¿Estimulador de nervio periférico para succinilcolina?, tranquilidad para pacientes y anestesiólogos / A peripheral nerve stimulator for succinylcholine? Peace of mind for patients and anaesthesiologists

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Unknown Pseudocholinesterase Deficiency in a Patient Undergoing TIVA with Planned Motor Evoked Potential Monitoring: A Case Report.

Pseudocholinesterase abnormalities are a genetic cause of aberrant metabolism of the depolarizing muscle relaxant succinylcholine. This article examines a case where succinylcholine was chosen to facilitate intubation due to its ultra short duration and the request of the surgeon to monitor motor evoked potentials. Following succinylcholine administration the neurophysiologist was unable to obtain motor evoked potentials. This case study highlights the intraoperative and postoperative management of an elderly patient with an unknown pseudocholinesterase deficiency.

Use of neuromuscular monitoring to detect prolonged effect of succinylcholine or mivacurium: three case reports.

Mutations in the butyrylcholinesterase gene can lead to a prolonged effect of the neuromuscular blocking agents, succinylcholine and mivacurium. If the anaesthesiologist is not aware of this condition, it may result in insufficient respiration after tracheal extubation. However, this can be avoided with the use of objective neuromuscular monitoring if used adequately. Three case reports of prolonged effect of succinylcholine or mivacurium were presented to illustrate the importance of neuromuscular monitoring during anaesthesia. In the first case, continuous intraoperative neuromuscular monitoring allowed a prolonged neuromuscular blockade to be discovered prior to tracheal extubation of the patient. The patient was extubated after successful reversal of the neuromuscular blockade. On the contrary, neuromuscular monitoring was not used during anaesthesia in the second patient; hence, the prolonged effect of the neuromuscular blocking agent was not discovered until after extubation. In the third patient, the lack of response to nerve stimulation was interpreted as a technical failure and the prolonged effect of succinylcholine was discovered when general anaesthesia was terminated. Both patients had insufficient respiration. They were therefore re-sedated, transferred to the intensive care unit and the tracheas were extubated after full recovery from neuromuscular blockade. We recommend the use of monitoring every time these agents are used, even with short-acting drugs like succinylcholine and mivacurium.

[Residual relaxant block due to pseudocholinesterase deficiency - First manifestation in an elderly patient]. / Kasuistik: Relaxansüberhang durch Pseudocholinesterasemangel - Erstmanifestation in höherem Alter.

Pseudocholinesterase or butyrylcholinesterase (BChE) inactivates the relaxant drugs mivacurium and suxamethonium. A deficiency in plasma activity of this enzyme may result in prolonged muscular paralysis and subsequently the need for an extended duration of mechanical ventilation. We report the case of a 65-year-old patient who was diagnosed with butyrylcholinesterase deficiency for the first time during elective surgery. Neuromuscular monitoring constitutes a central diagnostic asset in ensuring patient safety.

Utilización de rocuronio tras uso de sugammadex / Rocuronium used after sugammadex

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Pharmacokinetic properties of succinylmonocholine in surgical patients.

Intoxications with succinylcholine (SUX) lead to a potentially lethal respiratory paralysis, and forensic cases involving accidental or deliberate SUX-application have been reported. Detection of SUX as well as its metabolite succinylmonocholine (SMC) is difficult: both substances are analytically challenging, and the extremely short plasma half-life of SUX additionally hampers detection of the parent compound. Pharmacokinetic data are scarce on SUX and non-existent on SMC. To enhance forensic knowledge concerning SUX intoxications, plasma pharmacokinetics of SMC were investigated in anesthetized patients. Fifteen subjects scheduled for a surgical procedure were included in this study. Muscle-relaxation was initialized with a bolus injection of 80-100 mg SUX. Blood sampling was performed within 6 h after SUX application using paraoxonized tubes. Collected plasma was processed according to a validated isotope dilution high-performance liquid chromatography-tandem mass spectrometry method using ion-pair solid-phase extraction. Pharmacokinetic parameters were derived from a user-defined as well as a three-compartment model. For SMC, peak plasma concentrations were reached after 0.03-2.0 min. In contrast to SUX, SMC was more slowly and more extensively distributed, featuring triphasic plasma concentration time profiles. Pharmacokinetic key parameters were subject to interindividual variation of potential forensic importance, with terminal half-lives of 1-3 h indicating a detection interval of 8-24 h for SMC in plasma. SMC was proven to be the only realistic SUX marker in a forensic context. The present work defines meaningful detection windows for plasmatic SMC after SUX application and offers guideline values for forensic toxicological casework.

