Sugammadex in the management of rocuronium-induced anaphylaxis

Purpose Over the past three decades, many studies have shown a high proportion of patients in the recovery room with residual neuromuscular blockade after anesthesia. The purpose of this Continuing Professional Development module is to present the physiological consequences of residual paralysis, estimate the extent of the problem, and suggest solutions to prevent its occurrence. Principal findings Residual paralysis is defined as a train-of-four ratio (TOFR) \ 0.9 at the adductor pollicis. While tidal volume and, to a lesser extent, vital capacity are well preserved as the intensity of blockade increases, the probability of airway obstruction, impaired swallowing, and pulmonary aspiration increases markedly as TOFR decreases. In recent studies, incidences of residual paralysis from 4-57% have been reported, but surveys indicate that anesthesiologists estimate the incidence of the problem at 1% or less. The decision to administer neostigmine or sugammadex should be based on the degree of spontaneous recovery at the adductor pollicis muscle (thumb), not on recovery at the corrugator supercilii (eyebrow). The most important drawback of neostigmine is its inability to reverse profound blockade, which is a consequence of its ceiling effect. When spontaneous recovery reaches the point where TOFR [ 0.4 or four equal twitch responses are seen, reduced doses of neostigmine may be given. The dose of sugammadex required in a given situation depends on the intensity of blockade. Conclusion Careful monitoring and delaying the administration of neostigmine until four twitches are observed at the adductor pollicis can decrease the incidence of residual paralysis. The clinical and pharmacoeconomic effects of unrestricted sugammadex use are unknown at this time. ObjectivesAfter reading this module, the reader should be able to:1. Describe the physiological effects of residual neuromuscular blockade 2. Define and justify the current threshold used for residual paralysis 3. Interpret the information provided by qualitative and quantitative monitors 4. Decide the dose and timing of administration of neostigmine 5. Manage neuromuscular blockade and reversal during and after anesthesia.In 1979, Viby-Mogensen et al. 1 reported that 42% of patients receiving non-depolarizing neuromuscular blocking agents during anesthesia followed by neostigmine at the end of the procedure had neuromuscular weakness in the recovery room, as documented by a train-of-four ratio 123Can J Anesth/J Can Anesth (2013) 60:714-729 DOI 10.1007 (TOFR) \ 0.7. This first description of what was later termed residual paralysis, residual curarization, or postoperative residual curarization was followed by many other observations in many countries around the world and in different settings. The introduction of shorter-acting agents, such as vecuronium and atracurium and later rocuronium and cisatracurium, to replace the longer-acting agents available in 1979 led to a decrease in the incidence of residual paralysis. 2 Nevertheless, many lines of evidence now...

Section: Side Effectsmentioning

confidence: 99%

Section: Effets Secondairesunclassified

Residual paralysis: a real problem or did we invent a new disease?

Donati

2013

“…This hypothesis was reported for the first time through a case report. 9 The authors of that report described a serious anaphylactic reaction that occurred immediately after an induction sequence that included fentanyl, propofol, and rocuronium. There was sudden cardiac arrest -a grade IV reaction in the Ring and Messner classification.…”

mentioning

confidence: 99%

“…Cette hypothèse a été rapportée pour la première fois grâce à la publication d'un cas clinique. 9 Dans cette situation, les auteurs décrivaient une réaction anaphylactique sévère, survenant immédiatement après l'administration d'une séquence d'induction comprenant fentanyl, propofol et rocuronium avec un arrêt cardiaque d'emblée, soit un grade IV de la classification de Ring et Messner. 10 Malgré une prise en charge initiale conforme aux recommandations (massage cardiaque, adrénaline, remplissage vasculaire notamment) l'état hémodynamique ne s'améliorait pas.…”

unclassified

A new option for the treatment of anaphylaxis linked to steroidal neuromuscular blockers: How much value should we grant to case reports?

Plaud

2014

Neuromuscular blockers (NMBs) are commonly used in anesthesia to facilitate tracheal intubation and optimize surgical conditions. However, these compounds share a common side effect -the risk of an allergic reaction. Anaphylactic shock is a rare (approximately one case in 10,000-20,000 procedures) but life-threatening complication of anesthesia. 1 In France, various epidemiological studies over the last three decades have shown that the most common causal agents of anaphylaxis are NMBs. 2 In the event of anaphylactic shock, epinephrine is the first-line therapy. The dose is usually titrated -except in case of cardiac arrest -depending on the clinical presentation and based on heart rate and blood pressure, to avoid the occurrence of arrhythmia with large doses of epinephrine. 3 This symptomatic treatment, coupled with crystalloid fluid resuscitation, allows to counteract hemodynamic (decreased blood pressure and cardiac output) and respiratory (bronchoconstriction) effects of the numerous mediators that are released during the course of an anaphylactic reaction. Despite these measures, the outcome remains potentially lethal in approximately 10% of cases. 4 However, there is no specific therapy of NMBassociated anaphylaxis. Proposed therapies could involve a substance able to rapidly inhibit the anaphylactic reaction by masking or binding the causal allergen. A specific therapy for the anaphylactic reaction to dextran, used in some countries as a fluid therapy, was attempted during the 1980s with the arrival on the market of a dextran-inhibitor hapten. 5 This hapten was purported to reduce the allergystimulating effects of dextrans through specific inhibition. The effectiveness of this preventive strategy proved unreliable, notwithstanding the other adverse effects of dextrans, renal in particular. 6 Thus, there remains no specific strategy at this time regarding the prevention or treatment of allergic reactions to NMBs. Could this situation change with the recent availability of sugammadex? Sugammadex is a gammacyclodextrine that was modified by the addition of side chains that specifically encapsulate the steroidal core of the NMB, mainly through interactions between the negative charges of the cyclodextrine molecule and the positive charges of the quaternary ammonium ions. 7 Their binding at the centre of the cyclodextrine molecule, more specifically the sterol moiety, is strong and prolonged, implying the presence of various high-energy chemical bonds. Binding is rapid, and steroidal NMBs show a high affinity for sugammadex, especially rocuronium and to a lesser degree vecuronium. 8 Beyond the rapid reversal of NMBs allowed by sugammadex, 7 neutralizing the NMB molecules by masking the causal allergen (i.e., the quaternary ammonium ion) should also be considered when an NMB-related allergic event is suspected. This hypothesis was reported for the first time through a case report. 9 The authors of that report described a serious anaphylactic reaction that occurred immediately after an induction sequence that i...

