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A Critical Perspective on Trophic Feeding

Editor(s): Finkel, Yigael M.D., Ph.D.; Baker, , Robert D. Jr. M.D., Ph.D.; Rosenthal, Philip M.D.; Sherman, Philip M. M.D., F.R.C.P.C.; Sondheimer, Judith M. M.D.

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Journal of Pediatric Gastroenterology and Nutrition: March 2004 - Volume 38 - Issue 3 - p 237-238
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Trophic feeding is a concept viewed with an almost religious fervor in some nurseries, intensive care units and surgical wards. Indeed, the determination to give trophic feedings occasionally approaches fanaticism. Having just been told by a dietician that a neonate with a recent intestinal resection would experience rapid atrophy of his remaining 16 cm of small bowel if he didn't get immediate trophic feedings, I thought some perspective on this misunderstood concept was warranted.

The generally accepted definition of trophic feeding is a small volume of balanced enteral nutrition insufficient for the patient's nutritional needs but producing some positive gastrointestinal or systemic benefit. The volume of feeding considered trophic in most neonatal nurseries is 10–12 cc/Kg/d or 1cc/h. If more than 25% of the patient's nutritional needs are administered enterally, the feeding should no longer be considered trophic. The commonly identified benefits of trophic feeding in the intact intestine are maturation of neonatal intestinal digestive, absorptive, motor and immune function; improved neonatal feeding tolerance and eating behavior; maintenance of intestinal function during starvation and catabolic states; and prevention of intestinal bacterial overgrowth and bacterial translocation.

There is an extensive literature on the importance of luminal nutrition in promoting mucosal hypertrophy after intestinal resection. It may be semantic, but this kind of nutrition is not trophic either in volume or caloric content. Most animal experiments of post resection intestinal adaptation have used the maximum enteral feeding the animal can tolerate, generally more than 30% of nutritional needs. To date, no studies of post-resection intestinal adaptation in response to strictly defined trophic feedings have been performed. Part of the dietician's anxiety over the failure to institute enteral feedings quickly was her concern that there was a critical time beyond which intestinal adaptation would not occur. This is a misconception. The potential for hypertrophy of residual bowel in response to luminal nutrition is always there, ready to start up in response to luminal feedings even if they are delayed for months (or years?) after resection.

There are problems with the attractive concept of trophic feedings. First, the presumed benefits are poorly defined. For example, trophic feedings are said to promote intestinal immune function or intestinal maturation, both of which are incredibly complex processes. Animal and human studies on the role of trophic feedings in promoting these complex functions are inadequate to isolate a unique contribution of trophic feedings. Second, the catabolic impact of starvation on the organism and on the gastrointestinal tract is often not considered in the selection of controls in such studies. If the negative impact of withholding trophic feedings from the intestine is to be isolated from the catabolic impact of undernutrition or the absence of an essential luminal nutrient, then adequate nutrition by the parenteral route must be part of any human or animal study.

Animal Studies

Pythons eat huge meals and then fast for long periods during which intestinal villous atrophy develops. Histologic abnormalities, mucosal mass and mucosal nutrient transport all improve rapidly in the python when small, balanced, nutritionally inadequate feedings are given enterally, but not when glucose, lipid, bile or saline alone are given (Secor SM et al. Am J Physiol Gastrointest Liver Physiol 2002;283:G1298). In piglets, who experience very modest mucosal atrophy with fasting, it requires the enteral administration of at least 40% of the daily nutritional to produce any increase in villous height in the jejunum and 60% of daily needs to produce mucosal proliferation in the ileum (Basu R, et al. Am J Clin Nutr 2000;71:1603) This suggests that mucosal atrophy is a reflection of general undernutrition and not a result of the absence of trophic feedings since it is only reversed by a large enteral intake. In enterally fasted puppies nourished by total parenteral nutrition (TPN), it likewise takes an enteral feeding of at least 30% of daily nutritional needs to produce mucosal growth above that of controls. There does appear to be a more rapid development of mature motor activity in the stomach and upper small bowel of puppies receiving trophic feedings plus TPN than is observed in pups on TPN alone (Owens L et al. J Nutr 2002;132:2717).

Some claim that trophic feedings will prevent cholestasis or other liver injury associated with parenteral nutrition. The mechanisms for this benefit are said to be the prevention of bacterial overgrowth, bacterial translocation and enterotoxin absorption or the augmentation of intra and extrahepatic biliary excretion via positive impacts on mucosal integrity, motor function and hormone release. The animal data to support these assumptions is weak. One study in adult rats receiving TPN for 7 days showed that there was more glutathione in the liver of animals who received “targeted” trophic feedings of alanine when compared to animals receiving saline. Hepatic sensitivity to exogenously administered endotoxin was less in the animals who received alanine (Dzakovic A et al. J Pediatr Surg 2003;38:844). Alanine would not fit most people's definition of trophic feeding. It is more an essential precursor. The appropriate control would be an animal receiving extra alanine by vein. There is very little information about the impact of trophic feedings on biliary flow and gall bladder function.

