Imaging In Sub Arachnoid Hemorrhage (SAH)

1. IMAGING IN SAH
DR.SARATHMENON.R, MD(Med),DNB(Med),MNAMS
DM Resident
Dept.of .Neurosciences
Amrita Institute of Medical Sciences,Kochi

2. INTRODUCTION
 Definition
 Epidemology
 Grading system
 Imaging modalities
 Differentials

3. IMAGING MODALITIES
 NCCT/CTA
 MRI /MRA
 Angiography
 Nuclear imaging
 Neurosonography

4. SAH
What is it?
 Bleeding into the subarachnoid space (space between
the pia & arachnoid meningeal layers) where blood
vessels lie & CSF flows
Where does the blood come from?
 An aneursym on a blood vessel in the subarachnoid
space has ruptured (~70%)
 Unknown (~15%)
 AVM (~10%)
 Rare causes (e.g. tumour) (~5%)
Where does the blood go?
 Anywhere where CSF goes, may get hydrocephalus if
into ventricle & causes obstruction of CSF circulation

5. SAH
 Incidence = 1/7000 people
 Higher chance if:
 Female
 3rd trimester of pregnancy
 Middle-aged
 Abuse of stimulant drugs
 Connective tissue disorder
 Family history
 PCKD

6. SAH – THE PROBLEM
 80% in 40-65 year olds
 15% in 20-40 year olds
 It can kill quickly
 25% die within 24 hours
 50% will be dead at 6 months
 It causes significant disability
 Cognitive impairment
 Neurological disability depending on size of bleed &
complications encountered

7. GRADING OF SAH
 WFNS Grading :
 Grade GCS Motor Deficit
 I 15 Absent
 II 13-14 Absent
 III 13-14 Present
 IV 7-12 +/-
 V 3-6 +/-

8. MODIFIED H & H GRADING
Grade Description Mortalit
y (%)
Grade 0 Unruptured aneurysm --
Grade I Asymptomatic or minimal headache with normal
neurologic examination
2
Grade II Moderate to severe headache, nuchal rigidity, no
neurologic deficit other than cranial nerve palsy
5
Grade III Lethargy, confusion, or mild focal deficit 15 — 20
Grade IV Stupor, moderate to severe hemiparesis,
possible early decerebrate rigidity, vegetative
disturbances
30 — 40
Grade V Deep coma, decerebrate rigidity, moribund
appearance
50 — 80

9. CT GRADING SYSTEM OF FISHER
1 No subarachnoid blood detected
2 Diffuse or vertical layers < 1 mm thick
3 Localized clot and/or vertical layer > 1 mm
4 Intracerebral or intraventricular clot with diffuse or
no SAH

12. INVESTIGATIONS
 CT scan without contrast
 Lumbar puncture
 CTA
 Cerebral angiogram
 MRI/MRA
98% sensitive @ 12 hours
80% at day 3
50% at day 7
Also good to see if
any associated ICH
or hydrocephalus.
May help localise the
location of the
aneurysm if there is
more than 1 & may
also see AVM

17. CT SCAN- NCCT
 Evident in the largest subarachnoid spaces- suprasellar cistern
and Sylvian fissures.
 most conspicuous within 2-3 days of onset
 Acute SAH is typically 50-60 Hounsfield units (HU).
 The protein content of the hemoglobin molecule is predominantly
responsible for the attenuating effect of blood; absolute
measurement in HU varies with the hematocrit value
 localizing the source of bleeding-
- interhemispheric fissure,frontal lobe- Aco A
- Sylvian fissure- I/L MCA
- Posterior fossa- post.circulation aneurysm
NCCT- Sensitivity-93-100% in first 24 hrs

18.  • Scrutinize these areas systematically for SAH
 – Perimesencephalic cisterns
 – Sylvian fissures
 Dilation of temporal horns suggestive of
hydrocephalus, which raises a possibility of SAH
 CTA: Multislice CTA 90-95% + for aneurysm ~ 2 mm

24. CORTICAL SAH

25. SAH-CISTERNAL

26. A nonenhanced computed tomography scan of the
brain that demonstrates an extensive SAH filling the
basilar cisterns in a patient with a ruptured
intracranial aneurysm

28. SAH & LP
 CT & LP are critical to diagnosing SAH
 No need for LP if obvious blood in subarachnoid space
on CT
 If NCCT –ve, LP needed.
 Blood may not be evident on CT, especially if it is
performed > few days after bleed
 LP should only be performed after 12 hours of headache
onset
 If NCCT,LP –VE, CTA to r/o saccular aneurysm

