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Perioperative Management of the Patient Undergoing Abdominal Aortic Surgery

Miguel Cobas, MD, Todd J. Smaka, MD, and David A. Lubarsky, MD, MBA
Department of Anesthesiology, Perioperative Medicine and Pain Management Miller School of Medicine University of Miami Miami, Florida

PATHOPHYSIOLOGY OF AORTIC OCCLUSION AND REPERFUSION


Clamping and unclamping of the abdominal aorta has significant implications involving the cardiovascular and renal systems. There are major changes in hemodynamics and humoral factors that can occur with varying degrees of clinical relevance.

Cardiovascular Changes
Gelman et al.1 established the basis of our understanding of the pathophysiology of hemodynamic changes that occur with aortic clamping and unclamping. Aortic cross clamping increases mean arterial pressure and systemic vascular resistance (SVR) up to 50%. These sudden increases are due to an increase in mechanical afterload, activation of renin, and release of catecholamines, prostaglandins, and other vasoconstrictors. This increase in SVR causes an initial reflexive decrease in cardiac output (see Supplemental Digital Content 1, http://links.lww.com/ASA/A1).1,2 Some of the initial changes in hemodynamics associated with cross clamping can be offset by the sympathectomy caused by a thoracic epidural or with boluses of a vasodilator administered immediately before placement of the clamp. Short23

acting pharmacologic agents (e.g., 0.3-0.7 mcg/kg of nitroprusside, 80-200 mcg of nitroglycerin or 200-600 mcg nicardipine) offset the mechanical effect of cross clamping, allowing the body to adapt. Preload changes are more variable than changes in SVR. Higher central venous and pulmonary artery occlusion pressures occur with higher clamp placement due to central redistribution of blood.1,3 In the patient with coronary disease, nitrate therapy during cross clamp will not necessarily prevent wall motion abnormalities,1 and care should be exercised when using any vasodilator so that perfusion pressure below the aortic cross clamp remains sufficient to avoid visceral/spinal cord ischemia. We will allow a systolic blood pressure (SBP) as high as 180-200 mm Hg provided there is no contraindication and the surgeon has acceptable operating conditions. Relative hypotension (less than 20% below baseline mean arterial pressure) probably should be avoided unless other means, such as shunts, are used to provide perfusion below the clamp. The level of clamping and the chronicity of occlusive disease can dramatically affect the hemodynamic response. The hemodynamic response is greater when the clamp is more proximal along the aorta (proximal descending thoracic aorta 4 supraceliac 4 suprarenal 4 infrarenal). There is an even smaller hemodynamic response when

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applying a clamp in a patient with chronic aortic or iliac occlusive disease. Vasodilation above the level of the clamp can offset the mechanical impedance to aortic flow. Existing collateral circulation remains intact during clamping and is responsible for maintaining lower body perfusion despite aortic cross clamping.4 Unclamping the aorta, especially at higher levels, can result in severe arterial hypotension unless aggressive therapy is undertaken before unclamping. No single preventive therapy is superior to another. Most anesthesiologists administer a fluid load to the patient while the surgeon is grafting the aorta. Pure vasoconstrictors (phenylephrine 100-200 mcg), or drugs such as calcium chloride (300-500 mg) or norepinephrine (4-12 mcg) may also be used to offset the negative inotropic/dromotropic effects of an acute potassium and acid load (and possibly other mediators) on the heart and peripheral vasculature immediately after unclamping and reperfusion. Rapid administration of sodium bicarbonate (especially through a central line) is not advocated as it will not minimize the hypotension seen with unclamping and may worsen intracellular acidosis, further depressing myocardial function. Alternatives to pharmacologic manipulation include gradual unclamping, unclamping with sequential release of bilateral femoral pressure, or restoring flow to one leg at a time with aortobifemoral grafts. When perfusion is restored and hemostasis is achieved, some surgeons request that the BP be allowed to rise to pressures that might be seen in the intensive care unit, so that they may to check suture lines under direct vision. This should be discussed with the surgeon in advance.

