Abstract

The patient is a white female, age 34. Her family history is irrelevant. She gives a history of the usual diseases of childhood, excepting pertussis. She has been married for several years but has not been pregnant. Beginning in January, 1918, she has had an attack of acute respiratory infection each winter, each of which has been diagnosed influenza. No history of pneumonia or of symptoms suggesting tuberculosis was obtainable. In March, 1924, during a local epidemic of whooping-cough, she had a very severe attack of this disease which required hospitalization for a month. During this time she had many severe attacks of coughing, vomiting and choking. The present symptoms began with the attack of whooping-cough in 1924. Since then there has been a slight dyspnea on exertion, and, during the menstrual periods, a dull aching pain in the lower part of the right side of the thorax. Because of these, the patient was referred to me for examination of the lungs. A fluoroscopic examination showed the right lung to be partially collapsed, and a small amount of fluid in the right pleural cavity. The upper level of the fluid was an inch below the highest part of the right arch of the diaphragm. The excursions of the arches of the diaphragm were equal. The heart and aorta appeared normal. Stereoscopic radiograms showed the zone of air around the lung to be one and three-fourths inches wide at the apex, gradually decreasing to a width of three-fourths of an inch at the level of the eighth rib. There were no evidences of adhesions or thickening of any part of the right pleural membrane. The lung was clear of all evidences of tuberculosis or other inflammatory disease. Trunk markings immediately adjacent to the hilus were slightly accentuated, probably due to congestion. Not more than a slight displacement of the heart and other mediastinal contents toward the left was present. The left lung was clear. Physical examination of the chest gave the usual findings associated with pneumothorax. A few moist râles were heard over the right lung. Because of these râles one physician insisted that the patient had tuberculosis. In this case I believe that the rupture of the lung was due to the severe strain during the paroxysms of whooping-cough, and that a pre-existing pleural bleb was the site of the rupture. The formation of the valve of the visceral pleura that opens with coughing and on deep expiration could keep the lung collapsed indefinitely. I think that the patient does not have pulmonary tuberculosis, the râles probably being due to the congestion incident to the collapse of the lung. Emerson (1) mentions pleurobronchial fistulæ that may, by a valve-like action of the visceral pleura, keep air in the pleural cavity for years.

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