Hepatic artery stenosis (HAS) is not a very common vascular complication post-OLT with a reported incidence of 4–10 % (Duff et al. 2009). It may be due to narrowing at the anastomosis, trauma to the intimal layer due to catheter manipulation, and twisting or kinking of the hepatic artery. Although it is generally thought that HAS may lead to biliary ischemia or liver graft dysfunction and can progress to HAT, its clinical significance remains unclear as many patients remain asymptomatic without liver dysfunction. High flow velocity (>200 cm/s) at the site of stenosis with turbulence distal to the stenosis and low resistive index (RI) of <0.5 in the main, right, or left hepatic artery are typical Doppler ultrasound findings of HAS. Mild stenosis may not demonstrate any changes on Doppler ultrasound (Dodd et al. 1994). Percutaneous angioplasty is an alternative treatment to surgery for HAS. However, the former is not as effective as surgical resection of the stenotic segment with arterial reconstruction (Rostambeigi et al. 2012). Without intervention, more than half of cases may develop HAT.

Hepatic artery pseudoaneurysm (HAPA) is a rare, life-threatening complication after OLT with a reported incidence of 1–2 %, and usual occurrence of 2–3 weeks post-OLT (Marshall et al. 2001). They usually involve the extrahepatic portion of the hepatic artery and commonly originate from a local infection around the arterial anastomosis. Rarely, they may be located intrahepatically, and these are frequently due to percutaneous interventional procedures such as liver biopsy, percutaneous transhepatic cholangiography, or transhepatic drainage catheter placements (Zajko et al. 1990). The initial clinical presentation of HAPA may be nonspecific, i.e., unexplained fever, liver graft dysfunction, or decreasing hemoglobin level. Therefore, it is very important to have a high index of suspicion to make an early diagnosis and initiation of treatment for HAPA before they rupture and develop bleeding complications. Liver grafts can also be lost because of ischemia secondary to HAPA thrombosis. Rupture of an intrahepatic aneurysm can cause arterio-portal venous leading to portal hypertension or arteriobiliary fistula leading to hemobilia or gastrointestinal hemorrhage (Pawlak et al. 2003). Likewise, rupture of an extrahepatic aneurysm can lead to profound shock and massive intraperitoneal hemorrhage.

Color and spectral Doppler ultrasound is a useful diagnostic study to differentiate HAPA from a cystic mass close to the hepatic artery by demonstrating arterial flow within the cystic lesion (Crossin et al. 2003). CT scan may also demonstrate fluid collections and may identify HAPA and other pathologies. Arteriography remains the definitive study to identify and localize HAPA and aid in planning further treatment (Marshall et al. 2001). If discovered before bleeding complications occur, HAPAs are often treated with surgical resection of the aneurysm with revascularization using interposition vascular or arterial grafts. However, in the presence of acute hemorrhage, particularly HAPAs involving the extrahepatic arterial anastomosis, aneurysm inflow occlusion using coil embolization is necessary to control bleeding and stabilize patients in preparation for re-transplantation. The occurrence of HAPA after OLT is associated with a high mortality rate of 69 % (Marshall et al. 2001). The presence of prior poor graft function or complicated post-OLT course of the recipient further worsens outcome after revascularization and re-OLT for bleeding HAPA (see Fig. 2).

Portal vein thrombosis and stenosis are a rare vascular complication after OLT with a reported incidence of 1–2 % (Langas et al. 1991). Portal vein stenosis or thrombosis may be due to surgical technical errors, i.e., anastomotic stricture, portal vein twisting, compression or kinking due to redundant vein reconstruction or use of vein graft extension, low portal vein inflow, and recipient hypercoagulable state. They usually manifest with severe liver graft dysfunction associated with hypoglycemia, coagulopathy, lactic acidosis, massive ascites, bleeding esophageal varices, renal failure, and hemodynamic instability. Portal vein thrombosis shows absence of flow within the portal vein on color or spectral Doppler ultrasound, which is confirmed by angiography (Friedwald et al. 2003). Although thrombectomy and portal vein reconstruction in conjunction with thrombolytic and anticoagulant agents may be tried, urgent re-transplantation is the only treatment of choice in most cases. However, re-transplantation may be challenging, particularly in patients with extensive portal vein thrombosis involving the superior mesenteric vein.

Ultrasound findings of portal vein stenosis include focal narrowing of the portal vein to 2.5 mm with increased flow velocity at the site of stenosis and decreased flow velocity in the portal vein. Flow velocities of >150 cm/s or anastomotic to pre-anastomotic flow velocity ratio of >4:1 is specific for anastomotic portal vein stricture (Pawlak et al. 2003). The treatment of choice for portal vein stenosis is percutaneous balloon angioplasty which can be done via transhepatic or transjugular approach (Glanemann et al. 2001; Ko et al. 2007).

