Nursing assingment

ADVANCED PRACTICE

NURSING in the Care of Older Adults

SECOND EDITION

ADVANCED PRACTICE

NURSING in the Care of Older Adults SECOND EDITION

Laurie Kennedy-Malone , PhD, GNP-BC, FAANP, FGSA Professor of Nursing, School of Nursing

University of North Carolina at Greensboro

Greensboro, North Carolina

Lori Martin-Plank , PhD, FNP-BC, NP-C, GNP-BC, FAANP Clinical Associate Professor, College of Nursing

University of Arizona

Tucson, Arizona

Evelyn Groenke Duffy , DNP, AGPCNP-BC, FAANP Associate Professor

Director of the Adult-Gerontology Primary Care Nurse Practitioner Program

Associate Director of the University Center on Aging and Health

Frances Payne Bolton School of Nursing

Case Western Reserve University

Cleveland, Ohio

F. A. Davis Company 1915 Arch Street Philadelphia, PA 19103 www.fadavis.com

Copyright © 2019 by F. A. Davis Company

Copyright © 2019 by F. A. Davis Company . All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher.

Printed in the United States of America

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Senior Acquisitions Editor: Susan R. Rhyner Manager of Project and eProject Management: Catherine H. Carroll Senior Content Project Manager: Christine Abshire Design and Illustration Manager: Carolyn O’Brien

As new scientifi c information becomes available through basic and clinical research, recommended treatments and drug therapies undergo changes. The author(s) and publisher have done everything possible to make this book accurate, up to date, and in accord with accepted standards at the time of publication. The author(s), editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of the book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised always to check product information (package inserts) for changes and new information regarding dose and contraindications before administering any drug. Caution is especially urged when using new or infrequently ordered drugs.

Library of Congress Cataloging-in-Publication Data

Names: Kennedy-Malone, Laurie, 1957- author. | Plank, Lori Martin, author. | Duffy, Evelyn Groenke, author. Title: Advanced practice nursing in the care of older adults [electronic resource] / Laurie Kennedy-Malone,

Lori Martin-Plank, Evelyn Groenke Duffy. Description: 2nd edition. | Philadelphia : F.A. Davis Company, [2019] | Includes bibliographical references

and index. Identifi ers: LCCN 2018038367 (print) | LCCN 2018039007 (ebook) | ISBN 9780803694798 |

ISBN 9780803666610 (pbk.) Subjects: | MESH: Geriatric Nursing—methods | Advanced Practice Nursing | Palliative Care |

Geriatric Assessment Classifi cation: LCC RC954 (ebook) | LCC RC954 (print) | NLM WY 152 | DDC 618.97/0231—dc23 LC record available at https://lccn.loc.gov/2018038367

Authorization to photocopy items for internal or personal use, or the internal or personal use of specifi c clients, is granted by F. A. Davis Company for users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided that the fee of $.25 per copy is paid directly to CCC, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that have been granted a photocopy license by CCC, a separate system of payment has been arranged. The fee code for users of the Transactional Reporting Service is: 978-0-8036-6661- 0/19 0  +  $.25.

I dedicate this book to my husband Chris and my son Brendan for their unwavering support during the writing of this book. To my parents, Nancy and Edward Kennedy, you continue to be models of successful aging that motivate me to continue to be passionate about advanced practice gerontological nursing. To graduates that I have worked with over the years, your continued dedication and expertise in working with older adults is appreciated and admired; thanks to those who also served as contributors to this edition.

—L.K.-M.

To my husband Rick and daughter Erin, thank you both for your patience and encouragement throughout the writing of this book. To my patients, who are also my teachers, thank you for entrusting your health to me; it has been my honor and privilege to serve you and to learn from you.

—L.M.-P.

To my husband Mark who supported me as I worked on this book in New Zealand, England, Italy, Ireland, Colorado—on every vacation we have taken. To my children Patrick, Colin, and Caitlin and my fabulous GNP daughter-in-law Kristen—you bless me every day. To my Aunt Karleen Groenke Sime who inspired me to become a nurse. To my father John and my in-laws Shirley and Art, who continue to live vital lives in their late 80s. Finally, to all my patients who challenge me to be the best provider I can be and my students who motivate me to constantly be better.

—E. G. D.

vii

Preface

With the continued rapid growth of the older adult popu- lation, there remains an increased demand for health-care providers to deliver age-specifi c care and direct disease man- agement. Advanced Practice Nursing in the Care of Older Adults will serve as a guide for advanced practice nurses who are privileged to provide care to older adults. Designed as a text for students, as well as a reliable source of evidence-based prac- tice for advanced practice nurses, this book contains informa- tion on healthy aging, comprehensive geriatric assessment, and common symptoms and illnesses that present in older adults. Given the complexity of prescribing for older adults taking multiple medications, a new chapter on polyphar- macy is included. The book concludes with a chapter on care delivery for patients with chronic illnesses who face end-of- life care.

Throughout the book, case studies are included to provide further practice and review. An important feature of this book is the use of the Strength of Recommendation Taxon- omy (SORT) [Ebell, M. H., Siwek, J., Weiss, B. D., Woolf, S. H., Susman, J., Ewigman, B., & Bowman, M. (2004). Strength of recommendation taxonomy (SORT): A patient-centered approach to grading evidence in medical literature American Family Physician, 69 (3), 548–556], which provides a direct reference to evidence-based practice recommendations for clinicians to consider in the care of older adults.

In Unit I, “The Healthy Older Adult,” the fi rst chapter, “Changes with Aging,” addresses the normal changes of aging, expected laboratory values in older adults, presen- tation of illness, atypical disease presentation, bimodal conditions, and the impact of chronic illness on functional capacity. In the second chapter, “Health Promotion,” updated information pertaining to health promotion and disease pre- vention strategies for older adults from Healthy People 2020 and the U.S. Preventive Services Task Force (USPSTF) is pro- vided, including an immunization schedule and information on the Welcome to Medicare Visit. Also covered is an over- view of physical activity, sexual behavior, dental health, and substance use, as well as a section pertaining to the older traveler. Recommendations for exercise and safe physical activity are provided in this unit.

Unit II, “Assessment,” opens with a detailed chapter on comprehensive geriatric assessment. Information on phys- ical, functional, and psychological health is delineated, and information on quality of life measures is included. Next is the fi fth chapter, “Symptoms and Syndromes,” which pro- vides the clinician with a concise description of more than 20 symptoms prevalent in older adults. A rapid reference detail- ing common contributing factors and associated symptoms and clinical signs that should be worked up for each present- ing condition is included. Recommendations for diagnostic

tests with accompanying results are used to form a differen- tial diagnosis.

Unit III, “Treating Disorders,” provides 11 chapters of concise, updated information pertaining to disease manage- ment of illnesses common in older adults, presented by body systems. Each chapter opens with an assessment section that provides the reader with a focused review of systems and the physical examinations needed to obtain pertinent informa- tion for diagnosis and treatment of the older adult. Signal symptoms indicating atypical presentation of illness are highlighted at the beginning of each condition. The discus- sion of each problem and disorder follows a consistent mono- graph format:

■ Signal symptoms ■ Description ■ Etiology ■ Occurrence ■ Age ■ Ethnicity ■ Gender ■ Contributing factors ■ Signs and symptoms ■ Diagnostic tests ■ Differential diagnosis ■ Treatment ■ Follow-up ■ Sequelae ■ Prevention/prophylaxis ■ Referral ■ Education

Unit IV, “Complex Illness,” addresses complex manage- ment of patients requiring chronic illness management, pal- liative care, and supportive care at end of life, and includes a new chapter on polypharmacy. The text concludes with two appendices—“Physiological Infl uences of the Aging Process” and “Laboratory Values in the Older Adult”—both of which are ready references for the busy practitioner.

In addition to the content of the book, a Bonus Chapter, Nutritional Support in the Older Adult, selected Refer- ences, and other online resources to aid the user in practice and review of the key concepts are available at Davis Plus . Case studies are provided to support critical thinking and are available for users to complete on their own or for edu- cators to incorporate into their course requirements. To enhance the delivery of competency-based education, the case studies were mapped to the Adult-Gerontology Primary Care Nurse Practitioner Competencies (2016).

For the faculty, there are PowerPoint presentations and a well-developed test bank located on Davis Plus . The

viii Preface

Active Classroom Instructors’ Guide is an online faculty resource that maps the resources available with the text and includes lecture notes and additional case studies.

This book is written by and for advanced practice nurses involved in the care of older adults across multiple settings of care. While intended as a guide for the management of care for older adults, clinicians are encouraged to deliver individ- ualized, patient-centered care considering the latest clinical

practice guidelines on prevention and management of condi- tions common in older adults.

REFERENCE National Organization of Nurse Practitioner Faculties . ( 2016 ). Adult-

Gerontology Acute Care and Primary Care Nurse Practitioner com- petencies . Retrieved from http://c.ymcdn.com/sites/www.nonpf.org/ resource/resmgr/competencies/NP_Adult_Geri_competencies_4.pdf .

ix

Contributors

Sue A. Anderson, PhD, RN, FNP-BC Associate Professor, Family Nurse Practitioner

Program Coordinator Saint Mary ’ s College Notre Dame, Indiana

Epistaxis; Rhinitis; Asthma

Louann Bailey, CRNP Nurse Practitioner Inpatient Medical Services Akron, Ohio

Chest Pain

Tracy Ballard, MSN, GNP-BC Nurse Practitioner Optum Greensboro, North Carolina

Gastroenteritis

Judith A. Berg, PhD, RN, WHNP-BC, FAANP, FNAP, FAAN

Clinical Professor The University of Arizona College of Nursing San Diego, California

Atrophic Vaginitis; Breast Cancer

Sharon Biby, MSN, APRN, ANVP-BC, AGPCNP-BC Nurse Practitioner, Advanced-Practice Stroke Nurse Cone Health Greensboro, North Carolina

Stroke

Anna Wentz Boone, PhD, ANP-BC Adult Nurse Practitioner Rockingham Gastroenterology, Cone Health Medical

Group Reidsville, North Carolina

C. Diffi cile ; Cholecystitis; Peptic Ulcer Disease; Gastritis

Angela Brown, DNP, FNP-BC, ANP-BC, CDE Clinical Assistant Professor, Family Nurse Practitioner University of Arizona Tucson, Arizona

Cellulitis; Hearing Loss

Lisa Byrd, PhD, FNP, GNP, FAANP Practice Administrator Florida Health Care Plans Nurse Practitioner, Assistant Professor University of South Alabama Lake Mary, Florida

Bowel Incontinence; Diarrhea; Fatigue; Urinary Incontinence; Wandering

Carol Calianno, RN, MSN, CWOCN, CRNP Nurse Practitioner – Dermatology and Wound Ostomy

Continence Specialist Philadelphia VA Medical Center Philadelphia, Pennsylvania

Skin Cancer

Christina Coletta-Hansen, MSN, ANP-BC, ACHPN Palliative Care Nurse Practitioner Einstein Medical Center Montgomery Norristown, Pennsylvania

Palliative and End of Life Care

Kristin R. Curcio, DNP, AGPCNP-BC, AOCNP Nurse Practitioner Cone Health Cancer Center at Wesley Long Greensboro, North Carolina

Lung Cancer; Bladder Cancer; Liver Cancer; Brain Tumor; Pancreatic Cancer

Nancy Dirubbo, DNP, FNP-BC, FAANP, Certifi cate in Travel Health

Director Travel Health of New Hamsphire, PLLC Laconia, New Hampshire

Travel and Leisure

Brenda L. Douglass, DNP, APRN, FNP-BC, CDE, CTTS

DNP Program Director, Assistant Clinical Professor, Family Nurse Practitioner

Drexel University Philadelphia, Pennsylvania

Chronic Obstructive Pulmonary Disease

x Contributors

Janet DuBois, DNP, APRN, FNP-BC, FAANP, FNAP Associate Professor Loyola University New Orleans New Orleans, Louisiana

Pneumonia; Upper Respiratory Tract Infection

Kristen Tomblin Duffy, CRNP Nurse Practitioner Lehigh Valley Health Network Allentown, Pennsylvania

Dysphagia; Hematuria

Renee E. Edkins, DNP, ANP-C, Fellow, American Society of Lasers in Medicine & Surgery

Director Laser Surgery Program, UNC Division of Plastic & Reconstructive Surgery, Medical Laser Safety Offi cer

University of North Carolina, Department of Surgery Chapel Hill, North Carolina

Burns

Vaunette P. Fay, PhD, RNC, FNP, GNP Director, Continuing Education; Lead Nurse Planner;

Professor of Nursing The University of Texas Health Science Center at

Houston, Cizik School of Nursing Houston, Texas

Dehydration; Pruritus

Carrie Fernald, DNP, AGPCNP-BC Nurse Practitioner PACE of Triad Greensboro, North Carolina

Joint Pain; Osteoarthritis

Diana Filipek-Oberg, RN, BSN, MSN, AGACNP-BC Surgery APN Cooper University Hospital Camden, New Jersey Clinical Adjunct Faculty Drexel University Philadelphia, Pennsylvania

Chapter 7 Case Study; Assessment of the Respiratory System; Chapter 8 Case Study

Nancy A. Fisher, RN, MSN, GNP-BC Nurse Practitioner, Rheumatology Cleveland Department of Veterans Affairs Cleveland, Ohio

Gout; Rheumatoid Arthritis

Debra A. Friedrich, DNP, FNP-BC, CLS, BC-ADM, FNLA, FAANP

Diplomate, Accreditation Council for Clinical Lipidology

Assistant Professor University of South Florida College of Nursing Tampa, Florida

Hyperlipidemia

Cynthia Gerstenlauer, ANP-BC, GCNS-BC, CDE, CCD

Nurse Practitioner Troy Internal Medicine Troy, Michigan

Osteoporosis

Larry Ryan Gibson, MSN, AGNP-C Nurse Practitioner Alliance Urology Specialists Greensboro, North Carolina

Cystitis

Eric Gill, DNP, AGNP-C Nurse Practitioner Rockingham Gastroenterology Cone Health Medical

Group Reidsville, North Carolina

Cirrohsis; Esophagitis; Gastroesophageal Refl ux Disease; Irritable Bowel Syndrome; Acute Pancreatitis; Chronic Pancreatitis

Mary Jane Griffi th, RN, MSN, GNP-BC, ACHPN Nurse Practitioner LTC Health Solutions Columbia, South Carolina

Palliative and End of Life Care

Mary Guhwe, DNP, FNP-BC, SCRN Nurse Practitioner Duke University Hospital Durham, North Carolina

Dizziness

Candace Currie Harrington, PhD, DNP, APRN, AGPCNP-BC, CDP

Clinical Professor East Carolina University Greenville, North Carolina

Heart Failure

Melodee Harris, PhD, APRN, GNP-BC, AGPCNP-BC Assistant Professor University of Arkansas for Medical Sciences College of

Nursing Little Rock, Arkansas

Delirium; Dementia

Contributors xi

Theresa C. Hollander, CRNP Nurse Practitioner Jefferson Health Abington, Pennsylvania

Ischemic Heart Disease

Shelly Jesberger, MSN Nurse Practitioner Veterans Health Administration Cleveland, Ohio

Hemoptysis

Carol G. Kelley, PhD, AGPCNP-BC Associate Professor Frances Payne Bolton School of Nursing, Case

Western Reserve University Cleveland, Ohio

Falls

Nanette LaVoie-Vaughan, ANP-C, DNP Nurse Practitioner Geriatric Neuropsychiatry Services Raleigh, North Carolina

Agitation; Constipation; Failure to Thrive

Sheree L. Loftus, PhD, MSN, APRN-BC Nurse Scientist Mount Sinai Union Square New York, New York Investigator CHEAR Center Bronx, New York

Parkinson ’ s Disease; Restless Legs Syndrome

William J. Lorman, JD, PhD, MSN, PMHNP-BC, CARN-AP

Vice President & Chief Clinical Offi cer Livengrin Foundation Bensalem, Pennsylvania

Alcohol Abuse; Prescription Drug Abuse

Denise Lucas, PhD, FNP-BC, CRNP, FAANP Chair, Advance Practice Programs Duquesne University Pittsburgh, Pennsylvania

Benign Prostatic Hyperplasia; Drug-Induced Impotence; Prostate Cancer; Prostatitis

Rhonda W. Lucas, MSN, AGNPC House Calls Provider Optum United Healthcare Reidsville, North Carolina

Herpes Zoster

Donna Behler McArthur, PhD, FNP-BC, FAANP, FNAP

Adjunct Clinical Professor Vanderbilt University School of Nursing University of Arizona College of Nursing &

Department of Neurology, College of Medicine Tuscon, Arizona

Headache; Seizure Disorders

Sincere McMillan, ANP-BC Nurse Practitioner Memorial Sloan Kettering Cancer Center New York, New York

Colorectal Cancer

Laurie Lovejoy McNichol, MSN, RN, CNS, GNP, CWOCN, CWON-AP, FAAN

Clinical Nurse Specialist, WOC Nurse Cone Health Greensboro, North Carolina

Pressure Injuries

Jennifer Mondillo, MSN, MBA, CRNP Clinical Instructor Villanova University Villanova, Pennsylvania

Assessment of the Cardiovascular System

LaTroy Navaroli, DNP, FNP-BC, CWS Nurse Practitioner Would Specialist Navaroli Medical Warren, Pennsylvania

Oral Nutritional Supplementation

D. Che Navey, A-GNP, MSN, RN Neurohospitalist, Advanced Practice Clinician Novant Health Presbyterian Medical Center Charlotte, North Carolina

Tremor

Olivia Faith Ogburn, AGPCNP Nurse Practitioner Gastroenterology Oncology Clinic Wake Forest Baptist Medical Center Winston Salem, North Carolina

Gastric Cancer

Loretta Phillips, RN, NP-C, APRN, BC Nurse Practitioner Capital Nephrology Associates Raleigh, North Carolina

Acute Kidney Injury; Chronic Kidney Disease

xii Contributors

Sabrina Pickens, PhD, RN, ANP-BC, GNP-BC Assistant Professor – Tenure Track, Faculty University of Texas Health Science Center at Houston

Cizik School of Nursing Houston, Texas

Elder Abuse

Allen V. Prettyman, PhD, FNP-BC, FAANP Associate Professor – College of Nursing University of Arizona Tucson, Arizona

Pulmonary Tuberculosis

Catherine R. Ratliff, PhD, GNP-BC, CWOCN, CFN Nurse Practitioner/Clinical Associate Professor, School

of Nursing University of Virginia Health System Charlottesville, Virgina

Peripheral Vascular Disorders

Barbara Reall, MBA, MSN, CRNP Senior Clinical Services Manager Optum Horsham, Pennsylvania

Hypertension

Luann Richardson, PhD, DNP Associate Professor Robert Morris University Moon Township, Pennsylvania

Anxiety; Bipolar Disorder

Lauren Robbins, DNP, APRN, GNP-BC Nurse Practitioner Atlanta VA Healthcare System Decatur, Georgia

Bowel Obstruction

Mary Ellen E. Roberts, DNP, APN-c, FNAP, FAANP, FAAN

Director – Doctor of Nursing Practice Program Seton Hall University South Orange, New Jersey

Cardiac Arrhythmias; Myocardial Infarction

Barbara Rogers, CRNP, MN, AOCN, ANP-BC Nurse Practitioner Fox Chase Cancer Center Philadelphia, Pennsylvania

Leukemias

Susan D. Ruppert, PhD, RN, FNP-C, ANP-BC, FNAP, FCCM, FAANP, FAAN

Professor, Associate Dean of Graduate Studies Cizik School of Nursing at The University of Texas

Health Science Center at Houston Houston, Texas

Anemia of Chronic Disease; Anemia; Iron Defi ciency

Valerie K. Sabol, PhD, ACNP-BC, GNP-BC, ANEF, FAANP

Professor and Division Chair, Healthcare in Adult Populations

Duke University School of Nursing Adult Acute Care & Gerontology Nurse Practitioner Department of Medicine, Division of Endocrinology,

Metabolism and Nutrition Duke University Medical Center Durham, North Carolina

Obesity

Susan Kate Sandstrom, MSN, APRN-BC, ADCN Nurse Practitioner University Hospitals, Seidman Cancer Center Cleveland, Ohio

Oral Cancer

Jennifer Serafi n, RN, BSN, MS, GNP-BC Nurse Practitioner Kaiser Permanente South San Francisco, California

Endometrial Cancer; Ovarian Cancer

Terri Setzer, NP-C Nurse Practitioner Reidsville Clinic for GI Diseases, Cone Health Medical

Group Reidsville, North Carolina

Nonalcoholic Fatty Liver Disease

Kate Sheppard, PhD, RN, FNP, PMHNP-BC, FAAN, FAANP

Clinical Associate Professor, Retired PMHNP Specialty Coordinator University of Arizona, College of Nursing Tucson, Arizona

Depression

Tracey Sherrod, MSN, ANP-C, GNP BC Adult and Gerontological Nurse Practitioner Vidant Healthplex Wilson, North Carolina

Nephrolithiasis

Contributors xiii

Carroll M. Spinks, GNP-BC Nurse Practitioner Triad HealthCare Network Greensboro, North Carolina

Corns and Calluses

David V. Strider, DNP, MSB, APRN, CCRN, ACNP-BC Nurse Practitioner, Clinical Assistant Professor of

Nursing University of Virginia School of Nursing Charlottesville, Virginia

Peripheral Vascular Disorders

Ladsine Taylor, MSN, GNP-BC Gerontology Nurse Practitioner Bill Hefner VA Medical Center Community Living

Center Salisbury, North Carolina

Peripheral Neuropathy

Barbara A. Todd, DNP, CRNP, FAANP, FAAN Director, Graduate Nurse Education Demonstration Hospital University of Pennsylvania Philadelphia, Pennsylvania

Valvular Heart Disease

Renee Walters, PhD, RN, CCRN, FNP-BC Clinical Operations Manager, Clinical Associate

Professor Boise State University Boise, Idaho

Restrictive Lung Disease; Immune Thrombocytopenic Purpura

Jennifer L. Warren, MSN, NP-C Nurse Practitioner Anticoagulation Clinic Wake Forest Baptist Health High Point, North Carolina

Pulmonary Embolism

Tomika Williams, PhD, AGPCNP-C Assistant Professor of Nursing East Carolina University Greenville, North Carolina

Malnutrition

Colleen Wojciechowski, MSN, GNP-BC Nurse Practitioner, Retired Veteran Administration Durham Health Care System Cary, North Carolina

Cough

M. Catherine Wollman, DNP, GNP-BC, CRNP Consultant Ponte Vedra, Florida

Chronic Illness and the APRN

xv

Reviewers

Wendy Biddle, CFNP Program Director MSN-FP program South University Savannah, Georgia

Joan Blum, MSN, APRN Assistant Professor Clarkson College Omaha, Nebraska

Sharon Chalmers, PhD, CNE, APRN, FNP-BC Professor of Nursing University of North Georgia Dahlonega, Georgia

Claudia M. Chaperon, PhD, RN, APRN, BC Associate Professor College of Nursing University of Nebraska Medical Center Omaha, Nebraska

Valerie Flattes, APRN, MS, ANP-BC Assistant Professor University of Utah Salt Lake City, Utah

Stacy Harris, DNP, APRN Graduate Program Coordinator, Assistant Professor University of Central Arkansas Conway, Arkansas

Ann McDonald, DNP, MSN Assistant Professor Western Carolina University Cullowhee, North Carolina

Clarice Wasmuth, MSN, NP Professor Georgia State University Atlanta, Georgia

xvii

Acknowledgments

The second edition of this book would not be a reality if not for the kind assistance and guidance of some wonderful people whom we would like to thank. To Susan R. Rhyner, our Senior Acquisitions Editor, who believed in the timeli- ness of updating this edition given the impact that the APRN consensus model for advanced practice registered nurses has on nursing education and practice with the required inclu- sion of gerontology and geriatrics for all advanced practice nurses taking care of older adults. To Christine M. Abshire, our Senior Content Project Manager, who kept us on track and provided us order. To Teresa Wilson for your quick turn- around editing and to Sharon Y. Lee, Daniel Domzalski, and

crew for carrying us over the fi nish line, without which we would not have completed the charge. To Ashleigh Lucas, Amy Daniels, and Tyesha Harvey who assisted in informa- tion retrieval, thanks for your timely research. We are most appreciative to our dedicated contributors who believe in the importance of creating a reference specifi c to the care of older adults written by advanced practice registered nurses. We also would like to acknowledge those who have contributed to our previous books. We especially want to thank Kathleen Ryan Fletcher for being a part of the journey over the past 20 years; your expertise and dedication to advanced practice gerontological nursing will not be forgotten.

xix

Contents in Brief

Unit I The Healthy Older Adult 1 1 Changes With Aging 2

2 Health Promotion 6

3 Exercise in Older Adults 19

Unit II Assessment 25 4 Comprehensive Geriatric

Assessment 26

5 Symptoms and Syndromes 34

Unit III Treating Disorders 95 6 Skin and Lymphatic Disorders 96

7 Head, Neck, and Face Disorders 127

8 Chest Disorders 152

9 Peripheral Vascular Disorders 215

10 Abdominal Disorders 225

11 Urological and Gynecological Disorders 280

12 Musculoskeletal Disorders 305

13 Central and Peripheral Nervous System Disorders 328

14 Endocrine, Metabolic, and Nutritional Disorders 361

15 Hematological and Immune System Disorders 407

16 Psychosocial Disorders 428

Unit IV Complex Illness 469 17 Polypharmacy 470

18 Chronic Illness and the APRN 474

19 Palliative Care and End-of-Life Care 485

appendix A Physiological Infl uences of the Aging Process 499

appendix B Laboratory Values in the Older Adult 505

Index 507

xxi

Unit I The Healthy Older Adult 1 CHAPTER 1 Changes With Aging 2

Fundamental Considerations 2

Physiological Changes With Aging 2

Laboratory Values in Older Adults 3

Presenting Features of Illness/Disease in the Older

Adult 3

Chronic Illness and Functional Capacity 5

Summary 5

CHAPTER 2 Health Promotion 6 Primary, Secondary, and Tertiary Prevention 7

Healthy Lifestyle Counseling 7

Screening and Prevention 9

Immunizations 12

Travel and Leisure 12

Summary 17

Case Study 17

CHAPTER 3 Exercise in Older Adults 19 Available Resources 19

Barriers and Facilitators to Exercise for Older

Adults 20

Plan for Incorporating Exercise into Patient

Encounter 20

Key Guidelines for Safe Physical Activity (Physical

Activity Guidelines Advisory Committee,

2008) 21

Summary 22

Case Study 23

Unit II Assessment 25 CHAPTER 4 Comprehensive Geriatric

Assessment 26 Physical Health 26

Functional Health 30

Psychological Health 31

Socioenvironmental Supports 32

Quality of Life Measures 32

Summary 32

CHAPTER 5 Symptoms and Syndromes 34

Assessment 34

Bowel Incontinence 34

Chest Pain 38

Constipation 41

Cough 43

Dehydration 46

Diarrhea 47

Dizziness 51

Dysphagia 53

Falls 55

Fatigue 57

Headache 59

Hematuria 63

Hemoptysis 65

Involuntary Weight Loss 67

Joint Pain 72

Peripheral Edema 74

Pruritus 77

Syncope 78

Tremor 81

Urinary Incontinence 83

Wandering 88

Case Study 90

Unit III Treating Disorders 95 CHAPTER 6 Skin and Lymphatic

Disorders 96 Assessment 96

Burns 97

Cellulitis 103

Corns and Calluses 104

xxii Contents

Herpes Zoster 106

Pressure Injuries 109

Psoriasis 113

Skin Cancer 117

Superfi cial Fungal Infections 120

Case Study 125

CHAPTER 7 Head, Neck, and Face Disorders 127

Assessment 127

Cataract 128

Epistaxis 130

Glaucoma, Acute and Chronic 132

Glaucoma, Acute (Primary Angle-Closure) 132

Glaucoma, Chronic (Primary Open-Angle) 133

Hearing Loss 136

Hordeolum and Chalazion 138

Age-Related Macular Degeneration 139

Oral Cancer 141

Retinopathy 144

Rhinitis 146

Case Study 150

CHAPTER 8 Chest Disorders 152 Assessment of the Cardiovascular System 152

Assessment of Risk Factors for Coronary Artery

Disease 152

Clinical Examination Features 153

Assessment of the Respiratory System 154

Asthma 155

Cardiac Arrhythmias 160

Chronic Obstructive Pulmonary Disease 164

Heart Failure 170

Hypertension 175

Ischemic Heart Disease 179

Lung Cancer 185

Myocardial Infarction 187

Pneumonia 191

Pulmonary Embolism 196

Pulmonary Tuberculosis 199

Restrictive Lung Disease 203

Upper Respiratory Tract Infection 205

Valvular Heart Disease 207

Case Study 211

CHAPTER 9 Peripheral Vascular Disorders 215

Assessment 215

Abdominal Aortic Aneurysm 216

Chronic Lymphedema 218

Peripheral Vascular Disease 219

Venous Disease (Chronic Venous Insuffi ciency) 221

Case Study 223

CHAPTER 10 Abdominal Disorders 225 Assessment 225

Acute Kidney Injury 226

Bladder Cancer 230

Bowel Obstruction 231

Cholecystitis 233

Chronic Kidney Disease 235

Cirrhosis of the Liver 239

Clostridium diffi cile 242

Colorectal Cancer 245

Diverticulitis 249

Esophagitis 251

Gastric Cancer 253

Gastritis 256

Gastroenteritis 258

Gastroesophageal Refl ux Disease 260

Hernia 263

Irritable Bowel Syndrome 265

Liver Cancer 268

Nephrolithiasis 270

Nonalcoholic Fatty Liver Disease 272

Peptic Ulcer Disease 274

Case Study 276

CHAPTER 11 Urological and Gynecological Disorders 280

Assessment 280

Atrophic Vaginitis 282

Breast Cancer 284

Cystitis 289

Endometrial Cancer 292

Ovarian Cancer 293

Benign Prostatic Hyperplasia (Benign Prostatic

Hypertrophy) 295

Drug-Induced Erectile Dysfunction 297

Prostate Cancer 299

Prostatitis 301

Case Study 303

CHAPTER 12 Musculoskeletal Disorders 305

Assessment 305

Bursitis, Tendinitis, Soft Tissue

Syndromes 307

Fractures 310

Gout 312

Contents xxiii

Osteoarthritis 315

Polymyalgia Rheumatica 319

Rheumatoid Arthritis 322

Case Study 325

CHAPTER 13 Central and Peripheral Nervous System Disorders 328

Assessment 328

Brain Tumor 331

Parkinson’s Disease 333

Peripheral Neuropathy 336

Restless Legs Syndrome 344

Seizure Disorders 346

Stroke 352

Case Study 359

CHAPTER 14 Endocrine, Metabolic, and Nutritional Disorders 361

Assessment 361

Acute Pancreatitis 362

Chronic Pancreatitis 366

Diabetes Mellitus, Types 1 and 2 369

Failure to Thrive 377

Hyperlipidemia 379

Hyperthyroidism 384

Hypothyroidism 387

Malnutrition 389

Obesity 392

Osteoporosis 396

Pancreatic Cancer 402

Case Study 404

CHAPTER 15 Hematological and Immune System Disorders 407

Assessment 407

Anemia of Chronic Disease 408

Anemia, Iron Defi ciency 410

Immune Thrombocytopenic Purpura (Idiopathic

Thrombocytopenic Purpura) 413

Leukemias 414

Acute Lymphoblastic Leukemia 414

Acute Myeloid Leukemia 416

Chronic Lymphocytic Leukemia 419

Chronic Myeloid Leukemia 423

Case Study 426

CHAPTER 16 Psychosocial Disorders 428 Assessment 428

Agitation 429

Alcohol Misuse (Hazardous or Risky Drinkers) 431

Anxiety 434

Bipolar Disorder 436

Delirium 439

Dementia 443

Depression 451

Elder Abuse 456

Grief and Bereavement 459

Insomnia 461

Prescription Drug Misuse (Hazardous or Risky

Users) 463

Case Study 466

Unit IV Complex Illness 469 CHAPTER 17 Polypharmacy 470

Pharmacokinetic/Pharmacodynamic Changes 470

Tools to Assist Providers to Avoid PIMs and

Polypharmacy 472

Preventing Polypharmacy, Addressing

Polypharmacy 472

CHAPTER 18 Chronic Illness and the APRN 474

Defi nitions of Chronic Disease and Chronic

Illness 474

Demographics of Chronic Illness 474

Multiple Chronic Conditions 475

Economic Burden of Chronic Disease 477

Minorities and Chronic Disease 478

Function and Frailty 478

Evidence-Based Practice and Chronic Disease 479

Chronic Care Model of Quality Improvement 479

Legislation and Chronic Disease 480

Transitions of Care 480

Provider Reimbursement for Chronic Illness

Care 482

The Role of APRNs in Chronic Disease 482

Case Study 483

CHAPTER 19 Palliative Care and End-of-Life Care 485

Overview of Palliative Care 485

Symptom Management 486

Delirium 486

Dyspnea 488

Pain 490

The Dying Patient 493

Grief and Bereavement 496

Case Study 497

xxiv Contents

appendix A Physiological Infl uences of the Aging Process 499

appendix B Laboratory Values in the Older Adult 505

Index 507

unit I The Healthy Older Adult

2

CHAPTER 1 Changes With Aging

Laurie Kennedy-Malone

FUNDAMENTAL CONSIDERATIONS

The aged population continues to be incredibly diverse; it includes some individuals who are nearly twice as old as others and is refl ective of growing cultural diversity as well. Knowing what is expected in aging, what diseases are prev- alent in aging, and what constitutes successful aging is an immense challenge even for the most skillful advanced clini- cian. When assessing the aged individual, the advanced prac- tice nurse should be familiar with the range of normal and expected changes associated with aging so that older persons falling outside this range may be identifi ed and interventions taken appropriately and expeditiously.

In the past, wellness was considered the mere absence of disease, but with more information from longitudinal studies of aging, we are learning a great deal about the charac- teristics of successful physiological and psychosocial agers (O’Brien et al., 2009). A profi le of what constitutes suc- cessful aging is beginning to emerge, and the illness–health continuum continues to expand to include adults living into old age. This chapter focuses on familiarizing the advanced practice nurse with fundamental underpinnings that serve to guide the approach to assessment and management of the older adult. In addition to appreciating the physiological changes that come with aging, the advanced practice nurse needs to understand how aging changes infl uence reference laboratory values. Recognizing that presenting features of disease/illness may be different and having a greater aware- ness of the impact of chronic illness on functional capacity and quality of life provide the advanced practice nurse with a perspective in approaching the older adult that is different from that of younger adults.

PHYSIOLOGICAL CHANGES WITH AGING

The physiological changes associated with the usual aging process have been detailed by system, and the impact of these changes has been described. (These can be found in Appendix

A.) Although Appendix A uses a single-system approach, the clinician must be aware that all the systems interact and, in doing so, can increase the older person ’ s vulnerability to illness/disease. For example, the risk of respiratory infection in the geriatric population is considerable, and the physiolog- ical infl uences may include limited chest wall expansion, cilia atrophy, and alterations in the immune system. During the clinical decision-making process, the clinician knowledgeable about physiological changes with aging will be less likely to undertreat a treatable condition. For example, the astute cli- nician will use the diagnostic process to differentiate the more benign seborrheic keratosis from the more serious melanoma in the aged individual. While educating the older patient, the informed professional will be less likely to attribute a fi nding to the aging process alone. When clinicians associate fi ndings to aging alone, the older person may conclude that there is no point in changing behavior because the process is inevita- ble. Additionally, the clinician may take a fatalistic approach and undertreat common conditions such as heart failure and diabetes.

The major impact of these physiological changes can be highlighted with four primary points. First, there is a reduced physiological reserve of most body systems, particularly cardiac, respiratory, and renal. Second, there are reduced homeostatic mechanisms that fail to adjust regulatory systems such as temperature control and fl uid and electro- lyte balance. Third, there are the changes in the sympathetic response, which contribute to orthostasis and falls, as well as lack of hypoglycemic response. Fourth, there is impaired immunological function: infection risk is greater and auto- immune diseases are more prevalent. The clinician is advised not to be complacent in that some processes previously con- sidered normal, age-related changes are now being refuted. Historically, normal aging studies were conducted using a cross-sectional study method. Today, results are becoming increasingly available from longitudinal studies of aged pop- ulations, some of which began in the 1930s (Besdine, 2016; O’Brien et al., 2009).

This more reliable methodology provides some challenges to previously held conclusions. The clinician is encouraged to stay informed regarding the research in expected and successful aging so that this information may be carefully

Chapter 1 ■ Changes With Aging 3

considered, interpreted, and translated quickly into the clin- ical setting.

LABORATORY VALUES IN OLDER ADULTS

Healthy individuals of all ages often have asymmetrical dis- tribution of test results. Normality in a statistical sense may be extrapolated incorrectly to normality in terms of health. In addition, the standards previously available to the health- care worker with which to compare normal laboratory values have been based on randomly collected samples of younger healthy adults. Many factors can infl uence laboratory value interpretation in the older adult, including the physiolog- ical changes with aging, the prevalence of chronic disease, changes in nutritional and fl uid intake, lifestyle (including activity), and the medications taken (Dharmarajan & Pitchu- moni, 2012).

Clinicians may fi nd that reference ranges, therefore, may be preferable. Reference ranges or intervals, such as age, sex, or race, can be defi ned demographically. For example, the ref- erence range for older adults might be the intervals within which 95% of persons over age 70 fall. These may be further defi ned physiologically (e.g., fasting or activity status) or phar- macologically (e.g., medication, tobacco or alcohol use). Even this more precise method does not ensure a healthy sampled population as the standard, and using the reference range method may not differentiate normal aging from disease. The reference values presented for the older adult cohort (see Appendix B) are not necessarily desirable ones. Longitudinal chemical studies support the concept of biochemical indi- viduality; that is, each individual ’ s variation is often much smaller than that of the larger group. Biochemical individ- uality is of particular importance in detecting asymptomatic abnormalities in older adults. Signifi cant homeostatic dis- turbances in the same individual may be detected through serial laboratory tests, even though all individual test results may lie within normal limits of the reference interval for the entire group.

The clinician must determine whether a value obtained refl ects a normal aging change, a disease, or the potential for disease. Although abnormal laboratory fi ndings are often attributed to old age, rarely are they true aging changes. Mis- interpretation of an abnormal laboratory value as an aging change can lead to underdiagnoses and undertreatment in some situations (e.g., anemia or urinary tract infection) and overdiagnosis and overtreatment in others (e.g., hypergly- cemia or asymptomatic bacteriuria). At times, the result of a laboratory value may be within the appropriate reference range, yet indicate pathology for the older adult (Dharmara- jan & Pitchumoni, 2012). The serum creatinine level may be within the normal range, yet indicate renal impairment in a patient with inadequate protein stores, and different mea- sures might need to be considered. One value of signifi cance to the practitioner with prescriptive privileges is the calcula- tion of creatinine clearance in the estimation of renal func- tion, for instance when dosing enoxaparin (Shaikh & Regal, 2017).

Reduced renal function, particularly the glomerular fi l- tration rate (GFR), affects the clearance of many drugs, and

creatinine clearance provides an index of renal function for use in choosing doses of renally eliminated or nephrotoxic drugs (such as digoxin, H 2 blockers, lithium, and water- soluble antibiotics). The Modifi cation of Diet in Renal Disease (MDRD) and Cockcroft-Gault equations both provide useful estimates of the GFR (Boparai & Korc-Grodzicki, 2011). The performance of these two formulas was compared in an older adult population, and the Cockcroft-Gault formula was found to be inferior to the MDRD equation; however, the MDRD equation is not as practical and is more complex to use (Fliser, 2008). The use of serum drug concentration measurements (where these are available) or timed urine specimens is rec- ommended until more acceptable methods of calculating renal function in this population become available.

Finally, when considering which laboratory tests to order, it is worth remembering the doctrine primum non nocere, to do no harm. Excessive blood sampling may lower the hema- tocrit; repeated fasting tests may provoke nutritional com- promise; and extensive use of tests often requires drugs that may cause adverse reactions. Any risks involved in laboratory testing must be considered with respect to the patient ’ s clin- ical condition and weighed against the test ’ s expected ben- efi ts. The clinician should plan in advance the use for each test result value obtained, especially for less specifi c or less sensitive tests such as sedimentation rate and serum alkaline phosphatase levels. “Ordering a test requires assessing the likelihood that a patient has specifi c conditions prior to the order, along with the accuracy of test and as to how it will change management” (Dharmarajan & Pitchumoni, 2012, p. 267). Once laboratory tests are available for review, test results should be discussed with the patients, with abnormal test results interpreted for the aging individual and addressed with the patient and/or caregivers. In addition to under- standing the fundamental changes that accompany aging and their infl uence on interpreting laboratory values and medication management, the advanced practice nurse needs to understand the presenting features of illness/disease in older adults (Dharmarajan & Pitchumoni, 2012).

PRESENTING FEATURES OF ILLNESS/DISEASE IN THE OLDER ADULT

The manifestations of illness and disease in the older adult can be very different, even if the underlying pathological process is the same as in younger individuals. The advanced practice nurse should be aware of what can infl uence the presentation. Underreporting of symptoms by older adults may occur if they attribute the new sign or symptom to age itself (Amella, 2004). By erroneously associating aging with disease, disuse, and disability, older adults perceive this change as inevitable and either fail to present to the health-care pro- vider or, if they do, fail to challenge the assumption that this represents normal aging. At times an acute symptom such as pain or dyspnea is superimposed on a chronic symptom, and the older adult may not recognize that it represents a new or exacerbated pathology (Bell et al., 2016). The advanced practice nurse is well advised to never attribute something to normal aging without doing a careful and methodical search for a treatable condition.

4 Chapter 1 ■ Changes With Aging

Certain diseases are more common in the older adult and an understanding of the epidemiology is critical in the inter- pretation. Certain neoplasms and malignancies such as basal cell carcinoma, chronic lymphocytic leukemia, and prostate cancer have a high prevalence beginning in older adulthood. Neurological conditions such as Parkinson ’ s disease, demen- tias, stroke, and complex partial seizures are more common to have initial onset in older age. Polymyalgia rheumatica along with giant cell arteritis almost exclusively begins in patients over the age of 50 (Besdine, 2016).

Complicating the care of older adults is when patients develop geriatric syndromes that often involve multiple body systems and have more than one underlying cause (Bell et al., 2016). For patients presenting with one or more of new geriatric giants: frailty, anorexia of aging, sarcopenia, and cognitive impairment, the risk escalates for falls, delirium, injuries, and depression, subsequently placing these patients at dangers for iatrogenic events that could lead to hospital- ization, institutionalization, and subsequently, death (Morley, 2017).

Altered Presentation of Illness Advanced practice nurses managing the care of older adults are challenged to recognize altered, atypical, vague, or even nonspecifi c signs and symptoms of common conditions in older adults (Auerhahn & Kennedy-Malone, 2010). It is well documented that disease progress may be different for the older adult, especially the frail older adult (Bell et al., 2016). The failure to develop an elevated temperature or fever with an underlying infectious process differs greatly from pre- sentation of illness in a younger patient. The patient with depression may not present with a dysphoric mood but rather agitation and psychotic features. The older adult may present with cardiac manifestations of undiagnosed thyroid disease (Amella, 2004). Additional illustrative examples include jaundice, which is suggestive of viral hepatitis in younger individuals but may represent gallbladder disease or a malig- nancy in the older adult, and delusions or hallucinations, which are suggestive of bipolar disorder in younger individ- uals but may represent dementia or medication side effects in the older adult (Williams, 2008).

Because the symptoms or signs of illness or disease may be vague and nonspecifi c, even a modest change in functional level or behavior should alert the clinician to carefully explore the potential for a treatable condition. Family members or caregivers may report that a patient may no longer be coop- erating or participating in individual care. Unusual changes such as these become red fl ags to the beginning of an atypi- cal presentation of illness. In many cases the progression of the condition is insidious, often presenting as a change in cognition or an alteration in functional status. Other signif- icant changes in patients with altered presentation of illness often include new onset of falls, weakness, fatigue, anorexia, and unexplained tachypnea (Auerhahn & Kennedy-Malone, 2010). Table 1-1 depicts common conditions that often have altered presentation of illness in older adults.

Bimodality of Age of Onset of Clinical Conditions Understanding of the epidemiology of clinical conditions includes having the knowledge of etiology of the disease,

Presentation of Illness in Older Adults

ILLNESS ATYPICAL PRESENTATIONS

Acute abdomen Absence of symptoms or vague symptoms

Acute confusion

Mild discomfort and constipation

Some tachypnea and possibly vague respiratory

symptoms

Appendicitis pain may begin in right lower

quadrant and become diffuse

Depression Anorexia, vague abdominal complaints, new

onset of constipation, insomnia, hyperactivity,

lack of sadness

Hyperthyroidism Hyperthyroidism presenting as “apathetic

thyrotoxicosis,” i.e., fatigue and weakness; weight

loss may result instead of weight gain; patients

report palpitations, tachycardia, new onset of

atrial fi brillation, and heart failure may occur

with undiagnosed hyperthyroidism

Hypothyroidism Hypothyroidism often presents with confusion

and agitation; new onset of anorexia, weight

loss, and arthralgias may occur

Malignancy New or worsening back pain secondary to

metastases from slow growing breast masses

Silent masses of the bowel

Myocardial

infarction (MI)

Absence of chest pain

Vague symptoms of fatigue, nausea, and a

decrease in functional and cognitive status;

classic presentations: dyspnea, epigastric

discomfort, weakness, vomiting; history of

previous cardiac failure

Higher prevalence in females versus males

Non-Q-wave MI

Overall infectious

diseases process

Absence of fever or low-grade fever

Malaise

Sepsis without usual leukocytosis and fever

Falls, anorexia, new onset of confusion and/or

alteration in change in mental status, decrease in

usual functional status

Peptic ulcer

disease

Absence of abdominal pain, dyspepsia, early

satiety

Painless, bloodless

New onset of confusion, unexplained

tachycardia, and/or hypotension

Pneumonia Absence of fever; mild coughing without

copious sputum, especially in dehydrated

patients; tachycardia and tachypnea; anorexia and

malaise are common; alteration in cognition.

Pulmonary edema Lack of paroxysmal nocturnal dyspnea or

coughing; insidious onset with changes in

function, food or fl uid intake, or confusion

Tuberculosis (TB) Atypical signs of TB in older adults include

hepatosplenomegaly, abnormalities in liver

function tests, and anemia

Urinary tract

infection

Absence of fever, worsening mental or

functional status, dizziness, anorexia, fatigue,

weakness

Source: Amella, E. J. (2004); Bell et al., 2016; Besdine (2016); Chmura & Chan (2006); Peters (2010); Rehman & Qazi (2013); Rowe & Juthani-Mehta, M. (2014); Van Duin (2011); Wester, Dunlop, Melby, Dahle, & Wyller (2013); Williams (2008).

TABLE 1-1

Chapter 1 ■ Changes With Aging 5

prevalence and incidence rates, risk factors, age of onset, and gender distribution. There are a number of conditions that are known or suggested to have a bimodal age of onset. In some conditions the difference is not only the decade(s) in life that the disease more likely presents but the dominance of the gender that the condition presents. Myasthenia gravis is one condition that tends to present initially in younger females, with a preponderance in older males (Alkhawajah & Oger, 2015).

Often the presentation of the same illness is different for older adults as compared to their younger counterparts. The onset of the condition may be acute versus progressive, with different symptomatology and clinical signs. For instance, in patients with late onset rheumatoid arthritis the joint involvement is more often in the larger joints such as the shoulder and they experience constitutional symptoms such as fever, malaise, weight loss, and depression (Evcik, 2013). Knowledge of the bimodality of age onset of certain disease conditions will aid the advanced practice nurse in avoiding misdiagnosis or delay in diagnosis due to lack of recognition. Table 1-2 describes medical conditions that present differ- ently in younger versus older adults.

CHRONIC ILLNESS AND FUNCTIONAL CAPACITY

Approximately 80% of those 65 or older have one chronic disease, and 50% have two or more. The most common of these are related to heart disease, arthritis, respiratory prob- lems, cancer, diabetes, and stroke (U.S. Department of Health

and Human Services [USDHHS], Centers for Disease Control and Prevention [CDC], 2010). Treating patients with multi- morbidities can be very complex and can result in polyphar- macy. Patients with multimorbidities are known to have a treatment burden in terms of understanding and self-care management of their conditions. This burden entails not only patients managing the conditions but attending multi- ple appointments and comprehending and affording complex drug regimens (Wallace et al., 2015).

These conditions often impair functional capacity and limit the person ’ s ability to perform activities of daily living (ADLs) such as bathing and dressing, and instrumental activ- ities of daily living (IADLs) such as managing medications and traveling. More than 25% of community-dwelling Medi- care benefi ciaries report diffi culties performing ADLs, and 14% report diffi culties performing IADLs (USDHHS, Admin- istration on Aging [AOA], 2010).

SUMMARY ■ Assessment and management of older adults is different from

that of younger adults, and it is of critical importance that the advanced practice nurse working with the older adult has the knowledge, skill, and ability to recognize these differences and take them into consideration. This chapter highlighted how the approach of the clinician might be different based on an understanding of the physiological changes of aging and the impact of these changes on medication management and lab- oratory interpretation; how the presenting features of disease and illness may be different in the older adult; and how the older adult are disproportionately affected with chronic disease and functional impairments.

Select Bimodal Presentations of Illness in Younger Adults versus Older Adults

TYPE OF CONDITION YOUNGER ADULTS OLDER ADULTS

Dermatological

Psoriasis

Late teens to 20s

Irregular course which tends to generalize

Hereditary factors

50s—males

60s—females

Sporadic onset

Gastrointestinal

Infl ammatory bowel disease

Ulcerative colitis (UC)

Crohn ’ s disease (CD)

20–40 years old

Right lower UC

Insidious onset

>60–75 years old a second peak occurs

More often older women

Proctitis

Left-sided UC

Higher rates of anemia

May present as chronic diarrhea

Fistula development

Increased cases of associated malnutrition

Extraintestinal manifestations including: arthritis spondylitis,

uveitis, and erythema nodosum

More comorbid conditions

May be confused with other forms of colitis

Malignancies

Hodgkin ’ s lymphoma

20–30 years old

Possible infectious etiology

>50 years old

Increased mortality

Neurodegenerative

Myasthenia gravis (MG)

Women 20–40 years old

More thymus abnormalities

Men—50–70 years old

Women—70 years old

Dysphonia

More frequent ocular form MG

Increased rate of AChR seropositivity

Source: Alkhawajah & Oger (2015); del Val (2011); Henseler & Christophers (1985); Louis & Dogu (2007); Montero-Odasso (2006); Shenoy, Maggioncalda, Malik, & Flowers (2011); Smith (2013); Smith, Kassab, Payne, & Beer (1993); Wester, Dunlop, Melby, Dahle, & Wyller (2013); Woon & Lim (2003); Živkovi ć , Clemens, & Lacomis (2012).

TABLE 1-2

6

CHAPTER 2 Health Promotion

Lori Martin-Plank

The concept of health promotion includes activities to which an individual is committed and performs proactively to further his or her health and well-being. This includes not only pre- ventive and health-protective measures but also actualization of one ’ s health potential. The broadest defi nition, identifi ed by the World Health Organization (WHO), includes healthy lifestyle promotion, creation of supportive environments for health, community action, redirection of health services, and healthy public policy formulation. According to the WHO, by 2050 the world population of those over 60 years old will be at 22%, nearly double what it was in 2015 (WHO, Aging Facts, 2015). In its Global Strategy and Action Plan for Ageing and Health, the WHO identifi es fi ve priorities for member coun- tries: 1) A commitment to healthy ageing; 2) synchronizing the needs of older persons and health systems; 3) designing age-friendly environments, 4) developing long-term care systems; and 5) research (WHO, 2017). Within the United States, there are several resources for healthy aging, includ- ing the Centers for Disease Control and Prevention (CDC) and Health Promotion Web site on Healthy Aging ( https://www. cdc.gov/aging/aginginfo/index.htm ) and the American Geri- atrics Society Health in Aging Web site geared to consumers ( http://www.americangeriatrics.org/public ).

These resources are available and contain measures that are within the scope of practice for the nurse practitioner (NP) to enhance the visibility of the role while advancing the needs of patients. NPs are in a unique and pivotal position to guide and encourage health-promotion programs and individ- ual efforts. From our nursing background, we bring a holis- tic orientation to health and wellness, as well as knowledge of developmental tasks and the wellness–illness continuum. Our advanced practice education helps us diagnose and treat patients in a way that supports their return to optimal level of function and/or maximizes their coping abilities within the limits of their existing function. This particular blend of NP competencies is especially valuable in working with older patients. Heterogeneity increases with aging, presenting the NP with the challenge of individualizing health-promotion recommendations for each patient. Most of the literature on older adult health is devoted to treatment of frail older adults, those with geriatric syndromes and dementia (Friedman, Shah, & Hall, 2015). There is a need to develop programs and measure outcomes in promoting health in older adults.

Because older adults have only recently begun to partici- pate in studies on health promotion (Bleijenberg et al., 2017) and because single-focused interventions for health promo- tion often do not “fi t” with the interrelatedness of older adult health-promotion challenges, clear age-specifi c preventive health guidelines for the older population are scarce. Many disorders in older adults encompass multiple risk factors that involve several systems and interventions to achieve out- comes. This presents a challenge when measuring and syn- thesizing evidence and reporting outcomes (AGS Guide to Multimorbidity, 2012). Medicare will only pay for A and B level recommendations that meet the U.S. Preventive Services Task Force (USPSTF) stringent evidence guidelines, leaving other benefi cial interventions without coverage. Another confounding factor is the way that outcomes for screening are measured in terms of years of life saved. For older adults, quality of life or functional life is a more realistic goal (Fried- man, Shah, & Hall, 2015).

The Healthy People 2020 program has also set specifi c objectives for prevention in older adults. These include increased use of the Welcome to Medicare visit, an increased percentage of older adults who are up to date on all preven- tive services, and decreased use of the emergency department for falls by older adults, among others. Because of the focus on chronic disease management and the complexities of mul- tiple comorbidities in older adults, many primary health-care providers are not oriented toward the potential of healthy aging and discount the importance of health promotion in this age group (Friedman et al., 2015).

Current life expectancy is 78.8 years (CDC, National Center for Health Statistics [NCHS], 2017), with many people living to 100 years and beyond. It behooves us to focus on preven- tion and health promotion in our older patients to maximize the quality of these years. A collaborative plan should include consideration of the patient ’ s health beliefs and goals, present and anticipated levels of function, risks and benefi ts of pro- posed interventions, and effectiveness of specifi c preventive interventions for older adults. The Welcome to Medicare visit provides a good opportunity to focus solely on preventive services and health promotion; this is followed by the Medi- care-supported annual prevention visit. Health-promotion activities should be incorporated into every patient encoun- ter, as opposed to being addressed selectively, and should be

Chapter 2 ■ Health Promotion 7

individualized to the patient. Recent efforts are being focused on partnering population-based, community-centered pro- grams with personal health initiatives in older adults to make interventions more available and more economical, and to increase socialization opportunities and harness the power of group support.

PRIMARY, SECONDARY, AND TERTIARY PREVENTION

Preventive services are typically divided into the categories of primary, secondary, and tertiary. Primary prevention refers to those activities undertaken to prevent the occurrence of a disease or adverse health condition, including mental health. Health counseling and immunization are examples of primary prevention.

Secondary prevention refers to those tasks directed toward detection of a disease or adverse health condition in an asymptomatic individual who has risk factors but no detectable disease. Screening tests are examples of secondary prevention. The screening test must detect the condition at a stage where it is treatable and a positive outcome is expected after treatment. Mammography for breast cancer screening is an example of secondary prevention.

Tertiary prevention refers to management of existing conditions to prevent disability and minimize complications, striving for optimal level of function and quality of life. Pul- monary rehabilitation for a chronic obstructive pulmonary disease (COPD) patient is an example of tertiary prevention.

HEALTHY LIFESTYLE COUNSELING

The Welcome to Medicare visit (Centers for Medicare and Medicaid, 2011) provides an ideal opportunity for healthy lifestyle counseling. In addition to a thorough history (including some risk assessment, physical activity, diet, and tobacco and alcohol use), home safety and depression assess- ment are included. The Medicare MedLearn network has a link to guide providers covering all areas ( www.cms.gov/ Outreach-and-Education/Medicare-Learning-Network-MLN/ M L N P r o d u c t s / d ow n l o a d s / / M P S _ Q R I _ I P P E 0 0 1 a . p d f ) . Healthy lifestyle counseling should be addressed at each visit, using brief motivational interviewing (Lee, Choi, Royce, Yum, & Chair, 2016; Moral et al., 2015; Purath, Keck, & Fitzgerald, 2014).

Physical Activity Older adults are the least active age group, although recent trends show an increase in physical activity in older adults. The American College of Sports Medicine and the American Heart Association issued updated recommendations for phys- ical activity in all adults, with additional recommendations tailored to adults over age 65 and adults aged 50 to 64 with chronic conditions that are clinically signifi cant or result in functional limitations (Nelson et al., 2007). Counseling on physical activity should include any type of activity that the patient is able and willing to do. The health benefi ts of regular physical activity are well documented and include

fl exibility, increased muscle mass, maintenance of desirable weight, decreased insulin resistance, decreased peripheral vascular resistance, lower blood pressure, and a sense of well-being. Whenever possible, the components of aerobic activity (low to moderate), fl exibility, balance, and strength- ening (weight training) should be included, and the physical activity prescription should be individualized to the patient. Active hobbies, such as gardening, golfi ng, tennis, dancing, bowling, hiking, and swimming, are benefi cial. Tai chi and yoga are helpful for stretching and balance. Frail older adults or older adults with impaired mobility can benefi t from arm- chair exercises and modifi ed ambulation.

A recent study showed a decrease in risk of death in older adults with multiple morbidities who engaged in regular physical activity (Martinez-Gomez, Guallar-Castillon, Gar- cia-Esquinas, Bandinelli, & Rodriguez-Artalejo, 2017). Patients need to be reassured that expensive equipment or fi tness memberships are not necessary to increase physical activity; motivation is the key. There are also many commu- nity exercise programs targeted to older adults, as well as Web sites that can be shared if the patient has access to the Internet; these include Exercise is Medicine, the American Association of Retired Persons (AARP), the National Council on Aging (NCOA), and the National Institute on Aging (NIA). Many programs are now targeting exercise and brain health to prevent cognitive decline. Several government and com- munity group programs have handouts for patients.

Before embarking on an exercise program, all patients should have an evaluation of health history, including medications, present physical activity and functional level, potential barriers to exercise, and a physical examination. Older adults with known or suspected cardiac risk factors should have a stress test before engaging in vigorous exer- cise. All participants should be reminded of the need for ade- quate hydration and use of caution during extreme weather conditions.

Nutrition The heterogeneity of older adults is evident in the wide range of nutritional issues affecting them. Before initiating counseling on diet, obtain baseline information on current dietary intake and activity pattern, and combine this with height and weight data and other health status information. For patients in the long-term care setting, this information is obtained easily from chart documentation. For communi- ty-dwelling older adults, a brief nutrition screening tool such as the Mini Nutritional Assessment (MNA) can be helpful. The abbreviated MNA consists of six questions, and there is a patient self-questionnaire that can be downloaded or mailed in advance of the visit. The MNA Web site contains a section on tools for clinicians, including a user guide and streaming video ( www.mna-elderly.com/tools_for_clinicians.html ). It is available in multiple languages as well.

The importance of a healthy, balanced diet to the overall health of older adults cannot be overemphasized. Chronic illness and disability can interfere with the activities of daily living such as shopping or preparing meals. Financial hard- ship can limit food choices. Prescribed medications can affect absorption of nutrients, sense of taste, or appetite. Depression or social isolation can contribute to poor nutrition. Another problem commonly seen in community-dwelling older adults is obesity. Close to one-half of U.S. older adults are overweight

8 Chapter 2 ■ Health Promotion

or obese (Batsis et al., 2017). A recent systematic review of interventions targeting obesity in older adults found that pro- grams combining physical activity and diet had better out- comes, although the fi ndings were of low to moderate quality (Batsis et al., 2017). There is a need for further research to guide clinical interventions to decrease obesity. Overweight and obesity are associated with heart disease, certain types of cancer, type 2 diabetes, breathing diffi culties, stroke, arthritis, and psychological problems. Although there is a decline in the prevalence of overweight and obesity after age 60 years, it remains a problem for many older adults. It is a major risk factor for decreased mobility and functional impairment as well as a cardiovascular risk. General guidelines for dietary counseling include:

■ Limit fat and cholesterol. ■ Maintain a balanced caloric intake. ■ Emphasize the inclusion of grains, fruits, and vegeta-

bles daily. ■ Ensure an adequate calcium intake, especially for

women. ■ Limit alcohol, if used, to one drink daily for women and

two drinks daily for men: one drink = 12  oz beer, 5  oz wine, or 1.5 oz of 80-proof distilled spirits.

Safety Prevention of injury in the older adult is of paramount impor- tance to continuing functionality and quality of life. Part of this counseling involves reinforcement of extant recommen- dations, including wearing lap and shoulder seat belts in a motor vehicle, avoiding drinking and driving, having working smoke detectors in the residence, and keeping hot water set below 120°F. For older adults who drive a motor vehicle, peri- odic assessment of their ongoing ability to drive safely is vital to the older adult and the public at large. Most motor vehicle accidents involve young drivers and older drivers.

Two recommendations are especially important for ensur- ing the safety of the older adult. The fi rst involves the safe storage and removal of fi rearms. Possession of a fi rearm com- bined with depression, caregiver stress, irreversible illness, or decline in functional abilities can invite self-infl icted injury, suicide pacts, or other acts of violence. Counsel patients to avoid fi rearms in the home and to use alternative means for self-protection such as alarm systems and pepper mace spray. The second recommendation involves the prevention of falls, the leading cause of nonfatal injuries and unintentional death from injury in older persons. Certain combinations of phys- iological and environmental factors place some patients at increased risk. About 85% of falls occur at home, in the later part of the day. Offi ce-based providers can assess for falls by asking if there is a history of falling and by performing the Get Up and Go test in the offi ce. If indicated, evaluation of risk factors and a home safety assessment by a home health nurse or a geriatric assessment team can provide direction for preventive intervention and education. Potential recommenda- tions include exercise programs to build strength, modifi cation of environmental hazards, monitoring and adjusting of med- ications, external protection against falling on hard surfaces, and measures to increase bone density. If urinary incontinence is a contributing factor, a urological work-up may be indicated.

Falls are often alarming to patients and families. In some cases, family members may desire nursing home placement

for the patient because of a fall. In other cases, patients may be fearful of ambulation as a result of a fall. Falls also pose a challenge in the long-term care environment. Education and counseling combined with an assessment of the patient ’ s environment are helpful. Keeping water, call bell, telephone, and other necessities available and toileting regularly can minimize the potential for falling in nursing home patients. Several home safety checklists are available on the Internet and can be given to patients for self-assessment.

Aging in Place In the past few years technology such as SMART HOMES and sensors have been introduced to facilitate aging in place. Most of these technologies are still in their infancy but offer hope in delaying institutionalization and promoting healthy functioning at home. Other programs, primarily in European countries, are targeting at-risk “oldest old” and have designed comprehensive interventions to maintain them at home (Dahlin-Ivanoff et al., 2017). It is anticipated that more technological interventions will be implemented to promote healthy aging in place in the near future.

Sexual Behavior Assumptions regarding lack of sexual expression in the healthy older adult are unfounded. With the possibility of pregnancy eliminated, many mature adults feel less restraint. As a result of divorce or widowhood, they may seek satis- faction with new partners yet lack the knowledge to protect themselves from sexually transmitted diseases, especially HIV. More than 42% of those living with HIV in the United States in 2013 were people more than 50 years old (CDC, 2017); 39% of deaths from HIV in 2014 were in adults more than 55 years of age (CDC, 2017). Older adults need to be taught methods for safe sex with use of a barrier to avoid sexually transmitted diseases, including HIV and hepatitis B. Using the patient ’ s sexual history, explore patient needs, preferences, and medical or psychological obstacles to sexual expression. This exploration facilitates counseling and interventions to promote healthy sexual behavior.

Dental Health Counseling regarding dental health in the older adult includes the need for regular visits to the dental-care pro- vider, daily fl ossing, and brushing with fl uoride toothpaste. Many elders have dentures or dental implants and assume that dental checkups are no longer necessary. Oral screen- ing for cancer is still indicated, as is periodic assessment of denture fi t and functionality. Another concern is for the con- dition of the remaining teeth of some older adults. Periodon- tal disease, erosion of dentin, or other problems may render the teeth nonfunctional for chewing and a potential source for infection. Dependence on others for transportation or lack of available dental resources for patients in long-term care settings further complicates the problem. Caregivers simply may overlook this aspect of preventive health or fi nancial considerations may preclude treatment. Patient and family education regarding dental health is essential.

Substance Use Counseling about substance use (tobacco, alcohol, and drugs) and injury prevention can be combined naturally

Chapter 2 ■ Health Promotion 9

within the issue of safety. Smoking is the leading prevent- able cause of death in the United States. Smoking cessation yields many benefi ts to former smokers in terms of reduction of risk for several chronic illnesses and stabilization of pul- monary status. Clear and specifi c guidelines are available to help health-care providers advise tobacco users to quit and to provide them with follow-up encouragement and relapse pre- vention management. Quitting smoking may not be a choice for the institutionalized older adult but rather dictated by the policy of the institution. Health-care providers can offer support and encouragement, emphasizing the positive health changes that will result.

Counseling regarding alcohol or other drug use can be preventive or interventional, depending on the initial assess- ment. Use the Michigan Alcohol Screening Test (MAST), the CAGE questionnaire, or the Alcohol Use Disorders Identifi - cation Test (AUDIT) to assess risk. Emphasize the dangers of drinking and driving and the increased risk of falling while under the infl uence of alcohol or any drug that acts on the central nervous system. Teach patients about the coincidental

interactions between alcohol and many prescription drugs, over-the-counter preparations such as acetaminophen, and herbal remedies. The contribution of alcohol abuse to prob- lems such as insomnia, depression, aggressive behaviors, and deteriorating social relationships, should be addressed. Likewise, the problem of dependence on prescription drugs such as analgesics, hypnotics, tranquilizers, and anxiolytics, should be assessed and addressed. Counseling in the form of individual follow-up sessions, group support, or outpatient or inpatient rehabilitation may be indicated. In a group- living situation, the governing body (i.e., resident council) may become involved if the patient ’ s behavior threatens the safety or well-being of the other group members.

SCREENING AND PREVENTION

The following table contains the areas of screening and pre- vention that are covered by Medicare for older adults and the relevant evidence to support these initiatives.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The USPSTF concludes that the current evidence is insuffi cient to assess the balance of benefi ts and harms of screening for hearing loss in asymptomatic adults aged 50 years or older.

I Moyer for the USPSTF, 2012

The USPSTF recommends that clinicians screen for HIV infection in adolescents and adults aged 15 to 65 years. Younger adolescents and older adults who are at increased risk should also be screened.

A Moyer for the USPSTF, 2013

The USPSTF recommends that clinicians screen adults aged 18 years or older for alcohol misuse and provide persons engaged in risky or hazardous drinking with brief behavioral counseling interventions to reduce alcohol misuse.

B Currently under revision, 2017 https://www.uspreventiveservices taskforce.org/Page/Document/ UpdateSummaryDraft/unhealthy -alcohol-use-in-adolescents-and -adults-including-pregnant-women -screening-and-behavioral -counseling-interventions

The USPSTF recommends that clinicians ask all adults about tobacco use, advise them to stop using tobacco, and provide behavioral interventions and U.S. Food and Drug Administration (FDA)–approved pharmacotherapy for cessation to adults who use tobacco.

A Siu for the USPSTF, 2015

The USPSTF recommends screening for depression in the general adult population, including pregnant and postpartum women. Screening should be implemented with adequate systems in place to ensure accurate diagnosis, effective treatment, and appropriate follow-up.

B Siu for the USPSTF, 2016

Continued

10 Chapter 2 ■ Health Promotion

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The USPSTF recommends screening for high blood pressure in adults aged 18 years or older. The USPSTF recommends obtaining measurements outside of the clinical setting for diagnostic confi rmation before starting treatment.

A Siu for the USPSTF, 2015

The USPSTF recommends screening for abnormal blood glucose as part of cardiovascular risk assessment in adults aged 40 to 70 years who are overweight or obese. Clinicians should offer or refer patients with abnormal blood glucose to intensive behavioral counseling interventions to promote a healthful diet and physical activity.

B USPSTF, 2015

The USPSTF recommends that adults without a history of cardiovascular disease (CVD) (i.e., symptomatic coronary artery disease or ischemic stroke) use a low- to moderate-dose statin for the prevention of CVD events and mortality when all of the following criteria are met: 1) they are aged 40 to 75 years; 2) they have one or more CVD risk factors (i.e., dyslipidemia, diabetes, hypertension, or smoking); and 3) they have a calculated 10-year risk of a cardiovascular event of 10% or greater. Identifi cation of dyslipidemia and calculation of 10-year CVD event risk requires universal lipids screening in adults aged 40 to 75 years. See the “Clinical Considerations” section for more information on lipids screening and the assessment of cardiovascular risk.

B Bibbins-Domingo for the USPSTF, 2016

The USPSTF recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in men aged 65 to 75 years who have ever smoked.

Topic under revision, June 2017 by the USPSTF https://www.uspreventiveservices taskforce.org/Page/Name/topics-in -progress

The USPSTF recommends screening all adults for obesity. Clinicians should offer or refer patients with a BMI of 30 kg/m 2  or higher to intensive, multicomponent behavioral interventions.

Topic under revision, 2017 https://www.uspreventiveservices taskforce.org/Page/Document/ UpdateSummaryDraft/obesity-in -adults-interventions1

The USPSTF recommends biennial screening mammography for women aged 50 to 74 years.

B Siu for the USPSTF, 2016

The USPSTF concludes that the current evidence is insuffi cient to assess the balance of benefi ts and harms of screening mammography in women aged 75 years or older.

I Siu for the USPSTF, 2016

The USPSTF concludes that the current evidence is insuffi cient to assess the balance of benefi ts and harms of screening for impaired visual acuity in older adults.

I Siu for the USPSTF, 2016

Chapter 2 ■ Health Promotion 11

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The USPSTF recommends screening for osteoporosis in women aged 65 years and older and in younger women whose fracture risk is equal to or greater than that of a 65-year-old white woman who has no additional risk factors.

B USPSTE, 2018

Prostate cancer is common in older men. USPSTF update in progress, 2017 https://screeningforprostatecancer. org/

Screening for cognitive impairment in older adults.

USPSTF update in progress, 2017 https://www.uspreventiveservices taskforce.org/Page/Document/ UpdateSummaryDraft/cognitive -impairment-in-older-adults -screening1

The USPSTF recommends screening for colorectal cancer (CRC) starting at age 50 years and continuing until age 75 years (A recommendation).

A USPSTF, JAMA , 2016 ; 315(23):2564–2575. doi:10.1001/ jama.2016.5989

The decision to screen for colorectal cancer (CRC) in adults aged 76 to 85 years should be an individual one, taking into account the patient ’ s overall health and prior screening history (C recommendation).

C

The decision to initiate low-dose aspirin use for the primary prevention of CVD and CRC in adults aged 60 to 69 years who have a 10% or greater 10-year CVD risk should be an individual one. Persons who are not at increased risk for bleeding, have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefi t. Persons who place a higher value on the potential benefi ts than the potential harms may choose to initiate low-dose aspirin.

C Bibbins-Domingo for the USPSTF, 2016

The current evidence is insuffi cient to assess the balance of benefi ts and harms of initiating aspirin use for the primary prevention of CVD and CRC in adults aged 70 years or older.

I Bibbins-Domingo for the USPSTF, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

12 Chapter 2 ■ Health Promotion

IMMUNIZATIONS

Infl uenza vaccine is now recommended annually for all adults over 50 years old, unless contraindicated ( Table 2-1 ). Residents of long-term care facilities that house persons with chronic medical conditions are at especially high risk for developing the disease. Health-care workers also should receive the vaccine, preferably before the end of October (Resnick, 2018). Patients with a severe egg allergy or severe reaction to the infl uenza vaccine in the past and patients with a prior history of Guillain-Barré syndrome should talk with their health-care provider before getting the vaccine.

Tetanus-diphtheria toxoids with acellular pertussis (Tdap) vaccine is administered as a once-in-a-lifetime booster to every adult. Following this, a tetanus-diphtheria (Td) booster is recommended every 10 years.

Pneumococcal vaccine is recommended as follows: Administer a one-time dose to PCV13-naïve adults at age 65 years, followed by a dose of PPSV23 12 months later.

Hepatitis B vaccine is recommended for high-risk persons such as IV drug users, persons who are sexually active with multiple partners, those living with someone with chronic hepatitis B, patients less than 60 years old with diabetes, and all desiring protection from hepatitis B. The initial dose is given, followed 1 month later by the second dose, then the third dose is given 4 to 6 months after the second dose.

Shingrix is a new vaccine for zoster and is recommended over Zostavax. It is administered in two doses. The second dose can be given from 2 to 6 months after the initial one. Persons who have had Zostavax should now be immunized with Shingrix (Resnick, 2018). Those who have had a prior episode of zoster should be vaccinated (CDC, Adult Immuni- zation Schedule, 2017; www.immunize.org ).

TRAVEL AND LEISURE

Travel can be one of the most enjoyable experiences one can have. People travel to see new things, understand the world

and themselves better, visit friends and family, return to the land of their ancestors, volunteer, challenge themselves, and because it is fun. They travel alone, in groups, and with their families. They go on cruises and they go on safaris. They stay in fi ve-star resorts and in host family homes. They take planes, buses, trains, jeeps, and rickshaws. They scuba dive, hike the Himalayas, and bicycle in Tuscany. They teach and learn. They volunteer in Haiti, Ghana, and Honduras. But travel can pose some unique health risks for the older trav- eler. The gerontology NP in primary care can provide pre-trip advice to help ensure healthy and safe travel.

Travel Health and Nursing Travel health is an interdisciplinary specialty that has grown out of the need to protect travelers from illness and injury. It developed in the 1970s as infectious disease and tropical medicine clinicians treating returned travelers recognized that many of the problems they encountered could be pre- vented by pre-travel evaluations, immunizations, chemopro- phylaxis, and counseling about safety, food and water, and insect precautions.

In 1991 the International Society of Travel Medicine (ISTM) ( www.istm.org ) was formed and established an international body of knowledge to defi ne travel medicine. It is the only body offering an examination to demonstrate competences for physicians, NPs, registered nurses (RNs), physician assistants (PAs), and pharmacists. Those who pass are awarded a Certifi cate in Travel Health. The American Travel Health Nurses Association (ATHNA) ( www.athna.org ) was formed in 2004 to promote and support travel health nursing in North America. ATHNA provides many resources for nurses and NPs who specialize in travel health, as well as for those in primary care.

Travel health is rapidly evolving and growing as a spe- cialty but is also growing as a part of primary care. NPs will need to know how to evaluate older travelers and develop a plan of care to keep them healthy while they travel. They need to know how, when, and where to refer to a travel health specialist. The majority of travelers who could benefi t from pre-travel consultations do not receive them (Zuckerman,

2017 Adult Immunization Schedule for Older Adults

VACCINE AGE GROUP DOSING

PCV13 Over 65 Single dose; for those with chronic health conditions

may administer a dose before age 65 and boost with

a second dose after age 65

PPSV23 Over 65 Give 1 year after PCV13

Diphtheria-tetanus-pertussis (Tdap) Any adult—one time substitute for Td Single dose

Tetanus diphtheria (Td) Every 10 years after single dose of DTaP Single dose every 10 years

Infl uenza All adults Annual

Hepatitis B All with risk factors due to lifestyle, history of

diabetes mellitus

Three doses

Herpes zoster (HZV) Adults aged 50 years or older regardless of

whether they had a prior episode of herpes

zoster; immunize those who have had Zostavax

with Shingrix

Two doses age 50 or older (Shingrix)

See full details and recommendations for special populations and contraindications at: Recommended adult immunization schedule—2017. Retrieved from https://www.cdc.gov/vaccines/schedules/hcp/adult.html

TABLE 2-1

Chapter 2 ■ Health Promotion 13

Brunette, & Leggat, 2015). NPs are in a unique position to educate patients and the public about the benefi ts of this service.

Medical Tourism Some people travel abroad to receive medical care. The most common procedures sought outside the United States include joint replacements, cosmetic surgery, cataract lens replace- ment, cardiovascular surgery, and dental procedures. Some people travel for organ transplants, stem cell treatments, and anti-aging and cancer treatments not available or banned in the United States. While there are some options for high quality, less expensive health care abroad, the patient must do careful research to ensure safe, quality care is rendered by competent providers. Traveling with a patient advocate is advised, as elders recovering from surgery or who are in poor health are more vulnerable to complications and being taken advantage of (Brunette & Kozarsky, 2018).

The Older Traveler Some of the physiological and psychosocial changes that can occur with aging pose special risks during travel. How a patient functions at home may not be indicative of how well he or she will function in an unfamiliar environment. Dimin- ished musculoskeletal strength, agility, mobility, and endur- ance can affect a person ’ s ability to navigate safely. Travel often involves more walking and standing than an elder may be accustomed to. Many places abroad are not handicapped accessible. Uneven stairs and walkways, lack of handrails, and lack of elevators can be challenging.

Cardiopulmonary function can decrease with age and contribute to fatigue. Long fl ights in low humidity and lowered oxygen, in cramped seats, can increase risk of thromboembolic events. The older adults are at increased risk of altitude illness, which affects cardiac and cerebral func- tioning. Increased air pollution is a signifi cant problem in many countries and affects pulmonary function. The ability to tolerate temperature changes affects the older traveler. Heat and humidity can aggravate underlying conditions, and older travelers will become dehydrated more easily. They are more prone to thermal damage in colder climates. Central nervous system changes affect the older traveler ’ s ability to deal with the stresses of travel. It can be anxiety inducing to be in a place where everything is so different—the language, food, customs, and climate. Jet lag is harder to cope with as one ages. Any traveler can experience unexpected delays and be without food and sleep for hours. This can take an even greater toll on the older traveler.

Sensory changes may result in decreased hearing, which is especially diffi cult on airplanes or trains with background engine noise. Decreased vision can result in greater risk of injuries. Decreased night vision, longer reaction time, and driving on unfamiliar, poorly lit roads increase the risk of accidents. Bathroom stops may be at longer intervals than needed for an older traveler with diminished bladder capac- ity or any degree of incontinence. Some facilities may consist only of holes in the fl oor that the elder may have to balance over to use.

Older travelers have less robust immune systems. Fever is not always a reliable indicator of illness in the older adult. Seroconversion rates decrease with age, rendering some vac- cines less effective for older travelers. Although many older

travelers are very healthy, many have comorbidities that contribute to the development of health problems abroad. Patients with chronic disease that is well managed at home may decompensate in foreign environments because of heat, humidity, altitude, fatigue, changes in diet, and exposure to infectious diseases.

It is very important that older travelers know what to do if they become ill or injured away from home. Advise the traveler to obtain travel health insurance that includes emer- gency medical evacuation and repatriation of remains. Medi- care does not cover the cost of health care outside the United States. Have the patient bring a hard or electronic copy of his or her medical history, medication list, allergies, and copies of pertinent imaging studies or electrocardiograms (EKGs). The NP with expertise in gerontology can provide pre-travel care that will not only reduce the morbidity and mortality asso- ciated with travel but also enhance the elder ’ s travel expe- rience. When destinations or itineraries are complicated or when a patient ’ s condition poses special risks, a visit to or a consultation with a travel health specialist is warranted.

Preparing the Elder in a Primary Care Setting for Travel To develop an individualized pre-travel plan of care, the NP needs to evaluate the traveler, the destination, and the itiner- ary. Assessing the traveler consists of reviewing these areas:

■ Current health status—stability of preexisting conditions

■ Past medical history ■ Medications and allergies ■ Diet ■ Mental status ■ Immunization status

CURRENT MEDICAL STATUS

Ideally, the traveler should be seen at least 6 to 8 weeks before the trip to allow for time to optimize preexisting chronic disease and adequate immune response to vaccine-prevent- able diseases (Gerstenlauer, 2017). Evaluate the patient ’ s current medications. Simplifying medication schedules enhances compliance. Are there any that do not need to be taken on this trip? Are there any factors that will affect your patient ’ s ability to take any medications during travel? Does the patient know how to adjust medication schedules to accommodate air travel and time zone changes? All pre- scription medications should be brought in original bottles and not in unlabeled pill containers. If your patient gets his or her prescriptions in 90-day supplies, give the patient new prescriptions for smaller amounts for travel, including a few extra in case of delays. Does the patient need to bring a wheelchair, walker, glucometer, hearing aids, C Pap, or neb- ulizer? Remind them to check all batteries and bring extras. Is adequate electricity reliably available at a current that will work with the equipment? Will adapters be needed and will they work properly?

MEDICATIONS AND ALLERGIES

■ Is the patient taking any medication that could prove life threatening if lost or stolen? If so, is it accessible at the patient ’ s destination?

14 Chapter 2 ■ Health Promotion

■ Does the patient have any life-threatening allergies? ■ Does the patient take any medications that require

refrigeration? Decompose from heat and humidity? Require syringes? Need a nebulizer?

■ Is the patient on oxygen? If so, he or she must notify the airline well in advance of travel.

All medications should be packed in carry-on luggage, not in checked bags. Certain countries restrict bringing in any controlled substances and some other drugs whether legally prescribed in the United States or not. Caution patients about purchasing pharmaceuticals abroad which may be cheaper but also could be counterfeit.

DIET

Does the patient have any special dietary restrictions? Air- lines offer diabetic and vegetarian options but may not offer gluten-free or sodium-restricted comestibles. These must be ordered in advance. Cruise ships accommodate many spe- cialty diets but also offer many temptations. Restaurant menus in many countries do not list all the ingredients in the dishes offered, which can be problematic for those with severe food allergies.

MENTAL STATUS

Short-term memory decreases with age. Many elders cope with these changes by adhering to routines that travel may disrupt. Misplacing passports, room keys, or wallets or not remembering hotel names or addresses can be distressing. Family members or travel companions may need to offer additional assistance. Advise that elders carry a hotel ’ s busi- ness card that includes the hotel ’ s name, address, and phone number. Taking photographs of hotels, cruise ships, or tour company ’ s names can help the memory impaired who may become confused.

IMMUNIZATION STATUS

All routine immunizations should be current. This includes infl uenza, pneumococcal, Td/Tdap (tetanus, diphtheria, and acellular pertussis), zoster, and for some, hepatitis B vaccina- tion. The current schedule of adult vaccination recommen- dations from the CDC (updated February 2016) is available at http://www.cdc.gov/vaccines/schedules/hcp/adult.html . Certain vaccines may be recommended based on destina- tion, and some vaccines are required for entry into some African and South American countries ( Table 2-2 ) (Brunette & Kozarsky, 2018).

Yellow fever vaccinations can only be given by certifi ed yellow fever centers. If the patient is seeing a primary care provider before getting a yellow fever vaccine, be aware

of the live virus vaccine rule (Brunette & Kozarsky, 2018). Yellow fever and herpes zoster vaccine are the only live virus vaccines that people over age 50 receive. Immune response can be impaired if live virus vaccines are given within a 28- to 30-day interval of each other. Yellow fever vaccine is not effective until 10 days after administration. If the NP gives a patient a herpes zoster vaccine, that patient cannot receive a yellow fever vaccine for 30 days. If the patient is required to have a yellow fever vaccine for travel, he or she cannot enter a yellow fever country until 10 days after receiving the yellow fever vaccine (or 40 days after receiving a herpes zoster vaccine). If the administration of a herpes zoster vaccine precludes the administration of a time-sensi- tive yellow fever vaccine, travel plans could be interrupted, with serious fi nancial consequences for the traveler. If the NP has any questions about when to vaccinate a patient whose trip is imminent, discuss this with a travel health specialist. If a patient receives a yellow fever vaccine, he or she cannot receive a herpes zoster vaccine for 28 days. The patient may receive both vaccines on the same day with no decrease in immune response (Brunette & Kozarsky, 2018). Typhoid oral vaccine is a live bacterial vaccine and will not interfere with live viral vaccine administration.

After assessing the destination and itinerary (see the fol- lowing section), decide which vaccines to recommend for this specifi c patient for this specifi c trip. The most common vac- cines used for protecting travelers are hepatitis A, hepatitis B, typhoid fever, yellow fever, adult booster polio, Japanese encephalitis, meningococcal, and rabies. If the NP does not have access to these vaccines, referral to a travel health spe- cialist will be needed. To help the patient make an informed decision about which recommended vaccines to receive, con- sider the indications, contraindications, side effects, timing of doses for immune response, and costs. Medicare will cover hepatitis B in very limited patient populations and will not cover the cost of the other recommended vaccines (Offi cial U.S. Government Web site for Medicare, n.d.). Federal regu- lations require the NP to give patients Vaccine Information Statements (VISs), which are available in many different lan- guages at http://www.cdc.gov/vaccines/hcp/vis/index.html . The most important vaccine a traveler should receive is the infl uenza vaccine.

All patients should have a copy of their immunization record. If a patient has an incomplete vaccine series, con- tinue the series but do not restart it. For example, if a patient received one dose of hepatitis A several years ago but never received the second, fi nal injection, give the next and fi nal dose now. If the patient received only one dose of hepatitis B years ago, give the second dose now and the third dose 5 months from now, and the series will be complete (Immuni- zation Action Coalition, n.d.).

If a patient cannot complete a series before travel, partial immunization may confer enough protection. Some vac- cines can be given on an accelerated schedule; otherwise, do not give a vaccine sooner than the recommended interval between doses. One dose of hepatitis A given just before travel will confer enough protection to make it worth giving to the last-minute traveler. Hepatitis A and B vaccines are also available as a combined vaccine given at 0, 1, and 6 months. If there are at least 21 days before the patient ’ s departure, the vaccine can be given in an accelerated schedule of 0, 7, and 21 to 30 days with a booster at 12 months (Brunette

Adult Vaccinations for Travel

RECOMMENDED ADULT VACCINATIONS FOR TRAVEL

REQUIRED ADULT VACCINATIONS FOR TRAVEL

Hepatitis A; others are specifi c

to area where traveling

including hepatitis B, typhoid,

polio, meningococcal, Japanese

encephalitis, rabies

Yellow fever for some African

and South American countries

Meningococcal for Saudi Arabia

during the Hajj

TABLE 2-2

Chapter 2 ■ Health Promotion 15

& Kozarsky, 2018). Typhoid fever vaccine is available in two forms, a single-dose injectable and orally as a series of four capsules given every other day for 1 week. The oral vaccine then takes a week to be effective. The injectable vaccine needs to be boostered every 2 years and the oral vaccine at 5 years, if needed. Before prescribing the oral form, be sure the patient can comply with the proper administration (Brunette & Kozarsky, 2018).

Because of worldwide efforts to eradicate polio, only a few countries require adults to get a polio booster for travel. If your patient has had polio in the past, he or she does not need vaccination. If your patient has been fully vaccinated for polio, a single booster dose as an adult will protect him or her. Japanese encephalitis vaccine, meningococcal vaccine, and rabies pre-exposure vaccine are not usually administered to elders for travel in a primary care setting. Japanese enceph- alitis vaccine is only advised for long-term stays in high-risk areas. Meningococcal vaccine is only licensed for people ages 2 to 55. Depending on the country visited, length of stay, and potential exposure to rabid animals, decisions regarding rabies pre-exposure vaccine are usually made with a travel health specialist. Cost and vaccine availability play a role in deciding pre-exposure vaccination (Brunette & Kozarsky, 2018). It is important to warn travelers of the risk of rabies and to educate them in animal bite prevention strategies, especially concerning dogs, which are the biggest vector for rabies worldwide.

The CDC Yellow Book 2018 is an invaluable resource for vaccine administration and is available in paperback and online in its entirety for free and as a free app. Clinicians and travelers can research recommendations for specifi c coun- tries at http://wwwnc.cdc.gov/travel/ . The Advisory Council on Immunization Practice (ACIP) has a section on its Web site ( www.immunize.org ) called Ask the Expert that can be searched for answers to immunization questions. Listings for travel health specialists and clinics can be found at the ISTM Web site ( www.istm.org ) and the CDC Web site ( wwwnc.cdc. gov/travel/page/fi nd-clinic ).

ASSESSING THE DESTINATION AND ITINERARY

The NP needs to know where the traveler is going and what he or she will do there to provide anticipatory guidance for risk reduction. The NP may decide to refer to a travel clinic for the remainder of the pre-trip evaluation. Either way, the following overview will help the NP to understand what com- prises a comprehensive pre-travel evaluation.

Mexico, China, India, Peru, Kenya, Australia, Europe, and the Caribbean all pose different risks for the elder traveler. The time of year, duration of the trip, type of accommodations, modes of transportation, and purpose of the trip all infl u- ence travel risk. A 70-year-old couple going to the Dominican Republic who plan to stay at an all-inclusive resort will need different advice than a 70-year-old couple traveling to build an orphanage and staying in a host family home. There are Web sites that offer current advice about destinations that the NP can use. Some are free, such as the CDC Web site, and some are subscription based, such as Shoreland ( www. travax.com ) and Tropimed ( www.tropimed.com ).

The most common risks for travel to tropical, subtropical, and low-resource countries are trauma and food-, water-, and insect-borne diseases. Because so much information is relayed at the pre-travel visit, it is important to provide

written information for review at home. Handouts for insect, food, and water precautions are found on the CDC Web site.

SAFETY

Accidents and injuries are the most common cause of pre- ventable death and disability for travelers. Tourists are 10 times more likely to die from trauma than infectious disease (Brunette & Kozarsky, 2018). The most common risks travel- ers face from trauma result from motor vehicle, pedestrian, and water accidents; personal safety/crime; natural disasters and environmental hazards; and animal-related injuries.

In many parts of the world, roads and vehicles are poorly maintained. Seat belts and helmets are typically unavail- able. Roads are shared by pedestrians, animals, motorbikes, bicycles, trucks, buses, and rickshaws. Traffi c accidents are more common because the traveler is unfamiliar with the roads, may be driving on the opposite side of the road, and may need to drive to the left on roundabouts. Road signs and lighting are suboptimal. To help prevent accidents, always take these precautions:

■ Wear seat belts when available. ■ Avoid driving or riding at night in underdeveloped

countries. ■ Avoid motorcycles and mopeds altogether. ■ Do not drive impaired by alcohol or fatigue or ride with

someone who is. ■ Do not use cell phones or text or type on GPS systems

while driving. ■ Avoid overcrowded buses and vans. ■ Be alert when crossing the street.

The Association for International Road Travel (ASIRT) has a very helpful Web site with patient handouts for accident prevention ( www.asirt.org ).

Drowning is the leading cause of accidental death for U.S. travelers visiting countries where water recreation is a major activity (Brunette & Kozarsky, 2018). Warn travelers to avoid diving into shallow water or swimming or boating under the infl uence of alcohol and remind them to use life vests. Boating in unfamiliar waters, and in unfamiliar boats, increases risk of accidents. Many countries do not have laws and regulations concerning public safety to the same extent as the United States. Outfi tters may not be as careful about safety. Divers Alert Network (DAN) ( www.DAN.org ) pro- vides education, support, and travel and health insurance worldwide for scuba divers. They staff a 24-hour hotline for divers and health-care providers for medical support at 1-919-684-9111.

The U.S. Department of State Web site provides current information about worldwide safety and security at https:// travel.state.gov/content/travel/en.html . Personal crime rates vary from country to country. While risk of harm from ter- rorist activities is low, travelers should be aware of emergency exits and routes and know the location of the U.S. embassy in the countries they are in. Homicide was the second leading cause of death from injuries for U.S. citizens. In Honduras, Colombia, Guatemala, and Haiti, 38% to 52% of all deaths from injuries for U.S. travelers were homicides (Brunette & Kozarsky, 2018). Older adult travelers are seen as wealthy, vulnerable targets and can travel in high-poverty, high-crime areas. Travel during civil unrest or travel at night in unfamil- iar places increases the risk of assault.

16 Chapter 2 ■ Health Promotion

FOODBORNE AND WATERBORNE ILLNESSES

It is not safe to drink the water in many places in the world. Food and water precautions must be carefully adhered to for preventing disease. The easiest way for travelers to remember this is to tell them to boil it, peel it, cook it, or forget it. Bottled water; carbonated beverages without ice; and coffee, tea, and alcohol are safe to drink. Do not brush teeth or soak dentures in tap water. Some travelers tie a ribbon or small rope around the faucet to remind them not to drink the water. Despite best efforts, traveler ’ s diarrhea is common, and often the health- care provider will prescribe drugs for the traveler to take with him or her in the event that this occurs. Mild diarrhea can be treated with bismuth subsalicylate (BSS). Signifi cant diarrhea can be treated very effectively with azithromycin, 500 mg once daily for 1 to 3 days (Brunette & Kozarsky, 2018), as 90% of the cases are bacterial. Oral rehydration solution (ORS) packets or effervescent tablets help prevent dehydration.

INSECT-BORNE DISEASES

Dengue, chikungunya, and Zika viruses have spread through- out much of the temperate zones of the world, including Central America, the Caribbean, and southern areas of the United States, areas where large numbers of older travelers go for extended stays in the winter. When traveling to areas where insect-borne diseases are a risk, the older traveler should be advised to avoid bites day and night by using insect repellents on exposed skin, treating clothing with permethrin prior to packing, and covering up with clothing, hats, and footwear. Morbidity and mortality for Zika is greater in the older adult. Because there is still much to be learned about this infection, the NP needs to stay informed about new developments at https://www.cdc.gov/zika/ . NPs can subscribe to Morbidity and Mortality Weekly Review (MMWR) for free at http://www. cdc.gov/mmwr/mmwrsubscribe.html and receive the table of contents and links to articles when published.

Prevention of malaria is essential for any traveler going to a malaria-endemic area, regardless of age. Malaria is more severe in the older adult, and mortality risk from malaria increases with age (Zuckerman et al., 2015). When traveling to malaria-endemic areas, travelers should always practice bite avoidance and consider chemoprophylaxis depending on their specifi c itinerary and season of travel. Mosquitoes that transmit malaria bite from sunset to sunrise. If a traveler is taking a cruise and spends the day in port in a malaria- endemic area but returns to the ship before sunset, insect repellent and protective clothing may suffi ce.

Malaria chemoprophylaxis is generally well tolerated in the older adult. Drug choice depends on the destination, side effects, drug interactions, and cost. All medications are started before travel, taken during travel, and taken for a period of time after travel. The CDC provides maps of malar- ia-endemic areas and guidelines for prescribing (Brunette & Kozarsky, 2018). It is important for patients who are being evaluated for fever or fl u-like symptoms for up to a year post travel tell their health-care providers that they have traveled so that insect-borne diseases can be ruled out.

Motion Sickness Motion sickness can be prevented with pharmacological and nonpharmacological methods. Many large, modern

cruise ships are designed to greatly reduce motion sickness. Commonly used medications for motion sickness include dimenhydrinate, promethazine, diphenhydramine, and anti- cholinergic agents such as scopolamine. Review possible side effects and drug and alcohol interactions carefully. Methods such as closing your eyes, focusing on the horizon line, and acupressure wrist bands can also be helpful.

Jet Lag Jet lag can be mitigated by getting proper rest before travel and maintaining proper hydration during fl ight. Zolpidem has been shown to be more effective in the treatment of jet lag than melatonin (Suhner, Schlagenhauf, & Hofer, 2001). The patient should try a dose of zolpidem at bedtime at home before travel to test tolerance. Confusion, ataxia, and falls are potential side effects of zolpidem.

Heat and Humidity Hyperthermia occurs more frequently in the older adult. Acclimatization to heat and humidity may take several days. Many of the drugs frequently used by the older adult, such as antihistamines, anticholinergics, calcium channel block- ers and beta blockers, diuretics, and anti-Parkinson ’ s medi- cations, impair thermoregulation. The older adult traveler should use caution in hot and humid environments, drink adequate fl uids, avoid caffeine and alcohol, and avoid overex- ertion. Self-treatment measures may also include using ORS packets/tablets in clean bottled water.

Altitude Illness Altitude illness can range from mild shortness of breath to life-threatening acute mountain sickness (AMS). Prior toler- ance of altitude does not predict future tolerance. Those with underlying cardiopulmonary disease may experience greater hypoxia. Because the body ’ s normal response to lowered oxygen is to increase the pulse rate, beta blockers can reduce the body ’ s compensatory response. Acetazolamide is used to prevent AMS but needs to be started 24 to 48 hours before ascent, and side effects versus benefi ts need to be carefully evaluated. If symptoms of AMS develop, descent, if possible, is the best treatment. Many areas, such as Cusco, Peru, are experienced in treating AMS in tourists because it is such a common occurrence.

Respiratory Infections Low humidity from airline travel and exposure to crowds and air pollution will make the older adult more prone to respi- ratory infections during travel. If your patient has chronic pulmonary disease, consider giving him or her an antibiotic to self-treat, if infection occurs.

Sexually Transmitted Infections Older people may be at increased danger from sexually trans- mitted infections (STIs) because of the decreased perception of risk by both health-care providers and patients, resulting in less screening and treatment. Older adults are less likely to practice safe sex and use condoms. The rate of casual sex increases with travel (Jong & Sanford, 2008). Encoun- ters may be with fellow travelers, locals, or commercial sex workers. Many older women are told they do not need Pap smears based on their age alone. Current sexual history may

Chapter 2 ■ Health Promotion 17

determine the need for continued screening for STIs, human papillomavirus (HPV), and cervical cancer.

Fitness for Travel Travel can be strenuous. Airports and cruise ships are huge. If a trip involves a higher level of activity than what travelers are accustomed to, they need to be sure they are fi t for that trip. Tour operators will often give specifi c suggestions for fi tness for walking, hiking, or bicycling trips but not for sight- seeing tours. Each traveler should bring a fi rst aid kit and an emergency dental kit and have a plan for getting health care abroad if needed.

National and international travel by the older adult will continue to increase. A knowledgeable NP, either alone or in conjunction with a travel health specialist, can prepare the older patient to safely enjoy travel to many destinations around the world ( Table 2-3 ). It is imperative to not only protect our elder travelers but to help prevent the importa- tion of infectious diseases back to communities in the United States.

SUMMARY ■ Evidence-based health promotion for older adults is an evolv-

ing science. As the population of older adults increases, lifestyle management for prevention of chronic illness, self-management of chronic conditions, safety, and quality- of-life issues will be more at the forefront. NPs are well posi- tioned to advance health-promotion efforts and keep older adults healthy and functional (Gerstenlauer, 2017).

Online Resources for Travel Health Travel Clinic

Locator and

Certifi ed Yellow

Fever Centers

CDC: https://wwwnc.cdc.gov/travel/page/

fi nd-clinic

ISTM: http://istmsite.membershipsoftware.org/

AF_CstmClinicDirectory.asp

Practice Protocols

and Standing

Orders

ATHNA: www.athna.org

ISTM: www.istm.org

ACIP: www.immunize.org

Immunizations CDC: wwwnc.cdc.gov/travel

ACIP: www.immunize.org

Safety and Accident

Prevention

Association for International Road Travel:

www.asirt.org

U.S. Department of State: www.state.gov/

travel/

Continuing

Education in Travel

Health

ATHNA, nursing: www.athna.org

CDC, nursing: CDC: www2a.cdc.gov/

TCEOnline/

ISTM, general: www.istm.org

Vaccine Information

Statements

CDC: https://www.cdc.gov/vaccines/index.html

See quick link for Vaccine Information Sheets

(VIS).

Journals Journal of Travel Medicine: www.istm.org

Destination

Information—

subscription

Tropimed: www.tropimed.com

Shoreland—Travax: www.shoreland.com

Destination

Information—free

CDC: https://wwwnc.cdc.gov/travel

TABLE 2-3

C A S E S T U DY

J. S. is a 66-year-old African American woman who presents to your practice for a well-adult physical checkup. She is widowed and works part-time as a mental health technician to support herself. Family history includes father deceased from a stroke at age 50 years, mother living with hypertension and type 2 diabetes mellitus, a half-sister deceased with breast cancer, and a brother with pancreatic cancer and coronary artery disease and end- stage renal disease secondary to type 2 diabetes mellitus.

J. S. has not seen a health-care provider for several years because she had no health insurance. Now she has Medicare, so she is coming in for care. She is a former smoker who quit 5 years ago after smoking 1 pack per day since age 20 years. She has four grown children, all of whom live nearby, and she has eight grandchildren. Vital signs are blood pressure (BP) 150/92, heart rate (HR) 76 (reg), respiratory rate 18 breaths per minute (bpm) (afebrile), and body mass index (BMI) 32.1.

1. What additional subjective data are you seeking?

2. What additional objective data will you be assessing for?

3. What national guidelines are appropriate to consider?

4. What tests will you order?

5. Are there any screening tools that you want to use?

6. What are the priorities for primary, secondary, and tertiary prevention?

7. What is your plan of care?

8. Are there any Healthy People 2020 objectives that you should consider?

9. What additional patient teaching may be needed?

10. Will you be looking for a consultation?

18 Chapter 2 ■ Health Promotion

REFERENCES Bibbins-Domingo , K. on behalf of the U.S. Preventive Services Task Force .

( 2016 ). Aspirin use for the primary prevention of cardiovascular disease and colorectal cancer: U.S. Preventive Services Task Force rec- ommendation statement . Annals of Internal Medicine , 164 , 836 – 845 . doi:10.7326/M16-0577 .

Bibbins-Domingo , K. on behalf of the U.S. Preventive Services Task Force . ( 2016 ). Statin use for the primary prevention of cardiovascular disease in adults: U.S. Preventive Services Task Force recommendation statement . Journal of the American Medical Association , 316 ( 19 ), 1997 – 2007 . doi:10.1001/jama.2016.15450 .

Moyer , V. A. on behalf of the U.S. Preventive Services Task Force . ( 2012 ). Screening for hearing loss in older adults: U.S. Preventive Services Task Force recommendation statement . Annals of Internal Medicine , 157 , 655 – 661 .

Moyer , V. A. on behalf of the U.S. Preventive Services Task Force . ( 2013 ). Screening for HIV: U.S. Preventive Services Task Force recommenda- tion statement . Annals of Internal Medicine , 159 , 51 – 60 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2016 ). Screening for breast cancer: U.S. Preventive Services Task Force rec- ommendation statement . Annals of Internal Medicine , 164 , 279 – 296 . doi:10.7326/M15-2886 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2016 ). Screening for depression in adults: U.S. Preventive Services Task Force

recommendation statement . Journal of the American Medical Associa- tion , 315 ( 4 ), 380 – 387 . doi:10.1001/jama.2015.18392 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2015 ). Behavioral and pharmacotherapy interventions for tobacco smoking cessation in adults, including pregnant women: U.S. Preventive Ser- vices Task Force recommendation statement . Annals of Internal Medi- cine , 163 , 622 – 634 . doi:10.7326/M15-2023 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2015 ). Screening for high blood pressure in adults: U.S. Preventive Services Task Force recommendation statement . Annals of Internal Medicine , 163 , 778 – 786 . doi:10.7326/M15-2023 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2015 ). Screening for abnormal blood glucose and type 2 diabetes mellitus: U.S. Preventive Services recommendation statement . Annals of Inter- nal Medicine , 163 , 861 – 868 .

U.S. Preventive Services Task Force Recommendation Statement June 21 . ( 2016 ). Screening for colorectal cancer: U.S. Preventive Services Task Force recommendation statement. U.S. Preventive Services Task Force article information . Journal of the American Medical Association , 315 ( 23 ), 2564 – 2575 . doi:10.1001/jama.2016.5989 .

U.S. Preventive Services Task Force Recommendation Statement . ( 2018 ). Screening for osteoporosis to prevent fractures . Journal of the American Medical Association , 319 ( 24 ), 2521 – 2531 .

19

CHAPTER 3 Exercise in Older Adults

Lori Martin-Plank

Current population statistics ( www.agingstats.gov ) indicate that Americans over 65 years of age now represent the most rapidly growing segment of the U.S. population, comprising 15% of the population in 2014. As those born from 1946 to 1964 enter the over-65 age group, these numbers will increase exponentially, expected to reach 21% by 2030, and with that growth is an anticipated skyrocketing of medical costs for chronic health conditions. Lifestyle interventions at any stage can mitigate the effects of chronic illness (Hupin et al., 2015), but they are usually given short shrift during patient encounters (Weiss et al., 2012). Many providers feel inadequately prepared to initiate realistic discussions about lifestyle changes with older adult patients. Accord- ing to one report, less than 32% of primary care providers and health professionals offer exercise counseling or educate older patients on the benefi ts of physical activity during an offi ce visit and physical examination (Barnes & Schoenborn, 2012).

Recent statistics related to exercise in older adults (Federal Interagency Forum on Aging Statistics, 2016) show that 12% of adults over age 65 years had an exercise program that met federal physical activity guidelines in 2014, compared to 6% in 1998. This report (Older Americans, 2016) also reveals an increase in obesity in older adults, from 22% in 1988 to 1994 to 35% in 2011 to 2014. Women over 65 years old were more obese than men. These facts underscore the need for a new paradigm to promote increased physical activity in older adults as part of a program of lifestyle intervention for wellness and quality of life. Nurse practitioners are uniquely positioned to assume the primary role in health promotion of both healthy persons and those with chronic illness.

AVAILABLE RESOURCES

Guidelines and position statements for increasing phys- ical activity in adults and older adults have been issued by several authorities, including the American College of Sports Medicine (ACSM) (Chodzo-Zajko et al., 2009; Nelson et al., 2007 ), American Heart Association (AHA) (Artinian et al., 2010; Marcus et al., 2006), U.S. Preventive Services Task Force (Moyer, 2012), U.S. Department of Health and Human

Services (USDHHS) (Physical Activity Guidelines Advi- sory Committee, 2008). The Healthy People 2020 initiative has several sections dedicated to health promotion in older adults. Numerous agencies, such as the Centers for Disease Control and Prevention (CDC), American Osteopathic Asso- ciation (AOA), National Institute on Aging, and Center for Medicare and Medicaid, have programs to promote wellness and quality of life in older adults, including physical activ- ity projects. The ACSM has a Web site, Exercise is Medicine, with extensive resources for providers and the public ( http:// exerciseismedicine.org ), and the Preventive Cardiovascu- lar Nurses Association has a Heart Healthy Toolbox ( http:// pcna.net/clinical-tools/tools-for-healthcare-providers/heart- healthy-toolbox ) with a variety of free tools for use by clini- cians. Despite the availability of these tools, they are largely unknown to most health-care providers, who are focused on the day-to-day activities of disease management (Friedman, Shah, & Hall, 2015).

Since the publication of the exercise guidelines for older adults, several studies have demonstrated that adapting these guidelines to individuals and specifi c populations, such as the oldest old and those with frailty (Bleijenberg et al., 2017; Dahlin-Ivanoff et al., 2015; Lee & Kim, 2017 ; Tarazona-Santabalbina, 2016), can be successful. One large study at the Veterans Association (VA) also demonstrated the effectiveness of physical activity counseling in primary care in decreasing overall health-care costs (Cowper et al., 2017). Additional studies are now focusing on the relation- ship of physical activity and cognitive changes, some includ- ing diet and supplements (Jonasson et al., 2015; Kobe et al., 2016; Tarazona-Santabalbina et al., 2016; Tse, Wong, & Lee, 2015). While this area (cognitive benefi ts and exercise) is inconclusive, the future holds promise.

Another area that is being addressed is the relationship of exercise of any kind to a decrease in mortality, both with and without cardiovascular risk factors (Hupin et al., 2015; Kim et al., 2017; Martinez-Gomez et al., 2017; Morey, 2017; Villareal et al., 2017). Specifi c programs for older adults with osteoarthritis are also effective (Bartels et al., 2016; Fransen et al., 2015). Finally, the American Academy of Family Phy- sicians (AAFP) (Lee, Jackson, & Richardson, 2017; Pescatello, 2014; Zaleski et al., 2015) and other exercise professionals

20 Chapter 3 ■ Exercise in Older Adults

have given detailed descriptions of how to design an exercise program and write a prescription, as well as how to engage the patient. LeTorneau and Goodman (2014) and Lee and colleagues (2016) have addressed the role of motivational interviewing in facilitating older adult engagement in phys- ical activity and exercise.

BARRIERS AND FACILITATORS TO EXERCISE FOR OLDER ADULTS

In 2006, a subcommittee of the AHA Council on Nutri- tion, Physical Activity, and Metabolism undertook a review of existing physical activity intervention studies, focus- ing on subpopulations and settings to gain perspective on the state of the science and to help identify future goals (Marcus et al., 2006). Studies that focused on older adults and exercise found that short-term interventions, both indi- vidual and group, face-to-face and by phone, were effective in increasing physical activity when delivered as part of a multifaceted program of educational and cognitive-behav- ioral participation. Health education alone was ineffective in this population. Health-care personnel–recommended physical activity and an exercise prescription were effective in the short term. None of the studies reviewed had a long enough duration to measure persistence of effort (Marcus et al., 2006).

Patient Barriers

■ Lack of time ■ Perceived need for equipment ■ Perceived barrier to beginning exercise/physical

activity ■ Disability or functional limitation ■ Unsafe neighborhood or weather conditions ■ No parks or walking trails ■ Depression ■ High body mass index (BMI) ■ Lack of motivation ■ Interpersonal loss or signifi cant life event ■ Ignorance of what to do

Patient Facilitators ■ Social support ■ Positive self-effi cacy ■ Motivation to engage in physical activity ■ Good health, no functional limitations ■ Frequent contact with prescriber ■ Regular schedule, planned program ■ Satisfaction with program ■ Insurance incentive ■ Improvement in mobility or health condition ■ Staff (of exercise facility) support (Franco et al., 2015;

Lee et al., 2017 ; Simmonds et al., 2015)

Medical Contraindications for Exercise Therapy

■ Unstable angina ■ Uncompensated heart failure

■ Severe anemia ■ Uncontrolled blood glucose ■ Unstable aortic aneurysm ■ Uncontrolled hypertension or tachycardia ■ Severe dehydration or heat stroke ■ Low oxygen saturation

PLAN FOR INCORPORATING EXERCISE INTO PATIENT ENCOUNTER

The ACSM has designed a program for primary care pro- viders called Exercise is Medicine. The goal of this program is to counsel the patient at every visit to increase physical activity. In conjunction with the AHA, the ACSM has also issued guidelines for physical activity in older adults ( Nelson et al., 2007 ). These guidelines can be used to incorporate physical activity and exercise recommendations into patient encounters.

All authorities agree that whenever possible, older adults should engage in physical activities that strengthen muscles, maintain fl exibility, promote good balance, and are aerobic in nature; further qualifi cations include the development of a plan incorporating both preventive and therapeutic goals, and risk management and reducing sedentary lifestyle (Artinian et al., 2010; Chodzko-Zajko et al., 2009; National Institute on Aging, 2011; Nelson et al., 2007 ). The preferred amount of exercise is 30 minutes per day for 5 days a week of moderate exercise; if weight management is part of this, 60 minutes per day is advised (Villareal et al., 2016). This can be broken up into as little as 10-minute intervals throughout the day. Any increase in physical activity is desirable and has some value over sedentary behavior ( Nelson et al., 2007 ). If older adults with chronic health conditions cannot achieve the 150 minutes per week of aerobic activity recommended, they should be as physically active as possible within the constraints of their conditions and abilities (Chodzko-Zajko et al., 2009).

The initial Welcome to Medicare visit can focus on healthy lifestyle counseling, including assessment of current physical activity level and specifi c guidance or exercise prescription for the patient. In the case of a patient with disabilities or functional limitations, referral to physical therapy or a com- munity-based program targeting those with physical restric- tions is appropriate and more effective. For those who are already very active, an exercise physiologist or ACSM-certi- fi ed personal fi tness trainer can help them to maximize their program benefi ts. Following up at each visit will emphasize the importance of ongoing exercise in maintaining or pro- moting healthy aging. Health coaches from the insurance carrier can also be used to keep the patient engaged. Strate- gies, such as using motivational interviewing (LeTourneau & Goodman, 2014), can be helpful in persuading the patient to adopt a new behavior.

The annual Medicare wellness visit can also be used to reinforce or expand on the importance of lifestyle changes. Exercise prescriptions that are individualized to fi t the patient ’ s abilities and preferences are most likely to be imple- mented ( Lee et al., 2017 ; Zaleski et al., 2015). Actually

Chapter 3 ■ Exercise in Older Adults 21

handing the patient a program or exercise prescription is more effective than just speaking about it. Knowing resources that are available in the community for group exercise or individual walking programs is a valuable adjunct to coun- seling. Knowledge of Internet resources for computer-savvy patients is also helpful. Goal setting and self-monitoring by the patient are very effective. A clinician who is aware of some common excuses (e.g., lack of time, no equipment) can counter these with positive suggestions, such as acknowl- edging the 10-minute benefi t, using stairs in the home, or walking around the block.

Clinician judgment should be exercised in assessing the patient and prescribing an exercise routine. Major authori- ties agree that all adults who do not have symptoms and have no diagnosed chronic health condition, such as osteoarthri- tis, heart disease, or diabetes mellitus, do not need to consult with a health-care professional about increasing physical activity (Offi ce of Disease Prevention and Health Promotion, 2008). Patients with chronic conditions should consult a health-care provider for physical activity goals that are real- istic and safe (Physical Activity Guidelines Advisory Commit- tee, 2008). Healthy adult men over 45 years old and healthy women over 55 years old who are considering a vigorous exercise program need health-care provider screening and routine stress testing. Sedentary older adults and all adults with cardiac disease or strong risk factors should undergo screening and stress test if they are undertaking a vigorous exercise program ( Lee et al., 2017 ).

Examples of Common Health Conditions in Older Adults With Exercise Recommendations

HEALTH CONDITION: CONSIDER COMORBIDITIES FOR ALL

RECOMMENDED ACTIVITIES: START LOW INTENSITY, GO SLOW

COMMENTS: CONSIDER COMORBIDITIES FOR ALL

Osteoarthritis Walking, aquatic activities, tai chi, resistance

exercises, cycling

Vary type and intensity to avoid overstressing joints;

heated pool

Coronary artery disease Walking, treadmill walking, cycle ergometry Supervised program with BP and heart rate monitoring

Congestive heart failure Walking, treadmill walking, cycle ergometry Individualize to client; supervised program

Type 2 diabetes mellitus Resistive, aerobic, aquatic, recreational activities Proper shoe fi t; may need insulin reduction if insulin

dependent

Anxiety disorders Walking, biking, weight lifting If able to do high-intensity exercise, this benefi ts

anxiety

Depression Walking, cycling, recreational activities Group participation helpful to keep patient engaged

Fibromyalgia Aerobic, aquatic therapy, strengthening, tai chi, Pilates Heated pool, gentle stretches, counsel about possible

increased pain initially

Chronic obstructive

pulmonary disease

Cycle ergometer, treadmill walking; individualize Supervised program—consider pulmonary

rehabilitation program

Chronic venous insuffi ciency Walking, standing exercises Supervised program

Osteoporosis Weight-bearing exercises, weight training Assess balance and risk for falls before beginning

Parkinson ’ s disease Walking, treadmill walking, stationary bike, dancing,

tai chi, Pilates, boxing

Assess balance and risk for falls before beginning;

American Parkinson ’ s Disease Association resources

Peripheral arterial disease Lower extremity exercises, treadmill walking, walking Very short intervals initially, progress as tolerated

Age-related sleep disorders Tai chi, walking, aquatherapy, biking Assess balance and risk for falls before beginning

Dementia Walking, recreational activities Provide safe environment, assess fall risk and ability to

participate

Source: Adapted from Goodman, C., & Helgeson, K. (2011). Exercise prescriptions for medical conditions. Philadelphia: F.A. Davis.

KEY GUIDELINES FOR SAFE PHYSICAL ACTIVITY (PHYSICAL ACTIVITY GUIDELINES ADVISORY COMMITTEE, 2008)

To perform physical activity safely and reduce risk of injuries and other adverse events, people should:

■ Understand the risks and yet be confi dent that physical activity is safe for almost everyone.

■ Choose to do types of physical activities that are appro- priate for their current fi tness level and health goals, because some activities are safer than others.

■ Increase physical activity gradually over time whenever more activity is necessary to meet guidelines or health goals. Inactive people should “start low and go slow” by gradually increasing how often and how long activities are done.

■ Protect themselves by using appropriate gear and sports equipment, looking for safe environments, following rules and policies, and making sensible choices about when, where, and how to be active.

■ Be under the care of a health-care provider if they have chronic conditions or symptoms. People with chronic conditions and symptoms should consult their health- care provider about the types and amounts of activity appropriate for them.

22 Chapter 3 ■ Exercise in Older Adults

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

To promote and maintain health, older adults need moderate-intensity aerobic activity for a minimum of 30 min on 5 days each week or vigorous-intensity aerobic activity for a minimum of 20 min on 3 days each week.

A Nelson et al., 2007

To promote and maintain health and physical independence, older adults will benefi t from performing activities that maintain or increase muscular strength and endurance for a minimum of 2 days each week. It is recommended that 8–10 exercises be performed on two or more nonconsecutive days per week using the major muscle groups.

A Nelson et al., 2007

Participation in aerobic and muscle-strengthening activities above minimum recommended amounts provides additional health benefi ts and results in higher levels of physical fi tness.

A Nelson et al., 2007

To maintain the fl exibility necessary for regular physical activity and daily life, older adults should perform activities that maintain or increase fl exibility on at least 2 days each week for at least 10 min each day.

A Nelson et al., 2007

To reduce risk of injury from falls, community-dwelling older adults with substantial risk of falls (e.g., with frequent falls or mobility problems) should perform exercises that maintain or improve balance.

A Nelson et al., 2007 Lee & Kim, 2017

Older adults with one or more medical conditions for which physical activity is therapeutic should perform physical activity in the manner that effectively and safely treats the condition(s).

A Nelson et al., 2007 Lee & Kim, 2017

Older adults should have a plan for obtaining suffi cient physical activity that addresses each recommended type of activity. Those with chronic conditions for which activity is therapeutic should have a single plan that integrates prevention and treatment. For older adults who are not active at recommended levels, plans should include a gradual (or stepwise) approach to increase physical activity over time. Many months of activity at less than recommended levels is appropriate for some older adults (e.g., those with low fi tness), because they increase activity in a stepwise manner. Older adults should also be encouraged to self-monitor their physical activity on a regular basis and to reevaluate plans as their abilities improve or as their health status changes.

C Nelson et al., 2007

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about SORT evidence rating system, go to www. aafp.org/afpsort.xml .

SUMMARY ■ There is strong evidence from a variety of sources that increas-

ing physical activity in older adults will improve health and quality of life in both healthy adults and those with chronic health conditions (Avers, 2016; Bleijenberg et al., 2016; Dah- lin-Ivanoff et al., 2016; Fransen et al., 2016; Hupin et al.,

2015; Martinez-Gomez et al., 2017; Tarazona-Santabalbina, 2016). Primary care practitioners can play an important role in promoting physical activity for all older adult patients at every visit, using an individualized approach. Resources are available to assist with this effort; further research is needed regarding effective counseling methods and outcomes.

Chapter 3 ■ Exercise in Older Adults 23

REFERENCES Lee , S. H. , & Kim , H. S. ( 2017 ). Exercise interventions for preventing falls

among older people in care facilities: A meta-analysis . Worldviews on Evidence-Based Nursing , 14 ( 1 ), 74 – 80 .

C A S E S T U DY

A. G., a 72-year-old man, comes in for follow-up of laboratory test results. He has coronary artery disease (CAD), hypertension (controlled), impaired fasting glucose (IFG), benign prostatic hyperplasia, and mild degenerative joint disease (DJD). Since being diagnosed with IFG he has cut back on soda consumption and is also seeing a dietitian for counseling. He is a former smoker (last use 12 years ago) and admits to being a “couch potato.” Current medications: Lisinopril 20 mg orally (PO) daily, hydrochlorothiazide 12.5 mg PO daily, simvastatin 20 mg PO daily in the evening, and tamsulosin 0.4 mg PO daily. He has a prescription for nitroglycerin 0.4 mg sublingually as needed for chest pain but has never needed to use it. He occasionally takes Tylenol Arthritis Pain or Aleve if the DJD bothers him. Vital signs are blood pressure (BP) 134/72, heart rate (HR) 70 (reg), respiratory rate 18 breaths per minute (bpm) (afebrile), and BMI 34.2. Pulse oximetry is 99% on room air. Laboratory test results are unremarkable except for high-density lipoprotein (HDL) 32 and fasting blood sugar (FBS) 125. Mr. G expresses frustration at the lack of change in his fasting glucose

despite cutting back on soda. He asks you, “What else can I do? I don ’ t want to get diabetes.” You encourage him to increase his physical activity level gradually, beginning with walking.

1. What strategies will you use to promote increased physical activity in this patient?

2. What additional objective data will you be assessing for?

3. What national guidelines are appropriate to consider?

4. Will you need to order any tests before he begins this program? If so, what tests?

5. Are there any screening tools that you want to use?

6. What is your plan of care?

7. Are there any Healthy People 2020 objectives that you should consider?

8. What additional patient teaching may be needed?

9. How will you follow up on the planned increase in physical activity?

Nelson , M. E. , Rejeski , W. J. , Blair , S. N. , Duncan , P. W. , Judge , J. O. , King , A. C. , . . . Castaneda-Sceppa , C. ( 2007 ). Physical activity and public health in older adults: Recommendation from the American College of Sports Medicine and the American Heart Association . Medicine and Science in Sports and Exercise , 39 ( 8 ), 1435 – 1445 .

unit II Assessment

26

CHAPTER 4 Comprehensive Geriatric Assessment

Evelyn Duffy

Because older individuals represent a richly diverse popula- tion, the components of assessment may vary from person to person. People age at different rates and within one person organ systems age at different rates. Psychosocial adapta- tions, environmental supports, and functional ability can differ dramatically among individuals of the same chronolog- ical age. A comprehensive approach to geriatric assessment is recommended because the physical health of the older adult is inextricably related to functional ability, psychosocial health, and a safe and enabling environment. Older individ- uals who can benefi t the most from this approach are the vulnerable older adult (those at risk for decline) and the frail older adult (those already demonstrating decline). This pop- ulation has less physiological reserve and is at increased risk of iatrogenic complications. Comprehensive geriatric assess- ment (CGA) helps not only to diagnose treatable conditions and improve patient outcomes, but also to identify potentially preventable conditions. It facilitates the goal of patient-cen- tered care.

CGA has been defi ned as a multidimensional, interprofes- sional, diagnostic process to identify care needs, plan care, and improve outcomes for older people (Morley, Little, & Berg-Weger, 2017; Ramani, Furmedge, & Reddy, 2014). A recent Cochrane systematic review of inpatient CGA versus usual care of older adults admitted to acute care or inpatient rehabilitation concluded that older adults were more likely to be alive and in their own homes if they received a CGA (Ellis et al., 2017). These fi ndings were consistent with the work of Partridge, Harari, Martin, and Dhesi (2014) who noted that preoperative CGA is likely to positively impact postop- erative outcomes. CGA may be undertaken by an individual provider initially, with the interprofessional team called in for selected patients. Advanced practice nurses may be a part of a team that works together to complete a CGA, or may apply the concepts of CGA to their own patients. Domains of CGA include physical health, psychological health, socio-environ- mental supports, mobility, functional status, and measure of quality of life. A number of geriatric assessment instruments are focused on these domains. These tools can facilitate the assessment, diagnosis, and evaluation processes, and those

with the most clinical utility are highlighted in this chapter. Suggested dimensions within each CGA domain are identifi ed in Table 4-1 . Each of these domains is described in greater detail as follows.

PHYSICAL HEALTH

The physical assessment of the older adult includes all the components of a conventional medical history (chief com- plaint, history of present illness, past history, family and social history, and a review of systems), the conventional physical examination, and appropriate diagnostics based on the fi ndings. The approach to the physical assessment process, however, needs to be tailored to the older adult. Assessment begins with observation of the patient ’ s appear- ance, language, and behaviors. Does the individual look the stated age? Are they dressed appropriately? Is there evidence of neglect in self-care? What is the manner and content of speech? What behaviors are observed, including facial expressions, eye contact, gestures, or abnormal movements? If a family member or caregiver accompanies the patient, how do they interact?

Interviewing begins before the physical examination and typically continues throughout the examination. Many pro- viders send a geriatric history-taking form to the patient in advance so that they or their family can complete it and the details can be reviewed and expanded on during the visit. Any impairment in vision, hearing, speech, or cognition may affect the patient ’ s ability to communicate effectively. Impair- ments should be addressed and measures taken to accom- modate them during the visit, to prevent the common trap of talking to the family or caregiver rather than the older adult in order to facilitate the visit. The patient ’ s permission needs to be acquired before interviewing the family in most cases. The input of the family or caregiver may provide valu- able information about the patient ’ s behavioral or functional changes, which can indicate a change in the patient ’ s overall health status. It is important to address what the patient or

Chapter 4 ■ Comprehensive Geriatric Assessment 27

their family considers signifi cant, which often differs from what the provider considers signifi cant.

Many older adults suffer from multiple chronic diseases that require monitoring. There may not be a new chief concern, but if one is reported it is important to put it into the context of the patient ’ s previous health and illness. The history of chronic diseases should be identifi ed and updated with any symptoms of decompensation. If a new concern is identifi ed, a history of present illness is recorded using the seven dimensions of symptomatology as a guide (location and radiation, quantity and quality, aggravating and alle- viating factors, associated symptoms and signs, absence of associated symptoms and signs, evolution and course of the symptom, and effect of the symptom on normal daily activ- ities). After taking the history, the provider should summa- rize for the patient what was heard. This gives the patient the opportunity to clarify or deny any parts of the discussion.

Medication Medication review should be completed at every encounter. Because older adults are the population most likely to suffer from multiple chronic diseases, they are also most likely to take more medications, both prescribed and over the counter. The more medications a person is taking the more likely they are to have an adverse drug reaction. The most frequently used criteria for evaluating drug use are the Beers Criteria for Potentially Inappropriate Medication Use in Older Adults, fi rst published in 1991 and most recently updated in 2015 (Beers, 1997; American Geriatrics Society [AGS], 2015). A subse- quent scale was developed to address some of the limitations

of the Beers criteria, the Medication Appropriateness Index (Hanlon & Schmader, 2013; Hanlon et al., 1992; Table 4-2 ). It is a validated tool that can be used along with the Beers criteria to determine the appropriateness of prescribed medi- cations for older adult patients.

Appropriate prescribing often means that multiple med- ications are required for adequate management of chronic disease. Appropriate prescribing may actually require adding a medication, such as an angiotensin-converting enzyme (ACE) inhibitor for a patient with diabetes. Older versions of the Beers criteria had identifi ed limitations that led to the development of more explicit criteria, including the Screen- ing Tool of Older Persons’ Prescriptions (STOPP) and the Screening Tool to Alert Doctors to Right Treatment (START) (Gallagher et al., 2008). These tools address the issue of appropriate prescribing more specifi cally and are organized by organ system. The START tool includes medications that may need to be added, while the STOPP tool lists those that should be assessed for possible elimination. An updated version was published in 2015, STOPP/START Criteria for Potentially Inappropriate Prescribing in Older People: Version 2 (O’Mahony et al., 2015).

Examination The collection of objective data usually begins with the vital signs. These may be completed by ancillary staff, but any abnormalities need to be verifi ed by the provider. A common issue is the necessity to rule out orthostatic hypotension, which is prevalent in older adults due to volume depletion and medication effects. If concerns indicate the possibility of orthostatic drop, the provider needs to accurately measure the blood pressure (BP). The patient should lie down for 5 minutes and then have the BP and pulse rate measured. Have the patient stand and wait for a full minute, then repeat the BP and pulse rate measurements. Note any symptoms of light-headedness or dizziness and any drop in systolic BP greater than or equal to 20  mm  Hg or diastolic BP greater than or equal to 10  mm  Hg. An increase of heart rate of at least 30 beats per minute (bpm) is also abnormal. BP and pulse rate measurements should be repeated 3 minutes after standing, and if they have returned to baseline the patient has not demonstrated true orthostasis, but you will have con- fi rmed the cause of light-headedness or dizziness.

Pulse oximetry is now readily available in practice set- tings, and this gives a measure of oxygen saturation. If the respiratory rate is greater than 20 respirations per minute it is classifi ed as tachypnea and may be a sign of infection

Comprehensive Geriatric Assessment

DOMAINS OF COMPREHENSIVE GERIATRIC ASSESSMENT

DIMENSIONS OF COMPREHENSIVE GERIATRIC ASSESSMENT

Physical health History taking

Physical examination

Diagnostics

Nutritional assessment

Medication review

Functional health Activities of daily living

Instrumental activities of daily living

Sensory assessment (hearing, vision)

Gait and balance

Psychological health Cognitive disorders (delirium, dementia,

mild cognitive impairment)

Affective disorders (depression, anxiety)

Spiritual well-being

Socioenvironmental

supports

Social network and support

Living situation

Environmental safety

Economic resources

Quality of life measures Physical conditions

Social conditions

Environmental conditions

Personal resources (mental health, life

perspective)

Preferences for care

TABLE 4-1 Medication Appropriateness Index Criteria

Is there an indication for the drug?

Is the medication effective for the condition?

Is the dosage correct?

Are the directions correct?

Are the directions practical?

Are there clinically signifi cant drug–drug interactions?

Are there clinically signifi cant drug–disease/condition interactions?

Is there unnecessary duplication with other drugs?

Is the duration of therapy acceptable?

Is this drug the least expensive alternative compared with others of

equal usefulness?

TABLE 4-2

28 Chapter 4 ■ Comprehensive Geriatric Assessment

or sepsis, lung disease, heart failure, or a metabolic disorder. Weight is another measurement in which accuracy is import- ant, because it is a marker for both nutritional and fl uid status. Pain is the fi fth vital sign and quantifying pain can be accomplished in various ways, although older adults may prefer verbally descriptive scales.

The physical examination is of critical signifi cance in CGA. In examination of the older adult, functional assessment is as important as careful examination of each body system. In younger adults, neurological and musculoskeletal examina- tion may be less of a focus because health of those systems is obvious, but older adults may have unrecognized muscle weakness, limitations in range of joint motion, or contrac- tures requiring thorough examination. Sensory loss often precludes the ability of the older adult to live independently, and visual and hearing acuity is part of the functional assess- ment. Measured visual acuity (corrected with lenses) equal to or worse than 20/40 constitutes a visual impairment. Screen- ing for hearing loss can be accomplished using a handheld audiometer, which is more accurate than the whispered voice test. Abnormality in the six cardinal fi elds of gaze with nys- tagmus or lack of a downward gaze may reveal neurological disease. Otoscopic examination can identify cerumen impac- tion, a common cause of conductive hearing loss.

A comprehensive physical examination of the older adult is recommended, and a sample examination is identifi ed in Table 4-3 . After completing the examination, discuss the general fi ndings with the patient. Patient teaching should reinforce the positive behaviors taken to improve or maintain health and teach self-assessment and self-care management strategies.

Diagnostics Chapter 1 discusses the changes associated with aging that are refl ected in laboratory values. This section provides some general guidelines on when to order testing. The reader is referred to the disease sections of this text for more specifi c guidelines. Tests used to screen geriatric patients and tests used to aid in diagnosis have different objectives. Screening can be defi ned as the presumptive identifi cation of unrec- ognized disease or defect by the application of tests, exam- inations, or other procedures. The screening parameters for those over age 65 years, which include laboratory and diag- nostic testing, are covered in Chapter 2 , Health Promotion.

One of the considerations in ordering tests for diagnostic purposes is whether the test result will alter the diagnosis, prognosis, or management of a condition. Some guidelines for use of diagnostics in decision making include: What is the prevalence of the disease being screened for with the test?

Is the test necessary to make the diagnosis? Will the test be accepted and tolerated by the patient? Does the cost or benefi t of the test outweigh the risk? Is it the least invasive test avail- able? Can the results be interpreted? Will the results change the treatment of the patient? What is the sensitivity and spec- ifi city of the test?

To be of diagnostic value, a test for a given disease must produce patient results that differ substantially from normal results, as well as from results in patients with other diseases that may be mistaken for that disease. Even highly accurate tests produce false results when applied inappropriately and without a fi rm understanding of the concepts. Most import- ant, consider the test ’ s acceptability to the patient. This is especially signifi cant in the patient who cannot make a choice and give consent. In such individuals, a proxy is needed to gain permission to give the test. Although some patients may be unable to express themselves verbally, their behavior may give nonverbal expression to their feelings toward the test ’ s acceptability.

Nutritional Assessment Several age-associated changes infl uence the nutritional status of older adults. These primarily include the loss of lean body mass, a decrease in the basal metabolic rate, and an increase in body fat. Although overall caloric intake should decrease due to decreased metabolism and often decreased physical activity, certain nutrient needs may change as one ages. A nutrient-rich diet is required to meet these chang- ing needs. A nutritional assessment needs to be a part of the CGA, because inadequate intake is common in older adults. An estimated 5% to 30% of older adults living in the com- munity are malnourished; 23% to 60% of hospitalized older adults and 16% to 70% of those in long-term care facilities experience malnutrition (Guyonnet & Rolland, 2015).

Obesity is the most common nutritional disorder in the older adult living in the community, and undernutrition is most common in those in acute and long-term care facili- ties. The diagnosis of abnormal weight loss may be made if one or more of the following criteria are present: abnormal weight loss of 5% or greater in 1 month, 10% or greater in 6 months; body mass index (BMI) of less than 21 kg/m 2 ; and serum albumin concentration of less than 35 g/L (Guyonnet & Rolland, 2015). There are four components of nutritional assessment: 1) nutritional history using a validated tool; 2) food intake diary of 1 to 3 days; 3) physical assessment, including anthropometric measurements and signs of nutri- tional defi ciencies; and 4) biochemical markers, if applicable.

Screening for nutritional defi ciencies begins with the use of a standardized tool. Several assessment instruments have

Sample Focused Geriatric Physical Examination

SIGNS PHYSICAL SIGN OR SYMPTOM DIFFERENTIAL DIAGNOSES

Vital signs Blood pressure Hypertension Adverse effects from medication, autonomic dysfunction

Orthostatic hypotension Adverse effects from medication, atherosclerosis, coronary artery

disease

Heart rate Bradycardia Adverse effects from medication, heart block

Irregularly irregular heart rate Atrial fi brillation

Respiratory

rate

Increased respiratory rate >24 breaths

per min

Chronic obstructive pulmonary disease, congestive heart failure,

pneumonia

Temperature Hyperthermia, hypothermia Hyperthyroidism and hypothyroidism, infection

TABLE 4-3

Chapter 4 ■ Comprehensive Geriatric Assessment 29

SIGNS PHYSICAL SIGN OR SYMPTOM DIFFERENTIAL DIAGNOSES

General Unintentional weight loss Cancer, depression

Weight gain Adverse effects from congestive heart failure, medication

Head Asymmetrical facial or extraocular

muscle weakness or paralysis

Bell ’ s palsy, stroke, transient ischemic attack

Frontal bossing Paget disease

Temporal artery tenderness Temporal arteritis

Eyes Eye pain Glaucoma, temporal arteritis

Impaired visual acuity Presbyopia

Loss of central vision Age-related macular degeneration

Loss of peripheral vision Glaucoma, stroke

Ocular lens opacifi cation Cataracts

Ears Hearing loss Acoustic neuroma, adverse effects from medication, cerumen

impaction, faulty or ill-fi tting hearing aids, Paget ’ s disease

Mouth,

throat

Gum or mouth sores Dental or periodontal disease, ill-fi tting dentures

Leukoplakia Cancerous and precancerous lesions

Xerostomia Age-related, Sjögren ’ s syndrome

Neck Carotid bruits Aortic stenosis, cerebrovascular disease

Thyroid enlargement and nodularity Hyperthyroidism and hypothyroidism

Cardiac Fourth heart sound (S4) Left ventricular thickening

Systolic ejection, regurgitant murmurs Valvular arteriosclerosis

Pulmonary Barrel chest Emphysema

Shortness of breath Asthma, cardiomyopathy, chronic obstructive pulmonary disease,

congestive heart failure

Breasts Masses Cancer, fi broadenoma

Abdomen Pulsatile mass Aortic aneurysm

Gastro-

intestinal

Constipation Adverse effects from medication, colorectal cancer, dehydration,

hypothyroidism, inactivity, inadequate fi ber intake

Genital/

rectal

Fecal incontinence Fecal impaction, rectal cancer, rectal prolapse

Atrophy of the vaginal mucosa Estrogen defi ciency

Prostate enlargement Benign prostatic hypertrophy

Prostate nodules Prostate cancer

Rectal mass, occult blood Colorectal cancer

Urinary Urinary incontinence Bladder or uterine prolapse, detrusor instability, estrogen defi ciency

Extremities Abnormalities of the feet Bunions, onychomycosis

Diminished or absent lower extremity

pulses

Peripheral vascular disease, venous insuffi ciency

Heberden ’ s nodes Osteoarthritis

Swan neck deformity Rheumatoid arthritis

Pedal edema Adverse effects from medication, venous insuffi ciency, congestive

heart failure

Musculo-

skeletal

Diminished range of motion, pain Arthritis, fracture

Dorsal kyphosis, vertebral tenderness,

back pain

Cancer, compression fracture, osteoporosis

Gait disturbances Adverse effects from medication, arthritis, deconditioning, foot

abnormalities, Parkinson ’ s disease, stroke

Leg pain Intermittent claudication, neuropathy, osteoarthritis, radiculopathy,

venous insuffi ciency

Muscle wasting Atrophy, malnutrition

Proximal muscle pain and weakness Polymyalgia rheumatica

Skin Erythema, ulceration over pressure

points, unexplained bruises

Anticoagulant use, elder abuse, idiopathic thrombocytopenic

purpura

Premalignant or malignant lesions Actinic keratoses, basal cell carcinoma, malignant melanoma,

pressure ulcer, squamous cell carcinoma

Neurological Tremor with rigidity Parkinson ’ s disease

Source: From Elsay, B., & Higgins, K. E. (2011). The geriatric assessment. American Family Physician, 83 (1), 48–56.

Sample Focused Geriatric Physical Examination—cont’d TABLE 4-3

30 Chapter 4 ■ Comprehensive Geriatric Assessment

clinical utility in the nutritional evaluation of older adults. The Mini Nutritional Assessment Instrument, a tool that can identify older adults who have or are at risk for malnutri- tion, and the Nutrition Health Checklist, part of the Nutri- tional Screening Initiative project by the American Academy of Family Medicine, the American Dietetic Society, and the National Council on Aging for healthy older adults, are the two most often used and available online. A food diary com- pleted by the patient and reviewed by the provider can help to identify both the quantity and the quality of food and fl uid intake. MyPlate for Older Adults serves as a guide for evalua- tion ( Figure 4-1 ).

The physical examination may reveal some indicators of malnutrition, including weight loss, muscle wasting, dry and dull hair, mental impairments, and poor wound healing. In addition to calculating the BMI, there are other noninva- sive, quantitative techniques for determining an individual ’ s body fat composition by measuring, recording, and analyzing specifi c dimensions of the body (height and weight, skinfold thickness, and bodily circumference).

There is no gold standard for biomarkers of nutritional defi ciencies in the older adult, but some indicators include pre- albumin, transferrin, albumin, chemistries, complete blood count (CBC), vitamin B 12 , folate, 25(OH) vitamin D, and thyroid panel. As the understanding of the role of pro-in- fl ammatory cytokines on the acute phase protein response, albumin cannot be used as the sole indication of malnu- trition. The presence of infl ammation needs to be consid- ered when interpreting serum albumin results. A C-reactive protein can help to determine if malnutrition is the result of lack of intake or due to infl ammation and hypercatabolism (Guyonnet & Rolland, 2015).

FUNCTIONAL HEALTH

Although functional decline is common with advanced aging, the two are not synonymous. Although functional decline occurs in every system, the distinction between func- tional usual aging and functional successful aging remains

FIGURE 4-1. MyPlate for Older Adults. Copyright 2011, Tufts University. For details about MyPlate for Older Adults, please see http://www.nutrition.tufts.edu/research/myplate-older-adults .

Chapter 4 ■ Comprehensive Geriatric Assessment 31

unclear. The goal in geriatric care is to improve function, if possible, and, if not, to prevent functional decline or at least slow down the process of functional deterioration. The parameters of function include both activities of daily living (ADLs) and instrumental activities of daily living (IADLs). Basic ADLs include three components: basic self-care, mobil- ity, and continence. IADLs measure community interactions within the home and outside the home ( Table 4-4 ).

Two well-established tools used to evaluate function in older adults are the Katz Activities of Daily Living Scale (Katz et al., 1963) and the Lawton and Brody Scale for Instrumen- tal Activities of Daily Living (Lawton & Brody, 1969). It is important to be cautious about self-report of function (rather than direct observation of function) and to ask, “How do you . . . ?” or “Show me how you. . . .” instead of “Can you . . . ?” in order to determine if patients actually perform the activity. Bathing is often the fi rst ADL that poses problems for older adults.

Falls are a leading cause of death and disability in the older adult, and assessment of both intrinsic and extrinsic factors contributing to falls is important. Ask yourself the question, “Why did this patient fall today?” A valid tool for assessment of falls is the Hendrich II Fall Risk Model, which is useful in acute care, ambulatory, assisted living, long-term care (Hen- drich, Bender, & Nyhuis, 2003). In addition to identifying those at risk for falls, it helps to identify appropriate interven- tions to reduce their fall risk. Mobility can be screened with the Timed Get Up and Go Test. This test involves observing for unsteadiness as the patient gets up from a chair without using the arms, walks 10 feet, turns around, walks back, and resumes a seated position. Timing the process, which should take less than 16 seconds, enhances the sensitivity of this test (Podsiadlo & Richardson, 1991). Patient diffi culties perform- ing this test indicate mobility issues, weakness of the extrem- ities, and an increased risk for falling. Tinetti ’ s Performance Oriented Mobility Assessment is a task-oriented test that measures gait and balance abilities (Tinetti, 1986).

PSYCHOLOGICAL HEALTH

Cognitive and affective disorders, specifi cally dementia, delir- ium, and depression, are more prevalent in older adults, and

clinical defi nitions of these disorders are addressed in the Diagnostic and Statistical Manual of Mental Health Disorders (DSM), 5th ed. (2013). The DSM-5 describes the character- istics of delirium and mild or moderate neurocognitive dis- orders. There are a number of validated tools used to screen for cognitive dysfunction. For years the gold standard was the Mini Mental Status Examination (MMSE), but more recent tools have all been validated against that standard. Three tools used in clinical settings have comparable psychometric properties to the MMSE: the Mini-Cog, Montreal Cognitive Assessment (MoCA), and Saint Louis University Mental Status Examination (SLUMS) (Cummings-Vaugh et al., 2014; Tariq et al., 2006; Tsoi et al., 2015). The primary advantage of the Mini-Cog is that it is shorter than the MMSE and measures executive function. It is composed of a three-item recall and the Clock Drawing Test (CDT) and takes about 3 minutes to administer (Borson et al., 2011). Both the MoCA and SLUMS have comparable specifi city and sensitivity to the MMSE, but are better at identifying mild neurocognitive disorder and are available online; unlike the MMSE, which is copyrighted.

Older adults are at greater risk of delirium, which is under-recognized and underdiagnosed. There are a number of instruments designed to screen for delirium; however, the best evidence supports the use of the Confusion Assessment Method (CAM), which takes 5 minutes to administer (Inouye et al., 1990). The CAM diagnostic algorithm is based on four cardinal features of delirium: 1) acute onset and fl uctuat- ing course, 2) inattention, 3) disorganized thinking, and 4) altered level of consciousness (Shi, Warren, Saposnik, & Mac- Dermid, 2013).

Depression is also under-recognized in older adults. There are several screening tools for depression, though the most widely used in the clinical practice is the Geriatric Depression Scale: Short Form (GDS:SF). It consists of 15 questions requir- ing a “yes” or “no” response, so it can be completed quickly in any setting (Sheikh & Yesavage, 1986). It has been suggested that a single question sensitive to depression, such as “During the past 4 weeks, how often did you feel downhearted and depressed?” be the fi rst step in screening (Le Strat & Duber- tret, 2013). The PHQ-9 is a nine-item depression scale of the Patient Health Questionnaire that assesses depressive symp- toms and functional impairment, and screens for symptom severity (Kroenke & Spitzer, 2002).

A recent implementation of a program to improve the quality of spiritual care validated the use of three instru- ments: HOPE, FICA, and SPIRIT. These tools are effective means of determining the older patient ’ s spiritual beliefs and the comfort associated with these beliefs (Piotrowski, 2013). In that program, they chose to use the HOPE questionnaire with one additional question, “Are you at peace?”

HOPE (Anandarajah & Hight, 2001)

■ Sources of H ope, meaning, comfort, strength, peace, love, and connection

■ O rganized religion ■ P ersonal spirituality and practice ■ E ffects on medical care and end-of-life issues

FICA (Puchalski & Romer, 2000)

■ F aith or belief ■ I mportance or infl uence ■ C ommunity ■ A ddress

Selected Elements of Functional Independence/Dependence

ADLs IADLs

Bathing Food preparation

Dressing Household chores

Toileting Laundry

Feeding oneself Managing medications

Move from bed to a standing position or

chair

Using the telephone

Ability to walk with or without assistive

device

Managing fi nances

Continence of urine Shopping

Continence of stool Transportation

TABLE 4-4

32 Chapter 4 ■ Comprehensive Geriatric Assessment

SPIRIT (Ambuel, 2005)

■ S piritual belief system ■ P ersonal spirituality ■ I ntegration with a spiritual community ■ R itualized practice and restrictions ■ I mplications for medical care ■ T erminal event planning

SOCIOENVIRONMENTAL SUPPORTS

Social isolation in community-dwelling older adults is all too common. Estimates are as high as 43%, ranging from 10% to 43% (Nicholson, 2012). Social isolation has been shown to contribute to all-cause mortality. While social isolation is not always assessed in the primary care setting, it should be an essential component of a CGA. A valid instrument that is clinically practical in assessment of social support is the Lubben Social Network Scale—6-item version (Lubben et al., 2006). This validated scale can be an important contribution to the assessment of family and friendship relationships, and identifi es patients at risk for social isolation who can benefi t from intervention. In 1995, Kane recommended including the following statements in a geriatric assessment to help improve understanding of the patient ’ s social support:

■ Is there any one special person you could call or contact if you need help? (If yes, identify.)

■ In general, other than your children, how many rela- tives do you feel close to and have contact with at least once a month? (Number.)

■ In general, how many friends do you feel close to and have contact with at least once a month? (Number.)

Additional social and economic resources are assessed by exploring the following:

■ Living situation ■ Housing ■ Transportation ■ Income ■ Assets ■ Degree of fi nancial burden resulting from health

concerns

QUALITY OF LIFE MEASURES

Quality of life in aging individuals involves identifying the per- son’s general satisfaction with life in a number of the domains identifi ed in the CGA. The Medical Outcomes Study—Short- Form 36 (Stewart & Ware, 1992) is a tool that looks at three of these: the physical, mental, and social domains. Although not specifi cally designed for the older adult, it remains the gold standard of quality of life instruments because of its longevity, applicability, and ease of administration and anal- ysis. A fi nal assessment involves having a frank discussion with the older adult about preferences for care at present and at end of life, and encouraging the patient to complete an advance directive so these preferences are documented.

SUMMARY ■ CGA is a multidimensional process designed to identify care

needs, plan care, and improve outcomes for older adults. The domains of CGA include, but are not limited to, physical health, functional status, psychological health, socioenviron- mental supports, and measures of quality of life. This chapter covered both the tools and techniques that can be used to conduct a CGA and also highlighted the supportive research where it exists. The evidence of the value of CGA in general has been inconsistent. The evidence is clear that parts of the CGA do improve certain outcomes in older patients, but con- tinued rigorous research is indicated.

CLINICL RECOMMENDATION EVIDENCE RATING REFERENCES

The evidence is insuffi cient to assess the balance of benefi ts and harms of screening for hearing loss in asymptomatic older adults.

C Moyer for USPSTF, 2012a

Evidence shows that the benefi t of mammography screening increases with age, with women between 50 and 74 years old benefi ting the most. The best balance of benefi t to harm is when screening every 2 years. For women over 75 years old, evidence is insuffi cient and decision should be on an individual basis.

A Siu for USPSTF, 2016

For adults over age 65 who do not present with vision problems, evidence is insuffi cient to recommend screening in older adults.

C Chou et al. for USPSTF, 2016

The American Academy of Ophthalmology recommends every 1- to 2-year screening for older adults, while the American Optometric Association recommends screening annually.

C Teutsch, McCoy, Woodbury, & Welp, 2016

Chapter 4 ■ Comprehensive Geriatric Assessment 33

REFERENCES Chou , R. , Dana , T. , Bougatsos , C. , Grusing , S. , & Blazina , I. ( 2016 ).

Screening for impaired visual acuity in older adults updated evidence report and systematic review for the U.S. Preventive Services Task Force (USPSTF) . Journal of the American Medical Association , 315 ( 9 ), 915 – 933 . doi:10.1001/jama.2016.0783 .

Moyer , V. A. on behalf of the U.S. Preventive Services Task Force . ( 2012a ). Screening for hearing loss in older adults: U.S. Preventive Services Task Force recommendation statement . Annals of Internal Medicine , 157 ( 9 ), 655 – 661 . doi:10.7326/0003-4819-157-9-201211060-00526 .

Moyer , V. A. on behalf of the U.S. Preventive Services Task Force . ( 2012b ). Screening for prostate cancer: U.S. Preventive Services Task Force recommendation statement . Annals of Internal Medicine , 157 ( 2 ), 120 – 134 . doi:10.7326/0003-4819-157-2-201207170-00459 .

Qaseem , A. , Barry , M. J. , Denberg , T. D. , Owens , D. K. , & Shekel , P. ( 2013 ). Screening for prostate cancer: A guidance statement from the clinical

guidelines committee of the American College of Physicians . Annals of Internal Medicine , 158 ( 10 ), 761 – 769 .

Siu , A. L. on behalf of the U.S. Preventive Services Task Force . ( 2016 ). Screening for breast cancer: U.S. Preventive Services Task Force recommendation . Annals of Internal Medicine , 164 ( 4 ), 279 – 296 . doi:10.7326/0003-4819-151-10-200911170-00008 .

Teutsch , S. M. , McCoy , M. A. , Woodbury , R. B. , & Welp , A. ( Eds .). ( 2016 ). Toward a high-quality clinical eye and vision service delivery system. Making Eye Health a Population Health Imperative: Vision for Tomorrow ( pp . 325 – 379 ). Washington, DC : National Academies Press .

U.S. Preventive Services Task Force . ( 2011 ). Screening for osteoporosis: U.S. Preventive Services Task Force recommendation statement . Annals of Internal Medicine , 154 ( 5 ), 356 – 364 . doi:10.7326/0003-4819-154 -5-201103010-00307 .

CLINICL RECOMMENDATION EVIDENCE RATING REFERENCES

Women age 65 years and over, and younger women whose fracture risk is equal to theirs with no additional risk factors, should be screened for osteoporosis with dual-energy x-ray absorptiometry of the femoral neck.

B USPSTF, 2011

The USPSTF previously recommended against PSA-based screening in men over age 75, but they now recommend against PSA screening in all age groups.

C Moyer for USPSTF, 2012b

The American College of Physicians concurred with the recommendation.

C Qaseem et al., 2013

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

34

CHAPTER 5 Symptoms and Syndromes

Evelyn Duffy

ASSESSMENT

Assessment of a symptom based on the presentation of a concern or an evaluation of a geriatric syndrome in the older adult poses challenges to the health-care provider. Using a change in function as a measure of the impact of a symptom on the patient is an effective means of sorting out the dif- ferential. Heterogeneity increases with age, so there are a greater number of possibilities to consider in formulating a diagnosis, and the differential diagnosis can be quite broad. Working up a geriatric patient with a single symptom or cluster of symptoms using typical symptom analysis and clin- ical decision-making tools can be done, but it is often compli- cated by the fact that patients may ignore symptoms initially because they do not interfere with functional activities or because they attribute the symptoms to the aging process. Conversely, patients may fear loss of independence related to a subtle decline in functional abilities and deliberately choose to conceal this, or they may be unaware of a subtle decline until it becomes apparent to others.

Acuity of symptoms may be blunted because of changes in the effi ciency of certain physiological mechanisms. New symptoms often appear in one organ system as an offshoot of pre-existing disease in another organ system. Multiple symptoms may be present because of comorbidities. These factors can result in a delayed or atypical presentation. In many cases, the fi rst hint of illness may be a change in cog- nitive function or mental status. In the case of the patient with an underlying dementia, the refusal to eat or drink, or a

change in the patient ’ s behavior, may signal an acute illness. The term geriatric syndrome refers to conditions that have multiple underlying factors that may involve multiple organ systems; some of the most common are delirium, falls, diz- ziness, and incontinence. The literature refl ects that shared risk factors across geriatric syndromes include older age, cognitive impairment, functional impairment, and impaired mobility. For each presenting symptom, the following descrip- tors should be used to guide the diagnosis:

■ Mode of onset of the symptom (events coinciding with onset, similar past episodes, gradual or sudden, total duration)

■ Location of the symptom ■ Character of the symptom ■ Radiation of the symptom ■ Precipitating or aggravating factors ■ Relieving or ameliorating factors ■ Past treatment or evaluation (when, where, who;

studies done and results) ■ Course of the symptom ■ Effect of the symptom on normal daily activities

If the symptom or the patient ’ s demeanor indicates a problem in function or cognition, assess these areas. Perform a thorough medication history, including the use of over-the- counter (OTC) preparations, vitamins, herbal and homeo- pathic remedies, and any other dietary supplements, and consider their use in formulating diagnostic possibilities. Pharmacotherapeutic or other treatment modalities can complicate or even cause illness in older patients.

BOWEL INCONTINENCE

Description: Bowel incontinence or fecal incontinence (FI) is an involuntary passage of stool or the inability to control stool from expulsion. There are three types of FI: 1) urge incontinence: a person has a desire to defecate but cannot make it to the toilet despite attempts to avoid defecation; 2) passive incontinence: involuntary loss of gas or stool without

awareness; and 3) fecal seepage-leakage of stool after a normal bowel evacuation, usually presenting staining of clothing ( Shah et al., 2012 ). This condition can be costly due to use of adult briefs, as well as greater incidence of nursing home placement of individuals with FI (Taminini et al., 2015). It can also be a socially and emotionally devastating

Chapter 5 ■ Symptoms and Syndromes 35

situation that interferes with quality of life and leads to diminished self-esteem and depression.

Etiology: Defecation involves a complex series of events and factors: diet, stool consistency, anorectal sensation, muscle strength and function, as well as neurological integrity, cognition, and motivation ( Shah et al., 2012 ). The ability to defecate has two components: continence and defeca- tion. Continence is the ability to hold fecal material and is under the control of the autonomic and spinal cord nervous system, including the internal and external anal sphincter. Defecation is the evacuation of feces when a person con- sciously attempts to have a bowel movement ( Shah et al., 2012 ). FI occurs due to a number of reasons, from gastro- intestinal (GI) issues to cognitive or neurological diseases. A greater concern exists in a patient who is continent of urine but incontinent of stool. See Table 5-1 for a review of causes of fecal incontinence.

Occurrence: Prevalence in community-dwelling elders is 36% and up to 65% in nursing home residents. In the hospi- talized setting, there is reported to be 16% prevalence ( Shah et al., 2012 ).

Age: FI is found more frequently in older adults than in the general population.

Gender: FI occurs more commonly in women than men due to delivery of large babies or from obstetrical trauma related to childbirth ( Shah et al., 2012 ).

Ethnicity: Not signifi cant.

Contributing Factors: There are certain epidemiological risk factors in the older individual associated with FI. In men, kidney disease and urinary incontinence were associated with FI, and in women, depression, urinary incontinence, and chronic diarrhea were associated with FI ( Shah et al., 2012 ).

