Juxtarenal Aortic

Occlusion

S. SCOTT TAPPER, M.D.,* JUDITH M. JENKINS, R.N., M.S.N.,t WILLIAM H. EDWARDS, M.D.,* JOSEPH L. MULHERIN, JR., M.D.,*t RAYMOND S. MARTIN, III,*t and WILLIAM H. EDWARDS, JR., M.D.*t The authors' experience with 113 aortic occlusions in 103 patients during a 26-year period (1965 to 1991) is reviewed. The authors found three distinct patterns of presentation: group I (n = 26) presented with acute aortic occlusion, group II (n = 66) presented with chronic aortic occlusion, and group III (n = 21) presented with complete occlusion of an aortic graft. Perioperative mortality rates were 31%, 9%, and 4.7% for each respective group and achieved statistical significance when comparing group I with group II (p = 0.009) and group I with group III (p = 0.015). Group I presented with profound metabolic insults due to acute ischemia and fared poorly. Group II presented with chronic claudication and did well long-term. Group III presented with acute ischemia but did well because of established collateral circulation. The treatment and expected outcome of aortic occlusion depends on the cause. . . . le traitement ideal consisterait evidment a resequer la zone obliteree et a retablier la permeabilite si c'est possible . . ." R. LeRiche (deLyon) 1923

O CC LUSION OF THE juxtarenal aorta (JRA) may present as an acute vascular catastrophe, chronic lower extremity ischemia, or as an aortic graft occlusion, a sudden event superimposed on chronic ath-

erosclerotic occlusive disease. All of these scenarios produce formidable treatment challenges because of the potentially disastrous sequence of events associated with lower extremity ischemia. In 1923, LeRiche' described the condition of aortic occlusion and envisioned resection of the occluded segment as the treatment of choice. Unfortunately, he had neither the technique or the skill to see his vision to fruition. Reconstructive efforts began in 1947, when Dos Santos2 performed abdominal aortic endarterectomy, and Presented at the 103rd Annual Scientific Session of the Southern Surgical Association, Hot Springs, Virginia, December 1-4, 1991. Address reprint requests to William H. Edwards, M.D., 4230 Harding Road, Suite 705, Nashville, TN 37205. Accepted for publication December 26, 1991.

From the Department of Surgery, * Vanderbilt University Medical Center, and the Division of Vascular Surgery, t St. Thomas Hospital, Nashville, Tennessee

in 1950, Oudot3 replaced the terminal aorta with an arterial homograft for chronic occlusive disease. The ensuing years have seen numerous advances in the approach to aortic occlusion. The vascular surgeon's armamentarium is overflowing with creative solutions: embolectomy, thrombolytic therapy, and extra-anatomic bypass, using a variety of graft materials to revascularize the lower extremities. Despite these developments, the mortality rate of acute aortic occlusion (AAO) and disability from chronic occlusion (CAO) remains significant. To better understand the presentation, management, and expected surgical outcome, we have reviewed our experience with this multifaceted disorder. Methods During the years 1965 to 1991, 4126 aortic reconstructions were entered in the vascular registry at St. Thomas Hospital. Abdominal aortic aneurysm was the operative indication in 1774, whereas aorto-iliac occlusive disease was found in 2352. The male/female ratio was 3:1. One hundred three patients required 113 operations for JRA occlusion during this period. Retrospective analysis was obtained from the medical records, and followup was secured through clinical evaluation or phone interview. Follow-up ranged from 6 months to 24 years (mean, 5 years); no patient was lost to follow-up. The study population was composed of 64 men and 39 women, with a mean age of 59.2 years (range, 24 to 80 years). Associated risk factors (Table 1) are typical of other series.4'5 Cardiovascular surgical history was positive in 27%.

443

TABLE 1. Patient Profiles

ASHD HTN MI COPD DM CVA Cigarette abuse

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TAPPER AND OTHERS

444 AAO

CAO

GO

35% 38% 46% 15% 19% 23% 60%

20% 48% 17%

21% 37% 21% 11% 16% 5% 58%

11% 6% 8% 62%

AAO, acute aortic occlusion; CAO, chronic aortic occlusion; GO, graft occlusion; ASHD, atherosclerotic heart disease; HTN, hypertension; MI, myocardial infarction; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus; CVA, cerebrovascular accident.