“…[1][2][3] Nous décrivons après consentement, le cas d'une patiente qui a subi une réaction anaphylactique grave au rocuronium à l'induction de l'anesthésie et qui a bénéficié d'une administration de sugammadex en plus du traitement traditionnel.Une patiente de 52 ans (77 kg pour 1,59 m), était programmée pour le traitement chirurgical d'une tumeur rectale par laparoscopie. On notait dans ses antécédents un cancer du sein droit opéré, une hystérectomie totale et une césarienne.…”

unclassified

Un nouveau cas de choc anaphylactique induit par le rocuronium amélioré par le sugammadex

Badaoui¹,

Popov²,

Dupont³

2012

Au rédacteur en chef,Depuis la mise en marché du sugammadex, plusieurs cas d'anaphylaxie au rocuronium ont été traités avec succès par le sugammadex. [1][2][3] Nous décrivons après consentement, le cas d'une patiente qui a subi une réaction anaphylactique grave au rocuronium à l'induction de l'anesthésie et qui a bénéficié d'une administration de sugammadex en plus du traitement traditionnel.Une patiente de 52 ans (77 kg pour 1,59 m), était programmée pour le traitement chirurgical d'une tumeur rectale par laparoscopie. On notait dans ses antécédents un cancer du sein droit opéré, une hystérectomie totale et une césarienne. Il n'avait pas de notion d'allergie. Une antibioprophylaxie à la céfazoline 2 g est administrée 30 min avant le début de l'anesthésie. L'induction de l'anesthésie se réalise par l'injection de propofol 200 mg et de sufentanil 20 lg. Après vérification d'une ventilation manuelle sans difficulté, une injection de rocuronium 50 mg est administrée. Deux minutes plus tard, on constate une tension artérielle systolique à 50 mmHg avec tachycardie à 150 battementsÁmin -1 , puis rapidement une tension artérielle imprenable au brassard avec un érythème généralisé, une désaturation, une baisse de la concentration télé-expiratoire de CO 2 à 15 mmHg. Après intubation de la trachée avec ventilation manuelle en oxygène pur et un remplissage vasculaire (500 mL d'hydroxyéthylamidon et 500 mL Ringer lactate), une administration intraveineuse d'adrénaline en doses successives de 0,1 mg est débutée avec un relais à 0,5 mg/h en continu. Un bilan sanguin est prélevé en même temps. Vingt minutes après le début de la réanimation et malgré des doses supplémentaires d'adrénaline (6 mg au total) et un remplissage (30 mLÁkg -1 ), la tension artérielle reste à 70 mmHg avec apparition d'une bradycardie à 35 battementsÁmin -1 et de quelques troubles de rythme. On décide alors d'injecter du sugammadex 1000 mg dans l'hypothèse d'un choc anaphylactique dû au rocuronium, en espérant un bénéfice dans cette situation menaçant le pronostic vital. Cinq minutes plus tard, on note un pouls carotidien et radial, une restauration hémodynamique, ainsi qu'une recoloration cutanée. Sous adrénaline 0.7 mgÁh -1 , la tension artérielle est alors à 85/46 mmHg et la fréquence cardiaque à 97 battementsÁmin -1 . La patiente reçoit du midazolam comme sédation pour la mise en place d'une canule dans l'artère radiale gauche et d'un cathéter veineux central dans la jugulaire interne droite. La patiente est sevrée en catécholamines une heure après son admission en unité de surveillance continue. La trachée est extubée après arrêt de la sédation. La tension artérielle est alors à 103/47 mmHg et le pouls à 103 battementsÁmin -1 . La patiente quitte l'hôpital après 48 h. Le bilan biologique donne les résultats suivants: histamine [ 100 nmolÁL -1 (N \ 10 nmolÁL -1 ); tryptase: 102 lgÁL -1 (N \ 11,4 lgÁL -1 ); IgE spécifique au rocuronium: 46,33 % d'inhibition (positif). Les tests cutanés (pricks tests) sont positifs pour le rocuronium avec une papule de...