Malnutrition is a condition that develops from an imbalance of nutrient intake and the body's needs. It can manifest as protein-energy malnutrition (PEM) in various forms including kwashiorkor, marasmus, and marasmic-kwashiorkor. Kwashiorkor is characterized by edema and results from insufficient protein intake while marasmus is caused by lack of energy intake leading to wasting. PEM is assessed clinically through measurements, lab tests, and evaluating functional criteria to determine severity and appropriate treatment.

1. Malnutrition
Dr. Reza Parker (MD Romania)

2. MALNUTRITION
WHO defines Malnutrition as "the cellular
imbalance between the supply of nutrients
and energy and the body's demand for them
to ensure growth, maintenance, and specific
functions.“
Malnutrition is the condition that develops when
the body does not get the right amount of
the vitamins, minerals, and other nutrients it needs
to maintain healthy tissues and organ function.
Definitions

3. • PROTEIN ENERGY MALNUTRITION
It is a group of body depletion disorders which
include kwashiorkor, marasmus and the
intermediate stages
• MARASMUS
Represents simple starvation . The body adapts
to a chronic state of insufficient caloric intake
• KWASHIORKOR
It is the body’s response to insufficient protein
intake but usually sufficient calories for energy

4. • MEALS ON WHEELS
• Medications
• Emotional problems
• Anorexia
• Late-life paranoia
• Swallowing disorders
• Oral problems
• Nosocomial infections
• Wandering/dementia related activity
• Hyperthyroid/Hypoadrenalism
• Enteric disorders
• Eating problems
• Low-salt/Stones
Etiology

5. • Amongst the Social, Economic, Biological and
Environmental Factors the common causes are:
 Lack of breast feeding and giving diluted formula
 Improper complementary feeding
 Over crowding in family
 Ignorance
 Illiteracy
 Lack of health education
 Poverty
 Infection
 Familial disharmony

6. • Role of Free Radicals & Aflatoxin: Two new
theories have been postulated recently to
explain the pathogenesis of kwashiorkor. These
include Free Radical Damage & Aflatoxin
Poisoning . These may damage liver cells giving
rise to kwashiorkor.
• Age Of Host :
 Frequent in Infants & young children whose
rapid growth increases nutritional requirement.
 PEM in pregnant and lactating women can
affect the growth, nutritional status & survival
rates of their fetuses, new born and infants.
 Elderly can also suffer from PEM due to
alteration of GI System

7. Leading cause of death (less than 5 years of
age)
Primary PEM:
Protein + energy intakes below requirement for normal growth.
Secondary PEM:
 the need for growth is greater than can be supplied.
 decreased nutrient absorption
 increase nutrient losses
Linear growth ceases
Static weight
Weight loss
Wasting
Malnutrition and its signs
AETIOLOGY of PEM:

8. The clinical presentation depends upon the
type , severity and duration of the dietary
deficiencies. The five forms of PEM are :
1. Kwashiorkor
2. Marasmic-kwashiorkor
3. Marasmus
4. Nutritional dwarfing
5. Underweight child

9. Body weight
as percentage
of standard
Oedema Deficit in
weight for
height
Kwashiorkor 60 – 80 + +
Marasmic
kwashiorkor
< 60 + ++
Marasmus < 60 0 ++
Nutritional
dwarfing
< 60 0 Minimal
Underweight
child
60 – 80 0 +
Classification of PEM (FAO/WHO)

10. KWASHIORKOR
• The term kwashiorkor is taken from the Ga language of
Ghana and means "the sickness of the weaning”.
• Williams first used the term in 1933, and it refers to an
inadequate protein intake with reasonable caloric (energy)
intake.
• Kwashiorkor, also called wet protein-energy malnutrition, is a
form of PEM characterized primarily by protein deficiency.
• This condition usually appears at the age of about 12 months
when breastfeeding is discontinued, but it can develop at
any time during a child's formative years.
• It causes fluid retention (edema); dry, peeling skin; and hair
discoloration.

