Protein energy malnutrition (PEM) is caused by a deficiency of protein and energy intake and can have serious health consequences, especially for children. It manifests as conditions like marasmus, kwashiorkor, or a combination of the two. Marasmus is characterized by severe wasting while kwashiorkor involves edema in addition to wasting. Treatment involves resolving life-threatening conditions, restoring nutritional status, and ensuring rehabilitation to prevent recurrence. Diet and supplementation aim to increase calorie and protein intake depending on the severity of malnutrition. Addressing underlying socioeconomic causes is also important for long-term management of PEM.

1. Protein Energy Malnutrition

2. Protein energy malnutrition
is due to ‘food gap’ between
intake and requirement.
The average energy deficit was found to be 300 Kcal/day

3. INTRODUCTION
Protein energy malnutrition (PEM) is widely prevalent among young children (0-6
years) but is also observed as starvation in adolescents and adults, mostly lactating
women, especially during periods of famine or other emergencies. PEM has serious
consequences for the health of individuals particularly children and can even result in
death.
“PEM can be defined as a range of pathological conditions arising
from a deficiency of protein and energy and is commonly associated
with infections.” (WHO)
DEFINE

7. THE INDIAN
PROFILE
UNDER NUTRITION IN <5 years child 241365
(average as per 18 states calculated in INDIA)
33.13% of INDIAN children <5 years is
underweight.
In every 10 children 3 are underweight in
INDIA
INDIA is 17.5% of world’s population but 39%
of world’s undernourished children live in INDIA
1 in every 3rd undernourished child lives in
INDIA
(world bank report, UNICEF 2011)
NFHS 4 is averaged of 18 states of INDIA

8. AETIOLOGY
Socio
Economic
Factors
Biological
Factors
Environmental
Factors
Role of Free
Radicals and
Aflatoxins
Age of the
host

9. PEM
Inadequate
medical
facilities
Occult
infectious
diseases
Poverty
ignorance
and illiteracy
Early
weaning
from
breast
Maternal
Malnutrition
High birth
rate
Late
weaning
Increased
intestinal
losses and
Anorexia
Weak
implementatio
n of
government
Low birth
weight
Inadequate
intrafamilial
food distribution
Social mores of
feeding and
cultural
practices
Large no. of
children
Poor hygiene
sanitation
water supply
Inadequate
medical facilities

10. MULTIFACTORIAL CAUSATION OF
MALNUTRITION
Protein
Energy
Malnutritio
n
Food
availabilit
y
Increase
d
populatio
n
Low
purchasin
g power
Malabsorpti
on
Poor
utilization
of
nutrients
Socio-
cultural
backgrou
nd
Low
intake of
protein
and
energy

11.  ACUTE PEM: protein-energy malnutrition caused by recent severe food restriction;
characterized in children by thinness for height (wasting).
 CHRONIC PEM: protein-energy malnutrition caused by long-term food deprivation;
characterized in children by short height for age (stunting).
SEVERITY COURSE MAIN DEFICIT
Mild Acute Energy
Moderate Chronic Protein
Severe Both Both

12. Protein
Energy
Malnutrition
Kwashiorkor
Marasmus
Marasmic
Kwashiorkor

13. Marasmus: Marasmus is a condition characterized by very low body
weight for age, loss of subcutaneous fat (fat under the skin), gross
muscle wasting. It is observed more frequently in infants and very young
children.
Kwashiorkor: Kwashiorkor on the other hand is a condition characterized
by oedema (excessive accumulation of fluid in the intercellular spaces of
tissue) and very low body weight for age. The syndrome is most
frequently observed in children aged 1-3 and is precipitated by an
infection or more commonly by a series of infections.
There are also children who show some of the characteristic signs of
both Marasmus and kwashiorkor. Such children are said to suffer from
Marasmic Kwashiorkor.

14. Subclinical condition means that we do not see the clinical features of
the disease. These forms of the disease can be identified only on special
investigations or tests.
In the case of PEM, we can detect subclinical status by
measuring body weight.
In all the forms of PEM, remember, growth failure or low body weight is a
common sign.
Then there are children whose heights and weights are considerably below
that of healthy children of the same age. These children may not show any
typical clinical signs of either kwashiorkor or marasmus, and as such they
are placed in the category of SUBCLINICAL FORMS OF PEM which forms
a large proportion of the disease in the community.

15. KWASHIORKO
R
Ghanian word that describes the
“evil spirit that infects the first child
when second child is born.”
Kwashiorkor typically reflects a
sudden and recent deprivation of
food (acute PEM).
Also referred to as “WET PEM”

16. KWASHIORKOR
 Kwashiorkor typically sets in between 18 months and two years.
Kwashiorkor usually develops rapidly as a result of protein deficiency or,
more commonly, is precipitated by an illness such as measles or other
infection.
 Other factors, such as aflatoxins (a contaminant sometimes found in
moldy grains), may also contribute to the development of, or symptoms
that accompany, kwashiorkor.

