SEVERE MALNUTRITION

AND MICRO NUTRIENT DEFICIENCY

Boerhan Hidayat
Nutrition and Metabolic Diseases Division
Child Health Department
Medical Faculty-Airlangga University
Dr Soetomo General Hospital
Surabaya

02/08/2017 Nutrition Lecture Note 2016 1

 HUMAN NUTRITION
Nutrients are substances that are crucial for
human life, growth & well-being.
Macronutrients (carbohydrates, lipids,
proteins & water) are needed for energy and
cell multiplication & repair.
Micronutrients are trace elements &
vitamins, which are essential for metabolic
processes.
 HUMAN NUTRITION/2
Obesity & under-nutrition are the 2 ends of
the spectrum of malnutrition.
A healthy diet provides a balanced nutrients
that satisfy the metabolic needs of the body
without excess or shortage.
Dietary requirements of children vary
according to age, sex & development.
 Assessment of Nutr status

Direct
Clinical
Anthropometric
Dietary
Laboratory
Indirect
Health statistics
Ecological variables
 Macro-nutrients
Energy
Necessary for all bodily function
Protein
Necessary for structural development (muscle and
bone)
Fat
Necessary for cell membrane and skin cell
development
 Water soluble vitamins
Thiamin B
nervous system function, enzymatic energy release of carbohydrates (beef,
pork, liver, legumes, breads)
Riboflavin B2
Participants in enzymatic energy release of carbs, fat & protein (milk, dairy,
dark green vegetables, yogurt)
Niacin
Participates in enzymatic energy release of energy nutrients (beef, pork,
liver, breads, nuts)
Folate
Red blood cell formation, new cell division (veg, seeds)
Vitamin B12 (Cobalamin)
Red blood cell formation, nervous system maintainance (animal prod)
Pantothenic Acid
Biotin (Vitamin H, CoEnzyme R)
Vitamin B6 (Pyridoxine)
Vitamin C
 Fat soluble vitamins
Vitamin A
Essential to vision, fetal development, immune response
Found in dairy products, fish liver oils; as B-carotene found in many
plants (e.g. carrots, mango)
Vitamin D
Bone formation, calcium metabolism and absorption
Found in sunlight, egg yolk, dairy products and fish liver oil
Vitamin E
Cell membrane construction and maintenance
In fats and oils, green leafy vegetables, poultry, fish
Vitamin K
Blood clotting, protein synthesis
In green leafy vegetables, liver, cabbage
 Minerals
Major Bone Minerals Trace Minerals

Calcium (bones) Iodine (thyroid function)

Phosphorus (DNA) Iron (hemoglobin)
Magnesium (bones) Zinc (enzyme, hormone)
Sodium (nerve impulse) Copper (abs. of iron)
Chloride (fluid balance) Flouride (bone & teeth)
Potassium (prot. syn) Chromium (energy rel.)
Sulfur (some a.a.s) Molybdenum (enzymes)
Manganese (enzymes)
Selenium (antioxidant)
Cobalt (part of B12)
 Death from malnutrition
*

*At least 70%

* of childhood
diseases are
related with
one of these
conditions
*
*
Source: WHO, based on C.J.L. Murray and A.D. Lopez, The Global Burden of Disease, Harvard University Press,
Cambridge (USA) 1996 and American Journal of Public Health 1993-83.
 Causes of malnutrition
Child malnutrition
death and disability

Inadequate Disease
Diet

Poor water/ sanitation Inadequate

Insufficient
inadequate health maternal and
access to food
services child care
 Higher Impaired
mortality rate mental
development
Reduced Increased risk of
capacity adult chronic disease
Baby
to care
Low Birth Untimely/inadequate
Elderly for baby
Weight weaning
Malnourished
Frequent
Infections
Inadequate Inadequate
catch up food, health
Inadequate
Inadequate growth & care
fetal Child
food, nutrition
health Stunted
& care Reduced
mental
Woman capacity
Malnourished
Adolescent
Start here Pregnancy Inadequate
Stunted
Low Weight food, health
Gain & care