29. SAH & LP
 When blood enters the CSF (e.g. from SAH or during LP) the
red cells are broken down & oxyhaemoglobin is released
 It then takes 12 hours for the oxyhaemoglobin to be converted
into bilirubin – conversion is via an enzyme found in the brain.
 Bilirubin in the CSF, therefore, tells us that blood must have
been in the subarachnoid space for at least 12 hours
 Blood which entered the CSF during the LP would not
encounter the enzyme & could not produce bilirubin
 The CSF will look xanthochromic (yellowish discolouration) if
bilirubin is present which they will look for with spectroscopy in
the lab

31. CTA
subarachnoid hemorrhage and contrast
medium filling the right sylvian fissure,
the interhemispheric fissure, and the
lateral and third ventricles

32. CTA SPOT SIGN

33. MRI/MRA
 (FLAIR) is the most sensitive for the detection of SAH
 FLAIR images, SAH appears as high signal-intensity
(white) in normally low signal-intensity (black) CSF
spaces.
 In acute SAH, FLAIR and CT scanning have similar
findings.
 T2- and T2*- low signal-intensity in normally high signal-intensity
subarachnoid spaces.
 T1-weighted - intermediate-intensity or high-intensity
signal in the subarachnoid space

34.  MRA may be useful for evaluating aneurysms > 5mm
and other vascular lesions that cause SAH

35. LEVEL OF CONFIDENCE
 FLAIR MRI is as sensitive as or more sensitive than
CT scanning in the evaluation of acute SAH
 compared with LP, FLAIR MRI cannot exclude SAH.
 MRI -valuable in the subacute phase of SAH, in which
the density of hemorrhage on CT scans decreases.
 Magnetic field inhomogeneity - artifactual increase in
signal intensity in sulci over the cerebral convexities on
FLAIR images, which can mimic SAH.
 Hyperintensity in the subarachnoid space on FLAIR
images seen in meningitis or leptomeningeal
carcinomatosis

37. SAH appears hyperintense on the T2-weighted and fluid-attenuated inversion
recovery (FLAIR) images and isointense to hypointense on the T1-weighted
(T1W) image. Marked blooming is observed on the gradient-echo (GRE) image.
Findings in the right parietal region extend into cortical sulci and suggest
hyperacute or acute hemorrhage.

38. Sagittal T1-weighted image shows a right SDH (fig a). Axial fluid
attenuated inversion recovery image demonstrates SAH (arrows)
in the right parietal region (fig b).

39. NUCLEAR IMAGING
 not useful in the initial diagnosis of subarachnoid
hemorrhage (SAH), role in the diagnosis of related
vasospasm
 (SPECT) scanning with the radiopharmaceutical
technetium-99m (99m Tc) hexamethylpropyleneamine
oxime (HMPAO).
 semiquantitative and qualitative in that the cerebellum is
generally considered as a control value for normal
perfusion
 Space-occupying lesions such as cerebral hematoma
can cause perfusion defects on SPECT perfusion
imaging

40. ANGIOGRAPHY
 standard imaging -intracranial aneurysms, arteriovenous
malformations (AVMs), and fistulae
 (AP), lateral, and one or more oblique views of both
carotid and vertebral artery contrast injection studies
 submentovertical - the neck of a middle cerebral artery
bifurcation aneurysm or anterior communicating artery
aneurysm
 aneurysm location, shape, neck size, and neck-to-maximal
diameter ratio - the aneurysm is better treated with open
craniotomy or with an endovascular technique.

41. LEVEL OF CONFIDENCE
 high degree of accuracy
 false-negative rate in the range of 1-2%
 A repeat cerebral arteriogram at 10-14 - initial angiogram
negative
 B/l selective external and internal carotid artery
angiograms - exclude a dural arteriovenous fistula
 B/l vertebral arteriograms of the neck ( selective
thyrocervical trunk and/or careful injections of the right
superior intercostal artery) demonstrate the arterial and
venous circulation of the cervical spinal cord
 If thorough arteriographic studies do not demonstrate a
specific cause for an SAH, a presumptive diagnosis of
idiopathic perimesencephalic hemorrhage is sometimes
made

42. An angiogram showing a bilobed aneurysm of a
posteroinferior cerebellar artery immediately before
rupturing

43. onset of an aneurysmal rupture, with
extravasation of contrast material into the
subarachnoid space from the
anterosuperior aspect of a bilobed
aneurysm in a posteroinferior cerebellar
artery

44. later-phase angiogram of a rupturing bilobed
aneurysm of a posteroinferior cerebellar
artery shows progressive opacification of the
subarachnoid space in the posterior fossa

45. late angiogram demonstrating contrast
medium filling the posterior fossa
subarachnoid spaces, including the
ambient, prepontine, and perimedullary
cisterns

