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Evolution of Intracranial Hemorrhage

Best diagnostic clue

○ Hyperdense (50-70 HU) mass on CT; peripheral edema develops over 1st few days
○ Hematoma matures more slowly in center (core) than in periphery
○ MR: ICH staging based on T1 and T2 signal
○ MR as sensitive as CT in hyperacute phase and more sensitive in subacute and chronic phases


○ Supratentorial > infratentorial brain


○ Near microscopic to very large; solitary >> multiple


○ Ovoid; larger hematomas have more irregular shape and heterogeneous attenuation

CT Findings


Hyperacute and acute: Hyperdense mass (0-3 days)
– Immediate: Heterogeneous with 40-60 HU
– CT density increases to 60-80 HU over first few hours secondary to clot formation and retraction
– Clot maturation can increase density to 80-100 HU in hematoma core
– Isodense if Hgb < 8-10 (hemophilia, renal failure)
– Fluid-fluid levels seen in larger hematomas, mostly with coagulopathies or anticoagulation
– Edema and mass effect initially mild (< 3 hours)
– Swirl sign: Extraaxial collection with hyperdense clot and smaller hypodense area in swirled configuration (implies active bleeding)

Subacute: 3-10 days
– Progressive attenuation loss (↓ 1.5 HU/day)
– Edema peaks at ~ 5 days
– Isodense in 1-4 weeks, dependent on original size

Chronic: > 10 days
– Residua: ↓ attenuation foci (37%), no visible residua (27%), slit-like lesions (25%), Ca++ (10%)


○ Active bleeding: Contrast pooling; CTA "spot" sign
○ Subacute-chronic: Rim enhancement (3 days to 1 month)
○ Chronic: Enhancement disappears (2-6 months)

MR Findings

• T1WI

○ Hyperacute (< 24 hours): Isointense to mildly hypointense
○ Acute (1-3 days): Isointense to mildly hypointense
○ Early subacute ( 3-7 days): ↑ signal periphery, isointense center
○ Late subacute/early chronic (~ 1-2 weeks/4 weeks): Diffuse ↑ signal
○ Late chronic (> 1 month): Iso- to hypointense

• T2WI

○ Hyperacute: Hyperintense, may have subtle hypointense rim, hyperintense peripheral edema
○ Acute: Markedly hypointense, increased edema
○ Early subacute: ↓ hypointensity, ↑ edema
○ Late subacute/early chronic: Progressive central signal increase, peripheral hypointensity
○ Late chronic: Hypointense rim or cleft, no edema


○ Same as on T2WI. It May show subarachnoid extension of hemorrhage

• T2* GRE

○ Hyperacute: Typically hypointense margin; differentiates hemorrhage from other masses
○ Acute: Marked diffuse hypointensity
○ Early subacute: Hypointensity (> T2WI and FLAIR)
○ Late subacute/early chronic: Increasing low signal rim
○ Late chronic: Persistent marked hypointense nodule or cleft due to glial hemosiderin staining


○ Signal on DWI strongly affected by underlying T2 signal (T2 shine through and T2 "black out")
○ ADC shows diffusion restriction in core during hyperacute, acute, and early subacute phase

• T1WI C+

○ Peripheral enhancement can develop within a few days and persist for months

• SWI (susceptibility weighted imaging)

○ ↑ sensitivity for microscopic hemorrhage than GRE Imaging Recommendations

Best imaging tool

○ Initial diagnosis: NECT or MR
○ Staging/work-up: MR, MRA/MRV, or CTA/CTV
○ Angiography if no clear cause


Fat-Containing Lesions

• Lipoma, dermoid
• Mimics subacute ICH (↑ T1WI, ↑ T2WI)
• Chemical shift artifact, lack of edema, loss of intensity on fat-saturated images confirm diagnosis

Calcified Lesions

• Dural plaque, thrombosed aneurysm, meningioma
• Hypointense on T2WI and GRE, variable on T1WI Proteinaceous Fluid Collections
• Colloid cyst, Rathke cleft cyst, craniopharyngioma
• Mildly hyperintense on T1WI, hypointense on T2WI


• Etiology

Very common: HTN, cerebral amyloid angiopathy (CAA), trauma, hemorrhagic vascular malformations
Common: Infarct with reperfusion, coagulopathy, blood dyscrasia, drug abuse, tumor
Less common: Dural sinus thrombosis, eclampsia, endocarditis with septic emboli, fungal infection (aspergillosis, mucormycosis), encephalitis

• Genetics

○ ICH can occur sporadically or with familial syndromes (familial CAA, familial cavernous malformations)

• Associated abnormalities

○ Vasogenic edema forms rapidly, peaks at about 5 days
○ May decompress into ventricles/subarachnoid space

Staging, Grading, & Classification

• No consistent definition of hematoma stages for MR

  • Hyperacute: < 24 hours
  • acute: 1-3 days
  • early subacute: 3-7 days
  • late subacute: 1-2 weeks
  • chronic  > 1 month

Gross Pathologic & Surgical Features

Acute to early subacute: Blood-filled cavity surrounded by vasogenic edema, inflammation
Early subacute to early chronic: Organizing clot, vascularized wall
Late chronic: Hemosiderin scar with gliosis

Microscopic Features

• Immediate

○ Water-rich liquid hematoma; 95-98% oxy-Hgb

• Hyperacute

○ RBCs contain diamagnetic oxy-Hgb
○ High water content (↑ T2 and ↓ T1)
○ Peripheral vasogenic edema begins

