sepsis

Diagnoses

Pathophysiology

Patient’s related signs and symptoms

Diabetes Mellitus Type II

The cause is unknown, however, central obesity, genetic predisposition, and physical inactivity are three major contributing factors, as well as age, illness and medication. Insulin is the key that unlocks the cellular doors to let glucose into the cells to use for energy. In Type II Diabetes, the body’s cells become resistant to insulin, and the cell doors do not open or use the needed glucose. Then the pancreas creates more insulin in an attempt to keep trying to unlock the cells. In the process this creates increased levels of insulin in the blood along with the large amounts of unused glucose. Hyperinsulinemia and hyperglycemia are very damaging to the body and can cause many other problems including abnormal lipid synthesis. This leads to hypercholesterolemia that only adds more injury to the body. Two major complications of Diabetes Mellitus are microvascular disease and macrovascular disease. They can cause all of the following to occur: peripheral vascular disease, hypertension, cardiovascular diseases including coronary artery disease and myocardial infarction (MI), stroke, and atherosclersois. Diabetic neuropathies also occur such as paresthesias of the extremities, gastroparesis, retinopathy, neurogenic bladder, diabetic diarrhea or constipation, neurological changes, and nephropathy in the kidneys which is the number one cause of end-stage renal failure in the US. Other classic symptoms of diabetes include re-occurring infections, especially vaginal infections, wounds that are slow to heal, and fatigue (McCance & Hunter 2006).

The patient is experiencing:

· Three types of invading bacterial organisms causing infection in her body.

· Neuropathies include:

· End Stage Renal Failure related to (RT) nephropathy

· Visual difficulty RT retinopathy

· GERD, nausea, vomiting, and anorexia RT gastroparesis

· Current and reoccurring UTIs, urinary retention and patient is unaware of urine elimination needs RT neurogenic bladder

· Paresthesias in her extremities and bilateral AKAs as a result.

· Diabetic diarrhea

· Hypertension

· Hypercholesterolemia

· Ischemic cardiomyopathy, mitral regurgitation, sinus ventricular tachycardia RT macrovascular disease

· Hyperglycemia as evidenced by (AEB) serum glucose checks of 395, 386, 257, 153, and 266.

End-Stage Renal Disease

The progression of chronic renal failure leads to end-stage renal failure when less than 10% of the kidneys are capable of functioning. More specifically, it is an irreversible loss of function in the kidney nephrons, where the glomerular filtration rate (GFR) is characterized as being almost absent. Diabetes Mellitus contributes to renal failure by causing nephropathy, increased capillary pressure due to microvascular disease, and glomerulosclerosis. This leads to severe impairment in the kidney’s absorption and excretion capabilities, which then disrupts fluid, electrolyte, and acid-base balances, and affects non-renal organ systems. The effects of end-stage renal failure include: metabolic acidosis due to decreased ammonia synthesis and bicarbonate reabsorption, hyponatremia, hypocalcemia, hyperphospatemia, hyperkalemia, bone demineralization, hypertension, cardiac dysrrhythmias, congestive heart failure (CHF), peripheral neuropathy, GI bleeding, pancreatitis, anemia, signs of uremia (such as anorexia, nausea, vomiting, abnormal skin pigmentation, pruritus, diarrhea, weight loss, edema, and neurologic changes), increased risk of infection, defective platelet aggregation, proteinuria, increased BUN and creatinine levels, etc. (McCance & Hunter 2006).

The patient is experiencing:

· Hyponatremia

· Hypocalcemia

· Anemia AEB decreased red blood cells (RBC), hemoglobin (Hgb) and hematocrit (Hct) and a high red blood cell distribution width (RDW) count.

· Hypertension

· Cardiac dysrrhythmias AEB sinus ventricular tachycardia

· Peripheral neuropathy

· Increased risk of infection AEB patient currently has three types of invading bacterial organisms causing infection in her body.

· Defective platelet aggregation AEB high prothrombin time (PT), international normalized ratio (INR) and partial thromboplastin time (PTT) levels

· Proteinuria

· Uremia RT the accumulation of toxins in the plasma AEB

· Anorexia

· Nausea and vomiting

· Abnormal skin pigmentation particularly on hands, arms and neck.

· Pruritus

· Diarrhea

· Edema in her hands and arms.

· Foul breath

Peritonitis

Inflammation of the peritoneal cavity lining of the abdomen. The inflamed area is usually caused by a fluid leak from the abdominal organs onto the peritoneum, resulting in infection, ischemia or trauma to the peritoneal site. However in this case the peritonitis was a direct complication of the peritoneal dialysis, where there was an open site for bacterial invasion. Staphylococcus aureaus is one of the most common causes of peritonitis. When Staphylcoccus aureaus invades the PD site the dialysate drainage becomes cloudy as a result of infection. The patient will experience rebound tenderness and diffuse pain in the abdomen. Abscess formation may occur. Large amounts of protein are lost with peritonitis. Other symptoms include diminished peristalsis, nausea and vomiting, fever, increased pulse rate, elevated white blood cell (WBC) count, decreased hemoglobin (Hgb) and hematocrit (Hct) levels, and alterations in electrolytes such as potassium, sodium and chloride. Potential complications include widespread infection, sepsis, hypovolemia, and bowel adhesions (Smeltzer, Bare, Hinkle, & Cheever 2007).

