Acute Occlusive Mesenteric Ischemia: Surgical Management and Outcomes

Acute Occlusive Mesenteric Ischemia: Surgical Management and Outcomes Matthew S. Edwards, MD,1 Gregory S. Cherr, MD,1 Timothy E. Craven, MSPH,2 Amy W. Olsen, MD,1 George W. Plonk, MD,1 Randolph L. Geary, MD,1 John L. Ligush, MD,1 and Kimberley J. Hansen, MD,1 Winston-Salem, North Carolina

Acute mesenteric ischemia secondary to arterial occlusion (AMI) remains a highly lethal condition. To examine recent trends in management and associated outcomes, we examined our institutional experience over a recent 10-year period. All patients treated for AMI between January 1990 and January 2000 were identified (76 patients, 77 cases) and their medical records examined. At presentation, 64% demonstrated peritonitis and 30% exhibited hypotension. The interval from symptom onset to treatment exceeded 24 h in 63% of cases. Etiology was mesenteric thrombosis in 44 patients (58%) and embolism in 32 patients (42%). Thirty-five patients (46%) had prior conditions placing them at high risk for the development of AMI including chronic mesenteric ischemia (n = 26) and inadequately anticoagulated chronic atrial fibrillation (n = 9). Surgical management consisted of exploration alone in 16 patients, bowel resection alone in 18 patients, and revascularization in 43 patients, including 28 who required concomitant bowel resection. Overall, intestinal necrosis was present in 81% of cases. Perioperative mortality was 62% and long-term parenteral nutrition (TPN) was required in 31% of survivors. Peritonitis (odds ratio [OR] 9.4, 95% confidence interval [CI] 1.6, 54.0; p = 0.012) and bowel necrosis (OR 10.4, CI 1.9, 56.3; p = 0.007) at presentation were independent predictors of death or survival dependent upon TPN. We conclude that AMI remains a highly lethal condition due in large part to advanced presentation and inadequate recognition and treatment of patients at high risk.

INTRODUCTION Acute arterial occlusive mesenteric ischemia (AMI) has been recognized as a potential cause of abdom1 Division of Surgical Sciences, Section on Vascular Surgery, Wake Forest University School of Medicine, Winston-Salem, NC. 2 Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC. Presented at the Twenty-seventh Annual Meeting of the Peripheral Vascular Surgery Society, Boston, MA, June 8, 2002. Correspondence to: K.J. Hansen, MD, Department of General Surgery, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA, E-mail: kjhansen@wfubmc. edu.

Ann Vasc Surg 2003; 17: 72-79 DOI: 10.1007/s10016-001-0329-8 Ó Annals of Vascular Surgery Inc. Published online: 15 January 2003 72

inal catastrophe and death since 1875.1 Unfortunately, little has changed during the past 125 years to decrease the high rate of mortality associated with established acute ischemic events.2-12 These dismal rates of survival have been attributed to delays in definitive therapy leading to irreversible bowel ischemia and necrosis.3,12-14 Delays in treatment may be due to variable presentations, misdiagnoses, and lack of accurate tests for rapid diagnosis.3,13 Regardless of the cause, the high mortality associated with AMI is disconcerting, particularly when the incidence of AMI appears to be increasing secondary to the growing population of elderly patients with generalized atherosclerosis.2,13,15 This review examines our operative experience over a recent 10-year period and describes the eti-

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ology, presentation, management, and outcomes of patients with AMI. Questions of particular interest included (1) differences between patients with thrombotic versus embolic occlusions, (2) utility of the ‘‘second-look’’ laparotomy, and (3) predictors of morbidity, mortality, and postoperative dependence on parenteral nutrition (TPN).

