Anesthesia for Carotid Endarterectomy

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Anesthesia for Carotid Endarterectomy

  1. 1. Anesthesia for Carotid Endarterectomy Robert Y. Gumnit, MD Director of Clinical Education Burlington Anesthesia Associates
  2. 2. Carotid Endarterectomy <ul><li>Prophylactic intervention to prevent cerebral infarction and relieve symptoms of carotid artherosclerosis </li></ul><ul><li>Stroke incidence in USA- 160/100,000 people </li></ul>
  3. 3. Etiologies of Ischemic Stroke <ul><li>Thromboembolism from atherosclerotic large extracranial or intracranial arteries </li></ul><ul><li>Embolism from a cardiac source </li></ul><ul><li>Atherosclerotic disease in small cerebral vessels </li></ul>
  4. 4. Location of Carotid Disease <ul><li>Most likely site is at the carotid bifurcation with proximal internal carotid involvement </li></ul><ul><li>Carotid circulation supplies 80 to 90% of cerebral blood supply </li></ul><ul><li>Vertebral circulation supplies 10 to 20% of cerebral blood supply </li></ul>
  5. 5. Distal Circulation <ul><li>Internal carotid contributes to anterior and middle cerebral arteries </li></ul><ul><li>1 st intracranial branch of ICA is the ophthalmic artery </li></ul>
  6. 6. Important Anatomic Structures Near Carotid Dissection <ul><li>Hypoglossal nerve </li></ul><ul><li>Vagus Nerve </li></ul><ul><li>Recurrent Laryngeal Nerve </li></ul><ul><li>Mandibular Branch of Facial Nerve </li></ul><ul><li>Important to document preoperative neurologic examination </li></ul>
  7. 7. Clinical Presentation of Carotid Disease <ul><li>Varies by site of stenosis and distal embolization </li></ul><ul><li>Part of a generalized vascular disease </li></ul><ul><li>Transient Ischemic Event (TIA)/ Reversible Ischemic Neurologic Deficit(RIND) </li></ul>
  8. 8. Transient Ischemic Events <ul><li>Sudden onset of focal neurologic deficit which resolves within 24 hours </li></ul><ul><li>Contralateral motor or sensory deficits </li></ul><ul><li>Amaurosis Fugax </li></ul>
  9. 9. RIND’s <ul><li>Neurologic dysfunction greater than 24 hours but less than 2 weeks </li></ul><ul><li>Important to differentiate between carotid disease and posterior vertebro-basilar artery disease </li></ul>
  10. 10. Posterior Circulation Symptoms <ul><li>Binocular vision loss </li></ul><ul><li>Vertigo </li></ul><ul><li>“ Drop Attacks” </li></ul>
  11. 11. Differential Diagnosis of TIA <ul><li>Intracranial mass </li></ul><ul><li>Cardiac Disease- e.g. Atrial Fibrillation, Valvular Heart Disease, Cardiomyopathy) </li></ul><ul><li>Metabolic Encephalopathy/ Hyperglycemia </li></ul>
  12. 12. Risk Factors for Carotid Disease <ul><li>Advanced age </li></ul><ul><li>Hypertension </li></ul><ul><li>Diabetes </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Hypercoagulable states </li></ul><ul><li>Smoking </li></ul>
  13. 13. Diagnostic Imaging <ul><li>Ultrasound- 89% detection rate </li></ul><ul><li>Gold standard is cerebral angiography but there is a 1% chance of a neurologic deficit </li></ul>
  14. 14. Choice of Therapy <ul><li>Individualized assessment of stroke risk weighing medical management versus risk of perioperative stroke, death, or cardiac event </li></ul><ul><li>Large multicenter trials comparing medical versus surgical management comparing anti-platelet therapy versus surgery </li></ul>
  15. 15. Summary of Large Clinical Trials <ul><li>Depending on particular series, patients with between a minimum of 50% to 70% stenosis are candidates with ipsilateral disease and acceptable surgical risk </li></ul><ul><li>The greater the degree of stenosis, the greater the difference in outcome statistics compared to medical therapy </li></ul>
  16. 16. Preoperative Evaluation <ul><li>Comorbidities including advanced vascular disease, coronary artery disease- leading causes of perioperative death </li></ul><ul><li>Testing is useful if the only if results will impact on actual perioperative care </li></ul>
