Nutritional Considerations in Failure to Thrive

Nutritional Considerations in Failure to Thrive

No Results

No Results

processing….

Failure to thrive is an interruption in the normal pattern of growth, usually seen in younger children. While many anthropometric standards have been employed to define “growth,” (BMI, weight, or weight-for-height z-scores), serially comparing a child to appropriate standard growth curves is now commonly employed. 

Often exacerbating the effects of chronic infections, failure to thrive is perhaps the greatest contributor to worldwide childhood morbidity and mortality. Stunting with intellectual compromise is seen in children who survive long periods of inadequate growth. In the developed world, there is controversy regarding the long-term deficits seen in children who experience failure to thrive. However, the contribution that failure to thrive plays in contributing to the morbidity of pediatric pathologic states is being more appreciated.  

Failure to thrive can be secondary to inadequate intake of calories, inefficient utilization of ingested calories (emesis, malabsorption) or an increased basal metabolism (usually seen in oncology, infections, cardiopulmonary deficiencies, chronic inflammatory states, and hyperthyroidism). 

Comprehensive evaluation of children by multidisciplinary feeding teams has illustrated that frequently more than one entity is present in a single child with failure to thrive. One example would be the anorexia related to depression seen in children with chronic illnesses.

It has been long considered dogma that the overwhelming majority of children with growth impairment in the developing world have psychosocial issues that result in nonorganic failure to thrive. Multiple feeding teams have noted that among children with nonorganic failure to thrive, there is frequently a subtle organic problem such as dysphagia, gastroesophageal reflux, constipation, or food allergy/intolerance that has created pain and/or fear in this cohort. Recognition and therapy that addresses these issues have yielded improved outcomes.     

Failure to thrive (FTT) is both a descriptive term for various entities and a diagnosis. It is defined as a significant interruption in the expected rate of growth during early childhood. Because sequential measurements of growth are vital aspects of preventive pediatrics, FTT is a concern for all pediatric heath care providers. All standard pediatric textbooks have sections on this topic, [1] and numerous review articles have been written. [2, 3, 4, 5, 6] However, despite significant attention, the consequences of FTT on developmental outcomes in industrialized children is controversial as discussed in the section on prognosis below. It is easier to appreciate that in certain children, FTT can be a prelude to significant physical and cognitive morbidity, including stunting, and mortality. This is especially relevant throughout the developing world, in rural and impoverished inner city children, and in those with multiple chronic illnesses. Two significant developments in the approach to the child with FTT have begun to dramatically influence the approach to these children.

Firstly, while it is accepted that all children with failure to thrive have inadequate or worsening growth over time, one area of controversy is determining which anthropometric criteria should be utilized to define this term. [7] The most common definitions are weight less than the third to fifth percentile for age on more than one occasion or weight measurements that fall 2 major percentile lines using the standard growth charts of the National Center for Health Statistics (NCHS).

Some authors have included height measurements as part of the definition; however, height measurements more precisely describe short stature. If weight parameters are significantly compromised, height can also be secondarily affected in individuals with FTT. A European study examined a large cohort of children using various terms associated with pediatric growth compromise and documented a wide variance in the prevalence of this condition. [8] Although serial measurements of head circumference are important in the evaluation of infants and toddlers, isolated failure of the head to grow should not suggest the typical failure to thrive differential.

The American Society for Parenteral and Enteral Nutrition assembled a group of experts that recently published a comprehensive report on pediatric malnutrition based on a comprehensive analysis of literature published through 2011. [9] They organized their review, discussion, recommendations and definition around five key domains. The authors developed a novel definition of pediatric malnutrition that clearly overlaps with the term failure to thrive as employed in this article and by multiple other authors. Their proposed definition is an “imbalance between nutrient requirements and intake, resulting in cumulative deficits of energy, protein, or micronutrients that may negatively affect growth, development, and other relevant outcomes.”

To address the controversy of determining which anthropometric criteria should be utilized to define FTT, the group has recommended that z-scores be used to express individual anthropometric variables in relation to the population reference standard. The authors agree that this is the best approach to track serial measurements in a child being evaluated for FTT.

The second new development in the approach to a child with FTT is that especially since 2011, there have been a number of publications from multidisciplinary feeding groups from around the United States that have stressed the significant integration between physical issues and psychosocial problems that yield FTT (see pathophysiology section below).

The working group characterized failure to thrive as “a term used to describe children who are not growing as expected.” They note that more than 90% of cases in most studies do not have an underlying medical cause, and virtually all are identified by a careful history and physical exam. [10] The report also cites a paper describing an inner city academic center that only evaluated 75 children in their specialized clinics over a 40 month period. These authors and others have characterized virtually all of their referrals as having psychosocial etiologies for their FTT and recommended a reappraisal of how to provide resources for these children. [11]

Another recent study from a multidisciplinary feeding program at a US medical school also reports that 90% of their referrals had nonorganic failure to thrive. While they described a very short follow-up, they also report that children who adhered to their basic instructions were able to quickly gain significantly more weight than those were “nonadherent.” However, the 25% of the cohort who were unable to follow directions, may also include children who had unidentified issues. [12]

With the routine inclusion of comprehensive speech and feeding evaluations as part of the FTT work-up, psychosocial compromise is now recognized as most likely to yield failure to thrive in children with subtle swallowing dysfunction, or other primary organic conditions, especially those associated with visceral pain during feeds. [13] As this fundamental paradigm is reconsidered, [14, 15] the practicing provider evaluating a deprived child with failure to thrive must make every effort to illicit and correct discomfort (such as feeding refusal, grimacing, bloating, premature satiety) or dysphagia (such as coughing, choking, gagging, or extended meal times). Thus, a routine part of the evaluation of children with failure to thrive is identifying any pathophysiologic conditions that may contributing factors.  

