Lectures of Dr.

Al-Khorsani
Dr. Mohammed Al-Khorsani

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 Growth and Development

Definitions
Growth: Simple increase in the of the tissues and organs.
Development: Functional maturation of the tissues and organs and
acquisition of skills ’(development milestones).
Development" involves many aspects e.g.
1) Mental development
2) motor development.
3) Sexual development.

Stages of Growth and Development

I. Intrauterine stage (from the time of fertilization to the time of birth).
1) Embryonic period (the first 8 weeks of gestation): By the end of wk 8, the
gross structure of all major organ systems have developed.
2) Fetal period (9-40 weeks of gestation).
a) Early fetal period (9-24 weeks of gestation): By 24wk, primitive
alveoli have formed and lung surfactant production has begun; the
newborn delivered before that time can not survive.
b) Late fetal period (25-40 weeks of gestation).
II. Extrauterine (postnatal) period :
1) Newborn period (the first 28 days of life).
2) Period of infancy (the first 2 years of life).
a) Early infancy period (1-12 mo of age).
b) Late infancy period (the 2nd year of age)،
3) Period of childhood (2-12 years of age).
a) Early childhood or preschool years (2-5 years of age).
b) Late childhood or school-aged children (6-12 years of age).
4) Period of adolescence (10-20 years of age).

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 Aspects of Physical Growth
1. Weight. 2. Length or Height 3. Body proportions.
4. Head circumference 5. Cest circumference. 6. Teeth eruption.
7. Bony maturation. 8. Scutaneous fat thickness. 9. Physiologic and structural growth.

Weight

 A newborn’s weight may decrease up to 10% below birth weight in the 1st week.
Newborn should regain birth weight by 2 wk of age and should grow at ~30
gm/day during the neonatal period.
 Weight gain is~750 g/mo during the first 4 months of life. ~500g/mo during the
next 4 months (5-8 mo of age).~250 g/mo during the last 4 months of the first
year.
Formulas for Approximate Average Weight of Normal Infants Children
Weight Kilograms Pounds

At birth 3.25 7

3-12 mo Age(mo)+9 Age(mo)+11

2
1-6 yr {Age(yr) ×2 +8} Age(yr) × 5+17

7-12 yr {Age(yr) × 7-5} Age(yr) × 7+5

2

The weight at the age of 4 mo =4+9/2=6.5kg(~double the birth weight).

The weight at the age of 1 yr =12+9/2=10.5kg(~three times birth weight).
The weight at the age of 2 yr =2×2+8=12kg(~four times the birth weight).

Length or height
Definition: Length or height (the linear growth) is the crown-heal
measurement below the age of 5 years.
Height is that measure in the standing position and is applied to older children above
the age of 5 years.
Formulas for Approximate Average Length or Height of Normal Infants and
Children

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 Length or Height Centimeters Inches

At birth 50 20

At 1 year 75 30

2-12yr Age (yr)x6 + 77 Age (yr) X 2½+30

The length at the age of4 years = 4x6 +77 = 101 cm ("-double the birth length).
The height at the age of 12 years = 12x6 +77 = 149 cm (~ three times the birth length).

Body Proportions
Upper and Lower Segments
The length or the height of the individual is classified into two segments.
1) The upper segment (US) is the measure extending between the crown to the
symphysis pubis (the anterior iliac spine).
It reflects the growth of the short bones of the neck and trunk (vertebrae), as
well as the skull.
2) The lower segment (LS) is the measure extending between the symphysis
pubis to the t heel.
It reflects the growth of the long bones of the lower limbs.
The rate of growth of the long bones (including those of the lower limbs) is
much greater than the rate of growth of short bones forming the major part of
US measure.
At birth: The US to LS ratio is .1.7:1.
At 3 yr of age: The US to LS ratio is 1.3:1.
After 7 yr of age: The US to LS ratio is 1: 1.

Clinical application
1) Diseases which affect the general health of the body e.g., undernutrition
and hypothyroidism will affect the US and LS equally and the proportion
between them will / not be affected.
2) Diseases which affect mainly the long bones e.g., achondroplasia and rickets

Mohammed 3
 will affect the LS, thus increasing the US: LS ratio.
3) Diseases which affect the short bones of the trunk e.g., pott’s disease
(tuberculosis of the spine) will affect the us, thus lowering the US: LS ratio.

Arm Span and Height

The arm span is the distance between the(tips of the two middle ~fingers) of
the outstretched upper limbs.
It is made mainly by the long bones of the upper limbs. This is in contrary to
the height, which is made by both the long bones and short bones.
Normally, the height and span are nearly equal.
Clinical application
1) Diseases affecting mainly long bones will affect the span more than the
height.
2) Diseases affecting mainly the short bones will affect the height more
than the span.

Head Circumference
The skull circumference is measured by a tape from the forehead just above
the supra- orbital ridge, passing just above the auricles of the ears, to the
farthest point on the occiput.
o At birth: It is 35 cm.
o At 6 mo of age: It is 43 cm (8 cm increase).
o At 1 yr of age: It is 47 cm (4 cm increase).
o At 2 yr of age: It is 49 cm (2 cm increase).
o At 4 yr of age: It is 50 cm (1 cm increase).
o At 12 yr of ag: It is 52-55 cm.
The skull circumference increases about 14 cm during the first 2-years of age,
reflecting the rapid development of the brain during this period.

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 Chest Circumference

o At birth, the head circumference is greater than the chest circumference.

o By six months of age they become equal.

o At the of age one year the chest circumference becomes greater than that of
the head.

 At birth: It is 33 cm.
 At 6 mo of age : It is 43 cm.
 At 5 yr of age: It is 56 cm.

Teeth Eruption
Time of eruption of deciduous teeth

Mandibular Maxillary
Central incisor 6 ½ mo 7 ½ mo
Lateral incisor 7 mo 8mo
Canine 16-20 mo 16-20 mo
First molar 12-16 mo 12-16 mo
Second molar 20-30 mo 20-30 mo

Exfoliation begins at 6 years to 12 yrs.

Time of eruption of permanent teeth

Mandibular Maxillary Mandibular Maxillary
Central incisor 6-7 yr 7-8 yr 2nd premolars: 11-12 yr 10-12 yr
Lateral incisor 7-8 yr 8-9 yr 1st molar: 6-7 yr 6-7 yr
Canine 9-10 yr 11-12 yr 2nd molar: 11-13 yr 12-13 yr
1st premolar 10-12 yr 10-11 yr 3rd molar: 17-21 yr 17-21 yr

The timing of dental eruption is poorly correlated with other processes of growth
and maturation.

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 Bony Maturation
Bone age equals to the chronologic age of the normal individuals. Bone age is
determined by the time of appearance of the ossific centers and the time of
complete fusion. Reference standards for bone maturation facilitate estimation of
bone age.
Time of ossific centers appearance in the X-ray
1) At birth: The ossific centers at the lower end of femur and the upper end of
tibia are usually present at birth.
2) At the age of 3 weeks: The ossific center appears in the head of humerus.
3) At the age of~2 mo- 6 yr: The ossific centers of the carpal bones in the wrist
appear successively, approximately one center per year.
Bone age in years may be calculated as 1 + number of ossific centers in the
wrist.

Time of complete fusion in skeletal areas during adolescence

1) Elbow: It is complete fusion at 15 yr of age in boys (13yr in girls).
2) Knee: It is complete fusion at l8 yr of age in boys (16 yr in girls).
3) Shoulder and hip: It is complete fusion after the age of 18 yr in boys
(18yr in girls).
During adolescence, the skeletal maturation is linked more closely to sexual
maturity than to chronological age. It is more rapid in girls than boys.
Clinical application (discrepancy between the chronologic age and bone age)
1) Retardation of bone age: The bone age is lower than the chronologic age in

the following conditions; prematurity, undernutrition, rickets, and endocrine

hypofunction such-as hypoituitarism and hypothyroidism.
2) Advanced bone age: The bone age exceeds the chronologic age. Precocious

puberty (excess sex hormones enhances skeletal maturation) is the most

common cause.

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 Subcutaneous Fat Thickness

The thickness can be measured by a special device.

The skin fold over the triceps to assess the limb fat.
The skin fold over the anterior superior iliac spine.
The skin below the scapula to assess the trunk fat.
Clinical significance:
1) Increased amount of fat during the first year of life: The person may
become obese.
2) Cushing syndrome: The disease is associated with obesity, especially over the
trank.
3)Reduced amount of fat:
o The fat is the most adaptable organ to changes in nutritional state.
o Short-term stress (malnutrition or infection) is associated with decrease of the
contents of the adipose cells.
o long-term stress (malignancy) is associated with decreased number of the
adipose cells (cachexia).

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 physiologic and Structural Growth

(1)Average Pulse Rates, Respiratory Rates, and Blood Pressures at Rest

during Infancy, Childhood, and adolescence

Pulse Rate Respiratory Rate Blood Pressure

Age Group
(per min) (per min) (50th percentile )
Newborn 125 55 80/55
6 months 120 40 90/55
1 year 120 35 90/55
4 years 100 25 90/55
10 years 90 20 105/65
Adolescence (15 years) 80 20 115/65

(2)The lymphoid tissues develop rapidly, reaching adult size by 6 yr of age and
continuing to hypertrophy throughout childhood and early adolescence before
receding to adult size.
(3)The development of the paranasal sinuses continues throughout childhood.
 The ethmoids, maxillary, and sphenoid sinuses are present from birth.
 The frontal sinuses first appear radiologically around 6 yr of age.

(4)The serum alkaline phosphatase level increases during periods of rapid bone
growth.

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 Developmental Milestones
Mental Development

The following aspects of mental development are the most important.

1) Development of hearing, vision, and speeeh.
2) Development of sphincter control.
3) Social adaptation as smiling, recognition of parents and relatives, and
recognition of the surroundings.
4) Learning ability in school.
Brain development Is also important for the development of the motor system.

