Effect of adjunctive dexmedetomidine on anesthesia and analgesia requirement and recovery characteristics during Bispectral Index-guided anesthesia for cerebello-pontine angle surgeries: A randomized clinical trial.

BACKGROUND AND AIMS: The study was conceived to elucidate the effects of dexmedetomidine as an anesthetic adjunct to propofol (total intravenous anesthesia) on anesthetic dose reduction and anesthesia recovery parameters in cerebello-pontine angle (CPA) surgeries. MATERIAL AND METHODS: This prospective randomized study was conducted on 49 patients (25 with dexmedetomidine, 24 without). After standardized anesthetic induction, anesthesia was maintained using propofol (via target controlled infusion, titrated to maintain BIS between 40 and 60), fentanyl (0.5 µg/kg/hour) and either dexmedetomidine (0.5 µg/kg/hour) or a sham infusion. Neuromuscular blocking agents were excluded to allow cranial nerve EMG monitoring. Adverse hemodynamic events, recovery parameters (time to opening eyes, obeying commands, and extubation) and postoperative sedation score, shivering score, nausea, and vomiting score were recorded. RESULTS: Propofol and fentanyl utilization (as total dose, adjusted for duration of surgery and body weight, and number of extra boluses) was significantly lower in the dexmedetomidine group. There was no difference in any of the recovery parameters between the two groups. Incidence of bradycardia was significantly higher with dexmedetomidine, while no difference was found for hypotension, hypertension, and tachycardia. CONCLUSION: Dexmedetomidine-fentanyl-propofol anesthesia compares favorably with fentanyl-propofol anesthesia during CPA neurosurgical procedures with regard to anesthesia recovery times, but with lower intraoperative opioid and hypnotic utilization rates.

Multiple cranial nerve palsies following radiofrequency ablation for trigeminal neuralgia.

A 33-year-old man developed diffuse subarachnoid haemorrhage following attempted radiofrequency ablation for trigeminal neuralgia. Over the next 2 weeks, he progressively developed multiple bilateral cranial nerve palsies, bilateral cerebellar signs, hypotonia of all four limbs and diminished vision in both eyes. A visual-evoked potential study revealed anterior visual pathway defect. A possibility of demyelination was considered and he was treated with corticosteroids. His neurological deficits improved gradually over the next 4 months. He later underwent microvascular decompression uneventfully with good pain relief. This complication has not been reported earlier and needs to be kept in mind while performing radiofrequency ablation.

Cerebral Oxygen Saturation During Electroconvulsive Therapy: A Secondary Analysis of a Randomized Crossover Trial.

BACKGROUND: Electroconvulsive therapy (ECT) causes acute changes in cerebral perfusion and oxygenation. Near-infrared spectroscopy is a novel, noninvasive technique to assess cerebral oxygen saturation (cSO2). We hypothesized that cSO2 increases during ECT and more so with atropine premedication and decreases when systemic desaturation (peripheral oxygen saturation <90%) occurs during ECT. METHODS: We performed a secondary analysis of a randomized trial of patients undergoing ECT for psychiatric illness during a 6-month period. During the second ECT session, patients were randomly assigned to receive either 0.01 mg/kg IV atropine or no atropine. During the third ECT session, patients were crossed over. Standard anesthetic management was performed. Data with regard to heart rate, blood pressure, peripheral oxygen saturation, and cSO2 were collected at baseline and continuously examined for 5 minutes from delivery of ECT stimulus. RESULTS: Forty-one patients underwent 82 ECT sessions. ECT resulted in significant increase in cSO2 during both the atropine and the no-atropine sessions (P<0.001 for both) but no between-session difference was observed (mean difference, 1.9±2.0; 95% confidence interval, -2.0, 5.9; P=0.337). The cSO2 values were lower in patients who developed systemic desaturation when compared with the cSO2 values in those who did not (mean difference, 5.0±2.6; 95% confidence interval -0.1, 10.2; P=0.054). However, the mean cSO2 was >60% at any measured time point, even in those with systemic desaturation. CONCLUSIONS: ECT increased cSO2 irrespective of atropine premedication. cSO2 was lower when systemic desaturation occurred. Future studies should explore the effect of cerebral oxygenation changes during ECT on outcome of psychiatric conditions.

