Enteral Nutrition

The preferred route for the nutritional support of a sick child is via the alimentary canal. Enteral alimentation provides the most acceptable and effective method for maintaining and repleting the nutritional state of pediatric patients who have functioning gastrointestinal tracts. In this chapter, we discuss the background necessary for implementing successful enteral nutrition therapy as well as the steps preceding the initiation of enteral feeding, an approach to the actual feeding, steps to establishing a successful feeding regimen at home, and finally an approach to discontinuing the feedings.


The subspecialty of pediatric gastroenterology encompasses the practical application of basic nutritional principles necessary to maintain normal nutrition and, when necessary, guide repletion of nutritionally compromised infants and children. To successfully make use of the material presented in this chapter, it is necessary to understand the basic principles of gastrointestinal physiology and pathophysiology. An understanding of the mechanisms of normal absorption and malabsorption provides the basis for providing useable nutrients to the sick patient with primary gastrointestinal disease. To care for the patient with metabolic disease, or a very sick patient with a complex illness, a basic understanding of intermediary metabolism is necessary.

The nutritional management of the sick child includes an assessment of the nutritional status of the patient ( Chapter 86 ) with the primary goal of preventing malnutrition. When malnutrition already exists, whether primarily involving disease of the gastrointestinal tract or secondary to nongastrointestinal causes, pediatric gastroenterologists work with the rest of the medical team to prescribe and establish an appropriate and safe nutritional regimen for the patient. The nutritional assessment and estimation of nutritional needs is a primary obligation of the nutritional support team. From this initial assessment, a determination is made as to whether the gastrointestinal tract can be used to supply part or all of the patient’s nutritional needs.

The use of special nutritional regimens as primary therapy for specific diseases such as Crohn’s disease is receiving new and important attention in the United States. In Canada and Western Europe, the use of enteral nutrition as primary therapy for Crohn’s disease is widely accepted. The mechanism by which the therapeutic effect is accomplished is unknown. It seems plausible that any therapeutic effect of enteral nutrition may be accomplished by influencing the composition of the gut microbiome. Whether an altered gut microbiome ultimately is shown to predictably and significantly affect immune-mediated processes, or directly or indirectly affect metabolic processes, remains to be proven. A discussion of enteral nutrition as specific treatment for any specific disease is beyond the scope of this chapter.

Generally, nutritional regimens may be administered via the enteral pathway, that is, through the gastrointestinal (alimentary) tract, or via the parenteral route, that is, intravenously. The enteral pathway is universally the preferred route, when clinically feasible. Patients who require nutritional support include those with primary gastrointestinal disease, the secondary gastrointestinal side effects of a nongastrointestinal primary disease, or patients who are unable to ingest adequate nutrition by the oral route. See Box 89-1 for a brief list of conditions for which enteral nutrition may be indicated. A general approach to initiation of enteral feeds is outlined in Table 89-1 . If the gastrointestinal tract is not capable of supplying the prescribed nutrition, then partial or total parenteral nutrition is required ( Chapter 88 ).

TABLE 89-1


No Malabsorption Comment
Normal caloric requirements
Normal baseline stool Use regular feeds; a “blenderized” normal diet is ideal.
Diarrhea at baseline

  • Evaluate for etiology of diarrhea.

  • If hydration in not an issue, then diarrhea by itself is not an absolute contraindication for enteral feeding.

Constipation at baseline

  • Evaluate for cause of constipation.

  • Consider stool cleanout and starting a fiber supplement/bulk laxative or polyethylene glycol 3350 to increase water in stool.

  • Comorbid constipation can contribute to feeding intolerance.

Mild to moderate increase in caloric requirements Increase volume of normal feeding as tolerated.
Mild to moderate increase in protein needs Increase volume of normal feeding as tolerated.
Major increase in caloric needs

  • 1.

    Increase volume as tolerated.

  • 2.

    Consider adding long-chain (nml) fat supplement.

  • 3.

    Consider increasing the concentration of the feed.

Major increase in protein needs Initially increase volume as tolerated.

  • 1.

    Be certain that there are enough calories to ensure optimal protein utilization.

  • 2.

    If adequate calories, consider adding extra protein to feeding.

Delayed gastric emptying and normal intestinal absorption

  • 1.

    Consider decreasing fat content.

  • 2.

    Consider adjusting osmolarity downward if high.

  • High osmolarity is most often a problem with amino acid–containing formula and/or flavored formula.

Malabsorption Present
Obstructive jaundice (fat malabsorption) Increase percentage of fat from medium-chain triglycerides gradually up to 85%.

  • Must monitor for essential fatty acid and fat-soluble vitamin (A, D, E, and K) deficiencies.

Pancreatic insufficiency (potential fat, protein, and rarely CHO malabsorption) Consider using pancreatic enzyme replacement for exocrine pancreatic insufficiency or:

  • 1.

    Protein hydrolysate.

  • 2.

    Increased ratio of MCT-to-LCT.

  • 3.

    For CHO malabsorption consider avoiding complex CHO, possibly using disaccharides instead.

