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Macronutrient deficiency, Micronutrient deficiency and
Obesity in the Infant and Young Child
Karen Calixto-Mercado, MD
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Objectives• To discuss Malnutrition in the pediatric age
group, its forms, clinical manifestations and management.
• To discuss Obesity in the infant and child, its causes, diagnosis, clinical manifestations and management.
• To discuss Vitamin deficiency and excess, its causes, clinical presentation and management pertinent to the pediatric population.
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NutritionUndernutrition and
Obesity
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Severe Childhood Undernutrition(SCU)
Protein –Energy Malnutrition• Inadequate intakes of 2 nutrients= protein
and energy• Almost always accompanied by deficiencies
of other nutrients
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Primary Malnutrition• Results from inadequate food intake
Secondary Malnutrition• Results from increased nutrient needs,
decreased nutrient absorption or increased nutrient losses despite adequate dietary intake
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SCU• Underlying causes:
– Social & economic (Poverty & Ignorance)– Social (Food taboos, fad diets)– Biologic (Maternal malnutrition, inadequate intakes)– Environmental (overcrowding, poor sanitation)– Medical: N/PICU, burns, HIV, CF, failure to thrive,
chronic diarrhea syndromes, malignancies, bone marrow transplantation, inborn errors of malnutrition, etc.
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Severe Childhood Undernutrition (SCU)
• Spectrum:– Mild undernutrition (decrease in weight-for-age &/or
length-for-age)– Severe undernutrition (weight-for length)
• Severe forms:– Marasmus (non-edematous SCU with severe wasting)– Kwashiorkor (edematous SCU)– Marasmic-Kwashiorkor (wasting+edema)
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World Health Organization: Management of Severe Malnutrition: A Manual for Physicians and Other Senior Health Workers. Geneva, WHO, 1999.
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Non-edematous SCU (Marasmus): Clinical Manifestations
– Failure to gain weight and irritability Weight loss and listlessness
emaciation- Loss of subcutaneous fat and skin turgor- Loss of fat from sucking pads (wizened look): late sign- Constipated or starvation diarrhea (mucousy, small,
frequent)- Abdomen: distended or flat with visible intestinal pattern- Muscle atrophy hypotonia- Hypothermia- bradycardia
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Edematous SCU (Kwashiorkor): Clinical Manifestations
- Loss of muscle tissue- Edema- vomiting- Diarrhea- Anorexia- Flabby subcutaneous tissues- Increased susceptibility to infections Dermatitis: darkening
of irritated areas not exposed to light- Hair is sparse and thin, streaky red or gray - Lethargy, apathy and/or irritability
lack of growth/ stamina stupor, coma, death
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SCU: TreatmentWorld Health Organization: Management of
Severe Malnutrition: A Manual for Physicians and Other Senior Health Workers. Geneva, WHO, 1999.
Ashworth A, Khanum S et al. Guidelines for the inpatient treatment of severely malnourished children. Geneva, WHO, 2003.
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Step 6. Correct micronutrient deficiencies
• All severely malnourished children have vitamin and mineral deficiencies
• Vit A, Folic acid, zinc, copper, iron, multivits
• do NOT give iron initially for anaemia wait until the child has a good appetite and starts gaining weight (usually by the second week) as giving iron can make infections worse
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Dosage:Daily for at least 2 weeks
• Multivitamin supplement
• Folic acid 1 mg/d (give 5 mg on Day 1)
• Zinc 2 mg/kg/d
• Copper 0.3 mg/kg/d
• Iron 3 mg/kg/d but only when gaining weight
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Vitamin A
Oral dose to be given on Day 1
• for age >12 months, 200,000 IU
• for age 6-12 months, 100,000 IU
• for age 0-5 months, 50,000 IU (unless there is definite evidence that a dose has been given in the last month)
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Step 7. Begin Cautious Feeding
Step 8. Feed to achieve catch-up growth
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Refeeding Syndrome
• Occurs in undernourished children • During 1st week when refeeding is started• Severe hypophosphatemia ( 0.5 mmol/L)
from massive cellular uptake of phosphate • Weakness, rhabdomyolysis, neutrophil
dysfunction, cardiorespiratory failure, arrhythmias, seizures, altered sensorium or sudden death
• Mx: monitor and supplement
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Step 9. Provide sensory stimulation and emotional support
Provide:• tender loving care• a cheerful, stimulating environment• structured play therapy 15-30 min/d • physical activity as soon as the child is well
enough• maternal involvement when possible (e.g.
comforting, feeding, bathing, play)
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Step 10. Prepare for follow-up after recovery
• A child who is 90% weight-for-length (equivalent to -1SD) can be considered to have recovered.
• The child is still likely to have a low weight-for-age because of stunting.