Many different methods of renal protection have been advocated, most of them centering on improving renal blood flow or glomerular flow. These include dopamine (acting at the now discredited dopaminergic receptor dose of 2-3 mcg/kg/min),10 fenoldopam,11 angiotensin-converting enzyme inhibitors,12 prostaglandins,13 halogenated agents,14 thoracic epidurals (for renal arterial sympatholysis),15 vasodilators,16 isovolemic hemodilution (for increased blood flow in the face of increased vascular resistance),17 furosemide, and mannitol. Mannitol increases diuresis and even though it does not seem to decrease mortality, patients with a milder form of renal failure (nonoliguric) might benefit, as the mannitol may function as a hydroxyl-free radical scavenger and a diuretic. Outcomes, however, have never been shown to improve with its use.18 Dopamine has been shown to lack specific renal hemodynamic effects and does not diminish the risk of developing postoperative renal dysfunction.10 Fenoldopam is a highly specific DA-1 agonist which decreases renal oxygen demand by renovascular dilation and inhibits tubular resorption of sodium.11 However, in humans, it has been found to have no significant clinical benefits.19

Probably the most important factors for preventing postoperative renal failure and maintaining renal perfusion during both cross-clamp and post-clamp release are adequate volume resuscitation and BP preservation.
Probably the most important factors for preventing postoperative renal failure and maintaining renal perfusion during both cross-clamp and post-clamp release are adequate volume resuscitation and BP preservation. If prolonged renal ischemia is anticipated, direct renal arterial infusion of 41C Ringers lactate may decrease the incidence of postoperative renal impairment.20 Recently, Ali et al.,21 investigated the role of ischemic preconditioning on renal and myocardial injury in humans and found that intermittent cross-clamping of the internal iliac arteries before the insult reduced the incidence of renal insufficiency by 23%. The preconditioning is probably humorally mediated as the induced ischemia is occurring at a distance from the protected organ. Even though it has not been proven that statins can decrease postoperative renal failure after abdominal aortic aneurysm (AAA) surgery, these agents have been associated with improved outcomes in vascular surgery patients with renal impairment. One poorly controlled study of 2126 patients found that the use

Renal Hemodynamics and Renal Protection


There is no renal protective strategy proven to yield a superior outcome. The avoidance of prolonged hypotension and the level of aortic clamping are probably the most important factors that impact renal blood flow. Perioperative factors associated with acute renal failure include hypotension, low cardiac index, rhabdomyolysis, acute atrial fibrillation, and early reoperation.5 The incidence of acute renal failure after infrarenal clamping is approximately 5%, whereas the incidence after suprarenal clamping can approach 13%.6 Preoperative renal insufficiency and renal failure requiring dialysis are likely the strongest predictors of mortality.7 Postoperative mortality is up to five-fold higher in those who develop acute renal failure. With suprarenal occlusion, renal blood flow decreases by 80%. Blood flow is not only reduced with aortic cross-clamping, but it is also redistributed, favoring the cortical and juxtamedullary layers over the hypoxia-prone renal medulla.8 Even with an infrarenal aortic clamp, renal blood flow is reduced by 45% and renal vascular resistance is increased by 70%. These renal hemodynamic changes do not immediately revert after the release of the clamp and can persist for up to 30 minutes.8,9

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of statins was associated with a decrease in both short-term and long-term mortality at 30 days and 6 (73.7 years) in patients with a preoperative creatinine clearance less than 60 mL/minute.22

