Gastrointestinal Dysfunction

Chapter 41

Gastrointestinal Dysfunction

David Wilson

Nutritional Disorders

Reports of severe nutritional disorders in childhood in most developed countries are uncommon, yet small numbers of children who may experience a nutritional deficiency of some type often exist. The 2008 Feeding Infants and Toddlers Study (FITS) found that usual nutrient intake of infants, toddlers, and preschoolers (ages 0 to 47 months) met or exceeded energy and protein requirements based on the Dietary Reference Intakes (DRIs) and the 2005 Dietary Guidelines for Americans (Butte, Fox, Briefel, et al., 2010). According to the study, a small but significant number of infants were at risk for inadequate intake of iron and zinc. Dietary fiber intakes in toddlers and preschoolers were low, and saturated fat intakes exceeded recommendations for the majority of preschoolers (Butte, Fox, Briefel, et al., 2010). There are reports of an increased dependence on fortified foods and supplements in toddlers to meet nutritional requirements rather than meeting such needs with a wide variety of fruits, vegetables, and whole grains (Fox, Reidy, Novak, et al., 2006).

The findings of these studies and other similar reports are important for nurses who work with infants and children. Nurses must work to promote healthy nutrition habits early in children’s lives through proper education of families and children about healthy lifestyle habits, including diet and exercise for health promotion and prevention of morbidities associated with poor micronutrient intake and sedentary lifestyle.

Vitamin Imbalances

Although true vitamin deficiencies are rare in the United States, subclinical deficiencies are commonly seen in population subgroups in which either maternal or child dietary intake is imbalanced and contains inadequate amounts of vitamins. Vitamin D–deficiency rickets, once rarely seen because of the widespread commercial availability of vitamin D–fortified milk, increased before the turn of the century. Populations at risk include the following:

The American Academy of Pediatrics (AAP) (2008) recommends that infants who are breastfed exclusively receive 400 IU of vitamin D beginning shortly after birth to prevent rickets and vitamin D deficiency. Vitamin D supplementation should continue until the infant is consuming at least 1 L/day (or 1 quart/day) of vitamin D–fortified formula (AAP, 2008). Nonbreastfed infants who are taking less than 1 L/day of vitamin D–fortified formula should also receive a daily vitamin D supplement of 400 IU. Inadequate maternal ingestion of cobalamin (vitamin B12) may contribute to infant neurologic impairment when exclusive breastfeeding (past 6 months) is the only source of the infant’s nutrition. A correlation between the incidence of childhood upper respiratory infections and vitamin D deficiency has been found, but the implications of the findings have yet to be completely understood (Taylor and Camargo, 2011; Walker and Modlin, 2009).

Children may also be at risk for vitamin deficiencies secondary to disorders or their treatment. For example, vitamin deficiencies of the fat-soluble vitamins A and D may occur in malabsorptive disorders such as cystic fibrosis and short bowel syndrome. Preterm infants may develop rickets in the second month of life as a result of inadequate intake of vitamin D, calcium, and phosphorus. Children receiving high doses of salicylates may have impaired vitamin C storage. Environmental tobacco smoke exposure has been implicated in decreased concentrations of ascorbate in children; therefore increased intake of sources of vitamin C should be encouraged even in children minimally exposed to environmental tobacco smoke (Preston, Rodriguez, and Rivera, 2003). Children with chronic illnesses resulting in anorexia, decreased food intake, or possible nutrient malabsorption as a result of multiple medications should be evaluated carefully for adequate vitamin and mineral intake in some form (parenteral or enteral).

Children with sickle cell disease are reported to have suboptimal intakes (according to DRI recommendations) of vitamins E and D, folate, calcium, and fiber, which decrease significantly with increasing age. Poor dietary intake was a significant factor in the findings of the study (Kawchak, Schall, Zemel, et al., 2007). One study found that children with intestinal failure who were being transitioned from parenteral to enteral nutrition had at least one vitamin and mineral deficiency; vitamin D was the most common deficiency identified, and zinc and iron were the most common minerals identified as being deficient (Yang, Duro, Zurakowski, et al., 2011).

Vitamin A deficiency has been reported with increased morbidity and mortality in children with measles. However, a Cochrane review of studies wherein a single dose of vitamin A was administered to children with measles found no decrease in mortality. Children with measles younger than the age of 2 years who received two doses of vitamin A (200,000 IU) on consecutive days did have decreased mortality rates and a reduced rate of pneumonia-specific mortality (Huiming, Chaomin, and Meng, 2005). Complications from diarrhea and infections are often increased in infants and children with vitamin A deficiency. Although scurvy (caused by a deficiency of vitamin C) is rare in developed countries, cases have been reported in children who were fed an organic diet deficient in vegetables and fruits (Burk and Molodow, 2007).

An excessive dose of a vitamin is generally defined as 10 or more times the Recommended Dietary Allowance (RDA), although the fat-soluble vitamins, especially vitamins A and D, tend to cause toxic reactions at lower doses. With the addition of vitamins to commercially prepared foods, the potential for hypervitaminosis has increased, especially when combined with the excessive use of vitamin supplements. Hypervitaminosis of vitamins A and D presents the greatest problems because these fat-soluble vitamins are stored in the body. High intakes of vitamin A have been linked to physeal growth arrest, which can lead to osteoporosis, fracture, and metaphyseal irregularity (Saltzman and King, 2007). Chronic hypervitaminosis A may result in signs and symptoms of headache; vomiting; dry, itching desquamating skin; anorexia; fissures at the corner of the mouth; weight loss; bulging fontanels; and neurologic signs such as irritability and stupor (Zile, 2011). An excessive intake of vitamin A in pregnant women has also been linked to fetal defects (Zile, 2011). Vitamin D is the most likely of all vitamins to cause toxic reactions in relatively small overdoses. The water-soluble vitamins, primarily niacin, B6, and C, can also cause toxicity. Poor outcomes in infants (e.g., fatal hypermagnesemia) have been associated with megavitamin therapy with high doses of magnesium oxide, and severe anemia and thrombocytopenia have resulted from megadoses of vitamin A.

