A randomised controlled trial of oral chloral hydrate vs. intranasal dexmedetomidine before computerised tomography in children.

Chloral hydrate is commonly used to sedate children for painless procedures. Children may recover more quickly after sedation with dexmedetomidine, which has a shorter half-life. We randomly allocated 196 children to chloral hydrate syrup 50 mg.kg-1 and intranasal saline spray, or placebo syrup and intranasal dexmedetomidine spray 3 µg.kg-1 , 30 min before computerised tomography studies. More children resisted or cried after drinking chloral hydrate syrup than placebo syrup, 72 of 107 (67%) vs. 42 of 87 (48%), p = 0.009, but there was no difference after intranasal saline vs. dexmedetomidine, 49 of 107 (46%) vs. 40 of 87 (46%), p = 0.98. Sedation was satisfactory in 81 of 107 (76%) children after chloral hydrate and 64 of 87 (74%) children after dexmedetomidine, p = 0.74. Of the 173 children followed up for at least 4 h after discharge, 38 of 97 (39%) had recovered normal function after chloral hydrate and 32 of 76 (42%) after dexmedetomidine, p = 0.76. Six children vomited after chloral hydrate syrup and placebo spray vs. none after placebo syrup and dexmedetomidine spray, p = 0.03.

A randomised comparison of two intranasal dexmedetomidine doses for premedication in children.

We compared sedation levels in children following administration of intranasal dexmedetomidine. One hundred and sixteen children aged between 1 and 8 years were enrolled in this prospective, randomised trial. Children were assigned to receive either intranasal dexmedetomidine 1 µg.kg(-1) (Group 1) or 2 µg.kg(-1) (Group 2). Thirty-one (53%) patients from Group 1 and 38 (66%) patients from Group 2 were satisfactorily sedated at the time of anaesthetic induction. Logistic regression showed a significant interaction effect (p=0.049), with the odds ratio between Group 2 over Group 1 estimated as 1.1 (95% CI 0.5-2.7) for the 1-4 year age group, and 10.5 (95% CI 1.4-80.2) for the 5-8 year age group. Both doses produced a similar level of satisfactory sedation in children aged 1-4 years, whereas 2 µg.kg(-1) resulted in a higher proportion of satisfactory sedation in children aged 5-8 years. There were no adverse haemodynamic effects. We conclude that intranasal dexmedetomidine in a premedication dose of 2 µg.kg(-1) resulted in excellent sedation in children.

EMLA cream versus dorsal penile nerve block for postcircumcision analgesia in children.

We conducted a prospective, randomized, double-blinded trial comparing preoperative application of EMLA cream and sodium chloride solution dorsal penile block (n = 31) with placebo cream and bupivacaine dorsal penile nerve block (n = 32) for postcircumcision analgesia. Pain was assessed using modified Children's Hospital of Eastern Ontario Pain Scale and the duration of block by the time to requirement of first dose of postoperative analgesic. There was no difference in Children's Hospital of Eastern Ontario Pain Scale between the two groups, but bupivacaine dorsal penile nerve block resulted in longer analgesia (P = 0.003). There were no local or systemic complications related to either technique, and there was a very small incidence of vomiting. We conclude that preoperative application of EMLA cream is an effective and simple method to produce postcircumcision analgesia with a very small incidence of adverse effects.

Propofol effective concentration 50 and its relationship to bispectral index.

Sixty unpremedicated healthy adult patients were studied during induction of anaesthesia with intravenous propofol delivered by a 'Diprifusor' target-controlled infusion. Bispectral index (BIS) and spectral edge frequency (SEF95) were measured concurrently with the predicted blood and effect site propofol concentrations. Logistic regression was used to calculate the predicted propofol blood and effect site concentrations required to produce unconsciousness and no response to a noxious stimulus in 50% and 95% of patients and to correlate BIS with these end-points. The Diprifusor TCI software produces anaesthesia at consistent target concentrations. Bispectral index correlates well with clinical end-points and may be useful during propofol anaesthesia.

An audit of the safety of an acute pain service.

We audited and analysed the adverse effects and safety of postoperative pain management on 2509 consecutive patients under care of the Acute Pain Service at a tertiary referral teaching hospital over a 32-month period. Our standard respiratory monitoring consisted of continuous pulse oximetry, hourly respiratory rate counting, sedation scoring and intermittent arterial blood gas sampling. This protocol was reliable and detected six episodes of bradypnoea, 13 of hypercapnia and 23 of oxygen desaturation occurring in 39 patients (1.8% of all spontaneously breathing patients). Two patients required naloxone injection and none had long-term sequelae. Hypotension due to epidural bupivacaine 0.0625% and fentanyl 3.3 micrograms.ml-1 infusion occurred in four patients (1.2%), all with a sensory block higher than T5. They readily responded to fluid infusion and ephedrine (two patients). Postoperative nausea or vomiting occurred in 723 (28.8%) and 380 (15.1%) patients, respectively. Odds ratio analysis showed that the risk factors for postoperative nausea and vomiting were: female gender, gynaecological operations, nongeriatric patients and systemic analgesia. Postoperative nausea and vomiting decreased analgesic efficacy by discouraging the use of patient-controlled analgesia and was regarded as equally distressing as pain. Other side-effects included: pruritus in 182 patients; dizziness in 333 and lower limb weakness in 73 (21.2% of patients receiving epidural local anaesthetics). It is concluded that a standard monitoring and management protocol, an experienced nursing team and reliable Acute Pain Service coverage is mandatory for the safe use of modern analgesic techniques.

Recovery from mivacurium block with or without anticholinesterase following continuous infusion in obstetric patients.

