myaesthenia gravis
TRANSCRIPT
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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
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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 presentreUp to 25% of patients have a concurrent
thymoma, • About 10% have evidence for other
autoimmune diseases
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ors reduced to 30% of normal
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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
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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)
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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.
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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).
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Drugs aggravate Neuromuscular weakness
• Penicillamine • Nondepolarizing muscle relaxants • Aminoglycosides • Procainamide
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Some other DD s of myasthenia • Graves' disease• Eaton lambert syndrome • Cranial nerve palsies • Congenital myasthenic
syndromes
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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
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Treatment • Two problems • I. muscle weakness • Cholinesterase inhibitors
(neostigmine,• Pyridostigmine • (maximal dose )120 mg every 3
hours)
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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
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Anaesthetic challenges Preop evaluation
• preoperative interview that they may be intubated and ventilated when they awaken
• All routine investigations • ECG -- Cardiac arrhythmias and
myocarditis
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Preop preparation• pyridostigmine ↓• Bad response ↓ good response• Young old ↓ ↓• Steroids steroids + azathioprine• ↓ ↓• Imp. Not imp imp.→taper steroids →thy• ↓ ↓• Thy add plasma
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Preop preparation
• Only plasmapheresis
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Preop • Lung function testing• Respiratory and bulbar functions should
be carefully evaluated during the preoperative evaluation
• Preop neurologist evaluation • Preoperative plasmapheresis
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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.
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Premed
• Anticholinesterase to continue ??• Small dose benzodiazepine • Anticholinergics
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Anaesthetics-Nondepolarizing Neuromuscular Blockers
• Long acting NDNMB (pancuronium, pipecuronium, doxacuronium) :avoided
• Intermediate and short acting: used with careful monitoring..
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Depolarizers nondepolarizers
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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
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So regarding relaxants
• NDP s more sensitive • Depolarizers more resistant
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Inhaled Anaesthetics• Isoflurane , enflurane: decrease
TOF responses
• Sevoflurane at 2.5% depresses EMG responses
• effects of desflurane in MG ??
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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
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Anaesthesia -1 • IV induction • + inh. Drugs + • intubation • Maintain on N2O ,O2, Inh. Agent • No NonDepolarizers • Extubate without reversal
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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
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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
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Anaesthesia 3, 4• TIVA for the management of myasthenics
has been reported.
• Local anaesthesia is successful
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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
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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 !!
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Your icu ready
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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
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precipitants• infection.• Surgery• Pregnancy,• certain antibiotics (aminoglycosides,
erythromycin and azithromycin), cardiac drugs (beta-blockers, procainamide, and quinidine), and magnesium.
• TREAT VIGOROUS WITH POSSIBLE OPTIONS
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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.
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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.
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Cholinergic crisis• When muscarinic effects are obvious ,
diagnosis is easily made. Antimuscarinics and respiratory support are given
• EDROPHONIUM TEST WILL DIFFERENTIATE BOTH CRISES
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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.
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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
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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
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Thank you all