Key Points
- 1.
Patients who present for cerebrovascular, aortic, or peripheral arterial interventions are at elevated risk for concomitant coronary artery disease.
- 2.
A thorough preoperative assessment for cardiovascular disease and medical optimization of any comorbid conditions are essential before elective vascular surgery. This preoperative process is typically not possible for emergency vascular procedures. For urgent but not truly emergent procedures, an expedited workup and targeted medical optimization may aid in perioperative management.
- 3.
The most significant risk factor for future stroke in the setting of carotid stenosis is the presence of recent symptomatic neurologic symptoms. Symptomatic high-grade carotid stenosis should undergo repair. The benefit of intervention for patients with symptomatic but moderate stenosis or in asymptomatic patients with high-grade stenosis is statistically significant, although less robust.
- 4.
Because of the high mortality and morbidity associated with emergent repair, abdominal aortic aneurysms should be repaired if increasingly symptomatic or if rapidly expanding or the aneurysm diameter exceeds 5 cm.
- 5.
With aggressive medical management and lifestyle modifications, the natural history of claudication related to peripheral arterial disease is generally indolent and relatively benign. A small subset will progress to critical disease. In general, critical limb ischemia mandates surgical intervention. Timing for intervention in intermittent claudication should take into account the severity and tolerability of the symptoms as well as patient-specific risk factors.
- 6.
Endovascular interventions have become a mainstay of treatment for vascular disease. In general, short-term morbidity and mortality are improved with endovascular repair, although the early preoperative benefit is not always maintained in long-term follow-up.
- 7.
Endovascular interventions have their own unique complication profile and often warrant repeat intervention and life-time surveillance.
Cardiovascular disease (CVD) is the leading cause of death both in the United States and worldwide. The lifetime risk of developing CVD in the Framingham Heart Study has been estimated to be greater than 50% in men and nearly 40% in women. Although the total number of deaths attributable to CV events has declined over the past decade, CVD still accounts for nearly one in every three deaths in the United States.
Among the various disease processes that can lead to CVD, atherosclerosis is the most common. The process of atherosclerotic plaque formation is both complex and dynamic, involving lipid deposition, smooth muscle proliferation, and an inflammatory milieu ( Fig. 13.1 ). These lesions progress into fibrous plaques prone to rupture, erosion, and hemorrhage. The end result is a narrowed intravascular lumen that creates the potential for downstream ischemia caused by mismatch between oxygen supply and demand. Some risk factors for CVD, such as age, gender, ethnicity, and family history, are not modifiable. Others are controllable by lifestyle and pharmacologic measures. A large, international study identified nine potentially modifiable risk factors that contributed to greater than 90% of the patient-attributable risk of a cardiovascular event: hypertension, dyslipidemia, diabetes, smoking, abdominal obesity, regular physical activity, daily consumption of fruits and vegetables, regular alcohol consumption, and psychosocial factors.
Cardiovascular disease can be grouped into four major categories: coronary artery disease (CAD), cerebrovascular disease, aortic disease, and peripheral arterial disease (PAD). Depending on the location of the lesion, this can result in ischemia or infarction of the heart, brain, abdominal viscera, or limbs. Patients with atherosclerotic disease in one area are at increased risk of vascular disease in other major vascular beds ( Table 13.1 ). Noncoronary atherosclerotic disease is considered a CAD equivalent and confers a risk of a major adverse cardiac event equivalent to CAD. The 10-year risk of developing CAD in patients with noncoronary atherosclerotic disease is greater than 20%. Thus it is common to see significant CAD in patients undergoing major noncardiac vascular surgery and vice versa.
| Cerebrovascular Disease | Abdominal Aortic Disease | Peripheral Artery Disease | |
|---|---|---|---|
| Coronary artery disease | 8–40% | 30–40% | 4–40% |
| Cerebrovascular disease | — | 9–13% | 17–50% |
| — | — | 7–12% |
General Considerations for Perioperative Management for Vascular Surgery
Preoperative Assessment and Management
The goal of the preoperative assessment of the patient is to delineate the extent of underlying cardiac and noncardiac disease and medically optimize any underlying conditions. Because of the significant association of CAD, cerebrovascular disease, aortic degenerative disease, and PAD, a major focus of the preoperative assessment is to detect, evaluate, and optimize preexisting vascular comorbidities. Perioperative management must be tailored to the individual patient to protect any at-risk organ system. The association of smoking with CVD means that many patients have pulmonary comorbidities that may also increase their risk with surgery and anesthesia.
