Malnutrition is a term referring to poor or

inadequate nutrition.
Although it is generally thought of in terms of
undernutrition, it includes overnutrition.
The most severe states of undernutrition involve
protein and caloric deficiencies, such as
kwashiorkor and marasmus. Overnutrition may
be manifested as obesity.
Hunger is one of the worlds gravest and most
prevalent health problem. Three- fourth of the
world population suffer from some form of
malnutrition.
This problem is more prevalent in under-
developed countries. Although several factors
may contribute to the production of deficiency
diseases, 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 childrens nutrition.
: Kwashiorkor is a deficiency of protein with an
adequate supply of calories.
: It is a syndrome that develops in the first child,
usually between 1 and 3 years of age, when he
is weaned from the breast once the second child
is born.
: The infant is put on a diet which consists mainly
of carbohydrates, beside the excessive demand
of all nutrients at that age of rapid growth,
especially protein of high biological value.

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.
This occurs usually during weaning and post
weaning periods. The poverty, ignorance and
lack of basic health education and nutritional
knowledge are important factors in this mistake.
Etiology:
Acute infections like acute infantile diarrhea
and measles can precipitate the appearance of
kwashiorkor or in borderline cases due to:
Catabolic effect of the infections.
Anorexia, which usually accompanies
infections.

Precipitating Factor:

The bad habit of withholding food
during measles and diarrhea up to
the degree of starvation.

Malaria and severe parasitic
infestations may play a role in the
development of kwashiorkor in some
region of the world.

Assessment criteria
Occasional
manifestations
Constant
(or cardinal)
manifestations
Usual
manifestations
I. Constant (or cardinal)
manifestations.
Weight is markedly diminished (to 60-80% of
what is expected for childs age).
Retarded linear growth (length).
Head circumference may also be affected.
This is reflected by:

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 cheecks become bulky, pale and waxy
in appearance (doll-like cheecks).
Ascites is unusual.

e There is a generalized muscle wasting with
preservation of some subcutaneous fat.
e This can be demonstrated clinically by
measuring the mid-arm circumference which
is diminished in these cases.
e The children are often weak, hypotonic and
unable to stand and walk.
Infants with kwashiorkor have marked
apathy; misery and they lack interest in
the surrounding.
They dont move, look sad and never
smile.
Their cry is weak.

II-Usual Manifestations.
Hair is a sparse, especially over the temples and
occipital regions.
There is dyspigmetation of hair (hypochromotrichia).
The hair loses its black color and becomes reddish or
grayish. The cause of this dyspigmentation is obscure.
Deficiency of pantothenic acid and sulfur containing
amino- acids in the hair or a defect in the melanin
formation may be responsible for such
dyspigmentation.
Hair is also atrophic, easily pickable, having lost its curl
and tapered nearer to the scalp (like an exclamation
mark).
Anorexia sometimes associated with
vomiting, especially in severe cases.
Diarrhea is common and can be due
to:
1. Infection with intestinal pathogens or
parasites.
2. Reduction of intestinal and pancreatic
enzymes (e.g., amylase, lipase, trypsin..)
as a result of protein deficiency. This will
lead to inadequate digestion of food and
passage of loose stools as a
consequence.
3. Malabsorption of nitrogen, fat,
carbohydrates and minerals due to the
atrophy of villi.

III-Occasional Manifestations.
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.
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

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 hepatomegly.
It is due to:
Deficiency of protein, iron, zinc, copper, folic
acid and vitamins A, B, E and or C.
Infections may be responsible also by disturbing
the iron metabolism.

Riboflavin, Niacin, Thiamin, Vitamin D and C
deficiencies) and minerals as iron, copper, zinc
and magnesium.
Reduced total plasma protein (less than 4
gm/dl).
Reduced level of serum albumin (less than
2 gm/dl).
Urea in blood and urine is markedly
reduced because of deficient intake of
exogenous protein.
Total body sodium is higher than normal.
Serum sodium may be low due to the
excessive amount of water extracelluar
fluid compartment.

Low total body potassium due to
potassium losses by diarrhea.

Marasmus is a form of severe PEM occur due to
intake of badly balanced diet 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).
Loss of subcutaneous fat.
Gross muscle wasting.
Absence of edema.
Poor feeding habits due to improper training.
A physical defect e.g. cleft lip or cleft palate or
cardiac abnormalities, which prevent the infant
from taking an adequate diet.
The specific cause may be:
Diseases, which interfere with the assimilation
of food e.g. cystic fibrosis.
Infections, which produce anorexia.
Loss of food through vomiting and diarrhea.
Emotional problems e.g. disturbed mother-
child relationship.