One vitamin supplement that is recommended for all women of childbearing age is a daily dose of 0.4 mg of folic acid, the usual RDA. Folic acid taken before conception and during early pregnancy can reduce the risk of neural tube defects such as spina bifida by as much as 70%. Drugs such as oral contraceptives and antidepressants may decrease folic acid absorption; thus adolescent girls taking such medications should consider supplementation. (See Spina Bifida (Myelomeningocele, Chapter 49.)

Mineral Imbalances

A number of minerals are essential nutrients. The macrominerals refer to those with daily requirements greater than 100 mg and include calcium, phosphorus, magnesium, sodium, potassium, chloride, and sulfur. Microminerals, or trace elements, have daily requirements of less than 100 mg and include several essential minerals and those in which the exact role in nutrition is still unclear. The greatest concern with minerals is deficiency, especially iron deficiency anemia (see Chapter 43). However, other minerals that may be inadequate in children’s diets, even with supplementation, include calcium, phosphorus, magnesium, and zinc. Low levels of zinc can cause nutritional growth failure (failure to thrive [FTT]). Some of the macrominerals may be overlooked inadvertently when a child with intestinal failure or recent surgery is making the transition from total parenteral to enteral intake.

An imbalance in the intake of calcium and phosphorous may occur in infants who are given whole cow’s milk instead of infant formula; neonatal tetany may be observed in such cases. Whole cow’s milk is also a poor source of iron, and inadequate intake of iron from other food sources such as iron-fortified cereal may cause iron deficiency anemia.

The regulation of mineral balance in the body is a complex process. Dietary extremes of mineral intake can cause a number of mineral-mineral interactions that could result in unexpected deficiencies or excesses. For example, excessive amounts of one mineral such as zinc can result in a deficiency of another mineral such as copper even if sufficient amounts of copper are ingested. Thus megadose intake of one mineral may cause an inadvertent deficiency of another essential mineral by blocking its absorption in the blood or intestinal wall or competing with binding sites on protein carriers needed for metabolism.

Deficiencies can also occur when various substances in the diet interact with minerals. For example, iron, zinc, and calcium can form insoluble complexes with phytates or oxalates (substances found in plant proteins), which impair the bioavailability of the mineral. This type of interaction is important in vegetarian diets because plant foods such as soy are high in phytates. Contrary to popular opinion, spinach is not an ideal source of iron or calcium because of its high oxalate content. Factors that affect iron absorption are listed in Chapter 32.

Children with certain illnesses are at greater risk for growth failure, especially in relation to bone mineral deficiency as a result of the treatment of the disease, decreased nutrient intake, or decreased absorption of necessary minerals. Those at risk for such deficiencies include children who are receiving or have received radiation and chemotherapy for cancer; children with human immunodeficiency virus (HIV), sickle cell disease, cystic fibrosis, gastrointestinal (GI) malabsorption, or nephrosis; and extremely low–birth-weight (ELBW) and very low–birth-weight (VLBW) preterm infants.

Care Management

Identification of adequacy of nutrient intake is the initial nursing goal and requires assessment based on a dietary history and physical examination for signs of deficiency or excess (see Nutrition, Chapter 32, and Nutritional Assessment, Chapter 29). After assessment data are collected, this information is evaluated against standard intakes to identify areas of concern. DRIs are one source of standard nutrient intakes (see Chapter 32, Dietary Guidelines).

Standardized growth reference charts should be used in infants, children, and adolescents to compare and assess growth parameters such as height and head circumference with the percentile distribution of other children at the same ages. The World Health Organization (WHO) growth chart is a standardized growth reference now recommended for infants and toddlers up to 24 months of age. This growth chart includes head circumference, height, and weight references that were derived from healthy children in six different countries around the world. These growth standards are based on the growth of healthy breastfed infants throughout the first year of life. The Centers for Disease Control and Prevention (CDC) growth charts are now recommended for children 2 to 19 years of age (Grummer-Strawn, Reinold, Krebs, et al., 2010).

Infants should be breastfed for the first 6 months and preferably for 1 year, be introduced to some solid foods after about 4 to 6 months, and receive iron-fortified cereal for at least 18 months (see Chapter 31). Vitamin B12 supplementation is recommended if the breastfeeding mother’s intake of the vitamin is inadequate or if she is not taking vitamin supplements (Dunham and Kollar, 2006). If the infant is being breastfed exclusively after 4 months (when fetal iron stores are depleted), iron supplementation (1 mg/kg/day) is recommended until appropriate iron-containing complementary foods such as iron-fortified cereal are introduced (Baker, Greer, and AAP Committee on Nutrition, 2010). The introduction of solids for vegetarian infants may occur using the same guidelines as for other children (see Chapter 32). A variety of foods should be introduced during the early years to ensure a well-balanced intake. Infants who are identified as having particular nutritional deficits should be identified; a multidisciplinary approach should be taken for identifying the deficit and the etiology, and a plan established with the caregiver to promote adequate growth and development.

