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MALNUTRITION – Dra. Garcia’s Lecture HEIGHT FOR AGE

DEFINITION OF MALNUTRITION
 Malnutrition encompasses both ends of the
nutrition spectrum, from undernutrition
(underweight, stunting, wasting
micronutrient deficiencies) to overweight.
 Useful for assessing the nutritional status of
populations
 This measure of skeletal growth reflects the
cumulative impact of events affecting
and nutritional status that result in stunting.
 Index of chronic malnutrition.

DIFFERENT CRITERIA USED IN DEFINING WEIGHT FOR AGE or WASTING

MALNUTRITION:
1. GOMEZ – weight below % median weight for
age (WFA)
 Mild (grade 1) 75%-90% weight for
age
 Moderate (grade 2) 60%-74% weight
for age
 Severe (grade 3) <60% weight for age
2. WATERLOW – z scores (SD) below median
weight for height (WFH)
 Mild 80%-90% WFH
 Moderate 70%-80% WFH
 Severe <70% WFH
3. WHO (Wasting) – z scores (SD) below median
weight for height (WFH)
 Moderate -3 z score < -2
 Severe z score < -3
4. WHO (Stunting) – z scores (SD) below median
height for age (HFA)
 Moderate -3 z score <-2
 Severe z score <-3
5. KANAWATI – Middle upper arm
circumference (MUAC) divided
occipitofrontal head circumference.
 Mild < 0.31
 Moderate <0.28
 Severe <0.25
6. COLE – z scores of BMI for age
 Grade 1 z score <-1
 Grade 2 z score <-2
 Grade 3 z score <-3
*** The z-score system expresses the anthropometric
value as a number of standard deviation or z-scores
below or above the reference mean or median value.
Z SCORE
 Defined as the child’s height (weight) minus
the median height (weight) for the age and
sex of the child divided by the relevant
standard deviation.
( ) ( )

( )
 Is a measure of Acute Malnutrition
MID-UPPER ARM CIRCUMFERENCE (MUAC)
 Is often used for screening in lieu of weight
for height.
 During 1-5 years of age it remains reasonably
static between 15-17cms among healthy
children.
 It is conventionally measured over the left
upper arm, at a point marked midway
between acromion (shoulder) and olecranon
(elbow) with arm bent at right angle.
 The child is asked to stand or sit with the arm
hanging loose at the side.
 MUAC is measured with a fiber glass or steel
tape.
 If it is less than 12.5 cm it is suggestive of
severe malnutrition.
 If it is between 12.5-13.5 cm it is indicative of
moderate malnutrition.
BODY MASS INDEX (BMI)
by  BMI is calculated by dividing weight in
kilograms by the square of height in meters
OR
 Weight(kg) /stature(cm) x 10,000
OR
 Weight(lbs) / Stature (in.) x 703
BMI INTERPRETATION
 BMI below 18.5 – chronically energy deficient
 BMI greater than 25 – overweight
 BMI greater than 30 – Obese
MICRONUTRIENT DEFICIENCY:
1. IODINE DEFICIENCY
 Sequelae
i. Goiter
ii. Hypothyroidism
iii. Developmental disabilities
including severe mental
retardation
 Assessment:

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i. By clinical inspection of  Promoting key hygiene behaviour (e.g.

