Lescot T, Degos V, Zouaoui A, et al. Opposed effects of hypertonic saline on contusions and noncontused brain tissue in patients with severe traumatic brain injury

Université Pierre et Marie Curie-Paris 6, France.
Critical Care Medicine (Impact Factor: 6.31). 01/2007; 34(12):3029-33. DOI: 10.1097/01.CCM.0000243797.42346.64
Source: PubMed


The aim of this study was to quantify the effect of hypertonic saline solution on contused and noncontused brain tissue in patients with traumatic brain injury. We hypothesize that hypertonic saline would increase the volume of brain contusion while decreasing the volume of noncontused hemispheric areas.
Prospective observational study.
Neurosciences critical care unit of a university hospital.
Fourteen traumatic brain injury patients with increased intracranial pressure.
A computed tomography scan was performed before and after a 20-min infusion of 40 mL of 20% saline.
The volume, weight, and specific gravity of contused and noncontused hemispheric areas were assessed from computed tomography DICOM images by using a custom-designed software (BrainView). Physiologic variables and natremia were measured before and after infusion. Hypertonic saline significantly increased natremia from 143 +/- 5 to 146 +/- 5 mmol/L and decreased intracranial pressure from 23 +/- 3 to 17 +/- 5 mm Hg. The volume of the noncontused hemispheric areas decreased by 13 +/- 8 mL whereas the specific gravity increased by 0.029 +/- 0.027%. The volume of contused hemispheric tissue increased by 5 +/- 5 mL without any con-comitant change in density. There was a wide interindividual variability in the response of the noncontused hemispheric tissue with changes in specific gravity varying between -0.0124% and 0.0998%.
Three days after traumatic brain injury, the blood- brain barrier remains semipermeable in noncontused areas but not in contusions. Further studies are needed to tailor the use of hypertonic saline in patients with traumatic brain injury according to the volume of contusions assessed on computed tomography.

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Available from: Louis Puybasset, Mar 01, 2015
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    • "The principles of identifying areas of BBB compromise and edema can be translated into clinical practice . In 2006, Lescot et al. [19] used computed tomography to measure volume, weight, and specific gravity of contused and noncontused areas in patients with severe TBI. Recently, preclinical investigators using MRI with diffusion weighted imaging technology have been able to identify temporal and regional differences in edema after TBI in rabbits. "
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    ABSTRACT: Background: Blood brain barrier (BBB) compromise is a key pathophysiological component of secondary traumatic brain injury characterized by edema and neuroinflammation in a previously immune-privileged environment. Current assays for BBB permeability are limited by working size, harsh extraction processes, suboptimal detection via absorbance, and wide excitation fluorescence spectra. In this study, we evaluate the feasibility of Alexa Fluor 680, a far-red dye bioconjugated to dextran, as an alternative assay to improve resolution and sensitivity. Methods: Alexa Fluor was introduced intravenously on the day of sacrifice to three groups: sham, controlled cortical impact (CCI), and CCI treated with a cell based therapy known to reduce BBB permeability. The brains were sectioned coronally and imaged using an infrared laser scanner to generate intensity plot profiles as well as signal threshold images to distinguish regions with varying degrees of permeability. Results: Linear plot profile analysis demonstrated greater signal intensity from CCI than treated rats at corresponding injury depths. Threshold analysis identified rims of signal at low + narrow threshold ranges. The integrated signals from a treatment group known to preserve the BBB were significantly less than the groups with CCI injury alone. There was no significant difference at high + wide signal intensity threshold ranges. Conclusions: Alexa Fluor 680 infrared photodetection and image analysis can aid in detecting differential degrees of BBB permeability after traumatic brain injury and maybe particularly useful in demonstrating BBB preservation of at-risk regions in response to therapeutic agents.
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    • "First, there is no established dose of HTS or target serum sodium when instituting therapy. Hyperosmolarity from hypernatremia works in areas of “normal brain” where the blood–brain barrier remains intact and can result in increased brain volume in contusional areas [19]. Furthermore, the brain accommodates to HTS-induced sustained hypernatremia by intracellular idiogenic osmoles accumulation, which raises brain water content, restores brain volume, and leads to rebound increased ICP [12,20]. "
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