Abstract

Previous reports identified the presence of traumatic subarachnoid hemorrhage (tSAH) on admission computed tomographic (CT) scans as an independent prognostic factor in worsening outcomes. The mechanism underlying the link between tSAH and prognosis has not been clarified. The aim of this study was to investigate the association between CT evidence of tSAH and outcomes after moderate or severe head injuries. In a survey organized by the European Brain Injury Consortium, data on initial severity, treatment, and subsequent outcomes were prospectively collected for 1005 patients with moderate or severe head injuries who were admitted to one of the 67 European neurosurgical units during a 3-month period in 1995. The CT findings were classified according to the Traumatic Coma Data Bank classification system, and the presence or absence of tSAH was recorded separately in the initial CT scan forms. Complete data on early clinical features, CT findings, and outcomes at 6 months were available for 750 patients, of whom 41% exhibited evidence of tSAH on admission CT scans. There was a strong, highly statistically significant association between the presence of tSAH and poor outcomes. In fact, 41% of patients without tSAH achieved the level of good recovery, whereas only 15% of patients with tSAH achieved this outcome. Patients with tSAH were significantly older (median age, 43 yr; standard deviation, 21.1 yr) than those without tSAH (median age, 32 yr; standard deviation, 19.5 yr), and there was a significant tendency for patients with tSAH to exhibit lower Glasgow Coma Scale scores at the time of admission. A logistic regression analysis of favorable/unfavorable outcomes demonstrated that there was still a very strong association between tSAH and outcomes after simultaneous adjustment for age, Glasgow Coma Scale Motor Scores, and admission CT findings (odds ratio, 2.49; 95% confidence interval, 1.74-3.55; P < 0.001). Comparison of the time courses for 164 patients with early (within 14 d after injury) deaths demonstrated very similar patterns, with an early peak and a subsequent decline; there was no evidence of a delayed increase in mortality rates for either group of patients (with or without tSAH). These findings for an unselected series of patients confirm previous reports of the adverse prognostic significance of tSAH. The data support the view that death among patients with tSAH is related to the severity of the initial mechanical damage, rather than to the effects of delayed vasospasm and secondary ischemic brain damage.

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