Statistical Analysis. Chi square analysis using a twotail Fisher's exact test and actuarial survival curves were calculated for each presentation scenario.6'7 Presentation and Management Three distinct categories of JRA occlusion emerged on analysis: group I were patients with AAO; group II, CAO; and group III were those patients with aortic graft occlusion (GO). Group I had a statistically significant perioperative mortality rate when compared with the less acute conditions found in groups II (p = 0.009) and III (p = 0.015). Group I had an actuarial survival different from groups II (p < 0.0006) and III (p < 0.015). Groups II and III were statisfically similar. Because each group had a different clinical presentation, behavior, and management strategy, they demand separate attention for this discussion.

Group I Acute aortic occlusion was documented in 26 patients, 13 secondary to acute saddle embolus (ASE), and 13 due to thrombosis. Distribution was equally divided, with 13 men and 13 women, having a mean age of 66 years. Myocardial infarction (MI) was the primary risk factor (46%) (Table 1). Premorbid cardiac dysrhythmia was documented in 58%, requiring cardioversion in three patients. Ischemic rest pain was the salient clinical feature (92%), whereas 35% had sensory/motor dysfunction. Because of the acute nature of the process, many patients were critically, and ultimately, fatally ill. Of particular interest, four patients (15%) presented with evidence of multiple peripheral emboli, including acute renal failure in three (mortality rate, 75%), and three patients (12%) had AAO after acute MI without death. Operative management for AAO was determined by cause. Bilateral transfemoral embolectomy (TFE) was performed in 10 of the 13 patients (82%) with ASE; however, six required further revascularization to preserve distal perfusion. Of the remaining three patients, two had

aortofemoral bypass (AF) and one had axillo-femoral bypass (AxF). In contrast, TFE was attempted four times in 13 patients with thrombotic AAO, but was successful in only one patient with abdominal aortic aneurysm thrombosis secondary to blunt trauma. Eight patients required direct aortic reconstruction by AF (62%), whereas four (3 1%) had AxF. Group II Sixty-five patients presented with 66 CAO, 42 men and 23 women, with a mean age of 57 years. The medical profile is shown in Table 1. Fifteen patients (23%) had undergone previous cardiovascular surgery. The site of occlusion was documented by arteriography in all patients. Juxtarenal aorta occlusion occurred in 34 patients (52%), aortic bifurcation occlusion in 22 patients (33%), and occlusion ofthe suprarenal aorta in 10 (15%). Pathology was primarily atherosclerosis (95%); however, aortic coarctation, Takayasu's arteritis, and Buerger's disease each occurred in one patient. Disabling claudication was the primary clinical feature (92%), followed by rest pain (18%), ischemic ulceration (6%), and impotence (30% of men). No patient presented with acute symptoms. Direct aortic revascularization was the operative management of choice. Aortofemoral bypass was performed in 56 patients (85%), with 30 of these requiring proximal aortic thromboendarterectomy (TEA). Four patients, early in the series, had aorto-iliac TEA, and one reoccluded 10 years after operation, requiring AF bypass. Visceral revascularization was a component of 25% of the aortic reconstructions (10 renal, four mesenteric).

Group III Aortic GO occurred 21 times in 19 patients. There were 13 men and six women, with a mean age of 54 years. Comorbid conditions are listed in Table 1. Seven patients had previous cardiovascular surgery (37%). Symptoms of acute ischemia were present in 92%, whereas 8% had disabling claudication. Primary operations included one abdominal aortic aneurysm tube graft and 18 bifurcated grafts for occlusive disease. Graft size ranged from 12 to 19 mm, most commonly 14 mm (53%). Two grafts were on-lay anastomoses. Operative management for GO included AxF (48%), redo AF (43%), and graft thrombectomy (9%). Concomitant profundaplasty was necessary in 20% to improve pelvic and distal perfusion. Results

Group I Eight patients with AAO had significant morbidity (Table 2), most often multisystem organ failure, which

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445

AORTIC OCCLUSION TABLE 2. Morbidity

CAO

No.

No.

GO

No.

AAO Survival

-L*

100

AAO

- - CAO Survival

. .

