The patient was a 36-year-old man with liver cirrhosis secondary to chronic hepatitis B. Because the donor’s right hepatic artery (RHA) originated from superior mesenteric artery, a continuous end-to-end anastomosis of RHA with splenic artery was performed (6-0 prolene). Then, the confluence of proper hepatic artery and gastroduodenal artery of the recipient was anastomosed with the graft’s celiac trunk in a continuous end-to-end manner (6-0 prolene). Hepatic artery thrombosis (HAT) at anastomotic stoma was confirmed by angiography on postoperative day (POD) 5. After revascularization by injection of urokinase (150,000 U) directly into the thrombus, continuous administration of urokinase (100,000 U, q12h), argatroban (2.0 mg/hr), and papaverine (30 mg, every 12 hours [q12h]) was performed at anastomotic stoma. Twenty hours later, hemorrhage of anastomotic stoma occurred, which gradually ceased after stopping the thrombolysis and anticoagulation therapy. Successful thrombolysis with urokinase (100,000 U) was performed on POD 7 and 8, and continuous anticoagulation of argatroban (2.0 mg/hr) and papaverine (30 mg, q12h) was given without urokinase in case of hemorrhage. RHA was occluded on POD 9. Its revascularization was performed by urokinase (100,000 U). Ten hours later, left hepatic artery (LHA) was occluded. After the same management, argatroban (1.5 mg/hr) and papaverine (30 mg, q12h) were given combined with urokinase (100,000 U, q12h). The occlusion of LHA with bleeding at anastomotic stoma occurred on POD 11. After revascularization with urokinase (100,000 U), argatroban (1.0 mg/hr) and papaverine (30 mg, q12h) were continuously infused, and the hemorrhage was controlled soon. Although LHA was occluded again on POD 12, collateral circulation derived from RHA supplied the ischemic left hepatic lobe. Thrombolysis was not performed this time. Even though LHA was not recanalized from then on, the visualization of RHA and the collateral arteries was fine all along. The catheter remained in the hepatic artery for 27 days. The collateral vessels, including some thick trunks, were abundant in left hepatic parenchyma 1 month posttransplant (Fig. 1). Liver function was normal during thrombolysis therapy and no necrotic foci were found in hepatic parenchyma by computed tomography scanning. The patient was discharged on POD 50 and was in excellent health during the 12-month follow-up.FIGURE 1.: Angiograms at different time points after liver transplantation. (1) Complete occlusion of hepatic artery by thrombus at anastomotic stoma (postoperative day [POD] 5). (2) Relatively satisfactory revascularization with totally 150,000 U of urokinase (POD 5). (3) Bleeding at anastomotic stoma (POD 6). (4) Occlusion of right hepatic artery (RHA) with patent left hepatic artery (LHA) (POD 9). (5) Occlusion of LHA with patent RHA (POD 9). (6) Occlusion of LHA combined with bleeding at anastomotic stoma (POD 11). (7) Collateral circulation from RHA to left hepatic lobe (POD 12). (8) Plentiful collateral arteries in left hepatic parenchyma, including some thick trunks (POD 32).It was reported that HAT was identified again in three orthotopic liver transplantation patients after hepatic artery revascularization and immediate second thrombolysis with urokinase was performed successfully (1). We herein first described a patient who underwent HAT as many as seven times. Successful revascularization with urokinase was achieved each time except for the last one when urokinase was not used for the formation of collateral circulation. Argatroban, a synthetic direct thrombin inhibitor (2), was introduced for the treatment of HAT in this case. When argatroban was used for anticoagulation without urokinase, there was no bleeding, which showed its safety. It needs to be further investigated whether argatroban can be routinely used to prevent HAT after liver transplantation. Different from the cases previously reported (3, 4), the collateral circulation in this case ran within the hepatic parenchyma from RHA to left hepatic lobe. It appeared as early as 2 weeks after transplantation, hence saved the ischemic region. We speculated that the fact that the time required to form collateral circulation in our case was shorter than that in other cases was likely to be attributed to the highly developed vascular network in liver. Bing Han Chang Liu Department of Hepatobiliary Surgery The First Affiliated Hospital of Medical College Xi’an Jiaotong University Shaanxi Province, China Hongyan Tian Yamin Liu Department of Cardiopathy and Peripheral Angiopathy The First Affiliated Hospital of Medical College Xi’an Jiaotong University Shaanxi Province, China Liang Yu Xuemin Liu Bo Meng Department of Hepatobiliary Surgery The First Affiliated Hospital of Medical College Xi’an Jiaotong University Shaanxi Province, China Hongmei Wan Department of Cardiopathy and Peripheral Angiopathy The First Affiliated Hospital of Medical College Xi’an Jiaotong University Shaanxi Province, China Naiying Shen Haitao Zhu Yi Lu Department of Hepatobiliary Surgery The First Affiliated Hospital of Medical College Xi’an Jiaotong University Shaanxi Province, China