enlarged thyroids (goiter) Handwashing with soap)
ii. By testing iodine  Providing micronutrient interventions such as
concentrations in urine vitamin A and iron supplements for pregnant
(µg/L) and lactating women and young children.
 Sequelae  Presumptive treatment for malaria for
i. Poor mental and physical pregnant women in endemic malarial regions
development among and promoting long-lasting insecticide treated
children bed nets.
ii. Fetal losses  Deworming in endemic parasitic areas and
2. VITAMIN A DEFICIENCY oral rehydration in high-diarrhea regions.
 Is caused by low intake of retinol or  Fortifying commonly eaten food with
its precursor, beta-carotene. micronutrients (such as salt fortified with
 Absorption can be inhibited by a lack iodine) and staple food like wheat, oil and
of fats in the diet or by parasite sugar with iron, vitamin A and zinc.
infestations.
 Clinical deficiency – is estimated by INTERVENTIONS WITH SUFFICIENT EVIDENCE TO
combining night blindness and eye IMPLEMENT IN ALL COUNTRIES
changes – principally Bitot spots and
total xerophthalmia prevalence. Maternal and Birth Outcomes
 Subclinical deficiency – is assessed as  Iron folate supplementation
prevalence of serum retinal  Maternal supplements of multiple
concentrations <0.70 µmol/L micronutrients.
3. ANEMIA  Maternal iodine through iodization of salt.
 Low iron intakes  Maternal calcium supplementation.
 Poor absorption  Interventions to reduce tobacco consumption
 Result of illness or parasite infection or indoor air pollution.
 Severe protein-energy malnutrition Newborn Babies
and vitamin B12 or folate deficiency  Promotion of breastfeeding (individual and
can also lead to anemia. group counselling)
 Cut-offs to define Anemia: Infants and Children
i. 11 g/dL for children 6-59  Promotion of breastfeeding (individual and
mo. group counselling)
ii. 11.5 g/dL for children 5-11  Behaviour change communication for
yr. improved complementary feeding.
iii. 12 g/dL for children 12-14  Zinc supplementation
yr  Zinc in management of diarrhea
iv. 12 g/dL for non-pregnant  Vitamin A fortification or supplementation
women.  Universal salt iodization
v. 11 g/dL for pregnant women  Handwashing or hygiene interventions
vi. 13 g/dL for man  Treatment of severe acute malnutrition.
4. ZINC
 Zinc supplementation can reduce SEVERE ACUTE MALNUTRITION (PROTEIN ENERGY
child mortality, especially when MALNUTRTION)
combined with oral rehydration  Is manifested primarily by inadequate dietary
therapy for diarrheal disease. intakes of protein and energy.
 Either because the dietary intakes of these 2
nutrients are less than required for normal
KEY INTERVENTIONS
growth or because the needs for growth are
 Promoting exclusive breastfeeding. greater than can be supplied by what
 Promoting adequate and timely otherwise would be adequate intakes.
complementary feeding (at ~6 months of age)

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 PEM is almost always accompanied by present in internal organs before it is

deficiencies of other nutrients. recognized in the face and limbs.
 Liver enlargement can occur early or late in
The Most Severe Forms of Malnutrition: the course of disease.
 MARASMUS – non-edematous malnutrition  Dermatitis is common, with darkening of the
with severe wasting. skin in irritated areas (in contrast to pellagra
 KWASHIORKOR – edematous malnutrition. not in areas exposed to light)
 NON-EDEMATOUS MALNUTRITION – result  Depigmentation can occur after
primarily from inadequate energy intake or desquamation in these areas, or it may be
inadequate intakes of both energy and generalized.
protein.  The hair is sparse and thin, and in dark-haired
 EDEMATOUS MALNUTRITION – result children, it can become streaky red or gray.
primarily from inadequate protein intake.  Eventually, there is stupor, coma and death.
 MARASMIC KWASHIORKOR – has features of
both disorder (wasting and edema) COMPARISON OF THE FEATURES OF KWASHIORKOR
AND MARASMUS
CLINICAL MANIFESTATIONS OF SEVERE PROTEIN FEATURE KWASHIORKOR MARASMUS
CALORIE MALNUTRITION Growth Failure Present Present
Wasting Present Present,
Non-edematous Malnutrition (Marasmus) marked
 Failure to gain weight Edema Present Absent
 Irritability (sometimes mild)
 Weight loss Hair Changes Common Less Common
 Listlessness Mental Changes Very Common Uncommon
 Emaciation Dermatosis, Common Does not occur
 Skin loses turgor and becomes wrinkled and Flaky-paint
loose as subcutaneous fat disappears. Appetite Poor Good
 Loss of fat from sucking pads of the cheeks Anemia Severe Present, less
(occurs late in the course of the disease)  (sometimes) severe
eventually becomes shrunken and wizened. Subcutaneous Reduced but Absent
 Infants are often constipated or with Fat present
starvation diarrhea (frequent small stools Face May be Drawn in,
containing mucus) edematous monkey-like
 The abdomen may be distended or flat, with Fatty infiltration Present Absent
the intestinal pattern readily visible. of liver
 There is muscle atrophy and resultant
hypotonia. NOMA
 As condition progresses, the temperature  Is a chronic necrotizing ulceration of the
usually becomes subnormal and the pulse gingival and cheek.
slows.  It is associated with malnutrition and is often
Edematous Malnutrition (Kwashiorkor) preceded by debilitation illness (measles,
 Vague manifestations: lethargy, apathy, malaria, tuberculosis, diarrhea, ulcerative
and/or irritability gingivitis) in a nutritionally compromised host.
 Lack of growth Manifestations:
 Lack of stamina  Fever
 Loss of muscle tissue  Malodorous breath
 Increased susceptibility to infections  Anemia
 Vomiting, diarrhea, anorexia, flabby  Leukocytosis
subcutaneous tissues and edema  Signs of malnutrition
 The edema usually develops early and can  If untreated, it produces severe disfiguration.
mask the failure to gain weight. It is often