46. NEUROSONOGRAPHY
 Echoencephalography is useful for diagnosing germinal
matrix and intraventricular hemorrhage in the newborn
 transcranial Doppler USG - diagnosis and management of
vasospasm in patients with SAH.
 Serial transcranial Doppler USG - presence of vasospasm and
allow for the maximization of medical therapy for vasospasm
before the patient becomes symptomatic
 Flow measured in the middle cerebral arteries, which have
have flow velocities normally in the 30-80 cm/s range.
Elevation to 120 cm/s indicates moderate vasospasm, and
elevation to 200 cm/s indicates severe vasospasm
 sensitivity of transcranial Doppler ultrasonographic imaging for
the detection of vasospasm has been reported to be 85-90%

47. SAH: DIFFERENTIAL DIAGNOSIS
 Aneurysmal
 Nonaneurysmal
 “Pseudo-SAH”
 Reversible cerebral vasoconstriction syndrome
(RCVS)

48. ANEURYSMAL SAH
 • SAH caused by ruptured aneurysm
 • Worst headache of life
 • 40-60 years, M:F = 1:2
 • 50% mortality, 20% rebleed within 1st 2 weeks
 • Outcome inversely proportional to Hunt and Hess
(H&H) grade and WFNS grade
 • Severity of vasospasm/ischemia correlates with
Fisher CT grading (amount)
 – 1 = no SAH visible
 – 2 = diffuse, thin layer (< 1 mm)
 – 3 = localized clot or thick layer (> 1 mm)
 – 4 = intraventricular blood

49. ANEURYSMAL SAH
 • NCCT:
– May show culprit aneurysm as filling defect within
hyperdense SAH
– Effaced cistern, hydrocephalus, +/- IPH
 • CTA: 90-95% positive if > 2 mm
 • MRA TOF: 85-95% sensitive for aneurysm > 3 mm
 • DSA: current gold standard
 • Highest amount of blood near site of rupture
 ACoA aneurysm anterior interhemispheric fissure
MCA aneurysm Sylvian
 Basilar tip, SCA, PICA, VA prepontine cistern, foramen
magnum, 4th ventricle

51. Subarachnoid hemorrhage secondary to rupture of left
superior cerebellar artery aneurysm

52. NON-ANEURYSMAL SAH-PERIMESENCEPHALIC
 Hyperdense prepontine, perimesencephalic CSF
 Location: "Pretruncal" (anterior to pous, around
 midbrain)
 • CTA/MRA/DSA
- Angiography negative in 90-95% of pnSAH
- 5-10% prevalence of vertebrobasilar aneurysm in pnSAH
- DSA
 Saccular or blister-like aneurysm identified as cause of
pnSAH in 5-10%
 Vasospasm, hydrocephalus rare « < aSAH)

53. NON-ANEURYSMAL (PMSAH)

54. Small SAH, localized to interpeduncular cistern
• Presumed venous etiology with low
recurrence

55. REVERSIBLE CEREBRAL
VASOCONSTRICTION SYNDROME (RCVS)
 • Reversible, multifocal cerebral vasoconstrictions
 • Clinical thunderclap headache +/- neurodeficit
 • NCCT often negative: 20% with small cortical SAH +/-
IPH
 • Vasculitic pattern on CTA, MRA and DSA
 – Segmental arterial constriction
 – Interval DSA may show rapid improvement with
vasodilator Rx

56. BEWARE: CORTICAL SAH FROM VENOUS
SINUS THROMBOSIS
Small SAH with hyperdense clot of superior sagittal sinus on CT, absence
of flow voids on T2WI and loss of venous signal on MRV image

57. PSEUDO-SAH
Increased density in basal cisterns, frequently related to
cardiopulmonary arrest
• Hypodense brain (severe edema): cisternal effacement, distension +/-
thrombosis of vessels
•

58. two images suggest subarachnoid hemorrhage along the cisterns
with effacement of the quadrigeminal cisterns seen in meningitis

59. PSEUDO SAH
 Other causes: intrathecal contrast, meningitis
 polycythemia
 Falx cerebri
 Tentorium cerebelli
 Streak artifact –bone from skull base
 Motion artifact
 hyperintensity of SAH is reported to range between
60 and 70 Hounsfield units, whereas that of PSAH
is reported to range between 29 and 33 Hounsfield
units

60. SAH WITH INTRAVENTRICULAR
HEMORRHAGE

62. CONCLUSION
 • LP more sensitive than CT
 • Negative NCCT but still suspicious of SAH –still
need LP
 • MRI is sensitive to detect SAH using FLAIR, GRE and
SWI
 – But problematic in perimesencephalic cistern
 Persistent vasospasm – vessels can be permanently
narrow
 Etiologies of non-traumatic SAH
 – 80% ruptured aneurysm
 – 10% non-aneurysmal perimesencephalic SAH
 – 10% others (brain AVM, spinal AVM, DAVF, venous
infarct, tumor)

63. THANK YOU