It is incumbent upon the anesthesiologist to work with the patient’s surgical and medical teams to ensure medical optimization before surgery, including appropriate management of preoperative medications. As such, it is critical that the anesthesiologist recognize the potential benefits and risks of maintaining, stopping, or initiating medications in the perioperative period. As a general rule, most antihypertensive medications should be continued in the perioperative period. The preponderance of evidence suggests that patients on chronic β-blockers should be continued on the medication in the perioperative period, although β-blockers should not be instituted as new therapy on the day of surgery because of an increased risk of stroke and death. Current guidelines recommend that statin therapy should be continued in the perioperative setting, and perioperative statin therapy has been associated with the reduction of perioperative cardiac morbidity and mortality in vascular surgical patients. Management of antiplatelet agents must balance the risk of stopping medications versus the risk of bleeding in the perioperative period, particularly in the setting of recent percutaneous intervention with coronary stents. Although most recent clinical guidelines suggest that earlier discontinuation of dual-antiplatelet therapy may be considered in some cases, decisions about the duration of dual-antiplatelet therapy are best made on an individual basis based on an assessment of risk versus benefit and with input from a multidisciplinary team (surgery, anesthesiology, and cardiology).
Because of the risk of anemia, as well as a significant risk for blood loss, a complete blood count to assess starting hemoglobin and hematocrit should be obtained before vascular surgery. An active type and screen should be available, with blood products cross-matched as appropriate. A metabolic panel to assess baseline renal function is reasonable because of the likelihood of underlying renal insufficiency as well as risk for postoperative renal dysfunction. Coagulation studies should be considered for any patient who has been on anticoagulation and are mandatory if considering neuraxial manipulation either for anesthesia (e.g., spinal or epidural) or therapeutic intervention (e.g., spinal drain). A preoperative electrocardiogram (ECG) is often useful to serve as a baseline for evaluation of a perioperative insult. A preoperative echocardiogram is reasonable to assess baseline function for any patient with cardiovascular risk factors undergoing vascular surgery, particularly if there are new or worsening symptoms.
The American College of Cardiology (ACC) and American Heart Association (AHA) have released well-known guidelines regarding the perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery. The most recent recommendations from these guidelines simplify previous risk stratification before elective surgery ( Fig. 13.2 ; also see Chapter 1 ). The first step is to evaluate whether a clinical emergency exists; if so, the patient should proceed to surgery without delay with best medical optimization. The second step evaluates whether the patient has an acute coronary syndrome, which should be evaluated and optimized according to guideline-directed medical therapy before nonemergent surgery. Subsequent steps use a combination of surgical risk calculators, patient functional capacity, and clinical decision making to determine if further cardiac evaluation is warranted before surgery. In general, patients undergoing vascular surgery represent at least an intermediate (>1%) risk for an adverse perioperative cardiac event and may benefit from additional testing if it will change perioperative management (see Chapter 1 for further details).
Several observational studies previously suggested that preoperative cardiac revascularization improves patient outcomes before high-risk noncardiac surgery. The Coronary Artery Revascularization Prophylaxis (CARP) study was the first and only randomized controlled trial to evaluate outcomes following prophylactic cardiac revascularization before major vascular surgery. This study found no difference in outcomes in patients undergoing major vascular surgery who underwent routine revascularization by either coronary artery bypass grafting or percutaneous coronary intervention versus medical management. A subsequent analysis found that patients with unprotected left main disease may be the only subset of patients who benefits from prophylactic revascularization. In large part because of the CARP trial, cardiac revascularization is not typically recommended before surgery unless otherwise indicated according to current practice guidelines.
In general, most patients undergoing elective vascular surgery warrant cardiac evaluation because of their multiple comorbidities, high likelihood of concomitant CAD, and often difficult-to-quantity functional capacity related to vague symptomology (e.g., shortness of breath may be an anginal equivalent, related to concomitant pulmonary disease, or simple deconditioning) or other limiting factors (e.g., claudication before reaching 4 METs; previous amputations limiting exertion). Many vascular procedures are performed on an emergent basis, with little time for extensive workup. For urgent, but not emergent, procedures (e.g., peripheral intervention for critical limb ischemia), there may be time for limited workup and optimization. For true emergencies (e.g., ruptured aortic aneurysm), the case should proceed with best mitigation of perioperative risk ( Box 13.1 ).
Box 13.1- •
Rapidly evaluate patient for signs and symptoms of acute coronary syndrome or equivalent (e.g., crackles or peripheral edema suggestive of decompensated heart failure; harsh systolic murmur suggestive of undiagnosed or worsened stenotic valvular disease) and treat accordingly.
- •
Maintain patient on preoperative antiplatelet therapy if not contraindicated, particularly if a recent coronary stent is present.
- •
Avoid tachycardia (will increase myocardial oxygen demand while decreasing supply). Continue preoperative β-blocker, if applicable, if hemodynamically stable.
- •
Avoid extremes of both hypertension (increases left ventricular wall stress) and hypotension (may compromise perfusion to vital organs).
- •
Avoid anemia, particularly if there is evidence of end-organ compromise.
- •
Assure adequate pain control to minimize sympathetic stimulation.
- •
Maintain normothermia.
