Myasthenia gravis is caused by a decrease in the number of postsynaptic acetylcholine receptors (circulating antibodies to the receptors), resulting in a decrease in the margin of safety of neuromuscular transmission (exercise-induced weakness).
Medical Therapy
Anticholinesterase drugs are administered in an attempt to prolong the duration of action of acetylcholine. Whereas anticholinesterase overdose causes a cholinergic crisis (treat with IV atropine), underdose causes a myasthenic crisis (improves with edrophonium, 2–10 mg IV).
Plasmapheresis decreases antibody titers, resulting in transient improvement (also causes a decrease in plasma cholinesterase).
Thymectomy is considered the treatment of choice in most patients with myasthenia gravis. The gland is removed by a median sternotomy or transcervically using a technique similar to mediastinoscopy (lower incidence of postoperative ventilatory failure).
It is prudent to assume that even treated patients are sensitive to the effects of muscle relaxants and the initial dose should be decreased. One approach is to titrate to effect using a peripheral nerve stimulator, beginning with doses of muscle relaxant that are 1/10 to 1/20 the usual dose.
Sugammadex is designed to bind rocuronium and provide rapid, complete, and long-lasting antagonism of rocuronium-induced neuromuscular blockade.
Depolarizing Relaxants. Patients treated with anticholinesterases may be sensitive to succinylcholine, reflecting slowed metabolism of the muscle relaxant.
Nonrelaxant Techniques. Because of concerns over the use of muscle relaxants in patients with myasthenia gravis, there are many reports of successful use of techniques that do not include paralysis (propofol–nitrous oxide–fentanyl; sevoflurane–nitrous oxide–fentanyl).
Postoperative Care. The opioid dose should be decreased by one third because anticholinesterases may increase the analgesic effect of these drugs.