Health Problems During Infancy

• Children who are exclusively breast-fed by mothers with an inadequate intake of vitamin D or are exclusively breast-fed longer than 6 months without adequate maternal vitamin D intake or supplementation

• Children with dark skin pigmentation who are exposed to minimal sunlight because of socioeconomic, religious, or cultural beliefs or housing in urban areas with high levels of pollution

• Children with diets that are low in sources of vitamin D and calcium

• Individuals who use milk products not supplemented with vitamin D (e.g., yogurt,* raw cow’s milk) as the primary source of milk

Lacto-ovo vegetarians, who exclude meat from their diet but consume dairy products and rarely fish

Lactovegetarians, who exclude meat and eggs but drink milk

Pure vegetarians (vegans), who eliminate any food of animal origin, including milk and eggs

Macrobiotics, who are even more restrictive than pure vegetarians, allowing only a few types of fruits, vegetables, and legumes

Semivegetarians, who consume a lacto-ovo vegetarian diet with some fish and poultry (an increasingly popular form of vegetarianism that poses little or no nutritional risk to infants unless dietary fat and cholesterol intake are severely restricted)

1. Grains (cereal, rice, pasta) and legumes (beans, peas, lentils, peanuts)

2. Grains and milk products (milk, cheese, yogurt)

3. Seeds (sesame, sunflower) and legumes

Kwashiorkor

Kwashiorkor has been defined as primarily 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. Some evidence, however, supports a multifactorial etiology, including cultural, psychologic, and infective factors that may interact to place the child at risk for kwashiorkor. Penny (2003) suggests that kwashiorkor may result from the interplay of nutrient deprivation and infectious or environmental stresses, which produces an imbalanced response to such insults. Kwashiorkor 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 (Penny, 2003). 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 arachidonic acid seems to have an interactive role in its development (Penny, 2003).

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 (Fig. 13-1). 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 are common, especially iron, calcium, and zinc. 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

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 breast-feeding 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 suffers from 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 smaller head size and slower recovery after treatment.

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 (2003) proposes 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 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 the child who has been malnourished and refed too rapidly.

Vitamin and mineral supplementation are 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. Breast-feeding 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 (Penny, 2003).

The World Health Organization (2006) issued a statement recognizing the importance of breast-feeding for the first 6 months in developing countries where HIV is prevalent among childbearing women and children. The World Health Organization recognizes that appropriate sources of food and water for infants may not be available once the 6 months are concluded and that the risk for malnutrition is greater among such children than the theoretical risk of HIV. However, the organization does recommend that breast-feeding continue after 6 months with the introduction of complementary foods, provided these 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 will not tolerate a high-energy and high-protein source initially. A number of food sources may be provided to treat PEM. They include oral rehydration solutions (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 (Ciliberto, Sandige, Ndehka, et al, 2005; Amadi, Mwiya, Chomba, et al, 2005) (see Cultural Competence box).

Nursing Care Management

Because PEM appears early in childhood, primarily in children 6 months to 2 years of age, and is associated with early weaning, low-protein diet, delayed introduction of complementary foods, and frequent infections (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. Breast-feeding is the optimal method of feeding for the first 6 months. The immune properties naturally found in breast milk not only nourish the infant 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 the breast, 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 in infants too weak to breast- or bottle-feed. Oral rehydration with an approved oral rehydration solution 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). The 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 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 suffer from emotional starvation as well, care should be consistent with care of the child with growth failure (p. 534).

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

Systemic—Anaphylactic, growth failure

GI—Abdominal pain, vomiting, cramping, diarrhea

Respiratory—Cough, wheezing, rhinitis, infiltrates

Cutaneous—Urticaria, rash, atopic dermatitis

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; 80% of those children may outgrow the hypersensitivity by 4 years of age (Sampson, 2004). Recent studies reveal that milk allergy may persist and some children may not be able to tolerate milk until they are 16 years of age (American Academy of Pediatrics, 2009). (This discussion centers on cow’s milk protein contained in commercial infant formulas; whole milk is not recommended for infants <12 months of age.) The hypersensitivity 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 13-3). The diagnosis may initially 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 p. 532), diarrhea, vomiting, GI bleeding, gastroesophageal reflux, chronic constipation, or sleeplessness in an otherwise healthy infant.

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. It is rare and requires 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 varies. Ethnic groups with a high incidence of lactase deficiency include Asians, southern Europeans, Arabs, Israelis, and African-Americans, whereas Scandinavians tend to have the lowest. Lactose malabsorption manifests as lactose intolerance and is characterized by an imbalance between the ability of lactase to hydrolyze the ingested lactose and the amount of lactose ingested (Heyman and American Academy of Pediatrics, 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; or infections such as giardiasis, HIV, or rotavirus may cause 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 American Academy of Pediatrics, 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 (Goldberg, Folta, and Must, 2002).

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 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 American Academy of Pediatrics, 2006).

Treatment of lactose intolerance involves elimination of offending dairy products; however, some advocate decreasing amounts of dairy products rather than total elimination, especially in small children (Heyman and American Academy of Pediatrics, 2006; Goldberg, Folta, and Must, 2002). In infants lactose-free or low-lactose formula offers no special advantages over lactose-containing formula, except in the severely malnourished (Heyman and American Academy of Pediatrics, 2006).

One concern is that dairy avoidance in children and adolescents with lactose intolerance contributes to reduced bone mineral density and osteoporosis (Sibley, 2004). There is evidence that dietary lactose enhances calcium absorption and that lactose-free diets may negatively affect bone mineralization (Heyman and American Academy of Pediatrics, 2006). Individuals with lactose maldigestion who do not experience lactose intolerance symptoms should continue to consume small amounts of dairy products with meals to prevent reduced bone mass density and subsequent osteoporosis (Sibley, 2004). In one study a decreased intake of calcium-containing dairy foods in early adolescent girls with perceived lactose intolerance resulted in lower spinal bone mineral content than in girls without perceived milk intolerance; the researchers cautioned that decreased dairy intake in persons with lactose intolerance may increase the risk of osteoporosis in later life (Matlik, Savaiano, McCabe, et al, 2007). One option to meet calcium intake needs of adolescents with dairy restriction due to lactose intolerance is to consume one half to one and a half servings of calcium-fortified citrus juice per day; vitamin D supplementation and increased physical activity are also recommended to increase bone health (Gao, Wilde, Lichtenstein, et al, 2006). There is evidence 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; Zeisel and Erickson, 2003). 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 even in the presence of deficient lactase activity (Heyman and American Academy of Pediatrics, 2006) 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 hypersensitivity is that lactose intolerance does not manifest as an anaphylactic-type reaction.

• Feeding too much or too little food

• Feeding too often, especially during the night, or too infrequently

• Selecting inappropriate foods for the infant’s physiologic and motor development

• Incorrectly preparing formula

Regurgitation—Return of undigested food from the stomach, usually accompanied by burping

Spitting up—Dribbling of unswallowed formula from the infant’s mouth immediately after a feeding

Etiology

Among the theories investigated as potential causes are too rapid feeding, overeating, swallowing excessive air, improper feeding technique (especially in positioning and burping), and emotional stress or tension between parent and child. Although all these may occur, there is no evidence that one factor is consistently present. Infants with CMA symptoms have a high rate of colic (44%), and eliminating cow’s milk products from the infant’s diet can reduce the symptoms. However, there is considerable controversy about the role of allergy and colic because there does not appear to be an increased incidence of atopy in infants with colic (Sicherer, 2003).

