TextbookObstetrics & GynaecologyVenous Thromboembolism in Pregnancy

Venous Thromboembolism in Pregnancy

Venous thromboembolism (VTE) in pregnancy encompasses deep vein thrombosis and pulmonary embolism, representing a leading cause of direct maternal death in the UK.

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Key Facts

  • VTE is the leading direct cause of maternal death in the UK, accounting for approximately 1.13 per 100,000 maternities (MBRRACE-UK)
  • Pregnancy confers a 5-10 fold increased risk of VTE compared to non-pregnant women of the same age
  • LMWH (e.g. enoxaparin 1mg/kg BD or dalteparin 200 units/kg OD) is the treatment of choice in pregnancy
  • RCOG GTG 37a/b guides risk assessment and thromboprophylaxis in pregnancy and the puerperium
  • Risk factors include previous VTE, thrombophilia, BMI >30, immobility, pre-eclampsia, and caesarean section
  • Left leg DVT accounts for 85% of pregnancy-related DVT due to compression of the left iliac vein
  • Compression duplex USS is first-line for DVT; CTPA is preferred over V/Q scan for PE diagnosis in pregnancy
  • Thromboprophylaxis should be considered for 6 weeks postpartum in high-risk women (NICE NG133, RCOG GTG 37a)

Overview

Key Facts

Venous thromboembolism in pregnancy encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE). Pregnancy is a prothrombotic state due to Virchow's triad: hypercoagulability, venous stasis, and endothelial injury. VTE remains the leading direct cause of maternal death in the UK.

Epidemiology

  • Incidence: 1-2 per 1,000 pregnancies
  • Risk is present throughout pregnancy and the puerperium, with highest risk in the first 6 weeks postpartum
  • Accounts for approximately 1.13 deaths per 100,000 maternities in the UK (MBRRACE-UK 2020)
  • DVT is more common antepartum; PE is more common postpartum
  • Left-sided DVT predominates (85%) due to compression of the left common iliac vein by the right iliac artery

Aetiology

  • Hypercoagulability: increased levels of factors VII, VIII, X, fibrinogen, von Willebrand factor; decreased protein S; acquired resistance to activated protein C
  • Venous stasis: compression of pelvic veins by the gravid uterus; hormonally mediated venodilation
  • Endothelial injury: during delivery, particularly caesarean section
  • Additional risk factors: previous VTE, known thrombophilia (Factor V Leiden, prothrombin gene mutation, antithrombin deficiency, antiphospholipid syndrome), obesity (BMI >30), immobility, pre-eclampsia, dehydration, long-haul travel

Pathophysiology

  • Pregnancy induces a physiological hypercoagulable state to minimise blood loss at delivery
  • Venous stasis worsens as the uterus enlarges, compressing the IVC and iliac veins
  • Thrombus formation typically begins in the deep veins of the calf or iliofemoral segment
  • Embolisation to the pulmonary vasculature causes PE with ventilation-perfusion mismatch and, in severe cases, right ventricular failure

Clinical Presentation

Deep Vein Thrombosis

  • Unilateral leg swelling (>2 cm difference in calf circumference)
  • Pain and tenderness, particularly in the calf or thigh
  • Erythema and warmth
  • Left leg affected in 85% of cases
  • Symptoms may overlap with normal pregnancy-related leg swelling

Pulmonary Embolism

  • Sudden-onset dyspnoea (most common symptom)
  • Pleuritic chest pain
  • Tachycardia and tachypnoea
  • Haemoptysis
  • Collapse or cardiac arrest in massive PE

Red Flags

  • Sudden-onset dyspnoea with pleuritic chest pain
  • Haemodynamic instability (massive PE)
  • Oxygen saturations <94%
  • Signs of right heart strain
  • Unilateral leg swelling with pain at any stage of pregnancy or within 6 weeks postpartum

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
CellulitisErythema, warmth, fever, bilateral possibleBlood cultures, inflammatory markers
Ruptured Baker's cystSudden calf pain, posterior knee swellingUSS knee/calf
Musculoskeletal painPositional, mechanical, no swellingClinical assessment
Peripartum cardiomyopathyDyspnoea, orthopnoea, oedema in late pregnancyEchocardiogram, BNP
Amniotic fluid embolismSudden collapse, DIC, during/after deliveryClinical diagnosis
PneumoniaProductive cough, fever, consolidationCXR, sputum culture
Aortic dissectionTearing chest/back pain, BP differentialCT aortogram