Intraoperative Anesthetic Management
The primary anesthetic used during vascular surgery will depend on factors such as patient comorbidities, surgeon skill and comfort level, anatomic considerations, and the invasiveness of the surgical procedure. As such, anesthetic techniques for specific procedures are discussed in subsequent sections. Upon arrival to the operating room (OR), all patients should be placed on standard American Society of Anesthesiologists (ASA) monitors, including regular noninvasive blood pressure measurement, pulse oximetry, and continuous ECG. It is prudent to place an arterial catheter for invasive blood pressure monitoring for all but the most minor of vascular procedures because of the inherent risk for rapid hemodynamic changes and major blood loss. Patient comorbidities, cross-clamping on major vascular structures, and potential for hemorrhage all contribute to the hemodynamic instability frequently observed during these procedures. Invasive arterial monitoring also allows for frequent blood sampling to assess ventilation and oxygenation, ongoing blood loss and resuscitation needs, and overall metabolic milieu. Because induction of general anesthesia and endotracheal intubation are among the more hemodynamically labile periods, placing the arterial monitoring before induction of general anesthesia is wise.
Invasive monitoring with central venous or pulmonary arterial cannulation is not routine for most vascular procedures. Common exceptions include open aortic procedures or when patient comorbidities dictate utility. Large-bore intravenous (IV) access, either peripheral or central, is mandatory for any major vascular procedure because of the inherent risk of blood loss and need for resuscitation. An active type and screen and adequate blood product availability should be confirmed before undertaking any major vascular procedure.
Although transesophageal echocardiography (TEE) is the most sensitive method for detecting intraoperative myocardial ischemia, it has not supplanted clinical assessment and routine ECG for determination of patients at risk for myocardial ischemia during noncardiac surgery. The ASA, in conjunction with the Society of Cardiovascular Anesthesiologists, has released practice guidelines for the intraoperative use of TEE. In general, expert opinion has recommended that TEE should be considered in noncardiac surgery in the following circumstances: when the patient has CV pathology that may result in significant clinical compromise, when life-threatening hypotension is anticipated, and when persistent unexplained hypotension or hypoxia occurs. Furthermore, these practice guidelines recommended TEE should be strongly considered for major open abdominal aortic procedures, and TEE does not have a routine role during endovascular aortic and distal procedures.
Postoperative Management
In general, patients can undergo tracheal extubation uneventfully in the OR and recover in the postanesthesia care unit after most vascular surgical procedures. Patients undergoing major abdominal aortic procedures may benefit from close surveillance and management in an intensive care unit setting where mechanical ventilation is frequently continued after initial admission to the unit. In this case, sedation and analgesia should be provided with short-acting agents to facilitate rapid emergence and serial neurologic assessments. Common complications after major vascular surgery include myocardial ischemia, hemodynamic lability, stroke, coagulopathy, renal failure, respiratory failure, coagulopathy, hemorrhage, hypothermia, delirium, and metabolic disturbances.
Carotid Artery and Cerebrovascular Disease
An imbalance between blood supply and demand to the brain can result in permanent cerebral infarction (stroke) or transient ischemic attack (TIA), conventionally defined as focalized neurologic deficit lasting less than 24 hours with no evidence of permanent infarction. Although TIAs resolve, they are clinically important because they strongly predict for clinical stroke in the near future. Strokes can be defined as ischemic, caused by disruption of blood flow through a vessel, or hemorrhagic, caused by bleeding into the brain parenchyma or surrounding spaces. Approximately 87% of strokes in the United States are ischemic in origin, and at least 20% of ischemic strokes are related to extracranial atherosclerotic disease, such as carotid stenosis. The prevalence of carotid artery disease rises with age, male gender, and racial minorities.
Considerations for Intervention
The determination of when and how to intervene for carotid atherosclerotic disease is complex ( Box 13.2 ). The stroke risk related to the disease itself must be balanced with the inherent stroke risk due to intervention. Furthermore, surgical decision making must also take into consideration patient-specific risk factors and risk factors for open (carotid endarterectomy [CEA]) versus endovascular carotid artery angioplasty and stenting (CAS) management. Revascularization is achieved in CEA by opening the lumen of the cervical segment of the extracranial carotid artery and removing the atherosclerotic plaque (typically at the carotid bifurcation). CAS is a minimally invasive alternative, during which a stent is deployed across the atherosclerotic plaque to restore the patency of the vessel lumen.
Box 13.2- •
All patients should be aggressively treated with antiplatelet therapy, statins, and β-blockade, and should receive management of comorbid conditions per current clinical practice guidelines.
- •
Revascularization should occur within 2 weeks of stroke or TIA for further stroke prevention.
- •
Revascularization is recommended for patients with symptomatic stenosis greater than 50%. The more significant the stenosis, the stronger the indication for surgical intervention.
- •
CEA is preferred over CAS unless there are contraindications to CEA (e.g., decompensated heart disease, previous neck surgery or radiation, contralateral vocal cord paralysis from previous surgery or an atypical and/or surgically inaccessible lesion).
- •
In asymptomatic stenosis greater than 60%, CEA may be considered in acceptable risk candidates (i.e., predicted combined stroke and death rates <3%) in addition to best medical therapy.