Reduced
Inadequate mental
Higher
food, health capacity
maternal
& care
mortality
 Types of malnutrition
Severe Protein-Energy Malnutrition (>3 S.D.)
Kwashiorkor (low protein)
Marasmus (low calories)
Mild/moderate undernutrition (>2 S.D.)
Stunting
Underweight
Wasting
Micro-nutrient deficiency
Iodine
Iron
Vitamin A
Vitamin D
 Measurement of Malnutrition
STUNTING: Height for age height compared
to a reference population of the same age.
= represents long term growth retardation
UNDERWEIGHT: Weight for age weight
compared to age in a reference population

WASTING: Weight for height weight

compared to a reference population of the
same height.
PRECIPITATING FACTORS
LACK OF FOOD (famine, poverty)

INADEQUATE BREAST FEEDING

WRONG CONCEPTS ABOUT NUTRITION

DIARRHOEA & MALABSORPTION

INFECTIONS (worms, measles, T.B)

 CLASSIFICATION

A. CLINICAL ( WELLCOME )
Parameter: weight for age + oedema
Reference tandard (50th percentile)
Grades:
80-60 % without oedema is under weight
80-60% with oedema is Kwashiorkor
< 60 % with oedema is Marasmus-Kwash
< 60 % without oedema is Marasmus
 CLASSIFICATION (2)

B. COMMUNITY (GOMEZ)
Parameter: weight for age
Reference standard (50th percentile) WHO
chart
Grades:
I (Mild): 90-70
II (Moderate): 70-60
III (Severe) : < 60
 ADVANTAGES

SIMPLICITY (no lab tests needed)

REPRODUCIBILITY
COMPARABILITY
ANTHROPOMETRY+CLINICAL SIGN USED
FOR ASSESSMENT
 Kwashiorkor (low protein)
Decreased muscle mass (failure to gain weight and of linear
growth)
Swollen belly (edema and lipid build-up around the liver)
Changes in skin pigment (pellagra); may lose pigment where
the skin has peeled away (desquamated) and the skin may
darken where it has been irritated or traumatized
Hair lightens and thins, or becomes reddish and brittle.
Increased infections and increased severity of normally mild
infection, diarrhea
Apathy, lethargy, irritability

Death does not occur from actual starvation but from

secondary infection
 Kwashiorkor mechanisms
Occurs in reaction to emergency situations
(famine)
Kwashiorkor more likely in areas where
cassava, yam, plantain, rice and maize are
staples, not wheat
Increased carbohydrate intake with decreased
protein intake eventually leads to edema
(water) and fatty liver
CONSTANT FEATURES OF KWASH

OEDEMA

PSYCHOMOTOR CHANGES

GROWTH RETARDATION

MUSCLE WASTING
USUALLY PRESENT SIGNS

MOON FACE

HAIR CHANGES

SKIN DEPIGMENTATION

ANAEMIA
OCCASIONALLY PRESENT SIGNS

HEPATOMEGALY
FLAKY PAINT DERMATITIS
CARDIOMYOPATHY & FAILURE
DEHYDRATION (Diarrh. & Vomiting)
SIGNS OF VITAMIN DEFICIENCIES
SIGNS OF INFECTIONS
 DD of Kwash Dermatitis

Acrodermatitis Entropathica
Scurvy
Pellagra
Dermatitis Herpitiformis
Marasmus
Deficit in calories
marasmus comes from
Greek origin of word to
waste
Gross weight loss
Hyper-alert and ravenously
hungry
Children have no
subcutaneous fat or muscle

eventually starve to death

(immediate cause often is
pneumonia)
 Marasmus mechanism
Energy intake is insufficient for bodys requirements
body must draw on own stores
Liver glycogen exhausted in a few hours skeletal
muscle protein used via gluconeogenesis to maintain
adequate plasma glucose
When near starvation is prolonged, fatty acids are
incompletely oxidized to ketone bodies, which can be
used by brain and other organs for energy
High cortisol and growth hormone levels

