Not just monitoring; a strategy for managing neuromuscular blockade
2015; Wiley; Volume: 70; Issue: 10 Linguagem: Inglês
10.1111/anae.13219
ISSN1365-2044
AutoresG. Rodney, P. K. Raju, D. R. Ball,
Tópico(s)Nausea and vomiting management
ResumoAnaesthesiaVolume 70, Issue 10 p. 1105-1109 EditorialFree Access Not just monitoring; a strategy for managing neuromuscular blockade G. Rodney, G. Rodney Consultant Anaesthetist [email protected] Ninewells Hospital and Medical School, Dundee, UKSearch for more papers by this authorP. K. B. C. Raju, P. K. B. C. Raju Consultant Anaesthetist Ninewells Hospital and Medical School, Dundee, UKSearch for more papers by this authorD. R. Ball, D. R. Ball Consultant Anaesthetist Dumfries and Galloway Royal Infirmary, Dumfries, UKSearch for more papers by this author G. Rodney, G. Rodney Consultant Anaesthetist [email protected] Ninewells Hospital and Medical School, Dundee, UKSearch for more papers by this authorP. K. B. C. Raju, P. K. B. C. Raju Consultant Anaesthetist Ninewells Hospital and Medical School, Dundee, UKSearch for more papers by this authorD. R. Ball, D. R. Ball Consultant Anaesthetist Dumfries and Galloway Royal Infirmary, Dumfries, UKSearch for more papers by this author First published: 15 September 2015 https://doi.org/10.1111/anae.13219Citations: 25 You can respond to this article at http://www.anaesthesiacorrespondence.com AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL With great power comes great responsibility – variously attributed to Voltaire, Churchill and Spiderman's uncle The drugs we use for neuromuscular blockade are potent; they stop our patients breathing and moving, so we must provide gas exchange and prevent accidental awareness under general anaesthesia. The latter was the focus of the 5th National Audit (NAP5) 1, the vast majority (97%) of reported incidents involving neuromuscular blocking drugs (NBDs). At emergence and during recovery from anaesthesia, residual neuromuscular blockade accounted for 18% of reports 1. The revised Association of Anaesthetists of Great Britain and Ireland (AAGBI) guidelines (in preparation, see www.aagbi.org) on standards of monitoring are in broad agreement with the NAP5 report and leading editorials 2, 3 in calling for a safer approach to the management of neuromuscular blockade. There are a number of misconceptions about neuromuscular blockade, its reversal and its monitoring. These are related to the variability in onset and duration of NBDs' effects, the high incidence of residual neuromuscular blockade, and the inadequacies of both clinical assessment and conventional qualitative peripheral nerve stimulator monitoring as an indication of adequate recovery from neuromuscular block. The aims of this editorial are to discuss new developments in the monitoring and reversal of neuromuscular blockade, and to set out a strategy for the rational use of NBDs and reversal agents, providing safer conditions for patients through all phases of anaesthesia, with special emphasis on preventing residual neuromuscular blockade. Neuromuscular blocking drugs Nearly half of the general anaesthetics given in the UK include NBDs 1. Widely used intermediate-duration drugs, such as atracurium, vecuronium, rocuronium and cisatracurium – while safer than older-generation drugs – remain unpredictable and may cause prolonged neuromuscular blockade and patient harm 4. A significant but unpredictable number of patients experience prolonged duration of neuromuscular block; thus Debaene et al found that 37% of patients had evidence of inadequate spontaneous recovery (failure to return to a train-of-four (TOF) ratio > 0.9) two hours after administration of a single dose of atracurium, vecuronium or rocuronium 5. Reversal of neuromuscular blockade In a recent survey, only 18% of European and 34% of US anaesthetists routinely reversed neuromuscular blockade 6. This is despite wide variability in the duration of like-for-like doses of drugs 5, 7. Anticholinesterase agents include neostigmine, edrophonium and pyridostigmine. Edrophonium has a rapid onset but a short duration of action, and pyridostigmine a slow onset, rendering both unsuitable for routine reversal of neuromuscular blockade. Neostigmine, the drug most commonly used, has limitations in both efficacy and safety; animal, volunteer and clinical studies have shown that it may worsen muscle function if given after full recovery of the TOF ratio 8-11. Other shortcomings include: significant side-effects requiring co-administration of an anticholinergic drug; a slow onset and short duration; a variable effect; a ceiling effect; and inability to reverse deep neuromuscular blockade. A number of studies have reported prolonged reversal times 12-14, with potential inability to restore neuromuscular function in the timescale usually associated with awakening from anaesthesia 1. Sugammadex is a selective aminosteroid-binding reversal agent, recently introduced to clinical practice. It has a number of advantages over neostigmine, including rapid and predictable reversal of rocuronium and vecuronium from any depth of neuromuscular blockade 15. It is tempting to consider it the solution to all NBD reversal issues and to negate the need for monitoring; however, if used in the absence of peripheral nerve stimulation monitoring, there remains