Abstract
Intracerebral hemorrhage (ICH) is a medical emergency, which often leads to severe disability and death. ICH-related poor outcomes are due to primary injury causing structural damage and mass effect and secondary injury in the perihemorrhagic region over several days to weeks. Secondary injury after ICH can be due to hematoma expansion (HE) or a consequence of repair pathway along the continuum of neuroinflammation, neuronal death, and perihemorrhagic edema (PHE). This review article is focused on PHE and HE and will cover the animal studies, related human studies, and clinical trials relating to these mechanisms of secondary brain injury in ICH patients.
Highlights
Intracerebral hemorrhage (ICH) is a medical emergency, which often leads to severe disability and death [1]
This review article is focused on perihemorrhagic edema (PHE) and Hematoma expansion (HE), and will cover the animal studies, related human studies, and the clinical trials relating to these mechanisms of secondary brain injury in ICH patients
Perihemorrhagic edema is often seen in ICH patients and causes mass effect on adjacent brain structures, elevation in intracranial pressure (ICP), hydrocephalus, or brain herniation often leading to clinical deterioration
Summary
Intracerebral hemorrhage (ICH) is a medical emergency, which often leads to severe disability and death [1]. The hematoma cleaves or dissects neuronal tissue over several hours leading to the presenting symptoms. In survivors of ICH, the total extent of remodeled brain tissue may exceed the volume of the initial hematoma. This excess volume of remodeling serves as an evidence of secondary injury. Secondary injury after ICH can be separated into two major types: rebleeding causing HE and the consequences of repair pathways along the continuum of neuroinflammation and neuronal death, including perihemorrhagic edema (PHE), elevated intracranial pressure (ICP), hydrocephalus, and brain atrophy. Intracerebral Hemorrhage: Secondary Complications published by the American Heart Association/American Stroke Association (AHA/ASA) in 2015 did not recommend any current therapy for PHE or HE [1]
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