Severe brain injury. Part I. Pathophysiology

Severe head trauma, a common type of injury in veterinary patients, can be induced by motor vehicle accidents, falls, or attacks by humans or other animals. Trauma patients present with a variety of primary brain injuries, including cerebral lacerations caused by skull fractures, parenchymal contusions, neuronal and axonal damage, and compartmentalized hemorrhage (e.g., epidural, subdural, and subarachnoid hemorrhage). All of these factors influence the neurologic presentation and the prognosis for future function. Recently, secondary brain injuries have been increasingly recognized in relation to cerebral injury that occur after the initial impact injury and during the treatment period. These brain insults result from increased neuronal and cerebrovascular sensitivity, increased intracranial pressure, and episodes of systemic hypotension and hypoxemia. In brain-injured patients, uncontrolled glutamate release and failure of energy systems in neuronal and supporting tissues directly cause cell death mediated by high intracellular calcium. By developing an understanding of the pathophysiologic mechanisms of cerebral susceptibility to secondary brain injury, veterinarians will be better equipped to make treatment decisions that do not predispose patients to ongoing brain insults. Part I of this two-part presentation considers the extracranial and intracranial causes of secondary include increased sensitivity of cerebrovascular and neuronal tissue, elevations in intracranial pressure, and altered cerebrovascular reactivity. The second part will discuss specific treatment modalities (including fluid therapy, oxygen, corticosteroids, and hyperventilation) to be used in patients with severe brain injury.