Increased Sensitivity to Non-Depolarizing Neuromuscular Blockers in Myasthenia Gravis

Pathophysiological Mechanism

Myasthenia gravis is characterized by antibodies targeting nicotinic acetylcholine receptors, reducing the number of functional receptors at the neuromuscular junction 1
This reduction in functional receptors leads to impaired neuromuscular transmission at baseline, causing increased sensitivity to non-depolarizing NMBAs 3

Patients with myasthenia gravis require significantly reduced doses of non-depolarizing NMBAs to achieve the desired neuromuscular blockade 1, 3
A 50-75% reduction in the recommended dose is common with agents like atracurium and cisatracurium 4
The sensitivity to NMBAs correlates with the severity of myasthenia gravis 4

Peripheral nerve stimulation (PNS) with train-of-four (TOF) monitoring is essential when administering NMBAs to myasthenia gravis patients 1, 3
Assessment of neuromuscular function before administering NMBAs can help identify impaired transmission and guide appropriate dosing 3
If TOF ratio is less than 0.9 before neuromuscular blockade, sensitivity to muscle relaxants is greater and doses must be reduced further 4
Benzylisoquinoline muscle relaxants (atracurium/cisatracurium) are probably recommended due to their more predictable metabolism 4

Sugammadex is recommended for reversal of steroidal muscle relaxants (like rocuronium) in myasthenia gravis patients 4
Patients on cholinesterase inhibitors (like pyridostigmine) have reduced plasma cholinesterase activity, which can further prolong the effect of certain NMBAs 1

Discontinuing cholinesterase inhibitors on the day of surgery increases the risk of respiratory distress 1
Patients with primarily ocular disease may require higher doses of NMBAs than those with generalized disease 3