SAH- it's a neurological emergency

1. BY DR.MAULIK
SR- NEUROLOGY

2.  Sub-arachnoid hemorrhage is a
neurological emergency in which there is
sudden extravasation of blood occurs in
subarachnoid space between the pial
and arachnoid membranes – leading to
thunderclap headache , described by
patient as “ worst headache of my life”.

4.  Subarachnoid hemorrhage (SAH), mostly
from rupturing of intracranial aneurysms,
accounts for 5% to 10% of all stroke cases
and is related to greater fatality than the
other forms of strokes.
 Case fatality of aneurysmal SAH ranges
between about 30% and 70%, with an
average of approximately 50%.
 In more than half of SAH survivors, the
level of disability is major; 60% of those
patients never achieve the quality of life
they enjoyed before the aneurysm
ruptured

5.  Primary spontaneous SAH-
 Aneurysmal SAH (80%)& Non-aneurysmal SAH(20%)
 Traumatic SAH (most common)
 Secondary to cerebral hemorrhage

6.  The true incidence of intracranial aneurysms remains
unknown, but the reported incidence varies from as low
as 0.2% to 10% of the general population.
 There is a rising occurrence of intracranial aneurysms
associated with increasing age and female gender .
 In the United States, the peak age for aneurysm rupture
is between 50 and 60 years of age . Overall, the female-
to-male ratio is approximately 2 : 1 in adults.
 Pediatric aneurysms are rare and account for about 1%
to 3% of aneurysmal SAH

7. TABLE 1 Risk Factors for the
Formation of and Rupture of
Intracranial Aneurysms
7

8.  Unruptured, asymptomatic aneurysms
are much less dangerous than a recently
ruptured aneurysm. The annual risk of
rupture for aneurysms <10 mm in size is
~0.1%, and for aneurysms ≥10 mm in size
is ~0.5–1%
 Giant aneurysms, those >2.5 cm in
diameter, occur at the same sites as
small aneurysms and account for 5% of
cases
 Their risk of rupture is ~6% in the first year
after identification and may remain high
indefinitely

9. • Saccular The most common intracranial aneurysm
morphology is the saccular aneurysm, which is a rounded berry-like
outpouching arising from first- and second-order branches in the
circle of Willis
it account for approximately 90% of intracranial aneurysms and are
responsible for most of the morbidity and mortality from SAH
• fusiform aneurysm is defined as a circumferential dilatation in
a segment of an intracranial artery
they are generally associated with atherosclerosis,
• dissecting aneurysm is formed as a result of splitting or
dissection of an arterial wall by blood flow entering through a tear.
This may cause a ballooning out on one side of the artery, with
arterial narrowing (a classic radiographic appearance of pearl-and-
string sign),

11. Approximately 90 to 95 percent of saccular aneurysms lie on the
anterior part of the circle of Willis .
The four most common sites are
(1)the proximal portions of the anterior communicating artery,
(2) at the origin of the posterior communicating artery from the stem
of the internal carotid,
(3) at the first major bifurcation of the middle cerebral artery, and
(4) at the bifurcation of the internal carotid into middle and anterior
cerebral arteries.
(5) Other sites include the internal carotid artery in cavernous sinus,
at the origin of the ophthalmic artery, the junction of the posterior
communicating and posterior cerebral arteries, the bifurcation of the
basilar artery, and the origins of the cerebellar arteries.

13. three patterns:
(1)the patient is stricken with an excruciating generalized
headache and vomiting and falls unconscious almost
immediately;
(2) severe generalized headache develops in the same
instantaneous manner but the patient remains relatively lucid
with varying degrees of stiff neck— the most common
syndrome;
(3) rarely, consciousness is lost so quickly that there is no
preceding complaint.
If the hemorrhage is massive, death may ensue in a matter
of minutes or hours

14. Rupture of the aneurysm usually occurs while the
patient is active rather than during sleep,
• sexual intercourse,
• straining at stool,
•lifting heavy objects,
•or other sustained exertion

