Handbook of Clinical Anesthesia

Chapter 42

Anesthesia for Vascular Surgery

The outcome after vascular surgery is principally determined by patient factors (coronary artery disease [CAD]), surgical factors, and institution-specific factors (Mantha S, Roizen MF, Katz JC, Lubarsky DA, Ellis JE: Anesthesia for vascular surgery. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1108–1136). Low serum albumin values and high American Society of Anesthesiologists physical classification are predictors of morbidity and mortality after vascular surgery. New surgical techniques, such as angioplasty and endovascular repair with placement of stent grafts, have revolutionized vascular surgery.

  1. Vascular Disease: Epidemiologic, Medical, and Surgical Aspects
  2. Pathophysiology of Atherosclerosis.Atherosclerosis is a generalized inflammatory disorder of the arterial tree with associated endothelial dysfunction (Table 42-1).
  3. Natural History of Patients with Peripheral Vascular Disease.Atherosclerosis is a systemic disease that has important sequelae in many other regional circulations (carotid artery stenosis and stroke, aortic atherosclerosis and aneurysms, claudication).
  4. Medical Therapy for Atherosclerosis
  5. Medical therapy, including the use of antihypertensives (beta-blockers, angiotensin-converting enzyme inhibitors), statin drugs, aspirin, and control of hyperglycemia [hypoglycemia or the use of insulin] may reduce perioperative morbidity and mortality in vascular surgery patients (Table 42-2). Patients with high cardiac risk undergoing vascular surgery who receive preoperative statin therapy are less likely to die. Cessation of smoking may be the most effective medical therapy.

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Table 42-1 Risk Factors for Atherosclerosis

Predisposing Risk Factors (aspects of the metabolic syndrome)
Abdominal obesity
Atherogenic dyslipidemia
Increased blood pressure
Insulin resistance
Proinflammatory state
Prothrombotic state
Major Risk Factors
Cigarette smoking
Elevated LDL cholesterol level
Low HDL level
Family history of premature CAD
Aging
Emerging Risk Factors
Elevated triglycerides
Small LDL particles

CAD = coronary artery disease; HDL = high-density lipoprotein; LDL = low-density lipoprotein.

  1. Chronic Medical Problems and Managment in Vascular Surgery Patients
  2. Coronary Artery Disease in Patients with Peripheral Vascular Disease.The presence of uncorrected CAD appears to double the 5-year mortality rate after vascular surgery.
  3. Previous percutaneous transluminal coronary angioplasty (PTCA) and stenting may or may not protect against perioperative cardiac events after vascular surgery.
  4. Drug-eluting stents are slow to endothelialize, and the exposed stent material remains thrombogenic far longer than with bare-metal stents. Therefore, the duration of dual antiplatelet therapy (75 mg/day of clopidogrel and 325 mg/day of aspirin) is 1 month for bare metal stents and 12 months (perhaps forever) for drug-eluting stents.
  5. Whenever possible, noncardiac surgery should be delayed until 6 weeks after bare-metal stent placement (endotheliazation is usually complete by this time) and perhaps for 12 months after placement of a drug-eluting stent.

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Table 42-2 Management of Preoperative Drug Therapy

Medication

Side Effects of Potential Concern in the Perioperative Period

Recommendation for Perioperative Use

Aspirin

Platelet inhibition may increase bleeding

Continue until day of surgery, especially for carotid and peripheral vascular cases

Decreased glomerular filtration rate

Monitor fluid status and urine output

Clopidogrel

Platelet inhibition may increase bleeding

Hold for 7 days before surgery except for CEA and severe CAD

Rare thrombotic thrombocytopenic purpura

Consider additional cross-match of blood
Avoid neuraxial anesthesia for at least 7 days

HMG-COA reductase inhibitors (statins)

Liver function test abnormalities

Assess liver function tests and continue through the morning of surgery

Rhabdomyolysis

Check CPK if myalgias are present

Beta-blockers

Bronchospasm
Hypotension
Bradycardia
Heart block

Continue through the perioperative period

ACE inhibitors

Hypotension with induction

Continue through the perioperative period

Cough

Consider 50% the dose on the day of surgery

Diuretics

Hypovolemia

Continue through the perioperative period

Electrolyte abnormalities

Monitor fluid status and urine output

Calcium channel blockers

Perioperative hypotension, especially with amlodipine

Continue through the perioperative period (consider withholding amlodipine on the morning of surgery)

