Vascular Surgery Anesthesia Chapter 56 PDF

56 Anesthesia for Vascular Surgery AHMED SHALABI and JOYCE CHANG - KEY POINTS □ □ □ □ □ □ □ □ □ □ □ □ □ □ □  erioperative management of patients undergoing vascular surgery requires an understanding P of the underlying pathophysiology of the specific vascular lesion. Major vascular surgery is part...

56 Anesthesia for Vascular Surgery AHMED SHALABI and JOYCE CHANG - KEY POINTS □ □ □ □ □ □ □ □ □ □ □ □ □ □ □  erioperative management of patients undergoing vascular surgery requires an understanding P of the underlying pathophysiology of the specific vascular lesion. Major vascular surgery is particularly challenging to the anesthesiologist because these are high-risk operations in a patient population with a high prevalence of either overt or occult coronary artery disease, which is the leading cause of perioperative and long-term mortality after vascular surgery. Accurate clinical assessment of the pretest probability of significant coronary artery disease is necessary for prudent use and rational interpretation of preoperative cardiac testing. Guidelines on perioperative cardiovascular evaluation and care suggest that coronary intervention is rarely necessary to simply decrease the risk for surgery unless such intervention is indicated, irrespective of the preoperative context. Prophylactic coronary revascularization has not been shown to reduce perioperative or long-term morbidity after major vascular surgery. Medical therapy is the cornerstone for the management of coronary artery disease. Patients should take their usual cardiovascular medications throughout the perioperative period. Antiplatelet therapy requires special consideration and must be individualized to each patient. Prevention and treatment of perioperative myocardial ischemia require careful control of the determinants of myocardial oxygen supply and demand. ST-segment monitoring, particularly with computerized ST-segment analysis, should be used to detect myocardial ischemia during the perioperative period. Initiation of perioperative β-adrenergic blocker therapy has potential benefits and risks. All patients who require statin therapy on an ongoing basis should also receive statins in the perioperative period. The clinical usefulness of any intraoperative monitoring technique ultimately depends on patient selection, accurate interpretation of data, and appropriate therapeutic intervention. Maintenance of vital organ perfusion and function by the provision of stable perioperative hemodynamics is more important to overall outcome after aortic surgery than is the choice of anesthetic drug or technique. The pathophysiology of aortic cross-clamping and unclamping is complex and depends on many factors, including the level of the cross-clamp, the extent of coronary artery disease and myocardial dysfunction, intravascular blood volume and distribution, activation of the sympathetic nervous system, and the anesthetic drugs and techniques. The degree of preoperative renal insufficiency is the strongest predictor of postoperative renal dysfunction. Endovascular aortic surgery has become an established, less invasive alternative to conventional open aortic repair. Endoleak, or the inability to obtain or maintain complete exclusion of the aneurysm sac from arterial blood flow, is a complication specific to endovascular aortic repair. The primary clinical utility of cerebral monitoring during carotid endarterectomy is to identify patients in need of carotid artery shunting; second, such monitoring is used to identify patients who may benefit from an increase in arterial blood pressure or change in surgical technique. Postoperative hypothermia is associated with many undesirable physiologic effects and may contribute to adverse cardiac outcome. Preoperative Evaluation COEXISTING DISEASE Patients undergoing vascular surgery have a high incidence of coexisting disease, including diabetes mellitus, hypertension, renal impairment, and pulmonary disease, all of which should be assessed and, if possible, optimized before surgery. Because of the systemic nature of atherosclerotic disease, patients with vascular disease frequently have arterial disease affecting multiple vascular territories. Coronary artery disease (CAD) is the leading cause of perioperative mortality at the time of vascular surgery, and long-term survival after vascular procedures is significantly limited by the frequent 1825 Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1826 SECTION IV Adult Subspecialty Management occurrence of morbid cardiac events.1 Less than 10% of patients who undergo vascular surgery have normal coronary arteries, and more than 50% have advanced or severe CAD. Unrecognized myocardial infarction (MI) (determined by wall motion abnormalities at rest in the absence of a history of MI) and silent myocardial ischemia (determined by stress-induced wall motion abnormalities in the absence of angina) often occur in vascular surgery patients (23% and 28%, respectively) and are associated with increased longterm mortality and adverse cardiac events.2 Left ventricular systolic dysfunction (LVSD) is five times more common in patients with vascular disease than in matched controls.3 It is not clear whether any specific category of vascular disease is associated with a greater likelihood of coexisting CAD. Some investigators have shown a similar incidence and severity of CAD in patients with aortic, lower extremity, and carotid disease. Others have shown that patients with lower extremity vascular disease are more likely to have significant CAD and to experience perioperative morbidity. Medical therapy is the cornerstone of the management of CAD. PERIOPERATIVE AND LONG-TERM CARDIAC OUTCOMES Preoperatively, the potential for MI and death in patients undergoing vascular surgery must be considered (Table 56.1). Nonfatal and fatal MIs are the most important and specific outcomes that determine perioperative cardiac morbidity. When multiple recent studies are pooled, the overall prevalence of perioperative MI and death is 4.9% and 2.4%, respectively. When outcomes are assessed over the long term (2 to 5 years), the prevalence of MI and death is 8.9% and 11.2%, respectively. This perioperative and long-term morbidity and mortality persist despite aggressive medical and surgical therapy.4 TABLE 56.1 Rates of Myocardial Infarction and Death in Patients Undergoing Vascular Surgery Study MI (%) Death (%) Comments SHORT-TERM FOLLOW-UP (IN HOSPITAL OR 30-DAY) Ouyang et al.5 Raby et al.6 Mangano et A guideline-based approach to health care is relatively new and originated primarily in the United States. The American College of Cardiology (ACC) Foundation and the American Heart Association (AHA) jointly produced guidelines in the area of cardiovascular disease for more than 2 decades. The ACC/AHA Task Force on Practice Guidelines published “Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery” in 1996. This evidence-based approach to perioperative evaluation and management was updated in 2002, 2007,18 2009,19 and 2014.20 A stepwise approach (simplified from the 2007 guidelines) to perioperative cardiac evaluation and care for noncardiac surgery is provided in Chapter 31. The authors emphasize that the purpose of the preoperative evaluation is not to give medical clearance but rather to perform an evaluation of the patient’s current medical status; make recommendations concerning the evaluation, management, and risk for cardiac problems; and provide a clinical risk profile that the patient and caregivers can use in making treatment decisions that may influence perioperative and longer-term cardiac outcomes. The overriding theme of the perioperative guidelines is that intervention is rarely necessary to simply lower the risk associated with surgery unless such intervention is indicated, irrespective of the preoperative context. 0 Small study 2.3 0.06 Aortic, lower extremity, carotid 4.1 2.3 Vascular patient only reported Bode et al.8 4.5 3.1 All lower extremity Christopherson et al.9 4.0 2.0 All lower extremity Mangano et al.7 5.0 0 Vascular patient only reported 6.0 3.0 Vascular patient only reported Pasternack et al.11 4.5 1.0 Aortic, lower extremity, carotid Krupski et al.12 2.1 2.9 Aortic, lower extremity Baron et al.13 5.9 4.0 All aortic Norris et al.14 3.3 5.4 All aortic al.15 5.5 4.1 All aortic al.4 8.4 3.2 Aortic, lower extremity 4.9 2.4 Fleisher et Fleron et McFalls et al.10 Average LONG-TERM FOLLOW-UP (IN HOSPITAL AND AFTER DISCHARGE) Raby et al6 7.4 5.1 20-mo follow-up Mangano et al.7 4.7 3.5 15-mo follow-up Mangano et al.16 19.4 13.5 24-mo follow-up Hertzer et al.17 12 Krupski et al.12 3.9 McFalls et Average GUIDELINE‐BASED APPROACH al.7 8 al.4 60-mo follow-up 11.2 22 8.9 24-mo follow-up 30-mo follow-up 11.2 MI, Myocardial infarction. Thus, preoperative testing should not be performed unless it is likely to influence patient care. The particular challenge that the vascular surgery patient presents is emphasized throughout the document. Aspects of the updated guidelines and their evidence-based approach will be discussed throughout this chapter. CARDIAC RISK ASSESSMENT The preoperative cardiac assessment presents an opportunity to initiate and optimize pharmacologic management, perform appropriate diagnostic and therapeutic interventions, and adjust overall care to decrease not only perioperative risk but also long-term risks from cardiovascular events. The challenge for clinicians is to accurately assess risk for cardiac morbidity while maintaining a cost-effective, clinically relevant, and evidence-based strategy. The ACC/AHA stepwise approach considers vascular surgery distinct from other noncardiac surgical procedures and is reviewed in detail in Chapter 31. Only issues specific to vascular surgery are reviewed in this chapter. After assessment of cardiac risk, the additional challenge exists of modifying perioperative management to reduce Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1827 56 Anesthesia for Vascular Surgery risk by adjusting or adding cardiac medications (e.g., β-adrenergic blocker), direct coronary intervention (e.g., percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]), modifying or intensifying perioperative management (e.g., invasive hemodynamic monitoring), or changing preoperative plans (e.g., performing endovascular aneurysm repair [EVAR] rather than open aortic repair). Coordination is essential among surgeons, anesthesiologists, and cardiologists, each of whom may have different criteria for risk assessment and different objectives for risk modification. Clinical Risk Indices Assessing cardiac risk in patients before vascular surgery is a controversial and difficult task. Although risk indices are a cost-effective screening method for determining which patients may require further cardiac evaluation (i.e., additional risk stratification with noninvasive technologies), the high pretest probability of CAD in vascular surgery patients makes the risk index somewhat less useful. Vascular surgery-specific indices have been recently developed to optimize the prediction of perioperative mortality21 and cardiac morbidity22 in patients undergoing elective and urgent vascular surgery. Risk indices do not provide specific risk prediction for individuals, but rather place patients in general risk categories, most commonly designated as low (cardiac risk generally 5%). Clinical risk variables identified by logistic regression in vascular surgery cohorts can be used along with noninvasive cardiac testing to optimize preoperative assessment of cardiac risk before vascular surgery. From the registry of the Coronary Artery Revascularization Prophylaxis (CARP) trial, the absence of multiple preoperative cardiac risk variables identifies patients with the best long-term survival after elective vascular surgery.23 Noninvasive Diagnostic Cardiac Testing Accurate clinical assessment of the pretest probability of significant CAD is