ABIM - Pulmonary Embolism and Deep Vein Thrombosis

Here are key facts for American Board of Internal Medicine (ABIM) Examination from the Pulmonary Embolism & Deep Vein Thrombosis tutorial, focusing on clinical management and treatment decision-making that are essential for board certification. See the tutorial notes for further details and relevant links.

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1. Definition & Relationship: Pulmonary embolism (PE) occurs when the pulmonary arteries are obstructed, most often due to emboli from deep veins of thighs/pelvis; together with deep vein thrombosis (DVT), they comprise venous thromboembolism (VTE). 2. Epidemiology: PE is a leading cause of cardiovascular-related death. 3. Pathophysiologic Sequence: Clot forms in deep vein → fragment breaks off → travels through venous system → right heart → pulmonary arteries → obstructs blood flow → impaired gas exchange and hemodynamics. 4. Nonthrombotic Emboli: Air, fat, amniotic fluid, bacterial (septic), foreign bodies, and tumors can also cause PE. 5. Key Complications: Pulmonary hypertension, right heart failure, and pulmonary infarction. 1. Virchow's Triad: Three components predisposing to thrombosis:

• Endothelial injury: Fracture, surgery, trauma, previous DVT; triggers clotting cascade
• Venous stasis: Immobility, elevated central venous pressure, heart failure, obesity
• Hypercoagulable states: Pregnancy and postpartum period, smoking, cancer, hormonal medications, coagulation disorders (Factor V Leiden)

2. Combined Risk Assessment: Patients with multiple predisposing factors have significantly higher risk (e.g., pregnant women on bed rest). 3. Risk Stratification for PE:

• Massive (High Risk): Hemodynamically unstable with hypotension
• Intermediate (Submassive): Stable but with evidence of right ventricular dysfunction
• Low Risk: Hemodynamically stable without evidence of right ventricular dysfunction

4. Anatomic Classification:

• Saddle emboli: Located at pulmonary trunk bifurcation
• Lobar, segmental, subsegmental: Located in respective arterial branches

5. DVT-PE Relationship: DVT is the leading cause of pulmonary embolism. 1. DVT Manifestations: Unilateral leg swelling, tenderness, venous dilation; can occur in upper body (less common); post-thrombotic syndrome if venous valves are damaged. 2. PE Symptoms & Signs:

• Dyspnea and tachypnea (rapid breathing)
• Chest pain
• Hypoxemia and ventilation-perfusion mismatch
• Respiratory alkalosis
• Tachycardia and potential right heart failure
• Altered mental state, especially important to recognize in elderly patients

3. Clinical Probability Assessment:

• Wells Score for PE: ≥4 indicates PE likely; <2 low probability, 2-6 moderate, >6 high probability
• Wells Score for DVT: Based on swelling, edema, likelihood of alternative diagnosis

4. Pulmonary Infarction: Most often due to small emboli causing tissue ischemia, typically in lower lobes; may present with the wedge-shaped "Hampton Hump" on imaging. 5. Diagnostic Challenges: PE diagnosis can be difficult due to nonspecific symptoms and signs, requiring high clinical suspicion. 1. Laboratory Studies:

• D-dimer: >500 ng/mL suggests possible PE/DVT requiring further testing; useful to rule out low-probability cases
• Arterial blood gases: May show hypoxemia and respiratory alkalosis

2. Imaging for PE:

• CT angiography: Most widely used; visualizes disruption of blood flow in pulmonary arteries
• Ventilation-perfusion scan: Non-invasive test indicating blood clot presence
• Chest X-ray: May show atelectasis, Hampton hump (pulmonary infarction), Westermark sign (oligemic areas), pleural effusion

3. Imaging for DVT:

• Venous ultrasonography with compression: Verifies thrombus presence
• Contrast venography: Alternative method

4. ECG Findings:

• Sinus tachycardia
• S1Q3T3 pattern (S wave in lead I, inverted Q and T waves in lead III)

5. Histopathology: Premortem thrombi display lines of Zahn (layers of fibrin, red blood cells, and platelet deposition). 1. Supportive Therapy:

• Oxygen administration when saturation <90%
• Saline for fluid management
• Vasopressors if hemodynamically unstable

2. Anticoagulation Therapy:

• Short-term: Heparin, enoxaparin, or fondaparinux
• Long-term: Warfarin
• Monitoring: For efficacy and complications, including heparin-induced thrombocytopenia

3. Advanced Interventions:

• Embolectomy for mechanical removal of clot
• Clot dissolution (thrombolytics) to restore pulmonary arterial flow

4. DVT Prophylaxis in High-Risk Patients:

• Mechanical: Sequential compression devices (SCDs) to prevent venous stasis
• Pharmacologic: Low-dose enoxaparin or heparin