Protein-Energy Malnutrition (Severe Childhood Undernutrition)

Malnutrition continues to be a major health problem in the world today, particularly in children younger than 5 years of age. However, lack of food is not always the primary cause of malnutrition. In many developing and underdeveloped nations, diarrhea (gastroenteritis) is a major factor. Additional factors are bottle-feeding (in poor sanitary conditions), inadequate knowledge of proper child care practices, parental illiteracy, economic and political factors, climate conditions, cultural and religious food preferences, and simply a lack of adequate food. Müller and Krawinkel (2005) point out that poverty is the underlying cause of malnutrition. The most extreme forms, or protein-energy malnutrition (PEM), are kwashiorkor and marasmus. Some authorities suggest that severe malnutrition encompasses more than protein-energy deficits and thus prefer the term severe childhood undernutrition (SCU). Another term used is severe acute malnutrition (SAM). Entities such as the WHO continue to use the term protein-energy malnutrition. SCU may also be subdivided into edematous (kwashiorkor) and nonedematous (marasmus) types.

In the United States milder forms of PEM are seen as a result of primary malnutrition, although the classic cases of marasmus and kwashiorkor may also occur. Unlike in developing countries, where the main reason for PEM is inadequate food, in the United States PEM occurs despite ample dietary supplies (see Failure to Thrive, Chapter 31). It may also be seen in people with chronic health problems such as cystic fibrosis, renal dialysis, cancer, and GI malabsorption; in elderly adults who have chronic malnutrition; and in people with acute illnesses such as prolonged, untreated anorexia nervosa. Kwashiorkor has been reported in the United States in children fed only a rice beverage diet (Rice Dream) and few solid foods and in infants who were fed nonstandard infant diets such as flour water, corn porridge, molasses, and nondairy creamer (Katz, Mahlberg, Honig, et al., 2005; Tierney, Sage, and Shwayder, 2010). Kwashiorkor has also been reported in the United States when infants have been fed inappropriate food as a result of parental (caretaker) nutritional ignorance, a perceived cow’s milk–based formula intolerance, family social chaos, or cow’s milk intolerance. Therefore it is important that health care workers not assume that PEM cannot occur in developed countries; a comprehensive dietary history should be obtained in any child with clinical features resembling PEM.


Kwashiorkor has been defined primarily as a deficiency of protein with an adequate supply of calories. A diet consisting mainly of starch grains or tubers provides adequate calories in the form of carbohydrates but an inadequate amount of high-quality proteins. However, some evidence supports a multifactorial etiology, including cultural, psychologic, and infective factors, that may interact to place the child at risk for kwashiorkor. Some experts suggest that kwashiorkor may result from the interplay of nutrient deprivation, response to infection and oxidative stress, and environmental stresses, which combined produce an imbalanced response to such insults (Penny, 2008). It often occurs subsequent to an infectious outbreak of measles and dysentery. There is further evidence that oxidative stress occurs in children with kwashiorkor, resulting in free radical damage, which may precipitate cellular changes, resulting in edema and muscle wasting. The role of the essential fatty acid arachidonic acid in lipid metabolism, altered leukotriene production, and oxidative stress in kwashiorkor has yet to be fully understood, but abnormal essential fatty acid metabolism seems to have an interactive role in its development (Penny, 2008).

Taken from the Ga language (Ghana), the word kwashiorkor means “the sickness the older child gets when the next baby is born” and aptly describes the syndrome that develops in the first child, usually between 1 and 4 years of age, when weaned from the breast after the second child is born.

The child with kwashiorkor has thin, wasted extremities and a prominent abdomen from edema (ascites). The edema often masks severe muscular atrophy, making the child appear less debilitated than he or she actually is. The skin is scaly and dry and has areas of depigmentation. Several dermatoses may be evident, partly resulting from the vitamin deficiencies. Permanent blindness often results from the severe lack of vitamin A. Mineral deficiencies especially iron, calcium, and zinc, are common. Acute zinc deficiency is a common complication of severe PEM and results in skin rashes, loss of hair, impaired immune response and susceptibility to infections, digestive problems, night blindness, changes in affective behavior, defective wound healing, and impaired growth. Its depressant effect on appetite further limits food intake. The hair is thin, dry, coarse, and dull. Depigmentation is common, and patchy alopecia may occur.

Diarrhea (persistent diarrhea malnutrition syndrome) commonly occurs from a lowered resistance to infection and further complicates the electrolyte imbalance. Low levels of cytokines (protein cells involved in the primary response to infection) have been reported in children with kwashiorkor, suggesting that such children have a blunted immune response to infection. A large number of deaths in children with kwashiorkor occur in those who develop HIV infection. GI disturbances such as fatty infiltration of the liver and atrophy of the acini cells of the pancreas occur. Anemia is also a common finding in malnourished children. Protein deficiency increases the child’s susceptibility to infection, which eventually results in death. Fatal deterioration may be caused by diarrhea and infection or by circulatory failure.


Marasmus results from general malnutrition of both calories and protein. It is common in underdeveloped countries during times of drought, especially in cultures where adults eat first; the remaining food is often insufficient in quality and quantity for the children.

Marasmus is usually a syndrome of physical and emotional deprivation and is not confined to geographic areas where food supplies are inadequate. It may be seen in children with growth failure in whom the cause is not solely nutritional but primarily emotional. Marasmus may be seen in infants as young as 3 months of age if breastfeeding is not successful and there are no suitable alternatives. Marasmic kwashiorkor is a form of PEM in which clinical findings of both kwashiorkor and marasmus are evident; the child has edema, severe wasting, and stunted growth. In marasmic kwashiorkor the child has inadequate nutrient intake and superimposed infection. Fluid and electrolyte disturbances, hypothermia, and hypoglycemia are associated with a poor prognosis.

