A smooth ICU course after liver transplant is dependent on satisfactory graft function, which can be assessed by clinical parameters, such as wakefulness, normal mentation, improvement of muscle-power, stable respiratory effort, change in drain fluid from sero-sanguinous to ascites, improvement in urine-output, and lab parameters including improvement in acidemia, stable platelet counts, stable and improving INR without use of fresh-frozen plasma, improving serum lactate, declining transaminases, and normal flow patterns on Doppler.
Serum bilirubin concentration gradually falls to normal levels during the first week. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) peak during the first three days and slowly level off, from then, in case of a healthy uptake of the grafted liver. Gamma glutamyl transferase and alkaline phosphatase, which are canalicular enzymes rise to four to five times of normal and then return to normal in the next few days. Synthetic functions normalize after the third day. While all of the above parameters may remain equivocal, the deteriorating clinical condition with multi-organ dysfunction may be the main clue to the nonfunction of transplanted liver. In such situations, liver biopsy (percutaneous or transjugular) may provide the ultimate answer.
Hyperacute graft rejection is very rare in liver transplantation and occurs due to the presence of preformed antibodies. On the other hand, acute cellular rejection is as common as 15-25%.[2
] It can be present from within few days to a few years, and so in reality the term acute is inaccurate. Here a rise in serum bilirubin is associated with rise in aminotransferases and canalicular enzymes. Clinical symptomatology can be rather nonspecific with loss of appetite, pruritis, and fever without tachycardia. This picture is associated with increased hepatic artery resistive index on Doppler. The diagnosis is made on liver biopsy and treatment based on severity or the degree of rejection (Banff score).[4
] The so called “chronic” rejection can also occur at any time and is evidenced by cholestatic features clinically and advancing arteriopathy and degenerating bile ducts on liver histology, with terminal liver failure ensuing eventually. Chronic rejection is extremely uncommon, accounting for less than 5%[6
] of all cases of graft loss, and may occur due to untreated acute rejection, noncompliance to immunosuppression medication, or some immunological mechanisms which are not very well understood.
Various kinds of anastomotic problems can be present in the early postoperative days with varying incidence. Hepatic artery thrombosis, with incidence of 4-12%,[7
] can present as sudden deterioration in hemodynamics, ARDS, severe coagulopathy, sudden and marked elevation of aminotransferases, with commonly accompanying liver abscesses due to bile duct strictures. Complications involving the portal vein are seen in 1.7-6% of liver transplant recipients.[8
] Persistent ascites, enteric congestion and bleeding denoting portal hypertension, and later variceal hemorrhage may point to portal vein thrombosis. Doppler ultrasound followed by a traditional angiogram or magnetic resonance angiogram (MRA) will be diagnostic. Appropriate surgical or radiological intervention can be both, graft and life saving in these conditions. Patency of biliary tract can be jeopardized, either due to direct insult to the duct system or because of feeder vessel obstruction. Biliary tract complications account for up to 15% of postoperative surgical complications.[11
] These are more common in partial grafts than in whole liver grafts. Again surgical intervention and/or radiological intervention are imperative.
Mediators from the liver or intestine may lead to a reperfusion syndrome after the graft is revascularized, which may manifest as hypotension from peripheral vasodilation, bradycardia, hyperkalemia, and pulmonary hypertension.