To consolidate all of these nuances, some authors have gone from categorizing children as either one extreme or the other to describing a spectrum extending from pure nonorganic failure to thrive to pure organic failure to thrive, with individual children lying closer to one or the other. [16] In this view, medical, developmental, neurological, environmental issues are often found in a single child. [17]

Normal growth and growth charts of term and premature infants, as well as the etiology, evaluation, management, and outcome of failure to thrive are discussed in this article. For information on energy malnutrition, see the article Marasmus.

Organic FTT is secondary to inadequate intake, increased losses, compromised utilization of ingested calories, excessive metabolic demands, or combinations of these factors. Nonorganic failure to thrive is defined as a consequence of inadequate energy intake. However, the complexity of inadequate intake has now been studied in more detail. While classically viewed as a behavioral i.e. nonorganic problem, it is now appreciated that identifiable and treatable pathologies can be antecedents of this behavior and must be eradicated to reverse this situation. [18] Conversely, the increased prevalence of FTT in children with chronic medical conditions has been emphasized by the recent pediatric malnutrition working group which recommended that malnutrition be characterized explicitly with reference to the specific pathologic state. [9] The following examples illustrate the spectrum of potential interactions between organic and nonorganic features in FTT children. [19, 20, 21, 22, 23, 24, 25]

Factors contributing to childhood feeding difficulties were described in 340 out of 349 participants identified by an interdisciplinary feeding team. These included developmental disabilities, gastrointestinal problems, cardiopulmonary problems, neurological problems, renal disease and anatomical anomalies. The most prevalent condition was gastroesophageal reflux. [19]

In a review of 38 intervention studies of 218 children with food refusal, 212 had some form of a medical issue. The majority, 116 children (55%), had gastrointestinal disorders (e.g. gastroesophageal reflux) and 131 (62%) had a non-gastrointestinal medical disorder (e.g. bronchopulmonary dysplasia, seizure disorder). In this study  gastroesophageal reflux was the most common medical diagnosis while other diagnoses such as cardiopulmonary conditions (33%), neurological conditions (25%), food allergies (15%) anatomical anomalies (14%) and delayed gastric emptying (6%) were also reported. [20]

Another study examining sensory processing skills in a childhood feeding disorders group of toddlers with nonorganic failure to thrive concluded that sensory processing problems were more commonly observed in toddlers with feeding problems and growth deficiency. [21]

Out of a 143 subjects in a feeding clinic in a tertiary hospital, 65.5% (55/84) of children with a medical condition also had one or more feeding behavior disorders. This study by Jung et al also found no underlying medical disorder to explain the feeding disorders in 59 (41.3%) of the 143 subjects. Many of these children had feeding behavior disorders such as sensory food aversion and infantile anorexia with FTT. [22]

Dysphagia or odynophagia, caused by the inflammation of the esophagus (drug-induced, allergic, eosinophilic or induced by gastroesophageal reflux disease), motor dysfunction or structural anomaly of the upper gastrointestinal tract, is well recognized as a cause of food refusal as swallowing food becomes a triggering factor of pain. [23, 24]

In a study characterizing the feeding difficulty of 700 children referred for assessment of severe feeding difficulty, close to 50% of the children had a combined medical and oral condition underlying their feeding difficulties. More than half of the children were examined for gastrointestinal conditions, particularly gastroesophageal reflux disease. The results indicate that oral sensory-based feeding problems are related to past medical intervention. [25]

Normal growth in term infants

The average birth weight for a term infant is 3.3 kg. Weight drops as much as 10% in the first few days of life, secondary to loss of excess fluid. By 10-14 days of life, birth weight should be regained. Breastfed infants who are fed smaller volumes of colostrum for the first few days regain birth weight a little later than bottle-fed infants.

On average, infants gain 1 kg/mo for the first 3 months, 0.5 kg/mo from age 3-6 months, 0.33 kg/mo from age 6-9 months, and 0.25 kg/mo from age 9-12 months.  Expressed in another perspective, full term infants double their birth weight by 4-6 months of age and triple their weight by 12 months of age. A third approach to use is that term infants gain almost 30 g (1 oz) per day for 3 months and then almost 15 g (0.5 oz) per day for the next 6 months. From 9 months of age until the child is a toddler, the average weight gain is roughly 0.25 kg/mo (or 0.5 lb/mo). Afterwards, the weight gain is about 2 kg/y through early school age.

Caloric requirements to assure adequate intake in a normal infant is 100-110 kcal/kg/d for the first six months and decreases slightly to 100 kcal/kg/d for the second half of the first year. Beyond 10 kg, 50 kcal/kg/day is required until 20 kg and beyond 20 kg, 20 kcal/kg/d are necessary.

Term infants grow 25 cm in length during the first year, 12.5 cm in the second year, and then slow down to approximately 5-6 cm between 4 years of age and the onset of puberty, at which time, growth can increase up to 12 cm per year.

The average head circumference is 35 cm at birth and rapidly increases to 47 cm by age 1 year. The rate of growth then slows, reaching an average of 55 cm by 6 years of age.

Also, the upper-to-lower body segment ratio changes with growth. Normally, the ratio at birth is 1.7, the ratio at 3 years of age is 1.3, and the ratio by 7 years of age becomes 1.0 with the upper body segment and lower body segment being about equal. The lower body segment is measured from the symphysis pubis to the floor.

