cerebral aneurysm
TRANSCRIPT
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CEREBRAL ANEURYSM:
ANESTHETIC MANAGEMENT
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KEY TOPICS Introduction Anatomy Scoring systems Anaesthetic consideration Intervention General intensive care mx Prognosis Conclusion
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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%)
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Mortality 50% 25% dying before reaching hospital 1/3 of survivors dependent for care Almost ½ will have cognitive impairment
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RISK FACTORS Smoking Hypertension Alcohol intake FHx Genetics: Ehler Danlos, PCKD Recreational sympatomimetics drugs Multiple aneurysm : smoking, hpt, post
menopausal, hx of CVA, FHx
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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
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SX Asymptomatic Headache Neck stiffness Nausea & vomiting LOC Neurological deficit
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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
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TYPE OF CEREBRAL ANEURYSM
SHAPE SIZE
Saccular/ berry** Small ( < 11mm)
Lateral Large ( 11-25mm)
fusiform Giant ( > 25 mm)
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RUPTURED: Unruptured:1-2%/yr rupture Ruptured: 50% rerupture within 6/12
Vulnerable : vascular bifurcation Sites: anterior circulation ( 80-90% ) posterior circulation (10-20 % )
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SCORING Hunt & Hess WFNS Fischer staging
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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%
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WFNSGRADE GCS MOTOR
DEFICITREMARKS
0 15 - INTACT ANAEURSYM
1 15 -
2 13-14 -
3 13-14 +
4 7-12 +-
5 3-6 +-
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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
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DIAGNOSTIC IMAGING CT scan (no contrast) MRI with haemosiderin-sensitive
sequences LP CT angiogram – identify cause of SAH DSA –digital subtraction angiography
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ANAESTHETIC MX PERIOPERATIVE INTRAOPERATIVE POSTOPERATIVE
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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
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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
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IXblood radiological others
FbcPt/pttBuse/creatLft/cs/mg/po4RBSLftgxm
CxrCt brainCTADSATCD
12 lead ecgCEUrine NA/ osmolarity
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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
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INTRACRANIAL ANEURYSM RUPTURE Loss of consciousness Hydrocephalus Vasospasm Intracerebral & intraventricular
haematomas Cerebral oedema
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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
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INTRAOP MONITORING INDUCTION MAINTAINANCE EMERGENCE
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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
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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
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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
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POSTOPERATIVE BP control Pain & anxiety Seizure prophylaxis Vasospasm Rebleeding Glucose control VTE
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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% )
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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
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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
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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).
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Higher risk of vasospasm in:Poor grade SAHLarge subarachnoid blood load
Intraventricular haemorrhage
smokers
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PROGNOSIS
RUPTURED
UNRUPTURED
Morbidity 30-45% Morbidity 1 %
mortality 30-50% mortality 4.1 %
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RISK OF RUPTURED ANEURYSM:(ISUIA 1998) larger aneurysm posterior circulation prev hx of SAH inc age smoker aspect ratio( height and neck of
aneurysm)
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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
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