Myaesthenia gravis

1. Anaesthesia in
myasthenia
Dr. S. Parthasarathy
MD., DA., DNB, MD (Acu), Dip. Diab.
DCA, Dip. Software statistics, PhD
(physio)
Mahatma Gandhi Medical college
and research institute ,
puducherry India

2. What is myasthenia gravis
• MG is an autoimmune disorder –
• circulating antibodies to nicotinic
acetylcholine receptors at the neuromuscular
junction
• antibodies reduce the numbers of receptors
• Symptoms if only 30% receptors are present
reUp to 25% of patients have a concurrent
thymoma,
• About 10% have evidence for other
autoimmune diseases

3. ors reduced to 30% of normal

4. Clinical features
• muscle weakness -an overall fatigability
increases with exertion over the course of the day.
14:100,000
age 10 and 40. (bimodal )
Females are more frequently affected
• diplopia and ptosis resulting from weakness of the
ocular muscles.
• slowly spread to bulbar muscles, which may lead
to aspiration and respiratory failure, and later
affect the proximal extremities

5. Osserman and Genkins
• class I (ocular muscles only);
• class II (eye symptoms plus mild
generalize weakness);
• class III (eye plus moderate
weakness);
• class IV (eye plus severe
weakness);
• class V (intubation, ventilation)

6. How to diagnose ?
• blood tests for antibodies;
• electromyographic recordings;
• electrophysiologic evaluation is
often performed and shows a classic
decrement in the compound muscle
action potential after repetitive
nerve stimulation.

7. cholinesterase inhibitor test
(edrophonium test);
• Tensilon test (administration of an
anticholinesterase, e.g., edrophonium).
Improvement is usually seen within 5 minutes
after administration of the drug and lasts for
about 10 minutes
• Imaging (to identify thymoma).

8. Drugs aggravate Neuromuscular
weakness
• Penicillamine
• Nondepolarizing muscle relaxants
• Aminoglycosides
• Procainamide

9. Some other DD s of myasthenia
• Graves' disease
• Eaton lambert syndrome
• Cranial nerve palsies
• Congenital myasthenic
syndromes

10. Other autoimmune diseases
coexisting
• hyperthyroidism is present in
approximately 10% of patients with
myasthenia gravis.
• Rheumatoid arthritis, SLE, and
pernicious anemia occur more
commonly in MG

11. Treatment
• Two problems
• I. muscle weakness
• Cholinesterase inhibitors
(neostigmine,
• Pyridostigmine
• (maximal dose )120 mg every 3
hours)

12. Problem 2. immunosupression
• corticosteroids and
• immunosuppressive drugs (cyclosporine,
azathioprine)
• Plasmapheresis-(four to eight treatments
over 2 weeks
• thymectomy is performed if general
symptoms are present

13. Anaesthetic challenges
Preop evaluation
• preoperative interview that they may
be intubated and ventilated when they
awaken
• All routine investigations
• ECG -- Cardiac arrhythmias and
myocarditis

14. Preop preparation
• pyridostigmine
↓
• Bad response ↓ good response
• Young old
↓ ↓
• Steroids steroids + azathioprine
• ↓ ↓
• Imp. Not imp imp.→taper steroids →thy
• ↓ ↓
• Thy add plasma

15. Preop preparation
• Only plasmapheresis

16. Preop
• Lung function testing
• Respiratory and bulbar functions should
be carefully evaluated during the
preoperative evaluation
• Preop neurologist evaluation
• Preoperative plasmapheresis

17. Post op ventilation ??
 Four Factors
 disease duration of longer than 6 years,
 chronic obstructive pulmonary
disease(COPD) unrelated to myasthenia
gravis,
• a daily dose of pyridostigmine higher
than 750 mg,
• and a vital capacity less than 2.9 L.

18. Premed
• Anticholinesterase to continue ??
• Small dose benzodiazepine
• Anticholinergics

19. Anaesthetics-Nondepolarizing
Neuromuscular Blockers
• Long acting NDNMB (pancuronium,
pipecuronium,
doxacuronium) :avoided
• Intermediate and short acting: used
with careful monitoring..

20. Depolarizers nondepolarizers

21. Succinylcholine
• resistance to depolarizing agents.( ED95 :
2.6 times of control)
• because of the decreased number of
functional acetylcholine receptors
• more likely to develop phase II block
• decrease in cholinesterase activity
achieved by anticholinesterase
treatment

22. So regarding relaxants
• NDP s more sensitive
• Depolarizers more resistant

23. Inhaled Anaesthetics
• Isoflurane , enflurane: decrease
TOF responses
• Sevoflurane at 2.5% depresses
EMG responses
• effects of desflurane in MG ??