Normal growth in premature infants

When plotting growth charts for premature babies, a “corrected age” should be used. This corrected age can be calculated by subtracting the number of weeks of prematurity from the postnatal age. Special growth charts based on gestational age rather than chronological age have been developed for infants, beginning at 26 weeks’ gestational age. However, because these charts represent a compilation of a relatively small number of infants, they may not be completely reliable. Whichever technique is used for premature babies (eg, adjustment of age, using specific premature growth charts), consistency of methodology is essential. Once a method for plotting growth is chosen, that technique should be followed each time plotting occurs. Prior to 40 weeks’ gestation, some infants may require as much as 120 kcal/kg/d to ensure adequate weight gain.

Catch-up growth is attained at approximately 18 months of age for head circumference, 24 months of age for weight, 40 months of age for height. Subsequently, normal growth charts can be used. In some premature babies with very low birth-weight, catch-up growth does not occur until early school age.

Growth charts

Growth charts were developed by the NCHS based on data collected through the Third National Health and Nutrition Examination Survey. They have been used since 1977 and are available for males and females 0-36 months of age and 2-18 years of age. The growth charts for boys and girls 0-36 months of age include weight and height for age and head circumference; growth charts for both age groups include weight for stature.

These charts have been revised and are available from the Centers for Disease Control and Prevention (2000 CDC Growth Charts: United States). [26] The new charts are applicable to infants, children, and adolescents from birth to age 20 years and have 7 percentile curves (5th, 10th, 25th, 50th, 75th, 90th, 95th). Charts are available for use in subspecialty patients (eg, endocrine, gastroenterology), with additional third and 97th percentile curves. Body mass index (BMI) charts, which are available for individuals aged 2-20 years, have replaced the weight-for-stature charts. BMI is calculated by dividing weight in kilograms by height in meters squared.

Accurate measurements are essential to the interpretation of growth charts. Scales need to be regularly calibrated; length should be carefully measured, and head circumference should be measured using standardized techniques.

WHO has recommended the use of z-scores in expressing anthropometric measurements. Z-scores allow more precision in describing anthropometric status than does the customary placement “near” or “below” a certain percentile curve. [9]

Alternate growth charts are available for children who are breastfed and for children with multiple genetic conditions including Down syndrome, [27]  Turner syndrome, [28] achondroplasia, [29] meningomyelocele, low birth weight, and very low birth weight. No matter which growth chart is used, the most valuable information is obtained by careful measuring and plotting on the same chart over time. Infants and children should remain within 1-2 percentile curves over time.

Other anthropometric variables for assessing nutritional status

In acutely ill children, height and weight measurements may be challenging to accurately record due to difficulty in transporting critically ill children, or to fluid shifts that affect the measurement. Mid–upper arm circumference (MUAC) has been suggested as a proxy for weight and HC as a proxy for height. In patients with fluid shifts and edema, MUAC may be a better indicator than weight-for-height for classification of acute malnutrition. MAMC and triceps skinfold are other measurements that are useful in children where height and weight measurements are not easily acquirable. Mid-arm muscle circumference (MAMC) may be calculated from MUAC and triceps skin fold (TSF) using the formula MAMC = MUAC – (TSF × 0.314). [9]

United States

In reports from 1980-1989, failure to thrive accounted for 1-5% of tertiary hospital admissions for infants younger than 1 year. As many as 10% of children in primary care settings and 5% of US hospitalized children have been reported to show signs of failure to thrive. [30, 10]  The incidence is highest in children with prematurity and with other medical conditions. The proportion of nonorganic failure to thrive among all infants with failure to thrive is much higher in the United States and other industrialized countries than in the developing nation.

International

In underdeveloped countries, malnutrition manifesting as failure to thrive is more common. Worldwide, underweight prevalence was projected to decline from 26.5% in 1990 to 17.6% in 2015, a change of –34% (95% confidence interval [CI], –43% to –23%). In developed countries, the prevalence was estimated to decrease from 1.6% to 0.9%, a change of –41% (95% CI, –92% to 343%). In developing regions, the prevalence was forecasted to decline from 30.2% to 19.3%, a change of –36% (95% CI, –45% to –26%). In Africa, the prevalence of underweight was forecasted to increase from 24.0% to 26.8%, a change of 12% (95% CI, 8%-16%). In Asia, the prevalence was estimated to decrease from 35.1% to 18.5%, a change of –47% (95% CI, –58% to –34%). Worldwide, the number of underweight children was projected to decline from 163.8 million in 1990 to 113.4 million in 2015, a change of –31% (95% CI, –40% to –20%). Numbers are projected to decrease in all subregions except the subregions of sub-Saharan, Eastern, Middle, and Western Africa, which are expected to experience substantial increases in the number of underweight children. Thus, neither the world as a whole, nor the developing regions, achieved the Millennium Development Goals of decreasing the prevalence by 50% from 1990 to 2015. This is largely due to the deteriorating situation in Africa where all subregions, except Northern Africa, are expected to fail to meet the goal. [31]

Mortality/Morbidity

The global trend in chronic failure to thrive (referred to as stunting) prevalence and numbers affected is decreasing. Between 2000 and 2013 stunting prevalence declined from 33% to 25% and numbers declined from 199 million to 161 million. In 2013, about half of all stunted children lived in Asia and over one third in Africa. Globally, 51 million children under-five years of age were acutely malnourished (wasted) and 17 million were severely wasted. Globally, wasting prevalence in 2013 was estimated at almost 8% and nearly a third of that was for severe wasting, totaling 3%. Approximately two thirds of all wasted children lived in Asia and almost one third in Africa, with similar proportions for severely wasted children. [32]

Ultimate physical growth and cognitive development may be decreased in children with long standing failure to thrive, especially with an early onset. However, efforts to analyze the published data have not yielded unequivocal confirmation in children in the developing world. [33] Earlier publications have described more cognitive deficits in nonorganic than organic failure to thrive. [34]

In developing countries, malnutrition is a significant cause of mortality, whether directly or secondary to complications (eg, infection). Among children with certain illnesses, failure to thrive is an independent risk factor for premature mortality, such as with HIV infection  [35] and epidermolysis bullosa. [36]

Race

Failure to thrive can occur in all socioeconomic strata, although it is more frequent in families living in poverty. Studies indicate increased incidence in children receiving Medicaid, children living in rural areas, and children who are homeless.

