Contribution of increased cerebral blood volume to posttraumatic intracranial hypertension.

Overview

Cerebrovascular dysfunction following acute brain injury (BI) may be the critical mediator of excess morbidity and mortality after BI. Despite aggressive therapy, death often is caused by refractory intracranial hypertension (IH). An understanding of the contributions of cerebrospinal fluid (CSF) and vascular factors to IH after BI is essential for management of intracranial pressure (ICP). Marmarou et al. showed that CSF accounted for only one third of the ICP rise after BI. We hypothesized that a vascular mechanism is predominant. Cerebral cortical reflectance photoplethysmography (IP) and radioactively labeled red blood cells were employed to study cerebral blood volume (CBV) changes associated with increased ICP after BI in miniature swine. Immediate posttraumatic IH could be attributed almost entirely to increased CBV. An early elevation in ICP immediately after BI (t = 0) was accompanied by a large increase in CBV compared with pre-BI levels (19.2 +/- 4.9 vs. 8.9 +/- 2.7 mL/100 g tissue, p < 0.05). Decreased CBV corresponded to lower ICP within 1 hour, followed by a slow rise that paralleled the increase in ICP. The 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 BI and within 6 hours are predominantly caused by increased CBV.