L

MOF MI ARF Repeat EMB

3 1 1 1

Mesenteric ischemia Pulmonary MOF Pancreatitis Splenectomy SBO

2 2 1 1 1 1

1 MOF 1 Pulmonary Mesenteric ischemia 1 Ureteral injury I 1 DVT

80

Group II Eight complications occurred in 14 patients with CAO (Table 2), most commonly groin lymphocele (n = 6), groin infection (n = 3), and mesenteric ischemia (n = 2). Six patients died, resulting in a perioperative mortality rate of 9% (Table 3). There were three early graft thromboses, one an aortic GO, one AF limb occlusion, and one bilateral renal artery bypass. Follow-up showed 91% of patients alive at 1 year, 68% at 5 years, and 51% survival at 10 years (Fig. 1). The TABLE 3. Perioperative Mortality Rate

AAO (n = 8) MOF Cardiac Mesenteric ischemia Pulmonary embolus Unknown Mortality rate

CAO (n =6)

3

1

4

1 2 1

1 31%

1 9%

GO (n = 1)

GO Survival

* 1 -rn~~L

-

SURVIVAL

m______

-.-

40 20~

0

occurred in three patients (12%). Perioperative mortality rate (Table 3) was 31%, and was greater for ASE (39%) than for aortic thrombosis (23%). There was one early GO requiring AxF thrombectomy and distal revascularization to improve run-off. Follow-up demonstrates a 50% mortality rate at 1 year. Only 20% of the original cohort were alive at 10 years (Fig. 1). The cause of late death was most commonly cancer (n = 3) and cardiovascular disease (n = 3), followed by complications of diabetes (n = 1) and hip fracture (n = 1). Although survival rates are disconcerting, with a 31% perioperative mortality rate and only 20% alive at 10 years, this finding speaks to the complicated and devastating problem of AAO and the profoundly positive cardiac history. Two late graft limb failures were documented, and one AF thrombosis, necessitating AxF reconstruction.

....

60

(%)

AAO, acute aortic occlusion; CAO, chronic aortic occlusion; GO, graft occlusion; MOF, multisystem organ failure; MI, myocardial infarction; ARF, acute renal failure; EMB, embolism 2; DVT, deep venous thrombosis; SBO, small bowel obstruction.

t*-

2

4

6

8

10

12

14

TIME (years)

FIG. 1. Actuarial survival.

longest CAO survival was 24 years. Fourteen deaths occurred during the follow-up period, 11 secondary to MI and one each due to stroke, cancer, and multisystem organ failure. One patient developed a graft-enteric fistula 11 years after AF bypass, requiring AxF revascularization. There were three late graft limb occlusions, whereas six GO occurred during the follow-up period (0.2 to 8 years postoperatively), and are also included in the group III analysis. In addition, one patient occluded an AxF bypass and another occluded a celiac bypass. Group III

Morbidity rate for aortic GO is demonstrated in Table 2, including four amputations. One patient had an unrecognized ureteral injury during a third AF, which resulted in a urinoma. Nephrectomy was necessary because the ureter was not amenable to repair. There was one perioperative death in a patient who presented with GO complicated by a strangulated small bowel obstruction and peritonitis. Management necessitated AxF reconstruction with lysis of adhesions and bowel resection. Multisystem organ failure led to his death 60 days after operation. Long-term survival was 90% at 1 year, and 55% at both 5 and 10 years (Fig. 1). There were four deaths in the follow-up period, three from MI, one from stroke. Late graft thrombosis occurred in three patients, two graft limb occlusions, and one recurrent aortic GO. Discussion

1

Acute Aortic Occlusion 4.7%

AAO, acute aortic occlusion; CAO, chronic aortic occlusion; GO, graft occlusion; MOF, multisystem organ failure.

Acute aortic occlusion is a catastrophic event. It occurs in patients with severe cardiac disease and sets in motion a series of physiologic insults that continues to have a

high mortality.

