Deep vein thrombosis

• Deep vein thrombosis (DVT) is a blood clot (thrombus) forming in the deep veins of the legs, most often in the calf and propagating into the proximal veins; it is the commonest presentation of venous thromboembolism (VTE).
• It matters most because pieces of the clot can break off and travel to the lungs as a pulmonary embolism (PE), which is a leading cause of preventable hospital death.
• DVT is usually provoked (recent surgery, immobilisation, cancer, pregnancy, oestrogen, travel) but can be unprovoked; whether it was provoked decides how long to anticoagulate.
• Diagnosis rests on pre-test probability (Wells score) and D-dimer: DVT unlikely (score 1 or less) plus a negative D-dimer rules it out; DVT likely (score 2 or more) goes straight to proximal leg ultrasound, repeated in 6 to 8 days if the first scan is negative but suspicion remains.
• Treatment is anticoagulation (a DOAC or LMWH first), for at least 3 months, plus elevation and analgesia; thrombolysis only when the limb is threatened.

By the end of this page you should be able to:

1. Explain the three elements of the Virchow triad and how they produce a clot in a deep vein.
2. Take a history and examination for suspected DVT, distinguish proximal from isolated distal (calf) disease, and separate DVT from the other causes of a swollen leg.
3. Calculate the two-level Wells score for DVT and use D-dimer and duplex ultrasound to diagnose or exclude DVT.
4. Prescribe first-line anticoagulation with drug, dose, route, adjustment and duration, and state when thrombolysis or thrombectomy is justified.
5. Decide whether a DVT is provoked or unprovoked and use that to set the duration of treatment, secondary prevention and who needs investigation for cancer or thrombophilia.
6. Recognise cancer-associated and pregnancy-associated DVT and post-thrombotic syndrome, and what does and does not help the latter.
7. Manage DVT with renal impairment, extremes of body weight, and in low-resource settings.

Most clots start in the valve pockets of the calf veins and grow by accretion of platelets and fibrin; once they reach the proximal veins they can shed fragments that travel as pulmonary emboli. A "phlegmasia" (a swollen, blue, severely painful limb from massive venous outflow obstruction, sometimes with arterial ischaemia) is an emergency needing urgent reperfusion.

VTE occurs in about 1 to 2 people per 1000 each year, or about 300,000 to 600,000 events a year in the United States. About one third of patients with a new VTE have a PE. The incidence rises steeply with age, from about 1 in 10,000 in people under 20 to about 1 in 100 in people aged 80 or more. VTE is commoner in black people than in white people in most studies and less common in people of Asian descent. A large clot in the proximal leg veins is the common source of pulmonary embolism, although more than half of those who have a DVT have no symptoms of either. Post-thrombotic syndrome develops in 20 to 50 percent of patients after a DVT and is severe in up to 5 percent. ^[3]

Three interacting influences explain clot formation in veins: ^[3]

• Endothelial injury: damage to the vein lining, for example by surgery, trauma, a fracture or an indwelling central venous catheter.
• Stasis or turbulence of blood flow: slow or static blood in the deep veins, as in prolonged bed rest, lower-limb paralysis, a plaster cast or a long-haul flight; stasis lets platelets and fibrin accumulate instead of being washed away.
• Hypercoagulability: an excess of pro-coagulant forces or a lack of natural anticoagulants, from cancer, pregnancy, the oral contraceptive pill, hormone replacement, or an inherited or acquired thrombophilia.

Thrombi usually start as a platelet nidus in the valve pockets of the calf veins and grow by accretion; from there they can propagate into the popliteal and femoral veins. ^[3]

The most important clinical habit is to ask whether a DVT was provoked. ^[1] Risk factors are best grouped as transient (reversible), persistent, and unprovoked.

