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Surgery_Schwartz. after endovascular repair of AAA has been reported to be as high as 95%.41 The less invasive nature Brunicardi_Ch23_p0897-p0980.indd 92527/02/19 4:14 PM 926SPECIFIC CONSIDERATIONSPART IIof this procedure is appealing to many physicians and patients. In addition, virtually all reports indicate a decreased blood loss, transfusion requirements, and length of intensive care unit and hospital stay for endovascular repair of AAAs compared with the standard surgical approach.47 With the advent of bifurcated grafts and improved delivery systems in the future, the only real limitation will be cost. When evaluating the literature for results from clinical series, it is important to look at a comparison of endoluminal versus open repair and device-specific outcome and cost analysis studies.Early reports on results with endovascular repair were often flawed due to selection biases. This is because from its inception, endovascular repair has been used mostly in patients who are at higher risk


Surgery_Schwartz

Surgery_Schwartz. reports on results with endovascular repair were often flawed due to selection biases. This is because from its inception, endovascular repair has been used mostly in patients who are at higher risk for open repair. At the same time, only patients with favorable anatomy including less tortuosity and the presence of a suitable infrarenal neck were considered for endovascular repair. Randomization is also difficult because most patients who anatomically qualify for endovascular repair would withdraw from the study if randomized to open repair. Consequently, there are very few randomized controlled tri-als that have compared outcomes in patients with similar risk factors and anatomy who are eligible for both types of repair. Two such European trials have recently published short-term outcome data that are unbiased in design.The DREAM trial is a multicenter randomized trial that compared open versus endovascular repair among a group of 345 patients at 28 European centers using multiple


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Surgery_Schwartz. data that are unbiased in design.The DREAM trial is a multicenter randomized trial that compared open versus endovascular repair among a group of 345 patients at 28 European centers using multiple different devices including Gore, AneuRx, and Zenith.66 Patients were included only if they were considered to be candidates for both types of repairs. The operative mortality rate was 4.6% in the operative group versus 1.2% in the endoluminal group at 30 days. When looking at the combined rate of operative mor-tality and severe complications, there was an incidence of 9.8% in the open repair group versus 4.7% in the endoluminal group. The difference here was largely due to the higher frequency of pulmonary complications seen in the open group. There was a higher incidence of graft-related complications in the endolu-minal group. There was no difference in the nonvascular local complication rate among the two groups. The Endovascular Repair-1 (EVAR-1) trial is also a multicenter randomized


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Surgery_Schwartz. in the endolu-minal group. There was no difference in the nonvascular local complication rate among the two groups. The Endovascular Repair-1 (EVAR-1) trial is also a multicenter randomized trial that compared open to endoluminal repair.67 This study was con-ducted on 1082 patients at 34 centers in the United Kingdom using all available devices. Short-term mortality at 30 days was 4.7% in the open group and 1.7% in the endoluminal group. The in-hospital mortality rate was also increased in the open when compared to the endoluminal group (6.2% vs. 2.1%). As expected, the secondary intervention rate was higher in the endoluminal group (9.8% vs. 5.8%). Complication rates were not reported in the EVAR-1 trial. Criticisms can be applied to both of these trials. Patients had to be eligible for either type of repair in order to be included in the study. Consequently, these findings cannot be generalized to patients who are too sick to undergo open surgery or to patients whose anatomy


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Surgery_Schwartz. for either type of repair in order to be included in the study. Consequently, these findings cannot be generalized to patients who are too sick to undergo open surgery or to patients whose anatomy precludes them from undergoing endovascular repair.The Open Versus Endovascular Repair (OVER) Veter-ans Affairs Cooperative Study Group randomly assigned 881 patients with asymptomatic AAAs who were candidates for both procedures to either endovascular repair (n = 444) or open repair (n = 437) and followed them for up to 9 years.68 Reduction in perioperative mortality with endovascular repair was sustained at 3 years but not thereafter. There was no difference in pri-mary outcome of all-cause mortality. Endovascular repair and open repair resulted in similar long-term survival. Six aneurysm ruptures were confirmed in the endovascular repair group ver-sus none in the open repair group. Rupture after endovascular repair remains a concern. A significant interaction was observed between age and


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Surgery_Schwartz. were confirmed in the endovascular repair group ver-sus none in the open repair group. Rupture after endovascular repair remains a concern. A significant interaction was observed between age and type of treatment. Endovascular repair led to increased long-term survival among younger patients but not among older patients, for whom a greater benefit from the endo-vascular approach had been expected.Device-Specific Outcome. Matsumura and associates com-pared endoluminal versus open repair using the Excluder device.69 In their review, they demonstrated a 30-day mortality rate of 1% along with endoleak rates of 17% and 20% at 1and 2-year intervals, respectively. The limb narrowing, limb migra-tion, and trunk migration were all 1% at 2 years. There were no deployment failures or early conversions. There was an annual 7% reintervention rate. Aneurysm growth was demonstrated in 14% of patients at 2 years. The Zenith device by Cook has been studied by Greenberg and associates, who compared


Surgery_Schwartz

Surgery_Schwartz. There was an annual 7% reintervention rate. Aneurysm growth was demonstrated in 14% of patients at 2 years. The Zenith device by Cook has been studied by Greenberg and associates, who compared standard surgical repair with endoluminal repair in low-risk patients and endoluminal repair in high-risk patients.70 They reported a 30-day mortality rate of 3.5%, which was equal to the open group. The endoleak rates were 7.4% and 5.4% at 1and 2-year intervals, respectively. There was a 5.3% migration of 5 mm at 1 year. Freedom from rupture was 100% in the low-risk group and 98.9% in the high-risk endoluminal group at 2 years. Expe-rience with the AneuRx device has been reported by Zarins.71 In this 4-year review, they found a 30-day mortality rate of 2.8%. Endoleak rate at 4 years was 13.9%, aneurysm enlargement was 11.5%, and stent graft migration was 9.5%. Freedom from rup-ture was noted to be 98.4% at 4 years. Criado and associates have reported on their 1-year experience with the Talent


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Surgery_Schwartz. enlargement was 11.5%, and stent graft migration was 9.5%. Freedom from rup-ture was noted to be 98.4% at 4 years. Criado and associates have reported on their 1-year experience with the Talent LPS device by Medtronic.72 They report a 30-day mortality rate of 0.8%. Endoleak rate was 10%. Three deployment failures were noted, and freedom from rupture was 100%. Aneurysm growth and migration rates were divided into three different neck size groups. Patients with a wide neck (>26 mm) had a 3% growth and migration rate. Narrow-neck patients (<26 mm) had a 1% growth rate and a 2% migration neck. Interestingly, short-neck patients (<15 mm) had no aneurysm growths and a 2% migra-tion rate.Cost Analysis. The current climate of cost containment and limited reimbursement for healthcare services mandates a criti-cal analysis of the economic impact of any new medical technol-ogy on the market. The in-hospital costs for both endovascular and open repair include graft cost, operating room fees,


Surgery_Schwartz

Surgery_Schwartz. mandates a criti-cal analysis of the economic impact of any new medical technol-ogy on the market. The in-hospital costs for both endovascular and open repair include graft cost, operating room fees, radiol-ogy, pharmacy, ancillary care, intensive care unit charges, and floor charges. Despite the improved morbidity and mortality rates, several early studies have reported no cost benefit with the application of endovascular repair.73,74 The limiting factor appears to be the cost of the device. Despite commercializa-tion of endovascular repair, the device costs are still in the range of $5000 to $6000 with no signs of abating. A report by Angle and associated further corroborates previous studies.75 In their review, despite decreased hospital and intensive care unit stays and utilization of pharmacy and respiratory services, cost of endovascular repair was 1.74 times greater than the stan-dard surgical approach. In addition, these cost analysis stud-ies are centered on in-hospital costs


Surgery_Schwartz

Surgery_Schwartz. pharmacy and respiratory services, cost of endovascular repair was 1.74 times greater than the stan-dard surgical approach. In addition, these cost analysis stud-ies are centered on in-hospital costs and do not even begin to address secondary costs such as postoperative surveillance that is required with endovascular repair. In the OVER trial, endo-vascular repair was found to be a cost-effective alternative to Brunicardi_Ch23_p0897-p0980.indd 92627/02/19 4:14 PM 927ARTERIAL DISEASECHAPTER 23open repair in the U.S. Veterans Affairs healthcare system for at least the first 2 years.76 The primary outcomes were mean total healthcare cost per life-year and per quality-adjusted life-year. There were no differences found in survival, quality of life, and costs after 2 years between the endovascular and the open group. Although graft costs were higher in the endovas-cular group, length of stay was shorter, resulting in lower cost of AAA repair hospitalization in the endovascular group.


Surgery_Schwartz

Surgery_Schwartz. and the open group. Although graft costs were higher in the endovas-cular group, length of stay was shorter, resulting in lower cost of AAA repair hospitalization in the endovascular group. Costs remained lower after 2 years in the endovascular group, but the difference was no longer significant.Classification and Management of EndoleakAn endoleak is an extravasation of contrast outside the stent graft and within the aneurysm sac (Fig. 23-34). It can be pres-ent in up to 20% to 30% of all endovascular AAA repairs in the early postoperative period.77,78 In general, over half of these endoleaks will resolve spontaneously during the first 6 months, resulting in a 10% incidence of chronic endoleaks in all cases beyond the first year of follow-up. Endoleaks can be detected using conventional angiography, contrast CT (Fig. 23-35), MRA, and color-flow duplex ultrasound. Although there is no recognized gold standard, in practice, angiography is consid-ered the least sensitive but most


Surgery_Schwartz

Surgery_Schwartz. angiography, contrast CT (Fig. 23-35), MRA, and color-flow duplex ultrasound. Although there is no recognized gold standard, in practice, angiography is consid-ered the least sensitive but most specific for characterizing the Type I endoleak Type II endoleak Type III endoleak Type IV endoleakFigure 23-34. The four types of endoleak include the following: type I endoleak = attachment site leak; type II endoleak = side branch leak caused by lumbar or side branches; type III endoleak = endograft junctional leak due to overlapping device components; and type IV endoleak = endograft fabric or porosity leak.Figure 23-35. A computed tomography scan demonstrating an endoleak (small arrow) as evidenced by contrast flow outside the aortic endograft (long arrow).source of the endoleak, whereas the CT scan is the most sensi-tive but least specific. Widespread availability and reliability that is relatively independent of technique have made the CT