  17. 17. Conditions Requiring Some Workup <ul><li>Orthostatic hypotension </li></ul><ul><li>Coronary artery disease </li></ul><ul><li>Myocardial infarction </li></ul><ul><li>Congestive heart failure </li></ul><ul><li>Dysrhythmias, Implanted pacer, AICD’s </li></ul>
  18. 18. Assessment of Functional Capacity <ul><li>DM </li></ul><ul><li>Renal Insufficiency </li></ul><ul><li>Pulmonary disease </li></ul>
  19. 19. ACC/AHA Guidelines <ul><li>Stepwise approach to risk assessment </li></ul><ul><li>Functional capacity </li></ul><ul><li>Major markers: unstable coronary syndromes, MI, unstable angina, uncompensated CHF, severe valvular lesions </li></ul>
  20. 20. Intermediate Markers <ul><li>Mild angina </li></ul><ul><li>Previous MI </li></ul><ul><li>Compensated CHF </li></ul><ul><li>DM </li></ul><ul><li>Renal Insufficiency </li></ul>
  21. 21. Minor Clinical Predictors <ul><li>Advanced age </li></ul><ul><li>Abnormal EKG </li></ul><ul><li>Non-sinus rhythm </li></ul><ul><li>Low functional capacity </li></ul><ul><li>History of stroke </li></ul><ul><li>Uncontrolled hypertension </li></ul><ul><li>Cardiac and Long-term risks are increased in patients unable to meet a 4-MET demand </li></ul>
  22. 22. Surgery Specific Risks <ul><li>ACC/AHA define CEA as an intermediate risk procedure </li></ul><ul><li>Risk of cardiac death or non-fatal MI generally less than 5% </li></ul><ul><li>If surgery is to be performed in presence of high risk indicators, ACC recommends delaying surgical for further evaluation and treatment </li></ul>
  23. 23. Elective CEA with Intermediate Risk Predictors <ul><li>Consider functional capacity </li></ul><ul><li>Consider non-invasive testing </li></ul>
  24. 24. Indications for Further Testing <ul><li>Exercise tolerance < 4 METS </li></ul><ul><li>Symptomatic valvular lesions </li></ul><ul><li>Dilated or Hypertrophic Cardiomyopathy </li></ul><ul><li>Hemodynamically significant dysrhythmias </li></ul>
  25. 25. Simple Conservative Approach <ul><li>Assume presence of CAD </li></ul><ul><li>Treat with medically appropriate therapy </li></ul><ul><li>Coronary angiography and prophylactic revascularization has not been shown to reduce cardiac morbidity and should only be used in high risk cases </li></ul>
  26. 26. Hypertension <ul><li>Most treatable preoperative risk factor for stroke </li></ul><ul><li>Reduced blood pressure decreases probability of perioperative stroke </li></ul><ul><li>Poorly controlled BP increases risk of perioperative hemodynamic instability and significant neurologic events </li></ul><ul><li>BP meds continued right up to time of surgery </li></ul><ul><li>Rapid correction of BP preoperatively not advised </li></ul>
  27. 27. Delay Surgery if Not Emergent <ul><li>Uncontrolled hypertension </li></ul><ul><li>Uncontrolled diabetes </li></ul><ul><li>Uncontrolled coronary disease </li></ul>
  28. 28. Goals of Anesthetic Management <ul><li>Protect brain and heart from ischemic injury </li></ul><ul><li>Maintain hemodynamic stability </li></ul><ul><li>Ablate stimulatory and stress response to surgery </li></ul><ul><li>Awake, cooperative patient at end of procedure allowing clear neurologic evaluation </li></ul>
  29. 29. Standard Monitoring <ul><li>ECG- Leads II, V4-5 for rhythm and S-T segments </li></ul><ul><li>Continuous arterial pressure monitoring, arterial line </li></ul><ul><li>Pulse oximetry </li></ul><ul><li>Central lines generally not necessary but should not be placed in jugular area </li></ul>
  30. 30. Perioperative ß-Blockade <ul><li>Continue for patients already on this therapy </li></ul><ul><li>Those who are not already on ß-blockers can be started on them immediately if there is no contraindication for reduction of perioperative myocardial ischemia </li></ul>
  31. 31. Choice of Anesthetic Technique <ul><li>Largely dependent on preferences of: </li></ul><ul><li>Surgeon </li></ul><ul><li>Patient </li></ul><ul><li>Anesthesia Team </li></ul><ul><li>No strong data to clearly mandate any particular method or agents </li></ul>
  32. 32. General Anesthesia for CEA <ul><li>Maintain cerebral perfusion </li></ul><ul><li>Minimize myocardial work </li></ul><ul><li>Rapid and smooth emergence to allow immediate postoperative neurologic assessment </li></ul>