11. • Kwashiorkor was thought to be caused by
insufficient protein consumption but with
sufficient calorie intake, distinguishing it
from marasmus.
• More recently, micronutrient and
antioxidant deficiencies have come to be
recognized as contributory.
• Victims of kwashiorkor fail to
produce antibodies following vaccination against
diseases, including diphtheria and typhoid.
• Generally, the disease can be treated by
adding food energy and protein to the diet;
however, it can have a long-term impact on a
child's physical and mental development, and in
severe cases may lead to death.

12. SYMPTOMS
• Changes in skin pigment.
• Decreased muscle mass
• Diarrhea
• Failure to gain weight and grow
• Fatigue
• Hair changes (change in color or
texture)
• Increased and more severe
infections due to damaged
immune system
• Irritability
• Large belly that sticks out
(protrudes)
• Lethargy or apathy
• Loss of muscle mass
• Rash (dermatitis)
• Shock (late stage)
• Swelling (edema)

13. St.Ann's Degree College for Women

14. MARASMUS
• The term marasmus is derived from the Greek
word marasmos, which means withering or wasting.
• Marasmus is a form of severe protein-energy
malnutrition characterized by energy deficiency and
emaciation.
• Primarily caused by energy deficiency, marasmus is
characterized by stunted growth and wasting of muscle
and tissue.
• Marasmus usually develops between the ages of six
months and one year in children who have been
weaned from breast milk or who suffer from
weakening conditions like chronic diarrhea.

15. SYMPTOMS
• Severe growth retardation
• Loss of subcutaneous fat
• Severe muscle wasting
• The child looks appallingly thin and
limbs appear as skin and bone
• Shriveled body
• Wrinkled skin
• Bony prominence
• Associated vitamin deficiencies
• Failure to thrive
• Irritability, fretfulness and apathy
• Frequent watery diarrhoea and acid
stools
• Mostly hungry but some are anoretic
• Dehydration
• Temperature is subnormal
• Muscles are weak
• Oedema and fatty infiltration are
absent

16. St.Ann's Degree College for Women

17. CLINICAL
FEATURES
-MUSCLE
WASTING
-FAT WASTING
-EDEMA
-WEIGHT FOR HEIGHT
-MENTAL CHANGES
MARASMUS
Obvious
Severe loss of
subcutaneous fat
None
Very low
Sometimes quite and
apathetic
KWASHIORKOR
Sometimes
hidden by edema and
fat
Fat often retained but
not firm
Present in lower legs,
and usually in face and
lower arms
May be masked by
edema
Irritable, moaning,
apathetic
DIFFERENCE IN CLINICAL FEATURES BETWEEN MARASMUS AND KWASHIORKOR

18. CLINICAL FEATURES
-APPETITE
-DIARRHOEA
-SKIN CHANGES
-HAIR CHANGES
-HEPATIC ENLARGEMENT
MARASMUS
Usually good
Often
Usually none
Seldom
None
KWASHIORKOR
Poor
Often
Diffuse pigmentation,
sometimes ‘flaky paint
dermatitis’
Sparse, silky, easily
pulled out
Sometimes due to
accumulation of fat
DIFFERENCE IN CLINICAL FEATURES BETWEEN MARASMUS AND KWASHIORKOR

19. A severely malnourished child
with features of both
marasmus and Kwashiorkor.
• The features of
Kwashiorkor are severe
oedema of feet and legs
and also hands, lower
arms, abdomen and face.
Also there is pale skin and
hair, and the child is
unhappy.
• There are also signs of
marasmus, wasting of the
muscles of the upper arms,
shoulders and chest so that
you can see the ribs.
MARASMIC-KWASHIORKOR

20. • Some children adapt to prolonged
insufficiency of food-energy and protein by a
marked retardation of growth.
• Weight and height are both reduced and in
the same proportion, so they appear
superficially normal.
NUTRITIONAL DWARFING OR
STUNTING

21. • Children with sub-
clinical PEM can be
detected by their
weight for age or
weight for height,
which are significantly
below normal. They
may have reduced
plasma albumin. They
are at risk for
respiratory and gastric
infections
UNDERWEIGHT CHILD

