Sodium Bicarbonate Lowers Intracranial Pressure After Traumatic Brain Injury

Bourdeaux, Chris; Brown, Jules

doi:10.1007/s12028-010-9368-8

Cited by 28 publications

(11 citation statements)

References 20 publications

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“…Clinical decisions are supported by the analysis of head computed tomography (CT) and multimodal brain monitoring. In practice this high complexity is often simplified by ''ICP Management Protocols'' [8][9][10][11] that specify appropriate types and levels of interventions according to the underlying cause and the patient response to treatment. Among all the specific interventions, hyperosmolar therapy is recommended 12 as a non-surgical measure to manage high ICP due to brain edema either with mannitol or hypertonic saline.…”

Section: Introductionmentioning

confidence: 99%

Post-Traumatic Multimodal Brain Monitoring: Response to Hypertonic Saline

Dias

João

PereiraEduarda

et al. 2014

Journal of Neurotrauma

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Emerging evidence suggests that hypertonic saline (HTS) is efficient in decreasing intracranial pressure (ICP). However there is no consensus about its interaction with brain hemodynamics and oxygenation. In this study, we investigated brain response to HTS bolus with multimodal monitoring after severe traumatic brain injury (TBI). We included 18 consecutive TBI patients during 10 days after neurocritical care unit admission. Continuous brain monitoring applied included ICP, tissue oxygenation (PtO2) and cerebral blood flow (CBF). Cerebral perfusion pressure (CPP), cerebrovascular resistance (CVR), and reactivity indices related to pressure (PRx) and flow (CBFx) were calculated. ICM+software was used to collect and analyze monitoring data. Eleven of 18 (61%) patients developed 99 episodes of intracranial hypertension (IHT) greater than 20 mm Hg that were managed with 20% HTS bolus. Analysis over time was performed with linear mixed-effects regression modelling. After HTS bolus, ICP and CPP improved over time (p<0.001) following a quadratic model. From baseline to 120 min, ICP had a mean decrease of 6.2 mm Hg and CPP a mean increase of 3.1 mmHg. Mean increase in CBF was 7.8 mL/min/100 g (p<0.001) and mean decrease in CVR reached 0.4 mm Hg*min*100 g/mL (p=0.01). Both changes preceded pressures improvement. PtO2 exhibited a marginal increase and no significant models for time behaviour could be fitted. PRx and CBFx were best described by a linear decreasing model showing autoregulation recover after HTS (p=0.01 and p=0.04 respectively). During evaluation, CO2 remained constant and sodium level did not exhibit significant variation. In conclusion, management of IHT with 20% HTS significantly improves cerebral hemodynamics and cerebrovascular reactivity with recovery of CBF appearing before rise in CPP and decrease in ICP. In spite of cerebral hemodynamic improvement, no significant changes in brain oxygenation were identified.

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Section: Introductionmentioning

confidence: 99%

Post-Traumatic Multimodal Brain Monitoring: Response to Hypertonic Saline

Dias

João

PereiraEduarda

et al. 2014

Journal of Neurotrauma

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“…Second, it may be possible to alter brain pH in humans. Although brain pH was not measured, HCO 3 − has been administered to patients with severe TBI [74], [75]; hypertonic NaHCO 3 was given intravenously in place of hypertonic NaCl to reduce elevated intracranial pressures. While NaHCO 3 was as effective as saline at reducing intracranial pressure, brain pH was not measured and whether HCO 3 − administration had any additional long-term benefits remains uncertain.…”

Section: Discussionmentioning

confidence: 99%

Loss of Acid Sensing Ion Channel-1a and Bicarbonate Administration Attenuate the Severity of Traumatic Brain Injury

et al. 2013

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Traumatic brain injury (TBI) is a common cause of morbidity and mortality in people of all ages. Following the acute mechanical insult, TBI evolves over the ensuing minutes and days. Understanding the secondary factors that contribute to TBI might suggest therapeutic strategies to reduce the long-term consequences of brain trauma. To assess secondary factors that contribute to TBI, we studied a lateral fluid percussion injury (FPI) model in mice. Following FPI, the brain cortex became acidic, consistent with data from humans following brain trauma. Administering HCO3 − after FPI prevented the acidosis and reduced the extent of neurodegeneration. Because acidosis can activate acid sensing ion channels (ASICs), we also studied ASIC1a−/− mice and found reduced neurodegeneration after FPI. Both HCO3 − administration and loss of ASIC1a also reduced functional deficits caused by FPI. These results suggest that FPI induces cerebral acidosis that activates ASIC channels and contributes to secondary injury in TBI. They also suggest a therapeutic strategy to attenuate the adverse consequences of TBI.

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“…Although decompressive craniectomy reduces ICP and may reduce brain temperature, 241 it is unclear whether it impacts neurologic outcome. Hypertonic sodium bicarbonate reduces ICP without the development of hyperchloremic metabolic acidosis, 247 although its efficacy relative to hypertonic sodium chloride has not previously been evaluated. The former received bilateral frontotemporal parietal craniectomy with dural opening.…”

Section: Traumatic Brain Injurymentioning

confidence: 99%