Development of hearing

1. At birth: Hearing is impaired because the middle ear Is filled with amniotic fluid.
2. The 1st and 2nd months: The infant responds to loud sounds and noises by
sudden jerky movement (Moro reflex) and by crying.
3. The 3rd and 4th months: The infant responds to loud sounds and noises by
cessation of movements and stopping of crying.
4. The 5th and 6th months: The infant turns his head towards the direction of voice.
5. At 1 year of age: The hearing ability is fine.

Development of vision

1) Neonatal period: Doll’s eye movement of eyes on turning of the body.

2) At 2nd and 3rd months: The infant watches persons and follows moving objects
180 degrees.
3) After 8th month: The infants can differentiate different colors of light.

Mohammed 9
 Development of speeeh

It occurs in 3 successive stages:

(1) vocalization (2) babbling (3)true verbal articulation.
1) localization stage (the first 6 mo of age): Simple production of sounds by
the vocal cords. Crying and sounds of no meaning are examples of this stage.
2) Babbling stage (7-10 mo of age): Babbling begins with many syllable
(ba-da-ma), and then repetitive consonant sounds (mama, dada) are
articulated at the age of 10 mo.
3) True verbal articulation (words, proper speech)
The develment of proper speech depends on 3 integral functional units:
1. good hearing ability.
2. memorization (good mentality).
4) production of sounds that requires peripheral articulation (by the lips, tongue,
larynx,..etc):
Disturbances in any one of these will prolong the babbling stage and delay
the verbal communication.
 At the age of 1 year : Meaningful few words besides mama and dada" are formed.
 At the age of 15 mo: The infants use average 4-6 words and point to major body
parts. Most communication of wants and ideas continues to be nonverbal.
 At the age of 18 mo: Average 10-15 words and they name pictures.
 At the age of 2 year: The number of words increases to 50-100. The verbal language
marks this period; the children combine 3 words together “give me the ball
 At the age of 2 ½ year: The child knows his/her full name .
 At the age of 3 year: The child knows age and sxe; counts 3 objects correctly;
repeats 3 numbers or a sentence of 6 syllables.
 At the age of 5 year: The child names 4 colors, repeats sentence of 10 syllables,
counts 10 pennies correctly.
 At the school age: School makes increasing cognitive function, language

Mohammed 10
 development and learning abilities (reading , writing, basic mathematics skills).

Development of sphincter control

The development of sphincter control requires:
1. central nervous system maturation .
2. training.
3. encourage the child to go to the bathroom when ever he feels the urge to urinate
or defecate.
4. should not try to postpone this urge.
5. Avoid punishment and reward child for being dry (notification and smiles,
hugs, and kisses from every one in the family when the child is dry).
6. Refusal to defecate in the toilet or potty is relatively common:
 Defusing the issue by a temporary cessation of training (and return to diapers)
often allows toilet mastery to proceed.
 Bladder and bowel control emerge during the preschool years(average age 2 ½ yr).
 Day time bladder control typical precedes bowel control, and girls precede boys.
 Bed wetting is normal up to the age 4 yr in girls and 5yr in boys.

Development social adaptation

 At 2 mo of age : The infant smiles on social contact and listens to voice.
 At 3 mo of age : The infant continues social contact and listens to music.
 At 4 mo of age : The infant laughs out loud, may show displeasure if social
contact is broken, and become excited at sight of food.
 At 6 mo of age : The infant recognizes mother.
 At 10 mo of age : The infant responds to sound of name and waves bye-bye.
 At 1 mo of age : The infant plays simple ball game and makes postural
adjustment to،dressing.
 At 15 mo of age : The infant indicates some desires or needs by pointing.
 At 18 mo of age : The infant feeds self, seeks help when in trouble, may
complain when wet or soiled, and kisses parent.
 At 2 yr of age: The child handles spoon well, helps to undress, and listens to
stories with pictures.

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  At 3 yr of age: The child plays simple games, helps in dressing (unbuttons
clothing and puts on shoes), and washes hands.
 At 4 yr of age: The child plays with several children and goes to toilet alone.
 At 5 yr of age: The child dresses and undresses and asks questions about
meaning of words.
 At school years: The social and emotional development proceeds in three
contexts:
1) The home.
2) The school.
3) The neighborhood.
- The home remains the most influential. the parent-child relationship
'٧<
continues to provide a secure base from which children can venture forth.
- The beginning of school "coincides with a child’s further separation form
the family and the increasing importance of teacher and peer relationships.
- The friendships may persist for months or years, experience with a large
number of superficial friendships, and antagonisms contributes to a child’s
growing social competence and actual social skills.
[
During adolescence:
 In early adolescence, the trend toward separation from family with
increasing involvement in same-sex peer activities accelerates.
 puberty commonly results in strained relationships between adolescents and
their parents.
 As part of separation, adolescents may become distant from parents,
selecting adults outside of the family as role models (teacher or the parents
of other children), and redirecting- emotional and sexual energies toward
peer relationships.
 The need to belong to the same-sex declines.
 Physical attractiveness and popularity remain critical factors in both peer
relationships and Self – esteem.

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 Motor Development

The development of motor system depends entirely on three factors:

1. The development of central nervous system.
2. The development of the peripheral motor system (bones, joints and
muscles).
3. Training.
 Neonatal period: The infant lies in flexed attitude and turns head from side to
side.
 At 2 mo of age: The infant raises head slightly when on prone position and
the head lags on pulling the infant to sitting position when on supine
position.
 At 3 mo of age: The infant lifts head and chest when on prone position.
 At 4 mo of age: Head support and he enjoys sitting with full truncal support.
 At 6 mo of age: Sitting freely and leans forward on hands starting crawling.
 At 10 mo of age: The infant creeps or crawls and starts walking with support.
 At 1 yr of age: The infant stands up independently, walks with one hand held,
and takes several steps.
 At 15 mo of age: The infant walks alone and crawls up stairs.
 At 18 mo of age: The infant runs stiffly and walks up stairs with one hand
held.
 At 2 yr of age: The child runs well and walks up and down stairs (one step at
a time), opens doors, climbs on furniture, and jumps.
 At 2 ½ yr of age: The child goes UP stairs with alternating feet.
 At 3 yr of age: The child rides tricycle.
 At 6 yr of age and onwards: Muscular strength and coordination increase
progressively as does the ability to perform fine motor movements as writing
and drawing.

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 Sexual Development
Normal Embryonic Sexual Differentiation

During the first, 6 weeks of the embryonic period

1) The gonads: They are undifferentiated (ovotestis).
2) The internal sex organs: Two sets of primitive duct system are present:
 The Wollfian (male).
 Mullerian (female) duct systems.
3) The external genitalia:
1. A knob-like genital tubercle (that forms penis or clitoris).
2. urogenital groove flanked by urethral folds and labioscrotal swellings.
 The normal sexual differentiation occurs between 6th-14th weeks of
gestation..

Development of the male phenotype (genotype 46, XY)

 Maleness requires a Y chromosome which directs the undifferentiated
gonads to become a testis (at ~6th wk gestation).
 The testis secretes testosterone by Leydig cells and anti-mullerian hormone
(AMH) by Sertoli cells.
 The testosterone initiates the development of the Wollfian duct into the
internal sex organs (1.epididymis, 2.vas deferens and 3. seminal vesicle) and
is responsible for the differentiation of the external genitalia to develop as
penis ،fusion of urethral folds to form penile urethra) and scrotum (fusion of
the labioscrotal folds).
The AMH causes the Mullerian ducts to regress at 6th-7th wk of gestation.

Development of the female phenotype (genotype 46, XX)

1. In the absenee of ¥ chromosome, the undifferentiated gonads develop into
ovaries.
2. In the absence of ¥ chromosome, and testosterone, the wollfian duct system
will regress, and the external genitalia remain without virilization.
3. In the absence of AMH, the Mullerian duct system develops into:
1. two fallopian tubes.

Mohammed 14
 2. Uterus.
3. vagina.

The Puberty
Physiology of puberty
 The prepubertal stage: Between early childhood and approximately
8-9 yr of age, the hypothalamic-pituitary-gonadal axis is dormant as reflected
by undetectable serum concentrations of LH and sex hormones (estradiol in
girls and testosterones in boys).
 FSH is detectable in most children
 The peripubertal period: 1-3 yr before the onset of puberty becomes
clinically evident:
1. FSH and LH levels are low but measurable.
LH secretion occurs in pulsatile fashion during sleep due to episodic
discharge of gonadotropin-releasing hormone.
2. Adrenarche: Adrenal cortical androgens are responsible for the appearance of
sexual hairs (axillary and pubic hairs).
The androgens begin to rise before the earliest physical changes of puberty.
 With the onset of puberty (after the age of8yrin girls and 9 yr in boys)
LH and FSH increase progressively in the blood and they act synergistically
to promote enlargement and maturation of the gonads and the secretion of sex
hormones.

Factors affecting the age of onset of puberty :

1. Osseous maturation: The onset of puberty is more closely correlated with
osseous maturation than with chronologic age.
Diseases causing retardation of osseous maturation (bone age) can affect the
age of onset of puberty.
2. Genetie faetors: Familial.
3. Race: Black girls are more advanced in development of secondary sex
characteristics than white girls.
4. Environmental factors: Climate?
5. Nutrition and general health: Good nutrition and general health leads to

Mohammed 15
 earlier pubertal changes than children with bad nutrition and general health.
6. Body weight and composition: Girl athletes (swimmers, runners, gymnasts,
dancers) in whom leanness and strenuous physical activity have coexisted from
early childhood frequently exhibit a marked delay in puberty or menarche.

general features of puberty:

1) The enlargement of the internal sex (the somniferous tubules, epididymis,
seminal vesicles, and prostate in boys) and the ovaries, uterus, and
thickening of the vaginal mucosa in girls).
2) The development of the secondary sex characteristics (breast in girls) (
growth of testes and thinning of scrotum in boys) and (the sexual hairs in
both).
3) The adolescent growth spurt: Rapid increase in the height during the
period of adolescence.

