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Carotid Endarterectomy and Stenting. Mani K.C Vindhya M.D Asst Prof of Anesthesiology Nova Southeastern University. Introduction -- Stroke and Transient Ischemic Attacks (TIA's) Stroke statistics (Heart and Stroke Facts: 1997 Statistical Suppl. Dallas, TX: American Heart Association)
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Carotid Endarterectomy and Stenting Mani K.C Vindhya M.D Asst Prof of Anesthesiology Nova Southeastern University
Introduction -- Stroke and Transient Ischemic Attacks (TIA's) • Stroke statistics (Heart and Stroke Facts: 1997 Statistical Suppl. Dallas,TX: American Heart Association) • Stroke = third leading cause of death in U.S. • (after heart disease and cancer) • Over 500,000 new cases in U.S. each year (75% in carotid distribution) • Mortality: nearly 1/4 die • Morbidity: often significant and permanent disability
Types and causes of stroke: (Cummings RO (ed). ACLS. American HeartAssociation, 1997, pp. 10-1--10-20.) • Ischemic strokes (75%) – due to occlusion of a blood vessel to the brain • Anterior circulation strokes • = carotid territory strokes • usually involve the cerebral hemispheres • Posterior circulation strokes • = vertebrobasilar territory strokes • usually affect brain stem or cerebellum • Hemorrhagic strokes (25%) • Subarachnoid hemorrhage (SAH) • = bleeding onto surface of brain • Aneurysm = most common cause • Intracerebral hemorrhage • = bleeding into brain parenchyma • Hypertension = most common cause
Treatment of Stroke – now includes thrombolytic therapy • Thrombolytic agent = rt-PA • I.V. thrombolytic therapy is best initiated within 3 hours after onset of stroke symptoms.
Detection • Hallmark of stroke = sudden onset of focal brain dysfunction • Early recognition of “brain attack” signs and symptoms • Carotid (anterior) circulation ! unilateral paralysis ! visual disturbance ! numbness ! monocular blindness • language disturbance • Vertebrobasilar (posterior) circulation ! vertigo ! numbness ! visual disturbance ! dysarthria ! diplopia ! Ataxia ! paralysis
Dispatch – early activation of EMS • Delivery – prehospital transport and management • Minimize time in the field • Door • Immediate general assessment: <10 min from arrival • Immediate neurologic assessment: <25 min from arrival (often includes Glasgow Coma Scale and Hunt-Hess classification)
Data – Does the CT scan show intracerebral or subarachnoidhemorrhage? • If yes, consult neurosurgery. • If no, then probable ischemic stroke. • Review CT exclusions: are any oberved? • Repeat neurologic exam: are deficits variable or rapidly improving? • Review thrombolytic exclusions: are any observed? • Review patient data: is symptom onset now >3 hours? • Decision – Is the patient a candidate for thrombolytic therapy? • Drug – Begin thrombolytic therapy with i.v. rt-PA
Transient Ischemic Attack (TIA) • TIA = a reversible episode of focal brain dysfunction • Initial signs and symptoms of stroke • Lasts only a few minutes to hours before resolving • TIA = the most important forecaster of brain infarction • 5% will develop cerebral infarction within 1st month. • Risk = 12% at one year, and an additional 5% for each year after that • Treatments for TIA: • Carotid endarterectomy, angioplasty & stenting – if severe • (>70% narrowing) of internal carotid artery • Aspirin or ticlopamide • Oral anticoagulants – to prevent embolism to brain in patients with cardiac causes of stroke, especially atrial fibrillation
History of Carotid Endarterectomy (CEA) Surgery • Early history (Koller RL. Postgrad Med 90: 81-86, 1991.) • 1950's: CEA first used to treat cerebrovascular disease • 1971: 15,000 operations per year in U.S. • Mid-1980's: > 100,000 operations per year • 1984: CEA = 3rd most commonly performed operation in U.S. • Late 1980's: The appropriateness of CEA surgery was questioned. • "Only two prospective randomized trials had been carried out, neither of which demonstrated clear benefit." • In the patient with TIA's, which is better? • medical management, surgery, or both? • CEA: Perioperative mortality and morbidity = 10% in one large study (Winslow CM et al. N Engl J Med 318: 721-7, 1988). • C. Early 1990's: • Symptomatic carotid stenosis a. 3 clinical trials showed benefit of CEA (Easton JD, Wilterdink JL. Ann Neurol 35: 5-17, 1994). • NASCET (N Engl J Med 325: 445-53, 1991) • ECST (Lancet 337: 1235-43, 1991) • VA (Mayberg MR et al, JAMA 266: 3289-94, 1991) b. For > 60-70% stenosis, • CEA better than optimal medical care alone
CEA for symptomatic carotid stenosis (70-99%) [Rothwell P et al, Lancet 261: 107-16, 2003; Brown, M. (2008) “Carotid endarterectomy, angioplasty and stenting”, in Hachinski, V. (ed.), The Diagnosis, Treatment, and Prevention of Cerebrovascular Disease: A Prioritized Approach, The Biomedical and Like Sciences Collection, Henry Stewart Talks Ltd, London (online at http://www.hstalks.com/bio)]: • ! Surgical arm: 6-7% stroke or operative death in first few months, but then M&M levels off. • Medical arm: 25% had recurrence in 3 years, 33% recurrence in 10 years • Surgical treatment was better than medical treatment • Surgery is highly effective in preventing recurrent events • In patients treated medically, the highest risk for recurrence is in the first 3 years. • Surgery is only beneficial if performed soon after symptoms.