- •
Symptomatic patients with stenosis of <50% and asymptomatic patients with stenosis of <60% should be treated with best medical therapy and should not undergo intervention.
- •
Intervention is not indicated for patients with chronic total occlusion or patients with severe neurologic disability that precludes preservation of useful function.
CAS, Carotid artery angioplasty and stenting; CEA, carotid endarterectomy; TIA, transient ischemic attack.
Symptomatic carotid disease is defined as the onset of sudden and focal neurologic symptoms, either temporary or permanent, that are ipsilateral to the carotid pathology. The most important indicator of future stroke risk is the presence of symptoms within the previous 6 months. Several landmark trials have evaluated the benefit of CEA versus medical management for patients with symptomatic carotid disease. Pooled analyses of these trials found a consistent benefit was demonstrated for patients with greater than 70% stenosis, with a number needed to treat (NNT) of 6.3 to prevent one stroke over 5 years. A benefit was also demonstrated in patients with moderate (50%–69%) stenosis, although this benefit was less robust with an NNT of 22. CEA was not beneficial below 50% carotid stenosis and was found to be harmful for patients with less than 30% stenosis. There was no significant benefit of CEA with near-total occlusion of the internal carotid artery.
The role of CEA in asymptomatic carotid artery disease has also been extensively studied. A meta-analysis of the literature found a small absolute risk reduction of about 1% per year for the outcome of any stroke for patients with asymptomatic carotid disease who underwent CEA. The NNT to prevent one stroke at 3 years was approximately 33. The net benefit to CEA in asymptomatic patients is delayed because of perioperative morbidity; the early perioperative morbidity outweighs the modest reduction in stroke risk until 2 years or more after surgery. Thus asymptomatic patients must be carefully selected to have at least a 5-year expected survival to benefit from surgical intervention.
Carotid artery angioplasty and stenting is an alternative to open surgical intervention for patients with carotid atherosclerotic disease, particularly for patients considered to be poor candidates for surgery or anesthesia. Endovascular treatment of carotid disease has been extensively studied and compared to traditional CEA. The preponderance of evidence suggests similar long-term results in preventing disabling or fatal strokes between CEA and CAS; however, significant differences in short-term morbidity and mortality have been found between the two procedures, with a higher periprocedural stroke rate in patients undergoing CAS but a higher myocardial infarction (MI) rate in patients undergoing CEA. Examples of patients who are generally considered favorable candidates for CAS include those at a prohibitively elevated medical risk (e.g., contralateral occlusion, severe medical comorbidities) or surgical risk (e.g., previous radiation to the neck, history of previous neck dissection, intracranial or high extracranial location) to undergo open repair. Alternatively, severe aortic arch atheroma or significant carotid tortuosity typically increase the complication rate for CAS and are indications for CEA. The complication rate of the surgeon must also be taken into account when weighing the risk and benefits of carotid intervention for the individual patient.
Intraoperative Anesthetic Considerations and Management
Carotid revascularization can be performed under general anesthesia or under local anesthesia. The primary advantage of local anesthesia is the ability to continuously monitor neurologic function in an awake patient, which may more reliably detect cerebral ischemia than the neuromonitoring methods used under general anesthesia. Because the need for intraoperative intervention in an awake patient may be detected more promptly and reliably, it can minimize the risks of intervention such as embolic risk of shunt placement. Local anesthetic techniques may also avoid hemodynamic extremes and cardiorespiratory morbidity associated with general anesthesia. General anesthesia, on the other hand, has the benefits of increased patient comfort, decreased patient anxiety, and airway control. It also avoids the need for emergent intraoperative conversion because of complications such as seizure and airway compromise.
Patient outcomes after general versus local anesthesia have been the subject of extensive study. The largest and most well-known study is the General Anaesthesia versus Local Anaesthesia for carotid surgery (GALA) trial, which randomized more than 3500 patients undergoing CEA at 95 medical centers in 24 countries to either general anesthesia or local anesthesia. In this investigation, there were no differences in major adverse events between the two groups with respect to death, stroke, MI, length of stay (LOS), and quality of life. Patients undergoing general anesthesia were more at risk for hemodynamic instability and perioperative cognitive dysfunction; subsequent analysis, however, demonstrated that intraoperative shunting was the main risk factor variable associated with perioperative cognitive dysfunction. A recent large meta-analysis demonstrated that anesthetic technique had no effect on death, stroke, MI, postoperative cardiopulmonary complications, hospital LOS, or patient satisfaction after CEA. The available literature does not support the use of one anesthetic technique over another for carotid surgery, and survey of practice patterns suggests variability in perioperative practice for carotid surgery. The decision for general versus local anesthesia should consider both patient and surgeon preferences, as well as unique patient characteristics, that might favor one technique over another. Regardless of technique, the goals of the anesthetic are the same: maintain hemodynamic norms and ensure smooth, rapid recovery from anesthesia to allow for early neurologic assessment.