Oral hypoglycemics

Hypoglycemia given preoperatively and intraoperatively

When feasible, switch to insulin preoperatively

Lactic acidosis with metformin

Monitor glucose status perioperatively

ACE = angiotensin-converting enzyme; CAD = coronary artery disease; CEA = carotid endarterectomy; CPK = creatine phosphokinase; HMG-CoA = 3-hydroxy-3-methyl-glutaryl-CoA.

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Table 42-3 Definition of a New Myocardial Infarction

Rise and fall of a biochemical marker (troponin) of myocardial necrosis with one of the following clinical and ECG criteria:
   Ischemic symptoms
   Development of pathologic Q waves
   Ischemic ECG changes
   Coronary intervention

ECG = electrocardiogram.

  1. Perioperative myocardial infarction after vascular surgery may be early (resembling acute nonsurgical acute myocardial infarction that is most likely caused by plaque rupture and thrombosis of a coronary artery) or delayed (resembling an increase in oxygen demand in the presence of fixed coronary stenosis) (Table 42-3). Perioperative troponin screening is an effective means of surveillance for perioperative myocardial ischemia damage.
  2. Preoperative coronary revascularization(surgical or interventional) may be of no value in preventing cardiac events except in patients in whom revascularizations is independently indicated for acute coronary syndrome. The safe time intervals between surgical revascularization and vascular surgery is 4 to 6 weeks and is 2 weeks for PTCA (longer for stents).
  3. Management of Perioperative Myocardial Ischemia and Infarction in Vascular Patients(Table 42-4). Of the various pharmacologic risk reduction strategies, perioperative beta-blocker therapy in noncardiac surgery is useful to reduce rates of preoperative arrhythmias and myocardial ischemia but may not provide benefit regarding myocardial infarction, length of hospitalization, and mortality. Patients with few or no risk factors may not benefit from beta-blocker therapy and may have an increased risk of death, stroke, and clinically significant hypotension. Asthma, chronic obstructive airway disease, and cardiac conduction disease in the absence of a pacemaker are contraindications to beta-blocker therapy.
  4. High-dose opioid anesthetics reduce the stress response and may improve the overall outcome after major surgery.

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Table 42-4 Pharmacologic Prophylaxis Against Acute Vascular Events in Patients Undergoing Vascular Surgery

Intervention

Regimen and Comments

Recommendation*

Perioperative beta-blockade

Preoperative oral beta1 selective beta-blocker (bisoprolol, metoprolol, atenolol) initiated at least 30 days before surgery and IV and postoperative period (metoprolol, atenolol, esmolol)

Class I

§  In patients with ischemia on preoperative testing, in patients with three or more clinical risk factors, and in patients receiving beta-blockers for stable cardiac symptoms

§  In patients with one or two clinical risk factors and no cardiac symptoms

Patients with few or no risk factors may not benefit from beta blockade

Class IIa

α2-blockers

Pretreatment with oral clonidine 300 µg at least 90 minutes before surgery and therapy continued for 72 hours (oral or transdermal 0.2 mg/day)
IV clonidine 300 µg/day can also be administered for 72 hours

Class IIa

Statin therapy

Typical dose of atorvastatin is 20 mg/day initiated at least 45 days before surgery
Withdrawal of statin therapy for more than 4 days after vascular surgery is associated with an increased risk of cardiac complications
Administration of extended-release fluvastatin preoperatively appears ideal when prolonged postoperative ileus is expected
Use should be continued after surgery for at least 2 weeks

Statin use is associated with improved graft patency, limb salvage, and a decreased amputation rate in patients undergoing infrainguinal bypass

Class IIa

ACE inhibitors

Potential benefits include decreased stroke rate, limitation of ventricular remodeling that occurs after acute myocardial infarction, and decreased long-term mortality after infrainguinal bypass surgery

