The surgeons need to be aware of both recipient and donor anatomy and must also have a specific plan for how to manage any recipient anatomical problems including the hepatic artery (HA), portal vein (PV), hepatic vein (HV), and bile duct (BD). In addition, there must be a plan for how to maintain adequate portal inflow without portal flow steal in the presence of large portosystemic collaterals, massive splenomegaly with enlarged splenic artery, and small graft size with less than 1.0 graft-to-recipient weight ratio (GRWR).

Before beginning perihepatic dissection, a full laparotomy should be performed, and the decision made as to when the preoperatively planned interventions should be undertaken, i.e., splenic artery ligation, splenectomy, isolation of portosystemic collaterals, etc. Usually splenic artery ligation or isolation of splenorenal shunt causing portal flow steal is undergone at the initial stage because edematous changes of bowel and mesentery after liver graft implantation might hinder those procedures. Other tasks, such as interruption of portosystemic collaterals and splenectomy, are performed after engraftment.

Using electrocautery, both coronary and triangular ligaments are divided; the detachment should be performed along the avascular plane. In some cases, however, it is more effective to peel off the hepatic capsule by thorough cauterization of both diaphragmatic and hepatic surface and ligation of sizable diaphragmatic vessel so as to reduce intraoperative bleeding when perihepatic collateral vessels or dense adhesions are present, such as in salvage or re-transplantation. After adrenal detachment, hemostasis of the perihepatic area becomes easier, and there should be minimal bleeding before dissection of retrohepatic IVC is begun. The following step is often dissection of hepatic hilum prior to retrohepatic IVC dissection. This takes into consideration the possibility of significant bleeding and/or technical difficulty depending on the extent of caudate lobe hypertrophy, Budd-Chiari syndrome, etc. Early dissection and division of hilar structures can facilitate the following procedures with less bleeding, particularly in salvage LDLT patients who have undergone previous major hepatectomy or in secondary biliary cirrhosis patients who underwent repeated surgery for biliary problems. Venovenous bypass through the inferior mesenteric vein or PV or temporary portocaval shunt may be helpful to reduce bleeding and splanchnic congestion during total hepatectomy and the anhepatic phase.

The main technical principle of dissection of the hepatic hilum is to preserve implantation options by maintaining the length and integrity of all hilar structures. In particular, meticulous dissection of the hepatic artery to obtain a sufficient length and adequate diameter is very important in order to match with the small hepatic artery opening of the partial liver graft without tension and to avoid intimal dissection of the recipient hepatic artery, such as is often encountered during hilar dissection of a recipient with portal hypertension. Alternatives are not easily achievable because of the vessels’ small diameter of usually less than 3 mm, in contrast to the diameters of the BD and PV.

When cholecystectomy is performed, the cystic duct is divided close to the neck of the gall bladder in order to preserve as much of its length as possible in case the cystic duct might be necessary for duct-to-duct anastomosis of where two bile duct openings are present on the liver graft with a wide gap between them. When LL implantation is being planned, the left hepatic artery (LHA) is isolated first at the left hilum and then dissected up to the umbilical portion of the left hilum in order to get enough length and also to get the branch patch of hepatic segment 2 and 3 HAs to accommodate the often larger graft hepatic artery. When RL implantation is planned, this step is a type of insurance procedure, and it is important for a surgeon to proceed following dissection in a comfortable situation. Dissection of the middle and right HA should be performed with preservation of the periductal connective tissue encompassing the axial periductal microcirculation in order to avoid posttransplant biliary complications related to ischemia. The right hepatic artery (RHA) should be freed up to the anterior and posterior branches so as to overcome size disparity between the graft and the recipient HAs. Division of HAs without ligation in the recipient side is better than ligation of both sides in order to obtain longer hepatic arteries and to avoid intimal injury.

The division site of bile duct should be decided by size and number of ductal openings of the graft. Pre- and intraoperatively, there should be communication between the recipient and donor surgeons regarding the cholangiogram. If multiple ductal openings are expected and also situated widely apart in the graft, the Glisson tissue containing the duct in the recipient should be divided at a high level in the hepatic hilum in order to create multiple ductal orifices with wide distances between those of both corners.

