Contribution of Increased Cerebral Blood Volume to Post-Traumatic Intracranial Hypertension

Summary

Cerebrovascular dysfunction following traumatic brain injury (TBI) may be the critical mediator of excess morbidity and mortality after TBI. Despite aggressive therapy, death is often due to refractory intracranial hypertension (IH). Cerebral cortical reflectance photoplethysmoghraphy and radioactively labeled red blood cells were employed to study cerebral blood volume (CBV) changes associated with increased intracranial pressure (ICP) after TBI in miniature swine. An early elevation in ICP immediately after TBI (t=0) was accompanied by a large increase in CBV compared to pre-TBI levels (19.2±4.9 vs 8.9±2.7 mL/lOOg tissue, p<0.05). Decreased CBV corresponded to lower ICP within 1 hour, followed by a slow rise that paralleled the increase in ICP. CBV (16.1+3.3 vs 8.9±2.7, p<0.05) and ICP (23±2.2 vs 9±0.6, p <0.05) were higher at 6 hours than at baseline. Based on compartmental analysis, the data indicate that ICP changes immediately after TBI and within 6 hours are predominantly due to increased CBV.