Intraoperative-evoked Potential Monitoring: From Homemade to Automated Systems No abstract available |
Securing Endotracheal Tube in a Bearded Patient Undergoing Surgery for Cerebellopontine Angle Tumor in Lateral Position—A Different Approach No abstract available |
Hypotension and Hypocapnia During General Anesthesia in Piglets: Study of S100b as an Acute Biomarker for Cerebral Tissue Injury Background: Hypotension and/or hypocapnia might increase general anesthesia (GA)-related neuromorbidity in infants, but safe levels of perioperative blood pressure are poorly defined. Serum protein S100b has been used as screening, monitoring, and prediction tool in the management of patients with traumatic brain injury. Using an animal model, we investigated serum S100b as an acute biomarker of cerebral hypoperfusion and cerebral cell dysfunction during hypotension, hypocapnia, or combined hypotension/hypocapnia during GA. Methods: Fifty-seven sevoflurane-midazolam anesthetized piglets aged 4 to 6 weeks were randomly allocated to control (n=9), hypotension (n=18), hypocapnia (n=20), or combined hypotension and hypocapnia (n=10). Hypotension (target mean arterial blood pressure: 35 to 38 or 27 to 30 mm Hg) was induced by blood withdrawal and nitroprusside infusion, and hypocapnia by hyperventilation (target PaCO2: 28 to 30 and 23 to 25 mm Hg). Serum S100b and albumin were measured at baseline, before and 60 minutes after the interventions, and following 60-minute recovery. Results: Serum S100b concentrations decreased over time (P=0.001), but there was no difference in S100b between control piglets and those exposed to hypotension, hypocapnea, or a combination of the both (P=0.105). Albumin decreased in all 4 groups (P=0.001). Conclusion: S100b did not increase following 60 minutes of systemic hypotension and/or hypocapnia during GA in piglets. In this setting, the use of S100b as a biomarker of cerebral cell tissue dysfunction cannot be supported. The study is part of Mrs. Clausen's PhD project, which was awarded the ESA MAQUET GRANT at the annual meeting of the European Society of Anesthesia 2015. Mrs Clausen's project is further supported by funds provided by the Department of Anesthesiology and Intensive Care Medicine, University Hospital Odense. The authors have no conflicts of interest to disclose. Address correspondence to: Nicola G. Clausen, MD, PhD, E-mail: nicola@nicola.dk. Received September 9, 2018 Accepted March 14, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
Effects of Vasopressors on Cerebral Circulation and Oxygenation: A Narrative Review of Pharmacodynamics in Health and Traumatic Brain Injury The clinical use of vasoactive drugs aims to improve hemodynamic variables and thereby maintain or restore adequate perfusion and oxygenation in accordance with metabolic demands. A main focus in the management of patients with brain pathology during surgery and neurointensive care is restoring and/or maintaining adequate cerebral perfusion pressure in order to ensure cerebral blood flow in accordance with metabolic demands. One commonly used clinical strategy is the administration of vasoactive drugs aiming to increase mean arterial blood pressure and thereby cerebral perfusion pressure. Here, we first describe the anatomic and physiological basis for the cerebrovascular effects of vasopressor agents. Next, we review the pharmacodynamics of commonly used vasopressors under normal circumstances and in the presence of head injury. We further discuss the role of blood-brain barrier disruption and microvascular dysfunction with regard to the effects of the reviewed vasopressor agents. M.R. was funded by the Health Research Fund of Central Denmark Region, Viborg, Denmark. The remaining authors have no conflicts of interest to disclose. Address correspondence to: Mads Rasmussen, MD, PhD, Department of Anesthesia and Intensive Care, Section of Neuroanesthesia, Aarhus University Hospital, 8000 Aarhus C, Denmark (e-mail: mads.rasmussen@vest.rm.dk). Received December 7, 2018 Accepted February 27, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
Journal Club No abstract available |
Journal Club No abstract available |