Prolonged succinylcholine action during electroconvulsive therapy (ECT) after cytarabine, vincristine, and rituximab chemotherapy.

Succinylcholine is a depolarizing neuromuscular blocker frequently used during electroconvulsive therapy. In most patients, the duration of paralysis is brief, allowing for spontaneous respiration shortly after the therapy. We report a case of delayed return of neuromuscular function after succinylcholine administered during electroconvulsive therapy in a 72-year-old man receiving cytarabine, vincristine, and rituximab chemotherapy for chronic lymphocytic leukemia. We hypothesize that an interaction between succinylcholine and one of the chemotherapeutic agents caused the prolongation of paralysis and believe that this is the first reported case of prolonged duration of succinylcholine following this regimen of chemotherapy. Despite this unexpected prolonged neuromuscular blockade, the patient could be treated uneventfully, with attention paid to his respiratory support and with subsequent succinylcholine dose titration to effect.

Determination of suxamethonium in a pharmaceutical formulation by capillary electrophoresis with contactless conductivity detection (CE-C(4)D).

A simple method based on capillary electrophoresis with a capacitively coupled contactless conductivity detector (CE-C(4)D) was developed for the determination of suxamethonium (SUX) in a pharmaceutical formulation. A hydro-organic mixture, consisting of 100mM Tris-acetate buffer at pH 4.2 and acetonitrile (90:10, v/v), was selected as background electrolyte (BGE). The applied voltage was 30kV, and the sample injection was performed in the hydrodynamic mode. All analyses were carried out in a fused silica capillary with an internal diameter of 50 microm and a total length of 64.5cm. Under these conditions, a complete separation between SUX, sodium ions and the main degradation products (choline) was achieved in less than 4min. The presence of acetonitrile in the BGE allowed a reduction of SUX adsorption on the capillary wall. The CE-C(4)D method was validated, and trueness values between 98.8% and 101.1% were obtained with repeatability and intermediate precision values of 0.7-1.3% and 1.2-1.6%, respectively. Therefore, this method was found appropriate for controlling pharmaceutical formulations containing suxamethonium and degradation products.

Anestesia en terapia electroconvulsiva. Experiencia clínica / Anesthesia for electroconvulsive therapy: clinical experience

OBJETIVO: Valoramos el efecto de la anestesia con propofoly succinilcolina (Sch) en obtener convulsiones óptimasy mantener la seguridad del paciente durante laterapia electroconvulsiva (TEC).PACIENTES Y MÉTODOS: Realizamos un estudio prospectivoobservacional en pacientes sometidos a TECbajo anestesia general con propofol y Sch. Registramosvariables demográficas, dosis de propofol y Sch, númerode estímulos aplicados, duración electroencefalográfica(EEG) de las convulsiones y complicaciones. Utilizamosestadísticas descriptivas, análisis de correlación, t de studentpara muestras independientes, ANOVA de una víay Mann-Whitney.RESULTADOS: Estudiamos 108 pacientes, 62% mujeresy 38% hombres, 80% ASA I y 20% ASA II, sometidos a844 sesiones de TEC, con una edad de 39,95 ± 18,09años. Las dosis de propofol y Sch fueron 1,34 ± 0,32 mgkg-1 y 1,35 ± 0,26 mg kg-1, respectivamente. La duraciónEEG de la primera convulsión (29,87 ± 22,42 segundos)tuvo una correlación negativa con la edad (r = -0,12), notuvo correlación con la dosis de propofol (r = 0,06) ni conel peso corporal (r = 0,02). Los pacientes hombres y losportadores de esquizofrenia tuvieron convulsiones demayor duración (p < 0,01). Hubo complicaciones cardiovasculares(2,4%) y agitación psicomotora (1,4%); nohubo complicaciones respiratorias, ni traumatismosmusculoesqueléticos, ni náuseas ni vómitos.CONCLUSIONES: La TEC es un procedimiento segurorealizado en el quirófano o en un área similar, con anestesiageneral y bloqueo neuromuscular para prevenir eltrauma psicológico y musculoesquelético. A las dosisadministradas el propofol no afectó las convulsiones (AU)

