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Pediatrics Dr. Nawal
Under Nutrition
Anthropometric indices
1. height-for-age, (chronic malnutrition)
2. weight-for-age, reflects the combined effects of both recent and longer-term levels of
nutrition, clinicly less significant but easly measure.
3. weight-for-height. Acute malnutrition(wasting)
Gomez classification(WFA)
n Mild malnutrition 75-90%
n Moderate malnut. 60-74%.
n Sever malnut. < 60%
SEVERE CHILDHOOD UNDERNUTRITION (PROTEIN-ENERGY MALNUTRITION
PEM
Deficiency of nutrient.(macro, micro)
inadequate dietary intakes of protein and energy:-
1) dietary intakes of these nutrients are less than required for normal growth
2) the needs for growth are greater than can be supplied.
causes
A. primary malnutrition inadequate food intake.
B. secondary malnutrition resulting from increased nutrient needs, decreased nutrient
absorption, and/or increased nutrient losses.
classification
1. marasmus (non-edematous SCU with severe wasting), wt < 60% inadequate energy
intake or inadequate intakes of both energy and protein.
2. kwashiorkor (edematous SCU), was believed to result primarily from inadequate protein
intake. wt 60- 80%
3. marasmic kwashiorkor, has features of both disorders (wasting and edema). Wt <60%
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The 3 conditions have number of overlapping features.
1. A low plasma albumin concentration.
2. the underlying causes are quite similar:-
o social and economic factors:- such as poverty and ignorance, food taboos (family
believes).
o chronically ill patients; in neonatal or pediatric intensive care units , burns, HIV, cystic
fibrosis, chronic diarrhea syndromes, malignancies, bone marrow transplantation, and
inborn errors of metabolism
CLINICAL MANIFESTATIONS OF SCU
Marasmus
is characterized by failure to gain weight and irritability, followed by weight loss and
listlessness until emaciation results.
The skin loses turgor and becomes wrinkled and loose as subcutaneous fat disappears. Loss
of fat from the sucking pads of the cheeks often occurs late in the course of the disease.
constipation, may have starvation diarrhea, with frequent, small stools containing mucus.
The abdomen may be distended or flat, with the intestinal pattern readily visible.
muscle atrophy and resultant hypotonia.
temperature usually becomes subnormal and the pulse slows
kwashiorkor
lethargy, apathy, and/or irritability.
lack of growth, lack of stamina, loss of muscle tissue,
flabby subcutaneous tissues.
increased susceptibility to infections, GE
Edema: The edema usually develops early and may mask the failure to gain weight. It is
often present in internal organs before it is recognized in the face and limbs.
Liver enlargement may occur early or late in the course of disease.
Dermatitis is common, with darkening of the skin in irritated areas, Depigmentation may
occur after desquamation in these areas, or it may be generalized .
The hair is sparse and thin, it may become streaky red or gray.
Eventually, there is stupor, coma, and death
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Signs
Face: moon(k), simian(M)
Eye: dry, pale, periorbital odema, bitot spot
Hair: dull, sparse, brittle, hypopoigmented, allopecia
Mouth: angular stomatitism cheilitis, glossitis, spongy gum,
teeth: delay teeth eruption
Skin: hyper or hypopigmented lesion,
Abdomen: distended, hepatomegali
Cardiac: bradycardia, hypotension, low out put
Neurological: delayed development, loss of reflexes, apathy, irritable
Hematology: pallor, petichiae
Musculoskeletal: muscle wasting, chvostick sign +ve, deformity of bone
PATHOPHYSIOLOGY OF SCU
Many manifestations are adaptive responses to inadequate energy and/or protein
intakes.
activity and energy expenditure decrease.
fat stores are mobilized to meet the ongoing, albeit lower, energy requirement.
Once these stores are depleted, protein catabolism must provide the ongoing substrates
for maintaining basal metabolism
Why edematous SCU develops in some children and non-edematous SCU develops in others
is unknown
1) the variability among infants in nutrient requirements and in body composition at the
time the dietary deficit is incure.
