Malnutrition is endemic among infants and children with gastrointestinal disorders. The cause usually is loss of nutrients secondary to the specific derangement in gastrointestinal function, either diarrhea or vomiting. However, both diarrhea and vomiting are frequently treated by withholding all nutrients except water and electrolytes. This practice, of course, contributes to the development of malnutrition.
Acute diarrhea caused by most common organisms rarely persists for more than 4 to 5 days. During this time, the major goal of therapy is to ensure a normal state of hydration. This can be accomplished with use of oral rehydration solution (ORS), modified ORS for malnourished children, and/or special formulas (Table 71.1
), each with its own advantages and disadvantages (35
). Hospitalization and intravenous fluid therapy may be necessary, particularly if fever and/or vomiting accompany the diarrhea.
What to feed and whether to feed the child with acute diarrhea have been subjects of considerable controversy for many years, and both remain unresolved. In general, stool output is greater in the patient who is fed, but this does not mean necessarily that feeding should be proscribed. In most patients, at least some nutrient intake is possible; however, the nature of this intake must be selected, carefully taking into account the age of the patient as well as the severity and probable cause of the diarrhea. One approach is outlined later; other approaches, of course, may be equally successful, particularly in developing countries, where hospital resources may be limited, thus necessitating use of a
liquid milk-based diet, and/or a dry, solid, ready to use therapeutic food that can be eaten without adding water (e.g., Plumpy’nut; Nutriset, Malaunay, France), to minimize the risk of bacterial contamination (36
). A Working Group Report from the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition summarizes the latest advances in this field (37
TABLE 71.1 COMPOSITION (AMOUNTS OF MAJOR INGREDIENTS/100 kcal) OF SPECIAL FORMULAS FOR INFANTS WITH DERANGED OR IMMATURE INTESTINAL FUNCTION
(Soy protein isolate)
(Milk, whey protein concentrates)
(Nonfat milk, whey protein concentrates)
(Free L-amino acids)
(Free L-amino acids)
(Free L-amino acids)
(High oleic safflower, soy, coconut oils)
(MCT, soy, corn, high oleic safflower or sunflower oils)
(Palm olein, soy, coconut, high oleic sunflower oils)
(MCT, corn oil)
(Safflower, MCT, soy oils)
(High-oleic safflower, canola oils)
(Soy, high oleic safflower, MCT, coconut oils)
(Palm olein, coconut, soy, high oleic sunflower oils)
(High oleic safflower, MCT, soy oils)
(Palm kernel or coconut, high oleic sunflower, soy oils)
Lineoleic acid (mg)
1,663 (1, 000)
(Carbohydrate source selected by physician, usually glucose)
(Corn syrup solids, modified corn starch)
(Corn syrup solids, modified corn starch)
(Corn syrup solids, sucrose)
(Sucrose, modified tapioca starch)
(Sucrose, corn maltodextrin)
(Corn syrup solids, lactose)
(Corn syrup solids, modified tapioca starch)
(Corn syrup solids)
(Corn syrup solids)
Vitamin A (IU) (Retinol)
Vitamin D (IU) (Calciferol)
Vitamin E (IU) (Tocopherol)
Vitamin K (µg) (Phytonadione)
Vitamin B1 (µg) (Thiamin)
Vitamin B2 (µg) (Riboflavin)
Vitamin B3 (µg) (Niacin)
2.214 (1, 350)
Vitamin B5 (µg) (Pantothenic acid)
Vitamin B6 (µg) (Pyridoxal PO4)
Vitamin B7 (µg) (Biotin)
Vitamin B9 (µg) (Folic acid)
Vitamin B12 (µg) (Cobalamin)
Vitamin C (mg) (Ascorbic acid)
MCT, medium chain triglyceride; RCF, Ross Carbohydrate Free.
a Abbott Nutrition, Columbus, OH.
