Hepatitis B Annual

: 2008  |  Volume : 5  |  Issue : 1  |  Page : 117--133

Nutritional management of acute and chronic liver disease

Neeraj Saraf 
 Department of Gastroenterology and Hepatology, Sir Ganga Ram Hospital, New Delhi - 110 060, India

Correspondence Address:
Neeraj Saraf
UNOS Certified Liver Transplant Physician, Department of Gastroenterology and Hepatology, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi-110 060


Malnutrition is prevalent in all forms of liver diseases. A number of factors contribute to malnutrition in patients with hepatic failure. Early diagnosis of malnutrition is essential to allow appropriate treatment, since malnutrition is an important predictor of complications of liver disease and mortality. Disease-specific nutritional therapy should be considered for acute liver failure, sepsis, transplantation, and encephalopathy. This article provides an overview of the nutritional management of acute and chronic liver disease and discusses the need for further intervention studies before appropriate rational treatment guidelines can be formulated.

How to cite this article:
Saraf N. Nutritional management of acute and chronic liver disease.Hep B Annual 2008;5:117-133

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Saraf N. Nutritional management of acute and chronic liver disease. Hep B Annual [serial online] 2008 [cited 2021 Jul 26 ];5:117-133
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Full Text

 Malnutrition in Liver Disease

Malnutrition is prevalent in all forms of liver diseases; from 20% in compensated liver disease to more than 80% in those patients with decompensate disease. [1] Patients with alcoholic liver disease are reported to have a greater incidence of malnutrition than those with nonalcoholic disease. [2] Protein energy malnutrition has been reported in 100% of those who receive liver transplant and malnutrition is an independent risk factor for morbidity and mortality in these patients. Frequently, patients with end stage hepatic failure will present with muscle wasting, decreased fat stores and overt cachexia. However, many more patients will have subtle changes such as fat-soluble vitamin deficiencies, anemia from iron, folate, and pyridoxine deficiency, altered cell-mediated immune function, and slow loss of muscle mass. [1],[2],[3],[4]

Etiology of malnutrition

There are a number of factors that contribute to malnutrition in patients with hepatic failure [Table 1].

Decreased intake

Inadequate food intake is one of the primary causes of malnutrition and occurs in up to two-thirds of patients with chronic liver disease. Anorexia may result from increased circulating levels of tumor necrosis factor and leptin. [5] Patients with chronic liver disease also have delayed gastric emptying. [6] In patients with ascites, early satiety and fullness are common complaints. Frequent inpatient admissions, with periods of nothing by mouth (NPO), also contribute to decreased food intake.

Altered absorption

Reduced bile secretion due to cholestasis or compromised hepatic bile synthesis may impair micelle formation which is essential for digestion of fat by pancreatic and luminal enzymes. The fat-soluble vitamins (A, D, E, and K) are also dependent on micelle formation. Over one-third of adult patients with chronic cholestasis have vitamin A deficiency, and 20-50% of adults with primary biliary cirrhosis are deficient in vitamin D. [7],[9] Undiagnosed pancreatic exocrine insufficiency may be another contributing factor to altered absorption in those patients with alcoholic liver disease. Finally, patients with cirrhosis have also been reported to have an increased incidence of small bowel bacterial overgrowth.

The prevalence of small bowel bacterial overgrowth in populations with cirrhosis has been documented between 35-60% of patients, which may further alter nutrient absorption. [10]

Altered metabolism

Patients with hepatic failure have "accelerated starvation," with an early recruitment of alternative fuel sources. Cirrhotic patients demonstrate significantly increased fat oxidation and gluconeogensis with protein catabolism after an overnight fast. It would take a healthy adult approximately 72 hours of starvation to reach the same level of fat oxidation and protein catabolism as occurs in an overnight fast in a cirrhotic patient. [11],[12],[13] It is believed that the diminished hepatic and muscle glycogen stores that occur with cirrhosis is a factor in this accelerated rate of starvation. Patients without adequate glycogen stores utilize increased fat and muscle protein for fuel even during short-term fasting. This contributes to the loss of subcutaneous fat and muscle wasting that is the hallmark of malnutrition. Insulin resistance and decreased levels of insulin, like growth factor-1, are also believed to contribute to muscle wasting in cirrhosis. See [Table 2] for a list of some of the factors affecting metabolism in these patients.

