Pediatrics: Formula Feeding Amounts

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4/21/2022

Pediatrics
Infant Nutrition (Continued)

Formula feeding amounts

 Age method
 Can be used for healthy infants.
 Amount of milk per feed: 1st day = 10 cc, then increases 10 cc
everyday till the 7th day (70 cc / feed).
 Then increases 10 cc / feed / week till the age of 4 weeks = 100
cc / feed.
 Then amount/feed = age in months x 10+100
 Weight method
 Amount of milk/feed in cc = wt in kg x 20 + 20

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Formula feeding amounts

 Calorie method
 Most Accurate
 Calculate the total caloric needs / day (=C).
 Calculate the total amount of milk needed/day = ( C )x
100/67 cc.
 Calculate the amount of milk / feed.
 Caloric requirements
0-3 months - 116kcal./kg./d
3-12 months- 100kcal./kg./d

Caloric Requirements

Age Form KCal/kg/day


-------------------------------------------------------------
Low Birth wt Infants Enteral 150
Low Birth wt Infants Parental 80-100
Preterm Infants Parental 85-130
1- 7 years Enteral 75- 90
7-12 years Enteral 60- 75
>18 years Enteral 30- 60
BEE (men)= 66 +(13.7*wt)+(5.0*ht)-(6.8*age)
BEE (wom)=665+(9.6*wt)+(1.7*ht)-(4.7* age)

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Baby's Growth Charts


 This is an American system (released in November 2000 and based
on data from the National Center for Health Statistics, U.S. Public
Health Service).
 Charts are a vast improvement over earlier charts
 Baby's growth charts can give you a general picture of how ! baby
is developing physically
 By comparing baby's measurements — weight, length, and head
circumference — to national averages for children of the same age
and sex measurements from previous checkups
 There are charts for: weight, length, and head circumference.
 These charts measure baby growth in percentiles.
 What does "percentile" mean?

Baby's Growth Charts

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Weaning
 Definition: addition of any food other than milk to infant formula.
 At the time of weaning, the close relationship between the mother
and the baby begins to weaken; so this should be a gradual
process.
 Why
 Breast milk on its own is sufficient for most babies until 4-6 months of age,
 After 6 months of age, the baby's growing body demands are more
than the mother's milk can provide.
 When
 The appropriate time for weaning depends on several factors such as
the infant's state psychomotor and psychosocial development,
gastrointestinal function and the relationship of dietary energy to the
volume of feeds given to the infants, deeply held traditions and type of
the community (urban areas start earlier weaning than rural areas).

Weaning; How?
 To train the baby to chew and become accustomed to new foods, first
give 1-2 teaspoonfuls of freshly peeled mashed fruits e.g. orange,
apple.
 If the baby is reluctant to take food then he may be willing to try when
he is hungry.
 Use a spoon to feed the baby as this cleaner and safer than bottle and
hand feeding also to avoid nipple confusion.
 Gradually increase the amount of food offered. Within about two
weeks basic mixes and then multi-mixes should be introduced.
 Don’t force the infant to eat and don’t worry if he spits out the food.
 Once a new food is accepted give it frequently so that it becomes
familiar.
 As the baby grows he will be encouraged to try a new food and to eat
what he is given, if he is allowed to handle the food and try to feed
himself.

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Hazards of faulty weaning


 Time of weaning
 Early weaning → distention – colics – diarrhea (maldigestion). Early cessation of breast
feeding may lead to early return of fertility and undesirable pregnancy.
 Delayed weaning (prolonged exclusive breast feeding): →Decreased calories, proteins
→ Malnutrition diseases
 → Fe deficiency → Anemia.
 → Vit C deficiency → Scurvy.
 Amounts of food given
 Under nutrition
 Obesity
 Type of food
 Food allergy.
 Low protein + excess CHO; Kwashiorkor (PEM ).
 Low Vit D; rickets.
 Contamination; Gastroenteritis.

