nursing

1. by Racquel Burrowes-Blackwood

2. • 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.

3. • Identify treatment steps for PEM.
• Formulate nursing care plan for
malnourished infants.

4. DEFINITION
MALNUTRITION
• The World Health Organization (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."

5. What is Malnutrition?
• Malnutrition is a broad term refers to
under nutrition and over nutrition .
• People are malnourished if their diet
doesn’t provide adequate calories protein
for growth and maintenance or they are
unable to fully utilize the food they eat due
to illness (under nutrition).
• They are also malnourished if they
consume too many calories (over
nutrition). (UNICEF)

6. • " 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 associated
with infection

7. • 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

8. Anthropometric Measurement
• Underweight
– Measurements that fall below 2 standard
deviations under the normal weight for age.
• Stunting
– Measurements that fall below 2 standard
deviations below height for age.
• Wasting
– Measurements that fall below 2 standard
deviations below weight for height.

11. Protein Energy malnutrition
(Clinical diagnosis)
OK135 S056

12. Micronutrient deficiencies
• Iron: fatigue, anemia, decreased cognitive function,
glossitis and nail changes
• Iodine: Goiter, developmental delay, and MR
• Vitamin D: poor growth, rickets, and hypocalcemia
• Vitamin A: night blindness, xerophthalmia, poor growth,
and hair changes
• Folate: Glossitis, anemia

13. Clinical forms of PEM
• Marasmus: Severe weight loss or wasting
• Marasmic kwashiorkor: A combination of
both severe wasting and bi-lateral oedema.
• Kwashiorkor: Malnutrition with edema
[bloated appearance due to water
retention (bi-lateral oedema)]
• A rapid deterioration in nutritional status in
a short time can lead to marasmus, one
form of acute malnutrition.

14. Causes of PEM
• Early weaning
• Delayed introduction of complementary
food
• Low protein diet
• Severe or frequent infections.
Usually manifest between 6 months and 2
years of age

15. Direct and indirect causes of
malnutrition
Malnutrition
Marasmus, kwashiorkor
Micronutrient deficiency
Severe or
Frequent infections
diarrhea
Insufficient supply
Of protein, energy
Or micronutrients
Ill health
Unhealthy
enviournment
Insufficient
Child and
Maternal care
Insufficient
Household
Food security
War
Natural disaster
Civil disorder
Low status and
Little education
Of women
Poverty

16. Nutritional assessment
• Medical and dietary history
• Anthropometric evaluation and physical
examination
• Laboratory measurements

17. Medical and dietary history
• Medical history
– review of acute and chronic illnesses
– history of preexisting nutrient deficiencies
– social history (poverty, domestic violence, parental
employment, parental marital status, and parental substance
abuse)
• Dietary history
– quantity and quality of current intake
– in infants
• history of breast feeding pattern
• formula preparation
• volume consumed
• feeding techniques

18. • Marasmus is the most common form of
acute malnutrition in nutritional
emergencies and, in its severe form, can
very quickly lead to death if untreated.
• It is characterized by severe wasting of
fat and muscle which the body breaks
down to make energy. Occurs chiefly in
children between the 6 and 18 month old.
• Wasting can affect both children and
adults.

19. The child at risk for:
• Hypoglycemia
• Hypothermia
• Fluid overload/ heart failure
• Infection
• A wasted child can be classified as either
moderately or severely acutely malnourished
based on body measurements.

20. 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/ stunting.
5- finally, weight loss.

21. Etiology of Maramus
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 infant from taking an
adequate diet.
3. Diseases, which interfere with the
assimilation of food e.g. cystic fibrosis.

22. Etiology of Maramus
4. Infections, which produce anorexia.
5. Loss of food through vomiting and
diarrhea.
6. Emotional problems e.g. disturbed mother
child relationship.

23. Marasmus: Typical Findings
History
• decreased caloric intake over months to years
physical examination
– impression: cachectic, severely ill, “little old man”
irritable, apathetic, hungry
– underweight, growth retardation
– hair sparse, brittle, easily pulled out
– Corneal opacity

24. Marasmus: Typical Findings cont.d
– Poor skin turgor
– nails fragile , thin and fissured
– loss of subcutaneous tissue
– muscle wasting
– abdominal distension (muscular hypotonia)
– Rectal prolapse (loss of perianal fat)
– vital signs: hypothermia, hypotension, bradycardia
Anthropometry:
wasting or stunting, weight for height or height for age is
less than 65% of the mean average

25. 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.
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.

26. 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 old man.
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.

27. 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.
5. Chronic diarrhea with or without
vomiting.

28. 6. Intercurrent infections:Like otitis media,
bronchopneumonia, urinary tract infections.
7. Associated deficiencies of iron, vitaminA
and D.
8. Hypothermia due to loss of subcutaneous
fat.

30. 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.

31. • 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

32. • characterized by edema, irritability,
anorexia, ulcerating dermatoses, and an
enlarged liver with fatty infiltrates.
• The presence of edema caused by poor
nutrition defines kwashiorkor

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

34. • 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
• socio - economic status such as:
Poverty, ignorance.
• Inadequate weaning practice, lack of
basic health education and nutritional
knowledge and child abuse

35. 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.

