What

1. What�s New in Neuroanesthesia? Irene P. Osborn, MDAssociate Professor of AnesthesiologyMount Sinai Medical Center

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3. 4 Goals of Neuroanesthesia To maintain or improve intracranial dynamics To provide optimal operating conditions To produce an awake patient forneurologic evaluation

4. Neurosurgical Procedures: Challenges Vasospasm, ICP, neurologic deficit Ischemia, hyperemia Painful stimuli (laryngoscopy, intubation, mayfield clamp) Retractor pressure, temporary clipping

5. 6 What�s New? New procedures New anesthetic agents/ techniques New monitors New thinking

6. 7 What hasn�t changed? Intracranial components Intracranial elastance (compliance) curve Regulation of cerebral blood flow (CBF) by metabolic and chemical factors Autoregulation and "coupling" of CBF to metabolic activity

7. 8 The Adult Brain: Blood Flow CBF= 45-54 ml/100gm/min 750 ml/min CSF=150 ml, entire volume replaced 3-4 times/day

8. 9 Intracranial components Brain tissue- 80% Blood- 12% CSF- 8%

9. 10 Intracranial Elastance and Adverse Consequences of Increasing Intracranial Volume Increases in the volume of an intracranial compartment will eventually exhaust compensatory mechanisms (the flat part of the elastance curve). Gradual increases in intracranial volume are better tolerated than acute increases. As the "knee" of the curve is approached, small increments in intracranial volume generate large increases in intracranial pressure (ICP). Increasing intracranial volume, and therefore eventually increasing ICP, can lead to morbidity through a number of mechanisms: (1) Because of pressure differentials across brain compartments, brain tissue may herniate transluminally across the falx, through the foramen magnum or across a cranial defect. (2) Increased brain volume can make surgical exposure extremely difficult, leading to brain herniation through the dural incision and to retractor- induced ischemia. (3) Because cerebral perfusion pressure is determined by the difference between mean arterial pressure and ICP, intracranial hypertension may lead to underperfusion of cerebral tissue. Drummond JC, Patel PM. Neurosurgical anesthesia. In: Miller RD, ed. Anesthesia. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:1895-1933. Increases in the volume of an intracranial compartment will eventually exhaust compensatory mechanisms (the flat part of the elastance curve). Gradual increases in intracranial volume are better tolerated than acute increases. As the "knee" of the curve is approached, small increments in intracranial volume generate large increases in intracranial pressure (ICP). Increasing intracranial volume, and therefore eventually increasing ICP, can lead to morbidity through a number of mechanisms: (1) Because of pressure differentials across brain compartments, brain tissue may herniate transluminally across the falx, through the foramen magnum or across a cranial defect. (2) Increased brain volume can make surgical exposure extremely difficult, leading to brain herniation through the dural incision and to retractor- induced ischemia. (3) Because cerebral perfusion pressure is determined by the difference between mean arterial pressure and ICP, intracranial hypertension may lead to underperfusion of cerebral tissue. Drummond JC, Patel PM. Neurosurgical anesthesia. In: Miller RD, ed. Anesthesia. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:1895-1933.

10. 11 Cerebral blood flow Varies with metabolic activity 15-20ml/100g/min can produce flat EEG <10ml/100g/min associated with irreversible brain damage

11. Deliberate Hyperventilation CBF is proportional to arterial carbon dioxide tension Change in CBF of 2ml/100gm/minper 1mmHg PaCO2 change Lower limit produces vasoconstriction and tissue hypoxia Effect is mediated by increase in perivascular pH, which lasts about 6 hours

12. Management of hyperventilation

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14. Cerebral Perfusion Pressure (CPP) = MAP-ICP Normal CPP= 80 mmHgAvoid < 70 mmHg

15. 16 Methods To Acutely DecreaseIntracranial Pressure Head up position Deliberate hyperventilation Barbiturates/sedatives Osmotic/renal tubular diuretics CSF drainage

16. Drainage of cerebral venous blood Cerebral blood volume vs. body position

17. Perioperative morbiditysupratentorial craniotomy

18. Concepts of anesthesia in neurosurgeryA 2004 survey among neuroanesthesia departments in Germany

19. 20 Anesthetic Techniques Short-acting volatile agents for neurosurgical procedures Total intravenous anesthesia with remifentanil/propofol Dexmedetomidine as a component of anesthesia Use of nitrous oxide (?)

