https://www.youtube.com/watch?v=wCInmCltl0M

1. SAH
BY
Dr Mohammud Ibraheem

2. OUR POINTS
1) Anatomy of SA space
2) Histology of cerebral vasculature
3) Epidemiology
4) Risk factors of SAH
5) Types of SAH
6) Classification cerebral aneurysm
7) Grades of severity of SAH
8) Clinical presentation
9) Investigations

3. Anatomy

6. Histology

7. Intracranial arteries lack external elastic lamina,
which in the anterior circulation disappears in the
horizontal segment of the cavernous internal carotid
arteries.
Reduction and disappearance of the external elastic
lamina and of elastic fibers in the tunica media
occurs in the vertebral arteries as they enter the
skull.

9. Epidemiology

10. Epidemiology
SAH represent 1% - 6% of all strokes
SAH constitutes 1% - 4% of all ED visits for acute headaches
The most common cause of spontaneous SAH is a ruptured
cerebral aneurysm (85%).
The incidence of aSAH is 6.1/100,000 person-years
worldwide. Females affected 1.6 times more than males.
aSAH is with a case-fatality rate up to 51% and long-term
disability in 1/3 to 1/2 of all survivors. cognitive impairments
in half of survivors
0.3% of all unruptured intracranial aneurysms rupture per
year

11. Epidemiology
Risk factors of rupture of an unruptured intracranial aneurysm:
1. Hypertension
2. Females
3. Age (peaks in the 5th and 6th decades)
4. Larger aneurysm (6 mm-10 mm)
5. Aneurysm location (bifurcations, posterior circulation)
6. Aneurysm shape (irregular shape, with a daughter sac or
multilobuations )
7. Ethnic origin (common in African American, Hispanic, Japanese
and Finnish populations)
8. Family history and past history of SAH
9. Aneurysms that are growing or causing clinical symptoms

13. Epidemiology
location in the ICA and larger neck are the
protective factors against aneurysm rupture.
10% to 15% of patients with SAH do not have an
identifiable bleeding source; of these, 38% have
perimesencephalic SAH, which is a benign
variant of SAH with excellent prognosis.

14. Epidemiology
Over the past 2 to 3 decades, the SAH case-fatality
rate has decreased by 17% -50% worldwide due to
A. Advances in stroke systems of care
B. Diagnostic accuracy
C. Surgical techniques
D. Critical care support
Despite these, SAH remains a highly deadly and
morbid disease, with 30-day mortality as high as
35%.
The overall mortality of SAH is underestimated.

15. Risk factors

16. Risk factors of SAH
Modifiable
1. Hypertension (90% in AC,
10% in PC)
2. DM
3. Tobacco smoking
4. Cocaine use
5. Bacterial endocarditis
6. Fungal infection
7. Tuberous sclerosis
8. Coarctation of the aorta
9. Pheochromocytoma
Non modifiable
1. Age
2. Sickle cell anemia
3. Neurofibromatosis type 1
4. Carotid-vertebrobasilar
anastomoses
5. AD inherited polycystic kidney
disease
6. Fibromuscular dysplasia
7. Moyamoya syndrome
8. Pseudoxanthoma elasticum
9. α1-Antitrypsin deficiency
10. SLE
11. Ehlers-Danlos syndrome,
vascular type (type IV)

18. Risk factors of SAH
10% of AD polycystic kidney disease have
asymptomatic unruptured intracranial aneurysms.
AD polycystic kidney disease accounts for 0.3% of
all SAH.
Although familial clustering is seen in SAH,
variabilities in genetic loci account for 5% of the
hereditary risk of SAH, suggesting that familial
clustering may also be related to shared
environmental risk factors.

19. Risk factors of SAH
The risk in first-degree relatives of patients with
SAH is 3 to 7 times higher than in the general
population, but second-degree relatives have
risks similar to that of the general population.
the AHA/ASA SAH guidelines suggest screening
is considered in those with two or more first-
degree relatives with aneurysm or SAH.