extremely important. In general, noninvasive cardiac testing before vascular surgery is best directed at patients considered to be at intermediate clinical risk. Such testing should not be undertaken if it is unlikely to alter patient management and should not be considered as a preliminary step leading to coronary revascularization. A revascularization procedure is rarely needed solely for the purpose of getting a patient through the perioperative period. Extensive cardiac evaluation before vascular operations can result in morbidity, delays, and patient refusal to undergo vascular surgery. A complete review of this subject is found in Chapter 31. Cardiac Catheterization and Prophylactic Revascularization The largest series on outcome in vascular surgery patients is that of Hertzer and colleagues24 from the Cleveland Clinic. These investigators performed cardiac catheterization in 1000 consecutive patients scheduled to undergo peripheral vascular surgery (aortic aneurysm resection, carotid endarterectomy, and lower extremity revascularization). The incidence and severity of CAD were assessed according to the following classification: normal coronary arteries; mild-to-moderate CAD with no lesion exceeding 70% TABLE 56.2 Results of Coronary Angiography in 1000 Patients with Peripheral Vascular Disease CLINICAL CAD NONE SUSPECTED TOTAL Angiographic Classification No. % No. % No. % Normal coronary arteries 64 14 21 4 85 Mild‐to‐moderate CAD 218 49 99 18 317 32 Advanced, compensated CAD 97 22 192 34 289 29 Severe, correctable CAD 63 14 188 34 251 25 Severe, inoperable CAD 4 1 54 10 58 8.5 5.8 CAD, Coronary artery disease. Data from Hertzer NR, Beven EG, Young JR, et al. Coronary artery disease in peripheral vascular patients: a classification of 1000 coronary angiograms and results of surgical management. Ann Surg. 1984;199:223–233. stenosis; advanced, compensated CAD with one or more lesions exceeding 70% stenosis but with adequate collateral circulation; severe, correctable CAD with more than 70% stenosis in one or more coronary arteries; and severe inoperable CAD with greater than 70% stenosis in one or more coronary arteries and severe distal disease or poor ventricular function. The most remarkable findings were that only 8.5% of patients had normal coronary arteries and 60% had advanced or severe coronary lesions (>70% stenosis). Even when CAD was not suspected by the clinical history, more than a third of patients had advanced or severe coronary lesions (Table 56.2). In the Hertzer series, patients with severe correctable CAD were offered CABG before their vascular surgery, patients with normal or mild-to-moderate CAD went directly to vascular surgery, and those with severe inoperable CAD were treated on an individual basis. Combined mortality rates over the immediate- and long-term (4.6-year follow-up) postoperative period are shown in Table 56.3.17 Of the 216 patients who underwent coronary revascularization (CABG), 12 (5.5%) died after this surgery. This mortality rate is higher than that reported for patients undergoing CABG surgery without peripheral vascular disease (1% to 2%). Perhaps the risks associated with CABG should be seriously considered as part of the preoperative evaluation of these patients. When overall early and late mortality (>5 years) is considered, death occurred in 12% versus 26% of patients who did or did not undergo CABG. Although these data appear to support the beneficial effect of CABG on outcome, the mortality from CABG itself (5.5%) reduces its apparent benefits. Two randomized clinical trials have been performed to determine the impact of prophylactic coronary artery revascularization on outcome after open aortic and lower extremity arterial vascular surgery.4,25 Of the 5859 patients screened in the CARP trial, 41190 underwent coronary angiography based on a combination of clinical risk factors and noninvasive stress imaging data.26 The incidence and severity of CAD on these angiograms were 43% of patients had one or more major coronary arteries with at least a 70% stenosis suitable for revascularization (and were randomized to either revascularization or no revascularization before vascular surgery); 31% had Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1828 SECTION IV Adult Subspecialty Management TABLE 56.3 Perioperative and Late Cardiac Deaths after Peripheral Vascular Reconstruction in Patients Monitored over a 5-Year Period According to Coronary Angiographic Classification NORMAL OR MILD-TOADVANCED, MODERATE CAD COMPENSATED CAD SEVERE, CORRECTABLE CAD WITH CABG NO CABG SEVERE, INOPERABLE TOTAL CARDIAC CAD DEATHS Clinical Features Total No. of Patients No. % No. % No. % No. % No. % No. % Men 685 10/242 4.1 33/204 16 13/174 7.5 6/24 25 14/41 34 76 11 Women 315 5/160 3.1 12/85 14 12/42 29 3/11 27 8/17 47 40 13 Age 70 yr 278 5/74 6.8 16/91 18 6/68 8.8 6/15 40 9/30 30 42 15 Normotensive 403 7/185 3.8 15/102 15 8/82 9.8 2/15 13 8/19 42 40 9.9 Hypertensive 597 8/217 3.4 30/187 16 17/134 13 7/20 35 14/39 36 76 13 Nondiabetic 830 12/348 3.4 28/232 12 17/183 9.3 8/30 27 13/37 35 78 9.4 Diabetic 170 3/54 5.5 17/57 30 8/33 24 1/5 20 9/21 43 38 22 Total 1000 15/402 3.7 45/289 16 25/216 12 9/35 26 22/58 38 116 12 CABG, Coronary artery bypass grafting; CAD, coronary artery disease. Data from Hertzer NR, Young JR, Beven EG, et al. Late results of coronary bypass in patients with peripheral vascular disease. II. Five‐year survival according to sex, hypertension, and diabetes. Cleve Clin J Med. 1987;54:15–23. 1.0 Probability of survival No coronary artery revascularization ! 0.8 0.6 Coronary artery revascularization 0.4 0.2 P =.92 0 0 No. at Risk Revascularization No revascularization 1 2 3 4 5 Years after randomization 226 229 175 172 113 108 65 55 18 17 6 7 12 Fig. 56.1 Long-term survival in patients randomized to undergo coronary artery revascularization or no coronary artery revascularization before elective major vascular surgery (Coronary Artery Revascularization Prophylaxis trial). (From McFalls EO, Ward HB, Moritz TE, et al. Coronary-artery revascularization before elective major vascular surgery. N Engl J Med. 2004;351:2796–2804.) nonobstructed coronary arteries; 18% had coronary stenosis considered unsuitable for revascularization; and 5% had left main coronary artery stenosis of 50% or more. The CARP trial showed that prophylactic revascularization (by CABG or PCI) was generally safe but did not improve longterm outcome after vascular surgery. Long-term mortality (2.7 years) was 22% in the revascularization group and 23% in the group considered inappropriate for revascularization (Fig. 56.1). Although the trial was not designed to test the short-term benefit of prophylactic revascularization, perioperative outcomes were not decreased, including death (3.1% vs. 3.4%) and MI (12% vs. 14%). The CARP trial results can be applied to most of the vascular surgery patients; however, they cannot be extrapolated to patients with unstable cardiac symptoms, left main coronary artery disease, aortic stenosis, or severe left ventricular dysfunction because these conditions excluded patients from study participation. The DECREASE-V trial 26 screened 1880 vascular surgery patients, 430 of whom with three or more clinical risk factors underwent noninvasive stress testing using stress-echo or perfusion imaging. Patients with extensive stress-induced ischemia (26%) were randomly assigned to revascularization or no revascularization. Coronary angiography showed twovessel disease in 24%, three-vessel disease in 67%, and left main coronary artery disease in 8%. Prophylactic coronary revascularization (CABG or PCI) did not improve perioperative or long-term outcome (Table 56.4). The incidence of all-cause death or nonfatal MI at 30 days in patients who underwent revascularization or who did not was 43% versus 33%, respectively. The incidence of the composite end point at 1 year was similar, 49% versus 44%, respectively. As noted previously, this trial has come under scrutiny based on concerns of scientific misconduct by the principal investigator. The lack of benefit of prophylactic coronary revascularization in the CARP and DECREASE-V trials is difficult to reconcile with the more favorable data from Hertzer and co-workers 25 and other studies (Coronary Artery Surgery Study [CASS]27 and Bypass Angioplasty Revascularization Investigation [BARI]28). Clearly, issues are involved that go beyond critical coronary lesions; perhaps the current understanding of the pathophysiology of perioperative MI is incomplete. For example, perioperative MI may be caused by culprit lesions (i.e., vulnerable plaques with high likelihood of thrombotic complications) often located in coronary vessels without critical stenosis.29 For this type of MI (atherothrombotic), perioperative strategies aimed at reducing potential triggers of coronary plaque destabilization and rupture may be more appropriate than those leading to coronary revascularization. Demand ischemia is likely the predominant cause of perioperative MI, which has been confirmed by a recent angiographic study.30 Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery 1829 TABLE 56.4 Perioperative and Long-Term Patient Outcomes from the Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography (DECREASE)-V—V TRIAL HR (95% CI) P-value Revascularization No. (%) No Revascularization No. (%) NO. OF PATIENTS Events before surgery All-cause mortality Myocardial infarction Composite 49 2 (4.1) 1 (2.1) 3 (6.1) 52 0 0 0 Events up to 30 days after surgery All-cause mortality Myocardial infarction Composite 11 (22.5) 17 (34.7) 21 (42.9) 6 (11.5) 16 (30.8) 17 (32.7) 2.2 (0.74-6.6) 1.4 (0.73-2.8) 0.14 0.30 Events up to 365 days after surgery All-cause mortality Myocardial infarction Composite 13 (26.5) 18 (36.7) 24 (49.0) 12 (23.1) 19 (36.5) 23 (44.2) 1.3 (0.55-2.9) 1.2 (0.68-2.3) 0.58 0.48 0.23 0.11 CI, Confidence interval; HR, hazard ratio. From Poldermans D, Schouten O, Vidakovic R, et al. A clinical randomized trial to evaluate the safety of a noninvasive approach in high-risk patients undergoing major vascular surgery. The DECREASE-V Pilot Study. J Am Coll Cardiol. 2007;49:1763–1769. ASSESSMENT OF PULMONARY FUNCTION ASSESSMENT OF RENAL FUNCTION Postoperative pulmonary complications are potentially serious in patients undergoing vascular surgery, with the most significant morbidity seen in patients undergoing open aortic procedures (see also Chapter 54). The most important pulmonary complications are atelectasis, pneumonia, respiratory failure, and exacerbation of underlying chronic disease. Given the prevalence of cigarette smoking in this population, chronic obstructive pulmonary disease (COPD) and chronic bronchitis are common and, when present, place the patient at increased risk for postoperative pulmonary complications. When clinical assessment suggests severe pulmonary compromise, pulmonary function tests may be useful in evaluating and optimizing respiratory function (see also Chapters 32 and 41). Preoperative analysis of arterial blood gases should be used to establish a baseline for postoperative comparison. Baseline hypercapnia (partial pressure of arterial carbon dioxide >45 mm Hg) indicates a more frequent risk for postoperative morbidity. Bronchodilator therapy may be indicated on the basis of results of pulmonary function tests, although the risk for β-adrenergic agonist–induced arrhythmia or myocardial ischemia also must be considered. Preoperative treatment with a short course of glucocorticoids (prednisone 40 mg/day for 2 days) may be helpful for patients with significant COPD or asthma. Evidence of pulmonary infection should be treated with appropriate antibiotics. Although improved pulmonary outcome with regional anesthesia is not clear, patients with significant pulmonary disease may benefit from epidural techniques. Use of these techniques in the postoperative period helps to avoid respiratory depression from systemic opiates (see also Chapter 81). Pulmonary