Cervical Spine Movement During Awake Orotracheal Intubation With Fiberoptic Scope and McGrath Videolaryngoscope in Patients Undergoing Surgery for Cervical Spine Instability: A Randomized Control Trial Background: Cervical spine movement during intubation with direct laryngoscopy can predispose to new-onset neurological deficits in patients with cervical spine instability. While fiberoptic-guided intubation (FGI) is mostly preferred in such patients, this is not always possible. Videolaryngoscopy results in less cervical spine movement than direct laryngoscopy and may be an alternative to FGI in patients with cervical spine instability. The objective of this study was to compare cervical spine movement during awake FGI with those during awake McGrath videolaryngoscope-guided intubation (VGI) in patients undergoing surgery for cervical spine instability. Methods: Forty-six adult patients with upper cervical spine instability scheduled for stabilization surgery were randomized to awake FGI or awake VGI. Cervical spine movement during intubation was assessed by changes in lateral fluoroscopic-measured angles (α and β at C1/C2 and C3 levels, respectively) at 3 time points: T1, preintubation; T2, during intubation; T3, postintubation. Motor power was assessed before and after intubation. Results: Patient demographics and airway characteristics were similar between the 2 groups. Cervical spine motion (in degrees) during intubation was significantly greater with VGI than FGI at C1/C2 (T3-T1, −8.02±8.11 vs. −1.47±3.31; P<0.001) but not at C3 (T3-T1, −2.17±5.16 vs. −1.85±3.29; P=0.960). No patient developed new-onset motor deficits following intubation in either group. Conclusions: Compared with FGI, VGI results in a greater degree of cervical spine movement at C1/C2 but not at C3. The authors have no funding or conflicts of interest to disclose. Address correspondence to: Kamath Sriganesh, DM. E-mail: drsri23@gmail.com. Received November 25, 2018 Accepted February 21, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
Hyperlactatemia After Intracranial Tumor Surgery Does Not Affect 6-Month Survival: A Retrospective Case Series Background: Patients undergoing neurosurgery frequently exhibit hyperlactatemia. The aim of this study was to identify factors associated with hyperlactatemia and assess how hyperlactatemia impacts survival and hospital length of stay after intracranial tumor surgery. Materials and Methods: This retrospective cohort study included 496 adult patients that underwent surgery between January 1, 2014 and December 31, 2015. We evaluated patient characteristics, surgery characteristics, pH, lactate, and blood glucose from blood samples collected on admission to the high-dependency unit and the morning after surgery, and 6-month outcome data. Results: Hyperlactatemia (>2.0 mmol/L) occurred in >50% of patients, but only 7.7% had acidosis. Postoperative hyperlactatemia was not correlated with 6-month survival (P=0.987), but was correlated with (median [interquartile range]) longer hospital stays (6 [4 to 8.5] d vs. 5 [4 to 8] d; P=0.006), longer surgery duration (4:53 [4:01 to 6:18] h:min vs. 4:28 [3:33 to 5:53] h:min; P=0.001), higher dexamethasone dose (16 [16 to 35] mg vs. 16 [16 to 20] mg; P<0.001), and higher blood glucose concentration (8.4 [7.5 to 9.6] mmol/L vs. 8.0 [7.1 to 8.9] mmol/L; P<0.001). Patients that received total intravenous anesthesia developed hyperlactatemia less frequently than those that received balanced anesthesia with inhalational agents (48.4% vs. 61.5%, P=0.008). Hyperlactatemia was not associated with increased postoperative neurological deficits or the need for rehabilitation therapy. Conclusions: Hyperlactatemia was common after intracranial tumor surgery. It did not influence 6-month outcomes but was associated with longer hospital length of stay. Several potential causative factors for hyperlactatemia were identified. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0/ The authors have no funding or conflicts of interest to disclose. Address correspondence to: Peter P. de Smalen, MD, Department of Anesthesiology, Erasmus University Medical Center, Kamer Na-1718, Postbus 2040, 3000 CA Rotterdam, The Netherlands (e-mail: p.desmalen@erasmusmc.nl). Received April 2, 2018 Accepted February 22, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
Transient Neurological Events After Surgery for Pediatric Moyamoya Disease: A Retrospective Study of Postoperative Sedation Practices Background: Moyamoya disease is a cerebrovascular disease characterized by bilateral stenosis of the intracranial internal carotid arteries and an abnormal collateral vascular network at the base of the brain. Transient neurological events (TNEs), which are episodes of neurological dysfunction lasting <24 hours, are associated with stroke in pediatric patients with Moyamoya disease. Perioperative agitation often occurs in pediatric patients. We hypothesized that anesthetic technique and postoperative sedation would modify the association between TNE and superficial temporal artery-middle cerebral artery (STA-MCA) bypass in pediatric patients with Moyamoya disease. Methods: We retrospectively reviewed the medical records of patients with Moyamoya disease aged 15 years and below who underwent STA-MCA bypass