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Surgery_Schwartz. arrow).source of the endoleak, whereas the CT scan is the most sensi-tive but least specific. Widespread availability and reliability that is relatively independent of technique have made the CT scan the de facto standard imaging modality for postoperative surveillance. Conversely, routine use of duplex ultrasound and MRA has been limited by the lack of proper equipment and local expertise. On the other hand, investigational techniques such as time-resolved MRA may provide greater sensitivity and specificity than either angiography or CT in the future.Four types of endoleaks have been described (Table 23-10). Type I endoleak refers to fixation-related leaks that occur at the proximal or distal attachment sites. These represent less than 5% of all endoleaks and are seen as an early blush of contrast into the aneurysm sac from the proximal or distal ends of the device during completion angiography.77,78 Although seen as marker of poor patient selection or inadequate repair, over 80% of


Surgery_Schwartz

Surgery_Schwartz. contrast into the aneurysm sac from the proximal or distal ends of the device during completion angiography.77,78 Although seen as marker of poor patient selection or inadequate repair, over 80% of these leaks spontaneously seal in the first 6 months. Persistent type I endoleaks, on the other hand, require prompt treatment. Type II endoleak refers to retrograde flow originating from a lumbar, inferior mesenteric, accessory renal, or hypogastric artery. They are the most common type of endoleak, accounting for 20% to 30% of all cases, and about half resolve spontaneously. On angi-ography, they are seen as a late filling of the aneurysm sac from a branch vessel(s). Type II endoleaks carry a relatively benign natural history and do not merit intervention unless associated with aneurysm growth. Type III endoleaks refer to failure of device integrity or component separation from modular sys-tems. If detected intraoperatively or in the early perioperative period, it is usually from


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Surgery_Schwartz. growth. Type III endoleaks refer to failure of device integrity or component separation from modular sys-tems. If detected intraoperatively or in the early perioperative period, it is usually from inadequate overlap between two stent Table 23-10Endoleak classificationCLASSIFICATIONDESCRIPTIONType I endoleakAttachment site leakType II endoleakSide branch leak caused by lumbar or inferior mesenteric arteriesType III endoleakJunctional leak (of overlapping endograft components) and graft fabric defectType IV endoleakEndograft fabric porosity leakBrunicardi_Ch23_p0897-p0980.indd 92727/02/19 4:14 PM 928SPECIFIC CONSIDERATIONSPART IIgrafts, whereas in the late period, the endoleak may be from a fabric tear or junctional separation from conformational changes of the aneurysm. Regardless of the etiology or timing, these should be promptly repaired. Finally, type IV endoleak refers to the diffuse, early blush seen during completion angiography due to graft porosity and/or suture holes of


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Surgery_Schwartz. the etiology or timing, these should be promptly repaired. Finally, type IV endoleak refers to the diffuse, early blush seen during completion angiography due to graft porosity and/or suture holes of some Dacron-based devices. It does not have any clinical significance and usually cannot be seen after 48 hours and heparin reversal. Endoleaks that are initially considered type IV but persist become type III endoleaks by definition because this indicates a more significant material defect than simple porosity or a suture hole.Endotension Following Endovascular Aortic Aneurysm Repair. In approximately 5% of cases after an apparently suc-cessful endovascular repair, the aneurysm continues to grow without any demonstrable endoleak.79,80 This phenomenon has been described as endotension. Although it was initially thought that an endoleak was really present but simply not detected, case have been reported where the aneurysm has been surgically opened and the contents were completely devoid


Surgery_Schwartz

Surgery_Schwartz. it was initially thought that an endoleak was really present but simply not detected, case have been reported where the aneurysm has been surgically opened and the contents were completely devoid of any blood and no extravasation could be found. The mechanism of con-tinued pressurization of the aneurysm sac following successful exclusion from the arterial circulation remains unsolved at this time. One putative mechanism has been linked to a transuda-tive process related to certain expanded PTFE graft materials.81 More importantly, however, the natural history of these enlarg-ing aneurysms without endoleaks is unknown, but to date, there has been no evidence to suggest that they carry an increased risk of rupture. Conservatively speaking, until further long-term data become available, if the patient is a suitable surgical risk, elec-tive open conversion should be considered.Secondary Interventions Following Endovascular Aortic Aneurysm Repair. There is approximately 10% to 15% per year


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Surgery_Schwartz. patient is a suitable surgical risk, elec-tive open conversion should be considered.Secondary Interventions Following Endovascular Aortic Aneurysm Repair. There is approximately 10% to 15% per year risk of secondary interventions following endovascular AAA repair.62 These procedures are critical in the long-term success of the primary procedure in prevention of aneurysm rup-ture and aneurysm-related death. These secondary procedures, in order of frequency, include proximal or distal extender place-ment for migrations, highly selective or translumbar emboliza-tion for type II endoleaks, direct surgical or laparoscopic branch vessel ligations, bridging cuffs for component separations, and late open surgical conversions.Multiple large series have reported that an annual rupture rate of approximately 1% to 1.5% per year after endovascular repair.82,83 The EUROSTAR registry reports a rupture rate of 2.3% over 15.4 months in patients with an endoleak, compared with 0.3% in those


Surgery_Schwartz

Surgery_Schwartz. of approximately 1% to 1.5% per year after endovascular repair.82,83 The EUROSTAR registry reports a rupture rate of 2.3% over 15.4 months in patients with an endoleak, compared with 0.3% in those without.82,83 Various causes of late ruptures have been reported in the literature, although presence of a per-sistent endoleak with aneurysm enlargement remains a com-mon culprit for this complication. It has been shown that even successfully excluded aneurysms can lead to the development of attachment-site leaks and device failure, caused in part by aneurysm remodeling resulting in stent migration or kinking. Mehta and colleagues reported that 63% of delayed AAA rup-tures after endovascular repair were caused by type I endoleaks with endograft migration, 11% by type I without migration, 19% by type II, and the rest of unknown type.84Treatment of rupture may be open conversion or endo-vascular stent graft placement. May and associates reported a mortality rate of 43% in those patients who


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Surgery_Schwartz. type II, and the rest of unknown type.84Treatment of rupture may be open conversion or endo-vascular stent graft placement. May and associates reported a mortality rate of 43% in those patients who underwent open conversion.85 Emergent endovascular repair should be consid-ered in these patients since it is potentially much faster and less likely to cause physiologic stress than open conversion. Several reports have shown that endovascular repair can be performed successfully in patients previously treated with endoluminal prostheses.80,86MESENTERIC ARTERY DISEASEVascular occlusive disease of the mesenteric vessels is a rela-tively uncommon but potentially devastating condition that gen-erally presents in patients over 60 years of age, is three times more frequent in women, and has been recognized as an entity since 1936.87 The incidence of such a disease is low and repre-sents 2% of the revascularization operations for atheromatous lesions. The most common cause of mesenteric ischemia


Surgery_Schwartz

Surgery_Schwartz. as an entity since 1936.87 The incidence of such a disease is low and repre-sents 2% of the revascularization operations for atheromatous lesions. The most common cause of mesenteric ischemia is atherosclerotic vascular disease. Autopsy studies have dem-onstrated splanchnic atherosclerosis in 35% to 70% of cases.88 Other etiologies exist and include FMD, panarteritis nodosa, arteritis, and celiac artery compression from a median arcuate ligament, but they are unusual and have an incidence of one in nine compared with that of atherosclerosis.Chronic mesenteric ischemia is related to a lack of blood supply in the splanchnic region and is caused by disease in one or more visceral arteries: the celiac trunk, the superior mesen-teric artery, and the IMA. Mesenteric ischemia is thought to occur when two of the three visceral vessels are affected with severe stenosis or occlusion; however, in as many as 9% of cases, only a single vessel is involved (SMA in 5% and celiac trunk in 4% of


Surgery_Schwartz

Surgery_Schwartz. occur when two of the three visceral vessels are affected with severe stenosis or occlusion; however, in as many as 9% of cases, only a single vessel is involved (SMA in 5% and celiac trunk in 4% of cases).89 This disease process may evolve in a chronic fashion, as in the case of progressive luminal oblitera-tion due to atherosclerosis. On the other hand, mesenteric isch-emia can occur suddenly, as in the case of thromboembolism. Despite recent progress in perioperative management and bet-ter understanding of pathophysiology, mesenteric ischemia is considered one of the most catastrophic vascular disorders with mortality rates ranging from 50% to 75%. Delays in diagnosis and treatment are the main contributing factors in its high mor-tality. It is estimated that mesenteric ischemia accounts for 1 in every 1000 hospital admissions in this country. The prevalence is rising due in part to the increased awareness of this disease, the advanced age of the population, and the significant


Surgery_Schwartz

Surgery_Schwartz. for 1 in every 1000 hospital admissions in this country. The prevalence is rising due in part to the increased awareness of this disease, the advanced age of the population, and the significant comor-bidity of these elderly patients. Early recognition and prompt treatment before the onset of irreversible intestinal ischemia are essential to improve the outcome.Anatomy and PathophysiologyMesenteric arterial circulation is remarkable for its rich collat-eral network. Three main mesenteric arteries provide the arterial perfusion to the gastrointestinal system: the celiac artery (CA), the superior mesenteric artery (SMA), and the IMA. In gen-eral, the CA provides arterial circulation to the foregut (distal esophagus to duodenum), hepatobiliary system, and spleen; the SMA supplies the midgut (jejunum to mid-colon); and the IMA supplies the hindgut (mid-colon to rectum). The CA and SMA arise from the ventral surface of the infradiaphragmatic supra-renal abdominal aorta, whereas the IMA


Surgery_Schwartz

Surgery_Schwartz. (jejunum to mid-colon); and the IMA supplies the hindgut (mid-colon to rectum). The CA and SMA arise from the ventral surface of the infradiaphragmatic supra-renal abdominal aorta, whereas the IMA originates from the left lateral portion of the infrarenal aorta. These anatomic origins in relation to the aorta are important when a mesenteric angio-gram is performed to determine the luminal patency. In order to fully visualize the origins of the CA and SMA, it is necessary to perform both an anteroposterior and a lateral projection of the aorta since most arterial occlusive lesions occur in the proximal segments of these mesenteric trunks.Brunicardi_Ch23_p0897-p0980.indd 92827/02/19 4:14 PM 929ARTERIAL DISEASECHAPTER 23Because of the abundant collateral flow between these mesenteric arteries, progressive diminution of flow in one or even two of the main mesenteric trunks is usually tolerated, provided that uninvolved mesenteric branches can enlarge over time to provide sufficient


Surgery_Schwartz

Surgery_Schwartz. progressive diminution of flow in one or even two of the main mesenteric trunks is usually tolerated, provided that uninvolved mesenteric branches can enlarge over time to provide sufficient compensatory collateral flow. In contrast, acute occlusion of a main mesenteric trunk may result in profound ischemia due to lack of sufficient collateral flow. Collateral networks between the CA and the SMA exist primarily through the superior and inferior pancreaticoduodenal arteries. The IMA may provide collateral arterial flow to the SMA through the marginal artery of Drummond, the arc of Riolan, and other unnamed retroperitoneal collateral vessels termed meandering mesenteric arteries (Fig. 23-36). Lastly, collateral visceral vessels may provide important arterial flow to the IMA and the hindgut through the hypogastric arteries and the hemorrhoidal arterial network.Regulation of mesenteric blood flow is largely modulated by both hormonal and neural stimuli, which characteristically regulate