Class IIb

Calcium channel blockers

Reduced perioperative adverse cardiac events, including supraventricular tachycardia in patients undergoing noncardiac vascular surgery (primarily diltiazem)
Evidence is limited in patients undergoing vascular surgery

Class IIb

Nitroglycerin

Not indicated for prophylaxis or initial treatment of myocardial ischemia
May be used to treat arterial hypertension, elevated filling pressures, or suspected coronary vasospasm

Class III

*Class I: Evidence or general agreement that is useful or effective.
Class II: Conflicting evidence or a divergence of opinion regarding usefulness or efficacy.
Class IIa: Weight of evidence or opinion in favor of usefulness or efficacy.
Class IIb: Usefulness or efficacy is less well established by evidence or opinion.
Class III: Evidence that is not useful or effective.
Class I recommendations are the “dos,” class II recommendations are the “maybes,” and class III recommendations are the “do nots.”
ACE = angiotensin-converting enzyme; IV = intravenous.

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Table 42-5 Coexisting Medical Problems in Patients with Peripheral Vascular Disease

Hypertension (treat with oral doses of atenolol or metoprolol if poorly controlled)
Diabetes mellitus (increased incidence of postoperative death when autonomic neuropathy is present; intraoperative euglycemia may be particularly important during thoracic and carotid surgery)
Hypercoagulability
Chronic obstructive pulmonary disease (tobacco abuse)
Renal insufficiency

  1. Epidural anesthesia may reduce perioperative myocardial ischemia (reduced preload and afterload; decreased coagulation responses), but cardiac outcome has not been proven to be improved after abdominal aortic surgery, especially if heart rate is well controlled in the intensive care unit.
  2. Anemia (hematocrit <28%) may increase the incidence of postoperative myocardial ischemia in high-risk patients undergoing noncardiac surgery. (It is more likely to transfuse high-risk patients or those who demonstrate myocardial ischemia with packed red blood cells to augment the hematocrit to 30%.)
  3. Hypothermia is associated with increased adrenergic tone and postoperative myocardial ischemia in patients undergoing vascular surgery. (Patients should be aggressively warmed, and heat should be conserved during and after surgery.)
  4. Suctioning, tracheal extubation, and weaning from mechanical ventilation may produce myocardial ischemia (early tracheal extubation vs sedation and analgesia to permit tolerance of the tracheal tube).
  5. Other Medical Problems in Vascular Surgery Patients(Table 42-5)

III. Carotid Endarterectomy (CEA)

Carotid disease is primarily a problem of embolization and rarely occlusion or insufficiency. Carotid disease may manifest itself only as an asymptomatic bruit or as amaurosis fugax (transient attacks of monocular blindness) when the ophthalmic artery is embolized. Other patients may experience

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episodes of paresthesias, clumsiness of the extremities, or speech problems, which resolve spontaneously after a short period of time. The most common diagnostic noninvasive test is the duplex scan, which combines B-mode anatomic imaging and pulse Doppler spectral analysis of blood flow velocity. The accuracy of duplex scanning reaches 95% in experienced hands compared with angiography. Also, many surgeons use magnetic resonance angiography as the sole modality to detect disease. Combined administration of aspirin and dipyridamole, when compared with placebo, reduces the incidence of transient ischemic attacks more so than either drug alone. (Patients presenting for CEA must continue to receive aspirin, clopidogrel, or both in the perioperative period.)

  1. Preoperative Evaluation and Preparation.The long-term risks of adverse cardiac events after CEA are related to progression of CAD.
  2. Monitoring and Preserving Neurologic Integrity.The two main goals of intraoperative management are to protect the brain and heart.
  3. The rationale behind maintaining a stable, high-normal blood pressure throughout the procedure is based on the assumption that blood vessels in ischemic or hypoperfused areas of the brain have lost normal autoregulation. The judicious use of phenylephrine to increase blood pressure only in specific instances of electroencephalography (EEG)-detected reversible cerebral ischemia seems to be without detriment to the heart.
  4. Hypercapnia during CEA may be detrimental if it dilates vessels in normal areas of the brain while vessels in ischemic brain areas that are already maximally dilated cannot respond (“steal” phenomenon manifesting as a diversion of blood flow from hypoperfused brain regions to normally perfused brain regions). Most authorities recommend the maintenance of normocarbia or moderate hypocarbia.
  5. Moderate hyperglycemia may worsen ischemic brain injury, and hyperglycemia has a documented association with worse outcome after CEA (aggressive glucose control is recommended).
  6. Almost all commonly used anesthetic agents reduce cerebral metabolism, but the notion that reduced