2) giving excess CHO to non odematous PEM reverse the adaptive response to low protein
intake resulting in mobilization of body protein stores. Eventually, albumin synthesis
decreases, resulting in hypoalbuminemia with edema.
Fatty liver also develops secondary, perhaps, to lipogenesis from the excess
carbohydrate intake and reduced apolipoprotein synthesis
3) impaired renal function and decreased Na+ K+ ATPase activity.
4) free radical damage has been proposed as an important factor in the development of
edematous SCU.
Laboratory Features
Hemoglobin, PCV,RBC,MCV:
Degree of dehydration and anemia; type of anemia (iron/folate and vitamin B12
deficiency, hemolysis, malaria).
Glucose : Hypoglycemia.
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Electrolytes and alkalinity
Sodium: Hyponatremia, type of dehydration
Potassium : Hypokalemia.
Chloride, pH, bicarbonate: Metabolic alkalosis or acidosis.
Total protein, transferrin,(pre-)albumin: Degree of protein deficiency
Creatinine : Renal function
C-reactive protein, lymphocyte count, serology, thick and thin blood films : Presence of
bacterial or viral infection or malaria
Stool examination Presence of parasites
TREATMENT OF SCU
1) The initial phase (1–7 days) is a stabilization phase:-
1. dehydration, ORT is preferred, intravenous therapy if necessary.
2. control bacterial or parasitic infection.. antibiotic therapy is initiated.
3. Oral feedings high-calorie formula , F75 diet (75 kcal /100 mL), higher frequency and
smaller volumes, then frequency is reduced from 12 to 8 to 6 feedings/24 hr, 80–100
kcal/kg/day.
If diarrhea starts or fails to resolve:-
lactose intolerance is suspected, a non–lactose-containing formula. milk protein
intolerance suspected, soy protein hydrolysate formula.
2) Rehabilitation phase (wk 2–6)
may include
1) continued antibiotic therapy.
2) oral feeding: F100 diet, 100 kcal/kg/day.
3) Iron therapy .
iron not given in initial phase:-
a. may interfere with the protein's host defense mechanisms.
b. free iron during the early phase of treatment may exacerbate oxidant damage.
c. precipitating infections (malaria).
d. ppt. clinical kwashiorkor, or marasmic kwashiorkor in a child with clinical marasmus..
By the end of the 2nd phase:
1. any edema that was present has usually been mobilized.
2. infections are under control.
3. the child is becoming more interested in his or her surroundings.
4. appetite is returning
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3) Follow-up phase7-26 wk
a. feeding to cover catch-up growth .
b. the provision of emotional and sensory stimulation.
c. The child should be fed ad libitum..
this final phase is often carried out at home.
In all phases, parental education is crucial for continued effective treatment & prevention of
additional episodes
Elements in the MANAGEMENT
Hypothermia, Warm patient up.
Hypoglycemia, Monitor, provide oral (or intravenous) glucose.
Dehydration, oral solution containing less sodium and more potassium than standard
mix.
Micronutrients, Provide copper, zinc, iron, folate, multivitamins.
Electrolytes :- Supply plenty of potassium and magnesium
infection :- antibiotic and antimalarial therapy, even in the absence of typical symptoms
Starter nutrition Keep protein and volume load low.
Tissue-building nutrition dense in energy, protein, and all essential nutrients that is easy to
swallow and digest.
Stimulation, Prevent permanent psychosocial effects of starvation with psychomotor
stimulation.
Prevention of relapse, Start early to identify causes. involve the family and the
community in prevention
Refeeding syndrome
severe hypophosphatemia
1st week of starting to refeed.
Serum phosphate levels of ≤0.5 mmol/L . weakness, rhabdomyolysis, neutrophil
dysfunction, cardiorespiratory failure, arrhythmias, seizures, altered level of consciousness,
or sudden death.
Phosphate levels should be monitored , and if low, phosphate should be administered.