  • Monitor for essential fatty acid and fat-soluble vitamins (A, D, E, and K) deficiencies.

  • Pancreatic enzyme replacement, depending on preparation, may require acid suppression.

  • Enzymes may clog tubes. Use porcine pancreatic enzymes through a G-tube only, may cause severe ulceration if introduced to jejunum.

Terminal ileal disease

  • 1.

    If longstanding, check vitamin B 12 level.

  • 2.

    Check cholesterol: lower levels c/w fat malabsorption secondary to bile salt loss, i.e., decreased enterohepatic circulation.

  • 3.

    Monitor vitamin B 12 levels and fat-soluble vitamins (A, D, E, and K).

  • 4.

    Increase nonfat calories; consider using high fat first thing in the morning after a fast, when bile salt pools are maximum; then decrease fat in later feeds.

  • 5.

    If bile salts are depleted—increase MCT in place of LCT.

Mild disease

  • 1.

    May not tolerate bolus feeding of any formula.

  • 2.

    Check for CHO malabsorption.

    • a.

      If not significant, increase volume to meet maintenance fluid requirements.

      • Continue to increase volume as tolerated, before considering an increase in formula concentration.

    • b.

      If CHO is significant, assess grams of CHO/unit of time administered and dilute formula—to level of tolerance.

Moderate disease

  • 1.

    Slowly advance formula as a continuous feed until maintenance fluid requirements are met.

  • 2.

    Transition to bolus feeding as tolerated.

  • 3.

    Consider TPN

Severe disease

  • 1.

    “Severe” implies that TPN is necessary for at least some of the patient’s calories for a clinically significant amount of time.

  • 2.

    The establishment of a minimal amount of enteral feeds is a critical baseline from which the slow, continuous feeds increase.

Metabolic Implications of Enteral Versus Parenteral Route

There is evidence that regardless of the type of patients, there are specific advantages if nutrition is delivered through the gastrointestinal tract as opposed to the parenteral route. The enteral pathway maintains and, when necessary, helps to return the integrity of the gastrointestinal mucosa (which parenteral nutrition does not do), and it is safer than the parenteral route. Studies after experimental intestinal resection have shown that the return of normal gastrointestinal function is related to intraluminal (i.e., alimentary tract) nutrition. Studies of laboratory animals that were given identical nutritionally complete supplementation either orally or through the parenteral route have shown that the mucosal weight of the gastrointestinal tract as well as the total protein and DNA content were all greater in the animals receiving enteral nutrition. The brush border enzymes, which are important in digestion, were also higher in those animals that were fed. It has been shown that exclusive parenteral nutrition results in decreased intestinal mucosal cell turnover and thereby a decreased height of the mucosal villi. The infusion of small amounts of nutrients intraluminally (often referred to as “trophic feeds”) to patients receiving otherwise total parenteral nutrition is generally considered an appropriate strategy to “protect/maintain” the integrity of the intestinal mucosa, if tolerated.

Steps Preceding Initiation of Enteral Feeding

Before choosing the correct “diet” for a patient, it is essential to perform a subjective as well as an objective nutritional assessment. This will inform the prescribing team as to whether they are dealing with an undernourished child or a currently well-nourished child, and at least as importantly, what the nutritional outlook is for the child in the coming days, weeks, months, and sometimes years.

Prescribing special feeding regimens or “diets” provides for flexibility in nutrient composition, caloric density, and osmolarity as well as taste. The correct terminology to apply to these specialized diets has been a source of confusion. The variety of commercially available diets started to significantly increase in the 1970s. In 1975, at a “Conference on Defined-Formula Diets for Medical Purposes” sponsored by the American Medical Association in Chicago, the term used to describe these special formulas was “Defined-Formula Diets.” Today they are often and inappropriately referred to as “elemental” diets. The term “Defined Formula” seems the most rational but has never gained widespread popularity. Regardless of the term used to describe these “specialized diets,” it is essential to prescribe a nutritional regimen that is appropriate for each individual patient’s specific medical need.

Initially, it is necessary to determine whether the nutritional status of the child will require special attention based on the clinical picture. An inpatient dietitian, when available, often completes the initial nutritional assessment. Under appropriate circumstances, this initial assessment can be performed in the outpatient setting. Although the dietitian generally is skilled in applying the latest objective measures, a completely adequate assessment should include subjective input from the medical team. For example, a child may be well nourished at the time of his/her initial encounter; however, it may be evident that impending surgery or chemotherapy will result in either a prolonged recuperation, loss of appetite, loss of digestive function, or some other indicator or predictor of certain malnutrition.

The next step is generally recognition of the need for special intervention to support the child’s nutrition. The key question then arises: can the child receive all or at least a substantial amount of nutrition via the gastrointestinal tract? Successful alimentation may be achieved using the oral route or via a nasogastric, nasojejunal, gastrostomy, or jejunostomy feeding tube ( Chapter 87 ). If a tube feeding is considered, then the complications associated with this treatment must be taken into account ( Table 89-2 ). The choice of the route depends on the primary medical problem and the clinical status of the child being supported. The risks vary depending on the age, neurologic status, state of debility, and specific medical condition. There is no adequate, high-quality evidence to accurately quantify most of the risks, so a more empiric approach is required. The actual risk–benefit relationship still needs to be decided on an individualized basis by the nutrition support team.

