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By Dr. Mohamed Dorgham, MD Lecturer of Anesthesia, Critical Care medicine and Pain Therapy Carotid End Arterectomy
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Anatomy
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Pathophysiology Atheroscelerosis Carotid Artery Occlusive Disease Stroke TIA Amaurosis Fugax Asymptomatic Bruit Embolization Hypoperfusion
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Stroke Stroke is the 3 rd leading cause of Death and long term disability in USA Perioperative Stroke Carotid Stenosis > 50% Asymptomatic Carotid Bruit 1.0% 3.6%
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Indications North American Symptomatic CEA Trial North American Symptomatic CEA Trial European Carotid Surgery Trial 1992 Definitive results for symptomatic patients with high grade stenosis > 70% 9% # 26% 2.8% # 16.8% 70-99%
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CA Surgery Asymptomatic Narrowing Operation Versus ASA CA Surgery Asymptomatic Narrowing Operation Versus ASA Mayo Asymptomatic CEA Study 5 Randomized trials evaluated CEA in Asymptomatic Pts European Asymptomatic CA Surgery Trial CAS ~70% European Asymptomatic CA Surgery Trial CAS ~70% Asymptomatic CA (60%) Atherosclerosis Study Asymptomatic CA (60%) Atherosclerosis Study Depatment of veterans CEA + Aspirin Versus Asprin alone >or= 50% Depatment of veterans CEA + Aspirin Versus Asprin alone >or= 50% Largest Trial CEA is not indicated 50-90% stenosis Increased no. of MI & TIA In Surgical Group No difference in the incidence Of Stroke & Death 5 yrs risk of Ipsilateral Stroke CEA+ASA: 5.1% ASA alone: 11.0% CEA+ASA: 6.4% ASA alone: 11.8%
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Perioperative Morbidity and Mortality rates Perioperative Morbidity and Mortality rates Systematic review of 51 studies ( from 1980- 1995) reported the results below Systematic review of 51 studies ( from 1980- 1995) reported the results below 5.6% 1.6% 1.3% 3.8%
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Preoperative Evaluataion Correctable CAD 28% Severe Valvular Disease Severe Valvular Disease Decompensated CHF Decompensated CHF Recent MI Unstable Angina Systemic Atherosclerosis CAD Leading cause of Early & Late Mortalities Evaluation of Myocardial Function Evaluation of Myocardial Function
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Trials established that CEA prevents Stroke in selected patients Perioperative medical TTT is standard for all CEAs Further tests would have little potential to alter TTT Percutaneous angioplasty + Stenting may be an alternative in high risk pts CEA Remains the Gold Standard 1 2 3 No reduction in short term mortality with prophylactic revascularization Low overall rates of cardiac M & M It would be unlikely that further specialized tests would cancel the procedure It would be unlikely that further specialized tests would cancel the procedure 4
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Severe CAD (Unstable) + Severe Carotid Artery Occlusive disease (Symptomatic) Combined CEA + Coronary revascularization Role of Carotid Angioplasty + Stenting Before Staged CABG Still unproven
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Ablation of Stress responses Heart Protection Brain Protection Goals Anesthetic management Awake patient during or at the end of surgery For neurological examination HR & BP control Ablation of Surgical pain
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Regional Versus General Anesthesia No large scale prospective randomized trials evaluated the difference in Neurologic & Cardiac outcomes with Regional versus General Anesthesia Most reports indicate no difference in perioperative mortality rates on basis of anesthetic technique Rate of conversion from RA to GA 2-6% Decision to use one technique is based on: Surgeon’s & Anesthetist’s experience Patient pereference
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General Versus Regional Anesthesia No clinical neurological assessment Less BP stability 1.Inability to use pharmacological cerebral protection 2.Inadequate access to airway 3.Near toxic level of LA 4.Phrenic nerve paresis 5.Claustrophobia 6.Increased catechoamine level 1.Continuous neurological assessment 2.Greater stability of BP. 3.Reduced need for shunting 4.Avoidance of expensive monitoring & Reduced hospital costs 5.High patients preference (92%) Advantages Disadvantages 1.Difficult vascular anatomy Short neck High carotid bifurcation 2.Control of respiration 3.Brain protective measures 4.Avoids excessive neck palpitations Advantages
