imaging of intracranial hemorrhage sattam s. lingawi md, frcpc, abr assistant professor of radiology...

Imaging ofImaging of INTRACRANIAL INTRACRANIAL HEMORRHAGEHEMORRHAGE

Sattam S. Lingawi MD, FRCPC, ABR

Assistant Professor of Radiology – King Abdulaziz University

President of Radiological Society of Saudi Arabia

Acute hemorrhageAcute hemorrhage

A NECT should be done when there is a question of acute hemorrhage.

Acute hemorrhageAcute hemorrhage

There is linear relation between CT attenuation & hematocrit ,hemoglobin concentration.

Retracted clot has a high globin content, hence its hyperdensity compared to normal brain

Subacute hemorrhageSubacute hemorrhage

The attenuation of uncomplicated ICH decrease with time at an average of 1.5 HU/day.

Between 1-6 weeks subacute ICH becomes isodense with adjacent brain may show peripheral enhancement.

MR is much more sensitive for evaluation of subacute & chronic hemorrhage.

Chronic hemorrhageChronic hemorrhage

Unless re-bleeding has occurred ,chronic hematomas are hypodense copmared to adjacent brain

Rim enhancement of resolving hematoma (target sign) can be seen if re-bleeding takes place within an organizing hematoma.

Chronic hemorrhageChronic hemorrhage

Thin linear clot near the skull base or calvarial bones are difficult to detect.

Window width between 150-250 HU may be helpful in separating them from adjacent bony structures.

PitfallsPitfalls

Occasionally acute cerebral hematoma appears isodense with adjacent brain due to:

Sever anemia (Hb < 8g/dL) Coagulation disorders Thrombolytic therapy

Fluid-fluid level can occur in 50% of these clots.

PitfallsPitfalls

Hyperdense Hypodense

Fluid-Fluid level

The sequential oxidation products of hemoglobin affects the relaxation time of T1 & T2 due to changes in magnetic properties (magnetic susceptibility).

Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI

Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI

Time Time (Days)(Days)

RBCRBC Hb stateHb state T1T1 T2T2

Few Few hrs.hrs.

intact Oxy Hb Iso/dark bright

Up to 2 Up to 2 daysdays

intact Deoxy Hb Iso/dark Dark

2-142-14 intact IC Met Hb Bright Dark

10-2110-21 Lysed EC Met Hb Bright Bright

>21>21 Lysed Hemosiderin Iso/dark dark

Oxy Hg. Deoxy Hg. I.C Hg. E.C Hg. Hemosiderin

T 1 - / 0 0 1 1 0

T 2 1 0 0 1 0

Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI

Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI

I.C Hemoglobin

Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI

E.C Methemoglobin

CLASSIFICATIONCLASSIFICATION

Intra-axial hemorrhageExtra-axial hemorrhage

Intra-axial hemorrhageIntra-axial hemorrhage

Hypertensive hemorrhage is seen in: putamen 35-50% Subcortical white matter 30% Cerebellum15% Thalamus 10-15% Pons 5-10%

Amyloid angiopathy. Vascular malformation :

AVM cavernous malformation, Telangiectasias venous malformations.

Intra-axial hemorrhageIntra-axial hemorrhage

Amyloid angiopathy:parenchymal hemorrhage is of lobar nature. It is not associated with systemic vascular

amyloidosis.Affects elderly individuals.Associated infarcts & hemorrhage.

T2 FSE T2 GRE

Intra-axial hemorrhageIntra-axial hemorrhage

Named after its anatomic location.Etiology:

– HTN

– Anticoagulation

– Amyloid Angiopathy

– Vasculitis

Medical not Surgical.

Intra-axial hemorrhageIntra-axial hemorrhage

Putamenal Pontine Parenchymal

Intra-axial hemorrhageIntra-axial hemorrhage

I.V Extension Mass effect

Hemorrhagic Hemorrhagic TransformationTransformation

InfarctionInfarction

Arteriovenous malformation: 80-90 are seen supratentorial. AVM have 2-3 annual risk of bleeding.Angiography is the definitive method

of evaluation for an AVM anatomy.NECT will show a mixed attenuation

lesion.MR will show an AVM as a tangle of

enlarged vessels without mass effect.Contrast will increase conspicuity of

the AVM

Cavernous malformations:Thin walled sinusoidal vessels, not

seen on Angiogram. MR will show a reticulated enhancing

lesion.

Venous malformation (venous angiomas) seen in 1-2 % of patient studiedby contrast MR ,seen as an enhancing stellate lesion extending to the ventricle or cortex.

Extra-axial hemorrhageExtra-axial hemorrhage

Relationship to Meningeal reflection. Epi-dural (Extra-dural) Sub-dural Sub-arachnoid

Etiology: Trauma Aneurysm

Surgical not medical.

Extra-axial hemorrhageExtra-axial hemorrhage

EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

Hyperacute – Swirl Sign

EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

Venous Hemorrhage

SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

Acute

SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

SubacuteIso-dense

C+

SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

Acute on Chronic

SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)

Subarachnoid hemorrhageSubarachnoid hemorrhage

SAH is most commonly the result of:– aneurysm rupture 75-80% – AVM malformation 10-15%– Trauma, dissection – Drug abuse – Coagulopathies. – Congenital berry aneurysm (1-2%)– Risk increases with smoking and positive FH.

CT sensitivity:– > 95% for detection of acute SAH – Drops to 66% after 3 days.– 50% by the end of 1st wk.

