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Venous Thromboembolism and DVT

GMJ News knowledge hub · last reviewed August 2026 · Georgian Medical Journal

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Deep vein thrombosis and pulmonary embolism together constitute venous thromboembolism, a condition responsible for an estimated hundreds of thousands of deaths annually and, critically, one in which a substantial proportion of hospital-associated cases are preventable through systematic risk assessment and thromboprophylaxis — making failure to assess VTE risk on admission one of the most consequential omissions in inpatient care (WHO). Diagnosis follows a structured pathway of clinical probability scoring followed by D-dimer in low-probability patients and imaging in the rest, and treatment has been transformed by direct oral anticoagulants, which have largely replaced warfarin for most indications; but the decision that matters most in the long term is whether the event was provoked or unprovoked, since unprovoked VTE carries a recurrence risk of roughly 30% at five years after stopping anticoagulation and increasingly justifies extended low-dose therapy, while the substantial burden of post-thrombotic syndrome after DVT remains widely underestimated and undertreated.

Key messages

Hospital-associated VTE is largely preventable — and risk assessment is routinely omitted
A substantial proportion of venous thromboembolism is hospital-associated, arising during or within 90 days of an admission, and much of it is preventable by systematic VTE risk assessment on admission followed by appropriate pharmacological or mechanical prophylaxis. Failure to perform this assessment is one of the most consequential routine omissions in inpatient care, and mandatory risk assessment with audited compliance has been shown at national level to reduce VTE mortality. Prophylaxis must also be reconsidered at each change in clinical state, since risk is dynamic.
Diagnosis follows probability, then D-dimer, then imaging — in that order
Clinical probability scoring comes first: the Wells score for DVT and PE, or the revised Geneva score for PE. In LOW probability patients, a negative D-dimer excludes VTE without imaging. In moderate or high probability, D-dimer must not be used to exclude — proceed directly to imaging (compression ultrasound for DVT, CT pulmonary angiography for PE). Using D-dimer in the wrong probability group is the commonest diagnostic error, in both directions: false reassurance in high-probability patients, and unnecessary imaging generated by a raised D-dimer in patients who never needed the test. Age-adjusted D-dimer thresholds and the PERC rule reduce imaging further in appropriate populations.
Provoked versus unprovoked determines how long anticoagulation continues
The most consequential long-term decision. VTE provoked by a major transient risk factor — surgery, major trauma, immobilisation, pregnancy, oestrogen therapy — carries a low recurrence risk once the provoking factor resolves, and 3 months of anticoagulation is usually sufficient. UNPROVOKED VTE carries a recurrence risk of roughly 10% at one year and 30% at five years after stopping, which increasingly justifies extended anticoagulation, often at reduced dose (apixaban 2.5mg twice daily or rivaroxaban 10mg daily), shown in AMPLIFY-EXT and EINSTEIN-CHOICE to retain most of the protective effect with bleeding rates approaching placebo. Cancer-associated VTE is treated as a separate category requiring continuing therapy while cancer is active.
DOACs have replaced warfarin for most indications
Direct oral anticoagulants — apixaban, rivaroxaban, edoxaban and dabigatran — offer equivalent or superior efficacy with significantly less intracranial haemorrhage, no routine monitoring, and no dietary interaction, and are recommended first-line for most VTE. Important exceptions where DOACs should NOT be used: antiphospholipid syndrome, particularly triple-positive, where rivaroxaban performed worse than warfarin in the TRAPS trial; mechanical heart valves; severe renal impairment (thresholds differ by agent); pregnancy and breastfeeding, where low molecular weight heparin is used; and significant drug interactions with strong P-glycoprotein and CYP3A4 inducers such as rifampicin, carbamazepine and phenytoin.
Post-thrombotic syndrome is common, disabling and neglected
Up to 20-50% of patients develop post-thrombotic syndrome after proximal DVT — chronic limb pain, heaviness, swelling, skin pigmentation, and in severe cases venous ulceration — caused by persistent outflow obstruction and valvular reflux. It is a major determinant of long-term quality of life after DVT and is consistently under-recognised, in part because it develops months to years after the acute event when follow-up has ended. Prevention rests on adequate initial anticoagulation and early mobilisation; graduated compression stockings improve symptoms though the SOX trial did not show prevention of the syndrome itself. Catheter-directed thrombolysis reduces post-thrombotic syndrome in selected patients with extensive iliofemoral DVT, at the cost of bleeding risk.
Unprovoked VTE and cancer — screen sensibly, not exhaustively
Occult cancer is found in around 5-10% of patients with unprovoked VTE, usually within the first year. The SOME trial answered how hard to look: adding comprehensive CT of the abdomen and pelvis to a limited screening strategy — history, examination, basic bloods, chest radiograph and age-appropriate cancer screening — did not increase cancer detection or improve outcomes. The recommendation is therefore a thorough but limited evaluation with attention to ensuring routine screening is up to date, rather than extensive imaging that generates incidental findings, cost and anxiety without benefit. New unexplained VTE should nonetheless prompt careful review of any symptoms suggesting malignancy.