The signs of puberty

Girls: The first visible sign of puberty is the (1) appearance of breast buds (8-
13 yr) and breasts increase gradually in size with the development of the
areola and nipples. (2) Menses typically begin 2-21/2yr later (the mean age of
menarche is about 12 yr).
Boys: The first visible sign of puberty is the enlargement of testes which begins
as early as 9 ½ yr.
The prepubertal testicular volume is 1, 2, or 3 mL in volume or less than 2.5
cm in longest diameter.
The testicular volume increases during the pupertal period gradually from
4_mL to the adult size.
This is followed by pigmentation and thinning of the scrotum and growth of
penis.

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 Boys typically begin their linear growth acceleration (the height) 2-3 yr later
than girls and continue their linear growth for ~2-3 yr after girls have
stopped.
The growth accelerates up to 6-7 cm per year in boys and may continue
beyond 18 yr of age, whereas it is up to 8 cm per year in girls and then slows
to a stop at 16 yr.
The pubic hair in both sexes starts to appear as scanty, straight, and slightly
pigmented hairs and then it becomes darker and starts to curl.
The adult distribution is triangular and spreads to the medial surface of
thighs.

Factors Affecting Growth and Development

1) Genetic factors: They may affect:

A- The rate of growth.

B- The stature of the individual in adulthood.

C- The age of menarche, and the level of intelligence.

The race: It is closely linked to genetic factors; the growth rate and final height
differ greatly from one country to another (Japanese children differ in growth than
American children). Local growth charts are available for each country.

Certain genetic and hereditary diseases: They may affect the growth and
development e.g., trisomy 21, phenylketonuria, galactosemia, and congenital
myopathy. Some of them are treatable, and others can be avoided by genetic
counseling.

2) Sex: The growth rate of females differs than that of males. Growth charts are
available for boys and others for girls.

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 3) Perinatal factors: The perinatal factors may play a role in the future growth
and development. These factors include the maternal age and nutrition,
infections during the pregnancy, and duration of gestation and the birth weight.

4) Nutrition: Malnutrition results in growth retardation, delayed puberty, and may

affect the mental function (iron deficiency anemia).

5) Socioeconomic factors: These factors include the food supply, education,

housing, exposure of infections, and the availability of services.

6) Chronic systemic diseases: The cardiac, pulmonary, renal, and gastrointestinal

diseases as well as infections are usually associated with growth retardation.

7) Visual or auditory impairment usually hinders the development of the

children.

8) Endocrinal factors.
(a) Hormones with a direct effect on growth and development
 Growth hormone is responsible for the longitudinal growth of bones (the
linear growth).

 Thyroid hormone is essential for physical, mental, and sexual growth and
development.

 Sex hormones are essential for sexual growth and maturation.

(b) Hormones with an indirect effect on growth and development
 Insulin: It has a growth promoting effects on tissues and organs. Infant of
diabetic mother with hyperinsulinism is large for date.
 Glucocorticoids: They are required for optimum normal growth. However,
excessive amounts (e.g., Cushing syndrome) are associated with linear
growth retardation (short stature).

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 Assessment of Physical Growth

Growth assessment is an essential component of pediatric health surveillance.

The most powerful tool in growth assessment is the growth charts.

1) Growth curves: Curves demonstrating the different parameters of growth

(height, weight, and head circumference) of the same person in the successive
years.

a. Distance growth curve: The height attained at each year:

50 tm at birth, 75 cm at the age of 1 yr, 89 cm at the age of

2 yr, 100 cm at the age of4 yr,..etc.

b. Velocity growth curve: The height gain in cm per year: 25 cm during the first
year of life, 14 cm during the second year of life.

2) percentile growth curves: They are designed because of the wide range of
normal variations in growth parameters and the requirement to compare these
parameters to those of healthy children of the same age, sex, race, and
environment.

percentile growth curves are available for height, weight, and head
circumference for boys and others for girls.

How to create a percentile growth curve (an example is demonstrated)

 Bring 100 normal healthy children at the age of 6 yr (from the same school),
measure their heights, and categorize them in the following 7 groups (levels or
percentiles on the chart).

 50th percentile (the average = the median): The level at which 50% of these
heights are below it and 50% are above it.

 25th percentile (below average): The level at which 25% of these heights are
below it and 75% are above.
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  10th percentile (low normal): The level at which 10% of these heights are
below it and 90% are above it.

 5th percentile (lowest normal): The level at which 5% of these heights are
below it and 95% are above it.

 75th percentile (above average): The level at which 75% of these heights are
below it and 25% are above it.

 90th percentile (high normal): The level at which 90% of these heights are
below it and 10% are above it.

 95th percentile (highest normal): The level at which 95% of these height are
below it and 5% are above it.
The percentile growth curves measure the height, weight, and head circumference
of normal healthy children of the same age, sex, race, and environment.

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 See Causes in pediatric Neurology

CDC Growth Charts: United States

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 How to assess the physical development of a child

1. Is he normal?: Measure the height (for example) of the child and apply it on the
percentile growth curve; a normal child should lie between the 5th and 95th
percentiles.
Short stature is diagnosed when the height of this child lies below the 5th
percentile. Tall stature is documented when the height is above the 95th
percentile.
2. Is he growing normally?: Follow the height of the child on the curve (serial
estimations); a normal child should follow the same percentile level. Marked
deviation away from this percentile level is abnormal and should be
investigated.
3. All the growth parameters of this child (height, weight, and skull
circumference) should follow more or less the same percentile level (i.e., the
10th percentile).
4. Severity of malnutrition: When growth parameters fall below the 5th
percentile, it becomes necessary to express the values as percentages of the
median or average value (50th percentile). For example, a 12 mo old girl
weighing 6.2 kg is 65% of the median weight (9.5 kg at the 50th percentile) for
her age. The growth failure can be graded as moderate wasting from the
following grading system.

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 Severity of Malnutrition: Stunting and Wasting
Grade of Weight for Age Height for Age
Malnutrition (Wasting) (Stunting)

Normal >90% >95%

Mild 75-90% 90-95%

Moderate 60-74% 85-89%)

Severe <60% <8-5%

Weight for length or height curves: Weight for stature percentile curves are also
available with the weight in kilograms is plotted against length or height in
centimeters.
According to the chart, the standard weight for a girl measuring 110 cm is 18.6 kg
(at the 50th percentile).
Weight for height below the 5th percentile is the single best growth chart indicator
of acute undernutrition (the child loses weight during a recent condition with an
unaffected height). Children who have been chronically malnourished may be
short as well as thin, i.e., both parameters arc affected equally and their weight for
stature curves may appear relatively normal.

Body mass index (BMI): BMI can be calculated as weight per height when
weight is in kilograms and height is in meters. Growth percentile charts are
available for BMI.
 A BMI over the 95th percentile indicates overweight.
 Between 85th and 95th percentile is at risk of overweight.
 Below 5th percentile is underweight.

Mohammed 23
 Catch-up growth (canalization): It is the period of accelerated growth following a
period of growth arrest. This pattern of growth enables the infants or children
(through self regulatory mechanisms) to accelerate their growth velocity once the
insult is removed (recovery from gastroenteritis or malnutrition), so that they can
re-attain their target percentile of growth (complete catch-up growth).

Abnormal physical growth (<5th percentile or>95 percentile) include

1. Abnormalities of the height: Short stature and tall stature.
See causes in pediatric Endocrinology.
2. Abnormalities of the weight: Underweight and obesity.
See causes in Pediatric Nutrition.
3. Abnormalities of the skull eireumference: Microcephaly and macrocephaly.

Mohammed 24
 Assessmentof MentalorIntellectual Development

The assessment is made by The Following:

1) Evaluation of social development (in infancy).
2) Speech development (in early childhood).
3) Learning ability or school achievement(in late childhood).
 Screening for language delays (in early childhood 0-6 yr of age) is particularly
important because of the strong links between language and cognitive
development and later school performance.
 Another procedure that can be useful for developmental screening is the draw-
a-person test and the kinetic family drawing “draw your family, with everybody
doing something”.
Abnormality in development: Mental retardation (marked deviation from the
normal average) may occur due to several genetic or monogenetic causes.

AssessmentofMotorDevelopment
1) The assessment of motor development is made by:
(1) evaluation of gross motor Skills (in infancy).
(2) Refined motor skills (in early childhood).
(3) Fine motor skills (in late childhood).
2) Abnormality in development: Delayed motor development (marked deviation
from the normal average) may occur due to mental retardation, cerebral palsy,
or gross environmental factors (rickets or malnutrition).

Mohammed 25
 AssessmentOfSexualDevelopment

1) Examination for the enlargement of the internal sex organs by

ultrasonography.
2) The development of the secondary sex characteristics by apply the findings
to special grading systems (as sexual maturity rating {SMR} with 5 stages of
development; designed by Tanner JM, 1962).
3) The assessment of adolescent growth spurt by the percentile curves.
4) Abnormality in development: Delayed puberty and precocious puberty.

Mohammed 26
 Pediatric Nutrition
Nutritional Requirements
Adequate to nutrition during the is 1st year of life leading to dramatic growth and
development.
Failure to provide adequate nutrients during this time is likely to have adverse
effects on development as well as growth.
Adequate diet
An adequate diet should fulfill these basic criteria.
1. Adequate total caloric value (energy) according to the age and weight of the
individual.
2. Adequate quantity and proportions of proteins, carbohydrates, and fats.
3. Adequate amounts of vitamins, minerals, and electrolytes.
4. .Adequate amounts of water.

