Hepatic gas gangrene following liver transplantation

Abstract

A 45-year-old man presented with a 2-day history of diarrhea, fever, and progressing fatigue. The patient had undergone a liver transplantation for cryptogenic cirrhosis with Roux-en-Y hepaticojejunostomy 9 years earlier. No vascular complications had emerged in the posttransplant period. Immunosuppression was achieved initially with prednisolone and cyclosporine A, and was later switched to mycophenolate mofetil and prednisolone. Upon admission, the patient's blood pressure was 100/70 mm Hg, and his pulse was 115 beats per minute, with an oxygen saturation of 93% while breathing 6 liters of oxygen per minute through nasal cannula. Upon examination, the patient appeared somnolent, but his chest and abdomen were unremarkable. Laboratory investigations revealed procalcitonin of 56.8 μg/L, creatinine of 487 μmol/L, and aspartate aminotransferase of 1,502 U/L. Escherichia coli in the first blood culture prompted the administration of ceftriaxone plus metronidazole. A computed tomography scan of the abdomen revealed massive aerobilia (Fig. 1) and gas-filled cavity of the right hepatic lobe. During the next hours, the patient became anuric, and the hemodynamic situation deteriorated rapidly despite maximal treatment. Surgical debridement that might have ended up in hepatectomy was not regarded to be an option in the face of advanced multiorgan failure. The patient died shortly thereafter. A computed tomography scan of the abdomen revealing massive aerobilia (black arrow) and gas-filled cavity of the right hepatic lobe (white arrows). The postmortem examination revealed a large abscess formation within the right lobe of the liver, and portal-vein thrombosis. The necrotic hepatic parenchyma was infiltrated by gram-positive rods. Blood cultures tested positive for Clostridium perfringens shortly thereafter. C. perfringens is a member of the normal colonic flora. Spores in soil or food can enter the organism and cause food poisoning or gas gangrene with a high mortality rate.1C. perfringens appears as a short, plump, strongly gram-positive rod (2 to 4 μm long and 1 to 1.5 μm wide) that possesses a central or subterminal spore.2 Alpha toxin (phospholipase C) is one of at least 12 antigenic protein toxins of C. perfringens and induces hemolysis, platelet destruction, cardiogenic shock, and multiple organ failure.3 Spontaneous C. perfringens bacteremia has been associated with neoplastic diseases (mortality rate of 58% in a case series of 136 episodes) and liver cirrhosis (mortality rate of 30% in a case series of 73 episodes).4, 5 Hepatic involvement of C. perfringens infection can lead to pylephlebitis, which carries a bad prognosis and may come to attention by floating high amplitude ultrasound echoes within the extrahepatic and intrahepatic portal veins.6 In the current case, the cause of portal vein thrombosis, which was recognized post mortem but not seen on the initial computed tomography scan, remains unclear. The patient had not received vascular grafts during the transplantation. Moreover, the hepatic artery as well as the hepatic veins were patent on computed tomography imaging. Five cases of Clostridium infections following liver transplantation have recently been described in the literature.7-11 At least 2 patients died, another underwent immediate retransplantation. Although this strain of C. perfringens was sensitive to metronidazole, the antibiotic therapy was probably initiated too late to be effective. Broad-spectrum coverage with concomitant administration of penicillin G, aminoglycoside, and clindamycin is now recommended for C. perfringens infections.2, 12 Surgical debridement of all necrotic tissue should be performed immediately, and liver retransplantation has been suggested as a salvage therapy.10 The current case reminds us, however, that C. perfringens infections in transplant patients may come to attention too late to be effectively treated.