The patient is experiencing:

· Diffuse abdominal pain and tenderness

· Cloudy dialysate

· Diminished peristalsis, nausea and vomiting

· Elevated WBC count RT bacterial infection AEB Staphylococcus aureaus and step like cocci present in the PD site.

· Anemia AEB decreased Hgb and Hct levels

· Alterations in electrolytes:

· Hyponatremia

· Hypochloremia

· Hypokalemia

· CT scan shows presence of abdominal abscesses

Treatments and Medications:

Reason for Treatment, Patient’s Related Side Effects and Responses to Treatment

Aspirin Tab 81mg

1 Tablet 81mg

PO

QD

Antiplatelet use to decrease coagulation of the blood in order to treat history of ischemic cardiomyopathy and HTN.

Patient related side effects include nausea, vomiting, abdominal pain, anemia, and increased PT levels (Deglin & Vallerand 2007). The patient showed no signs of platelet coagulation.

sevelamer (Renagel) Tab 400mg

2 Tablets 800mg

PO

Q 8 hours

An electrolyte modifier that binds with phosphate in the GI tract. It reduces high phosphate levels in people with ESRD.

Patient related side effects include diarrhea, dyspepsia, nausea, and vomiting (Deglin & Vallerand 2007). The patient showed high levels of phosphate on one day only, and on the other days the lab values were controlled showing an apparent effectiveness of the drug.

Enalaprilat Inj 2.5mg

5mg / 4ml

IV

Q 6 hours

An angiotensin converting enzyme (ACE) inhibitor that blocks the conversion on angiotensin I to angiotensin II to lower the blood pressure by decreasing the afterload on the heart. Used to treat her history of sinus tachycardia with preventricular contractions (PVC), ischemic cardiomyopathy and HTN.

Patient related side effects include headache, tachycardia, anorexia, proteinuria, and renal failure (Deglin & Vallerand 2007). The patient continues to be sinus tachycardic with no PVCs and have hypertensive blood pressures.

esomeprazole (Nexium) INJ 40mg

40mg / 1ml

IV dilute with 5 ml of 0.9% normal saline, push over 3 minutes

QD

An antiulcer medication used to decrease the GI acid in the stomach and digestive tract in order to prevent ulcers and treat GERD.

Patient related side effects include headache, abdominal pain, diarrhea, dry mouth, nausea and vomiting (Deglin & Vallerand 2007). The patient continued to have nausea and vomiting.

insulin human regular (Novolin R) 100units

Give units on a sliding scale based on serum glucose level.

Subcutaneous injection

Q 6 hours

It’s an antidiabetic hormone used to control the serum blood glucose level in the body by increasing the cell’s uptake of glucose to use for energy.

Patient related side effects include pruritus (Deglin & Vallerand 2007). The patient’s glucose levels were still extremely high indicating a continued hyperglycemic state.

Insulin NPH Novol 100units Inj

20 units / 0.2ml

Subcutaneous injection

BIDWM

It’s an antidiabetic hormone used to control the serum blood glucose level in the body by increasing the cell’s uptake of glucose to use for energy.

Patient related side effects include pruritus (Deglin & Vallerand 2007). The patient’s glucose levels were still extremely high indicating a continued hyperglycemic state.

metoprolol (Lopressor) Inj 5mg

10mg / 10ml

IV

Q 6 hours

It’s a beta blocker used to decrease blood pressure and heart rate in order to treat the patient’s sinus tachycardia with PVC’s, history of ischemic cardiomyopathy and HTN.

Patient related side effects include fatigue, weakness, dizziness, GI pain, nausea, vomiting and hyperglycemia (Deglin & Vallerand 2007). The patient continues to be sinus tachycardic with no PVCs and have hypertensive blood pressures.

promethazine (Phenergan) Inj 25mg

12.5mg / 0.5ml

IV dilute with 10ml of 0.9% normal saline and push over 5 minutes

Q 4 hours and PRN

An antiemetic medication used to diminish nausea and vomiting RT the peritonitis, gastroparesis, and use of other medications listed including the use of Dilaudid.

Patient related side effects include sedation, dizziness, HTN, and tachycardia (Deglin & Vallerand 2007). The patient did experience relief from nausea and vomiting after administration of the drug.

hydromorphone (Dilaudid) Inj 1mg

0.5mg / 0.5ml

IV

Q 2 hours

An opioid analgesic used to decrease the patient’s sensation to the pain experienced in the abdomen RT the peritonitis.

Patient related side effects include sedation, dizziness, nausea, vomiting, urinary retention, physical dependence / tolerance (Deglin & Vallerand 2007). The patient did request pain management every 2 hours and rated her pain as a 9 out of 10 on the pain scale. Thirty minutes to an hour later during her pain evaluation she rated her pain at a 6 out of 10. The patient stated a desired pain level at a 4 out of 10 for comfort and tolerance.