b Note that this formula contains no carbohydrate, which accounts for its markedly different nutrient content vs. the other formulas shown. However, if 13 fl oz (390 ml) RCF is reconstituted with 54 g carbohydrate, e.g., glucose, and 12 fl oz (360 ml) water as the manufacturer recommends, the alternate values listed in (parentheses) will result, which approximates the carbohydrate content of most other formulas shown (i.e., approximately 2 g carbohydrate/fl oz of formula). As noted (see text), if other formulas are poorly tolerated (i.e., result in the resumption of diarrhea), the authors recommend initially reconstituting RCF with 12 g carbohydrate, e.g., glucose, and 12 fl oz (360 ml) water (i.e., approximately 0.5 g carbohydrate/fl oz of formula), before gradually increasing carbohydrate content, progressively reconstituting RCF with additional increments of 12 g carbohydrate, e.g., glucose, per 12 fl oz (360 ml) water, daily or every other day as tolerance for carbohydrate increases. Once full carbohydrate content (i.e., approximately 2 g carbohydrate/fl oz of formula) is tolerated, the patient usually can be switched to a carbohydrate-containing formula.
c Mead Johnson Nutrition, Evansville, IN.
d Note that this formula is designed for preterm infants.
e Nutricia North America, Gaithersburg, MD.
f Note that these formulas are hypoallergenic.
In general, the most common cause of acute diarrhea in developed countries is viral infection, chiefly resulting from contact with infected individuals; less common is bacterial infection, related either to socioeconomic dislocation or foreign travel (38
). Therefore, a stool culture to detect a specific pathogen usually is not helpful. The pathophysiology of most toxicogenic (i.e., enteropathogenic) bacterial diarrheas (e.g., Salmonella, Shigella,
spp., enteropathogenic Escherichia coli
serotype O157:H7) is secretory diarrhea resulting from stimulation of the adenylate cyclase system, as occurs in cholera) (40
); by contrast, the pathophysiology of most viral diarrheas (e.g., rotavirus) is both osmotic (inhibition of glucose transport as described for rotavirus) (41
) and secretory. As such, testing the stool for pH and the presence of reducing substances may be very helpful, because a low pH (<6.0) and the presence of reducing substances suggest carbohydrate intolerance, hence a viral origin. The stool is best tested after a period of adequate intake of a reducing sugar (e.g., a 5% glucose solution or ORS); in addition, the water content of the stool, rather than any solid matter, should be tested.
Carbohydrate malabsorption in acute diarrhea is common but fortunately transient in most cases. Malabsorption of all carbohydrates, including glucose, may occur. However, this should not preclude administration of ORS in acute diarrhea. Occasionally, the carbohydrate malabsorption persists, and the patient develops postinfectious gastroenteritis. Young infants in lower growth percentiles who present with metabolic acidosis are particularly vulnerable to postinfectious gastroenteritis. Before the inception of total parenteral nutrition (TPN), this entity carried a high case fatality rate. However, this condition can now be managed successfully in most cases with nutritional support through the parenteral route with careful introduction of elemental or semielemental formulas.
If the origin of the diarrhea seems to be osmotic, and reintroduction of a carbohydrate-containing formula results in resumption of the diarrhea, a carbohydrate-free formula (see Table 71.1
) usually is well tolerated. However, such formulas can result in ketosis and occasionally hypoglycemia; thus, some carbohydrate intake is necessary. In the hospitalized child, this can be provided intravenously. Most children who do not require hospitalization usually tolerate at least some sugar intake by the enteral route. In general, 0.5 g of glucose or sucrose per ounce of formula, provided intake is adequate but not excessive, is well tolerated and prevents ketosis and hypoglycemia. If this preparation is tolerated, the amount of carbohydrate can be increased daily or every other day as tolerance for carbohydrate increases. Once full carbohydrate content (i.e., approximately 2 g/oz) is tolerated, the patient usually can be switched to a carbohydrate-containing formula.
If the origin of the diarrhea is secretory, feeding usually does not affect the volume of stool output. In many cases, in fact, a glucose-electrolyte solution (e.g., ORS) seems to decrease the volume of stool output. In any event, fluid and electrolyte replacement must keep pace with intestinal losses until the diarrhea abates. Therefore, decisions concerning feeding must be based on clinical experience in such patients.
Regardless of the cause of the diarrhea, the tendency to avoid feedings containing lactose, especially breast milk, in most infants with diarrhea is unnecessary. In fact, continued breast-feeding should be encouraged. If stool pH is normal when the child is first seen and reducing substances are not present, lactase deficiency is an unlikely contributor to the diarrhea.
