Failure To ThriveFTT

Michal Kori M.D.

Pediatric Gastroenterology

Failure to thrive (FTT) is a sign that describes a particular problem rather than a diagnosis.

The term FTT is used to describe instances of growth failure or, more specifically, failure to gain weight appropriately.

In more severe cases, linear growth and head circumference also may be affected.

Definition There is no consensus regarding the definition

of failure to thrive. FTT may be attributed to a child with any of the

following: Weight <2nd percentile for age and sex on more than

one occasion Weight <80 percent of ideal body weight for age and

sex Weight that is depressed in proportion to height A weight trajectory that crosses two or more major

percentile lines over time A rate of daily weight gain less than expected for age

Daily weight gain expected for age

26 to 31 g/day for those 0 to 3 months 17 to 18 g/day for those 3 to 6 months 12 to 13 g/day for those 6 to 9 months 9 to 13 g/day for those 9 to 12 months 7 to 9 g/day for those 1 to 3 years

Expected changes in weight and length

Age months

Weight gr/day

Weight gr/month

Length cm/month

0-3 25-30 600-1000 2.7 3-6 20 600 2.1 6-9 15 450 1.5 9-12 10 300 1.2 12-18 8 240 1.2 18-24 6 180 1.0

Infants and young children with genetic short stature, constitutional growth delay, prematurity, or intrauterine growth restriction (IUGR) who have appropriate weight for length and normal growth velocity are not considered to have FTT.

Measurement and growth Accurate assessment of the child's weight,

length, and head circumference is essential. In the child < 2 years, the recumbent length,

should be obtained. Height (length), weight, weight for length, and

head circumference, should be plotted on a standardized growth chart.

Two growth charts are available; World Health Organization (WHO) growth charts (CDC/NCHS) Centers for Disease Control and

Prevention and National Center for Health Statistics growth charts

Growth trajectory The growth trajectory is assessed by plotting the

child's growth parameters at various ages on a growth chart standardized for sex, age, and medical condition (eg, Down syndrome).

Special attention should be paid to the timing of changes in the slopes of the weight, length, or head circumference trajectories. What happened at that point in the child's life:

initiation of complementary foods? Onset of diarrhea? Parental stressor

Normal growth parameters at birth deceleration in weight, followed by deceleration in stature z"stunting", and finally deceleration in head circumference is characteristic of inadequate nutritional intake. As stunting develops, the weight for length may return toward normal.

Normal growth parameters at birth with simultaneous deceleration in length and weight before two years of age and normal growth velocity after two years of age is suggestive of genetic short stature or constitutional growth delay. These normal growth patterns are often confused with FTT.

Deceleration of head circumference before deceleration in weight or length is suggestive of a neurologic disorder

Proportionality

Decreased weight in proportion to length ("wasting") reflects inadequate nutritional intake.

Decreased length in proportion to weight is suggestive of an endocrinologic abnormality.

Decreased length with a proportionate weight may be nutritional (if long-standing), genetic, or endocrine in origin.

When head circumference is impaired as much as, or more than, weight or length, intrauterine infection, teratogenic exposures, congenital syndromes, and other causes of microcephaly should be considered.

Risk factors for FTT Medical risk factors

Prematurity, (particularly when associated with IUGR) Developmental delay, Congenital anomalies (eg, cleft lip and/or palate), Intrauterine exposures (eg, alcohol, anticonvulsants, infection) Any medical condition that results in inadequate intake,

increased metabolic rate, maldigestion or malabsorption Psychosocial risk factors

Poverty, Certain health and nutrition beliefs, disordered feeding

techniques Social isolation Life stresses Poor parenting skills Substance abuse Psychopathology, violence, and abuse

Etiology- three major catagories

Inadequate dietary energy intake, Inadequate nutrient absorption, Increased energy requirements

The majority of cases in primary care practice are secondary to inadequate dietary energy intake, usually related to psychosocial factors or disturbance in feeding behavior.

Traditional classification of FTT

FTT

Organic Mixed Non- organic

Nutritional deprivation in infancy may be related to severe, irreversible developmental deficits and behavior problems.

The goal of the evaluation of a child with FTT is to identify the potential contributing factors so that each one may be addressed systematically.

The involvement of a dietitian, occupational or speech therapist, social worker, and/or developmental and behavioral pediatrician can be helpful in gathering this information and formulating a management plan.

Evaluation

Medical history Physical examination Social status and problems Nutritional evaluation Developmental evaluation

Medical History (1)

Perinatal- pregnancy, drugs, alcohol etc. Birth weight- LGA, SGA (IUGR,

symetrical, asymetrical), prematurity Postnatal problems- asphyxia, NEC, BPD Prior medical problems- infections,

hospitalizations, Family history of disease, FTT, weight and

height of parents and siblings.

Medical History (2)

Detailed information regarding nutritional intake and feeding should be obtained, including information related to the duration of mealtimes, the type of food, and the quantity of food consumed breast feeding / formula, amounts, preparation,

introduction of new foods (when?), mother child interaction during feeding, fatigue, crying etc.

Stools- number per day, consistency Vomiting

The psychosocial history should include an assessment of psychosocial stressors and family strengths and resources.

Children with FTT should undergo formal developmental and behavioral testing.