METHODS Patient Information Patients treated at our medical center for acute mesenteric ischemia between January 1990 and January 2000 were identified by CPT and ICD-9 codes. Diagnoses were confirmed by angiography, pathologic exam, or operative findings in all cases. In patients not undergoing angiography, the etiology of mesenteric occlusion was considered to be thrombotic if there was extensive necrosis without proximal jejunal sparing and embolic if necrosis involved proximal jejunal sparing with or without termination of ischemia in the transverse colon. Patients experiencing nonocclusive mesenteric ischemia or mesenteric venous thrombosis were excluded from further analysis. Hospital, vascular laboratory, and follow-up clinic records were examined for all patients with AMI. Medical risk factors and complications were evaluated and reported according to previously published guidelines.16 Mortality and cause of death data were obtained from the medical record and from a National Death Index search. The National Death Index is a computerized database containing death record information from state vital statistics offices and, at the time of our search, contained information on deaths through December 31, 1998.17 Follow-up data were complete for all patients. Statistical Methods Data were examined for the entire cohort and by etiologic group (i.e., thrombotic versus embolic arterial occlusion). Univariate tests of association for categorical data were performed using a Pearson’s chi-squared or Fisher’s exact test where appropriate. Differences in continuous data were assessed using Student’s t-test. Multivariate analysis was performed using logistic regression techniques. A backward stepwise elimination technique was used with all factors of interest included in the first step. Factors not significant at a 0.10 a-level were sequentially eliminated until all remaining factors were significant at a 0.10 a-level. Survival was examined by means of life-table methods.18

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RESULTS Etiology One hundred two patients treated for acute mesenteric ischemia were identified including 76 with AMI (75%), 18 with nonocclusive mesenteric ischemia (17%), and 8 with mesenteric venous thrombosis (8%). One patient experienced two episodes of AMI. Based on angiographic and/or operative findings, the etiology of AMI was thrombotic occlusion in 44 patients (58%) and embolic occlusion in 32 patients (42%). Patient Characteristics Demographics and medical comorbidities are presented in Table I. The mean patient age was 68 ± 13 years and women (n = 53) outnumbered men (n = 23) in both etiologic groups. Overall, clinically apparent ischemic heart disease was present in 63%, diabetes mellitus in 28%, chronic renal insufficiency in 32%, chronic pulmonary disease in 61%, and a history of tobacco use in 68% of patients. There were no significant differences in demographics or medical comorbidities according to the etiology of AMI. Clinical Presentation Clinical presentation and time to treatment are summarized in Table II. Twenty-four patients (32%) presented primarily to our institution and 52 (68%) were referred from other institutions. Abdominal pain was the presenting complaint in all patients. At the time of initial evaluation by a surgeon at our center, peritonitis was evident in 49 patients (64%) and hypotension in 23 patients (30%). A presumptive diagnosis of mesenteric ischemia was rendered in 48 patients (62%) who then proceeded to angiography prior to operation. The remainder underwent exploratory laparotomy without angiography. Eight additional arteriograms were performed after the initial operation revealed acute mesenteric ischemia. The interval from onset of abdominal pain to operation exceeded 24 h in 48 patients (63%). Two patients had an interval to operation exceeding 24 h following admission to our center. Interval to treatment could not be accurately assessed in one patient because of severe dementia. When examined according to the etiology of arterial occlusion, there were no significant differences in the presence of peritonitis or hypotension, accuracy of the initial diagnosis, or interval to treatment (Table II). Antecedent complaints consistent with chronic mesenteric ischemia (CMI) were reported by 26

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Table I. Patient demographics and medical risk factors

Variable

Gender Male Female Age (years) Mean Range Race Caucasian African American Other Coronary artery disease Congestive failure History of tobacco use Diabetes mellitus Chronic renal insuciency Hypertension Carotid disease Chronic obstructive pulmonary disease

Total group (n = 76) [n (%)]

Patients with thrombotic occlusions (n = 44) [n (%)]

Patients with embolic occlusions (n = 32) [n (%)]

23 (30) 53 (70)

11 (25) 33 (75)

12 (38) 20 (62)

68 ± 13 24-92

66 ± 12 37-91

70 ± 14 24-92

66 (87) 9 (12) 1 (1) 48 (63) 18 (24) 52 (68) 21 (28) 24 (32) 53 (70) 23 (30) 46 (61)

38 (87) 5 (11) 1 (2) 27 (61) 11 (25) 31 (70) 11 (25) 13 (29) 31 (70) 13 (30) 31 (70)

28 (88) 4 (12) 0 (0) 22 (69) 7 (22) 21 (66) 10 (31) 12 (38) 23 (72) 10 (31) 16 (50)

Table II. Clinical presentation and time to treatment

Peritonitis Hypotension Correct diagnosis Interval from symptom onset to operation <24 h 24-72 h >72 h

Total group (n = 76) [n (%)]