5. Long-Term Management: Risk factor modification, monitoring for post-thrombotic syndrome, prevention of recurrence.

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1. Diagnostic Strategy: Integration of clinical probability assessment, D-dimer testing, and appropriate imaging selection. 2. Risk Assessment Integration: Using both Virchow's Triad elements and PE severity classification to guide management. 3. Recognition of Atypical Presentations: Altered mental status in elderly with PE; upper extremity DVT. 4. Appropriate Threshold for Testing: Balancing overtesting against missed diagnosis based on risk stratification. 5. Differential Diagnosis Refinement: Distinguishing PE from other causes of acute dyspnea and chest pain. 1. D-dimer Utilization: High sensitivity but low specificity; most useful to rule out VTE in low-probability patients. 2. Imaging Selection Logic:

• CT angiography as first-line imaging for suspected PE
• Venous ultrasonography with compression for suspected DVT

3. Specific Imaging Findings:

• Hampton Hump: Wedge-shaped opacity indicating pulmonary infarction, typically in lower lobes
• Westermark Sign: Focal oligemia appearing as area of poor perfusion

4. ECG Pattern Recognition: S1Q3T3 pattern, though not sensitive or specific, can support diagnosis. 5. Clinical Probability Refinement: Using Wells scores appropriately to guide diagnostic workup and interpret test results. 1. Anticoagulation Initiation: When to start therapy based on clinical suspicion before confirmatory testing. 2. Management Based on PE Classification:

• Massive PE: Considering thrombolytics or embolectomy
• Submassive PE: Anticoagulation with consideration of advanced interventions if deterioration
• Low-risk PE: Anticoagulation alone, possible outpatient management

3. Intervention Selection: Determining appropriate anticoagulant based on patient characteristics and comorbidities. 4. Prophylaxis Decision-Making: Risk stratification to determine appropriate preventive measures. 5. Monitoring Requirements: Appropriate surveillance for treatment efficacy and complications. 1. Endothelial Injury Assessment: Evaluation of recent surgery, trauma, or prior DVT as risk factors. 2. Venous Stasis Identification:

• Immobility risk in hospitalized patients
• Heart failure contribution to reduced flow
• Obesity increasing intra-abdominal pressure

3. Hypercoagulability Evaluation:

• Pregnancy and postpartum risk periods
• Cancer-associated hypercoagulability
• Medication effects (hormonal contraceptives/therapies)
• Recognition of coagulation disorders

4. Compound Risk Assessment: Multiplicative risk with multiple Virchow's Triad elements. 5. Preventive Strategy Matching: Tailoring prophylactic measures to specific risk factors. 1. Pulmonary Infarction: Recognition of small emboli causing tissue ischemia; Hampton Hump on X-ray. 2. Right Heart Failure: Assessment and management of increased right ventricular afterload. 3. Heparin-Induced Thrombocytopenia: Monitoring platelet counts; recognition and management of this paradoxical complication. 4. Post-thrombotic Syndrome: Long-term complication of DVT due to venous valve damage. 5. Recurrent VTE: Assessment for underlying hypercoagulable conditions or inadequate anticoagulation.

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Below is information not explicitly contained within the tutorial but important for the American Board of Internal Medicine Examination. 1. Anticoagulation Selection: Direct oral anticoagulants (DOACs) vs. warfarin vs. low molecular weight heparin based on patient factors. 2. Extended Anticoagulation: Decision-making for duration based on risk factors for recurrence. 3. Thrombolytic Therapy: Specific indications, contraindications, and administration protocols. 4. Inferior Vena Cava Filters: Indications, placement timing, retrieval considerations. 5. Management of Anticoagulation Complications: Approaches to bleeding events and reversal strategies. 1. Cancer-Associated Thrombosis: Preferred anticoagulants and duration of therapy. 2. Pregnancy-Related VTE: Anticoagulation selection and monitoring during pregnancy and postpartum. 3. Elderly Patients: Balancing bleeding and thrombotic risks, dose adjustments. 4. Renal Impairment: Anticoagulant selection and dose modifications. 5. Thrombophilia: Testing indications and management implications. 1. Risk Assessment Models: PADUA, Caprini, and IMPROVE scores for hospitalized patients. 2. Extended Prophylaxis: Indications for continuing prophylaxis post-discharge. 3. Mechanical vs. Pharmacologic Methods: Comparative effectiveness and combination approaches. 4. Special Surgical Populations: Orthopedic, bariatric, neurosurgical prophylaxis considerations. 5. Travel-Related Thrombosis: Evidence-based recommendations for long-distance travelers. 1. Post-PE Syndrome: Chronic dyspnea and functional limitations after PE. 2. Chronic Thromboembolic Pulmonary Hypertension (CTEPH): Diagnostic approach and treatment options. 3. Post-Thrombotic Syndrome Management: Compression therapy and other interventions. 4. Quality of Life Assessment: Functional capacity evaluation and rehabilitation approaches. 5. Long-Term Surveillance: Monitoring for development of chronic complications. 1. VTE Prophylaxis Protocols: Hospital-based implementation strategies. 2. Care Transitions: Anticoagulation management across healthcare settings. 3. Quality Metrics: Hospital-acquired VTE rates as healthcare quality indicator. 4. Cost-Effective Diagnostic Strategies: Appropriate use criteria for imaging. 5. Interdisciplinary Management: Collaboration with interventional radiology, vascular medicine, and hematology.