Wide awake under anesthesia: Scoline apnoea update

Abstract

Butyrylcholinesterase (BChE) catalyses the hydrolysis of choline esters and thus deactivates muscle relaxants such as succinylcholine and mivacurium. The prolonged neuromuscular blockade following the use of succinylcholine, called scoline apnea, occurs in patients with significant BChE deficiency. It is proved that BChE activity can be reduced in certain physiological conditions, in a number of diseases and after the administration of certain drugs. Gene encoding butyrylcholinesterase (BChE, CHE1) is located on the locus 3q26.1-q26.2. This gene shows a high level of polyallelism and so far about 75 natural mutations of this gene have been documented. The development of modern genetics has provided more insight into the cause of this disorder and is now considered to be caused by a number of genetic variations in the BChE gene. The most commonly observed gene variant is 209A > G, Asp70Gly. If neuromuscular relaxants are used during anesthesia, the use of monitoring in the form of nerve stimulator is recommended. Scoline apnea should be investigated by conventional biochemical tests and molecular genetic tests. This testing should include the closest relatives of the patient if it is suspected to be inherited rather than acquired.

Keywords

• butyrylcholinesterase deficiency
• butyrylcholinesterase
• nucleotide polymorphism