Carotid/Cerebrovascular

Carotid/Cerebrovascular procedures include: 

• Carotid Endarterectomy (CEA) 
• Transcarotid Artery Revascularization (TCAR)
• Trans-femoral carotid stent (TFCAS)
• Subclavian artery stent (trans-femoral or trans-brachial/radial)
• Carotid subclavian artery bypass or transposition 
• Carotid–carotid bypass
• Vertebral artery interventions or bypass 
• Carotid body tumor.

Carotid disease 

Carotid artery atherosclerotic disease is a major cause of ischemic stroke, being an underlying  cause in 10% to 20% of cases.⁷⁴ It is important to assess symptom status to determine the need for  intervention as well as the type of intervention. Symptoms could be permanent (stroke), or  transient (TIA and amaurosis fugax). A transient ischemic attack (TIA) or mini stroke lasts less  than 24 hours, and amaurosis fugax involves the transient loss of vision in one or both eyes.  Patients with innominate artery disease can also present with anterior cerebral ischemic symptoms  due to reversal of flow in the carotid artery. 

It is important to assess for comorbidities to confirm the patient’s life expectancy of at least five  years at the time of planned intervention in asymptomatic patients.⁴⁸ 

Vertebrobasilar disease 

The diagnosis of vertebrobasilar disease is challenging due to conditions that mimic posterior circulation ischemia such as cardiac arrhythmias or orthostatic hypotension. Two main mechanisms are low-flow or embolic: low-flow presents with vertigo drop attacks, diplopia,  tinnitus, dysphagia, dysarthria, and ataxia. Similar positional symptoms can also occur due to vertebral artery compression. Significant bilateral vertebral artery stenosis is necessary to produce low-flow symptoms. 

In addition, patients with proximal subclavian artery stenosis may present with vertebrobasilar insufficiency due to reversal of flow in the vertebral artery. Patients with subclavian stenosis may  also present with arm claudication, rest pain, digital embolization, or coronary-subclavian steal 

Physical Examination 

A complete physical exam should be performed, with special attention paid to the neurologic exam, documenting existing deficits. Evaluation of the neck to determine prior surgical history is important to determine if surgical re-operation may be challenging (i.e., anatomic high risk).

Elicitation of other physical exam findings that suggest high medical risk is also important (e.g.,  oxygen dependence, lower extremity edema, elevated Jugular Venous Pressure [JVP], and irregular heart rhythm).  

A carotid bruit detected on auscultation is associated with an increased risk of cardiovascular mortality by 2-3-fold, but the positive predictive value for a greater than 50% Internal Carotid  Artery (ICA) stenosis is poor (less than 40%).^{75, 76} 

Imaging 

• Duplex Ultrasound (DUS) is the first-line imaging modality for carotid occlusive disease and is associated with high sensitivity and specificity. In asymptomatic patients with high grade carotid stenosis, DUS findings of echolucent, homogenous, ulcerated plaque can predict increased stroke risk and may benefit from intervention. In some expert centers,  DUS alone is adequate for planning prior to carotid endarterectomy.  
• Computed Tomography Angiography (CTA): CTA of the chest, neck, and head is appropriate prior to intervention in order to assess the anatomy of the vasculature,  especially if carotid stenting is performed. Magnetic resonance angiography (MRA) can also be performed but is prone to overestimation of the degree of stenosis. 
• Diagnostic Digital Subtraction Angiography (DSA): DSA is rarely indicated for diagnostic purposes only but can be performed if there is a discrepancy between different diagnostic modalities when assessing the degree of stenosis. In patients with chronic kidney disease and equivocal DUS imaging, DSA is preferred over CTA and MRA (by minimizing contrast load). DSA is also preferred in patients for whom CTA or MRA are technically inadequate or difficult (e.g., obesity, or indwelling ferromagnetic material). 

Medical Management and Lifestyle Changes  

In patients with carotid artery stenosis, treatment of hypertension, hypercholesterolemia, and efforts at smoking cessation are recommended to reduce overall cardiovascular risk and risk of stroke regardless of whether intervention is planned. Smoking cessation, antiplatelet/  anticoagulation therapy, blood pressure control, cholesterol and diabetes management can all impact the risk of stroke and should be aggressively managed. 