Energy Requirement
Calories taken by the body are needed for:
1. maintenance of basal metabolism(50% of total caloric intake).
2. Physical activity (25%).
3. Physical growth (12%).
4. Fecal loss in the form of unused food (8%).
5. Specific dynamic action of food(5%).
Energy should be supplied as]~ 50% from carbohydrates, 30% from triglycerides,
and less than 10% from saturated fatly acids (linoleic acid and a-linolenic
acid),portion 15%.

The Recommended Daily Total Caloric Intake for Different Age Groups

Pediatric Age Group Calories

Newborn 125 calories/ kg/ day
l-12mo 100 calories/ kg/ day
1-3 yr 85 calories/ kg/ day ‫م‬
Moderately active 4-6 yr old children 1,600 calories per day
Moderately active 6-10 yr old children 2,200 calories per day
Active teenage boys At least 2,800 calories per day
Adults 40 calories/ kg/day

Mohammed 27
 Protein Retirement
 Essential amino acids:
These include the (9) essential amino acids know for adults:
1.leucine.2.Isoleucine , 3.valine, 4.threonine,5.methionine, 6. phenylalanine,7.
tryptophan, 8. lysine, 9. Histidine, 10. Others 1.cysteine, 2.tyrosine, 3. Arginine.
they are necessary for building up new tissues.
They cannot be formed in the body.
Non essential amino acids:
 These amino acids can be synthesized in the body either from essential amino
acids or from carbohydrates.
 They should be taken in the diet because in their absence, more essential
amino acids will be needed to supply these amino acids.

High biological value proteins:

 They contain all essential amino acids in big amounts and in good
proportions.
 They are of animal origin e.g., milk, milk products, eggs, meat, fish, and live.
Low biological value proteins:
 They do not contain all essential amino acids or contain them in small
amounts or in unsuitable proportions.
 They are of plant origin e.g., cereals, and beans.

Daily Requirements:
 Protein requirement
 The recommended daily intake of protein is 2-2.2 g/ kg/ day for infants, less
amount is required during childhood (~1.5 g/ kg/ day), and ~1g/ kg/ day for
adolescents.
 The total protein content of human milk averages only approximately 1.2 g/ 100
mL(2OOmL human milk/ kg/ day should be ingested by the infant to meet the
daily requirement).
 The fresh bovine milk contains 3.5 g proteins/ 100 mL.
 The infant formula contains 1.7-3.4 g proteins/100kcal.
 The high quality and easy digestibility of human breast milk protein obviously
compensate for any quantitative deficiency.

Mohammed 28
 Carbohydrate Requirement
 The carbohydrates are the main source of energy.
 The minimal daily requirement of carbohydrates sufficient to prevent ketosis
and hypoglycemia is about 5g/ kg/ 24 hr. About 10 g/ kg/ 24 hr or more is
usually consumed.

Fat Requirement

 The fats are provide the essential fatty acids (linoleic acid and smaller amount
of a-linolenic acid).
 All are necessary for:
1. Energy production.
2. Development of central nervous system.
3. Development of Retinal photoreceptor membranes (cognitive and visual).
4. physical growth.
The daily requirement is 0.5-1 g/kg/24 hr.

Water Requirement

 a fluid intake of 150 mL/ kg/ 24 hr is recommended for infants, smaller

amounts are given for children and adolescents (l^70rnL/ kg/24hr).
 Because human milk and common formulas are at least 90% water, the infants
usually consume this amount during feeding and Usually need not additional
water for the first several months of life.

The Minerals and Vitamins Requirement

Calcium: It is essential for:

1. Mineralization of the bones and teeth.
2. cardiac action.
3. muscle contraction.
4. Nerve conduction.
5. Blood coagulation.

The daily requirement is~250 mg/24hr during infancy. 500 mg/ 24 hr for 1-3 yr old
children.750-1,000 mg 124hr thereafter.
Iron: lt is essential for the formation of:

Mohammed 29
  Blood hemoglobin and muscles hemoglobin.
 The normal infant is thought to have sufficient stores of iron to meet
requirements for4-6 mo.
 The daily requirement for infants 7mo of age or older and children is 10 mg/
24 hr.

Vitamin A: it is essential for healthy epithelium and formation of retinal pigments .

The daily requirement is 2,000 1U/ 24 hr.
Vitamin D: It is important for the regulation calcium-phosphorus metabolism and
daily mineralization of bone.
The daily requirement is 400-800 IU/ 24 hr.
Vitamin C: lt is essential for the formation of collagen fibers.
The daily requirement is 50 mg/24 hr.
Vitamin B1 (thiamine): The daily requirement is 0.5mg/24 hr.
Vitamin B2 (riboflavin): The daily requirement is 0.5mg/24 hr.
Folic acid: The daily requirement is 0.1-0.2mg/24 hr.
Vitamin B12 (riboflavin): The daily requirement is 0.5-1mg/24 hr.

Mohammed 30
 The Feeding of Infants during the First Year of Life
Types of milk feeding
I. Natural breast feeding
1. Mother’s milk.
2. Wet nurse milk.
II. Artificial bottle feeding
1. Powdered dried milk (infant formula).
2. Fluid animal milk.
III. Combined feeding
1. Complementary feeding.
2. Supplementary feeding.

Breast-feeding
Breast Feeding vs. Formula-feeding
 The most appropriate milk for the infant.
 Has practical and psychologic advantages.
 All mothers should be encouraged to at least consider breast-feeding her baby.

The breast gland

 The breast is a modified sebaceous gland made up of about (5-20 lobules)
separated by adipose tissues.
Each lobule consists of secretory alveoli (acini), each having a lactiferous
duct, which unite together forming a common lacteal duct which opens at the
nipple by a separate hole (l5-20 holes at the nipple).
 The size of the breast is mainly due to its fat and connective tissues content,
and this is not related to the secretory capacity of the breast.

Mohammed 31
 The lactation
1) Preparation of the breast during pregnancy
 This is achieved by the ovarian and placental hormones (estrogen and
progesterone).
 The main changes that occur in the breast during pregnancy are:
1. proliferation of duct epithelium.
2. Formation of new secretory alveoli.
3. Enlargement of the breast.
 Milk production does not occur during pregnancy because of the inhibitory
effects of ovarian and placental hormones on prolactin hormone secretion by
the anterior pituitary gland.

2) Initiation of milk secretion

Prolactin hormone: The milk production starts on the second day after delivery.
This is due to the release of prolactin hormone from the anterior pituitary gland after
lowering the estrogen and progesterone hormones levels as a result of placental
separation and delivery.

Other hormones: They are necessary to initiate and maintain milk production and
include :
1. Thyroxine hormone (general stimulant of cell metabolism).
2. Growth hormone (anabolic hormone).
3. Oxytocin hormone secreted by the posterior pituitary gland in response to
sucking the nipple and areola and is responsible for contraction of smooth
muscle fibers in the walls of the alveoli leading to expulsion of milk into the
ducts.

Mohammed 32
 3) Maintenance of milk sccretion.
This is affected by several factors
a. Regular and complete evacuation of the breast: This is the most important
stimulus of continuous milk secretion.
b. The nutritional state of the mother:
Milk from the mother will supply all the necessary nutrients, except fluoride,
vitamin D, vitamin K, and iron.
Weight-reducing diets should be avoided.
c. Psychological state of the mother:
 postpartum period is a time of great anxiety and insecurity, particularly
for the first-time mother because of the responsibilities of motherhood.
 Adequate continuous milk secretion requires desire of the mother to
breast-feed her baby and relaxed state of mind.
 Many women must be reassured that the breast Tone will be preserved
by the use of a properly fitted brassiere to support the breasts’during
the nursing period.

Mohammed 33
 Types of breast milk.

1. Colostrum (day 2-to-4).

2. Transitional breast milk (day 5-to-20)
3. Mature breast milk (the 4lh week onwards).

Colostrum

Definition: Colostrum is the secretion of the breasts during the first 2-to-4 days
after birth.
Advantages of colostrums feeding
1) Advantages related to colostrums itself.
 It is highly nutritive with high protein and mineral content and high caloric
value.
 It has a suitable composition: The composition of colostrums is close to that
of the tissues of the newborn, thus it represents a transition from intrauterine
nutrition to breast feeding.
2) Advantages related to sucking the breast early after delivery
1. Accustom the baby to the breast very early in life to promote maternal infant
bonding.
2. Stimulation of continuation of milk secretion via complete and regular
evacuation of the breast.
3. Involution of the uterus: This is due to the effect of oxytocin hormone.
4. Correction of minor deformities of the nipple e.g., small or inverted nipple.

Mohammed 34
 General characteristics
1. Color :Greyish yellow.
2. Consistency : Thick.
3. Reaction : Alkaline.
4. Amount : 40-60 mL/ day.
5. Caloric value : 1,500 calories/ day.
6. Composition
 Proteins : 4-8 g/100 mL (very high).
 Fats :3_g/100 mL (low).
 Carbohydrates :4g/ lOOmL (high).
 Minerals : 4 g/100 mL (high).

Mature Breast Milk

General characteristics
1. Color : White.
2. Consistency : Thin.
3. Reaction : Neutral.
4. Amount : Up to 1-2 liters/ day.
5. Caloric value : 67 calories/100 mL.
6. Composition
 Proteins : 1.2 g/ l00 mL.
: Lactalbumin and lactglobulin {whey}:casein is 80: 20
 Fats : 3.8 g/ 100 mL (triglycerides, linoleic acid, and a-linolenic acid)
 Carbohydrates : 7 g/100 mL (beta lactose is the main carbohydrate).
 Minerals : 7 g/100 mL (beta lactose is the main carbohydrate).
Water :0.5g/100 mp (low))
p
:90 mp/100 mp.

