الفهرس 
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Abstract
Myasthenia Gravis (MG) is an autoimmune disease characterized by weakness and fatigability of skeletal muscles, with improvement following rest. It may be localized to specific muscle groups or more generalized. MG is caused by a decrease in the numbers of postsynaptic acetylcholine receptors at the neuromuscular junction, which decreases the capacity of theneuromuscular end-plate to transmit the nerve signal. Initially, in response to a stimulus resulting in depolarization, acetylcholine is released presynaptically which results in a muscle action potential being generated. In MG, the number of activated postsynaptic receptors may be insufficient to trigger a muscle action potential. Further, with repeated stimulation, the decline in release of acetylcholine correlates with the characteristic fatigability.
Auto-antibodies develop against acetylcholine (ACh) nicotinic postsynaptic receptors. Cholinergic nerve conduction to striated muscle is impaired by a mechanical blockage of the binding site by antibodies and, ultimately, by destruction of the postsynaptic receptor. Patients become symptomatic once the number of ACh receptors is reduced to approximately 30% of normal. The antibodies to the acetylcholine receptor reduce the number of functional receptors by blocking the attachment of acetylcholine molecules, by increasing the rate of degradation of receptors and by complement induced damage to the neuromuscular junction. The cholinergic receptors of smooth and cardiac muscle have a different antigenicity than skeletal muscle and are not affected by the disease.
The prevalence of MG is approximately 100 per 100 000 population with incidence of 2-4 per 100 000 per annum. In the past, untreated MG had a mortality rate of 30-70%, now most patients with MG have a near-normal life expectancy. Morbidity results from intermittent impairment of muscle strength, which may cause aspiration, increased incidence of pneumonia and falls. In addition, the medications used to control the disease may produce adverse effects. With prompt diagnosis and treatment, the mortality rate of myasthenic crisis is less than 5%.
The cardinal features are weakness and fatigability of skeletal muscles, usually occurring in a characteristic distribution.
The weakness tends to increase with repeated activity and improve with rest. Ptosis and diplopia occur early in the majority of patients. Weakness remains localized to the extraocular and eyelid muscles in about 15 percent of patients.
Myasthenic patients may be at increased risk of developing postoperative respiratory failure. Several authors have proposed criteria for predicting which patients will require prolonged postoperative mechanical ventilation.
The anaesthetic management of the myasthenic patient must be individualized to the severity of the disease and the type of surgery. The use of regional or local anaesthesia seems warranted whenever possible. Whenever local or regional anaesthesia is used, the dose of the local anaesthetic may be reduced in patients to decrease the possible effects of anaesthetics on neuromuscular transmission.
This may be particularly important when ester local anaesthetics are administered to patients receiving anticholinesterase therapy (inhibit plasma cholinesterase). General anaesthesia can be performed safely, provided the patient is optimally prepared and neuromuscular transmission is adequately monitored during and after surgery.
Sugammadex is a selective NMBA-binding agent designed to reverse the effect of the steroidal NMBA rocuronium, which is also partially effective against vecuronium. Sugammadex decreases the amount of free NMBA molecules after administration by binding the molecules making them ineffective. This makes it possible to reverse a neuromuscular block in 3 min after administration of vecuronium or rocuronium and does not intervene with the nAChR or the anticholinesterases.