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Failure To Thrive FTT Michal Kori M.D. Pediatric Gastroenterology.

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Presentation on theme: "Failure To Thrive FTT Michal Kori M.D. Pediatric Gastroenterology."— Presentation transcript:

1 Failure To Thrive FTT Michal Kori M.D. Pediatric Gastroenterology

2 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.

3 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

4 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

5 Expected changes in weight and length

6 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.

7 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

8 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

9 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

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11 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.

12 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

13 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.

14 Traditional classification of FTT

15 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.

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

17 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.

18 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

19 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.

20 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

21 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

22 Laboratory evaluation Laboratory evaluation for organic disease should be guided by the signs and symptoms found in the initial evaluation. Basic routine testing;  CBC  Urine analysis  SMA (albumin)  Liver function

23 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

24 Therapy Therapy is directed at the major medical problem: malnutrition and its complication. Nutritional assessment, current daily intake, prescribe RDA calories and protein to allow “ catch-up” growth, add iron and vitamins when needed. Close follow-up. Attention to social problems.

25 Maldigestion and Malabsorption

26 Characterized clinically by by chronic diarrhea, distended abdomen and FTT

27 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

28 Carbohydrates Intraluminal 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)

29 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.

30 Absorption across the enterocyte carrier 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

31 Carbohydrate Malabsorption Fermentative diarrhea Distended abdomen Acidic stools- pH Unabsorbed reducing substances in the stool

32 Proteins Intraluminal 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.

33 Proteins Intraluminal digestion (cont.) Endopeptidases  trypsin- amino basic acids  chemotrypsin- aromatic a.a.  elastase- charged small a.a. Exopeptidases - frees terminal a.a. Carboxypeptidase A- aromatic, neutral, acid Carboxypeptidase B- basic

34 Hydrolysis at enteroctye membrane and 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.

35 Fat Intraluminal digestion Starts in the stomach with fundic lipase (pH ) 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)

36 Fat Micelle 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

37 Fat Cellular 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.

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