446

TAPPER AND OTHERS

Acute aortic occlusion is most commonly caused by ASE, which originates from a cardiac source. Today cardiac dysrhythmias and previous MIs are frequently encountered, whereas historically rheumatic valvular disease was a source of ASE. Additional causes of AAO include trauma, hypercoagulable states, dissection, and mycotic embolism. Thrombosis superimposed on occlusive disease is a common cause of AAO and may be difficult to distinguish from ASE. Diagnosis of AAO is straightforward. The universal symptom is acute pain accompanied by varying degrees of the classic six Ps, that is, pain, pallor, pulselessness, paresthesia, paresis, and poikilothermy. The degree of ischemia is dependent on the site of occlusion, proximal thrombosis, distal embolization, and collateral circulation. The distinction between ASE and acute thrombosis may be difficult and relies on such historical data as previous claudication, previous embolism, cardiac dysrhythmias, recent MI, low flow state, and evidence of multiple peripheral emboli. Angiography is not mandatory but is beneficial in situations of suspected renal or mesenteric embolism. Historically, von Bauer8 is credited with performing the first successful aortic embolectomy in 1913. Ravdin and Wood,9 in 1941, first reported removal of an ASE by the femoral approach. Albright and Leonard,'° in 1950, reviewed 193 cases of ASE, finding just 34 survivors. Eight patients were cured by nonoperative means, including anticoagulation, vasodilators, intermittent venous occlusion, lower extremity cooling to reduce metabolism, and Buerger's exercises. The remaining 26 survivors were managed by direct aortic embolectomy, aortectomy, and retrograde milking of emboli from the femoral artery. The overall mortality rate in this series was 75%, whereas the nonoperative mortality rate was 95%. In 1958, Dale and Mahoney" reviewed 64 successful aortic embolectomies and concluded that immediate operation was the treatment of choice. Willman and Hanlon'2 (1959) reported four successful saddle embolectomies through the femoral artery under local anesthesia without death. In 1962, Deterling et al."3 reported 22 cases of ASE with an operative mortality rate of 66%. The operative management of arterial embolism was forever changed by the introduction ofthe balloon-tipped embolectomy catheter by Fogarty et al (1963). '4 Porter et al.,'5 in 1966, reported a series including 16 "conventional embolectomies" compared with six catheter embolectomies. The catheter technique reduced operative time by 50% and transfusion requirements by 75%. More importantly, operative mortality rate dropped from 50% to 33%, and limb salvage rose from 44% to 100%. Recent reports4" 6 confirm the enhanced survival and limb salvage rates associated with balloon catheter TFE. Acute aortic thrombosis was described by Bell'7 (1967)

Ann.

Surg. * May

1992

terminal event associated with severe iliofemoral occlusive disease and progressive cardiac failure. He recognized the futility of thrombectomy and advocated bypass of the thrombosed segment from the infrarenal aorta to the femoral arteries. Despite these observations, his mortality rate was 100%. Danto et al.,'8 in 1972, however, treated eight patients with AAO using aortoiliac or AF bypass. Mortality rate was 25%, although the morbidity rate remained high. Thrombosis of abdominal aortic aneurysm was first reported in 1959 by Shumacker,'9 but Janetta and Roberts (1961)20 are usually credited. The largest series is by Johnson et al.,2' who, in 1974, reviewed 15 cases with an operative mortality rate of 53%. This series of 26 AAOs, having a limb salvage rate of 98% and mortality rate of 31%, compares with other large series. On diagnosis, systemic anticoagulation is begun with intravenous heparin sodium to inhibit proximal and distal thrombosis. Often patients are profoundly decompensated, displaying both local and systemic effects of ischemia, including variable degrees ofcardiac failure with intravascular volume depletion, acidemia, and hyperkalemia. They also may have acute renal failure or mesenteric ischemia. Aortography is not mandatory unless renal or mesenteric involvement is suspected, although it was performed in 50% ofthis series. Operation is imperative for survival. In our experience, TFE had a disappointingly low success rate as the sole means of revascularization. Even with ASE, TFE was enhanced with a bypass procedure in 60% of cases. Nonetheless, TFE using local anesthesia is, theoretically, the safest and most expeditious means to revascularize these critically ill patients. If TFE only clears one iliofemoral system, a femoral-femoral crossover should be used. If adequate inflow is impossible bilaterally, a judgment must be made regarding the potential for successful aortic reconstruction. Most circumstances dictate extra-anatomic bypass grafting through AxF, and the patient should be prepared for such a contingency at the as a

outset.

Anticoagulation is continued after operation. Patients must be evaluated for evidence of compartment

syn-

drome, acid washout from reperfused muscle and gut, myoglobinuria, and recurrent embolization. Cardiac complications and multisystem organ failure are the most frequent causes of death. Long-term anticoagulation with warfarin has been shown to prevent re-embolization.4 Patients in this series were not routinely managed with warfarin until 1982. One patient, however, required amputation while still hospitalized after reembolization while being treated with heparin. Acute aortic occlusion continues to present life-threatening surgical challenges. Rapid diagnosis, resuscitation,

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AORTIC OCCLUSION

and revascularization must occur, cognizant of the physiologic milieu of acute ischemia, to achieve survival. Despite advances in critical care medicine and surgical techniques, mortality rate remains high.

