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Intracranial aneurysm surgery and anesthesia

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this presentation will be very useful for the candidates of neuroanesthesia....

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Intracranial aneurysm surgery and anesthesia

  1. 1. Dr. Manoj Tripathi
  2. 2.  75% of subarachnoid hemorrhages 27,000 American/year 6-49 per 100,00 year depending on location Female predominance Age 40-60
  3. 3.  Ruptured intracranial aneurysm (IA) 20% morbidity 20% mortality Unruptured IA 4% morbidity 0-2% mortality
  4. 4.  More than 90% of cerebral aneurysm occur at thefollowing locations-1-The origin of the posterior communicating artery2- The region of the anterior communicating artery3- Middle cerebral artery bifurcation4- apex of basilar artery5- internal carotid artery bifurcation.
  5. 5.  Acquired vascular lesions secondary todegenerative changes in the muscular and elasticcomponents of the vessel wall. Usually occuring at the branching points of themajor cerebral vessels. A deficiency of type III collagen in arteries isassosiated with SAH.
  6. 6.  Congenital influences may play a role. Disease processes associated with an increasedrisk of IA Polycystic kidney Hypertension Coarctation of the aorta Ehler- Danlos syndrome Fibromuscular disease smoking
  7. 7.  Small – less than 12 mm 78% Large – 12-24 mm 20% Giant - 24mm 2% Majority of aneurysms that bleed are less than 1cm of diameter. Aneurysms that are less than .5 cm diameterhave less risk of bleeding.
  8. 8.  Hypertension Pregnancy Smoking Heavy drinking Strenuous activity
  9. 9.  Causes increase ICP Increased ICP causes decrease CBF Bleeding stops with decreased CBF Decreased consciousness 2 clinical scenarios are seen typically Return to normal ICP and CBF with return of function High ICP continues with low CBF
  10. 10.  Grade 0 - Aneurysm is not ruptured Grade 1 - Asymptomatic, min. headache and sl. nuchalrigidity Grade 2 - Moderate to severe headache, nuchal rigidity, butno neurologic deficit other than cranial nerve palsy Grade 3 - Drowsiness, confusion, mild focal deficits Grade 4 - Stupor, mild or severe hemiparesis, possible earlydecerebrate rigidity, vegetative disturbances Grade 5 - Deep coma, decerebrate rigidity, moribundappearance
  11. 11. WFNS Grade GCS Score Motor DeficitI 15 AbsentII 13-14 AbsentIII 13-14 PresentIV 7-12 P or AV 3-6 P or A
  12. 12.  It is very important to assess the degree of SAH.There are different grading scales for thispurpose. Modified Hunt and Hess grading scale is mostcommonly used because of ease of application. Extent of vasospasm is related to the amount ofsubarachnoid blood present. CT scan is graded according to the Fisher grade
  13. 13.  Grade 1 – No blood detected Grade 2- Diffuse thin layer of subarachnoidblood ( vertical layers less than 1 mm thick) Grade 3 – Localised clot or thick layer ofsuarachnoid blood( vertical layer = 1 mm thick) Grade 4 – Intracerebral or intraventricular bloodwith diffuse or no subarachnoid blood
  14. 14.  The clinical management of cerebral aneurysmscenters on the reduction of risk of hemorrhage inuruptured cases and of repeat hemarrhage inSAH. The major complications of SAH are –1- Aneurysmal rebleeding2- delayed cerebral ischemia secondary tovasospasm
  15. 15.  Incidence of rebleeding is 14-30 % . Peak incidence at the end of the first week ofSAH. High risk of rebleed during angiography Assosiated with high rate of mortality andmorbidity.
  16. 16.  Blood pressure control is of critical importancein reduction of risk of rebleeding. Antifibrinolytic agents have been usedsuccessfully to control rebleeding
  17. 17.  Vasospasm is the leading cause of morbidity andmortality in patients who initially survive SAH Radiological evidence of vasospasm is noted in upto70% of patients . Clinical vasospasm occur in almost 30% of patients Clinical vasospasm occur after 4-9 days of SAH It typically does not occur after 2 weeks ofaneurysmal rupture.
  18. 18.  Pathological changes occur are contraction ofvascular smooth muscles and thickening of thevessel wall Prostaglandins , biological amines , peptides , cyclicneucleotides , calcium , lipid peroxidation and freeredicals are implicated . Conventional cerebral angiography , xenon-enhanced CT and transcranial doppler is used toconfirm the presence of vasospasm
  19. 19.  There is a correlation between the amount ofsubarachnoid blood after aneurysmal rupture andthe occurrence and severity of vasospasm Because of this , extensive removal of subarachnoidblood by early surgery is attempted to decrease theincidence of vasospasm. Nimodipine , a calcium channel blocker issuccessfully used .