Surgery_Schwartz

Surgery_Schwartz. through the hypogastric arteries and the hemorrhoidal arterial network.Regulation of mesenteric blood flow is largely modulated by both hormonal and neural stimuli, which characteristically regulate systemic blood flow. In addition, the mesenteric cir-culation responds to the gastrointestinal contents. Hormonal regulation is mediated by splanchnic vasodilators, such as nitric oxide, glucagon, and vasoactive intestinal peptide. Certain intrinsic vasoconstrictors, such as vasopressin, can diminish the mesenteric blood flow. On the other hand, neural regulation is provided by the extensive visceral autonomic innervation.Clinical manifestation of mesenteric ischemia is pre-dominantly postprandial abdominal pain, which signifies that the increased oxygen demand of digestion is not met by the gastrointestinal collateral circulation. The postprandial pain fre-quently occurs in the mid-abdomen, suggesting that the diver-sion of blood flow from the SMA to supply the stomach impairs perfusion


Surgery_Schwartz

Surgery_Schwartz. gastrointestinal collateral circulation. The postprandial pain fre-quently occurs in the mid-abdomen, suggesting that the diver-sion of blood flow from the SMA to supply the stomach impairs perfusion to the small bowel. This leads to transient anaerobic metabolism and acidosis. Persistent or profound mesenteric ischemia will lead to mucosal compromise with release of intra-cellular contents and by-products of anaerobic metabolism to Figure 23-36. An aortogram showing a prominent collateral ves-sel, which is the arc of Riolan (arrow) in a patient with an inferior mesenteric artery (IMA) occlusion. This vessel network provides collateral flow between the superior mesenteric artery and IMA.the splanchnic and systemic circulation. Injured bowel mucosa allows unimpeded influx of toxic substances from the bowel lumen with systemic consequences. If full-thickness necrosis occurs in the bowel wall, intestinal perforation ensues, which will lead to peritonitis. Concomitant atherosclerotic


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Surgery_Schwartz. from the bowel lumen with systemic consequences. If full-thickness necrosis occurs in the bowel wall, intestinal perforation ensues, which will lead to peritonitis. Concomitant atherosclerotic disease in cardiac or systemic circulation frequently compounds the diag-nostic and therapeutic complexity of mesenteric ischemia.Types of Mesenteric Artery Occlusive DiseaseThere are three major mechanisms of visceral ischemia involv-ing the mesenteric arteries: (a) acute mesenteric ischemia, which can be either embolic or thrombotic in origin; (b) chronic mes-enteric ischemia; and (c) nonocclusive mesenteric ischemia. Despite the variability of these syndromes, a common anatomic pathology is involved in these processes. The superior mesen-teric artery (SMA) is the most commonly involved vessel in acute mesenteric ischemia. Acute thrombosis occurs in patients with underlying mesenteric atherosclerosis, which typically involves the origin of the mesenteric arteries while sparing the collateral


Surgery_Schwartz

Surgery_Schwartz. acute mesenteric ischemia. Acute thrombosis occurs in patients with underlying mesenteric atherosclerosis, which typically involves the origin of the mesenteric arteries while sparing the collateral branches. In acute embolic mesenteric ischemia, the emboli typically originate from a cardiac source and frequently occur in patients with atrial fibrillation or following myocar-dial infarction (Figs. 23-37 and 23-38). Nonocclusive mesen-teric ischemia is characterized by a low flow state in otherwise normal mesenteric arteries and most frequently occurs in criti-cally ill patients on vasopressors. Finally, chronic mesenteric ischemia is a functional consequence of a long-standing ath-erosclerotic process that typically involves at least two of the three main mesenteric vessels. The gradual development of the occlusive process allows the development of collateral ves-sels that prevent the manifestations of acute ischemia, but are not sufficient to meet the high postprandial intestinal


Surgery_Schwartz

Surgery_Schwartz. development of the occlusive process allows the development of collateral ves-sels that prevent the manifestations of acute ischemia, but are not sufficient to meet the high postprandial intestinal oxygen requirements, giving rise to the classical symptoms of postpran-dial abdominal pain and the resultant food fear.Several less common syndromes of visceral ischemia involving the mesenteric arteries can also cause serious debili-tation. Chronic mesenteric ischemic symptoms can occur due Figure 23-37. An anteroposterior view of a selective superior mesenteric artery angiogram shows an abrupt cutoff of the middle colic artery, which was caused by emboli (arrow) due to atrial fibrillation.Brunicardi_Ch23_p0897-p0980.indd 92927/02/19 4:14 PM 930SPECIFIC CONSIDERATIONSPART IIFigure 23-38. A lateral mesenteric angiogram showing an abrupt cutoff of the proximal superior mesenteric artery (SMA), which is consistent with SMA embolism (arrow).to extrinsic compression of the celiac artery by


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Surgery_Schwartz. lateral mesenteric angiogram showing an abrupt cutoff of the proximal superior mesenteric artery (SMA), which is consistent with SMA embolism (arrow).to extrinsic compression of the celiac artery by the diaphragm, which is termed median arcuate ligament syndrome or celiac artery compression syndrome. Acute visceral ischemia may occur following an aortic operation, due to ligation of the IMA in the absence of adequate collateral vessels. Furthermore, acute visceral ischemia may develop in aortic dissection, which involves the mesenteric arteries, or after coarctation repair. Finally, other unusual causes of ischemia include mesenteric arteritis, radiation arteritis, and cholesterol emboli.Clinical ManifestationsAbdominal pain out of proportion to physical findings is the classic presentation in patients with acute mesenteric ischemia and occurs following an embolic or thrombotic ischemic event of the SMA. Other manifestations include sudden onset of abdominal cramps in patients with


Surgery_Schwartz

Surgery_Schwartz. in patients with acute mesenteric ischemia and occurs following an embolic or thrombotic ischemic event of the SMA. Other manifestations include sudden onset of abdominal cramps in patients with underlying cardiac or ath-erosclerotic disease, often associated with bloody diarrhea, as a result of mucosal sloughing secondary to ischemia. Fever, nausea, vomiting, and abdominal distention are some common but nonspecific manifestations. Diffuse abdominal tenderness, rebound, and rigidity are late signs and usually indicate bowel infarction and necrosis.Clinical manifestations of chronic mesenteric ischemia are more subtle due to the extensive collateral development. How-ever, when intestinal blood flow is unable to meet the physio-logic gastrointestinal demands, mesenteric insufficiency ensues. The classical symptoms include postprandial abdominal pain, food fear, and weight loss. Persistent nausea and occasionally diarrhea may coexist. Diagnosis remains challenging, and most of the


Surgery_Schwartz

Surgery_Schwartz. ensues. The classical symptoms include postprandial abdominal pain, food fear, and weight loss. Persistent nausea and occasionally diarrhea may coexist. Diagnosis remains challenging, and most of the patients will undergo an extensive and expensive gastro-intestinal tract workup for the above symptoms prior to referral to a vascular service.The typical patient who develops nonocclusive mesenteric ischemia is an elderly patient who has multiple comorbidities, such as congestive heart failure, acute myocardial infarction with cardiogenic shock, hypovolemic or hemorrhagic shock, sepsis, pancreatitis, and administration of digitalis or vasocon-strictor agents such as epinephrine. Abdominal pain is only present in approximately 70% of these patients. When present, the pain is usually severe but may vary in location, character, and intensity. In the absence of abdominal pain, progressive abdominal distention with acidosis may be an early sign of isch-emia and impending bowel


Surgery_Schwartz

Surgery_Schwartz. severe but may vary in location, character, and intensity. In the absence of abdominal pain, progressive abdominal distention with acidosis may be an early sign of isch-emia and impending bowel infarction.Abdominal pain due to narrowing of the origin of the CA may occur as a result of extrinsic compression or impingement by the median arcuate ligament (Fig. 23-39). This condition is known as celiac artery compression syndrome or median arcuate ligament syndrome. Angiographically, there is CA compression that augments with deep expiration and poststenotic dilatation. The celiac artery compression syndrome has been implicated in some variants of chronic mesenteric ischemia. Most patients are young females between 20 and 40 years of age. Abdominal symptoms are nonspecific, but the pain is localized in the upper abdomen, which may be precipitated by meals.Diagnostic EvaluationThe differential diagnosis of acute mesenteric ischemia includes other causes of severe abdominal pain of acute


Surgery_Schwartz

Surgery_Schwartz. localized in the upper abdomen, which may be precipitated by meals.Diagnostic EvaluationThe differential diagnosis of acute mesenteric ischemia includes other causes of severe abdominal pain of acute onset, such as perforated viscus, intestinal obstruction, pancreatitis, cholecys-titis, and nephrolithiasis. Laboratory evaluation is neither sensitive nor specific in distinguishing these various diagnoses. Figure 23-39. A lateral projection of the magnetic resonance angi-ography of the aorta showing a chronic compression of the celiac artery by the median arcuate ligament (arrow).Brunicardi_Ch23_p0897-p0980.indd 93027/02/19 4:14 PM 931ARTERIAL DISEASECHAPTER 23In the setting of mesenteric ischemia, complete blood count may reveal hemoconcentration and leukocytosis. Metabolic acidosis develops as a result of anaerobic metabolism. Elevated serum amylase may indicate a diagnosis of pancreatitis but is also com-mon in the setting of intestinal infarction. Finally, increased lac-tate


Surgery_Schwartz

Surgery_Schwartz. develops as a result of anaerobic metabolism. Elevated serum amylase may indicate a diagnosis of pancreatitis but is also com-mon in the setting of intestinal infarction. Finally, increased lac-tate levels, hyperkalemia, and azotemia may occur in the late stages of mesenteric ischemia.Plain abdominal radiographs may provide helpful infor-mation to exclude other causes of abdominal pain such as intes-tinal obstruction, perforation, or volvulus, which may exhibit symptoms mimicking intestinal ischemia. Pneumoperitoneum, pneumatosis intestinalis, and gas in the portal vein may indicate infarcted bowel. In contrast, radiographic appearance of an ady-namic ileus with a gasless abdomen is the most common finding in patients with acute mesenteric ischemia.Upper endoscopy, colonoscopy, or barium radiogra-phy does not provide any useful information when evaluating acute mesenteric ischemia. Moreover, barium enema is con-traindicated if the diagnosis of mesenteric ischemia is being considered.


