Deep Vein Thrombosis (DVT) is the formation of a thrombus within the deep venous system, most commonly in the lower extremities. DVT is a major component of venous thromboembolism (VTE), which includes both DVT and pulmonary embolism (PE).

Approximately 90% of clinically significant PE originates from proximal DVT involving the popliteal, femoral, or iliac veins. Untreated DVT may propagate proximally, embolize to the pulmonary circulation, or lead to long-term complications such as post-thrombotic syndrome.

DVT pathogenesis is explained by Virchow’s triad: venous stasis, endothelial injury, and hypercoagulability.

Risk Factors

A. Venous Stasis

• Prolonged immobilization (bed rest, long-haul travel)

• Postoperative state (especially orthopedic surgery)

• Stroke with limb paralysis

• Heart failure

B. Endothelial Injury

• Trauma

• Surgery

• Central venous catheterization

C. Hypercoagulability

• Malignancy

• Pregnancy and postpartum

• Oral contraceptives or hormone replacement therapy

• Obesity

• Smoking

• Inherited thrombophilias (Factor V Leiden, Protein C/S deficiency)

• Antiphospholipid syndrome

• Previous history of VTE (strongest risk factor)

Clinical Presentation (Signs and Symptoms)

DVT may be asymptomatic or present with nonspecific symptoms.

Common Features

• Leg pain and tenderness

• Unilateral limb swelling

• Warmth and erythema

• A palpable cord representing thrombosed vein

• Dilated superficial veins

• Cyanosis (in severe cases)

Important: Clinical diagnosis alone is unreliable due to low specificity. Objective testing is required.

Diagnostic Criteria

Diagnosis is based on:

1. Clinical probability assessment (e.g., Wells score)

2. D-dimer testing (low/moderate probability cases)

3. Compression ultrasonography (first-line imaging)

DVT classification:

• Proximal DVT (popliteal vein or above) – high embolic risk

• Distal DVT (calf veins) – lower embolic risk

Investigations

Laboratory

• D-dimer (high sensitivity, low specificity)

• Baseline coagulation profile (PT, aPTT)

• Complete blood count

• Renal function tests (before anticoagulation)

Imaging

• Compression duplex ultrasonography (gold standard initial test)

• Venography (rarely used, invasive)

• CT or MR venography (selected cases)

Management

A. Non-Pharmacological

• Limb elevation

• Graduated compression stockings (reduce post-thrombotic syndrome)

• Early ambulation once anticoagulation is initiated

• Inferior vena cava (IVC) filter if anticoagulation contraindicated

B. Pharmacological

Long-term anticoagulation is required to prevent clot propagation, recurrence, and PE.

1. Initial Anticoagulation

Option 1: Warfarin-Based Regimen

• Warfarin 5 mg PO daily

• Overlap with heparin/LMWH for 4–5 days

• Continue overlap until INR 2.0–3.0 for at least 24 hours

Option 2: Low Molecular Weight Heparin (LMWH)

• Enoxaparin (Clexane) 1 mg/kg SC every 12 hours

Option 3: Unfractionated Heparin (UFH)

• 75 units/kg IV bolus

• Continuous infusion 18 units/kg/hour

• Adjust to achieve aPTT 1.5–2.5 times control

Monitoring

• Warfarin: Monitor INR after 5–7 days

  • Target INR: 2.0–3.0

• UFH: Monitor aPTT every 6 hours until therapeutic

• LMWH in pregnancy: Monitor anti-Xa levels

Special Populations

Adolescents / Children

• 15–25 units/kg/hour IV infusionOR

• 250 units/kg SC every 12 hours

Pregnant Women

• LMWH preferred (1 mg/kg SC twice daily)

• Warfarin contraindicated

• Monitor anti-Xa levels

Duration of Therapy

• Provoked DVT: 3 months

• Unprovoked DVT: ≥6 months

• Recurrent DVT: Long-term anticoagulation

• Cancer-associated thrombosis: LMWH or DOAC for at least 6 months

Complications

• Pulmonary embolism

• Post-thrombotic syndrome

• Chronic venous insufficiency

• Recurrent VTE

Prevention

Primary Prevention

• Early mobilization post-surgery

• Mechanical prophylaxis (compression devices)

• Prophylactic LMWH in high-risk hospitalized patients

Secondary Prevention

• Adequate anticoagulation duration

• Lifestyle modification (weight reduction, smoking cessation)