15. there are few if any focal neurologic signs
As occurs when a jet of blood emanating from an aneurysm
ruptures into the adjacent brain or insular cistern and
produces a hemiparesis or other focal syndrome.
transient focal acute syndrome that occasionally occurs
in the territory of the aneurysm-bearing artery due to
transitory fall in pressure in the circulation distal to the
aneurysm or some form of acute transient vasospasm

16. Convulsive seizures, usually brief and generalized,
occur in 10 to 25 percent of cases according to Hart and
associates (but far less often in our experience) in
relation to acute bleeding or rebleeding.
Past h/o of sentinel headache should be asked.
“sentinel headache” or warning leak refer to both a
headache that precedes subarachnoid hemorrhage and to
a small leakage prior to a major rupture

17. Grade Description
World Federation of Neurological Surgeons Scale
1 Glasgow coma scale 15, no motor deficit
2 GCS 13 to 14, no motor deficit
3 GCS 13 to 14, with motor deficit
4 GCS 7 to 12, with or without motor deficit
5 GCS 3 to 6, with or without motor deficit

18. Grade Description
Hunt and Hess Scale
1 Asymptomatic or minimal headache and slight
nuchal rigidity
2 Moderate to severe headache, nuchal rigidity, no
neurological deficit other than cranial nerve palsy
3 Drowsiness, confusion, or mild focal deficit
4 Stupor, moderate to severe hemiparesis, possible
early decerebrate rigidity and vegetative
disturbances
5 Deep coma, decerebrate rigidity, moribund
appearance

19.  Cavernous portion or
1st
part of MCA (M1)
 AICA or PICA
 Pcom- ICA OR Pcom-
PCA junction
 Supraclinoid portion of
ICA near its bifurcation
to ACA-MCA
 Orbit or retro-orbital
pain
 Ipsilateral occipital or
cervical pain
 Ipsilateral partial 3rd
CN
palsy with dilated pupil
 Mono-ocular visual
field defect

20.  Rebleeding
 Hydrocephalus—acute , subacute or
delayed, chronic (NPH)
 Vasospasm
 hyponatremia

21.  Rerupture. The incidence of rerupture of
an untreated aneurysm in the first month
following SAH is ~30%, with the peak in
the first 7 days.
 Rerupture is associated with a 60%
mortality rate and poor outcome

22. Hydrocephalus.
 Acute hydrocephalus --- stupor and coma
Rx--- placement of an external ventricular drain.
 subacute hydrocephalus ---progressive drowsiness or
slowed mentation (abulia) with incontinence.
 Hydrocephalus is differentiated from cerebral
vasospasm with a CT scan, CT angiogram,
transcranial Doppler (TCD) ultrasound, or
conventional x-ray angiography.
 Hydrocephalus may clear spontaneously or require
temporary ventricular drainage.
 Chronic hydrocephalus ( weeks to months )--- gait
difficulty, incontinence, or impaired mentation.
 Subtle signs may be a lack of initiative in
conversation or a failure to recover independence.

23. •Vasospasm: Delayed hemiplegia and other deficits because of
focal vasospasm usually appear 3 to 10 days after rupture and rarely
before or after this period.
•Fisher and coworkers (1980) have shown that the most severe
vasospasm occurs in arteries that are surrounded by collections of
clotted subarachnoid blood after 24 hours
•vasospasm appears to be a direct effect of some blood product on
the adventitia of the adjacent artery.
• the mechanism is presumed to be purely a reduction in blood flow
distal to the area of vasospasm but therefore influenced by systemic
blood pressure and by collateral circulation in the cortex.