  33. 33. Advantages of GA <ul><li>Allows for still, motionless patient </li></ul><ul><li>Early control of airway and ventilation </li></ul><ul><li>Ability to protect brain if ischemia develops </li></ul>
  34. 34. Blood Pressure Management <ul><li>Best range is individualized to each patient </li></ul><ul><li>Risk of either myocardial or cerebral ischemia is minimized if perfusion pressures are maintained in the patient’s high normal range </li></ul>
  35. 35. Choice of Induction Agent <ul><li>All available agents reduce cerebral metabolic rate in excess of reduction of cerebral blood flow </li></ul><ul><li>Pentothal provides best protection against focal ischemia </li></ul><ul><li>Most rapid awakening with Propofol </li></ul><ul><li>Etomidate has most favorable hemodynamic profile but may worsen ischemic neurologic injury (animal data) </li></ul>
  36. 36. Hemodynamic Response to Intubation/ Hypertension <ul><li>Short acting narcotic </li></ul><ul><li>Short acting beta-blocker </li></ul><ul><li>Nitroglycerin or Nitroprusside </li></ul>
  37. 37. Maintenance with a Volatile Agent <ul><li>All presently clinical available agents reduce cerebral metabolic rate </li></ul><ul><li>Isoflurane has the most pronounced effect with a minimum of myocardial depression </li></ul><ul><li>Newer agents allow for more rapid emergence ( Sevoflurane , Desflurane ) </li></ul><ul><li>Maintain at a lighter plane to allow rapid emergence and an easily interpretable EEG </li></ul>
  38. 38. Hypotensive Response to Induction <ul><li>Hypertensive patients often present in a mildly hypovolemic state </li></ul><ul><li>Small fluid boluses </li></ul><ul><li>Phenylephrine </li></ul>
  39. 39. Maintenance Events <ul><li>Cervical incision not especially stimulating </li></ul><ul><li>Rapid changes in pulse rate and blood pressure/ hemodynamic instability can be frequent </li></ul><ul><li>Role of short acting agents/ vasoactive drugs </li></ul>
  40. 40. Blood Pressure Management <ul><li>Phenylephrine- α-agonist with no direct effect on cerebral vasculature; cerebral perfusion increased by elevating perfusion pressure </li></ul><ul><li>Ephedrine- Mixed α and β activity </li></ul>
  41. 41. Stimulation of Carotid Baroreceptor <ul><li>Manipulation can result in sustained bradycardia </li></ul><ul><li>Infiltration with local agent in carotid sinus area </li></ul><ul><li>atropine </li></ul>
  42. 42. Tachycardia <ul><li>Not well tolerated in the beta-blocked patient </li></ul><ul><li>Short acting beta-blocker – e.g. esmolol </li></ul>
  43. 43. Management of Ventilation <ul><li>Maintain normocarbia </li></ul><ul><li>Hypercapnea may cause cerebral steal syndrome </li></ul><ul><li>Hypcapnea may decrease cerebral perfusion </li></ul><ul><li>LMA vs. ETT? </li></ul>
  44. 44. Emergence Issues <ul><li>Coughing </li></ul><ul><li>Hyperdynamic circulation </li></ul><ul><li>Stress on suture lines </li></ul><ul><li>Deep extubation? </li></ul><ul><li>Airway topicalization? </li></ul>
  45. 45. Neurologic Monitoring During GA <ul><li>No monitoring modality is as effective as watching an awake patient </li></ul><ul><li>Rational for monitoring is to identify which patients need shunting or selective blood pressure augmentation </li></ul>
  46. 46. Carotid Shunts Problems <ul><li>Carotid emboli </li></ul><ul><li>Intimal dissection </li></ul><ul><li>Limited surgical exposure </li></ul>
  47. 47. Commonly Used Monitors <ul><li>EEG </li></ul><ul><li>Somatosenory-evoked potentials SSEP’s </li></ul><ul><li>Transcranial Doppler </li></ul><ul><li>Internal carotid artery stump pressure </li></ul>
  48. 48. EEG Monitoring <ul><li>Measures electrical activity of cortical neurons </li></ul><ul><li>Cortical ischemia is manifested as ipsilateral cortical slowing, attenuation, or both </li></ul><ul><li>EEG signal is usually diminished when cerebral blow flow < 15 ml/ 100 gm of brain tissue </li></ul><ul><li>Below 12-15 ml/ 100 gm brain tissue there is the beginning of cortical ischemia </li></ul>
