Traumatic Brain Injury

Focal or diffuse cerebral edema of mixed types may develop following traumatic brain injury (TBI). Following contusion of the brain, the damaged BBB permits the extravasation of fluid into the interstitial space. Areas of contusion or infarction may release or induce chemical mediators that can spread to other regions. These potentially deleterious mediators include lysosomal enzymes, biogenic amines including serotonin and histamine, excitatory amino acids, arachidonic acid, and components of the kallikrein-kinin system. These factors activated during tissue damage are powerful mediators of extravasation and vasodilation. TBI is associated with a biphasic patho-physiologic response heralded by a brief period of vasogenic edema immediately following injury, followed after 45-60 min by the development of cytotoxic edema. Vasogenic edema may be detected by neuroi-maging modalities within 24-48 hr and reach maximal severity between Days 4 and 8. Although cerebral blood flow decreases for the initial few hours following head injury, a reactive hyperemic response that exceeds metabolic demands may exacerbate vasogenic edema. Autoregulatory dysfunction is a common sequela of TBI that may promote the formation of hydrostatic edema in regions where the BBB remains intact.

Recent efforts have also demonstrated a prominent role of cytotoxic edema in head-injured patients.

Figure 5 Multimodal MRI of cerebral venous thrombosis. Ischemic edema of the thalami manifest as hyperintensity on (a) T2-weighted sequences and (b) DWI. (c) ADC hypointensity corresponds to the cytotoxic component. (d) Focal hyperintensity suggests increased regional cerebral blood volume.

Tissue hypoxia with ischemic edema formation and neurotoxic injury due to ionic disruption contribute to this cytotoxic component. In addition, osmotic edema may result from hyponatremia, and hydrocephalic edema may complicate the acute phase of TBI when subarachnoid hemorrhage or infections predominate. Conspicuous diffuse axonal injury may produce focal edema in white matter tracts experiencing shear-strain forces during acceleration/deceleration of the head (Fig. 6). Arterial hypotension may aggravate the clinical expression of cerebral edema. Episodic hypotension is a common occurrence in the head-injured patient, exacerbated by hypovolemia and the cardio-depressant effect of sedative medications. When autoregulation is preserved, arterial blood pressure may have a significant effect on ICP levels. As CPP decreases with arterial hypotension, compensatory cerebral vasodilation leads to increased cerebral blood volume and thereby raises ICP. Conversely, therapeutic maintenance of CPP encourages vasoconstriction with subsequent reduction in ICP. These changes in cerebral blood volume influence the severity of edema through modulation of the overall water content of brain tissue. Although the degree of edema has not been directly correlated with outcome, ICP elevations illustrate the ability to predict poor clinical outcome. Raised ICP attributed to cerebral edema is the most frequent cause of death in TBI. The effects of herniation due to a traumatic epidural hematoma and diffuse axonal injury are demonstrated in Fig. 7. The pathogenesis of cerebral edema in the immature brain stands is the subject of much controversy in attempts to address the relatively higher frequency and severity of edema in pediatric head-injury patients. Sustained posttraumatic cerebral hypoperfusion and a greater susceptibility to excitoxic injury have been suggested as alleged factors in this process.

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