24.  Vasospasm causes fluctuating hemiparesis or
aphasia and increasing confusion that must be
distinguished from the effects of hydrocephalus
 Severe vasospasm is also visualized with MRA
and CT angiography.
 Transcranial Doppler ultrasonography –
measurement of blood flow velocity, the caliber
of the main vessels at the base of the brain
 progressive elevation of flow velocity in any one
vessel (especially if over 175 cm/s) suggests that
focal vasospasm is occurring.
 Should be performed daily or every other day in
patient with risk of developing vasospasm

25.  Severe cerebral edema in patients with
infarction from vasospasm may increase
the ICP enough to reduce cerebral
perfusion pressure.
 RX--- mannitol, hyperventilation, and
hemicraniectomy; moderate
hypothermia may have a role as well

26. Hyponatremia
 in the first 2 weeks following SAH.
 There is both natriuresis and volume depletion with
SAH, so that patients become both hyponatremic
and hypovolemic.
 Both atrial natriuretic peptide and brain natriuretic
peptide have a role in producing this “cerebral salt-
wasting syndrome.” Typically, it clears over the
course of 1–2 weeks and, in the setting of SAH,
should not be treated with free water restriction as
this may increase the risk of stroke

27.  CT BRAIN PLAIN
 LUMBAR PUNCTURE
 CT ANGIOGRAPHY OF BRAIN
 MRI BRAIN– FLAIR & GRE sequence
 CONVENTIONAL CATHETER
ANGIOGRAPHY

29.  Gold standard to detect SAH in acute
stage, detect blood in 95% cases in
acute stage ,sensitivity declines as
duration increases.
 predicting the location of the rupture site
 to predict the probability of vasospasm
 Can detect acute hydrocephalus.

30.  anterior interhemispheric fissure --
anterior communicating artery
aneurysm;
 sylvian fissure--- a middle cerebral artery
aneurysm;
 anterior perimesencephalic cistern---
posterior communicating or distal basilar
artery aneurysm

31. Group (Grade)
1
2
3
4
Description
No blood detected
A diffuse deposition or thin
layer with all vertical layers
of blood (interhemispheric
fissure, insular cistern,
ambient cistern) less than 1
mm thick)
Localized clots and/or
vertical layers of blood 1
mm or greater in thickness
Diffuse or no subarachnoid
blood, but with
intracerebral or
intraventricular clots

32. VASPSPASM
Subarachnoid
Blood
No.
Cases None
Slight-
Moderate Severe
Signs of
Severe Vasospasm
None 11 7 2 2 0
Diffuse
only
7 4 3 0 0
Clot or Thick
Layer
24 0 1 23 23
Diffuse or
None, with
Cerebral of
Ventricular
Blood
5 3 2 0 0
TOTAL 47 14 8 25 23

33.  if strong clinical suspicion for aneurysm rupture
but CT scan negative for SAH, lumbar
puncture should be performed.
 The sensitivity of lumbar puncture within 12
hours of hemorrhage is high .
 characteristics of cerebrospinal fluid (CSF) for
patients with SAH include increased red blood
cell count and xanthochromia.

34.  Lysis of the red blood cells and
subsequent conversion of hemoglobin to
bilirubin stains the spinal fluid yellow
within 6–12 h.
 This xanthochromic spinal fluid peaks in
intensity at 48 h and lasts for 1–4 weeks,
depending on the amount of
subarachnoid blood.

35.  the diagnosis of ruptured saccular aneurysm is
essentially excluded if blood is not present in
the CSF, provided the spinal fluid is examined
more than 30 min after the event.
 Xanthochromia is found after centrifugation if
several hours or more have elapsed from the
moment of the ictus.
 To determine whether xanthochromia is
present, fresh CSF must be centrifuged in a
tube with a conical bottom and the
supernatant compared to clear water in good
light or examined by spectrophotometric
techniques

36.  Collect CSF in several tubes & observe for
intensity of colour
 Opening pressure of CSF – usually increased
in SAH
 Xanthochromia s/o SAH
 In both a traumatic puncture and early in subarachnoid
hemorrhage, the proportion of WBCs to RBCs in the CSF is usually
the same as in the circulating blood (approximately 1:700), but in
some patients with genuine hemorrhage a brisk CSF leukocytosis
appears within 48 h, sometimes reaching more than 1,000
cells/mm3. The protein is slightly or moderately elevated and in
some instances glucose is reduced sometimes dramatically so.

