Analysis of the association of fluid balance and short-term outcome in traumatic brain injury

Zhao, Ziqi; Wang, Dong; Jia, Ying; Tian, Ye; Wang, Yi; Wei, Yingsheng; Zhang, Jianning; Jiang, Rongcai

doi:10.1016/j.jns.2016.03.007

Cited by 21 publications

(11 citation statements)

References 26 publications

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“…Following severe TBI, the blood brain barrier is disrupted, and the resulting cerebral oedema causes increases in intracranial pressure (ICP) and thus leads to poor outcomes (Zhao et al, 2016). Therefore, pharmacological therapies designed to slow the development of cerebral oedema and attenuate disruption of the BBB are expected to improve neurologic outcomes after TBI.…”

Section: Discussionmentioning

confidence: 99%

Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation

Sun

Wang

et al. 2017

Front. Cell. Neurosci.

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Traumatic brain injury (TBI) is one of the leading causes of trauma-induced mortality and disability, and emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, has been reported to act as an ER stress inhibitor and chemical chaperone and to have the potential to attenuate apoptosis and inflammation. To study the effects of TUDCA on brain injury, we subjected mice to TBI with a controlled cortical impact (CCI) device. Using western blotting, we first examined TBI-induced changes in the expression levels of GRP78, an ER stress marker, p-PERK, PERK, p-eIF2a, eIF2a, ATF4, p-Akt, Akt, Pten, Bax, Bcl-2, Caspase-12 and CHOP, as well as changes in the mRNA levels of Akt, GRP78, Caspase-12 and CHOP using RT-PCR. Neuronal cell death was assessed by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, and CHOP expression in neuronal cells was detected by double-immunofluorescence staining. Neurological and motor deficits were assessed by modified neurological severity scores (mNSS) and beam balance and beam walking tests, and brain water content was also assessed. Our results indicated that ER stress peaked at 72 h after TBI and that TUDCA abolished ER stress and inhibited p-PERK, p-eIF2a, ATF4, Pten, Caspase-12 and CHOP expression levels. Moreover, our results show that TUDCA also improved neurological function and alleviated brain oedema. Additionally, TUDCA increased p-Akt expression and the Bcl-2/Bax ratio. However, the administration of the Akt inhibitor MK2206 or siRNA targeting of Akt abolished the beneficial effects of TUDCA. Taken together, our results indicate that TUDCA may attenuate early brain injury via Akt pathway activation.

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Section: Discussionmentioning

confidence: 99%

Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation

Sun

Wang

et al. 2017

Front. Cell. Neurosci.

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“…Insufficient fluid administration in the early phase of TBI may lead to cerebral hypoperfusion or intensify brain oedema. Excessive fluid administration in the presence of a leaky BBB may lead to refractory intracranial hypertension while aggressive fluid removal and negative fluid balance may result in AKI [62]. Many clinicians still believe in the beneficial effects of a negative fluid balance in TBI patients, which can be achieved by high dose diuretics.…”

Section: Importance Of Daily and Cumulative Fluid Balancementioning

confidence: 99%

“…Many clinicians still believe in the beneficial effects of a negative fluid balance in TBI patients, which can be achieved by high dose diuretics. However, uncontrolled use of diuretics together with mannitol has been associated with a high incidence of AKI and increased risk of worse outcomes or death in TBI patients [62,63]. Several studies have also documented that a fluid balance lower than 0.5-0.8 L during 96 hours post-TBI is independently associated with poor outcomes [62,64].…”

Section: Importance Of Daily and Cumulative Fluid Balancementioning

confidence: 99%

“…However, uncontrolled use of diuretics together with mannitol has been associated with a high incidence of AKI and increased risk of worse outcomes or death in TBI patients [62,63]. Several studies have also documented that a fluid balance lower than 0.5-0.8 L during 96 hours post-TBI is independently associated with poor outcomes [62,64]. Mannitol intensifies extraction of water, Na + and other electrolytes via osmotic diuresis leading to temporary hyponatremia in TBI [63].…”

Section: Importance Of Daily and Cumulative Fluid Balancementioning

confidence: 99%

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The use of crystalloids in traumatic brain injury

Dąbrowski

Woodcock²,

Rzecki

et al. 2018

Anaesthesiol Intensive Ther

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Fluid therapy is one of the most important treatments in patients with traumatic brain injury (TBI) as both hypo- and hypervolaemia can cause harm. The main goals of fluid therapy for patients with TBI are to optimize cerebral perfusion and to maintain adequate cerebral oxygenation. The avoidance of cerebral oedema is clearly essential. The current weight of evidence in the published literature suggests that albumin therapy is harmful and plasma substitutes have failed to demonstrate superiority over crystalloids solutions. Crystalloids are the most common fluids administered in patients with TBI. However, differences in their composition may affect coagulation and plasma tonicity and acid-base homeostasis. The choice of the ideal crystalloid fluid in TBI should be made based on tonicity, type of buffer used and volume status. Hypotonic fluids buffered with substances altering blood coagulation should be avoided in clinical practice. The prescriber remains faced with choices about the tonicity and pH buffering capability of fluid therapy, which we review here.

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“…However, in some patients, particularly those with severe ARDS requiring high mean airway pressures for oxygenation, hypovolaemia may exacerbate hypoxaemia by virtue of increased intrapulmonary shunt, and clinical benefit may result from the careful administration of fluid boluses (98). Zhao et al (99) were the first to test the effect of fluid balance on short term TBI outcome and they demonstrated that both high © Journal of Thoracic Disease. All rights reserved.…”

Section: Fluid Balance and Hemoglobin Targetmentioning

confidence: 99%

Acute respiratory distress syndrome in traumatic brain injury: how do we manage it?

Torre¹,

Badenes²,

Corradi³

et al. 2017

J. Thorac. Dis.

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Traumatic brain injury (TBI) is an important cause of morbidity and mortality worldwide. TBI patients frequently suffer from lung complications and acute respiratory distress syndrome (ARDS), which is associated with poor clinical outcomes. Moreover, the association between TBI and ARDS in trauma patients is well recognized. Mechanical ventilation of patients with a concomitance of acute brain injury and lung injury can present significant challenges. Frequently, guidelines recommending management strategies for patients with traumatic brain injuries come into conflict with what is now considered best ventilator practice. In this review, we will explore the strategies of the best practice in the ventilatory management of patients with ARDS and TBI, concentrating on those areas in which a conflict exists. We will discuss the use of ventilator strategies such as protective ventilation, high positive end expiratory pressure (PEEP), prone position, recruitment maneuvers (RMs), as well as techniques which at present are used for 'rescue' in ARDS (including extracorporeal membrane oxygenation) in patients with TBI. Furthermore, general principles of fluid, haemodynamic and hemoglobin management will be discussed. Currently, there are inadequate data addressing the safety or efficacy of ventilator strategies used in ARDS in adult patients with TBI. At present, choice of ventilator rescue strategies is best decided on a case-by-case basis in conjunction with local expertise.

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Analysis of the association of fluid balance and short-term outcome in traumatic brain injury

Cited by 21 publications

References 26 publications

Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation

Administration of Tauroursodeoxycholic Acid Attenuates Early Brain Injury via Akt Pathway Activation

The use of crystalloids in traumatic brain injury

Acute respiratory distress syndrome in traumatic brain injury: how do we manage it?

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