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Anaerobic cellulitis as the result of Clostridium perfringens: A rare cause of vascular access graft infection
Anaerobic cellulitis as the result of Clostridium perfringens: A rare cause of vascular access graft infection Luc G. Y. Claeys, MD, and Ricardo Matamoros, MD, Herne, Germany Infection of prosthetic vascular access grafts is the second most common complication of vascular access and represents a challenge encountered by the vascular surgeon. Anaerobic graft infections are rare. We report on a case of a prosthetic vascular access graft infection with Clostridium perfringens. To our knowledge, only one other case with an infected arteriovenous shunt caused by C perfringens has been reported. The patient, a 67-year-old woman with end-stage renal failure as the result of polycystic renal disease, was seen with an infected pseudoaneurysm at the arterial puncture site of the loop graft on the left arm. There was associated purulence at the time of operation. Surgical management consisted of complete graft removal because of the presence of small tunnel abscesses. C perfringens was found in the resected pseudoaneurysm and graft material. Infected pseudoaneurysms most likely are attributable to repetitive punctures in one small area and to a break in sterile technique. A compromised vascular supply, not infrequent in patients for hemodialysis, may lower the oxidation reduction potential, which allows anaerobic bacteria, such as C perfringens, to cause infection. (J Vasc Surg 2002;35:1287-8.)
Infection of prosthetic vascular access grafts is the second most common complication of vascular access.1 Staphylococcus aureus is the most frequent causative organism, but other pathogens have been isolated. Infections of prosthetic vascular grafts, including prosthetic vascular access grafts, with Clostridium are rare. The clinical implications, natural history, and optimal therapy of such graft infections are unknown.2 A Medline review disclosed one case of an arteriovenous shunt infection as the result of Clostridium perfringens.3 This report represents our only encounter with clostridial infection of a vascular access graft. CASE REPORT A 67-year-old woman was admitted to the emergency room at the University Hospital Herne with a bleeding complication at the puncture site of the prosthetic vascular access graft. End-stage renal failure was caused by polycystic renal disease, and chronic hemodialysis had been performed since 1985. The medical history included a cholecystectomy, and mild arterial hypertension was shown to be in good control. The patient received a standard polytetrafluoroethylene-loop graft from the brachial artery to the cephalic vein of the left arm in 1994. Since that time, the patient underwent two thrombectomies and two angioplasties for stenosis and restenosis in the subclavian vein. Before admission to the hospital, the loop graft functioned well for 15 months. Five weeks before admission, the patient was seen with a painful swelling at the arterial punction site. At admission, the patient’s condition was From the Department of Vascular Surgery, University Hospital Herne, Ruhr-University Bochum. Competition of interest: nil. Reprint requests: Luc G.Y. Claeys, MD, Department of Vascular Surgery, University Hospital Herne, Ruhr-University Bochum, Hoelkeskampring 40, 44625 Herne, Germany (e-mail: [email protected]). Copyright © 2002 by The Society for Vascular Surgery and The American Association for Vascular Surgery. 0741-5214/2002/$35.00 ⫹ 0 24/4/122026 doi:10.1067/mva.2002.122026
afebrile, despite local signs of infection. Vital signs included a blood pressure of 135/80 mm Hg and a pulse of 83 beats per minute. Physical examination results were remarkable for localized cellulitis, erythema, tenderness, skin erosion, and persistent drainage of blood over the punction site. The swelling impressed as a pseudoaneurysm covered by a blood crust as the result of chronic bleeding. Empiric treatment with vancomycin hydrochloride was started. Preoperative blood test results were healthy except for renal parameters. At operation, the pseudoaneurysm was excluded and the roof of the aneurysm was opened. A defect of 1 ⫻ 0.5 cm was observed in the wall of the graft. Surgical management consisted of complete graft removal, because infection of the graft with small tunnel abscesses was manifest, debridement, and drainage. Samples were taken from the aneurysm wall and graft and inoculated into vials with aerobic and anaerobic conditions. The bacteriologic study results revealed a mixed type of infection with low counts of Escherichia coli and Pseudomonas aeruginosa and high counts of C perfringens. Antibiotic treatment consisted of vancomycin hydrochloride for 10 days and penicillin G when aneurysm tissue and graft cultures grew C perfringens. Penicillin G treatment was maintained for 4 weeks. X-ray results showed no evidence of osteitis. The postoperative course was uneventful. At discharge, laboratory and clinical findings were healthy. Evaluation results at 2 and 6 months after discharge did not reveal any symptoms or physical findings. Dialysis was performed with a Sheldon catheter, and 2 months later, an autologous arteriovenous shunt of a superficial femoral artery to long saphenous vein in the straight configuration was constructed.
