Pulmonary Infarction

Pulmonary infarction is necrosis of lung tissue caused by occlusion of the pulmonary arterial supply, most often by pulmonary embolism. It occurs in 10 to 30% of patients with pulmonary embolism, usually after embolism to small distal arteries, with weak collateral bronchial supply.

Risk factors are distal emboli, chronic heart failure or raised left atrial pressure, mitral stenosis, chronic lung disease (loss of bronchial collateral supply), older age, smoking and sickle cell disease. Other causes are septic emboli, fat and tumour emboli, vasculitis (granulomatosis with polyangiitis), pulmonary vein thrombosis or torsion, lung transplant complications, in situ thrombosis and sickle cell crisis.

Pathophysiology. Occlusion of a small peripheral artery causes ischaemia of the supplied segment. If the collateral bronchial supply is poor, necrosis occurs, followed by alveolar haemorrhage into the infarct, a wedge shaped haemorrhagic lesion abutting the pleura, with pleural inflammation. Infarcts then organise to a scar, or may cavitate or become infected.

Pleuritic chest pain (the commonest), dyspnoea, cough, haemoptysis (up to a third), low grade fever, leucocytosis and a pleural rub. Signs of the underlying pulmonary embolism and deep vein thrombosis (leg swelling) may be present. Small pleural effusions (often bloody) are common. The features are milder than massive embolism, and the patient is usually haemodynamically stable.

Haemodynamic instability, syncope, severe hypoxaemia or massive haemoptysis needs urgent assessment since the embolus burden may be large.

• CT pulmonary angiography: the test of choice, showing the occluded artery and a peripheral wedge shaped, pleura based consolidation with a convex border (Hampton hump), central lucency (the "bubbly" sign from preserved aerated lung), the "reversed halo" sign (ground glass surrounded by consolidation), and absent enhancement. A feeding vessel sign is seen in septic emboli.
• Chest radiograph: peripheral wedge shaped opacity (Hampton hump, in up to 20 to 25%), pleural effusion, elevated hemidiaphragm. It may be normal.
• Assessment of pulmonary embolism: D-dimer (low pretest probability), Wells score, leg compression ultrasound and echocardiography.
• Blood tests: full blood count, troponin and NT-proBNP for risk, and thrombophilia screening if unprovoked at a young age.
• Pleural fluid (if tapped) shows an exudate with blood.
• Features of infarct infection (cavitation, air fluid levels, persistent fever) need microbiology.

Differential diagnosis.

• Pneumonia (consolidation with fever and purulent sputum)
• Organising pneumonia
• Lung cancer or metastasis
• Septic emboli
• Pulmonary vasculitis or haemorrhage
• Pulmonary contusion

• Anticoagulation using the pulmonary embolism regimen: apixaban 10 mg twice daily for 7 days, then 5 mg twice daily, or rivaroxaban 15 mg twice daily for 21 days then 20 mg once daily with food. If DOAC cannot be used: enoxaparin 1 mg/kg twice daily (or 1.5 mg/kg daily) overlapped with warfarin to INR 2 to 3 for at least 5 days. Duration at least 3 months, and extended for unprovoked disease or persistent risk.
• Analgesia for pleuritic pain: paracetamol 1 g every 6 hours (maximum 4 g daily), and ibuprofen 400 mg every 8 hours with food in the absence of bleeding risk (caution with anticoagulation). Opioid (codeine 30 to 60 mg every 6 hours) for severe pain.
• Oxygen for hypoxaemia (target saturation 94 to 98%).
• Haemoptysis is not a contraindication to anticoagulation unless severe: monitor, and consider tranexamic acid 500 mg to 1 g orally three times daily for short use only when major bleeding is a risk, with specialist advice.
• Thrombolysis for haemodynamic instability (alteplase 100 mg over 2 hours, or 10 mg bolus then 90 mg over 2 hours), not for the infarct itself. Catheter directed or surgical embolectomy for unstable patients with contraindication to lysis.
• Infected infarct or abscess: antibiotics (amoxicillin-clavulanate 625 mg three times daily or 1.2 g intravenously three times daily for 7 to 14 days), with drainage when large.
• Large effusion: therapeutic thoracentesis (up to 1.5 L).
• Inferior vena cava filter only when anticoagulation is contraindicated.
• Treat underlying causes: heart failure, sickle cell crisis (oxygen, hydration, exchange transfusion in severe cases), and vasculitis.

Complications and prognosis. Infarcts resolve over weeks to months, leaving a linear scar or pleural thickening, and sometimes cavitation, infection, empyema or bloody effusion. Prognosis depends on the underlying embolism and risk class.

Monitoring. Review at 4 to 6 weeks and 3 months, with repeat radiograph or CT to confirm resolution, assessment for chronic thromboembolic disease if breathlessness persists (echocardiography and ventilation perfusion scan), and anticoagulation review at 3 months.

Referral and escalation. Refer to a pulmonary embolism response team or respiratory service for unstable or high risk disease, and to haematology for recurrent or unprovoked events.