Nutritional considerations in end-stage liver disease
- Simone I Strasser1,*, Helen Vidot2
Journal of Gastroenterology and Hepatology Volume 26, Issue 9, pages 1346–1348, September 2011
Protein–energy malnutrition (PEM) is a common feature of alcoholic and non-alcoholic liver disease, and might be present in 65–90% of patients with cirrhosis1 and in up to 100% of patients waiting for liver transplantation.2 Patients present with depleted fat stores and varying degrees of muscle wasting and reduced muscle strength.
Short-term survival is reduced in malnourished patients with cirrhosis, and PEM can adversely affect outcomes for patients on the waiting list for transplantation, as well as post-transplantation morbidity and mortality.3 Malnutrition in cirrhosis is implicated in increased risk for infection,4 increased severity of ascites,5 and the development of hepatic encephalopathy.6 Repeated episodes of overt hepatic encephalopathy might result in recurrent hospitalizations and persistent cumulative deficits in working memory, response inhibition, and learning.7
The mechanisms of PEM in cirrhosis are complex and multifactorial. They include reduced oral intake secondary to disease-related anorexia, restrictive diets, including overzealous sodium-restricted diets, altered taste sensations, nausea, early satiety, particularly in the presence of marked ascites, portal-hypertension associated malabsorption, insulin resistance, reduced glycogen storage capacity, increased gluconeogenesis, and alterations in fuel utilization. Repeated episodes of infection and endotoxemia as a result of alterations in gut barrier function might also contribute to the increased energy requirements and reduced intakes in this group via the pro-inflammatory cytokine response.8
Despite studies demonstrating that there is no benefit to a low-protein diet in patients with episodic or chronic hepatic encephalopathy,9 a protein-restricted diet is commonly recommended by health-care practitioners under the misapprehension that it is beneficial to patients. Protein restriction has further deleterious impacts on the severity of malnutrition,10 while a higher protein intake has positive benefits both on overall nutrition and possibly the severity of hepatic encephalopathy.11 Hospitalization, with frequent prolonged periods of fasting for diagnostic or therapeutic procedures, is another major contributory factor; thus, clinicians should make every effort to minimize periods of fasting and maximize nutritional intake in patients with cirrhosis while they are in hospital.
Accurate assessment of nutritional status might also be difficult in patients with cirrhosis. This is because many of the traditional markers of nutritional assessment are dependent on normal hepatic synthetic function. Weight is a poor indicator of nutritional status in the presence of ascites and/or peripheral edema. Nutritional assessment of the cirrhotic patient includes subjective global assessment—liver,12 anthropometrical measurements of mid-arm circumference, triceps skinfold thickness, and mid-arm muscle circumference. In addition, grip strength measurements are an accurate reflection of protein status in those with cirrhosis.13 It is particularly important to note that obese patients with cirrhosis might exhibit features of protein malnutrition that are not apparent in the absence of nutritional assessment.
In summary, regular review of nutritional status with appropriate nutritional advice should be included as part of the comprehensive care of all patients with cirrhosis. Referral to an accredited, practising dietitian, particularly one experienced in the management of end-stage liver disease, will assist in determining the nutritional status and oral intake of the patient with cirrhosis as well as providing expert advice about nutritional requirements and practical advice on how to meet these requirements. In 2006, the European Society for Enteral and Parenteral Nutrition updated its guidelines for the management of patients with cirrhosis. The recommendations are that patients with cirrhosis require 35–40 kcals/kg body weight/day and 1.2–1.5 g protein/kg body weight/day.14 Meeting these energy and nutritional requirements is a major challenge for patients, and the use of oral supplements is often essential to ensure reversal of malnutrition. In addition, supplementation with oral branched-chain amino acids might improve muscle mass and lead to the resolution of minimal hepatic encephalopathy, and might be of benefit in patients with recurrent hepatic encephalopathy, who are unresponsive to other measures.6,15
Another nutritional consideration in patients with cirrhosis, particularly those with hepatic encephalopathy, is dietary supplementation with probiotics (live microorganisms) or prebiotics (non-digestible food ingredients that selectively stimulate the growth or activity of beneficial colonic bacterial). Altered gut barrier function and gut flora contribute to systemic inflammation in cirrhosis. There is growing evidence that pro-inflammatory cytokines are involved in the development of encephalopathy, and that factors that reduce the rate of bacterial translocation across the intestine might reduce the level of encephalopathy.16 The use of synbiotics (a combination of probiotics and prebiotics) might result in improvements in encephalopathy and in overall liver function.17 Currently, there is no standardization in commercially-available probiotic or synbiotic preparations.
Hepatic glycogen stores are depleted in cirrhosis. The response to prolonged periods of fasting in cirrhotic patients is an alteration in the pattern of fuel utilization similar to that seen in starvation metabolism, with increased lipolysis and gluconeogenesis from amino acids. Repeated, prolonged periods of starvation for procedures should be avoided in the cirrhotic patient. The use of evening nutritional sip supplements is recommended to reduce the periods of fasting to less than 7 h.18 If patients with cirrhosis are unable to meet 70% of their requirements orally, then supplementary artificial feeding should be initiated, preferably via a fine bore feeding tube using a high-energy, high-protein feed.19 Parenteral feeding should only be considered if the patient is unable to tolerate oral intake or enteral feeding.13
Apart from energy and protein considerations in cirrhotic patients, vitamin and mineral deficiencies are also common, and these too are often poorly addressed. In this issue of the Journal of Gastroenterology and Hepatology, Abbott-Johnson and colleagues describe the results of their investigation of fat-soluble vitamin deficiencies in cirrhotic patients being assessed for liver transplantation.20 They identified that fat-soluble vitamin deficiency, particularly of vitamins A and D, is common in patients with end-stage liver disease awaiting liver transplantation, independent of the cause of liver disease.
Vitamin D deficiency might have many consequences in patients with liver disease. As Abbott-Johnson et al. point out, it is strongly linked to osteoporotic fractures, osteomalacia, and decreased muscle strength, but recent reports also implicate vitamin D deficiency in the progression of and response to antiviral therapy of hepatitis C-associated liver disease21 and in carcinogenesis.22 Vitamin D deficiency is also linked to the progression of chronic kidney disease and cardiovascular disease, type 2 diabetes mellitus, and insulin resistance, all of which are common in patients with chronic liver disease and after liver transplantation.23 Identification and correction of vitamin D deficiency is therefore essential in patients with cirrhosis.
As the authors have previously noted, vitamin A deficiency is also extremely common, and correction is recommended, particularly in those with impaired dark adaptation or night blindness.24
In conclusion, nutritional assessment and support is a critical part of the management of patients with end-stage liver disease. Identification of the increasing energy, protein, and vitamin requirements of cirrhotic patients and early intervention might prevent the severe cachexia and its associated complications that unfortunately remain common in these patients.
Jump to…Top of pageReferences References
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