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Imaging of CerebralHemorrhage

Prof. Dr. E. Turgut TaliPresident, World Federation of Neuroradiological Societies

President, Turkish Society of NeuroradiologyPast CEO, European Board of Neuroradiology

Past President, European 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 60-90 HU

Hyperdense massCould 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

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• May occur between 2-6 weeks

• Developing neovascularization aroundintracranial hemorrhage (ICH)

• Blood-brain barrier (BBB) breakdown in the vascularized capsule• DDx: Brain tumor / Abscess

Hematoma Volume MeasurementABC/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 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 Evacuation

CLEAR-IVH: Clot Lysis Evaluation of Accelerated Resolution of

Intraventricular Hemorrhage

Hematoma Volume Measurement• Intracerebral hemorrhage volume is probably more

important than GCS score in determining treatment. GCS score of at least 13 or when ICH volume is less than 30 mL, regardless of GCS score.

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 Intacranial HemorrhageT1 iso iso hyper hyper hyper hypo

T2 iso hypo hypo hypo hyper hypo

Oxy Hb Deoxy Hb Met Hb Hemosiderine

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T1

T2

Oxy Hb Edema Deoxy Hb

T1

T2

Edema Deoxy Hb Met Hb

T1

T2

Edema Deoxy Hb Met Hb

T1

T2

Edema Met Hb

Phacytes withhemosiderine and/or

ferritine

T1

T2

Phacytes withhemosiderine and/or

ferritine

Met HbHemosiderine

T1

T2

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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 RBCs.

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.

SWI: Hematoma vs Calcification

Phase map shows bright signal of hemorrhage.

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.

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DWI: Chronic Hematoma

Hypointense on DWI and hyperintense on ADC map

• Extraaxial• Epidural• Subdural• Subarachnoid• Intraventricular

Intracerebral Hemorrhage

Lobar 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 multiplanar

reconstructions 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

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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

Subdural Hematoma• Tearing of bridging cortical veins (as they

cross the subdural space to enter a duralvenous 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• 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• 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 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

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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

Subdural Hematoma Stages

Acute < 3 days

Sulcal effacement, subfalcial herniation, Shift

Chronic>2 weeks

Subacute 3 days-2 weeks

Left frontoparietal hyperdense, homogeneous, crescent-shaped

extraaxial collection

Acute subdural hematoma

Asymmetric hyperdensity along the left tentorium SDH can be difficult to

differentiate from adjacent parenchyma

Effacement of adjacent sulci, an important clue for subtleSDHs (suggested “subdural”

window width 130 andwindow level of 30)

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

a chronic

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

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• CTA, Angiography, MRA• Hyperdensities in sulci

• CTA, Angiography, MRA• Normal in 2 days• 2 days-2 weeks; vessel

narrowing, beading• MRI• Dirty sulci on T1, T2• Hyperintense sulci on FLAIR• Blooming hypointensity on

GRE, SWI

Subarachnoid Hemorrhage• 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

• 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 Hemorrhage