Pulmonary Embolism (PE)

BASICS

Definition: Acute cardiovascular disorder caused by obstruction of pulmonary vascular bed, resulting in acute right ventricular (RV) failure.
Severity Classification:
Low-risk PE: No clinical markers of adverse prognosis.
Submassive PE: No systemic hypotension, but with myocardial necrosis (elevated troponin) or RV dysfunction (dilated RV, RV/LV ratio >1 on CT, echo changes, elevated BNP/NT-proBNP, or ECG changes).
Massive PE: Hemodynamic instability (sustained hypotension, pulselessness, bradycardia, shock, acute RV failure).

3rd leading cause of vascular death (after MI, stroke).
Incidence: 30–80/100,000; increases with age; ~250,000 US hospitalizations/year; higher risk in orthopedic/cancer patients and pregnancy.
Prevalence: 17% in hospitalized adults admitted for first episode of syncope (2012–2014).

Virchow’s triad: Venous stasis, endothelial damage, hypercoagulability → thrombus
Most common source: Proximal lower extremity DVT (~85%)
Genetic risk: Factor V Leiden, prothrombin G20210A, rare: protein C/S, antithrombin deficiency
PE pathophysiology: Increased PVR, impaired gas exchange, decreased compliance, acute RV failure (main cause of death)

Older age, obesity, immobilization, surgery/trauma, malignancy, pregnancy/puerperium, previous VTE, antiphospholipid syndrome, estrogen therapy (OCPs commonest in women)
Genetic: Factor V Leiden, prothrombin G20210A
COVID-19, sepsis, recent hospitalization

Low risk: Early ambulation, compression devices
High risk (surgery, trauma, fracture, spinal cord injury, cancer): ≥10–35 days prophylaxis with LMWH, fondaparinux, DOACs, or UFH
Travel >8 hours: Hydration, walking, avoid constrictive clothes, calf exercises, compression stockings
Genetic thrombophilia without prior VTE: Prophylaxis not usually indicated

Tachycardia, tachypnea, dyspnea, hypoxemia, accentuated P2, pleuritic pain, DVT signs (leg swelling, tenderness), JVD, S3/S4, hepatomegaly

Pneumonia, pneumothorax, MI, pericarditis, CHF, aortic dissection, musculoskeletal chest pain

D-dimer: Sensitive, negative rules out PE in low risk; positive not diagnostic
Labs: CBC, creatinine, PT/aPTT, ABG (resp alkalosis/hypoxemia), consider hypercoagulability workup only in select patients
CXR: Westermark sign, Hampton’s hump, Fleischner sign, pleural effusion
ECG: S1Q3T3, RV strain
CT Pulmonary Angiography: Test of choice; sensitivity 96–100%, specificity 86–89%
V/Q scan: For patients with contraindications to contrast; high NPV/PPV for PE
Echo: For RV dysfunction, thrombus in transit
CUS (venous US): Confirms DVT source
Pulmonary Angiography: Gold standard but invasive; reserved for complex cases

Low risk + negative D-dimer: Rule out PE
Moderate/high risk or positive D-dimer: Proceed to CTPA or V/Q scan
Start anticoagulation if suspicion is high and bleeding risk low, even before confirmatory testing

First Line:
Rivaroxaban: 15 mg BID × 3 wks, then 20 mg QD
Apixaban: 10 mg BID × 7 days, then 5 mg BID
Warfarin: Start with bridging UFH/LMWH/fondaparinux; INR 2–3
LMWH/Fondaparinux: Enoxaparin 1 mg/kg BID or 1.5 mg/kg QD; dalteparin, fondaparinux per weight
Pregnancy: LMWH (dalteparin, enoxaparin, fondaparinux)
Cancer: LMWH or DOAC preferred

Anticoagulation + definite INR consult
Systemic thrombolysis (alteplase 100 mg IV over 1–2 hr) if shock/hypoperfusion/cardiac arrest & low bleeding risk
Contraindications: Intracranial hemorrhage, recent stroke/trauma, bleeding diathesis, recent neurosurgery

IVC filter: Only if absolute contraindication to anticoagulation or recurrent PE despite therapy
Catheter/embolectomy: For massive/submassive PE or contraindication to thrombolysis

Duration: Provoked PE: 3 months; unprovoked: at least 3 months (consider long-term if low bleeding risk); cancer-related: LMWH 3–6 months, then as long as cancer active
INR monitoring for warfarin
Compression stockings for DVT
Monitor aPTT/anti-Xa for UFH/LMWH as indicated

Mortality: Submassive 6–14%, Massive 15–60%
PESI score: Predicts 30-day mortality
Complications: Post-PE syndrome (chronic dyspnea, decreased exercise tolerance)

In low pretest probability, a negative D-dimer effectively rules out PE.
In moderate/high risk, obtain CT pulmonary angiography.
Start anticoagulation if clinical suspicion is high and risk of bleeding is low, even before diagnostic confirmation.