Asymptomatic carotid stenosis • Asymptomatic Carotid Atherosclerosis Study (ACAS) (JAMA 1421-28, 1995): • Surgery also of value for asymptomatic stenosis (>60%). • 53% reduction in risk of ipsilateral stroke and any perioperative stroke or death. • Asymptomatic carotid bruits are common. • Occur in 5% of population > age 45 • More common in women • Risk of stroke = 2% per year • ACST: Risk of Stroke or Death after CEA or Medical Treatment for Asymptomatic Carotid Stenosis (60-99%) (Halliday A et al, Lancet 363: 1491-1502, 2004): • Initial risk greater for surgical treatment (CEA) • Risk at 5 years greater for medical treatment • Surgical vs. medical: Risks cross at 2 years.
Carotid Angioplasty and Stenting • Carotid Angioplasty – Carotid and Vertebral Artery TransluminalAngioplasty Study (CAVITAS): Comparison of Endovascular vs. Surgical Treatment • (McCabe DJH et al, Stroke 36: 281-6, 2005) • The 5-year risk of stroke or death was the same. • Cranial nerve palsies or hematomas were more common with surgery. • The 5-year rate of restenosis was greater with endovascular treatment.
. Carotid Stenting – Stenting and Angioplasty with Protection in Patients atHigh Risk for Endarterectomy (SAPPHIRE) (Yadav JS et al, New Engl J Med 361: 1493-1501, 2004). • ! “...Carotid stenting with the use of an emboli-protection device is not inferior to carotid endarterectomy.”
Anesthetic Management of Carotid Angioplasty and Stenting (DrummondJ. Anesthesia for Carotid Endarterectomy / Stenting. Dannemiller Anesthesiology Review Course, 2008) • Dual antiplatelet treatment (aspirin and clopidogrel) • Usually transfemoral (sometimes transcarotid) • Usually MAC (neurologic exam) • Two stages: Dilatation and Stenting • Heparin to maintain ACT 250-300 • e.g. 500 units + 1000 units/hr • Prevent / treat bardycardia • independent arterial line • glycopyrrolate pre-treatment • atropine before dilatation (+/-) • external pacer (on and available) • Carotid stenting can cause severe bradycardia, hypotension, and cerebral hypoperfusion.
Preoperative Evaluation • Typical diagnostic workup for TIA/stroke (Koller RL. Postgrad Med 90: 81-96, 1991) • CT scan and/or MRI • Lab studies -- CBC, platelet count, PT/PTT • Carotid studies • Carotid ultrasound • Carotid angiography • Cardiac studies • Electrocardiogram • Echocardiography
Cardiac evaluation of patients with TIA's or stroke (Sirna Set al, Stroke14-23, 1990) • Strong association between carotid and coronary artery disease • Cardiac events often determine the fate of the TIA patient. • Abnormal exercise EKG's = 28% in patients with TIA's and no known cardiac symptoms. • Abnormal stress or dipyridamole thallium studies = 45% in patients with TIA or mild stroke and no apparent heart disease.
ACC/AHA Gudielines on Peri-operative Cardiovascular Evaluation and Care for Non-Cardiac Surgery (Fleisher LAet al, Circulation 116: e418-99, 2007) Active Cardiac Conditions • a. Unstable coronary syndromes • (unstable or severe angina, recent MI) • Decompensated heart failure • Significant arrhythmias • Severe valvular disease • (severe aortic stenosis, symptomatic mitral stenosis) • Functional Capacity • a. If there are no “active cardiac conditions” and the functional capacity is > 4 METs without symptoms, proceed with planned surgery. • b. If the functional capacity is < 4 METs or unknown: • CEA is considered to be “intermediate risk surgery” (reported cardiac risk = 1-5 %) • Clinical Risk Factors include: • H/o ischemic heart disease • H/o compensated or prior heart failure • H/o cerebrovascular disease (i.e., carotid stenosis) • diabetes mellitus • renal insufficiency • With 1 or more clinical risk factors, “Proceed with planned surgery with HR control or consider non-invasive testing if it will change management.”