Transient, major risk factors. Recent major surgery (risk remains elevated for at least 12 weeks after surgery), immobilisation, lower-limb fracture, major trauma, and hospitalisation for heart failure or acute myocardial infarction. ^[5]

Transient, minor risk factors. Prolonged travel, minor leg injury, brief hospitalisation. ^[5]

Persistent (chronic) risk factors. Active cancer, chronic heart or lung disease, inflammatory bowel disease, obesity, smoking, age, and thrombophilias. ^[5]

Unprovoked DVT: no identifiable risk factor is found in about 40 percent of patients with DVT or PE. ^[5]

A 2025 European review estimated that 96 percent of VTE patients have at least one recognised predisposing factor and 76 percent have two or more. ^[5] Major surgery is a common trigger, especially after orthopaedic procedures. ^[5]

Surgery is the single most common setting for DVT. Risk is highest after hip, pelvic and spinal operations and leg fractures, and stays raised for at least 12 weeks after any operation. ^[5] Immobility in a cast, on a long flight or during prolonged bed rest is enough on its own when other risks are present.

Active cancer is a persistent major risk factor for VTE and a reason to treat longer and to prefer LMWH or a suitable DOAC rather than warfarin. Cancer is often found first by the history, basic blood tests and examination; further searching (imaging, tumour markers) without symptoms or signs is not recommended. ^[4]

VTE risk is increased throughout pregnancy and is particularly high after delivery. PE is a leading cause of maternal death, with risk greatest in the third trimester and the first 6 weeks after delivery. ^[3] Treatment is with LMWH or UFH at full therapeutic dose; DOACs and warfarin are contraindicated in pregnancy and breastfeeding (see special groups). ^[1]

Oestrogen-containing contraceptives and postmenopausal hormone replacement increase the risk of VTE; the effect rises with dose and with age. ^[5] A patient with a personal or strong family history of VTE should not take combined oral contraception or hormone replacement therapy; progesterone-only or non-hormonal methods are preferred. ^[5]

Suspect hereditary thrombophilia in young patients, those with recurrent VTE, or with a family history. The commonest inherited states include factor V Leiden (resistance to activated protein C), deficiencies of protein C, protein S or antithrombin, the prothrombin gene mutation, raised factor VIII, dysfibrinogenaemia and disorders of plasminogen or plasminogen activator. ^[5] Acquired thrombophilias include antiphospholipid syndrome (triple-positive disease: warfarin rather than a DOAC), ^[4] myeloproliferative disease, paroxysmal nocturnal haemoglobinuria and heparin-induced thrombocytopenia. Routine thrombophilia testing is not recommended after a provoked DVT or while continuing anticoagulation. ^[4]

Upper-limb DVT is usually catheter-associated and has a lower risk of pulmonary embolism than lower-limb DVT. ^[5] A new swollen arm with a central venous catheter needs investigation with ultrasound.

Travel is a minor transient risk factor; the absolute risk is low and confined to people with other factors. Sensible measures are leg exercises, hydration and avoiding cramped immobility; pharmacological prophylaxis only for very high-risk travellers. ^[5]

Stasis in the sinusoids of the soleal plexus or in valve pockets triggers platelet activation; once thrombin forms, fibrin reinforces it. Clinically the affected segment drains badly, so the leg swells below the clot and becomes painful and tender; if the outflow is large and sudden the limb becomes massively swollen, tense and cyanosed (phlegmasia). Inflammation of the vein wall gives the warmth and erythema that mimic cellulitis.

The calf or thigh is swollen, painful, warm and tender, often with calf pain on dorsiflexion of the foot. Homans' sign is unreliable and should not be relied on. ^[4] Dilated superficial veins may be visible. Many DVTs cause few or no symptoms, and a DVT can first present with a pulmonary embolism. ^[3]

History. Ask about onset (hours to days), laterality (DVT is usually unilateral; bilateral swelling suggests systemic causes such as heart failure, nephrotic syndrome or lymphoedema), pain (aching or cramp, worse on standing and walking), swelling (ankle, whole calf or thigh), and any risk factor above. Ask about breathlessness or chest pain that would suggest an embolus.

Red flags. Sudden severe pain with a hugely swollen, cold, blue leg; absent pulses; compartment syndrome pain; any breathlessness or chest pain at rest; a swollen, painful arm with a central line.