Continuous electrocardiogram (ECG)

Has been used to monitor the patient’s heart rate and rhythm. She continues to have a sinus tachycardic rhythm. The patient appears to tolerate the treatment.

Discontinued Peritoneal Dialysis: Wound care at the PD site and of the inserted drainage tube on the right lower side of the patient’s back.

The patient seemed to have tolerated the previous procedures with no current complications. She tolerates the dressing change at the previous PD site. The skin appears intact and free of infection. The drainage tube site also appears free of infection and inflammation. The drainage fluid is yellow in color and clear with some sedimentation present.

Hemodialysis reinitiated

Hemodialysis prevents death in patients with chronic renal failure. It filters the blood to remove toxins and nitrogenous wastes, and control electrolyte and fluid imbalances. Dialysis can also buffer the system by providing bicarbonate to reverse metabolic acidosis. It contains heparin to prevent blood clots.

Patient related side effects include atherosclerosis, cardiovascular disease, coronary artery disease, peripheral vascular insufficiency, anemia, fatigue, increased calcium metabolism that leads to bone demineralization, infection, neuropathy, pruritus, and sleep disturbances. The patient appeared very fatigued and irritable after the hemodialysis treatment (Smeltzer, Bare, Hinkle, & Cheever 2007).

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

CBC with Differential

WBC

Nl: 4.6-10.2

17.6 H

13.2 H

12.4 H

15.8 H

12.8 H

The white cell count is usually high when peritonitis is present. WBCs fight infection, and there is infection present in the body, three possible organisms have been noted staph, strep, and a gram-negative rod. Stress can also cause a rise in the WBC count and this patient has experienced physical and emotional stress and depression. The patient has been on an aspirin therapy daily that can increase the WBCs. She has also been experiencing nausea and vomiting inducing dehydration that can create an increase in WBCs (Pagana & Pagana 2006).

RBC

Nl: F 4.0-5.0

M 4.5-6.1

4.61

3.62 L

3.87 L

3.67 L

3.15 L

Patient is anemic. She may have experienced GI blood loss as a result of peritonitis. She is also continuing to receive dialysis. During hemodialysis RBCs have a high likelihood of being destroyed in the process. She is experiencing re-occurring nausea and vomiting. Her nutrition has been poor decreasing the body’s ability to make RBCs related to iron or vitamin b deficiency. Decreased production of erythropoietin by the kidneys secondary to ESRD will decrease RBC production. Patient had a mitral valve repair completed that could cause trauma to RBCs as they pass through the heart (Pagana & Pagana 2006).

Hgb

Nl: F 12-16

M 13.5-17.5

13.1

10.3 L

10.8 L

10.1 L

8.6 L

Hct

Nl: F 36-46

M 41-53

39.1

30.8 L

33.1 L

31.5 L

26.5 L

MCV

Nl: 80-97

84.8

85.2

85.7

85.7

83.9

MCHC

Nl: 27-31.2

33.4

33.3

32.6

32.1

32.3

RDW

Nl: 11-14.5

16.5 H

17.2 H

17.6 H

17.2 H

16.9 H

RDW is a measure of variations of size in RBCs. Increases in RDW indicate anemia that could be related to iron or vitamin B deficiency due to poor nutrition and nausea and vomiting. The anemia could also be a result of post hemorrhage due to bleeding in the GI from peritonitis (Pagana & Pagana 2006).

MPV

8.5

8.2

7.8

7.2

7.8

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

MCH

Nl: 31-37

28.4

28.4

27.9

27.5

27.1

Platelets

Nl: 142-424

347

273

454 H

485 H

298

Iron deficiency anemia and post hemorrhagic anemia cause stimulation of the bone marrow which platelets easily respond too, however the platelets were only elevated on 2 days although the anemia is present for all labs collected (Pagana & Pagana 2006). So these results would have to be related to something else like possibly an invasive treatment such as where the patient had a removal of the PD catheter, placement of a drainage tube to relieve fluid from the peritonitis, and placement of the hemodialysis catheter.

Neut ABS

Nl: 2.0-6.9

16.4 H

10.4 H

13.10 H

10.9 H

Neutrophils increase with infection in order to phagocitize bacterial microorganisms. Other possible causes RT this patient are physical or emotional stress, and metabolic disorders like diabetes mellitus II and ESRD (Pagana & Pagana 2006).

Lymph ABS

Nl: 0.6-3.4

1.1

1.0

1.30

1.0

Mono Abs

Nl: 0-0.9

0.20

0.70

0.70

0.70

Eos ABS

Nl: 0-0.7

0.0

0.30

0.20

0.20

Baso ABS

Nl: 0-0.2

0.0

0.0

0.10

0.0

Auto Neut

Nl: 40-85

74 H

83.7 H

83.2 H

85.2 H

Neutrophils increase with infection in order to phagocitize bacterial microorganisms. Other possible causes RT this patient are physical or emotional stress, and metabolic disorders like diabetes mellitus II and ESRD (Pagana & Pagana 2006).

Auto Lymph

Nl: 5-46

6.0 L

8.0 L

8.4 L

8.1 L

The increase in the neutrophils is causing a decrease in the lymphocytes due to percentage ratio of the leukocytes in the blood (Pagana & Pagana 2006).