DISCUSSION Infection of prosthetic vascular access grafts is the second most common complication of vascular access, after thrombosis, and is responsible for 10% of all deaths in patients for chronic hemodialysis.1 The incidence rate of prosthetic vascular access graft infection varies from 5% to 1287
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20%.4 Gram-positive organisms predominate in graft infections, and more than 70% of all access-related infections are attributable to S aureus. Roughly 20% of vascular access infections are caused by gram-negative organisms, including Ps aeruginosa and E coli. Anaerobic infection of a vascular graft is rare.5,6 Clostridial vascular access graft infection is a case event. A compromised vascular supply, not infrequent in patients for hemodialysis, has been suggested to lower the oxidation-reduction potential, allowing anaerobic bacteria to cause infection.3 Clostridia are gram-positive, anaerobic, spore-forming, motile bacteria (family Bacillaceae) that are ubiquitous in nature. Most of the 60 recognized species are obligate anaerobes. However, few are aerotolerant. Clostridia are generally found in soil and in the gastrointestinal tract of humans and animals. Many toxigenic strains are pathogenic to humans and include C perfringens, C septicum, C fallax, and others. Infection associated with clostridia range from localized wound contamination to overwhelming systemic disease. Clinical symptoms develop when environmental conditions are conductive to the proliferation of these opportunists and the elaboration of the toxin.2 Despite the isolation of clostridial species from many serious traumatic wounds, the prevalence of severe infections caused by species of the genus Clostridium is low. Therefore, the diagnosis of clostridial infection, in association with positive cultures, must be primarly on the basis of clinical findings.7 Two main factors that appear to be essential to the development of severe disease are tissue necrosis and a low oxidation-reduction potential.2 C perfringens requires about 14 amino acids and at least six additional growth factors for optimal growth. These nutrients are present in necrotic tissue. Furthermore, immunocompromising conditions, such as in patients for chronic hemodialysis or transplant, appear to predispose to clostridial infections.8,9 Anaerobic cellulitis is a localized infection involving the skin and soft tissue and is caused by clostridia alone or with other bacteria. There are no systemic signs of toxicity, although the infection may invade locally, producing necrosis. These infections tend to be relatively indolent, spreading slowly to contiguous areas.7 In our case, the diagnostic criteria were fulfilled because localized suppurative infection of the skin and soft tissue was manifest and because bacteriology results revealed a mixed type of infection with high counts of C perfringens. The primary pathogen in this case was most likely C perfringens, whereas E coli and Ps aeruginosa were present as opportunists. Although some clostridial diseases may arise exogenously, the source of most is the patient’s own flora. Puncture site infections in patients for hemodialysis generally are most likely attributable to a break in sterile puncture technique, hematoma/pseudoaneurysm formation, or
other technical problems during cannulation. Infected pseudoaneurysms are a frequent complication of vascular access grafts and are potentially dangerous because they can lead to life-threatening hemorrhage. Puncture site infections manifest themselves with local tenderness, swelling, and erythema centered over the cannulation site. This type of infection can progress to skin erosion in which the graft is exposed without gross infection or erosions with localized infection or abscess formation.1 Once access site infection has developed, prompt treatment is important for any possibility of graft salvage and for prevention of sepsis. The initial treatment is administration of systemic antibiotics. Empiric treatment with vancomycin hydrochloride can be started until