20. 21 Inspired and Alveolar Anesthetic Concentrations The rate of rise of the alveolar concentration (FA) toward the inspired concentration (FI) increases with decreasing solubility (Yasuda et al). The rate of rise for nitrous oxide is augmented by the concentration effect (Eger). Yasuda N et al. Anesth Analg. 1991;72:316-324. Eger EI II. Desflurane (Suprane�). A Compendium and Reference. Rutherford, NJ: Healthpress Publishing; 1993. The rate of rise of the alveolar concentration (FA) toward the inspired concentration (FI) increases with decreasing solubility (Yasuda et al). The rate of rise for nitrous oxide is augmented by the concentration effect (Eger). Yasuda N et al. Anesth Analg. 1991;72:316-324. Eger EI II. Desflurane (Suprane�). A Compendium and Reference. Rutherford, NJ: Healthpress Publishing; 1993.

21. 22 Volatile Anesthetics andCerebral Blood Flow Autoregulation Over a wide range of arterial blood pressures, CBF does not change, due to autoregulation. When pressure is too low, autoregulation cannot cause dilation sufficient to maintain flow. In normal brain, blood flow is controlled by autoregulatory mechanisms. This is generally assumed to result in stable flow over a range of perfusion pressures from 50 to 150 mm Hg. Volatile anesthetics interfere with autoregulation in a dose-dependent manner. Even at moderate doses, CBF may become largely pressure-dependent. When autoregulation is impaired (in ischemia, brain trauma, vascular malformations, and brain tumors), increases in blood pressure may directly affect CBF and, presumably, cerebral blood volume and ICP. Volatile anesthetic agents may produce cerebral vasodilation, leading to increases in CBF and CSF pressure. Therefore, the CBF effects of halothane, isoflurane, and the newer inhalational agents desflurane and sevoflurane may influence important and critical neuroanesthetic parameters. Drummond JC, Patel PM. Cerebral physiology and the effects of anesthetics and techniques. In: Miller RD, ed. Anesthesia. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:695-733.Over a wide range of arterial blood pressures, CBF does not change, due to autoregulation. When pressure is too low, autoregulation cannot cause dilation sufficient to maintain flow. In normal brain, blood flow is controlled by autoregulatory mechanisms. This is generally assumed to result in stable flow over a range of perfusion pressures from 50 to 150 mm Hg. Volatile anesthetics interfere with autoregulation in a dose-dependent manner. Even at moderate doses, CBF may become largely pressure-dependent. When autoregulation is impaired (in ischemia, brain trauma, vascular malformations, and brain tumors), increases in blood pressure may directly affect CBF and, presumably, cerebral blood volume and ICP. Volatile anesthetic agents may produce cerebral vasodilation, leading to increases in CBF and CSF pressure. Therefore, the CBF effects of halothane, isoflurane, and the newer inhalational agents desflurane and sevoflurane may influence important and critical neuroanesthetic parameters. Drummond JC, Patel PM. Cerebral physiology and the effects of anesthetics and techniques. In: Miller RD, ed. Anesthesia. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000:695-733.

22. 23 Propofol Advantages: rapid onset of effect rapid recovery decrease CBF,ICP,CMRO2 neurophysiologic monitoring Disadvantages: potential hypotension ? prolonged action reliance on I.V. access Cost

23. 24 Remifentanil for Craniotomy Excellent control of BP and HR with easy titration Rapid emergence despite durationof case No increase in CBFor ICP Potential for hypotension in elderly, debilitated Must be controlled throughout (NIVA?) No residual analgesia

24. 25 TIVA forNeurosurgical Anesthesia Pts with decreased intracranial compliance Avoidance of nitrous oxide Neurophysiologic monitoring

25. Effect of Dexmedetomidine on ICP Animal model ICP was unchanged despite an increase in systemic blood pressure in rabbits ICP was decreased in the presence of intracranial hypertension Zornow MH et al, Anesth Analg 1992 Human study Dex has no effect on lumbar CSF pressure in patients undergoing transphenoidal pituitary tumor resection Talke P et al. Anesth Analg 1997

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27. �Scalp Block� Supplemental analgesia for craniotomy Ablation of hemodynamic response to pin fixation Anesthesia and analgesia for awake craniotomy Stereotactic biopsy Postoperative pain relief following craniotomy

28. Effect of ropivacaine skull block on perioperative outcomes in patients with supratentorial brain tumors and comparison with remifantanil: a pilot study Gazoni FM, Pouratian N, NemergutJ Neurosurg 2008 109:44.

29. Skull Block 30 patients received skull block or none Pts in skull block group did not have a significant increase in HR and MAP during �pinning� No difference in blood pressure variability between the groups No difference in VAS scores postoperatively

30. 31 Neurosurgical Positioning For surgical access Physiologic phenomena Potential for injury

31. Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation Ng I, Lim J, Wong HBNeurosurgery 2004; 54:593.

