Deep Vein Thrombosis & Pulmonary Embolism
Surgery · Vascular · lean revision notes
Deep Vein Thrombosis & Pulmonary Embolism
Venous thromboembolism (VTE) is a single disease spectrum: a clot forms in the deep veins (DVT), then a fragment embolises to the pulmonary arteries (PE). It cuts across surgery, medicine, and obstetrics and is one of the most consistently tested vascular topics in NEET PG—expect questions on Virchow's triad, Wells score, D-dimer logic, the investigation of choice, and the drug of choice.
Definition & Classification
Deep vein thrombosis (DVT) is thrombus formation within the deep venous system, most commonly the deep veins of the lower limb (calf/popliteal/femoral/iliac). Pulmonary embolism (PE) is obstruction of the pulmonary arterial tree by embolised thrombus, fat, air, or amniotic fluid—in the VTE context it is almost always thrombotic.
Anatomical classification of DVT:
| Type | Site | Significance |
|---|---|---|
| Distal (calf) DVT | Below the knee (peroneal, posterior tibial veins) | Lower embolic risk; ~25% propagate proximally if untreated |
| Proximal DVT | Popliteal vein and above (femoral, iliac) | High embolic risk; the classic source of PE |
| Iliofemoral DVT | Common iliac/femoral | Greatest swelling, highest post-thrombotic morbidity |
| Phlegmasia | Massive iliofemoral occlusion | Limb-threatening (see complications) |
PE is classified clinically by haemodynamic impact:
| Category | Definition | Key feature |
|---|---|---|
| Massive (high-risk) | Sustained hypotension (SBP <90 mmHg ≥15 min) or shock | Mortality >15%; thrombolysis indicated |
| Submassive (intermediate-risk) | Normotensive but RV strain (echo/CT) and/or raised troponin/BNP | Watch closely; sometimes thrombolysis |
| Low-risk | Normotensive, no RV dysfunction, normal biomarkers | Anticoagulation alone, consider outpatient |
High-yield: Most clinically significant PEs arise from proximal lower-limb DVT (popliteal and above), not from calf veins alone.
Etiology & Pathophysiology — Virchow's Triad
The cornerstone fact. Thrombosis results from one or more of three elements described by Rudolf Virchow:
- Venous stasis — immobilisation, long-haul travel ("economy class syndrome"), prolonged surgery, paralysis, heart failure, varicose veins.
- Endothelial injury — surgery (especially orthopaedic hip/knee), trauma, central venous catheters, previous DVT.
- Hypercoagulability — malignancy, pregnancy & puerperium, oestrogen (OCP/HRT), nephrotic syndrome, inflammatory states, and inherited thrombophilias.
Mnemonic for Virchow's triad — "SHE": Stasis, Hypercoagulability, Endothelial injury.
Inherited thrombophilias (NEET favourites):
- Factor V Leiden — commonest inherited thrombophilia; causes activated protein C (APC) resistance.
- Prothrombin G20210A mutation.
- Protein C, Protein S, and Antithrombin III deficiency — antithrombin deficiency gives heparin resistance.
- Antiphospholipid antibody syndrome (APLA) — acquired; arterial + venous thrombosis, recurrent fetal loss, paradoxically prolonged aPTT in vitro.
High-yield: Warfarin-induced skin necrosis occurs in Protein C deficiency because protein C (a natural anticoagulant with short half-life) falls faster than the clotting factors, producing a transient procoagulant state. Always bridge warfarin with heparin/LMWH.
Pathophysiology of PE: Embolus lodges in pulmonary arteries → increased pulmonary vascular resistance → RV pressure overload (acute cor pulmonale) → RV dilatation, septal bowing, reduced LV filling → hypotension and shock. Gas exchange is impaired by V/Q mismatch and dead-space ventilation, producing hypoxaemia with hypocapnia (tachypnoea blows off CO₂ → respiratory alkalosis).