Transitional Breast Milk

The milk is whiter and thinner than the colostrum, and the protein content is less
than that of colostrum.

Mohammed 35
 Quality of breast milk
1) Proteins: The amount of soluble proteins (lactalbumin and lactglobulin) is much
more than the amount of insoluble protein (casein). This factor renders the protein
of breast milk easily broken down and digested.
2) Fat :
 The fat globules are of small size, this renders them easily acted upon by the
digestive enzymes.
 High content of lipase enzyme helps the intestinal lipolytic enzyme in
digesting fat.
 It contains small amounts of volatile fatty acids (not irritant to GIT).
3) Carbohydrates: Beta lactose facilitates the growth of lactobacilli which prevent the
growth of pathogenic organisms.
they synthesize vitamins K and B complex.
4) Minerals content: Although small amounts of calcium and phosphorus are present,
optimal Ca/P ratio (2:1) is very suitable for their complete absorption and
utilization.

N.B : Although human milk contains less iron than most infant formulas, iron deficiency is
less common in breast-fed infants because of its higher bioavailability.
5) Adequate amounts of vitamins A and B complex.
6) Reaction: It is neutral and this fits very well with the weak acidity (hypochloridria)
of the infant’s stomach.

Advantages of breast feeding

1. Advantages related to milk itself

1) General advantages
 Availability: It is available whenever needed and wherever the mother may be.
 Proper temperature of the breast milk (no need for heating).
 Economic benefit: It is cheap.
 Sterilization: It is free from bacterial contamination.

2) Nutritional advantages .
 Adequate composition.
 Constant composition.
 Adequate quality.

Mohammed 36
 3) Protective advantages .
1. High antibody concentrations against bacteria and viruses
 Local GIT immunity: Secretary IgA prevents the microorganisms from adhering
to the intestinal mucosa, reducing the incidence of diarrhea among breast-fed
infants.
 Systemic immunity: Different immunoglobulin's account for the lower incidence
of otitis media, pneumonia, bacteremia, and meningitis during the 1st year of life
in breast-fed infants vs. formula-fed infants.
2. Substances that inhibit growth of many common viruse.
3. Macrophages in human milk may synthesize complement, lysozymes, and
lactoferrin.
 Complement is essential for immunity.
 Lysozymes are enzymes that attack the bacterial cell wall.
 Lactoferrin is has an inhibitory effect on the growth of E. coli in the intestine.

4. Bile salt-stimulated lipase: It kills Giardia lamblia and E. coli.

5. Low pH of the stool of breast-fed infants favors the growth of intestinal
flora (bifidobacteria and lactobacilli) which help protect against E. coli
infections.

II. Advantages related to sucking the breast and not taking the bottle
1. Less technical difficulties: No need for sterilization of the containers.
2. Psychological advantages: The mother is personally involved in the nutrition
of her baby, resulting in a feeling of being essential and a sense of
accomplishment while the infant is provided with a close and comfortable
physical relationship with the mother.
3. The amount is self-regulated (need no calculation).
4. Better physical care of the infant.
5. Better involution of the uterus.

Mohammed 37
 Disadvantages of breast feeding
1) Allergic reactions: They may occur either due to milk itself or due to
allergens ingested by the mother.
2) Minor gastrointestinal symptoms (colic or loose stool): They may occur on
ingestion of some foods by the mother (berries, tomatoes, onions, members of
the cabbage family, chocolate, spices, and condiments).
3) Transmission of microorganisms
o Transmission of viruses: AIDS (HIV) virus, cytomegalovirus, rubella
virus, hepatitis B virus, and herpes simplex virus.
o Transmission of bacteria: It can occur via infected fissured nipples or
mastitis.
4) Hemorrhagic disease of the newborn: It is due to low vitamin K content of
human milk.
5) Breast milk jaundice: See Neonatology.

Program of Breast Feeding

 Initiation of feeding
 Feedings should be initiated as soon after birth as possible. Glucose 5% in
water or sweetened fluids should be given initially to exclude tracheo-
esophageal fistula.
 Most infants can start breast-feeding shortly after birth, within 4-6 hr.
 In respiratory distress feedings should be withheld until the infant is carefully
evaluated.
 Intravenous fluids should be given if feedings must be withheld for several
hours.
 Demand feeding: Initially, the feeding schedule should be based on this
“self-regulation” by the infant, with considerable variation in the time
between feedings and in the amount taken per feeding.
 Regular feeding: Most infants will have established regular schedule by
1 mo of age (feeding about every 3 hr during the day and night).

Mohammed 38
 Technique of breast feeding
 At feeding time
The infant should be hungry, fully awake, dry, and warm.


 The baby should be held in a semi-sitting position to prevent vomiting with

eructation and should be supported comfortably with the face held close to the
mother’s breast by one arm and hand while the other hand supports the
breast, making the nipple easily accessible to the infant’s mouth without
obstructing nasal breathing .
 The infant’ lips should engage considerable areola as well as nipple.
 The mother should be comfortable and completely at ease.
 Several reflexes that facilitate breast feeding are present at hirth:
1) Rooting reflex is the first to come into play; when the infant smells milk or the
cheek is touched by a mother’s breast or nipple, the infant will turn toward the
breast and open his or her mouth in anticipation of grasping the nipple.
2) Sucking reflex is the process of squeezing the sinuses of the areola rather than
simply sucking on the nipple.
3) Swallowing reflex is stimulated when milk is in the infant’s mouth.
4) Let down or milk ejection reflex
 The breast-feeding infant’s sucking results in afferent impulses to the
mother’s hypothalamus and, then, to both anterior and posterior pituitary.
 Prolactin hormone stimulates milk secretion by the acini or alveoli of the
breast.
 Oxytocin hormone stimulates contraction of the myoepithelial cells
surrounding the alveoli and “squeezes” milk into the larger ducts, where it
is more easily available to the sucking infant. Milk flows from the opposite
breast as the infant begins to nurse.
 This reflex is often absent during the periods of pain, fatigue, or emotional
distress: i.e mother should avoid feeding.

 Duration of breast feeding

 The infants should be allowed to suck until satisfied. Some infants will empty a
breast in 5 min; others will_ nurse more leisurely, sometimes for 20 min or
longer. Most of the milk is obtained early in the feeding (i.e., 50% in the first 2
min and 80-90% in the first 4 min).

Mohammed 39
  One or both breasts per feeding
 Both breasts should be used at each feeding in the early weeks to encourage
maximal milk production.
 After the milk supply is established, the breasts may be alternated at successive
feedings. The infant will usually be satisfied with the amount obtained from one.
 If milk secretion becomes too great, both breasts may be offered at each feeding
but incompletely emptied, thereby decreasing milk production.

 At the end of nursing

Mothers should know that the infant who is not hungry will not search for the nipple
or suck. The infant should be held erect over the mother’s shoulder with gently
rubbing or patting the back to assist in expelling swallowed air (eructation of air).
 Frequency of feedings

 Most infants want to be fed every 2-4 hr (the time required for an
infant’s stomach to empty may vary from 1-4 hr during a single day).
 Nursing less than 2 hr may inhibit prolactin secretion and decrease
milk production.
 By the end of the 1st week of life, most healthy infants will want 6-9
feedings/ 24 hr, and by 9-12 mo of age, most will be satisfied with 3
meals/ day plus snacks.

Two-hourly feeding: It may be also indicated in the following conditions

 The first 2 weeks of life to:
1. stimulate milk production.
2. accustom the baby to the breast.
3. induce involution of the uterus.
 Premature infants to compensate for the small volume of the feed (easy
fatigability).
 Scanty breast milk.
 Protein-energy malnutrition.
 Weak sucking power.

Four-hourly feeding: It may be also indicated in the following conditions

Mohammed 40
  Infants over 4 mo of age.
 Abundance of breast milk.
 Overfed obese infants.

Mid-night feeding
The normal night break through from 12.00 mid night to 6.00 A.M. is essential
because it provides.
 General rest to the mother and local rest for her breast.
 General rest to the infant and local rest for his gastrointestinal tract.
 Sweetened fluids may be offered instead of breast if the infant cries.

 Expression of breast milk

It is useful to relieve engorgement of the breasts, and pointed by:

a. Manual expression of breast milk.
b. Battery-operated or electric breast pump.
 Pumping can increase milk production (complete evacuation of the breast)
and relieve sore (fissured or cracked) nipples. Breast milk can be safely stored
in the refrigerator and used for feed in the infant at a later time.

 Determining adequacy of milk supply

The amount of milk secreted by the breast can be evaluated from the following
clinical criteria
1) General behavior: Satisfied infant releases the breast spontaneously at the end
of feeding and sleeps 2-4 hr between feedings.

Unsatisfied infant does not go to sleep or awakens after 1-2 hr and becomes
irritable and crying all the time.
2) Weight gain: Adequate weight gain is noticed with good feeding (150-200
gm/ wk during the first 4 mo of life, -125 gm/ wk during the next 4 mo, and -60
gm/ wk during the last 4 mo of the 1st yr of life).
3) The number of motions and consistency of stools: Satisfied infants passes 1-
4 semisolid stools perday, Underfeeding is associated with constipation (one
motion every 36 hr or more) and small hard stools.

Mohammed 41
  Three possibilities should be excluded before assuming that a mother cannot
produce sufficient milk:
1. Errors in feeding technique.
2. Maternal factors related to diet, rest,or emotional distress.
3. Physical disturbances of the infant (diseases) that interfere with
nursing or with weight gain.
 Small gains may worry the mother and this may diminish her milk supply. In
addition, the mother may give the infant a bottle to reassure her, and this in
turn, further diminish milk production and may discourage breast-feeding.

