Effects of traumatic subarachnoid hemorrhage on pathological properties in diffuse brain injury: A comparison with aneurysmal subarachnoid hemorrhage

As a result of recent advances in continuous monitoring equipment, it has been reported that vasospasm (VS) and delayed ischemic neurological deficit (DIND) occur as frequently in traumatic subarachnoid hemorrhage (TSAH) as in subarachnoid hemorrhage due to ruptured intracranial aneurysm (ASAH), and these VS and DIND have been reported to affect the outcome of TSAH adversely in many cases. When we compared TSAH secondary to diffuse brain injury (DBI) with ASAH, however, these two conditions were evidently different from each other in nature. Then we compared laboratory data, clinical course, and outcomes of TSAH associated with DBI with those of ASAH, to determine whether TSAH results in poor outcomes of DBI. On CT scans, patterns of SAH distribution were different from each other, and SAH was detected in 76% of the patients with ASAH on day 4, whereas only 2.0% of the patients with TSAH had detectable SAH on day 3. The incidence rates of detectable SAH in both groups remained significantly different from each other after day 2. The cerebral blood flow (CBF) decreased to around 75% of the normal flow in the acute stage of ASAH, and it decreased further to around 65% in the subacute stage. In TSAH, in contrast, CBF varied widely among the patients. The average CBF decreased to about 70% in the acute stage, and then it increased to around the lower limit of the normal range in the subacute stage. The urinary output and serum concentration of low molecular protein compositions in TSAH were markedly different from those in ASAH. In addition, the contour of a low density area (LDA) in CT scans in the subacute-chronic stage was the same as that of the area supplied by the artery being constricted due to cerebro-vascular spasm in ASAH. In TSAH, in contrast, hardly any LDA had a form that was suggestive of this conjunction, with cerebro-vascular spasm and the incidence rate of LDAs was significantly different from that for ASAH. About 30% of the patients with ASAH had ventricular enlargement, which was diagnosed as normal pressure hydrocephalus by cisternography, in the chronic stage. Surgical shunting was effective for these patients. In TSAH, ventricular enlargement was observed in more than 50% of the patients, bur almost none of these patients underwent surgical shunting, because it resulted from cerebral atrophy. Regardless of causes of SAH, the severer SAH was, the more often patients had a poor our-come. The outcome of TSAH was, however, significantly poorer than that of ASAH. When SAH was traumatic, it disappeared by the time VS developed and, in addition, changes in CBF and the form and incidence rate of LDAs were different from those in ASAH. We concluded that, although TSAH is an adverse prognostic factor for DBI, it does nor contribute to poor outcomes of DBI by giving rise to DIND caused by VS.