Diarrhea from GI disease (colitis, irritable bowel syndrome [IBS]), infectious causes such as viral gastroenteritis or Clos- tridium diffi cile (C diff), or medication side effects can contrib- ute to acute, short-term bowel incontinence. C diff infections occur when a person is exposed to the pathogen while receiv- ing antibiotic treatment for another illness (Keller et al., 2014). Antibiotics suppress the normal bacteria in the colon, allowing malabsorbed carbohydrates or C diff to fl ourish,

producing toxins that cause a severe diarrhea. Damage to the colon can cause the individual to become septic and possibly cause death, especially in the older patient (Roos, 2015).

Signs and Symptoms: The fi rst step in the clinical appraisal is to inquire about bowel habits, including incidence of diarrhea and fecal continence. Determine the duration, fre- quency, severity, and character of the incontinence (gas, liquid, solid). Inquire if there is sensation of rectal fullness, awareness of passing stool or gas, and warning symptoms of cramping or urgency. Associated symptoms of abdomi- nal pain and bloating, anorexia, diarrhea or constipation, nausea and/or vomiting, rectal bleeding, and urinary incon- tinence should be ascertained. Review prescription and OTC medications carefully. Past medical history may be positive for diabetes, neurological and psychiatric diseases, GI dis- orders, cancers with radiation, and any condition limiting mobility. Surgical history may include hemorrhoidectomy, anal fi ssure repair, fi stulectomy, anal dilation, or colon resec- tion. Diet review may reveal high fi ber intake and excessive fl uid intake or foods that may cause irritation and worsen FI such as caffeine, alcohol, chocolate, greasy or spicy foods, dairy products, and various raw fruits and vegetables.

Physical examination includes assessing for signifi cant weight loss. The abdomen should be examined for disten- tion, hyperactive or absent bowel sounds, pain, masses, and bladder distention. The perineum is inspected for gaping of anus, an indication of severe sphincteric dysfunction, hem- orrhoids, dermatitis, surgical scars, fi ssures, and fi stulas. The clinician should check the “anal wink” (the refl ex contrac- tion of the anal sphincter when the skin around the anus is stroked bilaterally) to test sensation and pudendal nerve func- tion. Asking the patient to bear down will reveal rectal pro- lapse, if present. The digital rectal examination is performed to detect hemorrhoids or masses, and evaluate baseline and squeeze sphincter tone, as well as the amount and character of stool. Neurological examination includes assessment of gait, general mobility, motor strength, and sensory testing.

Diagnostic Tests: The results of data collected from the history and physical examination will dictate if additional testing is needed. Categorize the diarrhea as infl ammatory, fatty, or watery. When an infectious or foodborne cause is suspected, stool tests guided by the clinical presentation are indicated. Exclusion of fecal impaction, particularly in

Causes of Fecal Incontinence

DISEASE MECHANISM COMMENTS

Central Nervous System

Dementia Impairs awareness of need to defecate

Loss of inhibitory control

Manifestations depend on type and severity of dementia

Stroke Impaired awareness of anal control

Slowed motor processing communication with

frontal lobe damage

Dependent on size of infarct or hemorrhage within the brain

Brain tumor Similar to stroke Dependent on location of tumor

Multiple sclerosis Decreased external anal sphincter pressures

leading to decreased volumes of rectal

distention to inhibit the internal anal sphincter

TABLE 5-1

Continued

36 Chapter 5 ■ Symptoms and Syndromes

Causes of Fecal Incontinence—cont’d TABLE 5-1

Peripheral Nervous System

Cauda equina syndrome Compression of spinal nerves

Polyneuropathies Various mechanisms leading to destruction of

the axon and myelin

Causes include infection, autoimmune disease, hypothyroidism,

vitamin B 12 defi ciency, and medications

Diabetes mellitus Neuropathy of sensory and motor nerves

Internal anal sphincter dysfunction

Shy Drager syndrome Multisystem atrophy

Toxic neuropathy Destruction of nerve cells leading to loss of

sensation or motor control

Chemotherapy and radiation therapy

Traumatic neuropathy Chronic straining during evacuation

External anal sphincter weakness or pudendal

nerve neuropathy

Fecal impaction Altered rectal sensation

Liquid stool escaping around solid feces in colon

or higher in bowels

Gastrointestinal (GI)

GI disease GI dysfunction/disease with excessive stool

volume and rapid gut transit

Causes include viral or bacterial gastroenteritis, colitis, Crohn ’ s

disease, celiac disease, colon cancer, irritable bowel syndrome,

rectocele, and other GI diseases

* Clostridium diffi cile can cause severe diarrhea in the elderly and can lead to death

Rectal sphincter

dysfunction

Anal sphincter damage and/or pudendal

neuropathy affecting sphincters, puborectalis

muscle, and rectal sensation

Common causes include delivery of large baby, traumatic

childbirth, anal surgery, rectal prolapse, and prolonged

straining

Reservoir incontinence Loss of compliance of the rectal wall leading to

urgency, frequency, and leakage of stool

Associated with colectomy, infl ammatory bowel disease, chronic

rectal ischemia, and prostate/cervical radiation

Diminished colonic/rectal capacity is a less common type of FI

Medications

Laxatives Medications causing increased gastric motility or

increased water in stools

Fiber products Increase fl uid in the stool to keep it soft and

move easier but can lead to diarrhea and FI

Magnesium Draws fl uid into the bowels through osmosis Magnesium containing antacids and certain laxatives contain

signifi cant amounts of magnesium

Other medications Antibiotics can cause destruction of the colon ’ s

natural fl ora, leading to diarrhea

Other medications that can cause diarrhea

include proton pump inhibitors, SSRIs, and

NSAIDs

Other

Physical defi cits Inability to recognize need to defecate (cognitive

problems) or inability to ambulate to toilet

without assistance

Common causes of cognitive problems include dementia

Common causes of mobility problems include debilitating

arthritis, hemiplegia, or any condition affecting gait

Dietary causes Foods in susceptible individuals include a diet

high in fi ber, spicy foods, fatty/greasy foods,

cured meats, smoked meats, dairy products,

caffeine, or sorbitol

Sugar-free gum and artifi cial sweeteners can cause diarrhea and

FI

Avoidance of irritating foods can eliminate the FI

Obesity Inability to ambulate to defecate This is usually a reversible condition

Excessive fl uid intake Overhydration can lead to diarrhea and possibly

cause FI

Source: Barr & Smith ( 2014 ); Keller & Surawicz (2014); Nodrqvist (2014); Shah et al. ( 2012 ); Sweetser ( 2012 ).

DISEASE MECHANISM COMMENTS

Chapter 5 ■ Symptoms and Syndromes 37

nursing home patients, is essential. Plain abdominal radio- graph may show a high impaction when no hardened stool is felt in the rectal vault. If organic bowel disease is suspected (infl ammatory disease, ischemic colitis, neoplasm), stools for occult blood, fl exible sigmoidoscopy or colonoscopy is indicated. Anorectal manometry tests rectal sensation and compliance through the use of an intrarectal balloon and measures pressure, tone, and refl ex contraction of the inter- nal sphincter. It provides comprehensive information about anorectal function and is reasonable in the ambulatory and/ or healthy elder who has failed conservative interventions. Other tests that may be considered include colonoscopy, elec- tromyography, anal ultrasound, and magnetic resonance imaging (MRI).

Differential Diagnosis: The differential diagnosis includes fecal impaction, gastroenteritis, foodborne illness, ruptured diverticulum, infl ammatory bowel disease, ischemic colitis, irritable bowel syndrome, anal fi stula, diabetic neuropathy, rectal prolapse, upper motor neuron lesions secondary to cerebrovascular accident, multiple sclerosis, spinal cord com- pression, degenerative processes, dementia, depression with self-care defi cits, and functional impairment.

Treatment: Elimination of potentially offending agents is an important fi rst step. Fecal impaction requires disimpaction (manually, with enemas, and/or osmotic/stimulant laxatives) and establishment of a preventive bowel regimen (see section on constipation). With loose or liquid stools, a supplement of soluble dietary fi ber may be benefi cial (adding more bulk to stools); the ideal amount and type have yet to be deter- mined, and response varies greatly. Increasing fi ber gradually over a period of several days can help reduce symptoms of abdominal bloating and discomfort that may be associated with increased fi ber intake. In the setting of fecal reservoir incontinence, avoidance of dietary fi ber may be indicated. Habit training may be effective for elders with dementia and involves frequent and regular toileting, usually after a meal to take advantage of the gastrocolic refl ex. Once infection is ruled out, fecal impaction is excluded, and no clear cause is determined for FI with diarrhea, the antidiarrheal medication

Imodium (loperamide) may be tried. For rectosphincter dys- function, biofeedback with sphincter-strengthening exercises is an option for motivated, cognitively intact elders who have some degree of rectal sensation. Sacral nerve stimulation is also a promising, safe, minimally invasive treatment of FI related to rectosphincter dysfunction. Surgical sphincter repair may be considered when incontinence is severe, unre- sponsive to conservative interventions, and clearly related to anatomical defects, with best outcomes seen with repair of defi ned defects in the external sphincter.

Follow-Up: Follow-up is indicated to assess resolution of FI and the time frame will be dictated by the identifi ed cause, as well as the severity of the problem. Ongoing monitoring is needed in all cases.

Sequelae: Complications of FI include perineal dermatitis, pressure ulcers in the sacral/perineal area, non-healing wounds, recurrent urinary tract infections (UTIs), anxiety, social isolation, and depression. FI, along with urinary incon- tinence, is a leading cause of institutionalization of elders.

Prevention/Prophylaxis: Manage constipation. Optimize treat- ment of underlying medical conditions, such as diabetes and GI disturbances. Adjust diet and laxative use to address loose stools. Consider physical therapy/occupational therapy (PT/ OT) intervention to address mobility and toileting ability. Reinforce a regular toileting program for the cognitively impaired and physically frail.

Referral: Urgent spinal imaging/neurosurgical consultation for new-onset fecal/urinary incontinence with lower extrem- ity weakness and paresthesia to rule out spinal cord compres- sion. Additional evaluation with “alarm” symptoms: change in bowel habits, rectal bleeding, weight loss to rule out GI malignancy.

Education: Provide clear information on normal bowel func- tion, FI cause, and rationale for any diagnostic tests, pre- ventive strategies, and treatments. Instruct in appropriate dilution and need for adequate fl uid with fi ber supplements. Direct to appropriate resources for incontinence pads and briefs as needed.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

With loose or liquid stools, a supplement of soluble dietary fi ber may be benefi cial.

A Shah, Chokhavatia, & Rose, 2012

Habit training may be effective for elders with dementia and involves frequent and regular toileting.

B Nordqvist, 2014

Antidiarrheal medications, such as loperamide (drug of choice) and diphenoxylate, may be considered.

A Shah, Chokhavatia, & Rose, 2012

Provide biofeedback with sphincter-strengthening exercises.

B Shah, Chokhavatia, & Rose, 2012

Stimulate the sacral nerve. A Shah, Chokhavatia, & Rose, 2012

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

38 Chapter 5 ■ Symptoms and Syndromes

Description: Acute, nontraumatic chest discomfort, perceived as pain or as a sensation of tightness, pressure, or squeezing in the chest or thorax area; associated with actual or poten- tial tissue or organ damage.

Etiology: The many different pathophysiologies of chest pain (CP) may be attributed to segmental overlap of neurons of cardiopulmonary and noncardiopulmonary origin. CP may originate from organs within or outside of the thorax; cardiac, pulmonary, esophageal, large vessel, gastric, pancreas, biliary, musculoskeletal, skin, and psychological pathology may be implicated. Life-threatening or high acuity causes include acute coronary syndrome (ACS) (includes acute myocardial infarction [MI] and unstable angina), aortic aneurysm, tho- racic aortic dissection, spontaneous tension pneumothorax, pneumonia, pulmonary embolism, esophageal perforation, and esophagitis. Lower acuity causes of CP can be stable angina, pericarditis, myocarditis, gastroesophogeal refl ux disease/gastro-peptic, biliary disease, costochondritis, rib fracture/trauma, and herpes zoster (Gupta & Munoz, 2016).

Occurrence: CP is one of the most common causes of emer- gency department visits, with more than 6 million people evaluated yearly. Of those 6 million visits, approximately 15% are over the age of 65 years (Goldwater, 2014).

Age: The U.S. Census Bureau predicts that by the year 2030, 71 million Americans will be over 65 years of age and by 2050, almost 81 million Americans will be age 65 years or older (Goldwater, 2014). The probability for serious condi- tions increases with chronological age due to increasing prev- alence of coronary artery disease (CAD), hypertension, lung cancer, cardiac arrhythmias, diabetes, and conditions asso- ciated with immobilization. Age is a number and the geriat- ric population can be further defi ned as elderly (between 75 and 84 years old) and very elderly (85 years of age or older) (Goldwater, 2014). Associated with age is the assessment of frailty. One does not need to be old to be frail, but frailty will occur with aging and frailty must be considered when treat- ment modalities for CP are considered.

Gender: Atypical presentation of ACS is more common in females, the older adult, and the very older adult.

Ethnicity: African Americans report less typical anginal fea- tures than Caucasians. Hispanic women with MI report more prodromal chest pain/discomfort than African Americans and Caucasians. Studies show ethnicity and time to seek medical care for CP increases in many ethnic minorities. African Americans, Asians, Hispanics, and South Asians take longer than those of majority populations to seek care for CP.

Contributing Factors: Esophageal disease not only can mimic, but also coexists with MI in 50% of elders with CAD. A recent heavy, fatty meal can exacerbate refl ux esophagitis. Panic dis- order with a prevalence of 0.1% to 1.0% may manifest with hyperventilation, which has been linked to coronary artery and esophageal spasm. Medications, illicit drugs (metham- phetamines, cocaine, caffeine, stimulants), and prescriptions such as sildenafi l (Viagra) which may cause hypotension, and sumatriptan (Imitrex) through coronary vasoconstriction,

can trigger CP. Cancer, recent orthopedic surgery, and immo- bility may result in deep vein thrombosis (DVT), a risk factor for pulmonary emboli.

Signs and Symptoms: Pain of ACS may be retrosternal or poorly localized; may radiate to arms, back, neck, or jaw; may occur at rest; may last longer than 20 minutes; and is unrelieved with nitroglycerin. It may occur with nausea, vomiting, dia- phoresis, dyspnea, weakness, fatigue, light-headedness, and/ or anxiety. It may be precipitated by stress, exercise, or illness. Stable angina is substernal or precordial pressing, constrict- ing, or heaviness precipitated by exertion and relieved with nitroglycerin. Older adult or diabetic patients with altered pain perception or altered ability to localize the discomfort commonly have atypical presentations. An absence of chest pain with ACS in older adults is common. Dyspnea, not chest pain, is the most common presenting symptom of acute MI in patients over 85 years old.

Thoracic aortic dissection has abrupt onset and severe, retrosternal tearing pain that usually radiates to the back and both arms. Pulmonary embolism may present with acute dyspnea, cough, deep pleuritic chest pain that may not be severe, and hemoptysis. Tension pneumothorax is associ- ated with acute unilateral pleuritic chest pain and dyspnea. Esophageal spasm/gastroesophageal refl ux disease (GERD) may mimic myocardial ischemia, may be associated with eating, improves with upright position or antacids, and is accompanied by cough, hoarseness, and dysphagia. Acute pancreatitis may present with knifelike epigastric or lower chest pain radiating to the left shoulder associated with vom- iting and relieved by leaning forward. Musculoskeletal pain is usually persistent and is aggravated by movement, cough, or deep respirations. Herpes zoster is described as sharp pain or paresthesia in the mid-thorax unilaterally. Pain may precede rash by several days. History may be positive for CAD with or without angina or risk factors thereof, including hyperten- sion, diabetes, and hypercholesterolemia.

Anemia may predispose to ischemia. Atrial fi brillation is associated with pulmonary emboli, as is recent orthopedic surgery, recent immobilization, DVT, and cancers. GI disor- ders, degenerative joint disease, and anxiety disorders, as well as smoking and alcohol abuse, can be clues to diagno- sis. Signs of serious conditions include acute confusion or anxiousness, pallor/cyanosis, diaphoresis, tachycardia, bra- dycardia, tachypnea, and hypotension. A new S4 murmur or signs of heart failure (jugular venous distention, wet crackles, S3 murmur, extremity edema) suggest myocardial ischemia. Asymmetrical blood pressures, absent or asymmet- rical extremity pulses, and aortic bruit may be present with aortic dissection. Tracheal deviation, unilateral diminished or absent breath sounds, and palpable subcutaneous crepi- tus may reveal pneumothorax. Rapid, irregular apical pulse suggests atrial fi brillation, whereas unilateral lower extrem- ity swelling and tenderness suggests DVT. Fever suggests an infectious cause. Localized abdominal tenderness with guarding and rebound points to GI origins. Costochondritis pain is worse with chest movement, sneezing, or cough and is not associated with fever, shortness of breath, tachycardia, or other cardiopulmonary symptoms. Diffuse tenderness is

CHEST PAIN

Chapter 5 ■ Symptoms and Syndromes 39

usually seen over one or more costochondral joints. Vesicular rash in a unilateral thoracic dermatome suggests zoster.

Diagnostic Tests: If myocardial ischemia is suspected, imme- diate 12-lead electrocardiogram (EKG) is essential and may show ST-segment depression or elevation, T-wave inver- sion, new left bundle branch block (LBBB), or new Q waves. However, the EKG may not change for hours or sometimes not at all. Elevations in cardiac markers (troponins I and T) 3 to 6 hours (COR I LOE A) after the onset of pain indicate myocardial cell damage.

Additional tests include chest x-ray, which may reveal pul- monary edema, pneumothorax, pleural effusion, pneumonia, or lung mass. D-dimer and spiral computed tomography (CT) or ventilation/perfusion (V/Q) scan may confi rm pulmonary emboli. Lower extremity Doppler ultrasound diagnoses DVT. Additional testing is guided by the clinical situation, history, and physical fi ndings. Older adult patients with ACS are less likely to have typical EKG fi ndings (i.e., ST-segment eleva- tion). Unstable angina/non-ST elevation MI shows T-wave inversion, absent Q waves, and evolving ST-segment changes.

Differential Diagnosis: The differential diagnosis includes previously discussed emergent conditions, stable angina, pericarditis, pneumonia, pleurisy, lung/chest malignancy, esophageal spasm, esophagitis, GERD, cholecystitis, pan- creatitis, peptic ulcer disease, costochondritis, herpes zoster infection, and psychogenic causes.

Treatment: If there is high suspicion of emergent conditions such as ACS or aortic dissection, immediate transport to the emergency department by emergency medical services (EMS) is recommended. For institutionalized elders, conservative management of ACS in the facility may be reasonable. Imme- diate intervention and early hospital care for suspected ACS is supplemental oxygen, 160 to 325  mg chewed aspirin (if no allergy), and sublingual or IV nitroglycerin when blood pressure is greater than 90  mm  Hg systolic and heart rate is greater than 50 beats per minute (bpm). Nitrates should never be administered to patients with a non-ST elevation ACS who received phosphodiesterase inhibitors within 24 to 48 hours of onset of symptoms, or a precipitous fall in the blood pressure could lead to fatal outcomes. Supplemental oxygen to maintain oxygen saturation above 90% is indicated with other suspected emergent conditions.

Analgesic therapy may be recommended for pain control, and morphine IV can be used in a patient when not con- traindicated. Treatment of stable angina includes aspirin, beta blockers, angiotensin-converting enzyme (ACE) inhib- itors, nitrates, and statins. Long-acting calcium channel blockers may be used for symptom reduction if beta block- ers are ineffective or contraindicated. Although only mod- erately successful, treatment options for esophageal spasm include calcium channel blockers, tricyclic antidepressants (exercise caution with use in older adults), nitrates, botuli- num toxin, and dilation. Proton pump inhibitors, H 2 block- ers, and/or antacids are the mainstay for GERD. Weight loss is advised for the overweight patient. Costochondritis may respond to local cool or warm packs, rest, or topical or oral analgesics. Careful examination of the skin to detect herpes zoster requires oral antiviral medications and appro- priate pain management. Reassurance, cognitive-behav- ioral therapy, and/or antidepressants may be indicated for psychogenic causes.

Follow-Up: Follow-up is guided by diagnosis and response to treatment.

Sequelae: A 20% to 60% rate of unrecognized MI in older adults with inappropriate hospital discharge and delayed treatment results in poor outcomes and increased mortality.

Prevention/Prophylaxis: Optimize treatment of diabetes, hypertension, CAD, and atrial fi brillation. Encourage daily exercise and smoking cessation. For refl ux symptoms, rec- ommend controlling weight, elevating head of bed on blocks, staying upright after meals, and avoiding caffeine, chocolate, spicy foods, peppermint, cigarettes, and alcohol. Encourage the patient to get the Pneumovax and Zostavax vaccinations.

Referral: Suspected life-threatening conditions or unstable status may be referred to the emergency department depend- ing on the patient ’ s and family ’ s wishes. Physician consulta- tion is indicated with uncontrolled pain, uncertain diagnosis, and poor response to treatment.

Education: Teach patients and families to immediately seek medical care with acute new-onset CP or when a change in chronic CP is experienced. Carefully explain causes of pain, appropriate testing and treatment, prevention strategies, and indications for follow-up.

Alternate Differential Diagnosis for Angina for Patients With Chest Pain

NON-ISCHEMIC PULMONARY GI CHEST WALL PSYCHIATRIC

Cardiovascular

Aortic dissection

Pericarditis

Pulmonary

Embolism

Pneumothorax

Pneumonia

Pleuritic

Esophageal

Esophagitis

Refl ux

Biliary

Colic

Cholecystitis

Choledocholithiasis

Cholangitis

Peptic ulcer

Pancreatitis

Costochondritis

Fibrositis

Rib fracture

Sternoclavicular

arthritis

Herpes zoster

(before rash)

Anxiety disorder

Hyperventilation

Panic disorder

Primary anxiety

Affective disorders

Thought disorders

40 Chapter 5 ■ Symptoms and Syndromes

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

If there is a high suspicion of an emergent condition, immediate transport to emergency department.

B Amsterdam et al., 2014

Immediate interventions for suspected ACS: supplemental oxygen, 160–325 mg aspirin, sublingual nitroglycerin.

B Amsterdam et al., 2014

All patients with CAD should be taking the following medications unless contraindicated:

■ Aspirin A Amsterdam et al., 2014

■ Lipid lowering agent if low-density lipoprotein (LDL) is above target

A

■ Beta blocker for patients with a history of myocardial infarction (MI)

A

■ Beta blocker for patients without a history of MI B

For patients with CAD and diabetes mellitus (DM)/left ventricular systolic dysfunction, add: ACE inhibitor, unless contraindicated.

A

Immediate-acting nitroglycerin (sublingual/spray) provides relief of anginal symptoms.

B

Treatment of esophageal spasm: long-acting calcium channel blockers.

B Katz, Gerson, & Vela, 2013

Treatment of esophageal spasm: calcium channel blockers, tricyclic antidepressants, nitrates, botulinum toxin, dilation.

C

Treatment of GERD: proton pump inhibitors, H 2 -blocker, antacids.

A Katz, Gerson, & Vela, 2013

Treatment for GERD: controlling weight, elevating the head of the bed on blocks, staying upright after meals, avoiding specifi c foods and alcohol, smoking cessation.

C Katz, Gerson, & Vela, 2013

Treatment for costochondritis: NSAIDs for pain. C Ayloo, Cvengros, & Marella, 2013

Treatment for herpes zoster: antivirals. A Gan, Tian, & Tay, 2013

Treatment of psychogenic causes: cognitive-behavioral therapy.

A Campbell et al., 2017

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Chapter 5 ■ Symptoms and Syndromes 41

Description: Constipation is the presence of two or more of the following symptoms: decreased stool frequency, straining, hard stools, sensation of incomplete emptying or anorectal blockage, requirement for manual maneuvers to pass stool, and rarely, loose stools in absence of laxative use ( Ameri- can Gastroenterological Association, 2013 ). It is the most common digestive complaint and a symptom rather than a disease ( Basson, 2017 ).

Etiology: Colonic motility depends on the integrity of the nervous system impulses and circular smooth muscle tone, and motor complexes stimulated by increasing intralumi- nal pressure generated by bulk. Any pathophysiological process that interferes with this process can cause constipa- tion. It is thought that changes in colonic motility are not age related but are infl uenced instead by extrinsic factors such as insuffi cient fl uid, fi ber, and exercise (DiGiorgio et al., 2015).

Occurrence: The prevalence of constipation in the general population is 20%, although it can range from 2% to 27% depending on the defi nition used and the population ( Roque & Bouras, 2015 ).

Age: Constipation is a frequent complaint of older adults, with reports 20% higher than in younger patients. Older adults residing in long-term care facilities have a greater prevalence of constipation; up to 50% to 74% use laxatives daily ( Roque & Bouras, 2015 ).

Gender: At all ages, constipation is reported more frequently in women than in men. Older women are two to three times more likely to report constipation than their male counterparts.

Ethnicity: Not signifi cant.

Contributing Factors: The functional factors described earlier contribute to constipation if they are not the primary etiol- ogy. Medications that may contribute to constipation include calcium channel blockers, calcium supplements, narcotics, iron supplements, aluminum-containing antacids, anti-Par- kinson ’ s drugs, NSAIDs, and any drug that has anticho- linergic side effects. Certain types of laxatives also may be constipating, such as stimulant laxatives, which may cause cathartic colon and laxative dependency, and bulk laxatives taken with insuffi cient fl uids. Neurological disorders, such as Parkinson ’ s disease, stroke, spinal cord disorders, dementia, depression, metabolic factors, and nursing home placement, are also factors that increase the risk for constipation (Wald, 2016; Bardsley, 2016).

Signs and Symptoms: The fi rst part of an assessment should include the use of a tool to determine the person ’ s normal pattern of bowel function. The most common tool is the Bristol Stool Chart, which classifi es stools as hard to pass, ideal consistency, or diffi cult to control. Descriptions and pic- tures make it easy for patients to identify the type of stool. It is also helpful to include a food diary to determine dietary sources of the problem. Other considerations are mobility, which allows them to easily get on and off the toilet; proper environment for defecation; underlying medical conditions;

medications, including OTC and herbal supplements; and remedies already tried for relief ( Bardsley, 2015 ).

A thorough abdominal and rectal examination is neces- sary to rule out physical abnormalities and then the data is compiled. The ROME III diagnostic criteria are helpful in confi rming the diagnosis of constipation, which must include two or more of the following:

■ Straining at least at 25% of defecations ■ Lumpy or hard stools in at least 25% of defecations ■ Sensation of incomplete evacuation for at least 25% of

defecations ■ Sensation of anorectal obstruction/blockage for at least

25% of defecations ■ Manual maneuvers to facilitate at least 25% of defe-

cations (digital evacuation, support of the pelvic fl oor) ( Basson, 2017 )

Diagnostic Tests: All individuals should have a fecal occult blood test at the initial visit of a complaint of constipation. Additional diagnostic tests should be done if they can inform contributing causes or alter the treatment. Laboratory tests might include complete blood count (CBC), glucose, thy- roid-stimulating hormone, electrolytes, blood urea nitrogen (BUN), and creatinine. An abdominal radiograph may help to determine the extent and distribution of feces. Sigmoidos- copy or barium enema or both may be indicated in patients with a recent onset of constipation when a lesion is sus- pected. Checking colonic transit times may be indicated in patients who have a normal number of bowel movements but still complain of constipation. Colonic motility testing may be useful in identifying patterns of colonic activity. A colonos- copy should be done if the patient presents with alarm symp- toms, anemia, or positive fecal occult blood ( Roque & Bouras, 2015 )

Differential Diagnosis: The clinician then evaluates the eti- ology and contributing causes to rule out obstruction, fecal impaction, irritable bowel syndrome, or diverticular disease ( Bardsley, 2015 ).

Treatment: After the specifi c etiology is established and factors contributing to constipation are identifi ed, the appropriate pharmacological and nonpharmacological interventions are initiated. The primary aim of treatment is for the patient to have regular, predictable, and comfortable bowel movements. Ideally, this should be accomplished with diet and lifestyle changes. An increase in fi ber intake should be done gradu- ally to prevent bloating and fl atulence. Adults should eat 18 to 20 g of fi ber per day. Insoluble fi ber found in whole wheat, whole grains, vegetables, and wheat bran is the best choice. It may take up to 4 weeks for the effects to be noted, so the patient may need laxatives in the interim. An adequate fl uid intake of 1.5 to 2  L/day is also important. Fruits and fruit juices, especially prune and apricot, which are high in sorbi- tol, are an alternative for those who cannot increase the fi ber intake ( Bardsley, 2015 ).

Laxatives are recommended when diet and lifestyle changes are not suffi cient. The recommendation is to start with bulk-forming laxatives. Psyllium or polycarbophil are commonly recommended, but they require increased fl uid

CONSTIPATION

42 Chapter 5 ■ Symptoms and Syndromes

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Ask the patient about a feeling of incomplete evacuation, obstruction, digital manipulation, infrequent bowel movements, and abdominal bloating.

A Bardsley, 2015

Consider laboratory testing: CBC, electrolytes, BUN, creatinine, calcium, glucose, and thyroid-stimulating hormone if symptoms persist despite conservative treatment.

A Roque & Bouras, 2015

Patients with red fl ags for malignancy or complicated disease should have a colonoscopy.

A AGA, 2013

The initial management of symptomatic constipation is typically dietary modifi cation (high fi ber, exercise, and fl uid supplementation).

A Bardsley, 2015

Polyethylene glycol (PEG) and lubiprostone are effective for the management of chronic constipation.

A Izzy et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

intake, which may not be appropriate for some older adults with heart and kidney disease. Alternatives should be based on the presenting symptoms, the nature of the complaint, the side effects, speed of action, and patient acceptability. Stimulant laxatives, such as senna, cascara, or bisacodyl, increase peristalsis and mucus production. Osmotic laxatives such as polyethylene glycol or lactulose act by drawing fl uid from the body. Iso-osmotic laxatives increase water content and trigger peristalsis and defecation. They are becoming the fi rst-line treatment for chronic constipation ( Bardsley, 2015 ). Stool softeners are often prescribed for older adults. These are not laxatives and actually may contribute to constipation, “the mush without the push.” Discontinuing inappropriately prescribed stool softeners is an option for medication reduc- tion in polypharmacy.

Follow-Up: Chronically constipated individuals often need to have combined nonpharmacological with periodic pharma- cological intervention. When laxatives are prescribed, these individuals should be reevaluated every 3 months for the side effects and the responses to treatment ( Bardsley, 2015 ).

Sequelae: Constipation, although uncomfortable, is rarely life threatening. When associated with pain, distention, or vom- iting, constipation may be a sign of a life-threatening mes- enteric infarction or a partial or complete bowel obstruction. Straining in older adults may have serious effects on the cere- bral, coronary, and peripheral arterial circulation. If stool is not eliminated from the colon and the patient becomes dehydrated, stool may harden, resulting in fecal impaction, a large mass of compacted feces at the intestinal level that cannot be evacuated spontaneously. It is estimated that 7%

of long-term residents suffer from impactions yearly (Falcon et al., 2016).

Prevention/Prophylaxis: Adequate dietary fl uid and fi ber and regular exercise habits help to promote colonic mobility. Bowel elimination patterns should be monitored regularly in individuals who are unable to report bowel habits or bowel discomfort.

Referral: Hospitalization may be necessary in some cases of severe constipation and/or impaction, anorexia, dehydra- tion, or nausea or vomiting. Patients with recent-onset con- stipation associated with bleeding, anemia, or family history of colon cancer; patients with chronic constipation with anemia, abdominal pain, and weight loss; and patients with recent-onset fecal incontinence should be referred to a gas- troenterologist. Referral to a specialist also should be consid- ered when there is a failure to alleviate constipation despite escalating attempts ( Roque & Bouras, 2015 ).

Education: In addition to giving instruction in the dietary measures appropriate in preventing constipation, encourage older patients to maintain regular bowel habits and respond to the urge to defecate rather than suppress it. Patient educa- tion regarding diet and exercise is challenging when patients have cognitive impairments, mood disorders, uncontrolled pain, or signifi cant muscle weakness. Patients should be taught to take advantage of the gastrocolic refl ex, which is strongest about 30 minutes after meal consumption. All individuals should avoid the use of laxatives and OTC med- ications known to have constipating side effects ( Bardsley, 2015 ).

Chapter 5 ■ Symptoms and Syndromes 43

Description: Cough is the forceful expelling of air from the lungs involving the use of accessory muscles of the chest and constriction of the glottis.

Etiology: Cough is the voluntary or involuntary mecha- nism used to eject aspirants or noxious substances, includ- ing fl uids, solids, dust, and gases from the body ’ s upper and lower airways. Cough is also the body ’ s mechanism to remove mucus from the upper or lower respiratory tracts. Involuntary cough is regulated by the vagal afferent nerve, but higher central nervous system (CNS) cortical modulation can inhibit cough or allow for voluntary cough.

Occurrence: Cough is one of the most common complaints for seeking medical attention. It is divided into three catego- ries based on duration: acute, lasting less than 3 weeks; sub- acute, lasting between 3 and 8 weeks; and chronic, lasting more than 8 weeks.

Age: Cough occurs at any age.

Gender: There are no gender-specifi c differences, though females tend to seek medical attention more often.

Ethnicity: No direct ties to ethnicity have been documented.

Contributing Factors: Any stimulation, chemical or mechani- cal, that irritates the receptors of the cough refl ex are causes of cough. These receptors are located in the upper and lower respiratory tract, esophagus, pericardium, diaphragm, and stomach. Environmental exposure that causes cough includes multiple different types of irritants such as chemi- cals, dust, and pollen, along with infectious agents such as the common cold, tuberculosis (TB), or Bordetella pertussis. Trauma, including assault, motor vehicle accidents, or falls that lead to contusion of the lungs can cause cough. Medica- tions may cause cough, particularly ACE inhibitors (in 20% of users).

Smoking is a primary cause of chronic cough, but medical services are often not sought by smokers. Cigarette smoking is the most signifi cant preventable cause of disease, and lung cancer is the number one cause of cancer deaths of both men and women in the United States. Cough from chronic obstructive pulmonary disease (COPD) worsens in intensity and duration if the patient continues to smoke. Broncho- genic cancers are often associated with cough, but metastatic cancers to the lungs seldom result in cough until late in the course of the disease.

Signs and Symptoms: A thorough disease history is required, as multiple chronic diseases present with cough as a symptom. Risk factors and work and home environment assessment is essential in narrowing the cause of cough. Using a systematic anatomical approach provides ease in identifying the trigger and illness. Risk factors for cough include recent exposure, smoking, stroke, immigrant status, use of ACE inhibitors, HIV-positive status, and heart disease. The cough may be pro- ductive or nonproductive, and the sputum may be a variety of colors or tinged with blood. Identify the onset, including if it is episodic, continuous, or occurs only certain times of the day; the duration and character; and if it is associated

with other symptoms, including fever, tachycardia, dyspnea, weight loss, or pain.

The physical examination begins with vital signs that should include temperature, heart rate, respirations, and oxygen saturation. Next is a thorough examination of the nose and oropharyngeal mucosa. Tenderness to percussion of the facial and maxillary sinuses and swollen, mucus-covered, boggy turbinates indicate allergic rhinitis. A “cobblestone” appearance from chronic posterior pharynx and swollen eyelids are other indicators of an allergic origin. Loss of tooth enamel can indicate GERD. The chest must be assessed for adventitious breath sounds. Wheezes indicate bronchitis or asthma caused by mucus in or constriction of the airways. Rhonchi or crackles are suspicions for pneumonia or infi l- trates. Diminished or absent lung sounds by auscultation and dullness to percussion are highly suggestive of pneumonia ’ s consolidation. Rhonchi or crackles with cardiomegaly on x-ray or EKG indicate congestive heart failure and may not be accompanied by peripheral edema.

Diagnostic Tests: No specifi c tests are indicated when the patient has a cough. The selection and extent of testing depends on the fi ndings of the history and physical exam- ination, duration (acute, subacute, or chronic), and previous evaluations.

Acute cough associated with upper respiratory infec- tion does not require further diagnostic evaluation, unless infl uenza is suspected, then a rapid infl uenza diagnostic test may be benefi cial. Acute cough with physical fi ndings of life-threatening illness should be appropriately evaluated for the diagnosis of concern. A chest radiograph is appropri- ate for physical fi ndings consistent with pneumonia (fever, heart rate above 100  bpm, respiratory rate greater than 24 breaths/min, chest examination with fi ndings of local con- solidation). Viral cultures, serologic assays, and sputum anal- ysis should not be routinely performed in the diagnosis of acute bronchitis.

Subacute cough that has lasted more than 2 weeks without an apparent cause and is associated with post-tus- sive vomiting, inspiratory whooping, and paroxysms of coughing should have a nasopharyngeal aspirate or polymer swab of the nasopharynx for culture to confi rm the presence of B. pertussis, whooping cough. Bacterial isolation is the only certain way to confi rm the diagnosis. Testing for TB is indicated when there is an increased risk of the population becoming infected, such as in nursing homes or prisons; in a patient with a recent visit to a country with high prevalence of TB; or in an immunocompromised patient.

Chronic cough diagnostic testing in nonsmokers is guided by elimination through treatment of the most common dis- orders: upper airway cough syndrome (UACS), previously known as postnasal drip syndrome secondary to rhino- sinus diseases; GERD; and asthma. Medical history is crucial to determining progression of diagnostic tests for chronic cough. A chest radiograph is appropriate, though most often negative. An abnormal study would guide further diagnos- tics; a mass suggestive of lung cancer could be followed up with high-resolution computed tomography (CT) scan, bron- choscopy, and biopsy; congestive heart failure would lead

COUGH

44 Chapter 5 ■ Symptoms and Syndromes

to cardiovascular evaluation; evidence of infection such as TB would direct microbiologic diagnostics. UACS evaluation includes sinus imaging, either plain sinus fi lms or sinus CT scan. Scans or fi lms taken during the episode of a common cold are not diagnostic of bacterial sinus infection. Evalua- tion for asthma-induced chronic cough is bronchoprovo- cation challenge. GERD evaluation may include a barium swallow or 24-hour esophageal pH monitoring test.

Differential Diagnosis: The most important fi rst step is determining if the acute cough is potentially related to a life-threatening condition such as pneumonia, congestive heart failure, or pulmonary embolism. Most acute coughs are related to a respiratory tract condition such as the common cold, fl u, acute bronchitis, acute exacerbation of COPD, viral syndrome, or exposure to an environmental irritant.

Subacute cough is usually a cough that lingers on from a respiratory tract infection. A post-infectious cough can last 2 to 3 weeks after onset. Consider UACS, transient bronchial hyper-responsiveness, asthma, acute exacerbation of chronic bronchitis, and pertussis. If it appears to be a noninfectious cough, it should be managed and further evaluated as a chronic cough.

Chronic cough most commonly is UACS, asthma, or GERD. Other potential causes may include nonasthmatic eosinophilic bronchitis (NAEB), COPD, drug-induced cough, fungal infection, and mediastinal masses. A nocturnal cough associated with shortness of breath suggests heart failure, and without shortness of breath is more indicative of an allergy.

Diagnosis of unexplained cough or idiopathic cough requires an exhaustive evaluation by a specialist for uncom- mon causes before the diagnosis is used.

Treatment: Most often the source of the cough is isolated to the respiratory system and the condition is not life threaten- ing. The following treatments are recommended:

Common Cold, Postnasal Drip, and Throat Clearing: Treat with fi rst-generation antihistamine/decongestant preparation to decrease and hasten the resolution of the cough. Naproxen, an NSAID, may also be used to decrease cough. It is thought to work by inhibiting the infl ammatory process.

Acute Bronchitis: This diagnosis is applicable in persons without signs or symptoms of acute exacerbation of COPD, acute asthma, common cold, or pneumonia. In the older adult, a high suspicion of pneumonia should be considered until proved otherwise. Most acute bronchitis is viral and self-limiting; antibiotics do not shorten the course of the disease and should not be used. Beta-2 agonists are not rec- ommended for routine treatment unless there is an asthma component. Expectorants such as guaifenesin may be used. Dextromethorphan or codeine may be used for cough sup- pression for severe coughing, though research has only been done in chronic bronchitis. A cool mist humidifi er in the bedroom may be helpful.

Bacterial Pneumonia: Community-acquired pneumonia (CAP) is treated differently than health-care–associated pneumo- nia. It is of particular concern in older adult patients and those who are immunocompromised because their symp- toms may be less intense. Pneumonia most often is caused by Streptococcus pneumoniae, Staphylococcus aureus, Hemophilus

infl uenza, Moraxella catarrhalis, or Pseudomonas aeruginosa . If pneumonia is suspected, broad-spectrum antibiotic therapy should be initiated empirically. Patients with any respiratory distress and older adult patients with signifi cantly elevated white blood cell (WBC) counts may need to be hospitalized.

Chronic Bronchitis: Stable patients with a sudden change of symptoms, increase in cough, shortness of breath, purulent sputum, and increase in sputum production are considered to be having an acute exacerbation. Treatment includes a combination bronchodilator, beta-agonists, and ipratropium as an inhaler or as a nebulizer, antibiotics, and oral ster- oids. Dextromethorphan or codeine may be used for cough suppression. Diagnosis and chronic management of COPD is addressed elsewhere in this text.

TB: Antituberculosis drugs should be initiated if the tuber- culin skin test is positive and the patient referred to the local health department.

Drug Reaction: ACE inhibitor should be stopped and only restarted if there is compelling need for the category of drug.

Post-Infectious Cough: A treatment trial of inhaled ipratro- pium for a cough that is adversely affecting quality of life may be used. If ipratropium alone is not successful, use of inhaled corticosteroids can be considered. Antibiotics are not recommended. Severe symptoms may require use of an oral steroid for a short period while other causes of cough are being considered.

Chronic Cough Treatment: Treatment of UACS, asthma, and GERD in a stepwise, systematic approach is most likely to provide a high rate of success. Because UACS is the most common cause of chronic cough, a trial of fi rst-generation antihistamine and decongestant should be tried. Cough should improve in 1 to 2 weeks. If the response is positive, the medication should continue because it may take several weeks for marked improvement. A partial response indicates more than one cause of the cough, and evaluation and treat- ment for asthma or GERD is reasonable.

Follow-Up: The tenacity of follow-up depends on the severity of the illness and the impact on the patient ’ s life. For pneu- monia or bronchitis with minimal dyspnea, a call to check on the patient is appropriate. Rising temperature or increasing diffi culty breathing requires immediate attention or emer- gency department evaluation. Patients with resolving pneu- monia should be evaluated in 2 to 3 weeks; a repeat chest x-ray may be taken. Chronic cough may take multiple fol- low-up visits, evaluation, and treatment trials.

Sequelae: If a cough is caused by lung cancer, the progno- sis is ominous. Cough from COPD worsens in intensity and duration if the patient continues to smoke. In older adults, chronic cough can contribute to stress incontinence.

Prevention/Prophylaxis: Preventive measures include smoking avoidance or cessation intervention, evaluation of the work and home environment, and humidifi cation of the sleeping area with a cool mist humidifi er. Patients should be provided vaccinations following Centers for Disease Control and Pre- vention (CDC) guidelines, including annual fl u shots, Pneu- movax, and Tdap.

Chapter 5 ■ Symptoms and Syndromes 45

Referral: A referral to a specialist can be initiated anytime during the evaluation and treatment of a cough. Some results, such as lesions suspicious for cancer on radiography, require referral to a specialist immediately. A cough specialist, allergist, or pulmonologist referral is appropriate for a chronic cough that is persistent. Other specialists who may be helpful are a GI specialist for evaluation of GERD, an infectious

disease specialist for infections and immunocompromised patients, and a cardiologist for heart conditions.

Education: Recommend smoking cessation classes and aller- gen avoidance training. Cough can last longer than patient expects.

DIAGNOSIS CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Common cold, postnasal drip, and throat clearing

First-generation antihistamine/ decongestant preparation, naproxen

B Pratter, 2006a, 2006b Smith et al., 2014

Acute bronchitis without signs or symptoms of pneumonia, COPD exacerbation, acute asthma, or common cold

Most acute bronchitis is viral and self- limiting; antibiotics do not shorten the course of the disease and should not be used

B Braman, 2006a Holzinger et al., 2014

Bacterial pneumonia— community-acquired

Broad-spectrum antibiotic therapy should be initiated empirically; older adult patients with signifi cantly elevated WBC counts or patients with respiratory distress may need to be hospitalized

B Holzinger et al., 2014 Musher & Thorner, 2014

Chronic bronchitis— sudden change in symptoms

Combination bronchodilator, beta agonists, and ipratropium as an inhaler or as a nebulizer, antibiotics, and oral steroids; dextromethorphan or codeine may be used for cough suppression

A Irwin et al., 2006

Drug reaction ACE inhibitor should be stopped A Dicpinigaitis, 2006 Kahrilas et al., 2016

Post-infectious cough with other conditions ruled out

Treatment trial of inhaled ipratropium for cough if affecting quality of life; can consider inhaled corticosteroids or use 30–40 mg of prednisone for a limited period of time for severe paroxysms. Cough suppression for failure of other treatments. Antibiotics are not recommended.

B Braman, 2006b Iyer & Lim, 2013

Upper airway cough syndrome (UACS)

First-generation antihistamine and decongestant

C Iyer & Lim, 2013

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

46 Chapter 5 ■ Symptoms and Syndromes

Description: Dehydration, or fl uid volume depletion caused by too little fl uid intake, too much fl uid lost, or both, is a common condition in older patients. Fluid balance, intake equals output, is essential to health.

Etiology: Total body water decreases with age. The total body water of an adult age 61 to 74 years is approximately 40% compared with 60% for younger adults (Miller, 2015). Even small decreases in fl uid intake can cause dehydration quickly in an older adult, due to a smaller fl uid reserve. The ability of the kidneys to concentrate urine declines with age, so that even when deprived of water, urina- tion is not signifi cantly reduced. Also, thirst decreases as a person ages, which is an important self-regulation against dehydration.

Dehydration can be defi ned as a fl uid and electrolyte dis- turbance arising from either a water depletion or a sodium depletion in which there is accompanying water loss. It can be classifi ed into three different types based on the possible causes (see Table 5-2 ): isotonic, hypotonic, and hypertonic.

Occurrence: Dehydration has been reported to be the most common fl uid and electrolyte imbalance in older adults. The prevalence is increasing, with 23% of patients over 70 years of age and 34% of nursing home patients who were admitted to the hospital diagnosed with dehydration ( Theerthakaria & Madlon-Kay, 2016 ).

Age: Older people are particularly susceptible to dehydration because of age-related changes noted previously, with indi- viduals older than 85 years at the highest risk.

Gender: Not signifi cant.

Ethnicity: African Americans have a greater likelihood of dehydration than Caucasians (Stookey, Pieper, & Cohen, 2003).

Contributing Factors: The causes of dehydration are multi- factorial and include decreased mobility and the presence of

chronic diseases such as diabetes, cancer, and cardiovascu- lar and renal disease, which make older adults more sensi- tive to fl uid and electrolyte imbalance. Other risk factors for dehydration in older adults include dependency for eating or drinking, mouth pain, poorly fi tted dentures, and diffi culty swallowing. Vomiting, diarrhea, hemorrhage, and increased metabolic states that result in excess loss of fl uids (fever, infection, excess sweating, excess urination) are also contrib- uting factors. The use of certain medications, such as diuret- ics, anticholinergics, psychotropics, or laxatives, also may increase the risk. Dehydration is the most frequent secondary condition resulting from debilitating issues such as fever, con- fusion, pain, or pneumonia. Cognitive impairment (delirium, dementia, depression) has been associated with dehydration in older adults.

Signs and Symptoms: Assessing for hydration status in the clinical setting can be diffi cult, as there is no valid tool to assess for risk of dehydration in patients (Burns, 2016; Miller, 2016). A dry, furrowed tongue and mucous membranes; sunken eyes; headaches; dizziness on standing; confusion; concentrated or dark urine; weight loss; and upper body muscle weakness may indicate dehydration. Clinical signs may not appear, however, until dehydration is far advanced. In addition, the usual signs of constipation, disorienta- tion, dry mucous membranes, orthostatic hypotension, and weight loss may be caused by other factors. If one or more of these are present or are a change from baseline, dehydra- tion may be the cause. While poor skin turgor is an expected fi nding in older adults, it is also a classic sign of dehydration. Clinical assessment should include assessment of skin turgor at the sternum or dorsum of the hand and inspection of oral mucous membranes for dryness and tongue for dryness and longitudinal furrows (Miller, 2016; McCrow, 2016). Signs and symptoms of hypovolemic shock include altered mental status; hypotension; tachycardia; cold, clammy skin; and rapid, deep respirations.

Diagnostic Tests: Serum markers provide the most reliable indicators of dehydration and these include serum sodium, increased serum osmolality, and BUN–creatinine ratio. The serum albumin may be higher than normal when the patient is dehydrated.

Differential Diagnosis: When dehydration is identifi ed, it is important to identify the cause and contributing factors and address these. Weight gain and edema from congestive heart failure can conceal a patient ’ s dehydrated status.

Treatment: Individualize treatment, depending on the type of dehydration. The route of administration (oral or IV or sub- cutaneous) is determined by what is safe and effective. The recommended daily intake of fl uids for older adults should not be less than 1,600  mL/24 hours to ensure adequate hydration, and this is adjusted for climate and physical activ- ity ( Theerthakaria & Madlon-Kay, 2016 ). Regular presenta- tion of fl uids to bedridden individuals can maintain adequate hydration status. Provide continuous verbal cues to encour- age drinking fl uids. Fluids given with medication can be an important source of fl uids, so fl uids should be encouraged

DEHYDRATION

Types of Dehydration

TYPE OF DEHYDRATION DESCRIPTION

Isotonic A balanced loss of both sodium

and water causes extracellular fl uid

loss that increased blood viscosity.

Common causes: vomiting, diarrhea,

osmotic effects of glucose.

Hypertonic Excessive water loss results in raised

sodium levels and shifts from the

intracellular space to extracellular

space. Common causes: renal tubular

disease, osmotic diuresis, resistance

to vasopressin.

Hypotonic Excessive sodium loss results in

extracellular fl uid loss. Common

causes: overuse of diuretics, chronic

salt wasting.

TABLE 5-2

Chapter 5 ■ Symptoms and Syndromes 47

at this time. Determine the patient ’ s personal preferences of fl uid.

Follow-Up: The timing of patient follow-up depends on the seriousness of the identifi ed cause and the response to treatment.

Sequelae: Dehydration has severe consequences for older adults and can have a major impact on quality of life. Dehy- dration is associated with chronic health problems, including constipation, falls, medication toxicity, increased confusion, and infection. Inadequate fl uid intake can have serious medical consequences such as renal failure, hyperthermia, bowel obstructions, delirium, cardiovascular symptoms, and death. A primary or secondary diagnosis of dehydra- tion has been associated with poor outcomes and increased length of stay for older adults who are hospitalized. Older adults admitted with a primary diagnosis of dehydration have a 1-year mortality rate of 42% (El-Sharkawy et al., 2016).

Prevention/Prophylaxis: Educate patients, families, and care- givers that to prevent dehydration the body needs to adequate fl uid intake. All liquids are not the same in maintaining fl uid

balance. Water is the best and should be at least half of the daily intake of fl uid. Add milk, fruit and vegetable juices, and non-salty soups for variety. Decrease coffee, tea, alcohol, colas, and liquid diet supplements because they may cause dehydration. The use of a 24-hour fl uid balance chart can help determine if the patient is at risk or is dehydrated.

Referral: Refer as indicated by source of symptom. Hospital- ization is indicated when the patient has severe signs and symptoms such as dizziness, altered mental status, or leth- argy; is hemodynamically unstable; or cannot tolerate oral fl uids.

Education: Explain causes of symptoms and measures taken to determine cause and treatment. Aim for 1,600 mL of oral liquids per day unless contraindicated by certain medical con- ditions such as congestive heart failure. Allow adequate time for eating at mealtimes. Meals can provide two-thirds of daily fl uids. Offer fl uids regularly during the day. Encourage con- sumption of fl uids with medications. Staff education is criti- cal; staff should report any signifi cant weight loss, change in fl uid consumption, or other relevant symptoms, such as dry mucous membranes.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The recommended daily intake of fl uids should not be <1,600 mL/24 hours to ensure adequate hydration.

A Theerthakaria & Madlon-Kay, 2016

Hypodermoclysis is as effective as IV rehydration of older adults with mild-to-moderate dehydration.

A Theerthakaria & Madlon-Kay, 2016 Thomas et al., 2008

Verbal prompts have been shown to increase fl uid intake in nursing home residents.

A Oates & Price, 2017

Evidence-based practice guidelines for hydration management.

A Mentes & Kang, 2013

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

DIARRHEA

Description: Diarrhea is the passage of increased stool fre- quency, liquidity, or volume. It is objectively quantifi ed as passage of three or more loose or watery stools or increased stool weight of greater than 200  g or 200  ml per 24 hours ( Shah et al., 2012 ). Most episodes of diarrhea are caused by viral gastroenteritis, are short lived, and resolve without treatment ( Barr et al., 2014 ). Chronic diarrhea is defi ned as diarrhea that lasts longer than 4 weeks.

Etiology: In normal bowel motility, water is not actively trans- ported across the intestinal mucosa, it moves passively by osmotic forces generated by solutes such as electrolytes and

nutrients. Absorption and secretion take place simultane- ously, but when there is either a decrease in absorption or an increase in water within the intestinal lumen, diarrhea occurs. The fundamental cause of diarrhea is the incomplete absorption of water from the intestinal luminal contents. The pathophysiology mechanisms of diarrhea include osmotic, secretory, infl ammatory, and altered motility leading to food and liquids being passed too quickly through the body and being excreted through the colon as loose or watery stool. Diarrhea is often accompanied by abdominal cramping, as well as nausea. There are various causes of diarrhea (see Table 5-3 ). Note that Clostridium diffi cile infection should

48 Chapter 5 ■ Symptoms and Syndromes

Causes of Diarrhea

DISEASE MECHANISM COMMENTS

Physical Causes Contributing to the Incidence of Diarrhea

Dementia Impairs awareness of need to defecate, loss of inhibitory

control

Manifestations depend on type and severity of dementia

Stroke Impaired awareness of anal control, slowed motor

processing communication with frontal lobe damage

Dependent on size of infarct or hemorrhage within the

brain

Fecal impaction Altered rectal sensation, liquid stool escaping around

solid feces in colon

GI disease GI dysfunction/disease with excessive stool volume and

rapid gut transit

Causes include viral or bacterial gastroenteritis, colitis,

Crohn ’ s disease, celiac disease, colon cancer, irritable

bowel syndrome, rectocele, and other GI diseases

Clostridium diffi cile can cause severe diarrhea in the older adult individual and can lead to death

Medication Causes

Laxatives Medications causing increased gastric motility or

increased water in stools

Fiber products Increase fl uid in the stool to keep it soft and move

easier but can lead to diarrhea and FI

Magnesium Draws fl uid into the bowels through osmosis Magnesium containing antacids and certain laxatives contain

signifi cant amounts of magnesium

Other medications Antibiotics can cause destruction of the colon ’ s natural

fl ora, leading to diarrhea

Other medications that can cause diarrhea include

proton pump inhibitors, SSRIs, and NSAIDs

Other

Physical defi cits Inability to recognize need to defecate (cognitive

problems) or inability to ambulate to toilet without

assistance

Common causes of cognitive problems include dementia

Common causes of mobility problems include debilitating

arthritis, hemiplegia, or any condition affecting gait

Dietary causes Other foods in susceptible individuals include diet high

in fi ber, spicy foods, fatty/greasy foods, cured meats,

smoked meats, dairy products, caffeine, and sorbitol

Sugar-free gum and artifi cial sweeteners can cause diarrhea

and FI

Avoidance of irritating foods can eliminate the FI

Excessive fl uid intake Overhydration can lead to diarrhea and possibly cause FI

Source: Barr & Smith ( 2014 ); Keller & Surawicz (2014); Nodrqvist (2014); Shah et al. ( 2012 ); Sweetser ( 2012 ).

TABLE 5-3

be suspected as a cause of diarrhea in patients with watery diarrhea during or shortly after receiving antibiotic therapy or recent hospitalization.

Occurrence: In the United States, an estimated 48 million foodborne diarrheal illnesses occur annually, resulting in more than 128,000 hospitalizations and 3,000 deaths ( Barr et al., 2014 ). The greatest risk factor is contact with another individual with diarrhea.

Age: Diarrhea occurs at any age. The severity of illness and the mortality rate is increased in individuals more than 65 years old, especially if the individual has a concurrent medical illness (Wanke, 2016).

Gender: No gender-specifi c differences.

Ethnicity: No direct ties to ethnicity have been documented.

Contributing Factors: The following can be contribut- ing factors in the development of diarrhea: recent travel, family history of infl ammatory/bowel disorders, recent

antibiotic usage, exposures to either contacts or foods includ- ing tube feedings, whether or not the individual is immuno- compromised such as with HIV, recent hospitalization, age of more than 65 years, extended stay in hospital or nursing home, recent chemotherapy, recent GI surgery including post-pyloric tube feeding, and medications. The list of medi- cations that can cause diarrhea include diuretics, beta block- ers, NSAIDs, antibiotics, quinidine, chemotherapy, colchicine, laxatives, digitalis, theophylline, prostaglandins, cholinergic agents, and phenolphthalein.

Signs and Symptoms: The initial clinical assessment is to obtain a detailed history to include symptom assessment parameters, including onset, frequency, amount, and char- acter of the stool (the presence of blood, mucus, or atypi- cal color) and any associated symptoms such as abdominal pain, cramping, fever, nausea/vomiting, or bloating. Include the patient ’ s baseline bowel pattern, usual dietary intake, food intolerance history, exposure to others with illness, and any recent dining out experiences. A thorough medication

Chapter 5 ■ Symptoms and Syndromes 49

review including any OTC herbal remedies or laxatives needs to be conducted. A dietary history 3 to 5 days before onset of symptoms would be helpful, with particular attention to the ingestion of meat, dairy products, and seafood. The associated symptoms of fever, abdominal pain and disten- tion, vomiting, myalgias, and headache with abrupt onset suggest acute diarrhea etiology. In contrast, fatigue, muscle weakness, weight loss, alternating diarrhea and constipation, incomplete evacuation, abdominal pain, and protracted or recurring symptoms suggest chronic diarrhea etiologies.

Physical examination should include vital signs, weight, and assessing for the presence of postural hypotension. Assess the skin for turgor and the condition of the tongue and mucous membranes. Check for evidence of jaundice, rashes, or lesions. Examine the thyroid for enlargement or lesions. Perform a thorough examination of the abdomen for distention, rigidity, tenderness, bowel sounds, masses, hep- atomegaly, or splenomegaly. Perform a rectal examination to check for impaction, include hemoccult testing to assess for

bleeding, hemorrhoids, polyps, fi ssures, fi stulas, or evidence of malignancy. Include a general inspection for arthritis or lymphadenopathy. Stool should be examined for mucus and the presence of blood. Figure 5-1 describes an algorithm to assist in determining the appropriate work-up needed for diarrhea.

Diagnostic Tests: For most cases of diarrhea of acute onset, no diagnostic testing is warranted unless the individual appears acutely ill. If abnormal fi ndings are observed on physical examination or the individual has additional comor- bid conditions, then diagnostic testing may be necessary. CBC and complete metabolic panel (CMP) to include elec- trolytes and renal function will help identify an infectious process and any electrolyte imbalance, and the presence of dehydration. Abdominal x-rays are helpful to identify the presence of obstruction or ischemia. A barium enema can reveal malignancies, polyps, or abnormalities of the mucosal lining. Colonoscopy or sigmoidoscopy may be useful when

FIGURE 5-1. Algorithm to assist in determining the appropriate work-up needed for diarrhea.

Colon evaluation

Upper endoscopy with small bowel

biopsies

Inflammatory Fatty Mucosal

Stool Evaluation

Luminal Watery

Pancreatic insufficiency

Small bowel bacterial

overgrowth

Pancreatic insufficiency

Small intestinal bacterial

overgrowth

CT scan or esophageal ultrasound

CT scan or endoscopic

ultrasonogram

Breath test or aspirates

Secretory or osmotic

Consider both small bowel and colon evaluation

Type of Diarrhea Assessment Common Causes

Inflammatory diarrhea Frequent, small volume, bloody stools, and may be accompanied by fever and severe abdominal cramping May have leukocytes in stool Laboratory tests may demonstrate elevated C-reactive protein level or elevated sed rate (ESR), and low albumin level

Crohn’s disease Ulcerative colitis Ischemic colitis Infectious processes including C. Difficile, cytomegalovirus, tuberculosis, and Entamoeba histolytica

Fatty diarrhea History of weight loss Greasy or bulky appearing stools (may be difficult to flush and creates oily toilet requiring a brush to remove)

Malabsorption syndromes Celiac disease Chronic pancreatitis Inadequate bile acid concentration Small intestinal bacterial overgrowth Liver cirrhosis

Watery diarrhea Classified as osmotic or secretory in origin Differentiate: Fasting decreases stool production in osmotic diarrhea but does not affect secretory diarrhea

Osmotic diarrhea is due to poorly absorbed ions or sugars caused by ingestion of anions such as laxatives and antacids or ions such as magne- sium; or carbohydrate malabsorption of poorly absorbed sugars or sugar alcohols such as sorbitol or xylitol Secretory diarrhea is due to disruption of epithelial electrolyte transport caused most commonly by infectious processes—either viral or bacterial, as well as parasitic or peptide-secreting endocrine

50 Chapter 5 ■ Symptoms and Syndromes

symptoms are persistent and unexplained. If you suspect laxative abuse, you may order a stool laxative screen. Send a stool sample to test for occult blood, C. diffi cile, salmonella, Escherichia coli, lactoferrin, campylobacter, leukocytes, ova, and parasites. If the stool tests positive for leukocytes, the sample should be cultured to identify any bacterial etiology.

Differential Diagnosis: Distinguish fi rst between acute diar- rhea and chronic diarrhea. In acute diarrhea, consider infl ammatory bowel disease, fecal impaction, irritable bowel syndrome, diverticulitis, antibiotic-associated pseudomem- branous colitis, bowel ischemia, drug side effects, food poi- soning, and virus or bacteria exposure. In chronic diarrhea consider ulcerative colitis, Crohn ’ s disease, microscopic colitis, celiac disease, irritable bowel syndrome, bile acid mal- absorption, occult neoplasm, post-radiation entercolitis, and functional problems. A fecal specimen should be obtained for anyone in cases of severe, bloody, infl ammatory, or persistent diarrhea or if an outbreak is suspected.

Treatment: In many cases of diarrhea, replacing lost fl uid and electrolytes is the only treatment needed, but treatment is dependent on the cause. Frail older adult individuals are at increased risk for dehydration and multisystem failure. If diarrhea is severe, refer the patient for emergent evaluation and treatment. In the hospital, the older adult patient should be treated aggressively with IV fl uid therapy with close mon- itoring of the cardiopulmonary status, renal status, and elec- trolytes. In cases of acute-onset diarrhea in which a viral cause is likely, provide symptomatic treatment to maintain hydration and electrolyte balance. Use of medications to slow the intestinal motility and the diarrhea may actually extend the length of the illness.

Follow-Up: Scheduling follow-up visits will be determined based on the cause of the diarrhea. In the case of acute diarrhea, reevaluate the patient after 3 to 5 days of follow- ing the initial treatment plan. If diarrhea persists, diagnostic studies may be indicated and the patient ’ s hydration status reevaluated.

Sequelae: Depending on the cause and extent of the diar- rhea, complications may include dehydration, sepsis, shock,

anemia, fl uid and electrolyte imbalance, malnutrition, and peritonitis.

Prevention/Prophylaxis: Prevention depends on the cause. Oral replacement of fl uids is of highest priority, but in severe cases IV replacement may be warranted. Careful cooking and storage of food is important to avoid spoilage. Check expira- tion dates on dairy and meat products before using. Clean cutting boards and utensils. Educate about cross-contami- nation when cooking, such as with raw meats, to prevent exposure to pathogens. For individuals who are traveling to a foreign country, begin appropriate prophylactic treatment (World Health Organization, 2012). Caution travelers about avoiding undercooked foods, raw foods, buffet food, unpas- teurized dairy products, untreated water, and ice. Carbonated drinks, bottled water, and boiled water are considered safe for drinking and to use for oral hygiene.

Prevention of transmission of diarrhea to or from others (including young children), in hospitals, and in the long-term care facility is extremely important. Frequent hand washing by patients and health-care providers is the key to preventing transmission of infectious diarrhea. Avoidance of long-term laxative use and prudent use of antimicrobial agents are also important in preventing diarrhea.

Referral: Further work-up may be necessary in individuals who are exhibiting prolonged diarrhea, severe dehydration, recurrent episodes of diarrhea, and in individuals who report blood in stools. Refer to the hospital for consideration of an inpatient stay if IV fl uids and/or electrolyte replacements are needed, or if diarrhea persists. The patient may need to be evaluated by a gastroenterologist or an infectious disease specialist depending on the causative agent of the individu- al ’ s diarrhea. Complications may include dehydration, mal- nutrition, peritonitis, sepsis, shock, anemia, or electrolyte imbalances, which can be life threatening (such as with hypokalemia).

Education: Explain to the patient, family, and caregivers the cause of symptoms, diagnostic and treatment measures, fol- low-up, and preventive strategies. Emphasize the need for early intervention to prevent dehydration.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Classify diarrhea into three categories (watery, bloody, or fatty) based on the history, physical examination, and testing.

A Sweetser, 2012

Specifi c therapy depends on the underlying cause. C Barr & Smith, 2014 Sweetser, 2012

Teach patients the signs and symptoms of dehydration. C Barr & Smith, 2014 Arena et al., 2014

Metronidazole 500 mg PO 3 times a day for 10–14 days is the initial and most cost-effective treatment for C. diffi cile diarrhea.

A McDonald et al., 2018

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Chapter 5 ■ Symptoms and Syndromes 51

Description: Dizziness is an imprecise term commonly used to describe various subjective symptoms by lay persons, espe- cially older adults. The practitioner must understand the patient ’ s personal meaning of dizziness to determine etiology of the dizziness. Patients, however, tend to fi nd it diffi cult to articulate their symptoms well. Thus, establishing the time course, provoking or aggravating factors, concurrent symp- toms, age, pre-existing conditions, as well as interpreting physical examination fi ndings, are crucial in establishing a diagnosis. Despite a thorough history and physical exam- ination, the fi nal cause of dizziness is not identifi ed in some patients. The most common clinical categories of dizziness are vertigo, unsteadiness or gait instability, light-headedness, and disequilibrium.

Etiology: Dizziness may result from mixed pathologies; medi- cations; and neurological, otolaryngological, cardiovascular, or psychiatric causes. Benign paroxysmal positional vertigo (BPPV), a disorder arising from the inner ear, is the most common cause in individuals over age 70 years (Luscher, Theilgaard, & Edholm, 2014). People greater than age 70 years complaining of dizziness with associated neurological defi cits but lacking vertigo require a thorough investigation of the cause of their dizziness. Individuals without a neuro- logical defi cit and no defi nitive cause of dizziness identifi ed, can be diagnosed with presbystasis. This is age-related dis- equilibrium not attributed to any pathology and is character- ized by a gradual onset of diffi culty walking (Belal & Glorig, 1986).

Occurrence: Dizziness is a common symptom, with 45% of affected nonhospitalized patients seeking care from primary care providers (Sloane, 1989).

Age: Dizziness occurs in 30% of individuals over age 60 years and increases to more than 50% in individuals over age 85 years old (Jönsson, Sixt, Landahl, & Rosenhall, 2004).

Gender: Dizziness occurs more frequently in women.

Ethnicity: Not signifi cant.

Contributing Factors: Contributory medications include anti- hypertensives, anticonvulsants, psychotropic drugs, and oto- toxic drugs. Physiological changes occurring with age can affect equilibrium. Altered sensitivity of the baroreceptors, as well as diminished sensory and motor pathways over time, increase the vulnerability to syncope and gait instability.

Signs and Symptoms: The patient ’ s description of the symptom should help determine the type of dizziness experienced.

Vertigo: Vertigo is illusion of movement of the patient or the environment due to central or peripheral causes. Associ- ated symptoms may include nausea, vomiting, unsteadiness, or visual disturbances. The time course of vertigo assists in determining the appropriate diagnosis. Episodic vertigo fol- lowing a viral illness and lasting days with nausea and no associated symptoms is usually due to vestibular neuritis. Episodic vertigo lasting for seconds and associated with posi- tion changes is probably due to BPPV. Vertigo of sudden onset lasting for minutes can be due to migraine or cerebrovascular disease, especially if neurological defi cits are present. Vertigo

lasting hours associated with hydropic ear symptoms is prob- ably caused by Ménière ’ s disease. Older adults with head or neck pain post trauma can develop cervicogenic vertigo pro- voked by movement or sustained positions of the neck.

Presyncope: In presyncope, patients have the sensation of nearly fainting. Associated symptoms include perspiration, fatigue, pallor, palpitations, dimming of auditory or visual stimuli.

Disequilibrium: Patients with disequilibrium describe a sense of imbalance. Symptoms improve dramatically by bracing on a stationary object and are exacerbated by vision defi cits or uneven surfaces. Associated symptoms may include chronic hearing loss, chronic lower extremity sensation defi cits, poor coordination, and general weakness. Patients with acute gait instability need further evaluation for cerebrovascular disease.

Light-Headedness: Patients often describe presyncope symp- toms as light-headedness. This can often be associated with anxiety or depression.

Physical Examination: The physical examination should be comprehensive and include the following components:

General: Observe how the patient moves around. Does he or she hold onto the furniture or walls? Any signs or symptoms of fever?

Head, Eyes, Ears, Nose, and Throat: Test for extraocular move- ment, watching for nystagmus. Rotatory nystagmus suggests a peripheral cause of dizziness, but this alone is not a con- clusive fi nding. Vertical nystagmus suggests a central lesion and needs further investigation. In many clinical situations, rotatory nystagmus is superimposed on horizontal nystag- mus. Check the patient ’ s static monocular or binocular visual acuity and dynamic visual acuity. Evaluate visual fi elds. Perform a funduscopic examination, looking for papilledema and other abnormalities. Inspect the ears for accumulation of fl uid, tympanic membrane abnormalities, or presence of cerumen impaction. Perform Weber ’ s and Rinne ’ s tests if decreased hearing to conversational level auditory stimulus. Examine the neck for range of motion and fl exibility.

Cardiovascular: Evaluate central and peripheral function. Auscultate for heart sounds; evaluate for arrhythmias and murmurs. Evaluate the carotid arteries for bruits. Check vital signs, including orthostatic blood pressure and heart rate. A drop in systolic blood pressure of 20  mm  Hg or diastolic blood pressure of 10  mm  Hg is signifi cant, especially if it reproduces the patient ’ s symptoms.

Neurological: Test for coordination defi cits with fi nger to nose, heel to shin, past pointing, and rapid alternating move- ments. If coordination tests are abnormal, keep vestibular dysfunction or cerebrovascular insuffi ciency in the differen- tial. Test sensation including pain, temperature, vibration, proprioception, and Romberg. Patients with cerebellar disease have diffi culty standing with their feet together. Patients with decreased position sense or other sensory defi cits in their lower extremities are able to compensate with eyes open but

DIZZINESS

52 Chapter 5 ■ Symptoms and Syndromes

sway with eyes closed. Perform gait assessment, including tandem gait. Complete a motor examination and evaluate deep tendon refl exes. The inclusion of psychological tests (mental status, depression, anxiety) is appropriate if a psy- chogenic cause is suspected.

Special Diagnostic and Screening Tests: Forced hyperventilation involves asking the patient to breathe 20 to 30 times per minute for 2 to 3 minutes. This normally causes dizziness and fi nger and perioral numbness. If presenting sensations are reproduced, the dizziness may be related to anxiety.

Have the patient march in place for 30 seconds with the eyes closed and arms extended in front. Be careful not to orient the patient with any sounds (e.g., your voice or a ticking clock). Patients with absent or reduced vestibular function (from prior vestibular damage) rotate more than 30 to 45 degrees while marching.

For the Dix-Hallpike maneuver, assist the patient quickly to lie down on the examination table with the head hanging over the back of the table at an approximate 30-degree angle with the face turned 45 degrees to the right. While holding the patient ’ s head in place for 1 minute, observe the patient for nystagmus and ask whether this reproduces the dizziness (vertigo) symptoms. Bring the patient back to a sitting posi- tion and observe for 1 minute. Repeat the test with the head turned 45 degrees to the left. If vertigo is reproduced, the test should be repeated two or three times on the side that caused the most severe symptoms to determine if the nystagmus and symptoms begin to disappear. Patients with benign pos- tural vertigo (BPV) experience severe vertigo 5 to 15 seconds after the head is turned and nystagmus is induced. Position change must be completed in 2 seconds, as the signs typically fade in less than 1 minute, and repeated testing causes the symptoms to disappear. The safety of this test must be consid- ered if the patient is frail or has neck or back problems.

Diagnostic Tests: Diagnostic tests are dependent on the pre- senting symptoms, the history and physical examination, as well as comorbid factors. The HINTS (head-impulse, nys- tagmus, test of skew) examination can help distinguish peripheral from central etiologies, as well as delineate which patients may need diagnostic testing ( Muncie, Sirmans, & James, 2017 ). Select testing might include CBC for anemia, serum glucose for hypoglycemia, EKG or Holter monitoring for arrhythmia, audiometry if hearing loss is present, or ves- tibular function tests (such as videonystagmography or elect- ronystagmography). Neuroimaging (CT, CTA, MRI, or MRA) must be ordered if neurological symptoms are present to evaluate for a central lesion or vascular occlusions causing ischemia.

Differential Diagnosis: Differentiate between vertigo (a sensa- tion of movement), light-headedness (a sensation of being about to faint), and syncope (an actual loss of conscious- ness). If dizziness has a predictable pattern associated with it (e.g., mid to late morning, mid to late afternoon, 2 to 4 hours after eating), suspect hypoglycemia.

Treatment: Treatment is based on the cause of the dizziness. Physical therapy for balance training or vestibular rehabil- itation can be the primary treatment or it may supplement

other management approaches. Traditional vestibular reha- bilitation, although shown to be effective, requires face-to- face time, resulting in inconsistent completion rates. Recently, however, there are ongoing studies evaluating the effi cacy of blended online and face-to-face vestibular rehabilitation pro- tocols in the hope of improving access and promoting consis- tent completion rates ( Geraghty et al., 2014 ).

Patients with BPV can perform the Epley maneuver, which loosens particles out of the posterior semi-circular canal and back into the utricle. If the cause of light-headedness is med- ication side effects or volume defi ciencies, adjustments are indicated. Support stockings may alleviate symptoms from orthostatic hypotension. Appropriate management of car- diovascular, cerebrovascular, or psychogenic conditions is warranted.

Antihistamine medications like meclizine were initially shown to reduce the severity and frequency of attacks, as well as signs and symptoms associated with positional or con- tinuous vertigo of vestibular origin like vestibular neuritis. However, they have not been shown to be effective in patients with peripheral vestibular diseases like BPV or central vestib- ular diseases, despite their frequent use for these conditions (Cohen & DeJong, 1972). Benzodiazepines, despite the risk of somnolence and potential for dependency, are another class of drugs frequently used to treat associated symptoms of vertigo, although recent studies have shown no difference between meclizine and diazepam (Shih et al., 2017). These medications require caution, as they can worsen the symp- toms of dizziness and have other side effects, which are par- ticularly problematic in older adults.

Follow-Up: Patients should follow up if symptoms worsen, change from one type of dizziness to another, or do not resolve within 2 weeks.

Sequelae: Older adults with dizziness are at high risk for falls and injury, as well as self-induced immobility due to fear of falling. In patients younger than 80 years, the prevalence of falls is 16.5%, whereas in patients older than 80 years, the prevalence is 31.7% (Olsson Moller et al., 2013). Clinicians can view dizziness as a geriatric syndrome that requires spe- cifi c strategies to reduce signifi cant impairment and compli- cations (Tinetti, Williams, & Gill, 2000).

Prevention/Prophylaxis: Educate older adults to move extrem- ities before rising from positions held for any length of time to compensate for age-related changes in vascularity. Evalu- ate for medication side effects before adding medications to combat the dizziness.

Referral: Persistent symptoms with unknown etiology require a referral to neurology, cardiology, otolaryngology, or psychi- atry as appropriate.

Education: Explain the underlying cause, rationale for treat- ment, and importance of exercises. Teach the patient the exercises and ask for return demonstration. Explain that this condition may take time to completely resolve, but that it is important to seek care for worsening or persistent symptoms. Encourage the use of assistive devices for safety until the con- dition resolves.

Chapter 5 ■ Symptoms and Syndromes 53

Description: Dysphagia is a swallowing disorder involving the inability to get food from the mouth to the stomach. The problem is divided into oropharyngeal causes related to the inability to initiate the act of swallowing and esoph- ageal causes from disorders of impaired transit through the esophagus.

Etiology: The causes of dysphagia are multiple and diverse. Aging does not cause clinical dysphagia; however, some normal changes of aging, such as changes in nerve and sensory function, delay in pharyngeal swallow, loss of esoph- ageal sphincter tone, decreased lower esophageal sphincter relaxation, delayed emptying of the esophagus, decreased facial muscle and masticatory strength, and oral cavity changes (e.g., impaired masticatory function, reduced sal- ivary fl ow, xerostoma) can contribute to or aggravate any swallowing problems.

Oropharyngeal dysphagia is usually related to neuro- muscular impairments of the tongue, pharynx, and upper esophageal sphincter. Stroke is the most common cause of oropharyngeal dysphagia, but other causes include CNS disorders such as extrapyramidal syndromes, Alzheimer ’ s disease, myogenic disorders (e.g., myasthenia gravis or myop- athies), structural disorders (e.g., Zenker ’ s diverticulum, cricopharyngeal stenosis, or tumors). Xerostoma, dry mouth, is a common occurrence in older adults, affecting 16% of men and 25% of women, and adversely affects swallowing by impairing the ability to form an adequate bolus of food to allow for smooth transport of food/fl uid.

Esophageal dysphagia is usually a result of a motor disorder (e.g., muscular dystrophy, myasthenia gravis, scleroderma), motility or neurological disorders (e.g.,

achalasia, multiple sclerosis, amyotrophic lateral sclerosis), or an obstruction from either intrinsic (e.g., carcinoma, stric- ture, web, diverticula) or extrinsic (e.g., mediastinal tumors, vascular anomalies) sources. Achalasia is characterized by slow, progressive dysphagia for liquids and solids with weight loss, and its etiology is unknown. Esophagitis is another eti- ology, usually secondary to GERD, herpes virus, or a retained pill (primary offenders include NSAIDs, quinidine, potas- sium, ferrous sulfate, tetracycline, and alendronate). Drugs with dopamine antagonist action such as phenothiazine and metoclopramide can cause dystonia and dyskinesia, leading to dysphagia.

Age/Occurrence: Swallowing disorders occur in 13.5% of adults and are more common in older adults. Individuals over age 65 years account for up to two-thirds of all people with dysphagia. Forty percent to 60% of nursing home resi- dents develop dysphagia compared to 13% to 33% of nonin- stitutionalized older adults . Symptomatic dysphagia has been found to occur in 16% of individuals over 87 years old.

Gender: Dysphagia occurs equally in males and females.

Ethnicity: Not signifi cant.

Contributing Factors: Factors that contribute to dysphagia include changes with aging, including decreased body fl uid and facial muscle weakness, which decreases masticatory strength. Medications with anticholinergic side effects (e.g., antidepressants, opiates, sedatives, antipsychotics, anti- spasmodics, antihistamines, and some antihypertensives) may produce slowing or disruptions of the oral phase of swallowing and affect salivation. Other drugs can increase the likelihood of refl ux (e.g., calcium channel blockers,

CLINICAL RECOMMENDATIONS EVIDENCE RATING REFERENCES

Balance disorders and presence of dizziness in the elderly is a strong predictor of falls. Falls are the leading cause of accidental death in people older than 65 years.

A Fernández, Breinbauer, & Delano, 2015

Performing a medication history and review is important for adjusting medications to prevent/resolve medication-related dizziness.

A Shoair, Nyandge, & Slattum, 2011

No routine neuroimaging tests are indicated in the diagnosis of dizziness unless neurological symptoms are present. However, check glucose levels in diabetics and monitor cardiac rhythm in those >45 years old.

C Muncie, Sirmans, & James, 2017

Vestibular rehabilitation is effective for management of unilateral peripheral vestibular dysfunction. It is unclear at this time if Internet- based vestibular rehabilitation is superior to traditional vestibular rehabilitation.

B Geraghty et al., 2014

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

DYSPHAGIA

54 Chapter 5 ■ Symptoms and Syndromes

β -adrenergic agents, aspirin, theophylline, nitrates, vitamin C, and NSAIDs), particularly if the patient has inadequate fl uid intake.

Signs and Symptoms: Symptoms typically associated with oropharyngeal dysphagia include diffi culty initiating swal- lowing, food sticking in the throat, nasal regurgitation, and coughing during swallowing. The onset of symptoms may assist in the differential diagnosis because sudden onset may suggest a cerebrovascular event, whereas insidious onset is more characteristic of a myopathy, multiple sclerosis, or amy- otrophic lateral sclerosis. Voice changes (wet vocal quality) may be associated with swallowing incompetence. Patients with esophageal dysphagia most commonly present with a complaint that food is stuck in the chest (sternum or supra- sternal area) and may report choking or a sensation of pres- sure. Refl ux symptoms may be present. If total obstruction occurs, salivation increases, and vomiting may result. Weight loss and aspiration pneumonia may occur. Weight gain may be a sign of dysphagia if the patient consumes signifi cant amounts of processed foods, such as milkshakes, that have a higher calorie count.

Careful history helps to distinguish the type of dyspha- gia. It is important for the clinician to distinguish between diffi culty swallowing solids, liquids, or both. In general, patients with obstructions (e.g., strictures, webs) complain of solid rather than liquid dysphagia, which may progress to both solid and liquid dysphagia. The onset of signs and symptoms is important because rapid progression may indi- cate infection, irritation, or a food impaction, whereas a more insidious onset suggests dysmotility. Physical exam- ination consists of checking the oral cavity in conjunction with a neuromuscular examination. The mouth should be assessed for signs of irritation, ill-fi tting dentures, and any pharyngeal masses. The head and neck should be examined, checking for lymph node or thyroid enlargement. Dentures may block palatal mechanoreceptors, which can lead to poor bolus control, oral transit delays, and longer feeding times. Review all medications and address any that may decrease salivation.

Neurological evaluation must be comprehensive and include a mental status evaluation, cranial nerve examina- tion, and assessment for muscle weakness. A bedside swallow assessment to determine aspiration risk is often inadequate and misleading, so additional diagnostics may be indicated if increased suspicion of dysphagia persists.

Diagnostic Tests: Diagnostic tests are based on the medical history. Videofl uoroscopy (modifi ed barium swallow) is important to assess aspiration risk and guide therapy by a speech language pathologist and a radiologist. Other tests that may be indicated based on the history and physical include testing the stool for occult blood and a CBC with indices if associated esophagitis is suspected. Ambulatory 24-hour pH testing of intraesophageal pH and manometry has been found to be useful when evaluating for GERD. If malnutrition is suspected, a serum albumin level may be appropriate with the understanding that infl ammatory illnesses common in older adults may result in a low albumin unrelated to actual protein calorie malnutrition. Laboratory screening may be helpful to exclude metabolic, systematic, and myogenic dis- eases. Upper endoscopy is performed for evaluating structural causes; it also allows for tissue samples to determine etiology

and, if needed, therapeutic intervention (e.g., dilatation of esophageal ring). MRI or CT scan is used if a cerebrovascular event is suspected. Fiberoptic endoscopic evaluation of swal- lowing (FEES) is an option when the patient cannot be trans- ported to the radiology department for the modifi ed barium swallow and is done by a speech language pathologist and an otolaryngologist. FEES is diagnostic and therapeutic, allowing for biofeedback, as patients can be instructed in swallowing techniques and visually observe their swallowing function on a video monitor.

Differential Diagnosis: It is important to differentiate whether the patient has a feeding problem (inability to present food to the mouth) or a swallowing problem (inability to get food from the mouth to the stomach) or both. Cognitive impair- ments are frequently associated with feeding problems. Eval- uation for specifi c motor, neurological, or obstructive causes should be performed. For the patient complaining of burning associated with swallowing, refl ux esophagitis, esophageal infection, and pill esophagitis need to be explored.

Treatment: Treatment targets the specifi c cause, compensates for mechanical problems, and eliminates or minimizes aspira- tion risk. Therapeutic strategies include diet modifi cation and swallowing posture or techniques. Management of dyspha- gia after a stroke is directed toward increasing the sensory awareness of food and improving bolus movement by the chin-tuck and double-swallow technique. A percutaneous endoscopic gastrostomy or nasogastric tube may be used to feed stroke patients at high risk for aspiration, but there is no guarantee it will prevent aspiration. A nutritionist works to ensure appropriate consistency and nutritional content. Stable patients can be treated as outpatients. Hospitalization may be required when dysphagia is associated with total or near-total obstruction of the esophageal lumen. Esophageal dilation (pneumatic or bougie), surgical intervention for an esophageal stent, or laser therapy for late cancer also may be part of the treatment plan, depending on the etiology of the dysphagia. Patients with esophageal spasms can be given calcium channel blockers, and those with associated esophagitis may receive antacids or H 2 blockers, or, in cases of severe esophagitis, a proton pump inhibitor. Referral to a speech language pathologist for specifi c exercises, compensa- tory strategies, and recommendations for dysphagia can help to regain control over swallowing. A dental referral should be obtained to assess and treat problems with dentition that may be contributing to the dysphagia.

Follow-Up: Patient monitoring depends on the specifi c etiol- ogy of the dysphagia.

Sequelae: Complications from dysphagia depend on its cause. The most common complications are malnutrition, aspiration, pneumonia, and death. Of stroke patients with dysphagia, 45% to 68% die within 6 months, largely due to nutritional and pulmonary complications related to dysphagia.

Prevention/Prophylaxis: Patients with dysphagia should remain upright with the head midline and slightly fl exed when eating or drinking. Extremely hot or cold foods may worsen symptoms of dysphagia. Aspiration precautions include modifying food and fl uid consistencies, giving verbal and physical prompts, and allowing additional time for feeding to encourage double swallows and small amounts taken per mouthful.

Chapter 5 ■ Symptoms and Syndromes 55

Referral: Initial consultation with speech pathology for eval- uation can be essential in deciding on further assessment. Gastroenterology should be consulted if invasive diagnostic tests are indicated.

Education: Patients and caregivers should be encouraged to provide food and fl uids at appropriate consistency. All

foods, especially meat products, should be chewed thor- oughly. Patients also should be informed that it is important to swallow all medications with plenty of fl uid while in an upright position.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients with cough and their caregivers should be questioned regarding swallowing problems and if positive further evaluation for dysphagia is indicated.

C Amin & Belafsky, 2010

Patients with dysphagia should undergo clinical bedside assessment, endoscopy, or fl uoroscopy.

C Amin & Belafsky, 2010

First-line therapy for dysphagia is swallowing therapy, including simply tucking the chin.

C Amin & Belafsky, 2010 Welch et al., 1993

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

FALLS

Description: According to the World Health Organization (WHO), a fall is an event that results in a person coming to rest inadvertently on the ground, fl oor, or other lower level. Falls are commonly categorized by health-care providers as witnessed or unwitnessed, assisted or unassisted, and by loca- tion (community, hospital, or long-term care). In the Inter- national Statistical Classifi cation of Diseases and Related Health Problems (ICD-10), falls are categorized as slipping, tripping, and stumbling. Falls are the leading cause of both fatal and nonfatal injuries in older adults. Of serious injuries, fractures and traumatic brain injury are the most common, with falls as the cause for 95% of hip fractures. The total cost for fall injuries in 2013 was 34 billion dollars.

Etiology: The majority of falls are caused by an interaction of several intrinsic and extrinsic risk factors. Intrinsic factors include age, previous falls, weakness, gait/balance prob- lems, poor vision, postural hypotension, chronic medical conditions (e.g., arthritis, dementia, arrhythmia, neuropa- thies), an occult medical condition (e.g., pneumonia or UTI), and fear of falling. Extrinsic factors include conditions in the environment such as lack of handrails, grab bars, poor lighting, obstacles, slippery or uneven surfaces, psychoactive medications, or being on more than four medications. Addi- tional risk factors include inactivity, improper use of assistive devices, and risky behavior (e.g., use of a ladder).

Occurrence: Approximately 25% of persons 65 years and older and 50% of persons 80 years and older will fall each

year, although the true incidence of falling is likely to be higher due to the fact that many falls are not reported. Persons who reside in long-term care are twice as likely to fall as persons who live in the community.

Age: Normal physiological changes with aging can affect ves- tibular function, vision, and postural refl exes, which increase the risk of falling. Persons who are older than 85 years are four times more likely to fall as persons age 65 to 74 years.

Gender: Males and females are equally likely to fall; however, women are more likely to report falls and fall-related injuries than men. Women have an increased risk of falling due to decreased muscle mass and osteoporosis.

Ethnicity: According to data from the 2014 Behavioral Risk Factor Surveillance System survey, Caucasians and Amer- ican Indians/Alaskan Natives were more likely to fall com- pared with African Americans and Asian/Pacifi c Islanders. American Indians/Alaskan Natives were more likely to report a fall injury compared with all other racial/ethnic groups.

Contributing Factors: The risk of a fall increases as the number of fall risk factors increases, and risk factors increase with age.

Signs and Symptoms: Every older adult patient or their fam- ilies/caregivers should be questioned if there has been a fall in the past year. Half of patients or families may fail to mention a fall unless there was injury. In addition to asking

56 Chapter 5 ■ Symptoms and Syndromes

about falling, it is important to assess tripping, slipping, or stumbling but not falling, and fear of falling, as both increase risk of falling. For patients who report a fall, it is important to obtain information about the circumstances of the fall, including location, what the patient was doing, how the fall occurred, presence of pain after the fall, and symptoms at the time of the fall (e.g., chest pain, shortness of breath, dizzi- ness/light-headedness, vertigo, diaphoresis, numbness and weakness of extremities, loss of consciousness).

Diagnostic Tests: The details about the fall and symptoms associated with a fall will determine the need for diagnostic testing. Intracerebral injuries need to be considered in any patient on anticoagulants or antiplatelet drugs. Evidence of trauma to the head and loss of consciousness are predic- tive of intracranial injuries and should guide the decision to obtain diagnostic imaging. Because loss of consciousness is diffi cult to assess in unwitnessed falls or in persons with cognitive impairment, it is important to determine baseline mental status. It can be challenging to determine if loss of consciousness was the cause or result of the fall.

The decision to obtain radiographic imaging on elders who fall should be based on understanding that low-force mechanisms such as falling from a sitting or standing posi- tion has been shown to cause injury, primarily fractures in frail older adults. Hip fracture, one of the most common injuries, should be considered in a person with any of the following: pain in the groin region, inability to bear weight, external rotation and abduction of the affected hip, and the appearance of a shortened leg. A plain radiograph can detect fractures in the majority of persons, however, for patients with negative fracture on plain radiograph, ongoing pain, and inability to function at previous level, an occult frac- ture should be suspected. An MRI can identify occult frac- tures, soft tissue damage, and joint disease. For any injury, nondisplaced fractures may not be evident on initial radio- graphic imaging, so consideration of repeat imaging may be necessary.

For patients who have reported a fall, slipping, tripping, or stumbling in the past year, or who report fear of falling, gait, strength, and balance should be assessed. The timed Get Up and Go Test, 30-Second Chair Stand, or 4-Stage Balance Test can be done in the offi ce in 30 seconds or less. There are no standard laboratory recommendations for patients who are at increased risk of falling or who have fallen, although a suggested work-up would include a basic met- abolic panel, CBC, vitamins D and B 12 levels, thyroid func- tion, and EKG. Diagnostic testing should be individualized based on the history and physical examination fi ndings and comorbidities.

For patients with identifi ed gait and balance issues, it is important to assess multifactorial risks, including assess- ment for orthostatic hypotension or postural dizziness; cog- nitive evaluation, such as the Mini-Mental State Examination (MMSE); visual acuity assessment; and assessment of feet, footwear, and mobility aids.

Differential Diagnosis: Determining the cause of a fall can be complex because many falls are multifactorial, resulting from intrinsic and extrinsic factors. A differential diagnosis can be narrowed by assessment of these risk factors, along with subjective and objective fi ndings. Reports of light-head- edness, near-fainting, or legs giving out is consistent with

cerebral ischemia and would suggest orthostasis, arrhyth- mias, or other cardiovascular conditions. Diffi culty standing from a chair or feeling that legs are not supportive suggests deconditioning or neuromuscular disease. Disequilibrium or feeling the legs are not coordinated could suggest vestibulo- spinal tract or cerebellar lesions.

The physical examination can help narrow a differen- tial diagnosis or identify additional factors related to a fall. It is important to initially assess gait, strength, and balance; however, the differential diagnosis can be narrowed by including assessment of orthostatic vital signs, muscle tone to determine spasticity or rigidity, sensation, propriocep- tion, vibration to determine neuropathy or a somatosensory problem, cognitive status, and visual problems. The pattern of injury can help sort out the event leading to a fall. For example, a wrist fracture caused by a fall on an outstretched hand suggests that consciousness was preserved while falling, or bilateral wounds on knees could suggest drop attacks.

Treatment: Regardless of having a history of a fall, interven- tions should address intrinsic and extrinsic risk factors. All older adults with gait, strength, or balance problems should be encouraged to engage in routine exercise or be referred to a community falls prevention program.

Follow-Up: For patients who have fallen and those at risk of falling, ongoing management and monitoring of medical conditions associated with falling is important. Follow-up on exercise or the use of interventions to improve gait, strength, and balance serves as reminders or reinforcement of the importance of fall prevention.

Sequelae: Persons who fall are two to three times more likely to fall again. Approximately 5% to 10% of older adults who fall endure serious injury, including fractures and traumatic brain injury. Injuries result in decreased functional status, subsequent loss of independence, and possible nursing home placement. Falls can also have psychological and social consequences, such as fear of falling or post-fall anxiety syndrome, which can result in social isolation and loss of self-confi dence. Approximately 25% to 50% of elders will not ambulate at their previous level after a fall.

Prevention/Prophylaxis: Physiological changes that increase the risk of falling in older adults are inevitable; however, many falls are preventable. Factors associated with the risk of falls in older people need to be addressed and imple- mented, including optimizing medical conditions, tapering psychoactive medication when appropriate, annual review of all medications, and managing environmental issues (e.g., inappropriate lighting, lack of grab bars, ill-fi tting footwear, inappropriate assistive devices). Vitamin D supplementation is widely recommended for all older adults regardless of their history of falls or risk factors, however, the recommended dose varies. Exercise in general has been shown to reduce the prevalence of falls, although evidence on specifi c exer- cise at home is lacking. Muscle mass and leg strength can be increased with resistance strength training for older adults. Strength and balance exercise programs are available in many communities. The CDC and National Council on Aging provide resources to help identify and evaluate community falls prevention programs.

Referral: A home safety assessment is essential for patients with identifi ed gait and balance problems. The following

Chapter 5 ■ Symptoms and Syndromes 57

referrals are based on the risk factors for falling, the cause of the fall, and the history and physical examination: physical therapy, occupational therapy, podiatrists or subspecialty pro- vider such as cardiologist or neurologist.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Group and home-based exercise program, and home safety interventions reduce rate of falls and risk of falling.

A Gillespie et al., 2012

Exercise may help reduce fear of falling in community- dwelling adults.

A Kendrick et al. 2014

Exercise as a single intervention can prevent falls in community-dwelling older adults.

A Sherrington et al. 2016 El-Khoury et al., 2013

Vitamin D supplementation does not reduce falls. A Gillespie et al., 2012 Uusi-Rasi et al., 2015

Multifactorial assessment and intervention program reduce rate of falls but not risk of falling.

A Gillespie et al., 2012

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

FATIGUE

Description: Fatigue is a subjective state often described as a feeling of tiredness, weariness, lack of energy, or exhaustion that is unrelieved or only partially relieved by rest. It often results in an inability to initiate normal activity; a reduced capacity to maintain activity; and diffi culty with concen- tration, memory, and emotional stability ( Gambert, 2013 ). Occasional fatigue is common, but pathological fatigue may affect quality of life and impair independence. Chronic fatigue syndrome occurs when fatigue lasts longer than 6 months and is not relieved with rest. Fatigue could also be a symptom of another illness and any older person with this complaint should obtain a medical evaluation and work-up.

Etiology: Physiological fatigue occurs normally with inade- quate rest, excess exertion, or insuffi cient diet. Fatigue that interrupts the individual ’ s activities of daily living (ADLs) may have a physical or psychological cause and be either acute or chronic. Fatigue in older adults may be an early indicator of the aging process, as well as debility or another disorder (Tang & Chen, 2014; Hermans et al., 2014; Manty et al., 2014). See Table 5-4 for common causes of fatigue.

Occurrence: Fatigue occurs in about 25% of the U.S. popu- lation ( Gambert, 2013 ; Gluckman, 2014 ). Under-reporting and under-recognition make the actual prevalence unknown.

Age: Fatigue is common among the elderly, with reports of up to 65% of older patients complaining of fatigue at some point (Tang & Chen, 2014; Hermans et al., 2014; Manty

et al., 2014). Among elders living in the community and assisted living facilities, more than 50% report mild fatigue and 7% report severe fatigue on a chronic basis.

Gender: Fatigue is more common in women than in men.

Ethnicity: Not signifi cant.

Contributing Factors: Poor dietary habits, overexertion, alco- hol abuse, smoking, stress, chronic illness, drug interactions, misuse of drugs, and sleep apnea may contribute to fatigue symptoms. In the older adult individual it is compounded by a decrease in muscle strength, loss of muscle neurons, muscle atrophy, a decrease in hormone levels, and lack of exercise.

Signs and Symptoms: Obtain a complete medical history and perform a thorough physical examination when an individ- ual complains of fatigue because it may indicate various psychological or physiological illnesses. Conduct a complete symptom assessment, including the onset; duration; severity; and precipitating, aggravating, and relieving factors. Identify other indicators or associated symptoms of fatigue, which may include decreased energy expenditure, decreased endur- ance, sleep disturbance, attention defi cits, somatic complaints (aching body, tired eyes), dyspnea, and weakness. Carefully review the adequacy of the diet, all medications (evaluating for potential medication side effects), activity level (including degree of independence of ADLs), and potential causes or contributing factors. Identify the impact fatigue is having on the person ’ s ADLs and quality of life and current stressors.

Education: Patients and their families need to be informed that falls are preventable. They need to be encouraged to report all falls, near falls, or fear of falling to their health-care providers.

58 Chapter 5 ■ Symptoms and Syndromes

Common Causes of Fatigue Infectious causes Viral infections

• Hepatitis A, B, C

• Epstein-Barr virus (mononucleosis)

• HIV

Bacterial infections

• TB

• Lyme disease

• Occult endocarditis

• Osteomyelitis

Immunological/rheumatic

• RA

• Systemic lupus erythematous

Celiac disease

Fibromyalgia

Medication related NSAIDs

Tetracycline

Antipsychotics

Antidepressants

Sleep medications

Pain medications

Anxiolytics

Statin agents

Illicit drugs

Alcohol

Chronic fatigue

syndrome

No known cause but theories to the cause

include viral infections, immune system

problems, and hormonal imbalances

Physiological Inadequate sleep

Insuffi cient rest

Overactivity

Poor physical conditioning

Stress

Changes in diet, including decreased protein

intake

TABLE 5-4

Relocation of one ’ s home or change in job/

retirement

Frailty

Weight loss

Sarcopenia

Parkinson ’ s disease

Vitamin defi ciencies including vitamins B 12

and D

Endocrine related Hypothyroidism including subclinical

hypothyroidism

Hyperthyroidism

Perimenopausal/postmenopausal

Hypogonadism (low testosterone levels)

Neoplastic-related

disorders

Any form of cancer

Chemotherapy treatments

Radiation treatments

Anemia related to cancer, as well as its

treatment

Toxin-related

disorders

Exposure as well as toxicity to:

• Carbon monoxide, possibly caused by

wood-burning stove, kerosene lamps,

automobile exhaust, or coal-burning plants

• Lead

• Arsenic

Cardiovascular/

pulmonary diseases

Congestive heart failure

COPD

Psychogenic Depression

Anxiety

Somatoform disorders

Substance abuse (prescribed and

nonprescription drugs, alcohol)

Source: Gambert ( 2013 ); Combs et al. (2013); Tang & Chen (2014); Hermans et al. (2014); Manty et al. (2014); Patel, 2015.

The quality and quantity of sleep should always be evalu- ated. Distinguish between generalized fatigue and actual weakness by testing for muscle strength and presence of localized tenderness. A thorough physical examination will include a mental status examination to screen for dementia and rule out depression.

Diagnostic Tests: The benefi t of testing is limited when fatigue is the only symptom. Diagnostic tests on all patients with persistent unresolved fatigue should include CMP, CBC with differential, erythrocyte sedimentation rate (ESR), and/or C-reactive protein, because these are low cost and offer signif- icant screening capacity. Other tests that may be appropriate include thyroid function, urinalysis, and pulmonary function tests. If symptoms and signs indicate cardiac decompensa- tion, a B-type natriuretic peptide (BNP) may indicate degree of heart failure and an EKG may reveal cardiac arrhythmias, enlargement of the heart, myocardial infarction, or abnor- malities in the conduction system. Late-life hypothyroidism or masked hyperthyroidism may present with a chief com- plaint of fatigue.

Differential Diagnosis: Fatigue can be related to many psy- chological and physiological etiologies. Psychiatric disor- ders, including depression and generalized anxiety disorder, account for 70% of cases of fatigue. An underlying cause is determined in only 10% of all cases. Fatigue that cannot be relieved by rest or sleep is often a sign of disease.

Treatment: Treatment depends on the etiology identifi ed in the comprehensive work-up. Symptom management includes regular exercise, attention-restoring activities, psychosocial techniques, energy conservation measures, good sleep hygiene, improving diet, and possibly adding nutritional sup- plements. Pharmacological management is directed at the cause of the fatigue. Psychostimulants may be considered for opioid-related somnolence, cognitive impairment, and depression.

Follow-Up: Follow-up depends on the fi ndings. Monitor the patient periodically as indicated by diagnosis or symptoms, symptom persistence, and disability associated with the symptom. The symptom may be a subclinical one.

Chapter 5 ■ Symptoms and Syndromes 59

Sequelae: The potential for complications relates to the cause of fatigue and the impact the symptom has on the person ’ s function.

Prevention/Prophylaxis: Optimal health maintenance, in- cluding maintaining a healthy diet, regular exercise, and good sleep hygiene, may prevent or enable early recogni- tion of signs and symptoms of systemic or psychological illness.

Referral: Referral to a specialist may be indicated based on the results of the work-up.

Education: If the fatigue has a physiological cause, teaching should be related to the fi ndings; psychological counseling, changes in the environment, behavior modifi cation, and stress reduction may be needed. The goal of fatigue manage- ment is to provide the patient with self-help tools to eliminate or alleviate fatigue.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

A thorough history and physical examination are crucial in determining the differential diagnosis and identifying the causative agent.

C Gambert, 2013

Graded exercise has been shown to improve symptoms and physical function in patients with fatigue.

A Gluckman, 2014 Gambert, 2013

Cognitive-behavioral therapy is an effective treatment for adult outpatients with chronic fatigue syndrome.

A Gluckman, 2014

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

HEADACHE

Description: Headache refers to a symptom that occurs in the head, neck, or face. Headaches decline with aging and any new onset of headache should be considered serious until proved otherwise.

Etiology: The International Classifi cation of Headache Disorders (ICHD), 3rd edition, describes two categories of headache: primary and secondary (International Headache Society [IHS], 2013). Primary headaches include those in which there is an intrinsic dysfunction of the nervous system, often genetic in origin, which predisposes the older adult to increased vulnerability to headache attacks. Primary headaches include migraine, tension-type headache (TTH), cluster headache, and other trigeminal autonomic cephal- gias. In contrast, secondary headaches are those in which the headache is secondary to an organic or physiological process, intracranially or extracranially. Secondary head- aches include headaches attributed to trauma or injury to the head and/or neck; cranial or cervical disorder; nonvascu- lar intracranial disorder; substance abuse or its withdrawal; infection; disorder of homeostasis; disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cervical structures; and psychiatric disorder.

Occurrence: While the prevalence of headache decreases in the older adult, headaches remain a problem with approxi- mately 17% of older adults reporting “frequent headaches” (more than two headaches per month) ( Bravo, 2015 ; Dees, Coleman-Jackson, & Hershey, 2013 ). The majority of head- aches (approximately 66%) are primary, TTH, and migraine.

TTH is the most common type of headache in individuals over 65 years old and in the general population, with a lifetime prevalence of 78% (Crystal & Grosberg, 2009). Of greater signifi cance is that secondary headaches are more common in older adults over 65 years old, 15% of which are new-on- set headaches, which is signifi cantly increased from an esti- mated 1.6% for adults under 65 years old ( Bravo, 2015 ).

Age: The prevalence of primary headaches decreases with age; however, the prevalence of migraine in patients over 65 years old is still 10%. New-onset migraine in patients over 60 years old is rare and is a red fl ag indicating evaluation for a secondary cause ( Bravo, 2015 ).

Gender: TTH is more frequent in women in all age groups, regardless of race or education (Crystal & Grosberg, 2009). Generally, women are affected more often than men; 76% of women and 57% of men report one headache per month. Migraine headaches are more common in women than in men, tending to begin in early adulthood. Cluster headaches are more common in men than in women, with a mean age of onset at age 30 years. Giant cell arteritis is more com- monly seen in women.

Ethnicity: Giant cell arteritis is more common in Caucasian populations. Ethnicity does not appear to be related to other headache types.

Contributing Factors: Depending on the type of headache, multiple factors can contribute. Poor posture, cervical osteo- arthritis, ill-fi tting dentures, tooth pain, and jaw disorders

60 Chapter 5 ■ Symptoms and Syndromes

can contribute to tension headaches. Depression, anxiety, sleep disorders, and general pain syndromes can also con- tribute to most headache types. Medication side effects, par- ticularly with estrogen, calcium channel blockers, nitrates, anti-Parkinson ’ s drugs, indomethacin, and theophylline, can contribute to headaches. Alcohol can trigger or worsen head- aches. Migraines can be triggered by dietary factors such as aged or smoked cheese, chocolate, caffeine, and monoso- dium glutamate, as well as changes in sleep pattern, weather changes, and smoking. Genetics may play a role in migraine, cluster headache, and giant cell arteritis.

Signs and Symptoms: Headache types, presentation, and treatment options change as patients age ( Bravo, 2015 ). Tension headaches are the most common and are due to mostly extracranial causes, such as muscle tension. Migraine in older adults may appear with sensory or motor phenome- non and may be confused with transient ischemic attack or stroke. The reported symptoms change with age bilaterally or globally with decreasing associated symptoms such as photo- phobia, phonophobia, nausea, and vomiting. The older adult may complain of increased neck pain, bilateral rhinorrhea, and lacrimation ( Bravo, 2015 ). On a positive note, the older adult frequently has a better response to medication as com- pared with younger adults. A word of caution for patients who report new-onset auras without a headache; that is, visual, sensory, and/or speech symptoms that may mimic those of migraine headaches. These patients merit immediate referral for evaluation of secondary causes such as transient ischemic attack (TIA), seizure, and intracranial hemorrhage ( Bravo, 2015 ). Two rare primary headaches occurring in older adults are hypnic (developing only during sleep, lasting several hours) and primary cough or Valsalva maneuver headache (precipitated by cough or other Valsalva maneuver, lasting up to 2 hours).

The evaluation of an acute headache in adults is based largely on the history; the physical examination is often normal. Key responses in the history of present illness include the classic, “The worst headache in my life,” which may suggest subarachnoid hemorrhage (SAH), a medical emergency. Ask if the headache is “typical;” that is, migraine or TTH. If the typical headache did not improve with usual treatment, other diagnoses should be considered. The onset of the headache is very informative: sudden onset, unprovoked may be SAH or cerebrovascular accident (CVA); sudden onset provoked by agitation, orgasm, cough, or sneeze is usually benign and transient. Lastly, a subacute headache progress- ing over weeks may indicate an intracranial lesion, subdural hematoma, or hydrocephalus. For the older adult with their fi rst headache, always consider giant cell arteritis (Neblett, Hamilton, Jacobson, & Helseth, 2016). Location, duration, frequency, severity, character, triggering or aggravating factors, and alleviating factors must be considered. Specifi - cally address exacerbating factors such as posture, exertion or Valsalva, and foods (caffeine, monosodium glutamate).

A focused review of systems is important. For example, fever may suggest meningitis, brain abscess, viral syndrome, or dehydration. While vomiting is less common in older adults with migraine, if present, a CVA or SAH should be consid- ered. Visual complaints suggest a possible CVA, acute angle glaucoma, or giant cell arteritis. Other signifi cant fi ndings would be seizures, confusion, or change in mental status,

dizziness, weakness, neck pain, recent head trauma, recent travel (Lyme disease, Zika virus, dengue fever), facial pain or tenderness, and eye pain. Ask if other family members or pets are sick. Past medical history should address the patient ’ s immune status, recent change in medication, history of cancer, and hypertension. A family history of migraine or brain tumor may be signifi cant. Alcohol consumption and smoking should be examined, because they frequently inten- sify headaches. For recurrent/frequent headaches, having the patient keep a headache diary is helpful in identifying patterns and the impact the symptom has on function. Input from family and caregivers on the impact of the headaches on daily life may be helpful.

As noted, the physical examination is often normal, but several components of the examination, to include a focused neurological examination, deserve attention. Observe the patient ’ s general appearance, including facies, and evalua- tion of mental status. Any sudden change in mental status or mood should be evaluated swiftly. Assess vital signs for extremes in blood pressure, which suggest a neurological event, and temperature elevation, which suggests infection. Test the cranial nerves. Perform a funduscopic examina- tion to assess for papilledema, hemorrhages, exudates, and venous pulsations. Check for pupillary size and look at the cornea for haziness. Check extraocular movements and posi- tion of the eyelids. Evaluate gross and fi ne motor and sensory functions, including gait, balance, and tactile sense. Test deep tendon refl exes for presence and symmetry. Measure muscle strength for grading and equality.

Conduct an examination of the head and neck for lymph- adenopathy, thyroid enlargement, carotid bruits, trigger points, meningeal irritation, or limitation in normal range of motion. Palpate the head and neck for tenderness, which may suggest a TTH. Tenderness over the frontal and max- illary sinuses suggests sinusitis. Palpate over the temporal artery; tenderness suggests giant cell arteritis. Palpate the temporomandibular joint for alignment, mobility, and click- ing. Examine the ears, nose, throat, and teeth for contrib- uting problems. Evaluate the patient for postural alignment problems, muscle spasms, or trigger points in the back or shoulders.

Diagnostic Tests: Individualize diagnostic tests according to the suspected cause of the symptom. Neuroimaging some- times is indicated for emergency evaluation of suspected vas- cular, neoplastic, or infectious disease. If red fl ags are present, in addition to a full neurological evaluation, neuroimaging should be considered. ( Bravo, 2015 ). Generally, MRI is pre- ferred to CT scan. A CT scan of the brain may be indicated if the patient is immunocompromised, has a fever, or has a history of cancer (Neblett et al., 2016). MRI is considered if the headache is of sudden onset, severe, worsening, unre- sponsive to treatment, and associated with neurological or constitutional symptoms. Laboratory tests generally are not helpful, unless anemia, infection, or electrolyte imbalance is suspected. ESR or C-reactive protein may be indicated if an infl ammatory condition, such as giant cell arteritis, is under consideration. An elevated ESR warrants referral of the patient for temporal artery biopsy to confi rm diagno- sis. A lumbar puncture may be indicated after a negative CT scan without contrast if the patient has a “thunder-clap headache,” suggesting an SAH, fever, or neck stiffness

Chapter 5 ■ Symptoms and Syndromes 61

(Neblett et al., 2016). Sinus or cervical spine x-rays may be indicated.

Differential Diagnosis: There are numerous differential diag- noses to be considered based on the history and examination. Differentiating between urgent headaches in older adults is the fi rst step. Differential diagnoses of primary headaches include TTH, which is the most common, and may be trig- gered by lack of sleep and emotional or physical stress. The patient may complain of constant bilateral tightening pres- sure, which does not worsen with ADLs. The neurological examination will be normal. Migraine headaches, as noted previously, with or without aura, are rarely new-onset. Medication-induced headache must be considered, especially with medication overuse or misuse of barbiturate-analgesic- caffeine combinations, codeine, opioids, caffeine, acetamino- phen, aspirin, and NSAIDs. These patients may present with daily or near-daily headaches. Other potential diagnoses include sinusitis and cervical spine disease.

The cluster headache is characterized by severe unilat- eral orbital, periorbital, or temporal pain. The attacks are relatively short (15 to 180 minutes) but can recur up to eight times in one day. The pain is worse in the supine posi- tion, which makes the patient very restless, and the patient often wants to pace or rock back and forth during an attack. Autonomic symptoms are also associated with the pain and present as ipsilateral ptosis, miosis, lacrimation, rhinorrhea, nasal congestion, and facial swelling.

Urgent diagnoses include SAH, giant cell arteritis, stroke/ CVA, brain tumor, infection, and acute angle glaucoma. The most common acute cerebral bleed is a subarachnoid hemor- rhage, which has its highest incidence in women more than 70 years old, with a history including smoking, excessive alcohol ingestion, and hypertension. This individual generally presents with a “thunderclap” or the “worst headache of my life.” The pain may be associated with other symptoms, such as confusion, vomiting, and seizures. This individual should be transported to the emergency department for a CT scan and possibly surgery. More commonly, an older adult patient may present with a chronic subdural hematoma, which is defi ned as one that is more than 20 days old. The peak inci- dence is in ages 60 to 80 years, and up to 80% of the cases are in men. Most often a chronic subdural hematoma is asso- ciated with a fall or other type of minor trauma. Typically, they present with a headache and a change in mental status. The headache is described as mild and generalized all over the head. Although the individual does not appear to be in great distress, he or she should be transferred immediately, preferably to a location where neurosurgical consultation is possible.

Giant cell arteritis occurs predominantly in females over 50 years old who may have a history of polymyalgia rheu- matica. She may present with monocular vision loss, fl u-like symptoms, and jaw claudication. On examination, unilateral blindness may be present with tenderness in the temporal area. Optic nerve edema may be seen on funduscopic exam- ination. Headache may also warn of an impending stroke, but only in about 25% of all ischemic strokes. The incidence in hemorrhagic strokes is 40% to 60%. Infectious diseases, such as encephalitis and meningitis, may also present with a headache. Generally, both include other symptoms such as fever, altered mental status, and nuchal rigidity. The mortality

rate for meningitis in patients older than 65 years is as high as 50% to 70%. When infectious disease is suspected, the patient should be immediately transferred.

Acute angle-closure glaucoma is an emergency. The patient presents with acute unilateral eye and/or forehead pain, blurred vision, halos around lights, injected sclera, and nausea/vomiting. On examination, the pupil is mid-position and the cornea appears hazy. This presentation is considered a serious emergency, and the patient should be seen immedi- ately by an ophthalmologist because the main treatment is decreasing intraocular pressure.

To reiterate, red fl ags for possible secondary headaches includes systematic symptoms (fever, chills, weight loss), focal or mental status changes, sudden onset or thunderclap pre- sentation, onset over 50 years old, and a change in pattern to recurring headaches ( Bravo, 2015 ).

Treatment: Treatment of headache depends on the presumed etiology. Regardless, acute and preventative medications must be carefully scrutinized, considering the presence of comorbidities and the pathophysiological aspects of aging. The dearth of research studies including older adults limits best evidence. Acetaminophen, NSAIDs, and triptans, as well as combinations, have been established as effective for acute migraine treatment based on available evidence ( Marmura, Silberstein, & Schwedt, 2015 ). Vasoactive substances (trip- tans or dihydroergotamine) should not be prescribed to patients with cardiovascular disease (CVD), including stroke. If the patient is at low cardiovascular risk, triptans should be considered for acute episodes. Side effects must be recognized to include cognitive and autonomic signs/symptoms ( Bravo, 2015 ).

Management of TTH combines pharmacological and non- pharmacological measures. Analgesics, including NSAIDs and cyclooxygenase-2 inhibitors, are effective. NSAIDs must be used with caution because of the risk of GI ulceration, and renal and hepatic impairment. Concomitant use of aspirin or antiplatelet agents increases the risk of bleeding. Treat- ment should be limited to 2 days per week to avoid medica- tion overuse headaches. Prophylactic therapy is advised for patients experiencing two to three headache days per week. Tricyclic antidepressants (amitriptyline and nortriptyline) may be effective, but have the potential for anticholinergic side effects. Behavioral intervention such as relaxation, cog- nitive behavioral therapy, biofeedback, and other lifestyle modifi cations may be helpful as adjunctive therapy.

For recurrent headaches, most notably migraine, prophy- lactic therapy may be indicated. In addition to medication, patients should be advised to avoid triggers and to consider behavioral modifi cation. Regular meals, sleep hygiene, hydra- tion, and regular physical activity should be encouraged. Biofeedback and other relaxation techniques, as well as cog- nitive behavioral therapy, has been helpful for some adults. For older adults without predominant depression or aura, the most effective drugs are the same as those for younger adults. Medication is taken daily for a trial period (usually 1 to 2 months) to evaluate the effect on headache frequency and strength.

All categories of drugs should be started at low doses and incrementally increased to therapeutic dosing. Although beta blockers (propranolol [Inderal LA], 80  mg orally daily; atenolol [Tenormin], 50 to 100  mg orally daily; or nadolol

62 Chapter 5 ■ Symptoms and Syndromes

[Corgard], 40  mg orally daily) have been used prophylacti- cally for migraine and headaches, they are contraindicated in patients with a history of bronchospastic disease, asthma, diabetes, or congestive heart failure. Non-dihydropyridine calcium channel blockers (verapamil, 240  mg orally daily in divided doses, or nifedipine, 30 to 180  mg orally daily) also have been used prophylactically to prevent cluster headaches and are highly effective. Contraindications include congestive heart failure, heart block, hypotension, sick sinus syndrome, and atrial fi brillation. There is moderate evidence that antide- pressants are effective for prophylaxis. Low doses of tricyclic antidepressants (amitriptyline [Elavil], 25 to 50  mg orally daily, or desipramine [Norpramin], 50  mg orally daily) have been used for prevention, although these agents may be con- traindicated because of adverse effects on the cardiovascular system or anticholinergic effects.

Anticonvulsants have been found to be among the most effective agents for prophylaxis of migraine headaches. Val- proic acid (250 to 500 mg in daily divided doses), topiramate (25 to 200 mg in divided doses), and gabapentin (begin with 300  mg increasing to a maximum of 3,600  mg/day) have been used successfully, particularly for migraine manage- ment. Each anticonvulsant can increase fatigue, and base- line liver and kidney function studies should be obtained before initiation. Topiramate can cause kidney stones, so it is important that the patient increase fl uids while taking the medication.

For abortive treatment of mild to moderate migraine, nonprescription analgesics (NSAIDs or aspirin) with anti- emetics and hydration are the fi rst line of treatment. For more severe symptoms, early treatment with a triptan is indicated. Adjunct measures include antiemetics, hydration, and possibly magnesium. Combining NSAIDs with triptans improves the effi cacy (Neblett et al., 2016). Triptans are contraindicated in patients with CAD, peripheral vascular disease (PVD), or CVD. Likewise, they should not be used in patients with uncontrolled hypertension or severe hepatic impairment, limiting their use in older adults. Various forms of the triptans are available in oral, injectable, and nasal forms.

For cluster headache, subcutaneous sumatriptan 6  mg or sumatriptan nasal spray 20  mg are effective in improv- ing headache response, as is zolmitriptan nasal spray 5  mg ( Robbins, Starling, Pringsheim, Becker, & Schwedt, 2016 ). While less convenient, high-dose and high-fl ow oxygen is effective in the acute cluster headache, decreasing the intensity and duration. It is safe and not contraindicated in patients with hypertension or CVD. There is insuffi cient evidence that prednisone improves the headache response; however, corticosteroids may reduce remission within 24 to 48 hours. If not contraindicated, prednisone, 30 to 60  mg, can be administered orally daily for 1 week, then tapered off for another week. Intranasal lidocaine 4% topical solu- tion, 1 mL in the nostril corresponding to the location of the

headache, also has been effective in relieving migraine or cluster headaches. Ergotamine and dihydroergotamine (DHE 45) are effective in migraine treatment, but are contraindi- cated for older adults due to their effects on peripheral and central circulation. Botulinum toxin has been studied for the treatment of migraine and tension headaches; however, there is currently no evidence of effi cacy.

For giant cell arteritis, management requires larger doses of prednisone in order to prevent visual sequelae, 40 to 60  mg and even 80  mg/day. The dose is maintained until remission is reached, which may take 2 to 4 weeks before tapering (Kennedy, 2012). Monitor blood sugar and other side effects of corticosteroids, such as changes in cognition and mood.

Follow-Up: Monitoring depends on etiology and treatment strategies. Once the diagnosis has been made and manage- ment strategies identifi ed, patients should be monitored for effectiveness of treatment in person, via secure patient portals, or other preferred methods identifi ed by the patient.

Sequelae: Sequelae depend on cause. Missed diagnosis of acute, life-threatening symptoms can prove fatal. Most common causes have recurrence or chronicity, which affects quality of life. Potential for side effects from medications and medication overuse must be considered.

Prevention/Prophylaxis: Preventive measures include avoid- ance of triggers, early intervention with medication as soon as symptoms present, and stress reduction techniques as appropriate. Use of alcohol, tobacco, and caffeine in specifi c types of headache should be monitored.

Referral: Refer patients to an emergency department for urgent conditions when headaches may be a result of hemor- rhage, vasculitis, stroke, infectious disease, or acute angle-clo- sure glaucoma. Any abnormal MRI or CT scan results should be referred to a neurologist. Symptoms warranting immedi- ate referral for emergency evaluation include:

■ Headache associated with any neurological changes ■ Sudden change in mental status ■ Headache associated with a fall or other unusual event ■ New-onset migraine headache ■ Patient complaint of the “worst headache” ever

experienced

Education: Patient and family/caregiver education should be ongoing, specifi cally nonpharmacological management as well as pharmacological management. Evidence-based resources should be provided, as well as Web-based resources from organizations such as the American Headache Society. Provide a headache journal (templates available from the American Headache Society and other venues) for the patient with guidance on how to use. If medications are prescribed, ensure that the patient understands proper use and safety considerations.

Chapter 5 ■ Symptoms and Syndromes 63

Description: Hematuria is the presence of red blood cells (RBCs) in the urine. It can be classifi ed as either gross or microscopic. Gross hematuria is suspected when the urine appears either red or brown in color to the naked eye. Micro- scopic hematuria is identifi ed by laboratory analysis. The American Urological Association (AUA) defi nes clinically signifi cant microscopic hematuria as three or more RBCs per high-power fi eld on an accurately collected urine speci- men. All patients with hematuria require evaluation, as 5% of patients with microscopic hematuria are found to have a malignancy and 30% to 40% of patients with gross hematu- ria are found to have a malignancy.

Etiology: Hematuria may be renal or contamination from outside the urinary tract. Renal hematuria may result from glomerular or nonglomerular causes. The source of hema- turia may be the upper collection system (e.g., renal, ureter) and/or lower collection system (e.g., bladder, prostrate, urethra). Microscopic hematuria is a common fi nding on routine urinalysis and etiologies range from life threatening to benign incidental causes. The pathophysiology depends on the anatomical site from which blood loss occurred. In older adult patients the most common causes are malignancy or benign prostatic hyperplasia.

Occurrence: The prevalence of asymptomatic microscopic hematuria ranges from 2% to 31% in the adult population. In patients older than 50 years, the prevalence is estimated at 13%.

Age: Incidence of hematuria increases with age. Younger patients are less likely to have an etiology identifi ed.

Gender: There is a slightly higher incidence of hematuria in older women.

Ethnicity: Not signifi cant.

Contributing Factors: Infection, anticoagulation therapy, renal calculi, trauma, anatomical defects such as rectocele,

menstruation, atrophic vaginitis, renal disease, or recent urological procedures may all contribute to the presence of hematuria. Factors related to the development of a malig- nancy include age more than 35 years, male sex, current or past history of smoking, occupational exposures to chemi- cals or dyes (e.g., painters, printers, chemical plant workers), history of gross hematuria, history of chronic cystitis, history of pelvic irradiation, any exposures to cytotoxic agents such as cyclophosphamide or ifosfamide, plus any history of anal- gesic abuse.

Signs and Symptoms: A thorough history is important in the assessment of hematuria. Ask all patients about the presence of visible blood in their urine, history of vigorous exercise, recent prostate examination or procedure, recent trauma to the abdomen, recent catheterization, menstruation, renal disease, viral illness, and medications (analgesics, antibiotics, anticoagulants, NSAIDs). Gross hematuria would be recog- nizable by the red or brownish color of the urine, but there may not be any signs or symptoms related to microscopic hematuria. Symptomatic hematuria with associated fl ank pain, fever, chills, nausea or vomiting, abdominal pain, or renal colic may represent kidney disease or a kidney stone. A patient may report urinary frequency, lower abdominal pain or dysuria, which may indicate a UTI. Ask about symptoms of prostatic obstruction in males. A physical examination should focus on abdominal or fl ank pain, urogenital exam- ination, prostate examination, testicular examination, and/ or vaginal examination. Because the history and physical examination often fail to diagnose the etiology of hematuria, all patients need to be evaluated with diagnostic tests for glo- merular disease.

Diagnostic Tests: A urinalysis with microscopy should be obtained to confi rm hematuria. Urine dipstick evaluation may be misleading because it lacks the ability to distinguish RBCs from myoglobin or hemoglobin. Always confi rm a

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Relaxation, biofeedback, and cognitive therapy lead to signifi cant reductions in headache activity.

A Andrasik & Grazzi, 2014

Acetaminophen, ergots, NSAIDs, triptans are established as effective for acute migraine management. Medications must be individualized based on older adult patient ’ s risk factors.

A Dees et al., 2013 Marmura et al., 2015

Sumatriptan subcutaneous and via nasal spray is effective in improving headache response in cluster headaches.

A Robbins et al., 2016

Red fl ags for secondary headaches include fever, focal or mental status changes, sudden or thunderclap headache.

B Bravo, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

HEMATURIA

64 Chapter 5 ■ Symptoms and Syndromes

heme-positive dipstick with a microscopic urinalysis. Micro- scopic hematuria is defi ned as three or more RBCs per high- power fi eld in a urine collection. Other analysis may include a CMP to identify metabolic abnormalities. An elevated cre- atinine level may be indicative of acute or chronic renal disease and should be referred to nephrology. If the patient is on anticoagulation therapy, a prothrombin time (PT), international normalized ratio (INR), and CBC should be obtained. Always evaluate hematuria in patients receiving antiplatelet or anticoagulant therapy, as these medications are not a satisfactory explanation as a cause of the hematu- ria. Note if the patient is taking any other medications that would affect platelet function or decrease clotting abilities. If a glomerular source is ruled out, as well as benign issues, radiological imaging may be indicated to further assess the hematuria. A multiphasic CT urography or IV pyelogram is indicated if there is suspicion for a kidney stone, renal mass, or malignancy. Cystoscopy is indicated in patients older than 35 years of age, patients younger than 35 years if no other reason for hematuria is present, or patients at any age with risk factors for cancer. Cystoscopy is also used to diagnose bladder or prostatic cancers. On initial evaluation for hema- turia, urine cytology and urine markers for bladder cancer are not recommended.

Differential Diagnosis: Infection or supratherapeutic antico- agulation should be ruled out as reversible causes of hema- turia. More serious causes such as glomerular disease, renal calculi, trauma, anatomical defects, or malignancy must be ruled out.

Treatment: Treatment is directed at the cause. Asymptom- atic (isolated) hematuria generally does not require treat- ment. Appropriate antibiotic therapy for a UTI should resolve the hematuria. If the patient is on anticoagulation therapy, medication adjustment may resolve the problem. If a kidney stone is present, initial treatment may be pain management and oral hydration. The patient with urosepsis, acute kidney injury, anuria, unrelenting nausea, and vomiting should be referred immediately.

Follow-Up: A repeat urinalysis should be obtained 6 weeks after initial treatment for any infection, vigorous exercise, or trauma to make sure that the hematuria has cleared. Referral to a urologist is needed for gross and microscopic hematu- ria. For persistent hematuria with initial negative urological

work-up, a repeat urinalysis should be done yearly and a full repeat evaluation every 3 to 5 years for ongoing hematuria. Referral to a nephrologist may be needed if hematuria per- sists with renal impairment. Once any benign causes have been treated (e.g., anatomical abnormalities, viral illness, or vigorous exercise) the evaluation should be repeated after the cause has been excluded. Some organizations recommend three repeated analyses due to the potential intermittent nature of hematuria.

Sequelae: Hematuria without an obvious underlying cause is fairly common, particularly in young adults under the age of 35 years. Hematuria may be a sign of a malignancy and should not be ignored, even if it occurs transiently. Hematu- ria may indicate renal disease, especially when proteinuria is present and, if needed, referral to a nephrologist for a second opinion. A diagnosis of a kidney stone does not rule out the coexistence of a malignancy. Any patient on anticoagulant or antiplatelet therapy needs a full evaluation for hematuria.

Prevention/Prophylaxis: The U.S. Preventive Services Task Force does not endorse routine screening for asymptomatic hematuria due to lack of evidence. “ No major health organiza- tion recommends screening healthy, asymptomatic patients with urinalysis in the purpose of cancer detection.”

Referral: Primary care providers can initiate testing to verify the presence of hematuria and treat if diagnosis is clear. Referral to a nephrologist is indicated for the presence of proteinuria, RBC casts, dysmorphic RBCs, and/or elevated serum creatinine levels. Patients with hematuria persisting after treatment for a UTI or who are taking anticoagulants or in the absence of some benign cause need a referral to a urologist. Of patients referred for evaluation of hematuria or specialty care, 5% to 40% have a urological malignancy. Referral to a urologist is needed for gross and microscopic hematuria.

Education: Counsel patients and family members to seek medical advice about gross hematuria, plus signs and symp- toms to report, such as urinary frequency, dysuria, fl ank pain, and abdominal pain. Educate patients and families about side effects of OTC medications and prescribed medi- cations. Educate the patient about the effects of anticoagu- lation therapy and to call immediately if the patient notices any hematuria, because this may mean the patient ’ s drug levels are too high.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Further evaluation is need for patients with three or more RBCs per high-power fi eld for a urinalysis.

C Davis et al., 2012 Sharp, Barnes, & Erickson, 2013

Once benign causes are ruled out, patient should be referred to urologist for further evaluation of hematuria.

C Davis et al., 2012

Refer to a nephrologist for proteinuria, RBC casts, dysmorphic RBC, hypertension, and/or elevated serum creatinine levels.

C Davis et al., 2012

Chapter 5 ■ Symptoms and Syndromes 65

Description: Hemoptysis is coughing or spitting blood from the respiratory tract. This can range from blood-streaked sputum to frank bleeding. Coughing up more than 100 to 600 mL in 24 hours is indicative of massive hemoptysis.

Etiology: Hemoptysis refers specifi cally to bleeding from the lower respiratory tract, but sometimes bleeding from the upper respiratory tract or the upper GI tract may mimic hemoptysis. There are multiple potential causes for hemopty- sis including, but not limited to, airway disease and trauma, pulmonary infections or infl ammation, lung neoplasms, cardiac disease, cocaine use, and medication use (anticoag- ulants, antithrombotics, NSAIDs). The lungs receive blood from the pulmonary and bronchial arterial systems. The low-pressure pulmonary system produces small-volume hemoptysis, whereas the high-pressure bronchial system produces profuse bleeding. Infection causes mucosal infl am- mation that can lead to blood vessel rupture, and neoplasms cause mucosal invasion, which erodes the blood vessels. In the primary care setting the most common causes of hemop- tysis are acute and chronic bronchitis, pneumonia, TB, and lung cancer.

Occurrence: The most common cause of hemoptysis is airway disease. There is a strong seasonal trend with peak incidence in the spring and decreased incidence in late summer.

Age: Hemoptysis may occur at any age, but the mean age of occurrence is 62 years.

Gender: Male to female ratio is 2:1.

Ethnicity: No direct ties to ethnicity have been documented, but immigrants and persons living in poverty are at higher risk for TB and other pulmonary infections.

Contributing Factors: Smoking history (active or passive expo- sure); alcohol use; cocaine use; any history of trauma; envi- ronmental exposures; hypertension; comorbidities including diabetes or immunocompromised status; or medications such as aspirin, NSAIDs, or anticoagulants can either be caus- ative or contributing factors. Risk factors associated with an increased risk of fi nding a malignancy with bronchoscopy

include male, older than 40 years, greater than 40-pack- per-year smoking history, and duration of hemoptysis longer than 1 week.

Signs and Symptoms: The quantity, characteristics, and dura- tion of the hemoptysis should be established fi rst when assess- ing the patient. It is also important to know if it has increased in severity, if the cough is worse at night, and if there are any other associated symptoms. The amount of blood loss usually is overestimated by patients and physicians, but an attempt to determine the volume and rate of blood loss should be made. Hemoptysis of more than 100  mL in under 24 hours is potentially life threatening and requires assessment in an emergency department. Any sudden onset of hemop- tysis with or without any other associated symptoms can be caused by a pulmonary embolism and needs emergency treatment. A comprehensive history including the patient ’ s known risk factors and the work and home environment are all helpful in narrowing the cause of the hemoptysis. Estab- lish if there are any signs and symptoms of infection (fever, cough, sputum production), malignancy (cachexia, weight loss, smoking history), trauma or foreign body, or any history of immune defi ciency. A thorough medication review should also be completed.

Risk factors such as smoking, cocaine use, long-term alcohol abuse, stroke, older age, immigrant status, immuno- compromise, and any heart disease are important to assess in trying to fi nd the cause of bleeding. Use of tobacco with long-standing or increasingly severe hoarseness may indicate cancer of the mouth or throat. A history of persistent “heart- burn” may be a clue to possible esophageal erosion as the source of bleeding. Chronic cough, dyspnea, and/or sputum production may suggest pulmonary disease.

Vital signs should include oxygen saturation. Tachypnea, tachycardia, use of accessory muscles, cyanosis, fatigue, or altered mentation are signs of respiratory distress and should be treated as a medical emergency regardless of the amount of hemoptysis described or observed. The physical examina- tion should begin with a thorough examination of the nose and oropharyngeal mucosa. The neck, supraclavicular area, and axillae should be palpated for any enlarged lymph nodes,

HEMOPTYSIS

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Urinalysis is not recommended in the detection of cancer screening without any signs or symptoms.

C Sharp et al., 2013

Patients on antiplatelet and anticoagulation therapy need further evaluation by urologist and nephrology.

C Davis et al., 2012

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

66 Chapter 5 ■ Symptoms and Syndromes

a possible sign of infection, lymphoma, or other malignan- cies. Auscultation of the lungs may reveal a focal abnormal- ity consistent with pneumonia (crackles, rhonchi, wheezing); egophony is suggestive of consolidation and is often present in pneumonia. Heart sounds should be auscultated specifi - cally for a murmur, as mitral regurgitation or mitral stenosis can be associated with pulmonary edema or decompensated heart failure, especially in the setting of clinically apparent volume overload. An abdomen distended with ascites may be accompanied by esophageal varices.

Diagnostic Tests: The test of choice is the chest x-ray or chest CT scan. Diagnostic work-up may also include these labo- ratory tests: CBC, coagulation studies, CMP, arterial blood gas, sputum culture and smear, purifi ed protein derivative, INR, d-dimer, ESR, CT angiogram, or bronchoscopy. If no cause of hemoptysis can be isolated and the radiographic studies are normal, a fl exible bronchoscopy for airway exam- ination is still useful to rule out an endobronchial source of bleeding.

Differential Diagnosis: Determine fi rst if the blood is coming from the respiratory tract (hemoptysis) or from the GI tract (hematemesis). Patients with hematemesis typically have nausea and vomiting and a history of gastric or liver disease, and the sputum more likely will be coffee ground in texture and a brown-black color. In hemoptysis, however, the sputum is bright red or pink and a frothy liquid or clotted, and the patient has a history of lung disease. If the source of bleed- ing is determined to be the lung, consider the possibility of infection, infl ammation, malignancies, trauma, autoimmune disease, CVD, and coagulation disorders, among others.

Treatment: The goals of management include bleeding ces- sation, aspiration prevention, and treatment of underlying cause. If the source of the bleeding has been reasonably iso- lated to the respiratory system and the condition is not life threatening, and if an infectious or infl ammatory etiology is diagnosed, the following diagnoses might be considered.

Acute Bronchitis: Acute bronchitis is predominantly viral and antibiotics do not shorten the course of the disease. If the patient smokes, he or she should be counseled to quit or to cut back signifi cantly. Bronchodilators help open the airways; expectorants such as guaifenesin used to mobilize secretions are about as effective as drinking two additional glasses of water per day. Cough suppressants should be avoided except to help the patient sleep. A cool mist humidi- fi er in the bedroom is useful for loosening secretions.

Chronic Bronchitis: Chronic bronchitis needs a combina- tion bronchodilator as an inhaler or as a nebulizer. Because chronic bronchitis is usually a result of smoking, the patient should be counseled to stop. Antibiotics or oral steroids should be reserved for acute exacerbations heralded by increasing shortness of breath, change in color of the sputum to dark yellow or green, or fever.

Bronchiectasis: Permanent enlargement of some of the airways in the lungs caused by chronic infections, trauma, or immune system problems can result in intermittent hemopty- sis. The hemoptysis usually results from dilation of bronchial arteries. Because this is a chronic illness, antibiotic selection is generally based on previous sputum culture/susceptibility results.

Bacterial Pneumonia: Community-acquired pneumonia is most often caused by Streptococcus pneumoniae. Hemophilus infl uenza, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Legionella pneumophilia are other major bacteria that cause pneumonia in the otherwise healthy individual. If pneumo- nia is suspected, broad-spectrum antibiotics should be ini- tiated empirically. Immunocompromised patients, patients with any respiratory distress, and older adult patients with signifi cantly elevated or decreased WBC counts may need to be hospitalized. Patients with pneumonia caused by Staph- ylococcus aureus, Enterobacteriaceae, and Pseudomonas aeru- ginosa may present with a more severe illness and require hospitalization.

Fungal Infection: A fungal infection should be suspected if the pneumonia does not respond to conventional antibiotic therapy. Appropriate antifungal therapy may be initiated, and the patient should be referred to a pulmonologist.

TB: If TB is suspected based on history, signs/symptoms, and chest imaging, the diagnostic work-up should focus both on detecting the bacteria in sputum (acid-fast bacteria [AFB] culture and smear) and on protecting other individuals from contracting the infection. This may include admission to a negative pressure hospital room with airborne isolation for the diagnostic work-up. Treatment with an antituberculosis regimen can be started by the hospital or outpatient clinic; however, these patients need to be referred to the health department who will often manage treatment through directly observed administration of the antituberculosis regimen.

Follow-Up: The tenacity of follow-up depends on the sever- ity of the illness. For pneumonia or bronchitis with minimal dyspnea, a call to check on the patient is appropriate. Wors- ening temperature, bleeding, or diffi culty breathing requires immediate attention or emergency department evaluation. Patients with resolving pneumonia should be evaluated in 2 to 3 weeks, but bear in mind that radiographic resolution may take 6 to 8 weeks, especially in older adult patients or those with underlying lung disease. Mild hemoptysis recur- ring sporadically over a few years is common in smokers who have chronic bronchitis punctuated with superimposed acute bronchitis.

Sequelae: Death can occur if the etiology is not identifi ed quickly and treated, particularly if it causes cardiovascular collapse or acute respiratory insuffi ciency. The mortality rate depends on the etiology, and in patients with a malignancy and massive hemoptysis (more than 1,000 mL per 24 hours) the rate is 80%. Chronic lung disease may also result.

Prevention/Prophylaxis: Counseling patients and their fami- lies about the benefi ts of smoking cessation and to decrease alcohol intake are worthwhile. Discussions to promote a healthy lifestyle are important, stressing activity and weight loss.

Referral: Massive hemoptysis requires treatment in the inten- sive care unit and pulmonary and cardiovascular surgeon consultation. If hemoptysis persists or increases, the patient may need to be referred to a pulmonologist for either bron- choscopy or laryngoscopy. Radiological imaging such as CT scan may be needed to rule out neoplasm followed by a refer- ral to a surgeon or an oncologist.

Chapter 5 ■ Symptoms and Syndromes 67

Education: Discuss risk factors associated with pulmonary embolism, such as immobility or hormone replacement ther- apies. Provide patient education related to smoking cessation and cessation of street drugs and/or alcohol abuse. Patients

with COPD or bronchiectasis should be aware of their own clinical signs/symptoms of worsening or acute exacerbation and have an action plan should one occur.

CLINICAL RECOMMENDATIONS EVIDENCE RATING REFERENCES

Moderate hemoptysis has shown similar prognosis of recurrent hemoptysis and mortality to massive hemoptysis; therefore, the more aggressive fl exible bronchoscopy and bronchial artery embolization should be considered in moderate hemoptysis.

A Lee et al., 2014

The initial test of choice is a chest x-ray. Contrast-enhanced CT with angiography adds additional information and is the method of choice.

A Ittrich, Bockhorn, Klose, & Simon, 2017 Salamone et al., 2017

Patients with a mass on CT and those at risk for cancer should have a fl exible bronchoscopy.

A Bonlokke, Guldbrandt, & Rasmussen, 2015 Cordovilla et al., 2016

Massive hemoptysis is a respiratory emergency. CT angiography (CTA) can play a crucial role in assessing the cause and origin of hemoptysis and directing the interventional radiologist before treatment.

A Ittrich, Bockhorn, Klose, & Simon, 2017

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xtml .

INVOLUNTARY WEIGHT LOSS

Description: Weight loss is common among older adults and is associated with poor health outcomes and functional decline. Involuntary or unintentional weight loss is a condi- tion in which the patient does not purposefully set out to lose weight for any reason ( Wong, 2014 ). It may be a presenting concern of the patient, reported by the family, or fi rst noted by the provider. There is a well-established association between weight loss and mortality in older adults (Wijnhoven, van Zon, Twisk, & Visser, 2014). The Centers for Medicare and Medicaid Services (CMS) defi nes involuntary weight loss that must be clinically investigated as 5% in 1 month, 7.5% in 3 months, or 10% in 6 months.

Etiology: The causes of involuntary weight loss are not always clear. In 16% to 18% of patients no identifi able cause is found ( Gaddey & Holder, 2014 ). With aging there is a decline in bone mass and a decrease in muscle mass, which is responsible for a small decline in weight after the seventh decade of life, 0.2 to 0.4 pounds per year. Another age-re- lated phenomenon is a reduction in appetite called anorexia of aging (Wernette, White, & Zizza, 2011). Sarcopenia is a geriatric syndrome that includes decrease in muscle mass

and strength, and decline in physical performance related to aging. The resulting increased ratio of fat to muscle may con- tribute to further weight loss because of the relationship of adipose tissue to infl ammatory cytokines, which have been linked to cachexia and weight loss, including tumor necro- sis factor- α (THF- α ), interleukin-1 β , and interleukin-6. Cachexia is a metabolic disease characterized by the loss of muscle mass with or without the loss of fat. It may be diffi - cult to distinguish cachexia from sarcopenia and the two may coexist. Causes of weight loss may be the result of physiologi- cal factors, psychological factors, social factors, or a combina- tion of these (see Table 5-5 ). While often the primary concern is an undiagnosed malignancy, nonmalignant causes are the most common. Many medications can interfere with appetite and result in weight loss, but often medications are added as treatment rather than removed.

Occurrence: Involuntary or unintentional weight loss occurs in 15% to 20% of older adults ( Wong, 2014 ). Using the CMS criteria, the yearly incidence of weight loss is about 7% in the community. From 30% to 50% of long-term care res- idents have below-average body weight, but CMS nursing

68 Chapter 5 ■ Symptoms and Syndromes

Causes of Unintentional Weight Loss

PHYSIOLOGICAL FACTORS

Disease

Malignancy Lung, GI, pancreatic, hematological, prostate

Acute illness Infl uenza, pneumonia, clostridium diffi cile

GI disease Malabsorption, autoimmune, oral health

Endocrine Diabetes, hyperthyroidism

Cardiovascular Heart failure

Respiratory COPD, interstitial lung disease

Infectious disease HIV, TB

Neurological disease Dementia, stroke, Parkinson ’ s disease

Rheumatological

disease

RA, sarcoidosis, infl ammation

Renal disease Uremic cachexia

Previous surgery Malabsorption, pain

Chronic pain

Medications

See Table 5-6

Functional Issues

Decline in ADLs and

IADLs

Feeding, purchasing, and preparing food

Dysphagia Food avoidance, dietary restrictions

Sarcopenia Muscle weakness, decreased mobility

Falls Fracture, fear of falling

Psychological Factors

Depression

Anxiety

Grief

Substance abuse and

dependence

Alcoholism, tobacco, cocaine

Social Factors

Social isolation

Limited income

Abuse or neglect

Environment Food desert, transportation, safety

TABLE 5-5

home data using their criteria reported a 6% incidence when patients with end stage disease or on hospice were excluded (CMS, 2015).

Age: Old age is a risk factor for involuntary weight loss due to the normal physiological changes with aging combined with a higher prevalence of physiological, psychological, and social factors associated with involuntary weight loss.

Gender: No documented signifi cance; however, gender data are affected if the specifi c underlying disease causing the weight loss is more common in men or in women.

Ethnicity: Not signifi cant.

Contributing Factors: When considering all causes of invol- untary weight loss, nonmalignant causes are most common, but in up to 38% the cause is a malignancy. Nonmalignant GI disease is next, followed by psychiatric, endocrine, and cardiopulmonary; alcoholism; dementia; medications; loss of taste and smell; decreased functional status; chronic infec- tion; dentition; and smoking. Social factors such as isolation, abuse or neglect, location of residence (food deserts, safety concerns), lack of transportation, and fi nancial issues have an infl uence on adequate nutrition with resulting weight loss as well. Many medications contribute to factors related to weight loss and a careful review should be initiated (see Table 5-6 ). In the Amsterdam Longitudinal Study on Aging, weight loss due to medical reasons, unknown reasons, and a change in eating habits were all associated with increased mortality; however, no association to mortality was found when weight loss was due to intentional loss or social reasons (Wijnhoven, van Zon, Twisk, & Visser, 2014). Their interesting conclusion requires additional investigation. Because weight loss can cause skeletal muscle loss there is an increased risk for falls, functional impairment, protein calorie malnutrition, immune system compromise, anemia, and decreased cognition, all of which increase morbidity and mortality.

Signs and Symptoms: Weight loss may be reported by the patient, their family, or noted by the provider. If clinical doc- umentation is not available, a classic guideline introduced by Marton, Sox, and Krupp ( 1981 ) suggests that a change in clothing size, confi rmation of history by a family member, or ability of the patient to report exact weight change can

Medications That May Cause Weight Loss

MEDICATION EXAMPLES

Neurological Psychiatric Antidepressants, lithium, anticonvulsants,

stimulants, levodopa, dopamine agonists,

selegiline, phenothiazines, haloperidol,

benzodiazepines, cholinesterase inhibitors,

NMDA receptor antagonists

Cardiovascular Digoxin, ACE inhibitors, CCB, β blockers, α agonists, hydralazine, statins, diuretics, amiodarone, procainamide, spironolactone

GI Cimetidine, interferon, diphenoxylate-

atropine, proton pump inhibitors, laxatives

Anti-infective Metronidazole, griseofulvin, most

antibiotics, amantadine

Nutritional Calcium carbonate, iron, potassium, bile

acid sequestrants

Musculoskeletal

(including pain)

NSAIDs, bisphosphonates, colchicine,

penicillamine, aspirin, opiates, allopurinol,

colchicine, gold, hydroxychloroquine,

methotrexate

Pulmonary Theophylline, pseudoephedrine,

antihistamines

Endocrine Levothyroxine, Armour thyroid,

metformin

Other Anticholinergics

TABLE 5-6

Chapter 5 ■ Symptoms and Syndromes 69

be substituted. A thorough history and complete physical examination are required to identify any treatable underly- ing cause of the weight loss. History should include a review of cardiac, respiratory, GI, genitourinary, endocrine, hema- tological, or infectious disease symptoms. An assessment of depression, anxiety, cognitive impairment, substance abuse, and functional decline begin with the history. There should be a focus on oral concerns such as poor dentition, new den- tures, mouth lesions, dry mouth, dysphagia, or loss of taste. A review of medications both prescribed and OTC, including supplements, is necessary.

A functional cause of weight loss may be primary or sec- ondary to a physiological or psychological etiology. Determine if the patient has functional limitations that affect the ability to prepare and eat an appropriate diet and if adequate help is consistently available to assist with ADLs if necessary. The Mini Nutritional Assessment (MNA) is supported by evidence as useful in measuring nutritional risk. The tool is accessi- ble at www.mna-elderly.com where you can download the forms and the user ’ s guides at no charge. There is a training video and the possibility of integrating it into the electronic medical record. There are three versions of the MNA: Self MNA, the MNA for clinical use, and the original full MNA. They all include anthropometric measurements and general, dietary, and functional assessments.

Physical examination should include cardiovascular, respiratory, GI, genitourinary, dermatological, and musculo- skeletal systems. A comprehensive neurological examination and a mental status examination that includes assessment of mood, cognitive ability, and substance use are essential components. Patients with signifi cant weight loss appear pale and cachectic, with signs of malnutrition such as hair loss, muscle wasting, and loss of subcutaneous fat. Look for evidence of loose skin, petechiae, cyanosis, clubbing of the fi ngers, and edema. There may be temporal wasting, icterus, dry mucous membranes, and fl attened papillae of the tongue. The oral examination should note denture fi t; tooth and gum disease; and oral lesions such as ulcers, stomatitis, and candidiasis. Examination of the cardiorespiratory system may reveal loud or palpable murmurs and diminished breath sounds. The liver or spleen may be palpable. Check for masses in the abdomen, breasts, and rectum. Muscle wasting may be apparent on the extremities, and deep tendon refl exes may have a prolonged relaxation phase. Patients may have dimin- ished position and vibratory sense. Check women for ovarian masses, cervical lesions, and any obvious neoplasia. In men, examine the prostate gland for enlargement.

Diagnostic Tests: History and physical examination fi ndings guide the choice of diagnostic tests. The shot gun approach to gathering data that may or may not be signifi cant is no longer an option, as increasing emphasis is placed on evi- dence-based practice and testing that supports assumptions from the history and physical examination. In our current health-care environment it is more important than ever to remember the advice of Sir William Osler, “Listen to the patients, they will tell you the diagnosis.” It has been shown that 70% of the diagnosis can be made with history alone and the physical examination increases to 90% the likelihood of diagnosis.

Additional diagnostic tests serve to confi rm the assump- tions. Diagnostic screening tests are shown in Table 5-7 . A

nutritional or diet history and calorie counts add objective data to evaluate the amount and quality of food intake. After the results of the diagnostic work-up are available, consider a neoplastic origin when benign causes of weight loss appear unlikely. Malignant and nonmalignant GI disorders are the most prevalent cause of involuntary weight loss. Evidence of microcytic anemia on the CBC or a positive fecal occult blood result is a reason to refer for colonoscopy. With frail older adults it is important to address the question of treatment options with the patient and family before further invasive and expensive work-up is initiated. If the cause of weight loss is not clear from the diagnostic evaluation, watchful waiting is recommended; watch for further weight loss or specifi c symptoms and reconsider a functional cause of weight loss. If no abnormalities are detected from the history, physi- cal examination, and diagnostic tests, an organic cause is unlikely (less than 5%). When the fi ndings from the initial work-up are negative, psychological problems, particularly depression and anxiety, are among the most common reasons for weight loss.

Differential Diagnosis: For weight loss that occurs with increased food intake, consider diabetes, thyrotoxicosis, malabsorption, leukemia, lymphoma, and adrenal insuffi - ciency. For weight loss that occurs with normal or decreased food intake, consider alcoholism; malignancy; infection; GI, hepatic, renal, dental, endocrine, respiratory, cardiac, or psy- chological causes; anorexia nervosa; malnutrition; or a func- tional origin. After investigation, the cause of weight loss remains unknown in 16% to 28% of patients. Table 5-8 lists the causes of weight loss in the older adult.

Treatment: Treat or manage the identifi ed underlying cause. This will likely involve the inclusion of other disciplines. Regardless of the cause, a referral to a nutritionist should be a priority. Medicare offers specifi c nutritional benefi ts to patients with diabetes or chronic kidney disease. Den- tistry to assess oral health, speech to evaluate swallowing, occupational or physical therapy, and social work are all key to addressing the problem of involuntary weight loss. Nonpharmacological options should be initiated fi rst. Diet modifi cations should minimize dietary restrictions, address patient preferences, and accommodate problems of dentition or swallowing. Smaller, more frequent meals can be useful if the patient reports early satiety. Patients with demen- tia tend to consume most of their daily energy at break- fast, so high-energy foods should be served at this meal, and varying dietary texture can be helpful. Eating with assistance and in the company of others increases calorie intake. For elders in the community, home delivered meal programs are benefi cial. Oral nutritional supplements, such as high energy and high protein drinks, if initiated, should be consumed between meals. Evidence supports that their short-term use improves weight and diagnostic parame- ters, but data in support of their long-term use is lacking. Regular exercise, especially resistance training, stimulates appetite and can prevent increasing sarcopenia. Use of a multivitamin supplement should not be a fi rst-line inter- vention; nutrient-dense foods and improving intake are preferable. Oral supplements are rich in micronutrients and when added to the treatment plan are superior to a multi- vitamin. Multivitamins are preferred over individual vitamin supplements.

70 Chapter 5 ■ Symptoms and Syndromes

Diagnostic Screening Tests

TEST RESULTS INDICATING DISORDER

Albumin

Half-life of about 21 days

and refl ects level about 3

weeks in past

Albumin and pre-albumin are negative acute phase proteins and decrease in response to infl ammation. Many

chronic diseases in older adults have an infl ammatory component that can result in a low albumin and pre-

albumin with or without protein calorie malnutrition. Current consensus is that laboratory markers are not

reliable by themselves but need to be interpreted in the context of history and physical examination.

Historically albumin was interpreted as:

2.8–3.5 g/dl: Mild depletion

2.1–2.7 g/dl: Moderate depletion

<2.1 g/dl: Severe depletion

Pre-albumin

Short half-life: 2–3 days

Pre-albumin interpretation:

10–15 g/dl: Mild depletion

5–10 g/dl: Moderate depletion

<5 g/dl: Severe depletion

Transferrin

Half-life 10 days

Low in protein-calorie malnutrition, but also affected by iron status:

100–150 mg/dL: Mild depletion

150–200 mg/dL: Moderate depletion

<200 mg/dL: Severe visceral protein depletion

C reactive protein A positive acute phase reactant can be useful in interpreting the results of the albumin and pre-albumin.

Sedimentation rate Elevation indicates infl ammation and a very high sed rate can occur in temporal arteritis, polymyalgia rheumatic,

relapsed Hodgkin ’ s, or malignancy. The test needs to be interpreted in the context of other results and should

not be the sole indication of serious illness.

Serum cholesterol Total cholesterol <130 mg/dl when matched with albumin less than 3.15 g/dl was consistent with protein-

calorie malnutrition if signs/symptoms of poor nutrition present.

CBC with differential Low total lymphocyte count or an unexplained normocytic anemia may indicate malnutrition. A blood loss

anemia should raise concern of malignancy.

CMP Abnormal glucose, sodium, BUN, creatinine, AST, ALT, alkaline phosphatase may be indicative of disease links.

