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MALNUTRITION – Dra. Garcia’s Lecture HEIGHT FOR AGE

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

DIFFERENT CRITERIA USED IN DEFINING WEIGHT FOR AGE or WASTING

MALNUTRITION:  Is a measure of Acute Malnutrition
1. GOMEZ – weight below % median weight for
age (WFA) MID-UPPER ARM CIRCUMFERENCE (MUAC)
 Mild (grade 1) 75%-90% weight for  Is often used for screening in lieu of weight
age for height.
 Moderate (grade 2) 60%-74% weight  During 1-5 years of age it remains reasonably
for age static between 15-17cms among healthy
 Severe (grade 3) <60% weight for age children.
2. WATERLOW – z scores (SD) below median  It is conventionally measured over the left
weight for height (WFH) upper arm, at a point marked midway
 Mild 80%-90% WFH between acromion (shoulder) and olecranon
 Moderate 70%-80% WFH (elbow) with arm bent at right angle.
 Severe <70% WFH  The child is asked to stand or sit with the arm
3. WHO (Wasting) – z scores (SD) below median hanging loose at the side.
weight for height (WFH)  MUAC is measured with a fiber glass or steel
 Moderate -3 z score < -2 tape.
 Severe z score < -3  If it is less than 12.5 cm it is suggestive of
4. WHO (Stunting) – z scores (SD) below median severe malnutrition.
height for age (HFA)  If it is between 12.5-13.5 cm it is indicative of
 Moderate -3 z score <-2 moderate malnutrition.
 Severe z score <-3
5. KANAWATI – Middle upper arm BODY MASS INDEX (BMI)
circumference (MUAC) divided by  BMI is calculated by dividing weight in
occipitofrontal head circumference. kilograms by the square of height in meters
 Mild < 0.31 OR
 Moderate <0.28  Weight(kg) /stature(cm) x 10,000
 Severe <0.25 OR
6. COLE – z scores of BMI for age  Weight(lbs) / Stature (in.) x 703
 Grade 1 z score <-1
 Grade 2 z score <-2 BMI INTERPRETATION
 Grade 3 z score <-3  BMI below 18.5 – chronically energy deficient
*** The z-score system expresses the anthropometric  BMI greater than 25 – overweight
value as a number of standard deviation or z-scores  BMI greater than 30 – Obese
below or above the reference mean or median value.
MICRONUTRIENT DEFICIENCY:
Z SCORE 1. IODINE DEFICIENCY
 Defined as the child’s height (weight) minus  Sequelae
the median height (weight) for the age and i. Goiter
sex of the child divided by the relevant ii. Hypothyroidism
standard deviation. 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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 Cardiovascular
Polymicrobial Infection in NOMA o Bradycardia, hypotension, reduces
 Fusobacterium necrophorum cardiac output, small vessel
 Prevotella intermedia vasculopathy
 Neurologic
Treatment of Noma: o Global developmental delay, loss of
 Local wound care knee and ankle reflexes, impaired
 Pencillin memory
 Metronidazole  Hematologic
 Therapy for the underlying predisposing o Pallor, petechiae, bleeding diathesis
condition  Behaviour
o Lethargic, apathetic, irritable on
CLINICAL SIGNS OF MALNUTRITION handling
 Face
o Moon face (kwashiorkor), simian PATHOPHYSIOLOGY OF SEVERE PROTEIN CALORIE
facies (marasmus) MALNUTRITION
 Eye
o Dry eyes, pale conjunctiva, bitot Edematous or Non-edematous Malnutrition??
spots (vitamin A), periorbital edema  Variability among infants in nutrient
 Mouth requirements and in body composition at the
o Angular stomatitis, cheilitis, glossitis, time the dietary deficit is incurred.
spongy bleeding gums (vitamin C),  Giving excess carbohydrate to a child with
parotid enlargement non-edematous malnutrition reverses the
 Teeth adaptive responses to low protein intake 
o Enamel mottling, delayed eruption mobilization of body protein source 
 Hair albumin synthesis decreases 
o Dull, sparse, brittle hair, hypoalbuminemia with edema
hypopigmentation, flag sign  Fatty liver: due to lipogenesis from the excess
(alternating bands of light and carbohydrate intake and reduced
normal color), broomstick eyelashes, apolipoprotein synthesis
alopecia  Other causes if edematous malnutrition:
 Skin aflatoxin poisoning, diarrhea, impaired renal
o Loose wrinkled (marasmus), shiny function and decreased Na+/K+ ATPase
and edematous (kwashiorkor), dry, activity
follicular hyperkeratosis, patchy  Free radical damage may also be an important
hyper and hypopigmentation (crazy factor in the development of edematous
paving or flaky paint dermatosis), malnutrition. (low plasma methionine, a
erosions, poor wound healing dietary precursors of cysteine, which is
 Nails needed for synthesis of the major antioxidant
o Koilonychia (spoon nails), thin and factor, GLUTATHIONE.
soft nail plates, fissures or ridges
 Musculature MANAGEMENT OF SEVERE MALNUTRITION
o Muscle wasting particularly buttocks  Initial Phase (1-7 days) – stabilization phase
and thighs, Chvostek and Trosseau o dehydration is corrected
sign (hypocalcemia) o Treat or prevent hypoglycaemia and
 Skeletal hypothermia
o Deformities, usually as a result of o Correct electrolyte imbalance
calcium, Viatmin D or Vitamin C o Treat bacterial or parasitic infection
deficiencies o Oral rehydration therapy is preferred
 Abdomen o Oral feedings stated with specialized
o Distended, hepatomegaly with fatty high calorie formula.
liver, ascites may be present