TABLE 89-2


Feeding Related

  • 1.

    Excessive rate of feeding (or slow gastric emptying)

  • 2.

    Severe gastroesophageal reflux

  • 3.

    Inability to handle secretions unrelated to tube feeding

Overhydration Especially with concurrent intravenous hydration/medication or intravenous feeding
Hyperglycemia Especially with concurrent corticosteroid administration
Azotemia Especially with high protein and or highly concentrated feeds (inadequate hydration)
Hypovitaminosis K Occurs with longstanding antibiotic use
Dehydration Secondary to diarrhea concentrated formula/lack of free water
Mineral/electrolyte disorders Especially with vomiting/diarrhea
Failure to gain weight Secondary to inadequate energy absorption (either from too little intake or too much loss, i.e., malabsorption)
Nutrient deficiencies Secondary to formula errors in manufacture or preparation
Diarrhea Requires review of gut function and feed contents

  • 1.

    Inappropriate feeding

  • 2.

    Excessive volume/time period

  • 3.

    Excessive osmolarity

  • 4.

    Infection (exclude Clostridium difficile )

  • 5.


  • 6.

    Constipation (paradoxical diarrhea)

Nausea/vomiting Requires review of all enteral intake including medications

  • 1.

    Excessive feeding concentration

    • Check contents, osmolarity

  • 2.

    Secondary to unrelated medications

  • 3.

    Excessive rate of infusion and/or slow gastric emptying

  • 4.


Mechanical Tube Related

  • 1.

    Incorrect tube placement

  • 2.

    Tube migration or dislodgement

Clogging Usually result of trying to instill medication or other dense/viscous solution without adequate dilution or flushing
Spontaneous perforation of viscus Rarely reported in patients with soft silicone or polyurethane tubes, well-known problem with polyvinyl chloride tubes left in place for more than a few days

Once a decision to employ a tube feeding is reached, another key question arises: for how long will the patient be unable to take adequate nutrition by mouth? The clinical state of the patient and nutrition assessment should be reconciled to provide a general estimate of this time period. If expected to be temporary (weeks to months), then the suggested route of feeding would be via a nasogastric tube. Longer-term support (months to years) requires consideration of a more permanent gastrostomy tube.

An Approach to Selecting the Type of Enteral Feeding

Special Formula Diets

The large number of specialized diets commercially available provides the clinical dietitian with a diverse number of alternative regimens from which to choose. Although the use of prepared formulas has many advantages, it is necessary to be careful and rigorous in assessing new as well as reassessing established commercial formulas. Products with which the team may have significant familiarity may undergo changes in their formulations without the patient or practitioner being made fully aware of the changes. It is therefore inappropriate to select a formula by “name”; instead, it is preferable to consider the pertinent components of the diet first. Then those components should be sought in a particular formula. As a rule, the least synthetic and least “predigested” or “elemental” formula that meets the patient’s expected nutritional needs will be the safest and best formula. This generic approach is much more rational and appropriate than considering brand name. With regard to selecting the generic formula, an assessment of the integrity of the patient’s gastrointestinal tract, which is part of a thorough nutritional assessment, should reveal the known or suspected absorptive defects or other problems that might impede normal nutrition. The assessment of the gastrointestinal tract includes an assessment of the adequacy of absorption of carbohydrates, fats, proteins, vitamins, and minerals, as well as consideration of the effect of damaged or nonfunctional bowel on specific nutrients. For general reference, a list of the commonly used formulas is provided in Table 89-3 .

