Adult tube feeding formulas.
This independent study offering is designed for nurses and other health care professionals who care for and educate adult patients regarding tube feeding. The multiple choice examination that follows is designed to test your achievement of the following educational objectives. After studying this offering, you will be able to:
1. List the differences between the open and closed tube feeding delivery systems.
2. Categorize tube feeding products by their formula composition.
3. Describe characteristics of formulas designed for use in specific disease entities.
4. Apply knowledge of relevant factors when choosing a tube feeding administration schedule.
5. Identify the issues that affect reimbursement for home tube feedings.
Enteral tube feeding products come in a variety of forms and sizes, with at least 90 different types commercially available. Consequently, it can be overwhelming to the health care practitioner who needs to select or administer an appropriate product while keeping costs down. The purpose of this article is to familiarize the health care provider with the various enteral products, delivery systems, infusion schedules, starter regimens, and cost issues.
Depending on how a tube feeding product is packaged, infusion is via an "open" or "closed" delivery system.
Open delivery system. The open system utilizes either a large syringe or an open top container for tube feeding delivery. Products include flip-top cans, brick packs, or powder packages that require reconstitution with water. Clean technique should be used along with good hand washing to lessen significant bacterial contamination (Freedland, Roller, Wolfe, & Flynn, 1989). Maximum formula hang time is generally from 4 to 12 hours, depending on manufacturer guidelines. Medications, supplemental nutrients, and dyes may be added to the formula as long as they are compatible, dissolve readily, and are bacteria free. The addition of water to dilute tube feeding products is discouraged as this practice has been associated with increased abdominal distention (Freedland et al., 1989). This alteration in gastrointestinal function may be due to the increased risk of formula contamination when adding the water.
Closed delivery system. In the closed system, a container is prefilled with sterilized tube feeding product that is then spiked with tubing and attached to the enteral access device. The container usually contains at least one liter of product; formula hang time extends from 24 to 36 hours, as long as sterile technique is used. This method of delivery is generally used for continuous or cyclic feeding schedules. It may also be used for intermittent drip feedings as long as a pump is used to prevent an unintentional bolus infusion of product. Nothing should be added directly to the formula, unless a designated port is available for injections of sterile substances. Closed delivery systems cost more but this must be weighed against the benefits. Decreased formula contamination has been noted with the closed delivery system (Belknap Mickschl, Davidson, Flournoy, & Parker, 1990; Wagner, Elmore, & Knoll, 1994); however, this benefit may only hold true if medications and flushes are administered through a Y-port (Donius, 1993). Significant formula contamination is of clinical concern as it has been associated with diarrhea (Anderson, Norris, Godfrey, Avent, & Butterworth, 1984) and abdominal distention (Freedland et al., 1989). In addition, nursing time is saved with the closed delivery system due to the ease of delivery and the extended hang time (Wagner et al., 1994).
Tube feeding products are used as either the sole source of nutrition or as a supplement to inadequate oral intake. They generally are considered complete nutrition because they usually contain enough protein, carbohydrate, fat, vitamins, minerals, and trace elements to prevent deficiencies if total caloric need is met. Some disease-specific formulas may not be nutritionally complete. Certain medical disorders, such as renal and hepatic insufficiency, affect the metabolism and excretion of some nutrients or elements. Formulas designed to feed these patients are altered accordingly. Tube feeding products can be divided into generic categories, differentiated by the composition of the formula. Formula composition involves the percentage of protein/carbohydrate/fat calories, amounts of vitamins/minerals/ electrolytes, nutrient complexity, caloric density, osmolality, and special product features.
Percentage of Protein/Carbohydrate/Fat
Standard enteral products provide about 15% protein, 55% carbohydrate, and 30% fat calories. The protein content can range from 6% to 25% of the total calories. The lower protein formulas are intended for renal insufficiency and the higher protein formulas for burns and trauma. The carbohydrate content of formulas range about 30% in the pulmonary and diabetic type products to 82% in the elemental category. Fat, provided as essential fatty acids, make up at least 3% of the total calories in low-fat formulas, to prevent essential fatty acid deficiency. The higher fat formulas, promoted as either pulmonary or diabetic products, can provide up to 55% of the total calories as fat.
The volume of tube feeding product needed to meet the recommended daily allowance of vitamins and minerals ranges from about 950 mL to 1,900 mL per day. Formulas designed for renal or hepatic insufficiency tend to have a lowered amount of vitamins, minerals, and electrolytes due to the retention of these elements in the body.
Tube feeding products can be categorized according the complexity of the protein, carbohydrate, and fat ranging from complex to the simplest form.
1. Polymeric formulas. This is the most common of the formula categories and contains nutrients in the complex form, therefore requiring intact digestive and absorptive capabilities. The protein source is soy, casein whey, or lactalbumin; carbohydrate source is long-chain polysaccharides, starch, and some simple sugars; and the fat source is soy, vegetable oils, and some medium-chain triglycerides. These formulas are the least expensive and can be used by most people requiring tube feeding.
2. Peptide-based formulas. This category contains products with a protein source of mainly dipeptides and tripeptides and is considered semi-elemental or somewhat "predigested." These may be better absorbed with impaired absorptive capacity or hypoalbuminemia (Brinson & Kolts, 1988). Research has not, however, consistently shown a clinical benefit when these formulas are compared to polymeric formulas in hypoalbuminemic patients (Mowatt-Larrsen, Brown, Wojtysiak, & Kudsk, 1992).
3. Monomeric formulas. This product category is considered "truly elemental" and contains nutrients in their simplest forms. The protein is provided as individual amino acids, the carbohydrate as monosaccharides, and the fat content is very low. These formulas may be useful during periods of diminished digestive and absorptive capacity, pancreatitis, or chylothorax, but are not generally used on a chronic basis. Monomeric formulas have shown no benefit over polymeric formulas in patients fed early postoperatively (Ford, Hull, Jennings, & Andrassy, 1992).
The number of calories varies from 1.0 to 2.0 per mL of product. The more concentrated formulas are used in conditions that require fluid restriction such as fluid overload, renal insufficiency, syndrome of inappropriate antidiuretic hormone (SIADH), and congestive heart failure.
Osmolality of a solution represents the number of dissolved particles contained in the solution. The greater the number of particles, the higher the osmolality. If two feeding formulas of the same concentration are compared, the one with the smaller particle size will have the higher osmolality because there will be a greater number of particles present. Isotonic solutions have an osmolality close to that of body fluids -- 300 mOsm/L. One of the functions of the stomach and intestine is to maintain their contents at an osmolality of 300 mOsm/L; therefore the majority of the standard tube feeding products are isotonic. Elemental and concentrated formulas are more hypertonic due the increased number of particles present. Formulas can be diluted with water to decrease the osmolality. Hypertonic formulas at full strength can be given in both the stomach and small bowel but they should be initiated at low rates and advanced slowly while checking for gastrointestinal tolerance. Signs and symptoms of intolerance include abdominal cramping or distention, high feeding residuals, nausea, emesis, or diarrhea.
Special Product Features
In recent years, the evolution of formulas containing pharmacologic doses of some nutrients places tube feeding products beyond patient nourishment into the realm of disease prevention and treatment. Immunomodulary components are added to stimulate the immune response and increase wound healing. Nonsoluble and soluble fiber sources may be included to normalize bowel function and provide short-chain fatty acids to feed and maintain healthy colonocytes. Disease-specific products are available that provide nutrients tailored to treat or prevent nutritional and metabolic imbalances related to the disease entity. The following is a listing of some components added to enteral products and some of the disease-specific product categories along with the theories behind their use.
Using the traditional classification of Rose, glutamine is considered a nonessential amino acid (Lacey & Wilmore, 1990; Smith, 1990). It is synthesized by skeletal muscle, liver and lung, and it is the most abundant amino acid in the plasma (Smith, 1990; Souba, 1991). Nearly all mammalian cells utilize glutamine for energy and synthesis of purines, pyrimidines, Krebs' cycle intermediates, and the cellular antioxidant glutathione (Lacey & Wilmore, 1990). The gut, kidney, and immune cells seem to have the highest use of glutamine, though the amount of glutamine that the body, or specific organs, require is not known.