• Good feeding practices and sensory stimulation should be continued at home. Advise parent or carer to:
• bring child back for regular follow-up checks• ensure booster immunizations are given• ensure vitamin A is given every six months
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OBESITY
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Obesity
• Overweight = Obesity
• Increased prevalence in pediatrics
• Complications: DM, Hypertension, CVD
• Prevention and treatment by pediatrician
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Predictors of Childhood Overweight
• High BW (maternal obesity or GDM)
• Low BW
• Parental obesity
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Pathogenesis of Childhood Overweight
• Dysregulation of caloric intake/ appetite and energy expenditure
• Nature “&” nurture
• “thrifty genotype”: beneficial to prehistoric ancestors, detrimental to present day overabundance
• Environmental changes: advertising, convenience foods, sedentary life
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Pathogenesis of Childhood Overweight
• Short-term control of food intake ~
Long term control of adiposity
• Endogenous weight control mechanism: Satiety: CCK, GLP-1, PYY, vagal
afferentsAppetite: ghrelin
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Neuroendocrine feedback
Satiety• CCK• GLP-1• PYY• Vagal efferents• Leptin• adiponectin
Appetite• ghrelin
Hypothalamus
Arcuate nucleus
Brainstem
Solitary tract nucleus
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Obesity Genes
• > 600 genes, markers, chromosomal regions in humans
• Identical Twin studies: genes play a more important role in weight regulation than environmental factors
• <5% of cases of childhood obesity are associated with syndromes, genetic abnormality
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Diseases Associated with Childhood Obesity
• Leptin receptor gene mutation
• Prader-Willi Syndrome
• Pro-opiomelanocortin deficiency
• Cushing Syndrome
• Turner Syndrome
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Diagnostic Criteria for Overweight
• BMI: most reliable
• Kg/m2
• Overestimates adiposity in athletes, “maskulado”
• US, CT, MRI, DEXA, total body conductivity, air displacement plethysmography , skin fold thickness, waist-hip ratio, bioelectric impedance analysis
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Table 1: The International Classification of adult underweight, overweight and obesity according to BMI
Classification of BMI(kg/m2)
Principal cut-off points
Additional cut-off points
Underweight <18.50 <18.50
Severe thinness <16.00 <16.00
Moderate thinness 16.00 - 16.99 16.00 - 16.99
Mild thinness 17.00 - 18.49 17.00 - 18.49
Normal range 18.50 - 24.99 18.50 - 22.99
23.00 - 24.99
Overweight ≥25.00 ≥25.00
Pre-obese 25.00 - 29.99 25.00 - 27.49
27.50 - 29.99
Obese ≥30.00 ≥30.00
Obese class I 30.00 - 34.99 30.00 - 32.49
32.50 - 34.99
Obese class II 35.00 - 39.99 35.00 - 37.49
37.50 - 39.99
Obese class III ≥40.00 ≥40.00Source: Adapted from WHO, 1995, WHO, 2000 and WHO 2004.
ADULTS
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Underweight < 5th Normal Weight 5th- 84thAt risk for overweight 85th- 94thOverweight >/= 95th
Body Mass Classification of Children and Adolescents
Weight Status BMI percentile for Age
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Evaluation of the Overweight Child
• Can certain aspects in the family structure, habits and practices be altered?
• Is obesity primary or secondary?
• Are there current co-morbidities?
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Comorbidities of Overweight
• Cardiovascular disease• hypercholesterolemia• Hypertriglyceridemia• Hypertension• Insulin resistance• Type 2 Diabetes• Metabolic syndrome • Blount disease, slipped capital femoral epiphysis• Obstructive sleep apnea• NAFLD• Focal segmental glomerulosclerosis
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PE findings in Overweight
• Acanthosis nigricans (insulin resistance)
• Premature adrenarche
• Hirsutism, male pattern baldness, severe acne (polycystic ovary syndrome)
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Laboratory Evaluation in Overweight
• Glucose
• Insulin
• Hemoglobin A1c
• AST, ALT
• Total Cholesterol, LDL, HLD, Triglycerides
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Treatment of Overweight, Obesity
• Goal: weight maintenance vs weight loss
• Skeletally mature child, severe complications 1lb or ).5kg/ week, 10% weight loss maintained for 6 mos
• Lifestyle s: diet, exercise, behaviour
• Medication
• Surgery
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Management of Obesity
• Multidisciplinary vs clinic-based Mgt: MD, psychologist, dietitian, exercise specialist, nurse, counsellors
• Yearly BMI• Identify high-risk behaviours and problem-areas in family
dynamics and diet• Age-specific, Family-based behavioral tx• Methods: positive reinforcement, changes in home
environment, self-monitoring, goal-setting, contracting, parenting skills training
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Dietary Counselling
• Age-specific• 1-6 y/o: 4-6oz fruit juice/day• 7-18 y/o: 8-12oz• >2y/o shift to skim kilk• >10 repeated food exposure before a child
accepts new food as “regular”• Avoid skipping meals, sweet beverages, fad
diets, fast food • Low glycemic index foods: non-starchy
vegetables and whole grains
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Benton D. Role of parents in the determination of the food preferences of children and the development of Obesity. International Journal of Obesity (2004) 28, 858–869.
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• Green:
fruits and vegetables
Lo calorie, hi fiber,
nutrient-dense• Yellow:
lean meats, dairy,
starches, grains
Hi calorie, nutrient-
dense• Red: fatty meats,
sugar, fried foods
Hi-calorie, sugar & fat
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Medications
• Sibutramine: norepinephrine &serotonin uptake inhibitor
• Orlistat: Intestinal lipase inhibitor
• Topiramate: anti-epileptic, anorectic S/E
• Metformin
• Octreotide: hypothalamic obesity
* Need for clinical trials in pediatrics
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Bariatric Surgery
• BMI>40 + medical complication + failure of 6 mo multidisciplinary program
• Roux-en-Y gastric bypass, adjustable gastric band
• Mandatory change in lifestyle and eating habits
• Iron, folate, Vit B12, Thiamine, Vit D & Ca Deficiency => Wernicke’s encephalopathy, dry beriberi
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END of Chapter 1
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