ma nutrition

8/3/2019 Ma Nutrition

1/70


2/70


3/70

Malnutrition is a term referringto poor orinadequate nutrition.

Although it is generally thought of in terms ofundernutrition, it includes overnutrition.

The most severe states of undernutrition involve

protein and caloric deficiencies, such askwashiorkor and marasmus. Overnutrition maybe manifested as obesity.


4/70

Hunger is one of the worlds gravest and mostprevalent health problem. Three- fourth of the

world population suffer from some form ofmalnutrition.

This problem is more prevalent in under-developed countries. Although several factors

may contribute to the production of deficiencydiseases, the basic problem is usually a lack offood intake.

Sometimes there may be poor absorption of one

or more of food components. Other time, thecause is lack of parental education regardinginfants and childrens nutrition.


5/70


6/70

Kwashiorkor is a deficiency of protein with anadequate supply of calories.

It is a syndrome that develops in the first child,

usually between 1 and 3 years of age, when heis weaned from the breast once the second childis born.

The infant is put on a diet which consists mainly

of carbohydrates,beside the excessive demandof all nutrients at that age of rapid growth,especially protein of high biological value.


7/70

Dietary inadequacy occurs when there is a rapidperiod of transition from the balanced diet

supplied by the breast milk to an unbalancedinadequate diet, which is very low in protein,and consists mainly of carbohydrates.

This occurs usually during weaning and postweaning periods. The poverty, ignorance andlack of basic health education and nutritionalknowledge are important factors in this mistake.

Etiology:


8/70

Acute infections like acute infantile diarrhea

and measles can precipitate the appearance ofkwashiorkor or in borderline cases due to:

Catabolic effect of the infections.

Anorexia, which usually accompaniesinfections.

Precipitating Factor:


9/70

The bad habit of withholding food

during measles and diarrhea up tothe degree of starvation.

Malaria and severe parasiticinfestations may play a role in thedevelopment of kwashiorkor in someregion of the world.


10/70

Assessment criteria

Occasional

manifestationsConstant(or cardinal)

manifestations

Usualmanifestations


11/70

I. Constant (or cardinal)

manifestations.

Weight is markedly diminished (to 60-80% ofwhat is expected for childs age).

Retarded linear growth (length).

Head circumference may also be affected.

This is reflected by:


12/70

The main factor is hypoproteinemia.

It starts in the feet and lower parts of the legs

then becomes generalized.It is usuallysoft and pittingaffecting more thedependent parts (back and dorsum of hands and

feet). The cheecks become bulky, pale and waxyin appearance (doll-like cheecks).

Ascites is unusual.


13/70

There is a generalized muscle wasting withpreservation of some subcutaneous fat.

This can be demonstrated clinically bymeasuring the mid-arm circumference which

is diminished in these cases. The children are often weak, hypotonic and

unable to stand and walk.


14/70

Infants with kwashiorkor have marked

apathy; misery and they lack interest inthe surrounding.

They dont move, look sad and never

smile.Their cry is weak.


15/70

II-Usual Manifestations.

Hair is a sparse, especially over the temples andoccipital regions.

There is dyspigmetation of hair (hypochromotrichia).The hair loses its black color and becomes reddish orgrayish. The cause of this dyspigmentation is obscure.Deficiency of pantothenic acid and sulfur containingamino- acids in the hair or a defect in the melaninformation may be responsible for suchdyspigmentation.

Hair is also atrophic, easily pickable, having lost its curland tapered nearer to the scalp (like an exclamationmark).


16/70

Anorexia sometimes associated with

vomiting, especially in severe cases.

Diarrhea is common and can be due

to:

1. Infection with intestinal pathogens orparasites.


17/70

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 aconsequence.

3. Malabsorption of nitrogen, fat,

carbohydrates and minerals due to theatrophy of villi.


18/70

III-Occasional Manifestations.

Dermatosis:

The rash appears mainly in areas ofincreased pigmentation. These

pigmented areas subsequently

desquamate leaving atrophic,

hypopigmented and easily damage skinor even ulcerations.


19/70

The characteristic rash is usually seen on

the back of thighs and axillae; though

other parts of the body may be affected.

Sometimespetechiaemay be present,

particularly over the abdomen


20/70

It is caused by fatty infiltration of the liver,which is a constant pathological finding inkwashiorkor that may or may not be

accompanied by hepatomegly.


21/70

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.


22/70

Riboflavin, Niacin, Thiamin, Vitamin D and C

deficiencies) and minerals as iron, copper, zinc

and magnesium.


