Effect of 35°C Hypothermia on Intracranial Pressure and Clinical Outcome in Patients With Severe Traumatic Brain Injury

2009 ◽  
Vol 66 (1) ◽  
pp. 166-173 ◽  
Author(s):  
Takashi Tokutomi ◽  
Tomoya Miyagi ◽  
Yasuharu Takeuchi ◽  
Takashi Karukaya ◽  
Hiroshi Katsuki ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Clinical Outcome ◽  
Severe Traumatic Brain Injury

scholarly journals A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury

2013 ◽  
Vol 118 (6) ◽  
pp. 1317-1328 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
David A. Zaun ◽  
Jiannong Liu
Keyword(s):  
Clinical Trial ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Clinical Outcome ◽  
Severe Traumatic Brain Injury ◽  
Standard Care ◽  
Cerebral Metabolism ◽  
Control Group ◽  
Normobaric Hyperoxia

Object Preclinical and clinical investigations indicate that the positive effect of hyperbaric oxygen (HBO2) for severe traumatic brain injury (TBI) occurs after rather than during treatment. The brain appears better able to use baseline O2 levels following HBO2 treatments. In this study, the authors evaluate the combination of HBO2 and normobaric hyperoxia (NBH) as a single treatment. Methods Forty-two patients who sustained severe TBI (mean Glasgow Coma Scale [GCS] score 5.7) were prospectively randomized within 24 hours of injury to either: 1) combined HBO2/NBH (60 minutes of HBO2 at 1.5 atmospheres absolute [ATA] followed by NBH, 3 hours of 100% fraction of inspired oxygen [FiO2] at 1.0 ATA) or 2) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Intracranial pressure, surrogate markers for cerebral metabolism, and O2 toxicity were monitored. Clinical outcome was assessed at 6 months using the sliding dichotomized Glasgow Outcome Scale (GOS) score. Mixed-effects linear modeling was used to statistically test differences between the treatment and control groups. Functional outcome and mortality rates were compared using chi-square tests. Results There were no significant differences in demographic characteristics between the 2 groups. In comparison with values in the control group, brain tissue partial pressure of O2 (PO2) levels were significantly increased during and following combined HBO2/NBH treatments in both the noninjured and pericontusional brain (p < 0.0001). Microdialysate lactate/pyruvate ratios were significantly decreased in the noninjured brain in the combined HBO2/NBH group as compared with controls (p < 0.0078). The combined HBO2/NBH group's intracranial pressure values were significantly lower than those of the control group during treatment, and the improvement continued until the next treatment session (p < 0.0006). The combined HBO2/NBH group's levels of microdialysate glycerol were significantly lower than those of the control group in both noninjured and pericontusional brain (p < 0.001). The combined HBO2/NBH group's level of CSF F2-isoprostane was decreased at 6 hours after treatment as compared with that of controls, but the difference did not quite reach statistical significance (p = 0.0692). There was an absolute 26% reduction in mortality for the combined HBO2/NBH group (p = 0.048) and an absolute 36% improvement in favorable outcome using the sliding dichotomized GOS (p = 0.024) as compared with the control group. Conclusions In this Phase II clinical trial, in comparison with standard care (control treatment) combined HBO2/NBH treatments significantly improved markers of oxidative metabolism in relatively uninjured brain as well as pericontusional tissue, reduced intracranial hypertension, and demonstrated improvement in markers of cerebral toxicity. There was significant reduction in mortality and improved favorable outcome as measured by GOS. The combination of HBO2 and NBH therapy appears to have potential therapeutic efficacy as compared with the 2 treatments in isolation. Clinical trial registration no.: NCT00170352 (ClinicalTrials.gov).

scholarly journals Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Daniel Agustin Godoy ◽  
Rafael Badenes ◽  
Paolo Pelosi ◽  
Chiara Robba
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Acute Phase ◽  
Severe Traumatic Brain Injury ◽  
Safety Profile ◽  
Point Of View ◽  
Current Evidence ◽  
Potential Benefits ◽  
Sedation And Analgesia

AbstractMaintaining an adequate level of sedation and analgesia plays a key role in the management of traumatic brain injury (TBI). To date, it is unclear which drug or combination of drugs is most effective in achieving these goals. Ketamine is an agent with attractive pharmacological and pharmacokinetics characteristics. Current evidence shows that ketamine does not increase and may instead decrease intracranial pressure, and its safety profile makes it a reliable tool in the prehospital environment. In this point of view, we discuss different aspects of the use of ketamine in the acute phase of TBI, with its potential benefits and pitfalls.