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cerebral metabolism is associated with cerebral protection has been challenged. Volatile anesthetics may provide preconditioning and neuronal protection by inducing nitric oxide synthase.

  1. Barbiturates may offer a degree of brain protection during periods of regional ischemia. Thiopental decreases cerebral metabolic oxygen requirements to about 50% of baseline. These maximally achievable reductions in oxygen requirements correspond to a silent (isoelectric) EEG. Beyond this point, additional doses of barbiturates are neither necessary nor helpful. In cases of massive global ischemia in which basal cellular metabolism has already deteriorated, even high doses of barbiturates will not improve neurologic outcome.
  2. The use of a shunt is beneficial only if the cause of neurologic dysfunction is inadequate blood flow. (Most neurologic deficits during CEA are caused by thromboembolic events.)
  3. Anesthetic and Monitoring Choices for Elective Surgery(Table 42-6)
  4. Often on the day of surgery, patients present with hypertension despite having taken their morning antihypertensive and antianginal medications. These

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patients appear to be the most prone to hypotension after the induction of general anesthesia.

Table 42-6 Anesthetic and Monitoring Choices for Patients Undergoing Elective Carotid Endarterectomy

Intra-arterial catheter (before surgery, blood pressure in each arm should be compared)
Electrocardiography (leads II and V5 for ST segment changes)
TEE (consider in patients at high risk for intraoperative myocardial ischemia)
Preoperatively establish range of patient's blood pressure and heart rate
Continue chronic medications to the day of surgery
Avoid intraoperative fluid overload (may contribute to postoperative hypertension)
Restrict use of opioids (sedation may confound results of early neurologic assessment)
Avoid use of continuous infusions of phenylephrine (rely on the patient's endogenous pressure-sustaining responses)
Ask the surgeon to infiltrate carotid bifurcation with 1% lidocaine
Confirm neurologic integrity before leave the operating room

TEE = transesophageal echocardiography.

  1. The use of a cervical plexus block or surgeon-administered local anesthetic helps considerably in reducing to eliminating opioid requirements.
  2. There is no proof that any one general anesthetic technique or general anesthesia versus regional anesthesia provides a superior outcome. The choice of anesthetic technique should take into account the preference of the surgeon and the experience and expertise of the anesthesiologist.
  3. Carotid angioplasty and stenting (CAS)may be performed by vascular surgeons, cardiologists, or radiologists. In some cases, CAS involves sedation and monitoring provided by anesthesiologists; in other cases, no anesthesiologist will be involved. The patient needs to be arousable and responsive so that serial neurologic examinations can be conducted.
  4. Both CEA and CAS may cause blood pressure to decrease immediately after reperfusion and into the postoperative period because of alterations in baroreceptor function.
  5. Studies to date fail to show an outcome advantage of CAS over CEA.
  6. Postoperative Management(Table 42-7)
  7. Severe hypertension (systolic blood pressure >200 mm Hg) seems to occur more often in patients with poorly controlled preoperative hypertension.

Table 42-7 Postoperative Complications After Carotid Endarterectomy

New neurologic dysfunction (ability to move the extremities excludes the possibility of acute thrombosis of the endarterectomy site)
Hemodynamic instability (hypertension is more common than hypotension)
Hyperperfusion syndrome (manifests several days after surgery as ipsilateral headache that may progress to seizures; transcranial Doppler may predict susceptible patients; steroids may be used in treatment)
Respiratory insufficiency (recurrent laryngeal nerve palsy; carotid body denervation)
Wound hematomas (airway compression)

