TextbookCardiologyDeep Vein Thrombosis

Deep Vein Thrombosis

Blood clot formation in the deep venous system, most commonly in the lower limbs. Major risk is pulmonary embolism. Diagnosed with D-dimer and compression ultrasonography; treated with anticoagulation.

Key Facts

Virchow triad: venous stasis, endothelial damage, hypercoagulability — underlying pathophysiology Wells score for DVT: clinical probability assessment guiding investigation pathway D-dimer: highly sensitive but low specificity; negative D-dimer with low Wells score effectively excludes DVT Compression ultrasonography: diagnostic investigation of choice; non-compressible vein = DVT First-line treatment: DOAC (rivaroxaban 15mg BD for 3 weeks then 20mg OD, or apixaban 10mg BD for 7 days then 5mg BD) per NICE NG158 Proximal DVT (above knee) carries higher PE risk than distal (below knee) DVT Duration of anticoagulation: 3 months for provoked; 3-6 months or lifelong for unprovoked or recurrent Post-thrombotic syndrome: chronic complication (~30-50%) with leg swelling, pain, skin changes, venous ulceration

Overview

Key Facts

Deep vein thrombosis (DVT) is the formation of a blood clot in the deep venous system, most commonly in the lower limbs. It is part of the spectrum of venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE).

Epidemiology

  • VTE incidence: ~1-2 per 1,000 per year
  • DVT accounts for ~2/3 of VTE events
  • Increases with age: ~1 per 10,000 in young adults; ~1 per 100 in elderly
  • Recurrence rate: ~5-10% per year after first unprovoked DVT

Aetiology (Virchow's Triad)

Stasis:

  • Immobility (hospitalisation, long-haul travel, plaster cast), pregnancy, obesity

Endothelial damage:

  • Surgery (especially orthopaedic), trauma, IV catheterisation

Hypercoagulability:

  • Inherited: Factor V Leiden, prothrombin G20210A, protein C/S deficiency, antithrombin deficiency
  • Acquired: malignancy, OCP/HRT, pregnancy, antiphospholipid syndrome, myeloproliferative disorders, nephrotic syndrome

Pathophysiology

  • Thrombus typically originates in valve pockets of deep veins
  • Most commonly: calf veins → propagates proximally to popliteal/femoral/iliac veins
  • Proximal DVT: higher risk of PE (50% have asymptomatic PE at presentation)
  • Thrombus can embolise to pulmonary arteries → PE
  • Post-thrombotic syndrome: chronic venous hypertension from valve damage and residual thrombus → oedema, skin changes, ulceration

Clinical Presentation

Typical Presentation

  • Unilateral calf/leg swelling (most common presenting feature)
  • Pain and tenderness along the deep veins
  • Warmth and erythema of affected limb
  • May be asymptomatic (incidental finding)

Examination Findings

  • Unilateral leg oedema (>3 cm calf circumference difference is significant)
  • Tenderness along the course of the deep veins
  • Warmth, erythema
  • Homan sign (calf pain on dorsiflexion): poor sensitivity and specificity; not recommended
  • Dilated superficial veins (collateral drainage)

Special Presentations

  • Phlegmasia alba dolens: white swollen limb (massive iliofemoral DVT)
  • Phlegmasia cerulea dolens: blue, severely swollen limb; venous gangrene; may progress to arterial compromise — surgical emergency
  • Upper limb DVT: associated with central venous catheters, Paget-Schroetter syndrome (effort thrombosis)

Red Flags

  • Bilateral DVT: consider IVC thrombosis or malignancy
  • Phlegmasia cerulea dolens: emergency
  • Unexplained/recurrent DVT: screen for malignancy and thrombophilia
  • DVT in unusual sites: consider myeloproliferative disorder, paroxysmal nocturnal haemoglobinuria

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
CellulitisBilateral skin erythema, fever, no swelling asymmetryClinical, bloods
Ruptured Baker cystPosterior knee swelling, sudden calf pain/swellingUSS knee and calf
Musculoskeletal injuryTrauma history, localised tendernessClinical, X-ray
Superficial thrombophlebitisTender, palpable, erythematous cord along superficial veinClinical, USS
LymphoedemaNon-pitting oedema, skin thickening, chronicClinical, imaging
Heart failureBilateral oedema, dyspnoea, JVP elevationEcho, BNP