scholarly journals Correction to: Serum sodium and intracranial pressure changes after desmopressin therapy in severe traumatic brain injury patients: a multi-centre cohort study

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
A. Harrois ◽  
◽  
J. R. Anstey ◽  
F. S. Taccone ◽  
A. A. Udy ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cohort Study ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Serum Sodium ◽  
Collaborative Group ◽  
Full List ◽  
Pressure Changes

Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list:

Severe Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Kee D. Kim ◽  
Marike Zwienenberg ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Brain Oxygenation ◽  
Barbiturate Coma ◽  
Blast Traumatic Brain Injury ◽  
Penetrating Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

scholarly journals Experimental model of intracranial hypertension with continuous multiparametric monitoring in swine

2013 ◽  
Vol 71 (10) ◽  
pp. 802-806 ◽  
Author(s):  
Almir Ferreira de Andrade ◽  
Matheus Schmidt Soares ◽  
Gustavo Cartaxo Patriota ◽  
Alessandro Rodrigo Belon ◽  
Wellingson Silva Paiva ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Animal Model ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Severe Traumatic Brain Injury ◽  
Transcranial Doppler ◽  
Porcine Model ◽  
Cerebral Oximetry ◽  
Suitable Animal Model

Objective Intracranial hypertension (IH) develops in approximately 50% of all patients with severe traumatic brain injury (TBI). Therefore, it is very important to identify a suitable animal model to study and understand the pathophysiology of refractory IH to develop effective treatments. Methods We describe a new experimental porcine model designed to simulate expansive brain hematoma causing IH. Under anesthesia, IH was simulated with a balloon insufflation. The IH variables were measured with intracranial pressure (ICP) parenchymal monitoring, epidural, cerebral oximetry, and transcranial Doppler (TCD). Results None of the animals died during the experiment. The ICP epidural showed a slower rise compared with parenchymal ICP. We found a correlation between ICP and cerebral oximetry. Conclusion The model described here seems useful to understand some of the pathophysiological characteristics of acute IH.

scholarly journals Monitoring of Intracranial Pressure in Patients with Severe Traumatic Brain Injury: Review

2018 ◽  
Vol 4 (2) ◽  
pp. 63 ◽  
Author(s):  
LuisR Moscote-Salazar ◽  
AlexisR Narvaez-Rojas ◽  
Joulem Mo-Carrascal ◽  
Johana Maraby ◽  
GuruD Satyarthee ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury

Intracranial Pressure Waveform Morphology and Intracranial Adaptive Capacity

2008 ◽  
Vol 17 (6) ◽  
pp. 545-554 ◽  
Author(s):  
Jun-Yu Fan ◽  
Catherine Kirkness ◽  
Paolo Vicini ◽  
Robert Burr ◽  
Pamela Mitchell
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Adaptive Capacity ◽  
Severe Traumatic Brain Injury ◽  
Controlled Trial ◽  
Pressure Monitor ◽  
Data Set ◽  
Prime Concern ◽  
Intracranial Pressure Waveform

Background Intracranial hypertension due to primary and secondary injuries is a prime concern when providing care to patients with severe traumatic brain injury. Increases in intracranial pressure vary depending on compensatory processes within the craniospinal space, also referred to as intracranial adaptive capacity. In patients with traumatic brain injury and decreased intracranial adaptive capacity, intracranial pressure increases disproportionately in response to a variety of stimuli. However, no well-validated measures are available in clinical practice to predict the development of such an increase. Objectives To examine whether P2 elevation, quantified by determining the P2:P1 ratio (=0.8) of the intracranial pressure pulse waveform, is a unique predictor of disproportionate increases in intracranial pressure on a beat-by-beat basis in the 30 minutes preceding the elevation in patients with severe traumatic brain injury, within 48 hours after deployment of an intracranial pressure monitor. Methods A total of 38 patients with severe traumatic brain injury were sampled from a randomized controlled trial of cerebral perfusion pressure management in patients with traumatic brain injury or subarachnoid hemorrhage. Results The P2 elevation was not only present before the disproportionate increase in pressure, but also appeared in the comparison data set (within-subject without such a pressure increase). Conclusions P2 elevation is not a reliable clinical indicator to predict an impending disproportionate increase in intracranial pressure.

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