CHAPTER 21 Failure to Thrive
Failure to thrive (FTT) is a term given to malnourished infants and young children who fail to meet expected standards of growth. The term FTT is most often used to describe malnutrition that is related to environmental or psychosocial causes, although in many children with inadequate growth, organic, and environmental contributors coexist. It is important to assess the potential medical, nutritional, developmental, psychosocial, and environmental contributors to FTT.
FTT is diagnosed by weight that falls or remains below the third percentile for age; that decreases, crossing two major percentile lines on the growth chart over time; or that is less than 80% of the median weight for the height of the child. Caveats to these definitions exist. According to growth chart standards, 3% of the population naturally falls below the third percentile. These children, who typically have short stature or constitutional delay of growth, usually are proportional (normal weight for height). Additionally, in the first few years of life, large fluctuations in percentile position can occur in normal children. Changes in weight should be assessed in relation to height (length) and head circumference.
Weight that decreases from a disproportionately high percentile to one that is proportional causes no concern, but weight that decreases to a percentile that is disproportionately low is of concern. Allowances must be made for prematurity; weight corrections are needed until 24 months of age, height corrections until 40 months of age, and head circumference corrections until 18 months of age. Although some growth variants can be difficult to distinguish from FTT, growth velocity and height-for-weight determinations can be useful in distinguishing the cause of growth failure. In children with FTT, malnutrition initially results in wasting (deficiency in weight gain). Stunting (deficiency in linear growth) generally occurs after months of malnutrition, and head circumference is spared except with chronic, severe malnutrition. FTT that is symmetric (weight, height/length, and head circumference are proportional) suggests long-standing malnutrition, chromosomal abnormalities, congenital infection, or teratogenic exposures. FTT is a common problem in pediatrics, affecting 5% to 10% of young children, 3% to 5% of children admitted to teaching hospitals, and 15% of children living in poverty and foster care.
Diseases of any organ system can cause malnutrition. Because possible causes of growth failure are so diverse and often multifactorial, the management of FTT begins with a careful search for its etiology (Table 21-1). The common causes of FTT vary by age, which should be reflected in the evaluation (Table 21-2). In most cases, a comprehensive history and physical examination are sufficient to suggest or eliminate medical disease as the primary cause of FTT. Medical diseases are diagnosed in fewer than 50% of children hospitalized for growth failure and even less frequently in children managed in the outpatient setting. Growth failure is often a manifestation of more extensive family problems.
TABLE 21-1 Causes of Failure to Thrive
ENVIRONMENTAL (COMMON) |
Emotional deprivation |
Rumination |
Child maltreatment |
Maternal depression |
Poverty |
Poor feeding techniques |
Improper formula preparation |
Improper mealtime environment |
Unusual parental nutritional beliefs |
GASTROINTESTINAL |
Cystic fibrosis and other causes of pancreatic insufficiency |
Celiac disease |
Other malabsorption syndromes |
Gastrointestinal reflux |
CONGENITAL/ANATOMIC |
Chromosomal abnormalities, genetic syndromes |
Congenital heart disease |
Gastrointestinal abnormalities (e.g., pyloric stenosis, malrotation) |
Vascular rings |
Upper airway obstruction |
Dental caries |
Congenital immunodeficiency syndromes |
INFECTIONS |
Human immunodeficiency virus |
Tuberculosis |
Hepatitis |
Urinary tract infection |
Chronic sinusitis |
Parasitic infection |
METABOLIC |
Thyroid disease |
Adrenal or pituitary disease |
Aminoaciduria, organic aciduria |
Galactosemia |
NEUROLOGIC |
Cerebral palsy |
Hypothalamic and other central nervous system tumors |
Hypotonia syndromes |
Neuromuscular diseases |
Degenerative and storage diseases |
RENAL |
Chronic renal failure |
Renal tubular acidosis |
Urinary tract infection |
HEMATOLOGIC |
Sickle cell disease |
Iron deficiency anemia |
TABLE 21-2 Common Causes of Malnutrition in Early Life
NEONATE |
Failed breastfeeding |
Improper formula preparation |
Congenital syndromes |
Prenatal infections |
Teratogenic exposures |
EARLY INFANCY |
Maternal depression |
Improper formula preparation |
Gastroesophageal reflux |
Poverty |
Congenital heart disease |
Cystic fibrosis |
Neurologic abnormalities |
Child neglect |
LATER INFANCY |
Celiac disease |
Food intolerance |
Child neglect |
Delayed introduction of age-appropriate foods |
Juice consumption |
AFTER INFANCY |
Acquired diseases |
