Hemorrhage HypotensionHypoxia Ischemia

A high number of patients that suffer from head injury often present with accompanying severe injury to other parts of the body, with profound hemorrhage at the site of injury. Additionally, hypotensive episodes have been found to occur in head-injured patients despite intensive care. Due to the duration and/or extent of these secondary episodes (SEs) accompanied by profoundly impaired autoregulation after TBI, these events may or may not be associated with hypoxia or ischemia to the brain, however. To test for the contribution of these SEs to the posttraumatic cascade after TBI, a number of experiments have included volume- or pressure-controlled hemorrhage, hypoxia, or pharmaceutically induced hypotensive episodes in their study design. Additionally, models of cerebral ischemia or hypoxia have been added to produce secondary ischemic or hypoxic insults to the injured brain directed to evaluate for aggravation of trauma-induced changes after TBI. To date, the models of impact acceleration, fluid-percussion brain injury, or rigid indentation combined with episodes of either hemorrhage, hypotension, ischemia, or hypoxia (or a combination of more than one of these pathologic conditions) have been used to experimentally mimic these frequent complications of clinical TBI.

Due to the broad spectrum of different investigation protocols and numerous possible combinations of the previously mentioned pathologic conditions, comprehensive conclusions are difficult to draw at present. Evidence suggests that animals showed some ability to cope with these posttraumatic SEs without further damage to CNS structures or behavioral impairment if the SE does not occur for a prolonged period. In contrast, a substantial increase in injury-induced pathologic changes has been reported if the duration of the SE or its severity exceeded a certain level or if the animal was subjected to a combination of more than one SE after the traumatic CNS insult.

To date, an increase in cell death in selectively vulnerable brain regions has been reported when trauma and SE were combined. Additionally, tests for neurologic motor function or cognitive ability revealed increased impairment if SE was added to the experimental protocol after TBI. The time frame of exposure to SEs appears to influence the magnitude of additional damage to the CNS. Longer periods of ischemia result in more pronounced damage to the cortex and subcortical hippocampal structures. Moreover, another variable that has to be considered is the time point after the traumatic impact to the brain when the SE occurs. Whereas the subcortical regions seem to be affected in the early period after TBI (immediately until 1 hr), the extent of cortical contusion increased markedly when the ischemia occurred several hours after TBI, although these reports have been contested.

Taken together, the data support a detrimental role of these secondary pathologic events in the sequelae after TBI if they exceed a certain threshold that is dependent on a number of factors. Among others, the magnitude of the single SE, the number, the temporal course and the duration appear to play a crucial role in increasing TBI-induced damage and impairment.

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