OBJECTIVE: To assess the utility of propofol and succinylcholine in obtaining optimal convulsions and assuring patient safety during electroconvulsive therapy. PATIENTSANDMETHODS: This was a prospective observational study of patients undergoing electroconvulsive therapy under general anesthesia with propofol and succinylcholine. We recorded patient characteristics, doses of propofol and succinylcholine, electroencephalographically-recorded duration of convulsions, and complications. Descriptive statistics were compiled and the data were subjected to analysis of correlations, comparison with the Student t test for independent samples, the Mann-Whitney U test, and analysis of variance. RESULTS: We studied 108 patients, 62% women and 38% men, 80% classified as ASA 1 and 20% as ASA 2. The patients underwent 844 sessions of electroconvulsive therapy ;their mean (SD) age was 39.95 (18.09) years. The doses of propofol and succinylcholine were 1.34 (0.32) mg·kg–1 and 1.35 (0.26) mg·kg–1, respectively. The mean recorded duration of the first convulsion (29.87 [22.42] seconds) was negatively correlated with age (r = –0.12) and unrelated to propofol dose (r = 0.06) or body weight (r = 0.02). Male and schizophrenic patients had longer-lasting convulsions (P < .01). Cardiovascular complications occurred in 2.4% and psychomotor agitation in 1.4%; there were no respiratory complications, musculoskeletal injuries, nausea, or vomiting. CONCLUSIONS: Electroconvulsive therapy can be safely applied in an operating room or similar space under general anesthesia and with a neuromuscular blockade in order to prevent psychological or musculoskeletal trauma. Propofol did not affect the convulsions at the dosages administered (AU)

[Interaction between mivacurium and succinylcholine from a different point of view]. / Interacción entre mivacurio y succinilcolina: vista desde otra perspectiva.

OBJECTIVES: Succinylcholine (SCH) may first be used and continue with mivacurium (MIV). MIV has been suggested as a pretreatment. Conflicting results arises from studies on SCH-MIV interaction. The following trial revisits this interaction. PATIENTS AND METHODS: The patients were intubated after randomized administration of 100 microg x Kg(-1) of mivacurium (group 1) or 1 mg x Kg(-1) of succinylcholine and, after 50% recovery, 100 microg x Kg(-1) of mivacurium (group 2). A third group received the same regimen as group 2, preceded by pretreatment with 10 microg x Kg(-1) of mivacurium. Maximum effect (MAX), onset time, the 10%-25% recovery index, and duration of effect of mivacurium were determined by electromyography. In groups 2 and 3, the corrected MAX was defined as the difference between the actual MAX effect and the residual block after administration of succinylcholine, and speed of action was defined as the ratio between MAX or corrected MAX and onset time. Data were subjected to analysis of variance and Student-Newman-Keuls and t tests for bivariate comparisons. A value of P less than 0.05 was considered significant. RESULTS: Groups 2 and 3 had significantly greater MAX effects (97% and 98%, respectively) in comparison with group 1 (93%), shorter onset times (135 and 158 seconds in groups 2 and 3 vs 279 seconds in group 1), and greater speed of action without changes in duration of effect. MAX was halved when corrected (to 47% and 49% in groups 2 and 3, respectively), and speed of action was significantly reduced (from 1.34 and 1.62 seconds/% in groups 2 and 3 respectively, to 2.69 and 3.36 seconds/%). Mivacurium pretreatment did not produce relevant clinical changes. CONCLUSIONS: When mivacurium is used before the effects of succinylcholine disappear, a residual effect is not usually taken into consideration. This study corrected MAX and calculated speed of action, demonstrating a reduction in net block and speed of action, consistent with an antagonistic action when the 2 blockers are administered sequentially.

