Secondary Neurologic Injury Resulting from Nonhypotensive Hemorrhage Combined with Mild Traumatic Brain Injury
| Autor: | Matthew J. Fabian, Todd F. Glass, Joseph A. Weinberg, Kenneth G. Proctor, John B. Schweitzer |
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| Rok vydání: | 1999 |
| Předmět: |
Blood Glucose
Male medicine.medical_specialty Resuscitation Mean arterial pressure Subarachnoid hemorrhage Swine Traumatic brain injury Intracranial Hypotension Hemodynamics Central nervous system disease Cerebral contusion medicine Animals Lactic Acid business.industry Brain Hemorrhage Traumatic medicine.disease nervous system diseases Surgery nervous system Brain Injuries Anesthesia Female Neurology (clinical) Hypotension Intracranial Hypertension business |
| Zdroj: | Journal of Neurotrauma. 16:771-782 |
| ISSN: | 1557-9042 0897-7151 |
| DOI: | 10.1089/neu.1999.16.771 |
| Popis: | Although the emergency physician often treats patients with multiple injuries, there are relatively few clinically relevant models that mimic these situations. To describe the changes after a hemorrhagic insult superimposed on traumatic brain injury (TBI), anesthetized and ventilated juvenile pigs were 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 parameters were assessed for 48 h. In TBI, mean arterial pressure (MAP) was not significantly different from baseline. For TBI + 40H, MAP fell by 60% (p < 0.05). This was corrected with resuscitation. Interestingly, TBI + 35H did not 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 elevated for 60 min. ICP remained at baseline with 35 H. Hemorrhagic focal cerebal contusions at the gray-white interface were 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 demonstrated grossly discernible intraparenchymal injury. There was no evidence of intracranial injury in the 35H group. Only in animals receiving a secondary insult of hemorrhage following the primary TBI were cerebral contusions found. 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 pressure changes. |
| Databáze: | OpenAIRE |
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