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How Would You Feed this Patient ?Liver Cirrhosis with Variceal Bleeding

Matthias Pirlich, M.D.Div. of Gastroenterology, Hepatology & Endocrinology, Charit, Humboldt-Universitt, D-10098 Berlin,

Germany,phone +49-30-450-514 102, fax +49-30-450-514 923, email: matthias.pirlich@charite.de

Learning Objectives

To identify protein-energy malnutrition as a complication of liver cirrhosis

To explain basic principles of nutrition therapy in chronic liver disease

To balance the risks of nutritional therapy against encephalopathy and rebleedingepisodes in cirrhotic patients with esophageal varices

Malnutrition in Patients with Liver CirrhosisProtein-energy malnutrition (PEM) is a common finding in chronic liver disease and posi-tively related to advanced clinical stage independent of the etiology [1]. In patients withcirrhosis and esophageal varices, malnutrition is an independent predictor of both the firstbleeding episode and survival. PEM is also associated with muscle weakness, impairedliver function, with the presence of refractory ascites or the persistence of ascites, and withpostoperative morbidity and mortality.

Nutritional Support in Chronic Liver DiseaseAccording to the 1997 ESPEN guidelines for nutrition in liver disease [1], the majority ofpatients with chronic liver disease tolerate a normal diet and do not need any dietary re-

strictions. A modified eating pattern with six to seven meals including at least one lateevening meal rich in carbohydrate has been shown to improve nitrogen economy and sub-strate utilisation in stable cirrhosis.Nutritional therapy is recommended for those patients with malnutrition who are failing tomaintain an adequate oral nutrient intake especially if they are at risk of fatal complica-tions. Nutrition should be provided preferably by the oral or the enteral route, and the par-enteral approach should only be used when enteral feeding is not possible or impractable.In stable cirrhosis recommended intake of non-protein energy is 25-30 kcal/kg/d. In mal-nourished patients, intakes should be higher (35-40 %) in order to improve the nutritionalstate. Regarding protein or amino acids intake should be 1-1.2 g/kg/d. Most patients canbe treated with standard solutions. Especially in patients with fluid retention liquid enteral

formulae should be preferably of high energy density (1.5 kcal/ml) with a low sodium con-tent (40 mmol/d). Deficiency of water soluble vitamins, folic acid and some trace elementssuch as zinc is frequently observed in patients with liver cirrhosis. Since in clinical practice,micronutrient deficiency may be difficult to diagnose, supplementation should be providedliberally.

Dietary Protein and Hepatic EncephalopathyHepatic encephalopathy is a common neuropsychiatric complication in patients withchronic liver disease. The pathogenesis is unknown, but gut-derived toxins, such as am-monia, which are formed by degradation of ingested protein, are thought to be important in

its genesis. Upper GI bleeding is a major precipitating factor for encephalopathy [2].

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In the 1950s, several studies suggested that high protein intake could precipitate hepaticencephalopathy in cirrhosis. As a result of these studies, the practice of dietary proteinrestriction became widespread and is still commonly practised as an overprotective strat-egy even in patients without encephalopathy [3].There is now evidence, that long term protein restriction is not beneficial to the clinical out-

come of patients with chronic liver disease, but might even be harmful and further deterio-rate nutritional state, liver function, and mental state [1,4]. Moreover, in recent studies aprotein intake of up to 1.3-1.5 g/kg/d was tolerated by many patients without adverse ef-fects on encephalopathy and mental state [1,5]. Furthermore, patients with stable cirrhosisappear to have increased protein requirements of 1.2 g/kg/d to maintain nitrogen homeo-stasis as opposed to 0.8 g/kg/d in normal individuals [5]. Therefore, the ESPEN guidlines[1] recommended a rather high protein intake for patients with liver cirrhosis with the onlyexception of protein-intolerance.In patients with I-II encephalopathy, protein should only transiently be restricted to 0.5g/kg/d for a few days. After improvement of encephalopathy a stepwise increase in dietaryprotein is recommended (up to 1.01.5 g/kg/d) to reinstitute adequate nutrition. This ap-

proach also allows to identify patients who are protein intolerant. In proven protein-intole-rant patients, oral supplementation with branched chain amino acids (BCAA) at 0.25 g/kg/dmay be helpful in achieving an adequate nitrogen intake. Long-term BCAA supplementa-tion seems to be associated with better nitrogen accretion, improved liver function, andimproved mental state. The use of vegetable protein has also been recommended, butwith this approach it might be more difficult to achieve a sufficient protein intake. However,according to Ferenci [2], only a minority of patients with encephalopathy are truely proteinintolerant.Patients in coma (encephalopathy III-IV) can safely be treated with TPN regimens pro-viding 25-30 kcal/kg/d non-protein energy plus 0.5-1.2 g/kg/d BCAA-enriched amino acidsolutions. Contrary to the general belief that enteral feeding always is advantageous, arecent study showed that in patients with TIPS parenteral infusion of amino acids was as-sociated with significantly less systemic hyperammonemia then enteral infusion of isoni-trogenous amounts of the identical solution [6].

