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End-stage liver disease is a term that is applied to chronic liver disease that is associated with minimal liver function or severe complications that may lead to death. Cirrhosis represents a final common histologic pathway for a wide variety of liver diseases, being characterized by diffuse fibrosis and conversion of the normal liver architecture in to structurally abnormal nodules (Fig. 425-1). Often there is a poor correlation between histology and the clinical status of the patient. Some patients with cirrhosis are essentially asymptomatic whereas others have all of the sequelae of chronic liver disease discussed below. In the era of liver transplantation various attempts to measure the severity of chronic liver disease have been applied in order to determine to prioritize organ distribution for liver transplantation such that the sickest patients received organs. The measure now applied in North America is the Model of End-Stage Liver Disease, or MELD score. The MELD score is calculated using laboratory values including the bilirubin, INR and serum creatinine. The scoring system has been modified for children less than age 12 years (PELD score) such that it uses other measures of chronic disease relevant in children including serum albumin, bilirubin, INR, growth failure (based on gender, height and weight) and age at listing. Calculators to determine the MELD and PELD scores are available at: http://www.unos.org/resources/meldpeldcalculator.asp (accessed March 2, 2010).

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Figure 425-1.
Graphic Jump Location

Cirrhosis with architectural alteration resulting from fibrosis and nodular hepatocellular regeneration (Masson trichrome, 2x).

(From Fauci AS, Braunwald E, Kasper DL et al (eds). Harrison’s Principles of Internal Medicine. 17th ed. http://www.accessmedicine.com. Copyright © The McGraw-Hill Companies. All rights reserved.)

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The major complications of end-stage liver disease include malnutrition, portal hypertension, and its ensuing risk for variceal hemorrhage and ascites, infection, hepatic encephalopathy, and hepatorenal and hepatopulmonary syndrome.1 Early detection with appropriate management may prevent or ameliorate some of these chronic complications.

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Malnutrition and Specific Nutrient Deficits

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A variety of mechanisms may contribute to malnutrition in end-stage liver disease. These include poor dietary intake, malabsorption, increased intestinal protein losses, low protein synthesis, disturbances in substrate utilization, and hypermetabolism. Many of these are not fully understood. Diminished oral intake may be the result of anorexia of chronic disease; gastroesophageal reflux; nausea and early satiety secondary to abdominal distention exacerbated by tense ascites, organomegaly, delayed gastric emptying, small bowel dysmotility and bacterial overgrowth, and altered taste sensation (dysgeusia). Decreased concentrations of intraluminal bile acids and some medications (cholestryamine and antibiotics) predispose the patient to malabsorption of fat and fat-soluble vitamins. Altered protein metabolism and substrate utilization are manifested by hyperammonemia, hypoalbuminemia, reduced clotting factors, and hypoglycemia. Metabolic disturbances consequent to liver disease, such as increased energy expenditure, insulin resistance, and low respiratory quotient (indicating reduced glucose and increased lipid oxygenation), may contribute to malnutrition even in the early stages. Recurrent sepsis is ...

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