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Polymicrobial Infection in NOMA
 Fusobacterium necrophorum
 Prevotella intermedia
Treatment of Noma:
 Local wound care
 Pencillin
 Metronidazole
 Therapy for the underlying predisposing
condition
CLINICAL SIGNS OF MALNUTRITION
 Face
o Moon face (kwashiorkor), simian
facies (marasmus)
 Eye
o Dry eyes, pale conjunctiva, bitot
spots (vitamin A), periorbital edema
 Mouth
o Angular stomatitis, cheilitis, glossitis,
spongy bleeding gums (vitamin C),
parotid enlargement
 Teeth
o Enamel mottling, delayed eruption
 Hair
o Dull, sparse, brittle
hypopigmentation, flag
(alternating bands of light and
normal color), broomstick eyelashes,
alopecia
 Skin
o Loose wrinkled (marasmus), shiny
and edematous (kwashiorkor), dry,
follicular hyperkeratosis, patchy
hyper and hypopigmentation (crazy
paving or flaky paint dermatosis),
erosions, poor wound healing
 Nails
o Koilonychia (spoon nails), thin and
soft nail plates, fissures or ridges
 Musculature
o Muscle wasting particularly buttocks
and thighs, Chvostek and Trosseau
sign (hypocalcemia)
 Skeletal
o Deformities, usually as a result of
calcium, Viatmin D or Vitamin C
deficiencies
 Abdomen
o Distended, hepatomegaly with fatty
liver, ascites may be present
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 Cardiovascular
o Bradycardia, hypotension, reduces
cardiac output, small vessel
vasculopathy
 Neurologic
o Global developmental delay, loss of
knee and ankle reflexes, impaired
memory
 Hematologic
o Pallor, petechiae, bleeding diathesis
 Behaviour
o Lethargic, apathetic, irritable on
handling
PATHOPHYSIOLOGY OF SEVERE PROTEIN CALORIE
MALNUTRITION
Edematous or Non-edematous Malnutrition??
 Variability among infants in nutrient
requirements and in body composition at the
time the dietary deficit is incurred.
 Giving excess carbohydrate to a child with
non-edematous malnutrition reverses the
adaptive responses to low protein intake 
mobilization of body protein source 
albumin synthesis decreases 
hair, hypoalbuminemia with edema
sign  Fatty liver: due to lipogenesis from the excess
carbohydrate intake and reduced
apolipoprotein synthesis
 Other causes if edematous malnutrition:
aflatoxin poisoning, diarrhea, impaired renal
function and decreased Na+/K+ ATPase
activity
 Free radical damage may also be an important
factor in the development of edematous
malnutrition. (low plasma methionine, a
dietary precursors of cysteine, which is
needed for synthesis of the major antioxidant
factor, GLUTATHIONE.
MANAGEMENT OF SEVERE MALNUTRITION
 Initial Phase (1-7 days) – stabilization phase
o dehydration is corrected
o Treat or prevent hypoglycaemia and
hypothermia
o Correct electrolyte imbalance
o Treat bacterial or parasitic infection
o Oral rehydration therapy is preferred
o Oral feedings stated with specialized
high calorie formula.
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o The initial phase of oral treatment is REFEEDING SYNDROME