Mechanism is same as anorexia

 Severe Malnutrition: Consequences
Mental development
Lower IQ levels
Poorer school performance
Behaviors of recovered severely malnourished
children
shy, isolated, withdrawn
decreased attention span
immature, emotionally unstable
fewer peer relationships/reduced social skills
played less/stayed nearer to mothers
 Stunting Height for Age
Height for age reflects pre- and post- natal
linear growth
Stunting refers to shortness that is not
genetic, but due to poor health or nutrition
Most standard definition < 2 S.D.
Stunting is good cumulative measure of well-
being for populations of children (because
not affected by weight recovery)
 Stunting: Causes
Poor nutrition plays major role
Role of environment: improvements in
average height shown by populations over last
century (impact of genetic influence
subsumed by level of socio-economic
development)
In 1833, British children were as tall as
children today from India and Guatemala
All immigrant populations have same height
after 3 generations in US
 Stunting: Timing
Age of onset varies, but usually in first 2-3
years of life
First few months, infants in developing
countries grow just as quickly as children in
reference populations
Growth retardation starts from 2-6 month of life
(often associated with weaning)
Infants at risk during this time because of high
nutritional requirements and high rates of
infections (breast fed infants often protected)
 Stunting: Consequences
Cross-sectional associations Low height for
age associated with:
Reduced cognitive development
Poor motor skills
Poor neuro-sensory integration
Quiet, reserved, withdrawn, timid, passive
Difficulty making decisions
Decreased involvement with environment, toys,
tasks
Less able to deal with stressor such as hunger or
parasites
 Hypothesized Mechanisms
alterations in
development
of CNS

emotional poor mental

poor
reactivity, development &
nutrition impaired behavior
stress response

functional
isolation
 Severe Malnutrition
Medical & social disorder

End result of chronic nutritional & emotional

deprivation

Management requires medical & social

interventions
 Underlying causes of poor diet & excess
disease (UNICEF)

Insufficient access to food

Inadequate maternal & child care

Poor environment

Inadequate or lack of access to health services

 3 Phases of Management
Initial Treatment
Life threatening problems identified & treated
Specific deficiencies/metabolic abnormities corrected
Feeding begun
Rehabilitation
Intensive feeding
Emotional & physical stimulation
Mother trained
Follow-up
Prevention of relapse
Assure continued development
 Treatment Facilities
Initial treatment & beginning of rehabilitation
SAM with complication (anorexia, infection,
dehydration)
Residential care in special nutrition unit
SAM w/out complications, s/p inpt has appetite.
gaining weight, stable
Nutritional rehabilitation center:
day hospital,
1ary health center
CTC
 Evaluation of malnourished child
Nutritional status
WFH, HFA, edema
Moderate (-3<SD<-2) or severe (<3SD)
Hx & PE
Lab tests
Useful: glucose, blood smear (malaria), H/H, urine cx,
feces , CXR, PPD
Not useful: serum protein, HIV, electrolytes
 GENERAL PRINCIPLES FOR ROUTINE CARE
(the 10 Steps)
There are ten essential 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

These steps are accomplished in two phases:

# an initial stabilisation phase where the acute medical conditions are managed
# longer rehabilitation phase

Note that treatment procedures are similar for marasmus and kwashiorkor
 Initial Treatment
Hypoglycemia Dehydration
Cause death first days Reliable signs
Sign infection: ATB Diarrhea, thirst, hypoT, eyes,
weak pulse
Sign infrequent feedings
Clinical suspicion, treat Unreliable signs
MS, mouth/tongue/ tears/skin
50ml D10%, F75 PO/NG
elasticity
Never use bottles ReSoMal: 70-100ml/kg/12h
Hypothermia Breastfeed, F-75
Kangaroo Septic shock
Warm ATB broad spectrum
Treat for hypoglycemia Tx hypoGly, hypoT
Sign of infection, treat CHF, anemia, Vit K
Time frame for management
 ReSoMal
Severely malnourished children
K deficient, high Na levels
Mg, Zn, copper deficiency
Commercially available
Dilute 1 packet of standard WHO ORS in 2 l water +
50 g of sucrose (25g/l) + 40 ml (20ml/l) mineral mix
solution
5ml/kg PO/NG q30min
Cont till thirst & urine
 Formula diets for severely malnourished
children
Impaired liver & intestinal function + infection
Food must be given in small amounts, frequently (PO/NG)
Unable to tolerate usual amounts of dietary protein, fat, Na
Diet low in above, hi in carbohydrates

