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Chapter: Clinical Cases in Anesthesia : Myasthenia Gravis

Explain the treatment alternatives for MG

Historically, the similarity of symptoms between MG and curare poisoning led Jolly to propose in 1895 that physostig-mine, a cholinesterase inhibitor that was known to antago-nize curare, would be of therapeutic value in myasthenics.

Explain the treatment alternatives for MG.

 

Historically, the similarity of symptoms between MG and curare poisoning led Jolly to propose in 1895 that physostig-mine, a cholinesterase inhibitor that was known to antago-nize curare, would be of therapeutic value in myasthenics. In 1934, this was first attempted by Walker and has since been the mainstay of therapy in MG. Anticholinesterase therapy is aimed at increasing the amount of acetylcholine available to the reduced number of active receptors, thus increasing the likelihood of agonist–receptor interaction and therefore neuromuscular transmission. Neostigmine, edrophonium, pyridostigmine, and ambenonium are all effective acetylcholinesterase inhibitors. Physostigmine crosses the blood–brain barrier, producing central nervous system symptoms, and is not used in myasthenics for this reason. Pyridostigmine is the most common acetyl-cholinesterase inhibitor employed because it has the fewest muscarinic side-effects and a 3–6 hour duration of action. Pyridostigmine is administered either intravenously 2 mg or orally 60 mg. A sustained-release preparation is available that is active over several hours. This sustained-release prepara-tion is often used at night to ensure strength on awakening in the morning. Dose requirements vary from day to day. Patients usually learn to adjust doses appropriately.

 

Other medical treatments of MG are directed at decreasing the production of antibodies. Corticosteroids have been used for many years. Controlled studies reveal that corticosteroids promote clinical improvement in up to 80% of patients; however, prolonged therapy leads to a high incidence of unacceptable side-effects (cataracts, osteoporosis, hypertension, and peptic ulcers). Initiation of steroid therapy is often associated with an exacerbation of weakness that is due to a direct inhibitory effect on neuro-muscular transmission. Diminished antibody production and its consequent beneficial effects are delayed. Other immunosuppressive agents have also been used, such as azathioprine and cyclosporine.

 

Plasmapheresis has been used to remove circulating antibodies and temporarily improve clinical symptoms in 45% of patients. Several treatments are required, and improvement may last only 4 days or as long as 12 weeks. It should be noted that plasmapheresis also decreases pseudocholinesterase levels, which results in a prolonged duration of action of succinylcholine.

 

Thymectomy has provided significant long-term improvement in most patients. It probably decreases production, or the stimulus for production, of antibodies directed at the nicotinic acetylcholine receptor. Because the thymus contains myoid cells with nicotinic receptors and a number of myasthenics have thymic abnormalities, the thymus may be responsible for the initial pathogenesis. It may also be the source of autoreactive helper T-cells. Thymectomy is the preferred treatment in patients under 55 years of age; however, there is no age limit for this surgery if the patient is otherwise medically stable.

 

Controversy exists as to the benefits of different surgical approaches to the thymus. The transcervical approach interferes less with respiratory mechanics compared with transsternal approaches. Sternal incision may offer a greater likelihood of complete thymectomy. Incomplete thymec-tomy results in suboptimal clinical improvement. Advocates of the transcervical approach feel that complete thymectomy is possible with this incision. Improvement after thymec-tomy may take months. When thymoma is present, removal of the thymus gland via sternotomy is required.


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