TABLE 89-3


Premature Infant Formulas Term Infant Formulas Toddler Formulas Pediatric Formulas Adolescent/Adult Formulas
Milk-based, intact protein Milk-based, intact protein Milk-based, intact protein Milk-based, intact protein Milk-based, intact protein
Enfamil Premature 20 Cal Enfamil Newborn (birth to 3 months) Similac Go and Grow Milk Based (9-24 months) Boost Kid Essentials Jevity 1.0, 1.2 and 1.5
Enfamil Premature 24 Cal Enfamil Premium Infant Enfagrow Premium Toddler (9 months & up) Boost Kid Essentials 1.5 Osmolite 1.0, 1.2 and 1.5
Enfamil Premature 24 Cal High Protein Enfamil AR Boost Kid Essentials 1.5 with Fiber Promote
Enfamil Premature 30 Cal Similac Advance Carnation Breakfast Essentials Promote with Fiber
Enfamil EnfaCare (22 kcals/oz) Similac Advance Organic Partially Hydrolyzed Whey PediaSure Nutren 1.0, 1.5 and 2.0
Similac Expert Care NeoSure Similac for Spit–Up Gerber Graduates, Gentle (9-24 months) PediaSure Enteral 1.0 Nutren 1.0 with Fiber
Similac Special Care 20 with Iron Similac Sensitive (Reduced Lactose) Gerber Graduates, Protect (9-24 months) PediaSure with Fiber TwoCal HN
Similac Special Care 24 High Protein Similac Expert Care for Diarrhea Enfagrow Gentlease Toddler (9 months & up) PediaSure Enteral 1.0 with Fiber
Similac Special Care 24 with Iron Baby’s Only Organic (Dairy, Soy & LactoRelief) Enfagrow Premium Older Toddler Vanilla or Natural Milk Flavor (1 year & up) PediaSure SideKicks (0.63 kcal/ml) Peptide Based
Similac Special Care 30 with Iron PediaSure 1.5 Peptamen
Partially Hydrolyzed Whey Soy-protein Based PediaSure 1.5 with Fiber Peptamen with Prebio
Partially Hydrolyzed Whey Gerber Good Start Gentle Enfagrow Soy Toddler (9 months & up) Nutren Junior Peptamen 1.5
Gerber Good Start Premature 20 Gerber Good Start Protect Nutren Junior with Fiber Peptamen 1.5 with Fiber
Gerber Good Start Premature 24 Gerber Good Start Soothe Partially Hydrolyzed Soy Organic PediaSmart Dairy Peptamen 1.5
Gerber Good Start Premature 24 High Protein Enfamil Gentlease Gerber Graduates, Soy (9-24 months) Peptamen 1.5 with Prebio
Gerber Good Start Premature 30 Soy-protein Based Vital 1.0 and 1.5
Gerber Good Start Nourish (22 kcals/oz, postdischarge) Soy-protein based Casein Hydrolysate Bright Beginnings Pediatric Soy Drink
Enfamil ProSobee Nutramigen with Enflora LGG 2 Toddler (9-36 months) Organic PediaSmart Soy Amino-Acid Based
Gerber Good Start Soy Tolerex
Similac Soy Isomil Semi-Elemental Vivonex Plus
Pepdite Junior Vivonex RTF
Casein Hydrolysate Vivonex TEN
Nutramigen with Enflora 1 LGG Peptide Based
Pregestimil PediaSure Peptide 1.0 Blenderized
Similac Expert Care Alimentum PediaSure Peptide 1.5 Compleat
Peptamen Junior
Amino-Acid Based Peptamen Junior Fiber Specialized Formulas
EleCare for Infants Peptamen Junior with Prebio Glucerna (Diabetes)
Neocate Infant DHA/ARA
PurAmino Amino-Acid Based
EleCare Junior
Specialized Formulas Neocate Junior
Enfaport (Chylothorax, LCHAD Deficiency) Neocate Junior with Prebiotics
Similac PM 60/40 (Lower mineral intake) Vivonex Pediatric
Compleat Pediatric
Compleat Pediatric Reduced Calorie (0.6 kcal/mL)
Specialized Formulas
KetoCal 3:1 and 4:1 (ketogenic)
Portagen (fat malabsorption)
Suplena (kidney disease)
Nepro (kidney disease)

Product information is subject to change. Please check manufacturer product information for current composition and caloric value.

The variable contents from which the nutrition support team has to choose must be determined on a rational basis. Each advantage cited for any particular defined formula diet implies potential problems. For example, one problem that tends to limit nutrient density is osmolality. Our experience suggests that even the child without intrinsic gastrointestinal disease may begin to complain of gastrointestinal symptoms when the osmolality of the formula approaches 600 mOsm/L. This experience is consistent with that of investigators who have reported delayed gastric emptying when the osmolality of the duodenal contents is 560 mOsm/L.

In general, the specific therapeutic benefits of specialized formula diets are those that accrue from improved or good nutrition. As more data support special therapeutic effects of special enteral formula (as is occurring in Crohn’s disease), we should expect expanding claims of efficacy for many diseases, especially diseases of the gastrointestinal tract and diseases with gastrointestinal symptoms. Because of the general population’s interest in nutrition (and especially older patients and parents of sick children), it is incumbent on the nutritionally focused clinician to critically evaluate research and therapeutic claims. It will continue to be important to distinguish therapeutic benefits that derive from improved nutrition from those that directly affect the disease process.

Formulas can be designed with the physiology of the gastrointestinal tract in mind. For example, the protein content of the formula has been demonstrated to be directly proportional to its acid-secreting potential. Gastrin release itself is related to the presence of specific amino acids and small peptides. The administration of intragastric amino acids results in significant pancreatic stimulation, which can be minimized if the infusion is intrajejunal and at neutral pH. The decreased pancreatic output that results may be effective for the treatment of pancreatitis and high-output intestinal fistulas.

Other considerations regarding the fat and carbohydrate contents of the diets and routes of delivery may also be pertinent. Overall, it must be emphasized that the comparison of studies using different formulas under nonstandard conditions is usually not valid. It is evident that careful and critical evaluation of each apparently relevant report is essential to place it in its proper therapeutic role.