  49. 49. Causes of EEG Changes <ul><li>Ischemia from cross clamping </li></ul><ul><li>Shunt Malfunction </li></ul><ul><li>Hypotension </li></ul><ul><li>Contralateral carotid stenosis </li></ul><ul><li>Cerebral Emboli </li></ul>
  50. 50. Limits of EEG Monitoring <ul><li>Inability to detect subcortical injury </li></ul><ul><li>High false positive rate </li></ul><ul><li>Diminished sensitivity in patients with prior stroke </li></ul><ul><li>Majority of intraoperative strokes are embolic in nature </li></ul><ul><li>Most strokes occur postoperatively </li></ul>
  51. 51. SSEP’S <ul><li>Unlike EEG, it can detect deep brain and brainstem ischemia </li></ul><ul><li>Ischemia causes a detectable decrease in signal amplitude with a concomitant increase in signal latency </li></ul><ul><li>Data is unclear whether this is actually more sensitive than EEG </li></ul>
  52. 52. Transcranial Doppler <ul><li>Allows continuous noninvasive assessment of blood flow velocity </li></ul><ul><li>Can detect emboli in ipsilateral middle cerebral artery </li></ul><ul><li>In presence of a shunt, can determine shunt adequacy </li></ul>
  53. 53. Carotid Artery Stump Pressure <ul><li>Mean arterial pressure cephalad to carotid cross clamp </li></ul><ul><li>Needle artery and connect to pressure transducer </li></ul><ul><li>Pressure is generated by back pressure from Circle of Willis </li></ul><ul><li>Minimal pressures believed to be in the 25 to 70 mm Hg range </li></ul>
  54. 54. Other Neuro-Monitors <ul><li>Jugular bulb oxygen saturation </li></ul><ul><li>Cerebral blood flow measurements using injection of xenon-133 and calculation done with scintilography </li></ul>
  55. 55. Regional Anesthesia Techniques <ul><li>Requires the correct combination of surgeon, anesthesiologist and patient to be successful </li></ul><ul><li>Deep and Superficial Cervical Plexus Block </li></ul><ul><li>Epidural anesthesia </li></ul><ul><li>Local infiltration </li></ul>
  56. 56. Advantages of Regional Anesthesia <ul><li>Awake patient- allowing for repeated neurologic evaluations </li></ul><ul><li>Can avoid complicated neurologic monitors </li></ul><ul><li>Greater hemodynamic stability </li></ul><ul><li>Improved cross clamp tolerance </li></ul><ul><li>Reduced hospital stay and costs </li></ul><ul><li>Lower (?) incidence of stroke and cardiac morbidity </li></ul>
  57. 57. Disadvantages of Regional Anesthesia <ul><li>Inability to use pharmacologic cerebral protection </li></ul><ul><li>Requires a cooperative, non-claustrophobic patient </li></ul><ul><li>Possibility of seizures </li></ul><ul><li>Poor access to the airway if GA becomes necessary </li></ul><ul><li>Phrenic and superior laryngeal nerve block is common </li></ul>
  58. 58. Other Problems <ul><li>Conversion rate to GA reported to be around 3% </li></ul><ul><li>Patients who undergo CEA and develop neurologic changes under Cervical Plexus Block are 6 times more likely to suffer a stroke </li></ul>
  59. 59. Relevant Anatomy <ul><li>Cervical Plexus is formed by the 1 st 4 cervical nerves </li></ul><ul><li>Nerves pass laterally along respective vertebral transverse processes </li></ul><ul><li>At the tips of C-2 to C-4 the nerves divide into ascending and descending branches and form loops before uniting into deep and superficial branches </li></ul>
  60. 60. Anatomy Continued <ul><li>The plexus is situated in front of the levator scapulae and scalenus medius and covered by the sternocleidomastoid muscle </li></ul><ul><li>The deep branches are purely motor </li></ul><ul><li>The superficial branches are sensory and supply the skin and subcutaneous tissues of the neck and posterior aspect of the head </li></ul>
  61. 61. Sensory Anatomy <ul><li>The side of the neck may also derive sensation from the trigeminal nerve </li></ul><ul><li>The platysma receives some sensory innervation from cervical branches of the facial nerve </li></ul>
  62. 62. Cervical Plexus
  63. 63. Plexus Diagram
