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48 R. Azzolina, F.V.E. Russo et Al give you an idea of the need for postoperative ventilator support. The preoperative management of the patient can then be influenced by surgical technique and the choices of the anaesthesiologist. In some cases, you can stop the administration of anticholinesterases on the morning of the operation to reduce the need for the use of curare. Plasmapheresis or steroids can improve the preoperative condition of a patient with limited respiratory reserve. For myasthenia patients already receiving immunosuppressive treatment (corticosteroids, azathioprine, cyclophosphamide), the doses of drugs should not be changed due to the risk of triggering a poussèe of the disease. Use of anaesthetic drugs in myasthenia patients Curare drugs are potentially the most dangerous among those used for myasthenia. Curare relaxants are theoretically used in untreated myasthenia, although in some cases you may experience a relative resistance. During a patient’s recent treatment with anticholinesterases or plasmapheresis their use becomes random and their effects unpredictable with a high risk of establishing a curarizing prolonged block type II. Indeed electromyography studies have shown that the response to succinylcholine is difficult to predict in the case of myasthenia, whether treated or not. For these reasons it is appropriate to refrain from using them in the presence of myasthenia. The myasthenia patient is sensitive to no depolarizing curare, in fact the use of small doses as a priming or prior use of curare relaxants should be avoided because it may lead to a loss of airway protection and respiratory distress equivalent to that induced by normal doses in healthy individuals. Recommended doses are 4-8 times smaller, yet very different due to the evolution of the disease from person to person, the disparity in the muscle groups involved and the possibility of potentiating associated with drugs. No rule can be stated precisely. The use of curare in the course of no depolarizing myasthenia requires close monitoring. Sensitivity to no depolarizing curare has been described in patients with minimal impairment (ocular symptoms), those with apparent remission or in those with undiagnosed myasthenia. Longacting curare such as d-tubocurarine, pancuronium, pipercuronium and doxacurium should be avoided. Medium and short half-life curare can be used with extreme caution and with monitoring of neuromuscular transmission, preferably with a Electromyography (EMG) or meccanomiografia (MMG), which measures the electrical response or mechanical change to the stimulation of peripheral nerves. Although in literature individual doses are reported (e.g. vecuronium from 0.005 to 0, 03 mg / kg etc.) there is wide variability in response from patient to patient and it is difficult to predict the duration and effect even with short half-life curare such as mivacurium and pyridostigmine, which inhibits the metabolism of mivacurium. In the second case studies are reported which indicate the rapid onset of cisatracurium and a more prolonged cuarizing effect. Although the use of curare is possible through adequate monitoring, their use is seldom necessary. Barbiturates in experiments on animals have shown to moderately increase neuromuscular blockade induced by no depolarizing curare, without lengthening the duration. In humans few changes have been observed. In fact, it was demonstrated that these drugs increase the amount of acetylcholine released at the pre-synaptic, but decrease the sensitivity of the postsynaptic membrane. Balancing these two effects leads to no change of neuromuscular blockade. Ketamine leads to a desensitization of the postsynaptic membrane, but does not promote the release of acetylcholine. Its effects lead to more of an aggravation of neuromuscular blockade. Propofol has the theoretical advantage of a short duration of action with no effect on neuromuscular transmission. Morphinomimetics at usual doses do not interfere with neuromuscular transmission and can be used safely as anaesthesia for myasthenia patients although the danger of respiratory depression should be considered. Remifenatnil for the short half-life (9.5 minutes) could be considered the ideal analgesic, although in literature at present there are no data on its use. The use of benzodiazepines in myasthenia is not recommended and for some authors it is formally contraindicated, however, this does seem to be excessive. Their actions at the level of neuromuscular transmission are relatively small and comparable to those of barbiturates. Harmful properties of benzodiazepines are those muscle relaxants, an effect related to increasing level of medullar inhibitory GABA on muscle tone but not on neuromuscular transmission. The use of benzodiazepines during myasthenia is therefore possible with prudence and by decreasing the dosage. Droperidol has no effect
