Hematology

Deep Vein Thrombosis

DVT and pulmonary embolism — Virchow's triad in action

Deep vein thrombosis is clot formation in deep veins, usually of the legs. Virchow's triad describes the three pathogenic factors: venous stasis, endothelial injury, and hypercoagulability. The lethal sequela is pulmonary embolism (PE) when fragments break off and lodge in pulmonary arteries — fatal in ~10-30% if untreated. Annual incidence: 1-2 per 1000. Most clots start in calf veins; ~25% propagate proximally where embolism risk rises sharply. Anticoagulation prevents propagation; thrombolysis is reserved for hemodynamic compromise.

  • Virchow's triadStasis, endothelial injury, hypercoagulability
  • Annual incidence1-2 per 1000
  • PE mortality untreated~30%
  • Wells scoreClinical pre-test probability tool
  • D-dimerSensitive (>500 ng/mL); not specific
  • First-line treatmentDOAC (apixaban, rivaroxaban) or LMWH

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Why DVT/PE matters

  • Hospital prophylaxis. Mechanical and pharmacologic VTE prophylaxis prevents thousands of deaths.
  • Postoperative care. Major orthopedic surgery requires extended prophylaxis (10-35 days).
  • Cancer. Trousseau syndrome — migratory thrombophlebitis can herald malignancy.
  • Pregnancy. 5× increased risk; treat with LMWH (warfarin and DOACs cross placenta).
  • Long flights. Hydration, walking, compression stockings for high-risk travelers.
  • Bleeding management. Andexanet for factor Xa inhibitors; idarucizumab for dabigatran; vitamin K/PCC for warfarin.
  • Pulmonary hypertension. CTEPH (chronic thromboembolic) treated with pulmonary thromboendarterectomy.

Common misconceptions

  • Negative D-dimer in high-probability patient rules out PE. Sensitive only in low-probability patients.
  • Calf DVT is benign. ~25% propagate; serial ultrasound or treatment recommended.
  • Aspirin replaces anticoagulation. Aspirin doesn't prevent venous thrombosis effectively.
  • Bedrest is needed for DVT. Early ambulation reduces post-thrombotic syndrome without raising PE.
  • Warfarin is always safer than DOACs. DOACs have less ICH and don't need INR monitoring for most VTE.
  • IVC filter is a substitute for anticoagulation. Filters don't prevent clot formation, only embolization to lungs.

Frequently asked questions

Who gets DVT?

Risk factors stack. Surgery (orthopedic highest — hip/knee), trauma, immobilization, cancer (especially pancreatic, gastric, lung), pregnancy and 6 weeks postpartum, oral contraceptives/HRT, obesity, age >60, prior VTE. Inherited thrombophilia: factor V Leiden (5% Caucasians), prothrombin G20210A, antithrombin/protein C/S deficiency, antiphospholipid syndrome. Long-haul flights add small risk.

How does it present?

DVT: unilateral leg swelling, pain, warmth, erythema, palpable cord. Often asymptomatic — many discovered only after PE. Homan sign (calf pain on dorsiflexion) is unreliable. PE: dyspnea, pleuritic chest pain, tachycardia, hypoxia, hemoptysis. Massive PE: hypotension, syncope, right heart strain on echo. Sudden death in 25% of PE cases.

How is it diagnosed?

Wells score risk-stratifies. Low probability + negative D-dimer rules out DVT. Otherwise: compression ultrasound (lack of vein compressibility = clot). For PE: CT pulmonary angiography (CTPA) is gold standard; V/Q scan if contrast contraindicated. PERC rule excludes PE in low-probability outpatients without further testing.

How is it treated?

Anticoagulation 3 months minimum. DOACs (apixaban 10 mg BID × 7d, then 5 mg BID; rivaroxaban 15 mg BID × 21d, then 20 mg daily) preferred. Warfarin (INR 2-3) for antiphospholipid syndrome, mechanical valves. LMWH (enoxaparin 1 mg/kg BID) for cancer-associated thrombosis or pregnancy. Massive PE: tPA thrombolysis or catheter-directed therapy.

What about IVC filters?

Reserved for patients with PE who can't be anticoagulated (active major bleeding, CNS bleed) or who have recurrent PE despite therapeutic anticoagulation. Retrievable filters should be removed within months — long-term filters cause IVC thrombosis, fracture, migration. PREPIC trial: filters reduce early PE but increase DVT recurrence; no mortality benefit.

How long should anticoagulation continue?

Provoked (post-surgery, trauma): 3 months. Unprovoked first event: 3-6 months minimum, consider extended based on bleeding risk and patient preference. Recurrent unprovoked: indefinite. Cancer-associated: while cancer active. Antiphospholipid syndrome: indefinite. Reduced-dose DOAC (apixaban 2.5 mg BID, rivaroxaban 10 mg daily) for extended therapy after initial 6 months.

What is post-thrombotic syndrome?

Chronic complication in 20-50% of DVT survivors. Damaged valves cause venous reflux and hypertension; presents with leg pain, edema, pigmentation, and venous ulcers. Prevention: early ambulation, graded compression stockings (controversial, SOX trial negative), prompt anticoagulation. Treatment: compression, leg elevation, ulcer care.