Hemodynamic effects of dexmedetomidine during intra-operative electrocorticography for epilepsy surgery.

BACKGROUND: Dexmedetomidine, a predominant alpha-2-adrenergic agonist has been used in anesthetic practice to provide good sedation. The drug is being recently used in neuroanesthesia during awake surgery for brain tumors and in functional neurosurgery. MATERIALS AND METHODS: This prospective study analyzed the hemodynamic effects of dexmedetomidine infusion during electrocorticography in patients undergoing surgery for mesial temporal sclerosis. Dexmedetomidine infusion was administered during intra-operative electrocorticography recording, 15 minutes after the end tidal MAC of N2O and isoflurane were decreased to zero. Anesthesia was maintained with O2 : air mixture = 50:50, vecuronium and fentanyl. Heart rate (HR), mean arterial pressure (MAP) and end tidal carbon dioxide (ETCO2) were recorded across at induction, 2 min prior to dexmedetomidine (PreDEX), 5 min during dexmedetomidine infusion (DEX; 1 µg/kg), 5 min after stopping dexmedetomidine and 10 minutes after stopping dexmedetomidine. RESULTS: Forty patients with mesial temporal sclerosis (M: F = 27:13, mean age = 28.15 ± 10.9 years; duration of epilepsy = 12.0 ± 7.9 years) underwent anterior temporal lobe resection with amygdalohippocampectomy for drug-resistant epilepsy. Infusion of dexmedetomidine caused a transient fall in HR in 87.5% of patients and an increase in MAP in 62.5% of patients, which showed a tendency to revert back towards PreDEX values within 10 min after stopping the infusion. Sixty-five percent of the patients showed ≤25% reduction and 10% of them showed >25% reduction in HR. 47.5% of the patients showed ≤25% increase and 15% of them showed >25% increase in MAP. These changes were over a narrow range and within physiological limits. CONCLUSION: The infusion of dexmedetomidine for a short period causes reduction of HR and increase in MAP in patients, however the variations are within acceptable range.

Intraoperative bradycardia and postoperative hyperkalemia in patients undergoing endoscopic third ventriculostomy.

During our initial experience with endoscopic third ventriculostomies, we observed intraoperative bradycardia and postoperative hyperkalemia. The present study was carried out to verify the consistency of these initial observations. Intraoperative heart rate (HR) changes and postoperative serum K + changes were studied prospectively in 20 patients of endoscopic third ventriculostomy. Another 6 patients who underwent endoscopic procedures other than ventriculostomy acted as controls. The anaesthetic technique and intraoperative and postoperative fluid regimen were similar in all patients. Serum K + concentrations were measured intraoperatively and once a day for the next 5 days. The third ventriculostomy group exhibited a significant slowing of the heart rate during the fenestration of the floor of the third ventricle (112 +/- 26 to 101 +/- 28 bpm, p < 0.001) and also at the time of the reversal of the neuromuscular block at the end of surgery (104 +/- 29 to 96 +/- 33 bpm, p < 0.01). The control group did not exhibit similar changes in the heart rate. The postoperative increase in serum K + values in the ventriculostomy group (0.82 +/- 0.55 mmol/L) was higher than that in the control group (0.10 +/- 0.44 mmol/L) (p < 0.01). Endoscopic third ventriculostomy is associated with a significant bradycardia at the time of fenestration and at the time of reversal of the neuromuscular block. The procedure is also associated with a postoperative increase in serum K + values. We propose a mechanism involving distortion of the posterior hypothalamus, which accounts for the bradycardia and postoperative hyperkalemia.