Power point presentation
Diagnosis & management of pulmonary embolism
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Introduction
Purpose of Presentation:
Educate & Enhance clinician skills in diagnosing and managing Pulmonary Embolism
Overview epidemiology and new, evidence-based practice guidelines
Goal: Improve patient outcomes in acute care
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PATHOPHYSIOLOGY OF PULMONARY EMBOLISM
CLOT FORMATION
Virchow's Triad, Risk Factors, Precipitating Conditions
Thrombus forms superficial or deep
Deep Vein Thrombus becomes dislodged and embolizes
Embolus travels to the lung vasculature
PE obstructs the lung vasculature causing symptoms
Patient experiences Pulmonary Infarction, Impaired Gas Exchange, or Cardiopulmonary Compromise
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PATHOPHYSIOLOGY OF PULMONARY EMBOLISM
Hypoxemia:
V/Q mismatch:
Ventilation remains preserved, but perfusion is decreased in areas obstructed by emboli and increased in non-obstructed areas.
This leads to high V/Q units (ventilated but underperfused) and low V/Q units (ventilated but overperfused), resulting in inefficient gas exchange.
Surfactant dysfunction and atelectasis:
Inflammatory injury from PE damages alveoli, impairing surfactant production and function causing atelectasis.
Hypocapnia:
Results from increased respiratory drive due to hypoxemia and inflammation.
Leads to excessive CO₂ exhalation, causing respiratory alkalosis.
Right posterior oblique perfusion (top) and ventilation (bottom) showing wedge-shaped defects in a patient with PE Image source: Nuclear Medicine & Radiology Group https://www.nucsradiology.com/topics/diagnosis-of-pulmonary-embolism/
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PATHOPHYSIOLOGY OF PULMONARY EMBOLISM
Pulmonary Infarction:
Thrombi obstruct segmental or subsegmental vessels, leading to pulmonary infarction.
Pulmonary Infarction produces classic triad of symptoms:
Pleuritic Chest Pain
Hemoptysis
Pleural effusion
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PATHOPHYSIOLOGY OF PULMONARY EMBOLISM
Cardiopulmonary Compromise:
PE causes severe hypotension through diminished stroke volume and cardiac output.
PE causes increased pulmonary vascular resistance (PVR) via obstruction of the vascular bed
Increased PVR impedes right ventricular (RV) outflow and causes RV dilation
Together, these changes reduce left ventricular (LV) preload and LV volume, resulting in reduced cardiac output and hypotension.
When severe, this results in obstructive shock
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CLINICAL PRESENTATION
PE has a wide variety of symptom presentation, and up to 1/3rd of patients will be asymptomatic.
The most common symptoms that cannot be overlooked include:
Dyspnea at rest or with exertion
Pleuritic Pain
Cough
Calf or Thigh Pain/Swelling
Wheezing
Hemoptysis
Additionally, on examination of patient, common presenting signs include:
Tachypnea
Tachycardia
Rales
Decreased breath sounds
Jugular Vein Distention
Transient or Persistent Arrhythmias
Pleural Effusion
Calf Swelling, Erythema, Edema, Tenderness
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Special Populations & their risks: COVID-19
Thrombosis and Clinical Impact:
VTE was common early in the pandemic, especially in ICU patients, with rates up to 43%, often despite prophylaxis.
Rates have declined, likely due to improved management and early diagnosis.
Autopsy studies revealed microvascular thrombosis, endothelial damage, and microangiopathy in the lungs.
Additional Risk factors for VTE included age, male sex, obesity, CAD, and elevated D-dimer.
Hypercoagulability in Hospitalized COVID-19 Patients:
(1) Endothelial injury—SARS-CoV-2 directly invades endothelial cells, causing complement activation, inflammation & endotheliitis
(2) Venous Stasis due to hospitalization.
(3) Hypercoagulability—These patients have elevated D-dimer, fibrinogen, & platelet activation, reflecting both inflammation and disease severity.
Coagulation Abnormalities in COVID-19 Patients:
COVID-19-associated coagulopathy (CAC) has the presentation of elevated fibrinogen, Von Willebrand Factors (VWF), & Factor VIII and minimal consumption of clotting factors.
Thromboelastography (TEG) findings showed enhanced clot formation and suppressed fibrinolysis, especially in severe cases.