Rickets

 Rickets is a softening of bones in children potentially


leading to fractures and deformity.
 Rickets is among the most frequent childhood diseases
in many developing countries.
 The predominant cause is a Vitamin D deficiency, but
lack of Ca in the diet can also produce rickets

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Etiological classification

Vitamin D deficiency rickets (vitamin D sensitive


rickets; corrected by Vit D therapy); the most
common in Egypt.
Vitamin D resistant rickets (i.e. there is no
response to ordinary treatment of vitamin D)(
treat the cause)

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Vitamin D resistant rickets


 Renal rickets
 (rickets caused due to a renal disorder). Manifestations of the renal disease +
manifestations of rickets.
 Hepatic rickets
 (severe hepatic disease e.g. chronic hepatitis or obstructive jaundice, e.g. Biliary
atresia [absence or closure of ducts], leading to failure of vitamin D hydroxylation
in ! liver or reduced absorption of vitamin D due to bile deficiency.
 Manifestations of the hepatic dysfunction e.g. jaundice + manifestations of
rickets.
 Malabsorption rickets (celiac rickets):
 Caused by malabsorption syndrome.
 Manifestations of malabsorption + manifestations of rickets.
 Condition stimulating rickets
 e.g. hypophosphatasia [abnormal genetic inherited low phosphate in the body].

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Hypophosphatasia
 It is an autosomal inherited disorder that affects the
development of bones and teeth.
 Bone Constituents
 1. Bone Matrix
 2. Bone Cells:
 a. Osteoblasts (bone forming cells)
 They Secrete collagen around themselves which then ossifies.
 They increase the Ca x P product leading to mineralization (ossification).
 b. Osteocytes [Old Osteoblasts]: osteoblasts surrounded by ossified
matrix.
 C. Osteoclasts (Bone resorping cells): They resorp previously formed
bone (Wear& Tear).

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Ca and PO4 Homeostasis


Hormonal regulation
Parathyroid hormone
Vitamin D
Calcitonin
Growth hormone
Adrenal Steroids

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Vitamin D
 Calcitriol plays an important role in the maintenance of several
organ systems.
 Its major role is to increase calcium and phosphorus flow into the
bloodstream, by promoting their absorption from food in the
intestines, and reabsorption in kidneys; enabling normal
mineralization of bone and preventing hypocalcemic tetany.
 Generally, It is necessary for bone growth and bone remodeling by
osteoblasts & osteoclasts
 vitamin D stimulates differentiation of osteoclasts
 the crucial effect of vitamin D on bone is to provide the proper
balance of calcium and phosphorus to support mineralization.
 Nature and Absorption:
 Fat soluble vitamin absorbed in the upper part of the small intestine
utilizing bile.

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Daily needs

 In full term = 400IU/day starting from the 4th month.


 In preterm and LBW (low birth weight)= 800-1000IU/day
from ! 2nd month.(due to the decrease in the size of
stores).

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Sources

 Endogenous: (vit D3–cholecalciferol) formed in ! skin by


UVR (300 – 310 nm) from 7-dehydrocholesterol.
 Animal source: (D3)
 Fish liver oil and egg yolk (3-10 ug/gm).
 Cow milk and breast milk are poor sources.
 Plant source: (vit D2- ergocalciferol) from irradiated
green plants and vegetable oils.

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Calcium

 Normal level 9-11 mg%


 A) Non diffusible = Protein bound about 50%.
 Bound to albumin, prealbumin and globlin.
 Decreased in cases of hypoalbuminaemia B) Diffusible:
 B) Diffusible
 Ionized = 50% (active form) Increased by acidosis.
 Decreased by alkalosis; tetany

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Vit D. deficiency rickets


 Rachitogenic diet
 Cow milk: Low content of vit D, Ca/P ratio is not optimal for Ca
absorption
 Prolonged breast feeding without Vit D supplementation.
 Cereals rich in phytate and phosphate.
 Dec. acidity in gut (poor intake of vit C).
 Inc alkalinity (e.g. excess beverages).
 Increased stearic and palmitic acids in diet.
 Ca deficient diet [early weaning, cow milk allergy
 Inadequate exposure to sunlight

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Pathogenesis

 Vit D deficiency [1ry event] [no Ca abs]; initial


hypocalcemia; [low Ca levels stimulate PTH]. Secondary
hyperparathyroidism:
 a) increase Ca levels through mobilizing Ca from bones and
increased renal reabsorption
 b) hypophosphatemia through increased renal excretion

 Mobilizing Ca from bones: osteoclasts; increased bone


resorption; decreased bone density; weak bone liable
for fractures and deformities, and delayed teeth
eruption

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