Pulmonary Thromboembolism (PTE / PE)

Definition and Epidemiology

• Robbins & Kumar Basic Pathology, p. 93
• Grainger & Allison's Diagnostic Radiology, p. 381

Pathogenesis and Sources

1. Stasis (immobility, surgery, malignancy)
2. Hypercoagulability (thrombophilia, pregnancy, OCP)
3. Endothelial injury (trauma, catheters)

Anatomical distribution

Pathophysiology

• At least 30-50% of the pulmonary vascular bed must be obstructed to significantly raise pulmonary artery pressure (PAP).
• Humoral factors (serotonin, thromboxane A2) and reflex vasoconstriction also contribute.
• Abrupt rise in pulmonary vascular resistance → right ventricular (RV) dilatation → RV pressure overload → RV failure (primary cause of death in severe PE).
• Paradoxical embolism can occur when venous emboli cross an atrial or ventricular septal defect and enter systemic circulation.

• 60-80% of emboli: small, clinically silent; organize and incorporate into vascular wall (may leave fibrous webs).
• Large embolus occluding major pulmonary artery: sudden death.
• Medium-sized: ischemia without infarction (preserved bronchial artery flow); but if left-heart failure co-exists, infarction may occur.
• Recurrent emboli: progressive pulmonary hypertension → cor pulmonale.

Risk Factors

Clinical Presentation

• Pleuritic chest pain, tachypnea, dyspnea (most common)
• Cough, tachycardia (HR >100), fever
• Signs of DVT (leg swelling, tenderness)
• Syncope (suggests massive PE with hemodynamic compromise)
• Shock, hypotension, or cardiac arrest (severe/massive PE)

Classification by Severity

• Miller's Anesthesia, p. 5028

Diagnosis

Step 1: Pre-test Probability (Wells Score)

• Grainger & Allison's Diagnostic Radiology, p. 381

Step 2: D-Dimer Testing

• Very high negative predictive value (NPV) - a negative D-dimer with low/intermediate pre-test probability safely excludes PE in up to 51% of outpatients.
• Age-adjusted D-dimer cut-off above age 50: age × 10 μg/L (instead of standard 500 μg/L) - improves specificity while maintaining sensitivity.
• Positive D-dimer is non-specific (elevated with inflammation, surgery, trauma, malignancy, pregnancy).
• A negative D-dimer does NOT have 100% NPV and cannot absolutely exclude PE.

Step 3: Imaging

• Sensitivity: 83% (PIOPED II), Specificity: 96%
• Negative predictive value: 95-99%
• Requires adequate pulmonary arterial enhancement (≥300-350 HU)
• RV/LV ratio ≥1 on CTPA = independent predictor of adverse outcome
• Anticoagulation can be safely withheld with a negative CTPA (if concordant with clinical probability)

• Most useful in outpatients without known cardiopulmonary disease with a normal CXR
• Preferred in young patients (less radiation), pregnant patients
• Normal perfusion scan effectively excludes PE
• High-probability scan is 97% specific (PIOPED I)

• Proximal DVT on CUS is sufficient to initiate anticoagulation without further imaging

• Not diagnostic; useful to exclude MI, arrhythmia
• ECG: sinus tachycardia most common; S1Q3T3, RBBB, RV strain in massive PE
• ABG: hypoxemia, reduced PaCO2, widened A-a gradient

Treatment

Initial Management

• Airway and oxygen support
• Hemodynamic resuscitation (vasopressors if shocked)
• Anticoagulation is the cornerstone of therapy in all risk groups

Anticoagulation Options

• Low-molecular-weight heparin (LMWH) - preferred (e.g., enoxaparin 1 mg/kg SC q12h)
• Unfractionated heparin (UFH) - IV drip; preferred if renal failure, thrombolysis anticipated, or hemodynamically unstable
• Fondaparinux - subcutaneous, factor Xa inhibitor

• DOACs (rivaroxaban, apixaban, edoxaban, dabigatran) - now standard of care for most patients
• Warfarin with INR 2.0-3.0 (with bridging heparin)
• LMWH in pregnancy (does not cross placenta; warfarin is teratogenic)

Advanced Therapies (Massive and High-Risk Submassive PE)

Duration of Anticoagulation

Complications

Pulmonary Infarction

• Occurs when dual circulation is overwhelmed (usually with pre-existing cardiopulmonary disease)
• Hampton's hump on CXR (wedge-shaped pleural-based opacity)

Chronic Thromboembolic Pulmonary Hypertension (CTEPH)

• Occurs in up to 4% of patients with acute PE (typically within 2 years)
• Paradoxically, ~50% of CTEPH patients have no clinical history of acute PE
• Presents with progressive dyspnea, RV failure
• Diagnosis: V/Q scintigraphy (screening) → CTPA/conventional pulmonary angiography confirms

• Pulmonary thromboendarterectomy (PTE surgery) - treatment of choice for surgically accessible (proximal) disease
• Balloon pulmonary angioplasty (BPA) - for inoperable or distal disease
• Medical therapy (riociguat, macitentan) for inoperable/residual CTEPH
• Grainger & Allison's Diagnostic Radiology, p. 388

Key Summary Points

1. 95% of PEs originate from DVT in proximal leg veins - they share the same risk factors and pathophysiology (VTE spectrum).

2. 60-80% of emboli are clinically silent; massive PE causes sudden death.
3. Low/intermediate Wells score + negative D-dimer safely rules out PE.
4. CTPA is the gold-standard first imaging test; V/Q scan is preferred in pregnancy and young patients.
5. Anticoagulation is universal; choice of agent depends on severity, renal function, pregnancy, and bleeding risk.
6. Systemic thrombolysis is reserved for massive PE; CDT/mechanical thrombectomy for selected submassive cases.
7. CTEPH is a serious delayed complication requiring long-term follow-up after acute PE.