imaging of subarachnoid hemorrhage

1. IMAGING OF
SUBARACHNOID
HEMORRHAGE
Nagaraju.B

2. Bleeding into the subarachnoid space is termed
subarachnoid hemorrhage (SAH).
a) Causes
b) Distribution of SAH
c) Grading of SAH
d) Complications of SAH
e) Diagnosis & Investigation

3. a) Causes :
1-Trauma (Most common cause)
2-Ruptured Intracranial Aneurysm
3-Bleeding From Vascular Malformation
4-Extension From Parenchymal Hematoma
5-Perimesencephalic Hemorrhage
6-Miscellaneous

4. CLINICAL FEATURES
 Sudden, severe “explosive” headache, vomiting,
altered sensorium are common presentations.
 Usually the headache is described as “worst
headache of the life”.
 The usual age of presentation is 55- 60 years.
 M:F ratio is 1:2.

5. Traumatic SAH
 Traumatic SAH can occur with both direct
trauma to the skull and non-impact closed head
injury.
 Tearing of cortical arteries and veins, rupture of
contusions and lacerations into the contiguous
subarachnoid space, and choroid plexus bleeds
with intraventricular hemorrhage may all result
in blood collecting within the subarachnoid
cisterns.

6. IMAGING:
 NECT:
 Acute SAH seen as linear hyperdensities in
sulci adjacent to cortical contusions or under
epi- or subdural hematomas.
 Chronic tSAH may appear as hypodense fluid
that expands the affected sulci.

7.  MRI:
 T1WI: As acute blood is isointense with brain, it may be
difficult to detect. “Dirty” sulci with “smudging” of the
perisylvian cisterns is typical.
 T2WI: similar in SI to cisternal CSF.
 FLAIR: show hyperintensity in the affected sulci.
 “Blooming” with hypointensity can be identified on T2*
scans, typically adjacent to areas of cortical contusion.

8.  GRE or SWI: very hypointense signal intensity
surrounded by hyperintense CSF.
 Chronic tSAH causes focal superficial siderosis
that appears as curvilinear hypointensity along
gyral crests and sulci.

9.  ANGIOGRAPHY. CTA is typically normal for
the first several days after tSAH.
 Vasospasm may ensue from two to three days to
two weeks after trauma and is identified as
multifocal areas of vessel narrowing or
“beading.”
 DSA is rarely performed in acute brain trauma
unless vascular injury such as dissection or
pseudoaneurysm is suspected

11. Ruptured intracranial aneurysm :
Most common cause of non-traumatic SAH
-Potentially devastating condition with 50 %
immediate mortality and high long-term
morbidity

12. 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)

13. 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

14. 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)

15. 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)

16. 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)

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

18. DEFINETIVE MANAGEMENT OF aSAH
Microsurgical Clipping OR Endovascular coiling
should be performed as early as feasible in the
majority of patients to reduce the rate of rebleeding
Complete obliteration of the aneurysm should be
achieved whenever possible

19. COILING

22. COILING OR CLIPPING
 For patients with ruptured aneurysms judged to
be technically amenable to both endovascular
coiling and neurosurgical clipping
endovascular coiling should be considered

23. CLIPPING PREFERRED
 Patients presenting with large ICH and MCA
aneurysm
Aneurysm characteristics
Wide neck
Geometrically complex with incorporation of
branch artery
Partially thrombosed

24. COILING PREFERRED
 In elderly
 In poor-grade
 Aneurysms of basilar artery

25. 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
*The hemorrhage must be limited to the cisterns
directly anterior to the midbrain

26. *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

29. 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
headache
Grade IV : is the most severe with coma

30. -Fisher Grade classifies the CT appearance of
SAH :
Grade 1 : negative on CT
Grade 2 : < 1 mm thick
Grade 3 : > 1 mm thick
Grade 4 : Diffuse SAH or intraventricular or
parenchymal extension

33. 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
-

34. 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

35. 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

36. 2-Hydrocephalus :
-20-30 % of patients with SAH will develop acute
hydrocephalus due to obstruction of arachnoid
granulations, treatment is ventriculostomy

37. 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

38. 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)

39. e) Diagnosis & Investigation :
1-CT
2-Lumbar Puncture
3-MRI
4-Catheter Angiography

40. 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

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

43. 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

44. 3-MRI :
-In Late cases, 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
-

45.  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

47. 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.

48. 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)

49. -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

50. -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

51. 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

52. 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

53. (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)

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

55. (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

56. -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

57. *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 cisterns

58. c) 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

59. *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

60. -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

61.  -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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