In situ allograft replacement of infected infrarenal aortic prosthetic grafts: Results in forty-three patients☆

Article Outline

• Abstract
• Patients and methods
  • Population
  • Timing of allograft replacement
  • Procurement and preservation of allografts
  • Allograft implantation
  • Follow-up
• Results
  • Early results
  • Late results
• Discussion
• Discussion
• References
• Copyright

Abstract 

Purpose: Dissatisfaction with conventional methods of treatment of infected infrarenal aortic prosthetic grafts and excellent long-term results reported by heart surgeons after allograft replacement for management of infections involving the ascending aorta have prompted us to investigate allograft replacement in the management of arterial infections. Methods: From October 1988 to April 1992, 43 consecutive patients with infected infrarenal aortic prosthetic grafts underwent in situ replacement with preserved allografts obtained from cadavers as part of a program to retrieve multiorgan transplant tissue. Thirty-four patients had isolated prosthetic infections, whereas nine had aortoenteric fistulas. One patient had a concomitant below-knee amputation for septic arthritis of the ankle as a result of septic emboli. Nineteen patients had nonvascular-associated procedures, including 17 intestinal procedures. Results: Five patients (12%) died after operation: four of general causes and one of rupture of the native aorta as a result of persistent infection. Three patients successfully underwent repeat operation for allograft-related complications (one case each of occlusion, septic rupture, and graft-enteric fistula). All surviving patients were discharged after control angiography showed patent allografts. Two patients were unavailable for follow-up. The other 36 patients have been monitored with serial duplex and computed tomography scanning for a mean follow-up of 13.8 months (range 1 to 42 months). There were four late deaths: three were unrelated to the vascular operation, and one may have been caused by late persistent or recurrent infection. Nine patients (26%) have had pathologic changes in the allograft, with three (9%) requiring repeat operation. There were no early or late postoperative amputations in the entire series. Conclusions: Although complete protection against persistent or recurrent infection has not been achieved and late deterioration may be expected, in situ allograft replacement seems to be a major advance in the management of infected infrarenal aortic prosthetic grafts. (J VASC SURG 1993;17:349-56.)

Allograft aortic replacement, as studied experimentally by Alexis Carrel¹ early in this century, was introduced for clinical use in the early years of vascular surgery.², ³, ⁴ Although clinical results were encouraging, several drawbacks were soon recognized. Despite the organization of arterial banks in many major surgical centers, procurement and preservation of human allografts were flawed with difficulties. Secondary dilation and calcification caused by allograft degeneration were observed in a significant number of patients.⁵, ⁶, ⁷ Finally the development of suitable arterial prostheses led to abandonment of arterial allografts in the early 1960s.

Aortic reconstructions with Dacron prostheses have had gratifying results for more than 30 years.⁸, ⁹ Prosthetic infection soon appeared, however, as a rare but devastating complication. Although steady improvement in results has occurred during the last decade,¹⁰, ¹¹, ¹² prosthetic infection is still associated with high mortality and amputation rates, and its management remains a matter of controversy. Stimulated by excellent long-term results reported by heart surgeons after allograft replacement for management of infections that involve the ascending aorta,¹³ and by the availability of arterial allografts from a very active local program for retrieval of multiorgan transplant tissue, we decided to investigate allograft replacement in the management of arterial infections. We have previously reported on our first patient.¹⁴ In this article we report our total experience with 43 patients who have had in situ allograft replacement of infected infrarenal aortic prosthetic grafts, with a mean follow-up of more than 1 year.

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Patients and methods 

Population 

From October 8, 1988, to April 30, 1992, all patients with infected infrarenal aortic prosthetic grafts seen at the Department of Vascular Surgery of the Pitié-Salpétrière University Hospital in Paris, France, were treated by resection of the prosthesis followed by in situ allograft replacement.

There were 43 consecutive patients (36 men and 7 women) with a mean age of 61.9 ± 7.1 years (range 42 to 71 years). Nine patients (21%) had secondary aortoenteric fistulas, whereas 34 (79%) had isolated prosthetic graft infections. Thirteen patients had undergone initial operation in our center, whereas 30 were referred to us after an operation had been performed elsewhere. The initial operation had been performed for aortoiliac occlusive disease in 31 patients, aortic aneurysmal disease in 11 patients, and blunt aortic trauma in 1 patient. Mean interval between the initial operation and allograft replacement was 5.3 ± 4.7 years (range 24 days to 18 years). A mean of 3.2 ± 1.9 operations (range 1 to 8) had been performed before allograft replacement. Clinical events and types of aortic reconstruction before allograft replacement are described in Tables I and II, respectively.

