Contents
Lung tissue infarction due to thrombus lodging in segmental and subsegmental vessels usually in the setting of pulmonary embolism (PE).
History:
Hampton and Castleman provided the first accurate description of the radiologic appearance of pulmonary infarction. In their series of 370 patients with autopsy-proven pulmonary embolism (PE), pulmonary infarction was found in nearly 70%. The frequency of infarction was the highest among the patients who came to death with a history of longstanding heart failure. Ever since then, pulmonary venous hypertension, secondary to heart failure, has been regarded as a predisposing risk factor for pulmonary infarction in the setting of acute PE. Elevated pulmonary venous pressure is believed to hinder collateral blood flow via broncho-pulmonary anastomoses distal to embolized regions.
Aetiology
Pulmonary embolism (PE) (M/C)
PI occurs in nearly ⅓ of patients with PE, usually a small PE
Other causes:
- Infection, malignancy, surgical iatrogenesis, amyloidosis, sickle cell disease, vasculitis
Risk factors:
- Smoking
- Pulmonary venous hypertension
- Heart failure
Clinical features
- Dyspnea
- Chest pain
- Swelling/pain in unilateral lower extremity
- Fever
- Hemoptysis
Diagnosis
X-ray:
- Hampton’s hump (wedge-shaped consolidation at the lung periphery)
- Westermark’s sign (radiographic oligemia or increased lucency)
- Fleischer sign (prominent pulmonary artery)
- Atelectasis or focal consolidation
CT scan:
- Feeding vessel or “vessel sign” with central lucency and a semicircular shape
- No air bronchogram
Management
In addition to supportive management, treatment is guided by the underlying condition that has led to the PI.
Anticoagulant therapy:
- IV Heparin or LMW heparin (inpatient management)
- Warfarin or other oral-anticoagulants (outpatient management)
In patients with hemodynamic instability due to a sub-massive or massive PE:
- Catheter-based fibrinolytics
- Systemic fibrinolytics
- Surgical interventions