17. A fatty liver
develops due to a
lack of the protein
carriers that
transport fat out of
the liver.
The fatty liver lacks
enzymes to clear
metabolic toxins
from the body, so
their harmful effects
are prolonged.
Inflammation in response to
these toxins and to infections
further contributes to the
edema that accompanies
kwashiorkor.
Insufficient tyrosine to
make melanin, the
child’s hair loses its
color.
• Inadequate protein
synthesis leaves the
skin patchy and scaly,
often with sores that
fail to heal.
The lack of
proteins to carry
or store iron
leaves iron free.
Unbound iron is
common in children with
kwashiorkor:
• illnesses
• deaths
• promoting bacterial
growth
• free-radical damage.

18. Identifying child suffering from KHWASHIORKOR
Pitting
Oedema
Failure of
growth
Irritability
and Mental
Changes
Skin
changes
Flaky paint
dermatitis
Hair changes
Flaky
Alopecia
Moon Face
Associated
Deficiencies
Vitamin A &
B Complex
Associated
diseases

19. KWASHIORKAR
Stress of PEM Dysadapted
Cortisol not increased
Muscle Protein is not mobilised
Low plasma amino acid concentration
Increased Somatomedin C
Increased Growth Hormone
Increased Plasma free fatty acids
Reduced synthesis of lipo protein
Fatty liver, impaired hepatic function

20. Body weight as %
of standard
oedema
Deficit in weight
for height
Kwashiorkor 80-60 + +
Marasmus <60 0 + +
Marasmic
kwashiorkor
<60
+
+ +
Nutritional
dwarfing
<60 0 minimal
Underweight child 80-60 0 +

21. MARASMUS
Children below 2 years of age.
Consumption of diets marked by deficient in both
PROTEIN AND CALORIES.
Weight is below the third percentile for age or less than 80% of ideal weight
for age.

22. Stress of PEM Well Adapted
High Cortisol
Muscle Protein
Release of Amino Acids from muscle protein
Reduced synthesis of plasma protein
Β- lipo protein normal
Increased mobilisation of triglycerides from liver
No fatty liver
MARASMUS

23. Muscle
wasting
Failure to
thrive
Severe growth
retardation
Loose and
hanging skin
folds over
arms
Bony
prominence
Irritability,
fretfulness and
apathy
Frequent
watery
diarrhoea and
acid stools
Mostly hungry
but some are
anorexic
Temperature is
subnormal
Muscles are
weak
Identifying child suffering from MARASMUS

24. Children with sub clinical symptoms of PEM can be detected by their weight for age
or weight for height which is significantly below normal. These children growth smaller
than their genetic potential & they are at risk of gastroenteritis, respiratory and other
infections which can precipitate malnutrition.
Children adapt to prolonged insufficiency of food-energy and protein- by a marked
retardation of growth. Weight and height are both reduced resembling children a year
or more younger and they appear superficially normal.
Child showing mixture of symptoms of both Marasmus and kwashiorkor. The child is
not only extremely wasted as in MARASMUS but also has swelling in lower limbs as
in KWASHIORKOR.
MARASMIC
KWASHIORKOR
NUTRITIONAL DWARFING or
STUNTING
THE UNDERWEIGHT
CHILD

25. DIETARY MANAGEMENT
Mild and Moderate Conditions
Energy 1 ½ times of requirement –
150 kcal/kg body weight
Protein of high biological value-
3.5-4 g/kg
For pre-school children
130-150 kcal/kg
Protein 3-3.5g/ kg

26. SEVERE PEM
• 1 ½ times of normal, i.e. 150-170 kcal/kg body weight
ENERGY
• Two to four times than normal 3-7g/kg body weight
PROTEIN
• 40% of total calories
FAT
• Adequate in Ca, Fe, Na, K and Mg
MINERALS and VITAMINS

27. TREATMENTTREATMENT STRATEGY: 3
STAGES
Resolving life-
threatening conditions
Restoring nutritional
status without
disrupting homeostasis
Ensuring nutritional
rehabilitation
CRITERIA FOR
IMPROVEMENT
Disappearance of mental
apathy in 4-5 days
Disappearance of oedema
in 7 to 10 days
Weight gain in 3-4 weeks
Rise is serum albumin level
in about 2 weeks time

28. WHO and UNICEF recommend two major
approaches to the treatment
1. Facility/ hospital-based approach for clinical management using the WHO protocol.
2. Home/ community-based approach, an integrated public health response to acute
malnutrition without medical complications.
The three stages of treatment are-
Hospital Treatment
Dietary Management
Rehabilitation

29. Most deaths occur during first few days of treatment.
To reduce deaths it is recommended that treatment be divided into an initial
phase during which acute medical conditions are addressed.
HYPOGLYCEMIA:
10% Dextrose solution
4ml/kg body weight
initiated as early as
possible.
HYPOTHERMIA:
Hypothermia,
Hypoglycemia, gram
negative sepsis often
occur together. The
child should be kept
warm “bedding in” with
the mother.
DEHYDRATION AND
ELECTROLYTE
IMBALANCE:
HOSPITAL
TREATMENT