Glutamine, not glucose, is the primary fuel of the mucosal epithelial cells of the small bowel, particularly the villus and crypt cells of the jejunum (Windmueller, 1982). Work in primates showed that glutamine deficiency was associated with diarrhea, villous atrophy, mucosal ulcerations, and intestinal necrosis (Baskerville, Hambelton, & Benbough, 1980). A number of both animal and human studies have shown that glutamine-supplemented nutrition preserves gut morphology and function. Some studies have also indicated that oral glutamine protects the GI tract from damage caused by chemotherapy or radiation, while enhancing tumor kill (Fox et al., 1988; Klimberg et al., 1992; Klimberg, Souba, Dolson, et al., 1990; Klimberg, Souba, Salloum, et al., 1990).
Glutamine is also a significant fuel for immune cells, both as an energy source and for cell division (Ardawi & Newsholme, 1985). It is essential for phagocytosis and the secretion of interleukin-1 (IL-1) (Ogle et al., 1994; Wallace & Keast, 1992). In addition, glutamine can be used to form glutathione, an important cellular antioxidant (Hong, Rounds, Helton, Robinson, &Wilmore, 1992), and providing glutamine supplementation can improve glutathione levels in the gut (Harward, Coe, Souba, Klingman, & Seeger, 1994) and liver (Hong et al., 1992). Under metabolic stress, such as in sepsis, the body may need more glutamine than it can make, and a state of "glutamine deficiency" can develop, which can be lethal if severe (Baskerville et al., 1980; Roth et al., 1982). Therefore, any patient under conditions of metabolic stress may benefit from receiving glutamine. Doses of up to 0.5g/kg, or 30% of protein, have been suggested. There is no known toxicity to enteral glutamine.
The amount of glutamine in enteral nutrition products varies. Elemental and peptide-based products are likely to have less glutamine than formulas containing intact proteins, unless glutamine has specifically been added. When the individual amino acid ("free") glutamine is added to products, these products must come as a powder to avoid degradation of the glutamine in solution during storage. It is difficult to ascertain the amount of glutamine in most enteral products because product literature frequently reports a combination of "glutamine and glutamate nitrogen." They report this because while glutamate (glutamic acid) is quite soluble and stable, glutamine is relatively insoluble, heat labile, and unstable in solution (Hardy et al., 1993; Hornsby-Lewis et al., 1994; Lacey & Wilmore, 1990; Ziegler et al., 1990). With normal analytical techniques, most glutamine is degraded to glutamate. Hence, glutamate is easy to measure, but glutamine is not. But glutamine and glutamate are not the same amino acid, and they are not clinically equivalent, so knowledge of the nitrogen from the combination is of little use.
Arginine is classified as a nonessential amino acid. It can be synthesized by the body via a pathway that interacts very closely with the urea cycle enzymes. Arginine is used by all tissues for protein and nucleotide synthesis. It also has secretagogue activities on several endocrine glands; administration of arginine to humans results in increases in growth hormone, prolactin, insulin, glucagon (Barbul, 1986; Grant, 1994) and somatostatin (Daly, 1994; Grant, 1994). In growing or injured animals, arginine is primarily used for the synthesis of connective tissue, and arginine supplementation has improved wound healing and nitrogen retention in numerous animal (Barbul, 1986) and some human studies (Daly, 1994)
In conditions of metabolic stress, such as burns or abdominal sepsis, animals had increased survival on arginine supplemented diets, but only if the arginine is given prior to, or immediately at the time of insult (Grant, 1994). Not all studies demonstrate improved outcomes with arginine supplementation. In fact, some animal studies show significantly worse survival with higher doses of arginine (6% of nonprotein calories) given after sepsis had become established (Grant, 1994).
Arginine supplementation can decrease the thymic involution that occurs as part of the stress response in rodents, and increase the number of T-helper cells and T-cell mediated responses in animals and humans. In addition to improving immune response to recall antigens, many (but not all) animal studies have shown that arginine supplementation has an impact on cancer. Animals which received the supplement had improved survival or decreased cancer recurrence. The improvement in immune function may be due to increased macrophage and natural killer cell lysis of target cells. The increased cytotoxicity occurs by two mechanisms. One mechanism involves an increase in nitric oxide (NO) production; NO is one of the chemical substances released by immune cells to kill pathogens or tumor cells. Arginine also increases the production of interleukin-2 (IL-2) and IL-2 receptor activity; many immune responses depend on chemical signals such as IL-2 for immune responses to be elaborated (Daly, 1994; Grant, 1994). Thus, arginine may become a "conditionally-essential" amino acid after injury, in that arginine supplementation can improve nitrogen balance, wound healing, and immune function. Arginine is generally considered to have low toxicity, with humans tolerating oral doses up to 60 g/day, without untoward effects. However, severe hyperkalemia and hypophosphatemia can occur if arginine is given during severe alkalosis, or in patients with renal or hepatic insufficiency (Barbul, 1986). Since immune function maybe "upregulated," arginine may not be appropriate for patients who are purposely immunosuppressed, such as transplant recipients or those with autoimmune diseases. However, for patients at high risk of sepsis or those with cancer, arginine supplementation at 15-30 g/day is recommended (Grant, 1994). Animal data suggests that the timing and dosage of arginine are important, as a toxic effect may be seen at higher doses or if the supplement is given after sepsis is established.
Omega 3 Fatty Acids
Dietary fat is primarily composed of triglycerides and can also contain free fatty acids. A triglyceride molecule is three fatty acids esterified to a glycerol backbone. Fatty acids (FA) are straight hydrocarbon chains with a carboxyl group at one end and a methyl group at the other end. Fatty acids can be classified by several of their properties, including the length of the hydrocarbon chain, and the number and location of double bonds. Short-chain FAs have chains of 2 to 4 carbons, medium-chain FAs are 6 to 10 carbons in length, and long-chain FAs are 12 to 24 carbons long; saturated FAs have no double bonds, mono-unsaturated FAs have one, and polyunsaturated fatty acids (PUFAs) have more than one double bond. The location of the first double bond from the methyl end is denoted by the W or omega nomenclature system, such that an omega-6 FA has the first double bond at the 6th carbon from the methyl end (Krause & Arlin, 1992; Sardesai, 1992).
Fat is required by the body for a variety of functions, and several fats are essential in the diet. Fatty acids form the phospholipid bilayer of cell membranes. In addition, metabolites from fatty acids form compounds (sterols, prostaglandins, thromboxanes, prostacyclins, leukotrines) which regulate functions as diverse as reproduction, cardiovascular tone, blood clotting, immune responses, and the function and integrity of cell membranes. The few cases of essential fatty acid (EFA) deficiency that have been reported in adults occurred only in patients on fat-free parenteral nutrition. The patients developed alopecia, brittle nails, desquamating dermatitis, and an increased susceptibility to infection (Gottschlich, Alexander, & Bower, 1990; Krause & Arlin, 1992; Sardesai, 1992). While fat is essential for health, a high-fat diet is immunosuppressive (Endres, De Caterina, Schmidt, & Kristensen, 1995; Krause & Arlin, 1992; Sardesai, 1992).
There are two essential fatty acids (EFAs): linoleic acid, an omega-6 FA, and alpha-linolenic acid, an omega-3 FA. The dietary requirements for these EFAs have not been determined, but the estimated needs are 1% to 10% of calories for linoleic acid, and 0.2% to 0.3% of calories for alpha-linolenic acid (Gottschlich, Alexander, & Bower, 1990; Krause & Arlin, 1992; Sardesai, 1992). Some vegetable oils (rapeseed [canola] and soybean) are good sources of both, but most oils contain few omega-3 fats, and coconut and palm oils are not good sources of either EFA (Krause & Arlin, 1992). Certain deep ocean or cold water fish, and the oils from these fish, are high in omega-3 FA.