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Commonly used Induction agents Commonly used maintenance anesthetics Short to Intermediate acting NDMR Stable hemodynamics Awake patient at the end of procedure General Anaesthesia Sufentanil: 0.5-1.0 mcg/kg for sedation slow speech or delayed response to questions Thiopental / Etomidate / Propofol O2 50% + Low dose (< 0.5 MAC) inhaled Anesthetic Vecuronium Combined Remifentanil + Propofol infusion Isoflurane Low Critical rCBF Less EEG changes during CA clamping Sevoflurane Same Critical rCBF Rapid Emergence
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Stress of Laryngoscopy & Intubation Esmolol Used liberally during induction High normal BP Induced HTN Hemodynamic Fluctuation IV volume depletion Esmolol Nitroglycerine Nitroprusside Light anesthesia Phenylephrine Ephedrine Vasopressors IV fluids 5ml/Kg Titration of Anesthetics Immediate TTT Anesthetic Problems Phenylephrine 50-100 mcg Surgical manipulations of carotid sinus Infiltration of Carotid Biforcation Baroreceptors activation Hypotention & Bradycardia Intra & Postopertive Hypertension
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Anesthetic Problems CO2 management Poor Collaterals Poor Collaterals Chronic Hypo perfusion Chronic Hypo perfusion Vasomotor Paralysis Vasomotor Paralysis Hypercarbia Hypocarbia Steel Phenomenon Inverse steel Phenomenon Relation between hypercarbia & cerebral ischemia is unproven Normocapnia Or Mild Hypocapnia Little clinical evidence of Inverse steel PaCO2 23 mmHg increases risk of ischemia Vasoplegia significantly improve after CEA
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Anesthetic Problems Blood Sugar management Hyperglycemia increases ischemic injury Blood glucose > 200mg% Increase incidence of Stroke / TIA / MI / Death Maintain blood sugar < 200 mg% Avoid dangerous Hypoglycemia
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Anesthetic Problems Emergence Neurological Deficits Hypertension & Tachycardia Myocardial Ischemia Discuss with Surgeon Angioplasty Reoperation Aggressive pharmacological TTT Propofol # Isoflurane Control BP Propofol # Isoflurane Decreased pharmacological intervention during emergence Propofol > Isoflurane Decreased incidence of Myocardial ischemia during emergence All patients with myocardial ischemia on emergence had SBP>200mmHg
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Regional Anesthesia Blocking C2 to C4 dermatomes Superficial & Deep Cervical Plexus block 1.Requires Patient cooperation Constant communication Gentle handling of tissues 2.Supplemental infiltration of LA by surgeon especially at the lower border and ramus of mandible 3.Sedation must be kept to minimum 1.Assess conscious / speech / contralateral hand grip 2.Clamp test 2-3 mins in awake pt indicates the need of shunt placement 3.BP augmentation with phenylephrine if neurologic deficit During Clamp TestAfter shunt placement
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals Stump Pressure It’s the back pressure from the contralateral CA & vertebrobasilar system Easy Inexpensive Continously available Critical Stump pressure is Unknown <50mmHg is associated with hypoperfusion
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals Regional cerebral Blood Flow Iv or CA injection of Radioactive Xenon Detectors placed over the ipsilateral cortex supplied by MCA Before – During – After CA clamping Provided the relationship between Critical rCBF (ml/100gm/min) & EEG Isoflurane: 10 Enflurane:15 Sevofluran: 10 Halothane: 20 Limitations: Expenses & Expertise
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals Electroencephalogram Incidence of ischemic changes: 7.5- 20% Contralateral CA stenosis: 50% Ischemic changes: CA clamping Hypotension Shunt malfunction Cerebral emboli Limitations: Subcortical & small cortical infarcts False negative results Affected by: BP Temperature Anesthetic depth False +ve results perioperative strokes occur PO