In a few patients, the acute episode of diarrhea does not resolve in the usual 4 to 5 days. In these patients, nutritional management becomes a much more important consideration. Although most infants can tolerate a 4- to 5-day period with little or no nutritional intake, few can tolerate a period of more than 2 weeks without becoming malnourished and developing secondary intestinal changes caused by both persistent diarrhea and malnutrition. Such infants are much more likely to develop secondary deficiencies of mucosal disaccharidases (e.g., lactase deficiency, and less commonly, sucrase deficiency). Monosaccharide intolerance may also develop. In these infants, management without hospitalization is difficult. Choice of formula again must be made on the basis of the suspected or culture-proven cause of the diarrhea; in addition, the much greater likelihood of secondary mucosal hydrolase deficiencies must be taken into account. If small volumes of a particular formula are reasonably well tolerated, it frequently is possible to deliver sufficient amounts to meet nutritional needs by use of a continuous infusion technique (41
). Again, in small infants, this usually requires hospitalization.
Noninfectious causes of chronic diarrhea result from a spectrum of congenital or acquired abnormalities that include changes in villous structure (e.g., celiac disease), ultrastructural abnormalities (e.g., microvillous inclusion disease), and abnormalities at the molecular level (e.g., congenital chloride diarrhea). If not managed appropriately, these disorders frequently result in the same secondary changes in mucosal function observed in acute diarrheas. The nutritional management of the two most common illnesses associated with chronic diarrhea, celiac disease and inflammatory bowel disease, are described here. Nutritional management of other chronic diarrheas, in general, is similar to that described earlier and must be
tailored to the specific cause and pathophysiology of these conditions.
Celiac disease (gluten-sensitive enteropathy) has been recognized to be far more common than was previously thought (42
). Strict adherence to a gluten-free diet (GFD) is the cornerstone of therapy; a safe gluten threshold has been established for adults with celiac disease (44
). Foodstuffs must contain less than 20 ppm to be considered gluten free. Patients with celiac disease are restricted from eating products that contain wheat, barley, or rye. Compliance is problematic among children, especially among adolescents diagnosed through mass screening, who may lack the typical symptoms (45
). Fortunately, some oat cereals have been found to be a safe substitute for gluten-rich cereals and may facilitate management of children with this condition (46
). Adherence to a strict GFD is important for reasons other than symptom management. Achievement of adequate growth, maintenance of normal bone mineral density, and correction of iron deficiency anemia are but a few examples of the importance of adherence to a strict GFD (47
). Again, a Working Group Report from the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition describes the current approach to treatment of these patients (50
Inflammatory Bowel Disease.
Inflammatory bowel disease, including both ulcerative colitis and Crohn disease (regional enteritis, granulomatous colitis), is another condition associated with chronic diarrhea and growth failure that often becomes permanent despite appropriate nutritional intervention (51
). Because ulcerative colitis afflicts only the large intestine, thus leaving the absorptive functions of the small intestine fully intact, its effects on growth are limited. However, the pathophysiology of Crohn disease, which chiefly affects the distal ileum (although it can involve any area of the alimentary canal), is transmural inflammation; the precise cause remains uncertain, but it likely involves complex interactions among environmental, immunologic, and bacterial factors in genetically susceptible hosts. Inadequate nutrition and growth failure in Crohn disease, which may affect as many as 30% of children with the disease, are the result of inadequate intake and the cumulative effects of inflammation on growth; in fact, the disease is typically heralded by an unexplained slowing of linear growth before diagnosis (54
Anti-inflammatory (i.e., immunosuppressive) agents (e.g., 5-aminosalicylate derivatives) and immunomodulating agents (e.g., azathioprine) are the mainstays of therapy for induction as well as maintenance of remission; corticosteroids (e.g., prednisone) may also be prescribed, but long-term use is associated with an unacceptably high incidence of side effects in children.
The observation that patients prepared for surgical management of complications related to Crohn disease (e.g., intestinal obstruction, perforation, abscesses, fistulas) experienced improvement in symptoms led to the use of elemental and semielemental diets as a primary treatment. Although the precise mechanism of this improvement is unknown, it is clear that elemental enteral nutrition indexed to 133% of ideal body weight or 60 to 75 kcal/kg actual body weight may achieve treatment results in children, although not in adults, that are comparable to those obtained with anti-inflammatory agents (57
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