Auto Mono

Nl: 0-12

1.0 L

6.0

6.8

5.2

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

Auto Eos

Nl: 0-7

0.0

2.0

1.1

1.3

Auto Baso

Nl: 0-2.5

0.0

0.3

0.5

0.2

COAGULATION

PT

Nl: 9-11.5

64.4 H

The patient was on aspirin and coumadin therapy along with vitamin K deficiency due to poor nutrition may have dramatically increased the PT/INR levels. A salicylate intoxication due to renal impairment could increase PT time and INR. The patient may have liver disease secondary to ESRD and diabetes mellitus II metabolic diseases. Coagulation factors are synthesized in the liver and if liver damage is present PT/INR would be increased due to decreased synthesis causing an anticoagulating affect. Also this patient received blood transfusions due to decreased RBCs, Hgb and Hct. Anticoagulants are present in the banked blood causing increased PT time and INR (Pagana & Pagana 2006).

INR

Nl: <2

Therapeutic: Cardiac: 2-3

Valves: 2.5-3.5

6.80 CF

PTT

Nl: 24.7-34.9

72.0 H

54.1 H

31.6

SMA 7

Sodium

Nl: 136-145

131 L

134 L

134 L

136

Sodium may be low because of the following: Poor nutrition causing poor sodium intake. Diarrhea and vomiting causing GI sodium to be lost. Administration of diuretics and renal disease inhibit sodium reabsorption by the kidneys. Hyperglycemia increases the osmotic effect pulling fluid in diluting sodium. Peripheral edema also causes sodium levels to become diluted (Pagana & Pagana 2006).

Potassium

Nl: 3.6-5.1

3.3 L

3.1 L

3.2 L

3.1 L

Potassium can become low by poor nutrition, GI loss through vomiting and diarrhea, use of potassium wasting diuretics, and administration of insulin causes loss of serum potassium to the cells along with glucose. ESRD causes life-threatening increases in potassium, and can be lowered by dialysis treatment (Pagana & Pagana 2006).

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

Chloride

Nl: 98-107

91 L

91 L

101

98

Chloride follows sodium ions to produce neutrality. Sodium was low. Chloride loss would most likely be from reoccurring vomiting and diarrhea, diuretic therapy, and hypokalemia (Pagana & Pagana 2006).

CO2

Nl: 22-32

23

27

23

31

Glucose

Nl: 70-110

395 H

386 H

257 H

153 H

266 H

Patient has severe, long-term type II diabetes mellitus that causes a hyperglycemic state. Other causes that could increase glucose levels for this patient include: emotional and physical stress, renal failure decreases metabolization of glucagon which increases glucagon and glucose levels, diuretic therapy, antidepressant therapy and aspirin therapy (Pagana & Pagana 2006).

BUN

Nl: 8-20

30 H

44 H

19

14

Impaired renal function causes increased BUN and creatinine levels. Creatinine is specifically associated with kidney function and increases indicate renal disease chronicity. Other possible causes of elevated BUN and creatinine levels include urinary tract obstruction possibly RT UTI, ureteral blockages, and neurogenic bladder, diabetic nephropathy, decreased renal perfusion due to dehydration RT vomiting, diarrhea, poor nutrition and poor fluid intake (Pagana & Pagana 2006).

Creatinine

Nl: 0.6-1.3

5.5 H

6.3 H

4.4 H

5.4 H

LIVER PROFILE

Albumin

Nl: 3.5-4.8

1.4 L

1.2 L

1.2 L

Possible causes include: malnutrition decreases intake of protein for albumin synthesis, liver dysfunction would decrease synthesis of albumin, renal dysfunction where albumin can be lost through the kidneys / proteinuria, and third space losses including peripheral edema and increased peritoneal fluid RT PD peritonitis (Pagana & Pagana 2006).

Prealbumin

Nl: 20-40

13.0 L

Possible causes include: malnutrition, liver damage, and inflammation. Prealbumin levels decrease in the presence of inflammation (Pagana & Pagana 2006).

Alk Phos

Nl: 32-91

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

AST

Nl: 15-41

91

84

89

ALT

Nl: 14-63

Bilirubins:

Total

NlL 0.3-1.2

0.5

Direct/ Conjugated

Nl: 0.1-0.5

0.1

Indirect/

Unconjugated

Nl; 0-1

0.4

LIPID PANEL

No lipid panel was completed.

OTHER LABS

Total Protein

Nl: 6.1-7.9

Calcium

Nl: 8.9-10.3

8.8 L

7.3 L

7.1 L

6.2 L

Serum calcium is bound to and follows albumin. Since albumin is low so is calcium. Causes could be malnutrition and vitamin D deficiency, blood transfusions, malabsorption (due to nausea, vomiting, and diarrhea), and renal failure that cause excess ions to be present in the body and bind to the calcium (Pagana & Pagana 2006).

