Traumatic brain injury induced temperature dysregulation: What is the role of β blockers?

Asmar, Samer; Bible, Letitia; Chehab, Mohamad; Tang, Andrew; Khurrum, Muhammad; Castañón, Lourdes; Ditillo, Michael; Douglas, Molly; Joseph, Bellal

doi:10.1097/ta.0000000000002975

Cited by 5 publications

(7 citation statements)

References 25 publications

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“…From 7922 relevant citations, 17 studies met the inclusion criteria (2 prospective, 2 RCTs, and 13 retrospective) 8–12 14 15 17 22–30. A PRISMA flow diagram of the study selection is illustrated in figure 1.…”

Section: Resultsmentioning

confidence: 99%

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Beta blockers in traumatic brain injury: a systematic review and meta-analysis

Hart

Lannon

Chen

et al. 2023

Trauma Surg Acute Care Open

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BackgroundTraumatic brain injury (TBI) is a major cause of death and disability worldwide. Beta blockers have shown promise in improving mortality and functional outcomes after TBI. The aim of this article is to synthesize the available clinical data on the use of beta blockers in acute TBI.MethodsA systematic search was conducted through MEDLINE, Embase, and Cochrane Central Register of Controlled Trials for studies including one or more outcomes of interest associated with use of beta blockers in TBI. Independent reviewers evaluated the quality of the studies and extracted data on all patients receiving beta blockers during their hospital stay compared with placebo or non-intervention. Pooled estimates, CIs, and risk ratios (RRs) or ORs were calculated for all outcomes.Results13 244 patients from 17 studies were eligible for analysis. Pooled analysis demonstrated a significant mortality benefit of overall use of beta blocker (RR 0.8, 95% CI 0.68 to 0.94,I2=75%). Subgroup analysis of patients with no preinjury use of beta blocker compared with patients on preinjury beta blockers showed no mortality difference (RR 0.99, 95% CI 0.7 to 1.39,I2=84%). There was no difference in rate of good functional outcome at hospital discharge (OR 0.94, 95% CI 0.56 to 1.58,I2=65%); however, there was a functional benefit at longer-term follow-up (OR 1.75, 95% CI 1.09 to 2.8,I2=0%). Cardiopulmonary and infectious complications were more likely in patients who received beta blockers (RR 1.94, 95% CI 1.69 to 2.24,I2=0%; RR 2.36, 95% CI 1.42 to 3.91,I2=88%). Overall quality of the evidence was very low.ConclusionsUse of beta blockers is associated with decreased mortality at acute care discharge as well as improved functional outcome at long-term follow-up. Lack of high-quality evidence limits definitive recommendations for use of beta blockers in TBI; therefore, high-quality randomized trials are needed to further elucidate the utility of beta blockers in TBI.PROSPERO registration numberCRD42021279700.

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Section: Resultsmentioning

confidence: 99%

“…The majority of studies (11 of 17) broadly included all patients who received at least one dose of any beta blocker while in the hospital. Only three studies included information on specific dosing 23 27 29…”

Section: Resultsmentioning

confidence: 99%

Beta blockers in traumatic brain injury: a systematic review and meta-analysis

Hart

Lannon

Chen

et al. 2023

Trauma Surg Acute Care Open

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“…They also play a role in regulating lipolysis in white adipose tissue, thermogenesis in brown adipose tissue and mobilization of hematopoietic progenitor cells [212]. It has been shown that TBI patients experience sympathetic hyperactivity, causing a catecholamine surge [213][214][215][216][217][218]. This surge causes secondary insults, which manifest as posttraumatic hyperthermia [216,218], increased inflammation and leukocyte migration [219,220], impaired cerebral homeostasis and perfusion [217], and cardiovascular dysfunction [216], and has been associated with increased mortality [221].…”