  20. 20.  Triple H therapy – hypertension , hypervolumiaand hemodilution is used in treatment ofvasospasm. A new method for symptomatic vasospasmincludes use of cerebral angioplasty to dilateconstricted major cerebral vessels.
  21. 21.
  22. 22. PREOPERATIVE ASSESSMENTDETERMINATION OFANAESTHETIC STRATEGYPREOPERATIVEPREPARATIONINDUCTIONMAINTENANCEEMERGENCE
  23. 23.  Assesment of patients neuroloical condition andclinical grading of SAH A review of patient,s intracranial pathologicalconditions including CT scan and angiograms. Monitoring of ICP and transcranial dopplerultrasonography.
  24. 24.  Evaluation of patients other systemic functions ,premorbid as well as present Systems known to affected by SAH Communication with the neurosurgeon regardingpositioning and special monitoring Optimisation of patient,s condition by correctingany biochemical and physiological condition
  25. 25.  To assess the CNS , as we have discussed beforethere are grading scales-1. Modified Hunt and Hess grading2. WFNS grade scale3. Fisher grading of CT scan
  26. 26.  The greater the clinical grade , more likelyvasospasm , elevated ICP , impaired autoregulationand disordered response to hypocapnia will occur Worse clinical grade is also assosited with cardiacarrythmia , myocardial dysfunction , hypovolumiaand hyponatremia.
  27. 27.  ECG abnormalities Very common Many changes seen cannon t wave, Q-T prolongation, ST changes Autonomic surge may in fact cause somesubendocardial injury from increase myocardial walltension
  28. 28.  Cardiac dysfunction does not appear to affectmorbidity or mortality (studies from Zaroff andBrowers) Prolonged Q-T with increased incidence ofventricular arrhythmias PVC’s are seen in 80% ECG changes occur during the first 48 hrs of SAH andcorrelate with amount of intracranial bleed.
  29. 29.  ECG changes reflect the severity of neurogenicdamage and have not shown to contributeperioperative mortality and morbidity The decision to operate should not be influencedby these ECG changes.
  30. 30.  Hydrocephalous Seizures 13% Vasospasm may be cause Increased risk of rebleed Treat and prophylaxis Headache, visual field changes, motordeficits
  31. 31.  SIADH Cerebral salt wasting syndrome release of naturetic peptide hypovolemia, increased urine NA and volumecontraction Distinguish between the two and treataccordingly
  32. 32.  Neurogenic pulmonary edema 1-2% with SAH Hyperactivity of the sympathetic nervous system Pneumonia in 7-12% of hospitalized patients withSAH
  33. 33.  0-3 days post bleed appears to be optimal Improved outcome within 6 hours of rupturedespite high H/H grade If delayed, should be done after 10 days postbleed after fibrinolytic phase The results are worst with surgery performedbetween 7 to 10 days.
  34. 34.  Avoid abrupt changes in BP Maintain CBF with normal to high blood pressure Avoid increase of ICP Assess immobility & vital signs control Achieve brain relaxation Allow for swift emergence & neurologic assessment Be prepared for disaster
  35. 35.  Arterial blood pressure- beat to beat monitoringof MAP ECG- myocardial ischemia/ arrhythmia Pulse oximetry- systemic hypoxia EtCO2- trend monitor for Paco2/ detection of VAE Temperature- via oesophageal lead; to allowmodest, passive hypothermia(~35o C) Urine output- adequacy of renal function &hydration
  36. 36.  Blood glucose/ serum electrolytes/ osmolality-particularly if mannitol is used Hemoglobin & hematocrit- to estimate extentof bleeding/ permissible blood loss Jugular venous bulb monitoring- adequacy ofcerebral perfusion & oxygenation EEG- CMR/ cerebral ischemia/ depth ofanaesthesia
  37. 37.  Evoked potentials- intactness of specific CNSpathways Transcranial oximetry- noninvasive informationon regional cerebral oxygenation TCD ultrasonorgaphy
  38. 38.  TCD is a indirect measure CBF It is unreliable as a measure of CBF in patients ofSAH because of changes in vessel diameter But it has become valuable for diagnosingvasospasm noninvasively before the onset ofclinical symptoms TCD has been successfully used in theperioperative management of patients withcerebral aneurysm.
  39. 39.  Continuous TCD monitoring may improve the safetyof induced hypotension by correlating the bloodvelocity change to the decline in the bloodpressure. It has been used perioperatively to confirm thediagnosis of aneurysmal rupture.
  40. 40.  Patients should receive their regular dose ofnimodipine and dexamethasone Tab Loarazepam 1-2 mg and tab rantac 150should be given in night before surgery To relieve anxiety inj midazolam in incrementaldose of 1 mg is given in the morning of surgery.