Highly distractible child |
Juice consumption |
Autonomy struggles |
Inappropriate mealtime environment |
Inappropriate diet |
A medical history should include the history of prenatal care, maternal illnesses during pregnancy, identified fetal growth problems, prematurity, and birth size (weight, length, and head circumference). Indicators of medical diseases, such as vomiting, diarrhea, fever, respiratory symptoms, and fatigue, should be noted. A careful diet history is essential to the evaluation. Lactation problems in breastfed infants and improper formula preparation are frequent causes of growth failure early in infancy; the adequacy of the maternal milk supply or the precise preparation of formula should be evaluated. For older infants and young children, a detailed diet history is helpful, although it may be difficult to obtain. It is essential to evaluate intake of solid foods and liquids. Because of parental dietary beliefs, some children have inappropriately restricted diets. Others drink excessive amounts of fruit juice, leading to malabsorption or anorexia. The child’s daily schedule, including the timing, frequency, and location of meals, is important. Mealtime practices, especially distractions that interfere with completing meals, can influence growth. A complete psychosocial assessment of the child and family is required. Child factors (temperament, development), parental factors (depression, domestic violence, social isolation, mental retardation, substance abuse), and environmental and societal factors (poverty, unemployment, illiteracy, lead toxicity) all may contribute to growth failure. In some cases, the history provided by parents is inaccurate, which complicates the evaluation and management of the problem.
A complete physical examination and developmental screening should assess signs of inflicted injury; oral or dental problems; indicators of pulmonary, cardiac, or gastrointestinal disease; and dysmorphic features that may suggest a genetic or teratogenic cause for growth failure. A complete neurologic examination may reveal spasticity or hypotonia, both of which can have untoward effects on feeding and growth. Physical findings related to malnutrition include dermatitis, hepatomegaly, cheilosis, or edema (see Chapter 30). Additionally, children with FTT have more otitis media as well as respiratory and gastrointestinal infections than age-matched controls; severely malnourished children are at risk for a variety of serious infections.
The history and physical examination findings guide the laboratory evaluation, but an extensive search has no merit. Simple screening tests are recommended to identify common illnesses that cause growth failure and to search for medical problems that result from malnutrition. Recommended laboratory tests include screening for iron deficiency anemia and lead toxicity; urinalysis, urine culture, and serum electrolytes to assess renal infection or dysfunction; and a protein purified derivative test to screen for tuberculosis. Human immunodeficiency virus testing may be indicated for selected children. For children with diarrhea, abdominal pain, or malodorous stools, a stool sample for culture and ova and parasites may be indicated. Observation during feeding and home visitation, if possible, are of great diagnostic value in assessing feeding problems, food preferences, mealtime distractions, unusual or disruptive parent-child interactions, and the home environment.
Treatment must address the nutritional requirements of the child and the social issues of the family. Initial treatment should focus on the nutritional and medical management of the child while engaging the family in the treatment plan. Parents of malnourished children may feel personally responsible and threatened by the diagnosis of FTT. Parents may be so depressed or dysfunctional that they cannot focus on their child’s needs; they may not recognize the psychosocial and family contributors to the malnutrition. These issues can have a profound effect on the success of treatment, and, in the course of therapy, they need to be addressed.
Children with mild malnutrition whose cause is easily identified can be managed by the primary care physician and family. In more challenging cases, a multidisciplinary team, including pediatricians, nutritionists, developmental specialists, nurses, and social workers, improves nutritional outcome in children with FTT. Most children with FTT can be treated in the outpatient setting. Children with severe malnutrition, underlying diagnoses that require hospitalization for evaluation or treatment, or whose safety is in jeopardy because of maltreatment require hospitalization. Admitting children to the hospital to induce and document weight gain is not recommended unless intensive outpatient evaluation and intervention has failed or the social circumstances are a contraindication for attempting outpatient management.
