Abstract

Spontaneous intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, ≈4 times more common than subarachnoid hemorrhage and accounting for 15% of all strokes.1 ICH is associated with higher rates of morbidity and mortality than all stroke subtypes. Overall, mortality rates for ICH are estimated to be as high as 40% to 50%, with the vast majority of survivors disabled at 6 months. When ICH is associated with intraventricular hemorrhage (IVH), outcomes are even worse, with estimated rates of mortality between 50% and 80%.1 Current standards recommend that patients with cerebellar hemorrhages measuring >3 cm with associated neurological deterioration or significant mass effect be managed with emergency surgical decompression. Similarly, patients with supratentorial hemorrhage and impending herniation are frequently taken for surgical decompression with or without hematoma evacuation. ICH patients who do not fall into either of these 2 categories are, in the vast majority of cases, managed medically.2 With the exception of aggressive blood pressure normalization, no medical therapy has been shown to improve outcomes or reduce mortality in patients with ICH.2 In the absence of clinical evidence to guide therapy, many aspects of medical management are based on local practice patterns with significant variations between institutions. Spontaneous supratentorial ICH may be divided into 2 general categories based on anatomic location—deep (involving the deep gray matter nuclei) or lobar. Deep hemorrhages are generally caused by hypertension, whereas lobar hemorrhages are most often caused by either hypertension or amyloid angiopathy.3 Either type of hemorrhage may be caused or exacerbated by an inherent or pharmacologically induced coagulopathy.1 Brain injury caused by spontaneous ICH is believed to be a biphasic process. The initial hemorrhage dissects through the brain parenchyma, creating a direct traumatic injury to the regional neurons. Although some neurons are irreversibly injured …

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