Application of the Bair Hugger™ core body temperature at wrist region with upper body warming blanket: a prospective observational study.

BACKGROUND: Body temperature monitoring is essential during the perioperative period. However, core body temperature measurement requires invasive device that may cause complications. This study aimed to evaluate the accuracy of non-invasive Bair Hugger™ core body temperature monitoring system (BHTMS) at the wrist compared with esophageal temperature under general anesthesia. METHODS: Twenty adult patients of the American Society of Anesthesiologists physical status I or II were enrolled. BHTMS sensor was applied at wrist region. After tracheal intubation, an esophageal probe was inserted. Bair Hugger™ upper body warming blankets were used. Esophageal temperature (Teso) and BHTMS at wrist (Twrist) were recorded every 10 min. RESULTS: Total of 257 pairs of data sets were analyzed: Teso and Twrist had no statistically significant difference (P = 0.103). Median of Teso and Twrist were 36.5°C and 36.4°C. Bland-Altman analysis showed Teso - Twrist of 0.14°C ± 1.44. Subsequently, 99 pairs of 0-40 min data set were analyzed and showed significant difference at 0 and 10 min (P < 0.001) but no significant difference at 20, 30 and 40 min. Bland- Altman plot by times showed difference (Teso - Twrist) of 1.49°C ± 2.00, 0.82°C ± 1.30, 0.29°C ± 1.32, -0.03°C ± 0.84, and -0.12°C ± 0.82 at 0, 10, 20, 30 and 40 min respectively. CONCLUSIONS: BHTMS at wrist area under the upper body warming blanket is a potential alternative other than esophageal temperature for monitoring body temperature after 30 min of anesthesia induction.

Supraglottic airway devices as a strategy for unassisted tracheal intubation: A network meta-analysis.

We aimed to compare the effectiveness of supraglottic airway devices as a strategy for unassisted tracheal intubation. Accordingly, we searched the OVID-MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, KoreaMed, and Google Scholar databases to identify all relevant randomized controlled trials (RCTs) on supraglottic airway devices as a strategy for tracheal intubation published until May 2017. The primary outcome was the overall success rate of intubation by the intention to treat (ITT) strategy. The secondary outcomes of the study were the overall success rate of tracheal intubation by the per protocol (PP) strategy and the success rate of tracheal intubation at first attempt by ITT and PP. We conducted a network meta-analysis with a mixed-treatment comparison method to combine direct and indirect comparisons among supraglottic airway devices. Of 1396 identified references, 16 RCTs (2014 patients) evaluated unassisted intubation with supraglottic airway devices. Patients were grouped according to the type of device used: LMA-CTrach, LMA-Fastrach, Air-Q, i-gel, CobraPLA, Ambu-Aura, or single-use LMA devices. Based on the surface under the cumulative ranking curve, the three best supraglottic airway devices for use as a strategy for unassisted tracheal intubation were LMA-CTrach (which included video-assisted tracheal tube guidance), single-use LMA-Fastrach, and LMA-Fastrach. LMA-Fastrach showed a higher success rate of intubation than did i-gel, CobraPLA, Air-Q, and Ambu-Aura. However, this study was limited by the small number of eligible RCTs. Therefore, well-designed RCTs performed on large patient populations are required to increase the confidence of the results.

Myoclonic movement after general anesthesia: A case report and review of the literature.

RATIONALE: Myoclonic movement is a rare side effect after general anesthesia. Since we use various intravenous agents during general anesthesia recently, it is troublesome to find out the exact cause of this neurologic complication. PATIENT CONCERNS: A 31-year-old female patient without any past medical history underwent hip arthroscopic surgery under general anesthesia. DIAGNOSES: Although there was no specific event during the operation, she showed a sudden myoclonic movement confined to left upper extremity in recovery room. INTERVENTIONS: We administered anticonvulsant agents intrvenously, the myoclonus was stopped shortly but recurred over again. As we stopped the patient-controlled analgesia due to nausea, the symptom halted. OUTCOMES: There was no significant abnormality in electroencephalography or brain diffusion magnetic resonance imaging, which was taken after the event. LESSONS: Clinicians should carefully consider the pharmacologic characteristics and neurologic adverse effects of all administered agents when myoclonus occurs after general anesthesia.

Optimal dose of intravenous oxycodone for attenuating hemodynamic changes after endotracheal intubation in healthy patients: A randomized controlled trial.