Phosphorus

Nl: 2.4-4.7

7.3 H

3.7

4.2

In renal failure phosphate excretion is decreased and therefore increased in the blood. Phosphate has an inverse relationship with calcium which was low, however not all days show spikes when the calcium is low. A hyperphosphatemia may have been a result of cellular damage/lysis that moved intracellular phosphate into the bloodstream on or before that day. RT effects of renal dysfunction, peritonitis, invasive procedures, etc. Also administration of sevelamer is used to decrease hyperphosphatemia in people with renal disease (Pagana & Pagana 2006).

Lab/Diagnostic Test

8/11/20

8/13/20

8/18/20

8/22/20

8/26/20

Analysis

Magnesium

Nl: 1.8-2.5

1.7 L

1.9

Possible causes for low magnesium in this patient: administration of diuretics, antibiotics, and insulin, malnutrition, malabsorption (due to nausea, vomiting, and diarrhea), decreased levels occur in diabetics and in people with renal disease who can not reabsorb it in the kidneys (Pagana & Pagana 2006).

AGB’s

No AGB’s were complete.

URINALYSIS (UA)

PH

Nl: 4.5-8.0

8.0

8.0

Specific Gravity

Nl: 1.002-1.030

1.020

1.014

Nitrates

Nl: negative

Negative

Negative

Leuk. Esterace

Nl: negative

Moderate

500/UL

Positive results indicate a UTI. WBCs are present to fight infection (Pagana & Pagana 2006).

Blood

Nl: negative

Lg

70/UL

Blood in the urine indicates renal disease. This could also be caused by a UTI, or an aggressive anticoagulant therapy. This patient’s PT / INR are extremely elevated putting her at risk for bleeding (Pagana & Pagana 2006).

Protein

Nl: negative

>=300 AB

100mg/dL

Proteinuria due to lack of kidney function and an indicator of renal disease. Other possible causes could be diabetic glomerularsclerosis, bacterial pylonephritis, urethritis, and when protein is present with RBCs in the urine, a UTI could be the cause (Pagana & Pagana 2006).

GRAM STAIN

Date

Results

Analysis

Urine

8/11/20

Gram negative rods found.

Indicates a bacterial infection and UTI, possibly ecoli. Patient needs appropriate antibiotic therapy.

Stool

8/24/20

Negative for Clostridium difficile (C-diff)

No clostridium difficile found in the stool. No need for C-Diff precautions. Does not explain chronic diarrhea.

Abdominal wound

8/11/20

Positive for Staphlacoccus aureaus at opening for peritoneal dialysis site.

Indicates the wound has tested positive for the Staphylococcus aureaus bacteria and needs appropriate antibiotic therapy.

Peritoneal fluid

8/15/20

Rare for Streptococcus viridans.

Indicates peritonitis infection of fluid, but the result was rare and may be caused by contamination.

CULTURE/

SENSITIVITIES

CT

PELVIS W/CO:

Contrast-enhanced CT scan of the abdomen

8/21/07

Impression:

1. Minimal right pleural effusion and associated right basilar subsegmental atelectasis.

2. Moderate free fluid in the abdomen accompanied by a pneumoperitoneum, findings likely related to peritoneal dialysis.

3. The bilateral renal stents remain unchanged in position. Small upper pole renal calculi of both kidneys are redemonstrated.

4. Small ventral hernia, unchanged.

Impression Contrast-enhanced

1. Interval increase in size in the encapsulated or loculated fluid collection located in the pelvic cul-de-sac. This could conceivably represent an infected collection.

2. A small encapsulated fluid collection has developed in the lower pelvis anterior to the uterine fundus and is associated with inflammatory type changes in the adjacent fat planes. This also could represent an infected collection (abscess).

3. Free fluid is redemonstrated in the pelvis related to peritoneal dialysis.

There is a small amount of fluid present in the pleural space compressing the lung causing impaired gas exchange of the alveoli on the right lung. There is a moderate amount of fluid present in the abdomen indicating peritonitis. Renal stents and kidney stones are still present bilaterally, as well as a hernia located on the front of the abdomen as compared to previous findings.

Peritoneal fluid increased within the abdomen and indicates infection. Infected abscesses or puss pockets are located in the abdomen causing inflammation to the organs. This confirms peritonitis, infection and increased fluid in the peritoneal cavity related to dialysis.

CT

ASPIR ABD/R: CT-guided drainage of pelvic fluid collection

8/23/20

Impression:

1. Using CT guidance, 10 French pigtail drainage catheter was placed in the loculated pelvic fluid.

2. Cloudy white fluid was aspirated.

3. Total of 150 ml of fluid was removed.

A large amount of fluid was aspirated from the peritoneal cavity, with what appears to be containing infection. A specimen was sent to the lab for gram staining.

ULTRASOUND

of the Kidneys

8/24/20

R Kidney measures 9.8 x 4.5 x 5.7 cm.

L Kidney measures 8.3 x 3.3 x 4.4 cm.

Impression:

1. No hydronephrosis or mass lesion.

2. Chronic medical renal disease.

No fluid on the kidneys or any suspect cancer type mass or lesion. Positive results for chronic renal disease.

