Protein calorie malnutrition (PCM) is one of the main cause of poor prognosis for the liver patient, however, it remains generally undiagnosed due to the complications of liver disease such as edema and ascites, which poses a challenge in weight change detection of these patients. It has been reported that PCM occurs in at least 50% and up to 90% of patients with liver cirrhosis. Moreover, malnutrition is considered as an independent risk factor for predicting clinical outcomes in patients with liver disease and increases the risk of morbidity, mortality along with biochemical dysfunction, compromised immune function, respiratory function, decreased muscle mass, increased recovery time, and delayed wound healing.

Older data suggested that protein intake was contraindicated in the liver patient due to the effects of ammonia on the development of hepatic encephalopathy. Nevertheless, in current scenario, protein is vital component of the diet in cirrhosis and is significant so as to avoid PCM. Moreover, several studies have also debated regarding sodium restrictions, which is an important component of the cirrhosis diet and can contribute to PCM.

Various studies have been conducted to examine different aspects of protein intake such as the amount and source of the protein consumed. Evidences suggest that protein requirements of the cirrhotic patient are higher in comparison to those of their healthy counterparts due to PCM. Moreover, these patients may also have protein-losing enteropathy in which excessive intestinal protein is lost due to portal hypertension, which in turn, requires higher protein intake.

The American Society of Parenteral and Enteral Nutrition (ASPEN) and the European Society Parenteral and Enteral Nutrition (ESPEN) recommends that patients with cirrhosis should consume 25-40 kcal/kg/day based on their dry body weight and 1.0-1.5 g/kg protein per day to prevent muscle catabolism. However, patients with acute episodes of hepatic encephalopathy, a temporary protein restriction of 0.6-0.8 g/kg/day has to be implemented until its cause is eliminated, subsequently followed by a high protein intake.

Alteration of amino acid metabolism occurs in liver diseases as the body’s amino acid profile and the ratio of branch chained amino acids (BCAA): aromatic amino acids (AAA) changes to a higher AAA and lower BCAA, which can lead to several complications including hepatic encephalopathy. Thus, supplementation with BCAA can be helpful to normalize this ratio, while ASPEN recommend the use of BCAA for hepatic encephalophathy,along with other benefits such as relief from muscle cramps, improvement in immune function and inhibition of hepatocarcinogenesis.

Besides, patients with liver diseases may be recommended to increase their intake of vegetables proteins as well as other high biological value proteins such as eggs, lean animal meats like fish, chicken, turkey, and low fat dairy, while avoiding excessive red meat consumption.

Sodium is important for the regulation of blood volume, blood pressure, osmotic equilibrium and blood pH and may contribute to malnutrition in some patients. However, sodium restriction is usually the first diet intervention for a liver patient, due to its effects on water retention and the development of edema and ascites. Acites is considered as the hallmark of progression of liver disease and is a undesirable symptom, a strict sodium restriction may contributes to and may worsen PCM in cirrhotic patients. It can also lead to hypernatremia and diuretic-induced renal impairment. Hence, it is essential to monitor patients carefully and treat them in the best possible manner, based on their signs, symptoms, and severity of liver disease. The American Association for the Study of Liver Diseases’ (AASLD) recommendations for the management of ascites suggest that a dietary sodium restriction of ≤2000 mg/day is appropriate for the management of ascites in patient with liver disease.

Source: Eghtesad S, Poustchi H, Malekzadeh R. Malnutrition in Liver Cirrhosis:The Influence of Protein and Sodium. Middle East J Dig Dis. 2013 Apr; 5(2): 65–75.