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Hydroxyethyl starch 130/0.4 or hypertonic saline solution to decrease inflammatory response in hemorrhagic shock?
Critical Care volume 17, Article number: 457 (2013)
We read with great interest the study by Chen and colleagues highlighting interest in hydroxyethyl starch (HES) 130/0.4 in treatment after hemorrhagic shock to ameliorate oxidative stress and the inflammatory response in a rat model. Compared with HES 200/0.5 and succinylated gelatin, the authors showed that infusions of HES 130/0.4 significantly reduced malondialdehyde levels and myeloperoxidase activity and also inhibited about 50% of TNF-α production in the intestine .
However, we regret the lack of assessment of another resuscitative fluid: the hypertonic saline solution (HTS). In our level 1 trauma center, we chose to use HTS because we have some concerns about HES safety. Indeed, HES may induce coagulopathy and increase risk of renal-replacement therapy . HTS has several advantages due to its osmotic effects. Firstly, it leads to restoration of circulating volume with a smaller volume of fluid. Secondly, it reduces intracranial pressure in case of associated traumatic brain injury . In addition, HTS attenuates the increase in plasma concentration of IL-1β, IL-6, IFN-γ and TNF-α, suggesting that HTS may also limit the inflammatory response to hemorrhage and reperfusion . One of its inconveniences may be the increased risk of acute kidney injury due to hyperchloremic metabolic acidosis decreasing renal blood flow; however, this effect was especially demonstrated when using large amounts of 0.9% saline solution .
We suggest that, in 2013, studies on fluid resuscitation should compare all the available resuscitative fluids, and not just HES, currently under concern for safety reasons.
hypertonic saline solution
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The authors declare that they have no competing interests.
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Esnault, P., Prunet, B., Cotte, J. et al. Hydroxyethyl starch 130/0.4 or hypertonic saline solution to decrease inflammatory response in hemorrhagic shock?. Crit Care 17, 457 (2013) doi:10.1186/cc13043
- Traumatic Brain Injury
- Metabolic Acidosis
- Acute Kidney Injury