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Hypertonic saline infusion for treating intracranial hypertension after severe traumatic brain injury.

ABSTRACT: Traumatic brain injury (TBI) remains a major cause of mortality and disability. Post-traumatic intracranial hypertension (ICH) further complicates the care of patients. Hyperosmolar agents are recommended for the treatment of ICH, but no consensus or high-level data exist on the use of any particular agent or the route of administration. The two agents used commonly are hypertonic saline (HTS) and mannitol given as bolus therapy. Smaller studies suggest that HTS may be a superior agent in reducing the ICH burden, but neither agent has been shown to improve mortality or functional outcome. In a recently published analysis of pooled data from three prospective clinical trials, continuous infusion of HTS correlated with serum hypernatremia and reduced ICH burden in addition to improving 90-day mortality and functional outcome. This lays the foundation for the upcoming continuous hyperosmolar therapy for traumatic brain-injured patients (COBI) randomized controlled trial to study the outcome benefit of continuous HTS infusion to treat ICH after severe TBI. This is much anticipated and will be a high impact trial should the results be replicated. However, this would still leave a question over the use of mannitol bolus therapy which will need to be studied.

SUBMITTER: Mangat HS

PROVIDER: S-EPMC5820788 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Hypertonic saline infusion for treating intracranial hypertension after severe traumatic brain injury.

Mangat Halinder S HS

Critical care (London, England) 20180220 1

Traumatic brain injury (TBI) remains a major cause of mortality and disability. Post-traumatic intracranial hypertension (ICH) further complicates the care of patients. Hyperosmolar agents are recommended for the treatment of ICH, but no consensus or high-level data exist on the use of any particular agent or the route of administration. The two agents used commonly are hypertonic saline (HTS) and mannitol given as bolus therapy. Smaller studies suggest that HTS may be a superior agent in reduci ...[more]

PMID: 29463291

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Project description:To investigate the effect of the occurrence of early hyperchloremia on death or severe disability at 180 days in patients with severe traumatic brain injury (TBI).DesignPost hoc analysis of Resuscitation Outcomes Consortium Hypertonic Saline (ROC HS)-TBI trial.SettingA total of 114 North American emergency medical services agencies in the ROC.PatientsA total of 991 patients with severe TBI and Glasgow Coma Scale score of less than or equal to 8.InterventionsPrehospital resuscitation with single IV dose (250 cc) of 7.5% saline in 6% dextran-70, 7.5% saline (no dextran), or crystalloid.Measurements and main resultsPatients with increased serum chloride concentrations (110 mmol/L or greater) 24 hours after randomization were identified. Hyperchloremia was graded into one or greater than or equal to 2 occurrences in the first 24 hours. Logistic regression analyses were performed to determine the effects of hyperchloremia on: 1) death or severe disability at 180 days and 2) death within 180 days after adjusting for confounders. Compared with patients without hyperchloremia, patients with greater than or equal to 2 occurrences of hyperchloremia had significantly higher odds of death or severe disability at 180 days (odds ratio [OR], 1.81; 95% CI, 1.19-2.75) and death within 180 days (OR, 1.89; 95% CI, 1.14-3.08) after adjustment for confounders. However, the total volume of fluids administered during the first 24 hours was an independent predictor of death within 180 days; therefore, after adding an interaction term between the total volume of fluids administered during the first 24 hours and greater than or equal to 2 occurrences of hyperchloremia, patients with greater than or equal to 2 occurrences of hyperchloremia had significantly higher odds of death within 180 days (OR, 2.35; 95% CI, 1.21-4.61 d) but not of composite outcome of death or severe disability at 180 days.ConclusionsAfter modifying for the effect of the total volume of fluids administered during the first 24 hours, multiple occurrences of hyperchloremia in the first 24 hours were associated with higher odds of death within 180 days in patients with severe TBI.