ENDOSCOPY

8/21/2020

Diffuse esophagitis in the distal esophagus consistent with recurrent nausea, vomiting and reflux. Large amount of bilious liquid in the body and fundus of stomach. Mild antral gastritis status post biopsy.

Patient’s nausea, vomiting and reflux are being caused by esophagitis, gastritis, and diabetic gastroparesis.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

FORMCHECKBOX Nsg Dx

FORMCHECKBOX PC

DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

CT

Pelvis w/CO: Contrast-enhanced CT scan of the abdomen 8/21/07.

See chart.

Atelectasis, Pneumonia RT right pleural effusion and associated right basilar subsegmental atelectasis.

The nurse will manage and minimize complications of atelectasis pneumonia during hospitalization.

AEB The patient will have clear breath sounds, maintain a patent airway, and will have no complaints of difficulty breathing.

The Nurse will:

1. Assess vital signs Q 4 hours, especially heart rate and respirations.

2. Initiate and maintain ECG monitor to observe rate, rhythm, and abnormal occurrences of the heart due to hypoxia.

3. Monitor for signs and symptoms of inflammation in the lungs such as:

· Increased respiratory rate

· Fever and chills

· Diminished or absent breath sounds

· Dyspnea

· Decreased oxygen saturation levels

· Signs of shock

4. Administer supplemental oxygen as needed. (As oxygen may prevent dyspnea and pulmonary edema) (Carpenito-Moyet 2006).

5. Assist patient to a high fowler’s position and turn her often to promote movement of secretions.

6. Teach her diaphragmatic breathing and encourage cough and deep breathing techniques. (These strategies will increase tidal volume and reduce complications of atelectasis and pneumonia) (Carpenito-Moyet 2006).

7. Monitor and record intakes and outputs (I & O) and daily weights in patient chart.

· The patient lungs sounded clear to auscultation in all lung fields except for diminished sounds in the lowest base of the lungs.

· Respirations were slightly high with no complaints of chest pain, fever or signs of shock. Respirations could be high to compensate for metabolic acidosis related to renal failure too.

· No oxygen was needed patient was 98% saturated on room air.

· ECG and physical assessment revealed sinus tachycardia without PVCs.

· Patient was assisted to a high fowler’s position and ambulated with turning.

· RN encouraged patient to cough and deep breath.

· Continue interventions to manage and minimize complications of atelectasis pneumonia

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

FORMCHECKBOX Nsg Dx

FORMCHECKBOX PC

DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

See Nursing Diagnosis

Bleeding RT drug induced effects secondary to anticoagulation therapy, and the additive effects of heparin aspirin and coumadin on the hematological clotting system.

AEB increased PT, INR, and PTT levels as well as blood present in urine.

The nurse will manage complications of bleeding during this shift.

AEB The patient will experience no signs of spontaneous bleeding. RBC’s, Hgb, and Hct levels will not decrease further from the previous blood draw, but maintain or increase. The PT, INR and PTT levels / anticoagulation therapy will be maintained within the therapeutic range.

The Nurse will:

8. Assess vital signs Q 4 hours, especially blood pressure and pulse.

9. Wash hands and use aseptic technique when touching the patient and infection sites.

10. Inspect PD site, peritonitis drainage tube, IV and HD catheter sites for signs of redness, swelling, drainage, bleeding and pain Q 2-4 hours.

11. Monitor lab results for new RBCs, Hgb, Hct, PT, INR, and PTT levels and report significant changes to the doctor.

12. Monitor for signs and symptoms of spontaneous or excessive bleeding. (Assessing the patient regularly helps to identify bleeding early) (Carpenito-Moyet 2006).

13. Apply pressure for 5-10 minutes to venipuncture sites and then apply a pressure dressing to minimize bleeding (This helps the blood to clot and reduce bleeding) (Carpenito-Moyet 2006).

14. Prevent vomiting by administering antiemetics and reducing nausea. (GI bleeding can be caused by profuse vomiting) (Carpenito-Moyet 2006).

15. Consult with nutritionist and doctor about ordering a soft diet.

· The patient did not have any visible bleeding occurring during this shift.

· The patient’s RBCs, Hgb, and Hct remained low, in fact, they decreased further indicating possible internal bleeding.

· Consult the doctor regarding possible GI bleed evaluation.

· A new PT, INR, and PTT need to be completed and evaluated to determine improvement in levels. Consult the doctor to manage the order.

· Patient’s pain, nausea and vomiting were controlled with analgesics and antiemetics in order to decrease likelihood of GI bleeding.

· Continue interventions with additional interventions listed.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

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DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

Decreased RBCs, Hgb, Hct, sodium, potassium, chloride, albumin, prealbumin, calcium, and magnesium levels, and increased RDW, BUN, and creatinine levels.

Dysrhythmias RT electrolyte imbalance, anemia, and altered tissue perfusion.

The nurse will manage and minimize dysrhythmic episodes during hospitalization.

AEB The patient will experience minimal to no signs of dysrhythmic episodes. Patient will have serum blood levels, electrolytes, BUN and creatinine levels WNL.

The Nurse will:

16. Assess vital signs Q 4 hours, especially heart rate, blood pressure and pulses.

17. Monitor lab results for new blood counts, electrolytes, BUN and creatinine lab values, and report significant changes to the doctor.