• Smoking: Smoking increases stroke risk up to 50%; cessation is particularly advised for all patients with cerebrovascular disease. 
• The use of Antiplatelets/Anticoagulation for stroke reduction should be considered based  on published data: Aspirin or Plavix is the mainstay of antiplatelet therapy: 
  • ASA 75-100 mg/day reduces relative risk by ~25% compared to placebo.
  • Clopidogrel did not reduce stroke risk compared to ASA in CAPRIE trial.⁴⁸
  • DAPT did not reduce stroke risk compared to ASA alone in the CHARISMA  trial.⁴⁹ 
  • DAPT did not reduce stroke risk compared to Clopidogrel alone in the MATCH trial.⁷⁷ 
  • Adding Dipyridamole to ASA may provide only marginal benefit in the European  Stroke Prevention Study 2.⁷⁸ 
  • ASA+Dipyridamole had similar effect compared to Clopidogrel for noncardioembolic ischemic stroke in PRoFESS trial.⁷⁹ 
  • Vitamin-K Antagonist (VKA, Warfarin) reduces stroke risk only in patients with atrial fibrillation.  
• Antihypertensive management: 
  •  ~6 mmHg reduction in DBP reduces nonfatal stroke risk by 43%
  • Particular antihypertensive agent has not been shown to be associated with  reduction of stroke risk in HOPE⁸⁰ (ACEI), PROGRESS⁸¹ (ACEI), LIFE⁸² (ARB),  and ALLHAT⁸³ (Diuretics) studies. 
  • It is prudent to be cautious with BP reduction in patients with stroke, as J-shaped relationship with BP and Stroke risk and hypotension may lead to cerebral hypo perfusion and worsen stroke clinically.  
  • Cholesterol management: Statin use reduced relative risk of stroke by 25-30% in 4S,⁸⁴CARE,⁸⁵ HPS,⁸⁶ and SPARCL⁸⁷ studies. 
  • Diabetes management: Diabetes increases stroke risk by about three-fold. There are conflicting randomized controlled trial (RCT) results for intensive glycemic control and stroke risk. Glycemic control should be considered per the current guidelines of the  American Diabetes Association.¹⁸ 

Risk Stratification for Surgery (both physiologic and anatomic) 

A multidisciplinary approach to care can optimize outcomes. Medical specialists and team members can assist patients with risk factor modification, such as smoking cessation, maintaining glycemic control, normalizing blood pressure and lipid levels, maintaining antiplatelet therapy  and fostering participation in exercise programs, thereby promoting a positive patient experience.  Discharge planning should also be considered at time of surgical planning. 

Risk stratification for surgery is critical in patients with carotid stenosis, as it affects the decision  making to treat with revascularization vs medical therapy alone, and also impacts the choice of intervention in patients being considered for revascularization.⁸⁸ For patients being considered for  CEA, the 30-day perioperative CEA stroke and death rate should not exceed 6% for symptomatic patients and 3% for asymptomatic patients. 

The cardiac assessments should follow the general recommendation of the American College of  Cardiology/American Heart Association (ACC/AHA) guidelines.³¹ 

Cardiovascular and pulmonary disease remain the leading causes of early and late death in patients with peripheral vascular disease, and the first step should be to determine whether an active cardiovascular condition exists, which would mandate further assessment and management before planned intervention.⁸⁸ There are well-accepted, published guidelines from most of the  medical subspecialties to guide the preoperative evaluation, including those from the American Heart Association and the American College of Cardiology for the optimal preoperative cardiac  evaluation for patients undergoing major or moderate risk noncardiac surgery.³¹ 

Factors that may increase the risk of CEA include:  

• Medical comorbidities like advanced CHF, severe coronary artery disease (e.g., left main  or severe multivessel CAD, recent MI in last 6 weeks), and severe COPD  
• Anatomical features (such as high cervical or intrathoracic lesion) 
• History of neck surgery or radiation, contralateral ICA occlusion, ipsilateral CEA, tracheal  stoma, immobilized neck (e.g., from arthritis)  

Asymptomatic patients at high risk of complications after CEA and CAS may be managed medically. Patients should be on aspirin (75-100 mg daily). The addition of rivaroxaban 2.5 mg  twice daily to aspirin monotherapy may improve cardiovascular outcomes (COMPASS trial).⁸⁹

Preoperative Labs  

Standard CBC, chemistry profile and coagulation profile are recommended preoperatively.