Sex

Nonorganic failure to thrive is reported more commonly in females than in males. In certain areas of the world where there is nutrient shortage, distribution is sometimes gender based yielding greater prevalence in females.

Age

The term is mainly reserved for growth compromise in young children.

Multiple studies have investigated whether failure to thrive is associated with long-term cognitive deficits. [33, 37, 38] Two published meta-analyses looking at cognitive outcomes of published children with failure to thrive in developed countries found small differences consisting of 3-4 IQ points. [33, 38] Interestingly, one group concluded that this disparity was not enough to warrant an aggressive approach to identification and treatment of this entity. [33] The other authors suggested substantial population-based cognitive deficiencies could be attributed to failure to thrive. [38]

Another longitudinal population study of a large cohort found the same degree of IQ score difference when they examined a cohort with infantile failure to thrive. [39] A separate study that further divided nonorganic failure to thrive into those who had or had not experienced neglect defined a particularly vulnerable cohort; failure to account for this additional variable may explain some differences. [40]

A new area of research has been exploring whether aggressive refeeding or early malnutrition itself could impact future health parameters independent of simply changes in BMI and growth. The Barker or Fetal Origins Hypothesis is based on data accumulated over the last 20 years that has linked low birth weight to a subsequent increased risk for cardiovascular disease and type 2 diabetes. This theory states that in utero nutrient restriction results in epigenetic modifications that reprogram intermediary metabolism, glucose regulation, and blood pressure regulation. These genetic changes persist into adult life and yield increased susceptibility to disease.

A few epidemiologic studies have hypothesized that this principle could be extended to include malnutrition occurring in early postnatal life. A comprehensive review summarizes the published literature in this field and concludes that children with early-onset enteric infections, malnutrition, and stunting appear to be at increased risk to ultimately develop the metabolic syndrome. [41] A small observational study describes a cohort of young children with severe failure to thrive who received aggressive nutritional rehabilitation and ultimately developed obesity. [42] Whether this was a consequence of the primary deficit or the therapy is not addressed.

Potential long-term psychosocial consequences of stunting secondary to growth failure in early childhood in the developing world have been highlighted by a longitudinal study following a rural Guatemalan cohort. [43] Affected individuals went on to have profound consequences in adulthood related to economic status, marriage, and fertility. They scored worse on tests of reading and intelligence and had lower cognitive skills. Men had decreased likelihood of entry into higher-salaried positions. Individuals who were stunted often entered into relationships with poorer partners and were more likely to live in poorer households as adults. Women with stunting had their first child at a younger age and had more pregnancies and more children. While provocative, the potential for other economic, educational, or sociologic factors being the primary explanation for these outcomes still needs to be considered.

Although the goal of all pediatricians caring for children with organic failure to thrive is to incorporate measures into their management that are designed to preserve adequate growth, this may prove to be difficult. A greater appreciation for the significant prevalence of failure to thrive in children with multiple chronic illnesses including cerebral palsy (CP), congenital heart disease, cystic fibrosis, cirrhosis, HIV, inflammatory bowel disease, malignancy, and genetic diseases has been noted as well as the contribution of FTT to the ultimate outcomes in these patients.

Bauchner H. Failure to Thrive. Nelson Textbook of Pediatrics. 18th Ed. Philadelphia, PA: WB Saunders; 2007. 37;184-7.

Frank DA, Zeisel SH. Failure to thrive. Pediatr Clin North Am. 1988 Dec. 35(6):1187-206. [Medline].

Porter B, Skuse D. When does slow weight gain become ‘failure to thrive’?. Arch Dis Child. 1991 Jul. 66(7):905-6. [Medline].

Zenel JA Jr. Failure to thrive: a general pediatrician’s perspective. Pediatr Rev. 1997 Nov. 18(11):371-8. [Medline].

Hoare KJ. A baby presenting with failure to thrive in primary care: a case report. Cases J. 2009. 2(1):137. [Medline].

Leung DH, Chung CT. Cases in pediatric gastroenterology from The Children’s Hospital of Philadelphia: a 2-year-old boy with diarrhea, failure to thrive, and hepatomegaly. Medscape J Med. 2009. 11(1):13. [Medline].

Growth retardation indicators in children under 5 years old. Epidemiol Bull. 1998 Mar. 19 (1):13-6. [Medline].

Olsen EM, Petersen J, Skovgaard AM, et al. Failure to thrive: the prevalence and concurrence of anthropometric criteria in a general infant population. Arch Dis Child. 2007 Feb. 92(2):109-14. [Medline].

Mehta NM, Corkins MR, Lyman B, Malone A, Goday PS, Carney LN, et al. Defining pediatric malnutrition: a paradigm shift toward etiology-related definitions. JPEN J Parenter Enteral Nutr. 2013 Jul. 37 (4):460-81. [Medline].