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  2. Hypertension may precipitate acute myocardial ischemia (the incidence is increased in first few hours after surgery) and congestive heart failure and may lead to cerebral edema or hemorrhage. (Postoperative hypertension is associated with an increased incidence of neurologic deficits.)
  3. Causes of postoperative hypertension (pain, arterial hypoxemia, hypercarbia, and bladder distention should be ruled out) are unclear but may include denervation of the carotid sinus and overzealous administration of intravenous (IV) fluids.
  4. Hypertension usually peaks 2 to 3 hours after surgery but may persist for 24 hours in some individuals.
  5. Treatment of hypertension is with titration of short-acting drugs (nitroglycerin, labetalol, esmolol, tracheal lidocaine spray).
  6. Hypotension and bradycardia after CEA are less frequent than hypertension. (Surgical removal of the atheroma again exposes the carotid sinus baroreceptors to higher levels of transmural pressure, leading to brainstem-mediated vagal responses.)
  7. Chemical denervation of the carotid sinus with local anesthetic injected by the surgeon results in fewer hypotensive patients but increases the incidence of postoperative hypertension.
  8. The baroreceptors seem to adjust over 12 to 24 hours.
  9. Treatment may not be necessary in the absence of myocardial ischemia or changes in neurologic status. Nevertheless, blood pressure is often restored to a low-normal range with IV infusion of fluids or administration of drugs (ephedrine, phenylephrine, dopamine).
  10. Management of Emergent Carotid Surgery
  11. A patient who awakens with a major new neurologic deficit or who develops a suspected stroke in the immediate postoperative period represents a surgical emergency. (Prompt removal of a carotid thrombosis may produce significant neurologic improvement.)
  12. A wound hematoma occurring after CEA may be associated with airway obstruction and necessitate opening the operative site to remove pressure on the trachea before returning to the operating room.

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  1. Aortic Reconstruction
  2. Aneurysmal Disease.Aneurysms pose an ever-present threat to life because of their unpredictable tendency to rupture or embolize. Aggressive surgical management is warranted even in the absence of symptoms.
  3. Epidemiology and Pathophysiology of Abdominal Aortic Aneurysm (AAA).Risk factors for aneurysm include advanced age, smoking more than 40 years, hypertension, low serum high-density lipoprotein cholesterol, high level of plasma fibrinogen, and low blood platelet count. The risk of rupture of an AAA increases after the aneurysm is greater than 4.5 to 5 cm in diameter; surgical treatment is generally recommended.
  4. Pathophysiology of Aortic Occlusion and Reperfusion
  5. Cardiovascular Changes(Table 42-8)
  6. Renal Hemodynamics and Renal Protection.No renal protective strategy has been proven to yield a superior outcome. However, the level of aortic clamping and the avoidance of prolonged hypotension are probably the most important factors because they markedly impact renal blood flow. Intraoperative urinary output is not predictive of postoperative renal function; rather, preoperative renal function is the most powerful predictor of postoperative renal dysfunction.

Table 42-8 Hemodynamic Changes During Aortic Cross-Clamping and Unclamping

Increased MAP and SVR (reflecting increased afterload, activation of renin, and release of catecholamines and prostaglandins)
Decreased cardiac output in the presence of increased systemic vascular resistance (may be accompanied by increased cardiac filling pressures if underlying coronary artery disease)
Administration of a vasodilator (nitroprusside) concomitant with or immediately before placement of cross-clamp allows body to adapt
Level of clamping affects hemodynamic response (infrarenal clamping is better tolerated than suprarenal clamping)
Hypotension may accompany unclamping (pretreatment should be done with fluid loading with or without vasoconstrictors [phenylephrine] or calcium [high potassium and acid load]
Gradual unclamping is preferable

MAP = mean arterial pressure; SVR = systemic vascular resistance.