Preoperative Medication Adjustment  

It is reasonable to individualize the management of perioperative clopidogrel therapy. There is no clear information regarding the risks or benefits of continued clopidogrel monotherapy in the periprocedural period for CEA.  

Preoperatively:  

• ASA: Start ASA 75-100 mg/day. Clopidogrel can be used as an alternative in patients already on it prior to CEA. While DAPT with aspirin and clopidogrel may slightly reduce the risk of perioperative stroke, the incidence of perioperative bleeding events is significantly higher compared to monotherapy.  
• Statins: Start high-intensity statins: Atrovastatin 40-80 mg/day or Rosuvastatin 20-40  mg/day 
• Perioperative antibiotics: Prophylactic antibiotics for open procedure should be considered perioperatively as for any other surgery, and for endovascular interventions on a case-by-case basis. 
• Anticoagulation and its reversal: If patient is on oral anticoagulation preoperatively, then discontinue them before the procedure to minimize bleeding complication. DOACs should be held for 48-72 hours before procedure. Warfarin should be discontinued 3-5 days in advance. Please consider bridging with parenteral anticoagulation (UFH or LMWH) in appropriate patients with high thrombosis risk. 
• Nephropathy: Techniques to minimize contrast nephropathy for endovascular procedures in patients with CKD should be utilized. While many different agents have been studied with varying success, only fluid loading has been consistently reported to be associated with better renal outcomes. If there is no contraindication fluid administration pre, intra and post operatively is recommended. The issue to hold ACEs and ARBs is still not resolved and more research is needed.  
• Allergy: Patients with allergy to intravenous iodinated contrast and scheduled for  angiography should get premedication with prednisone 50 mg in 3 oral doses at 13 hours,  7 hours, and one hour prior to procedure, and Diphenhydramine 50 mg one hour prior to  procedure 
• ACE Inhibitors: If significant volume depletion is anticipated, it is suggested to hold ACE  inhibitors and angiotensin receptor antagonists on the morning of surgery and restarting these agents after the procedure, once euvolemia has been achieved. 
• Diabetes Mellitus: It is suggested to hold metformin at the time of administration of contrast material among patients with an eGFR of <60 mL/min or up to 48 hours before administration of contrast material if the eGFR is <45 mL/min and restarting no sooner than 48 hours after administration of contrast material as long as renal function has remained stable. Diabetic patients who receive intermediate or long-acting insulin should receive half the scheduled dose when nil per os (NPO) in preparation for surgery.  Glycemic control should be considered per the current guidelines of the American  Diabetes Association.¹⁸

General 

• Anesthetic technique: General anesthetic, regional or local per surgeon preference.  
• Hair is removed with clippers if needed.  
• Skin preparation with chlorhexidine gluconate/alcohol antiseptic. 
• Perioperative antibiotics are routinely used (cefazolin or vancomycin). 

a. Optimization and Risk Assessment  

The perioperative anesthesia process should include identifying potential perioperative risks,  since patients scheduled for carotid surgery are at high-risk for neurological and/or cardiovascular complications.^{90, 91} They are commonly older and have significant comorbid burden, including peripheral arterial disease, coronary artery disease, history of TIA or stroke, hypertension,  diabetes mellitus, chronic kidney disease, with poor functional status and extensive smoking history.⁹¹ 

b. Anesthesia Management 

i) Anesthesia Techniques  

Most carotid procedures can be safely performed under general anesthesia (GA), regional  anesthesia (RA), sedation, or a combination of the three, depending on the local clinical practice  as well as patient preferences.^92-94 

Despite theoretical advantages of RA and a plethora of well-designed clinical studies, the  question regarding safest anesthetic modality for carotid surgery remains controversial, though some more recent reports found GA to represent an independent risk factor for perioperative MI  and to be associated with higher mortality compared with RA.⁹⁵ 

The lack of clear and consistent evidence supporting one particular anesthetic approach has led to  development of a wide range of individual views on what constitutes “optimal anesthesia.” 