Micronutrient deficiencies in cirrhosis

Deficiency of water soluble vitamins is common in cirrhosis particularly in alcoholic cirrhosis. Deficiency of thiamine is well known to cause wernickes encephalopathy and korsokoffs dementia. [14] Thiamine deficiency also occurs in HCV related cirrhosis. [15] Fat soluble vitamin deficiency occurs more commonly in cholestatic liver disease. Vitamin A deficiency is described in cirrhosis and may be a risk factor in development of HCC. [16] Low levels of vitamin E and trace elements like selenium and zinc have been described. [17] Zinc deficiency in patients with chronic alcoholism is attributed to decreased intake and absorption and diuretic-induced increased urinary excretion. [18] Supplementation with zinc has been shown to improve glucose disposal in cirrhotic patients, and it's deficiency may contribute to the impaired glucose tolerance and diabetes commonly observed. Zinc deficiency is considered to precipitate hepatic encephalopathy; [19] however, trials of supplementation have shown conflicting results. [20],[21] Magnesium deficiency also occurs in alcoholic liver disease, and muscle magnesium is an independent predictor of muscle strength. [22] This is probably related to the reduced content of sodium-potassium pumps in skeletal muscle that accompanies magnesium deficiency. However, supplementation did not restore muscle magnesium or improve muscle function in patients with alcoholic liver disease. Serum levels 25-OH vitamins D are low in patients with liver disease and are a cause of osteoporosis. Hence it is recommended to treat vitamin D deficiency with vitamin D3 and calcium. [23]

Diagnosis and assessment

Early diagnosis of malnutrition is important to allow appropriate treatment, since malnutrition is predictor of complications of liver disease and mortality. [24] Body weight can be misleading in patients with ascites and peripheral edema, although one study has validated body mass index in cirrhotic patients with cut-off values of 22 kg/m [2] in non ascitic patients, 23kg/m 2 for patients with mild ascites, and 25 kg/m [2] for patients with tense ascites. [25] Commonly used bedside parameters like anthropometry and plasma protein concentration have significant drawbacks. Anthropometric techniques such as mid arm muscle circumference assess body composition. Fat-free mass (lean body weight; water, protein, and mineral) and fat mass are measured, and these techniques are referred to as two-compartment systems. Anthropometric techniques may be affected by edema and have been shown in one study to classify up to 20-30% of healthy controls as undernourished. [26], [27] However, several other studies have shown that anthropometric measurements and handgrip strength correlate well with more sophisticated assessments such as DEXA in cirrhotic patients. [28] Indeed, midarm muscle circumference was shown to be an independent predictor of mortality in advanced cirrhosis. Subjective global assessment uses clinical information obtained during history taking and examination to determine nutritional status without objective measurements and can determine outcome in patients with cirrhosis. [29] However, when compared with nutritional prognostic index and hand grip strength, hand grip strength was the only method that predicted a poorer clinical outcome. [30] The European Society for Clinical Nutrition and Metabolism guidelines state that bedside methods such as subjective global assessment, anthropometry, or handgrip strength are adequate for identification of under nutrition and composite scores do not add value. For quantitative analysis, the determination of phase angle or body cell mass using bio impedance analysis is recommended instead of anthropometry, despite limitations with ascites [31] [Figure 1].


An intake of 35-40 kcal/ kg/day (dry body weight) and 1.2-1.5g/kg/day of protein is recommended. Approach to nutritional treatment is given in [Table 3].

In severely malnourished patients with cirrhosis, feeding 40 Kcal/day over one month increases body fat mass irrespective of degree of liver damage. If nutritional supplementation is inadequate to maintain desired adequate calorie intake, then artificial nutrition should be initiated either via nasogastric tube or intravenously.

Enteral nutrition

A whole protein formula providing 35-40 K cal energy per day and 1.2 -1.5 gm/Kg /day protein is recommended for enteral feeding. [32] Four randomized trials concerning total enteral nutrition in cirrhosis have been reported. [33],[34],[35],[36] Three showed an increased dietary intake over conventional oral diet, and two showed improvement in liver function. One showed lower hospital mortality compared with conventional diet. The fourth was performed in well-nourished patients admitted with variceal bleeding and failed to show benefit in nutritional status or disease-related morbidity and mortality. [33] However, most of these patients were able to eat 2000 kcal/day from day 4. [32] In hospitalized patients with an inadequate dietary intake, enteral nutrition should be commenced as soon as possible, ideally within 24-48 hours of admission. This is illustrated by a prospective study in 396 patients showing that a decrease in dietary intake was an independent predictor of hospital mortality and corresponded with a deterioration of liver function.

Total parenteral nutrition

Use of TPN in chronic liver disease is controversial. One study concluded that small intestinal metabolism contributes to post feeding hyperammonemia which may worsen hepatic encephalopathy and in such cases parenteral nutrition may be superior to enteral nutrition. [37] The risks of mechanical complications (eg pneumothorax) and catheter-related sepsis are high in malnourished cirrhotic patients; it is essential that parenteral nutrition is administered via a dedicated line to reduce the incidence of sepsis. Also, the osmotic strength of parenteral mixtures requires the infusion of large amounts of fluid that may be excessive for patients with ascites. Thus, enteral feeding is the preferred mode of artificial nutrition in liver disease, and the parenteral route is reserved for intensive care patients with multiorgan failure and subsequent paralytic ileus that prevents successful enteral feeding. A randomized trial comparing the two in liver disease has never been performed.

