Delayed profound respiratory depression after premedication with trimeprazine

Delayed, profound respiratory depression occurred in a 4-year-old boy, who had been premedicated with trimeprazine 4 h after tonsillectomy. This is a rare, but potentially fatal idiosyncratic reaction.     

Delayed respiratory depression after risperidone overdose

Risperidone is an atypical antipsychotic drug used for the treatment of schizophrenia. Both positive and negative symptoms are prominent with its use. Metabolism occurs mainly in the liver, where risperidone is changed by CUP2D6 to an active metabolite, 9-hydroxyrisperidone. The half-lives of risperidone and its metabolite are 3 and 7 h, respectively. Genetic polymorphism is seen in the 6%-8% of white patients who are considered poor metabolizers. In poor metabolizers, the half-life extends to 20-30 h. We present an unusual case of unanticipated delayed respiratory depression after risperidone overdose.     

Oral midazolam premedication in preadolescents and adolescents.

We sought to determine the influence of preoperative oral midazolam on 1) sedation score, 2) measures of anesthetic emergence, 3) recovery times, and 4) bispectral index (BIS) measurements during sevoflurane/N(2)O anesthesia in adolescent patients. Fifty ASA I and II patients 10-18 yr of age were enrolled in a prospective double-blinded study. Patients were randomized to receive either 20 mg of midazolam (M group) or midazolam vehicle (P group) as premedication. Before the induction, sedation scores and BIS values were determined in all patients. After inhaled induction and intubation, expired sevoflurane was stabilized at 3% in 60% N(2)O and the corresponding BIS (BIS I) recorded. Upon completion of surgery, sevoflurane was stabilized at 0.5% and the BIS (BIS E) again recorded. Plasma midazolam levels were measured at the time of BIS I and BIS E. There were no significant differences between groups in awakening time, sevoflurane/N(2)O awakening concentrations, time to postanesthesia care unit discharge, or BIS I and BIS E measurements. Sedation scores and preinduction BIS values were significantly lower in Group M than in Group P, although only 40% of midazolam-treated patients exhibited detectable sedation, with marked interindividual variability in achieved plasma midazolam levels. Detectable preoperative sedation was predictive of delayed emergence. IMPLICATIONS: We demonstrated a measurable sedative effect of oral midazolam in adolescents which correlated with simultaneous bispectral index (BIS) measurement. Considering the overall group, midazolam premedication did not affect intraoperative BIS, emergence times, or recovery times compared with placebo controls. Detectable preoperative sedation, and not merely midazolam administration, was predictive of prolonged emergence.     

Effect of cimetidine premedication on morphine-induced ventilatory depression

The potential respiratory interaction between morphine and cimetidine was studied by determining resting ventilation, PETCO2 and ventilatory response to added carbon dioxide in eight healthy volunteers on three separate occasions following administration of : (1) cimetidine 600 mg p.o., (2) morphine 10 mg IM, (3) morphine 10 mg IM preceded by cimetidine 600 mg p.o. Individual entry into the study was randomized and separated by at least one week. All measurements were determined at time 0, 30, 60, 120, 180, 240, 360, 480, 600, 720 minutes and at the end of 24 hours. In addition, serum morphine levels were measured in six subjects during the first six hours following morphine administration. Cimetidine alone had negligible respiratory effects. Morphine alone reduced resting ventilation, elevated PETCO2 and reduced the ventilatory response to added CO2, while the morphine-cimetidine combination caused a more profound depression of the CO2 response and delay in its recovery. No significant difference between resting ventilation and PETCO2 was observed. We conclude that cimetidine premedication interacts with morphine to prolong the respiratory depression but the magnitude of this interaction is small and clinically insignificant in healthy subjects. Caution, however, should be exercised in susceptible patients.     

Salbutamol premedication in children with a recent respiratory tract infection

Background :  Premedication with β-2 agonists (e.g. salbutamol) is effective in preventing increases in total respiratory resistance and in decreasing the incidence of perioperative bronchospasm in asthmatic children. Because children with recent respiratory tract infection (RTI) exhibit bronchial hyperreactivity similar to that observed in asthmatic children, the use of salbutamol in children with RTI has become popular among pediatric anesthetists for the prevention of perioperative respiratory adverse events (PRAE). In a prospective observational study, we therefore assessed the usefulness of salbutamol premedication on the occurrence of PRAE.
Methods :  Results from 600 children (0–16 years) undergoing general anesthesia were analyzed: 200 children with a recent RTI who received preoperative salbutamol 10–30 min prior to surgery, 200 children with a recent RTI without salbutamol premedication, and 200 children without a RTI during the last 4 weeks. All PRAE (laryngospasm, bronchospasm, oxygen desaturation [<95%], severe coughing) were recorded.
Results :  Children with a recent RTI who received salbutamol demonstrated a significantly reduced incidence of perioperative bronchospasm (5.5% vs 11%, P  = 0.0270) and severe coughing (5.5% vs 11.5%, P  = 0.0314) compared with children who had an RTI but did not receive salbutamol. However, healthy children presented with the lowest rate (bronchospasm 1.5%, severe coughing 4.5%) of respiratory complications compared with children with a recent RTI independent whether or not they received salbutamol preoperatively.
Conclusions :  The results from this audit suggest that children with a history of a recent RTI have significantly less PRAE following a premedication with salbutamol compared with no premedication. Therefore, premedication with salbutamol might be considered in children with recent RTI.     

Time-course of respiratory depression after an alfentanil infusion-based anesthetic.

Postoperative respiratory depression after alfentanil administration has been described in several case reports. The effects of a prolonged alfentanil infusion on the CO2 response curve or cognitive function have not been studied. Twenty-one ASA physical status I or II patients were studied after a prolonged alfentanil infusion (> 90 min) to determine the incidence of postoperative respiratory depression, arterial O2 desaturation, and impairment of cognitive function. Each patient's recovery was observed at 30-min intervals for evidence of respiratory depression (utilizing the Read CO2 rebreathing method), desaturation by pulse oximetry (severe desaturation defined as arterial O2 saturation < 90%), and cognitive function (utilizing Trieger dot and digit substitution tests). Plasma samples were also examined for secondary elevations in alfentanil plasma concentrations. Significant depression of the CO2 response curve and cognitive function was found up to 1 h postoperatively. Arterial O2 desaturation was seen in 11 of 21 patients (52%). No correlation was found between arterial O2 desaturation and cognitive function scores or CO2 rebreathing results. Increased depression of the CO2 response curve was not necessarily associated with severe desaturation episodes. A secondary increase in plasma alfentanil concentration was detected in 5 of the 21 patients (24%), but these patients did not experience further depression of the CO2 response curve. We conclude that prolonged alfentanil administration may result in severe arterial O2 desaturation with significant depression of the hypercapnic respiratory drive during the first hour in the postanesthesia care unit, even though the majority of our patients were easily aroused in response to verbal stimuli.