Diagnosis / Investigation

Bedside

  • Oxygen saturations and ABG if PE suspected
  • ECG (sinus tachycardia most common; S1Q3T3 pattern, right axis deviation in PE)
  • Chest X-ray (to exclude other causes; often normal in PE)
  • Leg circumference measurements (>2 cm difference is significant)

Bloods

  • FBC, U&Es, LFTs
  • Coagulation screen
  • D-dimer is NOT reliable in pregnancy (physiologically elevated); do not use to exclude VTE
  • Thrombophilia screen (defer to 6 weeks postpartum; not done acutely)

Imaging

  • Compression duplex USS: first-line for suspected DVT; sensitivity >95% for proximal DVT
  • If USS negative but high clinical suspicion: repeat in 3-7 days or perform MR venography
  • CTPA: preferred investigation for PE in pregnancy (RCOG GTG 37b); higher sensitivity and specificity than V/Q scan
  • V/Q scan: alternative if CTPA contraindicated; lower radiation dose to maternal breast tissue

Special Tests

  • Echocardiography if massive PE (right ventricular dilatation, McConnell's sign)
  • MR venography for iliac vein thrombosis if USS equivocal

Management

Non-pharmacological

  • Elevate affected leg and apply graduated compression stockings (after excluding arterial disease)
  • Early mobilisation once anticoagulated
  • Adequate hydration
  • Risk assessment using RCOG VTE risk assessment tool at booking, during admission, and postpartum

Pharmacological

  • LMWH is the treatment of choice:
    • Enoxaparin 1mg/kg BD (treatment dose) or 1.5mg/kg OD
    • Dalteparin 200 units/kg OD or 100 units/kg BD
    • Tinzaparin 175 units/kg OD
  • Continue treatment dose LMWH throughout pregnancy and for at least 6 weeks postpartum (minimum total duration 3 months)
  • Switch to unfractionated heparin around delivery if epidural/spinal planned (shorter half-life)
  • Warfarin is teratogenic in first trimester (avoid); may be used postpartum (safe in breastfeeding)
  • DOACs are contraindicated in pregnancy and breastfeeding
  • Thrombolysis (alteplase 50mg IV) for massive PE with haemodynamic compromise

Surgical/Interventional

  • Surgical embolectomy or catheter-directed thrombolysis for life-threatening PE unresponsive to medical therapy
  • IVC filter in rare cases where anticoagulation is contraindicated and recurrent PE

Referral Criteria

  • Immediate referral to obstetric medicine/haematology for confirmed VTE
  • Anaesthetic review for delivery planning (timing of LMWH cessation)
  • Thrombophilia screening at 6 weeks postpartum
  • Postnatal review to determine duration of anticoagulation

Prognosis

  • Maternal mortality from PE: approximately 1-2% with treatment
  • Case fatality rate for untreated PE: 30%
  • Recurrence risk in subsequent pregnancies: 5-12% (higher with thrombophilia)
  • Post-thrombotic syndrome develops in 20-50% of DVT cases
  • Long-term anticoagulation may be required if recurrent VTE or high-risk thrombophilia
  • With appropriate thromboprophylaxis, risk of recurrence is significantly reduced

Other Relevant Information

RCOG VTE Risk Assessment

Risk LevelCriteriaThromboprophylaxis
High riskPrevious VTE (except single provoked)LMWH from first trimester + 6 weeks postpartum
Intermediate≥3 risk factors antenatallyLMWH from 28 weeks + 6 weeks postpartum
Lower risk<3 risk factorsMobilisation, hydration

LMWH Dosing for Thromboprophylaxis (Weight-Based)

WeightEnoxaparinDalteparinTinzaparin
<50 kg20mg OD2,500 units OD3,500 units OD
50-90 kg40mg OD5,000 units OD4,500 units OD
91-130 kg60mg OD7,500 units OD7,000 units OD
>130 kg0.5mg/kg OD75 units/kg OD75 units/kg OD

Peripartum LMWH Management

SituationAction
Prophylactic LMWHStop ≥12 hours before regional anaesthesia
Treatment LMWHStop ≥24 hours before regional anaesthesia
UFH infusionStop 4-6 hours before, check APTT
Restart postpartum≥4 hours after spinal removal