Interacción entre mivacurio y succinilcolina: vista desde otra perspectiva / Interaction between mivacurium and succinylcholine from a different point of view

OBJETIVOS: La succinilcolina (SC) puede utilizarseinicialmente para continuar con mivacurio (MIV), y estea su vez como precurarizante. Esta interacción da lugara contradicciones y revisarlas es nuestro propósito.PACIENTES Y MÉTODOS: Los pacientes fueron intubadostras utilizar aleatoriamente: MIV 100 µg Kg-1 (grupo 1),SC 1 mg.Kg-1 y al cabo de una recuperación del 50%,MIV 100 µg Kg-1 (grupo 2). En el grupo 3 el mismo régimenprecedido por una precurarización con MIV 10 µgKg-1. Electromiográficamente se determinaron: máximoefecto (MAX), tiempo de comienzo (TC), índice de recuperaciónentre 10-25% y duración clínica (DUR) delMIV. Como MAX corregido (©MAX) consideramos lasustracción del bloqueo remanente al valor actual en losgrupos 2 y 3 y como velocidad de acción (VA) la relaciónentre MAX o ©MAX y TC. Se utilizaron: análisis devarianza, pruebas de Student-Newman-Keuls y T paracomparaciones y p>0,05 como significancia.RESULTADOS: En los grupos 2 y 3 el MIV mostró unsignificativo incremento de MAX (97-98% vs 93), reducciónde TC (135-158 vs 279 segundos) y aumento de laVA, sin modificaciones en la DUR. Usando ©MAX seredujo a la mitad MAX (47-49%) y disminuyó VA (1,34-1,62 segundos/% vs 2,69-3,36). La precurarización noañadió cambios relevantes.CONCLUSIONES: Cuando se utiliza MIV antes de desaparecerlos efectos de la SC, habitualmente no se cuenta conel efecto remanente. Este ensayo corrigió el MAX y calculóla VA, reduciendo el bloqueo neto y la VA, representandoun antagonismo para la secuencia de ambos bloqueantes

OBJECTIVES: Succinylcholine (SCH) may first be usedand continue with mivacurium (MIV). MIV has beensuggested as a pretreatment. Conflicting results arisesfrom studies on SCH-MIV interaction. The followingtrial revisits this interaction.PATIENTS AND METHODS: The patients were intubatedafter randomized administration of 100 µg·Kg-1 of mivacurium(group 1) or 1 mg·Kg-1 of succinylcholine and,after 50% recovery, 100 µg·Kg-1 of mivacurium (group 2).A third group received the same regimen as group 2, precededby pretreatment with 10 µg·Kg-1 of mivacurium.Maximum effect (MAX), onset time, the 10%-25% recoveryindex, and duration of effect of mivacurium weredetermined by electromyography. In groups 2 and 3, thecorrected MAX was defined as the difference between theactual MAX effect and the residual block after administrationof succinylcholine, and speed of action was definedas the ratio between MAX or corrected MAX and onsettime. Data were subjected to analysis of variance and Student-Newman-Keuls and t tests for bivariate comparisons.A value of P less than 0.05 was considered significant.RESULTS: Groups 2 and 3 had significantly greaterMAX effects (97% and 98%, respectively) in comparisonwith group 1 (93%), shorter onset times (135 and 158seconds in groups 2 and 3 vs 279 seconds in group 1),and greater speed of action without changes in durationof effect. MAX was halved when corrected (to 47% and49% in groups 2 and 3, respectively), and speed of actionwas significantly reduced (from 1.34 and 1.62 seconds/%in groups 2 and 3 respectively, to 2.69 and 3.36seconds/%). Mivacurium pretreatment did not producerelevant clinical changes.CONCLUSIONS: When mivacurium is used before theeffects of succinylcholine disappear, a residual effect isnot usually taken into consideration. This study correctedMAX and calculated speed of action, demonstrating areduction in net block and speed of action, consistentwith an antagonistic action when the 2 blockers areadministered sequentially

[Infant boy with propionic acidemia: anesthetic implications]. / Implicaciones anestésicas en un niño afecto de acidemia propiónica.

