PURPOSE OF REVIEW: To summarize new pathophysiologic insights and recent advances in the treatment of intracerebral hemorrhage. RECENT FINDINGS: Emerging information of the physiopathologic mechanisms of injury that occur after intracerebral hemorrhage is available from current animal models and human studies. The effects of chronic vascular changes are fundamental to the genesis of the hematoma. Novel proposed mechanisms in the pathophysiology of hematoma expansion and worsening edema include harmful accumulation of excitotoxins and osmotically active electrolytes, followed by activation of leukocytes and platelets with production of inflammatory mediators such as interleukin-1, interleukin-6, intercellular adhesion molecule, tumor necrosis factor alpha, and vascular endothelial growth factor. Expression of metalloproteinases and the toxic effects of the complement, thrombin, and blood degradation products may play a role in late edema formation after intracerebral hemorrhage. Despite recent attempts to discern the pathophysiology of ICH, evidence-based therapies for intracerebral hemorrhage are not yet available. Treatment is primarily supportive, and outcomes remain poor. Blood pressure lowering, intracranial pressure monitoring, osmotherapy with adequate fluid balance, fever control, and seizure prophylaxis are usually done in the acute setting. Novel approaches currently under study include ultra early hemostatic therapy and thrombolytic therapy for intraventricular hemorrhage. Although the value of surgical treatment remains unclear, the results of a large, randomized study (the STITCH Trial) are forthcoming. SUMMARY: Prospective controlled studies are needed to develop novel medical and surgical therapies for ICH.
PURPOSE OF REVIEW: To summarize new pathophysiologic insights and recent advances in the treatment of intracerebral hemorrhage. RECENT FINDINGS: Emerging information of the physiopathologic mechanisms of injury that occur after intracerebral hemorrhage is available from current animal models and human studies. The effects of chronic vascular changes are fundamental to the genesis of the hematoma. Novel proposed mechanisms in the pathophysiology of hematoma expansion and worsening edema include harmful accumulation of excitotoxins and osmotically active electrolytes, followed by activation of leukocytes and platelets with production of inflammatory mediators such as interleukin-1, interleukin-6, intercellular adhesion molecule, tumor necrosis factor alpha, and vascular endothelial growth factor. Expression of metalloproteinases and the toxic effects of the complement, thrombin, and blood degradation products may play a role in late edema formation after intracerebral hemorrhage. Despite recent attempts to discern the pathophysiology of ICH, evidence-based therapies for intracerebral hemorrhage are not yet available. Treatment is primarily supportive, and outcomes remain poor. Blood pressure lowering, intracranial pressure monitoring, osmotherapy with adequate fluid balance, fever control, and seizure prophylaxis are usually done in the acute setting. Novel approaches currently under study include ultra early hemostatic therapy and thrombolytic therapy for intraventricular hemorrhage. Although the value of surgical treatment remains unclear, the results of a large, randomized study (the STITCH Trial) are forthcoming. SUMMARY: Prospective controlled studies are needed to develop novel medical and surgical therapies for ICH.
Authors: Sangeetha Sukumari-Ramesh; Melissa D Laird; Nagendra Singh; John R Vender; Cargill H Alleyne; Krishnan M Dhandapani Journal: Glia Date: 2010-11-15 Impact factor: 7.452
Authors: Berk Orakcioglu; Christopher Beynon; Julian Bösel; Christian Stock; Andreas W Unterberg Journal: Neurocrit Care Date: 2014-12 Impact factor: 3.210