Nutritional management is the cornerstone of treatment, regardless of the etiology. Children with FTT may require more than 1.5 times the expected calorie and protein intake for their age for catch-up growth. Children with FTT who are anorexic and picky eaters may not be able to consume this amount in volume and require calorically dense foods. For formula-fed infants, the concentration of formula can be changed from 20 cal/oz to 24 or 27 cal/oz (Table 21-3). For toddlers, dietary changes should include increasing the caloric density of favorite foods by adding butter, oil, sour cream, peanut butter, or other high-calorie foods. High-calorie oral supplements that provide 30 cal/oz are often well tolerated by toddlers. In some cases, specific carbohydrate, fat, or protein additives are used to boost calories by increasing calories without increasing volume requirements. They can be used to supplement formulas for infants and older children. In addition, vitamin and mineral supplementation is needed, especially during catch-up growth. In general, the simplest and least costly approach to dietary change is warranted.
TABLE 21-3 Infant Formula Preparation*
Amount of Powder/Liquid | Amount of Water (oz) | Final Concentration |
---|---|---|
1 cup powdered formula | 29 | 20 kcal/oz |
4 scoops powdered formula | 8 | 20 kcal/oz |
13 oz liquid concentrate | 13 | 20 kcal/oz |
1 cup powdered formula | 24 | 24 kcal/oz |
5 scoops powdered formula | 8 | 24 kcal/oz |
13 oz liquid concentrate | 9 | 24 kcal/oz |
1 cup powdered formula | 21 | 27 kcal/oz |
5.5 scoops powdered formula | 8 | 27 kcal/oz |
13 oz liquid concentrate | 6 | 27 kcal/oz |
* Final concentrations are reached by adding formula to water. One scoop of powdered formula = one measuring tablespoon. For healthy infants, formulas are prepared to provide 20 kcal/oz.
From Jew R, editor: Department of Pharmacy Services Pharmacy Handbook and Formulary, 2000–2001. Hudson, Ohio, 2000, Department of Pharmacy Services, p 422.
Depending on the severity of the malnutrition, initiation of catch-up growth may take 2 weeks. Initial weight gain of more than double normal growth can be seen. Weight improvement precedes improvement in stature. For children with chronic, severe malnutrition, many months are needed to reverse all trends in growth. Although many children with FTT eventually reach normal size, they continue to be at risk for developmental, learning, and behavioral problems.
Malnutrition causes defects in host defenses. Conversely, infection increases the metabolic needs of the patient and often is associated with anorexia. Children with FTT may suffer from a malnutrition-infection cycle, in which recurrent infections exacerbate malnutrition, which leads to greater susceptibility to infection. Children with FTT must be evaluated and treated promptly for infection and followed closely.
During starvation, the body slows metabolic processes and growth to minimize the need for nutrients and uses its stores of glycogen, fat, and protein to maintain normal metabolic requirements. During starvation, the body also generally maintains homeostasis and normal serum concentrations of electrolytes. With the rapid reinstitution of feeding after starvation, fluid and electrolyte homeostasis may be lost. Changes in serum electrolyte concentrations and the associated complications are collectively termed the refeeding syndrome. These changes typically affect phosphorus, potassium, calcium, and magnesium and can result in life-threatening cardiac, pulmonary, or neurologic problems. Infants and children with marasmus, kwashiorkor, and anorexia nervosa and who have had prolonged fasting are at risk for refeeding syndrome. Refeeding syndrome can be avoided by slow institution of nutrition, close monitoring of serum electrolytes during the initial days of feeding, and prompt replacement of depleted electrolytes.
Occasionally, children who live in psychological deprivation develop short stature with or without concomitant FTT or delayed puberty, a syndrome called psychosocial short stature. The signs and symptoms found in children with psychosocial short stature include polyphagia, polydipsia, hoarding and stealing of food, gorging and vomiting, drinking from toilet bowls, and other notable behaviors. Affected children are often shy and passive and are typically depressed and socially withdrawn. Endocrine dysfunction is often identified in affected children, who may have decreased growth hormone secretion and a muted response to exogenous growth hormone. Removal of the child from the adverse environment typically results in rapid improvement in endocrine function and subsequent rapid somatic and pubertal growth of the child. The prognosis for children with psychosocial short stature depends on the age at diagnosis and the degree of psychological trauma. Early identification and removal from the environment portends a healthy prognosis. Children who are diagnosed in later childhood or adolescence may not reach their genetic potential for growth and have a poorer psychosocial prognosis.