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Significance of Pulmonary Embolism
Acute Pulmonary Embolism (PE) is a form of Venous Thromboembolism (VTE) that obstructs the pulmonary artery or its branches, which leads to hemodynamic instability, respiratory collapse, and death if left untreated.
Other forms of emboli that can obstruct the pulmonary arteries include tumor, fat, and air, but the focus of this presentation will be on PE due to thrombus.
PE can be classified by:
Risk of Death from PE: Low, Intermediate, High
Temporal Pattern of Presentation: Acute, Subacute, Chronic
Anatomic Location: Saddle, Main, Lobar, Segmental, Subsegmental
Presence or Absence of Symptoms: Symptomatic or Asymptomatic
In the past, PE was previously classified as Stable or Unstable PE, however, it is now recommended to classify PE by Risk of Death.
Distinction of PE by Risk of Death guides how aggressive treatment is.
High-Risk patients require very aggressive treatment, as these patients have the highest risk of death from obstructive shock within the first two hours of symptom presentation.
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INCIDENCE & MORTALITY of Pulmonary Embolism
Population-Based Estimates:
Canada: 0.38 per 1000 person-years (2002–2012).
USA (2023): ~393,000 cases annually.
Europe: ~296,000 cases/year across 6 countries (population 310.4M
Life-time Risk:
8.1% by age 45
11.5% in Black individuals
10.9% in Obese individuals
Demographic Information
Incidence rises with age.
Males > Females
Annual Deaths:
U.S.: ~110,000 deaths/year
Europe: ~300,000 deaths/year
U.S. Mortality Data: (2002-2019)
Total deaths: 109,992
Higher mortality in:
Males
Black individuals
Rural areas vs. Urban
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Risk Factors PREVALENCE & VIRCHOW's TRIAD
Virchow's Triad:
Any one or combination of the three risk factors can precipitate a VTE
Venous Stasis
Hypecoagulability
Endothelial Damage
Heritability
Patients can have genetic predispositions for hypercoagulability which increases their risk for VTE.
Factor V Leiden Deficiency
Antithrombin Deficiency
Protein S or Protein C Deficiency
Provoked or Acquired Risks
Formation of VTE can be attributed to other acquired risk factors
Surgery, Major Trauma
Malignancy
Age > 65 years
Immobilization
Pregnancy
Cardiovascular Disease States
R. Sided HF at greatest risk
Chronic Inflammatory States
E.g., Chronic Liver Disease, Chronic IBD
Hormonal/Contraceptive Therapies
Kidney Disease (Chronic, End-stage)
Prior VTE
Anatomical Changes
Indewelling CVCs
E.g., Varicosities, Paget-Schroetter, IVC Agenesis
Hyperviscosity Syndromes
E.g., Sickle Cell, Myeloproliferative Disorder
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Special Populations & their risks: PREGNANCY
VTE is 4–50 times higher in incidence compared to nonpregnant women.
Though uncommon, it is a significant cause of maternal mortality, contributing to 10.5% of pregnancy-related deaths in the U.S.
VTE is more common postpartum than antepartum, with the highest risk during the first 6 weeks after delivery
During pregnancy, DVT is about 3x more common than PE.
Between 2000–2018 it was found that there 1.7 PE cases per 10,000 deliveries.
Pregnancy causes hormonal dilation of veins and mechanical compression by the uterus.
These changes reduce venous flow velocity, markedly on the left side, leading to pooling and increased clot risk
All three components of Virchow’s triad are present in pregnancy:
Venous stasis due to hormonal changes and uterine compression of major veins.
Endothelial injury from delivery trauma (especially with cesarean or forceps use).
Hypercoagulability from increased clotting factors and decreased anticoagulant proteins
Pregnancy increases multiple clotting factors and decreases natural anticoagulants.
Resistance to Protein C increases in late pregnancy.
Fibrinolytic inhibitors also increase contributing to a pro-thrombotic state
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Special Populations & their risks: CANCER
In a retrospective study of 497,180 Taiwanese patients with cancer, the VTE risk was 10-fold higher than the general population
Death from VTE + cancer vs VTE without cancer is significantly higher
In a review of 8 million patients admitted to the hospital for VTE, those with concurrent malignancy had a 94% probability of death within six months.
Those without cancer had a 29% probability of death within the same time period
In a Danish cohort study of 57,591 individuals, the incidence of VTE was highest within the first year after cancer diagnosis.
