Parenteral nutrition complications

It is common practice to discontinue oral feedings during an attack of acute pancreatitis. In theory, discontinuation of oral intake will decrease the secretory functions of the pancreas and minimize further complications from the disease. Some patients can be fed with minimal oral intake. Tube feeding delivered via a nasojejunal tube will feed the patient beyond the ampulla of Vater, minimizing stimulation of the pancreas.15,16 If oral intake is discontinued for a protracted period, total parenteral nutrition must be used to maintain adequate nutrition.17,18... 

Maintaining adequate nutritional status, especially during periods of illness and metabolic stress, is an important part of patient care. Malnutrition in hospitalized patients is associated with significant complications, including increased infection risk, poor wound healing, prolonged hospital stay, and increased mortality, especially in surgical and critically ill patients.1 Specialized nutrition support refers to the administration of nutrients via the oral, enteral, or parenteral route for therapeutic purposes.1 Parenteral nutrition (PN), also... 

Parenteral nutrition can be a lifesaving therapy in patients with intestinal failure, but the oral or enteral route is preferred when providing nutrition support ( when the gut works, use it ). Compared with PN, enteral nutrition generally is associated with fewer infectious complications (e.g., pneumonia, intraabdominal abscess, and catheter-related infections) and potentially improved outcomes.1-3 However, if used in appropriate patients (i.e., patients with questionable intestinal function or when the intestine cannot be used), PN can be used safely and effectively and may improve nutrient delivery.4 Indications for PN are listed in Table 97-1.1... 

Btaiche IF, Khalidi N. Metabolic complications of parenteral nutrition in adults, part 1 and part 2. Am J Health-Syst Pharm 2004 61 1938-1949, 2050-2059. 

Compare clinical efficacy, complications, and costs of enteral nutrition (EN) versus parenteral nutrition (PN). 

EN has replaced parenteral nutrition (PN) (see Chap. 60) as the preferred method for the feeding of critically ill patients requiring specialized nutrition support. Advantages of EN over PN include maintaining GI tract structure and function fewer metabolic, infectious, and technical complications and lower costs. 

Linoleic acid and alpha-linoleic acid are essential fatty acids that are provided in any long-term parenteral nutrition by administering fat emulsions at least twice a week. Fatty acid deficiency is a common complication of severe end-stage liver disease. The ability of short-term intravenous lipid supplementation to reverse fatty acid deficiencies has been studied in patients with chronic liver disease and low plasma concentrations of fatty acids (914). Shortterm supplementation failed to normalize triglycerides. 

McCowen KC, Friel C, Sternberg J, Chan S, Forse RA, Burke PA, Bistrian BR. Hypocaloric total parenteral nutrition effectiveness in prevention of hyperglycemia and infectious complications—a randomized clinical trial. Crit Care Med 2000 28(11) 3606-11. 

Peripheral PN (PPN) is a relatively safe and simple method of nutritional support. PPN candidates do not have large nutritional requirements, are not fluid restricted, and are expected to begin enteral intake within lOto 14days. Thrombophlebitis is a common complication this risk is greater with solution osmolarities greater than 600 to 900 mOsm/L (Table 60-2). Solutions for PPN have lower final concentrations of amino acid (3% to 5%), dextrose (5% to 10%) and micronutrients as compared to central parenteral nutrition (CPN). 

Alpers, D.H. Liver complications and failure in patients on home parenteral nutrition. Gastroenterology 2001 17 147—149... 

Gaddipati, K., Yang, P. Hepatobiliary complications of parenteral nutrition. Gastroenterologist 1996 4 98—106... 

Persons at risk for EFA deficiency tend to be the same as those at risk for vitamin E deficiency. Some signs are shared by both defidencies. Premature infants may be at risk for EFA deficiency because of their low stores of lipids and their rapid growth, especially when they are fed diets that do not contain EFAs. For example, fats have been omitted from diets used to feed preterm infants (to avoid a variety of complications). EFA deficiency may develop later in life with fat malabsorption syndromes, EFA deficiency has presented in adults fed by total parenteral nutrition for longer periods, where EFAs had not been included in the liquid diet. 

A major complication of intravenous infusion is thrombophlebitis, which is a principle limitation of peripheral parenteral nutrition. Its precise pathogenesis is unclear, but venospasm has been proposed as the most likely cause. However, in a study with ultrasound techniques to monitor vein caliber, there was no evidence to support this hypothesis, although thrombophlebitis was observed (10). The author suggested that the initiating event may be venous endothelial trauma, caused by the venepuncture itself, abrasion at the catheter tip, or the delivery of the feeding solution. 