• Acute

○ Deoxy-Hgb in intact RBCs
– Paramagnetic deoxy-Hgb with 4 unpaired electrons in intact RBC causes field gradient across cell membrane
→ ↓ T2WI and GRE
– Paramagnetic center of Hgb inaccessible to water molecules → no T1 shortening
○ Severe edema

• Early subacute

○ Deoxy-Hgb in intact RBCs oxidized to paramagnetic met- Hgb with 5 unpaired electrons
– Susceptibility induced gradient across cell membrane
→ T2WI and GRE hypointensity
○ Met-Hgb formation begins at hematoma periphery → T1 hyperintensity initially seen at margin

• Late subacute-early chronic

○ RBC lysis → release met-Hgb into extracellular space → loss of gradient across RBC membrane
– Loss of magnetic heterogeneity and increased water content → ↑ T2WI and FLAIR intensity
○ Persistent dipole-diploe interaction → T1 shortening
○ Edema and mass effect decrease

• Chronic

○ Lysed RBCs and clot taken up by macrophages
○ Met-Hgb converted into ferritin and hemosiderin
○ Residual cysts, clefts with hemosiderin scar, persist indefinitely in areas with intact blood-brain barrier
○ Edema, inflammation resolve


• Most common signs/symptoms
○ HTN (90%), vomiting (50%), ↓ consciousness (50%), headache (40%), seizures (10%)

• Clinical profile

○ HTN, ↑ age most important risk factors
○ Increasing incidence of anticoagulation-related ICH

• Incidence

○ about 30/100,000 (USA); 37/100,000 (Europe)

• Age

○ Risk increases with age (mean 63 [USA], 70 [Europe])

• Gender

○ Men < 65 years have 3.4x higher risk; > 65 years: No significant gender difference

• Ethnicity

○ Higher risk of ICH for African Americans (3.8x higher risk) and Hispanics (2.6x higher risk) compared with Caucasians

Natural History & Prognosis

• 1 or more rebleeds occur in 1/4 of cases
○ Rebleed: Increased mortality
– 70% died with 2nd or 3rd ICH

• Prognosis depends on size, initial level of consciousness, and location
○ Higher mortality with posterior fossa and lobar hemorrhage than with deep hemorrhage
○ Ventricular extension: Higher mortality for lobar hemorrhage, but lower mortality for thalamic bleeds
○ ICH with warfarin use correlates with higher mortality (2x as high at 3 months)

• 20% independent at 6 months


• Surgical evacuation as needed


• MR more sensitive, more accurate staging of ICH
• Large area of surrounding vasogenic edema more commonly seen with underlying neoplasm
• Marked heterogeneity of acute hematoma on CT predicts hematoma growth and mortality
• Swirl sign, contrast extravasation, and enhancement indicate hematoma growth and ↑ mortality
• Fluid-fluid levels: Question of underlying coagulopathy

Imaging gallery

graphic shows the evolution of parenchymal hemorrhage from 
  • Hyperacute (left upper image) :  (intracellular oxy-Hgb) 
  • Acute (right upper) :   (intracellular deoxy- Hgb with surrounding edema) .
  • Early and late subacute ( Intermediate two images) :  (intra- and extracellular met- Hgb respectively) 
  • chronic (lower images) : cystic cavity with a hemosiderin stain.

Axial NECT shows a hyperdense mass related to an acute left cerebellar hemorrhage with minimal surrounding edema in a patient with hypertension.

Hyperacute hemorrhage

 Axial T1WI MR in the previous patient shows the cerebellar hemorrhage is predominantly isointense and mildly hypointense to the surrounding brain parenchyma, indicating hyperacute blood products.

Axial T2WI MR in the previous  patient shows the hyperacute hemorrhage to be hyperintense to the surrounding brain parenchyma with a peripheral hypointense rim st. Intraparenchymal hemorrhage evolves from peripheral to central with the central core maturing more slowly.

Early subacute Hemorrhage

Axial T2WI MR shows a large hypertensive hemorrhage in the left basal ganglia, which shows early subacute blood products that are predominantly hypointense with surrounding edema . The anterior aspect of the hemorrhage shows hyperintense signal suggesting more acute blood products .

 Axial SWI shows the hypointense hemorrhage and multiple other foci of susceptibility (from hemosiderin) related to remote microhemorrhages from chronic hypertension.

 Hemorrhages in an amyloid angiopathy

Axial T1WI MR shows hemorrhages in an amyloid angiopathy patient. There is a hyperacute  (isointense) and an acute/early subacute  (hyperintense) left posterior hemorrhage as well as a late subacute (hyperintense) right temporal hemorrhage .

Axial T2WI MR shows heterogeneous bright signal in the hyperacute  portion and low signal in the acute/early subacute portion of the posterior hemorrhage. The late subacute  hemorrhage has bright T1 and T2 signal intensity.

Axial DWI MR 21 hours after initial imaging shows that the signal on DWI is mostly determined by underlying T2 effects with T2 shine through  in the right subacute hemorrhage and T2 blackout  in the acute/early subacute hemorrhage.

Axial ADC shows that signal on DWI is mostly determined by underlying T2 effects. Only the acute/early subacute hemorrhage shows low signal on ADC , while increased diffusivity is seen in the late subacute right temporal hemorrhage ..

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