Imaging of INTRACRANIAL HEMORRHAGE Sattam S. Lingawi MD, FRCPC, ABR Assistant Professor of Radiology...
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Transcript of 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
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Acute hemorrhageAcute hemorrhage
A NECT should be done when there is a question of acute hemorrhage.
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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
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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.
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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
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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
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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
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Hyperdense Hypodense
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Fluid-Fluid level
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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
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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
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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
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Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI
I.C Hemoglobin
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Evolution of hemorrhage by MRIEvolution of hemorrhage by MRI
E.C Methemoglobin
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CLASSIFICATIONCLASSIFICATION
Intra-axial hemorrhageExtra-axial hemorrhage
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Intra-axial hemorrhageIntra-axial hemorrhage
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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
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Amyloid angiopathy:parenchymal hemorrhage is of lobar nature. It is not associated with systemic vascular
amyloidosis.Affects elderly individuals.Associated infarcts & hemorrhage.
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T2 FSE T2 GRE
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Intra-axial hemorrhageIntra-axial hemorrhage
Named after its anatomic location.Etiology:
– HTN
– Anticoagulation
– Amyloid Angiopathy
– Vasculitis
Medical not Surgical.
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Intra-axial hemorrhageIntra-axial hemorrhage
Putamenal Pontine Parenchymal
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Intra-axial hemorrhageIntra-axial hemorrhage
I.V Extension Mass effect
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Hemorrhagic Hemorrhagic TransformationTransformation
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InfarctionInfarction
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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
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Cavernous malformations:Thin walled sinusoidal vessels, not
seen on Angiogram. MR will show a reticulated enhancing
lesion.
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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.
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Extra-axial hemorrhageExtra-axial hemorrhage
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Relationship to Meningeal reflection. Epi-dural (Extra-dural) Sub-dural Sub-arachnoid
Etiology: Trauma Aneurysm
Surgical not medical.
Extra-axial hemorrhageExtra-axial hemorrhage
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EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
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EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
Hyperacute – Swirl Sign
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EpiduralEpidural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
Venous Hemorrhage
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SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
Acute
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SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
SubacuteIso-dense
C+
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SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
Acute on Chronic
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SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
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SubduralSubdural(Extra-axial hemorrhage)(Extra-axial hemorrhage)
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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.
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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.
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Detailed selective 4 vessels angiogram is needed on initial evaluation.
Negative angio 15% of SAHRepeat is positive in 5%
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MR in SAHMR in SAH
T1:T2:FLAIR:GRE:The combination of MRI & MRA will
detect the vast majority of aneurysm greater > 3 mm.
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AneurysmAneurysm
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AneurysmAneurysm
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AneurysmAneurysm
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A. COMA. COM
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SubarachnoidSubarachnoid(Extra-axial hemorrhage)(Extra-axial hemorrhage)
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A. ComA. Com
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P.Com AneurysmP.Com Aneurysm
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PICA AneurysmPICA Aneurysm
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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%)
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Non-Aneurysmal HgNon-Aneurysmal Hg
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Non-Aneurysmal HgNon-Aneurysmal Hg
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Non-Aneurysmal SAHNon-Aneurysmal SAH
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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%
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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
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50% Mortality15% re-bleed within the first 24 hoursVasospasm: 3-10 days (70-90% patients)
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AVMAVM
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AVMAVM
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Speitz-Martin Grading Speitz-Martin Grading systemsystem0 1 2 3
Size <3 3-6 >6
Location NE E
Drainage Superficial Deep
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Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)
Pathology:– Discrete multiloculated lesions formed of
dilated endothelial spaces.– Multiple stages of hemorrhage.
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Cavernous AngiomaCavernous Angioma(Cavernoma)(Cavernoma)
Location:– 80% are supratentorial
(esp. frontal and temporal).– Spinal cord
involvement is rare.– Extra-axial &
intraventricular locations are rare.
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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
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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.
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Carotid DissectionCarotid Dissection
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ICA DISSECTIONICA DISSECTION
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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
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Dural Sinus ThrombosisDural Sinus Thrombosis EtiologyEtiology
Dural Sinus ThrombosisDural Sinus Thrombosis EtiologyEtiology
•Unknown•Infection •Coagulopathies•Behcet;’s disease •SLE •Tumors
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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 %
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N MILD
MODERATE SEVER
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Dural Sinus ThrombosisDural Sinus Thrombosis DiagnosisDiagnosis
Dural Sinus ThrombosisDural Sinus Thrombosis DiagnosisDiagnosis
– Clinical Presentation.– Radiological Findings.
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•NECT:
•Dense Sinus•Cord sign
•Venous infarction & Hemorrhage
Dural Sinus ThrombosisDural Sinus Thrombosis
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CECT: Empty Delta sign. Dural Sinus Filling Defect
Dural Sinus ThrombosisDural Sinus Thrombosis
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MRI:•MRI:
•Dense Sinus•Cord sign •Venous infarction•Filling Defect
Dural Sinus ThrombosisDural Sinus Thrombosis
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Dural Sinus ThrombosisDural Sinus Thrombosis
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Dural Sinus ThrombosisDural Sinus Thrombosis
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Dural Sinus –NORMAL MRVDural Sinus –NORMAL MRV
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Dural Sinus ThrombosisDural Sinus Thrombosis