Marasmus is characterized by gradual wasting and atrophy of body tissues, especially of subcutaneous fat. The child appears to be very old, with loose and wrinkled skin, unlike the child with kwashiorkor, who appears more rounded from the edema. Fat metabolism is less impaired than in kwashiorkor; thus deficiency of fat-soluble vitamins is usually minimal or absent. In general the clinical manifestations of marasmus are similar to those seen in kwashiorkor with the following exceptions: with marasmus there is no edema from hypoalbuminemia or sodium retention, which contributes to a severely emaciated appearance; no dermatoses caused by vitamin deficiencies; little or no depigmentation of hair or skin; moderately normal fat metabolism and lipid absorption; and a smaller head size and slower recovery after treatment. There is also an abnormal regulation of the sodium-potassium pump, resulting in an increase in intracellular sodium and a decrease in potassium (Penny, 2008).

The child is fretful, apathetic, withdrawn, and so lethargic that prostration frequently occurs. Intercurrent infection with debilitating diseases such as tuberculosis, parasitosis, HIV, and dysentery is common.

Therapeutic Management

The treatment of PEM includes providing a diet with high-quality proteins, carbohydrates, vitamins, and minerals. When PEM occurs as a result of persistent diarrhea, three management goals are identified:

Local protocols are used in developing countries to deal with PEM. Penny (2008) and Alderman and Shekar (2011) recommend a three-phase treatment protocol: (1) acute or initial phase in the first 2 to 10 days involving initiation of treatment for oral rehydration, diarrhea, and intestinal parasites; prevention of hypoglycemia and hypothermia; and subsequent dietary management; (2) recovery or rehabilitation (2 to 6 weeks) focusing on increasing dietary intake, iron fortification, and weight gain; and (3) follow-up phase, focusing on care after discharge in an outpatient setting to prevent relapse and promote weight gain, provide developmental stimulation, and evaluate cognitive and motor deficits. In the acute phase care is taken to prevent fluid overload; the child is observed closely for signs of food or fluid intolerance. The refeeding syndrome may occur if intake progresses too rapidly; cardiac failure may cause sudden death in a child who has been malnourished and refed too rapidly (Grover and Ee, 2009). Severe hypophosphatemia may develop during the first week of initiating feedings and is considered to be the hallmark of refeeding syndrome (Alderman and Shekar, 2011). Signs and symptoms include weakness, arrhythmias, altered levels of consciousness, seizures, cardiorespiratory failure, and sudden death.

Vitamin and mineral supplementation is required in most cases of PEM; vitamin A, zinc, and copper are recommended; iron supplementation is not recommended until the child is able to tolerate a steady food source. In addition, the child is observed for signs of skin breakdown, which should be treated to prevent infection. Breastfeeding is encouraged if the mother and child are able to do so effectively; in some cases partial supplementation with a modified cow’s milk–based formula may be necessary.

The WHO (2006) issued a statement recognizing the importance of breastfeeding for the first 6 months in developing countries where HIV is prevalent among childbearing women and children. It recognizes that appropriate sources of food and water for infants may not be available after the 6 months are concluded and that the risk for malnutrition is greater among such children than the theoretic risk of HIV. However, the organization does recommend that breastfeeding continue after 6 months with the introduction of complementary foods, provided they are safe for child consumption. In severely malnourished children a modest energy food source is given initially, followed by a high-protein and energy food source; severely malnourished children do not tolerate a high-energy and high-protein source initially. A number of food sources may be provided to treat PEM. They include ORSs (ReSoMal), amino acid–based elemental food, and ready-to-feed foods that do not require the addition of water (to minimize contaminated water consumption); parenteral and oral antibiotics are often part of the standard treatment for PEM (Amadi, Mwiya, Chomba, et al., 2005; Ciliberto, Sandige, Ndekha, et al., 2005).

Care Management

Because PEM appears early in childhood, primarily in children 6 months to 2 years of age, and is associated with early weaning, a low-protein diet, delayed introduction of complementary foods, and frequent infections (Grover and Ee, 2009; Müller and Krawinkel, 2005), it is essential that nursing care focus on prevention of PEM through parent education about feeding practices during this crucial period. Prevention should also focus on the nutritional health of pregnant women because this directly impacts the health of their unborn children. Breastfeeding is the optimal method of feeding for the first 6 months. The immune properties naturally found in breast milk not only nourish infants but also help prevent opportunistic infections, which may contribute to PEM. Providing for essential physiologic needs such as appropriate nutrient intake, protection from infection, adequate hydration, skin care, and restoration of physiologic integrity is paramount. Additional nursing care focuses on education about and administration of childhood vaccinations to prevent illness, promotion of nutrition and well-being for the lactating mother, encouragement and participation in well-child visits for infants and toddlers, appropriate food sources for children being weaned from breastfeeding, and education regarding sanitation practices to prevent childhood GI diseases.

Poor skin integrity further increases the chance of infections, hypothermia, water loss, and skin breakdown. Tube feedings may be required for infants too weak to breastfeed or bottle-feed. Oral rehydration with an approved ORS is commonly used in cases of PEM in which diarrhea and infection are not immediately life threatening.

One approach that has gained acceptance for treating childhood malnutrition in developing countries is the home-based use of ready-to-use therapeutic food (RUTF). RUTF is a paste based on peanut butter and dried skim milk with vitamins and minerals; it requires no mixing with water or milk. The packaged RUTF can be stored without refrigeration. Studies have demonstrated improved survival rates in malnourished children (Amthor, Cole, and Manary, 2009; Ciliberto, Sandige, Ndehka, et al., 2005). Some of the reported advantages of home-based (community-based) treatment include that children are not exposed to hospital-acquired infections and may receive the RUTF from village health aides (Kapil, 2009).