The use of commercially prepared formulas of a known composition facilitates the accurate measurement of nutrient intake. They are therefore of particular value in metabolic studies and in critical care situations, in which accurate intake measurements are necessary.

Because of the flexibility of these formulas, it is common to have constituents vary in relation to one another. Although most formulas are designed to provide for an apparently well-balanced nutritional regimen, many modulars can be added to change the balance and content of nutrients. The use of these additional modulars requires additional attention and monitoring. Munro has pointed out in a review of oral versus parenteral nutrient metabolism that major deviations that occur in parenterally nourished patients are often the result not of the route of delivery of the nutrient but rather of the unusual pattern of nutrients administered. The clear implication is that similar aberrations are to be expected through the injudicious use of the enteral pathway, as can be expected with total parenteral nutrition (TPN). Despite shortcomings of commercially available formulas for the child with special nutritional needs, they offer a standardized nutrient regimen that may be superior to complex prescriptions that require intense labor to create or to imaginative nonrigorously derived concoctions. In cases where modular additives are required to augment caloric density or protein content, specific attention should be paid to avoid possible mixing errors. Erroneously mixed formulas can result in hypocaloric or hyperosmotic products. Such errors represent the potential risk of feeding intolerance, metabolic derangements and, in rare cases, infectious complications due to poor sanitary conditions.

Principal Components of Specialized Formula Diets

Energy Requirements

In most clinical situations, energy requirements for children are estimated based on age. Actual energy requirements vary widely among healthy individuals and are even more variable in disease. For the healthy individual, most published charts report energy requirements from the guidelines provided by the National Academy of Sciences, National Research Council. Their published Dietary Reference Intakes (DRIs) for energy provides an “Estimated Energy Requirement” or “EER.” The EER is the average dietary energy intake that is predicted to maintain energy balance in a healthy adult of a defined age, gender, weight, height, and level of physical activity consistent with good health. In children and pregnant and lactating women, the EER is taken to include the needs associated with the deposition of tissues or the secretion of milk at rates consistent with good health. It is evident that these can only be rough estimates for healthy individuals and that for sick children they can at best be viewed as crude guesses of the energy requirement.

In the nutritionally stable, generally healthy child, the simple application of DRIs as a screening evaluation of caloric requirements may be sufficiently informative. They are not, and were never intended to be, an adequate tool for estimating the energy needs for sick or malnourished children, such as patients with the conditions listed in Box 89-1 .

Box 89-1

Indications for Enteral Nutrition

  • Chronic Illness:

    • FTT

    • Cancer

    • Liver Disease

      • Liver Failure

      • Cholestatic Liver Disease

      • Chronic Hepatitis

    • Renal failure

    • Congenital heart disease

    • Gastrointestinal Diseases

      • Short Bowel Syndrome

      • Gastrointestinal Fistula

      • Intractable Diarrhea (from any cause)

      • Liver Failure

      • Post Small Bowel Transplantation

      • Pancreatitis

      • Pancreatic Insufficiency (i.e., cystic fibrosis; CF)

      • Lymphangiectasia

      • Unexplained Malabsorption

      • Chronic Enteritis

  • Allergic Enteropathy

  • Autoimmune Enteropathy

    • Food Allergy

    • Intestinal Pseudo-obstruction

    • Inflammatory Bowel Disease

  • Specific Diseases:

  • IBD (Crohn’s Disease)

  • Metabolic Diseases

  • Special Situations:

    • Intensive Care Unit

      • Burns

      • Trauma

  • Anorexia

  • Anorexia Nervosa

  • As symptom of severe psychiatric illness

  • Chronic Immunodeficiency

  • Early Post-op Feedings

  • Renal Failure

  • Diagnostic Studies

  • Test Meals

  • Metabolic Challenge

  • Specific Metabolic Disease

  • Glycogen Storage Disease (as support)

    • Physically Unable to Eat

    • Neurologic Impairment

      • Dysfunctional Swallowing

  • Congenital/Acquired abnormalities of the upper gastrointestinal tract

  • Orofacial Dysplasias

  • Facial/Neck Trauma

  • Tumors obstructing enteral route

  • After surgical repair of oral/pharyngeal/esophageal/gastric pathway

When the determination of a sick patient’s energy requirement is crucial to medical management, it cannot be accurately determined by charts or “rule-of-thumb” calculations. Instead, after an informed target is set, adjustments will be necessary according to the response to feeding over time as measured by growth, weight change, other anthropometrics, various laboratory param­eters such as serum proteins, wound healing, and general sense of well-being. These adjustments will determine the success of the feeding regimen. Occasionally estimation of energy requirements is complicated by the presence of multiple processes occurring simultaneously, for example, when increased needs caused by infection complicate postoperative wound healing, or decreased needs result from inactivity or increased body fat. Extenuating circumstances such as these may warrant special assessment techniques such as indirect calorimetry. Indirect calorimetry may have a limited clinical roll in general, but may be particularly helpful in certain clinical situations. Nonetheless, the procedure needs to be performed under carefully controlled circumstances and interpreted with caution by experienced personnel. Even when appropriately performed, there are differing opinions about how to use and interpret the results. Activity and injury “factors” have been suggested for calculating the increase in energy expenditure with various types of injury in the patient population. Although these values have not been validated in the pediatric population, they have been used in the pediatric clinical setting to account for observed differences in energy needs during illness and stress.


