Macronutrient deficiency, Micronutrient deficiency and Obesity in the Infant and Young Child Karen...

Macronutrient deficiency, Micronutrient deficiency and

Obesity in the Infant and Young Child

Karen Calixto-Mercado, MD

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.

NutritionUndernutrition and

Obesity

Severe Childhood Undernutrition(SCU)

Protein –Energy Malnutrition• Inadequate intakes of 2 nutrients= protein

and energy• Almost always accompanied by deficiencies

of other nutrients

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

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.

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)

World Health Organization: Management of Severe Malnutrition: A Manual for Physicians and Other Senior Health Workers. Geneva, WHO, 1999.

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

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

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.

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

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

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)

Step 7. Begin Cautious Feeding

Step 8. Feed to achieve catch-up growth

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

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)

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

OBESITY

Obesity

• Overweight = Obesity

• Increased prevalence in pediatrics

• Complications: DM, Hypertension, CVD

• Prevention and treatment by pediatrician

Predictors of Childhood Overweight

• High BW (maternal obesity or GDM)

• Low BW

• Parental obesity

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

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

Neuroendocrine feedback

Satiety• CCK• GLP-1• PYY• Vagal efferents• Leptin• adiponectin

Appetite• ghrelin

Hypothalamus

Arcuate nucleus

Brainstem

Solitary tract nucleus

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

Diseases Associated with Childhood Obesity

• Leptin receptor gene mutation

• Prader-Willi Syndrome

• Pro-opiomelanocortin deficiency

• Cushing Syndrome

• Turner Syndrome

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

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

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

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?

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

PE findings in Overweight

• Acanthosis nigricans (insulin resistance)

• Premature adrenarche

• Hirsutism, male pattern baldness, severe acne (polycystic ovary syndrome)

Laboratory Evaluation in Overweight

• Glucose

• Insulin

• Hemoglobin A1c

• AST, ALT

• Total Cholesterol, LDL, HLD, Triglycerides

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

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

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

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.

• 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

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

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

END of Chapter 1