Examine with the patient supine, both legs exposed:

• limb circumference measured at a fixed point below the tibial tuberosity; a difference of at least 3 cm is one Wells criterion;
• tenderness along the deep veins;
• pitting oedema confined to the symptomatic leg;
• warmth and erythema;
• dilated collateral superficial (non-varicose) veins;
• pulses and capillary refill to exclude arterial disease; a cool blue leg suggests phlegmasia.

Electrocardiography and chest radiograph are not diagnostic of DVT; in suspected PE they help exclude mimics. Blood tests show no specific marker; D-dimer is the exclusion test.

Use the two-level Wells score before any test. ^[4]

D-dimer is a breakdown product of cross-linked fibrin: it is highly sensitive (a negative result reliably rules out thrombosis in a low-probability patient) but poorly specific (it rises with age, pregnancy, inflammation, cancer, infection and after surgery). ^[5]

• DVT likely (2 points or more): offer a proximal leg vein ultrasound scan with the result within 4 hours if possible; if not, a D-dimer test, interim therapeutic anticoagulation, and an ultrasound within 24 hours. If the scan is positive, start or continue anticoagulation; if negative but the D-dimer is positive, repeat the scan 6 to 8 days later; if the D-dimer is negative, think about alternative diagnoses. ^[4]
• DVT unlikely (1 point or less): offer a D-dimer test within 4 hours, or interim therapeutic anticoagulation while awaiting the result; if positive, a proximal leg vein ultrasound scan; if negative, alternative diagnoses. ^[4]

Consider a point-of-care D-dimer test if laboratory facilities are not immediately available, choosing a fully quantitative test, and an age-adjusted threshold (for example age times 10 ng per mL) in people over 50. ^[4]

• Compression duplex ultrasound of the proximal leg veins is the first-line imaging test. It is non-invasive, cheap and gives an immediate answer; absence of compressibility of the vein is diagnostic. A proximal positive scan is enough to diagnose DVT and start treatment. ^[4]
• Distal (calf-vein) ultrasound is more operator-dependent; isolated calf DVT has a lower embolic risk, and guidelines differ on whether to anticoagulate immediately or to repeat ultrasound in a week. If the first proximal scan is negative but the D-dimer is positive, repeat imaging in 6 to 8 days captures a propagating clot. ^[4]
• Whole-leg or extended ultrasound is used where available to see the calf veins in one visit.
• CT venography / MR venography are reserved for suspected ilio-caval or upper-extremity thrombosis, or when ultrasound is inconclusive (for example in a patient with a plaster cast or marked obesity). CT pulmonary angiography (CTPA) is the imaging of choice if a PE is suspected; see the separate pulmonary embolism topic.
• D-dimer plus ultrasound in pregnancy: reduce radiation by using serial ultrasound and, when needed, V/Q or low-dose CTPA; involve obstetrics.

A diagnostic flow:

When DVT is confirmed, or strongly suspected pending imaging, start therapeutic anticoagulation without delay. Add leg elevation above the level of the heart for symptom relief, analgesia (avoid intramuscular injections), and well-fitted graduated compression or an elastic bandage for symptom relief in the acute phase. Mobilisation is encouraged rather than bed rest once anticoagulation is started and pain allows.

For a limb-threatening DVT (phlegmasia), anticoagulation alone may not be enough; see thrombolysis below.

