Pharmacologic Management of the Patient With Traumatic Brain Injury

Ripley, David L.; Driver, Sangeeta; Stork, Ryan; Maneyapanda, Mithra B.

doi:10.1016/b978-0-323-54456-6.00011-6

Cited by 4 publications

(7 citation statements)

References 183 publications

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“…The administration of beta-adrenergic blockade has not been delineated in the TBI guidelines or recommendations provided by various trauma organizations, including the Trauma Brain Foundation, the American College of Surgeons, and the American Association for the Surgery of Trauma. [33][34][35] The accumulating evidence supporting the ability of beta-blockers to improve mortality rates and mitigate any paroxysmal sympathetic hyperactivity-related complications 36 indicates that there may be a need for updated recommendations to include beta-blocker therapy in the management of TBI patients. Given the variations in the choice of beta-blocker and regimen across the studies, we are unable to make recommendations regarding the efficacy of specific beta-blocker regimens.…”

Section: Discussionmentioning

confidence: 99%

Beta-Blocker Therapy in Patients With Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Zagales

Selvakumar

Ngatuvai

et al. 2022

The American Surgeon™

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Introduction Traumatic brain injury (TBI), a leading cause of morbidity and mortality among trauma patients worldwide, poses the risk of secondary neurological insult due to significant catecholamine surge. We aim to investigate the effectiveness and outcomes of beta-blocker administration in patients with severe TBI. Methods A search through PubMed, EMBASE, JAMA network, and Google Scholar databases was conducted for relevant peer-reviewed original studies published before February 15, 2022. A standard random-effects model was used, as justified by a high Cohen’s Q test. Results Twelve studies met inclusion criteria and were included in the meta-analysis. Severe TBI patients who were administered beta-blockers had a significantly reduced incidence of in-hospital mortality compared to the non-beta-blocker group (14.5% vs 19.2%). However, the beta-blocker group was reported to have a significantly greater number of ventilator days (5.58 vs 2.60 days). Similarly, intensive care unit (9.00 vs 6.84 days) and hospital (17.30 vs 11.02 days) lengths of stay (LOS) were increased in the beta-blocker group compared to those who were not administered beta-blocker therapy, but only the difference in hospital-LOS was significant. Conclusions Beta-blockers have significantly decreased in-hospital mortality in patients with severe TBI despite being associated with an increase in ventilator days and hospital-LOS. The administration of beta-blocker therapy in the management of severe TBI may be warranted and should be discussed in future guidelines.

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Section: Discussionmentioning

confidence: 99%

Beta-Blocker Therapy in Patients With Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Zagales

Selvakumar

Ngatuvai

et al. 2022

The American Surgeon™

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“…They do so by acting on GABA A Rs and thereby mediate sedative effects and anti-epileptic action ( 50 ). Benzodiazepines are commonly used as anesthetic/sedative agents in clinical TBI and also in the treatment of anxiety, insomnia, and seizures ( 14 , 18 , 50 ). By binding to the benzodiazepine receptor on the GABA A Rs, these drugs potentiate the effect of GABA by inducing a conformational change on the receptor ( 50 ).…”

Section: Benzodiazepinesmentioning

confidence: 99%

“…In clinical TBI, sedation through drugs still remains the first line of treatment to prevent further complications, normalize intracranial pressure (ICP), and reduce metabolic demand ( 14 , 16 ). Generally, the choice of anesthetic agents is decided by the treating physician based on the drug's hemodynamic factors, its ability to reduce ICP, cerebral metabolic rate, and the drug's potential to cause short-term and long-term side effects ( 15 , 17 , 18 ). Unfortunately, one factor that is often under-emphasized while selecting an anesthetic agent in clinical TBI is the ability of the drug to prevent cell death and reduce histological damage.…”

Section: Introductionmentioning

confidence: 99%

“…Here, in this study, I have reviewed the neuroprotective efficacy of a specific class of drugs that augment GABAergic neurotransmission (GABA A receptor agonists) from preclinical animal research studies. GABA A R agonists are commonly employed as anesthetic agents in clinical TBI owing to their safety profile and anti-epileptic efficacy ( 3 , 16 , 18 , 24 ). After performing an exhaustive literature search, only studies that reported direct metrics on histopathological damage or edema were included in the review ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

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Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies

Sudhakar¹

2023

Front. Neurol.

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Traumatic brain injuries (TBI) caused by physical impact to the brain can adversely impact the welfare and well-being of the affected individuals. One of the leading causes of mortality and dysfunction in the world, TBI is a major public health problem facing the human community. Drugs that target GABAergic neurotransmission are commonly used for sedation in clinical TBI yet their potential to cause neuroprotection is unclear. In this paper, I have performed a rigorous literature review of the neuroprotective effects of drugs that increase GABAergic currents based on the results reported in preclinical literature. The drugs covered in this review include the following: propofol, benzodiazepines, barbiturates, isoflurane, and other drugs that are agonists of GABAA receptors. A careful review of numerous preclinical studies reveals that these drugs fail to produce any neuroprotection after a primary impact to the brain. In numerous circumstances, they could be detrimental to neuroprotection by increasing the size of the contusional brain tissue and by severely interfering with behavioral and functional recovery. Therefore, anesthetic agents that work by enhancing the effect of neurotransmitter GABA should be administered with caution of TBI patients until a clear and concrete picture of their neuroprotective efficacy emerges in the clinical literature.

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“…), which is consistent with the literature, these patients have shorter length of stay, greater likelihood of discharge to less restrictive environments, and improved clinical outcomes. 6,7,8 This commentary considers ways in which restraints can be viewed as tools to support interdisciplinary best practices for patients with certain clinical conditions like Albert's, what factors can make clinical benefits of restraints outweigh their harms, and how restraints can be effectively and ethically regulated and applied.…”

Section: Commentarymentioning

confidence: 99%

Should One Kind of Freedom Be Restricted to Promote Another?

Feder

Firn

Stork

2021

AMA Journal of Ethics

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Due to restraints' consequences for personal liberty and dignity, the threshold to apply restraints is understandably high and heavily regulated. However, there can be clinical scenarios in which restraint use can facilitate a patient's freedom. This article considers such a case and examines conditions under which using restraints offers therapeutic benefit for patients with traumatic brain injuries.

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Pharmacologic Management of the Patient With Traumatic Brain Injury

Cited by 4 publications

References 183 publications

Beta-Blocker Therapy in Patients With Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Beta-Blocker Therapy in Patients With Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis

Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies

Should One Kind of Freedom Be Restricted to Promote Another?

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