It is imperative that nurses be at the forefront in educating and reinforcing healthy nutrition habits in parents of small children to prevent malnutrition. Because children with marasmus may experience emotional starvation as well, care should be consistent with that for children with FTT.

The WHO has published guidelines for the treatment and management of children with severe acute malnutrition (Ashworth, Khanum, Jackson, et al., 2003; Grover and Ee, 2009). These guidelines include a two-phase program with a 10-step guide to treating the child with malnutrition.

Food Allergy

In late 2010 the National Institute of Allergy and Infectious Diseases (NIAID), working with 34 other professional organizations, published new evidence-based guidelines for the diagnosis and management of food allergy. A food allergy is defined by the NIAID as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food” (Boyce, Assa’ad, Burks, et al., 2010, p. 1108). Food allergens are defined as specific components of food or ingredients in food such as a protein that are recognized by allergen-specific immune cells eliciting an immune reaction that results in the characteristic symptoms (Boyce, Assa’ad, Burks, et al., 2010). A food intolerance is said to exist when a food or food component elicits a reproducible adverse reaction but does not have an established or likely immunologic mechanism (Boyce, Assa’ad, Burks, et al., 2010). The example given suggests that a person may have an immune-mediated allergy to cow’s milk protein, but the person who is unable to digest the lactose in cow’s milk is considered to be intolerant, not allergic, to it. The NIAID guidelines classify food allergy according to the following: food-induced anaphylaxis, GI food allergies, and specific syndromes; cutaneous reactions to foods; respiratory manifestation; and Heiner syndrome (Boyce, Assa’ad, Burks, et al., 2010). The exact prevalence of food allergies in children is reported to be much lower than that which parents report. Approximately 6% of children may experience food allergic reactions in the first 2 to 3 years of life; 1.5% will have an allergy to eggs, 2.5% to cow’s milk, and 1% to peanuts (Sampson and Leung, 2011). Seafood allergies in children are reported to be low in the United States: 0.2% for fish and 0.5% for crustaceans (Boyce, Assa’ad, Burks, et al., 2010). Diagnosed allergy to milk and eggs was found to be 2.2% in a Danish study and 1.6% in a Norwegian study. The NIAID report further points out that most children will eventually be able to tolerate milk, eggs, soy, and wheat; far fewer will ever tolerate tree nut and peanuts (Boyce, Assa’ad, Burks, et al., 2010). The NIAID report indicates that 50% to 90% of all presumed food allergies are not actually allergies. The NIAID’s (Boyce, Assa’ad, Burks, et al., 2010) guidelines also recommend the following:

• Infants should be breastfed exclusively until 4 to 6 months of age.

• Soy formula is not recommended to prevent the development of food allergy.

• Introduction of complementary foods should not be delayed beyond 6 months of age.

• Hydrolyzed formula (versus cow’s milk) may be used in at-risk infants to prevent or modify food allergy.

• Maternal diet during pregnancy or lactation should not be restricted to prevent food allergy.

• Children should be vaccinated with the measles, mumps, and rubella (MMR) and measles, mumps, rubella, and varicella (MMRV) vaccines (even with egg allergy [unless severe reaction occurred]).

• Patients with severe egg allergy reactions should not receive the influenza vaccine without consulting the primary practitioner for an analysis of the risks versus benefits.

A summary of the NIAID guidelines is provided by McBride (2011).

The clinical manifestations of food allergy may be divided as follows (AAP, 2009):

Food allergies usually occur either as an immunoglobulin E (IgE)–mediated or non–IgE-mediated immune response; some toxic reactions may occur as a result of a toxin found within the food. Food allergy is caused by exposure to allergens, usually proteins (but not the smaller amino acids), that are capable of inducing IgE antibody formation (sensitization) when ingested. Sensitization refers to the initial exposure of an individual to an allergen, resulting in an immune response; subsequent exposure induces a much stronger response that is clinically apparent. Consequently food allergy typically occurs after the food has been ingested one or more times. The NIAID report (Boyce, Assa’ad, Burks, et al., 2010) indicates that sensitization alone is not sufficient to classify as a food allergy; rather an immune-mediated response and manifestation of specific sign and symptoms are necessary to categorize an individual as having a food allergy. The most common food allergens are listed in Box 41-1.

Box 41-1   Common Allergenic Foods and Sources

Nuts*—Some chocolates, candy, baked goods, cherry soda (may be flavored with a nut extract), walnut oil

Eggs*—Mayonnaise, creamy salad dressing, baked goods, egg noodles, some cake icing, meringue, custard, pancakes, French toast, root beer

Wheat*—Almost all baked goods, wieners, bologna, pressed or chopped cold cuts, gravy, pasta, some canned soups

Legumes—Peanuts,* peanut butter or oil, beans, peas, lentils

Fish or shellfish*—Cod liver oil, pizza with anchovies, Caesar salad dressing, any food fried in same oil as fish

Soy*—Soy sauce, teriyaki or Worcestershire sauce, tofu, baked goods using soy flour or oil, soy nuts, soy infant formulas or milk, soybean paste, tuna packed in vegetable oil, many margarines

Chocolate—Cola beverages, cocoa, chocolate-flavored drinks

Milk—Ice cream, butter, margarine (if it contains dairy products), yogurt, cheese, pudding, baked goods, wieners, bologna, canned creamed soups, instant breakfast drinks, powdered milk drinks, milk chocolate

Buckwheat—Some cereals, pancakes

Pork, chicken—Bacon, wieners, sausage, pork fat, chicken broth

Strawberries, melon, pineapple—Gelatin, syrups

Corn—Popcorn, cereal, muffins, cornstarch, corn meal, corn bread, corn tortillas, corn syrup

Citrus fruits—Orange, lemon, lime, grapefruit; any of these in drinks, gelatin, juice, or medicines

Tomatoes—Juice, some vegetable soups, spaghetti, pizza sauce, catsup

Spices—Chili, pepper, vinegar, cinnamon

*Most common allergens.

