Transcript
Page 1: Diagnostic Imaging of Subarachnoid Hemorrhage

C.N.S.Subarachnoid Hemorrhage

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Mohamed Zaitoun

Assistant Lecturer-Diagnostic Radiology Department , Zagazig University Hospitals

EgyptFINR (Fellowship of Interventional

Neuroradiology)[email protected]

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Knowing as much as possible about your enemy precedes successful battle

and learning about the disease process precedes successful management

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Subarachnoid Hemorrhagea) Causesb) Distribution of SAHc) Grading of SAHd) Complications of SAH e) Diagnosis & Investigation

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a) Causes :1-Trauma (Most common cause)2-Ruptured Intracranial Aneurysm3-Bleeding From Vascular Malformation4-Extension From Parenchymal Hematoma5-Perimesencephalic Hemorrhage6-Miscellaneous*N.B. :-No cause of the SAH is identified in up to 22 % of cases

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1-Trauma : Most common cause-Tends to have peripheral distribution in sulci

rather than concentrated in basal cisterns

2-Ruptured intracranial aneurysm : Most common cause of non-traumatic SAH

-Potentially devastating condition with 50 % immediate mortality and high long-term morbidity

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Traumatic SAH , high density blood (arrowheads) fills the sulci over the right cerebral convexity in this subarachnoid hemorrhage

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3-Bleeding from vascular malformation :-Cerebral or Spinal-5 %

4-Extension From Parenchymal Hematoma :-Often hypertensive bleed-5 %

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5-Perimesencephalic Hemorrhage :-Low pressure probable venous hemorrhage -Few symptoms and signs-Good prognosis

6-Miscellaneous :-Anticoagulants & Vasculopathy

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b) Distribution of SAH :-The pattern of SAH may provide a clue to the location

of the ruptured aneurysm, however, multiple aneurysms are seen in up to 20 % of patients with SAH and subarachnoid blood may redistribute if the patient was found down

1-Hemorrhage in the anterior interhemispheric fissure suggests an ACOM aneurysm (33 % of intracranial aneurysms)

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Ruptured ACOM aneurysm , (a) NECT shows small amount of blood in the anterior interhemispheric fissure and some sedimentation in the right occipital horn , (b) CTA shows a small aneurysm of the ACOM

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Ruptured ACOM aneurysm , (a) NECT shows nearly symmetric SAH & a small interhemispheric or midline parenchymal hematoma (white arrow) , (b) DSA confirms ACOM aneurysm (black arrow) suspected for rupture , small MCA & ICA aneurysms were also detected (black arrow heads)

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2-Hemorrhage in the suprasellar cistern suggests a PCOM aneurysm (also 33 % of intracranial aneurysms)

3-Hemorrhage in the sylvian fissure suggests a MCA aneurysm (20 % of intracranial aneurysms)

4-Perimesencephalic SAH :*Suggests either a basilar tip aneurysm (5 % of

intracranial aneurysms) or the relatively benign non-aneurysmal perimesencephalic SAH

*Perimesencephalic SAH is a type of nonaneurysmal SAH that is a diagnosis of exclusion with a much better prognosis than hemorrhage due to a ruptured aneurysm

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*The hemorrhage must be limited to the cisterns directly anterior to the midbrain

*95% of cases have a normal cerebral angiogram and the source of bleeding is not identified, the cause is thought to be a venous bleed, the other 5% of cases are due to a vertebrobasilar aneurysm and the prognosis is worse

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Ruptured MCA aneurysm , (a) NECT shows SAH in the sylvian fissure (white arrowhead & parenchymal hematoma (black arrowhead) , (b) CTA confirms MCA aneurysm ((white arrow) , a 2nd unruptured MCA aneurysm is present (open arrow)

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Ruptured MCA aneurysm , (a,b) NECT at 2 locations , show asymmetric SAH & focal hematoma , expanding the LT sylvian fissure

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1-Interhemispheric fissure2-Suprasellar cistern3-Sylvian fissure4-Interpeduncular cistern5-Ambient cistern6-Quadrigeminal cistern

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c) Grading of SAH :-Hunt & Hiss Score is the clinical grading scale for aneurysmal

SAH and is based solely on symptoms , without imaging Grade I : is the lowest grade with only mild headacheGrade IV : is the most severe with coma-Fisher Grade classifies the CT appearance of SAH :Grade 1 : negative on CTGrade 2 : < 1 mm thickGrade 3 : > 1 mm thickGrade 4 : Diffuse SAH or intraventricular or parenchymal

extension

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d) Complications of SAH :1-Vasospasm :-The most common cause of morbidity & mortality in

patients who survive the initial episode of SAH-The peak incidence of vasospasm occurs approximately