Eicosapentanoic acid (EPA) and docohexaenoic acid (DHA) are omega-3 fatty acids derived from alpha-linolenic acid; these are also the primary omega-3 FAs in fish oils. Although humans can form EPA and DHA from alpha-linolenic acid, it is an inefficient process (Sardesai, 1992). Interest in supplementing these FA in enteral formulas stems from knowledge of the metabolic fate of different FAs.
Prostaglandins, prostacyclins, thromboxanes, and leukotrienes are formed from the FA in cell membranes. Since the American diet is typically high in omega-6 FA and low in omega-3 FA, cell membranes are high in omega-6, and therefore the prostaglandins, prostacyclins, and thromboxanes are typically derived from the omega-6 FAs. These metabolites, when derived from omega-6 FAs, are more immunosuppressive, more vasoconstrictive, and cause more platelet aggregation than the prostaglandins, prostacyclins, and thromboxanes formed from omega-3 FAs. The caveat is that leukotrienes from omega-6 FAs are more immunostimulatory then those from omega-3 FAs, so not all the metabolites from omega-6 FAs are immunosuppressive.
Thus, the theory is that patients with autoimmune diseases, or those at high risk for infection, should be given less omega-6 FAs and more omega-3 FAs because omega-6 FAs are more immunosuppressive than omega-3 FAs. Most of the research on omega-3 FA efficacy has been done with animals. A number of small clinical trials in humans have been done with doses of 1.0 to 6.0 g/day of omega-3 FAs, with study time frames of weeks to years. The studies have shown decreased disease progression in IgA nephropathy, lower rejection rates and increased graft survival in renal transplant, decreased subjective complaints and medication requirements in rheumatoid arthritis, and decreased disease activity and reduction or discontinuation of steroid use in patients with ulcerative colitis (Endres et al., 1995). One study in AIDS patients showed improved weight gain in stable patients who added fish oil to their diets compared to those who did not (Hellerstein et al., 1996). However, omega-3 FA supplementation showed no benefit in patients with lupus nephritis, Crohn's disease, psoriasis, or atopic dermatitis (Endres et al., 1995). There have been no trials in critically ill humans in which the only variable was the amount of omega-3 FAs.
Fiber-containing formulas currently available on the market vary significantly in their fiber content. Depending upon which product is chosen, they may provide anywhere from 6 to 15 grams of fiber per liter. Fiber sources used include soy polysaccharide, oat fiber, partially hydrolyzed guar gum, and fruit and vegetable fiber as is found in blendarized formulas, with the most common being soy polysaccharide.
Dietary fiber is typically classified as either soluble or insoluble. Soluble fibers include pectins, gums, and mucilages. They slow gastric emptying, blunt postprandial glucose curves (Homann, Kemen, Fuessenich, Senkal, & Zumtobel, 1994; Spiller, 1994), and are rapidly fermented in the colon to form short-chain fatty acids (SCFA) (Lampe, Effertz, Larson, & Slavin, 1992; Spiller, 1994). SCFAs in turn, promote increased sodium and water absorption in the colon, thereby decreasing diarrhea (Homann et al., 1994; Lampe et al., 1992; Levine & Rosenthal, 1991; Roediger, 1994). Because soluble fibers are quickly fermented, they loose water-holding capacity and have little effect on fecal weight. Therefore, they have minimal effect on fecal transit time, rendering them poor therapy for constipation (Lampe et al., 1992).
Unfortunately, when soluble fibers are added to tube feeding formulas, they significantly increase the viscosity and therefore the potential risk for clogging feeding tubes (Homann et al., 1994; Lampe et al., 1992; Spiller, 1994). In response to this problem, modified guar gum was developed. It is 100% soluble, but has none of the gel-forming properties of native guar gum and can therefore be successfully added to tube feeding formulas. In addition to being highly fermentable with subsequent SCFA production, modified guar gum can significantly slow colonic transit time, resulting in a decreased incidence of diarrhea (Lampe et al., 1992). Although fiber-containing formulas have the potential to significantly decrease the incidence of diarrhea in tube-fed patients, it should be pointed out that the etiology of diarrhea is often not the tube feeding. Other causes are medications, infection, hypoalbuminemia, and/or multi-organ failure (Zarling, Edison, Berger, Leya, & DeMeo, 1994).
Insoluble fibers include celluloses, hemicelluloses, and lignins (Homann et al., 1994; Spiller, 1994). Unlike soluble fibers, these fibers have varying degrees of resistance to digestion and fermentation (Spiller, 1994) and, as a whole, are considered to be significantly less fermentable than soluble fibers. However, because insoluble fibers contain at least small amounts of soluble fiber, they can exhibit some of the properties inherent to soluble fibers (Deitch, 1994). Because insoluble fiber is less fermentable, it retains its water-holding capacity, or "bulking property," and is therefore an appropriate therapy for constipation. In addition, it is the bulk-forming properties attributed to insoluble fiber that have been implicated in stimulating gut trophic hormones responsible for maintaining enterocyte integrity and balance among intestinal microflora, thereby contributing to the prevention of bacterial translocation from the GI tract (Deitch, 1994; Spaeth, Specian, Berg, & Deitch, 1990).
Soy polysaccharide, the fiber source most commonly added to tube feeding products, is classified as an insoluble fiber, containing only 6% soluble fiber (Kapadia, Raimundo, Grimble, Aimer, & Silk, 1995; Lampe et al., 1992). Unlike other insoluble fibers it is highly fermentable and therefore exhibits the properties of soluble as well as insoluble fiber. Because of its fermentability it is not an effective treatment for constipation.
"Diabetic" tube feeding products were designed on the theory that carbohydrates, especially simple carbohydrates such as sucrose, make blood sugar control more difficult. Despite the fact that the American Diabetes Association's only diet recommendations are that fat comprise [is less than or equal to] 30% of calories, enteral supplements have been designed to be low in carbohydrates with [is greater than] 30% of calories as fat. Other hallmarks of these products are alterations in the type of carbohydrate and fat in the formulas. Fructose may be substituted for sucrose, even though there is no advantage of other nutritive sweeteners (fructose or sorbitol) over sucrose. These products frequently contain fiber of various types, which is fine, although the effects of fiber on blood sugar control are not well defined. Some diabetic products have a high proportion of the fat as mono-unsaturated fats. This is acceptable, as diets high in mono-unsaturates can reduce triglyceride levels in some individuals.
The commercial use of diabetic products is based primarily on the work of Peters and Davidson (1989), and several other studies, published only in abstract form. When a diabetic enteral product was first designed it was tested in type I diabetics. The patients sipped the product over 4 hours to simulate tube feeding. The product initially showed a significant improvement in blood sugar control compared to other enteral formulas. However, these same authors were unable to reproduce their own results, and 2 years later published a report stating that their initial findings may have been a statistical aberration (Peters & Davidson, 1991).
An abstract by Harley, Pohl, and Isaac (1989) used the same protocol that was used by Peters and Davidson (1989) in their study of type I diabetics, only Harley et al. used ten otherwise healthy, obese, type II diabetics (noninsulin requiring) as subjects. The authors found that blood sugar rose higher when patients consumed Ensure HN than when they consumed the diabetic product (205 mg/dL vs. 162 mg/dL, p [is less than] 0.03; no range or standard deviation given).
Galkowski, Silverstone, Brod, and, Isaac (1989) compared glycemic responses of five nursing home residents with type 11 diabetes given snacks of solid food, Ensure HN, or a diabetic product. All snacks increased blood glucose levels. Blood sugars after either solid food or the diabetic product were on average 195 mg/dL, but ranged from 108 to 280 mg/dL; after Ensure HN, blood sugars averaged 243 mg/dL, and ranged from 180 to 291 mg/dL. When one considers that a normal postprandial blood sugar is 110 to 150 mg/dL, it is obvious that the diabetic enteral product alone did not satisfactorily control blood sugar in most of these patients.