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o The initial phase of oral treatment is REFEEDING SYNDROME

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

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 Chronic partial sleep loss can increase risk for  ADINOPECTIN (a peptide with anti-
weight gain and obesity inflammatory properties) – occurs in reduced
EFFECTS OF SLEEP DEBT levels in obese patients
 Results in decreased glucose tolerance and
insulin sensitivity related to alterations in Low Adinopectin Levels Correlate with:
glucocorticoids and sympathetic activity  Elevated levels of free fatty acids
 Release of orexins (peptides synthesized in  Elevated levels of plasma triglycerides
the lateral hypothalamus)  increase feeding,  High BMI
arousal, sympathetic activity, and or  Adipocytes secrete peptides and cytokines
neuropeptide Y activity. into the circulation
 Proinflammatory peptides such as interleukin-
Role of Genetics in Obesity: 6 and TNF- occur in high levels in obese
 Rare single-gene disorders resulting in human patients.
obesity are known, including FTO (Fat Mass  IL-6 stimulates production if C-Reactive
and Obesity) and INSIG2 (insulin-induced gene Protein
2) mutations as well as leptin deficiency and  CRP is a marker of inflammation and might
pro-opiomelanocortin deficiency link obesity, coronary disease and subclinical
 Prader-Willi Syndrome inflammation