Diagnosis / Investigation

Wells Score for DVT

CriterionPoints
Active cancer (treatment within 6 months)+1
Paralysis, paresis, or recent plaster immobilisation of lower limb+1
Recently bedridden >3 days or major surgery within 12 weeks+1
Localised tenderness along deep venous system+1
Entire leg swollen+1
Calf swelling >3 cm compared to asymptomatic side+1
Pitting oedema confined to symptomatic leg+1
Collateral superficial veins (non-varicose)+1
Previously documented DVT+1
Alternative diagnosis at least as likely as DVT-2
  • ≤1: DVT unlikely → D-dimer → if negative, DVT excluded
  • ≥2: DVT likely → proximal leg vein USS within 4 hours (or D-dimer + interim anticoagulation if USS delayed)

Bloods

  • D-dimer: highly sensitive (>95%); low specificity; useful to exclude DVT in low-probability patients
  • FBC, U&Es, LFTs, coagulation: baseline
  • Thrombophilia screen: if unprovoked DVT in young patient (defer testing until after anticoagulation — Factor V Leiden, prothrombin mutation, antithrombin, protein C/S, antiphospholipid antibodies)
  • Cancer screen: CT CAP if unprovoked DVT (NICE recommendation), PSA, mammography as appropriate

Imaging

  • Compression ultrasonography: first-line imaging; sensitivity ~95% for proximal DVT, lower for distal
    • Positive: vein non-compressible
  • Whole-leg ultrasound: detects both proximal and distal DVT
  • CT venography: if USS inconclusive
  • MR venography: pelvic/IVC thrombosis

Management

Non-pharmacological

  • Early mobilisation: encouraged (bed rest not necessary)
  • Graduated compression stockings: NOT routinely recommended for post-thrombotic syndrome prevention (SOX trial negative); may be used for symptom relief

Pharmacological

Anticoagulation (NICE NG158):

  • DOACs first-line:
    • Rivaroxaban: 15mg BD for 21 days, then 20mg OD
    • Apixaban: 10mg BD for 7 days, then 5mg BD
    • No need for initial heparin bridging
  • Alternative: LMWH (enoxaparin 1.5mg/kg OD or dalteparin 200 IU/kg OD) + warfarin (target INR 2.0-3.0); stop LMWH when INR >2 for ≥24 hours
  • LMWH monotherapy: preferred in active cancer (or DOAC — NICE now permits edoxaban or rivaroxaban for cancer-associated VTE)

Duration:

  • Provoked DVT (transient risk factor): 3 months
  • Unprovoked DVT: ≥3-6 months, consider extended/lifelong (risk-benefit assessment)
  • Recurrent unprovoked DVT: lifelong anticoagulation
  • Cancer-associated: treat for duration of cancer/ongoing risk factor

Surgical/Interventional

  • Catheter-directed thrombolysis: for extensive iliofemoral DVT (phlegmasia) to preserve valve function and prevent PTS
  • Thrombectomy: for phlegmasia cerulea dolens with limb compromise
  • IVC filter: only if anticoagulation contraindicated and proximal DVT with high PE risk; retrieve when anticoagulation can resume

Referral Criteria

  • Phlegmasia: emergency vascular referral
  • Unprovoked DVT: cancer screening
  • Recurrent VTE or young patient: haematology for thrombophilia assessment
  • Pregnancy-related DVT: specialist obstetric/haematology care

Prognosis

  • With appropriate anticoagulation: PE risk is low (<3% during treatment)
  • Recurrence after provoked DVT: ~3% per year
  • Recurrence after unprovoked DVT: ~5-10% per year
  • Post-thrombotic syndrome: develops in ~30-50% of proximal DVT patients within 2 years
  • Mortality: DVT-related mortality is predominantly from PE (~1-2% of DVT cases)
  • Long-term anticoagulation reduces recurrence by ~80-90% but carries bleeding risk (~1-3% major bleeding per year)

Other Relevant Information

NICE NG158 DVT Pathway Summary

StepAction
1Calculate Wells score
2a (unlikely ≤1)D-dimer → if negative, exclude DVT
2b (likely ≥2)USS within 4 hours → if positive, treat
3If USS negative but high suspicion: repeat USS at 6-8 days
4Start DOAC (rivaroxaban or apixaban)

Duration of Anticoagulation

ScenarioDuration
Provoked (surgery, OCP, travel)3 months
Unprovoked (first episode)≥3-6 months, consider lifelong
Recurrent unprovokedLifelong
Cancer-associatedDuration of risk factor