High Versus Low Volume Fluid Resuscitation Strategies in a Porcine Model (Sus scrofa) of Combined Thermal and Traumatic Brain Injury.

BACKGROUND: Combined burn and traumatic brain injury (TBI) treatment priorities may not align due to opposing fluid resuscitation paradigms used in treating burns and TBI. We developed a porcine model of combined thermal injury/TBI and compared an "aggressive" fluid resuscitation strategy using the Parkland formula and a "restrictive" resuscitation strategy using the modified Brooke formula. METHODS: Twenty-eight swine were deeply anesthetized and received a 40% total body surface area full-thickness burn injury and TBI. Swine were then randomized to receive restrictive or aggressive resuscitation for 8 h after which time animals were euthanized and necropsy was performed. Volume of brain injury was assessed after analyzing segmental slices of brain tissue. RESULTS: There were no differences between the restrictive and aggressive resuscitation groups in blood pressure, heart rate, central venous pressure, intra-cranial pressure (ICP), or serum lactate levels after 8 h of resuscitation. Urine output was higher in the aggressive resuscitation group. The restrictive group had a significantly higher serum blood urea nitrogen (BUN) compared with baseline and compared with the aggressive group. There was no significant difference in size of brain injury between groups. CONCLUSIONS: Both restrictive and aggressive resuscitation demonstrated adequate resuscitation at 8 h postinjury. Increased serum BUN in the restrictive group may be an indicator of early acute kidney injury, despite adequate urine output. Resuscitation strategy did not appear to affect ICP or the size of brain injury.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) in a swine model of hemorrhagic shock and blunt thoracic injury.

PURPOSE: While resuscitative endovascular balloon occlusion of the aorta (REBOA) is contraindicated in patients with aortic injuries, this technique may benefit poly-trauma patients with less extreme thoracic injuries. The purpose of this study was to characterize the effects of thoracic injury on hemodynamics during REBOA and the changes in pulmonary contusion over time in a swine model. METHODS: Twelve swine were anesthetized, instrumented, and randomized to receive either a thoracic injury with 5 impacts to the chest or no injury. All animals underwent controlled hemorrhage of 25% blood volume followed by 45 min of Zone 1 REBOA. Animals were then resuscitated with shed blood, observed during a critical care period, and euthanized after 6 h of total experimental time. RESULTS: There were no differences between the groups at baseline. The only difference after 6 h was a lower hemoglobin in the thoracic trauma group (8.4 ± 0.8 versus 9.4 ± 0.6 g/dL, P = 0.04). The average proximal mean arterial pressures were significantly lower in the thoracic trauma group during aortic occlusion [103 (98-108) versus 117 (115-124) mmHg, P = 0.04]. There were no differences between the pulmonary contusion before REBOA and at the end of the experiment in size (402 ± 263 versus 356 ± 291 mL, P = 0.782) or density (- 406 ± 127 versus - 299 ± 175 HFU, P = 0.256). CONCLUSIONS: Thoracic trauma blunted the proximal arterial pressure augmentation during REBOA but had minimal impacts on resuscitative outcomes. This initial study indicates that REBOA does not seem to exacerbate pulmonary contusion in swine, but blunt thoracic injuries may attenuate the expected rises in proximal blood pressure during REBOA.