This document discusses protein-energy malnutrition (PEM) in infants and children. It defines malnutrition and the specific forms of PEM, including marasmus and kwashiorkor. For kwashiorkor, it covers the pathophysiology, etiology, clinical signs and symptoms, laboratory findings, and complications. For marasmus it discusses the definition, etiology, clinical assessment, and differences from kwashiorkor. The document also outlines the WHO's 10 steps for recovery from malnutrition and provides a nursing care plan to address malnutrition through dietary interventions and maintaining appropriate body temperature.

1. MALNUTRITION (PEM)
Marasmus/
Kwashiorkor
Najah Kh. Qasem
Qassim University
1

2. OBJECTIVES
 Define the definition of malnutrition,kwashiorkor, and
marasmus.
 Discuss pathphysiology of Kwashiorkor.
 List etiology factors for kwashiorkor, and marasmus.
 Explain assessment findings, laboratory findings in
kwashiorkor, and marasmus.
 Identify the complications of PEM.
 Identify treatment steps for PEM.
 Formulate nursing care plan for malnourished infants.
2

3. OVERVIEW OF PEM
 The term protein - energy malnutrition
has been adopted by WHO in 1976.
 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.
3

4. OVERVIEW OF PEM
" The term protein-energy
malnutrition (PEM) applies to a
group of related disorders. that
include marasmus, kwashiorkor, and
intermediate states of marasmus-
kwashiorkor.
• occurring most frequently in infants
and young children and commonly
4 associated with infection

5. OVERVIEW OF PEM
 Although several factors may
contribute to the production of PEM,
the basic problem is usually a lack of
food intake. Sometimes, there may be
poor absorption of one or more of food
components. Other time, the cause is
lack of parental education regarding
infants and children's nutrition
5

6. Mortality / Morbidity
 In 2000 WHO estimated that 32% of <5
years old children in developing countries
are underweight (182 million).
 Around 150 million children younger than
5 years are malnourished when measured
in terms of weight for age.
 The reciprocal interaction between PEM &
infection is the major cause of death &
morbidity in young children.
6

7. Cont..
 In south central Asia and
eastern Africa, about half the children have
growth retardation due to protein-energy
malnutrition. This figure is 5 times the
prevalence in the western world.
 Approximately 50% of the 10 million
deaths each year in developing countries
occur because of malnutrition in children
< than 5 years.
7

8. 8

9. Kwashiorkor - Definition
It is an acute form of childhood protein-energy
malnutrition characterized by inadequate
protein intake with reasonable caloric (energy)
intake; it tends to occur after weaning, when
children change from breast milk to a diet
consisting mainly of carbohydrates.
Studies suggest that kwashiorkor represents a
maladaptive response to starvation
9

10. Cont..
 characterized by edema, irritability, anorexia,
ulcerating dermatoses, and an enlarged liver
with fatty infiltrates.
 The presence of edema caused by poor
nutrition defines kwashiorkor
 The term Kwashiorkor is taken from the Ga
language of Ghana & means “the sickness of
the weaning” .
10

11. Pathophysiology_ Kwashiorkor.
 Decreased protein intake decreased
synthesis of visceral proteins.
 Decreased visceral protein hypo-
albuminemia contributes to
extravascular fluid accumulation.
 Impaired synthesis of B-lipoprotein
produced a fatty liver.
11

12. Etiology:
 Dietary Inadequacy:
occurs when there is a rapid period of transition
from the balanced diet supplied by the breast
milk to an unbalanced inadequate diet, which
is very low in protein, and consists mainly of
carbohydrates due to socio - economic
status such as:
12

13. Cont..
 Poverty
 Ignorance
 Inadequate weaning practice
 Lack of basic health education and nutritional
knowledge.
 Child abuse
13

14. Precipitating Factor:
i) Acute infections like acute infantile diarrhea and
measles due to:
 Catabolic effect of the infections.
 Anorexia, which usually accompanies infections.
 The bad habit of withholding food during measles and
diarrhea up to the degree of starvation.
ii) Malaria and severe parasitic infestations may play a
role in the development of kwashiorkor in some region
of the world.
14

15. Cont..
iii) Studies suggest that aflatoxin poisoning is an
important factor in the development of kwashiorkor.
 Aflatoxins are produced by molds and ingested with
moldy foods.
 Aflatoxins damage liver DNA.
15

16. Assessment (signs & symptoms)
The clinical assessment of
kwashiorkor is divided into 3 groups:
 Constant manifestation.
 Usual manifestations.
 Occasional manifestations
16

17. Clinical Manifistation
 Clinical manifistation is affected by:
• The degree of deficiency
• The duration of deficiency
• The speed of onset
• The age at onset
• Presence of conditioning factors
• Genetic factors
17

18. Constant Manifestations
1. Growth retardation: this is reflected by:
 Weight is markedly diminished.
 Retarded linear growth (length).
 Head circumference may also be affected.
 Bone age may be retarded.
18