F-75
75kcal or 315kj/100ml
Initial phase treatment, 130ml/kg/d
Feed q 2-3hr (8 meals/d)
F-100
100kcal or 420kj/100ml
Feed q 4-5 h (5-6 meals/d)
Rehabilitation phase (appetite returned)
 Composition F-75 and F-100
F-75 F-100
Dried skimmed milk 25g 80g
Sugar 70g 50g
Cereal flour 35g -
Vegetable oil 27g 60g
Mineral mix 20ml 20 ml
Vitamin mix 140ml 140 ml
Water 1l 1l
Protein 0.9g 2.9g
Lactose 1.3g 4.2g
K 3.6mmol 5.9mmol
Na 0.6mmol 1.9mmol
Mg 0.43mmol 0.73mmol
Zn 2.0mmol 2.3mmol
Copper 0.25mg 0.25mg
Osmolarity 333mOsmol/l 419mOsmol/l
Energy from protein 5% 12%
Energy from fat 32% 53%
Continue Breastfeeding
 Initial Treatment

Infections Vitamin deficiencies

fever, inflammation Folic acid
Measles vaccine
Vit mix: riboflavin, ascorbic acid,
1st line, all children pyridoxine, thiamine, fat soluble vit D, E,
Cotrimoxazole K
Complications: ampi + gent Vit A PO or IM
2nd line, > 48 hr ATB Eye pads NS solution
+ chloramphenicol
Tetracycline + atropine eye drops
Malaria, candidiasis Bandage eyes
Helminthiasis
TB Severe Anemia
Transfusion PRC/WB (CHF)
Dermatosis Kwashiorkor No Iron at this stage
1% K permanganate soaks
Nystatin CHF
Zinc + castor oil Overhydration (>48hr)
Stop feeds. Give furosemide
 Rehabilitation
Principles & criteria
Eating well
MS improved: smiles, responds to stimuli
Dev appropriate behavior
Nl temperature
No V/D
No edema
Gaining Wt: > 5g/kg of body wt/d x 3 days
Most important determinant of recovery:
Amount of energy consumed: calories, protein, micronutrients (K, Mg, I, Zn)
 Nutrition for children < 24 mo
F-100 diet q 4 hr (day & night)
each feed by 10ml
150-220 kcal/kg/d
Folic acid + Iron, Vit & Mineral mix
Attitude of care giver crucial
Decreasing edema
F-100 continued till Target Wt (-1 SD/ 90% of median NCHS/WHO reference
value for WFH)

Wt daily plotted on graph

Target wt usually reached 2-4 wks
 Nutrition for children > 24 mos
amounts F-100 (practical value in refugee camps, # different diets )

Introduce solid foods

Local foods should be fortified

content of Energy (oil), minerals &Vitamins (mixes)
Milk added (protein)
Energy content of mixed diets: 1kcal or 4/2kj/g
F-100 given between feeds of mixed diet
5-6 feeds /d

Folic acid (5mg on day 1, 1mg/d) + Iron ( 3mg/kg elemental iron/d x 3mo)
 Emotional & physical stimulation