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Surgery_Schwartz. radiogra-phy does not provide any useful information when evaluating acute mesenteric ischemia. Moreover, barium enema is con-traindicated if the diagnosis of mesenteric ischemia is being considered. The intraluminal barium can obscure accurate visu-alization of mesenteric circulation during angiography. In addi-tion, intraperitoneal leakage of barium can occur in the setting of intestinal perforation, which can lead to added therapeutic challenges during mesenteric revascularization.Diagnosis of chronic mesenteric ischemia can be more challenging. Usually prior to the evaluation by a vascular ser-vice, the patients have undergone an extensive workup for the symptoms of chronic abdominal pain, weight loss, and anorexia. Rarely, the vascular surgeon is the first to encounter a patient with the above symptoms. In this situation, it is advisable to keep in mind that mesenteric ischemia is a rare entity and that a full diagnostic workup that should include CT scan of the abdo-men and


Surgery_Schwartz

Surgery_Schwartz. with the above symptoms. In this situation, it is advisable to keep in mind that mesenteric ischemia is a rare entity and that a full diagnostic workup that should include CT scan of the abdo-men and evaluation by gastroenterologist should be performed. Mesenteric occlusive disease may coexist with malignancy, and symptoms of mesenteric vessel stenosis may be the result of extrinsic compression by a tumor.Duplex ultrasonography is a valuable noninvasive means of assessing the patency of the mesenteric vessels. Moneta and associates evaluated the use of duplex ultrasound in the diag-nosis of mesenteric occlusive disease in a blinded prospective study.90,91 A peak systolic velocity in the SMA >275 cm/s dem-onstrated a sensitivity of 92%, specificity of 96%, and overall accuracy of 96% for detecting >70% stenosis. The same authors found sensitivity and specificity of 87% and 82%, respectively, with an accuracy of 82% in predicting >70% celiac trunk ste-nosis. Duplex has been successfully


Surgery_Schwartz

Surgery_Schwartz. >70% stenosis. The same authors found sensitivity and specificity of 87% and 82%, respectively, with an accuracy of 82% in predicting >70% celiac trunk ste-nosis. Duplex has been successfully used for follow-up after open surgical reconstruction or endovascular treatment of the mesenteric vessels to assess recurrence of the disease. Finally, spiral CT with three-dimensional reconstruction (Fig. 23-40) and MRA (Fig. 23-41) have been promising in providing clear radiographic assessment of the mesenteric vessels.The definitive diagnosis of mesenteric vascular disease is made by biplanar mesenteric arteriography, which should be performed promptly in any patient with suspected mesenteric occlusion. It typically shows occlusion or near-occlusion of the CA and SMA at or near their origins from the aorta. In most cases, the IMA has been previously occluded secondary to dif-fuse infrarenal aortic atherosclerosis. The differentiation of the different types of mesenteric arterial occlusion may


Surgery_Schwartz

Surgery_Schwartz. the aorta. In most cases, the IMA has been previously occluded secondary to dif-fuse infrarenal aortic atherosclerosis. The differentiation of the different types of mesenteric arterial occlusion may be sug-gested with biplanar mesenteric arteriogram. Mesenteric emboli typically lodge at the orifice of the middle colic artery, which creates a “meniscus sign” with an abrupt cutoff of a normal Figure 23-40. Computed tomography angiogram of the abdomen with three-dimensional reconstruction provides a clear view of the celiac artery, superior mesenteric artery (SMA), and inferior mes-enteric artery (IMA).Figure 23-41. A cross-sectional view of a magnetic resonance angiogram provides a clear view of the luminal patency of the supe-rior mesenteric artery.proximal SMA several centimeters from its origin on the aorta. Mesenteric thrombosis, in contrast, occurs at the most proximal SMA, which tapers off at 1 to 2 cm from its origin. In the case of chronic mesenteric occlusion, the appearance


Surgery_Schwartz

Surgery_Schwartz. origin on the aorta. Mesenteric thrombosis, in contrast, occurs at the most proximal SMA, which tapers off at 1 to 2 cm from its origin. In the case of chronic mesenteric occlusion, the appearance of collateral circulation is typically present. Nonocclusive mesenteric isch-emia produces an arteriographic image of segmental mesenteric vasospasm with a relatively normal-appearing main SMA trunk (Fig. 23-42).Mesenteric arteriography can also play a therapeutic role. Once the diagnosis of nonocclusive mesenteric ischemia is Brunicardi_Ch23_p0897-p0980.indd 93127/02/19 4:14 PM 932SPECIFIC CONSIDERATIONSPART IIFigure 23-42. Mesenteric arteriogram showing nonocclusive mes-enteric ischemia as evidenced by diffuse spasm of intestinal arcades with poor filling of intramural vessels.made on the arteriogram, an infusion catheter can be placed at the SMA orifice, and vasodilating agents, such as papaverine, can be administered intra-arterially. The papaverine infusion may be continued


Surgery_Schwartz

Surgery_Schwartz. on the arteriogram, an infusion catheter can be placed at the SMA orifice, and vasodilating agents, such as papaverine, can be administered intra-arterially. The papaverine infusion may be continued postoperatively to treat persistent vasospasm, a common occurrence following mesenteric reperfusion. Trans-catheter thrombolytic therapy has little role in the management of thrombotic mesenteric occlusion. Although thrombolytic agents may transiently recannulate the occluded vessels, the underlying occlusive lesions require definitive treatment. Fur-thermore, thrombolytic therapy typically requires a prolonged period of time to restore perfusion, during which the intestinal viability will be difficult to assess.A word of caution would be appropriate here regarding patients with typical history of chronic intestinal angina who present with an acute abdomen and classical findings of peri-toneal irritation. Arteriography is the gold standard for the diagnosis of mesenteric occlusive disease;


Surgery_Schwartz

Surgery_Schwartz. of chronic intestinal angina who present with an acute abdomen and classical findings of peri-toneal irritation. Arteriography is the gold standard for the diagnosis of mesenteric occlusive disease; however, it can be a time-consuming diagnostic modality. In this group of patients, immediate exploration for assessment of intestinal viability and vascular reconstruction is the best choice.Surgical RepairAcute Embolic Mesenteric Ischemia. Initial management of patients with acute mesenteric ischemia includes fluid resus-citation and systemic anticoagulation with heparin to prevent further thrombus propagation. Significant metabolic acidosis not responding to fluid resuscitation should be corrected with sodium bicarbonate. A central venous catheter, peripheral arte-rial catheter, and Foley catheter should be placed for hemody-namic status monitoring. Appropriate antibiotics are given prior to surgical exploration. The operative management of acute mesenteric ischemia is dictated by the


Surgery_Schwartz

Surgery_Schwartz. catheter should be placed for hemody-namic status monitoring. Appropriate antibiotics are given prior to surgical exploration. The operative management of acute mesenteric ischemia is dictated by the cause of the occlusion. It is helpful to obtain a preoperative mesenteric arteriogram to confirm the diagnosis and to plan appropriate treatment options. However, the diagnosis of mesenteric ischemia frequently can-not be established prior to surgical exploration, and therefore, patients in a moribund condition with acute abdominal symp-toms should undergo immediate surgical exploration, avoiding the delay required to perform an arteriogram.The primary goal of surgical treatment in embolic mes-enteric ischemia is to restore arterial perfusion with removal of the embolus from the vessel. The abdomen is explored through a midline incision, which often reveals variable degrees of intestinal ischemia from the mid-jejunum to the ascending or transverse colon. The transverse colon is lifted


Surgery_Schwartz

Surgery_Schwartz. abdomen is explored through a midline incision, which often reveals variable degrees of intestinal ischemia from the mid-jejunum to the ascending or transverse colon. The transverse colon is lifted superiorly, and the small intestine is reflected toward the right upper quad-rant. The SMA is approached at the root of the small bowel mesentery, usually as it emerges from beneath the pancreas to cross over the junction of the third and fourth portions of the duodenum. Alternatively, the SMA can be approached by incising the retroperitoneum lateral to the fourth portion of the duodenum, which is rotated medially to expose the SMA. Once the proximal SMA is identified and controlled with vascular clamps, a transverse arteriotomy is made to extract the embolus, using standard balloon embolectomy catheters. In the event the embolus has lodged more distally, exposure of the distal SMA may be obtained in the root of the small bowel mesentery by isolating individual jejunal and ileal branches to


Surgery_Schwartz

Surgery_Schwartz. catheters. In the event the embolus has lodged more distally, exposure of the distal SMA may be obtained in the root of the small bowel mesentery by isolating individual jejunal and ileal branches to allow a more comprehensive thromboembolectomy. Following the restora-tion of SMA flow, an assessment of intestinal viability must be made, and nonviable bowel must be resected. Several methods have been described to evaluate the viability of the intestine, which include intraoperative intravenous fluorescein injection and inspection with a Wood’s lamp, and Doppler assessment of antimesenteric intestinal arterial pulsations. A second-look pro-cedure should be considered in many patients and is performed 24 to 48 hours following embolectomy. The goal of the proce-dure is reassessment of the extent of bowel viability, which may not be obvious immediately following the initial embolectomy. If nonviable intestine is evident in the second-look procedure, additional bowel resections should be


Surgery_Schwartz

Surgery_Schwartz. of bowel viability, which may not be obvious immediately following the initial embolectomy. If nonviable intestine is evident in the second-look procedure, additional bowel resections should be performed at that time.Acute Thrombotic Mesenteric Ischemia. Thrombotic mesenteric ischemia usually involves a severely atheroscle-rotic vessel, typically the proximal CA and SMA. Therefore, these patients require a reconstructive procedure to the SMA to bypass the proximal occlusive lesion and restore adequate mesenteric flow. The saphenous vein is the graft material of choice, and prosthetic materials should be avoided in patients with nonviable bowel, due to the risk of bacterial contamina-tion if resection of necrotic intestine is performed. The bypass graft may originate from either the aorta or iliac artery. Advan-tages from using the supraceliac infradiaphragmatic aorta as opposed to the infrarenal aorta as the inflow vessel include a smoother graft configuration with less chance of


Surgery_Schwartz

Surgery_Schwartz. or iliac artery. Advan-tages from using the supraceliac infradiaphragmatic aorta as opposed to the infrarenal aorta as the inflow vessel include a smoother graft configuration with less chance of kinking and the absence of atherosclerotic disease in the supraceliac aortic segment. Exposure of the supraceliac aorta is technically more challenging and time consuming than that of the iliac artery, which unless calcified is an appropriate inflow. Patency rates are similar regardless of inflow vessel choice.92Chronic Mesenteric Ischemia. The therapeutic goal in patients with chronic mesenteric ischemia is to revascularize mesenteric circulation and prevent the development of bowel infarction. Mesenteric occlusive disease can be treated successfully by either transaortic endarterectomy or mesenteric artery bypass. Brunicardi_Ch23_p0897-p0980.indd 93227/02/19 4:14 PM 933ARTERIAL DISEASECHAPTER 23Transaortic endarterectomy is indicated for ostial lesions of pat-ent CA and SMA. A left