Local Anesthesia Technique for Carotid Endarterectomy
Local anesthesia is performed with a nerve block, usually in conjunction with IV sedation to minimize patient discomfort and anxiety. It is important to limit sedation so as to maintain the ability to monitor the neurologic status. Local anesthetic options include cervical epidural or superficial cervical plexus block with or without deep cervical plexus block. Superficial cervical plexus block has been found to be as effective as a deep or combined block, while avoiding the complications of a deep cervical plexus block such as subarachnoid injection, phrenic nerve blockade, Horner syndrome, and increased risk of conversion to general anesthesia.
The ability to rapidly convert to a general anesthetic must be ensured before undertaking CEA under local anesthesia. Indications for conversion to general anesthesia include patient intolerance or request, accidental subarachnoid injection with brainstem anesthesia, seizure (related to intravascular injection of local anesthetic), airway compromise (from surgery or oversedation), or other hemodynamic or surgical complication. Patient selection is key for the success of local anesthesia. The patient cannot be claustrophobic (drapes are immediately adjacent to and across the patient’s face) and must be able to lie flat and still for the duration (arthritis, chronic obstructive pulmonary disease [COPD], heart failure [HF], and other comorbidities may make this difficult for patients). Consideration must be given to the fact that intraoperative conversion may require airway management after sterile draping and surgical incision. As such, it may be prudent to consider having advanced airway equipment readily available, such as video laryngoscopy, to minimize disruption or difficulty during an emergent intubation. Despite these concerns, the rate of conversion to general anesthesia has been reported to be relatively low, occurring in only 4% of patients in the GALA trial.
General Anesthetic Technique for Carotid Endarterectomy
A major goal during the induction and maintenance of a general anesthetic is to avoid hemodynamic extremes such as the lows (during induction with agents with vasodilatory effects) and the highs (during periods of intense sympathetic stimulation, such as intubation and surgical incision). To this end, a variety of anesthetic agents can and have been used. Typically a balanced anesthetic technique is used. Induction of general anesthesia should involve the slow titration of a short-acting hypnotic agent, titrated to effect. The addition of a short-acting opioid may blunt the hemodynamic response to endotracheal intubation. In general, endotracheal intubation is preferred because of limited access to the airway during the procedure and the greater ability to manipulate ventilation. Normocapnia should be maintained during the procedure to avoid both a decrease in cerebral blood flow associated with hyperventilation and vasoconstriction, as well as potential intracerebral “steal” during permissive hypercapnia. Invasive arterial blood pressure monitoring should be considered because of the potential for sudden hemodynamic changes as a result of anesthesia or surgical manipulation. General anesthesia can be maintained effectively with either volatile or IV agents. Anesthetics must be titrated to minimize interference with any intraoperative monitoring techniques such as electroencephalography (EEG).
Additional Intraoperative Monitoring
Stroke during carotid intervention may result from inadequate cerebral perfusion because of hypotension, thrombosis, embolism, or carotid clamping in the setting of insufficient collateral flow from the circle of Willis. Cerebral ischemia can be mitigated if the insult is detected in timely fashion and appropriate interventions are made. An intact neurologic examination in an awake patient remains the gold standard for neurologic monitoring and provides a rationale for carotid intervention under local anesthesia. In this setting, a baseline neurologic assessment is performed before administration of sedative medication. Thereafter the sedation is titrated to achieve both patient comfort and cooperation with serial neurologic evaluations during the procedure, especially during carotid manipulation and clamping. A change in neurologic function may require interventions to restore cerebral perfusion such as shunt placement or permissive systemic hypertension to augment collateral flow via the circle of Willis.
When a general anesthetic technique is chosen, a variety of neuromonitoring techniques are available to monitor for cerebral ischemia during carotid intervention such as EEG, carotid stump pressure, somatosensory evoked potentials, transcranial Doppler, and cerebral oximetry. Intraoperative EEG is a commonly used neuromonitoring modality. Unprocessed EEG is preferred over processed EEG (e.g., bispectral index) because bispectral index monitoring has not been reliably shown to predict cerebral ischemia in this patient population. Significant alterations during carotid intervention in the EEG tracings such as complete signal loss, a 50% decrease in background activity, or an increase in delta wave activity may indicate intraoperative ischemia and the need for intervention. The clinical studies supporting the utility of routine EEG monitoring during carotid intervention are limited and not conclusive. Because both IV and volatile anesthetic agents may affect the EEG tracings, close communication between the anesthesia and neuromonitoring teams remains essential to minimize this anesthetic interference and to maximize both the sensitivity and specificity of EEG to detect cerebral ischemia during the carotid procedure.