culture and sensitivity results return. In case of a clostridial infection, penicillin G has excellent activity against most strains of C perfringens and is the drug of choice for treatment of such infections.7 Graft infection with tunnel abscesses usually requires complete graft removal and drainage to control the infection. However, consideration of graft salvage should occur in each case of graft infection.10 In the case of an infection as the result of clostridia, complete graft removal is mandatory. REFERENCES 1. Kudva A, Hye RJ. Management of infectious and cutaneous complications in vascular access. Semin Vasc Surg 1997;10:184-90. 2. Holland FW, Darling RC, Chang BB, Shah DM, Leather RP. Clostridial aortic graft infection. Ann Vasc Surg 1994;8:387-9. 3. Oliveras A, Orfila A, In ˜igo V. Clostridium perfringens: an unusual pathogen infecting arteriovenous shunts for dialysis. Nephron 1998;80: 479. 4. Palder SB, Kirkman RL, Whittemore AD, Hakim RM, Lazarus JM, Tilney NL. Vascular accesss for hemodialysis: patency rates and results of revision. Ann Surg 1985;202:235-9. 5. Gorbach SL, Thadepalli H. Isolation of clostridium in human infections: evaluation of 114 cases. J Infect Dis 1975;131:581-5. 6. Brook I. Role of anaerobic bacteria in aortofemoral graft infection. Surgery 1988;104:843-5. 7. Kasper DL, Zaleznik DF. Gasgangrene, antibiotic-associated colitis, and other Clostridial infections. In: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, et al, eds. Harrison⬘s principles of internal medicine. 14th edition. New York: McGraw-Hill; 1998. p. 906-10. 8. Meer RR, Songer JG, Park DL. Human disease associated with Clostridium perfringens enterotoxin. Rev Environ Contam Toxicol 1997; 150:75-94. 9. West M, Rirenne J, Chavers B, Gillingham K, Sutherland DE, Dunn DL, et al. Clostridium difficile colitis after kidney and kidney-pancreas transplantation. Clin Transplant 1999;13:318-23. 10. Schwab DP, Taylor SM, Cull DL, Langan EM, Snyder BA, Sullivan TM, et al. Isolated arteriovenous dialysis access graft segment infection: the results of segmental bypass and partial graft excision. Ann Vasc Surg 2000;14:63-6. Submitted Aug 22, 2001; accepted Nov 28, 2001.
Infection of prosthetic vascular access grafts is the second most common complication of vascular access.1 Staphylococcus aureus is the most frequent causative organism, but other pathogens have been isolated. Infections of prosthetic vascular grafts, including prosthetic vascular access grafts, with Clostridium are rare. The clinical implications, natural history, and optimal therapy of such graft infections are unknown.2 A Medline review disclosed one case of an arteriovenous shunt infection as the result of Clostridium perfringens.3 This report represents our only encounter with clostridial infection of a vascular access graft. CASE REPORT A 67-year-old woman was admitted to the emergency room at the University Hospital Herne with a bleeding complication at the puncture site of the prosthetic vascular access graft. End-stage renal failure was caused by polycystic renal disease, and chronic hemodialysis had been performed since 1985. The medical history included a cholecystectomy, and mild arterial hypertension was shown to be in good control. The patient received a standard polytetrafluoroethylene-loop graft from the brachial artery to the cephalic vein of the left arm in 1994. Since that time, the patient underwent two thrombectomies and two angioplasties for stenosis and restenosis in the subclavian vein. Before admission to the hospital, the loop graft functioned well for 15 months. Five weeks before admission, the patient was seen with a painful swelling at the arterial punction site. At admission, the patient’s condition was From the Department of Vascular Surgery, University Hospital Herne, Ruhr-University Bochum. Competition of interest: nil. Reprint requests: Luc G.Y. Claeys, MD, Department of Vascular Surgery, University Hospital Herne, Ruhr-University Bochum, Hoelkeskampring 40, 44625 Herne, Germany (e-mail: [email protected]). Copyright © 2002 by The Society for Vascular Surgery and The American Association for Vascular Surgery. 0741-5214/2002/$35.00 ⫹ 0 24/4/122026 doi:10.1067/mva.2002.122026
