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• W2079455810 abstract "Many of the deaths in acute bulbar poliomyelitis have been attributed to pulmonary complications, among which are listed suppurative tracheobronchitis, pneumonia, atelectasis, mediastinal emphysema, and pneumothorax. The literature so far encountered, however, fails to reveal any report correlating these lesions, roentgenologically demonstrated, with the clinical course of the disease. This study was undertaken to evaluate, if possible, the various pulmonary complications and to alert clinicians and radiologists to the possible factors which predispose to their development. It has been observed by many (2, 4, 7, 15, 17) that symptoms of cerebral involvement in bulbar poliomyelitis, heretofore considered a result of actual virus infection, have cleared completely almost immediately after establishment of an unobstructed airway. Thus, the treatment and prevention of pulmonary acidosis and anoxia (1) have emerged as a most vital adjunct to therapy. Histopathologic studies reported by Courville (3) emphasize that it is extremely difficult to differentiate the pathological changes produced by the virus from those due solely to anoxia. This lends further emphasis to the need for the prevention of pulmonary acidosis and the maintenance of proper oxygenation of the central nervous system. There are two phases during which the absence of a free respiratory exchange of gases presents itself as a definite threat to the life of the patient with bulbar poliomyelitis (4). The first, or ventilatory phase, occurs during the early days of the disease, when respiratory muscular paralysis, laryngeal paralysis or spasm, and pharyngeal paralysis with secretional obstruction are presenting features. Here the signs of acidosis and oxygen lack are obvious and the symptoms dramatic. The second, or alveolar phase, occurs later, when pulmonary complications develop. During this period the changes are more insidious and persistent and, if unrecognized, frequently lead to death. The pathogenesis of acidosis and anoxia early in poliomyelitis depends upon an interesting series of events, many of which are etiologic factors in producing pulmonary complications. Pharyngeal paralysis, due to involvement of the 5th, 9th, 10th, 11th, and 12th cranial nerves, together with hypersecretion, which occurs commonly in these patients, results in the accumulation and pooling of secretions in the hypopharynx. With each respiratory cycle, the secretion may overflow into the trachea or, in those cases in which a respirator is used, may actually be sucked into the tracheobronchial tree. There are, however, other factors which lead to these changes. Acute obstruction of the larynx is not uncommonly produced by laryngeal paralysis but is more frequently caused by adductor spasm resulting from irritation by secretions. In addition, secretions frequently are retained in the tracheobronchial tree due to ineffectiveness of the cough reflex as a result of muscular paralysis." @default.
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• W2079455810 date "1951-11-01" @default.
• W2079455810 modified "2023-09-24" @default.
• W2079455810 title "Pulmonary Complications of Acute Bulbar Poliomyelitis" @default.
• W2079455810 doi "https://doi.org/10.1148/57.5.629" @default.
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