• G Cammu.
• Onze-Lieve-Vrouw Hospital, Moorselbaan 164, B-9300, Aalst. Guy.Cammu@olvz-aalst.be
• Acta Anaesthesiol Belg. 2001 Jan 1;52(4):357-63.

AbstractMany drugs interact with neuromuscular blocking drugs and often enhance the induced block; this is of clinical importance for volatile anaesthetics, antimicrobials, magnesium and some more specific drugs. Difficulty in reversing the block occurs with calcium-channel blockers and polymyxin. Phenytoin, carbamazepine and other anticonvulsants may cause resistance to neuromuscular blocking drugs. Moreover, clinically important interactions are found between individual neuromuscular blockers. Giving succinylcholine after a non-depolarizing neuromuscular blocking drug prolongs the onset of succinylcholine; when non-depolarizing drugs are administered after succinylcholine their effects are prolonged. The succinylcholine block is prolonged when the drug is administered during recovery from pancuronium or following neostigmine reversal. Drugs or diseases that decrease the activity of plasma cholinesterase may prolong a succinylcholine-induced block. Finally, liver dysfunction, renal failure, disturbances of acid-base balance, change in temperature and neurological diseases all have an effect on the profile of the neuromuscular blocking drugs; the response to an induced block may be altered in patients under intensive care and those with cancer. Although knowledge of the most important theoretical interactions of neuromuscular blocking drugs is favourable, the anaesthetist should be aware that pharmacological interactions can lead to an unpredictable induced neuromuscular block in many cases in daily clinical practice. Therefore anaesthetists should become familiar with the use of neuromuscular transmission monitoring in order to manage the block correctly.

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