afebrile, despite local signs of infection. Vital signs included a blood pressure of 135/80 mm Hg and a pulse of 83 beats per minute. Physical examination results were remarkable for localized cellulitis, erythema, tenderness, skin erosion, and persistent drainage of blood over the punction site. The swelling impressed as a pseudoaneurysm covered by a blood crust as the result of chronic bleeding. Empiric treatment with vancomycin hydrochloride was started. Preoperative blood test results were healthy except for renal parameters. At operation, the pseudoaneurysm was excluded and the roof of the aneurysm was opened. A defect of 1 ⫻ 0.5 cm was observed in the wall of the graft. Surgical management consisted of complete graft removal, because infection of the graft with small tunnel abscesses was manifest, debridement, and drainage. Samples were taken from the aneurysm wall and graft and inoculated into vials with aerobic and anaerobic conditions. The bacteriologic study results revealed a mixed type of infection with low counts of Escherichia coli and Pseudomonas aeruginosa and high counts of C perfringens. Antibiotic treatment consisted of vancomycin hydrochloride for 10 days and penicillin G when aneurysm tissue and graft cultures grew C perfringens. Penicillin G treatment was maintained for 4 weeks. X-ray results showed no evidence of osteitis. The postoperative course was uneventful. At discharge, laboratory and clinical findings were healthy. Evaluation results at 2 and 6 months after discharge did not reveal any symptoms or physical findings. Dialysis was performed with a Sheldon catheter, and 2 months later, an autologous arteriovenous shunt of a superficial femoral artery to long saphenous vein in the straight configuration was constructed.
DISCUSSION Infection of prosthetic vascular access grafts is the second most common complication of vascular access, after thrombosis, and is responsible for 10% of all deaths in patients for chronic hemodialysis.1 The incidence rate of prosthetic vascular access graft infection varies from 5% to 1287
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20%.4 Gram-positive organisms predominate in graft infections, and more than 70% of all access-related infections are attributable to S aureus. Roughly 20% of vascular access infections are caused by gram-negative organisms, including Ps aeruginosa and E coli. Anaerobic infection of a vascular graft is rare.5,6 Clostridial vascular access graft infection is a case event. A compromised vascular supply, not infrequent in patients for hemodialysis, has been suggested to lower the oxidation-reduction potential, allowing anaerobic bacteria to cause infection.3 Clostridia are gram-positive, anaerobic, spore-forming, motile bacteria (family Bacillaceae) that are ubiquitous in nature. Most of the 60 recognized species are obligate anaerobes. However, few are aerotolerant. Clostridia are generally found in soil and in the gastrointestinal tract of humans and animals. Many toxigenic strains are pathogenic to humans and include C perfringens, C septicum, C fallax, and others. Infection associated with clostridia range from localized wound contamination to overwhelming systemic disease. Clinical symptoms develop when environmental conditions are conductive to the proliferation of these opportunists and the elaboration of the toxin.2 Despite the isolation of clostridial species from many serious traumatic wounds, the prevalence of severe infections caused by species of the genus Clostridium is low. Therefore, the diagnosis of clostridial infection, in association with positive cultures, must be primarly on the basis of clinical findings.7 Two main factors that appear to be essential to the development of severe disease are tissue necrosis and a low oxidation-reduction potential.2 C perfringens requires about 14 amino acids and at least six additional growth factors for optimal growth. These nutrients are present in necrotic