Systemic Complications after Subarachnoid Hemorrhage

Aneurysmal subarachnoid hemorrhage (SAH) is a neurologic emergency that affects an estimated 10 individuals in a population of 100.000 annually, and is associated with high mortality rates and significant morbidity among survivors(1,2) . The most important independent determinants of outcome include neurological state on admission (3-8), age (3, 5,7-9) large aneurysm size (> 10 mm)(6), and aneurysm rebleeding(10-12). Actually, medical complications may have a considerable impact on neurological outcomes and survival (Tab. 1). They are very common, and in recent large prospective cohorts, the proportions of death directly attributable to extracerebral organ injuries was estimated between 23 and 42%(13-16). These are potentially modifiable derangements, that can exacerbate brain injury after SAH, and consist mainly in respiratory, cardiac, electrolyte and metabolic abnormalities. Recently, fever, anemia and hyperglycemia were found to be significantly independently associated with mortality and poor functional outcome (17); furthermore at 24 hours from the admission, hypoxemia, metabolic acidosis, hyperglycemia, and cardiovascular instability resulted to be the physiological abnormalities that independently predict poor outcome (15). Pathophysiological mechanisms are not completely understood. They are probably multifactorial and involve a massive catecholamine release at the time of the hemorrhage, and the activation of a remarkable inflammatory and immunological response, both within the brain and systemically. In this review the principle mechanisms of injury and the most important clinical features of prognostic relevant organ failures after SAH are described.