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July 2005 Better
Choices, Better Outcomes — Nutrition Support Update The right nutrition support can make a significant difference in quality of care, outcome of treatment, cost, length of hospital stay, and patient comfort. In the critically ill, it can influence morbidity and mortality. Choosing the type of nutrition support—enteral nutrition (EN) or parenteral nutrition (PN)—for the best patient outcome is not always easy or clear-cut since you cannot extrapolate from one type of patient or one disease state to another. In addition, it seems that new products and techniques emerge almost daily. In fact, we now speak of “specialized nutrition support” (SNS) to reflect the growing sophistication of the practice. The American Society for Enteral and Parenteral Nutrition (ASPEN) has established the following guidelines for the use of SNS:1 1. SNS should be used in patients who cannot meet their nutrient requirements by oral intake. 2. When SNS is required, EN should generally be used in preference to PN. 3. When SNS is indicated, PN should be used when the gastrointestinal (GI) tract is not functional or cannot be accessed and in patients who cannot be adequately nourished by oral diets or EN. 4. SNS should be initiated in patients with inadequate oral intake for seven to 14 days or in those patients in whom inadequate oral intake is expected over a seven- to 14-day period. We’ll explore what is known about SNS, discuss the pros and cons of EN vs. PN support, and provide guidance for their use. Let’s take a look at each type of nutrition support before we compare the two. Parenteral Nutrition Because PN is much more complex and expensive than EN therapies, its use must be closely monitored. Some of the conditions in which PN may be needed include massive small-bowel resection, small-bowel obstruction, enterocutaneous fistula, hyperemesis gravidarum, or in patients who have had major surgery, exhibit moderate stress caused by illness or injury, and cannot be fed through the GI tract for seven to 10 days. Patients who are unable to utilize their GI tracts over five to seven days and are also severely malnourished or catabolic should also be treated with PN, as it helps to alleviate nutrition depletion and aids in recovery.2 A VA study of 1,250 patients showed a 10% decrease in postoperative complications when severely malnourished patients were given TPN for seven to 10 days prior to surgery.3 The use of TPN should be limited to patients who truly require and would benefit from it. Well-nourished patients with minimal injury or stress, or those in the immediate postoperative period, seldom benefit from TPN. A functional GI tract is a contraindication, and TPN should not be used when the patient does not desire it or when the patient has a very poor prognosis. Access Central venous access can be attained via the subclavian, internal jugular, and femoral veins, via indwelling catheters. Peripherally inserted central (PICC) lines are more readily placed than the more invasive indwelling catheters. PICC lines are often used for the patient receiving TPN or intravenous antibiotics at home and increasingly while hospitalized. PICC lines are inserted in the arm and the catheter is fed into smaller peripheral veins to the superior vena cava or right atrium so central line concentrations can be used. PICC lines can be inserted by radiologists or trained nurses and, if cared for properly, can last up to two to three months. Because solutions with osmolality greater than 900 milliosmoles per deciliter require administration through a central line, the amount of nutrients provided in a peripheral vein is limited, unless the patient can tolerate large volumes of fluid. TPN administered through a central vessel (subclavian, internal, or external jugular veins) is usually more concentrated and can more easily provide adequate required nutrients. Complications A frequent complication of PN therapy associated with the critically ill patient is an alteration in glucose metabolism. Because of illness, the patient may be insulin-resistant or glucose-intolerant, and the introduction of a large dextrose load via TPN can exacerbate this problem. Hyperglycemia can be caused by overfeeding (excessive dextrose infusion) and is more likely to occur with diabetes, organ failure, and stress. It is believed that hyperglycemia may be the cause of increased infections in TPN-fed patients. Van den Berghe found decreased morbidity and mortality in mechanically ventilated TPN patients under tight glucose control—blood glucose levels maintained between 80 and 110 milligrams per deciliters with an insulin drip.4 Normally, blood sugar levels in TPN patients are maintained at 180 to 200 milligrams per deciliters, which in this study was associated with higher morbidity and mortality. Hyperlipidemia may occur when lipid emulsions are given to a patient with existing familial hyperlipidemia. Septic and critically ill patients may also develop difficulty with fat metabolism, resulting in an increase in serum triglyceride levels. If serum lipid levels are consistently high, more than 