complications in the postoperative period are difficult to avoid. Incentive spirometry and continuous positive airway pressure (CPAP) do provide benefit.31 Given proper pulmonary care, even patients with severe pulmonary insufficiency, however, may undergo aortic surgery with acceptable morbidity and mortality outcomes.32 Chronic renal disease is common in vascular surgery patients and is associated with an increased risk for death and cardiovascular disease (see also Chapters 30 and 42).33 Chronic renal disease strongly predicts long-term mortality in patients with symptomatic lower extremity arterial occlusive disease irrespective of disease severity, cardiovascular risk, and concomitant treatment.34 Cardiovascular disease is independently associated with a decline in renal function and the development of kidney disease.35 Serum creatinine and creatinine clearance are used to assess renal function perioperatively. A preoperative serum creatinine level more than 2 mg/dL is an independent risk factor for cardiac complications after major noncardiac surgery.36 Preoperative creatinine clearance less than 60 mL/min is an independent predictor of both short-term and longterm mortality after elective vascular surgery.37 Perioperative β-adrenergic blocker38 and statin37 administration decrease risk for death in vascular surgery patients with renal impairment. Atherosclerotic disease in the abdominal aorta or renal arteries may compromise renal blood flow and renal function. Conversely, renal artery stenosis causes hypertension through renin-induced and angiotensininduced vasoconstriction. Hypertension itself may cause renal insufficiency or failure. Diabetic nephropathy is also common (see also Chapter 32). Superimposed on baseline abnormalities in renal function are the preoperatively and intraoperatively administered angiographic dyes, which are directly nephrotoxic. Renal ischemia occurs with interruption of renal blood flow from aortic cross-clamping. Even with infrarenal aortic cross-clamps, renal blood flow may decrease despite normal systemic arterial blood pressure and cardiac output. Embolic plaque can be showered into the renal arteries, especially when suprarenal aortic cross-clamps are applied and released. Fluctuations in intravascular volume and cardiac output can compromise renal perfusion during the intraoperative and postoperative periods. In one series of more than 500 patients, the prevalence of acute renal failure was 7% after abdominal aortic reconstruction. Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1830 SECTION IV Adult Subspecialty Management PERIOPERATIVE β-ADRENERGIC BLOCKER THERAPY Perioperative β-adrenergic blocker therapy is an important and controversial topic, particularly in patients undergoing vascular surgery, and is reviewed more fully in Chapters 31 and 32. Patients receiving chronic β-adrenergic blocker therapy should continue taking β-adrenergic blockers throughout the perioperative period. However, β-adrenergic blockers should not be used as the initial or primary treatment of tachycardia caused by perioperative events, such as hypovolemia, anemia, pain, or infection, because these conditions require prompt treatment of the underlying cause. Treatment of tachycardia caused by the sympathetic stimulation associated with surgical stress should be considered in high-risk patients, particularly those with known ischemic potential (i.e., ischemia on preoperative testing). Hypotension and bradycardia should be avoided. Acute initiation of large-dose β-adrenergic blockade in the perioperative period should be avoided. If a decision is made to initiate β-blocker treatment in the perioperative period to reduce cardiac risk, the safest approach may be to initiate therapy with a small dose and titrate to effect over a 7- to 10-day period before the planned surgery. Perioperative β-adrenergic blocker therapy can decrease the number of patients referred for preoperative cardiac testing. However, such testing should not be eliminated, and its risk-to-benefit ratio should be carefully assessed. PERIOPERATIVE STATIN THERAPY In addition to their lipid-lowering properties, statins have beneficial anti-inflammatory, plaque-stabilizing, and antioxidant effects (see also Chapter 32). Over the last decade, statin use has emerged as a promising strategy for the prevention of perioperative cardiovascular complications in patients undergoing vascular surgery.39 This approach is supported by the double-blind, placebo-controlled DECREASE-III trial. Unfortunately, controversy exists regarding this trial because of scientific misconduct identified by a recent investigation by Erasmus University.40 Statin use can help preserve renal function after aortic surgery and improve graft patency after lower extremity bypass surgery. Although current guidelines recommend the use of statins in all patients with peripheral arterial disease, the optimal timing and dosing of statins for perioperative use have not been established. PERIOPERATIVE DUAL ANTIPLATELET THERAPY The timing of noncardiac surgery in patients treated with coronary stents with the risk of stent thrombosis if the dual antiplatelet therapy (DAPT) is discontinued versus the risk of increased intraoperative bleeding if DAPT is continued. 20,41 Previous recommendations regarding the duration of DAPT and timing of noncardiac surgeries were based on observations of those treated with first-generation stents. Currently, used newer generations of stents, particularly the newer drug eluting stents (DES), have lower risk of in-stent thrombosis and require a shorter minimum duration of DAPT.42 The safety of treating patients with newer generation DES treated for shorter durations of DAPT (3 to 6 months) has been demonstrated in a meta-analysis of four trials.43 Also, in the PARIS (Patterns of Nonadherence to Antiplatelet Regimens in Stented Patients) registry, interruption of DAPT based on the physician judgment in patients undergoing surgery at any point did not affect the risk of major cardiac events.44 Hence, the ACC/AHA guidelines were changed in 2016 to reflect those changes (see Chapters 31 and 32).45 Abdominal Aortic Reconstruction Anesthesia for conventional abdominal aortic reconstruction requires an understanding of the pathophysiology, extensive knowledge of the surgical procedure, the ability to interpret sophisticated hemodynamic data, and skillful pharmacologic control and manipulation of hemodynamics. Preoperative and intraoperative communication with the surgical team is essential. All open operative procedures on the abdominal aorta and its major branches require large incisions and extensive dissection, clamping and unclamping of the aorta or its major branches, varying duration of organ ischemia-reperfusion, significant fluid shifts and temperature fluctuations, and activation of neurohumoral and inflammatory responses. The major objectives of surgical treatment of the aorta are to relieve symptoms, reduce the frequency of associated complications, and in the case of aortic aneurysm, prevent rupture. Over the last two decades, the growth and development of catheter-based technology for the treatment of peripheral arterial disease have generated tremendous interest for less invasive methods to treat aortic disease. Endovascular aortic aneurysm repair (discussed later) has become an established, less invasive alternative to conventional open repair, and its use has expanded to more than 75% of elective repairs and 30% of rupture repairs.46 The endovascular field continues to evolve rapidly with new devices, innovations, and indications for aortic disease. NATURAL HISTORY AND SURGICAL MORTALITY Abdominal Aortic Aneurysm Abdominal aortic aneurysms (AAAs) occur frequently in elderly men, with an incidence approaching 8% (see also Chapter 65). Increasing age, smoking, family history of AAA, and atherosclerotic disease are established risk factors. Although the prevalence is less frequent in women, the risk factors for AAA resemble those in men. More than 30,000 deaths result from rupture of AAAs each year in the United States.47 The number of hospital discharges each year with the first diagnosis of aortic aneurysm is nearly 70,000. Approximately 40,000 patients undergo repair of AAA each year in the United States, at a cost likely to exceed a billion dollars. The incidence of AAA appears to be increasing and is age- and gender-dependent. AAA is a multifactorial disease associated with aortic aging and atherosclerosis. Although no unified concept of pathogenesis exists, genetic, biochemical, metabolic, infectious, mechanical, and hemodynamic factors may contribute to the development of AAA disease. Adventitial elastin degradation (elastolysis), a hallmark of AAA formation, may be the primary event. Chronic inflammation plays a Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery fundamental role in the destruction of connective tissue in the aortic wall. Concomitant aortoiliac occlusive disease is present in approximately 20% to 25% of patients with AAA. Approximately 5% of patients undergoing abdominal aortic resection have inflammatory aneurysms. Rare causes of AAA disease include trauma, mycotic infection, syphilis, and Marfan syndrome. Most AAAs are detected incidentally when imaging is performed for other reasons or through screening programs. The natural history of AAA disease is progressive enlargement and ultimate rupture and death. The diameter and rate of expansion of asymptomatic AAAs are the best predictors of the risk for rupture. Current guidelines emphasize that it is not possible to recommend a single threshold diameter for operative intervention that can be generalized to all patients. Yet, elective repair should be undertaken in all patients with AAA 6 cm or larger in diameter. Although some controversy exists regarding elective AAA repair when its diameter is in the 5.5- to 5.9-cm range, the risk for rupture of a 5.5-cm aneurysm (per year) is equal to or greater than the risk for perioperative mortality, and thus surgical repair is indicated. The 1-year incidence of probable rupture in patients refusing or unfit for elective repair is 9.4%, 10.2%, and 32.5% for aneurysms 5.5 to 5.9 cm, 6.0 to 6.9 cm, and 7.0 cm or greater, respectively.48 Over 90% of AAAs are less than the current threshold (5.5 cm) for surgical repair at the time of detection. Randomized controlled trials in patients with AAAs 4.0 to 5.5 cm in diameter have provided important insight into the natural history of small asymptomatic aortic aneurysms.49 Four trials have demonstrated that surveillance of small aneurysms (4.0 to 5.5 cm) is a safe management option and that early repair (open or endovascular surgery) did not result in any long-term survival benefit. Surgical repair is often considered if small aneurysms become symptomatic or expand more than 0.5 cm in a 6-month period. Although significant interest exists in medical treatment (e.g., antibiotics, β-adrenergic blockers, statins) to delay or reverse expansion of small aneurysms, evidence for a protective effect is limited.50 Aneurysms less than 4.0 cm in diameter are thought to be relatively benign in terms of rupture and expansion. Perioperative mortality from elective resection of infrarenal AAAs has progressively declined from 18% to 20% during the 1950s, 6% to 8% in the mid-1960s, 5% to 6% in the early 1970s, and 2% to 4% in the 1980s, at which time it plateaued. A publication of data from 1000 consecutive elective open infrarenal abdominal aneurysm repairs over a 15-year period reported a perioperative mortality rate of 2.4%.51 Hertzer and co-workers52 reported a mortality rate of 1.2% for 1135 consecutive elective open infrarenal abdominal aortic repairs at the Cleveland Clinic. This singlecenter mortality rate is considerably less than the mortality rates of 5.6% to 8.4% reported from large national data sets. These more frequent mortality rates on the national level suggest that all the technologic