Beta Blockers for Acute Traumatic Brain Injury: A Systematic Review and Meta-analysis

Alali, Aziz S.; McCredie, Victoria; Golan, Eyal; Shah, Prakesh S.; Nathens, Avery B.

doi:10.1007/s12028-013-9903-5

Cited by 50 publications

(46 citation statements)

References 34 publications

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“…(31–33) Furthermore, beta-blocker therapy has shown to confer a survival advantage to sTBI patients with elevated cardiac enzymes. (34,35) Despite growing evidence that suggest a potential link between cardiac dysfunction and TBI, only two studies have investigated the clinical outcomes of patients with cardiac dysfunction and TBI. Prathep et al reported abnormal echocardiogram, including reduced left ventricular rejection fraction and regional wall motion abnormality, was present in 22.3% of patients with isolated TBI and was independently associated with all cause in-hospital mortality.…”

Section: Discussionmentioning

confidence: 99%

The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury

Cai

Bonds

et al. 2016

Journal of Trauma and Acute Care Surgery

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Background cardiac dysfunction is frequently observed after severe traumatic brain injury (sTBI), however its significance is poorly understood. Our study sought to elucidate the association of cardiac troponin I (cTnI) elevation with all cause in-hospital mortality following isolated sTBI (brain AIS ≥ 3 and admission GCS ≤ 8, no AIS ≥3 to any other bodily regions). Methods we retrospectively reviewed all adult patients (≥ 18 years) with isolated sTBI admitted to a level one trauma center between June 2007 and January 2014. Patients must have cTnI values within 24 hours of admission. Mortality risks were examined by Cox proportional hazard model. Results of the 580 patients identified, 30.9% had detectable cTnI in 24 hours of admission. The median survival time was 4.19 days (IQR: 1.27 – 11.69). When adjusted for potential confounders, patients in the highest cTnI category (≥ 0.21 ng/mL) had significantly higher risk of in-hospital mortality (HR: 1.39; 95% CI: 1.04 – 1.88) compared to patients with undetectable cTnI. Mortality risk increased with higher troponin levels (p-trend < 0.0001). This association was more pronounced in patients ≤65 years (HR: 2.28; 95% CI: 1.53 – 3.40; p-trend < 0.0001), while interestingly, insignificant in those > 65 years (p-trend = 0.0826). Conclusions among patients with sTBI, cTnI elevation is associated with all cause in-hospital mortality via a non-linear, positive trend. Age modified the effect of cTnI on mortality. Level of Evidence level III retrospective study, Prognostic and Epidemiological

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Section: Discussionmentioning

confidence: 99%

The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury

Cai

Bonds

et al. 2016

Journal of Trauma and Acute Care Surgery

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“…From a clinical standpoint, treatment of humans with SAH with beta and alpha-adrenergic antagonists has been associated with improvements in neurologic outcomes 26 . In the TBI literature, a growing body of observational literature has demonstrated an improvement in outcomes with early exposure to beta-blockers 27,28 . Overall, the improvements in clinical outcomes associated with attenuation of the catecholamine response highlight the central role that elevated catecholamines play following neurologic injury.…”

Section: Catecholamine Excess After Traumatic Brain Injurymentioning

confidence: 99%

“…A meta-analysis of 4 observational cohort studies evaluating beta-blockers in the setting of TBI was recently published by Alali et al showed that beta-blockers exposure was associated with in-hospital mortality reduction (OR 0.35; 95%CI 0.27-0.45) 27 . Mosheni, et al demonstrated that non-exposure to beta-blockers in isolated TBI patients was associated with a 5-fold increase of mortality compared to patients exposed to beta-blockers, regardless of type or dose of beta-blocker (adjusted OR 5.0, 95% CI 2.7 – 8.5) 28 .…”

Section: Should Hypertension After Traumatic Brain Injury Be Treated?mentioning

confidence: 99%

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Krishnamoorthy

Chaikittisilpa

Kiatchai

et al. 2017

Journal of Neurosurgical Anesthesiology

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Traumatic brain injury (TBI) is a major public health problem, with severe TBI contributing to a large number of deaths and disability worldwide. Early hypotension has been linked with poor outcomes following severe TBI, and guidelines suggest early and aggressive management of hypotension after TBI. Despite these recommendations, no guidelines exist for the management of hypertension after severe TBI, although observational data suggests that early hypertension is also associated with an increased risk of mortality after severe TBI. The purpose of this review is to discuss the underlying pathophysiology of hypertension after TBI, provide an overview of the current clinical data on early hypertension after TBI, and discuss future research that should test the benefits and harms of treating high blood pressure in TBI patients.

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“…Either adverse effect can lead to hypotension, which is associated with poor outcomes in the TBI population (6–8). β-blockers have been evaluated mostly in retrospective cohort studies and a meta-analysis of the literature through mid-2013 demonstrated a potential mortality benefit with exposure to β-blockers (9). However, additional studies have been published since then and an updated systematic review is required to summarize the current evidence and offer guidance to clinicians.…”

Section: Introductionmentioning

confidence: 99%

Beta-blockers and Traumatic Brain Injury

et al. 2017

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OBJECTIVE To determine if beta-(β)-blockers improve outcomes after acute traumatic brain injury (TBI). BACKGROUND There have been no new inpatient pharmacologic therapies to improve TBI outcomes in a half-century. Treatment of TBI patients with β-blockers offers a potentially beneficial approach. METHODS Using MEDLINE, EMBASE, and CENTRAL databases, eligible articles for our systematic review and meta-analysis (PROSPERO CRD42016048547) included adult (age≥16 years) blunt trauma patients admitted with TBI. The exposure of interest was β-blocker administration initiated during the hospitalization. Outcomes were mortality, functional measures, quality of life, cardiopulmonary morbidity (e.g. hypotension, bradycardia, bronchospasm, and/or congestive heart failure). Data were analyzed using a random-effects model, and represented by pooled odds ratio (OR) with 95% confidence intervals (CI) and statistical heterogeneity (I2). RESULTS Data were extracted from 9 included studies encompassing 2005 unique TBI patients with β-blocker treatment and 6240 unique controls. Exposure to β-blockers after TBI was associated with a reduction of in-hospital mortality (pooled OR 0.39, 95%CI: 0.27–0.56; I2=65%, p<0.00001). None of the included studies examined functional outcome or quality of life measures, and cardiopulmonary adverse events were rarely reported. No clear evidence of reporting bias was identified. CONCLUSIONS In adults with acute TBI, observational studies reveal a significant mortality advantage with β-blockers; however, quality of evidence is very low. We conditionally recommend the use of in-hospital β-blockers. However, we recommend further high-quality trials to answer questions about the mechanisms of action, effectiveness on subgroups, dose-response, length of therapy, functional outcome, and quality of life after β-blocker use for TBI.

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Beta Blockers for Acute Traumatic Brain Injury: A Systematic Review and Meta-analysis

Abstract: The current body of evidence is suggestive of a benefit of beta blockers following TBI. However, methodologically sound randomized controlled trials are indicated to confirm the efficacy of beta blockers in patients with TBI.

Cited by 50 publications

References 34 publications

The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury

The role of cardiac troponin I in prognostication of patients with isolated severe traumatic brain injury

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

Beta-blockers and Traumatic Brain Injury

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