I conclude from animal studies that intestinal mucosal atrophy may accompany enteral fasting in some species with (pups, rats and piglets) or without (pythons) adequate IV nutrition and that feeding a mixed meal of significant caloric magnitude stimulates mucosal growth and function. There does not appear to be any impact of feedings providing less than 30% of daily nutritional needs except in the area of neonatal gastroduodenal motility.

Human Studies

Does mucosal atrophy actually occur in humans from whom enteral nutrition is withheld with or without IV nutritional support? Alpers reports that there at most a 10% decrease in the adult bowel wall thickness during catabolic states in the intensive care setting (Alpers DH. Curr Opin Clin Nutr Metab Care 2002;5:697). According to Alpers, reversal of this modest atrophy with trophic feedings has not been documented. Alpers feels, after a review of the adult ICU literature, that mucosal atrophy is simply a manifestation of a catabolic state as is muscle wasting and fat store depletion, which can be prevented by adequate IV nutrition with no unique contribution from trophic feeding.

In the 1980s several good studies evaluated trophic feedings in premature neonates. The primary objective was to see whether early small enteral feedings increased the incidence of necrotizing enterocolitis. Most studies confirmed that they did not. The unexpected result of these studies was that babies given adequate IV nutrition plus balanced minimal enteral feedings progressed faster to full enteral nutrition. Feeding behavior and tolerance were better and babies were discharged from the hospital faster than those not receiving minimal enteral feedings. In one study, hospital discharge was 22 days earlier than controls. Peak direct bilirubin was lower in premature neonates receiving trophic feedings (.7mg/dL vs 2.5mg/dL) and fewer days of phototherapy were required for indirect hyperbilirubinemia (6.8days vs 9.5 days) as well (Dunn L et al. J Pediatr 1988; 112:622–9). Voluntary energy intake was better in babies receiving early minimal enteral feedings even briefly, a result attributed to overall better feeding behavior. One study found that the weight of premature neonates who had received only 7 days of trophic feeding was 225g over birth weight at 30 days of age while the body weight of those receiving no trophic feedings was only 95g above birth weight. The average caloric intake of these babies was identical for the 30 days. Somatomedin levels were the same in the two groups, suggesting that maturation of hormone secretion was not the cause of better growth (Troche B et al. Biol Neonate 1995;67:172–81). The authors wondered whether efficiency of absorption was better in the neonates who got trophic feedings thus increasing their actual calorie intake. As in puppies, the use of minimal enteral nutrition in neonates is associated with an earlier appearance of a mature antro-duodenal motility pattern. Saline perfused controls have not been studied, so the impact of volume as opposed to luminal nutrient cannot be assessed (Berseth CL et al. Pediatrics 2003;111:529).

Trophic feedings are said to promote maturation of intestinal absorptive function, but hard data are scanty. One study has shown indirectly that absorption of leucine is better in preterms receiving trophic feedings (Saenz de Pipaon M et al. Ped Res 2003;53:281). There are very few other studies that have assessed the impact of minimal enteral nutrition on any aspect of digestive or absorptive function.

The claims for improved immunity in infants and adults receiving trophic feedings are weak, because of the complexity of the process and the inadequate scope of the outcome measures used. In one study of infants on TPN, bactericidal activity of neutrophils against coagulase positive staph and release of TNFα was better after 7 days of trophic feedings but neither function approached the level of enterally fed controls. The incidence of septic events in infants with and without trophic feedings is the same (Ocada Y et al. J Pediatr Surg 1998; 33:16). There are no studies evaluating intestinal responses to infectious agents, the development of food allergy or the nature of the intestinal immune function in infants receiving trophic feedings.

The Cochrane group reviewed the human literature on trophic feedings (defined as less than 25 calories /Kg for more than 5 days). They agreed that total hospital stay, days to achieve full enteral nutrition and days feedings were withheld because of intolerance were fewer in neonates who received trophic feedings. In all other clinical studies, they concluded that methodologic problems prevented the conclusion that trophic feedings had any other benefits and that enteral fasting until the child was ready for “real feedings” was still an appropriate clinical approach (Tyson JE et al. Cochrane Database Syst Rev 2: CD 000504,2000).

It would facilitate management planning in many clinical situations if the confusion between the three concepts of luminal nutrition, specific luminal nutrients essential for enterocyte function and trophic feeding were clarified and if words like atrophy and hypertrophy were used with more precision. Most of the supposed benefits of trophic feedings still require confirmation by good clinical studies. These studies are doable. I submit that assessing intestinal absorptive function is tedious but possible. Assessing the biochemical and histologic evidence of liver injury should be easy. Evaluating histologic changes before and after trophic feedings is possible in carefully selected situations, for example by monitoring the biopsies of the easily accessible distal small intestine in infants with ileostomies. The measures of immune function must be more carefully selected since endpoints like infection rate are too insensitive to reveal possible differences. The challenge to pediatric gastroenterology is evaluate the unconfirmed benefits of trophic feeding before insisting on its use in fragile patients who might be better off fasting and supported by TPN until truly ready to feed.

© 2004 Lippincott Williams & Wilkins, Inc.