7 days after the initial ictus-Vasospasm may lead to stroke or hemorrhage-The medical treatment of vasospasm is triple-H therapy

of hypertension, hypervolemia & hemodilution -Endovascular treatment of vasospasm involves intra-

arterial infusion of vasodilators

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Vasospasm , two coronal MIP from CTA , (a) shows severe narrowing of the basilar artery , left AICA (RT not visible) and distal vertebral arteries , (b) the follow up study was performed after endovascular treatment which shows a normal caliber of the basilar & LT vertebral arteries

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2-Hydrocephalus :-20-30 % of patients with SAH will develop acute

hydrocephalus due to obstruction of arachnoid granulations, treatment is ventriculostomy

3-Superficial Siderosis :-Is a condition caused by iron overload of pial

membrane due to chronic or repeated subarachnoid bleeding

-On imaging, the iron causes hypointensity on T2 outlining the affected sulci

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Superficial Siderosis , T2 show a thin hypointense interface at the junction of the sulcal surfaces & the subarachnoid space (arrows) of the basal cisterns (a) & the MCA territory temporal lobes (b)

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e) Diagnosis & Investigation :1-CT2-Lumbar Puncture3-MRI4-Catheter Angiography

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1-CT :-Most sensitive in first few days (98 % on day 1,

only 50 % positive by 7 days), CTA may be performed

-Noncontrast CT is the initial imaging modality in suspected SAH, on CT, subarachnoid blood appears as high attenuation within the subarachnoid space

-High attenuation material in the subarachnoid space may be due to SAH (by fat the most common cause), meningitis, leptomeningeal carcinomatosis or prior intrathecal contrast administration

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2-Lumbar Puncture :-Negative CT scan doesn’t exclude SAH,

especially if scan performed days after ictus, therefore lumbar puncture mandatory if CT negative to look for Xanthochromia

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3-MRI :-Late MRI more sensitive than CT -Proton Density, Gradient Echo T2 and FLAIR sequences most

sensitive-Acute SAH appears hyperintense on FLAIR & demonstrates

susceptibility artifact on gradient sequences-D.D. for increased FLAIR signal in the subarachnoid space is

similar to the differential for high attenuation subarachnoid material seen on CT including SAH, meningitis, leptomeningeal carcinomatosis and residual contrast material, note that meningitis & carcinomatosis will typically show leptomeningeal enhancement in addition to the abnormal FLAIR signal

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4-Catheter Angiography :-Now used less often in initial work-up as CTA

often used at time of diagnosis of aneurysmal SAH and for planning therapy (neurointerventional versus surgical)

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**N.B. Reversible Cerebral Vasoconstriction Syndrome :

-The pathophysiology of RCVS is not well-understood-Pregnancy, migraines, exposure to certain vasoactive

drugs (pseudoephedrine, selective serotonin reuptake inhibitors, triptans, ergot derivatives and cocaine) and trauma have been associated with this condition

-Not to be confused with posterior reversible encephalopathy syndrome (PRES)

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-A thunderclap headache is the usual main symptom, often occipital but also potentially diffuse, there may be a history of recurrent thunderclap headaches over days or weeks, headache may be associated with photophobia, nausea and vomiting, focal neurological deficits can occur secondary to ischemia

-Radiographic Findings :1-Angiography (CTA/MRA/DSA) demonstrated

multifocal narrowings in the circle of Willis branches or arteries forming circle of Willis, post stenotic segments show dilatation giving classical beaded appearance/sausage shaped arteries

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2-No CT evidence of SAH (although recent studies shown the association of SAH and intraparenchymal hemorrhage with RCVS more commonly SAH which is seen in about 11-25% of the cases, cortical SAH was the most common pattern seen)

3-Confirmation of the diagnosis rests on eventual resolution of angiographic findings within 12 weeks

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Marked narrowing of the basilar artery (measuring 1.1 mm in diameter) and proximal PCAs with beaded irregular areas of narrowing and dilation in the distal PCAs

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(a) MRA showing segmental narrowings (arrows) of the middle and anterior cerebral arteries , (b) DSA showing segmental narrowings of the branches of the anterior cerebral artery (arrows)

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FLAIR shows focal SAH blood in the precentral sulci and superior frontal sulci (arrow) , the cisterns and sylvian fissures were free

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(a) MRA at presentation shows segmental narrowing of the anterior , middle (arrow) and posterior cerebral arteries bilaterally , (b) 3 months follow-up angiogram shows resolution of arterial narrowing

