Carl M. Kirsch

Case Report:Hepatic Hydrothorax Without Ascites

Pleural effusion due to hepatic cirrhosis and ascites is well known. We describe three patients with right-sided hepatic hydrothorax in the absence of ascites. The formation of pleural fluid in these patients is probably a result of fluid movement from peritoneal to pleural space across diaphragmatic defects before ascites can form. The differential diagnosis of a right-sided transudative pleural effusion in a patient with chronic liver disease with or without ascites includes congestive left ventricular failure and nephrotic syndrome. These diseases are usually ruled out with standard clinical tests. Patients with hepatic hydrothorax should be treated with fluid restriction and diuretics. Patients with severe symptoms due to refractory hepatic hydrothorax might benefit from pleural sclerosis and surgical closure of diaphragmatic defects.

Analysis of Induced Sputum in the Diagnosis of Pneumocystis carinii Pneumonia

Sixty-two patients with possible AIDS-associated Pneumocystis carinii pneumonia (PCP) were studied to determine the diagnostic usefulness of sputum analysis and whether or not the results of sputum analysis are related to severity of disease. Induced sputum was stained with Gomori Methenamine silver and modified Wright Giemsa stains. Indicators of disease severity were: extent of chest roentgenographic infiltrate, serum lactic dehydrogenase activity, alveolar-arterial oxygen tension difference, and total blood lymphocyte count. All patients with sputum negative for Pneumocystis underwent bronchoscopy with bronchoalveolar lavage. Sputum analysis was 71% sensitive and 100% specific for the diagnosis of PCP. The negative predictive value of sputum analysis was 48%. There was no relationship between sputum results and the severity of PCP. This study led to the conclusions that sputum analysis is a sensitive, specific, rapid, and low-cost technique for the diagnosis of PCP, and that the sensitivity of sputum analysis for the detection of PCP is not affected by the severity of PCP.

Effects of platelet-activating factor on vascular permeability and granulocyte recruitment in the rat trachea

Platelet-activating factor (PAF) is a phospholipid mediator known to produce several features of airway inflammation. We examined the effects of intravenous PAF on vascular permeability and granulocyte recruitment in the rat trachea. To assess vascular permeability, anesthetized rats were given injections of Evans blue dye (30 mg/kg, iv) and PAF (1–10µg/kg, iv), and then their tracheas were removed and assayed spectrophotometrically for dye content. We found that a PAF dosage of 6µg/kg increased the tracheal dye content 7-fold compared to controls. The amount of extravasated dye in the tracheas was significantly increased 1 min after PAF injection, was maximal at 5 min, and had returned to control levels by 10 min. To assess granulocyte recruitment, anesthetized rats were given an injection of PAF (6µg/kg, iv), and then their tracheas were removed and stained to reveal myeloperoxidase-containing neutrophils and eosinophils. We found that the number of neutrophils in the tracheal mucosa was increased 7-fold from controls 5 min after PAF injection, but was not significantly increased 6 h later. The number of eosinophils in the tracheal mucosa was not significantly increased from controls at any time after PAF injection. We conclude that intravenous PAF causes a rapid but transient increase in vascular permeability in the rat trachea, and that intravenous PAF also causes a rapid but transient recruitment of neutrophils into the tracheal mucosa without a similar effect on eosinophils.

Cardiac arrest due to succinylcholine-induced hyperkalemia in a patient with wound botulism.

Cardiac arrest due to hyperkalemia is a known complication of succinylcholine administration in patients with neuromuscular disease, extensive burns, and prolonged immobility. We report a case of hyperkalemic cardiac arrest following the administration of succinylcholine in a patient suffering from wound botulism.