Hemoglobin A1c Refl ects average blood glucose over the last 90 days. Is not accurate in severe anemia.

Thyroid-stimulating hormone 1.9–5.4  μ IU/mL, normal reference range. Decreased levels in hyperthyroidism, often associated with weight loss. Increased levels in hypothyroidism, associated with weight change (usually gain, but loss also occurs in older adults).

Urinalysis Send only if clear indication for its usefulness to screen for blood, protein, or infection if patient exhibits

symptoms consistent with the revised McGeer criteria (Rowe & Juthani-Mehta, 2014).

Stool for occult blood The FIT or Cologuard screening tests are superior to the hemoccult test for screening.

TABLE 5-7

It is common in clinical practice for clinicians to order mirtazapine and other pharmacological agents to stimulate appetite; however, evidence underlying their use is limited, particularly in older adults, and none has gained approval from the U.S. Food and Drug Administration (FDA). Megestrol acetate has evidence for use in cancer or HIV, but studies in older adults have had equivocal results. The risk of DVT and pulmonary embolus is alarming and increasing in patients who are sedentary. Dronabinol is a synthetic form of THC, a naturally occurring component of cannabis sativa (mari- juana), which is FDA approved for chemotherapy-induced nausea and vomiting, and anorexia from AIDS or cancer. Only one study has been conducted in older adults, patients with dementia who were refusing food. The CNS side effects are a major risk in a population who has a more vulnerable CNS.

Follow-Up: If results of the standard tests listed earlier are negative, and the history and physical examination are neg- ative, the recommended approach is to watch for further weight loss and to reconsider functional causes. Have the patient or caregiver keep a daily record of food intake, activ- ity levels, and symptoms, and schedule a return visit in 2 to

4 weeks. Supplements may be added with the emphasis that they should be used between meals.

Sequelae: Malnutrition is the fi rst complication to consider in involuntary weight loss. Long-term unexplained weight loss may indicate failure to thrive and the beginning of a down- ward spiral in health and function. Many patients in acute and long-term care have unrecognized protein-calorie mal- nutrition. Protein-calorie malnutrition is a common iatro- genic complication of hospitalization.

Prevention/Prophylaxis: Discuss proper nutrition and the need for dental care, if appropriate. Address functional, fi nan- cial, and social issues that may affect nutrition (e.g., address depression; arrange for socialization at mealtime, if feasible; arrange home delivered meals).

Referral: Involuntary weight loss often has multiple factors and may require the assessment of multiple specialties to derive a diagnosis and plan for treatment. Include the patient and their family in discussions about goals of care. Referral for palliative care may be appropriate. Adult failure to thrive can no longer be used as the primary diagnosis for hospice admission; however consultation with hospice teams can

Chapter 5 ■ Symptoms and Syndromes 71

help in determining the primary diagnosis. Always consult a specialist for rapid or acute decline; for positive diagnostic test results indicating malignancy, thyrotoxicosis, or other acute organic illnesses requiring sophisticated diagnostic work-up or management; or for a patient condition beyond your current scope of practice. Refer patients for assistance if social or functional issues may be contributing to weight loss. Refer to an appropriate specialist as noted previously.

Education: Instruct patients about proper nutrition and hydration. Encourage exercise to improve strength or func- tion and to stimulate appetite. Teach patients about medica- tion side effects that may affect nutrition and about signs or symptoms of overmedication or undermedication.

Meals-on-Wheels Mnemonic for Causes of Weight Loss in the Older Adult

MNEMONIC CAUSES OF WEIGHT LOSS

M Medications

E Emotional problems (depression, anxiety)

A Alcoholism, anorexia tardive, abuse

L Late life paranoia

S Swallowing disorders (dysphagia)

O Oral problems

N Nosocomial infections No money (poverty)

W Wandering and other dementia-related behaviors

H Hyperthyroidism, hypercalcemia, hypoadrenalism

E Enteric problems (malabsorption)

E Eating problems (inability to feed oneself)

L Low-salt, low-cholesterol diet

S Social problems Shopping and meal preparation

Stones (cholecystitis)

Source: Morley & Silver (1995).

TABLE 5-8

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

There is a relationship between depressive symptoms and weight loss. Patients with weight loss should be screened for depression.

A Kim, Noh, Park, & Kwon, 2014

Oral nutritional supplementation is associated with weight gain and reduced mortality.

A Morley, 2012

Nutritional supplementation should be given between meals. A Morley, 2012

Loss of weight in obese older adults is associated with greater morbidity than in non-obese older adults even when they maintain loss or regain weight.

A Fabbri et al., 2015

If clinically documented weight loss is not available, a change in clothing size, confi rmation of history by a family member, or ability of the patient to report exact weight change can be substituted.

B Marton, Sox, & Krupp, 1981 classic study

Treatment should address the underlying cause. Involve a multidisciplinary team.

B Gaddey & Holder, 2014 Wong, 2014

Optimize caloric intake, minimize dietary restrictions, eat in the company of others.

B Gaddey & Holder, 2014 Morley, 2012

No medications have been shown to reduce mortality. Few studies have been done to determine effectiveness in older adults with involuntary weight loss, and all have considerable side effects.

B Gaddey & Holder, 2014 Wong, 2014

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

72 Chapter 5 ■ Symptoms and Syndromes

Description: Joint pain can be discomfort or infl ammation arising from any part of a joint, including the cartilage, bone, ligaments, tendons, or muscles. It is commonly referred to as arthralgia, which is infl ammation within the joint itself (Mayo Clinic, 2016).

Etiology: Any damage to the joints from disease or injury can interfere with movement and cause a lot of pain. Many dif- ferent conditions can lead to painful joints, including osteo- arthritis, rheumatoid arthritis (RA), bursitis, gout, strains, sprains, and other injuries. The description, location, onset, and associated symptoms are important to diagnosing the cause of joint pain. Clarifying the etiology of the pain depends on the clinical presentation, complete history, fi ndings from physical examination, and appropriate diagnostic testing. The pain can be mild (from strained muscles or ligaments that support the joint), chronic (lasting more than 6 months, from degenerative joint disease, arthritis, osteoarthritis), infl ammatory (from joint effusion, RA), or severe and acute (from trauma or infection). Drug-induced arthralgia can occur with some medications. Acute joint pain may become a chronic pain if posture, overuse, and weight bearing are not corrected or eased. For example, pain of osteoarthritis of the knee may initially occur intermittently during weight bearing and evolve into persistent chronic pain. Systematic causes of joint pain may include lupus, sarcoidosis, Lyme disease, hemophilia, fi bromyalgia, Raynaud ’ s disease, and Paget ’ s disease ( Kong, Lauche, & Chang, 2016 ).

Occurrence: In the United States, an estimated 52.5 million adults have provider-diagnosed arthritis, and 22.7 million report limitations due to their arthritis (CDC, 2015). Neogi (2013), reported that joint pain symptoms requiring medical attention are projected to increase to nearly 67 million by 2030.

Age: Joint pain is found more frequently in the older adult patient as a result of age-related muscle atrophy, demineral- ization of trabecular bone, atrophy of cortical bone, chronic disease, and loss of bone density. Arthritis (degenerative and infl ammatory) is the most common cause of disability in indi- viduals more than 75 years old, and it affects more than 80% of individuals in this age group, with joint pain being the dominant symptom.

Gender: Joint pain occurs more frequently in women than in men.

Ethnicity: Prevalence of certain types of infl ammatory disease and systematic disorders are higher in various ethnic groups.

Contributing Factors: Factors that may lead to joint pain include overuse or strain, previous injury or trauma to the joint, alterations in gait or balance, past surgery or joint replacement, known history of joint disease, and postmeno- pausal women with no hormone replacement therapy. Phys- ical stature, weight, smoking, and family history should be assessed in reviewing the risk factors for osteoporosis. Other contributing factors include obesity, poor nutritional habits, low calcium intake, alcohol consumption, medications, and personal exercise habits. Older adults with obesity may suffer from multi-site pain due to the strain caused by the pressure

of the additional weight on the joints. Longitudinal evidence shows that a high body mass index (BMI) precedes and inde- pendently predicts foot joint pain and knee pain. Deterio- ration of the normal gait and mobility may be affected by the combined stressors of lower body joint pain ( Zdziarski, Wasser, & Vincent, 2015 ).

Signs and Symptoms: Using a systematic method to obtain the history, such as the comprehensive OLDCART mnemonic, is essential to identifying the symptom of joint pain. The patient history should identify all joints affected and include the onset of the pain (sudden, insidious), character of the pain (dull, sharp), and duration and location of the pain (including radiation). Inquire about any associated symp- toms, alleviating or aggravating factors, and timing (e.g., worse in morning, better late in the day). Morning stiffness points toward an infl ammatory arthritis, whereas post-ex- ercise stiffness indicates a degenerative process. Symptoms associated with joint pain may include erythema, warmth, general weakness, stiffness, and decreased range of motion.

Discuss normal activity levels and the possibility of overuse, injury, and strain. Has the patient experienced any past or recent injury to the joint? Has the patient heard any popping, crepitus, or clicking? Discuss the limitation in joint mobility and note the presence of edema, redness, or fever. Review any associated muscle fatigue, joint deformity, or inability to perform certain movements. Red fl ags include unremitting pain, systematic symptoms (fever, chills, fatigue, weight loss), signifi cant disability, and change in function.

The physical examination includes a complete assessment of the patient. Inspect and palpate each joint and assess the proper range of motion, noting any pain or limitations in movement. Include additional diagnostic maneuvers, if indi- cated, such as the drawer sign for ligament injury, the McMur- ray test for meniscal tears, or the Thomas test for hip fl exion contracture. Assess the patient ’ s gait, balance, and posture. Inspect each joint, noting the musculature, any atrophy, con- tractures, nodules, asymmetry, or gross deformity. Note any erythema, infl ammation, or soft tissue swelling on or near the joint. Joints affected by RA usually involve the metacarpopha- langeal joints and the wrist, while distal involvement of the interphalangeal joints suggests osteoarthritis. Palpate for any tenderness or effusions at the joint and check for crepitus, clicking, or popping. Sensory testing may reveal neurological or vascular involvement (Neogi, 2013). Extra-articular signs (rashes, tophi, conjunctivitis, mouth ulcers) provide addi- tional information toward a differential diagnosis.

Diagnostic Tests: Diagnostic tests are not specifi cally indicated with a complaint of joint pain; they are useful to identify specifi c problems consistent with fi ndings from the history and physical examination. A CBC with differential will rule out infection and an ESR may support the concern of an infl ammatory process. Marked elevations in alkaline phos- phatase level are seen in patients with bone disease (e.g., Paget ’ s disease, metastatic bone disease). Hypercalcemia with marked alkaline phosphatase is seen in patients with hyperparathyroidism or bone carcinoma. Serum creatine kinase (CK) isoenzymes are elevated in persons with muscle trauma and progressive muscular disease. If indicated, obtain

JOINT PAIN

Chapter 5 ■ Symptoms and Syndromes 73

a complete electrolyte panel and urinalysis. Check BUN and creatinine levels to assess renal function. Rheumatoid factor may be of use, but it is negative in approximately 30% of all RA cases and the test has a high false-positive rate. A more specifi c test is the anti-cyclic citrullinated peptide (anti-CCP), which tests for an antibody present in most patients with RA. X-rays of the joint are not necessary routine, but can be useful to detect fracture, joint space destruction or nar- rowing, erosion, arthritic changes, and degeneration. Joint aspirations may be done to distinguish infl ammatory, non- infl ammatory, and infectious conditions, and may provide symptomatic relief.

Differential Diagnosis: Other conditions to consider include gout, pseudogout, psoriatic arthritis, connective tissue disease, Reiter ’ s disease, multiple myeloma, scleroderma, lupus, septic arthritis, polymyalgia rheumatic (PMR), cer- vical radiculopathy, fi bromyalgia, and spinal stenosis. PMR is not uncommon in older adults and should be considered when the large joints are involved and the onset of pain is sudden. PMR is diagnosed with symptoms and an elevated ESR.

Treatment: The goal in acute joint pain is to reduce pain and swelling, if present. If the pain is due to acute injury, the mne- monic PRICE is helpful: P rotection (brace or wrap), R est, I ce (15 minutes on and 15 minutes off for several times a day), C ompression (elastic wrap), and E levation (elevate the joint above the heart level). Emergency intervention is required if you suspect a fracture, avascular necrosis, or sepsis.

Nonpharmacological treatment should be the fi rst line of recommendation. Weight loss of even a small amount can make a difference in pain. Physical therapy can be used to develop a plan for treatment that includes exercise and muscle strengthening. The use of a cane to off load weight and provide stability is an option. Application of moist heat can help with both knee and back joint pain. The use of transcutaneous electrical nerve stimulation and acupunc- ture is increasing in application.

Pharmacological management should be based on the type and number of joints involved and the presence of comorbidities. Topical NSAID agents have been shown to be as effective as oral agents, especially with knee arthritis. Edwards and colleagues ( 2016 ) noted that the NSAID diclo- fenac sodium topical gel 1% applied up to four times a day resulted in 30% pain reduction of knee osteoarthritis pain. Capsaicin, an enzyme found in hot pepper, depletes substance P when applied to the painful area three times a day for several weeks. Side effects may include burning and erythema, and it should never be applied to open or irritated skin.

Oral NSAIDs are on the Beers’ Criteria for Potentially Inap- propriate Medication and if used with older adults should be considered for short-term use. Consider the selective Cox-2 inhibitors: moist heat, intra-articular steroid injections, assis- tive devices, and surgery. Acetaminophen, which was a cor- nerstone of treatment for osteoarthritis in older adults in the past, is no longer recommended as fi rst-line treatment based on the risk of toxicity and lack of evidence of pain relief. The total dose for an older adult should not exceed 3 g a day from all sources. Newer agents useful in infl ammatory arthritis include disease-modifying antirheumatic drugs and biolog- ical response modifi ers. Intra-articular injections can also provide short-term relief.

Polsunas and colleagues (2016) made the following rec- ommendations for dosing medications: acetaminophen 325 to 1,000  mg every 4 to 6 hours, maximum dosage 3  g per day; tramadol start 25  mg daily, increase 25 to 50  mg every 3 to 7 days to 100  mg every 6 hours. Side effects for trama- dol may include seizures and orthostatic hypotension, and tramadol is now a schedule IV medication which requires a U.S. Drug Enforcement Administration (DEA) number to pre- scribe. Opioid medications include hydrocodone/APAP 5/325 to 10/325  mg every 4 to 6 hours, maximum 3  g per day of APAP; oxycodone 5 to 10  mg every 4 hours. Side effects of this class include an increased risk of falls.

Follow-Up: Monitoring of patients depends on fi ndings. Patients with acute or severe joint pain may need emergency care and intervention. Monitor patients with chronic pain frequently until the clinical work-up is completed. Manage- ment of chronic joint pain requires routine visits to monitor the effectiveness of treatments and follow-up laboratory and diagnostic tests, if indicated.

Sequelae: The condition and prognosis relate to the etiology of joint pain.

Prevention/Prophylaxis: Weight reduction to decrease stress on the joint when possible; physical therapy and exercise for strengthening; and moist heat, topical medications, and steroid injections to reduce pain and spasms. Instruct the patient on joint protection and preservation. Alternative methods of pain control such as acupuncture, yoga, med- ication, or massage therapy may be recommended. Tai chi showed improvement in chronic pain conditions, including low back pain, fi bromyalgia, and osteoporosis ( Kong, Lauche, & Chang, 2016 ). These alternatives help with pain, fatigue, and feelings of helplessness of chronic joint symptom condi- tions such as RA, osteoarthritis, and fi bromyalgia. Assistive devices such as canes, crutches, or walkers should be dis- cussed to prevent falls. Information on nutrition, the use of calcium supplements, and smoking cessation should be dis- cussed for further measures.

Referral: Refer patients to a specialist pending the results of the work-up. Refer patients to the appropriate emergency service if you suspect sepsis, fracture, or avascular necrosis. Referral to physical or occupational therapy for exercises to reduce pain and improve strength and endurance is advised (Polsunas et al., 2016).

Education: Teach patients about the appropriate dose of medi- cations and the potential side effects that need to be reported. Instruct patients about appropriate follow-up and referrals. Tell the patient to report any persisting or worsening joint pain and any systemic involvement. Instruct patients on the appropriate methods for pain control. Review the use of any adaptive equipment and the role the patient plays in avoiding disability and slowing progression of the disease. Low-im- pact exercise is important for obese patients. Hermsen and colleagues ( 2016 ) noted education in cognitive appraisals and coping strategies have contributed to positive physical functioning for self-effi cacy. Patients with chronic joint pain conditions and higher social support have shown lower levels of depression ( Lee, Kahana, & Kahana, 2016 ). Neogi (2013) noted that joint pain also contributes to the socioeconomic burden, so providers should discourage nonevidence-based costly treatment measures.

74 Chapter 5 ■ Symptoms and Syndromes

Description: Peripheral edema is swelling due to an increase in the interstitial fl uid volume and is not clinically appar- ent until the interstitial volume has increased by 2.5 to 3  L. Lymphedema, or lymphatic obstruction, occurs when a com- promised lymphatic system causes localized fl uid retention and tissue swelling. There are numerous etiologies for periph- eral edema ranging from benign to life-threatening clinical conditions.

Etiology: Normally, the distribution of water between the blood and interstitial tissues is maintained by hydrostatic and oncotic pressures in each compartment. Starling ’ s concept— the osmotic pressure of the plasma proteins balances the hydrostatic pressure in the capillaries—helps in the under- standing of fl uid dynamics. Fluid fl ows from the vessels to the interstitial area in response to intravascular hydrostatic pressure and the colloid osmotic pressure of the interstitial fl uid. In the opposite direction, fl uid enters the blood because of the interstitial tissue tension and the oncotic pressure of the plasma proteins. Interstitial fl uid also is returned to the blood as lymph. Under steady-state conditions, net fl uid fl ux out of the capillary is balanced by lymph fl ow back into cir- culation. Alteration in any of these compartments (intravas- cular, extravascular, lymphatic) upsets the equilibrium, and edema occurs. Two basic steps occur in edema formation: sodium and water are retained, and capillary hemodynamics are altered.

Edema is common in older adults, has diverse etiolo- gies, and more than one disorder can be causing edema in the same patient. The most common cause in patients older than 50 years of age is venous insuffi ciency. Other common causes of edema include heart failure, DVT, cirrhosis, renal disease, and drug-induced edema. The swelling that results from lymphedema is nonpitting. It may be primary due to

congenital or inherited conditions, or secondary caused by damage to the lymphatic system; cancers (especially breast, ovarian, and prostate); infection; infl ammation; or obesity (see Table 5-9 ).

Occurrence: The frequency of occurrence depends on the underlying etiology.

Age: Peripheral edema occurs frequently in older adults.

Gender: No documented signifi cance is found, but gender statistics vary according to the specifi c etiology. Lymphedema and venous insuffi ciency are more common in women.

Ethnicity: While moderate edema does not have a notable ethnic difference, severe venous insuffi ciency is less common in African American women.

PERIPHERAL EDEMA

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Diclofenac sodium topical gel 1% applied up to four times a day resulted in 30% pain reduction of knee OA pain.

A Edwards et al., 2016

Education in cognitive appraisals and coping strategies have contributed to positive physical functioning for self-effi cacy.

A Hermsen et al., 2016

Tai chi showed improvement in chronic pain conditions including low back pain, fi bromyalgia, and osteoporosis.

A Kong, Lauche, & Chang, 2016

Patients with chronic joint pain conditions and higher social support have shown lower levels of depression.

A Lee, Kahana, & Kahana, 2016

Aerobic exercise, resistance exercise, or multimodal exercise programs (combination of the two types) can reduce joint pain in older obese adults in the range of 14%–71.4%.

A Zdziarski, Wasser, & Vincent, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Common Causes of Peripheral Edema

Unilateral, acute DVT, ruptured Baker ’ s cyst, compartment

syndrome

Bilateral, acute Allergic reaction, trauma, burns, bilateral

DVT, acute worsening of renal failure, or

congestive heart failure (CHF)

Unilateral, chronic Venous insuffi ciency, lymphedema, pelvic

tumor, and refl ex sympathetic dystrophy

Bilateral, chronic Venous insuffi ciency, pulmonary

hypertension, CHF, lymphedema,

medications, renal disease, idiopathic,

dependent edema, anemia

Source: Adapted from O’Brien, J. G., & Miles, T. P. (2013). Edema. Essential Evidence Plus . Retrieved from http://www.essentialevidenceplus.com.proxy.its. virginia.edu/content/eee/29

TABLE 5-9

Chapter 5 ■ Symptoms and Syndromes 75

Contributing Factors: Physiological age-related changes increase the vulnerability to fl uid retention. The older adult has a smaller amount of total body water overall (80% of body weight for a newborn, 60% for a young adult, 50% for an older adult), and of this, two-thirds is intracellular and one-third is extracellular. As more intracellular fl uid is lost over time, extracellular fl uid volume starts to comprise more body water. Risk factors for peripheral edema from age-re- lated changes include a decrease in:

■ Serum albumin—less than 2 g/dL can cause edema ■ Glomerular fi ltration rate ■ Hepatic blood fl ow ■ Sodium-concentrating ability of the kidney ■ Myocardial contractility and cardiac output ■ Baroreceptor sensitivity

Medications that are used to treat conditions common in older adults can cause peripheral edema:

■ NSAIDs cause increased sodium absorption in the kidney due to the blockage of prostaglandin.

■ Thiazolidinediones are used as treatment for diabetes (pioglitazone or rosiglitazone) and stimulate sodium reabsorption in the kidney; worsening heart failure is a known side effect.

■ Antihypertensives with mechanisms that cause vaso- dilation or activation of the renin-angiotensin-aldo- sterone sympathetic nervous system may increase peripheral edema (hydralazine, dihydropyridine calcium channel blockers, and alpha blockers).

Additional contributing factors include dependent position- ing of the lower extremities, excessive intake of sodium, and hot weather.

Signs and Symptoms: The patient may complain of fullness, discomfort, aching pain, shoes that are too tight, wounds, gait disturbance, self-image issues, or weight gain. The history should elicit the seven dimensions of the signs and symptoms of edema, emphasizing location (unilateral or bilateral) and chronological evolution (acute or chronic progression). Asso- ciated symptoms need to be elicited, particularly shortness of breath or awakening at night with diffi culty breathing. The presence or absence of pain is helpful in determining the differential diagnosis. Ask about aggravating and alleviating factors, including the effect of prolonged sitting or standing, and determine the effect of passive leg elevation. A history of malignancy, pulmonary, cardiac, renal, hepatic, endocrine, or PVD is important. Ask about recent weight loss or gain, changes in diet, salt intake, and alcohol use. A thorough review of medications (both prescribed and OTC), particu- larly new medications or a recent change in dosage is essen- tial. Has the patient been on a trip recently or had periods of prolonged standing or sitting?

The physical examination begins with weight. Assess skin changes, including pigmentation and thickening, lesions, discoloration, texture, temperature, and induration. Evaluate the venous and arterial circulation, checking pulses through- out; capillary refi ll; and dependent rubor. Varicose veins are usually readily apparent with the inspection of the legs while the patient stands. Assess the extremity for local or diffuse tenderness and for pitting or nonpitting edema. Measure and compare the circumference bilaterally from a fi xed reference

point above the ankle to the area of maximal edema (e.g., patella, calf, midcalf). Assess any localized enlargement.

Pitting edema has no universal scale for measurement. It is generally defi ned on a scale of 1 + to 4 + or brawny edema (which is chronic and may not be pitting). Edema is assessed by applying fi rm pressure with your thumb over the area of swelling. A commonly used scale for grading edema refers to the depth of the impression: 2  mm  =   1 + , 4  mm  =   2 + , 6  mm  =   3 + , and 8  mm  =   4 + . Another method adds the amount of time it takes for the impression to return to normal: 30 seconds or less  =   1 + , 30 to 60 seconds  =   2 + , 60 to 90 seconds  =   3 + , and 90 to 120 seconds  =   4 + . To assess whether nonpitting edema represents the presence of lymphedema, a technique that is recommended was defi ned by Kaposi and later by Stemmer. The Kaposi-Stem- mer sign suggests lymphedema when there is an inability to tent the skin over the dorsum of the foot at the base of the second toe.

The examination should also include body systems as indicated by the history, particularly pulmonary, cardiac, hepatic, renal, and endocrine. If arterial insuffi ciency is sus- pected, an ankle-brachial index (ABI) measurement should be performed. In unilateral edema, a 1-cm difference in size above the ankle or a 2-cm difference at the calf is signifi cant and should lead to further investigation.

Diagnostic Tests: Diagnostic tests depend on the probable etiology of peripheral edema. Cardiac causes may warrant a chest x-ray, EKG, or echocardiogram. Laboratory studies also depend on the diagnostic considerations: CBC for sus- pected anemia, with a differential if infection is a possibility; CMP, which includes electrolytes, glucose, BUN, creatinine, albumin, phosphorus, AST, ALT, and bilirubin. More tar- geted chemistries may be reasonable; for example, a basic metabolic, renal, or hepatic panel. Thyroid function can be assessed with a high sensitivity thyroid-stimulating hormone with a refl exive addition of free thyroxine if abnormal. Addi- tional studies could include ultrasound, venogram, venous Doppler studies, lymphoscintigraphy, or the more invasive lymphangiography. CT scans or ultrasound for pelvic masses and lymphoma may be indicated, as well as a CA-125. Urine studies quantify protein losses and urine electrolytes.

Differential Diagnosis: Peripheral edema is an important clin- ical sign and its causes are diverse. The differential diagno- sis is facilitated in part by noting if edema is unilateral or bilateral and recognizing distinctions between lymphedema, lipedema, and venous stasis. Lipedema is a bilateral, symmet- rical deposition of fat in the lower extremities that spares the feet (a distinguishing feature) and occurs exclusively in obese women. A multisystem approach that excludes major organ system dysfunction is useful, especially pulmonary, cardiac, endocrine, hepatic, and renal disease. An accurate diagnosis is important because the mainstay of treatment is reversing the underlying disorder, if possible.

Treatment: Always direct treatment at the cause of periph- eral edema: diuretics for heart failure, a high-protein diet for hypoalbuminemia, ACE inhibitors for proteinuria, and thrombolytics for acute DVT. Any drugs known to cause edema should be discontinued or decreased in dosage. Many patients expect that any edema should be treated with a diuretic, but if fl uid overload is not the issue, diuresis can

76 Chapter 5 ■ Symptoms and Syndromes

actually cause tissue death. Edema due to venous stasis, for example, should focus on that specific etiology, which may not require diuretics.

Compression Stockings: Compression stockings decrease the capillary filtration rate, thus decreasing edema. They are especially useful in patients with venous insufficiency. There is no evidence to indicate that high compression (30 to 40 mm Hg) is clinically more advantageous than medium compression (20 to 30 mm Hg), and patients are more com- pliant with medium compression. The stockings can be dif- ficult to pull on, and a stocking donner can be helpful. Give the patient a prescription for two sets to allow for laundering. They need to be replaced every 6 months because the com- pression properties decrease with wear. Stockings that zip are available. Send the patient to the medical supply store where trained fitters will ensure the proper fit. Compression stockings are not recommended for patients with peripheral artery disease (PAD), and if suspected, an ABI can be ordered to screen for PAD.

Behavioral modifications include intermittent periods of recumbency, the avoidance of environmental heat, and sodium and water restriction as indicated. Exercise improves the muscle pump action and strengthens leg muscles.

Follow-Up: Closely monitor patients for effectiveness of therapy and adverse events. Monitor the weight and limb cir- cumference measurements using the same reference points because a patient ’ s weight may increase 10% before pitting edema is clinically evident.

Sequelae: When administering diuretics, the health-care pro- fessional must be alert to potential volume depletion. Older adult patients are very sensitive to diuretics, and their admin- istration may result in falls, weakness, confusion second- ary to sodium and other electrolyte abnormalities, urinary

incontinence, gout attacks, volume depletion, and acute renal failure. Patients with edema as a result of deep venous insufficiency are prone to recurrent ulceration.

Prevention/Prophylaxis: For patients with recurrent lymphan- gitis and cellulitis, prescribe intermittent long-term antibiotic prophylaxis. For patients with leg swelling secondary to DVT, thrombolytics may limit the tissue loss, pulmonary embolus, and more extensive thrombosis of the deep venous system.

Referral: Referral to specialists depends on the diagnosis. It would be rare to hospitalize a patient for most causes of peripheral edema, thus treatment is almost always outpatient. Even DVTs are treated in the outpatient setting in consulta- tion with a vascular medicine specialist with low-molecu- lar-weight heparin (enoxaparin), warfarin, or non-vitamin K antagonist oral anticoagulant (NOAC) (rivaroxaban, dab- igatran, apixaban, and edoxaban). The NOACs offer benefits above warfarin because they do not require routine moni- toring, have predictable pharmacokinetics, fewer drug-drug interactions, and limited drug-food interactions.

Education: Patients need specific information related to the edema and the management of symptoms. Typically, the patient with edema is instructed to avoid highly salted foods (follow a 2 to 3 g sodium diet). If compression stock- ings are recommended, emphasize the importance of proper sizing and application technique to avoid excessive pressure. Instruct patients to elevate the legs above heart level to decrease peripheral vascular pressure for 10 to 15 minutes three to four times a day. Periodic active muscle contraction exercises are important for individuals who must sit for long periods. Teach patients with peripheral vascular disorders to avoid excessive heat and reduce weight if indicated. Special care of the skin, including proper shoes and prevention of trauma, is important.

CLINICAL RECOMMENDATIONS EVIDENCE RATING REFERENCES

When DVT is suspected, use the Wells Clinical Rule, D-dimer, and selective use of imaging to confirm the diagnosis.

A O’Brien & Miles, 2013

Begin by evaluating whether edema is unilateral or bilateral, painful or nonpainful, and acute or chronic.

B O’Brien & Miles, 2013 Trayes et al., 2013

Leg edema in immobile patients due to venous insufficiency can be adequately managed with compression and physical therapy alone.

B Suehiro et al., 2014

Brain natriuretic peptide (BNP) is helpful for distinguishing heart failure from other causes of leg edema.

B O’Brien & Miles, 2013

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Chapter 5 ■ Symptoms and Syndromes 77

Description: Pruritus is an unpleasant, irritating, or itching sensation on the surface of the skin that may lead to the desire to scratch. It may be localized or generalized. Pruritus may be acute (less than 6 weeks) or chronic (more than 6 weeks). Characteristic features include scratching and infl ammation.

Etiology: The pathophysiology of pruritus remains unknown. Infl ammation results from activation of the immune response. Immunoglobulin E (IgE) in the skin surface cells triggers an infl ammatory response in which histamines and other neurostimulators are released. Repetitive rubbing and scratching exacerbate the infl ammation. As the skin ages, integumentary and vascular changes lead to decreased skin moisture, sweat, and sebum production, all of which con- tribute to dry skin. The decline in immune function with age produces increased incidence of autoimmune diseases that can cause pruritus. Pruritus can be caused by infl amma- tory skin disease, exogenous trigger factors (scabies, mites, toxins, allergens, wind), endogenous trigger factors (medi- cations and pH changes), or systemic disease (diabetes, iron defi ciency anemia, chronic renal insuffi ciency, liver disease, tumors, HIV). Psychogenic pruritus (somatoform pruritus) is another common condition. Medications can induce pru- ritus, including antihypertensives (ACE inhibitors, calcium channel blockers), antibiotics, opioids, and psychotropics. Drug-induced pruritus may be localized or generalized and may start after the fi rst dose of a drug or many weeks or months after being on the drug.

Occurrence: There is no epidemiological data base for pruri- tus, therefore the overall incidence and prevalence unknown, but it is the most common symptom seen in dermatology, and various skin and systemic diseases are associated with it.

Age: Pruritus is the most common skin complaint in individ- uals more than 65 years old, and the incidence is about 20% in those more than 85 years old. Analysis of hospital admis- sion data indicates that 11.5% of older adults had a primary diagnosis of pruritus and two-thirds of patients in skilled nursing facilities experience it. Xerosis (dry skin) is the most common cause in older adults.

Gender: Pruritus is more prevalent in women than in men.

Ethnicity: Genetic variation may affect receptors for itch as well as response to anti-pruritic therapies. The prevalence of pruritis is greater in darker skin types (Hajdarbegovic & Thio, 2012).

Contributing Factors: Once a pattern for pruritus has been initiated, continued scratching causes a cascade of infl am- matory mediators that provoke the itch sensation and repeat scratching. Additional factors that contribute to dryness include winter weather (low environmental humidity), daily use of cleansers, and bathing without replacement emol- lients. Sleep deprivation can cause an increase in the release of an infl ammatory mediator, and though it is often a result of pruritus, it can also contribute to it.

Signs and Symptoms: A thorough history and physical exam- ination should be done in all patients with pruritus. Focused questions should include:

■ How did it start (sudden or gradual)? ■ Characterize the sensation—is it prickling, crawling,

burning, stinging? ■ How severe is it? ■ How frequently does it occur and for how long? ■ Does anything make it worse or better? ■ Where does it itch (local or systemic)?

Asking if and how it might interfere with activities or sleep is important. Asking patients what they think the cause might be might help. Find out about allergies and if there was an exposure to new creams or detergents. Ask about systemic-as- sociated symptoms such as weight loss, fever, heat/cold intol- erance (thyroid disease), nausea and vomiting (chronic renal failure), and polyuria/polydipsia (diabetes). Additional history of importance is past medical history, including previous skin conditions, skin care routine, and current medications. Brief psychological screening may provide some insights into the potential cause. A complete physical examination is war- ranted, examining all surfaces of the skin, including the hair and nails. Assess texture, temperature, moisture, and turgor of the skin. Assess lesions and document using drawings or photos accurately recording the location, shape, and charac- teristics. Look for secondary lesions such as lichenifi cation (the thickening of the skin from continued scratching). The general physical examination is focused on identifying poten- tial systemic causes and contributors to pruritus and includes palpating lymph nodes and the thyroid gland.

Diagnostic Tests: No specifi c tests are indicated for a com- plaint of pruritus, though it might include a CBC, ESR, and/ or C-reactive protein to determine infection/infl ammation. Patch testing or photo testing may be needed to establish a diagnosis. If a systemic disease is suspected, an appropri- ate thyroid panel, liver function tests, serum glucose levels, serum iron level, renal values (serum urea and creatinine), stool examination for parasite detection, and HIV testing may be done.

Differential Diagnosis: The differential diagnosis is quite broad and include dermatological causes, hypersensitivities, allergic reactions, scabies, lice, neuropathic and neurogenic causes, and psychiatric causes, as well as pruritus associated with systemic diseases. Pruritus is present in 80% to 100% of persons presenting with cholestasis and jaundice. There may be more than one cause, and frequently a cause is never determined.

Treatment: Treatment goals should be patient-specifi c and tailored to the patient ’ s physical and mental ability and any concurrent medical issues, severity of the symptoms, and potential for adverse effects of treatments. Goals of treatment include alleviating the itch and maintaining skin integrity. Treatment is aimed at the cause. Xerosis, the most common cause, is treated with emollients that rehydrate the skin and reduce infl ammation, and some may additionally include a mild anesthetic that helps decrease the sense of itching.

Topical Therapies: These are most useful with localized forms of pruritus. Topical steroids can reduce infl ammation and itching, though these are avoided for generalized itching

PRURITUS

78 Chapter 5 ■ Symptoms and Syndromes

or for prolonged periods because they cause skin thinning. An antihistamine topical cream may be used or a menthol cream, which has a cooling effect. Topical immunomodu- lators act on nerve fi bers, and capsaicin topically has been found to be helpful with neuropathic origins such as posther- petic neuralgia. Local anesthetics can decrease transmission in sensory fi bers.

Systemic Therapies: These are frequently used for treatment of generalized pruritus. Systemic medications that have anti- pruritic properties include serotonin and norepinephrine reuptake inhibitors (SNRIs), selective serotonin reuptake inhibitors (SSRIs), and tricyclic antidepressants. Mirtazapine (an SNRI), paroxetine (an SSRI), and doxepin (tricyclic anti- depressant) have antihistaminic and serotonergic effects and have been used to treat pruritus. The antidepressants may be helpful in psychogenic causes. Antihistamines, neuroleptics, and opioid agonists and antagonists can be helpful in some circumstances. First-generation antihistamines may help patients experiencing nocturnal pruritus sleep due to sop- orifi c effects; however, their anticholinergic properties are problematic in older adults. Gabapentin can be used instead, starting at 100 to 300 mg at bedtime, with a maximum dose of 1,800  mg in divided doses. Systemic steroids should only be used in acute, severe forms of pruritus.

Nonpharmacological Measures: These include removing any environmental allergens if identifi ed, using an occlusive dress- ing in a localized area to reduce scratching, cool dressings,

psychotherapy, and acupuncture. Phototherapy has been used for decades to treat various pruritic dermatoses.

Follow-Up: Monitor the patient frequently to evaluate the effectiveness of treatment, reinforce adherence, and watch for secondary complications.

Sequelae: Secondary infection is a risk when the skin is broken. Neglecting the symptom can have a negative effect on the patient ’ s quality of life, especially through sleep deprivation.

Prevention/Prophylaxis: Avoid triggering or exacerbating factors. Bathing less often in warm (not hot) water, increas- ing the humidity, and using a soft towel to pat dry gently rather than vigorous rubbing are advised. Apply emollients after bathing (and never in the tub due to fall risk), apply- ing them gently to avoid overstimulating the nerve endings. Eating a healthy diet and drinking plenty of water is advised.

Referral: Refer to a dermatologist or an allergist for severe cases or when treatment is ineffective.

Education: Education should include an explanation of the diagnosis and the triggering and exacerbating factors. In addition to bathing techniques and how and when to use moisturizers, educate the patient to keep fi ngernails short, wear light and loose clothing, avoid alkaline and alco- hol-based cleansers, maintain comfortable temperature and humidifi cation, and alleviate stress. Discussion of breaking the itch-scratch cycle is very important.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Keep cool, use emollients, and take short, tepid showers. Avoid soaking and use moisturizing soaps as opposed to antibacterial soaps.

C Valdes-Rodriguez, Stull, & Yosipovitch, 2015

First-generation and second-generation antihistamines have an antipruritic effect in management of chronic pruritus.

B Berger et al., 2013

In patients with chronic atopic dermatitis, exacerbating factors and appropriate treatment options are important and interventions that include educational interventions report signifi cant benefi ts.

A Arkwright et al., 2013

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

SYNCOPE

Description: Syncope is a sudden and transient loss of con- sciousness and postural tone resulting from a reduction in oxygen to the brain with immediate spontaneous recovery. While of short duration, it can result in physical injury, acci- dents, and a decreased quality of life.

Etiology: Etiologies for syncope range from trivial to lethal. In most instances, the loss of consciousness refl ects a temporary decrease in cerebral blood fl ow that is usually secondary to a fall in the systemic arterial blood pressure infl uenced by met- abolic regulation, chemical regulation, and autoregulation.

Chapter 5 ■ Symptoms and Syndromes 79

Refl ex-mediated and orthostatic causes are usually more benign, whereas cardiac and neurological causes are more dangerous. In the Framingham Heart Study, cardiac syncope doubled the risk of death compared to those without syncope. The most common cause of syncope is the neurocardiogenic refl ex or vasovagal syncope, which represents about one-third of all causes (da Silva, 2014). The second most common refl ex syncope that has the highest incidence in older adults is carotid sinus syncope, which is more common in men and repro- ducible with carotid massage. Other refl ex syncope is more situational, triggered by cough, micturition, or defecation. Car- diovascular causes of syncope include orthostatic hypotension, which is particularly common in older adults, and bradycardia or tachyarrhythmias. Valvular heart disease and pulmonary hypertension, while not common causes of syncope, can be treatable. Studies show that the cause of syncope remains elusive in 30% of cases of patients admitted for syncope.

Occurrence: The Framingham Heart Study showed that 3% of men and 3.5% of women had experienced at least one syncopal episode. Approximately one-third of the population will experience a syncopal event in their lifetime. Syncope accounts for about 3% to 5% of all emergency department visits and 1% to 6% of all hospital admissions.

Age: The lifetime incidence of syncope may be 25% in older adults, and 80% of all emergency department admissions for syncope are individuals older than 65 years of age. Some forms of syncope (i.e., vasovagal, carotid sinus hyper- sensitivity) are more common in younger persons than in older persons; other forms of syncope (i.e., cardiac, ortho- static, micturition related) occur more often in older than in younger individuals.

Gender: Among younger adults, women have nearly twice the rate of syncope as men; among older adults, men have the greater incidence. This likely refl ects the most common etiologies in the different age groups.

Ethnicity: Not signifi cant.

Contributing Factors: Cerebral blood fl ow has been reported to decline 25% with physiological aging, which is thought to be related to vascular stiffening. Hormonal regulation of extracellular volume may become impaired with age. Cardiac refl exes and baroreceptor sensitivity also may become impaired. The kidneys’ ability to conserve sodium and water declines. Chronic diseases, such as heart disease, diabetes, renal insuffi ciency, hypertension, and chronic pulmonary disease, are predisposing conditions. Medications used to treat these chronic diseases, such as diuretics, beta blockers, vasodilators, nitrates, antiarrhythmics, and antihyperten- sives, also may be offenders. Alcohol is a contributing factor in vasovagal syncope. An emotional response can cause neu- rally mediated syncope in susceptible individuals in stressful circumstances. Dehydration and orthostatic hypotension may be factors. Situational syncope can occur when the Valsalva maneuver is produced (micturition, defecation, cough, lifting heavy objects, or after meals related to postprandial hypoten- sion). Prolonged recumbency can contribute to micturition syncope, especially in men with prostate enlargement who awaken from a supine sleep and stand to urinate.

Signs and Symptoms: Sudden collapse with loss of motor tone, with or without injury, is the most common presentation of

syncope. Self-report and eyewitness accounts of transient loss of consciousness are often unreliable—even when the eyewitness is a health-care professional. The most import- ant fi rst step is determining if it is true syncope. Obtain the patient ’ s description of symptoms preceding the event and of activities that may have precipitated the event. Cardiac-re- lated syncope may be sudden and without warning. A brief prodrome of symptoms, such as nausea, pallor, or diaphore- sis, may suggest a vasovagal episode or a seizure. Many older adult patients report presyncopal episodes along with true syncopal events. Determine if any focal neurological symp- toms were present (i.e., diplopia, motor and sensory symp- toms). Review signifi cant past medical history, prior history of an event, all medications being used, and alcohol intake. Ask about family history for sudden cardiac event. Rapid onset and complete recovery are key diagnostic symptoms along with loss of motor tone. If any one of these symptoms is absent, nonsyncopal causes must be considered. It is possi- ble to have generalized jerking movements with syncope that occur after the loss of consciousness. Rapid reorientation can distinguish this presentation of syncope from a seizure dis- order. The recognition of this difference can save a patient from inaccurately being diagnosed with a seizure disorder ( Walsh, Hoffmayer, & Hamdan, 2015 ).

The physical examination should start with checking the patient for evidence of trauma, then focus on the cardiovas- cular and neurological components. Check blood pressure in both arms and positionally. Determine the compensatory pulse rate. Check the carotids for bruits. Carotid sinus com- pression sometimes is used to provoke symptoms, but this should be done cautiously and selectively and is contraindi- cated in patients with a bruit or a history of stroke or myo- cardial infarction. Examine the heart, assessing for murmurs, signs of arrhythmia, vascular disease, and left ventricular dysfunction. Check oxygen saturation rates. Perform a thor- ough neurological examination, paying particular attention to focal abnormalities that may suggest neurological syncope. Generalized anxiety disorders can cause hyperventilation and trigger a vasodepressor reaction; this should be evaluated during the physical examination.

Diagnostic Tests: The EKG is the most important diagnostic test with a focus on the rate and rhythm. Diagnosis of cause from the EKG is very low at 2% to 9%, but it is inexpensive and when positive for disease, critical to proper intervention. Positive fi ndings may include sinus bradycardia, prolonged PR interval, a bundle branch block, or ventricular ectopy. Cardiac diagnostic studies may include echocardiogram (valuable in estimating ejection fraction and valvular heart disease), ambulatory EKG monitoring, and electrophysio- logical studies. A stress test is not indicated unless the event occurred during exercise or was accompanied by chest pain. A chest x-ray, which may reveal cardiomyopathy, is indi- cated in patients with new abnormal fi ndings, patients with dyspnea, and patients without a recorded baseline. Electro- encephalogram and CT scan of the head are reserved for patients with focal neurological abnormalities. Vasovagal syncope may be induced with tilt-table testing, which may be done with or without isoproterenol. It is useful in patients with syncope of unknown etiology or patients with recurrent syncope. Laboratory evaluation is generally of low yield but may include a CBC with differential if infection or anemia is

80 Chapter 5 ■ Symptoms and Syndromes

suspected. Renal function studies and electrolytes may also be considered.

Differential Diagnosis: Distinguish syncope from seizures, diz- ziness, drop attacks, orthostasis, postprandial hypotension, carotid sinus sensitivity, and arrhythmias. Atypical presen- tations include myocardial infarction and pulmonary embo- lism. Dizziness does not involve a loss of consciousness and is often characterized further as vertigo, light-headedness, disequilibrium, or presyncope (sensation of impending loss of consciousness). Drop attacks are sudden drops without warning and may be due to transient basilar artery insuffi - ciency at times precipitated by head movement or neck hyper- extension. Metabolic disorders (hypoglycemia, hypoxemia) cause coma/somnolence rather than syncope. Orthostatic hypotension refl ects a drop in blood pressure of 20  mm  Hg systolic or 10 mm Hg diastolic after changing from a lying to a standing position and is taken 1 minute after standing and again 3 minutes after standing. Consider the relationship to meals with a drop in blood pressure. Carotid sinus sensitiv- ity and arrhythmias (atrioventricular block, sick sinus syn- drome, and supraventricular arrhythmias) increase with age. Supraventricular arrhythmias rarely cause syncope, but ven- tricular tachyarrhythmias, especially those with decreased ejection fraction, are a major concern.

Treatment: When you identify the specifi c cause of syncope, you can initiate the appropriate treatment. Hospitalization may be required when there is a high risk of death, recur- rence, or injury. Twenty-four-hour observation may be an option for patients with confusing presentation. Vasodepres- sor syncope is best addressed with volume expansion. Six factors predictive of adverse outcomes were noted in almost all research focused on risk stratifi cation: acute coronary syn- drome, heart failure, structural heart disease, abnormal EKG, anemia, or hemodynamic instability. Antiarrhythmic therapy is initiated, if indicated, and drug-induced or idiopathic orthostatic hypotension is treated appropriately. Cardiac pacing may be appropriate. Cardiac surgery is the treatment of choice for obstructive heart disease. Always correct under- lying anemia and metabolic imbalance, and optimize cardiac and pulmonary status in the older adult patient. Address any age-related, disease-related, or disuse-related changes that

impair the patient ’ s compensation for hypotensive stressors, such as dehydration, deconditioning, and orthostatic hypo- tension. Nonpharmacological approaches to vasodepres- sor syncope include tilt-table training and lower extremity muscle tensing.

Follow-Up: Unknown causes precipitate a high incidence of syncopal events and in one-third of patients, syncope is a recurring event. Because recurrences may refl ect lack of effective therapy or a failure to diagnose correctly, close mon- itoring is indicated.

Sequelae: Syncope from cardiovascular causes tends to be more dangerous. Sudden death with syncope has been attributed to arrhythmia. Patients with syncope are at risk for fall-related injury (fracture, subdural hematoma) and reduced functional capacity.

Prevention/Prophylaxis: Patients with vasovagal syncope are taught to avoid triggers and, if premonitory symptoms occur, to lie down immediately and elevate the feet higher than the chest. Adequate fl uid intake is a precaution, and for selected individuals with vasovagal syncope, a higher salt intake may be advised. Support hose may help prevent reduction in central plasma volume. Patients are encouraged to avoid a sudden change in position. For syncope caused by atrial fi brillation, low-dose warfarin or aspirin therapy may be pre- scribed. Micturition syncope can be avoided by advising men to sit down to urinate.

Referral: Hospitalization is necessary for patients in whom you suspect an arrhythmia or myocardial infarction as the cause of the syncope and for patients who sustain signifi cant injury during the syncopal event. Consultation may be appro- priate with a cardiologist for managing cardiac syncope and with a neurologist for managing neurally mediated syncope. If it is determined that outpatient evaluation is an option, it should occur within 3 to 5 days ( Puppala et al., 2015 ).

Education: In addition to teaching preventive strategies and the avoidance of triggering events, teach individuals with recurrent syncope safety precautions related to driving or the use of dangerous machinery. It is prudent for the health-care professional to understand the driving laws of the state rela- tive to loss of consciousness/syncope.

CLINICAL RECOMMENDATIONS EVIDENCE RATING REFERENCES

A 12-lead EKG in all patients coming to the emergency department for syncope should be done.

A Puppala, Dickinson, & Benditt, 2014 Puppala et al., 2015 Walsh, Hoffmayer, & Hamdan, 2015

Serious outcomes following syncope are unlikely if the following risk factors are absent: systolic blood pressure >90 mm Hg, shortness of breath, EKG with new changes or nonsinus rhythm, history of heart failure, hematocrit less than 30%.

A Puppala et al., 2015

If patient is not hospitalized after presenting to the emergency department for a syncopal event, outpatient follow-up should be scheduled in 3–5 days.

C Puppala et al., 2015

Chapter 5 ■ Symptoms and Syndromes 81

Description: Tremor is the most common form of involun- tary movement and is characterized by rhythmic oscillation of a body part that can be classifi ed according to the cir- cumstances under which it occurs. Only a small fraction of persons with tremor seek medical attention. Tremors may result from physiological or pathological processes.

Etiology: Because of the vast number of causes of tremor, etiological classifi cation is not helpful. Terms used to describe the clinical phenomenology of tremor include rest tremors and action tremors. Rest tremor occurs when muscle is not activated voluntarily, and the relevant body part is fully sup- ported against gravity; whereas action tremor is present with voluntary contraction of muscle. Action tremors can be sub- classifi ed further into postural, kinetic, and isometric tremor. Postural tremor is present while voluntarily maintaining a position against gravity. Kinetic tremor may occur during any form of voluntary movement of the affected body part . Iso- metric tremor occurs with muscle contraction against a rigid stationary object. The most common tremor is enhanced phys- iological tremor followed by essential tremor and then parkinso- nian tremor.

Occurrence: Tremor is the most common movement disorder encountered in clinical practice. Everyone has a low-ampli- tude physiological tremor that can be observed when the arms are extended. Present in all muscle groups, it persists throughout the waking state. Enhanced physiological tremor is a physiological tremor that comes and goes with anxiety, caffeine, and fatigue. Estimates suggest 7 million people (or 2.2% of the U.S. population) have essential tremor. Most do not seek help until later age because of slow progression.

In 50% of cases, the disease is familial (autosomal domi- nant, meaning 50% of an affected individual ’ s children have it). More than 70% of patients with Parkinson ’ s disease have tremor as the presenting symptom. Less common are cerebel- lar tremor, psychogenic tremor, dystonic tremor, and tremor associated with Wilson ’ s disease.

Age: Most studies report a signifi cant age-associated increase in the prevalence of essential tremor. Essential tremor begins in young to middle-aged people and gradually intensifi es with age. Tremors in older adults are more likely to be of the essential or parkinsonian type.

Gender: Tremor affl icts both genders equally, with perhaps slightly more frequency in men than in women.

Ethnicity: Tremor is more prevalent in Caucasians than in African Americans, and is of intermediate prevalence in Hispanics.

Contributing Factors: During times of stress, the amplitude of a physiological tremor increases. Fatigue, anxiety, hyperthy- roidism, systemic illness, use of medications, drug withdrawal (especially from alcohol), use of methylxanthines, and excess caffeine intake can exaggerate tremor. Medications that can cause or exacerbate tremor include those that stimulate the sympathetic nervous system and psychoactive medications.

Signs and Symptoms: The fi rst step in the evaluation of tremor is to categorize the tremor based on activation conditions, dis- tribution, and frequency. Determine the duration and age of onset of symptoms, exacerbating or alleviating factors, and any family history of tremor or other neurological disorders. Include any associated symptoms, such as bradykinesia or rigidity (suggesting Parkinson ’ s disease) or ataxia and nystag- mus (suggesting cerebellar disease). The patient ’ s medication history, any exposure to toxins, and the presence of illness should be noted. In assessment of the impact of tremor on patients’ lives, functional disability in performing ADLs and the patient ’ s subjective assessment of his or her quality of life are useful. History is important, but the diagnosis is based on clinical physical examination fi ndings. Tremor may occur in various body parts, such as the hands, head, facial structures (chin, tongue, lips, and ears), vocal cords, trunk, and legs. Of all tremors, 94% occur in the hands, either unilaterally or bilaterally.

On physical examination it is important to conduct a thor- ough tremor-focused neurological examination: muscle tone is checked throughout the body, cranial structures (including the mouth and jaw) are examined at rest and in action, and the tongue is observed during rest and protrusion. To distin- guish properly between resting and action tremors, patients should be evaluated while supine and when seated with the arms fully supported. (If patients are in a position that does not provide complete support, certain muscles may be active against gravity, producing a tremor that may be classifi ed improperly as a resting tremor.) Once rest tremor is ruled out, the patient performs other maneuvers.

The upper extremities are examined in an outstretched position with the hands supine (palms up), sideways (semi- prone), and then prone (palms down). The semi-prone posi- tion enhances essential tremor, whereas the supine position

CLINICAL RECOMMENDATIONS EVIDENCE RATING REFERENCES

Generalized jerking movements may occur after loss of consciousness with syncope. These are unlikely to represent a seizure if patient is rapidly reoriented.

C Walsh, Hoffmayer, & Hamdan, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

TREMOR

82 Chapter 5 ■ Symptoms and Syndromes

inhibits it. In the wing position (i.e., with apposition of the index fi ngers close to each other but not touching), prox- imal tremor may be identifi ed. Goal-directed activities are performed, such as fi nger-to-nose, heel-to-shin, and toe-to- fi nger movements. The patient is asked to recite a standard paragraph and enunciate a sustained vowel. Handwriting samples are obtained (e.g., script, numbers, Archimedes spirals). Gait is evaluated for shuffl ing and unsteadiness, and Romberg (station) and balance testing are conducted. Careful evaluation is performed for signs associated with tremor syndromes. Bradykinesia and postural abnormalities are evaluated by observing diffi culty rising from a seated posi- tion, decreased arm swing, and masked facies. Patients with essential tremor typically have handwriting that is shaky and large, whereas the handwriting of patients with Parkin- son ’ s disease initially may be of normal size and progressively become smaller (micrographia). Archimedes spirals drawn by essential tremor patients tend to illustrate natural fl uctua- tions in tremor magnitude.

Diagnostic Tests: No specifi c tests are routinely ordered for tremors. Electromyography is used to subdivide tremors according to their rate and their relationship to posture of limbs and volitional movement. Tremor frequency usually is categorized as low frequency (less than 4  Hz), medium fre- quency (4 to 6 Hz), and high frequency (greater than 6 Hz).

The diagnosis of tremor is primarily clinical; however, laboratory testing may be necessary to exclude certain con- ditions that may be associated with tremor, such as meta- bolic disturbances, including hyperthyroidism (e.g., through thyroid function tests) and Wilson ’ s disease. Brain imaging may be indicated for select patients, particularly patients with tremor that is unilateral, of sudden onset, or associated with atypical clinical features. For diffi cult cases, single-pho- ton emission computed tomography (SPECT) to visualize the integrity of dopaminergic pathways may be useful in diag- nosing Parkinson ’ s disease.

Differential Diagnosis: The differential diagnosis, in general practice, is almost always between Parkinson ’ s disease and essential tremor.

Physiological Tremor: A normal phenomenon, physiological tremor occurs in all contracting muscle groups. Although seldom visible to the naked eye, physiological tremor often may be detected when the fi ngers are fi rmly outstretched with a piece of paper placed over the hands.

Enhanced Physiological Tremor (or an Intensifi cation of Physiologi- cal Tremor to Detectable Levels): Physiological tremor may be enhanced under conditions of stress, anxiety, fatigue, exer- cise, cold, hunger, stimulant use, alcohol withdrawal, or metabolic disturbances such as hypoglycemia or hyperthy- roidism. Although the tremor is typically low in amplitude and high in frequency (8 to 12 Hz), it may be clinically indis- tinguishable from essential tremor.

Essential Tremor (4 to 12 Hz): Essential tremor is a persistent postural and kinetic tremor that predominantly affects the hands and forearms. Classically, to show the tremor, the patient is asked to extend the arms in front of the body. The legs are affected less often. Although less frequently involved, the presence of tremor in the head and/or voice is a strong indication of essential tremor and is especially useful in

differentiating the syndrome from Parkinson ’ s disease. Head tremor, which is also postural, disappears when the head is supported. Listening to the patient speak or having the patient hold a musical note as long as possible may reveal a quivering intonation. A resting component is present only rarely and typically occurs in the most advanced cases.

Parkinsonian Tremor Syndromes (4 to 6  Hz): Parkinsonian tremor syndromes involve resting tremor that is often asym- metrical. Tremor may be observed when muscles are relaxed, such as when the hands are resting on the lap, and may affect hands, feet, mandible, and lips. Tremor disappears during sleep. Typical is an alternating tremor of the thumb against the index fi nger— pill-rolling tremor. Although rest tremor is a diagnostic criterion for Parkinson ’ s disease, other forms of tremor also may be present.

Treatment: Tremor should be treated if it causes disability. First-line treatment for tremor is oral medication. Beta block- ers, anticholinergic medication, and levodopa are useful modalities for resting tremor. Kinetic tremor may respond to beta blockers, primidone, anticholinergics, and alcohol. When there is a lack of response to medical treatment or when tremor results in severe disability, a patient may be considered for neurosurgery. Specifi c treatments for the most common causes are noted next.

Physiological Tremor: Usually no treatment is required for physiological tremor. When exaggerated, however, it may interfere with activities requiring extreme precision. Identify and remove precipitating causes and contributing causes. If the precipitating cause cannot be removed, propranolol may be effective.

Essential Tremor: Varying degrees of control in essential tremor have been obtained with the beta blocker propranolol and the anticonvulsant agent primidone. Either agent may be considered an appropriate fi rst-line therapy for the symp- tomatic management of essential tremor. When appropriate, these agents may be administered in combination with ben- zodiazepines, such as lorazepam or clonazepam. If the med- ication is of no benefi t at a dose that causes adverse effects, dose levels should be tapered down gradually and eventually discontinued. If a medication is documented to be benefi cial, it may be continued at the regulated doses, and the next med- ication may be added to the drug regimen. If the response to a drug is adequate and the dose is well tolerated, you may continue to monitor tolerance and possibly increase the dose.

Physical and psychological measures may be helpful in managing mild tremor. Physical measures may include the application of weights to affected limbs to decrease tremor amplitude. Some patients have experienced benefi ts with biofeedback, relaxation methods, and other behavioral techniques through alleviation of anxiety or stress that may exacerbate tremor. Alcohol consumption may lead to transient improvement for many with essential tremor. The potential risk of alcohol dependence and abuse among essen- tial tremor patients who drink alcohol to control symptoms is controversial. Alcohol has no impact on the tremor of Par- kinson ’ s disease.

Parkinsonian Tremor: The tremor of Parkinson ’ s disease re- sults from a loss of striatal dopamine, and this is the rationale for treatment with either the dopamine precursor levodopa

Chapter 5 ■ Symptoms and Syndromes 83

or dopamine receptor agonists. Dopaminergic and anticho- linergic agents are equally effective, but dopaminergic sub- stances additionally improve other parkinsonian signs, and the potential side effects of anticholinergic medications make these drugs undesirable in the older adult. The combination of levodopa and carbidopa reduces levodopa-induced nausea; a typical starting dose is one tablet of Sinemet 25/100 three times daily. Levodopa-carbidopa intestinal gel (brand name Duopa) is a combination of levodopa and carbidopa that is dosed for 16 hours during wakefulness. It is administered via PEG-J tube supplied by an external box. This route of dosing decreases tremor by reducing plasma fl uctuations that pa- tients on oral levodopa and carbidopa might experience.

Patients with severe tremors that are resistant to phar- macotherapy may benefi t from ablative surgery and/or deep brain stimulation. For those essential tremor patients who fail medication treatment, transcranial magnetic res- onance-guided focused ultrasound thalamotomy (product name ExAblate Neuro) has been shown to be successful in the treatment of essential tremor. This procedure is noninvasive.

Follow-Up: Patients should be evaluated for therapeutic effects and side effects within 1 week of starting treatment. Annual monitoring for weight loss, depression, and decline in functional status is necessary.

Sequelae: Functional disabilities may occur in ADLs, includ- ing compromised eating, drinking, and preparing food.

Decreased caloric intake and weight loss may be observed. Ambulation, especially on stairs, may be hazardous. With- drawal from social situations may occur, and depression is common.

Prevention/Prophylaxis: Reduce factors that can exacerbate the tremor. Continue medication regimen.

Referral: A neurologist should be consulted for cerebellar tremors, mixed tremors, or Parkinsonian tremor, or when a focal neurological defi cit is identifi ed. An ophthalmologist should be consulted when Wilson ’ s disease is suspected. A mental health provider or psychiatrist should be consulted when a hysterical tremor is suspected. Physical therapy or occupational therapy may be helpful in advanced or disabling cases.

Education: Some patients, particularly patients with severe, disabling tremor, may limit their contacts. Patients must be encouraged to learn as much as they can about their disease to help them cope better with the condition ’ s progression. When a diagnosis has been established, the natural history of the condition should be explained to patients. It also may be appropriate to recommend counseling. Use of appropriate coping strategies may reduce stress substantially, preventing possible augmentation of tremor owing to anxiety. Referral to appropriate patient support organizations is helpful for most patients.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The diagnosis of tremor is based on clinical information from the history and physical examination.

C Deuschl et al., 1998 Sharma & Pandey, 2016

Propranolol and primidone are fi rst-line treatments for essential tremor.

A Sharma & Pandey, 2016

Tremor amplitude worsens over time if not treated. C Sharma & Pandey, 2016

Levodopa-carbidopa intestinal gel improves resting tremors. B Fernandez et al., 2016

Transcranial magnetic resonance-guided focused ultrasound thalamotomy successfully treats essential tremor.

B U.S. FDA, 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

URINARY INCONTINENCE

Description: Urinary incontinence (UI) is an involuntary loss of urine ( Gibson & Wagg, 2014 ). It is common in the older individual but often underreported. It can be distressing and affect a person ’ s overall quality of life (Berardelli, 2013). Acute UI is generally a result of illness or the effects of medi- cations and is self-limiting when the cause is determined and addressed. Chronic UI has different forms, including stress incontinence, urge incontinence, overfl ow incontinence,

and functional incontinence. Many older women manifest a combination of urge and stress symptoms resulting in mixed incontinence. Tables 5-10 and 5-11 describe the various types of UI and management strategies.

Etiology: The causes and management of UI are multifac- torial, depending on the type of incontinence and also the severity and impact on quality of life for the individual.

84 Chapter 5 ■ Symptoms and Syndromes

Types of Urinary Incontinence

TYPE SYMPTOMS TREATMENT OPTIONS

Stress

incontinence

Urine leakage associated with

increased abdominal pressure

from laughing, sneezing,

coughing, climbing stairs,

or other physical stressors

increasing abdominal pressure

Lifestyle

interventions

Behavioral

therapies

Urge

incontinence

Urine leakage associated by

or immediately preceded by

the feeling of an urgent need

to void

Lifestyle

interventions

Behavioral

therapies

Consider trial of

antimuscarinic

medications

Mixed

incontinence

A combination of stress and

urge incontinence, marked by

involuntary leakage associated

with urgency and also with

exertion, effort, sneezing, or

coughing

See Management of

Stress Incontinence

and Urge

Incontinence

Overfl ow

incontinence

Urine leakage when the

bladder is over-distended

and may result in incomplete

bladder emptying

Symptoms can present as

constant dribbling, frequency,

hesitation when initiating

urination, and nocturia

Often associated with bladder

outlet obstruction, such as

benign prostatic hypertrophy

in men and pelvic organ

prolapse in women

Neurogenic bladder

can also present as

overfl ow UI

Assess for the

cause such as

medication usage

and fl uid intake

Double voiding

to empty residual

urine from bladder

Functional

incontinence

The inability to hold urine

due to reasons other than

neurological and lower urinary

tract dysfunction including

delirium, psychiatric disorders,

UTI, impaired mobility

Treat underlying

cause

Source: Vasavada ( 2016 ); Luckacz (2016); Wagg et al. ( 2015 ).

TABLE 5-10 Lifestyle Measures and Behavioral Therapies for UI Management

Lifestyle

measures

Weight loss

Fluid management-restricting fl uids

Avoiding alcohol, caffeine, and carbonated beverages

Avoiding constipation

Behavioral

therapies

Pelvic fl oor exercises including Kegel exercises:

• Identify the muscle that starts and stops urination

through attempts to start and stop urinating

• Contract the identifi ed muscle for approximately

8–10 seconds, and then relax the muscles

• Perform 8 to 12 contractions

• Repeat 3–4 sets of repetitions daily

Bladder training:

• Prompted toileting: Ask the individual to void more

often

• Habit training: Identifying the toileting pattern

including UI episodes, schedule toileting routine to

prevent UI episodes

• Timed toileting: Scheduled toileting at fi xed intervals

• Combined toileting and exercise therapy:

Incorporates pelvic fl oor strengthening exercises

and bladder training interventions

• Double voiding: Empty bladder, relax for 1–2

minutes, then lean forward and/or press on bladder

and attempt to void again, emptying the remaining

urine from the bladder

Source: Luckanz (2016); Wagg et al. ( 2015 ).

TABLE 5-11

Anatomical changes, factors related to the individual ’ s medical history, lifestyle, and acute and chronic illnesses, in addition to medications, can result in incontinence that can be either reversible or a permanent condition. Cognitive as well as chronic mental illness, depression, and functional barriers to continence can also affect an individual ’ s ability to maintain urinary continence.

Occurrence: Urinary incontinence is often underreported, with the prevalence of UI being more common in women and increasing with age. Greater than 60% of older individ- uals experience UI, with the highest occurrence in women ( Gibson et al., 2014 ; da Silva et al., 2012 ). In the long- term care setting, this rate increases to an average of 85% of the population and is the cause of approximately one in ten nursing home admissions ( Vasavada, 2016 ). UI is not a cause, but it is associated with frailty and functional decline

in the older individual ( Gibson et al., 2014 ; da Silva et al., 2012 ; Omli et al., 2013 ; Wagg et al., 2015 ).

Age: Urinary incontinence affects all age groups, with the highest prevalence in older adults who are institutionalized, have cognitive impairment, and are physically frail with functional limitations. Despite popular belief, lifestyle mea- sures and behavioral therapies can be effective interventions when used for individuals, even in individuals with cognitive impairment.

Gender: UI is twice as prevalent in women as in men, and the incidence increases with age, with institutionalized individu- als, and those who have at least one defi cit in ADLs ( Wagg et al., 2015 ; da Silva et al., 2012 ). Women are at higher risk for stress incontinence; however, overfl ow incontinence is more prevalent in men as a result of hyperplasia of the prostate gland.

Ethnicity: Ethnicity is not signifi cant with regard to incon- tinence in general; however, some data indicate a higher prevalence of stress incontinence among Caucasian women, whereas African American women were found to be at higher risk for urge incontinence.

Contributing Factors: The many contributing factors for UI include pelvic muscle weakness, multiparity, estrogen deple- tion, pelvic organ prolapse, diabetes, stroke, multiple sclero- sis, Parkinson ’ s disease, spinal cord injury, benign prostatic hyperplasia, UTI, fecal impaction, poor fl uid intake or exces- sive fl uid intake, smoking, cognitive impairment, depression, immobility or impaired mobility, environmental barriers,

Chapter 5 ■ Symptoms and Syndromes 85

impaired dexterity, visual impairment, obesity, and high-im- pact physical activities. Incontinence can be a side effect of many medications, including cholinergics, anticholiner- gics, diuretics, antispasmodics, opiates, hypnotics, calcium channel blockers, ACE inhibitors, alcohol, and caffeine.

Signs and Symptoms: In screening for UI it is important to evaluate whether symptoms are transient or persistent in nature. A thorough history should include:

■ The severity and quantity of urine lost, including use of pads or adult briefs

■ Onset and duration of the problem and whether the UI is worsening

■ Triggering factors or events, including sneezing, cough- ing, laughing, or during activity

■ Constant versus intermittent urine loss ■ Associated frequency, urgency, dysuria, pain with a full

bladder ■ History of UTIs ■ Association with fecal incontinence or pelvic organ

prolapse ■ Additional medical problems, including current or past

cancers of the pelvic organs, congestive heart failure, COPD, cognitive impairment, and connective tissue disorders

■ Obstetrical history, including diffi cult deliveries, multi- parity, and large babies

■ History of pelvic surgeries or other urological proce- dures, including use of indwelling urinary catheters

■ History of spinal or CNS problems and/or surgeries ■ Lifestyle issues, including use of tobacco, alcohol, or

caffeine; occupational or recreational factors causing severe or repetitive increases in intra-abdominal pressure

■ Medications, including use of the following medications that have been associated with UI: cholinergic or anti- cholinergic agents, alpha blockers, OTC allergy medica- tions, estrogen replacement, beta-mimetics, sedatives, muscle relaxants, diuretics, and ACE inhibitors

■ Effect of these symptoms on ADLs, socialization, and relationships, including sexual activity ( Vasavada, 2016 )

Considering that approximately 10% of nursing home admis- sions are a result of UI, discussion with patients and caregiv- ers before long-term care placement about symptoms has the potential to prolong the individual ’ s ability to be maintained at home for an extended period of time.

Physical examination should include functional assess- ment with special attention to mobility, including ability to ambulate to the toilet and dexterity, including the per- son ’ s ability to remove necessary clothing in time to use the toilet. Vital signs should be completed, looking for the pres- ence of an elevated temperature. Respiratory rate and the presence of dyspnea on exertion may affect continence due to limited stamina to complete necessary tasks for main- taining continence. Mental status, including cognition and evidence of depression, should be assessed. The abdomen should be examined for clues such as bladder distention, pelvic masses, inguinal lymphadenopathy, or tenderness in the suprapubic region. Bladder distention can be found in overfl ow incontinence secondary to obstruction. In women,

malignancy, uterine fi broids, or organ prolapse in the pelvic region creates pressure on the bladder seen in urge, stress, or mixed incontinence. A vaginal examination may also reveal poor perineal hygiene, skin breakdown from urine soaking, or redness and thinning of tissue typical of atrophic changes. Prolapse of genitourinary structures or the rectum may also be seen.

To assess for pelvic fl oor muscle strength and relaxation, instruct the patient to bear down as though having a bowel movement, then tighten or squeeze by pulling up with the pelvic fl oor muscles. In patients with pelvic fl oor relaxation, you can see the inability to contract or weak contractions, and feel a lack of muscle tone when testing during the vaginal examination. Have the patient cough and determine if leakage occurs. Urethral discharge in male patients should also be assessed. Positive neurological fi ndings in the perineal area include hypersensation, hyposensation, or absence of the bulbocavernosus (anal wink) refl ex. A rectal examination may reveal fecal impaction, rectal prolapse, hemorrhoids, masses, or, in men, prostatic enlargement. Whenever possi- ble, the examiner should observe the patient voiding, having the patient void into a measurable receptacle. This should be followed by evaluation of a post-void residual (PVR) urine by catheterization or ultrasound of the bladder. Studies are inconclusive with respect to the amount of PVR that is sig- nifi cant, with values ranging from greater than 50  mL to greater than 200 mL.

Diagnostic Tests: Initial evaluation for UI should include a uri- nalysis to rule out infection and renal abnormalities. This has great signifi cance when UI has an acute onset. The presence of nitrites and leukocyte esterase in the urinalysis is usually indicative of an infectious process. When a UTI is suspected, a culture and sensitivity should be ordered to ensure appropri- ate antimicrobial therapy. Hematuria may indicate a number of differential diagnoses, including infection, obstruction, kidney stones, or malignancy. Proteinuria is revealing for renal disease and is often associated with poorly controlled diabetes. When renal, metabolic, or obstructive causes of urinary tract dysfunction are suspected, a basic metabolic panel is recommended to evaluate elevated BUN and creati- nine levels, and calculate estimated glomerular fi ltration rate (eGFR) to evaluate for renal disease. Measurement of PVR may reveal incomplete bladder emptying.

When symptoms and basic noninvasive evaluation does not clearly indicate the type of urinary tract dysfunction, and the individual indicates that UI is problematic enough to warrant further treatment, urodynamic testing and referral to a urologist or urogynecologist is indicated. Urodynamic testing evaluates all stages of lower urinary tract func- tion, including fi lling and storage, as well as bladder outlet abnormalities. Subjective reporting by the patient of sensa- tion such as urgency can also be evaluated with respect to bladder wall compliance, detrusor overactivity, pressure, and fl ow measurements during testing. Cystoscopy is indicated for evaluation of hematuria to visualize the bladder wall when cancer is suspected, and also when stricture or pros- tate enlargement is suspected with symptoms of urinary retention.

Differential Diagnosis: UI is a symptom, not a diagnosis. The two mnemonics DRIP and DIAPERS often are used to differen- tiate transient (acute) from persistent urinary incontinence:

86 Chapter 5 ■ Symptoms and Syndromes

Mnemonic: DRIP ■ D elirium ■ R estricted mobility ■ I nfection ■ P harmaceuticals, polyuria

Mnemonic: DIAPERS ■ D elirium ■ I nfection, impaction, infl ammation ■ A trophic vaginitis ■ P sychological, pharmaceuticals, psychotropics ■ E ndocrine problem ■ R estricted mobility ■ S tool impaction

Treatment: Management of UI will depend on the type of incontinence; the patient ’ s preference with regard to his or her perception of how UI affects his or her lifestyle; and the patient ’ s physical condition to tolerate treatments, surgical procedures, and risk for adverse effects, as well as complica- tions due to medications or treatment regimens. For transient UI, treating, eliminating, or modifying the cause usually alle- viates the symptom. Delirium or a mild elevation in tempera- ture from the patient ’ s baseline, rather than a fever, may be the fi rst indication of a UTI in the older adult. Appropriate antimicrobial therapy will generally resolve the UI as a result of the infection.

Lifestyle management using behavioral therapies and pelvic muscle exercises or Kegel exercises can be an effective treatment for stress and urge incontinence, performed alone or in combination with biofeedback, to help strengthen peri- urethral muscles. Toileting programs (see Table 5-11 ) can be effective interventions for decreasing the impact of or con- trolling UI, even in patients with cognitive impairment. Noc- turia can be a very annoying problem and cause signifi cant issues where quality of life is concerned. Control of comor- bidities and symptoms such as edema, in addition to limiting fl uids before bedtime, can be helpful to improve sleep hygiene.

Pharmacological treatment for urge incontinence with anticholinergic drugs is effective for symptoms; however, they are not without side effects, especially constipation, blurred vision, and cognitive changes in older adults. These medica- tions, such as tolterodine (Detrol) and oxybutynin (Ditropan), seem to be better tolerated in long-acting and transdermal forms. Drugs that are more selective for muscarinic-3 recep- tors, such as darifenacin (Enablex), solifenacin (Vesicare), and trospium (Sanctura), which do not appear to cross the blood-brain barrier, appear to have a better side effect profi le, and are better tolerated in the older adult population. In the STAR trial, with 70% of subjects more than 65 years old, effi - cacy and tolerability of solifenacin was found to have better outcomes with regard to incontinence than long-acting tolterodine.

Comorbidities such as narrow-angle glaucoma and poten- tial interactions with other medications are always a concern in the geriatric population and should be considered before prescribing a drug regimen for UI. Topical estrogen therapy (one-quarter applicator nightly) for 2 weeks, then three times a week ongoing, can be an effective remedy for UI as a result of vaginal atrophy. Studies have also indicated that the anti- depressant duloxetine can be an effective treatment for stress UI, with approximately a 50% reduction in incontinence episodes and improved quality of life; however, nausea as a

signifi cant adverse effect may reduce compliance with this treatment regimen.

For patients with overfl ow incontinence secondary to pros- tatic hypertrophy, 5-alpha-reductase inhibitors, fi nasteride (Proscar), or dutasteride (Avodart) are effective to reduce prostate volume by preventing the conversion of testosterone to dihydrotestosterone. These drugs should not be handled by women of childbearing age, because they can be harmful to the development of a male fetus. Selective alpha-adrener- gic antagonists such as tamsulosin (Flomax) relax smooth muscle to reduce urethral resistance and improve urine fl ow. Nonselective alpha-1 blockers such as doxazosin (Cardura) and terazosin (Hytrin) are effective for UI and can also be used in patients who also require antihypertensive therapy. The provider should consider, however, the cardiovascular side effects due to their nonselectivity, because orthostatic hypotension is an adverse reaction that can have serious consequences, such as increased fall risk and injuries, in the older adult patient. Post-prostatectomy incontinence can be treated long after surgery with behavioral therapy such as pelvic fl oor muscle training. Studies have found an average of 55% reduction in incontinence using these strategies.

Other treatments for UI include bulking agents such as col- lagen for stress incontinence, botulinum toxin, sacral nerve stimulation for urge incontinence, and surgical interventions for stress incontinence in women and for prostatic hypertro- phy in men. Referral to urology or urogynecology for surgical intervention is appropriate if the patient is inclined to con- sider surgical intervention and is physically able to tolerate the procedure. Surgical management for pelvic organ pro- lapse to improve organ support, such as retropubic suspen- sion, sling procedures, and vaginal mesh, are viable options; however, patient education with regard to the high failure rate (5% to 12%) should be discussed when considering these options. In 2008, the FDA warned of potentially serious com- plications associated with the use of surgical mesh, and in 2016 they changed the classifi cation from moderate risk to high risk when used for pelvic organ prolapse, a frequent cause of stress incontinence. When surgical treatment for UI as a result of pelvic organ prolapse is contraindicated, a pessary is a viable option. In addition to incontinence pads and briefs, pessaries, when properly fi tted within the vaginal vault to correct organ prolapse and reduce stress UI, can often be managed by the patient or cared for by a qualifi ed nurse at regular intervals. Nonsurgical management of per- sistent urinary overfl ow incontinence includes clean inter- mittent catheterization. Although the Centers for Medicare and Medicaid Services now reimburses for a single-use sterile catheter, there is no evidence to support a reduction in UTIs with the use of sterile versus clean urinary catheter.

Follow-Up: Follow-up visits will depend on the acuity and severity of symptoms. Treatment of infection and symptoms related to urinary retention requires closer and more frequent follow-up until the problem is resolved due to renal compli- cations that can result. Initially, medication management should be attempted but monitored closely for adverse effects, especially with anticholinergic medications. Side effects of these medications can result in signifi cant complications for the geriatric patient, such as blurred vision, dizziness, and somnolence, as well as contribute to fall risk. Long-acting medications appear to have a lower risk profi le, but individual

Chapter 5 ■ Symptoms and Syndromes 87

DIAGNOSIS CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Urinary incontinence

Combination behavioral therapy and medication management

A da Silva et al., 2012 Omli et al., 2013 Gibson & Wagg, 2014 Vasavada, 2016 Wagg et al., 2015

Stress urinary incontinence

Alpha-adrenergic medications, serotonin- norepinephrine reuptake inhibitors

A Gibson & Wagg, 2014 Wagg et al., 2015

Stress urinary incontinence

Surgical procedures A Omli et al., 2013

Urge urinary incontinence

Anticholinergic medications (antimuscarinic agents)

A Gibson & Wagg, 2014 Wagg et al., 2015

Overfl ow urinary incontinence

Treatment of underlying cause of bladder outlet obstruction, urinary catheterization

C Lucacz, 2016

monitoring is necessary to ensure patient safety. Additionally, dementia exacerbation can occur with the use of anticho- linergic medications, resulting in hallucinations, psychosis, or changes in behavior that can lead to injury to the indi- vidual or others. Constipation, a common adverse effect of anticholinergics, can exacerbate UI by causing a fecal impac- tion. Polypharmacy issues also need to be monitored closely with any medication change, requiring close follow-up when starting a new drug regimen.

Sequelae: Possible complications include UTI, hydronephro- sis (with overfl ow or obstruction), renal failure, adverse drug events, or failure of behavioral therapy. Skin breakdown is a signifi cant complication with persistent UI. Urosepsis can occur with unrecognized UTIs. Falls due to UI result from environmental factors or as a side effect of medication man- agement. Social isolation may be a result of uncontrolled UI having a signifi cant impact on quality of life and may lead to depression.

Prevention/Prophylaxis: Ways to help prevent incontinence include:

■ Early identifi cation of acute or transient UI ■ Teaching patients and family members/caregivers that

UI is not a normal part of the aging process and that treatment options are available

■ Referral to appropriate specialists for treatment options ■ Regular rectal examination in men to detect and treat

early prostatic hypertrophy ■ Recognition of polypharmacy and adverse reactions

when initiating new medications in the geriatric population

Referral: Referral to urogynecology for the female patient to explore treatment options is appropriate if behavioral inter- ventions and medication management are unsuccessful. It is also appropriate to refer to a specialty practice if the diag- nosis is uncertain. Refer men with overfl ow incontinence

for urological evaluation urgently if PVR urine volume is signifi cant, to prevent renal complications, and for surgical intervention, if indicated. Certifi ed continence nurse special- ists may be an appropriate referral for behavioral therapies, such as biofeedback or for electrical stimulation treatments to improve continence. Further work-up and referral to urology would be indicated if abnormalities in the urinalysis do not resolve after treatment for infection, such as persistent hema- turia or proteinuria, and if the patient has a past medical history that includes surgeries for genitourinary diagnoses, or a history of pelvic cancer with or without radiation therapy. Patients with neurogenic bladder as a result of injury or a chronic neurological condition should be followed by a neu- rologist in collaboration with the primary care provider.

Education: Teach patients, family, caregivers, and health- care providers, as well as the community, that UI is not a normal part of aging and it is a treatable medical problem in many individuals. Behavioral therapy can be provided in the primary care setting, such as Kegel exercises, as well as self-catheterization techniques. Written instructions given to the patient with possible adverse drug effects when starting a new medication can prevent serious consequences of drug effects/complications. Teach patients, especially women and men with bladder outlet obstruction, the signs and symptoms of UTI, including delirium as an indication of acute illness, and that in an older adult a fever may not occur even when there is a UTI. Dietary issues such as adequate fl uid intake, limiting bladder irritants such as caffeine and alcohol, and prevention of constipation to avoid fecal impaction can help avoid bladder symptoms and infections. The importance of good perineal hygiene, especially for women and patients who do self-catheterization, should be emphasized. When incontinence cannot be completely avoided, attention to skin care and instruction in the use of skin barriers such as zinc oxide or dimethicone-based products should be taught to the patient or caregivers to prevent skin breakdown.

Continued

88 Chapter 5 ■ Symptoms and Syndromes

Description: Wandering in older individuals with disorien- tation or cognitive impairment is characterized as locomo- tion (either ambulation or propelling in a wheelchair) in a seemingly aimless pattern. The behavior is often described as having observable patterns such as lapping, pacing, or random movements (Cipriani, Lucetti, & Danti, 2014). The behavior may be frequent, repetitive, temporally disordered, and possibly spatially disordered in nature.

Etiology: Although poorly understood, there are many hypotheses to the causes of wandering behaviors. A medical hypothesis suggested right parietal dysfunction, which leads to spatial perception and memory lapses resulting in these types of behaviors. Another theory is the individual has unmet needs or environmental triggers leading to wandering behaviors ( Cipriani et al., 2014 ; Bright Foundation, 2016) (see Table 5-12 ).

Wandering behaviors occur in individuals who experience looseness of thoughts, most noticeably in individuals experi- encing confusion—either temporary in states of delirium or in individuals with a dementia, most commonly during the middle to later stages of the dementia process. Delirium is an extreme confusion, an acute episode of fl uctuating attention, worsening of cognition, and change in level of consciousness, which frequently results in agitated and wandering behaviors (Huang, 2016). Most delirium is reversible but occurs more often in individuals with dementia. Common causes of delir- ium include illness, medications, and environmental factors (Huang, 2016) (see Table 5-13 ).

The many causes of dementia include Alzheimer ’ s disease, vascular disease, Lewy Body dementia, Parkinson ’ s disease, alcoholic encephalopathy, normal pressure hydrocepha- lus, and frontotemporal dementia (also referred to as Pick ’ s disease) (Huang, 2016).

Occurrence: Dementia was estimated to affect 44 million older people worldwide in 2013, with the number expected to explode to 74 million by the year 2030 and 135 million by 2050 (Kales, Gitlin, & Lyketsos, 2015). Wandering behaviors occur in one out of every fi ve individuals with dementia at some point during their illness ( Cipriani et al., 2014 ).

DIAGNOSIS CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Functional urinary incontinence

Scheduled toileting A Gibson & Wagg, 2014 Wagg et al., 2015

Mixed urinary incontinence

Anticholinergic medications (antimuscarinic agents)

A Gibson & Wagg, 2014 Wagg et al., 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

WANDERING

Potential Causes of Wandering Behaviors

Unmet personal needs • Internal discomfort: need for toileting,

hunger, thirst

• Loneliness

• Perceived threat to the individual ’ s safety

• Past history of walking behaviors

Environmental triggers • Noisy environment

• Increased visual distractors

• Visualizing other individuals leaving

• Shadowing a caregiver

Source: Cipriani et al. ( 2014 ); Bright Foundation (2016).

TABLE 5-12

Common Causes of Delirium in the Older Individual

Illness • UTI

• Upper respiratory infections (URIs) including

pneumonia

• Sepsis

• Severe constipation as well as intestinal

obstruction

• Meningitis

• Dehydration

• Electrolytes imbalances, especially low sodium

and low calcium levels

• Severe malnutrition

• Hypoxia

• Terminal illness

Potential

medications

• Medications with anticholinergic properties

• Certain antipsychotics

• Pain medications, especially when the individual

is toxic

*See the Beer ’ s list of potentially inappropriate

medications frequently prescribed in the older

patient

Overstimulation • Loud noises or multiple conversations

• Bright or blinking lights

• Large number of people

• Change in routine of an individual with

cognitive impairment

• Overly tired individual with a diagnosis of

dementia

Source: AGS (2016); Bright Foundation (2016).

TABLE 5-13

Chapter 5 ■ Symptoms and Syndromes 89

Age: Wanderers do not differ in age (although some studies suggested it occurs more frequently in younger elders) or gender (although some reports suggested it occurs more fre- quently in males) ( Cipriani et al., 2014 ).

Gender: Women are diagnosed more often with Alzheimer ’ s disease. Women generally live longer than men and therefore are more likely to live to the age when Alzheimer ’ s disease is more common.

Ethnicity: Prevalence related to ethnicity showed frequency of occurrence to be 58% in Caucasians, 67% in African Ameri- cans, and 63% in Hispanics.

Contributing Factors: Wandering behaviors occur in over half of individuals with a diagnosis of dementia in the moderate to late stage of this cognitive impairment process. The great- est percentage of wandering occurrence has been reported in seniors residing in a nursing home setting ( Cipriani et al., 2014 ). The most frequent occurrence is between 5:00 pm and 7:00 pm, but it has been reported as early as 2:00 pm and late into the night, which is often referred to as “sun- downing” ( Cipriani et al., 2014 ; Bright Foundation, 2016).

Signs and Symptoms: Wandering may be accompanied with agitation and anxiety, causing the individual to be diffi cult to redirect. Individuals who are anxious and those who are delusional appear to exhibit wandering behaviors more fre- quently. The consequences of wandering may include falls, exhaustion, malnutrition, anxiety and aggression, elope- ment, and becoming lost from the individual ’ s home environ- ment ( Lin, Zhang, Chen, Ni, & Zhou, 2014 ; Cipriani et al., 2014 ; Tilly, 2015 ; Nagamatsu, Kam, Liu-Ambrose, Chan, & Handy, 2013 ).

Diagnostic Tests: In an older person who seems to wander aimlessly or become confused or lost, a full medical eval- uation should be conducted, including an evaluation for dementia, particularly Alzheimer ’ s disease. A work-up includes a review of the individual ’ s medications; diet, nutri- tion, and use of alcohol; as well as medications (prescription and nonprescription/street drugs); vital signs and pain level; laboratory tests (blood and urine); and a thorough physi- cal examination including an in-depth geriatric neurolog- ical examination. Although no singular test is available for dementia, multiple cognitive assessments are recommended, including the MMSE, the Montreal Cognitive Assessment, the St. Louis University Mental Status Exam, Mini-Cog test, Clock Drawing test, and Memory Impairment Screening. The Mini-Cog test is a short screening test that incorporates a three-item recall within 5 minutes and a clock drawing test. The MMSE, a 30-item test, had been the most widely used test to assess an individual ’ s level of cognitive functioning. Wandering behaviors have been shown to be common in individuals who score a 13 or less on the MMSE ( Cipriani et al., 2014 ).

Treatment: A person-centered approach to assessment, plan- ning, and delivery of care is the key to managing wandering behaviors ( Tilly, 2015 ). When possible, attempt to identify why the person is wandering, and when developing a plan of care, involve the person with dementia in decision making. Identify triggers to the behavior and modify the individual ’ s routine to minimize the triggers; decrease distractions, espe- cially in the afternoon and evening hours or when the person

is tired; and do not vary the day-to-day routine. Attempt to engage the individual in nondemanding activities during the time of day the wandering behaviors most frequently occur. Nonpharmacological interventions should be attempted, but when the individual is severely agitated, aggressive, exhausted, or otherwise at risk for harm to self or others, and distraction and redirection are unsuccessful, pharmacologi- cal intervention may become necessary.

Sequelae: Consequences of wandering behaviors include accidents, getting lost, fatigue, sleep disturbances, social iso- lation, injury, and death ( Cipriani et al., 2014 ). Falling with hip fractures and head injuries are common consequences in these individuals. Malnutrition can also occur as a result of an inability to sit for a meal or excessively wandering, which increases caloric requirements and leads to weight loss. Wandering behaviors often lead to early institutionalization in a nursing home when families are unable to manage the individual in the community setting. Disruptive activities are associated with wandering such as agitation, screaming, physical aggression, and disturbed nighttime sleep.

Prevention/Prophylaxis: Care is aimed at balancing a person ’ s need for autonomy with the need to minimize risks. The goal is to provide a pleasant and safe environment where an individual will not wander away, fall, or become exhausted. Wandering is not always problematic if the person is able to ambulate without falling, the behavior does not lead to aggression, or the person does not wander away and become lost. To maximize safety, the living environment needs to be surveyed and modifi cations made, when necessary, and the area is familiar (minimize changes) and uncluttered. Assure ample lighting, maintain clutter-free walkways, and keep harmful objects out of reach from the confused individual. Other considerations may include putting locks on cabinets and ovens, unplugging dangerous appliances when neces- sary, removing wall hanging mirrors (the confused may mis- interpret the refl ection as another person in the room), and providing exits with safety mechanisms. Wandering behavior can be diminished with the installation of simple childproof door knob covers, possibly more complex door locks, or even in-house alarms or bells.

If an individual wanders, identify where the person usually wanders to, what activity the person is usually engaged in when wandering occurs, and what time of day the behavior usually occurs. Identifi cation bracelets or necklaces may help minimize the hazardous consequences if wandering off does occur and the individual becomes lost. Also include identifi - cation in clothing and keep a recent photograph of the indi- vidual when assistance is needed to locate the person. When wandering occurs, caregivers should approach the individual slowly, speaking softly and in a nonthreatening manner. Act in a nonjudgmental, matter-of-fact manner. Validate the per- son ’ s feeling with positive, open statements such as “You look concerned” or “What can I do to help?” Distract the individ- ual by refocusing the person ’ s attention on something differ- ent, such as looking at old pictures or discussing the weather. Redirect the person in a reassuring manner by saying, “I know you are concerned; let ’ s sit and talk and have a cup of coffee.” Possibly suggest going for a walk in the direction you wish the person to go instead of the individual leaving that environment. Avoid asking the person to explain the behav- ior. In summary, validate, redirect, distract, and redirect the

90 Chapter 5 ■ Symptoms and Syndromes

wandering or confused person to abort the behavior (Jong, 2016).

Referral: Caregivers need to determine the abilities of the wandering individual and create an environment that pro- vides for autonomy as much as possible and ensures safety. Referrals may be made to geriatric care specialists for evalu- ation and management, home health agencies for assistance in the home setting, and community resources for support groups and available educational resources. When necessary, consideration for a more structured living arrangement may be advised when safety becomes a major concern. Options

include sitters in the home setting, adult day cares, assisted living facilities, and nursing homes. In extreme situations, when the elder is at risk for harming self or others, referral to a psychiatrist may be indicated for evaluation.

Education: Educating caregivers, both family and friends, of the wanderer, as well as paid caregivers (nurses, aides, staff), is essential to provide optimal care. The essential information includes the causes of dementia and wandering behaviors and how to identify triggers of this behavior, create a safe environment, and manage wandering individuals while pro- moting quality of life and patient autonomy.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Falls are associated with an increased tendency to engage in tasks unrelated thoughts that commonly occur in individuals with dementia.

A Nagamatsu, Kam, Liu- Ambrose, Chan, & Handy : Psychology and Aging, 2013

Elders with dementia frequently engage in wandering behaviors and attempt to exhibit exit-leaving behaviors leading to elopement or becoming lost as a consequence of wandering behaviors.

B Tilly : Administration on Aging, 2015

The occurrence of wandering in older individuals with dementia, comparison of characteristics, and researchers’ theories on causes of wandering behaviors.

A Cipriani, Lucetti, Nuti, & Danti : Psychogeriatrics, 2014

Defi nitions of delirium and dementia, discussion of causes and manifestations of these conditions that often lead to wandering behaviors in individuals with cognitive impairment.

C Huang, 2016

Discussion of consequences of wandering behaviors and strategies to manage.

B Lin, Zhang, Chen, Ni, & Zhou : International Journal of Gerontology, 2014

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

C A S E S T U DY

J. B. is a 77-year-old man who is known to your practice. He is brought in today by his daughter, who reports a new onset of confusion accompanied by UI (fi rst noticed bed was wet a few nights ago). When you see the patient today, he is oriented to place and person (knows you and your offi ce), but not to time, and does not recall much about events of the past few days. He says that he is eating and drinking as usual (but daughter is shaking her head to the contrary). He denies any change in bowel function, but is fearful of sleeping because he might “wet the bed.” Daughter states that he has been drinking a lot more water than usual and urinating more frequently. He denies any pain, other than arthritis. He was a regular attendee at the local senior center but has not been there for a week and seems to have forgotten about it.

Past medical history: Known CAD, hypertension, hyperlipidemia, impaired fasting glucose, osteoarthritis of knees.

Medications: Lisinopril 20 mg orally PO once daily in evening; hydrochlorothiazide 12.5 mg PO once daily in morning; metoprolol 50 mg PO once daily in morning; simvastatin 20 mg PO once daily. OTC medications include Aleve, 2 tablets every 12 hours when needed for severe knee pain (infrequent use); topical Icy Hot for knee pain daily; glucosamine-chondroitin preparation daily for joint health; multivitamin for male more than 50 years daily.

Vital signs: Blood pressure (BP) 130/84 mm Hg; heart rate (HR) 60 beats per min, regular; respiratory rate 16 breaths/min; temperature 99.2°F orally; BMI 38.

Chapter 5 ■ Symptoms and Syndromes 91

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Physical fi ndings are unremarkable. Using the guide to characterizing a symptom located in

this chapter, focus on the following questions:

1. What additional subjective data are you seeking?

2. What additional objective data will you be assessing for?

3. What national guidelines are appropriate to consider?

4. What tests will you order? How will you decide on prioritizing in this patient with multiple symptoms?

5. What are the differential diagnoses that you are considering? For each one, map out your clinical reasoning for and against it and make a tentative plan to confi rm it or rule it out.

6. Will you be looking for a consultation?

C A S E S T U DY — c o n t ’d

92 Chapter 5 ■ Symptoms and Syndromes

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Ittrich , H. , Bockhorn , M. , Klose , H. , & Simon , M. ( 2017 ) The diagnosis and treatment of hemoptysis . Deutsches Arzteblatt International , 114 , 371 – 381 . doi:10.3238/arztebl.2017.0371 .

Lee , M. K. , Kim , S. H. , Yong , S. J. , Shin , K. C. , Kim , H. S. , Yu , T. S. , . . . Lee , W. Y. ( 2014 ). Moderate hemoptysis: Recurrent hemoptysis and mor- tality according to bronchial artery embolization . Clinical Respiratory Journal , 9 ( 1 ), 53 – 64 . doi:10.1111/crj.12104 .

Salamone , I. , Cavallaro , M. , Visalli , C. , Velo , M. , Barbaro , U. , Galletta , K. , Andò , F. ( 2017 ). Embolization of a bronchial artery aneurysm in a chronic obstructive pulmonary disease patient with non-massive hemoptysis . Polish Journal of Radiology , 82 , 174 – 178 .

Involuntary Weight Loss Fabbri , E. , Tanaka , T. , An , Y. , Zoli , M. , Bandinelli , S. , Guralnik , J. M. ,

. . . Ferruci , L. ( 2015 ). Loss of weight in obese older adults: A bio- marker of impending expansion of multimorbidity? Journal of the American Geriatrics Society , 63 ( 9 ), 1791 – 1797 . doi:10.1111/jgs. 13608 .

Gaddey , H. I. , & Holder , K. ( 2014 ). Unintentional weight loss in older adults . American Family Physician , 89 ( 9 ), 718 – 722 .

Kim , J. , Noh , J.-H. , Park , J. , & Kwon , Y. D. ( 2014 ). Body mass index and depressive symptoms in older adults: A cross-lagged panel analysis . PLOS ONE , 9 ( 12 ), e114891 . doi:10.1371/journal.pone.0114891 .

Morley , J. E. ( 2012 ). Undernutrition in older adults . Family Practice , 29 suppl 1 , i89 – i93 . doi:10.1093/fampra/cmr054 .

Marton , K. I. , Sox , H. C. , & Krupp , J. R. ( 1981 ). Involuntary weight loss; Diagnostic and prognostic signifi cance . Annals of Internal Medicine , 95 ( 5 ), 568 – 574 .

Wong , C. J. ( 2014 ). Involuntary weight loss . Medical Clinics of North America , 98 ( 3 ), 625 – 643 . doi:10.1016/j.mcna.2014.01.012 .

Joint Pain Edwards , R. R. , Dolman , A. J. , Martel , M. O. , Finan , P. H. , Lazaridou ,

A. , Corneius , M. , & Wasan , A. D. ( 2016 ). Variability in conditioned pain modulation predicts response to NSAID treatment in patients with knee osteoarthritis . BMC Musculoskeletal Disorders , 17 , 284 . doi:10.1186/s12891-016-1124-6 .

Hermsen , L. A. , Van der Wouden , J. C. , Leone , S. S. , Smallbrugge , M. , Van der Horst , H. E. , & Dekker , J. ( 2016 ). The longitudinal association of cognitive appraises and coping strategies with physical functioning in older adults with joint pain and comorbidity: A cohort study . Geriat- rics , 16 ( 29 ). doi:10.1186/s12877-016-0204-7 .

Kong , L. J. , Lauche , R. , & Chang , Y. W. ( 2016 ). Tai chi for chronic pain conditions: A systematic review and meta-analysis of randomized con- trolled trials . Scientifi c Reports , 6 ( 25 ), 325 . doi:10.1038/srep25325 .

Chapter 5 ■ Symptoms and Syndromes 93

Lee , J. E. , Kahana , B. , & Kahana , E. ( 2016 ). Social support and cogni- tive functioning as resources for elderly persons with chronic arthritis pain . Aging and Mental Health , 20 ( 4 ), 370 – 379 . doi: http://dx.doi.org/ 10.1080/13607863.2015.1013920 .

Zdziarski , L. A. , Wasser , J. G. , & Vincent , H. K. ( 2015 ). Chronic pain management in the obese patient: A focused review of key challenges and potential exercise solutions . Journal of Pain Research , 8 , 63 – 77 . doi: https://doi.org/10.2147/JPR.S55360 .

Peripheral Edema O’Brien , J. G. , & Miles , T. P. ( 2013 ). Edema . Essential Evidence Plus .

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Trayes , K. P. , Studdiford , J. S. , Pickle , S. , & Tully , A. S. ( 2013 ). Edema: Diagnosis and management . American Family Physician , 88 ( 2 ), 102 – 110 .

Pruritus Arkwright , P. D. , Motala , C. , Subramanian , H. , Spergel , J. , Schneider ,

L. C. , & Wollenberg , A. ( 2013 ). Management of diffi cult-to-treat atopic dermatitis . Journal of Allergy and Clinical Immunology: In Practice , 1 , 142 – 151 . http://dx.doi.org/10.1016/j.jaip.2012.09.002 .

Berger , T. G. , Shive , M. , & Harper , M. ( 2013 ). Pruritus in the older patient: A clinical review . Journal of the American Medical Association , 310 ( 22 ), 2443 – 2450 .

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Urinary Incontinence da Silva , V. , & D’Elboux , M. ( 2012 ). Factors associated with urinary

incontinence in elderly individuals who meet frailty criteria . Texto & Contexto-Enfermagem , 21 ( 2 ). Retrieved from http://dx.doi. org/10.1590/S0104-07072012000200011 .

Gibson , W. , & Wagg , A. ( 2014 ). New horizons: Urinary incontinence in older people . Age and Aging , 43 ( 2 ), 157 – 163 . doi:10/1093/ageing/ aft214 .

Lucacz , E. ( 2016 ). Patient education: Urinary incontinence treatments for women (beyond the basics) .

Omli , R. , Hunskar , S. , Myleturn , A. , Romild , U. , & Kuhry , E. ( 2013 ). Urinary incontinence and risk of functional decline in older women: Data from the Norwegian HUNT study . BMC Geriatrics , 13 ( 47 ), 1 – 6 . doi:10.1186/1471-2318-13-47 .

Vasavada , S. ( 2016 ). Urinary incontinence . Medscape . Retrieved from http://emedicine.medscape.com/article/452289-overview .

Wagg , A. , Gibdson , W. , Ostaszkiewicz , J. , Johnson , T. , Markland , A. , Palmer , M. , . . . Kirschner , R. ( 2015 ). Urinary incontinence in frail elderly persons: Report from the 5th international consultation on incontinence . Neurology and Urodynamics , 34 , 398 – 406 .

Wandering Cipriani , G. , Lucetti , C. , Nuti , A. , & Danti , S. ( 2014 ). Wandering and

dementia . Psychogeriatrics , 2 , 135 – 142 . Haung , J. ( 2016 ). Online Merck Manual for Professionals: Delir-

ium . Retrieved at http://www.merckmanuals.com/professional/ neurologic-disorders/delirium-and-dementia/delirium .

Lin , Q. , Zhang , D. , Chen , L. , Ni , H. , & Zhou , X. ( 2014 ) Managing elders’ wandering behavior using sensors-based solutions: A survey . Interna- tional Journal of Gerontology , 8 , 40 – 55 .

Nagamatsu , L. , Kam , J. , Liu-Ambrose , T. , Chan , A. , & Handy , T. ( 2013 ). Mind-wandering and falls risk in older adults . Psychology and Aging , 28 ( 3 ): 685 – 691 .

Tilly , J. ( 2015 ). Responding to the wandering and exit-seeking behaviors of people with dementia . Administration on Aging , Retrieved from http://www.aoa.acl.gov/AoA_Programs/HPW/Alz_Grants/docs/ BH-Brief-WanderingExit-Seeking.pdf .

unit III Treating Disorders

96

CHAPTER 6 Skin and Lymphatic Disorders

Laurie Kennedy-Malone

ASSESSMENT

Proper assessment of an older adult ’ s skin, hair, and nails reveals the patient ’ s history of sun exposure, nutrition, socio- economic status, and education, as well as his or her surgical and medical history. The largest organ of the body, the skin, undergoes certain normal changes with age. The number of cells in the epidermis, such as Langerhans’ cells, which are responsible for immune surveillance, begin to decline. Mela- nocytes also decrease, thereby reducing the skin ’ s natural protection from the sun (Resnick, 2016; Williams, 2009).

Changes With Aging As people age, the skin tends to be very thin, fragile, and often transparent (Gray-Vickrey, 2010). Skin renewal turn- over time increases to approximately 87 days in older adults, compared with 20 days during youth. This fact becomes an important consideration in surgical and dermatological healing. The subcutaneous tissue that houses the eccrine, sebaceous, and apocrine glands thins, thereby providing less protection from heat exposure and less insulation, energy storage, and shock absorption. Secretions aiding tempera- ture control, moisturization, and odor production are also reduced. The skin of older adults therefore tends to be very dry (xerosis). Fat is generally redistributed to the abdomen and thighs, leaving bony surfaces, such as the face, hands, and sacrum, exposed to potential injury, especially skin tears from shearing and friction forces and pressure ulcer develop- ment (Doughty & McNichol, 2015). The skin ’ s repair system becomes impaired, with delayed cell regeneration and poor circulation (Resnick, 2016).

Common benign skins lesions in older adults include seborrheic keratoses, cherry angiomas, acrochorda (skin tags), and senile lentigo (Gray-Vickrey, 2010; Williams, 2008). Although the capillaries in older adults tend to be fragile, making the skin of older adults more susceptible to bruising, it is important to discern the cause of the ecchy- mosis, whether it is trauma-, pressure-, or medication-in- duced, as in patients taking anticoagulants or corticosteroids (Gray-Vickrey, 2010). It is important to note, however, that “sudden appearance of seborrheic keratoses, telangiectasia

or pigmented warty lesions (known as Leser-Trelat sign) may suggest internal malignancy” (Williams, 2008, p. 305).

All of these tissue changes represent a near-catastrophic scenario of aged skin poorly protected from the environment (especially the sun, heat, and cold) and slow to respond to immunological challenges, producing minimal or delayed urticaria and swelling.

Evaluation of Skin and Lymphatics Assessment of the skin begins with the chief complaint and history, including the dermatological problem ’ s onset, dura- tion, location, size of lesion, color, associated pain or itching, and lost or heightened sensation to touch.

■ Investigate associated symptoms such as wheezing, loss of appetite, fever, malaise, headaches, and change in temperature perception.

■ Question current and chronic medication history, com- plete a focused nutritional assessment, and ask about relevant childhood diseases (especially asthma, atopic dermatitis, and chickenpox).

■ Ask about contact with chemicals, lifetime occupa- tions, level of lifetime sun exposure, family history of skin cancer, contact with animals, change in environ- mental habits (e.g., plants, insects, water) or internal habits (e.g., change in soap or laundry detergents, use of any lotions or creams, recent travel, change in diet to include cooking products, exposure to new clothing items or metals such as nickel).

■ Ask whether the person has been treated for a similar condition in the past and, if so, ask about the results.

■ Note whether the patient appears uncomfortable or pruritic.

■ Observe overall hygiene and grooming (Williams, 2008).

■ Is the patient incontinent? (Doughty & McNichol, 2015) ■ Has the patient had the Zostavax vaccine? ■ Is the patient taking any anticoagulation medications?

(Elsawy & Higgins, 2011)

Proper equipment for inspection includes good overhead and tangential lighting, a magnifying glass, blades, and collec- tion devices for biopsies and microscopic study. Gloves should

Chapter 6 ■ Skin and Lymphatic Disorders 97

be readily available. Inspect the skin for possible signs of neglect, abuse, or decreased function. Poorly healing wounds or chronic pressure ulcers may signal a problem not only with the patient but with the caregiver ’ s ability to provide adequate care. Welts, lacerations, burns, and distinctive markings may indicate a need for intervention (Gray-Vickrey, 2010; Williams, 2008).

Inspect the hair and nails. The hair may be graying and thinner than in youth. Normally, nails start to form ridges after age 80. A recent (in the past year) change in quality of hair and nails is a signifi cant fi nding. For example, the hair may have become dryer, duller, and thinner or the nails pitted or brittle, which may be indicative of a systemic condition or nutritional defi ciency (Gray-Vickrey, 2010).

Inspection of the skin for even color and overall quality and care is important. Lesions require close scrutiny, descrip- tion, and classifi cation. Description by type, shape, arrange- ment, and distribution is a widely accepted and usable format.

■ Type: Is the lesion a macule or papule? Is it eroded, excoriated, or hyperpigmented or hypopigmented?

■ Shape: Is the periphery of the lesion round, ulcerated, or linear?

■ Arrangement: Are multiple lesions grouped (serpigi- nous, zosteriform, arciform, iris, or bull ’ s-eye pattern) with or without defi nable borders? (LeBlond, Brown, Suneja, & Szot, 2015).

■ Distribution: Is the extent of the lesions isolated, regional, or generalized? Is the pattern symmetrical or over pressure sites, hairline, or sun-exposed areas? Is the distribution characteristic of scabies, seborrheic dermatitis, contact dermatitis, herpes zoster, or lupus?

■ Is there any unexplained bruising that could be indica- tive of elder abuse or neglect? (Elsawy & Higgins, 2011).

The lesion may be classifi ed as primary or secondary. Primary lesions (vesicles, tumors, burrows) arise from normal tissue. Secondary lesions (infections, crusts, and lichenifi - cation) arise from changes to the primary lesion (LeBlond et al., 2015). Palpate for moisture, temperature, mobility, and turgor. Testing skin turgor in older patients can be done by pinching the skin on the sternum or forehead. The skin should move easily and return back to place after release; a

slower return of the skin may be indicative of dehydration. Lax skin may indicate weight loss, whereas fi xed skin may be associated with sclerotic or scarred tissue. Lesions should also be palpated to check whether they are fl uctuant, hard, or fi xed. At the end of the examination, consider associated pathology, especially thyroid disorders, diabetes, autoimmune conditions, and anemia. Provide wellness instructions, including those concerning proper nutrition, moisturizing, and sun protection. Awareness of the high susceptibility of the elderly to hyperthermia and hypothermia secondary to reduced thermoregulation in the skin should be emphasized (Williams, 2008).

Guidelines for Prescribing Topical Medications Lesions that concern you or the patient should be exam- ined through biopsy. Lesions that warrant biopsy are those that have changed, bleed, or are painful. Treatment for skin lesions must take impaired absorption, duration, dosage, and delivery method (e.g., cream, powder, ointment, lotion) into consideration. Patients for whom treatment plans fail initially should be referred to a dermatologist.

When prescribing topical treatments it can be a challenge to determine the quantity necessary to dispense. A guideline for determining the quantity was fi rst described by Long and Finlay in 1991 with the introduction of the “fi ngertip unit.” One fi ngertip unit (FTU) is the amount of ointment or cream dispensed from a tube with a 5-mm opening from the tip of the fi nger to the fi rst crease. One FTU is equal to approxi- mately 0.5 g. Along with the concept of FTUs, the “Rule of Hand” was developed. This rule says that the body surface of the front and back of an adult hand requires 1 FTU for cov- erage. Each body part is described by its equivalent surface area in hands. Each arm is equal to three hands, the front torso is seven hands, and so are the back and buttocks. Each leg is equal to six hands, and each foot is two hands. So, if you are treating lesions on one foot, a total of 2 FTUs will be required, or 1 g per treatment. For treatments that are pre- scribed as twice a day (bid) for 2 weeks, a total of 28 g will be necessary. This guideline results in a more quantitative prescription than writing “dispense 1 week ’ s supply” (Long & Finlay, 1991).

BURNS

Signal Symptoms: Erythema, blistering, serous exudates, eschar, pain, carbonaceous sputum, hypertrophic, pruritus.

Description: Burn injury can be caused by multiple mech- anisms. Flame and hot liquids are obvious sources of burn injury. Other causes of burn damage can occur from electric- ity from high power lines, household current, or lightning strike; radiation or sun exposure; and chemical corrosion. Patients may present varying degrees and depth of tissue damage along with underlying trauma, thus requiring a very thorough physical examination. In addition to what is con- sidered a true burn injury, many exfoliative and necrotizing skin disorders can present in a similar fashion and must be

ruled out. Although these skin disorders are not true burns, they are increasingly treated in burn care facilities.

Etiology: Skin forms the largest organ in the body and is constantly in contact with a changing environment. It is composed of three layers: the epidermis, the dermis, and the subcutaneous tissue or hypodermis. The epidermis is the thin outermost layer of the skin. It contains keratinizing cells that migrate from the basal cell membrane and even- tually shed over a 2- to 4-week period (Lewis, Heimbach, & Gibran, 2012). At this level of the skin, melanocytes produce melanin, which affects skin color and provides protection from ultraviolet (UV) radiation. The dermis consists of a

98 Chapter 6 ■ Skin and Lymphatic Disorders

dense connective tissue that forms the bulk of the skin. This layer is vascular, with its deeper layer containing hair folli- cles, associated muscle fi bers, cutaneous glands, and nerve fi bers. The subcutaneous layer or hypodermis is largely com- posed of adipose tissue, which provides padding and thermal regulation. Burn injury can affect all of these skin levels in addition to deeper structures, including muscle and bone.

As one ages, there are signifi cant changes in the skin, which becomes thinner, providing a less effective barrier to external stimuli. The dermis atrophies with aging. There are fewer appendages and decreased vascularity. Thus, older adults are at particular risk for burns. Thinner skin combined with decreased vascularity and diminished nerve function often result in a higher incidence of deeper burns. Advanced age results in a weakened immune system. All of these factors, along with the burden of various comorbidities, lead to delayed wound healing and reepithelialization after burn injury in the elderly population (Porro, Deming, Pereira, & Herndon, 2012).

Occurrence: An estimated 2.5 million injuries, 60,000 requiring hospitalization, and 6,000 deaths occur annually in the United States from burns.

Age: Between 2007 and 2011, those aged 65 years and older made up 13% of the U.S. population, but accounted for 30% of fatal home fi re victims. This represents an increase from 1980 by 31%. Between ages 65 and 75 years, the mortal- ity rate from burns is twice that of the national average (M. Ahrens, 2014). The Centers for Disease Control and Preven- tion (CDC, 2016) data indicates that from 2001 to 2014, fi re-related burn injury was the twelfth leading cause of non- fatal injury for individuals 65 years and older.

Gender: The American Burn Association ’ s (ABA ’ s) National Burn Registry reported that between 2009 and 2015, across all age categories, males sustained a higher rate of burn injury than women, except for those individuals 80 years and older.

Ethnicity: The ABA ’ s National Burn Registry outlines the following breakdown of reported ethnicity in burn injuries: 58.4% Caucasian, 20.7% African American, 13.0% His- panic, 4.5% other, 2.5% Asian, and 0.9% Native American. When analyzed by age group, it was found that minorities were overrepresented among those with burn injuries 4 years and younger. As the population ages into adulthood, this characteristic shifts and minorities were no longer found to predominate.

Contributing Factors: Nearly 84% of all burn-related deaths occur in the home (Haynes, 2015). Smoke- and toxic-fume– induced inhalation injury associated with house fi res is a larger contributor to death than the burn itself. Inhalation injury is particularly lethal when victims are more than 65 years of age (Peck, 2011). Among the major causes of house fi res are cooking equipment, home heating systems, and electrical wiring. Smoking is the leading cause of home fi re deaths and has been found to increase the risk of burn injury six-fold (M. Ahrens, 2015; Low, Meyer, Willebrand, & Thomas, 2012 ). In home fi res related to smoking, the risk of death is further compounded by the use of home oxygen.

Human judgment plays a large role in activities that are related to burn injury. Older adults have slow response times and may show impaired judgment due to illness or

medications. The ability to sense fi re decreases and dis- abilities can impede escape. Comorbidities such as cardiac disease, renal disease, diabetes mellitus, dementia, or psy- chological impairment may complicate outpatient care and these individuals may require initial hospital admission for burn assessment and stabilization ( Low et al., 2012 ; Warner, Coffee, & Yowler, 2014 ). Many older adult individuals live alone or are dependent on an aging spouse for support. This isolation further increases the risk of burn injury.

Signs and Symptoms: A thorough history and physical exam- ination should be undertaken and will provide a majority of the information needed to assess a burn injury and its appro- priate management. Ascertain the time and mechanism of the burn injury, as well as duration of contact with the offending agent, and any steps taken to manage the injury. This will assist in determination of wound depth and suit- ability for outpatient management. Burn injury constitutes trauma, and as such, the initial evaluation should always consist of a primary survey, including the ABCs: airway, breathing, and circulation, followed by a secondary survey including a head-to-toe assessment. After these assessments are completed, it is time to focus on burn depth. Burn inju- ries involve a graduating zone of damage that occurs along a time continuum, making it diffi cult to estimate the depth of a burn when fi rst evaluated.

■ First-degree burns involving the epidermis are erythe- matous and painful, but do not blister. Most sunburns fall into this category and are not considered when esti- mating total burn size.

■ Second-degree (partial thickness) burns ■ Superfi cial dermal burns involve the dermis and are

characterised by blisters. The underlying tissue is pink, moist, and hypersensitive to touch. The tissue will blanch with pressure and is associated with dilatation. Superfi cial dermal burns will often heal within 2 to 3 weeks.

■ Deep dermal burns extend further into the dermis, present with blistering, but the tissue surface appears mottled, pink and white immediately after injury. Capillary refi ll is slow and usually by the second day from injury the wound bed appears white and dry. Pain is often described more as pressure. Partial thickness burns that are not healed by 3 weeks should be excised and grafted.

■ Third-degree (full thickness) burns involve the full dermis extending into the subcutaneous tissue. The burn appears dry, white, charred, and leathery. There is no sensation to pinprick in the wound bed. There may be mottling that does not blanch with pressure. There may be visible coagulated vessels on the surface. Full thickness burns require early excision and autograft.

■ Indeterminate burn wounds may hold components of both partial thickness and full thickness, and should be evaluated daily over a period of days to determine the need for excision and autograft (Lewis et al., 2012).

After determining the extent of the burn injury, it is neces- sary to estimate the total body surface area (TBSA) involved. Small area burns in healthy individuals can be easily managed in the outpatient setting. However, it must be kept in mind that the larger the TBSA involved, the higher the likelihood

Chapter 6 ■ Skin and Lymphatic Disorders 99

of a poor prognosis. This is particularly salient in the older adult population due to comorbidities and the psychosocial components of managing a burn injury at home. There are several methods for determining burn size, which can be as complex as laser-assisted mapping to simple visual estimates. The Lund and Browder technique was fi rst published in 1944 and takes into account body surface area in light of age. This is particularly important with infants and small children, as the head occupies a larger surface area. The estimated surface area stabilizes by 15 years of age through adulthood ( Table 6-1 ). A more simple method for estimating the burn size utilizes the patient ’ s palm as representative of 1% of their TBSA. This involves the patient ’ s palm, digits, and thumb in adduction.

After your patient assessment is completed, a decision must be made to transfer to a higher level of care or to con- tinue management in the outpatient setting. The ABA has established criteria for burn center referral to improve patient outcomes ( Table 6-2 ). An important caveat is that any case of suspected elder abuse should be transferred via the emer- gency medical system to the appropriate emergency depart- ment to ensure proper follow-up and reporting. Suspicion of abuse should be triggered by any of the following:

■ Burn patterns that do not match the reported event ■ Straight or smooth transitions between the area burned

and healthy skin, resulting in a stocking- or glove-like appearance

■ A long delay between burn injury and request for treatment

Diagnostic Tests/Tools: Laboratory and diagnostic testing should be guided by patient presentation and, if warranted, may be an indication for hospital based evaluation. Of note, smoke inhalation injury may be masked by standard pulse oximetry monitoring. Most systems are designed to detect full saturation of a hemoglobin molecule and cannot differenti- ate between oxygen and carbon monoxide, resulting in mis- leading saturation levels (Nitzan, Romem, & Koppel, 2014). A carboxyhemoglobin (COHb) blood level should be obtained whenever an inhalation injury is suspected.

Differential Diagnosis: ■ Toxic epidermal necrolysis ■ Scalded skin syndrome

Treatment: Initial Care: First, stop the burn. This should include

removing and isolating the causative agent responsible for the injury while protecting the patient and your staff. If a scald has occurred, be certain that soaked clothing has been removed. If chemicals are suspected, irrigate the wounds with copious amounts of water (Lloyd, Rodgers, Michener, & Williams, 2012). Isolate clothing to be sure that others are not contaminated. In evaluating older adult burn patients, it is imperative to consider their physiological differences from younger adults, along with any associated comorbidities. If it is determined that transfer to a higher level of care is appropriate, activate the emergency medical system; do not delay for wound debridement. Cover wounds with dry, clean sheets or towels. Maintain a warm environment to minimize the risk of hypothermia. IV access should be obtained with lactated Ringer ’ s solution as the preferred replacement agent.

Adult Burn Size Estimation

AREA ADULT (>15 YRS.)

SECOND- DEGREE INJURY

THIRD- DEGREE INJURY TOTAL

Head 7

Neck 2

Anterior trunk 13

Posterior trunk 13

Right buttock 2.5

Left buttock 2.5

Genitalia 1

Right upper arm 4

Right lower arm 3

Right hand 2.5

Left upper arm 4

Left lower arm 3

Left hand 2.5

Right thigh 9.5

Right lower leg 7

Right foot 3.5

Left thigh 9.5

Left lower leg 7

Left foot 3.5

TOTAL

Note: Lund and Browder technique for those greater than 15 years of age. Adapted from Care of the outpatient burn by C. E. Hartford ( 2012 ), in D. N. Herndon (Ed.), Total burn care (4th ed., pp. 81–92). Edinburgh; New York: Saunders Elsevier.

TABLE 6-1 American Burn Association Transfer Criteria

1. Partial-thickness burns greater than 10% of TBSA

2. Burns that involve the face, hands, feet, genitalia, perineum, or

major joints

3. Third-degree burns in any age group

4. Electrical burns, including lightning injury

5. Chemical burns

6. Inhalation injury

7. Burn injury in patients with pre-existing medical disorders

that could complicate management, prolong recovery, or affect

mortality

8. Any patient with burns and concomitant trauma in which the

burn injury poses the greatest risk of mortality or morbidity;

if trauma poses the greater immediate risk, the patient may be

stabilized in a trauma center before transfer to a burn unit

9. Burned children in hospitals without qualifi ed personnel or

equipment for the care of children

10. Burn injury in patients who will require special social, emotional,

and/or long-term rehabilitative intervention

From Guidelines for the operation of burn centers. (2007). Journal of Burn Care and Research, 28 (1), 134.

TABLE 6-2

100 Chapter 6 ■ Skin and Lymphatic Disorders

Oxygen by nasal cannula would be appropriate for moder- ate-to-major burns and in any case where pulmonary dis- tress is evident. In cases of suspected inhalation injury, 100% via a nonrebreather mask is indicated.

Wound Care: Burn wounds are frequently colonized with bacteria from the local environment. These wounds are rou- tinely managed with topical antibiotics; systemic antibiotic therapy is not generally indicated ( Table 6-3 ). After admin- istration of appropriate pain medication, wounds should be initially doused with cool tap water to disperse any remaining heat in the tissue. The use of cold fl uids is not advised, because this may cause further tissue damage as well as hypother- mia. For routine wound care, tepid water is advised. Wounds should be cleaned with a mild soap and rinsed. Antibacterial soaps are not indicated. There are varying approaches to the management of blisters. One theory is that if left in place, the blister provides a protective covering and will allow the wound to heal more quickly. Alternatively, plasmin inhibitors in the fl uid of the blister may delay healing while the fl uid itself can provide a medium for infection ( Hartford, 2012 ). For small surface area burns, a good guide is to remove what tissue is loose during cleansing and allow intact blisters to remain ( Warner et al., 2014 ). Gently wipe the wound in a circular manner, debriding any loose devitalized tissue and debris during this process. Wounds should be washed in this manner on a daily basis.

The goal of wound dressings is threefold: absorb drain- age, provide protection, and decrease pain. Keeping this in mind, the dressings used for small burn wounds should be simple, affordable, and manageable by patients and caregiv- ers. There are virtually no objective comparisons of dressings

for small burn wounds, and anecdotal evidence leans heavily toward coverage with simple petroleum-infused mesh with or without antibiotic ointment. When wrapping a burn wound, it is important to consider function. Digits should be wrapped individually to allow for gentle range of motion exercises. Elevate extremities at rest and utilize an ace wrap or com- pression garments to prevent edema.

Burn wound care utilizes clean rather than sterile tech- nique. Patients and families should be taught proper cleaning techniques, including frequent hand washing and manage- ment of supplies within their environment. Wounds should be examined daily during care for redness, swelling, purulent drainage, or odor. This should be reported promptly to the health-care provider, and the addition of systemic antibiotics should be considered.

Patients should be instructed to minimize exposure to UV light. This should include the use of protective clothing and sunscreen over healed burn wounds. They should continue to utilize compression garments in the rehabilitative phase to minimize swelling and scar formation.

Follow-Up: Outpatients should be reevaluated 24 hours after the burn injury. Examine the condition of the wound and surrounding tissues for signs of healing or impending infection. Reexamine respiratory status of patients with an inhalation injury to detect diffuse wheezing and rhonchi. Determine the adequacy of the current pain management regimen. Have the patient or signifi cant other demonstrate proper dressing techniques. Depending on the severity of the burn, the patient may be asked to return once a week until progressive healing is noted; daily visits may be nec- essary. Have patients return periodically about every 4 to

Topical Agents and Dressings for Burn Wounds

NAME USAGE APPLICATION

Topical antibiotic

ointment (bacitracin,

mupirocin)

Small area burns: prevention and treatment of infection with

gram-positive and some gram-negative bacteria. Mupirocin is

active against most strains of MRSA.

Ophthalmic preparations without a dressing

are preferred for facial wounds. Apply a thin

layer daily to wound, cover with a petroleum

impregnated mesh and suffi cient gauze as needed

to absorb exudate.

Hydrocolloid dressings Provide a moist protective covering and barrier against

exogenous bacteria. Effective for small-area, partial-thickness

burns. Not indicated for wounds with large amounts of exudate.

Occlusive dressings may be left in place for 5–7

days for patients with low risk for complication.

Silver sulfadiazine 1% Prevention and treatment of infection in second- and third-

degree burns with eschar burden. Can delay wound healing by

impeding epithelialization. Discontinue use once necrotic tissue

has sloughed from wound. Contraindicated in those with sulfa

allergies or pregnant women.

Do not apply to face, cover burn area with a layer

approximately 1/16-inch thick, wrap with suffi cient

gauze to absorb exudates, change daily.

Petroleum gauze/mesh

(Adaptic ® , Xeroform ® ) Protective covering, 3% bismuth tribro-mophenate in a

petrolatum blend (Xeroform ® ) has bacteriostatic action, can be used with topical antibiotic ointments.

May be used in cases of sulfa allergy.

Apply daily, cover with gauze wrapping suffi cient to

manage exudate.

Aquacel Ag Hydrofi ber silver impregnated antimicrobial dressing. Conforms

to wound surface and can absorb high amounts of exudate with

autolytic properties.

May be left in place for up to 14 days. Cover with

secondary dressing such as hydrogel, foam dressing,

or gauze. Not compatible with oil-based products.

Care should be taken to monitor function if placed

over joints.

Adapted from Warner, P. M., Coffee, T. L., & Yowler, C. J. (2014). Outpatient burn management. Surgical Clinics of North America, 94 (4), 884–885 and Hartford, C. E. (2012). Care of outpatient burns. In D. N. Herndon (Ed.), Total burn care (4th ed., pp. 81–92). Edinburgh; New York: Saunders Elsevier.

TABLE 6-3

Chapter 6 ■ Skin and Lymphatic Disorders 101

6 weeks to determine healing, assess progress/compliance with any physical therapy if required, and assess coping mechanisms.

Sequelae: Pain: There is benefi t in utilizing medications with different

mechanisms of action to address pain in burn patients. This is especially true for burn patients undergoing any type of procedure that can include wound care or physical therapy ( Edkins et al., 2015 ; Meyer, Wiechman, Woodson, Jaco, & Thomas, 2012 ). It should be anticipated that for small burns the need for narcotics will be short lived as the wound heals. With deeper or larger burns, there may be a benefi t to adding pharmacological agents that act on neuropathic pain, such as gabapentin and pregabalin, while acetaminophen and NSAIDs are benefi cial to manage pain and infl ammation ( McIntyre, Clifford, Maani, & Burmeister, 2016 ; Retrou- vey & Shahrokhi, 2015 ; Warner et al., 2014 ). Evaluation of renal function should be assessed with dosages adjusted accordingly.

Pruritis: The process of healing triggers the mobilization of multiple agents, including cytokines and histamine, into the wound bed. These agents, among others, can result in intense pruritus. While multiple additional causes for pru- ritus have been suggested, the exact causation remains unknown ( Hartford, 2012 ). Signifi cant disruption to wound healing can result through the process of scratching. This can be particularly challenging in the older adult popula- tion, because antipruritic agents, such as diphenhydramine or hydroxyzine, can be sedating. Adequate analgesia in con- junction with these agents can be effective, but care must be taken to avoid oversedation. Agents that selectively block H 1 receptors, such as cetirizine or loratadine, can be more effec- tive with less sedating effects and are best administered on a scheduled basis ( Warner et al., 2014 ). The use of mois- turizers can aid in management of pruritus in healed burn scars and are essential to prevent drying and cracked skin. As the burn scar begins to mature, it is anticipated that pru- ritus will begin to diminish over a period of approximately 6 months.

Hypertrophy and Contracture: In healing wounds, the produc- tion of collagen is increased. This can be even more exag- gerated in infected wounds or in individuals prone to keloid formation. Wounds that remain open for 2 weeks or longer tend to be particularly prone to the development of hypertro- phic scarring ( Hartford, 2012 ). Hypertrophy can lead to pain and loss of function through distortion of normal anatomy. The utilization of appropriate topical agents and dressings that act to facilitate a wound ’ s timely closure will help prevent hypertrophy. In addition, the use of pressure garments over nearly closed or healed wounds will aid normal scar progres- sion. Although the action is not completely understood, the use of silicone sheeting over areas of hypertrophy has been a successful adjunct to normal scar progression in some individuals.

Management of scar bands that compromise function should include an evaluation for surgical release. The phe- nomenon of web creep occurs when hypertrophic scars begin to compromise the web spaces of the fi ngers and toes. Con- tractures and underlying tendon damage in the hands may result in impairments, such as Boutonniere deformities. The

resulting loss of function can often be restored through sur- gical intervention. Healed scars at least 6 months out from injury that remain hyperemic and hypertrophic may benefi t from resurfacing with a pulsed dye laser, alternated with a fractional carbon dioxide laser, to diminish infl ammation and soften scars (Hultman, Edkins, Wu, Calvert, & Cairns, 2013; Hultman, Friedstat, Edkins, Cairns, & Meyer, 2014). Additionally, fat grafting to burn scars that remain chron- ically painful have shown some benefi t (Fredman, Edkins, & Hultman, 2015). Bands and contractures can develop many years after injury, and scars should be monitored for progression.

Prevention/Prophylaxis: In order for a burn injury to occur, multiple factors must come together at one time. These factors include the host, the environment, and the vector. For example, an elderly patient falls asleep while smoking, his sheets ignite, and he is burned in a resulting house fi re. It is the relationship between man, his environment, and a potentially hazardous agent that can result in injury. The nurse practitioner can affect each of these components and possibly prevent the initial burn injury from occurring. By using three dimensions of prevention, primary, secondary, and tertiary, the nurse practitioner, by virtue of education, clinical expertise, and anticipatory guidance, plays a vital role in burn prevention ( Grant, 2004 ).

Primary prevention constitutes product design, regula- tion, and legislation. This also includes educational programs designed to educate the public on safety. In the previous example, the individual smoking in bed would hopefully benefi t from smoking cessation programs in his commu- nity. Regulation and product design in this scenario would affect the combustibility of clothing, linen, and housing materials exposed to the smoldering cigarette. During an annual physical examination, the nurse practitioner should include education on sound living habits and home safety. Included in this discussion should be a review of home fi re safety protocols, including the proper use of smoke alarms, removal of hazards such as frayed electrical cords, visual aids for those with impaired sight, and the appropriate tem- perature setting for home hot water heaters. This is also an excellent opportunity to discuss the advantages of smoking cessation.

Secondary prevention includes actions that would serve to limit the extent of damage done by a burn, such as cooling wounds initially to mitigate deeper tissue damage. Occupa- tional therapists provide compression garments and ensure proper splitting technique to maintain function. Physical therapists assist with mobilization though stretching and exercise programs. The injury has occurred, but these actions work to limit the scope of damage.

Lastly, tertiary prevention addresses recovery and reha- bilitation. Individuals continue to work with therapists to maximize function. Management of healed burn scars with moisturizers and sunscreen can prevent further skin damage. Through tertiary prevention, the individual optimizes his or her level of functioning and minimizes disability resultant from the burn injury.

The nurse practitioners are instrumental in developing and/or referring clients to community-based programs that promote home safety for the elderly ( Grant, 2004 ). Excellent educational programs are available through agencies such as

102 Chapter 6 ■ Skin and Lymphatic Disorders

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Education regarding fi re safety and prevention is the most effective intervention to prevent loss of life and injury due to home fi res and should be promoted at every visit.

A American Burn Association Prevention Campaign, 2014 Grant, 2004

Initial pain management for burn injuries with low- dose narcotics suffi cient to allow for wound care and therapy. Adjunct therapy with NSAIDs and neuropathic pain modulators as indicated.

A Edkins et al., 2015 Meyer, Wiechman, Woodson, Jaco, & Thomas, 2012 McIntyre, Clifford, Maani, & Burmeister, 2016 Retrouvey & Shahrokhi, 2015 Warner et al., 2014

Topical antibiotic use for burn wounds with avoidance of prophylactic systemic antibiotics.

C Warner, Coffee, & Yowler, 2014 Hartford, 2012

Systematic daily care of burn wounds using clean technique, with goal of 1 month for wound closure.

C Warner, Coffee, & Yowler, 2014 Hartford, 2012

Pressure garments and silicone sheeting to prevent swelling, decrease pruritus, and minimize hypertrophic scar formation.

C Warner, Coffee, & Yowler, 2014 Hartford, 2012

Evaluation for comorbidities including dementia and other psychiatric disorders associated with burn injury.

C Low et al., 2012 Warner, Coffee, & Yowler, 2014

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

the National Fire Protection Association, the CDC, the ABA Prevention Campaign, and verifi ed burn centers.

Referral: Burns often require complex care and the involve- ment of multiple disciplines. In the older adult population, even a small burn may require fl uid resuscitation that could complicate care due to pre-existing comorbidities and con- comitant medications. The absence of support systems or the suspicion of elder abuse should prompt considerations for hospitalization and possible referral to a specialized burn care facility. The ABA has developed a list of criteria that should signal the need for referral to a burn center (see Table 6-2 ). A burn center verifi ed by the ABA can provide ser- vices to a burn patient through all phases of the patient ’ s care.

For rehabilitation concerns related to nerve compres- sion, development of scar bands, or contractures, it would be advantageous to make a referral to a plastic and recon- structive surgeon. Reconstruction after burn injury should also include evaluation of mature scars that have remained hyperemic and hypertrophic for possible photoablation with laser therapy. Occupational therapy and physical therapy are

crucial in preserving and maintaining form and function for burn victims (Lloyd et al., 2012). Referral for these ser- vices should be made early in the care of the burn patient. A referral for social services or in-home assistance may be indicated to promote safe return to a living environment. Contact your nearest burn center for referral information. An excellent resource for patient and family support is the Phoenix Society, a national nonprofi t organization dedicated to empowering those affected by a burn injury ( https://www. phoenix-society.org/ ).

Education: Education is an ongoing component of patient care. The nurse practitioner should identify early on who will be providing wound care. This individual, or the patient if able, should demonstrate the ability to perform wound care before leaving the clinic or hospital setting. Patients should be provided with appropriate written instructions in clear language for wound care, indicators for infection or tissue compromise, and contact information should questions arise. In addition to wound care, there should be written instructions on medications, including dosing and possible side effects.

Chapter 6 ■ Skin and Lymphatic Disorders 103

Signal Symptoms: Erythema, warmth, blisters, local tender- ness, erysipelas.

Description: Cellulitis is an infection of the deep dermis and subcutaneous tissues of the skin; it is most commonly caused by groups A, B, C, and G beta-hemolytic streptococci, Staph- ylococcus aureus (both methicillin-susceptible [MSSA] and methicillin-resistant [MRSA]), and occasionally a gram-neg- ative organism ( IDSA, 2014 ). Cellulitis can also be caused by human or animal bite pathogens.

Etiology: Cellulitis usually occurs when an organism enters the skin through an open area. However, a clear site of entry may not be evident in patients with obesity, edema, or lymph- edema ( Salmon, 2015 ).

Occurrence: In the United States, 14.5 million cases of cel- lulitis are diagnosed annually, with over 650,000 hospital admissions per year attributed to the diagnosis ( Raff & Kro- shinsky, 2016 ).

Age: Cellulitis can occur at any age. Facial cellulitis is most common in people 50 years and younger and lower extrem- ity cellulitis is more common in older individuals with lymph- edema and venous stasis ulcers ( Compton, 2013 ).

Gender: Cellulitis occurs equally among men and women.

Ethnicity: Cellulitis occurs in all ethnic groups.

Contributing Factors: Predisposing factors include arterial or venous insuffi ciency, diabetes mellitus, lacerations, obesity, lower extremity edema, lymphedema, human or animal bites (cat bites), tinea infections, recurring cellulitis, burns, trauma, stasis ulceration, ischemia, toe web maceration, IV drug use, and puncture wounds ( Compton, 2013 ; Salmon, 2015 ). Any break in the skin or mucous membranes is a potential bacterial pathogen port of entry (Dunphy et al., 2015). Acute and chronic sinusitis can lead to periorbital or orbital cellulitis. Consider cellulitis in patients who are on immunosuppressive medications, immunocompetent (HIV infection and AIDS), have drug or alcohol abuse issues, or are prescribed long-term use of corticosteroids or cancer chemo- therapy (Dunphy et al., 2015). The fragile skin of the elderly is predisposed to skin tears and edema which increases risk of cellulitis ( Compton, 2013 ).

Signs and Symptoms: Cellulitis in the elderly often presents with atypical symptoms ( Compton, 2013 ). Signs include complaints of trauma or injury to the skin, pre-existing skin conditions, recurrent cellulitis, and worsening of ery- thema, edema, tenderness, and pain over the past few days. Symptoms are usually sudden and include rapidly spreading warmth, localized tenderness, erythema, edema, and pain ( Raff & Kroshinsky, 2016 ). Systemic symptoms that indicate serious toxicity include fever, hypotension, tachycardia, leuko- cytosis, lymphadenopathy, and lymphangitis (Dunphy et al., 2015). Cellulitis may be purulent or nonpurulent.

Diagnostic Tests: Unless pus has formed in the wound, a tissue culture is usually not necessary ( IDSA, 2014 ). In cases of extensive infection or suspected systemic toxicity, blood cultures and a complete blood count (CBC) with differential

should be obtained to determine the severity of illness and to identify the organism, including methicillin-resistant Staph- ylococcus aureus (MRSA) ( IDSA, 2014 ). C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) may be ele- vated in patients with severe cellulitis. Patients with diabetes mellitus should have a radiograph of the area and an ESR to rule out the presence of osteomyelitis. Skin biopsies may be necessary to rule out the presence of fungal, viral, parasitic, or mycobacterial etiologies (ISDA, 2014).

Differential Diagnosis: ■ Lipodermatosclerosis (tender red plaque on the medial

lower legs with venous stasis or varicosities) ■ Acute severe contact dermatitis (superfi cial edema,

itching) ■ Acute gout (synovial fl uid aspiration contains monoso-

dium urate crystals) ■ Necrotizing fasciitis (determined by magnetic resonance

imaging [MRI] or computed tomography [CT]; diffuse swelling of an arm or leg with bullae (clear or serosan- guineous fl uid, crepitus, and intense pain)

■ Deep vein thromboses (DVTs) (lower extremity Doppler ultrasound)

■ Pseudogout (synovial fl uid aspiration contains calcium pyrophosphate crystal deposition)

■ Osteomyelitis (diagnosed by radiographs, MRI, CT) ■ Pyomyositis (diagnosed by radiographs, MRI, CT) ■ Early herpes zoster ■ Atypical drug eruptions ■ Erysipelas (superfi cial cellulitis represented by red area) ■ Venous or varicose eczema (limited or localized ery-

thema, absence of systemic symptoms) (Dunphy et al., 2015)

Treatment: Ask when the patient ’ s last tetanus toxoid booster was given if an open wound is present. If the most recent booster was 10 years ago, 0.5 mL of tetanus toxoid should be administered immediately (CDC, 2016). If the wound is grossly contaminated and the patient ’ s last tetanus booster was 5 to 10 years ago, the practitioner should con- sider giving another booster at this time (CDC, 2016). An older adult who has not had primary immunization requires tetanus toxoid and tetanus immune globulin (CDC, 2016).

Patients with mild cellulitis may be given oral antibiot- ics ( IDSA, 2014 ). The drugs of choice (typically for 7 days) include one of the following: dicloxacillin 500 mg four times daily; clindamycin 300 mg four times daily; amoxicillin/ clavulanate 875 mg/125 mg twice daily; and a fi rst-gener- ation cephalosporin such as Cephalexin 250 to 500 mg four times daily (ISDA, 2014). For streptococcal cellulitis, penicil- lin is the drug of choice ( IDSA, 2014 ). Treatment of MRSA (total duration of therapy is 7 to 14 days) should be guided by wound culture results and/or considered when the patient has higher risk factors for MRSA or cellulitis is nonrespon- sive to primary choice of treatment ( IDSA, 2014 ). Antibiotic choices include one of the following: clindamycin 300 to 600 mg four times daily; doxycycline 200 mg once followed by 100 mg every 12 hours; trimethoprim-sulfamethoxaz- ole 160 mg/800 mg 1 to 2 tablets twice daily; or linezolid

CELLULITIS

104 Chapter 6 ■ Skin and Lymphatic Disorders

600 mg every 12 hours ( IDSA, 2014 ). Consider the patient ’ s renal function before prescribing any medication. Patients with complications or severe symptoms (especially systemic) should be hospitalized for monitoring and to receive IV anti- biotics ( IDSA, 2014 ).

Follow-Up: Outpatients should be requested to contact their health-care providers within 1 week if no improvement with antibiotic use or within 48 hours if fever or infl ammation continues.

Sequelae: In patients with cellulitis of the lower extremi- ties there is an increased risk of DVT. Further issues caused by cellulitis include bacteremia, bullae, lymphangitis, and necrosis of the affected area (Herchline, 2015).

Prevention/Prophylaxis: Prevention of cellulitis includes good hand washing, avoidance of injury/trauma, minimizing edema, prevention of peripheral vascular disease, and con- trolling diabetes.

Referral: The following patients should be hospitalized: those with high fever, diabetes, alcoholism, HIV, anaerobic cellulitis,

necrotizing fasciitis, or cellulitis of the orbit or face, or those experiencing extreme pain ( IDSA, 2014 ). Consultation with an infectious disease specialist may be necessary. A surgical consultation may be required for incision and drainage of abscesses and débridement of necrotic tissue.

Education: Patients with cellulitis must adhere to antibiotic dose, frequency, and duration of antibiotic treatment for optimal results. Avoid trauma to the area, keep the area clean, and elevate the affected area if able (especially if edema is present). If there are no contraindications, patients may use NSAIDs and Tylenol for pain relief. If there is no DVT, patient may use compression bandages to decrease edema (especially if edema causes recurrent cellulitis). As with any infection, blood glucose levels may need to be monitored in those with diabetes. There is an increased risk of DVT associated with cellulitis, and education should include signs and symptoms of DVT (report immediately if they occur).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Guidelines were updated to improve diagnosis and treatment of soft tissue and skin infections (cellulitis).

C IDSA, 2014

Increasing awareness of differential diagnoses associated with red legs improves accuracy of cellulitis diagnosis.

C Salmon, 2015

Cellulitis is a common skin infection in the elderly. Choosing the right empiric therapy is important.

C Compton, 2013

Treatment of cellulitis should cover Streptococcus and MRSA. Expand coverage for MRSA if risk factors are present. Five days of treatment is recommended with extension if no improvement.

A Raff & Kroshinsky, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

CORNS AND CALLUSES

Signal Symptoms: Thickened skin or hyperkeratotic area on the foot or hand that is often painful. This section will focus on those occurring on the foot.

Description: Corns and calluses are benign skin lesions on the foot. Corns (helomas) can be soft (heloma molle) or hard (heloma duram). They have distinct borders as compared to callosities. Soft corns are spongy and most often found between the fourth and fi fth toes. Hard corns form from calluses over time. They have a central core that is painful with weight bearing. They occur on the plantar surface of the foot at the metatarsal heads and on the interphalangeal joints. A callus (tyloma) is a hardened area on the foot ’ s plantar surface. These usually are seen at the metatarsal

heads, medially to the fi rst metatarsal head and laterally to the fi fth metatarsal head. Melo and colleagues (2015) report lesser-toe deformities including hammer toes, claw toes, and mallet toes, predispose individuals to callus formation on the second through fi fth distal surface of the toes.

Etiology: Mechanical forces of compression, shear, and torsion (Hashmi, 2013) put stress on the stratum corneum of the epidermis. This triggers a protective and infl ammatory response. The stratum corneum cells form either a plaque (callus) that is superfi cial or cone shape (corn), which is pointed and deep (Hashmi, 2013).

Occurrence: Corns and calluses are the most common foot ailment seen by podiatrists (26%) in the United Kingdom

Chapter 6 ■ Skin and Lymphatic Disorders 105

(Farndon, 2015). Concannon and Stephens (2015) reported that corns can be found in 14% to 48% of the population.

Age: Corns and calluses are common with increasing age (Feldman, 2017). Older adults have a higher incidence, as the aging process reduces fatty tissue and bones become more prominent (Nordqvist, 2014).

Gender: Females are affected more often than men. This is predominately related to women wearing high heels. Farndon (2015) found that the ratio of females to males seeing a podi- atrist for any foot problem was 74% versus 25% in a given day.

Ethnicity: African Americans report 30% greater occurrence than Caucasians (Feldman, 2017).

Contributing Factors: Intrinsic: Bony prominences, foot deformity, mobility alter-

ations, obesity, diabetes, peripheral neuropathy, peripheral arterial disease, anhidrosis, and hyperhidrosis.

Extrinsic: Poor fi tting shoes, not wearing socks or wearing socks that fi t poorly, high heels, thin-soled shoes, walking barefoot and standing, walking or running for prolonged periods of time.

Signs and Symptoms: Pain can be the cardinal symptom of both lesions, however, calluses are usually asymptomatic, although they may be of cosmetic concern. Corns are often painful and interfere with daily activities, which is frequently the chief complaint in podiatry practices (Frandon et al., 2015).

Diagnostic Tests: Clinical examination and history taking is usually the method of discovery, however, radiographs may be ordered to assess bone anatomy and foot deformity. Hashmi (2013; Hashmi et al., 2006) reports ultrasound has been used but resolution is poor. Dermatology practices are using optical coherence tomography (OTC) to assess before and after treatment (Hashmi, 2013; Baillie et al., 2011).

Differential Diagnosis: ■ Plantar wart (Feldman, 2017) ■ Foreign body granuloma (Ramano, 2016) ■ Porokeratosis (Mitnick, 2006-2016) ■ Underlying ulcer (Feldman, 2017) ■ Fungal infection (Feldman, 2017; Mitnick, 2016;

Ramano, 2016)

Treatment: Self-maintenance of minor calluses can be done by soaking the feet in warm water and sanding the affected area with a pumice stone. Calluses may be softened with emollients (with and without urea). Barrier creams and occlusive materials, such as silicone sleeves may reduce

friction (Hashimi, 2013) and prevent callus and corn for- mation. Crest pads, off-loading pressure with padding will reduce pressures (Curran, 2015). Salicylic acid plasters and mechanical debridement or paring with a 15-blade scalpel are two successful treatments for removing corns (Fardon, 2013). High-risk patients with some toe deformities may require surgery. Percutaneous digital fl exor tendon tenot- omy used to straighten a toe when conservative treatment has been unsuccessful (Bus et al., 2016) and electrosurgery are two other methods recognized by Hashmi (2013). Dia- betic patients and those with neuropathy should be advised to never use a chemical treatment on their feet. This could damage normal skin without them knowing it (Ramano, 2016).

Follow-Up: Follow-up is determined by the intervention type. Use of salicylic acid plasters usually demand a follow-up appointment within 1 week to assess the progress of the chemical debridement, the need for mechanical debridement of affected skin, and to assess for any complication (Fardon et al., 2013).

Sequelae: Untreated corns and calluses usually result in extended periods of pain, possible alteration in mobility that could result in falls, and a general decline in quality of life. According to the CDC (2015), diabetic patients are especially at risk as these lesions may ulcerate, become infected, and worst-case scenario, require amputation.

Prevention/Prophylaxis: Encourage self-awareness and inspec- tion of the feet as a basic self-care measure. Providers should inspect diabetic feet at every visit. Proper footwear is essen- tial. The shoe must be the proper size and not cause any fric- tion. If a problem area is identifi ed, inspect the inside of the shoe for problems. Lamb ’ s wool and toe pads of felt or silicone may be used to protect the affected area. Prescribed orthotic inserts or therapeutic shoes may be necessary.

Referral: Primary care providers can address the problems associated with corns and calluses; however, podiatric or orthopedic referral for patients with complicated corns and calluses should be made when treatment prescribed has not alleviated or improved the problem. It is recommended that diabetic patients see a podiatrist annually (CDC, 2015) and with more frequency if high risk factors or problems exist.

Education: Advise patients to maintain good foot hygiene: washing feet regularly, keeping toenails clipped, and wearing clean socks and shoes that fi t properly. Diabetic patients should be instructed to wash and inspect their feet daily, looking for problematic areas, and to seek medical assistance when lesions are apparent. Counsel patients on the preven- tion measures mentioned previously.

106 Chapter 6 ■ Skin and Lymphatic Disorders

Signal Symptoms: Cutaneous eruption of a dermatome distri- bution; burning, itching, or tingling skin sensation.

Description: Herpes zoster is an acute vesicular eruption caused by a virus histologically identical to the varicella (chickenpox) virus. Herpes zoster is human (alpha) herpes virus 3 (varicella-zoster virus [VZV]), a member of the herpes virus group.

Etiology: Recurrent VZV infection causes herpes zoster. The patient has initial contact with VZV in the form of chick- enpox. The DNA virus resides within the neurons. A rash, beginning as maculopapular lesions, develops when the VZV reactivates in the dorsal ganglia. VZV migrates to adjacent sensory dermatomes. The vesicles form scabs within 10 days ( Cohen et al., 2013 ). Older adults have a decrease in cell-me- diated immunity, which contributes to the risk of developing herpes zoster and post-herpetic neuralgia (PHN) (Barakzai & Fraser, 2008; Ganty, 2013). If herpes zoster affects adjacent dermatomes, crossing the midline of the body, it is consid- ered to be disseminated herpes zoster. Ten percent to 40% of people who are immunocompromised will contract dissemi- nated VZV (Yoon et al., 2013).

Although chickenpox is one of the most readily communi- cable diseases, herpes zoster has a much lower rate of trans- mission. Nonimmune persons are considered contagious 8 to 21 days after exposure to VZV. Mode of transmission is coming into contact with the vesicle fl uid. Patients with herpes zoster may be sources of infection for 1 week after the appearance of vesicle lesions. Nonimmune individuals can transmit the infection and should avoid contact with patients with herpes zoster (Fashner & Bell, 2011).

Occurrence: Herpes zoster occurs worldwide, more com- monly in older adults. Incidence increases markedly in those 60 years old or older as a result of impaired cell-mediated immunity (Epps et al., 2015). Ten cases of herpes zoster occur for every 1,000 older adults. This increase is, in part, due to older adults living longer (CDC, 2016; Gargliadi et al., 2016). It is estimated that the risk of contracting herpes zoster is greater than 50% for those 85 years of age or older. Approximately 1 million cases occur in the United States each year (CDC, 2016). There was an increase in reported episodes of herpes zoster from 1997/1998 to 2013/2014 by 49.5% (Friesen et al., 2016).

Age: This infection is most common in adults over 55 years old. The risk of herpes zoster increases with age (Dworkin et al., 2009; Sundström, 2015).

Gender: Women are diagnosed with 60% of the cases of herpes zoster (Insinga et al., 2005).

Ethnicity: Herpes zoster is 50% less common in the African American population (CDC, 2016).

Contributing Factors: Individuals are more likely to develop herpes zoster if they are more than 55 years old, have dia- betes mellitus, have had an organ transplant, are immu- nosuppressed (e.g., HIV-infected patients), have certain malignancies, are receiving long-term corticosteroids, are receiving chemotherapy, or are taking radiation treatments. Physiological or psychological stressors can precipitate the development of herpes zoster (Fashner & Bell, 2011; Johnson, Wasner, Saddier, & Baron, 2008; CDC, 2016; Cohen et al., 2013 ).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Emollients with 25% urea are more effective than those with 10% urea in softening and removing calluses.

A Young & Jones, 2015

Crest pads offl oad pressure from the distal area of the toes in patients with lesser toe deformities, improving, minimizing, and preventing callus formation.

A Melo et al., 2015

Seven mm felt padding reduces plantar pressure as compared to lesser depth felt padding.

B Curran, Ratcliffe, & Campbell, 2015

Corn plasters are an effective treatment to reduce and resolve corns as compared to scalpel debridement on appropriate patients.

A Farndon et al., 2013

Gold standard treatment to reduce corns and calluses is scalpel debridement.

C Hashmi, Nester, Wright, & Lam, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

HERPES ZOSTER

Chapter 6 ■ Skin and Lymphatic Disorders 107

Signs and Symptoms: Patients usually experience hyperes- thesia with an itching, burning, or tingling pain at the site 4 to 5 days before the eruption appears. Pain in a dermato- mal pattern may precede the appearance of the vesicles by weeks, however. Allodynia, the presence of pain without a painful stimulus applied to the area, may also be experi- enced ( Ganty, 2014 ). Patients often experience a sense of anxiety, malaise, headache, fever, and fl u-like symptoms with the onset of herpes zoster. Patients may report sleep distur- bances, decreased appetite, and depression. There may be a sense of dysesthesia and paresthesia along the dermatome (Ferri, 2007; Cohen et al., 2013 ). Some patients complain of intense itching in the involved area (Dworkin et al., 2009). There may be reported pain around the eye if ophthalmic herpes zoster later develops. The eruption is maculopapular for a few hours and then becomes characterized as grouped vesicles on an erythematous base over one dermatome (usually). The vesicles are clear at fi rst and then become cloudy within 3 to 5 days. T5 and T6 are the most common vertebral dermatomes involved, followed by cervical and sacral dermatomes. As vesicles age, they become pustular, then crust over after 7 to 10 days, fi nally healing in 2 to 4 weeks (CDC, 2016; Ganty, 2014 ).

Lesions may appear in irregular crops and are typi- cally unilateral. Scarring and change in pigmentation may occur following the healing of the crusted vesicles. The most common distributions are on the trunk or face in elderly. Regional lymph nodes may or may not be swollen and tender (Fashner & Bell, 2011). The pain can last 6 to 12 months after disappearance of the rash (PHN). Ocular complications occur in about one-half of patients with involvement of the ophthalmic division of the trigeminal nerve. These compli- cations may include keratitis, anterior uveitis, and corneal ulceration. Herpes zoster ophthalmicus occurs in 5% to 10% of patients with herpes zoster; permanent loss of vision or cranial nerve palsies can occur (Dworkin et al., 2009). Ves- icles on the tip of the nose, known as Hutchinson ’ s sign, have been found to be a precursor to ocular involvement in herpes zoster (Sampathkumar et al., 2009; Cohen et al., 2013 ). Cutaneous or visceral dissemination, the appearance of numerous varicella-like lesions in extradermatomal sites, may cause pneumonitis, encephalitis, meningitis, myelitis, and hepatitis (Fashner & Bell, 2011; CDC, 2016). The reac- tivation of VZV in the geniculate ganglion produces vesicles in the mucocutaneous distribution of the peripheral nerves. Known as Ramsey-Hunt syndrome, patients may experience vesicles in the pharynx and external auditory canal, tinnitus, vertigo, one-sided hearing loss, nausea and vomiting, invol- untary eye movements and often paralysis on one side of the face (Sampathkumar et al., 2009; Cohen et al., 2013 ).