A study of 235,149 cancer cases from a United States cancer registry reported the following:
A diagnosis of VTE in 1.6 %
12 % of VTE events occur at the time of diagnosis.
Across all cancer types, diagnosis of VTE was a significant predictor for decreased survival during the first follow-up year
Patients with cancer are hypercoagulable.
Tumor-specific procoagulant factors and patient-specific co-morbidities contribute to VTE risk.
VTE risk is higher in solid cancer tumors such as pancreatic cancer and brain cancer
Types of interventions increase VTE Risk, such as chemotherapy, major surgeries, and presence of CVC
VTE most commonly presents as DVT and/or PE.
Up to 10% of cancer patients develop VTE
Arterial thrombosis can account for a large number of deaths in cancer patients receiving chemotherapy.
A review of 4,466 ambulatory patients with cancer reported that the majority of the deaths related to thromboembolic disease were due to arterial thrombosis (eg, myocardial infarction, stroke) versus VTE while receiving chemotherapy.
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SPECIAL POPULATIONS: Pregnancy
Treatment of DVT/PE in pregnancy mirrors that in non-pregnant individuals.
Pregnant patients are treated with anticoagulation however assessing bleeding risk for these patients is necessary due to obstetric factors (e.g., abruption or hemorrhage)
Anticoagulation of choice is LMWH due to safety and efficacy
DOACs and Warfarin is avoided due to fetal risks
Length of therapy is at least 3 months total and at least 6 weeks post-partum
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SPECIAL POPULATIONS: MALIGNANCY
Anticoagulation is the treatment for cancer-associated VTE; however, cancer patients face higher risks of both VTE recurrence and bleeding which makes the decision to anticoagulate an individualized approach
DOACs are preferred in stable cancer patients without renal dysfunction, bleeding contraindications, or malabsorption.
LMWH is equal in efficacy, but DOACs are preferred due to oral dosing
Eliquis is most favored for its monotherapy and potential lower GI bleeding risk.
LMWH is a first-line option in the setting of impaired oral intake, GI cancer, high bleeding risk, or when reversal may be needed.
LMWH matches DOACs in efficacy and safety.
Unfractionated heparin and Warfarin are reserved for patients with severe renal impairment, obesity, hemodynamic instability, extensive clot burden, or expected need for rapid reversal.
Treatment should last 3-6 months but can continue beyond 6 months if the patient has metastatic disease/active cancer and a high risk of recurrence
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ABNORMALITIES IN LABS, EKG, & Radiography
Laboratory tests are NOT diagnostic of PE but provide information if PE is present.
Labs will reveal:
Leukocytosis
Increased ESR
Elevated Serum Lactate Dehydrogenase
ABGs demonstrate hypoxemia, respiratory alkalosis, and hypocapnia
Elevated D-Dimer
BNP, pro-BNP, and Troponin can be elevated
ABGs usually reveal Hypoxemia and Hypocapnia
Chest XR will show nonspecific findings (atelectasis, effusion, etc)
EKGs will show sinus tachycardia and nonspecific ST-segment or T-wave changes
S1Q3 pattern, RBBB, and Q waves can indicate a poor prognosis in PE
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PE DIfferential
The major competing diagnoses in patients with s/s for PE include:
Heart Failure
Myocardial Ischemia/Infarction
Pneumothorax
Pneumonia
Pericarditis
MSK Pain
Acute on Chronic Exacerbations of Lung Disease
Unexplained tachycardia prompts consideration for PE
Acute Pleuritic chest pain is highly suspicious for PE
Unilateral leg swelling favors a PE workup, and should not be missed
Dyspnea that is abrupt or disproportionate to the patient's lung function favors PE workup
Especially if hemoptysis, hypoxemia, and pleaurisy is present
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WELLS SCORE
The Wells score is the preferred tool to assess clinical probability of PE in patients:
Based on the total score, the clinical probability for PE can be categorized as
Low (<2 points)
Intermediate (2–6 points)
High (>6 points)
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Modified geneva scORE
The Modified Geneva score is a tool used to estimate the likelihood of a pulmonary embolism (PE)
It is not as validated as the Wells score, but it is useful in categorizing patients into
Low risk (less than 4 points)
Intermediate risk (4–10 points)
High risk (more than 10 points)
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DETERMINING CLINICAL PROBABILITY OF PE
Determining the clinical probability of PE (low, intermediate, or high) can be determined by using:
Wells Score (preferred & most validated)
Modified Geneva Score
Clinical Assessment/Judgement
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PERC Rule
The PERC Rule is a rule-out criterion that determines if a patient has a low-probability of PE
The PERC Rule is only valid in patients with a very low likelihood of PE (estimated to be < 15%)
The PERC Rule is valid for NON-hospitalized patients
PERC Rule is not applied for hospitalized patients, rather directly performing a d-dimer is best practice
All 8 criteria must be met for PE to be unlikely
If at least 1 criterion is NOT met, then the patient has an increased probability of PE, and necessary testing for PE should go underway
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Application of the pesi
The PESI
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WHEN PE PROBABILITY IS low
PERC Rule (Pulmonary Embolism Rule-out Criteria) for Outpatient:
Used in non-hospitalized patients with low clinical suspicion.