PREOPERATIVE PREPARATION
The Coronary Artery Revascularization Prophylaxis trial showed that coronary artery revascularization before elective major vascular surgery does not improve longterm survival or short-term outcomes, when compared with medical therapy of b blockers, statins and aspirin. It also showed no improvement in outcome between patients with one or two clinical risk factors randomized to preoperative testing and revascularization versus those undergoing medical therapy with b blocker driven heart rate control, although heart rates were not reported.23 A meta-analysis, in early 2007, suggested that perioperative b blockers should be routinely administered in patients at high risk for perioperative myocardial ischemia or infarction.24 Additional literature in AAA patients showed that the use of b blockers in high-risk patients resulted in a significant reduction in adverse perioperative cardiac events.25,26 Recently, the benefits of b blocker therapy in the perioperative setting have been called into question. The Perioperative Ischemic Evaluation study of 8351 patients showed that perioperative b blocker administration, significantly decreased cardiac risks including myocardial infarction but it carried an increased risk of death from noncardiac causes and stroke.27 The starting dose was 100 mg of metoprolol given 2-4 hours before surgery and again 0-6 hours after surgery; the medication was withheld only if SBP was less than 100 mm Hg or heart rate was below 50 bpm. This starting dose is two to eight times the commonly prescribed initial daily dose. It is not great surprise that the administration of b blockers without consideration of coexisting morbidities, and the administration of b blockers to an endpoint of a SBP of 100 mm Hg without regard to initial preoperative BP, might result in iatrogenic harm, as the Perioperative Ischemic Evaluation study showed. A large retrospective study by Lindenauer et al.28 suggested that patients with few or no risk factors might actually have higher morbidity and mortality if started on b blockers in the perioperative setting. This study considered a dose of b blocker to be prophylactic if given postoperatively the same day of surgery or the first postoperative day, even when the b blocker was possibly given to treat a cardiac problem. This methodologic flaw makes it impossible to draw strong conclusions about any increased danger of b blockers. In contrast, prophylactic b blockers clearly benefited those who had multiple cardiac risk factors. There are a number of reasons why conflicting data exist. Heart rate control may be only one aspect of b blocker therapy, and it is possible that an antiinflammatory or a plaque stabilizing effect exists which

confers greater protection with longer duration of therapy.29 In addition, withdrawal of b blocker therapy in the days after surgery may be associated with greater risks for cardiac ischemia. Redelmeier et al.,30 found that atenolol, as opposed to metoprolol, provides greater myocardial protection after surgery, possibly because of its longer halflife. Finally, consideration must be given to the differences in pharmacogenomics that exist among patients. Patients with particular phenotypes may be more protected by b blocker therapy, whereas others may simply be nonresponders. Additional research is needed to elucidate these questions and help to determine which patients will benefit from perioperative b blocker therapy. We still routinely use b blockers in AAA surgical repairs, both endovascular and open, seeking to achieve a heart rate (HR) less than 70 in the operating room, but do not singlemindedly dose the drug to drive the BP down to untenable levels. We also recommend to our surgical colleagues that they continue b blockers when they are started. There are no data about the impact of withdrawal after the initial postoperative period. In summary, patients with significant risk factors for perioperative cardiac events benefit the most from b blocker therapy with appropriate heart rate control but this may not necessarily be the mechanism of protection. The literature suggests that starting this therapy before the surgical intervention (1 week to 37 days) may offer the best protection31 (see Supplemental Digital Content 2, http://links.lww.com/ASA/A3). Further studies on pharmacogenomics may help the clinician determine who would benefit and who would be harmed by instituting b blocker therapy.32 We are fairly aggressive with a goal resting HR of 60 bpm, and intraoperative HR less than 75 bpm, even if the patient has not been on the drug for the optimal period of time. We monitor critical organ perfusion and alter b blocker dosing as indicated by consideration of comorbidities. Randomized controlled trials (RCTs) of statins in the perioperative period are still lacking (see Supplemental Digital Content 3, http://links.lww.com/ASA/A4). One of the first studies revealing possible beneficial effects of statin therapy in the outcome of acute coronary syndromes was the Global Registry of Acute Coronary Events. In addition to their lipid lowering properties, statins have beneficial effects that including anti-inflammatory effects, improved endothelial function through a variety of mechanisms, plaque stabilizing actions, and antioxidant effects. Poldermans et al.33 observed in a non-RCT that the perioperative mortality rate among vascular surgery patients treated with statins was reduced 4.5-fold when compared with patients not treated with them. Lindenauer et al.34 observed in another non-RCT that statin therapy was associated with a reduced risk of postoperative death. It has been suggested that acute withdrawal of statins can triple the risk of perioperative MI35,36 (see Supplemental Digital Content 4, http://links.lww.com/ASA/A5). Careful attention to continuing statins perioperatively is