Diagnostic Tests: Diagnosis usually is based on clinical appear- ance and distribution of the eruption and on a careful history of when the rash appeared. The direct immunofl uorescence with fl uorescein-tagged antibody (DFA) or polymerase chain reaction (PCR) (if available) is preferred over the old standard Tzanck smear. These tests have far greater sensitivity and specifi city than the Tzanck smear and allow differentiation between herpes simplex virus (HSV) and VZV infections. The DFA and PCR are useful in complicated cases and epidemio- logical studies, especially in immunocompromised individu- als who may not present with a rash (Sampathkumar et al.,

2009; Ganty, 2014 ). PCR is an expensive test, however, and the results of the test generally are not known for at least a day (Dworkin et al., 2007).

Differential Diagnosis: When the pain of pre-eruptive herpes occurs, the differential diagnosis depends on the dermatome involved:

■ Migraine ■ Myocardial infarction ■ Acute abdomen ■ Renal colic ■ Pericarditis ■ Pleuritis ■ Pulmonary embolism

Once the rash or eruption appears:

■ Contact allergic dermatitis (linear vesicles) ■ Grouped vesicles (viral infection) (Fashner & Bell, 2011;

Sampathkumar et al., 2009)

Treatment: Antiviral agents are recommended in the presence of signifi cant pain, serious herpes zoster, or involvement near the eye. PHN is not prevented by antiviral therapy, but these agents may decrease PHN duration. These antivirals block the virus’ DNA and block viral cell replication ( Beuscher et al., 2017 ). Give acyclovir 800 mg fi ve times a day for 7 to 10 days; famciclovir 500 mg orally every 8 hours for 7 days, or valacyclovir 1,000 mg orally every 8 hours for 7 days (Fashner & Bell, 2011; Cohen et al., 2013 ). These drugs must be given within 72 hours after onset of rash to be effective, and their use must be monitored in patients with reduced renal function ( Tyring, Beutner, Tucker, Anderson, & Crooks, 2000 ; Beuscher et al., 2017 ). IV acyclovir 10 mg/kg every 8 hours is the treatment of choice for herpes zoster in these patients. Patients should be encouraged to stay hydrated and avoid scratching (Cadogan, 2010). Patients with dis- seminated disease and those who are immunocompromised may need IV antiviral medications (Cadogan, 2010). Topical agents are also effective in treating herpes zoster. The use of cool compresses with 1:20 Burow ’ s solution, calamine lotion, and topical lidocaine (Xylocaine) is recommended for the soothing local effect.

Analgesics may be necessary for the initial prodromal pain associated with herpes zoster. Acetaminophen is recom- mended initially, but around the clock dosing is needed for optimal pain control. Tramadol, NSAIDs, and opiates are also used as recommended for severe pain. Acute pain may be diminished if antiviral treatment is begun within 72 hours ( Cohen et al., 2013 ).

Gabapentin and pregabalin are recommended for the treatment of PHN. The initial dose of gabapentin is 300 mg on the fi rst day and is titrated up gradually until pain relief is safely reached. The maximum does of gabapentin is 3,600 mg per day. Treatment with gabapentin with 1,800 mg per day was shown to signifi cantly reduce PHN for up to 4 weeks in a study by Fan and colleagues (2014). Pregabalin is also recommended for the treatment of PHN and can be admin- istered 50 mg three times a day or 75 mg twice a day. The dosage can be increased to 300 mg daily after 3 to 7 days as tolerated, followed by 150 mg every 3 to 7 days. The maximum recommended dose is 600 mg per day. Caution is advised when prescribing gabapentin and pregabalin to older

108 Chapter 6 ■ Skin and Lymphatic Disorders

adults, given the side effects of dizziness and ataxia. Dosage adjustment for both of these medications is required for patients at risk for renal impairment (Christo, Hobelmann, & Maine, 2007; Cohen et al., 2013 ).

The secondary amine tricyclic antidepressants, nortripty- line 10 mg orally or desipramine 10 to 25 mg orally, both given at bedtime, may be helpful, and it may be necessary to gradually increase the dosage until reduction of pain occurs; however, because of the anticholinergic side effects, caution is warranted (Ahmad & Goucke, 2002). It is also rec- ommended to have a baseline EKG done before treatment is begun with tricyclic antidepressants due to possible cardiac side effects (Gundy et al., 2014).

The use of opioids (e.g.., oxycodone) in the treatment of PHN alone or in combination with other therapies has also been studied; greater pain relief was experienced by patients when a combined regimen was prescribed over a single agent ( Gilron et al., 2005 ; Liang et al., 2015 ). The 5% lidocaine patch has been shown to be the fi rst line in treatment of the pain of PHN; one to three patches are applied in a 24-hour period. Common side effects are skin irritation and rash ( Cohen et al., 2013 ). For PHN pain, capsaicin (Zostrix cream) has been proved benefi cial in clinical trials and can be applied topically ( Cohen et al., 2013 ). The capsaicin 8% patch can be applied by a health-care professional to the most painful skin areas (Christo et al., 2007). In cases of severe pain, a transcutaneous electrical nerve stimulator unit may be tried (Christo et al., 2007). Alternative treatments including acu- puncture, cupping, and meditation have been shown to be benefi cial in reducing pain as well ( Cohen et al., 2013 ).

Follow-Up: Patients should be reexamined in 2 to 4 weeks to monitor progression of rash and as needed for follow-up of PHN.

Sequelae: PHN is the primary complication, occurring almost exclusively in people over 60 years old. Twenty percent of people over the age of 85 years diagnosed with herpes zoster develop PHN (Ganty et al., 2014). This pain persists at least 6 weeks after skin lesions. The pain, characterized as constant, severe, sharp, or burning, may develop into a long-stand- ing, debilitating problem. PHN usually lasts 1 year or less. Some patients experience a post-herpetic itching sensation rather than pain (Dworkin et al., 2009; Oaklander, 2008). Another consequence of herpes zoster is secondary bacterial

infection leading to cellulitis, caused by staphylococcus group A or group A β -hemolytic streptococcus. There is also an increased risk of an acute cardiovascular event, such as a cerebrovascular accident or myocardial infarction in the weeks to months after an episode of herpes zoster (Minassian et al., 2015).

Prevention/Prophylaxis: The new vaccine for herpes zoster (Shingrix) is available and is recommended for patients age 50 years and older. Even those people who have had herpes zoster should receive the vaccine to help prevent future occurrences of the disease (Resick, 2018). The immunization may be given without any serological testing, history of var- icella, or history of herpes zoster. The vaccine is given in two doses, with the second dose to be given 2 to 6 months after the fi rst dose. Patients should be scheduled for the second visit (Resnick, 2018). With the protection of the Zostavax vaccination waning within the fi rst 5 years and protection uncertain (CDC, 2016), it is recommended that patients are covered with the Shingrix vaccination even if they have had the Zostavax vaccine in the past (Resnick, 2018). Prac- titioners are advised to review the listed contraindications before administering the herpes zoster vaccine. High-risk individuals, such as immunosuppressed patients and individ- uals who have not had chickenpox, should be kept from expo- sure to patients with herpes zoster. Second cases of herpes zoster are rare in immunocompetent patients given that one incidence of herpes zoster boosts immunity and prevents subsequent outbreak (Dworkin et al., 2009).

Referral: Because of probable ocular involvement, patients with lesions on the nose or in the eye area should be referred to an ophthalmologist. Patients with disseminated herpes zoster should be referred to a specialist. Refer patients with severe uncontrollable PHN to a neurologist or pain manage- ment clinic (Christo et al., 2007).

Education: Emphasize to the patient the need to stay home and get plenty of rest. Teach patients proper infection control measures and proper disposal of dressings or items of clothing that contain vesicle fl uid, especially if they have known contacts that are vulnerable for developing varicella. Patients should avoid contact with immunosuppressed indi- viduals, pregnant women, and individuals who have not had chickenpox.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Antiviral therapy should be initiated within 72 hours of onset of the maculopapular lesions to increase the healing of the herpes zoster and decrease the duration of PHN.

A Tyring et al., 2000 Beuscher et al., 2017

Regular participation in tai chi boosted the cell-mediating effects of the herpes zoster vaccine.

B Irwin et al., 2007

In the treatment of PHN, combined use of certain opioids and anticonvulsant drugs provided patients greater pain relief over a prescribed single agent.

A Gilron et al., 2005 Liang et al., 2015

Chapter 6 ■ Skin and Lymphatic Disorders 109

Pressure injuries are classifi ed through the use of staging systems. These systems describe the degree of tissue loss and the clinical presentation of the injury caused by pres- sure and/or shear. Pressure injury staging has become the basis for treatment, comparison of outcomes, and, if applica- ble, reimbursement. It is noteworthy that in April 2016 the National Pressure Ulcer Advisory Panel (NPUAP) updated the Pressure Injury Classifi cation System following a rigorous literature review by a NPUAP-appointed task force, solicited input from stakeholders and the public, and the consensus conference held in Rosemont, Illinois with over 400 stake- holders in attendance. The revisions refl ect current scientifi c and clinical understanding of the etiology of pressure inju- ries, as well as clarify and make the system more accurate and easy to use (Edsberg et al., 2016).

Only pressure injuries should be staged with the NPUAP Staging System. Non-pressure-related ulcers and wounds are subject to unique staging or classifi cation systems based on wound type: diabetic foot ulcers (Wagner Classifi ca- tion System), venous leg ulcers (Clinical Etiology Anatomy Pathophysiology [CEAP]), skin tears (International Skin Tear Advisory Panel [ISTAP]), medical adhesive or tape injuries (Medical Adhesive Related Skin Injury [MARSI] categories), and burn classifi cation (total body surface area). It is essen- tial to confi rm the presence of pressure and/or shear as a causative factor prior to using the NPUAP Staging System for an injury. Because the NPUAP Staging System is based on the extent of tissue damage, an understanding of anatomy is required prior to evaluating tissue types found in wounds. Finally, to ensure an accurate assessment, pressure injury staging should take place only after a wound has been thor- oughly cleansed. In 2016, several revisions, which follow, were made to the NPUAP Staging System.

Ulcer Versus Injury: The 2016 NPUAP Pressure Injury Staging System used the term injury instead of ulcer. After an intensive review, the panel determined that the term ulcer did not accurately describe the clinical presentation of a stage 1 pressure injury or a deep tissue pressure injury (DTPI). In

short, an ulcer cannot be present without an injury, but an injury can be present without an ulcer.

Roman Versus Arabic Numerals: Roman numerals were changed to Arabic numerals in each of the numbered stages. This change was made to clarify and reduce the potential for confusion between similar terms used in health care, such as Stage IV and intravenous (IV).

Artwork: Artwork was created to illustrate the features of each stage of pressure injury. It is a graphic representation of the tissues present and is to be used for teaching about the extent of injury and the tissues present or absent within each stage of pressure injury. It is available for free color download on the NPUAP website at www.npuap.org .

Suspected Removed, Pressure Inserted in DTPI: The word sus- pected has been removed from the term deep tissue injury and the word pressure inserted for consistency with the revisions of the other terms.

Teaching Points: Teaching points (key elements of under- standing) have been included with each stage. Educators and those responsible for the accuracy, as well as the interrater reliability of serial assessments, can use these teaching points as elements of an orientation or skills competency program for bedside care providers.

Signal Symptoms: Intact skin with a localized area of non- blanchable erythema may be present, which may appear differently in darkly pigmented skin. It is usually over a bony prominence or related to a medical device. Presence of blanchable erythema or changes in sensation, temperature, or fi rmness may precede visual changes. Partial thickness involves loss of skin with exposed dermis, intact serum- fi lled blister. Full thickness loss of skin with visible adipose (fat) tissue and/or deeper structures such as fascia, muscle, tendon, ligament, cartilage, or bone may be exposed. Wound edges may be open or present with epibole (closed or rolled edges). Depth may be obscured by the presence of necrotic

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The herpes zoster vaccine (Zostavax), unless contraindicated, should be given to persons >60 years old to prevent an outbreak of herpes zoster and subsequent development of PHN.

B Hurley et al., 2010 Lu et al., 2009 Oxman et al., 2005 Cohen et al., 2013

The use of the high-concentration capsaicin patch provided sustained relief from pain in patients with PHN.

B Irving et al., 2011 Ganty, 2014

The lidoderm 5% patch provided relief to patients experiencing pain from PHN.

B Binder et al., 2009 Cohen et al., 2013

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

PRESSURE INJURIES

110 Chapter 6 ■ Skin and Lymphatic Disorders

tissue, resulting in an unstageable pressure injury until such time when the wound bed becomes visible and the degree of tissue damage can be determined. Intact or nonintact skin may be present with a purple or maroon discoloration and/ or an epidermal separation revealing a dark wound bed or blood-fi lled blister (NPUAP, 2016).

Description: A pressure injury is localized damage to the skin and underlying soft tissue usually over a bony prominence or related to a medical device. The injury can present as intact skin or an open ulcer and may be painful. The injury occurs as a result of intense and/or prolonged pressure or pressure in combination with shear. The tolerance of soft tissue for pressure and shear may also be affected by microclimate, nutrition, perfusion, comorbid conditions, and condition of the soft tissue. Common terms for pressure injury include pressure ulcer, decubitus ulcer, bedsore, and pressure sore. There are six pressure injury stages and two categories pertaining to etiology based on anatomical location (Edsberg et al., 2016):

■ Stage 1: Intact skin with a localized area of nonblanch- able erythema, which may appear differently in darkly pigmented skin. Presence of blanchable erythema or changes in sensation, temperature, or fi rmness may precede visual changes. Color changes do not included purple or maroon discoloration; these may indicate DTPI.

■ Stage 2: Partial thickness loss of skin with exposed dermis. The wound bed is visible, pink or red, moist, and may also present as an intact or ruptured serum- fi lled blister. Adipose (fat) is not visible and deeper tissue is not visible. Granulation tissue, slough, and eschar are not present. These injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel.

■ Stage 3: Full thickness skin loss in which adipose (fat) is visible in the ulcer and granulation tissue and epibole (rolled wound edges) is often present. Slough and/ or eschar may be visible. The depth of tissue damage varies by anatomical location: areas of signifi cant adi- posity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage, or bone is not exposed. If slough or eschar obscures the extent of tissue loss, this is an unstageable pressure injury.

■ Stage 4: Full thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled wound edges), undermin- ing, and/or tunneling often occur. Depth varies by ana- tomical location. If slough or eschar obscures the extent of tissue loss, this is an unstageable pressure injury.

■ Unstageable: Full thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confi rmed because it is obscured by slough or eschar. If slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. Stable eschar (i.e., dry, adherent, intact without erythema or fl uctu- ance) on ischemic limbs or heels should not be softened or removed.

■ DTPI: Intact or nonintact skin with localized area of persistent nonblanchable deep red, maroon, purple discoloration, or epidermal separation revealing a dark

wound bed or blood-fi lled blister. Pain and temperature change often precede skin color change. Discoloration may appear differently in darkly pigmented skin. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury or may resolve without tissue loss. If necrotic tissue, subcutaneous tissue, granulation tissue, fascia, muscle, or other underlying structures are visible, this indicates a full thickness pressure injury (unstageable, stage 3, or stage 4). Do not use DTPI to describe vascular, traumatic, neuropathic, or dermato- logical conditions.

Etiology: While the science regarding the etiology of pres- sure injuries has supported the role of tissue deformation, microclimate, nutrition, perfusion, and tissue tolerance, the exact mechanism of pressure ulcer development is poorly understood (Edsberg et al., 2016). Classic references by Kottner, Balzer, Dassen, and Heinze (2009) describe four causation theories: ischemia caused by occlusion of the cap- illaries leading to vascular insuffi ciency, tissue anoxia, and cell death; reperfusion injury (i.e., cellular injury resulting from the reperfusion of blood to previously ischemic tissue); impairment of lymphatic function leading to a build-up of metabolic waste products; and mechanical deformation of tissue cells. The type of tissue involved is also important, with epidermis and dermis being more resilient to the effects of pressure than muscle (Kottner et al., 2009). Also, the type of force or combination of forces (i.e., pressure, shear, fric- tion) exerted on the tissue is important. Pressure and shear- ing forces mainly affect deeper tissue layers, with moisture, pressure, and friction affecting primarily superfi cial layers (Kottner et al., 2009). Consequently, pressure is believed to be the major causative factor in pressure injury formation. Several factors play a role, however, in determining whether pressure is suffi cient to create an injury. The pathological effect of excessive pressure on soft tissue can be attributed to intensity of pressure, duration of pressure, and tissue tol- erance (the ability of skin and its supporting structures to endure pressure without adverse sequelae). Injury occurs to the skin and underlying tissues. Ischemia and hypoxia result as the pressure is applied to the area. Waste products accu- mulate as the ischemia continues, which produces toxins that cause further tissue breakdown.

Medical Device-Related Pressure Injury: Medical device-related pressure injuries result from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant pressure injury generally conforms to the pattern or shape of the device. The injury should be staged using the 2016 NPUAP Pressure Injury Staging System.

Mucosal Membrane Pressure Injury: Mucosal membrane pres- sure injuries are found on mucous membranes with a history of a medical device in use at the location of the injury. Mucosal tissues are especially vulnerable to pressure from medical devices such as oxygen tubing, endotracheal tubes, bite blocks, orogastric and nasogastric tubes, indwelling urinary catheters, and fecal containment devices. Because the 2016 NPUAP Pressure Injury Staging System for cutane- ous injuries is based on the anatomy of the skin, it cannot be used to stage mucosal pressure injury.

Chapter 6 ■ Skin and Lymphatic Disorders 111

Occurrence: Defi nitive information on the occurrence of pressure injuries is limited. Studies to date have been encum- bered by methodological issues such as variability in describ- ing the lesions and in differentiating pressure injuries from lesions of other etiologies. Consequently, pressure injuries are common; increase patient morbidity and mortality; and are costly for patients, their families, and the health-care system (Bauer et al., 2016).

The incidence in hospitalized patients ranges from 2.7% to 29% and the prevalence in hospitalized patients ranges from 3.5% to 69%. Patients in critical care units have an increased risk of pressure injuries, as evidenced by a 33% incidence and 41% prevalence. Elderly patients admitted to acute care hospitals for nonelective orthopedic procedures, such as hip replacement and treatment of long bone fractures, are at even greater risk, with a 66% incidence (Engels et al., 2016)

In the nursing home environment, the prevalence of pressure injuries is in the range of 2.6% to 24%. The inci- dence has been as high as 25% in residents admitted from an acute care hospital. Patients with pre-existing pressure injuries demonstrate a 26% incidence of additional pressure injury formation over a 6-month period. The incidence in chronic care hospitals is reported to be 10.8%, whereas 33% of those admitted to a chronic care hospital have pressure injuries. Long-term follow-up demonstrates that most inju- ries healed within a year. Persons with spinal cord injury and associated comorbidity are also at increased risk. The inci- dence of pressure injuries in this population is in the range of 25% to 66%.

Age: It has long been believed that comorbid conditions are associated with pressure injuries, and age is considered a comorbid state. Recent literature reviews suggest, however, that age is a confounding factor and a general indicator of likely defi cits in the main areas of risk, including mobility/ activity, skin status, perfusion and oxygenation, nutrition, and skin moisture (NPUAP, 2014). Prevalence of pressure injuries in the older adult population is 11.6% to 27.5%, with the increased risk being assigned to those of advancing age. The incidence in skilled care and nursing home facilities is approximately 25%. Patients admitted to a hospital geriatric unit have similarly high prevalence rates: of patients under 70 years of age, only 6% have pressure injuries; of patients over 70 years of age, the prevalence almost doubles to 11.6%.

Gender: Pressure injuries occur equally in men and in women.

Ethnicity: Cited in the literature and mentioned in the NPUAP 2016 Staging System Update is that there may be some dif- fi culty in detecting stage 1 pressure injuries in persons with darker skin pigmentation, as the red-hued changes may appear more subtly in persons with darker skin tones.

Contributing Factors: The main contributing factors to pres- sure injury development are pressure, shear, adverse micro- climate, and malnutrition. Moisture is cited as a related condition because it alters the resiliency of the epidermis to external forces. The primary offending source of moisture is incontinence, and more fecal incontinence than urinary incontinence due to the signifi cantly higher pH of feces (liquid greater than solid) when compared to that of urine. The skin ’ s pH is an acid mantle (i.e., 5.5). Understanding the concept and presentation of moisture associated skin damage

(MASD), particularly the two subcategories of incontinence associated dermatitis (IAD) and intertriginous dermatitis (ITD), are essential in the differential diagnosis of pressure injuries from those partial thickness tissue injuries that are not resultant from pressure (Gray et al., 2011).

Signs and Symptoms: A detailed history of the injury should be obtained from the patient or caregiver, including chronic illness, hygiene, nutritional status, immobility, presence and type of prolonged moisture, ability to perform activities of daily living (ADLs), psychological impact of injury, and sources of available support. Ask the patient if he or she has pain over or near bony prominences or beneath medical devices.

Clinical presentation can vary from nonblanching ery- thema to partial thickness tissue loss and frank tissue necro- sis. Nonblanching erythema results from damage to blood vessels and extravasation of blood into the tissue. Its presence suggests that more extensive tissue damage is imminent or has already occurred. The color of the skin can be varying hues of pink to red to darker toned hues of maroon or purple. Pressure-induced nonblanching erythema is occasionally misdiagnosed as a hematoma or ecchymosis. When DTPI is also present, the area is often either indurated or boggy when palpated. Note the injury size; obtain serial measure- ments of length, width, and depth; note the characteristic of the wound edge (open or epibole [rolled]); note the pres- ence and character of exudate, epithelialization, granula- tion tissue, deeper structures, and fi ndings such as necrotic tissue, sinus tracts, undermining, tunneling, and other signs of infection, such as induration, warmth, and/or advancing erythema.

Diagnostic Tests: General laboratory tests for the patients with a pressure injury include wound culture and sensitivity. Par- ticularly look for any of the following:

■ Signs of local infection (erythema, edema, change in exudate to include purulent or foul-smelling drainage, pain, crepitus)

■ Signs of systemic infection (fever, leukocytosis); bone involvement (due to risk of osteomyelitis)

■ Presence of chronicity to determine if there is a caus- ative, elusive organism

Evaluation of nutritional status should include total protein, albumin, and prealbumin; in patients with a pres- sure injury, often these clinical indicators are decreased because of inadequate nutritional stores present for tissue repair. A CBC may reveal increased red blood cell distribution, decreased lymphocyte count (malnutrition), and elevated leukocyte count (osteomyelitis). The erythrocyte sedimen- tation rate will be increased. X-rays of the appropriate area often reveal bony rarefaction (decreased density), periosteal elevation, and new bone formation.

Differential Diagnosis: ■ Skin cancers (neoplasms) ■ Fungal or yeast infections ■ Herpes simplex (HSV-2) ■ Herpes zoster (shingles) ■ Lower extremity wounds (venous, arterial, mixed etiol-

ogy, and neuropathic etiology in origin) ■ MASD, particularly IAD and ITD ■ Burns (thermal injuries) (Doughty & McNichol, 2015)

112 Chapter 6 ■ Skin and Lymphatic Disorders

Treatment: Effective pressure injury treatment with topical dressings requires consideration of numerous factors. Con- sider use of the mnemonic I DIP A MOP:

■ I nfection (eliminate, reduce bioburden) ■ D ebride necrotic tissue (consider: surgical/conservative,

sharp, mechanical, enzymatic, biological, autolytic) ■ I nsulate the wound ■ P rotect periwound tissue ■ A bsorb excess exudate ■ M aintain a constant moisture level ■ O bliterate dead space ■ P revent further injury

Pharmacological Management: Most moisture-retentive dress- ings are available without a prescription. Some antimicro- bials (e.g., silver sulfadiazine, mupirocin), some antifungals (e.g., fl uconazole), and some enzymatic debriding agents (e.g., collagenase) are prescriptive.

Follow-Up: Practitioners need to objectively evaluate the patient ’ s progress toward healing at least weekly using stan- dardized methods of assessment (e.g., wound measurements in three dimensions, amount of exudate, patient comfort, etc.). Immediate intervention is indicated if wound deterio- ration is observed sooner. If the wound deteriorates, is it in accordance with a decline in the patient ’ s overall condition? It is important to communicate this decline as an expected result to patient, caregivers, and staff. The patient ’ s general health and nutritional intake, the stability of the comor- bid conditions, the need for psychological support, and the patient ’ s comfort level should be monitored. Signs and symp- toms of complications need to be reported and recorded accurately.

Sequelae: Complications include, but are not limited to, cellu- litis, bacteremia, osteomyelitis, and sepsis (secondary to pres- sure injuries).

Prevention/Prophylaxis: Conduct a valid and reliable risk assessment tool (e.g., Braden, Norton) at the fi rst encounter

and at regular intervals thereafter for patients at risk. Spe- cifi c interventions are to be directed at the fi rst encounter and at regular intervals following initial appraisal of skin and should be targeted toward improving subscale scores in any areas in which the patient ’ s score falls below normal. Enlist the support of an interdisciplinary care team (e.g., nurse, physician, physical therapist, caregiver, dietitian, pharmacist) to ensure all goals of care are addressed adequately. Consider support surfaces for bed and/or chair when decreased mobil- ity and moisture are risk factors (McNichol et al., 2015).

Referral: Consider referral to a wound care specialist (wound, ostomy, and continence [WOC] nurse, plastic surgeon, infec- tious disease practitioner, dermatologist) if wounds fail to progress in spite of evidence-based interventions consistent with the overall plan of care.

Education: Practitioners should provide patients and their caregivers with information that highlights the applicable contributing factors to the development of pressure injury formation and information about techniques being used (or those attempted, but not tolerated by the patient) pertaining to mitigation of those contributing factors.

■ Review available and appropriate treatment modalities for each identifi ed stage of wound progression, as well as expected outcomes and anticipated time frames for healing.

■ Discuss reportable signs and symptoms of infection and complications.

■ Discuss advances in technology and dispel myths that may exist regarding wound care.

■ Identify informative Web-based resources and explain that information available via electronic means and/ or from well-meaning individuals may not be evidence based.

■ Discuss hand hygiene and disposal of soiled dressings. ■ Review the importance of positioning, sources of

dietary protein, and the amount to be consumed during the wound repair process.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Use a structured approach to risk assessment that includes assessment of activity/mobility and skin status.

B NPUAP/EPUAP/ PPPIA, 2014

Consider the impact of the following factors on an individual ’ s risk of pressure ulcer (injury) development: • Perfusion and oxygenation • Poor nutritional status • Increased skin moisture

C NPUAP/EPUAP/ PPPIA, 2014

Assess localized pain as part of every skin assessment. C NPUAP/EPUAP/ PPPIA, 2014

Inspect the skin under and around medical devices at least twice daily for the signs of pressure injury on the surrounding tissue.

C NPUAP/EPUAP/ PPPIA, 2014

Consider applying a polyurethane foam dressing to bony prominences (e.g., heels, sacrum) for the prevention of pressure ulcers (injuries) in anatomical areas frequently subjected to friction and shear.

B NPUAP/EPUAP/ PPPIA, 2014

Chapter 6 ■ Skin and Lymphatic Disorders 113

Signal Symptoms: There are several forms of psoriasis. The most common is plaque psoriasis, with erythematous patches, papules, and plaques with silvery scales that may be pruritic. Other forms include inverse psoriasis in intertrig- inous areas that appears as a smooth plaque; guttate, which is a rare form that presents with pustules; erythrodermic, which can be deadly with generalized rash; and rheumatoid varieties with joint involvement.

Description: Psoriasis is a disease of abnormal keratin syn- thesis. Infl ammation in the lesions results in hyperprolifera- tion with a shortening of the cell cycle that results in 28 times the normal production of epidermal cells ( Habif, 2016 ; Wolff, Johnson, Saavedra & Roh, 2017). This results in the development of papules with a fi ne scale that coalesce and form distinctive, well-demarcated, round to oval plaques with a silvery scale. If the scale is removed traumatically, the presence of bleeding points, Auspitz sign, is noted. When the lesion is present in intertriginous areas, the moist environ- ment macerates the scale, so the lesion appears as a smooth plaque. This is referred to as inverse psoriasis. Other less common forms of psoriasis include the guttate or acute erup- tive psoriasis, which presents with small papules that are gen- eralized over the trunk and extremities. Pustular psoriasis, in contrast to papular types, include pustular psoriasis of the palms and soles or generalized pustular psoriasis (Zumbus- ch ’ s psoriasis), which is an acute systemic illness that may be fatal. Frequently, those with psoriasis have involvement of either the fi ngernails or toenails. Fingernail involvement is more common ( Habif, 2016 ; Wolff et al., 2013).

Psoriasis can also affect the joints, causing a seronegative spondyloarthropathy, psoriatic arthritis. Other autoimmune diseases, such as infl ammatory bowel disease, may also be present (Ferri, 2018). Generally, symptoms occur in those age 30 to 55 years. Joint symptoms occur before skin psoria- sis in about 15% of cases. Symptoms include early morning stiffness; warm, red joints; and effusions.

John Updike is credited with fi rst describing the “heart- break of psoriasis.” The phrase was used in advertisement in the 1960s, but it is a genuine concern because psoriasis may have a more profound effect on the emotional health of patients than on the physical health. The skin changes and stigma of psoriasis can result in depression, and depression can exacerbate psoriasis ( Ferreira, Abreu, Reis, & Figueiredo, 2016 ).

Etiology: Recent understanding of the pathogenesis includes the probability of psoriasis being an immune-mediated dis- order. This is supported by the responsiveness of psoriasis to treatment with immunosuppressive drugs. Although there appears to be a genetic link to psoriasis, it is a polygenic trait with an 8% incidence when one parent has psoriasis, and it increases to a 41% rate if both parents have been affected. About one in three patients with psoriasis has a family history of the disease. In addition to the genetics, environmental factors are often the trigger, including skin trauma (Koebner phenomenon), streptococcal or viral infection, stress, medi- cations, smoking, and alcohol consumption ( Ferreira et al., 2016 ; Patterson, 2016).

Occurrence: Psoriasis affects about 2% of the population of the United States, or about 7.5 million Americans. Most have less than 5% of their body surface affected. About 30% of those also have psoriatic arthritis (National Psoriasis Foun- dation, 2017). Chronic stable plaque psoriasis is the most common type, affecting 80% to 90% of those with psoriasis. Guttate psoriasis most often occurs in younger adults and represents about 10% of patients with psoriasis.

Age: The peak incidence of psoriasis occurs at 22.5 years of age, although it can occur even in childhood and may have a later onset at age 55 years or over. Women tend to have earlier onset, and earlier onset is associated with more sever- ity of the disease. Psoriatic arthritis occurs most often in

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Offer fortifi ed foods and/or high-calorie, high-protein oral nutritional supplements between meals if nutritional requirements cannot be achieved by dietary intake.

B NPUAP/EPUAP/ PPPIA, 2014

Turn and reposition all individuals at risk for or with existing pressure ulcers (injuries), unless contraindicated.

A NPUAP/EPUAP/ PPPIA, 2014

Use a high-specifi cation, reactive foam mattress for all individuals assessed for being at risk for pressure ulcer (injury) development.

A NPUAP/EPUAP/ PPPIA, 2014

Consider pressure redistribution prior to and after surgery. C NPUAP/EPUAP/ PPPIA, 2014

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

PSORIASIS

114 Chapter 6 ■ Skin and Lymphatic Disorders

those between the ages of 30 and 50 years (National Psoria- sis Foundation, 2017).

Gender: There is an equal incidence of the disease in males and in females.

Ethnicity: Prevalence is highest among Scandinavians, with low incidence in West Africans, Japanese, and Inuits. There is a very low incidence among North and South American Indians. African Americans also have a low incidence of 1.3% compared with 2.5% of Caucasians.

Contributing Factors: Classic links to the development of pso- riasis include drugs, physical trauma (Koebner ’ s phenome- non), infection, and stress. A streptococcal or viral infection often precedes the onset of guttate psoriasis by 2 weeks. Drugs that may precipitate or exacerbate psoriasis include lithium, beta blockers, antimalarial agents, and systemic steroids. Several lifestyle factors or behaviors have been asso- ciated with a higher rate of psoriasis. Smoking was reported by 37% of those with psoriasis, and 78% of those reported smoking before they were diagnosed. This compares to a rate of smoking of only 13% in the general population. Psoria- sis is more prevalent in those who abuse alcohol and may increase the severity of the disease. Multiple studies have noted a relationship between obesity and the development of psoriasis ( Menter et al., 2011 ).

Signs and Symptoms: Patients may present with a papular rash that is getting worse, with shiny scales on the lesions. They may complain of pruritus. In guttate psoriasis, the lesions are distinct small papules with thin scales over the trunk and extremities. Chronic plaque psoriasis may involve a few plaques or may have many plaques scattered over the entire body. If the patient presents with a sudden onset of lesions, it is important to elicit a history of possible upper respiratory infection 2 to 3 weeks before the onset of the lesions.

Physical examination will reveal well-demarcated erythe- matous lesions with silvery scales. The scales may be thin or very thick. They are not easily removed, and if forcefully removed there may be points of bleeding, known as the Auspitz sign. The lesions of plaque psoriasis are generally symmetrical in distribution and may be located on the scalp, trunk, and buttocks, often affecting the extensor surface of the extremities. When the lesions form in the skinfolds, the moisture affects the development of scales, and the surface may be shiny. This inverse pattern psoriasis may be diffi cult to distinguish from Candida or tinea. The distinct demarcated border is helpful in differentiation. Nails also may be affected with the presence of pitting, onycholysis, subungual hyper- keratosis, red-brown coloring (oil drop sign), and nail plate dystrophy.

Diagnostic Tests: The distinct presentation of the lesions of psoriasis makes a clinical diagnosis possible. When fungal infections are a possibility, KOH tests are the gold standard for that diagnosis. Biopsies to confi rm the diagnosis of psoriasis are rare, but when they are necessary, it is essential to take the sample from an intact lesion that has not been scratched and is not bleeding. If biopsy is required, a referral to a der- matologist will ensure accurate testing.

Laboratory testing, including blood chemistry profi le, liver function tests, serum uric acid, a CBC with differential, anti- nuclear antibody titer, or rheumatoid factor, is directed at

the infl ammatory process and to rule out the possibility of infection. If the patient is presenting with guttate-type pso- riasis, a throat culture to screen for streptococcus should be considered.

Differential Diagnosis: Plaque psoriasis: ■ Seborrheic dermatitis ■ Nummular eczema ■ Tinea corporis ■ Lichen planus ■ Pityriasis rubra pilaris ■ Mycosis fungoides ■ Atopic dermatitis

Guttate Psoriasis: ■ Secondary syphilis ■ Pityriasis rosea ■ Maculopapular drug eruption

Inverse Psoriasis: ■ Candidiasis ■ Tinea

Psoriatic Nails: ■ Tinea unguium ■ Onychomycosis caused by yeast or molds

Treatment: While treatment decisions will generally be made by the dermatologist or, in the case of psoriatic arthritis, by the rheumatologist, the primary care provider is always responsible for the oversite of the patient ’ s care. Knowledge of contraindications, side effects, adverse drug reactions, and drug-drug interactions are all a critical responsibility of the advanced practice nurse provider. Establishing good com- munication with the specialist is a necessity. It is also crucial that comorbidities which are common with psoriasis are opti- mally managed. The staging of psoriasis helps to determine the choice of treatment:

■ Mild, affecting less than 5% of the body ■ Moderate, affecting more than 5% but less than 10% of

the body ■ Severe, affecting more than 10% of the body

The hand is representative of about 1% of the body. When hands, feet, face, or genital areas are involved, because of the possible effect on ADLs, even with less percent involvement it may be considered more severe ( Menter et al., 2011 ). The emotional impact of psoriasis is also considered in determin- ing the severity and may increase the ranking even with less severe involvement. Eighty percent of patients have mild-to-moderate disease.

In addition to severity, the age of the patient and the type of psoriasis needs to be considered. To ensure the appropriate choice of treatment, referral to a dermatologist should be ini- tiated. Dermatologists are the experts who treat and manage the multiple nuances of this disease. However, primary care providers need to be knowledgeable regarding the treat- ment options, because the treatments have implications for ongoing primary follow-up.

Topical Treatments: Topical treatments are the fi rst line of treatment and recommended for mild-to-moderate psoriasis. For most patients in that category, the topical treatments are safe and effective. The treatments are also used as adjunctive

Chapter 6 ■ Skin and Lymphatic Disorders 115

therapy for patients with more extensive disease who are receiving phototherapy or systemic therapy. When making a choice of topical treatments, the patient ’ s goals are import- ant to consider. The vehicle for the medication should be chosen to match those goals and the severity of the disease. Problems with topical treatments include the time needed for application, the need for prolonged treatment, and incom- plete clearance of lesions. All of these factors infl uence the patient ’ s likelihood of adherence to therapy. Patients may be on concurrent topical therapy with the use of more than one topical agent. Agents include corticosteroids, vitamin D analogues, retinoids, calcineurin inhibitors, salicylic acid, anthralin, coal tar, and nonmedicated topical moisturizers ( Table 6-4 ) ( Menter et al., 2011 ).

Phototherapy: Phototherapy requires treatment by a der- matologist. Narrow-band ultraviolet B (UVB) is often used in combination with topical therapies and offers the possi- bility of home therapy. A more aggressive treatment is che- mophototherapy with psolarens (an oral medication) and long-wavelength UV light (PUVA). The treatment inhibits mitosis by stopping DNA replication. It increases the risk of squamous cell carcinoma and possibly melanoma. It also induces photoaging. Although it has more risk than UVB, it is more effective ( Menter et al., 2011 ).

Systemic Therapy: Systemic therapy is reserved for those patients with severe disease and requires management by a dermatologist with expertise in treatment of psoriasis. Meth- otrexate is very effective but has the potential for hepatotox- icity and should be avoided in renal impairment (this will eliminate many older adults). Drug interactions are common. Biologicals include T-cell and tumor necrosis factor (TNF)

inhibitors. Baseline laboratory data are essential and need to be repeated frequently to monitor for toxicities. Live vaccines must be avoided in patients being treated with biologicals. All of the TNF inhibitors carry the increased risk of infection, especially upper respiratory infection. Coordinating the care of older adults on systemic therapy with the dermatologist is essential to adequate management ( Menter et al., 2011 ).

Follow-Up: Follow-up should be on a case-by-case basis. A key to follow-up is coordination with the dermatologist, who, in other than the mildest cases, should be managing the disease process. It is important to consider the “heartbreak of psoriasis.” The incidence of depression and suicidal ideation is higher in psoriasis and may not be directly related to the severity of the disease. All patients should be screened for depression. Patients with psoriasis have a higher incidence of arthritis, heart disease, diabetes, cancer, and hypertension, and all of these are increased in older adults as well ( Menter et al., 2011 ).

Sequelae: Psoriasis is a chronic disease with exacerbations and remissions. In a small percentage of those with psoriasis, more serious types, such as psoriatic erythroderma or gen- eralized acute pustular psoriasis, may occur. These diseases have much higher morbidity and may even result in death. Five percent of those with psoriasis will develop psoriatic arthritis.

Prevention/Prophylaxis: Triggers should be avoided: smoking, excess alcohol use, and skin trauma. Keeping the skin dry but well hydrated may decrease pruritus and the urge to scratch. Drugs known to exacerbate psoriasis should be avoided. Stress management, adequate rest, and a well-balanced diet to achieve ideal body weight are all important.

Topical Treatment for Psoriasis

TOPICAL TREATMENT MECHANISM OF ACTION SIDE EFFECTS/PRECAUTIONS

Corticosteroids Anti-infl ammatory, antiproliferative, immunosuppressive,

vasoconstrictive

Skin atrophy, telangiectasia, striae distensai, acne, folliculitis, and

purpura

May exacerbate some superfi cial skin conditions: rosacea, tinea

Rebound of psoriasis

With high potency, possible systemic side effects

Vitamin D

analogues

Binds to vitamin D receptors Burning, pruritus, edema, peeling, dryness, erythema may

improve with continued treatment

Calcipotriene

topical

Inhibition of keratinocyte proliferation and

enhancement of differentiation

Rarely systemic effects of hypercalcemia and parathyroid

suppression; apply after UVA therapy

Retinoids

Tazarotene topical

Normalizes abnormal keratinocyte differentiation,

diminishes hyperproliferation

Local irritation, may be reduced with lower concentrations;

combine with moisturizers or topical steroids

Decreases infl ammation

Calcineurin

inhibitors

Pimecrolimus

topical

Block the synthesis of infl ammatory cytokines Burning and itching reduced with continued therapy

Cautious use with light therapy

Not FDA approved for psoriasis

Salicylic acid Keratolytic; reduce keratinocyte-to-keratinocyte binding Risk of systemic toxicity; do not use with oral salicylates

Reduce pH stratum corneum Use after UVA therapy

Anthralin Prevent T lymph activation

Normalize keratinocyte differentiation

Skin irritation and staining

TABLE 6-4

116 Chapter 6 ■ Skin and Lymphatic Disorders

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Psoriasis is associated with depression and suicidal ideation. In one study of 217 patients with psoriasis, almost 10% indicated a wish to be dead, with 7.2% of patients with severe psoriasis indicating active suicidal ideation. This compares to a rate of 2.4%–3.3% in the general medical patient population. The recommendation to screen patients with psoriasis for depression and suicidal ideation is supported.

A Gupta & Gupta, 1998 Ferreira, B. I. R. C. et al., 2016

Early studies of topical calcineurin inhibitors, tacrolimus, and pimecrolimus did not show effi cacy, but when used under occlusion, they were effi cacious. The conclusion that they lacked the ability to penetrate thick plaque was supported by their successful use in the treatment of thin lesions on the face and in intertriginous areas. Although not FDA-approved for treatment of psoriasis, two double-blind studies strongly support their effectiveness in treating psoriasis on the face or intertriginous areas, without the skin atrophy common with chronic steroid treatment.

A Gribetz et al., 2004 Menter et al., 2011

Vitamin D analogue calcitriol, used in topical treatment of plaque psoriasis, was found to have slower onset of action but a longer disease-free period than betamethasone dipropionate. The risks of toxicity are minimal compared to topical steroids.

A Menter et al., 2011

Tumor necrosis factor (TNF) inhibitors are an effective treatment for severe psoriasis and psoriatic arthritis. Side effects may discourage their use. However, for treatment of psoriasis, TNF inhibitors are only approved as monotherapy while they are often combined with methotrexate in the treatment of rheumatoid arthritis and infl ammatory bowel disease. The risks associated with the combination therapy may overestimate the risk when using TNF inhibitors alone.

C Menter et al., 2011

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Referral: Except in the mildest cases of psoriasis, the patient should be co-managed with a dermatologist.

Education: In addition to ways to avoid triggers that can cause exacerbations, patients need to understand the treat- ment options and partner with providers to make choices that increase adherence. Teaching needs to include informa- tion regarding medication side effects and special consider- ations, such as the importance of not getting live vaccines

if currently being treated with biologicals. In the current health-care environment, retail clinics and pharmacies are offering vaccines, so patients need to be especially conscious of the recommendations related to their treatments and the guidelines regarding vaccines. The emotional toll of this disease needs to be acknowledged, offering patients connec- tion to support groups. Patients also need to be informed of reputable Internet sources on psoriasis.

Chapter 6 ■ Skin and Lymphatic Disorders 117

Signal Symptoms: Poikiloderma refers to telangiectasia, reticulate hyperpigmentation and atrophy. These are signs of long-term sun exposure and indicate signifi cant risk for development of skin cancer. Squamous cell carcinoma (SCC) skin cancer may evolve from actinic keratosis, which present as discrete lesions or a cluster of crusted, scaly papules on sun-exposed skin. These are called actinic keratosis and may be tender or itchy. Any lesion with changing pigment, abnor- mal symmetry, crusting, bleeding, or tenderness is a possible skin cancer.

Description: Neoplasms of the skin are the most common type of cancers in humans. Non-melanoma skin cancers (NMSCs) are basal cell carcinoma (BCC), which arises from the basal keratinocyte layer of the epidermis and SCC, which originates in the squamous cells of the epithelium. Malignant melanoma (MM) is a tumor arising from pigmented cells. Melanoma causes abnormal proliferation of specialized cells that produce melanin in the skin, eyes, and hair.

Etiology: The major risk factor for the development of skin cancers is exposure to UV radiation (Welsh et al., 2011). Patients who have or had an occupation requiring them to spend extensive time outdoors are susceptible to the develop- ment of skin cancer. There is a high recurrence rate for BCC.

Occurrence: Skin cancer is the most common form of cancer in the United States. The incidence of NMSCs has increased by 100% in the Medicare population and by 35% in the fee-for- service population from 2006 to 2012 (Rogers, Weinstock, Feldman & Coldiron, 2015). BCCs have long been thought to be more prevalent than SCCs. Current research indicates changing trends. Rogers and colleagues (2015) found a 1:1 ratio in BCCs to SCCs in the United States, and global trends are similar. Each year, more than 1 million new cases of skin cancer are diagnosed in the United States. Melanoma occurs less frequently but is responsible for more deaths. It is esti- mated that over 9,000 persons will die of MM each year (Guy et al., 2015; U.S. Cancer Statistics Working Group, 2016). The incidence of MM has doubled from 1982 to 2011 (Guy et al., 2015). Melanoma, though deadly in the later stages of development, has an excellent prognosis if treated early (Guy et al., 2015).

Age: The incidence of all types of skin cancers increases with age and the degree and intensity of sun exposure.

Gender: SCC presents three times more frequently in men than in women (Nolen, Beebe, King, Bryn, & Limaye, 2011). MM is equally prevalent in men and in women. It poses sig- nifi cant mortality risks for both (Guy et al., 2015).

Ethnicity: Skin cancers are more prevalent in fair-skinned persons, blue-eyed persons (especially people with blonde, red, or light brown hair), and people of Celtic ancestry. In the United States, residents of states where year-round sun- shine is abundant are at a high risk, especially those people who spend an extended amount of time outside. The highest incidence of BCC in the world occurs in Australia (Nolen et al., 2011). SCC is more common than BCC in darker skinned persons. Acral lentiginous melanomas (ALMs) are the most

common melanoma subtype in dark skinned persons (Mar- chetti, Chung, & Halpern, 2015). They are characterized by location and are found on the palms, plantar surface of feet, and subungually. A pigmented streak of the cuticle, longitu- dinal melanonychia, is diagnostic (Marchetti et al., 2015).

Contributing Factors: Certain patient phenotype characteris- tics are associated with risk for developing skin cancer: albi- nism, hair and eye color, tendency to burn, and skin freckling (Lin et al., 2011). UV sun exposure is the most signifi cant contributing factor to the development of skin cancer (Welsh et al., 2011). Other factors include tanning bed use, late sequelae to burns, scars, chronic ulcers, genetic disorders, and exposure to radiation (Welsh et al., 2011). Patients who report severe sunburns in childhood are at risk for develop- ing skin cancer. Patients who have had ionizing radiation, whether as a treatment for a condition such as acne or acci- dental exposure, are at risk for developing BCC and SCC. Inor- ganic arsenic, pitch, tar, and radium exposure also have been linked to the development of skin cancer (Welsh et al., 2011). Patients who have had a renal transplant and immunosup- pression are at risk for developing skin cancer and cancer of the lips (Nolen et al., 2011). Presence of multiple and atyp- ical nevi are contributing factors (Welsh et al., 2011), but a recent study of over 500 persons with melanoma showed younger patients had few nevi and no atypical nevi preced- ing the diagnosis of melanoma (Geller et al., 2016). Human papillomavirus and xeroderma pigmentosum may also play a role in the development of SCC. Certain genetic predispo- sitions can contribute to the development of skin cancer, and there is a familial tendency to develop melanoma. For patients diagnosed with familial atypical mole and melanoma syndrome or dysplastic nevus syndrome, there is a very high lifetime risk of developing melanoma (Haenssle et al., 2016).

Signs and Symptoms: Question patients about any new or changing lesions. Is the lesion painful? Does it itch or bleed? Has it healed and then reappeared? Ask about past history of any previous actinic keratosis, excised or treated lesions, and prior diagnosed skin of cancer. Question patients about any family history of skin cancers. Ask about their history of sun exposure, severe sunburn, burns, scars, ulcers, radiation der- matitis, use of tanning beds, current and prior occupations, and family history of skin cancer.

Presentation of the skin cancer will depend on the type of tumor. There are several types of BCCs. The most common are nodular, morpheaform, and superfi cial. Nodular BCC initially presents fi rst as a dome-shaped papule that is white- to-pink with a raised pearly border and prominent telangi- ectasia (James, Elston, Berger, & Andrews, 2011). Over time, these lesions may develop a central erosion and bleed easily (James et al., 2011). BCCs can also be pigmented, with a brown glossy appearance, which comprise 6% of all BCCs (James et al., 2011). Patients may describe this lesion as a pimple that did not heal. Superfi cial BCC often appears on the trunk and extremities. Characteristics of superfi cial BCCs are the presence of a well-circumscribed translucent or bright pink to red patch of skin surrounded often by telangiecta- sia. This type of BCC resembles other chronic skin conditions

SKIN CANCER

118 Chapter 6 ■ Skin and Lymphatic Disorders

such as psoriasis, eczema, discoid lupus erythematous, and Bowen ’ s disease. The least common type of BCC is the scle- rosing or morpheaform tumor. Found on the head and neck and occasionally the trunk of the body, the lesion appears to be a hypopigmented tumor that eventually is surrounded by irregular telangiectasia with atrophic scar-like appearance (Nolen et al., 2011).

SCC often originates at sites of chronic infl ammation or old scars. Actinic keratoses, precursors to SCC, appear as round or irregular-shaped erythematosus or tan plaques with a scaly or rough surface. Other precursor lesions of SCC include cutaneous horn, leukoplakia, and keratoacanthoma. These are often rapidly growing lesions that may arise from another benign, pre-malignant, or malignant lesion (James et al., 2011). Signs of malignancy of SCC include elevation, ulceration, or infl ammation of the lesion; the original lesion also may have enlarged in size. In later stages of SCC, the surface may appear crusted, and a horn of keratin forms. SCC appears on sun-exposed as well as on non–sun-exposed areas of the body. They may be tender to touch, owing to their rapid growth and infl ammatory process. Common loca- tions are the scalp, ears, lower lip, and dorsa of the hands.

For patients with suspected melanoma, the mnemonic ABCDE guides the clinician in determining if the clinical characteristics of a suspicious lesion warrant close surveil- lance and/or biopsy for histological evaluation.

■ Asymmetry ■ Border irregularity ■ Color variation ■ Diameter greater than 6 mm ■ Elevation of a previously fl at lesion, evolving, and

enlarging (Bibbins-Domingo et al., 2016)

It is important to note that the classic ABCDE pattern of MM development is not always present. The tool is used to alert patients and nondermatologists about suspicious lesions (Rastrelli et al., 2013). Melanoma can mimic benign lesions.

Major Signs: Change in size, change in shape, change in color. If one or more major signs exist, refer for expeditious biopsy.

Minor Signs: Infl ammation, crusting or bleeding, sensory change, diameter of greater than 6 mm. If three or four minor signs exist with a major sign, consider referral.

Patients may be concerned about a new, pigmented lesion or a change in an already existing one. Patients may report associated itching, burning, or pain in a mole. Superfi cial spreading melanoma is a fl at to slightly raised pigmented lesion with irregular borders, commonly found on the backs of men and the lower legs of women. Lentigo maligna mel- anoma, an irregularly pigmented macula with notched borders, occurs on sun-exposed areas, especially on the faces of older adults. Nodular melanoma, brown or black papules usually located on the trunk, head, and neck, is characterized by rapid growth. Clinical evaluation for skin cancer includes a total body skin examination and palpation of regional lymph nodes, liver, and spleen (Rastrelli et al., 2013).

Diagnostic Tests: Skin cancer is diagnosed through biopsy. Biopsy of the suspected lesion is necessary to confi rm the diagnosis via histological examination of the tissue. An adequate tissue sample should be excised, and an elliptical

excision generally is necessary for larger lesions. Excisional biopsy is recommended for any pigmented lesion (Rastrelli et al., 2013; Nolen et al., 2011).

Differential Diagnosis: ■ Actinic keratoses ■ Seborrheic keratoses ■ Keratoacanthoma ■ Atypical nevi ■ Blue nevus ■ Dermatofi broma ■ Venous lakes ■ Pyogenic granulomas ■ Intradermal nevus ■ Sebaceous hyperplasia ■ Molluscum contagiosum ■ Psoriasis ■ Eczema ■ Discoid lupus erythematous ■ Bowen ’ s disease (Nolen et al., 2011)

Treatment: Several factors need to be considered before skin cancer therapy begins: the patient ’ s age and general health, whether or not the patient is immunocompromised, size and location of the tumor, the pathology of the tumor, and the cosmetic concerns of the patient. BCC may be treated by excisional surgery, electrodessication and curettage, cryo- therapy, ionizing radiation, and Mohs’ micrographic surgery (MMS). A chemotherapeutic agent such as 5-fl uorouracil, interferon, and retinoids are topical agents for superfi cial or small BCCs and early-diagnosed SCC. SCC may be treated in the same manner as BCC; however, because of its more truc- ulent growth pattern, wider excision and MMS are the pre- ferred methods of treatment. Recurrent BCC and SCC should be treated with surgical excision (Nolen et al., 2011). Treat- ment of MM is surgical. An excisional margin surrounding the tumor is made, depending on the thickness of the tumor. Chemotherapy and radiation are used for palliative measures in the treatment of metastatic disease.

A number of different treatment options are available for the management of actinic keratosis (AK), including cryo- therapy, topical chemotherapy using 5-fl uorouracil, immu- nomodulators, and photodynamic therapy, all of which have been shown to reduce lesion count in patients with AK (Patel, Armstrong, & Eisen, 2014; Englet & Hughes, 2012). Cryotherapy, topical 5-fl uorouracil, and photodynamic therapy are the most commonly used treatments for AK. A meta-analysis by Patel and colleagues (2014) found photo- dynamic therapy had a larger treatment effect on thin AKs of the scalp and face compared to cryotherapy and topical che- motherapy. It is relatively easy to use and is an effective treat- ment. Other treatments can include electrodessication and curettage or photodynamic therapy. Combination therapies can include both fi eld-directed and lesion-directed therapy (Huang & Clark, 2011).

Follow-Up: Follow-up for a patient with diagnosed skin carci- noma is essential, because the recurrence rate of skin cancer is high; 50% of persons with BCC and SCC have a reappear- ance of a cancerous lesion within 5 years. A person who is susceptible to skin cancer may develop another cancerous lesion at any time. Precancerous lesions should be exam- ined regularly every 6 to 12 months using a head-to-toe

Chapter 6 ■ Skin and Lymphatic Disorders 119

skin examination, including a careful inspection of the previous site of a lesion. In patients with SCC, palpation of regional lymph nodes is suggested. During subsequent visits of patients with malignant melanoma, a thorough review of systems is imperative to elicit clinical signs and symptoms of metastasis.

Sequelae: BCC rarely metastasizes; however, if it is not treated early, the carcinoma may invade the surrounding tissue and bone. Advanced SCC lesions of the lips, pinna, and genita- lia often metastasize. Recurrent NMSC has a higher rate of recurrence and eventually may lead to the development of metastatic disease (Nolen et al., 2011). The larger the NMSC in size, the higher the rate of recurrence. The anatomical location of the NMSC also infl uences the recurrence rate; lesions on the face, ears, vertex, and scalp are known as high-risk cancer areas. Five-year prognosis for MM is deter- mined by the thickness of the tumor. Tumors less than 0.76 mm are associated with a 98% 5-year survival rate; tumors 0.76 to 1.49 mm, with an 87% to 94% 5-year survival rate; and tumors 1.50 to 3.99 mm, with a 66% to 83% 5-year survival rate. Patients with tumors greater than 4.0 mm have a less than 50% 5-year survival (American Cancer Society, 2016).

Prevention/Prophylaxis: Because the incidences of all skin cancers increase with age, it is important to discuss sun care protective behaviors with all older adults (Lin et al., 2011). The CDC recommends easy options for sun protec- tion. Because UVR exposure increases the risk for skin cancer with all skin types, individuals need to seek shade when UVR is strongest, during the hours of 10:00 a.m. to 4:00 p.m., and avoid burning. According to the Skin Cancer Founda- tion, sunscreen should have a sun protective factor (SPF) of at least 30 or higher, broad spectrum, and water resis- tant for extended outdoor activity. Tanning beds or booths should be avoided, as they pose a signifi cant risk for the development of melanoma (Biniol, Boyle & Gandini, 2012; CDC, 2016).

Areas of the body for sunscreen application include head, neck, and ears; exposed areas of the front of torso; back of torso; each arm; dorsum of hand and shoulder; each upper and lower leg; and each foot. One teaspoon of sunscreen should be applied separately to the upper leg and one tea- spoon applied to the lower leg. It is necessary to reapply sunscreen after toweling off from swimming or exercise and after heavy sweating. Wide-brim hats that shade the face, head, ears, and neck; long-sleeved shirts; and long pants are recommended. Sunglasses that are wrap-around type should be worn and can be purchased to block up to 100% of UVR (U.S. Cancer Statistics Working Group Department, 2014).

Patients need to be routinely asked about their ability to conduct skin self-examinations. Recommending partner par- ticipation can enhance one ’ s thoroughness in examining hard-to-reach areas of the body. Providing individuals with printed directions on how to position mirrors to examine the body, the use of good lighting, and suggesting magnify- ing lenses for those with impaired eyesight can help ensure a thorough examination has been carried out by the patient. Taking the time to give patients adequate instructions in skin self-examination has been found to be a successful strategy in ensuring older adults routinely conduct or seek assistance in regular skin examinations and the use of sunscreen (Janda et al., 2011). High-risk patients can be provided body maps to record areas of suspicious lesions to bring with them at the time of clinical examinations. These patients should be ques- tioned if they are regularly being followed by a dermatology practice. If not, primary care providers are well positioned to begin triaging (to include referring patients to a derma- tologist) patients who present with suspicious skin lesions (Goulart et al., 2011).

Yearly physical examinations should include assessment of the head, scalp, and skin, and an accurate recording of descriptions of any suspicious lesions. Patients should be fully undressed, to complete an accurate physical. New, unusual, or changing lesions or moles should be evaluated by a dermatologist. Lesions that have variegated colors, irreg- ular elevations, or irregular borders should be examined by biopsy. Immunosuppressed organ recipients are at high risk for developing skin cancer at rates faster than the general patient population and should be scheduled for regular skin examinations.

Referral: When a suspicious lesion is found, referral to a der- matologist for evaluation and possibly biopsy is necessary. Whole-body photographs and dermoscopy may be used to follow patients with suspicious lesions. A tutorial on dermos- copy is available on the Internet at http://www.dermoscopy. org . Oncology referral is needed for metastatic SCC and MM.

Education: Advise older patients that skin cancers are a common occurrence as one ages, especially for patients at risk. Older adults should perform a monthly self-evalua- tion of the skin. Any suspicious lesion that does not heal in a reasonable time needs to be examined by a primary care provider. Patients also need to report any slow-growing, fl esh-colored, or pigmented lesion, noting if the lesion has irregular borders, changes in color, ulceration, bleeding, or horn formation. Sun exposure, especially during the hours of 10:00 a.m. to 4:00 p.m., should be avoided. Year-round broad-spectrum sunscreen that blocks UVA and UVB light is recommended. Vulnerable areas, such as the head and neck, should be covered with protective clothing.

120 Chapter 6 ■ Skin and Lymphatic Disorders

SUPERFICIAL FUNGAL INFECTIONS

Etiology: Dermatophytes: The dermatophytes are a group of fungi

that infect the dead keratin of the stratum corneum, hair, and nails. They are limited to these areas because they require keratin for growth. They are responsible for most of the fungal infections of the skin, hair, and nails. Patients who are chronically infected may have a genetic predisposition to dermatophyte infection. One way to classify dermatophytes is by the origin of the infection: anthropophilic, transmis- sion from person to person by fomites or direct contact; zoophilic, transmission from animal to person by fomites or direct contact; or geophilic, from the soil. The latter two sources result in a more rapid and more severe infl ammatory response. Another classifi cation is based on the tissue primar- ily involved: epidermomycosis when the epidermis is infected, trichomycosis when it involves the hair or hair shaft, and onychomycosis when the nail is affected. The dermatophytes within the stratum corneum disrupt the horny layer, lead to scaling, and create an infl ammatory response. Three fungal species are primarily responsible for the infection: Tricho- phyton, Epidermophyton, and Microsporum. T. rubrum are the most common cause of skin and nail infection, with Tricho- phyton responsible for 80% of infections (Clinard & Smith, 2015; Wolff, Johnson, Saavedra, & Roh, 2017).

Cutaneous Candidiasis: Candida albicans is an oval, yeast-like fungus that lives in the normal fl ora of the mouth and gastro- intestinal tract. It reproduces through budding, the develop- ment of pseudohyphae, and true hyphae. Conditions that compromise the immune system or alter the normal body fl ora contribute to the development of Candida infections. The yeast infects the outer layer of the skin with the primary

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

In outdoor occupational settings the provision of information regarding sun protection to workers through instruction, small media, or both increase sun protective behaviors.

C Guide to Community Preventive Services, August 2013

Multicomponent community wide interventions including a combination of: • Individual directed strategies • Mass media campaigns • Policy changes Is effective in increasing sunscreen use.

C Guide to Community Preventive Services, August 2013

In high school and college education through class instruction, use of brochures/fl yers, and participation in an educational program did improve self-care practices, including increased use of sunscreen and sunglasses.

B Guide to Community Preventive Services, August 2013

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml . Source: U.S. Department of Health and Human Services. The Surgeon General ’ s Call to Action to Prevent Skin Cancer.

Signal Symptoms Dermatophyte Infection (Tinea): Erythema, scale, raised border,

clearing center, may present with vesicles if infl ammatory.

Candidiasis (Moniliasis): Pustules, red, denuded, glistening surface with a scaling border and satellite pustules. In the oral cavity and vagina, the scale and infl ammatory cells form the classic “cottage cheese curds.”

Tinea Versicolor (Pityriasis Versicolor): Hypopigmented macules and patches or scaly red or shades of brown macules or patches may be slightly pruritic.

Description: Superfi cial fungal infections include the derma- tophytes, candidiasis, and tinea (pityriasis) versicolor. The warm, moist surface of the skin allows fungal infections to survive. Fungal infections are not self-limiting and without treatment will spread (Salmon & Fuller, 2013). Dermato- phyte infections are referred to clinically as tinea followed by the region of the body that is infected: tinea capitis (the head), tinea barbae (the beard area), tinea facea (the face except for the beard area), tinea manuum (the hand), tinea corporis (the body), tinea cruris (the groin), tinea pedis (the foot), and when there is nail involvement, tinea unguium or onychomycosis. Lay terms for the dermatophytes include ringworm, jock itch, and athlete ’ s foot.

Candidiasis may be termed monilia, yeast, or thrush and generally presents in intertriginous areas or on mucous membranes. Tinea versicolor, which in almost all other coun- tries is referred to as pityriasis versicolor, is not caused by a dermatophyte, and is therefore not a true tinea. It is a chronic scaling change in color that affects the areas of the body with increased sebaceous activity.

Chapter 6 ■ Skin and Lymphatic Disorders 121

lesion, a pustule that dissects under the outer skin layer and peels it away. The result is a glistening surface with a scaling, advancing border and often the presence of satellite lesions. Candida grows best in warm, moist environments, and often the lesions end as they meet the area of dry skin.

Tinea Versicolor: Tinea versicolor is caused by organisms in the Malassezias species. (Wolff et al., 2017). The organisms are lipophilic yeasts that reside in the keratin and hair folli- cles, areas with increased sebaceous activity ( Habif, 2016 ; Wolff et al., 2017). It is not known to be contagious, but is an overgrowth of a normal fl ora. As sebum production declines later in life, the incidence of tinea versicolor also declines.

Occurrence: Immunosuppressed patients are at higher risk for fungal infections of all kinds and are more likely to have infections that do not resolve. Older adults are at higher risk for many fungal infections because of the decline in the immune system with aging, as well as the increased incidence in comorbidities and the use of multiple medications. Func- tional compromise can lead to a decline in personal hygiene, which also increases the risk factors for fungal infection. Der- matophyte infections are increasing as there is an increase in travel, migration, and international sports (Salmon & Fuller, 2013). Tinea versicolor is more common in young adults due to its link to sebum production (Wolff et al., 2017).

The feet and nails are the most common areas of the body affected by dermatophytes in the older adult. Onychomycosis due to tinea unguium increases in incidence with advanc- ing age, while toenail onychomycosis due to Candida albicans declines with aging. When the dermatophytes are inaccu- rately diagnosed and treated with topical steroids, a phe- nomenon called tinea incognito may occur. The rash initially disappears, but when treatment with steroids is discontinued, the rash returns with much more extensive involvement and may appear without scale. It is not responsive to subsequent topical steroid treatment, and a thorough history is neces- sary to make the proper diagnosis of tinea.

Candida most often causes intertriginous infections in those over 65 years old, but it can also be the cause of ony- chomycosis. Although it seldom causes infection in toenails, it may be the identifi ed cause in half of all fi ngernail infec- tions, especially in women and those who often immerse their hands in water (Gelotar, Vachhani, Patel, & Makwana, 2013). Tinea versicolor thrives in heat and humidity. It has an estimated prevalence in the U.S. population between 2% and 8%, however, the actual prevalence may be much higher because many of those with the disease do not seek medical evaluation.

Age: Tinea of the scalp and face (tinea capitis and tinea facialis) are primarily diseases of children. Tinea of the body, trunk, and extremities (tinea corporis) can occur at any age. The initial presentation of tinea pedis (athlete ’ s foot) is most common in adults aged 20 to 50 years, and the initial presen- tation of tinea unguium (onychomycosis) commonly occurs in those age 45 to 54 years. Tinea unguium can affect any age, but the incidence in toenails increases with aging and is most common in the oldest old. Approximately 50% of those over 70 years old are affected (Wolff et al., 2017).

Candida of the skin occurs more often in older adults because of the decline in immune response with aging, as well as a decline in hygiene among many older adults. While

not a common cause of toenail infection, when it occurs it is more likely in an older adult, while fi ngernail fungus is rarely seen in older adults.

Tinea versicolor is more common when sebaceous glands are most active during puberty and in young adults ages 15 to 24 years. Tinea versicolor is less common in those over 65 years old because sebum production declines with age (Wolff et al., 2017).

Gender: Tinea barbae is an infection that only occurs in males and is more common in rural areas. Males also more often experience tinea cruris and tinea pedis, and are more likely to have toenails infected with dermatophytes than females, while females are more likely to have Candida- infected fi nger- nails . Gender differences have not been found in cases of Candi- da in other parts of the body or in cases of tinea versicolor.

Ethnicity: Although African Americans are less likely than other races to be diagnosed with dermatophytosis, African American children are at highest risk for tinea capitis. This is attributed to genetic and cultural factors, as well as socio- economic status. Ethnic differences have not been noted for either Candida or tinea (pityriasis) versicolor.

Contributing Factors: Fungal infections are more common in warmer climates. Excessive sweating increases risk. Any of the diseases that compromise the immune system, atopy, and topical and systemic steroids increase risk. Diabetics are of noted higher risk and those with abnormalities of the keratin, as in psoriasis and ichthyosis (Nenoff et al., 2013). Age alone increases the risk, particularly of onychomycosis. Tinea manuum is rare in individuals who do not also have tinea pedis. A common presentation is two feet–one hand syndrome, which is believed to be a result of the patient touching or scratching the infected feet. Tinea pedis occurs more frequently in those who wear occlusive footwear that promotes warmth and sweating, the perfect environment for fungal growth. Socioeconomic status also appears to contrib- ute to the incidence of dermatophyte infections, with tinea pedis more prevalent in developed countries and tinea capitis more prevalent in poorer countries.

Cutaneous candidiasis is more common in adults with diseases that compromise the immune system, those taking medications that cause immune decline, adults treated with broad-spectrum antibiotics, and those with poor hygiene that results in moisture in intertriginous areas ( Habif, 2016 ; Wolff, et al., 2017). Other contributing factors include hot, humid weather; tight underwear; poor hygiene; and infl am- matory diseases occurring in skinfolds.

Like other fungal infections, tinea (pityriasis) versicolor is more common in an environment of heat and humidity. It grows best where sebaceous activity is highest and may be more common in those with oily skin. Immune-compromised individuals and those on steroids are also more susceptible. While the color change may be more noticeable on black skin, there is no noted racial difference ( Habif, 2016 ; Wolff et al., 2017).

Signs and Symptoms: Well-defi ned borders with scale are a hallmark of each of the superfi cial fungal infections. Tinea is often dry and scaly, while Candida presents with initial pus- tules that become eroded, confl uent, and evolve into patches with sharply demarcated borders and fi ne scale, surrounded by satellite pustules. Either can also be noted in thickened,

122 Chapter 6 ■ Skin and Lymphatic Disorders

discolored nails, onychomycosis. As the infection in the nail progresses, the nail becomes brittle, splinters easily, and the nail plate may pull away from the nail bed (onycholysis).

Tinea capitis presents as hair loss (alopecia). Gray patch tinea capitis often is circular in shape with the presence of many broken-off hairs and the scalp assumes a dull gray color due to the arthrospores that are formed by the fungi. Black dot tinea capitis occurs when hairs break off near the surface and give the appearance of dots. The dots may be scattered over the scalp and not form a classic round patch. A kerion is an infl ammatory mass on the scalp that is painful and may include pustules and result in cervical or occipital adenopathy.

Tinea of the face and body presents as the classic ring- worm pattern with a clearing center and a raised, scaling leading edge. Tinea cruris presents as an erythematous pru- ritic rash that begins in the groin and spreads onto the thighs. It is usually unilateral and rarely involves the scrotum. The lack of scrotum involvement can help to differentiate tinea from Candida of the groin, where scrotum involvement is common ( Habif, 2016 ).

Tinea pedis, athlete ’ s foot, is a common dermatophyte infection and presents with many different signs and symp- toms. Habif ( 2016 ) notes that although it may present in the classic ringworm pattern, involvement between the toes or on the soles of the feet is more common. Three primary types are interdigital, moccasin type, and vesicular.

■ Interdigital tinea pedis results in erythema and scaling present between the fourth and fi fth toes, although any interdigital space can be affected. Secondary infection with bacteria is more common in the macerated toe space.

■ Moccasin-type tinea pedis affects the entire sole of the foot, and the chronic silvery white scale may also occur on the palms of the hands, where it is referred to as painter ’ s palm. The creases of the palms and the soles of the feet are thickened and the creases are white in color, hence the appearance of paint that was not fully washed away. Because of the mild nature of this infec- tion and its subtle presentation, it may be present for years before the patient seeks treatment.

■ Vesicular-type tinea pedis may appear on the sole or the top of the foot and may represent a secondary bacte- rial infection in someone with chronic interdigital tinea pedis. It can also occur as an id reaction to the fungal infection, in which case the blisters may even involve remote sites.

Toenails are most often infected with dermatophytes, and there are three classic presentations:

■ Distal and lateral subungual onychomycosis (DLSO), which presents with onycholysis (the pulling away of the nail plate from the nail bed), hyperkeratosis, and yellow-brown discoloration.

■ Superfi cial white onychomycosis (SWO), in which the dermatophyte invades the surface of the nail and the dorsal nail plate is chalky white.

■ Proximal subungual onychomycosis (PSO) appears as a chalky, white color at the base of the nail.

When a patient presents with a nail problem it is important to think broadly about the differential, as only 50% of nail problems are onychomycosis (Westerberg & Voyak, 2013). Not every toenail with abnormal appearance is infected with

fungus. Other common considerations should be trauma, fre- quent immersion in water, psoriasis, atopic dermatitis, or HIV infection.

Cutaneous candidiasis occurs intertrigo, in large skin- folds and interdigital areas, as well as in nails. Habif (2010) describes two presentations of Candida : 1) Pustules form, become macerated in the skinfold, and develop papules with a fringe of moist scale at the border and intact pustules outside the intertriginous area; 2) Red, moist, and shiny lesions form that lack the pustules, because they macerate as soon as they form. Small intact pustules appear outside the border, and these satellite lesions are helpful in making the diagnosis.

Tinea (pityriasis) versicolor appears as macular, well-de- marcated lesions that are light brown on untanned skin and white on tanned skin. The lesions vary in size and may become confl uent and cover large areas of the body. They are fi nely scaled and sometimes pruritic. The trunk is the most common area of the body affected, but the lesions can spread to the upper arms, neck, and face.

Diagnostic Tests: History of the concern is critical in diagno- sis, because in most superfi cial fungal infections diagnosis is primarily presumptive, based on clinical presentation. The fungal lesions evolve and for the most part are asymptomatic, so they may be found coincidentally by the provider on phys- ical examination or presented by the patient when self-treat- ments have failed. Taking the history along with inspection is recommended. Asking the patient to identify what part of the lesion looks like the initial presentation allows for identifi - cation of the primary lesion and can sort out confusing signs of lesions that are secondary and may mask the primary disease.

For fungal skin involvement, the gold standard of diagno- sis is direct microscopic examination of a potassium hydrox- ide wet mount preparation ( Habif, 2016 ). Scale is obtained using a surgical blade and placed on a slide. Although fungal infection in the hair or nails may need to be cultured, most tinea does not require culture because treatments are effec- tive against any of the specifi c species. Culture may also be needed for defi nitive diagnosis of lesions on the foot. Because nail involvement will require prolonged oral treatment to eradicate the infective agent, clinical diagnoses should be confi rmed by laboratory testing. Approximately 90% of nail infections are due to dermatophytes; 8% are caused by a mold, Scopulariopsis; and 2% are due to a yeast, Candida, that may not respond to treatments useful in treating der- matophytes ( Habif, 2016 ; Westerberg & Voyak, 2013). Gar- cia-Doval and colleagues (2010) present a clinical diagnostic rule for tinea unguium. In their study, they found that if the patient with suspected onychomycosis had greater than 25% involvement of the sole of the foot with plantar desquama- tion and the presence of interdigital tinea pedis, the positive predictive value of the rule was 81%, which is higher than that of laboratory tests.

Differential Diagnosis: Scalp Lesions: ■ Seborrheic dermatitis ■ Psoriasis ■ Atopic dermatitis ■ Alopecia areata ■ Bacterial folliculitis ■ Neoplasia needs to be considered with presence of a

kerion

Chapter 6 ■ Skin and Lymphatic Disorders 123

Lesions on the Trunk: ■ Allergic contact dermatitis ■ Atopic dermatitis ■ Nummular eczema ■ Psoriasis ■ Pityriasis rosea ■ Tinea (pityriasis) versicolor ■ Early presentation of herpes zoster

Lesions in the Groin: ■ Intertrigo ■ Psoriasis ■ Seborrheic dermatitis ■ Erythrasma

Lesions on the Feet: Between the toes: ■ Bacterial infections: erythrasma, impetigo, Pseudomonas ■ Candida intertrigo

Moccasin type:

■ Allergic contact dermatitis ■ Atopic dermatitis ■ Dyshidrotic eczema ■ Psoriasis

Vesicular:

■ Allergic contact dermatitis ■ Dyshidrotic eczema ■ Bacterial infection ■ Bullous disease

Nail Involvement: Distal and lateral subungual onychomyco- sis (DLSO):

■ Psoriatic nails ■ Onychogryphosis (thickening and hardening) ■ Onychauxis (overgrowth or thickening)

Superfi cial white onychomycosis (SWO):

■ Trauma ■ Contact or irritant dermatitis

Tinea Versicolor: ■ Vitiligo ■ Pityriasis alba ■ Seborrheic dermatitis ■ Secondary syphilis ■ Pityriasis rosea

Treatment: In older adults, response to treatment may be decreased due to slower cell turnover and comorbid condi- tions, particularly diabetes and peripheral vascular disease. Tables 6-5 and 6-6 offer topical and systemic treatment options, respectively. For topical agents, the treatment is twice a day for 2 to 4 weeks and should be continued for 1 week after the lesions clear. Application should extend beyond the leading edge of the lesion. Within a class of medication, the options are comparable and should be selected based on cost and the preferred base (lotion, cream, ointment). Topical treatments are not useful for tinea capitis, and failure is common in tinea manuum and tinea unguium.

Newer agents are more likely to cure tinea pedis than the older generation of antifungals, including clotrimazole, which is fungistatic, whereas terbinafi ne is fungicidal. Terbi- nafi ne 1% cream applied twice daily for 1 week has a high

cure rate for interdigital tinea pedis and butenafi ne twice a day for a week is also very effective ( Habif, 2016 ). Econazole and ciclopirox also have antibacterial properties and may be the drugs of choice if bacterial involvement is suspected.

When tinea pedis is vesicular, the use of aluminum acetate solution (Burow ’ s solution) compresses applied for 30 minutes several times a day is a helpful drying agent and facilitates the penetration of the topical antifungal treatment. Oral antifungal drugs may be used to treat the acute infection ( Habif, 2016 ). In hyperkeratotic, moccasin-type tinea, kera- tolytic agents, such as ammonium lactate lotion or topical urea, can reduce the hyperkeratosis and allow for improved penetration. Applying a plastic occlusive dressing over the keratolytic agents enhances their effectiveness. Oral terbina- fi ne daily for 4 weeks may result in cure rates of 95% ( Habif,

Topical Treatment for Superfi cial Fungal Infections

DRUG CLASS PREPARATION USE

Azoles Clotrimazole Dermatophytes of the

trunk or extremities

Miconazole Cutaneous candidiasis

Ketoconazole Tinea (pityriasis) versicolor

Econazole

Oxiconizole

Sulconizole

Allylamines Naftifi ne Dermatophytes of the

trunk or extremities

Terbinafi ne Tinea (pityriasis) versicolor

Butenafi ne

Naphthionates Tolnaftate Dermatophytes of the

trunk or extremities

Pyridone Ciclopirox Dermatophytes of the

trunk or extremities

Candidiasis

Tinea (pityriasis) versicolor

Onychomycosis SWO

Polyene Nystatin Candidiasis

TABLE 6-5

Systemic Treatment for Superfi cial Fungal Infections

DRUG CLASS PREPARATION USE

Allylamines Terbinafi ne Tinea corporis, cruris,

capitis, pedis

Onychomychosis

Azoles Itraconazole Dermatophyte infections

Fluconazole Tinea (pityriasis) versicolor

Onychomychosis

Mitotic inhibitor Griseofulvin Tinea corporis, cruris,

capitis, pedis

Tinea (pityriasis) versicolor

TABLE 6-6

124 Chapter 6 ■ Skin and Lymphatic Disorders

2016 ). For tinea pedis it is important to assess the condition of the nails and treat any reservoir that may be present.

Topical treatments are rarely useful in the treatment of tinea unguium, except for SWO. In the United States, three topical treatments are approved by the FDA. Ciclopirox topical (Penlac Nail Lacquer) is the oldest; new agents include tavaborole (Kerydin) and efi naconazole (Jublia). Ciclopirox alone has a clinical cure rate of only 6% to 9%, however, it is also used in combination with oral agents and in that combination had a complete cure rate of 68% (Westerberg & Voyak, 2013). An intriguing alternative was presented by Derby, Rohal, Jackson, Beutler, and Olsen ( 2011 ). In a small study (including only 18 subjects) of the effectiveness of the lay treatment of onychomycosis with Vicks VapoRub applied topically once a day for 48 weeks, 83% of the participants reported satisfactory results, with 27.8% experiencing a complete clinical and mycological cure; 56% had partial clearance, and 17% had no improvement.

An alternative treatment of tinea (pityriasis) versicolor is selenium sulfi de 2.5% lotion or shampoo applied for 10 to 15 minutes followed by showering off for 2 weeks. Weekly appli- cation for several additional months may prevent recurrence. The skin color alterations may take 1 to 2 months to resolve completely.

Research supports a variety of dosing options for all of the oral treatments, from daily to once-a-month pulse therapy. The duration of therapy depends on the site of involvement as well as the response. Although oral terbinafi ne is least toxic of the antifungals, all of the agents have the potential of serious side effects. Before recommending any oral treatment, consultation is recommended.

Mechanical treatments of nails infected with fungus offer another option for resolution of the infection. Total nail removal is an option, but can have unintended consequences.

Follow-Up: Follow-up of the patient with superfi cial fungal infections needs to be addressed on a case-by-case basis. A fol- low-up in 4 weeks is a reasonable option, especially for those patients on oral therapy, where hepatitis may appear after 4 weeks of treatment (Baran et al., 2008). For oral therapy, a baseline CBC and liver function tests are recommended with retesting every 4 to 6 weeks ( Habif, 2016 ). Infection of the toenails requires 6 weeks or longer to judge results, and in tinea versicolor 1 to 2 months are required before the lesions resolve. Patient education regarding expected outcomes and possible side effects can help in the assessment of when or even whether follow-up is necessary.

Sequelae: The superfi cial fungal infections for the most part do not present a serious health threat to older adults. Their lack of symptoms is one reason they are often chronic before they are addressed. In older adults, onychomycosis can result

in cellulitis and foot ulcers. The risk of superinfection with bacteria and resulting severe consequences is greatest in those with diabetes, peripheral vascular disease, or immune compromise. The Candida species may have systemic conse- quences and are often painful; treatment and prevention are key. The side effects of the treatments may be more concern- ing than the disease, and these risks are important to weigh in decision making. Serious consequences include hepatic toxic- ity, CyP-450 interactions, neutropenia, and agranulocytosis.

Prevention/Prophylaxis: All fungus grows best in warm, humid environments. The key to prevention of all types is to keep the skin cool and dry. Avoiding occlusive footwear, wearing absorbent materials, and practicing good hygiene offer the best primary prevention. Tinea pedis, tinea manuum, and onychomycosis are diffi cult to completely eradicate; recur- rence is common, and the diseases may become chronic in nature. The interdependence of these infections requires the complete resolution of all three in order to prevent recur- rence. Tinea versicolor is the result of the conversion of the normal Malassezia skin fl ora to a mycelial form that is pathological and causes the scaly lesions. Older age actually decreases the risk of this disease, because sebaceous activity declines with age. Prophylactic therapy with topical or oral antifungals has been effective in preventing recurrence. The Candida species are part of the normal fl ora in the mouth, gut, and vaginal tract. The key to prevention of recurrence is keeping the skinfolds dry. Use of a hairdryer to thoroughly dry the area after bathing, the use of aluminum acetate solu- tion (Burow ’ s solution), and the application of antifungal or absorbent powder have all been shown to prevent recurrence ( Habif, 2016 ; Wolff et al., 2017).

Referral: When defi nitive diagnosis is needed for suspected fungal infections of the skin, hair, or nails, referral is often necessary so that direct visualization of a wet mount prepa- ration can be performed. When the hair or nails are affected, systemic treatment is usually required. A culture is necessary to rule out the other diseases that can mimic fungal infection and determine the causative organism.

Education: Patient education should center on the cause of the infection and the risk of reinfection/recurrence. Prevention requires avoidance of situations that cause occlusive, warm, moist environments. This can be accomplished by wearing absorbent materials, loose clothing, and open-toe shoes in the summer, and wearing protective footwear in showers and around pools. Patients can be reassured that tinea versicolor is the result of a change in the normal body fl ora and not contagious, and that coloration changes will resolve with treatment. Prophylactic antifungal therapy may be required, especially for tinea pedis, tinea manuum, or onychomycosis.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

A rule for the clinical diagnosis of onychomycosis was developed. Data supported that the rule was at least as accurate as laboratory tests. When dermatologists considered onychomycosis was the most likely diagnosis and plantar desquamation affected >25% of the sole of the foot, treatment could be started without further confi rmation. The rule needs to be validated with primary care practitioners.

B Garcia-Doval et al., 2010

Chapter 6 ■ Skin and Lymphatic Disorders 125

C A S E S T U DY

Mrs. Jones is a 70-year-old woman you are admitting to the skilled nursing facility after a total hip replacement. When you obtain her past medical history, she reports a problem with a chronic rash under her breasts and in her supragluteal fold. She has tried a number of topical antifungal treatments without success. She has never seen a dermatologist. While she fi nds the rash a nuisance and experiences an occasional increase in itchiness, it is something she can live with. Her primary care provider diagnosed the rash as Candida and encouraged her to keep the area clean and dry and to use antifungals. Recently, her 42-year-old daughter was diagnosed with psoriasis and asked about a family history of the disease. Mrs. Jones was unaware of anyone in her or her husband ’ s family with that diagnosis.

On physical examination, you note a shiny, erythematous lesion with symmetrical distribution under both breasts. It is well demarcated without drainage and without the presence of any satellite lesions. Examination of the gluteal fold reveals a similar well-demarcated, shiny, erythematous lesion without drainage. On close inspection of the rest of the body around the umbilicus,

you note an erythematous patch with silvery scale. You ask Mrs. Jones about the lesion, and she states that it has been there for years. The lesion is worse in the winter, but she attributes this to the closures on her skirts and pants causing irritation. She reports some improvement when applying OTC hydrocortisone cream, although when she stops using the cream, the lesion returns. For this case, the answers and rationale for your decision making need to be provided.

1. What clues in Mrs. Jones’ history can help you determine her diagnosis?

2. What signs on physical examination are most helpful to defend or refute the differential?

3. How would you classify the severity of Mrs. Jones’ disease? Be specifi c in your explanation.

4. What would be the treatment(s) of choice in her case?

5. What are some important points to include in patient education?

6. What would require a referral to a dermatologist?

REFERENCES Burns American Burn Association . ( 2014 ). Prevention Campaigns . Retrieved

November 26, 2016 from http://www.ameriburn.org/prevention EdRes.php .

Edkins , R. E. , Hultman , C. S. , Collins , P. , Cairns , B. , Hanson , M. , & Carman , M. ( 2015 ). Improving comfort and throughput for patients undergoing fractionated laser ablation of symptomatic burn scars . Annals of Plastic Surgery , 74 ( 3 ), 293 – 299 . doi:10.1097/SAP .0000000000000367 .

Grant , E. J. ( 2004 ). Burn prevention . Critical Care Nursing Clinics of North America , 16 ( 1 ), 127 – 138 . doi:10.1016/j.ccell.2003.09.005 .

Hartford , C. E. ( 2012 ). Care of the outpatient burn . In D. N. Herndon ( Ed .), Total burn care ( 4th ed. , pp . 81 – 92 ). Edinburgh; New York : Saun- ders Elsevier .

Low , A. J. , Meyer , W. J. , Willebrand , M. , & Thomas , C. R. ( 2012 ). Psy- chiatric disorders associated with burn injury . In D. N. Herndon ( Ed .), Total burn care ( 4th ed. , pp . 733 – 741 ). Edinburgh; New York : Saunders Elsevier .

McIntyre , M. K. , Clifford , J. L. , Maani , C. V. , & Burmeister , D. M. ( 2016 ). Progress of clinical practice on the management of burn-associated

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Oral ketoconazole is not a recommended treatment for dermatophyte infections. Newer antifungals are more effective, and it is the most toxic antifungal with the risk of hepatitis and drug interactions.

A Habif, 2016

A small study of topical Vicks VapoRub applied to nails affected with fungus confi rmed by microscopy and culture was found to be as effective as topical ciclopirox 8%, the only FDA-approved treatment for onychomycosis. Participants were followed for 48 weeks, and the outcome measure was clinical and mycological cure. Patient satisfaction was also measured. The cost of treatment is less than one-fourth that of the prescription treatment.

B Derby et al., 2011

White socks are not useful in the prevention of tinea pedis. The color of the socks does not make a difference; the fabric does. Cotton socks are preferable to synthetics.

C Habif, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

126 Chapter 6 ■ Skin and Lymphatic Disorders

pain: Lessons from animal models . Burns . doi:10.1016/j.burns.2016 .01.023 .

Meyer , W. J. , Wiechman , S. , Woodson , L. C. , Jaco , M. , & Thomas , C. R. ( 2012 ). Management of pain and other discomforts in burned patients . In D. N. Herndon ( Ed .), Total burn care ( 4th ed. , pp . 715 – 731 ). Edinburgh; New York : Saunders Elsevier .

Retrouvey , H. , & Shahrokhi , S. ( 2015 ). Pain and the thermally injured patient: A review of current therapies . Journal of Burn Care and Research , 36 ( 2 ), 315 – 323 . doi:10.1097/bcr.0000000000000073 .

Warner , P. M. , Coffee , T. L. , & Yowler , C. J. ( 2014 ). Outpatient burn management . Surgical Clinics of North America , 94 ( 4 ), 879 – 892 . doi:10.1016/j.suc.2014.05.009 .

Cellulitis Compton , G. A. ( 2013 ). Bacterial skin and soft tissue infections in older

adults . Clinics in Geriatric Medicine , 29 , 443 – 459 . Infectious Disease Society of America (IDSA) . ( 2014 ). Practice guidelines

for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America . Clinical Infectious Disease , 63 ( 4 ). doi:10.1093/cid/ciu296 .

Raff , A. B. , & Kroshinsky , D. ( 2016 ). Cellulitis: A review . Journal of the American Medical Association , 316 ( 3 ), 325 – 337 .

Salmon , M. ( 2015 ). Differentiating between red legs and cellulitis and reviewing treatment options . British Journal of Community Nursing , 20 ( 10 ), 474 – 480 .

Corns and Calluses Curran , M. J. , Ratcliffe , C. , & Campbell , J. ( 2015 ). A comparison of types

and thicknesses of adhesive felt padding in the reduction of peak plantar pressure of the foot: A case report . Journal of Medical Case Reports , 9 , 203 . doi:10.1186/s13256-015-0675-8 .

Melo , M. , Bernecker , T. , McCullough , J. , Hong , J. , Trumbauer , J. S. , & Miller , M. E. ( 2015 ). A pilot study investigating the utilization of crest pads for treatment of toe callus and ulceration . Journal of Vascular Nursing , 33 ( 4 ), 157 – 163 .

Farndon , L. J. , Vernon , W. , Walters S. J. , Dixon , S. , Bradbum , M. , Concan- non , M. , & Potter , J. ( 2013 ). The effectiveness of salicylic acid plasters compared with “usual” scalpel debridement of corns: A randomized controlled trial . Journal of Foot and Ankle Research , 6 , 40 . Retrieved from http://www.jfootankleres.com/content/6/1/40 .

Hashmi , F. , Nester , C. J. , Wright , C. R. F. , & Lam , S. ( 2016 ). The evalu- ation of three treatments for plantar callus: A three-armed random- ized, comparative trial using biophysical outcome measures . Trials , 17 , 251 . doi:10.1186/s13063-0160137 .

Young , M. , & Jones , S. ( Eds .). ( 2015 ). Proceedings from the 15th Annual Scottish Conference of The Diabetic Foot Journal in Glasgow .

Herpes Zoster Beuscher , L. , Reeves , G. , & Harrell , D. ( 2017 ). Managing herpes zoster in

older adults: Prescribing considerations . The Nurse Practitioner , 42 ( 6 ), 24 – 29 .

Binder , A. , Bruxelle , J. , Rogers , P. , Hans , G. , Bosl , I. , & Baron , R. ( 2009 ). Top- ical 5% lidocaine (lignocaine) medicated treatment for post-herpetic neuralgia: Results of a double-blind, placebo-controlled, multinational effi cacy and safety trial . Clinical Drug Investigation , 29 ( 6 ), 393 – 408 .

Cohen , K. R. , Salbu , R. L. , Frank , J. , & Israel , I. ( 2013 ). Presentation and management of herpes zoster (shingles) in the geriatric population . Pharmacy and Therapeutics , 38 ( 4 ), 217 – 227 .

Ganty , P. ( 2014 ). Management of pain in the elderly patient with herpes zoster . Nursing Prescribing , 12 ( 1 ), 32 – 37 .

Gilron , I. , Bailey , J. M. , Tu , D. , Holden , R. R. , Weaver , D. F. , & Houlden , R. L. ( 2005 ). Morphine, gabapentin, or their combination for neuro- pathic pain . New England Journal of Medicine , 352 ( 13 ), 1324 – 1334 .

Hurley , L. P. , Lindley , M. C. , Harpaz , R. , Stokley , S. , Daley , M. F. , Crane , L. A. , . . . Kempe , A. ( 2010 ). Barriers to the use of herpes zoster vaccine . Annals of Internal Medicine , 152 ( 9 ), 555 – 560 .

Irving , G. A. , Backonja , M. N. , Dunteman , E. , Blonsky , E. R. , Vanhove , G. F. , Lu , S. P. , & Tobias , J. ( 2011 ). A multicenter, randomized,

double-blind, controlled study of NGX-4010, a high concentration capsaicin patch for the treatment of postherpetic neuralgia . Pain Medi- cine , 12 ( 1 ), 99 – 109 . doi:10.1111/j.1526-4637.2010.01004.x .

Irwin , M. R. , Olmstead , R. , & Oxman , M. N. ( 2007 ). Augmenting immune responses to varicella zoster virus in older adults: A randomized, con- trolled trial of tai chi . Journal of the American Geriatrics Society , 55 ( 4 ), 511 – 517 . doi:10.1111/j.1532-5415.2007.01109 .

Liang , L. , Li , X. , Zhang , G. , Sun , Y. , Yu , H. , & Jiao , J. ( 2015 ). Pregabalin in the treatment of herpetic neuralgia: Results of a multicenter Chinese study . Pain Medicine , 16 ( 1 ), 160 – 167 . doi:10.1111/pme.12564 .

Lu , P. J. , Euler , G. L. , Jumaan , A. O. , & Harpaz , R. ( 2009 ). Herpes zoster vaccination among adults aged 60 years or older in the United States, 2007: Uptake of the fi rst new vaccine to target seniors . Vaccine , 27 ( 6 ), 882 – 887 .

Oxman , M. N. , Levin , M. J. , Johnson , G. R. , Schmader , K. E. , Straus , S. E. , Gelb , L. D. , . . . Shingles Prevention Study Group . ( 2005 ). A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults . New England Journal of Medicine , 352 ( 22 ), 2271 – 2284 .

Tyring , S. K. , Beutner , K. R. , Tucker , B. A. , Anderson , W. C. , & Crooks , R. J. ( 2000 ). Antiviral therapy for herpes zoster: Randomized, con- trolled clinical trial of valacyclovir and famciclovir therapy in immu- nocompetent patients 50 years and older . Archives of Family Medicine , 9 ( 9 ), 863 – 869 .

Pressure Injuries National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advi-

sory Panel, and Pan Pacifi c Pressure Injury Alliance . Emily Haesler ( Ed .). ( 2014 ). Prevention and treatment of pressure ulcers: Clinical practice guideline . Cambridge Media : Osborne Park, Western Australia .

Psoriasis Ferreira , B. I. R. C. , Abreu , J. L. P. D. C. , Reis , J. P. G. D. , and Figueiredo , A.

M. D. C. ( 2016 ). Psoriasis and associated psychiatric disorders . Clinical and Aesthetic Dermatology , 9 ( 6 ), 36 – 43 .

Gribetz , C. , Ling , M. , Lebwohl , M. , Pariser , D. , Draelos , Z. , Gottlieb , A. B. , . . . Menter , A. ( 2004 ). Pimecrolimus cream 1% in the treatment of intertriginous psoriasis: A double-blind, randomized study . Journal of the American Academy of Dermatology , 51 ( 5 ), 731 – 738 .

Gupta , M. A. , & Gupta , A. K. ( 1998 ). Depression and suicidal ideation in dermatology patients with acne, alopecia areata, atopic dermatitis and psoriasis . British Journal of Dermatology , 139 ( 5 ), 846 – 850 .

Menter , A. , Korman , N. J. , Elmets , C. A. , Feldman , S. R. , Gelfand , J. M. , Gordon , K. B. . . . Bhushan , R. ( 2011 ). Guidelines of care for the treatment of psoriasis and psoriatic arthritis. Section 6. Guidelines of care for the treatment of psoriasis and psoriatic arthritis: Case-based presentations and evidence-based conclusions with topical therapies . Journal of the American Academy of Dermatology , 65 ( 1 ), 137 – 174 . doi: http://dx.doi.org/10.1016/j.jaad.2010.11.055 .

Skin Cancer Guide to Community Preventive Services . ( August 2013 ). Preventing

skin cancer: Interventions in outdoor occupational settings . Retrieved from www.thecommunityguide.org/cancer/skin/education-policy/ outdooroccupations.html .

Superfi cial Fungal Infections Derby , R. , Rohal , P. , Jackson , C. , Beutler , A. , & Olsen , C. ( 2011 ). Novel

treatment of onychomycosis using over-the-counter mentholated ointment: A clinical case series. [Research Support, Non-U.S. Govern- ment.] Journal of the American Board of Family Medicine , 24 ( 1 ), 69 – 74 . doi:10.3122/jabfm.2011.01.100124 .

Garcia-Doval , I. , Cabo , F. , Monteagudo , B. , Alvarez , J. , Ginarte , M. , Rodríguez-Alvarez , M. X. , . . . & Florez , A. ( 2010 ). Clinical diagnosis of toenail onychomycosis is possible in some patients: Cross-sectional diagnostic study and development of a diagnostic rule . British Journal of Dermatology , 163 ( 4 ), 743 – 751 .

Habif , T. P. ( 2016 ). Superfi cial fungal infections . Clinical dermatology ( 6th ed .). St. Louis, MO : Elsevier .

127

CHAPTER 7 Head, Neck, and Face Disorders

Lori Martin-Plank

ASSESSMENT

A systematic and thorough examination of the head and neck begins with the inspection of the face, head, and scalp. Assess the shape, size, and symmetry of the patient ’ s fea- tures. Examine the shape of the skull, palpating the bones of the head for any anatomical irregularities, masses, or areas of tenderness. Inspect the hair for distribution, quantity, and any balding patterns, noting any uniform alopecia, nits, or seborrhea. The scalp should be carefully inspected for any skin lesions on sun-exposed areas, noting pigment changes, tenderness, scales, or lumps. Assess for scars or bruising patterns. Note the symmetry of the patient ’ s features, facial expressions, the presence of involuntary tics or tremors, peri- orbital edema, or facial drooping; palpate over the temples for any abnormality or tenderness in the temporal arteries. The presence of pain and nodules on palpation is not a normal fi nding even in very old individuals. Cranial nerve VII (facial nerve) should also be assessed at this time, noting any facial asymmetry, weakness, drooping of the lower eyelid, and uni- lateral paralysis (Bickley & Szilagyi, 2012; LeBlond, Brown, Suneja & Szot, 2015).

Eyes Begin the inspection of the eyes by noting the position and symmetry of the surrounding skin and tissue, as well as the presence and position of the eyebrows and eyelashes. Screen visual acuity before proceeding with any other examination of the eye. Using a Snellen chart from 20 feet, or a hand- held chart approximately 12 inches from the patient, assess visual acuity in each eye separately, then together; if the patient wears corrective lenses, he or she should have them on for this test. Note the condition of the skin around the eyes, check the sclera, and note the color of the conjunctiva. Assess the presence of exophthalmos, xanthelasma, pinguec- ula, ptosis, edema, and skin lesions. The lids should be care- fully examined for the presence of hordeolum, chalazion, ectropion, and entropion, which is most common among elderly persons. Examine the cornea for any scarring, pres- ence of pterygium, corneal arcus, and opacities. Note that basal and squamous cell carcinomas are common around the

eye. Palpate for any tenderness over the lacrimal gland and assess the patency of the lacrimal duct. Examine the extraoc- ular motions of the eye (cranial nerves III, IV, and VI). Check the visual fi elds (cranial nerve II), corneal refl exes (cranial nerve V), and pupillary reactions (cranial nerves II and III) with direct and consensual reactions. Carefully perform a funduscopic examination; most elderly patients need dilation for accurate assessment of the fundus. If you see the fundus, note the narrow, pale appearance of the arterioles common in elderly persons. Be careful to note any abnormalities in blink- ing (Parkinson ’ s disease), dull or blank staring (hypothyroid- ism), residual facial paralysis (Bell ’ s palsy or cerebrovascular accident), and skin changes. Decreased elasticity and turgor is a normal aging pattern; the skin around the eyes becomes thin and wrinkles appear. This is a normal change in older adults and makes skin turgor a poor determinant of hydra- tion status (Bickley & Szilagyi, 2012; LeBlond et al., 2015).

Sinuses Inspect and palpate over the frontal and maxillary sinus areas. Note any gross tenderness or infl ammation in the sinus area or around the eyes.

Nose Inspect the external nose for any asymmetry, infl ammation, gross septal deviation, or deformities. If applicable, assess the function of the olfactory nerve (cranial nerve I) by having the patient identify a familiar-smelling item with the eyes closed. The olfactory sense greatly diminishes as a normal part of aging. Assess for patency of each nostril. Examine the inter- nal nose, noting any discharge, bleeding, or edema. Check the status of the turbinates and position of the septum using a large otoscope speculum. The color and consistency of the inferior and middle turbinates as well as the presence of any polyps should be noted (Bickley & Szilagyi, 2012).

Ears Carefully examine the external ears, noting their position and symmetry on the head, as well as any abnormal lesions, defor- mities, and the presence of tophi, keloids, or cysts. Estimate auditory acuity (cranial nerve VIII) by using the whisper test, testing each ear separately. Use the Weber and Rinne tests

128 Chapter 7 ■ Head, Neck, and Face Disorders

to assess for any conductive or sensorineural hearing loss. Palpate the tragus for any tenderness, as well as for any pre- auricular or postauricular adenopathy. When examining the middle ear, note any infl ammation, discharge, erythema, or cerumen in the canal. If visible, inspect the tympanic mem- branes and surrounding landmarks for abnormalities. Note any foreign bodies, dull membranes, alterations in the cone of light refl ex, and presence of fl uid or scarring. Be careful to inspect the posterior ear and helix for any skin lesions or carcinomas (LeBlond et al., 2015).

Oral Cavity Perform a complete assessment of the lips, mouth, oral mucosa, and pharynx, noting the color, moisture, and pres- ence of any abnormal lesions on and around the lips. Assess for any herpes simplex I, chancres, angular stomatitis, mucous retention cysts, angioedema, and fi ssures. Check oral mucosa for color, nodules, ulcers, or white patches (Bickley & Szilagyi, 2012). If the patient has dentures, these should be removed to do a complete oral examination. Examine the fi t of the dentures and assess the consistency of the gums under the dentures. If natural teeth are present, note any loose or broken teeth as well as caries. Because periodontal disease is the primary cause of tooth loss in the adult, do a careful oral and gum examination. Examine the gums for bleeding, discoloration, swelling, and retractions. Note the attrition of the teeth (exposed dentin) and enamel loss from years of chewing.

Note the condition of the hard palate and the presence of torus palatinus, thrush, or other lesions. Assess the gag refl ex and rise of the palate (cranial nerves IX and X). Care- fully examine the tongue for symmetry, enlargement (hypo- thyroidism), growths, protrusions, or abnormal movements (cranial nerve XII) and the dorsum for any papillary atrophy. A swollen, red, painful tongue may indicate vitamin B or ribofl avin defi ciency. Note any infl ammation or obstruction in the parotid (Stensen) or submaxillary (Warton) ducts.

Thoroughly examine the area underneath the tongue, the fl oor of the mouth, and the tonsils, soft palate, uvula, and pos- terior pharynx, noting any lesions, infl ammation, or exudate and the color. Examine the strength and movement of the temporal and masseter muscles (cranial nerve V), as well as any crepitus in the mandible junction. Complete assessment should also include evaluation of the voice (cranial nerve X) and speech (cranial nerves V, VII, X, and XII).

Neck Inspect the neck for symmetry, masses, scars, tracheal posi- tion, and deviation. Look for the presence of thyroid infl am- mation or goiters. Carefully palpate for any lymphadenopathy, noting that loss of lean muscle makes it easier to feel nodes in the cervical region of elderly persons. Assess supracla- vicular, tonsilar, superfi cial, deep, and posterior cervical chains and submaxillary, submental, occipital, preauricular, and postauricular nodes, noting any infl ammation, tender- ness, or change in size, position, or shape. Hard, fi xed nodes imply malignancy; tender nodes are typical of infl ammation (Bickley & Szilagyi, 2012). Gently palpate and auscultate the carotid arteries one side at a time for any nodularity or bruits. Note any jugular vein distention that occurs when the patient is seated. Check to see if the patient uses any neck muscles to breathe. Carefully inspect and palpate the thyroid gland, noting any infl ammation or nodules (unilateral). Exam- ination of the range of motion of the neck should include fl exion, extension, rotation, and lateral bending. Check the strength of the trapezius and sternomastoid muscles (cranial nerve XI).

A complete and thorough detailed examination of the head and neck has the potential to allow the examiner to dis- cover multiple variants from the normal. Develop a clear and concise pattern of examination to ensure appropriate eval- uation of these areas. Keep in mind the normal variants of the older person and how these differ from pathological or abnormal fi ndings.

Signal Symptoms: Diminished vision in one or both eyes, poor night vision, sensitivity to glare. Because progression is gradual, changes may go unnoticed until visual loss is advanced.

Description: A cataract is an opacifi cation of the lens that interferes with the passage of light through the lens, decreas- ing visual acuity. The location, size, and density of this opacity infl uence the degree of visual impairment (Harper, 2018; Liu et al., 2017). Nuclear sclerotic cataracts affect contrast sensitivity, progress slowly, and tend to preserve functional reading vision while frequently causing nearsight- edness. In contrast, posterior subcapsular cataracts progress more rapidly and interfere with reading vision.

Etiology: Most cataracts are related to the aging process. The gradual thickening or hardening in the lens is believed to be caused by oxidative damage to the lens protein.

Occurrence: The rate of visually signifi cant cataracts in persons 50 to 59 years old is 6.8%. Of persons over 80 years old, 68.3% have cataracts (Harper, 2018). Cataracts tend to be bilateral, although the rate of progression varies between the eyes.

Age: Although subtle changes in visual acuity related to cat- aract formation occur by age 50, people over 75 years old experience most visually signifi cant cataracts.

Gender: Cataracts occur equally in men and women.

Ethnicity: Not signifi cant.

Contributing Factors: Diabetes mellitus, hypertension, poor nutrition, cigarette smoking, high alcohol intake, trauma to the eye, long-term exposure to ultraviolet (UV) B radi- ation (sunlight), and a strong family history of cataracts are risk factors. Use of certain substances, including oral

CATARACT

Chapter 7 ■ Head, Neck, and Face Disorders 129

glucocorticoids, also contributes to cataracts. An association between cataracts and glaucoma and intraocular infl amma- tion exists ( Jacobs, 2016 ).

Signs and Symptoms: The patient with a cataract initially may present with an improvement in near vision, requiring a new prescription for corrective lenses; distance vision will worsen (Harper, 2018). Patients also may experience blurred vision or sensitivity to glare from bright light or from automobile headlights during night driving. Complaints of having dif- fi culty reading and distinguishing contrast sensitivities and of seeing a yellow tint or washed-out colors are common. Some patients may not seek evaluation of their symptoms by a health-care provider owing to denial or fear of loss of independence (driver ’ s license being revoked), whereas other patients seek prompt assessment in the hope of early inter- vention. A recent history of falls, accidents, or injury is suspi- cious. On physical examination, visual acuity test results are abnormal for one or both eyes (evaluate near and distance vision). Examine the eye using an opaque light for opacifi ca- tion of the lens. The cataract may be visible to the naked eye. The red refl ex may be absent, or the cataract may appear as a black area.

Diagnostic Tests: No diagnostic testing is required other than that for visual acuity and examination of the eye, unless other visual problems are suspected. Refer the patient to an ophthalmologist for complete evaluation after initial screen- ing. Pupillary dilation and slit lamp examination will reveal white, gray, or brownish opacities if the cataract is developed. Dark areas on the red refl ex in a dilated eye indicate small cataracts; the red refl ex may not be visible if the cataract is large ( Jacobs, 2016 ).

Differential Diagnosis:

■ Corneal scarring ■ Retinal detachment ■ Macular degeneration ■ Chronic glaucoma ■ Diabetic retinopathy

Treatment: Treatment is determined after full evaluation by the ophthalmologist. Ultimately, surgical intervention is required with extraction of the cataract and immediate implantation of a plastic intraocular lens, unless contrain- dicated by other disease conditions ( Thompson & Lakhani, 2015 ). Standard treatment is phacoemulsifi cation. Recently, laser has been added to assist with this, but outcomes are no better with laser (Day, Gore, Bunce, & Evans, 2016). A variety of types of implantable lenses are used depending on patient vision assessment and lifestyle. These include lenses that adjust for astigmatism and refractive errors. Patients with posterior capsular opacifi cation may require neodymium:yt- trium-aluminum-garnet (Nd:YAG) laser capsulotomy. This should not be performed at the same time as other cataract surgery. Collaboration with the ophthalmologist is indicated for patients with severe cardiac, respiratory, or neuromuscu- lar conditions that may prevent the patient from lying still or supine as required during the surgery. Patients with dia- betes and hypertension should be instructed in medication use preoperatively. Patients receiving anticoagulant therapy also should be managed collaboratively and individually. Patients on clopidogrel after cardiac stent are encouraged to delay surgery until the clopidogrel is no longer needed ( Jacobs, 2017 ). There is no hard and fast rule for patients

on aspirin or warfarin maintenance ( Jacobs, 2017 ). Patients receiving anticoagulant therapy also should be managed col- laboratively and individually. Patients who are or have been on alpha receptor therapy, such as tamsulosin for prostatic enlargement, may experience intraoperative fl oppy iris syn- drome (IFIS). Treatment of these patients may require special techniques during surgery to prevent this (Olson et al., 2016; Thompson & Lakhani, 2015 ). Although still considered an alternate practice pattern, intracameral antibiotic injection during surgery is becoming more common and has been shown to reduce rates of endopthalmitis (Hashemian et al., 2016; Herrinton et al., 2016; Javitt, 2016).

The degree of visual impairment and its infl uence on the patient ’ s usual daily functioning determine the timing of the surgery (Preferred Practice Panel-Cataract, 2016; Thompson & Lakhani, 2015 ). Initially, a conservative treatment plan may include a prescription for glasses and periodic reevalu- ation by the ophthalmologist, coupled with a plan for envi- ronmental safety and optimization of the patient ’ s functional abilities within his or her visual limitations. Surgery is per- formed in an outpatient or short procedure unit, with the patient returning home immediately after discharge. With the advent of multifocal implantable lenses and toric lenses for astigmatism, glasses may not be required after surgery, however, insurers currently only support monofocal lenses. More research needs to be done before multifocal lenses are perfected (Alio et al., 2017; deSilva et al., 2016; Harper, 2018; Lawless et al., 2016; Thompson & Lakhani, 2015 ).

Follow-Up: Immediate postsurgical care includes eye pro- tection and application of topical agents prescribed by the ophthalmologist. The patient may be cautioned to avoid straining, lifting, or bending. Postoperative follow-up is usually within 24 to 48 hours. The family or health-care team should heighten precautions for environmental safety to avoid injury. Intensive supervision of mentally compro- mised patients is required to prevent damage to the operative site. Future follow-up includes a reevaluation of visual acuity, prescription of corrective lenses if indicated, and monitoring of the unaffected eye for cataract development.

Sequelae: Possible sequelae to cataract surgery include faulty wound closure with aqueous humor leakage, blindness sec- ondary to choroidal hemorrhage, endophthalmitis, toxic anterior segment syndrome (TASS), infl ammation, retinal detachment, prolapse of the iris into the corneal wound, and secondary glaucoma (Preferred Practice Panel-Cataract, 2016; Thompson & Lakhani, 2015 ).

Prevention/Prophylaxis: The patient should be protected from exposure to UVB radiation by wearing sunglasses designed for this and by wearing a hat with a wide brim.

Referral: After the initial visual screening, refer the patient to an ophthalmologist for complete examination and treatment, including postsurgery follow-up.

Education: Provide the patient with information on age-re- lated visual changes and the importance of protecting the eyes from sunlight with UV-blocking sunglass lenses; main- taining a nutritionally balanced diet including green, leafy vegetables; avoiding tobacco and high alcohol intake; and having periodic eye examinations every 2 years. Instruct the patient to seek prompt evaluation of any vision changes, and reassure the patient that with proper treatment cataracts do not result in permanent loss of visual acuity ( Jacobs, 2017 ).

130 Chapter 7 ■ Head, Neck, and Face Disorders

Signal Symptoms: Bleeding from the nose or into the posterior nasopharynx.

Etiology: Ninety percent of the time the bleeding is the result of a spontaneous rupture of a blood vessel in the anterior septum in Kiesselbach ’ s plexus (Morgan & Kellerman, 2014). Local causes of epistaxis include trauma, irritation or infl am- mation of the nasal mucosa, a septal defect, or paranasal tumors. Systemic causes include arteriolosclerosis, hemato- logical disorders, or hereditary hemorrhagic telangiectasias (Nguyen, 2016; Scott, 2014). Approximately 10% of nose- bleeds are idiopathic.

Occurrence: Most people have at least one episode of minor, nonrecurring epistaxis. Because self-treatment is often effec- tive and the episode is not reported, statistical data are scarce. Several sources indicate a lifetime incidence of 60% with fewer than 10% requiring medical intervention (Morgan & Kellerman, 2014; Nguyen, 2016). Typically, people older than age 50 years have more serious bleeding that requires medical attention (Morgan & Kellerman, 2014).

Age: Epistaxis occurs most frequently in young children and in elderly persons (Nguyen, 2016).

Gender: Epistaxis occurs more frequently in males than in females (Nguyen, 2016).

Ethnicity: Not signifi cant.

Contributing Factors: Local trauma to the anterior por- tions of the nose (digital, as in nose picking, and blunt, as in nasal fractures) is usually the cause of epistaxis. Low humidity in desert climates or from central heating, foreign bodies, intranasal polyps or neoplasms, irritants (smoking),

intranasal steroids, infl ammation from rhinosinusitis, and systemic medications such as NSAIDs, anticoagulants, and antiplatelets may contribute secondarily to the occurrence of epistaxis. Septal abnormalities also are contributing factors. Systemic diseases including hypertension; bleeding disorders such as aplastic anemia, leukemia, and thrombocytopenia; liver disease; and hereditary coagulopathies may contribute to the occurrence of epistaxis (Blomgren, 2014; Morgan & Kellerman, 2014; Nguyen, 2016).

Signs and Symptoms: Usually no signs or symptoms are associ- ated with epistaxis other than external bleeding or an aware- ness of blood dripping down the posterior nasopharynx.

Diagnostic Tests: No laboratory studies are indicated for minor and nonrecurring epistaxis. For more substantial or recurrent epistaxis, a complete blood count (CBC) includ- ing platelet count, bleeding time, prothrombin time (PT), and partial thromboplastin time may be useful. In a patient who is on warfarin therapy, an international normalized ratio (INR) should be drawn if epistaxis occurs (Ruhl & Swindell, 2015). If bleeding is severe and the need for blood replacement is anticipated, type and crossmatch also should be done.

Differential Diagnosis:

■ Trauma ■ Infl ammation due to rhinitis or infection ■ Vascular disorders ■ Clotting disorders and blood dyscrasias ■ Intranasal foreign bodies ■ Hereditary telangiectasia ■ Tumors

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

There is no evidence from randomized, controlled trials (RCTs) that supplementation with antioxidant vitamins (beta carotene, vitamin A, or vitamin E) prevents or slows the progression of age-related cataract.

A Olson et al., 2016

The decision to recommend cataract surgery should be based on consideration of the following factors: visual acuity, visual impairment, and the potential for functional benefi ts.

B Thompson & Lakhani, 2015 Olson et al., 2016

Ophthalmologists and other physicians managing patients taking alpha antagonists should be aware of the risks of intraoperative fl oppy iris syndrome (IFIS).

B Jacobs, 2017 Thompson & Lakhani, 2015

Extracapsular cataract surgery by phacoemulsifi cation with intraocular lens (IOL) implantation provides safe and effective treatment for patients with cataract.

A Olson et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

EPISTAXIS

Chapter 7 ■ Head, Neck, and Face Disorders 131

Treatment: Most episodes of epistaxis are mild and self-lim- ited, resolving spontaneously. Epistaxis may be controlled by pinching the nostrils together for 5 to 10 minutes, keeping the patient in an erect sitting position with head tilted forward to prevent blood from going down the posterior nasopharynx. Anterior bleeding that does not stop with manual pressure alone may be controlled with two sprays of oxymetazolone 0.05% applied directly to the bleeding site followed by 10 to 15 minutes of manual pressure (Morgan & Kellerman, 2014). The mucous membrane can be topically anesthetized with 4% lidocaine, and a silver nitrate stick then applied to the bleeding site once it is located. Other devices include nasal tampons such as Merocel or balloons for packing (Scott, 2014). The user must be skilled in handling these devices properly. If packing is needed, adequate pain management must be prescribed and it should be removed within 2 to 3 days (Ruhl & Swindell, 2015).

Follow-Up: For recurrent episodes, follow-up visits are rec- ommended as needed. If medications have been implicated as likely causes, follow-up by a home health nurse for medi- cation management education may be helpful. Posterior epi- staxis, comorbidities, or recurrent bleeding may necessitate admission or referral to an ear, nose, and throat (ENT) spe- cialist for management (Ruhl & Swindell, 2015).

Sequelae: Anemia can be a complication of excessive or fre- quent bouts of epistaxis. Infection can result from nasal packing. Severe blood loss can exacerbate existing diseases. Older patients must be assessed for dyspnea, chest pain/pres- sure, and syncope (Morgan & Kellerman, 2014).

Prevention/Prophylaxis: Discourage patients from nose picking and rubbing, and excessive forceful blowing of the nose;

advise them to increase the humidity in the home, especially in winter months. Some patients may be prescribed bacitra- cin, saline gel, or petrolatum to apply twice weekly in the area of Kiesselbach ’ s plexus (Nguyen, 2016; Scott, 2014).

Referral: Consultation with an ENT specialist is indicated for the following conditions:

■ Bleeding that is not controlled after 15 minutes of compression

■ Evidence of massive bleeding ■ Recurrent bleeding within the fi rst hour ■ Second episode of epistaxis within 1 week ■ Uncontrolled bleeding from the posterior nasopharynx

The consulting physician may initiate interventions, such as the insertion of Merocel nasal tampons or an intranasal balloon to control bleeding. Intractable epistaxis may require transantral arterial ligation or embolization (Nguyen, 2016).

Education: Discourage picking of the nose and advise patients to increase the humidity in the home, especially in winter months, by means of a humidifi er. Petrolatum or saline gel may be rubbed over the nasal septum twice daily to decrease dryness of mucosa. Teach the patient how to manage simple epistaxis at home, with instructions to seek medical atten- tion for excessive (bleeding for more than 1 hour) or recur- rent epistaxis. Use of nasal saline spray for humidifi cation is encouraged. Prolonged hot showers and hot, spicy foods should be avoided. Instruct the patient to avoid nose blowing and to open the mouth when sneezing (Nguyen, 2016).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Simple measures are helpful in stopping most nosebleeds: nose blowing to clear clots, pinching the nose for 15 minutes, and topical decongestants.

C Ruhl & Swindell, 2018

Cauterizing visible bleeding vessels with silver nitrate (AgNO 3 ) or electrocautery are equally effective.

B Ruhl & Swindell, 2018

Patients with resistant or posterior bleeds are likely to need posterior packing, surgery, or embolization.

C Ruhl & Swindell, 2018

Routine coagulation tests for epistaxis are not useful unless the patient is taking an anticoagulant.

B Ruhl & Swindell, 2018

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

132 Chapter 7 ■ Head, Neck, and Face Disorders

Glaucoma encompasses several different eye diseases charac- terized by progressive neuropathy of the optic disc, leading to loss of vision. The optic disc is composed of vascular, neural, and connective tissue. The axons of the retinal ganglion cells form a rim around a shallow cup in the optic disc. Apopto- sis of the ganglion cells of the retina leads to a thinning of the nerve fi bers in the inner layer and axons, with atrophy of

the disc and the appearance of cupping or expansion of the cup/disc ratio (Salmon, 2017; Weinreb, Aung, & Medeiros, 2014 ). The two most common glaucomas are primary angle closure with acute or chronic closure and primary open- angle (POAG). Current research has identifi ed specifi c genetic associations, but research in this area is ongoing.

GLAUCOMA, ACUTE AND CHRONIC

GLAUCOMA, ACUTE (PRIMARY ANGLE-CLOSURE)

Signal Symptoms: Unilateral eye pain, visual blurring with halos around lights, conjunctival injection, and photopho- bia; nausea and vomiting may also occur. Approximately two-thirds of patients with angle-closure glaucoma will have vision loss without experiencing an acute episode.

Description: Acute glaucoma, also known as angle-closure or narrow-angle glaucoma , is an obstruction to the outfl ow of aqueous humor from the posterior to the anterior chamber through the trabecular meshwork, canal of Schlemm, and associated structures. It typically results in an elevation of intraocular pressure, damaging the optic nerve and causing loss of peripheral vision, eye pain, and redness. This type of glaucoma is uncommon but may occur as a primary disease or secondary to other conditions, and constitutes an ophthal- mic emergency ( Hoffman, 2018 ; Salmon, 2017; Weinreb et al., 2014 ). Associated presenting symptoms may compli- cate diagnosis or result in misdiagnosis.

Etiology: The precise pathophysiology of angle-closure glau- coma is unknown. It is a disorder of the lens, iris, and retro- lenticular system. In the acute form, pupillary blockage limits the progress of the aqueous humor through the trabecular network. The peripheral iris, which blocks the trabecular meshwork, is displaced forward (Mantravadi & Vadhar, 2016; Weinreb et al., 2014 ).

Occurrence: Uncommon; accounts for 10% of all glaucoma. This is more common in families with prior history.

Age: The predominant age range for acute glaucoma is 60 to 70 years old.

Gender: Acute glaucoma occurs more often in women.

Ethnicity: Acute and primary angle-closure glaucoma are more common in Inuit and Asian populations.

Contributing Factors: Contributing factors include an ana- tomically narrow anterior chamber angle, requiring identifi - cation with the use of a special examination technique called gonioscopy . This examination technique is beyond the scope of the primary care practitioner, but the condition can be evaluated during the comprehensive eye examination. Other risk factors include hyperopia; small cornea; shallow ante- rior chamber; Asian ancestry; female gender; family history of glaucoma (fi rst-degree relatives have a 2% to 5% risk over

a lifetime); and use of antihistamines, a/b-Adrenergic ago- nists, tricyclic antidepressants, SSRIs and SNRIs, anticholin- ergics and cholinergic agents—these drugs may precipitate an acute episode (Mantravadi & Vadhar, 2016; Prum et al., 2015).

Signs and Symptoms: The presentation is often dramatic, but the diagnosis can be missed because of the associated symptoms. The history reveals severe, unilateral eye pain; blurred vision; lacrimation; reports of seeing colored halos around lights; and a red eye. Headache, nausea, and vomit- ing frequently accompany eye pain, causing eye pain to be overlooked. Emotional stress also is common. Examination reveals circumcorneal, conjunctival injection, tearing, and a fi xed mid-dilated pupil that is nonreactive to light; the cornea is steamy or cloudy. Visual acuity, if evaluated, shows a loss in the affected eye.

Diagnostic Tests: Immediately refer patients for a complete ophthalmic examination (Mantravadi & Vadhar, 2016; Weinreb et al., 2014 ).

Differential Diagnosis:

■ Conjunctivitis ■ Hyphema ■ Uveitis ■ Corneal trauma or infection

Treatment: The patient with acute glaucoma needs an imme- diate consultation with and referral to an ophthalmologist. Permanent visual loss occurs within 2 to 5 days if this con- dition is untreated. Surgical treatment includes peripheral iridectomy or laser iridotomy. Intraocular pressure must be lowered preoperatively, which may require the use of an osmotic diuretic intravenously or orally and miotic eye drops. As the primary health-care provider, you must communicate to the specialist any medical conditions that need monitoring with the use of these agents. Bilateral treatment is indicated, because patients are at risk for developing the same problem in the other eye (Mantravadi & Vadhar, 2016; Prum et al., 2015)

Follow-Up: The ophthalmologist treating the patient deter- mines follow-up treatment. Periodic eye examinations are recommended by preventive guidelines.

Chapter 7 ■ Head, Neck, and Face Disorders 133

Sequelae: If treated promptly, acute glaucoma is not asso- ciated with sequelae. If untreated, permanent visual loss occurs.

Prevention/Prophylaxis: Knowing the risk factors for acute angle-closure glaucoma, the health-care provider should educate patients about those risk factors (see under Edu- cation). Periodic eye examinations are recommended for prevention.

Referral: Refer the patient immediately on presentation and evaluation of symptoms.

Education: Teach patients with known risk factors (see under Contributing Factors) the importance of regular eye exam- inations and reporting of symptoms.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Acute angle-closure glaucoma is an ocular emergency that requires immediate lowering of IOP with topical/oral/parenteral medications, usually followed by iridectomy or laser iridotomy.

A Prum et al., 2016

For acute angle-closure glaucoma, topical and systemic agents are usually necessary to adequately decrease the IOP, and laser iridotomy is the defi nitive surgical treatment.

A Prum et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

GLAUCOMA, CHRONIC (PRIMARY OPEN-ANGLE)

Signal Symptoms: None initially: silent; tunnel vision, night blindness, halos around lights.

Description: Chronic open-angle or primary open-angle glaucoma is an insidious optic neuropathy characterized by increased intraocular pressure (IOP) severe enough to damage the optic nerve. Progressive over time with a gradual visual fi eld loss, chronic glaucoma is called the silent blinder , because it often goes unnoticed until the later stages. Variants occur in which IOP does not increase, but the optic nerve still becomes damaged; this is termed normal tension glaucoma and is common in Asian populations ( Jacobs, 2016 ; Mantravadi & Vadhar, 2016; Salmon, 2017). Conversely, some patients have increased IOP but show no optic nerve changes or visual defects; these are referred to as glaucoma suspects (Prum et al., 2015) or those with ocular hypertension (Mantravadi & Vadhar, 2016)). Secondary glaucomas are the result of prior or concurrent ocular disease or trauma; they may have open angles caused by steroid-induced pressure increases.

Etiology: The etiology of chronic glaucoma is unknown, but the disease is associated with increased IOP, optic nerve degeneration, and visual fi eld loss. Because IOP is the one factor that can be measured, most reevaluation and treat- ment decisions are infl uenced by this measurement (Mantra- vadi & Vadhar, 2016).

Occurrence: Prevalence of chronic glaucoma increases in persons over 40 years old, approaching 15% by age 75; 80% of cases are the open-angle type. Primary open-angle glaucoma causes 15% to 20% of all blindness in the United States and is the primary cause of blindness in African Amer- icans (Salmon, 2017). In 2010, there were 2.8 million in the

United States with POAG and this is predicted to rise to 3.4 million by 2020 ( Jacobs, 2016 ).

Age: The incidence increases in persons over 40 years old, with another increase in incidence in persons between ages 60 and 75 years. Onset is earlier in African Americans.

Gender: Chronic glaucoma occurs equally in both men and women.

Ethnicity: African Americans, Afro-Caribbeans, and Hispan- ics are at a higher risk than the general population for devel- oping chronic glaucoma (Salmon, 2017).

Contributing Factors: Risk factors include older age, a positive family history, African American ancestry or Latino/Hispanic ethnicity, type 2 diabetes mellitus, hypertension, myopia, low ocular perfusion, thinner central cornea, and genetic muta- tions ( Jacobs, 2016 ). There is some association with migraine headache, but further research is needed to confi rm this. Risk factors for secondary open-angle glaucoma include long- term use of topical or oral corticosteroids. It is important to note if the patient had prior LASIK surgery, because this can alter corneal thickness. Cataract surgery can also lower IOP, so this history is essential ( Mantravadi & Vadhar, 2015 ).

Signs and Symptoms: The disease is asymptomatic in the early stages. By the time symptoms develop, signifi cant neural damage has occurred. Eye health specialists frequently dis- cover chronic open-angle glaucoma during routine eye examinations. Patients may present with a complaint of blurred vision, a request for new corrective lenses, or occa- sionally a report that they see a halo around lights ( Jacobs, 2016 ; Weinreb et al., 2014 ).

134 Chapter 7 ■ Head, Neck, and Face Disorders

On routine vision screening, visual acuity may be normal or unchanged from previous screening; visual fi elds may be decreased, however. The skilled examiner may detect changes in the cup-to-disc ratio on funduscopic examination—a cup with a diameter of more than 50% of the vertical disc diam- eter is highly suspect for glaucoma ( Jacobs, 2016 ). Because it is diffi cult to perform a funduscopic examination on older patients without the benefi t of a mydriatic agent, referral for specialized ophthalmological examination is essential. The ophthalmological examination may reveal increased IOP or signs of optic nerve damage without increased pressure.

Diagnostic Tests: Visual acuity should be measured and compared with prior measurements; pupillary assessment should be included. A dilated funduscopic examination and slit lamp examination of the anterior segment is conducted, assessing cup-to-disc ratio, asymmetry between discs, or other abnormalities. Applanation tonometry with the Gold- mann applanation criterion standard should be measured to determine IOP. IOP has a circadian rhythm and is highest in the morning. Time of day, method, and measurements in both eyes are noted and compared with any prior measure- ments. If glaucoma is suspected, pachymetry should be used to measure central corneal thickness. If corneal thickness is outside of an established normal range, an adjustment in the IOP number is made based on this, raising or lowering the number. Because a thin central cornea is a risk factor, those with thicker central corneas but increased IOP have a cor- rection factor calculated into the adjusted IOP (Prum et al., 2015).

Automated visual fi eld testing is done to rule out any visual fi eld defi cits (visual fi eld assessment by confrontation is of no value) ( Jacobs, 2016 ). Gonioscopy is done to rule out other causes of IOP increase, including angle-closure glau- coma. Various imaging modalities, including fundus pho- tography, optical coherence tomography, and scanning laser polarimetry, are used to preserve a permanent visual picture of the optic disc and are to be repeated later for comparison or evidence of disease progression ( Jacobs, 2016 ).

Differential Diagnosis:

■ Cerebral neoplasia ■ Other optic neuropathies ■ Vascular occlusive disease ■ Trauma

Treatment: Chronic open-angle glaucoma cannot be cured. The goal of treatment is to halt progression of the disease and preserve existing vision as follows:

■ IOP control within an identifi ed range ■ Stable visual fi elds ■ No further progression of optic nerve damage

Mainstay treatment modalities include:

■ Topical eye drops that reduce aqueous production or encourage outfl ow

■ Laser trabeculoplasty ■ Trabeculectomy or fi ltering surgery

Medical treatment with eye drops is usually fi rst-line therapy, unless there are contraindications. Consultation between primary care provider and ophthalmologist may be indicated for patient safety and accurate identifi cation of comorbidities and current medications ( Table 7-1 ).

If topical ophthalmic agents do not effectively lower IOP, systemic carbonic anhydrase inhibitors are added. These also may be used before surgery to lower the IOP. If medical therapy is unsuccessful, selective laser trabeculoplasty or fi l- tration surgery (trabeculectomy) to improve aqueous outfl ow is indicated. The laser treatment is considered for elderly patients who cannot tolerate surgery, although the outcome is not as desirable as with surgery. In either case, medication still may be required after surgery ( Jacobs, 2017 ; Prum et al., 2015).

The U.S. Food and Drug Administration (FDA) has approved the use of a miniscule device called the Glaukos iStent ® Trabecular Micro-Bypass Stent for patients with glau- coma and cataract. At the conclusion of cataract surgery, this stent is inserted into the canal of Schlemm, allowing the aqueous humor to bypass trabecular obstruction and drain directly from the anterior chamber into Schlemm ’ s canal, lowering IOP ( Jacobs, 2017 ; Mantravadi & Vadhar, 2015 ).

Follow-Up: Monitor patients for compliance with the treat- ment regimen. If eye drops are used, ensure that the patient can instill these, or teach a family member or neighbor to do it. Monitor medications for adverse effects; the range and frequency of side effects to glaucoma medications are signif- icant. Ensure that patients have regular ophthalmological follow-up visits. If visual loss is severe, evaluate the environ- ment for safety and risk of falls or injury. If the patient is still a licensed motor vehicle operator, driver ’ s license retesting may be indicated in the interest of public safety.

Sequelae: If initial presentation is monocular, the other eye may become affected. Changes in the patient ’ s overall health may have implications for the treatment plan.

Prevention/Prophylaxis: The U.S. Preventive Services Task Force (USPSTF) found insuffi cient evidence to recommend screening for glaucoma ( USPSTF, 2013 ). Primary care pro- viders need to be aware of risk factors and discuss these with patients who have not been diagnosed but are at risk. Patients who are glaucoma suspects or have actual primary open-angle glaucoma must be reminded of the need for eye examinations, continued monitoring, and adherence to the prescribed regimen. African Americans should have peri- odic eye examinations every 3 to 5 years, beginning at age 40 years. Anyone with a family history of glaucoma should have an annual eye examination, beginning at age 40 years. Patients with hypertension or diabetes should have regular eye examinations, as recommended by their health-care pro- vider. All patients over 65 years old should have annual eye examinations (Prum et al., 2015).

Referral: Refer patients initially for ophthalmological exam- ination and diagnosis. Collaborate on the management plan if the patient has signifi cant medical conditions that affect treatment options, particularly pharmacological choices. Refer patients for periodic follow-up eye examinations or for treatment of complications if they arise.

Education: Educate the patient about the chronic and progres- sive nature of the disease, the need to follow the treatment regimen as prescribed, and the need for regular follow-up eye examinations and reporting of symptoms, if any. Reas- sure the patient that, although the disease is not curable, it can be managed. Educate patients with known risk factors about the need for eye examinations despite the absence of

Chapter 7 ■ Head, Neck, and Face Disorders 135

symptoms. Asymptomatic patients may question the need for regular treatment. Explain that treatment is preventing disease progression, which is why there are no symptoms.

The frequency or complexity of the medication regimen may infl uence compliance. Reinforce the role of medication in controlling IOP and preventing visual loss.

Glaucoma Drugs

DRUG CLASS ACTION EXAMPLES SIDE EFFECTS CONTRAINDICATIONS

Prostaglandin analog Lower IOP 25%–30% by

increasing trabecular or

uveoscleral outfl ow

Once-daily dosing

Lantanoprost

Travoprost

Bimatoprost

Tafl uprost

Iris color change,

uveitis, eyelash growth,

conjunctival injection

History of herpes keratitis, macular

edema

Beta blockers Decrease aqueous

production; lower IOP

20%–25%

Betaxalol

Carteolol

Levobunolol

Metipranolol

(OptiPranolol)

Timolol gel

Fatigue, bronchospasm,

hypotension, bradycardia,

corneal toxicity,

depression, impotence

Congestive heart failure (cardiology

consult)

Nonselective are contraindicated in

asthma, chronic obstructive pulmonary

disease

Hypotension, >fi rst-degree heart block

Adrenergic agonists Decrease aqueous

production, enhance

aqueous outfl ow; lower

IOP 20%–25%

Apraclonidine

Brimonidine

Dipivefrin

Epinephrine

Conjunctival injection,

fatigue, headache

Use of monoamine oxidase inhibitors

Parasympathomimetic

agents

Increase trabecular

outfl ow; lower IOP

20%–25%

Pilocarpine

Carbachol

Corneal toxicity

Increased myopia

Cataract

Decreased vision

Other types of malignant glaucoma

Carbonic anhydrase

inhibitors (primarily

oral route)

Decrease aqueous

production; lower IOP

15%–20%

Topical: Dorzolamide

Brinzolamide

Oral: Acetazolamide

Acetazolamide

sustained release

Dichlorphenamide

Methazolamide

Topical: Corneal edema, metallic

taste, conjunctivitis

Oral: Stevens-Johnson syndrome

Metallic taste

Renal calculi

Aplastic anemia

Thrombocytopenia

Sulfa allergy

Sickle cell disease

Renal calculi

Thrombocytopenia

TABLE 7-1

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Prostaglandin analogs are the most effective drugs at lowering IOP and can be considered as initial medical therapy unless other considerations, such as cost, side effects, intolerance, or patient refusal, preclude this.

A Li et al., 2016 Mantravadi & Vadhar, 2015

Measurement of central corneal thickness (CCT) aids the interpretation of IOP readings and helps to stratify patient risk for ocular damage.

B Prum et al., 2016

The IOP can be lowered by medical treatment, laser therapy, or incisional glaucoma surgery (alone or in combination). The choice of initial therapy depends on numerous considerations, and discussion of treatment with the patient should include the relative risks and benefi ts of the three options.

B Prum et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

136 Chapter 7 ■ Head, Neck, and Face Disorders

Signal Symptoms: Cannot hear or hears but does not under- stand (especially in a group); turns up radio or television louder to hear (noted by family, friends, or neighbors); inabil- ity to hear in one ear; tinnitus; feeling like people are “mum- bling.” Because presbycusis is gradual and insidious, hearing loss may go unnoticed until it has progressed signifi cantly.

Description: Hearing loss is the decreased ability or complete inability to hear. The loss may involve the external, middle, or inner ear and can be unilateral or bilateral.

Etiology: Sensorineural: A lesion in the organ of Corti or in the central

pathways, including the eighth nerve and auditory cortex, causes sensorineural hearing loss. Presbycusis, noise-induced hearing loss, and ototoxic drug-related hearing loss all are sensorineural. Because there is no cure for this, amplifi cation is usually required (Contrera et al., 2016).

Conductive: Conductive hearing loss is caused by a lesion involving the outer and middle ear to the level of the oval window. Various structural abnormalities, cerumen impac- tion, perforation of the tympanic membrane, middle ear fl uid, damage to the ossicles from trauma or infection, otosclerosis, tympanosclerosis, cholesteatoma, middle ear tumors, tempo- ral bone fractures, injuries related to trauma, and congenital problems are some of the causes.

Mixed: Mixed hearing loss includes sensorineural and con- ductive components.

Retrocochlear: Retrocochlear hearing loss is caused by a lesion between the cochlea and the brain, such as an acoustic neuroma or a meningioma.

Occurrence: Occurs in about 25% of adults more than 50 years old and in over 80% of those more than 80 years old. It is the most common sensory defi cit in older adults (Walker et al., 2013).

Age: Sensorineural hearing loss increases with age.

Gender: Presbycusis is more severe in men than in women. This is attributed to environmental causes.

Ethnicity: Not signifi cant.

Contributing Factors: Exposure to loud noises; heredity; ototoxic drugs, such as aminoglycoside antibiotics, salicy- lates, loop diuretics, cisplatin, and quinine; eustachian tube obstruction; chronic middle ear infections; and chronic cerumen impaction are contributing factors. Most cases of sudden unilateral hearing loss in older adults are due to thrombotic or embolic obstruction of the internal auditory artery.

Signs and Symptoms: The patient may complain that people mumble. There may be diffi culty hearing associated with pain, pressure, discomfort, vertigo, or loss of balance. Asso- ciated symptoms may include tinnitus, dizziness, blockage, popping, pressure, crackling, trouble hearing distant sounds, or stiffness. A history of noise exposure, prior ear problems, or familial hearing problems is signifi cant.

Otoscopic examination and inspection of the external auditory canal and middle ear may reveal redness, foreign objects, discharge, scaling, lesions, fl uid, or cerumen impac- tion. Expect to see minimal cerumen, a pink color, and hairs in the outer one-third of the ear. The tympanic membrane should have no perforations and should be a translucent pearly gray. Changes in the tympanic membrane may be con- sistent with conductive hearing loss.

Diagnostic Tests: Primary care provider awareness requires asking about or screening for hearing loss in older adults (Walker et al., 2013). The self-administered Hearing Handi- cap in the Elderly (HHIE-S) is a 10-question instrument that can be given to patients in the waiting room or administered in the long-term care setting (Gross, 2016). Alternatively, asking a single question—“Do you have a hearing problem now?”—can be effective in uncovering a problem. Use of a portable pure-tone audiometer in the primary care offi ce is also a quick screening test, and a medical assistant or offi ce nurse can be instructed in how to administer the test and record results. Anyone with a hearing threshold of 40  dB or greater should be referred to audiology for evaluation. If there is a history of trauma or sudden hearing loss, urgent consultation with an otolaryngologist is warranted, and a computed tomography (CT) scan may be ordered. The Weber and Rinne are not good screening tests for hearing loss, but they can help to identify if the loss is sensorineural or con- ductive (Weber, 2015).

Differential Diagnosis:

■ Ménière ’ s disease ■ Acoustic neuroma (unilateral, with tinnitus) ■ Cholesteatoma (unilateral) ■ Embolic or thrombotic phenomenon, associated with

hypertension (sudden onset, unilateral) ■ Meningioma (unilateral) ■ Trauma (history of ear trauma, unilateral) ■ Otitis media with effusion (retracted tympanic mem-

brane, fl uid behind tympanic membrane) ■ Acute otitis media (unilateral, ear pain; bulging, immo-

bile tympanic membrane) ■ Central auditory processing disorder (seen in dementia)

Treatment: Treat the cause or refer the patient as appropriate. Encouragement, follow-up, and support are important for the patient with hearing loss.

Cerumen Impaction: Treat the patient with cerumenolytic agents, manual removal, or irrigation followed by manual removal as needed (AAFP, 2013). If cerumen impaction is a chronic problem, instruct the patient on instillation of an over-the-counter agent to soften cerumen.

Acute Otitis Media: Antibiotic treatment; an analgesic, such as acetaminophen or an NSAID, may be indicated for pain initially. In the presence of tympanic perforation, ossicle damage, tumor, tympanosclerosis, otosclerosis, sudden hearing loss, or temporal bone injury, refer the patient to a specialist (Weber, 2016a).

HEARING LOSS

Chapter 7 ■ Head, Neck, and Face Disorders 137

Presbycusis: Educate and support the patient so that no further damage occurs. Have the patient reduce noise expo- sure and avoid ototoxic medications. Refer to an audiologist for hearing aid evaluation. Refer the patient for lip-read- ing instruction when appropriate, and instruct the family to speak clearly. Consult a hearing rehabilitation company about the availability of special audio equipment. Patients with profound hearing loss should also be evaluated for suit- ability for cochlear implant (Mosnier et al., 2015).

Follow-Up: See patients as indicated by the cause of the symptom.

Sequelae: Possible complications depend on the cause of the symptom but may include permanent hearing loss. The patient may need a hearing aid or assistive listening device. Middle ear problems may progress to chronic ear problems, such as perforations and cholesteatoma. Social isolation and depression may result from inability to communicate.

Prevention/Prophylaxis: Advise the patient to use protec- tive devices to guard against occupational or recreational hearing loss, to equalize ear pressure when diving, to chew gum or use decongestants in airplanes, to avoid fl ying or diving if upper respiratory infection is present, and to avoid ototoxic medications. Teach the patient proper techniques for cerumen removal and avoidance of Q-tip–type ear swabs or other foreign bodies in the ear. Hearing screening tests are recommended for persons over 65 years old and persons who report hearing diffi culty. The USPSTF recently revised its rec- ommendation and does not recommend periodic screening for hearing loss in asymptomatic adults ( USPSTF, 2013 ).

The American Speech-Language-Hearing Association rec- ommends screening every 3 years for adults more than 50 years of age (American Speech-Language-Hearing Associa- tion, 1997). Residents of long-term care facilities should be screened for hearing loss on admission and as needed there- after (Echalier, 2013).

Referral: Refer to or consult with appropriate specialist as indicated by cause of symptom. All patients with unex- plained hearing loss should have an otoscopic and audiomet- ric evaluation.

Education: Explain cause of symptoms, measures taken to determine the cause, and symptomatic treatment, if any. Advise the patient when to seek medical care. Teach the importance of using hearing aids, if indicated, because this can make a signifi cant difference in the patient ’ s quality of life. Older patients with multiple comorbidities may require the services of a multidisciplinary team to learn how to use a hearing aid effectively (Weinstein & Taylor, 2015). Advise the patient to contact rehabilitation centers to learn lip-read- ing skills or sign language if a hearing aid is not indicated. Hearing rehabilitation services can also assess the need for assistive devices such as fl ashing smoke detector alarms, an amplifi ed telephone, or an amplifi ed television device. Provide support and help the patient resist the temptation to with- draw socially. Caution the patient to avoid solicitation by hearing aid salespeople, particularly if they are offering a device without proper testing of the patient or a device that is very inexpensive. For patients in a long-term care setting, education of staff is essential to enhance communication and improve quality of life (Echalier, 2013).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

In 2012, the U.S. Preventive Service Task Force concluded that the current evidence is insuffi cient to assess the balance of benefi ts and harms of screening for hearing loss in asymptomatic adults ≥ 50 years. This recommendation applies to asymptomatic adults ≥ 50 years. It does not apply to persons seeking evaluation for perceived hearing problems or for cognitive or affective symptoms that may be related to hearing loss. These persons should be assessed for objective hearing impairment and treated when indicated.

B USPSTF, 2013

Sudden hearing loss warrants urgent evaluation and treatment by a specialist.

C Gross, 2018a

Patients who report hearing loss should be referred for full audiometry. C Gross, 2018a

Order imaging and/or ears, nose, and throat referral if vertigo, sudden onset, neurological symptoms, unilateral loss, or primarily low- frequency loss.

C Gross, 2018a, 2018b

Patients with presbycusis may benefi t from amplifi cation or assistive listening devices.

C Gross, 2018b

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

138 Chapter 7 ■ Head, Neck, and Face Disorders

Signal Symptoms: Increased lacrimation with lump on eyelid.

Description: A hordeolum (stye) is an acute, purulent area of infl ammation in the meibomian gland or gland of Zeis, commonly referred to as a “stye.” The hordeolum typically contains Staphylococcus aureus bacteria; it can occur inter- nally (underside of the eyelid) or externally at the lid margin (Ghosh & Ghosh, 2017); and some styes are sterile. A chal- azion is a sterile mass on the eyelid caused by an infl amma- tion and obstruction of a meibomian (oil-secreting) gland of the upper or lower eyelid. Meibomian glands lubricate the lid margins. The chalazion is more chronic in nature, pain- less, and lipogranulomatous without erythema. It can inter- fere with vision at times and develops a rubbery consistency (Vagefi , 2018).

Etiology: Blockage in a duct leading to the eyelid surface from the meibomian gland or obstruction of the gland of Zeis results in infl ammation or infection (usually from Staphylo- coccus ) called hordeolum. If the blockage becomes chronic, progressing to the formation of a hard, granulomatous mass, it is called a chalazion.

Occurrence: Common.

Age: Can occur at any age.

Gender: Occur equally in both men and women.

Ethnicity: Not signifi cant.

Contributing Factors: Previously unresolved blepharitis, poor hygiene, immunosuppression, and skin conditions, such as acne rosacea or seborrheic dermatitis, all are contributing factors to development of hordeolum or chalazion (Fort, 2018; Vagefi , 2018).

Signs and Symptoms: A hordeolum is painful and erythe- matous; it may present initially as a grossly swollen and tender eyelid, then localize ( Walker & Adhikari, 2016 ). A chalazion is a slow-developing, painless hard mass, with infl ammation of the meibomian gland and possible involve- ment of the surrounding tissue. Physical examination with inversion of the eyelid reveals a red, elevated mass that may become large and press against the cornea (Vagefi , 2018).

Diagnostic Tests: None unless recurrent, then biopsy of lesion to rule out malignancy.

Differential Diagnosis:

■ Foreign body ■ Contact dermatitis ■ Rosacea ■ Atopic dermatitis ■ Blepharitis

■ Orbital cellulitis ■ Acute dacriocystitis ■ Sebaceous cell, meibomian gland, or basal cell carci-

noma (Ghosh & Ghosh, 2017; Vagefi , 2018)

Treatment: Warm compresses are applied to the affected eyelid for 10 minutes, four times daily, to facilitate opening and drainage. Allow purulent lesions to drain without squeez- ing them. Massage of the eyelid after warm compresses may help to soften secretions. Many lesions resolve spontaneously without treatment. In cases of secondary infection, antibiotic eye drops or ointment may be used; combination antibiotic and steroid should be used only by an ophthalmologist. If the hordeolum progresses to preseptal cellulitis, prescribe a sys- temic antibiotic, such as dicloxacillin (Fort, 2018). Treatment of chalazion includes warm compresses for 15 minutes four times a day. Incision and drainage by an ophthalmologist may be needed if there is no resolution after 2 months. Antibiot- ics are not indicated because it is granulomatous in nature (Ghosh & Ghosh, 2017). A large nondraining hordeolum or chalazion may require emergency treatment if cellulitis occurs (Vagefi , 2018; Walker & Adhikari, 2016 ). Cochrane reviews on use of acupuncture in acute external hordeolum report low level certainty of effectiveness in China (Cheng et al., 2017). Another Cochrane review on the use of nonsurgi- cal interventions for acute internal hordeolum found no evi- dence for or against nonsurgical treatment (Lindsley, Nichols, & Dickersin, 2017).

Follow-Up: See patient in 2 to 4 weeks to evaluate treatment.

Sequelae: Complete resolution may take several weeks to months; frequent recurrence may indicate underlying malig- nancy (Ghosh & Ghosh, 2017).

Prevention/Prophylaxis: Prevention strategies include advis- ing the patient to perform proper lid hygiene (helps prevent recurrence) by gently scrubbing lids with diluted baby shampoo daily or directly applying baby shampoo with cot- ton-tipped applicator, then rinsing. Frequent hand washing is advised. Warm compresses should be initiated at the fi rst sign of eyelid irritation or if chalazion starts to return; a clean cloth should be used for each warm compress to eye (Ghosh & Ghosh, 2017).

Referral: Refer to or consult with an ophthalmologist if the patient has a visual change, eye pain, or impairment to the eye, or if the chalazion does not heal spontaneously in 6 weeks, because surgical removal may be necessary.

Education: Explain the problem and treatment. Discuss pre- vention strategies.

HORDEOLUM AND CHALAZION

Chapter 7 ■ Head, Neck, and Face Disorders 139

Signal Symptoms: Age-related macular degeneration (AMD) is the leading cause of blindness in adults. It is a disease that results in a loss of central vision, which is most crucial for activities of daily living (ADLs) and instrumental activities of daily living (IADLs). The severity of central vision loss varies depending on the type of macular degeneration. Most recently, efforts have been made to standardize the terminol- ogy and classifi cation of AMD by defi ning it as one disease with three stages: early, intermediate, and late. Late AMD is characterized by signifi cant vision loss, which may occur with gradual loss due to “dry” macular geographic atrophy, or with rapid onset as a result of the neovascularization of “wet” macular degeneration ( Wenick, Bressler, & Bressler, 2018 ).

Dry, Nonexudative or Atrophic Macular Degeneration: Gradual loss of central vision in one or both eyes, with complaints of diffi culty reading or driving, blurred or fuzzy vision (late), and the concern that straight lines appear wavy. In early dry AMD there is the presence of drusen, yellow deposits under the retina. In the intermediate stage, pigmentary distur- bances in the retinal pigment epithelium (RPE) occur, and in the late stage there is geographic atrophy (GA) with severe central vision loss.

Wet, Exudative or Neovascular Macular Degeneration (NVAMD): This characterizes one form of late AMD with accelerated central vision loss in a period of weeks to a couple of months. The fragility of the neovasculature results in subretinal hem- orrhage or fl uid accumulation that destroys the visual center. The disease usually presents in one eye initially, but there is a greater than 40% risk of development in the other eye within 5 years.

Description: The macula in the center of the retina comprises millions of photoreceptor cells containing visual pigments for central vision. These are nourished by the retinal pigment epithelium (RPE), part of a complex basement membrane that becomes sclerotic with age. AMD is defi ned as early, intermediate, and late, depending on the severity of vision loss and pathological fi ndings. Dry AMD is most common,

accounting for 90% of cases. Onset of visual loss is gradual and may not be noticed if only one eye is affected. The cause is unknown, but there is the presence of drusen, disintegra- tion of the RPE and light-sensing cells. Late AMD with neo- vasculature occurs in 10% of cases of AMD but accounts for 90% of all AMD blindness. Patients with early and interme- diate forms of AMD may develop neovascularization of the choroid area with leakage of new blood vessels and fl uid into the retinal pigment epithelium, which causes scarring and additional damage to the macula. The risk ranges from 2% to 20% depending on the size of drusen present. The presence of GA does not protect against the development of NVAMD, with an incidence of 16%, which increases to 36% if NVAMD is present in the other eye ( Wenick et al., 2018 ).

Etiology: A challenge in identifying the cause of dry AMD is the diffi culty in distinguishing the early form from normal changes with aging and the lack of symptoms at this stage. As the macula ages, the RPE, Bruch ’ s membrane, and cho- roidal vessels are all affected. Hard drusen may by noted in almost all older eyes. It is the increase in size and number of drusen that is one indication of early AMD. Genetic predis- position and risk factors certainly contribute to the develop- ment of AMD. The role of infl ammation in the development of AMD is the focus of research on the role of the comple- ment pathway (Gemenetzi & Lotery, 2016). NVAMD has been more aggressively studied in attempts to understand the origin of the angiogenesis. As a result of these studies, several pro-angiogenic factors have been identifi ed. The vas- cular endothelial growth factor (VEGF) is the most important in intraocular angiogenesis and its role has resulted in new treatment options for NVAMD (Velez-Montoya et al., 2014).

Occurrence: Common; macular degeneration is the leading cause of legal blindness in adults more than 55 years old. Risk rises with age; occurrence is 30% in adults over 75 years old. In North America, 15 million people have nonexudative AMD and 1.7 million have NVAMD. These numbers may be an underestimate, as those with early AMD may have no visual changes and may not have been diagnosed. Those with early AMD and NVAMD are at low risk of increasing visual

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Initial treatment includes warm compresses 4 times daily and topical erythromycin ointment for hordeolum.

C Wolter, 2017

Lesions refractory to treatment should be referred for incision and drainage (both hordeolum and chalazion).

C Walker & Adhikari, 2016 Wolter, 2017

Sebaceous carcinoma should be suspected in patients who are middle-aged and older with persistent chalazia.

C Wolter, 2017

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

AGE-RELATED MACULAR DEGENERATION

140 Chapter 7 ■ Head, Neck, and Face Disorders

loss, with only one-third progressing to intermediate AMD in the next 5 years ( Wenick et al., 2018 ).

Gender: Occurs with equal frequency in males and females.

Ethnicity: Caucasians are more likely to experience visual loss from AMD than are African Americans.

Contributing Factors: The primary risk factor for AMD is advancing age. Other risk factors include family history, smoking, exposure to sunlight, nutritional defi cits, and car- diovascular disease. History of AMD in one eye is a risk factor for developing it in the other eye ( Brady, Bressler & Bressler, 2018 ).

Signs and Symptoms: In early AMD there may be no symp- toms, particularly if it is monocular. Later, patients may note a decrease in visual acuity or blurred vision that improves in bright light. In late NVAMD, straight lines appear wavy, and there may be a hole in central vision. White-yellow drusen spots are seen on funduscopic examination. Until recently, the primary screening device for NVAMD was the Amsler grid test, which, when administered, may reveal wavy lines or missing lines in central vision; however, it has low sensitiv- ity (a high number of false negatives). New perimetry devices are now available for both clinical and home monitoring with better sensitivity and specifi city for identifying NVAMD ( Wenick et al., 2018 ). On funduscopic examination of those with NVAMD, choroidal neovascular membranes (CNVMs), subretinal fl uid, hemorrhage, and subretinal lipid deposits may be present.

Diagnostic Tests: All patients should have a comprehensive eye examination by an ophthalmologist, including visual acuity with best correction, funduscopic examination, Amsler grid or perimetry assessment, fl uorescein angiogra- phy, and fundus photos, including optical coherence tomog- raphy ( Brady et al., 2018 ; Wenick et al., 2018 ).