and treatment advances over the last 2 decades have not had an impact on outcomes of patients requiring open AAA repair. Regionalization of patient care and endovascular treatments currently hold the most promise for improvement in operative mortality. For ruptured AAAs, perioperative mortality has not changed significantly over the last 4 decades and remains nearly 50%, with few exceptions. Including patients with 1831 rupture who die before reaching a hospital, the overall mortality rate after rupture may very well exceed 90%. The long-term durability of open infrarenal AAA repair is excellent and well established. The incidence of late graft complications is infrequent (0.4% to 2.3%). Postoperative survival rates after repair of non-ruptured AAA are 92% at 1 year and 67% at 5 years. Aortoiliac Occlusive Disease The infrarenal aorta and the iliac arteries are two of the most common sites of chronic atherosclerosis. Because of the diffuse and progressive nature of aortoiliac atherosclerosis, plaque enlargement may reduce blood flow to the lower extremities below a critical level and result in symptoms of ischemia. Unlike patients with aortic aneurysmal disease, patients undergo surgery for aortoiliac occlusive disease only if they are symptomatic. Surgical intervention is indicated for disabling intermittent claudication and limb-threatening ischemia. Intervention is directed toward restoring peripheral pulsatile circulation to relieve claudication and toward preventing amputation. Patients with localized aortoiliac occlusive disease typically have claudication because collateral circulation adequate to prevent critical lower extremity ischemia usually exists. Perioperative mortality is lower in patients undergoing aortoiliac reconstruction than in those undergoing abdominal aortic surgery. Therapeutic options for managing aortoiliac occlusive disease include anatomic or direct reconstruction (i.e., aortobifemoral bypass), extra-anatomic or indirect bypass grafts (i.e., axillofemoral bypass), and catheter-based endoluminal techniques (i.e., percutaneous transluminal angioplasty [PTA] with or without stent insertion). Aortobifemoral bypass is viewed as the gold standard in treating aortoiliac occlusive disease. Extra-anatomic bypass grafts are generally reserved for specific indications, usually patients with infection, failure of previous reconstruction, or prohibitive risk. Reduced long-term patency and inferior functional results are frequently the trade-off for lower perioperative morbidity and mortality. Catheter-based endoluminal techniques, such as PTA, are used for relatively localized disease and may be reasonable alternatives to aortobifemoral bypass in 10% to 15% of patients with aortoiliac occlusive disease. Renal and Visceral Arterial Insufficiency Atherosclerosis is the most common cause of renal artery stenosis. Occlusive lesions are located almost exclusively in the proximal segment and orifice of the renal artery and are usually an extension of aortic atherosclerosis. Fibromuscular dysplasia is an important, but less common, cause of renal artery stenosis and most frequently involves the distal two thirds of the renal arteries. Hemodynamically significant renal artery stenosis may cause hypertension by activation of the renin-angiotensin-aldosterone system, and bilateral involvement may result in renal failure. Patients with renovascular hypertension frequently have poorly controlled hypertension despite maximal medical therapy. These patients often have severe bilateral renal artery stenosis and may have recurrent congestive heart failure or flash pulmonary edema. Indications for intervention include control of hypertension and salvage of renal function. Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1832 SECTION IV Adult Subspecialty Management Operative interventions include aortorenal bypass, extraanatomic bypass (hepatorenal or splenorenal bypass), or transaortic endarterectomy. Suprarenal or supraceliac aortic cross-clamping is frequently required for open operative interventions. PTA with stenting of the renal artery is used as the first-line treatment in selected patients. Stenosis at the origin of the celiac and mesenteric arteries occurs as a result of extension of aortic atherosclerosis. The inferior mesenteric artery is by far the most commonly involved, followed by the superior mesenteric artery and the celiac artery. Occlusion of a single vessel rarely causes ischemic symptoms because of the extensive nature of visceral collateralization. However, occlusion or significant stenosis of any two vessels may compromise collateral flow sufficiently to give rise to chronic visceral ischemia. Operative repair of visceral artery stenosis is reserved for symptomatic patients. Operative interventions include transaortic endarterectomy and bypass grafts, which frequently require supraceliac aortic cross-clamping. Mortality rates for such procedures range from 7% to 18%. To avoid the high mortality associated with open repair, PTA with stenting has increasingly been applied in patients with chronic visceral ischemia. Acute visceral artery occlusion can be caused by an embolus or, less commonly, by thrombosis. To avoid the extremely high mortality associated with acute visceral ischemia, diagnosis and surgical intervention must occur before gangrene of the bowel develops. AORTIC CROSS CLAMPING The pathophysiology of aortic cross-clamping is complex and depends on many factors, including level of the cross-clamp, status of the left ventricle, degree of periaortic collateralization, intravascular blood volume and distribution, activation of the sympathetic nervous system, and anesthetic drugs and techniques. Most abdominal aortic reconstructions require clamping at the infrarenal level. However, clamping at the suprarenal and supraceliac levels is required for suprarenal aneurysms and renal or visceral reconstructions and is frequently necessary for juxtarenal aneurysms, inflammatory aneurysms, and aortoiliac occlusive disease with proximal extension. These higher levels of aortic occlusion have a significant impact on the cardiovascular system, as well as on other vital organs rendered ischemic or hypoperfused. Ischemic complications may result in renal failure, hepatic ischemia and coagulopathy, bowel infarction, and paraplegia. With EVAR now common, an increasing proportion of patients undergoing open repair have anatomically complex aneurysms, many of which require suprarenal cross- clamping.53 Hemodynamic and Metabolic Changes The hemodynamic and metabolic changes associated with aortic cross-clamping are summarized in Box 56.1. The magnitude and direction of these changes are complex, dynamic, and vary among experimental and clinical studies. However, several important factors must be considered (Box 56.2). The systemic cardiovascular consequences of aortic cross-clamping can be dramatic, depending primarily on the level at which the cross-clamp is applied. Arterial hypertension above the clamp and arterial hypotension BOX 56.1 Physiologic Changes With Aortic Cross-Clamping* and Therapeutic Interventions Hemodynamic Changes ↑ Arterial blood pressure above the clamp ↓ Arterial blood pressure below the clamp ↑ Segmental wall motion abnormalities ↑ Left ventricular wall tension ↓ Ejection fraction ↓ Cardiac output†,‡ ↓ Renal blood flow ↑ Pulmonary occlusion pressure ↑ Central venous pressure ↑ Coronary blood flow Metabolic Changes ↓ Total body oxygen consumption ↓ Total body carbon dioxide production ↑ Mixed venous oxygen saturation ↓ Total body oxygen extraction ↑ Epinephrine and norepinephrine Respiratory alkalosis Metabolic acidosis Therapeutic Interventions Afterload reduction Sodium nitroprusside Inhalational anesthetics Amrinone Shunts and aorta-to-femoral bypass Preload reduction Nitroglycerin Controlled phlebotomy Atrial-to-femoral bypass Renal protection Fluid administration Distal aortic perfusion techniques Selective renal artery perfusion Mannitol Drugs to augment renal perfusion Other Hypothermia ↓ Minute ventilation Sodium bicarbonate *These changes are of greater significance with longer duration of crossclamping and with more proximal cross-clamping. †Cardiac output may increase with thoracic cross-clamping. ‡When ventilatory settings are unchanged from pre-clamp levels. below the clamp are the most consistent components of the hemodynamic response to aortic cross-clamping at any level. The increase in arterial blood pressure above the clamp is primarily due to the sudden increase in impedance to aortic blood flow and the resultant increase in systolic ventricular wall tension or afterload. However, factors such as myocardial contractility, preload, blood volume, and activation of the sympathetic nervous system also may be important.54 Cross-clamping of the aorta at or above the diaphragm results in the most profound increases in arterial blood pressure unless diverting circulatory support or IV vasodilators are used. Changes in cardiac output and filling pressure with aortic cross-clamping are not consistent and require an integrated approach in understanding Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery BOX 56.2 Factors That May Influence the Magnitude and Direction of Physiologic Changes Occurring With Aortic Cross-Clamping TABLE 56.5 Percent Change in Cardiovascular Variables on Initiation of Aortic Occlusion Level of aortic cross-clamp Species differences Anesthetic agents and techniques Use of vasodilator therapy Use of diverting circulatory support Degree of periaortic collateralization Left ventricular function Status of the coronary circulation Volume status Neuroendocrine activation Duration of aortic cross-clamp Body temperature Cardiovascular Variable Supraceliac Impedance to Ao flow R art Preload* Afterload Coronary flow Contractility ~I If coronary flow and contractility increase CO I I SuprarenalInfraceliac Infrarenal Mean arterial blood pressure 54 5* 2* Pulmonary capillary wedge pressure 38 10* 0* End-diastolic area 28 2* 9* End-systolic area 69 10* 11* Ejection fraction −38 −10* −3* 33 0 92 *Statistically different (P <.05) from group undergoing supraceliac aortic occlusion. From Roizen MF, Beaupre PN, Alpert RA, et al. Monitoring with two-dimensional transesophageal echocardiography: comparison of myocardial function in patients undergoing supraceliac, suprarenal-infraceliac, or infrarenal aortic occlusion. J Vasc Surg. 1984;1:300–305. Catecholamines (and other vasoconstrictors) Active venoconstriction proximal and distal to clamp PERCENT CHANGE AFTER OCCLUSION Patients with wall motion abnormalities AoX Passive recoil distal to clamp 1833 I'-------~ If coronary flow and contractility do not increase Fig. 56.2 Systemic hemodynamic response to aortic cross-clamping. Preload (asterisk) does not necessarily increase with infrarenal clamping. Depending on splanchnic vascular tone, blood volume can be shifted into the splanchnic circulation and preload will not increase. Ao, Aortic; AoX, aortic cross-clamping; CO, cardiac output; R art, arterial resistance. the direction and magnitude of such changes (Fig. 56.2). Cross-clamping of the proximal descending thoracic aorta increases mean arterial, central venous, mean pulmonary arterial, and pulmonary capillary wedge pressure by 35%, 56%, 43%, and 90%, respectively, and decreases the cardiac index by 29%.55 Heart rate and left ventricular stroke work are not significantly changed. Supraceliac aortic cross-clamping increases mean arterial pressure by 54% and pulmonary capillary wedge pressure by 38%.56 Ejection fraction, as determined by two-dimensional echocardiography, decreases by 38%. Despite normalization of systemic and pulmonary capillary wedge pressure with anesthetic agents and vasodilator therapy, supraceliac aortic cross-clamping causes significant increases in left ventricular end-systolic and end-diastolic area (69% and 28%, respectively), as well as wall motion abnormalities indicative of ischemia in 11 of 