Subarachnoid hemorrhage

1. SUBARACHNOID HEMORRHAGE
AND ANEURYSMS
Moderator- Dr. Johny Prasad MDRD
Presentor- Dr. Gowthami

2. Subarachnoid Hemorrhage
• Causes-
1. Trauma (MCC)
2. Ruptured intracranial aneurysm (MCC of spontaneous SAH)
3. Bleeding from vascular malformation
4. Extension from parenchymal hematoma
• No identifiable cause in 10-12% cases of ntSAH

3. Presentation of aSAH
• Sudden onset of severe excruciating headache
• Mass effects- Cranial nerve palsies (3rd nerve palsy with PCOM
aneurysm)
• Thromboembolic events

4. Aneurysmal SAH
• The typical location –
• Basal cisterns
• Sylvian fissure
• Interhemispheric fissure
• MCC- rupture of saccular/ berry aneurysm

5. Distribution of SAH
• May provide a clue to the location of ruptured aneurysm.
1. Hemorrhage in anterior interhemispheric fissure- ACOM aneurysm
2. Suprasellar cistern- PCOM aneurysm
3. Sylvian fissure- MCA aneurysm
4. Perimesencephalic – basilar artery aneurysm
5. 4th ventricle, prepontine cistern- Vertebrobasilar system

6. • However, in 20% of cases
subarachnoid blood may
redistribute if the patient was
found down and multiple
aneurysms may be present.
• IVH may be present in 50%

7. Grading of SAH
• Based on clinical findings-
• Hunt and Hess scale
• World Federation of Neurological Societies scale
• Based on the CT findings-
• Modified Fisher CT grade

8. • C

9. • C

10. • C

11. Factors associated with unfavourable
outcome
• Aneurysm size
• Large amount of SAH on initial CT scan
• Parenchymal hematoma
• Intraventricular hemorrhage
• Increase in Modified Fischer grade have a linear relationship with the
risk of vasospasm, delayed infarction and poor clinical outcome

12. Imaging of SAH
• CT-
• Best for screening in patients with thunderclap headache and
suspected aSAH.
• Most sensitive- 100% if performed in the first 6 hours after ictus

13. • Hyperdense basal cisterns
and sulci
• IVH can be present
• Hyperdense subarachnoid
blood surrounds and
outlines the comparatively
hypodense appearing
aneurysm sac in some
cases

14. Imaging of SAH
• MRI
• T1W- isointense with brain and CSF
cisterns appear smudged or dirty
• FLAIR is the best sequence to depict aSAH
• Hyperintense CSF in the sulci and cisterns is
present but nonspecific
• Other causes of bright CSF- meningitis,
neoplasm, artifact

15. Imaging of SAH
• Angiography
• CT Angiography- positive in 95% in
detecting 2mm or larger aneurysm
• DSA- in cases with CTA negative
SAH

16. Complications of SAH
1. Cerebral ischemia and vasospasm
2. Obstructive hydrocephalus
3. Neurodegeneration
4. Tearson syndrome
5. Superficial siderosis

17. Cerebral ischemia and vasospasm
• Major cause of morbidity and mortality
• 2 types-
• Immediate/ Acute
• Delayed/ subacute

18.  Immediate cerebral ischemia
• Acute vasoconstriction can develop within minutes
• Early ischemic changes can be detected within first 3 days following
aSAH
 Delayed cerebral ischemia
• Vasospasm and delayed ischemia develop usually after 4-10 days
• Patients with large volume SAH are at high risk for developing
symptomatic vasospasm and delayed cerebral ischemia

19. Imaging post aSAH complications
• MRI- Most sensitive for detecting early ischemic changes following
aSAH
• CT angiography and DSA- multiple segments of vascular constriction
and irregularly narrowed vessels are typical findings in cerebral
vasospasm

20. Obstructive hydrocephalus-
• Develop within hours and exacerbated by the presence of IVH
• Imaging show periventricular extracellular fluid with blurred lateral
ventricle margins
Tearson syndrome-
• Intraocular haemorrhage in 12% cases
• Associated with more severe SAH grades

