Prehospital Plasma Is Noninferior to Whole Blood for Restoration of Cerebral Oxygenation in a Rhesus Macaque Model of Traumatic Shock and Hemorrhage

Abstract

Traumatic shock and hemorrhage (TSH) is a leading cause of preventable death in military and civilian populations. Using a TSH model, we compared plasma with whole blood (WB) as prehospital interventions, evaluating restoration of cerebral tissue oxygen saturation (CrSO 2 ), systemic hemodynamics, colloid osmotic pressure (COP) and arterial lactate, hypothesizing plasma would function in a noninferior capacity to WB, despite dilution of hemoglobin (Hgb). Methods: Ten anesthetized male rhesus macaques underwent TSH before randomization to receive a bolus of O(−) WB or AB(+) plasma at T0. At T60, injury repair and shed blood (SB) to maintain MAP > 65 mm Hg began, simulating hospital arrival. Hematologic data and vital signs were analyzed via t test and two-way repeated measures ANOVA, data presented as mean ± SD, significance = P < 0.05. Results: There were no significant group differences for shock time, SB volume, or hospital SB. At T0, MAP and CrSO 2 significantly declined from baseline, though not between groups, normalizing to baseline by T10. Colloid osmotic pressure declined significantly in each group from baseline at T0 but restored by T30, despite significant differences in Hgb (WB 11.7 ± 1.5 vs. plasma 6.2 ± 0.8 g/dL). Peak lactate at T30 was significantly higher than baseline in both groups (WB 6.6 ± 4.9 vs. plasma 5.7 ± 1.6 mmol/L) declining equivalently by T60. Conclusions: Plasma restored hemodynamic support and CrSO 2 , in a capacity not inferior to WB, despite absence of additional Hgb supplementation. This was substantiated via return of physiologic COP levels, restoring oxygen delivery to microcirculation, demonstrating the complexity of restoring oxygenation from TSH beyond simply increasing oxygen carrying capacity.

Assessment of abnormal skeletal muscle perfusion by contrast-enhanced ultrasound with parametric imaging in rats after severe injury, hemorrhagic shock, and whole blood resuscitation

“…This is consistent with current resuscitation practices and avoids the hemodilution that impairs hemostasis and does not play a causal role in MBF derangement (32). The model produces a loss of coherence between macrohemodynamics and microhemodynamics, which is consistent with clinical observations and can be difficult to capture with other methods of measuring MBF (33). It also produces coagulopathy and a drop in platelet count, which are consistent with clinical observations and could be important aspects of the pathophysiology underpinning MBF derangement.…”