RESUMO
Diagnostic and monitoring procedures for patients with head injury are aimed at early detection of mass lesions and secondary insults. Our therapeutic approach is based on our understanding of pathophysiologic mechanisms that cause secondary brain damage, and includes evacuation of mass lesions and prevention of secondary insults. Basic research has greatly increased our knowledge of these pathophysiologic mechanisms and has prompted the development of many neuroprotective agents, targeted to selected mechanisms. Unfortunately, it has proved difficult to demonstrate the benefit of such agents in the overall population of head-injured patients. Clinical research has emphasized the importance of ischemia in head injury and has demonstrated the deleterious effect of secondary insults on outcome. Medical management of patients with head injury has consequently focused on prevention of secondary insults, treatment of raised intracranial pressure, and maintenance of adequate cerebral perfusion pressure. The introduction of new monitoring techniques in head-injured patients offers the possibilities of more targeted therapy in individual patients, in contrast to the current practice of a staircase approach to treatment of raised intracranial pressure.In the US, an evidence-based approach has resulted in the wide acceptance of general principles, but at the same time highlighted the lack of hard evidence for the use of many therapeutic modalities. Practical guidelines, developed and published by the European Brain Injury Consortium, are based on expert opinion and consensus. Surveys have shown considerable variation in monitoring techniques and treatment. There is still considerable need for further improvements, both from a medical scientific perspective and from an organizational aspect. Particularly relevant are early resuscitation and stabilization at the scene of the accident, the organization of emergency services, admission policy to the intensive care unit, and improved policy for early identification of patients with operable intracranial hematoma. Further dissemination and general acceptance of already published guidelines may be expected to significantly improve care in head injury.
RESUMO
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.