Duration of breast feeding

Breast feeding can be continued for2years. Exclusive breast milk for(more)than 6

mo of age without supplementation is associated with iron deficiency anemia and
rickets.
 Fresh animal milk can be provided after the age of 1 yr.
Hygiene
 Proper hygiene will help prevent irritation and infection of the nipples. The
breasts should be washed at least once a day, using a non drying soap.
 The nipple area should be kept as dry as possible. The mothers are more
comfortable, wearing a properly fitted brassiere day and night and an
absorbent pad or clean cloth ,should be placed inside the brassiere to
absorb any leaked milk.
 Mcdicinal supplements

Vitamin D, iron, and extra calcium supplement should be administered on the 4th mo
of age onwards to compensate for their deficiencies in the breast milk.

Minor problems during the first weeks of breast feeding

1- Fissuring or cracking of the nipples (tender or sore nipples):
 Improper hygiene of the nipples, leaving nipples wet after nursing,
improper positioning of the infant during nursing, or breast
engorgement lead to sore nipples.

Mohammed 42
  If nipple tenderness is sufficient to make the mother apprehensive, the
milk ejection reflex may be delayed, that, in turn, leads to increasingly
vigorous nursing, which further injures the nipple and areolar area.

Management:
1. Exposing the nipples to air.
2. frequent feeding the infants and in different positions.
3. manual expression of the breast.
4. keeping the breast dry between feedings.
5. appropriate cream application.
6. avoidance of irritant agents (soap, alcohol, tincture of benzoin).

Breast engorgement: Maternal or infant illness, sore nipples, or improper feeding

technique lead to incomplete evacuation of the breast that, in turn, can reduce milk
production.
Management: Expression of breast milk (manually or by a pump) can avoid this
condition.
Insufficient breast milk: Infants who awaken and cry consistently at short intervals
may not be receiving enough milk. It is important to appreciate that infants cry tor
reasons other than hunger (e.g., too much clothing; colic; soiled, wet, or
uncomfortable diapers; swallowed air “gas”; an uncomfortably hot or cold
environment; illness) and that they do not need to be fed every time they cry.

Management:
1) The breast-feeding mother's diet should contain enough calories and other
nutrients to compensate for those secreted in the milk as well as for those
required to produce it.
 A varied diet sufficient to maintain weight and generous in fluids, vitamins,
and minerals is important.
 Milk is an important component of the mother’s, diet to supply sufficient
calcium and other nutrients.
2) Frequent feeding the infant (8- 10 times per day to compensate for the small
amount sucked by the infant).

Mohammed 43
 3) Expression of breast milk after nursing is important to stimulate milk
production.
4) Breast-milk jaundice.

Difficulties in breast feeding

1.Difficulties on the part of the mother
1) Developmental anomalies.
 Breast: Very small breast with scanty milk production, pendulous, or very
huge breast.
 Nipple: Absence of the nipple, flat nipple, or retracted nipple (drawing the
nipple out).
2) Painful conditions
 Breast: Acute mastitis or breast abscess.
 Nipple: Fissuring of the nipples or ulceration with secondary infection.
II. Difficulties on the part of the infant
1. Developmental anomalies: Hare lip, cleft palate, micrognathia (small
mandible), macroglossia (large tongue), and congenital nasal obstruction.
2. Painful conditions: Stomatitis or traumatic ulcers.
3. Weak sucking power: Prematurity, facial palsy (traumatic), and brain anoxia
4. Respiratory distress: Respiratory distress syndrome, pneumonia, and other
causes.
Degree of difficulties
1. Mild difficulties: They do not affect largely the process of sucking and swallowing
and so breast feeding can be continued and more time and patience can be allowed
i.e., prematurity, flat nipple, and nasal obstruction.
2. Moderate difficulties: These will contraindicate breast feeding temporarily such as
breast abscess and stomatitis of infant mouth. Breast feeding can be re-established
when the difficulty is overcome.
3. Severe difficulties: These will contraindicate breast feeding permanently because
they carry a high risk for the infant such as large cleft palate for fear of aspiration.

Contraindications of breast feeding

I. Maternal contraindications.

Mohammed 44
 1. Useless mother
 Very scanty breast milk.
 Markedly inverted, Assuring, or cracking of the nipples.
 Chronic debilitating conditions: Marked anemia, diabetes, heart
disease, and chronic renal diseases.

2. Harmful mothers
 Pulmonary infectious diseases: Influenza, pharyngitis, bronchitis,
pneumonia, and open tuberculosis. Infection of the baby occurs by the
droplet way and not by passag‘e of organisms through milk.
 Local inflammatory conditions of the breast: Infected fissures and
ulcers of the nipples or breast abscess opening into a lacteal duct. The
infant is infected via swallowing milk.
 Maternal drug therapy: Breast feeding may be temporarily or
permanently contraindicated when the mother is receiving anti-thyroid
medications, anti-cancer agents, isoniazid, diagnostic
radiopharmaceuticals, chloramphenicol, metronidazole, sulfonamides,
and anthraquinone-derivative laxatives. Smoking cigarettes and
drinking alcoholic beverages should be discouraged during breast
feeding.
 Allergy: Allergens to which the infant is sensitized can be conveyed in
the milk. The allergen can be identified and removed from the mother’s
diet.
 Substance abuse and neurologic diseases (severe neuroses or
psychoses) of the mother.

II. Contraindications related to the infant

1- Moderate and severe difficulties of the breast feeding.

2- Metabolic diseases: Galactosemia and phenylketonuria. Such diseases
necessitate special types of artificial formula.
Duration of contraindications

Mohammed 45
 1- Temporary contraindications: Diseases such as Influenza, pharyngitis,
and mastitis.
2- Permanent contraindications: Conditions such as metabolic diseases of
the baby and severe difficulties of breast feeding.

Mohammed 46
 Respiratory Failure
( Pa O2  Pa O2 )
I. Respiratory Distress.
II. Hypoventilation.

Lung failure Pump failure

 Type I respiratory failure.  Type II respirator/ failure.
Other names
 Peripheral respiratory failure.  Central respirator/ failure.

Basic defect  Poor arterial oxygenation.  Alveolar hypoventilation.

Causes Causes of respiratory distress. Respiratory pump failure.

 Pulmonary causes.  Respiratory depression (deep coma).
 Extra pulmonary causes.
 Respiratory paralysis.
 Respiratory fatigue (severe lung failure).

Clinically Respiratory distress Chest Shallow breathing, cyanosis Coma or

signs. paralysis.

Blood gases Arterial hypoxemia (low PaO2) Hypoventilation (high PaCO2).

± hypoventilation (high PaCO2) ± arterial hypoxemia (low PaO2).
 Acute respiratory acidosis
 Acute respiratory acidosis
Therapy Oxygen therapy Assisted ventilation
± assisted ventilation ± oxygen therapy

I. Respiratory Distress (R.D)

 Causes:
1. Pulmonary.
2. Extra-Pulmonary.
I. Pulmonary Causes of R.D.
1. Pneumonia.
2. Acute Bronchiolitis.
3. Acute Asthmatic attack.
4. Aspiration Syndromes.
5. Pulmonary oedema.
6. Adult respiratory distress syndrome [A.R.DS].

Mohammed 47
 7. Pleural effusion.
8. Pneumothorax.
9. Localized obstructive emphysema.
10. Massive lung callapse.
11. organic phosphorus poisoning.
12. Bronchopulmonary Displasia.
13. Bronchiolitis cbliterance.
14. Respiratory paralysis
II. Extra pulmonary Causes of R.D

1. Acute Congestive heart Failure (All Causes).

2. Acute metabolic acidosis (All Causes).
3. Acute Severe anaemia.

Causes of pump failure (Hypoventilation)

Central respiratory depression

 Primary brain lesion: Hemorrhage, infection, convulsions.

 Secondary brain lesion: Hypoxic encephalopathy, CNS depressant drugs.

 Central hypoventilation syndrome or Ordine's curse: Congenital or acquired.

Respiratory muscle paralysis

 Acute: Poliomyelitis, Guillain Barre syndrome, botulism, spinal cord trauma,

phrenic nerve injury.

 Chronic: Werdnig-Hoffmann disease, myasthenia gravis, muscular dystrophies.

Respiratory musde fatigue

 Severe pneumonia, severe acute bronchiolitis, severe acute asthma.

 Other pulmonary causes of respiratory distress.

Mohammed 48
 Degree OF Respiratory Distress
1. Grade ɪ (mild distress):
o Rapid respiration (tachypnea) and working alaenasi.
2. Grade ɪɪ (moderate distress):
Intercostal and subcostal retraction.
o

3. Grade ɪɪɪ (severe distress ):

o Expiratory Grunting.
4. Grade ɪV (Advanced distress):
 Central cyanosis and disturbed consciousnen.
 Respiratory failure with PaO2 below 35 mmHg.
 Al tered consciousness i.e severe hypoxemia and andCo2narcosis with PaCo2
>60mmHg.

Grades of metabolic acidosis

Normal blood gases Grade of metabolic acidosis
pH 7.35 7.4 pH Bicarbonate
Bicarbonate 20-24mEq/litre Mild Below 7.3 Below 16mEq/litre
PaCO2 35-40mmHg Moderate Below 7.2 Below 13mEq/litre
PaCO2 90-100mmHg Severe Below 7.1 Below 10mEq/litre
N.B: For assessment of acid- base Profound Below 7.0 Below 7mEq/litre
Status, venues are satisfactory

Mohammed 49
 Components of the respiratory pump

Brain (The central controller)

 Cerebral cortex: Responsible for voluntary control.

 Brainstem (Pons and medulla): Responsible for involuntary control.

Respiratory neuromuscular system

Spinal cord.
Respiratory nerves and muscles
 Cervical nerves (C2 - C4): Accessory muscles.

 Phrenic nerve (C3 - C5): Diaphragm.