Patients with thrombotic occlusions (n = 44) [n (%)]

Patients with embolic occlusions (n = 32) [n (%)]

49 (64) 23 (30) 47 (61)

31 (70) 15 (34) 25 (57)

18 (56) 8 (25) 22 (69)

28 (37) 17 (22) 31 (41)

13 (30) 11 (25) 20 (45)

15 (47) 6 (19) 11 (34)

patients (59%) with acute thrombotic mesenteric occlusions, with an average premorbid symptom duration of 7.8 months. Among patients with embolic occlusions, a documented history of recent arrhythmia was present in 17 patients (53%) and simultaneous peripheral artery embolization occurred in 10 patients (31%). The most common arrhythmia was chronic atrial fibrillation (n = 9), and the most common site of peripheral embolization was the lower extremity (n = 9). Among confirmed sources of emboli (n = 19), the heart was the most common site of origin (n = 17, 89%).

superior mesenteric artery (SMA), or its branches, was noted in all cases. The distribution of occlusive disease among patients experiencing thrombotic occlusions is presented in Table III. Multiple mesenteric vessels were occluded in 87% of these patients. In patients with antecedent symptoms of CMI, multiple vessels were occluded in 96%. Among patients experiencing embolic occlusions, concomitant non-SMA visceral embolization occurred in six patients (splenic, renal, inferior mesenteric, common hepatic) and an isolated branchlevel SMA embolization occurred in one patient.

Angiographic Findings

Surgical Management

Angiography was performed in 56 patients, including 33 (75%) with thrombotic occlusions and 23 (72%) with embolic occlusions. Occlusion of the

All patients underwent operation. Sixteen patients underwent exploration alone when findings at operation revealed extensive intestinal infarction

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Acute occulsive mesenteric ischemia 75

Table III. Angiographic findings in patients with thrombotic mesenteric occlusions

Arteries involved Number 1 2 3 Distribution Celiac only SMA only IMA only Celiac and SMA SMA and IMA Celiac, SMA, and IMA

Patients with antecedent chronic mesenteric angina (n = 24) [n (%)]

Patients without antecedent chronic mesenteric ischemia (n = 33) [n (%)]

1 (4) 11 (46) 12 (50)

4 (12) 15 (45) 14 (43)

0 (0) 1 (4) 0 (0) 9 (38) 2 (8) 12 (50)

0 (0) 4 (12) 0 (0) 12 (36) 3 (9) 14 (43)

IMA, inferior mesenteric artery; SMA, superior mesenteric artery.

Table IV. Revascularization procedures (n = 43) Procedure

n

SMA embolectomy Aorta to celiac and SMA bypass Aorta to SMA bypass Patch angioplasty Endoluminal angioplasty and stent SMA and celiac endarterectomy Aorta to celiac axis bypass Aorta to SMA and common hepatic artery bypass Celiac endarterectomy and SMA patch angioplasty SMA and IMA embolectomy SMA Reimplant with IMA patch angioplasty

17 9 4 3 2 2 2 1 1 1 1

IMA, inferior mesenteric artery; SMA, superior mesenteric artery.

believed to be incompatible with survival. Eighteen patients underwent bowel resection alone, including four patients with unreconstructable vascular disease and six with limited segment bowel necrosis. Revascularization was performed in 43 patients, with 28 requiring concomitant intestinal resection. In all cases requiring resection, small bowel necrosis was present. There was no difference in the prevalence of any intestinal necrosis or limited intestinal necrosis (<1 m) at the time of operation between etiologic groups. Revascularization procedures are summarized in Table IV. All embolectomy procedures were performed through the root of the small bowel mesentory and all bypass grafts were constructed in an antegrade fashion. Single- and multiple-vessel bypass procedures were performed in six and ten patients, respectively. In all single-vessel bypasses