19. Constant Manifestations
2. Edema:
 The main factor is hypoproteinemia. It starts
in the feet and lower parts of the legs then
becomes-generalized. It is usually soft and
pitting, affecting more the dependent parts
(back and dorsum of hands and feet). The
cheeks become bulky, pale and waxy in
appearance (doll-like cheecks). Ascites is
unusual.
19

20. Constant Manifestations
3. Disturbed muscle/ fat ratio
(Muscle wasting)
There is a generalized muscle wasting with
preservation of some subcutaneous fat. This
can be demonstrated clinically by measuring
the mid-arm circumference which is
diminished in these cases. The children are
often weak, hypotonic and unable to stand
and walk.
20

21. Constant Manifestations
4. Psychomotor changes:
Infants with kwashiorkor have marked apathy;
misery and they lack interest in the
surrounding. They don't move, look sad and
never smile. Their cry is weak.
21

22. Usual Manifestations
1 Hair Changes;
 Hair is a spates, especially over the temples and
occipital regions.
 There is depigmetation of hair. The hair loses its
black color and becomes reddish or grayish.
Deficiency of pantothenic acid and sulfur containing
amino- acids in the hair or a defect in the melanin
formation may be responsible for such
depigmentation.
22

23. Usual Manifestations
 Hair is also atrophic, having lost its curl and
tapered nearer to the scalp (like an
exclamation mark).
2- Gastro-intestinal Manifestations:
 Anorexia sometimes associated with
vomiting, especially in severe cases.
23

24. Usual Manifestations
 Diarrhea is common and can be due to:
- infection with intestinal pathogens or parasites.
- Reduction of intestinal and pancreatic enzymes
(e.g., amylase, lipase) as a result of protein
deficiency. This will lead to inadequate digestion
of food and passage of loose stools as a
consequence.
- Malabsorption of nitrogen, fat, carbohydrates
and minerals due to the atrophy of villi.
24

25. Occasional Manifestations
1.Skin Changes:
Dermatosis:
 The rash appears mainly in areas of increased
pigmentation. These pigmented areas
subsequently desquamate leaving atrophic,
hypopigmented and easily damage skin or
even ulcerations.
25

26. Occasional Manifestations
1.Skin Changes:
 The characteristic rash is usually seen on the
back of thighs and axillae; though other parts
of the body may be affected.
* Sometimes petechiae may be present,
particularly over the abdomen.
26

27. Occasional Manifestations
2. Hepatomegly:
 It is caused by fatty infiltration of the liver,
which is a constant pathological finding in
kwashiorkor that may or may not be
accompanied by hepatomegty.
27

28. Occasional Manifestations
3. Anemia: due to:
 Deficiency of protein, iron, zinc, copper, folic
acid and vitamins A, B, E and or C.
 Infections may be responsible by disturbing
the iron metabolism.
4. Poor resistance and liability to
infections.
28

29. Occasional Manifestations
5. Associated deficiencies of several types
of nutrients
(Riboflavin, Niacin, Thiamin, Vitamin D and C
deficiencies) and minerals as iron, copper,
zinc, and magnesium, particularly those
involved with anti-oxidant protection
(glutathione, albumin, vitamin E,
and polyunsaturated fatty acids)
29

30. Laboratory Findings:
1.Reduced total plasma protein (less than 4
gm/dl).
2.Reduced level of serum albumin (less than 2
gm/dl).
3. Urea in blood and urine is markedly reduced
because of deficient intake of exogenous
protein.
30

31. Laboratory Findings:
4. Total body sodium is higher than normal.
Serum sodium may be low due to the
excessive amount of water extracellular fluid
compartment.
5. Low total body potassium due to potassium
losses by diarrhea
31

32. Marasmus - Definition
Marasmus is a form of severe PEM occur as result from a
negative energy balance that may occur at any age,
particularly in early infancy and is characterized by:
 Severe wasting (body weight is less than 60% of the
expected), the body utilizes all fat stores before using
muscles.
 Loss of subcutaneous fat.
 Gross muscle wasting.
 Absence of edema.
“marasmus” comes from Greek origin of word “to waste”
32

33. Cont..
 Studies suggest that Marasmus represents
an adaptive response to starvation
 Children adapt to an energy deficiency with:
1- a decrease in physical activity.
2- lethargy.
3- a decrease in basal energy metabolism.
4- slowing of growth.
5- finally, weight loss.
33

34. Etiology:
The specific cause
may be:
1. Poor feeding habits due to improper training.
lack of breast feeding and the use of dilute
animal milk.
2. A physical defect e.g. cleft lip or cleft palate
or cardiac abnormalities, which prevent the
34 infant from taking an adequate diet.

35. Etiology:
3. Diseases, which interfere with the
assimilation of food e.g. cystic fibrosis.
4. Infections, which produce anorexia.
5. Loss of food through vomiting and diarrhea.
6. Emotional problems e.g. disturbed mother-
child relationship.
35

36. Assessment (S&S)
 Beside the history taking,
emphasizing the actual foods
taken by the child,
the presence of any of the
following manifestations
should be assessed:
36

37. Assessment (S&S)
1. Growth retardation:
 Weight is less than 60% of expected for age
and sex.
 Length, head, chest, and abdominal
circumferences are also affected but to a
lesser extent than weight.
37

38. Assessment (S&S)
2. Loss of Subcutaneous Fat from:
 The abdominal wall leading to loss of skin elasticity
 The limbs (thighs and buttocks): the skin becomes
wrinkled and hanging into longitudinal folds.
 The buccinators pad of fat is the last to disappear.
This leads to hollowing these cheeks, which leads
to triangle face and an appearance resembling the
38
old man.