A small study by Grahm, Harrington, and Isaac (1989) concluded that a diabetic product was superior in preventing a rise in blood sugar after acute head injury when compared to an elemental formula. However, several issues make this work difficult to interpret. First, the "control" was an elemental product which was inappropriate in this patient population. In addition, the authors claim that there was a significant difference in blood sugars, and that those on the diabetic product did not require insulin, while those on the elemental product did. But other than the fact that both groups of patients were hyperglycemic prior to the initiation of tube feedings, no blood sugar results are actually reported.
In summary, diabetic enteral products cannot replace oral hypoglycemic agents, insulin, and blood glucose monitoring. Stable patients with very mild glucose intolerance are probably the only ones who would benefit from these products. However, there is a great deal of variability in patients' blood glucose responses, so this type of product may be worth trying if the patient has mild glucose intolerance on standard enteral products.
The theory for the development of these products is based in biochemistry. It involves how much carbon dioxide is produced compared to the oxygen consumed when different substrates are used for energy in the body. This is called the respiratory quotient (RQ). Using only fat as a fuel source produces the least [CO.sub.2] for the oxygen consumed, and has the lowest RQ (0.7); pure protein has a RQ of 0.8, and utilizing pure carbohydrate (CHO) produces the most [CO.sub.2], with a RQ of 1.0. However, the body typically utilizes a mixture of all fuel types, which produces a RQ of about 0.85 to 0.9. Feeding an excessive amount of calories results in lipogenesis, which uses the most oxygen, produces the most [CO.sub.2] and results in a RQ [is greater than] 1.0. In people with normal respiratory mechanisms, the amount of [CO.sub.2] produced is inconsequential, because their bodies will compensate automatically by altering their breathing. However, a belief developed that patients with lung conditions such as emphysema or bronchitis, or those requiring mechanical ventilation, would benefit from a low-carbohydrate, high-fat tube feeding to reduce [P.sub.a][CO.sub.2].
Much of the original "supporting evidence" for providing lower carbohydrate feedings to pulmonary patients were case reports of high [p.sub.a][CO.sub.2], respiratory distress, or inability to wean from mechanical ventilation when patients received very high caloric loads (50-80 Kcal/kg, or 2-4 times the resting energy needs), most or all of which was in the form of intravenous dextrose (in one case, nearly 4,000 Kcal/day was given as dextrose) (Askanazi, Elwyn, Silverberg, Rosenbaum, & Kinney, 1980; Covelli, Black, Olsen, & Beckman, 1981).
A commonly cited study is one by Angelillo et al. (1985). This group studied 14 ambulatory patients with COPD. Patients were fed three liquid diets at a caloric level of resting energy expenditure x 1.3, with varying compositions: 28% CHO/55% fat, 53% CHO/30% fat, and 74% CHO/9.4% fat. Each patient received each diet for 5 days, and diets were given in random order. All of the diet regimens resulted in [CO.sub.2] production less than baseline and all patients lost weight. Baseline [p.sub.a][CO.sub.2] was 49 torr; [p.sub.a][CO.sub.2] on the various diets ranged from 47.5 torr to 49.2 torr, which the authors stated was statistically significant. Even if these changes in [p.sub.a][CO.sub.2] are statistically significant, it is doubtful that they would be clinically significant.
Talpers, Romberger, Bunce, and Pingleton (1992) studied ten clinically stable, mechanically ventilated ICU patients on parenteral nutrition. The first study used three different substrate mixes: 40% CHO/40% fat, 60% CHO/20% fat, and 75% CHO/5% fat. All regimens provided calories at basal energy needs x 1.3. The authors found no difference in [P.sub.a][CO.sub.2] or [P.sub.a][O.sub.2] between regimens. They then studied ten more similar ventilated ICU patients on parenteral nutrition with 60% CHO/20% fat, but altered the total caloric loads. Calories were given at basal energy expenditure (BEE), BEE x 1.5, and BEE x 2.0, in random order. All feedings raised [CO.sub.2] production compared to fasting levels; feeding at BEE x 2.0 raised [CO.sub.2] production significantly more than feeding at either of the lower calorie levels.
One study suggests that [O.sub.2] consumption is higher for ambulatory COPD patients on a higher carbohydrate regimen when the patients are bolus fed one-third of their daily caloric requirement; blood gas values were not given (Kuo, Shiao, & Lee, 1993). Since other studies have not shown an effect of formula composition on blood gases, perhaps the lesson here is not to bolus large amounts of any formulas into the pulmonary compromised patient.
In summary, studies show no significant advantage to a high-fat feeding for patients with pulmonary compromise when caloric load is not excessive. Higher carbohydrate loads may increase [CO.sub.2] production, but the patients studied to date, whether normal controls, injured ICU patients, or patients with pulmonary compromise, increased minute ventilation to compensate for the increased [CO.sub.2] production; and blood gases were not significantly affected. Only overfeeding (regardless of formula composition) affects [p.sub.a][CO.sub.2] and [P.sub.a][O.sub.2]. Disadvantages to high-fat diets include immune suppression and gastrointestinal side effects such as abdominal discomfort and diarrhea (Kuo et al., 1993). The high-fat diet should not routinely be prescribed for all patients with pulmonary compromise, but may be worth trying in a select few who are malnourished and have extremely limited capacity to increase minute ventilation.
Renal Failure Formulas
Enteral formulas designed for use in patients with renal failure vary in composition. All are calorie dense (they provide 2.0 calories per mL of formula), thus enabling patients calorie needs to be met with relatively small volumes of formula. Some of these formulas are low in protein while others supply a more moderate protein load. Vitamin, mineral, and electrolyte content varies significantly among formulas. In deciding which formula to use, it is necessary to define the specific needs of the population being treated. Those with nondialyzed chronic renal failure (CRF) will have different needs than those undergoing maintenance dialysis. Patients with acute renal failure (ARE;) are yet another population with special needs.
Nutritional and metabolic consequences of CRF include: altered protein metabolism with resultant azotemia and/or uremia; decreased ability to excrete a large salt load or to conserve salt when dietary sodium is restricted; decreased ability to excrete water, potassium, magnesium and phosphate; decreased intestinal absorption of calcium and possibly iron; increased risk for vitamins B6, C, D, and folic acid deficiency; and increased accumulation of aluminum and glucose intolerance (Kopple, 1994). If a patient is maintained without dialysis, a diet low in protein (0.55-0.6 gm/kg/day with 50%-70% of this as high biological value protein) is recommended. A low-protein diet can improve uremic symptoms and slow the progression of CRF (Kopple, 1994; Lamberto, Rugiu, & Maschio, 1994). When protein is provided in such minimal amounts, adequate calories must be provided to prevent nitrogen wasting (Lamberto et al., 1994). In this instance, a low-protein formula with reduced quantities of those electrolytes known to be poorly disposed of would be appropriate. Once a patient is placed on dialysis, protein intake can be liberalized to 1.0 to 1.2 gm/kg/day for hemodialysis (HD) patients and 1.2 to 1.5 gm/kg/day for peritoneal dialysis (PD) patients. Protein is lost into the dialysate of both forms of dialysis, but more so into that of PD (Kopple, 1994). Once protein intake is liberalized, it is appropriate to switch to a more moderate protein-containing formula. Once on dialysis these patients typically tolerate more liberal amounts of electrolytes as well. Fluid status should be assessed on an individual basis and restricted or supplemented as needed.