ENDOCRINE AND NEURAL PHYSIOLOGY OBESITY ASSOCIATED COMORBIDITIES

GI Hormones that Promote Satiety: Cardiovascular

 Cholecystokinin  Dyslipidemia – HDL <40, LDL >130, Total
 Glucagon-like peptide 1 Cholesterol >200
 Peptide YY  Hypertension – SBP >95% for sex, age, height
 Vagal Neuronal Feedback  promote satiety
 Ghrelin – stimulates appetite ENDOCRINE
 Adinopectin – secreted by adipocytes –  Type 2 DM – Acanthosis nigricans, polyuria,
reduced levels in response to obesity and polydipsia, Fasting Blood Glucose >110
increased levels in response to fasting  Metabolic Syndrome – Central adiposity,
 Leptin – is directly involved in satiety  low insulin resistance, dyslipidemia, hypertension
leptin levels stimulate food intake and high  Polycystic Ovary Syndrome – irregular
leptin levels inhibit hunger menses, hirsutism, acne, insulin resistance,
hyperandrogenemia
Neuropeptide in the Brain that Affect Appetite GASTROINTESTINAL
Stimulation:  Gallbladder Disease Abdominal Pain,
 Neuropeptide Y vomiting, jaundice
 Agouti-related peptide  Nan-alcoholic Fatty Liver Disease –
 Orexin hepatomegaly, abdominal pain, dependent
 Melanocortins and α-melanocortin edema, increased transaminase, can progress
Stimulating Hormone – are involved in satiety to fibrosis, cirrhosis
 The neuroendocrine control appetite and NEUROLOGIC
weight involves a negative feedback system,  Pseudomotor Cerebri- headaches, vision
balanced between short term control of change, papilledema
appetite (including ghrelin, PPY) and long ORTHOPEDIC
term control of adiposity (including leptin)  Blount Disease (Tibia Vera) – severe bowing of
tibia, knee, pain, limo
OBESITY AND CHRONIC INFLAMMATION  Musculoskeletal problems – back pain, joint
 There is increase evidence that obesity may pain, frequent strains in sprains, limp, hip,
be associated with chronic inflammation groin pain, leg bowing
 Slipped Capital Femoral Epiphysis – hip pain,
knee pain, limp, decreased mobility of hip

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PSYCHOLOGICAL  Bariatric surgery??

 Behavioral Complications – anxiety,  Meal should be based on fruits, vegetables,
depression, low self-esteem, disordered whole grains, lean meat, fish and poultry.
eating, signs of depression, worsening school  Traffic-Light diet groups food into those that
performance, social isolation, problems with can be consumed without any limitations
bullying or being bullied (Green), in moderation (Yellow), or reserved
PULMONARY for infrequent treatment (Red).
 Asthma – SOB, wheezing, coughing, exercise  Increasing physical activity → decrease risk for
intolerance cardiovascular disease, improve well-being, ad
 Obstructive Sleep Apnea – snoring, apnea, contribute to weight loss
restless sleep, behavioural problems  Referral to multi-disciplinary, comprehensive
pediatric weight-management program is
EVALUATION ideal for obese children whenever possible.

 examination of the growth chart for weight, ADJUCTIVE THERAPY

height, and BMI trajectories
 consideration of possible medical causes of  Sibutramine - appetite suppressant:
obesity combined norepinephrine and serotonin
 detailed exploration of family eating, reuptake inhibitor.
nutrition, and activity patterns  S/E: Modest increases in heart rate and blood
 A complete pediatric history → is to uncover pressure, nervousness, insomnia.
comorbid disorders.  Orlistat - Lipase inhibitor: decreased
 The family history focuses on the adiposity of absorption of fat
other family members and the family history  S/E: Diarrhea, flatulence, bloating, abdominal
of obesity-associated disorders. pain, dyspepsia

PHYSICAL EXAMINATION SHOULD BE THOROUGH: SUGGESTIONS FOR PREVENTING OBESITY

 Careful screening for hypertension PREGNANCY

 Systemic examination of the skin: Acanthosis
nigricans (insulin resistance), hirsutism  Normalize body mass index before pregnancy.
(polycystic ovary syndrome)  Do not smoke.
 Tanner staging can reveal premature  Maintain moderate exercise as tolerated.
adrenarche secondary to advanced sexual  In gestational diabetics, provide meticulous
maturation in overweight and obese girls. glucose control.

POSTPARTUM AND PREGNANCY

LABORATORY TESTING:
 Breast-feeding is preferred for a minimum of
 Fasting plasma glucose 3 mos.
 Triglycerides  Postpone the introduction of solid foods and
 Low-density lipoproteins (LDL) sweet liquids.
 High-density lipoproteins (HDL)
FAMILIES
 Cholesterol
 Liver function test  Eat meal as a family in a fixed place and time.
 Do not skip meals, especially breakfast.
INTERVENTION  No television during meals.
 Use small plates, and keep serving dishes
 A combine nutritional advice, exercise and away from the table.
cognitive behavioral approaches usually work  Avoid unnecessary sweet or fatty and soft
best. 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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