If all 8 PERC criteria are met → PE is excluded; no D-dimer or imaging needed.
If any PERC criteria are not met → perform high-sensitivity D-dimer.
Not valid in inpatients or settings with PE prevalence >15%.
D-dimer Testing For Low-Probability Hospitalized Patients:
If D-dimer <500 ng/mL → PE excluded.
If D-dimer ≥500 ng/mL → proceed to CT pulmonary angiography (CTPA).
Age-Adjusted D-dimer Cutoff:
Used to reduce false positives in older adults.
Formula: Age × 10 ng/mL (for age >50).
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WHEN PE PROBABILITY IS INTERMEDIATE
D-dimer Testing:
If D-dimer <500 ng/mL → PE excluded.
If D-dimer ≥500 ng/mL → proceed to CTPA.
In these patients, it is worth assessing the cardiopulmonary reserve since patients that have limited cardiopulmonary reserve, experts suggest to go straight to CTPA testing
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WHEN PE PROBABILITY IS HIGH
Skip D-dimer, go directly to CTPA
Even with a negative D-dimer, PE risk remains >5% in the group of people that tested HIGH in the Wells or Geneva Score screenings
The first-choice diagnostic test for suspected PE is CTPA:
High sensitivity and specificity.
Detects clot burden and RV strain (prognostic value).
May identify alternate diagnoses (e.g., pneumonia, aortic dissection).
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When CTPA is contraindicated
Use V/Q scan as an alternative if CTPA is contraindicated due to renal function.
Allergies to contrast is not an absolute contraindication, and the patient should be pre-medicated before the scan
If PE risk is high and CTPA is delayed by more than 2 hours, initiate empiric anticoagulation and consider leg ultrasound.
Diagnostic accuracy for PE varies with clinical context:
High clinical suspicion + high-probability scan → 96% chance of PE
Low clinical suspicion + normal scan → <4% chance of PE
Intermediate scenarios often require more testing
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OTHER TESTING FOR PE
Magnetic Resonance Pulmonary Angiography (MRPA):
Used when CTPA and V/Q scans cannot be performed
Less sensitive than CTPA
Catheter-Based Pulmonary Angiography:
Historically the gold standard, now used rarely
Best Use is only when diagnosis and treatment (e.g., thrombolysis/embolectomy) are combined.
Echocardiography:
Not diagnostic for PE
Best performed via transesophageal echo for direct thrombus visualization.
The best use of this is to stratify the risk of mortality with patients that have confirmed PE since Right Ventricular Strain is associated with high mortality in already confirmed PE
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TREATMENT GUIDELINES
After PE has been confirmed, treatment is based on stratifying risk of mortality
In the way suspicion for PE is grouped into low, intermediate, and high, treatment is categorized by low, intermediate, and high risk of mortality
Low-Risk:
Anticoagulation
Intermediate-Risk:
Anticoagulation, Hospitalization, Potential Thrombolysis
High-Risk:
IVC Filter, Reperfusion Therapy, Procedures, Embolectomy
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LOW-RISK PE Treatment
Treatment of choice for low-risk patients is anticoagulation
Anticoagulation reduces the risk of embolization and PE-related death
Direct Oral Anticoagulants (DOACs) like apixaban or rivaroxaban are typically preferred in hemodynamically stable patients who have a low risk of bleeding due to their convenience and favorable safety profiles.