Project description:BackgroundAmong people who have suffered a traumatic brain injury, increased intracranial pressure continues to be a major cause of early death; it is estimated that about 11 people per 100 with traumatic brain injury die. Indomethacin (also known as indometacin) is a powerful cerebral vasoconstrictor that can reduce intracranial pressure and, ultimately, restore cerebral perfusion and oxygenation. Thus, indomethacin may improve the recovery of a person with traumatic brain injury.ObjectivesTo assess the effects of indomethacin for adults with severe traumatic brain injury.Search methodsWe ran the searches from inception to 23 August 2019. We searched the Cochrane Central Register of Controlled Trials (CENTRAL; 2019, Issue 8) in the Cochrane Library, Ovid MEDLINE, Ovid Embase, CINAHL Plus (EBSCO), four other databases, and clinical trials registries. We also screened reference lists and conference abstracts, and contacted experts in the field.Selection criteriaOur search criteria included randomised controlled trials (RCTs) that compared indomethacin with any control in adults presenting with severe traumatic brain injury associated with elevated intracranial pressure, with no previous decompressive surgery.Data collection and analysisTwo review authors independently decided on the selection of the studies. We followed standard Cochrane methods.Main resultsWe identified no eligible studies for this review, either completed or ongoing.Authors' conclusionsWe found no studies, either completed or ongoing, that assessed the effects of indomethacin in controlling intracranial hypertension secondary to severe traumatic brain injury. Thus, we cannot draw any conclusions about the effects of indomethacin on intracranial pressure, mortality rates, quality of life, disability or adverse effects. This absence of evidence should not be interpreted as evidence of no effect for indomethacin in controlling intracranial hypertension secondary to severe traumatic brain injury. It means that we have not identified eligible research for this review.

Project description:ObjectiveWhile existing guidelines support the treatment of intracranial hypertension in severe traumatic brain injury (TBI), it is unclear when to suspect and initiate treatment for high intracranial pressure (ICP). The objective of this study was to derive a clinical decision rule that accurately predicts intracranial hypertension.MethodsUsing Delphi methods, the authors identified a set of potential predictors of intracranial hypertension and a clinical decision rule a priori by consensus among a group of 43 neurosurgeons and intensivists who have extensive experience managing severe TBI without ICP monitoring. To validate these predictors, the authors used data from a Latin American trial (n = 150; BEST TRIP). To report on the performance of the rule, they calculated sensitivity, specificity, and positive and negative predictive values with 95% confidence intervals. In a secondary analysis, the rule was validated using data from a North American trial (n = 131; COBRIT).ResultsThe final predictors and the clinical decision rule were approved by 97% of participants in the consensus working group. The predictors are divided into major and minor criteria. High ICP would be considered suspected in the presence of 1 major or ≥ 2 minor criteria. Major criteria are: compressed cisterns (CT classification of Marshall diffuse injury [DI] III), midline shift > 5 mm (Marshall DI IV), or nonevacuated mass lesion. Minor criteria are: Glasgow Coma Scale (GCS) motor score ≤ 4, pupillary asymmetry, abnormal pupillary reactivity, or Marshall DI II. The area under the curve for the logistic regression model that contains all the predictors was 0.86. When high ICP was defined as > 22 mm Hg, the decision rule performed with a sensitivity of 93.9% (95% CI 85.0%-98.3%), a specificity of 42.3% (95% CI 31.7%-53.6%), a positive predictive value of 55.5% (95% CI 50.7%-60.2%), and a negative predictive value of 90% (95% CI 77.1%-96.0%). The sensitivity of the clinical decision rule improved with higher ICP cutoffs up to a sensitivity of 100% when intracranial hypertension was defined as ICP > 30 mm Hg. Similar results were found in the North American cohort.ConclusionsA simple clinical decision rule based on a combination of clinical and imaging findings was found to be highly sensitive in distinguishing patients with severe TBI who would suffer intracranial hypertension. It could be used to identify patients who require ICP monitoring in high-resource settings or start ICP-lowering treatment in environments where resource limitations preclude invasive monitoring.Clinical trial registration no.: NCT02059941 (clinicaltrials.gov).