Although EEG is the most commonly used monitor, other options are available to detect cerebral ischemia. Although an intraoperative carotid stump pressure less than 50 mm Hg may predict for stroke after carotid intervention, it has limited utility as the sole method for detecting intraoperative cerebral ischemia and the need for interventions such as shunting. Transcranial Doppler (TCD) measures blood velocity in the middle cerebral artery for detection of significant intraoperative microemboli. This alert may prompt the surgical team to avoid further carotid manipulation that could lead to stroke. Although TCD can detect cerebral ischemia, it is not always accurate. Cerebral oximetry is another monitoring modality that uses near-infrared spectroscopy to detect cerebral oxygen saturation; however, data to support its use for carotid surgery are mixed.
Given the current neuromonitoring choices for detection of stroke during carotid intervention under general anesthesia, it is clear that no technique is perfect. The primary role for neuromonitoring during CEA under general anesthesia is to guide decision for selective shunting. In the setting of routine shunting for CEA, there is less of a role for these modalities, given that the shunt maintains cerebral perfusion despite the clamped segment of the carotid artery. Ultimately, the choice of neuromonitoring technique—and whether to routinely use neuromonitoring at all—is left to the discretion and expertise of the operative team.
Anesthesia for Carotid Artery Stenting
Carotid artery stenting is a minimally invasive procedure that can usually be performed under local anesthesia or monitored anesthesia care (MAC). Sedation is carefully titrated to allow for continuous neurologic examination throughout the procedure. If a general anesthetic technique is used, short-acting agents are typically used to allow for a rapid emergence and neurologic evaluation. Because peripheral endovascular access is obtained rather than direct surgical manipulation of the head and neck, a laryngeal mask airway may be chosen rather than endotracheal intubation to attenuate the hemodynamic lability encountered on induction and emergence of general anesthesia. As with any endovascular technique, it may become necessary to convert to open repair. As such, monitoring and vascular access should be planned accordingly.
Perioperative Challenges
Both CEA and CAS may be associated with hemodynamic lability of both heart rate and blood pressure because of altered baseline carotid baroreceptor sensitivity as well as intraoperative manipulation of the carotid baroreceptors. Carotid baroreceptor manipulation, either directly or via endovascular manipulation, may result in a profound parasympathetic response with bradycardia and hypotension. Conversely, periods of significant stimulation (such as endotracheal intubation or surgical dissection) may lead to increased sympathetic outflow with resultant hypertension and tachycardia, which may not be well tolerated by patients with concomitant CAD. Hemodynamic lability may continue into the postoperative period because of continued altered baroreceptor function or uncontrolled pain.
Carotid cross-clamping may precipitate ipsilateral cerebral ischemia from decreased carotid blood flow and inadequate collateral flow via the circle of Willis. Blood pressure should be maintained in a normal to slightly higher-than-baseline range before cross-clamping to optimize cerebral blood flow. Carotid unclamping may be complicated by impaired autoregulation and disrupted baroreceptor function, resulting in increased cerebral blood flow.
Cerebral hyperperfusion syndrome is a rare but clinically important complication, which results from impaired cerebral autoregulation after relief of high-grade stenosis. The clinical presentation may progress from severe headache to seizure to, at worst presentation, intracerebral hemorrhage. Thus it is important to monitor the patient closely for complaint of headache in the postoperative period. Management is supportive with strict control of blood pressure to minimize the risk of intracerebral hemorrhage.
Postoperative hematoma after CEA is usually a result of diffuse oozing after heparin administration and concurrent antiplatelet therapy. Although a relatively uncommon occurrence, with a reported incidence of 0.5% to 3%, it can result in life-threatening airway compromise. Injury to the recurrent or superior laryngeal nerve may result in paralysis of the ipsilateral vocal cord.
Carotid artery angioplasty and stenting may present unique concerns such as stent kinking, stent thrombosis, carotid dissection, or atheroembolism. Technical issues with the stent may often be amenable to observation or additional stent placement, and acute thrombosis typically necessitates immediate conversion to open CEA. The incidence of clinically important embolization has significantly decreased with the use of embolic protection devices. In the event of significant distal embolization, management options include catheter-directed thrombolysis, aspiration thrombectomy, and aggressive anticoagulation.
Abdominal Aortic Disease
The aorta is the major arterial conduit from the heart to the systemic circulation and provides vascular inflow to all of the major abdominal and pelvic organs as it traverses the abdomen. The abdominal aorta is a retroperitoneal structure that begins at the diaphragmatic hiatus and ends at the level of the fourth lumbar vertebra, where it bifurcates into the common iliac arteries. The aorta tapers gradually from the thorax to the abdomen such that its normal diameter at the level of the renal arteries is approximately 2.0 cm. An aneurysm is typically defined as a greater than 50% dilation of the expected normal arterial diameter. Aortic aneurysm occurs most commonly in the abdominal aorta. Aneurysms of the thoracic and thoracoabdominal aorta occur far less commonly.
Abdominal aortic aneurysms (AAAs) are classified by location as infrarenal (originating below the level of the renal arteries), juxtarenal (originating at the level of the renal arteries), or suprarenal (originating above the renal arteries). This distinction is important because it dictates the complexity of the surgical repair as well as the potential for hemodynamic derangements, particularly with open intervention and the accompanying aortic cross-clamp. Whereas the majority of AAAs are infrarenal, approximately 5% to 15% involve the suprarenal aorta.