  64. 64. Technique of Cervical Plexus Block <ul><li>Superficial block requires infiltration along posterior border of sternocleidomastoid muscle </li></ul><ul><li>Deep plexus requires block of the nerve roots are they pass through the intervertebral foramina of C-2,C-3,& C-4 </li></ul>
  65. 65. Superficial Plexus Block
  66. 66. Deep Plexus Block
  67. 67. Materials for Block <ul><li>Regular length #25 spinal needle </li></ul><ul><li>Short (1-1.5 inch) spinal needle </li></ul><ul><li>Intermediate acting local anesthetic- 1% lidocaine, 0.5% bupivicaine, etc. </li></ul><ul><li>Use 10 to 20 cc of anesthetic for superficial plexus </li></ul><ul><li>3 to 5 cc at C-2, C-3, C-4 </li></ul>
  68. 68. Superficial vs. Deep Plexus Block <ul><li>3 different randomized trials (205 patients) could not demonstrate clear benefit if deep block was done with superficial block or not </li></ul><ul><li>Same VAS scores </li></ul><ul><li>Same need for additional supplementation </li></ul><ul><li>Some authors question if there is a real anatomic basis for any difference </li></ul>
  69. 69. Supplemental Block <ul><li>Manibular branch of trigeminal nerve </li></ul>
  70. 70. Surgical Approach <ul><li>Ventrojugular approach is standard surgical technique </li></ul><ul><li>This approach improves patient tolerance </li></ul><ul><li>This technique is associated with a higher transient incidence ipsilateral vocal cord motility impairment because of a need for greater vagal nerve mobilization </li></ul>
  71. 71. Cervical Plexus Complications <ul><li>Deep plexus block : </li></ul><ul><ul><li>Intravascular injection </li></ul></ul><ul><ul><li>Subarachnoid injection with brain stem anesthesia </li></ul></ul><ul><ul><li>Phrenic nerve block </li></ul></ul><ul><ul><li>Recurrent laryngeal nerve block </li></ul></ul><ul><ul><li>Vagus nerve block </li></ul></ul><ul><ul><li>Horner’s syndrome </li></ul></ul>
  72. 72. Cervical Plexus Complications <ul><li>Superficial plexus block </li></ul><ul><ul><li>Intravascular injection </li></ul></ul><ul><ul><li>Recurrent laryngeal nerve block if injection is made deeper than the inferior border of the SCM muscle </li></ul></ul><ul><ul><li>Partial brachial plexus block has been reported </li></ul></ul>
  73. 73. Incidence of Problems <ul><li>Pandit et al did not find a single incidence of serious complications related to superficial block in a review of 2500 cases collected from several publications </li></ul><ul><li>In this review serious complications defined as life threatening occurred in only 0.25% of patients (inadvertent subarachnoid injection, respiratory distress from phrenic or laryngeal nerve block) </li></ul><ul><li>Br J Anaesth 2007,99:159-169 </li></ul>
  74. 74. Additional Problems <ul><li>Deep blocks done alone are associated with a higher conversion rate to GA (2.1% vs. 0.4%) </li></ul><ul><li>When deep and superficial blocks are done together the incidence of ipsilateral hemidiaphragmatic paralysis is 55 to 61% </li></ul>
  75. 75. Choice of Local Anesthetic <ul><li>Bupivicaine 0.5% provides the longest time to request for first analgesia </li></ul><ul><li>Ropivicaine is probably the least cardiotoxic </li></ul><ul><li>Use the least possible amount of total anesthetic in any case. </li></ul>
  76. 76. Outcomes: Local vs. GA <ul><li>One series of 548 cases </li></ul><ul><li>Local was 10 cc lidocaine for skin, 10 cc for platysma </li></ul><ul><li>GA was thiopental with isoflurane, nitrous-oxide/oxygen, fentanyl maintenance </li></ul><ul><li>No differences in postoperative stroke or death rate </li></ul><ul><ul><ul><li>Watts et al Am. J Surg 2004; 188:741-747 </li></ul></ul></ul>
  77. 77. Outcomes: Patient Satisfaction Local vs. GA <ul><li>Prospective randomized study of 176 patients comparing CEA under local or GA </li></ul><ul><li>Only the recovery was significantly better with the local group </li></ul><ul><li>No differences in anxiety or satisfaction </li></ul><ul><li>McCarthy et al. Eur J Vasc Endovasc Surg 2001; 27:654-659 </li></ul>
