Emergence agitation is common after nasal surgery. We investigated the effects of intraoperative dexmedetomidine infusion on emergence agitation and quality of recovery after nasal surgery in adult patients. One hundred patients undergoing nasal surgery were randomized into two groups. The dexmedetomidine group (Group D, n=50) received dexmedetomidine infusion at a rate of 0.4 μg kg(-1) h(-1) from induction of anaesthesia until extubation, while the control group (Group C, n=50) received volume-matched normal saline infusion as placebo. Propofol (1.5-2 mg kg(-1)) and fentanyl (1 μg kg(-1)) were used for induction of anaesthesia, and desflurane was used for maintenance of anaesthesia. The incidence of agitation, haemodynamic parameters, and recovery characteristics were evaluated during emergence. A 40-item quality-of-recovery questionnaire (QoR-40) was provided to patients 24 h after surgery. The incidence of agitation was lower in Group D than Group C (28 vs 52%, P=0.014). Mean arterial pressure and heart rate were more stable in Group D than in Group C during emergence (P<0.05). Time to extubation, bispectral index, and respiratory rate at extubation were similar between the groups. Global QoR-40 score at 24 h after surgery was higher in Group D (median [range], 183 [146 -198]) compared with Group C (178 [133-196]) (P=0.041). Intraoperative infusion of dexmedetomidine provided smooth and haemodynamically stable emergence. It also improved quality of recovery after nasal surgery.

BACKGROUND: In this study, we examined the relationship between postoperative cognitive dysfunction (POCD) and intraoperative regional cerebral oxygen saturation (rSO₂) in elderly patients undergoing spinal surgery. METHODS: We enrolled 87 patients older than 65 years. All patients were tested using a battery of cognitive function tests (Korean Mini-Mental State Examination and visuomotor test of Dynamic Lowenstein Occupational Therapy Cognitive Assessment–Geriatric Version) the day before their surgical operation and on the seventh postoperative day. Our threshold for defining POCD for a given patient was a Reliable Change Index score of <−1.96 occurring on 2 tests. RESULTS: POCD was detected in 20 patients (23%) at the seventh postoperative day. Between-patient baseline characteristics, surgical data, and baseline cognitive function were similar for both those who developed POCD and those who did not. A univariate analysis that included age, female sex, education level, presence of diabetes, and duration of intraoperative decline in rSO₂ to a level of <60% of baseline revealed that only diabetes and duration of rSO₂ <60% (odds ratio, 1.01; 95% confidence interval [CI], 1.005–1.010) were found to be risk factors for POCD. After multivariate logistic regression analysis of these 2 variables, only the duration of rSO₂ <60% (odds ratio, 1.006; 95% CI, 1.00–1.01, P = 0.014) remained as an independent risk factor for POCD. The area under the receiver operation characteristic of the duration of rSO₂ <60% was 0.70 (95% CI, 0.57–0.82; P = 0.008). The optimal cutoff value was 157 minutes with a sensitivity of 75% and specificity of 72%. CONCLUSIONS: This study showed that the duration of decline in rSO₂ <60% during lumbar spinal surgery was correlated with the development of POCD at the seventh postoperative day in elderly patients.

Volatile sedation in the intensive care unit (ICU) may reduce the number of adverse events and improve patient outcomes compared with intravenous (IV) sedation. We performed a systematic review and meta-analysis comparing the effects of volatile and IV sedation in adult ICU patients. We searched the PubMed, Embase, Cochrane Central Register, and Web of Science databases for all randomized trials comparing volatile sedation using an anesthetic-conserving device (ACD) with IV sedation in terms of awakening and extubation times, lengths of ICU and hospital stay, and pharmacologic end-organ effects. Thirteen trials with a total of 1027 patients were included. Volatile sedation (sevoflurane or isoflurane) administered through an ACD shortened the awakening time [mean difference (MD), −80.0 minutes; 95% confidence intervals (95% CIs), −134.5 to −25.6; P = .004] and extubation time (MD, −196.0 minutes; 95% CIs, −305.2 to −86.8; P < .001) compared with IV sedation (midazolam or propofol). No differences in the lengths of ICU and hospital stay were noted between the 2 groups. In the analysis of cardiac effects of sedation from 5 studies, patients who received volatile sedation showed lower serum troponin levels 6 hours after ICU admission than patients who received IV sedation (P < .05). The effect size of troponin was largest between 12 and 24 hours after ICU admission (MD, −0.27 μg/L; 95% CIs, −0.44 to −0.09; P = .003). Compared with IV sedation, volatile sedation administered through an ACD in the ICU shortened the awakening and extubation times. Considering the difference in serum troponin levels between both arms, volatile anesthetics might have a myocardial protective effect after cardiac surgery even at a subanesthetic dose. Because the included studies used small sample sizes with high heterogeneity, further large, high-quality prospective clinical trials are needed to confirm our findings.

