A comparison of the combination of aprepitant and dexamethasone versus the combination of ondansetron and dexamethasone for the prevention of postoperative nausea and vomiting in patients undergoing craniotomy.

BACKGROUND: Postoperative nausea and vomiting (PONV) occur commonly after craniotomy. In patients receiving prophylaxis with ondansetron and dexamethasone, vomiting occurred in 45% of patients at 48 hours. In addition to causing patient discomfort, the physical act of vomiting may increase intracranial pressure or cerebral intravascular pressure, jeopardizing hemostasis and cerebral perfusion. Aprepitant is a neurokin-1 receptor antagonist with a long duration of action and no sedative side effect. In a large multicenter study in patients undergoing abdominal surgery, aprepitant was significantly more effective than was ondansetron in preventing vomiting at 24 and 48 hours postoperatively. We hypothesized that the combination of aprepitant with dexamethasone will decrease the incidence of postoperative vomiting when compared with the combination of ondansetron and dexamethasone in patients undergoing craniotomy under general anesthesia. METHODS: Patients scheduled to undergo craniotomy under general anesthesia were enrolled in this prospective, double-blind, randomized study. Patients were randomized to receive oral aprepitant 40 mg (or matching placebo) 1 to 3 hours before induction of anesthesia or ondansetron 4 mg IV (or placebo) within 30 minutes of the end of surgery. All patients received dexamethasone 10 mg after induction of anesthesia. The anesthetic technique was standardized. Data were collected at regular intervals by blinded personnel for 48 hours after surgery. Statistical analysis was performed using Wilcoxon's ranked sum test and χ(2) test. P < 0.05 was considered statistically significant. RESULTS: One hundred four patients completed the study. The cumulative incidence of vomiting at 48 hours was 16% in the aprepitant group and 38% in the ondansetron group (P = 0.0149). The incidence of vomiting was also decreased in the aprepitant group at 2 hours (6% vs. 21%, P = 0.0419) and 24 hours (14% vs. 36%, P = 0.0124). From 0 to 48 hours, there was no difference between the aprepitant and ondansetron groups in the incidence of nausea (69% vs. 60%), nausea scores, need for rescue antiemetics (65% vs. 60%), complete response (no PONV and no rescue, 22% vs. 36%), or patient satisfaction with the management of PONV. CONCLUSION: The combination of aprepitant and dexamethasone was more effective than was the combination of ondansetron and dexamethasone for prophylaxis against postoperative vomiting in adult patients undergoing craniotomy under general anesthesia. However, there was no difference between the groups in the incidence or severity of nausea, need for rescue antiemetics, or in complete response between the groups.

Neurophysiological intraoperative monitoring of the glossopharyngeal nerve: technical case report.

OBJECTIVE: Neurophysiological intraoperative monitoring of the glossopharyngeal nerve has been performed only with needle electrodes inserted into the pharyngeal muscles or soft palate. We describe a noninvasive method of monitoring this cranial nerve. METHODS: A 30-year-old man who presented with headache, as well as speech and swallowing difficulty, underwent surgical resection of a right vagus nerve schwannoma. Neurophysiological intraoperative monitoring of multiple lower cranial nerves, including the glossopharyngeal and vagus nerves, was performed. RESULTS: The glossopharyngeal nerve was monitored with an adhesive surface electrode mounted on the cuff of a laryngeal mask airway, and the vagus nerve was monitored with a similar electrode mounted on the endotracheal tube. Successful monitoring allowed separation of the glossopharyngeal nerve from the tumor, and there was no postoperative swallowing deficit. CONCLUSION: Monitoring of the glossopharyngeal nerve with surface electrodes is possible and reliable, but it must be combined with vagus nerve monitoring.

Induction of hypothermia after intraoperative hypoxic brain insult.

Hypoxic brain injury can be a devastating complication of anesthesia. Fortunately, it has become increasingly rare. Here we report a case of suspected intraoperative hypoxic brain injury treated with moderate hypothermia. Anesthesiologists should be aware of the option of using this therapy and how to employ it in the setting of suspected hypoxic brain injury.

A retrospective analysis of a remifentanil/propofol general anesthetic for craniotomy before awake functional brain mapping.

UNLABELLED: We performed this study to summarize drug dosing, physiologic responses, and anesthetic complications from an IV general anesthetic technique for patients undergoing craniotomy for awake functional brain mapping. Review of 98 procedures revealed "most rapid" IV infusion rates for remifentanil 0.05, 0.05-0.09 microg x kg(-1) x min(-1) and propofol 115, 100-150 microg x kg(-1) x min(-1). The infusions lasted for 78, 58-98 min. Intraoperative emergence from general anesthesia was 9 (6-13) min after discontinuing IV infusions to allow for brain mapping and was independent of infusion duration and duration of craniotomy before mapping. Spontaneous ventilation was generally satisfactory during drug infusion, as evidenced by Sao(2) = 95% (92%-98%) and Paco(2) = 50 (47-55) mm Hg. However, we recorded at least one 30-s epoch of apnea in 69 of 96 patients. Maximum systolic arterial blood pressure was 150 (139-175) mm Hg and minimal systolic arterial blood pressure was 100 (70-150) mm Hg during drug infusion. Three patients experienced intraoperative seizures. Two patients did not tolerate the awake state and required reinduction of general anesthesia. No patients required endotracheal intubation or discontinuation of surgery. This general anesthetic technique is effective for craniotomy with awake functional brain mapping and offers an alternative to continuous wakefulness or other IV sedation techniques. IMPLICATIONS: An IV general anesthetic technique using remifentanil and propofol is an effective method allowing for reliable emergence for intraoperative awake functional brain mapping during craniotomy.

