Pathophysiology of traumatic brain injury

Werner, Christian; Engelhard, Kristin

doi:10.1093/bja/aem131

Cited by 1,319 publications

(1,036 citation statements)

References 73 publications

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“…1,2 When intracranial compliance is limited, any increase in volume (e.g., cerebral edema or contusion) can lead to a precipitous rise in intracranial pressure (ICP), resulting in impaired cerebral blood flow and secondary ischemia. 1,3 The duration and magnitude of elevated ICP consistently portends worse neurologic outcomes following TBI. [4][5][6] As such, treatment of elevated ICP remains a cornerstone in the management of severe TBI, with the Brain Trauma Foundation recommending keeping ICP below 20 mmHg.…”

Section: Résumémentioning

confidence: 99%

The effect of continuous hypertonic saline infusion and hypernatremia on mortality in patients with severe traumatic brain injury: a retrospective cohort study

Tan

Kolmodin

Sekhon

et al. 2016

Can J Anesth/J Can Anesth

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Purpose Hypertonic saline (HTS) is used to control intracranial pressure (ICP) in patients with traumatic brain injury (TBI); however, in prior studies, the resultant hypernatremia has been associated with increased mortality. We aimed to study the effect of HTS on ICP and mortality in patients with severe TBI. Methods We performed a retrospective cohort study of 231 patients with severe TBI ( [CI], 0.56 to 2.05; P = 0.84) nor hypernatremia (HR, 1.31; 95% CI, 0.68 to 2.55; P = 0.42) was associated with hospital mortality. There was no effect modification by either HTS or hypernatremia on each another. Patients who received HTS observed a significant decrease in ICP during their ICU stay compared with those who did not receive HTS (4 mmHg; 95% CI, 2 to 6; P \ 0.001 vs 2 mmHg; 95% CI, -1 to 5; P = 0.14). Conclusions Hypertonic saline and hypernatremia are not associated with hospital mortality in patients with severe TBI. RésuméObjectif Une solution saline hypertonique (HTS) est utilisée pour contrô ler la pression intracrânienne (PIC) chez les patients ayant subi un traumatisme cérébral (TC); toutefois, dans des études précédentes, l'hypernatrémie

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Section: Résumémentioning

confidence: 99%

The effect of continuous hypertonic saline infusion and hypernatremia on mortality in patients with severe traumatic brain injury: a retrospective cohort study

Tan

Kolmodin

Sekhon

et al. 2016

Can J Anesth/J Can Anesth

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“…The accumulation of blood-borne immune cells within the parenchyma has been reported in both head-injured patients and in animal models of brain trauma. 2 These activated cells release mediators including prostaglandins, free radicals, complement factors, and pro-inflammatory cytokines, 10 which in turn induce the expression of chemokines and cell adhesion molecules and mobilize immune and glial cells to the injured site. 11 Over time, subsequent production of anti-inflammatory mediators suppresses both humoral and cellular immune activation.…”

Section: Introductionmentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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Summary:Despite dramatic improvements in the management of traumatic brain injury (TBI), to date there is no effective treatment available to patients, and morbidity and mortality remain high. The damage to the brain occurs in two phases, the initial primary phase being the injury itself, which is irreversible and amenable only to preventive measures to minimize the extent of damage, followed by an ongoing secondary phase, which begins at the time of injury and continues in the ensuing days to weeks. This delayed phase leads to a variety of physiological, cellular, and molecular responses aimed at restoring the homeostasis of the damaged tissue, which, if not controlled, will lead to secondary insults. The development of secondary brain injury represents a window of opportunity in which pharmaceutical compounds with neuroprotective properties could be administered. To establish effective treatments for TBI victims, it is imperative that the complex molecular cascades contributing to secondary injury be fully elucidated. One pathway known to be activated in response to TBI is cellular and humoral inflammation. Neuroinflammation within the injured brain has long been considered to intensify the damage sustained following TBI. However, the accumulated findings from years of clinical and experimental research support the notion that the action of inflammation may differ in the acute and delayed phase after TBI, and that maintaining limited inflammation is essential for repair. This review addresses the role of several cytokines and chemokines following focal and diffuse TBI, as well as the controversies around the use of therapeutic anti-inflammatory treatments versus genetic deletion of cytokine expression.

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“…Furthermore, increased glutamatergic release into the extracellular milieu following injury causes marked increases in glucose use and accumulation of extracellular lactate [53,[74][75][76][77][78][79]. This deregulated cerebral metabolism leads to decreased ATP production causing the failure of ATP-dependent ion channels and proteins leading to ionic osmotic alterations that result in cell swelling and culminating in necrosis [80]. Mitochondrial dysfunction may be central to the pathophysiology of TBI through metabolic derangements, oxidative stress, and apoptosis.…”

Section: Mechanisms Of Neural Injury In the Traumatic Penumbramentioning

confidence: 99%

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

Regner¹,

Meirelles²,

Simon³

2018

Traumatic Brain Injury - Pathobiology, Advanced Diagnostics and Acute Management

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Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Understanding the pathophysiology of TBI is crucial for the development of more effective therapeutic strategies. At the moment of the traumatic impact, transfer of kinetic forces causes neurologic damage; this primary injury triggers a secondary wave of biochemical cascades, together with metabolic and cellular changes, called secondary neural injury. These areas of ongoing secondary injury, or areas of "traumatic penumbra," represent crucial targets for therapeutic interventions. This chapter is focused on the interplay between progression of parenchymal injury and the neuroprotective and neurorestorative processes that are emerging and developing subsequently to traumatic impact. Thus, we emphasized the role of traumatic penumbra in TBI pathogenesis and suggested a crucial contribution of the neurovascular units (NVUs) and paracrine effects of exosomes and miRNAs in promoting neurological recovery.

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Pathophysiology of traumatic brain injury

Cited by 1,319 publications

References 73 publications

The effect of continuous hypertonic saline infusion and hypernatremia on mortality in patients with severe traumatic brain injury: a retrospective cohort study

The effect of continuous hypertonic saline infusion and hypernatremia on mortality in patients with severe traumatic brain injury: a retrospective cohort study

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

Traumatic Penumbra: Opportunities for Neuroprotective and Neurorestorative Processes

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