Schwartz ID. Failure to thrive: an old nemesis in the new millennium. Pediatr Rev. 2000 Aug. 21 (8):257-64; quiz 264. [Medline].

Atalay A, McCord M. Characteristics of failure to thrive in a referral population: implications for treatment. Clin Pediatr (Phila). 2012 Mar. 51 (3):219-25. [Medline].

Larson-Nath CM, Goday PS. Failure to Thrive: A Prospective Study in a Pediatric Gastroenterology Clinic. J Pediatr Gastroenterol Nutr. 2016 Jun. 62 (6):907-13. [Medline].

Reilly SM, Skuse DH, Wolke D, Stevenson J. Oral-motor dysfunction in children who fail to thrive: organic or non-organic?. Dev Med Child Neurol. 1999 Feb. 41(2):115-22. [Medline].

Olsen EM, Skovgaard AM. [Psychosomatic failure-to-thrive in infants and toddlers]. Ugeskr Laeger. 2002 Nov 25. 164(48):5631-5. [Medline].

Skuse DH. Non-organic failure to thrive: a reappraisal. Arch Dis Child. 1985 Feb. 60(2):173-8. [Medline].

Manikam R, Perman JA. Pediatric feeding disorders. J Clin Gastroenterol. 2000 Jan. 30(1):34-46. [Medline].

Black MM, Tilton N, Bento S, Cureton P, Feigelman S. Recovery in Young Children with Weight Faltering: Child and Household Risk Factors. J Pediatr. 2016 Mar. 170:301-6. [Medline].

Manikam R, Perman JA. Pediatric feeding disorders. J Clin Gastroenterol. 2000 Jan. 30 (1):34-46. [Medline].

Field D, Garland M, Williams K. Correlates of specific childhood feeding problems. J Paediatr Child Health. 2003 May-Jun. 39 (4):299-304. [Medline].

Williams KE, Field DG, Seiverling L. Food refusal in children: a review of the literature. Res Dev Disabil. 2010 May-Jun. 31 (3):625-33. [Medline].

Yi SH, Joung YS, Choe YH, Kim EH, Kwon JY. Sensory Processing Difficulties in Toddlers With Nonorganic Failure-to-Thrive and Feeding Problems. J Pediatr Gastroenterol Nutr. 2015 Jun. 60 (6):819-24. [Medline].

Jung JS, Chang HJ, Kwon JY. Overall Profile of a Pediatric Multidisciplinary Feeding Clinic. Ann Rehabil Med. 2016 Aug. 40 (4):692-701. [Medline].

Wu YP, Franciosi JP, Rothenberg ME, Hommel KA. Behavioral feeding problems and parenting stress in eosinophilic gastrointestinal disorders in children. Pediatr Allergy Immunol. 2012 Dec. 23 (8):730-5. [Medline].

Dellon ES, Gonsalves N, Hirano I, Furuta GT, Liacouras CA, Katzka DA, et al. ACG clinical guideline: Evidenced based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). Am J Gastroenterol. 2013 May. 108 (5):679-92; quiz 693. [Medline].

Rommel N, De Meyer AM, Feenstra L, Veereman-Wauters G. The complexity of feeding problems in 700 infants and young children presenting to a tertiary care institution. J Pediatr Gastroenterol Nutr. 2003 Jul. 37 (1):75-84. [Medline].

[Guideline] Centers for Disease Control and Prevention. CDC Growth Charts. August 4, 2009. [Full Text].

[Guideline] Cronk C, Crocker AC, Pueschel SM, et al. Growth charts for children with Down syndrome: 1 month to 18 years of age. Pediatrics. 1988 Jan. 81(1):102-10. [Medline].

[Guideline] Lyon AJ, Preece MA, Grant DB. Growth curve for girls with Turner syndrome. Arch Dis Child. 1985 Oct. 60(10):932-5. [Medline].

[Guideline] Horton WA, Rotter JI, Rimoin DL, Scott CI, Hall JG. Standard growth curves for achondroplasia. J Pediatr. 1978 Sep. 93(3):435-8. [Medline].

Daniel M, Kleis L, Cemeroglu AP. Etiology of failure to thrive in infants and toddlers referred to a pediatric endocrinology outpatient clinic. Clin Pediatr (Phila). 2008 Oct. 47(8):762-5. [Medline].

de Onis M, Blössner M, Borghi E, Frongillo EA, Morris R. Estimates of global prevalence of childhood underweight in 1990 and 2015. JAMA. 2004 Jun 2. 291 (21):2600-6. [Medline].

Levels & Trends in Child Malnutrition: UNICEF-WHO-The World Bank Joint Child Malnutrition Estimates. WHO. Available at http://www.who.int/nutgrowthdb/summary_jme_2013.pdf?ua=1. 2014; Accessed: December 1, 2016.

Rudolf MC, Logan S. What is the long term outcome for children who fail to thrive? A systematic review. Arch Dis Child. 2005 Sep. 90(9):925-31. [Medline].

Drewett RF, Corbett SS, Wright CM. Cognitive and educational attainments at school age of children who failed to thrive in infancy: a population-based study. J Child Psychol Psychiatry. 1999 May. 40(4):551-61. [Medline].

Prazuck T, Tall F, Nacro B, et al. HIV infection and severe malnutrition: a clinical and epidemiological study in Burkina Faso. AIDS. 1993 Jan. 7(1):103-8. [Medline].

Lechner-Gruskay D, Honig PJ, Pereira G, McKinney S. Nutritional and metabolic profile of children with epidermolysis bullosa. Pediatr Dermatol. 1988 Feb. 5(1):22-7. [Medline].

