The medical community has been interested in intravenously administered nutrition since the 1600s; however, reliable sources of IV nutrients were not established until the 1960s. As a young intern, Stanley Dudrick, MD, struggling to save patients who could not be nourished orally or via tube feeding, dedicated himself to finding a way to supply nutrients to patients lacking a functional GI tract.1 He was able to demonstrate that IV nutrition could support growth and development in beagle puppies. Continuing to refine his nutrient solution, he began administering his nutrient solution intravenously to select human patients.1
Another challenge was finding adequate venous access for administration of the hypertonic nutrition. Dudrick found that using subclavian vein cauterization allowed nutrients to be quickly diluted within the central venous system, thereby decreasing the likelihood of thrombotic complications. In 1968, Dudrick discharged a 36-year-old patient with a nonfunctioning GI tract to home with his newly developed IV nutrition support. The patient had metastatic end-stage ovarian cancer; however, she was likely to die sooner from starvation than disease progression. The home nutrition support extended her life expectancy and improved her quality of life.
The development of parenteral nutrition (PN) contraindicated a long-held belief that nutritional administration entirely through the veins was impossible, impractical, or unaffordable. The ability to supply nutrients to patients lacking a functional GI tract ultimately saved lives that would have otherwise been lost to malnutrition.
Early PN formulas consisted of dextrose and protein hydrolysates of either casein or fibrin, which were later replaced with crystalline amino acids. Intravenous lipid infusions were not available until the 1970s. In the 1980s, IV lipid emulsions became a source of calories. At the same time, the FDA approved total parenteral nutrition (TPN), nutrient admixtures of fat emulsions combined with other nutrients in one mixture. Today, PN is a complex mixture of up to 40 different chemicals or nutrient components. As with any complex formulation, stability and compatibility problems can occur. Improper compounding or contamination can result in harm or even death. Complications of PN include venous catheter infections, hepatobiliary disease, and glucose disorders. Complications can be minimized through careful patient selection. This article addresses the nutritional merits of PN and its use in oncology.
ENTERAL VS PARENTERAL NUTRITION
Specialized nutrition support (SNS) is available in two forms: parenteral nutrition and enteral nutrition. Both forms are used to prevent malnutrition in patients otherwise unable to satisfy estimated nutritional requirements via the oral route.
Patients at risk for malnutrition who are candidates for SNS experience an involuntary weight loss of more than 10% over a 2- to 3-month period, weigh less than 75% of his or her ideal or usual weight, and laboratory test results indicate prealbumin of less than 10 mg/dL, or have a history of inadequate oral intake for more than 7 days.
Enteral nutrition provides requisite nutrients to patients who have a functioning GI tract but cannot ingest nutrients orally. Enteral nutrition requires inserting a feeding tube directly to the GI tract to provide liquid nutrition via pump, bolus, or gravity feeding. It is recommended for patients in whom access to the GI tract does not cause trauma.
Parenteral nutrition provides requisite nutrients to patients intravenously, thereby bypassing a nonfunctional GI tract. The PN formulation provides energy, fluid, and various medications via peripheral or central venous access. PN is recommended for patients who may become or are malnourished and are not candidates for enteral nutrition. Parenteral nutrition should not be used routinely in patients with an intact GI tract. PN is associated with more infectious complications, does not preserve GI tract function, and is more expensive than enteral nutrition.
INDICATIONS FOR PARENTERAL NUTRITION
American Society of Parenteral and Enteral Nutrition (ASPEN) guidelines suggest that patients who cannot, should not, or will not eat enough to maintain adequate nutritional status and have the potential to become malnourished are appropriate candidates for PN.2 These patients have failed enteral nutrition trials with postpyloric tube placement. PN is also indicated for patients with short bowel syndrome, particularly if less than 150 cm of small bowel remains after surgery and GI fistula except when enteral access can be placed distal to the fistula or volume output is less than 200 mL/day. Critically ill patients who cannot receive enteral nutrition and nothing-by-mouth status will last for more than 4 to 5 days are candidates for PN. It is also initiated in cancer patients with treatment-related symptoms that affect oral intake (eg, mucositis, stomatitis, esophagitis) if the symptoms last for more than 7 days (Table 1). Parenteral nutrition is not well-tolerated in cases of severe hyperglycemia, azotemia, encephalopathy, hyperosmolarity, and severe electrolyte and fluid imbalance, and it should be withheld until improvement is observed.
Carbohydrates are the primary source of energy for the human body. The brain and neural tissues, erythrocytes, leukocytes, the lens of the eyes, and the renal medulla either require glucose or use it preferentially. The base of all PN solutions is carbohydrates, most commonly dextrose monohydrate. Dextrose provides 3.4 kcal/kg and is available in concentrations from 5% to 70%, with higher concentrations used primarily for patients on fluid restrictions.
Protein is necessary to maintain cell structure, tissue repair, immune defense, and skeletal muscle mass. Protein is provided in the form of crystalline amino acids in concentration ranging from 3% to 20%. Amino acids provide 4 kcal/kg.
Amino acid solutions are usually a physiologic mixture of both essential and nonessential amino acids. Disease-specific amino acid solutions are available and are primarily used for renal and hepatic disease. Patients with declining kidney function who are not yet candidates for dialysis are at risk for urea nitrogen accumulation when infused with nonessential amino acids. These patients receive only essential amino acids. Patients with severe hepatic encephalopathy may benefit from branch-chain amino acids (BCAAs). BCAAs are oxidized primarily in the muscle, rather than the liver, preserving hepatic metabolic pathways in case of liver failure. In general, disease-specific amino acid solutions offer an incomplete amino acid profile and should not be used for more than 2 weeks.
Lipids in oil-in-water emulsion concentrations ranging from 10% to 30% provide fats in PN. Lipid solutions currently available in the United States contain long-chain triglycerides (LCT) in the form of soybean or safflower oil, egg phospholipids as an emulsifier, water, and glycerol to create an isotonic solution.
Inclusion of lipids in IV nutrition prevents essential fatty acid (EFA) deficiency. Solutions that provide up to 4% of total calories from linoleic acid or 10% of total calories from safflower oil-based emulsions will meet daily EFA requirements. Patients who receive PN without lipids, usually those with an egg allergy, should be monitored for EFA deficiency. Excessive hair loss, poor wound healing, dry and scaly skin, and laboratory test results for a triene:tetraene ratio of more than 0.2 are indicators of EFA deficiency. In patients with egg phospholipid allergy, oil can be applied to the skin to prevent EFA deficiency. Recommended dosage is 2 to 3 mg/kg/d safflower seed oil for 12 weeks.