  41. 41.  There is risk of rupture of aneurysm at the timeof induction due to high blood pressure duringtracheal intubation As a general principle , the patients bloodpressure should be reduced by 20-25% below thebaseline value and hypertensive response to thetracheal intubation should be alleviated.
  42. 42.  Another useful approach is to balance the risk ofischemia from a decrease in CPP against thebenefit of a reduced chance of aneurysmalrupture from a decrease TMP. Conceptually induction phase is consisting of 2partsInduction to achieve loss of consciousness Thiopental ( 3- 5 mg/kg ) or propofol (1-2.5mg/kg ) in combination with fentanyl (3-7 ug/kg)or sufentanil(.3-.7 ug/kg) is suitable
  43. 43.  Other alternatives include etomidate (.3-.4 mg/kg)and midazolam ( .1-.2mg/kg)Prophylaxis against rise in BP during laryngoscopy Many agents have been used successfully toalleviate hypertensive response of intubation.Fentanyl ( 5-10 ug/kg)Sufentanil ( .5-1 ug/kg)Esmolol (.5 mg/kg)Labetolol (10-20 mg)Intraveous or topical lidocaine (1.5-2 mg/kg)Second dose of thiopental ( 1-2 mg/kg)
  44. 44.  Intravenous adjuncts are preferred in patientswith poor SAH grades whereas deep inhalationalanesthetics are preferred in patients with goodSAH grades.
  45. 45. Choice of muscle relaxant Vecuronium is most hemodyanamically stableand suitable muscle relaxant. Succinylcholine causes incease in ICP. Atracurium may cause hypotension. Pancuronium causes tachycardia andhypertension
  46. 46.  The location and size of aneurysm generallydetermine the position of patient. Anterior circulation aneurysm are usuallyapproached using fronto-temporal incision with thepatient in supine position Basilar tip aneurysms are approached usingsubtemporal incision with the patient in lareralposition
  47. 47.  Vertebral and basilar trunk aneurysms approached usingsuboccipital incision with the patient in sitting or parkbench position Avoid extreme positioning (extreme rotation or flexionof neck to avoid IJV compression) Padding/ fixing of regions susceptible to injury bypressure/ abrasion/ movement -groin, breasts, axillaryregion-falling extremities-knees kept in mild flexion to preventbackache postoperatively Mild head-up position (to aid venous cerebral drainage)
  48. 48.  Elevation of contralateral shoulder by wedge/ roll(to prevent brachial plexus stretch injury if head isturned laterally) Meticulous attention to specific problems in prone/lateral/ parkbench/ sitting positions Care of ETT –easy intraoperative accessibility-fixed & packed securely toprevent accidental extubation, or abrasionsresulting from movement
  49. 49.  Care of eyes- taped occlusively to prevent cornealdamage (from exposure/ irrigation with antisepticsolutions)APPLICATION OF SKULL PIN HOLDER FRAME Pain- provides maximal nociceptive stimulus- must be blocked adequately byi. deepening of anaesthesia (i.v. bolus ofthiopentone 1mg/kg or propofol 0.5 mg/kg)ii. analgesia (i.v. bolus of fentanyl 1-3mcg/kg or alfentanil 10-20 mcg/kg or remifentanil 0.25-1mcg/kg)
  50. 50. iii. local anaesthetic infiltration at pin siteiv. antihypertensive β-blockers e.g.Esmolol 1 mg/kg or Labetalol 0.5-1 mg/kg VAE- may occur with pin insertion
  51. 51.  Positioning of Anaesthetist-optimal patient monitoring-access to airway/ intravenous & intraarteriallines
  52. 52. The goals during maintainance of anesthesia are -- To provide a relaxed or ‘slack’ brain that will allowminimum retraction pressure To maintain perfusion to the brain To reduce TMP if necessary during dissection of theaneurysm and final clipping Allow prompt awakening and assessment ofpatients with good SAH grades
  53. 53.  MaintenanceCHOICE OF TECHNIQUEVolatile agents Intravenous agentsAdvantages Controlability/ predictability/ earlyawakeningGood control of CBF, ICP, & brainbulk-cerebrovasoconstriction↓ in ICPDisadvantages Poor control of CBF, ICP, & brainbulk-cerebrovasodilation↑ in ICPProlonged/ unpredictableawakeningMay interfere with D/D of delayedawakeningMay require emergent CT scanto rule out surgical complicationsType ofsurgerySimple, low risk of ↑ed ICP Complex, high risk of ↑ed ICP