23/70


24/70

Reduced total plasma protein (less than 4gm/dl).

Reduced level of serum albumin (less than2 gm/dl).

Urea in blood and urine is markedly

reduced because of deficient intake ofexogenous protein.


25/70

Total body sodium is higher than normal.Serum sodium may be low due to theexcessive amount of water extracelluarfluid compartment.

Low total body potassium due topotassium losses by diarrhea.


26/70


27/70

Marasmus is a form ofsevere PEM occur due tointake of badly balanced diet that may occur atany 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.


28/70

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:


29/70

Diseases, which interfere with the assimilationof food e.g. cystic fibrosis.

Infections, which produce anorexia.

Loss of food through vomiting and diarrhea. Emotional problems e.g. disturbed mother-

child relationship.


30/70

Beside the history taking, emphasizing the actual

foods taken by the child, the presence of any ofthe following manifestations should be assessed:

Assessment criteria


31/70

1-Growth Failure:

Weight is less than 60% of expected for age and sex.

Length, head, chest, and abdominal circumferencesare also affected but to a lesser extent than weight.


32/70


33/70

2-Loss of Subcutaneous Fat from:

The abdominal wall leading to loss of skin elasticity.

The limbs (thighs and buttocks): the skin becomeswrinkled and hanging into longitudinal folds.

The buccinator pad of fat is the last to disappear(probably due to different chemical composition ofits fat). This leads to hollowing these checks, whichleads to triangle face and an appearance resemblingthe old man.


34/70

3- Marked Wasting of Muscles:

This together with the loss of subcutaneous fat

leads to: Sticklike appearance of limbs.

Scaphoid abdomen with marked thinning of

abdominal wall.


35/70

Marasmic infants look anxious, irritable,

excessively cry and sleep little. However, theylook less miserable than the cases ofkwashiorkor. Marasmic infants are usually

hungry and have good appetite. Sometimes,there is anorexia and poor feeding.

4-Psychic Changes


36/70

Chronic diarrhea with or without vomiting.

Intercurrent infections:

Like otitis media, bronchopneumonia, urinarytract infections are commonly present.

Associated deficiencies of iron, vitamin A

and D.

Hypothermia due to loss of subcutaneous

fat.


37/70

No hair changes.No fatty infiltrationof the liver (hepatomegly).

No edema.No dermatosis.

Characteristically cases ofMarasmus have


38/70

Laboratory findings:

Plasma protein may be normal or slightlylowered. This is because marasmic infants liveon their own muscle protein.

Blood urea is low since the protein utilized bythe infant is totally endogenous protein.

Blood glucose level is low due to deficient

glycogen stores in the liver.


39/70

Diarrhea, dehydration, electrolyte and acid basedisturbances.

Infections, such as, thrush stomatitis,bronchopneumonia, empyema, T.B, urinary tractinfection.

Hypoglycemia.

Hypothermia.

Early prolonged malnutrition may lead to mentalsubnormality.

Complications of Protein-Energy

Malnutrition


40/70

The basic principle in the treatment is toimprove 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 mineralssupplementation).

Treatment of complications infection,

diarrhea, parasitic infestation and anemia.

Therapeutic management of Protein-

Energy Malnutrition


41/70

Altered nutrition: less than bodyrequirements related to knowledge deficit,

physical defect, infection, disease

interferes with the assimilation of food oremotional problems.

Body temperature alteration (hypothermia)related to diminished food intake.

Skin integrity impaired related todeficiencies of vitamins intake.

Nursing Care Plan: (PEM Infants)


42/70

High risk for infection related to low body

resistance

Fluid volume deficit related to diarrhea.

(Refer to G.I.T. lecture).


43/70

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

Prevention ofMalnutrition


44/70

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


45/70

Breast milk must end slowly at 2 years

A good food is mixed food

Sick children need food.


46/70

Young children at risk of malnutrition need tohave well balanced diet and avoid prolongedbreast feeding

School children need 3 meals a day and

break down food taboos

Bottle-feeding should not be used exceptif it is a necessity.


47/70

2. Immunization of children against measles andwhooping 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.


48/70


49/70

It is a metabolic disorder of infancy and childhoodcaused by vitamin D deficiency and affecting thegrowing bones (defective mineralization, slow

growth), the skeletal muscles (hypotonia) andsometimes the nervous system (tetany).


50/70

It may occur if vitamin D intake isinadequate.

Lack of skin exposure to ultraviolet rays.

Vitamin D (the sunshine vitamin) is a fat-solublevitamin. It is the common name for a group ofsteroids, the most important ones are:

D2 is formed by ultraviolet irradiation of ergosterolin green plants.