Low Molecular Weight Heparin (LMWH) or Unfractionated Heparin (UFH) is used when DOACs are contraindicated (e.g., pregnancy, severe renal impairment, or GI absorption issues) or when inpatient therapy is required for monitoring or rapid reversal.
To classify a patient as low-risk, clinical judgement, absence of RV dysfunction, hemodynamic stability, and the simplified Pulmonary Embolism Severity Index (sPESI) are factored in.
sPESI:
Age >80 years
History of cancer
Chronic Cardiopulmonary Disease
Pulse >= 110/min
Systolic BP < 100
Arterial Oxygen Saturation <90%
Low Risk = 0
High Risk >= 1
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INTERMEDIATE-RISK PE Treatment
Anticoagulation
First-line treatment, similar to low-risk PE patients
Helps prevent further embolization and reduces mortality
Close Monitoring
Monitor closely for signs of clinical deterioration
Tachycardia >120 bpm
Decreasing oxygen saturation
Early signs of hypotension
Thrombolysis or Thrombectomy
Considered in intermediate-high risk patients (both RV dysfunction and elevated BNP/troponin)
Intermediate-low risk patients (only one of these findings) are less likely to benefit
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HIGH-RISK PE Treatment
High-Risk patients are those who are hemodynamically unstable
1st-Line – Systemic Thrombolysis:
Indicated in most unstable patients unless contraindications exist
Rapidly restores perfusion and improves survival
Catheter-Based or Surgical Embolectomy:
Used when thrombolysis is contraindicated
Indicated if thrombus is trapped in:
Right atrium
Right ventricle
Patent foramen ovale
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SUPPORTIVE CARE
Supplemental Oxygen:
Administer oxygen to maintain SpO₂ ≥ 90%.
Mechanical Ventilation:
Reserved for severe hypoxemia or impending respiratory/cardiac arrest.
Patients with RV failure are at risk of hemodynamic collapse during induction.
Hemodynamic Support
Extracorporeal Support (ECMO)
Considered for patients with refractory RV shock who do not respond to fluids and vasopressors.
Used as a bridge to reperfusion therapies (e.g., thrombolysis or embolectomy)
IV Fluids:
Use small boluses (250–500 mL NS) for hypotension & to avoid RV overload / ischemia
Vasopressors: Norepinephrine is 1st-line for hypotension and maintaining perfusion with minimal tachycardia
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When ANTICOAGULATION IS CONTRAINDICATED
Indications for IVC Filter Placement
Used when patients have contraindications to anticoagulation (e.g., active bleeding, high bleeding risk).
IVC filters can be life-saving when anticoagulation is not feasible, especially in unstable PE.
Routine use in stable patients is not supported by evidence.
Lower fatality rate in unstable PE patients treated with thrombolytics (8% vs. 18%) and without thrombolytics (33% vs. 51%)
Once the contraindication resolves, anticoagulation should resume and the filter should be removed.
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Decision tree FOR LOW PROBABILITY OF PE
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Decision tree FOR INTERMEDIATE PROBABILITY OF PE
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Decision tree FOR HIGH PROBABILITY OF PE
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Distal lower leg dvt – to anticoagulate or not?
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Decision tree for distal lower leg dvt
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Decision tree for PROXIMAL lower leg dvt
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Patient education: MEDICATION
Understanding Medication
Anticoagulants do not break up existing clots, but they prevent new clots from forming and existing clots from growing
Medication Adherence
Take the medication exactly as prescribed and discuss missed doses with the doctor for instructions
Discuss OTC medications, herbs, supplements as well since these can interact with the medication.
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Patient education: ADHERENCE & prevention
Preventing Clots During Travel or Inactivity
Get up and move every hour on long trips
Shift positions and move your legs frequently
Wear loose-fitting clothing and compression stockings if advised
Avoid alcohol or medications that cause drowsiness
Avoid smoking before travel
Emphasize the following:
Poor medication compliance increases the risk of recurrent blood clots, stroke, and death
Remain diligent to follow up with the doctor so they can monitor the response to treatment, and adjust dose if needed
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Patient education: SIGNS OF AN EMERGENCY
Signs of an Embolized Clot to the Lungs
Sudden shortness of breath or panting
Sharp chest pain, especially when breathing in or straining
Coughing or coughing up blood
Rapid or irregular heartbeat
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