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IntracerebralHemorrhage

Prof. Dr. E. Turgut Tali

President, World Federation of Neuroradiological Societies President, Turkish Society of Neuroradiology

Head, Division of NeuroradiologyGazi University School of Medicine

Ankara, Turkeyturgut.tali@gmail.com

When a patient • Focal neurological deficits• Severe headache• Vomiting• High systolic blood pressure greater than 220 mm. Hg• Decreased consciousness with a sudden onset• Symptoms progression over minutes‐hours

Intracerebral hemorrhage (ICH) should be the first condition considered in the 

diagnosis! 

Red Flags!

ACR Appropriateness Criteria ACR Appropriateness Criteria

ACR Appropriateness Criteria ACR Appropriateness Criteria

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• Brain computed tomography (CT) 

• The gold standard for identifying acute hemorrhage 

• Subacute and chronic stages may be occult

ICH Imaging

• Magnetic resonance imaging (MRI) 

• An alternative with an advantage of being able to differentiate between the acute and chronic stages of hemorrhage 

• Hyperacute stage 

• T2* and susceptibility‐weighted (SWI) are as sensitive as CT for detection of acute hemorrhage and are more sensitive for identification of prior hemorrhage 

ICH Imaging

Blood   =    Plasma +  Cells

35‐45%     55‐65%

35‐45 HU        0‐10 HU          60‐90HU

Hyperdense mass

Could be isodense; if hemoglobine < 8-10 g/dl or with bleeding diatheses (e.g., hemophilia)

Attenuation decreases 1.5 HU/day Chronic stage; hypodense lesion, sequela gliosis, hemosiderin

Intracerebral Hemorrhage

Effacement of adjacent sulci, an important clue for subtle

SDHs

Central hypodensity possible: Rapidly accumulating hematoma & unretractedsemiliquid clot; "swirl sign"

Enhancing spots inside thehematoma shows extravasation

Hemorrhagic sedimentationlevel; hematocrite effect, bloodserum-settled blood cells

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CECT: Intracerebral Hemorrhage

• No enhancement in the acute phase• Enhancement may occur between 2-6

weeks• Developing neovascularization around

intracranial hemorrhage (ICH)• Blood-brain barrier (BBB) breakdown in

the vascularized capsule• DDx: Brain tumor / Abscess

Hematoma Volume Measurement

ABC/2 method; A: Maximal hematoma diameter on the axial slice with largest hematoma areaB: Maximal hematoma diameter perpendicular to A C: The number of CT slices with hematoma multiplied by slice thickness (ignoring slices with <25% of hematoma area compared with the reference slice)

Alastair JS, Stroke 2015

Hematoma Volum Measurement

A: 4,27 B: 4,39 C: 0.5 x 10 =5ABC = 93,5 / 2 = 46,75 mL

Hematoma Volume Measurement• ABC/2 scores are sufficiently accurate to categorize

ICH volume and assess eligibility for the CLEAR-III and MISTIE III studies, and moderately accurate for change in ICH volume

• Accuracy decreases with large, irregular, or lobar clots. Attempts to improve the accuracy of volume measurements could provide additional clinical value.

MISTIE-II: Minimally Invasive Surgery Plus Recombinant Tissue-Type Plasminogen Activator for Intracerebral Hemorrhage EvacuationCLEAR-IVH: Clot Lysis Evaluation of Accelerated Resolution of Intraventricular Hemorrhage

Hematoma Volume Measurement• Intracerebral hemorrhage volume is probably more

important than Glascow Coma Scale score (GCS) in determining treatment

Cho DY Surg Neurol 2008

• Operation is to be the preferred choice of treatment for the cases GCS≥6 and for large hematomas (>40ml volume)

Anik I, Turkish Neurosurg 2011

MRI in Intracerebral Hemorrhage

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Parenchymal Hemorrhage Stages Hemorrhagic infarct can be shown byMRI

Blood ageing or degradation can be followed by MRI

Non-EnhancedMRI

T1 iso iso hyper hyper hyper hypo

T2   iso hypo hypo hypo hyper      hypo

Oxy Hb Deoxy Hb Met Hb Hemosiderine

T1

T2  

Oxy Hb Edema Deoxy Hb

T1

T2  

Edema Deoxy Hb Met Hb

T1

T2  

Edema Deoxy Hb Met Hb

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T1

T2  

Edema Met Hb 

Phagocytes withhemosiderine and/or

ferritine

T1

T2  

Phagocytes withhemosiderine and/or

ferritine

Met Hb

Hemosiderine

T1

T2  

Siderosis

SWI: Hyperacute & Acute Hematoma

Even at early stage, some transition to deoxyhemoglobin formation may cause rim hypointensity

Loss of signal due to T2* dephasing from paramagnetic deoxy-Hb confined to red blood cells (RBC).

SWI: Subacute & Chronic HematomaMarked hypointensity at periphery of hematoma noted due to ferritin/hemosiderin accumulation.

Loss of signal due to T2* dephasing from paramagnetic met-Hb confined to RBCs. Even more hypointensity is seen at periphery due to accumulation of ferritin and hemosiderin.

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SWI: Hematoma vs Calcification

Phase map shows bright signal of hemorrhage. Phase map shows signal void of calcification 

SWI: Hematoma vs Calcification

DWI: Hyperacute Hematoma

Restricted diffusion in the hematoma center due to reduced extracellular space and increased viscosity.

DWI: Acute Hematoma

Both have dark centers, due to strong paramagnetic artifacts and the T2‐blackout effect. Susceptibility artifacts make accurate calculation of ADC values difficult.

DWI: Subacute Hematoma

Both have dark centers, due to strong paramagnetic artifacts and the T2‐blackout effect. Brighter susceptibility artifacts is present at periphery of trace image. 

