Abnormal liver function tests in the parenteral nutrition fed patient

Abstract

Liver dysfunction is common in individuals receiving parenteral nutrition (PN) and particularly in neonates and infants. Abnormalities of liver function tests in patients receiving short term PN are usually transient but in individuals receiving long term PN, substantial liver damage and ultimately end stage liver disease may occur. The aetiology is complex, involving a large number of patient related and nutrition related factors. The terminology intestinal failure associated liver disease (IFALD) is therefore more appropriate than PN associated liver disease. Effort should be made to prevent liver dysfunction by managing sepsis, avoiding parenteral overfeeding, employing cyclical parenteral feeding and encouraging enteral nutrition where possible. Intake of soybean based parenteral lipid emulsions should be reduced in individuals with established IFALD, possibly to be replaced by lipid emulsions containing medium chain triacylglycerol, monounsaturated fatty acids or fish oil although larger clinical studies are needed. Similarly, evidence supporting the widespread use of parenteral choline and taurine supplementation in the prevention or treatment of IFALD remains limited. There are more data to support the use of oral antibiotics to treat bacterial overgrowth and oral ursodeoxycholic acid in neonates. Ultimately, severe IFALD may necessitate referral for small intestine and/or liver transplantation.

Review article: the management of long‐term parenteral nutrition

“…The aetiology of IFALD is broad and not limited solely to PN, but often has multiple aetiological contributing factors. 86 Nonnutritient causes of IFALD Patients receiving PN with abnormal liver function test should be assessed and treated for nonnutrient-related abnormalities such as drugs, sepsis, biliary obstruction, bacterial overgrowth, hepatotoxic medications and underlying intrinsic liver disease, while evaluating nutritient-related factors. 86 Care should be taken to ensure that patients receiving PN receive the correct daily amount of both calories (25-35 kcal/kg) and protein (0.8-1.5 g/kg) as both malnutrition and overfeeding can lead to steatosis.…”

“…86 Nonnutritient causes of IFALD Patients receiving PN with abnormal liver function test should be assessed and treated for nonnutrient-related abnormalities such as drugs, sepsis, biliary obstruction, bacterial overgrowth, hepatotoxic medications and underlying intrinsic liver disease, while evaluating nutritient-related factors. 86 Care should be taken to ensure that patients receiving PN receive the correct daily amount of both calories (25-35 kcal/kg) and protein (0.8-1.5 g/kg) as both malnutrition and overfeeding can lead to steatosis. 100,103 Steatosis is the commonest initial histological finding in liver disease associated with PN, followed by later by the development of persistent intrahepatic cholestasis, fibrosis and cirrhosis.…”

The future developments in nutrition

“…IFALD represents an important indication for small-bowel transplantation in patients dependent on HPN 28. While mildly abnormal liver function is common in patients receiving long-term PN, the incidence of advanced liver disease varies widely 28.…”

“…While mildly abnormal liver function is common in patients receiving long-term PN, the incidence of advanced liver disease varies widely 28. IFALD is a multifactorial entity, resulting, for example, from a variety of nutrient excesses and/or deficiencies.…”

“…IFALD is a multifactorial entity, resulting, for example, from a variety of nutrient excesses and/or deficiencies. Lipid excess, in particular, can be especially hepatotoxic,29 and recent evidence suggests that the use of more sophisticated lipids (eg, medium chain triglyceride/long-chain triglyceride mixtures and monounsaturated fatty acids, or fish-oil based lipid emulsions) may further attenuate hepatic injury 28. A key challenge over the next few years is to identify patients at risk of developing IFALD at an early stage to facilitate, for example, the early targeted use of these second/third generation lipids, before patients with IF develop end-stage liver disease necessitating multivisceral transplantation.…”