Krom, Ruud A. F.

A 59‐year‐old female developed symptoms of graft‐versus‐host disease 3½ weeks after liver transplantation for primary biliary cirrhosis. Symptoms of graft‐versus‐host disease included fever, erythroderma with bullae formation, and mucosal surface ulceration. Donor lymphocytes were present in the peripheral blood. Despite treatment with equine antilymphoblast globulin, steroids and, eventually, cyclosporine withdrawal, she developed neutropenia and succumbed to sepsis. At autopsy, she had marked lymphocyte depletion involving the bone marrow and both native and donor origin lymph nodes. As expected, the liver was normal. The clinical and pathological features were remarkably similar to those of the few other reported cases of graft‐versus‐host disease after liver transplantation and transfusion‐associated graft‐versus‐host disease; therapy is usually ineffective, and progression of disease leads to pancytopenia and death from sepsis.

Biliary tract complications are a significant risk following orthotopic liver transplantation (OLT). We reviewed the biliary tract complications of the first 50 liver transplants in 44 recipients performed in our institution. The mean follow‐up was 8 months (range 1 to 16 months). Biliary tract complications that required surgical or instrumental intervention developed in 17 of the 50 (34%) transplants. No deaths were attributable to biliary tract complications. Hepatic artery thrombosis caused the biliary tract complication in 3 transplants (1 stenosis, 2 anastomotic leaks) and a cystocele of the cystic duct remnant caused 1 common bile duct obstruction. The other 13 complications were associated either with the type of anastomosis performed or type of stent used. An end‐to‐end choledochocholedochostomy was performed in 31 transplants and 2 developed biliary tract complications (6.5%). One developed a biliary leak and the other developed a stenosis at the anastomosis. Nineteen of these choledochocholedochostomies were stented with a straight tube and 6 developed stent‐related complications. Twelve were stented with a T‐tube and only 1 stent complication occurred. An end‐to‐side choledochojejunostomy with a Roux‐en‐Y loop was performed in 19 patients. Only 1 early biliary complication occurred (5%), which was an anastomotic leak. However, 2 developed a stenosis of the entire donor extra‐hepatic duct, 12 and 13 months following transplantation. All anastomoses were stented with a straight tube and only 1 leak developed at the entrance site of the stent into the Roux‐Y. We conclude that the choledochocholedochostomy and the choledochojejunostomy with a Roux‐en‐Y loop are safe methods of biliary reconstruction following OLT. We recommend that a T‐tube be used for stenting the choledochocholedochostomy, and a hepatic artery thrombosis must be excluded when biliary tract complications develop.

We prospectively studied the utility of the amplification of cytomegalovirus (CMV) DNA in the sera of liver transplant recipients in order to predict symptomatic CMV infection, thus enabling preemptive therapy with antiviral agents. Serum samples obtained at biweekly intervals from 20 sequential liver transplant recipients for at least 8 weeks following transplantation were tested by the PCR amplification procedure. Results were correlated with blood and urine cultures, histopathological findings from infected organs, and clinical manifestations. Six patients (30%) developed symptomatic CMV infection; in five (83%) of these patients, CMV DNA was detected prior to symptomatic CMV infection, and in one (17%) of these patients, CMV DNA was detected at the time of symptomatic CMV infection. CMV DNA was detected a mean of 13 days (range, 0 to 23 days) prior to the onset of symptomatic CMV infection. In addition, CMV DNA was detected in the sera of four of five patients with asymptomatic viremia and two patients with asymptomatic viruria. Lastly, the PCR was negative for sera from seven patients with no evidence of CMV infection. We found that PCR was able to detect the presence of CMV DNA in the sera of liver transplant recipients at a sensitivity of 92% and a specificity of 100% for CMV infection, while the sensitivity and specificity for symptomatic infection were 100 and 57%, respectively.

Significant hemostatic abnormalities can occur during orthotopic liver transplantation (OLT). This study addressed three goals: 1)evaluation of the hemostatic mechanism at each stage of the OLT; 2) the relationship of the coagulation process with the thrombelastograph (TEG); and 3) comparison of results in patients requiring retransplantation or who died, with the overall pattern. To evaluate hemostasis during 50 consecutive OLTs, a detailed coagulation and TEG study was done. The surgical procedure was divided into the following stages: Stage I--induction of anesthesia to occlusion of blood flow to the patient’ s diseased liver; Stage II—occlusion of blood flow to the patient’ s diseased liver to reperfusion of the patient’ s new liver; and Stage III—reperfusion of the new liver until skin closure. 28 ml of arterial blood were sampled at the beginning and end of each stage and up to five days posttransplantation for the following: platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin, factors V, VII, IX, and X, plasminogen, antiplasmin, antithrombin III (functional and immunologic), fibrinolytic split products, and TEG. The patient’ s core temperature and amount of blood products transfused were obtained intraoperatively during each of the six data times. The ischemia time of the donor liver was recorded. Significant hemostatic abnormalities developed during each of the 50 OLTs, especially during reperfusion of the donor liver. In some instances, this was corrected within one hour, but platelet counts continued to fall, and a number of coagulation factors rebounded only partially. The TEG values correlated with laboratory data and blood loss, but the correlations were not strong. The patient’ s requirement for red cells varied with the operative drop in temperature; however, the donor liver ischemia time and length of Stage II made no significant difference. It is concluded that 1) significant deterioration of coagulation factors occurs during OLT, 2) the TEG is an effective screening test that affords prompt information, 3) aggressive measures should be taken to maintain the patient’ s body temperature at 37°C, 4) patient outcome was not predicted by intraoperative hemostatic evaluation.

Successful replacements of the superior vena cava (SVC) using autogenous saphenous or superficial femoral vein or prosthetic grafts have been previously performed, but the use of allograft for treatment of SVC syndrome has not been reported. The patient treated by the authors was a forty-one-year-old woman who presented with severe venous congestion of the head and neck caused by fibrosing mediastinitis. In addition, she had sclerosing cholangitis and chronic liver failure. To treat her SVC syndrome and provide access for fluid and blood transfusion and for possible venovenous bypass, SVC reconstruction was performed concomitant to orthotopic liver transplantation. A left innominate vein-right atrial bypass was inserted using an iliocaval allograft. The patient had an uncomplicated recovery, and at six months after surgery her SVC allograft is widely patent and her transplanted liver is functioning well. The venous allograft is an excellent conduit for those patients who are receiving immunosuppression therapy to avoid rejection of a transplanted organ.