Chronic Aortic Occlusion The clinical presentation, management, and outcome of CAO contrasts that of AAO. Chronic occlusive disease of the terminal aorta has been recognized to cause claudication and impotence at least since LeRiche' described the syndrome in 1923; however, CAO is rare, noted only in 0.15% of 33,216 autopsies.22 Manifestations of CAO include bilateral lower extremity claudication and absent femoral pulses. There is a predilection toward males with a strong history of tobacco abuse. Other features include ischemic rest pain and impotence. Acute ischemia is not a clinical finding because of the progressive nature of the disease and the opportunity for the development of collateral circulation. As such, these patients do not have the physiologic insult found in AAO and may be evaluated and managed electively. In 1963, Bergan and Trippell23 recognized JRA occlusion as a terminal stage of LeRiche syndrome because of continued proximal thrombosis. They described JRA endarterectomy with distal revascularization by bypass graft or TEA. They advised renal cross-clamping before aortic manipulation to avoid embolization and, further, advocated hypothermia and mannitol infusion for renal protection from ischemic injury. Chavez et al.,24 in 1968, reported three cases of successful proximal aortic TEA for juxtarenal CAO using temporary occlusion of the renal arteries without hypothermia. Starrett and Stoney22 (1974) reviewed a large experience with JRA occlusion receiving either medical or surgical management. The nonoperative group had documented proximal propagation of thrombosis into the renal and mesenteric circulation with ensuing visceral ischemia. In the operative group (n = 40), 17 extensive aortic TEAs demonstrated the primary occlusive lesion to be distal to the inferior mesenteric artery or in the origin of the common iliac arteries. They noted that occlusion proximal to the primary lesion was due to thrombosis, often in the absence of significant aortic intimal hyperplasia. Followup disclosed an 85% patency at 10 years; however, 10year survival was only 37%. Several published accounts appeared in the early 1 970s describing remote bypass procedures designed to treat proximal aortic occlusive disease. Nunn and Kamal,25 in 1972, first reported a descending thoracic to femoral artery bypass using a retroperitoneal approach. The authors recommended that this procedure only be considered in lowrisk patients. In 1974, Frantz et al.26 described an ascending aorta to femoral artery bypass for a singular pa-

447

tient in whom the abdominal aorta was found to be unsuitable for grafting. This approach requires a median sternotomy and, as such, has not been widely used. Such remote bypass procedures, including AxF, have been condemned for the management of CAO because they do not eliminate the risk of proximal thrombosis. In one report, extension of thrombosis to the level of the renal or mesenteric arteries accounted for a 46% mortality rate in untreated patients, compared with a 10% operative mortality rate.22 Liddicoat et al.27 (1975) reported standardized operative techniques for proximal aortic TEA and onlay AI or AF bypass. Perioperative mortality rate was 4.6%, with a low morbidity rate and favorable long-term results in 64 patients. A fundamental debate concerned the need for in-line aortic reconstruction to remove the thrombus and prevent proximal propagation. Although Starrett and Stoney22 demonstrated devastating complications and death from proximal thrombosis, others found the antithesis true. In one group of patients with CAO treated medically or with AxF, none of the 13 patients available for follow-up demonstrated proximal thrombosis of visceral vessels.28 The debate continued regarding the risk of proximal thrombosis, as Deriu and Ballotta29 (1983) demonstrated arteriographic and pathologic evidence for progressive ascending thrombosis of the occluded aorta. This controversy is not likely to be settled without a prospective, randomized trial to include nonoperative therapy, direct aortic reconstruction, and extra-anatomic bypass. Follow-up would involve serial arteriography to document the nature of disease progression. Because a study of this nature is unlikely to be performed, it is prudent to acknowledge the potential for clot propagation and consequential acute renal failure or mesenteric ischemia, and recommend direct in-line aortic reconstruction. Aortic Graft Occlusion There exists a large body of literature discussing aortic graft limb occlusion, but there is little concerning complete occlusion of an aortic graft. Robiscek et al.30 (1985) dispelled an early myth that woven and knitted grafts had dissimilar failure rates, concluding that graft thrombosis is rare and is usually related to poor technique, disease progression, and chronic cigarette abuse.3' Naylor et al.32 reported 46 GOs in 28 of 241 patients evaluated after AF. There were five bilateral occlusions, not otherwise distinguished from the single limb occlusions. Others confirm these observations in longitudinal studies of AF effi-

cacy.33'34 We believe this experience of 21 aortic GOs is the largest yet presented. Five grafts were implanted at another institution, leaving 16 implanted by this practice. During