Nutritional management in specific conditions

Alcoholic hepatitis

Severe alcoholic hepatitis, defined by a Maddrey score 32, has a significant mortality rate. Although corticosteroids remain the mainstay of treatment [38] there have been several studies of nutritional support. A multicenter, randomized, controlled trial that compared four weeks of treatment with total enteral nutrition or corticosteroids showed no difference in mortality during treatment between the two groups. [37] Deaths were found to occur earlier in the enteral nutrition group. However, 10 of the survivors treated with corticosteroids died in the first year of follow-up compared with two of 24 who received enteral nutrition; majority of these deaths were due to sepsis. The investigators hypothesized that the increase in infection seen with prolonged immunosuppression could be reduced by improving gut barrier function and thus reducing bacterial translocation. They went on to examine the combination of enteral nutrition with corticosteroid treatment in a pilot study in 13 patients and found no deaths related to infection. [39]

Hepatic encephalopathy

Traditionally, a restricted protein diet has been considered a mainstay of treatment. However, cirrhotic patients exhibit increased protein requirement to achieve balanced nitrogen metabolism, and normal protein diets have been given safely to patients with hepatic encephalopathy. [40] Thus, restriction is rarely required but, if necessary, usually for no more than 48 hours. It should be noted that the recommended protein supplementation is based on "dry" body weight and may need alteration in edematous patients. Importantly, the risk of aspiration pneumonia in patients with advanced hepatic encephalopathy during tube feeding must be weighed against the potential complications of parenteral nutrition

Variceal bleed

The European Society for Parenteral and Enteral Nutrition guidelines support insertion of fine bore nasogastric tubes in patients with esophageal varices. [41] This has been addressed only in one study in which 22 patients with esophageal varices after bleeding and endoscopic treatment were randomized to either nasogastric feeding or no oral diet for three days. Recurrent bleeding occurred in three patients from the nasogastric tube group but none of the controls. In light of these findings, it has been suggested that the guidelines should state that tube feeding is dangerous in patients with esophageal varices that have bled before and that in patients without former bleeding, there is a tendency for an adverse effect. The European Society for Clinical Nutrition and Metabolism authors responded that endoscopic therapies in this study were unbalanced between the two groups, which might have influenced outcome, with a higher proportion of injection sclerotherapy in the feeding group as opposed to a greater number of band ligations in controls. [42] They also referred to a small series of tube fed cirrhotic patients in which fine bore tubes did not provoke variceal hemorrhage and a trial of low/normal protein diet via fine bore tube in hepatic encephalopathy in which gastrointestinal bleeding occurred in only one of 30 patients. They concluded "if patients are unable to maintain adequate oral intake, tube feeding is recommended (even in presence of esophageal varices)." They acknowledged that there is concern in the immediate days following a bleed. It is probably best to wait at least 24 hours following endoscopic therapy for a bleed and then insert a nasogastric tube and commence feeding.

Acute liver failure

A patient of acute liver failure is generally not malnourished at presentation, since there is no preceding illness. The aim of treatment is to maintain a nutritional balance in presence of an increased catabolic state due to liver failure and coexistent sepsis. Hypoglycemia is common due to impaired gluconeogenesis, depletion of hepatic glycogen and hyperinsulinemia. Administration of IV glucose 1.5-2 gm/kg/day is recommended. There is great disparity amongst liver units in using nutritional regimens. A recent European survey was conducted on 33 hepatology units attending two to 170 cases of acute liver failure per year. All units used specific nutrition regimens, but these varied considerably and mostly resembled those used in critically ill patients with near-normal liver function. Eight units preferentially used enteral feeding and 25 parenteral. Two-thirds used standard parenteral regimens containing amino acids, although plasma amino acid levels are already greatly elevated due to liver failure and increased protein catabolic rate. [43]

Role of branched chain amino acids

Use of the branched chain amino acids (leucine, isoleucine, and valine) has been the subject of interest. [39] These are essential amino acids; which cannot be synthesized de novo, but must be obtained from the diet and are largely metabolized by muscle rather than liver. In cirrhosis, there is a likely reduced total body pool of BCAAs due to reduced lean muscle mass and defective use secondary to hyperinsulinemia. [44] Conversely, amino acids metabolized by the liver are elevated in cirrhosis (e.g., the circulating aromatic amino acids phenylalanine, tryptophan, and tyrosine). BCAAs compete with the serotonin precursor tryptophan for the same amino acid transporter in the blood-brain barrier, and the imbalance between the two in cirrhosis probably influences brain ammonia levels directly or indirectly. This is considered an important mechanism underlying the development of hepatic encephalopathy, and so supplementation with BCAAs may reduce brain uptake of tryptophan and improve encephalopathy. Additionally, both enteral and parenteral BCAA supplementation improved cerebral perfusion in cirrhotic patients, which again may improve encephalopathy; the underlying mechanism is unclear. [43]