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necessary because traditional advice had been to withhold them in the perioperative period and most preoperative nurses and surgeons remain unaware of the need to continue statins when writing preoperative or postoperative orders.

SURGICAL PROCEDURES FOR AORTIC RECONSTRUCTION


Perioperative (i.e., 30 day) mortality in elective aortic surgery ranges between 0 and 12% with a much higher probability of death in emergency surgery, especially in those situations with preoperative hypotension (SBP less than 90 mm Hg). Hypotension increases the risk of mortality threefold; whereas preexisting heart disease, including coronary artery disease and congestive heart failure, increases the risk 2.5-fold to 5-fold.24 Other identifiable risks for increased mortality are female sex, serum creatinine above 2 mg/dl, and age greater than 80 years. Some studies have reported that the size of the aneurysm alone does not appear to influence operative mortality.7 However, a recent study looking at almost 4400 patients found that patients with a large aneurysm (greater than 6.5 cm) treated with endovascular aneurysm repair (EVAR) had an increased rate of aneurysm related and unrelated death, and an increased rate of rupture, compared with those with a smaller aneurysm (4.0 to 5.4 cm).37 Expeditious surgery with better graft materials, minimal clamp time, and blood conservation, along with better understanding of the pathophysiology of the disease, have made aortic surgery safer.

Collagen impregnated polyesther fibers (Dacron grafts) compose the majority of implanted grafts. Dacron grafts seem to be associated with rare episodes of anaphylactic reactions, which may be related to the stabilizers used in their manufacture. Polytetrafluoroethylene grafts are less porous and are gaining more widespread use. Aortobiiliac, aortobifemoral, and aortoiliac/femoral grafts are used in most cases. Nonbifurcated grafts constitute approximately 30% of cases.

Endovascular Approach. EVAR was developed with the


goal of placing a stent into the aorta to exclude the aneurysm sac from the systemic circulation and to avoid an open surgical intervention. In 1991, Parodi et al.40 performed the first endovascular stent insertion for an infrarenal aortic aneurysm. Initially, this surgical plan was carried out only for patients deemed too sick to undergo open aortic surgery. Now, with the advent of new stent designs and improved surgical techniques, this therapy is now offered to a wide spectrum of patients. EVAR has a less than 2% associated risk of aneurysm-related death and rupture at 1 year.41 EVAR may be carried out under almost any type of anesthesia including local, neuraxial, and general techniques.38,42 Our preferred method is local anesthesia with moderate sedation. The anesthetic technique selected will depend on preoperative factors such as clopidogrel or low molecular weight heparin use or concomitant illness such as severe chronic obstructive pulmonary disease, and on intraoperative factors such as anticipated duration. Blood loss and hemodynamic changes should be minimal when EVAR is performed by an experienced surgeon. Consideration must be given to the need for conversion to general anesthesia and/or for massive volume resuscitation, although the incidence of this is very low at approximately 0.6%.43,44 Elective and emergent AAA repairs have been carried out using EVAR.45 A meta-analysis of elective EVARs over the last 12 years showed that as technical experience improved, there was a reduction in operative mortality, postoperative rupture, and the incidence of leak requiring surgical intervention.46 Although it has been reported that up to 37% of patients may not be suitable candidates for an EVAR for their infrarenal AAA,4749 new stent technology with smaller modular designs may allow a number of these patients to undergo EVAR. Successful stent deployment occurs in more than 90% of patients adequately evaluated for EVAR. Whether the same success can be achieved with emergent repairs depends on the preoperative assessment by the surgeon and operator experience.50,51 Studies have shown decreased morbidity and mortality with EVAR for ruptured AAAs, over open repairs.52 Despite the minimally invasive nature of the technique, there are several complications unique to EVAR that must be anticipated. Endoleak is the most common complication which occurs in more than 30% of patients, in some studies. An endoleak is defined as persistent blood flow