21. Superficial siderosis
• Seen in chronic repeated SAH
• Due to iron overload of pial membrane
• Best identified on T2* (GRE, SWI) MR imaging
• Seen as hypointensity outlining the affected sulci

22. DDs of aSAH
• tSAH- focal, adjacent to cortical contusions and seen in superficial
sulci
• Perimesencephalic nonaneurysmal SAH
• Convexal SAH
• Pseudo-SAH

23. Perimesencephalic nonaneurysmal SAH
• Benign SAH subtype confined to perimesencephalic and prepontine
cisterns
• Venous bleed is the most likely cause
• Imaging- CT scan shows focal accumulation of SAH around the
midbrain and in front of pons
• Clinically benign and uneventful course

24. Convexal SAH
• Isolated spontaneous ntSAH that involves the
sulci over the vertex
• Restricted to hemispheric convexities, sparing
the basal and perimesencephalic cisterns
• Etiology- Reversible cerebral vasoconstriction
syndrome, cerebral amyloid angiopathy,
cortical vein thrombosis

25. Convexal SAH
• CT findings- Unilateral, involving one or
several dorsolateral convexity sulci
• MRI-
• Focal sulcal hyperintensity on FLAIR
• T2* (GRE, SWI) shows blooming in the
affected sulci
• Hypointense cord sign may be present
in dural sinus or cortical vein occlusion

26. Aneurysm
• Abnormal dilatation of artery
• Types
• Saccular aneurysm
• Fusiform aneurysm
• Pseudoaneurysm

27. Saccular/ Berry aneurysm
• Most common type
• Arise eccentrically at vessel
branch points
• Mostly acquired- weakened
arterial wall due to
abnormal hemodynamics,
shear stress

28. Saccular/ Berry aneurysm
• Increased incidence
1. Anomalous vessels- Persistent trigeminal artery, Fenestrated ACOM
2. Vasculopathies, syndromes-
• Marfan syndrome
• Ehler-Danlos syndrome
• ADPKD
• Fibromuscular dysplasia
3. Familial history

29. • Location –
• 90% in anterior circulation
• Circle of Willis, MCA bifurcation
• ACoA, ICA/PCoA junction- MC
• Size- Tiny (1-2 mm ) to giant (>2 cm)
• Multiple in 15-20%
• F>M

30. Saccular aneurysm
• Increased risk of rupture-
• >5 mm greater risk than 2-4 mm
• Nonsaccular shape
• Vertebrobasilar, ICA-PCoA location
• Imaging
• Round/ lobulated arterial outpouching

31. Fusiform aneurysm
• Involves long, nonbranching vessel segments
• Focal dilatation that involves the entire
circumference of a vessel
• Mostly caused by atherosclerosis
• More common in vertebrobasilar artery

32. Pseudoaneurysm
• Caused by a specific inciting event eg-
trauma, infection, surgery
• Arterial wall completely disrupted
• Often contained only by cavitated
clot
• Inflammatory changes are common
• 15-20% are intracranial- cavernous/
paraclinoid ICA

33. Pseudoaneurysm
• Imaging
• Irregularly shaped outpouching
• Neck usually absent
• CTA- may show “spot sign” (focus of contrast enhancement within
rapidly expanding hematoma)

34. Blood blister like aneurysm
• Lethal subtype of intracranial
pseudoaneurysm
• Broad based blister covered by thin
friable tissue cap.
• Dorsal wall of supraclinoid ICA most
common site
• Easily rupture, may cause catastrophic
aSAH
• Rupture at earlier age and smaller size

35. Imaging
• CT
• Aneurysm- extra-axial mass in subarachnoid space
• Enhances if patent
• May be thrombosed/ have calcifications
• CTA – site and morphology of aneurysm. Allow treatment planning

36. Imaging
• MRI
• Patent aneurysm will show flow void
• Giant or partially thrombosed aneurysm can show complex flow
pattern with heterogenous signal

37. Thank you