HYPEREMIA FOLLOWING TRAUMATIC BRAIN INJURY - RELATIONSHIP TO INTRACRANIAL HYPERTENSION AND OUTCOME

The role of posttraumatic hyperemia in the development of raised intra cranial pressure (ICP) has important pathophysiological and therapeuti c implications. To determine the relationship between hyperemia (cereb ral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measureme nts of ICP and CBF (xenon-133 method) were obtained in 59 patients wit h moderate and severe head injury. Hyperemia was associated with an in creased incidence of simultaneous intracranial hypertension compared t o nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0. 059). However, in 78% of blood flow studies in which ICP was greater t han 20 mm Hg. CBF was less than or equal to 55 ml/100 g/minute. At lea st one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individ uals with hyperemia without simultaneous intracranial hypertension, IC P was greater than 20 mm Hg for an average of 11 +/- 16 hours and favo rable outcomes were seen in 75% of patients. In contrast, in eight ind ividuals with hyperemia and at least one episode of hyperemia-associat ed intracranial hypertension, ICP was greater than 20 mm Hg for an ave rage of 148 +/- 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the coh ort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores ( all less than or equal to 6), and having the highest incidence of effa ced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypert ension, their clinical profile suggests the occurrence of a severe ini tial insult with resultant gross impairment of metabolic vasoreactivit y and pressure antoregulation. In a minority of these patients, howeve r, high CBF may be coupled to a hypermetabolic state, given their resp onsiveness to metabolic suppressive therapy. In patients with hyperemi a but without intracranial hypertension, elevated CBF is also likely t o be a manifestation of appropriate coupling to increased metabolic de mand consistent with a generally favorable outcome. This study support s the concept that there are multiple etiologies of both elevated bloo d flow and intracranial hypertension after head injury.