Parental smoking, strained parent-infant interaction, lactase deficiency, difficult infant temperament, difficulty regulating emotions, overstimulation, central nervous system immaturity, and neurochemical dysregulation in the brain have also been proposed as potential causes of colic (Ellett, 2003; Neu and Robinson, 2003). A positive association between consumption of fruit juices (carbohydrate malabsorption) and colic has been demonstrated in some cases (Duro, Rising, Cedillo, et al, 2002). Some experts have suggested that gastroesophageal reflux is a cause of colic, but studies have not supported this theory (St. James-Roberts, 2008). The consensus of many experts who study colic is that it is multifactorial and that no single treatment for every colicky infant will be effective in alleviating the symptoms.

Therapeutic Management

Management of colic should begin with an investigation of possible organic causes, such as CMA, intussusception, or other GI problem. If a sensitivity to cow’s milk is strongly suspected, a trial substitution of another formula such as an extensively hydrolyzed (Nutramigen, Alimentum, Pregestimil), whey hydrolysate, or amino acid (Neocate, EleCare) formula is warranted. Soy formulas are usually avoided because of the possibility of sensitivity to soy protein as well (American Academy of Pediatrics, 2009). Oral administration of Lactobacillus reuteri to colicky breast-fed infants decreased symptoms within 1 week of initiation in one small study (Savino, Pelle, Palumeri, et al, 2007).

When no specific inciting agent can be found, the supportive measures discussed under Nursing Care Management are employed.

The use of drugs, including sedatives, antispasmodics, antihistamines, and antiflatulents, is sometimes recommended. The most commonly used sedatives are phenobarbital, hydroxyzine hydrochloride (Atarax), and chloral hydrate. Simethicone (Mylicon) may also help allay the symptoms of colic. However, in most controlled studies none of these drugs completely reduced the symptoms of colic. Herbal (chamomile) tea offered at the onset of crying and up to three times daily has proved effective in relieving the symptoms of colic in some infants (Weizman, Alkrinawi, Goldfarb, et al, 1993); however, parents are to be cautioned regarding the unknown safety of this treatment (Crotteau, Wright, and Eglash, 2006). Behavioral interventions have not proved effective at reducing symptoms of colic but have helped parents deal with the crying infant in a more positive manner. The addition of lactase to infant formula has produced mixed results as far as abatement of overall symptoms.

One study found that a combination of interventions—massage, herbal tea, sucrose solution, and hydrolyzed formula—decreased crying in reported colicky infants; the administration of the hydrolyzed formula achieved best results, whereas massage was least effective at reducing crying (Arikan, Alp, Gozum, et al, 2008).

An extensive review of a wide variety of interventions for colic indicates there are no specific safe remedies to alleviate symptoms of colic in every infant. Dietary changes, such as eliminating cow’s milk protein from the lactating mother’s diet, and behavioral interventions were shown to be effective in helping parents reduce stimulation and respond to the infant’s crying, yet these interventions are perceived only as moderately effective (Joanna Briggs Institute, 2008). Administering sucrose was effective at reducing crying in colicky infants for a short period (3 to 30 minutes) (Joanna Briggs Institute, 2008).

The literature on colic contains many behavioral remedies for treatment; however, none has proved entirely effective at reducing the symptoms of colic in all infants treated. Studies on infant massage for relieving the symptoms of colic demonstrated no advantage, and the practice is not recommended (Roberts, Ostapchuk, and O’Brien, 2004). The Internet offers a variety of remedies for colic. Parents should be aware of the sources of information and use home remedies such as herbal teas or natural remedies touted for colic relief cautiously.

A survey of pediatric nurse practitioners (PNPs) and pediatricians managing infants with colic found that the PNPs were more likely to suggest behavioral or environmental modification strategies, whereas the pediatricians predominantly suggested pharmacologic interventions or formula changes (Lobo, Kotzer, Keefe, et al, 2004). The study emphasized the lack of understanding and consensus regarding the etiology and management of infant colic.

Nursing Care Management

The initial step in managing colic is to take a thorough, detailed history of the usual daily events. Areas that should be stressed include (1) the infant’s diet; (2) the diet of the breast-feeding mother; (3) the time of day when crying occurs; (4) the relationship of crying to feeding time; (5) the presence of specific family members during crying and habits of family members, such as smoking; (6) activity of the mother or usual caregiver before, during, and after crying; (7) characteristics of the cry (duration, intensity); (8) measures used to relieve crying and their effectiveness; and (9) the infant’s stooling, voiding, and sleeping patterns. Of special emphasis is a careful assessment of the feeding process via demonstration by the parent.

If cow’s milk sensitivity is suspected, breast-feeding mothers should follow a milk-free diet (see Box 13-3) for a minimum of 3 to 5 days in an attempt to reduce the infant’s symptoms. Caution mothers that some nondairy creamers may contain calcium caseinate, a cow’s milk protein. If a milk-free diet is helpful, lactating mothers may need calcium supplements to meet the body’s requirement. Bottle-fed infants may improve with the same dietary modifications as for the child with CMA (see p. 530).

One important nursing intervention (before or after organic cause has been eliminated) is reassuring both parents they are not doing anything wrong and that the infant is not experiencing any physical or emotional harm. Parents, especially mothers, become easily frustrated with the infant’s crying and perceive this as a sign that something is horribly wrong. Additionally, colicky infants may be at increased risk for being shaken by the caregiver and experiencing traumatic brain injury. A survey of fathers of colicky infants revealed that professional assistance was limited. The fathers described the experience of having a colicky infant as like falling into an abyss from which they had to climb with the assistance of family and friends, thus reinforcing the importance of empathetic nurses (Ellett, Appleton, and Sloan, 2009). An empathetic, gentle, and reassuring attitude, in addition to suggestions for treatment, will help allay parents’ anxieties, which are usually exacerbated by loss of sleep and preoccupation over the infant’s welfare. Colic disappears spontaneously, usually by 3 to 4 months of age, although guarantees should never be given, since it may continue for much longer. Other support persons and extended family members may be enlisted to support the parents during this difficult time.*

When no specific organic or behavioral cause can be identified, it is preferable to determine the time of the onset of crying and attempt to manipulate the circumstances associated with it. For example, some infants have episodes of colic around the family’s dinner time, when all household members are home and often tired and busy. The overstimulating, tense atmosphere may upset the infant. Changing the evening routine, such as encouraging someone other than the mother or primary caregiver to prepare dinner, preparing dinner earlier in the day, and feeding the infant in a quieter area of the house, may help. Other approaches for relieving colic are listed in the Family-Centered Care box and shown in Fig. 13-2. Encourage parents to try as many of these approaches as possible, since not all are effective for every infant.

One author suggests that a problem-solving discussion with the parents, in addition to acknowledgment that the infant has colic, is an optimal strategy for helping parents manage the infant with colic until a cure is found (Ellett, 2003). Nurses must also be aware that once colic symptoms are resolved, family function may be negatively impacted by residual feelings and emotions experienced during the acute phase of the colic (Ellett, Schuff, and Davis, 2005). Practical parental support interventions include the provision of a colic hotline (mother-to–nurse practitioner or nurse) and nurse-managed colic support groups (Ellett, Schuff, and Davis, 2005).