Neostigmine antagonism after suxamethonium followed by mivacurium chloride bolus and infusion was studied. Thirty ASA group I or II patients were given mivacurium 0.15 mg/kg followed by infusion during nitrous oxide-enflurane-pethidine anaesthesia. Train of four (TOF) stimuli were applied to the ulnar nerve at the wrist and TOF twitch height and ratio measured by TOF-GUARD nerve stimulator. Mivacurium infusion was titrated to give a 90% block of first twitch height. Patients were randomized into two groups. Group I patients recovered from the mivacurium block spontaneously while Group II patients were given neostigmine 0.05 mg/kg and atropine 0.02 mg/kg. Time to reach train of four ratio (TOFR) of 25%, 50% and 70% were measured. This study demonstrated a mean infusion rate of 5.1 +/- 1.8 micrograms/kg/min to maintain a 90% neuromuscular block. In the spontaneous recovery group, time to reach TOFR of 25%, 50% and 70% were 9.3 +/- 2.7 min, 13.5 +/- 3.0 min and 16.7 +/- 3.0 min respectively while the corresponding times in the neostigmine group were 5.2 +/- 1.7 min, 10.9 +/- 2.2 min and 16.1 +/- 7.4 min respectively. There were significant differences in the time taken to TOFR of 25% (P < 0.0001) and 50% (P < 0.05) but no difference in the time taken for TOFR to return to 70%. We concluded that mivacurium is suitable for use in caesarean section despite a decrease in plasma cholinesterase activity. Neostigmine antagonism is not required as a routine.

Additive interactions between propofol and ketamine when used for anesthesia induction in female patients.

BACKGROUND: Propofol and ketamine may be paired for anesthesia induction and for total intravenous anesthesia. The nature of any sedative interactions occurring between propofol and ketamine are unknown. The combination when used for anesthesia induction in female patients was studied. METHODS: Quantal dose-response curves were determined in 180 female patients to whom the drugs were administered individually and in combination. Two minutes after administering the drugs, two endpoints were assessed. First, loss of response to verbal command (hypnosis) and then, in those who failed to respond to this endpoint, loss of response to a 5-s transcutaneous tetanus (anesthesia). Interactions were analyzed by fitting the data to a mathematical model in which response was analyzed in terms of the doses of the two drugs and an additional term included to describe nonadditive interactions. The incidences of apnea, arterial pressure, and heart rate changes during the first 5 min were recorded. RESULTS: At the hypnotic endpoint, the ED50s were 1.10 mg/kg propofol (95% CIs 0.93-1.27), 0.39 mg/kg ketamine (95% CIs 0.27-0.46), and the combination of 0.63 mg/kg propofol and 0.21 mg/kg ketamine (95% CIs 0.53/0.18-0.73/0.24). At the anesthetic endpoint, the ED50s were 1.85 mg/kg propofol (95% CIs 1.58-2.36) 0.66 mg/kg ketamine (95% CIs 0.58-0.77), and the combination of 1.05 mg/kg propofol and 0.35 mg/kg ketamine (95% CIs 0.88/0.29-1.27/0.42). The effects were additive at both endpoints; there was no evidence of an interaction. The ED50s for apnea were 1.61 mg/kg propofol (95% CIs 1.39-1.94), greater than 0.85 mg/kg ketamine and for the combination 1.50 mg/kg propofol and 0.50 mg/kg ketamine (95% CIs 1.15/0.38-3.09/1.03). The addition of ketamine did not significantly alter the ED50 for apnea of propofol. There was a significant difference in the arterial pressures among the three groups (P < 0.001). Using the combination, the cardiostimulant effects of ketamine balanced the cardiodepressant effects of propofol. There was no change in arterial pressure or heart rate after the noxious stimulus. CONCLUSIONS: When using the combination, doses were additive at hypnotic and anesthetic endpoints. Ketamine had no influence on the incidence of apnea after propofol, and the net hemodynamic effects were minimal.

Hypnotic and anesthetic interactions between ketamine and midazolam in female patients.

BACKGROUND: Midazolam, if used with ketamine for induction and maintenance of anesthesia, may attenuate hyperdynamic circulatory effects and prevent undesirable emergenic reactions. The nature of the interaction between midazolam and ketamine used for anesthesia induction was studied in female patients. METHODS: Quantal dose-response curves were determined in 170 female patients for the drugs, individually and in combination. Two endpoints were assessed, loss of response to verbal command (hypnosis) and loss of response to a 5-s transcutaneous tetanus (anesthesia). At the hypnotic endpoint, interactions were analyzed by fitting the data to a mathematical model in which the response was analyzed in terms of the doses of the two drugs, and an additional term was included to describe nonadditive interactions. At the anesthetic endpoint, the decrease in ED50 of ketamine in the presence of midazolam was assessed because dose-related effects could not be demonstrated for midazolam alone. RESULTS: At the hypnotic endpoint, the ED50s were: 0.15 mg/kg midazolam (95% CIs 0.11-0.38 mg/kg), 0.37 mg/kg ketamine (95% CIs 0.08-0.44 mg/kg), and the combination of 0.086 mg/kg midazolam and 0.27 mg/kg ketamine (95% CIs 0.07/0.22-0.10/0.31 mg/kg), respectively. The hypnotic effects were found to be additive, and there was no evidence of an interaction. At the anesthetic endpoint, the ED50 of ketamine alone was 0.57 mg/kg (95% CIs 0.47-0.69) and the ED50 for ketamine in the presence of midazolam was also 0.57 mg/kg (95% CIs 0.48-0.79); 0.18 mg/kg midazolam was given at this point. Midazolam had no influence on the anesthetic dose of ketamine. CONCLUSIONS: When using the combination, doses employed should be adjusted according to the depth of central nervous system depression that is required.