Hepatic artery thrombosis: Conservative management or retransplantation?

1. Early HAT and late HAT continue to be challenges. 2. There is a role for daily ultrasound in early recognition. 3. Computed tomography angiography is the key to management decisions. 4. There is a role for early revascularization. 5. Morbidity and mortality are associated with early retransplantation. 6. Conservative management should be used in cases of late recognition with collateralization. Hepatic artery thrombosis (HAT) is the most feared surgical complication after liver transplantation (LT). It occurs most commonly in the first 10 days after LT, but it can present even many years later. A single definition of early HAT is not universally accepted, with the time of presentation varying from 2 weeks to 3 months. However, for practical purposes, HAT within 1 month of LT is a clinically useful definition. Late HAT, occurring more than 3 months after LT, is less common, its causes are less well defined, and it may have a different evolution and outcome. The mean incidence of early HAT has been reported to be 3.9% (median 5 4.4%). It occurs in 2.9% of adult LT cases and in 8.3% of pediatric LT cases. An era effect can be observed: the reported incidence was 6.9% for 1982-1996 and 3.8% for 1993-2006. A higher incidence of HAT has been reported from lower volume centers (5.8% with <30 LT cases/year versus 3.2% with >30 LT cases/year). No data are available for the performance of individual surgeons with respect to the number of LT procedures performed or center activity. Early HAT is usually silent and is often identified during a routine postoperative ultrasound examination before the development of complications. HAT should be suspected if there is a fever spike and a positive blood culture for a gram-negative organism in the first month after LT. If HAT is unrecognized, then the subsequent clinical course will depend on the potential for and the efficiency of developing a collateral arterial circulation and supervening infection within the compromised biliary tree. Liver dysfunction may occur with modest transaminitis and subsequent cholestasis. The clinical picture can mimic early rejection. With the development of parenchymal ischemia, the transaminitis becomes more pronounced. Increasing cholestasis and the onset of cholangitis mark the development of significant biliary ischemia and cholangiolitic abscesses with associated parenchymal necrosis. Untreated, this can progress to liver failure and death. A more protracted course of recurrent cholangitis and chronic ill health is less common. The pathognomonic sign of HAT is the development of a nonanastomotic/complex biliary stricture, most commonly at the hilum. The ischemic biliary tree sheds damaged biliary epithelium, and densely adherent casts form on the ulcerated surfaces. These casts and duct ischemia predispose the patient to recurrent cholangitis and obstructions with the development of biliary abscesses and liver infarction. Patients who survive long enough and are not suitable for radiological or surgical interventions may become malnourished and chronically unwell. Factors influencing the likelihood of spontaneous, effective collateral formation are poorly understood