Klein GL, Snodgrass WR, Griffin MP, Miller NL, Alfrey AC. Hypocalcemia complicating deferoxamine therapy in an infant with parenteral nutrition-associated aluminum overload evidence for a role of aluminum in the bone disease of infants. J Pediatr Gastroenterol Nutr 1989 9(3) 400-3. 

Two children developed neurological complications of fat emulsion therapy, including focal and generalized seizures, weakness, and altered mental status, before any systemic findings were in evidence (15). Biopsy and autopsy findings included cerebral endothehal and intravascular lipid deposition. These complications are potentially reversible with alteration of the parenteral nutrition content, highlighting the importance of their early recognition. 

Since chronic renal insufficiency is frequently complicated by rises in serum potassium, phosphate, and magnesium, parenteral nutrition solutions used to treat malnourished patients with chronic renal insufficiency are usually prepared with little supplementation of these cations. Four patients with chronic renal insufficiency developed significant hypophosphatemia 3-5 days after starting parenteral nutrition. Other electrolyte abnormalities included hypomagnesaemia (n = 1) and hypokalemia (n — 3) (50). Hypophosphatemia may be the most significant of the electroljde risks in this clinical setting, and the electrolytes of such patients should be monitored closely when nutritional support is begun. 

Patients who develop cholestatic jaundice during chronic parenteral nutrition can develop significant hematological complications due to hypocupremia. 

Intestinal transplantation is combined with liver transplantation in 46% of cases, because of terminal liver failure (93). Of 78 patients who had received parenteral nutrition for more than 2 years n — 66) and/ or had short bowel syndrome and could not be weaned from parenteral nutrition (n = 12), 58 developed chronic cholestasis and 37 developed one or more severe liver complication (serum bilirubin concentration 60 pmol/l, factor V (proaccelerin) 50%, portal hypertension, encephalopathy, ascites, bleeding from the gastrointestinal tract, or histological findings consisting of extensive fibrosis and cirrhosis) after 6 (3-132) months and 17 (2-155) months respectively. Liver disease was responsible for deaths in 6.5% of the patients (22% of deaths). 

The role of lipid emulsions in cholestasis associated with long-term parenteral nutrition has been investigated retrospectively in 10 children with a total of 23 episodes of cholestasis, associated with thrombocytopenia in 13 cases (104). Changes in lipid delivery, associated with increased daily amounts, preceded complications in more than half the cases, while temporary reduction in lipid administration led to normalization of bilirubin in 17 episodes. The authors concluded that lipid supply is one of the risk factors for cholestasis associated with parenteral nutrition. They recommended that when cholestasis occurs, lipid should be temporarily withdrawn, especially if there is associated thrombocytopenia. 

Priapism has been reported as a complication of parenteral nutrition (160). 

Three different mechanisms have been postulated for this complication of parenteral nutrition ... 

Since the introduction of parenteral nutrition in hospital care the potential microbiological risks associated with the manufacture, preparation, and administration of these products have abated but not disappeared (133,152). Fatal infectious complications still occur. The parenteral nutrition mixture is a good growth medium for microorganisms, more conducive to microbial growth than glucose or amino acid solutions. Storage of mixtures... 

Janigan DT, Percy B, Marrie TJ, Chiasson PM, Hirsch D. Skin necrosis an unusual complication of hyperphosphatemia during total parenteral nutrition therapy. J Parenter Enteral Nutr 1997 21(l) 50-2. 

Duerksen DR, Ahmad A, Doweiko J, Bistrian BR, Mascioli EA. Risk of symptomatic central venous thrombotic complications in AIDS patients receiving home parenteral nutrition. J Parenter Enteral Nutr 1996 20(4) 302-5. 

Baker AL, Rosenberg IH. Hepatic complications of total parenteral nutrition. Am J Med 1987 82(3) 489-97. 

Kelly DA. Liver complications of pediatric parenteral nutrition—epidemiology. Nutrition 1998 14(l) 153-7. 

Cavicchi M, Crenn P, Beau P, Degott C, Boutron MC, Messing B. Severe liver complications associated with long-term parenteral nutrition are dependent on lipid parenteral input. Transplant Proc 1998 30(6) 2547. 

Complications from parenteral nutrition support therapy are ... 

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