a 10% incidence of residual neuromuscular blockade 16, 17. Routine use is limited by cost, lack of availability in some countries such as the USA and ineffectiveness against benzylisoquinoline drugs such as atracurium. Some caution remains regarding the potential for allergic responses 18 and cost-effectiveness 19. However, availability of sugammadex is a key component of a strategy for use of NBDs, in conjunction with a quantitative peripheral nerve stimulator to ensure recovery and cost effectiveness. Monitoring of neuromuscular block Clinical tests of recovery from neuromuscular blockade, such as sustained head lift or hand grip, are widely used, but are unreliable. Sustained tongue depressor test is the most specific, but achieves a sensitivity of only 13-22% in predicting a TOF ratio < 0.9. Overall, clinical tests cannot exclude residual paralysis unless the TOF ratio is < 0.5 20. Importantly, these tests require a degree of patient co-operation and wakefulness to perform them, and this exposes patients to the risk of significant harmful effects from residual neuromuscular blockade 1. The absence of observed or tactile fade in response to TOF stimulation does not indicate adequacy of recovery from neuromuscular blockade. Train-of-four fade (of fourth relative to first twitch) is indistinguishable, even to experienced observers, once the TOF ratio (see Table 1 21, 22) exceeds 0.4 23. For double-burst stimulation, fade (of second relative to first tetanic twitch) is indistinguishable once the TOF ratio exceeds 0.6-0.7 24. Table 1. Neuromuscular blockade monitoring and reversal strategy 21, 22. Other factors include the surgical requirement for depth of neuromuscular blockade and patients' risk factors such as age, and physiological status Type of stimulus Phase (depth) of neuromuscular block Reversal (sugammadex availablea) Reversal (sugammadex unavailable) Post tetanic count 50-Hz stimulus for 5 s followed by up to 20 single 1-Hz stimuli Intense (count < 3) Deep (count > 3) Sugammadex 4-16 mg.kg−1 Sugammadex 4 mg.kg−1 Wait till TOF count 4 Wait till TOF count 4 TOF count Four stimuli delivered every 0.5 s with 2-Hz frequency) Intermediate (TOF count 1-3) Recovery (TOF count 4) With fadeb Without fadeb Sugammadex 2 mg.kg−1 Neostigminec 50 μg.kg−1 Neostigminec 30 μg.kg−1 Wait till TOF count 4 Neostigminec 50 μg.kg−1 Neostigminec 30 μg.kg−1 TOF ratio Measurable using a quantitative monitor only, once the fourth twitch has returned on TOF stimulation Recovery (TOF count 4) TOF ratio 0-0.8 TOF ratio > 0.9 Neostigminec 30-50 μg.kg−1 No reversal Neostigminec 30-50 μg.kg−1 No reversal Double-burst stimulus Two short-duration 50-Hz stimuli separated by 750-ms interval) Recovery (TOF count 4) Fade (on 2nd stimulus) No fade (on 2nd stimulus) Neostigminec 50 μg.kg−1 Neostigminec 30 μg.kg−1 Neostigminec 50 μg.kg−1 Neostigminec 30 μg.kg−1 TOF, train-of-four a Sugammadex is an option if available and if steroidal neuromuscular blocking drugs have been used. b Absence of visible or tactile fade on TOF delivery cannot reliably differentiate a TOF ratio between 0.4 and 1.0. c If neostigmine is used without a quantitative monitor, wait for recovery to TOF count 4, and allow at least 15 min after administration, before full awakening. Neostigmine reversal from deeper neuromuscular block (TOF count < 4) should only be attempted if guided by a quantitative monitor. d Absence of visible or tactile fade after double-burst stimulation cannot reliably differentiate a TOF ratio between 0.6 and 1.0. Most peripheral nerve stimulators in clinical use are simple, qualitative devices, delivering one or more of a set pattern of stimulation modes (Table 1). Until recently, quantitative nerve stimulation has been the preserve of researchers, but devices employing it are now commercially available, usually using the principle of acceleromyography, in which a piezo-electric transducer attached to the stimulated muscle measures the force produced by that muscle after nerve stimulation. The key differentiating feature that quantitative peripheral nerve stimulators provide is measurement and display of the TOF ratio. This is of crucial importance in measuring recovery to a TOF ratio > 0.9 and in ensuring an adequate return of muscle function. Without the use of quantitative monitors, there is a 'neuromuscular function monitoring gap'. This exists once four twitches return on TOF monitoring, and there is an absence of clinically detectable fade (~a TOF ratio of 0.4), often recorded as 'four strong twitches present'. At this point, the TOF ratio could be anywhere between 0.4 (with the risk of residual neuromuscular blockade and patient harm) and 0.9 or greater (adequate recovery). Studies have demonstrated that fewer patients enter the recovery room with a TOF ratio < 0.9 when acceleromyography is used, compared with conventional nerve stimulators, with fewer associated respiratory adverse events and reduced symptoms of weakness 25, 26. Residual neuromuscular blockade The modern definition of residual neuromuscular blockade is failure to achieve a TOF ratio > 0.9. This is necessary for recovery of the most sensitive muscle groups including the pharyngeal, masseter and genioglossus muscles, allowing upper airway recovery and the reduction of aspiration risk 27. This target replaces an earlier