2.  Introduction
 Anatomy
 Scoring systems
 Anaesthetic consideration
 Intervention
 General intensive care mx
 Prognosis
 Conclusion

3.  1-6% of the populations
 SAH in 8-10:100,000 persons per year
 1-2% risk of haemorrhage for unruptured
aneurysms
 85% of non traumatic SAH- Ruptured
intracranial aneurysm
 Age 40-60
 Female (60%)

4.  Mortality 50%
 25% dying before reaching hospital
 1/3 of survivors dependent for care
 Almost ½ will have cognitive impairment

5.  Smoking
 Hypertension
 Alcohol intake
 FHx
 Genetics: Ehler Danlos, PCKD
 Recreational sympatomimetics drugs
 Multiple aneurysm : smoking, hpt, post
menopausal, hx of CVA, FHx

6.  endovascular
services
 the volume of
SAH
 type of facility in
which thepatient
is first evaluated
severity of initial
hemorrhage
age
sex
time to treatment
medical
comorbidities
size,
location in the
posterior
circulation
morphology
PATIENT ANEURYSM INSTITUTION
ISUIA- International Study Of Unruptured Intracranial aneurysm

7.  Asymptomatic
 Headache
 Neck stiffness
 Nausea & vomiting
 LOC
 Neurological deficit

8.  Congenital or acquired-85% intracranial
aneurysms ( internal elastic lamina)
 AV malformations
 Trauma
 Rare – Moyamoya disease
 Increase risk of SAH:
 Hypertension, atherosclerosis, cocaine, alcohol abuse,
smoking
 Autosomal-dominant polycystic kidney ds
 Ehlers Danlos Type 4
 Familiail intracerebral aneurysms

9. SHAPE SIZE
Saccular/ berry** Small ( < 11mm)
Lateral Large ( 11-25mm)
fusiform Giant ( > 25 mm)

10.  RUPTURED:
 Unruptured:1-2%/yr rupture
 Ruptured: 50% rerupture within 6/12
 Vulnerable : vascular bifurcation
 Sites:
 anterior circulation ( 80-90% )
 posterior circulation (10-20 % )

12.  Hunt & Hess
 WFNS
 Fischer staging

13. GRAD
E
FEATURES MORBIDI
TY
MORTALI
TY
0 unruptured aneurysm 0-2% 0-2%
1 Asymptomatic, min. headache and sl.
nuchal rigidity
2-5 % 2%
2 Moderate to severe headache, nuchal
rigidity, but no neurologic deficit
other than
cranial nerve palsy
5-10% 7 %
3 Somnolence, confusion, medium focal
deficits
5-10% 25%
4 Stupor, hemiparesis medium or
severe,
possible early decerebrate rigidity,
vegetative disturbances
25-30% 25%
5 Deep coma, decerebrate rigidity,
moribund appearance
40-50% 30-40%

14. GRADE GCS MOTOR DEFICIT REMARKS
0 15 - INTACT
ANAEURSYM
1 15 -
2 13-14 -
3 13-14 +
4 7-12 +-
5 3-6 +-

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

16. CT scan (no contrast)
MRI with haemosiderin-sensitive sequences
LP
CT angiogram – identify cause of SAH
DSA –digital subtraction angiography

17.  PERIOPERATIVE
 INTRAOPERATIVE
 POSTOPERATIVE

18.  General and specific cdtn related to cerebral
anaeurysm
 History, physical ex, relevant ix
 Detail neurological assessment
 Cx of SAH:
 Rebleeding
 Vasospasm
 Hydrocephalus (EVD, ICP monitoring )
 Seizure

19. Systemic problems related to SAH :
 CVS
 Electrolyte abnormalities eg hyponatraemia
 Related medication:
 Antiepileptic
 Stress ulcer prophylaxis
 Intravascular volume status
 Premedications:
 Anxiolytics agent
 Acid aspiration prophylaxis

20. blood radiological others
Fbc
Pt/ptt
Buse/creat
Lft/cs/mg/po4
RBS
Lft
gxm
Cxr
Ct brain
CTA
DSA
TCD
12 lead ecg
CE
Urine NA/ osmolarity

21.  ECG abnormalities
 25-100% of SAH patients
 higher in poor grade patients
 T wave inversion & ST depression (most
common)-neurogenic stress/ stunned
myocardium
 Prolong QT (arterial & ventricular dysrhytmias)
 Q waves
***sympathetic cathecolamine release & posterior
hypothalamus injury