Reif S, Beler B, Villa Y, Spirer Z. Long-term follow-up and outcome of infants with non-organic failure to thrive. Isr J Med Sci. 1995 Aug. 31(8):483-9. [Medline].

Corbett SS, Drewett RF. To what extent is failure to thrive in infancy associated with poorer cognitive development? A review and meta-analysis. J Child Psychol Psychiatry. 2004 Mar. 45(3):641-54. [Medline].

Emond AM, Blair PS, Emmett PM, Drewett RF. Weight faltering in infancy and IQ levels at 8 years in the Avon Longitudinal Study of Parents and Children. Pediatrics. 2007 Oct. 120(4):e1051-8. [Medline].

Mackner LM, Starr RH Jr, Black MM. The cumulative effect of neglect and failure to thrive on cognitive functioning. Child Abuse Negl. 1997 Jul. 21(7):691-700. [Medline].

DeBoer MD, Lima AA, Oría RB, Scharf RJ, Moore SR, Luna MA, et al. Early childhood growth failure and the developmental origins of adult disease: do enteric infections and malnutrition increase risk for the metabolic syndrome?. Nutr Rev. 2012 Nov. 70(11):642-53. [Medline]. [Full Text].

Kim GJ, Furman LM. Obesity Outcomes in Children With a History of Failure to Thrive. Clin Pediatr (Phila). 2013 May 15. [Medline].

Hoddinott J, Behrman JR, Maluccio JA, et al. Adult consequences of growth failure in early childhood. Am J Clin Nutr. 2013 Nov. 98(5):1170-8. [Medline]. [Full Text].

Berwick DM, Levy JC, Kleinerman R. Failure to thrive: diagnostic yield of hospitalisation. Arch Dis Child. 1982 May. 57(5):347-51. [Medline].

Genero A, Moretti C, Fait P, Guariso G. [Non-organic failure to thrive: retrospective study in hospitalized children]. Pediatr Med Chir. 1996 Sep-Oct. 18(5):501-6. [Medline].

Homer C, Ludwig S. Categorization of etiology of failure to thrive. Am J Dis Child. 1981 Sep. 135(9):848-51. [Medline].

Crossin R, Cairney S, Lawrence AJ, Duncan JR. Adolescent inhalant abuse leads to other drug use and impaired growth; implications for diagnosis. Aust N Z J Public Health. 2016 Oct 23. [Medline].

Yoo SD, Hwang EH, Lee YJ, Park JH. Clinical Characteristics of Failure to Thrive in Infant and Toddler: Organic vs. Nonorganic. Pediatr Gastroenterol Hepatol Nutr. 2013 Dec. 16(4):261-8. [Medline]. [Full Text].

Oates RK. Similarities and differences between nonorganic failure to thrive and deprivation dwarfism. Child Abuse Negl. 1984. 8(4):439-45. [Medline].

Skuse DH. Non-organic failure to thrive: a reappraisal. Arch Dis Child. 1985 Feb. 60(2):173-8. [Medline].

Shams N, Mostafavi F, Hassanzadeh A. Determinants of complementary feeding practices among mothers of 6-24 months failure to thrive children based on behavioral analysis phase of PRECEDE model, Tehran. J Educ Health Promot. 2016 Jun 23. 5:24. [Medline].

Wu YP, Franciosi JP, Rothenberg ME, Hommel KA. Behavioral feeding problems and parenting stress in eosinophilic gastrointestinal disorders in children. Pediatr Allergy Immunol. 2012 Dec. 23 (8):730-5. [Medline].

Vohr BR, Stephens BE, McDonald SA, et al. Cerebral palsy and growth failure at 6 to 7 years. Pediatrics. 2013 Oct. 132(4):e905-14. [Medline]. [Full Text].

Schwarz SM, Corredor J, Fisher-Medina J, Cohen J, Rabinowitz S. Diagnosis and treatment of feeding disorders in children with developmental disabilities. Pediatrics. 2001 Sep. 108(3):671-6. [Medline].

Tannenbaum GS, Ramsay M, Martel C, Samia M, Zygmuntowicz C, Porporino M. Elevated circulating acylated and total ghrelin concentrations along with reduced appetite scores in infants with failure to thrive. Pediatr Res. 2009 May. 65(5):569-73. [Medline].

Wali P, King J, He Z, Tonb D, Horvath K. Ghrelin and obestatin levels in children with failure to thrive and obesity. J Pediatr Gastroenterol Nutr. 2014 Mar. 58(3):376-81. [Medline].

Velasco P, Clemente M, Lorite R, et al. The role of leptin in diencephalic syndrome. Pediatrics. 2014 Jan. 133(1):e263-6. [Medline].

Järvinen KM, Nowak-Wegrzyn A. Food protein-induced enterocolitis syndrome (FPIES): current management strategies and review of the literature. J Allergy Clin Immunol Pract. 2013 Jul-Aug. 1(4):317-22. [Medline].

Puls HT, Hall M, Bettenhausen J, Johnson MB, Peacock C, Raphael JL, et al. Failure to Thrive Hospitalizations and Risk Factors for Readmission to Children’s Hospitals. Hosp Pediatr. 2016 Aug. 6 (8):468-75. [Medline].

Wright CM, Garcia AL. Child undernutrition in affluent societies: what are we talking about?. Proc Nutr Soc. 2012 Nov. 71(4):545-55. [Medline].

Mash C, Frazier T, Nowacki A, Worley S, Goldfarb J. Development of a risk-stratification tool for medical child abuse in failure to thrive. Pediatrics. 2011 Dec. 128(6):e1467-73. [Medline].