the SMA was revascularized. Bypass conduit was saphenous vein in seven cases, Dacron in six cases, and polytetrafluoroethylene (PTFE) in three cases. Endoluminal methods of revascularization were employed in two individuals, one of whom had pancreatic cancer with vascular involvement and the other with a densely calcified aorta and aortoiliac occlusive disease deemed unreconstructable by traditional open surgery. Following the restoration of mesenteric perfusion, clinical examination and continuous-wave Doppler assessment were used to evaluate bowel viability. Only frankly necrotic intestine was resected at the initial operation. No patient deemed to have viable bowel required subsequent laparotomy for complications of ongoing intestinal ischemia. Second-look procedures (SLP) were performed at an interval of 48 to 72 h when residual intestinal viability was in question. Overall, 34 patients (44%) underwent SLP, including 19 patients with thrombotic occlusions (42%) and 15 patients with embolic occlusions (47%). Additional resection of gangrenous bowel was necessary in 50% of these procedures. Patients with embolic occlusions were significantly more likely than patients with thrombotic occlusions to require repeat bowel resection at the time of SLP (73% vs. 32%, p = 0.037). Morbidity, Mortality, and Survival Significant postoperative morbidity occurred in 42 patients (55%). Patients with embolic occlusions had a higher rate of morbidity than patients with thrombotic occlusions (69% vs. 46%, p = 0.044). Permanent parenteral nutrition (TPN) was required

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Table V. Survival according to surgical treatment

Treatment

Total group (n = 77) [n (%)]

Patients with thrombotic occlusions (n = 45) [n (%)]

Patients with embolic occlusions (n = 82) [n (%)]

Exploration only Intestinal resection only Revascularization total Concomitant resection No resection necessary

0/16 (0) 6/18 (33) 23/43 (53) 13/28 (46) 10/15 (67)

0/10 (0) 2/9 (22) 11/26 (42) 8/18 (44) 3/8 (38)

0/6 (0) 4/9 (44) 12/17 (71) 5/10 (50) 7/7 (100)

Fig. 1. Estimated survival curves for individuals with acute, arterial occlusive mesenteric ischemia by etiology (n = 76).

in 9 of 29 survivors (31%), including 4 of 6 survivors treated with isolated intestinal resection. There was no difference in postoperative TPN dependence between etiologic groups. Survival according to operative therapy is presented in Table V. Overall perioperative mortality was 62%–70% in the thrombotic occlusion group and 50% in the embolic occlusion group. Causes of perioperative mortality included multisystem organ failure secondary to the acute ischemic event (n = 31, 65%), delayed multisystem organ failure secondary to sepsis (n = 12, 25%), pulmonary failure/pneumonia (n = 4, 8%), and hemorrhagic stroke (n = 1, 2%). There was a trend toward improved perioperative survival among patients with

embolic occlusions as opposed to thrombotic occlusions (p = 0.069). In patients with and without frank intestinal necrosis at initial operation, perioperative mortality was 69% and 33%, respectively (p = 0.033). Survival curves are depicted in Figure 1. Estimated 5-year survival for both etiologic groups was 18%. The median survival for patients in both etiologic groups was less than 1 month and the median survival for patients surviving to hospital discharge was 52 months. There were 4 deaths among the 29 survivors during follow-up. One patient who underwent surgical bypass suffered a fatal recurrence of AMI secondary to graft occlusion. The remaining late deaths were secondary to

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atherosclerotic coronary disease (n = 2) and malignancy. There were no known recurrences of embolic mesenteric occlusion. Predictors of Morbidity, Mortality, and TPN Dependence Logistic regression analysis demonstrated that the use of SLP (odds ratio [OR] 0.08, 95% confidence interval [CI] 0.02, 0.41; p = 0.002) and intestinal necrosis at the time of initial operation (OR 2.5, CI 0.95, 6.62; p = 0.063) were independently associated with perioperative morbidity. Peritonitis (OR 22.9, CI 2.3, 225.2; p = 0.007) at presentation and preoperative hypotension (OR 14.9, CI 1.4, 160.6; p = 0.026) were significant, independent predictors of perioperative mortality. Peritonitis (OR 9.4, CI 1.6, 54.0; p = 0.012) at presentation and intestinal necrosis (OR 10.4, CI 1.9, 56.3; p = 0.007) at the time of initial operation were significant, independent predictors of perioperative mortality or survival dependent upon TPN. Of note, concomitant peripheral embolism, antecedent symptoms of CMI, need for repeat bowel resection at second look, and increasing interval to treatment were not associated with increased mortality, morbidity, or TPN dependence by univariate or multivariate analyses.

