Pulmonary Embolism — Wells Score, S1Q3T3, CTPA and Management

Acute pulmonary embolism (PE) occurs when a blood clot that formed elsewhere blocks the pulmonary arteries. Most emboli start as a deep vein thrombosis (DVT) of the lower limb; PE and DVT together make up venous thromboembolism (VTE). Rarely the embolus is air, fat or tumour cells. Because the symptoms (dyspnoea, chest pain, syncope) overlap with many cardiac and respiratory diseases, PE is easy to miss, which is why exams test the scoring and diagnostic pathway more than the textbook description.

Risk factors follow Virchow's triad — hypercoagulability, venous stasis and endothelial injury (see Virchow's triad). Genetic causes include factor V Leiden, prothrombin gene mutation, protein C or S deficiency and hyperhomocysteinaemia. Acquired causes include bed rest of more than 3 days, travel of more than 4 hours, recent orthopaedic surgery, malignancy, central venous catheters, pregnancy and the postpartum period, oral contraceptives, hormone replacement, smoking and obesity. Pancreatic, haematological, lung, gastric and brain cancers carry the highest VTE risk.

Emboli are usually multiple, more often in the lower lobes, and bilateral involvement is common. A large embolus lodges at the main pulmonary artery bifurcation as a saddle embolus; smaller peripheral emboli can cause pulmonary infarction (intra-alveolar haemorrhage). Obstruction leaves ventilation unchanged but reduces perfusion, creating dead-space ventilation and a V/Q mismatch with hypoxaemia. Mediators such as serotonin add vasospasm, and inflammatory mediators stimulate respiratory drive, so many patients hyperventilate and develop hypocapnia with respiratory alkalosis.

The haemodynamic effect decides the outcome. Pulmonary vascular resistance rises from mechanical obstruction plus hypoxic vasoconstriction; pulmonary artery pressure climbs once more than 30–50% of the pulmonary arterial bed is occluded. The right ventricle dilates against the raised afterload, the septum bows into the left ventricle, left ventricular filling falls, cardiac output drops and the patient becomes hypotensive. Acute right ventricular failure is the primary cause of death in severe PE.

• Symptoms: dyspnoea, pleuritic chest pain, cough, haemoptysis, syncope — all non-specific.
• Signs: tachypnoea and tachycardia (common but non-specific), calf swelling or tenderness, raised JVP, a loud P2, right-sided gallop, right ventricular parasternal heave.
• Sudden collapse: PE is a recognised cause of sudden cardiac arrest (about 8%).
• Chronic sequel: persistent dyspnoea in the first 3 months to 2 years should prompt a search for chronic thromboembolic pulmonary hypertension (CTEPH), which affects up to 5% of patients.

The Wells score converts bedside findings into a pre-test probability so you can choose the right test. It is the most examined number in PE.

PERC (Pulmonary Embolism Rule-out Criteria) is used in the emergency department for patients whose clinical suspicion is already low. If all eight are met, the likelihood of PE is low enough that no further testing is needed: age under 50, heart rate under 100, oxygen saturation of 95% or more, no haemoptysis, no oestrogen use, no prior DVT/PE, no unilateral leg swelling, and no surgery or trauma needing hospitalisation in the last 4 weeks.

Biomarkers help prognosis, not diagnosis. Troponin is raised in 30–50% of moderate to large PE and predicts deterioration; BNP and NT-proBNP rise with right ventricular dysfunction. Neither confirms or excludes PE.

Choose the next step from the pre-test probability and the patient's haemodynamic state.

• Pregnancy and PE: V/Q scan is preferred when the chest X-ray is normal.
• Renal failure or contrast anaphylaxis: V/Q scan.
• Abnormal chest X-ray: V/Q results become unreliable, so go to CTPA.
• MR angiography: not first-line (low sensitivity, availability, many inconclusive scans).

First classify by haemodynamics. Haemodynamically unstable PE (formerly 'massive') means systolic BP under 90 mmHg, a fall of 40 mmHg or more from baseline, or hypotension needing vasopressors. 'Massive' refers to the effect, not the clot size. Stable PE ranges from small, low-risk emboli to intermediate-risk (submassive) PE, which causes right ventricular dysfunction without hypotension.

The PESI and simplified PESI (sPESI) predict 30-day mortality and identify patients who can be treated as outpatients. sPESI scores 1 point each for age over 80, cancer, chronic heart failure or lung disease, pulse of 110 or more, systolic BP under 100 and oxygen saturation under 90%.

Anticoagulation is the mainstay of treatment. For suspected PE it is started before imaging in stable patients with high clinical suspicion, and also in intermediate suspicion if imaging will be delayed. In low suspicion, wait for imaging if it can be done within 24 hours.

• Choice of anticoagulant: LMWH or fondaparinux are preferred (less major bleeding and less heparin-induced thrombocytopaenia). Unfractionated heparin is used in haemodynamic instability, when reperfusion may be needed, and in renal impairment. Oral options are DOACs or vitamin K antagonists. See heparin, warfarin and DOACs.
• Unstable PE: primary reperfusion, usually systemic thrombolysis. Be cautious with large volumes of IV fluid: aggressive resuscitation can over-distend the failing right ventricle and reduce output.
• Thrombolysis timing: preferred within 48 hours of symptom onset, still beneficial up to 14 days. The PEITHO trial showed fewer haemodynamic collapses in stable intermediate-risk PE but more major bleeding.
• Absolute contraindications to thrombolysis: prior intracranial haemorrhage, known structural intracranial vascular disease or malignant intracranial tumour, ischaemic stroke within 3 months, suspected aortic dissection, active bleeding or bleeding diathesis, recent brain or spinal surgery, recent significant head or facial trauma.
• If thrombolysis is contraindicated or fails: catheter-directed therapy (up to about 87% success in studies) or surgical pulmonary embolectomy.
• IVC filter: only for VTE with an absolute contraindication to anticoagulation, or recurrent VTE despite anticoagulation. Use a retrievable filter and anticoagulate once safe.