Approximately 15-20 % of patient with SAH will have multiple aneurysm

Detailed selective 4 vessels angiogram is needed on initial evaluation.

The combination of MRI & MRA will detect the vast majority of aneurysm greater > 3 mm.

Detailed selective 4 vessels angiogram is needed on initial evaluation.

Negative angio 15% of SAHRepeat is positive in 5%

MR in SAHMR in SAH

T1:T2:FLAIR:GRE:The combination of MRI & MRA will

detect the vast majority of aneurysm greater > 3 mm.

AneurysmAneurysm

AneurysmAneurysm

AneurysmAneurysm

A. COMA. COM

SubarachnoidSubarachnoid(Extra-axial hemorrhage)(Extra-axial hemorrhage)

A. ComA. Com

P.Com AneurysmP.Com Aneurysm

PICA AneurysmPICA Aneurysm

Non-Aneurysmal HgNon-Aneurysmal Hg

Perimesencephalic non-aneurysmal SAH. Benign clinical entity with SAH.

Hydrocephalus and vasospasm are very rare. Recurrence < 1%.

Blood location: perimesencephalic and prepontine cisterns. Blood does not extend to Sylvian fissure.

Angiogram: Negative(90-95%). Vertebrobasilar aneurysm (5-10%)

Non-Aneurysmal HgNon-Aneurysmal Hg

Non-Aneurysmal HgNon-Aneurysmal Hg

Non-Aneurysmal SAHNon-Aneurysmal SAH

Hunt & Hess ClassificationHunt & Hess ClassificationGrade Description % Vasospasm

0 Un-ruptured Aneurysm O%

1 Asymptomatic or mild H/A & slight nuchal rigidity 22%

2 Cr. N Palsy (e.g. III, VI) moderate to severe H/A, nuchal rigidity.

33%

3 Mild focal deficit, lethargy, or confusion. 52%

4 Stupor, moderate to severe hemiparesis, early decerebrate rigidity

53%

5 Deep coma, decerebrate rigidity, moribund appearance

74%

Fisher GradingFisher Grading

Group Blood in CT % Vasospasm

1 NO blood detected 0

2 Diffuse layer < 1mm 0

3 Focal or Diffuse layer > 1mm 23

4 Intraventricular / intracerebral 0

50% Mortality15% re-bleed within the first 24 hoursVasospasm: 3-10 days (70-90% patients)

AVMAVM

AVMAVM

Speitz-Martin Grading Speitz-Martin Grading systemsystem0 1 2 3

Size <3 3-6 >6

Location NE E

Drainage Superficial Deep

Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)

Pathology:– Discrete multiloculated lesions formed of

dilated endothelial spaces.– Multiple stages of hemorrhage.

Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)

Location:– 80% are supratentorial

(esp. frontal and temporal).– Spinal cord

involvement is rare.– Extra-axial &

intraventricular locations are rare.

Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)

Incidence:– The most common vascular

anomaly (0.4%).– 50% - 80% are multiple.

Age: – 20-40 yrs.

Symptoms:– Seizure, Neuro. Deficit, H/A.

Hemorrhage: – 1% per yr.– Previous large hg. & post.

Fossa location

Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)

Angio.: – Angiographically occult.

CT: – Iso or hyperdense with Ca+

+.– No enhancement.

MRI: (GRE > T2 > T1)– Well defined mass of

multiple intensities.– High signal core and low

signal rim “popcorn”.– Presence of surrounding

edema = recent hg.

Carotid DissectionCarotid Dissection

ICA DISSECTIONICA DISSECTION

Dural Sinus ThrombosisDural Sinus ThrombosisDural Sinus ThrombosisDural Sinus Thrombosis

Incidence: Unknown

– Uncommon cause of stroke, requires a high index of clinical suspicion to diagnose.

Sex: Female > Males

venous : Arterial 1 : 62.5

Dural Sinus ThrombosisDural Sinus Thrombosis EtiologyEtiology

Dural Sinus ThrombosisDural Sinus Thrombosis EtiologyEtiology

•Unknown•Infection •Coagulopathies•Behcet;’s disease •SLE •Tumors

Dural Sinus ThrombosisDural Sinus Thrombosis Clinical presentationClinical presentation

Dural Sinus ThrombosisDural Sinus Thrombosis Clinical presentationClinical presentation

Headache 75 %Papillodema 49 %Focal deficit 34 %Cranial palsy 12%LOC , Coma 30 %Seizures 37 %Meningeal sings 0 %Amnestic syndrome 12 %

N MILD

MODERATE SEVER

Dural Sinus ThrombosisDural Sinus Thrombosis DiagnosisDiagnosis

Dural Sinus ThrombosisDural Sinus Thrombosis DiagnosisDiagnosis

– Clinical Presentation.– Radiological Findings.

•NECT:

•Dense Sinus•Cord sign

•Venous infarction & Hemorrhage

Dural Sinus ThrombosisDural Sinus Thrombosis

CECT: Empty Delta sign. Dural Sinus Filling Defect

Dural Sinus ThrombosisDural Sinus Thrombosis

MRI:•MRI:

•Dense Sinus•Cord sign •Venous infarction•Filling Defect

Dural Sinus ThrombosisDural Sinus Thrombosis

Dural Sinus ThrombosisDural Sinus Thrombosis

Dural Sinus ThrombosisDural Sinus Thrombosis

Dural Sinus –NORMAL MRVDural Sinus –NORMAL MRV

Dural Sinus ThrombosisDural Sinus Thrombosis