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Canadian Journal of Anesthesia, Vol 13, 550-556, Copyright © 1966 by Canadian Anesthesiologists' Society
1 Departments of Anaesthesia and Clinical Laboratory Services, University of Alberta Hospital, Edmonton, Alberta
Pseudocholinesterase is essential for the rapid breakdown of succinylcholine. If pseudocholinesterase is quantitatively or qualitatively deficient, prolonged apnoea may result after administration of succinylcholine. Normal pseudocholinesterase activity is dependent upon allelic genes E1u. There now appear to be two atypical variant alleles and a silent allele. In anaesthetic practice the homozygous atypical pseudocholinesterase variants may be expected to be encountered with a frequency of about 1:3000.
The cornerstone of treatment of prolonged succinylcholine apnoea is adequate ventilation with maintenance of physiological levels of pH, PCOCO2 and bicarbonate, and avoidance of hypoxia.
Patients experiencing prolonged apnoea should be biochemically investigated. Knowledge of a low pseudocholinesterase level will certainly be of interest. However, as is evident from the cases described here, this by itself will not reveal whether low activity is due to a low but normal type of enzyme, or to a genetic mutant. As certain drugs and illnesses may produce a low enzyme level, and such causes may only be temporary, it is of more than academic interest to determine the nature of the defect. If it is of genetic origin, it is a permanent defect and such persons should receive a warning card to alert physicians regarding this biochemical abnormality.
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