CC BY-NC-ND 4.0 · Indian Journal of Neurosurgery 2021; 10(01): 001-005
DOI: 10.1055/s-0041-1726865
Editorial

Surgery for Spontaneous Intracerebral Hemorrhage: Current Concept

Partha S. Ray
1  Department of Neurology and Clinical Neurophysiology, The Walton Centre for Neurology, National Health Service, Liverpool, United Kingdom
› Author Affiliations

Spontaneous intracerebral hemorrhage (ICH) into the brain parenchyma and into the ventricles presents as a severe stroke with high mortality,[1] with uncontrolled hypertension, cerebral amyloid angiopathy, and more recently the anticoagulant-induced cerebral bleeds representing the main risk factors.[2] [5] Unfortunately, interventions to stop hematoma expansion by rapid reduction of blood pressure, the use of recombinant activated factor eight, or the administration of tranexamic acid have not shown improvement in functional outcome.[6] [8]

The theoretical advantages of evacuating the hematoma and preventing the acute effects of the blood products on the surrounding healthy brain tissue are counterbalanced by the risks of reaching out to the location of the bleeds in the deep basal ganglia structures and the thalamus through healthy cerebral tissue and the additional burden of postsurgical complications.[9]

There is the need for emergency lifesaving surgical evacuation of large lobar hemorrhages and hematomas in the posterior fossa to avoid cerebral or brainstem herniation, and in such situations comparison of best medical management with surgical interventions does not lend itself to a randomized clinical trial (RCT) opportunity for an evidence-based assessment.

In about two-thirds of patients, acute hemorrhage into the brain parenchyma results in stoppage of bleeding through disruption and mass effect within the cerebral tissue. In the remaining one-third, hematoma expansion results in midline shift and an adverse outcome.[10] The best medical management and neuro intensive care with interventions of recombinant activated factor eight reduced hematoma growth but did not decrease mortality or improve functional outcome. The use of tranexamic acid reduced hematoma expansion but did not improve the functional outcome at 90 days. Two large trials of blood pressure lowering—INTERACT-2[11] and ATACH-II[6]—demonstrated that maintaining a systolic blood pressure around 120 to 130 mm Hg in the first 24 hours might result in improved functional outcome.[12]

Hematoma volume greater than 30 mL had statistically unfavorable outcome and a volume greater than 60 mL with Glasgow Coma Scale (GCS) score lower than 8 had greater than 90% predicted 30-day mortality. A volume greater than 150 mL through abrupt increase in intracranial pressure (ICP) and critical reduction of cerebral perfusion pressure (CPP) leads to death.[13] [14] Much smaller hematoma volumes in the posterior fossa due to obvious limitations of space to expand leads to brainstem herniation/compression with hydrocephalus and clinical deterioration when hematoma evacuation is of lifesaving consequence.[15] [16]

Additional adverse effects of the blood products from the hematoma and secondary inflammation and edema resulting from the same would compound the mass effect, midline shift and decreasing cerebral perfusion consequent to rising ICP.[17] [18]



Publication History

Publication Date:
26 March 2021 (online)

© 2021. Neurological Surgeons’ Society of India. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial-License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/).

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