Premium
MALIGNANT HYPERPYREXIA IN AUSTRALIA AND NEW ZEALAND
Author(s) -
KING J. O.,
DENBOROUGH M. A.
Publication year - 1973
Publication title -
medical journal of australia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 131
eISSN - 1326-5377
pISSN - 0025-729X
DOI - 10.5694/j.1326-5377.1973.tb110542.x
Subject(s) - medicine , rhabdomyolysis , halothane , malignant hyperthermia , metabolic acidosis , incidence (geometry) , anesthesia , myoglobinuria , general anaesthesia , physics , optics
In a survey of malignant hyperpyrexia in Australia and New Zealand, 19 well documented cases were found. The patients were all males, and 14 were aged between 6 and 25 years. There were 16 cases in Australia, and they occurred in all States except Queensland and Tasmania. There were three cases in New Zealand. The episodes occurred between 1955 and 1971, and the incidence increased after 1967. Eight cases occurred during emergency surgery and 11 during elective procedures, four of which were for orthopaedic reasons. Eleven of the 19 individuals had had previous general Anæsthesia, and only two had a family history of anæsthetic deaths suggestive of malignant hyperpyrexia. In 16 instances, halothane and succinylcholine were given in combination. Failure of relaxation with succinylcholine occurred in eight of the 16 cases in which the drug was used, and is a useful early warning sign. Muscular rigidity was observed In 15 instances. Biochemical data In the early stages of the reaction in four cases revealed acidosis, hypercapnia and hyperkalæmia, and in one individual serial monitoring demonstrated increasing serum levels of muscle enzymes, particularly creatine Phosphokinase, and a fall in serum calcium level. Terminal bleeding states were recorded in six cases. Seventeen of the 19 patients required treatment apart from cessation of Anæsthesia. In addition to cooling and oxygen therapy, a wide range of agents were used. Twelve of the 19 patients (63%) died, seven suddenly from cardiac arrests and five after prolonged resuscitation. The mortality was highest in cases in which the maximum temperature was higher than 41° C, and in which the first abnormality, apart from failure of relaxation with succinylcholine, was noted more than 30 minutes after induction of Anæsthesia. Routine temperature monitoring of patients under general Anæsthesia appears to be the most effective method of reducing the mortality of the reaction. Local, spinal or regional Anæsthesia should be used in susceptible individuals, but if general Anæsthesia Is unavoidable, thiopentone sodium, nitrous oxide and d‐tubocurarine are the only agents which at present appear to be safe.