Basic pathophysiology

The reader is referred elsewhere for a detailed discussion of the pathological features of acute traumatic brain injury (TBI; also referred to as diffuse axonal injury).[1] However, it is important to appreciate that the severity and type of impact will substantially influence the structural lesions that ensue (Fig. 44.1). The acceleration–deceleration forces that ensue from impact during falls and motor vehicle accidents can produce axonal dysfunction and injury, brain contusions, and axial and extra-axial hematomas. The generation of such macroscopic injury is associated with microscopic and ultramicroscopic changes, including ischemic cytotoxic edema, astrocyte swelling and dysfunction, microglial activation, and recruitment and blood–brain barrier disruption. The pathophysiological processes underlying these changes have been extensively discussed in other publications [2] and will not be addressed in detail here.

These varied consequences are reflected by sequential changes in cerebrovascular physiology. Cerebral blood flow (CBF) is thought to show a triphasic behavior (Fig. 44.2),[3] and these time-varying hemodynamic responses also define the vascular contribution to intracranial pressure elevation in time. Immediately after head injury, there is no vascular engorgement, and though a transient blood–brain barrier leak has been reported in the first hour after impact in animal models, there are no data regarding this in humans. Apart from mass lesions, intracranial pressure elevation during this phase is assumed to be the consequence of cytotoxic edema. Increases in CBF and cerebral blood volume (CBV) from the second day post-injury onwards make vascular engorgement an important contributor to intracranial hypertension.