Table I. Clinical events in 43 patients with infected aortic prosthetic graft

Table II. Types of aortic reconstructions with infection in 43 patients

There were 40 Dacron bypasses, two polytetrafluoroethylene bypasses, and one aortic Dacron patch angioplasty. Bypasses extended from the descending thoracic aorta in three patients, from the infrarenal aorta in 36 patients, and from one common iliac artery in three patients. In addition, eight patients had 10 femoropopliteal bypasses with prosthetic grafts, and two patients had secondary grafts that originated from their infected prostheses (one prosthetic graft to the hypogastric artery and one vein graft to the superior mesenteric artery).

Timing of allograft replacement 

As a result of acute bleeding or septic complications, allograft aortic replacement was performed as an emergency procedure in 12 (28%) patients, whereas it was a planned procedure in 31 (72%) patients. In the former group allografts were not always available. In seven (58%) of these patients, acute complications called for an emergency operation with an in situ or extraanatomic prosthetic replacement while awaiting availability of an allograft, which was inserted as a second-stage procedure 7 to 45 days later. In the latter group a delay of a few days or weeks allowed optimal preparation of the patient and procurement of a suitable allograft in all cases. Matching blood and tissue compatibility between recipient and donor was not attempted.

Procurement and preservation of allografts 

Arterial allografts were harvested from cadavers as part of a program to retrieve multiorgan transplant tissue. Bacteriology and virology tests were routinely performed for donors. The whole length of the descending thoracic aorta, aortic bifurcation, and iliac and femoral arteries were obtained. Small collateral branches were transected a few millimeters distal to their origin to facilitate later ligation or suture. Hypogastric and deep femoral arteries were transected 2 to 3 cm distal to their origins to allow revascularization of the corresponding arteries of the recipient. A fragment of the retrieved arterial allograft was routinely cultured for bacteriologic control. After being flushed with heparinized saline solution to eliminate any residual intraarterial blood, allografts were stored at 4° C in 500 ml of a preservation medium that contained heparin and antibiotics (Table III).

Table III. Preservation medium for arterial allograft storage

Allografts were implanted after a minimum interval of 48 hours to decrease cellular antigenicity and a maximum interval of 21 days to avoid late degenerative changes.

Allograft implantation 

A fragment of allograft and a few milliliters of the preservation medium were sent to the bacteriology laboratory. The allograft was rinsed with heparinized saline solution. The collateral branches of the graft were carefully ligated with 5-0 polypropylene sutures.

After heparin (50 IU/kg) was administered systemically, the aorta was cross-clamped. Thoracic, supraceliac, suprarenal, infrarenal, and iliac clamping was performed in 1, 9, 7, 24, and 2 patients, respectively. The left renal vein had to be transected in four patients. The aortic stump and periprosthetic infected tissues were carefully debrided to obtain macroscopically normal tissues. The periprosthetic fluid and part of the infected prosthetic graft were subjected to bacteriologic culture. Infection was due to a variety of organisms; Staphylococcus was the most frequent cause of infection (Table IV).

Table IV. Organisms grown from infected aortic prosthetic grafts in 43 patients

Multiple organisms grew in 12 patients, whereas no organisms were cultured in three patients.

The allograft was implanted in situ, with polypropylene running sutures for proximal and distal anastomoses. It was tunneled to the distal anastomotic site by way of either the previous pathway or a new pathway in close proximity to the previous one. Types of allograft aortic reconstruction are indicated in Table V.

Table V. Types of allograft aortic reconstructions in 43 patients

The allograft revascularized both lower extremities in 40 patients and only one extremity in three patients. Proximal anastomosis was end-to-side to the descending thoracic aorta in one patient, end-to-end to the infrarenal aorta in 35 patients, end-to-side to the infrarenal aorta in four patients, and end-to-side to one common iliac artery in two patients. All infected prosthetic material was usually removed at the same operation. Associated reconstructions of lower limb or visceral arteries were performed in 20 patients (Table VI).