Changes in hematocrit based on incremental blood sampling: mathematical models perform poorly.

PURPOSE: Excessive blood sampling, with its inherent risks, is of growing concern among clinicians. We performed this study to measure the changes in hematocrit (Hct) during a laboratory investigation where multiple blood samples are collected. The performance of a simple mathematical model, used in clinical practice to predict Hct changes, is evaluated. METHODS: Eight healthy male volunteers participated in this study. The equation Hct(f) = Hct(i)*(EBV-BL)/EBV is used to predict changes in Hct. Where Hct(f) and Hct(i) are, respectively, the final and initial Hct, EBV is the estimated blood volume and BL is the blood loss. RESULTS: Thirty-five pharmacokinetic samples per subject were collected totalling 314 mL of BL. The Hct decreased from 44.2% +/- 2.2% to 39.9% +/- 2.5% (P = 0.001). On average, model predictions tended to have a discrete tendency to underestimate the Hct changes (-0.5% points of bias). While the predictions of the Hct were very accurate in 50% of the subjects, the discrepancy of the Hct predictions was clinically significant in the other 50% of the subjects. CONCLUSION: Consistent with the model prediction, this study demonstrated a significant reduction in the Hct values in healthy subjects undergoing incremental phlebotomy. On average, the model successfully predicted the decrease in Hct. However, the inter- and intra-individual variabilities in the Hct changes are clinically significant. In clinical settings, which are not well controlled environments, the variability is likely to be greater and the clinical use of the model cannot replace the need to monitor the Hct.

Dexmedetomidine pharmacodynamics: part I: crossover comparison of the respiratory effects of dexmedetomidine and remifentanil in healthy volunteers.

BACKGROUND: Dexmedetomidine, a highly selective alpha2-adrenoceptor agonist used for short-term sedation of mechanically ventilated patients, has minimal effect on ventilation. METHODS: This study compared the respiratory effect of dexmedetomidine to that of remifentanil. The authors measured and compared respiratory responses of six healthy male volunteers during (1) a stepwise target-controlled infusion of remifentanil, (2) a stepwise target-controlled infusion of dexmedetomidine, and (3) a pseudonatural sleep session. RESULTS: Compared with baseline, remifentanil infusions resulted in respiratory depression as evidenced by a decrease in respiratory rate and minute ventilation, respiratory acidosis, and apnea episodes resulting in desaturations. Remifentanil disturbed the natural pattern of breathing and flattened the distribution of ventilatory timing (inspiratory time/ventilatory cycle time). The respiratory effects of dexmedetomidine markedly contrasted with those of remifentanil. When compared with baseline, during dexmedetomidine infusions, the respiratory rate significantly increased, and the overall apnea/hypopnea index significantly decreased. The distribution of inspiratory time/ventilatory cycle time showed an increased peak. In addition, dexmedetomidine seemed to mimic some aspect of natural sleep. While the subjects were breathing a 5% CO2 mixture, hypercapnic arousal phenomena (documented by the Bispectral Index, the electroencephalogram, and sudden increase in the minute ventilation) were observed during dexmedetomidine infusions. Similar phenomena during natural sleep have been reported in the literature. CONCLUSIONS: In comparison with remifentanil, dexmedetomidine infusions (1) did not result in clinically significant respiratory depression, (2) decreased rather than increased the apnea/hypopnea index, and (3) exhibited some similarity with natural sleep.

Dexmedetomidine pharmacodynamics: Part II: Crossover comparison of the analgesic effect of dexmedetomidine and remifentanil in healthy volunteers.

BACKGROUND: Dexmedetomidine is a highly selective alpha2-adrenoceptor agonist used for short-term sedation of mechanically ventilated patients. The analgesic profile of dexmedetomidine has not been fully characterized in humans. METHODS: This study was designed to compare the analgesic responses of six healthy male volunteers during stepwise target-controlled infusions of remifentanil and dexmedetomidine. A computer-controlled thermode was used to deliver painful heat stimuli to the volar side of the forearms of the subjects. Six sequential 5-s stimuli (ranging from 41 degrees to 50 degrees C) were delivered in random order. The recorded visual analog scale was used to fit an Emax model. RESULTS: Compared to baseline, remifentanil infusions resulted in a right shift of the sigmoid curve (increased T50, the temperature producing a visual analog scale score of 50% of the maximal effect, from 46.1 degrees C at baseline to 48.4 degrees and 49.1 degrees C during remifentanil infusions) without a change of the steepness of the curve (identical Hill coefficients gamma during baseline and remifentanil). Compared to baseline, dexmedetomidine infusions resulted in both a right shift of the sigmoid curve (increased T50 to 47.2 degrees C) and a decrease in the steepness of the curve (decreased gamma from 3.24 during baseline and remifentanil infusions to 2.45 during dexmedetomidine infusions). There was no difference in the pain responses between baseline and after recovery from remifentanil infusions (identical T50 and gamma). CONCLUSION: As expected, dexmedetomidine is not as effective an analgesic as the opioid remifentanil. The difference in the quality of the analgesia with remifentanil may be a reflection of a different mechanism of action or a consequence of the sedative effect of dexmedetomidine.