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-Differential Diagnosis :1-The presence of SAH necessitates differentiating vasospasms secondary to

aneurysmal rupture from those secondary to RCVS*In RCVS, at the time of presentation, the patient has the multifocal

vasospasms which are characteristic of the same, however, in cases of aneurysmal rupture with SAH, there was delayed vasospasm in a time setting of about 1-2 weeks after hemorrhage

*Ruptured aneurysmal SAH has various patterns depending on the region of involvement :

a) ACOM aneurysm is suggested by blood in the cisterna lamina terminalis, anterior pericallosal cistern and interhemispheric fissure

b) PCOM aneurysm : blood is usually seen diffusely within the cisternsc) MCA aneurysm is characterized by blood in the sylvian fissure and a

hematoma in the temporal lobe which may rupture into the adjacent temporal horn

d) Posterior fossa aneurysms mostly have no characteristic localizing findings on CT

*In RCVS, the blood is found in the cortical sulci*Vasospasms can also occur in correlation to a ruptured aneurysm, these

spasms are most commonly seen in the vessels closest to the site of leakage

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2-Primary angitis of the CNS :-Has no characteristic radiological findings, it can have

diffuse white matter lesions, multiple infarctions involving multiple vascular territories and multiple intraparenchymal hemorrhages

-The differentiation from RCVS is predominantly based on the clinical presentation, Primary angitis of the CNS tends to have a dull aching pain of insidious onset and is progressive in nature, in RCVS there is a sudden and severe onset of headache

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Cerebral Cisterns & Subarachnoid Spaces 1-Premedullary cistern2-Prepontine cistern3-Cerebellopontine cistern4-Cisterna magna5-Superior cerebellar cistern6-Interpeduncular cistern7-Ambient cistern8-Quadrigeminal cistern9-Suprasellar cistern

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sagittal T11-Premedullary cistern2-Pons3-Medulla4-Cerebellum

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axial T11Premedullary cistern2-Medulla3-Cerebellum

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coronal T11-Basilar artery in premedullary cistern2-Spinal cord3-Hippocampus

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sagittal T11-Prepontine cistern2-Pons3-Medulla4-Cerebellum5-Splenium, corpus callosum

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axial T11-Basilar artery in prepontine cistern2-Pons3-Cerebellum4-Cranial nerve V

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coronal T11-Basilar artery in prepontine cistern2-Hippocampus 3-Lentiform nucleus

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axial cut (magnification) T2-1-Cerebellopontine cistern2-Pons3-Internal acoustic meatus4-Fourth ventricle5-Cerebellar hemisphere

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coronal cut (magnification) T21-Cerebellopontine cistern2-Temporal lobe (right side)3-Pons4-Hippocampus5-Internal acoustic meatus

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sagittal T11-Cisterna magna2-Medulla3-Pons4-Midbrain5-Cerebellum

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axial T11-Cisterna magna2-Cerebellum3-Medulla

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coronal T11-Cisterna magna2-Cerebellum3-Corpus callosum

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sagittal T11-Superior cerebellar cistern2-Tentorium cerebelli3-Cerebellum4-Pons5-Midbrain

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axial T11-Superior cerebellar cistern2-Cerebral aqueduct

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coronal T11-Superior cerebellar cistern2-Lateral ventricle3-Cerebellar hemisphere4-Tentorium cerebelli

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sagittal T11-Interpeduncular cistern2-Midbrain3-Pons4-Medulla5-Fourth ventricle6-Cerebellum7-Third ventricle8-Corpus callosum

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Axial T11-Interpeduncular cistern2-Cerebral aqueduct3-Hippocampus

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coronal T11-Interpeduncular cistern2-Hippocampus3-Third ventricle4-Lateral ventricle

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sagittal T11-Ambient cistern2-Splenium, corpus callosum 3-Cerebellum4-Pons

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coronal T11-Ambient cistern2-Cerebral aqueduct3-Lateral ventricle

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axial T11-Ambient cistern2-Lateral ventricle3-Fourth ventricle4-Cerebellar hemisphere

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sagittal T11-Quadrigeminal cistern2-Midbrain3-Pons4-Medulla5-Cerebellum

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axial T11Quadrigeminal cistern2-Cerebral aqueduct3-Optic chiasm

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coronal T11-Quadrigeminal cistern2-Lateral ventricle3-Fourth ventricle4-Cerebellar hemisphere

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sagittal T11-Suprasellar cistern2-Pituitary gland3-Pons4-Third ventricle 5-Corpus callosum

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axial T11-Suprasellar cistern2-Pituitary stalk 3-Cerebral aqueduct4-Hippocampus

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coronal T11-Suprasellar cistern2-Anterior cerebral artery3-Lateral ventricle4-Caudate nucleus

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