22.  Loss of consciousness
 Hydrocephalus
 Vasospasm
 Intracerebral & intraventricular haematomas
 Cerebral oedema

23.  International subarachnoid aneurysm trial (ISAT)
 Multicentre randomized controlled trial
Clipping reserved for aneurysms not suitable for coiling
 those with wide neck, MCA
Endovascular
coiling
Surgical clipping
Primary outcome
(risk of death or
dependence at
1yr)
23.7% 30.9%
Long term:
delayed
retreatment
higher lower

24.  MONITORING
 INDUCTION
 MAINTAINANCE
 EMERGENCE

25. Good SAH grade
 Near normal ICP
 Less prone to develop
ischemia
 More chance of
rupture
 Can tolerate fall in BP
up to 30-35%
 Can not tolerate
much fall in CBF:
don’t hyperventilate
Poor SAH grade
 Raised ICP
 Relatively protected
against rupture
 More at risk of
ischemia
 Can not tolerate
much fall in BP
 Hyperventilation
improves CPP

26.  1. Minimizing the degree and duration of
intraoperative hypotension during aneurysm
surgery is probably indicated
(Class IIa, Level of Evidence B).
 2. There are insufficient data on
pharmacological strategies and induced
hypertension during temporary vessel occlusion
to make specific recommendations, but there
are instances when their use may be considered
reasonable(Class IIb, Level of Evidence C).
 3. Induced hypothermia during aneurysm surgery
may be a reasonable option in some cases but is
not routinely recommended (Class III, Level of
Evidence B).***IHAST trial 2005

27.  Incidence
-Aneurysm leak: 6%
-Frank rupture: 13%
-Combined incidence: 19%
 When does it occur?
-Before dissection (7%)
-During dissection (48%)
-During clip placement (45%)
 Increases overall mortality & morbidity
 Better prognosis if occurs after opening of dura

28.  BP control
 Pain & anxiety
 Seizure prophylaxis
 Vasospasm
 Rebleeding
 Glucose control
 VTE

29.  Rate of rebleeding:
 4% during the first 24 hrs
 1.5% per day
 19% first 2 weeks
 50% first 6 months
 3% per year
 Mortality ( 78% )

30.  13.5% of mortality & morbidity.
 cerebral ischaemia & infarction
 Rare in the first 72 hrs after SAH,
 Peaks 5-7 days, resolves after 14 days
 Angiographic vasospasm 40-60%
 Symptoms in 20-30%
 Aetiology
 Vasoactive substances (free oxyHb)
 Stimulation of Endothelin1& inhibition of Nitric Oxide

31.  Calcium channel blocker (Nimodipine)-British
nimodipine trial
 Intraop clot removal
 Hypervolaemic Hypertensive Haemodilution
(triple H)-???
 Clot lysis(1-Transluminal angioplasty 2-Intra-
arterial papaverine)
 Mg (IMASH trial)
 Statin tx ( STASH trial )
 Antiplatelet tx

32.  1. Oral nimodipine is indicated to reduce poor outcome
related to aneurysmal SAH (Class I, Level of Evidence A).
 2. Treatment of cerebral vasospasm begins with early management
of the ruptured aneurysm, and in most cases,maintaining normal
circulating blood volume and avoiding hypovolemia are probably
indicated (Class IIa, Level of Evidence B).
 3. One reasonable approach to symptomatic cerebral vasospasm
is volume expansion, induction of hypertension,and hemodilution
(triple-H therapy) (Class IIa, Level of Evidence B).
 4. Alternatively, cerebral angioplasty and/or selective intraarterial
vasodilator therapy may be reasonable after,together with, or in the
place of triple-H therapy, dependingon the clinical scenario (Class IIb,
Level of Evidence B).

33. Higher risk of vasospasm in:
Poor grade SAH
Large subarachnoid blood
load
Intraventricular
haemorrhage
smokers

34. RUPTURED UNRUPTURED
Morbidity 30-45% Morbidity 1 %
mortality 30-50% mortality 4.1 %

35.  larger aneurysm
 posterior circulation
 prev hx of SAH
 inc age
 smoker
 aspect ratio( height and neck of aneurysm)

36.  Early vs delay surgical
intervention(International Cooperative study on
the timing of aneurysm surgery (1990)
 HHH tx
 Anticonvulsant prophylaxis
 Antifibrinolytic tx
 Family screening( level C)
 Optimal glucose level
 Pyrexia
 Statin tx
 MG tx