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals SSEP Based on the response of sensory cortex “supplied by MCA” to peripheral sensory nerve stimulation Decreased CBF: Decrease amplitude Increase latency or both CBF<12ml/100gm/min: Abolished response Limitations: Affected by: BP Hypothermia Anesthetics False –ve results Validity not definitively established
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals Transcranial Doppler Continuous measurement of mean blood flow velocity: Detects microemblic events in MCA Shunt function Need of early CA clamping Detects early asymptomatic CA occlusion Hyperperfusion syndrome Limitations: High rate of technical failure Improved outcome not yet reported
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Monitoring Prevent IO Strokes Identify need of shunting Identify benefit from BP augmentation Goals Cerebral Oxygenation Jugular Bulb Venous monitoring Cerebral Oximeter Global cerebral O2 Metabolism: Arterial – Jugular venous O2 content SjvO2 Global cerebral O2 Metabolism: Arterial – Jugular venous O2 content SjvO2 Continuous regional cerebral SO2 Through Scalp Limitations: Wide Pt to Pt variability Lack of clinical threshold Continuous regional cerebral SO2 Through Scalp Limitations: Wide Pt to Pt variability Lack of clinical threshold
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Postoperative Considerations 1.Neurological Complications Thromboembolic Major mechanism Hemodynamic 21% HypoperfusionHyperperfusion Syndrome of abrupt increased blood flow + Loss of autoregulation in surigically reperfused brain Headache Seizures Focal neurological signs Brain edema Intracerebral hage 1-5 days PO (0.4-2.0%) Risk Factors Post operative HTN Preop. severe CA stenosis Recent contralateral CEA
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Postoperative Considerations 2.Post operative Hypotension Occurs as frequent as HTN Carotid sinus hypersensitivity and reactivation More common after regional anesthesia Carotid sinus hypersensitivity and reactivation More common after regional anesthesia Myocardial ischemia & Cerebral ischemia COP: Normal or elevated SVR: reduced Judicious fluids + Vasopressors Resolves within 12-24 hrs
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Postoperative Considerations 3.Cranial & Cervical nerve dysfunction Recurrent Laryngeal Nerve Superior Laryngeal Nerve Hypoglossal Nerve Marginal Mandibular Nerve
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Postoperative Considerations 4.Carotid Body Denervation Unilateral Bilateral Due to Surgical manipulation Impaired ventilatory response to mild hypoxemia Impaired ventilatory response to mild hypoxemia Loss of normal ventilatory responses Loss of normal arterial pressure Responses to acute hypoxia Loss of normal arterial pressure Responses to acute hypoxia Increased resting PaCO2 Central chemoreceptors are the primary sensors for maintaining ventilation Serious respiratory depression in response to opioid administration
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Postoperative Considerations 5.Wound Hematoma North American Symptomatic CEA Trial: 5.5% Most of cases due to venous oozing North American Symptomatic CEA Trial: 5.5% Most of cases due to venous oozing External Compression Aggressive BP control Immediate evacuation
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Endovascular Intervention Management of carotid artery stenosis By percutaneous intervention Femoral or CCA Management of carotid artery stenosis By percutaneous intervention Femoral or CCA AngioplastyStenting GA with short acting drugs GA with short acting drugs Sedation With MAC Sedation With MAC Heparin........> ACT= 250-300 sec Protective devices against embolization Anticholinergics Intolerance to antiplatelets Aortic arch disease CA torsiousity Calcification / Heavy thrombus burden / Unstable plaque Considerations Contraindications
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1.Manifestations: of CAD (Asymptomatic bruit...> Stroke) 2.Indications: Symptomatic Pt. +/- High grade stenosis 3.Further evaluation of myocardial function 4.Combined versus Staged operation 5.Goals of anesthetic management 6.Regional versus GA 7.Anesthetic problems 8.Postoperative considerations 9.Endovascular intervention Summary
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