الفهرس 
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Abstract
Total parenteral nutrition (TPN) is a continuous infusion of a hypertonic solution of glucose, amino acids, electrolytes, minerals and vitamins as well as lipids to maintain tissues and promote growth. The guiding principle of nutrition support is to use the least invasive and most physiological method of feeding. Infusing chemicals directly into the bloodstream is the least preferred method of providing nutrition support.
Parenteral nutrition (PN) may be a life-saving therapy for patients who cannot support their nutritional needs via the enteral route. parenteral nutrition allows the introduction of nutrients and associated additives directly into the blood stream. This process results in three different problems related to the fact that the protective effect of the gut is breached. These are first the almost unlimited ability to infuse nutrients such as glucose and lipid, second to infuse additives such as preservatives and additives and finally introduce bacteria. The liver, as the target organ of these aspects of parenteral nutrition (PN), is subjected to significant complications in the form of PN-associated liver dysfunction which can be seriously damaged causing fibrosis and hepatic failure.
Presentation of liver dysfunction associated with parenteral nutrition differs between adults and infants; steatosis is the most common complication of adults, whereas cholestasis occurs frequently with children.
The etiology of PN-associated liver dysfunction seems to be multifactorial and includes patient-dependent factors such as extreme SBS, severe protein malnutrition, and local and systemic sepsis. Furthermore, nutrition-dependent factors, most importantly the absence of gastrointestinal stimulation and excess energy intake and lipid supply appear to be among the risk factors for PN-associated cholestasis.
Recently, evidence has been brought forward that a change in the parenteral lipid emulsion, from a predominance of n-6 fatty acids (FAs) within the parenteral regimen, to the inclusion of n-3 fatty acids from fish oil, seems to improve liver function in adult and pediatric patients and may be effective in the treatment of PNALD in patients with SBS
In many patients who receive parenteral nutrition there is less than a 2-fold elevation above normal of aspartate and alanine transaminase as well as alkaline phosphatase. These abnormalities, if stable, are of little clinical consequence. If progressive, and in particular if the bilirubin level rises, there is need to exclude the standard causes of such abnormalities including drug toxicity, biliary disease and viral hepatitis. If investigations show no other cause than PN, it is necessary to review the nutrient intake and mix so as to avoid the excessive infusion of fat and carbohydrate as well as total calories. In addition, a search should be undertaken for systemic sepsis and bacterial overgrowth in the intestine. Reduction of calories and treatment of sepsis and/or bacterial overgrowth often solves the problem.
Elevations in liver function tests can occur within 2 weeks of initiation of PN, studies suggest development of steatosis is primarily due to excessive calories/overfeeding,
Cholestasis, impaired secretion of bile or frank biliary obstruction that occurs predominantly in children, can also occur in adults on long term PN, Presents as an elevation of AP, GGT, and direct bilirubin with/without jaundice. AST and ALT may also be elevated. An elevated direct bilirubin (>2 mg/dL) is considered a prime indicator of cholestasis “PN-Associated Cholestasis” (PNAC) may progress to cirrhosis and liver failure ,progressive elevations in serum conjugated bilirubin and persistent jaundice is associated with high mortality risk.
Gallbladder stasis, during PN therapy may lead to gallstones or gallbladder sludge, with subsequent cholecystitis which can occur in both adult and pediatric patients. Lack of oral/enteral intake leads to decreased cholecystokinin (CCK) release and impaired bile flow and gallbladder contractility .The duration of PN therapy correlates with development of biliary sludge.
Management includes, trial of enteral nutrition, use the enteral route as soon as possible, provide as much enteral nutrition as tolerated, even small volumes of enteral feeds are beneficial. Avoid overfeeding, limit total calories from dextrose to 65%or lesse .Optimize lipid emulsions. Optimize amino acid infusions. prevent sepsis and bacterial translocation. prevent choline,carnitine,taurine deficiency. Supplement with glutamine. Trial of Ursodeoxycholic acid, infusion of IV Cholecystokinin-octapeptide .