BACKGROUND: Intravenous oxycodone has been used as an adjunct to anesthetic agents. This study aimed to assess the optimal dose of intravenous oxycodone for the attenuation of the hemodynamic responses to laryngoscopy and endotracheal intubation. METHODS: A prospective, randomized, double-blind study was conducted. Ninety-five patients were randomly divided into 5 groups based on the oxycodone dose: 0, 0.05, 0.1, 0.15, 0.2 mg/kg. After administering the assigned dose of intravenous oxycodone, anesthesia was induced with thiopental. Heart rate (HR) and blood pressure (BP) were measured at baseline, before intubation, and 1, 2, and 3 minutes after intubation. The percentage increase of BP was calculated as (highest BP after intubation - baseline BP)/baseline BP × 100 (%). The percentage increase of HR was calculated in same formula as above. Hypertension was defined as a 15% increase of systolic BP from baseline, and probit analysis was conducted. RESULTS: Hemodynamic data from 86 patients were analyzed. The percentage increase of mean arterial pressure after intubation in groups 0.05, 0.1, 0.15, and 0.2 was significantly different from that in the control (P < 0.001). For HR, the percentage increase was lower than control group when oxycodone was same or more than 0.1 mg/kg (P < 0.05). Using probit analysis, the 95% effective dose (ED95) for preventing hypertension was 0.159 mg/kg (95% confidence interval [CI], 0.122-0.243). In addition, ED50 was 0.020 mg/kg (95% CI, -0.037 to 0.049). However, oxycodone was not effective for maintaining the HR in our study dosage. There were no significant differences in the incidence of hypotension during induction between groups. CONCLUSIONS: Using 0.1 mg/kg of intravenous oxycodone is sufficient to attenuate the increase of BP and HR during induction period in healthy patients. The ED95, which was 0.159 mg/kg, can be useful to adjust the dosage of IV oxycodone for maintain stable BP during induction of general anesthesia.

Palonosetron and Ramosetron Compared for Effectiveness in Preventing Postoperative Nausea and Vomiting: A Systematic Review and Meta-Analysis.

Previous randomized controlled trials have reported conflicting findings on the superiority of palonosetron over ramosetron for preventing postoperative nausea and vomiting (PONV). Therefore, the present systematic review was registered in PROSPERO (CRD42016038120) and performed to compare the efficacy of perioperative administration of palonosetron to that of ramosetron for preventing PONV. We searched MEDLINE, EMBASE, and CENTRAL to identify all randomized controlled trials that compared the effectiveness of perioperative administration of palonosetron to that of ramosetron. The primary endpoints were defined as the incidence of postoperative nausea (PON), postoperative vomiting (POV), and PONV. A total of 695 patients were included in the final analysis. Subgroup analysis was performed through administration times which were divided into two phases: the early phase of surgery and the end of surgery. Combined analysis did not show differences between palonosetron and ramosetron in the overall incidence of PON, POV or PONV. Palonosetron was more effective than ramosetron, when the administration time for the 5-HT3 receptor antagonist was during the early phase of the operation. Otherwise, ramosetron was more effective than palonosetron, when the administration time was at the end of surgery. However, the quality of evidence for each outcome was low or very low and number of included studies was small, limiting our confidence in findings.

Dexmedetomidine-Induced Neuroapoptosis Is Dependent on Its Cumulative Dose.

BACKGROUND: Dexmedetomidine (DEX) has inherent neuroprotective properties that have been attributed to the activation of prosurvival kinases. However, the impact of supraclinical doses of DEX on neuroapoptosis and neuronal viability has not been determined. METHODS: Rat pups and primary neuronal cells were treated with DEX or ketamine (KET) alone or in combination. Neuroapoptosis was measured by cleaved-caspase-3 expression and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining in brain sections. Expression of prosurvival kinases was measured by Western blot. We measured the impact of DEX with and without α1-adrenergic receptor blockade on the viability of primary neuronal cell cultures. RESULTS: Increasing the cumulative dose of DEX resulted in elevated levels of neuroapoptosis in vivo. Low doses increased, whereas high dose decreased phosphorylation of the prosurvival kinases. KET alone and in combination with DEX produced a greater degree of apoptosis and reductions in expression of these protein kinases than DEX alone. Increasing concentrations of DEX decreased, while coadministration of an α1-adrenergic receptor blocker preserved neuronal viability in vitro. CONCLUSIONS: Although DEX is neuroprotective at clinical doses, high cumulative doses and concentrations induce neuroapoptosis, in vivo and in vitro, respectively. Because the current dosing schedules used in humans yield plasma levels that are substantially below concentrations that induce neurotoxicity, low-dose DEX should not be neurotoxic and has the potential to be a neuroprotective adjuvant.

Noxious stimulation attenuates ketamine-induced neuroapoptosis in the developing rat brain.

BACKGROUND: Ketamine induces neuroapoptosis in neonatal rodents. However, these experimental paradigms were performed without concurrent noxious stimulation, a condition that does not reflect the interaction of anesthesia and surgical stimulation. Noxious stimulation with and without concurrent analgesic drugs has been shown to have divergent patterns of neuronal activation and cell death. We hypothesized that concurrent noxious stimulation would attenuate ketamine-induced caspase-3 activation. METHODS: Postnatal day 7 Sprague-Dawley rat pups were randomized to a 6-h exposure to ketamine with and without peripheral noxious stimulation by intraplantar injection of complete Freund's adjuvant. A cohort of naïve rat pups with and without complete Freund's adjuvant injections served as control subjects. Neuroapoptosis was measured by cleaved caspase-3 expression and terminal deoxynucleotidyl-transferase mediated 2'-deoxyuridine 5'-triphosphate nick end labeling staining. In order to determine if concurrent noxious simulation altered the expression of cell survival and cell cycle proteins, levels of protein kinase B and glycogen synthase kinase-3ß and cyclin D1 were measured. RESULTS: Ketamine induced a significant increase in cleaved caspase-3 expression and terminal deoxynucleotidyl-transferase mediated 2'-deoxyuridine 5'-triphosphate nick end labeling staining with increases in cyclin D1 levels. Concurrent noxious stimulation with ketamine attenuated caspase-3 activation and maintained cyclin D1 levels. Phosphorylation of protein kinase B and glycogen synthase kinase-3ß was not definitively altered under these conditions. CONCLUSION: The administration of ketamine with concurrent noxious stimulation results in the attenuation of the neuroapoptotic response. These findings suggest that concurrent surgery and procedural pain attenuates ketamine-induced neuroapoptosis.