18. Initiate and maintain ECG monitor to observe rate, rhythm, and abnormal occurrences of the heart.

19. Monitor for signs and symptoms of dysrhythmia such as:

· Abnormal rate and rhythm

· Palpitations

· Chest pain

· Decreased oxygen saturation levels

20. Administer supplemental oxygen as needed. (As oxygen increases in the body, cardiac workload decreases) (Carpenito-Moyet 2006).

21. Administer metoprolo, enalaprilat, and aspirin medication as ordered by the doctor to decrease blood pressure and heart rate in order to treat the patient’s sinus tachycardia with PVC’s, history of ischemic cardiomyopathy and HTN.

22. Monitor and record intakes and outputs (I & O) and daily weights in patient chart.

· The patient did experience a tachycardic rhythm with occasional PVCs during her hospital stay.

· The patient’s RBCs, Hgb, and Hct remained low, in fact, they decreased further indicating possible hypoxia and decreased tissue perfusion that leads increased risk of heart dysrhythmias.

· There was an improvement to normal levels with several of the electrolytes and BUN levels.

· The potassium, calcium, and albumin levels decreased further, and the creatinine level was inconsistent. These levels have the greater impact on the heart and could result in more dysrhythmic episodes.

· No oxygen was needed.

· ECG and physical assessment revealed sinus tachycardia without PVCs.

· Continue interventions with additional interventions listed as the patient only experienced minimal signs of dysrhythmic episodes.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

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DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

See Nursing Diagnosis

Risk of deep vein thrombosis (DVT) RT increased platelet count, immobility, and peripheral venous insufficiency.

The nurse will manage and minimize complications of DVT during hospitalization.

AEB The patient will experience no signs of localized redness, inflammation, or pain in the extremities. Platelet levels will not increase further from the previous blood draw, but maintain or decrease. Anticoagulation therapy will be maintained within the therapeutic range.

The Nurse will:

23. Assess vital signs Q 4 hours, especially blood pressure and pulses.

24. Monitor lab results for new platelet, PT, INR, and PTT levels and report significant changes to the doctor.

25. Monitor for signs and symptoms of DVT such as localized redness, inflammation, or pain in the extremities.

26. Monitor I & Os, daily weights and serum osmolality to assess hydration and provide adequate hydration as needed. (Dehydration causes increased blood viscosity that could lead to thrombus formation) (Carpenito-Moyet 2006).

27. Elevate edematous extremities above the heart. (Above the heart positioning can reduce thrombus formation by promoting venous return to the heart, reducing blood stasis in the extremities) (Carpenito-Moyet 2006).

· The patient did not have any visible signs or symptoms of DVT.

· The patient’s platelets returned to normal range by end of laboratory collection.

· A new PT, INR, and PTT need to be completed and evaluated to determine if the levels are in the therapeutic range. Consult the doctor to manage the order.

· Continue interventions with additional interventions listed.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

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DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

See Nursing Diagnosis

Infection RT increased susceptibility of the host to bacterial invasion, secondary to diabetes mellitus type II, ESRD, PD catheter site for bacterial invasion, and urinary tract site for bacterial invasion due to urinary retention.

AEB increased WBC’s, neutrophils, serum glucose, BUN, creatinine, leukocyte esterase in the urine, blood in the urine, proteinurea, decreased lymphocytes, gram-negative rods in urine culture, Staphlyococcus aureaus at the PD site culture, and Streptococcus viridans in the peritoneal fluid culture.

The patient will experience normal wound healing and improved signs and symptoms of local and systemic infection during her hospitalization.

AEB having temperature within normal limits (WNL), WBCs WNL, urine analysis WNL, negative future cultures from infection sites listed, and the PD site will be free of drainage, inflammation, redness, bleeding and pain.

The Nurse will:

28. Assess vital signs Q 4 hours, especially temperature.

29. Wash hands and use aseptic technique when touching the patient and infection sites.

30. Inspect PD site, peritonitis drainage tube, IV and HD catheter sites for signs of redness, swelling, drainage, bleeding and pain Q 2-4 hours.

31. Monitor lab results for new WBC counts and report significant changes to the doctor.

32. Administer antibiotics as ordered to treat infection.

33. Collect specimens from sites of infection for future and culture and sensitivity tests according to doctor orders.

34. Monitor serum glucose AC / HS and administer oral antidiabetic medication and insulin as ordered.

· The patient’s WBC count did begin to improve however remained above normal range, which could indicate infection still present in the body.

· Vitals were assessed and a low-grade fever was present.

· Used aseptic technique at all times.

· None of the sites with documented infections appeared to worsen. No presence of redness, blood or inflammation was observed. Patient did continue to complain of pain in the abdomen, and the only drainage noted was contained in the drainage tube from the peritoneal site.

· No new sites of infection were observed.

· Urine specimen still needs to be collected and cultured.

· Glucose levels remained high throughout treatment with oral antidiabetics and insulin. Consult doctor to reevaluate hyperglycemic treatments.

