Abstract

Perioperative hyperthermia is a serious and potentially life-threatening condition. The least common but most serious type, malignant hyperthermia (MH), is well documented in the literature. Some more common causes of perioperative hyperthermia include septicernia,' neuroleptic malignant syndrome.' thyrotoxic crisis, iatrogenic causes, and idiosyncratic drug reactions. With the exception of MH, these conditions are usually diagnosed by history and clinical examination and are rarely present initially during general anesthesia. Postoperative hyperthermia, probably the result of an episode of MH, was reported in the literature as early as 1900 by Moschowitz' and again by Ombredanne in 1929 and Guedel in 1937. Since that time, numerous articles have contributed to the understanding, diagnosis, and treatment of this rare genetic problem. MH is characterized by a hypennetabolic state following the administration of a anesthetic that results in an increase in carbon dioxide production, heart rate, and later core temperature. This potentially life-threatening reaction is caused by a defect in the calcium-control mechanism in the sarcoplasmic reticulum of skeletal muscle. Under the appropriate triggering conditions, there is an increase in the concentration of myoplasmic calcium, failure of the sarcoplasmic reticulum to take up the calcium, and subsequent sustained muscle contraction associated with hypermetabolism. The adenosine triphosphate pump mechanism responsible for recycling calcium in the sarcoplasmic reticulum exhausts the available ox-

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