tissue. Furthermore, immunocompromising conditions, such as in patients for chronic hemodialysis or transplant, appear to predispose to clostridial infections.8,9 Anaerobic cellulitis is a localized infection involving the skin and soft tissue and is caused by clostridia alone or with other bacteria. There are no systemic signs of toxicity, although the infection may invade locally, producing necrosis. These infections tend to be relatively indolent, spreading slowly to contiguous areas.7 In our case, the diagnostic criteria were fulfilled because localized suppurative infection of the skin and soft tissue was manifest and because bacteriology results revealed a mixed type of infection with high counts of C perfringens. The primary pathogen in this case was most likely C perfringens, whereas E coli and Ps aeruginosa were present as opportunists. Although some clostridial diseases may arise exogenously, the source of most is the patient’s own flora. Puncture site infections in patients for hemodialysis generally are most likely attributable to a break in sterile puncture technique, hematoma/pseudoaneurysm formation, or
other technical problems during cannulation. Infected pseudoaneurysms are a frequent complication of vascular access grafts and are potentially dangerous because they can lead to life-threatening hemorrhage. Puncture site infections manifest themselves with local tenderness, swelling, and erythema centered over the cannulation site. This type of infection can progress to skin erosion in which the graft is exposed without gross infection or erosions with localized infection or abscess formation.1 Once access site infection has developed, prompt treatment is important for any possibility of graft salvage and for prevention of sepsis. The initial treatment is administration of systemic antibiotics. Empiric treatment with vancomycin hydrochloride can be started until culture and sensitivity results return. In case of a clostridial infection, penicillin G has excellent activity against most strains of C perfringens and is the drug of choice for treatment of such infections.7 Graft infection with tunnel abscesses usually requires complete graft removal and drainage to control the infection. However, consideration of graft salvage should occur in each case of graft infection.10 In the case of an infection as the result of clostridia, complete graft removal is mandatory. REFERENCES 1. Kudva A, Hye RJ. Management of infectious and cutaneous complications in vascular access. Semin Vasc Surg 1997;10:184-90. 2. Holland FW, Darling RC, Chang BB, Shah DM, Leather RP. Clostridial aortic graft infection. Ann Vasc Surg 1994;8:387-9. 3. Oliveras A, Orfila A, In ˜igo V. Clostridium perfringens: an unusual pathogen infecting arteriovenous shunts for dialysis. Nephron 1998;80: 479. 4. Palder SB, Kirkman RL, Whittemore AD, Hakim RM, Lazarus JM, Tilney NL. Vascular accesss for hemodialysis: patency rates and results of revision. Ann Surg 1985;202:235-9. 5. Gorbach SL, Thadepalli H. Isolation of clostridium in human infections: evaluation of 114 cases. J Infect Dis 1975;131:581-5. 6. Brook I. Role of anaerobic bacteria in aortofemoral graft infection. Surgery 1988;104:843-5. 7. Kasper DL, Zaleznik DF. Gasgangrene, antibiotic-associated colitis, and other Clostridial infections. In: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, et al, eds. Harrison⬘s principles of internal medicine. 14th edition. New York: McGraw-Hill; 1998. p. 906-10. 8. Meer RR, Songer JG, Park DL. Human disease associated with Clostridium perfringens enterotoxin. Rev Environ Contam Toxicol 1997; 150:75-94. 9. West M, Rirenne J, Chavers B, Gillingham K, Sutherland DE, Dunn DL, et al. Clostridium difficile colitis after kidney and kidney-pancreas transplantation. Clin Transplant 1999;13:318-23. 10. Schwab DP, Taylor SM, Cull DL, Langan EM, Snyder BA, Sullivan TM, et al. Isolated arteriovenous dialysis access graft segment infection: the results of segmental bypass and partial graft excision. Ann Vasc Surg 2000;14:63-6. Submitted Aug 22, 2001; accepted Nov 28, 2001.