Renal impairment and extremes of body weight:

• CrCl 15 to 50 mL per min: offer apixaban or rivaroxaban, or LMWH for at least 5 days followed by edoxaban, or dabigatran if CrCl is at least 30, or LMWH or UFH with a vitamin K antagonist (VKA). Dose adjustments follow the SPC. ^[4]
• CrCl under 15 mL per min: LMWH, UFH, or LMWH or UFH with a VKA, then VKA alone. ^[4]
• CrCl 15 to 50 mL per min or body weight 60 kg or less: edoxaban dose reduces to 30 mg daily. ^[5]
• Weight under 50 kg or over 120 kg: use therapeutic-level monitoring to ensure effective anticoagulation. ^[4]

DOAC-vs-DOAC: there is no evidence that one DOAC is superior to another. ^[3] Choice is driven by the need for lead-in parenteral therapy, once-versus-twice-daily dosing, cost, renal function, interacting drugs and the presence of cancer. ^[3]

• Provoked by a major reversible factor (surgery, trauma, immobilisation): at least 3 months, then stop; the risk of recurrence is low once the provoking factor has resolved. ^[2][3][4]
• Unprovoked: at least 3 months, then re-assess; many guidelines favour continuing indefinitely in patients with low bleeding risk, because the benefit usually outweighs the risk. ^[2][3][4]
• Persistent risk factor or chronic disease: indefinite antithrombotic therapy in many cases. ^[3]
• Active cancer: 3 to 6 months initially, reviewed at 3 to 6 months; LMWH or a DOAC (dabigatran, apixaban, edoxaban, rivaroxaban) rather than warfarin. ^[4][5]
• Extended (secondary) prevention after the initial 3 to 6 months: anticoagulation is preferred over aspirin; if a VKA is used the target INR is 2.0 to 3.0; with a DOAC a lower-dose regime may be used (rivaroxaban 10 mg daily or apixaban 2.5 mg twice daily). ^[3][4]
• Recurrent DVT despite treatment: investigate adherence and other sources of hypercoagulability; switch or increase the dose. ^[4]

Major bleeding occurs in about 1 to 3 percent of patients on a VKA each year, with about a 30 percent lower relative risk on a DOAC. ^[3]

The HAS-BLED score can be used to estimate the risk of major bleeding during long-term anticoagulation; a score of 4 or more that cannot be modified argues for stopping. ^[4] Avoid, reduce or correct risk factors: treat hypertension, review interacting drugs (antiplatelets, NSAIDs), limit alcohol and prevent falls.

• DOACs: no routine monitoring is required, but renal function must be checked and the dose adjusted. Overdose or serious bleeding: stop the drug, give supportive care, tranexamic acid, and the specific reversal if available (idarucizumab for dabigatran, andexanet alfa for the factor Xa inhibitors), with prothrombin complex concentrate as an alternative. Follow local protocol and product labelling.
• LMWH and UFH: protamine reverses most of the effect.
• Warfarin: vitamin K plus prothrombin complex concentrate for serious bleeding; hold doses and give vitamin K for an elevated INR without bleeding, depending on level and risk. Blood components as for massive haemorrhage.

For most proximal DVTs, anticoagulation alone is preferred. ^[3] Thrombolysis is reserved for limb-threatening (phlegmasia) disease and for selected younger patients at low bleeding risk with symptomatic DVT involving the iliac and common femoral veins (higher risk of post-thrombotic syndrome), and is considered for extension of ischaemic venous obstruction. ^[3] For DVT meeting criteria, catheter-directed thrombolysis is preferred over systemic thrombolysis. ^[3] NICE advises considering catheter-directed thrombolytic therapy only for symptomatic iliofemoral DVT with symptoms lasting less than 14 days, good functional status, life expectancy of 1 year or more and low bleeding risk. ^[4]

Pharmacological systemic thrombolysis is not recommended for DVT itself outside these settings, and is certainly not for routine proximal DVT. ^[3]

An inferior vena cava (IVC) filter is not used routinely for a DVT treated with anticoagulation. It is reserved for DVT or PE when anticoagulation is contraindicated, or for recurrent embolism despite appropriate anticoagulation; a retrievable filter is preferred and should be removed as soon as anticoagulation is established. ^[3][4] Put a strategy for removal in place before fitting. ^[4]

Superficial thrombophlebitis (a tender, palpable cord in a superficial vein) is common and usually benign, but thrombus can extend into the deep system at the sapheno-femoral junction. Manage with anti-inflammatory analgesia, compression and mobilisation; for extensive disease above the knee or near the junction with the deep system, 45 days of fondaparinux or an intermediate dose of LMWH reduces thrombotic complications (ESC recommendations). ^[1] Always ultrasound the proximal extension if the process is close to the sapheno-femoral junction or the patient has risk factors.

