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Myasthenia: Muscle relaxant effects
Last updated: 03/05/2015
Myasthenia gravis is caused byIgG 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 arelesssusceptible to succinylcholine andmoresusceptible 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.
Myasthenia Gravis
- Lesssusceptible to SCh,moresusceptible 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
Other References
- Keys to the Cart: October 16, 2017; A 5-minute video review of ABA Keywords Link
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