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