Clinical Features
DVT: Unilateral limb swelling, calf pain/tenderness, warmth, erythema, dilated superficial collateral veins, and a palpable cord.
- Homans' sign — calf pain on passive dorsiflexion of the foot (low sensitivity/specificity; classically asked but unreliable).
- Moses' sign — calf tenderness on squeezing against the tibia.
PE: Sudden-onset pleuritic chest pain, dyspnoea, tachypnoea (most common sign), tachycardia, haemoptysis, and in massive PE—syncope, hypotension, raised JVP, and a loud P2/right parasternal heave. Tachypnoea and tachycardia are the most consistent findings; "classic triad" of haemoptysis + pleuritic pain + dyspnoea is uncommon.
High-yield: Sinus tachycardia is the commonest ECG finding in PE. The famous S1Q3T3 (S wave in lead I, Q wave + inverted T in lead III) indicates RV strain but is seen in only a minority.
Diagnosis — Pre-test Probability First
The exam logic is always: clinical probability (Wells) → D-dimer or imaging → definitive imaging.
Wells Score for DVT
| Criterion | Points |
|---|---|
| Active cancer | +1 |
| Paralysis/recent immobilisation of leg | +1 |
| Bedridden >3 days or major surgery <12 weeks | +1 |
| Localised tenderness along deep veins | +1 |
| Entire leg swollen | +1 |
| Calf swelling >3 cm vs other leg | +1 |
| Pitting oedema (symptomatic leg) | +1 |
| Collateral superficial veins | +1 |
| Previous documented DVT | +1 |
| Alternative diagnosis as likely | −2 |
Interpretation: ≥2 = DVT likely; <2 = DVT unlikely.
Wells Score for PE
| Criterion | Points |
|---|---|
| Clinical signs of DVT | 3 |
| PE is the most likely diagnosis | 3 |
| Heart rate >100/min | 1.5 |
| Immobilisation/surgery in previous 4 weeks | 1.5 |
| Previous DVT/PE | 1.5 |
| Haemoptysis | 1 |
| Malignancy (treated within 6 months) | 1 |
Interpretation (dichotomised): >4 = PE likely; ≤4 = PE unlikely.
High-yield: D-dimer has high sensitivity but low specificity. A negative D-dimer in a low/unlikely pre-test probability patient safely excludes VTE—it is a rule-OUT, never a rule-IN test. It is raised in pregnancy, malignancy, sepsis, post-op, and the elderly (use age-adjusted cut-off: age × 10 µg/L for >50 years).
Investigation of choice
- DVT — Compression (Doppler) ultrasonography is the investigation of choice. Diagnostic hallmark = non-compressibility of the vein under probe pressure. Venography is the historical gold standard but is invasive and rarely used.
- PE — CT Pulmonary Angiography (CTPA) is the investigation of choice/gold standard. Shows intraluminal filling defects.
- V/Q scan is preferred when CTPA is contraindicated—renal failure (avoid contrast), contrast allergy, and pregnancy/young women (lower breast radiation, especially with perfusion-only scanning).
Stepwise approach to suspected PE:
Suspected PE → assess haemodynamics → if unstable → bedside echocardiography (RV strain) ± empirical treatment → if stable → Wells score → unlikely → D-dimer (negative ⇒ excluded; positive ⇒ CTPA) → likely → straight to CTPA.
High-yield: In a haemodynamically unstable patient too sick for CT, bedside echocardiography showing RV dilatation/dysfunction supports the diagnosis and justifies thrombolysis. McConnell's sign = RV free-wall akinesia with apical sparing.
Supportive (not diagnostic) tests: ABG (hypoxaemia + hypocapnia), ECG (sinus tachycardia, S1Q3T3), CXR (often normal; Hampton's hump = peripheral wedge opacity, Westermark sign = focal oligaemia), troponin and BNP for risk stratification.
