A febrile course coupled with pleural fluid examinations

COMMUNICATIONS TO THE EDITOR 243 O’Donohue the pleural manifestation occurred by accident, not associated with the common etiologic relationship of the yellow nail syndrome, namely, the primarily defective lymphatic circulation. The history data on their patient as having profound mental retardation and being under continuous use of anticonvulsants and sedatives, suggests a propensity toward the development of aspiration episodes from which pneumonitis or lung abscess with empyema might concur. A febrile course coupled with pleural fluid examinations showing an initial count of 240 cells/cu mm, predominantly polymorphonuclear leukocytes, which ultimately became frank pus, was consistent with an infective process. It is here remarked that previous cases of the yellow nail syndrome exhibited lymphocytic effusions.1,7,8 Subsequent isolation of anaerobic pathogenic organisms in the case reported by Angelillo and O’Donohue, Jr., provided further support to the preliminary diagnosis of pneumonia by aspiration with parapneumonic effusion. Additional information that “no parenchymal infiltrates were observed on chest roentgenograins,” did not rule out concurrent lung inflammation, but rather reflected the interpretation of follow-up films after effective treatment. The mechanisms for low glucose levels in the pleural exudate are an excessive utilization by inflammatory cells and the impairment of diffusion across the thickened inflammatory membrane lining the pleural cavity. Results of thoracocenteses performed 60 and 90 minutes after loading with glucose and showing no rise in glucose levels supported the idea of an undue delay in glucose transportation from the blood to the pleural fluid.