We introduce a Feasible Artificial Intelligence with Simple Trajectories for Predicting Adverse Catastrophic Events (FAST-PACE) solution for preparing immediate intervention in emergency situations. FAST-PACE utilizes a concise set of collected features to construct an artificial intelligence model that predicts the onset of cardiac arrest or acute respiratory failure from 1 h to 6 h prior to its occurrence. Data from the trajectory of 29,181 patients in intensive care units of two hospitals includes periodic vital signs, a history of treatment, current health status, and recent surgery. It excludes the results of laboratory data to construct a feasible application in wards, out-hospital emergency care, emergency transport, or other clinical situations where instant medical decisions are required with restricted patient data. These results are superior to previous warning scores including the Modified Early Warning Score (MEWS) and the National Early Warning Score (NEWS). The primary outcome was the feasibility of an artificial intelligence (AI) model predicting adverse events 1 h to 6 h prior to occurrence without lab data; the area under the receiver operating characteristic curve of this model was 0.886 for cardiac arrest and 0.869 for respiratory failure 6 h before occurrence. The secondary outcome was the superior prediction performance to MEWS (net reclassification improvement of 0.507 for predicting cardiac arrest and 0.341 for predicting respiratory failure) and NEWS (net reclassification improvement of 0.412 for predicting cardiac arrest and 0.215 for predicting respiratory failure) 6 h before occurrence. This study suggests that AI consisting of simple vital signs and a brief interview could predict a cardiac arrest or acute respiratory failure 6 h earlier.

Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood–brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inflammatory mediators, which are associated with tissue damage, while those of M2 phenotype release anti-inflammatory mediators, which are related to tissue recovery. Moreover, late inflammation continually stimulates immune cell infiltration and leads to brain infarction. Therefore, regulation of M1/M2 phenotypes under persistent inflammatory conditions after cerebral ischemia is important for brain repair. Herein, we focus on apoptosis signal-regulating kinase 1 (ASK1), which is involved in apoptotic cell death, brain infarction, and production of inflammatory mediators after cerebral ischemia. We hypothesized that ASK1 is involved in the polarization of M1/M2 phenotype and the function of microglia and macrophage during the late stage of ischemia/hypoxia. We investigated the effects of ASK1 in mice subjected to middle cerebral artery occlusion and on BV2 microglia and RAW264.7 macrophage cell lines subjected to oxygen-glucose deprivation. Our results showed that ASK1 silencing effectively reduced Iba-1 or CD11b-positive cells in ischemic areas, suppressed pro-inflammatory cytokines, and increased anti-inflammatory mediator levels at 7 days after cerebral ischemia. In cultured microglia and macrophages, ASK1 inhibition, induced by NQDI-1 drug, decreased the expression and release of M1-associated factors and increased those of M2-associated factors after hypoxia/reperfusion (H/R). At the gene level, ASK1 inhibition suppressed M1-associated genes and augmented M2-associated genes. In gap closure assay, ASK1 inhibition reduced the migration rate of microglia and macrophages after H/R. Taken together, our results provide new information that suggests ASK1 controls the polarization of M1/M2 and the function of microglia and macrophage under sustained-inflammatory conditions. Regulation of persistent inflammation via M1/M2 polarization by ASK1 is a novel strategy for repair after ischemic stroke.

Kim JM, et al. Korean J Anesthesiol. 2018 Feb;71(1):48-56. https://doi.org/10.4097/kjae.2018.71.1.48