Differential Diagnosis:

■ Unexplained loss of visual acuity ■ Diabetic retinopathy ■ Ocular histoplasmosis ■ Trauma with scar ■ Hypertension

Treatment: The Age-Related Eye Disease Study (AREDS) found that patients at high risk of late AMD lowered their risk by 25% when treated with high doses of vitamin C, vitamin E, beta carotene, zinc oxide, and cupric oxide. This effect was confi rmed through 10 years of follow-up. The effi cacy of this was demonstrated for those with intermediate AMD or late monocular AMD to prevent further loss or involvement of the other eye. It is not recommended for those without AMD or those with early AMD who have a low 5-year risk of worsening vision. The risk versus benefi ts of this high-dose vitamin treatment needs to be evaluated for each patient. The AREDS2 evaluated the effect of substituting the carot- inoids, lutein and zeaxanthin, as well as omega-3 (DHA) and eicosapentaenoic acid (EPA) for beta carotene and a lower zinc dose on progression of AMD (AREDS2 Research Group, 2013). The conclusion after 5 years was that elimi- nating beta carotene and lowering zinc did not make a dif- ference in progression to advanced AMD, and the addition of lutein and zeaxanthin, DHA, and EPA did not further reduce

progression. However, they concluded that there may be value in substituting lutein and zeaxanthin for beta carotene, as beta carotene increased the risk of developing lung cancer, especially in smokers. Trials are currently underway for the use of intravitreal injections of lampalizumab for the treat- ment of GA. The initial data seems promising and this would be a breakthrough for treatment of advanced nonexudative or dry macular degeneration (Bohadorani & Singer, 2017). Low-vision enhancement aids are available to help patients with dry AMD. For patients with bilateral advanced and end stage untreatable AMD, a visual prosthetic implant may be considered.

First-line therapy for NVAMD includes monoclonal anti- bodies that have anti-VEGF abilities. These drugs are injected directly into the vitreous area of the eye and bind with the angiogenic VEGF or receptor and interrupt the neovascu- larization. They are not able to repair the basic defect or attack the source of VEGF, so they must be used repeatedly to suppress the angiogenic process ( Brady et al., 2018 ). Ran- ibizumab and bevacizumab are two humanized monoclonal antibodies that are used to treat NVAMD successfully ( Brady et al., 2018 ). They are injected intravitreally at monthly intervals; current focus is on determining optimal spacing and length of treatment for best results. Local side effects include eye pain, uveitis, and endophthalmitis. There are also potential systemic cardiovascular and thrombotic effects from these drugs, although they have proved minimal. Afl ibercept is a newer agent that improves visual outcomes with less fre- quent injections; preliminary studies show it to be as effective as ranibizumab, with better outcomes in visual acuity and less frequent dosing or maintenance; further studies are in progress (Arroyo, 2017b).

Laser photocoagulation therapy is no longer fi rst-line treatment since the advent of anti-VEGF therapies. Photo- dynamic therapy is now being studied as a possible combi- nation therapy with anti-VEGF treatment (Arroyo, 2017b). Research into surgical options has yielded disappointing results; likewise, use of statins for AMD has not shown pos- itive results, but recent studies with a small number of par- ticipants showed some promise (Arroyo, 2017b; Leung et al., 2018 ). Research is currently underway to fi nd safe, effective treatments for both dry and wet AMD. Research into treat- ment using stem cells is actively being pursued with some recent success (Janigian, 2018).

Follow-Up: All patients with AMD should be seen periodically by an ophthalmologist for reevaluation of disease progres- sion and, where applicable, further treatment. Patients may be given an Amsler grid or the newest option of an at-home perimetry monitor to use weekly or monthly to check for visual changes.

Sequelae: Loss of central vision limits functional capacity and ability to read. Most AMD patients cannot drive. Environ- mental safety also is compromised; falls and hip fractures can occur in patients with AMD. Patients using high-dose vitamin and mineral therapy may have yellowing of skin. Smokers are at increased risk of lung cancer from beta carotene included in the fi rst AREDS vitamin supplement formula.

Prevention/Prophylaxis: There is no specifi c prevention. The USPSTF has determined that there is not enough evidence to support visual screening of older adults for AMD (USPSTF,

Chapter 7 ■ Head, Neck, and Face Disorders 141

2014). Annual eye examinations in persons over 65 years old can facilitate early detection and, in the case of wet AMD, early intervention to limit visual loss. Smokers should be encouraged to quit.

Referral: All patients more than 65 years old should be referred to an ophthalmologist for an annual eye examina- tion. Patients less than 65 years old with visual symptoms also should be referred. Patients with AMD should be referred

to the local chapter of the Blind Association for services, vision enhancement devices, and support groups.

Education: Teach patients the importance of seeking eval- uation for visual symptoms as soon as they occur. Explain disease process and community support services. Educate the family about the need for environmental safety. Caution patients to avoid unproven remedies. Enforce the role of smoking as an independent risk factor in AMD.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Anti-VEGF injections are fi rst-line agents to treat wet AMD. A Brady, Bressler, & Bressler, 2018 Leung et al., 2018

Antioxidant formulations as used in the AREDS and AREDS2 trials should be recommended to those with intermediate or advanced AMD.

A Wenick, Bressler, & Bressler, 2018 Leung et al., 2018

There is inadequate to support the use of antioxidant formulations in those without AMD or with early AMD.

A Wenick, Bressler, & Bressler, 2018

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

ORAL CANCER

Signal Symptoms: Nonhealing sore in the mouth or lip, unex- plained lymph node swelling in head/neck area, diffi culty chewing or swallowing.

Description: Oral cancer is a malignant tumor of the oral squamous epithelium, which includes the lip, buccal mucosa, upper and lower alveolar ridge, fl oor of the mouth, retromolar trigone, hard palate, and anterior two-thirds of the tongue. The oropharynx includes the soft palate at the back of the mouth, part of the throat behind the mouth, tonsils, and base of the tongue ( Figure 7-1 ). The oral cavity has a rich lymphatic supply with initial spread to lymph nodes in levels I to III of the neck. The risk for lymphatic spread in cancers of the lip is lower than other oral cancers ( NCCN, 2016 ).

Etiology: Oral cancer is associated with chronic irritation of the squamous epithelial lining of the oral cavity. Tobacco and heavy alcohol use have previously been the primary risk factors in the development of oral cancers. In recent years, there has been a global increase in the incidence of human papilloma virus (HPV)-related oral cancers, particularly in North America and Northern Europe (ACS, 2016; Gillison, Chaturvedi, Anderson, & Fakhry, 2015). In certain subsets of oropharyngeal cancers, HPV, especially HPV-16, is now considered to be the leading cause of the increased incidence (Gillison et al., 2015). HPV-associated head and neck cancers are commonly confi ned to the oropharynx and are associ- ated with improved prognosis and response to treatment (van Monsjou et al., 2013).

FIGURE 7-1. Oral anatomy.

Lower lip

Upper lip Hard palate Soft palate

Palatine tonsil

Buccal mucosa

Base of the tongue

Uvula

Retromolar trigone

Tongue

Floor of mouth

Occurrence: The National Cancer Institute Surveillance Epi- demiology and End Results (SEER) estimates that in 2016, 48,330 people in the United States will be diagnosed with oral cancer, with estimated deaths from this disease at 9,570 (SEER Stat Fact Sheet, 2016). The incidence of new cases has been rising on average 0.6% each year over the last 10 years and from 2009 through 2013. The Caucasian and non-His- panic population had the highest incidence, followed by the African American population (SEER, 2016). The lowest inci- dence was seen in Hispanics. Death rates for oral cancers

142 Chapter 7 ■ Head, Neck, and Face Disorders

have not changed signifi cantly from 2004 through 2013; the overall 5-year survival rate in the United States is about 64% (SEER, 2016). If cancer has spread to a distant part of the body, the 5-year survival rate is 38% ( Cancer.net , 2016).

Age: The median age at diagnosis for oral cancers from 2009 through 2013 in the United States (including all races and both sexes) was 62 years of age; the median age for death from this cancer was 67 years old, with death rates higher in men of African American descent (SEER, 2016).

Gender: Men are almost three times more likely to develop oral cancer than women, with the number of new cases of oral cavity and pharynx cancer 11.1 per 100,000 in men and women combined per year based on 2009 through 2013 cases (SEER, 2016).

Contributing Factors: Tobacco use and heavy alcohol con- sumption, alone or synergistically, are strongly related to the development of oral cancer. Pipe smoking and sun exposure have been implicated in lip cancer. Leukoplakia and erythro- plasia are often precursors to oral cancer. In addition to HPV, relationships between oral cancer and Epstein-Barr virus, herpes simplex virus, and immunodefi ciency states also have been found (ACS, 2016). Ill-fi tting dentures are a risk factor for development of oral cancer, however, duration of denture use in general is not (Manoharan, Nagaraja & Eslick, 2014). In Asian populations, several genetic polymorphisms, combined with environmental carcinogens such as betel quid chewing, have been implicated in the development of oral cancer (Guha1, Warnakulasuriya, Vlaandere, & Straif, 2014).

Signs and Symptoms: Nonhealing, ulcerative lesions on the lip, tongue, or oral mucosa usually are noted fi rst. Leukopla- kia, a white patch on the mucosa that cannot be rubbed off, is the most common precancerous lesion. There is often no pain, so detection is contingent on a careful soft tissue exam- ination by a dentist. Erythroplasia is a nonpainful, fl at, or even depressed erythematous change of the mucosa without a patch lesion with high risk for malignant transformation (Yardimci, Kutlubay, Engin, & Tuzun, 2014). Presenting symptoms of oral cancers may include a lump or thickening in the mouth, soreness or a feeling that something is caught in the throat, diffi culty chewing or swallowing, ear pain, dif- fi culty moving the jaw or tongue, hoarseness, numbness of the tongue or other areas of the mouth, or swelling of the jaw causing dentures to fi t poorly or become uncomfortable (NIDCR, 2013). Oral pain, bleeding lesions, and unexplained weight loss are usually late signs of malignancy. Patients may complain of numbness in the skin around the chin when the lesion involves a nerve. Enlarged submandibular or submen- tal lymph nodes may be found in advanced disease.

Diagnostic Tests: More than 90% of all oral cancers are squa- mous cell carcinomas and involve lesions on the mucosal surfaces (Schiff, 2016). The challenge is to differentiate can- cerous lesions from a number of benign lesions that also occur in the oral cavity. Defi nitive diagnosis depends on tissue biopsy and is recommended after 2 weeks of nonhealing. Endoscopy may also be performed to evaluate extent of the lesion. Depending on location and potential extent of oral cancer, and the possibility of second primary site or distant metastases, various diagnostic strategies will be employed by the specialist seeing the patient. Magnetic resonance imaging

(MRI), CT scan, positron emission tomography (PET), or PET/ CT scan will show extent of infi ltration, regional lymph node spread, second primary tumors, or distant metastases. CT scan is superior in detecting early bone invasion and lymph node metastasis, but MRI is preferred for evaluating the extent of soft tissue involvement and for providing a three- dimensional image of the tumor. (Poon & Stenson, 2016). Other adjunctive studies include vital cytology staining, bio- logical markers, routine dental radiographs, and thorough dental examination.

Differential Diagnosis:

■ Oral candidiasis (white patches are scraped off and bleed underneath)

■ Melanocytic lesions ■ Oral lichen planus (lacy white lesions on buccal

mucosa) ■ Oral hairy leukoplakia ■ Viral or idiopathic lesions (herpes, aphthous ulcers,

mucositis) ■ Gingivitis ■ Oral cysts ■ Intravascular/extravascular blood lesions (Finkelstein,

2016)

Staging: The tumor, node, metastases (TNM) staging system of the American Joint Committee on Cancer (AJCC) staging system and the Union for International Cancer Control (UICC) system is used by oncology specialists in the staging of oral cancers (AJCC, 2016; Sobin, Brierley, & Gos- podarowicz, 2015). The TNM system describes the anatom- ical extent of disease by the size of the primary tumor, the presence or absence of regional nodal involvement, and pres- ence or absence of metastatic disease (Sobin et al., 2016) (see Figure 7-2 ). Additionally, oral cancers are given a histologi- cal grading, GX to G4 (cell differentiation of the tumor) and stage grouping (stage 0 to stage IVC) (AJCC, 2016; Cancer. net , 2016).

Treatment: Treatment for oral cancers ideally requires a mul- tidisciplinary approach with three main treatment options: surgery, radiation therapy, and chemotherapy, or a combina- tion of one or all of these. Treatment depends on the extent of disease, comorbid illness, potential side effects, and functional outcomes. Surgery and radiation therapy are the standard of care for early-stage and resectable locally advanced cancers ( NCCN, 2016 ). Radiation therapy may be the primary treat- ment modality, particularly in early stage disease, unresect- able tumors, and as adjuvant therapy after surgery to prevent recurrence or if there is possible microscopic residual disease. Radiation treatment is generally given 5 days per week, for 6 to 7 weeks (Gross et al., 2016). Chemotherapy is not con- sidered a fi rst-line therapy in early-stage oral cancers, but may be used in conjunction with radiation therapy in more advanced cases (Gross et al., 2016).

Follow-Up: Post-treatment surveillance is recommended for lifetime with more frequent follow-up the fi rst 2 to 4 years, as 80% to 90% of all recurrences in patients treated for curative intent will occur in this timeframe ( NCCN, 2016 ). The 5-year overall survival rate is approximately 70% for stage I and II oral cancer (Gross et al., 2016) and 83.3% for localized oral cavity and pharynx cancer (SEER, 2016). During the 1 to 2 years, the patient should be seen frequently for focused oral

Chapter 7 ■ Head, Neck, and Face Disorders 143

examinations and to assess for recurrence of symptoms and late effects of treatment, in addition to yearly complete phys- ical examinations. Thereafter, follow-up visits should occur per recommendation of the surgeon or oncologist.

Sequelae: Complications and late effects from oral cancer treatment include disfi gurement and oral problems such as chronic xerostomia, dental problems, diffi culty chewing or swallowing, chronic pain, hypothyroidism, and malnutrition. Cosmetic and functional outcomes are often very good with advanced surgical reconstruction techniques and microsur- gery ( NCCN, 2016 ). Regardless of the treatment modality, patients undergoing treatment for oral cancers may have substantial side effects, loss of function, and changes in appearance with signifi cant impact on quality of life (Sand- strom et al., 2016). Other complications may include second- ary infections, second primary cancers, or metastases to the lungs, regional lymph nodes, or adjacent organs.

Prevention/Prophylaxis: The most effective way to control oral cancer is to combine early diagnosis with timely and appropri- ate treatment. Smoking cessation, treatment for alcoholism, adequate nutrition, and yearly oral examinations (see Figure 7-3 ) can help prevent oral cancer. Edentulous patients should remove dentures for oral examination. Wearing a hat with a brim or using lip gloss with sunscreen can prevent sun expo- sure of lips. Routine dental examination of asymptomatic and symptomatic patients can lead to detection of earlier stage cancers and premalignant lesions, however, there is no defi nitive evidence that shows screening can reduce oral cancer mortality (NIH, 2016). The USPSTF (Moyer, 2014), Cochrane Database of Systematic Reviews (Brocklehurst et al., 2010), and American Dental Association Council on

Scientifi c Affairs Expert Panel (Rethman et al., 2010) all agree that there is insuffi cient evidence to justify screening for oral cancer in the general population. The American Dental Association does recommend that providers screen for signs of potentially malignant lesions early-stage cancer during routine oral examinations, particularly for patients who use tobacco or have heavy alcohol consumption (Moyer, 2014). A review by Omaña-Cepeda and colleagues (2016) found substantial evidence that with proper training, dentists and the dental team can be very effective in counseling patients to quit smoking and are essential to implement guidelines that help patients quit.

Referral: Refer the patient to an otolaryngology surgeon and/ or oncologist. Initial consultation with a dentist who special- izes in oral cancer detection may also be indicated. Also refer the patient and family to the National Cancer Institute Help- line (1-800-4-CANCER) for information about resources and support, and to a local support group if available. If nutrition is a problem, refer to a nutritionist who works with cancer patients. Many cancer programs, particularly academic and comprehensive cancer centers, have multidisciplinary teams that include surgeons, medical and radiation oncologists, nurses, advance practice clinicians, dieticians, and social workers to manage the complex care that may be required for these patients.

Education: Teach patients about the risk factors for develop- ing oral cancer, including smoking, chewing tobacco, alcohol abuse, HPV transmission, and poor nutrition. Discuss strate- gies to help the patient deal with these issues. Advise patients to report any nonhealing oral lesion within 2 weeks of onset.

FIGURE 7-2. Oral cancer staging.

T1 (�2 cm)

T3 (�4 cm)

T2 (2–4 cm)

T4a (invasive)

144 Chapter 7 ■ Head, Neck, and Face Disorders

Signal Symptoms: Blurred vision, painless visual loss, poor night vision, poor color vision, fl oaters.

Description: Retinopathy, a disease of the retina, includes several types: hypertensive, diabetic, and, less commonly in older adults, sickle cell; polycythemia vera; and infectious causes such as toxoplasmosis or cytomegalovirus in HIV.

Etiology: The pathology of the retinopathy relates to the underlying cause. Systemic causes common to older adults include hypertension (arteriosclerotic retinopathy), diabetes

(diabetic retinopathy), and AMD (see previous discussion). Hypertensive or arteriosclerotic retinopathy is related to the severity of the hypertension. Diabetic retinopathy is a highly specifi c microvascular complication of type 1 and 2 diabetes. It is related directly to the duration of diabetes, the patient ’ s age at onset, and glycemic control. Diabetic retinop- athy is either proliferative or nonproliferative. Nonprolifera- tive retinopathy is most common in type 2 diabetics and is characterized by dilation of veins, microaneurysms, retinal edema and hemorrhages, and hard exudates. Proliferative

FIGURE 7-3. Oral cancer screening.

Gingiva Mucosa

1

Lip

2

Buccal mucosa

Posterior gingiva

3 Mucosa

Anterior gingiva

Vestibule

4

5

Hard palate

6

Soft palate

Tonsillar area

7

Floor of mouth

Ventral surface of tongue

8

Lateral border of tongue

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Curative treatment for oropharyngeal cancer typically consists of surgery, radiation therapy, or radiation therapy in combination with chemotherapy.

A National Comprehensive Cancer Network Guidelines, 2016

Current evidence is insuffi cient to assess the balance of benefi ts and harms of screening for oral cancer in asymptomatic adults.

I Moyer, 2014

Patients presenting with metastatic disease or very advanced disease may benefi t from systemic chemotherapy, local radiation to palliate symptoms, or both.

A National Comprehensive Cancer Network Guidelines, 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

RETINOPATHY

Chapter 7 ■ Head, Neck, and Face Disorders 145

retinopathy is common in type 1 diabetics and includes neo- vascularization, vitreous hemorrhage, and retinal detach- ment; secondary glaucoma also can occur because of blockage of outfl ow channels by new vessels. Diabetic reti- nopathy often coexists with hypertensive retinopathy.

Occurrence: Diabetic retinopathy is the leading cause of new blindness in people 20 to 74 years old. Up to 27% of people with type 1 diabetes have some retinopathy present in 5 to 10 years of diagnosis, and after 10 years the prevalence is 70% to 90% ( Yanoff & Cameron, 2016 ). Nearly 80% people with type 2 diabetes develop retinopathy after 15 to 20 years and it is present in one-third at the time of diagnosis (Hammes, Lemmen, & Bertram, 2014). Diabetic retinopathy develops earlier in older patients, but proliferative retinopathy is less common. Proliferative retinopathy is more common with insulin use. According to the National Eye Institute, dia- betic retinopathy affects 7.7 million people age 40 years and older. Hypertensive retinopathy is seen with poorly controlled hypertension.

Age: Older adult patients are more likely to have hypertensive or diabetic retinopathy because of the increase in chronic disease with age. Approximately one-half of all diabetes cases occur in persons over 55 years old.

Gender: Men develop diabetic retinopathy sooner than women.

Ethnicity: Diabetes is more common in Native Americans, Asian Americans, African Americans, Hispanic Americans, and Pacifi c Islanders than in Caucasians. Hypertension is also more prevalent among African Americans.

Contributing Factors: Contributing factors in diabetic retinop- athy include age at onset, type of diabetes, duration of disease, poor glycemic control (persistent elevated hemoglo- bin A1c), arterial hypertension, dyslipidemia, nephropathy, smoking, and stage at which retinopathy is detected (early detection of nonproliferative is preferred) (Hammes et al., 2014). Duration of disease is the best predictive factor for retinopathy ( Yanoff & Cameron, 2016 ). Causes of other types of retinopathy include poorly controlled hypertension and AMD. Multiple sclerosis, sarcoidosis, and coagulopathies are also associated with proliferative retinopathy (Bearelly, Mathura, & Jampol, 2008).

Signs and Symptoms: Retinopathy usually develops without symptoms until advanced stages of the disease. If present- ing with symptoms, they may be the insidious painless onset of decreased visual acuity. Patients may report blurred vision, poor night vision, poor color vision, or “fl oaters and fl ashers.” The ophthalmoscopic examination may be the fi rst point of detection in an asymptomatic patient. All patients with known diabetes or hypertension should have regular comprehensive eye examinations, including a fun- duscopic examination. The funduscopic changes seen in patients with hypertension include arteriolar narrowing, arteriovenous nicking, changes in arteriolar light refl ex, and tortuosity of vessels. Classic nonproliferative changes in patients with diabetes are microaneurysms and hard and soft exudates. Clinical fi ndings in patients with proliferative retinopathy are cotton-wool spots, deep hemorrhages, and neovascularization.

Diagnostic Tests: Dilated funduscopic examination and com- prehensive eye examination, fundus photos, ocular coher- ence tomography (OCT), and fl uorescein angiography are used to diagnose diabetic retinopathy (Crandall & Shamoon, 2016; Janigian, 2018). Hypertensive retinopathy is a clini- cal diagnosis based on physical examination fi ndings during slit-lamp examination. Hypertensive retinopathy presents as disc edema and can be classifi ed by ophthalmology using the Keith-Wagener-Barker or the recent simplifi ed Mitch- ell-Wong grading system (Aissopou et al., 2015; Downie et al., 2013). The intent of these grading systems was to cor- relate hypertensive retinopathy with a systemic disease such as left ventricular heart failure, pulmonary edema, stroke, or myocardial infarction. Although not specifi c for the diagnosis of retinopathy, regular monitoring of hypertension and blood glucose is essential in disease management and prevention of complications.

Differential Diagnosis:

■ Retinal detachment ■ Cytomegalovirus retinitis (usually associated with HIV) ■ Toxoplasmosis (associated with latent infection) ■ Retinal vasculitis ■ Retinal vein occlusion ■ Hyperviscosity syndromes

Treatment: Prevention and early detection are fundamental to preserving vision. Annual ophthalmological examinations are required. For patients with diabetes, the goal is to optimize glucose control. Patients with hypertension or hypertension and diabetes should be treated to control blood pressure (goal is 130/80  mm  Hg for those with diabetes, 140/90  mm  Hg without diabetes). Blood pressure reduction should be slow and deliberate to minimize end-organ damage; treatment of the underlying pathology is essential. The parameters and goal of treatment in patients with hypertension and diabetes should be clear and concise.

For patients who have diabetes with nonproliferative retinopathy, macular edema is responsible for most vision loss. If macular edema is clinically signifi cant, treatment with anti-VEGF is superior to laser therapy, but intravit- real steroid injection may also be used ( Yanoff & Cameron, 2016 ). For those with diabetes with severe nonproliferative disease, panretinal laser photocoagulation can lower the risk of progression to proliferative diabetic retinopathy (Crandall & Shamoon, 2016). For patients who have diabetes with vitreous hemorrhage and advanced neovascularization, vit- rectomy can be of signifi cant benefi t (Crandall & Shamoon, 2016).

Follow-Up: Follow-up depends on the fi ndings. A retinal spe- cialist should follow up with patients with retinopathy. The primary care provider is responsible for regular disease man- agement. The staging of retinopathy and the treatment plan require specialty follow-up.

Sequelae: Not all retinopathy is progressive. The condition and its outcome are related to the cause of the retinopathy and the degree of successful disease management. For hyper- tensive retinopathy, arteriovenous nicking and arteriolar narrowing are irreversible.

Prevention/Prophylaxis: Older adult patients should have an annual ophthalmological examination. During routine offi ce

146 Chapter 7 ■ Head, Neck, and Face Disorders

visits, perform a funduscopic examination on the eyes of patients with diabetes and hypertension. Promptly refer the patient to a retinal specialist at the earliest report of vision change or abnormal examination fi ndings. Patients with diabetes and hypertension should be aware of the goals of treatment and the need to control blood pressure and blood glucose. Home monitoring of blood glucose and blood pres- sure may be advised.

Referral: A retinal specialist should see all patients with retinopathy. All patients with diabetes and hypertension

need to see an ophthalmologist annually. Communication between the specialist and primary care provider is essential for optimal patient treatment.

Education: Patients should report any alteration in vision. Patients should know how the goals of blood pressure and blood glucose control relate to prevention of complications. Finally, patients should understand the importance of fol- low-up care. The goals of treatment should be a partnership between patient and health-care provider.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCE

Refer patients with macular edema, severe nonproliferative retinopathy, or any degree of proliferative retinopathy to an ophthalmologist immediately for treatment.

A Yanoff & Cameron, 2016 AAO, 2016

Patients with type 1 diabetes should have annual screenings beginning 5 years after diagnosis. Those with type 2 diabetes should have annual screenings beginning at the time of diagnosis.

A AAO, 2016

Optimal glycemic control reduces the risk and progression of retinopathy.

A Diabetes Control and Complications Trial (DCCT) Research Group, 1993

Optimal glycemic control and blood pressure control reduces the risk and progression of retinopathy.

A Yanoff & Cameron, 2016

Laser photocoagulation reduces the risk of vision loss in patients with proliferative retinopathy, clinically signifi cant macular edema, and some cases of severe nonproliferative retinopathy.

A ACCORD Study Group & ACCORD Eye Study Group, 2010

In macular edema that is clinically signifi cant, treatment with anti-VEGF is superior to laser therapy, but intravitreal steroid injection may also be used.

A Yanoff & Cameron, 2016 AAO, 2016

Aspirin therapy does not prevent the progression of retinopathy, nor is it contraindicated for prevention of cardiovascular disease in the presence of retinopathy, because it does not increase the risk of retinal hemorrhage.

A AAO, 2016 ACCORD Study Group & ACCORD Eye Study Group, 2010

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

RHINITIS

Signal Symptoms: Clear rhinorrhea (anterior or posterior drainage), nasal congestion and itching, and sneezing. May also present with itching of the palate, ear canals, eyes, and reduced olfaction.

Description: Rhinitis is an infl ammation of the nasal mucosa and includes allergic rhinitis (AR), nonallergic rhinitis (NAR),

and nonallergic rhinitis with eosinophilia syndrome (NARES) (McCullan, 2014).

Etiology: AR is classifi ed by pattern (e.g., seasonal or peren- nial), symptom frequency, severity, and evidence of immuno- globulin E (IgE) sensitization to an allergen. Symptoms occur due to the response of the nasal mucosa to airborne allergens

Chapter 7 ■ Head, Neck, and Face Disorders 147

in genetically predisposed individuals. The mechanism of the three-phase type 1 hypersensitivity response experienced in AR is due to IgE-mediated mast cell degranulation and acti- vation (Welch & Kau, 2014). In the sensitization phase, the genetically predisposed person inhales an allergen, which is presented by dendritic cells to T cells in lymph nodes (Rote & McCance, 2014). This causes T-helper 2 cells to increase and release cytokines, causing B cells to class-switch into plasma cells that produce antigen-specifi c IgE antibodies (Settipane & Schwindt, 2013). During the challenge phase, cross-link- ing of mast cells initiates degranulation of the mast cell and release of symptom-eliciting mediators. The fi nal phase, elic- itation, has an early and late-stage response. The early phase response (sneezing, itching, rhinorrhea), occurring within 5 to 30 minutes of exposure, is primarily due to histamines. The late phase response (primarily nasal congestion) occurs 2 to 8 hours after exposure and is due to the infl ux of baso- phils, eosinophils, and T-lymphocytes into the nasal mucosa. Priming is a process in which a susceptible person becomes more sensitive to smaller amounts of the allergen and more reactive to nonallergic substances such as irritants (Settipane & Schwindt, 2013).

AR may be seasonal, caused by pollens from trees, grass, or weeds pollinating in the spring or fall. Pollen from fl owers is rarely allergenic, because the pollen is heavier and is carried by bees from plant to plant (American Academy of Allergy, Asthma, & Immunology, n.d.). Perennial AR is often related to environmental exposure to pollutants, animal dander, dust, and indoor and outdoor molds. Response to irritants such as cigarette smoke, pollution, and odors such as perfumes and diesel may cause rhinitis but is not IgE mediated.

NAR is not mediated by the production and interaction of IgE, yet symptoms are similar to AR (rhinorrhea and nasal congestion). However, the patient usually does not experi- ence itching, sneezing, or conjunctival symptoms ( McMul- lan, 2014 ; Settipane & Kaliner, 2013). The subtypes of NAR include vasomotor, atrophic nonallergic, rhinitis medica- mentosa, drug-induced, hormonal, gustatory, infectious, or NARES. The cause of NAR is not well understood, but is thought to be due to atopy, nociceptive nerve sensor and ion channel protein dysfunction, and autonomic dysfunction (Settipane & Kaliner, 2013).

Vasomotor rhinitis symptoms have been linked to tem- perature changes, inhaled irritants, bright lights, and strong odors. Atrophic NAR is probably due to degeneration and atrophy of nasal membranes and bony structures. Rhinitis medicamentosa is frequently due to the overuse of topical over-the-counter (OTC) nasal decongestants. Drug-induced rhinitis may occur with use of alpha-receptor agonists, angio- tensin-converting enzyme (ACE) inhibitors, aspirin, beta blockers, NSAIDs, oral contraceptives, and phosphodiester- ase—5 selective inhibitors. Hormonal rhinitis may occur in patients with hypothyroidism, who are menstruating, or are pregnant. Gustatory rhinitis can occur after food or alcohol ingestion and is thought to be mediated vagally. Infectious rhinitis is most commonly caused by acute viral syndrome. Chronic infectious rhinitis results from a secondary bacterial infection. Marked by sneezing fi ts, profuse rhinorrhea, nasal itching, and reduced olfaction, NARES is thought to be a pre- cursor to asthma, aspirin-aggravated respiratory disease, and nasal polyps ( McMullan, 2014 ; Settipane & Kaliner, 2013).

Occurrence: AR occurs in 10% to 30% of adults (approxi- mately 60 million people) in the United States. NAR occurs in 7% of the population, affecting 22 million people (Settipane & Kaliner, 2013; Settipane & Schwindt, 2013).

Age: AR is most common between ages 10 and 39 years, declining after age 40 years. NAR is a condition of adulthood and is more common in older adults.

Gender: Adult men and women have an equal incidence of rhinitis ( McMullan, 2014 ). Women who are 40 years old and older have a higher incidence of NAR (Settipane & Kaliner, 2013).

Ethnicity: Not signifi cant.

Contributing Factors: Most important, AR usually is asso- ciated with a strong family history of atopic disorders, including asthma, atopic eczema, urticaria, food allergy, stinging-insect-venom allergy, and anaphylaxis. Exposure to airborne allergens in the environment, such as animal dander, dust mites, molds, or seasonal pollens, triggers AR. A variety of factors are thought to contribute to NAR including anatomical abnormalities, infections, medications (especially in the elderly), immunodefi ciency, tumors of the nasophar- ynx and paranasal sinuses, pregnancy, hypothyroid disease, granulomatous disease (Wegener ’ s disease and sarcoidosis), and leakage of cerebrospinal fl uid. Vasomotor rhinitis can be triggered by strong odors or fumes, temperature or baromet- ric pressure changes, and psychological factors. Age-related changes in the geriatric population should be considered, because physiological changes in this age group, as well as medication side effects and drug–drug interactions, may contribute to the development of symptoms (Hellings et al., 2013; Settipane & Kaliner, 2013).

Signs and Symptoms: Patients with seasonal AR report rhi- norrhea, sneezing, obstructed nasal passages, and pru- ritic eyes, nose, and oropharynx during the spring and fall. Patients with perennial AR have similar symptoms associated with exposure to environmental allergens, typically in their homes.

Review of Symptoms: Questions to ask patients with symp- toms of rhinitis include: Does the patient associate the symp- toms with a season, place, time of day, or activity? Is there a family history of allergic diseases? Do symptoms seem to occur during times of stress or during weather or tempera- ture changes? What is the patient ’ s quality of life (sleep disturbance, fatigue, missed work)? Does the patient use intranasal drugs such as cocaine?

Physical Examination: Although the patient history is key in establishing the diagnosis, the physical examination will assist in ruling out other differential diagnoses. A full head, eyes, ears, nose, and throat (HEENT), skin, and respiratory examination should be performed. Objective fi ndings con- sistent with AR includes atopic dermatitis, scleral erythema and injection, allergic shiners and Dennie ’ s lines (infraorbital hyperpigmentation and creasing), salute sign (creasing of the nasal dorsum), swollen and pale turbinates, and tonsillar enlargement. As asthma often accompanies AR, the patient also must be assessed for wheezing ( McMullan, 2014 ).

Postnasal discharge and congestion are common com- plaints in vasomotor rhinitis; symptoms associated with AR

148 Chapter 7 ■ Head, Neck, and Face Disorders

may coexist. Individuals with atrophic rhinitis report a bad taste along with congestion and thick postnasal discharge. In AR, pink-to-red, dry nasal mucosa is found on exam- ination. Symptoms of infection such as fever and purulent nasal discharge should be ruled out on history and physical examination.

Diagnostic Tests: Skin testing involves scratching the surface of the skin with a single stylus for each allergen. Depending on the practice, providers may begin with skin prick testing and proceed to intradermal testing if the results are neg- ative (Hollander, 2014). It is important to note that some medications (antihistamines, tricyclic antidepressants, oral and topical corticosteroids, and leukotriene antagonists) will interfere with skin allergy testing. Total serum IgE testing may be used when skin testing is not possible due to medi- cations or skin conditions; however, mild elevation of IgE is not useful in the diagnosis of allergies and serum IgE testing should not be used as a screening test (Hollander, 2014). Radiographic sinus fi lms or CT scan should not be used in the absence of recurrent infection ( Seidman et al., 2015 ). Patients with chronic rhinitis may be referred for evaluation of obstructive sleep apnea in the presence of sleep-disordered breathing ( Seidman et al., 2015 ).

Differential Diagnosis:

■ Viral or bacterial upper respiratory infection ■ Acute or chronic sinusitis ■ Otitis media ■ Nasal polyps ■ Deviated nasal septum ■ Hypothyroid disease ■ Tumor ■ Foreign body in the nose

Treatment: Allergic Rhinitis: Pharmacological therapy is directed at

control of the specifi c patient symptoms. Avoid fi rst-gener- ation antihistamines, such as diphenhydramine, because of safety issues related to sedating effects. The lowest possible dose of these medications should be used in older adults to avoid excessive sedation. Because of their anticholinergic effects, these drugs may worsen certain conditions that are common in the older adult patient, such as benign prostatic hypertrophy, bladder neck obstruction, and narrow-angle glaucoma.

Intranasal corticosteroid nasal sprays are the most effec- tive treatment for AR due to their ability to prevent early and late phase responses ( McMullan, 2014 ). It is best to begin treatment with intranasal sprays or in combination with oral antihistamines. Oral leukotriene receptor antagonists such as monelukast are not considered fi rst-line treatment but may be effective for patients with asthma and seasonal AR ( McMullan, 2014 ; Seidman et al., 2015 ). Topical intranasal antihistamine preparations are helpful in avoiding systemic side effects but may cause local irritation and dryness of the nasal mucosa.

Intranasal Antihistamines: ■ Azelastine (Astelin) nasal spray, two sprays each nostril

twice daily ■ Olopatadine (Patanase), two sprays each nostril twice

daily

Intranasal Corticosteroids: ■ Beclomethasone dipropionate (Qnasl), two sprays each

nostril once daily ■ Budesonide (Rhinocort), two sprays each nostril twice

daily ■ Ciclesonide (Omnaris, Zetonna), two sprays each nostril

once daily ■ Flunisolide (Nasarel, Nasalide), two sprays each nostril

twice daily ■ Fluticasone furoate (Veramyst), two sprays each nostril

once daily ■ Fluticasone propionate (Flonase), two sprays each

nostril once daily or one spray each nostril twice daily ■ Mometasone furoate (Nasonex), two sprays each nostril

once daily ■ Triamcinolone acetonide (Nasacort), two sprays each

nostril once daily

While second-generation antihistamines are not as effective as intranasal steroids, some patients cannot tolerate nasal sprays and fi nd the once-daily dosing and rapid symptom relief to be advantageous. Most have few side effects, however, cetirizine and levocetirizine may be sedating ( Seidman et al., 2015 ).

Second-Generation Antihistamines: ■ Loratadine (Claritin), 10  mg once daily (10  mg every

other day in hepatic or renal insuffi ciency with glomer- ular fi ltration rate less than 30 mL/min)

■ Desloratadine (Clarinex), 5  mg once daily (give every 48 hours to start with hepatic or renal insuffi ciency)

■ Cetirizine (Zyrtec), 10  mg once daily (5  mg once daily with hepatic or renal insuffi ciency)

■ Levocetirizine (Xyzal) 5 mg once daily ■ Fexofenadine (Allegra), 180 mg once daily, 60 mg twice

daily (60 mg once daily with decreased renal function)

These antihistamines should not be prescribed for patients taking antifungal medications, macrolide antibiotics, tricy- clic antidepressants, or class Ia antiarrhythmics, because their interaction with these drugs may cause life-threaten- ing cardiac dysrhythmias. They also are contraindicated for patients with a history of congestive heart failure, coronary artery disease, or liver disease.

Nonallergic Rhinitis: ■ Avoid known irritants. ■ Nasal corticosteroids (see earlier) for NARES. ■ Nasal corticosteroids and elimination of topical decon-

gestant sprays in rhinitis medicamentosa. ■ Ipratropium bromide (Atrovent) nasal spray 0.03%,

0.06%, two sprays each nostril two to four times daily, is an anticholinergic for local control of rhinorrhea.

■ Pseudoephedrine, 30 to 60  mg orally every 4 hours, a decongestant, decreases nasal mucosa swelling but has little effect on other rhinitis symptoms; it is best used briefl y and intermittently because of central nervous system (CNS) side effects. It is contraindicated in older adult patients with poorly controlled hypertension, cor- onary artery disease, and a history of cerebrovascular accident.

■ Oral corticosteroids are recommended only for severe nasal obstruction, such as that caused by rebound rhi- nitis or nasal polyps, and require individualized dosing.

Chapter 7 ■ Head, Neck, and Face Disorders 149

Follow-Up: The patient should return in 2 to 4 weeks after beginning therapy to review the response to medications and the effectiveness of environmental control.

Sequelae: Epistaxis, acute and chronic sinusitis, and the development of nasal polyps are complications of rhinitis.

Prevention/Prophylaxis: Teach patients with AR to avoid irri- tants and to try to control environmental risk factors. Discuss the need to take intranasal steroid sprays and/or antihista- mines regularly to control symptoms.

Referral: When symptoms persist or worsen, or are accompa- nied by comorbidities such as nasal polyps or asthma, refer the patient to an otolaryngologist or allergist ( McMullan, 2014 ). In patients with chronic rhinitis, the otolaryngologist may prescribe a short-term course of antibiotics along with oral prednisone. Sinus surgery may be indicated in order to correct obstruction, a major component of recurrent sinus- itis. An allergist may skin prick test patients in order to determine their sensitivities and place the patient on allergy immunotherapy.

Education: Avoid the use of OTC nasal sprays for more than 3 consecutive days, and warn patients about the sedating side effects of fi rst generation antihistamines. Teach the patient with perennial allergies to use their medications (intranasal steroid sprays and second-generation antihistamines) regu- larly. Waiting until symptoms have progressed may result in the lack of effi cacy of either the oral antihistamine and/or the intranasal steroid spray.

Discuss specifi c environmental control with the patient. For patients with house dust mite sensitivity, advise them to use mite-impermeable mattress covers, wash fl oors each day, wash bedding in hot water twice weekly, and remove upholstered furniture from the bedroom. For control of sea- sonal pollen from trees and grass in the spring, and weeds in the summer and fall, it is essential that patients keep their windows closed and air conditioning on during periods of high pollen counts, especially from 5:00 am to 10:00 am. Pollen easily enters the screens of windows and deposits on furniture and bedding. High-effi ciency particulate air (HEPA) fi lters can be used in bedrooms and living areas. Patients should also be encouraged to shower and change their clothes when coming in from the outside. Clothes should be dried in an automatic dryer, not outdoors. Outdoor mold exposure can be decreased by avoiding areas of decaying plants, rotting leaves, and other debris. Wearing a mask when working outside also may be benefi cial (National Institute of Environmental Health Sciences, n.d.; Seidman et al., 2015 ).

Patients with animal dander sensitivity can be more diffi - cult to treat if the family chooses to keep the pet. Pets must be kept out of the patient ’ s room at all times, and a HEPA fi lter should be run in the bedroom. Because animal dander is sticky, bed clothes should be clean before entering the bedroom. Washing the hands and face after pet exposure also is advised (National Institute of Environmental Health Sci- ences, n.d.). There may be some benefi t gained from washing dogs twice weekly for 5 minutes and then blowing them dry; no such benefi t has been found with bathing cats ( Seidman et al., 2015 ).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Topical corticosteroid intranasal sprays are the most effective treatment of AR when used regularly.

A Seidman et al., 2015

Oral second-generation antihistamines are effective, either alone or in conjunction with intranasal steroid sprays, for treatment of AR with sneezing and itching.

A Seidman et al., 2015

Patients with comorbidities such as asthma, atopic dermatitis, sleep-disordered breathing, conjunctivitis, and otitis media should receive further testing.

A McMullan, 2014

Patients should implement environmental controls such as frequent washing of bedding and fl oors, using mite-impermeable mattress covers and HEPA fi lters, keeping pets out of the bedroom, and keeping the windows closed.

B Seidman et al., 2015

Mold exposure can be decreased by eliminating sources of moisture, avoiding areas of decaying plants, rotting leaves, and other debris. Wearing a mask when working outside can also be of benefi t.

A National Institute of Environmental Health Sciences, 2018

Specialized allergy testing (skin or blood testing) may be performed on patients who do not respond to empiric treatment.

B Seidman et al., 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

150 Chapter 7 ■ Head, Neck, and Face Disorders

REFERENCES Cataract Jacobs , D. S. ( 2017 ). Cataract in adults . UpToDate . Olson , R. J. , Braga-Mele , R. , Chen , S. H. , Miller , K. M. , Pineda S. , II ,

Tweeten , J. P. , & Musch , D. C. on behalf of the American Academy of Ophthalmology Preferred Practice Pattern Cataract and Anterior Segment Panel . ( 2016 ). Cataract in the adult eye preferred practice pattern . Ophthalmology , 124 ( 2 ), P1 – P119 .

Thompson , J. , & Lakhani , N. ( 2015 ). Cataracts . Primary Care Clinics in Offi ce Practice , 42 , 409 – 423 .

Epistaxis Ruhl , T. S. , & Swindell , A. E. ( 2018 ). Epistaxis and nosebleeds . Essen-

tial evidence . John Wiley & Sons, Inc . Retrieved from http://www. essentialevidenceplus.com .

Glaucoma, Acute (Primary Angle-Closure) Hoffman , R. S. ( 2018 ). Glaucoma, primary angle-closure . In Ferri ’ s clini-

cal advisor ( pp . 521 – 521.e1 ). Elsevier . Mantravadi , A. V. , & Vadhar , N. ( 2015 ). Glaucoma . Primary Care in Offi ce

Practice , 42 ( 3 ), 437 – 449 . Prum , B. E. Jr. , Herndon , L. W. Jr , Moroi , S. E. , et al. ( 2016 ). Primary

angle closure preferred practice pattern guidelines . Ophthalmology 2016 , 123 , 1 – 40 .

Weinreb , R. N. , Aung , T. , & Medeiros , F. A. ( 2014 ). The pathophysiology and treatment of glaucoma: A review . Journal of the American Medical Association , 311 ( 18 ), 1901 – 1911 . doi:10.1001/jama.2014.3192

Glaucoma, Chronic (Primary Open-Angle) Hoffman , R. S. ( 2018 ). Glaucoma, open-angle . In Ferri ’ s clinical advisor

( pp . 519 – 520.e3 ). Jacobs , D. S. ( 2016 ). Open-angle glaucoma: Epidemiology, clinical pre-

sentation, and diagnosis . UpToDate . Jacobs , D. S. ( 2017 ). Open-angle glaucoma: Treatment . UpToDate . Li , T. , Lindsley , K. , Rouse , B. , Hong , H. , Shi , Q. , Friedman , D. S. , . . . Dick-

ersin , K. ( 2016 ). Comparative effectiveness of fi rst-line medications for primary open angle glaucoma – A systematic review and network meta-analysis . Ophthalmology 2016 , 123 ( 1 ), 129 – 140 .

Mantravadi , A. V. , & Vadhar , N. ( 2015 ). Glaucoma . Primary Care in Offi ce Practice , 42 ( 3 ), 437 – 449 .

Prum , B. E. Jr , Rosenberg , L. F. , Gedde , S. J. et al. ( 2016 ). Primary open-angle glaucoma preferred practice pattern guidelines . Ophthal- mology 2016 , 123 , P41 – 111 .

Weinreb , R. N. , Aung , T. , & Medeiros , F. A. ( 2014 ). The pathophysiology and treatment of glaucoma: A review . Journal of American Medical Association , 311 ( 18 ), 1901 – 1911 . doi:10.1001/jama.2014.3192

Hearing Loss Gross , S. R. ( 2018a ). Hearing loss . Essential evidence . John Wiley & Sons,

Inc. Retrieved from http://www.essentialevidenceplus.com Gross , S. R. ( 2018b ). Presbycusis . Essential evidence . John Wiley & Sons,

Inc. Retrieved from http://www.essentialevidenceplus.com U.S. Preventive Services Task Force . ( 2013 ). Screening for hearing loss

in older adults: U.S. Preventive Services Task Force Recommendation Statement . American Family Physician , 87 ( 2 ). Retrieved from http:// www.aafp.org/afp/2013/0115/od1.html

Hordeolum and Chalazion Walker , R. A. , & Adhikari , S. ( 2016 ). Hordeolum and chalazion . In J. E.

Tintinalli , J. S. Stapczynski , O. J. Ma , D. M. Yealy , G. D. Meckler , & D. M. Cline ( Eds .), Tintinalli ’ s emergency medicine: A comprehensive study guide, 8e . McGraw-Hill Education .

Wolter , B. R. ( 2017 ). Hordeolum and chalazion . Essential evi- dence plus . John Wiley & Sons, Inc. Retrieved from http://www. essentialevidenceplus.com .

Age-Related Macular Degeneration Brady , C. J. , Bressler , N. M. , & Bressler , S. B. ( 2018 ). Neovascular (exu-

dative or “wet”) age-related macular degeneration . In A. P. Schachat , S. R. Sadda , D. Hinton , C. P. Wilkinson , & P. Wiedemann ( Eds .), Ryan ’ s retina ( pp . 1345 – 1372 ). Philadelphia, PA : Elsevier .

Leung , L-S. B. , Zarbin , M. A. , Rosenfeld , P. J. , Toy , B. , Martin , D. F. , & Blu- menkranz , M. S. ( 2018 ). Pharmacotherapy of age-related macular degeneration . In A. P. Schachat , S. R. Sadda , D. Hinton , C. P. Wilkin- son , & P. Wiedemann ( Eds .), Ryan ’ s retina ( pp . 1373 – 1414 ). Philadel- phia, PA : Elsevier .

Wenick , A. S. , Bressler , N. M. , & Bressler , S. B. ( 2018 ). Age-related macular degeneration: Non-neovascular early AMD, intermedi- ate AMD, and geographic atrophy . In A. P. Schachat , S. R. Sadda , D. Hinton , C. P. Wilkinson , & P. Wiedemann ( Eds .), Ryan ’ s retina ( pp . 1293 – 1344 ). Philadelphia PA : Elsevier .

C A S E S T U DY

A 76-year-old woman presents today with complaints of nasal drainage, clearing of throat, and occasional nasal congestion, especially on waking in the morning. She has recently moved into an independent living center after living in her home for 40 years. She states that, although she has had these symptoms before, generally the symptoms appeared in the spring, and she associated the nasal drainage with pollination. Because it is winter, she could not identify the trigger of her symptoms.

Chief complaint: Persistent “runny nose” for 3-week duration, associated clearing of throat, and nasal congestion on awakening in the morning.

Objective data: Blood pressure (BP) 130/84, temperature 98.6, pulse 78, respiratory rate 20.

1. How will you use this information to prepare for today ’ s visit?

2. What additional subjective data are you seeking, to include history of any allergies?

3. What additional objective data will you be assessing for?

4. What are the differential diagnoses that you are considering?

5. What laboratory tests will help you rule out some of the differential diagnoses?

6. What is your treatment, and what specifi c information about the prescription will you give to this patient?

7. What are the potential complications from the treatment ordered?

8. What additional specifi c laboratory tests will you consider ordering?

9. What additional patient teaching may be needed?

10. What type of specialist will you be consulting for this patient?

Chapter 7 ■ Head, Neck, and Face Disorders 151

Oral Cancer Moyer, V. A. on behalf of the USPSTF . ( 2014 ). Screening for oral cancer:

U.S. Preventive Services Task Force Recommendation Statement . Ann Intern Med , 160 , 55 – 60 .

National Comprehensive Cancer Network (NCCN) Guidelines . ( 2016 ). Version 2.2016: Cancer of the oral cavity . Retrieved October 2016 from www.nccn.org .

Retinopathy ACCORD Study Group & ACCORD Eye Study Group . ( 2010 ). Effects of

medical therapies on retinopathy progression in type 2 diabetes . New England Journal of Medicine , 363 ( 3 ), 233 – 244 .

American Academy of Ophthalmology (AAO) Retina/Vitreous Panel. Preferred Practice Pattern Guidelines . ( 2016 ). Diabetic retinopathy . San Francisco, CA : American Academy of Ophthalmology. Retrieved from www.aao.org/ppp .

Diabetes Control and Complications Trial (DCCT) Research Group . ( 1993 ). The effect of intensive treatment of diabetes on the devel- opment and progression of long-term complications in insulin- dependent diabetes mellitus . New England Journal of Medicine , 329 ( 14 ), 977 – 986 .

Yanoff , M. , & Cameron , J. D. ( 2016 ) Diseases of the visual system . In L. Goldman , & A. I. Shafer ( Eds .), Goldman-Cecil medicine (25th ed.) ( pp . 2556 – 2573 ). Philadelphia, PA : Elsevier/Saunders .

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S. Joo & A.L. Kau ( Eds .), The Washington manual of allergy, asthma, and immunology subspecialty consult (The Washington Manual subspecialty consult series (2nd ed.) (Kindle version) . Philadelphia, PA : Lippincott, Williams & Wilkins .

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152

CHAPTER 8 Chest Disorders

Lori Martin-Plank

ASSESSMENT OF THE CARDIOVASCULAR SYSTEM

Key symptoms for cardiovascular assessment include dizzi- ness, syncope, orthopnea, angina, edema, and claudication ( Bickley, 2013 ; Kane, Ouslander, Resnick, & Malone, 2018). Differentiating normal from abnormal cardiac function in an older adult can be a challenge because one in two older persons has cardiac disease. More specifi cally, almost one- half of all individuals older than age 60 years have severe coronary artery narrowing with a respective increase in myocardial demand. Of these, less than 50% have clinical signs and symptoms of this process. Cardiovascular disease is the most prominent cause of disability in this age group and the leading cause of death, accounting for about one-half of all deaths among older adults.

ASSESSMENT OF RISK FACTORS FOR CORONARY ARTERY DISEASE

Although some risk factors for coronary artery disease (CAD) can be remedied, others cannot. The two most important risk factors for atherosclerosis that cannot be remedied are advanced age and male gender. The major remediable risk factors are high blood pressure (BP), cholesterol levels, and smoking.

Nearly 13 million Americans have CAD, and the incidence increases with age (Keller, Sabatino, Winland-Brown, Porter, & Keller, 2015). Since the 1970s, the mortality rate from CAD has shown a pronounced decline in the United States. Most of this decline can be attributed to changes in lifestyle and improved technologies such as thrombolytic drugs. The decline in cardiovascular disease has occurred in older as well as younger age groups, suggesting that the effects of risk factor modifi cation persist well into later life.

Blood Pressure The systolic blood pressure (SBP) rises with age; the dia- stolic blood pressure (DBP) remains the same or drops a bit.

Established hypertension is a risk factor for cardiovascular disease in the geriatric age group, with systolic elevations posing a greater risk than diastolic elevations. Overall, the risk for both genders of experiencing a cardiovascular event or death is two to three times higher in those with signifi cant hypertension than in those who are normotensive. Isolated systolic hypertension (ISH) is defi ned as an SBP greater than 160 mm Hg and a DBP of less than 90 mm Hg. Aggressive treatment of ISH has demonstrated a signifi cant reduction in stroke, myocardial infarction (MI), and sudden cardiac death.

Cholesterol Serum cholesterol levels rise with age, up to age 60 years; thereafter, these levels begin to drop. The risk of the effects of an elevated cholesterol level persists from middle age to extreme old age. Aggressive efforts are often indicated to lower low-density lipoprotein (LDL) levels and raise high- density lipoprotein (HDL) levels for cardiac protection. Con- troversy exists about the role of statins in primary prevention of low-risk older adults (Keller et al., 2015; Patterson, Gaz- ziano, & Greenland, 2014).

Smoking Smoking is an independent signifi cant risk factor for ath- erosclerosis and coronary heart disease (CHD) ( Carter et al., 2015). Smoking cessation is strongly advised as both primary prevention (Patterson et al., 2014) and secondary prevention for those with known CAD or peripheral vascular disease (American Heart Association [AHA]/American College of Cardiology [ACC], 2013).

Additional proven or postulated risk factors for cardiovas- cular disease in older adults include obesity, lack of exercise, left ventricular hypertrophy, and impaired glucose tolerance. Older adult individuals are most likely to have a combination of risk factors, which has a cumulative effect of increasing the risk of CAD. Control of hypertension is clearly the most potentially remediable risk factor. Evidence is compelling for discontinuation of cigarette smoking at any age. More infor- mation is needed regarding the effectiveness and feasibility of lowering cholesterol levels, weight reduction, improved exercise plans, and strict control of blood glucose levels, with respect to the incidence of CHD, particularly in those of most advanced age.

Chapter 8 ■ Chest Disorders 153

Cardiac risk assessment tools, including the Global Framingham Risk Assessment, are available at https:// www.nhlbi.nih.gov/health-pro/guidelines/in-develop/ cardiovascular-risk-reduction/risk-assessment/. Assessment for metabolic syndrome and obesity, including body mass index (BMI) and waist circumference, also enhances risk assessment.

Physiological Changes The size of the heart remains essentially unchanged, although some increase in left ventricular wall thickness has been demonstrated, even in older individuals who do not have cardiovascular disease. Left ventricular hypertrophy is usually due to increased cardiac demand, most likely caused by an increase in peripheral resistance. Peripherally, the vessels become atherosclerotic and arteriosclerotic, and the SBP increases with age. Structural and physiological changes in the aging cardiovascular system cause decreased capacity to endure stresses, decline in physical activity performance, and limited functional reserve capacity (Keller et al., 2015). Fat deposits accumulate around the sinoatrial (SA) node. The number of pacemaker cells usually has decreased by age 75 years. Baroreceptors become less sensitive with age, and the response to changes in BP often is blunted.

These physiological changes have little functional impact on the aging heart at rest, but with exercise or stress, they render the aging heart less capable of increasing and sus- taining an increase in cardiac output. The maximal heart rate declines approximately 30% between ages 20 and 80 years. Cardiac dilation and increased stroke volume compen- sate somewhat for the diminished heart rate during exercise (Keller et al., 2015).

Symptom Assessment Using the Onset, Location, Duration, Characteristics, Aggra- vating factors, Relieving factors, Timing (OLDCART) mne- monic or Precipitating/Palliating factors, Quality, Radiation, Severity, Timing (PQRST) mnemonic, ask the patient about chest pain, shortness of breath, dizziness, palpitations, or edema. Establish the patient ’ s usual baseline activities of daily living (ADLs) and activity level and ask how symptoms are affecting this. Some older adults experience palpitations as a nervous feeling, so include that in your questioning. Chest pain may be presented as heartburn or indigestion, particu- larly if the patient also has gastroesophageal refl ux disease (GERD). Shortness of breath may be felt as anxiety but is a more common presentation of an acute coronary event than chest pain. Atypical presentation for MI includes vague symptoms such as nausea, decreased ADL status, and fatigue without chest pain (Cash & Gunter, 2016; Keller et al., 2015).

CLINICAL EXAMINATION FEATURES

In the actual physical assessment of the older adult, the apical impulse is diffi cult to locate, as the chest wall under- goes changes due to the intercostal muscles weakening, resulting in an increased anteroposterior diameter (Bickley, 2017).

Auscultation in the geriatric patient frequently reveals changes in normal heart sounds, extra heart sounds, bruits, and murmurs. The S 1 is more easily heard, and splits of the fi rst heart sound are more easily detected because of an ejec- tion sound that occurs when the aortic valve cusp tissue fails to fold into the vessel wall during ejection. A change in the loudness of S 1 , accompanied by a slow heart rate, may indi- cate heart block. The S 2 split on inspiration is narrower or absent because of decreased compliance of the pulmonary vasculature. An opening snap occurs when the mitral or tri- cuspid valve produces minor vibrations of increased inten- sity caused by more rapid cusp movement or a resistance to infl ow caused by cusp fusion (Bickley, 2017). An audible opening snap is the best physical sign of mitral stenosis, but it becomes less obvious in the older adult whose valves are rigid and calcifi ed.

Ventricular fi lling sounds, best heard with the stetho- scope bell, are caused by the halting of the ventricle after ventricular fi lling. The physiological S 3 , heard most clearly at the apex, disappears by the fourth decade as the ventri- cle stiffens and fi lling becomes less rapid. An S 3 in an indi- vidual more than 50 years old is usually pathological and refl ects an increased fi lling rate, indicating heart failure or mitral regurgitation (Bickley, 2017). Early diastolic fi lling is reduced in healthy older adults resulting in an end-diastolic volume maintained by an increase in atrial contribution to left ventricular fi lling. This condition may cause an S 4 , which in the absence of other fi ndings, is considered normal in older adults.

The carotid arteries should be assessed routinely for the presence of bruit. Asymptomatic carotid bruit is a risk factor for stroke (Bickley, 2017). Studies demonstrate that a vessel is occluded more than 50% by the time a bruit can be heard. In older adults assess the top level of the internal jugular pul- sation when evaluating jugular venous pressure. Do not use the external jugular veins, because they may be sclerosed and appear to be falsely distended or may yield a falsely low pres- sure reading.

Prolonged extra heart sounds (murmurs), particularly sys- tolic ones, are quite common in elderly individuals. Systolic murmurs, which often indicate aortic valve disease, occur in more than 50% of individuals over age 70 years. The soft sys- tolic ejection murmur is due to the dilation and the decrease in compliance of the aorta caused by stiffening of the aortic cusps without obstruction (aortic sclerosis). Loud murmurs, which usually indicate aortic stenosis, are often accompa- nied by a slow rising carotid pulse and left ventricular hyper- trophy. An apical pansystolic or late systolic murmur also occurs frequently in older persons, resulting from fl oppy valves that become regurgitant over time. The two most common causes of mitral regurgitation are papillary muscle dysfunction (usually due to MI) and mitral annular calcifi ca- tion. Diastolic murmurs, which are almost always patholog- ical in elderly persons, may be caused by heart block, aortic regurgitation, or mitral stenosis ( LeBlond, Brown, Suneja, & Szot, 2014 ).

In the older adult, additional features of cardiac disease may be seen on physical examination of systems other than the heart. The eye examination may reveal the thick corneal arcus seen with lipid abnormalities or the funduscopic fi nd- ings of atherosclerosis. The skin may demonstrate xantho- mas or cholesterol nodules and changes in skin temperature,

154 Chapter 8 ■ Chest Disorders

indicating a metabolic or peripheral vascular disease causing or contributing to cardiac disease. The presence of edema must be determined. The clinical cardiac examination fea- tures in the geriatric patient are:

■ Structural wall changes are common. ■ S 1 is more easily heard. ■ S 2 split is narrower. ■ S 4 is common. ■ Systolic murmurs are common. ■ Bruits (carotid, abdominal) are common.

ASSESSMENT OF THE RESPIRATORY SYSTEM

Key symptoms warranting evaluation include increasing dyspnea and persistent cough (Kane et al., 2018). In order to assess the respiratory system accurately in the older adult, the nurse practitioner must be familiar with changes in tissue and in the musculoskeletal and respiratory systems that are caused by aging.

The aging process is characterized by a loss of elasticity and fl exibility in collagen and elastin tissue components; this impedes the normal expiratory recoil of the lung. The con- current decrease in body water composition dries mucous membranes and interferes with the protective functions of the upper airway in expelling foreign material. Loss of elastin also affects the alveoli and the basement membrane of the capillary wall, where gas exchange occurs. A thick- ening occurs in both areas, limiting the amount of diffusion (Bickley, 2017; Shanker, Rojas & Caufi eld, 2017). Musculo- skeletal changes, including calcifi cation of costal cartilage and weakening of inspiratory muscles, result in a relaxation of the skeletal contours and an increased anteroposterior diameter, causing a barrel chest, although not as pronounced as that found in patients with chronic obstructive pulmonary disease (COPD). An exaggeration of the thoracic curvature may also occur, with some tracheal displacement. Expiratory muscles must work harder because expiration is no longer a passive act, resulting in use of accessory muscles. The resid- ual capacity of the lungs is increased and inspiratory reserve capacity lessened. Air tends to fi ll the apices and not the bases. Because of decreased muscular strength, the cough refl ex is not as forceful or as effective. All of these changes occur gradually and are hardly noticeable unless a physi- ological challenge or stress arises. Even in such an event, exertional dyspnea may be the only observed change in the healthy older adult. Healthy lifestyle behaviors also serve to mitigate these age-related changes.

Healthy older adults or those with stable, chronic prob- lems are unlikely to seek care unless there is a change in functional capabilities related to breathing, such as decreased exercise tolerance, shortness of breath with exertion, or easy fatigability. In frail older adults an increase in respira- tions, sweating, or anorexia may be the only indication of a respiratory problem. History questions should address the symptom(s) using the OLDCART or PQRST symptom analy- sis formats. Is there a prior history of the problem(s) or of any respiratory problem(s)? Does the patient use tobacco, or has he or she used it in the past? Is there a history of

occupational exposures or lung problems? Has the possibility of tuberculosis (TB) been eliminated? Is the patient a silent aspirator? Any changes in medications, including the use of over-the-counter (OTC), herbal, and homeopathic remedies, should be addressed. Is there a cough, sputum production, or hemoptysis? Is the patient wheezing? If there is pain, have cardiac or musculoskeletal causes been ruled out? If there is dyspnea, is it related to activity, or does it occur at rest or when lying down? How many pillows are used? Specifi c ques- tions about changes in endurance, stair-climbing, or ADLs are necessary to quantify the extent of the problem. Does the problem interfere with eating? Has there been a 10-pound weight loss or gain in the past 6 months? Has the patient received the infl uenza vaccine and pneumococcal vaccine? Is HIV a consideration?

Physical assessment of the respiratory system begins with general observation of the patient: rate and ease of respi- rations at rest, conversational ability (limited by breathing problems), use of accessory muscles, posture, color, pursed lips, circumoral or nail bed cyanosis, and capillary refi ll. The chest and upper back should be exposed for full inspection and examination. Are both sides symmetrical, with equal respiratory effort and diaphragmatic movement? Is there any evidence of kyphosis, lordosis, or scoliosis? Rapid respiratory rates are common with pneumonia, fever, or COPD.

Palpation of the posterior chest to confi rm equal chest expansion is done by placing the thumbs on the chest wall near the vertebrae at T9 and T10 and spreading the hands. A small fold of skin should be between the thumbs. When the patient takes a deep breath per your instruction, the thumbs should move apart symmetrically. If pneumonia or consolida- tion is suspected, palpating for tactile fremitus may be helpful. Using the ball of the hand (metacarpophalangeal area of the palm) or the ulnar side of the hand, feel the vibrations in a side-to-side pattern while the patient says “ninety-nine.” The vibrations should feel the same on either side and should be stronger in the upper areas. Increased fremitus occurs with marked consolidation, such as lobar pneumonia. Percussion of the posterior chest for resonance and symmetry is the next step, again using a side-to-side approach. Dullness is indic- ative of increased density, as found with pneumonia, tumor growth, or pleural effusion. Hyperresonance is found with air trapping in emphysema or with pneumothorax. Auscultation of posterior breath sounds for symmetry, presence or absence of adventitious sounds, and air movement is done with the patient seated and the arms resting on the knees to retract the scapulae. The patient is instructed to take a deep breath through the mouth, with the mouth open, inhaling and exhaling. Decreased breath sounds are common with emphy- sema, pleurisy, or pleural effusion. Wheezing is commonly heard with asthma or acute bronchitis, although it may also be part of the background of chronic bronchitis or COPD. Crackles are heard with congestive heart failure (CHF), pul- monary edema, or pneumonia; basilar crackles that clear with coughing or deep breathing are not pathological. Older patients become light-headed with deep breathing and may need this part of the examination to be spaced out over time. If pneumonia is suspected, vocal fremitus techniques such as bronchophony, egophony, or whispered pectoriloquy may be indicated. Examination of the anterior chest follows the same sequence. The right middle lobe is auscultated anterolaterally.

Chapter 8 ■ Chest Disorders 155

ASTHMA

Signal Symptoms: Wheezing, shortness of breath, cough (especially at night), chest tightness.

Description: The Global Initiative for Asthma (GINA) provides an operational defi nition of asthma as a chronic infl amma- tory disorder of the airways in which many cells and cellular elements play a role. The chronic infl ammation is associated with airway hyperresponsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or early in the morning. These episodes are usually associated with widespread, but variable, airfl ow obstruction within the lung that is often reversible either spontaneously or with treatment (Global Strategy for Asthma Management and Prevention, 2016 update).

Etiology: Both GINA and the National Asthma Education and Prevention Program Expert Panel Report–3 (NAEPP-EPR-3) (2007) cite a lack of agreement on defi nition and etiology due to the complexity and variation in manifestation of asthma as well as the lack of identifi cation of the phenotype qualities of asthmatics. Characteristics that are agreed on are infl ammation, airway hyperresponsiveness, airway obstruc- tion, and clinical symptoms (NAEPP-EPR-3, 2007).

Occurrence: In the United States, asthma is more prevalent in African Americans—the age-adjusted rate for those over 18 years of age is 8.7%; the rate for Caucasians is 7.6%; and the rate for Hispanics/Latinos is 5.8% (U.S. Department of Health and Human Services, Centers for Disease Control and Prevention [CDC], 2016 , March). Worldwide, it is estimated that asthma affects up to 334 million people and is respon- sible for 346,000 deaths each year (Global Asthma Network, 2014; Global Strategy for Asthma Management and Preven- tion, 2016 update).

Age: The age-adjusted rate for adults 65 to 74 years old is 6.9%; for age 75 and older it is 6.2% (U.S. Department of Health and Human Services, CDC, National Center for Health Statistics, 2016).

Gender: In adult asthma there are more females with the disease than males (Wheaton et al., 2016). The age-adjusted rate for females over 18 years old is 9.7%; for males it is 5.4% (U.S. Department of Health and Human Services, CDC, National Center for Health Statistics, 2016).

Ethnicity: African Americans have a higher rate of asthma in the United States.

Contributing Factors: Exposure to allergens, respiratory infec- tions, family history/genetic predisposition, atopy, occupa- tional irritants, tobacco smoke (smoking and passive smoke exposure)), high levels of indoor and outdoor pollution, and obesity; rhinitis is a specifi c factor in older adults (Global Strategy for Asthma Management and Prevention, 2016 update; Miller & Sawlani, 2013; Tarasidis & Wilson, 2015). Multiple genes contribute to the development of asthma in different ethnic groups; research into genetic phenotypes is ongoing (Global Strategy for Asthma Management and Pre- vention, 2016 update; Toskala & Kennedy, 2015).

Signs and Symptoms: Recurrent wheezing, cough (especially occurring at night), recurrent chest tightness, and recurrent

breathing diffi culty (Miller & Sawlani, 2013). Symptoms may occur in conjunction with a respiratory infection, weather changes, contact with environmental allergens, strong emo- tional reactions, animal fur, mold, exercise, or other triggers. Medications including aspirin, NSAIDs, and beta blockers can exacerbate symptoms. Older adults are less likely to sense dyspnea related to airway obstruction, even in the presence of cough, chest tightness, or wheezing (Vaz Fragoso, 2016). Other symptoms may include rhinorrhea with postnasal drip.

Diagnostic Tests: Spirometry or pulmonary function testing, particularly forced expiratory volume in 1 second (FEV 1 ), FEV 6 , forced vital capacity (FVC), and FEV 1 /FVC ratio before and after bronchodilator challenge, showing an improve- ment of 12% and 200 mL, indicates reversible airway obstruction (Brigham & West, 2015). This is helpful in differ- entiating asthma from COPD, particularly in an older adult with a prior smoking history. A history of atopy or allergen testing may establish an allergic component. In a patient with dyspnea, measurement of brain natriuretic peptide, also known as B-type natriuretic peptide (BNP), and a chest x-ray may be needed to eliminate other conditions. If spirometry is near normal, bronchoprovocation such as a methacholine challenge test may help to differentiate other conditions with a similar presentation (NAEPP-EPR-3, 2007; Vaz Fragoso, 2016). Older adults tend to have increased hyperrespon- siveness to bronchoprovocation even when adjusting for the baseline amount of airway obstruction, atopy, or smoking status (Vaz Fragoso, 2016). Vaz Fragoso (2016) suggests that in response to a low provocative challenge (PC-20), a PC-20 threshold for hyperresponsiveness should be decreased to less than 4 mg/mL in lieu of the standard less than 8 mg/ mL. The American Thoracic Society (ATS) has endorsed the use of FeNO, the fractional nitrous oxide measurement in exhaled breath, as a biomarker for eosinophilic infl ammation and a complimentary tool to assess airway disease, including asthma (Bjermer et al., 2014). At the present time, use and utility of this test are still evolving.

Differential Diagnosis:

■ COPD ■ CHF ■ Pneumonia ■ Upper respiratory infection (URI) ■ Pulmonary embolism (PE) ■ Anxiety disorder ■ Vocal cord dysfunction (VCD) ■ Cough secondary to drugs ■ GERD ■ Allergic bronchopulmonary aspergillosis (ABPA)

Treatment: The NAEPP-EPR-3 (2007) has identifi ed four components of asthma management:

■ Assessment and monitoring measures, including patient history, physical examination, and objective testing, such as spirometry, to diagnose asthma and determine severity and initial and ongoing level of control

156 Chapter 8 ■ Chest Disorders

■ Patient, family, and professional education for partner- ship in asthma management

■ Control of comorbidities and environmental factors affecting asthma

■ Pharmacotherapy

Treatment in older adults may need to be individualized based on comorbidities.

Recommendations from the NAEPP-EPR-2 (1997) rel- evant to older adults that are incorporated into current asthma guidelines include:

■ Review of patient technique in using inhaler medica- tions/devices is essential; functional, visual, or cognitive impairments may require more intense and prolonged instruction for safe and effi cacious use.

■ A comprehensive medical history is essential to safely integrate asthma medications without aggravating

pre-existing medical conditions such as osteoporosis, glaucoma, or cardiac problems. Conversely, medications such as beta blockers or aspirin prescribed for a pre-ex- isting condition may need to be reevaluated if they are exacerbating the asthma.

■ COPD may coexist with asthma; a trial of systemic corticosteroids will establish reversibility and benefi t.

Initial assessment of severity is optimized when the patient has not been started on long-term controller therapy. Asthma is classifi ed as intermittent or persistent; persistent is further classifi ed as mild, moderate, or severe based on certain parameters (NAEPP-EPR-3, 2007) (see Figure 8-1 ).

Once the severity is established, treatment goals at all levels aim to control asthma and evaluate responsiveness to the plan of care ( Figure 8-2 ) using a stepwise approach to management ( Figure 8-3 ).

Intermittent

Components of Severity

Impairment

Normal FEV 1 /FVC:

8–19 yr 85% 20–39 yr 80% 40–59 yr 75% 60–80 yr 70%

Moderate Severe

Classification of Asthma Severity ≥12 years of age

Persistent

Mild

Symptoms

Nighttime awakenings

Short-acting beta

2 -agonist use

for symptom control (not

prevention of EIB)

Interference with normal activity

Lung function

≤2 days/week

≤2x/month

≤2 days/week

None

• Normal FEV 1

between exacerbations • FEV

1 >80%

predicted • FEV

1 /FVC normal

0–1/year

�2 days/week but not daily

Daily Throughout the day

3–4x/month 1x/week but not

nightly Often 7x/week

Several times per day

Daily �2 days/week

but not daily, and not more than 1x on any day

Minor limitation Some limitation Extremely limited

• FEV 1 >80%

predicted • FEV

1 /FVC normal

• FEV 1 >60% but

<80% predicted • FEV

1 /FVC

reduced 5%

• FEV 1 <60%

predicted • FEV

1 /FVC

reduced 5%

Consider severity and interval since last exacerbation. Frequency and severity may fluctuate over time for patients in any severity category.

Relative annual risk of exacerbations may be related to FEV 1 .

Step 3 Step 4 or 5

≥2/year Exacerbations requiring oral

systemic corticosteroids

Risk

Step 2Step 1 Recommended Step for

Initiating Treatment

and consider short course of oral systemic corticosteroids

In 2–6 weeks, evaluate level of asthma control that is achieved and adjust therapy accordingly.

Assessing severity and initiating treatment for patients who are not currently taking long-term control medications

Key: FEV 1 forced expiratory volume in 1 second; FVC, forced vital capacity; ICU, intensive care unit

FIGURE 8-1. Classifying asthma severity and initiating treatment in youths ≥ 12 years of age and adults. FEV 1 , forced expiratory volume in 1 second; FVC, forced vital capacity. (National Asthma Education and Prevention Program [2007, August]. Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. Section 4 : Stepwise approach for managing asthma in youths ≥ 12 years of age and adults. Bethesda, MD: National Heart, Lung, and Blood Institute. Available from www.ncbi.nlm.nih.gov/books/NBK7222 .)

Chapter 8 ■ Chest Disorders 157

Components of Control

Impairment

Not Well Controlled

Very Poorly Controlled

Classification of Asthma Control ≥12 years of age

Well Controlled

Symptoms

Nighttime awakenings

Short-acting beta 2 -agonist

use for symptom control (not prevention of EIB)

Interference with normal activity

Validated questionnaires

ATAQ ACQ ACT

≤2 days/week >2 days/week Throughout the day

≤2x/month 1–3x/week ≥4x/week

Extremely limitedSome limitation

≤2 days/week

None

>2 days/week Several times per day

0 ≤0.75* ≥20

Exacerbations requiring oral systemic corticosteroids

Risk

Recommended Action for Treatment

FEV 1 or peak flow <60% predicted/

personal best 60%–80% predicted/ personal best

>80% predicted/ personal best

1–2 ≥1.5 16–19

3–4 N/A ≤15

0–1/year ≥2/year

Consider severity and interval since last exacerbation.

Progressive loss of lung function

Treatment-related adverse effects

Evaluation requires long-term follow-up care

Medication side effects can vary in intensity from none to very troublesome and worrisome. The level of intensity does not correlate to specific levels of control but should be considered in the overall assesment of risk.

• Maintain current step. • Regular follow-ups every 1–6 months to maintain control. • Consider step down if well controlled for at least 3 months.

• Step up 1 step. • Reevaluate in 2–6 weeks. • For side effects, consider alternative treatment options.

• Consider short course of oral systemic corticosteroids. • Step up 1–2 steps, and • Reevaluate in 2 weeks. • For side effects, consider alternative treatment options.

*ACQ values of 0.76–1.4 are indeterminate regarding well-controlled asthma. Key: EIB, exercise-induced bronchospasm; ICU, intensive care unit

FIGURE 8-2. Assessing asthma control and adjusting therapy in youths ≥ 12 years of age and adults. EIB, exercise-induced bronchospasm. (National Asthma Education and Prevention Program [2007, August]. Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. Section 4 : Stepwise approach for managing asthma in youths ≥ 12 years of age and adults. Bethesda, MD: National Heart, Lung, and Blood Institute. Available from www.ncbi.nlm.nih. gov/books/NBK7222 .)

Asthma is a chronic health problem, just as hyperten- sion and diabetes are. Regular chronic maintenance visits are required for optimal management. Depending on level of control, patients should be seen every 1 to 6 months for reevaluation. An interval symptom history is highly import- ant in ongoing monitoring of control and adjustment of stepped treatment. An increase in symptoms indicating that asthma is not well controlled necessitates stepped up man- agement and more frequent monitoring.

All patients who are able to read and comprehend should have an asthma action plan that is updated whenever changes in treatment are made (Apter, 2015). A printable asthma action plan including information on controlling environmental triggers is available at www.nhlbi.nih.gov/ health/public/lung/asthma/asthma_actplan.pdf. The plan may need to be adapted to older adults who cannot or will not perform peak expiratory fl ow rate (PEFR) monitoring.

Although one study in 2006 found no additional benefi t of PEFR monitoring in terms of health-care utilization, lung function, or quality of life (Buist, Vollmer, Wilson, Frazier, & Hayward, 2006), it is recommended that patients with mod- erate to severe asthma use a diary every day to record the PEFR and their symptoms (Bailey & Gerald, 2016). Pharma- cotherapy for asthma follows the guidelines in the NAEPP- EPR-3 (2007) outlined in Figure 8.3 .

Patients who experience symptoms less than twice per month may be managed with a short-acting beta agonist (SABA) such as albuterol used as required for symptoms. Lev- albuterol is an alternative with fewer side effects than albu- terol. Patients are instructed to contact their primary care provider if symptoms increase, necessitating more frequent use of the SABA, or if their use of the medication does not alleviate symptoms. Prior to a step-up in treatment, inhaler adherence and technique must be assessed.

158 Chapter 8 ■ Chest Disorders

Intermittent Asthma

Persistent Asthma: Daily Medication Consult with asthma specialist if step 4 care or higher is required.

Consider consultation at step 3.

Step 3

Preferred: Low-dose ICS + LABA

OR

Medium-dose ICS

Alternative: Low-dose ICS + either LTRA, theophylline, or zileuton

Each step: Patient education, environmental control, and management of comorbidities. Steps 2–4: Consider subcutaneous allergen immunotherapy for patients who have asthma.

Quick-Relief Medications for All Patients • SABA as needed for symptoms. Intensity of treatment depends on severity of symptoms: up to 3 treatments at 20-minute intervals as needed. • Use of SABA >2 days a week for symptom relief (not prevention of EIB) generally indicates inadequate control and the need to step up treatments.

Step 2

Preferred: Low-dose ICS

Alternative: Cromolyn, LTRA, nedocromil, or theophylline

Step 1

Preferred: SABA PRN

Step 4

Preferred: Medium-dose ICS + LABA

Alternative: Medium-dose ICS + either LTRA, theophylline, or zileuton

Step 5

Preferred: High-dose ICS + LABA

AND

Consider omalizumab for patients who have allergies

Step 6

Preferred: High-dose ICS + LABA + oral corticosteroid

AND

Consider omalizumab for patients who have allergies

Step up if needed

(first, check adherence,

environmental control, and

comorbid conditions)

Assess control

Step down if possible

(and asthma is well controlled

at least 3 months)

Alphabetical order is used when more than one treatment option is listed within either preferred or alternative therapy. EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting inhaled beta2-agonist; LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta2-agonist

FIGURE 8-3. Stepwise approach for managing asthma in youths ≥ 12 years of age and adults. EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting inhaled beta-2 agonist; LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta-2 agonist. (National Asthma Education and Prevention Program [2007, August]. Third Expert Panel on the Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. Section 4 : Stepwise approach for managing asthma in youths ≥ 12 years of age and adults. Bethesda, MD: National Heart, Lung, and Blood Institute. Available from www.ncbi.nlm.nih.gov/books/NBK7222 .)

For persistent asthma, initiate stepwise therapy with the goal of well-controlled asthma. For patients with mild per- sistent asthma by severity classifi cation, Step 2 therapy with a low-dose inhaled corticosteroid (ICS) such as fl uticasone should be initiated. The patient should be followed up in 2 to 6 weeks to evaluate level of control and modify treatment as indicated.

Patients with moderate persistent asthma should be started on Step 3 therapy with either a medium-dose ICS or a combined low-dose ICS and long-acting beta agonist (LABA) such as fl uticasone/salmeterol, budesonide/formoterol, or momentasone/formoterol. Follow up at 2 to 6 weeks for evaluation of response and adjustments to therapy. Referral should be considered for patients requiring Step 3 or higher therapy.

Patients with severe persistent asthma should be started on Step 4 treatment with a medium-dose ICS and LABA

combination and reassessed at 2 to 6 weeks for response and level of control.

For Steps 2 through 4 alternative treatments include a leukotriene modifi er antagonist (LTRA) such as montelukast, either alone (Step 2) or in combination with an ICS (Steps 3 through 4). A recent Cochrane review (Chauhan & Ducha- rme, 2014) found that LTRAs were safe but not as effective as monotherapy ICS for asthma. Research continues into the role of leukotrienes in asthma (Singh, Tandon, Dastidar, & Ray, 2013). Theophylline is also listed as an alternative treat- ment in Steps 2 through 4. Vaz Fragoso (2016) discourages the use of this medication in older adults due to toxicity and adverse effects. Other considerations in older adults with comorbidities include individualizing therapy; for example, for a patient with heart disease, increasing the dose of ICS and avoiding a LABA is prudent; for a patient with glaucoma or osteopenia, adding a LABA or LTRA instead of increasing

Chapter 8 ■ Chest Disorders 159

the dose of ICS is preferable (Saag, Furst, & Barnes, 2016; Vaz Fragoso, 2016). In short, guidelines are not meant to be absolute and do not preclude the use of clinical judgment.

Patients with severe persistent asthma should be referred for add-on treatment. Treatment at Step 5 is usually with a high-dose ICS/LABA and possible addition of omalizumab for patients with an allergic component. Studies have demon- strated that omalizumab, a humanized monoclonal antibody, is safe and effective for diffi cult-to-control asthma in older adults who meet allergic criteria. Treatment with omalizumab should be discontinued if the patient has not responded to the therapy within 4 months of initiation (Chang et al., 2014). Practitioners must be prepared to treat anaphylaxis in the unlikely event that it occurs.

Step 6 is reserved for patients who are not well controlled at Step 5. Therapy includes high-dose ICS and LABA and oral corticosteroid. Omalizumab also should be considered for those with an allergic component. Close follow-up of these patients is essential to avoid further morbidity and even mor- tality due to asthma. Oral corticosteroid therapy should be limited to short “bursts” to avoid drug-related events.

Asthma exacerbations in older adults frequently result in emergency department visits or hospital admissions. Aggressive treatment with SABAs and systemic (IV or oral) glucocorticoids is the standard of care, along with frequent spirometric assessment (Fanta, 2016.). Patients who do not respond well within 4 to 6 hours should be hospitalized (Fanta, 2015). It is critical to encourage patients to adhere to prescribed medication regimens. Evidence indicates that only 30% to 40% of patients currently take their asthma medica- tions as prescribed (Sumino & Cabana, 2013).

Stepping down therapy is a gradual process compared to stepping up treatment. If a patient has been stable and well controlled for 3 months or more, it is generally safe to decrease the dose of ICS by 25% to 50% (GINA, 2016; Hagen, 2014).

Follow-Up: Regular monitoring should be done 1 to 3 months after initiation of treatment, and then every 3 to 12 months, depending on the level of control and severity. Patients should be seen within 1 week after an asthma exacerbation, and within 2 to 6 weeks when changes are made in stepwise management (Fanta, 2016; GINA, 2016; Khalid, 2015). Treatment step-down can be considered if the patient has had good control for 3 months; follow-up should be sched- uled every 1 to 3 months after treatment step-down has been initiated (GINA, 2016).

Sequelae: Asthma in older adults is associated with increased bronchial hyperresponsiveness and a more rapid decline in lung function than in older adults without asthma (Hanania & Busse, 2016; Vaz Fragoso, 2016). Older adults also have increased treatment-related adverse events. Comorbidities such as COPD, cardiovascular disease, osteoporosis, glau- coma, diabetes mellitus, and other health problems com- plicate management and may limit treatment options. Older adults have the highest rate of asthma-associated mortality.

Prevention/Prophylaxis: There is no known strategy to prevent asthma. Patients with asthma should be given an infl uenza vaccine annually. Immunization with the pneumococcal pneumonia vaccine is also advised if the patient has not already been immunized. Partnership with the patient/family in education to recognize triggers, identify changes in status, and seek prompt medical assistance to avoid complications is key to success. Avoidance of environmental factors is also essential.

Referral: According to the NAEPP-EPR-3 (2007) report, consultation with an asthma specialist is advised at Step 4, with a suggestion to consider a consultation at Step 3. Older adults who have multiple comorbidities, have been treated in the emergency department, or have been hospitalized due to an asthma exacerbation within the past year should also be managed in collaboration with an asthma specialist. Patients who require ongoing oral corticosteroids or more than two courses of oral corticosteroids in a year should be referred to an asthma specialist. Patients having any complications that affect asthma or those who require further testing should also be referred (Fanta, 2016; GINA, 2016; NAEPP-EPR-2, 1997); patients with characteristics of both asthma and COPD fall into this category (Fanta, 2016; GINA, 2016). Patients/families may also be referred to a community-based asthma education program, although many of these initia- tives are more focused on childhood asthma. Referral to case management through local Area Agency on Aging services can be helpful if the patient has unmet care needs or fi nan- cial problems with obtaining medications.

Education: Patient/family education is an important compo- nent of asthma management in older adults. In addition to educating patients on the disease and the need for frequent monitoring and immediate reporting of increased symptoms, a written asthma action plan should be initiated, detailing how to identify and deal with environmental triggers, med- ications (including dosage and frequency), and when to seek emergent care. Instruction in use and care of inhalers and spacers, if used, is also important. If the patient is on an ICS, instruct on the need for daily use and oral hygiene to prevent a fungal infection. Clarifi cation of the action and role of quick relief inhaler versus daily controller therapy is essential for medication adherence. The role of patient as partner in asthma management should be emphasized (Peláez, Bacon, Lacoste, & Lavoie, 2016).

Risk factors predictive of uncontrolled asthma in adults are African American race, less education, living in poverty, a BMI of more than 30 kg/m 2 , insurance status, history of gas- troesophageal symptoms, prior exacerbations, and current tobacco use (Miller & Sawlani, 2013; Schatz et al., 2013). Gearing education to the health literacy level of the patient is critical to gaining patient understanding and partnership. Patients who are still smoking should receive brief motiva- tional counseling at each visit and referral to a Quitline or community-based smoking cessation program when ready to quit. Referral to the local Area Agency on Aging for assis- tance with insurance issues may also be benefi cial.

160 Chapter 8 ■ Chest Disorders

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The hallmark of asthma is partial reversibility of airfl ow obstruction on spirometry following beta-2 agonist administration.

C Kraft & Oppong, 2015

Short-acting beta-2 agonists (SABAs) are indicated only as needed rather than on a scheduled basis for all levels of asthma severity.

A Kraft & Oppong, 2015

ICSs are the preferred controller medication for all but mild intermittent asthma.

A Kraft & Oppong, 2015

Long-acting beta agonists (LABAs) are the preferred add-on agent due to lack of control, but they should never be used as monotherapy without ICSs.

A Kraft & Oppong, 2015

It is important to educate patients on the proper technique for inhaled medications and trigger avoidance.

B Kraft & Oppong, 2015

The best strategy for management and improved outcomes is early treatment of asthma exacerbations.

A Humphrey, 2016

Initial treatment (of asthma exacerbation) should include oxygen for most patients, SABA for all patients, ipratropium bromide for severe exacerbations, and systemic corticosteroids for most patients.

A Humphrey, 2016

Initial treatment response in the emergency department, rather than severity of attack presentation, is a better predictor of need for hospitalization.

C Humphrey, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

CARDIAC ARRHYTHMIAS

Signal Symptoms: No symptoms at times; feeling of heart “beating out of the chest.”

Description: An arrhythmia is a disturbance of cardiac rhythm. Cardiac arrhythmias, which occur in either the presence or absence of underlying heart disease, may be life threatening or may be an incidental fi nding. Arrhythmias may be differentiated by type or mechanism.

Atrial fi brillation (AF) is the most common sustained rhythm disorder. AF consists of numerous fi brillatory P waves that vary in shape, size, and timing. The ventricular response is often chaotic and rapid if the atrioventricular (AV) conduc- tion is intact. AF can be clinically classifi ed as follows:

■ Paroxysmal: less than 7 days self-terminating or with intervention; episodes may occur with varied frequency

■ Persistent: greater than 7 days and requires interven- tion to terminate

■ Long-standing persistent: continuous AF more than 12 months

■ Permanent: used when the patient and clinician make a joint decision to stop further attempts to restore or maintain sinus rhythm

■ Nonvalvular: in the absence of rheumatic mitral steno- sis, a mechanical or bioprosthetic heart valve or mitral valve repair ( January et al., 2014 )

Other prevalent forms of arrhythmias in a geriatric pop- ulation are:

Sick Sinus Syndrome: 1) Pathological bradyarrhythmia with an alternating supraventricular tachyarrhythmia (brady- cardia-tachycardia syndrome); 2) supraventricular tachyar- rhythmia—three primary categories.

Arrhythmias Primarily of Atrial Origin: Atrial premature beats, ectopic atrial rhythms, multifocal atrial tachycardia, atrial fl utter, and AF.

Arrhythmias Arising Primarily Within the AV Node: AV nodal reen- trant tachycardia, junctional premature beats, and nonpar- oxysmal junctional tachycardia.

Arrhythmias Partially Supraventricular in Origin: Pre-excitation syndromes.

Ventricular Arrhythmias: Ventricular ectopic beats are the most common variety.

Chapter 8 ■ Chest Disorders 161

Etiology: Most arrhythmias are thought to be caused by abnormalities either in impulse formation (disordered auto- maticity) or in impulse conduction (allowing reentry), or by a combination of the two. Increased automaticity is an accen- tuation of the inherent ability of many cardiac tissues to gen- erate an independent rhythm. Reentry consists of a wave of excitation repeatedly circulating around a fi xed anatomical obstacle. Triggered arrhythmias are caused by altered cellu- lar depolarization.

Occurrence: Studies show that asymptomatic older patients with no known structural heart disease have an incidence of up to 40% of sinus arrhythmia, supraventricular or ventricu- lar premature beats, or supraventricular tachycardia.

Age: The prevalence of ventricular arrhythmia increases with age, occurring in 80% of healthy older adults ages 60 to 85 years. AF is diagnosed in 4.8% of women and 6.2% of men over age 65 years at baseline examination, and its prev- alence is strongly associated with advanced age, particularly in women. Although no specifi c data are available, the inci- dence of junctional arrhythmias and tachycardias related to the accessory pathway may be lower in older adult individu- als because of an age-related reduction in accessory pathway conduction.

Gender: Arrhythmias occur slightly more often in men than in women (see also section on Age).

Ethnicity: Not signifi cant.

Contributing Factors: Pre-existing heart disease is a contrib- uting factor to arrhythmias, with structural disease becom- ing more prevalent with age. The muscular response and contractility decreases as the patient ages. The patient expe- riences a reduction in cardiac function and contractility. This reduction is responsible for a decreased stroke volume and ejection fraction. The average older adult does not expe- rience adverse symptoms with normal everyday activities. However, stressors (whether they are physical, psychological, environmental, or social) can increase the risk of illness in the patient. These illnesses are taxing to the patient ’ s system, and the increased energy demands place an increased demand on the cardiac system. The aging process can also have an adverse effect on the cardiac valves. The valves tend to become thick and stiff secondary to arteriosclerosis and atherosclerotic plaques. Fibrosis or calcifi cation in the vicin- ity of the AV node causes conduction disturbances. Atrial arrhythmias may be caused by a mechanical obstruction to atrial emptying with subsequent left atrial dilation, myocar- dial ischemia, and increased sympathetic activity.

An age-related factor associated with tachyarrhythmias is increased left atrial size. This enlargement may contrib- ute to the increase in supraventricular ectopy. Increases in ventricular ectopic beats may be related to left ventricular enlargement. The overload of ionized calcium in the older myocardium may contribute to ectopy. Age-related factors associated with bradyarrhythmias include an age-related decline in the number of pacemaker cells and the presence of fat deposits around the SA node. His bundle cells are replaced with fi brous tissue, and adipose tissue and amyloid are depos- ited; this is also associated with conduction disturbance.

Systemic diseases (i.e., thyrotoxicosis, infection, hypox- emia, hypercapnea) can cause circulatory disturbances

that may provoke an arrhythmia. Drugs that can cause an arrhythmia include digitalis and other antiarrhythmics, aminophylline, and alcohol. Electrolyte disturbances, par- ticularly hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia, can precipitate ectopic beats. Family history of sudden cardiac death may indicate a predisposing factor for rhythm disorder, such as hypertrophic obstructive cardiomy- opathy, congenital prolonged QT syndrome, or the presence of an aberrant conduction pathway.

Signs and Symptoms: The history, physical examination, and electrocardiogram (EKG) studies represent the cornerstone to evaluation of arrhythmias. Arrhythmias may cause symp- toms due to a reduced blood fl ow or inadequate cardiac pump function. In the history, the patient may describe sensations that accompany abnormal cardiac rhythm such as pounding, racing, or skipped beats. Older adults are less likely to com- plain of palpitations and more likely to present with mani- festations of heart failure or hypoperfusion (i.e., impaired mental function, dizziness, syncope). There appears to be a peak in syncopal episodes after age 65 years in both men and women. The Framingham study showed an increased incidence of syncope after age 70 years, from 5.7 events per 1,000 person-years in men ages 60 to 69 years, to 11.1 events in men ages 70 to 79 years ( Moya et al., 2009 ). Along with the history of present illness, previous diagnosis and treatment for arrhythmia and cardiac disease should be elicited.

In the physical examination, concentrate on the cardiac and peripheral vascular systems. Check the pulses for 1 full minute to determine rate and regularity (Bickley & Szi- lagyi, 2013; Goolsby & Grubbs, 2015). Assess normal and extra heart sounds. S 1 intensity may provide information about the relation of atrial to ventricular contraction. The longer the PR interval, the softer the S 1 . Note intermittent extra heart sounds (S 3 and S 4 ). The jugular vein must be assessed. In AV dissociation (when the atria and ventricles contract independently), giant A waves (cannon waves) may be observed. Provoking maneuvers should not be attempted by the advanced practice nurse but may be attempted by a cardiologist. These maneuvers include carotid massage (for atrial arrhythmias only), mild exercise, psychological stress, pharmacological stress, and electrical programmed stimula- tion (EPS).

Other indicators of hemodynamic response to an arrhyth- mia include level of consciousness and skin temperature and color. The history should guide the remainder of the episodic examination because it is also helpful in identifying the contributing factors that may precipitate or aggravate an arrhythmia.

Diagnostic Tests:

TEST RESULTS INDICATING DISORDER

Rhythm strip Rhythm disturbance may be present, or if

transient, it may be absent

12-lead EKG Acute MI or ischemia, prolonged QT

intervals, and pre-excitation may be

identifi ed as precipitators of an

arrhythmia

Continued

162 Chapter 8 ■ Chest Disorders

TEST RESULTS INDICATING DISORDER

Ambulatory EKG

monitoring

Quantifi es arrhythmias with reference to

symptoms

Identifi es patients at risk for sudden death by

documenting ventricular arrhythmias and heart

rate variability

Implantable loop

recorder

In infrequent syncope this long-term device

(14 months) may identify the precipitant

Echocardiogram Identifi es structural, functional, and

hemodynamic abnormalities in the

cardiovascular system

Cardiac

electrophysiological

study

Evaluates specifi c arrhythmias to distinguish

these, determine location and characteristics,

and guide therapy

Implantable

cardioverter-

defi brillator (ICD)

ICD fi rings may be due to recurrent

arrhythmia

Electrolyte panel Identify electrolyte disturbance (i.e.,

hypokalemia, hyperkalemia, hypomagnesemia,

hypocalcemia) that may be causative or

contributory

Coronary and LV

angiography

Identifi es CAD and LV function

Cardiac MRI Especially useful in recognizing arrythmogenic

RV dysplasia, or infi ltrative diseases

Diagnostic testing includes a 12-lead EKG done with a rhythm strip, lasting at least 2 to 3 minutes. Include exercise testing for those with a clinical history suggesting exercise-induced arrhythmia. Ventricular arrhythmias can occur in individu- als with or without cardiac disorders. The standard resting 12-lead EKG is indicated in all patients who are evaluated for ventricular arrhythmias (Domino, 2017; Pedersen et al., 2014). An ambulatory 24-hour EKG (Holter monitoring) helps to quantify arrhythmias with reference to symptoms. Ambulatory EKG is indicated when there is a need to clarify the diagnosis by detecting arrhythmias, QT interval changes, T-wave alternans, or ST changes; to evaluate risk; or to judge therapy (Pedersen et al., 2014). Event recorders are best suited for documenting less-frequent but more-prolonged bouts of arrhythmias, although not used with as much fre- quency. Patient-activated loop memory devices, which record the EKG before the symptomatic event, are most useful. His bundle electrograms involve the insertion of a transvenous electrode catheter into the right ventricle, to record depolar- izations and the intervals. This method is most useful for dis- tinguishing AV block from an ectopic focus.

Echocardiography is recommended in patients with ven- tricular arrhythmias who are suspected of having struc- tural heart disease (Domino, 2017; Pedersen et al., 2014). An echocardiogram is used more commonly than magnetic resonance imaging (MRI) or cardiac computed tomogra- phy (CT) scan because it is inexpensive in comparison. The echocardiogram is a useful tool in assessing for valvular disorders, left ventricular function and wall motion, and the ejection fraction. The electrophysiological (EP) testing is performed using intracardiac recordings, electrical stimula- tion, and drugs to assess and document ventricular tachy- cardia, guide ablations, and evaluate loss of consciousness in patients with arrhythmias as the suspected cause. EP testing

is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyar- rhythmias, including palpitations, presyncope, and syncope (Domino, 2017; Pedersen et al., 2014). EP testing is recom- mended in patients with syncope of unknown cause with impaired left ventricular function or structural heart disease (Domino, 2017; Pedersen et al., 2014).

In EPS, multipolar catheter electrodes are introduced into the venous or atrial circulation and advanced to various in- tracardiac positions to monitor the electrical activity or to induce an arrhythmia. EPS is most useful for determining sinus node dysfunction, AV block, intraventricular conduc- tion disturbances, pre-excitation syndromes, supraventric- ular tachycardia, ventricular tachycardia, and unexplained syncope or palpitations. It is used also to monitor cardiac activity in survivors of sudden cardiac death.

Differential Diagnosis: Clarify the diagnosis with precision. Note reversible and precipitating causes of an arrhythmia and coexisting diseases.

Treatment: The incidence of asymptomatic arrhythmias of questionable clinical signifi cance is high. Arrhythmias are never treated in isolation; some are benign and some are lethal. Patients with hemodynamic compromise resulting from arrhythmia need to be hospitalized as soon as possible. Prehospital care for threatening hemodynamic instability secondary to tachyarrhythmia may include direct current cardioversion, and the nurse practitioner should be skilled in this intervention. After thorough investigation, the goals of arrhythmia treatment include the alleviation of bothersome symptoms, the prevention of complications from sustained arrhythmias, and the avoidance of sudden death associated with certain arrhythmias.

The risk of treatment is considerable. Aggressive thera- peutic treatment is indicated when patients are symptom- atic and the urgency of therapy depends on the associated hemodynamic disturbance. A comprehensive treatment plan must address the three cornerstones of AF management: rate control, rhythm control, and prevention of thromboem- bolism. Goals of the therapy should be to obtain symptom control, stroke prevention, and a reduction in hospital recid- ivism ( January et al., 2014 ). Three major factors determine how well a patient tolerates an arrhythmia: heart rate, dura- tion of the arrhythmia, and presence and severity of asso- ciated underlying heart disease. Arrhythmias often cannot be controlled unless underlying cardiac problems are discov- ered and treated. No antiarrhythmic “wonder drug” exists, and the bothersome and potentially dangerous side effects necessitate determination of clear indications and use of the utmost caution. Pharmaceutical agent selection is based on the electrophysiology of the rhythm disturbance, the mecha- nism of action, and the side effects of the drug. Several new drugs are useful as an alternative to warfarin for the preven- tion of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically signifi cant valve disease, severe renal failure, or advanced liver disease ( January et al., 2014 ). Conditions common in older adults that can affect the choice, dosing, effi cacy, and safety of antiarrhythmic therapy include decreased hepatic or renal function, decreased serum albumin levels, and electrolyte abnormalities.

Chapter 8 ■ Chest Disorders 163

The broad categories of arrhythmia treatment include medications, pacemakers, antitachycardia devices, implant- able automatic cardioverter-defi brillators, catheter abla- tive procedure, and specifi c maneuvers. Defi brillation is the required intervention in ventricular fi brillation or pulseless ventricular tachycardia and is the most important deter- minant of survival in cardiac arrest. Patients defi brillated within 2 minutes have a 60% hospital discharge survival rate (Hansen et al., 2014). Vagal maneuvers (carotid massage or the Valsalva maneuver) may terminate or slow AV nodal reentry or AV reentry types. These maneuvers are associated with a high risk of emboli dislodgment. The carotid arteries should be assessed for bruit before administering massage. Because of the high mortality rate associated with antiar- rhythmic surgery, it is not recommended in older adult indi- viduals. The specifi cs of treatment are not detailed in this text, because all assessment and management must be done in close collaboration with a physician specialist; much of the treatment is initiated by the specialist in the hospital setting.

Follow-Up: Because of their low therapeutic ratio, drug dosing and plasma concentrations of the antiarrhythmics are based on therapeutic monitoring. Side effects are signif- icant and include the negative inotropic effect, which can precipitate heart failure or proarrhythmia in the presence of structural heart disease. Extracardiac side effects can also be signifi cant, including anticholinergic effects, gastrointestinal effects, and neurological toxicity with some antiarrhythmic agents. Monitor patients after pacemaker insertion with regular follow-up appointments and EKG testing, specifi cally looking for pacemaker failure, infection, thromboembolism, perforation or dislodgment, and complicating arrhythmias.

Sequelae: Regardless of age, the nature and severity of under- lying heart disease are of much greater prognostic signif- icance than the arrhythmia alone. The following rhythm disturbances have been reported to carry a poor prognosis in patients with CAD: frequent ventricular premature con- tractions (VPCs) (greater than 10 per min), multiform VPCs, ventricular couplets, R-on-T phenomenon, and ventricular tachycardia.

Syncope can occur secondary to asystole. Syncope is an intermittent symptom that may be caused by an underlying

arrhythmia with or without cardiac disease. Treatment goals are prevention of symptom recurrence, improvement of quality of life, and prolongation of survival. Permanent cardiac pacing may relieve the symptoms but may not affect the survival rate. Syncope recurs in approximately 20% of the patients ( Moya et al., 2009 ; Saklani, Krahn,  & Klein, 2013). Bradycardia can contribute to complete heart block and to the development of heart failure in patients with associated ventricular dysfunction. Tachycardia can precipitate angina and circulatory arrest in patients with CAD. Bradyarrhyth- mias or tachyarrhythmias can cause systemic embolism and stroke. AF can result in heart failure and a low cardiac output state. The risk of stroke related to AF increases with age. The Cardiac Arrhythmia Suppression Trial (CAST) demonstrated that patients treated for prognostically signifi cant arrhyth- mias may have a higher mortality rate from sudden cardiac death if Class IC (fl ecainide and encainide) agents are used (Greenberg et al., 1995).

Prevention/Prophylaxis: All patients with AF should be con- sidered for long-term low-intensity warfarin or the newer anticoagulant therapy. Aspirin, though less effective in pre- venting stroke, is an alternative for some patients in whom warfarin is contraindicated. Electrolyte imbalances should be monitored and metabolic disturbances treated. Patients receiving digitalis should be monitored for toxicity.

Referral: All patients with treatable arrhythmias require col- laborative management. Clinically signifi cant ventricular arrhythmias or any symptomatic arrhythmia is managed by the specialist in the coronary care unit. A primary care provider may handle many atrial arrhythmias and low-grade ventricular arrhythmias; however, a specialist should be con- sulted for all clinically signifi cant ventricular arrhythmias, arrhythmias resistant to routine therapy, or arrhythmias whose clinical signifi cance is in doubt.

Education: Carefully instruct all patients receiving antiar- rhythmics about the therapeutic effects, side effects, and potentially adverse effects of these medications. Because patients with pacemakers are vulnerable to external electri- cal fi elds, they should be instructed to recognize this potential and avoid exposure. Patients with pacemakers must also be aware of signs and symptoms of pacemaker failure.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Oral anticoagulants are useful as an alternative to warfarin for the prevention of stroke and systemic thromboembolism in patients with paroxysmal to permanent AF and risk factors for stroke or systemic embolization who do not have a prosthetic heart valve or hemodynamically signifi cant valve disease, severe renal failure, or advanced liver disease. Based on shared decision making.

B January et al., 2014

A 1-minute delay in defi brillation is associated with a reduction in odds of survival of up to 21%.

C Scottish Intercollegiate Guidelines Network, 2007

Continued

164 Chapter 8 ■ Chest Disorders

Signal Symptoms: Dyspnea, chronic cough with or without sputum production, decreased activity tolerance, wheezing.

Description: COPD is defi ned by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as “a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airfl ow limitation that is due to airway and/or alveolar abnormalities usually caused by signifi cant exposure to noxious particles or gases” ( GOLD, 2017 , p. 2). Cardinal symptoms of COPD include dyspnea, chronic cough, and/or sputum production (GOLD 2017; Han, Dransfi eld, & Martinez, 2016).

A characteristic of COPD is chronic airfl ow limitation resulting from a parenchymal destruction (emphysema) and small airways disease (e.g., obstructive bronchiolitis) that vary among individuals and evolve at different intervals over time ( GOLD, 2017 ). Chronic infl ammation is responsi- ble for structural changes, narrowed passages of the small airways, and lung parenchyma destruction, leading to loss of alveolar attachments to the small airways and a reduc- tion in lung elastic recoil ( GOLD, 2017 ). The ability of the airways to remain open is diminished during expiration as a result. Characteristics of COPD are airfl ow limitation and

mucociliary dysfunction, both of which are likely attributed to loss of small airways ( GOLD, 2017 ).

The most signifi cant risk factor for COPD is cigarette smoking ( CDC, 2016 , Sept. 16; GOLD, 2017 ). Long-term cumulative exposure to noxious particles and gases, in com- bination with various other host factors such as airway hyperresponsiveness, inadequate lung growth and develop- ment during childhood, genetics, occupational/industrial gases or fumes, and indoor/outdoor air pollution are all con- tributing risk factors for COPD ( GOLD, 2017 ; GOLD, 2017a; Liu, Li, Ding, Wang, & Wen, 2016; World Health Organiza- tion [WHO], 2017). Long-term asthma has been attributed to some cases of COPD and advancing age is a factor with symptoms presenting often after the ages of 40 to 50 years old (WHO, 2017). Patients with symptoms and/or exposure to risk factors for COPD should be considered ( GOLD, 2017 ). The presence of persistent airfl ow limitation with lung func- tion measurements (spirometry) is required to confi rm the diagnosis of COPD ( GOLD, 2017 ).

Etiology: The most signifi cant etiological factor in the devel- opment of COPD and the progression of the disease is ciga- rette smoking ( CDC, 2016 , Sept. 16; GOLD, 2017 ). However,

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Permanent cardiac pacing may relieve the symptoms but may not affect the survival rate. Syncope recurs in approximately 20% of the patients.

C Moya et al., 2009

EP testing is recommended in patients with syncope of unknown cause with impaired left ventricular function or structural heart disease.

C Pedersen et al., 2014

EP testing is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope.

C Pedersen et al., 2014

Echocardiography is recommended in patients with ventricular arrhythmias who are suspected of having structural heart disease.

B Pedersen et al., 2014

Ambulatory EKG is indicated when there is a need to clarify the diagnosis by detecting arrhythmias, QT-interval changes, T-wave alternans, or ST changes, to evaluate risk.

C Pedersen et al., 2014

The standard resting 12-lead EKG is indicated in all patients who are evaluated for ventricular arrhythmias.

B Pedersen et al., 2014

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chapter 8 ■ Chest Disorders 165

individuals who are non-tobacco users may also develop airfl ow limitations and COPD ( GOLD, 2017 ). Long-term asthma has been attributed to some cases of COPD and advancing age is a factor with symptoms presenting often after the ages of 40 to 50 years old (WHO, 2017).

Occurrence: COPD is a chronic disease with substantial mor- bidity and mortality worldwide, lending to social and eco- nomic burdens, long-term disability, and premature death (American Lung Association [ALA], 2017; Criner et al., 2015 ; GOLD, 2017 ). COPD is the third leading cause of death in the United States, with over 3 million or 5% of all deaths globally attributed to COPD ( CDC, 2016 , Sept. 16; GOLD, 2017 ). An approximate 15.7 million Americans or 6.4% have been diagnosed with COPD ( CDC, 2016 , Sept. 16). Over one-half of adults with abnormally low pulmonary function tests were unaware they had COPD, thus the prevalence of COPD may be underrepresented ( CDC, 2016 , Sept. 16; Criner et al., 2015 ).

Age: Individuals aged 65 to 74 years and age 75 years and older have the highest incidence of COPD ( CDC, 2016 , Sept. 16). COPD development occurs gradually over time and most commonly becomes apparent after 40 to 50 years of age (WHO, 2017). Advancing age is a risk factor for COPD, although the evidence is unclear if healthy aging leads to COPD or if it is a result of the cumulative sum of exposures throughout life ( GOLD, 2017 ).

Gender: Anatomical and physiological differences between the male and female gender infl uence the course of respira- tory disease and treatment response (Pinkerton et al., 2015).

Women have an increased prevalence of COPD ( CDC, 2016 , Sept. 16; GOLD, 2017 ), although some studies have suggested women are more susceptible to the detrimental effects of smoking than men, leading to greater severity of disease and burden of small airway disease despite a similar history of tobacco exposure ( GOLD, 2017 ; Jenkins, 2017; Pinkerton et al., 2015). Evidence reveals that women who have COPD and have fewer pack-years of smoking than men have demonstrated an early-onset of COPD, experienced greater dyspnea, and progress to severe COPD more rapidly than men ( GOLD, 2017 ; Jenkins, 2017). When compared to men, women with comparable pack-year history smoking have shown more loss of lung function, airfl ow obstruction, and exercise intolerance than men ( GOLD, 2017 ; Jenkins, 2017). The differences found in women are presumably a result of the manner in which tobacco smoke is metabolized in women differently than men, rendering more higher and more prolonged toxic exposure to tobacco smoke (Pinkerton et al., 2015).

Ethnicity: Native Americans/Alaska Natives and multiracial non-Hispanic individuals have been found to have the great- est prevalence of COPD ( CDC, 2016 , Sept. 16).

Contributing Factors: Cigarette smoking is the most import- ant risk factor for COPD (CDC, 2017; GOLD, 2017 ). Inhaling other pollutants and exposure to particles (e.g., second-hand smoke, pipe, water pipe, or cigar use), environmental and occupational exposures (e.g., biomass fuel exposure, chem- icals, dust, fumes), and genetic determinants (e.g., alpha-1 antitrypsin defi ciency) are other causative factors in COPD ( GOLD, 2017 ; Liu et al., 2016; WHO, 2017). Chronic

bronchitis and frequent respiratory infections have been associated with a greater risk of COPD ( GOLD, 2017 ).

Signs and Symptoms: COPD is a complex, chronic disease and therefore requires a comprehensive assessment of symp- toms. Symptoms may include dyspnea, chronic cough with or without sputum production, recurrent lower respiratory infections, wheezing, chest tightness, fatigue, weight loss, and/or anorexia ( GOLD, 2017 ; GOLD, 2017a). Signs may include increased anteroposterior diameter of the thorax, use of accessory muscles for respiration, prolonged expiration, hyperresonance on percussion, decreased heart and breath sounds, tachypnea, neck vein distention during expiration in absence of heart failure, ruddy or cyanotic skin color, and clubbing of nail beds (Bickley, 2017). Nocturnal and seasonal exacerbation of symptoms are common. Weight loss, fatigue, and anorexia pulmonary cachexia are commonly associated with severe to very severe COPD ( GOLD, 2017 ). Symptoms of anxiety or depression may be present when assessed and are attributed to an increased risk of COPD exacerbations and less than optimal health ( GOLD, 2017 ).

“Chronic and progressive dyspnea is the most character- istic symptom of COPD” ( GOLD, 2017 , p. 25). Dyspnea is considered a cardinal symptom described by COPD patients as breathlessness, air hunger, chest heaviness, or gasping for breath ( GOLD, 2017 ). Chronic cough is commonly an initial symptom of COPD, and in about 30% of patients cough with tenacious sputum production is present ( GOLD, 2017 ). Because the COPD patient usually has several manifestations of COPD, symptoms often vary.

A thorough history to include pattern of symptom devel- opment, past medical history, family history, exposure to risk factors, history of exacerbations, and/or hospitalizations for respiratory conditions aid in establishing the diagnosis of COPD ( GOLD, 2017 ). The impact of symptoms such as activ- ity limitations, socioeconomic impact (e.g., missed work days) and comorbid conditions (e.g., cardiovascular heart disease, heart failure, osteoporosis) are supportive in developing the diagnosis of COPD.

The severity of symptoms and airfl ow limitation associ- ated with COPD are contributing factors impacting quality of life and ADLs. Limitations of functional activities vary daily, such as physical exertion, daily function, lifestyle man- agement, social activities, household chores, sleep, and work performance ( GOLD, 2017 ).

Physical examination is not typically diagnostic in early COPD and may be normal ( GOLD, 2017 ). This does not preclude a diagnosis of COPD and can aid in establishing a baseline and identifying comorbidities ( GOLD, 2017 ). In the early to middle stages, chest auscultation may reveal longer expirations, with wheezing on forced expiration. Wheezes can sometimes be heard (most frequently with chronic bron- chitis); the presence of crackles suggests possible pulmonary edema or pneumonia.

As the severity of the disease progresses, signs of airway limitations are more apparent on physical examination ( GOLD, 2017 ). Physical examination with advancing disease may reveal decreased breath sounds, hyperinfl ation (e.g., resonance to percussion), use of accessory muscles of respi- ration, wheezes, crackles in the lung bases, pursed lip breath- ing, and/or distant heart sounds (Bickley, 2017; Han et al., 2017). Hyperinfl ation restricts diaphragmatic movement and

166 Chapter 8 ■ Chest Disorders

the chest takes on a barrel-like appearance (Bickley, 2017). As the cardiovascular system attempts to compensate, tachy- cardia or a gallop rhythm commonly occurs. Right-sided heart failure and cor pulmonale seen in the later stages may present as jugular venous distension, hepatomegaly, or peripheral edema (Bickley, 2017). Patients frequently present for treatment due to health-related issues, such as upper or lower respiratory infections, thus presenting an opportunity for the clinician to assess symptomatology of COPD.

Diagnostic Tests: Spirometry is the gold standard for measur- ing airfl ow limitation ( GOLD, 2017 ; Guirguis-Blake, Senger, Webber, Mularski, & Whitlock, 2016). Airfl ow limitation that is not fully reversible is evident if post-bronchodilator FEV 1 /FVC is less than 0.70 and FEV 1 is less than 80% pre- dicted (refer to Table 8-1 ) (GOLD, 2017a). The U.S. Preventive Services Task Force (USPSTF) recommends spirometry only in symptomatic patients, as there was no direct evidence to support screening asymptomatic individuals (Guirguis-Blake et al., 2016). Symptoms for considering a diagnosis and per- forming spirometry include dyspnea, cough, chronic sputum production, recurrent lower respiratory tract infections, history of risk factors, family history of COPD, and/or child- hood factors (GOLD, 2017a). Although the GOLD guidelines (2017) are focused on spirometry results, FEV 1 decreases with age and, therefore, the age-related change needs to be factored into interpretation of spirometry results ( GOLD, 2017 ). Spirometry has good sensitivity, although a peak expiratory fl ow measurement alone is unreliable when used as the only diagnostic tool because of weak specifi city ( GOLD, 2017 ). Because there is a weak correlation between FEV 1 , symptoms, and impairment impacting an individual ’ s health status, a more formal assessment of symptoms is indicated.

The updated 2017 GOLD guidelines added important multidimensional recommendations regarding COPD man- agement and treatment. In addition to results of spirome- try, assessing the impact of COPD, the burden of disease, the risk of disease progression, and COPD exacerbation risk are integral components ( GOLD, 2017 ; Karloh et al., 2016). Thirteen disease-specifi c instruments have been identifi ed as COPD assessment tools (Karloh et al., 2016). The most com- prehensive disease-specifi c questionnaires with reliability and validity focused on health status include the Chronic Respi- ratory Questionnaire (CRQ) and the St. George ’ s Respiratory Questionnaire (SGRQ) ( GOLD, 2017 ; Karloh et al., 2016).

Both tools are comprehensive, but are lengthy, and the scoring systems are too complex to use for clinical settings ( GOLD, 2017 ; Karloh et al., 2016). Brief and simple, yet valid and reliable assessment tools recommended for clinical prac- tice include the COPD Assessment Test (CAT) and the COPD Control Questionnaire (The CCQ) ( GOLD, 2017 ; Karloh et al., 2016). Of the two, the CAT is widely utilized, applicable worldwide, and useful to predict clinical correlation of dis- ease-related impact ( GOLD, 2017 ; Karloh et al., 2016).

Radiographic imaging with a chest x-ray alone is not diagnostic of COPD but can provide value in excluding dif- ferential diagnoses, detecting the presence of concomitant pulmonary disease (bronchiectasis, pleural diseases, pul- monary fi brosis), pneumonia, or cardiac diseases (e.g., car- diomegaly) ( GOLD, 2017 ). Chest radiography in early COPD appears normal (Dunphy, Winland-Brown, Porter, & Thomas, 2015). Abnormalities associated with COPD may be present on a chest x-ray, such as lung hyperinfl ation, hyperlucency of the lungs, or tapering of vascular markings ( GOLD, 2017 ). Structural lung disease may be seen on chest imaging (e.g., emphysema, gas trapping, or airway wall thickening) con- sistent with COPD fi ndings. A chest x-ray in those having advanced COPD with emphysema may reveal hyperinfl ation, bullae or blebs, and a fl at hemidiaphragm. A chest x-ray is not recommended for screening of lung cancer. The USPSTF (2017) recommendations for lung cancer screening include an annual screening with low-dose computed tomography (LDCT) in adults age 55 to 80 years with a 30 pack-year smoking history and who currently smoke or have smoked in the past 15 years.

Pulse oximetry is a noninvasive intervention to assess a patient ’ s arterial oxygen saturation and need for supplemen- tation oxygen therapy ( GOLD, 2017 ). If pulse oximetry is less than 92%, arterial or capillary blood gases are recommended ( GOLD, 2017 ).

Laboratory tests should include a complete blood count (CBC) with differential to rule out anemia, polycythemia (occurs in advanced COPD with hypoxemia), detecting the presence of infection consistent with an increased white blood cell (WBC) count, or if eosinophilia is present, con- sidering an allergic or asthmatic component (Dunphy et al., 2015). Serum alpha 1 -antitrypsin levels are recommended for individuals presenting with COPD at early ages (less than 45 years of age), in non-tobacco users with clinical emphysema, and individuals with a family history of COPD at a young onset (Dunphy et al., 2015).

An EKG is recommended as a baseline in patients with signs of advanced COPD or with concurrent cardiac disease. In COPD patients and older adults of any age, atrial arrthy- mias are common (Dunphy et al., 2015). Peaked P waves in leads II, III, and aVF are often apparent in patients with pulmonary disease (Dunphy et al., 2015). If concomitant cardiac involvement is severe, an EKG in advanced COPD may demonstrate evidence of right-axis deviation, sinus tachy- cardia, and pulmonary hypertension with the presence of ongoing S waves in the lateral precordial leads.

Differential Diagnosis: Carcinoma of the lung, asthma, inter- stitial lung disease, heart failure, pneumonia, bronchiecta- sis, TB, obliterative bronchiolitis, diffuse panbronchiolitis, chronic rhinitis, chronic sinusitis, obstructive sleep apnea, and/or PE.

Global Initiative for Chronic Obstructive Lung Disease: Post-Bronchodilator Fev 1 Classifi cation of Severity of Airfl ow Limitation

Patient Criteria: FEV 1 /FVC <0.70

FEV 1 ≥ 80% predicted GOLD 1: Mild

50% ≤ FEV 1 <80% predicted GOLD 2: Moderate

30% ≤ FEV 1 <50% predicted GOLD 3: Severe

FEV 1 <30% predicted GOLD 4: Very Severe

Adapted from GOLD Pocket Guide to COPD Diagnosis, Management, and Prevention, A Guide for Health Care Professionals , 2017.

TABLE 8-1

Chapter 8 ■ Chest Disorders 167

Treatment: Individualize treatment goals according to the stage of disease, assessment of symptomatology, patient goals, comorbidities, and risk COPD exacerbation. Treatment is targeted toward improvement of health status and func- tional status, quality of life, prevention of disease progres- sion, avoidance of exacerbations or complications, prevention of treatment side effects, and management of exacerbations ( GOLD, 2017 ). The GOLD syllabus identifi es four segments of a COPD management program: 1) diagnosis and assessment, 2) prevention and maintenance therapy, 3) management of stable COPD, and 4) management of COPD exacerbations. Because diagnosis and assessment has been addressed in the Assessment/Diagnostic Tools section, the remaining seg- ments will be focused on prevention and management.

Prevention and Prophylaxis: ■ COPD is almost 100% preventable by avoidance of

smoking. Early detection of COPD may alter the course and progression ( CDC, 2016 ).

■ All COPD patients should have annual infl uenza vac- cines unless allergic (CDC, 2017a). The pneumococ- cal polysaccharide vaccine (PPSV23) is recommended for all patients at age 65 years (CDC, 2017a). Prior to age 65, adults 19 to 64 years of age at high risk (e.g., cigarette smoking, chronic conditions, COPD) are rec- ommended to have the PPSV23 (CDC, 2017a). For indi- viduals who receive a PPSV23 prior to age 65 years, revaccination is recommended with PPSV23 at age 65 years (CDC, 2017a).

Risk Factor Reduction: ■ Identifi cation and reduction of exposure to risk factors

is key in the prevention and treatment of COPD ( GOLD, 2017 ).

■ Smoking cessation is the most effective and cost-ef- fective intervention and should be promoted at every visit (CDC, 2017; GOLD, 2017 ). Counseling (brief or intensive), educational, and community resources are helpful. Pharmacotherapy (e.g., nicotine replace- ment therapy, buproprion, varenicline, or combination therapy) consistently should be offered as a component of an intervention program (CDC, 2017; GOLD, 2017 ).

■ Identify and reduce personal exposure to occupational or environmental risk factors (fumes, gases, dust, indoor/outdoor air pollutants).

■ Vaccination for infl uenza and pneumococcal (PCV13 and PPSV23) are recommended unless contraindicated.

■ Adequate hydration and nutrition are important.

Management of Stable COPD: ■ Individualize assessment to reduce current symptoms

and risk of exacerbations. Tailor plan for escalating/ de-escalating treatment-based interventions dependent on symptomatology and COPD exacerbation risk.

■ Establish a partnership facilitating patients to become active partners in their care. Educate patients on the nature of the disease process, chronicity, and risk factors for progression. The role of self-management and the health-care team is recognition of instability and when to seek medical assistance. Adherence to treatment regimen should be included in education provided.

■ Discussion of healthy living, nutrition, and physical activity is essential.

■ Pulmonary rehabilitation is recommended in patients with high symptom burden to reduce symptomatology and risk of exacerbations ( GOLD, 2017 ; McCarthy et al., 2015). Pulmonary rehabilitation has been shown to be a highly effective therapeutic intervention to improve dyspnea, health status, and exercise intolerance ( Criner et al., 2015 ; GOLD, 2017a).

■ Long-term supplemental oxygen therapy in patients with severe resting hypoxemic COPD has been shown to improve survival (GOLD, 2017a). Additional ben- efi ts include reductions in nocturnal hypoxemia and arrhythmias, reduction in polycythemia, dyspnea, increased exercise tolerance, and improved cognitive status. Criteria for oxygen therapy include PaO 2 = 55 mm Hg or SaO 2 = 88% with or without hypercapnia confi rmed twice over a 3-week period; or PaO 2 = 55 to 60 mm Hg or SaO 2 = 88% if there is evidence of pulmo- nary hypertension, polycythemia, or peripheral edema suggesting heart failure ( GOLD, 2017 ).

Anxiety and depression are comorbidities associated with COPD and attributed to poor health outcomes (Panagioti, Scott, Blakemore, & Coventry, 2015). Assess for symptoms and provide psychological interventions as indicated. Holistic care can facilitate self-management and self-care. Pharmaco- logical management is the cornerstone of COPD treatment and is directed at symptom reduction, reducing the risk and severity of COPD exacerbations, and improving exercise tol- erance and health status ( GOLD, 2017 ). The GOLD (2017) guidelines recommend initiation therapy along with sub- sequent escalation and/or de-escalation pharmacological management.

When dyspnea is unrelieved by medications and inter- feres with functioning and quality of life, consider evaluation for surgical options. Lung volume reduction therapy, lung resections, transplants, and laser bullectomy are available in selected circumstances ( GOLD, 2017 ).

Clinician–patient communication should include a dis- cussion of disease progression and patient choices for care, including high technology (intensive care unit [ICU], venti- lator), subacute, long-term ventilator dependent, long-term care, home care, and surgical options. End-of-life care to include advance directives, resuscitation, palliative care and hospice considerations, and place of death preferences are important components.

Management of COPD Exacerbations: COPD exacerbations are defi ned as “an acute worsening of respiratory symptoms that result in additional therapy” (GOLD, 2017a, p. 31). They are attributed to progression of disease, worsening health status, and mortality (Wedzicha, 2015). Most commonly, COPD exacerbations are precipitated by respiratory tract infections ( GOLD, 2017 ).

COPD exacerbations are classifi ed as mild, moderate, or severe (GOLD, 2017a). Interventions aligned with severity include: mild (short-acting bronchodilator [SABDs]; treat- ment only; moderate (SABDs and/or oral corticosteroids); or severe (emergency department visit or hospitalization required) (GOLD, 2017a). Severe exacerbations may be asso- ciated with acute respiratory failure, which can be non-life threatening or life-threatening ( GOLD, 2017 ).

Treatment modalities include short-acting beta 2 -agonists with or without anticholinergics, long-acting bronchodilators,

168 Chapter 8 ■ Chest Disorders

systemic corticosteroids, antibiotics, noninvasive mechanical ventilation, and/or invasive mechanical ventilation (GOLD, 2017a).

Individualized COPD action plans for management of COPD exacerbations with a brief patient educational session has been found to signifi cantly reduce the risk of hospital- ization (Howcroft, Walters, Wood-Baker, & Walters, 2016). Goals for treatment include minimizing the negative impact relative to the current exacerbation and preventing future events ( GOLD, 2017 ).

Pharmacological Management Pharmacological therapy for COPD has a signifi cant role in reducing symptoms, reducing exacerbation frequency and severity, along with improving exercise tolerance, health status, and quality of life (Dunphy et al., 2015; GOLD, 2017 ). Individualized treatment regimens are required based on assessment of symptoms severity, airfl ow limitation, and/or severity of COPD exacerbation ( GOLD, 2017 ). A step-wise approach to therapy is utilized in the treatment of COPD. No current drug therapy has been proved to infl uence the long-term, progressive decline in COPD lung function ( GOLD, 2017 ). Classes of medications to in the treatment of COPD are:

Inhaled Beta 2 -Agonist Bronchodilators: Bronchodilators are widely used in the treatment of COPD to reverse bron- choconstriction by relaxing smooth muscles in the airways ( GOLD, 2017 ). Acute bronchospasms lead to permanent airway remodeling and, therefore, prevention is paramount (Dunphy et al., 2015). There are two types of beta 2 -agonists: SABAs and LABAs. SABAs, known as “rescue” inhalers, are prescribed for intermittent symptoms on an as-needed basis. SABAs include medications such as albuterol or levalbuterol. Onset is rapid, about 15 to 30 minutes, and duration of action is 4 to 6 hours.

Beta-agonists are sympathomimetic agents with adverse effects that may include transient tachycardia, nervous- ness, palpitations, and and/or arrhythmia ( GOLD, 2017 ). SABAs are not recommended for regular use and in patients who have recurrent symptoms. Modifi cation of the treat- ment regimen with a step-wise approach would be indicated ( GOLD, 2017 ).

LABAs in COPD are used for maintenance therapy to prevent acute bronchospasms and not for relief of acute symptoms (Dunphy et al., 2015). The duration of LABAs is about 12 hours ( GOLD, 2017 ). Formoterol and salmeterol are two examples of LABAs that have demonstrated improve- ment in COPD patients (Ferguson & Make, 2017).

Inhaled Anticholinergic/Antimuscarinic Bronchodilators: Inhaled antimuscarinic bronchodilators block the bronchoconstric- tion effects of acetylcholine on muscarinic cholinergic recep- tors in the smooth muscle of the airways ( GOLD, 2017 ). The short-acting antimuscarinic (SAMA) agent, ipratroprium, has a duration of 6 to 8 hours and is used in long-term and acute COPD management ( Criner et al., 2015 ; Fergu- son & Make, 2017). Tiotropium, a long-acting anticholin- ergic/antimuscarinic, is used for maintenance treatment of COPD. Duration of action is about 24 hours. Tiotropium has been shown to decrease symptoms of dyspnea along with the frequency of COPD exacerbations and hospitalizations ( Criner et al., 2015 ; Ferguson & Make, 2017). Tiotropium

demonstrated more benefi ts, such as fewer COPD exacerba- tions, reduced hospital admissions, and improved quality of life, as compared to ipratropium ( Cheyne, Irvin-Sellers, & White, 2015 ). Antimuscarinic agents have anticholinergic properties and should be used cautiously in patients with narrow-angle glaucoma, prostatic hypertrophy, or bladder neck obstruction, and are contraindicated in patients who are allergic to atropine (Dunphy et al., 2015).

Combination Bronchodilator Therapy: When used in combina- tion, bronchodilators with different mechanisms of action may improve the degree of bronchodilation with a lower risk of increasing a monotherapy agent ( GOLD, 2017 ). Combi- nation inhaled therapy with LABAs, ICSs, or long-acting inhaled anticholinergics are used for stable COPD patients with symptoms and may be more effective than the agents as individual components ( Farne & Cates, 2015 ). In patients with stable, moderate to very severe COPD, a maintenance combination of an ICS/LABA or ICS and inhaled long-acting anticholinergic therapy are recommendations ( Criner et al, 2015 ). For patients with severe COPD and persistent symp- toms, triple therapy is recommended with a combination ICS/LABA and inhaled long-acting anticholinergic (Ferguson & Make, 2017).

Glucocorticoids: Glucocorticoids are utilized in the manage- ment of COPD for the anti-infl ammatory effects on COPD-as- sociated infl ammation ( Criner et al., 2015 ). Two types of glucocorticoids are available: ICSs and systemic corticoster- oids. ICSs are used in combination with LABAs for optimal symptom management in persistent symptoms. Flutica- sone/salmeterol and budesonide/formoterol are examples of combination pharmacological agents available. Instruct the patient to rinse the mouth after using. ICSs are not recom- mended for use as monotherapy due to greater effi cacy when combined with a LABA ( GOLD, 2017 ). In a large meta-analy- sis reviewing 71 randomized controlled studies with 73,062 individuals, lung function and quality of life was improved on combination inhalers (LABA and ICS) as compared to monotherapy with ICS ( Kew, Dias, & Cates, 2014 ).

Systemic corticosteroids (e.g., prednisolone) have nonspe- cifi c anti-infl ammatory properties and are used for short-term treatment in the management of an acute COPD exacerba- tion. Systemic corticosteroids are associated with numerous side effects and, therefore, have no role in long-term manage- ment of COPD ( GOLD, 2017 ).

Methylxanthines: Theophylline, a nonspecifi c phosphodies- terase inhibitor, is the most common of methylxanthines, although its use has decreased signifi cantly. Theophylline is an oral bronchodilator that has been found to be modestly effective with a small therapeutic range, potential for toxic- ity, many drug-to-drug interactions, and wide range of toxic adverse effects ( GOLD, 2017 ).

Inhaled Delivery Technique: Delivery of inhaled pharmacolog- ical agents in COPD management is user dependent and has been identifi ed as a long-term issue in COPD management (Sanchis, Gich, & Pederson, 2016).

Follow-Up: A newly diagnosed patient should be seen fre- quently until an optimal treatment plan is in place and disease education has been completed. For stable patients, routine reassessment every 3 to 6 months is advisable, with

Chapter 8 ■ Chest Disorders 169

instructions to the patient or caregiver to schedule an interim visit if there is a change in status, increased symptoms, or an infectious process. For stable patients with other signifi cant comorbidities, visits every 3 months are advisable. A team model for chronic care is optimal for COPD management. Periodic reassessment of pulmonary function and assess- ment of patient report of breathing status can guide therapy. Patients who are unstable or have had an acute exacerbation will need more frequent follow-up visits initially. Collabora- tive management with these patients is strongly advised. During the immediate post-acute period, a pulmonary spe- cialist should manage the patient. Pulmonary rehabilitation is helpful in moderate to severe disease ( GOLD, 2017 ).

Sequelae: COPD is a multisystem disease and can lead to infections, particularly respiratory (pneumonia, recurrent bronchitis, viral infections), cor pulmonale, pulmonary hypertension, malnutrition, acute or chronic respiratory failure, steroid-induced myopathy or Cushing ’ s syndrome, bullous lung disease, polycythemia, and sleep-related hypox- emia. Depression is frequently associated with COPD (Remels et al., 2007; Shapiro et al., 2010).

Prevention/Prophylaxis: Avoidance of tobacco, smoking cessa- tion, and avoidance of second hand smoke are helpful.

Referral: Collaborative management is advised in all patients. Refer patients to a pulmonary specialist during instability, for hospital and post-acute care, and for oxygen therapy eval- uation. Refer patients to a surgeon if the option of surgery is deemed appropriate. Refer patients to physical therapy for reconditioning; occupational therapy may also be helpful in teaching breathing techniques and energy-conserving mea- sures. Consult with a dietary health professional when appli- cable. Post-acute COPD patients in the community should be referred for home care. Refer all patients to community resources and support groups. Palliative care and hospice options are considerations.

Education: Teach the patient, family, and/or caregivers about the disease process and its management; the association of risk factors such as smoking and importance of cessation; pharmacological therapy; oxygen therapy and precautions; and seeking early care with symptoms of exacerbation or infectious processes ( GOLD, 2017 ). Self-management edu- cation and coaching are integral components of a chronic care model approach ( GOLD, 2017 ). Self-management skills patients need to learn include monitoring and managing signs and symptoms of COPD; treatment adherence; and maintaining regular follow-up with health-care providers.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Smoking cessation is the most effective and cost-effective intervention and should be promoted at every visit.

A GOLD, 2017 CDC, 2016

In patients with respiratory symptoms, particularly dyspnea, spirometry should be performed to diagnose airfl ow obstruction. Spirometry should not be used to screen for airfl ow obstruction in asymptomatic individuals.

B GOLD, 2017 Guirguis-Blake et al., 2016

Pulmonary rehabilitation consisting of exercise training, muscle strengthening, nutritional counseling, energy conservation, ADLs, breathing modifi cations, medication education (including use of inhaler devices), and oxygen use is benefi cial, particularly in moderate-to-severe COPD.

A GOLD, 2017

Supplemental oxygen therapy in patients with hypoxemic COPD improves survival.

A GOLD, 2017

Bronchodilators are the foundation of symptomatic management; they are given on an as-needed basis for symptom management.

A GOLD, 2017

ACP, ACCP, ATS, and ERS recommend that clinicians prescribe monotherapy using either long-acting inhaled anticholinergics or long-acting inhaled beta agonists for symptomatic patients with COPD and FEV 1 <60% predicted. Clinicians should base the choice of specifi c monotherapy on patient preference, cost, and adverse effect profi le.

A GOLD, 2017 Cheyne et al., 2015 Farne et al., 2015 Kew et al., 2014

Long-term monotherapy with oral corticosteroids is not recommended in COPD.

A GOLD, 2017

Continued

170 Chapter 8 ■ Chest Disorders

Signal Symptoms: Dyspnea on exertion, orthopnea, parox- ysmal nocturnal dyspnea, progressive activity intolerance, weakness, progressive edema.

Description: As a cardiac syndrome, heart failure is a sec- ondary process associated with multisystem pathophysiol- ogy involving neurochemical regulation, abnormal cardiac muscle structure, and/or wall function. The older term con- gestive heart failure does not represent symptom presentation in all heart failure patients; therefore, the preferred term is heart failure.

Etiology: CAD and hypertension are the most common etiol- ogies of heart failure. Other causes of heart failure include valvular heart disease, dysrhythmias (e.g., AF), COPD, obstructive sleep apnea, fl uid volume overload, and hyper- or hypometabolic disorders (e.g., diabetes, anemia, thyroid disease, infection). Heart failure with reduced left ventricu- lar ejection fraction (HF r EF), previously referred to as systolic heart failure, is due to a large, thin left ventricular wall that has lost the elasticity required to effectively eject enough blood to maintain normal cardiac output ( Yancy et al., 2013 ). In con- trast, heart failure with preserved LVEF (HF p EF), previously referred to as diastolic heart failure , is caused by thick, stiff- walled ventricles and may occur with normal or near-normal LVEF ( Yancy et al., 2013 ).

Occurrence: Prevalence of heart failure with preserved and reduced LVEF are evenly distributed, with 650,000 new cases diagnosed each year ( Mozzafarian et al., 2016 ). The lifetime risk of developing heart failure is 20% for those over 40 years of age or older. The 5-year mortality rate is approximately 50% ( Mozzafarian et al., 2016 ). Heart failure is the fourth most common hospital discharge diagnosis in those over age 65 (CMS, 2015). Hospital readmissions within the fi rst 30 day are correlated with increased mortality risk (Krumholz et al., 2013).

Age: More common in older adults.

Gender: More common in men in the general population, but higher in women within the long-term care setting.

Ethnicity: African Americans have higher rates of heart failure.

Contributing Factors: Nonmodifi able risk factors include gender and race. Advanced age is an independent risk factor for heart failure. Modifi able risk factors for heart failure are tobacco use, SBP of more than 140 mm Hg, fasting glucose of more than 125 mg/dL, elevated cholesterol, obesity, diet, and physical inactivity. Use of NSAIDs, COX-2 inhibitors, glucocorticoids, and thiazolidinediones are common precip- itating factors for heart failure in the geriatric population (Maxwell & Jenkins, 2011; Trelle et al., 2011 ; Yancy et al., 2013 ).

Heart failure is caused by myocardial structural or func- tional damage. To maintain cardiac output, stroke volume, and vital organ perfusion, the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) are acti- vated to release neurohormones. Angiotensin II, the end product of the RAAS and a potent vasoconstrictor, leads to increased systemic vascular resistance, enhances the release of catecholamines from noradrenergic nerve endings, and directly stimulates the adrenal cortex to increase secretion of aldosterone. Vasopressin (antidiuretic hormone) and aldosterone secretion cause sodium and fl uid retention with subsequent increase in blood volume. Increased systemic vascular resistance, decreased arterial pressure, increased venous pressure, increased blood volume, and decreased venous compliance further increase ventricular wall stress and myocardial oxygen demand. Ultimately, these normal physiological responses become maladaptive and result in damage to the heart, cardiopulmonary, renal, and systemic vasculature, and cause progression of heart failure.

Signs and Symptoms: Geriatric patients with severe heart failure may be asymptomatic, whereas others with mild disease can suffer incapacitating symptoms (Ahmed, 2011).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Regular treatment with ICSs improves symptoms, lung function, and quality of life and reduces exacerbations in COPD patients with an FEV 1 <60% predicted.

A GOLD, 2017 Cheyne et al., 2015 Criner et al., 2015 Farne et al., 2015 Kew et al., 2014

Education improves patient response to exacerbations. B GOLD, 2017

Prospective end-of-life discussions can lead to effective end-of-life decisions as a result of understanding advance directives.

B GOLD, 2017

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

HEART FAILURE

Chapter 8 ■ Chest Disorders 171

Left ventricular heart failure leads to pulmonary venous congestion, subsequent right ventricular dysfunction, and portal and systemic venous congestion. Clinical symptoms of dyspnea on exertion or at rest, orthopnea, dry cough (worse in recumbent position), and/or paroxysmal nocturnal dyspnea indicate increased pulmonary venous congestion. Progressive lower extremity edema (not due to venous insuf- fi ciency or hypoalbuminemia) and abdominal symptoms (pain, distention, nausea) related to hepatic enlargement are symptoms suggestive of right ventricular failure or systemic venous congestion.

Signs that suggest heart failure include weight gain, tachycardia, S 3 or S 4 heart sound, laterally displaced point of maximum impulse (PMI), neck vein distention, rales in bilateral lower lobes that are not due to atelectasis, positive hepatojugular refl ux, and ascites. Cognitive impairment is common in older adults with heart failure.

Heart failure classifi cation is based on risk, cardiac struc- tural changes, symptom presentation, and functional impair- ment. The New York Heart Association (NYHA) classifi es heart failure based on functional limitation ( Yancy et al., 2013 ). This system is diffi cult to use with the elderly popu- lation, who may have functional decline related to comor- bid conditions. The heart failure rating system is based on risk factors, structural changes, and history of heart failure symptoms. The ACC/AHA system classifi es heart failure in four stages as the syndrome progresses along the natural tra- jectory and is used in conjunction with, not as a replacement for, the NYHA functional classifi cation system. Stages A and B refer to risk factors and present opportunities for primary and secondary prevention measures.

■ Stage A: Risk factors are present for heart failure without structural changes, history of signs or symp- toms, or functional limitations.

■ Stage B: Risk factors and structural changes in the heart are present without signs or symptoms of heart failure.

■ Stage C: Risk factors, structural changes in the heart, and past or current signs or symptoms of heart failure are present. At this stage, the patient is diagnosed with heart failure that does not regress back to former stages.

■ Stage D: Heart failure is refractory despite maximum medical management. Patients are symptomatic at rest or with minimal exertion.

Diagnostic Tests: Two-Dimensional Echocardiography Combined With Doppler Flow

Studies: Two-dimensional echocardiogram is considered the most useful diagnostic tool for evaluation of ventricular ejec- tion fraction and structural abnormalities for prognostic and interventional purposes (Ahmed, 2011; Yancy et al., 2013 ). Two-dimensional echocardiograms are essential to accurate diagnosis and treatment plan development. Echocardiogram is essential for those with unknown history of heart failure and clinical presentation to evaluate ventricular function, size, wall thickness, wall motion, and valve function crite- ria. Diagnosis of HF p EF is supported by 1) evidence of clin- ical heart failure symptoms, 2) normal or mildly abnormal LV systolic function, and 3) evidence of abnormal LV relax- ation, fi lling, diastolic distensibility, or diastolic wall function (Nugeuh et al., 2016).

Electrocardiography: EKGs may indicate left atrial enlarge- ment, left ventricular hypertrophy, arrhythmias, or ST-T wave changes associated with MI or ischemia.

Cardiac Angiography: Cardiac catheterization may benefi t geriatric patients who are candidates for revascularization and may reveal hemodynamic abnormalities, the presence and severity of valvular heart disease, or CAD.

Chest X-Ray: Chest x-ray may reveal cardiomegaly, increased pulmonary vascularity, interstitial or pulmonary edema, and assists in evaluating alternative etiologies that may contribute or cause heart failure-like symptoms.

Brain Natriuretic Peptide (BNP) or N-Terminal proBNP (NT-proBNP): BNP and NT-proBNP are helpful in narrowing differential diagnoses or establishing prognosis. BNP elevation occurs slowly; therefore, levels are not helpful in acute heart failure episodes. BNP levels of less than 100 pg/mL indicate that heart failure is unlikely. Levels between 100 and 500 pg/ mL are indeterminate. Levels of more than 500 pg/mL may suggest heart failure, but are not appropriate as “stand- alone” tests.

Blood Chemistries and CBC: CBC, comprehensive metabolic profi le (CMP), and thyroid-stimulating hormone (TSH) levels should be obtained initially and periodically to evaluate renal, liver, metabolic, and hemodynamic status.

Serial Cardiac Enzymes: Cardiac enzymes (CK-MB, tropo- nin) may reveal myocardial ischemia or infarction. Cardiac enzymes require time-sensitive processing; therefore, have limited value in the long-term care setting. If the presenta- tion is questionable, transport via emergency medical ser- vices to an acute care facility is appropriate.

Differential Diagnosis: Atypical symptom presentation in geri- atric patients necessitates a thorough health history that includes evaluation of risk factors with correlation to physi- cal examination fi ndings and diagnostic test results. Dyspnea on exertion, the most common heart failure symptom, may be caused by numerous disease processes, including asthma, COPD, anemia, renal failure, dysrhythmias, cardiomyopa- thies, valvular heart disease, primary pulmonary hyperten- sion, PE, abdominal masses, deconditioning, and anxiety neurosis. Differentiation between heart failure with pre- served LVEF or reduced LVEF is crucial and best determined by two-dimensional echocardiography (Ahmed, 2011; Yancy et al., 2013 ).

Treatment: Treatment options for heart failure are targeted at symptom management, treatment of the causative disease process(es), and the resulting multisystem pathophysiology. Fragility, multiple comorbid disease processes, polypharmacy, age-related changes in pharmacokinetics and pharmacody- namics, and prevalence of geriatric syndromes require indi- vidualized treatment plans.

Angiotensin-Converting Enzyme Inhibitors: Unless contrain- dicated, angiotensin-converting enzyme (ACE) inhibitors (ACEIs) are fi rst-line agents in the treatment of asymptomatic HF r EF or in patients with recent or remote history of MI regardless of LVEF. ACEI contraindications include unilateral or bilateral renal artery stenosis, hypersensitivity to ACEIs, angioedema, pregnancy, serum potassium more than 5.5

172 Chapter 8 ■ Chest Disorders

mEq/L that cannot be reduced, and hypotension in patients at risk for cardiogenic shock. ACEI therapy should be discon- tinued as a last resort in heart failure patients due to cardio- protective properties. All ACEIs should be started at low doses and gradually titrated over several weeks to achieve target doses daily based on renal function, potassium levels, BP, and tolerance. Obtain baseline serum potassium, serum creati- nine, and blood urea nitrogen (BUN) levels before initiation and with dosage adjustments. Dosage adjustments should be made accordingly for symptoms of dizziness, light-head- edness, or unsteadiness. ACEI cough is a common side effect and is characterized as a dry nonproductive cough that starts as a tickling cough, may be worse at night, and can occur at any point in treatment. ACEI cough is a classwide side effect and is not dose dependent.

Angiotensin II Receptor Blockers: Angiotensin II receptor block- ers (ARBs) are an appropriate substitute for ACEIs, as they do not inhibit kininase and are associated with lower incidence of cough and angioedema ( Yancy et al., 2013 ). Isosorbide dinitrate and hydralazine combination therapy is an appro- priate alternative in patients who experience hypotension, hyperkalemia, angioedema, or renal insuffi ciency with ACEI or ARB therapy, and those who do not respond to treatment with ACEIs and beta blockers.

Angiotensin Receptor/Neprilysin Inhibitors: Angiotensin receptor/ neprilysin inhibitors (ARNIs) are ARBs combined with an inhibitor of neprilysin, an enzyme that degrades natriuretic peptides, bradykinin, adrenomedullin, and other vasoactive peptides ( McMurray et al., 2014 ). ARNIs are approved as a substitute for ACEIs or ARBs in those with symptomatic HF r EF and should be not used concomitantly with these agents and with a 3-day washout period ( McMurray et al., 2014 ). Clinical trials have shown 20% reduction in cardio- vascular death or heart failure hospitalization ( McMurray et al., 2014 ; Yancy et al., 2016 ).

Beta-Adrenergic Blockers: Carvedilol, metroprolol succinate, and bisoprolol are the only beta blockers indicated for treat- ment of heart failure and with evidence to support morbid- ity and mortality reductions in heart failure patients. Unless otherwise contraindicated (heart block, bradycardia, hypo- tension, severe respiratory disease), beta blockers are rec- ommended for patients with recent or remote history of MI regardless of LVEF. Use of carvedilol or metoprolol succinate has been shown to decrease morbidity and mortality in heart failure patients and is recommended in patients with Stage C heart failure and/or a history of MI regardless of LVEF.

Beta blockers are strongly associated with reduced risk of mortality and reduced rehospitalization during 30-, 60-, and 90-day follow-up periods. Carvedilol is the best option in those with advanced heart failure. Beta blockers should be used in combination with ACEIs, if possible, for synergistic effect. Monitor geriatric patients closely for volume status, emotional side effects, and functional decline. Contraindi- cations include bronchospastic lung disease (e.g., asthma), symptomatic bradycardia, or advanced heart block without a pacemaker. Beta blocker initiation should be started only in a euvolemic patient. Initial dosages should be low and titrated slowly based on response to treatment and toler- ance. Carvedilol may have a greater hypotensive effect in the geriatric patient due to the vasodilatory effect of alpha-1

receptor blockade properties. Metoprolol succinate may be better tolerated in those with lower baseline BP levels. Con- sider carvedilol or bisoprolol in patients who require crushed medications.

Diuretic Therapy: Loop diuretics are used to reduce symp- toms of peripheral or pulmonary congestion. Loop diuretics inhibit the Na + /K + /Cl- symporter in the ascending loop of Henle, whereas thiazide-type diuretics affect the Na + /Cl- in the distal convoluted tubules. Use of diuretics in the treat- ment of heart failure without ACEIs, ARBs, or beta blockers activates the RAAS and may hasten progression of heart failure. Most heart failure patients are resistant to the effects of hydrochlorothiazide; therefore, loop diuretics are preferred diuretics in heart failure treatment. When used in equipotent dosages, loop diuretics appear to have comparable diuretic effects (1 mg bumetanide = 40 mg furosemide = 10 to 20 mg torsemide). Furosemide should be initiated at 20 mg daily oral dosage in the older adult patient with mild symptoms, with dosage titration based on effect and tolerance. Bumeta- nide is 40 times more potent than furosemide and is less oto- toxic, but it is associated with myalgias in some patients.

Fluid overload refractory to loop diuretics results from downregulation in renal response and sodium retention (Trullás et al., 2016). The addition of a thiazide diuretic to a loop diuretic may be an indicated and effi cacious option to reduce acute heart failure symptoms if a sub-therapeutic response to loop diuretic dosage increase is noted (Trullás et al., 2016). Metolazone (2.5 to 5 mg daily), a thiazide-like agent, is a long-acting diuretic that is effective in increasing the effects of loop diuretics if given 30 minutes before the loop diuretic dosage. Combination therapy with metolazone requires close monitoring of potassium and magnesium levels. Torsemide may be advantageous, because absorp- tion is unimpaired and the response is less variable than the other loop diuretics. Amiloride, triamterene, and ethacrynic acid should only be considered if there is a life-threatening allergy to sulfa due to side effects and inability to protect against damaging neurohormonal activity. Spironolactone, an ARB, is an effective therapy in conjunction with ACEIs or ARBs to more completely block the deleterious effects of the RAAS in patients with Stage C and D Class III–IV HF r EF and in patients with LVEF of 40% or less who have adequate renal function without hyperkalemia. Additionally, providers should consider ability to monitor for renal dysfunction and hyperkalemia before initiation of therapy.

Aldosterone Antagonists: Aldosterone antagonists are recom- mended at low dosages once daily and should not be initi- ated in men with serum creatinine levels of 2.5 or more; in women with serum creatinine levels of 2.0 or more; or potas- sium levels of more than 5.0.

Digoxin: Digoxin is recommended in the treatment of heart failure patients without bradycardia as a fourth-line agent in those who have persistent symptoms despite optimal therapy with diuretics, ACEIs, and beta blockers. In addition, digoxin may be helpful to control ventricular response due to AF in men with heart failure with LVEF of less than 50% ( Yancy et al., 2013, 2016 ). To reduce morbidity and mortality, lower therapeutic range (0.5 to 0.9 ng/mL) is advised ( Yancy et al., 2013). Evidence from several trials supports the use of digoxin to improve functional status and decrease heart failure

Chapter 8 ■ Chest Disorders 173

hospitalization without improvement in mortality. Geriatric dosages should not exceed 0.125 mg daily (American Geriat- rics Society, 2015; Beers Criteria Update Expert Panel, 2015). In geriatric patients with renal dysfunction, every-other-day dosage may be appropriate. ACEIs, beta blockers, diuretics, nitrates, calcium channel blockers (CCBs), and aldosterone antagonists are helpful in treating HF r EF. Concurrent treat- ment with beta blockers and non-dihydropyridine calcium channel antagonist agents is contraindicated. There is no evi- dence supporting the use of CCBs in the treatment of heart failure ( Yancy et al., 2013 ).

Follow-Up: Fatigue and weakness without vital sign changes may occur with titration of any medication, but are tran- sient and should resolve within several days following dosage titration. Ask the patient about the presence of symptoms of heart failure as noted previously. Asking specifi c questions specifi c to triad symptoms (nocturnal dyspnea, orthopnea requiring two or more pillows, and dyspnea with exertion) is considered an optimal approach to symptom recognition. Ask general questions related to the patient ’ s quality of life such as sleep patterns, sexual diffi culties, symptoms of depres- sion, and coping behaviors. Assess for caregiver overburden. Immediate follow-up post-hospitalization and frequent fol- low-up may reduce readmission rates ( Boxes 8-1 and 8-2 ).

Sequelae: Complications of heart failure involve hepatic and renal end-organ disease. Fifty percent of heart failure suf- ferers die from sudden cardiac death. All patients with heart failure should have an advance care plan and documented goals of care, including the Medical Orders for Scope of Treatment.

Prevention/Prophylaxis: Reducing cardiac risk factors in older adult affects coronary disease as strongly as it does in younger age groups. Encourage risk factor reduction using age-spe- cifi c guidelines to facilitate changes in lifestyle. Patients with heart failure are at risk for a vascular event, although there is confl icting evidence regarding effi cacy of prophylactic antithrombotic treatment (aspirin or warfarin) without other indications.

Referral: Referral for interprofessional team and chronic care case management should be considered for all patients with

heart failure. Warning signs for the need for hospitalization include weight gain that is resistant to diuresis, palpita- tions, persistent or recurrent dizziness, agitation or cognitive changes, inability to sleep because of paroxysmal nocturnal dyspnea, abdominal pain, and inability to walk.

Practice of best evidence involves shared decision making between an experienced, well-coordinated, proactive primary care team in a patient-centered palliative care model. Refer- ral to cardiology is indicated when the diagnosis is unclear, if the patient remains symptomatic despite appropriate therapy, and in those with signifi cant cardiac disease. Hospice should be considered when a patient has Stage D Class IV heart failure, has an ejection fraction of 20% or less, is unable to tolerate optimal therapy due to hypotension or renal failure, or has symptoms that are not controlled with maximized medical management.

Education: Education and use of support groups are import- ant for patients with heart failure, because noncompliance is a major cause of morbidity and unnecessary hospital admissions. Instruct patients and their families about the natural progressive trajectory of heart failure, necessary medications, dietary restrictions, heart failure symptoms that necessitate contact with provider, and prognosis. Dis- cussions regarding advance directives should begin early in the trajectory. Explain typical symptoms of worsening heart failure (orthopnea, paroxysmal dyspnea, leg edema, or exer- cise intolerance) and instruct patients to contact their health- care provider if these occur. Mild aerobic exercise increases functional capacity and improves the quality of life for heart failure patients, but should be undertaken with provider supervision. Dietary sodium should be restricted to 2 or 3 g per day. Discourage alcohol use and tobacco use. Fluid restriction is not necessary unless there is hyponatremia, but patients with heart failure should avoid excessive fl uid intake. Advise patients to contact the health-care provider if weight increases more than 2 pounds in a day or 4 pounds in a week. Nurse practitioners should recommend that patients with heart failure receive vaccination against infl uenza and pneumococcal disease.