The last structure in the hilum to be further identified is the PV. The PV is usually dissected toward the right and left bifurcation of the main PV. For dual-graft LDLT and/or obtaining autogenous vessel graft to use for graft implantation, the PV needs to be dissected toward and beyond the takeoff of the right anterior, posterior, and left portal branches up to the umbilical portion. As for the extent of PV dissection to the opposite side, the PV is mobilized down at least 2 cm in length from the portal bifurcation toward the superior margin of the head of the pancreas.

During the anhepatic phase in LDLT, portal bypass is usually not the preferred procedure because most recipients tolerate portal clamping without hemodynamic instability due to maintaining caval flow, and construction of hepatic and portal vein anastomoses requires less than 60 min. LDLT using a right lobe graft , excluding extended right lobe, left lobe, and dual-lobe LDLTs, does not require systemic bypass because the piggyback technique allows partial clamping of the vena cava with a side-biting clamp and without hemodynamic instability.

The next step is division of the gastrohepatic ligament. At the time of left liver or dual-graft LDLT, if a LHA arises from the left gastric artery, this should be dissected as long as possible for arterial reconstruction of the implanted liver graft. The caudate lobe of the liver is detached from the IVC using a left-side approach in order to enhance the retrohepatic dissection as much as possible.

Considering the harvest time of donor graft and the duration of the bench procedures, the diseased liver is removed as late as possible to reduce anhepatic phase. Hepatic veins (HVs) are divided individually using a vascular clamp instead of an endovascular stapler because the recipient’s HV openings should be used for anastomosis with the graft HVs after venoplasty.

Virtually all living donor liver grafts in adult recipients are relatively small-for-size (SFS) and require optimal portal inflow for immediate graft regeneration, particularly when GRWR is less than 0.7–0.8 %. Portal hyperperfusion can cause excessive shear stress against sinusoidal cell of a SFS graft, which is known to be the primary cause of the SFS syndrome (Troisi et al. 2005). Various remedial procedures such as splenic artery ligation, splenectomy, and small-caliber hemiportocaval shunt (HPCS) creation have been utilized to modulate portal inflow (Kiuchi et al. 2003). High portal pressure is related however to not only to portal blood flow, but also to liver graft outflow resistance. The safest and most effective way to manage portal hyperperfusion in a SFS graft is provision of good HV outflow and modulation of high portal venous flow (PVF) and pressure (PVP) by splenic artery ligation or splenectomy (Ito et al. 2003; Ogura et al. 2010). Splenectomy is usually not indicated to decrease portal hyperperfusion because of its inherent complications such as bleeding, pancreatic fistula, abscess formation, PV thrombosis, and serious postsplenectomy infections. HPCS may trigger portal hypoperfusion and result in encephalopathy, graft atrophy, and even allograft necrosis, which may occur during the first 2 weeks postoperatively due to portal flow steal (Moon et al. 2008); thus, permanent HPCS is not an appropriate choice for resolving portal hypertension. In the author’s experience, PVF ≥250 mL/min/100 g graft weight or early elevation of PVP ≥20 mmHg after reperfusion is not associated with poor outcomes in SFS grafts as long as perfect venous outflow is provided and portal flow steal is completely interrupted. Considering portal flow steal phenomenon, it is not an issue limited to small-for-size grafts having less than GRWR <0.8 % undergoing HPCS, but a common issue in the field of LDLT using partial liver grafts with more than GRWR ≥0.8 % and having sizable spontaneous portosystemic collaterals (Lee et al. 2007; Moon et al. 2008).

Intraoperative Doppler ultrasound (IOUS) has been used to ensure hemodynamics of the implanted liver graft. IOUS however has difficulty in evaluating correct anatomical and hemodynamics parameters of portosystemic collaterals. Even when IOUS showed adequate portal inflow during LDLT, portal flow steal syndrome can manifest a few days after LDLT. To overcome the limitation of IOUS, IOCP has been used to evaluate portal flow to liver graft and to detect stealing hepatofugal flow through persistent portosystemic collaterals (Moon et al. 2007) (Fig. 2). In addition, IOCP is therapeutically utilized to complete interruption of surgically inaccessible portosystemic collaterals by coil embolization and to treat PV stenosis interfering with hepatopetal flow by stent placement (Kim et al. 2007). Measurement of PVP and PVF is stopped after introduction of IOCP and MHV reconstruction. To properly manage the potential small-for-size graft syndrome that may develop, both modulation of graft hyperperfusion by excessive portal hypertension and abolishment of portal flow steal through spontaneous or surgically created portosystemic collaterals are equally important.