How Would You Feed this Patient ?
Liver Cirrhosis with Variceal Bleeding
Matthias Pirlich, M.D.
Div. of Gastroenterology, Hepatology & Endocrinology, Charité, Humboldt-Universität, 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 rebleeding
episodes in cirrhotic patients with esophageal varices
Malnutrition in Patients with Liver Cirrhosis
Protein-energy malnutrition (PEM) is a common finding in chronic liver disease and positively related to advanced clinical stage independent of the etiology [1]. In patients with
cirrhosis and esophageal varices, malnutrition is an independent predictor of both the first
bleeding episode and survival. PEM is also associated with muscle weakness, impaired
liver function, with the presence of refractory ascites or the persistence of ascites, and with
postoperative morbidity and mortality.
Nutritional Support in Chronic Liver Disease
According to the 1997 ESPEN guidelines for nutrition in liver disease [1], the majority of
patients with chronic liver disease tolerate a normal diet and do not need any dietary restrictions. A modified eating pattern with six to seven meals including at least one late
evening meal rich in carbohydrate has been shown to improve nitrogen economy and substrate utilisation in stable cirrhosis.
Nutritional therapy is recommended for those patients with malnutrition who are failing to
maintain an adequate oral nutrient intake especially if they are at risk of fatal complications. Nutrition should be provided preferably by the oral or the enteral route, and the parenteral 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 malnourished patients, intakes should be higher (35-40 %) in order to improve the nutritional
state. Regarding protein or amino acids intake should be 1-1.2 g/kg/d. Most patients can
be 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 content (40 mmol/d). Deficiency of water soluble vitamins, folic acid and some trace elements
such as zinc is frequently observed in patients with liver cirrhosis. Since in clinical practice,
micronutrient deficiency may be difficult to diagnose, supplementation should be provided
liberally.
Dietary Protein and Hepatic Encephalopathy
Hepatic encephalopathy is a common neuropsychiatric complication in patients with
chronic liver disease. The pathogenesis is unknown, but gut-derived toxins, such as ammonia, 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].
In the 1950´s, several studies suggested that high protein intake could precipitate hepatic
encephalopathy in cirrhosis. As a result of these studies, the practice of dietary protein
restriction became widespread and is still commonly practised as an overprotective strategy even in patients without encephalopathy [3].
There is now evidence, that long term protein restriction is not beneficial to the clinical outcome of patients with chronic liver disease, but might even be harmful and further deteriorate nutritional state, liver function, and mental state [1,4]. Moreover, in recent studies a
protein intake of up to 1.3-1.5 g/kg/d was tolerated by many patients without adverse effects on encephalopathy and mental state [1,5]. Furthermore, patients with stable cirrhosis
appear to have increased protein requirements of 1.2 g/kg/d to maintain nitrogen homeostasis 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 only
exception of protein-intolerance.
In patients with I-II° encephalopathy, protein should only transiently be restricted to 0.5
g/kg/d for a few days. After improvement of encephalopathy a stepwise increase in dietary
protein is recommended (up to 1.0–1.5 g/kg/d) to reinstitute adequate nutrition. This approach also allows to identify patients who are protein intolerant. In proven protein-intolerant patients, oral supplementation with branched chain amino acids (BCAA) at 0.25 g/kg/d
may be helpful in achieving an adequate nitrogen intake. Long-term BCAA supplementation seems to be associated with better nitrogen accretion, improved liver function, and
improved mental state. The use of vegetable protein has also been recommended, but
with 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 protein
intolerant.
Patients in coma (encephalopathy III-IV°) can safely be treated with TPN regimens providing 25-30 kcal/kg/d non-protein energy plus 0.5-1.2 g/kg/d BCAA-enriched amino acid
solutions. Contrary to the general belief that enteral feeding always is advantageous, a
recent study showed that in patients with TIPS parenteral infusion of amino acids was associated with significantly less systemic hyperammonemia then enteral infusion of isonitrogenous amounts of the identical solution [6].
Nutritional Therapy in Patients with Variceal Bleeding
Variceal bleeding is a life-threatening complication of chronic liver disease and requires
immediate intervention by an experienced endoscopist. These patients are at risk for developing encephalopathy due to the enteral load with a protein of an unbalanced amino
acid 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 application of lactulose either orally or in combination with enema.
We must keep in mind that patients with complicated liver cirrhosis are likely to be malnourished, and that malnutrition further increases the risk of complications and poor outcome. 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 bleeding
considerations regarding the optimal route of nutritional support are secondary and the
immediate institution of nutritional support should be envisaged.
There are two main concerns regarding nutritional support in patients with variceal
bleeding:
 the potential risk of worsening encephalopathy,
 the potential risk of rebleeding episodes using tube-feeding.
Regarding encephalopathy, withholding energy and protein/amino acids puts the patient at
an 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 hemorrhage. If encephalopathy is of advanced stage (II-IV°), then TPN-regimens with BCAAenriched 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 with
cirrhosis demonstrated that tube feeding is not associated with an increased incidence of
upper GI bleeding episodes [8-10] even in patients with a history of previous variceal
bleeding.
In a further randomized controlled study safety and efficacy of early enteral feeding was
investigated in patients with recent variceal bleeding [11]. The treatment group received
early tube-feeding (from day 1) after bleeding from esophageal varices. The control group
were on nil-by-mouth, and on day 4, all patients received oral diet. The authors found no
difference 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 not
surprising given the short period of metabolic intervention.
Summary
Patients with complicatios of cirrhosis such as variceal hemorrhage are likely to be malnourished. Nutritional support should primarily consider the energy and protein requirements to improve the nutritional state. Variceal bleeding is not an absolute contraindication
to the generally preferable enteral route of feeding. Protein restriction should be instituted
only on a short-term basis in patients with clinically overt encephalopathy. Patients with
variceal bleeding and high-grade encephalopathy should be treated with TPN-regimens
providing BCAA-enriched amino acid solutions.
References
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