| | Prosthetic stent graft infection after endovascular abdominal aortic aneurysm repairReceived 1 March 2007; accepted 7 May 2007. ObjectiveThe purpose of this report is to discuss the incidence, diagnosis, and management of stent graft infections after endovascular aneurysm repair (EVAR). MethodsData were collected from the hospital database and medical case notes for all patients with infected endografts after elective or emergency EVAR for abdominal aortic aneurysm (AAA) during the last 8 years in two university teaching hospitals in Northern Ireland. The data included the patient’s age, gender, presentation of sepsis, treatment offered, and the ultimate outcome. The diagnosis of graft-related sepsis was established by a combination of investigations including inflammatory markers, labelled white cell scan, computed tomography (CT) scan, microbiology cultures, and postmortem examination. ResultsGraft-related septic complications occurred in six of 509 patients, including 433 elective repairs and 76 emergency endografts for ruptured AAA. Two patients presented with left psoas abscess and were treated successfully with extra-anatomic bypass and removal of the infected stent graft. Two more patients presented with infected graft without other evidence of intra-abdominal sepsis: one underwent successful removal of the infected prosthesis with extra-anatomical bypass, and the other was treated conservatively and died of progressively worsening sepsis. The fifth patient presented with unexplained fever and died suddenly, with a postmortem diagnosis of aortoenteric fistula and ruptured aneurysm. The last patient presented with an aortoenteric fistula, was treated conservatively in view of concurrent myelodysplasia, and died of possible aneurysm rupture. ConclusionThis report emphasizes the need for continued awareness of potential graft-related septic complications in patients undergoing EVAR of AAA. Attention to detail with regard to sterility and antibiotic prophylaxis during stent grafting and during any secondary interventions is vital in reducing the risk of infection. In addition, early recognition and prompt treatment are essential for a successful outcome. Prosthetic aortic graft infection after open repair of abdominal aortic aneurysm (AAA) has been well reported during the last 3 decades with a range of clinical manifestations and therapeutic options,1 but infective complications involving endografts after endovascular aneurysm repair (EVAR) have received little attention. Most EVAR surveillance concentrates on the technical aspects of the procedure, including endoleaks, device migration, neck dilatation, and rupture.2, 3, 4, 5 So far, there is limited knowledge on infective complications after EVAR. Since Chalmers et al6 described the first case of an infected stent in 1993, more centers have reported graft-related septic complications, usually in the form of single case reports. A recent multicenter retrospective study of 65 patients with infected endografts7 failed to provide enough data for statistical analysis. The purpose of this short series is, therefore, to simply examine our experience of infective complications after EVAR at two university centers rather than define the broad principles in the management of infected endovascular grafts. Patients and methods  Data were collected from the hospital database for all patients undergoing elective or emergency EVAR for AAA during the last 8 years in the only two university teaching hospitals undertaking endovascular stenting in Northern Ireland, with a population of 1.7 million. Patients undergoing EVAR were followed up in the vascular clinics at 1, 3, and 12 months and at yearly interval thereafter, unless there was a reason for earlier follow-up. At each visit, patients underwent four views of plain abdominal radiographs (anteroposterior, lateral, right anterior oblique, and left anterior oblique) to assess the mechanical integrity of the stent, contrast-enhanced computed tomography (CT) scan, and a blood test for levels of serum urea, creatinine, and electrolytes. Those patients who were reviewed in the follow-up clinic ≤15 months of the date of data collection were considered to be compliant with the follow-up. If a patient failed to attend follow-up, the general practitioner was contacted. All deaths were identified through the hospital system, the general practitioner, and the Registry Office for Deaths in Northern Ireland. In addition, we were notified of any patient who became unwell and was admitted to another hospital for any reason. In view of a closely linked community, all patients live ≤100-mile radius from the two hospitals performing EVAR. Therefore, the follow-up arrangements are adequate to identify any graft-related complications in a closely monitored EVAR population. We were familiar with the six patients who presented with infective complications in this series. The data collected for these patients included age, gender, comorbidities, type of stent graft used, prophylactic antibiotic regimen, adjuvant endovascular interventions, presentation