Clamp Level
In general, deleterious physiologic effects and the chance of a poor outcome are directly related to the level of the clamp. Infrarenal aortic clamping carries the lowest risk for patients; supraceliac clamping carries the highest. Anesthesiologists should be aware that 10-20% of infrarenal aortic disease will actually necessitate suprarenal clamping. Ruptured aneurysms often must be controlled initially by supraceliac clamping in an effort to gain hemodynamic control and allow the patient to be stabilized. Then, the priority shifts toward expeditious repair to restore distal blood flow and minimize ischemic time. Atheromatous material can be dislodged into the renal arteries or other tributaries during surgical manipulation and clamping, further complicating renal and bowel perfusion.

Infrarenal Operations. Reconstruction of the infrarenal


aorta is performed by exposing the relevant portion of the aorta and the iliac arteries. Although it is generally recognized that distal ischemic complications are embolic (dislodged atheromatous material), and that the systemic use of heparin in the absence of distal occlusive disease is unnecessary, many centers still religiously employ heparin before aortic clamping.38,39 Aortic repair is carried out by interposition of a graft with an end-to-end anastomosis.

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Table 1. EVAR Endoleak Classification System


Type 1 Classification High-flow leak adjacent to a stent that is not sealing the sac from the systemic circulation (requires immediate intervention) Low flow due to arterial branches which have been excluded by the position of the stent (can be treated with embolization) Resulting from a failure with the stent itself or at its junction with another stent (requires immediate recognition and treatment) Resulting from porosity in the stent (often resolves with reversal of anticoagulation)
EVAR endovascular aneurysm repair.

There are specific renal implications of endovascular interventions. A significant dye load may be administered during angiography. Therapies for renal protection such as adequate preoperative hydration, N-acetyl cysteine, and NaHCO3 have shown some benefit in minimizing contrast-induced nephropathy.58,59 However, these have not been shown to influence the incidence of renal dysfunction after AAA surgery.60 Consideration must also be given to the proximity of the renal arteries and the region of planned stent deployment. Although complete renal artery occlusion is unusual, there are reports of thrombosis and renal infarction after EVAR.61

Comparing Open to Endovascular Repairs


The decision of whether to treat a large AAA with EVAR, open repair or medical treatment generally depends on three variables: AAA size, AAA morphology, and patient surgical risk. The threshold of when to intervene has changed because an AAA is now often seen as a manifestation of widespread vascular disease caused by multiple medical comorbidities instead of a distinct disease by itself. The association between aortic diameter and severity of vascular disease has been studied. A 10-year follow-up study that screened 4734 patients over 65 years of age with abdominal ultrasound found that an infrarenal aortic diameter greater than 2 cm was associated with increased risk of future coronary vascular disease and mortality. Although the risk/benefit ratio for open surgery to repair small AAAs is not supported, there is an emerging discussion to reevaluate treating smaller AAAs with EVAR due to the ability to intervene before additional comorbidities make the operation riskier.37,62