20. Types of SAH

21. Primary SAH
1) aSAH (85%): SAH due to
rupture of intracerebral
aneurysm
2) Nonaneurysmal SAH
(perimesencephalic SAH)
(10%): SAH with no evidence
of cerebral aneurysm or other
vascular malformations
3) SAH due to other vascular
malformations (5%): SAH due
to bleeding from cerebral or
spinal AVM, dural
arteriovenous fistula, arterial
dissection, moyamoya
disease, or other
malformation
Secondary SAH
1) Trauma
2) RCVS
3) PRES
4) Cerebral amyloid angiopathy
5) Pituitary apoplexy
6) Cerebral vasculitis
7) Primary ICH with 2nd extension to
SA space
8) Cerebral venous sinus thrombosis
9) Tumor
10) Coagulopathy
11) Sympathomimetic drug use
12) Alcohol use
13) Endocarditis

22. Classification of
Intracranial
Aneurysms

23. By Morphology
A. Saccular (90%)
B. Fusiform (associated with
atherosclerosis).
Dolichoectatic fusiform
aneurysms is a variety of
fusiform A
C. Dissecting (associated with
trauma or an underlying
vasculopathy)
D. Mycotic (mortality of up to
80%)
By Size
A. <3 mm (small)
B. 3–6 mm (small)
C. 7–12 mm (small-medium)
D. 13–25 mm (large)
E. >25 mm (giant)

25. SAH Clinical and
Radiographic Severity
Scores

26. The initial clinical severity of SAH presentation varies
from very mild to critical.
SAH clinical severity is measured using:
a. The Hunt and Hess Scale
b. The World Federation of Neurological Surgeons
Scale (WFNSS)
c. Modified Fisher Scale

27. Hunt and Hess Scale
GRAD Hunt and Hess Scale
1 Asymptomatic or mild headache, minimal or no nuchal
rigidity
2 Moderate to severe headache, nuchal rigidity, and no
neurologic deficit other than cranial nerve palsy
3 Mild alteration in mental status (confusion, lethargy), with
or without mild focal neurologic deficit
4 Stupor and/or hemiparesis
5 Comatose and/or decerebrate rigidity and/or no motor
response

28. World Federation of Neurological
Surgeons Scale (WFNSS)
GRAD WFNSS
1 GCS score of 15, motor deficit absent
2 GCS score of 13-14, motor deficit absent
3 GCS score of 13-14, motor deficit present
4 GCS score of 7-12, motor deficit absent or
present
5 GCS score of 3-6, motor deficit absent or
present

29. Modified Fisher Scale
GRADE CHARACTERS
0  no SAH
 no IVH
 incidence of symptomatic vasospasm: 0%
1  focal or diffuse, thin SAH
 no IVH
 the incidence of symptomatic vasospasm: 24%
2  focal or diffuse, thin SAH
 IVH present
 the incidence of symptomatic vasospasm: 33%
3  thick SAH
 no IVH
 the incidence of symptomatic vasospasm: 33%
4  thick SAH
 IVH present
 the incidence of symptomatic vasospasm: 40%

30. Clinical
presentation
A. Neurological symptoms and signs
B. Non-neurologic symptoms and signs

31. Symptoms
1. Worst headache of life: sudden onset of severe
headache, this presentation accounts for only 10–50%
of patients with acute non-traumatic SAH
2. Sentinel headache: a new headache without other
associated SAH symptoms, leading to diagnosis of
aSAH(40%)
3. A change in headache characteristics
4. Nausea, often with vomiting
5. Sudden loss of consciousness, transient syncope
6. Acute onset or progressive altered mental status

32. Neurologic examination findings
1) Altered mental status
2) Abnormal Glasgow Coma Scale score
3) Focal cranial nerve palsies and ophthalmoplegia (eg, 3rd
nerve palsy from PcomA aneurysm, 6th nerve palsy from
increased ICP)
4) Meningismus: neck stiffness, photophobia
5) Terson syndrome: intraocular extension of SA blood
6) Focal neurologic deficits; Acute hemiparesis
7) Bilateral leg weakness and abulia due to mass effect from
hematoma in the interhemispheric fissure
8) Seizure or seizurelike events
9) Papilledema (18% of patients develop Terson syndrome)

34. Systemic manifestations
A. Acute hypertension
B. Cardiac dysrhythmia
C. Cardiac arrest
D. Hypotension/shock from neurogenic stunned
myocardium
E. Hypoxia from aspiration, respiratory
depression, or neurogenic pulmonary edema

35. Ottawa SAH Rule
A. Age ≥40 years
B. Neck pain or stiffness
C. Witnessed loss of consciousness
D. Onset during exertion
E. Thunderclap headache
F. Limited neck flexion on examination
Ottawa SAH Scale has 100% sensitivity (rule out
test)