of sepsis, time interval between EVAR and graft sepsis, treatment offered, and the ultimate outcome. The diagnosis of graft-related sepsis was established by a combination of investigations, including inflammatory markers, labelled white cell scan, CT scan, microbiology cultures, and postmortem examination. Statistical analysis Kaplan-Meier life-table analysis was used for freedom from graft-related sepsis using SPSS 14.0.1 (SPSS Inc, Chicago, Ill) for Windows (Microsoft Inc, Redmond, Wash). Patients were censored if they were converted to open repair, underwent axillofemoral graft, died during the course of follow-up, or failed to comply with the follow-up protocol. Results From November 1998 to January 2007, 509 patients underwent EVAR for AAA, including 433 elective repairs and 76 emergency endografts for ruptured AAA. During this period, stent graft–related sepsis was encountered in six patients, for a total follow-up duration of 968 person-years. The incidence of graft-related sepsis was 6.2/1000 person-years (6/968 × 1000). The average duration of follow-up was 1.9 years (range, 0 to 8.2 years), with only 15.1% (77/509) lost to follow-up (Table I). The cause of death in patients undergoing elective and emergency EVAR is summarized in Table II. Life-table analysis demonstrating freedom from graft-related sepsis is illustrated by Kaplan-Meier curve (Fig 1). The outcomes of the six patients who presented with graft-related sepsis are summarized (Table III). | | |  | Cause of death | Patients, n | |
|---|
| Elective EVAR repair | 108 | | |  Cardiac | 22 | | | Malignancy | 19 | | | Multiple organ failure | 14 | | | Respiratory failure | 12 | | | Renal failure | 7 | | | Stroke | 4 | | | Bowel ischemia | 3 | | | Systemic sepsis | 3 | | | Ruptured AAA after EVAR | 3 | | | Endograft infection | 2 | | | Bleeding diverticular disease | 1 | | | No record available | 18 | | | Emergency EVAR for ruptured AAA | 38 | | | Multiple organ failure | 12 | | | Cardiac | 7 | | | Uncontrolled rupture | 4 | | | Coagulopathy | 3 | | | Acute renal failure | 3 | | | Respiratory tract infection | 2 | | | Stroke | 2 | | | Type III endoleak | 1 | | | Bowel ischemia | 1 | | | Malignancy | 1 | | | Endograft infection | 1 | | | No record available | 1 | | | | |
| | | | Variable | Patient 1 | Patient 2 | Patient 3 | Patient 4 | Patient 5 | Patient 6 | |
|---|
| Age at graft infection | 71 | 75 | 77 | 76 | 67 | 70 | | | Gender | Male | Male | Male | Male | Male | Male | | | Pre-existing risks | Angina, NIDDM, smoking | Angina, CABG, COAD, smoking, hypertension | Ex-smoking, prostatism | NIDDM, hypertension, chronic renal impairment | MI, CVA, smoking, hypertension, COAD | CABG, Crohn disease | | | Immunodeficiency | Nil | Nil | Nil | Nil | Nil | Myelodysplasia | | | Urgency | Elective | Elective | Elective | Elective | Emergency | Elective | | | Device | Aortobiiliac | Aortobiiliac | Aortobiiliac | Aortobiiliac | Aortouniiliac | Aortobiiliac | | | Manufacturer | Zenith | Zenith | Zenith | Talent | Talent | Zenith | | | Procedure setting | OR | OR | OR | IR | IR | IR | | | Antibiotic prophylaxis | Cefuroxime, 1.5 g | Cefuroxime, 1.5 g | Cefuroxime, 1.5 g | Cefuroxime, 1.5 g | Cefuroxime, 1.5 g | Cefuroxime, 1.5 g | | | IV single dose | Teicoplanin, 400 mg | — | — | Teicoplanin, 400 mg | Teicoplanin, 400 mg | — | | | Anesthesia | General | General | General | General | Local | General | | | Adjuvant procedures | Coil embolization of left IIA | Nil | Thrombin injection, coil embolization | Nil | Nil | Nil | | | Presentation | Left psoas abscess | Left psoas abscess | Endograft infection | Endograft infection | AEF | AEF | | | Interval between EVAR sepsis diagnosis | 6 months | 12 months | 61 months | 12 months | 10 months (PM) | 5 months | | | Microbiology culture | Propionibacterium avidum (blood) | Streptococcus spp; coliforms (abscess) | Staphylococcus epidermidis (blood) | Staphylococcus aureus (blood) | Nil | Nil | | | Treatment | EAB, removal of infected graft | EAB, removal of infected graft | EAB, removal of infected graft | Conservative | Nil | Conservative | | | Outcome | Survived | Survived | Survived | Died, systemic sepsis (8 wks postdiagnosis) | Died, rupture | Died, possible rupture | | | Duration of follow-up from graft removal to date/death | 3 months, alive | 53 months, died of diverticular bleeding | 35 months, alive | — | — | — | | | | |