22. Assessment of Nutrition Status
–Clinical
–Anthropometric
–Dietary
–Laboratory

23. Investigations for PEM
• Full blood counts, inflammatory markers;
• Blood glucose profile, lipidic profile
• Iron, vitamin levels;
• Microbiology: septic screening,stool & urine for parasites &
germs;
• Electrolytes, Ca, Ph & Mg;
• Serum proteins, protein electrophoresis;
• immunological status: cellular immunity - decreased T cell,
interferon, IDR lack of response to tuberculin; humoral
immunity - low IgA (secretory IgA), IgM - high, low IgG.
• Decrease complement C3;
• Exclude HIV & malabsorption.

24. Investigations for PEM
In essence:
• decrease serum albumins → edema;
• decrease apoproteins (lipoproteins carrier);
• storage of fat in the liver (fatty infiltration);
Clinical outcomes: oedema, hepatomegaly
(fatty liver), changes in hair growth and skin
(areas of hypo-or hyperpigmentation, fissures),
diarrhea (villous atrophy), predisposition to
infection (humoral and cellular immunity
disturbed).

25. Anthropometric assessment of
malnutrition
anthropometric criteria :
 percentiles method (normal 10-90).
 standard derivations method (normal + / - 2 SD).
 ponderal index (PI)
PI = actual weight of the child / ideal weight (W of child of
the same age located on the 50th percentile of the growth
curve).
After the PI values ​​: 3 degrees of PEM(Gomez)
 degree I (PI = 0.89 to 0.76);
 degree II (PI = 0.75 to 0.60);
 degree III ( PI = 0.60).
PI = 0.90- underweight or child at risk of malnutrition.

26. Anthropometric assessment of
malnutrition
The protein malnutrition are two degrees:
 degree I PI = 0.8-0.6 - KWASHIORKOR;
 degree II PI= 0.6 – MARASMIC KWASHIORKOR
Nutritional index (NI) - index diets.
• NI = actual weight / weight appropriate waist.
After this indicator there are 3 degrees of malnutrition:
• grade I (NI= 0.89 to 0.81);
• grade II (NI= 0.80 to 0.71);
• grade III (NI= 0.70).
Head circumference (HC) - highlights the true growth in the first two years.
Midarm circumference (measured at the ½ distance between the acromion
and olecranon) pathological - under 13 cm - available in children over 2
years.

27. Assessment of malnutrition- functional criteria
Appreciation of the digestive tolerance:
• paradoxical reaction to hunger (disproportionate
weight loss);
• food paradoxical reaction (weight loss to increased
food intake, sometimes diarrhea);
• sensitivity to fasts - by spacing meals: hypoglycaemia,
especially nocturnal → apnea, sudden death.
• immunological reactivity :
- increased responsiveness to infection;
- reactivity collapsed (serious infection without fever,
leukocytosis, sometimes opportunistic).

28. Assessment of malnutrition
Neuropsychological development:
• Archaic reflexes;
• Muscle tone;
• Posture;
• Mobility;
• Development of language;
• Affection.
They are affected differently depending on the
severity of malnutrition .

29. • Significant findings in kwashiorkor include
hypoalbuminemia (10-25 g/L), hypoproteinemia
(transferrin, essential amino acids, lipoprotein), and
hypoglycemia.
• Plasma cortisol and growth hormone levels are high, but
insulin secretion and insulinlike growth factor levels are
decreased.
• The percentage of body water and extracellular water is
increased.
• Electrolytes, especially potassium and magnesium, are
depleted.
• Levels of some enzymes (including lactase) are decreased,
and circulating lipid levels (especially cholesterol) are low.
•
BIOCHEMICAL & METABOLIC CHANGES

30. • Ketonuria occurs, and protein-energy
malnutrition may cause a decrease in the
urinary excretion of urea because of
decreased protein intake.
• In both kwashiorkor and marasmus, iron
deficiency anemia and metabolic acidosis are
present.
• Urinary excretion of hydroxyproline is
diminished, reflecting impaired growth and
wound healing.