Acute renal failure (ARF) is characterized by the same metabolic and protein derangements as CRF, with the added element of calorie/protein malnutrition associated with the underlying disease that precipitated the ARF (trauma, surgery, sepsis). They are hypermetabolic with increased calorie and protein needs in the setting of decreased tolerance to fluid and protein. These patients tend to have increased serum levels of phosphate, sulfate, magnesium, and potassium resulting from release of these elements from damaged tissue and decreased ability to excrete them. Edema, hyponatremia, and metabolic acidosis are also typical (Freund, 1987). The appropriate tube feeding formula in this situation is one that will provide adequate calories to blunt urea synthesis and partially blunt protein catabolism. A mixture of essential amino acids (EAA) and nonessential amino acids (NEAA) is preferred as it is more effective in promoting protein synthesis (Lamberto et al., 1994). These patients are often volume restricted as well.
The use of EAA vs. a mixture of EAA and NEAA is controversial. The theoretical basis for an exclusively EAA feeding is based on the premise that EAA decrease urea production and enhance recycling of the abundant urea nitrogen present for use in the synthesis of NEAA (Freund, 1987). This is not, in fact, what happens. Recent studies have shown that nitrogen derived from urea does not support nitrogen balance. It is simply recycled for further urea synthesis. NEAA may, in fact, be a superior source of nonspecific nitrogen needed for protein synthesis. Both EAA and NEAA are of equal importance in renal failure (Freund, 1987). Early studies with providing EAA as sole protein source showed positive results in terms of decreased BUN levels, decreased endogenous protein catabolism, decreased dialysis requirement, and decreased duration of ARF. Recent studies have failed to confirm a significant advantage to the use of EAA vs. a mixture of EAA and NEAA (Freund, 1987; Matarese, 1994).
Dialysis, whether it be HD or PD, can lead to vitamin deficiencies. Some of the water-soluble vitamins, particularly vitamins C and B6 and folic acid, are lost in the dialysate. Whether or not thiamin is cleared by dialysis is controversial. Fat-soluble vitamins are not cleared by dialysis (Work, 1993). The renal formulas on the market vary in vitamin and mineral content. Therefore, it is prudent to be aware of the product's precise vitamin and mineral content.
Hepatic Failure Formulas
The number of tube feeding formulas on the market specifically designed for patients with hepatic failure is limited. Those that are available differ dramatically in composition. Therefore, it is important to understand the nutritional ramifications of hepatic failure in order to choose the most appropriate one.
Muscle wasting is common in this population due to decreased intake and utilization of calories and protein (Kondrup, Nielsen, & Hamberg, 1992). The capacity of the liver to store postprandial glucose and fat is decreased. The ability of the liver to produce glucose from glycogen is diminished as well. Consequently, glucose production from gluconeogenesis is increased, resulting in an increased daily protein requirement. The liver's capacity to store protein is not hindered (Kondrup et al., 1992); however, the patient's ability to meet this increased protein need is often due to decreased appetite and/or the concern on the part of caregivers that high-protein intake will lead to hepatic encephalopathy.
Much work has been done using branched chain amino acids (BCAA) for treating or preventing hepatic encephalopathy. Unfortunately the results are controversial. Hepatic failure leads to decreased metabolism of the aromatic amino acids (AAA) and failure to detoxify ammonia. This then leads to increased serum levels of both AAA and ammonia with a concomitant decrease in serum BCAA and subsequent increased potential for new onset or worsening of already present hepatic encephalopathy. Early studies advocated the use of BCAA-enriched formulas for treating or preventing hepatic encephalopathy.
It is important to keep in mind that these formulas are BCAA enriched, not pure BCAA. More recent studies have been unable to confirm that BCAA-enriched formulas are of benefit in treating hepatic encephalopathy (Kondrup et al., 1992) with the exception of one meta-analysis indicating that BCAA-enriched TPN was beneficial and had significant effect on recovery from hepatic encephalopathy (Naylor, O'Rouke, Detsky, & Baker, 1989). Although the usefulness of treating hepatic encephalopathy with BCAA is questionable, there is some evidence which indicates that the use of BCAA may improve nitrogen balance and enhance protein synthesis in peripheral tissue (Chin, Shepard, & Thomas, 1992)
A reduction in bile acid production as well as reduction in the bile salt pool size also accompanies hepatic failure. This leads to impaired fat absorption and impaired fat-soluble vitamin absorption (Kondrup et al., 1992). For this reason, formulas that provide part of the fat as medium-chain triglycerides (MCTs), which do not require bile for absorption, may be preferable. The supplementation of fat-soluble vitamins is of variable benefit (Kondrup et al., 1992). Vitamin content beyond that required to meet the RDA should not be a strong priority when choosing a hepatic failure formula (Kondrup et al., 1992)
Patients with liver cirrhosis are prone to electrolyte depletion resulting from vomiting, diarrhea, and inadequate food intake. They are particularly at risk for potassium depletion as a result of the above plus losses from the use of potassium wasting diuretics and the inability to replete potassium stores as a consequence of hyperaldosteronism, commonly seen in cirrhotics. One study even suggests a correlation between low potassium levels and increased ammonia levels (Zavagli, Ricci, & Bader, 1993).
It should be kept in mind that BCAA-enriched formulas are significantly more expensive than standard tube feeding formulas. For this reason, they are typically reserved for those patients who have failed conventional amino acid therapy.
Immune-enhancing formulas currently available on the market can be divided into two categories. First, those that are specifically designed for use with HIV/AIDS patients and second, those that are designed for critically ill ICU patients who are immunosuppressed as a normal sequelae of their underlying disease.
Weight loss is a significant component of the clinical syndrome in HIV-infected patients. These patients can also present with depleted serum albumin levels, multiple GI symptoms such as nausea, diarrhea, and pharyngitis, and decreased oral intake. Chlebowski et al. (1989) showed that nutritional status is strongly associated with survival in the AIDS population and that a decreased serum albumin level correlated with a decreased length of survival. This would appear to indicate that efforts should be made at maintaining adequate nutritional status, as much as possible, starting when a patient is first diagnosed with HIV.
A subsequent study by Chlebowski et al. (1993), compared the effectiveness of supplementing the oral diets of largely asymptomatic, early-stage HIV-infected patients with either a standard enteral supplement or a peptide-based enteral supplement enriched with omega 3 fatty acids, fiber, beta carotene, and increased levels of vitamins B6, B12, E, C, and folic acid. Calorie intake among the two groups was essentially the same with a net 21% increase in total calorie intake by both groups. In spite of isocaloric intake, the group receiving the enriched formula maintained their weight, while those receiving the standard enteral formula lost weight. Those receiving the supplemented formula also had fewer hospital admissions and fewer work days missed than those receiving the standard enteral formula. There were no differences noted in albumin levels, electrolyte levels, or onset of GI symptoms. Based on the results of the above study, it would appear that the enriched enteral supplement is superior to a standard enteral supplement when used early on in HIV-infected patients. Unfortunately we do not know its efficacy once a patient progresses to the later stages of HIV/AIDS and becomes more symptomatic.
Immune-enhancing formulas designed for use in critically ill ICU patients are enriched with omega 3 fatty acids, nucleotides, arginine, selenium, and vitamins E, C, and A ("Specialized enteral," 1993). Because nosocomial infections are a major concern in this patient population and significantly contribute to length of ICU stay as well as overall hospital stay, it is hoped that these formulas will decrease the incidence of such infections and thus decrease ICU and overall length of stay. A recent study by Bower et al. (1995) compared the use of one such formula with a common use formula in critically ill patients whose precipitating event was either trauma, operation, or new onset of infection that required ICU admission. Patients received a minimum of 60 cc/hr of either formula plus additional calories to meet their needs based on indirect calorimetry. The two formulas were not isonitrogenous and therefore neither were the feeding regimens of the two groups; however, this difference in nitrogen intake was considered not to be a factor in the overall results. Patients receiving the enriched formula had decreased length of both ICU as well as overall hospital stay, as well as decreased use of antibiotics. Based on their results, the authors concluded that the enriched formula decreased the probability of an infection that resulted from a high-illness severity score and had an indirect benefit of reducing the length of stay by decreasing the probability of such infections (Bower et al., 1995). It should be noted that patients in both studies were fed within 48 hours of their ICU-precipitating event. This would negate the notion that early feeding alone is responsible for these results. It should also be pointed out that these formulas are significantly more expensive than standard tube feeding formulas and should probably be reserved for patients in the ICU setting.
