Magnetic Resonance Angiogram Showing the Close Association between the Aortic Graft and the Terminal Duodenum (Arrow).). Four days later, the patient was taken to the operating

Room for an exploratory laparotomy. A periprosthetic enteric fistula measuring 2 cm by 2 cm was found between the terminal duodenum and the proximal right limb of the aortobifemoral bypass graft (Figure Figure 2

Intraoperative Findings.

Figure 2

Intraoperative Findings.). Bile staining and erosion of the proximal right limb of the graft

Were observed.

No overt purulence at the site was seen, but the graft was noted to be very densely adherent to the surrounding tissues. The aortobifemoral and femoral–popliteal bypass grafts were removed, and the defect in the duodenum was repaired. The aortobifemoral graft was replaced with an end-to-side anastomosis of the abdominal aorta with cryopreserved allogeneic femoral-vein conduits, and the femoral–popliteal bypass graft was replaced with autologous saphenous vein. C. albicans was isolated in multiple intraoperative cultures of the excised aortobifemoral graft. The patient's postoperative course was complicated by acute renal failure that required hemodialysis for approximately 1 month before he was discharged home with a slight increase in his baseline creatinine level. He completed a 6-week course of fluconazole. He was doing well 6 months after surgery.

Commentary

At the outset of the case, the lack of blood cultures before the patient received antibiotic therapy on multiple occasions clouded the clinician's ability to make the diagnosis of recurrent bacteremia. However, the history of recurrent low-grade fevers and malaise despite antibiotic therapy and eventual multiple, positive blood cultures prompted a strong clinical suspicion of an endovascular infection. The fact that the organisms identified were not adequately covered by the antibiotics that were given empirically underscores the risks of this approach. The focus shifted to gastrointestinal and aortic disease after the serial isolation of multiple gut pathogens. According to Bayesian reasoning,1 the elimination of a given diagnosis is linked to the elevation of the probability of an alternative diagnosis. Thus, since the negative radiologic, endoscopic, and nuclear medicine studies did not suggest an alternative diagnosis, the diagnosis of aortoenteric fistula became likely. Indeed, the patient underwent exploratory laparotomy almost entirely on the basis of the finding of recurrent bacteremia in the appropriate clinical setting.

In patients with recurrent bacteremia, the bacteriologic findings can provide clues to the ultimate cause. The time required to sterilize blood cultures in response to appropriate antibiotic therapy can vary depending on the disease state, but even in complicated cases of endocarditis, serial blood cultures can be expected to become negative in 1 to 2 weeks. Persistent or recurrent monomicrobial bacteremia should prompt an investigation for an occult source.2 In hospitalized patients, common sources include an infected indwelling catheter or prosthesis, septic thrombophlebitis, or another endovascular infection. Recurrent bacteremia with multiple organisms suggests a different clinical problem. For example, patients with terminal complement deficiency are susceptible to bacteremia from encapsulated organisms, including Neisseria meningitidis and Streptococcus pneumoniae.3 Recovery of enteric pathogens suggests a breach of gastrointestinal integrity,4 which, in this patient, was related to a prosthetic graft infection.

An aortoenteric fistula is a potentially catastrophic clinical entity5 that can be categorized as primary or secondary according to the cause. Primary fistulas are sometimes seen in patients with an abdominal aortic aneurysm, whereas secondary fistulas are more common and are manifested as complications of previous aortic surgery. The usual site is the third or fourth portion of the duodenum because of its retroperitoneal position and proximity to the aorta, although the small bowel, colon, or esophagus can also be involved.6 A secondary aortoenteric fistula is a complication of up to 2% of aortic-graft surgeries, and the rate of death can be as high as 50%. Risk factors include urgent or emergent intervention during the initial surgery, early wound dehiscence or infection, multiple previous vascular procedures,7 or the failure to separate the graft and bowel with healthy omentum. Although a catastrophic acute hemorrhage may be the first sign of a fistula, the bleeding can be indolent and manifested only as iron-deficiency anemia. In some patients, there may not be any evidence of bleeding. Aortoenteric fistulas can also mimic subacute bacterial endocarditis, with low-grade fevers, malaise, and weight loss.

Making the diagnosis requires a high index of suspicion. Upper gastrointestinal endoscopy may reveal a luminal defect in the duodenum. Contrast-enhanced CT of the abdomen may show signs of perigraft inflammation and infection, whereas unenhanced CT may reveal gas in the perienteric graft space. Because the bleeding may be intermittent, the sensitivity of conventional angiography is limited. Leukocyte scintigraphy detects more than 80% of graft infections, but it has relatively low sensitivity for simple fistulas unless there is considerable infection.7,8 Given the absence of an overt abscess surrounding the fistula in this patient, the negative scan is not surprising.

Treatment typically entails removal of the graft and any infected tissue, revascularization, and closure of the bowel fistula.9 Data regarding the duration and choice of antibiotic therapy are limited; recommendations for treatment are largely based on experience with bacterial endocarditis and generally involve the use of adjunctive antibiotic therapy for 4 to 6 weeks after surgery. This therapy is directed against organisms recovered from blood cultures, the graft tissue, or both. In this patient, the timing of surgical intervention was key. Without this “stitch in time,” the outcome could have been catastrophic.

No potential conflict of interest relevant to this article was reported.

We thank Chip Chambers, M.D., for his critical review of an earlier draft of the manuscript.

Source Information

From the Division of Infectious Diseases, Department of Medicine, University of California at San Francisco, San Francisco.

Address reprint requests to Dr. Graber at the Division of Infectious Diseases, Department of Medicine, San Francisco General Hospital, Bldg. 30, Rm. 3300, Box 0811, 1001 Potrero Ave., San Francisco, CA 94110, or at christopher.graber@ucsf.edu.

Date: 2015-12-11; view: 867