Intracranial hemorrhage (ICH) evolves through predictable biochemical stages, reflected as signal changes of hemoglobin breakdown products. Knowing these helps radiologists estimate the age of bleed.
🕒 Stages of Hemorrhage & MRI Signal Characteristics
| Stage | Timeframe | Biochemistry | T1 signal | T2 signal | Key Features |
|---|---|---|---|---|---|
| Hyperacute | < 24 hours | Oxyhemoglobin (intracellular) | Isointense to brain | Hyperintense | Difficult to detect; best on GRE/SWI |
| Acute | 1–3 days | Deoxyhemoglobin (intracellular) | Iso- to hypointense | Hypointense | Susceptibility blooming on GRE/SWI |
| Early Subacute | 3–7 days | Methemoglobin (intracellular) | Hyperintense | Hypointense | “T1 bright, T2 dark” – classic |
| Late Subacute | 7–14 days | Methemoglobin (extracellular) | Hyperintense | Hyperintense | “T1 bright, T2 bright” |
| Chronic | > 14 days | Hemosiderin, ferritin (in macrophages) | Hypointense | Hypointense rim (with central gliosis, CSF-like signal) | Peripheral dark rim on T2* (hemosiderin) |
🧠 Teaching Points
- T1 hyperintensity → appears in subacute stage (methemoglobin).
- T2 hypointensity → hallmark of acute and early subacute bleeds.
- Blooming artifact (GRE/SWI) → seen at all stages, accentuated in acute and chronic stages.
- Chronic bleeds often leave a hemosiderin rim (low signal on T2*/SWI).
- Always correlate with clinical history & CT (especially hyperacute bleeds, better seen on CT).
