Figure 1 Metabolic risk factors, pathophysiological mechanisms, and therapeutic strategies related to spontaneous intracerebral hemorrhage(1) Metabolic risk factors for spontaneous intracerebral hemorrhage (SICH) include obesity, hypertension, and hyperglycemia. (2) Pathophysiological mechanisms of metabolic abnormalities in SICH are as follows. Phase 1 (indicated by circle 1 in purple): In the acute phase of SICH, hematoma compression induces tissue necrosis, accompanied by the activation of local inflammatory cells. This process leads to the release of pro-inflammatory cytokines, including IL-6 and TNF-α, which contribute to neuronal dysfunction. Phase 2 (indicated by circle 2 in purple): A substantial accumulation of hemoglobin and hemolytic byproducts in the cerebrospinal fluid (CSF), including inflammasome component caspase-1, occurs following ICH. Concurrently, neuronal release of high-mobility group box 1 (HMGB1) significantly induces neuroinflammation and cerebral vasospasm, exacerbating microcirculatory damage. Phase 3 (indicated by circle 3 in purple): Capillary constriction leads to microcirculatory dysfunction, often manifesting as segmental arteriolar spasms or a “string-of-beads” pattern. Hemolysis-related factors, including hemoglobin, bilirubin oxidation end products (BOX), propentdyopents (PDP), and free iron, further exacerbate vasoconstriction, microvascular occlusion, and cognitive impairment. Additionally, the release of neutrophil extracellular traps (NETs) promotes microthrombosis formation, creating a vicious cycle of thrombosis and inflammation. Phase 4 (indicated circle 4 in purple): Hyperglycemia can exacerbate mitochondrial damage through oxidative stress, thereby amplifying the inflammatory response following ICH. (3) The intervention strategies targeting metabolic factors in SICH are neurocritical care and hypervolemia, hemodilution, and hypertension therapy. Hemodynamic management uses hypervolemia, hemodilution, and hypertension therapy to optimize cerebral perfusion. Metabolic intervention via the Sirt3 pathway involves activation of Sirt3 by (Honokiol can attenuate hyperglycemia-induced brain injury). CSF metabolic monitoring involves the integration of neuroimaging, electrophysiological assessments, and machine learning-assisted analysis to refine individualized therapeutic strategies. (Created with BioRender.com).