448

TAPPER AND OTHERS

the study period, a total of 4126 aortic graft procedures were performed, 1073 tube grafts and 3053 bifurcation grafts. The thrombosis rate for tube grafts (n = 1) is 0.09%, compared with 0.5% for bifurcated grafts (n = 15). Two onlay grafts occluded and were replaced by in-line grafts. The importance of the profunda femoris artery in maintaining graft patency has been emphasized previously,35 and profundaplasty accompanied five of nine redo AFs. Graft occlusion occurred early (median, 1.3 years) but, once corrected, reasonable survival and limb salvage can be expected. Patients with aortic GO represent a hybrid group that manifest features of acute ischemia, albeit less severe than AAO. This insult is tolerated well, with a lower perioperative mortality rate and good long-term survival. Most patients had original reconstructive procedures for occlusive disease; hence there was already well-developed collaterals to maintain limited perfusion to the pelvis and lower extremities. Seven of 21 GOs occurred after previous aortic occlusions (six CAO, one AAO). Presentation did not include the poor cardiac function and end-organ ischemia found in AAO. Preoperative management included early anticoagulation with heparin sodium, arteriography, and expeditious revascularization. Bilateral TFE was performed in two patients, though it proved to be a temporizing measure because both patients subsequently returned with another aortic GO. Aortic GO must be viewed as a technical failure secondary to redundant graft, a distal anastomotic problem, or the result of progressive outflow occlusive disease. Simple graft thrombectomy will not correct the underlying problem. Revascularization requires redo AF or extraanatomic bypass. In either case, attention to the profunda femoris artery is important in providing run-off for proximal graft patency, because many patients have concomitant superficial femoral artery occlusion. The long-term patency of redo aortic grafts should approach that of primary aortic reconstructions and, thus, afford an improved functional result when compared with AxF. Conclusion In summary, JRA occlusion can be viewed as a spectrum of disorders ranging from AAO in a profoundly ill patient, through acute lower extremity ischemia found in GO, to chronic vascular insufficiency in CAO. The presentation, management, and expected outcome vary by cause. Despite advances in critical care medicine and specialized vascular and anesthetic techniques, AAO still has a poor prognosis. The principles of current therapy include rapid diagnosis, operative management, and anticoagulation. The future holds improved survival as we learn to pharmacologically manipulate ischemic physiology and preserve end-organ function.

Ann.

Surg. May 1992 -

In contrast, patients with acute GO and CAO survive their insults reasonably well. In-line aortic reconstruction for CAO results in durable limb preservation with improved function. Graft occlusion should continue to be managed with anticoagulation and expeditious revascularization. Attention must be directed, however, to the identification and correction of the underlying cause of graft failure. Long-term limb salvage and preservation of function can be achieved with diligence.

Acknowledgment The authors thank Robert D. Moses, M.D., for assistance with the statistical analysis.

References 1. LeRiche R. Des obliterations arterielles (obliteration de la terminason de l'aorta) comme causes des insuffisances circulatiores des membres inferieunes. Bull Soc Chir 1923; 49:1404-1406. 2. Dos Santos JC. Sur los desobstruction des thromboses arterielles anciennes. Mex Acad Chir 1948; 73:409. 3. Oudot J. La greffe vasculaire dans les thromboses du carrefour aortique. La Presse Medicale 1951; 59:234-236. 4. Busuttil RW, Keehn G, Milliken J, et al. Aortic saddle embolus. A twenty-two year experience. Ann Surg 1982; 197:698-706. 5. Traverso LW, Baker JD, Dainko EA, Machleder HI. Infrarenal aortic occlusion. Ann Surg 1977; 187(4):397-401. 6. Mantel N. Evaluation of survival data and two new rank order statistics arising in its consideration. Cancer Chemotherapy Reports 1966; 50:163-170. 7. Peto R, Pike MC, Armitage P, Breslow NE, Cox DR, Howard SV, Mantel N, McPherson K, Peto J, Smith PG. Design and analysis of randomized clinical trials requiring prolonged observation of each patient. II. Analysis and examples. Br J Cancer 1977; 35: 1-39. 8. Von Bauer F. Fall von embolus aortae abdominalis heiling. Zentralbl Chir 1913; 40:1945. 9. Ravdin IS, Wood FC. The successful removal of a saddle embolus of the aorta eleven days after acute coronary occlusion. Ann Surg 1941; 114:834-839. 10. Albright HL, Leonard FC. Embolectomy from the abdominal aorta. N Engl J Med 1950; 242:271-277. 11. Dale WA, Mahoney EB. Aortic saddle embolism. AMA Arch Surg

