[Ovarian cancer with hydrothorax].
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We report two cases of pleural effusion in which a subdiaphragmatic cause was noted. In both cases it was necessary to obliterate a defect in the diaphragm via a thoracic incision. In one case, a left chylothorax occurred in a patient with hepatic cirrhosis. In this case, it was postulated that the normal lymphatic pathway through the right hemidiaphragm could have been stopped by pleural sequelae from right lobectomy. In the other case, a right pleural effusion occurred after peritoneal dialysis. It is a well known pathological entity: the structural defect can be observed by separation of collagen bundles in the tendinous diaphragm. This type of pleuro-peritoneal communication is well known in women suffering from menstrual pneumothorax or in patients treated by peritoneal dialysis.
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Four patients on continuous ambulatory peritoneal dialysis (CAPD) developed large, symptomatic pleural effusions after commencing peritoneal dialysis. Pleuroperitoneal fistula in each case was diagnosed by the presence of a high glucose content in pleural fluid, with a normal corresponding blood sugar, and was confirmed by isotope or contrast peritoneography. Two patients had their effusions drained percutaneously, and then underwent pleural sclerosis with intracavitary tetracycline. Two patients had a thoracotomy performed, of which no fistula was identified in one case, and the other patient underwent pleurectomy. All four patients successfully recommenced CAPD several weeks after therapy, without recurrence of effusions. We conclude that pleuroperitoneal connections associated with CAPD do not mandate cessation of peritoneal dialysis and conversion to maintenance haemodialysis. Definitive diagnosis requires aspiration of pleural effusions for glucose estimation. Contrast or isotopic peritoneography is helpful in localising the fistula, but in our experience did not alter management. Simple sclerotherapy is effective and avoids the need for a formal thoracotomy.
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A 64-year-old woman with Idiopathic Portal Hypertension was hospitalized for severe respiratory distress. Chest X-ray film showed a massive pleural effusion in the right hemithorax. Though repeated thoracentesis was performed, the patient was suffering from dyspnea frequently. A pleurovenous shunt was inserted. Follow up chest X-ray films showed resolution of pleural effusion and the patient remained free of symptoms. Two months after the placement of the shunt pleural effusion again began to develop with systemic edema caused by development of chronic renal failure. Reduction of effusion was obtained by hemodialysis. Pleurovenous shunting may provide satisfactory palliation for intractable pleural effusions.
The principal focus of this study was to evaluate the hypothesis that increased interstitial fluid pressures served to stimulate de novo vesicle formation in pulmonary capillary endothelium. Direct measurements of interstitial fluid pressures within the alveolar septa pose great technical difficulty. The pleural space and subpleural capillaries are easily accessible, and thus, provide a more feasible model to test this hypothesis. After hydrostatic pressure of pleural space fluid was increased by periodic saline infusions into the pleural cavity, vesicle numerical densities were significantly increased in portions of the subpleural capillary endothelium. Those segments of the endothelium that directly apposed the interstitium of the visceral pleura displayed de novo vesicle formation. The endothelial segments located immediately adjacent to the alveolar epithelium were not affected by the elevated interstitial fluid pressures. In addition to the increased vesiculation, those same segments of the endothelium were characterized by increased attenuation of their cytoplasmic compartments. These conformational changes in the plasmalemma of portions of the subpleural capillary endothelium provide support to the tentative hypothesis, however, whether the increased numbers of vesicles contribute to a potential transendothelial transport system or expand a possible static network of membrane invaginations remains uncertain.
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