12 patients (Table 56.5). Aortic cross- clamping at the suprarenal level causes similar but smaller cardiovascular changes and clamping at the infrarenal level is associated with only minimal changes and no wall motion abnormalities. The marked increases in ventricular filling pressure (preload) reported with high aortic cross-clamping have been attributed to increased afterload and redistribution of blood volume, which is of prime importance during thoracic aortic cross-clamping. The splanchnic circulation, an important source of functional blood volume reserve, is central to this hypothesis. The splanchnic organs contain nearly 25% of the total blood volume, nearly two thirds (>800 mL) of which can be autotransfused from the highly compliant venous vasculature into the systemic circulation within seconds.57 Primarily because of smaller splanchnic venous capacitance, blood volume is redistributed from vascular beds distal to the clamp to the relatively noncompliant vascular beds proximal to the clamp (Fig. 56.3). Both passive and active mechanisms lower splanchnic venous capacitance with thoracic aortic cross-clamping. Cross-clamping the aorta above the splanchnic system dramatically reduces splanchnic arterial flow, which produces a significant reduction in pressure within the splanchnic capacitance vessels.58 This decreased pressure allows the splanchnic veins to passively recoil and increase venous return to the heart and blood volume proximal to the clamp. Thoracic aortic cross-clamping also results in significant increases in plasma epinephrine and norepinephrine, which may enhance venomotor tone both above and below the clamp. The splanchnic veins are highly sensitive to adrenergic stimulation. The major effect of catecholamines on the splanchnic capacitance vessels is venoconstriction, which actively forces out splanchnic blood, reduces splanchnic venous capacitance, and increases venous return to the heart.58 Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1834 SECTION IV Adult Subspecialty Management Control Upper body Occlusion of aorta Occlusion of aorta and IVC Shunt PVS SVC LV IVC Lower body PVI Fig. 56.3 Schematic drawing of the circulation. Compliant regions (dashed lines) of the upper and lower part of the body and end-diastolic volumes of the left ventricle in control state (left panel) are shown after occlusion of the aorta alone (middle panel) and combined occlusion of the aorta and inferior vena cava (right panel). IVC, Inferior vena cava; LV, left ventricle; PVS and PVI, pressure in compliant regions of the upper and lower body, respectively; Shunt, physiologic shunt; SVC, superior vena cava. Several animal studies support the blood volume redistribution hypothesis. Cross-clamping the thoracic aorta in dogs results in marked increases in mean arterial pressure and end-diastolic left ventricular pressure (84% and 188%, respectively) and no significant change in stroke volume.59 In this same experimental model, simultaneous crossclamping of the thoracic aorta and the inferior vena cava resulted in no significant change in mean arterial pressure or preload (see Fig. 56.3). Stroke volume was reduced by 74%. By transfusing blood (above the clamps) during this period of simultaneous clamping, the authors reproduced the hemodynamic effect of thoracic aortic cross-clamping alone. This study also demonstrated that thoracic aortic cross-clamping is associated with a significant and dramatic increase (155%) in blood flow above the level of the clamp whereas no change in blood flow occurred with simultaneous aortic and inferior vena cava clamping. In other animal models, the proximal aortic hypertension and increased central venous pressure (CVP) occurring after thoracic aortic cross-clamping were completely reversed by phlebotomy.60 Aortic cross-clamping at the thoracic and suprarenal levels in dogs both resulted in proximal aortic hypertension, but only occlusion at the thoracic level increased central venous pressure.61 In this study, thoracic aortic occlusion increased blood volume in organs and tissues proximal to the clamp whereas no such increase occurred with suprarenal aortic cross-clamping. These experimental data strongly support the hypothesis of blood volume redistribution during aortic cross-clamping and help explain the marked differences in hemodynamic responses observed after aortic cross-clamping at different levels.56 Afterload-dependent increases in preload also occur with aortic cross-clamping, usually in the setting of impaired myocardial contractility and reduced coronary reserve. The impaired left ventricle may respond to increased afterload with an increase in end-systolic volume and a concomitant reduction in stroke volume (afterload mismatch). The reduction in stroke volume may be due to limited preload reserve, myocardial ischemia, or inability of the heart to generate a pressure-induced increase in contractility (the Anrep effect). If right ventricular function remains normal, the pre-clamp right ventricular stroke volume added to the increased left ventricular end-systolic volume results in left ventricular dilation and elevated end-diastolic volume. If corrective measures are not undertaken, overt left ventricular overload may result, with severe peripheral organ dysfunction and pulmonary edema. Most clinical studies indicate that cardiac output decreases with thoracic aortic cross-clamping (without vasodilator therapy or diverting circulatory support), whereas most animal studies show no significant change or an increase in cardiac output. However, the status of the left ventricle clearly plays a major role. Whereas a normal intact heart can withstand large increases in volume without significant ventricular distention or dysfunction, an impaired heart with reduced myocardial contractility and coronary reserve may respond to such increase in volume conditions with marked ventricular distention as a result of acute left ventricular dysfunction and myocardial ischemia. Although impaired myocardial contractility and reduced coronary reserve are rare in animal experiments, such disorders are frequent in the elderly population undergoing aortic reconstruction. The increase in ventricular loading conditions seen with thoracic and supraceliac cross-clamping55,56 in the clinical setting may increase left ventricular wall stress (afterload), with resultant acute deterioration of left ventricular function and myocardial ischemia. Impaired subendocardial perfusion caused by high intramyocardial pressure may be the cause of wall motion abnormalities and changes in ejection fraction. Reflex mechanisms causing immediate feedback inhibition may also explain the reduction in cardiac output with aortic cross-clamping. For example, baroreceptor activation resulting from increased aortic pressure should depress the heart rate, contractility, Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery and vascular tone. Thoracic aortic cross-clamping with the use of vasodilator therapy to normalize ventricular loading conditions maintains or increases cardiac output.65 The metabolic effects of aortic cross-clamping are summarized in Box 56.1. Cross-clamping of the thoracic aorta decreases total-body O2 consumption by approximately 50%. For reasons that are unclear, O2 consumption decreases in tissues above the clamp. In clinical studies, increased mixed venous O2 saturation occurs with aortic cross-clamping above the celiac axis. This increase in mixed venous O2 saturation may be explained by a reduction in O2 consumption that exceeds the reduction in cardiac output, thus decreasing total body O2 extraction. Central hypervolemia and increased arteriovenous shunting in tissues proximal to the aortic clamp may play a role in reducing total body O2 extraction. Arterial blood pressure, blood flow, and O2 consumption distal to a thoracic aortic cross-clamp decrease by 78% to 88%, 79% to 88%, and 62%, respectively, from baseline values before clamping. Blood flow through tissues and organs below the level of aortic occlusion is dependent on perfusion pressure and is independent of cardiac output. Administration of sodium nitroprusside to maintain proximal aortic pressure above the cross-clamp at pre-clamp levels has been shown to further reduce arterial pressure distal to the clamp by 53%. As discussed later, these data have significant implications regarding vital organ protection during aortic cross-clamping. The cardiovascular response to infrarenal aortic crossclamping is less significant than with high aortic crossclamping (see Table 56.5). Although several clinical reports have noted no significant hemodynamic response to infrarenal cross-clamping, the hemodynamic response generally consists of increases in arterial pressure (7% to 10%) and systemic vascular resistance (20% to 32%), with no significant change in heart rate. Cardiac output is most consistently decreased by 9% to 33%. Reported changes in ventricular filling pressure have been inconsistent. Blood volume redistribution may affect preload with infrarenal aortic crossclamping (see Fig. 56.3). In this situation, blood volume below the clamp shifts to the compliant venous segments of the splanchnic circulation above the clamp, thereby dampening the expected increase in preload. The preload changes with infrarenal aortic cross-clamping also may depend on the status of the coronary circulation. Patients with severe ischemic heart disease responded to infrarenal aortic cross-clamping with significantly increased central venous (35%) and pulmonary capillary (50%) pressure, whereas patients without CAD had decreased filling pressure. Echocardiographically detected segmental wall motion abnormalities occur in up to 30% of patients during infrarenal aortic reconstruction, with over 60% occurring at the time of aortic cross-clamping. Patients with aortoiliac occlusive disease may have less hemodynamic response to infrarenal aortic cross-clamping than do patients with AAA disease, perhaps as a result of more extensive periaortic collateral vascularization. RENAL FUNCTION AND PROTECTION Preservation of renal function is highly important during aortic reconstructive surgery. Acute renal failure occurs in approximately 3% of patients undergoing elective infrarenal 1835 aortic reconstruction, and mortality resulting from postoperative acute renal failure is more frequent than 40%. Despite significant improvements in the perioperative care of these patients, the frequent incidence of morbidity and mortality resulting from acute renal failure has remained largely unchanged over the last several decades. Most of the morbidity associated with significant postoperative renal dysfunction is nonrenal. The adequacy of renal perfusion “cannot” be assumed by urine output. Although urine output is closely monitored and often augmented during aortic surgery, intraoperative urine output does not predict postoperative renal function. Procedures requiring aortic cross-clamping above the renal arteries dramatically reduce renal blood flow. Experimental studies report an 83% to 90% reduction in renal blood flow during thoracic aortic cross-clamping. Infrarenal aortic cross-clamping in humans is associated with a 75% increase in renal vascular resistance, a 38% decrease in renal blood flow, and a redistribution of intrarenal blood flow toward the renal cortex. These rather profound alterations in renal hemodynamics occurred despite no significant change in systemic hemodynamics, and they persisted after unclamping. The sustained deterioration in renal perfusion and function during and after infrarenal aortic cross-clamping has been attributed to renal vasoconstriction, but the specific pathophysiologic process remains unknown. Renal sympathetic blockade with epidural anesthesia to a T6 level does not prevent or modify the severe impairment in renal perfusion and function that occurs during and after infrarenal aortic cross-clamping. Although plasma renin activity is increased