Inadequate caloric intake—Incorrect formula preparation, neglect, food fads, excessive juice consumption, poverty, behavioral problems affecting eating, or central nervous system problems affecting intake

Inadequate absorption—Cystic fibrosis, celiac disease, vitamin or mineral deficiencies, biliary atresia, or hepatic disease

Increased metabolism—Hyperthyroidism, congenital heart defects, or chronic immunodeficiency

Defective utilization—Genetic anomaly such as trisomy 21 or 18, congenital infection, or metabolic storage diseases

Diagnostic Evaluation

Diagnosis is initially made from evidence of growth failure. If FTT is recent, the weight, but not the height, is below accepted standards (usually the 5th percentile); if FTT is longstanding, both weight and height are low, indicating chronic malnutrition. Perhaps as important as anthropometric measurements are a complete health and dietary history (including perinatal history), physical examination for evidence of organic causes, developmental assessment, and family assessment. A dietary intake history, either a 24-hour food intake or a history of food consumed over a 3- to 5-day period, is also essential. In addition, explore the child’s activity level, parental height, perceived food allergies, and dietary restrictions. An assessment of household organization and mealtime behaviors and rituals is important in the collection of pertinent data. It is often helpful to obtain the growth patterns of the affected child’s parents and siblings; these can be compared with norm-referenced standards to evaluate the child’s growth (Markowitz, Watkins, and Duggan, 2008). An assessment of the home environment and child-parent interaction may be helpful as well. Other tests (lead toxicity, anemia, stool-reducing substances, occult blood, ova and parasites, alkaline phosphatase, and zinc levels) are selected only as indicated to rule out organic problems. In most cases laboratory studies are of little diagnostic value (American Academy of Pediatrics, 2009). To prevent the overuse of diagnostic procedures, consider FTT early in the differential diagnosis. To avoid the social stigma of FTT during the early investigative phase, some health care workers use the term growth delay (or failure) until the actual cause is established.

Therapeutic Management

The primary management of FTT is aimed at reversing the cause of the growth failure. If malnutrition is severe, the initial treatment is directed at reversing the malnutrition. The goal is to provide sufficient calories to support “catch-up” growth—a rate of growth greater than the expected rate for age. The following formula may be used to calculate required caloric intake:

In this formula ideal weight for height is the median weight for the child’s height based on the current National Center for Health Statistics weight-for-height growth charts.

In addition to adding caloric density to feedings, the child may require multivitamin supplements and dietary supplementation with high-calorie foods and drinks. Any coexisting medical problems are treated.

In most cases of FTT an interdisciplinary team of physician, nurse, dietitian, child life specialist, occupational therapist, pediatric feeding specialist, and social worker or mental health professional is needed to deal with the multiple problems. Make efforts to relieve any additional stresses on the family by offering referrals to welfare agencies or supplemental food programs. In some cases family therapy may be required. Temporary placement in a foster home may relieve the family’s stress, protect the child, and allow the child some stability if insurmountable obstacles are preventing appropriate family function. Behavior modification aimed at mealtime rituals (or lack thereof) and family social time may be required. Hospitalization admission is indicated for (1) evidence (anthropometric) of severe acute malnutrition, (2) child abuse or neglect, (3) significant dehydration, (4) caretaker substance abuse or psychosis, (5) outpatient management that does not result in weight gain, and (6) serious intercurrent infection (American Academy of Pediatrics, 2009; Block, Krebs, and Committee on Child Abuse and Neglect and Committee on Nutrition [American Academy of Pediatrics], 2005).

Prognosis

The prognosis for FTT is related to the cause. If the parents have simply not understood the infant’s needs, teaching may remedy the child’s limited caloric intake and permanently reverse the growth failure. Inadequate or infrequent feeding periods by the infant’s primary caretaker, in conjunction with family disorganization, are often observed to be the cause of FTT.

Few long-term studies provide data on the prognosis for children with FTT; however, some studies indicate that children who had FTT as infants had shorter heights, lower weights, and lower scores on measures of psychomotor development than peers (Black, Dubowitz, Krishnakumar, et al, 2007; Rudolf and Logan, 2005). Factors related to poor prognosis are severe feeding resistance, lack of awareness in and cooperation from the parent(s), low family income, low maternal educational level, adolescent mother, preterm birth, intrauterine growth restriction, and early age of onset of FTT. Because later cognitive and motor function is affected by malnourishment in infancy, many of these children are below normal in intellectual development, have poorer language development and less well-developed reading skills, attain lower social maturity, and have a higher incidence of behavioral disturbances (Markowitz, Watkins, and Duggan, 2008). Such findings indicate that a long-term plan and follow-up care are needed for the optimum development of these children.

Nursing Care Management

Caring for the child with FTT presents many nursing challenges, whether treatment takes place in the hospital, clinic, or home. Providing a positive feeding environment, teaching the parent successful feeding strategies, and supporting the child and family are essential components of care.

Nurses play a critical role in the diagnosis of FTT through their assessment of the child, parents, and family interactions. Knowledge of the characteristics of children with FTT and their families is essential in helping identify these children and hastening the confirmation of a diagnosis. Accurate assessment of initial weight and height and daily weight, as well as recording of all food intake, is mandatory. The nurse documents the child’s feeding behavior and the parent-child interaction during feeding, other caregiving activities, and play. One available feeding observation instrument is the Nursing Child Assessment Satellite Training (NCAST) Feeding Scale, which is designed to assess the feeding interaction of infants up to 12 months of age (Barnard, Hammond, Booth, et al, 1993).* (See Nutritional Assessment, Chapter 6.)

The nurse should assess the approximate developmental age on admission by administering an appropriate developmental test. Only after objective measurements are available is a care plan for stimulation outlined. The nursing admission history and ongoing assessment should also focus on the following characteristics that have been identified in many of these children and their parents.

Nutritional Management

Four primary goals in the nutritional management of FTT are to (1) correct nutritional deficiencies and achieve ideal weight for height, (2) allow for catch-up growth, (3) restore optimum body composition, and (4) educate the parents or primary caregivers regarding the child’s nutritional requirements and appropriate feeding methods (Corrales and Utter, 2005; Maggioni and Lifshitz, 1995). For infants, 24 kcal/oz formulas may be provided to increase caloric intake; older children (1 to 6 years) may benefit from a 30 kcal/oz formula (American Academy of Pediatrics, 2009). Other carbohydrate additives include fortified rice cereal and vegetable oil. Because vitamin and mineral deficiencies may occur, multivitamin supplementation, including zinc and iron, is recommended. For toddlers, a high-calorie milk drink such as PediaSure may be used to increase caloric intake. Carefully monitor for signs of intolerance to the formula. Usually only in extreme cases of malnourishment are tube feedings or intravenous therapy required.

Because maladaptive feeding practices often contribute to growth failure, give parents specific step-by-step directions for formula preparation, as well as a written schedule of feeding times. Avoid juices in children with growth failure until adequate weight gain has been achieved with appropriate milk sources; thereafter give no more than 4 oz/day of juice.

Behavior-modification techniques may be used with older infants and toddlers to interrupt poor feeding patterns. Feeding times may actually involve “struggles of will” in cases of maladaptive feedings that result in FTT. These behaviors are different from the occasional toddler behavior of food refusal, which is primarily developmental, not pathologic. The association of appropriate food with good or bad behaviors and consequent rewards may be part of the complex problem. In severe cases of malnourishment, tube feedings or intravenous therapy may be required.

In addition to attending to the child’s physical needs, the interdisciplinary team must plan care for appropriate developmental stimulation. After an approximate developmental age is established, a planned program of play is begun. Ideally a child life specialist is involved to implement and supervise the stimulation program. Every effort is made to teach the parent how to play and interact with the child.

