Anaesthetic-induced malignant hyperpyrexia and a method for its prediction.

SUMMARY The clinical sundrome of anaesthetic-triggered malignant hyperpyrexia occurring in pigs is described. This condition in the pig is considered to be the same “explosive thermal idiosyncrasy” to general anaesthesia that is manifested by humans. The condition has a strong genetic factor occurring in 25 per cent of Landrace pigs used by us. Sex has no influence on its appearance. The clinical syndrome consists of: (1) tachycardia; (2) muscle rigor; (3) tachypnoea and hyperventilation progressing to apnoea; (4) blotchy cyanosis of the skin; (5) rapid, sustained and extreme rise in temperature; (6) gross acidosis. Prognosis, once the condition is well established, is extremely poor. All attempts at treatment have failed. Histological investigation has shown change in muscle only. The significance of this change is unknown. The muscle of affected pigs shows, in comparison to normal pigs, an abnormal fall in ATP content in response to incubation an to “in vitro” exposure to halothane. This reaction provides a method of predicting the development of the syndrome. Halothane, chloroform and suxamethonium have been identified as triggering agents. The mechanism of heat production is unknown.

[1]  B. Britt,et al.  Hereditary aspects of malignant hyperthermia , 1969, Canadian Anaesthetists' Society journal.

[2]  D. White,et al.  Hyperpyrexia during anaesthesia. , 1968, British medical journal.

[3]  A. Hawthorne,et al.  Fulminating hyperthermia and general anaesthesia. , 1968, British medical journal.

[4]  R. Havel.  The Autonomic Nervous System and Intermediary Carbohydrate and Fat Metabolism , 1968, Anesthesiology.

[5]  G. Kenny,et al.  Metabolic effects of volatile anesthetics in cell culture. , 1968, Anesthesiology.

[6]  D. Traber,et al.  Malignant hyperpyrexia with anesthesia. , 1967, JAMA.

[7]  L W Hall,et al.  Unusual reaction to suxamethonium chloride. , 1966, British medical journal.

[8]  L. E. Davies,et al.  Hyperpyrexia and death associated with general anaesthesia , 1966, Canadian Anaesthetists' Society journal.

[9]  P. J. Snodgrass,et al.  The effects of halothane on rat liver mitochondria. , 1966, Biochemistry.

[10]  T. Dent,et al.  Disturbances of the Oxidative-Phosphorylation Mechanism as a Possible Etiological Factor in Sudden Unexplained Hyperthermia Occurring During Anesthesia , 1966 .

[11]  P. A. Maplestone,et al.  ANAESTHETIC DEATHS IN A FAMILY , 1962, British journal of anaesthesia.

[12]  F. Depocas.  The calorigenic response of cold-acclimated white rats to infused noradrenaline. , 1960, Canadian journal of biochemistry and physiology.

[13]  L. D. Carlson,et al.  Role of the sympathetic nervous system in the control of chemical regulation of heat production. , 1957, The American journal of physiology.

[14]  J. Raventós.  The action of fluothane; a new volatile anaesthetic. , 1956, British journal of pharmacology and chemotherapy.

[15]  R E Hinkley,et al.  Effects of general anaesthetics on microbutules. , 1970, Lancet.

[16]  T. Slater.  The inhibitory effects in vitro of phenothiazines and other drugs on lipid-peroxidation systems in rat liver microsomes, and their relationship to the liver necrosis produced by carbon tetrachloride. , 1968, The Biochemical journal.

[17]  D. Challoner.  Hypermetabolic states. , 1966, Lancet.

[18]  W. Cullen.  Malignant hyperpyrexia during general anaesthesia , 1966, Canadian Anaesthetists' Society journal.

[19]  E. E. Bagwell,et al.  Determination of blood halothane levels by gas chromatography , 1965 .