with F75 diet (75kcal or 315
kJ/100mL)
o Feedings are initiated with higher
frequency and smaller volumes.
o Over time, the frequency is reduced
from 12 to 8 to 6 feedings per 24
hours.
o The initial calorie intake is estimated
at 80-100 kcal/kg/day
o Another approach: Use of ready to
use therapeutic food (RUTFS)
o RUTF is oil based paste that has little
water content and a similar nutrient
profile but a higher calorie density
and is equally palatable to F100.
o RUTF is a mixture of powdered milk,
peanuts, sugar, vitamins and
minerals
 Rehabilitation Phase (week 2-6)
o Continued antibiotic therapy with
appropriate changes, if the initial
combination was not effective.
o Introduction of the F100 or RUTF diet
with a goal of at least 100
kcal/kg/day
o This phase usually lasts an additional
4 weeks.
o Iron therapy – usually not started
until rehab phase of treatment
o Iron can interfere with the proteins’
host defense mechanism.
o Free iron during the early phase of
treatment might exacerbate oxidant
damage, precipitating infection
(malaria), clinical kwashiorkor or
marasmic kwashiorkor in a child with
clinical marasmus.
nd
o Expectations after 2 Phase:
 Any edema that was present
has usually been mobilized.
 Infections are undercontrol.
 The child is becoming more
interested in his or her
surroundings.
 Appetite is returning.
 Final Follow-up Phase (weeks 7-26)
o Feeding to cover catch up growth
o Providing emotional and sensory
stimulation
o The child should be fed ad libitum.
 Can complicate the acute nutritional
rehabilitation.
 Hallmark of refeeding syndrome:
development of severe hypophosphatemia
after the cellular uptake of phosphate during
st
the 1 week of starting to refeed.
Serum Phosphate Level of ≤ 0.5 mmol/L:
 Weakness
 Rhabdomyolysis
 Neutrophil dysfunction
 Cardiorespiratory failure
 Arrhythmias
 Seizures
 Altered level of consciousness
 Sudden death
OVERWEIGHT AND OBESITY
 Health care professional define obesity or
increased adiposity using the BMI, which is an
excellent proxy for more direct measurement
of fat.
 ( ) ( )
 Adults
o Obesity – BMI=≥30
o Overweight – BMI 25-30
For Children >2 Years Old
Obesity and overweight are defined using BMI
Percentiles
 Obesity – BMI ≥95 percentile
th
 Overweight – BMI between the 85 and 95
th th
percentiles
ETIOLOGY
 Obesity results from an imbalance of caloric
intake and energy expenditure
Individual Adiposity is the result of a complex
interplay:
 Genetically determined body habitus
 Appetite
 Nutritional intake
 Physical activity
 Energy expenditure
Environmental factors determine:
 Levels of available food
 Preferences for types of food
 Levels of physical activity
 Preferences for types of activities
 Work is increasingly sedentary