36. 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.

37. Kwashiorkor: Typical Findings
History
– decreased calorie intake over weeks to months
Physical Examination
– may look well nourished, even “fat”, apathetic,
irritable, anorexic
– moon facies, pitting edema
– overall fatness
– thin upper arm

38. Kwashiorkor: Typical Findings cont.d
– flaking paint rash, pellagrous lesions, fissures,
ulcerations
– mucosal thinnes, mild anemia
– lifeless, thin, pale, weak, or dry hair
– fragile and thin nails
– Hepatomegaly (steatosis)
– Vital signs: hypothermia, hypotension
• Anthropometry
– usually underweight; occasional fat
appearance

39. Kwashiorkor: Typical Findings cont.d

41. • The clinical assessment of kwashiorkor
is divided into 3 groups:
• Constant manifestation.
• Usual manifestations.
• Occasional manifestations

42. Clinical manifestation 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

43. 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.

44. • 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.

45. • 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.

46. • 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.

47. 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.
• Hair is also atrophic, having lost its curl
and tapered nearer to the scalp (like an
exclamation mark).

48. 2- Gastro-intestinal Manifestations: Anorexia
sometimes associated with vomiting,
especially in severe cases.
• 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.

49. Usual Manifestations
- Malabsorption of nitrogen, fat,
carbohydrates and minerals due to the
atrophy of villi.
• 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

50. 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
2. Hepatomegaly:
• 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 hepatomegaly.

51. 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.

52. • 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)

54. 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.

55. 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

56. • Promotion of exclusive breast feeding
for the first 6 months of the baby’s life
• 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

58. Assessment of Severely
Malnourished Child
• Dehydration
• Infection
• Intake of food & drinks & degree of anorexia
• Blood glucose
• Hemoglobin or hematocrit
• Urine examination
• Stool examination for giardia
• CXR & PPD if TB is suspected.

59. General principle of treatment
Monitor & treat
Hypoglycemia
Hypothermia
Dehydration
Infection
Specific treatment for all children
Electrolytes
Micronutrients
Sensory stimulation
Initial feeding
Feeding to achieve catch-up growth

60. Stabilization or Acute Phase
• Correction of shock & dehydration
– i.v if shocked
– ORS (low osmolarity with extra potassium)
• Life threatening complications:
– Hypoglycemia (<54 mg/dl)
– Hypothermia (<350 c). Keep the child well
clothed, with the head covered, in a warm
enviourment
– Two hourly feeding (day & night)
• Treatment of infections
• Electrolytes imbalance: K+, mg++

61. Stabilization or Acute Phase
• Micronutrient deficiencies
– Vit A & Zinc (impair immune function & have direct
effect on the structure & function of the mucosa.
– Iron
– Folic acid
– Copper (neutropenia, bone abnormalities,
microcytic anemia)
– Selenium ) impaired cardiac function)
• Dietary treatment
– Feeding should be started as soon as possible
– Diet should have low osmolarity and low lactose
– The child should be fed every two hours-or every
three hours

62. Rehabilitation phase
• The return of appetite heralds the
rehabilitation phase and usually occurs a
week after treatment is started.
• The goal is to achieve weight gain
>10g/kg/day until the patient is fully
recovered.
• Increase in energy & proetein intake
should be gradual to avoid cardiac failure.
• A child is considered to have recovered on
reaching a weight foe height that is 90% of
the Median.

63. 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.

64. Nursing Management: (PEM Infants)
1. 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.
• Feed the infant orally, either by breast, cup
and spoon. If it is impossible feed him
through nasogastric tube (gavage feeding).

65. • Introduce a positive feeding environment.
Give feeding slowly as the child is
irritable.
• Avoid interruption of feeding with other
activities, such as laboratory tests or
radiography.
• Weight daily and record to ascertain
weight gain.

66. • Place the infant in a warm humidified
incubator, radiant warmer or warmly
clothed in open crib.
• Avoid situations that might predispose
infant to heat loss, such as, exposure to
cool drafts, bathing or cold scales.
• Monitor temperature hourly in unstable
infants.
• Check infant's temperature in relation of
the heating unit.

67. Nursing Management: (PEM Infants)
• Use hot water bottles, dress infant with
extra- clothes. these provide additional
warmth due little or no subcuteous fat,
the patient is at great risk for
hypothermia.
• Observe for signs of collapse
(temperature drop, coldness of
extremities, slow pulse, cyanosis or
gray white color of skin.)

68. • 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.
• Feeding equipments must be sterile to avoid
danger of contracting thrush.

69. Marasmus is severe malnutrition
characterized by energy deficiency.
Kwashiorkor is a protein deficiency
disorder with adequate energy intake,
whereas Marasmus is inadequate energy
intake including proteins.

71. References
• Campbell,V., & Sinha, D.(1997).
Nutrition made simple. CFNI.
• Dudek, S. (1993). Nutrition handbook
for nursing practice. Philadelphia: J. B.
Lippincott Company.
• Jackson, D. & Saunders, R. (1993).
Child health nursing. Philadelphia:
Lippincott.
• Martin, E. (2003). Oxford dictionary of
nursing. Oxford: Oxford University
Press.

72. GOD BLESS YOU