Why is myasthenia gravis resistance to succinylcholine?
In myasthenia gravis, the destruction of acetylcholine receptors creates succinylcholine resistance and increased sensitivity to nondepolarizing agents.
Can you use succinylcholine with myasthenia gravis?
To summarize, though not directly studied, the anesthesiology literature subjectively supports the use of succinylcholine as needed for intubation in patients with myasthenia gravis, perhaps with slight increase in RSI dose (2.0mg/kg). There is not theoretical risk or report of hyperkalemic response.
Why are myasthenia gravis patients resistant to depolarizing muscle relaxants?
Depolarizing neuromuscular blocking agents — Patients with MG are resistant to neuromuscular blockade with depolarizing NMBAs (eg, succinylcholine), possibly because they have a decreased number of acetylcholine receptors [27,28].
How does anesthesia affect myasthenia gravis?
Surgery and anaesthesia in myasthenic gravis patients are associated with an increased risk of death and severe complications. The risk is mainly related to a markedly higher sensitivity to muscle relaxants observed in this group of patients, even in periods of complete remission [5].
What is the mechanism of action of succinylcholine?
Mechanism of Action A depolarizing neuromuscular blocking agent, succinylcholine adheres to post-synaptic cholinergic receptors of the motor endplate, inducing continuous disruption that results in transient fasciculations or involuntary muscle contractions and subsequent skeletal muscle paralysis.
What drugs are contraindicated in myasthenia gravis?
Answer
- Antibiotics – Macrolides, fluoroquinolones, aminoglycosides, tetracycline, and chloroquine.
- Antidysrhythmic agents – Beta blockers, calcium channel blockers, quinidine, lidocaine, procainamide, and trimethaphan.
- Antipsychotics – Phenothiazines, sulpride, atypicals.
How does succinylcholine affect muscle contraction?
Succinylcholine, commonly used in anesthesia, paralyzes normal skeletal muscles by blocking transmission at the myoneural junction, but in denervated muscle, it produces sustained muscle contractions lasting several minutes.
How does succinylcholine cause depolarization?
Succinylcholine is comprised of two acetylcholine molecules joined together and acts as a depolarizing neuromuscular blocker by binding acetylcholine receptors at the post-synaptic neuromuscular junction end plate.
Which of the following should not be administered to a patient with myasthenia gravis?
These antibiotics have black box warnings and should not be used for individuals with myasthenia gravis: Fluoroquinolones (Ciprofloxacin (“Cipro”), levofloxacin, gatifloxacin, femifloxacin, norfloxacin, ofloxacin) Ketek (telithromycin)
What can worsen myasthenia gravis?
Factors that can worsen myasthenia gravis
- Fatigue.
- Illness or infection.
- Surgery.
- Stress.
- Some medications — such as beta blockers, quinidine gluconate, quinidine sulfate, quinine (Qualaquin), phenytoin, certain anesthetics and some antibiotics.
- Pregnancy.
- Menstrual periods.
How does succinylcholine relax muscles?
Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations.
Why does succinylcholine cause hyperkalemia?
Systemic succinylcholine, in contrast to acetylcholine released locally, can depolarize all of the up-regulated AChRs leading to massive efflux of intracellular potassium into the circulation, resulting in hyperkalemia.