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 Chronic partial sleep loss can increase risk for
weight gain and obesity
EFFECTS OF SLEEP DEBT
 Results in decreased glucose tolerance and
insulin sensitivity related to alterations in
glucocorticoids and sympathetic activity
 Release of orexins (peptides synthesized in
the lateral hypothalamus)  increase feeding,
arousal, sympathetic activity, and or
neuropeptide Y activity.
Role of Genetics in Obesity:
 Rare single-gene disorders resulting in human
obesity are known, including FTO (Fat Mass
and Obesity) and INSIG2 (insulin-induced gene
2) mutations as well as leptin deficiency and
pro-opiomelanocortin deficiency
 Prader-Willi Syndrome
ENDOCRINE AND NEURAL PHYSIOLOGY
GI Hormones that Promote Satiety:
 Cholecystokinin
 Glucagon-like peptide 1
 Peptide YY
 Vagal Neuronal Feedback  promote satiety
 Ghrelin – stimulates appetite
 Adinopectin – secreted by adipocytes –
reduced levels in response to obesity and
increased levels in response to fasting
 Leptin – is directly involved in satiety  low
leptin levels stimulate food intake and high
leptin levels inhibit hunger
Neuropeptide in the Brain that Affect Appetite
Stimulation:
 Neuropeptide Y
 Agouti-related peptide
 Orexin
 Melanocortins and α-melanocortin
Stimulating Hormone – are involved in satiety
 The neuroendocrine control appetite and
weight involves a negative feedback system,
balanced between short term control of
appetite (including ghrelin, PPY) and long
term control of adiposity (including leptin)
OBESITY AND CHRONIC INFLAMMATION
 There is increase evidence that obesity may
be associated with chronic inflammation
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 ADINOPECTIN (a peptide with anti-
inflammatory properties) – occurs in reduced
levels in obese patients
Low Adinopectin Levels Correlate with:
 Elevated levels of free fatty acids
 Elevated levels of plasma triglycerides
 High BMI
 Adipocytes secrete peptides and cytokines
into the circulation
 Proinflammatory peptides such as interleukin-
6 and TNF- occur in high levels in obese
patients.
 IL-6 stimulates production if C-Reactive
Protein
 CRP is a marker of inflammation and might
link obesity, coronary disease and subclinical
inflammation
OBESITY ASSOCIATED COMORBIDITIES
Cardiovascular
 Dyslipidemia – HDL <40, LDL >130, Total
Cholesterol >200
 Hypertension – SBP >95% for sex, age, height
ENDOCRINE
 Type 2 DM – Acanthosis nigricans, polyuria,
polydipsia, Fasting Blood Glucose >110
 Metabolic Syndrome – Central adiposity,
insulin resistance, dyslipidemia, hypertension
 Polycystic Ovary Syndrome – irregular
menses, hirsutism, acne, insulin resistance,
hyperandrogenemia
GASTROINTESTINAL
 Gallbladder Disease Abdominal Pain,
vomiting, jaundice
 Nan-alcoholic Fatty Liver Disease –
hepatomegaly, abdominal pain, dependent
edema, increased transaminase, can progress
to fibrosis, cirrhosis
NEUROLOGIC
 Pseudomotor Cerebri- headaches, vision
change, papilledema
ORTHOPEDIC
 Blount Disease (Tibia Vera) – severe bowing of
tibia, knee, pain, limo
 Musculoskeletal problems – back pain, joint
pain, frequent strains in sprains, limp, hip,
groin pain, leg bowing
 Slipped Capital Femoral Epiphysis – hip pain,
knee pain, limp, decreased mobility of hip
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PSYCHOLOGICAL
 Behavioral Complications – anxiety,
depression, low self-esteem, disordered
eating, signs of depression, worsening school
performance, social isolation, problems with
bullying or being bullied
PULMONARY
 Asthma – SOB, wheezing, coughing, exercise
intolerance
 Obstructive Sleep Apnea – snoring, apnea,
restless sleep, behavioural problems
EVALUATION
 examination of the growth chart for weight,
height, and BMI trajectories
 consideration of possible medical causes of
obesity
 detailed exploration of family eating,
nutrition, and activity patterns
 A complete pediatric history → is to uncover
comorbid disorders.
 The family history focuses on the adiposity of
other family members and the family history
of obesity-associated disorders.
PHYSICAL EXAMINATION SHOULD BE THOROUGH:
 Careful screening for hypertension
 Systemic examination of the skin: Acanthosis
nigricans (insulin resistance), hirsutism
(polycystic ovary syndrome)
 Tanner staging can reveal premature
adrenarche secondary to advanced sexual
maturation in overweight and obese girls.
LABORATORY TESTING:
 Fasting plasma glucose
 Triglycerides
 Low-density lipoproteins (LDL)
 High-density lipoproteins (HDL)
 Cholesterol
 Liver function test
INTERVENTION
 A combine nutritional advice, exercise and
cognitive behavioral approaches usually work
best.
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 Bariatric surgery??
 Meal should be based on fruits, vegetables,
whole grains, lean meat, fish and poultry.
 Traffic-Light diet groups food into those that
can be consumed without any limitations
(Green), in moderation (Yellow), or reserved
for infrequent treatment (Red).
 Increasing physical activity → decrease risk for
cardiovascular disease, improve well-being, ad
contribute to weight loss
 Referral to multi-disciplinary, comprehensive
pediatric weight-management program is
ideal for obese children whenever possible.
ADJUCTIVE THERAPY
 Sibutramine - appetite suppressant:
combined norepinephrine and serotonin
reuptake inhibitor.
 S/E: Modest increases in heart rate and blood
pressure, nervousness, insomnia.
 Orlistat - Lipase inhibitor: decreased
absorption of fat
 S/E: Diarrhea, flatulence, bloating, abdominal
pain, dyspepsia
SUGGESTIONS FOR PREVENTING OBESITY
PREGNANCY
 Normalize body mass index before pregnancy.
 Do not smoke.
 Maintain moderate exercise as tolerated.
 In gestational diabetics, provide meticulous
glucose control.
POSTPARTUM AND PREGNANCY
 Breast-feeding is preferred for a minimum of
3 mos.
 Postpone the introduction of solid foods and
sweet liquids.
FAMILIES
 Eat meal as a family in a fixed place and time.
 Do not skip meals, especially breakfast.
 No television during meals.
 Use small plates, and keep serving dishes
away from the table.
 Avoid unnecessary sweet or fatty and soft
drinks.
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 Remove televisions from children’s bedroom;  Ban advertising of fast foods directed at pre-
restrict times for television viewing and video school children, and restricts advertising to
games. school-aged children.

