Pulmonary Artery Thrombosis: Roentgen Manifestations

Abstract

Thrombosis of the pulmonary arterial tree may result in the production of a pulmonary infarct, which customarily involves only a portion of the area supplied by the thrombosed vessel, or extensive thrombosis may be present without causing pulmonary infarction. The roentgenographic detection of pulmonary infarct is a frequent problem for the roentgenologist. In the absence of infarction, the detection of vascular changes in the lung resulting from embolism or thrombosis may sometimes be possible. When infarction is present, there is additional cause to suspect and search for evidence of thrombosis in the pulmonary arteries. Although an extensive literature exists on the pathologic and clinical aspects of pulmonary thrombosis, only a few authors have concerned themselves with its roentgen manifestations. Thrombosis in the pulmonary arterial tree, especially in the smaller vessels, is relatively frequent; as a rule it does not result in infarction (16, 24, 35, 36). Extensive studies have been made by Møller (24), who found arterial thrombosis in 29 per cent of 176 postmortem examinations, and by Brenner (6), who reported an incidence of 28 per cent in 100 consecutive routine autopsies. The most common etiologic factor in pulmonary arterial thrombosis is embolism from the systemic veins or from the right heart. Infection (10, 15, 28, 31), phlebothrombosis and thrombophlebitis (1, 6, 8, 10, 20), cardiac disease (28), age, and surgery (1, 8), all contribute to the formation of pulmonary thrombi. Thrombosis may occur in situ in the pulmonary arterial tree in (a) cases of parenchymal disease of the lung such as tuberculosis (21, 26, 28), silicosis (28), sarcoidosis (32), chronic (28) or acute (11) infection, and carcinoma (3), and (b) in cases of altered circulation of the pulmonary tree. The latter include rheumatic heart disease (8, 28), tetralogy of Fallot (27), interauricular septal defect (34), patent ductus (14, 29), Eisenmenger's complex (30), interventricular septal defect (7), and congenital dilatation of the pulmonary artery (13). When congenital or rheumatic heart disease is present, super-imposed subacute bacterial endocarditis may be the immediate cause of the thrombus formation (14, 29). Some of the less common causes of pulmonary thrombosis in situ are sickle-cell anemia (37), trauma to the chest (17), thrombo-angiitis obliterans of the pulmonary artery (18), measles complicated by pneumonia (11), and polycythemia (19, 25, 38). The sex incidence of pulmonary thrombosis appears to be about equal, as was found by Savacool and Charr (28) in a series of 100 cases. Although persons in the older age groups are more apt to be afflicted, a number of cases in infants and children have been reported (11, 15, 17, 31). Clinically the initial signs and symptoms of the disease may be either insidious or of dramatic onset (22, 23, 28).