1977
DOI: 10.1056/nejm197706232962503
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Pulmonary Embolism, Pulmonary Hemorrhage and Pulmonary Infarction

Abstract: 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 tha… Show more

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Cited by 200 publications
(84 citation statements)
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“…Cavitary parenchymal nodules may be caused by septic occlusion of small peripheral PA branches [186]. Pulmonary infarction is uncommon when the emboli obstruct the central arteries but is frequent when distal arteries are occluded [187]. This may be explained by collateral flow from the bronchial arterial circulation that enters the PA distal to the site of an obstruction [186].…”
Section: Pathophysiologymentioning
confidence: 99%
“…Cavitary parenchymal nodules may be caused by septic occlusion of small peripheral PA branches [186]. Pulmonary infarction is uncommon when the emboli obstruct the central arteries but is frequent when distal arteries are occluded [187]. This may be explained by collateral flow from the bronchial arterial circulation that enters the PA distal to the site of an obstruction [186].…”
Section: Pathophysiologymentioning
confidence: 99%
“…14). Initial wurde es bei der invasiven pulmonalen Aspergillose als Manifestation perifokaler Hämorrhagien beschrieben [21], es ist jedoch unspezifisch und kommt auch bei Hämorrhagien anderer Ursache [22] wobei die Basis der Pleura anliegt und die Spitze in Richtung des Hilus gerichtet ist [23,24]. Die radiologisch sichtbaren Verände-rungen entsprechen überwiegend pulmonalen Hämorrhagien infolge des Infarkts, eventuell auch einer Nekrose.…”
Section: Halozeichenunclassified
“…At about 24 to 27 hours the natural evolution leads to surfactant loss and collapse of the alveoli consequently with the appearance and progression of lamellar atelectasis and to local edema with alveolar infiltrates that look like typical pneumonia. The reperfusion of the affected territory makes both processes to disappear after a few days (19).…”
Section: Acute Pementioning
confidence: 99%