BOX 8-1

R U Watching?

R - Reconcile medications post hospital

U - Up-titrate medication to target dosages as tolerated (document failure attempts)

Watching

■ Daily weight until stable x 4 weeks, then weekly

■ Notifi cation parameters (Call >3 # daily or >5 # weekly)

© 2016 Candace Harrington, DNP, ARPN, AGPCNP-BC

BOX 8-2

ABCs of Transitions

A - ACEI/ARB or ARNI

B - Beta antagonist Restart when stable on follow-up

C - Closely monitor labs

D - Diet (no added salt) Teach families to read nutrition labels

E - Exacerbation plan

F - Follow-up visit within 7 days post hospitalization; telephone follow-up within 3 days

© 2016 Candace Harrington, DNP, APRN, AGPCNP-BC

174 Chapter 8 ■ Chest Disorders

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

ACEIs are recommended for all patients with HF r EF unless contraindicated.

A Yancy et al., 2013, 2016 Muth, Gensichen, Beyer, Hutchinson, & Gerlach, 2009

ARBs are an appropriate option for those who have HF r EF are intolerant to ACEIs.

A Pitt et al., 1999 Yancy et al., 2013, 2016 Zannad et al., 2010

ARNIs are an appropriate substitute in those who have HF r EF and cannot tolerate ACEIs or ARBs

A Yancy et al., 2013, 2016 McMurray et al., 2014

Beta blockers should be used in combination with ACEIs if possible for synergistic effect.

A Poole-Wilson et al., 2003 Muth et al., 2009 Yancy et al., 2013

Beta blocker initiation should be started only in a euvolemic patient. Initial dosages should be low and titrated slowly based on response to treatment and tolerance. Transient fatigue is common with initiation and dosage titration.

A Rienstra et al., 2013 Yancy et al., 2013

Beta blockers (1 of the 3 specifi ed) are recommended for patients with or without recent or remote history of MI, regardless of LVEF.

A Rienstra et al., 2013 Yancy et al., 2013

Avoid use of diuretics in the treatment of heart failure without ACEIs, ARBs, or beta blockers (activates the renin-angiotensin-aldosterone system and may hasten progression of heart failure).

C Harrington, 2016 Triposkiadis et al., 2009

Aldosterone antagonist is recommended in HF r EF/ NYHA Class II–IV given appropriate renal function (>30 ml / min/1.73m 2 ) and serum potassium is less than 5 mEq/L. Class II patients should have a history of prior hospitalization and elevated natriuretic peptides for consideration of therapy. Providers should consider ability to monitor for renal dysfunction and hyperkalemia before initiation of therapy. Renal function and electrolytes should be checked in 2 to 3 days and again in 7 days following initiation or dosage adjustment.

A Pitt et al., 1999 Yancy et al., 2013 Zannad et al., 2010

Isosorbide dinitrate and hydralazine combination therapy is an appropriate alternative in patients who experience hypotension, hyperkalemia, angioedema, or renal insuffi ciency with ACEI or ARB therapy, in African Americans with NYHA class III–IV HF r EF receiving optimal therapy with ACEIs and beta blockers, unless contraindicated.

B A

Yancy et al., 2013

Combined use of ACEI, ARB, and aldosterone antagonist is potentially harmful in those with HF r EF.

B Cohn & Tognoni, 2001 Yancy et al., 2013 Zannad et al., 2010

Chapter 8 ■ Chest Disorders 175

Hypertension is one of the most important preventable contributors to cardiovascular disease and death. With the growing number of the world population over the age of 60 years and an increase in life expectancy, clinicians will be treating more and more patients with hypertension (William- son et al., 2016).

Signal Symptoms: Hypertension is usually asymptomatic, except in the case of hypertensive crisis, and is often referred to as the “silent killer” (Basile & Bloch, 2016).

Description: The ACC/AHA 2017 guidelines for the detec- tion, evaluation, and management of hypertension in adults incorporate new information regarding BP-related risk factors for cardiovascular disease and new BP thresh- olds for initiating antihypertensive drug therapy (Whelton et al., 2017). According to the new guidelines, BP should be defi ned as normal, elevated, or stages one or two (Whelton et al., 2017). Normal BP is defi ned as less than 120/less than 80 mm/Hg. Elevated BP is defi ned as 120 to 129/less than 80 mm/Hg. Stage one is defi ned as SBP 130 to 139 mm/Hg or DBP 80 to 89 mm/Hg. Stage two is defi ned as SBP greater than or equal to 140 mm/Hg or DBP greater than or equal to 90 mm/Hg (see Table 8-2 ) (Whelton et al., 2017).

Although hypertension is generally asymptomatic, it is a key risk factor for cardiovascular disease and contributes to approximately 45% of deaths due to heart disease and 51%

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Digoxin may be helpful in those with HF r EF to reduce hospitalization to control ventricular response due to AF as an add-on agent for control of heart failure symptoms resistant to ACEIs, beta blockers, and diuretics without contraindication.

A Yancy et al., 2013

Dietary sodium restriction of 3 g/day is reasonable. Fluid restriction is not necessary unless there is hyponatremia or Stage D Class IV symptom management.

C Yancy et al., 2013

Discourage alcohol use and tobacco use. C AHA, 2016 Mozzafarian et al., 2016 Yancy et al., 2013

Use of NSAIDs, COX-2 inhibitors, glucocorticoids, and thiazolidinediones are common precipitating factors for heart failure in the geriatric population.

A Trelle et al., 2011 Yancy et al., 2013

Vaccination against infl uenza and pneumococcal disease is recommended unless contraindicated for heart failure patients.

A ACIP, 2016 Moberley, Holden, Tatham, & Andrews, 2008

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

HYPERTENSION

Classifi cation of Hypertension

SYSTOLIC BLOOD PRESSURE

DIASTOLIC BLOOD PRESSURE CLASSIFICATION

130–139 mm Hg or 80–89 mm Hg Stage 1

hypertension

≥ 140 mm Hg or ≥ 90 mm Hg Stage 2 hypertension

<120 mm Hg and <80 mm Hg Normal

120–129 mm Hg and <80 mm Hg Elevated

Adapted from Whelton et al., 2017.

TABLE 8-2

of deaths due to strokes (Kjeldsen et al., 2014). Hypertension is a prevalent disorder in older adults and is one of the most common diagnoses seen in primary care (James et al., 2014).

Both SBP and DBP rise with age (Logan, 2011). However, the diastolic component of BP usually begins to level off around the age of 50 years and slowly declines over time (Logan, 2011). Isolated systolic hypertension is very common in older adults. It is defi ned as an SBP of 160 mm Hg or greater and is associated with a higher risk of MI and stroke (Logan, 2011). Hypertension is a major risk factor for

176 Chapter 8 ■ Chest Disorders

cardiovascular and renal disease, but is a modifiable cause of mortality (Logan, 2011).

Numerous clinical trials, including studies in older adults, document effective treatment and management of hyper- tension to improve survival rates with cardiovascular ben- efits (Alhawassi, Krass, & Pont, 2015). There are multiple, robust, randomized controlled trials that provide solid evi- dence-based treatment guidelines for hypertension in older adults (Alhawassi et al., 2015). When making a diagnosis of hypertension, it is also important to screen and manage other cardiovascular disease risk factors such as smoking, diabetes, hyperlipidemia, overweight, lifestyle factors, and sleep apnea (Whelton et al., 2017).

Etiology: Hypertension develops in response to an increase in cardiac output or an increase in peripheral resistance. The exact etiology of primary hypertension remains unclear but is thought to be the result of a number of genetic and envi- ronmental factors that affect cardiovascular and renal struc- ture and function. Secondary hypertension results from some known causes such as renal disease, obstructive sleep apnea, prescription and OTC medications, alcohol, and primary aldosteronism (Whelton et al., 2017). Uncommon causes of secondary hypertension include Cushing ’ s syndrome, hypo- thyroidism, hyperthyroidism, primary hyperparathyroidism, and acromegaly (Whelton et al., 2017).

Occurrence: It is estimated that 29% to 31% of adults in the United States have hypertension. With an aging population, the number is likely to grow, as hypertension occurs in the majority of persons over the age of 65 years (www.cdc.gov).

Age and Gender: Gender differences are noted in both younger and older populations. Men under the age of 45 years are more likely to develop hypertension than women. However, after the age of 60 years women are more likely than men to develop hypertension (Alhawassi et al., 2015).

Ethnicity: Hypertension is more common in African Ameri- can adults than in Caucasians and Hispanics, and develops at a younger age (www.cdc.gov).

Contributing Factors: Contributing factors in the develop- ment of hypertension include genetics, obesity, stress, life- style factors, loss of elasticity of blood vessels, and age (Basile & Bloch, 2016).

Aging is a major contributing factor to hypertension. As one ages, there is associated BP elevation caused by changes in arterial vessel structure and function (Logan, 2011). Col- lagen in blood vessels becomes more rigid, leading to sclero- sis and fibrosis of the vessels (Logan, 2011). This stiffening of the blood vessels causes a widening of the pulse pressure, commonly found in older adults (Logan, 2011). Furthermore, structural changes in blood vessels amplify systolic pressure with each heartbeat, causing an increase in systolic pressure and a fall in diastolic pressure (Logan, 2011).

Older adults are also more sensitive to salt due to reduced ability to excrete sodium. This increased salt sensitivity is caused by a decline in renal function and reduced generation of natriuretic substances, such as prostaglandin E2 and dopa- mine, resulting in elevated blood pressure (Logan, 2011). The prevalence of diabetes and glucose intolerance also increases with age and is a contributing factor to vascular injury and subsequent elevation in BP (Logan, 2011). Progressive renal

dysfunction as part of the aging process may contribute to the pathophysiology of hypertension in the geriatric popula- tion (Logan, 2011).

Secondary causes of hypertension such as renal artery ste- nosis, sleep apnea, primary hyperaldosteronism, and thyroid disorders should be considered and ruled out in older adults before assuming a diagnosis of hypertension (Logan, 2011).

Diagnostic Tests: All adults 18 years and older should be screened for elevated BP. Before labeling an individual with a diagnosis of hypertension, the clinician should use an average of two or more readings obtained on two or more occasions (Whelton et al., 2017). Out of office and self-moni- toring of BP measurements are recommended to confirm the diagnosis of hypertension (Whelton et al., 2017). As part of the evaluation and work-up for primary hypertension, the following studies should be considered:

■ CMP ■ CBC ■ Lipid panel ■ Thyroid panel ■ Urinalysis ■ EKG ■ Echocardiogram, uric acid level, urinary albumin to

creatinine ratio (optional) (Whelton et al., 2017)

Differential Diagnosis: Differential diagnoses to consider are drug-induced hypertension, chronic kidney disease, obstruc- tive sleep apnea, hyperaldosteronism, hypothyroidism, hyper- thyroidism, hyperparathyroidism, and Cushing syndrome when confirming a diagnosis of hypertension (Basile & Bloch, 2016). Accurate diagnosis of hypertension and identification of other cardiovascular risk factors is important to identify patients who would benefit from BP management (Kjeldsen, 2014). Health-care provider measurement of BP tends to be poor and often fails to look for the white-coat effect, masked hypertension, orthostatic hypotension, or postprandial hypo- tension, which leads to overestimation of BP and inappropri- ate treatment (Morley, 2014).

White coat hypertension in older adults is described as having an elevated office BP with a normal ambulatory or home BP with the patient receiving antihypertensive treat- ment. Research finds that medications do not have a signifi- cant effect on lowering BP in individuals with true white-coat hypertension (Franklin et al., 2012).

Masked hypertension is described as having a normal office BP with an elevated out-of-office BP, determined by ambulatory or home BP monitoring. Studies indicate 15% to 30% of older adults have masked hypertension with associ- ated increased cardiovascular risks (Peacock, 2014).

Orthostatic hypotension is defined as a significant fall in BP when moving from a supine or sitting to a standing posi- tion. Because orthostatic hypotension is a significant risk factor for falls and fractures in older adults, screening for orthostatic hypotension should be an important part of the clinician ’ s work-up for hypertension (Shaw & Clayton, 2014). Orthostatic testing involves a measurement of BP from two different body positions, with the most common sitting then standing. Orthostatic hypotension is present with a decrease in systolic pressure of 20 mm Hg or a decrease in diastolic pressure of 10 mm Hg within 3 minutes of standing when compared with BP from a sitting or supine position (Shaw & Clayton, 2014).

Chapter 8 ■ Chest Disorders 177

Postprandial hypotension is another important consider- ation in the work-up for hypertension in older adults. Post- prandial hypotension is a drop in SBP within 2 hours of a meal, which can also increase the risk for falls in older adults (Nair, Visvanathan, & Piscitelli, 2016).

Although a single, carefully taken BP may be a predic- tor of future cardiovascular risk, the AHA recommends using ambulatory or home BP readings in conjunction with offi ce monitoring as a better method for diagnosing hyper- tension and for subsequent guidance in treatment decisions (Logan, 2011). The USPSTF also recommends obtaining BP measurements outside of the clinical setting for diagnostic confi rmation before starting treatment (National Guideline Clearinghouse, 2015).

Ambulatory or home BP monitoring is considered a better predictor of cardiovascular risk and provides better data for clinicians to make treatment decisions than a few offi ce readings (Crabtree & Stuart-Shor, 2014). Evidence-based guidelines recommend home BP monitoring along with offi ce monitoring, as it helps with patient engagement with treatment and improvement in shared decision making (Crabtree & Stuart-Shor, 2014). The clinician should assess the patient ’ s capability of doing home BP monitoring and provide adequate instructions.

Sleep apnea, pain, nocturnal hypoglycemia, excessive aldosterone production, and pheochromocytoma should all be considered as causes of hypertension in older patients and should be ruled out before initiating treatment for hyperten- sion (Morley, 2014). Lifestyle risk factors such as smoking, excessive alcohol consumption, and lack of exercise should also be discussed with the patient. Before initiating treatment for hypertension, a diagnostic work-up is recommended, including EKG, urinalysis, CMP, lipid panel, CBC, TSH, and free T4 (Morley, 2014).

Treatment: Treatment of hypertension is recommended for noninstitutionalized, ambulatory, community-dwelling adults (65 years of age or older) with an average SBP greater than or equal to 130 mm Hg (Whelton et al., 2017). Treat- ment goal should be SBP less than 130 mm Hg (Whelton et al., 2017). For older adults (65 years of age or older), both community dwelling and those residing in long-term care facilities with complex comorbid conditions and/or limited life expectancy, treatment should be based on clinical judge- ment, goals of care, and a team approach to determine risk/ benefi t for intensity of BP targets and choice of antihyperten- sive medications ( Table 8-3 ) (Whelton et al., 2017).

There is scant research for treatment of hypertension for those ages 80 years or older, although some evidence exists for a BP goal of less than 150/90 mm Hg in this age group (James et al., 2014). Management of hypertension in geri- atric patients can be challenging. These patients often have organ damage or cardiovascular disease, leading to a differ- ent response to treatment than in younger patients (James et al., 2014). Clinical judgment must play an important role in using evidence-based guidelines regarding treatment deci- sions and must be individualized for each patient in the geri- atric population (Logan, 2011).

Poor adherence to a medication regimen due to pill burden, the cost of medications, or cognitive impairment is common in older adults (Jones, 2016). This is often the cause of poorly controlled BP and a major predictor for nursing

home placement in frail older adults (Jones, 2016). Hyper- tensive therapy often involves a high number of medications, usually with an assortment of classes (Jones, 2016). Studies provide strong evidence that as the number of medications increase, patient adherence falls (Jones, 2016). It is import- ant to complete a medication reconciliation during each visit and specifi cally ask about how prescriptions are being fi lled and medications are being taken (Jones, 2016). To increase compliance, clinicians should prescribe once-a-day medica- tions whenever possible, as frequency of dosing contributes to poor medication adherence (Jones, 2016). Lack of medi- cation adherence should not be mistaken for treatment-resis- tant hypertension (Jones, 2016).

Hypertension in older adults is treated with the same medications as with younger patients, but the clinician must take into account age-related changes in metabolism and pharmacodynamics (Sherman, 2013). Before any consider- ation of antihypertensive medication therapy the clinician should fi rst consider nonpharmacological interventions for BP reduction. Weight loss and reduction of sodium intake can be effective therapy in many older adults (DeSimone & Crowe, 2009). Other lifestyle modifi cations such as smoking cessation, exercise, and moderation in alcohol consumption should be discussed with the patient (Sherman, 2013).

When initiating antihypertensive drug therapy, fi rst- line agents include thiazide diuretics, CCBs, and ACEIs or ARBs (Whelton et al., 2017). Simultaneous use of an ACEI and ARB is contraindicated and potentially harmful to the patient (Whelton et al., 2017). The goal of the 2017 ACC/ AHA guidelines is to facilitate evidence-based practice in the management of hypertension in adults ( Table 8-4 ).

Medications should be started at the lowest dose and gradually increased to meet the targeted BP goal. Most older

2017 ACC/AHA Guidelines for the Treatment of Hypertension in Adults

Normal blood pressure Evaluate yearly.

Elevated blood pressure

or Stage 1 hypertension

with estimated

cardiovascular risk less

than 10%

Start treatment with nonpharmacological

interventions and reevaluate in 3 to 6

months. Nonpharmacological interventions

should include: weight loss, heart healthy

diet, sodium reduction, potassium

supplement unless contraindicated due

to chronic kidney disease or use of

drugs that inhibit potassium excretion,

increased activity, moderation in alcohol

consumption, and smoking cessation. Goal

of treatment <130/80 mm Hg.

Stage 1 hypertension

with estimated

cardiovascular risk 10%

or greater

Initial treatment should include

nonpharmacological interventions and

antihypertensive drug therapy and

reevaluate in 1 month. Goal of treatment

<130/80 mm Hg.

Stage 2 hypertension Initial treatment should include

nonpharmacological interventions and

antihypertensive drug therapy with two

agents of different classes and reevaluate

in 1 month. Goal of treatment

<130/80 mm Hg.

Adapted from Whelton et al., 2017.

TABLE 8-3

178 Chapter 8 ■ Chest Disorders

adults will require more than one medication along with lifestyle changes to reach the BP goal (Sherman, 2013). Review of the literature indicates 70% of older adults require two or more drugs to reach BP goals (Sherman, 2013). Specifi c comorbid illnesses may guide the initial and subse- quent choice of drug therapy (Sherman, 2013). ACEIs are recommended for patients with renal disease and diabetes. Beta blockers are recommended for those with CAD or CHF (National Guideline Clearing House, 2015).

Follow-Up: Follow-up is important, as the majority of patients with hypertension are not adequately controlled. Per

ACC/AHA guidelines, once treatment has been started for hypertension, low-risk adults with elevated BP or stage one hypertension with low cardiovascular risks should be reeval- uated in 3 to 6 months (Whelton et al., 2017). Adults with stage one and stage two hypertension with high cardiovas- cular risks should be reevaluated in 1 month (Whelton et al., 2017). Comorbid conditions such as diabetes, heart failure, and chronic kidney disease will infl uence the frequency of follow-up visits.

Sequelae: Hypertension is associated with serious adverse effects, such as left ventricular hypertrophy, heart failure, stroke, and kidney disease (Basile & Bloch, 2016).

Prevention/Prophylaxis: One of the primary preventative mea- sures for hypertension is lifestyle modifi cation. Excess weight, excess sodium intake, inadequate physical activity, smoking, inadequate intake of fruits and vegetables, and excessive alcohol consumption are all modifi able factors that can con- tribute to the onset of hypertension (Basile & Bloch, 2016).

Referral: The clinician should consider referring to a hyper- tension specialist when the BP goal cannot be attained or for the management of complicated patients who may benefi t from consultation (James et al., 2014).

Education: Patient education is important in preventing hypertension and/or adhering to treatment once diagnosed. There are many patient education resources available for health-care professionals. The AHA has disease-specifi c pocket guides available for health-care professionals to give to their patients, or patients can be referred to their website. UpToDate also has patient education materials available on hypertension. Lifestyle modifi cations and medication adher- ence must be reinforced with every patient.

Clinicians should refer to evidence-based guidelines, such as those provided by ACC/AHA, when assessing and treating older adults with hypertension, but recommendations are not a substitute for clinical judgment for individual patients. Older adults often have comorbid conditions or lifestyle prac- tices that may impact treatment outcomes. Balancing com- peting risk factors for hypertension-related risk of stroke, MI, and heart failure with treatment-related risks, such as fall-related fractures and adverse reactions to medications, is challenging and requires a patient-centered approach to treatment in older adults (Williamson et al., 2016).

Evidence-Based Dosing for Antihypertensive Agents

MEDICATION STARTING DAILY DOSE

TARGETED DOSE IN RANDOMIZED CONTROLLED TRIALS

Thiazide Diuretics

Hydrochlorothiazide 12.5–25 mg 25–100 mg

Chlorothiazide 12.5 mg 12.5–25 mg

Indapamide 1.25 mg 1.25–2.5 mg

ARBs

Lorsartan 50 mg 100 mg

Valsartan 40–80 mg 160–320 mg

ACEIs

Enalapril 5 mg 20 mg

Lisinopril 10 mg 40 mg

CCBs

Amlodipine 2.5 mg 10 mg

Diltiazem ER 120–180 mg 360 mg

Beta Blockers

Metoprolol 50 mg 100–200 mg

Atenolol 25–50 mg 100 mg

Source: James et al., 2014.

TABLE 8-4

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

In patients older than 50 years, SBP more than 140 mm Hg is a much more important risk factor for cardiovascular disease than DBP.

A Campbell-Scherer, Green, & Barry, 2017

Self-monitoring of BP at home or work is a practical way to assess differences between out of offi ce and offi ce readings.

B Campbell-Scherer, Green, & Barry, 2017

Most patients with hypertension have essential hypertension, and more extensive testing for secondary hypertension is not necessary unless BP control is not achieved or if the patient has symptoms of catecholamine excess, bruits, or unprovoked hypokalemia.

B Campbell-Scherer, Green, & Barry, 2017

Chapter 8 ■ Chest Disorders 179

Signal Symptoms: Angina pectoris is the initial manifestation of ischemic heart disease (IHD). Typical angina is substernal chest discomfort associated with physical exertion or emo- tional stress and relieved with rest or nitroglycerin (Fihn, 2012). Women report epigastric discomfort; nausea; radia- tion of discomfort to the arms, neck, and interscapular areas; dyspnea;and fatigue (Mieres, 2014).

Description: IHD is also referred to as coronary heart disease and occurs when there are one or more signs or symptoms of inadequate supply of blood to the myocardium. The most common problems resulting in IHD are related to obstruction of the epicardial coronary arteries due to atherosclerosis. Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply. Patients are considered stable when symptoms are manageable with either medical or revascular- ization therapy (Kannam, 2016). IHD is a chronic disorder that typically cycles through defi ned phases: asymptomatic, stable angina, accelerating angina, and acute coronary syn- drome (ACS)/unstable angina/acute MI. The progression of the disease is not necessarily linear (Fihn, 2012).

Etiology: Atherosclerosis involving the coronary arteries is the common etiology of IHD. Evidence supports a multi- factorial pathophysiology of coronary atherosclerosis that includes obstruction of the coronary arteries, reducing the quantity of oxygen-rich blood to the myocardium, and dys- function of the coronary microvasculature and endothelium.

Occurrence: Cardiovascular disease is the number one cause of death in both men and women. Among persons 60 to 79 years of age, approximately 25% of men and 16% of woman have IHD. It is projected that in 2016 there will be

approximately 660,000 Americans who have a new cor- onary event, either a fi rst hospitalization for an MI or CHD death, and about 305,000 will have a recurrent event. Silent MIs are estimated to involve 160,000 additional persons (Mozzafarian, 2016). There are trends indicating that MI has declined signifi cantly over time, including over the past decade. Mean predicted 10-year risk for CHD among adults aged 30 to 74 years has decreased from 7.2% during 1999 to 2000, to 6.5% during 2009 to 2010.

Age: The prevalence of CHD increases with age. The average age at fi rst MI is 65.1 years for men and 72 years for women.

Gender: Men have CHD at a younger age. Women lag behind men by 10 years. In those 40 to 59 years of age, men 6.3%, women 5.6%; in those 60 to 79 years of age, men 19.9%, women 9.7%; and in those 80 years of age and older, men 32.2%, women 18.8%.

Ethnicity: In a meta-analysis involving 17 population-based cohorts worldwide, 60,211 participants without cardiovas- cular disease at baseline were studied. The 10-year event rate for formation of carotid intima-media thickness was 6.7% in Asians, 7.8% in Hispanics, 8.1% in Caucasians, and 9.2% in African Americans. Ethnicity appears to signifi cantly modify the association between risk factors and atheroscle- rotic disease. The association between increase in age and atherosclerotic disease was weaker in African American and Hispanic populations. SBP elevations in Asians were strongly related to onset of disease. HDL cholesterol and smoking were associated less with disease onset in African Americans (Gijs- berts, 2015).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Lifestyle modifi cation (smoking cessation, sodium restriction, exercise, weight control, etc.) lowers BP and should be encouraged in all patients with all stages of hypertension.

A Campbell-Scherer, Green, & Barry, 2017

Thiazide diuretics (e.g., chlorthalidone and hydrochlorothiazide) are the drugs of fi rst choice for most patients given their enormous cost-effectiveness advantage and lack of evidence of superiority of any other medications.

A Campbell-Scherer, Green, & Barry, 2017

While diuretics are the cornerstone for treating hypertension, patients with diabetes, chronic kidney disease, heart failure, and CAD should have tailored treatment.

B Campbell-Scherer, Green, & Barry, 2017

Reducing the number of daily doses increases adherence to BP lowering medication.

A Campbell-Scherer, Green, & Barry, 2017

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

ISCHEMIC HEART DISEASE

180 Chapter 8 ■ Chest Disorders

Contributing Factors: In the absence of an established model to predict outcome, consider the following risks:

1. Sociodemographic: Age is the single, strongest determi- nant of survival. Sex and ethnicity have fewer effects on risk. Lower socioeconomic status is associated with worse outcome.

2. Cardiovascular: Smoking, hypertensions, dyslipidemia, family history of premature CAD, obesity, and seden- tary lifestyle have the greatest risk of complications.

3. Coexisting medical conditions: Diabetes, chronic kidney disease, chronic pulmonary disease, and malig- nancy infl uence the prognosis.

4. Cardiovascular comorbidities: Heart failure, peripheral artery disease, and cerebrovascular disease are strong risk factors for mortality.

5. Psychosocial characteristics: Depression is strongly associated with worse survival rates. Poor social support, poverty, and stress are associated with poor outcome.

6. Health status: Patient ’ s symptoms, functional capacity, and quality of life are associated with poor survival and incidence of ACS.

7. Anginal frequency: The more frequent the angina, the stronger prediction of ACS and hospitalization.

8. Cardiac disease severity: The degree and distribution of stenosis are meaningful predictors of outcome. (Fihn, 2012)

Signs and Symptoms: A detailed assessment of chest pain includes the quality, location, severity, and duration of pain; radiation; associated symptoms; and provoking and alleviat- ing factors. The quality of chest pain associated with IHD is most often described as squeezing, gripping, suffocating, or heavy. Women and older adults can present with atypical symptoms such as nausea, vomiting, mid-epigastric discom- fort, or sharp pain. Anginal pain typically lasts minutes; is located in the substernal area with pain that may radiate to the neck, jaw, epigastrium or arms; often is aggravated by exertion or emotional stress; and relieved with rest or nitro- glycerin. Patients with angina must be categorized as stable or unstable. Unstable angina is defi ned as new onset increas- ing in frequency, intensity, duration, or at rest.

Physical examination may be normal or nonspecifi c. The patient may present with heart failure, valvular disease, or cardiomyopathy. Bruits over vascular areas and/or dimin- ished pulses might suggest vascular disease. Elevated BP or xanthomas may indicate risk factors for IHD (Fihn, 2012).

Diagnostic Tests: A resting EKG is the initial test, followed by stress testing.

TEST RESULTS INDICATING DISORDER

EKG ST-segment depression or elevation or T-wave

inversion in the absence of left ventricular

hypertrophy supports the diagnosis of

ischemia

Q waves may be evidence of an old MI

Exercise stress

testing

Reproduces ischemic symptoms

Defects in myocardial perfusion with exercise

TEST RESULTS INDICATING DISORDER

Exercise stress

testing

Cardiac risk identifi ed in patients with a

decrease in the BP, S 3 , rales, or prolonged

downsloping ST-segment depression after

exercise

Myocardial perfusion

imaging

Perfusion defects

Left ventricular dysfunction

Echocardiogram Assesses the severity of left ventricular

dysfunction

Stress

echocardiogram

Multiple reversible wall motion abnormalities

Cardiac

catheterization

For patients who fail pharmacological therapy,

have had an MI, or have unstable angina, to

determine the severity of disease

Differential Diagnosis: Aortic dissection, pericarditis, PE, pneumothorax, pneumonia, pleuritic, esophagitis, spasm, refl ux, biliary colic, cholecystitis, choleolithiasis, peptic ulcer, pancreatitis, costochondritis, fi brositis, rib fracture, herpes zoster, anxiety, panic disorder, affective disorders (depression) (Fihn, 2012).

A resting EKG is recommended in patients when there is suspected cardiac cause of chest pain (Evidence Rating B). Those with evidence of prior MI, especially Q waves in mul- tiple leads or an R wave in V1; persistent ST-T-wave inver- sions particularly in leads V1 to V3; left bundle-branch block or bifascicular block, second or third-degree atrioventricu- lar block, or ventricular tachycardias or hypertrophy have a worse prognosis than those with a normal EKG (Fihn, 2012).

When the evaluation is complete, the determination of the probability of IHD is suffi cient to recommend further testing. The typical angina pain and the older age of the patient have a high likelihood of IHD. Diabetes has the greatest infl uence on increasing the probability of IHD (Fihn, 2012).

For those who have suspected IHD and a prior MI, Q waves or symptoms of heart failure, complex ventricular arrhyth- mias, or an undiagnosed heart murmur, an echocardiogra- phy to evaluate the LV systolic and diastolic function and heart structures is recommended (Fihn, 2012).

If there is a probability that IHD may be present, stress testing is the most common noninvasive test used to diagnose IHD. Stress testing is used to induce ischemia either by exercise or pharmacological stress agents. However, the production of ischemia is dependent on the stress imposed and submaximal exercise testing can fail to produce ischemia. Coronary artery stenosis under 70% may be undetectable. For those able to exercise, standard exercise EKG testing is recommended. The patient must have an interpretable EKG and a moderate phys- ical ability to exercise. For those unable to exercise, pharma- cological stress with nuclear myocardial perfusion imaging (MPI) or echocardiography is recommended.

Those patients who have survived sudden cardiac death, life-threatening ventricular arrhythmias, or heart failure should undergo coronary angiography (Fihn, 2012). Angi- ography is useful in patients with unacceptable ischemic symptoms despite guideline-directed medical therapy (Fihn, 2014). However, it should not be offered to those who are unwilling or are not candidates for revascularization.

Chapter 8 ■ Chest Disorders 181

MEDICAL THERAPY TO PREVENT MI AND DEATH

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

CHOLESTEROL MANAGEMENT

Lifestyle modifi cation including physical activity and weight management. B Fihn, 2012

Dietary therapy inclusive of reduction of saturate fats of <7% of total calories, trans fatty acids to <1% of total calories, and cholesterol to <200 mg/d.

B Fihn, 2012

Moderate or high dose of a statin should be prescribed if not contraindicated.

A Fihn, 2012

For those who do not tolerate statins, bile acid sequestrants, niacin or both are reasonable.

B Fihn, 2012

BLOOD PRESSURE MANAGEMENT

Lifestyle modifi cation including weight control, physical activity, alcohol moderation, sodium reduction; increased consumption of fresh fruits, vegetables, and low-fat dairy products.

B Fihn, 2012

Antihypertensive drug therapy should be started for BP 140/90 mmHg or higher.

A Fihn, 2012

DIABETES MANAGEMENT

For those with short duration of diabetes, a goal HbA1c of 7% or less. B Fihn, 2012

A HbA1c between 7% and 9% is reasonable for patients according to age, history of hypoglycemia, presence of microvascular or macrovascular complications, or presence of coexisting medical conditions.

C Fihn, 2012

Therapy with rosiglitazone should not be initiated. C Fihn, 2012

PHYSICAL ACTIVITY

30–60 minutes of moderate-intensity aerobic activity at least 5 days a week.

B Fihn, 2012

Physical activity history and an exercise test to guide prognosis and prescription.

B Fihn, 2012

Cardiac rehabilitation and physician-directed, home-based programs. A Fihn, 2012

Complementary resistance training at least 2 days per week. C Fihn, 2012

WEIGHT MANAGEMENT

BMI and/or waist circumference should be assessed at every visit, and encouragement for weight maintenance or reduction to maintain or achieve BMI 18.5 to 24.9 and a waist circumference less than 40 inches in men and less than 35 inches in women.

B Fihn, 2012

Initial goal of weight loss should be to reduce body weight by approximately 5% to 10% from baseline.

C Fihn, 2012

Treatment:

Continued

182 Chapter 8 ■ Chest Disorders

SMOKING CESSATION

Smoking cessation and avoidance of exposure to second hand smoke. B Fihn, 2012

MANAGEMENT OF PSYCHOLOGICAL FACTORS

Screen for depression B Fihn, 2012

ALCOHOL CONSUMPTION

Limit alcohol to 1 drink (4 ounces of wine, 12 ounces of beer, or 1 ounce of spirits) a day.

C Fihn, 2012

ANTIPLATELET THERAPY

ASA 75 to 162 mg daily in the absence of contraindication. A Fihn, 2012

Treatment with clopidogrel when ASA is contraindicated. B Fihn, 2012

Dipyridamole is not recommended. B Fihn, 2012

BETA BLOCKER

Beta-blocker therapy should be started and continued for 3 years in all patients with normal LV function after MI or ACS.

B Fihn, 2012

Beta-blocker therapy should be used in all patients with LV systolic dysfunction (EF ≤ 40%) with heart failure or prior MI (carvedilol, metoprolol succinate, or bisoprolol have been shown to reduce risk of death).

A Fihn, 2012

Beta blockers considered for chronic therapy for all other patients with coronary or other vascular disease.

C Fihn, 2012

RENIN-ANGIOTENSIN-ALDOSTERONE BLOCKER THERAPY

ACEIs for patients who have hypertension, diabetes, LVEF ≤ 40%, or chronic kidney disease.

A Fihn, 2012

ARBS for patients with hypertension, diabetes, LV systolic dysfunction, or chronic kidney disease who are intolerant of ACEIs.

A Fihn, 2012

Infl uenza vaccine is recommended. B Fihn, 2012

Estrogen therapy; vitamin C, E, and beta-carotene, folate or vitamin B 6 and B 12 , chelation therapy, garlic, coenzyme Q10, selenium or chromium.

No benefi t Fihn, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

Chapter 8 ■ Chest Disorders 183

MEDICAL THERAPY FOR SYMPTOM RELIEF

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

ANTI-ISCHEMIC MEDICATIONS

Beta blockers for initial therapy for symptom relief. B Fihn, 2012

CCBs or long-acting nitrates for symptom relief in those intolerant to beta blockers or contraindicated.

B Fihn, 2012

Sublingual nitroglycerin spray for immediate relief of angina. B Fihn, 2012

Long-acting nondihydropyridine CCB instead of beta blockers as initial therapy.

B Fihn, 2012

Ranolazine as a substitute for beta blockers if initial treatment with beta blockers leads to unacceptable side effects or is ineffective.

B Fihn, 2012

Ranolazine in combination with beta blockers if beta blockers alone is not successful.

A Fihn, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

MEDICAL THERAPY FOR SYMPTOM RELIEF IN PATIENTS WITH REFRACTORY ANGINA

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Enhanced external counterpulsation (EECP) B Fihn, 2012

Spinal cord stimulation C Fihn, 2012

Transmyocardial revascularization B Fihn, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

REVASCULARIZATION DECISION TO IMPROVE SURVIVAL

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Recommended in patients with unprotected left main or complex CAD. C Fihn, 2012

CABG to improve survival in patients with signifi cant ( ≥ 50% diameter stenosis) left main.

B Fihn, 2012

PCI is an alternative to CABG in stable patients with signifi cant unprotected left main who may have low risk of PCI complications or have a signifi cantly increased risk of adverse surgical outcomes.

B Fihn, 2012

CABG is benefi cial in patients with signifi cant ( ≥ 70) stenosis in two major coronary arteries with severe or extensive myocardial ischemia.

B Fihn, 2012

Continued

184 Chapter 8 ■ Chest Disorders

REVASCULARIZATION DECISION TO IMPROVE SURVIVAL

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

CABG is reasonable in patients with mild to moderate LV systolic dysfunction (EF 35%–50%) and signifi cant stenosis when viable myocardium is present.

B Fihn, 2012

CABG is recommended over PCI to improve survival in patients with diabetes, multivessel CAD, particularly if a left internal mammary artery (LIMA) graft can be used on the left anterior descending artery (LAD)

B Fihn, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

Follow-Up: See patient at regular intervals for chronic health management; instruct in emergency measures and lifestyle management.

Sequelae: IHD remains a major public health problem with more than 10 million people with angina. Survival rates of patient have been improving; however, it is still the number one cause of death in men and women. Patients with symp- toms of angina have MIs at a rate of 3% to 3.5% per year. Many people with IHD do not return to work after coronary revascularization and 15% to 20% rate their health as fair or poor. IHD continues to be associated with considerable morbid- ity despite the decrease in mortality rate. The costs of caring for patients with IHD are estimated at $156 billion in the United States for both direct and indirect costs (Fihn, 2012).

Prevention/Prophylaxis: Healthy, active lifestyle; control of hypertension, diabetes, cholesterol.

Referral: There are certain medical conditions, such as HIV and connective tissue disease, which may result in increased IHD. These patients need to be referred to Infectious Disease and Rheumatology to provide optimum management of these disorders. Ongoing reassessment of the patient ’ s adherence to the therapy, adverse events, treatment goals, effectiveness of interventions, and risk factor reduction should be done. For those who have not met their goals, especially in the manage- ment of diabetes, depression, smoking cessation, and chronic kidney disease, referral to an appropriate specialist may be considered. If angina becomes unstable, the patient should know to seek emergency medical care (Fihn, 2012).

Education:

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

INDIVIDUALIZED EDUCATION PLAN INCLUDING:

Importance of medication adherence for managing symptoms and slowing disease progression.

C Fihn, 2012

Explanation of medication management and cardiovascular risk reduction strategies.

C Fihn, 2012

Comprehensive review of therapeutic options. B Fihn, 2012

Description of appropriate levels of exercise. C Fihn, 2012

Information on recognition of worsening cardiovascular symptoms and appropriate actions.

C Fihn, 2012

Adherence to diet that is low in saturated fat, cholesterol and transfat; high in fresh fruits, whole grains and vegetables; reduction in sodium intake.

B Fihn, 2012

Common symptoms of stress and depression and techniques to minimize. C Fihn, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

Chapter 8 ■ Chest Disorders 185

Signal Symptoms: Cough, dyspnea, weight loss, anorexia, hemoptysis.

Description: Lung cancer is a malignant neoplasm originat- ing in the parenchyma of the lung or airways (Midthun, 2015). Approximately 95% of all lung cancer is classifi ed as non–small cell lung cancer (NSCLC) or small cell lung cancer (SCLC) ( Latimer & Mott, 2015 ; Midthun, 2015). NSCLC com- prises 80% of cancer diagnoses and includes adenocarci- noma, squamous cell cancer, and large cell cancer ( Latimer & Mott, 2015 ; Midthun, 2015).

Etiology: Research has shown conclusively that approxi- mately 90% of lung cancer cases are associated with tobacco smoking (CDC, 2016b; Mannino, 2016). Additional risk factors have also been identifi ed. Radiation therapy can increase the risk of a second primary lung cancer in patients who have received this for other malignancies (Mannino, 2016). Environmental toxins such as radon, asbestos, and second-hand smoke are also risk factors (CDC, 2016b; Mannino, 2016; Samet, 2016). Patients with pre-existing diseases that involve the lungs, such as COPD, prior lung cancers, sarcoidosis, and scleroderma, are at increased risk for developing lung cancer. Studies have shown that patients with pulmonary fi brosis have a sevenfold increased risk for developing lung cancer (Tomassetti et al., 2015). Genetic pre- disposition to carcinoma of the lung continues to be studied, but there is growing evidence that genetics can affect the risk of developing lung cancer and the prognosis (Mannino, 2016; Midthun, 2015).

Occurrence: Lung cancer is the most common cause of can- cer-associated deaths in the United States. It is the second most common cancer among men and women. Annually, more than 200,000 new cases are diagnosed (CDC, 2016a). Lung cancer is responsible for 26.5% of all cancer deaths (National Cancer Institute, 2016).

Age: Lung cancer can occur at any age, but there is a dra- matic increase in new diagnosis after age 40 years. Most recent statistics show 32.4% diagnosed between 65 and 74 years, 27.4% between 75 and 84 years, and 9.3% among those more than 84 years old (National Cancer Institute, 2016).

Gender: More men have lung cancer than do women, but the incidence rate for women is rising.

Ethnicity: African American men have a higher incidence of lung cancer than Caucasian men. No signifi cant difference exists between African American and Caucasian women.

Contributing Factors: The cumulative dose or pack-years for cigarette smoking is related directly to the risk of devel- oping lung cancer. The more cigarettes smoked per day and the longer the individual has smoked, the higher the risk of developing lung cancer. The risk of lung cancer is 30 times higher in smokers than in nonsmokers. Cigar and pipe smokers and passive smokers have double the risk. The risks of developing NSCLC steadily decline for people who quit smoking and approach that of a nonsmoker after 15 years of abstinence. Individuals who have smoked for more than 20

years probably always will have a slightly increased risk of developing the disease, even after 15 years as a nonsmoker. There is no change in risk of SCLC with smoking cessation; early age at beginning to smoke is a signifi cant risk factor. Asbestos exposure alone increases the risk of developing pulmonary carcinoma, but when combined with smoking, the risk increases to 100 times that of a nonsmoker. Other inhaled agents implicated in the development of the disease are radon, arsenic, nickel, chromates, halo ethers, alkylating compounds, and polycyclic aromatic hydrocarbons. Radon is a risk factor; air pollution also is thought to contribute to the development of lung cancer. Sarcoidosis carries a threefold increased risk; scleroderma increases risk of bronchoalveolar cancer.

Signs and Symptoms: Signs and symptoms of lung cancer are usually present only after the disease has progressed beyond the early stages. Routine screening for the disease with chest x-ray and/or sputum cytology is not recommended because it is neither specifi c nor sensitive (Deffebach & Humphrey, 2016 ). Low-dose chest CT scan can identify early-stage asymptomatic lung cancer. The USPSTF (2013) and National Comprehensive Cancer Network (NCCN) (2016a) recom- mend that adults age 55 to 80 years who have a 30 pack- year history and currently smoke or have quit within the past 15 years, undergo a low-dose CT scan to screen for lung cancer. Screening should be discontinued once the person has not smoked for 15 years or develops a health problem that can substantially limit life expectancy or undergoes cura- tive surgery. Symptoms suggestive of lung cancer include a new or changing cough, hoarseness, hemoptysis, anorexia, cachexia, unexplained weight loss, dyspnea, hypoxia, wheez- ing, unresolving pneumonia, and chest wall pain ( Latimer & Mott, 2015 ; Midthun, 2015). Patients initially may present with symptoms related to extrathoracic disease, including tracheal obstruction, esophageal obstruction with dyspha- gia, laryngeal nerve paralysis, phrenic nerve paralysis with elevated hemidiaphragm, sympathetic nerve paralysis or Horner ’ s syndrome, pleural effusion owing to lymphatic obstruction, Pancoast ’ s syndrome involving the eighth cer- vical and fi rst and second thoracic nerves, or superior vena cava syndrome from vascular obstruction (Midthun, 2015).

Patients with pericardial and cardiac extension of tumor may have symptoms of arrhythmia, tamponade, or failure. The presenting illness in patients with lung cancer may be paraneoplastic syndromes, including hypercalcemia, hypo- phosphatemia, hyponatremia with syndrome of inappro- priate antidiuretic hormone, and hypercoagulable states (Midthun, 2015). Occasionally, skeletal-connective syn- dromes, clubbing, and osteoarthropathy are initial symptoms of lung cancer.

Diagnostic Tests: After a history and physical examination suggestive of disease, the following tests are recommended (note that tissue biopsy results are required for diagnosis):

Noninvasive Testing: ■ Chest x-ray: This may show nonspecifi c abnormalities,

hilar masses, atelectasis, pleural effusions or masses, and infi ltrates.

LUNG CANCER

186 Chapter 8 ■ Chest Disorders

■ CT scan, preferably with contrast: CT scan can assist in defi ning the characteristics, size, and location of the primary tumor, lymphadenopathy if present, and any abnormalities of the liver and adrenal glands ( Latimer & Mott, 2015 ).

■ Fluorodeoxyglucose positron emission tomography (FDG-PET): This is a test that measures the metabolic uptake of glucose by cells; lung cancer cells have a higher cellular glucose uptake than normal cells. It is helpful in diagnosing metastatic disease ( Latimer & Mott, 2015 ).

■ MRI of the brain, with contrast: An MRI can assist in identifi cation of brain metastases (NCCN, 2016b; NCCN, 2017).

Invasive Testing: ■ Sputum for cytology: This is positive in most centrally

located tumors. ■ Transthoracic needle aspiration is usually reserved for

specifi c circumstances. ■ Fiberoptic bronchoscopy with biopsies has a very high

sensitivity rating for diagnosis. ■ Bronchoscopy with CT-guided transbronchial needle

aspiration has an important role in diagnosis and staging of lung cancer.

■ Endoscopic ultrasound, endobronchial ultrasound, and mediastinoscopy also contribute to staging; mediasti- noscopy is considered the gold standard for identifying mediastinal involvement ( Latimer & Mott, 2015 ).

■ If abnormalities suggest more extensive cancer, further testing will be conducted looking for extrathoracic, met- astatic disease.

Staging: NSCLC staging was revised in 2009 and follows the tumor, node, metastasis (TNM) classifi cation (Edge et al., 2009). Correct staging is essential at diagnosis to iden- tify treatment options, prognosis, and potential for recur- rence. An updated version of TNM staging is scheduled to be released in late 2017.

SCLC staging follows the two-stage Veterans Adminis- tration Lung Study Group staging system of limited disease (LD) and extensive disease (ED). Limited disease is confi ned to one hemithorax, the mediastinum, and the supraclavicular lymph nodes on the same side as the tumor. Extensive disease is any disease extending beyond this, including disease in the contralateral nodes or pleural effusion (Glisson & Byers, 2014).

Differential Diagnosis: TB, infectious granuloma, pneumonia, empyema, bronchiectasis, abscess, sarcoidosis, pneumonitis, and asbestosis all can mimic lung cancer.

Treatment: Surgical resection, radiation therapy, and che- motherapy are indicated for NSCLC; the stage of the disease, patient ’ s functional status, and histology of the tumor deter- mine the treatments. Recent advances in genotyping and targeting of altered signal mechanisms in lung cancer have allowed targeted treatment with immunotherapy, mono- clonal antibodies, anti–vascular endothelial growth factor (anti-VEGF) agents, and other modalities (NCCN, 2016b, 2017). The EGFR gene is mutated in 15% to 30% of non- Asian patients and 30% to 60% of Asian patients with ade- nocarcinoma, which is associated with improved response

to tyrosine kinase inhibitors (Midthun, 2015). Multimodal chemotherapy and radiation is the treatment of choice for limited stage SCLC; cisplatin and etoposide are the preferred agents (NCCN, 2016b). Prophylactic cranial irradiation is done in select patients. In some patients with very limited disease, surgical resection may be done (NCCN, 2016b). Treatment of extensive stage SCLC is chemotherapy alone with cisplatin or carboplatin, up to six cycles, then watchful waiting. Use of prophylactic cranial irradiation is recom- mended in patients who have a complete or partial response to initial therapy (NCCN, 2016b). Treatment after relapse is dependent on response to initial chemotherapy. If there is a positive response, repeating the treatment is done. If nonre- sponsive to initial chemotherapy, “salvage chemotherapy” with a nonplatinum, single agent such as topotecan, gemcit- abine, or a taxane is attempted (NCCN, 2016b). Clinical trials are now underway with other chemotherapy agents. Treat- ment for older adults should be individualized. A compre- hensive geriatric assessment is often conducted and used in determining treatment options. The Karnofsky Performance Scale is also used by some specialists (www.hospicepatients. org/karnofsky.html).

Follow-Up: Follow-up is individualized; generally, patients should be seen for follow-up every 3 to 4 months after treat- ment for lung cancer. During years 3 to 5, follow-up should be every 6 months. Yearly examinations are advised thereafter.

Sequelae: Disability and death are the chief sequelae of lung cancer. The 5-year survival rate is 17.7% (National Cancer Institute, 2016).

Prevention/Prophylaxis: Prevention of lung cancer should focus on smoking cessation. Ask about and record the tobacco use status of every patient, advise patients who smoke to quit, and offer smoking cessation treatment at every offi ce visit. Screening for lung cancer in asymptomatic patients is not advised. Screening in high-risk patients has not demonstrated any decrease in mortality; newer methodologies studying biomarkers have not been proved to date. The National Com- prehensive Cancer Network (NCCN, 2016a) and the USPSTF (2013) have issued guidelines endorsing screening with low- dose helical CT scan in high-risk patients. There is currently no recommended chemoprevention for lung cancer (Keith & Miller, 2014).

Referral: On suspecting lung cancer, refer the patient to a pulmonary specialist. At a later stage, referral to palliative care or hospice may be indicated. Give patient information on the American Lung Association Information Line (1-800- LUNGUSA). Referral to a mental health specialist is indicated in severe depression unresponsive to treatment.

Education: Many smoking cessation programs are available. Examples include the National Cancer Institute Tobacco Quitline, the American Academy of Family Physicians Stop Smoking Kit, various pamphlets from the American Cancer Society, and A Healthy Beginning Counseling Kit from the American Lung Association; the Web site www.smokefree. gov is another resource. The primary health-care provider can assess the smoker ’ s motivation to quit and offer brief motivational interventions at each visit. Provide information about support groups and community programs available to help with smoking cessation.

Chapter 8 ■ Chest Disorders 187

Once the patient is diagnosed with lung cancer, education about type of cancer, treatment options, and prognosis is very important. This is typically done by the oncology team,

Atherosclerotic plaque formation has been noted in persons younger than 20 years of age. Gradually, this athero- genic plaque builds up inside the intimal linings of the coro- nary artery(ies), resulting in both hardening of the arterial walls and narrowing of the coronary vessels. This atheroscle- rotic plaque contains lipid (cholesterol)–rich content, covered by a fi brous cap, which can ulcerate or fi ssure. Rupture of this vulnerable plaque can result in thrombosis, which par- tially or totally occludes the lumen of the affected artery(ies), either at the location where the thrombus formed or further downstream where a smaller artery could be blocked. The results are essentially the same—an abrupt decrease in cor- onary blood fl ow to the myocardium, termed myocardial ischemia. Prolonged myocardial ischemia can lead to tissue death and MI. Although there are other causes of MI due to reduced myocardial blood fl ow, including hypotension and prolonged coronary vasospasm, or severe hyperthyroidism (which can increase the heart ’ s demand for oxygen), the most frequent cause of MI is due to atherosclerosis. Another factor that plays an important role in ACS is platelet activation and aggregation (Amsterdam, 2014; Riffo, 2015). Damaged blood vessels result in exposed collagen fi ber in the basement membrane. Platelets subsequently adhere to this collagen

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Low-dose CT scan should be used to screen high risk individuals for lung cancer.

B USPSTF, 2013 NCCN, 2016a

Surgery is the treatment of choice for patients with local or only locally advanced non-small cell carcinoma (Stage I through Stage IIIA).

C Latimer & Mott, 2015 NCCN, 2017

Treatment for unresectable non-small cell carcinoma may involve radiotherapy and chemotherapy.

C NCCN, 2017

Chemotherapy, combined with radiotherapy in limited disease, is the mainstay of treatment for small cell carcinoma.

B NCCN, 2016b

Both radiotherapy and chemotherapy are used in treatment of superior vena cava (SVC) syndrome because of non-small cell or small cell lung cancer.

B NCCN, 2016b NCCN, 2017

Early palliative care results in improved quality of life and a decreased incidence of depression in patients with newly diagnosed non-small cell lung cancer.

B Latimer & Mott, 2015

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

but primary care providers can monitor for patient questions and communicate this to the specialty team.

MYOCARDIAL INFARCTION

Signal Symptoms: Typical symptom is prolonged chest pain (more than 20 minutes’ duration); atypical symptoms include shortness of breath, neurological symptoms (confu- sion, weakness), and worsening of heart failure.

Description: Reeder and Kennedy (2016) defi ne MI as a pathological clinical episode, triggered by myocardial ische- mia, manifesting in myocardial injury or necrosis. MIs can be classifi ed as acute ST elevation MI (STEMI) or non–ST eleva- tion MI (NSTEMI).

Etiology: The hallmark of ACS is the sudden imbalance between myocardial oxygen consumption (MVO2) and demand, which is usually the result of coronary artery obstruction. This imbalance may also be caused by other con- ditions, including excessive myocardial oxygen demand in the setting of a stable fl ow-limiting lesion; acute coronary insuf- fi ciency due to other causes such as vasospastic angina, cor- onary embolism, coronary arteritis; noncoronary causes of myocardial oxygen supply-demand mismatch include hypo- tension, severe anemia, hypertension, tachycardia, hyper- trophic cardiomyopathy, severe aortic stenosis; nonischemic myocardial injury and multifactorial causes that are not mutually exclusive (Amsterdam, 2014, p. 16).

188 Chapter 8 ■ Chest Disorders

fi ber and become activated. On activation, platelets then release chemicals, including adenosine diphosphate (ADP) and thromboxane (a vasoconstrictor), which causes addi- tional platelet aggregation. A platelet plug (or clot) is formed, which decreases blood fl ow to the blood vessel (Amsterdam, 2014; Riffo, 2015).

Occurrence: When looking at all-cause mortality, coronary disease is the most frequent cause of death in the United States. In persons age 55 to 74 years in the United States, coronary disease occurs more frequently in men, with a median age of 68 years (Amsterdam, 2014). Women of all ages have a greater risk of longer hospitalizations and com- plications (Amsterdam, 2014). In persons older than 75 years, coronary disease contributes to signifi cant morbidities and mortality (Amsterdam, 2014). In persons age 75 years or older who present with MI, more than 60% have NSTEMI with associated in-hospital mortality, accounting for approx- imately 80% of all in-patient hospital deaths (Kyriakides, Kourouklis, & Kontaras, 2007; Tullman, Haugh, Dracup, & Bourguignon, 2007). In addition, persons older than 65 years with MI are associated with higher post-discharge mortality, theoretically because of the higher incidence of diffuse coronary disease and existing poor myocardial per- fusion. Data published by the CDC (2011) on coronary disease and MI found that males overall had a signifi cantly higher myocardial rate than females; however, with suc- cessive age groupings, the prevalence of MIs signifi cantly increased. When identifying level of education with MI and coronary disease, persons who had less than a high school diploma experienced almost twice the occurrences of these conditions when compared with those who had college education.

Age: In 2010, the prevalence of CHD was greatest among persons aged 65 years and older (19.8%). Postmortem studies show that coronary atherosclerosis is widespread, even among asymptomatic adults. Aging itself may be a risk factor for MI in both men and women (CDC, 2011).

Gender: Before menopause, due to estrogenic cardiopro- tective effect, women have a lower occurrence of MI than men. Coronary disease is much more prevalent in men than in women up to age 74 years, after which the occur- rence increases steeply with age in both genders. On average, women develop heart disease 10 years later than men and suffer MIs and sudden death 20 years later than men. Thus, by age 75 years, postmenopausal women have an equal risk to men of coronary disease and MI.

Ethnicity: The incidences and occurrences of patients having MIs and CHD by race and ethnicity have been reported by the CDC (2011). Specifi c groups were identifi ed at increased risk, including those persons who are multiracial, Native Ameri- cans, and Alaskan natives, who have substantially higher prevalence of MI than non-Hispanic Caucasians or African Amerians (CDC, 2011). Overall, in patients with NSTEMI, African American patients (when compared to Caucasians) were younger, with concomitant comorbidities including hypertension, renal insuffi ciency, diabetes, and heart failure (CDC, 2011).

Contributing Factors: Risk factors for heart disease and MI in elderly individuals are essentially the same as in the younger population. Risk factors include hypertension,

hyperlipidemia, diabetes, insulin resistance, physical inac- tivity and sedentary lifestyle, overweight or obesity, family history of heart disease, poor diet, sleep apnea, alcohol, and stress (www.nhlbi.nih.gov/health/health-topics/topics/hd). Cigarette smoking is associated with new coronary events for elderly men and women. The risks of MI drop rapidly after smoking cessation and, at 5 years, the risk for new coronary events is similar to that of a nonsmoker (Mendis, Puska, & Norrving, 2011).

Aging alters the cardiovascular system in ways that reduce cardiac reserve and effi ciency, thus compromising the ability to respond to stress or illness. The cardiovascular system becomes less compliant as diastolic fi lling of the ven- tricles declines and afterload increases secondary to increased stiffness in the ascending aorta. The result is moderate left ventricular hypertrophy, which creates a more precarious balance between myocardial oxygen supply and demand. Other changes in the elderly cardiovascular system include decreased responsiveness to beta-adrenergic stimulation, decreased baroreceptor sensitivity, and an increased depen- dence on a higher end-diastolic volume to maintain cardiac output (NIH, 2015).

Signs and Symptoms: With advancing age, the presentation of acute MI will be less likely to include the classic symp- toms of crushing substernal chest pain, nausea, vomiting, and diaphoresis. Rather, atypical symptoms such as a vague ache or discomfort may be present. Elderly persons may not recognize that throat, shoulder, arm, jaw, or abdomi- nal pain may be referred cardiac pain or angina equivalent. Dyspnea is the second most common symptom of MI in both younger and older populations. For patients 85 years and older, syncope, acute confusion, or stroke may be the only presenting symptom. Some elderly patients may present only with faintness, weakness, giddiness, or restlessness (Domino, 2016).

On physical examination, the patient may be anxious and weak and may appear cyanotic. Arrhythmias may be noted on the EKG. The skin may be diaphoretic, cold, and clammy. Thrills, heaves, and an abnormal PMI may be palpated. Peripheral pulses may be irregular, slow, fast, or thready. Auscultation may reveal an S 3 or S 4 , pericardial friction rub, murmurs, or crackles. The physical examination must focus on ruling out diagnoses other than MI.

Diagnostic Tests: Along with a chest x-ray examination, CBC, clotting profi le, electrolytes, and cardiac biomarkers includ- ing troponin, evaluation for acute MI includes serial 12-lead EKGs (Amsterdam, 2014; Domino, 2016). Changes on the EKG indicative of STEMI include ST-segment elevation in leads facing the infarction. ST-segment depression is some- times present. With the increased incidence of NSTEMI, the presence of a single normal EKG does not rule out MI, and therefore serial EKGs are necessary. However, EKG fi ndings may be nondiagnostic or diffi cult to interpret in older adults because of possible abnormalities, such as left bundle branch block, left ventricular hypertrophy, and previously unrecog- nized MIs.

In older adults, the cardiac enzyme profi le may be atypical. Creatine kinase (CK), an enzyme found in myocardial cells, is released into the bloodstream when cells are damaged, approximately 6 to 8 hours after the onset of pain. Because the baseline CK in elderly patients may be signifi cantly

Chapter 8 ■ Chest Disorders 189

lower than normal, even those with MI may not develop CK levels high enough to be interpreted as abnormal, owing to decreased muscle mass. CK-MB, an isoenzyme of CK, is released on the death of myocardial cells and not during ischemia. The presence of CK-MB is also found in skeletal muscle, which can result in false-positive results from noncar- diac conditions such as renal failure, head or chest trauma, PE, acute and chronic muscular disorders, hypothyroidism, or hyperventilation. Therefore, CK-MB measurements do not provide additional information to the algorithms of STEMI and are not preferred over cardiac troponins (Rains, 2014). Cardiac troponin T (cTnT) is a cardiac-specifi c marker for MI, with rises in concentration levels soon after chest symptoms begin (Rains, 2014). Although elevations may not occur for 6 to 12 hours after onset of symptoms, in approximately 80% of patients use of cTnT alone can result in a defi nitive diagnosis of STEMI. Lactate dehydrogenase levels are occa- sionally useful in patients with delayed presentation because this enzyme remains elevated for several days. Other tests for MI may include echocardiography or stress thallium scans (Rains, 2014).

Differential Diagnosis: The pain from MI can be similar to that of acute pericarditis, PE, acute aortic dissection, or costo- chondritis. Many conditions can present as cardiac disease in the elderly, including cor pulmonale, pneumonia, esophageal spasm, GERD, hiatal hernia, gallbladder disease, osteoarthri- tis of the spine, infl ammation at the chondrocostal junction, muscle injury, and panic disorder (McPhee & Papadakis, 2016).

Treatment: The ACC and AHA have examined pharma- cological and interventional treatments for acute MI and established guidelines for care. Nitrates, the cornerstone of therapy for ischemic pain, reduce preload and improve coro- nary perfusion. Chest pain should be treated with sublingual nitroglycerin, repeated three times, 5 minutes apart, unless the patient is hypotensive, has right ventricular infarction, or has aortic stenosis ( Amsterdam et al., 2014 ). IV nitrates have been shown to limit infarct size and reduce pain, complica- tions, and mortality. IV nitroglycerin is started at 5 mcg/min on an infusion pump and titrated to desired effect. Frequent monitoring is required because harmful effects can be seen if the SBP drops below 90 mm Hg. Morphine sulfate, 2 to 4 mg IV, repeated at 5- to 15-minute intervals, is also effective for pain relief and can be given with anxiolytics ( Amster- dam et al., 2014 ). Supplemental oxygen (2 to 6 L/min nasal cannula) should be given if oxygen saturation is less than 94% or arterial oxygen saturations are low.

Thrombolytics: Reperfusion in patients who present to hos- pitals with percutaneous coronary angioplasty and inter- vention (PCI) capability has become the standard of care ( Amsterdam et al., 2014 ). In hospitals without PCI capability and where patients cannot be transferred to a hospital with PCI capability within 90 minutes, treatment with fi brino- lytic (thrombolytic) therapy initiated within 30 minutes of presentation should be performed unless contraindicated (HAA, 2014). The use of thrombolytics in STEMI patients has been shown to decrease mortality by up to 30% (Amster- dam, 2014; Morse et al., 2009). Thrombolytic agents include tissue-type plasminogen (tPA) and streptokinase (SK). Indi- cations for thrombolysis are based on the existence of chest

pain and specifi c EKG changes. Studies show that this therapy is frequently omitted for elderly patients. Reasons for this include frequent delay in seeking medical care, atypical pre- sentation of MI, and a higher prevalence of NSTEMIs. Fear of hemorrhage following use of thrombolytics must be weighed against the proven gains in survival for all age groups, espe- cially for those presenting early with MI. A variety of studies suggest that SK may be as benefi cial as tPA in treating the elderly MI patient, which is considerably less expensive (Morse et al., 2009).

Aspirin: Aspirin therapy in post-PCI STEMI patients without demonstrated aspirin resistance should be initiated at 162 to 325 mg daily and, depending on the type of stent implanted, the recommended maintenance dose to be used with Tica- grelor is 81 mg (Amsterdam, 2014). In patients at risk for increased bleeding after stent implantation, lower-dose aspirin is reasonable. Aspirin (non-enteric coated) should be given as soon as possible if there is no obvious contra- indication. Patients taking nonselective NSAIDs (excluding aspirin) and cyclooxygenase-2 inhibitors should have these agents discontinued at the time of presentation with STEMI and not readministered during the course of hospitalization due to increased risk of mortality, reinfarction, myocardial rupture, heart failure, shock, or hypertension ( Amsterdam et al., 2014 ).

Thienopyridines: Concurrent use of dual antiplatelet therapy (aspirin and thienopyridines) in MI patients (STEMI or NSTEMI) following PCI with stent implantation is the gold standard for secondary prevention of subsequent cardiovas- cular events. Use of thienopyridines, including clopidogrel or prasugrel, is important to decrease the risk of death and stroke, and to prevent reinfarction or in-stent thrombosis ( Amsterdam et al., 2014 ). Thienopyridines should be initi- ated as a loading dose early, either before or at the time of primary or nonprimary PCI, and continued for a minimum of 12 months after bare metal stent placement in patients who are not at high risk for bleeding ( Amsterdam et al., 2014 ). In patients for whom nonemergent coronary artery bypass is planned, thienopyridine therapy should be discon- tinued for a minimum of 5 days for those patients receiving clopidogrel and 7 days for those patients receiving prasugrel ( Amsterdam et al., 2014 ).

Parenteral anticoagulants are recommended in all patients with acute coronary syndrome or myocardial patients regardless of whether or not reperfusion therapy was received. Low-molecular-weight heparin (LMWH), unfrac- tionated heparin, bivalrudin, enoxaparin, or fondaparinux is recommended in patients undergoing PCI ( Amsterdam et al., 2014 ). If coronary artery bypass grafting is planned, antico- agulants should be withheld for 5 to 7 days before the proce- dure due to risks of excessive bleeding.

For patients not receiving thrombolytics, low-dose sub- cutaneous heparin or LMWH is indicated for prophylaxis of deep venous thrombosis. Older adult patients with large anterior MIs and heart failure, as well as those with docu- mented left ventricular thrombus, should receive full heparin anticoagulation.

Angiotensin-Converting Enzyme Inhibitors: ACEIs reduce mortal- ity in post-MI patients. ACEIs are recommended and should be continued indefi nitely for every patient recovering from an

190 Chapter 8 ■ Chest Disorders

STEMI and for those with MI with an LVEF less than 40% and no obvious contraindication(s) to their use. For patients with preserved LVEF with hypertension, chronic kidney diseases, or diabetes, ACEIs are recommended unless contraindicated ( Amsterdam et al., 2014 ).

Angiotensin Receptor Blockers: ARBs are recommended in those patients who are intolerant of ACEIs, who have heart failure with LVEF of 40% or less, or who have hypertension.

Aldosterone Blockade: Aldosterone blockade is recommended for post-MI patients without severe renal dysfunction or hyperkalemia, with heart failure, with LVEF of 40% or less, or with diabetes who are already on a therapeutic dose of ACEI and beta blockade ( Amsterdam et al., 2014 ).

Beta Blockers: Beta blockers have been shown to limit infarct size, decrease chest pain, improve prognosis, and reverse car- diovascular remodeling. They are generally well tolerated in patients ages 65 to 75 years. “The use of B-Blockers in this population should be tailored based on other concomitant cardiovascular conditions and completeness of revascular- ization” (Motivala, 2016). Conditions that contraindicate the use of beta blockers in the elderly include bronchospas- tic lung disease, marked bradycardia, hypotension, depres- sion, acute heart failure, and diabetes. “B-Blockers have consistently been shown to improve outcomes in a variety of cardiovascular settings and therefore remain widely used” (Motivala, 2016).

In acute MI, metoprolol or atenolol is given 2.5 to 5 mg IV every 5 minutes, for a total of 15 mg and 10 mg, respectively. Beta blockers should be initiated in the emergency depart- ment before PCI and within 24 hours in patients presenting with STEMI, MI, acute coronary syndrome, or left ventricu- lar dysfunction with or without heart failure, unless contra- indicated. Beta blocker use in this population has increased over time (Motivala, 2016). Contraindications to beta blocker therapy include heart failure, evidence for a low cardiac output state, or risk for cardiogenic shock ( Amsterdam et al., 2014 ).

Statins and Lipid-Lowering Therapy: A lipid profi le that includes total cholesterol, LDL, HDL, and triglycerides should be per- formed and assessed on all acute coronary syndrome or MI patients within 24 hours of admission. Lipid-lowering therapy is recommended before discharge, with the LDL goal to be less than 100 mg/dL, preferably with further LDL reduction to less than 70 mg/dL ( Amsterdam et al., 2014 ). Dietary therapy is recommended for all patients, including consumption of omega-3 fatty acids, weight management, and physical activity.

CCBs have limited use in STEMI and NSTEMI patients. Hypotension-induced tachycardia has been associated with the use of short-acting CCBs. Long-acting CCBs should be used sparingly, if needed, with additional precautions in those patients already taking digoxin or beta blockers (Kyriakides et al., 2007).

In terms of interventional management of elderly MI patients, guidelines by both the AHA and ACC have estab- lished “door to needle” time of less than 30 minutes and “door to balloon” time within 90 minutes of initial presen- tation to the hospital for the best possible outcomes ( Amster- dam et al., 2014 ). Percutaneous transluminal coronary

angioplasty (PTCA) with PCI may be a valuable alternative in those for whom thrombolytics are contraindicated. Coro- nary artery bypass graft (CABG) is preferred for patients with left main stenosis and those with moderately severe left ven- tricular depression. Emergency PTCA or CABG in older adult patients presenting with cardiogenic shock or heart failure is associated with high morbidity and mortality.

Glucose Control: Hyperglycemia (defi ned as blood sugar greater than 180 mg/dL) in patients with STEMI has been associated with adverse outcomes, including increased mor- bidity and mortality, as well as prolonged hospitalizations ( Amsterdam et al., 2014 ). Maintaining glucose control may decrease the infl ammatory response and improve LVEF ( Amsterdam et al., 2014 ).

Follow-Up: Risk stratifi cation for future cardiac events follow- ing stabilization from MI is necessary. Tests to evaluate for ischemia or myocardium at risk include low-level exercise test, nuclear perfusion scanning, and dobutamine echocardiogra- phy. Left ventricular function can be determined by echocar- diography or radionuclide ventriculogram. Routine coronary angiography is not recommended for all MI patients, but should be performed on patients with demonstrable ische- mia. Patients at high risk for sudden death from arrhythmias should undergo electrophysiology (EP) evaluation.

Sequelae: Increasing age is associated with more complica- tions after MI, including heart failure, arrhythmias, pulmo- nary edema, cardiogenic shock, cardiac rupture, and death.

Prevention/Prophylaxis: Secondary prevention in the older adult MI patient includes use of aspirin, beta blockers, and ACEIs, unless there are absolute contraindications to these agents. Lipid-lowering therapy is also benefi cial. Reduction of risk factors is necessary. Cardiac rehabilitation can be as benefi cial in older MI patients as in younger ones. Emotional support remains important.

Referral: Suspicion of acute MI should prompt transfer of the patient to an environment equipped with cardiac monitoring and the ability to administer advanced cardiac life support. As hospitalization continues, consultation with a variety of disciplines, such as surgery, social work, and physical therapy, may be necessary.

Education: Individualized teaching following MI for each patient and family should be provided, using age-specifi c teaching methods. Teach the basic defi nitions of CAD, angina, and MI. Patients need information on the healing process fol- lowing MI, when to return to work or resume normal daily activities, and when to resume sexual relations. Give an exer- cise prescription. Involve patients and families in a discussion of the psychological adjustment following MI. Encourage risk factor reduction. Health-care practitioners should work with patients to set goals and design plans. Give patients informa- tion on community resources, such as the AHA or support groups in their area. Smoking cessation should be strongly encouraged and pharmacological and nonpharmacologi- cal therapies discussed. Medication teaching and review are very important. Health-care providers should be aware of all medications prescribed for the patient and any OTC med- ications, including vitamins, minerals, and supplements. Patients should bring in all of their medications at each visit. Teach patients about the desired effects and common

Chapter 8 ■ Chest Disorders 191

side effects of their medications. Emphasize the importance of taking aspirin and anticoagulants as directed to prevent in-stent thrombosis. Review what to do if medication cannot be taken or obtained. Discuss the use of nitrates for any chest pain, while avoiding the usage of nitrates in patients taking medications such as sildenafi l, tadalifi l, or vardenafi l, due to sudden drops in BP, resulting in hypotension.

Teach older adult patients about altered pain perception that can occur with age and with diseases such as diabetes. Teach patients and their families about warning signs such as chest pain or pressure, shortness of breath, indigestion, choking, sweating, dizziness, palpitations, severe weakness, and loss of consciousness. Establish a clear plan for obtaining prompt medical attention.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The presence of elevated cardiac enzymes associated with clinical or EKG evidence of ischemia is diagnostic for MI.

A Amsterdam et al., 2014

Treat all patients with oxygen, pain control medications, and antiplatelet therapy including aspirin and heparin (or enoxaparin).

A Amsterdam et al., 2014

Nitroglycerin may be given to relieve ischemic chest pain, except in patients with hypotension and right ventricular infarction.

A Amsterdam et al., 2014

Give thrombolysis within 30 minutes when PCI is not available or when >90 minutes of delay is expected in door to balloon time.

A Amsterdam et al., 2014

Treat most patients with aspirin or clopidogrel, beta blockers, and statins (LDL target of 70–100 mg/dL) if no contraindications are noted.

A Amsterdam et al., 2014

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

PNEUMONIA

Signal Symptoms: Chills or hyperthermia, fever, sweating, chest discomfort or dyspnea, a new cough with or without sputum production or with chronic cough, a change in sputum color. Nonspecifi c symptoms include fatigue, abdomi- nal pain, headache, myalgias, loss of appetite, and worsening of other chronic illnesses. In older adults, initial symptoms may not include a cough or chest pain but fever and confu- sion. Atypical pneumonia symptoms generally have a more gradual onset and may include a dry, hacking cough with more constitutional symptoms such as headache, coryza, shaking chills, myalgias, and sore throat ( Wunderink & Waterer, 2014 ; Musher & Thorner, 2014 ).

Description: Community-acquired pneumonia (CAP) is an acute lower respiratory tract infection of the lung paren- chyma in which consolidation occurs as exudate fi lls the alveoli. CAP is usually infectious, can be bacterial or viral, and refers to pneumonia that begins outside of the hospital or is diagnosed within 48 hours of admission without recent (14 day) residence in a long-term care facility. Health-care– acquired pneumonia (HAP) is acquired from a hospital or nursing home (Donovan, 2015).

Ventilator-associated pneumonia (VAP) is the most fre- quently acquired infection in the ICU in mechanically ven- tilated patients, with the highest risk occurring in the fi rst

5 days post intubation. Multiple factors contribute to VAP, including micro aspiration, bacterial laden tube, secretions around the cuff, impairment of clearance of secretions within the airway, and pathogenic material from surround- ing structures (mouth, sinuses, stomach) ( Kalanuria, Zai, & Mirski, 2014 ).

Etiology: The most common cause of bacterial CAP in patients who were admitted to the hospital was streptococcus pneumoniae , followed by mycoplasma pneumoniae, Staphylo- coccus aureus, legionella pneumophilia , and enterobacteriacaea . Pneumococcal pneumonia was found in only 5% of CAP inpatient cases ( CDC, 2016 ; Jain et al., 2015).

HAP in older patients is caused by a variety of organisms ( Pseudomonas aeruginosa, Klebsiella pneumoniae, S. pneumoniae, Escherichia coli, Sarratia proteus, and Enterobacter) and it is common to have a mixture of multiple organisms . In nursing home residents S. Aureus , MRSA, S. pneumoniae , and H. infl uenza are reported more often as the causative organism (Marrie & File, 2016). The most common pathogens found in VAP differ depending on the length or ventilation ( Kalanuria et al., 2014 ).

Occurrence: Pneumonia and infl uenza together are the eighth leading cause of death in the United States, and CAP is the leading cause of death due to infectious disease. The

192 Chapter 8 ■ Chest Disorders

annual occurrence rate of CAP in the United States is about 5.6 to 6.11 cases per 1,000 persons, with the highest rates among adults 65 years or older (Marrie & File, 2016). Esti- mated annual deaths from CAP is over 55,000 (Kochanek, Murphy, Xu & Tejada-Vera, 2016). The incidence of CAP for each pathogen increased with age. In the EPIC study ( CDC, 2016 ), 93% had radiographic evidence of pneumonia and yet a pathogen was identifi ed in only 38%. About 23% of pathogens were viral and 11% were bacterial. Rhinovirus, infl uenza A or B, and streptococcus pneumonia were the most common pathogens identifi ed in the study.  Persons 65 to 79 years old had a rate of hospitalization approximately nine times that of those under 50 years, and persons 80 years and older were 25 times more likely to be hospitalized (Jain et al., 2015).

The mortality rate for CAP is dependent on the treating site but generally is less than 3% in the outpatient setting, 5% to 10% in hospitalized patients, and as high as 25% in intubated ICU patients. In ICU patients on vasopressors, the mortality rate may be as high as 50% (Restrepoa, Faverioa, & Anzueto, 2013).

Age: Pneumonia is the most common cause of death from infectious disease in older patients. Elderly persons experi- ence a more signifi cant increase in risk than that of younger adults from dying of pneumonia (Jain et al., 2015; Restrepoa et al., 2013).

Gender: More men than women are diagnosed with pneumonia.

Ethnicity: Not signifi cant.

Contributing Factors: Comorbidities, infl uenza, chronic pul- monary conditions, smoking, alcoholism, malnutrition, colonization of the oropharynx by gram-negative bacteria, institutional setting, decline in immune function, hospitaliza- tion, use of sedating medications, recent surgery or trauma, and diminished cough refl ex may contribute to development of pneumonia (Marrie & File, 2016; Restrepoa et al., 2013; Torres, Peetermans, Viegi, & Blasi, 2013).

The main risk factor for HAP is mechanical ventilation. Other signifi cant risk factors according to File (2016b, p. 1) include:

■ Age 70 years or older ■ Chronic lung disease ■ Depressed consciousness ■ Aspiration ■ Chest surgery ■ The presence of an intracranial pressure monitor or

nasogastric tube ■ Agents that increase gastric pH (H 2 blockers, antacids,

proton pump inhibitors) ■ Transport from the ICU for diagnostic or therapeutic

procedures ■ Previous antibiotic exposure, particularly to third-gen-

eration cephalosporins ■ Reintubation or prolonged intubation ■ Hospitalization during the fall or winter season ■ Mechanical ventilation for acute respiratory distress

syndrome ■ Frequent ventilator circuit changes ■ Paralytic agents ■ Underlying illness

The most common risk factors in pneumonia-related deaths are respiratory disease, cardiovascular disease, and cancer. Other common risk factors for increased mortality include older age, severity of pneumonia, and either existing or new onset of comorbidities such as cardiovascular, respi- ratory, neurological, diabetes, COPD, and acute kidney injury (Holter et al., 2016).

The CURB-65 score ( Table 8-5 ) and the CAP index are used to stratify risk in patients with CAP. The fi ve indicators that comprise the CURB score include elevated BUN levels, low DBP, a rapid respiratory rate, confusion, and age greater than 65 years. There is a 21-fold increase in mortality if patients have two or more of these symptoms. The pneumo- nia severity index (PSI) was designed to predict the 30-day mortality rate of patients with CAP and assigns points to con- tributing factors such as comorbidities, age, gender, nursing home residence, physical examination, and laboratory and radiographic fi ndings to determine which patients may need to be hospitalized ( File, 2016d ).

Signs and symptoms associated with pneumonia-related mortality include dyspnea, chills, altered mental status, tachypnea, hypotension, hypothermia, and hyperthermia. Laboratory abnormalities associated with increased mortality are hyponatremia, hyperglycemia, abnormal liver function studies, hypoalbuminemia, azotemia, hypoxemia, and azo- temia. Risk factors for drug-resistant S. pneumoniae (DRSP) include age of more than 65 years, alcoholism, antimicro- bial therapy within the past 3 months, exposure to children in day care, multiple comorbidities, or immunocompromise ( Musher & Thorner, 2014 ; Wonderink & Warterer, 2014).

Risk factors for VAP include the insertion of an endotra- chial tube and device-related issues, immunocompromise, adult respiratory distress, COPD, patient positioning, medica- tions, and personnel related (breach in technique) ( Kalanuria et al., 2014 ).

Signs and Symptoms: Typical symptoms include fever, chills, cough, and rusty or thick sputum, with associated gastro- intestinal upset or anorexia, malaise, and diaphoresis; pleu- ritic chest pain may also be present. These symptoms are frequently absent in the frail and elderly, leading to a lag time before diagnosis. In the older patient, mental status changes (i.e., confusion), new onset or increased frequency of falls, increased respiratory rate, hypotension, anorexia, a marked functional decline, and new onset of urinary incontinence

CURB-65 Criteria for Evaluation of Pneumonia Severity and Treatment Site

CLINICAL FACTOR POINTS SCORING

C onfusion (new disorientation) 1 Scoring 0-1: Low risk; consider

outpatient treatment

2: Brief hospitalization

or closely monitored

outpatient treatment

≥ 3: Severe, hospitalize and possible ICU

B U N >19 ng/dL 1

R espiratory rate ≥ 30 breaths/min

1

B P: Systolic <90 mm Hg OR Diastolic <60 mm Hg

1

Adapted from Dunphy, Winland-Brown, Porter, & Thomas. (2015). Primary care: The art and science of advanced practice nursing (4th ed.). Philadelphia: F.A. Davis.

TABLE 8-5

Chapter 8 ■ Chest Disorders 193

are typical symptoms (High, 2016). Physical examination of the chest reveals crackles that do not clear with cough or deep breathing. Increased respiratory rate (more than 24 breaths/min) is typical. A fever of 100°F with tachycar- dia may be present and signs of dehydration may occur. The patient may appear anxious, restless, or withdrawn (Marrie & Toumanen, 2016; Musher & Thorner, 2014 ; Wonderink & Warterer, 2014).

Symptoms of VAP include new or increasing pulmonary infi ltrate, decreased oxygenation with an increased respira- tory rate, and a decreased tidal volume. Fever and increased purulent secretions are common, and patients usually have diffuse rhonchi with an inability to mobilize secretions and may have either leukocytosis or leukopenia. Crackles, dimin- ished breath sounds, and tachypnea, as well as wheezing and hemoptysis, are common fi ndings ( Kalanuria et al., 2014 ; Kollef, 2016).

Diagnostic Tests: The diagnosis of CAP may be diffi cult in patients with underlying chronic comorbidities, especially those with pulmonary fi brosis, lung cancer or other chronic lung diseases, and heart failure. Recommendations for diag- nostic testing continue to be controversial, however, the chest x-ray is considered the gold standard for the diagno- sis of pneumonia (File, 2006d; Mandell et al., 2007 ). Other routine testing for patients treated on an outpatient basis is not recommended. Newer recommendations include testing for changes in C-reactive protein (CRP) and/or urine specifi c antigen when there is a question about when, or if, to start antibiotic therapy ( Bel et al., 2015 ; CDC, 2016 ; File, 2016a; National Institute for Health and Care Excellence [NICE], 2014 ). CT scan of the chest is often ordered and is more accu- rate than a chest x-ray, especially in the emergency depart- ment setting. Studies have shown that ultrasound of the chest has better sensitivity and specifi city than a chest x-ray and is equal to that of a CT scan (Bourcier et al., 2014). Pul- monary infi ltrate, lobular consolidation, or opacities found on chest x-ray, CT scan, or ultrasound confi rm the diagno- sis of pneumonia; however, newer studies demonstrate that chest x-rays have a low sensitivity and low positive predictive rate, but a high specifi city rate and high negative predictive value ( Bartlett, 2016 ; Self, Courtney, McNaughton, Wunder- ink, & Kline, 2013). Both the CPIS and CURB-65 are useful tools that may aid in predicting the severity of CAP and the need for hospital admission. The use of the PSI tool for use in risk stratifi cation and decision making has been validated in multiple studies (Yealy & Fine, 2015).

Other diagnostic tests are usually reserved for candidates admitted to the hospital following the Infectious Disease Society of America/American Thoracic Society (IDSA/ATS) guidelines (2007). Sputum for gram stain is recommended for all patients but is diffi cult to obtain in practice, particu- larly in an outpatient setting. For hospital patients, a urinary antigen test for pneumococcal disease is indicated ( Mandell et al., 2007 ).

Diagnostic testing for VAP includes chest x-ray or CT scan, and endotrachial aspirate for culture. There is little evidence to support invasive sampling over noninvasive sampling of sputum and secretions. In addition, the guidelines suggest that positive cultures from noninvasive samplings and clini- cal criteria should be the basis for treatment in VAP ( Kalil et al., 2016 ). The updated ISDA guidelines do not recommend

the use of biomarkers or CRP values when deciding to start antibiotic treatment. While only about 15% of VAP patients have positive blood cultures, they are still recommended as they may reveal other infectious processes not related to VAP ( Kalanuria et al., 2014 ; Kalil et al., 2016 ).

Differential Diagnosis: The differential diagnoses of CAP are dependent on the results of the chest x-ray. Differentials for those with a positive chest x-ray include:

■ Aspiration pneumonitis ■ Pulmonary infarction ■ Heart failure ■ Exacerbation of pulmonary fi brosis or bronchiectasis ■ Acute eosinophilic pneumonia ■ Pulmonary vasculitis ■ Hypersensitivity pneumonitis ■ Injury from cocaine use

For those without an abnormal chest x-ray the differen- tials are:

■ COPD exacerbation ■ Infl uenza ■ Pertussis ■ Acute bronchitis ■ Viral syndrome in asthmatic patients ( Wunderink &

Waterer, 2014 )

Early stage VAP occurs within 48 hours of intubation, while later stage VAP emerges after the fourth day of intuba- tion and is more likely to be associated with multi-drug resis- tant (MDR) bacteria. Differential diagnosis for VAP includes ventilator-associated respiratory infection (VARI) and ven- tilator-associated tracheobronchitis (VAT) ( Kalanuria et al., 2014 ; Kalil et al., 2016 ).

Treatment: A crucial element in treatment is determining the severity of the illness and the setting, but other factors includ- ing oral intake, adherence, substance abuse, mental illness, cognitive impairment, patient function, and living situation ( File, 2016d ). For community-dwelling older patients, the presence of a responsible caregiver and a supportive home environment is necessary. Temporary measures to increase support and monitor status of response may be introduced by ordering home health services. If the patient fails to recover or deteriorates despite these interventions, hospitalization should be contemplated. IDSA/ATS guidelines advocate the use of the pneumonia patient outcome research team (PORT) PSI prediction rule as a guideline for determining outpatient treatment versus hospitalization (which can be accessed at http://pda.ahrq.gov/clinic/psi/psicalc.asp).

Use of any prediction rule or tool should be tempered by clinical judgment. Objective criteria for hospital admission include ( File, 2016c ; Kalanuria et al., 2014 ; Kalil et al., 2016 ):

■ Inability to take oral medications or fl uids ■ Acute mental status changes ■ Severe acute metabolic, hematological, or electrolyte

abnormalities ■ Acute concomitant medical condition (e.g., malignancy,

hepatic disease, renal insuffi ciency, cardiac disease) ■ Hypoxemia on room air (PaO 2 less than 60 mm Hg) ■ Multilobular involvement on chest x-ray ■ Secondary suppurative infection

194 Chapter 8 ■ Chest Disorders

■ Severe vital sign abnormality (SBP less than 90 mm Hg, pulse greater than 125/min, respirations greater than 30/min)

The latest consensus guidelines from the IDSA/ATS for CAP, as well as recent studies, support the following recommendations:

■ Outpatient treatment for previously healthy adults with no risk factors for DRSP should consist of a macrolide or doxycycline.

■ Outpatient treatment for healthy adults who have been on an antibiotic in the previous 3 months should consist of a macrolide or respiratory fl ouroquinolone.

■ For those with comorbidities, including diabetes mel- litus, malignancies, alcoholism, chronic lung disease, cardiovascular disease, chronic liver or renal disease, immunosuppressive conditions or immunosuppressive drugs, or risk for DRSP, treatment should consist of a respiratory fl uoroquinolone or a combination of a beta-lactam and a macrolide.

■ For those in an area with more than 25% macrolide-re- sistant S. pneumoniae, consider treating with a beta-lac- tam plus either a macrolide or doxycycline.

■ For inpatient treatment outside the ICU, a respiratory fl uoroquinolone or a beta-lactam and macrolide con- currently; cefotaxime, ceftriaxone, and ampicillin are preferred.

■ For severe CAP requiring ICU admission, treat with a beta-lactam antibiotic, plus azithromycin or a respira- tory fl uoroquinolone.

■ Patients with risk factors for Pseudomonas should be treated with a beta-lactam antibiotic (piperacillin/tazo- bactam, imipenem/cilastatin, meropenem, doripenem, or cefepime), plus an aminoglycoside and azithromycin or an antipseudomonal fl uoroquinolone (levofl oxacin or ciprofl oxacin).

■ For risk factors for MRSA, treat with vancomycin or linezolid (Watkins & Lemonovich, 2011).

■ Treatment should be instituted as soon as possible and transition from IV to oral therapy should occur as soon as the patient is hemodynamically stable, shows clinical improvement, can ingest oral medications, and has no gastrointestinal tract problems. Duration of therapy is 5 to 7 days, provided the patient is afebrile for 48 to 72 hours (Donovan, 2015; File, 2016d ; Kalil et al., 2016 ; Lee, Giesler, Gellad, & Fine, 2016; Mandell et al., 2007 ; Wunderink & Waterer, 2014 ).

Treatment for HAP and VAP is guided by the IDSA/ATS guidelines ( Kalil et al., 2016 ). Once the potential for HAP/ VAP is identifi ed and specimens have been obtained, rapid empirical treatment with local antibiogram-driven choice of antimicrobial should be started. Knowledge of local resis- tance patterns, extent of MRSA, and other regional factors is essential. Treatment should be tailored to optimize antibiotic therapy and prevent resistance using pharmacokinetic and pharmacodynamic data (blood levels). In addition, patients on IV antimicrobial therapy should be switched to oral therapy

as soon as possible ( Kalil et al., 2016 ; Mandel, 2007). The use of glucocorticoids in the treatment of HAP/VAP has had varying results and should be reserved for patients who may benefi t from their anti-infl ammatory effects, ICU patients who are severely ill and have an elevated CRP, and patients whose risk for adverse effects from their use is limited ( File, 2016c ).

Follow-Up: Follow-up depends on comorbidities and response to prescribed treatment regimen. All patients diagnosed with CAP should schedule a follow-up offi ce visit within a few days after the initial diagnosis, as well as after completion of treat- ment, with future follow-up as needed. Patients should be instructed to call if symptoms worsen, if no response occurs after 3 to 5 days of treatment, or if symptoms reoccur. In most cases, follow-up chest x-ray is not necessary. In patients with comorbidities, smokers, and those over 40 years old, a repeat chest x-ray after 7 to 12 weeks may be indicated ( File, 2016c ).

Sequelae: The older patient with comorbidities is especially prone to complications and has a higher long-term mortality rate than those without comorbidities (Restrepoa et al., 2013). Serious complications can occur with CAP, including respi- ratory failure, pleural effusions, septic shock, renal failure, and empyema. Increased mortality is largely attributed to comorbidities and underlying disease, especially vascular and cardiac disease, COPD, diabetes, and renal disease. HAP and VAP patients are at risk for pneumonitis, CHF, acute respira- tory syndrome, atelectasis, and pleural effusion (Holter et al., 2016; Kalanuria et al., 2014 ; Restrepoa et al., 2013).

Prevention/Prophylaxis: Older patients and all health-care workers should have an annual infl uenza vaccine unless highly allergic. Latest guidelines recommend that the pneu- mococcal polysaccharide vaccine 23 and the pneumococcal conjugate vaccine  be administered in patients 65 years and older. Patients who are hospitalized for pneumonia may be immunized before discharge (Musher, 2016).

Prevention of VAP is facilitated by maintaining endo- tracheal tube cuff pressure, elevating the head of the bed, using chlorhexidine for oral care, performing a daily sedation assessment, and providing deep vein and ulcer prophylaxis ( Kalanuria et al., 2014 ).

Referral: Physical therapy measures for strengthening and ambulation may be initiated during the acute recovery period and continued during convalescence or replaced by restorative nursing measures. For those with chronic comor- bidities, follow-up or referral to the appropriate specialist is indicated.

Education: Provider education regarding appropriate pre- scribing of antibiotics is helpful in decreasing drug-resistant organisms. Teach groups of older adults (especially adults with comorbidities) about preventive measures including care after discharge, follow-up, and possible vaccination. Educate patient and caregivers about the importance of nutrition, hydration, deep breathing exercises, and smoking cessation (UpToDate, 2016).

Chapter 8 ■ Chest Disorders 195

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Consider pneumonia in patients with cough, dyspnea, or sputum production, especially if accompanied by fever, altered breath sounds, or rales.

C Bartlett, 2016

Perform a chest x-ray to confi rm the diagnosis of pneumonia. Newer studies suggest US and CT are more accurate.

C C

Bartlett, 2016 Bel, Hausfater, Chenevier- Gobeaux, Blanc, Benjoar, Ficko, . . . ..& Le Bel, 2015 CDC, 2016 File, 2016d NICE, 2014

Routine diagnostic tests are optional for outpatients, because most do well with empirical antibiotic treatment.

C C

Bartlett, 2016 Wunderink & Waterer, 2014

Sputum gram stain and culture, as well as legionella and pneumococcal antigen testing, are recommended for inpatients, particularly those with severe pneumonia, in whom identifi cation of an organism is more likely to prompt a change in the antibiotic agent.

C Kalil et al., 2016

The Pneumonia Severity Index and CURB-65 are validated prognostic models that may be used to help determine site of treatment in patients with CAP.

A C

Mandell et al., 2007 File, 2016c

Administer antibiotic therapy as soon as possible after the diagnosis is made and before leaving the emergency department if the person is being admitted.

C C

Mandell et al., 2007 Moran, Rothman, & Volturo, 2013

Treat previously healthy outpatients with a macrolide or doxycycline.

B C

Mandell et al., 2007 Musher & Thorner, 2014 Wunderink & Waterer, 2014

Treat outpatients with comorbidities or recent antibiotic use with levofl oxacin or moxifl oxacin alone or a beta lactam plus a macrolide.

B C

Mandell et al., 2007 Musher & Thorner, 2014

Treat inpatients empirically until pathogen is identifi ed with a 2 nd or 3 rd generation bata lactam plus a macrolide, or a respiratory fl uoroquinolone.

A C

Mandell et al., 2007 Wunderink & Waterer, 2014

VAP EVIDENCE

In the absence of medical contraindications, elevate the head of the bed at an angle of 30 to 45 degrees for a patient at high risk for aspiration (e.g., a person receiving mechanically assisted ventilation and/or who has an enteral tube in place).

A C

Institute for Clinical Systems Improvement (ICSI), 2011 Kalanuria, Zai, & Mirski, 2014

Cuff pressure should be maintained at 20 to 25 cm H 2 O. Minimal leak technique is discouraged.

B American Thoracic Society (ATS) Documents, 2004 ICSI, 2011

Effective infection control measures: staff education, compliance with alcohol-based hand disinfection, and isolation to reduce cross-infection with multidrug- resistant pathogens should be used routinely.

A C

ATS Documents, 2004 File, 2016c

Continued

196 Chapter 8 ■ Chest Disorders

Signal Symptoms: Acute onset dyspnea, tachypnea, tachy- cardia, pleuritic type chest pain, anxiety, symptoms of deep vein thrombosis (DVT).  Diffi cult to diagnose due to variabil- ity in presentation ( Belohlavek, Dytrych, & Linhart, 2013 ). Symptoms are nonspecifi c; some pulmonary emboli are asymptomatic. Clinical symptoms alone should not be used to confi rm or exclude PE ( Ho & Smouse, 2015 ).

Description: PE is the occlusion of the pulmonary artery or one of its branches by a traveling thrombus originating from elsewhere in the body (Thompson, 2016). A blood clot is the most common embolism, although fat, air, bone marrow, tumor cells, and foreign material also can occlude the pul- monary vasculature ( Konstantinides et al., 2014 ). PE is one component of venous thromboembolism (VTE), which also encompasses DVT.

Etiology: PE usually is caused by a dislodged thrombus from one of the veins of the legs or pelvis (DVT). Most emboli are believed to arise from areas of decreased blood fl ow in the lower extremity proximal veins (iliac, femoral, popliteal). More than 50% of patients with proximal vein DVT also present with PE (Thompson, 2016).

Occurrence: Estimated incidence of 60 to 70 per 100,000 in general population; PE can develop in as many as 40% to 50% of patients with DVT ( Belohlavek et al., 2013 ).  Seventy percent of patients presenting with PE are also found to have DVT in the legs (Wilbur & Shian, 2012). PE is the third leading cause of vascular death after MI and stroke (Gold- haber & Bounameaux, 2012). The estimated mortality rate in patients with PE is 12% (Wilbur & Shian, 2012).

Age: The incidence of PE increases steadily with age; however, in older age the incidence of PE is higher in men than in women ( Lavorini et al., 2013 ).

Gender: Overall prevalence of PE is similar in males and females, but there is a higher recurrence rate in men (Rob- ert-Ebadi et al., 2010).  Women of reproductive age have slightly increased incidence of PE because of the association of PE with pregnancy and increased risk with oral contracep- tive use ( Lavorini et al., 2013 ).

Ethnicity: Incidence varies by race; highest incidence is in those of African American descent, with Europeans in North

America and Europe almost as prevalent. There is lower inci- dence in Hispanic, Asian, and Native American populations (Zakai & McClure, 2011).

Contributing Factors: Risk factors for PE are indicated by Virchow ’ s triad of stasis or prolonged immobility, hyper- coagulation, and venous trauma (endothelial injury with infl ammation of the vessel lining). Stasis may be occupational or medical (e.g., CHF, postsurgical paralysis, chronic illness or debilitation, tumor compression). Venous trauma damaging the deep veins of the legs; prolonged immobility for less than 48 hours; orthopedic procedures from arthroscopy to hip, knees, or pelvic repair; or trauma from falls, burns, or crush injuries may contribute to thrombus formation and lead to PE ( Ho & Smouse, 2015 ). Medical disorders that increase PE risk include heart failure, ischemic stroke, acute respiratory failure or intubation, sepsis, acute rheumatic disease, and infl ammatory bowel disease ( Lavorini et al., 2013 ). Presence of a central venous catheter and insertion of a pacemaker, use of estrogen, advanced age, obesity, and malignancy are also risk factors. A past history of DVT or PE is associated with recurrence. Cardiovascular risk factors for PE include hypertension, diabetes, cigarette smoking, and increased cholesterol ( Ozaki & Bartholomew, 2012 ). A rare but strong risk factor for PE includes defi ciencies of natural coagulation inhibitors like antithrombin, Protein C and S. These usually account for about 1% of PE cases ( Lavorini et al., 2013 ). A small proportion of cases have been associated with Factor V Leiden and prothrombin (Factor II) G20210A.  Pregnancy can lead to a fi ve-fold increased risk of PE. Hormone replace- ment therapy (HRT) is believed to increase PE risk by two- to four-fold ( Lavorini et al., 2013 ). Although patient risk factor identifi cation is crucial in the initial diagnostic work-up, up to 30% of PE cases develop idiopathically ( Belohlavek et al., 2013 ).

Signs and Symptoms: Signs and symptoms of PE tend to be nonspecifi c.  Less than 20% of patients present with classic symptoms of chest pain, dyspnea, or hemoptysis. The Pro- spective Investigation of Pulmonary Embolism Diagnosis (PIOPED II) study showed that 97% of patients had more than one of the symptoms of dyspnea, pleuritic chest pain, and tachypnea. The variation in presentation may occur when these symptoms are attributed to aging or existing

VAP EVIDENCE

Intensive insulin therapy is recommended to maintain serum glucose levels between 80 and 110 mg/dL in ICU patients to reduce nosocomial bloodstream infections, duration of mechanical ventilation, ICU stay, morbidity, and mortality.

A ATS Documents, 2004

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

PULMONARY EMBOLISM

Chapter 8 ■ Chest Disorders 197

comorbidities ( Ho & Smouse, 2015 ). Dyspnea can range from acute to severe. Severe dyspnea, as seen with central PE, is usually described as having typical angina-type char- acter.  Dyspnea seen with a small peripheral PE is usually mild and transient, making PE diffi cult to diagnose ( Konstan- tinides et al., 2014 ). Other fi ndings may include anxiety or apprehension, cough, tachypnea, and accentuation of the pulmonic component of S 2 and may be accompanied by dia- phoresis, syncope, tachycardia, S 3 or S 4 gallop, hypoxemia, or hemoptysis ( Ozaki & Bartholomew, 2012 ). Auscultation of the lungs may be normal or may show localized wheez- ing, consolidation, or friction rub. Jugular venous distention and atrial arrhythmia may be present. Examination of the legs, especially of the iliofemoral and popliteal areas, may reveal signs of DVT. The arms, abdomen, and pelvic areas also should be examined for pain, erythema, or palpable vein cords. In the case of a massive PE, hypotension, circulatory instability, and cyanosis may be present.

Diagnostic Tests: Clinical judgment in conjunction with clinical prediction scoring tools and diagnostic studies is recommended. The Wells Clinical Prediction Scoring Tool for Pulmonary Embolism (www.mdcalc.com/wells-criteria- for-pulmonary-embolism-pe) considers clinical symptoms, tachycardia, recent immobility or surgery, hemoptysis, malignancy, and prior DVT/PE to help assign a pretest prob- ability of PE (low, intermediate, or high) (Wilbur & Shian, 2012). The Revised Geneva Score is sometimes used to strat- ify patients by probability of PE. The Simplifi ed Pulmonary Embolism Severity Index (PESI) (www.mdcalc.com/simplifi ed- pesi-pulmonary-embolism-severity-index) is a prediction rule for 30-day mortality from symptomatic PE; this tool is used more selectively as appropriate. No matter what scoring method is used, it is helpful to determine pretest probability in order to categorize patients into subgroups to determine like- lihood of presence of PE. Future research is needed to develop standardized models of predictability ( Lavorini et al., 2013 ).

The chest x-ray is often abnormal, but usually nonspecifi c. It is used primarily to rule out other causes of symptoms such as pneumonia or CHF. EKG changes that show signs of right ventricular strain, T-wave inversion in leads V1 to V4, QR pattern in V1, new-onset right bundle branch block, or S1Q3T3 complex can sometimes be seen in severe cases of PE. Mild PE cases may only reveal sinus tachycardia or atrial arrhythmias such as AF ( Konstantinides et al., 2014 ). In a patient deemed to be at low or intermediate risk of PE, a negative enzyme-linked immunosorbent assay (ELISA) D-dimer test can rule out the possibility of PE. The ELISA or ELISA-derived D-dimer assays have a sensitivity of 95% and can exclude PE in patients with a low to intermediate pretest probability ( Konstantinides et al., 2014 ). The sensitivity of D-dimer testing also increases with the extent of PE; highest concentrations are seen in patients with perfusion scan defects involving 50% of the pulmonary circulation ( Lavorini et al., 2013 ).   The specifi city of D-dimer tests decreases with increased age, to only 10% in patients older than 80 years. D-dimer can also be elevated in the patient with cancer, during hospitalization, and in pregnant patients.  Some studies suggest age-adjusted cut-offs to improve D-dimer testing in the elderly ( Konstantinides et al., 2014 ). Patients with intermediate to high pretest probability would require further testing to rule out PE ( Ozaki & Bartholomew, 2012 ).

Pulmonary catheter angiography has long been consid- ered the gold standard to diagnose PE, but the Multidetector CTA (MDCTA) is often used as the test of choice because it is noninvasive and has a lower rate of complications com- pared to pulmonary catheter angiography ( Ho & Smouse, 2015 ). The advancements in the quality of MDCTA has led to increased usage ( Belohlavek et al., 2013 ). MDCTA is widely available, and when used with IV contrast, the MDCTA can outline thrombi in the pulmonary arteries. MDCTA has almost replaced lung scanning and angiography as the stan- dard for PE diagnosis ( Lavorini et al., 2013 ). Limitations for using a MDCTA include patients with renal dysfunction, allergy to contrast media, possible pregnancy, critical illness, requiring ventilator support, or recent MI. In this case, a ven- tilation/perfusion (V/Q) scan may be done. If there is a high suspicion of PE but a negative MDCTA, a V/Q scan may be ordered also. However, most clinicians feel more comfortable with MDCTA as a diagnostic tool due to its ability to provide anatomical demonstration of presence of a clot versus relying on the V/Q scans to assess the probability of embolism based on V/Q mismatch ( Lavorini et al., 2013 ). V/Q scanning is done in the nuclear medicine department and may not be as readily available as MDCTA in many cases ( Belohlavek et al., 2013 ).

Echocardiography is not recommended to diagnose PE, but can help determine risk of mortality or adverse outcome. An echocardiogram can evaluate right ventricular function and detect a free-fl oating thrombus in the right heart, which can be associated with PE and increased mortality ( Ho & Smouse, 2015 ).  In patients with a massive PE, transesophageal echo- cardiography (TEE) should be done to assess right ventricular function.

The myocardial markers, including cardiac troponin levels and BNP or NT-proBNP have no role in the diagnosis of PE. These markers indicate a biochemical response to PE. They have been shown to forecast right ventricular dysfunction and mortality. Elevated troponin levels have been shown to refl ect severity of PE and have been associated with increased mortality ( Belohlavek et al., 2013 ).

Differential Diagnosis:

■ Pneumonia ■ MI ■ Pericarditis ■ CHF ■ Pleural effusion ■ Panic attacks ■ Hyperventilation syndrome ■ Pneumothorax ■ Esophageal rupture ■ Gastritis ■ Gastric or duodenal ulcer ■ GERD ■ Asthma ■ Musculoskeletal pain ■ Mediastinitis

Treatment: Anticoagulation is the cornerstone of treatment. Goal of anticoagulation is to prevent early death, recur- rence, or fatal VTE/PE. If no contraindications, anticoagu- lation should be initiated immediately in patients with high or moderate suspicion of PE while awaiting diagnostic test

198 Chapter 8 ■ Chest Disorders

results ( Lavorini et al., 2013 ). Acute phase therapy includes unfractionated heparin (UFH), low-molecular weight heparin (LMWH), or fondaparinux. Parenteral heparin should overlap with initiation of vitamin K antagonist (VKA) ( Konstan- tinides et al., 2014 ).

In patients with a massive PE, acute RV failure and low systemic output is the leading cause of death. Treatment should be individualized and supportive, and may include the use of vasopressors. Oxygen administration and/or mechan- ical ventilation may be needed to reverse hypoxia ( Konstan- tinides et al., 2014 ). Pharmacological treatments, including thrombolytic drugs or surgical or interventional reperfusion treatments such as surgical or catheter embolectomy proce- dures may also be considered in hemodynamically unstable patients ( Lavorini et al., 2013 ).

In patients at low risk for bleeding, LMWH, subcutaneous (SQ) fondaparinux, IV or SQ unfractionated heparin (UFH) can be used. LMWH or fondaparinux is preferred due to lower risk of inducing major bleeding or heparin-induced throm- bocytopenia (HIT) ( Konstantinides et al., 2014 ). In patients with severe renal impairment (creatinine clearance less than 30 mL/min), UFH is preferred because of ease in monitor- ing via activated partial thromboplastin time (aPPT) testing ( Lavorini et al., 2013 ). UFH is recommended in patients in whom thrombolysis is being contemplated, morbidly obese patients (questionable subcutaneous absorption), or those at high risk of bleeding because of the short half-life of UFH and the ability to rapidly reverse UFH with protamine ( Konstantinides et al., 2014 ).  Oral anticoagulation should be initiated simultaneously with or shortly after parenteral anticoagulation. Warfarin (Coumadin) has been the gold standard VKA for over 50 years and is monitored by measur- ing the international normalized ratio (INR). UFH, LMWH, or fondaparinux should be continued for at least 5 days and until INR is within the 2 to 3 range for 2 consecutive days to ensure adequate anticoagulation ( Konstantinides et al., 2014 ). Warfarin can be used for long-term maintenance of 6 months or more. INR monitoring should begin with baseline measurement, then again 2 to 3 days after initiation.  Mon- itoring then tapers to twice weekly until the INR is within the therapeutic range, then once weekly or every other week, and fi nally, monthly. ACCP guidelines allow clinicians to con- sider INR monitoring up to every 12 weeks in patients who are stable. Dosage is adjusted based on INR results (Wigle et al., 2013).

Dabigitran, rivaroxaban, apixaban, and edoxaban are the new oral anticoagulants (NOACs).  They are not vitamin K dependent and are approved for treatment of PE. NOACs overcome some limitations of standard therapy, such as the need for regular monitoring and dose adjustments ( Lavorini et al., 2013 ). Studies have shown NOACs have similar effi - cacy and safety profi les compared to traditional therapies in terms of initial and long-term treatment of PE ( Ho & Smouse, 2015 ). CHEST 2016 guidelines recommend the use of NOACs over VKA therapy in patients with PE and no cancer (Kearon et al., 2016). VKA therapy is suggested over LMWH in patients with PE and no cancer who are not treated with NOACs. The decision to use NOACs can be infl uenced by whether cost is covered by insurance plans and patient and physician satisfaction with current therapy ( Lavorini et al., 2013 ). Currently, NOAC therapy can be very expensive (Gool- am-Mahomed, 2013).

LMWH may be used long term in patients with cancer associated with PE due to greater compatibility with chemo- therapy ( Lavorini et al., 2013 ). LMWH is used for PE treat- ment during pregnancy because VKAs are teratogenic.

Routine use of venous fi lters to prevent PE recurrence is not recommended. Filters may be indicated in cases if anti- coagulation is contraindicated or if PE has recurred despite adequate anticoagulation. It is recommended that the fi lter be removed as soon as possible to avoid secondary vena cava thrombosis or thromboembolism ( Lavorini et al., 2013 ).

Follow-Up: Follow-up visits are on an individualized basis. Anticoagulation usually is continued for a minimum of 3 to 6 months after PE. Experts differ on optimal length of therapy and dosing adjustments in specifi c situations. CHEST 2016 guidelines recommend at least 3 months of anticoag- ulant therapy for provoked or unprovoked PE. The risk-ben- efi t ratio should be evaluated after 3 months of therapy for the unprovoked PE. For the unprovoked fi rst-time VTE with low to moderate bleeding risk, CHEST guidelines recommend extended anticoagulant therapy (no scheduled stop date). If bleeding risk is high, 3 months of anticoagulant therapy is recommended.  In any case of extended anticoagulant therapy, risk–benefi t for continued treatment should be reas- sessed at periodic intervals (i.e., annually). Extended therapy is recommended for the patient with active cancer and PE regardless of bleeding risk, keeping in mind the need to reas- sess risk–benefi t periodically (Kearon et al., 2016).

Sequelae: Unrecognized PE can be fatal and is associated with overall mortality of up to 30% (Thompson, 2016); many are diagnosed at autopsy. Most deaths occur within the fi rst week of diagnosis and are usually due to recurrent VTE and shock (Thompson, 2016). After acute PE, symptoms may resolve or can lead to chronic thromboembolic pulmonary hyperten- sion, which can progress to right heart failure if untreated (Goolam-Mahomed, 2013). Other complications include alveolar collapse, atelectasis, and pulmonary infarction. Complications from anticoagulation include uncontrolled bleeding and hematoma.

Prevention/Prophylaxis: PE is one of the most common pre- ventable causes of hospital deaths in the United States, but only one-third of hospitalized patients receive adequate pro- phylaxis ( Ozaki & Bartholomew, 2012 ). Patients should avoid controllable risk factors for PE such as sedentary lifestyle, obesity, and smoking. Encourage frequent ambulation, use of antiembolic stockings or graded compression hose, safety precautions to avoid injury to lower extremities, evaluation of possible hypercoagulation pathology, and prophylactic anticoagulation after orthopedic surgery of hip or knee. Pro- longed sitting should be avoided. Consideration of prophylac- tic anticoagulation in any immobilized hospitalized patient and use of sequential compression devices (SCDs) may be helpful.  In select patients with very increased DVT/PE risk and bleeding, a temporary IVC fi lter is an option (Tapson, 2015).

Referral: Refer patients to internal medicine or emergency medicine for emergent evaluation and initial treatment plan. When stable, patients can be managed on warfarin or NOAC therapy.  Health-care professionals skilled in initiation and assessment of warfarin therapy and adjustments can greatly infl uence outcomes (Wigle et al., 2013). Although no regular

Chapter 8 ■ Chest Disorders 199

monitoring of NOAC therapy is required for dosing, compli- ance is of utmost importance in order to achieve adequate therapeutic anticoagulant benefi ts (ten Cate, 2013).

Education: Provider education about awareness of PE in differential for chest pain or dyspnea is needed. Teach the patient, family, or caregiver about risk factors and preven- tive measures, disease pathology, monitoring for signs of

recurrence, and need for compliance with anticoagulation therapy. Instruct the patient to use a soft toothbrush and an electric razor and to report bleeding gums, hemoptysis, and any blood in stool or urine. Advise patients to avoid aspirin, to consult with their health-care provider before taking any OTC medications, and to take precautions to avoid bumping or bruising.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Prevention of VTE should be considered according to the patient ’ s baseline risk.

A Ozaki & Bartholomew, 2012

Diagnosis begins with estimating probability based on a validated clinical decision rule, then using a validated diagnostic algorithm integrating fi ndings from D-dimer, ventilation/perfusion (V/Q) scan, lower extremity ultrasound, and spiral (helical) CT scanning with IV contrast (i.e., CT pulmonary angiography [CT-PA]).

A Belohlavek et al., 2013 Ho & Smouse, 2015 Konstantinides et al., 2014 Lavorini et al., 2013

In patients with acute PE, we recommend early initiation of vitamin K antagonist (VKA) (e.g., same day as parenteral therapy is started) over delayed initiation, and continuation of parenteral anticoagulation for a minimum of 5 days and until the INR is 2.0 or above for at least 24 hours.

Studies have shown NOACs have similar effi cacy and safety profi les compared to traditional therapies in terms of initial and long term treatment of PE in some patient populations.

B Ho & Smouse, 2015 Konstantinides et al., 2014 Lavorini et al., 2013

In patients with acute PE, we recommend initial treatment with parenteral anticoagulation (LMWH, fondaparinux, IV UFH, or subcutaneous UFH) over no such initial treatment.

A Konstantinides et al., 2014 Lavorini et al., 2013

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

PULMONARY TUBERCULOSIS

Signal Symptoms: Productive, prolonged cough; fatigue; low- grade fever; night sweats; poor appetite; weight loss.

Description: Pulmonary TB is a chronic necrotizing infection caused by a slow-growing acid-fast bacillus (AFB), Mycobac- terium tuberculosis . TB is the most important, fatal infection among humans. The primary site for most cases of TB is the lungs. Extrapulmonary TB can affect any organ or tissue.

Etiology: The infection spreads by inhalation of airborne par- ticles or droplets produced by persons with active pulmonary or laryngeal TB during coughing, sneezing, singing, and other expiratory efforts. The development of infection after exposure depends on the exposed person ’ s ability to mount

an effective immune response on the cellular level. In the initial 2 to 4 weeks before cellular immunity response occurs, direct pulmonary infection may develop, or lymphohema- togenous circulation may lead to miliary, meningeal, or TB adenitis. When T cells recognize the specifi c antigen, they become sensitized, engaging the macrophages in destroy- ing or containing the tubercle bacilli. This leads to healing, with no residual or calcifi ed lymph nodes in the pulmonary or tracheobronchial areas. This latent stage is typical of 90% to 95% of infected persons, leaving them at lifelong risk for reactivation. Tuberculin skin testing documents exposure at 2 to 10 weeks after exposure.

Occurrence: TB is one of the world ’ s deadliest diseases.

200 Chapter 8 ■ Chest Disorders

■ One-third of the world ’ s population is infected with TB. ■ In 2015, 10.4 million people around the world became

sick with TB. There were 1.8 million TB-related deaths worldwide.

■ TB is a leading killer of people who are HIV-infected.

A total of 9,557 TB cases (a rate of 3.0 cases per 100,000 persons) were reported in the United States in 2015. The overall number of TB cases in the United States increased over the previous year in 2015, after having declined yearly during 1993 through 2014. Despite a slight increase in case count, the TB incidence rate per 100,000 persons has remained relatively stable at approximately 3.0 since 2013.

Age: Children and adolescents are more likely to have primary disease; adults and older adults are more likely to have recru- descent disease. TB disease in children under 15 years of age (also called pediatric TB) is a public health problem of special signifi cance because it is a marker for recent transmission of TB. Also of special signifi cance, infants and young children are more likely than older children and adults to develop life-threatening forms of TB disease (e.g., disseminated TB, TB meningitis). Among children, the greatest numbers of TB cases are seen in children less than 5 years of age and in ado- lescents older than 10 years of age.

Gender: TB occurs in men more frequently than in women.

Ethnicity: ■ Native Americans or Alaska Natives: 6.1 TB cases per

100,000 persons ■ Asians: 18.2 TB cases per 100,000 persons ■ African Americans: 5.0 TB cases per 100,000 persons ■ Native Hawaiians and other Pacifi c Islanders: 18.2 TB

cases per 100,000 persons ■ Hispanics or Latinos: 4.8 TB cases per 100,000 persons ■ Caucasians: 0.6 TB cases per 100,000 persons

Risk Factors: Overall, about 5% to 10% of infected persons who do not receive treatment for latent TB infection will develop TB disease at some time in their lives. For persons whose immune systems are weak, especially those with HIV infection, the risk of developing TB disease is much higher than for persons with normal immune systems. Persons who are at increased risk include those with:

■ HIV infection ■ Substance abuse issues (especially IV drug use) ■ Recent infection with M. tuberculosis (less than 2 years

ago) ■ Chest x-ray fi ndings suspicious of previous TB with no

treatment or ineffective treatment ■ Diabetes mellitus ■ Silicosis ■ Prolonged corticosteroid therapy ■ Other immunosuppressive therapy ■ Cancer of the head and neck ■ Hematological and reticuloendothelial diseases ■ End-stage renal disease ■ Intestinal bypass or gastrectomy ■ Chronic malabsorption syndromes ■ Low body weight (less than 10% ideal body weight)

Other factors associated with increased risk include home- lessness, residence in a congregate setting (e.g., nursing

home, boarding home, prison, mental health facility), low socioeconomic status, and health-care work in a high-risk area.

Signs and Symptoms: Typical presentation includes cough, hemoptysis, weight loss, anorexia, adenopathy, fever, night sweats, decreased activity level, and pleuritic pain ( Table 8-6 ). In the average population, the onset is gradual and may go undetected for some time. In the older patient, these fi ndings are not usually present, or they are so subtle and so intermingled with other chronic illness symptoms as to be undistinguishable. Weight loss, dyspnea, or anorexia may be the only symptoms. Typical simulations include pneumonia, bronchitis, or CHF with pleural effusion. Extrapulmonary TB may manifest with symptoms typical to the site involved (e.g., urinary incontinence or frequency and urgency for bladder TB).

Diagnostic Tests: Tuberculin Skin Test (TST): The TST is used to determine if a

person is infected with M. tuberculosis. If a person is infected, a delayed-type hypersensitivity reaction is detectable 2 to 8 weeks after infection. The skin test is administered intrader- mally using the Mantoux technique by injecting 0.1 ml of 5 TU purifi ed protein derivative (PPD) solution. The reading and interpretation of TST reactions should be conducted within 48 to 72 hours of administration. For more informa- tion about tuberculin skin testing, visit the CDC website for additional resources (see Resources) and refer to Appendix C.

Differentiating Between Latent TB Infection and TB Disease

LTBI TB DISEASE

No symptoms or physical

fi ndings suggestive of TB

disease.

Symptoms may include one or

more of the following: fever, cough,

chest pain, weight loss, night sweats,

hemoptysis, fatigue, and decreased

appetite.

TST or IGRA result usually

positive.

TST or IGRA result usually positive.

Chest radiograph is typically

normal.

Chest radiograph is usually

abnormal. However, may

be normal in persons with

advanced immunosuppression or

extrapulmonary disease.

If done, respiratory specimens

are smear and culture

negative.

Respiratory specimens are usually

smear or culture positive. However,

may be negative in persons with

extrapulmonary disease or minimal

or early pulmonary disease.

Cannot spread TB bacteria to

others.

May spread TB bacteria to others.

Should consider treatment for

LTBI to prevent TB disease.

Needs treatment for TB disease.

Note: Physical examination may be unrevealing: Nonspecifi c signs such as fever or weight loss may be the only fi ndings. In some persons, a positive tuberculin test reaction is the only manifestation. Chest examination may show post-tussive apical rales. If pleural effusion is present, percussion in the area may be dull. Source: https://www.cdc.gov/tb/topic/testing/default.htm

TABLE 8-6

Chapter 8 ■ Chest Disorders 201

Key Points: ■ Training is essential for health-care providers to gain

profi ciency in the administration and interpretation of the TST.

■ The TST should not be performed on a person who has written documentation of either a previous positive TST result or treatment for TB disease.

■ Patients or family members should never measure TST results; this should only be done by a trained health- care professional.

■ Interpretation of the TST result is the same for persons who have had BCG vaccination because a majority of BCG cross-reactivity wanes with time.

■ A TST that was not measured and recorded in millime- ters (mm) of induration must be repeated.

Interferon–Gamma Release Assays (IGRAs): IGRAs are used to determine if a person is infected with M. tuberculosis by mea- suring the immune response to TB proteins in whole blood. Specimens are mixed with peptides that simulate antigens derived from M. tuberculosis and controls. In a person infected with M. tuberculosis, the white blood cells recognize the simu- lated antigens and release interferon-gamma (IFN- γ ); results are based on the amount of IFN- γ released. As noted earlier, there are two U.S. Food and Drug Administration (FDA) approved IGRAs commercially available in the United States:

■ QuantiFERON ® -TB Gold-in-Tube test (QFT-GIT) ■ T-SPOT ® TB test

Key Points: ■ Advantages of IGRAs include:

■ Requires a single patient visit to conduct the test. ■ Does not cause booster phenomenon. ■ Laboratory test not affected by health-care worker

perception or bias. ■ Results can be available within 24 hours.

■ Unaffected by BCG and most environmental mycobacteria.

■ Limitations of IGRAs include: ■ Blood sample must be processed within 8 to 30 hours

after collection. ■ Limited data exist on use in groups such as chil-

dren younger than 5 years of age, persons recently exposed to TB, immunocompromised persons, and those who will be tested repeatedly (serial testing).

For more information, see Latent Tuberculosis Infection: A Guide for Primary Health Care Providers at https://www.cdc. gov/tb/publications/ltbi/.

Differential Diagnosis: Pneumonia, lymphoma, fungal infec- tions, CHF, pleural effusion, and lung cancer can mimic TB.

Treatment: Before treatment, obtain baseline values for liver function, bilirubin, CBC, BUN, creatinine, and serum uric acid. If ethambutol (EMB) is used, baseline visual acuity should be measured. The goal of treatment is safety and effi - cacy in the shortest time period. For newly diagnosed, active TB, initial treatment consists of combined therapy using four fi rst-line drugs: isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), and EMB, until culture results are complete. Follow-up cultures should be done, usually monthly, until negative, to determine response to treatment. If the culture is not neg- ative after 3 months, suspect drug resistance or noncompli- ance and reevaluate. After culture is negative, obtain one further culture at treatment completion. For drug-resistant TB, different culture guidelines apply. Several treatment options are available. The most commonly used options are presented in Table 8-7 (for further information, consult with the CDC).

Note: HIV-positive individuals require specifi c modifi ca- tions in therapy and CDC guidelines should be consulted. Multidrug-resistant TB also requires different regimens (see CDC guidelines).

Latent TB Infection Treatment Regimens

DRUGS DURATION INTERVAL COMMENTS

Isoniazid 9 months Daily Preferred treatment for:

• Persons living with HIV

• Children aged 2 to 11 years

• Pregnant women (with pyridoxine/vitamin B 6 supplements)

Twice weekly * Preferred treatment for:

• Pregnant women (with pyridoxine/vitamin B 6 supplements)

Isoniazid 6 months Daily

Twice weekly *

Isoniazid and

Rifapentine

3 months Once weekly * Treatment for:

• Persons 12 years or older

Not recommended for persons who are:

• Younger than 2 years old

• Living with HIV/AIDS taking antiretroviral treatment

• Presumed infected with INH or RIF-resistant M. tuberculosis

• Women who are pregnant or expect to become pregnant within the 12-week regimen

Rifampin 4 months Daily

* Use directly observed therapy (DOT). Note: Due to the reports of severe liver injury and deaths, CDC recommends that the combination of rifampin (RIF) and pyrazinamide (PZA) should generally not be offered for the treatment of latent TB infection.

TABLE 8-7

202 Chapter 8 ■ Chest Disorders

Daily for 2 months: INH 5 mg/kg (300 mg maximum) RIF 10 mg/kg (600 mg maximum) PZA 15 to 20 mg/kg (2 g maximum) EMB 15 to 25 mg/kg (1 g maximum)

Then daily for 4 months: INH and RIF (see preceding dosage schedule)

In lieu of daily therapy for 4 months, the same agents (INH, RIF) can be used as follows:

INH 15 mg/kg (900 mg maximum) two or three times weekly by directly observed therapy (DOT)

RIF 10 mg/kg (600 mg maximum) two or three times weekly by DOT

The basis for treatment is availability of two drugs to which the bacterium is susceptible. Prolonged treatment is needed. Compliance is key to successful control of disease.

Follow-Up: See Culture Guidelines. Follow-up chest x-ray examination may be done at therapy termination to evaluate response. Periodic liver enzymes are necessary, especially if the patient is taking INH, to monitor for effects on hepato- toxicity. For the frail, older adult in a long-term care facility, more frequent monitoring for adverse effects of treatment, including anorexia, polyneuropathy, or development of med- ication-induced hepatitis, is warranted. DOT is normally used in these settings, so compliance is less of a concern. Refer community-dwelling older adults to the local or state health department for follow-up, monitoring of medication com- pliance and side effects, patient and family education, and testing of close contacts. TB is a reportable disease.

Many agencies charged with monitoring and control have outreach services, such as home visits. Emphasize to patients that compliance is crucial to successful control. If no fol- low-up visitation is available through the monitoring agency, see the patient for monthly follow-up visits in the offi ce.

Sequelae: Possible complications include development of drug-resistant organisms, particularly if a patient is noncom- pliant with the prescribed treatment. Secondary infection of cavitary lesions and development of treatment-associated hepatitis or polyneuropathy are possible. If treatment is inef- fective, spread of disease to other close contacts can occur.

Prevention/Prophylaxis: For older patients residing in long- term care facilities, PPD testing before admission to the facility is required unless there is documented evidence of a positive test result in the past. Two-step testing is recom- mended initially. Annual retesting is recommended. Patients with a positive PPD reaction need a chest x-ray to evalu- ate for active or latent disease. Staff members are required to have tuberculin skin testing at initial employment and annually.

When targeted testing reveals a positive tuberculin skin reaction but no evidence of active TB, it is often referred to as latent tuberculosis infection. The person has been exposed to and infected with M. tuberculosis but does not have active disease and cannot infect others.

The decision to institute chemoprophylaxis is a clinical judgment, based on a comparison of individual factors with the risk of developing TB (see Contributing Factors) versus the risk of INH toxicity. Chemoprophylaxis is with INH, 300 mg orally daily for 6 months in an otherwise healthy person; 9 months is considered optimal if compliance is not an issue. Alternatively, INH, 15 mg/kg orally twice weekly by DOT, may be substituted. For HIV-positive persons or close contacts of patients with drug-resistant tuberculosis, see CDC recom- mendations. A shorter course of RIF and PZA previously recommended has been associated with fatal and severe liver injuries and so is no longer recommended.

Referral: Patients may be referred to a government-associated community agency, such as the health department, or to an infectious disease or pulmonary specialist for initial evalua- tion and management recommendations. Refer patients with concurrent positive HIV status or confi rmed AIDS to special- ized treatment services, or collaborate in management with specialists in this area. Refer patients with severe anorexia or malnutrition to a dietitian.

Education: Teach patient, caregivers, close contacts, and paraprofessional providers about the nature of the disease, its mode of transmission, screening and control measures, and follow-up required. Teach the patient or caregiver about medications, drug actions and possible side effects, length of treatment, and need for compliance.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

We recommend performing an interferon- γ release assay (IGRA) rather than a tuberculin skin test (TST) in individuals 5 years or older who meet the following criteria: 1) are likely to be infected with MTB, 2) have a low or intermediate risk of disease progression, 3) it has been decided that testing for LTBI is warranted, and 4) either have a history of BCG vaccination or are unlikely to return to have their TST read.

Remarks: A TST is an acceptable alternative, especially in situations where an IGRA is not available, too costly, or too burdensome.

A Lewinsohn et al., 2017 ISDA Guideline

We recommend that acid-fast bacilli (AFB) smear microscopy be performed, rather than no AFB smear microscopy, in all patients suspected of having pulmonary TB.

A Lewinsohn et al., ISDA Guideline

Chapter 8 ■ Chest Disorders 203

Signal Symptoms: Rapid, shallow respirations; dyspnea; decreased activity tolerance; easy fatigability; nonproductive, irritating cough provoked by deep breathing or exertion.

Description: Restrictive lung disease refers to a heterogeneous group of disorders that share a common abnormal ventila- tory function. Restricted breathing is characterized by small tidal volume and rapid rate. The hallmark restrictive pattern is a decrease in lung volumes, principally total lung capacity and vital capacity (Lutfi , 2017; Kanaparthi, 2012).

Etiology: Restrictive lung diseases, which have a variety of etiologies, are divided into subgroups based on the location of the pathology.

Restrictive/Parenchymal/Interstitial/Intrinsic: In addition to a decrease in total lung capacity and vital capacity, resid- ual volume is decreased. Forced expiratory fl ow rates are maintained.

■ Sarcoidosis ■ Idiopathic pulmonary fi brosis ■ Pneumoconiosis

■ Occupational lung disease ■ Drug/radiation-induced interstitial lung disease

Restrictive/Extraparenchymal/Extrinsic: Abnormalities can be predominantly in inspiration or in inspiration and expiration.

Neuromuscular: ■ Diaphragmatic weakness/paralysis ■ Myasthenia gravis (limitations may be inspiratory and

expiratory) ■ Muscular dystrophies (limitations may be inspiratory

and expiratory) ■ Cervical spine injuries (limitations may be inspiratory

and expiratory) ■ Guillain-Barré syndrome (limitations may be inspira-

tory and expiratory)

Chest Wall: ■ Kyphoscoliosis ■ Obesity ■ Ankylosing spondylitis (limitations may be inspiratory

and expiratory)

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

While both IGRA and TST testing provide evidence for infection with MTB, they cannot distinguish active from latent TB. Therefore, the diagnosis of active TB must be excluded prior to embarking on treatment for LTBI. This is typically done by determining whether symptoms suggestive of TB disease are present, performing a chest radiograph and, if radiographic signs of active TB (e.g., airspace opacities, pleural effusions, cavities, or changes on serial radiographs) are seen, then sampling is performed and the patient managed accordingly.

A Lewinsohn et al., 2017 ISDA Guideline

Guidelines recommend that persons at low risk for MTB infection and disease progression NOT be tested for MTB infection. We concur with this recommendation. However,we also recognize that such testing may be obliged by law or credentialing bodies. If diagnostic testing for LTBI is performed in individuals who are unlikely to be infected with MTB despite guidelines to the contrary: ■ We suggest performing an IGRA instead of a TST in individuals 5

years or older Remarks: A TST is an acceptable alternative in settings where an IGRA is unavailable, too costly, or too burdensome. ■ We suggest a second diagnostic test if the initial test is positive in

individuals 5 years or older. Remarks: The confi rmatory test may be either an IGRA or a TST. When such testing is performed, the person is considered infected only if both tests are positive.

C Lewinsohn et al., 2017 ) ISDA Guideline

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

RESTRICTIVE LUNG DISEASE

204 Chapter 8 ■ Chest Disorders

The mnemonics P leural, A lveolar, I ntrinsic, N euromuscular, T horacic (PAINT) and S pace, P leural, I nterstitial, C hest Wall, E xtrathoracic (SPICE) are helpful reminders of the possible causes of restrictive lung disease.

Occurrence: The incidence of restrictive lung disease is unde- terminable because several distinct entities are involved. Statistics are available for select causes of restrictive lung disease. Studies reference an overall prevalence of three to six cases per 100,000 persons for intrinsic lung diseases. Prevalence of idiopathic pulmonary fi brosis (IPF) is 27 to 29 cases per 100,000 persons; in adults over age 75 years, the prevalence increases to over 175 cases per 100,000 persons (Kanaparthi, 2012). Occupational lung diseases are common in farmers and in people who work with silica, asbestos, beryllium, organic solvents, or cotton. The prevalence of sar- coidosis in the United States is 10 to 40 cases per 100,000 persons.

Age: Occupationally induced disease and IPF are seen pre- dominantly in the older population; other restrictive lung dis- eases may occur at any age.

Gender: The incidence is higher in men than women for occupational types of restrictive lung disease.

Ethnicity: African Americans in the United States have a prevalence of sarcoidosis that is 10 to 17 times greater than Caucasians.

Contributing Factors: Risk factors vary with etiology, includ- ing exposure to occupational dust, abnormalities in skele- tal structure, genetics, and autoimmune disorders (King, 2012).

Signs and Symptoms: Patients have a gradual onset of dyspnea, initially occurring only with exertion and progressing to dyspnea at rest. The breathing pattern is rapid and shallow. A nonproductive cough may be present (Behr, 2012). A careful, detailed history is essential, including prior systemic diseases, occupational or environmental exposures, family history, social history, and history of drug use (Alhamed & Cosgrove, 2011). Amiodarone, nitrofurantoin, hydralazine, gold, chemotherapeutic agents, and procainamide can cause drug-induced disease (Kanaparthi, 2012). Prior radiation can result in fi brosis. Use of tobacco should also be ascer- tained; it is common for patients to have a mixed pattern of obstructive and restrictive disease. Physical fi ndings may reveal skeletal abnormalities, such as kyphoscoliosis, lim- iting lung expansion. The initial presentation of breath- ing problems often occurs after an acute respiratory viral infection.

Physical assessment of the lung initially may be unre- markable. In intrinsic disease, with progression of the disease, inspiratory crackles (“Velcro”) typically are heard at the bases. Cyanosis and clubbing of fi ngers and toes may occur in IPF. In the end-stages, signs of right-sided heart failure, including cor pulmonale, appear (Behr, 2012; Kanaparthi, 2012; King, 2012).

Diagnostic Tests: Because of the diverse nature of the condi- tions leading to restrictive lung disease, it is challenging to address diagnostic testing and results. Many results are spe- cifi c to the causative condition. Routine testing including CBC, chemistry profi le, and liver function tests is standard.

TEST RESULTS INDICATING DISORDER

PFT Normal FEV 1 /FVC ratio but decreased FVC

and FEV 1 ; decreased total lung capacity, residual

volume, and functional residual capacity. Residual

volume–to–total lung capacity ratio is normal

to low. Most have a gas exchange problem with

marked decrease in single breath diffusing lung

capacity for carbon monoxide. Diagnosis of

restriction and extent of restriction is based on

total lung capacity (Kanaparthi, 2012).

Chest x-ray Increased interstitial markings, especially in lower

fi elds. Hilar and mediastinal lymphadenopathy in

sarcoidosis, some lymphomas, and silicosis. Pleural

effusion and thickening with collagen-vascular

disease, lymphoma, and asbestosis. A scattered

reticulonodular pattern and ground glass opacities

are common (Behr, 2012).

High-resolution

CT scan

In idiopathic pulmonary fi brosis, patchy, peripheral

bibasilar reticular abnormalities in the subpleural

area; with advanced disease, subpleural fi brosis and

honeycomb pattern are present.

In the late stages, arterial blood gases help to identify the degree of hypoxemia and carbon dioxide retention. In select cases, bronchoscopy and biopsy may be indicated (Gulati, 2011).

Differential Diagnosis:

■ Infectious or neoplastic diseases ■ COPD ■ CHF ■ Wegener granulomatosis ■ Goodpasture syndrome ■ Bechet disease ■ Sjögren syndrome ■ Systemic sclerosis ■ Pneumoconiosis ■ Tuberous sclerosis ■ Eosinophilic pneumonia

Treatment: Therapy depends on the cause of disease; spe- cifi c diagnosis obtained from clinical evaluation, imaging, and lung biopsy; and the disease progression. Occupational exposures should be avoided. Therapy with corticosteroids, cytotoxic agents, and immunosuppressive agents has been the primary treatment for most interstitial diseases. Duration of treatment is still unknown, and objective data to support use of cytotoxics and immunosuppressants is lacking or low quality (Kanaparthi, 2012). Cytotoxic agents, including aza- thioprine (Imuran) and cyclophosphamide (Cytoxan), are given concurrently with prednisone or in place of it if the patient cannot tolerate high-dose prednisone therapy (Kana- parthi, 2012).

The ATS and other global organizations’ offi cial state- ment on the evidence-based treatment of IPF was issued in 2011 and updated in 2015 (Raghu et al., 2011; 2015), citing the weakness of the evidence for current treatments including corticosteroids, cytotoxics, immunosuppressants, and other miscellaneous drugs, and encouraging individual patient and specialist discussion before implementing any drug therapy. The ATS statement recommends against treat- ment of IPF with corticosteroids alone or in combination

Chapter 8 ■ Chest Disorders 205

with cytotoxics or immunosuppressants (Raghu et al., 2015). Nintedanib, a tyrosine kinase inhibitor, and pirfeni- done received conditional support for use in the 2015 Update (Raghu et al., 2015). Research indicates that IPF is related more to fi broblastic proliferation than infl ammation (Daccord & Maher, 2016; Cerri, Spagnolo, Luppi, & Richeldi, 2012). Lung transplantation is the only treatment to prolong sur- vival in IPF (Puglisi, 2016; King, Pardo, & Selman, 2011); post-transplant the patient will be on immunosuppression for life (Whelan, 2012). Studies using stem cells are ongoing. Prior studies with tumor necrosis factor inhibitors and other atypical drugs have proven unsuccessful (Puglisi, 2016; King et al., 2011). In the end stage of restrictive lung diseases, administer supplemental oxygen for supportive care; consider palliative care and hospice.

Follow-Up: Follow-up visits are scheduled as indicated by symptoms and comorbidities. Periodic chest x-rays or pulmo- nary function tests (PFTs) may help to chart diseases course and evaluate response to treatment.

Sequelae: Use of corticosteroids or immunosuppressives may result in increased risk of infection. Pulmonary hypertension and right-sided heart failure may occur. Restrictive lung dis- eases are chronic and there is no known cure.

Prevention/Prophylaxis: Give patients the pneumococcal pneumonia and infl uenza vaccines. Advise patients to avoid known exposures, tobacco use, and persons with acute, infectious upper respiratory illness.

Referral: Initially refer patients to a pulmonary specialist for bronchoscopy and possible biopsy; thereafter, collaborative management is appropriate. If immunosuppressives are used, refer the patient for initial recommendations and periodic reevaluation.

Education: Teach the patient and family about chronic disease management, regular self-care habits, and early intervention in acute illness. Discuss prognosis and preferred choices for end-stage disease.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Interstitial lung disease diagnosis can be made with a chest x-ray, pulmonary function tests (PFTs) consistent with restrictive lung disease, and typical fi ndings on high-resolution CT. Lung biopsy is necessary in atypical cases.

C ATS, 2002

No treatment has been shown to have consistent benefi t. C Reust, 2011

Corticosteroids, supplementary oxygen, and pulmonary rehabilitation may provide symptomatic relief.

C Reust, 2011

Standard treatment regimens have included corticosteroids plus azathioprine or cyclophosphamide. However, a recent Cochrane review concluded that there is little good-quality information on the effi cacy of noncorticosteroid agents for IPF.

C Davies, Richeldi, Walters, & Davies, 2007

At present, there is no evidence for an effect of corticosteroid treatment in patients with IPF. On the other hand, other fi brotic lung diseases, such as nonspecifi c interstitial pneumonia (NSIP), are reported to show a better response to corticosteroids. Making a clear distinction between IPF and other entities grouped under the umbrella term interstitial lung disease is, therefore, essential, because this may have therapeutic and prognostic implications.

C Richeldi, Spagnolo, Davies, et al., 2010

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

UPPER RESPIRATORY TRACT INFECTION

Signal Symptoms: Nasal congestion, rhinorrhea/mucopu- rulent discharge, sneezing, sore throat, cough, headache, malaise, low-grade fever.

Description: Upper respiratory tract infection (URI), most frequently the common cold, is a self-limited infection of the upper respiratory track, usually caused by a virus which

206 Chapter 8 ■ Chest Disorders

results in infl ammation of the nasal passages. Most URIs are self-limiting and accompanied only by minor somatic com- plaints. In addition to the common cold, acute laryngitis, acute rhinosinusitis, and acute pharyngitis are included as URIs.

Etiology: The majority of URIs are caused by a virus, most commonly rhinovirus, infl uenza, cornonavirus, and respi- ratory syncytial virus. However, there are over 200 viruses associated with the common cold and 100 subtypes of the rhinovirus alone. New viruses, including the metapneumovi- rus and bocaviruses, have recently been identifi ed. There are three modes of transmission: hand to hand (most common), small particle droplet, and large particle droplet. The incuba- tion period is 1 to 3 days, but could last as long as 2 weeks.

Occurrence: URIs are the third most common reason for offi ce visits in the United States, with approximately 500 million noninfl uenza viral respiratory infections annually ( Sexton & McClain, 2016 ).

Age: Occur much more frequently in children than in adults and decrease with age.

Gender: Occur equally in men and women.

Ethnicity: Not signifi cant.

Contributing Factors: Risk factors for developing URIs include exposure to infected individuals, psychological stress, lack of sleep, smoking, and contact between nose or conjunctiva and contaminated fi ngers. Older persons with diabetes contract more frequent URIs than the general population.

Signs and Symptoms: The most common signs and symp- toms include nasal obstruction and stuffi ness, sneezing, and scratchy throat. Other signs and symptoms include cough, hoarseness, malaise, headache, and fever higher than 100°F (less than1%). Physical examination may reveal mucopu- rulent nasal drainage, nasopharyngeal mucosal swelling, and lymphadenopathy (Sexton & McLain, 2016). Symptoms lasting more then 7 to 10 days, reports of facial pain with purulent nasal discharge, sudden onset of symptoms, or high fever may be indicative of a bacterial infection ( Aring & Chan, 2016 ).

Diagnostic Tests: No diagnostic tests are indicated for the nonspecifi c URIs. Diagnosis is clinical based on symptoms. If symptoms persist for more than 7 to 10 days or are indicative of a bacterial infection, an erythrocyte sedimentation rate and CRP may aid in the diagnosis ( Aring & Chan, 2016 ). A rapid strep or culture should be obtained if strep pharyngitis is suspected.

Differential Diagnosis:

■ Infl uenza ■ Allergic rhinitis ■ Chronic or bacterial sinusitis ■ Foreign body ■ Streptococcosis ■ Catarrhal phase of pertussis (Turner, 2015)

Treatment: URIs usually are managed on an outpatient basis. Patients with signifi cant COPD or cardiac disease should be evaluated on an individual basis. URIs are treated with rest, increased fl uid intake, and symptom relief measures, such as humidifi ed air (not recommended for asthma patients).

OTC medications may be taken for pain, fever, congestion, or cough relief. A recent Cochrane review found some benefi t to various OTC combination agents, including analgesics, anti- histamines, and decongestants, in terms of limiting duration and symptoms when compared to no treatment (DeSutter, van Driel, Kumar, Lesslar, & Skrt, 2012). Antihistamine-de- congestant combinations were most effective, although more side effects occurred in those who used combination therapy. Controversy still remains about the use of antihistamines for viral illness unless an allergic component has been identifi ed (DeSutter, Saraswat, & van Driel, 2015).

Topical nasal steroids may be used; however, in a recent Cochrane review (Hayward et al., 2015) studies demon- strated no benefi t from using them. Topical and oral decon- gestants are available but topical preparations are preferred, owing to fewer systemic side effects, and should be discon- tinued after 3 days. Nasal and oral decongestants are asso- ciated with elevated BP and should be used cautiously in older adults. A Cochrane review on the use of nasal saline irrigation for acute URIs found limited benefi t for symptom alleviation (King, Mitchell, Williams, & Spurling, 2015). Like- wise, a Cochrane review of echinacea products for preven- tion or treatment (limiting duration of symptoms) of URIs was confounded by the variability of echinacea products on the market. There was some evidence that Echinacea purpurea administration limited duration of symptoms (Karsch-Völk et al., 2014).

Antibiotics are not indicated for viral URIs (Chow et al., 2012; Institute for Clinical Systems Improvement [ICSI], 2011; Khandelwal, Lathren, & Sloane, 2012; Sexton & McLain, 2016; Spellberg et al., 2011). Guidelines are in agreement that consideration of bacterial illness should be deferred until the patient has had symptoms for 1 week or more that are worsening despite self-care measures. If a reevaluation at that time determines that a bacterial infec- tion is likely, treatment with amoxicillin or amoxicillin clavu- lanate is instituted. The overprescribing of antibiotics for viral infections is of global concern and should be avoided in URIs. Watchful waiting is often advised before starting antibiotic therapy ( Aring & Chan, 2016 ; Essak & Pignatari, 2013).

Follow-Up: The patient should return if symptoms last more than 7 to 10 days or if he or she develops a high fever asso- ciated with systemic symptoms, diffi culty breathing, or facial pain with purulent nasal drainage ( Aring & Chan, 2016 ).

Sequelae: Possible complications include lower respiratory tract infection, sinusitis, and aggravation of asthma symp- toms. In older individuals with comorbidities, URI may con- tribute to the exacerbation of other symptoms (e.g., COPD, hyperglycemia, CHF) or may lead to pneumonia.

Prevention/Prophylaxis: Advise the patient to perform fre- quent proper hand washing, avoid touching the face, and avoid contact with infected people. Pneumococcal and infl u- enza vaccinations are recommended for all older adults.

Referral: Usually neither referral nor consultation is neces- sary if the patient has an uncomplicated URI.

Education: Provider Education: Diagnosis of nonspecifi c URI or acute

rhinopharyngitis denotes an infection that is typically viral

Chapter 8 ■ Chest Disorders 207

and in which sinus, pharyngeal, and lower airway symptoms may be present but not prominent ( Sexton & McClain, 2016 ; University of Michigan Health System, 2011).

Antibiotic treatment of adults with nonspecifi c URI does not improve illness resolution and is not recommended. There are no studies specifi cally testing the impact of anti- biotic treatment on complications of acute URIs in adults. Life-threatening complications of URIs are rare.

Purulent nasal or pharyngeal secretions (commonly seen in patients with uncomplicated URIs) do not predict bacterial

infection and do not benefi t from antibiotic treatment ( Aring & Chan, 2016 ).

Patient Education: Explain the disease process, signs and symptoms, and treatment (including side effects of medica- tions). Discuss prevention strategies, including hand washing and when to contact a health-care provider. Educate patients and families about the dangers of antibiotic resistance owing to inappropriate prescribing ( Sexton & McClain, 2016 ; Uni- versity of Michigan Health System, 2011).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

The diagnosis of upper respiratory tract infection is based on clinical signs and symptoms. This is an acute infection that is typically viral in origin and in which sinus, pharyngeal, and lower airway symptoms are present but not prominent.

B C

Wong, 2009 Sexton & McClain, 2016

Purulent nasal discharge or sputum does not predict bacterial infection or benefi t from antibiotics.

A C

Wong, 2009 Aring & Chan, 2016

Antibiotics are ineffective for the treatment of the common cold in children and adults.

B C C

Wong, 2009 Sexton & McClain, 2016 Aring & Chan, 2016

Antihistamine and decongestant combinations may help alleviate nasal symptoms in older children and adults. Newer-generation nonsedating antihistamines are ineffective.

B C

Wong, 2009 Sexton & McClain, 2016

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

VALVULAR HEART DISEASE

Signal Symptoms: Asymptomatic in early stage; fatigue and dyspnea are common later.

Description: Valvular heart disease (VHD) is damage to a valve or valves of the heart, causing cardiac dysfunction. The most prevalent types of VHD in elderly persons are the result of calcifi c and degenerative valve disease. The most prevalent VHD disorders in the elderly are aortic stenosis and mitral regurgitation. VHD may be defi ned in terms of stages of disease progression from A to D. Patients with stage A VHD are defi ned as at risk for development of the disease; stage B VHD is defi ned as progressive mild to moderate disease but asymptomatic; stage C is defi ned as severe asymptomatic and may be further stratifi ed into C1 and C2, with C1 representing compensation by the ventricle and C2 representing decom- pensation; and stage D is defi ned as severely symptomatic. As defi ned in the stages, patients may be asymptomatic in early stages, but fatigue and exertional dyspnea are common (Nishimura et al., 2014).

Aortic Stenosis In aortic stenosis (AS), there is obstruction of the left ventric- ular outfl ow tract, which may be supra- or sub-valvular. AS is graded as mild, moderate, severe, or critical as defi ned by aortic gradient and area. Mild AS is defi ned as aortic valve area of 1.5 cm 2 and mean pressure gradient of less than 20 mm Hg; moderate AS is defi ned as aortic valve area of 1.0 to 1.5 cm 2 and mean pressure gradient of 20 to 40 mm Hg; severe AS is defi ned as aortic valve area less than 1 cm 2 and mean pressure gradient greater than 40 mm Hg; and critical AS is defi ned as aortic valve area less than 0.5 cm 2 /m 2 BSI and mean pressure gradient of greater than 80 mm Hg. The hemodynamic hallmark of AS is pressure overload, left ven- tricular hypertrophy with a resultant gradient.

Etiology: AS diagnosed before age 60 years is usually caused by a congenital bicuspid valve, whereas AS after age 60 years is usually caused by calcifi c degeneration of the valve. Occa- sionally, a patient after 60 years of age may present with a

208 Chapter 8 ■ Chest Disorders

calcifi c bicuspid or unicuspid aortic valve. Other less common causes of AS include rheumatic fever, endocarditis, systemic lupus erythematous, and Fabry ’ s disease.

Occurrence: In the absence of a congenitally malformed valve, occurrence increases with age due to focal thickening or calcifi cation of the valve. At the time of surgical interven- tion, 40% of patients older than 70 years will be noted to have a bicuspid valve, while it will be much higher in the age group younger than 70 years (Roberts & Ko, 2005).

Age: Congenital valvular heart disease is present at birth; acquired valvular heart disease is found in older age.

Gender: More prevalent in males.

Ethnicity: Not signifi cant.

Contributing Factors: Factors associated with degenerative aortic valve stenosis include age, male gender, current cig- arette smoker, high serum concentrations of lipoprotein (a), and history of hypertension (Mohty & Pislaru, 2016).

Signs and Symptoms: Many of these patients are asymp- tomatic. Prognosis is poor for patients who exhibit symp- toms. The triad of symptoms that may be associated are syncope, angina, and dyspnea (Otto, 2016). The survival rate decreases to 2 to 3 years for the patients who exhibit symptoms (Yeo & Low, 2007) and do not have appropriate intervention. Angina is an early and more common symptom and can occur in the presence or absence of CAD. Presyn- cope followed by effort syncope occurs in about one-third of the patients with symptoms and is related to a fi xed cardiac output due to the obstruction of the left ventricle created by AS. Exertional dyspnea indicates left ventricular dysfunction and heart failure.

Physical Examination Findings: The classic crescendo-decre- scendo systolic murmur is heard at the second right inter- costal space and radiates to the carotids. The murmur in the elderly may radiate to the apex (Soriano, Fernandez, Cassel, & Leipzig, 2007). This murmur, which peaks in intensity in mid to late systole, may also be associated with a thrill if greater than grade IV. The murmur intensity does not correlate with the severity of AS; often in the setting of heart failure the AS murmur may become softer as the cardiac output falls. S 1 is often soft, and the aortic component of S 2 is soft or absent. The S 2 may also be paradoxically split due to the late closure of the aortic valve. An S 4 is common, representing forceful atrial contraction in the setting of left ventricular hypertro- phy. Other fi ndings may include delayed carotid upstroke, a carotid and apical pulse lag time, systemic hypertension, prominent “A” waves in the jugular venous pulse, and a sustained and forceful apical impulse (O’Gara & Loscalzo, 2015).

Diagnostic Tests: In AS, the EKG is abnormal in most cases, demonstrating QRS or T-wave changes refl ecting left ven- tricular hypertrophy. Chest x-ray examination is not rec- ommended in routine screening of asymptomatic patients, but may provide information on valve calcifi cation, cardiac chamber sizes, and pulmonary vasculature. Chest fi lms may show cardiac enlargement when heart failure is advanced.

Echocardiography is the standard test for assessing aortic valve stenosis and may demonstrate thickening and calci- fi cation of the aortic valve with decreased mobility of the

leafl ets. Doppler measurement of intracardiac blood velocity can help determine hemodynamic severity. The echocardio- gram is useful for providing detail on the valve morphology. Useful questions that can be answered include, but are not limited to: Is there congenital absence of valve cusp, degree of valve calcifi cation, valve cusp mobility, aortic valve area, aortic valve pressure gradient, size of aortic root, left ventric- ular size, ejection fraction, posterior and septal left ventricu- lar wall thickness, and concomitant valvular dysfunction and estimation of pulmonary artery pressures?

The frequency of echocardiogram assessment of AS is dependent on the degree of severity and symptoms. Exer- cise testing has limited utility in the evaluation of patients with AS. Pharmacological echocardiogram may be done in patients with low gradient AS and can help to risk stratify patients in this category. Cardiac catheterization measure- ment of the systolic pressure gradient across the aortic valve is the defi nitive method for assessing AS in patients being con- sidered for surgery or when there is a discordance between the clinical fi ndings and the diagnostic tests. In patients with congenital AS there may also be abnormalities noted in the coronary arteries, which can be evaluated with the left heart catherization. Right heart catherization will provide informa- tion on hemodynamics. Cardiac MRI may be used to stratify patients with AS and assess the effect of chronic left venticle pressure overload, volume, and overall function.

Treatment: No medical therapies are available to delay the progression of AS. The patient with asymptomatic AS will need to be frequently monitored for the development of symptoms and progression of disease (Bonow et al., 2008; European Task Force, 2007). Symptoms of aortic stenosis (angina, heart failure, syncope) are associated with substan- tial valvular obstruction and a risk of sudden death; therefore, surgical management is necessary. Aortic valve replacement is associated with a higher mortality rate (9% to 12%) in older adults than in younger individuals. Factors associated with greater operative risk include emergency surgery, left ventricular dysfunction, right-sided heart failure, female gender, signifi cant coronary disease, cachexia, additional valve replacement, renal insuffi ciency, or concomitant CABG. The proper selection of the type of valve is important in older adult patients. The bioprosthetic valves have fewer structural failures and are advantageous in that their use obviates the need for long-term anticoagulation (which is associated with substantial morbidity and mortality in older adults). The disadvantage of this valve type is that the tissue degrades and many patients may require reoperation in 10 years. Mechanical valves are more durable and have better hemo- dynamic profi les, but these require lifelong anticoagulation therapy.

Aortic balloon valvuloplasty should be considered as an alternative method of treatment; however, because it is asso- ciated with rapid restenosis and signifi cant residual outfl ow obstruction, it is reserved as a palliative procedure for the symptomatic patient who is not a surgical candidate or as a bridge to surgery.

Secondary to advanced age, 30% of the patients with symp- tomatic, severe AS are not able to undergo surgery to replace the aortic valve. There has been a rapid growth in the use of a new procedure called transcatheter aortic valve implan- tation. This procedure involves implanting a bioprosthetic

Chapter 8 ■ Chest Disorders 209

valve within the diseased aortic valve through a catheter. The option of this procedure is becoming more common in cardiac centers across the nation. Early results from the Transcatheter Valve Therapy Registry indicate decrease in

30-day operative mortality and 1 year mortality (Grover et. al, 2017).

The AHA and ACC 2014 guideline recommendation for AS intervention include:

CLINICAL RECOMMENDATION RECOMMENDATION REFERENCES

Surgical AVR in patient with low or intermediate surgical risk. A Nishimura et al., 2014

Transcatheter aortic valve replacement (TAVR) for patients who have a prohibitive surgical risk and a predicted post TAVR survival greater than 12 months.