Section: Beta-blockersmentioning

confidence: 99%

Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies

El Baassiri,

Raouf,

Badin

et al. 2024

J Neuroinflammation

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Traumatic brain injury (TBI) is a chronic and debilitating disease, associated with a high risk of psychiatric and neurodegenerative diseases. Despite significant advancements in improving outcomes, the lack of effective treatments underscore the urgent need for innovative therapeutic strategies. The brain-gut axis has emerged as a crucial bidirectional pathway connecting the brain and the gastrointestinal (GI) system through an intricate network of neuronal, hormonal, and immunological pathways. Four main pathways are primarily implicated in this crosstalk, including the systemic immune system, autonomic and enteric nervous systems, neuroendocrine system, and microbiome. TBI induces profound changes in the gut, initiating an unrestrained vicious cycle that exacerbates brain injury through the brain-gut axis. Alterations in the gut include mucosal damage associated with the malabsorption of nutrients/electrolytes, disintegration of the intestinal barrier, increased infiltration of systemic immune cells, dysmotility, dysbiosis, enteroendocrine cell (EEC) dysfunction and disruption in the enteric nervous system (ENS) and autonomic nervous system (ANS). Collectively, these changes further contribute to brain neuroinflammation and neurodegeneration via the gut-brain axis. In this review article, we elucidate the roles of various anti-inflammatory pharmacotherapies capable of attenuating the dysregulated inflammatory response along the brain-gut axis in TBI. These agents include hormones such as serotonin, ghrelin, and progesterone, ANS regulators such as beta-blockers, lipid-lowering drugs like statins, and intestinal flora modulators such as probiotics and antibiotics. They attenuate neuroinflammation by targeting distinct inflammatory pathways in both the brain and the gut post-TBI. These therapeutic agents exhibit promising potential in mitigating inflammation along the brain-gut axis and enhancing neurocognitive outcomes for TBI patients.

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“…ese findings only translated to a shorter ICU stay and lower mortality in the subgroup of patients with head Abbreviated Injury Scale ≥4. [10] A consolidated research effort is being put into the development of effective neuroprotective agents that can improve long-term outcomes after TBI. e discussion of the potential neuroprotective role of beta-blockers merits a short discussion of another promising neuroprotective agent: amantadine.…”

Section: Anti-seizure Prophylaxis and Neuroprotectionmentioning

confidence: 99%

“…These findings only translated to a shorter ICU stay and lower mortality in the subgroup of patients with head Abbreviated Injury Scale ≥4. [ 10 ]…”

Section: Anti-seizure Prophylaxis and Neuroprotectionmentioning

confidence: 99%

Initial neurocritical care of severe traumatic brain injury: New paradigms and old challenges

El-Swaify

kamel

Ali

et al. 2022

Surgical Neurology International

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Background: Early neurocritical care aims to ameliorate secondary traumatic brain injury (TBI) and improve neural salvage. Increased engagement of neurosurgeons in neurocritical care is warranted as daily briefings between the intensivist and the neurosurgeon are considered a quality indicator for TBI care. Hence, neurosurgeons should be aware of the latest evidence in the neurocritical care of severe TBI (sTBI). Methods: We conducted a narrative literature review of bibliographic databases (PubMed and Scopus) to examine recent research of sTBI. Results: This review has several take-away messages. The concept of critical neuroworsening and its possible causes is discussed. Static thresholds of intracranial pressure (ICP) and cerebral perfusion pressure may not be optimal for all patients. The use of dynamic cerebrovascular reactivity indices such as the pressure reactivity index can facilitate individualized treatment decisions. The use of ICP monitoring to tailor treatment of intracranial hypertension (IHT) is not routinely feasible. Different guidelines have been formulated for different scenarios. Accordingly, we propose an integrated algorithm for ICP management in sTBI patients in different resource settings. Although hyperosmolar therapy and decompressive craniectomy are standard treatments for IHT, there is a lack high-quality evidence on how to use them. A discussion of the advantages and disadvantages of invasive ICP monitoring is included in the study. Addition of beta-blocker, anti-seizure, and anticoagulant medications to standardized management protocols (SMPs) should be considered with careful patient selection. Conclusion: Despite consolidated research efforts in the refinement of SMPs, there are still many unanswered questions and novel research opportunities for sTBI care.

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Traumatic brain injury induced temperature dysregulation: What is the role of β blockers?

Cited by 5 publications

References 25 publications

Beta blockers in traumatic brain injury: a systematic review and meta-analysis

Beta blockers in traumatic brain injury: a systematic review and meta-analysis

Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies

Initial neurocritical care of severe traumatic brain injury: New paradigms and old challenges

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