Surgery_Schwartz

Surgery_Schwartz. artery bypass. Brunicardi_Ch23_p0897-p0980.indd 93227/02/19 4:14 PM 933ARTERIAL DISEASECHAPTER 23Transaortic endarterectomy is indicated for ostial lesions of pat-ent CA and SMA. A left medial rotation is performed, and the aorta and the mesenteric branches are exposed. A lat-eral aortotomy is performed encompassing both the CA and SMA orifices. The visceral arteries must be adequately mobi-lized so that the termination site of endarterectomy can be visu-alized. Otherwise, an intimal flap may develop, which can lead to early thrombosis or distal embolization.For occlusive lesions located 1 to 2 cm distal to the mes-enteric origin, mesenteric artery bypass should be performed. Multiple mesenteric arteries are typically involved in chronic mesenteric ischemia, and both the CA and SMA should be revascularized whenever possible. In general, bypass grafting may be performed either antegrade from the supraceliac aorta or retrograde from either the infrarenal aorta or iliac artery. Both


Surgery_Schwartz

Surgery_Schwartz. be revascularized whenever possible. In general, bypass grafting may be performed either antegrade from the supraceliac aorta or retrograde from either the infrarenal aorta or iliac artery. Both autogenous saphenous vein grafts and prosthetic grafts have been used with satisfactory and equivalent success. An antegrade bypass also can be performed using a small-caliber bifurcated graft from the supraceliac aorta to both the CA and SMA, which yields an excellent long-term result.93Celiac Artery Compression Syndrome. The decision to intervene in patients with CA compression syndrome should be based on both an appropriate symptom complex and the finding of celiac artery compression in the absence of other findings to explain the symptoms. The treatment goal is to release the ligamentous structure that compresses the proximal CA and to correct any persistent stricture by bypass grafting. Some sur-geons advocate careful celiac plexus sympathectomy in addition to arcuate ligament


Surgery_Schwartz

Surgery_Schwartz. structure that compresses the proximal CA and to correct any persistent stricture by bypass grafting. Some sur-geons advocate careful celiac plexus sympathectomy in addition to arcuate ligament decompression to ensure good treatment outcome.102 The patient should be cautioned that relief of the celiac compression cannot be guaranteed to relieve the symp-toms. In a number of reports on endovascular management of chronic mesenteric ischemia, the presence of CA compres-sion syndrome has been identified as a major factor of techni-cal failure and recurrence. Therefore, angioplasty and stenting should not be undertaken if extrinsic compression of the CA by the median arcuate ligament is suspected based on preop-erative imaging studies. Open surgical treatment should be performed instead. A study that analyzed the outcome of lapa-roscopic and open median arcuate ligament release cases in the literature showed both approaches to be effective in symptom relief (85%), with no difference in


Surgery_Schwartz

Surgery_Schwartz. study that analyzed the outcome of lapa-roscopic and open median arcuate ligament release cases in the literature showed both approaches to be effective in symptom relief (85%), with no difference in late symptom recurrence rate (6.8% in the open group and 5.7% in the laparoscopic group).94Endovascular TreatmentChronic Mesenteric Ischemia. Endovascular treatment of mesenteric artery stenosis or short segment occlusion by bal-loon dilatation or stent placement represents a less invasive therapeutic alternative to open surgical intervention, particu-larly in patients whose medical comorbidities place them at a high operative risk category. Endovascular therapy is also suited in patients with recurrent disease or anastomotic steno-sis following previous open mesenteric revascularization. Pro-phylactic mesenteric revascularization is rarely performed in the asymptomatic patient undergoing an aortic procedure for other indications. However, the natural history of untreated chronic


Surgery_Schwartz

Surgery_Schwartz. Pro-phylactic mesenteric revascularization is rarely performed in the asymptomatic patient undergoing an aortic procedure for other indications. However, the natural history of untreated chronic mesenteric ischemia may justify revascularization in some minimally symptomatic or asymptomatic patients if the operative risks are acceptable, since the first clinical presenta-tion may be acute intestinal ischemia in as many as 50% of the patients, with a mortality rate that ranges from 15% to 70%.95 3This is particularly true when the SMA is involved. Mesenteric angioplasty and stenting is particularly suitable for this patient subgroup given its low morbidity and mortality. Because of the limited experience with stent use in mesenteric vessels, appro-priate indications for primary stent placement have not been clearly defined. Guidelines generally include calcified ostial stenoses, high-grade eccentric stenoses, chronic occlusions, and significant residual stenosis >30% or the presence of


Surgery_Schwartz

Surgery_Schwartz. have not been clearly defined. Guidelines generally include calcified ostial stenoses, high-grade eccentric stenoses, chronic occlusions, and significant residual stenosis >30% or the presence of dissection after angioplasty. Restenosis after PTA is also an indication for stent placement.96Acute Mesenteric Ischemia. Catheter-directed thrombo-lytic therapy is a potentially useful treatment modality for acute mesenteric ischemia, which can be initiated with intra-arterial delivery of thrombolytic agent into the mesenteric thrombus at the time of diagnostic angiography. Various thrombolytic medi-cations, including urokinase (Abbokinase; Abbott Laboratory, North Chicago, IL) or recombinant tissue plasminogen acti-vator (Activase; Genentech, South San Francisco, CA), have been reported to be successful in a small series of case reports. Catheter-directed thrombolytic therapy has a higher probabil-ity of restoring mesenteric blood flow success when performed within 12 hours of symptom


Surgery_Schwartz

Surgery_Schwartz. be successful in a small series of case reports. Catheter-directed thrombolytic therapy has a higher probabil-ity of restoring mesenteric blood flow success when performed within 12 hours of symptom onset. Successful resolution of a mesenteric thrombus will facilitate the identification of the underlying mesenteric occlusive disease process. As a result, subsequent operative mesenteric revascularization or mesen-teric balloon angioplasty and stenting may be performed elec-tively to correct the mesenteric stenosis. There are two main drawbacks with regard to thrombolytic therapy in mesenteric ischemia. Percutaneous catheter-directed thrombolysis does not allow the possibility to inspect the potentially ischemic intes-tine following restoration of the mesenteric flow. Additionally, a prolonged period of time may be necessary in order to achieve successful catheter-directed thrombolysis, due in part to serial angiographic surveillance to document thrombus resolution. An incomplete or


Surgery_Schwartz

Surgery_Schwartz. period of time may be necessary in order to achieve successful catheter-directed thrombolysis, due in part to serial angiographic surveillance to document thrombus resolution. An incomplete or unsuccessful thrombolysis may lead to delayed operative revascularization, which may further necessitate bowel resection for irreversible intestinal necrosis. Therefore, catheter-directed thrombolytic therapy for acute mesenteric ischemia should only be considered in selected patients under a closely scrutinized clinical protocol.Nonocclusive Mesenteric Ischemia. The treatment of non-occlusive mesenteric ischemia is primarily pharmacologic with selective mesenteric arterial catheterization followed by infu-sion of vasodilatory agents, such as tolazoline or papaverine. Once the diagnosis is made on the mesenteric arteriography (see Fig. 23-42), intra-arterial papaverine is given at a dose of 30 to 60 mg/h. This must be coupled with the cessation of other vaso-constricting agents. Concomitant


Surgery_Schwartz

Surgery_Schwartz. on the mesenteric arteriography (see Fig. 23-42), intra-arterial papaverine is given at a dose of 30 to 60 mg/h. This must be coupled with the cessation of other vaso-constricting agents. Concomitant intravenous heparin should be administered to prevent thrombosis in the cannulated vessels. Treatment strategy thereafter is dependent on the patient’s clini-cal response to the vasodilator therapy. If abdominal symptoms improve, mesenteric arteriography should be repeated to docu-ment the resolution of vasospasm. The patient’s hemodynamic status must be carefully monitored during papaverine infusion as significant hypotension can develop in the event that the infu-sion catheter migrates into the aorta, which can lead to systemic circulation of papaverine. Surgical exploration is indicated if the patient develops signs of continued bowel ischemia or infarction as evidenced by rebound tenderness or involuntary guarding. In these circumstances, papaverine infusion should be contin-ued


Surgery_Schwartz

Surgery_Schwartz. if the patient develops signs of continued bowel ischemia or infarction as evidenced by rebound tenderness or involuntary guarding. In these circumstances, papaverine infusion should be contin-ued intraoperatively and postoperatively. The operating room Brunicardi_Ch23_p0897-p0980.indd 93327/02/19 4:14 PM 934SPECIFIC CONSIDERATIONSPART IIshould be kept as warm as possible, and warm irrigation fluid and laparotomy pads should be used to prevent further intestinal vasoconstriction during exploration.Techniques of Endovascular Interventions. To perform endovascular mesenteric revascularization, intraluminal access is performed via a femoral or brachial artery approach. Once an introducer sheath is placed in the femoral artery, an anteroposte-rior and lateral aortogram just below the level of the diaphragm is obtained with a pigtail catheter to identify the origin of the CA and SMA. Initial catheterization of the mesenteric artery can be performed using a variety of selective angled


Surgery_Schwartz

Surgery_Schwartz. of the diaphragm is obtained with a pigtail catheter to identify the origin of the CA and SMA. Initial catheterization of the mesenteric artery can be performed using a variety of selective angled catheters, which include the RDC, Cobra-2, Simmons I (Boston Scientific/Meditech, Natick, MA), or SOS Omni catheter (Angiodynam-ics, Queensbury, NY). Once the mesenteric artery is cannulated, systemic heparin (5000 IU) is administered intravenously. A selective mesenteric angiogram is then performed to identify the diseased segment, which is followed by the placement of a 0.035-inch or less traumatic 0.014to 0.018-inch guidewire to cross the stenotic lesion. Once the guidewire is placed across the stenosis, the catheter is carefully advanced over the guide-wire across the lesion. In the event that the mesenteric artery is severely angulated as it arises from the aorta, a second stiffer guidewire (Amplatz or Rosen Guidewire, Boston Scientific) may be exchanged through the catheter to