one of ≥ 0.7, the threshold for recovery of normal vital capacity and inspiratory force 28. Many studies have found a high incidence of residual neuromuscular blockade after anaesthesia and surgery 29-33, with a range of 4-64%. Naguib et al.'s meta-analysis of 24 studies demonstrated a pooled incidence of 41% 31. Surveys confirm that anaesthetists consistently underestimate the incidence of residual neuromuscular blockade and under-use peripheral nerve stimulation monitors 6, 34, 35. In one such survey, over half of the respondents gave the incidence of residual neuromuscular blockade as < 1% 6. There are many studies of NBDs' effects on healthy awake subjects. At a TOF ratio of 0.8-0.9, volunteers experience diplopia, muscle weakness and pharyngeal dysfunction affecting speech and swallowing. At a TOF ratio of 0.5-0.8, decreased inspiratory flow, impaired hypoxic ventilatory drive and partial upper airway obstruction occur 36-38. The question is whether these effects cause patients harm or distress. For some patients, the likelihood of residual paralysis and the potential for harm increases; these include the elderly, females and patients with obesity, sleep apnoea, hypothermia and reduced physiological reserve. Clinical and cohort studies demonstrate harm, including serious respiratory events and increased mortality. Six decades ago, Beecher and Todd 39 reported a six-fold increase in mortality when NBDs were used. Arbous et al. found an incidence of 0.09% (among 900 000 patients) for an outcome of unexpected coma or death for patients receiving NBDs. There was a 90% reduction in a matched cohort of patients who received reversal of NBDs 40. In a case control study, Murphy et al. found the overall incidence of significant adverse respiratory events in the recovery room to be 0.8%; 90% of these patients had TOF ratios < 0.7 on acceleromyography 41. A large cohort study found that modern NBDs were associated with an increased incidence of arterial oxygen desaturation < 90% (5%) and tracheal re-intubation (0.8%) 8. Residual neuromuscular blockade is entirely preventable if anaesthesia is maintained until there is documented evidence of return to a TOF ratio > 0.9. The only guaranteed way to achieve this is to use a quantitative peripheral nerve stimulator, as discussed above, which is encouraged in the revised AAGBI guidelines. However, a comprehensive strategy for managing neuromuscular blockade is likely to be most effective. Strategy for neuromuscular blockade A strategy for neuromuscular blockade, such as that described by Baillard et al. 42, requires education and training to be effective 43. Such a strategy should include use of a quantitative peripheral nerve stimulator throughout all phases of anaesthesia. The device should be activated after induction of anaesthesia and before administration of NBDs, to confirm its correct position and function. It may be tempting to reduce the use of NBDs at induction 1 but there is evidence of harm (vocal cord injury) after tracheal intubation without adequate neuromuscular blockade 44, 45. Additional benefits of using and monitoring NBDs include ensuring adequate neuromuscular blockade, aiding mask ventilation 46 and optimising difficult airway management 47. The need for further administration of NBDs during surgery should be individualised and planned. For many surgical procedures, ongoing deep neuromuscular blockade is not required, but for some surgical procedures, deeper levels are required to optimise surgical conditions. These include abdominal surgery, especially that requiring diaphragmatic paralysis, and surgery where patients' movement would have profound adverse consequences for surgical outcomes, e.g. intracranial or upper airway endoscopic surgery. Use of a quantitative peripheral nerve stimulator is key to prevent residual neuromuscular blockade and patient harm. This allows tailoring of neuromuscular blockade to patients' and surgical needs, and a choice at the end of surgery, including: no reversal required (spontaneous recovery of TOF ratio > 0.9), or use of neostigmine or sugammadex. Rational choice will depend on drug availability, clinical factors and depth of neuromuscular blockade (Table 1). Confirmation of a TOF ratio of > 0.9 must be achieved, before awakening and tracheal extubation. Conclusion Problems with the use of NBDs, the monitoring of neuromuscular blockade and effective reversal are underrated as an issue by anaesthetists. We propose that a strategy should be adopted and use of a quantitative peripheral nerve stimulator should be mandatory throughout anaesthesia, for all patients receiving NBDs. An achievable challenge is no less than the elimination of residual neuromuscular blockade. Competing interests No external funding declared. GR is a member of the AAGBI Recommendations for Standards of Monitoring during Anaesthesia and Recovery Working Party. References 1Pandit JJ, Andrade J, Bogod DG, et al. 5th National Audit Project (NAP5) on accidental awareness during general anaesthesia: summary of main findings and risk factors. Anaesthesia 2014; 69: 1089– 101. 2Eriksson LL. Evidence based practice and neuromuscular monitoring. Its time for routine quantitative assessment. Anesthesiology 2003; 98: 1037– 9. 3Brull SJ, Prielipp RC. 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