1950; 76:930-943. 12. Willman VL, Hanlon CR. Safer operation in aortic saddle embolism: Four consecutive successful embolectomies via the femoral arteries under local anesthesia. Ann Surg 1959; 150:568-574. 13. Deterling RA Jr, Vargas LL, McAlister FF. Follow-up studies of patients with embolic occlusion of the aortic bifurcation. Ann Surg 1962; 155:383-391. 14. Fogarty TJ, Cranley JJ, Krause RJ, et al. A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963; 116: 241-244. 15. Porter JM, Acinapura AJ, Silver D. Aortic saddle embolectomy. Arch Surg 1966; 93:360-364. 16. Littooy FN, Baker WH. Acute aortic occlusion: a multifaceted catastrophe. J Vasc Surg 1986; 4:211-216. 17. Bell JW. Acute thrombosis of the subrenal abdominal aorta. Arch Surg 1967; 95:681-684. 18. Danto LA, Fry WJ, Kraft RO. Acute aortic thrombosis. Arch Surg 1972; 104:569-572. 19. Shumacker HD. Surgical treatment of aortic aneurysms. Postgrad Med 1959; 25:535-548. 20. Janetta PJ, Roberts B. Sudden complete thrombosis of an aneurysm of the abdominal aorta. N Engl J Med 1961; 264:434-436. 21. Johnson JM, Gaspar MR, Movius HJ, Rosenthal JJ. Sudden com-

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26. 27.

28.

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plete thrombosis of aortic and iliac aneurysms. Arch Surg 1974; 108:792-794. Starrett RW, Stoney RJ. Juxtarenal aortic occlusion. Surg 1974; 76: 890-897. Bergan JJ, Trippell OH. Management ofjuxtarenal aortic occlusions. Arch Surg 1963; 87:60-68. Chavez CM, Conn JH, Fain WR, Gee HL. Surgical treatment of high aortoiliac occlusion. Surgery 1969; 65:757-762. Nunn DB, Kamal MA. Bypass grafting from the thoracic aorta to femoral arteries for high aortoiliac occlusive disease. Surgery 1972; 72:749-755. Frantz SL, Kaplitt MJ, Beil AR Jr, Stein HL. Ascending aorta-bilateral femoral artery bypass for the totally occluded infrarenal abdominal aorta. Surgery 1974; 75:471-475. Liddicoat JE, Bekassy SM, Dang MH, DeBakey ME. Complete occlusion of the infrarenal abdominal aorta: management and results in 64 patients. Surgery 1975; 77:467-472. McCullough JL, Mackey WC, O'Donnell TF, Millan VG, Deterling RA, Callow AD. Infrarenal aortic occlusion: a reassessment of surgical indications. Am J Surg 1983; 146:178-182.

DIscuSSION

DR. LARRY H. HOLLIER (New Orleans, Louisiana): I appreciate Dr. Edwards sending me a copy of this paper. I am glad he did in advance because it has so much information in it. It really is a massive work, Bill, and I think you are to be congratulated; and your colleagues who did a lot of the background work in reviewing this information are certainly to be congratulated. It represents one of the most extensive experiences and is very well documented. I have several questions about this. How many were lost to follow-up over that period, and would it make any difference in your survival rates? Secondly, in the acute occlusion patients, you have noted throughout the study fair morbidity and mortality rates. Although they seem to be high, they are actually what is expected and are almost the same mortality and morbidity rates that we have seen in our own patients with acute problems. These patients are sick, and multi-organ problems do occur. In view of the high mortality rate despite early and aggressive therapy, what are your thoughts concerning any role that there might be for lytic therapy in these patients? Do you think that that would make a difference? About 10 or so years ago, Jack Wiley, Stoney, and Ehrenfeld commented about the risk of renal artery occlusion in patients with complete aortic obstruction. You noted in your presentation and in the paper that no patient presented with renal failure. But did you see evidence that would confirm Wiley's expectation that these would progress up and occlude? And, finally, in the graft occlusion group, it is my own experience that end-to-side anastomoses in the aorta would appear to have a higher rate of graft failure from hemodynamic disturbances and neointimal fibroplasia. Could you tell any difference in these patients? Were these primarily end-to-end, end-to-side, or were they mixed? Thank you. DR. STANLEY 0. SNYDER, JR. (Norfolk, Virginia): Dr. Edwards, I enjoyed your presentation and the opportunity to review this large manuscript also. As Larry said, the magnitude ofthis series is impressive and is "Houstonoid." I think the results are truly commendable, and I would like to comment on a couple of points and ask several questions. The mortality rate for acute aortic occlusions was actually quite good at 31 %, despite the increased requirements perhaps surgically for aortofemoral reconstruction in two thirds of the thrombotic occlusions and in two of three of the unsuccessful embolectomy patients. I think the increased operative risk in the elective chronic aortic occlusion is highlighted by your 9% mortality rate, compared with only a 2.6% mortality rate in the remaining 4100 patients in this series. The adjunctive 10 renal and four mesenteric revascularizations attest to the severity of disease and may have contributed to the increased mortality rate in this group. A somewhat disturbing finding in the chronic occlusive group was postoperative graft occlusion in six of the 66 patients, compared with only eight occlusions in the remaining 4100 patients in the series. My questions

