Muscle Relaxants, Myasthenia, and Mustards?

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Abstract
Pancuronium was used in management of myasthenic patients and was chosen for use in this case. After explanation to the patient, the muscle relaxant was titrated into the patient to the desired endpoint before anesthesia was induced. While there is no proof which of these suppositions was the cause, various drugs, each of which by itself or in combination, could have accentuated the myasthenic state were used. While the patient was diagnosed as having group IIa myasthenia, her myasthenia was really of group III-IV, a fulminant disease where a fatal outcome could be expected. This is likely when the 6 mo. history is considered. The use of succinyldicholine in combination with anticancer drugs was investigated, and reports of prolonged apnea resulting from this can be found. Thiotepa has an ID50 [median inhibitory dose] of 7.9 .times. 10-3 M with benzolycholine as the substrate. Progressive muscular paralysis may follow the administration of drugs in the nitrogen mustard group. These drugs, which are similar to acetylcholine in structure, may produce this paralysis by prolonged depolarization of the motor endplates. Irreversible chemical bonding between the transformed mustard and the receptor substance could also occur. Absorption of thiotepa from mucosal surfaces is known to occur. Peritoneal absorption was not studied, but it is known to occur with many other drugs. This case report suggests that thiotepa may have caused or potentiated neuromuscular blockade from pancuronium, and alkylating drugs (nitrogen mustards) should be considered a possible hazard when given to patients during anesthesia involving the use of muscle relaxants. The presence of myasthenia gravis may have been the predisposing and critical factor in this complication.

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