Individual modular supplements are commercially available and may be added to enteral products, increasing the concentration of certain nutrients without significantly increasing formula volume. Protein powders can be added to tube feeding products to increase the percentage of protein calories delivered. These protein modules contain either casein, whey, or soy to be added to polymeric formulas or hydrolyzed protein that is compatible with the peptide elemental products. Glucose polymers in both powder and liquid forms are available to increase the carbohydrate content of formulas. Fat can be added to formulas in the form of MCTs or essential fatty acids. Medium-chain triglycerides are readily absorbed into the portal vein to the liver for metabolism but don't contain essential fatty acids. A fat supplement derived from safflower oil, which contains essential fatty acids, may be added to tube feedings to prevent or treat essential fatty acid deficiency.
Tube Feeding Administration Schedules
Enteral tube feeding administration can be accomplished by one of several different feeding schedules.
Bolus feedings. The simplest method is by bolus delivery and uses either a large syringe or gravity feeding bag. A predetermined amount of formula is delivered over a relatively short period of time, usually over 15 to 20 minutes, several times per day. The enteral feeding device is flushed with water after each feeding. This method may be tolerated well in the healthy individual (Heitkemper, Martin, Hansen, Hanson, & Vanderburg, 1981) but slower rates are recommended for the patient who is at aspiration risk. An example of this method would be 480 mL of full-strength formula qid followed by a 100 mL water flush qid.
Intermittent drip feedings. In the intermittent drip feeding schedule, the formula is infused at a slower rate over a defined period of time, several times per day. The feeding is followed by a significant fasting period. A water flush is given after each feeding. Tube feeding orders following this schedule could read 480 mL of full-strength formula over 2 hours qid followed by a 100 mL water flush qid (Note: Many drip feedings are given over 30 to 60 minutes).
Cyclic feedings. Cycled continuous feedings are given continuously over a portion of the day. Administration is usually over the nighttime hours to free the patient of tubing during the daytime hours. This schedule may be used to help promote an appetite during the daytime hours but total caloric intake should be calculated to ensure that nutrition needs are being met. A feeding pump is recommended to regulate the delivery of the formula. The feeding schedule may be written as full-strength formula at 200 mL per hour over 10 hours preceded and followed by a 200 mL water flush.
Continuous feedings. Continuous tube feedings are the delivery of formula by a slow drip over a 24-hour period. Delivery rate is regulated by an enteral feeding pump and water flushes are given at intervals throughout the infusion to prevent tube clogging. The feeding prescription might read full-strength formula at 80 mL per hour around the clock with a 60 mL water flush every 4 hours.
Initiating tube feedings. Starter regimens for enteral feedings depend on the location of the enteral feeding device in the gastrointestinal tract, the patient's clinical status, and the length of time a patient has been NPO. Gastric feedings can be started at full strength and full volume if the patient is clinically stable, the gastrointestinal tract is functioning normally, and NPO status has not been prolonged (Keohane, Attrill, & Love, 1984; Rees, Keohane, & Grimble, 1986). Slower infusion rates are used for those patients who are: just beginning tube feedings after a prolonged NPO status, at risk for aspiration (Ciocon, Galindo-Ciocon, Tiessen, & Galindo, 1992), having diarrhea or abdominal upset (Ciocon et al., 1992; Hiebert, Brown, Anderson, Rodeheaver, & Edlich, 1981), or being fed via the small bowel. Even in these conditions, formulas do not require dilution and may be initiated at full strength (Zarling, Parmar, & Mobarhan, 1986). It may be prudent, however, to begin at a slow rate of 10 to 25 mL per hour and advance by 10 to 15 mL increments every 8 to 12 hours until goal rate is achieved. In our experience, even hypertonic formulas at full strength are well tolerated in the small bowel with this infusion schedule.
Tube feeding formula selection and reimbursement in the home setting. Product cost, disease state, and the method of delivery affect formula selection for the home setting. Reimbursement for formulas and enteral delivery systems vary according to patients' insurance and other resources. Generally, health maintenance organizations will only cover enteral feeding delivery systems and associated supplies. Coverage for an enteral feeding pump generally requires documentation of its necessity, such as small bowel access. Feeding formulas are usually not covered as they are considered substitutes for food. This can be problematic for a patient who has a chronic ailment, such as pancreatitis, and can only tolerate a specialized disease-specific product. These specialized formulas tend to be 2 to 5 times more expensive than standard polymeric products and are unaffordable by the general public. In this situation, patients often need to switch insurance plans to obtain adequate coverage. Currently (as of 7/96), Medicare will cover enteral tube feeding formulas and associated supplies as long as there is documentation of an anatomic or motility disorder that will interfere with oral intake for at least 3 months. This includes specialty products and tube feeding infusions that may not be the sole source of nutrition, as long as there is documentation of medical necessity. Each patient's insurance plan should be evaluated individually to determine coverage as regulations can change daily. It's important that practitioners involved in nutrition support document need for tube feedings, pumps, or specialty products and any efforts made to optimize nutrition by the oral route.
With the plethora of enteral tube feeding products available, health care practitioners should familiarize themselves with the product categories and the indications for use. Choices should be based on the documented value a product has for a given disease state, keeping in mind that specialty or elemental type products are significantly more expensive. If tube feeding products are begun at full strength with a progressive advancement at least every 8 to 12 hours, most patients should be able to achieve goal feedings in a couple of days. This will facilitate, in a timely manner, the goal of adequate enteral nutritional support and the potentially positive impact on patient outcome (Grahm, Zadrozny, & Harrington, 1989; Kudsk et al., 1992; Moore, Moore, & Jones, 1986).
Anderson, K.R., Norris, D.J., Godfrey, L.B., Avent, C.K., & Butterworth, C.E. (1984). Bacterial contamination of tube-feeding formulas. Journal of Parenteral and Enteral Nutrition, fl 673-678.
Angelillo, V.A., Sukhdarshan, B., Durfee, S., Dahl, J., Patterson, A.J., & O'Donohue, W.J. (1985). Effects of low and high carbohydrate feedings in ambulatory patients with chronic obstructive pulmonary disease and chronic hypercapnia. Annals of Internal Medicine, 103, 883-885.
Ardawi, M.S.M., & Newsholme, E.A. (1985). Glutamine metabolism in lymphocytes and its importance in the immune response. Essays in Biochemistry 21, 1-44.
Askanazi, J., Elwyn, D.H., Silverberg, P., Rosenbaum, S.H., & Kinney, J.M. (1980). Respiratory distress secondary to a high carbohydrate load: A case report. Surgery 87, 596-598.
Barbul, A. (1986). Arginine: Biochemistry, physiology, and therapeutic implications. Journal of Parenteral and Enteral Nutrition, 10(2), 227-238.
Baskerville, A., Hambleton, P., & Benbough, J.E. (1980). Pathologic features of glutaminase toxicity. British Journal of Exp Path, 61,132-138.
Belknap Mickschl, D., Davidson, L.J., Flournoy, D.J., & Parker, D.E. (1990). Contamination of enteral feedings and diarrhea in patients in intensive care units. Heart & Lung, 19, 362-370.
Bower, R.H., Cerra, F.B., Bershadsky, B., Lacari, N.J., Hoyt, D.B., Jensen, G.L., VanBuren, C.T., Rothkopf, M.M., Daly, J.M., & Adelsberg, B.R. (1995). Early enteral administration of a formula (Impact) supplemented with arginine, nucleotides, and fish oil in intensive care unit patients: Results of a multicenter, prospective, randomized, clinical trial. Critical Care Medicine, 23, 436-449.
Brinson, R.R., & Kolts, B.E. (1988). Diarrhea associated with severe hypoalbuminemia: A comparison of a peptide-based chemically defined diet and standard enteral alimentation. Critical Care Medicine, 16, 130-136.