Response to anaesthetic drugs in myasthenia patients 49 on neuromuscular transmission while phenothiazines appear to interfere with neuromuscular transmission as a result of postsynaptic desensitization. All halogenated anaesthetic agents can depress the function of the tractor units muscles. This effect can be significant and occur at several levels: central depressant effects, stabilizing effect of the membrane with a decrease in membrane conductance of calcium channels and above all depressant effects on the functioning of the postsynaptic membrane. They do not seem to have a direct action on ach receptors. In practice, they determine a depolarizing block, with a more pronounced effect in the case of halothane rather than enflorano or the isofluorane. In healthy subjects they allow for a decrease of 25% to 50% in the need for curare, while in myasthenia patients they often determine an acceptable muscle relaxant for the duration of surgery. If nitrous oxide has no documented effect on neuromuscular transmission and can be used in such patients without any precaution, isofluorane reduces T1 and train of four, T1 on T4 relationship with an effect of muscle relaxant two times higher than halothane. Enflorano instead can lead to muscle relaxant with varying and heavily dependent on the severity of myasthenia. Sevofluorane 2.5% suppresses the electromyographic response to T1/Tc with 47% and T4/T1 at 57% so much so that it has been used in some cases of thymectomies by transternale both as vapour and as a muscle relaxant anaesthetic. In normal patients undergoing anaesthesia with desflorane the curare request is reduced, and this gas due to its low solubility and its subsequent rapid washout may have interesting implications in myasthenia, both for muscle relaxant properties that would allow for the surgical procedure without the addition of curare, and for the rapid elimination. Local anaesthetics act as agents for rapid ion channel blockers, suppressing the propagation of nervous transmission, the release of Ach, the sensitivity of the postsynaptic membrane and the exciting of muscle cell. Local anaesthetics also increase neuromuscular blockade of all no depolarizing curari and seem able to decrease neuromuscular transmission in myasthenia gravis. Loco-regional or local anaesthesia should be practiced using smaller doses of local “amid” anaesthetics with the “Estereo” group (procaine, tetracaine), already widely out of use, should not be used in myasthenia treated with anticholinesterases as they are metabolized by plasma cholinesterase, with an increase in the rate of serum and with it toxic effects. The blocking of the nerves of the intercostals is not advised due to deficiency of respiratory dynamics, and recently there have been reports of epidural anaesthesia in thymectomies by trasternale. Discussion The considerable progress in anaesthesia, in recent years has allowed for the use of new drugs such as propofol, mivacurium, cisatracurium, sevorane, desfluorane and remifenatanil, due to their easy handling and reduced side effects allow for the execution of a balanced anaesthesia or a TIVA without risks in myasthenia patients. Volatile anaesthetics and curare with longer half-life make the approach even more secure in myasthenia patients. Studies previously mentioned and the experience gained in the field led to the embrace of surgery such as the attitude of “Miniinvasive Anaesthesiology”or rather minimal “Pharmacological Aggression” in patients with myasthenia. Current guidance is designed to favour recently introduced drugs such as propofol and remifentanil, intravenous anaesthesia (TIVA) in accordance with the more recent method of infusion (TCI site effect or plasma concentration), the desfluorane or sevorane if the choice is to use a balanced anaesthesia. These drugs are united by the following common properties; easy handling, a rapid wash-in, low half-life, and therefore rapid wash-out with fast elimination and minimal side effects. References 1) Abel M, Eisenkraft JB. Anesthetic Implication of Myasthenia Gravis. The mountsinai journal of medicine January/March 2002: 32-36. 2) Jaretzki A III, Barohn R J, Ernstoff R M. Myasthenia gravis: Recommendations for clinical research standards. Neurology Vol 55 (1), 12 July 2000: 16-23. 3) Kawamata M, Miyabe M, Nakae Y, et al. Contunuous thoracic epidural blockade in combination with general anaesthesia with nitrous oxide, oxygen, and sevoflurane in two patients with myasthenia gravis. Masui 1993; 42: 898-901. 4) Leventhal S R, Orkin F K, Hirsh R A. Prediction of the need for post-operative mechanical ventilation in myasthenia gravis. Anestesiology, 1980, 53: 26-30.
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