Traumatic subarachnoid hemorrhage: our current understanding and its evolution over the past half century.

Traumatic brain injury (TBI) is a common cause of morbidity and mortality in the US, especially among the young. Primary injury in TBI is preventable, whereas secondary injury is treatable. As a result, considerable research efforts have been focused on elucidating the pathophysiology of secondary injury and determining various prognosticators in the hopes of improving final outcome by minimizing secondary injury. One such variable, traumatic subarachnoid hemorrhage (tSAH), has been the focus of many discussions over the past half century as numerous clinical studies have shown tSAH to be associated with adverse outcome. Whether the relationship of tSAH with poorer outcome in TBI is merely an epiphenomenon or a result of direct cause and effect is unclear. Some investigators believe that tSAH is merely a marker of severer TBI, while others argue that it directly causes deleterious effects such as vasospasm and ischemia. At the present time, no proven treatment regimen aimed specifically at decreasing the detrimental effects of tSAH exists, although calcium channel blockers traditionally thought to target vasospasm have shown some promises. Given that tSAH may primarily be an early indicator of associated and evolving brain injury, vigilant diagnostic surveillance including serial head CT and prevention of secondary brain damage owing to hypotension, hypoxia and intracranial hypertension may be more cost-effective than attempting to treat potential adverse sequelae associated with tSAH.