Abstract
Hemorrhagic Shock (HS) after Traumatic Brain Injury (TBI) is common and lethal among military and civilians. Blood transfusion has been the resuscitation gold standard procedure for many years. However, only 3% of age‐eligible individuals donate blood, which limits blood availability and cannot meet current blood demands. This study was compared the efficacy to resuscitate from HS after TBI via infusion of Lactated Ringer’s solution (LR, electrolyte solution used to restore the loss of blood volume), fresh blood (Blood, autologous blood drawn during the hemorrhage), or Polymerized Hemoglobin [PolyHb, a Hemoglobin Based Oxygen Carrier (HBOC) that shows promise in increasing oxygenation]. Fifteen Wistar rats (350–400g) were instrumented with catheters in the femoral artery and vein and subjected to TBI through a pneumatic controlled cortical impact (CCI) (Leica Biosystems, Vista, CA). To induce TBI, a 5mm craniotomy over the right cerebral cortex was performed, and the scalp was impacted at a velocity of 5m/s and dwell time of 200ms. The scalp was subsequently closed and animals were given 10 min to stabilize before performing HS. HS was induced by blood withdrawal from the femoral artery catheter to achieve a mean arterial pressure (MAP) between 35–40mmHg, and the hypotensive state was maintained for 90 min before resuscitation. Animals were separated into 3 groups based on the resuscitation solution: Blood, LR, or PolyHb. Animals were monitored for an additional 120 min before euthanasia. Measurements were taken at baseline (BL), 90 min into HS (HS), and 30 min (R1) and 2 hours (R2) after resuscitation. The MAP, systolic blood pressure (SBP), and diastolic blood pressure (DBP) were decreased equally in all groups during HS. Blood and PolyHb groups increased MAP compared to the LR group at R1. The MAP was not different between Blood and PolyHb at R2. The SBP was increased only for the Blood group as compared to the LR group at R1. Moreover, DBP was increased for both Blood and PolyHb compared to the LR group at R1 and R2. As expected, hematocrit decreased in all groups after HS, with only the Blood group recovering hematocrit after resuscitation. Total hemoglobin (tHb) decreased after HS, and increased after resuscitation for the Blood and PolyHb groups but not in the LR group. Oxygen saturation was decreased for the Blood and PolyHb groups compared to the LR group at R1 and R2. The oxygen saturation was increased on the Blood group compared to PolyHb group at R2. After HS all groups increased lactate, after R1 just Blood and LR group recovered lactate to BL levels, and PolyHb did not decreased lactate concentration at R2 compared to the blood group. In conclusion, our results show that PolyHb was effective to resuscitation from HS after TBI, restoring blood pressure similarly to Blood group and could be a good alternative to transfusion for field resuscitation from HS after TBI.Support or Funding InformationThis work was supported by the NIH Heart Lung and Blood Institute under Grant, R01‐HL126945, and the DOD DMRDP under Grants W81XWH‐18‐1‐0059, W81XWH‐17‐2‐0047
Highlights
Traumatic brain injury (TBI) is often accompanied by hemorrhage, and treatment of hemorrhagic shock (HS) after TBI is challenging because the two therapeutic treatment strategies for TBI and HS often conflict
This study evaluated the efficacy of large molecular weight polymerized human hemoglobin (PolyhHb) to restore blood pressure after resuscitation from hemorrhagic shock post-TBI compared to lactated Ringer’s solution (LR, electrolyte solution used to restore the loss of blood volume), and fresh whole blood (Blood, autologous blood drawn during hemorrhage)
The systolic blood pressure (SBP) was significantly higher for the Blood and PolyhHb groups compared to the LR group 30 min into resuscitation and remained significantly higher in the Blood group at the end of the resuscitation period
Summary
Traumatic brain injury (TBI) is often accompanied by hemorrhage, and treatment of hemorrhagic shock (HS) after TBI is challenging because the two therapeutic treatment strategies for TBI and HS often conflict. Treatment of HS after TBI is challenging as the therapeutic regimens for the two individual conditions may conflict, since ischemia/reperfusion injury associated with resuscitation from HS can be exaggerated due to a loss of local and systemic autoregulatory mechanisms following T BI3. Cerebral edema is one of the most prominent pathophysiological factors associated with death and unfavorable outcomes after T BI9–11 While neurotraumas affect both systemic and cerebrovascular hemodynamic regulatory mechanisms, TBI exacerbates the cardiovascular instability observed during H S12. The systemic pathophysiological changes attributed to HS exacerbate the inflammatory response induced by TBI, negatively affecting the control of inflammatory mediators and oxidative stress, which in turn affects all organs[16] These pathways contribute to organ failure through microvascular shunting, coagulopathy, blood stasis, capillary occlusion, and a cidosis[17,18]. The optimal treatment goal for HS after TBI is ambiguous, especially since various strategies have been proposed without clear consensus[3]
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