500 milligrams, lipid emulsions may need to be limited to every other day or once weekly, depending on the patient’s caloric needs and serum triglycerides level.5 Electrolyte imbalances may occur during TPN. The uptake of glucose into the cell occurs with the uptake of potassium into the cell, which may result in hypokalemia, common during refeeding and insulin therapy. Increased potassium losses may occur because of diarrhea, vomiting, and/or fistulas and as side effects of such drugs as steroids, potassium-wasting diuretics, and certain antibiotics. Adequate potassium levels can be maintained through supplementation. Malnourished patients are frequently at risk for the development of hypophosphatemia. This occurs during refeeding due to inadequate phosphorus administration (because of the role phosphorus plays in glycolysis and synthesis of new cells). Elevation of liver function tests may occur with some patients on TPN after one to two weeks of therapy. The increase may be a result of overfeeding or cholestasis. Generally, these levels return to normal once oral or enteral feedings are reinstituted, but they should be closely monitored to ensure that liver failure does not ensue. If liver function is severely altered and/or changes in the liver have occurred, TPN may need to be discontinued or reduced. With careful monitoring and the avoidance of overfeeding and hyperglycemia, TPN is an appropriate medical nutrition therapy for the patient with a nonfunctioning GI tract who is unable to eat. Enteral Nutrition “If the gut works, use it!” This is the mantra for nutrition support of hospitalized patients, as, over the years, we have come to realize the importance of the GI tract as a metabolic and immune organ participating in amino acid metabolism and the immune response. Maintaining the health and integrity of the GI tract can prevent complications and speed up the healing process. During normal and catabolic states, the gut (mainly the small intestine) works in conjunction with the liver and skeletal muscles in maintaining amino acid homeostasis. During severe stress following surgery, the metabolic role of the gut is even more important. The GI tract is a major immunologic organ, containing 70% to 80% of all immune-secreting cells. Twenty-five percent of the GI tract is lymphoid tissue, immunologically active. Since most of the micro-organisms that threaten the body enter via the mouth and nose, the GI tract is a main line of defense, protecting the internal environment of the body. Malnutrition adversely affects the GI tract—structurally, immunologically, and metabolically—and feeding the gut properly maintains its immunologic and metabolic functions. When determining who is a candidate for EN, the primary criteria used are the inability to ingest adequate nutrients by mouth and a GI tract that can be used safely and effectively. Indications and contraindications for EN support are as follows: Indications Contraindications Chronically ill patients can benefit from EN during a hospitalization. Many of these individuals have chronically poor intake. The added stress of an illness coupled with increased nutrient needs and no reserves to meet these increased needs results in a further decline in nutritional status and malnutrition. However, very few of these needy patients receive EN. Enteral feedings are contraindicated for the patient with bowel obstruction, intractable vomiting, severe diarrhea, some forms of GI bleeding, persistent aspiration, and problems with access that cannot be overcome.1,6 Contrary to what many think, postoperative ileus does not always prevent the use or tolerance of enteral feedings. Small bowel motility returns within four to six hours of surgery while gastric motility is resumed within 12 to 24 hours of surgery. Ileus in the colon can last as long as five days, but enteral feedings can still be accomplished.7 If a feeding tube is placed in the small intestine during surgery and feedings are begun shortly thereafter, it does not matter whether there is an ileus in the stomach. Benefits of Enteral Feedings When EN is not utilized, immune response lessens (decreased immunoglobulin A secretion), with a resultant increase in bacterial growth.8 Bacterial translocation may occur with gut villi atrophy and bacterial overgrowth. Glutamine, available in enteral feedings and supplemented in elemental feedings—and generally not available in TPN—appears to be preferentially utilized by the small intestine for fuel in the starved or stressed state.9 The presence of an energy source for the gut is important in preventing gut atrophy. The benefits of EN can be enhanced by starting feedings as early in the hospitalization as possible, as soon as the patient can tolerate it. The less time the GI tract is without nutrient stimulation the better, and there is less likelihood of gut atrophy and bacterial translocation. Another benefit of EN is the number of formulas available to patients, generally classified into four categories: intact nutrients, predigested or elemental, disease-specific, and modular. Most formulas contain adequate vitamin/mineral supplementation once