Cerebral aneurysm.

Cerebral aneurysms-types, treatment and otcome.

1. Cerebral Aneurysm: Anesthetic Management

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

3. 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%)

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

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

6. Outcome Of SAH( ISUia 1998) 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. SX Asymptomatic Headache Neck stiffness Nausea & vomiting LOC Neurological deficit

8. 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 ds Ehlers Danlos Type 4 Familiail intracerebral aneurysms

9. TYPE OF CEREBRAL ANEURYSM 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. SCORING Hunt & Hess WFNS Fischer staging

12. HUNT & HESS GRADE FEATURES MORBIDITY MORTALITY 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%

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

14. Fischer Staging 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

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

16. ANAESTHETIC MX PERIOPERATIVE INTRAOPERATIVE POSTOPERATIVE

17. 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

18. 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

19. IX 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

20. 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 & posterior hypothalamus injury

21. Intracranial Aneurysm rupture Loss of consciousness Hydrocephalus Vasospasm Intracerebral & intraventricular haematomas Cerebral oedema

22. 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

23. INTRAOP MONITORING INDUCTION MAINTAINANCE EMERGENCE

24. 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

25. 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

26. 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

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

28. 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% )

29. 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

30. 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

31. AHA 2009 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).

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

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

34. Risk of ruptured aneurysm :(ISUIA 1998) larger aneurysm posterior circulation prev hx of SAH inc age smoker aspect ratio( height and neck of aneurysm)

35. 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