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 Introduction 
 Anatomy 
 Scoring systems 
 Anaesthetic consideration 
 Intervention 
 General intensive care mx 
 Prognosis 
 Conclusion
 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%)
 Mortality 50% 
 25% dying before reaching hospital 
 1/3 of survivors dependent for care 
 Almost ½ will have cognitive impairment
 Smoking 
 Hypertension 
 Alcohol intake 
 FHx 
 Genetics: Ehler Danlos, PCKD 
 Recreational sympatomimetics drugs 
 Multiple aneurysm : smoking, hpt, post 
menopausal, hx of CVA, FHx
PATIENT ANEURYSM INSTITUTION 
 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 
ISUIA- International Study Of Unruptured Intracranial aneurysm
 Asymptomatic 
 Headache 
 Neck stiffness 
 Nausea & vomiting 
 LOC 
 Neurological deficit
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
SHAPE SIZE 
Saccular/ berry** Small ( < 11mm) 
Lateral Large ( 11-25mm) 
fusiform Giant ( > 25 mm)
 RUPTURED: 
 Unruptured:1-2%/yr rupture 
 Ruptured: 50% rerupture within 6/12 
 Vulnerable : vascular bifurcation 
 Sites: 
 anterior circulation ( 80-90% ) 
 posterior circulation (10-20 % )
 Hunt & Hess 
 WFNS 
 Fischer staging
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%
GRADE GCS MOTOR DEFICIT REMARKS 
0 15 - INTACT 
ANAEURSYM 
1 15 - 
2 13-14 - 
3 13-14 + 
4 7-12 +- 
5 3-6 +-
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
CT scan (no contrast) 
MRI with haemosiderin-sensitive sequences 
LP 
CT angiogram – identify cause of SAH 
DSA –digital subtraction angiography
 PERIOPERATIVE 
 INTRAOPERATIVE 
 POSTOPERATIVE
 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
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
blood radiological others 
Fbc 
Cxr 
Pt/ptt 
Ct brain 
Buse/creat 
CTA 
Lft/cs/mg/po4 
DSA 
RBS 
TCD 
Lft 
gxm 
12 lead ecg 
CE 
Urine NA/ osmolarity
 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
 Loss of consciousness 
 Hydrocephalus 
 Vasospasm 
 Intracerebral & intraventricular haematomas 
 Cerebral oedema
 International subarachnoid aneurysm trial (ISAT) 
 Multicentre randomized controlled trial 
Endovascular 
coiling 
Clipping reserved for aneurysms not suitable for coiling 
 those with wide neck, MCA 
Surgical clipping 
Primary outcome 
(risk of death or 
dependence at 
1yr) 
23.7% 30.9% 
Long term: 
delayed 
retreatment 
higher lower
 MONITORING 
 INDUCTION 
 MAINTAINANCE 
 EMERGENCE
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
 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
 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
 BP control 
 Pain & anxiety 
 Seizure prophylaxis 
 Vasospasm 
 Rebleeding 
 Glucose control 
 VTE
 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% )
 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
 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
 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).
Higher risk of vasospasm in: 
Poor grade SAH 
Large subarachnoid blood 
load 
Intraventricular 
haemorrhage 
smokers
RUPTURED UNRUPTURED 
Morbidity 30-45% Morbidity 1 % 
mortality 30-50% mortality 4.1 %
 larger aneurysm 
 posterior circulation 
 prev hx of SAH 
 inc age 
 smoker 
 aspect ratio( height and neck of aneurysm)
 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
Cerebral aneurysm.

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Cerebral aneurysm.

  • 1.
  • 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. PATIENT ANEURYSM INSTITUTION  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 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 % )
  • 11.
  • 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 Cxr Pt/ptt Ct brain Buse/creat CTA Lft/cs/mg/po4 DSA RBS TCD Lft gxm 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 Endovascular coiling Clipping reserved for aneurysms not suitable for coiling  those with wide neck, MCA 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