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 American Academy of Pediatrics (AAP) (2008) recommends that infants who are exclusively breastfed 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). Non-breastfed 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, 2006). Children with chronic illnesses resulting in anorexia, decreased food intake, or possible nutrient malabsorption as a result of multiple medications should be carefully evaluated 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 study’s findings (Kawchak, Schall, Zemel, and others, 2007). One study found that children with intestinal failure who were being transitioned from parenteral nutrition 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, and others, 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 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). 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, Chapter 32.)

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 whose exact role in nutrition is still unclear. The greatest concern with minerals is deficiency, especially iron-deficiency anemia (see Chapter 26). 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 inadvertently overlooked when a child with intestinal failure or recent surgery is making the transition from total parenteral intake 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 by 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.

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.

Nursing 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 12, and Nutritional Assessment, Chapter 6). After assessment data are collected, this information is evaluated against standard intakes to identify areas of concern. One source of standard nutrient intakes is the Dietary Reference Intakes (see Chapter 12).

Standardized growth reference charts are 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 (Chumlea, 2005). The World Health Organization (WHO) growth chart is a standardized growth reference now recommended for infants and toddlers up to age 24 months. This growth chart includes head circumference, height, and weight references which 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’s growth charts are now recommended for children 2 to 19 years of age (Grummer-Strawn, Reinold, Krebs, and others, 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 10). 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 exclusively breastfed 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 Nutrition, Chapter 10). A variety of foods should be introduced during the early years to ensure a well-balanced intake. Infants who have particular nutritional deficits should be identified; a multidisciplinary approach should be taken to identify the deficit and the etiology, and to establish a plan 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 of malnutrition, 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 Growth Failure [Failure to Thrive], p. 362). PEM may also be seen in persons with chronic health problems such as cystic fibrosis, renal dialysis, cancer, and GI malabsorption; in elderly adults who have chronic malnutrition; and in persons 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 (Katz, Mahlberg, Honig, and others, 2005; Tierney, Sage, and Shwayder, 2010). The rice drink contains 0.13 g of protein per ounce (compared with the 0.5 g found in human milk and infant formulas) and is an inadequate source of nutrition for children. Other reported cases of kwashiorkor in developed countries involved infants who were fed nonstandard infant diets such as flour water, corn porridge, molasses, and nondairy creamer (Katz, Mahlberg, Honig, and others, 2005). 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 (Liu, Howard, Mancini, and others, 2001). 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.

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 (Boyce, Assa’ad, Burks, and others, 2010) as “an adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food” (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, and others, 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, and others, 2010). 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 to cow’s milk, not allergic as is the first person described. 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, and others, 2010). The exact prevalence of food allergies in children is reported to be much lower than what 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 1.0% 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, and others, 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, but far fewer will ever tolerate tree nut and peanuts (Boyce, Assa’ad, Burks, and others, 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, and others, 2010) guidelines also recommend the following:

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, and others, 2010) indicates that sensitization alone is not sufficient to classify as a food allergy; rather, an immune-mediated response and manifestation of specific signs and symptoms are necessary to categorize an individual as having a food allergy. The most common food allergens are listed in Box 11-1.

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 (2–48 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 allergy have a 50% or greater risk of developing allergy; children who have both parents with allergy have up to a 100% risk of developing allergy. 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 (5–30 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 then acute recurrence of symptoms (Simons, 2009) (see Nursing Alert and Drug Alert). Children with extremely sensitive food allergies should wear a medical identification bracelet and have an injectable epinephrine cartridge (EpiPen) readily available. (See Anaphylaxis, Chapter 25.) Any child with a history of food allergy or previous severe reaction to food should have a written emergency treatment plan, as well as 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. About 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 be safely added to the diet. Foods that are associated with severe anaphylactic reactions, however, continue to present a lifelong risk and must be avoided.

Growth Failure (Failure to Thrive)

Growth failure, or failure to thrive (FTT), is a sign of inadequate growth resulting from an inability to obtain or use calories required for growth. FTT has no universal definition, although one of the more common criteria is a weight (and sometimes height) that falls below the fifth percentile for the child’s age. Another definition of FTT includes a weight for age (height) z value of less than −2.0 (a z value is a standard deviation value that represents anthropometric data normalizing for sex and age with greater precision than growth percentile curves [Markowitz, Watkins, and Duggan, 2008]). A third way to define FTT is a weight curve that crosses more than 2 percentile lines on a standardized growth chart after previous achievement of a stable growth pattern. Weight for length is reported to be a better indicator of acute undernutrition (Cole and Lanham, 2011). Growth measurements alone are not used to diagnose children with FTT. Rather, the finding of a pattern of persistent deviation from established growth parameters is cause for concern. In addition to lack of consensus on the precise definition of FTT, some advocate for a change in terminology; thus, terms such as growth failure and pediatric undernutrition are used in the literature for FTT (Locklin, 2005). Another term seen in the literature is weight or growth faltering. According to Cole and Lanham (2011), approximately 5% to 10% of children in primary care in the United States have FTT with the majority presenting before the age of 18 months.

Some experts suggest that the previously used classifications of organic FTT and nonorganic FTT are too simplistic because most cases of growth failure have mixed causes; they suggest that FTT be classified according to pathophysiology in the following categories (Krugman and Dubowitz, 2003):

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