• General Anesthesia: The majority of carotid procedures in the US are performed under general endotracheal anesthesia.⁹² It offers airway protection, cerebral protection (volatile anesthetic agents), and arterial carbon dioxide control (cerebral perfusion). Endotracheal tube  (ETT, “tube”) provides better protection from aspiration and thus may be preferred over  Laryngeal Mask Airway (LMA) (high co-morbid burden may increase the risk of aspiration).  GA can be maintained using either: (1) inhalational agent (“gas”): Sevoflurane, with a “sweet”  smell, is commonly used compared to Desflurane as the latter has a more pungent smell/taste  (i.e., avoid in patients with irritable airway). Desflurane was however reported to be associated with a faster emergence;^{96, 97} (2) TIVA (total intravenous anesthesia; commonly  consisting of a combination of infusions, e.g., propofol, opioid, lidocaine, ketamine) offers another approach to maintain general anesthesia. TIVA was found to reduce nausea/anesthesia  (propofol).⁹⁸ 
• Regional Anesthesia: This offers intact cerebral autoregulation with easy assessment of neurological function during carotid cross-clamping, lower shunt insertion rate, reduced blood loss, lower risk of thromboembolic events, less hemodynamic instability with a reduction of cardiac- and respiratory-related morbidity, shorter hospital stay, and lower cost compared with  GA.^99-102 Most carotid procedures require a blockade of C1-4 dermatomes using either (1)  superficial cervical plexus block, (2) deep cervical plexus block, or, (3) local infiltration by  the surgeon (alone or in combination).^103-105 Of note, up to half of the patients with deep cervical block present with an unintended phrenic nerve block.¹⁰⁶ All anesthetic nerve blockades can be done safely under ultrasound guidance. Choice of local anesthetic drug will depend on expected duration of surgical procedure. Mepivacaine is suitable for procedures of up to 2 hours, Ropivacaine or Bupivacaine may be preferred for procedures expected to take longer than 2 hours.¹⁰⁴ 
• Sedation: All local or regional anesthetic techniques can be supplemented with light to moderate sedation such as propofol or dexmedetomidine drips for patient comfort.^107-109 On the other hand, avoidance of perioperative benzodiazepines has been recommended to reduce the risk of postoperative delirium.¹¹⁰ Opioids may be added for analgesia/sedation as well.  Sedation should be adjusted during cross-clamping to allow neurological assessment and should be minimized in patients undergoing TCAR or TFCAS. 

ii) Monitoring and Access 

All patients require the standard mandated by the American Society of Anesthesiologistsincluding oxygenation (peripheral oxygen saturation [SpO2]), ventilation (CO2 monitor),  circulation (ECG and BP), and temperature monitoring.⁶⁷ 

In addition, all patients need adequate IV access and continuous oxygen supply.

Several techniques have been introduced to monitoring cerebral perfusion including internal carotid artery stump pressure, EEG, transcranial Doppler, somatosensory-evoked potentials  (SSEP), Bispectral index (BIS) monitoring, or cerebral oximetry, with none showing consistently  improved outcome.^111-115 As such, many surgeons choose to routinely shunt all patients under GA  during cross-clamping. Of note, even patients undergoing carotid surgery under regional or local anesthesia who display a significant drop in brain regional oxygen saturation as measured with a  cerebral oximeter after cross-clamping, may fail to present immediate neurologic symptoms.¹¹⁶ 

Indwelling arterial catheter may be considered in patient with cardiac, pulmonary, renal, or metabolic conditions requiring continuous hemodynamic monitoring and/or blood sampling. 

