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Myasthenia gravis

Neuroanesthesia and neuromuscular·~4 min read· Physician-reviewed✓ Sourced · 3

Stem

A 38-year-old woman, 64 kg, with generalized acetylcholine-receptor antibody–positive myasthenia gravis is scheduled for video-assisted thoracoscopic thymectomy. She has mild ptosis, tires when chewing, and has had no crisis. She takes pyridostigmine 60 mg every four hours and has taken prednisone 10 mg daily for eight months. CT shows thymic hyperplasia without a mass, and her vital capacity is near normal.

Question

How will you plan her anesthetic, including your approach to neuromuscular blockade?

Ideal answer

HeadlineHer disease sits at the receptor I manipulate, so the goal is no residual weakness: relaxant avoided or minimized, measured, reversed with sugammadex.

  1. Optimize with neurology; continue pyridostigmine; stress-dose steroids. Pyridostigmine through the morning of surgery avoids added bulbar and respiratory weakness; she has had more than 5 mg prednisone for over three weeks. No sedative premedication.1
  2. Propofol, remifentanil, double-lumen tube without a relaxant. If conditions allow; volatile agent adds relaxation.1
  3. If needed, small incremental rocuronium, quantitatively monitored. She is exquisitely sensitive to nondepolarizers; adductor pollicis, baseline before dosing.1
  4. Sugammadex 2 mg/kg, about 130 mg, not neostigmine. With the second twitch back;2 neostigmine can tip her into cholinergic crisis.1
  5. Extubate fully awake, train-of-four ratio ≥0.9.3 With adequate cough and vital capacity; multimodal, opioid-sparing analgesia.

Watch for: in a monitored bed, weakness, rising CO2 and tachypnea meaning reintubation.1

Breaking down the answer

  • Fewer receptors, two opposite responses — antibodies to nicotinic receptors in about 85%; she resists succinylcholine and risks a phase II block, yet is very sensitive to nondepolarizers.1
  • Avoid, reduce or monitor — Changes if: sugammadex is unavailable, I avoid relaxants entirely if possible.1
  • Never stop pyridostigmine to "clean up" the block — it trades a cleaner twitch for bulbar weakness and aspiration risk.1
  • Why thymectomy — about 75% of patients have an abnormal thymus, and about 75% achieve remission or improvement after it.1 Changes if: a mass, which adds an anterior mediastinal airway problem.
  • Measured extubation — the 0.9 threshold applies doubly here because clinical tests are unreliable.3

Follow-up question

Two hours after extubation in the PACU she is weak, anxious, drooling and short of breath, with a heart rate of 48 and fasciculations. The nurse gave her home pyridostigmine an hour ago because she seemed weak. What do you do?

Follow-up answer

HeadlineRespiratory failure from either a myasthenic or a cholinergic crisis; extra pyridostigmine plus bradycardia, salivation and fasciculations point to cholinergic. I call for help.

I tell the team and hold all anticholinesterases. Airway first: oxygen, suction, and if she cannot protect her airway or her CO2 is rising, I intubate without a relaxant or with a small dose of rocuronium. Glycopyrrolate or atropine for the muscarinic effects. No edrophonium test; it is no longer used due to bradycardia risk.1 Neurology, ICU ventilation, and pyridostigmine reintroduced at a reduced dose once she recovers; if this proves to be myasthenic crisis, plasmapheresis or immunoglobulin follows.

Pitfalls that cost points

  • Calling a weak, salivating patient "residual block" and giving more anticholinesterase: muscarinic signs mean cholinergic crisis.1
  • A standard intubating dose of rocuronium with no monitor, or heavy opioid or benzodiazepine premedication.1
  • Discharging her to a ward without respiratory monitoring.

Rapid-fire

Q: How does Lambert-Eaton differ? A: About 60% have a malignancy, usually small-cell lung cancer, and patients are sensitive to both depolarizing and nondepolarizing relaxants.1

Q: What happens to her baby if she becomes pregnant? A: Transient neonatal myasthenia occurs in 10–20% of infants from transplacental antibodies.1

Q: Which antibodies cause receptor-antibody–negative myasthenia? A: MuSK, LRP4, agrin and others.1

Q: Why monitor the adductor pollicis rather than the eye? A: Eye muscles overestimate recovery, and the guideline recommends against them.3

Q: What do muscarinic signs suggest in a weak patient? A: Cholinergic crisis, from excess anticholinesterase.1

Numbers to know

Item Value
AChR antibody positive About 85%1
Stress-dose steroid threshold ≥5 mg prednisone for >3 weeks in prior 6 months1
Sugammadex, T2 present 2 mg/kg2
Extubation threshold TOF ratio ≥0.93
Neonatal myasthenia 10–20% of infants1

Sources

  1. 1.Myasthenia gravis · OpenAnesthesia (IARS) · openanesthesia.org
  2. 2.BRIDION (sugammadex) injection prescribing information · FDA / DailyMed · dailymed.nlm.nih.gov
  3. 3.New Practice Guidelines for Neuromuscular Blockade · APSF, 2023 · apsf.orgReproduces the recommendations of the 2023 ASA Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade.

Facts on this page were checked against these sources on Oct 15, 2026. Guidelines change; confirm doses against current institutional protocols.

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