24. Intravenous Anaesthetic Agents
• Propofol √
• -- no effect on NMJ
• Etomidate, althesin and ketamine :
Reports of uneventful anesthesia.
• Opioids
– do not appear to depress NM transmission in
MG muscle.
– Central respiratory depression may be a
problem

25. Anaesthesia -1
• IV induction
• + inh. Drugs +
• intubation
• Maintain on N2O ,O2, Inh. Agent
• No NonDepolarizers
• Extubate without reversal

26. Anaesthesia - 2
• Propofol
• Scoline
• N2O ,O2, Inh. Agent
• Nondepolarizers (10% dose with NMJ monitor)
• unsuccessful extubation, longer postoperative
mechanical ventilation and hospital stay
• Suggamadex or post op ventilation

27. Regional Anesthesia
• Ester anesthetics, metabolized by
cholinesterase, may present particular
problems in patients taking
anticholinesterases.
• Use reduced doses of amide (lidocaine,
bupivacaine) to avoid high blood levels.
• Remember drugs and coexisting
diseases

28. Anaesthesia 3, 4
• TIVA for the management of myasthenics
has been reported.
• Local anaesthesia is successful

29. Postoperative considerations
• Weakness
• Pain (local ,epidural opioids )
• Myasthenic crisis
• Cholinergic crisis
• Resume the anticholinergic therapy as soon as possible
after surgery. The postop requirements may be
different from the routine preoperative dose and
• careful titration because the IV dose is only about 1/30
to 1/120

30. Post op problems
• Nerve stimulator - bulbar Vs limb muscles
• Inspiratory force of > - 25 cm is OK
• Trans sternal thymectomy – 50 % req.
ventilation
• Trans cervical thymectomy OR
• video-assisted thorascopic (VATS)–
• less post op ventilation ,remission more ??
• Early thymectomy better !!

31. Your icu ready

32. Myasthenic crisis
• Myasthenic crisis is a life-threatening
condition, which is defined as weakness
from acquired myasthenia gravis (MG)
that is severe enough to necessitate
intubation

33. precipitants
• infection.
• Surgery
• Pregnancy,
• certain antibiotics (aminoglycosides,
erythromycin and azithromycin), cardiac
drugs (beta-blockers, procainamide, and
quinidine), and magnesium.
• TREAT VIGOROUS WITH POSSIBLE OPTIONS

34. Cholinergic crisis
• excess of cholinesterase inhibitors (ie,
neostigmine, pyridostigmine, physostigmine)
• resembles organophosphate poisoning.
• excessive ACh stimulation of striated muscle at
nicotinic junctions produces flaccid muscle
paralysis that is clinically indistinguishable from
weakness due to MG.

35. Cholinergic crisis
• Miosis and the SLUDGE syndrome (ie,
salivation, lacrimation, urinary incontinence,
diarrhea, GI upset and hypermotility, emesis)
also may mark cholinergic crisis.
• Despite muscle weakness, deep tendon
reflexes are preserved.

36. Cholinergic crisis
• When muscarinic effects are obvious ,
diagnosis is easily made. Antimuscarinics
and respiratory support are given
• EDROPHONIUM TEST WILL DIFFERENTIATE
BOTH CRISES

37. Myasthenia and pregnancy
• Exacerbations of myasthenia must be
anticipated during pregnancy
• Epidural analgesia and anaesthesia can be
used for labour and delivery
• Muscle relaxation induced by regional
anaesthesia may compound the weakness
caused by myasthenia.

38. Myasthenic syndrome
• Acq. Disorder
• Small cell ca of lungs
• IgG antibodies to pre synaptic voltage dep.
Calcium channels
• Abn. Vesicular release
• Exercise improves
• Diaminopyridine improves
• Sensitive to both DPs and NDPs
• anticholinesterase agent - not dependable

39. SUMMARY
• Preop bulbar? Anticholinestrase ,
plasmapheresis , premed atropine
• GA with propofol, inh. agents ,no NDPs
• Post op ventilation
• Or GA, relaxants, suggamadex, ventilation
• Other surgeries – possible RA, LA
• Post op epidural opioids, muscle weakness

40. Thank you all