Post-thrombotic syndrome (PTS) is chronic pain, heaviness, swelling and sometimes venous ulceration after a DVT, present in up to 20 to 50 percent and severe in up to 5 percent. ^[3] Routine graduated compression stockings do not prevent PTS; this is now the consensus (the early SOX trial evidence did not hold up in the ASH 2020 review). ^{[3] [4]} Stockings may still be worn to relieve oedema and pain in selected patients, and patients should be taught how to put them on and replace them. ^[3][4] Early, regular walking and calf-muscle exercise help. Keep weight normal and treat venous ulcers with compression and skin care; escalate to a vascular service for severe disease.

In active cancer, anticoagulate for 3 to 6 months and review. ^[4][5] Choose LMWH (or a DOAC such as edoxaban or rivaroxaban in patients without gastrointestinal cancer) over warfarin. ^[4][5] Take into account the tumour site, drug interactions (especially with chemotherapy), and bleeding risk. ^[4] Central venous catheter thrombosis is treated with anticoagulation and the catheter is usually left in place if it is still needed. ^[3]

Use LMWH (or UFH if delivery is imminent or renal failure is present) at full therapeutic dose, and avoid warfarin and DOACs in pregnancy and breastfeeding. ^[1][4] Anticoagulate through pregnancy and for at least 6 weeks postpartum, for a minimum of 3 months in total. ^[4] If delivery is approaching and a thrombolytic or anticoagulant reversal is needed, plan with obstetrics, haematology and anaesthetics. Regional anaesthesia should not be given while on therapeutic LMWH; coordinate timing with the anaesthetist.

All admitted patients should be assessed for VTE and bleeding risk, with pharmacological thromboprophylaxis offered when not contraindicated. In medical inpatients at increased risk, low-dose LMWH (or fondaparinux) is the standard; in surgical patients the choice and duration follow the procedure (LMWH for higher-risk surgery in addition to early mobilisation and adequate hydration). ^[5] Mechanical prophylaxis (intermittent pneumatic compression) is used when anticoagulation is contraindicated. Re-assess risk at every change in clinical status.

Unprovoked DVT: many guidelines advise continuing anticoagulation indefinitely in patients with low bleeding risk, because the balance usually favours treatment; shared decision-making and an annual review of benefits and risks. ^[3][4] Provoked DVT with a resolved trigger usually stops at 3 months. ^[4] Aspirin 75 or 150 mg daily is a fallback for patients who decline anticoagulation. ^[4]

• Pulmonary embolism, the most serious: see the separate pulmonary embolism topic in the pulmonary chapter for diagnosis, risk stratification and thrombolysis. A DVT in the proximal veins is the common source of PE.
• Post-thrombotic syndrome (see above): the commonest long-term complication.
• Recurrence: roughly 10 percent by 2 years and over 30 percent by 10 years after an unprovoked VTE, falling substantially with extended anticoagulation but at the cost of bleeding. ^[3]
• Bleeding from anticoagulation (see above).
• Phlegmasia and venous gangrene if untreated or late.
• Chronic thromboembolic pulmonary hypertension can follow PE in up to 5 percent. ^[3]
• Heparin-induced thrombocytopenia with UFH or LMWH is treatable and must be excluded if the platelet count falls.
• Incidental DVT found on imaging for another reason still carries the same thrombotic risk if propagating.