Nursing care of these children involves a “family systems” approach. In other words, for the entire family to become healthy, each member must be helped to change. Care of the parents is aimed at helping them improve their self-esteem by acquiring positive, successful parenting skills. Initially this necessitates providing an environment in which they feel welcomed and accepted. Depending on the cause of FTT, many children are treated on an outpatient basis.

Pathophysiology and Clinical Manifestations

Diaper dermatitis is caused by prolonged and repetitive contact with an irritant, principally urine, feces, soaps, detergents, ointments, and friction. Although the obvious irritant in the majority of incidences is urine and feces, the specific components that contribute to irritation include a combination of factors (Fig. 13-4).

Prolonged contact of the skin with diaper wetness affects several skin properties. Continuous moisture exposure enhances permeability to exogenous materials, produces maceration, increases susceptibility to friction damage, increases transepidermal permeability, and increases microbial counts. Irritant exposure also affects the epidermal barrier structure and function, further increasing permeability and inflammation. Therefore healthy skin, specifically the stratum corneum, becomes less resistant to potential irritants.

Although ammonia was once thought to cause diaper rash because of the association between the strong odor on diapers and dermatitis, ammonia alone is not sufficient. The irritant quality of urine is related to an increase in pH from the breakdown of urea in the presence of fecal urease. The increased pH promotes the activity of fecal enzymes, principally proteases and lipases, which act as irritants. Fecal enzymes also increase the permeability of skin to bile salts, another potential irritant in feces. Researchers believe the decreased incidence of diaper dermatitis in breast-fed infants is related to this interaction between pH and fecal enzymes, since feces from breast-fed infants have lower fecal enzyme activity and lower pH.

The eruption of diaper dermatitis occurs primarily on convex surfaces or in the folds (intertriginous areas), and the lesions can represent a variety of types and configurations. Eruptions commonly involve the skin in most intimate contact with the diaper (e.g., the convex surfaces of buttocks, inner thighs, mons pubis, and scrotum). However, lesions not involving the folds are likely to be caused by chemical irritants, especially from urine and feces (Fig. 13-5). Other causes are detergents or soaps from inadequately rinsed cloth diapers or the chemicals (alcohol) in disposable wipes. Dyes in disposable diapers have also been cited as causing diaper dermatitis.

Perianal involvement is usually the result of chemical irritation from feces, especially diarrheal stools. Candida albicans infection produces bright red, confluent lesions with raised borders and often with satellite lesions (Fig. 13-6). The infected area usually includes the folds and is painful. Risk factors for development of Candida infection are an altered immune status and antibiotic therapy.

Therapeutic Management

Treatment is primarily aimed at prevention of diaper dermatitis. A number of interventions are discussed under Nursing Care Management. For inflammations that do not respond to these interventions, topical glucocorticoid preparations are sometimes required. If steroids are prescribed, their use is limited to low-potency preparations, such as a 0.5% or 1% hydrocortisone cream. Potential side effects include striae, epidermal atrophy, suppression of the pituitary-adrenal axis, cessation of longitudinal growth, and Cushing syndrome from chronic use. Topical antifungals are used to treat candidal infections and include clotrimazole, miconazole, ketoconazole, and nystatin ointment. When C. albicans is present elsewhere, oral administration of a fungicide is advised because the GI tract is usually the source of infection. (See Candidiasis, Chapter 9.)

Nursing Care Management

Nursing interventions are aimed at altering the three factors considered to produce dermatitis: wetness (hydration), pH, and fecal irritants. The most significant factor amenable to intervention is the moist environment created in the diaper area. Changing the diaper as soon as it becomes wet eliminates a large part of the problem, and removing the diaper to expose intact skin to air facilitates drying as long as fecal contamination of the skin does not occur, in which case the skin is again exposed to possible injury. However, avoid rubbing or washing the skin frequently (unless fecal matter is present), since frequent washing or rubbing may also disrupt the barrier function of the skin. Many commercial diaper wipes contain alcohol and other products that are detrimental to the natural skin barrier and should be avoided.

The use of a hair dryer or heat lamp is not recommended because they can cause burns. Also, on denuded skin, dry heat delays healing. Instead, occlusive (barrier) ointments or dressings are applied to provide a moist healing environment for open wounds and to protect the skin from further irritation. (See Ostomies, Chapter 27.) Recommended barrier ointments include white petrolatum ointment, Aquaphor (contains lanolin), and zinc oxide. A protective barrier such as zinc oxide prevents skin injury and allows the skin to heal. In the event of diaper dermatitis caused by fungal and contact irritants, a layer of antifungal powder (nystatin [Mycostatin] powder) or cream under a zinc oxide–based skin barrier ointment may be used, but providers must take care to avoid mixing the two preparations together. A combination of products may provide better results for some children; combining a protective powder such as Stomahesive Protective Powder with karaya or cornstarch powder may be helpful (Borkowski, 2004). Some diaper pastes called butt balm or cream may be helpful with some cases of diaper dermatitis, but parents should check to ensure that the ingredients are safe for use in this age-group. Also, such pastes are often expensive (Borkowski, 2004). A Cavilon No-Sting Barrier Film may be used on infants older than 30 days (Baharestani, 2007). Other products include iLEX Skin Protectant Paste and Sureprep No-Sting Protective Barrier Wipe. Once a barrier paste has been applied, it is recommended that the paste not be removed when soiling occurs because this further disrupts the integrity of the skin; instead wipe off the stool or contaminated portion only, leaving as much barrier paste intact as possible.

A 1 : 1 mixture of iLEX paste and petroleum jelly applied liberally to the affected area is reported to be very effective in healing diaper dermatitis within 24 to 48 hours; as noted above, wipe off only excess stool, leaving as much paste in place as possible, and then reapply more as necessary (Hodge, 2009).

Diaper construction has a significant impact on the incidence and severity of diaper dermatitis. Superabsorbent disposable diapers reduce diaper dermatitis because they contain an absorbent gelling material that binds water tightly to decrease skin wetness, maintains pH control by providing a buffering capacity, and decreases skin irritation by preventing mixing of urine and feces in the diaper (Visscher, 2009). The improved containment of urine and feces is also an important factor in decreasing contamination of the environment, such as in daycare centers, and spread of disease.

Another advance in diapers is the addition of an inner layer or top sheet that is impregnated with petrolatum or zinc oxide. The liner transfers the petrolatum to the skin, where it acts as a barrier to moisture and irritants. Guidelines for controlling diaper rash are presented in the Family-Centered Care box.

Some caregivers may choose to apply a powder that may contain either talc or cornstarch. A common misconception about using cornstarch on skin is that it promotes the growth of C. albicans. Both cornstarch and talc do not support growth of the fungi under conditions normally found in the diaper area; however, the use of powders in the hospital nursery is not recommended (Association of Women’s Health, Obstetric and Neonatal Nurses, 2007).

An objective assessment of diaper dermatitis may be performed using the scale in Box 13-4.

Nursing Care Management

When seborrheic lesions are present, direct the treatment mainly at removing the crusts. White petrolatum may be applied to the scalp to assist with the removal of the scaly patches; another remedy involves soaking the scalp several hours in vegetable oil then removing the scales (O’Connor, McLaughlin, and Ham, 2008). Tar-containing shampoos are more expensive but may be effective. Teach parents the appropriate procedure to clean the scalp, which may necessitate a demonstration. Shampooing should be done daily with a mild soap or commercial baby shampoo. Medicated shampoos are usually not needed, but an antiseborrheic shampoo containing sulfur and salicylic acid may be used. The shampoo is applied to the scalp and allowed to remain on until the crusts are softened, and then the scalp is thoroughly rinsed. Using a fine-tooth comb or a soft facial brush after shampooing helps remove the loosened crusts from the strands of hair. If shampoos are not effective, an antifungal cream (ketoconazole) or shampoo may be helpful.