38.  to reveal and characterize the size,
location, and morphology of
intracranial aneurysms -- MRA, CTA,
and conventional catheter
angiography.
 For the purpose of screening or as an
initial method for evaluating
unruptured intracranial aneurysms, less
invasive imaging modalities, either
MRA or CTA, are preferred

39.  in a case of clear SAH with negative CTA,
four-vessel conventional catheter
angiography with 3D reconstruction has
to be considered.
 If four-vessel angiography and/or CTA
does not reveal any source of the
hemorrhage, six-vessel angiography
(including external carotid injections)
should be performed to rule out rare
causes of hemorrhage such as a dural
fistula or venous pathology.

40.  In approximately 10% to 15% of patients
with SAH, no aneurysm or other source of
hemorrhage can be detected.
 If the amount of SAH is small and its
distribution is perimesencephalic, the
diagnosis of benign perimesencephalic
SAH may be established, and the prognosis
is often good.
 It is believed that benign
perimesencephalic SAH results from
spontaneous rupture of perimesencephalic
veins.

41.  In a patient with an extensive SAH but
negative angiography(may be due to
severe vasospasm) repeating the
imaging studies, including catheter
angiography or CTA, is mandatory.
 The repeat study should be performed 1
to 2 weeks after the initial study, paying
particular attention to identifying small
dissections.

42.  A negative angiogram may be
followed by a MRI scan of the brain
with cervical spine, to rule out other
sources of SAH.
 A tumor or vascular lesion, such as a
cavernous malformation in the
posterior fossa or upper cervical
spine, would not be visible on a
cerebral angiogram.

43.  Non-aneurysmal subarachnoid
hemorrhage is defined as nontraumatic,
spontaneous SAH of unknown etiology.
 The term angiographically negative SAH,
often used interchangeably with NASAH,
refers to the fact that conventional
cerebral angiography fails to reveal a
source for the hemorrhage
 Half of cases –due to perimesencephalic
SAH.

44. Perimesencephali
c NASAH is
characterized by
a distinctive
pattern of blood
seen on an initial
CT scan
performed within
hours of symptom
onset.
The subarachnoid
blood is confined
to the midbrain
cisterns, with no
evidence of
intraventricular or
intracerebral
hemorrhage

45.  younger and male.
 Gradual onset of headache.
 Loss of consciousness at onset is rare
 Benign course & a favorable prognosis
 very low risk of rebleeding,
hydrocephalus, or delayed cerebral
ischemia
 No need of repeat angiography
 No need of nimodipine
 Less morbidity & mortality

46.  Medical management
 Surgical management- “clipping” done
by neurosurgeons requiring craniotomy &
brain retraction. Metal clips are placed
across aneurysm neck.
 “coiling” done by endovascular surgeons
. A microcatheter is placed in the dome
of an aneurysm, and it is tightly packed
with a variety of coils to induce thrombosis

47.  surgical clipping has proven to be highly
effective, with reported rates of
complete aneurysm occlusion of
approximately 90% to 95%.
 High risk factors for surgery:
 intracranial aneurysms of the posterior circulation, such as the upper
basilar region,
 advanced patient age,
 large or giant aneurysms,
 a past history of ischemic cerebrovascular disease, and
 symptomatic aneurysms other than rupture.

48.  aneurysms not amenable to surgical
clipping.
 treat aneurysms located at the upper
basilar and paraclinoid regions, where
the surgical exposure of aneurysm is
challenging
 older-age patients and those with serious
comorbid medical conditions

49.  Current evidence supports that either
conventional open surgery or
endovascular treatment should be
performed as soon as possible after the
onset of SAH unless contraindicated
 it prevents devastating rebleeding and
enables aggressive hypervolemia/
hypertension/hemodilution (triple-H)
therapy for cerebral vasospasm.