Intraoperative management • Three main goals of anesthesia for CEA surgery -- to protect the heartfrom ischemia, to protect the brain from ischemia, and to have the patient awaken quickly at the end of surgery (Roizen MF, Anesthesia for Vascular Surgery, In: Barash PG et al (eds.), Clinical Anesthesia, 1989, pp. 1015-47). • Protect the heart from ischemia. • Maintain normal hemodynamics, oxygenation, and ventilation. • Myocardial oxygen supply and demand balance (Thys DM, Kaplan JA. Cardiovascular Physiology. In: Miller RD (ed), Anesthesia, 3rd. Ed. NewYork: Churchill-Livingstone, 1990, pp. 551-83.) • Avoid factors that decrease myocardial O2 supply • Avoid factors that increase myocardial O2 demand
. A high percentage of CEA candidates have coexisting severe or advanced CAD, even with no history or EKG evidence
Protect the brain from ischemia. Some guidelines: (Wendling WW,Carlsson C. Guidelines for anesthesia and cerebral protection in neurovascular surgery. In: Rosenwasser RH et al (eds.), Cerebral Ischemia: Clinical Implications andTherapeutics. Commack, NY: Nova Scientific Publishers, 1994, pp. 77-100) • Maintain a normal or high normal blood pressure. • Maintain normocarbia or slight hypocarbia. • Avoid extreme hyperglycemia. • Monitor for cerebral perfusion. • Treat cerebral ischemia if it occurs. • Have the patient awaken quickly after the operation.
Premedication -- "light" premedication is recommended, to permit: • Neurologic assessment during regional anesthesia. • Fast "wakeup" after general anesthesia.
Monitors: Use routine monitors as reminder for additional monitors.
Does regional or general anesthesia for CEA have a better outcome? • Results of the GALA (General Anaesthesia vs. Local Anaesthesia) Trial (GALA Trial Collaborative Group. Lancet 372: 2132-42, 2008): • Primary outcome (stroke, MI, or death) – no significant difference • General anesthesia (4.8 %) • Local anesthesia (4.5 %) • 4.4 % of patients under local anesthesia had complications that led to cancellation of surgery or conversion to GA. • Stroke was a more common complication than MI after CEA.
Advantages and Disadvantages of Regional or General Anesthesia • Regional anesthesia. • a. Advantages • Awake patient • Airway reflexes preserved • Intraoperative neurologic exam is possible. • Less post-op BP problems (?) • Shorter ICU stay (?) • Shorter hospitalization (not borne out by GALA trial)
b. Disadvantages (Roizen MF. Anesthesia goals for operations to relieve or prevent cerebrovascular insufficiency. In: Roizen MF (ed), Anesthesia for Vascular Surgery. New York: Churchill-Livingstone, 1990, pp. 103-22.) • Need for patient cooperation • Possible loss of patient cooperation, with onset of new neurologic deficit, because of: • confusion • panic • seizures • Inability to secure airway if panic, seizure, or oversedation occur • ! An unexpected delayed deficit may occur sometime after the test period. • ! Inability to administer drugs such as thiopental that might protect the brain against ischemia
General anesthesia • a. Advantages • Anesthetized, motionless patient • Control of airway -- endotracheal intubation • Able to administer drugs such as thiopental to protect brain against ischemia. • b. Disadvantages • Intra-op neurologic assessment impossible • Need sensitive and reliable monitoring for cerebral perfusion in place of awake neurologic assessment.
Regional Anesthesia for CEA • Techniques • Local infiltration by surgeon • Superficial cervical plexus block • Deep cervical plexus block • Combined superficial and deep cervical plexus blocks
Superficial cervical plexus block (Carron H et al. Regional anesthesia:Techniques and Clinical Applications. Orlando, FL: Grune & Stratton, 1984, pp. 10-15) • Landmarks? Crossing of... • External jugular vein and • Posterior border of sternocleidomastoid muscle • Possible complications include: • Accidental injection into internal jugular vein. • Hematoma formation (tear in wall of vein) • Venous air embolus • Anatomy • Superficial cervical space communicates with the deep cervical plexus space. • Inject below the investing fascia, not just subcutaneously (Pandit et al. Brit J Anaesth 91: 733-5, 2003).