31. OT ROLE IN Malnutrition
• Occupational therapy offers patients goal-
directed activity to increase their functional
mobility and self-care abilities.
• Psychological problems may emerge during
hospitalization; pain, fear, and change in medical
status will influence motivation and activity
tolerance. Patients may attempt to avoid activity
because they are generally deconditioned from
prolonged illness and bedrest

32. • A program of individualized activity should be
instituted if nutritional intake is used
appropriately, and it should result in increased
strength and endurance.
• Physical activity or exercise enhances the
synthesis of protein into skeletal muscle.
Because the body does not store protein,
unused calories are stored only as fat or, to a
lesser extent, carbohydrates.

33. Treatment strategy can be divided into three
stages.
• Resolving life threatening conditions
• Restoring nutritional status
• Ensuring nutritional rehabilitation.
TREATMENT

34. 3 stages of TX
There are three stages of treatment.
1. Hospital Treatment
The following conditions should be corrected. Hypothermia,
hypoglycemia, infection, dehydration, electrolyte imbalance, anaemia
and other vitamin and mineral deficiencies.
2. Dietary Management
The diet should be from locally available staple foods - inexpensive,
easily digestible, evenly distributed throughout the day and increased
number of feedings to increase the quantity of food.
3. Rehabilitation
The concept of nutritional rehabilitation is based on practical
nutritional training for mothers in which they learn by feeding their
children back to health under supervision and using local foods.

35. TREATMENT
General principles:
The recovery of PEM (II and III degree) :
I. The initial phase
•Correction of water & electrolyte imbalance;
• Treatment of infectious complications.
II. Repair phase
• Dietary therapy;
• Correction of deficiencies (anemia, rickets, hypovitaminosis, etc).
III. Convalescence phase
• Restoration of body composition;
• Enhancing healing.
Optimal objective is to resume growth after 2-3 weeks of starting the
diet and clinical recovery in 6-8 weeks.

36. TREATMENT
I)Parenteral nutrition for 2-3 days → enteral nutrition with
flow probe using hyperproteic and hypercaloric solutions ;
II) Early initiation of oral nutrition :
– hypoallergenic preparations rich in proteins and calories, low
osmolarity: Alfare, PeptiJunior, Pregestimil, Nutramigen,
Pregomin or amino acid formulas, such as Neocate .
– Keep in parallel parenteral intake of carbohydrates, amino
acids, lipids.
– Simultaneously treating infections, hypoproteinemia, anemia,
multivitamins deficiencies .
– This variant is also little used because it requires specials
dietetics and carefully monitorization of nutritional therapy .

37. TREATMENT
III) after fluid replacement and electrolyte - digestive tolerance :
- with carrot soup or rice mucilage (in various concentrations ) in a dose of
150-200 ml / kg ( not exceeding 1000 ml / day)
- carbohydrates were obtained from glucose 5%, 7 %, 10 % and chicken
mixed proteins ( hypoallergenic, 100g , 17g protein).
- after normalization of the stools ( 7 days) :oil gradually (3-4 ml / day ) and
after 10 days from the beginning of enteral diet →hypoallergenic
preparation can be inserted (!preparations lactose free- can induce cow's
milk protein intolerance ) .
- week 4 :sugar (restoring lactose tolerance is difficult , 3-4 months);
- flour products containing gluten will not enter until full recovery;
- increases in protein - calorie intake by parenteral administration of
carbohydrates , amino acids and proteins;
- treat the infection , iron or vitamin deficiencies .

38. Education
•Patient
•Family
•Community
•WHO

39. • Promotion of breast feeding
• Development of low cost weaning
• Nutrition education and promotion of
correct feeding practices
• Family planning and spacing of births
• Immunization
• Food fortification
• Early diagnosis and treatment
PREVENTION

40. • Hypoglycemia
• Hypothermia
• Hypokalemia
• Hyponatremia
• Heart failure
• Dehydration & shock
• Infections (bacterial, viral & thrush)
Complications