Acute subacute and chronic haemorrhagic stroke
Reading File
Reading File
Finding Sources
Finding Sources
Searching PubMed
intracerebral hemorrhage AND imaging
Searching the Web
AHA ASA guideline spontaneous intracerebral hemorrhage neuroimaging CT MRI
Reading File
Reading File
Finding Sources
Reading Web Page
https://www.stroke.org/-/media/Files/Professional/Quality-Im…
Reading File
Reading File
Haemorrhagic stroke: acute, subacute, and chronic stages
This classification usually describes the time-dependent evolution of an intracerebral hematoma on MRI, driven by changes in hemoglobin products. Haemorrhagic stroke includes intracerebral haemorrhage (ICH) and subarachnoid haemorrhage (SAH), but the table below applies chiefly to ICH.
| Stage | Approximate time | Predominant blood product | T1 MRI | T2 MRI | Key point |
|---|---|---|---|---|---|
| Hyperacute | 0-6 hours | Intracellular oxyhaemoglobin | Isointense/gray | Hyperintense or light gray | CT is best and fastest initial test |
| Acute | 1-3 days | Intracellular deoxyhaemoglobin | Isointense/gray | Hypointense/dark | Deoxyhaemoglobin has susceptibility effects |
| Early subacute | 3-7 days | Intracellular methaemoglobin | Hyperintense/bright | Hypointense/dark | T1 becomes bright first |
| Late subacute | About 7 days to 1 month | Extracellular methaemoglobin | Hyperintense/bright | Hyperintense/bright | Both T1 and T2 appear bright |
| Chronic | Usually >14 days, evolves over weeks to months | Hemosiderin and ferritin at periphery, with gliosis/cavity | Dark or variable | Dark rim, often black on T2*/SWI | Persistent hemosiderin rim; may leave a CSF-like cavity |
Source: Neuroanatomy through Clinical Cases, 3rd ed., p. 121.
Why MRI appearances change
- Oxyhaemoglobin is initially intracellular.
- It converts to deoxyhaemoglobin, producing T2 shortening, so the hematoma becomes dark on T2.
- Conversion to methaemoglobin causes T1 shortening, producing T1 brightness.
- With red-cell lysis, methaemoglobin becomes extracellular, causing brightness on both T1 and T2.
- Finally, macrophages leave hemosiderin at the margins, producing a dark rim, especially conspicuous on T2*-GRE and susceptibility-weighted imaging (SWI).
Practical imaging approach
- Suspected acute stroke: obtain urgent non-contrast CT (NCCT). It is fast, widely available, and highly sensitive for acute intracranial blood.
- CTA: useful early when a structural lesion or active hematoma expansion is suspected. A contrast “spot sign” can indicate higher expansion risk.
- MRI with GRE/T2 or SWI:* sensitive for small, old, or chronic haemorrhages, cerebral microbleeds, and cortical superficial siderosis, such as in cerebral amyloid angiopathy.
- For spontaneous ICH, the AHA/ASA guidance supports rapid CT or MRI to establish the diagnosis and serial CT within the first 24 hours in selected patients to detect hematoma expansion or complications such as hydrocephalus. See the AHA/ASA clinical update.
Important caveats
- Exact timings overlap. The age of a bleed cannot be determined from MRI alone with complete precision.
- Rebleeding, variable oxygenation, anemia, clot heterogeneity, and the MRI sequence used can create mixed appearances.
- CT density also evolves: acute blood is typically hyperdense, then becomes isodense over roughly 1-2 weeks and hypodense later.
Neuroimaging is required because symptoms alone cannot reliably distinguish haemorrhagic from ischaemic stroke. Non-contrast CT is generally preferred initially in the emergency setting. Frameworks for Internal Medicine, p. 576.
This is a shared conversation. Sign in to Orris to start your own chat.