1ary/2ary prevention DD, MR, ED

Start during rehabilitation
Avoid sensory deprivation
Maternal presence
Environment
Play activities, peer interactions
Physical activities
 Rehabilitation
Parental teaching
Correct feeding/food preparation practices,
Stimulation, play, hygiene
Treatment diarrhea, infections
When to seek medical care
Preparation for D/C
Reintegration into family & community
Prevent malnutrition recurrence
 Criteria for D/C
Child
WFH reached -1SD
Eating appropriate amount of diet that mother can prepare at home
Gaining wt at normal or rate
Vit/mineral deficiencies 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, ARI
Health worker
Able to ensure F/U child & support for mother
 Follow up
Child usually remains stunted w/ DD
Prevention of recurrence severe malnutrition
Strategy for tracing children
F/U: 1,2, 4 weeks, then 3 & 6 mos, then 2x/yr till
age 3yrs
WFH no less than -1SD
Assess overall health, feeding, play
Immunizations, treatments, vitamin/minerals
Record progress
 Failure to respond Criteria

1ary failure to respond

Failure to regain appetite by day 4
Failure to start to lose edema by day 4
Edema still present by day 10
Failure to gain at least 5g/kg/d by day 10

2ary failure to respond

Failure to gain at least 5g/kg/d during rehabilitation
 Failure to respond
Problems with treatment facilities
Poor environments
Insufficient or inadequately trained staff
Inaccurate weighing machines
Food prepared or given incorrectly
 Failure to respond
Problems w/ individual children
Insufficient food given
Vitamin or mineral deficiency
Malabsorption of nutrients
Rumination
Infections
Diarrhea, dysentery, OM, LRI, TB, UTI, malaria, intestinal helminthiasis,
HIV/AIDS
Serious underlying disease
Congenital abnormalities, inborn errors metabolism, malignancies,
immunological diseases
Iodine deficiency - thyroid

Simple goiter is the easiest of all

known diseases to prevent . . .
It may be excluded from the list of
human diseases as soon as
society determines to make the
effort David Marine 1923
 Iodine Deficiency Disorders

Source: State of the Worlds Children, 1998

 Causes of Iodine Deficiency
Mountainous areas at risk (soils leached by
high rainfall, melting snow, flooding)

Culturally induced behavioral change

Tasmanian Aboriginals migrated every season until
European invasion, became sedentary and had
incidence of thyroid problems
 Iodine Deficiency: Severe

Goiter: most commonly recognized

consequence (enlarged thyroid)
Occurs when thyroid gland is unable to meet the
metabolic demands of the body through sufficient
hormone production thyroid compensates by
enlarging (works in short term)
Cretenism: proximal pyramidal signs,
intellectual impairment, primitive reflexes
Only occurs with severe fetal iodine deficiency
 Iodine Deficiency: Moderate
Studies comparing 2 Villages
Consistent results: meta-analysis showed 13.5 IQ
point difference between groups
Intervention Studies
Prenatal supplementation (esp. 1st trimester):
clear impact prevents cretenism, and affects
mental development in children
Childhood supplementation: many mediocre
studies, but positive impact
 Iron deficiency - anemia
80
70
South Central
60 Asia
%
West Africa
50
40 East Africa
30
Eastern
20 Europe
10 Oceania

0
% pregnant women

Source:UN ACC-SCN-IFPRI - 4th Report on

World Nutrition Situation
Source: UN-ACC-SCN-IFPRI-4 Report on World Nutrition Situation
 Iron Deficiency
Iron is critical for body:
Carries oxygen to tissues from lungs
Transports electrons within cells
Integral part of important enzyme reactions
Anemia is caused most commonly by iron
deficiency (anemia is found in 40-60% of
women and children in developing countries)
 Iron Deficiency Consequences
Iron deficiency results in:
Decreased work capacity and work productivity
Permanently impaired development
Psychomotor development of anemic children will be
reduced by 5-10 IQ points
Increased morbidity and mortality from infections
Decreased growth
Vitamin A Deficiency

Vitamin A is important
because it is essential to
vision, fetal development,
immune response

250 million children of pre-

school age lack sufficient
Vitamin A in their diet.
350,000 become blind each
year, and half of them die
within a year of becoming
blind.
 Vitamin A Deficiency
Associated with blindness and increased
severity of infections such as measles and
diarrhoeal disease

WHO estimates that 2.8 million children under

5 years old have signs of clinical xerophthalmia
(childhood blindness)

WHO estimates that 14 million pre-school

children already have some eye damage from
Vitamin A deficiency