Venous outflow complications due to vena cava or hepatic vein outflow stenosis are relatively uncommon with reported incidence of between 1 % and 6 % depending on anastomotic technique and transplant type (Darcy 2007). Hepatic vein stenosis is slightly more common than vena caval stenosis with higher incidence (6 %) reported in living compared to deceased donor OLT pediatric recipients (Egawa et al. 1993). It usually presents early post-OLT and may be due to technical complications, i.e., tight anastomosis, big donor-recipient vein size discrepancy, vein twisting, extrinsic compression of hepatic vein or vena cava, or intimal vein flap formation. The usual presentation of venous outflow obstruction may be similar to patients with portal hypertension, i.e., massive ascites, lower extremity edema, abdominal pain due to ascites or hepatomegaly, and sometimes variceal bleeding. Patients commonly develop renal insufficiency and liver graft dysfunction. Doppler ultrasound examination is the most commonly used initial diagnostic test to detect venous outflow obstruction, while venography with pressure gradient measurement is used to confirm the diagnosis (Egawa et al. 1993; Darcy 2007). Typical findings on Doppler ultrasound may include decreased hepatic and portal vein mean velocities and dampened hepatic vein wave forms. A pressure gradient of greater than 10 mmHg is a commonly used threshold to confirm the diagnosis (Raby et al. 1991; Borsa et al. 1999; Weeks et al., 2000). The treatment of choice for hepatic vein and caval stenosis is percutaneous transjugular balloon angioplasty with stent placement. However, repeated sessions of angioplasty may be necessary to achieve long-term patency due to the increased incidence of recurrent stenosis after a single angioplasty. The use of stents after angioplasty is reported to have an increased long-term patency rate (Borsa et al. 1999). Surgical revision of the anastomosis may be warranted in cases that cannot be dilated with percutaneous balloon angioplasty. Surgical technique involves dissecting around the cava, which may include opening the diaphragm around the cava for better exposure and access. Other surgical options include the use of caval patch venoplasty and bypass.

Biliary complications such as biliary leak or stricture occur in 1.6–19 % of cases after OLT (Hintze et al. 1997; Rabkin et al. 1998). Biliary leakage usually occurs within the first month post-OLT, and surgical technical errors, i.e., undue tension at the anastomosis and bile duct necrosis due to HAT, are the most common causes. They can originate from the biliary anastomotic site, T-tube exit site, cystic duct remnant, bile duct damage after liver biopsy, bile duct necrosis due to HAT, or cut surface of the liver in split liver or living donor liver transplantation. Biliary anastomotic leak and T-tube exit site leak account for more than 80 % of all bile leakages (Greif et al. 1994; Boraschi et al. 2001). Patients with biliary leak can be asymptomatic, but when symptomatic, they usually present with fever and abdominal pain and elevated liver enzymes. Doppler ultrasound of the liver should be performed initially to rule out HAT as a possible cause of bile leak. The diagnosis of bile leak may be suggested by HIDA scan but the definitive diagnosis can be confirmed by T-tube cholangiogram. In the absence of a T-tube, ultrasonography and HIDA scan can be used to detect bile leaks. However, ERCP can be used to diagnose and treat bile duct leaks in recipients with duct-to-duct anastomosis, while MRCP is the most appropriate diagnostic tool for recipients with Roux-en-y choledochojejunostomy (Thuluvath et al. 2003). Percutaneous transhepatic cholangiography (PTCD) may also be used in these cases, although oftentimes unsuccessful due to difficulty in accessing non-dilated intrahepatic ducts. Small, asymptomatic anastomotic bile leaks may be treated by opening the T-tube to decompress the biliary tree with follow-up cholangiogram after 2 weeks to check for resolution of bile leak. On the other hand, most persistent and symptomatic bile leaks post-T-tube removal can be managed successfully by ERCP and bile duct stent placement, with or without sphincterotomy. Biliary reconstruction by converting to Roux-en-Y choledochojejunostomy is the treatment of choice for bile leaks that do not respond to endoscopic or percutaneous approach. In patients with primary Roux-en-Y choledochojejunostomy with large bile leak or nonresponse to PTCD, revision of the Roux-en-Y anastomosis is the treatment of choice (see Fig. 3).

Biliary anastomotic strictures have a reported incidence of 5–10 %, majority of which occur within the first-year post-OLT (Verdonk et al. 2006). They may be associated with surgical technical complications, bile duct ischemia, previous bile duct leakage, and hepatic arterial flow problems, i.e., HAS or HAT. They manifest with progressive elevation of total bilirubin and canalicular enzyme levels. Although MRCP can be used to diagnose biliary strictures, T-tube cholangiogram, ERCP, or PTCD is still considered the gold standard in diagnosis of biliary anastomotic strictures. A simple bile duct stricture may be treated by dilatation and stent placement. However, biliary reconstruction with conversion to a Roux-en-y choledochojejunostomy may be the only treatment for long bile duct strictures, ampullary dysfunction, or failure of endoscopic and percutaneous techniques. Since bile duct complications may be secondary to hepatic artery thrombosis or stenosis, ultrasound Doppler studies should be part of the work-up to evaluate hepatic artery patency (see Fig. 4).

Most post-OLT complications occur in the first month after OLT and can cause significant morbidity and mortality. Early recognition, diagnosis, and treatment of post-OLT complications are critical to successful short- and long-term graft and patient survival outcomes after OLT.