1. Anesthesia For Intracranial Vascular Lesions

3.  Epidemiology  Understand pathophysiology of aneurysms  Presentation of I.C aneurysms  complications of I.C aneurysms

4.  Recognize the different treatment modalities of intracranial aneurysms  Understand the basic anesthetic management of intracranial aneurysm clipping  Select an anesthetic plan utilizing medications and or therapies designed to reduce brain injury during cerebral aneurysm repair.

6.  Incidence : 1 to 6%  Incidence of ruptured aneurysm: 12/100,000  Age: any age, peaks 40 - 60  Sex: M/F 2:3  Sites : 30% ICA 40% ACA 20% MCA,10% Vertebro-basilar systems

8.  Causes  Risk Factors  Classification  Locations  Neuronal injury and death

9. Causes Intracranial aneurysms are most likely to develop over the course of an individual’s life, with only 10%accountable to a genetic/familial cause, it is primarily acquired 90%.

10. Inherited RF Others  Polycystic kidney disease Over 50 years of age  Type IV Ehler Danlos syndrome Female gender  Pseudoxanthoma elasticum Smoking  Neurofibromatosis type 1 Infection of vessel wall  Alpha 1 antitrypsin deficiency Head trauma  Coarctation of the aorta Septic emboli  Fibromuscular dysplasia Hypertension  Pheochromocytoma Alcohol abuse  Klinfelter’s syndrome Oral contraceptive pills  Tuberous sclerosis hypercholesterolemia

11.  True or false  By size: Small: ≤ 10mm Large: 11 to 25mm Giant: > 25mm

12.  By shape: –Saccular –berry aneurysm –Fusiform

14. Brain Ischemia Global Focal Hypoperfusion contains tworegions Vasospasm. 1 st region receives no blood flow. 2 nd receives collateral flow and is partially ischemic.

15.  Early is excitotoxicity.

16.  Delayed Is death caused by apoptosis

18. Ruptured Unruptured (SAH) asymptomatic ICP Hydrocephalus Global,focal neurological deficits Meningeal irritation (initially may be due intracerebral bleeding, or from herniation).

20.  Rebleeding  Vasospasm  Hydrocephalus  Seizure(seizure prone for 18 months after SAH)

21. Aneurysmal Rebleeding: Risk : 4% during the first 24 hrs and then 1.5% per day Intraoperative 7% High mortality (78%) IMPAIRED AUTOREGULATION Risk of rebleeding proportional to transmural pressure (MAP-ICP) MAP AVOID

22. Peaks 5-7 days, resolves after 14 days Angioplasty vasospasm 70%,symptoms 30% Transcranial droppler (TCD) blood velocity changes cerebral ischaemia & infarction Presentation Reversability Severity frequancy

23. Management: Triple H therapy + Nimodipine ↑ perfusion pressure & ↓ blood viscosity → CBF ↑  SBP 120-150 mmhg in unclipped 160-200 mmHg in clipped aneurysm.  CVP 8-12mmHg  HCT 30-35%

24. Nimodipine V.D OF Collarerals Ca influx 60mg orally every 4 hours, continued for 21days. I.V 1mg/h up to 2mg/h after 6 h SBL.P NOT LESS THAN 150-130 Balloon angioplasty Intraarterial papaverine

25. Early Late IC H VASOSPASM BLOOD CSF CO2 VS Vasospasm CSF Drainage VS ICP (Rebleed)

28. Coiling Clipping VS Poor HUNT&HESS Co morbidity Basilar Artery

29. Surgical Treatment- Clipping Aim: isolate the weakened vessel area from the blood supply

30. Direct Clipping When the surgeon can visualize the surrounding structures, parent vessel and perforators and when the neck is soft

31. Temporary Clipping SURGICAL PHARMACOLOGY temporary clip is placed on the parent vessel permanent clip is placed on the aneurysm neck temporary clip is removed from the parent vessel

32. Timing of surgery Late surgery reduces the risk of a further bleed provide excellent operating condition 30% of patients did not survive Early surgery

34. CVS complications of SAH sympathetic cathecolamine release posterior hypothalamus injury  systemic and pulmonary hypertension, cardiac arrhythmias,  myocardial infarction, and pulmonary oedema.

