A 25-year-old Caucasian male underwent orthotopic liver transplantation in June 2000 because of Caroli's disease. He was retransplanted in May 2001 due to intractable chronic rejection. Retransplantation was performed with a conventional technique using veno-venous bypass, anastomosis between the hepatic artery of the graft and the common hepatic artery of the recipient, and a Roux-en-Y choledochojejunostomy. An episode of acute rejection was diagnosed in the second postoperative week that responded to high-dose steroids, and the patient was discharged 34 days after retransplantation. No significant abnormality in the graft function was detected until June 2003, when the patient developed fever and leukocytosis associated with biochemical signs of cholestasis followed by jaundice; transaminases remained normal or showed minimal increase. Hepatic ultrasonogram revealed moderate dilatation of the intrahepatic bile ducts with 2 small bilomas, while Doppler US showed normal intraparenchymal arterial resistive index and systolic acceleration time.
Abdominal computed tomography scan confirmed diffuse dilatation of the bile ducts with hypodense areas consistent with biloma (Fig. 1). Selective celiac arteriography showed a complete obstruction of hepatic artery (Fig. 2), while the arteriogram of the superior mesenteric artery demonstrated the presence of compensatory collateral vessels recruited from the jejunal vascular arcade of the Roux limb (Fig. 3). Despite antibiotic treatment, the patient developed recurrent episodes of cholangitis with persistent jaundice and is now listed for retransplantation.
Hepatic artery thrombosis (HAT) after orthotopic liver transplantation still represents one of the main causes of failure of liver transplantation, with an incidence ranging from 3 to 9% in adult recipients.1
When it occurs in the early postoperative period, unless promptly recognized and treated, HAT is normally associated with graft loss.2, 3 Late HAT typically has been associated with less severe complications and may even be asymptomatic.4 This fact is normally attributed to the development of arterial collaterals, possibly due to the gradual progression of arterial stenosis prior to HAT.5 Development of arterial collaterals has been reported in pediatric liver transplant recipients6–8 probably due to the more common presence of Roux-en-Y choledochojejunostomy, but has been rarely described in adults.9, 10 However, in these patients, even in those rare cases where arterial flow is still detectable, Doppler ultrasonogram always shows gross abnormalities with low resistive index and very high systolic acceleration time (almost always above 100 milliseconds).10, 11
In the present case, probably due to the considerable size of the vessels that revascularized the liver after hepatic artery occlusion, doppler signal was normal. As previously reported the rearterialization spared the graft function while permanent damage to intrahepatic bile tree was observed.5 In our patient the suspicion of liver ischemia was induced by the features of the intrahepatic bile tree. Hepatic angiogram is recommended in the presence of unexplained cholestasis, even when the normal arterial signal is detected at Doppler ultrasonogram.