during aortic cross-clamping, pretreatment with converting enzyme inhibitors before infrarenal aortic cross-clamping does not attenuate the decreased renal blood flow and glomerular filtration rate. Other mediators, such as plasma endothelin, myoglobin, and prostaglandins, may contribute to the decreased renal perfusion and function after aortic cross-clamping. Acute tubular necrosis accounts for nearly all the renal dysfunction and failure after aortic reconstruction. The degree of preoperative renal insufficiency remains the strongest predictor of postoperative renal dysfunction. In addition to aortic cross-clamping-induced reductions in renal blood flow, ischemic reperfusion injury, intravascular volume depletion, embolization of atherosclerotic debris to the kidneys, and surgical trauma to the renal arteries all contribute to renal dysfunction. Mannitol, loop diuretics, and dopamine are used clinically to preserve renal function during aortic surgery. Significant controversy exists regarding the use of these drugs, as well as the mechanisms by which they may offer a protective effect. Although not proved, pharmacologic “protection” before aortic cross-clamping is believed to be beneficial and is therefore given. The use of mannitol 12.5 g/70 kg to induce osmotic diuresis before aortic cross-clamping is ubiquitous in clinical practice. Mannitol improves renal cortical blood flow during infrarenal aortic cross-clamping and reduces ischemia-induced renal vascular endothelial cell edema and vascular congestion. Other mechanisms by which mannitol may be beneficial include acting as a scavenger of free radicals, decreasing renin secretion, and increasing renal prostaglandin synthesis. Loop diuretics and low-dose dopamine (1 to 3 μg/kg/min) are used to Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1836 SECTION IV Adult Subspecialty Management protect the kidneys from aortic cross-clamp-induced injury by increasing renal blood flow and urine output intraoperatively. Routine use of these drugs is common for patients with preoperative renal insufficiency and for procedures requiring suprarenal aortic cross-clamping. Intraoperative use of these drugs requires increased surveillance of intravascular volume and electrolytes during the postoperative period. Therapy with these drugs could actually be harmful because of hypovolemia and resultant renal hypoperfusion. In addition, dopamine’s positive inotropic and chronotropic activity may cause tachycardia and increase myocardial O2 consumption in patients with limited coronary reserve. Fenoldopam mesylate, a selective dopamine type 1 agonist that preferentially dilates the renal and splanchnic vascular beds, has shown some promise as a renoprotective drug. However, its role in the prevention of renal dysfunction after aortic surgery is not known. Statin use is associated with preserved renal function after aortic surgery requiring suprarenal aortic cross-clamping.63 Remote ischemic preconditioning reduces the incidence of renal impairment after open aortic surgery.64 Optimal systemic hemodynamics, including maintenance of intravascular volume and hematocrit, is generally considered the most effective means of renal protection during and after aortic cross-clamping. The goal is to achieve a preload adequate to allow the left ventricle to cope with cross-clamping-induced changes in contractility and afterload while maintaining cardiac output. However, in providing such therapy, excessive intravascular volume should be avoided because it may lead to inappropriate increases in preload or pulmonary edema in patients with decreased myocardial reserve. THERAPEUTIC STRATEGIES Patients with preexisting impaired ventricular function and reduced coronary reserve are most vulnerable to the stress imposed on the cardiovascular system by aortic crossclamping. Rational therapeutic strategies to prevent the deleterious effect of aortic cross-clamping primarily include measures to reduce afterload and maintain a normal preload and cardiac output. Vasodilators, positive and negative inotropic drugs, and controlled intravascular volume depletion (i.e., phlebotomy) may be used selectively. Patients with impaired ventricular function requiring supraceliac aortic cross-clamping are the most challenging. Myocardial ischemia, reflecting an unfavorable balance between myocardial O2 supply and demand, may result from the hemodynamic consequences of aortic crossclamping. Controlled (i.e., slow clamp application) supraceliac aortic cross-clamping is important to avoid abrupt and extreme stress on the heart. Both afterload and preload reduction are often required. Afterload reduction, most commonly accomplished with the use of sodium nitroprusside or clevidipine (predominantly arteriolar dilators), is necessary to unload the heart and reduce ventricular wall tension. In a large series of patients requiring cross-­clamping of the descending thoracic aorta, stable left ventricular function was maintained with sodium nitroprusside during cross-clamping. Sodium nitroprusside most likely allowed adequate intravascular volume before unclamping, which resulted in stable unclamping hemodynamics. A normal preload is equally important and involves careful IV fluid BOX 56.3 Physiologic Changes With Aortic Unclamping* and Therapeutic Intervention Hemodynamic Changes ↓ Myocardial contractility ↓ Arterial blood pressure ↑ Pulmonary artery pressure ↓ Central venous pressure ↓ Venous return ↓ Cardiac output Metabolic Changes ↑ Total body oxygen consumption ↑ Lactate ↓ Mixed venous oxygen saturation ↑ Prostaglandins ↑ Activated complement ↑ Myocardial-depressant factor(s) ↓ Temperature Metabolic acidosis Therapeutic Interventions ↓ Inhaled anesthetics ↓ Vasodilators ↑ Fluid administration ↑ Vasoconstrictor drugs Reapply cross-clamp for severe hypotension Consider mannitol Consider sodium bicarbonate *These changes are of greater significance with longer duration of crossclamping and with more proximal cross-clamping. titration and vasodilator administration. Nitroglycerin can be used because it increases venous capacity more than does sodium nitroprusside. In patients without evidence of left ventricular decompensation or myocardial ischemia during supraceliac aortic cross-clamping, a proximal aortic mean arterial pressure of up to 120 mm Hg is acceptable. The surgeon may request lower proximal arterial pressure if friable aortic tissue is encountered. Blood flow below the aortic clamp depends on pressure and decreases further during therapy with vasodilators. In this setting, vital organs and tissues distal to the clamp are exposed to reduced perfusion pressure and blood flow. Though infrequent, maintenance of adequate cardiac output may require active intervention with inotropic drugs. AORTIC UNCLAMPING The hemodynamic and metabolic effects of aortic unclamping are listed in Box 56.3. The hemodynamic response to unclamping depends on many factors, including the level of aortic occlusion, total occlusion time, use of diverting support, and intravascular volume. Hypotension, the most consistent hemodynamic response to aortic unclamping, can be profound, particularly after removal of a supraceliac cross-clamp (Fig. 56.4). Reactive hyperemia in tissues and organs distal to the clamp and the resultant relative central hypovolemia are the dominant mechanisms of the hypotension. Washout of vasoactive and cardiodepressant mediators from ischemic tissues, as well as humoral factors, Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery 1837 AoX Distal tissue ischemia “Mediators” release Distal vasodilation Cven R art Permeability (by end of clamping period) Unclamping “Mediators” production and washout Myocardial contractility Distal shift of blood volume I t Rpv Central hypovolemia Pulmonary edema Loss of intravascular fluid Venous return Cardiac output Hypotension Fig. 56.4 Systemic hemodynamic response to aortic unclamping. AoX, Aortic cross-clamping; Cven, venous capacitance; R art, arterial resistance; Rpv, pulmonary vascular resistance. may also contribute to the hemodynamic responses after unclamping the aorta. These humoral factors and mediators, which may also play a role in organ dysfunction after aortic occlusion, include lactic acid, renin-angiotensin, O2 free radicals, prostaglandins, neutrophils, activated complement, cytokines, and myocardial-depressant factors.54 Avoidance of significant hypotension with unclamping requires close communication with the surgical team, awareness of the technical aspect of the surgical procedure, and appropriate administration of fluids and vasoactive drugs. It is essential that correction of preoperative fluid deficits, maintenance of intraoperative fluid requirements, and replacement of blood loss be accomplished before unclamping. Vasodilators, if used, should be gradually reduced and discontinued before unclamping. The inspired concentrations of volatile anesthetics should be decreased. Moderate augmenting of intravascular volume by administration of fluids (∼500 mL) during the immediate prerelease period is indicated for infrarenal unclamping. More aggressive intravascular fluid administration is required in the period immediately preceding supraceliac unclamping. Maintaining increased central venous or pulmonary capillary wedge pressure during the cross-clamp period is not indicated and may result in significant overtransfusion of fluids and blood products. If significant hypotension results, gradual release of the aortic clamp and reapplication or digital compression are important measures in maintaining hemodynamic stability during unclamping. Although vasopressor requirements are minimal after release of the infrarenal clamp, significant support is often needed after the removal of supraceliac clamps. Caution must be observed when vasopressor support is used in this setting because profound proximal hypertension may occur if reapplication of the cross-clamp is required above the celiac axis. In addition, hypertension should be avoided to prevent damage to or bleeding from the vascular anastomoses. ANESTHETIC MANAGEMENT Intraoperative Monitoring The potential for significant and rapid blood loss cannot be underestimated. A central line and two peripheral lines are usually used as intravenous (IV) access. The choice of the type and the size of the central line can be decided on a case-by-case basis. Placement of an arterial catheter should be routine in all patients undergoing aortic reconstruction. Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1838 SECTION IV Adult Subspecialty Management As with other vascular procedures, the radial artery is most commonly selected for cannulation because of its superficial location, easy accessibility, and low complication rate. A noninvasive blood pressure cuff should be placed on the arm contralateral to the arterial catheter in the event of catheter malfunction. A central venous catheter should be used for all open aortic procedures. It allows monitoring of CVP and administration of drugs directly into the central circulation. The routine, nonselective use of pulmonary artery catheter monitoring is not recommended. It should be reserved for patients with severely limited cardiopulmonary function or complex aortic reconstruction. In patients with good left ventricular and pulmonary function, CVP correlates well with left ventricular filling pressure. The invasive monitoring catheters can be placed before or after induction of general anesthesia. The advantage of preinduction catheter placement is assessment of the patient’s awake (i.e., baseline) cardiovascular status, which allows correction of significant abnormalities in cardiac filling and function before induction. With selective use, accurate interpretation of data, and rational treatment strategies, pulmonary artery catheter monitoring may be beneficial in high-risk patients undergoing complex aortic reconstruction. Yet the clinical value of pulmonary artery catheter monitoring in high-risk patients has not been established.65 Clinical studies over the last 2 decades have yielded quite conflicting and variable results, including both increases and decreases in mortality. The National Heart, Lung and Blood Institute and the Food and Drug Administration (FDA)66 sponsored a large prospective, randomized trial that compared goal-directed therapy guided by a pulmonary artery catheter with standard care without the use of a pulmonary artery catheter in high-risk surgical patients. The result found no benefit in treatment guided by a pulmonary artery catheter.67 Yet this study did not find an increase in mortality with insertion and use of a pulmonary artery catheter. Transesophageal echocardiography (TEE) has been used intraoperatively to assess global ventricular function, guide intravascular fluid therapy, and monitor for myocardial ischemia. Patients requiring supraceliac aortic cross-clamping have significant increases in the end-diastolic area and significant decreases in ejection fraction on echocardiography that are not completely normalized with vasodilators and frequently are not detected by pulmonary artery catheter monitoring.56 The optimal intraoperative monitoring techniques for patients undergoing abdominal aortic reconstruction have not been established. Existing clinical studies offer insufficient data to conclusively answer the question of whether pulmonary artery catheter or TEE monitoring improves outcome. The clinical usefulness of any monitoring technique ultimately depends on patient selection, accurate interpretation of data, and appropriate therapeutic intervention. Cell Salvage Intraoperative cell salvage is a widely used technique combined with allogenic blood transfusion and in some centers is considered routine. The equipment is expensive and requires significant training and expertise. An early, nonrandomized study reported a 75% reduction in the number of allogeneic red blood cell (RBC) units transfused during elective aortic surgery with the use of cell salvage. Later randomized studies have reported conflicting results. The routine use of cell salvage during aortic surgery may not be cost-effective and thus it may best be reserved for a select group of patients with an expected large blood loss. A costeffective option is to use the cell salvage reservoir for blood collection and activate the full salvage process only if large blood loss occurs. Anesthetic Drugs and Techniques Various anesthetic techniques, including general anesthesia, regional (epidural) anesthesia, and combined techniques, have been used successfully for abdominal aortic reconstruction. Combined techniques most commonly use a lumbar or low thoracic epidural catheter in addition to general anesthetic. Local anesthetics, opioids, or, more commonly, a combination of the two may be administered by bolus or continuous epidural infusion. Maintenance of vital organ perfusion and function by the provision of stable perioperative hemodynamics is more important to overall outcome than is the choice of anesthetic drug or technique.14 Therefore, the specific anesthetic technique for patients undergoing abdominal aortic reconstruction is important insofar as it allows rapid and precise control of hemodynamic parameters. Given the frequent incidence of cardiac morbidity and mortality in patients undergoing aortic reconstruction, factors that influence ventricular work and myocardial perfusion are of prime importance. Induction of general anesthesia should ensure that stable hemodynamics are maintained during loss of consciousness, laryngoscopy and endotracheal intubation, and the immediate postinduction period. A variety of IV anesthetics (propofol, etomidate, thiopental) are suitable. The addition of a short-acting, potent opioid such as fentanyl or sufentanil usually provides stable hemodynamics during and after induction of anesthesia. Volatile anesthetics may be administered in low concentrations before endotracheal intubation during assisted ventilation as an adjunct to blunt the hyperdynamic response to laryngoscopy and endotracheal intubation. Esmolol 10 to 25 mg, sodium nitroprusside 5 to 25 μg, nitroglycerin 50 to 100 μg, or clevidipine 100 mcg and phenylephrine 50 to 100 μg should be available for bolus administration during induction if needed to maintain appropriate hemodynamics. Maintenance of anesthesia may be accomplished with a combination of a potent opioid (fentanyl or sufentanil) and an inhaled anesthetic (sevoflurane, desflurane, or isoflurane) (i.e., balanced anesthesia). Patients with severe left ventricular dysfunction may benefit from a pure opioid technique, but a balanced anesthetic technique allows the clinician to take advantage of the most desirable characteristics of potent opioids and inhaled volatile anesthetics while minimizing their undesirable side effects. Nitrous oxide can be used to supplement either an opioid or an inhaled anesthetic. Various regional anesthetic and analgesic techniques have been used effectively during and after aortic reconstruction. For over 2 decades, interest has focused on the use of regional anesthetic and analgesic techniques to reduce the incidence of perioperative morbidity in patients undergoing aortic reconstruction. The benefits of combined Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery general and epidural anesthesia intraoperatively, with or without epidural analgesia continued into the postoperative period, remain controversial.13,14,68-71 Moreover, studies that have reported improved outcome do not determine whether the benefit results from the intraoperative anesthetic technique or the postoperative analgesic regimen (or a combination of the two). In a randomized trial using epidural morphine in patients undergoing aortic surgery, Breslow and associates72 found attenuation of the adrenergic response and a less frequent incidence of hypertension in the postoperative period. A large randomized trial reported no reduction in nonsurgical complications with the use of intrathecal opioid.15 The effects of the anesthetic or analgesic technique on the incidence of perioperative myocardial ischemia have received considerable attention. Four randomized trials, with nearly 450 combined patients undergoing aortic reconstruction, failed to demonstrate a reduction in the incidence of perioperative,14,73 intraoperative,74 or postoperative70 myocardial ischemia when epidural techniques were used. Additionally, randomized trials have not demonstrated a reduction in the incidence of cardiovascular, pulmonary, or renal complications after aortic surgery with the use of epidural techniques.13,14,69,70,75 The duration and intensity of postoperative care after aortic surgery are critically dependent on the physiologic derangements incurred during the perioperative period (i.e., depression of consciousness, hypothermia, excessive intravascular fluids, incisional pain, ileus, and respiratory depression), as well as on the development of certain less common, but more severe postoperative complications (i.e., MI, pneumonia, sepsis, renal failure, and decreased tissue perfusion). Length of hospital stay may therefore be considered the outcome variable most directly proportional to an integrated final negative effect of all significant perioperative morbidity (excluding in-hospital death) and the variable most likely to be altered by the anesthetic or analgesic technique. Randomized trials have not demonstrated any reduction in length of hospital stay after aortic surgery with the use of regional techniques. Norris and colleagues14 reported the results of a randomized clinical trial comparing alternative combinations of intraoperative anesthesia (i.e., general or combined epidural and general) and postoperative analgesia (i.e., IV patient-controlled analgesia [PCA] or epidural PCA) with respect to length of stay after abdominal aortic surgery. Two unique features of the trial included a factorial design (Fig. 56.5), which allowed the inclusion of all four combinations of intraoperative anesthesia and postoperative analgesia and the ability to separate the influence of time period and technique, and a double-blind design, which helped eliminate investigator and treating physician bias. The study rigorously protocolized perioperative management, standardized postoperative surgical care, and optimized postoperative pain management. Although the overall length of stay was much shorter (median, 7.0 days) than that reported in other studies,13,68,70,75 they were not able to demonstrate a reduction in length of stay or direct medical costs based on anesthetic or analgesic technique (Table 56.6). The overall incidence of postoperative complications in the trial was low and not different based on anesthetic or analgesic technique. Postoperative pain was well controlled overall, with similar pain scores in both analgesic treatment groups. Thus, if perioperative care and 1839 Abdominal Aortic Surgery General anesthesia IV PCA Epidural PCA Epidural-supplemented general anesthesia IV PCA Epidural PCA Fig. 56.5 Outline of factorial study design. This design allows the inclusion of all four possible combinations on intraoperative anesthesia and postoperative analgesia and the ability to separate the influences of time period and technique. Data analysis by treatment group, intraoperative treatment, postoperative treatment, and any epidural activation, as well as simultaneous consideration of both intraoperative and postoperative treatments in the same model (factorial analysis), is possible and allows improvement in outcome to be attributed to the intraoperative anesthesia, postoperative analgesia, the combination of the two, or to unrelated factors. IV, Intravenous; PCA, patient-controlled analgesia. pain relief are optimized, epidural anesthetic and analgesic techniques for aortic surgery offer no major advantage or disadvantage over general anesthesia and IV PCA. The use of epidural local anesthetics in combination with general anesthesia during aortic reconstruction poses several problems, including hypotension at the time of aortic unclamping and the need for increased intravascular fluid and vasopressor requirements. Supraceliac aortic crossclamping may significantly exaggerate these disadvantages, and, as a result, some clinicians avoid running local anesthetics in the epidural around the period of aortic clamping and unclamping. Epidural opioids without local anesthetics can be used in the interim and local anesthetic can be given later, after aortic unclamping, when hemodynamics and intravascular volume have stabilized. Although elective aortic reconstruction via the retroperitoneal approach using straight epidural anesthesia (no general anesthetic) has been reported, this technique is not recommended for routine use. Hypertension and tachycardia are aggressively controlled during emergence by the use of short-acting drugs such as esmolol, nitroglycerin, clevidipine, or sodium nitroprusside. Emergence from anesthesia should be conducted after restoration of circulation and establishment of adequate organ perfusion. Hemodynamic, metabolic, and temperature homeostasis must be achieved before extubation; otherwise, patients should be transported intubated to the intensive care unit (ICU). Temperature Control Postoperative hypothermia is associated with many undesirable physiologic effects and may contribute to adverse outcomes (see also Chapter 80). Normothermia should be maintained before skin incision by increasing ambient temperature in the operating room, applying warm cotton blankets, and warming IV fluids. If significant hypothermia occurs early in the procedure, normothermia is extremely difficult to achieve, and emergence and tracheal extubation may be delayed. During surgery, all fluids and blood products should be warmed before administration. A forced-air warming blanket should be applied over the upper part of the body. The lower part of the body should not be warmed Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1840 SECTION IV Adult Subspecialty Management TABLE 56.6 Duration of Hospital Stay and Direct Medical Costs by Randomized Treatment Assignment for Patients Surviving to Discharge after Abdominal Aortic Surgery GA-IVPCA RSGA-IVPCA GA-EPCA RSGA-EPCA Total P-value No. of Patients 35 36 36 44 151 Duration of hospital stay (days)* Range 95% CI 7.0 (2.2) 4‐43 7.0‐13.3 8.0 (2.8) 5‐28 7.4‐10.2 7.0 (2.0) 5‐20 6.9‐8.8 7.0 (2.8) 5‐18 7.6‐9.6 7.0 (2.2) 4‐43 7.9‐9.7.833† Direct medical costs (US$ 1997)* Inpatient 12,413 (2867) 13,786 (4413) 12,492 (3111) 13,767 (3900) 12,793 (3777).242 Physician 10,394 (5993) 10,288 (4538) 9609 (3866) 9790 (3567) 9934 (4072).459 Total 22,674 (8783) 23,001 (6079) 22,182 (3914) 22,727 (3961) 22,674 (4903).851 CI, Confidence interval; GA‐EPCA, general anesthesia and epidural patient-controlled analgesia; GA‐IVPCA, general anesthesia and intravenous patientcontrolled analgesia; RSGA‐EPCA, regional supplemented general anesthesia and epidural patient-controlled analgesia; RSGA‐IVPCA, regional supplemented general anesthesia and intravenous patient-controlled analgesia. From Norris EJ, Beattie C, Perler B, et al. Double-masked randomized trial comparing alternate combinations of intraoperative anesthesia and postoperative analgesia in abdominal aortic surgery. Anesthesiology. 