Intracranial bleed that occurs within the brain tissue or ventricles.
Classification
Primary ICH:
M/C cause (80%): Hypertensive arteriosclerosis and cerebral amyloid angiopathy (CAA)
Secondary ICH:
Pathophysiology
Cascade of neural injury initiated by intracerebral haemorrhage: The steps in the first 4 h are related to the direct effect of the haematoma, later steps to the products released from the haematoma. | BBB=blood–brain barrier. MMP=matrix metallopeptidase. TNF=tumour necrosis factor. PMN=polymorphonuclear cells. | Qureshi, A. I., Mendelow, A. D., & Hanley, D. F. (2009). Intracerebral haemorrhage. Lancet (London, England), 373(9675), 1632–1644. https://doi.org/10.1016/S0140-6736(09)60371-8Progression of haemotoma and oedema on CT: Top: hyperacute expansion of haematoma in a patient with intracerebral haemorrhage on serial CT scans. Small haematoma detected in the basal ganglia and thalamus (A). Expansion of haematoma after 151 min (B). Continued progression of haematoma after another 82 min (C). Stabilisation of haematoma after another 76 min (D). Bottom: progression of haematoma and perihaematomal oedema in a patient with intracerebral haemorrhage on serial CT scans. The first scan (E) was acquired before the intracerebral haemorrhage. Perihaematoma oedema is highlighted in green to facilitate recognition of progression of oedema. At 4 h after symptom onset there is a small haematoma in the basal ganglia (F). Expansion of haematoma with extension into the lateral ventricle and new mass-effect and midline shift at 14 h (G). Worsening hydrocephalus and early perihaematomal oedema at 28 h (H). Continued mass-effect with prominent perihaematomal oedema at 73 h (I). Resolving haematoma with more prominent perihaematomal oedema at 7 days (J). | Qureshi, A. I., Mendelow, A. D., & Hanley, D. F. (2009). Intracerebral haemorrhage. Lancet (London, England), 373(9675), 1632–1644. https://doi.org/10.1016/S0140-6736(09)60371-8
