Intracerebral Hemorrhage: Perihemorrhagic Edema and Secondary Hematoma Expansion: From Bench Work to Ongoing

Manoj K Mittal1, Aaron LacKamp2

  • 1Department of Neurology, University of Kansas Medical Center , Kansas City, KS , USA.

Frontiers in Neurology
|December 6, 2016
PubMed

Insights

Intracerebral hemorrhage (ICH) causes severe disability. This review examines secondary brain injury mechanisms, focusing on hematoma expansion and perihemorrhagic edema in ICH patients.

Area of Science:

  • Neurology
  • Neurosurgery
  • Neuroscience

Background:

  • Intracerebral hemorrhage (ICH) is a critical neurological emergency with high mortality and disability rates.
  • Poor outcomes in ICH are attributed to primary structural damage and secondary injury mechanisms.
  • Secondary injury involves hematoma expansion (HE) and perihemorrhagic edema (PHE), contributing to neuroinflammation and neuronal death.

Approach:

  • This review synthesizes findings from animal studies, human observational studies, and clinical trials.
  • It specifically focuses on the pathophysiological mechanisms of PHE and HE in the context of ICH.
  • The review examines the continuum of neuroinflammation, neuronal death, and edema formation post-ICH.

Key Points:

  • Perihemorrhagic edema (PHE) is a significant contributor to secondary brain injury after ICH.
  • Hematoma expansion (HE) exacerbates primary damage and influences secondary injury progression.
  • Understanding these mechanisms is crucial for developing targeted therapies for ICH patients.

Conclusions:

  • Secondary injury, particularly PHE and HE, plays a critical role in the poor outcomes associated with intracerebral hemorrhage.
  • Further research into these mechanisms, supported by diverse study types, is essential for improving clinical management of ICH.
  • This review provides a comprehensive overview of current knowledge on PHE and HE in ICH, highlighting areas for future investigation.