Fat has the highest caloric density of the nutrients. The intake of fat is important because our experience suggests that for most pediatric patients the limiting nutrient is energy (or caloric) intake. Patients who have unusual losses of protein-rich fluid will require increased amounts of protein, but even in those patients, providing adequate energy intake will ultimately be most challenging. Triglycerides, composed of glycerol esterified to long-chain fatty acids, yield approximately 9 calories per gram when oxidized. They are, therefore, highly desirable nutrients for any nutritionally depleted patient. The major considerations with regard to choosing the amount or type of dietary fat include the following: (1) the use and absorption of long-chain triglycerides; (2) the use and absorption of synthetic medium-chain triglycerides; and (3) the requirements for essential fatty acids (all of which are long-chain fatty acids.)

Dietary fat consists predominantly of long-chain triglycerides. The process of digestion and absorption of long-chain triglycerides is reviewed in Chapter 31 on fat absorption. Briefly, within the lumen of the gastrointestinal tract, the long-chain fat must be emulsified and acted on by gastrointestinal (predominantly pancreatic) lipases. The lipases break down the triglyceride to free fatty acids and glycerol. Bile salts from the liver are necessary to form micelles to solubilize the free fatty acids for transport in the intestinal lumen to the brush border of the intestinal mucosa. Once within the enterocyte, fatty acids are re-esterified with glycerol to form a triglyceride again. With the addition of apolipoproteins, phospholipid, cholesterol ester, and cholesterol, chylomicrons are formed which are then released into the lymphatics. The lymphatics in turn empty into the thoracic duct and then the left subclavian vein.

From this brief description of the assimilation of long-chain fat, many of the pathologic processes that will require special attention from the nutrition team are evident. For example, pancreatic insufficiency results in decreased lipases; bile duct obstruction or hepatitis results in decreased bile flow to the intestine and thereby decreased micelle formation; gastrointestinal mucosal damage results in decreased surface area for absorption of fatty acids; metabolic derangements inhibit the formation of chylomicrons; and diseases or obstruction of the lymphatics inhibit the transport of lymph back into the circulation. All of these represent specific situations requiring special nutritional considerations. In some circumstances, it is acceptable to allow the increased fat malabsorption that results from increased fat intake to take advantage of the increased caloric density of the fat that does get absorbed. In other circumstances, long-chain fat must be largely excluded from the diet.

Medium-chain triglycerides are synthetic fats that contain a glycerol backbone esterified to fatty acids that are 8 to 10 carbons in length. Medium-chain triglycerides yield 8.3 calories per gram on oxidation and are therefore essentially as useful as long-chain fat from an energy point of view. Medium-chain triglycerides are hydrolyzed more rapidly than long-chain fats in the small intestine when pancreatic lipases are present and are then converted almost exclusively into free fatty acids and glycerol. If no pancreatic lipase is present, the medium-chain triglyceride can be found in the intestinal mucosa mainly as unhydrolyzed triglyceride. Thus, even in the absence of pancreatic lipase and bile salts, medium-chain triglycerides are transported intact through the intestinal lumen and through the brush border into the enterocyte. The unusual behavior of medium-chain triglyceride in the intestinal lumen and its absorption characteristics are due to the greater water solubility of medium-chain triglyceride and its products. The lower interfacial tension of the smaller triglyceride molecules with water facilitates its emulsification, so the formation of micelles is not necessary.

The exact mechanism and the rate-limiting step in the absorption of these different fats are unknown. The relatively high solubility of intact medium-chain triglycerides enhances their diffusion to the brush border of the healthy enterocyte. The triglyceride and the medium-chain free fatty acids are readily taken up into the enterocyte. Within the enterocyte, the triglyceride is acted on by intracellular lipases, and the resulting free fatty acids are released directly into the portal circulation, bypassing the lymphatic channels. The clinical indications for the use of medium-chain triglycerides are based on these characteristics. For example, patients with cholestatic liver disease and disrupted enterohepatic circulation often require a formula high in medium-chain triglycerides as they are otherwise unable to process and assimilate long-chain fats.

There are circumstances under which one, the other, or both types of fat become highly desirable as constituents of the prescribed diet. It has been demonstrated that the maximum absorption of long-chain fat is decreased when medium-chain triglycerides are added. The total amount of triglycerides absorbed when both are present, however, is greater than the maximum absorption of either alone. Absorption of medium-chain triglycerides from the rat cecum and the dog colon has been reported. The importance of this phenomenon and whether it has any implications for humans is unclear.

