Venous Thromboembolism and Pulmonary Vascular Disease — UKMLA-oriented extension, mapped to the GMC content map applying from September 2026. Emergencies are recognition-and-escalation teaching: follow local protocols and current specialist guidance.
11.01 Deep Vein Thrombosis: Presentation and Risk
DVT results from venous stasis, endothelial injury and hypercoagulability (Virchow triad). Risk factors include recent surgery, immobilisation, active cancer, prior VTE, oestrogen exposure, pregnancy and inherited thrombophilia. Presentation usually comprises unilateral swelling, calf or thigh tenderness, warmth and erythema, but these are non-specific and cellulitis or ruptured Baker cyst may resemble DVT. Examine for circulatory compromise and assess for coexisting PE symptoms.
11.02 DVT: Wells Score and Diagnostic Pathway
Use the two-level DVT Wells score to estimate probability: ≥2 = likely; ≤1 = unlikely. For likely DVT, arrange proximal leg vein ultrasound within 4 hours if possible; if delayed, NICE directs D-dimer testing, interim therapeutic anticoagulation if suitable, and scanning within 24 hours. For unlikely DVT, use D-dimer first and scan if positive. A negative initial proximal scan with a positive D-dimer requires a repeat proximal scan after 6–8 days under the NICE pathway.
MLA trap: D-dimer is useful to exclude VTE in a suitable low-probability patient, not to establish the diagnosis when positive.
11.03 Pulmonary Embolism: Presentation and Severity
PE causes ventilation–perfusion mismatch, hypoxaemia, increased pulmonary vascular resistance and sometimes acute RV failure. Typical features are sudden dyspnoea, pleuritic pain, tachycardia, haemoptysis or syncope; massive obstruction may cause obstructive shock, raised JVP and cardiac arrest. ECG may show sinus tachycardia or RV strain, but a normal ECG does not exclude PE; chest radiography is often non-diagnostic. Assess clinical severity, oxygenation, haemodynamics and alternative causes such as ACS, pneumonia and pneumothorax.
11.04 PE: Wells Score, PERC, D-dimer and Imaging
Use the two-level PE Wells score: >4 = PE likely and proceed to urgent CT pulmonary angiography (CTPA), or appropriate V/Q imaging when CT contrast/radiation issues require it. If PE is unlikely (≤4), use D-dimer and image if positive; consider PERC only when pretest clinical suspicion is genuinely low and criteria apply. Age-adjusted D-dimer thresholds may be considered for people over 50 according to the validated assay/pathway. If definitive imaging is delayed, consider interim therapeutic anticoagulation in the NICE pathway after bleeding-risk assessment.
11.05 Anticoagulation and Duration after DVT or PE
For confirmed proximal DVT or PE, NICE generally recommends apixaban or rivaroxaban as initial options, except when there are contraindications or particular situations such as severe renal impairment, pregnancy or triple-positive antiphospholipid syndrome. Treat for at least three months, then reconsider extension based on provoked versus unprovoked event, bleeding risk and patient preferences; active cancer and persistent risk factors may alter the plan. Document renal function, body weight, drug interactions and anticoagulant counselling, including bleeding warning signs and missed doses.
11.06 High-Risk PE and Thrombolysis
High-risk PE is defined by haemodynamic instability such as persistent hypotension, obstructive shock or cardiac arrest, not clot size alone. It requires resuscitation, urgent senior/PERT or critical-care input and consideration of systemic thrombolysis when appropriate; catheter intervention or embolectomy may be considered in selected cases. Stable patients with RV strain require monitored risk stratification rather than routine thrombolysis because the bleeding risk may outweigh the benefit. Pregnancy, previous intracranial haemorrhage and recent surgery modify treatment options and require specialist decisions.
11.07 Hospital and Perioperative VTE Prevention
Assess VTE and bleeding risk on admission and when clinical circumstances change, following NICE NG89 and local policy. Promote mobilisation and hydration when appropriate; pharmacological prevention with LMWH or an alternative depends on the balance of risks, kidney function and procedure. Mechanical measures may help when anticoagulants are contraindicated, but avoid unsuitable stockings in significant PAD. Discharge documentation should explain intended prophylaxis duration and warning symptoms of DVT/PE.
11.08 Chronic Venous Insufficiency and Varicose Veins
Valvular reflux and calf-pump dysfunction cause ambulatory venous hypertension, leading to ankle oedema, aching, varicose veins, skin pigmentation, lipodermatosclerosis and often shallow exudative gaiter-region ulcers. Examine with the patient standing when possible and assess pedal pulses/ABPI before compression. Duplex ultrasound identifies reflux and helps plan endovenous ablation, foam sclerotherapy or surgery for symptomatic varicose veins. Contrast with arterial ulcers, which are typically painful, distal and associated with impaired perfusion.
11.09 Post-thrombotic Syndrome and Chronic Thromboembolic Disease
After DVT, damaged venous valves and residual obstruction can cause chronic swelling, heaviness, hyperpigmentation and ulceration. A minority of patients after PE develop chronic thromboembolic pulmonary hypertension (CTEPH), with persistent dyspnoea, exercise intolerance and RV strain despite anticoagulation. Persistent symptoms after PE warrant assessment rather than simply labelling the patient deconditioned; ventilation–perfusion scanning is sensitive for chronic thromboembolic obstruction. Specialist therapies include pulmonary endarterectomy, balloon pulmonary angioplasty and selected medicines.
11.10 Pulmonary Hypertension: Classification and Assessment
Pulmonary hypertension is elevated pulmonary arterial pressure measured by right-heart catheterisation; causes include pulmonary arterial hypertension (group 1), left-heart disease (2), lung disease/hypoxia (3), chronic thromboembolic obstruction (4), and multifactorial mechanisms (5). Typical symptoms are progressive breathlessness, fatigue, syncope and peripheral oedema with a loud P2 or RV heave. Echocardiography estimates probability and assesses RV function, but cannot definitively establish type or haemodynamic classification. Treat the underlying disorder and refer suspected PAH/CTEPH for expert evaluation; PAH vasodilators are not interchangeable with routine therapy for left-heart-related PH.
11.11 Superior Vena Cava Obstruction
SVCO develops when extrinsic compression or thrombosis impairs upper-body venous drainage, most commonly from intrathoracic malignancy or central venous devices. Patients develop facial/neck/upper-limb swelling, venous distension, cough and dyspnoea, sometimes worse on bending forward; stridor or neurological compromise indicates an emergency. Raise the head of the bed, assess airway and oxygenation, and obtain urgent imaging and oncology/respiratory/vascular advice. Treatment depends on cause and may involve endovascular stenting, oncological therapy or anticoagulation for thrombotic obstruction.