· Patient finished one round of antibiotics prior to this analysis. No antibiotics were ordered during this time. Consult doctor to evaluate need for another round of antibiotics.

· Continue interventions with additional interventions listed, as symptoms for wound healing and infection do seem to be improving.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

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DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

See Nursing Diagnosis

Imbalanced Nutrition: Less than body requirements RT to decreased dietary intake, vomiting, and impaired digestion secondary to esophagitis, gastritis, and diabetic gastroparesis due to diabetes mellitus type II, ESRD, and peritonitis.

AEB signs and symptoms of anemia, decreased reserve to fight infection, decreased RBCs, Hgb, Hct, sodium, potassium, chloride, albumin, prealbumin, calcium, and magnesium levels, and increased RDW, BUN, and creatinine levels.

The patient will improved dietary intake of vitamins and nutrients in order to meet the metabolic needs of the body to heal during hospitalization.

AEB showing decreased nausea, vomiting and signs of fatigue, increased appetite, and having serum blood levels, electrolytes and other nutrients WNL.

The Nurse will:

35. Consult with nutritionist and doctor about ordering a diet with appropriate caloric intake to meet metabolic needs.

36. Administer analgesics and antiemetics as ordered to treat GI pain, nausea and vomiting.

37. Administer antibiotics as ordered to treat infection to improve physical state and appetite, and decrease nausea and vomiting.

38. Encourage eating several small meals throughout the day instead of 3 large ones.

39. Encourage resting prior to meals to prevent fatigue during eating.

40. Monitor lab results for new blood counts, electrolytes and other nutrient lab values, and report significant changes to the doctor.

41. Administer nutritional supplements according to doctor orders.

42. Monitor serum glucose levels AC / HS and administer antidiabetic medication and insulin as ordered by the doctor to control hyperglycemia and it’s effects.

43. Monitor and record intakes and outputs (I & O) and daily weights in patient chart.

· The nutritionist established appropriate caloric guidelines and the doctor ordered the diet needed to meet the patients needs for healing.

· Patient’s pain, nausea and vomiting were controlled with analgesics and antiemetics. That aided in her ability to ingest and absorb food and liquids.

· The patient’s physical state did improve some, however her appetite did not improve.

· The patient did eat more but not very well, even with several smaller meals throughout the day.

· The patient did rest throughout the day, but it did not prevent fatigue while eating.

· Lab values were monitored. RBCs, Hgb, and Hct continued to remain low and worsened over the course of treatment that would indicate that the anemia is more a result of RBC destruction or GI bleeding.

· Consult the doctor regarding possible GI bleed evaluation.

· Administered supplements, oral antidiabetic medication and insulin as ordered, and monitored glucose AC / HS. Serum glucose remained high throughout treatment. Consult doctor on reevaluation of hyperglycemic treatments.

· Monitored I & O’s and daily weight. Patient has little fluid intake or urine output, and she had several episodes of diarrhea which continued to result dehydration and electrolyte imbalance.

· Continue interventions as nutrition intake did improve, however include additional interventions listed, as the patient is not meeting the metabolic demands of the body for healing.

RELATED LAB DATA

AND TEST RESULTS

DIAGNOSTIC STATEMENT

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DESIRED OUTCOME

INTERVENTIONS with Rationale and Citation for each intervention

EVALUATION of Patient Problems, Interventions and Desired Outcomes

See Nursing Diagnosis

Urinary Retention RT impaired afferent pathways secondary to neurogenic bladder due to diabetes mellitus type II.

AEB history of chronic UTIs, gram negative bacteria, leukocyte esterase, RBCs, and protein currently present in her urine, and the patient stated no longer feeling the urge to urinate.

The patient will meet personal expectations for dryness during her hospitalization.

AEB learning how to use bladder emptying methods, post void retention measurements of less than 50 ml, and voluntary voiding,

The Nurse will:

44. Administer analgesics to treat GI pain.

45. Administer antibiotics as ordered to treat infection.

46. Monitor labs for new urinalysis results, and report significant changes to the doctor.

47. Monitor and record intakes and outputs (I & O) and daily weights in patient chart.

48. Clean the patient and change the patient’s sheets and gown immediately after incontinence is observed.

49. Complete post void measurements as ordered.

50. Encourage the patient to attempt voiding q 2 hours.

51. Collect a clean catch urine specimen for urinalysis to evaluate improvement from leukocyte esterase, hematuria, and proteinuria levels.

52. Complete patient education on methods for emptying the bladder

· Abdominal strain

· Valsalva maneuver

· Crede’s maneuver

(teach all methods to find out which

method is most effective for her to use)

(Carpenito-Moyet 2006).

· Patient’s pain, was controlled with analgesics.

· Urinalysis values were monitored. Consult doctor to order another urinalysis in order to evaluate improvement of UTI.

· Monitored I & O’s and daily weight. Patient has little fluid intake or urine output, and she had several episodes of diarrhea which continued to result dehydration and electrolyte imbalance.

· Immediate assistance was given to incontinence episodes.

· Consult doctor to obtain orders for post void measurements.

· Patient too fatigued to fully learn bladder emptying methods.

· Continue all interventions and include additional interventions listed.