Cavitary pulmonary infarction--a rare cause of spontaneous pneumothorax.
Department of Pathology, Seth G.S. Medical College, Mumbai.
Department of Pathology, Seth G.S. Medical College, Mumbai.
A 14-year old female was admitted to the hospital with a diagnosis of resolving myocarditis and dilated cardiomyopathy. She developed spontaneous right-sided pneumothorax. Autopsy, revealed rupture of cavitary pulmonary infarction to be the cause of the pneumothorax, a rare finding.
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Vaideeswar P. Cavitary pulmonary infarction--a rare cause of spontaneous pneumothorax. J Postgrad Med 1998;44:99-100
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Vaideeswar P. Cavitary pulmonary infarction--a rare cause of spontaneous pneumothorax. J Postgrad Med [serial online] 1998 [cited 2023 Mar 27 ];44:99-100
Available from: https://www.jpgmonline.com/text.asp?1998/44/4/99/364
Pulmonary infarction is an infrequent complication of pulmonary thrombo-embolism owing to the dual blood supply and rich capillary anastomosis. Liquefaction of the pulmonary infarct-cavitary infarcts is an unusual phenomenon. This can be a rare cause of spontaneous pneumothorax. We report cavitary lung infarcts in a 13 year-old-female, one of which was responsible for spontaneous pneumothorax.
A 13-year-old female was admitted for progressively increasing breathlessness, oedema of the feet, puffiness of the face and upper abdominal pain. She had a history of fever accompanied by icterus in the recent past following which she developed the above symptoms. On examination, she had generalized anasarca, tachycardia, tachypnoea, raised jugular venous pressure, basal crepitations, audible third heart sound, and tender hepatomegaly. Chest radiography revealed cardiomegaly and pulmonary oedema. Poor progression of 'R' wave and low complexes were the features on electrocardiogram. Two-dimensional echocardiography showed global hypokinesia, a left ventricular ejection fraction of 15%, left ventricular apical thrombus and mild pericardial effusion. Laboratory investigations revealed mild neutrophilia, mild elevations of the hepatic enzymes (PAST 751 and PALT 427 IU/ml), absent HBsAg and negative Paul Bunnell test.
With a clinical diagnosis of myocarditis progressing to dilated cardiomyopathy, the patient was administered anti-coagulants, anti-failure drugs and antibiotics. On the tenth day of admission, the patient developed decreased air entry on the right side; chest x-ray revealed hydropneumothorax. An intercostal drain was inserted. Later owing to accidental displacement of the drain, the patient developed interstitial emphysema, cyanosis and cardiac arrest.
A complete autopsy was performed. In-situ examination showed a right hydropneumothorax. The fluid was serosanguineous. The right lung was covered by a thick layer of fibrinous exudate. A remarkable finding was an irregular ragged defect, measuring 3X1.5 cm over the postero-basal segment of the right lower lobe. The defect communicated with the underlying large (5X4X4 cm.) cavitary haemorrhagic infarction [Figure:1]. An additional cavitary infarct (4X4X3 cm.) was also seen in the lateral basal segment. The oblique fissure had blood clots. Histologically, the infarcts were bland. The left lung had no infarcts. Both lungs had features of interstitial pneumonitis. The heart weighed 250 gm with moderate biventricular enlargement with mural thrombi, and had characteristics of resolving lymphocytic myocarditis, progressing to dilated cardiomyopathy. These mural thrombi lead to pulmonary infarction as well as right renal infarction.
Pulmonary infarction occurs in only 10% of patients of pulmonary thrombo-embolism. Patients with a pre-existing cardio-pulmonary disease are especially predisposed1. Morphologically, the infarct is typically haemorrhagic with coagulative necroses of the parenchymal framework, which heals with minimal fibrosis. On the other hand, liquefactive necrosis is unusual with an incidence of 2 to 4% though a higher incidence of 7% has also been noted. The liquefaction usually follows septic thrombo-embolism, though bland thrombi have also been implicated,,. The first case of bland liquefaction necrosis secondary to pulmonary infarction was first described by Bigger et al in 19354. The patient in the present case had necessary pre-requisites for pulmonary infarction namely resolving myocarditis and dilated cardiomyopathy with mural thrombi. There were two infarcts in the right lower lobe, both of which had cavitated.
There is a general agreement that cavitation occurs when the infarct is more than 4 cms. It chiefly involves the upper and middle zones of the lungs with only 20% involvement of the lower lobes, as was seen in our case. Cavitation is said to occur due to superadded infection, invasive monitoring, abnormal perfusion especially in patients with adult respiratory distress syndrome and barotrauma,,. In the present case, interstitial pneumonitis could have lead to poor capillary perfusion thereby leading to liquefactive tissue necroses as an extension of the effect of pulmonary thrombo-embolism.
If cavitary pulmonary infarction is rare, then spontaneous pneumothorax caused by it is even rarer,. The autopsied case had a ragged defect over a cavitary infarct that had resulted in sudden onset respiratory distress. Hence it is important to remember that cavitary pulmonary infarction forms one of the differential diagnosis for cavitary lung lesions and is a rare cause of pneumothorax.
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