A 12-month-old boy diagnosed with propionic acidemia underwent gastrostomy. The patient's general state was good and he was alert, but with reduced muscular tone (unstable when seated with support, floppy head) and with dystonic movements in all extremities. An electroencephalogram showed slightly slowed brain activity. The patient was being treated with a low protein diet, phenobarbital, L-carnitine, L-isoleucine, and biotin. Surgery was carried out in satisfactory conditions with general anesthesia without opioids combined with infiltration of the surgical wound with local anesthetic. Recovery from anesthesia was rapid and free of complications. Propionic acidemia is caused by mitochondrial propionyl coenzyme carboxylase deficiency. Most patients have episodes of severe metabolic ketoacidosis as a result of excessive protein intake, delayed development, vomiting, gastroesophageal reflux, lethargy, hypotonia, and convulsions. The anesthetic approach involves avoiding triggers of metabolic acidosis (such as fasting, dehydration, hypoxemia, and hypotension) and preventing airway complications. Agents that metabolize propionic acid (such as succinylcholine, benzylisoquinoline neuromuscular blocking agents, and propofol) are not used, as they can exacerbate acidemia. We also believe that using local or regional anesthesia in combination with general anesthesia without opiates is safe and effective for controlling pain during surgery and postoperative recovery, as that combination avoids respiratory depression in these patients, who are highly sensitive to opiates.

Implicaciones anestésicas en un niño afecto de acidemia propiónica / Infant boy with propionic acidemia: anesthetic implications

Un niño de 12 meses de edad con diagnóstico de acidemia propiónica fue intervenido para gastrostomía. El paciente presentaba buen estado general y sensorio despejado, tono muscular disminuido, sedestación inestable con apoyo, sostén cefálico incompetente y movimientos distónicos de las cuatro extremidades. El EEG mostraba una actividad bioeléctrica cerebral discretamente enlentecida. El paciente estaba siendo tratado con dieta hipoproteica, fenobarbital, L-carnitina, L-isoleucina y biotina. La cirugía fue realizada bajo anestesia general sin opioides combinada con infiltración de la herida quirúrgica con anestésico local, que proporcionó condiciones quirúrgicas satisfactorias y una recuperación de la anestesia rápida y sin complicaciones. La acidemia propiónica se produce como consecuencia de la actividad deficiente de la enzima mitocondrial propionilCo-A carboxilasa. La mayoría de los pacientes presentan episodios de cetoacidosis metabólica severa secundaria a la excesiva ingesta proteica, retraso del desarrollo, vómitos, reflujo gastroesofágico, letargia, hipotonía y crisis convulsivas. La conducta anestésica se dirige a evitar los precipitantes de acidosis metabólica (ayuno, deshidratación, hipoxemia e hipotensión arterial) y las complicaciones de la vía aérea, así como no utilizar agentes anestésicos que se metabolizan a ácido propiónico como la succinilcolina, bloqueantes neuromusculares bencilisoquinoleínicos y el propofol, ya que pueden contribuir a la acidemia. Además, consideramos que el empleo de anestesia locorregional combinada con anestesia general sin opioides es segura y efectiva para el control del dolor durante la intervención y en el postoperatorio, ya que evitaría la depresión respiratoria en estos pacientes con elevada sensibilidad a los opioides