Beside the history taking, emphasizing the actual
foods taken by the child, the presence of any of
the following manifestations should be assessed:

Assessment criteria
1-Growth Failure:
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.
The buccinator pad of fat is the last to disappear
(probably due to different chemical composition of
its fat). This leads to hollowing these checks, 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
leads to:
Stick like appearance of limbs.
Scaphoid abdomen with marked thinning of
abdominal wall.
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.

4-Psychic Changes
O Chronic diarrhea with or without vomiting.
O Intercurrent infections:
Like otitis media, bronchopneumonia, urinary
tract infections are commonly present.

O Associated deficiencies of iron, vitamin A
and D.
O Hypothermia due to loss of subcutaneous
fat.
No hair changes.
No fatty infiltration
of the liver (hepatomegly).

No edema.
No dermatosis.

Characteristically cases of
Marasmus have
Laboratory findings:
Plasma protein may be normal or slightly
lowered. This is because marasmic infants live
on their own muscle protein.
Blood urea is low since the protein utilized by
the infant is totally endogenous protein.
Blood glucose level is low due to deficient
glycogen stores in the liver.
Diarrhea, dehydration, electrolyte and acid base
disturbances.
Infections, such as, thrush stomatitis,
bronchopneumonia, empyema, T.B, urinary tract
infection.
Hypoglycemia.
Hypothermia.
Early prolonged malnutrition may lead to mental
subnormality.
Complications of Protein-Energy
Malnutrition
The basic principle in the treatment is to
improve the childs nutritional status as soon
as possible:
Provide a diet high in quality protein and/or
carbohydrates.
Parental fluids and blood transfusions.
Vitamin (A, B, C, D and minerals
supplementation).
Treatment of complications infection,
diarrhea, parasitic infestation and anemia.

Therapeutic management of Protein-
Energy Malnutrition
Altered nutrition: less than body
requirements related to knowledge deficit,
physical defect, infection, disease
interferes with the assimilation of food or
emotional problems.
Body temperature alteration (hypothermia)
related to diminished food intake.
Skin integrity impaired related to
deficiencies of vitamins intake.

Nursing Care Plan: (PEM Infants)
High risk for infection related to low body
resistance
Fluid volume deficit related to diarrhea.
(Refer to G.I.T. lecture).

1-Nutrition Education:
The Ten recommendations (rules) to be taught, which are:

Prevention of Malnutrition
A child must start eating solid food
when he is about 4-5 months old.
Plain starchy pudding (rice pudding, mehalabia..etc)
is not enough
Plain starchy pudding (rice pudding,
mehalabia..etc) is not enough
Breast-feeding is the best
Breast milk must end slowly at 2 years
A good food is mixed food
Sick children need food.
Young children at risk of malnutrition need to
have well balanced diet and avoid prolonged
breast feeding
School children need 3 meals a day and
break down food taboos
Bottle-feeding should not be used except
if it is a necessity.
2. Immunization of children against measles and
whooping cough in particular as they are often
associated with PEM.
3. Teaching about family planning or child
spacing, to allow sufficient time for satisfactory
breast-feeding and childs care.
4. Early treatment of defects or associated
diseases.
5. Prevention of emotional disturbances.
It is a metabolic disorder of infancy and childhood
caused by vitamin D deficiency and affecting the
growing bones (defective mineralization, slow
growth), the skeletal muscles (hypotonia) and
sometimes the nervous system (tetany).
O It may occur if vitamin D intake is
inadequate.
O Lack of skin exposure to ultraviolet rays.

