Lipids are useful for replacing excessive dextrose calories in cases of uncontrolled hyperglycemia or delayed weaning from mechanical ventilation due to hypercapnia. Lipids containing medium-chain triglycerides (MCT), fish oil, and olive oil have been available in Europe since 1984, but are just now available for research in the United States. Comparisons of the two emulsions indicate one MCT exerts less stress on the liver, improves plasma antioxidant capacity, reduces generation of proinflammatory cytokines, and improves oxygenation.
Essential vitamins and trace elements that are necessary for normal metabolism and cellular function are also added to PN solutions. The dosing requirements for vitamins and trace elements are generally higher than enteral requirements as patient needs are higher secondary to malnutrition.
PARENTERAL NUTRITION SOLUTIONS
PN solutions are classified as either total or peripheral based on route of administration and macronutrient composition. Total parenteral nutrition is delivered via a large-diameter central vein, usually the superior vena cava. Central access allows for the use of highly concentrated, hypertonic solutions and is preferred because the rate of blood flow rapidly dilutes the hypertonic feeding formulation to that of body fluids. Patients receiving PN for more than 2 weeks generally require central vein infusion via a temporary central venous catheter (CVC). Long-term usage requires a tunneled catheter, an implanted port, or a peripherally inserted central catheter (PICC). TPN offers greater choices in formula selection, but is associated with increased risk of catheter-related bloodstream infections. Specific conditions warrant caution when administering TPN (Table 2).
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Peripheral parenteral nutrition (PPN) uses a peripheral vein for access rather than a central vein. Because it is administered into a peripheral vein, the osmolarity of PPN must be less concentrated than TPN and should not exceed 900 mOsm/L. Patients receiving PPN are at risk for vein damage and thrombophlebitis. PPN is not recommended for severely malnourished patients but rather for those with mild to moderate malnutrition who need repletion for not more than 2 weeks.
COMPLICATIONS
Metabolic The most common metabolic complications of PN are hyperglycemia and hypoglycemia. Limiting the amount of dextrose to less than 300 g/day can reduce the risk for hyperglycemia. Hypoglycemia is generally caused by sudden cessation of TPN solutions. To prevent hypoglycemia, PN should be decreased to half rate for 1 hour and then discontinued.
Refeeding syndrome is a severe alteration of electrolyte balance caused by a rapid increase in nutrient intake in malnourished patients; it is a less common but more serious complication. Limiting the amount of calories, particularly dextrose to start, can reduce the risk of refeeding syndrome. Fluid status, potassium, phosphorus, and magnesium status need to be checked and corrected until stable at full PN rate. PN should be increased gradually over 2 to 3 days.
Other metabolic disturbances associated with long-term parenteral nutrition are metabolic bone disease such as osteomalica and osteoporosis. Hepatic disease, biliary disease, and renal disease (such as decreased glomerular filtration rate) have been noted in patients on long-term parenteral nutrition, as well as gastrointestinal disturbances, including gastroparesis.
Cholestasis, gallbladder stasis, and cholelithiasis are gallbladder-related potential complications of PN administration. Patients with short-bowel syndrome are particularly at risk for gallstone formation. If possible, a transition from parenteral to enteral nutrition can stimulate the gallbladder, which can help avoid gallbladder-related complications. Otherwise, the use of cyclic PN, carbohydrate restrictions, and avoidance of overfeeding will help minimize possible side effects.
Parenteral nutrition is associated with GI atrophy. The lack of enteral stimulation causes villus hypoplasia, colonic mucosal atrophy, decreased gastric function, impaired gastrointestinal immunity, bacterial overgrowth, and bacterial translocation. A reduction in mass of both the small and large intestine has been associated with PN. Reduced stimulation by gastric hormones and inadequate pancreatic and gallbladder secretions contribute to PN-associated gastrointestinal atrophy. Enteral feedings should be initiated if feasible. Beneficial effects have been seen in animal models with enteral administration in amounts as small as 10% to 25% of total caloric requirements.
PN provides postoperative nutrition support for patients who have had intestinal resections. These patients often receive long-term PN, particularly when less than 150 cm of small bowel is remaining after resection. This group of patients is prone to a high volume of acidic gastric secretions, depending on the length of bowel resected. Gastric hypersecretion can lead to peptic ulcers and hemorrhagic gastritis. Histamine, H2 receptor antagonists, cimetidine (Tagamet, generics), ranitidine (Zantac, generics), and famotidine (Pepcid, generics) are used to reduce gastric output and prevent ulcers after extensive small bowel resections. These medications can be added to the PN solution and administered over a 24-hour period.
Infectious The vascular access devices can be the source of infectious complications. These complications are typically associated with endogenous flora, contamination of the catheter hub, seeding of the device from a distant site, and contamination of the PN solution.
Mechanical Venous thrombosis is noted in patients receiving long-term PN. Catheter occlusion may also occur during long-term PN administration.
MALNUTRITION IN ONCOLOGY
Malnutrition is the most common secondary diagnosis in cancer patients. Even patients who are eating can become malnourished because of specific biochemical and metabolic changes associated with cancer. These metabolic changes impair nutritional status and contribute to cancer-related malnutrition, anorexia, and cachexia. At least 50% of cancer patients are cachetic.3 Recent reviews indicate cachexia is even more widespread among patients with advanced cancer.4
Cachexia is derived from the Greek word meaning “bad condition,” and is characterized by anorexia (loss of appetite), weight loss, muscle wasting, and chronic nausea. Other noted effects are changes in body composition, alterations in carbohydrate, protein, and lipid metabolism, and depression. Cancer-related metabolic changes lead to preferential depletion of lean body mass as a source of calories. In this way cachexia differs from simple starvation, where the body will metabolize fat stores and protect lean body mass.
Anorexia, the loss of appetite and food intake, is noted in 50% of newly diagnosed cancer patients. Early satiety, taste and smell alterations, food aversions, nausea, and vomiting are contributory factors to anorexia.
Cancer treatments such as chemotherapy and radiation treatment often cause nausea, vomiting, diarrhea, mucositis, and taste alterations (dysguesia). These treatment effects can lead to malabsorption. Cancer operations may result in decreased intake, particularly in the case of surgery to the mouth and neck, which may cause dysphagia. The GI tract can develop physical obstructions, which are often the result of tumor burden. GI obstructions result in decreased intake and are associated with emesis after oral intake. Finally, the depression that frequently accompanies the diagnosis of cancer leads to decreased intake. Eating, which is considered a pleasant experience for most, is no longer pleasant because of side effects, stress, and worry.
NUTRITIONAL ASSESSMENT
Malnutrition is associated with an increase in postoperative morbidity and mortality. A thorough clinical assessment and frequent reassessments are important steps to guarantee timely nutrition interventions. Various tools are available to assess nutritional risk.
The patient-generated subjective global assessment (PG-SGA) is a nutrition assessment tool designed to identify malnutrition in cancer patients.5 Sections on short-term weight status, food intake changes, symptoms that impact nutrition intake, and functional capacity are completed by the patient. A three-part physical assessment that includes evaluation of metabolic demands, degree of metabolic stress, and evaluation of fat stores is completed by the clinical practitioner.