Therapeutic Management

The major goals of management are to (1) hydrate the skin, (2) relieve pruritus, (3) reduce flare-ups or inflammation by avoiding triggers, (4) prevent and control infection, and (5) live as near as normal a childhood as possible. Most of the general measures for managing AD serve to reduce pruritus and other aspects of the disease. General management includes:

There are a number of ways to enhance skin hydration and prevent dry, flaky skin, depending on the child’s skin characteristics and individual needs. A tepid bath with a mild soap (Dove or Neutrogena), no soap, or an emulsifying oil, followed immediately by application of an emollient (within 3 minutes), assists in preventing moisture loss. Avoid bubble baths and harsh soaps. The bath may need to be repeated once or twice daily, depending on the child’s status. Excessive bathing without emollient application only dries out the skin. Some lotions are not effective, and emollients should be chosen carefully to prevent excessive skin drying. Aquaphor, Cetaphil, and Eucerin are acceptable for skin hydration. A nighttime bath, followed by emollient application and dressing in soft cotton pajamas, may alleviate much of the nighttime pruritus.

Moderate or severe pruritus is usually relieved by administration of oral antihistamine drugs (hydroxyzine or diphenhydramine), with the amount tailored to the individual child. Nonsedating antihistamines such as loratadine (Claritin) or fexofenadine (Allegra) may be preferred for daytime pruritus relief. Because pruritus increases at night, a mildly sedating antihistamine may be needed.

Topical corticosteroids are now considered first-line treatment for AD (Leung, 2007; Williams, 2005). Occasional flare-ups require the use of topical steroids to diminish inflammation. Low-, moderate-, or high-potency topical corticosteroids are prescribed, depending on the degree of involvement, the body area to be treated, the child’s age, potential for local side effects (striae, skin atrophy, and pigment changes), and the type of vehicle to be used (e.g., cream, lotion, ointment). Medical management of secondary skin infections with systemic antibiotics is an important part of the treatment of AD. Coal tar preparations may also be used to hydrate the skin yet are considered cumbersome because they stain clothing.

Two calcineurin inhibitors (immunomodulators) used in children with AD are tacrolimus and pimecrolimus (Elidel). Tacrolimus is available in two ointment strengths (0.03% and 0.1%); these have been approved for use in children 2 years of age and older. Pimecrolimus is available in a 1% cream that has no systemic accumulation or effects; this drug has been approved for children ages 2 years and older.

Acute flare-ups may require the use of wet wraps. One method is to apply a light coat of topical corticosteroid, then wrap the child in cool wet towels for 10 minutes (warm towels slightly in the winter to prevent heat loss). Once the towels are removed, the steroid ointment is reapplied, followed by a moisturizer. Be careful, however, not to use excessive wet wraps, since these may cause skin maceration and secondary infections.

Controversy exists regarding prevention of AD by limiting the exposure of infants at risk to allergens both prenatally and postnatally. Studies have shown a decrease in atopic eczema in infants at risk for atopy whose mothers breast-fed at least 4 months; avoiding highly allergenic foods during lactation may or may not help reduce the incidence of atopy. Infants who are not breast-fed and who are at risk for AD may benefit from extensively hydrolyzed formula (Greer, Sicherer, Burks, et al, 2008). Although conclusive evidence for preventive strategies is lacking, the precautions in the Nursing Care Guidelines box on p. 530 may be recommended.

Nursing Care Management

The child with AD presents a nursing challenge. Controlling the intense pruritus is imperative if the disorder is to be successfully managed, since scratching leads to the formation of new lesions and may cause secondary infection. In addition to the medical regimen, other measures can prevent or minimize the scratching. Keep fingernails and toenails short and clean, and file them frequently to prevent sharp edges. Gloves or cotton socks can be placed over the hands and pinned to shirtsleeves.

Also, eliminate conditions that increase itching when possible. Remove woolen clothes or blankets, rough fabrics, and furry stuffed animals. Because heat and humidity cause perspiration, which intensifies the itching, proper dress for climatic conditions is essential. Pruritus is often precipitated by exposure to the irritant effects of certain components of common products such as soaps, detergents, fabric softeners, perfumes, diaper wipes, and powders. Most children experience less itching when soft cotton fabrics are worn next to the skin. Avoid exposure to latex products, such as gloves and balloons. Launder clothes and sheets in a mild liquid detergent and rinse them thoroughly in clear water (without fabric softeners or antistatic chemicals); use a second rinse cycle to further reduce residual detergent. The use of skin cleansers with minimal defatting activity and a neutral pH is preferred over the usual soaps.

Preventing infection is usually accomplished by preventing scratching. Maintain personal hygiene as described previously. Give baths as prescribed, keeping the water tepid, and avoid soaps (except as indicated), bubble baths, oils, and powders. Skinfolds and diaper areas need frequent cleansing with plain water. A room humidifier or vaporizer may benefit children with extremely dry skin. The lesions are examined for signs of infection—usually honey-colored crusts with surrounding erythema. Report any signs of infection to the practitioner.

Wet soaks or compresses are applied as needed, and medications for pruritus or infection are administered as directed. The nurse gives the family explicit written instructions on the preparation and use of soaks, special baths, and topical medications, including the order of application if more than one is prescribed. If children have difficulty remaining still for a 10- or 15-minute soak, bath, or dressing application, perform these at nap time or when the child is watching television, listening to a story, or playing with tub toys.

No particular diet is recommended for children with AD. When a hypoallergenic diet is prescribed, parents need help in understanding the reason for the diet and guidelines for avoiding hyperallergenic foods (see Box 13-2). Because hypoallergenic diets take time before visible effects are apparent, parents need reassurance that results may not be seen immediately. If airborne allergens also worsen the eczema, the family is counseled regarding measures to “allergy proof” the home. (See Asthma, Chapter 32.)

Etiology

Numerous theories have been proposed regarding the etiology of SIDS; however, the cause remains unknown. One compelling hypothesis is that SIDS is related to a brainstem abnormality in the neurologic regulation of cardiorespiratory control. This maldevelopment affects arousal and physiologic responses to a life-threatening challenge during sleep (American Academy of Pediatrics, 2005). Abnormalities include prolonged sleep apnea, increased frequency of brief inspiratory pauses, excessive periodic breathing, and impaired arousal responsiveness to increased carbon dioxide or decreased oxygen. However, sleep apnea is not the cause of SIDS. The vast majority of infants with apnea do not die, and only a minority of SIDS victims have documented apparent life-threatening events (ALTEs) (see Apnea and Apparent Life-Threatening Events, p. 546). Numerous studies indicate that there is no association between SIDS and any childhood vaccine.

A genetic predisposition to SIDS has been postulated as a cause. In one study a genetic mutation on chromosome 6q 22.1-22.31 was positively linked to a syndrome of SIDS and dysgenesis of the testis (Puffenberger, Hu-Lince, Parod, et al, 2004).

Recently there has been increased interest in infection and inflammation as a possible cause of SIDS (Blood-Siegfried, 2009; Highet, 2008; Mitchell, 2009).