Surgery_Schwartz

Surgery_Schwartz. event that the mesenteric artery is severely angulated as it arises from the aorta, a second stiffer guidewire (Amplatz or Rosen Guidewire, Boston Scientific) may be exchanged through the catheter to facilitate the place-ment of a 6-French guiding sheath (Pinnacle, Boston Scientific).With the image intensifier angled in a lateral position to fully visualize the proximal mesenteric segment, a balloon angioplasty is advanced over the guidewire through the guiding sheath and positioned across the stenosis. The balloon diameter should be chosen based on the vessel size of the adjacent nor-mal mesenteric vessel. Once balloon angioplasty is completed, a postangioplasty angiogram is necessary to document the proce-dural result. Radiographic evidence of either residual stenosis or mesenteric artery dissection constitutes suboptimal angioplasty results that warrants mesenteric stent placement. Moreover, ath-erosclerotic involvement of the proximal mesenteric artery or vessel orifice should be


Surgery_Schwartz

Surgery_Schwartz. dissection constitutes suboptimal angioplasty results that warrants mesenteric stent placement. Moreover, ath-erosclerotic involvement of the proximal mesenteric artery or vessel orifice should be treated with balloon-expandable stent placement. These stents can be placed over a low-profile 0.014or 0.018-inch guidewire system. It is preferable to deliver the balloon-mounted stent through a guiding sheath, which is posi-tioned just proximal to the mesenteric orifice while the balloon-mounted stent is advanced across the stenosis. The stent is next deployed by expanding the angioplasty balloon to its designated inflation pressure. The balloon is then deflated and carefully withdrawn through the guiding sheath.Completion angiogram is performed by hand injecting a small volume of contrast though the guiding sheath. It is criti-cal to maintain the guidewire access until satisfactory comple-tion angiogram is obtained. If the completion angiogram reveals suboptimal radiographic results, such


Surgery_Schwartz

Surgery_Schwartz. the guiding sheath. It is criti-cal to maintain the guidewire access until satisfactory comple-tion angiogram is obtained. If the completion angiogram reveals suboptimal radiographic results, such as residual stenosis or dis-section, additional catheter-based intervention can be performed through the same guidewire. These interventions may include repeat balloon angioplasty for residual stenosis or additional stent placement for mesenteric artery dissection. During the procedure, intra-arterial infusion of papaverine or nitroglycerine can be used to decrease vasospasm. Administration of antiplatelet agents is also recommended for at least 6 months or even indefinitely if other risk factors of cardiovascular disease are present.Complications of Endovascular Treatment. Complica-tions are not common and rarely become life threatening. These include access site thrombosis, hematomas, and infection. Dissection can occur during PTA and is managed with place-ment of a stent. Balloon-mounted


Surgery_Schwartz

Surgery_Schwartz. common and rarely become life threatening. These include access site thrombosis, hematomas, and infection. Dissection can occur during PTA and is managed with place-ment of a stent. Balloon-mounted stents are preferred over the self-expanding ones because of the higher radial force and the more precise placement. Distal embolization has also been reported, but it never resulted in acute intestinal ischemia, likely due to the rich network of collaterals already developed.Clinical Results of Interventions for Mesenteric IschemiaThe first successful percutaneous angioplasty of the SMA was reported in 1980.97 Since 1995, multiple series and scattered case reports have reported results from endovascular manage-ment of mesenteric occlusive disease.92,96 A literature review by AbuRahma and colleagues in 2003 showed that endovascu-lar intervention had an overall technical success rate of 91%, early and late pain relief rates of 84% and 71%, respectively, and 30-day morbidity and mortality


Surgery_Schwartz

Surgery_Schwartz. in 2003 showed that endovascu-lar intervention had an overall technical success rate of 91%, early and late pain relief rates of 84% and 71%, respectively, and 30-day morbidity and mortality rates of 16.4% and 4.3%, respectively. The average patency was 63% during an average 26-month follow-up.98In our review of the literature from published series since 1995, restenosis developed in 22% of patients during 24.5 months of average follow-up.92 The long-term clinical relief without reintervention was 82%. Among the patients who experienced a technical failure, 15 were ultimately diagnosed with median arcuate ligament syndrome and underwent suc-cessful surgical treatment, an observation that emphasizes the need for careful patient selection. Interestingly, the addition of selective stenting after PTA that was started in 1998, while it slightly increases the technical success rate, is not correlated with any substantial overall clinical benefit or improved long-term patency rates.In


Surgery_Schwartz

Surgery_Schwartz. after PTA that was started in 1998, while it slightly increases the technical success rate, is not correlated with any substantial overall clinical benefit or improved long-term patency rates.In contrast to endovascular treatment, open surgical tech-niques have achieved an immediate clinical success rate that approaches 100%, a surgical mortality rate of 0% to 17%, and an operative morbidity rate that ranges from 19% to 54% in a number of different series.89,93,99 AbuRahma and colleagues reported their experience of endovascular interventions of 22 patients with symptomatic mesenteric ischemia due to either SMA or CA stenosis.98 They noted an excellent initial technical and clinical success rates, which were 96% (23 of 24 patients) and 95% (21 of 22 patients), respectively, with no periopera-tive mortality or major morbidity. During a mean follow-up of 26 months (range, 1–54 months), the primary late clinical suc-cess rate was 61%, and freedom from recurrent stenosis was 30%. The


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Surgery_Schwartz. mortality or major morbidity. During a mean follow-up of 26 months (range, 1–54 months), the primary late clinical suc-cess rate was 61%, and freedom from recurrent stenosis was 30%. The freedom from recurrent stenosis rates at 1, 2, 3, and 4 years were 65%, 47%, 39%, and 13%, respectively. The authors concluded that mesenteric stenting, which provides excellent early results, is associated with a relative high inci-dence of late restenosis.Several studies have attempted to compare the endovas-cular with the standard open surgical approach.89,100 The results of the open surgery appear to be more durable, but it tends to be associated with higher morbidity and mortality rates and an overall longer hospital stay. In one study that compared the clin-ical outcome of open revascularization with percutaneous stent-ing for patients with chronic mesenteric ischemia, 28 patients underwent endovascular treatment and 85 patients underwent open mesenteric bypass grafting.99 With both patient


Surgery_Schwartz

Surgery_Schwartz. with percutaneous stent-ing for patients with chronic mesenteric ischemia, 28 patients underwent endovascular treatment and 85 patients underwent open mesenteric bypass grafting.99 With both patient cohorts having similar baseline comorbidities and symptom duration, there was no difference in early in-hospital complication or mortality rates. Moreover, both groups had similar 3-year cumu-lative recurrent stenosis and mortality rates. However, patients Brunicardi_Ch23_p0897-p0980.indd 93427/02/19 4:14 PM 935ARTERIAL DISEASECHAPTER 23treated with mesenteric stenting had a significantly higher inci-dence of recurrent symptoms. The authors concluded that opera-tive mesenteric revascularization should be offered to patients with low surgical risk.Based on the above results one could argue that mesen-teric angioplasty and stenting demonstrate an inferior technical and clinical success rate. Long-term patency rates appear to also be superior with the open technique. There is a general


Surgery_Schwartz

Surgery_Schwartz. that mesen-teric angioplasty and stenting demonstrate an inferior technical and clinical success rate. Long-term patency rates appear to also be superior with the open technique. There is a general con-sensus, however, that the endovascular approach is associated with lower morbidity and mortality rates and is therefore more suitable for high-risk patients. One should also keep in mind that practices representing standard of care for stent placement today were absent in the early era of endovascular experience. These include perioperative heparinization and short-term anti-platelet therapy, use of stents with higher radial force, routine use of postoperative surveillance with arterial duplex and early reintervention to prevent a high-grade stenosis from progressing to occlusion, and placement of drug-eluting stents. One such example is a recent nonrandomized study to compare the out-comes of mesenteric angioplasty using covered stents or bare metal stents in patients undergoing


Surgery_Schwartz

Surgery_Schwartz. placement of drug-eluting stents. One such example is a recent nonrandomized study to compare the out-comes of mesenteric angioplasty using covered stents or bare metal stents in patients undergoing primary or reintervention for chronic mesenteric ischemia. The study showed that covered stents are associated with less restenosis (18% vs. 47%), symp-tom recurrence (18% vs. 50%), and reintervention (9% vs. 44%) at 24 months and better primary patency at 3 years (92% vs. 52%) than bare metal stents in the primary intervention group.101 Similar results were found in the reintervention group as well.RENAL ARTERY DISEASEObstructive lesions of the renal artery can produce hypertension, resulting in a condition known as renovascular hypertension, which is the most common form of hypertension amenable to therapeutic intervention, and affects 5% to 10% of all hyperten-sive patients in the United States.102 Patients with renovascular hypertension are at an increased risk for irreversible


Surgery_Schwartz

Surgery_Schwartz. amenable to therapeutic intervention, and affects 5% to 10% of all hyperten-sive patients in the United States.102 Patients with renovascular hypertension are at an increased risk for irreversible end-organ dysfunction, including permanent kidney damage, if inadequate pharmacologic therapies are used to control the blood pressure. The majority of patients with renal artery obstructive disease have vascular lesions of either atherosclerotic disease or fibro-dysplasia involving the renal arteries. The proximal portion of the renal artery represents the most common location for the development of atherosclerotic disease. It is well established that renal artery intervention, either by surgical or endovascular revascularization, provides an effective treatment for controlling renovascular hypertension as well as preserving renal function. The decision for intervention is complex and needs to consider a variety of anatomic, physiologic, and clinical features, unique for the individual


Surgery_Schwartz

Surgery_Schwartz. hypertension as well as preserving renal function. The decision for intervention is complex and needs to consider a variety of anatomic, physiologic, and clinical features, unique for the individual patient.EtiologyApproximately 80% of all renal artery occlusive lesions are caused by atherosclerosis, which typically involves a short seg-ment of the renal artery ostia and represents spillover disease from a severely atheromatous aorta (Fig. 23-43).102 Atheroscle-rotic lesions are bilateral in two thirds of patients. Individuals with this disease commonly present during the sixth decade of life. Men are affected twice as frequently as women. Atheroscle-rotic lesions in other territories such as the coronary, mesenteric, cerebrovascular, and peripheral arterial circulation are common. When a unilateral lesion is present, the disease process equally affects the right and left renal arteries.Figure 23-43. Occlusive disease of the renal artery typically involves the renal ostium (arrow) as


Surgery_Schwartz

Surgery_Schwartz. unilateral lesion is present, the disease process equally affects the right and left renal arteries.Figure 23-43. Occlusive disease of the renal artery typically involves the renal ostium (arrow) as a spillover plaque extension from aortic atherosclerosis.The second most common cause of renal artery stenosis is FMD, which accounts for 20% of cases and is most frequently encountered in young, often multiparous women. FMD of the renal artery represents a heterogeneous group of lesions that can produce histopathologic changes in the intima, media, or adventitia. The most common variety consists of medial fibro-plasia, in which thickened fibromuscular ridges alternate with attenuated media producing the classic angiographic “string of beads” appearance (Figs. 23-44 and 23-45). The cause of medial fibroplasia remains unclear. Most common theories involve a modification of arterial smooth muscle cells in response to Figure 23-44. Abdominal aortogram reveals a left renal artery fibromuscular