36. INVESTIGATIONS
I. NCCT
II. Lumbar puncture
III. Vessel imaging
IV. Laboratory tests

37. Noncontrast head computed tomography
(NCCT)
NCCT is the most common modality that identifies the
presence of acute blood in the SA space.
It is most sensitive for SAH in the first 6 - 12h following
vessel rupture, with a sensitivity of 93% - 100%.
Diagnostic sensitivity by CT degrades over time,
declining to 60% at 7 days post-SAH.
For subacute or chronic SAH, MRI with GRE, SWI, or
FLAIR sequences have superior sensitivity compared to
NCCT
Secondary SAH has different CT characteristics and
tends to be present in the high cerebral convexity and
not centered around the basal cisterns as in aSAH

38. Characteristic CT Appearance of aSAH
CT features Aneurysmal location
Preponderance of SA blood in the basal
cisterns
All
SA blood along the sylvian fissure More common with MCA aneurysms
SA blood in the interhemispheric fissure More common with AcoA or ACA aneurysms
SA blood in the interpeduncular cistern All
SA blood in prepontine area, 4th ventricular
outlet, and foramen magnum
Posterior circulation aneurysms
Focal anterior temporal lobe intracerebral
hematoma
More common with MCA aneurysms
Focal frontal lobe intracerebral hematoma More common with AcoA or ACA aneurysms
Focal subarachnoid blood in the prepontine
area
Perimesencephalic SAH with no
cerebrovascular malformations identified

42. Lumbar Puncture and CSF Analysis
In cases of negative or equivocal imaging and high
clinical suspicion for SAH, lumbar puncture for
diagnostic CSF analysis can assist in the diagnosis of
acute SAH, although the value of lumbar puncture
has been questioned. The classic diagnostic
criterion is presence of xanthochromia on
laboratory spectrophotometry analysis.
Lumbar puncture offers the opportunity to measure
an opening pressure as a surrogate for ICP.

44. Lumbar Puncture and CSF Analysis
Xanthochromia + headache ➡subarachnoid
hemorrhage (SAH)
DD of xanthochromia
1) hyperbilirubinemia
2) previous traumatic tap
3) hypercarotenemia
4) Subarachnoid hemorrhage
5) Excess protein (> 150mg/dl)
6) free Hb

45. Vessel Imaging
CTA is the 1st-line vessel imaging modality. A negative
CTA is insufficient to rule out the presence of an
aneurysm, particularly when the aneurysm is < 4 mm
Cerebral CTA has 90% -97% sensitivity compared to
DSA with 3D reconstructions, which is the gold
standard diagnostic modality for cerebral aneurysms.
When cerebral aneurysms are detected on CTA,
patients still proceed to DSA, which is also a potential
therapeutic modality for endovascular treatment of
the aneurysm.

51. CTA
Advantages:
1) Less cost and radiation, easy to
perform, readily available
2) Time saving
3) Good sensitivity and specificity
4) Can predict patients needing
surgical clipping and avoid DSA
Disadvantages :
1. Poor sensitivity for small
aneurysms (<3 mm)
2. Poor detection of aneurysms
near the base of the skull
3. Poor negative predictive value,
needing DSA for confirmation
4. Poor detection of culprit
aneurysm in cases with multiple
aneurysm
DSA
Advantages:
1) The gold standard to detect
aneurysms
2) Can reliably predict neck
width
3) 2 negative DSA 7 days apart
exclude aneurysms
4) Better modality in cases with
a diffuse pattern of SAH
Disadvantages:
1. High radiation and iodine
dose
2. Invasive, involving risks of
complications such as arterial
puncture, emboli, dissection,
hemorrhage and septicemia

52. Magnetic Resonance Imaging
On FLAIR images, SAH appears as high signal-
intensity (white) in normally low signal-intensity
(black) CSF spaces.
FLAIR and CT scanning have similar findings
MRI is a useful to diagnose AVMs.
MRI can detect aneurysms 5 mm and is useful for
monitoring the status of small, unruptured
aneurysms.
MRI evaluate the degree of intramural thrombus in
giant aneurysms.

53. Magnetic Resonance Imaging
Magnetic resonance angiography offers benefits
such as its lower cost and the absence of
procedure-associated risk of stroke and arterial
injury.
MRA is an effective diagnostic procedure to
detect cerebrovascular disease

57. Laboratory studies
1. Serum chemistry panel
2. Complete blood count
3. PT/activated partial thromboplastin time
(aPTT)
4. Blood typing/screening
5. Cardiac enzymes
6. Arterial blood gas (ABG) determination

58. THANK YOU