Oral allergy syndrome occurs when a food allergen (commonly fruits and vegetables) is ingested and there is subsequent edema and pruritus involving the lips, tongue, palate, and throat. Recovery from symptoms is usually rapid. Immediate GI hypersensitivity is an IgE-mediated reaction to a food allergen; reactions include nausea, abdominal pain, cramping, diarrhea, vomiting, anaphylaxis, or all of these. Additional food allergies seen in young children include allergic eosinophilic esophagitis, allergic eosinophilic gastroenteritis, food protein–induced proctocolitis, and food protein–induced enterocolitis.

Food allergy or hypersensitivity may also be classified according to the interval between ingestion and the manifestation of symptoms: immediate (within minutes to hours) or delayed (2 to 48 hours) (AAP, 2009).

Food allergies can occur at any time but are common during infancy because the immature intestinal tract is more permeable to proteins than the mature intestinal tract, thus increasing the likelihood of an immune response. Allergies in general demonstrate a genetic component: children who have one parent with an allergy have a 50% or greater risk of developing one; children who have both parents with an allergy have up to a 100% risk of developing one. Allergy with a hereditary tendency is referred to as atopy. Some infants with atopy can be identified at birth from elevated levels of IgE in umbilical cord blood.

Deaths have been reported in children who experienced an anaphylactic reaction to food. Onset of the reactions occurred shortly after ingestion (5 to 30 minutes). In most of the children the reactions did not begin with skin signs such as hives, red rash, and flushing but rather mimicked an acute asthma attack (wheezing, decreased air movement in airways, dyspnea). Watch children with food anaphylaxis closely because a biphasic response has been recorded in a number of cases in which there is an immediate response, apparent recovery, and acute recurrence of symptoms (Simons, 2009) (see Nursing Alert and Emergency box). Children with extremely sensitive food allergies should wear a medical identification bracelet and have an injectable epinephrine cartridge (EpiPen) readily available. (See Anaphylaxis, Chapter 42.) Any child with a history of food allergy or previous severe reaction to food should have a written emergency treatment plan and an EpiPen. Note that Benadryl and cetirizine are effective for cutaneous and nasal manifestations but not for airway manifestations (Keet, 2011).

Although the reason is unknown, many children “outgrow” their food allergies, especially to milk and eggs. Approximately 50% of all infants who are intolerant to cow’s milk usually develop tolerance by 3 to 5 years of age (Sampson and Leung, 2011). More than half (60%) of infants have an IgE-mediated reaction to cow’s milk, and 25% retain sensitivity until the second decade of life. Children who are allergic to more than one food may develop tolerance to each food at a different time. The most common allergens such as peanuts are outgrown less readily than other food allergens. Because of the tendency to lose the hypersensitivity, allergenic foods should be reintroduced into the diet after a period of abstinence (usually ≥1 year) to evaluate whether the food can safely be added to the diet. However, foods that are associated with severe anaphylactic reactions continue to present a lifelong risk and must be avoided.

Diagnosis and Therapeutic Management

The diagnosis of food allergy is made based on a number of factors, including the occurrence of anaphylaxis or any combination of 37 symptoms listed in the NIAID guidelines within minutes to hours of ingesting food or if such symptoms have occurred after the ingestion of a specific food on one or more occasions. The gold standard is the double-blind, placebo-controlled food challenge; the skin prick test and serum IgE (sIgE) measurements may be used as an adjunct to diagnose food allergy but singly should not be used for the diagnosis. The atopy patch test, intradermal test, and sIgE test are not recommended for establishing a diagnosis. A single oral food challenge may be used in certain circumstances (Boyce, Assa’ad, Burks, et al., 2010). The management of food allergy consists of avoiding the specific food or ingredient that causes the manifestations. Because children with food allergies (usually two or more) are at risk for inadequate nutrient intake and growth failure, it is recommended that they have an annual nutritional assessment to prevent such problems.

Care Management

Nursing care of children with potential food allergy consists of helping to collect vital health assessment data for the establishment of a diagnosis and helping with diagnostic tests. It is important for nurses to be informed about food allergy and provide parents, caregivers, and older children with accurate information regarding food allergy.

Educate parents, teachers, and day care workers regarding signs and symptoms of food allergy and reactions. People with food allergy should avoid unfamiliar foods and restaurants that do not disclose food ingredients. New labeling guidelines require that food additives such as spices and flavoring be labeled clearly on commercially sold, store-bought foods. Hidden ingredients in prepared foods are also potential sources of food allergy.

Children with a history of food allergy may spend a considerable amount of time in day care; therefore people working in day care centers and other children’s settings need to be educated properly regarding recognition and management of severe anaphylactic reactions (see Critical Thinking Case Study).

image Critical Thinking Case Study

Food Allergy Anaphylaxis

A group of nursing students is holding a health promotion fair at a local elementary school for first, second, and third graders. The nursing students have several booths set up in the school cafeteria. Three second-grade boys are horseplaying in front of one of the booths when one of the boys, Jason, an 8-year-old child, suddenly starts coughing and clutching his throat. The students also observe that he is developing red splotches on his face, neck, and throat and that he is scratching. Jason says, “I can’t breathe!” The school nurse is nearby and comes over to see what’s causing the commotion. One of the boys with Jason says, “We didn’t mean any harm; we were just goofing around when we put peanuts in his trail mix.” One of the student nurses says, “He’s in obvious distress. What should we do?”