The true capacity of the gastrointestinal tract to absorb fat has not been precisely measured. It is generally accepted that the rate of fat absorption is proportional to the amount of fat ingested, and the more fat ingested the more absorbed.

If there are no specific defects in fat absorption demonstrated or anticipated, the fat of choice for a special formula diet is regular, long-chain (dietary) fat. The use of medium-chain triglycerides in patients who have intact mechanisms for the normal digestion of fat can lead to osmotic diarrhea resulting from the rapid lipolysis of the medium-chain triglycerides to glycerol (and medium-chain free fatty acids). This diarrhea may exacerbate the symptoms for which the formula was originally prescribed resulting in unforeseen iatrogenic consequences. In addition, there are a few patients who seem to have an unexplained or idiosyncratic reaction resulting in severe diarrhea when they ingest even a small amount of medium-chain triglycerides. A mixture of both medium-chain triglycerides and long-chain triglycerides may conceivably help patients who require increased calories. Ideally, fecal fat determination can be used as a guide to determine the optimal combination of medium-chain triglyceride, long-chain triglyceride, or both, to be given to the patient. In lieu of fecal fat determinations, careful clinical monitoring of nutritional repletion may suffice.

Essential fatty acids are all long-chain fatty acids and therefore absent in medium-chain triglycerides. Because the administration of medium-chain triglycerides may decrease the absorption of long-chain triglycerides, the addition of a small amount of linoleic acid to a medium-chain triglyceride formula may be insufficient to prevent essential fatty acid insufficiency. An adequate intake (AI) was established for essential fatty acids based on the median intake of healthy individuals. The AI for infants is based on the total fat from human milk until 6 months old and fat from human milk and complementary foods from 7 to 12 months of age. Clinicians must be cautious to guard against the development of essential fatty acid deficiency. If long-chain fat absorption is severely compromised, the parenteral administration of lipid emulsions containing essential fats must be considered.


Complex carbohydrates such as starch are initially broken down by salivary and pancreatic amylases. The contribution of the various amylases in health and disease to carbohydrate digestion remains a subject of study. Once carbohydrates are reduced to disaccharides, they are further hydrolyzed to individual monosaccharides by the brush border oligosaccharidases. The individual monosaccharides are then absorbed into the enterocytes via specific transport systems. There are four distinct brush border oligosaccharidases: maltase (glucoamylase); sucrase-isomaltase (sucrase α-dextrinase); and lactase. The fourth, trehalase (acts on the sugar trehalose, which is found only in young mushrooms and insects), is of little clinical significance.

Maltase (glucoamylase) is the most abundant oligosaccharidase in the gastrointestinal tract. Sucrase is present in intermediate amounts, and lactase, which splits lactose into glucose and galactose, is present in the least quantities.

All the disaccharidases may be expected to be depressed when there is mucosal disease of the small intestine. Lactase appears to be the most sensitive to injury and the last of the disaccharidases to recover full activity after mucosal damage. Because disaccharidases are present in older enterocytes, any process that causes rapid intestinal regeneration and repopulation of the intestinal villi with young cells (i.e., recovery from acute gastroenteritis) will represent a period of relative disaccharidase deficiency for the patient. In addition, inflammatory conditions such as celiac disease and small bowel Crohn’s disease can result in villous blunting/destruction. Starvation alone may be sufficient to lower disaccharidase activity, as it results in decreased cell turnover, mucosal hypotrophy, and therefore decreased surface area. It may therefore be important to transiently limit dietary sources of lactose in the malnourished child or in the child recuperating from gastrointestinal insult for a short period given the risk of developing secondary lactose intolerance. Restriction beyond a brief period necessary to demonstrate mucosal recovery is typically not warranted. Breath hydrogen testing (when clinically indicated) is a noninvasive method to determine the status of carbohydrate absorption (i.e., lactose, sucrose), so resumption of acceptable amounts of dietary carbohydrates is not delayed.

In selecting a carbohydrate for a special (defined) formula diet, it is important to note that the use of glucose significantly increases the osmotic concentration of a formula. A disaccharide will provide, on a gram basis, one-half the osmotic load of a monosaccharide. The use of synthetic glucose polymers may contribute as little as one fifth to the total osmotic load of a similar amount of glucose. Many specialized formula diets, therefore, use glucose polymers and long-chain starches as their carbohydrate source. The assimilation of these long-chain carbohydrates appears to proceed so that the osmolarity of the intestinal contents is not adversely affected. Although there is evidence that sucrose or fructose feedings may cause increases in the intestinal level of sucrase and maltase, no such dietary effect on lactase activity has ever been demonstrated.

It is important to document the existence of carbohydrate malabsorption when it is suspected and a formula change is contemplated. This may be done by testing for the presence of hydrogen in breath samples or by searching for reducing substances in fresh stool. If the patient’s formula contains a nonreducing sugar (i.e., sucrose), it must first be hydrolyzed or the stool may be misleadingly reported as not having reducing substances present. Generally, if carbohydrate fermentation products are present in the stool of an infant with diarrhea, the stool has an acidic pH and it seems to “burn” the infant’s diaper area regardless of how meticulous the caretaker is. This finding is not invariably present.


