ABSTRACT
The antagonism of steroidal nondepolarizing neuromuscular blockers (NDMBs) moved forward recently with the introduction of sugammadex, the only drug able to immediately reverse the effects of curarization produced by NDMBs. This advance has necessitated reflection on the future role of pseudocholinesterase. In spite of the side effects of succinylcholine and published opinions on its use, this NDMB continues to be used in clinical anesthesia. Pseudocholinesterase is mainly found in the liver, plasma, and nervous system. The enzyme is synthesized in the liver in greater amounts than required although certain conditions lead to deficiency, which is usually asymptomatic. The only clinical expression is the apnea which develops after administration of succinycholine because this NDMB cannot be metabolized. In some patients, slight reductions in the antagonism of succinylcholine lead to rising neuromuscular concentrations of the drug in accordance with the degree and duration of the blockade. We review the various forms of pseudocholinesterase deficiency, including a discussion of genetic variants, clinical manifestations, and management. In addition to discussing the diagnosis of this condition and the clinical implications, we highlight the importance of practice protocols and access to a referral laboratory if one is not available within the immediate hospital.
Subject(s)
Cholinesterases/physiology , Cholinesterases/deficiency , Cholinesterases/genetics , Deficiency Diseases/therapy , HumansABSTRACT
Las novedades recientemente manifestadas en el campo de la antagonizacion de los relajantes neuromusculares no despolarizantes (BNMND) esteroideos, nos ha hecho revisar cual es o seguirá siendo en el futuro el rol que realizaran las enzimas plasmáticas seudocolinesterasas (CP SC) Con la introducción del sugamadex única molécula capaz de antagonizar de forma inmediata los efectos de la curarizacion producida por este tipo de bloqueantes neuromusculares (BNM) A pesar de sus efectos colaterales y la opinion encontrada de numerosos autores, la succinilcolina (SCH) sigue siendo un bloqueante neuromuscular despolarizante (BNMD) utilizado en el mundo de la anestesia clínica. La colinesterasa plasmática (CP), se encuentra presente principalmente en el hígado, plasma y sistema nervioso. Es sintetizada en el hígado en cantidades supriores a las necesarias. Asimismo puede presentarse en cantidades menores en diferentes situaciones patológicas. Los pacientes con déficit de CP son generalmente asintomáticos, y sólo tiene expresión clínica, mediante la aparición de apnea succinilcolínica, tras la administración de succinilcolina, por imposibilidad de metabolizar este fármaco. En algunos sujetos pequeñas disminuciones de la inactivación de la succinilcolina, producen un gran incremento del fármaco en la placa neuromuscular, del grado y duración del bloqueo. En esta revisión hacemos un repaso de los déficit de CP sus diferentes alteraciones por variantes genéticas, su clínica y su tratamiento. Además de sus implicaciones clínicas y método de diagnostico sin olvidar la importancia de tener elaborados protocolos de actuación y posibilidad de tener un laboratorio de referencia si no se determinan en nuestro medio hospitalario(AU)
The antagonism of steroidal nondepolarizing neuromuscular blockers (NDMBs) moved forward recently with the introduction of sugammadex, the only drug able to immediately reverse the effects of curarization produced by NDMBs. This advance has necessitated reflection on the future role of pseudocholinesterase. In spite of the side effects of succinylcholine and published opinions on its use, this NDMB continues to be used in clinical anesthesia. Pseudocholinesterase is mainly found in the liver, plasma, and nervous system. The enzyme is synthesized in the liver in greater amounts than required although certain conditions lead to deficiency, which is usually asymptomatic. The only clinical expression is the apnea which develops after administration of succinycholine because this NDMB cannot be metabolized. In some patients, slight reductions in the antagonism of succinylcholine lead to rising neuromuscular concentrations of the drug in accordance with the degree and duration of the blockade. We review the various forms of pseudocholinesterase deficiency, including a discussion of genetic variants, clinical manifestations, and management. In addition to discussing the diagnosis of this condition and the clinical implications, we highlight the importance of practice protocols and access to a referral laboratory if one is not available within the immediate hospital(AU)