 Intercostal nerves (T1-T12): Intercostal muscles.
 Lower thoracic nerves (T6 - L2): Abdominal muscles.

 Muscles of inspiration are the diaphragm, external intercostal muscles and the
accessory muscles while muscles of expiration are the abdominal muscles and
internal intercostal muscles.
 Cranial nerves IX (Pharynx), X (larynx) and XII (tongue) are responsible for
airway patency.

Diagnosis OF R.D:
 History.

 Examination.
 Investigations
 CXR (IN all cases)
 Blood gases (IN all cases)
 Sepsis screen (CBC,ESR,CRP with suspected pneumonia .
 Renal function.
 Blood sugar.
 Echocardiography.

Mohammed 50
 Diagnosis of pump failure

1. Clinical Diagnosis.
 In control Respiratory depression.

 In Respiratory muscle paralysis.

 In Respiratory muscle fatigue.
2. Arterial blood gases.
3. Pulmonary function.
(below 5ml/kg and Low minute ventilation

Management of Respiratory Faiture

I. Management OF R.D

I. Respiratory monitoring.
 clinical monitoring.

 .Arterial oxygen saturation Sao2 by pulse oxmeter.

 Arterial blood gases
II. Respiratory support
1. O2 therapy
2. Aerosol therapy
3. Chest Physio therapy and suctioning
4. Positive pressure support
 Manual ventilating Support.
 Mechanical ventilating Support.

III.Specific treatment: treat the cause.

II. Management of pump failure

1. Nonspecific Respiratory support

 Chest physio therapy and suctioning
 Mechanical Ventilating
 Treatment of complications.

Mohammed 51
 Specific Management
1. Drug therapy.
 Theophyllin.
 Naloxone .
2. Plasma pheresis .
3. Phrenic nerve Stimulation.

Mohammed 52
 Infant Formula (Artificial) Feeding
(Dried Powdered Milk)

Composition of infant formulas

 All formulas must contain minimum amounts of all nutrients known or thought
to be required by infants and no more than a reasonable maximum content of
each.
 The formula is manufactured safely and hygienically.

Proteins:
 They are usually a mixture of bovine milk protein and soy protein, or a variety
of hydrolyzed protein.
 The protein content ranges between 1.7-3.4g/ 100 kcal.

Carbohydrates: Lactose and/or other sugars.

 The carbohydrate content ranges between 9-13 g/100 kcal.
 Lactose-free milk is available to be used in case of post-enteritis
Malabsorption.

Fats: A mixture of vegetable oils.

 Fats contain considerable amounts of essential fatty acids, including linoleic
acid and a-linolenic acid.
The fat content ranges between 4.6- 6.4 g/100 kcal.

Electrolytes (i.e., sodium, potassium, chloride).

 Minerals (i.e., calcium, phosphorus, magnesium, iron, zinc).
 All vitamins.

Quality of infant formula

 Modern infant formulas are excellent substitutes for human milk as they have
adequate and constant composition for feeding infants.

Mohammed 53
  They are fortified by all minerals and vitamins in optimal quantities that
support normal growth and - development for at least the first 4mo of life.

Reconstitution of powdered milks

Powdered milks are reconstituted by diluting one measure to 60 mL sterile
water (American milks; S-26, Similac, Isomil, Promil) or one measure to 30mL
sterile water (European, Japanese, or Korean milks such as Bebelac, Aptamil,
Nan, Enfamil).
The preparation of milk should be under complete aseptic condition.
The dried milk should be properly reconstituted, as diluted milk formula will
lead to protein caloric malnutrition and concentrated formula will lead to
vomiting, diarrhea, and colic.

Caloric value
Most infant formulas provide 67 calories/ 100 mL. Preterm infant formulas
provide more calories necessary for their optimal growth.
Indications of infant formula feeding
1. All contraindications of breast feeding, including metabolic diseases of the
infant which necessitate special types of milks.
2. Absence of the mothers as in traveling, engagement in job, or death.
3. Scanty breast milk.
4. Twin delivery necessitating larger amounts of milk than that which can be
supplied by the mother.

Mohammed 54
 Types of infant formulas

1) Humanized milks(Milk – Adapted Formula).

 They are nearest, may be identical, in composition and quality to human
milk.
 They are enriched with good amounts of vitamins and minerals
 . They are the best for feeding normal infants in whom artificial feeding is
indicated for some reason.
2) Lactose- free milks: They are used for feeding infants with galactosemia and
lactose intolerance (including post-enteritis malabsorption).
Example: Alacta, Isomil.
3) Hypoallergenic milks: They are used for feeding infants allergic to both
human and animal protein. ,The protein content of hypoallergenic milk is of
vegetable (soy) origin.
Example: Nursoy, Prosobee, Isomil.
4) Salt-free milks: They are used for feeding infants with nephritis and heart
failure.
Example: Lonalac.
5) Phenylalanine-free milks: They are used for feeding infants with
phenylketonuria.
Example: Lofenalac.
6) Protein milks: They are special types of milks with a protein content much
higher than usual (i.e., Promil and Progress milks and prolac) They can be
used for feeding normal infants and children.
- This is prepared by addition of dry casein to Butter milk, it has a low CHO,
and low Caloric value.
- Its composition is as follows : Protein : 5 gm ; CHO : 3.5 gm ; Fat: 2.5
gm/dL.
- It cannot be used for a prolonged time due to :

Mohammed 55
 1. Its bad taste
2. Causes constipation.
3. Expensive.
4. Has low caloric value.
- Indications :
1. Diarrheal diseases (especially fermentative diarrhea).
2. Debilitated infants.
3. Preterm babies.
4. Marasmus and Kwashiorkor.
Preparation:1:10 in rice water, to keep the milk in suspension + adding some
calories.
7) Premature milk formulas: They are prepared by special procedures to provide
more calories (~80 calories/ 100 mL), more protein content, fats mainly
medium-chain triglyceride (need not bile for absorption), monosaccharides as
glucose (due to deficiency of lactase enzyme in the preterm infant’s gut),
minerals, and vitamins in optimal concentrations for feeding the premature
infants with limited digestive and absorptive capacities (i.e., Low-birth weight
S-26 formula, and Pre-Nan, Semitic special care , Enfamil LBW)
8) A predigested formula (Pregestimil): It is indicated in post-enteritis
malabsorption; an elemental formula is indicated with intolerance to feeding
with a predigested formula.
9) Other Dried Milks :
A) Cream milks :
1. Full cream :Fat content 4 % .
Indicated in completely healthy infants over 4 months age, also in cold
weather.
Example : Nestogen full cream, Guigoz full cream.
Preparation: 1:8
2. Half cream : Fat content 2-3 %.
Indicated in healthy infants less than 4 months age.
Example : Nestogen half cream, Bebelac Z12.

Mohammed 56
 Preparation: 1:8
3. Skimmed milk : Fat content 1/2 - lgm/dL
Indicated in :
1) Fat intolerance and malabsorption.
2) Convalescence from diarrheal diseases.
3) Prematurity.
Example : Cow and Coat separated milk.
B) Acidified milks.
Method of acidification :
1) Chemical : Lactic acid
2) Biological : By fermentation using Lactobacillus acidophilus, or
Lactobacillus bulgaricus.
NB : Yogurt(‫)اﻟﺰﺑﺎدي‬is a biologically acidified cows milk.
Advantages :
1. Easy digestion, need less gastric HC1 for digestion.
2. Casein is altered into fine curd.
3. Acidity enhances Ca++ absorption.
4. Disinfectant effect on GIT.
5. Shorter stay in stomach (in cases of vomiting).
Indications.:
1. infants with digestive troubles.
2. Recovery from diarrheal diseases.
3. Premature and low birth weight.
4. Protein caloric malnutrition,
5. Habitual vomiting

Mohammed 57
 Combined complementary or supplementary feedings

Complementary feedings
Definition: It means giving both the breast and the bottle at one and the same feed.
Indications: It is indicated whenever the amount of milk secreted by the breast
becomes insufficient for the needs of the infant. It is also indicated in
feeding of twins
Precautions
1) The infant formula should be prescribed only when it is surely indicated.
2) The breast should be given first and should be evacuated completely, followed
by the bottle.
3) infant formula should be one of the humanized milk.
4) The milk used should never be sweetened and the holes of the teat should not be
unduly large.

Supplementary feeding
Definition: It means the replacement of one or few of the breast feeds by bottle
feeds.

Mohammed 58
 Indications
3. Absence of the mother for some time of the day (engagement in the work).
4. Twin delivery: One infant is given the breast and the other is given a bottle at the
same feeding time. Alternating breast and bottle feedings are indicated in the
next nursings.
Precautions: The supplementary feeds are better given at fixed times of the day.
Total substitution of breast milk by infant formula is indicated for permanent
contraindications of breast milk feedings.
Program of Infant Formula (Artificial) Feeding

The following items should be taken into consideration

1. Technique of formula feeding.
2. Type of milk to be given.
3. Strength of milk.
4. Frequency of feeding.
5. Amount of milk per feed.
I. Technique of formula feeding
 The infant should be hungry, fully awake, dry, and warm.
 The temperature of the milk may be tested by dropping milk onto theorist.
 The setting for formula-feeding should be similar to that for breast-feeding.
 The nipple holes should be of a size that allows the milk to drop slowly, and
the bottle should be held so that milk, not air, channels through the nipple.
 Eructation of air swallowed during feeding is important for avoiding
regurgitation and abdominal discomfort.
 A feeding may last from 5-25 min, depending on the age and the vigor of the
infant.
 The excess milk should be discarded.
II. Type of milk :

Mohammed 59
 3. Normal infants: Humanized milks.
4. Diseased infants: Special types of milk as:
 Lactose-free milk: Galactosemia or lactose intolerance.
 Hypoallergenic milk: Milk allergy.