A Nishimura et al., 2014

TAVR for patient who have high surgical risk. B Nishimura et al., 2014

TAVR is not recommended in patients in whom comorbidities would preclude the expected benefi t from treatment of AS.

B Nishimura et al., 2014

Balloon aortic valvuloplasty (BAV) as a bridge to surgical AVR or TAVR in severely symptomatic patients.

C Nishimura et al., 2014

Adapted from Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, et al. 2014 AHA/ACC Guideline for the Management of Patients with Valvular Heart Disease: Executive Summary: A report of the American College of Cardiology/American Heart Association Task Force of Practice Guidelines. Circulation. 2014 June 10. 129 (23): 2440-92. A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

Other Class I recommendations for AVR in patients with AS include: patients with high gradient AS who have symp- toms by history or on testing (stage D1), asymptomatic patients with severe AS (stage C2) and left ventricular frac- tion less than 50%, and patients with severe AS (stage C or D) when undergoing other cardiac surgery (Nishimura et. al, 2014).

Mitral Regurgitation Mitral regurgitation (MR) is retrograde blood fl ow during systole from the left ventricle into the left atrium through an incompetent mitral valve. The mitral valve apparatus consists of mitral valve annulus, chordae tendineae, and papillary. Distortion of either of these structures may lead to an incom- petent mitral valve and thus mitral regurgitation. MR is cat- egorized by grades A to D. Grade A is patients at risk for MR, grade B is progressive MR, grade C is asymptomatic severe MR, and grade D is symptomatic severe MR. The progression of untreated disease may lead to pulmonary hypertension and a failing left ventricle.

Etiology: Some of the common causes of MR are rheumatic heart disease, mitral valve prolapse, and ischemic heart disease (Maganti, Rigolin, Sarano, & Bonow, 2010). In the older adult population, the most common causes of signifi - cant MR are myxomatous degeneration and ischemic heart disease. Congenital MR is rare, but may be seen with cleft mitral valve in persons with Down ’ s syndrome. MR may be further delineated as acute or chronic. Common causes of acute MR include chordal rupture, papillary muscle rupture, leafl et perforation, and trauma. Common causes of chronic MR include rheumatic fever, mitral leafl et prolapse, CAD,

papillary muscle dysfunction, congenital heart disease, left ventricular dilatation, myxomatous degeneration, and hypertension.

Signs and Symptoms: The symptoms associated with MR can be quite variable from a state of asymptomatic to symptoms of left ventricular dysfunction, shortness of breath, paroxys- mal nocturnal dyspnea, fatigue, as well as concomitant right- sided heart failure.

Physical Examination Findings: The murmur of MR is a holo- systolic murmur heard at the apex and may radiate to the axillae and may be associated with an S 3 gallop. Due to the dilatation of the left atrium, may of the patients will have AF. Other examination fi ndings may include edema, displaced apical impulse, and crackles on lung examination (Maganti et al., 2010).

Diagnostic Tests: In MR, the EKG shows left atrial enlarge- ment or AF and the chest x-ray examination shows left ven- tricular dilation; in nonrheumatic forms of MG these are less distinctive. Echocardiography delineates overall ventricular function and Doppler studies show the jet and severity of the regurgitation, as well as the mechanism. Transesophageal echocardiography is a more precise way of visualizing the regurgitant jet.

Treatment: Medical management of MR includes use of ACEIs, digitalis, diuretics, and vasodilators to reduce the symptoms of heart failure and reduce the regurgitant volume. Antico- agulation may be needed if the patient has AF. Mitral valve surgery is considered in asymptomatic and symptomatic patients with progressive disease before signs of irreversible left ventricular dysfunction are present. The mortality rate

210 Chapter 8 ■ Chest Disorders

associated with mitral valve replacement could be as high as 14% in the elderly patient. Mitral valve repair is associated with a lower operative mortality than mitral valve replace- ment and is preferred, as preservation of the existing valve architecture allows synchrony of left ventricular contrac- tion. When mitral annular calcifi cation is the cause, medical therapy is prudent because the operative risk is substantially

higher in patients with this disease process. Acute MR from papillary muscle rupture or chordal rupture requires patient stabilization followed by surgery, which still carries a high mortality rate. Other therapeutic options for repair or the mitral valve may include MitraClip (O’Riordan, 2013).

The AHA and ACC 2014 guideline recommendations for MG intervention include:

CLINICAL RECOMMENDATION RECOMMENDATION REFERENCES

MV surgery is recommended for symptomatic patients with severe primary MR (Stage D) and ejection fraction greater than 30%.

B Nishimura et al., 2014

MV surgery is recommended for asymptomatic patients with severe primary MR and left ventricular dysfunction (ejection fraction 30% to 60% and/or systolic diastolic dimension greater than 40 mm.

B Nishimura et al., 2014

MV repair is recommended when procedure is limited to posterior leafl et in the setting of chronic severe primary MR.

B Nishimura et al., 2014

MV repair is recommended over MV replacement in patients with chronic MR involving anterior or posterior leafl ets.

B Nishimura et al., 2014

If patient undergoing other cardiac surgery and has chronic primary MR, they should also have MV repair or replacement surgery at the same setting.

B Nishimura et al., 2014

Adapted from Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA, et al. 2014 AHA/ACC Guideline for the Management of Patients with Valvular Heart Disease: Executive Summary: A report of the American College of Cardiology/American Heart Association Task Force of Practice Guidelines. Circulation. 2014 June 10. 129 (23): 2440-92. A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

General Principles

Diagnosis: Often the fi rst indication of VHD may be the aus- cultation of a cardiac murmur. It is important for advanced practice nurses to have good cardiovascular assessment skills. Auscultatory and other associated fi ndings are listed in the table that follows and can be a useful guide in approaching the cardiovascular examination of all patients.

VALVULAR HEART DISORDER MURMUR

OTHER CARDIAC FINDINGS

Aortic

stenosis

Systolic murmur

heard at second right

intercostal space

and may radiate to

carotids

Decreased cardiac

upstroke. Best heard with

patient sitting up and

exhaling.

Aortic

regurgitation

Diastolic blowing

murmur at left

sternal border

Rapidly collapsing pulse

(Corrigan ’ s pulse),

preservation of A2

component of second

heart sound, widened pulse

pressure.

VALVULAR HEART DISORDER MURMUR

OTHER CARDIAC FINDINGS

Mitral

stenosis

Diastolic rumble May be associated with

signs of right heart failure

including edema, ascites,

elevated jugular venous

pressure.

Mitral

regurgitation

Holosystolic murmur

heard at apex and

may radiate to axilla

AF, ventricular gallop (S 3 ),

displaced apical impulse

laterally, crackles on lung

examination.

Mitral valve

prolapse

Mid-systolic click

heard at apex

May be associated with

mitral regurgitation.

Tricuspid

stenosis

Mid-diastolic rumble

heard at left sternal

border; may increase

with inspiration

Very rare fi nding but

may be associated with

right atrial myxomas or

carcinoid syndrome.

Tricuspid

regurgitation

Holosystolic murmur

heard at right sternal

border and increase

with inspiration

May be associated with

signs of right heart failure

including edema, ascites,

elevated jugular venous

pressure.

Chapter 8 ■ Chest Disorders 211

VALVULAR HEART DISORDER MURMUR

OTHER CARDIAC FINDINGS

Pulmonic

stenosis

Harsh mid-systolic

murmur heard at the

2nd left interspace

and may radiate to

the left carotid

May be associated with a

palpable thrill. The second

heart sound is widely split.

Pulmonic

regurgitation

High-pitched diastolic

murmur

Accentuated P2 of the

second heart sound. May

be louder in setting of

pulmonary hypertension.

Follow-Up: For patients treated medically for valvular disease, close follow-up to monitor the effectiveness of treatment, adverse effects of medication, and progressiveness of the disease process is indicated. Medication therapy, particu- larly the use of anticoagulation therapy, requires meticulous attention. Surgically treated patients are monitored for valve function, fl uid balance, and anticoagulation. Periodic echo- cardiographic, electrocardiographic, and chest x-ray moni- toring may be indicated.

Sequelae: Untreated VHD may lead to progressive heart failure, dysrhythmias, and death. Valve replacement risks include thrombus formation, infection, or rupture at the attachment points to the valve ring. Infective endocarditis, which may occur with artifi cial valves, has a high risk of mor- tality and requires reoperation. There is a high prevalence of gallstones in patients with prosthetic valves, thought to be due to low-grade intravascular hemolysis. In patients who are not surgical candidates, the symptoms of heart failure are progressive and disabling. Even in surgical patients, the symptoms of heart failure may recur or persist.

Prevention/Prophylaxis: In patients with prosthetic valves, the risk of thromboembolism decreases with an individualized

antithrombotic regimen. The specifi c therapy is determined based on the comorbid state and the patient ’ s overall status. Consider prophylactic antibiotic therapy (endocarditis pro- phylaxis) before any surgical or dental procedures in all patients with valvular disease, especially patients with valve replacement, rheumatic heart disease, aortic regurgitation, or mitral valve prolapse with signifi cant MR murmurs.

Referral: All patients with symptoms of progressive valvular disease must be managed collaboratively with the physician. Many require further collaboration with a cardiologist and or cardiac surgeon. The Practice Guidelines for Cardiotho- racic Surgery Concerning Valvular Heart Disease include the indications for surgery. In general, these include symptoms that cannot be controlled with medical therapy or indications of a threat to survival (i.e., angina, dyspnea, effort syncope or progressive impairment of ventricular contractility, and infective endocarditis).

Education: Older adults constitute 40% to 60% of all cases of endocarditis. Instruct all at-risk patients in the importance of good oral hygiene and antibiotic prophylaxis. Patients should be taught to monitor and report febrile illness.

Teach all patients with valve disease requiring medication therapy to report lack of therapeutic effect or any adverse effects of the drugs. Teach patients to be aware of drug-food interactions (e.g., green leafy vegetables and anticoagulants). Teach patients to have prothrombin time/INR checked on a regular basis if they are taking anticoagulant medications. Teach the patient with disabling heart failure about ener- gy-conservation measures. Patients with hemodynamically signifi cant valvular heart disease may need to limit vigorous physical activity. Deterioration may be rapid and symptoms insidious, so patients are taught to report any changes in condition.

C A S E S T U DY

You are assigned to see R. G., a 66-year-old man known to the practice where you have your clinical experience. When you go to review his chart it is in the inactive fi le because he has not been seen for more than 7 years. His last visit was for bronchitis, and he was prescribed albuterol metered-dose inhaler (MDI) as needed. He was given laboratory slips for a complete metabolic profi le, EKG, and PFTs, but there are no results on the chart. A follow-up postcard was sent to him 2 months after the visit.

On review of his chart you note that he has never come for a comprehensive visit, only episodic problems. He was diagnosed with hypertension 10 years ago and prescribed hydrochlorothiazide, 12.5 mg orally once daily; his last refi ll was 2 years ago. History is sketchy since he was seen mainly for sick visits. Here is what you can obtain from the record:

Divorced; worked as a carpenter, also did handyman jobs

Last insurance through carpenters’ union

Signifi cant family history: Father died from heart problem at age 42; mother died from lung cancer at age 60; younger brother has type 2 diabetes mellitus, heart disease

Smoker, 1-1/2 packs/day since age 15 years

Occasional alcohol; during military service drank four six- packs of beer every weekend

Denies any drug use, uses OTC Advil for “aches and pains on the job”

Reported that he had a tetanus booster in the emergency department 8 years ago for a work-related injury

Last visit: BP 130/84, heart rate (HR) 76, respiratory rate (RR) 18, BMI 28

Continued

212 Chapter 8 ■ Chest Disorders

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taking ( 11th ed ). Lippincott, Williams, & Wilkins : Wolters Kluwer Health .

LeBlond , R. F. , Brown , D. D. , Suneja , M. , & Szot , J. F. ( Eds .). ( 2014 ). DeGow- in ’ s diagnostic examination (10th ed.) . New York, NY : McGraw-Hill .

Asthma Humphrey , D. A. ( 2016 ). Asthma (acute exacerbation) . Essential evi-

dence plus . Retrieved from http://www.essentialevidenceplus.com Kraft , W. , & Oppong , Y. ( 2015 ). Asthma (chronic management) . Essen-

tial evidence plus . Retrieved from http://www.essentialevidenceplus. com

Cardiac Arrhythmias January , C. T. , Wann , L. , Alpert , J. S. , et al. ( 2014 ). AHA/ACC/HRS guide-

line for the  management of patients with atrial fi brillation: Executive summary: A report of the American College of Cardiology/American Heart Association task force on practice guidelines and the Heart Rhythm Society .  Journal of the American College of Cardiology , 64 ( 21 ), 2246 – 2280 . doi:10.1016/j.jacc.2014.03.021

Moya , A. , Sutton , R. , Ammirati , F. , Blanc , J. , Brignole , M. , Dahm , J. , & Wieling , W. ( 2009 ). Guidelines for the diagnosis and management of syncope. Version 2009 . European Heart Journal , 30 ( 21 ), 2631 – 2671 .

Pedersen et al. ( 2014 ). EHRA/HRS/APHRS expert consensus on ven- tricular arrhythmias . Europace , 16 ( 9 ), 1257 – 1283 . doi:10.1093/ europace/euu194

Scottish Intercollegiate Guidelines Network . ( 2007, February ). Cardiac arrhythmias in coronary heart disease. A national clinical guideline . Edin- burgh, Scotland : Scottish Intercollegiate Guidelines Network .

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Chronic obstructive pulmonary disease (COPD) . Retrieved from https:// www.cdc.gov/copd/index.html

Cheyne , L. , Irvin-Sellers , M. , & White , J. ( 2015 ). Tiotropium versus ipratropium bromide for chronic obstructive pulmonary disease . Cochrane Database of Systematic Reviews (Cochrane Airways Group) , 9 ( CD009552 ). doi:10.1002/14651858.CD009552.pub3

Criner , G. , Bourbeau , J. , Diekemper , R. , Ouellette , D. , Goodridge , D. , Her- nandez , P. , . . . Stickland , M. ( 2015 ). Prevention of acute exacerba- tions of COPD . Chest , 147 ( 4 ), 894 – 942 . doi:10.1378/chest.14-1676

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alone for chronic obstructive pulmonary disease . Cochrane Database of Systematic Reviews (Cochrane Airways Group) , 10 ( CD008989 ). doi:10.1002/14651858.CD008989.pub3

Global Initiative for Chronic Obstructive Lung Disease . Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Ini- tiative for Chronic Obstructive Lung Disease (GOLD) . ( 2017 ). Retrieved from www.goldcopd.org

Guirguis-Blake , J. , Senger , C. , Webber , E. , Mularski , R. , & Whitlock , E. ( 2016 ). Screening for chronic obstructive pulmonary disease: Evi- dence report and systematic review for the U.S. Preventive Services Task Force . Journal of the American Medical Association , 315 ( 13 ), 1378 – 1393 .

Kew , K. , Dias , S. , & Cates , C. ( 2014 ). Long-acting inhaled therapy (beta- agonists, anticholinergics, and steroids) for COPD: A network meta- analysis . Cochrane Database of Systematic Reviews (Cochrane Airways Group) , 3 ( CD010844 ). doi: 10.1002/14651858.XS010844.pub2

Heart Failure Advisory Committee for Immunization Practices (ACIP) . ( 2016, Febru-

ary ). Vaccines that might be indicated for adults aged 19 years or older based on medical and other indications . Retrieved from https://www. cdc.gov/vaccines/schedules/hcp/imz/adult-conditions-shell.html

Cohn , J. N. , & Tognoni , G. ( 2001 ). A randomized trial of the angioten- sin-receptor blocker valsartan in chronic heart failure [Val-HeFT trial] . New England Journal of Medicine , 345 ( 23 ), 1667 – 1675 . doi:10.1056/ NEJMoa010713 20160809175852664330005

Harrington , C. C. ( 2016 ). Nurse practitioner practice patterns for the management of heart failure in long-term care facilities. Journal of Doc- toral Nursing Practice , 9 ( 1 ), 73 – 80 . doi:10.1891/2380-9418.9.1.73 201608072017301589980007

McMurray , J. J. , Packer , M. , Desai , A. S. , Gong , J. , Lefkowitz , M. P. , Rizkala , A. R. , . . . Zile , M. R. ( 2014 ). Angiotensin–neprilysin inhi- bition versus enalapril in heart failure . New England Journal of Medicine , 371 ( 11 ), 993 – 1004 . doi:10.1056/NEJMoa1409077 20160807141431217793583

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Mozzafarian , D. , Benjamin , E. J. , Go , A. S. , Arnett , D. K. , Blaha , M. J. , Cushman , M. , . . . Turner , M. B. ( 2016 ). Heart disease and stroke sta- tistics—2016 update: A report from the American Heart Association . Circulation , 133 ( 4 ), e38 – e360 .

Muth , C. , Gensichen , J. , Beyer , M. , Hutchinson , A. , & Gerlach , F. M. ( 2009 ). Systematic guideline review: Method, rationale, and test on

1. How will you use this information to prepare for today ’ s visit? Today ’ s Visit: Chief Complaint: “I ’ m really feeling my age these

days. There are times when I feel like I can ’ t catch my breath. [Pause to breathe] I know I ’ ve put on a few pounds but I didn ’ t think I ’ d feel so winded. This retirement is for the birds; I can ’ t seem to get into the groove.” [Pause to breathe]

Objective: BP 160/92, HR 110, RR 28, BMI 27 66-year-old Caucasian male, ruddy

complexion, fi ngertips yellowed, prominent sternocleidomastoids, looks older than stated age

Diminished breath sounds, crackles at bases of lungs bilaterally

Heart sounds distant, possible S4

Feet cyanotic when dependent, + 2 edema bilaterally 2. What additional subjective data are you seeking?

3. What additional objective data will you be assessing for?

4. What national guidelines are appropriate to consider?

5. What tests will you order?

6. What are the differential diagnoses that you are considering?

7. What is your plan of care?

8. Are there any Healthy People 2020 objectives that you should consider?

9. What additional patient education may be needed?

10. Will you be looking for a consultation?

C A S E S T U DY — cont’d

Chapter 8 ■ Chest Disorders 213

chronic heart failure . BMC Health Services Research , 9 ( 74 ), 1 – 15 . 20160807124646410349488

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Poole-Wilson , P. , Swedberg , C. , Cleland , J. F. , Di Lenarda , A. , Hanrath , P. , Komjada , M. , . . . Skene , A. ( 2003 ). Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the carvedilol or metoprolol European trial (COMET): Randomised controlled trial . The Lancet , 362 ( 9377 ), 7 – 13 . doi:10.1016/S0140- 6736(03)13800-7 201608071932591439628959

Rienstra , M. , Damman , K. , Mulder , B. A. , Van Gelder , I. C. , McMur- ray , J. , & Van Veldhuisen , D. J. ( 2013 ). Beta-blockers and outcome in heart failure . Journal of American College of Cardiology , 1 ( 1 ), 21 – 28 . Retrieved from http://dx.doi.org/10.1016/j.jchf.2012.09.002 20160807195206225395679

Trelle , S. , Reichenbach , S. , Wandel , S. , Hildebrand , P. , Tschannen , B. , Villiger , P. M. , . . . Juni , P. ( 2011 ). Cardiovascular safety of non-steroi- dal anti-infl ammatory drugs: Network meta-analysis . British Medical Journal , 342 , 1 – 14 . Retrieved from http://www.bmj.com/content/ bmj/342/bmj.c7086.full.pdf

Triposkiadis , F. , Karayannis , G. , Giamouzis , G. , Skoularigis , J. , Louridas , G. , & Butler , J. ( 2009 ). The sympathetic nervous system in heart failure physiology, pathophysiology, and clinical implications . Journal of the American College of Cardiology , 54 ( 19 ), 1747 – 1762 . doi:10.1016/j. jacc.2009.05.015 201608072028571540446997

Yancy , C. W. , Jessup , M. , Bozkurt , B. , Butler , J. , Colvin , M. M. , Drazner , M. H. , . . . Westlake , C. ( 2016 ). 2016 ACC/AHA/HFSA focused update on new pharmacological therapy for heart failure: An update of the 2013 ACCF/AHA guideline for the management of heart failure . Journal of Cardiac Failure , doi:10.1016/j.jacc.2016.05.011 201608071424171053765297

Yancy , C. W. , Jessup , M. , Bozkurt , B. , Butler , J. , Casey , D. E. , Drazner , M. H. , . . . Wilcoff , B. L. ( 2013 ). 2013 ACCF/AHA guideline for the manage- ment of heart failure. A report of the American College of Cardiology Foundation/American Heart Association task force on practice guide- lines . Journal of the American College of Cardiology , 62 ( 16 ), e147 – e239 . doi:10.1016/j.jacc.2013.05.019 20160807122335445784807

Zannad , F. , McMurray , J. , Drexler , H. , Krum , H. , Van Veldhuisen , D. J. , Swedberg , K. , . . . Pitt , B. ( 2010 ). Rationale and design of the Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure (EMPHASIS-HF) . European Journal of Heart Failure , 12 ( 6 ), 1879 – 1844 . doi:10.1093/eurjhf/hfq049 201608071942001332595110

Hypertension Campbell-Scherer , D. , Green , L. A. , & Barry , H. C. ( 2017 ). Hypertension

(essential) . In Essential evidence plus & AHFS DI essentials . John Wiley & Sons .

Ischemic Heart Disease Fihn , S. D. , Gardin , J. M. , Abrams , J. , Berra , K. , Blankenship , J. C. , Aposo-

tolos , P. D. , . . . Williams , S.V. ( 2012 ). ACCF/AHA/ACP/AATS/PCNA/ SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: A report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, Amer- ican Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons .  Journal of the Ameri- can College of Cardiology , 60 , e44 – e164 .

Lung Cancer Latimer , K. M. , & Mott , T. F. ( 2015 ). Lung cancer: Diagnosis, treat-

ment principles, and screening . American Family Physician , 91 ( 4 ), 250 – 256 .

National Comprehensive Cancer Network . ( 2016a ). Lung cancer screen- ing – Version 1.2017 . Retrieved from http://www.nccn.org .

National Comprehensive Cancer Network . ( 2016b ). Small cell lung cancer – Version 2.2017 . Retrieved from http://www.nccn.org .

National Comprehensive Cancer Network . ( 2017 ). Non-small cell lung cancer – Version 4.2017 . Retrieved from http://www.nccn.org .

The U.S. Preventive Services Task Force . ( 2013 ). Lung cancer : Screening. Retrieved from https://www.uspreventiveservicestaskforce.org/Page/ Document/UpdateSummaryFinal/lung-cancer-screening

Myocardial Infarction Amsterdam , E. A. , Wenger , N. K. , Brindis , R. G. , et al. ( 2014 ). AHA/

ACC guideline for the  management of patients with  non–st-elevation acute coronary syndromes: A report of the American College of Car- diology/American Heart Association task force on practice guidelines . Journal of the American College of Cardiology , 64 ( 24 ), e139 – e228 . doi:10.1016/j.jacc.2014.09.017

Pneumonia Bartlett , J. ( 2016 ). Diagnostic approach to community-acquired pneu-

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C. , . . . Le Bel , J. ( 2015 ). Diagnostic accuracy of C-reactive protein and procalcitonin in suspected community-acquired pneumonia adults visiting emergency department and having a systematic thoracic CT scan .  Critical Care ,  19 , 1 – 12 . doi:10.1186/s13054-015-1083-6

CDC . ( 2016 ). Pneumococcal disease: Diagnosis and medical manage- ment . Retrieved from http://www.cdc.gov/pneumococcal/clinicians/ diagnosis-medical-mgmt.html

File , T. ( 2016c ). Treatment of community-acquired pneumonia in adults who require hospitalization . UpToDate. Retrieved from https://www. uptodate.com

File , T. ( 2016d ). Treatment of community-acquired pneumonia in adults in the outpatient setting . UpToDate. Retrieved from https://www.upto date.com

Institute for Clinical Systems Improvement . ( 2011 ). Prevention of ventila- tor-associated pneumonia. Health care protocol . Bloomington, MN : Insti- tute for Clinical Systems Improvement . Retrieved from https://www. icsi.org/_asset/y24ruh/vap-interactive1111.pdf

Kalanuria , A. , Zai , W. , & Mirski , M. ( 2014 ). Ventilator-associated pneu- monia in the ICU . Critical Care 2014 , 18 , 208 . doi: 10.1186/cc13775 . Retrieved from https://ccforum.biomedcentral.com/articles/10.1186/ cc13775

Kalil , A. , Metersky , M. , Klompas , M. , Muscedere , J. , Sweeney , D. , Palmer , L. , . . . Brozek , J. ( 2016 ). Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guide- lines by the Infectious Diseases Society of America and the American Thoracic Society . Clinical Infectious Diseases. Retrieved from http://cid. oxfordjournals.org/content/eary/2016/07/06/cid.ciw353.full

Mandell , L. , Wunderink , R. , Anzueto , A. , Bartlett , J. , Campbell , G. , Dean , N. , . . . Whitney , C. ( 2007 ). Infectious Diseases Society of America/ American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults . Clinical Infectious Dis- eases , 44 ( Suppl. 2 ), S27 – S72 . doi:10.1086/511159

Moran , G. J. , Rothman , R. E. , & Volturo , G. A. ( 2013 ). Emergency man- agement of community-acquired bacterial pneumonia: What is new since the 2007 infectious diseases society of America/American tho- racic society guidelines .  American Journal of Emergency Medicine ,  31 ( 3 ), 602 – 612 . doi:10.1016/j.ajem.2012.12.002

Musher , D. , & Thorner , A. ( 2014 ). Community-acquired pneumonia . New England Journal of Medicine , 371 , 1619 – 1628 . doi:10.1056/ NEJMra1312885

National Institute for Health and Care Excellence (NICE) . ( 2014 ). Pneu- monia in adults: Diagnosis and management . Retrieved from https:// www.nice.org.uk/guidance/cg19

Wunderink , R. , & Waterer , G. ( 2014 ). Community-acquired pneu- monia . New England Journal of Medicine , 370 , 6 . doi:10.1056/ NEJMcp1214869

Pulmonary Embolism Belohlavek , J. , Dytrych , V. , & Linhart , A. ( 2013 ). Pulmonary embo-

lism, part 1: Epidemiology, risk factors and risk stratifi cation,

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pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism .  Experimental & Clinical Cardiology Journal , 18 ( 2 ), 129 – 138 . Retrieved from   http://www.ncbi.nlm.nih.gov/pmc/ articles/PMC3718593/

Ho , D. , & Smouse , B. ( 2015 ). Updates in diagnosis and treatment in acute pulmonary embolism:  A review article . Journal of Clinical Trial Results , 1 ( 1 ).  Retrieved from   http://journalofclinicaltrialresults.com/ updates-on-diagnosis-and-treatment-in-acute-pulmonary-embo- lism-a-review-article/

Konstantinides , S. , Torbicki , A. , Agnelli , G. , Danchin , N. , Fitzmaurice , D. , Galie , N. , . . . Zompatori , M. ( 2014 ). 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism .  European Heart Journal , 35 ( 43 ), 3033 – 3069 .  Retrieved from   http://www.ncbi. nlm.nih.gov/pubmed/25173341

Lavorini , F. , Di Bello , V. , De Rimini , M. , Lucignani , G. , Marconi , L. , Palar- eti , G. , . . . Pistolesi , M. ( 2013 ). Diagnosis and treatment of pulmonary embolism:  A multidisciplinary approach . Mulitdisciplinary Respiratory Medicine 8 ( 75 ).  Retrieved from   https://mrmjournal.biomedcentral. com/articles/10.1186/2049-6958-8-75

Ozaki , A. , & Bartholomew , J. ( 2012 ). Venous thromboembolism (deep venous thrombosis and pulmonary embolism) . Cleveland clinic center for continuing education .  Retrieved from   http://www.cleveland clinicmeded.com/medicalpubs/diseasemanagement/cardiology/ venous-thromboembolism/

Pulmonary Tuberculosis Lewinsohn , D. , Leonard , M. , LoBue , P. , Cohn , D. , Daley , C. , Desmond , E. ,

. . . Woods , G. ( 2017 ). Offi cial American Thoracic Society/Infectious

Diseases Society of America/Centers for Disease Control and Preven- tion clinical practice guidelines: Diagnosis of tuberculosis in adults and children . Clinical Infectious Diseases , 64 ( 2 ), 111 – 115 . doi:10.1093/ cid/ciw778

Restrictive Lung Disease American Thoracic Society & European Respiratory Society . ( 2002 ).

American Thoracic Society/European Respiratory Society inter- national multidisciplinary consensus classifi cation of the idiopathic interstitial pneumonias . American Journal of Respiratory and Critical Care Medicine , 165 ( 2 ), 277 – 304 .

Davies , H. R. , Richeldi , L. , Walters , E. H. , & Davies , H. R. ( 2007 ). Immu- nomodulatory agents for idiopathic pulmonary fi brosis (Cochrane review) . In The Cochrane Library 2007 , Issue 1 . Chichester, UK : John Wiley & Sons .

Reust , C. M. ( 2011 ). Interstitial lung disease . Essential evidence plus . Retrieved from http://www.essentialevidenceplus.com

Richeldi , L. , Davies , H. R. , Spagnolo , P. , & Luppi , F. ( 2010 ). Corticoste- roids for idiopathic pulmonary fi brosis . Cochrane Database of Systematic Reviews , 2 , CD002880 .

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nusitis . American Family Physician. Retrieved from www.aafp.org Sexton , D. , & McClain , M. ( 2016 ). The common cold in adults: Treat-

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infection . Essential evidence plus . Retrieved from http://www. essentialevidenceplus.com

215

CHAPTER 9 Peripheral Vascular Disorders

Catherine Ratliff and David Strider

ASSESSMENT

A comprehensive vascular assessment may be integrated into the general history and physical examination for the patient with vascular disease. A systematic head-to-toe examination, done consistently for each vascular patient, will minimize the chance of missing subtle signs related to vascular defi cits.

The clinician should begin with auscultation of the carotid arteries bilaterally. Cardiac murmurs will usually radiate into the carotid arteries, and an underlying bruit may not be dis- cerned. The subclavian arteries should then be auscultated over the upper anteromedial chest area. During this phase of the examination, the jugular veins should be inspected for jugular vein distention. This can best be appreciated when the patient is lying down with the head of the bed elevated 15 degrees.

The clinician should proceed to the palpation of the bra- chial, radial, and ulnar arteries. Such palpation should be scored on a scale of 0 to 4 (4  =  pulsatile, bounding; 3  =  easily palpable with full triphasic pulse; 2  = biphasic pulse that may be a bit harder to locate initially; 1  =   monophasic pulse that may come and go depending on position of fi ngertips; and 0  =  absent pulse by palpation, which may be detected by Doppler ultrasound). All palpable pulses should be graded in the assessment and documented.

The clinician should evaluate any pain, coolness, pares- thesia, motor weakness, discoloration, or tissue loss in the hands. Careful inspection of the distal fi ngers and the nail beds may reveal signs of end tissue malperfusion. The fi nger joints should be inspected for cyanosis and/or petechiae. The fi ngernails should be checked for clubbing, which portends chronic hypoxemia. Routinely, in any patient confi rmed or suspected to have vascular disease, blood pressure should be checked in both arms at this point.

The heart should then be auscultated to permit delinea- tion of rhythm regularity, S 1 , S 2 , and any extrasystolic sounds such as S 3 , S 4 , or pericardial rub. Murmurs should be noted and classifi ed as per the cardiac assessment guidelines. The abdomen should be auscultated for celiac artery, superior mesenteric artery, and renal artery bruits, which are best heard 4 to 8  cm above the umbilicus and 1 to 2  cm to the right and left of midline abdomen. Then the clinician should

listen to the femoral artery in each groin for the presence of bruits. Following this, the abdomen should be lightly pal- pated just to the left of midline, approximately 4  cm above the umbilicus, to evaluate for a pulsatile abdominal aorta. In slender individuals, the abdominal aorta is often fairly easy to palpate. A bounding, pulsatile abdominal aorta in an individ- ual may suggest aneurysmal formation. The clinician should note and document any tenderness or guarding associated with the abdominal palpation. There are many other causes for abdominal tenderness that the clinician should be aware of, in addition to arterial and venous disease, to include pan- creatitis, liver contusions, cholecystitis, appendicitis, splenic infarction, pyelonephritis, cystitis, gastroenteritis, peptic ulcer, and small bowel obstruction.

Once the abdominal examination is complete, the cli- nician should progress to the vascular assessment of the lower extremities. The femoral arteries should be palpated over the groin area and documented on the scale of 0 to 4. Any pulse defi cits should be followed up with a Doppler examination. The popliteal fossa should be inspected and palpated bilaterally in order to locate the popliteal artery and assess for the possibility of popliteal artery aneurysms. The clinician should inspect the calves and feet for edema, skin turgor, and skin pigmentation. Thick, hyperpigmented skin in the lower calves and feet may be an indication of chronic venous insuffi ciency, whereas thin, shiny, pale skin is more consistent with peripheral arterial insuffi ciency. The dorsalis pedis and posterior tibial pulses should be palpated. If those pulses are not palpable, Doppler ultrasound should be used. Any Doppler signals should be located and identifi ed with an indelible marker pen. At this time, the heel, the medial and lateral malleoli, and the toes of each foot should be inspected for breakdown. As in the hands, any pedal pain, coolness, paresthesia, motor weakness, discoloration, or tissue loss should be documented. Dorsal and plantar fl exion of the feet should be assessed and recorded with muscular strength graded on a scale of 1 to 5.

The vascular examination then turns to a careful eval- uation of the cranial nerves (CNs), usually focusing on CN II to CN XII. Evaluation of pupillary light and accommoda- tion response (CN II and III); following the eyes in a lateral, medial, superior, and inferior gaze (CNs III, IV, and VI); and evaluation of facial smile, scowl, and opening eyes against

216 Chapter 9 ■ Peripheral Vascular Disorders

pressure (CNs V and VII) should be completed. Gross hearing assessment, with follow-up by Weber and Rinne testing, may ascertain any CN VIII defi cits. Evaluating the tongue protru- sion, uvula rise, cough refl ex, gag refl ex, and shoulder shrug will provide information on the integrity of CNs IX, X, XI, and XII. Document the conformation of the uvula, which may be bifi d or singular (some connective tissue disorders have asso- ciated bifi d uvula).

Completion of the CN examination provides the health- care team with an excellent neurological baseline before interventions for carotid artery disease. Assessment fi ndings related to vertebrobasilar insuffi ciency may include balance problems, dizziness, and coordination defi cits. Focal neuro- logical defi cits such as arm, leg, and/or facial weakness on one side of the body; loss of speech; diffi culty speaking or swallowing; and unilateral or partial vision loss signify tran- sient cerebral ischemia that may be related to severe carotid artery stenosis (Dua, Romanelli, & Upchurch, 2016).

Following the neurological examination, the clinician should ascertain any specifi c end organ perfusion defi cits, as shown by the following signs and symptoms:

■ Pain in the feet, calves, thighs, and or buttocks, either at rest or with ambulation (peripheral arterial disease [PAD])

■ Any open wounds or blisters on the distal aspects of feet and/or hands (PAD or chronic venous stasis ulcers)

■ Abdominal pain, nausea, vomiting, and/or diarrhea after a meal (mesenteric ischemia)

■ Persistent abdominal/back pain (abdominal aortic aneurysms or dissection)

■ Acute unilateral CN defi cits (carotid artery disease) ■ Acute balance/coordination defi cits (possible verte-

brobasilar malperfusion) ■ Acute chest and/or back pain (after ruling out myo-

cardial ischemia and pulmonary embolus, one needs to quickly and thoroughly evaluate the patient for tho- racic aortic dissection and/or expanding aneurysm)

Once the focused vascular assessment and abbreviated history are completed, the clinician will have achieved a very sound baseline with which to guide future interventions to delineate and treat vascular lesions.

ABDOMINAL AORTIC ANEURYSM

Signal Symptoms: Persistent or intermittent pain in the middle or lower abdomen, often radiating to the lower back, which is characteristic of a rapidly expanding, leaking, or rup- tured abdominal aortic aneurysm (AAA). Most AAAs are asymptomatic.

Description: The abdominal aorta is the large artery that pro- vides blood to the digestive organs, liver, kidneys, spleen, and lower extremities. It extends inferiorly from the descending aorta to the iliac arteries. An AAA is a dilation of the abdom- inal aorta that is one and one-half to two times greater than the size of the nondilated proximal or distal aorta. The AAA involves all three layers of the arterial wall.

Etiology: Most AAAs are atherosclerotic in nature; other causes include trauma, infection, and infl ammation. Con- nective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome, predispose the patient to AAA formation ( Strider et al., 2013 ; Yip & Sawatxky, 2014). Most AAAs are infrarenal (65%), occurring below the renal arteries. Patients with AAAs are more likely to have arterial aneurysms in other locations such as the thoracic aorta, the common iliac arteries, the common femoral arteries, and the popliteal arteries.

Occurrence: AAAs are the thirteenth leading cause of death in the United States. Mortality rates for ruptured aneurysms are 70% to 90%, compared with 5% operative mortality for elective open surgical repair and 2% to 3% for endovascular stent AAA exclusion.

Age: More frequent in adults over 50 years old; prevalence rate is 2% to 4%.

Gender: Onset occurs around age 50 years for men and 60 years for women. Incidence steadily increases with age and peaks at age 80 years. AAA is fi ve times more likely in men than in women.

Ethnicity: There is no dominant ethnic group that develops AAA, but there is a familial history associated with AAA development.

Contributing Factors: Risk factors for developing AAA include arteriosclerotic heart disease and arteriosclerotic changes of other vessels, smoking history, hypertension, chronic obstruc- tive pulmonary disease, obesity, family history of AAA, dia- betes mellitus, cystic medial necrosis, Marfan syndrome, and previous spinal cord injury ( Schermerhorn et al., 2015 ; Sodem, Zetterwal, & Ultee, 2016 ). Aortic dissection involves a splitting apart of the aortic wall layers, such that two or more blood fl ow channels are created within the aorta. Acute aortic dissection may produce intimal fl aps that occlude major take-off vessels, leading to end-organ ischemia. Pro- gressive dissection may lead to weakening of the entire aortic wall, resulting in aneurysm formation and possible rupture. Isolated celiac and/or superior mesenteric artery dissection may occur, although this is much less likely than the initial aortic dissection (Dimusto, Oberdoerster & Criado, 2015).

Signs and Symptoms: Most patients with AAAs are asymp- tomatic (66% to 75%), except in the presence of dissection, rupture, or impending rupture. A pulsatile abdominal mass at or slightly above the umbilicus in the epigastrium, as noted by palpation of the abdomen, is consistent with but not conclu- sive for an AAA. These are easier to palpate in thin individu- als; however, if noted in an obese individual, they are usually quite large. AAA should be suspected in individuals with a femoral or popliteal aneurysm, because 30% of individuals with a peripheral aneurysm also have an AAA. In patients with symptomatic AAAs, the complaints include mild-to-se- vere abdominal, fl ank, or lower back pain. Other symptoms may include nausea and vomiting, gastrointestinal bleeding, and lower extremity ischemia. Rupture is the most lethal clin- ical presentation, with symptoms including sudden onset of

Chapter 9 ■ Peripheral Vascular Disorders 217

severe abdominal and back pain, hypotension, and the pres- ence of a pulsatile, expanding mass. There is a high mortality rate associated with ruptured AAAs; therefore, the possibility of ruptured AAA in the differential diagnosis should be con- sidered in any adult patient with acute abdominal or fl ank pain ( Schermerhorn et al., 2015 ).

Diagnostic Tests: The best initial screening test is an ultra- sound of the abdominal aorta. In cases where surgery is planned, angiography and computed tomography (CT) scan with IV contrast are indicated to size the aneurysm and diag- nose any tears or perforations.

Differential Diagnosis: It is important to evaluate for and treat hypertension and heart disease, because basic and early steps in AAA management include blood pressure control and recognition or enhancement of cardiac function. An ectatic abdominal aorta without aneurysm may be palpated and confused with AAA. Other acute causes of abdominal and back pain may mimic a ruptured AAA and must be ruled out. Major imaging modalities for a patient with suspected or known AAA include abdominal ultrasound, CT scan, mag- netic resonance angiogram (MRA), and angiogram.

Treatment: The rate of AAA growth for an individual is unpredictable. Some aneurysms may remain stable for long periods, whereas others may enlarge quickly. Medical man- agement of an asymptomatic, small AAA should include blood pressure control, regulation of heart rate, and smoking cessation. Beta blockers have been shown to slow the long- term growth of aortic aneurysms. Angiotensin receptor blockers (ARBs), such as losartan, may also have a major role in critical blood pressure and heart rate control for patients with aortic aneurysms and/or dissections.

Initial treatment for symptomatic AAA, whether rup- tured or not, involves aggressive blood pressure control. Mean arterial pressure should be maintained between 60 and 70  mm  Hg, and systolic blood pressure should be kept between 100 and 120  mm  Hg. Arterial pressure monitoring is recommended, and IV antihypertensive agents, such as esmolol, nicardipine, nitroprusside, labetalol, and/or nitro- glycerin, should be used to rapidly and consistently main- tain blood pressure in these ranges. Cardiology should be consulted, and a transthoracic echocardiogram should be done to assess heart function. If the patient is to be medically managed, transition to oral antihypertensive agents should begin, using beta blockers, calcium channel blockers, clon- idine, ARBs, and labetalol as needed to maintain very tight blood pressure control.

The two invasive options for excluding an AAA when it becomes symptomatic or becomes more than 5 cm in diame- ter include open surgical repair and endovascular repair. Elec- tive operative repair has a mortality rate of 2% to 5%. Urgent repair (where cardiac and other known risk factors have not been optimized) of an intact symptomatic AAA has a mor- tality rate of 15% to 20% ( Cooper, 2014 ; Schermerhorn et al., 2015 ). In emergent repair in which the AAA has rup- tured, there is a 50% mortality rate in patients who reach the hospital. Average postoperative length of stay for an elective AAA surgical repair is 5 days. The major cause of death after AAA repair is myocardial infarction. Other complications include renal failure, limb ischemia, ischemic colitis, hem- orrhage, pneumonia with prolonged ventilator dependence,

and paraplegia (Buck, Ultee & Zetterwall, 2016; Yiu & Cheesy, 2016).

Endovascular grafts are a more recent addition to the treatment modalities for elective AAA repair. The graft is deployed through the femoral or the iliac artery. Not all AAAs are anatomically appropriate for stenting. Experimental AAA stent trials began in 1993 in the United States. Current success rates are higher than 90%, with a mortality rate of less than 2%. Most patients are discharged from the hospi- tal in 1 to 2 days ( Gordon & Toursarkissian, 2014 ). Compli- cations after endovascular treatment may include arterial injury at site of access, arterial embolization, endoleak (blood fl ow outside the lumen of the graft but within the original aneurysmal sac), post-implant syndrome (back pain and fever without elevated white blood cell count or other signs of infection), and graft limb distal thrombosis ( Schermerhorn et al., 2015 ).

Follow-Up: Initial management of patients with small aneu- rysms (fewer than 4 cm) should include serial evaluation with ultrasound every 3 to 6 months. Any symptomatic AAA or any asymptomatic AAA larger than 5 cm in diameter should be repaired using either open surgical or endovascular tech- nique ( Sodem, Zetterwall, & Ultee, 2016 ; Cooper, 2014 ).

Sequelae: The most common complication of AAA is rupture. Infrequent complications are thrombi to the lower extremi- ties and preexisting infection of the aneurysm (referred to as a mycotic aneurysm), with Salmonella and Staphylococ- cus aureus being the most commonly identifi ed organisms. Fungal infections of the aorta pose signifi cant challenges and require long-term IV antimycotics, such as fl uconazole after 6 weeks of an IV course of antifungal agents, until a defi ni- tive surgical repair is done.

Prevention/Prophylaxis: Because most AAAs are atheroscle- rotic in nature, the same long-term preventive measures for reducing coronary artery disease should be applied. These include lifestyle modifi cation, control of hypertension, beta blockade and/or ARB therapy, statin therapy, daily aspirin, and maintenance of euglycemia if diabetic (Sodem, Zetterwall & Ultee, 2016 ). Early abdominal ultrasonographic screening is recommended for fi rst-degree relatives of individuals who already have been diagnosed with an AAA. The prevalence of AAA in the fi rst-degree relatives of affected families is reported to be 15% to 33%. Large studies in Western Europe and North America support the selective ultrasonographic screening of men over age 65 years for AAA and all women and men over the age of 50 years if a fi rst-degree relative has been diagnosed with an AAA ( Schermerhorn et al., 2015 ).

Referral: Referral to a vascular surgeon is essential for all patients with symptomatic AAAs. Furthermore, any patient with a known AAA, even if not symptomatic, should be screened with serial ultrasound imaging at least once a year.

Education: Patients and their families should be taught the importance of follow-up; ways to manage hypertension, hypercholesterolemia, smoking, and other risk factors; and the signs and symptoms that should be reported to the phy- sician immediately (sudden onset of abdominal or back pain, dizziness). The risks of operative versus nonoperative treat- ment should be explained thoroughly to the patient and his or her family.

218 Chapter 9 ■ Peripheral Vascular Disorders

Signal Symptoms: Swelling of the affected body part, usually the limb, because of impaired fl ow of lymph fl uid.

Description: Lymphedema is a progressive condition of abnormal lymph accumulation in the interstitial tissues due to a disruption of lymph fl ow. The lymph system is a low-pres- sure system that includes capillaries and depends on muscle movement to advance the fl uid to the vascular system. Most of the lymph drains into the thoracic duct on the left side of the body and into the brachiocephalic vein.

Etiology: Lymphedema is swelling caused by impaired lymph transport, which results in an accumulation or pooling of protein-rich fl uid in the interstitial space. Lymphedema is most commonly caused by surgery, radiation, or infection that damages the lymphatic system.

Occurrence: Lymphedema may be classifi ed as primary (idio- pathic) or secondary (acquired). Primary lymphedema is congenital absence or abnormalities of the lymphatic system. It affects 1 to 2 million individuals in the United States. Sec- ondary lymphedema affects 2 to 3 million individuals in the United States (Ratliff, 2016). One of the most common causes of secondary lymphedema in the United States is related to treatment of cancer.

Age: Not confi rmed as a risk factor for lymphedema.

Gender: With primary or congenital lymphedema, females are affected twice as often as males. With secondary lymph- edema in the United States, females may be affected more often, but that is because a common cause of secondary lymphedema is breast cancer, which is primarily a woman ’ s disease.

Ethnicity: Not signifi cant.

Contributing Factors: The types of cancer associated with secondary lymphedema include breast cancer, gynecolog- ical cancer, lymphoma, melanoma, and urological cancers. Surgery, radiation, trauma, infection, malignancy, or scar tissue can cause secondary lymphedema by obstructing the lymphatic system. For example, patients with a history of breast cancer with axillary node dissection or radiation, groin node dissection or radiation, and a postoperative infection have an increased risk for developing lymphedema. Morbid obesity can also increase the rate of secondary lymphedema (Ratliff, 2016).

Signs and Symptoms: Swelling or edema is the characteristic symptom of lymphedema. Additional symptoms may include heaviness or tightness, aching and fatigue in the affected limb, restricted range of motion, recurring cellulitis in the affected extremity, and hardening and thickening of the skin. The Stemmer sign (or Kaposi-Stemmer ’ s sign) is another clinical indication of lymphedema in which one is unable to pinch a fold of skin at the base of the second toe on the dorsal aspect of the foot or between the second and third fi nger. Skin that does not fold up into a pinch is considered a positive sign of lymphedema (Ratliff, 2016; Lewis & Walsh, 2014).

Diagnostic Tests: Diagnosis of lymphedema is typically made through clinical presentation and medical history, such

as a cancer diagnosis. Lymphoscintigraphy is the imaging gold standard for lymphedema (Lewis & Walsh, 2014); however, it is expensive and invasive, and so only indicated if the patient is a surgical candidate. Bioimpedance spec- troscopy (BIS) measures the composition of tissues (e.g., fl uid such as lymph) and may be used for early diagnosis as well as determining the effectiveness of therapy (Ratliff, 2016).

Differential Diagnosis: Knowing if the patient had a prior history of comorbid conditions that can cause swelling of the extremities, such as cardiac disease, venous ulcer disease, renal disease, hepatic disease, trauma, and infection, is also important. Patients with rheumatoid arthritis, obesity, lipedema (painful fat syndrome), and venous ulcer disease are at greater risk for lymphedema because these conditions add additional stress to the impaired lymphatics. Lymph nodes are located around most joints, so patients undergo- ing such surgical procedures as total knee replacements may be at greater risk for developing lymphedema because lymph nodes can become injured during the surgery. Also, proce- dures such as vein stripping can exacerbate mild lymph- edema (Lewis & Walsh, 2014).

Treatment: Complete decongestive physiotherapy (CDP) is the gold standard for lymphedema management. CDP is a spe- cialized massage technique designed to stimulate the lymph vessels, break up subcutaneous fi brous tissue, and redirect the lymph fl uid to areas where lymph fl ow is normal. It involves four steps: manual lymph drainage (MLD), compres- sion bandaging, exercises, and skin care.

Conservative Treatment: The use of multilayer compression bandages and/or compression stockings is an important component for all patients with lymphedema to prevent the reaccumulation of lymph fl uid in the limb.

Pharmacological Treatment: Diuretics are not benefi cial with lymphedema because they draw off excess water in the interstitial spaces but not the protein. Lymphedema is a high-protein edema, and the high osmotic pressure from the increased protein in the interstitial space causes rapid reac- cumulation of edema. In addition, the higher concentration of protein in the edema fl uid causes increased fi brosis and induration of the skin. Diuretics are not contraindicated for the treatment of other conditions in lymphedema patients, but they should not be used as primary treatment for lymphedema.

Surgical Treatment: Surgery is reserved for individuals with a positive lymphoscintigram who do not respond to more con- servative methods such as CDP. Reconstructive or restorative procedures create lymph-venous shunts or autologous vessel transplantations. Debulking procedures remove excess tissue to reduce the size and weight of the limb (Lewis & Walsh, 2014).

Follow-Up: Patients with lymphedema need regular follow-up by health-care providers to make sure that the CDP is effec- tive and adequate and, if not, appropriate modifi cations can then be made to the care plan.

CHRONIC LYMPHEDEMA

Chapter 9 ■ Peripheral Vascular Disorders 219

Sequelae: Lymphangitis and cellulitis are complications seen with lymphedema. Once patients develop these infections, they are at greater risk for developing them again.

Prevention/Prophylaxis: Lifelong CDP is essential to prevent worsening of the lymphedema and to avoid complications.

Referral: Patients with lymphedema should be referred to a lymphedema specialist.

Education: It is important to teach patients with lymph- edema about the disease process, its lifelong treatment with compression bandaging, the importance of avoiding com- plications such as lymphangitis, and about resources, such as the National Lymphedema Network, that are available to them.

PERIPHERAL VASCULAR DISEASE

Signal Symptoms: Pain, intermittent claudication of the feet, tissue loss in affected leg/arm.

Description: Peripheral vascular disease (PVD) refers to a disease or process that alters blood fl ow to or from the extrem- ities and vital organs other than the heart. These processes may involve the arterial, venous, or lymphatic systems, but most often are due to enlarging atherosclerotic plaques in the distal aorta or in major bifurcations or areas of angulation in the iliac, femoral, and popliteal arteries. Most activity lim- itations and limb loss are associated with peripheral arterial disease (PAD).

Etiology: Atherosclerotic plaques may be fatty streaks, fi brous plaques, or complicated calcifi ed lesions. Fatty streaks are early lesions that occur in the intima of arteries. Fibrous plaques and areas of intimal thickening are the most fre- quently occurring type of lesion. Complicated (heteroge- neous) plaques, as well as calcifi ed fi brous plaques with potential for necrosis and thrombosis, are associated most often with symptoms in PAD patients ( Dua & Lee, 2016 ).

Occurrence: PAD is referred to as an age-related disease. More diabetics than nondiabetics are diagnosed with PAD. The prevalence of PAD for the U.S. adult population is 12%, with an annual incidence of 2.4%. The prevalence of criti- cal limb ischemia (CLI) for the same population is 1.3%, with an annual incidence of 0.4%. This percentage is expected to increase as the number of older adults in the population increases ( Dua & Lee, 2016 ).

Age: Nearly 20% of individuals who are more than 70 years old have PAD, compared with less than 8% of individuals who are younger than 70 years old.

Gender: Symptomatic PAD is two to fi ve times more prevalent in men than in women.

Ethnicity: There are few available data to support an ethnic predisposition for the development of PAD.

Contributing Factors: Smoking remains the most important risk factor, with up to 80% of cases of intermittent claudica- tion associated with tobacco use. Diabetes mellitus is another important risk factor. More than 80% of diabetics surviving 20 years from the time of diagnosis have some type of arte- rial disease. Of patients with a gangrenous lesion of the feet requiring amputation, more than 50% are diabetic. Other associated risk factors include hypertension, high serum cholesterol, obesity, sedentary lifestyle, strong family history, vasculitis, and hypercoagulopathy ( Pomposelli et al., 2015 ; Shirasu, Hoshima, & Nishiyama, 2016; Moain, Dabrn, & Steffen, 2016).

Signs and Symptoms: Intermittent claudication is the early symptom of PAD. It is described as a painful cramping of the muscles of the leg during walking. It goes away when the patient stops walking and resumes after the patient starts walking again. It also may be described as a sensation of tiredness or fatigue. One-third of patients with proven arte- rial stenosis report symptoms of claudication. Ischemic rest pain occurs constantly and is differentiated easily from clau- dication. It is described as a burning sensation and localizes to the metatarsal heads or to an ischemic ulcer. Pain is often worse at night when the leg is elevated. Relief may occur with dependency of the foot. Ischemic rest pain requires immediate attention. Ulceration or gangrene develops at an area of external pressure or at the site of a minor injury, with gangrene representing the end-stage of PAD. Acute arterial ischemia results from arterial thrombosis, embolism, or trauma, with symptoms that are sudden in onset. It often causes the fi ve Ps: pain, pallor, pulselessness, paresthesia, and paralysis. Other symptoms may include decreased sensation and mottling of the extremity. Acute arterial ischemia may be due to thrombus from the left atrium, sudden onset of atrial fi brillation, dislodging of calcium plaque in the aorta, and/or intrinsic hypercoagulopathy. A thorough patient history and physical examination are essential to determine the stage and type of vascular disease (Cucato, Ritti-Dias, & Franco, 2016; Johnston, Robinson, & Tracci, 2016).

Diagnostic Tests: Ankle-brachial index and systolic arterial pressure measurement with continuous-wave Doppler are fi rst-line tests. In cases where surgical intervention is being considered, angiography is indicated. Assessment of distal arterial system patency can be done by Doppler ultrasound, which can also detect and pinpoint occluded areas (Alahdab, Wang, & Elraihyah, 2015).

Differential Diagnosis: Buerger ’ s disease and Raynaud ’ s phe- nomenon also should be considered when diagnosing PAD. Buerger ’ s disease may occur in individuals less than 35 years old who are smokers, and it may affect the upper as well as the lower extremities. This rare disease causes infl ammation of the blood vessels, which can result in clot formation. Ray- naud ’ s phenomenon affects the fi ngertips, the tips of the ears and nose, and the feet. Patients with Raynaud ’ s phenomenon have symptom exacerbation with any cold temperatures. Other diagnoses that mimic the symptoms of PAD include gout, arthritis, diabetic neuropathy, sciatica, and severe venous insuffi ciency ( Dua & Lee, 2016 ).

The hallmark signs and symptoms of venous ulcers include distal lower extremity edema; warmth of the foot; large, irregular, copiously draining ulcers in the distal calf

220 Chapter 9 ■ Peripheral Vascular Disorders

or foot dorsum; and hyperpigmentation of the surround- ing skin. Arterial insuffi ciency ulcers usually are found over the medial or lateral malleolus, heel, or distal aspect of the toes. Wounds associated with arterial ischemia are small and drain minimally, but are extremely painful.

Treatment: The main goal of PAD treatment is to slow the progression of the disease. Treatment may be conservative, pharmacological, operative, or endovascular. Risk factor rec- ognition and lifestyle modifi cation are the central tenets for managing patients with long-term PAD.

Conservative Treatment: Conservative treatment involves modifi cation of risk factors, including smoking, blood pres- sure control, and diet (Hirsch et al., 2005). Smoking is the number one modifi able risk factor, and there are numerous methods available to help individuals stop smoking (Zkhari, 2013; VanDevanter, Zhou, & Katigbak, 2016; Arens, White, & Masengill, 2014 ). In addition, managing diabetes and hyperlipidemia are key measures. Exercise is an essential element of PAD management because collateral vessels are strengthened and stimulated to grow with the onset of an exercise program such as walking. Formalized vascular reha- bilitation programs exist; however, they are not currently rec- ognized by insurers and rarely are reimbursed. Home exercise programs should focus on exercising three or more times per week for at least 30 minutes per day. Patients should be instructed to walk until pain develops, walk a few steps more through the pain, rest until pain goes away, then resume walking. Over time, the patient should be able to walk farther with fewer rest breaks. Meticulous foot care is important to prevent complications of ulceration and gangrene. Patients should be instructed about wearing properly fi tted footwear, daily inspection of feet and legs, avoidance of walking bare- foot, application of lotion on feet and legs, and meticulous toenail trimming. Podiatrist consultation is recommended for patients with fungal overgrowth and/or ingrown toe- nails. (Han, Sadarangani, & Wyatt, 2016; Moyer-Harris, 2015).

Pharmacological Treatment: Pharmacological treatment is pro- vided with conservative treatment. Currently, aspirin (81 to 325  mg daily) is one of the mainstays for such treatment. Aspirin has been shown to prevent progression of disease in patients with claudication. Cilostazol (Pletal) may be effective in relieving symptoms of claudication. The use of pentoxifyl- line (Trental) is also available for treatment of claudication; however, studies have not shown signifi cant improvement in claudication symptoms and cilostazol has superiority (Stevens et al., 2012). Vasodilators and anticoagulants have not proved effective in relieving pain symptoms. Clopidogrel (Plavix) 75  mg daily is an antiplatelet medication that helps reduce the risk of stroke, heart attack, and other atheroscle- rotic problems. Clopidogrel is frequently used for at least 3 months after peripheral arterial stents have been placed. Medications for the management of hypertension, diabetes, and hyperlipidemia should be used with the goals of euglyce- mia, normotension, and attainment of a healthy lipid profi le

(Iannito, Dickman, & Lakhani, 2014; Mackey & Whitaker, 2015; Moyer-Harris, 2015). Most patients with cardiovascu- lar disease benefi t signifi cantly from a statin, a beta blocker, an aspirin, daily multivitamins with B-complex vitamins, vitamin E, and calcium supplements ( Pomposelli et al., 2015 ; Sherrod, Sherrod, & Cheek, 2015 ).

Surgical Treatment: Surgical treatment of PAD involves revascularization of the affected extremity. Surgical options should be considered when pain limits the patient ’ s lifestyle or when ulceration or gangrene is present. Surgical options involve using vein graft or synthetic graft material. Long- term patency rate is dependent on smoking cessation, exer- cise, antiplatelet therapy, and vigilant diabetic control, as well as the location, length, and diameter of the graft.

Endovascular Treatment: Endovascular options for the treat- ment of PVD include balloon angioplasty and endoluminal stents, which are minimally invasive for the patient. Angio- plasty involves infl ating a balloon across a stenotic lesion. Stents are devices that are deployed in a stenotic lesion to keep the vessel open. Other interventions include thrombol- ysis with fi brin-degrading infusions, mechanical thrombec- tomy, atherectomy, and subintimal recanalization.

Follow-Up: Follow-up should include evaluating the patient ’ s response to pharmacological intervention and the progres- sion of risk factor modifi cation. Pulse volume recording should be done at least once a year to assess lower extremity perfusion.

Sequelae: A history of intermittent claudication approxi- mately doubles the risk of mortality resulting from ischemic heart disease. In patients with claudication, 25% develop worsening symptoms and 5% require an amputation over their lifetime. There appears to be differences in the presenta- tion of PAD in men versus women, however many of the risk factors and treatments are similar for both genders (Tomczyk & Treat-Jacobson, 2009).

Prevention/Prophylaxis: Prevention of PAD focuses on slowing the progression of disease in patients with symptoms. This can be accomplished through risk factor modifi cation, as dis- cussed earlier. Good foot care, in conjunction with exercise, smoking cessation, glucose management if diabetic, and lipid management can prevent the development of tissue loss or gangrene.

Referral: Referral for surgical or endovascular treatment should occur when claudication becomes disabling to the patient, when ischemic rest pain or gangrene is present, or when nonhealing ulceration is present.

Education: Education needs to focus on proper follow-up and the modifi cation of risk factors as discussed earlier; patients also need to be taught to report any new onset of symp- toms, including nonhealing ulcers. There is a need for more research on the differences between the treatment for PAD in men and in women (Cucato, Ritti-Dias, & Franco, 2016; Han, Sadarangani, & Wyatt, 2016; Dua & Lee, 2016 ).

Chapter 9 ■ Peripheral Vascular Disorders 221

Signal Symptoms: May be asymptomatic but could also present with swelling that subsides with elevation of lower extremi- ties, eczematous skin changes, dull ache in lower extremities, and presence of varicosities.

Description: Venous leg ulcers (also known as chronic venous insuffi ciency ulcers, venous stasis ulcers, lower extremity venous ulcers, or varicose ulcers) are the most common leg ulceration. They typically occur over the medial malleolus, but can also occur over the lateral malleolus. The ulcers are irregular and shallow with granulation tissue and fi brin present in the wound bed. Exudate is moderate to heavy, but if there is an arterial component, the amount of exudate may be decreased. These wounds often have a foul odor as well. The area around the wound often presents with dermatitis from the increased permeability of the venous capillaries causing protein to leak into the interstitial space, becoming irritating to the epidermis and dermis. The loss of protein and red blood cells into the subcutaneous tissue results in a brownish discoloration of the skin referred to as hemosiderin staining. Over time, the induration and hyperpigmentation is associated with fi brosis of the adipose tissue of the leg, which is called lipodermatosclerosis.

Etiology: Venous disease is caused by ambulatory venous hypertension. Normally, blood fl ows from the superfi cial veins to the deep veins. Unidirectional valves and contraction of the calf muscles assist in blood fl owing from the super- fi cial to the deep veins. If there are any abnormalities (i.e., valvular incompetence, deep vein thrombosis, and/or failure of calf muscle pump), the deep and superfi cial veins become distended, increasing venous pressures.

Occurrence: Venous ulcers are the most common leg ulcers, accounting for up to 90% of all leg ulcers (Ratliff, 2016). In the United States, it is estimated that approximately 2.5 million people have clinical symptoms of chronic venous insuffi ciency (Lal, 2015; O’Donnell et al., 2014). Venous leg ulcers are estimated to affect 4% of adults 65 years of age or older, or about 600,000 people in the United States (Lal, 2015).

Age: As one ages, the incidence of venous ulcers increases (Alavi et al., 2016).

Gender: Women are affected more than men, with multiple pregnancies or pregnancies close together increasing the risk.

Ethnicity: There are no data to support an ethnic predisposi- tion to venous disease.

Contributing Factors: Risk factors for venous leg ulcers include advanced age, obesity, pregnancy, thrombophilia, systemic infl ammation, anticardiolipin antibody, venous thromboem- bolism (VTE)/phlebitis, varicose veins, pulmonary embolus, sedentary lifestyle or occupation, reduced mobility, simul- taneous insuffi ciency of two out of three venous systems, trauma/surgeries/leg fractures, impaired calf muscle pump, restricted range of motion of the ankle, family history of venous disease, injection drug user, and previous leg wound (WOCN, 2013). The presence of comorbid conditions such as

heart failure, lymphedema, and orthopedic procedures can also increase the risk of venous leg ulcers (WOCN, 2013).

Signs and Symptoms: Edema that worsens with standing and decreases with leg elevation is the classic sign of venous leg ulcers. The edema may be pitting or nonpitting. Other signs include hemosiderosis (hemosiderin staining), venous derma- titis (manifested as erythematous, scaly, pruritic skin), ankle fl aring (cluster of spider veins), varicose veins, scarring from previous ulcers, and lipodermatosclerosis.

Diagnostic Tests: In many cases of venous ulcers, diagnosis may be made by clinical assessment alone, which includes skin changes in the leg, extent and location of edema, capil- lary refi ll less than 2 seconds, and palpation of pedal pulses. Duplex ultrasonography imaging with or without color has become the standard diagnostic tool for assessing venous disease. Duplex imaging produces images of blood fl ow and its direction through vessels, pinpointing the anatomical site of refl ux or obstruction; thickened, abnormal vein walls; and the presence and age of a thrombus. Duplex scanning can be used to calculate the superfi cial venous pressures and allows for quantifi cation of venous refl ux and valve closure times. An ankle-brachial pressure index is also recommended to rule out signifi cant arterial disease, especially before applica- tion of compression therapy.

Differential Diagnosis: Lower leg edema, which is one of the classic signs of venous disease, is also seen with other dis- eases as well. Deep vein thrombosis usually presents with pain and the presence of a thrombus on ultrasound. Patients with heart failure usually present with dyspnea, orthopnea, and a decreased ejection fraction. Patients with cirrhosis will have abnormal liver functions, and those in renal failure will have proteinuria. The diagnosis of venous disease can be nar- rowed by categorizing the edema according to its duration (acute or chronic), distribution (unilateral or bilateral), and accompanying symptoms (e.g., pain, itching, skin changes).

Treatment: Treatment for venous ulcers includes manage- ment with compression therapy, leg elevation, medications, and surgery.

Conservative Treatment: Compression therapy is the gold standard for venous ulcers and is used by those with chronic venous disease to manage the edema and increase venous return. Compression has been shown to improve healing of venous ulcers when compared to no compression (O’Don- nell et al., 2014; O’Meara et al., 2012 ), as well as reducing venous ulcer recurrence (Ratliff, 2016; Mauck et al., 2014 ; O’Donnell et al., 2014). Compression is also effective in the improvement of symptoms of chronic venous disease, reduc- tion of edema and pain, and improvement of quality of life (Sippel, Seifert, & Hafner, 2015).

Compression can be achieved with the use of a single layer wrap (bandage) or the use of multiple layer wraps (bandages) ( Mauck et al., 2014 ). There are also compression garments such as the reusable Velcro wraps like CircAid ® , sleeves like tube-shaped Tubigrip™, compression stockings, and inter- mittent pneumatic compression pumps (Ratliff, 2016).

VENOUS DISEASE (CHRONIC VENOUS INSUFFICIENCY)

222 Chapter 9 ■ Peripheral Vascular Disorders

Another feature of compression products is based on the type of material in the wrap (bandage). Elastic (adapts to changes in limb size) should be prescribed for those who are sedentary, versus inelastic (will not change with limb size), which should be prescribed for those who frequently ambu- late. For patients with mixed venous and arterial disease (ankle-brachial index of greater than 0.5 to 0.8), a trial of supervised modifi ed light compression up to 30  mm  Hg may help decrease edema and promote ulcer healing (Ratliff, 2016). Leg elevation above the heart for 30 minutes three or four times per day when used with compression can also help reduce edema (Robinson & Melo, 2014).

Pharmacological Treatment: Horse chestnut seed extract (HCSE) in a dose of 300  mg twice daily may reduce edema and pain in venous leg ulcers (Pittler & Ernst, 2012). People with bleeding disorders, kidney disease, or liver disease should not take HSCE. There may also be interactions with certain medications, such as lithium, diabetic drugs, and anticoagu- lants, that might result in low blood sugars and slower blood clotting (WebMD, 2016). Aspirin may be effective when used with compression therapy with the recommended dosage of 300  mg per day, as long as there are no contraindications to its use (Kimmel & Robin, 2013). Pentoxifylline (Trental) 400  mg three times per day has been used to treat venous ulcers. It has been shown effective when used with compres- sion and may be benefi cial as monotherapy in those patients who cannot tolerate compression (Jull et al., 2012). Topical steroids may provide short-term improvement of venous der- matitis. Oral antibiotics are only warranted in cases of sus- pected cellulitis (Carmel & Bryant, 2016).

Surgical Treatment: Surgery should be considered when topical therapy and compression are not able to heal the venous ulcer. Surgical options to treat venous disease include interruption of the perforating veins with subfascial endo- scopic perforator surgery (SEPS), laser ablation, radiofre- quency ablation (RFA), and sclerotherapy (Carmel & Bryant,

2016; Robinson & Melo, 2014). Surgical procedures available for valvular incompetence include artifi cial valve insertion, direct valvuloplasty, and autogenous vein valve transplanta- tion (Carmel & Bryant, 2016). Skin grafts and bioengineered human skin equivalents may be used for those with large or refractory venous ulcers, but they must be used in conjunc- tion with compression therapy to improve healing (Carmel & Bryant, 2016).

Follow-Up: The goals of care are to reduce edema, promote ulcer healing, and prevent reoccurrence of the ulcer (Robin- son & Melo, 2014).

Sequelae: Compliance with compression, ulcer size, and dura- tion of the ulcer affect ulcer healing. Ulcers larger than 5 cm 2 and present for more than 6 months are predictive for non- healing, so early assessment and treatment with compression therapy is important to reduce complications such as infec- tion from nonhealing ulcers (Carmel & Bryant, 2016).

Prevention/Prophylaxis: The daily use of compression therapy for the rest of one ’ s life is recommended to promote healing and reduce the chance of reoccurrence.

Referral: Patients with venous leg ulcer disease with impaired calf muscle pump function may benefi t from physical therapy that includes fl exion and extension exercises, as well as walking programs to improve calf muscle pump function (Robinson & Melo, 2014).

Education: Patients with venous ulcer disease should be instructed to use compression stockings every day for the rest of their lives and replace these compression stockings at least every 6 months. They should elevate the affected leg or legs above the heart several times a day. Physical activity is recommended to increase venous return and should be per- formed based on the patient ’ s medical condition, but may include ankle fl exion exercises, brisk walking, and sitting in a rocking chair and using the feet to push down to plantar fl ex the ankles.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Smoking cessation, dietary management, exercise, and diabetic management are key treatments to slow the progression of peripheral arterial disease.

A Zakhari, 2013 Arens, White, & Masengill, 2014 Cucato, Ritti-Dias, & Franco, 2016 Iannito, Dickman, & Lakhani, 2014 Mackey & Whitaker, 2015 Conte et al., 2015 Dua & Lee ( 2016 )

Hypertension treatment is an essential treatment for patients with known abdominal aortic aneurysms.

A Scher, Drew, & Cottrell, 2015 Gordon & Toursarkissian, 2014

Patients with known abdominal aortic aneurysms should receive periodic ultrasound, magnetic resonance imaging, or CT-guided images at least once a year.

A Sodem, Zetterwal, & Ultee, 2016 Strider, Keeling, & Tullmann, 2013 Cooper, 2014

Chapter 9 ■ Peripheral Vascular Disorders 223

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Endovascular grafts for complex aortic aneurysms permit a lower perioperative risk profi le than does the open surgical procedure for such patients. After the procedure, nursing profi ciency with aortic endograft is key to the patient ’ s safe postoperative progression.

A Buck, Ultee, & Zetterwall, 2016 Sodem, Zetterwall, & Ultee, 2016 Cooper, 2014 Schermerhorn, Buck, & O’Malley, 2015

Compression improves healing of venous leg ulcers compared to no compression.

A O’Meara et al., 2012 Mauck et al., 2014

Compression stockings reduce the chance of venous ulcer recurrence when compared with no compression.

A Mauck et al., 2014

Manual lymph drainage may offer an additional benefi t to compression bandaging for swelling reduction in breast cancer-related lymphedema.

A Ezzo et al., 2015

Clinicians should prescribe one or more of the following for patients diagnosed with peripheral arterial disease: aspirin, beta blocker, statin agent.

B Iannito, Dickman, & Lakhani, 2014 Mackey & Whitaker, 2015 Conte et al., 2015 Sherrod, Sherrod, & Cheek, 2015 Dua & Lee, 2016 Lewis, Dindyal, & Raynor, 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml.

C A S E S T U DY

M. J. is a 76-year-old woman who lives on the side of a very steep mountain. The home health nurse has visited her once a week for the last year. She has running water, electricity, and a coal stove with back-up oil heat for very cold winter nights. She uses the telephone for communication. She has diabetes mellitus, hypertension, hypothyroidism, and is in atrial fi brillation. She has never been in the hospital before.

Her current medications include metformin (250 mg twice a day), losartan (50 mg/day), levothyroxine sodium (Synthroid) (50 mcg/day), digoxin (0.125 mg/ day), furosemide (Lasix) (10 mg/day), aspirin (81 mg/ day), simvastatin (20 mg/day), and warfarin (Coumadin) (4 mg/day, with 6 mg on Sundays). Allergies are to penicillin (hives) and to metoprolol (hypotension and dizziness). M. J. stopped smoking 5 years ago, but until then she smoked one-half pack a day.

Last laboratory test results (1 week ago) were: hemoglobin A1C (Hgb A1C) 8.3, international normalized ratio (INR) 1.7, sodium 129, potassium 5.8, chloride 102, CO 2 20, blood urea nitrogen (BUN) 45, creatinine 1.5,

glucose 289, white blood cell (WBC) count 6.8, Hgb 10.1, hematocrit 30.2, platelets 215,000.

The home health nurse calls you from the patient ’ s house, where she notes that the patient had a 5-minute spell of visual loss in her right eye. It has not recurred. During this period, M. J. noted that her left hand and left leg felt “funny,” and her left foot and leg were so weak that she could not walk.

M. J. has a heart murmur, described by the home health nurse as loudest over the right sternal border and more prominent in the systolic phase. Furthermore, the home health nurse tells you that she hears bruits on both sides of the neck, with the right being louder than the left. The blood pressure in the right arm is 135/72 mm Hg and 110/66 mm Hg in the left arm. Heart rate is irregular at 75 to 90 beats per minute. The left hand and fi ngers have always been cooler than the right. Lungs are remarkable for wheezes. The patient has no fever. Oxygen saturations at room temperature are 90% to 92%, which has been her baseline.

Continued

224 Chapter 9 ■ Peripheral Vascular Disorders

REFERENCES Arens , C. R. , White , T. L. , & Masengill , N. ( 2014 ). Attitudinal factors pro-

tective against youth smoking . Journal of Nursing Scholarship , 46 ( 3 ), 167 – 175 .

Buck , D. , Ultee , K. , Zetterwall , S. , Soden , P. A. , Darling , J. , Wyers , M. , . . . Schermerhorn , M. L. ( 2016 ). Transperitoneal vs. retroperito- neal approach for open abdominal aortic aneurysm repair . Journal of Vascular Surgery , 64 ( 3 ), 585 – 591 .

Conte , M. S. , Pomposelli , F. B. , Clair , D. G. , Geraghty , P. J. , McKinsey , J. F. , Mills , J. L. , . . . Sidawy , A. N. ( 2015 ). Society for Vascular Surgery guidelines for atherosclerotic occlusive disease of the lower extremi- ties: Management of asymptomatic disease and claudication . Journal of Vascular Surgery , 61 , 2s – 41s .

Cooper , A. ( 2014 ). Cochrane review summarizing the endovascular repair of abdominal aortic aneurysms . Critical Care Nurse , 34 ( 4 ), 87 – 92 .

Cucato , G. G. , Ritti-Dias , R. M. , Franco , F. B. , De Mattos , L. D. , Cendoro- glo , M. S. , . . . de Carvalho , J. A. ( 2016 ). Infl uence of peripheral arterial disease on daily living activities in elderly women . Journal of Vascular Nursing , 34 , 39 – 43 .

Dua , A. , & Lee , C. J. ( 2016 ). Epidemiology of peripheral arterial disease and critical limb ischemia . Techniques in Vascular and Interventional Radiology , 19 ( 2 ), 91 – 95 .

Ezzo , J. , Manheimer , E. , McNeely , M. L. , Howell , D. M. , Weiss , R. , Johans- son , K. I. , . . . Karadibak D. ( 2015 ). Manual lymphatic drainage for lymphedema following breast cancer treatment . Cochrane Database of Systematic Reviews , ( 5 ), CD003475 . doi:10.1002/14651858. CD003475.pub2 .

Gordon , P. , & Toursarkissian , B. ( 2014 ). Care of the patient with abdom- inal aortic aneurysm . Association of periOperative Registered Nurses Journal , 11 ( 2 ), 241 – 259 .

Iannito , J. M. , Dickman , K. , Lakhani , R. H. , & So , M. J. ( 2014 ). Telehealth insulin program: Managing insulin in primary care . Journal for Nurse Practitioners , 10 ( 8 ), 567 – 573 .

Lewis , J. , Dindyal , S. , & Raynor , H. ( 2016 ). A “preamputation care pathway” reduces mortality for lower limb amputation . Journal of Vas- cular Nursing , 34 , 54 – 58 .

Mackey , P. , & Whitaker , M. ( 2015 ). Diabetes mellitus and hyperglycemia management in the hospitalized patient . Journal for Nurse Practitioners , 11 ( 5 ), 531 – 537 .

Mauck , K. F. , Asi , N. , Elraiyah , T. A. , Undavalli , C. , Nabhan , M. , Altayar , O. , . . . Murad , M. H. ( 2014 ). Comparative systematic review and meta-analysis of  compression modalities for the promotion of venous ulcer healing and reducing ulcer recurrence . Journal of Vascular Surgery , 60 ( 2S ), 71S – 90S.e2 . doi:10.1016/j.jvs.2014.04.060 .

O’Meara , S. , Cullum , N. , Nelson , E.A. , & Dumville , J. C. ( 2012 ). Com- pression for venous leg ulcers . Cochrane Database of Systematic Reviews , ( 11 ), CD000265 . doi:10.1002/14651858.cd000265.pub3 .

Scher , H. E. , Drew , M. L. , & Cottrell , D. M. ( 2015 ). Treatment of resistant hypertension in the patient with chronic kidney disease . Journal for Nurse Practitioners , 11 ( 6 ), 597 – 604 .

Schermerhorn , M. , Buck , D. , O’Malley , A. , Curran , T. , McCallum , J. , Darling , J. , & Landon , B. ( 2015 ). Long term outcomes of abdominal aortic aneurysm in the Medicare population . New England Journal of Medicine , 373 ( 4 ), 328 – 338 .

Sherrod , M. M. , Sherrod , N. M. , & Cheek , D. J. ( 2015 ). Reducing cardio- vascular risk with statins . Nursing , 45 ( 6 ), 41 – 46 .

Sodem , P. , Zetterwall , S. L. , & Ultee , K. ( 2016 ). Outcomes of a symp- tomatic abdominal aortic aneurysm population . Journal of Vascular Surgery , 64 ( 2 ), 297 – 305 .

Strider , D. , Keeling , A. , Tullmann , D. , Reigle , J. , & Cherry , K. J. ( 2013 ). Marfan syndrome teaching algorithm . Journal of Vascular Nursing , 31 , 1 – 11 .

Zakhari , R. ( 2013 ). Smoking: Harm reduction versus abstinence . Journal of the American Academy of Nurse Practitioners , 25 ( 1 ), 1 – 2 .

1. What concerns do you have regarding M. J. at this point?

2. Do you need to see M. J. fairly soon, or can she come to see you at her regularly scheduled appointment in 3 weeks?

3. If you were to see M. J. in the next 24 hours, what additional tests would you perform?

4. Based on the laboratory results given, what changes would you make in her medication profi le?

5. Which arm will you use for blood pressure recordings in the future?

6. What systolic blood pressure range would you order for M. J., as a general target?

7. If M. J. has a repeat episode of right eye blindness, lasting 30 minutes this time, what would you do?

C A S E S T U DY — cont’d

225

CHAPTER 10 Abdominal Disorders

Laurie Kennedy-Malone

ASSESSMENT

Accurate history taking of abdominal complaints is essential for completing an assessment of the older adult. The physical examination is often unremarkable, and laboratory fi ndings may not provide diagnostic information because the presen- tation of illness in an older adult is usually subdued.

Gathering the Abdominal History Generally, the chief complaints of abdominal conditions can be categorized into symptom cluster areas for further explo- ration: abdominal pain/discomfort, gastroesophageal refl ux disease (GERD)/regurgitation symptoms, nausea/vomiting, diarrhea/incontinence, and diffi cult defecation and constipa- tion (Crowell et al., 2015; Koloski et al., 2017). Explore with the patient any episodes of anorexia, dyspepsia, dysphagia, heartburn, nausea, regurgitation, vomiting, painful or diffi - cult defecation, diarrhea, tenesmus, or constipation. Deter- mine the sequence of events that triggered each symptom. Inquire about precipitating factors such as a meal, position of the body, use of caffeine, alcohol use, or smoking. Were any other symptoms present that can be clustered to form a differential diagnosis? It is important to discern from patients what therapeutic measures they have initiated to alleviate the symptoms (Saccomano & Ferrara, 2013). Determine if the treatment is a previously prescribed regimen, an over- the-counter (OTC) medication, an herbal product, or a home remedy. Ask the patient when the last time a fecal occult blood test was performed and if he or she has had a recent colonoscopy or sigmoidoscopy examination.

Abdominal Symptoms Although abdominal pain is a common acute problem with which patients present to their health-care providers, older adults may not experience the typical symptoms of abdomi- nal disorders that younger patients report. If patients present with abdominal pain, it is important to discern the charac- teristic of the pain. How quickly did the pain begin? Was the pain abrupt? Is the pain progressive or intermittent? Has the patient ever experienced this type of pain before and, if so, what was the diagnosis and treatment? Has the patient noted

any improvements with self-treatment, positioning, vomiting, or defecation? What is the referral pattern? Is the pain worse at night or during the day? Is it relieved or aggravated by food? If the patient reports triggers to abdominal pain by food, ask more specifi c questions pertaining to food to discern if the patient is having a specifi c food intolerance(s) or possible food poisoning. Does the patient have any associated symptoms of regurgitation, refl ux, cough, nausea, vomiting, constipation, or diarrhea? You can ask about the severity of pain by asking the patient to rate the pain on a scale from 1–10, however, realizing that in older adults pain may be blunted despite the underlying pathology (Saccomano & Ferrara, 2013). Gather a history of previous abdominal surgeries. Inquire about alcohol use or drug abuse. Inquire about any history of jaun- dice, heart disease, or peripheral vascular disease. Review all current medications (Spirit, 2010).

Inspection The physical examination of the abdomen begins with inspection, checking for overall symmetry while observing the patient lying down. The practitioner can consider the abdomen to be divided into four quadrants, visualizing an imaginary vertical line from the sternum to the pubis passing though the umbilicus and a horizontal line drawn through the umbilicus. In addition to being familiar with the under- lying organ systems and referred pain in the four quadrants, the nurse practitioner should be familiar with other anatom- ical landmarks, such as epigastric, periumbilical, suprapubic, and McBurney ’ s point, which is one-third of the distance from the right anterior superior iliac spine to the umbilicus (Rabinowitz & Roberts, 2015).

Carefully examine for scars, lesions, dilated veins, or other marks. If surgical scars are detected, review with patient surgical history if not recorded. Determine if the abdomen is concave or protuberant. Is an umbilical, abdominal wall, inci- sional, or inguinal hernia present? If a hernia is suspected, have the patient raise the head and note if there is presence of a bulge. (O’Laughlen, 2009). Is a lift noticeable? Is there abdominal distention? If so, is the distention local or general- ized? Causes of generalized distention include abdominal fat, peritoneal fl uid, or gaseous distention, whereas local disten- tion often is indicative of obstruction, or organ or structural enlargement. Examine the umbilicus. Signs of ascites include

226 Chapter 10 ■ Abdominal Disorders

a fl at or everted umbilicus (Williams, 2008). Check for any bulging in the fl anks as a sign of ascites.

Examine the skin of the abdomen for color, noting if there is any jaundice found in liver disease or biliary tract obstruc- tion, bruising, or telangiectasias (O’Laughlen, 2009). If a bluish discoloration is detected around the umbilicus this is known as Cullens’ sign, which is often found in patients with bleeding in the peritoneum. If the bluish discoloration is on the fl anks, this is known as Grey Turner ’ s sign and is often indicative of retroperitoneal bleeding, as in pancreati- tis (Rabinowitz & Roberts, 2015). Jaundice in the area of the umbilicus is known as Ransohoff ’ s sign and is a result of a ruptured common bile duct (Williams, 2008). Note if there are any pulsatile movements across the abdomen. If present, this sign may be indicative of a vascular aneurysm or a wide arterial pulse pressure (Williams, 2008). Visible intestinal peristalsis may be indicative of bowel obstruction (Rabino- witz & Roberts, 2015).

Auscultation Auscultations follow inspection of the abdomen. Using the diaphragm, place the stethoscope lightly against the skin. Listen for bowel sounds, vascular bruits, and rubs. Bowel sounds are produced by peristalsis. A murmur heard in the abdomen may be an aortic aneurysm. A constant systolic- diastolic bruit may occur when the patient has an arterio- venous fi stula in the renal vessels. Other sites to auscultate for bruits during abdominal examination include the iliac arteries and the femoral arteries.

When auscultating bowel sounds, take the time to listen for presence of bowel sounds. Generally, people who are hungry have active bowel sounds. Bowel sounds described as high pitched, rumbling, or tinkling are known as borborygmi. A rushing sound is associated with bowel obstruction. If bowel sounds are absent, listen for 5 minutes. Suspect peritonitis, mesenteric thrombosis, or advanced intestinal obstructions when bowel sounds are absent (O’Laughlen, 2009). Listen for a loud succussion splash over the abdomen of a patient in whom you suspect a gastric obstruction or dilations (Wil- liams, 2008). Nurse practitioners should not, however, rely on auscultation alone for diagnostic purposes, as studies have refuted the usefulness of auscultation when differentiating patients who have normal versus pathological bowel sounds (Felder, Margel, Murrell, & Fleshner, 2014).

Percussion Percussion of the abdomen is performed to determine the density of tissue of the abdominal organs by the sounds emitted when tapped (LeBlond, Brown, Suneja, & Szot, 2015).

It is normal to hear tympanic sounds over the stomach, whereas dullness is expected over a distended bladder, the liver, and the spleen (O’Laughlen, 2009). Dullness noted over other areas of the abdomen is a deviation from the norm. Defi nitive percussion is used to ascertain the size and shape of the liver and spleen. Because the liver decreases in size starting at about age 50 years, the normal range of the liver size in an older person is 6 to 12 cm (Williams, 2008).

Palpation Perform light palpation to discern abdominal masses; enlarged organs such as liver, spleen, and kidneys; and areas of tenderness. If a mass is detected, the nurse practitioner needs to determine if the mass is intra-abdominal or within the abdominal wall. Using the palm and extended fi ngers of the right hand, press about 21  cm deep. If a patient has complained of abdominal pain, always palpate in a quadrant away from the identifi ed location. (Rabinowitz & Roberts, 2015).

Once you discover the tender area, maintain pressure over the area to determine the consistency of the pain. If the pain diminishes despite the applied pressure to the area, infl am- mation is unlikely. If you suspect intra-abdominal tender- ness, proceed to deep palpation. Check for referred rebound tenderness by applying pressure with the tips of the fi ngers to a site distant from the areas of questionable tenderness, and then quickly remove them from the abdomen (Saccomano & Ferrara, 2013). Assessment of the patient ’ s facial expression is warranted, especially in older adults with diffi culty with communication (O’Laughlen, 2009). If tenderness is elic- ited remote from the areas palpated after release of pressure, consider peritoneal irritation (LeBlond et al., 2015). Spe- cifi c maneuvers to detect tenderness can lead the examiner to making a differential diagnosis; for instance, tenderness medial to McBurney ’ s point (Rabinowitz & Roberts, 2015) suggesting a Meckel diverticulum should be distinguished from typical appendicitis tenderness. A mass detected in the lower abdomen on palpation warrants further rectal and/or pelvic examination.

Palpation of the kidneys should include checking for costovertebral angle tenderness, which is often indicative of renal disease, but also may be musculoskeletal in origin (O’Laughlen, 2009). While the bladder is not normally pal- pable, it may be detected on palpation if bladder distention is suspected. Rectal examination includes determining presence or absence of stool, checking for presence of hemorrhoids, and testing sphincter tone and guaiac. Ask the patient to strain gently as if having a bowel movement to relax the anal sphincter.

ACUTE KIDNEY INJURY

Signal Symptoms: Fatigue, altered mental status, anorexia, shortness of breath.

Description: Acute kidney injury (AKI), previously known as acute renal failure (ARF), is defi ned as the abrupt loss of kidney function over a period of hours to days ( Palev- sky, 2012 ). This can be either a minimal loss without any

residual effects, with the patient ’ s renal function returning to previous baseline before the injury, or can result in chronic kidney disease (CKD). In addition, any episode of AKI will increase the risk for CKD later in life. AKI has now been clas- sifi ed as one of a number of acute kidney diseases and dis- orders (AKDs), and can occur with or without other acute/ chronic kidney diseases (KDIGO, 2012).

Chapter 10 ■ Abdominal Disorders 227

Etiology: Renal function with urine formation is based on four steps that occur in specifi c areas of the kidney. First, blood from the renal arteries is delivered to the glomeruli and fi ltered, resulting in an ultrafi ltrate. The ultrafi ltrate, free of protein and blood elements, then fl ows into the renal tubules, which reabsorb and secrete solute and/or water from the ultrafi ltrate. The fi nal tubular fl uid, urine, leaves the kidney, draining through the renal pelvis and ureter and into the bladder, leaving the body through the urethra. Any disrup- tion in the process of urine formation can result in the deteri- oration of renal function and AKI.

AKI is defi ned as an increase in serum creatinine by 50% within 7 days or an increase in serum creatinine by 0.3 mg/ dl in 2 days or urine volume of less than 0.5  ml/kg/hr for 6 hours (KDIGO, 2012). Serum creatinine is a by-product of muscle metabolism that is excreted unchanged by the kidneys. Assessment of renal function is made by estima- tion of the glomerular fi ltration rate (eGFR) (KDIGO, 2012). Serum creatinine alone should not be used to determine renal function (Levey, 2015). eGFR is the most widely accepted and most useful overall index of kidney function (KDIGO, 2012). Changes in serum creatinine and urine output are indicators of a change in eGFR. Normal eGFR varies accord- ing to age, sex, and body size. In young adults, it is 120 to 130  mL/min and declines with age starting after 40 years. AKI can occur before a change in the serum creatinine or urine output is noted. eGFR is best calculated using the 2009 Chronic Kidney Disease Epidemiology Collaboration (CKD- EPI) (KDIGO, 2012).

The formula is as follows:

eGFR S S

if Cr Cr

Age= × × × ×

−141 1 1 0 993

1 018

1 209min( , ) max( , ) .

. [

.κ κα

ffemale if African American] . [ ]×1 159

eGFR is less accurate in patients who have AKI due to the rapid changes in kidney function. Patients who have extremes of muscle mass, such as the frail older adult, the critically ill, cancer patients, body builders, or those with unusual diets, will also have inaccurate eGFR. Creatinine clearance, where urine is collected over 24 hours and the amount of creati- nine is measured, is a more accurate indicator of the eGFR in these patients.

The causes of AKI can be grouped into three categories:

■ Prerenal, caused by reduced renal perfusion ■ Intrinsic, in which there is damage to the renal

parenchyma ■ Postrenal, where there is obstruction to the fl ow of

urine

Furthermore, AKI can be characterized as:

■ Oliguric, which is less than 400 mL urine output in 24 hours

■ Nonoliguric, which is greater than 400  mL urine output in 24 hours

■ Anuric, which is less than 100  mL urine output in 24 hours (Safi rstein, 2005)

Anuria is uncommon and may be caused by complete obstruction or a major vascular event such as aortic dissec- tion or ruptured aortic aneurysm in AKI. Prerenal, intrin- sic, and postrenal all present clinically with either oliguria or nonoliguria. A nonoliguric state is associated with much better renal prognosis and recovery of renal function.

Occurrence: Although risk for AKI increases with age, it can occur at any age or ethnicity.

Age: Although AKI can occur at any age, its incidence is highly associated with older adults, and risk increases across the age span, most notably in those age 85 years and older (Silver et al., 2015; USRDS, 2015).

Gender: Across age groups, a higher percentage of men are affected by AKI than women (USRDS, 2015).

Ethnicity: The rates of diagnosing AKI across all ethnic groups has doubled since 2013 (USRDS, 2015).

Contributing Factors: A prior history of CKD and/or diabetes mellitus increases the risk for an AKI event (USRDS, 2015). AKI can also be caused by volume depletion, certain medica- tions, cardiac issues, major surgery, trauma, sepsis, poison- ous plants, and animals. After sustaining a severe burn, it is very common to develop AKI (Wu et al., 2016).

Use of radioopague dye can induce AKI, which is also known as contrast-inducted nephropathy (Zuo et al., 2016). Factors that predispose the patient to vascular disease and a detailed history of hypertension, diabetes mellitus, smoking, hyperlipidemia, claudication, stroke, myocardial infarction, and atrial fi brillation should be noted. Patients with atrial fi brillation may develop acute renal infarction as the precur- sor to AKI (Yousuf et al., 2016).

In prerenal AKI, any condition in which there is volume depletion can lead to renal hypoperfusion, including vomit- ing, diarrhea, hemorrhage (either surgical or gastrointestinal [GI]), excessive diuresis, and burns. Volume depletion and decreased cardiac output are the main causes of prerenal AKI. Sepsis, hypoxemia, anaphylactic shock, pancreatic disease, and liver disease may also cause AKI. In addition, any condition that affects the renal vascular system, such as renal artery stenosis, renal vein thrombosis, hepato- renal syndrome, NSAIDs, and angiotensin-converting enzyme (ACE) inhibitors/angiotensin blockers, also can induce AKI.

Conditions that cause intrinsic AKI are focused on the area of the kidney that is damaged. These include the glom- eruli, tubules, and interstitium. The most common cause of damage to the structures of the kidney is prolonged hypo- perfusion and nephrotoxins such as radiopaque contrast agents or certain medications. Vascular damage to the kidney from ischemia or vasculitis leads to glomerular AKI. Systemic lupus erythematosus, antineutrophil cytoplasmic antibody (ANCA)-associated granulomatous polyangiitis, Goodpas- ture ’ s syndrome, cryoglobulinemia, postinfectious glomeru- lonephritis, polyarterisnodosa, hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP) hep- atitis B virus, and HIV are all conditions that can lead to the development of glomerular AKI. Tubules of the kidney may be damaged by ischemia, cellular edema, or interstitial edema, or become obstructed by cellular debris. AKI in this area of the kidney is called acute tubular necrosis (ATN). Any severe and prolonged prerenal cause of AKI will cause ATN. In addition, cyclosporine, tacrolimus, amphotericin B, aminoglycosides, ethylene glycol, radiopaque contrast agents, high-dose vitamin C, and Fleet ’ s Phosphosoda (a commonly used bowel prep) can lead to ATN. Rhabdomyolysis causes tubular damage by accumulation of a greater quantity of myoglobulin than can be fi ltered by the kidney. Interstitial

228 Chapter 10 ■ Abdominal Disorders

infl ammation or nephritis is usually caused by an immu- nological or allergic reaction and can be caused by certain medications.

Postrenal causes of AKI include any condition in which there is an impediment of the excretion of urine anywhere from the collecting tubules to the urethra. In the tubules, crystal or protein particles can precipitate, causing obstruc- tion. This is associated with tumor lysis, myeloma, and calcium oxalate from ethylene glycol (antifreeze) ingestion and rhabdomyolysis. Ureteral obstruction can be caused by calculi, clots, fungus balls, tumors, or trauma. Bladder obstruction, either mechanical or chemical, will also cause postrenal AKI. Prostatic disease, either hypertrophy or cancer, is the most common type of postrenal AKI.

Signs and Symptoms: Predominant symptoms are usually those of the underlying illness or injury, which then leads to AKI. The patient may have symptoms directly resulting from alterations in kidney function, such as decreased to no urine output, fl ank pain, edema, or hypertension. The patient may have noticed a change in his or her urine consistency or color, such as foamy urine, which indicates proteinuria, or dark brown/red urine that could be indicative of red blood cells (RBCs). Patients may have nausea, vomiting, and diarrhea, leading to volume depletion. Specifi c questions regarding use of medications that can cause renal injury, including NSAIDs and antihypertensive medications such as ACE inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), as well as recent antibiotic use, need to be asked of the patient. Factors that predispose the patient to vascular disease and a detailed history of hypertension, diabetes mellitus, smoking, hyper- lipidemia, claudication, stroke, myocardial infarction, and atrial fi brillation should be noted. In addition, ask patients whether they have experienced any fatigue, arthritis, weight loss, cough, hemoptysis, arthralgias, or sinus symptoms, which may indicate a systemic illness, such as vasculitis or systemic lupus erythematosus. Use of illicit drugs, such as cocaine, ecstasy, and heroin, can also cause AKI. In addition, ask about any past history of drug use, tattoos, and piercings, which increase the risk for hepatitis B, hepatitis C, and HIV and can cause glomerular disease.

Use of radiopaque dye can also induce AKI, which is known as contrast-inducted nephropathy (Zuo et al., 2016). Past history of cancer, specifi cally prostate, cervical, or bladder cancer, may be indicative of an obstruction. Any family history of kidney disease increases the risk of a patient developing kidney disease in his or her lifetime as well. Patients with signs and symptoms of renal failure such as weakness, easy fatigability, anorexia, altered mental status, weight loss, dysgeusia, nausea, cold intolerance, neuropathy, tremor, asterixis, seizures, and uremic fetor, where the patient has an ammonia-like or urine-like odor to the breath, may be suffering from end-stage renal disease (ESRD) and need hos- pital admittance for further evaluation.

Physical examination includes assessment of weight, orthostatic blood pressures, mucous membranes, and skin turgor and neck veins for the presence of volume depletion or overload. A funduscopic examination positive for atrioventric- ular nicking, exudates, or arterial narrowing is indicative of hypertension. Cardiac examination may reveal an S 3 , indic- ative of volume overload or congestive heart failure, and the presence of a pericardial rub may indicate pericarditis, a late

fi nding in ESRD. Lung assessment may reveal tachypnea and rales. Skin assessment should include inspection for any rash, skin lesions, livedo reticularis, or purpura that may indicate vasculitis or autoimmune disease. Periorbital, lower extrem- ity or pretibial, and presacral edema can indicate advancing renal disease from any cause. Abdominal assessment should include auscultation for renal or abdominal bruits, as well as evaluation for abdominal masses, costovertebral angle ten- derness, and bladder distention. Assess for asterixis, a tremor of the wrist when it is extended, often seen in patients with ESRD.

Diagnostic Tests: Urinalysis is a noninvasive tool that can provide information regarding AKI. Urine is analyzed for sed- iment, specifi c gravity, urine sodium, urine protein, and urine creatinine levels. The appearance of certain urinary casts are cylindrical particles associated with certain diseases, assist- ing in determination of the cause of the AKI. Specifi c gravity refl ects the ability of the kidney to concentrate urine and can refl ect a patient ’ s volume status. Patients who have impaired urine concentrating ability, such as those with ATN, will have low specifi c gravity. Urine sodium can assist in differentiating between ATN and volume depletion but can be falsely ele- vated in patients on diuretics. Further laboratory tests may show hyperkalemia, hypocalcemia, hyponatremia, and aci- dosis. A complete blood count (CBC) should also be drawn to evaluate for leukocytosis and anemia.

Radiographic studies are performed to assist in the diag- nosis and cause of AKI. Renal ultrasound is most common and can be used to assess kidney size, obstruction, and the presence of masses. In AKI, kidneys will be of normal size, as compared to CKD, where they are small. If masses are noted on the kidneys with ultrasound, an abdominal com- puted tomography (CT) scan will help to identify the lesion. Renal biopsy is only performed when laboratory data have been unrevealing and no reversible causes could be identi- fi ed as to the cause of AKI. It is performed percutaneously, and the most common complication is bleeding. Assess- ment of the patient ’ s activated partial thromboplastin time (aPTT), prothrombin time (PT)/international normalized ratio (INR), and platelet count must be performed before the kidney biopsy. Renal biopsy is avoided in patients who have a “solitary” kidney, either from congenital absence or acquired absence, such as nephrectomy for renal cell carcinoma.

Differential Diagnosis:

■ Hypovolemia ■ Low cardiac output ■ Sepsis ■ Glomerulonephritis ■ Ischemic nephritis ■ Hyperkalemia ■ Urethral obstruction ■ CKD (Rahman, Shad & Smith, 2012).

Treatment: Treatment is indicative of the cause of AKI. In volume depletion, fl uid resuscitation with isotonic saline and/or packed RBCs to reestablish circulating volume, as well as use of vasopressors to maintain blood pressure, may be needed. Withdrawal of the offending medication and avoid- ance of other nephrotoxic agents are of the utmost impor- tance. Dose adjustment of renally metabolized medications is needed as well. Antihypertensive medications should be

Chapter 10 ■ Abdominal Disorders 229

judiciously titrated to avoid any further renal hypoperfusion. In obstructive AKI, treatment of the obstruction often results in renal recovery. Usually, rapid correction of prerenal and postrenal causes leads to full recovery of kidney function. Avoidance of exogenous sources of potassium, such as nutri- tional supplementation and IV fl uids, should be discontin- ued. Treatment of hyperkalemia includes administration of IV calcium gluconate, insulin, beta-2 agonists (albuterol), dextrose, and occasionally kayexalate. Hyperphosphatemia may also occur in AKI, and calcium acetate or calcium car- bonate can be used to reduce absorption of phosphorus from the GI tract. Platelets are often dysfunctional in AKI and may require use of DDAVP to activate platelets. Due to lower levels of circulating erythropoietin and decreased bone marrow responsiveness, anemia is often found in AKI, requiring transfusion of RBCs to increase oxygen-carrying capacity to the kidney.

In the event that there is no recovery in kidney function after correction of the cause of the AKI, hemodialysis may need to be initiated. This is especially important in the face of continued acid-base disturbances, electrolyte abnormali- ties, volume overload, and uremia. Studies have found that early initiation of renal replacement therapy for patients with severe AKI reduced overall mortality during the fi rst 90 days after diagnosis (Zarbock et al., 2016). The risk of developing ESRD is higher in patients who already have CKD and sustain dialysis-requiring AKI.

Follow-Up: Patients who are unable to fully recover to their previous level of kidney function will need to be closely mon- itored and followed by a nephrologist. For Medicare patients age 66 years and older with an AKI hospitalization in 2011, the cumulative probability of a recurrent AKI hospitalization within 2 years was 48% (USRDS, 2015). Unfortunately, only 20% of patients had a nephrology visit within 1 year of a hospital admit for AKI. Among patients without pre-exist- ing CKD or diabetes, less than 5% had nephrology follow-up within 1 year (USRDS, 2015). Follow up with a nephrologist 3 to 4 weeks after discharge to evaluate serum creatinine is important. Patients who have a new diagnosis of CKD stages

1 through 5 will require follow-up with a nephrologist for the remainder of their lives. With patients with concomitant conditions of hypertension, diabetes, and strict disorders it is highly advised that current practice guidelines are followed for these patients (Silver et al., 2015).

Sequelae: CKD is a direct result of AKI if there is no return to previous level of function. Patients with CKD are at an increased risk for stroke and peripheral vascular disease. In addition, they are at an increased risk for cardiovascular death, left ventricular hypertrophy, coronary artery disease, and congestive heart failure. Management of CKD includes management of anemia of chronic disease, secondary hyper- parathyroidism, cholesterol, and hypertension.

Prevention/Prophylaxis: Prevention of AKI begins fi rst with identifying those at risk for CKD. Close monitoring of GFR and urine for albuminuria, especially in older adults, is par- amount. When there is a decline in GFR, prompt referral to a nephrologist is of the utmost importance. Avoidance of nephrotoxic medications, such as NSAIDs, as well as poly- pharmacy, will decrease risk of AKI. Recognition of medica- tions that need adjustment for levels of kidney dysfunction is also very important in the prevention of episodes of AKI.

Referral: All patients who have AKI need to be hospitalized. Evaluation and management by a nephrologist is warranted. After resolution of the AKI and discharge from the hospital, follow-up with a nephrologist is needed in 2 to 4 weeks to evaluate serum creatinine and eGFR until recovery or pla- teauing occurs.

Education: Patients should be educated on signs of congestive heart failure as well as avoidance of certain OTC medications such as NSAIDs, cimetidine, and phosphate enemas. Patients should be instructed to avoid diets high in salt and to strive for less than 2 grams of sodium per day (Silver et al., 2015). In addition, tight glycemic control, with hemoglobin A1c (HbA1c) of less than 7%, as well as optimal blood pressure control of less than 130/80  mm  Hg, is paramount. Smoking cessation and maintenance of healthy body weight are also important.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

GFR is the best indicator of kidney function. C Palevsky, 2012

Assessment of renal function is made by EGFR. C KDIGO, 2012

A prior history of CKD and/or diabetes mellitus increases the risk for an AKI event.

C USRDS, 2015

Serum creatinine alone should not be used to determine renal function.

C Levey, 2015

Serum creatinine alone should not be used to monitor kidney function. eGFR should also be used.

C

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

230 Chapter 10 ■ Abdominal Disorders

Signal Symptoms: Painless hematuria (most common pre- senting symptom), urinary frequency or urgency, urinary tract infection, fl ank pain, mild suprapubic pain; often asymptomatic.

Description: The majority of bladder cancers are transitional urothelial cell cancer; 3% are squamous cell cancer; and the rest are adenocarcinoma or small cell tumors (National Comprehensive Cancer Network [NCCN], 2016). In bladder cancer, the posterior and lateral walls of the bladder are involved more frequently than the superior wall. Bladder cancer can be categorized as superfi cial , invasive , and meta- static . Superfi cial, or early, bladder cancer occurs when the lesion is located on the surface of the mucosa or when the tumor penetrates the mucosa and submucosa only. Invasive bladder cancer develops when lesions pervade the bladder muscularis or the perivesical fat. Metastatic bladder cancer is characterized by lymph node, visceral, or bone tissue involvement.

Etiology: Bladder cancer has been linked to smoking, chem- ical exposure, and exposure to certain medications such as cyclophosphamide. There is a relationship between HPV infection and urothelial cancer. Squamous cell bladder cancer has been linked to chronic infection with Schistosoma haematobium (Hussein et al., 2016).

Occurrence: In the United States, each year more than 75,000 new cases of bladder cancer are diagnosed, and more than 16,000 deaths can be attributed to bladder cancer. Bladder cancer is the sixth most common type of cancer (National Cancer Institute, 2016).

Age: Median age of diagnosis is 69 years in men and 71 years in women. Bladder cancer is rarely diagnosed in patients under the age of 40 years. The age of onset is younger in current smokers than in never-smokers (American Cancer Society [ACS], 2016).

Gender: Bladder cancer is three times more common in men than in women (ACS, 2016).

Ethnicity: In the United States, Caucasian males have the highest risk, with roughly twice the incidence seen in African American and Hispanic men (ACS, 2016).

Contributing Factors: Smokers are three times more likely to develop bladder cancer as compared with non-smokers. Women exposed to second-hand smoke are at increased risk for bladder cancer. Some industrial chemicals have been linked with bladder cancer, including benzidine and beta-naphthylamine. Additionally, painters, machinists, printers, hairdressers, and truck drivers are at increased risk due to chemical exposure. Pelvic irradiation, certain drugs (e.g., cyclophosphamide), and abnormal tryptophan metabo- lism contribute to the development of bladder cancer. Exces- sive coffee consumption, use of some artifi cial sweeteners (e.g., saccharin sodium and cyclamate sodium), and overuse of phenacetin-containing analgesics have been suggested risk factors. S. haematobium infection is prevalent in Africa and the Middle East and has been associated with the development of bladder cancer, particularly in patients who smoke (Antoni

et al., 2016). Exfoliation of cancer cells by cystoscopy, brush- ing, or transurethral biopsy or resection may spread bladder cancer cells to other sites within the bladder or may cause irritation from instrumentation. There is an association with developing bladder cancer and a long history of indwelling catheters and urinary calculi.

Signs and Symptoms: Gross, painless hematuria, pyuria, burning, and urinary frequency are common in the presen- tation of bladder cancer. The presence of unexplained hema- turia in a patient over the age of 40 years denotes urothelial cancer until proved otherwise. Symptoms of advanced cancer may include pelvic or fl ank pain and lower extremity edema, resulting from lymphatic or venous blockage. Patients also may complain of abdominal pain, anorexia, and bone pain.

The physical examination may be normal in most patients; however, the clinician should palpate the pelvic area to iden- tify a solid pelvic mass, palpate and percuss for evidence of any kidney enlargement, and perform a prostate examination on men and a pelvic examination on women. Additionally, the examination should be directed toward searching for pos- sible sites of metastasis in the lungs, liver, bone, and lymph nodes.

Diagnostic Tests: Cystoscopy is the gold standard for the initial diagnosis and staging of bladder cancer (NCCN, 2016). Cys- toscopy can miss tumors during the initial transurethral resection of bladder tumors (TURBT); therefore, a repeat cys- toscopy is performed. The procedure begins with a bimanual examination under anesthesia (EUA) to determine whether or not a palpable mass is present and, if present, whether or not it is mobile. An EUA during cystoscopy is effective at iden- tifying locally advanced disease, which may present as gross extravesical extension, invasion of adjacent organs, or pelvic sidewall involvement. If a mass is felt, the bimanual examina- tion is repeated after the resection to see if it is still present. Fluorescence cystoscopy uses an intravesical photoactive pro- toporphyrin, which accumulates in neoplastic rather than normal tissue. Studies have shown that this test can detect more tumors than regular cystoscopy, but the cost is higher and there is a slightly higher false-positive rate (Kotodziej, Krajewski, Matuszewski, & Tupikowski, 2015). Urine-based tumor markers that look at tumor-related proteins, DNA, or RNA have been developed and are used to supplement cystos- copy but are not suffi ciently sensitive to replace cystoscopy.

Imaging studies may be used to defi ne the location and the extent of the tumor, as well as to detect sites of multifocal disease. CT scan is replacing the IV pyelogram (IVP) as the procedure of choice, but IVP remains an appropriate alterna- tive where CT scan is not readily available. CT scans should include both the abdomen and pelvis; scans need to be done with and without contrast, and they should include delayed images to identify defects in the collecting system. Although CT scan provides better visualization of tumors than ultra- sound, it may miss tumors less than 1 cm in size, particularly those in the bladder trigone or dome, and it cannot differ- entiate depth of bladder wall invasion (i.e., mucosal versus lamina propria or muscularis propria). Magnetic resonance imaging (MRI) is as reliable as CT scan for staging of invasive or locally advanced disease.

BLADDER CANCER

Chapter 10 ■ Abdominal Disorders 231

Urine dipstick, cytology, and screening for tumor-specifi c molecular markers in the urine have been used for screen- ing but are not recommended for screening asymptomatic patients due to low specifi city, low sensitivity, and cost, respectively (Cho & Dana, 2010).

Laboratory studies should include an alkaline phospha- tase, CBC, and chemistry profi le. If the alkaline phosphatase is elevated, a bone scan should be considered (NCCN, 2016).

Differential Diagnosis:

■ Neurogenic bladder ■ Nephrolithiasis ■ Urinary tract infection ■ Benign prostatic hypertrophy ■ Other genitourinary cancers (Xiong, Jia, & Wang,

2016)

Treatment: Management of bladder cancer depends on the stage of the disease. Initially, surgical intervention to remove the bladder tumors is warranted. Some patients may require a cystectomy with a urostomy, continent urostomy, or a replacement bladder. For patients with multiple recurrent superfi cial bladder tumors, the urologist may request collab- oration with an oncologist for chemotherapy after surgery. Recent clinical trials of checkpoint inhibitors have indicated effi cacy in the treatment of advanced and metastatic bladder cancer (Apolo, Vogelzang, & Theodorescu, 2015). Advanced disease generally requires surgery, radiation, and chemother- apy with combination agents. The patient ’ s age and health

status at the time of diagnosis must be considered in the man- agement of bladder cancer (Hall et al., 2014; NCCN, 2016).

Follow-Up: Patients with superfi cial low-grade bladder cancer require a cystoscopy at designated intervals, although the value of repeated testing has been questioned. The need for supplemental nutritional support, pain management, pre- vention of complications such as skin breakdown, and an advance directive should be discussed during future follow-up care. Patients with a urostomy may need assistance from an ostomy nurse.

Sequelae: Metastasis to other parts of the body can occur. Survival of the untreated patient may be less than 2 years.

Prevention/Prophylaxis: Encourage patients who smoke to quit, and exhort all patients to decrease exposure to harmful chemicals.

Referral: Refer patients with clinically signifi cant hematu- ria to a urologist. An oncologist also may be involved in the patient ’ s management of the disease. Patient and family support is important at this time; information pertaining to hospice services should be provided. Patients with a urostomy may seek support from a local chapter of the United Ostomy Associations of America (UOAA) at 1-800-826-0826 or http://www.ostomy.org/Home.html .

Education: Older adults with bladder cancer may need to be educated about palliative support measures when the disease becomes terminal.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Urine dipstick is not recommended for screening of bladder cancer in the general population due to lack of specifi city.

A ACS, 2016 ; NCCN, 2016

Routine screening for bladder cancer is not recommended for the general population.

B NCCN, 2016

Patients should be counseled to eliminate active and passive smoking for prevention of bladder cancer.

B ACS, 2016 ; NCCN, 2016

Cystoscopy is recommended in all patients with symptoms suggestive of bladder cancer. It cannot be replaced by cytology or by any other noninvasive test.

A NCCN, 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

BOWEL OBSTRUCTION

Signal Symptoms: Cramping abdominal pain, nausea, vomit- ing, obstipation.

Description: Bowel obstructions are classifi ed as mechanical or nonmechanical and partial or complete, and are located in either the small or large bowel (Ansari, n.d.; Bordeianou & Ye, 2017). The acute development of a large bowel obstruction

(LBO) is considered an abdominal emergency (Jaffe & Thomp- son, 2015).

Etiology: Normal fl ow of gastric and intestinal contents is interrupted (Bordeianou & Ye, 2017). A mechanical bowel obstruction results when there is a complete or partial blockage of the lumen of the bowel by an adhesion, tumor,

232 Chapter 10 ■ Abdominal Disorders

or hernia (Di Saverio et al., 2013). Postoperative adhesions cause approximately 60% to 70% of small bowel obstruction (SBO) (Di Saverio et al., 2013). Signs of an LBO are subtle compared to acute onset of SBO symptoms (Jaffe & Thomp- son, 2015). Bowel distention in LBO leads to bowel ischemia and perforation if not treated.

Occurrence: An estimated 300,000 admissions annually are due to SBO in the United States (Frasure, Hildreth, Takhar, & Stone, 2016; Taylor & Lalani, 2013).

Age: Bowel obstruction from all causes, except intussuscep- tion, is more prevalent in older adults.

Gender: Occurs equally in men and women.

Ethnicity: Not signifi cant.

Contributing Factors: Previous abdominal or pelvic surgery with formation of adhesions is common in SBO (Bordeianou & Ye, 2017). Additional causes for mechanical obstruction include “diverticulitis, foreign bodies (including gallstones), volvulus (twisting bowel on its mesentery), and intussuscep- tion (telescoping of one segment of bowel into another), and fecal impaction” (Ansari, n.d., para. 3).

Signs and Symptoms: Older adults often present for evalua- tion late in their illness and often have atypical or nonspecifi c complaints ( Springer, Bailey, Davis, & Johnson, 2014 ). The most common symptoms reported are cramping abdominal pain, nausea, vomiting, and obstipation (Ansari, n.d; Bor- deianou & Ye, 2017).

Inspect the abdomen for evidence of surgical scars and external hernias; the level of the obstruction determines the amount of abdominal distention (Bordeianou & Ye, 2017). Auscultate bowel sounds. In acute mechanical bowel obstruc- tion the bowel sounds are hyperactive and are described as “high-pitched tinkling” (Bordeianou & Ye, 2017). Palpa- tion of the abdomen may reveal abdominal wall or groin hernias. Patients with a strangulating bowel may have a tender abdomen, continuous pain, and absent bowel sounds (Ansari, n.d.). In mechanical obstruction of the large bowel, symptoms are similar to an SBO, but appear more gradually. The patient complains of persistent constipation leading to abdominal distention; vomiting is uncommon. Physical examination reveals loud borborygmi, no abdominal ten- derness, and an empty rectal vault. Perform a digital rectal examination to determine if fecal impaction or rectal mass is a source of the obstruction (Bordeianou & Ye, 2017).

Diagnostic Tests: Standard laboratory evaluation include CBC with differential and a metabolic panel to assess the patient for presence and severity of hypovolemia, leukocytosis, and metabolic abnormalities (Bordeianou & Ye, 2017).

The initial imaging of a patient with a suspected bowel obstruction is the plain abdominal x-ray with fl at and upright views ( Khan, n.d. ). Plain fi lms can identify “multiple air-fl uid levels, distention of small bowel loops and the absence of gas in the colonic section” (Di Saverio et al., 2013, p. 3). If x-rays do not show an obstruction and there is a high index of sus- picion, CT scan should be used to further evaluate. CT scan is found to have as much as a 90% sensitivity in identifying the presence of bowel strangulation and can identify the etiology and the site of the obstruction ( Khan, n.d. ). Ultrasonography is often used in the evaluation of acute abdominal pain and can be used to identify obstruction along with its cause.

Differential Diagnosis:

■ Cholecystitis ■ Constipation ■ Diverticulitis ■ Gallstones ■ Abdominal hernia ■ Appendicitis (Nobie, n.d.).

Treatment: SBO is a common reason for older adults to be admitted under general surgery and may be treated by non- operative management (NMO) or surgery ( Springer et al., 2014 ). Initial treatment of a bowel obstruction consists of hospitalization for nasogastric suctioning and IV fl uid admin- istration (Di Saverio et al., 2013). In the absence of clinical sign of strangulation or peritonitis, the patient can be treated with NMO up to 72 hours. Systematic signs of “tachycardia, fever, focal tenderness, and elevated lactate levels can indi- cate intestinal ischemia” (Di Saverio et al., 2013, p. 6). Imme- diate surgical intervention is indicated for suspected vascular insuffi ciency, perforation, or strangulation of the bowel.

Follow-Up: Di Saverio and colleagues (2013) recommend NMO should be attempted for 3 to 5 days, then surgical man- agement used for unresolved obstructions.

Sequelae: Delay in surgery may increase morbidity and mor- tality outcomes in older adults (Di Saverio et al., 2013).

Prevention/Prophylaxis: Caregivers must understand the importance of avoiding fecal impactions in patients at risk for this condition.

Referral: Immediate surgical referral with suspected bowel strangulation or after 3 days if no resolution after NMO (Di Saverio et al., 2013).

Education: Inform older adults with diagnosed, untreated internal and external hernias of the possible complication of bowel obstruction.

Chapter 10 ■ Abdominal Disorders 233

Signal Symptoms: Acute onset of right upper quadrant and/ or epigastric pain that is persistent, with radiation to back or shoulders, and usually related to history of fatty meal intake prior to onset ( Abraham, Rivero, Erlikh, Griffi th, & Konda- mudi, 2014 ).

Description: May fall into one of three categories: acute gallbladder infl ammation related to cystic duct obstruction by gallstones, acalculous cholecystitis without presence of stones or sludge, or chronic gallbladder infl ammation (Kata- bathina, Zafar, & Suri, 2015).

Etiology: Gallstones are mainly comprised of cholesterol, and stone formation is associated with high caloric intake, diagno- ses of diabetes mellitus, dyslipidemia, obesity, and the meta- bolic syndrome ( Abraham et al., 2014 ). Cholecystitis usually occurs when a gallstone obstructs the cystic duct; however, acalculous cholecystitis may be found in approximately 10% of cases, specifi cally in critically ill states (Katabathina et al., 2015). Trapped bile caused by the blockage of the cystic duct leads to infl ammation, impaired circulatory fl ow, and ische- mia. The risk of bacterial infection climbs, reaching 70% by 7 days with lack of appropriate treatment. Common culprit organisms include Escherichia coli , Enterobacter , Klebsiella , and Enterococcus . Acute acalculous cholecystitis (AAC) is precipitated by stagnant bile and ischemic states. The criti- cally ill patient who has suffered trauma, recent surgery, shock, sepsis, and total parenteral nutrition is at risk for AAC. Additional comorbid diagnoses of heart failure or dehydrated states may contribute to AAC. The possibility of undetected gallbladder cancer needs to be considered in all older adults presenting with symptoms of cholelithiasis (Makino, Yama- guchi, Nariatsu, Toshiaki, & Ichiro, 2009).

Occurrence: Gallstones may be an incidental fi nding via imaging, and 10% to 20% of these individuals may exhibit symptoms 5 to 20 years after imaging (Abraham et al., 2015). Ninety percent of cholecystitis cases are associated with gallstones. In the older adult, cholecystitis can present with atypical features and likely a complicated disease course (Bergman et al., 2015).

Age: During reproductive years, women are more prone to gallstones than men (Dua et al., 2013). As age increases, the risk for gallstones increases regardless of gender (Kuy, Sosa, Roman, Desai, & Rosenthal, 2011). Thirty percent of those older than 70 years are at risk for gallstones (Demehri & Alam, 2016).

Gender: Twice as many women as men have cholecystitis (Dua et al., 2013).

Ethnicity: A high prevalence for cholecystitis exists in older Native Americans and Caucasians; the disease is less prev- alent in African Americans. The prevalence of gallbladder disease is highest in the Pima, Hopi, and Navajo groups ( Abraham et al., 2014 ).

Contributing Factors: Nonmodifi able risk factors for cholecys- titis include advancing age, female gender, race, and family history of gallbladder disease ( Abraham et al., 2014 ). Obesity is a known predisposing factor to cholecystitis ( Abraham et al., 2014 ; Lee, Han, & Min, 2009). Diabetes, alcoholic cirrho- sis, infl ammatory bowel disease, chronic hemolysis, pancre- atic insuffi ciency, and hyperlipidemia predispose patients to gallstone development. Gallstone formation may be attributed to use of exogenous estrogens prescribed for postmenopausal hormone replacement, and clofi brate, used to treat hyperlip- idemia. Either past or current use of thiazide diuretics is asso- ciated with a modest increase in the formation of gallstones (Gorroll, 2014). Gallbladder stasis, a precursor to gallstone formation, occurs with extended total parenteral nutrition. Patients who experience rapid weight loss are at high risk for the development of gallstones. Cholelithiasis is common in patients who have undergone bariatric surgery (Decker, Swain, Crowell, & Scolapio, 2007).

Signs and Symptoms: The most common type of presenta- tion includes the acute onset of right upper quadrant and/ or epigastric pain that is moderate to severe in nature, per- sistent, and without any relieving factors ( Abraham et al., 2014 ). Associated symptoms may include nausea, vomiting, malaise, fever, and poor appetite. A change in mental status in the older adult may be the only outward sign. Physical

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

SBO is routinely diagnosed with plain fi lm radiographs that show distended small bowel loops, air-fl uid levels, and decreased large bowel air.

C Khan, n.d.

CT scan should be done when radiography is inconclusive or strangulation is suspected.

C Khan, n.d.

Discretion should be used when deciding to use nonoperative management beyond 24–48 hours in older adults.

C Springer et al., 2014

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

CHOLECYSTITIS

234 Chapter 10 ■ Abdominal Disorders

examination may reveal right upper quadrant subcostal ten- derness, guarding, and pain on inspiration (Murphy ’ s sign) ( Adedeji & McAdam, 1996 ; Katabathina et al., 2015). The absence of Murphy ’ s sign does not exclude the acute illness. Biliary colic pain can localize to the midepigastric region; thus, it is important to question the patient about general- ized upper abdominal pain (Trowbridge, Rutkowski, & Sho- jania, 2003). In a patient who has reported symptoms for days, rebound tenderness may suggest perforation. Jaundice on examination would raise concern for complicated clinical course secondary to biliary obstruction.

Diagnostic Tests: Mild leukocytosis with increased band for- mation is the most common abnormality seen on laboratory studies; however, white blood cell (WBC) counts may not be elevated in the older adult (Katabathina et al., 2015). Signif- icant leukocytosis would raise concern for complicated cho- lecystitis secondary to perforation or gangrene ( Abraham et al., 2014 ). Elevation in lipase, amylase, and elevated liver function tests would prompt further evaluation for gallstone pancreatitis. In chronic cholecystitis, however, laboratory values may be normal.

Real-time ultrasonography of the gallbladder and biliary tree is the diagnostic procedure of choice for both acute and chronic cholecystitis, showing gallstones, thickening of the gallbladder wall, and if the common bile duct is obstructed, dilation of the biliary tract ( Abraham et al., 2014 ). An addi- tional imaging modality called the hepatobiliary iminodiacetic acid scan (HIDA) is useful if there is concern for cystic duct obstruction or biliary dyskinesia. CT scan is often performed in evaluation of acute abdominal pain when diagnosis is unclear; yet, it is less sensitive at identifying gallstones than an ultra- sound. In situations where choledocholithiasis is questioned, a magnetic resonance cholangiopancreatography (MRCP) is highly sensitive and specifi c (97% and 98%, respectively) for biliary tree obstruction. Elevated bilirubin greater than 4 mg/ dL and a common bile duct dilated greater than 6 millimeters should prompt evaluation with MRCP to exclude the presence of choledocholithiasis. In cases where this is confi rmed, an endoscopic retrograde cholangiopancreatography (ERCP) is warranted for stone extraction; however, an ERCP may also be used as a diagnostic tool if the clinical picture remains unclear but high suspicion exists for biliary obstruction.

Differential Diagnosis:

■ Perforated peptic ulcer in older adults ■ Appendicitis ■ Liver abscess ■ Diverticulitis ■ Hepatitis ■ Acute pyelonephritis ■ GI carcinoma ■ Acute pancreatitis ■ Myocardial ischemia ■ Herpes zoster ■ Left lower lobe pneumonia ■ Gastritis ■ Cholangitis ■ Irritable bowel syndrome ■ GERD (Gorroll, 2014)

Treatment: Acute episodes require hospital admission in preparation for cholecystectomy; at this time antibiotics are

given intravenously and selected based on targeting enteric pathogens. For uncomplicated cases in which there is no penicillin allergy, evidence of multi-organ involvement, or other hospital-acquired infection, agents such as amoxicillin/ clavulanic acid or ceftriaxone and metronidazole are given (Demehri & Alam, 2016). Laparoscopic cholecystectomy should be undertaken in 24 to 48 hours, and delay of surgery for resolving infl ammation is no longer indicated. Supportive measures to include analgesics and antiemetics may be given as needed. The risk of conversion to open cholecystectomy is linked with male gender, older age (greater than 60 years), and prior abdominal surgeries ( Abraham et al., 2014 ).

A cholecystectomy for acalculous cholecystitis in the critically ill patient may be on hold and delayed until health improves, with a percutaneous cholecystostomy tube as an initial approach to treatment (Demehri & Alam, 2016; Macrì et al., 2006 ; Winbladh, Gullstrand, Svanvik, & Sand- ström, 2009). The general surgeon may weigh risks and benefi ts of a permanent cholecystostomy versus interval cholecystectomy in a patient with multiple comorbidities ( Fuks et al., 2015 ). The recurrence risk of events following conservative management of cholecystitis is high; there- fore, surgical intervention should be undertaken if there are no contraindications. In the event of choledocholitha- sis, an ERCP may be indicated for stone extraction prior to cholecystectomy (Demehri & Alam, 2016). If the clinical status is unknown regarding choledocholithiasis, a chole- cystectomy with intraoperative cholangiogram is indicated to ensure no occult stones remain. Cholangitis requires prompt recognition in order to provide IV antibiotics, biliary decompression via ERCP, and close monitoring for sepsis. Subsequent cholecystectomy is indicated after biliary decompression.

Although used less often now than in the past, oral ursode- oxycholic acid may be considered for dissolution of gallstones if surgery is contraindicated; however, the gallbladder must be functioning and the cystic duct patent ( Abraham et al., 2014 ). Recurrence rate of stones is more than 50%, even with ursodeoxycholic acid. Extracorporeal shock wave litho- tripsy is a possible alternative in nonsurgical candidates, yet potential complications to include biliary pancreatitis and hematomas may raise concern for the procedure.

Follow-Up: Postoperative management of routine cholecys- tectomy includes monitoring for impending infection, adverse drug reactions and interactions, and changes in functional and mental status. For the frail older adult who has under- gone percutaneous cholecystostomy, observation for com- plications is crucial. The catheter of a cholecystostomy tube should be replaced every 3 months if used for long-term pur- poses, and the catheter should be fl ushed with normal saline every 24 hours (Katabathina et al., 2015). For older women, the dosages of estrogen preparations may need to be reduced, if applicable, due to the idea that estrogen may contribute to gallstone development (Demehri & Alam, 2016).

Sequelae: Complications of acute cholecystitis include ische- mia and infl ammation within the gallbladder lumen ( Fuks et al., 2015 ), gallbladder necrosis with perforation and/or abscess, sepsis, choledocholithiasis, cholangitis, and pancre- atitis (Katabathina et al., 2015). Frail older adults, especially those who are diabetic, are at high risk for complications from cholecystitis (Gorroll, 2014).

Chapter 10 ■ Abdominal Disorders 235

Prevention/Prophylaxis: The importance of resting and avoid- ing risk factors after acute cholecystitis or an exacerbation of chronic cholecystitis needs to be emphasized.

Referral: A surgical consultation is necessary if acute chole- cystitis is suspected. A gastroenterologist should be consulted for the frail older adult who is not a surgical candidate, or in the clinical scenario of choledocholithiasis. Biliary pain in patients with a prior history of a cholecystectomy should be evaluated for a retained common bile duct stone. Referral

to a gastroenterologist for evaluation by ERCP, MRI, or endo- scopic ultrasonography is highly recommended (Agrawal, Morrissey, & Thakkar, 2012).

Education: To prevent complications, encourage patients with chronic cholecystitis and patients for whom surgery is contraindicated to report early signs and symptoms of an acute attack. Patients also should be educated that gall- stones could recur in the common bile duct, despite prior cholecystectomy.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

For patients with cumulative risk factors for cholecystitis, early cholecystectomy is recommended before there is a progression of the disease leading to complications of acute cholecystitis.

B Cho, Han, Yoon, & Ahn, 2010 Riall, Zhang, Townsend, Kuo, & Goodwin, 2010

Laparoscopic cholecystectomy is the preferred treatment for cholecystitis, barring any clinical contraindications.

A Abraham et al., 2014

A positive Murphy ’ s sign is a useful diagnostic tool when examining older adults presenting with symptoms of acute cholecystitis; a negative sign, however, should be cautiously interpreted.

C Adedeji & McAdam, 1996 Abraham et al., 2014

Older adults who underwent ultrasonograpahic percutaneous cholecystostomy for the treatment of acute cholecystitis had complete resolution of symptoms within 48 hours.

B Macrì et al., 2006

There was a negative correlation between BMI and the severity of cholecystitis; more complicated disease was found in males who were not obese.

B Hyeon Kook, Ho-Seong, & Seog Ki, 2009

Older adult patients who underwent an early laparoscopic cholecystectomy did not experience any more complications or infections than younger adults who had the same procedure.

A Fuks, Duhaut, Mauvais, Pocard, Haccart, Paquet, . . . Regimbeau, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

CHRONIC KIDNEY DISEASE

Signal Symptoms: Fatigue, anorexia, altered mental status, weakness, dysgeusia, pruritis, nausea, vomiting, edema.

Description: CKD continues to be a growing worldwide problem. According to CDC data, the prevalence of CKD was 25% higher from 2007 through 2014 than in 1988 through 1994 (CDC, 2015). Healthy People 2020 has developed 14 objectives to attempt to reduce new cases, complications, and economic costs of CKD. CKD, when left untreated, results in ESRD, which requires dialysis in order for the patient to survive. It is estimated that 25% of the Medicare budget is spent on CKD (CDC, 2015). With the increased prevalence of

diabetes and an aging population, incidence of CKD will con- tinue to rise. Unfortunately, many people are unaware that they have CKD.

Etiology: CKD is defi ned as abnormalities of kidney structure or function, present for more than 3 months (Inker, 2014). Markers of kidney damage include albuminuria, urine sedi- ment abnormalities, electrolyte abnormalities, abnormalities detected by histology or imaging, or a history of kidney trans- plantation. CKD is then further classifi ed based on cause, GFR category, and albuminuria category (KDIGO, 2013). Follow- ing are the stages of CKD:

236 Chapter 10 ■ Abdominal Disorders

■ Stage 1: GFR is greater than or equal to 90  mL/min with other evidence of CKD damage

■ Stage 2: GFR 60 to 89 mL/min ■ Stage 3a: GFR 45 to 59 mL/min ■ Stage 3b: GFR 30 to 44 mL/min ■ Stage 4: GFR 15 to 29 mL/min ■ Stage 5: GFR less than 15 mL/min or on dialysis

Diabetes is the leading cause of kidney failure, followed by hypertension. Other causes of kidney disease include glomer- ulonephritis, inherited polycystic disease, autoimmune dis- eases, infections, and urological diseases.

Occurrence: The CDC estimates that more than 20 million people in the United States have CKD (CDC, 2015).

Age: Although CKD can affect any age group, incidence increases with age. For U.S. adults age 30 to 49, 50 to 64, and 65 years or older with no CKD at baseline, the residual lifetime incidences of CKD are 54%, 52%, and 42%, respec- tively (CDC, 2015). The prevalence of CKD in adults 30 years or older is projected to increase from 13.2% currently to 14.4% in 2020 and 16.7% in 2030 (CDC, 2015).

Gender: CKD affects females more than males (CDC, 2015).

Ethnicity: African Americans have a higher prevalence of CKD than Caucasians, according to USRDS data. This is closely fol- lowed by Hispanics/Mexican Americans (CDC, 2015).

Contributing Factors: Diabetes mellitus is the leading cause of CKD and is the leading risk factor in the development of CKD. This is followed closely by hypertension, both a cause and a consequence of renal disease. Infl ammatory diseases, such as systemic lupus erythematosus, and malignancy, such as renal tumors or multiple myeloma, also increase the risk of kidney failure. Vascular disease, chronic pyelonephritis, urinary stones, systemic infections, gout (Roughley, Belcher, Mallen, & Roddy, 2015; Zhe & Hang, 2016), certain medications, and radiopaque dye also heighten the risk of developing CKD. AKI often predisposes a patient to the development of CKD. A family history of renal disease is an important risk factor in the development of CKD. Racial and ethnic minorities have an increased risk of CKD and are more likely to progress from CKD to ESRD. In addition, the presence of inherited disease, such as autosomal dominant polycystic kidney disease, will lead to development of CKD.

Exposure to toxins can also play a role in the develop- ment of CKD. Exposure can be occupational, environmen- tal, or recreational. There is a strong association between smoking and development of CKD. Chronic smoking causes nephrosclerosis, which is caused by microvascular ath- erosclerosis, resulting in hypertension. Illicit substances associated with CKD include heroin and cocaine. Recently, methamphetamines and ecstasy use have been associated with CKD. Cocaine use is associated with acute rises in blood pressure, leading to AKI from hypertension. Although heroin use was initially thought to cause focal glomerulosclerosis, it is now thought that substances mixed with the heroin or even transmittable diseases, such as hepatitis and HIV asso- ciated with IV injection of street drugs, are the cause of the CKD (Connor, 2011). Methamphetamines cause acceler- ated hypertension, causing renal damage. Ecstasy use can lead to rhabdomyolysis, drug-induced vasculitis, and severe hyponatremia. Recurrent episodes of rhabdomyolysis injury

could lead to CKD for the patient (Connor, 2011). Exposure to heavy metals such as lead, cadmium, mercury, and organic solvents has been strongly linked to CKD; thus, screening for occupational hazards is a must.

Signs and Symptoms: Unfortunately, CKD does not produce symptoms until renal injury is quite advanced. It is often known as a silent disease. Many individuals are unaware that they have CKD until it progresses to stages 3 or 4. In stages 1 and 2, BUN and creatinine levels are normal or nearly normal, and acid-base, fl uid, and electrolyte balances are maintained through the adaption of remaining nephrons. In stage 3, there is moderate impairment of GFR, and BUN and creatinine levels begin to increase. The patient usually remains asymptomatic, but levels of erythropoietin and para- thyroid hormone are abnormal. Early symptoms of kidney disease, if any, may be similar to other illnesses. Only when the patient develops stage 4 or 5 of kidney disease do more profound symptoms of CKD occur. These include fatigue, loss of appetite and weight loss, dyspnea, edema in upper and lower extremities, confusion and diffi culty with concen- tration, pruritus, dysgeusia, and foul-smelling breath (CDC, 2015).

Although diagnosis of kidney disease is based heavily on laboratory data and diagnostic imaging, a careful history may lead to clues associated with the diagnosis of CKD. Careful review of any kidney disease in the family is impera- tive, including questions relating to any hereditary diseases, such as autosomal dominant polycystic kidney disease. If the patient has a past history of pregnancy, ask whether there were any complications, including proteinuria or preeclamp- sia. Any past urological conditions could indicate postrenal causes of CKD.

Any history of diabetes mellitus or hypertension should immediately raise a strong suspicion for the presence of CKD. In addition, the patient should be questioned regarding any history of congestive heart failure, cirrhosis, or GI symptoms that may cause prerenal CKD. Disorders of the urinary tract, recent systemic infections, unusual rashes, or skin lesions should also raise suspicion of CKD. A through medication history should also be obtained to identify medications that may be contributing to CKD.

Diagnostic Tests/Tools: As stated previously, estimation of eGFR is the best indicator to level of kidney function and functioning renal mass. GFR declines after damage to the kidney structurally. GFR and albuminuria should be assessed yearly in patients with CKD and with increased frequency in those patients who have high risk of rapid progression of CKD. Serum creatinine alone as a decline in eGFR may occur before any rise in creatinine is noted. eGFR is best calculated using the 2009 Chronic Kidney Disease Epidemiology Collab- oration (CKD-EPI) (KDIGO, 2013).

The formula is as follows:

eGFR S S

if Cr Cr

Age= × × × ×

−141 1 1 0 993

1 018

1 209min( , ) max ( , ) .

. [

.κ κα

ffemale if African American] . [ ]×1 159

eGFR in CKD is more accurate than those in patients with AKI because of their steady state of kidney function. A creat- inine clearance, in which a volume of urine is collected over 24 hours and the amount of creatinine secreted is measured, is a more accurate indicator of eGFR because it is a direct measurement.

Chapter 10 ■ Abdominal Disorders 237

Albuminuria, defi ned as the abnormal loss of albumin in the urine, is also indicative of CKD. Albumin is a plasma protein that is the principal component in most kidney dis- eases. It is a very common fi nding in CKD, indicative of glomerular diseases. Albuminuria of more than 30  mg/24 hours for 3 months is indicative of CKD (KDIGO, 2013).

In addition to albuminuria, there are other markers that indicate damage to the kidneys. These include abnormali- ties in urinary sediment and abnormal fi ndings on imaging studies. Examination of the urinary sediment for WBCs, RBCs, or casts may indicate the presence of acute or chronic kidney disease and requires further investigation. Imaging studies should also be performed to suggest the cause of CKD. Ultrasound examination may indicate the presence of kidney stones, hydronephrosis, cysts, or masses. Small kidneys on ultrasound suggest CKD, whereas “large” kidneys may indi- cate tumors, cysts, or infi ltrating diseases. CT scan may reveal tumors, obstructions, cysts, or calculi.

Further laboratory data that should be assessed in patients with possible CKD include CBC and electrolytes. Fasting lipids and HbA1c should be evaluated in the diabetic patient. Serum calcium, phosphorus, parathyroid hormone, and vitamin D levels should be drawn to evaluate for the changes in mineral metabolism and bone structure that begin early in CKD. Iron studies, vitamin B 12 , and folate should also be completed and replacement begun, if warranted.

Differential Diagnosis:

■ Acute kidney injury ■ Cirrhosis ■ Uropathic obstruction ■ Nephrotic syndrome ■ Tubulointerstitial disease (Bazari, 2014)

Treatment: Referral to a nephrologist should occur if 1) GFR is less than 30  mL/min, 2) there is a decline in GFR greater than 3 mL/min, 3) albuminuria is present, 4) it is diffi cult to control hypertension, and 5) there is unexplained anemia with GFR less than 60  mL/min (Johnson, 2011). Further investigation using the previous diagnostic tests will assist the nephrologist in the determination of the cause of the CKD. Once the stage of CKD is identifi ed, management of CKD is aimed primarily at preventing progression of the disease through medications, risk factor reduction, lifestyle changes, and education of the patient and family regarding kidney disease. Eventually there is decline in kidney function to ESRD. Patients then must decide between renal replace- ment therapy—hemodialysis or peritoneal dialysis—in order for the patient to survive, or opt for no renal replacement therapy and end-of-life care.

Patients with CKD have a greater risk for cardiovascular disease than those without. As stated previously, hyperten- sion is both a cause and a sequela of kidney disease. It is asso- ciated with a faster decline in kidney function by increasing albuminuria and furthering the development of cardiovascu- lar disease. Thus, reducing the risk of progression of CKD and advancement of cardiovascular disease is paramount. Reduc- tion of blood pressure to target levels is the most import- ant treatment step in managing CKD. The targeted blood pressure for patients with hypertension as recommended by KDIGO is systolic blood pressure less than 140  mm  Hg and diastolic blood pressure less than 90 mm Hg (2012). Patients who are at greatest risk for complications or already have

evidence of cardiovascular disease may need more aggressive hypertension.

Multiple medications are frequently required in CKD patients to achieve goal blood pressure. ACEIs and ARBs are fi rst-line treatment as antihypertensive medications. These agents reduce albuminuria and slow the rate of decline in kidney function in both diabetic and nondiabetic kidney disease. When beginning a patient on an ACEI or ARB, serum creatinine and GFR should be measured at 1 week and 4 weeks after initiation of therapy. If the initial rise in creatinine is more than 30% above the baseline value, the ACEI or ARB should be discontinued. ACEIs or ARBs should also be withdrawn if serum potassium concentration exceeds 6  mmol/L despite dose reduction, potassium diet restriction, and diuretic therapy. In addition, treatment response to ACEIs or ARBs can be monitored by albuminuria. Reduction in urinary albumin excretion will decrease risk of develop- ment of end-stage kidney disease and cardiovascular disease. Furthermore, sodium restriction of less than 2  g per day is recommended for blood pressure control. This is especially important in “salt sensitive” groups; for example, African Americans, older individuals, and those with diabetes, hyper- tension, and CKD. These groups are more salt sensitive and have a greater response in their blood pressure with increased intake of salt.

Because of the increased salt and water retention with CKD, use of a diuretic should be included in the antihyper- tensive regimen of the CKD patient. Thiazide diuretics often become less effective as GFR falls below 40  mL/min due to decreased renal blood fl ow. Usually a loop diuretic, such as furosemide, torsemide, or bumetanide, is used. Side effects of loop diuretics include hypokalemia and hypomagnesia, which can lead to increased cardiovascular risk of arrhyth- mias. Thus, serum electrolytes should be monitored, and the patient should be instructed to report any paresthesias, rash, or tinnitus. Beta blockers such as carvedilol, metoprolol, or bisoprolol should be used in patients with CKD when a proper dose of ACEI, ARB, or diuretic is not enough to lower blood pressure. Although these agents do not provide any renopro- tective effects, they do assist in reducing cardiovascular mor- tality in high-risk patients. Beta blockers should be avoided in patients with bradycardia or heart block.

Calcium channel blockers (CCBs) are also effective agents that can be used to lower blood pressure in CKD patients; however, there are differences between these medications’ effects on reducing proteinuria. Nondihydropyridine CCBs (verapamil, diltiazem) reduce proteinuria among patients with advanced nephropathy, whereas dihydropyridine CCBs (nifedipine, felodipine, amlodipine) will not have this effect unless coupled with an ACEI or ARB (Kalitzidis, 2011). They should not be used as monotherapy in CKD patients but in combination with an ACEI or ARB to achieve optimal blood pressure control. Central alpha-adrenergic agonists decrease the effects of sympathetic activity to lower blood pressure. Vasodilators such as hydralazine and minoxidil are often used as fourth-line agents when other antihypertensive treat- ments have failed. Vasodilator therapy does not reduce pro- teinuria and has not been shown to improve renal outcomes. Side effects of minoxidil include increased hair growth and risk of pericardial effusion. Hydralazine is the leading cause of drug-induced lupus syndrome and should be avoided in any patient with an autoimmune disease.

238 Chapter 10 ■ Abdominal Disorders

Tight glycemic control in CKD patients reduces cardio- vascular disease and CKD progression risk in both type 1 and 2 diabetes mellitus. An HbA1c of less than 7.0% is the goal of patients with diabetes and CKD (KDIGO, 2012). Although achieving this can be diffi cult for some patients and is associated with increased risk of hypoglycemia, tight control reduces not only albuminuria but also retinopathy and neuropathy. Insulin can be used to treat diabetes in CKD, and doses should be tailored to attain the goal HbA1c while avoiding hypoglycemia. Insulin types and doses should be individualized to each patient and to the patient ’ s level of CKD. First-generation sulfonylureas are metabolized in the kidney and may lead to longer half-lives with greater risk of hypoglycemia and, thus, should be avoided in CKD. Metformin, a biguanide, is also metabolized in the kidney and increases risk for lactic acidosis and so should also be avoided. Exenatide (Byetta) is not recommended for use in patients with a GFR less than 30  mL/min and has actually been found to cause renal failure in a number of patients (Hahr, 2011).

Anemia is a common complication of CKD. It worsens as kidney function declines, becomes prevalent in CKD stage 3, and continues through stage 5 into ESRD. The primary cause of anemia is decreased secretion of eryth- ropoietin from decreased functioning renal cells, resulting in fatigue, decreased exercise capacity, decreased cognition, and impaired immunity, leading to decreased quality of life. Workload of the heart is increased with anemia, leads to left ventricular hypertrophy and cardiomyopathy, and increases the patient ’ s risk of death from ischemic heart disease and heart failure. Target hemoglobin goals are 11 to 12  g/dL in patients with CKD (KDIGO, 2012). In addition, iron studies should be completed to evaluate for a true iron defi ciency or functional iron defi ciency. Iron replacement is given orally as ferrous sulfate. IV iron is usually reserved for those patients severely iron depleted or those patients on hemodialysis. Erythropoietin-stimulating agents can be given once iron defi ciency is corrected, other causes of anemia have been excluded or treated, and hemoglobin is consistently below 10 g/dL. Epoetin alfa and darbepoetin alfa are two genetically engineered agents that can be administered to CKD patients to increase bone marrow production of RBCs.

Changes in mineral metabolism and bone structure begin early in CKD. This not only encompasses bone disease but also vascular and soft tissue calcifi cation. As kidney func- tion worsens and GFR continues to decline, the kidney must work harder to excrete phosphorus. This then reduces the formation of the active form of vitamin D (1,25D). Low levels of 1,25D, coupled with low serum calcium levels from decreased gut absorption, lead to a rise in parathyroid hormone. This leads to secondary hyperparathyroidism due to hypocalcemia, hyperphosphatemia, and low 1,25D levels. The increased parathyroid hormone affects bone metabolism and increased bone turnover, causing decreased cortical bone and bone strength. This increases risk of fracture and causes increased “bone pain” in CKD patients. Development of sec- ondary hyperparathyroidism can be decreased by dietary restriction of high-phosphate foods such as fast food, dairy products, colas, and processed food products. A phosphate binder, which binds to the phosphate in food and is eliminated in the bowel movement, is also prescribed. Calcium acetate, lanthanum carbonate, and sevelemer carbonate are the

common phosphate binders used today. In addition, admin- istration of vitamin D (Rocaltrol, Hectoral, and Zemplar) also helps to reduce parathyroid hormone secretion.

Patients with CKD are also at increased risk for malnutri- tion and hypoalbuminemia. These are associated with poor outcomes when the time comes for the patient to initiate dialysis. The restriction of protein in the CKD population has been a topic of ongoing debate. Current recommendations from KDIGO (2012) include a protein intake of 0.8  gm/kg/ day in patients with CKD. Patients need to be monitored for malnutrition with serum albumin levels and body weight assessments.

Smoking cessation is strongly encouraged in patients with CKD. Smoking compounds the risk for cardiovascular mor- tality in patients with CKD and hastens progression of kidney disease. It should be addressed with each offi ce visit and risks reviewed with the patient.

Unfortunately, despite optimal treatment and practices by the patient, kidney disease may continue to progress until kidney failure occurs. Patients then develop uremia, which is the accumulation of toxins within the blood. This leads to anorexia, nausea, vomiting, asterixis, muscle weakness, platelet dysfunction, pericarditis, mental status changes, and possibly coma. At this point, dialysis is initiated to “clean” the blood of these toxins and will need to continue throughout the patient ’ s lifetime.

Follow-Up: Care of the patient with CKD is in the hands of the nephrologist for the rest of the patient ’ s life span. Unfor- tunately, timely referral to help keep the patient from pro- gression to ESRD is often not done. In addition, some patients are not aware that they have CKD. It has been found that the worse the patient ’ s kidney function is, the more aware they are of their disease (CDC, 2012). According to KDIGO, any patient with the following criteria should be referred to nephrology for further evaluation:

■ AKI or abrupt sustained fall in GFR ■ eGFR less than 30 ml/min/1.73 m2 ■ A consistent fi nding of signifi cant albuminuria (ACR

greater than 300 mg/g [greater than 30 mg/mmol]) or AER greater than 300 mg/24 hours

■ Progression of CKD ■ Urinary RBC casts, RBC 420 per high power fi eld sus-

tained and not readily explained ■ CKD and hypertension refractory to treatment with

four or more antihypertensive agents ■ Persistent abnormalities of serum potassium ■ Recurrent or extensive nephrolithiasis ■ Hereditary kidney disease

The nephrologist continues to manage the patient in an attempt to avoid any further progression of CKD. Tight glycemic control, optimal blood pressure control, dietary phosphate restriction, and management of anemia are para- mount. Patient education of CKD continues with every offi ce visit as well. In addition, once the patient reaches stage 4, “options classes” are held with the family and the patient to discuss dialysis modalities (i.e., peritoneal dialysis or hemo- dialysis). Referral for renal transplant should be made before the patient begins dialysis. If the patient chooses not to proceed with dialysis, referral should be made for palliative care to discuss end-of-life decisions.

Chapter 10 ■ Abdominal Disorders 239

Sequelae: The major sequela of CKD is ESRD. In addition, CKD is associated with an increased risk for cardiovascular disease. Thus, lifestyle changes, such as maintaining healthy body weight, restriction of salt and high-fat diet, active par- ticipation in an exercise program, smoking cessation, limited alcohol intake, and tight glycemic and blood pressure control are important, not only to reduce cardiac risk, but also to slow progression of kidney disease.

Prevention/Prophylaxis: Early screening for albuminuria in patients at risk for CKD is paramount. In addition, other risk factors associated with CKD, including level of GFR, level of albuminuria, age, sex, race/ethnicity, elevated blood pressure, hyperglycemia, dyslipidemia, smoking, obesity, history of car- diovascular disease, ongoing exposure to nephrotoxic agents,

and others should not be ignored (KDIGO, 2012). Tight gly- cemic control, optimal blood pressure control, tobacco ces- sation, low-salt diet, avoidance of nephrotoxic medications, and optimal weight with healthy lifestyle all assist in reduc- tion of risk of CKD.

Referral: All patients with CKD should be referred to a nephrologist for ongoing monitoring.

Education: Patients with CKD are educated regarding their disease and the manifestations of this disease. Continued education of low sodium and low protein diet, compliance with medications, tight glycemic control, and avoidance of NSAIDs and contrast dye is important. Patients are encour- aged to continue to follow up with their primary care physi- cian for other aspects of their health care.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Assessment of renal function is made by eGFR. C KDIGO, 2012

Albuminuria of >30 mg/24 hours for 3 months is indicative of CKD. C KDIGO, 2012

Patients with or without diabetes mellitus should be treated primarily with an ACEI or ARB to decrease albumineria.

C KDIGO, 2012

Target hemoglobin A1c for people with diabetes should be <7%. C KDIGO, 2012

A = consistent, good-quality, patient-oriented evidence; B = inconsistent or limited-quality, patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

CIRRHOSIS OF THE LIVER

Signal Symptoms: Jaundice, fatigue, spider angiomas, palmar erythema, nodular liver.

Description: Cirrhosis occurs when there is chronic insult to the liver, resulting in fi brous and nodular regeneration of the existing hepatocytes. Forty percent of patients are asymptomatic initially when cirrhosis is diagnosed as part of a routine examination (Heidelbaugh & Bruderly, 2006). Cirrhosis is the eighth leading cause of death in the United States and a signifi cant fi nancial burden, with annual direct costs of approximately $2 billion and indirect costs of $10 billion (Ge & Runyon, 2016).

Etiology: Chronic alcoholism, viral hepatitis, and nonal- coholic fatty liver disease (NAFLD) are the most common causes of cirrhosis, together accounting for 80% of patients on the wait list for liver transplant from 2004 through 2013 (Wong et al., 2015). However, nonalcoholic steatohepatitis is expected to become the number one indication for liver trans- plant due to the increasing prevalence of fatty liver disease (Ge & Runyon, 2016). The cause of primary biliary cirrho- sis, a chronic infl ammatory disease of the liver in which the intrahepatic bile duct is destroyed, is unknown. Other less common causes include autoimmune hepatitis, primary scle- rosing cholangitis, medications, Wilson ’ s disease, Alpha-1 antitrypsin defi ciency, right-sided heart failure, and others (Heidelbaugh & Bruderly, 2006).

Occurrence: In the United States, data from 1999 through 2010 estimated the prevalence of cirrhosis at 0.27%, or approximately 633,323 adults (Scaglione et al., 2015). True estimates are diffi cult to derive, as many patients with cirrho- sis are asymptomatic, and an estimated 69% of patients are unaware that they have liver disease.

Age: Cirrhosis, which has an increase in onset in older adults, is the twelfth leading cause of death, predominantly in patients with alcoholic liver disease (Heidelbaugh & Bru- derly, 2006; Starr & Raines, 2011). Onset of primary biliary cirrhosis usually occurs before age 65 years.

Gender: Overall, being male is independently associated with cirrhosis (Scaglione et al., 2015). However, cirrhosis of the liver is equally prevalent in men and women with chronic alcoholism.

Ethnicity: The overall prevalence of cirrhosis is higher in non-Hispanic African Americans and Mexican Americans (Scaglione et al., 2015).

Contributing Factors: Chronic alcohol consumption, com- bined with a poor nutritional intake, contributes to cirrho- sis. Drug-induced cirrhosis can occur in patients taking large doses of vitamin A, aldomet, isoniazide, and methotrexate. Certain infectious diseases (tertiary syphilis, brucellosis, schis- tosomiasis) have predisposed patients to a risk of developing

240 Chapter 10 ■ Abdominal Disorders

cirrhosis. Patients with Wilson ’ s disease, sarcoidosis, heart failure, and hemochromatosis may go on to develop cirrho- sis (Heidelbaugh & Bruderly, 2006). A history of the follow- ing chronic conditions can contribute to the development of biliary cirrhosis: biliary obstruction, cystic fi brosis, primary sclerosing cholangitis, and congenital biliary cysts (Heidel- baugh & Bruderly, 2006). Chronic hepatitis B and C viruses also place patients at risk for developing cirrhosis (Chen, Chu, Yeh, & Liaw, 2007; Starr & Raines, 2011). Risk factors for developing cryptogenic cirrhosis, which occurs in patients with NAFLD, include obesity, diabetes mellitus, hypertri- glyceridemia, and signifi cant weight loss in patients who have had jejunoileal bypass surgery (Gill & Wu, 2006; Riley, Taheri, & Schreibman, 2009).