2001;95:1054–1067. during the cross-clamp period because doing so can increase injury to ischemic tissue distal to the cross-clamp by increasing metabolic demands. THORACOABDOMINAL AORTIC SURGERY Open repair of the thoracoabdominal aorta is widely regarded as the most challenging surgical procedure in terms of overall anesthetic and perioperative management. Surgical repair is required for a spectrum of disease, including degenerative aneurysm, acute and chronic dissection, intramural hematoma, mycotic aneurysm, pseudoaneurysm, penetrating aortic ulcer, coarctation, and traumatic aortic tear. Since the first thoracoabdominal aortic aneurysm (TAA) repair in 1955, tremendous advances have been made in the field. These advances have led to significant reductions in operative mortality and perioperative complications. However, even in centers where numerous procedures are performed, morbidity and mortality are frequent, especially in patients with dissecting or ruptured aneurysms. To successfully care for these patients, the anesthesiologist must be knowledgeable in the areas of one-lung ventilation; extracorporeal circulatory support, including circulatory arrest; renal and spinal cord protection; induced hypothermia; invasive hemodynamic monitoring, including TEE; massive transfusion; and management of coagulopathy. Intraoperative management requires a team effort with intimate cooperation among surgeons, anesthesiologists, perfusionists, nurses, and electrophysiologic monitoring staff. Endovascular stent-graft repair of lesions that affect the descending thoracic and thoracoabdominal aorta is evolving rapidly. As discussed later, accumulating experience with stent-graft repair of thoracic aortic aneurysm, dissection, and traumatic tear has demonstrated this modality to be an effective alternative to open repair for select patients. ETIOLOGY AND CLASSIFICATION Aneurysms of the thoracoabdominal aorta occur primarily because of atherosclerotic degenerative disease (80%) and chronic aortic dissection (17%).76 The remainder are caused by either trauma or connective tissue diseases involving the aortic wall from conditions such as Marfan syndrome, cystic medial degeneration, Takayasu arteritis, or syphilitic aortitis. The true incidence of TAA is unknown, but population studies suggest a prevalence much less than that of infrarenal AAA. Degenerative and dissecting TAAs differ in their associated risk factors, extent of aortic involvement, and natural history. Thus complete characterization of each TAA is required to formulate a comprehensive treatment plan. Development of both degenerative and dissecting TAAs is ultimately related to weakening of the aortic wall. Although the natural history of TAA without surgery is uncertain, enlargement tends to be progressive and nonoperative management is generally associated with a poor prognosis. With progressive enlargement, nutritional blood flow to the aorta is compromised. The increasing diameter is associated with increased wall tension, even when arterial pressure is constant (law of Laplace). The frequent incidence of associated systemic hypertension enhances aneurysm enlargement. Degenerative and dissecting TAAs are symptomatic at initial evaluation in 57% and 85% of patients, respectively. The most common initial complaint is back pain. Additional symptoms can be caused by compression of organs or structures adjacent to the aneurysm. Aortic rupture, as a manifestation of TAA, occurs with equal frequency (9%) in both degenerative and dissecting aneurysms. Rupture of the thoracic and abdominal segments occurs with equal frequency and primarily in patients with aneurysms larger than 5 cm. Surgical repair is usually recommended when aneurysm diameter exceeds 6 cm, but earlier repair may be offered to patients with Marfan syndrome and those with a strong family history of an aortic aneurysm. In addition to cause, aneurysms of the thoracoabdominal aorta may be classified according to their anatomic location. In 1986, Crawford and colleagues,76 recognizing the correlation between aneurysm extent and clinical outcome, proposed a classification based on the extent of aortic involvement (Fig. 56.6). The Crawford classification defines aneurysms as types I, II, III, and IV and is appropriately applied to aneurysms of all causes (degenerative and dissecting). Type I aneurysms involve all or most of the descending thoracic aorta and the upper abdominal aorta. Type II aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta. Type III aneurysms involve the lower portion of the descending thoracic aorta and most of the abdominal aorta. Type IV aneurysms involve all or most of the abdominal aorta, including the visceral segment. Types II and III are the most difficult to repair because they involve Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 56 Anesthesia for Vascular Surgery I II III 1841 IV Fig. 56.6 The Crawford classification of thoracoabdominal aortic aneurysms is defined by anatomic location and the extent of involvement. Type I aneurysms involve all or most of the descending thoracic aorta and the upper abdominal aorta; type II aneurysms involve all or most of the descending thoracic aorta and all or most of the abdominal aorta; type III aneurysms involve the lower portion of the descending thoracic aorta and most of the abdominal aorta; and type IV aneurysms involve all or most of the abdominal aorta, including the visceral segment. both the thoracic and the abdominal segments of the aorta. Patients with Crawford type II aneurysms are at greatest risk for paraplegia and renal failure from spinal cord and kidney ischemia during cross-clamping. Even with extracorporeal circulatory support, an obligatory period occurs when blood flow to these organs is interrupted because the origin of the blood flow is between the cross-clamps. For this reason, protective measures to prevent ischemic injury are important in reducing morbidity. Aortic dissection, with or without aneurysm formation, has likewise been classified according to the extent of aortic involvement. The most widely used classification, proposed by DeBakey and colleagues, defines aortic dissection as types I, II, and III (Fig. 56.7). Type I aneurysms begin in the ascending aorta and extend throughout the entire aorta. These lesions are usually repaired via a two-stage approach, with the first procedure on the ascending aorta and aortic arch and the second procedure on the descending thoracic aorta. Type II aneurysms are confined to the ascending aorta. Both types I and II often involve the aortic valve and cause aortic regurgitation, and sometimes they involve the ostia of the coronary arteries. Type III aneurysms begin just distal to the left subclavian artery (SCA) and extend either to the diaphragm (type IIIA) or to the aortoiliac bifurcation (type IIIB). Another commonly used classification of aortic dissection is the Stanford classification. This more simplified classification divides aortic dissection into those that involve the ascending aorta (Stanford type A) and those that do not involve the ascending aorta (Stanford type B). Aortic dissection is also classified by duration, with those less than 2 weeks classified as acute and those greater than 2 weeks classified as chronic. This classification has very significant mortality implications, with much higher mortality in the acute phase. Acute aortic dissection involving the ascending aorta (DeBakey types I and II, Stanford type A) is a surgical emergency that requires immediate cardiac surgical repair (see also Chapter 54). Acute dissections involving the descending aorta Type I Type III Type II Fig. 56.7 The DeBakey classification of dissecting aneurysms of the aorta. Type I has an intimal tear in the ascending aorta with dissection extending down the entire aorta. Type II has an intimal tear in the ascending aorta with dissection limited to the ascending aorta. Type III has an intimal tear in the proximal descending thoracic aorta with dissection either limited to the thoracic aorta (type IIIA) or extending distally to the abdominal aorta or aortoiliac bifurcation (type IIIB). (DeBakey type III, Stanford type B) are most often treated conservatively (i.e., arterial blood pressure, heart rate, and pain control) because surgical repair has no proved benefit over medical or interventional treatment in stable patients. Early surgical intervention may be required for a variety of reasons, including aneurysmal formation, impending rupture, organ or leg ischemia, and inadequate response to medical therapy. In approximately 20% to 40% of patients with chronic aortic dissection, significant aneurysmal dilatation of the descending thoracic or thoracoabdominal aorta will develop. Downloaded for alex arman davidson ([email protected]) at Florida International University from ClinicalKey.com by Elsevier on October 21, 2019. For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved. 1842 SECTION IV Adult Subspecialty Management MORBIDITY AND MORTALITY Despite tremendous development in surgical and anesthetic technique, mortality and complication rates remain frequent for open surgical repair of TAA. Patients who undergo replacement of the entire thoracoabdominal aorta (Crawford extent type II) have the most frequent perioperative risk. Contemporary mortality rates reported from large institutions range from 5% to 14%. Statewide and nationwide mortality rates may be considerably more frequent (∼20%). The perioperative mortality rate may significantly underestimate the risk associated with TAA repair. In a large statewide series, the mortality with elective TAA repair was 19% at 30 days and 31% at 365 days.77 The incidence of paraplegia or paraparesis in patients undergoing surgical repair of TAA is reported to be 3.8% to 40%, depending on complex factors such as anatomic location, the duration of cross-clamping, the use of protective measures, the degree of dissection, and whether the aneurysm has ruptured. Extensive dissecting TAA repair carries the highest risk for neurologic deficit. A contemporary report of 210 consecutive open TAA repairs reported three patients with paraplegia and two with temporary paraparesis for an overall rate of neurologic deficit of 2.4% (1.4% permanent).78 Renal failure occurs in 3% to 30% of patients, depending on similar factors noted earlier. Overall, approximately 6% of patients need postoperative dialysis after TAA repair, which is associated with high mortality (30% to 60%). Gastrointestinal complications occur in approximately 7% of patients and are associated with a mortality approaching 40%. Not surpri