Liver transplantation with the preservation of the recipient inferior vena cava, the so-called “piggyback” technique described by Tzakis in 1989 [21], has been recently adopted in the majority of cases instead of the conventional technique, avoiding the dissection of the retrocaval space, the use of venovenous bypass, and reducing blood loss and renal impairment [22].

In spite of its advantages, this technique does not perfectly restore the physiological situation and may increase the risk of venous outflow stenosis or obstruction, which is the only drawback compared to the conventional caval anastomosis [23]. Cavo-caval side-to-side anastomosis and piggyback technique using the stump of the three major hepatic veins are the best-performing techniques to reduce/avoid postoperative complications [23, 24]. With these techniques, the incidence of complications might be around 1 %. The kinking or stricture of the anastomosis may cause an early Budd-Chiari syndrome or a chronic outflow obstruction. This latter may present with refractory ascites, jaundice, and alterations of coagulator factors with a normal liver and which are not justified by liver biopsy or presence of a liver disease. The diagnosis suspected by percutaneous ultrasound showing the absence of the physiological triphasic waves must be confirmed by cavography and measurement of pressure gradients (see also Chap. 13).

In the case of stenosis/kinking, the percutaneous approach with balloon dilatation and, if necessary, stent placement may solve the problem in almost 80 % of patients (see Chap. 13). In a few cases, a second infracaval termino-lateral cavo-cavostomy is required in order to solve the problem and save the organ [25]. When surgical or percutaneous approaches do not solve the problem or a Budd-Chiari syndrome develops, retransplantation can be required in nearly half the cases [23].

Anastomotic stenosis of the portal vein is a rare complication after liver transplantation (occurring in 0.5–3 % of cases), but it is a potential cause of graft loss if not treated [26–28]; the majority of cases have been reported after living donor or split liver transplantation and in pediatric recipients. In these cases, alterations of biochemical liver function tests may be present, but the diagnosis must be confirmed by Doppler ultrasound and portography. In the past, these complications were usually treated by surgical reconstruction of the anastomoses or retransplantation, while nowadays the percutaneous approach is the treatment of choice (see Chap. 13) [29].

Preoperative portal vein thrombosis in recipients is no longer considered a contraindication for OLT [30]. However, in these patients postoperative re-thrombosis may appear in up 10 % of patients [31]; postoperative prophylaxis using low-dose heparin has been suggested to reduce the incidence of re-thrombosis [31].

These are probably the most complex anastomoses, since thrombosis of the hepatic artery is a life-threatening complication after OLT and an important cause of retransplantation and/or mortality. Early hepatic artery thrombosis is associated with bile duct necrosis followed by intrahepatic abscess and septic complications. In the case of late thrombosis, the presence of collaterals mainly derived from the phrenic arteries can prevent these dreaded complications [32]. A systematic review in 2009 showed that the median incidence of hepatic artery thrombosis was 4.4 %; it was higher among pediatric recipients and in low-volume transplant centers (less than 30 cases/year) [32]. The median time to detection was 6.9 days after surgery through Doppler ultrasound screening protocol performed daily or more frequently at least for the first week. In cases of suspected thrombosis, a CT scan or direct relaparotomy was performed. Revascularization can be successful in almost half of cases, but re-OLT is required in 50 % of cases [33]; mortality rates as high as 33 % have been reported. Several causes have been analyzed, but there is not agreement in all cases. There is a general consensus regarding the fact that the following are considered potential risk factors for postoperative occurrence of arterial thrombosis: presence of anatomical variants which may often require arterial reconstruction, donor age, retransplantation, and when the recipient’s weight is significantly higher than the donor’s weight [33–36]. In our experience, even the use of the infrarenal aortic conduit using an iliac cadaveric graft has a negative impact on hepatic artery patency [33, 37]. To avoid the use of an infra-aortic iliac conduit, alternative techniques such as arterial reconstruction on the splenic artery or microsurgery for end-to-end anastomoses with early administration of antiplatelet agents seem to reduce the incidence of this severe complication [36, 37].

It should be emphasized that intimal dissection of the artery due to a vigorous manipulation of the anastomotic sites, either of the donor or the recipient, can lead to intimal flap causing early thrombosis. For other situations such as ABO incompatibility, the use of reduced/split grafts, and cold ischemia time, no consensus has been found in the literature.

If arterial thrombosis is recognized early, surgical revascularization may be attempted with good long-term results and organ saving [38]. This technique may decrease the need for retransplantation. If revascularization fails or intrahepatic abscesses are present at the time of relaparotomy, retransplantation remains the only chance of cure. This strategy tries to save the number of organs as much as possible due to their shortage.

Risk factors for late arterial thrombosis have been reported as low donor weight, previous surgery, and long operative time for transplantation. In these cases, the presence of collateralization from phrenic arteries may ensure satisfactory perfusion of the liver, saving the organ from retransplantation; ischemic cholangiopathy can be treated by interventional radiology (see also Chap. 13).