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Surgery_Schwartz. fibroplasia remains unclear. Most common theories involve a modification of arterial smooth muscle cells in response to Figure 23-44. Abdominal aortogram reveals a left renal artery fibromuscular dysplasia (arrows) with a characteristic “string of beads” appearance.Brunicardi_Ch23_p0897-p0980.indd 93527/02/19 4:14 PM 936SPECIFIC CONSIDERATIONSPART IIFigure 23-45. Magnetic resonance angiography of the abdominal aorta reveals the presence of a left renal artery fibromuscular dys-plasia (arrows).estrogenic stimuli during the reproductive years, unusual trac-tion forces on affected vessels, and mural ischemia from impair-ment of vasa vasorum blood flow. Fibromuscular hyperplasia usually affects the distal two thirds of the main renal artery, and the right renal artery is affected more frequently than the left. Other less common causes of renal artery stenosis include renal artery aneurysm (compressing the adjacent normal renal artery), arteriovenous malformations, neurofibromatosis,


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Surgery_Schwartz. than the left. Other less common causes of renal artery stenosis include renal artery aneurysm (compressing the adjacent normal renal artery), arteriovenous malformations, neurofibromatosis, renal artery dissections, renal artery trauma, Takayasu’s arteritis, and renal arteriovenous fistula.Clinical ManifestationsRenovascular hypertension is the most common sequela of renal artery occlusive disease. Its prevalence varies from 2% in patients with diastolic blood pressure greater than 100 mmHg to almost 30% in those with diastolic blood pressure over 125 mmHg.103 Clinical features that may indicate the presence of renovascular hypertension include the following: (a) systolic and diastolic upper abdominal bruits; (b) diastolic hypertension of greater than 115 mmHg; (c) rapid onset of hypertension after the age of 50 years; (d) a sudden worsening of mild to moder-ate essential hypertension; (e) hypertension that is difficult to control with three or more antihypertensives; (f)


Surgery_Schwartz

Surgery_Schwartz. of hypertension after the age of 50 years; (d) a sudden worsening of mild to moder-ate essential hypertension; (e) hypertension that is difficult to control with three or more antihypertensives; (f) development of renal insufficiency after angiotensin-converting enzyme inhibi-tors; and (g) development of hypertension during childhood.103All patients with significant hypertension, especially ele-vated diastolic blood pressure, must be considered as suspect for renovascular disease. Young adults with hypertension have a great deal to gain by avoiding lifelong treatment if renovascular hypertension is diagnosed and corrected. Appropriate diagnostic studies and intervention must be timely instituted to detect the possibility of renovascular hypertension in patients with pri-mary hypertension who present for clinical evaluation.Diagnostic EvaluationThe diagnostic requisites for renovascular hypertension include both hypertension and renal artery stenosis. Impairment of the renal function


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Surgery_Schwartz. who present for clinical evaluation.Diagnostic EvaluationThe diagnostic requisites for renovascular hypertension include both hypertension and renal artery stenosis. Impairment of the renal function may coexist, although the occurrence of renal insufficiency prior to the development of hypertension is uncommon. Nearly all diagnostic studies for renovascular hypertension evaluate either the anatomic stenosis or renal parenchymal dysfunction attributed to the stenosis. The follow-ing section provides an overview of the strengths and limitations of the most common tests used in the diagnostic evaluation of the patient with suspected renovascular hypertension prior to intervention.Captopril renal scanning is a functional study that assesses renal perfusion before and after administration of the angioten-sin-converting enzyme inhibitor captopril. Captopril inhibits the secretion of angiotensin II. Through this mechanism, it reduces the efferent arteriole vasoconstriction and, as a result,


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Surgery_Schwartz. angioten-sin-converting enzyme inhibitor captopril. Captopril inhibits the secretion of angiotensin II. Through this mechanism, it reduces the efferent arteriole vasoconstriction and, as a result, the glo-merular filtration rate (GFR). The test consists of a baseline renal scan and a second renal scan after captopril administra-tion. A positive result indicates that captopril administration (a) increases the time to peak activity to more than 11 minutes or (b) the GFR ratio between sides increases to greater than 1.5:1 compared to a normal baseline scan. Significant parenchymal disease limits the reliability of this study.Renal artery duplex ultrasonography is a noninvasive test of assessing renal artery stenosis both by visualization of the vessel and measurement of the effect of stenosis on blood flow velocity and waveforms. The presence of a severe renal artery stenosis correlates with peak systolic velocities of greater than 180 cm/s and the ratio of these velocities to those in


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Surgery_Schwartz. on blood flow velocity and waveforms. The presence of a severe renal artery stenosis correlates with peak systolic velocities of greater than 180 cm/s and the ratio of these velocities to those in the aorta of greater than 3.5 (Table 23-11). Renal artery duplex is a techni-cally demanding exam, requiring a substantial amount of opera-tor expertise. In addition, the presence of bowel gas and obesity make the exam difficult to perform and interpret. However, in experienced hands and with appropriate patient selection, it can be a high-yield exam and is typically the initial screening test for patients with suspected renal artery occlusive disease.Selective catheterization of the renal vein via a femoral vein approach for assessing renin activity is a more invasive test of detecting the physiologic sequelae of renal artery stenosis. If unilateral disease is present, the affected kidney should secrete high levels of renin while the contralateral kidney should have low renin production. A


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Surgery_Schwartz. sequelae of renal artery stenosis. If unilateral disease is present, the affected kidney should secrete high levels of renin while the contralateral kidney should have low renin production. A ratio between the two kidneys, or the renal vein renin ratio (RVRR), of greater than 1.5 is indica-tive of functionally important renovascular hypertension, and it also predicts a favorable response from renovascular revascu-larization. Since this study assesses the ratio between the two kidneys, it is not useful in patients with bilateral disease because both kidneys may secrete abnormally elevated renin levels.The renal:systemic renin index (RSRI) is calculated by subtracting systemic renin activity from individual renal vein renin activity and dividing the remainder by systemic renin activity. This value represents the contribution of each kidney to renin production. In the absence of renal artery stenosis, the Table 23-11Renal duplex diagnostic criteriaRENAL ARTERY DIAMETER REDUCTIONRENAL


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Surgery_Schwartz. value represents the contribution of each kidney to renin production. In the absence of renal artery stenosis, the Table 23-11Renal duplex diagnostic criteriaRENAL ARTERY DIAMETER REDUCTIONRENAL ARTERY PSVRARNormal<180 cm/s<3.5<60%≥180 cm/s<3.5≥60%≥180 cm/s≥3.5OcclusionNo signalNo signalPSV = peak systolic velocity; RAR = renal-to-aortic ratio.Brunicardi_Ch23_p0897-p0980.indd 93627/02/19 4:14 PM 937ARTERIAL DISEASECHAPTER 23renal vein renin activity from each kidney is typically 24% or 0.24 higher than the systemic level. As the result, the total of both kidneys’ renin activity is usually 48% greater than the sys-temic activity, a value that represents a steady state of renal renin activity. The RSRI of the affected kidney in patients with renovascular hypertension is greater than 0.24. In the case of unilateral renal artery stenosis with normal contralateral kid-ney, the increase in ipsilateral renin release is normally balanced by suppression of the contralateral kidney renin


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Surgery_Schwartz. In the case of unilateral renal artery stenosis with normal contralateral kid-ney, the increase in ipsilateral renin release is normally balanced by suppression of the contralateral kidney renin production, which results in a drop in its RSRI to less than 0.24. Bilateral renal artery disease may negate the contralateral compensatory response, and the autonomous release of renin from both dis-eased kidneys may result in the sum of the individual RSRIs to be considerably greater than 0.48. The prognostic value of RSRI remains limited in that approximately 10% of patients with favorable clinical response following renovascular revas-cularization do not exhibit contralateral renin suppression. As a result, the use of RSRI must be applied with caution in the management of patients with renovascular hypertension.MRA with intravenous gadolinium contrast enhancement has been increasingly used for renal artery imaging because of its ability to provide high-resolution images (Figs. 23-46 and


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Surgery_Schwartz. hypertension.MRA with intravenous gadolinium contrast enhancement has been increasingly used for renal artery imaging because of its ability to provide high-resolution images (Figs. 23-46 and 23-47) while using a minimally nephrotoxic agent. Flow void may be inaccurately interpreted as occlusion or stenosis in MRA. Therefore, unless the quality of the image analysis soft-ware is superior, MRA should be interpreted with caution and used in conjunction with other modalities prior to making plans for operative or endovascular treatment.DSA remains the gold standard to assess renal artery occlusive disease. A flush aortogram is performed first so that any accessory renal arteries can be detected and the origins of all the renal arteries are adequately displayed. The presence of collateral vessels circumventing a renal artery stenosis strongly supports the hemodynamic importance of the stenosis. A pres-sure gradient of 10 mmHg or greater is necessary for collateral Figure 23-46. Magnetic


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Surgery_Schwartz. circumventing a renal artery stenosis strongly supports the hemodynamic importance of the stenosis. A pres-sure gradient of 10 mmHg or greater is necessary for collateral Figure 23-46. Magnetic resonance angiography of the abdominal aorta reveals bilateral normal renal arteries.Figure 23-47. Magnetic resonance angiography of the abdominal aorta reveals bilateral ostial renal artery stenosis (arrows).vessel development, which is also associated with activation of the renin-angiotensin cascade.Treatment IndicationsThe therapeutic goals in patients with renovascular disease include: (a) improved blood pressure control, in order to prevent end-organ damage on systems such as the cerebral, coronary, pulmonary, and peripheral circulations; and (b) preservation and possibly improvement of the renal function (Table 23-12).Table 23-12Indications for renal artery revascularizationAngiography Criteria• Documented renal artery stenosis (>70% diameter reduction)• Fibromuscular dysplasia


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Surgery_Schwartz. of the renal function (Table 23-12).Table 23-12Indications for renal artery revascularizationAngiography Criteria• Documented renal artery stenosis (>70% diameter reduction)• Fibromuscular dysplasia lesion• Pressure gradient >20 mmHg• Affected/unaffected kidney renin ratio >1.5 to 1Clinical Criteria• Refractory or rapidly progressive hypertension• Hypertension associated with flash pulmonary edema without coronary artery disease• Rapidly progressive deterioration in renal function• Intolerance to antihypertensive medications• Chronic renal insufficiency related to bilateral renal artery occlusive disease or stenosis to a solitary functioning kidney• Dialysis-dependent renal failure in a patient with renal artery stenosis but without another definite cause of end-stage renal disease• Recurrent congestive heart failure or flash pulmonary edema not attributable to active coronary ischemiaBrunicardi_Ch23_p0897-p0980.indd 93727/02/19 4:14 PM 938SPECIFIC CONSIDERATIONSPART IIThe