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  2. Dopamine has been shown to lack specific renal hemodynamic effects and does not appear to improve postoperative renal dysfunction. Fenoldopam, despite its specific DA-1 activity, has not been shown to be of clinical benefit.
  3. One of the most important factors for preventing postoperative renal failure remains good hydration (the most important factor for maintaining renal blood flow) during clamping and postclamp release.
  4. Humoral and Coagulation Profiles.Although the most evident factor contributing to hypotension after removal of the clamp is volume redistribution to the lower body, many humoral mediators are released from the underperfused areas and contribute to the hemodynamic changes.
  5. Administration of bicarbonate does not prevent immediate hypotension after unclamping. Mannitol administration before and after unclamping may be beneficial because of its function as a hydroxyl-free radical scavenger.
  6. Sequestration of microaggregates and neutrophils contributes to postoperative pulmonary dysfunction.
  7. Visceral and Mesenteric Ischemia.Bowel ischemia during cross-clamping is associated with increased mortality and leads to increased gut permeability and bacterial translocation.
  8. Central Nervous System and Spinal Cord Ischemia and Protection.The definitive measures for preventing spinal cord ischemia are short cross-clamping time, fast surgery, maintenance of normal cardiac function, and higher perfusion pressures. In high aortic clamping, other methods should be considered (Table 42-9)
  9. Some surgeons place a Gott shunt (heparinized tube most often from the ascending aorta to the descending aorta) that can decompress the heart and provide distal perfusion.
  10. A markedly reduced incidence of neurologic deficits has been reported when distal aortic perfusion is combined with drainage of cerebrospinal fluid (CSF).
  11. Endovascular techniques represent an alternative therapy when anatomy permits; lower paraplegia

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rates have been reported compared with open surgery.

Table 42-9 Strategies to Protect the Spinal Cord During Descending Thoracic Aortic Surgery

Limitation of cross-clamp duration
Use of distal circulatory support (Gott shunt)
Reattachment of critical intercostal arteries
CSF drainage
Hypothermia
Maintenance of proximal blood pressure
   Pharmacotherapy
   Systemic (corticosteroids, barbiturates, calcium channel antagonists, oxygen free radical scavengers, NMDA antagonists, mannitol, magnesium, vasodilators)
   Intrathecal (papaverine, magnesium, tetracaine)
Avoidance of postoperative hypotension
Sequential aortic clamping
Enhanced monitoring for spinal cord ischemia
   SSEPs
   MEPs

CSF = cerebrospinal fluid; MEP = motor evoked potential; NMDA = N-methyl-D-aspartic acid; SSEP = somatosensory evoked potential.

  1. Traditional “Open” Surgical Procedures for Aortic Reconstruction.Perioperative (30-day) mortality in elective aortic surgeries ranges between 0% and 12%, with a much higher probability of death in emergent surgery, especially in situations in which preoperative hypotension (systolic blood pressure <90 mm Hg) exists.
  2. Approach.Abdominal aortic reconstruction can be performed through a transperitoneal or retroperitoneal exposure.
  3. Clamp Level.Infrarenal aortic clamping carries the lowest risk for patients; supraceliac clamping carries the highest risk.
  4. Thoracic Aneurysm Repair(see Table 42-9). These operations are among the most challenging for anesthesiologists. Coincident CAD and chronic obstructive pulmonary disease are common.
  5. Lung isolation (double-lumen tube, bronchial blocker) is required to facilitate surgical access to the aneurysm and to avoid an iatrogenic pulmonary contusion in the left lung.
  6. Because edema of the head and neck frequently occurs after high cross-clamping (even with distal

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perfusion), reintubation may be difficult at the end of the procedure.

  1. Aortomesenteric Revascularization.Chronic mesenteric ischemia occurs because of atherosclerosis, and surgical revascularization is indicated only in patients with symptomatic disease. Partial cross-clamping of the aorta is preferred if possible and may mitigate the hemodynamic changes.
  2. Aortorenal revascularizationcan be performed by several surgical techniques (endarterectomy, reimplantation, bypass, and ex vivo renal artery reconstruction).
  3. Infrarenal Operations.Although it is generally recognized that distal ischemic complications are caused by dislodgment of atheromatous material off the diseased aorta and that the systemic use of heparin in the absence of distal occlusive disease is unnecessary, many centers still use heparin before aortic clamping.
  4. Thoracic Aortic Surgery and Endovascular Repair.Mortality from thoracic aortic surgery may approach 20%, making endovascular thoracoabdominal aortic aneurysm repair an alternative to open surgery. Although paraplegia may still occur, its incidence seems reduced compared with open thoracic aortic aneurysm repair. One approach to attempt to lessen paraplegia after endovascular repair is to place a temporary stent under somatosensory evoked potential (SSEP) monitoring (if SSEP is unchanged, a permanent stent may be placed). However, motor evoked potential monitoring seems more appropriate for monitoring function of the anterior spinal column. Another possibility that has been shown to confer protection in animal models is intermittent aortic cross-clamping.
  5. Endovascular Abdominal Aortic Repair (EVAAR)