The effects of changing from isoflurane to desflurane on the recovery profile during the latter part of anesthesia.

It is not known whether changing from isoflurane to desflurane during the latter part of anesthesia shows early emergence and recovery in long surgery. We therefore evaluated the effects of changing isoflurane to desflurane on emergence and recovery. Eighty-two patients were randomly assigned to receive isoflurane (Group I) or desflurane (Group D) or to change from isoflurane to desflurane anesthesia (Group X). At the point when there was an hour until the operation would end, isoflurane was replaced with 1 MAC of desflurane in Group X, and isoflurane and desflurane were maintained at 1 MAC in Groups I and D. When the operation ended, we compared the emergence and recovery characteristics among the 3 groups. Compared with Group I, Group X showed faster emergence and recovery. Group X and Group D showed similar emergence and recovery. In conclusion, changing isoflurane to desflurane during the latter part of anesthesia improves emergence and recovery.

Spontaneous pneumothorax during laparoscopy-assisted Billroth-I gastrectomy -A case report-.

Pneumothorax associated with a pneumoperitonium in laparoscopic surgery is rare but can cause life-threatening complications. A 62-year-old man was scheduled for a laparoscopy-assisted Billroth-I gastrectomy under general anesthesia. Approximately 70 minutes after insufflating carbon dioxide into the intraabdominal cavity at a pressure of 12 mmHg, the peak inspiratory pressure increased, while the oxygen saturation decreased. The pneumothorax of the left lung was evident on the intraoperative chest radiograph. The pneumothorax improved after inserting a catheter into the affected area. The cause of the pneumothorax was unknown but an anatomical defect is believed responsible. This report shows that pneumothorax developed under an intraabdominal pressure in the conventional safety range. Careful monitoring and immediate treatment is necessary to prevent the condition from worsening.

The effects of dantrolene on hypoxic-ischemic injury in the neonatal rat brain.

BACKGROUND: The pathophysiology of brain damage from hypoxia or ischemia has been ascribed to various mechanisms and cascades. Intracellular calcium overload and a calcium excitotoxic cascade have been implicated. It has been suggested that disturbances of endoplasmic reticulum calcium homeostasis are involved in the induction of neuronal cell injury. Two types of intracellular Ca2+-release channels, involving the ryanodyne receptor and the inositol (1,4,5)-triphosphate receptor, are essential for Ca2+ signaling in cells. Dantrolene, which is used for the treatment of malignant hyperthermia syndrome, has been reported to inhibit Ca2+ release through ryanodyne receptors from the endoplasmic reticulum into the cytosol. We designed this study to investigate the neuroprotective effects of dantrolene on hypoxic-ischemic brain damage in the neonatal rat brain. METHODS: Seven-day-old Sprague-Dawley rats were assigned into two groups; control group (n = 69) and dantrolene group (n = 60). Dimethyl sulfoxide was administered intracerebroventricularly in the control group, and dantrolene in dimethyl sulfoxide was similarly administered to the dantrolene group, before hypoxic-ischemic brain injury (HII). HII was induced by the ligation of the common carotid artery under isoflurane anesthesia, followed by exposure to about 2.5 h of hypoxia (oxygen concentration was maintained at 7%-8%). 1H magnetic resonance spectroscopy was performed 1 day after HII. This noninvasive method evaluated apoptotic processes in the brain after HII. Morphologic score analyses and the calculated percentage of infarct areas after 2,3,5-triphenyltetrazolium chloride staining 14 days after HII were also used to evaluate the effects of dantrolene on HII. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining was performed 1 day after HII using 24 more rats. RESULTS: The lipid/creatine ratios in the right hemispheres in the dantrolene group 1 day after HII were significantly lower than those of the control group (P < 0.05). There was no significant difference between the two groups in the N-acetylaspartate/creatine ratios. The gross morphologic scores were lower in the dantrolene group than in the control group (P < 0.05), and infarct area (%) after 2,3,5-triphenyltetrazolium chloride staining was less in the dantrolene group than in the control group (P < 0.05) 14 days after HII. Further work with 24 rats showed no significant difference, however, in the number of TUNEL positive cells on the two groups. CONCLUSIONS: Our results show that dantrolene, administered intracerebroventricularly before HII, had a neuroprotective effect in HII model of the neonatal rat brain.