Table VI. Associated reconstructions of lower limb and/or visceral arteries in 20 patients

This included 12 patients in whom hypogastric arteries were revascularized to restore pelvic flow and avoid colonic ischemia. One patient had a concomitant below-knee amputation for septic arthritis of the ankle as a result of septic emboli. A total of 27 associated nonvascular procedures were performed in 19 patients (Table VII), including left colectomy for colonic ischemia in one case and ureteral repair for iatrogenic injury in two cases.

Table VII. Associated nonvascular procedures in 19 patients

Coverage of the allograft replacement used pedicled omentoplasty in 21 patients. Retroperitoneal and inguinal drainage was used routinely. The skin incisions were loosely approximated to avoid superficial abscesses. In cases with major fibrosis or infection of the inguinal region, the skin was left open and the graft was covered with a myoplasty with the sartorius muscle.

All patients received broad-spectrum antibiotics during operation, which were replaced by selective antibiotics after responsible organisms were identified. Administration of antibiotics was continued for at least 6 weeks. No patients received long-term or indefinite antibiotic therapy.

Follow-up 

All surviving patients underwent arteriography with digital subtraction or conventional techniques before discharge. Routine late follow-up included clinical and duplex scanning at 3-month intervals. Late computed tomography (CT) scanning or aortography was performed depending on the results of duplex scanning. Six patients underwent late aortography at 6, 7, 12, 13, 17, and 22 months, respectively. CT scans were obtained in 14 patients from 4 to 42 months after operation.

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Results 

Early results 

Five patients (12%) died during the early (30 days) postoperative period. One patient died of uncontrollable coagulopathy during operation. One patient with an aortoenteric fistula with Klebsiella and Proteus prosthetic graft infection died 13 days after operation of septic rupture of his native aorta proximal to the allograft anastomosis. Autopsy showed an intact allograft. The probable causes of this complication were high-grade virulence of the causative organism and insufficient debridement of the infected aorta. One patient died of septic shock on postoperative day 2. One patient died of intestinal infarction on postoperative day 4. Finally, one patient with angiographically documented, severe, inoperable coronary artery disease died of myocardial infarction on postoperative day 2.

Nineteen (50%) of the 38 surviving patients had one or more non-allograft-related complications (Table VIII).

Table VIII. Postoperative nonallograft-related complications in 38 surviving patients

These included septic shock in two patients and peritonitis from colonic necrosis that necessitated repeat operation for colectomy in one patient. There were three allograft-related complications, including one thrombosis on postoperative day 4, two consecutive septic ruptures of the graft in the same patient on postoperative days 6 and 11, and a graft-to-right colon fistula in one patient on postoperative day 11. All three patients successfully underwent repeat operation by thrombectomy, allograft replacement, and allograft suture, respectively.

Routine aortography before discharge demonstrated patent allograft reconstructions in all 38 surviving patients.

Late results 

Two patients were unavailable for follow-up after 1 and 12 months, respectively. The mean follow-up period was 13.8 months (range 1 to 42 months). Ten patients were monitored for less than 6 months, nine patients from 6 to 12 months, seven patients from 12 to 18 months, three patients from 18 to 24 months, four patients from 24 to 30 months, two patients from 30 to 36 months, and three patients from 36 to 42 months.

Four patients died during late follow-up. One patient died of myocardial infarction 3 months after operation. One patient died of stroke 9 months after operation. One patient died suddenly of high fever and lumbar pain of several weeks' duration 10 months after operation while undergoing a work-up at another hospital. Autopsy was not performed. Aortic rupture caused by persistent or recurrent infection cannot be excluded in this case. The last patient died of liver failure 16 months after operation.

Eight patients had late non-allograft-related complications. Two patients had cardiac complications, ischemic colitis, and secondary ureteral obstruction. One patient had iliocaval venous thrombosis at 2 months. In one patient a recurrent abscess of the femoral triangle developed 3 months after operation. Repeat operation demonstrated a small fragment of the previously infected prosthesis, which was removed uneventfully and without damage to the adjacent allograft.

