Nutritional Considerations in Failure to Thrive Clinical Presentation

The most important part of the evaluation of a child with failure to thrive (FTT) is obtaining a careful, detailed history. Once identified, the history can reveal whether the failure to thrive is organic, nonorganic (no identifiable physical conditions contributing to the problem),^{[20, 21, 22]} or has components of both.

The next step is to establish whether the parent of a child with organic failure to thrive feels that it is related to decreased intake, increased losses (eg, diarrhea, emesis) or abnormal metabolism (chronic illnesses, especially cardiopulmonary illnesses that increase the basal metabolic rate). Often times, multiple factors can contribute in a single patient.

The history should include the following:

• Prenatal history: This should include information regarding smoking, alcohol use, use of medications, illnesses (including rashes), and any data on prenatal growth.
• A review of the events in the nursery: This should include feeding problems and medical conditions, especially those that delay discharge.
• Detailed feeding history (with a documentation of how many ounces or liters are consumed in a 24-hour period rather than 3 oz every 3 h): Breast-fed babies should have 7 or more wet diapers per day and regular passage of stools.
• Description of how the mother prepares any formula which is not ready to feed: Improperly prepared formula can result in failure to thrive and serious electrolyte imbalances. The use of any supplements to formulas and/or substitutes for formulas should be identified.
• Description of the type of solid foods eaten (including the quantitative composition and frequency of meals and snacks): If a detailed history is difficult to obtain, parents should bring in a 3-day food diary, as well as the jars and/or labels from foods that the child is eating. Nutritionists are helpful in interviewing parents and calculating the exact number of calories consumed.
• Previously charted growth: Old growth charts should be referred to when analyzing the data. If any changes in rate of weight gain are noted, the primary care taker should be asked about changes in feeding and additional changes, including introduction of new foods, change in formula, change from breast milk to formula, and changes in the primary individuals responsible for feeding the child. Finally, any changes in family dynamic should be investigated.
• Details about any illnesses that occurred since the neonatal period (particularly those that require hospitalization or are chronic and/or permanent)
• Medical problems that can compromise eating (eg, cleft palate, cerebral palsy, spasticity, seizures, and delayed development) and require closer scrutiny regarding caloric intake
• Family and social history: This should include growth and eating pattern of other siblings, living conditions, stressors, and data on parents' growth history.

The first thing that pediatricians should do in all health assessments is to plot the head circumference, height, and weight on a growth chart. Previous growth parameters should be used to detect trends in growth rather than relying on measurements at one particular visit. If weight, height, and head circumference are all compromised, this suggests an in utero insult and/or genetic or chromosomal abnormality (see the image below).

If weight and height growth are delayed with a normal head circumference, endocrinopathies (see the first 2 images below) or constitutional delay (see the third image below) should be suspected.

This pattern also can occur in long-standing failure to thrive. Ultimately, head circumference is delayed, emphasizing the importance of following these growth parameters over time. When only weight gain is delayed, this usually reflects recent energy (caloric) deprivation (see the image below).

Vital signs are usually within the reference range, but blood pressure, respiration rate, pulse rate, and oxygen saturation may provide important clues regarding the etiology.

The physical examination may reveal the following abnormalities in children with organic basis for failure to thrive:

• Edema including ascites - Renal disease, liver disease, protein-losing enteropathy
• Wasting - Cancer, HIV, CP, poorly controlled inflammatory disease
• Hepatomegaly - Liver infiltration by tumor, storage disease, or cirrhosis
• Heart murmur - Congenital heart disease
• Respiratory compromise -Cystic fibrosis, bronchopulmonary dysplasia
• Rash or skin changes - HIV, congenital syphilis, cow's milk protein allergy, lupus
• Hair color and texture changes - Zinc deficiency, Menkes kinky hair disease
• Mental status changes - CP
• Signs of vitamin deficiency -Celiac disease, parasites, other enteropathy

Decreased weight secondary to marasmus (caused by insufficient caloric intake) should be distinguished from decreased weight secondary to acute dehydration. Only the latter is characterized by decreased skin turgor, sunken anterior fontanelle, dry mucous membranes, absence of tears, and acutely ill appearance.