Chin, S.E., Shepard, R.W., & Thomas, B.J. (1992). Nutritional support in children with end-stage liver disease: A randomized crossover trial of a branched-chain amino acid supplement. American Journal Clinical Nutrition, 56, 158-163.
Chlebowski, R.T, Beall, G., Grosvenor, M., Lillington, L., Weintraub, N., & Ambler, C. (1993). Long-term effects of early nutritional support with new enterotropic peptide-based formula vs. standard enteral formula in HIV-infected patients: Randomized prospective trial. Nutrition, 9, 507-512.
Chlebowski, R.T, Grosvenor, M.B., Bernhard, N.H., Morales, L.S., Bulcavage, L.M., Richards, E.W., Abbruzzese, B.C., McCamish, M.A., & Cope, F.O. (1989). Nutritional status, gastrointestinal dysfunction, and survival in patients with AIDS. American Journal of Gastroenterology 84(10), 1288-1293.
Ciocon, J.O. Galindo-Ciocon, D.J., Tiessen, C., & Galindo, D. (1992). Continuous compared with intermittent tube feeding in the elderly. Journal of Parenteral and Enteral Nutrition, 16, 525-528.
Covelli, H.D., Black, J.W., Olsen, M.S., & Beckman, J.F. (1981). Respiratory failure precipitated by high carbohydrate loads. Annals of Internal Medicine, 95, 579-581.
Daly, J.M. (1994). Specific nutrients and the immune response: From research to clinical practice. Journal of Critical Care Nutrition, 2(1), 24-29.
Deitch, E.A. (1994). Bacterial translocation: The influence of dietary variables. GUT (Supp.1), S23-S27.
Donius, M. (1993). Contamination of a prefilled ready-to-use enteral feeding system compared with a refillable bag. Journal of Parenteral and Enteral Nutrition, 17, 461-464.
Endres, S., De Caterina R. Schmidt E.B., & Kristensen, S.D. (1995). n-3 polyunsaturated fatty acids: Update 1995. European Journal of Clinical Investigation, 25, 629-638.
Ford, E.G., Hull, S.F., Jennings, L.M., Andrassy, R.J. (1992). Clinical comparison of tolerance to elemental or polymeric enteral feedings in the postoperative patient. Journal of the American College of Nutrition, 11(1), 11-16.
Fox, A.D., Kripke, S.A., DePaula, J., Berman, J.M., Settle, R.G., & Rombeau, J.L. (1988). Effect of glutamine supplemented enteral diet on methotrexate-induced enterocolitis. Journal of Parenteral and Enteral Nutrition, 12(4), 325-331.
Freedland, C.P., Roller, R.D., Wolfe, B.M., & Flynn, N.M. (1989). Microbial contamination of continuous drip feedings. Journal of Parenteral and Enteral Nutrition, 13,18-22.
Freund, H.R. (1987). Renal failure. In C. Lang (Ed.), Nutritional support in critical care (pp. 315-327). Rockville, MD: Aspen Publishers.
Galkowski, J., Silverstone, F.A., Brod, M., & Isaac, R.M. (1989). Use of a low carbohydrate with fiber enteral formula as a snack for elderly patients with type II diabetes, abstracted. Clinical Flesearch, 37, 89A.
Gottschlich, M., Alexander, J.W., & Bower, R.H. (1990). Enteral nutrition in patients with burns or trauma. In J.L. Rombeau & M.D. Caldwell (Eds.), Clinical nutrition: Enteral and tube feeding (2nd ed.) (pp. 312-317). Philadelphia: Saunders.
Grahm, T.W., Harrington, TR., & Isaac, R.M. (1989). Low carbohydrate (CHO) with fiber enteral formula impedes development of hyperglycemia in patients with acute head injury, abstracted. Clinical Research, 37,138A.
Grahm, T.W., Zadrozny, D.B., & Harrington, T (1989). The benefits of early jejunal hyperalimentation in the head-injured patient. Neurosurgery 25, 729-735.
Grant, J.P. (1994). Nutritional support in critically ill patients. Annals of Surgery 220(5), 610-616.
Hardy, G., Bevan, S.J., McElroy, B., Palmer, f, Griffiths, R.D., & Braidwood, C. (1993). Stability of glutamine in parenteral feeding solutions. Lancet, 342(8864), 186.
Harley, J.R., Pohl, S.L., & Isaac, R.M. (1989). Low carbohydrate with fiber versus high carbohydrate without fiber enteral formulas: Effect on blood glucose excursion in patients with type 11 diabetes. Clinical Research, 37(1), 141A.
Harward, T.R., Coe, D., Souba, W.W, Klingman, N., & Seeger. J.M. (1994). Glutamine preserves gut glutathione levels during intestinal ischemia/reperfusion. Journal of Surgical Research, 56(4), 351-355.
Heitkemper, M.E., Martin, D.L., Hansen, B.C., Hanson, R., & Vanderburg, V. (1981). Rate and volume of intermittent enteral feeding. Journal of Parenteral end Enteral Nutrition, 5, 125-129.
Hellerstein, M.K., Wu, K., McGrath, M., Faix, D., George, D., Shackleton, C.H.L., Horn, W., Hoh, R., & Neese, R.A. (1996). Effects of n-3 fatty acid supplementation in men with weight loss associated with acquired immune deficiency syndrome: Relation to indices of cytokine production. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology, 11(3), 258-270.
Hiebert, J.M., Brown, A., Anderson, R.G., Rodeheaver, G.T., & Edlich, R.F. (1981). Comparison of continuous vs intermittent tube feedings in adult burn patients. Journal of Parenteral and Enteral Nutrition, 5, 73-75.
Homann, H.H., Kemen, M., Fuessenich, C., Senkal, M., & Zumtobel, V. (1994). Reduction in diarrhea incidence by soluble fiber in patients receiving total or supplemental enteral nutrition. Journal of Parenteral and Enteral Nutrition, 18, 486-490.
Hong, R.W., Rounds, J.D., Helton, W.S., Robinson, M.K., & Wilmore, D.W. (1992). Glutamine preserves liver glutathione after lethal hepatic injury. Annals of Surgery, 215, 114-119.
Hornsby-Lewis, L., Shike, M., Brown, P., Klang, M., Peatlestone, D., & Brennan, M.F. (1994). L-glutamine supplementation in home total parenteral nutrition patients: Stability, safety, and effects on intestinal absorption. Journal of Parenteral and Enteral Nutrition, 18(3), 268-273.
Kapadia, S.A., Raimundo, A.H., Grimble, G.K., Aimer, P., & Siik, D.B.A. (1995). Influence of three different fiber-supplemented enteral diets on bowel function and short-chain fatty acid production. Journal of Parenteral and Enteral Nutrition, 19, 63-68.
Keohane, P.P., Attrill, H., & Love, M. (1984). Relationship between osmolality of diet and gastrointestinal side effects in enteral nutrition. British Medical Journal, 288, 678-680.
Klimberg, V.S., Pappas, A.A., Nwokedi, E., Jenson, J.C., Broadwater, J. R., Lang, N.P., & Westbrook, K.C. (1992). Effect of supplemental dietary glutamine on methotrexate concentrations in tumors. Archives of Surgery 127, 1317-1320.
Klimberg, V.S., Souba, W.W., Dolson, D.J., Salloum, R.M. Hautamaki, R.D., Plumey, D.A., Mendenhall, W.M., Boom, F.J., Kahn, S.R., Hackett, R.L., Bland, K.I., & Copeland, E.M. (1990). Prophylactic glutamine protects the intestinal mucosa from radiation injury. Cancer, 66, 62-68.
Klimberg, V.S., Souba, W.W., Salloum, R.M., Plumey, D.A., Cohen, F.S., Dolson, D.J. Bland, K.I., & Copeland E.M. (1990). Glutamine-enriched diets support muscle glutamine metabolism without stimulating tumor growth. Journal of Surgical Research, 48, 319-323.