DISCUSSION The primary question posed by these results is: what changes in management can diminish the morbidity and mortality of AMI? In this series, AMI was most commonly caused by thrombosis of preexisting multivessel occlusive disease. Overall perioperative mortality was 62%, with 31% of survivors requiring lifelong TPN. An advanced presentation was common, as greater than 80% of patients had gangrenous intestine at the time of operation. Peritonitis, hypotension, and intestinal necrosis were significant predictors of adverse outcome, including perioperative morbidity, mortality, and postoperative TPN dependence. While these results are dismal, they do suggest future strategies for improvement and provide support for selected management concepts concerning the diagnosis and surgical treatment of AMI. Given the prohibitive mortality of AMI complicated by intestinal gangrene, prevention seems to be the most logical strategy to improve outcomes if high-risk groups can be identified. In this series, nearly two-thirds of patients with thrombotic

Acute occulsive mesenteric ischemia 77

occlusions reported prior complaints of CMI and nearly one-third of patients with embolic occlusions had inadequately treated chronic atrial fibrillation. Previous reports have demonstrated that chronic visceral ischemia can be surgically treated with durable results in terms of both symptom alleviation and prevention of acute ischemic events.19-23 Similarly, treatment of chronic atrial fibrillation with anticoagulation or cardioversion has been demonstrated to significantly reduce thromboembolic complications.24 Among patients in this series, adequate premorbid treatment of CMI and chronic atrial fibrillation could have potentially prevented 35 cases of AMI, 20 deaths, and 5 cases of lifelong TPN dependence. With regard to the treatment of established AMI, diagnostic accuracy and expediency may minimize intestinal ischemia and hasten appropriate treatment. Although the results presented here demonstrated no beneficial effect on survival with shorter intervals to treatment, it is likely that the high percentage of patients with established intestinal necrosis at the time of presentation precluded our ability to detect such a difference. With that point aside, an accurate early diagnosis requires a high index of clinical suspicion, as the principal complaints are usually nonspecific.3 In this series, all patients presented at our institution with complaints of abdominal pain and the majority exhibited peritonitis, rendering the concept of pain out of proportion to physical exam findings useless. However, most patients exhibited associated signs or symptoms referable to the etiology of the acute ischemic event (i.e., symptoms of CMI, peripheral emboli, or arrhythmia). Such findings should be considered highly suspicious for AMI and result in a prompt evaluation to confirm or rule out this diagnosis. Although angiography is the current mesenteric vascular imaging procedure of choice, CT and/or magnetic resonance angiography may soon become viable alternatives. In addition to confirming the diagnosis, mesenteric angiography also defines the etiology and proper revascularization procedure. In this series, multiple mesenteric arterial occlusions were observed in 90% of patients with thrombotic AMI and synchronous, nonSMA visceral emboli were present in nearly 20% of patients with embolic AMI. These points underscore the need for a high index of suspicion in all high-risk patients with acute abdominal pain and demonstrate the importance of definitive vascular imaging in all patients with AMI as a potential diagnosis. It cannot be overstated that any individual with acute abdominal pain and a prior history of CMI, recent arrhythmia, valvular heart disease, or

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generalized atherosclerosis must be considered to have AMI until proven otherwise. Once the diagnosis of AMI is made, revascularization, assessment of intestinal viability, and resection of necrotic bowel are necessary. Revascularization can be achieved using either endovascular or open techniques. Endovascular therapy offers the potential advantages of intervention at the time of angiographic diagnosis, provides an intraarterial route of administration for thrombolytic agents or other pharmacologic therapies, and avoids the use of prosthetic graft material in a potentially contaminated field. Endovascular revascularization does not, however, eliminate the need for assessment of bowel viability. Eighty percent of patients in this series had intestinal necrosis at the time of initial operation. Moreover, objective measures of long-term patency for mesenteric angioplasty are lacking. Consequently, all but two revascularization procedures were performed in this series via open techniques. Embolectomy procedures were performed through the root of the small bowel mesentory and all bypass grafts were constructed in an antegrade fashion. An antegrade bypass orientation was employed to minimize conduit length, turbulent flow, and the potential for graft kinking, although other groups have described excellent results with retrograde graft orientation.12,20,21,23 The supraceliac aorta was employed as the preferred source of inflow to take advantage of the relative absence of atherosclerotic disease in this portion of the aorta. Saphenous vein was the preferred conduit in the presence of peritoneal contamination. Otherwise, Dacron or PTFE was the conduit of choice. When possible, at least two mesenteric vessels were revascularized to ensure complete visceral revascularization and protect against future ischemia.25 Following the restoration of mesenteric perfusion, clinical examination and continuous-wave Doppler assessment were used to evaluate bowel viability. This combined technique proved to be extremely specific as no patient deemed to have satisfactory bowel viability at the time of initial operation required subsequent reoperation for ongoing ischemia. Only frankly necrotic intestine was resected at the initial operation and all patients with questionable viability of the remaining intestine underwent second-look laparotomy. At the time of the second look, 50% patients required additional resection of ischemic bowel that had progressed to full-thickness necrosis. The use of a second-look laparotomy was independently associated with a reduction in perioperative morbidity and additional intestinal resection was not associ-

