On the other hand, late HAT, occurring more than 1 month after OLT, is a less common event and it may have a different evolution and outcome. This discrepancy in outcome between early and late HAT can be explained by the presence of arterial collaterals. After OLT, these collaterals (mainly derived from the phrenic arteries) are initially absent, but have been demonstrated angiographically as early as 2 weeks after OLT [40] (Fig. 14.2). Collaterals probably prevent biliary ischemic lesions in the case of late HAT [39, 40].

Factors reported to reduce the incidence of eHAT include the use of microvascular surgical techniques, the use of Doppler ultrasound (DUS) immediately after surgery and daily scans for the first week, a low hematocrit, and the use of antiplatelet prophylaxis [31, 41]. The usual pattern of screening performed in our center is via routine DUS during the first postoperative week, while in cases of a suspicion of eHAT, a computed tomography angiography should be performed.

Various therapeutic options for managing HAT, including surgical revascularization [31, 32, 42, 43], portal vein arterialization [44], and endovascular treatments [45], are available, but re-OLT is still the treatment of choice for HAT [39]; in fact, alternative procedures (both radiological and surgical) to re-OLT can be complicated by the occurrence of biliary complications, among which biliary cast syndrome (BCS) is the most fearful. BCS, first described in 1975, is defined as the presence of a hardened, dark material within the biliary ductal system that takes the physical shape of the bile ducts [46] and is clinically characterized by fever, jaundice, and cholestatic liver enzyme elevation. Although endoscopic/interventional radiology techniques are successful and safe in the removal of biliary casts [47], BCS can ultimately cause substantial injury to the liver, with some transplant recipients requiring re-OLT (Fig. 14.3).

The 1-year patient and graft survival rates after re-OLT for eHAT are 20–60 % [38, 45, 48] and 50 %, respectively [49]. Asymptomatic eHAT detected by DUS and treated with early revascularization shows promising results [31, 32, 41–44]. It is, however, important to detect eHAT while the patient is still asymptomatic, because graft survival after revascularization is much better in this group compared to symptomatic patients (81.8 % versus 40 %, respectively) [50].

Portal vein thrombosis (PVT) is a rare but severe complication that typically occurs early after OLT and is often related to abnormal venous reconstruction during surgery in patients with preexisting PVT [51] or to the presence of spontaneous/surgical portosystemic shunts determining graft hypoperfusion [52]; its incidence ranges from 2.1 to 13 % [51–54]. When PVT occurs soon after OLT, urgent surgical management may be necessary for PV thrombectomy or the placement of interposition grafts because allograft survival and potentially patient survival may be negatively affected without restoration of PV flow. Other possible approaches to PVT are percutaneous thrombolysis, angioplasty, and stent placement. Re-OLT is rarely needed, especially in split-liver grafts/pediatric recipients experiencing early PVT, for the development of allograft failure [55].

Hepatic vein outflow obstruction after OLT is uncommon and occurs in less than 2 % of cases, but it is life-threatening if left untreated [56, 57]. The most common causes of hepatic vein thrombosis are anastomotic complications following OLT (30 %) [55]; although the majority of cases are managed conservatively with balloon angioplasty or transjugular intrahepatic portosystemic shunt placement, approximately 30 % of patients require re-OLT due to liver insufficiency [56].