Patient 1 A 71-year-old man was admitted for elective repair of aortic and bilateral common iliac artery aneurysms. The right internal iliac artery was already thrombosed, but the left was aneurysmal and patent. This vessel was coil-embolized 3 days before EVAR. The stent graft procedure was performed uneventfully using a Zenith aortobiiliac stent (Cook Europe, Bjaeverskov, Denmark), and a routine follow-up CT scan 1 month after the primary repair was satisfactory. The patient was admitted 6 months later with left flank and back pain, and a pyrexia of 38°C. The leukocyte count was 9000/mm3, C-reactive protein (CRP) level was 191 mg/L, and the erythrocyte sedimentation rate (ESR) was 127.0 mm/h. Propionibacterium avidum was found on blood culture, and a labelled white cell scan showed increased uptake in relation to the distal part of the main body of the stent graft (Fig 2). Intravenous piperacillin/tazobactam was started based on sensitivities obtained from blood cultures. A CT scan showed an area of low density in the left psoas muscle with peripheral enhancement suggestive of an acute abscess (Fig 3). Under CT guidance, 250 mL of pus was aspirated from the abscess cavity and a drain was left in situ. The culture of aspirated pus failed to show any growth, however. Bilateral axillofemoral bypasses were done before the exposure of the aneurysm through a midline approach. A suprarenal aortic clamp was applied before the pus-filled aneurysm sac was opened (Fig 4). Because the stent graft was barbed, the upper end was crimped down before it was pulled down. The iliac limbs of the graft were well incorporated into the native vessel and were removed surgically. Oversewing of aorta and both iliac arteries was done using a single layer of nonabsorbable sutures, without the need for double rows, which could weaken the aortic stump. A drain was left in the aneurysm sac. Culture of the stent graft and pus did not show any growth. Intravenous antibiotics were continued until the patient was discharged at 3 weeks, followed by a further course of oral antibiotics as an outpatient. At 3 months, his inflammatory markers had returned to normal and a follow-up CT scan was unremarkable. The antibiotics were stopped at this stage. Patient 2 A 75-year-old man underwent uneventful endovascular repair of an inflammatory AAA using an aortobiiliac Zenith stent graft. The follow-up CT scan at 4 months showed a small, well-circumscribed collection anterior to the left psoas muscle. This yielded thick pus at aspiration, and despite aggressive antibiotic treatment with intravenous piperacillin/tazobactam, it progressively enlarged and extended to the left limb of the stent graft. At 12 months after primary repair, he became progressively more septic with pyrexia, a leukocyte count of 18,800/mm3, CRP level of 156.0 mg/L, and a blood culture showing Streptococcus constellatus. At surgery, a supraceliac aortic balloon was positioned in the descending aorta through the transfemoral route. Laparotomy revealed an inflammatory mass surrounding the neck of the aneurysm. The supraceliac balloon was inflated before the aneurysm sac was opened and the infected graft was explanted. The aortic stump and both common iliac arteries were oversewn. A further abscess was located close to the left iliac limb of the graft extending over the left psoas. The procedure was completed by an axillobifemoral bypass after the abdomen was closed and redraped. In this particular case, the operating surgeon preferred to insert the axillofemoral graft after the removal of the infected endograft to diminish bacteremia and prevent possible infection of the axillofemoral graft. The periendograft pus grew coliforms and streptococci, and the patient was treated with intravenous piperacillin/tazobactam for 3 weeks postoperatively, followed by a further course of oral ciprofloxacillin. His postoperative recovery was complicated by dialysis-dependent renal failure and atrial fibrillation requiring long-term anticoagulation. His inflammatory markers returned to baseline at 9 months after graft removal (leukocytes 7000/mm3 and CRP <7 mg/L) at which stage his antibiotics were stopped. He remained on dialysis and died 4.5 years later from a massive bowel hemorrhage secondary to diverticular disease. Patient 3 A 77-year-old man underwent elective EVAR for a 6.8-cm AAA using an aortobiiliac Zenith stent graft. Postoperatively, a type II endoleak from a lumbar artery caused slow sac expansion. By 4 years after the primary repair, the sac had expanded to 7.9 cm, and he underwent unsuccessful ultrasound-guided percutaneous thrombin injection into the sac in an attempt to seal the leak. Nine months later, with continued expansion of the sac to 8.1 cm, coil embolization was done for the persistent type II endoleak. Both adjuvant procedures were done in the interventional radiology suite without prophylactic antibiotic cover. The patient was readmitted 12 days after the coil embolization with a 1-week history of backache and pyrexia. The leukocyte count was 9500/mm3, CRP level was 305.3 mg/L, and the ESR was 127.0 mm/h. A CT scan demonstrated soft-tissue thickening and air in the right anterolateral aspect of the aneurysm sac suggestive of graft infection. A blood culture grew coagulase negative Staphylococcus, and he was started on intravenous piperacillin/tazobactam and teicoplanin. He underwent right axillobifemoral bypass and excision of the infected graft with oversewing of the aortic stump and both common iliac arteries. Cultures of the pus collected intraoperatively and the excised graft were negative, and intravenous antibiotics were continued for 2 weeks, followed by a further course of oral doxycycline and rifampicin until his CRP level returned to base line. The patient