Nutritional Therapy in Patients with Variceal BleedingVariceal bleeding is a life-threatening complication of chronic liver disease and requiresimmediate intervention by an experienced endoscopist. These patients are at risk for de-veloping encephalopathy due to the enteral load with a protein of an unbalanced aminoacid pattern [2,7]. Therefore, after control of the bleeding and hemodynamic stabilisation,

an immediate therapeutic goal is the elimination of the ingested blood for instance by ap-plication of lactulose either orally or in combination with enema.We must keep in mind that patients with complicated liver cirrhosis are likely to be mal-nourished, and that malnutrition further increases the risk of complications and poor out-come. Therefore, many patients with variceal bleeding are in need of nutritional support,preferably by the enteral route. In the acute situation during or immediately after bleedingconsiderations regarding the optimal route of nutritional support are secondary and theimmediate institution of nutritional support should be envisaged.

There are two main concerns regarding nutritional support in patients with varicealbleeding:

the potential risk of worsening encephalopathy, the potential risk of rebleeding episodes using tube-feeding.

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Regarding encephalopathy, withholding energy and protein/amino acids puts the patient atan even higher risk for protein catabolism and thus an increased risk of encephalopathy.Also, the above cited recommendations [1] are valid also in patients with variceal hemor-rhage. If encephalopathy is of advanced stage (II-IV), then TPN-regimens with BCAA-enriched amino acid solutions should be used. In patients with low-grade encephalopathy

the enteral route with short term protein restriction is adequate.Regarding the risk of rebleeding a few number of studies on tube-feeding in patients withcirrhosis demonstrated that tube feeding is not associated with an increased incidence ofupper GI bleeding episodes [8-10] even in patients with a history of previous varicealbleeding.In a further randomized controlled study safety and efficacy of early enteral feeding wasinvestigated in patients with recent variceal bleeding [11]. The treatment group receivedearly tube-feeding (from day 1) after bleeding from esophageal varices. The control groupwere on nil-by-mouth, and on day 4, all patients received oral diet. The authors found nodifference in the number of rebleeding episodes between tube fed and control patients.The authors observed no favourable effect of short-term enteral nutrition on nutritional

status, liver function and mortality during the observation period of 35 days, which is notsurprising given the short period of metabolic intervention.

SummaryPatients with complicatios of cirrhosis such as variceal hemorrhage are likely to be mal-nourished. Nutritional support should primarily consider the energy and protein require-ments to improve the nutritional state. Variceal bleeding is not an absolute contraindicationto the generally preferable enteral route of feeding. Protein restriction should be institutedonly on a short-term basis in patients with clinically overt encephalopathy. Patients withvariceal bleeding and high-grade encephalopathy should be treated with TPN-regimensproviding BCAA-enriched amino acid solutions.

References

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2. Ferenci P. Hepatische Enzephalopathie: Ernhrung als Ursache oder Therapie. Z Gastroenterol 1996; Suppl5: 32-34

3. Soulsby CT, Morgan MY. Dietary management of hepatic encephalopathy in cirrhotic patients: survey of currentpractice in United Kingdom. Br Med J 1999; 318: 1391

4. Morgan TR, Moritz TE, Mendenhall CL Haas R, and VA coooperatve Study Group #275. Protein consumption andhepatic encephalopathy in alcoholic hepatits. J Am Coll Nutr 1995; 14: 152-158

5. Kondrup J, Mller MJ. Energy and protein requirements of patients with chronic liver disease. J Hepatol 1997; 27:

239-2476. Plauth M, Roske A-E, Romaniuk P, Ziebig R, Lochs H. Post-feediing hyperammonaemia in patients with transjugular

intrahepatic portosystemic shunt and liver cirrhosis: role of small intestinal ammonia release and rout of nutrient ad-ministration. Gut 2000; 46: 849-855

7. van Berlo CLH, van de Bogaard EJM, van der Heijden MH, van Eijk HMH, Janssen MA, Bost MCF, Soeters PB. Isincreased ammonia liberation after bleeding in the digestive tract the consequence of complete absence of iso-leucine in hemoglobin? A study in pigs. Hepatology 1989; 10: 315-323

8. Keohane PP, Attrill H, Grimble G, Spiller R, Frost P, Silk DB. Enteral nutrition in malnourished patients with hepaticcirrhosis and acute encephalopathy. JPEN 1983; 346-350

9. Cabr E, Gonzalez-Huix F, Abad-Lacruz A, et al. Effect of total enteral nutrition on the short-term outcome of se-verely malnourished cirrhotics. Gastroenterology 1990; 98: 715-720

10. Kearns PJ, Young H, Garcia G, et al. Accelerated improvement of alcoholic liver disease with enteral nutrition.Gastroenterology 1992; 102: 200-205

11. de Ledinghen V, Beau P, Mannant PR et al. Early feeding or enteral nutrition in patients with cirrhosis after bleeding

from esophageal varices? A randomized controlled study. Dig Dis Sci 1997; 42: 536-541