D3 (cholecalciferol) is produced by the effect ofsunlight on sterol substances in the skin (i.e.ultraviolet irradiation of 7-dehydrocholesterol).


51/70

Vitamin D2 and D3 are biologically inactive

forms. They are transported to the liver tobe hydroxylated (addition of hydroxylgroup OH) to 25 hydroxy- vitD.

Further hydroxylation takes place in therenal tubules to 1.23 dihydroxy- vitD(calcitriol). Which is the biologically activeform.


52/70

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.


53/70

Food sources of vitamin D are limited; the richestsource is fish liver oils (e.g. cod liver oils) andfish (e.g. herring, salmon, tuna or sardines).

Less efficient sources are milk, egg yolk and butter.Exposure to ultraviolet light either directly fromthe sun or from a lamp is an excellent source

since it converts provitamine D3 (inactive) tocholecalciferol.


54/70

To produce enough vitamin D to meet the

children daily needs they must be exposed tomid-day sun for about 15 minutes. So, the more

the sunrays are vertical, the more they are

effective for the natural formation of vitamin Din adequate amounts. However, theeffectiveness of sunrays is minimal when:


55/70

The rays are oblique i.e. before or afternoon.

They pass through clouds, dust, smoke orordinary window glass because they preventultra-violet rays from reaching the babys skin.

Also, adequate exposure of the skin is further

hampered by clothing and by the fact thatchildren spend much time indoors, especially

during the cold seasons.


56/70

The frequency of rickets in Arab Countries isstill high in spite of the knowledge of its etiologyand its response to treatment.


57/70

Heredity:Dark-skinned individuals absorb lessvitamin D through their skin because deeperpigmentation 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, enoughsunshine and he is growing slowly.


58/70

Diet:It is more common in artificial fed babies

if they do not receive enriched formulas. Abreast fed infant is not likely to suffer from

rickets, provided that his mother is receivingan 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 toaccommodate the rapid growth rate.


59/70

Season:The incidence is greater in late winter and earlyspring months due to the low level of sunlight.

Geographical distribution:It depends upon the diet givenand the climate condition e.g. sunrays is not so muchavailable in polar regions, but enough cod liver oil issupplied. While in the tropics excess ultraviolet raysexist. Thus rickets is less frequent in these tworegions. But in subtropical regions there is enough

vitamin D in the neither diet nor enough ultra-violet

rays and consequently rickets is more common


60/70

Beside the history taking, emphasizing the

actual foods taken by the child and if there isany exposure to sun-shine, the presence of anyof the following manifestations should be

observed:


61/70

Head appears enlarged and square when viewedfrom above.

Anterior fontanel is late in closure.

Craniotabes: Cranial bone is soft and making soundunder pressure. Craniotabes is the earliest bonychange to be observed. Its greater incidence is from3 to 8 months of age. This sign cant be elicited after

the first year of life.

Teeth eruption is usually delayed.


62/70

Ricketic Rosary: Beading of the ribs at thecostochondral junction and is seen as a raw ofnodules about the size of cherries extending

down and backwards along the line ofcostochondarl junction.

Harrisons groove, which is a bilateral

depression at the sites where the diaphragm isattached to the ribs.


63/70

Lack of muscular tone, where the infant assume

poor sitting posture. When the infant does sit upalone there is often apparent smooth curvature

(Kyphosis).

Scoliosis (lateral curvature of the spine) withdeformities of the pelvic occurs frequently.

Infant is delayed in sitting, standing and walking

due to poor muscular tone.


64/70

Pot belly is caused by relaxed abdominalmuscles.

The child may be constipated due to loss of the

strength in the abdominal muscles.


65/70

Epiphyseal enlargment of wrist and ankles.

Relaxation of ligaments helps to producedeformities and partly accounts for knock

knees and bowlegs.


66/70

Nutritional anemia may be evident (pallor,tachycardia, palpitationetc.

Low resistance, therefore he is liable to

infection, specially respiratory tract infection andits complication (Running nose, cough, sorethroat).


67/70

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


68/70

Therapeutic Management of

Infantile Rickets:

A daily administration of 1600 I.U. will producehealing 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 of600.000 I.U. (15 mg once monthly) one, two orthree injections may be needed. In ordinary

cases, one injection is enough, if to be repeatedblood examination for calcium should be done.


69/70

Nursing Care Plan

Skeletal system impaired related to diminishintake of vit. D.

High risk for infection related to deficient

immunologic defenses.


70/70

ma nutrition

Documents