We compared 41 patients with angiographic proof of pulmonary embolism and clinical signs of pulmonary infarction (as evidenced by an infiltrate on x-ray study and pleuritic pain in the area of the embolus) with 24 patients with pulmonary embolism but without infarction. Only 18 of the 41 patients with pulmonary infarction had associated heart disease. Pulmonary infarction was uncommon when emboli obstructed central arteries but frequent when distal arteries were occluded. Follow-up x-ray examination showed that the infiltrates resolved in the patients with pulmonary infarction without heart disease, but persisted when heart disease was present. We suggest that obstruction of distal arteries results in pulmonary hemorrhage owing to an influx of bronchial arterial blood at systemic pressure. Hemorrhage causes symptoms and x-ray changes usually attributed to pulmonary infarction. However, hemorrhage resolves without infarction in patients without, but progresses to infarction in those with, heart disease. (N Engl J Med 296:1431–1435, 1977) When pulmonary embolism occurs, it may or may not cause pulmonary infarction. Virchow1 was the first to realize that necrosis of the lung may occur in areas distal to pulmonary embolic obstruction. Hampton and Castleman described pulmonary infarction with particular clarity.2 They demonstrated that areas distal to embolic obstruction of a pulmonary artery may show a sequence that begins with hemorrhage into, and edema of, the alveoli. Within 24 to 48 hours, the extravasated red cells begin to break down into hemosiderin. At this point, actual necrosis of the alveolar walls and the surrounding lung parenchyma begins, and “true” infarction.
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