made a good recovery, and 12 months later, his CT scan showed no evidence of residual sepsis, with a CRP level of 14 mg/L and functioning axillofemoral bypass. Patient 4 A 76-year-old man was admitted 12 months after a successful elective EVAR with a Talent aortobiiliac device (Medtronic, Inc, Minneapolis, Minn). He presented with lower abdominal pain, fever, leukocytosis (24,000/mm3), and high CRP level (240 mg/L). Three consecutive blood cultures grew Staphylococcus aureus, and a CT scan showed marked thickening of the aortic wall at the neck of AAA, with adjacent lymphadenopathy and stranding of the surrounding fat planes suggestive of intense inflammatory response (Fig 5). He had an acute coronary event during his hospital stay and was considered unsuitable for graft removal in view of his deteriorating general condition, impaired renal function, and poor cardiac reserve. In view of his comorbidities, he was treated with intravenous flucloxacillin and oral rifampicin based on the sensitivities from blood culture. Unfortunately, he died from systemic sepsis and progressively deteriorating cardiac function at 8 weeks from the diagnosis of his graft infection. A postmortem examination confirmed an intact stent graft without evidence of rupture and severe coronary artery disease. Patient 5 A 67-year-old man underwent successful EVAR for a ruptured AAA using an aortouniiliac Talent device, an occluder in the contralateral iliac artery, and a femorofemoral bypass. Results of follow-up CT scans at 2 and 6 months were unremarkable. He was admitted 10 months after with profuse sweating, backache, and a feeling of malaise. The patient’s hemodynamic parameters were stable on admission, with hemoglobin level of 9.4 gm/dL, leukocyte count of 16,800/mm3, CRP level of 185 mg/L, and creatinine level of 269 μmol/L. An urgent CT scan was arranged, but before this could take place, the patient suddenly collapsed with massive hematemesis. Resuscitation was unsuccessful, and a postmortem examination revealed aortic inflammation with adhesions and a fistulous communication between the duodenum and anterior aortic wall. Patient 6 This last patient, a 70-year-old man with a history of Crohn’s disease, has previously been reported.8 He underwent endovascular repair using a bifurcated Zenith stent graft and presented 4 months later with epigastric discomfort, fever, and melena. The presence of an aortoenteric fistula (AEF) was confirmed by CT scan and a barium meal. He was treated conservatively with intravenous antibiotics in view of his concurrent aggressive myelodysplastic condition and poor prognosis. A repeat CT scan 8 months after the initial repair showed complete destruction of the aneurysm sac. Two months later, he suddenly collapsed and died in the hospital. The family declined a request for postmortem examination. Discussion Conventional open repair of AAA has a reported graft infection rate of 0.5% to 3%.9 In this series, the incidence of stent graft–related sepsis was 6.2/1000 person-years. Ducasse et al7 reported a mean frequency of infection at 0.43% based on 42 cases of infected endografts within an overall experience of 9739 endovascular procedures. This frequency does not represent the true incidence of stent graft infections, however, because information on completeness of follow-up and deaths is not included. Nevertheless, the Ducasse series includes a much larger database from multiple centers than our report and thus might be a more reliable source for patient-based incidence of EVAR infection. So far, the association between adjuvant endovascular procedures and the risk of stent graft infection is unclear. Two patients in this series underwent an associated endoluminal procedure. The coil embolization of the left internal iliac artery aneurysm was done 3 days before EVAR in patient 1, and a left psoas abscess and graft infection later developed. In this case, it is difficult to ascertain whether the coil embolization was responsible for the subsequent events. However, coil embolization for type II endoleak in patient 3 was clearly followed by a rapid onset of graft sepsis during the course of the next 10 days, with no previous evidence of graft infection for >5 years. It was interesting to note that graft sepsis was associated with AEF in two patients. Anecdotally, we thought that the excessive anterior neck angulation in patient 5, with possible extra pressure on the duodenum, could have contributed towards the fistulization; however, the Talent stent graft used had no intramural barbs. Although the suprarenal component of the Zenith stent graft has barbs, it is unlikely that it contributed to the formation of an AEF in patient 6. The AEF is more likely to be related to the presence of small bowel Crohn’s disease. These interpretations are unsupported speculations, however, and it is still most likely that a primary stent graft infection led eventually to erosion of an adherent segment of bowel. Other causes of AEF in association with the aortic stent graft described in recent literature include stent migration,10, 