CEREBRAL ANEURYSM:

ANESTHETIC MANAGEMENT

KEY TOPICS Introduction Anatomy Scoring systems Anaesthetic consideration Intervention General intensive care mx Prognosis Conclusion

INTRODUCTION 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

RISK FACTORS Smoking Hypertension Alcohol intake FHx Genetics: Ehler Danlos, PCKD Recreational sympatomimetics drugs Multiple aneurysm : smoking, hpt, post

menopausal, hx of CVA, FHx

OUTCOME OF SAH(ISUIA 1998)

endovascular services

the volume of SAH

type of facility in which thepatient is first evaluated

severity of initial hemorrhage agesextime to treatment medical comorbidities

size, location in the posterior circulation morphology

PATIENT ANEURYSM INSTITUTION

ISUIA- International Study Of Unruptured Intracranial aneurysm

SX Asymptomatic Headache Neck stiffness Nausea & vomiting LOC Neurological deficit

PATHOPHYSIOLOGY 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 dsEhlers Danlos Type 4Familiail intracerebral aneurysms

TYPE OF CEREBRAL ANEURYSM

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 % )

SCORING Hunt & Hess WFNS Fischer staging

HUNT & HESSGRADE

FEATURES MORBIDITY

MORTALITY

0 unruptured aneurysm 0-2% 0-2%

1 Asymptomatic, min. headache and sl.nuchal rigidity

2-5 % 2%

2 Moderate to severe headache, nuchalrigidity, but no neurologic deficit other thancranial nerve palsy

5-10% 7 %

3 Somnolence, confusion, medium focaldeficits

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%

WFNSGRADE GCS MOTOR

DEFICITREMARKS

0 15 - INTACT ANAEURSYM

1 15 -

2 13-14 -

3 13-14 +

4 7-12 +-

5 3-6 +-

FISCHER STAGINGGRADE FINDINGS

1 No blood visualized

2 diffuse deposition or thin layer with all verticallayers of blood (interhemispheric fissure, insularcistern, ambient cistern) less than 1 mm thick

3 Localized clots and/or vertical layers of blood 1 mmor greater in thickness

4 Diffuse or no subarachnoid blood, but withintracerebral or intraventricular clots

DIAGNOSTIC IMAGING CT scan (no contrast) MRI with haemosiderin-sensitive

sequences LP CT angiogram – identify cause of SAH DSA –digital subtraction angiography

ANAESTHETIC MX PERIOPERATIVE INTRAOPERATIVE POSTOPERATIVE

PERIOPERATIVE 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

IXblood radiological others

FbcPt/pttBuse/creatLft/cs/mg/po4RBSLftgxm

CxrCt brainCTADSATCD

12 lead ecgCEUrine NA/ osmolarity

CVS COMPLICATIONS OF SAH

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 &

posteriorhypothalamus injury

INTRACRANIAL ANEURYSM RUPTURE Loss of consciousness Hydrocephalus Vasospasm Intracerebral & intraventricular

haematomas Cerebral oedema

MANAGEMENT OF RUPTURED ANEURYSM

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

INTRAOP MONITORING INDUCTION MAINTAINANCE EMERGENCE

INDUCTION 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

AHA( 2009) 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

INTRA-OP ANEURYSM RUPTURE 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

POSTOPERATIVE BP control Pain & anxiety Seizure prophylaxis Vasospasm Rebleeding Glucose control VTE

ANEURYSMAL REBLEEDING 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% )

CEREBRAL VASOSPASM 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

CEREBRAL VASOSPASM 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

AHA 2009 1. Oral nimodipine is indicated to reduce poor outcomerelated to aneurysmal SAH (Class I, Level of Evidence A). 2. Treatment of cerebral vasospasm begins with early

managementof 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 vasospasmis volume expansion, induction of hypertension,and hemodilution (triple-H therapy) (Class IIa, Level of Evidence B). 4. Alternatively, cerebral angioplasty and/or selective intraarterialvasodilator 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 SAHLarge subarachnoid blood load

Intraventricular haemorrhage

smokers

PROGNOSIS

RUPTURED

UNRUPTURED

Morbidity 30-45% Morbidity 1 %

mortality 30-50% mortality 4.1 %

RISK OF RUPTURED ANEURYSM:(ISUIA 1998) larger aneurysm posterior circulation prev hx of SAH inc age smoker aspect ratio( height and neck of

aneurysm)

CONTROVERSY 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