Pulmonary embolism-infarct is ischemic necrosis that develops in the distal lung parenchyma as a result of thromboembolic occlusion of the pulmonary artery. Approximately 10-15% of pulmonary embolisms are complicated by infarction — dual blood supply (pulmonary + bronchial artery) usually provides collateral circulation. Infarction is located in the lower lobes and peripherally. Hampton hump (wedge-shaped pleural-based opacity) is the classic radiological finding. Filling defect in pulmonary artery branches on CT angiography is diagnostic.
Age Range
30-80
Peak Age
55
Gender
Equal
Prevalence
Uncommon
Pulmonary embolism usually originates from deep vein thrombosis (DVT) of the lower extremities — thrombus detaches and embolizes to pulmonary arteries. Pulmonary arteries show terminal branching and perfusion stops at the distal occlusion site. Normally, bronchial arteries provide collateral blood supply and infarction is prevented. However, in heart failure, chronic lung disease, or small artery occlusions, collateral circulation is insufficient and infarction develops. The infarct area is hemorrhagic in character — blood seeps into parenchyma and appears as peripheral wedge-shaped consolidation (Hampton hump) on CT. Pleural-based location results from the visceral pleura being in the bronchial artery supply zone — infarction starts peripherally and progresses centrally. Westermark sign reflects focal oligemia distal to the embolic occlusion with decreased perfusion.
Pleural-based, wedge (triangular) shaped peripheral consolidation. Base at the visceral pleura, apex pointing toward the hilum. Specific to hemorrhagic infarction following pulmonary arterial occlusion. Usually in lower lobes, showing homogeneous density, and may be accompanied by ground-glass halo in the acute phase.
Hypodense filling defect in pulmonary artery branches on CT pulmonary angiography (CTPA). In acute embolism, thrombus is centrally located and surrounded by contrast ('polo mint sign' axial, 'railway track sign' coronal). Thrombus is not adherent to the artery wall.
Report Sentence
Acute thromboembolic filling defect is noted in the right/left pulmonary artery __ branch/branches on CT pulmonary angiography.
Pleural-based, wedge (triangular) shaped peripheral consolidation — Hampton hump. Base is at the pleural surface, apex points toward the hilum. Usually in lower lobes, with homogeneous soft tissue attenuation. Reflects hemorrhagic consolidation of infarction.
Report Sentence
A pleural-based, wedge-shaped peripheral consolidation (Hampton hump) is noted in the right/left lower lobe, consistent with pulmonary infarction.
Focal oligemia distal to embolic occlusion — decreased vascularity and increased translucency. The affected segment/lobe appears more lucent compared to the other side on CT. More conspicuous in large artery occlusions.
Report Sentence
Focal oligemia is noted distal to the embolic occlusion (Westermark sign), suggesting perfusion defect in the corresponding segment.
Right ventricular (RV) dilatation (RV/LV ratio >1) and bowing of the interventricular septum toward the left side in massive pulmonary embolism. These findings indicate acute right heart strain/failure and are poor prognostic indicators.
Report Sentence
Right ventricular dilatation (RV/LV ratio: __) and leftward bowing of the interventricular septum are noted, consistent with acute right heart strain.
Infarct evolution: homogeneous consolidation in acute phase → shrinkage and cavitation may develop in subacute phase → linear scar or focal fibrosis in chronic phase. Cavitation increases risk of superinfection (abscess).
Report Sentence
Shrinkage/cavitation/scar development is noted in the consolidation previously consistent with infarction, compatible with infarct evolution.
Ipsilateral pleural effusion frequently accompanies pulmonary embolism-infarct (30-50%). Usually small to moderate in size and exudative. May be hemorrhagic effusion.
Report Sentence
Small/moderate pleural effusion is noted ipsilateral to the infarction area.
Criteria
0-7 days: pleural-based wedge-shaped consolidation, homogeneous density, ground-glass halo, acute filling defect in pulmonary artery
Distinct Features
Anticoagulant therapy should be initiated. In massive PE, thrombolytic therapy or catheter-directed thrombectomy is considered. Infarct area may enlarge in the first 48-72 hours.
Criteria
1-4 weeks: consolidation begins to shrink, cavitation may develop, 'melting ice sign', thrombus begins to organize
Distinct Features
Anticoagulant therapy continues. If cavitation develops, monitoring for superinfection is needed. 'Melting ice sign' — shrinkage of infarct area from periphery to center — supports infarct diagnosis.
Criteria
>4 weeks: linear scar or focal fibrosis, parenchymal band, pleural thickening, organized thrombus or recanalization
Distinct Features
Anticoagulant therapy duration is determined by clinical status (usually 3-6 months). Risk of chronic thromboembolic pulmonary hypertension (CTEPH) should be evaluated — pulmonary artery pressure monitoring by echocardiography is recommended.
Distinguishing Feature
Adenocarcinoma usually presents as a nodule/mass, is spiculated, and enhances. Pulmonary infarct shows pleural-based wedge-shaped consolidation, concurrent pulmonary artery filling defect is present, and shrinks on follow-up (melting ice sign).
Distinguishing Feature
Organizing pneumonia shows peripheral consolidation and ground-glass opacities, migratory pattern may be seen, and air bronchograms are prominent. Pulmonary infarct is pleural-based wedge-shaped with concurrent filling defect. Pulmonary artery filling defect is not expected in organizing pneumonia.
Distinguishing Feature
Lung abscess is a round cavitary lesion with thick smooth wall and air-fluid level. Pulmonary infarct cavitation may be irregular and concurrent filling defect is present. Abscess is usually accompanied by fever and leukocytosis.
Urgency
emergentManagement
medicalBiopsy
Not NeededFollow-up
3-monthPulmonary embolism is a medical emergency — anticoagulant therapy should be initiated immediately. In massive PE (hemodynamic instability, RV failure), thrombolytic therapy or catheter-directed thrombectomy is indicated. In submassive PE (RV dilatation, troponin elevation), close monitoring is required. Anticoagulant duration is 3 months for first provoked PE episode, long-term/lifelong for unprovoked or recurrent PE. Echocardiographic evaluation is recommended at 3-6 months for CTEPH risk assessment. DVT source should be investigated (lower extremity venous Doppler US).
Anticoagulation therapy is the mainstay. Thrombolytic therapy or mechanical thrombectomy may be needed for massive PE. Infarct area may organize and leave a scar over time. Underlying DVT should be investigated.