Management — Drug of Choice & Beyond
Anticoagulation is the mainstay for confirmed VTE (and started empirically if clinical suspicion is high while awaiting imaging, provided bleeding risk is acceptable).
Initial anticoagulation
- Low-molecular-weight heparin (LMWH, e.g. enoxaparin) is the preferred initial parenteral agent—subcutaneous, weight-based, no routine monitoring (monitor anti-Xa only in renal failure, pregnancy, extremes of weight).
- Unfractionated heparin (UFH) — preferred when rapid reversibility is needed, in severe renal failure (CrCl <30), or in massive PE/peri-thrombolysis. Monitored by aPTT; reversed by protamine sulphate.
- Fondaparinux — synthetic factor Xa inhibitor; used in HIT.
Long-term anticoagulation
| Agent | Monitoring | Reversal | Notes |
|---|---|---|---|
| Warfarin (VKA) | INR target 2–3 | Vitamin K, FFP, PCC | Needs heparin bridging (avoids skin necrosis); teratogenic |
| DOACs (rivaroxaban, apixaban, dabigatran, edoxaban) | None routine | Dabigatran → idarucizumab; Xa inhibitors → andexanet alfa | First-line in most non-cancer VTE; oral, fixed-dose |
| LMWH | Anti-Xa if needed | Partial (protamine) | Preferred in pregnancy and cancer-associated VTE |
High-yield: LMWH is the anticoagulant of choice in pregnancy because warfarin is teratogenic (warfarin embryopathy: nasal hypoplasia, stippled epiphyses) and DOACs cross the placenta. In cancer-associated VTE, LMWH or an oral factor Xa inhibitor (apixaban/rivaroxaban/edoxaban) is preferred.
Duration: provoked VTE (transient risk factor like surgery) → 3 months; unprovoked or recurrent/ongoing risk (cancer, thrombophilia) → extended/indefinite based on bleeding risk.
Heparin-induced thrombocytopenia (HIT)
High-yield: HIT is an immune (anti–PF4–heparin antibody) reaction occurring typically days 5–10 after heparin, causing a >50% platelet drop and paradoxical thrombosis. Diagnosed with the 4Ts score. Management: STOP all heparin, start a non-heparin anticoagulant (argatroban, bivalirudin, fondaparinux). Do NOT give platelets; do NOT start warfarin until platelets recover.
Reperfusion / interventional options
- Systemic thrombolysis (alteplase/tPA, streptokinase) — indicated in massive (high-risk) PE with haemodynamic instability, and in selected submassive PE with deterioration. Major contraindication: active bleeding, recent haemorrhagic stroke, recent major surgery.
- Catheter-directed thrombolysis (CDT) — lower-dose thrombolytic delivered directly into the clot; used in extensive iliofemoral DVT and in PE where systemic lysis is risky. Reduces post-thrombotic syndrome.
- Surgical/catheter embolectomy — for massive PE when thrombolysis fails or is contraindicated.
- IVC (Inferior Vena Cava) filter — mechanically prevents emboli reaching the lungs. Indication = anticoagulation contraindicated/failed in a patient with proven VTE (e.g., active bleeding, or recurrent PE despite adequate anticoagulation). Retrievable filters preferred; a filter does NOT treat the clot, only prevents embolism.
High-yield: An IVC filter is indicated when anticoagulation is contraindicated or has failed—it is not a substitute for anticoagulation and does not prevent DVT formation.
Adjuncts: early mobilisation, graduated compression stockings (reduce post-thrombotic syndrome), and prophylaxis in high-risk patients (LMWH, mechanical pneumatic compression) per surgical risk scores (Caprini score).
Complications
- Pulmonary embolism — the dreaded acute complication of DVT.
- Post-thrombotic (post-phlebitic) syndrome — chronic venous insufficiency after DVT: pain, oedema, hyperpigmentation, venous ulceration. Reduced by compression stockings and early recanalisation.