A 12-month-old boy diagnosed with propionic acidemia underwent gastrostomy. The patient's general state was good and he was alert, but with reduced muscular tone (unstable when seated with support, floppy head) and with dystonic movements in all extremities. An electroencephalogram showed slightly slowed brain activity. The patient was being treated with a low protein diet, phenobarbital, L-carnitine, L-isoleucine, and biotin. Surgery was carried out in satisfactory conditions with general anesthesia without opioids combined with infiltration of the surgical wound with local anesthetic. Recovery from anesthesia was rapid and free of complications. Propionic acidemia is caused by mitochondrial propionyl coenzyme carboxylase deficiency. Most patients have episodes of severe metabolic ketoacidosis as a result of excessive protein intake, delayed development, vomiting, gastroesophageal reflux, lethargy, hypotonia, and convulsions. The anesthetic approach involves avoiding triggers of metabolic acidosis (such as fasting, dehydration, hypoxemia, and hypotension) and preventing airway complications. Agents that metabolize propionic acid (such as succinylcholine, benzylisoquinoline neuromuscular blocking agents, and propofol) are not used, as they can exacerbate acidemia. We also believe that using local or regional anesthesia in combination with general anesthesia without opiates is safe and effective for controlling pain during surgery and postoperative recovery, as that combination avoids respiratory depression in these patients, who are highly sensitive to opiates

Concentration-effect relation of succinylcholine chloride during propofol anesthesia.

BACKGROUND: The pharmacokinetics and pharmacodynamics of succinylcholine were studied simultaneously in anesthetized patients to understand why the drug has a rapid onset and short duration of action. A quantitative model describing the concentration-effect relation of succinylcholine was proposed. The correlation between hydrolysis in plasma and elimination was also examined. METHODS: Before induction of anesthesia, blood was drawn for analysis in seven adults. Anesthesia was induced with propofol and remifentanil. Single twitch stimulation was applied at the ulnar nerve every 10 s, and the force of contraction of the adductor pollicis was measured. Arterial blood was drawn frequently after succinylcholine injection to characterize the front-end kinetics. Plasma concentrations were measured by mass spectrometry, and pharmacokinetic parameters were derived using compartmental and noncompartmental approaches. Pharmacokinetic-pharmacodynamic relations were estimated. RESULTS: The mean degradation rate constant in plasma (1.07 +/- 0.49 min(-1)) was not different from the elimination rate constant (0.97 +/- 0.30 min(-1)), and an excellent correlation (r2 = 0.94) was observed. Total body clearance derived using noncompartmental (37 +/- 7 ml x min(-1) x kg(-1)) and compartmental (37 +/- 9 ml x min(-1) x kg(-1)) approaches were similar. The plasma-effect compartment equilibration rate constant (k(eo)) was 0.058 +/- 0.026 min(-1), and the effect compartment concentration at 50% block was 734 +/- 211 ng/ml. CONCLUSION: Succinylcholine is a low-potency drug with a very fast clearance that equilibrates relatively slowly with the effect compartment. Its disappearance is greatly accountable by a rapid hydrolysis in plasma.

[Succinylcholine--update]. / Succinylcholin-Update.

The action profile of succinylcholine is unmatched even 50 years after its introduction into anaesthestic practice. This is probably why succinylcholine, despite its many and partly life-threatening side-effects, is still considered to be indispensable by many anaesthetists and emergency doctors. The main indication for succinylcholine--the facilitation of endotracheal intubation in patients considered to be at an increased risk of aspiration of gastric fluid, e.g. patients undergoing a Caesarean section or presenting with an ileus--remains undisputed. Some of the side-effects of succinylcholine can be diminished by precurarisation. However, just like priming, this technique holds some considerable dangers (such as a clinically significant attenuation of the protective reflexes) and has become a matter of increasing controversy. Rocuronium (> or = 1 mg/kg) is currently the best alternative to succinylcholine for rapid sequence induction. The routine use of succinylcholine as a relaxant for intubation is questionable, mainly because there are a number of modern anaesthetic techniques (laryngeal mask airway) and new drugs (rocuronium, mivacurium, remifentanil) which make succinylcholine quite dispensable except for a few situations (e.g. re-positioning of fractures). In the case of an expected difficult airway no muscle relaxant should be given, because severe hypoxaemia in these patients probably can only be prevented by a professional airway management. Succinylcholine is no longer an option in elective paediatric anaesthesia. The drug, however, retains its value in critical situations where a rapid onset but a short duration of action is of prime importance.