**9. Renal dysfunction**

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].

**201**

*Management of Patients with Liver Transplantation in ICU*

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**).

Acute cellular rejection (ACR), usually mediated by T-cells, has decreased in recent years with the use of improved potent immunosuppressants, but still ranges from 15 to 25% and usually occurs 7–14 days after surgery [94]. Hyperacute liver rejection is controversial, but undoubtedly early accelerated rejection occurs in the first 7 days and is associated with preformed antibodies. Risk factors include adequacy, type, and level of immunosuppression, underlying immune disease, biliary complications, certain transplant-related features such as donor-negative recipient-positive CMV mismatch, sex mismatch with a female donor. ACR is not significantly associated with long-term graft failure unless it concerns HCV-positive patients in which case it may result in corticosteroid-resistant rejection and graft loss. Early ACR is associated with better graft outcomes [95]. It is even hypothesized that such activation of the immune system may be beneficial and may induce a degree of tolerance. Manifestations of ACR include elevated levels of aminotransferase, alkaline phosphatase, bilirubin, and fever in later stages. Hepatic artery or portal vein thrombosis, biliary leak, CMV infection, and delayed graft function should be excluded. Diagnosis is finally confirmed by percutaneous liver biopsy prior to initiation of treatment, which depends on patient severity and current immunosuppression [94]. Cyclosporine is converted to tacrolimus or the sub-therapeutic levels of tacrolimus are increased and/or mycophenolate mofetil is added. In moderate to severe ACR, high doses of corticosteroids, usually methylprednizolone, are administered as a first-line medicine in a dose ranging from 500 to

Cirrhotic cardiomyopathy (CCM) is defined as cardiac dysfunction in patients with cirrhosis characterized by a blunted contractile responsiveness to stress and/ or diastolic dysfunction and electrophysiological abnormalities in the absence of known cardiac disease [96]. Diagnostic features include a reduced ejection

1000 mg for 1–3 days depending on the center protocol [94].

**12. Cardiac complications after LT**

*DOI: http://dx.doi.org/10.5772/intechopen.89435*

**10. Primary graft dysfunction**

**11. Rejection**
