3.2. malnutrition ppt. Pediatrics for malnutrition.
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Feb 27, 2025
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About This Presentation
Medics
Size: 2.04 MB
Language: en
Added: Feb 27, 2025
Slides: 38 pages
Slide Content
HYPOTROPHY: MALNUTRITIONAND
GROWTHINHIBITIONINCHILDREN
Ovsyannikov D.Yu.
Khaled M.
DEFINITIONOFMALNUTRITION
”People are malnourished if their diet does not
provide adequate calories and protein for growth
and maintenance or they are unable to fully utilize
the food they eat due to illness (undernutrition).
They are also malnourished if they consume too
many calories (overnutrition).” (Unicef)
NCHS 1978
CHILDGROWTHREFERENCES
Measures made 1960-75
American Children-geographically
restricted area.
With formula milk
High socioeconomic background
WHO 2006
CHILDGROWTHSTANDARDS1997-2003
Boys at age 11 with high, normal, reduced
nutrition (left to right)
NUTRITIONAL DEFICIENCY DISEASES
On global scale the five principal nutritional deficiency
diseases are:
1.Kwashiorkor
2.Marasmus
3.Xerophthalmia
4.Nutritional anemia
5.Endemic goiter
7
MANIFESTATIONS OF OVERNUTRITION
In the more developed countries of the world, over
nutrition is encountered much more frequently than
under nutrition.
The health hazards from over nutrition are:
1.Obesity,
2.Diabetes,
3.Hypertension,
4.Cardiovascular diseases,
5.Renal diseases,
6.Disorders of liver and gall bladder.
8
MALNUTRITION(HYPOTROPHY)
Intrauterine (intrauterine growth retardation) IUGR
Failure of the fetus to chieve the expected weight for a
given gestation
Newborn with intrauterine
growth retardation
(left)
and with normal physical
development (right)
IUGR, REASONS
poor diet, chronic diseases in pregnant, smoking
and alcohol consumption, exposure to industrial
hazards
pathological course of pregnancy, accompanied by
blood circulation in the placenta
intrauterine infection of the fetus, genetic
syndromes
Which maternal medical conditions result in IUGR?
•HPT
•PET
•DM with vascular involvement
•SLE
•Anemia
•Sickle cell disease
•Antiphospholipid syndrome
•Renal disease
•Malnutrition
•Inflammatory bowel disease
•Intestinal parasites
•Cyanotic pulmonary disease
What infections result in IUGR?
Congenital infections:
•CMV
•Rubella
•Herpes
•Vericella zoster
•Toxoplasmosis
•Malaria
•Listeriosis
5-10% of IUGR
Which drugs can result in IUGR?
•Alcohol
•Cigarette smoking 3-4X
•Heroin & coccaine
•Methotrexate
•Anticonvulsants
•Warfarin
•Antihypertensives /ß-blockers
•Cyclosporin
What are the genetic disorders that can result in IUGR?
•Down’s syndrome T21
•Trisomy 13,18
•Turner syndrome
•Neural tube defects
•Achondroplasia
•Osteogenisis imperfecta
•Abdominal wall defects
•Duodenal atresia
•Renal agenesis/ Poter’s S
15% of IUGR
CLINIC
trophic disorders
Changes in the functional status of CNS
Reduction of food tolerance
Reduction of immunobiological reactivity
PHYSICALAPPEARANCE:
•Heads are disproportionately large for their trunks and
extremities
•Facial appearance has been likened to that of a
“wizened old man”.
•Long nails.
•Scaphoid abdomen
COMPLICATION
Hypoxia
-Perinatal asphyxia
-Persistent pulmonary hypertension
-meconium aspiration
Thermoregulation
-Hypothermia due to diminished subcutaneous fat and elevated
surface/volume ratio
Metabolic
-Hypoglycemia
-result from inadequate glycogen stores.
-diminished gluconeogenesis.
-increased BMR
-Hypocalcemia
-due to high serum glucagon level, which stimulate calcitonin
excretion
COMPLICATIONS
Hematologic
-hyperviscosity and polycythemia due to increase
erythropoietin level sec. to hypoxia
Immunologic
-IUGR have increased protein catabolism and
decreased in protein, prealbumin and
immunoglobulins, which decreased humoral and
cellular immunity.