Intra- and postoperative use of vasoactive drips may require the placement of a central venous line. 

iii) Intraoperative Concerns 

• Neurological deficit after cross-clamping: (1) Presentation: contralateral motor weakness, loss  or altered consciousness, agitation, confusion, dysphasia, and/or seizures; (2) Prevention:  While the commonly applied augmentation of arterial pressure to > 20% above preoperative  baseline after cross-clamping has been shown to reduce the incidence of postoperative  cognitive dysfunction, it may trigger myocardial ischemia; (3) Treatment: (a) augmentation  of arterial pressure to > 20% above preoperative baseline; (b) Administration of high  concentrations of oxygen, (c) release of the carotid cross-clamp followed by shunt placement  (4) Post-unclamping: Avoidance of hypertension (hyperperfusion syndrome).^{58, 99, 117} 
• Myocardial infarction: Recent evidence reported higher incidence of MI in patients undergoing CEA under general anesthesia.⁹⁵ 

d. General and Procedure-Specific Concerns 

General interoperative concerns: Skin preparation (CHG wipe timeout for three minutes to dry),  Foley placed by trained staff, shaving performed with clippers, normothermia intra op. 

Steps Prior to Discharge 

• General: Avoid hypotension or hypertension, which may precipitate a neurologic event or bleeding.  
• Monitoring:  
  • Perform close physical examination and frequent neurologic checks in the immediate postoperative period in order to evaluate for new neurologic deficits or cranial nerve injuries.  
  • Conduct strict blood pressure monitoring in order to detect and treat cerebral hyperperfusion syndrome, which may lead to intracranial hemorrhage. This can also manifest initially as ipsilateral headache. Particular care should be taken in patients with high-grade or bilateral high-grade carotid artery stenosis. 
• Medication: 
  • Administer aspirin monotherapy after CEA (typically performed) 
  • Administer dual antiplatelet therapy (e.g., aspirin plus clopidogrel) after CAS  (standard treatment)  
  • Narcotics are typically avoided for pain control as they can lead to mental status changes, and pain control is often adequate with over-the-counter agents.  
• Discharge: Most asymptomatic patients can be discharged safely on the first postoperative day after carotid revascularization. 

Steps After Discharge 

• General: 
  • Instruct patients to contact the surgeon if swelling develops at the operative site, there are signs of infection (e.g., erythema, purulence), worsening pain at the surgical site or if ipsilateral headaches develop. Hyperperfusion syndrome can occur several days after CEA and can manifest as new onset headache.  
  • Factors associated with restenosis include continued smoking, small ICA  diameter, operative defect detected at intraoperative assessment, and primary closure after CEA. 
  • Smoking cessation and abstinence 
• Follow-up: Conduct a one-month follow-up visit with carotid duplex ultrasound to assess for patency.  
• Office / Telehealth Visit:  
  • Follow-up within a month with a postoperative, unless indicated sooner.
  • Surveillance carotid duplex ultrasound at 1 month, at 6 months (if >50%  stenosis), and then yearly after CEA 
  • Surveillance carotid duplex ultrasound at 1 month, 6 months, and yearly after  carotid stenting to assess stent patency and for to assess for development of  new or contralateral lesions 
  • Specific carotid duplex US velocity criteria must be used post CAS to detect a  hemodynamically significant stenosis post CAS, per local interpretation criteria. 
• Medication: The use of long-term medications can be coordinated with the patient’s primary care physician and can include the use of statins or a PCSK9 inhibitor in order to achieve optimal LDL control. In addition, anti-platelet agents, anti-hypertensive agents, and agents for glycemic control should be prescribed, as indicated.  o Reasonable antiplatelet regimens: 
  • ASA 81 mg/day or 
  • Clopidogrel 75 mg/day or 
  • ASA+Dipyridamole (25-200 mg) twice a day (BID) 
  • DAPT w ASA+Clopidogrel for at least 30 days in patients who underwent carotid stenting 
  • Statin – high intensity if tolerated 
  • Atrovastatin 40-80 mg/day or 
  • Rosuvastatin 20-40 mg/day 
  • PCSK9 inhibitor if LDL-C is not at goal <70 with maximum therapy with a high potency statin. 
  • Anti-hypertensive management is similar to that for the normal population with cardiovascular disease. Strict control is especially recommended in patients at high risk for hyperperfusion syndrome.
  • Diabetes medications – optimal glucose control recommended

References