Signs and Symptoms: Many patients can be asymptomatic until advanced disease sets in. Symptoms may include anorexia, fatigue, generalized pruritus, jaundice, and easy bruising of the skin. When questioned, reports of weight loss, weakness, and GI bleeding may be common. An assess- ment tool, such as the AUDIT (Alcohol Use Disorders Iden- tifi cation Test) or the CAGE Questionnaire (Ewing, 1984), is recommended to discern alcohol-related problems. It allows the practitioner to explore the patient ’ s history of chronic alcohol use and the status of functional impairment. Physi- cal examination may reveal evidence of scleral icterus, Kay- ser-Fleischer ring around the cornea of the eye, xanthoma, palmar erythema, spider angiomas, dilated abdominal veins (caput medusae), clubbing of fi ngers, changes in the nail bed (Terry ’ s nails, with two-thirds of the nail bed appear- ing white), Dupuytren ’ s contracture, asterixis, and in men, decreased body hair, gynecomastia, and testicular atrophy. Palpation of the liver may reveal a fi rm, nodular liver; sple- nomegaly; and ascites (Heidelbaugh & Bruderly, 2006; Starr & Raines, 2011).

Diagnostic Tests: CBC with indices may reveal anemia, which is typically multifactorial in nature. Potential etiologies, depending on etiology and manifestation of the underlying liver disease, may include chronic GI bleeding, alcohol toxic- ity, folate defi ciency, anemia of chronic disease, splenomeg- aly, suppression of bone marrow, and hemolysis. A decreased serum albumin level and prolonged PT/INR occur in cir- rhosis. The serum aspartate aminotransferase (AST) level is elevated; the alanine aminotransferase (ALT) level is usually above normal but not to the degree of the AST. The ALT is a more specifi c test for recognizing liver disease than the AST (Duke, 2012). The ammonia level is elevated in patients with hepatic encephalopathy. The alpha-fetoprotein (AFP) level is elevated in patients with hepatitis C and is also a tumor marker for hepatocellular carcinoma (Duke, 2012; Starr & Raines, 2011).

Abdominal ultrasound can be ordered initially when cirrhosis is suspected, given clinical symptom presentation and other diagnostic studies as surface nodularity, ascites, increased parenchymal echogenicity of the liver, and the direction of portal blood fl ow can be detected using Doppler scanning (Heidelbaugh & Bruderly, 2006). Liver biopsy, either percutaneous or transjugular, is the gold standard for diagnosing liver cirrhosis, with a sensitivity between 80% and 100% (Bravo, Sheth, & Chopra, 2001). However, biopsy may be unnecessary if clinical assessment, laboratory fi nd- ings, and imaging results signifi cantly suggest cirrhosis and

biopsy would not alter patient management. Additionally, noninvasive measures such as liver ultrasound elastography and laboratory studies like AST to platelet ratio and Fibrotest/ Fibrosure have emerged, although a standard has not been identifi ed (Chou & Wasson, 2013; Lin et al., 2016).

Differential Diagnosis:

■ Liver cancer ■ Alcoholic hepatitis ■ Congenital hepatic fi brosis ■ Portal hypertension ■ Schistosomiasis ( O’Shea, Dasarathy, & McCullough,

2010 )

Treatment: Treatment of cirrhosis is primarily dependent on the cause of the disease. Cessation of all alcohol intake is imperative in all cases ( O’Shea, Dasarathy, & McCullough, 2010 ). Patients should also avoid or have dose-reduction with hepatotoxic medications such as NSAIDs, acetamino- phen, systemic antifungals, and statins. Herbal medications have also been shown to be hepatotoxic, including german- der, mistletoe, green tea extracts, kava kava, and others (Pittler & Ernst, 2003). Review the patient ’ s immunizations and determine the need for infl uenza, hepatitis A and B, and pneumococcal pneumonia vaccines. Nutritional therapy is of the essence, as 20% to 60% of cirrhosis patients suffers from malnutrition (Ge & Runyon, 2016). Nutritional support includes at least 1.0 to 1.5  g protein/kg dry body weight; cirrhosis patients with ascites should have a 2,000  mg daily sodium restriction. It is highly recommended that patients with cirrhosis have small, frequent nutritious feedings, including a small snack at bedtime and a small morning meal, to improve overall nitrogen balance without exacerbat- ing hepatic encephalopathy. Multiple-vitamin supplements should be prescribed, including adequate intake of vitamins A, D, and K. It is recommended, however, that a multiple vitamin without iron be recommended, unless iron-defi ciency anemia is present ( O’Shea et al., 2010 ).

Treatment for complications of cirrhosis may include antibiotics for infections such as spontaneous bacterial peri- tonitis, diuretics if the patient has ascites, beta blockers for portal hypertension, and symptomatic relief of pruritus (Heidelbaugh & Bruderly, 2006). For hepatic encephalopa- thy treatment or prevention, lactulose and/or Rifaximin are commonly used (NeSmith, Ahn, & Flamm, 2016). Therapeu- tic paracentesis may be needed for recurrent, especially large volume, ascites and eventually a transcutaneous intrahepatic portosystemic shunt (TIPS) may be necessary. Esophagogas- troduodenoscopy (EGD) can be used to screen for esophageal varices, especially in patients who cannot undergo nonselec- tive beta blocker prophylaxis. Variceal banding can be utilized to prevent or treat variceal hemorrhage, which has been associated with a mortality rate near 15% (Cabrera, Tandon, & Abraldes, 2016).

Follow-Up: Surveillance of the older adult with cirrhosis depends on the stability of the patient and the presence of complications. Stable older adults should have repeat CBCs, complete metabolic profi le, and PT/INR 6 months to 1 year after initial diagnosis and every 6 months to identify cirrho- sis complications such as anemia, thrombocytopenia, coag- ulopathy, metabolic derangements, and others. Additionally, model for end-stage liver disease (MELD) score should be

Chapter 10 ■ Abdominal Disorders 241

calculated every 6 months (Harrison, Hogan, Floros, & Davies, 2016). Unstable patients may need to be monitored more frequently.

All adults with cirrhosis should undergo liver ultrasonog- raphy of CT imaging every 6 months to screen for hepato- cellular carcinoma (HCC) ( Bruix & Sherman, 2011 ; Ge & Runyon, 2016). The use of alpha fetoprotein laboratory test in conjunction with ultrasonography for HCC detection remains controversial, as it results in increased detection rates, but also increased costs and false positives. All cirrhosis patients should undergo EGD for esophageal variceal screen- ing and guideline-based repeat EGD for surveillance (Ge & Runyon, 2016). On return visits, observation and testing for changes in mental status and depression may be indicated. Other complications of cirrhosis, listed under Sequelae, will require additional medical therapy.

Sequelae: Complications from cirrhosis include ascites, spon- taneous bacterial peritonitis resulting from uncontrolled ascites, portal hypertension, hepatopulmonary syndrome, portopulmonary hypertension (Kochar, Nevah, Moises, & Fallon, 2011), esophageal variceal bleeding, renal failure, and hepatic encephalopathy and hepatorenal syndrome. Patients with ascites and cirrhosis are at risk for developing an umbil- ical hernia ( Eker et al., 2011 ). The incidence of developing cholelithiasis increases in patients with cirrhosis (Pessaux & Lermite, 2008). There is a very high risk of developing hepa- tocellular carcinoma, at approximately 5% per year, which is the leading cause of death for patients with cirrhosis, and therefore surveillance (as stated previously) is necessary (Ge & Runyon, 2016).

Alcoholic hepatitis may occur with cirrhosis and is gen- erally defi ned as alcohol-related acute onset of symptomatic hepatitis. Severity is measured with calculation of discrimi- nant function (DF), which is a score based on PT and serum bilirubin (Gholam, 2016). General management of these patients includes alcohol abstinence, fl uid management, nutritional support, and acid suppression (such as proton pump inhibitors [PPIs] or H 2 receptor blockers) to prevent mucosal bleeding (Saberi, Dadabhai, Jang, Gurakar, & Mezey, 2016). Patients with moderate to severe alcoholic hepatitis have 1 month mortality rates as high as 23% (Yu, Xu, Ye, Li, & Li, 2010). In severe alcoholic hepatitis (DF greater than or equal to 32), the use of nonselective beta blockers has been associated with increased risk of acute kidney injury

and should therefore be discontinued (Sersté et al., 2015). Additionally, patient with severe alcoholic hepatitis should be treated with a 4-week course of prednisolone (40 mg/day for 28 days, typically followed by discontinuation or a 2-week taper), unless steroid therapy is contraindicated, as this has been shown to reduce mortality rates in these patients (Thursz et al., 2015).

Prevention/Prophylaxis: Cessation of alcohol consumption is crucial to the prognosis of cirrhosis. Avoidance of hepa- totoxic medications, especially NSAIDs, is recommended for patients with cirrhosis. All patients with cirrhosis should be given the hepatitis A and B vaccines, unless they are shown to be immune to the diseases. The polyvalent pneumococ- cal vaccine and annual infl uenza vaccines also are recom- mended for these patients. Preventive strategies for patients with cirrhosis need to focus on the prevention of complica- tions by instituting measures such as routine follow-up with laboratory testing and abdominal imaging, as well as endo- scopic screenings for varices and variceal prophylaxis, unless contraindicated.

Referral: A gastroenterologist should be consulted when varices are suspected and variceal bleeding occurs. An EGD is performed to manage complicated patients. Patients present- ing with a new onset of ascites need to be referred for con- sideration of diagnostic paracentesis (Starr & Raines, 2011). Referral to a hepatologist for patients with cirrhosis should be considered early on to plan management for complications and formulate plans for end-stage liver disease. Additionally, all patients with a MELD score greater than or equal to 15 or complications of cirrhosis should be referred to a transplant center for evaluation ( Kanwal et al., 2010 ; Runyon & AASLD Practice Guidelines Committee, 2009 ).

Education: Instruct patients to eliminate all alcohol con- sumption. Recommend an alcohol treatment program and provide the telephone number for the nearest chapter of Alcoholics Anonymous. Patients should be requested not to self-medicate with OTC medications, including herbal prod- ucts. Patients with cirrhosis should eat small, frequent meals of a balanced diet containing 1.0 to 1.5  mg protein/kg body weight per day, unless contraindicated by advanced disease. Patients with encephalopathy should not be driving. For patients with end-stage liver disease, palliative care measures should be initiated.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients who have cirrhosis associated with a MELD score of 15 or greater or with complications of cirrhosis should be referred to a transplant center.

A Kanwal et al., 2010 Runyon & AASLD Practice Guidelines Committee, 2009

Patients with severe alcoholic hepatitis with or without hepatic encephalopathy and lacking contraindications to steroid use should be considered for a 4-week course of prednisolone (40 mg/day for 28 days, typically followed by discontinuation or a 2-week taper).

A O’Shea et al., 2010 Uribe et al., 1978

Continued

242 Chapter 10 ■ Abdominal Disorders

Signal Symptoms: Profuse, watery, malodorous diarrhea; abdominal discomfort; fever.

Description: Clostridium diffi cile -associated diarrhea (CDAD) and colitis are a consequence of the colonization and subse- quent infection of the colon by this organism following a dis- ruption of the normal fl ora of the gut by antibiotic exposure (Keller & Surawicz, 2014). Once established in the colon, C. diffi cile produces two potent toxins, Toxin A and Toxin B, that cause fl uid secretion, infl ammation, and injury to the colonic mucosa, resulting in diarrhea and/or colitis. Due to increas- ing antibiotic usage, new and dangerous strains continue to emerge (Trier, 2009). Intestinal colonization by toxigenic C. diffi cile strains does not always result in infection or clin- ical symptoms, meaning some individuals may be asymp- tomatic carriers. Clinical presentation of C. diffi cile diarrhea varies from mild diarrhea as the only symptom to fulminant, life-threatening colitis.

Etiology: CDAD is no longer a hospital-acquired infection only, as outpatient incidences are rising (Lessa et al., 2015). Risk factors include antibiotic exposure, older adults, and health- care facility exposure; however, the presence of infl amma- tory bowel disease, compromised immunity, liver and kidney disease, and prior GI procedures also play a role in increasing the risk for CDAD (Keller & Surawicz, 2014; Surawicz et al., 2013). Less-known risk factors include intensive care admis- sion, prior hospitalization within several months, ventila- tory support, enteral feedings, use of histamine blockers and PPIs, malnourished states, and hypoalbuminemia (Kim, Lee, & Jeong, 2010; Morrison et al., 2011; Tleyjeh et al., 2013).

Bacterial spores are spread via the fecal-oral route and thrive on surfaces such as toilets, hospital equipment, and door handles (Keller & Surawicz, 2014). These spores have the potential to survive for months, even in harsh circum- stances (Jump, Pultz, & Donskey, 2007; Keller & Surawicz,

2014). Asymptomatic carriage of the organism by patients is not uncommon and may hinder adequate infection control measures. The transfer of patients harboring C. diffi cile infec- tion (CDI) from one hospital or long-term care facility to another enables spread of the infection within geographical regions ( Cohen et al., 2010 ; Kee, 2012).

Occurrence: Recent estimations report 29,000 individuals with CDAD succumbed to the illness in 2011, with around 453,000 cases per year (CDC, 2015). Two-thirds of the cases per year are associated with hospital or nursing home admis- sion, while the remaining population may be without any recent health-care exposure. The incidence rate of outpatient infections is increasing, and the overall incidence of CDAD has doubled in prevalence from 2000 to 2015 (Lessa et al., 2015). The incidence in long-term care patients varies from 4% to 50% (Kee, 2012).

Recurrence and risk of death are more common with hos- pital-acquired infections (Lessa et al., 2015). Recurrence of CDAD is defi ned by the presence of diarrhea and a positive stool test, usually occurring 1 to 3 weeks after treatment completion for CDAD (Chopra & Krishna, 2014). Different strains of the bacteria may be responsible for recurrent infec- tion, as 50% of reinfections are a different bacterial strain of C. diffi cile .

Age: Although the infection is diffi cult to manage in all ages, older adult patients can be particularly challenging to treat. Individuals 65 years and older have an increased risk for CDAD along with severe disease manifestations (Keller & Surawicz, 2014; Louie et al., 2013; Surawicz et al., 2013). Advancing age correlates with diffi culty in successful treat- ment, while recurrence risk also increases with advancing age. The concern for decreased immunity in the older adult population is felt to contribute to complicated disease course (Louie et al., 2013).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients should be highly encouraged to abstain from drinking any alcohol.

B Borowsky, Strome, & Lott, 1981

It is highly recommended that patients with cirrhosis have small, frequent, nutritious feedings, including a small snack at bedtime and a small morning meal, to improve overall nitrogen balance.

A

Ascites should be treated with salt restriction and diuretics.

A Kanwal et al., 2010 Licata et al., 2009

Persistent hepatic encephalopathy should be treated with disaccharides or rifaximin (Xifaxan).

B Kanwal et al., 2010 Bass et al., 2010

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

CLOSTRIDIUM DIFFICILE

Chapter 10 ■ Abdominal Disorders 243

Gender: Females have been shown to have higher incidence rate of CDAD than males (Lessa et al., 2015).

Ethnicity: CDAD occurs in all ethnic groups, but Caucasians have been found to have higher incidence rates than other ethnicities (Lessa et al., 2015).

Contributing Factors: The main contributing factor to the development of CDAD is antibiotic exposure. All antibiotics, including antibiotics used in treatment for CDAD, have the potential to stimulate the development of CDAD. Common offending antibiotics include fl uoroquinolones, broad-spec- trum penicillin agents, clindamycin, and second- and third-generation cephalopsorins (Clark & Wiselka, 2008; Hensgens, Goorhuis, Dekkers, & Kujper, 2012; Hessen, 2010; Keller & Surawicz, 2014). Further characterization of anti- biotic offenders (Clark & Wiselka, 2008) may be classifi ed by tier, with clindamycin, second- and third-generation cephalo- sporins, pencillins, and quinolones as high risk; macrolides, tetracyclines, and aminoglycosides noted to be medium risk; and metronidazole and vancomycin rare risk for CDAD. Flu- oroquionolones are associated with a strain identifi ed in the older population known to have diffi culty with treatment response and increased recurrence (Keller & Surawicz, 2014; Surawicz et al., 2013).

Advancing age is a known risk factor. Patients with pro- longed length of stay in a health-care facility can be exposed to the infection, especially if they share common toilets, have severe underlying disease (malignancies), use PPIs and H 2 blockers, need tube feeding, require ventilatory support, are malnourished, and show poor host immune response (Hessen, 2010; Kim, Lee, & Jeong, 2010; Morrison et al., 2011; Tleyjeh et al., 2013). Patients with prior GI surgeries are at risk. The use of perioperative antibiotic prophylaxis has been known to contribute to CDAD (Carignan et al., 2008; Cohen et al., 2010 ). Advanced age, limited mobility and dif- fi culty with activities of daily living, history of depression, heart failure, immunocompromised status, and prior history of CDAD are associated with severe disease in the older adult (Rao et al., 2013).

Signs and Symptoms: The incubation period has not been established. Symptoms can appear immediately after begin- ning antibiotic therapy, or they may not develop until several weeks to months after completion of antibiotic therapy (Trier, 2009). Older adults can present atypically, with lack of fever; alteration in mental status or confusion can be an early sign (Bartlett & Gerding, 2008; Crogan & Evans, 2007).

Mild cases may present with only crampy lower abdominal pain and watery stool; moderate to severe cases present with profuse, watery diarrhea; abdominal pain and tenderness; tenesmus; nausea; anorexia; leukocytosis; hypoalbuminemia; and malaise (Surawicz et al., 2013). Complicated cases are characterized by at least one of the following criteria: inten- sive care, hypotension, ileus, mental status changes, fever, WBC count greater than 35,000 or leukopenia, serum lactate greater than 2.2  mmol/l, and organ failure (Surawicz et al., 2013). High suspicion for megacolon or perforation should be raised if marked tenderness to palpation; toxin injury to the colon results in lost functionality and decreased/absent peristalsis (Carter, Rood, & Lyras, 2012). Sepsis secondary to bacteremia may occur, with 20% mortality rate (Johnson et al., 2012). Other complications include chronic diarrhea,

electrolyte imbalance, hypoalbuminemia with anasarca, and reactive arthritis (Kee, 2012). Endoscopic evaluation via colonoscopy or fl exible sigmoidoscopy may be undertaken when diagnosis is uncertain. The presence of adherent white and yellowish plaques that may coalesce, termed pseudo- membranous colitis, are highly specifi c for C. diffi cile infection (Kee, 2012). However, the absence of pseudomembranous colitis does not exclude the presence of C. diffi cile.

Diagnostic Tests: The triad of leukocytosis, abdominal disten- sion, and hypoalbuminemia raises concern for severe CDAD in a patient with profuse, watery diarrhea (Keller & Surawicz, 2014; Surawicz et al., 2013). Suspicion for CDAD should prompt obtaining stool samples as soon as possible, with the nucleic acid amplifi cation test (NAAT) by polymerase chain reaction (PCR) as the best option for confi rming CDAD (Sur- waricz et al., 2013). This is approved by the U.S. Food and Drug Administration (FDA) and notable for providing quick results. False-negative results of stool specimens have been documented if empirical treatment was commenced prior to obtaining the stool sample; therefore, delay in diagnostic testing could present unclear results (Sunkesula, Kundrapu, Muganda, Sethi, & Donskey, 2013).

The European Society of Clinical Microbiology and Infec- tious Diseases recently completed a large review of existing literature regarding diagnostic methods, with updated guide- lines encouraging the use of a two-step approach to diag- nosing the disease (Crobach et al., 2016). Commercial tests evaluated included two enzyme immunoassays (EIAs) and NAATs. The authors concluded that stand-alone tests may not be suffi cient for correct diagnosis of C. diffi cile infection . This newer approach recommends starting with NAAT by PCR or glutamate dehydrogenase EIA (GDH EIA), with nega- tive results likely true negatives. Positive results of the NAAT or GDH EIA would prompt an EIA with toxin A/B, with posi- tive indicating likelihood of infection and negative indicating possibility of carrier status (Crobach et al., 2016). Peri-rec- tal swabs for diagnosis of infection may also be used in the clinical scenario of paralytic ileus. If suspicion remains high for CDAD despite negative testing, providers must use their best clinical judgment and treat appropriately (Crobach et al., 2016).

Initial baseline laboratory studies should include a CBC with differential; complete metabolic panel; thyroid panel; stool samples to include cultures, ova, and parasites; lactic acid; and a CT scan if concerning abdominal examination or subjective symptoms to exclude megacolon or perfora- tion. Endoscopic evaluation via colonoscopy or fl exible sig- moidoscopy may be indicated if persistent diarrhea and/or worsening clinical status occurs despite appropriate medical treatment. Diagnostic endoscopic evaluation is also helpful when the diagnosis is unclear, such as negative stool studies but persistent symptoms despite medical therapy.

Differential Diagnosis:

■ Acute diarrhea caused by salmonella ■ Shigella ■ Campylobacter jejuni ■ E. coli 0157:H7 ■ Cryptosporidium ■ Giardia ■ Microsporida

244 Chapter 10 ■ Abdominal Disorders

■ Isospora ■ Cyclospora ■ Diarrhea associated with hyperthyroidism or diabetic

neuropathy ■ Irritable bowel syndrome ■ Dietary causes, including nonabsorbable carbohydrates,

caffeine, lactose intolerance, and gluten sensitivity ■ Microscopic and collagenous colitis ■ Pancreatic insuffi ciency ■ Antibiotic-induced chemical effects ■ Known antibiotic effects of bacterial and fungal

overgrowth ■ Food poisoning ■ Bacterial or viral gastroenteritis ■ Infl ammatory bowel disease (Yassin, Young-Fadok,

Zein, & Pardi, 2001)

Treatment: Contact isolation must be employed for hospi- talized individuals who have suspected or known CDAD. Enteric isolation must continue until resolution of diarrhea or discharge (Surawicz et al., 2013). Supportive measures to include oral and IV fl uid replacement, low residue diet, and pharmacological therapy such as antiemetics are indicated. The offending antibiotic agent must be discontinued if clini- cally possible. A coexisting infection (e.g., urinary tract infec- tion, pneumonia) would preclude complete discontinuation of all antibiotic therapy, as these conditions would still need treatment. In this scenario, less-known offending antibiotics such as ampicillin, sulfonamides, erythromycin, tetracycline, and fi rst-generation cephalosporins may be cautiously used (Hessen, 2010). Antidiarrheals should be avoided due to risk of megacolon (Surawicz et al., 2013).

Treatment of choice for non-severe episodes is vancomycin 125 mg orally four times a day for 10 days ( McDonald et al., 2018 ). Fidaxomicin is an alternative antibiotic that may be used for initial non-severe or even severe episodes; however, if vancomycin or fi daxomicin is unavailable, metronidazole may be given 500  mg orally three times a day for 10 days. A fulminant presentation, which would be characterized by shock, ileus, hypotension, or megacolon, would require van- comycin 500  mg orally four times a day and intravenous metronidazole 500 mg three times a day. If an ileus is present or the individual is unable to receive oral medications, van- comycin enemas would be indicated for direct topical therapy ( McDonald et al., 2018 ; Surawicz et al., 2013). Subsequent recurrences should be treated similar to original episode if uncomplicated. Repeated recurrences may require vanco- mycin in a pulse dosed fashion or tapering. Fecal microbiota transplants (FMTs) are indicated after the third recurrence and show promising results for long-standing resolution.

Metronidazole and vancomycin are best absorbed via the oral route, but complicated clinical courses may require administration via other routes. Vancomycin is not highly effective intravenously, which leads to the need for colonic enemas. Fidaxomicin is also an FDA-approved antibiotic

therapy for CDAD, with similar effectiveness to vancomycin; however, cost remains a barrier to obtaining it in some facil- ities and as an outpatient (Cornely et al., 2012; Crawford, Husgen, & Danziger, 2012; Louie et al, 2013).

Emerging therapies for CDAD include FMT, which uti- lizes donor stool that is transplanted to the recipient ’ s colon, most commonly via colonoscopy (Yoon & Brandt, 2010; Musgrave, Bookstaver, Sutton, & Miller, 2011). Other routes include nasogastric tube, enemas, or upper endoscopy. Oral formation of C. diffi cile strains in capsules holds promise for the future, with further studies needed (Gerding et al., 2015).

Follow-Up: The fi rst month following treatment has been shown as crucial due to colonic fl ora disruption, raising concern for recurrence (Kelly, 2012). Recurrence is identi- fi ed as prior resolution with new onset diarrhea and a pos- itive stool sample. Repeated stool testing during the same episode is not necessary, and a “test of cure” via negative stool studies is not recommended (Crobach et al., 2016, p. S79). Risk factors for relapse following treatment for CDAD include renal insuffi ciency, antibiotic exposure during active CDAD, severe strains of C. diffi cile, and advanced age (Louie et al., 2013). Individuals with diabetes and/or sepsis are at risk for metronidazole treatment failure ( Jung et al., 2010 ). Therapeutic response should be based on clinical signs and symptoms, not repeat diagnostic testing.

Sequelae: Chronic colonization, paralytic ileus, toxic mega- colon and fulminating colitis, chronic diarrhea, electrolyte imbalances, hypoalbuminemia, and reactive arthritis are complications of CDI.

Prevention/Prophylaxis: Infection control in health-care set- tings and reduction of risk factors are paramount. Contact isolation should be implemented without delay. The use of electronic rectal thermometers should be avoided ( Cohen et al., 2010 ). Dedicated hospital equipment for the individ- ual is necessary to prevent spread of infection. Proper hand washing is imperative. Equipment and rooms must be sani- tized with bleach cleaning agents to kill spores, per facility protocol.

Referral: Signs and symptoms of ileus or fulminating colitis, failure to respond to conventional therapy, and persistent diarrhea that is unexplained require referral. Inpatient older adults with signs of acute abdomen need a surgical referral. Gastroenterology consultation is recommended for bloody diarrhea, concern for secretory diarrhea, fecal incontinence, and failure to improve symptomatically with pharmacologi- cal therapy.

Education: Avoid unnecessary antibiotics. Universal precau- tions include utilizing hand washing with soap and water, along with bleach cleaning agents to sanitize all surfaces at home and in hospital settings. Do not use antidiarrheal agents. Contact provider if recurrent diarrhea persists after treatment for CDAD.

Chapter 10 ■ Abdominal Disorders 245

Signal Symptoms: A change in bowel habits, persistent diar- rhea, bleeding from the rectum, blood in the stool, unexplained anemia, bloating, unexplained abdominal pain, increased gas, abdominal distention, vomiting, weight loss, fatigue, persistent constipation or feeling that the bowels do not completely empty, rectal pressure, rectal pain, and/or reduction in diam- eter of stool (National Cancer Institute, 2016).

Description: Approximately 50% of neoplasms in the colon occur in the sigmoid and descending colon (54%) (Wasif, Etzioni, Maggard, Tomlinson, & Ko, 2011). Approximately 95% of colorectal cancers are adenocarcinomas (World Cancer Research Fund International, 2012). Leiomyosar- comas account for less than 2% ( Sarcoma Alliance, 2006 ), lymphomas around 0.5% (ACS, 2007), and melanomas are rare, with incidence of less than 2% (Kayhan & Turan, 2003). Neuroendocrine tumors with subsets, including aggressive and indolent, are less than 2% ( Bernick et al., 2004 ).

Etiology: Colorectal cancer results from complex interactions between inherited susceptibility and environmental factors, but the exact nature and contribution of these factors con- tinues to be researched (National Cancer Institute, 2016). Nutritional factors play an important role in its development. High-fat, high-carbohydrate diets with highly processed sugars and carbohydrates and high intakes of red meat, processed meats, and alcohol (which may block the absorp- tion of folic acid) and low-fi ber diets appear to be factors. Smoking, inactivity, obesity, high insulin levels, and excessive adipose tissue centrally located all appear to infl uence the risk of colon cancer ( Giovannucci, 2003 ).

Occurrence: Colorectal cancer is the third most common malignant neoplasm worldwide and the second leading cause of cancer deaths in men and women combined in the United States (National Cancer Institute, 2016). Worldwide, 917,000 deaths occur yearly from colon cancer ( Jonker et al., 2007 ). Colon and rectum cancer represent 8.0% of all new cancer cases in the United States. Approximately 90% of all colorectal cancers occur after age 50 ( American Cancer Institute, 2012 ). Colorectal cancer incidence and mortality rates have been declining, largely attributable to the contri- bution of screening for prevention and early detection (Smith et al., 2015). Cancer rates vary in levels of education (Albano et al., 2007).

Age: The incidence of colorectal cancer increases with age. Ninety percent of the cases of colorectal cancer occur in people over 50 years old, with a peak incidence in those in their seventies (ACS, 2012).

Gender: Men are more likely to be diagnosed with colon cancer than women of the same age (Jemal et al., 2009).

Ethnicity: African Americans have a higher incidence of new colorectal cancer diagnosis and higher mortality rates from colorectal cancer than non-Hispanic Caucasians (SEER 18 2009-2013, Age-Adjusted) with Native Americans and Latino Americans below 2% (Agrawal et al., 2005).

Contributing Factors: Lifestyle, education, and specifi c genetic disorders (familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer) are associated with high risk of developing colorectal cancer (Lynch et al., 1993) and infl ammatory bowel diseases.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Reducing the frequency and duration of antimicrobial therapy can reduce the risk of recurrence of CDI.

A Cohen et al., 2010

Vancomycin is the drug of choice for initial episodes of uncomplicated cases of CDI.

A McDonald et al., 2018

Removing the provoking antimicrobial agent may reduce the rate of CDI recurrence.

A Cohen et al., 2010

Low serum albumin was found to be associated with relapse of C. diffi cile colitis following initial treatment.

B Nair, Yaday, Corpuz, & Pitchumni, 1998

Diabetes mellitus and sepsis were identifi ed as independent risk factors for metronidazole treatment failure in CDI.

B Jung et al., 2010

Removal of environmental sources (electronic thermometers with disposal covers) can reduce the spread of CDI.

B Cohen et al., 2010

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

COLORECTAL CANCER

246 Chapter 10 ■ Abdominal Disorders

American Cancer Society Guidelines on Screening and Surveillance for the Early Detection of Colorectal Adenomas and Cancer—Women and Men at Increased Risk or at High Risk

RISK CATEGORY AGE TO BEGIN RECOMMENDATION COMMENT

Increased Risk

People with a single small

(<1 cm) tubular adenoma

5–10 years after the baseline

colonoscopy, assuming

that all visible polyps were

completely removed

Colonoscopy If the examination is normal, the patient can

thereafter be screened as per average risk

guidelines.

People with a large (1 cm + ) adenoma, multiple adenomas

(greater than 3), or adenomas

with high-grade dysplasia or

villous change

Within 3 years after the

baseline colonoscopy

assuming that all visible

polyps were completely

removed

Colonoscopy If normal, repeat examination in 3 years; if normal

then, the patient can thereafter be screened as per

average risk guidelines.

Personal history of curative-

intent resection of colorectal

cancer

Within 1 year after cancer

resection

Colonoscopy After the 1-year colonoscopy the interval to the

next colonoscopy should be 3 years (i.e., 4 years

after surgery) and then 5 years (i.e., 9 years after

surgery). Subsequent colonoscopies should occur

at 5-year intervals until the benefi t of continued

surveillance is outweighed by diminishing life

expectancy (Kahi et al., 2016).

TABLE 10-1

Signs and Symptoms: Clinical symptoms include rectal pres- sure, passing bright red blood, constipation, bloating, diar- rhea, weight loss, melenonic stools, nausea, and loss of appetite. Patients presenting in the clinic with microcytic anemia should be evaluated for rectal bleeding and possible colorectal cancer.

Diagnostic Tests: Initial screening tests that primarily detect cancer include fecal occult blood tests (FOBTs) such as Hemoccult SENSA (Beckman Coulter, Inc.), immunochem- ical-based fecal occult blood tests (FITs), and stool tests for exfoliated DNA (sDNA) (Smith et al, 2015). Flexible sigmoid- oscopy and colonoscopies can detect cancer and advanced lesions and are used for a biopsy and diagnosis. Additional work-up can include digital rectal examination to palpate for any identifying masses, CBC with differential, chemistry panel, carcinoembryonic antigen (CEA), C-reactive protein (CRP), CT scan to determine metastases, and a positron emis- sion tomography (PET) scan for staging purposes. A new screening method, CT colonography or virtual colonoscopy, is a procedure that allows imaging the colorectal region by CT radiographs.

Differential Diagnosis:

■ Diverticulitis ■ Weight loss ■ Blood in the stool ■ Mass in the colon ■ Prostatic carcinoma ■ Sarcoma ■ Infl ammatory bowel disease ■ Hemorrhoids ■ Benign colonic polyps ■ Peptic ulcer disease (PUD) ■ Functional bowel disorders (Tamparo, 2016)

Treatment: The extent of treatment for colorectal cancer depends on how invasive the cancer is in the colon and sur- rounding sites, and the condition of the patient at the time of

diagnosis. The most widely used staging system among clini- cians is the TNM system maintained by the American Joint Committee on Cancer (AJCC) and the International Union for Cancer Control (UICC). This system can be used for many types of cancer (Edge & Compton, 2010). The staging of colorectal cancer is predicted using the Dukes classifi cation. Patients should be referred to a surgeon for consideration of a radical resection. Presence of metastatic disease does not rule out surgery. The chemotherapeutic agent 5-fl uorouracil combined with Avastin is an effective adjuvant therapy after a surgical resection of stage III colorectal cancer, even in older adults.

Follow-Up: After curative surgery, oncology follow-up is essential, which may include CT scan and CEA markers reg- ularly, depending on stage of cancer. Primary care providers will need to closely monitor for symptoms of fatigue, weight loss, and change in bowel habits with annual FOBTs, and colonoscopy within 1 year. Annual physical examinations are encouraged.

Sequelae: Complications of colorectal cancer include obstruc- tion and perforation, and possible colostomy. Post-resection recurrence of colorectal cancer is common. Radiation proc- titis with burning and diarrhea may occur. Bowel adhesions and chronic pain may also be a complication. The liver and bone are two sites known for metastasis after colorectal cancer.

Prevention/Prophylaxis: The ACS recommends that begin- ning at age 50 years all asymptomatic individuals with no risk factors should have an annual FOBT. FOBT at home is recommended over FOBT with a single stool sample col- lected by the clinician during a digital rectal examination (DRE) or a guaiac-based toilet bowel FOBT test. FITs may be more patient friendly (Smith et al., 2015). Clinicians should educate patients that stool tests require annual commitment. The gold standard for screening is delineated in Table 10-1 (ACS, 2012). Prolonged prophylactic use of aspirin, calcium,

Chapter 10 ■ Abdominal Disorders 247

American Cancer Society Guidelines on Screening and Surveillance for the Early Detection of Colorectal Adenomas and Cancer—Women and Men at Increased Risk or at High Risk—cont’d

TABLE 10-1

RISK CATEGORY AGE TO BEGIN RECOMMENDATION COMMENT

Increased Risk

Either colorectal cancer or

adenomatous polyps, in any

fi rst-degree relative before age

60, or in two or more fi rst-

degree relatives at any age (if

not a hereditary syndrome)

Age 40 or 10 years younger

than age at diagnosis of the

youngest affected relative

(Rex et al., 2009)

Colonoscopy Every 5 years (Rex et al., 2009). Colorectal cancer

in relatives more distant than fi rst-degree does not

increase risk substantially above the average risk

group.

High Risk

Family history of familial

adenomatous polyposis (FAP)

Puberty Early surveillance with

endoscopy, counseling

to consider genetic

testing

If the genetic test is positive, colectomy is indicated.

These patients are best referred to a center with

experience in the management of FAP.

Family history of Lynch

syndrome (hereditary

nonpolyposis colon cancer

[HNPCC])

Age 2 (?) Colonoscopy and

counseling to consider

genetic testing

If the patient has not had genetic testing,

colonoscopy every 1–2 years starting by age 25

years or 5–10 years before the age of earliest

colorectal cancer diagnosed in the family, whichever

is younger. At age 40 begin annual colonoscopy.

If the patient has a positive gene test, yearly

colonoscopy is recommended (Johns Hopkins

Medicine, 2016).

These patients are best referred to a center with

experience in the management of HNPCC.

Infl ammatory bowel disease,

chronic ulcerative colitis,

Crohn ’ s disease

Cancer risk begins to be

signifi cant 8 years after the

onset of pancolitis or 12–15

years after the onset of left-

sided colitis

Colonoscopy with

biopsies for dysplasia

Every 1–2 years. These patients are best referred

to a center with experience in the surveillance and

management of infl ammatory bowel disease.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Prevention of colorectal cancer by screening is cost effective, and if caught early, colorectal cancer is curable. Recommend annual FOBT; screening colonoscopy at age 50 based on meta-analysis of research studies involving colonoscopy and annual screenings; 75% of colorectal tumors do not appear to be due to inherited genetic mutations. Some experts suggest screening African Americans beginning at age 45 (Rex et al., 2009).

A ACS, 2012

and vitamin D supplementation may reduce the risk of colon cancer, as might weight loss and a diet high in fruits and vegetables.

Referral: A gastroenterologist should be consulted for colon- oscopy and a biopsy of the lesion should be obtained to determine the kind of cancer. A surgical consultation with a cancer surgeon, usually found at a major medical center, is advised. A team including a radiologist, oncologist, cancer

surgeon, nutritionist, pharmacist, and nurse will develop a plan of care individualized to the patient and type of cancer. The team, along with valuable input from the patient and family, will then decide the treatment. Hospice may be a nec- essary choice and is available in all communities.

Education: Teach older adults about the importance of routine surveillance for rectal bleeding and to report any change in bowel habits.

Continued

248 Chapter 10 ■ Abdominal Disorders

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

An adenoma is a polyp that resembles the normal lining of the colon but differs microscopically. They can occur without symptoms and may be precursors to adenocarcinoma of the colon. Fewer than 10% of all adenomas become cancerous, however, more than 95% of colorectal cancers develop from adenomas. Many can be detected radiographically. Patients have many choices in deciding kinds and costs of screening tools; shared decisions should be made after appropriate counseling.

B Buetow & Buck, 2006 Association of Directors of Anatomic and Surgical Pathology, 2014

Rare cancer (<2%). Routine screening recommended unless diagnosed, then annually.

A Sarcoma Alliance, 2006

Colorectal cancer (advanced neoplasia) is signifi cantly higher in men than in women. This could warrant refi nement of the screening recommendations for colorectal cancer.

A Regula et al., 2006

Diet and body weight with hyperinsulinemia are important risk factors for colorectal cancer. The majority of colon cancers may be prevented by consuming foods that are higher in dietary fi ber, such as fruits and vegetables; keeping BMI within normal ranges and avoiding smoking have been proven to reduce the incidence of colorectal cancer.

A Giovannucci, 2003

The most modifi able determinants of cancer risks are weight control, dietary choices, and levels of activity. Recommendations are to maintain a healthy weight, get regular physical activity, limit processed meat and red meat, and avoid alcohol and tobacco. Collaborative work in communities to promote healthy worksites, schools, and marketing of foods and beverages that have good nutritional value, particularly to youth, is advised.

A American Cancer Institute, 2012

Appropriate staging of colorectal cancer improves outcomes and allows for appropriate follow-up. Established guidelines are correlated to the staging of colorectal cancer and provide practitioners a better prognostic picture.

A

Colorectal cancer mortality rate is declining, but incidence rates are increasing. Obesity, diabetes, and diets high in processed foods all seem to correlate to higher rates. Providing patients with facts on colorectal cancer risks and preventive measures may reduce the incidence.

A Jonker et al., 2007

The USPSTF recommends screening for colorectal cancer using fecal occult blood testing, sigmoidoscopy, or colonoscopy beginning at age 50. Diagnosing colorectal cancer early has improved mortality rates.

USPSTF, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Chapter 10 ■ Abdominal Disorders 249

Signal Symptoms: Impaired cognitive status, lower quadrant pain.

Description: Diverticulitis is an infl ammatory condition that involves perforation of one or more colonic diverticula, which are herniations of the mucosa through the muscularis of the colon. It usually occurs in the sigmoid or descending colon. Infl ammation of the diverticulum begins at the apex when the narrow opening of the lumen is exposed to fecal residue. Mucosal erosion within the diverticulum also can occur, leading to diverticulitis.

Etiology: Diverticula are common in older adults. Age-related changes in the elastic matrix of the colon and the resulting sluggish fecal mass are thought to cause increased intralu- minal pressure of the colon. Diverticular disease is rare in societies that consume high-fi ber diets. It is thought that a low-fi ber diet produces less bulky stool and increased intra- colonic pressure. Diverticulitis is thought to develop when one or more diverticula are perforated (macroperforation or microperforation). A pseudodiverticulum occurs when only the mucosa and submucosa of the colon are affected (Sheth, Longo, & Floch, 2008). Approximately 85% of all cases of diverticulitis involve the left colon and sigmoid. Because this perforation is usually a localized process, free intraperitoneal air or diffuse peritoneal signs are usually not evident; their presence would indicate a more severe case and the possible need for surgical consultation.

Occurrence: An estimated 70% of older adults develop diver- ticulosis by age 85 years, with the prevalence rising to 80% for adults in their nineties. Approximately 10% to 25% of the population with diverticulosis goes on to develop symptoms of diverticulitis, which is usually most severe in older adults (Hall, 2014).

Age: Diverticulitis is found most commonly in older adults, most commonly in the sixties to eighties.

Gender: Diverticulitis occurs more commonly in women than men (Commane, Arasardnam, Mills, Mathers, & Brad- burn, 2009).

Ethnicity: Diverticulitis is found almost exclusively in Western- ized countries or populations that have begun to consume a refi ned Western diet. People of Asian descent are more likely to have right-sided diverticulitis (Kvansnovsky, Papagrigor- idia, & Bjarnason, 2014).

Contributing Factors: While there are patients who may not have been diagnosed with diverticulosis prior to an acute case of diverticulitis, it is important for the nurse practi- tioner to recognize known risk for developing diverticulo- sis. Obesity, as well as sedentary lifestyle, has been found to contribute to diverticular disease. One study, however, found a relationship between the development of diverticulosis in patients who had seven bowel movements a week as com- pared to patients who had less than seven; suggesting, too, that a diet high in fi ber was not protective of the formation of diverticulosis (Perry & Sandler, 2013). Patients who reg- ularly consumed processed and red meat were found to have

a high prevalence of diverticular disease; whereas regular inclusion of fruits and cereal in the diet has been shown to reduce the risk for developing diverticulosis. In one Danish study, there were high indications of developing diverticu- lar disease among siblings, however, there may be more of a connection because of shared environmental risks (Strate, Erichsen & Barron, 2013).

Advancing age is the primary nonmodifi able risk factor for developing diverticulitis (Commane et al., 2009). Chronic constipation and the need to strain to defecate contribute to diverticulitis. These two conditions lead to colonic wall weakness and raise the intraluminal pressure (Jacobs, 2007). Long-term use of NSAIDs, aspirin, antiplatelets, and immu- nosuppressant drugs increases the incidence of diverticu- litis (Nagate, Niikurs, & Aoki, 2014). The development of diverticulitis also has been associated with chronic cigarette smoking and adult polycystic kidney disease. There is a rela- tionship between physical inactivity and the development of diverticulitis (Mulligan, 2015). A recent study also indicated a connection between increased body mass index (BMI) in men (over 30 years) and diverticulitis ( Strate, Liu, Syngal, Aldoori, & Giovannucci, 2008 ). Similarly, patients with increased waist circumference have a tendency to develop diverticular disease ( Strate et al., 2008 ).

Signs and Symptoms: Clinical presentation of diverticulitis in an older adult may be suppressed despite the presence of severe disease. Mental confusion may be the fi rst overt indi- cation of diverticulitis in older adults with known divertic- ular disease. Patients also may report recent anorexia. They may report a low-grade fever. History of left lower quadrant pain aggravated by movement and fever may be present. They may report that the pain is precipitated by eating and describe a colicky pain (Salzman & Lillie, 2005). Pain also may be reported in the fl ank, back, or right side of the abdomen. Patients may describe the pain as dull, aching, and intermittent. A sensation of “bloating” may be the initial complaint offered. Associated complaints of nausea and vomiting suggest obstruction (Wilkins, Embry, & George, 2013). Obstipation, constipation, or diarrhea; abdominal cramping without the abdominal pain; and fever also may occur (McQuaid, 2010). Patients may experience abdominal or perirectal fullness. If the bowel is infl amed adjacent to the bladder, the presentation may mimic a urinary tract infec- tion, especially if the patient reports dysuria. Joint pain may be reported in the hip, knee, and/or thigh (Frattini & Longo, 2006). Acutely ill patients with a moderate-to-severe episode of diverticulitis may present with lethargy, refl ecting signs of fl uid depletion and sepsis.

Bowel sounds may be normal in mild disease; however, bowel sounds become hypoactive until there is an obstruc- tion, when a tinkling sound may be heard. Hyperresonance may refl ect intestinal obstruction. Localized tenderness is usually present in the left lower quadrant. Rebound tender- ness, involuntary rigidity, and guarding are signs of perito- nitis (Wilkins, Embry, & George, 2013). A mass palpated in the left lower quadrant may indicate an abscess. Occult rectal bleeding occurs in about 25% of patients with diverticulitis. Tenderness may be elicited during the rectal examination.

DIVERTICULITIS

250 Chapter 10 ■ Abdominal Disorders

Patients in acute distress may have pyrexia, tachycardia, and impending signs of hypovolemia (Jacobs, 2007).

Diagnostic Tests: A CBC, amylase, lipase, urinalysis, C-reactive protein sedimentation rate, and plain abdominal radiographs can be initially ordered (Mulligan, 2015, Wilkins, Embry, & George, 2013). Leukocytosis may be present. Normal amylase and lipase will help distinguish diverticulitis from other causes of acute abdominal pain. Urinalysis may reveal sterile pyuria due to adjacent colonic irritation; however, if mixed colonic fl ora are present, consider the presence of a colovesical fi stula (McQuaid, 2010). Abdominal x-rays may reveal perforation (free air) and bowel obstruction. Patients should be scheduled for a CT scan of the abdomen and pelvis. CT scans performed with oral, IV, and rectal contrast can enhance the accuracy of the diagnostic image (Rafferty, Shellito, Hyman, & Buie, 2006). Sigmoidoscopy, colonoscopy, and barium enema are usually avoided during acute diver- ticulitis because these tests may cause further perforation or leakage of bowel contents (Jacobs, 2007). These tests may be performed several weeks after the resolution of the acute episode. Gram stain and testing for C. diffi cile should be con- sidered in patients with diarrhea ( Strate et al., 2008 ).

Differential Diagnosis:

■ Acute appendicitis—suspect if right lower quadrant symptoms or nonresolution with medical therapy

■ Infl ammatory bowel disease (Crohn ’ s disease) ■ Complicated PUD—suspect if pneumoperitoneum or

peritonitis ■ Ischemic colitis—suspect if high-risk patient, bloody

diarrhea, or thumb printing ■ Pseudomembranous colitis—suspect if antibiotic use or

diarrhea ■ Vascular ectasia—consider leaking abdominal aortic

aneurysm ■ Carcinoma of the colon—suspect if weight loss or

bleeding ■ Urological disorders, such as infection or ureteric colic ■ Gynecological carcinomas or abscesses ■ Pelvic infl ammatory disease ■ Infectious colitis ■ Small bowel obstruction ■ Endometriosis ■ Ovarian cyst ■ Testicular torsion ■ Gastroenteritis ■ Bowel obstruction ■ Irritable bowel syndrome ■ Kidney stone (Wilkins, Embry & George, 2013)

Treatment: Diverticulitis is found to be polymicrobial and results from bacteria normally found in the GI tract (Spirit, 2010). The selection of antibiotics for the treatment of diver- ticulitis needs to consider the most common bacteria found in the colon, which are gram-negative aerobic rods and anaer- obic microorganisms (Rafferty et al., 2006). For mild cases, use broad-spectrum antibiotics such as ciprofl oxacin 250 to 500  mg every 12 hours or levofl oxacin 500  mg or moxifl ox- acin 400  mg once a day, plus metronidazole 250 to 500  mg three times a day for 7 to 10 days. An alternative choice is amoxicillin and clavulanate potassium 875  mg twice a day for 7 to 10 days. It is important to follow up with the patient

within 48 to 72 hours and inquire about pain, ability to tol- erate clear liquid fl uids, and if the patient has become febrile (McQuaid, 2010), because improvement should occur if a medication regimen such as this is followed (World Gastroen- terology Organization, 2007). Before recommending outpa- tient treatment, ensure that there is a reliable support system available. Patients treated at home should be able to tolerate oral fl uids and lack peritoneal signs (Lutwak & Dill, 2013). The diet can be advanced if there has been improvement in symptoms during this time (Alonso et al., 2010).

Hospitalization should be considered for older adults with diverticulitis, owing to the uncertainty of the severity of the disease because of possibly subdued presentation and comor- bid diseases (Lutwak & Dill, 2013). Acute treatment for hos- pitalized patients consists of bedrest; restriction of any fl uids by mouth; nasogastric suction if nausea, vomiting, or other indication of obstruction is present; and IV fl uids and elec- trolytes. It is recommended to try a single-agent parenteral antibiotic for adequate coverage of bowel fl ora for the treat- ment of severe diverticulitis. Selection of antibiotics used in the treatment of acute diverticulitis include:

■ Ciprofl oxacin 250 to 500  mg IV every 12 hours plus metronidazole 500 mg IV every 6 hours

■ Ceftizoxime 2 g IV every 12 hours ■ Cefoxitin 2  g IV every 8 hours plus metronidazole

500 mg IV every 6 hours ■ Moxifl oxacin 400 mg IV every 24 hours ■ Ampicillin-sulbactam 3 g every 6 hours ■ Piperacillin-tazobactam 3.375 g every 6 hours or 4.5 g

every 8 hours ■ Ticarcillin-clavulanate 3.1 g every 4 hours

Pay special attention to the patient ’ s renal function and creatinine clearance level. Aminoglycosides should only be considered in patients with normal renal function (Rafferty et al., 2006). Antibiotics may need to be adjusted following culture from any drainage or aspiration.

Follow-Up: Older adults with mild cases treated at home with prescribed therapy should expect improvement by the third day. If, however, patients are not able to tolerate fl uids and/or fail to respond to narcotic analgesics, refer for hos- pitalization. Hospitalized patients require daily monitoring for persistent signs and symptoms of diverticulitis, labora- tory values, and response to treatment. Patients need to be aware of the high rate of recurrence; approximately 30% of patients with diverticulitis have a recurrence (Mulligan, 2015). Surgical consultation may be necessary if the patient does not respond to treatment and continues to have an elevated WBC count, fever, rebound tenderness, pain, and tachycardia. Approximately 25% of patients with divertic- ulitis require surgical intervention. Once the acute divertic- ulitis has resolved, consider referring the patient for further diagnostic imaging studies such as colonoscopy or contrast enema x-ray (Lau et al., 2011; McQuaid, 2010; Rafferty et al., 2006).

Sequelae: Complications include anemia, bowel perforation, peritonitis, pericolonic or intramesenteric abscess, coloves- ical fi stula (most common fi stula in patients with diver- ticulitis), hemorrhage, and bowel obstruction. Of patients with diverticulitis, more than 50% eventually have bowel obstruction (Wilkins, Embry, & George). Complications from

Chapter 10 ■ Abdominal Disorders 251

diverticulitis tend to be most severe in patients who are immunocompromised, including those with diabetes, CKD, cirrhosis, or those on immunosuppressant therapies (Hall et al., 2011). Risk of bleeding in diverticular disease increases in patients taking anticoagulants and antiplatelets, aspirin, CCBs, steroids, and NSAIDs (Mulligan, 2015).

Prevention/Prophylaxis: Recognition of early signs and symp- toms of diverticulitis helps prevent severe cases (Maconi, Barbara, Bosetti, Cuomo & Annibale, 2011). The use of a symbiotic mixture was found to be benefi cial in prevent- ing recurrence of constipation-related abdominal pain in patients with diverticulum disease ( Lamiki et al., 2009 ). Evidence does not support that the inclusion of nuts, seeds, corn, and popcorn in the diet contributes to the development of diverticulitis ( Strate et al., 2008 ).

Referral: Severe episodes of diverticulitis require consultation with a gastroenterologist for hospitalization. Patients with localized abscesses need to be referred for consideration of a CT scan-guided percutaneous drainage (Mulligan, 2015). Repeated episodes may require surgical consultation for an elective sigmoid resection.

Education: Provide information on a high-fi ber diet or fi ber supplementation or both ( Strate et al., 2008 ; Tarleton & DiBaise, 2011). Teach patients to increase their fl uid intake, unless otherwise cautioned, especially when taking fi ber sup- plements. Diverticulitis recurs in approximately one-third of all patients who receive medical management only. Encour- age obese older adults to consider weight reduction, as obesity has been found to be a contributing factor to complicated cases of diverticulitis (Wilkins, Embry, & George, 2013).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Despite long-time popular belief, current evidence is lacking to show that including nuts, seeds, corn, and popcorn in one ’ s diet contributes to the development of diverticulitis.

B Strate, Liu, Syngal, Aldoori, & Giovannucci, 2008

Regular intake of fi ber may be benefi cial in the prevention and recurrence of diverticular disease.

B Tarleton & DiBaise, 2011

Patients with known diverticular disease benefi ted from taking a prescribed symbiotic mixture; recurrence of diverticular disease was prevented in patients with constipation-predominant symptoms.

B Lamiki et al., 2009

CT scan of the abdomen and pelvis is highly recommended as the imaging study of choice in patients with suspected acute diverticulitis.

A Ambrosetti, Jenny, Becker, Terrier, & Morel, 2000

Regular use of NSAIDs or aspirin has been associated with an increased risk of developing diverticulitis and diverticular bleeding.

B Strate, Liu, Huang, Giovannucci, & Chan, 2011

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

ESOPHAGITIS

Signal Symptoms: Dysphagia, regurgitation, pyrosis.

Description: Esophagitis is an infl ammation of the lining of the esophagus.

Etiology: There are a number of different causes for esoph- agitis. Patients may develop esophagitis if they ingest med- ication improperly; have chronic medical conditions; ingest caustic chemicals; are exposed to radiation treatments; have a bacterial, viral, or fungal infection (especially those patients who are immunocompromised); or have a history of GERD

(Aparanji, Annavarappu, Russell, & Dharmarajan, 2012). Candida albicans is the most common fungal infection (Klie- mann, Pasqualotto, Falavigna, Giaretta, & Severo, 2008). The herpes simplex virus type 1 also can cause esophagitis, as can cytomegalovirus. Bacterial esophagitis is rare but can coincide with a fungal or viral infection, making it diffi cult to diagnose. In GERD, esophagitis is a common complica- tion. Hiatal hernia, an intrinsic factor to the development of refl ux esophagitis, increases in incidence with increasing age ( Masaoka, Kondo, Yano, Araki, & Nobutomo, 2012 ).

252 Chapter 10 ■ Abdominal Disorders

Eosinophilic esophagitis results from infl ammation and is clinically evident by dense esophageal eosinophilia with severe squamous epithelial hyperplasia.

Occurrence: It is estimated that as much as 59% of the general population experiences some symptoms of esophagi- tis (Cohen et al., 2014). One study found as many as 19% of the population suffers from asymptomatic esophagitis ( Lee et al., 2016 ).

Age: Esophagitis can occur at all ages.

Gender: Esophagitis occurs equally in men and women.

Ethnicity: Not signifi cant.

Contributing Factors: In older adults, normal aging changes such as decreased salivation, gastric motility, and delayed gastric emptying can contribute to the development of esoph- agitis. Obesity and conditions that contribute to limited upper body mobility, such as spinal cord injuries, may increase the risk of esophagitis. Infectious agents are known to cause esophagitis in patients with certain viral, bacterial, parasitic, and fungal infections. Predisposing factors for patients who develop Candida esophagitis include radiation therapy, che- motherapy, certain hematological malignancies, AIDS, alco- holism, and malnutrition. Swallowing certain medications such as aspirin, antibiotics, ferrous sulfate, certain chemo- therapeutic agents, NSAIDs, quinidine, steroids, alendronate, alprenolol, vitamin C, phenytoin, calcium preparations, the- ophylline, and potassium chloride contributes to pill esoph- agitis due to chemical irritation of the esophageal mucosa. Patients often report that insuffi cient fl uid intake and not remaining upright after the medication is taken contributed to the symptoms of esophagitis (Aparanji et al., 2012).

Substances that can weaken the lower esophageal sphinc- ter (coffee, peppermint, alcohol, spicy foods, citric fruits, chocolate, nifedipine, verapamil, and progesterone) can contribute to esophagitis. Several systemic disorders place patients at risk for esophagitis, including pemphigus vul- garis, bullous pemphigoid, Stevens-Johnson syndrome, lichen planus, infl ammatory bowel disease, sarcoidosis, scleroderma, chronic granulomatous disease, and motility disorders of the esophagus. Patients with left atrial enlargement may experi- ence esophagitis due to the pressure of the left atrium exerted on the distal esophagus (Aparanji et al., 2012).

Signs and Symptoms: A history of dysphagia and pain on swallowing is common. Associated pyrosis, regurgitation, coughing, wheezing, and progressive hoarseness may occur. A fever may be present in patients with an infectious process. Patients should be questioned about medication usage, history of radiation treatments, smoking, and intake of sub- stances that weaken the lower esophageal sphincter; sleeping habits; and use of any tight or restrictive clothing. Review patient medical history for chronic conditions that can con- tribute to esophagitis.

Physical examination usually produces no positive fi nd- ings for simple esophagitis, but can be used to rule out other etiologies of abdominal pain. Oral thrush may be found in patients with C. albicans . Palpate for any upper abdominal masses or tenderness. Perform a rectal examination to detect any frank bleeding and stool guaiac to detect occult blood. Examine the oral cavity for sores and the skin for signs of immunosuppression or systemic diseases like scleroderma (Devuni & Birk, 2017a).

Diagnostic Tests: If suspicion was aroused on the physical examination, stool should be checked using the guaiac test to determine if there has been any intestinal bleeding. Labora- tory studies are not required when antacids, position change, or both relieve pyrosis. For older adults who complain of persistent dysphagia or odynophagia with or without fever, a barium swallow or an endoscopy (with brush and biopsy if structural mucosal damage is suspected), or both are ordered. pH monitoring studies may be considered; however, in patients with eosinophilic esophagitis, the results are usually normal and, as such, pH monitoring can be utilized to rule out GERD over eosinophilic esophagitis in differential diagnosis (Akhondi, 2017).

Differential Diagnosis:

■ Esophageal stricture (upper GI sinus) ■ Esophageal carcinoma ■ Cholecystitis and biliary colic ■ GI foreign body ■ Acute coronary syndrome ■ Angina pectoris ■ Myocardial infarction ■ PUD (Devuni & Birk, 2017b)

Treatment: For infectious esophagitis, temporary symptom- atic relief can be obtained with sucralfate slurry, 1  g/10  mL orally four times daily. Viscous lidocaine (2%), 15  mL orally every 4 hours as needed to swish and swallow, can be used for short-term temporary relief, unless contraindicated by poten- tial drug interactions or history of cardiac or hepatic disease. For mild cases of C. albicans infection, nystatin oral suspen- sion, 400,000 to 600,000 units four times daily spaced evenly over 24 hours, is prescribed. Ketoconazole should not be given at the same time as antacids or H 2 blockers. For severe cases of herpes simplex virus–induced esophagitis, IV acyclovir may be given, adjusting the dosage for the patient ’ s weight and creatinine clearance. Esophagitis from radiation can be treated with viscous lidocaine. For erosive esophagitis, use of PPIs is recommended for 4 weeks, followed by reevalu- ation. In moderate to severe cases, PPIs have been found to be consistently superior to other options, including H 2 receptor blockers, in esophageal healing; however, agent selection and dose should be tailored to each patient ( Kroch & Madanick, 2017 ).

Follow-Up: Patients should report progress at least 1 week after treatment. An endoscopy may be repeated if the patient is still symptomatic but compliant after the initial treatment. Yearly endoscopy is recommended thereafter for patients with severe cases of esophagitis. Patients with eosinophilic esophagitis generally do not respond to treatment with PPIs (Akhondi, 2017).

Sequelae: Ulceration and bleeding, if refl ux esophagitis is present, can occur after esophagitis. Barrett ’ s esophagus with possible adenocarcinoma may be a long-term complication ( Erichsen et al., 2012 ).

Prevention/Prophylaxis: Because of the high recurrence rate of esophagitis, patients should be instructed to follow all nonpharmacological measures unless otherwise instructed. Maintenance therapy for esophagitis may be prescribed for an extended time, although the dose and need should be peri- odically evaluated (Freedberg, Kim, & Yang, 2017).

Chapter 10 ■ Abdominal Disorders 253

Referral: A gastroenterologist should be consulted for the endoscopy and for patients with severe or nonresponsive esophagitis.

Education: Patients with refl ux esophagitis should be instructed to raise the head of the bed 4 to 6  in. with shock blocks. Factors that increase abdominal pressure, such as

wearing tight restrictive clothing, should be avoided. The patient should avoid smoking and ingestion of fatty foods, coffee, chocolate, mints, citric juices, alcohol, and large quantities of fl uids with meals. Remind patients not to break or crush extended-release or delayed-release tablets. Teach the patient the importance of swallowing medications with an adequate amount of fl uids.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients with erosive refl ux disease are at increased risk for developing adenocarcinoma.

B Erichsen et al., 2012

The incidence of hiatal hernia was found to increase with age.

B Masaoka et al., 2012

Hiatal hernia is an independent risk factor for asymptomatic erosive esophagitis

B Lee et al., 2016

PPIs have been found to be superior to H 2 receptor blockers in esophageal healing, preventing relapse of symptoms at 6 months, and maintaining symptom remission for more than 6 months.

A Kroch & Madanick, 2017

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

GASTRIC CANCER

Signal Symptoms: Weight loss and incessant abdominal pain are the most frequent symptoms at the time of diagnosis, reported by greater than 52% of patients (Mansfi eld, 2017). Weight loss is usually a consequence of decreased intake, and may be derived from dyspepsia, anorexia, nausea, and/or dysphagia. A palpable abdominal mass is the most common physical fi nding in gastric cancer and is usually indicative of advanced disease (Mansfi eld, 2017).

Description: Gastric cancer develops when cells in the stomach begin to grow rapidly and uncontrollably. Eventu- ally, this rapid cell growth will begin to interfere with the normal functions of the stomach. Adenocarcinoma accounts for approximately 90% to 95% of gastric cancers. Adenocar- cinoma arises from the stomach mucosa. About 4% of gastric cancers are classifi ed as lymphoma and are usually found in the wall of the stomach. Carcinoid tumors are found in the hormone-generating cells of the stomach and make up 3% of stomach cancers. Carcinoid tumors are unlikely to metastasize to other organs. GI stromal tumors (GISTs) form in the interstitial cells of Cajal in the stomach wall. GIST tumors can be cancerous or noncancerous. Additional types of gastric cancer include small cell carcinoma, leiomyosar- coma, and squamous cell carcinoma, however, these types of cancer very rarely present in the stomach (ACS, 2016). Gastric cancers are then further subdivided by histopatholog- ical and anatomical criteria. Recent work has identifi ed that

further subgroupings by gene expression exist and suggest a new classifi cation of gastric tumors (Shah et al., 2011).

Early gastric cancers generally are confi ned to the mucosa or submucosa. Advanced gastric carcinomas penetrate the muscularis propria with lymph node involvement. Gastric cancer usually begins in the distal portion of the stomach and spreads via the lymph, circulatory system, peritoneal seeding, and direct extension (Rowser, 2013).

Etiology: The etiology of gastric cancer is multifactorial. The difference in type and/or location of gastric cancer may also yield different etiologies. Intestinal-type gastric cancer accounts for 70% to 80% of gastric cancers (Cornett & Dea, 2015). It is strongly linked to environmental factors and is thought to progress from chronic gastritis to atrophic gas- tritis, intestinal metaplasia, dysplasia, and fi nally, adenocar- cinoma (Chan & Wong, 2016). An infection by the bacteria Helicobacter pylori allows the microbes to tunnel into the mucosal lining of the stomach and cause infl ammation and cellular damage (Jenks, 2015). It is estimated that gastritis caused by H. pylori infection is attributable to 60% to 90% of gastric cancers (Cornett & Dea, 2015; Li et al., 2014 ).

Diffuse-type gastric cancers are most derivable from an acquired or hereditary mutation in the cell adhesion protein E-cadherin. “Familial diffuse gastric cancers account for 1% to 3% of gastric cancers” (Cornett & Dea, 2015, p. 1603). Proximal gastric tumors differ from more distal tumors in

254 Chapter 10 ■ Abdominal Disorders

that they are not associated with severe gastritis, and carci- nomas in the cardia of the stomach are more strongly asso- ciated with environmental and chemical carcinogens than distal carcinomas (Chan & Wong, 2016).

Gastric cancer is additionally associated with the interac- tion of bacterial, dietary, environmental, lifestyle, and host risk factors. Patients who regularly consume diets contain- ing highly salted and preserved foods (salted, pickled, and/ or smoked) and foods high in refi ned carbohydrates have an increased risk for gastric cancer (Compare et al., 2001). Smoking is also associated with gastric cancers. It has been suggested that diet and lifestyle factors account for one-third to one-half of all gastric cancers (Chan & Wong, 2016).

Occurrence: Each year in the United States, more than 22,220 new cases of gastric carcinoma are diagnosed. Of those, approximately 10,990 will die from the disease (Chang & Wong, 2015). The incidence worldwide is much greater. In Japan and the developing regions of Eastern Asia, Eastern Europe, Chile, Colombia, and Central America the incidence is estimated at 70 per 100,000 people, compared to 6.7 per 100,000 people in the United States (ACS, 2017; Cornett & Dea, 2015). Causing 754,000 deaths a year, gastric cancer is the fourth highest cause of cancer death worldwide (World Health Organization [WHO], 2017).

The incidence of gastric cancer worldwide has diminished greatly over the past few decades ( Li et al., 2014 ). The decline began even before the recognition of certain risk factors, such as H. pylori infections. It has been proposed that the world- wide decrease in gastric cancers may be in part be due to the popularization of refrigerator use, which decreased the use of salt-based food preservation techniques and hindered food contamination by bacterial or fungal sources (Chan & Wong, 2015). Refrigeration additionally allowed people to preserve fresh fruits and vegetables, making them more available. Studies have shown that consuming fruits and vegetables is protective against gastric cancer (Chan & Wong, 2016).

Age: The average age at onset of gastric cancer is 69 years. Of patients diagnosed with gastric cancer, approximately 60% are over 65 years of age (ACS, 2017a).

Gender: Gastric cancer is found predominantly in men with a ratio of 3:2 in both developed and developing countries (Chan & Wong, 2015; Jemal et al., 2011Ford). The ACS (2017b) estimates that in the United States in 2017 there will be 17,750 new cases of gastric cancer in men and 10,250 new cases in women. In 2017, it is also estimated that 6,720 men and 4,240 women will die of gastric cancer in the United States (ACS, 2017b).

Ethnicity: Ample differences have been found in the incidence of gastric cancer among people of different ethnic groups, even when living in the same region (Chan & Wong, 2015). Within the United States, the annual incidence of gastric cancers is highest in Asian and Pacifi c Islanders (11/100,000), followed closely by non-Hispanic African Americans (10.7/100,000), Hispanic persons (10.1/100,000), Native American and Alaska Natives (8.6/100,000), and non-Hispanic Caucasians (5.5/100,000) (ACS, 2017b).

Contributing Factors: As previously mentioned, gastric cancer is associated with bacterial, dietary, environmental, lifestyle, and host risk factors. It is estimated that one-half of the world ’ s population is infected with H. pylori; however,

individual risk for developing gastric cancer is 2%. The longer the duration of H. pylori infection, the higher the risk of devel- oping gastric cancer, as the bacteria can cause signifi cant DNA damage over time. This may contribute to the increased incidence of gastric cancers in developing countries where individuals are more likely to become infected with H. pylori at a young age and carry the disease to old age untreated (Jenks, 2015). Chronic H. pylori gastritis increases the “rela- tive risk of gastric carcinoma 3.5 to 20 fold” (Cornett & Dea, 2015, p. 1603).

It is unknown why some individuals infected with H. pylori develop gastric cancers while some develop ulcers, while still most are symptomatically unaffected. Inherited traits may have some infl uence over if someone infected with H. pylori will go on to develop gastric cancer (ACS, 2016). Numerous studies strongly suggest that a diet high in salt and salt-preserved foods, such as salted fi sh and cured meat, increases the risk of developing gastric cancer. High dietary salt intake damages the stomach mucosa, making it easier for carcinogens, such as H. pylori, to invade. Some studies suggest a synergistic effect between H. pylori and salt intake in causing gastric cancer (Chan & Wong, 2016). In 2015, the WHO declared a positive association between eating pro- cessed meat and stomach cancer. This is thought to be due to the dietary nitrates contained in “sausages, bacon, ham, beef jerky, corned beef, and other smoked, salted, fermented, or cured meats” (Chan & Wong, 2016, para. 26). Additionally, diets high in fried foods and low in fruits and vegetables are also associated with an increased gastric cancer risk.

There has been some linkage proposed between occupa- tions in coal and tin mining, steel and iron processing, and manufacturing rubber with an increased risk of gastric cancer; however, further research is needed to determine the overall effect of these environmental effects and developing gastric cancer (Raj, Mayberry, & Podas, 2003). Regular inges- tion of alcohol has not been consistently associated with an increased gastric cancer risk; a European study advised that daily consumption of wine may even be protective. Cigarette smoking has, however, been linked to 18% of gastric cancers (La Torre et al., 2009) and recent studies have linked water pipe smoking with increased incidence of gastric cancer (Lai, Koriyama, Tokudome, Tran, Tran, & Nandakumar, 2016). Individuals with a low socioeconomic status have a twofold increase in risk of distal gastric cancers, while those with a higher socioeconomic status are at a higher risk of proximal gastric tumors.

Obesity, defi ned as having a BMI greater than or equal to 25  kg/m 2 , was correlated with an increased risk of gastric cancer, and there was a positive correlation with occurrence of gastric cancer and the individual’s BMI increasing (Kyrgiou et al., 2017). Other medical conditions associated with an increased risk for gastric cancer include gastric polyps, gastric ulcers, pernicious anemia, and Epstein-Barr virus. History of previous abdominal radiation and having undergone gastric surgery, especially a partial gastrectomy (Billroth I or II), also increases an individual ’ s risk for developing gastric cancer. Aggregation of gastric cancers within families account for 10% of incidences, while gastric cancers which are truly hereditary are culpable for 1% to 3% worldwide. Lastly, indi- viduals with blood type A have a 20% increase in developing gastric cancer when compared to those with blood types O, B, or AB (Chan & Wong, 2016).

Chapter 10 ■ Abdominal Disorders 255

Signs and Symptoms: Early detection of gastric cancer is often diffi cult because of the absence of clinical presentation. Patients often describe a vague sensation of fullness after a meal that is relieved by belching, nonspecifi c complaints of abdominal pain of varying intensities, nausea, anorexia, dys- pepsia, vomiting, and evidence of GI blood (hematemesis and melena), and changes in bowel habits. Epigastric discomfort is present in more than 75% of patients, and the presenta- tion may be similar to that of a gastric ulcer. Weight loss and pallor, if the patient is anemic, may be the only signs noted during physical examination. Examination of the skin may reveal diffuse seborrheic keratosis. A palpable mass in the abdomen is felt in less than 20% of patients.

Many patients with gastric cancer do not become symp- tomatic until their disease becomes metastatic. Metastatic distribution most commonly involves the liver, peritoneal surface, and distant lymph nodes. Liver involvement is usually diffuse and not singularly palpable, however, it is often associated with an elevated serum phosphatase level. Ascites is often the fi rst sign of peritoneal spread. Because gastric cancers can be spread through the lymphatic system, patients with metastatic disease often have enlargement of the left supraclavicular lymph nodes (Virchow ’ s node), a periumbilical nodule (Sister Mary Joseph ’ s node), and left axillary node (Irish node) (Mansfi eld, 2017). Additionally, in advanced disease a rigid rectal mass may be palpated (Blumer ’ s shelf) and/or an enlarged ovary may be detected in females (Krukenberg ’ s tumor). The patient ’ s stool may also be found to be guaiac-positive (Cornett, 2015).

Diagnostic Tests: For patients presenting with symptoms of gastric cancer, the following laboratory studies should be con- sidered: CBC with indices to determine presence of anemia, comprehensive chemistry profi le, and FOBT to detect bleed- ing in the intestinal tract. Patients will need to be referred for an endoscopy with a biopsy and cytological examination (Mocellin & Pasquali, 2015).

A chest abdominopelvic CT scan with oral and IV contrast should be used to evaluate for metastasis, especially if the provider is concerned about disease in the liver, adnexa, distal lymph nodes, or ascites. A paracentesis should be performed on patients with ascites and the fl uid should be examined for cytology and chemical evaluation. If metastatic disease is found on CT scan, the suspected lesion must be confi rmed by biopsy due to the risk of false-positive fi ndings. CT scans can miss peritoneal and hematogenous metastases smaller than 5  mm and do not precisely evaluate the depth of primary tumor invasion and existence of lymph node involvement. In the absence of distant metastatic disease, endoscopic ultraso- nography (EUS) is the preferred tool to determine the depth of invasion of primary gastric tumors, as well as to accu- rately evaluate for nodal staging and occult metastases (Man- sfi eld, 2017; NCCN, 2016). Additionally, epidermal growth factor receptor 2 (HER2) testing should be performed on the tumor biopsy if metastatic adenocarcinoma is documented or strongly suspected (NCCN, 2016). HER2 determination can be used to guide treatment choices in advanced disease.

Differential Diagnosis:

■ Chronic/acute gastritis ■ Functional dyspepsia ■ PUD

■ Esophageal stricture ■ Esophageal carcinoma ■ Refl ux esophagitis ■ Lymphoma ■ Malignant neoplasms of the small intestine ■ Crohn ’ s disease ■ Sarcoidosis ■ Mesenteric ischemia ■ Gastroenteritis ■ Irritable bowel syndrome ■ Gastric ulcers (Cabebe, 2017)

Treatment: A partial or complete gastric resection with adja- cent lymph nodes is the treatment of choice for gastric cancer. The NCCN recommends resecting 15 or more regional lymph nodes at the time of tumor resection (Cornett & Dea, 2015). One systematic review found that extended surgery carries increased mortality risks associated with spleen and pancreas resection (McCulloch, Nita, Kazi, & Gama-Rodrigues, 2007). Extensive cancer or metastases negate the need for “curative” surgery, however, surgery is sometimes used as a palliative treatment to relieve pain, bleeding, or a blockage caused by the cancer. Chemotherapeutic agents (most commonly, 5-fl uorouracil) have been used alone or in combination with other treatments, such as radiation. Targeted therapies such as monoclonal antibodies (trastuzumab [Herceptin] and ramucirumab [Cyramza]) attack cancer cells without affect- ing healthy cells, unlike standard chemotherapy in patients whose tumors carry the amplifi cation of the epidermal growth factor receptor 2 (HER2) (Cornett & Dea, 2015). Tar- geted therapy is used in gastric cancer for patients with stage IV disease or with a recurrence of disease.

Follow-Up: Patients who have undergone a gastric resection should be seen by their provider for continued surveillance to monitor for complications and cancer recurrence or met- astatic disease every 3 to 6 months for the fi rst 1 to 2 years after surgery, followed by every 6 to 12 months for the next 3 to 5 years, then annually. Evaluation with a CBC and chem- istry profi le, along with a CT scan of the chest and abdomen with contrast, should be assessed at each visit. Additionally, patients should be monitored for nutritional defi ciencies, including B 12 and iron insuffi ciency (NCCN, 2016). Serolog- ical cancer markers can be elevated in patients with gastric cancers; however, these tests have low rates of sensitivity and specifi city, hindering their use as diagnostic tests, and are rarely used for monitoring unless the patient is undergoing neoadjuvant therapy (Mansfi eld, 2017).

Sequelae: Malnutrition, hemorrhage, obstruction, possibly evasive cancer, metastases, and recurrence are complications from gastric cancer. Additionally, patients may experience refl ux, dumping syndrome, hypoglycemia, and diarrhea fol- lowing a gastric resection (Jeon, Choi, Lee & Noh, 2016).

Prevention/Prophylaxis: Patients should eliminate the use of food products that contain nitrates and are highly salted. Screening for H. pylori in high-risk populations has been advocated ( Li et al., 2014 ). Consumption of fruits, espe- cially citrus fruits, and vegetables has been found to protect against gastric cancer, possibly because of their vitamin C content. Vitamin C is thought to decrease the accumulation of carcinogenic agents in the stomach (Chan & Wong, 2016). Dietary fi ber and folate have also been shown to reduce the

256 Chapter 10 ■ Abdominal Disorders

risk of gastric cancers in some studies, but further inves- tigation is needed. The use of NSAIDs has been shown to inversely associate with distal gastric cancer risk. This is most evident in patients with a history of H. pylori infection (Chan & Wong, 2016).

Referral: A gastroenterologist should be consulted for the endoscopy and complicated management problems, includ- ing annual follow-up endoscopy. Patients with stages I to III disease should be seen by a surgeon for possible resection. After receiving a surgical resection, patients may need to be followed by a nutritionist. Additionally, patients with gastric cancer should see a medical oncologist to evaluate for the role of neoadjuvant, adjuvant, or palliative chemotherapy. Given

the advanced age and the cognition of patients with gastric cancer, careful attention to emotional support and their quality of life measures need to be considered when caring for older adults (Baldacci, 2015). For patients with advanced disease, referral for palliative care or local hospice should be made (Cornett & Dea, 2015).

Education: After partial and complete gastrectomy, teach patients about the importance of adequate nutrition. Con- suming six small meals a day may be necessary instead of the usual three. Supplementation with vitamins, especially vitamin B 12 , and minerals, such as calcium and iron, should be prescribed. Patients may prefer taking nutritional supple- ments in place of one or more meals each day.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Epidermal growth factor receptor 2 (HER-2) testing should be performed on the tumor biopsy if metastatic adenocarcinoma is documented or strongly suspected.

A NCCN, 2016

Treatment of H. pylori reduced the incidence of gastric cancer, suggesting the benefi ts of treatment in preventing gastric cancer.

A Li et al., 2014

Upper GI endoscopy with biopsy is the recommended initial diagnostic test.

C Mocellin & Pasquali, 2015

Persons with diets high in salted and preserved foods (salted, pickled, and/or smoked) and in refi ned carbohydrates have an increased risk for gastric cancer.

C Compare et al., 2011

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

GASTRITIS

Signal Symptoms: Anorexia, nausea and vomiting, epigastric pain, or discomfort with tenderness.

Description: Gastritis is an infl ammation of the mucosal lining of the stomach. A number of conditions can cause gastritis, including infection, autoimmune disorders, exoge- nous substances, and stress. Patients may be asymptomatic; however, dyspepsia and GI bleeding are common fi ndings in older adults (Zayouna & Piper, 2016).

Etiology: Gastritis represents a group of disorders character- ized by infl ammation of the stomach lining. Each disorder has distinct clinical attributes, pathogeneses, and histologi- cal features. Gastritis is divided fi rst into erosive and noner- osive types; a possible infl ammatory process within each group may be categorized as acute or chronic. It is also clas- sifi ed according to the area of the stomach involved (i.e., cardia, body, antrum). Gastritis may be caused by infectious agents such as H. pylori, E. coli, Staphylococcus aureus, Clos- tridium perfringens, and Streptococcus and viruses such as

cytomegalovirus (CMV), herpes virus, and Epstein-Barr virus. Candida may be found in immunocompromised patients, but also in alcoholic patients or those who have ingested corro- sive chemicals (Lauwers, Fujita, Nagata, & Shimizu, 2010). Acute erosive gastritis occurs when there is damage to the surface epithelium of the stomach. Erosion results from contact from exogenous agents such as NSAIDs, acetylsali- cylic acid, chemotherapeutic agents, and alcohol; infections; or bile secretions (Pilotto, Sancarlo, Addante, Scarcelli, & Franceschi, 2010). In the case of burns, trauma, sepsis, or prolonged hypotension, mucosal hypoxia occurs, leading to acute erosive gastritis (Pilotto et al., 2010).

Chronic gastritis can be classifi ed further as nonatrophic, atrophic, and specifi c types related to precipitating factors, such as chemical or radiation gastritis. Chronic nonspecifi c gastritis results from ongoing injury to the gastric mucosa causing chronic infl ammation and gastric atrophy (Chen, Ying, Kong, Zhang & Li, 2013). It is estimated that 90% of patients with chronic gastritis have been exposed to H.

Chapter 10 ■ Abdominal Disorders 257

pylori (Chey & Wong, 2007). There are a number of types of uncommon chronic gastritis, including autoimmune, reac- tive chemical, noninfectious granulomatous, lymphocytic, eosinophilic, radiation, and ischemic (Franceschi, Di Mario, Leandro, Maggi, & Pilotto, 2009).

Occurrence: Exact incidence of gastritis is unknown.

Age: Although gastritis occurs in all ages, it is a common occurrence in older adults. Although patients of all ages can be infected with H. pylori , extensive atrophic damage gen- erally occurs after age 50 years (Chen et al., 2013; Mapel, Roberts, Overhiser, & Mason, 2012). Pernicious anemia can develop as a result of long-standing autoimmune atrophic gastritis, which often occurs around the sixth decade (Orton, 2012).

Gender: Atrophic gastritis occurs equally in men and women; autoimmune gastritis is more prevalent in females (3:1 ratio). In a study by Mapel and colleagues (2012), women were found to have increased incidence of gastritis over men, espe- cially in the fi fth decade of life.

Ethnicity: Worldwide, the risk for developing H. pylori infec- tion is greatest among Asians and Hispanics. Chronic gastri- tis resulting from H. pylori infection is higher in the United States among African Americans than Caucasians. Autoim- mune atrophic gastritis occurs more frequently in individuals of northern European descent (Zayouna & Piper, 2016).

Contributing Factors: Many factors can precipitate the devel- opment of gastritis. Acute gastritis can be caused by physi- ological stressors, hypovolemic shock, portal hypertension, aspirin, NSAIDs, alcohol, radiation, chemotherapy, gastric lymphoma, Crohn ’ s disease, and H. pylori and other bacterial, viral, and fungal infections. Stress, trauma, and burns can trigger this acute condition (Wehbi & Dache, 2016). Patients on mechanical ventilation are at risk for developing acute gastritis. Patients with atrophic gastritis from long-term H. pylori infection and chronic damage to the intestinal mucosa generally also are found to have pernicious anemia (Zayouna & Piper, 2016). Autoimmune gastritis is related to the loss of parietal and chief cells and includes achlorhydria, hyper- gastrinemia, loss of pepsin and pepsinogen, and anemia. Chronic gastritis can develop because of gastric atrophy, H. pylori infection, bile and pancreatic secretions, and pernicious anemia. Exposure to long-term smoking makes the stomach lining more vulnerable to the development of chronic gas- tritis. Most patients who have had a previous gastrectomy develop gastritis (Chen et al., 2013).

Signs and Symptoms: Anorexia, nausea (with or without vom- iting), and epigastric distress (dyspepsia) often aggravated by eating are common with gastritis (Mapel et al., 2012).

Halitosis may be noted. Patients may report a bloating sensation and early satiety ( Huang, Sun, Wang, Tao, Wang, & Tan, 2015 ). Physical examination may be unremarkable in cases of chronic gastritis. Palpate for abdominal masses and liver tenderness. Perform a rectal examination to test for occult blood. Any unexplained weight loss should be noted. GI bleeding may be exhibited by coffee-ground vomitus, melena, hematochezia, or the passing of bright red blood in a nasogastric tube. Any patient suspected of GI bleeding should be examined for changes in mental status; coolness of the extremities; and pallor of the nail beds, mucous membranes,

and conjunctiva. Assessment should include watching for any changes in cardiac output, such as decreasing blood pressure and increased heart rate.

Diagnostic Tests: Diagnostic studies include CBC with indices to detect blood loss and anemia, stool guaiac test, and endo- scopic gastroduodenoscopy with a biopsy, which is the defi nitive diagnostic test for gastritis. If H. pylori infection is suspected, noninvasive testing includes antibody testing, urea breath tests (UBTs) 13 C and 14 C, and fecal antigen tests (Gurney, Carvalho, Gonzalez, Galaviz, & Sonstein, 2014). Though more costly, UBTs and fecal antigen tests have excel- lent sensitivity and specifi city (95%) and can be used for diag- nosis and post-therapy evaluation. PPI use will need to be restricted for 14 days and antibiotics for 28 days before UBT and fecal antigen testing (not serology) to ensure more accu- rate diagnosis and avoid false-negative results (Chey & Wong, 2007; Fashner & Gitu, 2015; Gurney et al., 2014). The sero- logical testing for H. pylori is not able to distinguish between prior exposure or active infection; therefore, the utility of this test is limited in clinical scenarios. During endoscopy, a biop- sy-based H. pylori test can be ordered and remains the gold standard for diagnosis.

Differential Diagnosis:

■ GERD ■ Biliary tract disease ■ Food poisoning ■ Functional dyspepsia ■ PUD ■ Perforated or penetrated ulcer ■ Gastric carcinomas ■ Pancreatic disease ■ Esophageal rupture ■ Myocardial colic (McQuaid, 2017)

Treatment: Patients with acute gastritis should avoid offen- sive agents such as alcohol, NSAIDs, aspirin, and cigarettes (Wehbi & Dache, 2016). Acute hemorrhagic gastritis requires hospitalization for IV fl uids, IV PPIs, nasogastric aspiration, transfusion of blood products as necessary, and monitoring of vital signs. H 2 blockers, such as famotidine, ranitidine, or nizatidine, can be given for 6 to 8 weeks. An oral dose of ranitidine 300 mg or nizatidine 300 mg daily at bedtime can be ordered. The dosage of the H 2 blockers may have to be reduced, however, depending on renal status of the patient. If treatment for H. pylori is indicated, treatment options are delineated in Table 10-2 (Chey & Wong, 2007; Gurney et al., 2014).

Follow-Up: A repeat endoscopy is advised after 6 weeks for patients who had severe gastritis or who continue to have symptoms despite treatment. Obtain a CBC and check stool for occult blood at subsequent offi ce visits every 3 to 6 months after the diagnosis of gastritis. At each follow-up appointment, review all drugs, including OTC medications and home remedies. (Wehbi & Dache, 2016).

Sequelae: Acute hemorrhagic gastritis has a high mortality rate in older adults. For the patients with H. pylori , there is a risk for developing gastric carcinoma; after eradication, the risk decreases (Adamu, Abdullahi, Weck, Gao, & Brenner, 2010; Carrasco & Corvalan, 2013). Patients with auto- immune gastritis may develop pernicious anemia, given the

258 Chapter 10 ■ Abdominal Disorders

loss of parietal cell mass and subsequently anti-intrinsic factor antibodies ( Miceli et al., 2012 ). It is important to note that unexplained or refractory iron defi ciency anemia can develop in patients with either H. pylori –associated atrophic gastritis or autoimmune atrophic gastritis.

Prevention/Prophylaxis: Prophylaxis with acid-suppressive drugs can reduce the incidence of acute stress gastritis. Older adults who are high-risk intensive care unit patients, includ- ing those with severe burns, central nervous system trauma, coagulopathy, sepsis, shock, multiple trauma, mechanical ventilation for longer than 48 hours, hepatic or renal failure, and a history of peptic ulcer or GI bleeding, benefi t from pro- phylaxis medication to prevent acute gastritis. Critically ill older adults need to be monitored for signs and symptoms of hypovolemic shock secondary to acute gastric bleeding (Wehbi & Dache, 2016). Alternative anti-infl ammatory or nonnarcotic analgesics should be considered in the treatment of pain or infl ammation in older adults with a history of gastritis, dyspepsia, or other upper GI clinical events ( Laine, Curtis, Cryer, Kaur, & Cannon, 2010 ).

Referral: Older patients with acute hemorrhagic gastritis require hospitalization, probably with intensive care unit admission. Consultation with a gastroenterologist for endos- copy and management of complicated cases of gastritis is recommended.

Education: Advise patients to report any black, tarlike stools or frank bleeding to the health-care practitioner immediately. All alcohol, caffeine, salicylates, tobacco, and NSAID product use should be discontinued.

H elicobacter Pylori Regimens

PATIENT CHARACTERISTICS FOR TREATMENT MEDICATION AND DOSAGE

Patients who are not allergic to

penicillin and have not previously

received a macrolide

Standard dose PPI twice daily

plus clarithromycin 500 mg

twice daily, and amoxicillin 1,000 

mg twice daily for 10–14 days

Patients who are allergic to

penicillin and who have not

previously received a macrolide

or metronidazole or are unable

to tolerate bismuth quadruple

therapy

Standard dose PPI twice daily,

clarithromycin 500 mg twice

daily, metronidazole 500 mg

twice daily for 10–14 days

Patients who are allergic to

penicillin, failed a course of

prior therapy, or have previously

received a macrolide

Bismuth subsalicylate 525 mg

or subcitrate 420 mg four times

daily, metronidazole 250 mg four

times daily, tetracycline 500 mg

four times daily, standard dose

PPI twice daily for 10–14 days

TABLE 10-2

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

A strong association between H. pylori and developing chronic atrophic gastritis exists.

B Weck, Gao, & Brenner, 2009

Vitamin B 12 defi ciency was found in patients diagnosed with autoimmune atrophic gastritis.

B Miceli et al., 2012

Patients with asymptomatic chronic gastritis predisposed patients taking metformin to experience GI side effects from the medication.

A Huang et al., 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

GASTROENTERITIS

Signal Symptoms: Sudden onset of diarrhea, abdominal pain with distention, fl atulence, vomiting.

Description: An infectious response of the GI tract to various microorganisms that can be viral, bacterial, or parasitic in origin.

Etiology: Caused by exposure to toxins and drugs or viruses, bacteria, and parasites:

■ Viruses such as norovirus, formerly called the Nor- walk-like virus and astrovirus

■ Bacteria such as Salmonella, Campylobacter, Shigella, E. coli, and Vibrio cholerae

■ Parasites such as Giardia lamblia

Occurrence: Approximately 30% to 40% of gastroenteritis diarrhea in the United States is thought to be viral in origin. Exact incidence of infectious gastroenteritis is unknown because of underreporting of symptoms. Noroviruses cause approximately 23 million cases of acute gastroenteritis each year and are the leading cause of outbreaks of gastroenteritis.

Chapter 10 ■ Abdominal Disorders 259

Norovirus outbreaks peak in the winter months. Norovirus accounts for around 19 to 21 million illnesses, 56,000 to 71,000 hospitalizations, and 570 to 800 deaths annually (Wikswo et al., 2015).

Age: Occurs at all ages, but its incidence and the mortal- ity rate from infectious diarrhea are higher in older adults. Epidemic cases of gastroenteritis occur in nursing home populations and long-term care facilities are the most fre- quently reported settings of outbreaks transmitted through person-to-person contact or environmental contamination (Wikswo et al., 2015).

Gender: Equally prevalent in both sexes, although diarrhea is more common in women.

Ethnicity: Not signifi cant.

Contributing Factors: Specifi c to the older adult popula- tion, age-related factors such as decreased motility, mucosal atrophy, and decreased gastric acidity inhibit natural defense mechanisms against infectious agents. The use of H 2 block- ers, PPIs, antacids, anticholinergic drugs, and narcotics increases the potential for developing gastroenteritis (Reuben et al., 2016). Gastroenteritis also can be caused by emotional stress, viral or bacterial infection, food intolerance, and organic (shellfi sh, certain mushrooms) or inorganic (sodium nitrate) poisons. Travel to another country with a change in surroundings or to an area of poor sanitation standards and facilities can contribute to the development of gastroenteri- tis. Nursing home populations are susceptible to epidemics because of contact with health-care workers who may not use proper hand washing techniques. Some viruses, such as norovirus, can be transmitted by an airborne route. Fecal-to- oral contact has been identifi ed as a mode of transmission of organisms (Wikso et al., 2015).

Signs and Symptoms: History of possible fecal-to-oral contact; exposure to other patients with gastroenteritis; and ingestion of certain food products such as mayonnaise, custards, fried rice, vegetables, beef, poultry, bean sprouts, or raw seafood should be explored. Try to estimate the length of time that has elapsed since the patient ingested the food product suspected of contamination. Travel to a foreign country or region that may have contaminated water should be recorded, as should any previous history of diarrhea and related symptoms, and the duration of the current episode. A sudden onset of diar- rhea, abdominal pain with distention, fl atulence, and vomit- ing may be reported. Associated anorexia, headache, fatigue, dizziness, and myalgias are also symptoms of gastroenteri- tis. Fever may or may not occur in the older adult. Mental confusion may result from dehydration. The stool ’ s color, odor, amount, and frequency should be described, and the presence of any blood or mucus in the stool should be dis- cerned. Patient use of prescription drugs, OTC medications, and home remedies need to be included in the history. In the physical examination, the skin is checked for signs of rashes or dehydration, and the lymph nodes are assessed for lymph- adenopathy. Abdominal examination may reveal distention, hyperactive bowel sounds, and tenderness. Perform a rectal examination to note any bleeding, the color of the stool, and to check for an impaction (Reuben et al., 2016).

Diagnostic Tests: CBC with differential should be ordered. WBC shift to the left may suggest an infection, and a

decreased hemoglobin value indicates anemia from probable blood loss. Serum electrolyte evaluation shows an increased sodium level in dehydrated patients and decreased potas- sium resulting from the diarrhea. Elevated serum creatinine and BUN levels also occur in dehydration. Stool samples for blood, ova and parasite, leukocytes, and bacteria are ordered to try to identify the microorganism in patients with bloody diarrhea, dehydration, or signs of infl ammatory disease, and symptoms lasting more than 3 to 7 days. Cultures in immu- nosuppressed patients are also warranted. Cultures may be obtained in traveler ’ s diarrhea (Barr & Smith, 2014).

Differential Diagnosis:

■ Fecal impaction ■ Fecal incontinence ■ Colorectal cancers ■ Adverse reaction to medications ■ Diverticulitis ■ Malabsorption ■ Pseudomembranous colitis if the patient has been

prescribed an antibiotic within 2 months of onset of symptoms

■ Clostridium diffi cile (Reuben et al., 2016; Swita, Winter, & Christensen, 2015)

Treatment: Lost fl uids and electrolytes must be replaced. Clear liquids and specially formulated rehydration liquids, such as Gatorade, should be given as tolerated. Clear broths and crackers may be added to the diet as tolerated. Early refeed- ing decreases symptom duration and improves nutritional outcomes (Barr & Smith, 2014). Patients should avoid caf- feine, dairy products, alcohol, fruits, bran, vegetables, and red meats. Solid foods should be added gradually, starting with rice or potatoes (Swita, Winter, & Christensen, 2015). Physi- cal activity should be limited, to avoid unnecessary exertion. Care should be taken to prevent any skin excoriation or pres- sure sores. Antibiotic therapy is specifi c to the bacterial or parasitic organisms identifi ed from the stool culture:

■ Campylobacter strains have been shown to have fl uo- roquinolone resistance and are best treated by azith- romycin or other macrolides. For all antibiotics, either single-dose therapy or 3 days of therapy are suffi cient for resolution of symptoms ( Riddle et al., 2016 ).

■ G. lamblia infection is treated with metronidazole, 250 mg three times daily for 5 to 7 days.

■ Severe cases of traveler ’ s diarrhea (enterotoxigenic E. coli ) can be treated with azithromycin 500 mg daily for 3 days ( Riddle et al., 2016 ).

Follow-Up: Contact outpatients 4 days after the onset of symptoms to determine progress. Request nursing home staff to provide a verbal report of the patient ’ s condition on the third or fourth day. Note any further outbreak of gastro- enteritis. When contacting the patient at home, question if there have been any additional symptoms, including fever and neurological developments such as paresthesia, motor weakness, and cranial nerve palsies. For older adults with chronic diarrhea or other persistent GI symptoms, refer to a gastroenterologist (Reuben et al., 2016).

Sequelae: Dehydration, anemia, metabolic acidosis, and hypo- volemic shock could occur in untreated cases of severe infec- tious diarrhea.

260 Chapter 10 ■ Abdominal Disorders

Prevention/Prophylaxis: Older adults with travel plans to foreign destinations should be counseled to avoid contam- inated water and other high-risk beverages and foods to prevent traveler ’ s diarrhea ( Riddle et al., 2016 ).

Referral: Refer to a specialist when symptoms persist beyond 4 days, when severe dehydration develops, or when the patient has bloody stools.

Education: Gastroenteritis, although generally self-limiting, can be debilitating. Infections with some microorganisms, such as G. lamblia, can become chronic and result in lactose intolerance, which is common in older adults. Any new case of diarrhea not resolved in 3 to 4 days requires health-care provider intervention. Use of OTC antiperistaltic agents, such as loperamide, is contraindicated in infectious diarrhea, but may be used for adjunctive therapy in patients receiving anti- biotics for traveler ’ s diarrhea ( Riddle et al., 2016 ).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Balanced electrolyte rehydration is favored over other oral options in the older adult with severe diarrhea. Other individuals can keep up with electrolyte replacement by using water, juices, soups, sports drinks, and saltine crackers.

A Riddle et al., 2016

Oral rehydration is the fi rst, preferred step in treating acute diarrhea.

C Barr & Smith, 2014

Antibiotics reduce the duration and severity of traveler ’ s diarrhea, A Barr & Smith, 2014

Testing for Clostridium diffi cile toxins Aand B should be performed in patients who develop unexplained diarrhea after a hospitalization of 3 days or more.

C Barr & Smith, 2014

Routine testing for ova and parasites in acute diarrhea is not needed in developed countries unless the patient is in a high-risk group (diarrhea >7 days, immunocompromised, travel, infants in daycare, bloody diarrhea with few fecal leukocytes).

C Barr & Smith, 2014

Probiotics and prebiotics are not recommended for prevention of traveler ’ s diarrhea.

C Riddle et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

GASTROESOPHAGEAL REFLUX DISEASE

Signal Symptoms: Regurgitation, pyrosis, hoarseness, chronic cough, atypical chest pain.

Description: GERD is a common disorder characterized by various symptoms ranging from mild heartburn to more severe physical complaints caused by the refl ux of gastric contents into the esophagus. These symptoms may or may not occur in patients who present with laryngopharyn- geal and/or respiratory symptoms. Infl uencing factors in the development of GERD include a weakened lower esoph- ageal sphincter (LES) pressure, hiatal hernia, abnormal esophageal clearance, slowed esophageal peristalsis, esoph- ageal mucosal resistance, and delayed gastric emptying (Hart, 2013).

Etiology: The presentation of GERD is a complex problem than involves reduction in the tone of the lower esopha- geal sphincter, episodic relaxation of the lower esophageal

sphincter at inappropriate times, decreased secondary peri- stalsis, and faulty mucosal resistance to caustic fl uids.

Occurrence: GERD affects more than 20% of the U.S. pop- ulation (El-Serag, Sweet, Winchester & Dent, 2014). Addi- tionally, it is estimated that at least 50 million Americans experience heartburn at least twice a week ( Kroch & Mada- nick, 2017 ).

Age: Approximately 10% to 30% of older adults experience weekly symptoms of heartburn or regurgitation.

Gender: The ratio of men to women with GERD is equal. Severe esophagitis is more common in men than in women (2:1). Barrett ’ s esophagus is more common in men than in women (10:1) (Kubo et al., 2013).

Ethnicity: Severe esophagitis is more common in Caucasians than in non-Caucasians.

Chapter 10 ■ Abdominal Disorders 261

Contributing Factors: Intrinsic factors that contribute to the development of GERD include LES incompetence, hiatal hernia, esophageal motility disorders, delayed gastric empty- ing, and gastric distention. Certain medications can trigger GERD. Nitrates, CCBs, benzodiazepines, tricyclic antidepres- sants, beta agonists, and anticholinergics lower the LES tone. NSAIDs, aspirin, steroids, iron sulfates, gelatin cap- sules, antibiotics, potassium chloride tablets, vitamin C, qui- nidine, and bisphosphonates contribute to esophagitis, local erosions, or ulcers. Additional medications that contribute to GERD due to decreased esophageal motility include the- ophylline, sedatives, and narcotics. Substances that weaken the LES pressure include caffeine, mints, chocolate, alcohol, spicy foods (including yellow onions and garlic), and citrus fruits. Smoking, alcohol, obesity, and certain dietary products (food substances that contain lactose in some patients lead to gastric distention) may contribute to the development of the symptoms of GERD (Hart, 2013). There is an increased risk in developing nonerosive esophagitis in patients with meta- bolic syndrome. Patients with nasogastric tubes are known to be at risk for having symptoms of GERD. Patients with certain medical conditions that affect gastric motility such as stroke, diabetes, scleroderma, myasthenia gravis, and Par- kinson ’ s disease are at risk for developing GERD (Basheshati, Hejazi, Andrews & Storr, 2014).

Signs and Symptoms: Determine from patients precipitating factors related to the development of GERD, length of time they have been experiencing symptoms, and what regimens and/or lifestyle changes they have tried. Patients should be questioned about medication usage, smoking, and intake of substances that can weaken the LES; sleeping habits; and use of any tight or restrictive clothing. Determine if any activ- ity triggers GERD, such as bending over, exercise, or being recumbent. Review the patient ’ s dietary habits and elicit if there are food products that the patient regularly ingests that aggravate symptoms of GERD.

Question the patient about history of heartburn, pyrosis, belching, halitosis, regurgitation, nausea, atypical chest pain (radiation of pain to back, neck, and/or jaw), hoarse- ness, recurrent laryngitis, cough, choking, pharyngeal tight- ness, globus sensation, sense of fullness, persistent clearing of the throat, sore throat, recent dental caries, dysphagia, odynophagia, anorexia, weight loss, vomiting, otitis media, bronchospasms, chronic bronchitis, and asthma (Becker et al., 2014; Richter, 1996). Determine if the patient ’ s sleep is disturbed because of GERD symptoms. Review the medi- cations the patient is taking to determine if any medications reduce the LES pressure, decrease the LES pressure, and/or irritate the esophageal mucosa. Question the patient about any previous history and/or treatment for H. pylori . Ask about any family history of esophageal cancer or hiatal hernia (Basheshati et al., 2014).

Physical examination usually produces no positive fi nd- ings. Conduct a thorough examination of the oral cavity and a respiratory examination. Palpate for any upper abdominal masses or tenderness. Perform a rectal examination to detect any frank bleeding.

Diagnostic Tests: If suspicion was aroused on the physical examination, stool should be checked using the guaiac test to determine if there has been any intestinal bleeding. Labora- tory studies are not required when antacids, position change,

or both relieve pyrosis. For older adults who complain of persistent dysphagia or odynophagia with or without fever, barium swallow or an endoscopy (with brush and biopsy if structural mucosal damage is suspected) or both are ordered. Any patient presenting with laryngopharyngeal symptoms of GERD should be considered for a laryngoscopy (Hart, 2013). A majority of GERD patients have a negative endoscopy.

Differential Diagnosis:

■ Nonulcer dyspepsia ■ Esophageal spasms ■ Esophagitis ■ Esophageal stricture (upper GI sinus) ■ Esophageal carcinoma ■ Cholecystitis ■ PUD (Hart, 2013)

Treatment: The goals for the treatment of GERD include reducing symptoms, healing esophagitis, managing esoph- ageal healing, improving quality of life, and preventing complications ( Kroch & Madanick, 2017 ). Important to the management of GERD are the lifestyle changes or non- pharmacological measures that patients need to incorporate along with the medication regimen. These include avoidance of smoking, alcohol, and food products such as chocolate, mints, spicy or acidic foods, and caffeine. For older adults, PPIs remain the mainstay of treatment, given the rapid relief of GERD symptoms and esophageal healing that result from PPI treatment. Once-a-day dosing is benefi cial to aid in med- ication compliance. It is important to note that older adults will require long-term maintenance therapy for GERD. A step-down approach can be initiated in patients with GERD by reducing the dosage of the PPI or by adding an H 2 blocker in the evening. While PPIs can be used long-term in patients who are unable to sustain remission without them, agent and dosage should be tailored to the individual patient with the dosage and need for the drug periodically reviewed in order to use the lowest effective dose (Freedberg et al., 2017; Kroch & Madanick, 2017 ). The use of prokinetic agents is not recom- mended in older adults given the serious side effects. Pharma- cological recommendations are listed in Table 10-3 .

Follow-Up: Review lifestyle changes and the impact modifi ca- tions have had on the patient ’ s symptoms of GERD (Daniele, Oh, O’Donnell & Clark, 2015). Evaluate compliance with the medication regimen. Determine if the patient has experi- enced any complications or alarming changes in status since the last evaluation.

Sequelae: Ulceration and bleeding, if refl ux esophagitis is present, can occur after esophagitis. In esophagitis with esophageal stricture, Barrett ’ s esophagus with possible ade- nocarcinoma may be a long-term complication (Bansal & Fitzgerald, 2013). GERD itself is associated with a 10% to 15% risk of Barrett ’ s esophagus ( Shaheen, Falk, Iyer, Gerson, & American College of Gastroenterology, 2016 ). Abdominal obesity, not specifi cally increased BMI, was found to be asso- ciated with the development of Barrett ’ s esophagus in both men and women (Kubo et al., 2013). Older adults are also at risk for developing pulmonary complications of GERD, such as chronic cough, recurrent pneumonitis, and aspira- tion pneumonia. Patients who present with otolaryngological symptoms of GERD may develop chronic laryngitis, laryngeal polyps, laryngotracheal stenosis, and laryngeal carcinoma

262 Chapter 10 ■ Abdominal Disorders

(Patrick, 2011). Given the refl ux of gastric content to the pharynx, dental erosions are also a common consequence of laryngopharyngeal refl ux. The risk of chronic sinusitis has also been found in patients with laryngopharngeal refl ux (Lin, Chang, Yao & Li, 2015).

Prevention/Prophylaxis: Prevention of GERD should be aimed at eliminating or at least modifying the extrinsic factors that contribute to the development of the condition. Patients

should be encouraged to make lifestyle adjustments and avoid potentially harmful medications to prevent further complications.

Referral: A gastroenterologist should be consulted for the endoscopy and for patients with anemia, severe or non- responsive refl ux disease, dysphagia, odynophagia, unex- plained weight loss, or evidence of hemorrhage. When a patient presents with laryngopharyngeal refl ux, he or she should be referred for an indirect or direct laryngoscopy. If a patient presents with dysphagia, odynophagia, unexplained weight loss, or GI bleeding, or if a patient did not respond to initial therapy, refer to a gastroenterologist (Katz, Gerson, & Velva, 2013; Müller, Gockel, Konig, Kuhr, & Eckardt, 2011; Bashashati et al., 2014; Galindo, Vassalle, Marcus & Triada- fi lopoulos, 2013).

Education: Patients with refl ux esophagitis should be instructed to raise the head of the bed 4 to 6  in. with shock blocks or a foam wedge that can be placed at the head of the bed. While there has been limited evidence to suggest that making lifestyle changes to decrease abdominal pressure, such as avoiding tight, restrictive clothing, counteracts the symptoms of GERD, medical practitioners should encour- age patients to adopt this strategy, especially given the small number of patients in studies that made this recommenda- tion (Katz et al., 2012). The patient should avoid smoking and ingestion of fatty foods, coffee, chocolate, mints, citric juices, alcohol, and large quantities of fl uids with meals. Remind patients not to break or crush extended-release or delayed-release tablets. Patients should avoid eating a meal for at least 3 hours before becoming recumbent. Teach the patient the importance of swallowing medications with an adequate amount of fl uids. An oral PPI needs to be ingested 60 minutes before a meal. It is suggested to then wait 30 minutes after the PPI has been taken before eating.

Pharmacological Recommendations for G astroesophageal Refl ux Disease

Treatment of Erosive or Nonerosive Gastroesophageal Refl ux Disease

Proton Pump Inhibitors

DRUG DOSAGE

Dexlansoprazole 30 mg daily

Esomeprazole 40 mg daily

Lansoprazole 15 to 30 mg daily

Omeprazole 20 to 40 mg daily

Pantoprazole 40 mg daily

Rabeprazole 20 mg daily

H 2 -Receptor Antagonists

Nizatidine 150 mg q12h

Famotidine 20 mg q12h

Ranitidine 150 mg q12h

Cimetidine * 400 mg four times

daily or 800 mg q12h

* Cimetidine is not recommended for use in older adults.

TABLE 10-3

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Older adults reported typical symptoms of GERD at postprandial times.

B Furuta et al., 2012

Despite negative results of pH monitoring indicating no evidence of GERD, patients were found to continue PPI use.

B Gawron et al., 2012

Screening for Barrett ’ s esophagus can be considered in men with more than 5 years of GERD symptoms and/or frequent GERD symptoms who also have two or more risk factors: age >50, Caucasian, central obesity, smoking history, and history of Barrett ’ s esophagus and/or esophageal adenocarcinoma in a fi rst- degree relative.

B Shaheen et al., 2016

Patient ’ s with Barrett ’ s esophagus should receive once-daily PPI, unless twice daily therapy is needed to adequately control symptoms.

B Shaheen et al., 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

Chapter 10 ■ Abdominal Disorders 263

Signal Symptoms: A dual dragging sensation with an ingui- nal hernia; male patients may report pain and swelling in the scrotum; patients with strangulated abdominal hernia usually have a tender mass with associated fever, nausea, and vomiting.

Description: A hernia is the protrusion of tissue through a weakened section in the abdominal wall. Abdominal wall hernias usually occur at the groin (inguinal) and umbilicus. Hernias are classifi ed by their severity as reducible, incar- cerated, or strangulated. A reducible hernia moves easily through the anatomical defect. An incarcerated hernia does not return to a normal position automatically or when manipulated externally. A strangulated hernia results when an incarcerated hernia develops edema with ischemia to the entrapped bowel.

In addition to these classifi cations, inguinal hernias may be either direct or indirect. A direct inguinal hernia passes through the posterior inguinal wall, whereas an indirect or congenital inguinal hernia enters in through the internal abdominal inguinal ring along the spermatic cord through the inguinal passage, to exit out the external inguinal ring.

Etiology: Hernia development has been linked to recurrent Valsalva maneuvers and dysfunctional connective tissue resulting from malnutrition or long-term steroid use. In older women, a history of multiple pregnancies and relaxation of the pelvic musculature, combined with loss of extraperito- neal fat, are considered etiological factors in the development of an obturator hernia (Haraguchi et al., 2007).

Occurrence: In the United States, more than 700,000 her- niorrhaphies are performed annually. The most common type of hernia is the inguinal hernia, which accounts for 80% of all cases, followed by the femoral hernia, which is 5% of all hernias. The remaining 15% include umbilical, epigas- tric, obturator, and those resulting from a surgical incision (Greenfi eld, 2001).

Age: The incidence of femoral and obturator hernias in women increases with age (Haraguchi et al., 2007). The inci- dence of male indirect (congenital) hernias decreases with age, but that of direct inguinal hernias increases.

Gender: Indirect inguinal hernias are eight to ten times more common in men than in women, yet the indirect ingui- nal hernia is the most common type of hernia in women. Older women are three to fi ve times more likely than men to develop a femoral hernia. The obturator hernia is a rare condition that occurs predominantly in women (Haraguchi et al., 2007; Kielar, Duigenan, & McInnes, 2014).

Ethnicity: Not signifi cant.

Contributing Factors: A chronic cough, ascites, abdominal surgery, obesity, and symptomatic prostatism can contribute to development of a hernia because of the associated risk factor of increased intra-abdominal or intrathoracic pres- sure (Kielar et al., 2014; Lau, Kim, Haigh & Tejirian, 2012 ). Incisional abdominal hernias can be found in patients with abdominal organ transplants (Smith et al., 2015). Chronic straining for bowel movements, straining to urinate, and

lifting heavy objects may be precursors to hernia formation. For women, a weakened pelvic fl oor after childbirth can contribute to the development of femoral herniation. Older women who are underweight and have a history of chronic illness can develop obturator hernias (Haraguchi et al., 2007). Hernias also may form at the site of a surgical inci- sion or a large scar. Patients with known liver cirrhosis with ascites have a 20% chance of developing an umbilical hernia ( Eker et al., 2011 ). Family history of organ herniation is also recognized as an intrinsic factor contributing to the develop- ment of hernias.

Signs and Symptoms: When patients present with signs and symptoms suggestive of a hernia, question them about how long the discomfort (swelling, pain, mass) has been present. Ask if the pain is aggravated by any activity, such as heavy lifting or positioning. Inquire about abdominal surgical history (LeBlanc, LeBlanc, & LeBlanc, 2013). Question if there is a family history of hernias. Patients may report a dual dragging sensation with an inguinal hernia (Kielar et al., 2014). Male patients may report pain and swelling in the scrotum. Hernias may be asymptomatic, only to be dis- covered as part of a routine physical examination. A reduc- ible hernia presents as a nontender mass that becomes more pronounced after a Valsalva maneuver. An incarcerated hernia, also a nontender soft mass, is found in the abdomi- nal, femoral, or inguinal area and remains even after gentle manipulation. Patients with strangulated abdominal hernia usually have a tender mass with associated fever, nausea, and vomiting. No attempt should be made to reduce a strangu- lated hernia.

Physical examination reveals decreased fl atus, high- pitched or tinkling bowel sounds, abdominal distention, and tenderness of the mass. When examining a patient with a suspected hernia, assess the patient in both the supine and standing position, fi rst observing the suspected mass before change in position. Have the patient also perform the Valsalva maneuver. If possible, attempt to identify the location of the hernia sac and the fascial opening of the hernia when palpat- ing the abdomen (Kielar et al., 2014). Identify the border of the suspected hernia (LeBlanc et al., 2013). Although rare, a patient with a chest wall bulge on the lower chest wall may have an abdominal intercostal hernia (Erdas, Licheri, Calò, & Pomata, 2014). For a suspected inguinal hernia, ask the patient to fl ex the leg on the side you will examine and then gently palpate the groin area. Then, with fi ngertips placed over the femoral area, external ring and internal ring should be inserted up into the inguinal canal (LeBlanc et al., 2013).

Gross screening for an inguinal hernia in a male patient is made easier with the patient coughing because “hernia bulges can be felt either against the examining fi nger (direct hernia) or at the tip of the fi nger, as it approaches the internal ring (indirect hernia)” (Amerson, 1990, p. 484). A femoral hernia can often be elicited by having a patient cough or strain; the bulge will be felt below the inguinal ligament (LeBlond et al., 2015). A positive Howship-Romberg, which is pain experienced with internal rotation of the hip along with intestinal obstruction, has been found in patients diagnosed with an obturator hernia ( Ramser, Messmer, Zbinden, Von

HERNIA

264 Chapter 10 ■ Abdominal Disorders

Holzen, & Nebiker, 2014 ). A mass is detected in the femoral triangle; patients experience pain down the medial aspect of the thigh all the way to the knee as a result of compression of the obturator nerve (LeBlond et al., 2015).

Diagnostic Tests: In an uncomplicated asymptomatic hernia, laboratory and diagnostic tests are unwarranted. If there is questionable strangulation from a prolonged incarcerated hernia, laboratory studies for complications may reveal leu- kocytosis, elevated serum amylase, and guaiac-positive stool. The use of higher-resolution multidetector CT scan allows for a clearer image of the anatomy studied. Axial CT scan should be requested fi rst if a hernia is suspected (Kielar et al., 2014). Abdominal series are done postoperatively to look for signs of perforation (free air) or obstruction of the bowel (multiple air-fl uid levels). Ultrasonography may be ordered for a patient with a suspected recurring hernia or hydrocele (LeBlanc et al., 2013).

Differential Diagnosis:

■ Femoral lymphadenopathy ■ Femoral artery aneurysm ■ Psoas abscess ■ Undescended testicle ■ Muscle strain (LeBlanc et al., 2013)

Treatment: Surgical repair of strangulated inguinal, umbili- cal, and femoral hernias is recommended immediately unless the patient is a poor surgical risk. These patients need to be hospitalized, receive IV solutions, and remain on NPO status. Small, direct inguinal hernias and painless, indirect inguinal hernias do not need immediate attention; however, surgery generally is recommended within 1 week of diagno- sis. Patients who are not surgical candidates can be fi tted for a truss and monitored for signs of prolonged incarceration. Patients with a small, direct, nonpainful hernia should be observed for reduction of the hernia when supine.

Follow-Up: For patients with reducible hernias, observation of the hernia during subsequent physical examination is rec- ommended ( Fitzgibbons et al., 2006 ). Patients suspected of having an incarcerated hernia should be followed up within 1 week to determine if they are experiencing any tenderness of the mass and if a general surgeon has seen them. For the postoperative patient who has had a herniorrhaphy, assess

for wound healing and recurrence of the hernia. The mor- tality rate is increased for patients who have undergone an emergent hernia repair (Altom et al., 2011).

Sequelae: An untreated inguinal, umbilical, or femoral hernia may become incarcerated and strangulated, with sub- sequent intestinal gangrene. The likelihood of incarceration is greatest for femoral hernias (Kielar et al., 2014). Post- surgical complications of a herniorrhaphy include wound hematomas and superfi cial wound infections. In one study, 17% of patients who had laparoscopic ventral hernia repair needed subsequent abdominal surgery for reasons such as unplanned bowel obstruction (Patel, Love, Ewing, Warren, Cobb, & Carbonell, 2017). Nerve entrapment is a serious complication of an inguinal herniorraphy. Approximately 50% of hernia recurrence occurs within 5 years, and an additional 20% occurs 15 to 20 years after surgical repair (Sevonius, Gunnarsson, Nordin, Nilsson, & Sandblom, 2011; Slater et al., 2014).

Prevention/Prophylaxis: Cessation of cigarette smoking is rec- ommended to reduce intrathoracic pressure from chronic coughing. Encourage the use of fi ber, fl uids, and stool soft- eners for patients who strain with defecation. Patients should avoid lifting heavy objects without proper support. As a preventive measure, encourage weight reduction for obese patients, especially those who have had prior abdominal surgery ( Lau et al., 2012 ).

Referral: Refer the patient to a general surgeon when a hernia is detected. A strangulated hernia requires immediate attention.

Education: Inform the patient with a reducible hernia of the potential complications of an untreated hernia and the importance of reporting immediately any new clinical signs and symptoms, such as increase in pain, swelling, and/or fever. Teach patients to avoid straining to defecate or urinate. Encourage smoking cessation to reduce the probability of a chronic cough. Instruct the patients on proper techniques for lifting heavy objects. Weight reduction should be encouraged for obese patients. Patients also should be advised to discuss with their surgeon postoperative restrictions and plan for rehabilitation and home support given the probable restric- tions to activity (Ritcher, 2014).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

In a retrospective review of patients with laparoscopic ventral hernia repair, 17% of the 733 patients required a subsequent abdominal operation.

A Patel, Love, Ewing, Cobb, Carbonell, A., . . . Carbonell, A. M., 2017

Both increasing BMI and older age were found to directly related to incarceration of noninguinal abdominal wall hernias.

A Lau, Kim, Haigh, & Tejirian, 2012

A positive Howship-Romberg sign, which is pain elicited with internal rotation of the hip, is common in older patients with an obturator hernia.

C Ramser, Messmer, Zbinden, Von Holzen, & Nebiker, 2014

Chapter 10 ■ Abdominal Disorders 265

Signal Symptoms: Abdominal pain (may be described as colicky, pain relieved by defecation), abdominal distention, mucus in the stool, and the sensation of incomplete evacua- tion; patients often complain of associated symptoms such as fatigue, fl atulence, headache, backache, and dyspepsia.

Description: Irritable bowel syndrome (IBS) is a chronic func- tional GI disorder characterized by chronic abdominal pain and altered bowel function, in the absence of an attributable organic cause (Longstreth et al., 2006). The subtypes of IBS are diarrhea prominent (IBS-D), constipation prominent (IBS-C), or mixed diarrhea and constipation (IBS-M), and unspecifi ed (IBS-U) (Capili, Anastasi, & Chang, 2016). IBS is generally felt to be caused by alterations in GI motility and visceral hypersensitivity (increased gut sensitivity to stimuli) (Capili et al., 2016; Kanazawa et al., 2016).

Etiology: Although IBS is felt to be due to multiple interact- ing factors, the exact etiology remains uncertain (Camilleri, 2012). While the focus remains on distortions, intestinal motility, and altered visceral sensation, research has begun to investigate other contributing factors such as infl ammation, changes in intestinal fl ora, food sensitivities, and genetic pre- dispositions (Capili et al., 2016; Jeffery et al., 2012; Lembo, Zaman, Jones, & Talley, 2007; Liebregts et al., 2007). There has also been an association made between increased stress and IBS (Chang, 2011; Kanazawa et al., 2016).

Occurrence: A common presentation for patient referral, IBS accounts for approximately 30% of all referrals to a gastroen- terologist (Drossman, Camilleri, Mayer, & Whitehead, 2002). It is estimated that 5% to 15% of the general population suffer from IBS (Capili et al., 2016).

Age: Of cases of IBS, 50% are diagnosed before age 35 years. Because most cases of IBS present by age 50 years, this syn- drome is often a chronic condition in older adults. A new diagnosis of IBS in the sixth decade or later is extremely rare (Kurniawan & Kolopaking, 2014).

Gender: Prevalence of IBS is twice as great in women as in men in the United States (Kurniawan & Kolopaking, 2016).

Ethnicity: IBS has a higher prevalence among Caucasians than among other ethnic groups (Minocha, 2008).

Contributing Factors: Female gender and family history of IBS are associated with the development of IBS. Traumatic life events, such as physical or sexual abuse, may trigger the onset of IBS (Koloski, Talley, & Boyce, 2005; Perona et al., 2005). Stressful psychosocial situations may hasten an exacerbation of IBS. IBS is common in patients who also have diagnosed anxiety or depression (Kurniawan & Kolopa- king, 2014). Small bowel overgrowth is a common fi nding in older adults with IBS (Chatterjee, Park, Low, Kong, & Pimen- tel, 2007; Lupascu et al., 2005). Recent fi ndings have indi- cated that the 5-HT (serotonin) concentration was higher in patients who had diarrhea predominant IBS than those with constipation dominant IBS (Kurniawan, & Kolopaking, 2014).

Certain food products such as fructose, sorbitol, and lactose, have been known to alter bowel motor function. Review any new prescribed and OTC medications to deter- mine if side effects include constipation or diarrhea. Given the increased prevalence of diverticulosis and intra-abdom- inal surgeries such as hysterectomy and cholecystectomy, it has been suggested that these conditions may cause or con- tribute to symptoms that occur in IBS in older adults. It is important to note that common medical conditions such as diabetes, stroke, and Parkinson ’ s disease are known to alter defecation patterns (Minocha, 2008). Symptoms of IBS have been found in about one-fourth of patients who have had a prior GI infection (Kurniawan & Kolopaking, 2014).

Signs and Symptoms: A thorough dietary history is essential to establish a differential diagnosis of IBS, ruling out the possibility of food intolerance. Review recent travel history with the patient. Explore the patient ’ s psychosocial history to determine the relationships between stressful events and exacerbation of IBS. Determine the onset of symptoms, including the time of day when the pain and GI disturbances usually occur. A thorough GI review of systems is important in patients with IBS because GI conditions such as GERD, nonobstructive dysphagia, and functional dyspepsia are often found in patients presenting with IBS symptoms (Kurniawan & Kolopaking, 2014). A report of postprandial abdomi- nal pain suggests biliary tract disease, pancreatitis, or PUD. Patients often report loose and frequent stools or alternating

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients with cirrhosis and ascites benefi t from elective umbilical hernia repair.

B Eker et al., 2011

No signifi cant difference was found in patients with inguinal hernias with mild symptoms who delayed surgical repair and those who did not.

B Fitzgibbons et al., 2006

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

IRRITABLE BOWEL SYNDROME

266 Chapter 10 ■ Abdominal Disorders

constipation and diarrhea. Abdominal pain may be described as colicky. Pain often is relieved by defecation. Abdominal dis- tention, mucus in the stool, and the sensation of incomplete evacuation are other presenting symptoms.

Patients often complain of associated symptoms such as fatigue, bloating, fl atulence, headache, backache, and dys- pepsia. It is common for older adults to present with non- GI-related symptoms such as lethargy, back pain, headache, or urinary frequency ( Agrawal, Khan, & Whorwell, 2009 ). Older adults tend to have greater incidence of rectal urgency with fecal incontinence than younger patients (Minocha, 2008). If patients report fever, unexplained weight loss, dys- phagia, or rectal bleeding, these are not symptoms of irritable bowel and should be evaluated closely, especially with a past personal history of any malignancy and a family history of colon cancer.

The physical examination is usually unremarkable (Kur- niawan & Kolopaking, 2016). Abdominal tenderness may be elicited, especially in the left lower quadrant, but is not pro- nounced. Presence of an abdominal mass, lymphadenopathy, hepatosplenomegaly, or ascites in a patient with IBS should prompt further investigation. A routine digital rectal exam- ination generally reveals a tender rectum that is either empty or full of hard, fi rm feces. It is important to discern if there are any disorders that may contribute to diffi cult or painful defecation, such as fi ssures, external hemorrhoids, or rec- tocele. Detection of a rectal mass on digital rectal examina- tion is concerning and must be further evaluated to rule out malignancy.

Diagnostic Tests: The Rome III criteria for the diagnosis of irritable bowel has been simplifi ed. It is important to discern from the patient the time frame of symptom presentation and duration to help distinguish IBS from other conditions that can mimic this chronic functional disorder of the bowel (see Table 10-4 ). A new presentation of IBS in older adults is one of the alarm symptoms, so when ordering diagnostic tests in older adults, determine the length of time since the last evaluation and the nature of the current symptoms. There is no biological indicator for IBS. In general, a CBC and eryth- rocyte sedimentation rate can rule out anemia and infl am- mation (Furman & Cash, 2011). If diarrhea is the presenting symptom, stool culture and examination for occult blood, ova and parasites, bacteria, and celiac sprue in patients with diarrhea are recommended. A test for Clostridium diffi cile should also be ordered in acute onset of diarrhea, especially in the setting of recent confi nement to a health-care facil- ity, recent antibiotic use, or other causes of altered GI fl ora, such as intestinal infection. For patients with constipation, plain abdomen x-ray series and colonic transit markers may

be useful in determining functional causes, as well as stool burden (Minocha, 2008).

Patients with documented involuntary weight loss equal to or more than 5% within a 6-month period, or with signs of obstruction, should have an abdominal CT scan and a small bowel series. Colonoscopy with biopsies may be con- sidered in patients with diarrhea-predominant symptoms to rule out microscopic colitis (Furman & Cash, 2011). Patients with persistent constipation should be evaluated for hypothy- roidism, which can contribute to constipation. If the present- ing symptoms are bloating and abdominal distention with cramping and diarrhea, a 3-week trial of a lactose-free diet is recommended to rule out lactose intolerance.

Differential Diagnosis:

■ Food intolerance ■ Diverticular disease ■ Parasitic diseases ■ Biliary tract disease ■ Colonic polyps ■ Neoplasms ■ Pancreatic disease ■ Abuse of cathartics ■ Latent celiac disease ■ Crohn ’ s disease ■ Ulcerative colitis ■ Ischemic colitis ■ Chronic prostatitis ■ Thyroid dysfunction ■ GI infection (viral or bacterial) ■ Lactose malabsorption (Furman & Cash, 2011;

Minocha, 2008)

Treatment: The management of IBS depends on the presen- tation of the patient ’ s condition. In all patients with mild symptoms that do not signifi cantly impair quality of life, life- style and dietary changes should be initiated. If symptoms do not respond, or are moderate to severe, pharmacological interventions can supplement diet and lifestyle modifi cation. Treatment should begin with education and reassurance that, while this is a chronic disease, there is no increase in malignancy. Dietary modifi cations should include avoiding foods that trigger symptoms.

Additionally, improvement of symptoms has been demon- strated with a traditional IBS diet (avoiding high fat, caffeine, gas-producing foods, insoluble fi ber, and large meals) (Böhn et al., 2015 ). Also, a trial of gluten avoidance and lactose avoid- ance can be instituted to assess improvement. If the patient presents predominantly with constipation, psyllium has been shown to improve symptoms (Ford & Talley, 2012). It should be initially prescribed at one-half to one tablespoon daily, to prevent gas and bloating side effects, and then titrated up until effective. For diabetic patients who choose bulk-forming products, caution should be given regarding using any prod- ucts that have high sugar content. Patients should be warned that increased bloating might occur initially with fi ber prod- ucts, but usually resolves in 2 to 3 weeks.

Polyethylene glycol (PEG) 3350 is an FDA-approved osmotic laxative used for short-term constipation; however, while it has been shown to improve constipation, it has little effect on abdominal discomfort (Chapman, Stanghell- ini, Geraint, & Halphen, 2013). PEG should be started at

Rome III Criteria for the Diagnosis of Irritable Bowel Syndrome

Symptoms present for at least 3 days per month in the past 3

months (with symptom onset at least 6 months previously) with at

least two of the following features:

• Improved with defecation

• Onset associated with a change in stool frequency

• Onset associated with a change in stool form (appearance)

Source: Ford et al., 2014.

TABLE 10-4

Chapter 10 ■ Abdominal Disorders 267

17  g in 8 ounces of water per day, and titrated up or down (maximum 34  g a day) for effect. Lubiprostone is a chloride channel activator used in the treatment of IBS-C; a dose of 8 to 24 mcg twice a day with food, to prevent nausea, is rec- ommended. Results of clinical trials show effi cacy in reduc- ing chronic constipation and abdominal pain with bloating in patients with IBS-C ( Lembo et al., 2011 ). Another agent is Linaclotide, a guanylate cyclase agonist that stimulates intestinal fl uid secretion and transit that has been shown to be effective in treatment of IBS-C (Chey et al., 2012; Rao et al., 2012). It is dosed in 290 mcg and 145 mcg once daily on an empty stomach, at least 30 minutes prior to the fi rst meal of the day to avoid diarrhea. Because it is a newer medication and long-term effects are still unknown, it is usually used in IBS-C patients who have failed PEG treatment. The most common side effect is diarrhea, although this tends to resolve after a few weeks of treatment.

Alosetron, a selective 5-HT(3) antagonist, is FDA approved for IBS-D treatment in females only, but signifi cant adverse side effects such as ischemic bowel and toxic megacolon limits this use in routine practice (Bleser, 2011). Historically, this drug resulted in adverse effects, but updated prescribing guidelines by the FDA has improved the safety profi le. Provid- ers who choose to prescribe this must be aware of all risks, benefi ts, and have a dedicated prescribing outline in order to meet safety requirements. Close follow-up is recommended, and prescribing should be done by an experienced provider who is familiar with the full ramifi cations of this drug.

Foods that may exacerbate IBS-D should be avoided (e.g., caffeinated beverages, histamine-releasing foods like wine and beer, sorbitol-containing candies or gums, citrus fruits for persons with fructose intolerance, and milk products for persons who have known lactose intolerance) (Bohn, Storsrud, Törnblom, Bengtsson, & Simren, 2013).

Antispasmodics are not recommended for treatment of IBS-D in older adults because of the anticholinergic side effects of these medications. If diarrhea is severe, loperamide 2 mg every 4 to 8 hours can be taken, but antidiarrheal med- ications are not benefi cial in treating global IBS-D symptoms. Another treatment often used for IBS-D is bile acid seques- trants, as up to 50% of IBS-D patients have been found to have bile salt malabsorption (Wedlake et al., 2009). Early studies point to the use of rifaximin, an antibiotic, for consid- eration of the treatment of IBS without constipation and can be considered in patients who have failed other treatments ( Menees, Maneerattannaporn, Kim, & Chey, 2012 ).

A newer agent recently approved for the treatment of IBS-D is a combination mu-opioid receptor agonist and del- ta-opioid receptor antagonist named Eluxadoline, in doses of 100  mcg and 75  mcg to be given twice a day with food. This has been shown effective in improving both the diarrhea and abdominal pain symptoms associated with IBS-D ( Lembo et al., 2016 ). It should be noted that pancreatitis developed in 0.3% of study patients and any patient on Eluxadoline

who experiences pancreatitis-like symptoms should stop the medication and notify their provider. Eluxadoline is also contraindicated in individuals with chronic alcohol abuse, chronic history of pancreatitis, known or concern for biliary duct obstruction, sphincter of Oddi disease, pancreatic struc- tural diseases, known mechanical obstruction, or severe liver impairment (Child-Pugh Class C).

Follow-Up: With chronic IBS patients, a positive relationship between the health-care provider and the patient is mutu- ally benefi cial. Dietary intervention and stress-reduction techniques should be reviewed and evaluated. In patients with newly diagnosed IBS, evaluation of persistent symp- toms is necessary because IBS is a diagnosis of exclusion. Patients with IBS have been found to have multiple comor- bidities that need to be considered. Functional dyspepsia and depression were the most common comorbidities in patients with chronic constipation (Nellesen, Chawla, Oh, Weissman, Lavins & Murray, 2013).

Sequelae: Older adults with a chronic history of IBS may have a concomitant illness, such as diverticulosis ( Agrawal et al., 2009 ; Minocha, 2008). Complications may develop because of other pathological processes mistaken for IBS symptoms. Patients with uncontrollable diarrhea are at risk for dehy- dration because of fl uid and electrolyte loss; this is especially true in older adults. Fecal impaction may result from chronic constipation, especially in an immobile, cognitively impaired older patient.

Prevention/Prophylaxis: The patient should use stress reduc- tion techniques during emotionally stressful situations. Patients should avoid all food products that are known to irritate their bowels (Bohn et al., 2013). Patients with known food intolerance must read nutrition labels and be informed of the inactive contents of medications, which may contain irritating substances.

Referral: Refer patients to a gastroenterologist for colono- scopic imaging. Refer again if patients exhibit persistent abdominal pain or uncontrollable diarrhea despite compli- ance with treatment and if signs of GI bleeding are present. Patients may benefi t from psychotherapy, biofeedback, or hypnosis. Cognitive behavioral treatment is a very common nonpharmacological treatment in patients with IBS (Kurni- awan & Kolopaking, 2014).

Education: Inform patients that because the increase of dietary fi ber could aggravate their IBS symptoms, they should increase gradually to the recommended dose. It may take 3 to 4 weeks to reach a therapeutic level suffi cient to produce results. Eating smaller, frequent meals may ease the IBS symptoms in older adults and enhance overall quality of life (Kurniawan & Kolopaking, 2014). Inform patients with chronic IBS that although the disease itself does not lead to a more serious illness, any change in symptoms should be reported to the health-care practitioner.

268 Chapter 10 ■ Abdominal Disorders

Signal Symptoms: Cachexia, jaundice.

Signal Description: The liver is the most common organ in the body for metastasis from other cancers. Common sites of primary tumors that metastasize to the liver are the lungs, colon, pancreas, stomach, breast, and gallbladder. Hepatocel- lular cancer is associated with cirrhosis of the liver.

Etiology: The hepatic fi ltration of arterial and portal venous blood is a major reason for the high prevalence of metastases from primary cancerous sites in the body to the liver. Metas- tases also may result from an extension from an abdominal tumor or through the lymphatic system. Malignant tumors of the liver are primarily adenocarcinomas.

Occurrence: Primary liver cancer, rare in the United States, accounts for about 2% of all cancers or approximately 39,000 cases per year (National Cancer Institute, 2016b). A malignant lesion is 20 times more likely to be from a meta- static source than from a primary lesion.

Age: Mean age of diagnosis is between 50 and 60 years.

Gender: More prevalent in males than in females (ACS, 2016).

Ethnicity: Primary liver cancer is prevalent in people from Africa and Asia because of the widespread occurrence of hepatitis B virus and hepatitis C virus (ACS, 2016).

Contributing Factors: The incidence of liver cancer increases for patients who have a history of cirrhosis of the liver, hep- atitis B virus, and hepatitis C virus. Hemochromatosis, por- phyria cutanea tarda, alpha-1 antitrypsin defi ciency, and Wilson ’ s disease place patients at higher risk of developing liver cancer (NCCN, 2016).

Signs and Symptoms: Complaints of weakness, malaise, weight loss, sweating, and anorexia may be reported. Pain in the upper abdomen can be associated with the cancer and also may be reported. Physical examination reveals cachexia. Auscultation may reveal a bruit over the tumor

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Patients with IBS without constipation treated for 2 weeks with rifaximin versus placebo experienced signifi cantly less bloating and other global symptoms of IBS than before the treatment started.

A Pimentel et al., 2011

A systematic review and meta-analysis of randomized controlled trials (RCTs) that tested the use of rifaximin against placebo in patients with IBS without constipation showed the effi cacy of rifaximin in reducing global symptoms of IBS, including bloating.

A Menees et al., 2012

Older adults diagnosed with IBS presented with noncolonic symptoms such as lethargy, headache, joint pain, and back pain.

B Agrawal, Khan, & Whorwell, 2009

Women with IBS reported greater psychological stress with the increased severity of abdominal pain/discomfort regardless of the bowel pattern.

B Heitkemper et al., 2011

Lubiprostone has been well tolerated in patients with chronic constipation.

A Drossman et al., 2009 Lembo et al., 2011

Eluxadoline reduced symptoms of IBS with diarrhea in men and women, with sustained effi cacy over 6 months with 100 mg dosed twice daily.

A Lembo et al., 2016

Implementation of the traditional IBS diet (avoidance of large meals, high-fat foods, caffeine, insoluble fi bers, and gas-producing foods) was associated with improvement in IBS symptoms.

A Böhn et al., 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

LIVER CANCER

Chapter 10 ■ Abdominal Disorders 269

and tenderness of the liver. Hepatomegaly and ascites may be present. A mass may be palpable. In more advanced cases, jaundice may appear (NCCN, 2016).

Diagnostic Tests: Laboratory fi ndings may be nonspecifi c and are related to the underlying liver disease. Findings may include thrombocytopenia, hypoalbuminemia, hyperbiliru- binemia, and hypoprothrombinemia. Additionally, patients may have mild anemia and electrolyte disturbances (ACS, 2016). Serum alkaline phosphatase, AST, ALT, and gam- ma-glutamyl transpeptidase (GGT) are often abnormal in a nonspecifi c pattern. PT/INR may be elevated.

Patients at high risk for hepatocellular carcinoma (HCC) should be screened using ultrasound every 6 months ( Bruix & Sherman, 2011 ; NCCN, 2016). Identifi cation of a liver nodule that is smaller than 1  cm should be reimaged with an ultra- sound in 3 months. Nodules that are larger than 1 cm should be reimaged with contrast-enhanced MRI. Nodules that demonstrate arterial hypervascularity and venous or delayed phase washout are consistent with HCC. Those nodules that do not demonstrate arterial hypervascularity and venous or delayed phase washout should be reimaged with another con- trast-enhanced study such as a CT scan or MRI. Lesions that demonstrate arterial hypervascularity and venous or delayed phase washout are diagnostic for HCC. Lesions that do not demonstrate arterial hypervascularity and venous or delayed phase washout should undergo percutaneous biopsy.

An elevated serum α -fetoprotein is not specifi c to liver cancer (National Cancer Institute, 2016a). A rise in the α -fetoprotein is concerning for the development of HCC in patients with cirrhosis. Elevated serum α -fetoprotein found at levels of more than 500  g/L in patients with cirrhosis is diagnostic for HCC. However, HCC is often found with lower levels of α -fetoprotein when high-risk patients are undergo- ing routine screening.

Differential Diagnosis:

■ Cirrhosis ■ Chronic hepatitis B or C infection ■ Metastatic malignancy of the liver

Treatment: Advancements in the surgical treatment of hepatic metastatic cancers include tumor ablation and micro- scopic glass beads containing a radioactive element. Surgical resection of the liver is benefi cial only if the patient has a resectable tumor; even so, the survival rate remains low. Liver transplant may be considered in patients with early stage liver cancer, as well as advanced disease. Intrahepatic che- motherapeutic agents, such as 5-fl uorouracil and fl oxuridine, may alter the growth of the tumor, but the prognosis remains the same. Sorafenib can be used for patients with unresect- able or metastatic disease. Older patients with known renal function impairment may require a reduced dosage of these agents compared with younger patients, however, often the treatment is palliative at best (NCCN, 2016).

Follow-Up: Patients and family members should be given the opportunity to explore adjunctive methods of pain relief and relaxation. After diagnosis of liver cancer, the focus should be on holistic palliative care, including the intervention of hospice and services provided by the ACS.

Sequelae: The prognosis is poor because the tumor grows rapidly and often metastasizes to the lungs or bones. The sur- vival rate is only 4 to 6 months.

Prevention/Prophylaxis: Hepatitis vaccine is recommended for high-risk patients. Avoidance of chemical exposure, as part of occupational safety, is suggested. Annual ultrasound screening for patients with chronic hepatitis B or cirrhosis should be considered as a preventive measure for liver cancer.

Referral: Refer the patient to an oncologist when the diag- nosis of liver cancer is suspected. Local hospice care services should be contacted for care for the patient and family.

Education: Although no further medical treatment is aimed at reversal of the disease, the patient needs to know that you will collaborate with the hospice nurses to provide for the patient ’ s comfort throughout the disease process. The patient can be referred to http://www.liverfoundation.org/support/ for basic information about liver cancer.

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

Prevention of HCC should focus on preventing infection with hepatitis B virus (HBV) and hepatitis C virus (HCV), treating patients with viral hepatitis who are candidates for treatment, avoiding environmental toxins, and attempting to prevent the development of cirrhosis in patients with liver disease.

A ACS, 2016 NCCN, 2016

Patients with chronic HBV infection who are at increased risk for HCC should undergo routine surveillance.

A Bruix & Sherman, 2011 NCCN, 2016

All patients with cirrhosis, regardless of etiology, should undergo surveillance for HCC.

B Bruix & Sherman, 2011 NCCN, 2016

Surveillance in high-risk patients should be performed with ultrasonography every 6 months rather than annually.

B Bruix & Sherman, 2011 NCCN, 2016

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

270 Chapter 10 ■ Abdominal Disorders

Signal Symptoms: Vague fl ank pain, hematuria, renal colic, abdominal pain.

Description: In the Western hemisphere, most cases of neph- rolithiasis, or kidney stones, are calcium salts, uric acid, cys- teine, and struvite. These substances begin to form crystals and become attached to the kidney, eventually developing into stones. Calculi range in size from microscopic to several centimeters in diameter. Nephrolithiasis often attempt to travel through the urinary system and out through the urine. Pain occurs when the calculi become lodged ( Curhan, Aronson, & Preminger, 2015 ).

Etiology: Kidney stones develop from the supersaturation of urine with stone-forming salts that occurs either by overex- cretion of salt or underexcretion of urine. Some preformed nuclei form to create a calculus. Abnormal crystal growth inhibitors are formed as well because of hypocitraturia or magnesium defi ciency. Approximately 80% of diagnosed kidney stones contain calcium; 10% to 20% are struvite stones, resulting from urinary tract infections; 10% to 15% are uric acid calculi; and 1% contain cystine.

Occurrence: One out of 11 Americans will be diagnosed with a kidney stone in their lifetime. Approximately 50% of patients who have had previous urinary calculi have a recur- rence in 5 to 10 years.

Age: Episode onset often occurs between 20 and 60 years of age. The incidence of kidney stones for women peaks around age 55 years.

Gender: Men are more likely than women to form uric acid and calcium stones; struvite stones are more common in women due to the higher incidence of urinary tract infec- tions. Cystine stone formation occurs equally in men and women (Han, Segal, Seifter, & Dwyer, 2015).

Ethnicity: The incidence of kidney stones in Caucasians is three to four times greater than in African Americans; however, the prevalence in African Americans has recently increased 150%. Asian women have the lowest occurrence of kidney stones.

Contributing Factors: A major contributing factor to the development of calculi is decreased fl uid intake leading to high concentration of urine. Certain food substances that augment the formation of kidney stones include dairy prod- ucts, chocolate, green leafy vegetables (calcium oxalate stones) and eggs, fi sh, poultry, peanuts, and wheat (cystine stones). Certain medications such as triamterene, indinavir, acetazolamide, acyclovir, and sulfa can contribute to the development of nephrolithiasis ( Curhan et al., 2015 ; Tan & Lerma, 2015 ). A history of hyperparathyroidism, sarcoid- osis, Cushing ’ s syndrome, Paget ’ s disease, and immobilization may contribute to the development of calcium phosphate stones. Chronic urinary tract infections may be precursors to struvite stone formation. Family history has also been found to contribute to stone formation, as well as increased oxalate absorption. Bowel disorders that cause chronic acidic urine states, such as patients that have undergone bariatric surgeries, can increase nephrolithiasis frequency. Individuals

with metabolic syndrome or those that encompass four to fi ve traits of the disease are more likely to experience kidney stones ( Richman, O’Bell, & Pareek, 2014 ; Tan & Lerma, 2015 ).

Signs and Symptoms: Patients may have abrupt, severe, colicky pain in either fl ank or pain that originates in the fl ank and radiates to the groin. The pain sensation can begin as vague fl ank pain. Pain spreading downward suggests movement of the stone along the ureter. Associated nausea and vomiting may occur. Hematuria is also common ( Curhan et al., 2015 ; Januchowski, Dabecco, & Verdone, 2014).

Physical examination may reveal local abdominal and costovertebral angle tenderness. Men complaining of groin pain should have a testicular examination to rule out testic- ular torsion, prostatitis, or epididymitis. Women with pain radiating to the labia should have a pelvic examination to rule out possible ovarian torsion, cysts, pelvic infl ammatory disease, or tumors.

Diagnostic Tests: For patients who have not yet passed a stone, urine collection for recovery of stones or gravel should be ordered. A urinalysis (UA) reveals the presence of leu- kocytes, bacteria, and blood, which can be indicative of a urinary tract infection. The presence of crystals in a UA can aid in the determination of the type of stone present. Although abdominal plain fi lms are inexpensive and quick, they can fail to detect radiolucent stones, small stones, or obstructions ( Curhan et al., 2015 ). It has been found that patients that undergo an ultrasound initially do not need further imaging studies; similar results are found with ultra- sound when compared to CT scans with decreased radiation exposure ( Smith-Bindman et al., 2014 ; Tan & Lerma, 2015 ). The ability to view the entire urinary system is provided by IVP; however, there is a large amount of radiation exposure with IVP, lower sensitivity than CT scans, and multiple fi lms may be required over several hours ( Curhan et al. 2015 ; Tan & Lerma, 2015 ). A noncontrast helical CT scan is still the gold standard for nephrolithiasis detection. The helical scan is quick and often detects stones and obstructions not seen on other imaging studies ( Curhan et al., 2015 ; Han et al., 2015; Januchowski et al., 2014; Tan & Lerma, 2015 ).

Differential Diagnosis:

■ Papillary necrosis ■ Hydronephrosis ■ Ileus ■ Diverticulitis ■ Appendicitis ■ Bowel obstruction ■ Mesenteric ischemia ■ Ovarian cyst ■ Testicular torsion ■ Constipation ■ Arterial aneurysm ■ Cholecystitis ■ Acute cystitis ■ Pyelonephritis ■ Ectopic pregnancy

NEPHROLITHIASIS

Chapter 10 ■ Abdominal Disorders 271

■ Prostatitis ■ Renal cell carcinoma ■ Narcotic seekers

Treatment: Size and location of the stone, coupled with the length of time since the onset of symptoms, directs treatment. Stones less than or equal to 4 mm usually pass on their own; stones 4 to 5  mm have a 50% chance of passing without intervention. A stone of more than 10  mm requires refer- ral to a urologist for possible intervention that may include extracorporeal shock-wave lithotripsy, ureteroscopy, or per- cutaneous nephrolithiotomy. IV fl uids have not been found to aid in stone passage, but are recommended if patients are dehydrated ( Curhan et al., 2015 ; Januchowski et al., 2014). Patients not in distress and without obstruction should drink at least 2  L of fl uid daily and strain the urine until a stone has passed ( Tan & Lerma, 2015 ). NSAIDs have been found to be as effective in pain management as narcotics (Han et al., 2015). CCBs and alpha adrenergic blockers, such as Tamsulosin, relax smooth muscle and are often prescribed to aid in stone passage ( Curhan et al., 2015 ; Januchowski et al., 2014).

Follow-Up: A 24-hour urine collection 3 to 6 months after treatment for nephrolithiasis is recommended. At this time, also review with the patient the need for compliance with dietary restrictions and fl uid requirements.

Sequelae: Immediate complications of unresolved kidney stones include obstruction, urinary tract infection, and sepsis. A high incidence of recurrence of kidney stone forma- tion exists. Metabolic causes of kidney stones need to be ruled out when dietary measures are unsuccessful. Additional

complications of nephrolithiasis include renal failure, ure- teral perforation, perinephric abscess, pyelonephritis, and sepsis (Januchowski et al., 2014).

Prevention/Prophylaxis: An adequate daily fl uid intake is essential. Patients should be encouraged to increase their fl uid intake during heavy exercise or when traveling long distances. To prevent recurrent stones, review the patient ’ s dietary habits to discern if there are any excessive food prod- ucts that may be factors in kidney stone formation (calcium, purine, protein).

Referral: Refer the patient to a urologist when:

■ Obstruction is detected. ■ The stone is more than 5 mm. ■ The stone has not passed within 24 to 48 hours of the

onset of pain. ■ The patient has complicated diagnostic reports. ■ The patient has severe nausea and vomiting, intractable

pain, urosepsis, anuria, or renal failure.

Education: Inform all patients with nephrolithiasis that there is a high probability of a second occurrence of a kidney stone. Advise the patient, if possible, to strain urine with the provided strainer when experiencing symptoms of kidney obstruction. A daily fl uid intake of 2 to 3 L is recommended. Explain to patients that fl uid intake needs to be increased when urine appears dark yellow. Provide information about any food restrictions that may be deemed necessary to prevent specifi c stone formation ( Curhan et al., 2015 ; Elmahdy & Persad, 2014; Han et al., 2015; Richman et al., 2014 ; Shah & Camillo Calle, 2016; Tan & Lerma, 2015 ).

CLINICAL RECOMMENDATION EVIDENCE RATING REFERENCES

A noncontrast helical CT scan is the gold standard for nephrolithiasis detection; however, initial ultrasonography reduces radiation exposure with no signifi cant difference in outcomes.

B Smith-Bindman et al., 2014

Alpha adrenergic blockers and CCBs aid in stone passage by relaxation of smooth muscle.

B Curhan et al., 2015

There is an increased risk of stone development in patients with 4 to 5 traits of metabolic syndrome.

B Richman et al., 2014

NSAIDs and narcotics have been found to be benefi cial for pain relief in kidney stone sufferers.

B Tan & Lerma, 2015

A  =  consistent, good-quality, patient-oriented evidence; B  =  inconsistent or limited-quality, patient-oriented evidence; C  =  consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml .

272 Chapter 10 ■ Abdominal Disorders

Signal Symptoms: Fatigue, right upper quadrant pain or full- ness, possible hepatomegaly.

Description: Nonalcoholic fatty disease (NAFLD) is the most common liver disease in Western countries (Byrne & Targher, 2015). NAFLD refers to a spectrum of liver disorders that include simple steatosis (fatty liver), and nonalcoholic steato- hepatitis (NASH). NASH is characterized by hepatocyte injury, infl ammation, and fi brosis, which can ultimately lead to cir- rhosis and end-stage liver disease (Byrne & Targher, 2015). Risk factors for the development of NASH include elevated fasting blood glucose, low high-density lipoprotein (HDL), and elevated fasting cholesterol (Wilkins, Tadkoh, Hepburn, & Schade, 2013). Alcohol use must be minimal to meet the criteria for NAFLD (Bayard, Holt, & Buroughs, 2006). The maximum intake of alcohol is two standards drinks a day for men and one for women.

Etiology: Risk factors for the development of NAFLD include obesity, insulin resistance, hypertension, and dyslipidemia (Dyson, Anstee, & McPherson, 2015). Insulin resistance is the most important risk factor for the development of NAFLD. It has been suggested that there may be a genetic predisposi- tion to NAFLD, especially in patients who also develop meta- bolic syndrome (Croke & Sampson, 2012).

Occurrence: NAFLD is the most common liver disease in Western countries (Byrne & Targher, 2015). It has been pre- dicted that NAFLD will become the most frequent indication for liver transplantation by 2030. In the United States, it is estimated that 95 million adults are affected by NAFLD and the prevalence will continue to rise (Malhotra & Beaton, 2015). It is estimated that up to one-third of the population has evidence of steatosis on imaging (Dyson et al., 2015).

Age: The majority of patients initially diagnosed with NAFLD are in their forties or fi fties (Sheth & Chopra, 2016a). The risk of nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma is increased in the elderly with NAFLD (Bertolotti et al., 2014).

Gender: NAFLD is more common in men than women (Byrne & Targher, 2014). The incidence of NAFLD is approximately 30% to 40% in men and 15% to 20% in women (Bryne & Targher, 2015).

Ethnicity: Hispanics have the highest rate of NAFLD and non-Hispanic African Americans have the lowest incidence of NAFLD (Pan & Fallon, 2014). African Americans have been found to have less steatosis than Caucasians.

Contributing Factors: The most common risk factors associ- ated with the development of NAFLD are obesity, hyperten- sion, dyslipidemia, and insulin resistance (Sheth & Chopra, 2016a). Aging was found to be a risk factor for the devel- opment of NAFLD in premenopausal women, but the same could not be said for men (Hamaguchi et al., 2012). NAFLD may be present in patients who have jejunoileal bypass or gastric bypass, or who have experienced starvation and/or protein energy malnutrition. Also at risk are patients on total parental nutrition (Sheth & Chopra, 2016a). Drug-induced NAFLD can be caused by aspirin, cocaine, valproate, highly

active antiretroviral, tetracycline, NSAIDs, amiodarone, tamoxifen, methotrexate, and corticosteroids (Patel & Sanyal, 2013). In patients with coexisting conditions, such as ulcer- ative colitis, Graves’ disease, or type 1 diabetes, consider an autoimmune cause for NAFLD (Croke & Sampson, 2012). There is evidence that NAFLD is linked to other chronic disease such as sleep apnea, colorectal cancer, osteoporosis, psoriasis, and endocrine diseases such as polycystic ovary syndrome (Bryne & Targher, 2015).

Signs and Symptoms: Most patients with NAFLD are asymp- tomatic (Wilkins et al., 2013). Patients may present with fatigue, jaundice, pruritus, right upper quadrant discom- fort or fullness, and muscle weakness (Wilkins et al., 2013). Inquire about weight loss. On examination, look for evidence of jaundice of the skin, scleral icterus, and spider angiomas. Patients with more advanced cases may also have anorexia and nausea. Patients may have unexplained abnormal liver blood tests as part of a routine physical or drug monitor- ing, such as statins. On physical examination, patients with NAFLD may have hepatomegaly (Sheth & Chopra, 2016a). Patients with more advanced illness may present with asterixis and caput medusa radiating from around the umbi- licus (Sheth & Chopra, 2016a).

Diagnostic Tests: NAFLD is a diagnosis of exclusion. The most common abnormal laboratory tests are elevated ALT and AST (Sheth & Chopra, 2016a). ALT and AST may be elevated two to fi ve times the upper limits. It is important to exclude other causes of elevated transaminases levels. Hepatitis A, B, and C need to be ruled out, as does autoimmune hepatitis. NAFLD is the most common reason for elevated transaminases (Vernon, Baranova, & Younossi, 2011). Hemochromatosis needs to be ruled out. It may be useful to rule out Wilson ’ s disease, thyroid disease, celiac disease, and alpha-1 antitryp- sin defi ciency. A fasting glucose, lipid panel, PT, albumin, and total bilirubin should be obtained (Wilkins et al., 2013). An ultrasonography of the liver will assist in the diagnosis of NAFD by identifying fatty infi ltration in the liver (Wilkins et al., 2013). An ultrasonography of the liver has a sensitivity of 82% to 89% and a specifi city of 93% for identifying a fatty liver. For patients suspected of liver fi brosis, commercially available serologic markers are available to order (Wilkins et al., 2013). A liver biopsy should be considered for patients who are likely to have a more advanced liver disease, includ- ing morbid obesity, diabetes, advanced age, and an AST/ ALT ratio greater than 1. Patients with persistent elevations in liver enzymes despite lifestyle changes may be considered for liver biopsy. Patients should be screened for alcohol and drug use.

Differential Diagnosis:

■ Alcoholic hepatitis ■ Auto immune hepatitis ■ Hepatitis B ■ Hepatitis C ■ Thyroid disease ■ Alpha 1 antitrypsin disease ■ Medication induced hepatitis

NONALCOHOLIC FATTY LIVER DISEASE