Historical clues to potential organic causes of failure to thrive

Diarrhea

Chronic constipation Recent travel to developing

country, camping, housing in shelter, day care

Chronic otitis media

Snoring or mouth breathing History of wheezing

Vomiting or spitting up

Gagging, tactile hypersensitivity, prolonged feeding time

Polyuria, polydipsia, polyphagia Frequent infections

Malabsorption -celiac disease, cystic fibrosis, lactase deficiency)

May cause decreased appetite Infectious diarrhea (eg, giardiasis,

nematodes, enteric pathogens)

Immune deficiency; structural abnormality that impairs intake

Adenoidal hypertrophy Mechanical obstruction, chronic

pulmonary disease Gastroesophageal reflux, delayed

gastric emptying, intestinal obstruction Oral motor dysfunction

Diabetes Immune deficiency

Physical Examination

Observation- general appearance, signs of neglect, hygiene

Malnutrition- decreased subcutaneous fat bony prominence, protuberant abdomen, flat buttocks, muscle wasting, poor tone.

Full physical exam Anthropometric measurements

Laboratory evaluation

Laboratory evaluation for organic disease should be guided by the signs and symptoms found in the initial evaluation.

Basic routine testing;CBCUrine analysisSMA (albumin)Liver function

More detailed testing

Cholesterol +TG Blood Gases Immunoglobulins HIV TSH, T4 Fe, ferritin Folic acid, B12

Zn Stool culture and

parasites xylose Celiac screen Sweat test GH studies

Therapy

Therapy is directed at the major medical problem: malnutrition and its complication.

Nutritional assessment, current daily intake, prescribe 1.5-2 RDA calories and protein to allow “ catch-up” growth, add iron and vitamins when needed.

Close follow-up. Attention to social problems.

Maldigestion and Malabsorption

Maldigestion and Malabsorption

Characterized clinically by by chronic diarrhea, distended abdomen and FTT

The stages of digestion and absorption Luminal hydrolysis and solubilization of

carbohydrates, fat and proteins by enzymes secreted from salivary glands, the gastric mucosa and the pancreas

Hydrolysis at the enterocyte membrane (of peptides and disaccarides by border enzymes)

Absorption across the enterocyte membrane and cellular processing

Uptake from the enterocyte into the blood and lymph

CarbohydratesIntraluminal digestion

Carbohydrates that undergo intraluminal digestion :Starch (50-60%) -amylose, amylopectin

(both are high MW polymers of glucose) they are broken down by amylase (saliva, gastric, pancreatic) to maltose, maltriose, and branched alpha limit dextrins.

Sucrose (30-40%) Lactose (40-50%- infants, 0-20% adults)

Brush border disacharridases

Glucoamylase- Breaks down 20-25% of maltose to free glucose. Releases free glucose from gl-polymers.

Sucrose-isomaltose 1. Splits 100% of sucrose to gl + fructose 2. Splits 75-80% of maltose in to free gl.

Lactase -phlorizine - splits lactose into glucose + galactose.

Absorption across the enterocytecarrier molecules

Glucose-galactose -Na dependent by an electromechanical gradient which is maintained by an Na-K ATPase on the basolateral membrane.

Fructose Carrier - non Na dependent

Carbohydrate Malabsorption

Fermentative diarrhea Distended abdomen Acidic stools- pH 4.0-5.5 Unabsorbed reducing substances in the

stool

ProteinsIntraluminal digestion Starts in the stomach with denaturation of

protein by gastric acid. Pepsinogen I and II become activated. In the duodenum: enterokinase activates

trypsinogen into trypsin which activates zymogens in to active proteases.

ProteinsIntraluminal digestion (cont.) Endopeptidases

trypsin- amino basic acidschemotrypsin- aromatic a.a.elastase- charged small a.a.

Exopeptidases - frees terminal a.a. Carboxypeptidase A- aromatic, neutral,

acid Carboxypeptidase B- basic

Hydrolysis at enteroctye membraneand absorption

There are at least 8 brush border peptidases Most amino acids are absorbed as dipeptides

and tripeptides. There are at least 4 amino acid transport

systems which are all active- Na dependent. No specific defect of peptide digestion and

absorption by intestinal mucosa is known. There are specific defects that are diagnosed

due to aminoaciduria.

FatIntraluminal digestion Starts in the stomach with fundic lipase

(pH- 3.5-5.5) In the duodenum:

1. Pancreatic enzymes- lipase, co-lipase 2. Bile acids (cholic, chenodeoxycholic acid, are synthesized in the liver) (absorbed in the terminal ileum by Na dependent carrier mediated process)

FatMicelle formation and absorption Mixed micelles contain FFA,

monoglycerides diglycerides, cholesterol esters, fat soluble vitamins.

Micelles diffuse into the enterocyte. In the cell FFA bind to carrier proteins FABP in the endoplasmic reticulem.

Long chain FA are activated by acyle CoA to monoglycerides

FatCellular processing MTP- Microsomal TG Transfer Protein,

passes resynthesized TG from the ER to the golgi adding PL, Cholesterol and apo-proteins (B48).

In the golgi cylomicrones are formed and are secreted from the cell by exocytosis to the lymphatic system.