LIVER TRANSPLANTATION 20:493–494, 2014
LETTER FROM THE FRONTLINE
Fatal Massive Infectious Gas Gangrene in a Liver Transplant Recipient Received November 22, 2013; accepted December 26, 2013.
TO THE EDITORS: Massive liver gas gangrene is a rare but devastating complication. Very few cases of liver gas gangrene have been reported in liver transplant recipients, with the main specific cause being hepatic artery thrombosis with subsequent biliary tree necrosis.1 In these cases, treatment required the use of specific antibiotics and eventually retransplantation. Here we describe a case of fulminant massive liver gas gangrene that occurred 2 days after transplantation because of the contamination of the cold-storage liquid. A 59-year-old man was admitted to our unit for liver transplantation. The indication for transplantation was genetic hemochromatosis complicated by hepatocellular carcinoma. His liver function was normal, and the patient underwent right hepatectomy before transplantation. During his stay on the waiting list, the patient had no specific treatment. The liver graft was harvested from an 81-year-old man. The cause of death was cerebral hemorrhaging. The donor’s hospital stay was 3 days, and his liver function was normal. The combined liver and kidney retrieval was reported to be simple, without any intestinal injury. The liver graft was implanted orthotopically with standard vessel reconstruction. The procedure lasted 10 hours, and the recipient received blood transfusions (5 U). The perioperative antibiotics were amoxicillin and cefazolin during the induction of anesthesia. A routine direct examination of the preservation fluid was positive for gram-negative bacteria. Once a preservation-fluid antibiogram was available, the antibiotics were changed to piperacillin and tazobactam for gram-negative coverage. The cold ischemia time was 13 hours; this was explained by a hepatectomy that was difficult because of important surgical adhesion after a previous right hepatectomy. The time for anastomoses was 69 minutes (caval, portal, and
arterial anastomoses). The liver was flushed out with cold (4 C) human albumin (5%). The patient was extubated 6 hours after transplantation and was rapidly fully conscious. The urine output was satisfactory, and the liver immediately produced normal, dark “motor-oil” bile. On day 2 after transplantation, the patient became febrile; Enterobacter cloacae was detected in both blood and bile samples from the recipient. A posteriori, the same bacteria were found in the graft’s preservation fluid. The liver function was suboptimal with declining blood transaminase levels and an increasing prothrombin time. The patient’s creatininemia remained normal (95 lmol/L). Because routine duplex ultrasound was not informative, abdominal computed tomography was performed. It showed massive gaseous infiltration of intrahepatic portal veins and suprahepatic veins. There were no signs of intestinal ischemia, and the main portal vein and artery were patent in the graft hilum (Fig. 1). An infectious etiology was then suggested as the cause of hepatic gas gangrene (HGG). At that moment, because the patient was in good clinical condition with moderately elevated leukocytosis (15,600/lL) and decreasing transaminase blood levels, the decision was made to wait and evaluate the patient’s clinical and hemodynamic condition hourly. Urgent liver retrieval and retransplantation were planned in case of any signs of failure. Unfortunately, on the morning of day 3, the patient suddenly went into cardiac arrest and eventually died despite 35 minutes of resuscitation maneuvers. During a postmortem examination, complete liver necrosis was observed. There were no signs of intestinal ischemia or superior mesenteric vessels, and the hepatic artery and the portal vein were patent. The patients who received the 2 kidneys retrieved from the same donor had preservation fluid infected with a gram-negative bacillus (E. cloacae). Both had an uneventful course.
The study protocol received a prior approval by the review committee of our institution. The authors have no conflicts of interest to declare. Address reprint requests to Karim Boudjema, M.D., Ph.D., Department of Hepatobiliary and Digestive Surgery, University Hospital Center of Rennes, University of Rennes 1, 2 rue Henri Le Guilloux 35033 Rennes cedex 9, Rennes, France. Telephone: 1332 99 28 98 41; FAX: 1332 99 28 41 29; E-mail: [email protected] DOI 10.1002/lt.23821 View this article online at wileyonlinelibrary.com. LIVER TRANSPLANTATION. DOI 10.1002/lt. Published on behalf of the American Association for the Study of Liver Diseases
C 2014 American Association for the Study of Liver Diseases. V
494 LETTER FROM THE FRONTLINE
LIVER TRANSPLANTATION, April 2014
Figure. 1. (A) Portal venous phase. A massive gas presence in the entire liver vein was observed. (B) Computed tomography coronal reconstruction. There was evidence of extrahepatic portal flow without gas inside the vessel (arrow). No abdominal cause of the massive hepatic gas presence was found.