SCHOOLS
ESTABLISHING HEALTHY HABITS IN CHILDREN
 Eliminate fundraisers with cookie and candy
 Do not punish a child during mealtimes with
sales.
regard to eating. Interactions during meals
 Review the contents of vending machines and
should be pleasant and happy.
replace with healthier choices.
 Do not use food as a reward.
 Install water fountains.
 Parents, siblings and peers should model
 Educate teachers, especially physical
healthy eating, tasting new foods, and eating
education and science faculty, about basic
a well-balanced meal.
nutrition and benefits of physical activity.
 Children should be exposed to a wide range of
HEALTH CARE PROVIDERS food, tastes, and textures.
 Food should be offered multiple times.
 Explain the biologic and genetic contribution Repeated exposure to initially disliked foods
to obesity. will break down resistance.
 Give age-appropriate expectations for body  Forcing a child to eat certain food will
weight in children. decrease his or her preference for that food.
 Work toward classifying obesity as a disease  Do not force children to “clean their plate”.
to promote recognition, reimbursement for
care, and willingness and ability to provide SUMMARY
treatment.
 Malnutrition
INDUSTRY  Criteria used in defining malnutrition
 Micronutrient deficiencies
 Mandate age-appropriate nutrition labelling  Protein Energy Malnutrition (Marasmus and
for products aimed at children (ex. Red/Green Kwashiorkor)
light food, with portion sizes.)  Overweight and Obesity
 Encourage marketing of interactive video
games in which children must exercise in
order to play.
 Use celebrity advertising directed at children
for healthful foods to promote breakfast and
regular meals.

GOVERNMENT AND REGULATORY AGENCIES

 Classify obesity as a legitimate disease.

 Find novel ways to fund healthy lifestyle
programs (ex. With revenues from food and
drink taxes.)
 Provide financial incentives to school that
initiate innovative physical activity and
nutrition programs.
 Allow tax deductions for the cost of weight
loss and extreme exercise programs.
 Provide urban planners with funding to
establish bicycle, jogging, and walking paths.

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