Neuromuscular disease and anaesthesia

What it is

Diseases of the motor nerve, the neuromuscular junction and muscle alter the response to neuromuscular blocking drugs, weaken the respiratory and bulbar muscles, and sometimes affect the heart. Myasthenia gravis, caused by antibodies against acetylcholine receptors, leaves fewer working receptors: patients are resistant to suxamethonium but very sensitive to non-depolarising blockers, which are avoided or given in reduced amounts under quantitative monitoring; sugammadex reverses rocuronium reliably, while neostigmine is unpredictable on top of chronic anticholinesterase treatment. Bulbar weakness raises the risk of aspiration, and long-standing or severe disease predicts the need for ventilation after surgery; myasthenic and cholinergic crises must be told apart. Lambert-Eaton syndrome makes patients sensitive to both types of blocker. In muscular dystrophies such as Duchenne, and in denervation, burns or long immobilisation, suxamethonium can cause severe hyperkalaemia and cardiac arrest, and volatile agents can cause rhabdomyolysis in dystrophies. Myotonic dystrophy brings sensitivity to sedatives and opioids, conduction defects, and myotonic contraction with suxamethonium, cold or shivering. Some congenital myopathies are linked to malignant hyperthermia susceptibility. Regional techniques and short-acting drugs are useful, with careful documentation of existing deficits.

What changes in this patient

• Fewer functional acetylcholine receptors in myasthenia mean small amounts of non-depolarising blocker cause profound, long weakness.
• Upregulated, immature receptors after denervation or immobilisation release large amounts of potassium with suxamethonium.
• Bulbar weakness impairs swallowing and cough, raising the risk of aspiration and postoperative pneumonia.
• Respiratory muscle weakness and a low vital capacity predict the need for ventilation after surgery.
• Dystrophies and myotonic dystrophy often involve the heart: cardiomyopathy and conduction disease.
• Myasthenic crisis (too little effect, weakness) and cholinergic crisis (too much anticholinesterase, secretions and weakness) both threaten breathing.

Anaesthetic plan (and why)

1. Assess bulbar and respiratory function: swallowing, cough, vital capacity, recent crises — this predicts aspiration and postoperative ventilation.
2. Optimise before elective surgery, with neurology; plasma exchange or immunoglobulin may be used before thymectomy — stronger muscles breathe better.
3. Continue the patient's anticholinesterase and immunotherapy as planned, and give steroid cover if needed — stopping can trigger a crisis.
4. Prefer regional anaesthesia or techniques without neuromuscular block when possible — this avoids the unpredictable relaxant response.
5. If a blocker is needed, give a small titrated amount of a short or intermediate agent — myasthenic muscle is very sensitive.
6. Avoid suxamethonium in dystrophies, denervation, burns and long immobilisation — the potassium surge can stop the heart.
7. Use quantitative neuromuscular monitoring throughout — clinical signs miss residual block in weak patients.
8. Reverse rocuronium with sugammadex where available — neostigmine adds to anticholinesterase therapy and its effect is unpredictable.
9. Keep the patient warm and avoid drugs that worsen weakness — cold triggers myotonia; aminoglycosides and magnesium weaken myasthenia.
10. Extubate only when fully reversed, awake and strong, and monitor closely after surgery — weakness can return or worsen.

Response to neuromuscular blockers by disease

Risks and complications

• Prolonged weakness and respiratory failure after surgery from residual block or the disease itself.
• Aspiration and pneumonia from bulbar weakness.
• Myasthenic or cholinergic crisis around surgery, both presenting with weakness that threatens breathing.
• Hyperkalaemic cardiac arrest after suxamethonium in dystrophies, denervation or immobilisation.
• Rhabdomyolysis with volatile agents in muscular dystrophies; malignant hyperthermia in susceptible myopathies.
• Myotonic contraction making ventilation or intubation difficult, and arrhythmias from conduction disease.

Next step

• Discuss with neurology before elective surgery and plan optimisation and the perioperative medicine schedule.
• Book an intensive care or high-dependency bed when respiratory or bulbar weakness is significant.
• Call a senior at once for unexpected prolonged weakness, falling vital capacity or a suspected crisis.
• Record the neuromuscular disease and the drugs to avoid in the anaesthetic record and on the patient's alert card.
• Refer the family for genetic counselling and testing when an inherited myopathy or malignant hyperthermia risk is found.

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Elsewhere in DurgiPedia

• Neuromuscular junction: motor end plate and acetylcholine receptors
• Myasthenia gravis: the neuromuscular junction

Connections

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Educational content; it does not replace supervised training, your institution's protocols or the anaesthetist's or intensivist's decision. It contains no doses and no ventilator or infusion settings.

Sources: Anesthesia for Patients With Myasthenia Gravis (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.