Protein requirements, as with energy requirements, must be approximated for any specific patient. Protein requirements will vary with energy intake. If energy intake is inadequate, the amino acids supplied from the protein will be deaminated, with the resulting carbon skeletons burned for energy. If energy intake is adequate, protein intake can be estimated according to the patient’s age and gender. For patients who might be pregnant or lactating, their protein requirements should be further adjusted. Protein requirements in the first 6 months of life have been estimated based on the amount of protein ingested from mother’s milk by healthy growing infants. Estimates beyond 6 months are similarly based on intake of normal infants, toddlers, and children, with few high-quality experimental data available. Overall, the range of estimates for protein requirements in healthy infants and children varies between 0.8 and 1.5 g/kg per day. For critically ill children in the intensive care unit, it has been shown that the daily protein requirement is approximately 1.5 g/kg per day, on average. The ultimate value, however, should be determined by the medical team based on the clinical status of the child. Some patients will have markedly elevated protein losses (i.e., patients with significant burn injury) and thus require increased protein intake. For all ill patients in whom there is any question of adequacy or excess protein intake, additional monitoring of serum proteins and serum urea will be necessary to ensure appropriate intake.

A child’s protein requirements may be met by using intact proteins, protein hydrolysates, individual amino acids, or a combination of these. Patients who have no known deficiency of the exocrine pancreatic function and no suspected major absorptive defect or protein allergy should receive high-quality intact protein. Intact protein is considerably less expensive than other dietary forms, is much more palatable, and does not contribute significantly to a formula’s osmolarity. Within a given volume and osmolarity, the formula containing intact protein will allow for significantly greater nutrient density. Patients who are unable to tolerate intact protein because of milk-protein allergy, exocrine pancreatic deficiency/insufficiency, or severe intestinal mucosal disease should receive a protein hydrolysate, a more readily absorbed form of protein.

There has been a significant increase in the number of infants demonstrating allergic reactions to the oligopeptides present in conventional formulas containing protein hydrolysate. Although it is not completely clear why this is occurring, it is clear that there are some infants who require their protein in the form of amino acids.

For many years, it was assumed that amino acids represented the optimal form of predigested protein for everyone and that a protein source containing only amino acids would be more easily absorbed. This was an oversimplified and incorrect view of the mechanism of protein absorption. The absorption of small peptides, especially dipeptides, has been shown to play a significant role in the digestion of protein. Perhaps one-fourth of the absorbed protein in health is absorbed in the form of oligopeptides. The oligopeptides, especially dipeptides, are absorbed and then hydrolyzed by brush border and cytoplasmic hydrolases to free amino acids. The mechanism of transport of the individual amino acids has been shown to be energy dependent and active and in many cases dependent on true carrier proteins with some degree of specificity for neutral, basic, and acidic amino acids. A lack of competition between amino acid uptake and the uptake of peptides suggests the separate carriers for absorption are present. It has thus become clear that in the severely damaged mucosa, the ideal form of protein for absorption will be found in a mixture of oligopeptides and individual free amino acids.

The clinical importance of peptide transport has been demonstrated in certain diseases; for example, in patients with Hartnup’s disease (in which there is a specific inability to transport some neutral amino acids such as tryptophan), normal development can occur, and this has been similarly demonstrated in cystinuria (another disorder involving amino acid transport). It is conceivable that in the damaged mucosa, similar other transport mechanisms are important. Some investigators have shown that in surgically shortened intestines, there are marked decreases in capacity to absorb free amino acids. Furthermore, there appears to be significantly less impairment in the absorption of dipeptides. Rats with exocrine pancreatic deficiency have been shown to use a diet containing 85% of the protein as oligopeptides significantly better than when fed a similar diet, as either intact protein or as free amino acids.

From a practical point of view, it is necessary first to determine the appropriate form of protein to be fed. When possible, this should be high-quality intact protein. There is no evidence that the use of formulas containing only synthetic amino acids offers any advantage to patients with compromised protein absorption. On the contrary, evidence suggests that such formulas may represent a significant problem for some patients. These formulas may be poorly tolerated because of either bad taste or high osmolar load. The use of oligopeptides (protein hydrolysates) and formulas that are mixtures of oligopeptides and free amino acids is usually adequate for the enteral support of most patients in need of the specialized defined formula diets who cannot tolerate intact proteins.

Vitamins and Minerals

Vitamin and mineral requirements for the pediatric population are listed in Tables 89-4 and 89-5 . In general, individuals who consume a varied diet that is adequate for the macronutrients (total energy, protein, and fat) are at low risk for vitamin and mineral deficiencies. Potential vitamin and mineral deficiencies in the pediatric population may occur even with adequate caloric intake, in the presence of fat malabsorption, drug–nutrient interactions, and with prolonged tube feeding with highly specialized diets.

Jul 24, 2019 | Posted by in GASTROENTEROLOGY | Comments Off on Enteral Nutrition

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