Failure to thrive can be organized into nonorganic failure to thrive, organic failure to thrive, and a combination of nonorganic and organic failure to thrive. The relative incidence of each category completely depends on the population that the study examines. A study from a United States University hospital Pediatric endocrinology clinic found that half of the patients had a purely nutritional deficiency and another quarter had short stature.^[23] As indicated above, many of the children from older articles who were considered to have nonorganic failure to thrive actually had subtle organic problems that contributed to their poor growth.

Nonorganic failure to thrive

Nonorganic failure to thrive, the most written about form of failure to thrive results from adverse environmental and psychosocial factors.^[24] The onset is almost always prior to age 5 years. It is often associated with abnormal interactions between the caregiver and the infant or child. At times, it can be part of a more global pattern of child abuse. The result is an inadequate provision of food and/or inadequate intake of food. It is most common in the setting of poverty.

Prenatal causes of nonorganic failure to thrive include the following:

• Some mothers who are malnourished during pregnancy can have babies who are malnourished and small. This is more common in teen pregnancies, in lower socioeconomic locations, and with multiple gestations.
• Maternal eating disorders (eg, anorexia, bulimia) can affect the growth of fetuses as well. Whether the failure to thrive in these infants is related to hormonal factors in addition to nutrient deprivation is open to debate.

Postnatal causes of nonorganic failure to thrive include the following:

• Traditionally, nonorganic postnatal causes of failure to thrive were thought to be due to maternal rejection or neglect. Skuse suggested that clinicians inquire about more than just the nutrition offered to children.^[25] He found behavior at meals and psychosocial issues to be important variables that affected whether children obtained sufficient energy.
• Poor parenting and family dysfunction can negatively affect a child's energy intake. Families characterized by less adaptive relationships, higher levels of family conflict, maternal drug abuse, maternal depression, lack of maternal education, and less emotional support for the mother have an increased rate of children with failure to thrive. The term psychosocial deprivation was created for these types of situations.
• Other classical nonorganic reasons for failure to thrive in younger children include a failure to signal hunger, a poor suck, difficulty in weaning, or a refusal to eat. An organic basis that plays a large role in these behaviors is now noted.
• Rarely in infants and toddlers, but more commonly in older children, eating disorders (eg, anorexia, bulimia) may lead to severe growth disturbances. Although infants and toddlers do not have the classical disturbed body image that characterizes the adolescents with eating disorders, all are involved in a struggle over control with food as the medium.
• Although the typical groups with nonorganic failure to thrive are infants and toddlers, the younger the child is, the more likely they are to have some organic pathology that contributes to the aberrant feeding behavior. If mild dysphagia is present, the infant may be a slow or fussy feeder, which can lead to parental frustration and their lack of persistence. Conversely, pain related to gastroesophageal reflux or enteropathy or fear of aspiration may lead to feeding aversion by the infant that becomes a more significant problem than the organic one.

Nonorganic causes of failure to thrive usually include combinations of the following:

• Poverty
• Dysfunctional family interactions (especially maternal depression or drug use)
• Difficult parent-child interactions
• Lack of parental support (eg, no friends, no extended family)
• Lack of preparation for parenting
• Family dysfunction (eg, divorce, spouse abuse, chaotic family style)
• Difficult child (prior to this characterization, the provider should seek out explanations as to why, including subtle dysphagia)
• Child neglect
• Emotional deprivation syndrome
• Poor feeding or feeding skills disorder
• Feeding disorders (eg, anorexia, bulimia)

Organic failure to thrive

Prenatal onset of organic failure to thrive involves the following:

• Prenatal causes of failure to thrive are often associated with complications of prematurity. Premature babies have an increased incidence of many medical conditions, including renal disease, heart disease, lung disease, and CNS disorders. All of these disorders can lead to intrauterine failure to thrive.
• Most premature babies catch-up to the growth of term babies by the time they are aged 2-4 years. Intrauterine growth retardation (IUGR) is diagnosed when an infant is born below the expected weight (usually < 3%) for their gender and gestational age. Some premature (as well as full term) babies, particularly those with concomitant IUGR, have failure to thrive.
• Whether premature babies are small because of prematurity or whether they have permanent failure to thrive is sometimes difficult to determine. If infants double their birth weight by age 4-6 months and triple their birth weight by 1 year, then full catch-up growth can be anticipated.
• Other causes of the prenatal onset of failure to thrive include exposure to toxins, environmental influences, maternal factors, intrauterine infection, and placental or chromosomal abnormalities.
• The most important prenatal exposures compromising growth are tobacco, which is known to produce placental insufficiency, and alcohol ingestion. Prenatal ingestion of drugs of abuse (eg, cocaine, amphetamines) can also play a role in the prenatal onset of failure to thrive. Because these drugs are often taken together, separating the effects of each drug may be difficult. Also, maternal exposure to certain medications (eg, hydantoin, phenobarbital) can lead to in utero failure to thrive.
• Certain maternal illness (eg, hypertension, preeclampsia, heart disease, anemia, advanced diabetes mellitus) can lead to uteroplacental insufficiency and can result in smaller babies.

Although the differential diagnosis of postnatal organic failure to thrive is vast, dividing the etiology is useful. The etiology can be divided into the following 3 general areas: inadequate energy intake, compromised use (usually vomiting or malabsorption and/or excessive losses), and excessive metabolic demands. An astute mother recognizes the category to which her baby belongs. The astute physician recognizes patterns that encompass more than one of these categories.

Causes of inadequate energy intake include the following:

• These causes can result from mechanical problems (eg, neuromuscular abnormalities, craniofacial abnormalities), lack of appetite, breathing difficulties, significant developmental delay, and primary GI disease or dysfunction. Medical therapy itself can sometimes significantly affect intake.
• Mechanical problems can cause a poor suck or defective swallowing. Hypotonia (eg, Wernig-Hoffman syndrome, Prader-Willi syndrome), neuromuscular or CNS system disease, and CP (most commonly) lead to incoordination of feeding. Structural defects related to craniofacial abnormalities (eg, severe micrognathia, cleft palate, cleft lip) make coordinating an oral bolus difficult. Children with developmental disabilities are often malnourished; however, a systematic approach can identify specific problems. Once corrected, a considerable benefit is realized.^[26]
• Children who have chronic illnesses are often too sick or too apathetic to maintain good oral intake. A lack of appetite is seen in renal failure, malignancy, tuberculosis, and HIV infection, which are associated with increased circulating levels of cachectin (also known as tumor necrosis factor [TNF]).
• Chronic cardiopulmonary compromise can make feeding exhausting and can attenuate caloric intake. Examples include congenital heart disease that leads to congestive heart failure (CHF) or chronic lung disease (eg, bronchopulmonary dysplasia, cystic fibrosis).
• Conditions that cause abdominal pain with eating (eg, gastroesophageal reflux, celiac disease, inflammatory bowel disease, other enteropathies), and those that include impaired peristalsis (eg, achalasia, gastroparesis, pseudoobstruction) all decrease ingestion.
• Ghrelin is a hormone that enhances appetite and induces a positive energy balance. An investigation to examine the role of ghrelin in failure to thrive revealed higher circulating concentrations but paradoxically lower appetite scores.^[27]

Inadequate use of ingested energy includes the following:

• This can cause failure to thrive even when oral intake is adequate. This is usually secondary to emesis, or malabsorption, which is sometimes secondary to compromised digestion.
• Children with metabolic diseases, drug toxicities, gastroesophageal reflux, eosinophilic, viral, or traumatic esophagitis may experience considerable vomiting and may be unable to salvage adequate quantities of their ingested caloric intake.
• Malabsorption may be secondary to compromised villous surface area, such as in celiac disease (gluten enteropathy), tropical sprue, cow's milk allergy and (less commonly) soy protein allergy, postviral enteropathy, chronic giardiasis and other chronic parasites, immunoglobin A (IgA) deficiency, radiation enteritis, Crohn disease, severe iron or zinc deficiency, acrodermatitis enteropathica, small bowel lymphoma, bacterial overgrowth, Zollinger-Ellison syndrome, Whipple disease, and abetalipoproteinemia.
• Anatomic defects of the small intestine (eg, short gut syndrome, blind loop syndrome, bacterial overgrowth, Hirschsprung disease) are frequently associated with failure to thrive.
• Digestion must precede absorption and any diseases that compromise this process can lead to wasting of energy and failure to thrive. Examples include pancreatic insufficiency including cystic fibrosis and (less commonly) Shwachman-Diamond syndrome and chronic cholestasis (seen primarily in children with hepatobiliary disease, especially biliary atresia) and cirrhosis secondary to metabolic disease and intrauterine infection
• Excessive losses of protein from the gut can disrupt growth and is discussed in the eMedicine article Protein-Losing Enteropathy.

Illnesses that increase metabolic demands include the following:

• Cancer, HIV, inflammatory bowel disease, certain collagen vascular diseases, and cardiopulmonary deficits that lead to tachypnea and hyperthyroidism can increase the amount of basal energy expenditure and thus increase the amount necessary to achieve normal growth.
• Many illnesses simultaneously have 2-3 features that cause failure to thrive. Children with CHF or bronchopulmonary dysplasia have both decreased intake of nutrients and increased metabolic demands. In addition, right-sided heart failure leads to digestive tract edema that compromises digestion and absorption. Children with cystic fibrosis often have tachypnea, frequent intercurrent illnesses that rob them of their appetite, and fat malabsorption. These children may also suffer from depression, which introduces another important contributor to failure to thrive.

An important part of the evaluation of all children is observation of the infant while feeding. Observing infants while they are feeding sheds light on maternal-infant interactions, the infant's ability to suck and swallow, and on the fatigability of the child.

Genetic short stature and constitutional delay of growth are 2 conditions associated with decreased growth that must be distinguished from failure to thrive. From birth to about age 2 years, a baby's weight changes to follow the genetic predisposition of the parents' height and weight. During this time of transition, children with genetic short stature may cross percentiles downward and still be considered normal. However, most children in this category find their true growth curve by age 3 years. Although children with genetic short stature are often below the third percentile on the growth chart, they have normal weight-to-height ratios and bone ages equal to their chronological ages.

The other condition associated with short stature that must be distinguished from failure to thrive is constitutional growth delay, another variation of normal growth. Children with short stature resulting from constitutional delay often have a family history of delayed growth and puberty. They have a deceleration of growth in the first 2 years that can be confused with failure to thrive, but then grow parallel to but below the third percentile. Puberty is delayed, but ultimate height may be normal. A distinguishing point from genetic short stature is that bone age is delayed.

Table 1. Summary of Organic Causes of Failure to Thrive (Open Table in a new window)

Combined organic and nonorganic failure to thrive

Failure to thrive is now commonly recognized as the result of both organic and nonorganic reasons.^{[10, 11]} Among the many infants with psychosocial deprivation, those with growth compromise often exhibit subtle evidence of dysphagia.

Conversely, some children with chronic illnesses who have failure to thrive may be less likely or less able to obtain adequate treatment for their primary organic disease. Reasons for this may be dysfunctional or ill caretakers, who may have psychological or behavioral co-morbidities themselves. Illnesses in children, particularly chronic illnesses, can take their toll on families. Stresses from coping with chronic illnesses may lead to parental dysfunction, such as depression, alcohol or drug abuse, divorce, or chaotic home environments. Parental dysfunction and the resultant negative atmosphere in which children are reared affect their food intake.

Children may also undergo personality changes when they have chronic diseases. Medications (eg, steroids) are well known to cause behavioral changes, but the mere presence of a chronic illness can also result in resistance or noncompliance in many aspects of a child's life, including consumption of proper energy intake. This is most common when the chronic illness includes the GI tract (eg, Crohn disease) or is especially debilitating (eg, HIV, difficult to treat neoplasia). As psychologists identify a greater proportion of children with chronic diseases who have depression as a comorbidity, this possible cause of failure to thrive should not be overlooked.