- Chronic thromboembolic pulmonary hypertension (CTEPH) — long-term sequel of unresolved PE; treated with pulmonary endarterectomy.
- Phlegmasia — massive iliofemoral DVT:
- Phlegmasia alba dolens ("white leg") — swelling with arterial compromise before frank cyanosis.
- Phlegmasia cerulea dolens ("blue leg") — massive venous occlusion with cyanosis, threatening venous gangrene; a surgical/thrombolysis emergency.
- Recurrent VTE and anticoagulant-related bleeding.
High-yield: Phlegmasia cerulea dolens is a limb-threatening emergency requiring urgent thrombolysis/thrombectomy and limb elevation—risk of venous gangrene and amputation.
Key Differentials
For DVT (unilateral leg swelling):
- Ruptured Baker's cyst — sudden calf pain, "crescent sign" of bruising at ankle; ultrasound differentiates.
- Cellulitis — erythema, fever, raised inflammatory markers, often a portal of entry.
- Muscle tear/haematoma, lymphoedema (usually bilateral, non-pitting late), chronic venous insufficiency.
For PE (acute dyspnoea/chest pain):
- Acute coronary syndrome, pneumonia, pneumothorax, aortic dissection, pericarditis, musculoskeletal pain, and anxiety/hyperventilation.
| Feature | DVT | Cellulitis | Ruptured Baker's cyst |
|---|---|---|---|
| Onset | Sub-acute | Sub-acute, with fever | Sudden after activity |
| Skin | Mild erythema, warm | Marked erythema, hot, tender | Bruising near ankle |
| Fever/CRP | Usually normal | Raised | Normal |
| Diagnostic test | Compression USG (non-compressible vein) | Clinical | USG showing cyst |
Recently asked / exam angle
- Investigation of choice questions: "Compression USG for DVT" and "CTPA for PE" are repeatedly tested; V/Q scan when CTPA contraindicated (pregnancy/renal failure).
- Anticoagulant of choice in pregnancy = LMWH; warfarin teratogenicity features.
- IVC filter indication = anticoagulation contraindicated/failed.
- HIT scenario: platelet drop on day 5–10 of heparin → stop heparin, start argatroban/fondaparinux; do not give platelets.
- Warfarin skin necrosis ↔ Protein C deficiency; heparin resistance ↔ antithrombin III deficiency.
- Factor V Leiden = commonest inherited thrombophilia (APC resistance).
- ECG/imaging signs: S1Q3T3, McConnell's sign, Hampton's hump, Westermark sign.
- D-dimer logic: rules out VTE in low probability; age-adjusted cut-off in elderly.
- Massive PE management: thrombolysis; unstable + can't do CT → bedside echo.
- Caprini/Wells scoring application questions.
Rapid revision
- Virchow's triad = Stasis + Hypercoagulability + Endothelial injury (SHE).
- Compression Doppler USG = IOC for DVT; hallmark is a non-compressible vein.
- CTPA = IOC/gold standard for PE; V/Q scan if contrast contraindicated or in pregnancy.
- D-dimer rules OUT VTE in low pre-test probability; never rules in.
- Wells DVT ≥2 = likely; Wells PE >4 = likely.
- LMWH is initial anticoagulant of choice and the agent of choice in pregnancy and cancer-associated VTE.
- Warfarin INR target 2–3; bridge with heparin to avoid skin necrosis (Protein C deficiency).
- DOAC reversal: dabigatran → idarucizumab; Xa inhibitors → andexanet alfa.
- IVC filter when anticoagulation is contraindicated or has failed—does not treat the clot.
- Thrombolysis for massive (high-risk) PE with hypotension/shock.
- HIT (day 5–10, >50% platelet fall, thrombosis) → stop heparin, use argatroban/fondaparinux; no platelets.
- Factor V Leiden = commonest inherited thrombophilia; antithrombin deficiency = heparin resistance; phlegmasia cerulea dolens = limb-threatening emergency.