Molecular, Pathological, Clinical, and Therapeutic Aspects of Perihematomal Edema in Different Stages of Intracerebral Hemorrhage

Figure 3

The evolution of PHE and its potential therapeutic targets. Clot retraction, activation of thrombin in the coagulation cascade, and toxicity of RBC degradation products can contribute to PHE formation after acute ICH. Furthermore, abnormal electrolyte and water transport and thrombin and RBC lysis-induced inflammatory and oxidative stress responses are critical in the formation of PHE. PHE can be classified as ionic (cytotoxic) and vasogenic edema according to the mechanisms and imaging characteristics. Although various variables, including cerebral venous drainage and the glymphatic system, can affect the severity of PHE, more accurate methods for quantifying PHE should be developed. PHE can aggravate the severity of brain injury, but the relationship between PHE and functional outcomes after ICH was conflicting. Strategies to alleviate PHE warrant further exploration by targeting ICP, thrombin, lysis of the RBC, inflammation, controlling blood pressure, reducing hematoma volume, etc. Abbreviations: PHE: perihematomal edema; RBC: red blood cell; MMPs: matrix metallopeptidases; AQP4: aquaporin 4; BBB: blood-brain barrier; ICP: intracranial pressure.