50.  For a patient with a ruptured aneurysm in
the anterior circulation and Hunt and
Hess or World Federation of
Neurosurgeons (WFNS) grades 1 to 3,
surgical treatment is usually considered.
 Surgical treatment for a patient with
Hunt and Hess or WFNS grades 4 and 5 is
controversial owing to the overall poor
outcome regardless of the surgery

51.  VASOSPASM--Angiographic vasospasm is seen in
70% of patients with aneurysmal SAH. clinically
symptomatic in about 30% of those patients
 New neurological signs or worsening of
preexisting neurological deficits suggest
symptomatic vasospasm
 Daily TCD monitoring can provide useful
information at the bedside in this setting. An
elevation of blood flow velocity on TCD and/or
high pulsatility index suggest cerebral vasospasm

52.  The main goal of treatment is to prevent
permanent deficits from ischemia, not to treat
angiographic vasospasm.
 Studies have shown that nimodipine reduces
morbidity from delayed ischemia due to
vasospasm . On the other hand, those studies
also demonstrated that nimodipine did not
reduce the actual frequency of vasospasm
itself. Explanations could be the
neuroprotective effect of nimodipine or the
dilatation of smaller distal arterioles

53.  Tab.Nimodipine 60mg QDS should be
started within 4 days of onset and
continued for 21 days.
 Prophylactic AED: in those with acute
seizure –continue for 6 months.
 Without seizure– should be given in those
with unsecured aneurysm/ large
concentration of blood at cortex.

54.  aggressive triple-H therapy is used to
improve cerebral perfusion in those
patients whose ruptured aneurysms are
treated by either surgical clipping or
endovascular coiling
 Prophylactic triple-H therapy for
asymptomatic vasospasm patients
remains controversial due to known
complications including cardiac failure,
pulmonary edema, hemorrhagic
transformation of infarcted tissue, and
worsening of cerebral edema

55.  Endovascular treatment: angioplasty using
a microballoon and superselective injection
of vasodilator into the affected arteries.
 balloon angioplasty--effect lasts longer
than vasodilator inj & used for relatively
proximal arteries
 superselective injection of
vasodilators(papaverine, verapamil, fasudil
hydrochloride) is most useful for distal spasm
 Although they improve angiographic
vasospasm but don’t improve clinical
outcome– so remains controversial.

56.  Hyponatremia– careful monitoring of
fluid level in body & S.Na level daily or
twice daily in first 2 weeks required
 Whenever hyponatremia found in
patient with symptomatic vasospasm–
treat with 3% NS.

57.  Hydrocephalus:
 Acute hydrocephalus– non-
communicating type– should be
differentiated from vasospasm &
hyponatremia by CT BRAIN.
 RX--- ventriculostomy with CSF drainage
in selected patients.
 Chronic hydrocephalus- communicating
type-
 RX-- lumbar puncture, ventricular
drainage, and surgical insertion of a

58. Using a discriminant function analysis, the relative importance of factors
prognostic for outcome was, in order of importance:
1. Whether the patient was treated surgically:
Patients subjected to definitive obliteration of the aneurysm (65%) did
much better than those whose aneurysms were not clipped, with a
mortality of 25% compared to 86% (P<0.001)
2. Neurological grade on admission:
a) Hunt and Hess: Mortality increased with worsening neurological grade,
being 23% for Grade III, 44% for Grade IV and 91% for Grade V. Good
outcome occurred in 30% of Grade III, 14% of Grade IV and no Grade V
patients (P<0.001)
b) GCS: Mortality was inversely related to admission GCS at 29% for GCS
11 to 14, 42% for GCS 7 to 10 and 70% for GCS 3 to 6. Good outcome
occurred in 29% for GCS 11-14, 14% for GCS 7-10 and 7% for GCS 3-6
(P=0.01)

59. 3. Age:
Younger patients had more good outcomes and lower
mortality. The mean age for good outcome was 46 and
for death, 58 years.
4. Initial systolic blood pressure:
When categorized by initial systolic BP (<141, 141-180,
>180), patients with higher systolic BP were less likely to
have a good outcome and had a higher mortality rate
(P<0.05)
5. Aneurysm size:
A bad outcome was seen in 72% of patients with
aneurysm diameter >21 mm and 56% with aneurysm
diameter 4-6 mm
Prognostic Factors in Aneurysmal SAH .../cont’d