Maternal smoking during pregnancy has emerged in numerous epidemiologic studies as a major factor in SIDS, and tobacco smoke in the infant’s environment after birth has also been shown to have a possible relationship to the incidence of SIDS (American Academy of Pediatrics, 2005). Data show that exposure to tobacco smoke increased an infant’s risk for SIDS 1.9 times over infants not exposed; 59% of SIDS deaths in smoke-exposed infants were attributed to maternal smoking (Anderson, Johnson, and Batal, 2005). It has been postulated that 12% of all SIDS deaths could be prevented with prenatal maternal smoking cessation (Pollack, 2001). One mechanism that has been proposed as a link between maternal smoking and SIDS is a decrease in the ability to arouse to auditory stimuli in infants of mothers who smoked prenatally (Franco, Groswasser, Hassid, et al, 1999). Exposure to maternal smoking has recently been positively correlated with decreased arousal potential in infants (Richardson, Walker, and Horne, 2009). Increased nicotine concentrations in lung tissue were found in children who died from SIDS compared with a group of control children (McMartin, Platt, Hackman, et al, 2002).

Cosleeping, or an infant sharing a bed with an adult or older child on a noninfant bed, has been reported to have a positive association with SIDS. One survey found a high association between infant deaths, nonstandard beds (sofa, day bed), and bed sharing; a large percentage of infants were found dead on their backs when bed sharing, suggesting suffocation (Unger, Kemp, Wilkins, et al, 2003). A study from Scotland indicates that the risk for SIDS when bed sharing is significantly increased for infants less than 11 weeks of age (Tappin, Ecob, and Brooke, 2005). Vennemann, Bajanowski, Brinkmann, and colleagues (2009) identified infant sleeping in the house of a friend or relative and sleeping in the family living room as significant risk factors for SIDS. Other studies correlated higher incidences of SIDS and infant cosleeping with maternal smoking, cosleeping with multiple family members, sleeping on a couch, use of a pillow in the infant’s bed, maternal overweight, soft bedding, and unintentional asphyxiation resulting from adult intoxication (overlaying) (American Academy of Pediatrics, 2000, 2005; Blair, Sidebotham, Evason-Coombe, et al, 2009; Hauck, Herman, Donovan, et al, 2003; Carroll-Pankhurst and Mortimer, 2001; Li, Zhang, Zielke, et al, 2009; Person, Lavezzi, and Wolf, 2002; McGarvey, McDonnell, Chong, et al, 2003).

A study by Hauck, Herman, Donovan, and colleagues (2003) found that bed sharing and SIDS correlated positively only in cases where the infant was sleeping with someone other than the parent; a high number of SIDS cases involved sleeping on a sofa. There are reports of a greater incidence of SIDS among African-American and non-Caucasian infants. In a population-based study Hauck, Herman, Donovan, and colleagues (2003) found that SIDS occurred more frequently among African-American infants. The prone sleep position was associated with twice (2.4% odds ratio) the rate of SIDS compared with infants placed nonprone to sleep. It has been suggested that the higher SIDS deaths among non-Caucasian infants is related to a higher incidence of prone sleep positioning (American Academy of Pediatrics, 2005; Hauck, Herman, Donovan, et al, 2003).

Cosleeping with infants in the age range when most SIDS deaths occur has not been shown to be preventive. The latest recommendation for cosleeping from the American Academy of Pediatrics (2005) is that the infant’s crib or bassinette be placed in close proximity to the mother’s bed and that the infant be placed in the adult bed only for breast-feeding, then placed to sleep in his or her own crib once the feeding session is completed.

Mesich (2005) notes that the current scientific literature fails to provide definitive guidance regarding mother-infant sleeping together in relation to safety or nonsafety; certain sleep environments (prone sleeping, tobacco smoke exposure, soft bedding, noninfant bed surface, use of certain drugs by cosleeper, and thermal stress), however, are known to increase the risk for SIDS.

Studies from countries other than the United States link sleep habits with an increased risk of SIDS. Prone sleeping may cause oropharyngeal obstruction or affect thermal balance or arousal state. One study found that healthy full-term infants had significantly impaired arousal from active and quiet sleep states when sleeping prone (Horne, Ferens, Watts, et al, 2001). Rebreathing of carbon dioxide by infants in the prone position is also a possible cause for SIDS. Infants sleeping prone and on soft bedding may not be able to move their heads to the side, thus increasing the risk of suffocation and lethal rebreathing. Evidence from other countries and the United States shows an increased incidence of SIDS in infants placed in a side-lying position; thus the side-lying position is no longer recommended for infants sleeping at home, daycare, or hospitals (unless medically indicated). Most preterm infants being discharged from the hospital should be placed in a supine sleeping position unless special factors predispose them to airway obstruction.

One postulated cause of SIDS has been a prolonged Q-T interval; however, there has been no strong evidence to support this as a cause of SIDS or universal testing of newborns for prolonged Q-T interval (American Academy of Pediatrics, 2005).

Soft bedding such as waterbeds, sheepskins, beanbags, pillows, or quilts should be avoided for infant sleeping surfaces. Bedding items such as stuffed animals or toys should be removed from the crib while the infant is asleep. Head covering by a blanket has also been found to be a risk factor for SIDS, thus supporting the recommendation to avoid extra bed linens or other items (Mitchell, Thompson, Becroft, et al, 2008).

One study indicated that breast-feeding during the first 16 weeks of life decreased the likelihood of SIDS (Alm, Wennergren, Norvenius, et al, 2002). Some studies have found pacifier use in infants to be a protective factor against the occurrence of SIDS; the data for pacifier use in infants in the first year of life are said to be more compelling than data linking pacifier use to the development of dental complications and the inhibition of breast-feeding (American Academy of Pediatrics, 2005). Therefore the American Academy of Pediatrics recommends using a pacifier at naptime and bedtime, using a pacifier only if the infant is breast-feeding successfully, not using a sweetened coating on the pacifier, and avoiding forcing the infant to use the pacifier.

The American Academy of Pediatrics (2005) recommends that healthy infants be placed to sleep in the supine (on the back) position. Since the Back to Sleep campaign in 1992 advocating nonprone sleeping for infants, an increased incidence of positional plagiocephaly has been observed. (See Chapter 11 and Fig. 11-9.) It is recommended that an infant’s head position be alternated during sleep time to prevent plagiocephaly. Infants may be placed prone during awake periods to prevent positional plagiocephaly and to encourage development of upper shoulder girdle strength (American Academy of Pediatrics, 2005).

Although the cause of SIDS is unknown, autopsies reveal consistent pathologic findings, such as pulmonary edema and intrathoracic hemorrhages that confirm the diagnosis. Consequently, autopsies should be performed on all infants suspected of dying of SIDS, and findings should be shared with the parents as soon as possible after the death. Postmortem findings in SIDS and accidental suffocation or intentional suffocation such as in Munchausen syndrome by proxy (see Child Maltreatment, Chapter 16) are practically the same. Individuals with less experience and training in performing autopsies, such as coroners instead of medical examiners, may not correctly identify some deaths as SIDS. Therefore mortality statistics can vary in different regions.

Infants at Risk for SIDS

Certain groups of children are at increased risk for SIDS:

Factors that are often listed as being protective against SIDS include:

No diagnostic tests exist to predict which infants, including those in the above groups, will survive, and home monitoring is no guarantee of survival. Whether subsequent siblings of one SIDS infant are at increased risk for SIDS is unclear. Even if the risk is increased, families have a 99% chance that their subsequent child will not die of SIDS. A review of sibling deaths attributed to SIDS in England failed to ascertain a precise risk of recurrence; previous studies suggested a recurrence risk range of 1.7 to 10.1, yet the researchers concluded the studies had too many methodologic flaws to draw any firm conclusions (Bacon, Hall, Stephenson, et al, 2008). Others report that recurrence risks for a SIDS death in a family with a previous infant SIDS death range from 2% to 6% (American Academy of Pediatrics, 2005). Home monitoring is not recommended for this group of children, but it is often used by practitioners and may even be requested by parents (American Academy of Pediatrics, 2005). Monitoring is best initiated on an individual basis.