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29. Deriu GP, Ballotta E. Natural history of ascending thrombosis of the abdominal aorta. Am J Surg 1983; 145:652-657. 30. Robiscek F, Daugherty HK, Cook JC, et al. Patency rate of bifurcated aortic grafts: comparative analysis of woven versus knitted prosthesis in the same patient. Ann Thorac Surg 1985; 40:172-174. 31. Robiscek F, Daugherty HK, Mullen DC, et al. The effect of continued cigarette smoking on the patency of synthetic vascular grafts in LeRiche syndrome. J Thorac Cardiovasc Surg 1975; 70:107-112. 32. Naylor AR, Ah-see AK, Engeset J. Graft occlusion following aortofemoral bypass for peripheral ischemia. Br J Surg 1989; 76: 572-575. 33. Malone JM, Moore WS, Goldstone J. The natural history of bilateral aortofemoral bypass grafts for ischemia of the lower extremities. Arch Surg 1975; 110: 1300-1306. 34. Sladen JG, Gilmour JL, Long RW. Cumulative patency and actual palliation in patients with claudication after aortofemoral bypass. Am J Surg 1986; 152:190-195. 35. Edwards WH, Jenkins JM, Mulherin JL, Martin RS, Edwards WH Jr. Extended profundaplasty to minimize pelvic and distal tissue loss. Ann Surg 1990; 211:694-702.

are, do you have a standard preoperative cardiac or medical evaluation to help to determine whether aortic reconstruction versus axillofemoral bypass might be best? Secondly, do all patients with chronic aortic occlusion require elective reconstruction? And, if not, in light of Dr. Stoney's and Dr. Hollier's comments today, do you think that these patients should be on chronic anticoagulation? The other question concerns whether you know what the cause of graft occlusion was? You only had to do a profundaplasty in 20% of the patients who had aortic graft failure. I wondered about the possible cause for the other 80%. And, lastly, as with Larry, I would like to know if you think there is a role for thrombolytic therapy in these patients who are not in jeopardy for limb loss. Thank you. DR. WILEY F. BARKER (Los Angeles, California): Mr. President, Members and Guests, I want to compliment Dr. Edwards and his group on this presentation. And I have three slides that I would offer that I hope will be complementary to this. The first slide shows an acute occlusion of the kind that he is talking about. Well, it was not that acute; the patient was a very big and husky oil field worker with about 5 weeks of acute, occlusive symptoms and ischemia, and we were astonished to find a 5- or 6-cm aneurysm in this man. There is nothing further to say about him, except that a few weeks later we saw a patient whom I can show better in this artist's drawing. There was a slight infundibulum showing below the renal artery, and we thought we had a classical infrarenal occlusion. When we entered the abdomen, that little infundibulum just tapered off into some fibrous bands that trickled down and finally joined what turned out to be a reconstitution of the iliac arteries with the extensive collateral. These are two quite different patterns of juxtarenal occlusion. I would point out that this man was in his 50s and had had no evidence of renal disease, perhaps a comment on the questions that were raised about the risk of renal involvement. The third slide then is probably the oldest slide shown in any of these meetings recently; this is a sketch from an 1835 paper by a man named Barth, who described the first patient, as far as I am aware, in which clinical claudication was clearly manifest. The patient happened to die of natural heart disease rather than of this, but was severely handicapped. If this is an acute and proper representation, this either represents a chronic and neglected aortic occlusion or a form of the hypoplasia that I showed in the second slide. I thought this might be of some interest because it probably even antedates the Houstonian work in this area. I want to compliment you again, and thank you for the privilege of discussing it. DR. CARLOS M. CHAVEZ (Brownsville, Texas): Dr. Ochsner, Dr. Jones, I think this is another well-structured and well-presented paper by Dr. Edwards' group. It contains a lot of information. I have not had a chance to review the paper, but I am going to limit my comments to those cases

of juxta-aortic occlusion.

Juxtarenal aortic occlusion.

The authors' experience with 113 aortic occlusions in 103 patients during a 26-year period (1965 to 1991) is reviewed. The authors found three distinc...
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