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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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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 ...