It has recently been recognized that the process of aneurysm formation is a distinct degenerative progression from atherosclerotic disease, with features such as vessel wall infiltration by macrophages, destruction of elastin and collagen, loss of smooth muscle cells, and neovascularization. Although inflammation and macrophage infiltration are common to both atherosclerotic and aneurysmal disease, atherosclerosis is primarily noted within the intima and media, but aneurysmal disease typically affects the media and adventitia. Although the overwhelming majority of AAAs are caused by degenerative disease, less common etiologies include infection, inflammatory diseases, trauma, and congenital conditions.
Considerations for Intervention
The single greatest risk factor for aneurysm rupture is size. Current evidence-based guidelines suggest repair when aneurysm diameter exceeds 5.0 to 5.5 cm. Rapid aneurysm growth, defined as greater than 10 mm per year, is also an indication for intervention. Urgent repair is recommended in the setting of symptomatic nonruptured AAA, regardless of size. In the setting of excessive perioperative risk, medical rather than surgical management may be considered in patients with multiple significant comorbidities.
Historically, open repair has been the definitive treatment for AAA. Open AAA repair is associated with significant perioperative morbidity and mortality. Although clinical outcomes have steadily improved because of ongoing refinements in perioperative management, including advances in anesthetic and surgical techniques, current estimates of perioperative mortality rates for elective open AAA repair range from 1 to 5%, with perioperative mortality rates for emergent repair reported to be as high as 30%. Perioperative morbidity may result from all major organ systems, including cardiovascular complications, renal failure, respiratory failure, mesenteric ischemia, bleeding, and infection.
With ongoing improvements in endovascular technology and proceduralist skill, endovascular aortic repair (EVAR) has become the mainstay of treatment for AAA. Even complex AAAs involving abdominal viscera may be candidates for endovascular repair using advanced techniques such as fenestrated stent grafts or snorkel techniques. Multiple high-quality randomized controlled trials comparing endovascular with open abdominal aortic repair have demonstrated a significant difference in 30-day mortality rates and major morbidity for patients who undergo EVAR. This perioperative survival advantage has not been sustained in intermediate- to long-term follow up. Furthermore, follow-up studies suggest a significantly higher rate of reintervention in patients who undergo EVAR, although the majority were also endovascular-based procedures associated with low mortality. In the current era, open AAA repair tends to be reserved for patients who are not candidates for EVAR, but the decision for open versus endovascular repair for the individual patient depends on multiple factors such as aortic anatomy, urgency, patient preference, and surgical expertise.
Intraoperative Anesthetic Considerations and Management
Open Abdominal Aortic Aneurysm Repair
General anesthesia is the most commonly used technique for open AAA repair. Surgical exposure is obtained by either a midline transabdominal or lateral retroperitoneal incision. Given the extensive incision and frequency of concomitant COPD, epidural analgesia should be considered in this setting to facilitate high-quality pain control, to limit the side effects of parenteral narcotics, and to preserve respiratory function. A recent meta-analysis has suggested that this strategy can decrease major complications in AAA repair such as postoperative mechanical ventilation, MI, gastrointestinal morbidity, and renal injury.
Although general anesthesia can be induced by a variety of agents, particular consideration is given to maintaining the patient’s baseline hemodynamics in order to maintain adequate end-organ perfusion (typically within 20% of baseline values), while minimizing sympathetic stimulation to noxious events such as endotracheal intubation and placement of invasive monitors. Moderate doses of narcotics and/or IV lidocaine upon anesthetic induction may prove useful in this regard. Volatile and/or IV anesthesia may be used for maintenance of general anesthesia. Although recent evidence suggests a cardioprotective effect of volatile agents in cardiac surgery, this benefit is less clear in AAA repair.
Invasive blood pressure monitoring is mandatory for tight control of blood pressure during periods of hemodynamic instability and rapid blood loss. Consideration should be given to placement of an arterial catheter before the induction of general anesthesia to guide titration of induction agents to ensure steady hemodynamics during this labile period. Reliable large-bore IV access is required and should also be present before surgical incision. Adequate blood product availability and assisted means for expeditious transfusion should be available as needed. Cell-saving techniques may decrease the amount of autologous blood needed and mitigate the risks of transfusion. Central venous access should be obtained to facilitate monitoring of overall volume status and to ensure rapid and reliable administration of vasoactive drugs. Invasive monitoring of cardiac output (CO), either by pulmonary artery catheter or TEE, is reasonable, especially in high-risk patients and those undergoing complicated surgical repairs requiring high or prolonged aortic cross-clamp times.