With treatment, the 30-day mortality of related VTE is low for uncomplicated DVT; untreated proximal DVT carries a serious risk of PE and death. Recurrence risk dominates long-term: roughly 10 percent by 2 years and over 30 percent by 10 years after an unprovoked event, and fell substantially with extended therapy. ^[3] Extended anticoagulation largely removes recurrence at the cost of bleeding at 1 to 3 percent on a VKA each year. ^[3]

Older adults. VTE incidence rises steeply with age; bleeding risk on anticoagulation also rises, so frailty, falls and renal function decide drug and dose. ^[3]

Pregnancy and postpartum. Use LMWH or UFH only; warfarin and DOACs are contraindicated in pregnancy and breastfeeding. ^[1][4] Treat from diagnosis, through delivery and for at least 6 weeks postpartum (a minimum of 3 months in total). Stop LMWH 24 hours before planned induction or caesarean, and restart after haemostasis and after catheter removal if a neuraxial block was used. ^[4]

Cancer. See cancer-associated thrombosis above. Dose and drug choice, especially in gastrointestinal cancers and with chemotherapy interactions.

Renal impairment. Use the adjustments above; below the respective thresholds switch to heparin-based regimens and involve a pharmacist. ^[4][5]

Children. VTE in children is rare and usually has a clear cause (central line, serious illness, inherited thrombophilia). ^[5] Paediatric haematology input is needed; DOACs have weight-based dosing in children now licensed in several regions.

Obesity. Use weight-adjusted LMWH; for extreme weight use anti-Xa monitoring. ^[4]

• A bedside clinical assessment and D-dimer where available, plus duplex ultrasound of the proximal veins, makes the diagnosis. Where ultrasound is unavailable, use clinical probability and treat presumptively when probability is high and the risk of missing DVT is worse than the risk of treatment.
• Unfractionated heparin by infusion or monitored subcutaneous regimen is cheap, widely available and rapidly reversible; it is a legitimate alternative to LMWH and DOACs when those are unaffordable or bleeding risk is high. ^[5]
• Warfarin is inexpensive and effective once the INR is controlled; its use depends on reliable INR testing and on patient education.
• Compression stockings for comfort and donated ultrasound machines in emergency departments can be high-value interventions.
• Leg elevation, analgesia and early walking are always available and should not be forgotten.

• DVT is a clot in the deep veins, usually of the leg; proximal DVT is the common source of pulmonary embolism. ^[3]
• Think Virchow: endothelial injury, stasis and hypercoagulability explain why surgery, immobility, cancer, pregnancy, oestrogen and thrombophilias matter. ^[3]
• About 40 percent of DVT and PE are unprovoked, but many more have at least one risk factor. ^[5]
• Diagnose with Wells (2 or more = likely) plus D-dimer plus duplex ultrasound; DVT unlikely plus a negative D-dimer rules it out. ^[4]
• Apixaban or rivaroxaban is first choice in NICE; LMWH or fondaparinux as parenteral options, warfarin (INR 2.0 to 3.0) when DOACs are unsuitable. ^[4][3]
• Standard total dose: apixaban 10 mg twice daily for 7 days then 5 mg twice daily; rivaroxaban 15 mg twice daily for 3 weeks then 20 mg once daily; warfarin to INR 2.0 to 3.0. ^[5]
• Treat provoked major-trigger DVT for 3 months; unprovoked DVT for at least 3 months and often indefinitely if bleeding risk is low. ^[3][4]
• Cancer: 3 to 6 months initially, reviewed; LMWH or a suitable DOAC over warfarin. ^[4][5]
• IVC filters, thrombolysis and catheter therapy are for limb- or life-threatening disease only. ^[3]
• Graduated compression stockings do not prevent post-thrombotic syndrome. ^[3][4]
• Major bleeding is 1 to 3 percent per year on warfarin and about 30 percent lower with DOACs. ^[3]
• Unprovoked recurrence is about 10 percent by 2 years and 30 percent by 10 years. ^[3]

• Pulmonary embolism (pulmonary chapter) — the most serious complication and the same disease continuum.
• Heart failure, ECG interpretation and cardiac physical examination may help exclude cardiac mimics of a swollen leg in complex patients. Heart failure is a cause of bilateral leg oedema; ECG interpretation and cardiac physical examination are useful when cardiopulmonary disease is suspected.
• Lymphoedema, chronic venous insufficiency and superficial vein thrombosis are the main local mimics.