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

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 (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 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

• 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 !!

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

• 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