Annals of Vascular Surgery

ated with an increased risk of perioperative morbidity, mortality, or postoperative TPN dependence. Interestingly, additional resection was more commonly required among patients with embolic occlusions. These findings support the liberal use of second-look procedures in all patients with questionable intestinal viability following revascularization, regardless of etiology, and have led our group to use planned second-look procedures in all patients with AMI. A final point concerning the utility of aggressive surgical treatment in patients with AMI relates to the life expectancy for patients surviving the acute event. Among patients surviving to hospital discharge the median survival was 52 months. This finding suggests that these patients can experience prolonged survival despite the major physiologic challenge of AMI and their multiple coexistent medical comorbidities. This series represents a large contemporary experience with AMI at a single tertiary referral center. Although the number of patients identified allowed for the analysis of multiple issues, several significant limitations remain. As a retrospective series, there are inherent selection and treatment biases. Only patients with recognized diagnoses were identified, and treatment was individualized according to patient condition and anatomy as well as surgeon preference. These factors may have led to noncausal correlations and limit the ability to draw definitive conclusions from these results. Finally, 76 patients afford limited power to detect outcome differences associated with infrequent occurrences. Unfortunately, given the relative rarity of this condition, prospective evaluations of a priori hypotheses are unlikely. In summary, AMI remains a highly lethal clinical entity most commonly caused by the thrombosis of preexisting occlusive disease. Patients tend to present with advanced intestinal ischemia or necrosis, both of which are independent predictors of adverse outcome. Improvement in these results will require the identification and treatment of patients at high risk for AMI prior to the onset of acute ischemia and/or development of intestinal necrosis as well as optimal management of patients with established ischemic events. REFERENCES 1. Litten M. Uber die Folgen des Verschlusses der Arteria Mesaraica Superior. Arch Pathol Anat 1875;63:289. 2. Brandt LJ, Boley SJ. AGA technical review on intestinal ischemia. Gastroenterology 2000;118:954-968. 3. Williams LF. Mesenteric ischemia. Surg Clin North Am 1988;68:331-352.

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16. Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity ischemia: revised version. J Vase Surg 1997;26:517-538. 17. Sathiakumar N, Delzell E, Abdalla O. Using the National Death Index to obtain underlying cause of death codes. J Occup Environ Med 1998;40:808-813. 18. SAS Institute, Inc. SAS/STATÒ User’s Guide, Version 8. Cary, NC: SAS Institute Inc., 1999. 19. Moawad J, McKinsey JF, Wyble CM, et al. Current results of surgical therapy for chronic mesenteric ischemia. Arch Surg 1997;132:613-619. 20. Mateo RB, O’Hara PJ, Hertzer NR, et al. Elective surgical treatment of symptomatic chronic occlusive disease: early results and late outcomes. J Vasc Surg 1999;29:821-832. 21. Gentile AT, Moneta GL, Taylor LM, et al. Isolated bypass to the superior mesenteric artery for intestinal ischemia. Arch Surg 1994;129:926-932. 22. Johnston KW, Lindsay TF, Walker PM, Kalman PG. Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia. Surgery 1995;118:1-7. 23. Foley MI, Moneta GL, Abou-Zamzam AM, et al. Revascularization of the superior mesenteric artery alone for treatment of intestinal angina. J Vasc Surg 2000;32:37-47. 24. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. Circulation 2001;104:2118-2150. 25. Shanley CJ, Ozaki K, Zelenock GB. Bypass grafting for chronic mesenteric ischemia. Surg Clin North Am 1997;77: 381-395.