calorie/protein requirements are met. Complications and Monitoring Diarrhea is invariably blamed on the tube feeding. However, diarrhea may also be caused by medications, including sorbitol-based medications, antibiotics, and certain antacids. Diarrhea may occur from contamination, a problem that should decrease with the use of closed systems, a method for enteral feedings in which the formula is provided in a sealed container or bottle that is spiked and hung for feeding without being opened. Other causes of diarrhea include hypoalbuminemia, lack of fiber, malabsorption with short bowel syndrome, ulcerative colitis, Crohn’s disease, and AIDS. Aspiration pneumonia is also a risk for the enterally fed patient, especially if the tube is placed into the stomach or upper portion of the duodenum; for this reason, tubes should be placed distal to the ligament of Treitz, if possible. Patients with a previous history of aspiration, head injury and decreased level of consciousness, depressed or absent cough or gag reflex, mechanical ventilation, and/or delayed gastric emptying are at increased risk for aspiration.10 Refeeding syndrome is another potential complication for the enterally fed patient, especially if he or she was quite malnourished or starved for a number of days. Start slowly with feeding to reduce risk of refeeding syndrome. Comparison of EN and PN Keep in mind that neither form of nutrition support is all good or bad. Studies have shown that patients meet their target nutrient goals more often with PN than EN. In addition, there are complications with EN such as high gastric residuals, increased risk of aspiration pneumonia, and colonization of the stomach with bacteria that limit its use.11 TPN appears to induce bacterial translocation (BT) while EN can as well, but to a much lesser degree. Lipman reviewed the relationship of EN to bacterial translocation and found that TPN, “oral” TPN solutions, and many forms of elemental diets induced or facilitated BT.12 He concludes that EN has not been proven to prevent BT in humans. Haskel has also shown that enteral or “liquid” diets induced BT in animals.13 In reviewing the studies that have shown increased septic complications with TPN over EN, Jeejeebhoy and MacFie conclude that the increase in septic complications was due to overfeeding dextrose, which led to hyperglycemia.14,15 In comparing studies of EN and PN when subjects were fed similar calories, there is no difference in septic complications.14 In addition, they believed there was no difference in bacterial translocation and gut atrophy between EN and PN, which is counter to the long-held belief that TPN and not EN causes bacterial translocation and gut atrophy. In a meta-analysis of EN compared with PN, Braunschweig found that there were decreased infectious complications in EN compared with PN, but that the number of nutrition support complications were higher in the enterally fed group.16 In studies where blood glucose levels were available, the TPN-fed patients had a significantly higher incidence of hyperglycemia. Woodcock has similar results to Braunschweig in a prospective study comparing EN with PN. He found no difference in septic morbidity between TPN and EN.17 There was a higher complication rate in EN, related to the delivery system and a higher incidence of inadequate intake. In critically ill patients, a review of the literature found that the use of EN compared with PN was associated with a significant decrease in infectious complications and cost.18 There were no differences in mortality rate, number of days on the ventilator, or length of stay. Jeejeebhoy, MacFie, and Braunschweig, with many researchers and clinicians, are beginning to question the long-held belief that EN is far superior to PN. We know that if a patient has a functioning gut, we should use EN. But if you can’t reach the nutrient requirements by EN alone, use the peripheral route. If the gut is not working, as long as the patient is not overfed, TPN will not increase septic morbidity.14,18,19 It’s interesting to note that of 106 U.S. academic medical centers, one-fourth to one-half used excessive glucose in TPN-fed patients.20 While the septic complication rate may be the same, there may be benefits of EN independent of bacterial translocation and related to the preservation of gut immune function and promotion of cellular growth. These benefits may translate into shorter hospital stays. Nutrients presented directly to the gut may stimulate the production of hormones such as bombesin and growth factors such as IGF-1 necessary for enterocyte metabolism and cellular growth.21,22 Feeding the gut early (within 12 to 24 hours of injury) may account for additional benefits of EN. By feeding early, the gut may not have a chance to atrophy and gut immunity can stay intact to prevent bacterial overgrowth and an influx of neutrophils that will undergo priming.12 Summary — Dale Ames Kline, MS, RD, CNSD, LD, is president of Nutrition Dimension, Inc. A former hospital chief clinical dietitian and nutrition educator in the WIC program, she has written and edited continuing education home study courses since 1984.
