Myasthenia: Muscle relaxant effects
Myasthenia gravis is caused by IgG antibodies to nicotinic ACh receptors. Most patients are on anticholinesterases, but may progress to steroids, thymectomy, immunosuppression, and plasmapheresis depending on the severity of the disease. IV immunoglobulin can be used for acute exacerbations.
Because there are functionally fewer nicotinic receptors, patients with MG are less susceptible to succinylcholine and more susceptible to nondepolarizing muscle relaxants.
A significant fraction of these patients will require up to 48 hours of post-operative ventilatory assistance. Predictive factors include disease duration (longer than 6 years), COPD, > 750 mg pyridostigmine daily, and a vital capacity < 40 mL/kg.
NMBDs are further complicated by pyridostigmine (which can decrease the efficacy of SCh and non-depolarizing agents), and chronic steroid therapy, which can produce resistance to non-depolarizing agents (at least vecuronium). Thus, quantitative twitch monitoring and careful titration is prudent.
- Less susceptible to SCh, more susceptible to non-depolarizing NMBDs
- Pyridostigmine and steroids complicate response to NMBDs
- Titrate small doses of NMBDs to quantitative twitch monitoring
- Post-op ventilation: > 6 yrs of disease, > 750 mg/day pyridostigmine, VC < 40 mL/kg