Endovascular Abdominal Aortic Aneurysm Repair
Endovascular aortic repair can be successfully performed under local anesthesia, neuraxial anesthesia, or general anesthesia. Very limited evidence exists on the best choice of anesthesia for a standard EVAR, and even less for complex endovascular repair. No randomized controlled trials have been performed that compare anesthetic techniques for EVAR. The data that exist are limited to retrospective analyses that must be interpreted cautiously because of the inherent risk for selection biases. A recent meta-analysis of the existing data found no difference in 30-day mortality or major morbidity rates among techniques. Locoregional anesthesia was associated with shorter procedural times, hospital LOS, and lower likelihood of ICU admission. Both the Society for Vascular Surgery as well as the European Society for Vascular Surgery practice guidelines suggest the use of locoregional techniques; however, wide variability exists in practice patterns.
Surgical access is obtained via surgical cutdown or percutaneous access of the femoral vessels. Locoregional anesthesia may be provided by neuraxial anesthesia (single-shot spinal, continuous spinal, or epidural catheter), regional blocks (ilioinguinal and hypogastric nerve blocks or bilateral transversus abdominis plane blocks), or surgical skin infiltration. As delivery devices improve, the need for surgical cutdown has decreased significantly, increasing the likelihood of success with local infiltration. Locoregional anesthesia has several potential intraoperative benefits for EVAR. Avoiding the myocardial depressant effects of general anesthetic agents and the potentially stimulating periods of induction and emergence may afford better intraoperative hemodynamic stability. Pulmonary outcomes may be improved by avoiding mechanical ventilation and maintaining baseline respiratory mechanics. An awake, conversant patient may also serve as an early monitor for complications such as anaphylactic reactions to iodinated contrast agents (e.g., pruritus or dyspnea) or arterial rupture (e.g., sudden retroperitoneal pain) that may not be immediately evident in an unconscious patient. Locoregional anesthesia may require supplementation with titrated sedation. Small doses of short-acting agents should be titrated carefully to provide adequate cooperation, sedation, analgesia, and anxiolysis. Care must be taken to avoid oversedation, airway obstruction, and hypoxemia. The ability to convert rapidly and safely to a general anesthetic remains important in the case of either surgical or anesthetic misadventure.
General anesthesia eliminates concerns regarding patient comfort, anxiety, and the ability to lie immobile and flat for a prolonged duration. It also obviates emergent conversion to general anesthesia, although the reported conversion rate from locoregional to general anesthesia (usually precipitated by surgical complication) is less than 1%. Additional advantages of general anesthesia include dampened bowel peristalsis and precise control of respiration, which may enhance the quality of intraoperative imaging to facilitate accurate stent deployment.
Both surgical factors and patient preference should be considered when choosing an anesthetic technique. Anatomically complex lesions requiring advanced endovascular techniques may be lengthy operations and can be associated with significant blood loss despite the minimally invasive nature. As such, complex endovascular repairs may be better suited for general anesthesia. Certain patient populations may also be unsuitable candidates for locoregional anesthesia, including patients with significant anxiety, medical comorbidities that preclude their ability to lie flat, and patients with whom communication is limited (e.g., baseline cognitive dysfunction or language barrier).
There is typically less hemodynamic instability during EVAR than an open aortic intervention because the need for aortic cross-clamping is avoided, although periods of ballooning and stent deployment are analogous to the placement of an endoclamp and may result in transient lability. Thus, from this perspective, the requirement for invasive arterial blood pressure monitoring is less imperative for EVAR. The ability to place an arterial catheter rapidly in an emergency situation is limited in EVAR, however, because both arms are usually tucked to allow intraoperative fluoroscopy, and both groins are usually surgically accessed for the repair. Given these constraints, elective direct arterial blood pressure monitoring is often selected as a precaution in case of arterial rupture and conversion to open repair. Continuous arterial pressure monitoring may also allow for more precise hemodynamic manipulation during critical periods such as stent positioning and deployment, although there are no studies to suggest benefit compared with noninvasive blood pressure monitoring.
Although EVAR has a lower risk of bleeding and transfusion compared with open aortic intervention, large-bore peripheral IV access is still preferred because of the small, but real, risk of conversion to an open approach. Central venous access is typically not required unless a significant need for vasoactive medication is anticipated or reliable large-bore peripheral access cannot be established.
Perioperative Challenges
Hemodynamic Management of Aortic Clamping and Unclamping
Hemodynamic management during open AAA repair is challenging and requires constant communication with the surgical team ( Box 13.3 ). Hemodynamic perturbations during open AAA repair are influenced by factors such as aortic clamping (AXC), rapid blood loss, significant fluid shifts, and acute cardiac dysfunction. The application of an AXC initiates an array of physiologic derangements governed primarily by the level at which the clamp is applied ( Fig. 13.3 ). Increases in mean arterial pressure (MAP) and systemic vascular resistance (SVR) caused by impeded arterial flow are the most consistent responses to AXC, with an increase in arterial pressure of 10% or more with infrarenal aortic cross-clamping. The potential for substantially greater increases exists if the aorta is clamped at a higher level such as above the celiac axis where flow to the abdominal viscera is also interrupted.
Box 13.3
