ABSTRACT
OBJECTIVE: To study the relation between cerebrospinal fluid (CSF) glucose levels, the highest level of sensory block, and the duration of motor block after intrathecal injection of 2 mL of hyperbaric bupivacaine. To determine CSF glucose levels upon recovery from motor block. PATIENTS AND METHODS: A prospective study of 34 patients administered a spinal anesthetic in continuous infusion through a 22-gauge catheter. CSF samples were extracted through the catheter 5, 10, 15, 20, 30, 45, and 60 minutes after start of infusion and upon motor recovery. After each extraction the intensity of the motor block was assessed; the intensity of the sensory block was assessed after each extraction up to 20 minutes. RESULTS: Glucose concentrations in CSF tended to decrease from 5 minutes (1027.07 [SD 349.04] mg dL(-1)) until full motor recovery (247.50 [20.39] mg dL(-1)). The probability of finding a motor block at a CSF glucose concentration of 287.5 mg dL(-1) or higher was less than 5%. We identified a positive correlation between the highest level of sensory block and the duration of full motor block (r=0.62, P<0.01) and between CSF glucose levels at the moment of greatest sensory block and upon full motor recovery (r=0.50, P<0.01). CONCLUSIONS: After continuous spinal anesthesia with hyperbaric bupivacaine, glucose concentrations in CSF are directly related to the highest level of sensory block, the course of the blockade, and its reversal.
Subject(s)
Anesthesia, Spinal , Anesthetics, Local/pharmacokinetics , Bupivacaine/pharmacokinetics , Glucose Solution, Hypertonic/pharmacokinetics , Glucose/cerebrospinal fluid , Movement/drug effects , Sensation/drug effects , Aged , Anesthesia Recovery Period , Anesthetics, Local/administration & dosage , Bupivacaine/administration & dosage , Drug Interactions , Female , Glucose Solution, Hypertonic/administration & dosage , Humans , Hydrogen Bonding , Injections, Spinal/methods , Male , Prospective Studies , SolubilityABSTRACT
A 75-years-old man with Alzheimer's disease, treated with the cholinesterase inhibitor donepezil for 14 months, was scheduled for left colectomy under general anesthesia. During the procedure, succinylcholine-induced relaxation was prolonged and the effect of atracurium besylate was inadequate even at higher doses than those indicated for the patient's weight. Cholinesterase blood tests performed 10 months, 1 month and 10 days before surgery had demonstrated a gradual decrease in the duration of activity of the enzyme. Such an effect, which has been described for cholinesterase inhibitors like neostigmine and donepezil, would explain the prolonged effect of succinylcholine. After ruling out other causes for resistance to atracurium, we conclude that donepezil or its metabolites acted on muscle plaque, blocking acetylcholine hydrolysis and antagonizing atracurium.
Subject(s)
Alzheimer Disease/drug therapy , Atracurium/antagonists & inhibitors , Cholinesterase Inhibitors/pharmacology , Indans/pharmacology , Nootropic Agents/pharmacology , Piperidines/pharmacology , Succinylcholine/antagonists & inhibitors , Acetylcholine/metabolism , Aged , Alzheimer Disease/complications , Anesthesia, General , Atracurium/administration & dosage , Cholinesterase Inhibitors/therapeutic use , Colectomy , Diverticulum, Colon/complications , Diverticulum, Colon/surgery , Donepezil , Drug Interactions , Drug Therapy, Combination , Humans , Indans/therapeutic use , Lorazepam/therapeutic use , Male , Mianserin/therapeutic use , Nootropic Agents/therapeutic use , Piperidines/therapeutic use , Succinylcholine/administration & dosageABSTRACT
Un paciente de 75 años que padecía enfermedad de Alzheimer, por lo que estaba en tratamiento desde hacía 14 meses con donepezilo (inhibidor de la acetilcolinesterasa) fue programado para intervención de colectomía izquierda bajo anestesia general, y presentó en el transcurso de la misma un alargamiento del tiempo de relajación por succinilcolina, así como una relajación posterior inadecuada por besilato de atracurio que requirió una dosificación mayor de la prevista por su peso.Al paciente se le habían realizado tres tipificaciones de colinesterasa diez meses, un mes y una semana previas a la intervención, que mostraban una disminución progresiva en el tiempo de la actividad total de la enzima, esto que ya ha sido descrito como una acción de los inhibidores de la colinesterasa como la neostigmina, también es un efecto del donepezilo y explicaría el alargamiento de la acción de la succinilcolina. La resistencia al atracurio, después de descartar otras causas, creemos que fue debida a un efecto del donepezilo o sus metabolitos sobre la placa muscular, en la que actuó bloqueando la hidrólisis de la acetilcolina y antagonizando el efecto del atracurio. (AU)
