Chest
Volume 60, Issue 4, October 1971, Pages 399-401
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Fatal Pulmonary Edema and Pneumonitis After Reexpansion of Chronic Pneumothorax

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In some instances, the reexpansion of a chronic pneumothorax results in pulmonary edema and, in the case presented, resulted in a fatality. The exact mechanism is unknown; however, the condition seems to be associated with (1) the chronic collapse of an entire lung, (2) sudden re-expansion of the lung, and (3) edema involving the chronically collapsed lung. Hypoxia was the cause of the patient's death and is related to perfusion of a lung without gaseous exchange. This condition can be treated by allowing the pneumothorax to recur or reducing perfusion of the involved lung by means of a balloon catheter placed in the pulmonary artery.

Section snippets

TECHNIQUE

Our standard technique consists of introducing a trocar through the second intercostal space of the affected pleural cavity and inserting an 18-French rubber catheter through the trocar. Suction is applied to the catheter during its insertion to produce rapid reexpansion of the lung and, in so doing, carries the catheter to the apex of the pleural space, the most desirable position. Then suction of about 20 to 25 cm of water is maintained to the intercostal tube.

CASE REPORT

A 69-year-old man suffered spontaneous pneumothorax June 13, 1969. Initial treatment was expectant, but reexpansion did not occur. The patient entered his local hospital for a short time, during which period 500 ml of air was aspirated from the right pleural space. Improvement was brief, but progressive shortness of breath prompted referral to us and admission to St. Joseph's Hospital, Marshfield, Wisconsin on September 3, 1969, 81 days after the initial event.

The patient's medical history

AUTOPSY

The principal pathologic changes were found in the lungs. The right weighed 800 gm and showed pronounced edema, more in the lower than in the upper lobes. The bronchial system contained frothy material. A 3-cm bleb at the apex of the upper lobe undoubtedly accounted for the pneumothorax. The left lung was somewhat congested but weighed only 450 gm. Thrombi and emboli were absent from the arterial and venous systems of both lungs.

Microscopically, the right lung revealed severe acute passive

DISCUSSION

Ziskind1 reported a similar but not fatal case in 1965. He postulated that the high negative pressure in the intrapleural space accounted for the pulmonary edema which was thought to be bilateral on a clinical basis, but was radiographically unilateral. A similar mechanism was ascribed to the use, in the distant past, of the Potain apparatus for the aspiration of pleural fluid, although, with this apparatus, bilateral pulmonary edema was not uncommon.

These explanations are not completely

REFERENCES (2)

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