  54. 54.  MaintenanceCHOICE OF TECHNIQUEVolatile agents Intravenous agentsEarly institution ofmoderatehyperventilationMandatory OptionalConcurrent use withN2OIdeal agentUsually avoided-synergistic effects in ↑ing CBF &CMR-if used, ensure ↓in ICP byi. hyperventilationIi. osmotic diureticsIii. BP controlIv. adequate positioning/ cerebralvenous drainagev. lumbar drainageVi. Use of < 1 MAC (e.g. < 1.15% ofisoflurane)NoCan be used withoutsignificant problemsYes
  55. 55. Fluid Therapy Fluid therapy should be guided by intraoperative bloodloss, urine output and CVP/PAWP The aim is to maintain normovolumia beforeaneurysmal clipping and slight hypervolumia andhypertension after clipping. Avoidance of hyperglycemia (worsens consequences ofcerebral ischemia)
  56. 56.  Avoidance of hypoosmolality – can cause brainoedemai. Target osmolality: 290-320 mOsm/kg)ii. Colloid oncotic pressure plays no significant rolein brain oedemaiii. Avoidance of glucose-containing & hypoosmolarsolutions (e.g. Ringer’s lactate, 254 mOsm/kg) Preferred solutions – crystalloids: 0.9% NaClcolloids: 6% HES (304 mOsm/kg)
  57. 57.  Hematocrit- Target for >28% Warming of I.V. solutions– may be avoided topermit establishment of mild hypothermia (~350 C)for neuroprotection-must be essentially warmed at the end ofprocedure to ensure normothermia for emergencefrom anaesthesia
  58. 58.  Hemodynamic control-Undesirable CNS arousal & hemodynamic activation mayoccur despite adequate depth of anaesthesia &analgesia-Consider use of i. Esmolol (1mg/kg: initial dose)ii. Labetalol (0.5-1mg/kg: initialdose)iii. Clonidine (0.5-1mcg/kg: initialdose) Moderate hypothermia (~350C)-may confer a degree of brain protection if ischemicevent occurs
  59. 59.  Prevention1. No over hydration2. Sedation/ analgesia/ anxiolysis3. Avoidance of application of any noxious stimulus withsedation/ local anaesthesia4. Head-up position5. Osmotic agents (mannitol/ hypertonic saline)6. β-blockers/ clonidine/ lignocaine
  60. 60. 7. Adequate hemodynamics: MAP, CVP, PCWP, HR8. Adequate ventilation: PaO2>100mmHg;PaCO2~35mmHg9. Minimal possible intrathoracic pressure10. Hyperventilation on demand (before induction)11. Use of total I.V. anaesthestic agents for induction& maintenance12. Avoidance of cerebral vasodilators (e.g.nitroglycerine)
  61. 61.  Treatment1.Hyperventilation2.Osmotic agents3.CSF drainage (if ventricular/ lumbar catheter in situ)4.Augmentation of anaesthesia with I.V. anaestheticagents (e.g. propofol, thiopentone, etomidate)5.Adequate muscle relaxation6. Venous drainage (head-up/ avoidance of PEEP/reduction of inspiratory time)7.Mild controlled hypertension (if autoregulation ispresent)
  62. 62.  5-7 minutes of occlusion with prompt reperfusionare usually well tolerated but this duration isinsufficient for clipping difficult or giant aneurysms A number of regimens have been used to extendthe occlusion duration High dose Mannitol 2g/kg SENDAI COCKTAIL - mannitol (500 ml of 20%solution) + vitamin E (500 mg) + dexamethasone(50 mg)
  63. 63.  Pharmacological metabolic suppression bythiopentone ( 5-6 mg/kg) or etomidate (.4-.5mg/kg) Etomidate is preferred over thiopental due togreater hemodyanmic stability Moderate hypothermia has also been to extend theduration of tolerable occlusion
  64. 64.  If the surgical procedure is uneventful , SAH grade Iand II patients should be extubated. Because hypertensive therapy is useful in reversingdelated cerebral ischemia from vasospasm , modestlevel of postoperative hypertension (<180mm hg )should not be aggressively treated. Depending on preoperative ventilatory status andduration and difficulty of surgical procedure
  65. 65.  SAH grade III patients may or may not be extubated. Patients with preoperative SAH grade IV and Vusually require postoperative ventilatory support andneurointensive care.
  66. 66.  In the postoperative period blood pressure should bemaintained above 140-150 mm hg and less than 180mm hg. To distinguish residual anesthesia from surgicalcause following general guidelines are useful1- Anesthesia causes global depression and any newfocal neurological deficit should alert to a surgicalcause
  67. 67. 2-The effect of potent inhaled anesthetics shouldhave larly dissipated after 30-60 minutes3- patients whose pupils are midsized and having norespiratoty depression are unlikly to experience anarcotic overdose.4- unequal pupils not present before surgery alwayssuggest a surgical cause. Neurological assessment should be done every 15minutes in the recovery room.
  68. 68. Thank you

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