Overall Bottom Line
- The risk of malnutrition is shown to correlate with severity of disease in cirrhotic patients. PEM is frequently found in decompensated cirrhotic patients at the time of liver transplantation.
- Malnutrition is linked to an increased risk of complications and death in cirrhotic patients awaiting liver transplantation. Poor nutritional status affects the transplant surgical outcome and post-transplant survival.
- Early recognition and treatment of malnutrition are important in the management of cirrhotic patients, especially those who are listed for transplantation.
Section 1: Background
Definition of disease
- Malnutrition is the condition where the human body does not get or process the right amount of the vitamins, minerals and other nutrients necessary to maintain health of tissues and organ function.
Disease classification
- Malnutrition can be classified into macronutrient and micronutrient deficiencies. The macronutrients include protein, lipid and carbohydrate which are cellular building blocks. The micronutrients include mineral (trace elements), electrolytes and vitamins which are key factors for many metabolic regulatory processes.
- The most common form of macronutrient deficiency in ESLD is protein–energy malnutrition (PEM which is also called protein–calorie malnutrition) characterized by wasting of muscle mass and loss of fat stores.
Incidence/prevalence
- Prevalence for malnutrition is varied; however, virtually all cirrhotic patients at the time of liver transplantation have a form of malnutrition.
- Most studies suggest that malnutrition is routinely under-diagnosed and under-treated in cirrhotic patients.
Economic impact
- There is no clear data on the economic impact of malnutrition. However, it has been shown that cirrhotic patients with PEM have an increased risk of infection, encephalopathy, prolonged hospitalization and death before and after liver transplantation.
Etiology
- The etiology of malnutrition in cirrhosis is complex and multifactorial.
- Protein, carbohydrate, and lipid metabolism are all affected by liver disease.
- Poor nutritional intake, impaired absorptive function, altered metabolism and iatrogenic effect from medical treatment are all thought to contribute to malnutrition in cirrhosis.
Pathology/pathogenesis
- Poor dietary intake is common in cirrhotic patients with ascites. This is often due to anorexia and early satiety associated with large ascites affecting gastric emptying and motility.
- Patients often complain of loss of appetite due to strict sodium restriction imposed by clinicians for treatment of ascites. A low sodium diet makes food unpleasant to taste.
- Cholestasis from cirrhosis or cholestatic liver disease leads to a decreased amount of bile flow which is necessary for digestion and absorption of fat and fat-soluble such as vitamins A, D, E and K.
- The use of laxatives such as lactulose and non-absorbable antibiotics for treatment of encephalopathy further increase the risk of malabsorption of protein, fat and micronutrients such as calcium and zinc. These patients frequently have occult steatorrhea which is a clinical sign of fat digestion and malabsorption.
- Gastrointestinal mucosal edema from portal hypertension and low gastric acid output state from portal gastropathy or from use of PPIs further make intestinal absorption of various nutrients such as iron, calcium and protein difficult.
- The liver is a key organ responsible for metabolism of macronutrients such as protein, carbohydrate and lipid. Metabolism and processing of these macronutrients are affected by hepatic dysfunction caused by cirrhosis.
- There is impaired storage of glycogen in the liver which affects glycogenolysis and gluconeogenesis in the fasting state. This leads to accelerated starvation with early recruitment of alternative fuel sources such as protein first, followed by fat second. This leads to a catabolic state with negative nitrogen balance. This is a central reason why cirrhotic patients develop PEM with loss of muscle and fat mass.
- Liver cirrhosis is a hyperinsulinemic state due to impaired clearance of insulin and peripheral insulin resistance. Peripheral insulin resistance with abnormal glucose is seen early in the course of cirrhosis. As the severity of hepatic dysfunction worsens, patients often develop nocturnal hypoglycemia due to impaired hepatic gluconeogenesis in the fasting state.
Predictive/risk factors
- The severity of hepatic dysfunction in cirrhosis correlates with the degree of malnutrition.
- Other risk factors for malnutrition include alcoholic liver disease and cholestatic liver diseases such as PBC, PSC and biliary atresia.
Section 2: Prevention
Bottom Line/Clinical Pearls
- It is important to identify and screen patients at risk of developing malnutrition.
- Clinicians should assume that inadequate dietary intake and PEM are present in almost all cirrhotic patients.
- Nutritional assessment, screening, counseling and treatment should be offered to all cirrhotic patients routinely.
- Balanced diet, exercise and nutritional supplements can prevent and treat malnutrition.
Screening
- A thorough nutritional assessment should be performed routinely in patients with cirrhosis and cholestatic liver disease. These patients should be routinely screened for fat soluble vitamins (A, D, E, K) and for anemia (iron, folate and vitamin B12).
- Patients with hepatic encephalopathy, chronic renal insufficiency and lactulose-induced diarrhea should be screened for zinc deficiency.
- Serum nutritional markers become less reliable as the severity of hepatic dysfunction and cirrhosis worsens.
Primary prevention
- Nutritional screening for malnutrition and dietary education should be offered to all patients with chronic liver disease.
Secondary prevention
- Periodic assessment should be undertaken to evaluate overall nutritional status.
Section 3: Diagnosis
Bottom Line/Clinical Pearls
- The approach to patients with chronic liver disease includes a thorough history including nutritional assessment, physical examination and appropriate laboratory studies.
- Body weight can be misleading in patients with ascites and peripheral edema.
- Protein catabolism is a hallmark of advanced cirrhosis. Assessment of plasma proteins such as albumin and pre-albumin are less reliable in cirrhosis due to impaired visceral protein synthesis in the liver.
- Several studies have shown that anthropometric measurements to assess muscle and fat mass and hand grip strength assessments are well correlated to other sophisticated tests such as bioelectrical impedance and dual X-ray absorptiometry.
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53: Recurrent Disease Post-Liver Transplantation: Autoimmune Diseases, Hepatitis B and NASH
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