Clostridial Aortic Graft Infection Fred Wilson Holland, MD, R. Clement Darling III, MD, Benjamin B. Chang, MD, Dhiraj M. Shah, MD, and Robert P. Leather, MD, Albany, New York
Aortic graft infection represents one of the most formidable challenges encountered by the vascular surgeon. Current principles of treatment are based on experience primarily derived from infection with Staphylococcus and enteric bacteria. Anaerobic prosthetic infection is a case event. Infection with Clostridium has heretofore been reported only twice. An additional case of clostridial infection of an aortic prosthesis is presented with review of the literature. Its clinical significance and management are discussed. (Ann Vasc Surg 1994;8:387389.)
Aortic graft infection w i t h anaerobic bacteria is an u n c o m m o n occurrence. The clinical implications, n a t u r a l history, a n d optimal t h e r a p y of anaerobic infections are u n k n o w n . Extensive review of the literature disclosed only t w o cases of clostridial aortic graft infection. 1'2 There are infreq u e n t reports of aortic graft infection b y anaerobic bacteria. T M This report represents our only e n c o u n t e r w i t h clostridial infection of a n aortic graft. The significance a n d p a t h o g e n i c i t y of this isolate are presented.
CASE R E P O R T A 75-year-old man with a history of hypertension and aortic stenosis was admitted for elective repair of an asymptomatic infrarenal abdominal aortic aneurysm. Preoperatively he had no symptoms or laboratory signs consistent with sepsis. Through a left retroperitoneal exposure, a bifurcated polytetrafluoroethylene graft was placed with exclusion of the abdominal aortic aneurysm. The right limb was placed anatomically to the right common femoral artery. The left lower ex-
From the Department of Vascular Surgery, Albany Medical College, Albany, N.Y. Reprint requests: Dhiraj M. Shah, MD, Albany Medical College, Vascular Surgery, A-61 VA, 47 New Scotland Ave., Albany, NY 12208.
tremity was reperfused by an external iliac anastomosis. The common iliac arteries were excluded. The postoperative course was complicated by multiple episodes of intermittent fever, leukocytosis, and nonoliguric renal failure. In addition to perioperative vancomycin (penicillin allergy), empiric treatment with ciprofloxacin was instituted. Blood cultures obtained during this interval were unremarkable. Intermittent fever continued, the renal failure resolved, and on the twenty-third postoperative day the patient had mild abdominal discomfort. Subsequently, an abdominal CT scan showed gas in the native aortic sac (Fig. 1). He was then transferred to our care for definitive treatment. At operation, through a midline approach, the native aortic sac contained a hematoma with no evidence of purulent debris. It was debrided and then copiously irrigated. Intraoperative Gram stain demonstrated gram-positive rods and many leukocytes. The duodenum, cecum, and sigmoid colon were mobilized. There was no evidence of colonic injury or retroperitoneal extension. A Silastic drain was placed within the native aorta and the abdomen was closed. Intraoperatire culture isolated Clostridia (not perfringens, species not identified) and Bacteroides fragilis. The patient's fever was reduced on the first postoperative day. There was complete resolution of the abdominal pain and the white blood count returned to normal. Antibiotics were continued for 6 weeks postoperatively (imipenem, 500 ml intravenously every 12 hours). 387
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Fig. 1, Preoperative CT scan shows air within the native aorta.
ENTERIC 41
OTHER 7
NAEROBIC 3 G R A M POSI i iv,'49
Follow-up CT scan demonstrated resolution of the abscess. A radiolabeled white blood cell scan was unremarkable. The patient has remained asymptomatic during 7 months of follow-up.
DISCUSSION Anaerobic infection of a n aortic prosthesis is a n u n c o m m o n event responsible for 3% of all graft infections. The incidence of aortic graft infection is only i% to 2%, w i t h enteric organisms and
Staphylococcus a c c o u n t i n g for 90% of the p a t h o gens isolated 3"~ (Fig. 2). E x t e n s i v e review of the literature disclosed only two additional cases of prosthetic aortic graft infection w i t h clostridial species. Gorback a n d Thadepalli 1 first reported clostridial aortic graft infection, w h i c h p r e s e n t e d as a n inguinal fistula. At operation, a n appendicular abscess was f o u n d in c o m m u n i c a t i o n w i t h the graft. C. perfringens and Staphylococcus epidermidis were cultured f r o m the fistula.