Endovascular Abdominal Aortic Repair is now being used more commonly in patients who would otherwise undergo an open repair. Patient eligibility for EVAAR depends on (1) the shape of the aneurysm, including involvement of the renal and iliac arteries and the size and shape of the neck of the aneurysm; (2) the feasibility of delivering the device through the femoral or iliac arteries; and (3) the ability of the patient to compensate for vascular exclusion (aortic branches that will not be supplied after the stent graft is in place).

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  1. Outcome and Complications.New onset or worsening of pre-existing renal failure is a significant source of perioperative morbidity and mortality in patients undergoing EVAAR. Nonperfusion of the hypogastric artery can lead to abdominal complaints. The inferior mesenteric artery is occasionally excluded, and bowel ischemia may result if flow through the superior mesenteric artery is compromised. The artery of Adamkiewicz is typically excluded, which may increase the risk of distal spinal cord ischemia, particularly in patients who have undergone thoracic aortic replacement.
  2. Anesthetic Techniques.The selection of anesthetic technique is based on the preferences of the patient, anesthesiologist, and surgeon. Before device insertion, systemic anticoagulation is produced with heparin. Surprisingly, EVAAR has not reduced the cost of AAA repair.
  3. Conversion from EVAAR to Open Aortic Repair.Primary conversion, or the immediate alteration of the surgical plan from an endovascular approach to an open one, occurs in the setting of aneurysm rupture, stent migration or malposition, access site disruption with arterial wall dissection, and poor anatomic parameters for endovascular repair. For anesthesiologists, the complexity of the operation increases dramatically. Hemodynamic instability may ensue with hemorrhage, aortic cross–clamping, or both.
  4. Monitoring and Anesthetic Choices for Aortic Reconstruction
  5. Arterial catheters are placed in patients undergoing aortic reconstruction. In patients undergoing thoracic aortic clamping with distal perfusion, distal arterial pressure and CSF pressure may be measured. A pulmonary artery catheter is placed at the discretion of the anesthesiologist in patients undergoing suprarenal aortic cross-clamping but rarely in patients when the clamp will be infrarenal. However, recent large, randomized trials and observational studies have not been able to demonstrate any improvements in outcome with the use of pulmonary artery catheters.
  6. Virtually all anesthetic techniques and drugs have been used for aortic reconstructive surgery.

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  1. Perhaps the most important reason to routinely include volatile anesthetics is the increasing awareness that these drugs improve preconditioning mechanisms and reduce the size of a myocardial infarction if it occurs.
  2. Combined general–epidural and general–spinal anesthetics have been used successfully for aortic reconstruction. (The issue of heparinization is a consideration.) For patients requiring thoracotomy, the analgesia provided by thoracic epidural infusion of opioids or local anesthetics may be particularly helpful.

VII. Management of Elective Aortic Surgery

  1. Prehydration may limit variations in blood pressure on induction of anesthesia. The anesthetic management is planned to keep the patient's vital signs within 20% of their normal range, as long as the heart rate does not exceed 80 to 90 bpm and signs of organ ischemia are absent. Increases in blood pressure or heart rate may be treated with 10 to 50 µg of sufentanil.
  2. For the half-hour immediately before cross-clamping and aortic occlusion, the patient is kept slightly hypo-volemic by examining the ventricular volume by means of echocardiography or by keeping pulmonary capillary wedge pressure at 5 to 15 mm Hg. At the time of occlusion, a vasodilating drug is available for immediate use if needed. Alternatively, the concentration of volatile anesthetic may be increased or local anesthetics may be injected into the epidural catheter.
  3. Immediately before removal of the cross-clamp, vasodilators are discontinued. The surgeon then opens the aorta gradually to ensure that severe hypotension or bleeding does not develop.
  4. During emergence from anesthesia, infusions of nitroglycerin and esmolol or another β-adrenergic blocking agent are used if necessary to prevent hemodynamic variations outside the patient's normal range.