DWI: Chronic Hematoma

Hypointense on DWI and hyperintense on ADC map 

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• Extraaxial• Epidural

• Subdural

• Subarachnoid

• Intraventricular

Intracerebral HemorrhageLobar Thalamocapsular 

Thalamic Caudate

• Intraaxial• Lobar• Thalamocapsular• Thalamic• Caudate

IntracerebralHemorrhage

• Trauma ‐> fracture & concussion • Tearing/stripping of both layers from inner table 

• Because the dura is especially tightly attached to sutures, rarely cross suture lines

• Laceration of outer periosteal layer • Laceration of meningeal vessels artery 90%, venous 10%

• Blood between naked bone and dura • Normal arterial pressure continues to dissect periosteum from bone

• Inner (meningeal dura) intact 

Epidural Hemorrhage

•Usually acute clinical presentation 

•Young patients, usually < 40 •Dura firmly fixed in older patients 

•Usually unilateral•85‐95% associated with skull fracture 

Epidural Hemorrhage

• NECT is the procedure of choice • Soft tissue, bone, and multiplanarreconstructions should be obtained (useful in identifying vertex epidural hematomas) 

• Hyperdense (60‐90 HU) lentiformextraaxial collection 

• Hypodense component (“swirl” sign) is seen in about one‐third of cases and indicates active, rapid bleeding with unretracted clot

• Air seen in 20% of cases

Epidural Hemorrhage Subdural Hematoma• Subdural hematoma > Epidural hematoma 

• Acute, subacute, chronic presentation• May be bilateral• Causes

• Trauma is common cause, 15% occur as “Contre‐coup” injuries, no particular association with fracture

• Aneurysm rupture, skull/dura‐arachnoid metastases from vascular extracranial primary neoplasms, and spontaneous hemorrhage in patients with severe coagulopathy

• Rarely, an acute spontaneous SDH of arterial origin occurs in someone without any traumatic history or vascular anomaly

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Subdural Hematoma• Tearing of bridging cortical veins as they cross the subdural space to enter a duralvenous sinus most common etiology

• Cortical vein lacerations either a skull fracture or the sudden changes in velocity and brain rotation that occur during non‐impact closed head injury

Subdural Hematoma• Tearing of bridging cortical veins (as they cross the subdural space to enter a dural venous sinus) 

• Cortical vein lacerations (either a skull fracture or the sudden changes in velocity and brain rotation that occur during non‐impact closed head injury

Subdural Hematoma

• Isolated SDH in infants and elderly

• More atrophy (larger spaces) more freedom of movement

• Larger subarachnoid space –more movement – more SDH

Subdural Hematoma• Vast majority of SDHs are associated with traumatic subarachnoid hemorrhage, significant parenchymal injuries; cortical contusions, brain lacerations, diffuse axonal injuries 

Subdural Hematoma• “Currant jelly” clot

• Under bulging dura

• Spreads diffusely• Covers brain• Often spreads over tentorium• May cross sutures, not dura• Extends into interhemispheric fissure

• NECT• Crescent shape • 60% hyperdense, 40% mixed • Swirl sign• Dots and lines of CSF trapped• CECT are helpful in detecting small isodense aSDHs. The normally enhancing cortical veins are displaced inward by the extraaxial fluid collection

Left frontoparietal hyperdense, homogeneous, crescent-shaped

extraaxial collection

Acute subdural hematoma

Asymmetric hyperdensity along the left tentorium

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SDH can be difficult to differentiate from adjacent

parenchymaEffacement of adjacent sulci, an important clue for subtle

SDHs (suggested “subdural” window width 130 and

window level of 30)

Isodense acute subdural hematoma: transition phase during from an acute SDH to

a chronic

Hypodense collection

Subdural Hematoma Stages

Acute < 3 days

Sulcal effacement, subfalcial herniation, Shift

Chronic>2 weeks

Subacute 3 days‐2 weeks

Utility of Multiplanar Reformats for Small Acute Subdural Hematoma

If Falx is too thick: Subdural Hematoma Iso-hypointense collection

Hyperintense collection of rebleeding

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Hemorrhagic sedimentationlevel; hematocrite effect, bloodserum-settled blood cells

• LP more sensitive than CT• Trauma is most common cause for RBC’S in CSF 

• Not seen as easily or as often on CT SAH on CT 

• Causes• Usually Aneurysm / AVM• Uncommon cause: neoplasm• Uncommon cause: spinal disease 

• Morbidity• Vasospasm • Mass Effect (parenchymal hematoma) 

• Hydrocephalus 

Subarachnoid Hemorrhage

Thick Falx with zig zags: SAH

• Intraventricular hemorrhage is present in nearly half of all patients with aSAH

• The presence of intraventricular blood together with thick SAH is designated a grade 4 bleed

• Increases in modified Fisher grade have a moderately linear relationship with the risk of vasospasm, delayed infarction, and poor clinical outcome

Intraventricular Hemorrhage

Intraventricular Hemorrhage

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• CT• Initial imaging modality

• Subacute and chronic stages may be occult

• MRI

• T2* and/or susceptibility‐weighted (SWI) are as sensitive as CT

Imaging of Intracerebral Hemorrhage

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Hemorrhage Visualized on CT but Not Interpreted as Acute Blood on MRI

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Hemorrhage Visualized on CT but Not Interpreted as Acute Blood on MRI

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Hemorrhage Visualized on MRI but Not on CT 

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Hemorrhage Visualized on MRI but Not on CT 

AIDOCArtificial 

IntelligenceAI

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Imaging of Hemorrhage

Hyperdense Left vertebral a.

Imaging of Hemorrhage

Thank you for your attention!