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Brook 2 described aortic graft infection with an unidentified Clostridium, which presented as a pseudoaneurysm. This was treated by graft removal. This report represents our only encounter with clostridial graft infection or more precisely perigraft infection. The early occurrence and isolation of B. fragilis in conjunction with a Clostridium suggests a technical error with unrecognized coIonic injury. Clostridia are gram-positive, anaerobic, sporeforming bacilli. Of the more than 60 strains, most are obligate anaerobes; however, few are aerotolerant. Clostridia are ubiquitous in nature and in the gastrointestinal tract of humans. Many toxigenic strains are pathogenic to humans and include C..perfringens, C. novyi, C. septicum, C. histolyticure, C. sordellii, and C. fallax. However, same clostridia show little pathogenicity and their isolation is of questionable clinical significance. Ls Infection with clostridia and its clinical presentation are determined by the elaboration of the toxin. Unlike the highly invasive Staphylococcus and Streptococcus, clostridia are comparatively noninvasive. Clinically significant disease develops w h e n environmental conditions are conducive to the proliferation of these opportunists and the subsequent elaboration of the toxin. Knowledge of infection with clostridia is derived from experience with myonecrosis and obstetric complications, s'6 In wounds from which clostridia are isolated, only a small proportion develop clinically significant disease. The corollary is that the majority of clostridial isolates are of no clinical importance. Isolation of clostridia from vascular prostheses in patients without systemic manifestations or contiguous soft tissue involvement is most likely coincidental and may herald infection with more invasive pathogens. The primary pathogen in the present case was most likely B. fragilis, whereas clostridia were present only as opportunists. Gorback and Thadepalli ~ isolated S. epidermidis in conjunction with Clostridium. The pathogenicity of the former bacterium and its role in aortic graft infection is well documented?-~2 The natural history and optimal treatment of anaerobic graft infection is yet to be determined.
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There is evidence of successful treatment with antibiotic therapy alone without graft removal. ~3 The present case lends further support to this concept. However, additional studies, both clinical and animal, are necessary to establish optimal therapy. Until then, patients selected for antibiotic therapy require meticulous surveillance with frequent examinations. Other useful parameters and adjunctive studies for surveillance include complete blood count, sedimentation ratio, ultrasonography, CT, and radiolabeled white cell scans.
CONCLUSION Aortic graft infection with anaerobic bacteria represents a clinical entity distinct from infection with enteric bacteria and Staphylococcus. Isolation of clostridia is most likely a coincidental event that is of tittle consequence. Optimal treatment and the natural history of anaerobic graft infection are still in the evolutionary stage. REFERENCES 1. Gorback SL, Thadepalli H. Isolation of clostfidium in human infections: Evaluation of 114 cases. J Infect Dis 1975;131: 581-585. 2. Brook I. Role of anaerobic bacteria in aortofemoral graft infection. Surgery I988;105:843-845. 3. Wilson SE, Veith FJ, Hobson RW, et al. Vascular Surgery: Principles and Practice. New York: McGraw-HiU, 1987, p 894. 4. Leather RP, Chang BB, Shah DM, et al. Diagnosis and Treatment of Infected Vascular Prosthetic Grafts. Complications in Surgery (in press). 5. Zissner SH. Microbiology, ed 16. Clostridium perfringens and Other Clostfidia of Wound Infections. New York: AppletonCentury-Crofts, 1976, pp 657-669. 6. Ahrenholz DH. Necrotizing soft tissue infections. Surg Clin North Am 1988;68:199-214. 7. Edwards MJ, Richardson JD, Klamer TW. Management of aortic prosthetic infections. Am J Surg 1988;155:327-330. 8. Bunt TJ. Synthetic vascular graft infections. I. Graft infections. Surgery 1983;93:733-746. 9. Schmitt DD, Bandyk DF, Pequet AJ, et al. Mucin production by Staphylococcus epidermidis. Arch Surg 1986;121:89-95. 10. Bandyk DF, Berni GA, Theile BL, et al. Aortofemoral graft infection due to Staphylococcus epidermidis. Arch Surg 1984; 119:102-108. 11. Conn JH, Hardy JD, Chavez CM, et al. Infected arterial grafts. Ann Surg 1970;I71:704-714. 12. Edwards WH, Martin RS, Jenkins JM, et al. Primary graft infections. J Vasc Surg 1987;6:235-239. 13. Bodner SJ, Koenig MG, Goodman JS. Bacteremic Bacteroides infections. Ann Intern Med 1970;73:537-544.