Spontaneous intracerebral hemorrhage (ICH), i.e., nontraumatic hemorrhage into the brain
parenchyma with or without ventricles, is a severe type of stroke with high mortality
rates. Systemic arterial hypertension and cerebral amyloid angiopathy represent the two
main risk factors of primary ICH. (1) ICH is understood to injure surrounding brain
tissue through the direct pressure effects of an acutely expanding mass lesion and
through secondary physiological and cellular pathways triggered by the hematoma and its
metabolized blood products. Direct pressure effects can include both local compression of
immediately surrounding brain tissue and more widespread mechanical injury caused by
increased intracranial pressure (ICP), hydrocephalus, or herniation. Early hematoma
expansion, possibly driven by mechanical shearing of surrounding vessels by the initial
hematoma, is common and a consistent predictor of worse ICH outcome. Secondary
physiological and cellular injury mechanisms postulated to be triggered by ICH include
cerebral edema, inflammation, and biochemical toxicity of blood products such as
hemoglobin, iron, and thrombin. Several of the major medical therapies for ICH such as BP
lowering and reversal of anticoagulation are aimed at limiting hematoma expansion. The
search for effective medical treatments for protecting tissue from secondary post-ICH
injury, like the search for effective neuroprotectants for ischemic stroke, has to date
been unsuccessful. Surgical hematoma evacuation through craniotomy or minimally invasive
approaches is aimed at both preventing further pressure-related injury and protecting
against secondary physiological and cellular injury. (2) Hematoma evacuation may have
therapeutic potential, based on the theoretical advantages of preventing or correcting
the acute effects of hematoma and its blood products into the surrounding healthy brain
parenchyma. However, because the most common sites of spontaneous ICH are the deep brain
structures, such as the basal ganglia and the thalamus, a large layer of healthy brain
tissue would be damaged. Additionally, neurosurgical procedures are not free of risks and
adverse effects. Post-surgical complications (e.g., hemorrhages and infections) are
common in this clinical scenario and carry high rates of morbidity and mortality. (3)
Recent meta-analyses suggested the benefits of neurosurgical hematoma evacuation,
especially when performed earlier and done using minimally invasive procedures. In MISTIE
III (Minimally invasive surgery plus alteplase for intracranial hematoma evacuation), to
confirm hemostasis and reduce the risk of rebleeding, the mean time from onset of ICH to
surgery was 47 hours while the mean time from onset of ICH to treatment completion was
123 hours. Theoretically, the earlier the hematoma is removed, the better the outcome.
Therefore, a higher rate of hematoma reduction within an earlier time course may be
beneficial. (4) Although the role of open surgery to treat patients with spontaneous ICH
remains controversial, the use of craniotomy for intracerebral hematoma drainage is the
most common strategy applied in most centers and also the most studied approach so far.
(5) Controversy remains over the efficacy of surgery for ICH, particularly in the early
(<12 hours) and very early (<8 hours) time windows. Further data are needed before
definitive conclusions can be reached. However, the sum of preclinical and clinical data
strongly suggests that early evacuation may be a necessary component of any successful
surgical approach. Furthermore, recent data have suggested improved safety of such
procedures using modern minimally invasive approaches. Such approaches may minimize
collateral injury, allow safe management of intraoperative bleeding, and prevent
postoperative rebleeding, all of which may facilitate the potential value of early ICH
evacuation. (6)