DISCUSSION HGG can be identified with plain radiography, computed tomography, and ultrasound. Among these imaging modalities, computed tomography is the most sensitive and specific examination for detecting hepatic portal venous gas and for demonstrating associated intra-abdominal problems and coexisting abnormal air.2 Ischemic and inflammatory bowel disease, obstructive airway disease, connective tissue disease, chemotherapy, and organ transplantation are known causes of hepatic portal venous gas.3 The clinical situation is often complex with no unequivocal identification of the underlying causes. In the present case, an infection due to E. cloacae was considered to be the etiology. The infection was passed from the preservation graft fluid to the recipient. Enterobacter is a facultative anaerobic gramnegative bacterium. In an ischemic liver, it can switch from aerobic metabolism to anaerobic metabolism as the oxygen tension decreases, and this can result in HGG.4 Only a few cases of HGG have been reported in the literature,5 and they have occurred from 1 day to 9 years after transplantation. In these cases, HGG was due to hepatic artery thrombosis or bowel ischemia and required either retransplantation or bowel resection, and the results were devastating (100% mortality). Infection of the preservation fluid has never been reported as a cause of HGG. We believe that in our case, an immediate total hepatectomy with a temporary portocaval shunt during the wait for urgent retransplantation would have been a better therapeutic option.
Hepatic portal venous gas is a life-threatening complication after liver transplantation. Urgent retransplantation is the only possible chance for a favorable outcome. Giovanni Battista Levi Sandri, M.D. Michel Rayar, M.D. Laurent Sulpice, M.D. Pauline Houssel-Debry, M.D. Karim Boudjema, M.D., Ph.D. Department of Hepatobiliary and Digestive Surgery University Hospital Center of Rennes University of Rennes 1 Rennes, France
REFERENCES 1. Patrick LE, Atkinson GO, Dodson TF, Niemer P. Gas gangrene limited to the right lobe of the liver after orthotopic liver transplant: sonographic, plain film and CT findings. Pediatr Radiol 1994;24:340-341. 2. Abboud B, El Hachem J, Yazbeck T, Doumit C. Hepatic portal venous gas: physiopathology, etiology, prognosis and treatment. World J Gastroenterol 2009;15:3585-3590. 3. Nelson AL, Millington TM, Sahani D, Chung RT, Bauer C, Hertl M, et al. Hepatic portal venous gas: the ABCs of management. Arch Surg 2009;144:575-581. 4. Hall TR, Poon A, Yaghsczian H, Boechat MI. Gas gangrene: an unusual cause of graft failure in an orthotopic pediatric liver transplant. Pediatr Radiol 1992;22:579581. 5. Doblecki-Lewis S, Palaios E, Bejarano PA, Tzakis AG, Selvaggi G, Morris MI. Hepatic gas gangrene following orthotopic liver transplantation: three cases treated with re-transplantation and a review of the literature. Transpl Infect Dis 2008;10:280-285.
LETTER FROM THE FRONTLINE
Fatal Massive Infectious Gas Gangrene in a Liver Transplant Recipient Received November 22, 2013; accepted December 26, 2013.
TO THE EDITORS: Massive liver gas gangrene is a rare but devastating complication. Very few cases of liver gas gangrene have been reported in liver transplant recipients, with the main specific cause being hepatic artery thrombosis with subsequent biliary tree necrosis.1 In these cases, treatment required the use of specific antibiotics and eventually retransplantation. Here we describe a case of fulminant massive liver gas gangrene that occurred 2 days after transplantation because of the contamination of the cold-storage liquid. A 59-year-old man was admitted to our unit for liver transplantation. The indication for transplantation was genetic hemochromatosis complicated by hepatocellular carcinoma. His liver function was normal, and the patient underwent right hepatectomy before transplantation. During his stay on the waiting list, the patient had no specific treatment. The liver graft was harvested from an 81-year-old man. The cause of death was cerebral hemorrhaging. The donor’s hospital stay was 3 days, and his liver function was normal. The combined liver and kidney retrieval was reported to be simple, without any intestinal injury. The liver graft was implanted orthotopically with standard vessel reconstruction. The procedure lasted 10 hours, and the recipient received blood transfusions (5 U). The perioperative antibiotics were amoxicillin and cefazolin during the induction of anesthesia. A routine direct examination of the preservation fluid was positive for gram-negative bacteria. Once a preservation-fluid antibiogram was available, the antibiotics were changed to piperacillin and tazobactam for gram-negative coverage. The cold ischemia time was 13 hours; this was explained by a hepatectomy that was difficult because of important surgical adhesion after a previous right hepatectomy. The time for anastomoses was 69 minutes (caval, portal, and
arterial anastomoses). The liver was flushed out with cold (4 C) human albumin (5%). The patient was extubated 6 hours after transplantation and was rapidly fully conscious. The urine output was satisfactory, and the liver immediately produced normal, dark “motor-oil” bile. On day 2 after transplantation, the patient became febrile; Enterobacter cloacae was detected in both blood and bile samples from the recipient. A posteriori, the same bacteria were found in the graft’s preservation fluid. The liver function was suboptimal with declining blood transaminase levels and an increasing prothrombin time. The patient’s creatininemia remained normal (95 lmol/L). Because routine duplex ultrasound was not informative, abdominal computed tomography was performed. It showed massive gaseous infiltration of intrahepatic portal veins and suprahepatic veins. There were no signs of intestinal ischemia, and the main portal vein and artery were patent in the graft hilum (Fig. 1). An infectious etiology was then suggested as the cause of hepatic gas gangrene (HGG). At that moment, because the patient was in good clinical condition with moderately elevated leukocytosis (15,600/lL) and decreasing transaminase blood levels, the decision was made to wait and evaluate the patient’s clinical and hemodynamic condition hourly. Urgent liver retrieval and retransplantation were planned in case of any signs of failure. Unfortunately, on the morning of day 3, the patient suddenly went into cardiac arrest and eventually died despite 35 minutes of resuscitation maneuvers. During a postmortem examination, complete liver necrosis was observed. There were no signs of intestinal ischemia or superior mesenteric vessels, and the hepatic artery and the portal vein were patent. The patients who received the 2 kidneys retrieved from the same donor had preservation fluid infected with a gram-negative bacillus (E. cloacae). Both had an uneventful course.
