Sleep apnea syndromes: mechanisms and therapy.
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Biomedical subjects
Publications and source records attributed to J B Gee.
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The perioperative course of three patients with obstructive sleep apnoea who underwent tracheotomy is presented as illustrative of the potentially life-threatening complications of management. It is concluded that this disease demands strict adherence to basic principles of airway management and close observation extending into the period after operation.
We compared the elastase and lysozyme activities of cells obtained by bronchoalveolar lavage from normal smokers and nonsmokers. After total and differential cell counts were obtained for the initial lavage cell population, we determined the enzyme activities of the total lavage cell population, the culture vessel's adherent alveolar macrophage cell fraction, and the cell culture supernatant medium. Our data indicated that macrophages, particularly from smokers, synthesized a calcium-dependent activity against a synthetic elastase substrate, succinyl-trialanine-p-nitroanilide. This activity was enhanced in smokers and was distinct from the polymorphonuclear leukocyte elastase as measured with this synthetic substrate. Measurements using insoluble elastin labeled with 3H demonstrated that smokers' macrophages also contained a serine-proteinase activity whose inhibitor profile resembled that of polymorphonuclear leukocyte elastase. Finally, macrophages from smokers secreted 5 times more lysozyme and contained more lactate dehydrogenase activity than did nonsmokers' macrophages. We suggest that pulmonary macrophages take up the polymorphonuclear leukocyte elastase and contain a synthetic substrate, "elastase". The biologic significance of this elastase activity is unclear. The enhanced lysozyme secretion by smokers' alveolar macrophages indicated increased biosynthetic activity by these cells.
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In a 66-year-old patient with chronic obstructive pulmonary disease (COPD) complicated by arterial hypoxemia and repeated episodes of respiratory and right ventricular failure, a satisfactory level of oxygenation could not be maintained despite controlled oxygen therapy. To enable oxygen to be administered without depression ventilation, artificial respiration by means of phrenic nerve stimulation (diaphragm pacing) has been employed. Evidence of clinical improvement since pacing was begun 32 months ago include fewer episodes of respiratory failure and better control of congestive heart failure despite a gradual worsening of pulmonary function.
We studied 89 patients in whom the clinical diagnosis of sarcoidosis was supported by the findings on tissue biopsy. A chest roentgenogram in 14 of the patients showed one of the following atypical features: large pulmonary nodules, an alveolar parenchymal pattern or a pleural effusion. Diagnoses of infection, malignancy or vasculitis were suggested by interpretations of atypical chest roentgenograms in eight of these 14 patients. Nonspecific and misleading clinical information contributed. The diagnosis of sarcoidosis was corroborated by extrathoracic tissue biopsies in 11 of the 14 patients. Over an average observation period of 38 months, the 14 patients remained classified as having sarcoidosis. This suggests that an extrathoracic tissue biopsy, whose findings are consistent with sarcoidosis, is often sufficient to support a clinical diagnosis of some forms of roentgenographically atypical pulmonary sarcoidosis.
Six patients with documented pulmonary sarcoidosis were selectively studied with the ACTA scanner. The CT scans were correlated with the standard chest radiographs of these patients. CT scans readily confirmed adenopathy, calcification, and pleural disease. Likewise, diffuse and isolated parenchymal disease was detected and in some cases unexpected lung involvement was noted.
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