35.  cardiogenic shock. Investigations may reveal an abnormal ECG and elevated cardiac troponin levels.  Management is mainly supportive (inotropes, ventilation), and cardiac dysfunction is reversible in most cases

36. ECG abnormalities  25-100% of SAH patients  higher in poor grade patients  T wave inversion & ST depression (most common),  Prolong QT (arterial & ventricular dysrhytmias)  Q waves

37.  Preop echo  serial cardiac enzymes  invasive haemodynamic monitoring & treatment Respiratory system Most common non-neurological cause of death in SAH  Neurogenic Pulmonary oedema  Atelectasis & pneumonia  Aspiration risk (Loss of consciousness)  Pulmonary embolism (immobility)

38. Fluid status More than one third of patients have decrease IV volume  reduced fluid intake, vomiting  diuretic effect of IV contrast  vasodilatory effect of nimodipine exacerbates vasospasm & cerebral ischaemia CVP monitoring in poor grade patients

39. Electrolytes disturbances Hypopnatraemia 1. Cerebral salt wasting Secretion of brain and atrial natriuretic peptide IV volume depletion Fluid replacement (normal or hypertonic saline) 2. SIADH Accumulation of excess water with a high CVP Fluid restriction Hypokalaemia,Hypocalcaemia & Hypomagnesaemia

40. Radiological evaluation Cerebral Angiogram  Site of the aneurysm  Prepare for intraop positioning, surgical exposure &monitoring CT scan Increase ICP from IC haemorrhage, hydrocephalous or cerebral oedema TCD facilitate vasospasm management.

41. Monitoring  Standard monitoring  Intra-arterial line preinduction under LA  Central venous catheter for CVP monitoring Fluid status & resuscitation, post op Triple H therapy The use of neurophysiological monitoring, such as evoked potentials,EEG, has not been shown to improve outcome.  poor predictive value  affected by the use of volatile anaesthetic agents.

42. SSEPS ANT&POST ANEUYRISM BAEPS POST ANEUYRISM Guide safeTemporary Clipping Detect burst supression

43. Jugular venous bulb monitoring has also not been established and may interfere with cerebral venous drainage. CBF MONITOR Transcranial droppler (TCD)

44. Premedication  Continue all usual medications  Pre op sedative medications are best ICP omitted(Paco2 &CBF) Sedate Poor grade patients : intubated,ventilated & stable haemodynamic

45.  Avoid increases in transmural aneurysm pressure  Provide good conditions for the aneurysm surgery a) "slack" brain b) reduce aneurysmal pressure during clipping Induced hypotension Temporary clips  Brain protection The principles

46. Transmural aneurysm pressure Risk of ruptureRisk of ischemia

47. Prevent changes in transmural pressure (TMP) TPMG= CPP = MAP-ICP Minimise TPMG to reduce risk of rupture Optimise CPP to prevent ischemia Maintain BP at pre op levels until the aneurysm is secured ↓ BP by 20-30% tolerable in good grade patients but not in poor grade patients (with ICP ↑& CPP ↓)

48. Prophylaxis against increased BP during laryngoscopy /intubation IV narcotics, IV lignocaine Antihypertensives (e.g labetolol or esmolol) Ensure full relaxation prior to intubation

49. Ensure optimal depth of anesthesia Maintenance of anesthesia IV technique (TIVA/TCI) Low dose volatile agents< 1 MAC + Opoiod Infusion

50. Highly stimulating interventions:  placement of the pin head holder  raising of the bone flap  dural incision, skin incision & closure bolus dose of anaesthetics (propofol, thiopentone) antihypertensives (esmolol, labetolol) IV narcotics

51. slack brain

52. TPMG= CPP = MAP-ICP ICP AVOID TILL DURA OPENED sudden ↓ICP precipitates aneurysm rupture

53. Lumbar Subarachnoid Catheter (Amount accutely drained should not exceed 20- 30 ml) Hyperventilation ↓ CBF AVOID ISCHEMIA (mild hypocapnia (PCO2 30-35mmHg) prior to dural opening & moderate hypocapnia (PaCO2 25-30mmHg) if needed after dural opening)