Nursing Care Management

Nurses have a vital role in preventing SIDS by educating families about the risk of prone sleeping position in infants from birth to 6 months of age, the use of appropriate bedding surfaces, the association with maternal smoking, and the dangers of cosleeping on noninfant surfaces with adults or other children. Additionally nurses have an important role in modeling behaviors for parents to foster practices that decrease the risk of SIDS: placing infants in a supine sleeping position in the hospital and using a pacifier at nap and bedtime. Data indicate that a small percentage of nurses still place healthy infants in a side-lying position in the hospital (Bullock, Mickey, Green, et al, 2004; Thompson, 2005). Statistics for infants being placed in a prone sleeping position in the United States decreased from 70% in 1992 to 13% in 2004 (American Academy of Pediatrics, 2005). One study of neonatal intensive care nurses indicated that 52% routinely provided discharge instructions that promote supine sleep positions at home; common nonsupine positions recommended by the nurses included either supine or side or exclusive side-lying sleep position (Aris, Stevens, Lemura, et al, 2006). Nurses must be proactive in further decreasing the incidence of SIDS; postpartum discharge planning, newborn discharges, follow-up home visits, well-baby clinic visits, and immunization visits provide excellent opportunities to educate parents in these matters.

Many health care workers are concerned that infants placed on the back to sleep will aspirate emesis or mucus, yet studies fail to show an increase in infant deaths, spitting up during sleep, aspiration, asphyxia, or respiratory failure as a result of supine sleep positioning (Malloy, 2002; Tablizo, Jacinto, Parsley, et al, 2007).

Loss of a child from SIDS presents several crises with which the parents must cope. In addition to grief and mourning the death of their child, the parents must face a tragedy that was sudden, unexpected, and unexplained. The psychologic intervention for the family must deal with these additional variables. This discussion focuses primarily on the objectives of care for families experiencing SIDS, rather than on the process of grief and mourning, which is explored in Chapter 23.

Research findings have important implications for practices that may reduce the risk of SIDS, such as avoiding smoking during pregnancy and near the infant; using the supine sleeping position; avoiding soft, moldable mattresses, blankets, and pillows; avoiding bed sharing; breast-feeding; and avoiding overheating during sleep. The infant’s head position should be varied to prevent flattening of the skull (positional plagiocephaly).

The first persons to arrive at the scene may be the police and emergency medical service personnel. They should handle the situation by asking few questions; giving no indication of wrongdoing, abuse, or neglect; making sensitive judgments concerning any resuscitation efforts for the child; and comforting the family members as much as possible. A compassionate, sensitive approach to the family during the first few minutes can help spare them some of the overwhelming guilt and anguish that commonly follow this type of death.

The medical examiner or coroner may go to the home or place of death and make the death pronouncement; until then the sleep environment should remain as it was when the infant was initially found (Koehler, 2008). If the infant is not pronounced at the scene, he or she may be transported to the emergency department to be pronounced dead by a physician. Usually there is no attempt at resuscitation in the emergency department. While they are in the emergency department, parents are asked only factual questions, such as when they found the infant, how he or she looked, and whom they called for help. The nurse avoids any remarks that may suggest responsibility, such as “Why didn’t you go in earlier?” “Didn’t you hear the infant cry out?” “Was the head buried in a blanket?” or “Were the siblings jealous of this child?” It is the coroner’s responsibility to document these findings at the scene rather than have parents recount the experience in the emergency department (Koehler, 2008). Parents may also express feelings of guilt about administering cardiopulmonary resuscitation (CPR) correctly or the timing of CPR in relation to finding the infant.

At this time the physician should initiate the discussion of an autopsy, often with the nurse being present to support the family. The physician or medical examiner, depending on the circumstances, emphasizes that a diagnosis cannot be confirmed until the postmortem examination is completed. Nurses may balk at the idea of requesting an autopsy because of the parents’ emotional state; however, an autopsy may clear up possible misconceptions regarding the death. Instructions about the autopsy and funeral arrangements may need to be repeated or put in writing. If the mother was breast-feeding, she needs information about abrupt discontinuation of lactation. The nurse or physician should contact the primary care practitioner for the infant and the mother to avoid any miscommunications or telephone calls at a later date inquiring about the child’s health status.

A review of 60 studies shows that parents experiencing perinatal death perceive health care workers’ responses as having a significant impact on the parents’ grieving process; parents perceived the behavior of many health care workers as thoughtless or insensitive. The findings suggest that nurses and physicians would benefit from more bereavement training (Gold, 2007).

An important aspect of compassionate care for these parents is allowing them to say good-bye to their child. These are the parents’ last moments with their child, and they should be as quiet, meaningful, peaceful, and undisturbed as possible. Encourage parents to hold their infant before leaving the emergency department. Because the parents leave the hospital without their infant, it is helpful to accompany them to the car or arrange for someone else to take them home. A debriefing session may help health care workers who dealt with the family and deceased infant to cope with emotions that are often engendered when a SIDS victim is brought into the acute care facility. Comprehensive guidelines have been published for health professionals involved in SIDS investigations to assist the family and at the same time to determine that the infant’s death was not the result of other factors such as child maltreatment (American Academy of Pediatrics, 2001).

When the parents return home, a competent, qualified professional should visit them as soon after the death as possible. They should receive printed material that contains excellent information about SIDS (available from the national organizations*).

During the initial visit help the parents gain an intellectual understanding of the condition. The nursing objectives are to assess what the parents have been told about SIDS; what they think happened; and how they explained this to the other siblings, family members, and friends. One question that the nurse will never be able to answer and therefore should not attempt to is, “Why did this happen to our baby?” or “Who is responsible for this tragedy?” These and other questions may linger in the parents’ minds for months or even years.

When the unexpected death of a child occurs, it is not uncommon for one parent to blame the other for the child’s death. Parents may also experience guilt over the child’s death; if they had checked earlier, the child might still be alive. It is important that the nurse assist parents in working through these feelings to prevent marital disruption in addition to the loss of the loved child.

Some parents are able to discuss their feelings openly, and the nurse supports this coping skill. However, others may be reluctant to express their grief, and the nurse can encourage the expression of emotions by asking about crying and feeling sad, angry, or guilty. This is an attempt to provoke a display of emotion, not just an admission of a feeling. During this session, help the parents explore their usual coping mechanisms and, if these are ineffectual, to investigate new approaches. For example, one parent may refrain from discussing the death for fear of upsetting the other parent, but each may need to hear how the other feels.

Ideally, the number of visits and plans for subsequent intervention need to be flexible. Parents facing the question of a subsequent child will need support. Both the birth of a subsequent child and the survival of that child, especially past the age of death of the previous child, are important transitional stages for parents.

Diagnostic Evaluation

An essential component of the diagnostic process includes a detailed description of the event—who witnessed the event, where the infant was during the event, and what, if any, activities were involved (such as during or after a feeding, riding in a car seat restraint, presence of siblings or any minor children, what clothing the infant was wearing). In addition, a prenatal and postnatal history must be obtained. A short period of observation in the emergency department may be appropriate to observe the infant’s respiratory pattern and response to feeding. A careful evaluation of the preterm infant in the car restraint currently in use is essential; upper airway occlusion and subsequent apnea and cyanosis may occur if the infant is not positioned properly. Reported diagnoses in infants with ALTE include a neurologic event such as a seizure (30% of cases seen); GI problem, including gastroesophageal reflux (50%); respiratory conditions (20%); and metabolic conditions, cardiac anomaly, or child abuse (each <5%). In some cases, multiple diagnoses may be made (Hall and Zalman, 2005).