VIII. Anesthesia for Emergency Aortic Surgery

The most common cause of emergency aortic reconstruction is a leaking or ruptured aortic aneurysm. (Symptoms

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include pain in the back or abdomen.) Ruptures most commonly occur into the retroperitoneum, resulting in a life-saving tamponade effect.

  1. Shock frequently accompanies rupture. However, the absence of hypotension does not rule out the possibility of rupture, and shock may occur suddenly.
  2. Rapid diagnosis with immediate laparotomy and control of the proximal aorta are the highest priorities.
  3. Because of hypothermia from massive fluid resuscitation and the placement of the aortic cross-clamp above the hepatic artery, replacement blood may not pass through the liver in amounts adequate to allow for metabolism of citrate.
  4. As opposed to elective aortic reconstruction, in which preserving myocardial function is the primary goal, in emergency resection, the crucial factor for patient survival is first rapid control of blood loss and reversal of hypotension and then preservation of myocardial function.
  5. Lower Extremity Revascularization

The prevalence of intermittent claudication increases with age, affecting more than 5% of patients older than 70 years of age. The incidence of claudication doubles or triples in patients with diabetes. Advances in minimally invasive percutaneous interventions have made endovascular procedures the primary modality for revascularization in most patients.

  1. The three clinical indications for elective surgery for chronic peripheral occlusive disease are claudication, ischemic rest pain or ulceration, and gangrene.
  2. During surgery, tunneling of the graft may be more stimulating than other parts of the procedure and may cause hypertension or movement under general anesthesia.
  3. The patient is usually given heparin during the procedure. In most cases, the heparin effect is not antagonized because bleeding problems are rare and graft reocclusion is a concern.
  4. Anesthetic Management of Elective Lower Extremity Revascularization
  5. Morbidity and mortality after traditional distal operations approach those after infra-aortic reconstruction and are mainly of cardiac origin. Most cardiac problems arise during the postoperative

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period, and pain relief and correction of hemodynamic and fluid disequilibria are most likely to be needed.

Table 42-10 Choice of Anesthesia for Lower Extremity Revascularization

Anesthetic Technique

Advantages

Disadvantages

Regional

Effective blockade of stress response
Postoperative analgesia
Patient serves as a monitor for myocardial ischemia (angina, dyspnea)
Possible prevention of postoperative hypercoagulability
Improved graft blood flow

Time consuming, especially for postoperative management
Sympathectomy requires volume loading
Respiratory depression of block level becomes high or the patient becomes oversedated
Patient discomfort while lying down during long procedures
Rare neurologic sequelae
Precludes thrombolytic therapy
Technically difficult in patients with obesity, kyposcoliosis, or previous laminectomy

General

Hemodynamics are easily controlled during surgery

Hyperdynamic state after surgery usually must be treated

No patient discomfort during long procedures
Reliable

Postoperative hypercoagulability not inhibited

  1. The choice of anesthetic for surgical lower extremity revascularization is individualized for each patient (Table 42-10).
  2. Anesthesia for Emergency Surgery for Peripheral Vascular Insufficiency.Emergency surgery for peripheral vascular insufficiency is required when acute arterial occlusion results in severe ischemia and threatens the viability of a limb. (The involved extremity suddenly becomes cold and pulseless, and the patient usually complains of coldness, pain, numbness, and paresthesias.)

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  1. Serum potassium levels can change quickly because of cell death and release of intracellular potassium into the circulation. Myoglobin may also be released into the circulation, and the development of a compartment syndrome is possible.
  2. Anticoagulants are commonly administered to patients suspected of having peripheral vascular occlusion. If a patient has received anticoagulants, the appropriateness of using regional anesthesia is controversial.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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