2. An increase in liver enzymes in a patient
on TPN can be a sign of which of the following? 3. Hyperglycemia is often a problem in the critically
ill TPN-fed patient for which of the following reasons? 4. Electrolyte imbalances occur during TPN. Which
of the following nutrients can fall to dangerously low levels if
refeeding syndrome occurs? 5. Which of the following patients meets the
criteria to use enteral nutrition (EN) support? 6. Which of the following is a contraindication
to EN? 7. A postoperative ileus always prevents the
use of EN. 8. EN can maintain a healthy gut. Which nutrient
does the gut use to maintain its structure and function and as a
source of energy? 9. Which of the following can cause diarrhea
in a tube-fed patient? 10. EN is preferable to parenteral nutrition
for which of the following reasons:
2. Skipper A. Parenteral nutrition. In: Shronts EP, Ed. Nutrition Support Dietetics. ASPEN, Rockville, Md., 1989. 3. Veterans Affairs Total Parenteral Nutrition Cooperative Study Group: Perioperative total parenteral nutrition in surgical patients. N Engl J Med. 1991;325:525-532. 4. Van de Berghe G, Wouters P, Weekers F, et al: Intensive insulin therapy in critically ill patients. N Engl J Med. 2001;344:1359. 5. Banks P. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 1997; 92:377-386. 6. Kudsk KA. Enteral vs. parenteral nutrition: advantages and disadvantages. J Crit Care Nutr. 1996;3(2):3-9. 7. Mueller CM. Enteral nutrition management: Gastroparesis, ileus, pseudo-obstruction, diarrhea. Current Issues in Enteral Nutrition Support, Report of the First Ross Enteral Device Conference. Columbus, Ohio. 1996; 55-58. 8. Border JR. Gut-origin septic states. The Gastrointestinal Response to Injury, Starvation, and Enteral Nutrition. Ross Laboratories, Columbus, Ohio. 1988. 9. Bell SJ, Pasulka SP and Blackburn GL. Enteral formulas. In: Skipper A, Ed. Dietitian’s Handbook of Enteral and Parenteral Nutrition. Aspen Publ., Rockville, Md: 1989. 10. Hamaoui E, Kodsi R. Complications of enteral feeding and their prevention. In: Rombeau J Rolandelli R, Eds. Clinical Nutrition, Enteral and Tube Feeding, 3rd ed. W.B. Saunders, Philadelphia: 1997. 11. Heyland DK, Dhaliwal R, Drover JW et al. Canadian Clinical Practice Guidelines for Nutrition Support in Mechanically Ventilated, Critically Ill Adult Patients. JPEN. 2003;27(5):355-373. 12. Lipman TO. Bacterial translocation and enteral nutrition in humans: an outsider looks in. JPEN. 1995;19(2):156. 13. Haskel Y, Udassin R, Freund HR, et al. Liquid enteral diets induce bacterial translocation by increasing cecal flora without changing intestinal motility. JPEN. 2001;25(2):60-64. 14. Jeejeebhoy KN. Total parenteral nutrition: Potion or poison? Am J Clin Nutr. 2001;74:160-163. 15. MacFie J. Enteral versus parenteral nutrition: The significance of bacterial translocation and gut-barrier function. Nutrition. 2000;16(7/8):606-611. 16. Braunschweig CL, Levy P, Sheean PM, et al. Enteral compared with parenteral nutrition: a meta-analysis. Am J Clin Nutr. 2001;74:534-542. 17. Woodcock NP, Zeigler D, Palmer MD, et al. Enteral versus parenteral nutrition: A pragmatic study. Nutrition. 2001;17:1-12. 18. Gramlich L, Kichian K, Pinilla J, et al. Does enteral nutrition compared to parenteral nutrition result in better outcomes in critically ill adult patients? A systematic review of the literature. Nutrition. 2004;20(10):843-849. 19. Bistrian BR. Update on total parenteral nutrition. Am J Clin Nutr. 2001;74:153-154. 20. Schloerb PR. TPN or intravenous food poisoning? Nutrition. 2001;17(7/8):680-681. 21. Haskel Y, Xu D, Lu Q, et al.: The modulatory role of gut hormones in elemental diet and intravenous total parenteral nutrition-induced bacterial translocation in rats. JPEN. 1994;18(2):159-166. 22. Chen K, Okuma T, Okamura K, et al. Insulin-like growth factor-I prevents gut atrophy and maintains intestinal integrity in septic rats. JPEN. 1995;19(2):119-124. |
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