In the event that an underlying diagnosis such as those mentioned previously is not established, home monitoring may be recommended. The most commonly used monitoring is continuous recording of cardiorespiratory patterns (cardiopneumogram, or pneumocardiogram). Four-channel pneumocardiograms (or multichannel pneumogram) monitor heart rate, respirations (chest impedance), nasal airflow, and oxygen saturation. A more sophisticated test, polysomnography (sleep study), also records brain waves, eye and body movements, esophageal manometry, and end-tidal carbon dioxide measurements. However, none of these tests can predict risk. Some children with normal results may still have subsequent apneic episodes.

Therapeutic Management

The treatment of the infant with an ALTE depends on the underlying condition (see above). Treatment of recurrent apnea (without an underlying organic problem) usually involves continuous home monitoring of cardiorespiratory rhythms and in some cases the use of methylxanthines (respiratory stimulant drugs, such as theophylline or caffeine). The decision to discontinue the monitoring is based on the infant’s clinical condition. A general guideline for discontinuation is when infants with ALTEs have gone 2 or 3 months without significant numbers of episodes requiring intervention.

Newer home apnea monitors allow download of information that assists the practitioner in deciding when to discontinue home monitoring. It is imperative to remember, however, that the home apnea monitor will not predict or prevent SIDS deaths. Furthermore, impedance-based monitors detect chest wall movement and will not detect obstructive apnea unless the episode involves significant bradycardia (see Family-Centered Care box).

Nursing Care Management

The diagnosis of an ALTE engenders great anxiety and concern in parents, and the institution of home monitoring presents additional physical and emotional burdens. Parents of infants on home apnea monitors report experiencing emotional distress, especially depression and hostility, during the first few weeks after hospital discharge (Abendroth, Moser, Dracup, et al, 1999). For parents of a SIDS victim who have a new infant on home apnea monitoring, the anxiety is compounded by the uncertainty of the future of the living child and grief for the lost child. Home apnea monitoring may offer some predictability and control over the current child’s survival through the period of uncertainty.

If home monitoring is required, the nurse can be a major source of support to the family in terms of education about the equipment; education regarding observation of the infant’s status; and instructions regarding immediate intervention during apneic episodes, including CPR. Several reports indicate that the first week to month after discharge is the most stressful for parents, particularly when the rate of false alarms is high (Bennett, 2002). To help the family cope with the numerous procedures they must learn, adequate preparation before discharge and written instructions are essential. In the first few weeks after discharge, parents may benefit by having a practitioner readily available to answer questions regarding false alarms and for other technical assistance (Abendroth, Moser, Dracup, et al, 1999).

Several types of home monitors are available and are set up by either a home monitor equipment company or home health staff. Nurses, especially those involved in the care at home, must become familiar with the equipment, including its advantages and disadvantages. Safety is a major concern because monitors can cause electrical burns and electrocution. The following precautions are recommended:

Siblings should also be supervised when near the infant and taught that the monitor is not a toy. Other safety practices include informing local utility and rescue squads of the home monitoring in case of an emergency. Telephone numbers for these services should be posted near all telephones in the home.

Caregivers need detailed information regarding proper attachment of the electrodes to the infant’s chest with impedance monitors that detect chest movement. The electrodes are placed in the midaxillary line, at a space one or two fingerbreadths below the nipple. For home use, electrodes attached to a belt that is placed around the child’s trunk are preferred (Fig. 13-8). The belt is positioned so that the electrodes contact the skin in the same area. Monitors may have memory chips that allow for event recording, which can be an effective tool in evaluating the use of the monitor, events immediately before and after the ALTE, and reported frequency of alarms.

Monitors are effective only if they are used. They do not prevent death but alert the caregiver to the ALTE in time to intervene. The need to use the monitor and to respond appropriately to alarms must be stressed. Noncompliance can result in the infant’s death.

Family Support

Many of the stresses observed during the monitoring period are characteristic of those of families with chronically ill children. The child with an apnea or cardiorespiratory monitor may have additional health care needs such as a gastrostomy, tracheostomy, ostomy, and myriad medications or treatments that exacerbate the parents’ stress. Parents report increased stress, including concern for the child’s survival, fear of incompetence in assuming home responsibility, inadequate respite care, lack of time for other children and spouse, social isolation from friends and extended family, constant work, and fatigue. The monitored child is at risk for vulnerable child syndrome, which may lead to lack of parental separation and preferential treatment, causing further family disruption (Bennett, 2002). To deal with these potential effects, nurses need to employ the same interventions as those discussed for children with chronic illness and be aware of the need for referral when difficulties are suspected.

To lessen the continuous responsibility of monitoring, other family members, such as grandparents, should be taught how to manipulate the equipment, read and interpret the signals, and administer CPR. They are encouraged to stay with the infant for regular periods to allow parents respite. Support groups of other families who have successfully completed monitoring can also be of benefit. Because reliable baby-sitters are difficult to locate, support group members or nursing students may be potential sources of qualified caregivers.

• Common nutritional disturbances of infancy include vitamin and mineral disturbances, some types of vegetarian diets, childhood malnutrition, and food hypersensitivity or intolerance.

• Mineral disturbances may be caused by mineral-mineral interactions and mineral-diet interactions.

• Nurses should counsel parents to provide the RDA of vitamins and minerals through appropriate foods instead of depending on supplements.

• Nutrient consumption varies among vegetarians; therefore a detailed dietary assessment is essential for planning AIs, particularly in children and pregnant and lactating women.

• PEM (SCU) may occur as a complication of social unrest when the child lacks food as a result of an underlying disease, a fad diet, lack of parental education about infant nutrition, inappropriate management of food allergy, incorrect preparation of formula, or poor food storage and handling.

• Food intolerance encompasses food allergies and food sensitivities during infancy, the most serious of which is CMA.

• Food hypersensitivity may cause a severe anaphylactic reaction in some children; a ready-to-administer dose of intramuscular epinephrine should be carried at all times by such children.

• Common feeding difficulties in the infant include regurgitation, spitting up, and colic.

• Treatment of colic may involve change in feeding practices, correction of a stressful environment, and support of the parent. Medications may or may not relieve some of the symptoms of colic.

• Behavioral interventions aimed at helping parents deal with the colicky infant may be more helpful than changing feeding practices or medications.

• Common skin disorders of infancy are diaper dermatitis, seborrheic dermatitis, and AD.

• Growth failure, or FTT, may occur in children who have a chronic illness, or it may occur in a family environment wherein healthy infant feeding practices are poorly managed or understood. FTT is not always associated with a pattern of disturbed maternal-infant relationship.

• SIDS is the third leading cause of infant death in the United States.

• Factors that place the infant at high risk for SIDS include prone sleeping position, soft bedding, sleeping in a noninfant bed with an adult or older child, and maternal prenatal smoking.

• The primary nursing responsibility in care associated with sudden infant death is educating the family of newborns about the risks for SIDS, modeling appropriate behaviors in the hospital such as placing the infant in a supine sleep position, and providing emotional support of the family that has experienced a SIDS loss.

• Infants with ALTEs are carefully evaluated for clues to the underlying cause.

• Home apnea or cardiorespiratory monitors do not prevent SIDS.