32. Head position �Positioning is everything!� Avoidance of neck flexion

33. 34 Subarachnoid Hemorrhage:Evolution of Technique 1980�s Late surgery Restrict fluids Induced hypotension 1990�s Urgent surgery Emphasis on cerebral perfusion Temporary clips HHH therapy

34. 35 Anesthetic Technique Avoidance of acute hypertension Provision of intraoperative brain relaxation Maintenance of perfusion pressure to prevent critical reduction of CBF Ability to perform precise manipulations of MAP as surgeon attempts to clip or control bleeding

35. 36 Mannitol Osmotic diuretic Causes reduction of brain water Onset- 15-20 min Duration of effectiveness- hrs to days

36. Fluid Management Increased emphasis on cerebral perfusion Isotonic solutions to maintain hemostasis and replace diuresis Use of normal saline and hypertonic saline Packed RBC�s for blood replacement

37. 38 Brain Injury & Glucose Hypo-osmolar glucose (D5W) Increases Cerebral Edema Increases ICP Induces Hyperglycemia Which Exacerbates Ischemic Injury

38. 39 Temperature &Cerebral Metabolism Cerebral Metabolism is Decreased 6 � 7 % Per 1? C Decrease In Temperature. Fever is Known To Worsen Postoperative Ischemic Outcome

39. 40 IHAST Trial 1000 patients for aneurysm clipping Randomized to receive normothermia vs. moderate hypothermia (33.3 �) Patients warmed by end of surgery No difference in outcome betweenthe groups

40. Hypothermia and Cerebral Aneurysm surgery IHAST-2

41. 42 How do we protect the brain? Appropriate anesthetics and doses Avoidance of ischemia (normocarbia) Avoidance of hyperthermia Maintainance of cerebral perfusionpressure Communication (keeping control)with neurosurgeon

42. 43 Aneurysm rupture! Decrease MAP(with a bolus of thiopental or propofol) Increase oxygen Open fluids Apply ipsilateral carotid pressure

43. 44 Radiology Suite vs. OR Location / anatomy of the aneurysm Age and grade of the patient Skill of the facility Luck of the draw

44. 45 Endovascular Coiling Anterior or posterior circulation aneurysm Medical contraindications to surgery Advanced age Pt. preference (unruptured)

45. Anesthesia for aneurysm coiling GA with ETT (possible LMA) Patient must NOT move Normocapnia and stable VS Radial artery line, especially if acute SAH 46

46. More indications for general anesthesia Inducing coma with pentobarbital Treatment of status epilepticus Emergency craniotomy

48. 49 Embolization of AVM

49. Emergence from anesthesia Should occur if patient lucid before surgery Should be �smooth� with minimal Couching, straining, hypertension Facilitate with IV lidocaine, betablockers, propofol if necessary

50. �Why isn�t he patient waking up?� Anesthetic agents Metabolic state Temperature Intraoperative problems

51. Decision time Not breathing Breathing but comfortable Fighting, bucking but not responsive to commands

52. Pain in neurosurgical patients:A prospective observational study More painful than anticipated Anticipated pain independent of operation type or preoperative pain intensity Preoperative pain promotes postoperative analgetic requirements ivPCA better than on demand

53. 54 Advantages of Airway Control with ETT Controlled ventilation decreased ICP decreased CBF Prevention of aspiration Facilitates positioning

54. 55 Awake craniotomy Careful monitoringof drug effects Response to stimulation Improved ability to awaken patients

55. 56 Awake Craniotomy Requires: Sufficient depth of anesthesia during openning and closing bone flap Full consciousness during cortical mapping Smooth transition between anesthesia and consciousness Adequate ventilation Patient immobility and comfort throughout

56. 57 Complications of Awake Craniotomy Hypoventilation Hypoxemia Seizures Nausea

57. Anaesthesia for awakecraniotomy-evolution of atechnique that facilitatesawake neurological testing Sarang A, Dinsmore JBJA 2003; 90:161 58

58. Anesthetic agents for deep brain stimulation Nothing! Propofol Remifentanil Dexmedetomidine 59

59. 60 Trends Out: Deep hypothermia Prolonged hyperventilation Certain anesthetic agents Hypovolemia Nitroprusside In: Short acting agents Rapid recovery Emphasis on cerebral perfusion pressure Appropriate fluid replacement Nicardipine

60. 61 Conclusions Future of neurosurgery Goals for neuroanesthesia Careful understanding and evaluation of patients Communication and cooperation with neurosurgeons

61. 62 Thank you!