Secondary neurologic injury resulting from nonhypotensive hemorrhage combined with mild traumatic brain injury

Although the emergency physician often treats patients with multiple injuri es, there are relatively few clinically relevant models that mimic these si tuations. To describe the changes after a hemorrhagic insult superimposed o n traumatic brain injury (TBI), anesthetized and ventilated juvenile pigs w ere assigned to 35% hemorrhage (35H), TBI (via fluid percussion); TBI + 35H , and TBI + 40H (40% hemorrhage). Animals were resuscitated with shed blood and crystalloid. Hemodynamic, metabolic, behavioral, and histologic parame ters were assessed for 48 h. In TBI, mean arterial pressure (MAP) was not s ignificantly different from baseline. For TBI + 40H, MAP fell by 60% (p < 0 .05). This was corrected with resuscitation. Interestingly, TBI + 35H did n ot show a fall in MAP, while in 35H, MAP was reduced similarly to the TBI 40H group. ICP was elevated only initially in the TBI group. In TBI + 40H and TBI + 35H, ICP increased markedly with resuscitation, remaining elevate d for 60 min. ICP remained at baseline with 35 H. Hemorrhagic focal cerebal contusions at the gray-white interface we:re observed in 3/5 of TBI + 40H and 5/7 of TBI + 35H. Despite the presence of subarachnoid hemorrhage (SAH) in all the animals in the TBI alone group, none of these animals demonstra ted grossly discernible intraparenchymal injury. There was no evidence of i ntracranial injury in the 35H group. Only in animals receiving a secondary insult of hemorrhage following the primary TBI were cerebral contusions fou nd. These experiments demonstrate the evolution of cerebral contusions as a form of secondary neurologic injury following resuscitation from traumatic brain injury and hemorrhage, even in the absence of significant blood pres sure changes.