11 erosion of the aorta and duodenum by embolization coils,12, 13 fabric rupture,14 inflammatory nature of the aneurysm,15 and bacterial aortitis with chronic duodenal erosion.16 Reports have shown that patients with infected stent grafts who are managed conservatively with antimicrobial therapy and percutaneous drainage can still survive.7 In this series, however, two of the three patients without surgical treatment died of ruptured aneurysm. In patient 5, the death was sudden, and treatment options could not be exercised; in fact, the diagnosis of AEF was only made at the postmortem examination. The third patient treated conservatively died of progressive sepsis and cardiac failure. Although conservative treatment of high-risk patients has been proposed by some authors, most would agree that the infected stent graft should be removed if the patient’s condition permits.17 The three patients in the current series who underwent removal of the infected prosthesis and axillobifemoral bypass survived. Ducasse et al7 reported 16% mortality with extra-anatomic bypass in this situation. Although the three patients undergoing graft removal in our series had extra-anatomic reconstruction, recent studies have questioned the choice of this approach. The duration of the antimicrobial treatment in patients undergoing removal of the infected prosthesis in this series was guided by serial estimation of CRP level. Because no current guidelines exist on the exact duration of treatment in this situation, our regimen was based on expert consensus involving local microbiologist, vascular surgeons, and the interventional vascular radiologists. Another change in our protocol for antibiotic prophylaxis was made after the finding of graft-related sepsis in patient 3, where thrombin injection without antibiotic cover was followed a week later by graft infection. We now routinely cover all secondary interventions in EVAR patients by a single intravenous dose of teicoplanin and cefuroxime. Our case series has two main limitations. First, the number of infected patients still remains very small, but endograft-related sepsis is an uncommon event. In view of the small numbers, the contribution of different risk factors toward the etiology of graft infection is difficult to evaluate. As the duration of follow-up increases beyond the first decade, more cases may come to light. Second, this series is insufficient to provide a comparative data set to allow assessment of the effectiveness of different treatment modalities in endograft infections. Conclusion The incidence of stent graft–related sepsis is currently low. Nevertheless, as more patients are treated by endovascular technique, there is an increasing need to be vigilant for the risk of graft infection. Better appreciation of the potential risk of stent graft infection and an obsession to detail in patient preparation and surgical technique, along with timely use of appropriate antibiotic regimens during primary and secondary interventions, may help to minimize the risk of graft-infection. A high index of suspicion is also required for diagnosis because the clinical presentation could be varied. Removal of the infected prosthesis and restoration of the blood flow to the lower extremities is recommended when possible. Author contributions Conception and design: MS, BL, CS Analysis and interpretation: MS, LL, CS Data collection: MS, PE, AC, PB Writing the article: MS, CS Critical revision of the article: MS, ML, LL, PE, AC, PB, CS Final approval of the article MS, BL, LL, PE, AC, PB, CS Statistical analysis: MS Obtained funding: Not applicable Overall responsibility: CS We offer our greatest appreciation to all the consultant vascular surgeons and interventional vascular radiologists at Belfast City Hospital and Royal Victoria Hospital for contributing cases, which led to the successful completion of this study. We also thank Patrick Comiskey, Medical Photography Department, Belfast City Hospital, for providing technical support in production of the images shown in this article. References 1. 1O’Connor S, Andrew P, Batt M, Becquemin JP. A systemic review and meta-analysis of treatments for aortic graft infections. J Vasc Surg. 2006;44:38–45. Abstract | Full Text |
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17. 17Zegelman M, Gunther G. Infected grafts require excision and extra-anatomic reconstruction: against the motion. In: Greenhalgh RM editors. The evidence for vascular or endovascular reconstruction. Philadelphia, Pa: WB Saunders; 2002;p. 235–245. a Department of Vascular and Endovascular Surgery, Belfast City Hospital, Belfast, United Kingdom b Department of Vascular Surgery, Royal Victoria Hospital, Belfast, United Kingdom.  Reprint requests: Muhammad Anees Sharif, FRCS, Department of Vascular and Endovascular Surgery, Belfast City Hospital, Lisburn Rd, Belfast BT9 7AB, UK.
Competition of interest: none. PII: S0741-5214(07)00945-7 doi:10.1016/j.jvs.2007.05.027 © 2007 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved. | |
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