Sills RH. Failure to thrive. The role of clinical and laboratory evaluation. Am J Dis Child. 1978 Oct. 132(10):967-9. [Medline].

Larson-Nath CM, Goday PS. Failure to Thrive: A Prospective Study in a Pediatric Gastroenterology Clinic. J Pediatr Gastroenterol Nutr. 2016 Jun. 62 (6):907-13. [Medline].

Sheiko MA, Feinstein JA, Capocelli KE, Kramer RE. Diagnostic yield of EGD in children: a retrospective single-center study of 1000 cases. Gastrointest Endosc. 2013 Jul. 78(1):47-54.e1. [Medline].

Thompson RT, Bennett WE Jr, Finnell SM, Downs SM, Carroll AE. Increased length of stay and costs associated with weekend admissions for failure to thrive. Pediatrics. 2013 Mar. 131(3):e805-10. [Medline].

Hyman P. Role of Development in Infant and Toddler Food Refusal. SIG 13 Perspectives on Swallowing and Swallowing Disorders (Dysphagia). October 2010. 19:64-67.

Arvedson J, Brodsky L. Pediatric Swallowing and Feeding , Assessment and Management. Second Edition. Singular Publishing Co.; 2002.

American Speech-Language-Hearing Association. Roles of speech-language pathologists in swallowing and feeding disorders: Position statement. 2002. ASHA Supplement 22:73.

Williams KE, Field DG, Seiverling L. Food refusal in children: a review of the literature. Res Dev Disabil. 2010 May-Jun. 31 (3):625-33. [Medline].

Piazza CC, Carroll-Hernandez TA. Assessment and Treatment of Pediatric Feeding Disorders. Encyclopedia on Early Childhood Development. March 11, 2004. 1-7. [Full Text].

Addison LR, Piazza CC, Patel MR, Bachmeyer MH, Rivas KM, Milnes SM, et al. A comparison of sensory integrative and behavioral therapies as treatment for pediatric feeding disorders. J Appl Behav Anal. 2012 Fall. 45 (3):455-71. [Medline].

Seiverling L, Kokitus A, Williams K. A clinical demonstration of a treatment package for food selectivity. The Behavior Analyst Today. 2012. 13(2):11-16.

Seiverling L, Harclerode W, Williams KE. The Effects of a Modified Treatment Package With and Without Feeder Modeling on One Child’s Acceptance of Novel Foods. Education and Treatment of Children. August 2014. 37(3):477-493.

Williams KE, Seiverling LJ. The assessment and treatment of feeding problems among children with autism spectrum disorders. Patel VB, Preedy VR, Marin CR. Comprehensive Guide to Autism. Springer; 1973-1993.

Black MM, Tilton N, Bento S, Cureton P, Feigelman S. Recovery in Young Children with Weight Faltering: Child and Household Risk Factors. J Pediatr. 2016 Mar. 170:301-6. [Medline].

Bentovim A, Elliott I. Hope for children and families: targeting abusive parenting and the associated impairment of children. J Clin Child Adolesc Psychol. 2014. 43(2):270-85. [Medline].

Maggioni A, Lifshitz F. Nutritional management of failure to thrive. Pediatr Clin North Am. 1995 Aug. 42(4):791-810. [Medline].

Black MM, Dubowitz H, Krishnakumar A, Starr RH Jr. Early intervention and recovery among children with failure to thrive: follow-up at age 8. Pediatrics. 2007 Jul. 120(1):59-69. [Medline].

Black MM, Dubowitz H, Hutcheson J, Berenson-Howard J, Starr RH Jr. A randomized clinical trial of home intervention for children with failure to thrive. Pediatrics. 1995 Jun. 95(6):807-14. [Medline].

Prenatal causes

Prematurity with complications

Maternal malnutrition

Toxic exposure in utero

Alcohol, smoking, medications, infections

IUGR

Chromosomal abnormalities

Postnatal causes

Inadequate intake

Lack of appetite (chronic illness)

Inability to suck or swallow

Vomiting

Therapy used to treat primary illness (eg, chemotherapy)

Developmental delay

GI pain or dysmotility

Poor absorption and/or use of nutrients

Malabsorption

Anatomical GI problems

Pancreatic and cholestatic conditions

Inborn errors of metabolism

Chronic GI infections

Increased metabolic demand

HIV infection

Malignancy

Cardiopulmonary diseases and inflammatory conditions

Renal failure

Hyperthyroidism

Product

Calories

Source

Medium-chain triglyceride (MCT) oil

7.7 kcal/mL

Fractionated coconut oil

Microlipid

4.5 kcal/mL

Safflower oil

Corn oil

8.4 kcal/mL

Corn

ProMod (protein powder)

28 kcal/scoop (4.2 kcal/g)

5 g/scoop

Whey protein with lecithin

Polycose (powder or liquid)

Powder – 23 kcal/tbsp

Liquid – 30 kcal/tbsp

Powder – Hydrolyzed cornstarch

Liquid – Glucose polymers derived from hydrolyzed cornstarch

Rice cereal (powder)

15 kcal/tbsp

Rice flour

Nonfat dry milk powder

15 kcal/T (1.5 g protein)

Cow’s milk

Powder infant formula

40 kcal/tbsp

Cow’s milk

Liquid concentrated infant formula

40 kcal/oz

Cow’s milk

Product, 30 kcal/oz

CHO, g/100 mL

Protein, g/100 mL

Fat, g/100 mL

Osmolality

Nutrient Sources

Nutren Junior

(Clintec)

12.8

3

4.2

350

CHO – Maltodextrin, sucrose

Protein – Casein, whey

Fat – Soy, MCT, and canola oils

(Vanilla, also available with fiber)