under general anesthesia at a single cerebrovascular center in Japan between January 1999 and March 2016. The primary outcome was TNE. Mixed-effects logistic regression was used to evaluate whether postoperative sedation and anesthetic agents were associated with TNE. Results: Among 277 hemispheres in 154 pediatric patients who underwent STA-MCA bypass, 107 patients (39%) experienced TNE within 1 week after surgery. Crying (adjusted odds ratio, 3.11; 95% confidence interval, 1.01-9.59; P=0.048) was an independent risk factor for TNE. Postoperative sedation was associated with a lower incidence of TNE (adjusted odds ratio, 0.514; 95% confidence interval, 0.264-0.997; P=0.049), but premedication and anesthetic agents were not associated with TNE. Conclusion: In pediatric patients with Moyamoya disease, crying was associated with increased TNE and postoperative sedation is associated with decreased TNE. The authors have no funding or conflicts of interest to disclose. Address correspondence to: Kenji Yoshitani, MD, Department of Anesthesiology, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan (e-mail: ykenji@ncvc.go.jp). Received November 17, 2018 Accepted February 11, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
Near-Infrared Spectroscopy–derived Cerebral Autoregulation Indices Independently Predict Clinical Outcome in Acutely Ill Comatose Patients Objective: Outcome prediction in comatose patients with acute brain injury remains challenging. Regional cerebral oxygenation (rSO2) derived from near-infrared spectroscopy (NIRS) is a surrogate for cerebral blood flow and can be used to calculate cerebral autoregulation (CA) continuously at the bedside from the derived cerebral oximetry index (COx). We hypothesized that COx derived thresholds for CA are associated with outcomes in patients with acute coma from neurological injury. Methods: A prospective cohort study was conducted in 88 acutely comatose adults with heterogenous brain injury diagnoses who were continuously monitored with COx for up to 3 consecutive days. Multivariable logistic regression was performed to investigate association between averaged COx and short (in-hospital and 3 mo) and long-term (6 mo) outcomes. Results: Six month mortality rate was 62%. Median COx in nonsurvivors at hospital discharge was 0.082 [interquartile range, IQR: 0.045 to 0.160] compared with 0.042 [IQR: −0.005 to 0.110] in survivors (P=0.012). At 6 months, median COx was 0.075 [IQR: 0.27 to 0.158] in nonsurvivors compared with 0.029 [IQR: −0.015 to 0.077] in survivors (P=0.02). In the multivariable logistic regression model adjusted for confounders, average COx ≥0.05 was associated with both in-hospital mortality (adjusted odds ratio [OR]=2.9, 95% confidence interval [CI]=1.15-7.33, P=0.02), mortality at 6 months (adjusted OR=4.4, 95% CI=1.41-13.7, P=0.01), and severe disability (modified Rankin Score ≥4) at 6 months (adjusted OR=4.4, 95% CI=1.07-17.8, P=0.04). Area under the receiver operating characteristic curve for predicting mortality and severe disability at 6 months were 0.783 and 0.825, respectively. Conclusions: Averaged COx ≥0.05 is independently associated with short and long-term mortality and long-term severe disability in acutely comatose adults with neurological injury. We propose that COx ≥0.05 represents an accurate threshold to predict long-term functional outcome in acutely comatose adults. C.H. and W.C.Z. are senior authors. C.H. is the PI on an NIH-sponsored clinical study (R01 HL 92259). C.H. receives research funding from Medtronic/Covidien, Dublin, IR, and he serves as a consultant to Medtronic/Covidien and Ornim Medical Inc., Foxborough, MA. L.R.-L. is the PI on an American Academy of Neurology/American Brain Foundation and grant from Medtronic/Covidien, Dublin, IR. The remaining authors have no conflicts of interest to disclose. Address correspondence to: Lucia Rivera-Lara, MD, MPH, Department of Neurology, Anesthesiology and Critical Care Medicine, The Johns Hopkins School of Medicine, 600 N Wolfe Street, Phipps 455, Baltimore, MD 21287 (e-mail: lriver14@jhmi.edu). Received July 27, 2018 Accepted January 17, 2019 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved |
ΩτοΡινοΛαρυγγολόγος Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,
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Σάββατο 27 Απριλίου 2019
Neurosurgical Anesthesiology
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Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
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00302841026182,
00306932607174,
alsfakia@gmail.com,
Anapafseos 5 Agios Nikolaos 72100 Crete Greece,
Medicine by Alexandros G. Sfakianakis
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