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Malnutrition = imbalance between energyintake and energy expenditure
Under nutrition:
Protein energy
malnutrition / PEM Micro-nutrient deficiency /
hidden hunger
Over nutrition:
obesity
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EXCESS NUTRITION(Energy, fat, cholesterol, carbohydrate, salt, vitamins)
NORMAL NUTRITION
DEFICIENCYPRIMARY(Lack of food, poverty,
ignorance, refusal totake food, fad diet,alcoholism,drug addiction,loneliness etc)
SECONDARY(Malabsorption,
defective metabolism,increased destruction,increased excretion)
TISSUE DEPLETION
BIOCHEMICAL LESION
CLINICAL SIGNS
Blood and urinestudies: reducednutrient levels,abnormal metabolites,enzyme changes)
(Robinson & Weigley, 1984)
Pathophysiology of malnutrition
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Classification of PEM
Based on the severity of deficiency:
Mild
Moderate .. no specific clinical sign Severe PEM:
Kwashiorkor
Marasmus
Marasmic-Kwashiorkor
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Characteristics of
Kwashiorkor and MarasmusKwashiorkor
Age usually over 18 months
Lacks protein-rich foods and othernutrients
Relatively more often in tropicalcountries
wet malnutrition
Any edema means severemalnutrition, child is not fat
Swollen belly from fatty liver, edemaand/or parasites
Marasmus
Usually under 1 year old
Lacks energy-rich foods andother nutrients
Often in dry climate/disaster/war
dry malnutrition
Classified as severe malnutrition
May be swollen belly fromparasites or weak muscle
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Clinical manifestation of Kwashiorkor
Mental changes: irritable,apathies
Flag sign
Moon face
Liver enlargement (fatty liver)
Crazy pavement dermatosis
Potbelly (swollen abdomen)
Edema
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Clinical manifestation of Marasmus
Loss of subcutaneous fat and
muscle wasting
Old man face / monkey face
Piano ribs
Baggy pant
Hungry
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Edema in kwashiorkor
Pitting edema
Pathophysiology:
Low protein intake
hypoalbuminemialow
plasma oncotic pressure
fluids extravasations to
interstitial tissue
Edema most commonly
occurs in the feet
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Diagnosis
Based on:
Clinical:
Anamnesis
Physical examination
Anthropometry
Laboratory
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Clinical
Anamnesis:
Dietary history
A detail dietary history mustbe taken
Quality and quantity of foodingested must be assessed
Medical history
Antenatal and perinatalhistory
Family history of atopic
Previous illness andhospitalization
Physical exam
Symptoms and signs ofkwashiorkor and marasmus
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Anthropometry
Commonly use: body weight and body height
Indicator:
Weight for age (W/A) Height for age (H/A)
Weight for height (W/H)
For adolescent (10-18 years) and adult:
Body mass index (BMI): weight (kg) / height (m) square Criteria for severe malnutrition:
Adolescent: BMI for age less than 5thpercentile
Adult: BMI less than 16
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Criteria of diagnosis
Clinical Anthropometry Diagnosis
With edema W/H between -3SD
and -2SD
Kwashiorkor
With edema W/H < -3SD Marasmic-Kwashiorkor
Without edema W/H < -3SD Marasmus
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WHO growth standardchart
For example:
Boy, BW 7 kg,
H 75 cm
anthro < -3SD
Clinical sign
without
edema
Diagnosis
marasmus
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WHO growth standardtable
Boy, 7 kg
and 75 cm
Anthro < -
3SD
Clinical
sign with
edema
Diagnosis:marasmic-
kwashiork
or
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Laboratory
Blood analysis:
white blood cell, electrolytes, sugar,plasma protein
Urine analysis:
culture, ketone
Stool analysis:
for parasites
X-rayfor chest and heart
Tuberculintest for TB
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Management
general principles (ten steps)1. Treat/prevent hypoglycemia
2. Treat/prevent hypothermia
3. Treat/prevent dehydration
4. Correct electrolyte
imbalance
5. Treat/prevent infection
6. Correct micronutrient
deficiencies
7. Start cautious feeding
8. Achieve catch-up growth
9. Provide sensory stimulation
and emotional support
10. Prepare for follow-up after
recovery
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Initial treatment
Hypoglycemia
Blood glucose < 3 mmol/L or 5g/kg of body weight/d x 3 days
Most important determinant of recovery:
Amount of energy consumed: calories, protein,
micronutrients (K, Mg, I, Zn)
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Rehabilitation
Parental teaching
Correct feeding/food preparation practices
Stimulation, play, hygiene Treatment diarrhea, infections
When to seek medical care
Preparation for outpatient care
Reintegration into family & community
Prevent malnutrition recurrence
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Criteria for outpatient care
Child
W/H reached -1SD
Eating appropriate amount of diet that mother can prepare at home
Gaining weight at normal rate
Vitamin & mineral deficiency treated/corrected Infections treated
Full immunizations
Mother
Able & willing to care for child
Knows proper food preparation Knows appropriate toys & play for child
Knows home treatment fever, diarrhea, respiratory tract infection
Health worker
Able to ensure follow up child & support for mother
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Follow up
Child usually remains stunted
Prevention of recurrence severe malnutrition
Follow up: 1,2,4 weeks, then 3 & 6 mos, then 2x/y
W/H no less than -1SD
Assess overall health, feeding, play
Immunizations, treatments, vitamin/minerals
Record progress
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Time frame for management
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Childhood Obesity
I Gusti Lanang SidiarthaSpesialis Anak Konsultan Nutrisi dan Penyakit Metabolik
Bagian Ilmu Kesehatan Anak FK UNUD/RSUP Sanglah
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Definition
Childhood Obesity is a condition where excess body
fat negatively affects a childs health or wellbeing.