60. Genetics of Intracranial Aneurysms
Ref. Neurosurgery clinics of North America, July 1998, pp 485-493
Observations to suggest genetic involvement:
Association of various heritable disorders with ICA
The familial aggregation of ICA in the absence of known systemic
disorder
Heritable Disorders associated with ICA:
Heritable CT disorder account for at least 5% of the cases of ICA
True frequency may be higher due to variability in phenotypic expression
and negative family history due to new mutation
The most important ones are:
Ehlers-Danlos type IV
Marfan’s syndrome
NF1
ADPKD

61. Screening for familial ICA
Why?
Poor prognosis once ruptured
Low surgical risk for the nonruptured (5% morbidity, 2% mortality)
Caveat: aneurysms may develop over short period of time
Indication for surgery for asymptomatic ICA is still unclear (critical size)
Who?
Families with two or more affected members
Restricted to first-degree relatives (yield 9-29%)
Monozygotic twin
When?
Screening between the ages of 35-65
Youngest patient with familial ICA is 6 years old
De novo aneurysms occur at a rate of 2% per year
Repeat screening at 6-month to 5-year intervals

62. Screening for familial ICA …/cont’d
How?
MRA is the most widely used
Critical size for detection 3-5 mm
Helical CT angiography
Coventional angiography
ICA gene
Current approaches
Screen the human genome for ICA gene by testing a large number of
distinct highly pleomorphic genetic markers
Analyze variations in the sharing of marker alleles among affected
sibling pairs
Candidate gene sequence analysis e.g., PKD1 or COL3A1

63. Disorder Inheritance
Pattern
Locus Gene Gene Product
Achondroplasia AD 4p16.3 FGFR3 Fibroblast growth
factor receptor 3
Alkaptonuria AR 3q2 AKU ?
ADPKD AD 16p13.3 PKD1 Polycystin
Cohen syndrome AR 8q22 CHS1 ?
Ehlers-Danlos
Syndrome type I
AD 9q COL5A1 Ollagen type V
Ehlers-Danlos
Syndrome type IV
AD 2q31 COL3A1 Collagen type III
Fabry disease AR XL-R Xq22.1 -galactosidase A
Kahn syndrome AR ? ? ?
Marfan’s syndrome AD 15q21.1 FBN1 Fibrillin-1
NF1 AD 17q11.2 NF1 Neurofibromin
Noonan syndrome AD 12q22 NS1 ?

64. 1. BRADLEY’S NEUROLOGY IN CLINICAL PRACTICE- 7TH
EDITIION
2. ADAMS & VICTOR’S PRINCIPLE OF CLINICAL NEUROLOGY –9TH
EDITION
3. Avoiding Pitfalls in the Diagnosis of Subarachnoid Hemorrhage. JA
Edlow and LR Caplan. N Engl J Med 342:29-36, 2000
4. 2. Unruptured Intracranial Aneurysms - Risk of Rupture and Risks of
Surgical Intervention. ISUIA Investigators. N Engl J Med; 339: 1725-33,
1998
5. 3. Intracranial Aneurysms and Subarachnoid Hemorrhage: An
Overview. B Weir and RL Macdonald. Chapter 214 (pp 2191-2213) in
Neurosurgery, 2nd edition, volume II, 1996, editors RH Wilkins and SS
Rengachary, published by McGraw-Hill
6. 4. Relation of Cerebral Vasospasm to Subarachnoid Hemorrhage
Visualized by Computerized Tomographic Scanning. CM Fisher JP
Kistler and JM Davis. Neurosurgery, 6:1-9, 1980
7. 5. Factors Influencing the Outcome of Aneurysm Rupture in Poor
Grade Patients: A Prospective Series. L Disney, B Weir, M Grace et al
Neurosurgery 23: 1-9 1988

69. (2)Most common aneurysm causing
aSAH
(a) berry aneurysm
(b)dissecting aneurysm
(c) fusiform aneurysm
(d)mycotic aneurysm

76.  Wednesday long case– Dr.RAJENDRA
PANDEY
 Thursday – journal presentation