1. Evidence—Is there sufficient evidence to draw any conclusions at this time about Jason’s condition?

2. Assumptions—Describe some underlying assumptions about the following:

3. What implication for nursing care exists in this situation after an intervention in the previous question has been chosen and implemented?

4. Describe the potential results of taking a “Let’s observe Jason for a few minutes before we do anything” stance in this scenario.

5. Is there evidence to support your immediate and secondary nursing interventions? Provide objective evidence to support your decisions for action.

Breastfeeding is now considered a primary strategy for avoiding atopy in families with known food allergies; however, there is no evidence that maternal avoidance (during pregnancy or lactation) of cow’s milk protein or other dietary products known to cause food allergy prevents food allergy in children (AAP, 2009; Boyce, Assa’ad, Burks, et al., 2010). Researchers indicate that delaying the introduction of highly allergenic foods past 4 to 6 months of age may not be as protective for food allergy as previously believed (Greer, Sicherer, Burks, et al., 2008). Likewise studies have shown that soy formula does not prevent allergic disease in infants and children (AAP, 2009).*

Cow’s Milk Allergy

Cow’s milk allergy (CMA) is a multifaceted disorder representing adverse systemic and local GI reactions to cow’s milk protein. Approximately 2.5% of infants develop cow’s milk hypersensitivity, with 60% of these being IgE mediated. It is estimated that 50% of these children may outgrow the hypersensitivity by 3 to 4 years of age (Sampson and Leung, 2011). Some studies suggest that milk allergy may persist and some children may not be able to tolerate milk until they are 16 years of age (AAP, 2009). (This discussion centers on cow’s milk protein contained in commercial infant formulas; whole milk is not recommended for infants younger than 12 months of age.) The allergy may be manifested within the first 4 months of life through a variety of signs and symptoms that may appear within 45 minutes of milk ingestion or after several days (Box 41-2). The diagnosis initially may be made from the history, although the history alone is not diagnostic. The timing and diversity of clinical manifestations vary greatly. For example, CMA may be manifested as colic (see Chapter 31), diarrhea, vomiting, GI bleeding, gastroesophageal reflux (GER), chronic constipation, or sleeplessness in an otherwise healthy infant.

Diagnostic Evaluation.

A number of diagnostic tests may be performed, including stool analysis for blood, eosinophils, and leukocytes (both frank and occult bleeding can occur from the colitis); sIgE levels; skin-prick or scratch testing; and radioallergosorbent test (RAST) (measures IgE antibodies to specific allergens in serum by radioimmunoassay). Both skin testing and RAST may help identity the offending food, but the results are not always conclusive. No single diagnostic test is considered definitive for the diagnosis (AAP, 2009). In breastfed infants cow milk protein products should be eliminated (by the mother) to improve the diagnostic results (Kattan, Cocco, and Järvinen, 2011).

The most definitive diagnostic strategy is elimination of milk in the diet followed by challenge testing after improvement of symptoms. A clinical diagnosis is made when symptoms improve after removal of milk from the diet and two or more challenge tests produce symptoms (Ewing and Allen, 2005; Kattan, Cocco, and Järvinen, 2011). Challenge testing involves reintroducing small quantities of milk in the diet to detect resurgence of symptoms; at times it involves the use of a placebo so the parent is unaware of (or “blind” to) the timing of allergen ingestion. A double-blind, placebo-controlled food challenge is the gold standard for diagnosing food allergies such as CMA, yet it may not be used often for diagnosing CMA because of the expense, time involved, and risk for further exposure and anaphylactic reaction (Ewing and Allen, 2005). Careful observation of the child is required during a challenge test because of the possibility of anaphylactic reaction.

Therapeutic Management.

Treatment of CMA is elimination of cow’s milk–based formula and all other dairy products. For infants fed cow’s milk–based formula, this primarily involves changing the formula to a casein hydrolysate milk formula (Pregestimil, Nutramigen, or Alimentum) in which the protein has been broken down into its amino acids through enzymatic hydrolysis. Although the AAP (2009) recommends the use of extensively hydrolyzed formulas for CMA, many practitioners may start a soy formula instead because of the expense of the hydrolyzed formulas. Approximately 50% of infants who are sensitive to cow’s milk protein also demonstrate sensitivity to soy, but soy is less expensive than protein hydrolysate formula. Other choices for children who are intolerant to cow’s milk–based formula are the amino acid–based formulas Neocate or EleCare, but their cost is a major consideration. Goat’s milk (raw) is not an acceptable substitute because it cross-reacts with cow’s milk protein, is deficient in folic acid, has a high sodium and protein content, and is unsuitable as the only source of calories. Some suggest that goat’s milk infant formula may be a suitable substitute for cow’s milk formula (Basnet, Schneider, Gazit, et al., 2010). Infants usually remain on the milk-free diet for 12 months, after which time small quantities of milk are reintroduced.

Children who have CMA may tolerate extensively heated cow’s milk (Nowak-Wegrzyn, Bloom, Sicherer, et al., 2008). One study reports that these children became tolerant to uncooked milk products over time after consuming baked milk products (Kim, Nowak-Wegrzyn, Sicherer, et al., 2011).

Care Management

The principal nursing objectives are identification of potential CMA and appropriate counseling of parents regarding substitute formulas. Parents often interpret GI symptoms such as spitting up and loose stools or fussiness as indications that the infant is allergic to cow’s milk and switch the infant to a variety of formulas in an attempt to resolve the problem.

