Caine1 suggested that death following anesthesia induced with nitrogen monoxide may be the result of cerebral injury. This has been confirmed anatomically by the recent studies of Löwenberg, Waggoner and Zbinden2 and those of Courville.3 The present report is a histopathologic study of 4 cases of postanesthetic encephalopathy, in 2 of which the condition followed the use of nitrogen monoxide and oxygen, in 1 that of avertin (tribromethanol) in amylene hydrate and in 1 that of cyclopropane. Anatomic evidence is submitted to support the idea that the cerebral damage in such cases is the result of deprivation of oxygen, regardless of the type of anesthetic used. The type of cellular change, the distribution of the lesions in the brain and the local selectivity of the degeneration in the cerebral cortex are analyzed.
REPORT OF CASES
—A white man aged 37, with evidence of increased intracranial
STEEGMANN AT. ENCEPHALOPATHY FOLLOWING ANESTHESIA: HISTOLOGIC STUDY OF FOUR CASES. Arch NeurPsych. 1939;41(5):955–977. doi:10.1001/archneurpsyc.1939.02270170093005
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