Transcript 1 MB - myaesthenia gravis - Anesthesia Slides, Presentations and

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
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
ors reduced to 30% of normal
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
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)
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.
cholinesterase inhibitor test
(edrophonium test);
• Tensilon
test
anticholinesterase,
(administration
e.g.,
of
an
edrophonium).
Improvement is usually seen within 5 minutes
after administration of the drug and lasts for
about 10 minutes
• Imaging (to identify thymoma).
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Drugs aggravate Neuromuscular
weakness
Penicillamine
Nondepolarizing muscle relaxants
Aminoglycosides
Procainamide
Some other DD s of myasthenia
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Graves' disease
Eaton lambert syndrome
Cranial nerve palsies
Congenital myasthenic
syndromes
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
Treatment
• Two problems
• I. muscle weakness
• Cholinesterase inhibitors
(neostigmine,
• Pyridostigmine
• (maximal dose )120 mg every 3
hours)
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
Anaesthetic challenges
Preop evaluation
• preoperative interview that they may
be intubated and ventilated when they
awaken
• All routine investigations
• ECG -- Cardiac arrhythmias and
myocarditis
Preop preparation
• pyridostigmine
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↓
Bad response ↓
good response
Young
old
↓
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Steroids
steroids + azathioprine
↓
↓
Imp. Not imp
imp.→taper steroids →thy
↓
↓
Thy add plasma
Preop preparation
• Only plasmapheresis
Preop
• Lung function testing
• Respiratory and bulbar functions should
be carefully evaluated during the
preoperative evaluation
• Preop neurologist evaluation
• Preoperative plasmapheresis
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.
Premed
• Anticholinesterase to continue ??
• Small dose benzodiazepine
• Anticholinergics
Anaesthetics-Nondepolarizing
Neuromuscular Blockers
• Long acting NDNMB (pancuronium,
pipecuronium,
doxacuronium) :avoided
• Intermediate and short acting: used
with careful monitoring..
Depolarizers nondepolarizers
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
So regarding relaxants
• NDP s more sensitive
• Depolarizers more resistant
Inhaled Anaesthetics
• Isoflurane , enflurane: decrease
TOF responses
• Sevoflurane at 2.5% depresses
EMG responses
• effects of desflurane in MG ??
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
Anaesthesia -1
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IV induction
+ inh. Drugs +
intubation
Maintain on N2O ,O2, Inh. Agent
No NonDepolarizers
Extubate without reversal
Anaesthesia - 2
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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
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
Anaesthesia 3, 4
• TIVA for the management of myasthenics
has been reported.
• Local anaesthesia is successful
Postoperative considerations
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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
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 !!
Your icu ready
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
precipitants
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infection.
Surgery
Pregnancy,
certain antibiotics (aminoglycosides,
erythromycin and azithromycin), cardiac
drugs (beta-blockers, procainamide, and
quinidine), and magnesium.
• TREAT VIGOROUS WITH POSSIBLE OPTIONS
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.
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.
Cholinergic crisis
• When muscarinic effects are obvious ,
diagnosis is easily made. Antimuscarinics
and respiratory support are given
• EDROPHONIUM TEST WILL DIFFERENTIATE
BOTH CRISES
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.
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
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
Thank you all