Kindercal

(Mead Johnson)

13.5

3.4

4.4

310

CHO – Maltodextrin, sucrose

Protein – Caseinates, milk protein concentrate

Fat – Canola, MCT, and high-oleic sunflower oils

Contains soy fiber 6.3 g/L

(Vanilla)

PediaSure

(Ross)

11

3

5

310

CHO – Corn syrup solids, sucrose

Protein – Caseinate, whey protein concentrate

Fat – High-oleic safflower, soy, and MCT oils

(Vanilla, also available with fiber)

Boost

(Mead Johnson)

17.4

4.3

1.7

590-620

CHO – Sucrose, corn syrup solids

Protein – Milk protein concentrate

Fat – Canola, sunflower, corn oils

(Chocolate, chocolate mocha, strawberry, vanilla)

Simon S Rabinowitz, MD, PhD, FAAP Professor of Clinical Pediatrics, Vice Chairman, Clinical Practice Development, Pediatric Gastroenterology, Hepatology, and Nutrition, State University of New York Downstate College of Medicine, The Children’s Hospital at Downstate

Simon S Rabinowitz, MD, PhD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Gastroenterology, American Gastroenterological Association, American Medical Association, New York Academy of Sciences, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Genie Rogers, MA, CCC-SLP, BRS-S Speech-Language Pathologist, Infant and Child Learning Center, Neonatal Intensive Care Unit, Downstate University Hospital; Clinical Supervisor, Speech Therapy Services, Step by Step Infant Development Program

Genie Rogers, MA, CCC-SLP, BRS-S is a member of the following medical societies: American Speech-Language-Hearing Association

Disclosure: Nothing to disclose.

Navneetha Unnikrishnan, MBBS Resident Physician, Department of Pediatrics, State University of New York Downstate College of Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jatinder Bhatia, MBBS, FAAP Professor of Pediatrics, Medical College of Georgia, Georgia Regents University; Chief, Division of Neonatology, Director, Fellowship Program in Neonatal-Perinatal Medicine, Director, Transport/ECMO/Nutrition, Vice Chair, Clinical Research, Department of Pediatrics, Children’s Hospital of Georgia

Jatinder Bhatia, MBBS, FAAP is a member of the following medical societies: Academy of Nutrition and Dietetics, American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Society for Nutrition, American Society for Parenteral and Enteral Nutrition, Society for Pediatric Research, Southern Society for Pediatric Research

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Nestle<br/>Serve(d) as a speaker or a member of a speakers bureau for: Nestle<br/>Received income in an amount equal to or greater than $250 from: Nestle.

Jatinder Bhatia, MBBS, FAAP Professor of Pediatrics, Medical College of Georgia, Georgia Regents University; Chief, Division of Neonatology, Director, Fellowship Program in Neonatal-Perinatal Medicine, Director, Transport/ECMO/Nutrition, Vice Chair, Clinical Research, Department of Pediatrics, Children’s Hospital of Georgia

Jatinder Bhatia, MBBS, FAAP is a member of the following medical societies: Academy of Nutrition and Dietetics, American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Society for Nutrition, American Society for Parenteral and Enteral Nutrition, Society for Pediatric Research, Southern Society for Pediatric Research

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Nestle<br/>Serve(d) as a speaker or a member of a speakers bureau for: Nestle<br/>Received income in an amount equal to or greater than $250 from: Nestle.

Maria Rebello Mascarenhas, MBBS Professor of Pediatrics, Perelman School of Medicine at the University of Pennsylvania; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support Service, Medical Director, Integrative Health Program, Children’s Hospital of Philadelphia

Maria Rebello Mascarenhas, MBBS is a member of the following medical societies: American Society for Parenteral and Enteral Nutrition, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition

Disclosure: Received research grant from: Kabi Fesinius<br/>Faculty member, DIGEST and member DSMB for: Cystic Fibrosis Foundation.

Rita Alvarez, MD Resident Physician, Department of Pediatrics, State University of New York Downstate Medical Center, Brooklyn

Rita Alvarez, MD is a member of the following medical societies: American Medical Student Association/Foundation

Disclosure: Nothing to disclose.

Reda W Bassali, MBChB Associate Professor, Departments of General Pediatrics and Adolescent Medicine, Medical College of Georgia

Reda W Bassali is a member of the following medical societies: Ambulatory Pediatric Association and American Academy of Pediatrics

Disclosure: Nothing to disclose.

John Benjamin, MD Chief, General Section of Pediatrics and Adolescent Medicine, Vice Chair for Clinical Activities, Professor, Department of General Pediatrics, Medical College of Georgia

Disclosure: Nothing to disclose.

Mohammad F El-Baba, MD Associate Professor of Pediatrics, Division of Pediatric Gastroenterology, Wayne State University School of Medicine; Divison Chief of Pediatric Gastroenterology, Children’s Hospital of Michigan

Mohammad F El-Baba, MD is a member of the following medical societies: American Gastroenterological Assocation and North American Society for Pediatric Gastroenterology and Nutrition

Disclosure: Nothing to disclose.

Madhavi Katturupalli, MD Resident Physician, Department of Pediatrics, New York Medical College, Richmond University Medical Center

Madhavi Katturupalli, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Ruby Mehta, MD Fellow, Division of Pediatric Gastroenterology, Children’s Hospital of Michigan

Disclosure: Nothing to disclose.

Nutritional Considerations in Failure to Thrive

Research & References of Nutritional Considerations in Failure to Thrive|A&C Accounting And Tax Services
Source