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

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

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

Pt/ptt

Buse/creat

Lft/cs/mg/po4

RBS

Lft

gxm

Cxr

Ct brain

CTA

DSA

TCD

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

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

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 theplace 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