Project description:Hypertonic saline (HTS) is a commonly administered agent for intracranial pressure (ICP) control in traumatic brain injury (TBI). The literature on its use is mainly in moderate/severe TBI where invasive ICP monitoring is present. The role of HTS in patients with moderate TBI (mTBI) outside of the intensive care unit (ICU) setting remains unclear. The goal of this scoping review was to provide an overview of the available literature on HTS administration in patients with mTBI without ICP monitoring, assessing its impact on outcome and transitions in care. We performed a scoping systematic review of the literature of MEDLINE, Embase, Scopus, BIOSIS, and the Cochrane Databases from inception to July 31, 2020. We searched for those published articles documenting the administration of HTS in patients with mTBI with recorded functional outcome or transitions in hospital care. A two-step review process was conducted in accordance with methodology outlined in the Cochrane Handbook for Systematic Reviews of Interventions. There were many studies with combined moderate/severe TBI populations. However, most failed to document subgroup analysis for patients with mTBI. Our search strategy identified only one study that documented the administration of HTS in mTBI in which subgroup analysis for mTBI and outcomes were provided. This retrospective cohort study assessed patients with mTBI who did/did not receive prophylactic HTS, finding that those not receiving HTS demonstrated a deterioration in Glasgow Coma Scale (GCS) score in the first 48 h. However, the HTS group did demonstrate a trend to longer hospital stay and pneumonia. Our scoping review identified a significant gap in knowledge surrounding the use of HTS for patients with mTBI without invasive ICP monitoring. The limited identified literature suggests prophylactic administration prevents clinical deterioration, although this is based on a single study with data available for mTBI sub-analysis. Further studies on HTS in non-monitored patients with mTBI are required.

Project description:To evaluate the clinical effectiveness of bolus-dose fentanyl and midazolam to treat episodic intracranial hypertension in children with severe traumatic brain injury.Retrospective cohort.PICU in a university-affiliated children's hospital level I trauma center.Thirty-one children 0-18 years of age with severe traumatic brain injury (Glasgow Coma Scale score of ? 8) who received bolus doses of fentanyl and/or midazolam for treatment of episodic intracranial hypertension.None.The area under the curve from high-resolution intracranial pressure-time plots was calculated to represent cumulative intracranial hypertension exposure: area under the curve for intracranial pressure above 20 mm Hg (area under the curve-intracranial hypertension) was calculated in 15-minute epochs before and after administration of fentanyl and/or midazolam for the treatment of episodic intracranial hypertension. Our primary outcome measure, the difference between predrug and postdrug administration epochs (?area under the curve-intracranial hypertension), was calculated for all occurrences. We examined potential covariates including age, injury severity, mechanism, and time after injury; time after injury correlated with ?area under the curve-intracranial hypertension. In a mixed-effects model, with patient as a random effect, drug/dose combination as a fixed effect, and time after injury as a covariate, intracranial hypertension increased after administration of fentanyl and/or midazolam (overall aggregate mean ?area under the curve-intracranial hypertension = +17 mm Hg × min, 95% CI, 0-34 mm Hg × min; p = 0.04). The mean ?area under the curve-intracranial hypertension increased significantly after administration of high-dose fentanyl (p = 0.02), low-dose midazolam (p = 0.006), and high-dose fentanyl plus low-dose midazolam (0.007). Secondary analysis using age-dependent thresholds showed no significant impact on cerebral perfusion pressure deficit (mean ?area under the curve-cerebral perfusion pressure).Bolus dosing of fentanyl and midazolam fails to reduce the intracranial hypertension burden when administered for episodic intracranial hypertension. Paradoxically, we observed an overall increase in intracranial hypertension burden following drug administration, even after accounting for within-subject effects and time after injury. Future work is needed to confirm these findings in a prospective study design.

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Hypertonic saline infusion for treating intracranial hypertension after severe traumatic brain injury.

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Hypertonic saline infusion for treating intracranial hypertension after severe traumatic brain injury.

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