30. CONDITION SUPPLEMENTATION
ORAL
REHYDARTI
ON
THERAPY
With diarrhoea, no dehydration ORS after each stool
Mild to moderate dehydration
70ml/kg ORS in 4 hrs sip by sip or as intra gastric
drip
Severe dehydration 100ml/kg sodium saline or Ringer Lactate in 3-6 hrs
Oedematous children
70ml/kg as slow ration: half calculated fluid as
Sodium saline and rest as 10% glucose
POTASSIU
M
SUPPLEME
NT
kwashiorkor
2-4 mEq/kg/day continued for 1-2 weeks. Fruit juice
can be encouraged along with this
SODIUM Restricted to 2-3 mEq
SODIUM

31. HOSPITAL
TREATMENT Continued.....
VITAMIN AND MINERAL DEFICIENCES:
10% Dextrose solution 4ml/kg body weight initiated as early as possible.
NUTRIENT DOSE OR CONDITION
Vitamin A Standard age related doses (50,000 IU, 1,00,000 IU or 2,00,000 IU) & repeat on 2- 14 days
Later the child is initaited to Vitamin A Prophylaxis Programme
Vitamin K 2-5 mg per day for 2-3 days
Packed
cell
transfusion
To treat severe anemia (5-10 ml/kg slowly along with fursemide)
Mild to moderate anemia 6 mg/kg
Magnesiu
m
If there is seziures due to tetany or apathy. 0.8 mEq/ kg/ day divided in two doses for 1-3
days
Zinc 20 mg daily

32. INITIATING REFEEDING AND FACILITATE CATCH-UP GROWTH:
This phase is for restoration of weight for height. This is the second and
often first step in those with mild to moderate PEM
HOSPITAL
TREATMENT Continued.....
ORS
HIGH ENERGY
MILK
Milk100 ml Sugar1tsp Oil2g
Total100ml
MILK CEREAL MILK
Milk100ml Sugar1tsp
CerealFlour1tsp Total100ml
FAMILY POT
FEEDING
CEREAL
PULSE MILK
Milk100ml
LowCostWeaningFood
(cereal+Pulse+Sugar)
Total100ml

33. Dietary Management is same for all types of PEM
DIETARY
MANAGEMENT
1. Locally available staple food.
2. Inexpensive, easily digestible
3. Minimum 100 ml milk/day, if affordable eggs can be
included
4. 5:1 cereal pulse combination
5. All five food groups, evenly distributed through out
the day
6. Number of feedings to increase quantity of food
7. High in calories by adding oil and banana
8. Groundnuts can be given to older children
 Improvement in
mental apathy in 3-
4 days
 Increase in
appetite and the
child gains weight
for age
 Oedema
disappears by 7-10
days
 Diarrhoea and
respiratory

34. Follow up studies show that 1/3 of children who had been treated for PEM at hospital
were dead within a year from the disease for which they had been successfully treated
and still others were malnourished.
REHABILITATION
Causes are poverty
and failure to involve
mother in treatment
or recovery.
Residential Units
Day-care centres
Domiciliary rehabilitation
Home/ community based management of
SAM
• Low cost recipes
• Concentrated food supplement
RUTF Ready to use
therapeutic foods
Roasted Peanut
powder: Milk powder:
Sugar (30:28:25) along
with 15g gingelly oil

35. The addition of complementary
foods was delayed in 46% of the
children.
Weaning or complete withdrawal
from breastmilk before one year
of age occurred in 35% of the
children.
The main reasons for weaning
were the illness of the baby,
illness of the mother and another
pregnancy. Complementary and
supplementary foods such as
milk, porridge, soup and family
food were improperly prepared.

38. Today, the relationship between low birth
weight and the later-age risk of T2DM is
the best understood one. The association
between these two factors is closely linked
to the so-called catch-up growth of infants
whose intrauterine development occurred
under the IUGR conditions. Catch-up
growth accounts for disproportionately
high growth rate for adipose tissue
compared to the other tissues. The main
mechanisms involved in these processes
are suppression of thermogenesis and
establishment of thrifty phenotype
characterized by insulin and leptin
resistance. Children born small for
gestational age reveal abnormalities in the
growth hormone/insulin-like growth factor-
1 (IGF-1) axis, and these compounds are
known to play a pivotal role in human
growth and development [19]. Such IGF-1
abnormalities in children with catch-up
growth are thought to be closely related

39.  Roy, S. K., Fuchs, G. J., Mahmud, Z., Ara, G., Islam, S., Shafique, S., ... & Chakraborty, B. (2005).
Intensive nutrition education with or without supplementary feeding improves the nutritional status
of moderately-malnourished children in Bangladesh. Journal of Health, Population and Nutrition,
320-330.

40. LET’S
FIGHT
AGAINST
MALNUTRI
TON