Ongoing Endothelial Cell Dysfunction Following Hemorrhagic Shock: Crystalloids are the Culprit

Current data demonstrate that early blood product resuscitation and minimization of crystalloid improve outcomes. However, there is little data on crystalloid use after hemorrhage control. We hypothesized that administration of crystalloid during early post resuscitation care may contribute to ongoing endothelial dysfunction.

As part of a prospective observational study of patients in hemorrhagic shock, crystalloid data were collected upon arrival, in the operating room and during the first 24, 48, and 72 hours in the intensive care unit (ICU). Blood samples were collected on arrival and in a subset of patients at 24 hours. Indicators of inflammation, endothelial dysfunction, and coagulation were evaluated by Luminex. Demographics, physiological data, outcomes, blood product, and resuscitation data were abstracted.

A total of 69 patients met the inclusion criteria. The mean crystalloid volume in the first 24 hours was 4.7 L (3.5-7 L): 0.5 L (0-1.5 L) during trauma resuscitation, 2.5 L(1.7-3.5 L) in the operating room and 1.5 L in the ICU. Cumulative total was 6.9 L (4.5-9.2 L) at 48 hours and 7.7 L (6.2-9.8 L) at 72 hours. At admission, patients had increases in endothelial, coagulation, and inflammatory markers compared with minimally injured controls. There was a correlation between crystalloid and syndecan-1 and INR at 24 hours, suggesting ongoing endothelial dysfunction. At 48 and 72 hours crystalloid totals correlated with sequential organ failure scores, ICU length of stay, and ventilator days.

We continue to rely on crystalloids after hemorrhage control. This practice is associated with ongoing endothelial and coagulation dysfunctions and suggests the need for alternative resuscitation strategies in the post hemorrhagic phase of care.