Abstract
A case of prolonged apnoea after suxamethonium is described in which misleading evidence was obtained from studies of neuromuscular conduction with a Medilec nerve stimulator. Estimations of esterase activity, dibucaine number and fluoride number were within the range expected in individuals possessing only “atypical” serum cholinesterase. Electromyographic studies showed a normal response to decamethonium, but a severe and prolonged neuromuscular block after suxamethonium. The block was apparently depolarizing for at least 1½ hours. After a review of other prolonged apnoeas the role of neostigmine in the prolongation of the apnoea is highlighted, and it is suggested that the demonstration of post-tetanic facilitation does not necessarily imply that the block will be improved by anticholinesterase drugs. Two types of theory are outlined to explain this type of case, and precautions against inadvertently making matters worse are suggested.