Nine patients (25% of 36 survivors who underwent late follow-up) had 10 late allograft-related complications. One patient had an occluded aortofemoropopliteal allograft 13 months after operation, which was probably a result of late deterioration of the distal runoff. Allograft thrombectomy and popliteal-to-tibial artery bypass with a new allograft were performed. Limb salvage was achieved despite early postoperative thrombosis of the distal graft. In four patients late stenoses that were diagnosed at 6, 6, 9, and 26 months, respectively, developed in their allograft-to-femoral artery anastomosis. One of the patients underwent a second operation at 7 months. The resected stenosed segment was replaced with a new allograft. One patient with bilateral femoral stenoses was treated by use of vein patch angioplasty 6 months after operation. Histopathologic examination showed typical signs of chronic rejection in the latter two cases: intimal proliferation mainly composed of myofibroblastic cells, medial smooth muscle cell necrosis, and adventitial inflammatory cell infiltration. Moreover, medial calcification was present in one case. The two remaining patients with femoral stenoses have not undergone a second operation. There were no late amputations in the series.

Ultrasonography and CT scanning demonstrated aortic dilation to 3.5 cm with mural thrombus in two patients 38 and 42 months after operation. In both patients, allografts of descending thoracic aorta had been used to replace the infrarenal aorta. To date, neither patient has undergone a second operation. Two other patients have moderate mural thrombus within their aortic allograft without dilation of the latter.

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Discussion 

Our experience with in situ allograft replacement suggests that this technique is a major improvement in the management of infected infrarenal aortic prosthetic grafts. The early mortality rate in our series was 12%, comparing favorably with the best results of recent series that used conventional methods.¹⁰, ¹¹, ¹² More important, there were no early or late amputations in our patients, an outcome that was not matched by any of the conventional methods.

Allografts seem to have optimal resistance to infection, which allows in situ replacement. In situ replacement avoids complications related to aortic stump disease and occlusion or infection of prosthetic extraanatomic bypass grafts.¹⁵ Relatively good results have been recently reported after in situ prosthetic replacement in selected patients with aortoenteric fistulas or low-grade prosthetic infections.¹⁶, ¹⁷, ¹⁸ However, in most cases, in situ prosthetic replacement entails a high risk of persistence or recurrence of infection, which is largely avoided by the use of allografts. Furthermore, the immediate availability of long bifurcated grafts makes the procedure feasible in all cases and technically much easier than autogenous in situ reconstructions with endarterectomy, venous or arterial autografts, or combinations of these.¹⁹ Associated visceral arterial reconstructions (if indicated) are feasible with allografts or autogenous material.

The high resistance of allograft to infection in our series correlates well with the results of experimental studies²⁰ and with clinical results of allograft replacement of the infected proximal ascending aorta.¹³ However, resistance of allograft to infection cannot be considered complete, especially when dealing with highly virulent organisms and incompletely debrided infected tissues. In our series two patients had proven persistent or recurrent infection that was discovered at autopsy in one case and led to emergency repeat operation in the other. In another patient infection was believed to be the primary cause of late death. Careful debridement, coverage of allograft with viable tissue such as omentum, administration of appropriate antibiotics for 4 to 6 weeks, and close clinical and ultrasonic surveillance are important adjuncts to in situ allograft replacement in contaminated fields.

Allograft replacement of an infected infrarenal prosthetic graft entails a repeat laparotomy with the possibility of important blood losses and long operative times along with the necessity of suprarenal clamping in a significant number of patients. Some of our patients at high risk who did not have emergency indications for the direct management of intraabdominal complications might have benefited from a conventional two-stage operation. The first stage includes extraanatomic bypass and distal ligation of the graft; a second procedure includes replacement with aortic allograft and removal of all prosthetic materials after adequate preparation of the patient.

Finally, our choice of the method of allograft preservation may have been less than optimal. We did not completely eliminate allograft antigenicity, because undisputable histologic signs of rejection were found in two of our patients. More important, secondary and late deterioration of arterial allografts has remained a major concern. Its incidence may be expected to increase with longer follow-up, making close surveillance of these allografts an obvious necessity. As already described by Szilagyi et al.,⁶, ⁷ the differences in histologic structures between the elastic aorta and common iliac arteries on one hand and the muscular external iliac and femoral arteries on the other hand probably account for differences in the deterioration patterns (dilation vs occlusive disease). Although indications for late repeat operations will probably arise more frequently, arterial allograft will have served as a bridge to a new in situ prosthetic replacement, a sequence that has already been introduced clinically by Snyder et al.,²¹ who used venous allografts. We believe, however, that the mechanical durability of arterial allografts should be better than that of venous allografts, and the longer interval between allografting and insertion of a new prosthetic graft is probably better. Finally, our short-term preservation method has made allografts unavailable to a significant number of patients who needed emergency operations. On the other hand, a few allografts that had not been used within a few weeks after retrieval had to be discarded.

