Date post: | 24-Dec-2015 |
Category: |
Documents |
Upload: | edith-berry |
View: | 216 times |
Download: | 0 times |
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 presentreUp to 25% of patients have a concurrent
thymoma, • About 10% have evidence for other
autoimmune diseases
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 (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).
Drugs aggravate Neuromuscular weakness
• Penicillamine • Nondepolarizing muscle relaxants • Aminoglycosides • Procainamide
Some other DD s of myasthenia
• 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 ↓• Bad response ↓ good response• Young old ↓ ↓• Steroids steroids + azathioprine• ↓ ↓• Imp. Not imp imp.→taper steroids →thy• ↓ ↓• Thy add plasma
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.
Anaesthetics-Nondepolarizing Neuromuscular Blockers
• Long acting NDNMB (pancuronium, pipecuronium, doxacuronium) :avoided
• Intermediate and short acting: used with careful monitoring..
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
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
• IV induction • + inh. Drugs + • intubation • Maintain on N2O ,O2, Inh. Agent • No NonDepolarizers • Extubate without reversal
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
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• 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 !!
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
• 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