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R. K. Richards, M.D.; Theodore Koppanyi, Ph.D.
JAMA. 1954;154(5):438-439. doi:10.1001/jama.1954.02940390062025.
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To the Editor:—  The Oct. 3, 1953, issue of The Journal carries an article by Dr. Lloyd H. Mousel entitled "Cerebral Edema and Its Relation to Barbituric Acid Poisoning." This article is timely in view of the continued controversy regarding the advisability of the use of analeptics in the treatment of barbiturate poisoning. It is not possible to enter an exhaustive discussion of the subject at this time, but it appears desirable to comment on the data that Dr. Mousel presents and the conclusions he draws from them. The thesis presented by Dr. Mousel consists of the assumption that, since cerebral hypoxia may result in cerebral edema, acute barbiturate poisoning will cause the same complications. In a properly managed case of acute barbiturate intoxication, however, a satisfactory oxygen supply to the central nervous system can usually be maintained. One of the main features of the pathological physiology of acute barbiturate


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