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Intestinal transplantation is indicated in instances of intestinal failure, which is defined as the irreversible inability of the intestine to sustain the body’s nutritional, electrolyte, and fluid balance (Molmenti et al., 2005). Liver and small-bowel grafts are considered in cases of irreversible liver failure, and the liver is transplanted with the intestine in a “piggyback” fashion (Molmenti et al., 2005).
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The first combined liver–intestinal transplantation was described in London for a 41-year-old woman with short-gut syndrome due to antithrombin III deficiency (Grant et al., 1990).
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Intestinal transplantation is indicated in any cases of intestinal failure, which is defined as the irreversible inability of the intestine to sustain the body’s nutritional status. (Molmenti et al., 2005)
Irreversible intestinal failure can be the result of loss of surface area, functional disturbances, or presence of unresectable tumors involving the intestine. (Molmenti et al., 2005.)
It has been found that <20% of adults with <100 cm of intestine or end jejunostomy will be able to maintain nutritional requirements in the absence of total parenteral nutrition (TPN). (Molmenti et al., 2005)
The most commonly cited incidence of patients needing a combined liver–intestine transplantation involves the use of parenteral nutrition (PN) (Molmenti et al., 2005).
Failure of PN criteria includes impending or overt failure due to TPN-induced liver injury; thrombosis of 2 or more central veins; development of 2 or more episodes of systemic sepsis secondary to line infection per year that require hospitalization; single episode of line-related fungemia, septic shock, and/or acute respiratory distress; and frequent episodes of severe dehydration despite intravenous fluid resuscitation (Molmenti et al., 2005).
Abnormalities in liver function tests are common in patients who are on PN; however, the concern is whether long-term PN causes chronic and possibly irreversible liver disease (Buchman et al., 2006).
It is now recognized that serum hepatic aminotransferases become elevated between 1.5 and 3 times the normal levels during the first 3 weeks of PN. (Buchman et al., 2006). The etiology of this is likely multifactorial and may be related to cytokine release driven by the patient’s underlying illness, as well as decreased or absent oral intake (Buchman et al., 2006).
The total bilirubin level might start to increase in some patients after about 10 weeks of PN use (Buchman et al., 2006). There might also be increases in serum alkaline phosphatase, which can be attributed to metabolic bone disease that occurs in patients on long-term PN (Buchman et al., 2006).
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Histologically, patients often present with:
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Steatosis or cholestasis
Ballooning of hepatocytes
Kupffer cell hyperplasia
Bile duct plugging
Extramedullary hematopoiesis
PN-associated liver disease (PNALD) is the most devastating complication of long-term PN therapy and is often recognized too late because its progression is insidious (Buchman et al., 2006).
When end-stage liver disease (ESLD) develops in these patients, most interventions are futile except for transplantation of both the intestine and ...