  78. 78. Anesthetic Technique and Surgical Stress Response <ul><li>Prospective trial of 109 patients </li></ul><ul><li>Cortisol, ACTH, prolactin, and C-reactive protein were measured before and after carotid cross clamping and then daily for 3 days after </li></ul><ul><li>Cortisol and ACTH levels were higher in the regional group but this effect was abolished if a shunt was used </li></ul><ul><li>Marrocco-Trischitta et al. J Vasc Surg 2004; 39:1295-1304 </li></ul>
  79. 79. Conclusions: Regional vs. GA <ul><li>No clear data to suggest improved outcome in perioperative neurologic problems </li></ul><ul><li>GA can be combined with plexus block and can result in greater hemodynamic stability and shorter operating times </li></ul><ul><ul><ul><li>Reg Anesth Pain Med 2008;33:340-345 </li></ul></ul></ul>
  80. 80. Complications: PACU Issues/ Postoperative Care <ul><li>Hypertension </li></ul><ul><li>Hypotension </li></ul><ul><li>Myocardial ischemia or infarct </li></ul><ul><li>Cranial nerve injury </li></ul><ul><li>Recurrent Laryngeal Nerve injury </li></ul><ul><li>Stroke </li></ul><ul><li>Bleeding </li></ul>
  81. 81. Postoperative Hypertension <ul><li>Can be secondary to local infiltration around the carotid sinus or its nerve- can be profound in 20% of patients </li></ul><ul><li>Patients with poorly controlled BP are at risk </li></ul><ul><li>Severe hypertension is associated with increased mortality, increased cardiac and neurologic morbidity </li></ul>
  82. 82. Management Options for Postoperative Hypertension <ul><li>Short acting agents such as esmolol and nitroglycerin are considered 1 st line agents </li></ul><ul><li>IV titration of labetolol or hydralazine </li></ul><ul><li>Nitroprusside infusion </li></ul><ul><li>Nicardipine infusion </li></ul>
  83. 83. Postoperative Hypoperfusion Syndrome <ul><li>Somewhat uncommon </li></ul><ul><li>Results from impaired cerebral autoregulation in the surgically reperfused hemisphere </li></ul><ul><li>Manifested as headache, seizure, neurologic deficit, cerebral edema, or hemorrhage. </li></ul><ul><li>CT scan- intracerebral hemorrhage, white matter edema </li></ul>
  84. 84. Hypotension <ul><li>May be related to carotid baroreceptor hypersensitivity after plaque removal </li></ul><ul><li>Can result in myocardial or cerebral ischemia </li></ul><ul><li>Consider judicious amounts of fluid replacement and sympathomimetic agents for support </li></ul>
  85. 85. Postoperative Respiratory Insufficiency <ul><li>Massive hematoma formation (active bleeding, coagulopathy) </li></ul><ul><li>Bilateral recurrent laryngeal nerve injury </li></ul><ul><li>Soft tissue swelling, supraglottic mucosal edema </li></ul>
  86. 86. Carotid Body Denervation <ul><li>Secondary to surgical manipulation </li></ul><ul><li>Results in impaired response to hypoxia </li></ul><ul><li>Can be clinically significant in presence of agents which depress respiration </li></ul><ul><li>May be exaggerated with moderate to severe COPD </li></ul><ul><li>Consider using non-narcotic analgesia </li></ul>
  87. 87. Cranial Nerve Dysfunction <ul><li>Generally secondary to surgical traction not transection </li></ul><ul><li>Generally transient- resolution within 6 months </li></ul><ul><li>Dysphagia/ Hoarseness- recurrent laryngeal nerve injury </li></ul><ul><li>Tongue deviation – hypoglossal nerve injury </li></ul>
  88. 88. Myocardial Infarction <ul><li>A major cause of morbidity </li></ul><ul><li>Symptoms and EKG changes should be investigated promptly </li></ul><ul><li>Hemodynamic instability </li></ul><ul><li>Arrhythmia </li></ul><ul><li>Maximize the balance between myocardial oxygen supply and demand </li></ul>
  89. 89. Parting Thoughts <ul><li>CEA requires a multi-disciplinary team approach from the pre-op period through convalescence </li></ul><ul><li>CEA is a prophylactic procedure requiring careful patient selection </li></ul><ul><li>Close intraoperative communication </li></ul><ul><li>There is no data to strongly support any specific anesthetic approach as long as CBF is maintained and hemodynamic stress is limited </li></ul>

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