The study protocol received a prior approval by the review committee of our institution. The authors have no conflicts of interest to declare. Address reprint requests to Karim Boudjema, M.D., Ph.D., Department of Hepatobiliary and Digestive Surgery, University Hospital Center of Rennes, University of Rennes 1, 2 rue Henri Le Guilloux 35033 Rennes cedex 9, Rennes, France. Telephone: 1332 99 28 98 41; FAX: 1332 99 28 41 29; E-mail: [email protected] DOI 10.1002/lt.23821 View this article online at wileyonlinelibrary.com. LIVER TRANSPLANTATION. DOI 10.1002/lt. Published on behalf of the American Association for the Study of Liver Diseases
C 2014 American Association for the Study of Liver Diseases. V
494 LETTER FROM THE FRONTLINE
LIVER TRANSPLANTATION, April 2014
Figure. 1. (A) Portal venous phase. A massive gas presence in the entire liver vein was observed. (B) Computed tomography coronal reconstruction. There was evidence of extrahepatic portal flow without gas inside the vessel (arrow). No abdominal cause of the massive hepatic gas presence was found.
DISCUSSION HGG can be identified with plain radiography, computed tomography, and ultrasound. Among these imaging modalities, computed tomography is the most sensitive and specific examination for detecting hepatic portal venous gas and for demonstrating associated intra-abdominal problems and coexisting abnormal air.2 Ischemic and inflammatory bowel disease, obstructive airway disease, connective tissue disease, chemotherapy, and organ transplantation are known causes of hepatic portal venous gas.3 The clinical situation is often complex with no unequivocal identification of the underlying causes. In the present case, an infection due to E. cloacae was considered to be the etiology. The infection was passed from the preservation graft fluid to the recipient. Enterobacter is a facultative anaerobic gramnegative bacterium. In an ischemic liver, it can switch from aerobic metabolism to anaerobic metabolism as the oxygen tension decreases, and this can result in HGG.4 Only a few cases of HGG have been reported in the literature,5 and they have occurred from 1 day to 9 years after transplantation. In these cases, HGG was due to hepatic artery thrombosis or bowel ischemia and required either retransplantation or bowel resection, and the results were devastating (100% mortality). Infection of the preservation fluid has never been reported as a cause of HGG. We believe that in our case, an immediate total hepatectomy with a temporary portocaval shunt during the wait for urgent retransplantation would have been a better therapeutic option.
Hepatic portal venous gas is a life-threatening complication after liver transplantation. Urgent retransplantation is the only possible chance for a favorable outcome. Giovanni Battista Levi Sandri, M.D. Michel Rayar, M.D. Laurent Sulpice, M.D. Pauline Houssel-Debry, M.D. Karim Boudjema, M.D., Ph.D. Department of Hepatobiliary and Digestive Surgery University Hospital Center of Rennes University of Rennes 1 Rennes, France
REFERENCES 1. Patrick LE, Atkinson GO, Dodson TF, Niemer P. Gas gangrene limited to the right lobe of the liver after orthotopic liver transplant: sonographic, plain film and CT findings. Pediatr Radiol 1994;24:340-341. 2. Abboud B, El Hachem J, Yazbeck T, Doumit C. Hepatic portal venous gas: physiopathology, etiology, prognosis and treatment. World J Gastroenterol 2009;15:3585-3590. 3. Nelson AL, Millington TM, Sahani D, Chung RT, Bauer C, Hertl M, et al. Hepatic portal venous gas: the ABCs of management. Arch Surg 2009;144:575-581. 4. Hall TR, Poon A, Yaghsczian H, Boechat MI. Gas gangrene: an unusual cause of graft failure in an orthotopic pediatric liver transplant. Pediatr Radiol 1992;22:579581. 5. Doblecki-Lewis S, Palaios E, Bejarano PA, Tzakis AG, Selvaggi G, Morris MI. Hepatic gas gangrene following orthotopic liver transplantation: three cases treated with re-transplantation and a review of the literature. Transpl Infect Dis 2008;10:280-285.