outside the wall of the stent graft into the aneurysm sac. Endoleak exposes the weak aneurysm wall to continued flow that may lead to rupture. White et al.,53 proposed the classification system shown in Table 1. Other problems related to EVAR include problems with arterial access; migration or malpositioning of the stent; obstruction of renal, mesenteric, or other major vascular ostia; contrast-induced nephropathy; and aneurysm rupture. Understanding surgical concerns will help prepare the anesthesiologist for potential problems. Severely atherosclerotic vessels may be difficult to cannulate and access. Percutaneous access may not be feasible in obese patients, or in patients who have had previous groin surgery, necessitating open groin access and arteriotomy. Aggressive attempts to negotiate less than ideal anatomy may lead to retroperitoneal hematoma and significant morbidity and mortality.54 Conversion from EVAR to an open procedure is associated with significant morbidity and mortality and may occur in the setting of aneurysm rupture, stent migration, stent malposition, vessel dissection at the arterial access site, and poor anatomic parameters for EVAR.37 For the anesthesiologist, conversion in this setting may involve the emergent induction of general anesthesia and the need for adequate resuscitative equipment such as cell saver and rapid infusion devices, which must be readily available in centers performing EVARs. A primary conversion is classified as an open reoperation within 30 days after an EVAR, and is most commonly associated with type 1 leak. A secondary conversion is classified as an open reoperation after 30 days after an EVAR and is usually performed for continuing enlargement of the aneurysm sac or for a persistent endoleak. Another indication for secondary conversion is aneurysm rupture despite successful sac exclusion. Although the occurrence of some of these complications is low, the associated mortality is quite high.55 The incidence of secondary conversion is between 0.6 and 2%,44 but it carries a perioperative mortality of 27%, up to 50% if the aneurysm ruptured.56 Primary conversion has a mortality of up to 18%, which is greater than the mortality from an initial open repair.57

The decision of whether to treat a large AAA with EVAR, open repair or medical treatment generally depends on three variables: AAA size, AAA morphology, and patient surgical risk.
Outcomes of endovascular repairs have been directly compared with open surgical interventions. In the EVAR-1 trial, patients deemed fit for open AAA repair were randomly assigned to either open repair or EVAR. Thirty-day mortality was significantly decreased in the EVAR group (1.6% EVAR vs. 4.6% open). However, reintervention rates were significantly higher in the EVAR group. Long-term morbidity, mortality, and quality of life were the same at 2 and 4 postprocedure years.63 Reasons for reintervention included endovascular repair of endoleak, open repair, reexploration of open repair, and other surgery not specified.64

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Some of the limitations found in the analysis of the EVAR-1 trial are (1) only 23% of those assessed for eligibility were ultimately randomized, (2) the average delay from randomization to actual treatment was 57 days despite a mean AAA size of 6.7 cm, and (3) only 24% of participant data were included in the 4-year cutoff point for analysis. These limitations make it difficult to definitively generalize the results obtained from this trial. As a minimally invasive technique, it would seem that EVAR, as compared with open AAA repair, would be better suited for patients who have multiple comorbidities. The EVAR-2 trial was designed to compare maximum medical therapy versus EVAR in those patients who were too unstable for open repair. No difference in mortality was found between the two groups in a 4-year follow-up.65 The major limitations of this trial relate to delays in receiving the assigned treatment and the high rate of patient crossover to the EVAR arm, both of which may have biased the results against EVAR. Furthermore, 8% of the patients were assigned to EVAR died while awaiting treatment; yet the analysis seems to have included them as receiving EVAR. Another relatively large trial of 345 patients, the Diabetes Reduction Assessment with Ramipril and Rosiglitazone Medication trial, compared open AAA repair to EVAR and showed no significant difference in 1-year moderate-to-severe morbidity and overall survival.66 A recent randomized, multicenter trial of 881 patients showed low mortality rates for both open repair and EVAR, 3 and 0.5%, respectively. Although there was a statistically significant difference in mortality in the perioperative period, there was no difference in mortality, quality of life, and erectile dysfunction after 2 years of follow-up.67 In summary, there are no RCTs showing long-term superiority of EVAR over open AAA surgery, yet EVAR may allow treatment of older, sicker, patients who are at risk of rupture and who would have not been considered for repair when open surgery was the only choice. The technique has become commonplace in most tertiary care centers, and nearly 60% of all AAA repairs in the United States are now EVAR.68

REFERENCES
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