Cryopreservation is probably the optimal solution to these problems. Organization of allograft arterial cryopreservation banks would allow better management of the available allografts. It would also make it possible to match blood and tissue compatibility between donor and recipient, which is an important concept that could not be applied in our series.

Secondary and late deterioration of allografts is probably partly immunologic in origin.²², ²³ Because immunosuppressive treatment is obviously contraindicated in infected patients, allograft manipulation to decrease antigenicity is the only possibility to avoid rejection and achieve close recipient/donor matching. In our series preservation of allograft at 4° C for more than 48 hours was aimed at allowing death of endothelial cells while preserving the extracellular matrix of the media. Other available methods to reduce allograft antigenicity include physical or chemical destruction of the cellular component of the arterial wall.²⁴ Further experimental work is needed to assess the long-term mechanical behavior of such pretreated allografts.

Although we are far from an optimal answer to the basic problems surrounding arterial allografting, the gratifying results obtained in this clinical series encourage us to continue to offer in situ allograft replacement to patients with infected arterial prosthetic grafts.

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Discussion 

Dr. David C. Brewster (Boston, Mass.). Conventional treatment of aortic graft infection usually consists of graft removal, aortic ligation, and extraanatomic revascularization, which often results in a substantial incidence of death, limb loss, or late, often lethal, complications. Therefore the proposed management scheme of Dr. Kieffer et al. and their encouraging early results certainly merit our very serious consideration.

There are several possible alternatives to traditional therapy. One option is to reconstruct autogenous tissue, which presumably is more resistant to infection, in the contaminated field. A second possible modification is in situ replacement of the infected graft with a new prosthetic conduit, with the hope that surgical debridement and intensive antibiotic therapy can avoid reinfection of the new prosthesis. The appeal of in situ graft replacement, which has been pointed out by Dr. Kieffer et al., consists mainly of simplification of the procedure and perhaps reduction in the acknowledged risk of aortic stump blowout. The major concern, of course, is failure to eradicate the infection and the resultant reinfection of the new prosthesis, which will require yet another operation, a tertiary procedure that surely will be even more difficult than the initial reoperative procedure. Indeed, in many cases the surgeon may have only one good chance of secure infrarenal closure of the aortic stump.

The procedure suggested by Dr. Kieffer et al. borrows important theoretic concepts from both alternative management strategies. Although autogenous tissue is not used, fresh allografts have been established experimentally as a biomaterial of low infectability as compared with prosthetic materials. By use of in situ graft replacement they have reduced the complexities and some of the potential problems associated with conventional management. Their early results seem to be quite successful and noteworthy, with reduced mortality rates, no amputations, and what seems to be a low incidence of persistent infection. One obvious concern, of course, is whether longer follow-up will reveal a higher incidence of recurrent infection or more significant degenerative changes in the allografts than have been manifest to date. Nonetheless, their mean follow-up period of more than a year, with nine of their grafts being observed for up to 2 years, is generally reassuring in this regard.

Even advocates of in situ replacement have acknowledged that the extent of infection and nature of the microorganism are important determinants of the outcome. In situ graft replacement is ideally used in circumstances of limited contamination as a result of low-virulence pathogens such as Staphylococcus epidermidis. Do you advocate in situ allografts in all cases, or are there clinical situations in which standard treatment might still be preferred?

Do you have any suggestions on the procurement and storage of allografts that could improve the availability of suitable conduits for emergency use?

Can you speculate a bit further on whether future modifications in allograft preparation may lessen the problem of antigenicity and reduce the anticipated later degenerative changes that have certainly marred the long-term effectiveness of homografts in the past?

Dr. Edouard Kieffer. In our patients we have applied the treatment in all patients consecutively, but obviously one or two patients who had extensive infections and pus that surrounded the prosthetic grafts would probably have fared better with conventional treatment followed by in situ allograft replacement in a second procedure. We had two patients who had septic shock, which was probably the result of aggressive local treatment.

I believe cryopreservation should be the major focus of progress in this field, and this would allow availability of allografts in all situations, including emergencies.

The future modifications we intend to apply to those allografts are the result of experimental works now in progress in France. We are very hopeful that cellular degradation in the allograft will allow us to reduce antigenicity and have better long-term results, because it seems that most of the late degenerative changes are of immunologic origin.