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Surgery_Schwartz. congestive heart failure or flash pulmonary edema not attributable to active coronary ischemiaBrunicardi_Ch23_p0897-p0980.indd 93727/02/19 4:14 PM 938SPECIFIC CONSIDERATIONSPART IIThe indications for endovascular treatment for renal artery occlusive disease include 70% or greater stenosis of one or both renal arteries and at least one of the following clinical criteria:• Inability to adequately control hypertension despite appropri-ate antihypertensive regimen.• Chronic renal insufficiency related to bilateral renal artery occlusive disease or stenosis to a solitary functioning kidney.• Dialysis-dependent renal failure in a patient with renal artery stenosis but without another definite cause of end-stage renal disease.• Recurrent congestive heart failure or flash pulmonary edema not attributable to active coronary ischemia.Prior to 1990, the most common treatment modality in patients with renal artery occlusive disease is surgical revascu-larization, with either renal artery


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Surgery_Schwartz. not attributable to active coronary ischemia.Prior to 1990, the most common treatment modality in patients with renal artery occlusive disease is surgical revascu-larization, with either renal artery bypass grafting or renal artery endarterectomy. The advancement of endovascular therapy in the past decade has led to various minimally invasive treatment strategies such as renal artery balloon angioplasty or stenting to control hypertension or to preserve renal function.Surgical ReconstructionThe typical approach for surgical renal artery revasculariza-tion involves a midline xiphoid-to-pubis incision. The posterior peritoneum is incised, and the duodenum is mobilized to the right, starting at the ligament of Treitz. The left renal hilum can be exposed by extending the retroperitoneal dissection to the left along the avascular plane along the inferior border of the pancreas. Mobilization of the left renal vein is essential in these cases and can be achieved by dividing the gonadal,


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Surgery_Schwartz. to the left along the avascular plane along the inferior border of the pancreas. Mobilization of the left renal vein is essential in these cases and can be achieved by dividing the gonadal, ilio-lumbar, and adrenal veins. The proximal portion of the right renal artery can be exposed through the base of the mesentery by retraction of the left renal vein cephalad and the vena cava to the right. Accessing the most distal portion of the right renal artery requires a Kocher maneuver and duodenal mobiliza-tion. Another approach useful for treating bilateral renal artery lesions involves mobilization of the entire small bowel and the right colon, with a dissection that starts at the ligament of Treitz and proceeds toward the cecum and then along the line of Todd in the right paracolic gutter. Simultaneous dissection along the inferior border of the pancreas provides additional visualization of the left renal artery. Finally, division of the diaphragmatic crura that encircle the suprarenal


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Surgery_Schwartz. Simultaneous dissection along the inferior border of the pancreas provides additional visualization of the left renal artery. Finally, division of the diaphragmatic crura that encircle the suprarenal aorta may sometimes be neces-sary to achieve suprarenal clamping.Types of Surgical Reconstruction. Aortorenal bypass is the most frequently performed reconstruction of ostial occlu-sive renal artery disease. After proximal and distal control is obtained, an elliptical segment of the aorta is excised, and the proximal anastomosis is performed in end-to-side fashion. Autologous vein is the preferred conduit. If the vein is not suit-able, then prosthetic material can be used. An end-to-end anas-tomosis is then performed between the conduit of choice and the renal artery using either a 6-0 or 7-0 polypropylene suture. The length of the arteriotomy needs to be at least three times the diameter of the renal artery to prevent anastomotic restenosis. In the event that the surgeon plans to perform


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Surgery_Schwartz. polypropylene suture. The length of the arteriotomy needs to be at least three times the diameter of the renal artery to prevent anastomotic restenosis. In the event that the surgeon plans to perform a side-to-side anasto-mosis between the conduit and the renal artery, this is performed first, and the aortic anastomosis follows.Endarterectomy, either transrenal or transaortic, is an alter-native to bypass for short ostial lesions or in patients with mul-tiple renal arteries. The transrenal endarterectomy is performed with a transverse longitudinal incision on the aorta that extends into the diseased renal artery. After plaque removal, the arteri-otomy is closed with a prosthetic patch. Transaortic endarter-ectomy is well suited for patients with multiple renal arteries and short ostial lesions. The aorta is opened longitudinally and aortic sleeve endarterectomy is performed, followed by ever-sion endarterectomy of the renal arteries. Adequate mobiliza-tion of the renal arteries is


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Surgery_Schwartz. lesions. The aorta is opened longitudinally and aortic sleeve endarterectomy is performed, followed by ever-sion endarterectomy of the renal arteries. Adequate mobiliza-tion of the renal arteries is essential for a safe and complete endarterectomy.Hepatorenal and splenorenal bypass are alternative options of revascularization for patients who might not tolerate aortic clamping or for those with calcified aorta that precludes ade-quate control. For hepatorenal bypass, a right subcostal inci-sion is used, and the hepatic artery is exposed with an incision in the lesser omentum. A Kocher maneuver is performed, the right renal vein is identified and mobilized, and the right renal artery is identified and controlled posteriorly to the vein. Greater saphenous vein is the conduit of choice. The anastomosis is per-formed end-to-side with the common hepatic artery, and end-to-end with the renal artery anterior to the inferior vena cava. The splenorenal bypass is performed via a left subcostal


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Surgery_Schwartz. anastomosis is per-formed end-to-side with the common hepatic artery, and end-to-end with the renal artery anterior to the inferior vena cava. The splenorenal bypass is performed via a left subcostal inci-sion. The splenic artery is mobilized from the lesser sac, brought through a retropancreatic plane, and anastomosed end-to-end to the renal artery.Reimplantation of the renal artery is an attractive option of reconstruction in children or in adults with ostial lesions. A redundant renal artery is a prerequisite for the procedure. After mobilization, the artery is transected and spatulated, eversion endarterectomy is performed if necessary, and an end-to-side anastomosis with the aorta is created.Clinical Results of Surgical RepairResults reflect the need for performance of renal artery bypass in high-volume and experienced centers. In a review from a large tertiary center, 92% of the patients with nonatherosclerotic vascular disease had improvement in hypertension, but only 43% were


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Surgery_Schwartz. in high-volume and experienced centers. In a review from a large tertiary center, 92% of the patients with nonatherosclerotic vascular disease had improvement in hypertension, but only 43% were completely cured and taken off antihypertensives.104 Patients younger than age 45 fair better, with a cure rate of 68% and improvement rate of 32%. In patients with atherosclerotic renal artery disease, the cure rate was even smaller (12%), and the overall response to hypertension rate was 85%. The opera-tive mortality rates were 3.1% and 0% in the atherosclerotic and nonatherosclerotic groups, respectively.Renal function improvement occurs within the first week of the operation in approximately two-thirds of patients. A pro-gressive decrease in the GFR is seen after this initial improve-ment, but the rate of decrease is less compared with patients who did not respond at all to operative intervention. Up to three-quarters of patients were permanently removed from dialysis in a large series.105


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Surgery_Schwartz. the rate of decrease is less compared with patients who did not respond at all to operative intervention. Up to three-quarters of patients were permanently removed from dialysis in a large series.105 Favorable response of renal function to revas-cularization improves overall survival.Endovascular TreatmentEndovascular treatment of renal artery occlusive disease was first introduced by Grüntzig who successfully dilated a renal artery stenosis using a balloon catheter technique. This tech-nique requires passage of a guidewire under fluoroscopic control typically from a femoral artery approach to across the stenosis in the renal artery. A balloon dilating catheter is passed over the guidewire and positioned within the area of stenosis and inflated to produce a controlled disruption of the arterial wall. Alternatively, a balloon-mounted expandable stent can be used Brunicardi_Ch23_p0897-p0980.indd 93827/02/19 4:14 PM 939ARTERIAL DISEASECHAPTER 23to primarily dilate the renal artery


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Surgery_Schwartz. arterial wall. Alternatively, a balloon-mounted expandable stent can be used Brunicardi_Ch23_p0897-p0980.indd 93827/02/19 4:14 PM 939ARTERIAL DISEASECHAPTER 23to primarily dilate the renal artery stenosis. Completion angiog-raphy is usually performed to assess the immediate results. The technical aspect of an endovascular renal artery revasculariza-tion is discussed in the following section.Techniques of Renal Artery Angioplasty and Stenting. Access to the renal artery for endovascular intervention is typi-cally performed via a femoral artery approach, although a bra-chial artery approach can be considered in the event of severe aortoiliac occlusive disease, aortoiliac aneurysm, or severe cau-dal renal artery angulation. Once an introducer sheath is placed in the femoral artery, an aortogram is performed with a pigtail catheter placed in the suprarenal aorta. Additional oblique views are frequently necessary to more precisely visualize the orifice of the stenosed renal artery and


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Surgery_Schwartz. is performed with a pigtail catheter placed in the suprarenal aorta. Additional oblique views are frequently necessary to more precisely visualize the orifice of the stenosed renal artery and thoroughly assess the presence of accessory renal arteries. Noniodinated contrast agents, such as carbon dioxide and gadolinium, can be used in endovascular renal intervention in patients with renal dysfunction or history of allergic reaction.After systemic heparinization, catheterization of the renal artery can be performed using a variety of selective angled cath-eters, including the RDC, Cobra-2, Simmons I, or SOS Omni catheter. A selective renal angiogram is then performed to con-firm position, and the lesion is crossed with either 0.035-inch or a 0.018to 0.014-inch guidewires. It is important to main-tain the distal wire position without movement in the tertiary renal branches during guiding sheath placement to reduce the possibility of parenchymal perforation and spasm. A guiding sheath or


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Surgery_Schwartz. main-tain the distal wire position without movement in the tertiary renal branches during guiding sheath placement to reduce the possibility of parenchymal perforation and spasm. A guiding sheath or a guiding catheter is then advanced at the orifice of the renal artery and provides a secure access for balloon and stent deployment.Balloon angioplasty is performed with a balloon sized to the diameter of the normal renal artery adjacent to the stenosis. Choosing a balloon with diameter 4 mm is a reasonable first choice. The luminal diameter of the renal artery can be further assessed by comparing it to the fully inflated balloon. Such a comparison may provide a reference guide to determine whether renal artery dilatation with a larger diameter angioplasty balloon is necessary.Once balloon angioplasty of the renal artery is completed, an angiogram is performed to document the procedural result. Radiographic evidence of either residual stenosis or renal artery dissection constitutes