Deep Cervical Plexus Block (Carron H et al. Regional anesthesia:Techniques and Clinical Applications. Orlando, FL: Grune & Stratton, 1984, pp. 10-15) • Landmarks? • Line between mastoid process and suprasternal notch • Aim perpendicularly for transverse processes of C2-C4. • Possible complications? • Recurrent laryngeal nerve paralysis = most common • Stellate ganglion block = next most common • Cervical subarachnoid block with possible phrenic nerve block • Direct injection of local anesthetic into vertebral artery, resulting in seizures or apnea
General Anesthesia for CEA • A. Induction. Goal = to avoid extreme changes in blood pressureand heart rate. One suggested regimen: • Preoxygenate • Defasciculating or priming dose of non-depolarizing muscle relaxant. • Titrate anesthetics slowly. One possible regimen: • Fentanyl • Lidocaine • Propofol or etomidate • Esmolol • Institute controlled ventilation with 100% O2. • Muscle relaxant for intubation: • Succinylcholine (unless patient has hemiplegia) • Vecuronium or rocuronium (alternate choices) • Aim for smooth intubation
Maintenance. "Balanced anesthesia" = a reasonable choice • Volatile inhalational agent (isoflurane, sevoflurane, or desflurane) • Nitrous oxide (?) • Narcotic (fentanyl) • Nondepolarizing muscle relaxant (vecuronium or rocuronium)
Two Potential Intraoperative Complications • Cardiac arrhythmias: Bradycardia -- during neck dissection • Most likely cause = compression of carotid baroreceptor • Mechanism? Reflex involving: • CN IX (Glossopharyngeal) = afferent • CN X (Vagus) = efferent • Lidocaine injection of carotid baroreceptor by surgeon • Evidence of decreased cerebral perfusion -- during carotid clamping • Is monitoring for cerebral perfusion even necessary? • These monitors have not been shown to improve outcome. • Logic dictates that monitoring techniques assuring adequate cerebral function at the lowest myocardial work have a place in CEA surgery (Roizen MF, 1990). • Types of cerebral perfusion monitors • Raw 16-20 lead encephalogram (EEG) • Considered to be the "gold standard" monitor • Disadvantages: • Need specially trained personnel • Electrically "noisy" OR environment • Bulky equipment • Significant change = • > 50% reduction in EEG amplitude • flattening of EEG
Processed EEG only monitors 2-4 channels. • EEG electrodes placed on "watershed" areas • Still may miss ischemia during clamping • Somatosensory evoked potentials (Lam AM et al. Anesthesiology 75: 15-21, 1991) • a) "Subtracts out" background EEG activity, leaving only the evoked potential from: • median nerve (wrist) • posterior tibial nerve (ankle) • Significant change = • > 50% reduction in amplitude • flattening of SSEP • Similar sensitivity and specificity to EEG • Both SSEP's and EEG are associated with a considerable false positive rate.
Stump pressures • Surgeon measures pressure in stump of carotid artery above cross-clamp. • Significant reduction = stump pressure < 50 mm Hg • Problem = poor correlation with EEG findings: • False positives = stump pressure < 50 mm Hg with normal EEG • False negatives = stump pressure > 50 mm Hg with "ischemic" EEG • May not adequately assess cerebral perfusion after stroke or RIND • Regional cerebral blood flow (Xenon washout) • only available in certain centers • indicates global well-being rather than focal cerebral ischemia • Jugular venous oxygen saturation • ! global well-being rather than focal ischemia • Transcranial Doppler (to detect emboli or ischemia) • Neurologic assessment under regional anesthesia
Responses to evidence of decreased cerebral perfusion. • Surgeon can unclamp the carotid artery and insert shunt. a) Shunting during carotid endarterectomy -- three schools of practice: • Shunt routinely. • Shunt never, or very rarely. • Shunt selectively, based on monitoring to detect cerebral ischemia. • Advantage -- preserves carotid flow • Potential risks: • Thromboembolism • Intimal dissection • Thrombus formation • Air embolism • Obstruction of surgical field
Increase the mean arterial pressure • Increases cerebral perfusion pressure • Increases cardiac afterload and may precipitate myocardial ischemia. • So follow ST segments on EKG • Pharmacologic cerebral protection with thiopental • Used more commonly for clipping of intracerebral aneurysms than for carotid endarterectomy • Thiopental was cerebroprotective in one prospective randomized study in humans (Nussmeyer NA et al. Anesthesiology 64: 165-70, 1986). • Emergence -- Main concerns: • Smooth and rapid awakening from general anesthesia, in order to obtain a neurologic assessment. • Control of blood pressure
Post-operative considerations.Potential postoperative complicationsoccur in 4 locations: • “In the arm.” • Hypertension = a very common complication • Incidence was 19% in one study. • More common if patient was hypertensive preoperatively. • Hypotension – in approximately 5% of patients • In the neck. Problems secondary to surgery on the neck: • Wound hematoma – occurred in 5.5% of NASCET patients • Paralysis of cranial nerves (VII, IX, X, or XII) • Carotid body dysfunction • In the head. Cerebrovascular complications include: • Carotid artery thrombosis • Emboli • Stroke • Hyperperfusion syndrome • Manifests as severe unilateral headache, which is postural • Related to preoperative hypoperfusion and loss of autoregulation • Seizures – relatively uncommon • D. In the chest. Myocardial infarction often occurs