MANAGEMENT
Antenatal diagnosis and management is the key to
proper management of IUGR
Delivery and Resuscitation
-appropriate timing of delivery
-skilled resuscitation should be available
-prevention of heat loss
Early feeding and caloric intake should be
100-120 kcal/kg/d
Developmental and growth f/u in all IUGR
infants
EVALUATIONOFSGA NEWBORN
Careful physical examination
Measure & plot head circumference &
length
CBC with differential and platelet count
Monitor glucose carefully
Further evaluation?
Urine for CMV
TORCH titers
Liver function tests
Head Ultrasound
WEIGHTANDGROWTHRATE
Evaluated in term infants
Ratio of the mass (g) to body length
(cm)
Standard: 60 –80
1 degree IUGR -55-59
2 degree IUGR -51-54
3 degree IUGR -less than 50
FETALORIGINSOFADULTDISEASES?
Coronary artery disease correlates inversely with
birth weight
Rate of non-insulin dependent diabetes mellitus is
highest in the “thinnest” babies at birth (low ponderal
index)
High serum cholesterol are linked to disproportionate
size at birth (body smaller than head)
Increased rate of hypertension in infants who were
thin, short, &/or proportionately small at birth
POSSIBLEMECHANISMS
Violation of DNA methylation
Permanent anatomical changes in structure of
organs
CLASSIFICATION OF PEM
By wellcome -to assess a child
with edema
According to Gomez -Comparison of
patient weight to body weight of a normal
child (50th percentile) of the same age, in%
% Of
predicted
body weight
with edemawithout
edema
60-80% kwashiorkorUnderweight
< 60 % marasmus
kwashiorkor
marasmus
interpretation
90-110 % norm
75-89 % I degree -mild
60-74 % II degree -
moderate
< 60 % III degree -severe
Malnutrition, kwashiorkor and
nutritional marasmus
SEVEREMALNUTRITION
W/H <70% or bilateral oedema
Impaired immune system and electrolyte inbalance
Kwashiorkor
Marasmus
KWASHIORKOR
2-4yrs
Comes suddenly after some time of
Moderate Malnutrition
Low protein intake
http://www.asnom.org/image/510_nutrition/116_327_kwashiorkor.jpg
Symtoms:
•Bilateral Oedema
•Apathy
•Depigmented corse hair, easy to pull.
•Skin lesions
•Poor aptetite
•Diarrhoea
Mechanism of Swelling
blood consists of water, blood cells and proteins
Dissolved proteins hold water within bloodstream,
preventing it from leaking into body tissues.
As blood protein falls to low levels, water leaks
from circulation into your tissues, causing
swelling.
With kwashiorkor, the levels of sodium and
potassium in bloodstream become unbalanced,
further contributing to tissue swelling.
MARASMUS
•1st year of life, often failure to
breastfeed.
•Lack of proteins and calories.
•Body creates energy by dissolving
its own tissuesLoss of
subcutanous fat and muscles.
Symtoms:
•Wasting W/H <70%
•Face o an old person
•Pot belly due to lack of abd. muscles.
•Anorexia, irritability.
•Hunger
Time Magazine, August, 2008
1.Hypoglycemia
2.Hypothermia
3.Dehydration
4.Infection
5.Severe anemia
Direct causes of death:
POSSETING(REGURGITATION)
Physiological
not abundant
Within 2 hours after
feeding
First 6 months.
Not more often 4-6
times a day
Pathological
abundant
Later than 2 hours after
feeding
After 6 months.
More than 6 times a
day
CORRECTION OFREGURGITATION
Burp your baby more often (usually after one to two
ounces of formula).
Avoid overfeeding.
Feed your infant smaller portions more frequently.
Keep your baby in an upright position after feeding.
Don’t jostle the baby after feeding, as this can cause the
stomach contents to reflux.
Wait 30 minutes after feeding before putting the infant to
sleep, as positioning can affect reflux symptoms.
Dietary (antireflux mix -Frisovom, Nutrilon
antireflyuks)
Prokinetics (procaine, motilium)