Oral BCAAs have been shown to benefit patients with hepatic encephalopathy; moreover, a large multicenter study showed that oral BCAAs given for 1 year improved the Child score, reduced hospital admissions, and prolonged event-free survival. A further large trial showed improved event-free survival and quality of life in Japanese patients treated with BCAAs for two years compared with controls. However, a cochrane analysis based on 11 trials of oral supplementation and 556 patients found no convincing evidence of benefit. [45] Although no toxicity was reported, many patients stop supplementation because of the taste and amount of water required. Importantly, no benefit of BCAA supplementation was observed in protein-tolerant patients.

Parenteral administration of BCAAs to patients with acute liver failure-related encephalopathy within intensive care units has been advocated because these patients have increased total amino acids but reduced BCAAs. However, there have been no controlled studies. The use of BCAAs remains controversial, and they are not widely available in many centers due to their expense and unpalatability. European Society for Parenteral and Enteral Nutrition guidelines recommend that enteral feed enriched with BCAAs is reserved for patients who develop encephalopathy with enteral feeding despite appropriate treatment.

Nutrition in liver transplantation

Various authors have examined the impact of preoperative nutrition on outcome after transplantation. A series of 100 patients six months post transplantation found that muscle wasting was one of six variables associated with reduced survival. [46] Other studies have shown that preoperative malnutrition impacts negatively on post transplantation outcome. [47],[48],[49] These include a prospective study of 150 patients who underwent transplantation for cirrhosis and who could be divided into high risk and low-risk groups, with survival rates of 54% and 88%, respectively, based on preoperative nutrition and resting energy expenditure. Other studies have shown higher rates of complications and mortality in cirrhotic patients with malnutrition compared with those with adequate nutrition who undergo transplantation.

More recently, however, this has been questioned. A prospective series of 53 patients from the Mayo Clinic who underwent transplantation failed to show an association between any preoperative nutritional parameters and survival or global resource utilization. In this series, the postoperative mortality was quite low after 1 year (7.5%), as was the frequency of preoperative malnutrition (9.4%), and patients were offered preoperative nutritional support.

Thus, this study could be interpreted as showing either that adverse outcome after transplantation is associated with factors other than preoperative nutritional state, or that preoperative nutritional support can overcome the adverse effect of malnutrition on outcome. An older study used a prognostic nutritional index based on serum albumin and transferring levels, triceps skin fold thickness, and delayed hypersensitivity responses to assess malnutrition and outcome post transplantation. All patients were found to be malnourished pre transplantation, but there was no correlation between this index and mortality or morbidity post transplantation. A further prospective series of 61 candidates for transplantation showed poor correlation between nutritional parameters and the Child score and Model of End-Stage Liver Disease score. Interestingly, a retrospective study in patients examined risk factors for acute rejection and found that the only significant predictor on multivariate analysis of a reduction in acute cellular rejection was decreased mid arm muscle circumference, that is, malnourished patients had a lower incidence of acute rejection.

To date, no controlled trial has shown that preoperative intervention improves clinically relevant outcomes. A study of 82 patients randomized to enteral supplementation (750 kcal, 20 g protein, and 34 g fat) and conventional diet or conventional diet alone showed an improvement in handgrip strength and mid arm muscle circumference but not outcome. The difference in overall survival at six months post transplantation almost reached significance, and a larger sample size might have shown benefit. Two studies have examined nutritional support following transplantation. Early postoperative enteral nutrition, within 12 hours, reduced the rate of viral infections and showed a trend toward a lower rate of bacterial infections. Postoperative parenteral nutrition compared with intravenous administration of fluid and electrolytes reduced the length of intensive care stay.

Immunonutrition, supplementation with nutrients shown to beneficially influence immunologic or inflammatory parameters in clinical or laboratory studies (eg, glutamine), has shown positive results in other gastrointestinal surgery. A pilot study of 15 patients given an immunomodulatory diet containing arginine, n-3 fatty acids, and nucleotides before and after transplantation showed an increase in total body protein and a trend to reduction in infections compared with historical controls receiving standard nutrition.


Nutritional support improves outcome in patients unable to maintain an intake of 35-40 kcal/kg/day and 1.2-1.5 g/kg/day protein. Simple methods of assessment such as subjective global assessment, mid arm muscle circumference, and calorie counting are useful, and standard enteral products may be used in the majority of patients. Future research should be aimed at answering these questions. In particular, disease-specific nutritional therapy should be considered for acute liver failure, sepsis, transplantation, and encephalopathy. Further large scale intervention studies are required before treatment guidelines can be based on a formal meta analysis.


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