Obesity results from excessive caloric intake,decreased energy expenditure and/or from a
combination of the two.
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Criteria for obesity based on BMI (WHO)
BMI (Body Mass Index) = Weight (kg) / Height (m)2
Underweight : < 18.5
Healthy weight : 18.524.9 Overweight (Grade I obesity) : 25.029.9
Obese (Grade II) : 30.039.9
Morbidly obese (Grade III) : 40 or above
Super obese (Grade IV) : > 50
for Adult
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forchildren and adolescence
Percentile of BMI-for-age and
gender
Underweight : < P-5
Healthy weight : P-5P-85
Overweight : P-85P-95
Obese : P-95P-97
Super obese : > P-97
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Classifications
Nutritional:
High
No mental retardation
No dismorphic
Normal bone age
Non-nutritional:
Endocrine: short
Hypothyroidism
Growth hormone deficiency
Genetic:
Prader-Willi
Turner
CNS conditions: hypothalamicdamage
Medications:
Glucocorticoids
Phenothiazine
Lithium, etc.
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Etiology
Heterogeneous and multifactorial
Environmental
Psychosocial
Genetic
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Genetics vs. Environment
Weight of adopted children correlate
better with biological parents
BMI of identical twins reared apart =together
Monozygotic twins more similar in fat
deposition and weight than dizygotic
twins.
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Environmental factors: Increased energy input
High caloric-density food
Supersized portions
Eating out
Working parents
Advertising
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Environmental factors: decreased energyexpenditure
TV: prevalence of obesity increases
2%/hour of viewing
Computers
Transportation
Inadequate safe areas for physical
activity
Sedentary lifestyle
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Complications
Diabetes type 2
Hypertension and heart
disease
Neurologic complications
Respiratory disease
Orthopedic condition
Psychosocial disorders
Hyperlipidemia
GI manifestations
Menstrual disorders
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Metabolic syndrome
Clustering of CV risk factors
related to insulin resistance
Including: Insulin resistance
Dyslipidemia
Hypertension
Obesity
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Obesity: respiratory diseases
Causes both restrictive and
obstructive disease
Sleep apnea 7-33%
Asthma ~ 30%
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Obesity: GI manifestations
Steatohepatitis
Fatty infiltration of the liver
Abnormal insulin metabolism
10% obese teens increased LFT
Can progress to fibrosis and cirrhosis
Gall bladder disease
Increased cholesterol excretion ~30% of gallstones in children
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Obesity: orthopedic conditions
Genu varum/valgus deformities
Blount disease
Bowing of legs
Tibial torsion
50-80% obese
Slipped capital femoral epiphysis (SCFE)
Femoral epiphysis slips off of metaphysis
60% obese
Associated with hypothyroidism,
hypogonadism & GH deficiency
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Neurologic complications: Pseudotumor cerebri
Increased ICP
Vomiting, diplopia, blurred vision
30-80% obese
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Obesity: psychological disorders
Difficult to quantitate
Stigmatization
Low self esteem
Depression
Discrimination
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Management
Prevention is the Key and prevention easier than cure
Team work
Individualized goal of weight loss; lifelong weight control
Components:
Education & motivation
Diet modification: decrease energy intake
Increased activity: increase energy expenditure
Parents are role models
Medicines & surgery
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Education
Need to educate family
Parents impose their lifestyle
+ family support improves weight loss
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Dietary therapy
Weight loss determined by # calories consumed
relative to expended
Healthy diet:
55% carbohydrates
30% fat
15% protein
Avoid fad diets
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Dietary therapy
Fat vs Carbs
Carb converted to fat 30% of energy consumed
Little energy used in absorbing fats
Glycemic Index
High carb diets
Leads to increased serum insulin
Promotes excessive food intake
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Physical activity
Physical activity essential for weight loss
Physical activity decreases 50% during adolescence
(girls > boys)
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Pharmacotherapy
Anti-obesity drugs not approved for pediatrics
None of drugs tested for:
Long term use Pediatric age groups
Drug options:
Appetite suppressants
Serotonin agonists
Inhibitors of fat absorption
Anti-hyperglycemic agents
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Bariatric surgery or weight loss surgery
Works in three basic ways:
1. Restricting how much food
the stomach can hold at anytime
2. Preventing the digestive
system from absorbing all
the nutrition in the food
3. Combination of these two
ways
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Surgery indications
BMI greater than 40 (obese
class III)
BMI of 35-40 for people withheart disease, diabetes, high
cholesterol, or obstructive
sleep apnea
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Types of weight loss surgery
Gastric banding and
gastroplasty (stomach
stapling): restrictive or
decrease the stomach sizefrom about six cups to one.
Gastric bypass (Roux-en-Y)
: reduces the size of the
stomach and prevent theabsorption of calories in the
small intestine.
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Risks of bariatric surgery
The risk of dying is less than 1%
Serious complications are rare
The risk including:
Vomiting from eating more than the stomach pouch canhold
The band disintegrating
Band and staples fall apart, reversing the procedure
Stomach contents leaking into the abdomen
Nutritional deficiencies and health problems: reducedabsorption of vitamin B-12, iron, and calcium.
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Thanks for your attention
Any question ?