54. Mannitol ( Osmotic diuresis & decrease CSF production ) IV infusion (1.5gm/kg), over 20 min fluid overload & pulmonary oedema Furosemide(0.3mg/kg) may be given with mannitol

55. Reduce aneurysmal pressure during clipping Induced hypotension Temporary clips

56. Decrease TMP (wall stress) of the aneurysm No longer used routinely impair global perfusion risk of vasospasm Facilitate dissection & clip placement degree of hypotension…… MAP 50mmHg Monitor cerebral function Agents Inhalational, SNP,GTN, Esmolol & Metaprolol

57. Temporary Surgical clipping Of artery feeding the aneurysm Risk of regional cerebral ischaemia Duration should not exceed 20 min (monitor clamp time) BP maintained at high normal or slightly above baseline to ensure adequate collateral blood flow

58. Fluid therapy  Maintain normovolaemic until the aneurysm isclipped  Maintain adequate filling pressures & BP prevent postop vasospasm  Fluid therapy according to blood loss, urine output,CVP & PCWP  isotonic balance salt solutions (Normal saline)  Avoid IV solution containing glucose

59. Intraoperative aneurysms rupture Management  Volume resuscitation to maintain normovolaemia  Temporary occlusion of cerebral arteries proximal &distal to the aneurysm(preferred technique)  BP management↓ MAP to 40-50mmHg (risk profound cerebral ischaemia. when temporary occlusion is not possible)

60. Emergence Rapid to allows neurologic assessment Prevent post op hypertension (cough) opioid infusion IV lidocaine, or in ET tube PONV prophylaxis! post op pain treatment BP 10-20% > baseline in patients at risk of cerebral vasospasm Antihypertensive (labetolol & esmolol)

61. Postoperative intubation & ventilation:  Higher grades  Intraoperative aneurysm rupture  vertebrobasilar aneurysms

62. Post op problems are : Vasospasm (delayed cerebral ischaemia) Re bleeds Infarction either due to the clip occluding a vessels or to thrombosis Pulmonary complications in high risk group ICU management & repeat angiography

63. Brain Protection

64.  Glucose control  Corticosteroids  Barbiturates BURET SUPPRESSION  Hypothermia Glucose> 150mg/dl Intracellular acidosis decrease ICP, CBF and Metabolic rate Etomidate or propofol alternatives, more hemodynamic stability

66.  Moderate hypothermia determined to be protective in some animal studies (33-35 degrees)  Mild hypothermia (35.5) found to improve outcome but not statistically significant  Deep hypothermic arrest for giant aneurysms

67.  Thiopental  Propofol  Fentanyl, Sufentanil, remifentanyl  Etomidate  Isoflurane, Desflurane  Rocuronium, vecuronium, vs atracurium, cisatracurium

68.  Ma gnesium sulfate  Methylene Blue  Anti epileptic drugs  Free radical scavengers  Antioxidants (Tirilazad)  Dexmedetomidine

69. Arteriovenous malformation congenital vascular malformation Dilated arteries and veins without communicating capillaries AVMs are more common in males than females Presentation: hemorrhage epilepsy Focal neurological deficit Feeding arteries Draining veins Peds: hydrocephalus, heart failure

70. AVM-Hemorrhage Peak age: 15-20 y/o 10 % mortality; 30-50% morbidity ICH(80%)/IVH/SAH Small AVMs are more lethal than larger ones 7% of pts with AVMs have aneurysms 75% are located on major feeding artery

71. Surgery Stereotactic Radiosurgery Embolisation Treatment Anesthesia-related Considerations for Cerebral AVMs Extensive blood loss Post-resection NPPB Occlusive Hyperemia Rebleeding Induced Hypotension Safe

72. Normal Perfusion Pressure Breakthrough post-op swelling or hemorrhage loss of autoregulation CBF prevent post-op hypertension BP control SBP< 120mmHg Pre and intra op BB & good pain control Diuritics Occlusive Hyperemia immediate: obstruction of venous outflow delayed: venous or sinus thrombosis adequate post-op hydration