Malnutrition in End Stage Liver Disease: Recommendations and Nutritional Support

Eleni T. Tsiaousi; Apostolos I. Hatzitolios; Sotirios K. Trygonis; Christos G. Savopoulos

Disclosures

J Gastroenterol Hepatol. 2008;23(4):527-533. 

In This Article

Causes of Malnutrition in Liver Cirrhosis

The majority of cirrhotic patients unintentionally follow a low caloric diet, a fact that is attributed to various side-effects observed in cirrhosis. Loss of appetite, which is currently attributed to the presence of cytokines such as tumor necrosis factor α (TNF- α),[10] or alcohol-induced anorexia, are the most common reasons. Also, early satiety due to impaired gastric accommodation[11,12] and impaired expansion capacity of the stomach due to the presence of clinically evident ascites[10] quite often lead to an inadequate nutrient intake.

Patients with chronic liver diseases experience abdominal pain, nausea and bloating[3] and are found to have altered gut motility,[13] all of which lead to the development of functional dyspepsia. As is excellently stressed by Kalaitzakis etal.,[3] there is an increased severity of gastrointestinal symptoms associated with recent weight loss and impaired health-related quality of life and the severity of liver disease.

One other important factor is the presence of impaired digestion and nutrient absorption due to portal hypertension, suggesting that controlling the pressure in the portal vein either by transjugular intrahepatic portocaval shunts (TIPS) or medication could improve the patients' nutritional status.[10] Cholestatic liver disease is another reason for impaired absorption, especially of fat-soluble vitamins such as A,D,E and K, due to the reduced intraluminal bile salt concentrations.[14,15]

Furthermore, conditions such as bacterial overgrowth, coexistent small intestinal disease (inflammatory bowel disease, celiac sprue), pancreatic insufficiency, mucosal congestion and villus atrophy contribute to the impaired absorption and utilization of nutrients.

Unfortunately, we should keep in mind that too many physicians tend to prescribe a low protein diet in order to avoid hepatic encephalopathy leading to poorer nutritional status. Other iatrogenic causes for protein and caloric loss include the multiple hospitalizations which may lead to loss of regular meals for reasons of pending examinations and procedures.[10]

The well-recognized hyperdynamic circulation in cirrhosis leads to a systematic vasodilatation and to an expanded intravascular blood volume. As a direct effect, a higher heart blood volume and therefore a greater use of macro- and micronutrients is one of the most common causes of high energy expenditure and demand.

Among cirrhotic patients, 34% are considered hypermetabolic[16] with a resting energy expenditure 120% of the expected value.[1] Elevated pro-inflammatory and anti-inflammatory cytokine levels[17,18] point to a cytokine-driven hypermetabolism in cirrhosis.

On various occasions, patients are driven from a normometabolic state to a speeding catabolic state without any obvious reason. One should keep in mind, however, that compromised gut barrier function in affected patients results in bacterial translocation. Possible effects of this are a spontaneous bacterial peritonitis, deterioration in hepatic encephalopathy or the presence of fever of unknown origin, complications that promote the increased degradation of protein and energy expenditure. In these circumstances, patients may experience deterioration in their general health and nutritional status and may shift to a higher grade in the Child–Pugh classification.[10]

Other important factors in the loss of body protein are the inadequate synthesis of various proteins from the affected liver, the diminished storage capacity of the cirrhotic liver and the affected enterohepatic circle. If we add to these conditions, the portal hypertensive enteropathy which leads to an impaired absorption of nutrients we can easily come to the conclusion that providing the cirrhotic patient with the proper amount of energy is far from easy.

It has been observed that among cirrhotic patients, after an overnight fast, an early switch to gluconeogenesis from amino acids originating from body proteins is often the rule. The lack of sufficient amounts of hepatic glycogen reserves, due to the impaired synthetic capacity of hepatic cells, results in the mobilization of amino acids from the skeletal muscles so that the proper amount of glucose is provided. This condition is observed in healthy individuals after a fasting period of approximately 3 days[19,20] depicting the great amount of hepatic damage that cirrhotic patients suffer.

Furthermore, deficiency in vitamins and trace minerals is often observed in liver cirrhosis. As has been mentioned earlier, cholestasis and portal hypertensive enteropathy may cause impaired absorption of fat and fat-soluble vitamins. This can result in specific deficiencies such as vitamin A deficiency, osteoporosis as a result of calcium loss and vitamin D malabsorption, deficiencies in folate, riboflavin, nicotinamide, pantothenic acid, pyroxidine, vitamin B12 and thiamine.[14,15] Decreased levels of zinc, magnesium, sodium and phosphorus are not rare.[1,14] It is worth mentioning that zinc deficiency impairs wound healing, immune reaction, protein metabolism and alters appetite and taste.[15]

Loss of protein and minerals is a common clinical condition in ESLD resulting from complications of cirrhosis or iatrogenic interventions. The most common iatrogenic interventions are the use of diuretics in order to cope with ascites and fluid retention, the quite often prescribed lactulose which is used in order to alter the intestinal flora, and the performance of multiple paracentesis. Last but not least, the occult or overt blood loss from esophageal and gastric varices and the intestinal lumen due to ulcerations or portal enteropathy are some of the main reasons for protein loss.[1]

Apart from the established portal hypertensive enteropathy, other conditions such as altered intestinal flora and lesser synthesis and secretion of bile salts and pancreatic enzymes are also significant causes of nutrient loss.

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