Key statistics

~30%
recurrence risk at 5 years after stopping anticoagulation for unprovoked VTE
ISTH/ACCP
Risk assessment
systematic VTE risk assessment on admission is the key preventable-harm intervention
NICE/WHO
20-50%
develop post-thrombotic syndrome after proximal DVT — under-recognised and disabling
ISTH/Blood
Low probability only
D-dimer excludes VTE only in low clinical probability — never in high probability
ESC/NICE
5-10%
of unprovoked VTE patients have occult cancer — limited screening suffices (SOME trial)
NEJM 2015
Not in APS
DOACs performed worse than warfarin in triple-positive antiphospholipid syndrome (TRAPS)
Blood 2018

VTE recurrence risk at 5 years after stopping anticoagulation, by provoking factor

Source: ISTH/ACCP. The provoked-unprovoked distinction determines duration of therapy.

Glossary of key terms

Wells score and clinical probability
DiagnosisFor DVT, the Wells score allocates points for active cancer, paralysis or recent immobilisation of the leg, recent bedrest over 3 days or major surgery within 12 weeks, localised tenderness along the deep venous system, entire leg swelling, calf swelling more than 3cm greater than the other side, pitting oedema confined to the symptomatic leg, collateral superficial veins, and previous DVT — with 2 points subtracted if an alternative diagnosis is at least as likely. Two or more points indicates DVT likely; one or fewer, unlikely. For PE, the Wells and revised Geneva scores serve the same function. The point of these scores is not to diagnose but to determine whether D-dimer can be used to rule out, and to prevent the systematic error of applying a rule-out test to a patient whose pre-test probability is too high for a negative result to be meaningful.
Thrombophilia testing — when it changes nothing
HaematologyInherited thrombophilias include factor V Leiden and prothrombin G20210A (common but weak), and deficiencies of antithrombin, protein C and protein S (rare but stronger). Testing is far more often performed than justified, because in most cases the result does not change management: the decision to continue anticoagulation after unprovoked VTE rests on the clinical circumstances and bleeding risk, not on thrombophilia status, and a negative result does not lower recurrence risk. Testing also has pitfalls — protein C and S and antithrombin levels are unreliable during acute thrombosis and on anticoagulation. It is appropriate in selected situations: suspected antiphospholipid syndrome, which genuinely changes drug choice away from DOACs; unusual site thrombosis; and occasionally for family counselling regarding contraception and pregnancy.
Antiphospholipid syndrome
Immunology/HaematologyAn acquired autoimmune thrombophilia defined by persistent antiphospholipid antibodies — lupus anticoagulant, anticardiolipin, anti-beta-2-glycoprotein I, confirmed at least 12 weeks apart — with arterial or venous thrombosis or defined pregnancy morbidity (recurrent early miscarriage, fetal death, or severe pre-eclampsia or placental insufficiency causing premature birth). Triple positivity carries the highest risk. It is the single most important thrombophilia to identify, because it changes management: warfarin rather than a DOAC, since the TRAPS trial found excess arterial events with rivaroxaban in triple-positive patients; consideration of hydroxychloroquine and statin as adjuncts; and, in pregnancy, aspirin with low molecular weight heparin. Catastrophic antiphospholipid syndrome, with multi-organ thrombosis over days, carries high mortality and requires anticoagulation, corticosteroids, plasma exchange or immunoglobulin.
Cancer-associated thrombosis
Oncology/HaematologyMalignancy substantially increases VTE risk through tumour procoagulants, immobility, surgery, central venous catheters and chemotherapy, and VTE is a leading cause of death in cancer patients. Low molecular weight heparin was historically preferred, but the SELECT-D, Hokusai-VTE Cancer and Caravaggio trials established that DOACs are effective alternatives, with the important caveat of increased major and clinically relevant non-major bleeding with edoxaban and rivaroxaban in patients with luminal gastrointestinal and genitourinary malignancy — apixaban showed a more favourable bleeding profile in Caravaggio. Anticoagulation continues while cancer is active or under treatment. Thromboprophylaxis in ambulatory cancer patients is guided by the Khorana score, with intermediate or high scores supporting prophylaxis in the absence of bleeding risk.
Pulmonary embolism risk stratification
Emergency/CardiologyManagement of PE depends on haemodynamic status rather than clot burden. High-risk (massive) PE: sustained hypotension, shock or cardiac arrest — mortality above 15%, requiring systemic thrombolysis, or catheter-directed therapy or surgical embolectomy where thrombolysis is contraindicated. Intermediate-risk (submassive): normotensive but with right ventricular dysfunction on imaging and raised troponin — managed with anticoagulation and close monitoring, since routine thrombolysis in the PEITHO trial reduced haemodynamic decompensation but caused excess major and intracranial bleeding. Low-risk: normotensive with no right ventricular strain and low sPESI score — increasingly managed as outpatients with a DOAC, which is safe in appropriately selected patients and avoids admission entirely.
Travel-related and situational risk
PreventionProlonged immobility during long-haul travel increases VTE risk modestly, with the effect concentrated in flights over approximately 8 hours and in people who already have risk factors — previous VTE, recent surgery, cancer, pregnancy, oestrogen use, obesity or thrombophilia. For most travellers, reassurance plus movement, calf exercises and hydration is sufficient; graduated compression stockings reduce asymptomatic thrombosis and are reasonable for those at higher risk; aspirin is not recommended, and prophylactic anticoagulation is reserved for individuals at particularly high risk. Other situational contexts requiring specific attention: combined hormonal contraception and menopausal hormone therapy, where the route matters — transdermal oestrogen carries substantially lower VTE risk than oral — and pregnancy and the puerperium, when risk is highest in the six weeks after delivery.

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Venous thromboembolism overviewCancer-associated thrombosisAntiphospholipid syndromePregnancy and hormonal VTE riskHospital-acquired VTE preventionTravel-related thrombosis

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