Prospective evaluation of early propranolol after traumatic brain injury

Murry, Jason; Hoang, David M.; Barmparas, Galinos; Harada, Megan Y.; Bukur, Marko; Bloom, Matthew B.; Inaba, Kenji; Margulies, Daniel R.; Salim, Ali; Ley, Eric J.

doi:10.1016/j.jss.2015.06.045

Cited by 28 publications

(44 citation statements)

References 28 publications

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“…There was no significant difference between both groups in terms of the incidence of the other outcomes including hypotension, bradycardia, congestive heart failure and bronchospasm (Table 1A). In the Murry et al (53) cohort, there was no significant difference in the rate of hypotensive events but more bradycardia episodes (defined as heart rate < 60 beats/min) were recorded in the control group relative to the patients who received propranolol. It was not reported whether these bradycardia events were clinically significant and symptomatic (i.e.…”

Section: Resultsmentioning

confidence: 93%

“…Two studies assessed for potential cardiopulmonary adverse events associated with β-blockers therapy in TBI patients (47, 53). Compared to the placebo group in the RCT by Cruickshank et al (47), the atenolol group had a lower proportion of patients with abnormally high CK-MB cardiac biomarker level (2/27 vs. 9/30, p=0.05) and a lower incidence of supraventricular tachycardia (6/46 vs. 28/49, p<0.0001).…”

Section: Resultsmentioning

confidence: 99%

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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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Section: Resultsmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Beta-blockers and Traumatic Brain Injury

et al. 2017

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“…Zangbar, et al conducted a retrospective propensity-matched cohort study evaluating patients exposed to metoprolol after TBI compared to patients with no beta-blocker exposure (n=356), and determined that metoprolol exposure was associated with a survival advantage (p=0.01) independent of heart rate 50 . A recent small prospective observational study (n=38) in moderate to severe TBI patients concluded that low-dose propranolol administration within 12 hours of ICU admission was associated with a reduced ICU and hospital length of stay, but not mortality 51 .…”

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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“…β-blockers do not appear to significantly decrease heart rate variability or blood pressure among patients with TBI, though overall effects on cardiac output have not been directly measured in this patient population. (25, 27, 28) Currently, there is evidence to suggest a benefit of β-blockers following TBI but there is a lack of well-designed controlled trials to address important functional outcomes, quality of life, and long-term mortality in TBI patients. In addition, there is a lack of uniformity on which β-blocker should be given.…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

β-Blockade use for Traumatic Injuries and Immunomodulation

Loftus

Efron

Moldawer

et al. 2016

Shock

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Sympathetic nervous system activation and catecholamine release are important events following injury and infection. The nature and timing of different pathophysiologic insults have significant effects on adrenergic pathways, inflammatory mediators, and the host response. Beta adrenergic receptor blockers (β-blockers) are commonly used for treatment of cardiovascular disease but recent data suggests that the metabolic and immunomodulatory effects of β-blockers can expand their use. β-blocker therapy can reduce sympathetic activation and hypermetabolism as well as modify glucose homeostasis and cytokine expression. It is the purpose of this review to examine either the biologic basis for proposed mechanisms or to describe current available clinical evidence for the use of β-blockers in traumatic brain injury (TBI), spinal cord injury (SCI), hemorrhagic shock, acute traumatic coagulopathy, erythropoietic dysfunction, metabolic dysfunction, pulmonary dysfunction, burns, immunomodulation, and sepsis.

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Prospective evaluation of early propranolol after traumatic brain injury

Cited by 28 publications

References 28 publications

Beta-blockers and Traumatic Brain Injury

Beta-blockers and Traumatic Brain Injury

Hypertension After Severe Traumatic Brain Injury: Friend or Foe?

β-Blockade use for Traumatic Injuries and Immunomodulation

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