39. Assessment (S&S)
3. Marked Wasting of Muscles:
This together with the loss of subcutaneous fat
lead to
 Scaphoid abdomen with marked thinning of
abdominal wall.
 Stick -like appearance of limbs.
39

40. Assessment (S&S)
4. Psychic Changes:
 Marasmic infants look anxious, irritable,
excessively cry and sleep little. However, they
look less miserable than the cases of
kwashiorkor.
 Marasmic infants are usually hungry and have
good appetite. Sometimes, there is anorexia
and poor feeding.
40

41. Assessment (S&S)
5. Chronic diarrhea with or without vomiting.
6. Intercurrent infections:
Like otitis media, bronchopneumonia, urinary
tract infections.
7. Associated deficiencies of iron, vitamin A
and D.
8. Hypothermia due to loss of subcutaneous
fat.
41

42. Characteristically cases of Marasmus
 No edema.
 No dermatosis.
 No hair changes.
 No fatty infiltration of the liver (hepatomegly).
42

43. Laboratory Findings:
1. Plasma protein may be normal or slightly
lowered. This is because marasmic infants
live on their own muscle protein.
2. Blood urea is low since the protein utilized
by the infant is totally endogenous protein.
3. Blood glucose level is low due to deficient
glycogen stores in the liver,
43

44. Complications of PEM:
1. Diarrhea, dehydration, electrolyte and acid
base disturbances.
2. Infections, such as, bronchopneumonia, T.B,
urinary tract infection.
3. Hypoglycemia.
4. Hypothermia.
5. Early prolonged malnutrition may lead to
mental retardation.
44

45. The WHO’s Ten Steps to Recovery
in Malnourished Children
45

46. Nursing Care Plan: (PEM Infants)
1. Nursing diagnosis:
 Altered nutrition: less than body
requirements related to knowledge deficit,
physical defect, infection, disease interferes
with the assimilation of food or emotional
problems.
Goal:
 The patient will gain weight.
46

47. Nursing Care Plan: (PEM Infants)
Intervention:
 Give high quality protein and adequate
carbohydrates in form of milk formula (first
skimmed milk then later whole milk). Give
the infant breast feeding if still on breast.
 Start with liquid food, then semi-solid other
chewable food as eggs, beans and meat.
47

48. Nursing Care Plan: (PEM Infants)
Intervention:
 Feed the infant orally, either by breast, bottle
or spoon. If it is impossible feed him through
nasogastric tube (gavage feeding).
 Give feeding slowly as the child is irritable.
 Introduce a positive feeding environment.
Avoid interruption of feeding with other
activities, such as, laboratory tests or
48
radiography.

49. Nursing Care Plan: (PEM Infants)
Intervention:
 Weight daily and record to ascertain weight
gain.
Expected Outcome:
 Infant exhibits weight gain appropriate to his
age.
49

50. Nursing Care Plan: (PEM Infants)
2. Nursing diagnosis:
Body temperature alteration (hypothermia)
related to diminished food intake.
Goal:
The infant will maintain suitable body
temperature.
50

51. Nursing Care Plan: (PEM Infants)
Intervention:
 Place the infant in a warm humidified
incubator, radiant warmer or warmly clothed
in open crib.
 Use hot water bottles.
 Dress infant with extra- clothes.
 Monitor temperature hourly in unstable
infants.
51

52. Nursing Care Plan: (PEM Infants)
Intervention:
 Avoid situations that might predispose infant
to heat loss, such as, exposure to cool drafts,
bathing or cold scales.
 Check infant's temperature in relation of the
heating unit.
 Observe for signs of collapse (temperature
drop, coldness of extremities, slow pulse,
52
cyanosis or gray white color of skin.)

53. Nursing Care Plan: (PEM Infants)
Expected Outcome:
 Infant's axillary temperature remains within
normal range (36.5- 37.2°C).
53

54. Nursing Care Plan: (PEM Infants)
3. Nursing diagnosis:
Skin integrity impaired related to deficiencies of
vitamins intake.
Goal:
Infant will maintain skin integrity.
54

55. Nursing Care Plan: (PEM Infants)
Intervention:
 Cleanse skin with clear water and apply oil if
needed.
 Care of buttocks if infant has diarrhea.
 Frequent change of infant's position to
prevent skin ulcer.
Expected Outcome:
 Skin remains clean and intact with no
55 evidence of irritation or injury.

56. Nursing Care Plan: (PEM Infants)
4. Nursing diagnosis:
High risk for infection related to low body
resistance.
Goal:
Infant will be protected from-infection,
Intervention:
 Feeding equipments must be sterile to avoid
danger of contracting thrush. Infant should
56 be kept out of draft.

57. 57