SMALL-FOR-SIZE SYNDROME (SFSS) IN LIVING DONOR LIVER TRANSPLANTATION (LDLT)
SFSS is characterized by the presence of hyperbilirubinemia, coagulopathy, ascites, and (in advanced stages) sepsis and encephalopathy occurring in the first week after transplantation. It is especially common when the graft-to-recipient weight ratio (GRWR) is <0.8.1
SFSS has a multifactorial genesis: a combination of donor factors (graft volume/quality and hepatic artery buffer response) and recipient factors (portal hyperperfusion, spleen-to-liver volume ratio, venous outflow, and stage of liver disease) leads to allograft dysfunction after partial liver transplantation.2 The following measures should be taken to prevent SFSS.
Improving the Quality and Quantity of Liver Grafts
We do not accept livers from donors with abnormal liver function or from donors with steatosis > 20% in cases of right lobe donation or > 30% in cases of left lobe donation.3 Our minimum acceptable limit for GRWR is 0.8. In select cases with compensated liver disease, we accept lower GRWR grafts with a portal pressure–reducing measure.4, 5
Pretransplant Recipient Status
We do not use donor livers of borderline quality or volume in sick recipients.
Good Venous Outflow
We ensure complete venous drainage [including drainage of the middle hepatic vein (MHV) territory] in all right lobe grafts. Our policy for MHV outflow reconstruction is as follows. We retain the MHV in a majority (approximately 75%) of right lobe grafts (Fig. 1). As we recently reported,3 various MHV lengths are retrieved, and we make sure that the distal MHV with any significant segment IVa veins is preserved in the donor. The MHV can usually be retained with the right lobe because there is sufficient segment IVb drainage into the left hepatic vein in 93% of cases, and there is adequate segment IVa drainage into the left hepatic vein in 80% of cases. When the venous anatomy suggests otherwise, there is >10% steatosis, or the remnant is <32%, the MHV is retained with the donor. In that case, separate segment V and VIII veins are isolated and preserved during transection, and they are later extended via vascular conduits and drained directly into the inferior vena cava.
Prevention of Portal Hyperperfusion and Hepatic Artery Buffer Response
In patients with small-for-size grafts, portal hyperperfusion and increased portal pressure may be observed in the immediate posttransplant period after partial grafting, and they can lead to sinusoidal congestion and hemorrhagic necrosis of perisinusoidal hepatocytes within minutes.6 An elevated portal pressure produces a reciprocal reduction in arterial perfusion via the hepatic artery buffer response, which further augments the hepatocyte damage.7
We routinely measure the portal pressure and the portal flow during the recipient's surgery. With low-GRWR grafts (<0.8), we aim for a portal pressure ≤18 mm Hg by using splenic artery ligation and/or a hemiportocaval shunt with a flow of one-half to two-thirds of the graft's portal flow. The ideal portal flow into the graft should be 100 to 300 mL/minute/100 g of liver tissue. These measures also prevent a hepatic artery buffer response.
Spleen-to-Liver Volume Ratio
Some have recommended prophylactic splenic artery ligation in patients whose spleen-to-liver volume ratio is greater than 0.5 (ie, patients with big spleens).8 However, we believe that the spleen-to-liver volume ratio is just a surrogate marker of the degree of portal hypertension rather than an independent predictor of SFSS. Paying attention to the portal hemodynamics (as discussed previously) is more directly beneficial.