Albumin Saturated With Fatty Acids Prevents Decompensation in a Rat Hemorrhagic Shock Trauma Model With Tourniquet and Hypotensive Resuscitation

Abstract

Decompensation is a major prehospital threat to survival from trauma/hemorrhage shock (T/HS) after controlling bleeding. We recently showed higher than expected mortality from a combat-relevant rat model of T/HS (27 mL/kg hemorrhage) with tourniquet (TQ) and permissive hypotensive resuscitation (PHR) with Plasmalyte. Mortality and fluid requirements were reduced by resuscitation with 25% albumin presaturated with oleic acid (OA-sat) compared with fatty-acid -free albumin or Plasmalyte. The objective of this follow-up analysis was to determine the role of decompensation and individual compensatory mechanisms in those outcomes. We observed two forms of decompensation: slow (accelerating fluid volumes needed to maintain blood pressure) and acute (continuous fluid administration unable to prevent pressure drop). Combined incidence of decompensation was 71%. Nearly all deaths (21 of 22) were caused by acute decompensations that began as slow decompensations. The best hemodynamic measure for predicting acute decompensation was diastolic arterial pressure. Decompensation was due to vascular decompensation rather than loss of cardiac performance. Albumin concentration was lower in decompensating groups, suggesting decreased stressed volume, which may explain the association of low albumin on admission with poor outcomes after trauma. Our findings suggest that acute decompensation may be common after trauma and severe hemorrhage treated with TQ and PHR and OA-sat albumin may benefit early survival and reduce transfusion volume by improving venous constriction and preventing decompensation.

CD226 deficiency promotes glutaminolysis and alleviates mitochondria damage in vascular endothelial cells under hemorrhagic shock

“…Except for plasma resuscitation, other HS treatments cannot effectively improve the cell function failure and metabolism disorders of vascular ECs after HS 11–14 . However, the supply of blood products is limited, and patients with decompensated HS would progress to systemic inflammatory response syndrome, multiple organ failure, and even death 38,39 . Hence, it is of great significance to develop targeted therapy for energy metabolic disorders and damages of vascular ECs at the early stage of HS.…”

“…[11][12][13][14] However, the supply of blood products is limited, and patients with decompensated HS would progress to systemic inflammatory response syndrome, multiple organ failure, and even death. 38,39 Hence, it is of great significance to develop targeted therapy for energy metabolic disorders and damages of vascular ECs at the early stage of HS. In this study, in vivo animal models showed that CD226 knockout mice had alleviated pathological damage and inflammatory response after HS.…”

What's New in Shock, June 2021?

“…We shift gears now onto a discussion of hemorrhagic shock and its sequalae. Penn et al (13) studied a rat model of hemorrhagic shock with tourniquet application and prolonged hypotensive resuscitation to describe different types of decompensation encountered after severe hemorrhagic shock. The authors suggest that decompensation does not seem to be driven by intrinsic cardiac factors but rather of loss of preload from inability of venous vasculature to constrict combined with a loss of oncotic pressure.…”