Kondrup, J., Nielsen, K., & Hamberg, O. (1992). Nutritional therapy in patients with liver cirrhosis. European Journal of Clinical Nutrition, 46, 239-246.
Kopple, J.D. (1994). Nutrition, diet, and the kidney. In M.E. Shils, J.A. Olson, & M. Shike. Modem nutrition in health and disease (8th ed.) (pp. 1102-1134). Philadelphia: Lea and Febiger.
Krause, M.L., & Arlin, M. (1992). Lipids. In Krause's food, nutrition and diet therapy (8th ed.). Philadelphia: Saunders.
Kudsk, K.A., Croce, M.A., Fabian, T.C., Minard, G., Tolley, E.A., Poret, H.A., Kuhl, R., & Brown, R.O. (1992). Enteral vs parenteral feeding: Effects on septic morbidity following blunt and penetrating trauma. Annals of Surgery 215, 503-51 3.
Kuo, C.D., Shiao, G.M., & Lee, J.D. (1993). The effects of high fat and high carbohydrate loads on gas exchange and ventilation in COPD patients and normal subjects. Chest, 104,189-196.
Lacey, J.M., & Wilmore, D.W. (1990). Is glutamine a conditionally essential nutrient? Nutrition Review, 48(8), 297-309.
Lamberto, O., Rugiu, C., & Maschio, G. (1994). Nutrition and the kidney: How to manage patients with renal failure. Nutrition in Clinical Practice, 9(1), 3-10.
Lampe, J.W., Effertz, M.E., Larson, J.L., & Slavin, J.L. (1992). Gastrointestinal effects of modified guar gum and soy polysaccharide as part of an enteral formula diet. Journal of Parenteral and Enteral Nutrition, 16, 538-544.
Levine, G.M., & Rosenthal, J. (1991). Effects of fiber-containing liquid diets on colonic structure and function in the rat. Journal of Parenteral and Enteral Nutrition, 15, 526-529.
Matarese, L.E. (1994). Rationale and efficacy of specialized enteral nutrition. Nutrition in Clinical Practice, 9(2), 58-64.
Moore, F.A., Moore, E.E., & Jones, TN. (1986). Benefits of immediate jejunostomy feeding after major abdominal trauma: A prospective randomized study. Journal of Trauma, 26, 874-881.
Mowatt-Larrsen, C.A., Brown, R.O., Wojtysiak, S.L., & Kudsk, K.A. (1992). Comparison of tolerance and nutritional outcome between a peptide and a standard enteral formula in critically ill, hypoalbuminemic patients. Journal of Parenteral and Enteral Nutrition, 16, 20-24.
Naylor, C.D., O'Rouke, K., Detsky, A.S., & Baker, J.P. (1989). Parenteral nutrition with branched-chain amino acids in hepatic encephalopathy; a meta-analysis. Gastroenterology 97,1033-1042.
Ogle, C.K., Ogle, J.D., Mao, J.X., Simon, J., Noel J.G., Li, B.G., & Alexander, W. (199i). Effect of glutamine on phagocytosis and bacterial killing by normal and pediatric burn patient neutrophils. Journal of Parenteral and Enteral Nutrition, 18(2), 128-133.
Peters, A.L., & Davidson, M.B. (1989). Lack of glucose elevation after simulated tube feeding with a low-carbohydrate, high-fat enteral formula in patients with type I diabetes. American Journal of Medicine, 87,178-182.
Peters, A.L., & Davidson, M.B. (1991). Effects of various enteral feeding products on postprandial blood glucose response in patients with type I diabetes. Journal of Parenteral and Enteral Nutrition, 16, 69-74.
Rees, R.G.P., Keohane, RR, & Grimble, G.K. (1986). Elemental diet administered nasogastrically without starter regimens to patients with inflammatory bowel disease. Journal of Parenteral and Enteral Nutrition, 10, 258-262.
Roediger, W.E.W. (1994). Famine, fiber, fatty acids, and failed colonic absorption: Does fiber fermentation ameliorate diarrhea? Journal of Parenteral and Enteral Nutrition, 18, 4-8.
Roth, E., Funovics, J., Mulbacher, F., Schemper, M., Mauritz, W., Sporn, P., & Fritsch, A. (1982). Metabolic disorders in severe abdominal sepsis: Glutamine deficiency in skeletal muscle. Clinical Nutrition, 1, 25-41.
Sardesai, V.M. (1992). The essential fatty acids. Nutrition in Clinical Practice, 7(4), 179-186.
Smith, R.J. (1990). Glutamine metabolism and its physiologic importance. Journal of Parenteral and Enteral Nutrition, 14, 40S-44S. Souba, W.W. (1991). Glutamine: A key substrate for the splanchnic bed. Annual Review of Nutrition, 11, 285-308.
Spaeth, G., Specian, R.D., Berg, R.D., & Deitch, E.A. (1990). Bulk prevents bacterial translocation induced by the oral administration of total parenteral nutrition solution. Journal of Parenteral and Enteral Nutrition, 14, 442-447.
Specialized enteral feedings boost immune system. (1993, April, 2-3). Symposia Monitor.
Spiller, R.C. (1994). Pharmacology of dietary fibre. Pharmacology and Therapeutics, 62, 407-427.
Talpers, S.S., Romberger D.J., Bunce S.B., & Pingleton, S.K. (1992). Nutritionally associated increase in carbon dioxide production - excess total calories vs high proportion of carbohydrate. Chest, 102, 551-555.
Wagner, D.R., Elmore, M.F, & Knoll, D.M. (1994). Evaluation of "closed" vs "open" systems for the delivery of peptidebased enteral diets. Journal of Parenteral and Enteral Nutrition, 18, 453-457.
Wallace, C., & Keast, D. (1992). Glutamine and macrophage function. Metabolism, 41(9), 1016-1020.
Windmueller, H.G. (1982). Glutamine utilization by the small intestine in advances in enzymology 53.
Wolk, R. (1993). Micronutrition in dialysis. Nutrition in Clinical Practice, 8(6), 267-276.
Zarling, E.J., Edison, T, Berger, S., Leya, J., & DeMeo, M. (1994). Effect of dietary oat and soy fiber on bowel function and clinical tolerance in a tube feeding dependent population. Journal of the American College of Nutrition, 13(6), 565-568.
Zarling, E.J., Parmar, J.R., & Mobarhan, S. (1986). Effect of enteral formula infusion rate, osmolality, and chemical composition upon clinical tolerance and carbohydrate absorption in normal subjects. Journal of Parenteral and Enteral Nutrition, 10, 588-590.
Zavagli, G., Ricci, G., & Bader, G. (1993) The importance of the highest normokalemia in the treatment of early hepatic encephalopathy. Miner Electrolyte Metab, 19, 362-367.
Ziegler, T.R., Benfall, K., Smith, R.J., Young, L.S., Brown, E., Ferrari-Baliviera, E., Lowe, D.K., & Wilmore, D.W. (1990). Safety and metabolic effects of L-glutamine administration in humans. Journal of Parenteral and Enteral Nutrition, 14(4), 137S-146S.
Linda M. Lord, MS, RN,C, CNSN, is a Nurse Practitioner, Nutrition Support Service, University of Rochester Medical Center, Rochester, NY, and a Clinical Associatte, University of Rochester School of Nursing, Rochester, NY.
Joanna Lipp, MS, RD, CS, CNSD, CDE, is a Clinical Nutrition Specialist, Nutrition Support Service, University of Rochester Medical Center, Rochester, NY.
Sue Stull, RD, CNSD, is a Clinical Nutrition Specialist, Nutrition Support Service, University of Rochester Medical Center, Rochester, NY.
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|Title Annotation:||includes test and answer form for continuing education credit|
|Author:||Lord, Linda M.; Lipp, Joanna; Stull, Sue|
|Date:||Dec 1, 1996|
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