Vitamin D (the sunshine vitamin) is a fat-soluble
vitamin. It is the common name for a group of
steroids, the most important ones are:
D2 is formed by ultraviolet irradiation of ergosterol
in green plants.
D3 (cholecalciferol) is produced by the effect of
sunlight on sterol substances in the skin (i.e.
ultraviolet irradiation of 7-dehydrocholesterol).
Vitamin D2 and D3 are biologically inactive
forms. They are transported to the liver to
be hydroxylated (addition of hydroxyl
group OH) to 25 hydroxy- vitD.
Further hydroxylation takes place in the
renal tubules to 1.23 dihydroxy- vitD
(calcitriol). Which is the biologically active
form.
Promotes calcium (Ca) and phosphorus (P)
absorption in the small intestine.
Increase Ca and P reabsorption from the kidney.
It affects Ca and P reabsorption from old bones
and deposition in newly formed bone and teeth.
Food sources of vitamin D are limited; the richest
source is fish liver oils (e.g. cod liver oils) and
fish (e.g. herring, salmon, tuna or sardines).
Less efficient sources are milk, egg yolk and butter.
Exposure to ultraviolet light either directly from
the sun or from a lamp is an excellent source
since it converts provitamine D3 (inactive) to
cholecalciferol.
To produce enough vitamin D to meet the
children daily needs they must be exposed to
mid-day sun for about 15 minutes. So, the more
the sunrays are vertical, the more they are
effective for the natural formation of vitamin D
in adequate amounts. However, the
effectiveness of sunrays is minimal when:
The rays are oblique i.e. before or afternoon.
They pass through clouds, dust, smoke or
ordinary window glass because they prevent
ultra-violet rays from reaching the babys skin.
Also, adequate exposure of the skin is further
hampered by clothing and by the fact that
children spend much time indoors, especially
during the cold seasons.
The frequency of rickets in Arab Countries is
still high in spite of the knowledge of its etiology
and its response to treatment.
Heredity: Dark-skinned individuals absorb less
vitamin D through their skin because deeper
pigmentation prevents penetration of
ultraviolet light.
Age: It is rarely seen below 3 months, the
maximal incidence is between 3 to 18 months,
after the second year it get less frequent
because the child receives mixed diet, enough
sunshine and he is growing slowly.
Diet: It is more common in artificial fed babies
if they do not receive enriched formulas. A
breast fed infant is not likely to suffer from
rickets, provided that his mother is receiving
an adequate amount of sunshine or vitamin D.
Prematurity and twins: They are liable to be
affected because they are born with inadequate
calcium and phosphorus stores to
accommodate the rapid growth rate.
Season: The incidence is greater in late winter and early
spring months due to the low level of sunlight.
Geographical distribution: It depends upon the diet given
and the climate condition e.g. sunrays is not so much
available in polar regions, but enough cod liver oil is
supplied. While in the tropics excess ultraviolet rays
exist. Thus rickets is less frequent in these two
regions. But in subtropical regions there is enough
vitamin D in the neither diet nor enough ultra-violet
rays and consequently rickets is more common
Beside the history taking, emphasizing the
actual foods taken by the child and if there is
any exposure to sun-shine, the presence of any
of the following manifestations should be
observed:
Head appears enlarged and square when viewed
from above.
Anterior fontanel is late in closure.
Craniotabes: Cranial bone is soft and making sound
under pressure. Craniotabes is the earliest bony
change to be observed. Its greater incidence is from
3 to 8 months of age. This sign cant be elicited after
the first year of life.
Teeth eruption is usually delayed.
Ricketic Rosary: Beading of the ribs at the
costochondral junction and is seen as a raw of
nodules about the size of cherries extending
down and backwards along the line of
costochondarl junction.
Harrisons groove, which is a bilateral
depression at the sites where the diaphragm is
attached to the ribs.
Lack of muscular tone, where the infant assume
poor sitting posture. When the infant does sit up
alone there is often apparent smooth curvature
(Kyphosis).
Scoliosis (lateral curvature of the spine) with
deformities of the pelvic occurs frequently.
Infant is delayed in sitting, standing and walking
due to poor muscular tone.
Pot belly is caused by relaxed abdominal
muscles.
The child may be constipated due to loss of the
strength in the abdominal muscles.
Epiphyseal enlargment of wrist and ankles.
Relaxation of ligaments helps to produce
deformities and partly accounts for knock
knees and bow legs.
Nutritional anemia may be evident (pallor,
tachycardia, palpitationetc.
Low resistance, therefore he is liable to
infection, specially respiratory tract infection and
its complication (Running nose, cough, sore
throat).
Infantile rickets can be prevented by:
Daily exposure to effective ultraviolet rays.
Daily oral does of 400 I.U. of vit. D in the form
of cod liver oil.
The daily prophylactic does of vit. D
recommended for premature infant and twins is
1000 I.U./ day.
Vit. D should be given to pregnant and lactating
mothers.
Therapeutic Management of
Infantile Rickets:
A daily administration of 1600 I.U. will produce
healing in 2 to 4 weeks, demonstrable in x-rays.
In cases of vit. D refractory rickets (cases do not
respond to rickets) massive therapy consisted of
600.000 I.U. (15 mg once monthly) one, two or
three injections may be needed. In ordinary
cases, one injection is enough, if to be repeated
blood examination for calcium should be done.
Nursing Care Plan
Skeletal system impaired related to diminish
intake of vit. D.
High risk for infection related to deficient
immunologic defenses.