Cerebral aneurysm

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Cerebral aneurysm

  1. 1.  Introduction  Anatomy  Scoring systems  Anaesthetic consideration  Intervention  General intensive care mx  Prognosis  Conclusion
  2. 2.  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%)
  3. 3.  Mortality 50%  25% dying before reaching hospital  1/3 of survivors dependent for care  Almost ½ will have cognitive impairment
  4. 4.  Smoking  Hypertension  Alcohol intake  FHx  Genetics: Ehler Danlos, PCKD  Recreational sympatomimetics drugs  Multiple aneurysm : smoking, hpt, post menopausal, hx of CVA, FHx
  5. 5.  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
  6. 6.  Asymptomatic  Headache  Neck stiffness  Nausea & vomiting  LOC  Neurological deficit
  7. 7.  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
  8. 8. SHAPE SIZE Saccular/ berry** Small ( < 11mm) Lateral Large ( 11-25mm) fusiform Giant ( > 25 mm)
  9. 9.  RUPTURED:  Unruptured:1-2%/yr rupture  Ruptured: 50% rerupture within 6/12  Vulnerable : vascular bifurcation  Sites:  anterior circulation ( 80-90% )  posterior circulation (10-20 % )
  10. 10.  Hunt & Hess  WFNS  Fischer staging
  11. 11. 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%
  12. 12. GRADE GCS MOTOR DEFICIT REMARKS 0 15 - INTACT ANAEURSYM 1 15 - 2 13-14 - 3 13-14 + 4 7-12 +- 5 3-6 +-
  13. 13. 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
  14. 14. CT scan (no contrast) MRI with haemosiderin-sensitive sequences LP CT angiogram – identify cause of SAH DSA –digital subtraction angiography
  15. 15.  PERIOPERATIVE  INTRAOPERATIVE  POSTOPERATIVE
  16. 16.  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
  17. 17. 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
  18. 18. 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
  19. 19.  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
  20. 20.  Loss of consciousness  Hydrocephalus  Vasospasm  Intracerebral & intraventricular haematomas  Cerebral oedema
  21. 21.  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
  22. 22.  MONITORING  INDUCTION  MAINTAINANCE  EMERGENCE
  23. 23. 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
  24. 24.  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
  25. 25.  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
  26. 26.  BP control  Pain & anxiety  Seizure prophylaxis  Vasospasm  Rebleeding  Glucose control  VTE
  27. 27.  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% )
  28. 28.  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
  29. 29.  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
  30. 30.  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).
  31. 31. Higher risk of vasospasm in: Poor grade SAH Large subarachnoid blood load Intraventricular haemorrhage smokers
  32. 32. RUPTURED UNRUPTURED Morbidity 30-45% Morbidity 1 % mortality 30-50% mortality 4.1 %
  33. 33.  larger aneurysm  posterior circulation  prev hx of SAH  inc age  smoker  aspect ratio( height and neck of aneurysm)
  34. 34.  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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