Dr. David S. Rosengarten (Melbourne, Victoria, Australia). At the Alfred Hospital in Melbourne we have inserted 76 arterial homografts in the infrainguinal or femorofemoral position for either critical ischemia in revision surgery or for sepsis when leg or arm veins are unavailable.

Five of these were inserted to replace infected grafts. Like you, we have been pleased with the case of handling homografts, and we have been delighted to be able to eradicate sepsis in all cases so far without septic recurrence, secondary hemorrhage, or false aneurysms, which has resulted in limb salvage in all cases and no perioperative deaths.

We create a bank of arteries removed at the time of multiorgan harvest and store them at −70° C without cryopreservatives. We believe that we are inserting a mandrel rather than a tube with viable cells.

Do you believe it is necessary to insert a viable graft, and would you comment on whether your technique of preservation actually maintains viability of the homograft?

Dr. Daniel J. Reddy (Detroit, Mich.). Do you have any experience or opinion about the application of this technique in the treatment of primary infections of the aorta? Analogous to the problems encountered when managing prosthetic graft infections, both alternative treatment methods, namely, in situ prosthetic graft replacement and extraanatomic bypass, have their own disadvantages when used to reestablish arterial continuity after excision of the infected aorta.

Dr. Jerry Goldstone (San Francisco, Calif.). I noticed in your presentation there were 12 patients who underwent hypogastric revascularizations. Would you comment on the indications for those procedures?

Dr. Lazar J. Greenfield (Ann Arbor, Mich.). How many of your patients no longer receive antibiotics? I noticed that you mentioned prolonged retroperitoneal drainage. Would you comment further on the length of time for the drainage and whether or not that introduced any added problems of infection?

Dr. Calvin B. Ernst (Detroit, Mich.). There is no reason to believe that a homograft will function any better now than it did 40 years ago when it was first introduced. Therefore I will be very interested in your long-term results beyond the short-term follow-up, because the natural history of a homograft is one of progressive deterioration. Indeed, its use for primary aortic reconstruction is of historical interest only.

Dr. Szilagyi and I have a mutual patient we have been monitoring who has had a well-functioning aortic homograft for more than 30 years, but this is the exception rather than the rule. So, Professor Kieffer, although from early results this seems to be a valuable and innovative approach to a complex problem, I would caution you to wait for prolonged and extensive follow-up before adopting it. However, I think you did imply that this may be a reasonable bridge alternative to definitive therapy, perhaps with a prosthetic graft in the future. How many of your patients have you converted from this bridge to a permanent replacement with a Dacron prosthesis?

Dr. Kieffer. Regarding the use of allografts in the infrainguinal position, we also have a smaller experience with this type of operation. Our experience was not as successful as Dr. Rosengarten's experience, because when infection was cured the midterm results with patency were rather poor. We would not accept this as a substitute to the vein or even prosthetic grafts for infrainguinal reconstruction.

We have used allograft replacement in primary infections but not in the infrarenal position. We have done two descending thoracic aortas with mycotic aneurysms and had two long-term successes. We had done reconstructions for innominate artery infection and one carotid bifurcation infection, all with success, but I have no reason not to use allograft replacement in primary infection of the aorta.

Dr. Goldstone asked about hypogastric arteries. We tended to revascularize hypogastric arteries because the risk of colonic ischemia seemed to be very important in those patients with long-segment replacement of the infrarenal aorta. The hypogastric artery is easier to revascularize than the usual small inferior mesenteric artery, and we have done many hypogastric arteries for that reason and not only for treating impotence or avoiding impotence.

None of our patients received antibiotics for more than 6 weeks as a treatment, and retroperitoneal drainage was limited to 24 or 48 hours to avoid hematomas and secondary infections around the allografts.

I believe the preparation of our allografts is quite different from what was used by Jacques Oudot more than 40 years ago when he performed the first operation, and that close attention to immunologic problems may be the response to the possibility of late deterioration. We did not expect an indefinite cure of infection or arterial problems in our patients; instead, allograft replacement was mainly thought of as a bridge to another prosthetic operation. Our first patient underwent operation in 1988. None of the patients has undergone prosthetic replacement, but obviously there will be some cases in the future.

With this operation, with its limited mortality rates, we have done no amputations in 43 patients; therefore this operation should be considered, we believe, as a progress in the management of this complication.

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