Parents need much reassurance regarding the needs of nonverbal infants with such an array of symptoms. Endless nights of lost sleep and a crying infant may promote feelings of parenting inadequacy and role conflict, thus aggravating the situation. Nurses can reassure parents that many of these symptoms are common and the reasons are often never found, yet the child does achieve appropriate growth and development. Report acute symptoms to the practitioner for further evaluation. Parents need reassurance that the infant will receive complete nutrition from the new formula and will have no ill effects from the absence of cow’s milk.

When solid foods are started, parents need guidance in avoiding milk product. Carefully reading all food labels helps avoid exposure to prepared foods containing milk products. Although labeled as nondairy, milk, cream, and butter substitutes may contain cow’s milk protein (Kattan, Cocco, Järvinen, et al., 2011).

Lactose Intolerance

Lactose intolerance refers to at least four different entities that involve a deficiency of the enzyme lactase, which is needed for the hydrolysis or digestion of lactose in the small intestine; lactose is hydrolyzed into glucose and galactose. Congenital lactase deficiency occurs soon after birth after the newborn has consumed lactose-containing milk (human milk or commercial formula). This inborn error of metabolism involves the complete absence or severely reduced presence of lactase, is extremely rare, and requires a lifelong lactose-free or extremely reduced lactose diet.

Primary lactase deficiency, sometimes referred to as late-onset lactase deficiency, is the most common type of lactose intolerance and is manifested usually after 4 or 5 years of age, although the time of onset is variable. Ethnic groups with a high incidence of lactase deficiency include Asians, southern Europeans, Arabs, Israelis, and African-Americans; Scandinavians tend to have the lowest incidence. Lactose malabsorption manifests as lactose intolerance and is characterized by an imbalance between the ability for lactase to hydrolyze the ingested lactose and the amount of lactose ingested (Heyman and AAP Committee on Nutrition, 2006).

Secondary lactase deficiency may occur secondary to damage of the intestinal lumen, which decreases or destroys the enzyme lactase. Cystic fibrosis; sprue; celiac disease; kwashiorkor; and infections such as giardiasis, HIV, or rotavirus may cause a temporary or permanent lactose intolerance.

Developmental lactase deficiency refers to the relative lactase deficiency observed in preterm infants of less than 34 weeks of gestation (Heyman and AAP Committee on Nutrition, 2006).

The primary symptoms of lactose intolerance include abdominal pain, bloating, flatulence, and diarrhea after the ingestion of lactose. The onset of symptoms occurs within 30 minutes to several hours of lactose consumption. Lactose intolerance is often perceived as an allergy; and, in several studies with reports of acute GI symptoms ascribed to lactose intolerance, measurement of lactase activity is normal.

Lactose intolerance may be diagnosed on the basis of the history and improvement with a lactose-reduced diet. The breath hydrogen test is used to positively diagnose the condition. Breath samples in lactose-deficient individuals yield a higher percentage of hydrogen (≥20 parts per million [ppm] above baseline). In infants lactose malabsorption may be diagnosed by evaluating fecal pH and reducing substances; fecal pH in infants is usually lower than in older children, but an acidic pH may indicate malabsorption (Heyman and AAP Committee on Pediatrics, 2006).

Treatment of lactose intolerance is elimination of offending dairy products; however, some advocate decreasing amounts of dairy products rather than total elimination, especially in small children (Heyman and AAP Committee on Nutrition, 2006). In infants lactose-free or low-lactose formula offers no special advantages over lactose-containing formula except in those who are severely malnourished (Heyman and AAP Committee on Pediatrics, 2006).

One concern is that dairy avoidance in children and adolescents with lactose intolerance contributes to reduced bone mineral density and osteoporosis (AAP, 2009; Suchy, Brannon, Carpenter, et al., 2010). Evidence indicates that dietary lactose enhances calcium absorption and that lactose-free diets may negatively affect bone mineralization (Heyman and AAP Committee on Nutrition, 2006). It is recommended that individuals with lactose maldigestion who do not experience lactose intolerance symptoms continue to consume small amounts of dairy products with meals to prevent reduced bone mass density and subsequent osteoporosis. Some evidence indicates that probiotics (food preparations containing microorganisms such as Lactobacillus, which alter the GI microflora and thus are beneficial to the host) improve lactose intolerance when live cultures are fermented in dairy products (de Vrese and Schrezenmeir, 2008). The positive attributes of probiotics for those with lactose maldigestion include delayed GI transit (slower than milk), positive effects on intestinal and colonic microflora, and a reduction of maldigestion symptoms.

Most people are able to tolerate small amounts of lactose (≈1 cup of milk per day) even in the presence of deficient lactase activity (Heyman and AAP Committee on Nutrition, 2006; Suchy, Brannon, Carpenter, et al., 2010) and should be encouraged to continue their intake of dairy products in small amounts to obtain much-needed nutrients. Milk taken at meals may be better tolerated than when taken alone (see Family-Centered Care box). Pretreated milk (with microbial-derived lactase) is reported to be effective in improving lactose absorption. Because dairy products are a major source of calcium and vitamin D, supplementation of these nutrients is needed to prevent deficiency. Yogurt contains inactive lactase enzyme, which is activated by the temperature and pH of the duodenum; this lactase activity substitutes for the lack of endogenous lactase. Fresh, plain yogurt may be tolerated better than frozen or flavored yogurt; hard cheeses, lactase-treated dairy products, and lactase tablets taken with dairy products are also viable options. An important distinction between lactose intolerance and food allergy is that lactose intolerance does not manifest as an anaphylactic-type reaction.

Sep 16, 2016 | Posted by in NURSING | Comments Off on Gastrointestinal Dysfunction

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