**10. Primary graft dysfunction**

*Liver Disease and Surgery*

**8. Nutritional support in liver transplant recipients**

also considered a risk factor for these disorders [83].

**9. Renal dysfunction**

Post-LT nutritional support in ICU is an essential adjunct to transplant recovery. Malnutrition, which characterizes many patients with ESLD being evident at rates of up to 80%, deteriorates with the progression of liver failure, and affects the patients' outcome [80]. On the other hand, it is associated with prolonged ICU and hospital stay, infections, respiratory complications, graft impairment, and mortality. Sarcopenia, defined as severe muscle wasting, is also a determining factor of the outcome, and it can be easily diagnosed with bioelectrical impedance. Patients with cirrhosis often present carbohydrate, fat, and protein disorders, characterized by elevated levels of aromatic amino acids and methionine while lowering plasma levels of branched-chain amino acids are detected [81, 82]. The immediate postoperative energy demands are increased, especially in patients with a high MELD score [82]. Factors such as operational stress, release of catabolic hormones, administration of immunosuppressants, mainly corticosteroids, as well as ICU factors including mechanical ventilation and hemodialysis, contribute to increased metabolic needs. For the above reasons, the aim is to ensure adequate intake of protein and calories in addition to protein breakdown protection [81]. An increase in nonprotein calories, estimated at 25–35% kcal/kg per day, is recommended when indirect calorimetry is not available. It should always be in accordance with the metabolic and inflammatory status, and it should be reviewed in hemodynamically unstable patients [83]. Due to elevated protein catabolism, it is necessary to obtain 1.5–2 g/kg of protein. Enteral nutrition (EN) has the edge over the parenteral one, assisting in maintaining intestinal integrity, by supporting the diversity of the microbiome, and helping the immune and metabolic response. The rapid onset of EN even 12 h after LT is recommended by some authors. It has been reported to reduce viral infections and contribute to a better N2 balance. If postoperative encephalopathy remains, the amount of protein intake is not reduced but the type of nutrition is altered by the addition of branched-chain amino acid (BCCA) enriched formulae, while the administration of immunonutrition remains under discussion. Frequent screening of electrolytes is required to prevent and correct disorders, while re-feeding syndrome is

Renal impairment is a very common complication after LT. Its presence ranges from 19 to 64%. Even with the application of the RIFLE and AKIN criteria, the percentage reaches from 39 to 54% [84, 85]. In cases of living donors, acute kidney injury (AKI) has been estimated at around 23% [86]. AKI occurrence is complex and multifactorial in origin, depending on the existence of the preoperative hepatorenal syndrome as well as various intraoperative and postoperative factors. High MELD score, perioperative transfusions, hemodynamic instability, vasoactive agents, graft dysfunction, infections, and nephrotoxic agents are mainly accountable for renal function deterioration [87]. Systematic evaluation of renal function is required with close monitoring of urine output, fluid balance, and hemodynamic parameters [18]. The treatment is mainly supportive and includes: restoring CO with sufficient preload for optimization of renal perfusion, administering loop diuretics, and efforts to avoid nephrotoxic agents. Renal replacement therapy is recommended in cases of volume overload, electrolyte disturbances, and acidemia in an attempt to avoid pulmonary edema and hepatic congestion. Immunosuppressants, antibiotics, and contrast agents are commonplace nephrotoxic agents. The dosage of CNIs should be minimized or they should be converted into mTOR inhibitors combined with anti-proliferative agents. In ICU, CVVDHF is the renal

replacement therapy of choice and favors the outcome of patients [88].

**200**

Primary graft dysfunction (PGD) is a major complication after LT and is associated with prolonged hospital and ICU stay jeopardizing graft viability, being responsible for its high rejection rates as well as higher mortality and morbidity. It describes different degrees of graft impairment which begins intraoperatively, divided into early or initial poor function (IPF) and primary nonfunction (PNF) [89–91]. IPF represents the clinical phenotype of severe ischemia-reperfusion injury due to various donor and/or recipient-related factors. Expanding the criteria to marginal donors has increased the use of allografts with a higher likelihood of initial malfunction. It affects the survival of both graft and patient, whether the transplant comes from living or deceased donors. Dysfunction may be transient and possibly reversible with appropriate supportive treatment. There are no clear definitions, nevertheless, there are suggested scores, such as MEAF and LGrAFT, that could help in early detection and classification of early hepatic impairment [92, 93]. On the contrary, PNF is a catastrophic injury characterized by hepatic necrosis, aminotransferase elevation, coagulation disorders, lactate elevation, hemodynamic instability, persistent hypoglycemia, and respiratory and renal failure with an incidence ranging from 0.9 to 7%. The treatment is immediate re-transplantation. There are certain risk factors related to donors, recipients, intraoperative events, and allograft preservation [91] (**Table 2**).
