Pulmonary Embolism

Pulmonary Embolism (PE) is a critical diagnosis in UK finals, often presenting as an acute medical emergency. It's a major cause of sudden death, particularly in hospitalised patients. The vast majority of PEs originate from Deep Vein Thrombosis (DVT), usually in the lower limbs or pelvis, driven by Virchow's Triad: endothelial injury, hypercoagulability, and venous stasis. Key risk factors include recent surgery, malignancy, immobility, pregnancy, and hormonal contraception/HRT. Clinical presentation is highly variable, from asymptomatic to sudden cardiovascular collapse. The diagnostic pathway is crucial for exams: use the Wells Score for clinical probability. If PE is 'unlikely' (Wells score ≤4), a D-dimer test can rule out PE if negative. If PE is 'likely' (Wells score >4) or D-dimer is positive, urgent CT Pulmonary Angiography (CTPA) is the gold standard. For patients with contraindications to CTPA (e.g., severe renal impairment, contrast allergy), a Ventilation/Perfusion (V/Q) scan is the alternative. In pregnancy, a lower limb duplex ultrasound is often the initial step to minimise radiation exposure, followed by V/Q scan or CTPA if DVT is not found. Haemodynamically unstable patients (systolic BP <90 mmHg) with suspected PE require immediate assessment, often with bedside echocardiography showing right heart strain, to guide emergency thrombolysis. First-line treatment for stable PE is a Direct Oral Anticoagulant (DOAC) for at least 3 months. The duration of anticoagulation depends on whether the PE was provoked or unprovoked, and the presence of ongoing risk factors like malignancy.

PE occurs when a thrombus dislodges from a peripheral vein, travels through the right heart, and lodges in the pulmonary arterial tree. A large 'saddle embolus' can block the main pulmonary artery bifurcation, leading to acute right heart failure and cardiogenic shock. Pathophysiologically, PE causes a ventilation-perfusion (V/Q) mismatch: areas of the lung are ventilated but not perfused, leading to increased alveolar dead space and hypoxaemia. This also triggers reflex bronchoconstriction and vasoconstriction in the affected lung segments. Massive PE causes an abrupt increase in pulmonary vascular resistance, leading to acute right ventricular (RV) pressure overload. The RV dilates, causing interventricular septal bowing into the left ventricle, impairing left ventricular filling (reduced preload) and leading to systemic hypotension and cardiogenic shock. Release of vasoactive mediators (e.g., serotonin, thromboxane A2) from platelets within the thrombus further exacerbates pulmonary vasoconstriction.

PE should be considered in any patient presenting with acute dyspnoea, pleuritic chest pain, or unexplained syncope. Other common symptoms include cough and haemoptysis (suggests larger emboli). Clinical signs include tachypnoea, tachycardia, and low-grade fever. In severe PE, look for signs of right heart strain: raised JVP, loud P2 heart sound, and hypotension. Unilateral leg swelling and tenderness may indicate an underlying DVT. Important differentials include myocardial infarction, pneumothorax, pneumonia, and acute exacerbation of asthma/COPD. Early recognition and management are crucial to prevent mortality and long-term complications like Chronic Thromboembolic Pulmonary Hypertension (CTEPH), which can develop in up to 4% of survivors. The Pulmonary Embolism Severity Index (PESI or sPESI) helps identify low-risk patients who may be suitable for outpatient management, a common SBA topic.

Bedside: ECG (most common finding is sinus tachycardia; look for T-wave inversion in V1-V4, RBBB, or the classic but rare S1Q3T3 pattern indicating right heart strain). SpO2 (often reduced). Bloods: D-dimer (age-adjusted cut-offs for patients >50 years are crucial for interpretation: age x 10 ng/mL). Troponin and Pro-BNP are useful biomarkers of right ventricular strain and prognosis. FBC, U&Es, and clotting screen are standard. Imaging: CTPA is the definitive diagnostic test. V/Q scanning is an alternative if CTPA is contraindicated (e.g., severe renal impairment, contrast allergy, or in pregnancy to reduce maternal breast radiation). Chest X-ray is often normal in PE, but may rarely show a Westermark sign (oligemia distal to embolus) or Hampton's hump (wedge-shaped pleural-based opacity). Lower limb duplex ultrasound is indicated if DVT is suspected or as an initial step in pregnancy. Echocardiography can show signs of right ventricular dysfunction, such as McConnell's sign (RV free wall hypokinesis with apical sparing).

Acute Management: Administer oxygen to maintain SpO2 >94%. Provide IV fluids cautiously to avoid RV overload. If haemodynamically unstable (systolic BP <90 mmHg), immediate thrombolysis (e.g., Alteplase) is indicated, or surgical embolectomy in selected cases. Anticoagulation (Stable PE): Initiate immediately if PE is suspected and diagnosis is pending. First-line for most stable patients are Direct Oral Anticoagulants (DOACs) such as Apixaban or Rivaroxaban. Second-line or in specific circumstances (e.g., severe renal impairment, drug interactions) is LMWH followed by Warfarin (target INR 2-3). For malignancy-associated PE, DOACs are generally preferred over LMWH. In pregnancy, LMWH (e.g., Dalteparin) is the anticoagulant of choice, continued throughout pregnancy and for 6 weeks postpartum. Duration of anticoagulation: 3 months for provoked PE (e.g., post-surgery). Consider indefinite anticoagulation for unprovoked PE, recurrent PE, or in patients with persistent risk factors (e.g., active cancer, thrombophilia).