III. Strength of milk:

1. Normal infants: Normal dilution during reconstitution.
2. Diseased infants: The powdered milk may be initially reconstituted as half
strength; formula for fear of intolerance and then increase the concentration
gradually until full strength formula with normal dilution is reached within few
days.
IV. Frequency of feeding:
1. Three-hourly feeding is the usual feeding schedule.
2. Two-hourly feeding: It is indicated in the following conditions:
 Premature infants to compensate for the small volume of the feed.
Other causes of weak sucking power.
 Protein-energy malnutrition.
3. Four-hourly feeding: It is indicated in the following conditions:
 Infants over 4mo of age.
 Overfed obese infants.
V. Amount of milk per feed :
1. Weight method:
 Amount of milk =wt in kg × 20+20,ML / Feed.
Example: For an infant weighing 5.5kg, the amount of milk needed is :
5.5× 20+20=130 ML.
 Another easy method in knowing that:
Every 1kg needs about 100 cal  present in 150 ML milk / day.
So amount of milk needed / day = wt. in kg × 150.
So amount of milk needed / feed= wt. in kg× 150/No. of feeds.
2. The weight method (caloric method)
Mohammed 60
  It is not simple, but definitely accurate and should be the method of choice.
 It is usually applied for infants whose actual weights are less than expected
for age.
 The total caloric requirement per day is calculated =

Weight in kg X 100 (calories/ kg/ day)

 The total amount of reconstituted milk required per day is then calculated =
Total calories required X 100/67 (3/2) as 100 mL of milk provide 67
calories.
 The amount of fluid milk per feed is then calculated =

The total amount required per day / Number of feeds.

3. The age method
 It is more easy, but less accurate than the weight method.
 It used only for normal infants whose weights are considered normal for
their ages.

Mohammed 61
 1st day :10 mL/ feed
2nd day :20 mL/ feed
3rd day :30 mL/ feed
4th day :40 mL/ feed There is an increase of 10 mL/ feed per day
5th day :50 mL/ feed
6th day :60 mL/ feed
7th day :70 mL/ feed

2nd week :80 mL/ feed

3rd week :90 mL/ feed There is an increase of 10 mL/ feed per week
4th week :100 mL/ feed

2nd month :120 mL/ feed

3nd month :130 mL/ feed There is an increase of 10 mL/ feed per month
4nd month :140 mL/ feed During the First year of life.

N.B:
- During the first year of life the following equation is used:
Amount of milk / feed = Age in month × 10+100 ML Feed.
Example: An infant 4 months age, weight is 6kg.
A. Age method :
Amount of milk / Feed = Age in months × 10+100 ML
= 4 × 10 + 100 = 140 ml.
B. Weight method :
Amount of milk / Feed = wt in kg × 20+20 ML
6 × 20 + 20 = 140 ml.
C. Caloric method :
Caloric needs of the infant = 6 × 110= 660 cal/d
100 ml  67.
? 660 Cal.
Amount of milk / day = 660 × 100/67
Amount of milk / Feed =990/6 = about 160 ml/ Feed.

Mohammed 62
 Disadvantages of infant formula feeding

I. Disadvantages related to milk itself

1. General disadvantages
 Availability: It is not available whenever needed and wherever the mother
may be.
 Temperature: The need for heating.
 Economic aspect: It is expensive.
 Sterilization: Bacterial contamination may occur.

2. No protective benefits as in case of breast milk feeding

II. Disadvantages related to sucking the bottle and not taking the breast
1. More technical difficulties: The need for sterilization of the containers.
2. Psychological aspect: Less psychological advantages.
3. The amount: It is not self-regulated and should be calculated.
4. Less physical care of the infant.
5. Less involution of the uterus.

Fresh Animal Milks

Sources
Cow’s (bovine) milk (most common), Buffalo’s milk (in Egypt), and Goat’s milk.
Composition and quality of fresh animal (cow’s) milk
1) Proteins:
 The amount is 3.5 g/100 mL (higher than the recommended intake, this
may represent a burden on the kidneys).
 The amount of insoluble protein (casein) is much more than the amount
of soluble proteins (lactalbumin and lactglobulin); it is 2:1. This factor
renders the protein of animal milk difficult to be broken down and
digested,.

Mohammed 63
  The cow’s milk protein may lead to food allergy(dietary protein
intolerance).
2) Fat:
 The amount is 4 g/100 mL.
 The fat globules are 10-20 times larger than those of human milk.
 They are, difficult to be suspended and acted upon by the intestinal lipolytic
enzymes.
 The linoleic acid content is low (50% of the recommended intake), which is
insufficient for growth and development of the central nervous system. The
high content of volatile fatty acids makes animal milk very irritant to the
infant’s gastrointestinal tract.
3) Carbohydrates:
 The amount is 4.8 g/ 100 mL.
 The carbohydrates of animal milk do not facilitate the growth of lactobacilli
which prevent the growth of pathogenic organisms, and also the vitamin
production in the intestine is diminished.
4) Minerals content: The calcium and phosphorus are present in comparison to
human milk, but Ca/P ratio (1.1:1) is not optimal for their complete absorption and
utilization.
 Animal milk contains more iron than breast milk, but iron deficiency anemia
is common because of its less bioavailability.
 Other causes of iron deficiency anemia include deficient amount of iron (2/3
of the recommended intake) and intestinal blood loss as a manifestation of
cow’s milk protein allergy.
5) Low amounts of vitamins C and D.
6) Electrolytes (sodium): Infants fed bovine milk, on average ingest about 50% more
sodium than the upper limit of the safe range of intake.
7) Reaction: It is alkaline, and this further reduces the weak acidity (hypochloridria)
of the infant’s stomach, interfering with digestion.

Mohammed 64
 Disadvantages of fresh animal milk feeding

IV. Disadvantages that are similar to those of infant formula feeding.

V. Food allergy: The manifestations include:
A. Gastrointestinal manifestations (nausea, vomiting, crampy abdominal pain,
diarrhea, proctocolitis, and intestinal blood loss).
B. Cutaneous manifestations (urticaria, eczema) .
C. Respiratory manifestations (asthma and rhinoconjunctivitis).

VI. Exclusive animal milk feeding without supplementation leads to iron deficiency
anemia, rickets, and high incidence of essential fatty acid deficiency.

Weaning

Definition: It means addition of extra food to milk to the infant’s diet.

Justifications of early weaning
 Early and gradual feeding of the infant with semi-solids is the method of choice in
weaning.
 Weaning should be started as early as 4-6 mo of life. This is because of the
following
1. By 6 mo of age, the infant’s capacity to digest and absorb a variety of dietary
components as well as to metabolize, utilize, and excrete the absorbed products of
digestion is near the capacity of the adult.
Moreover, teeth are beginning to erupt and the infant is able to sit unassisted.
2. Developing the habit of tasting other foods early in life otherwise the infant will not
accept them and will stick to the breast “milk addiction”.
3. The amount of milk secreted by the breast, its caloric value, and the protein content
are no more sufficient for the requirements of the infant after the 4th mo of life.
4. Diminished stores of iron and vitamin D, which are supplied by the mother during
pregnancy.

Basic principles of weaning

1. The infant: The infant should not be diseased or during convalescence period from
a recent disease.

Mohammed 65
 2. The characters of the added food
 Added food should be freshly prepared; not stored and then re-heated before
serving.
 Added food should be sieved, strained, and pursed.
 Avoid salts and spices.
3. Technique of feeding
 Additional foods should be given at fixed times of the day.
 The amount of added food should be small at first following the milk, and then
gradually increased with a corresponding decrease in the milk feed (start it as a
complementary food and then proceed to be a supplementary {replacement} food).
 Additional foods should be given with a spoon and not through the bottle.
 Only one new food should be introduced at a time, and additional new foods
should be spaced by at least 3-4 days to allow detection of any adverse reactions to
each newly introduced food.
 Added food should be omitted if the baby dislikes its taste, to be tried some weeks
later.

Suggested schedule of weaning

1) At 4 mo of age: Cereal food (at 12.00 Noon) should usually be the first such food
given. Cereals are good source of protein and iron.
2) At 5 mo of age: Vegetable soup (potatoes, carrot, marrow ) at 3.00 PM are added
and introduced next.
3) At 6 mo of age: Fruits (fresh apples or banana) and yogurt (at 6.00 PM) are added
to the above mentioned foods.
4) At 7 mo of age: Chicken is added to the vegetable soup.

Egg yolk (hard and boiled, at 9.00 AM). However, the intake is delayed, particular
important if there is a family history of food allergy.
5) At 8 mo of age: Meat is added to the vegetable soup.
6) At 9-12 mo of age: Other types of foods are tried separately and gradually.
7) At 1 yr of age: Ordinary family food.

Mohammed 66
 Hazards of weaning

1. Gastrointestinal troubles: Colic, abdominal distension, diarrhea, or constipation,

2. Food allergy.
3. Gastroenteritis: It is due to administration of contaminated food.

Mohammed 67
 Feeding Problems during the First Year of Lift
Underfeeding

Etiology: It results from the infant's failure to take a sufficient quantity of food.
1. Breast-fed infants:
a) Scanty breast milk.
b) Difficulties in feedings (i.e. hare lip of infant, flat nipple).
2. Bottle-fed infants:
a) Small volume of feeds.
b) Highly diluted milk formula.
c) Difficulties in feedings (i.e., cleft palate of the infant. too small holes in the
teat).
3. In both breast- and bottle- ted infants:
a) Nursing errors (infrequent feedings, inadequate eructation of air).
b) Abnormal mother-infant "bonding".
c) Systemic disease in the infant.

Clinical manifestations

1. Behavior: Underfed infants do not sleep well and continuously cry between feeds.
2. Underweight:
 The infant fails to gain weight properly, then the weight becomes stationary. and
finally actual loss of weight occurs.
 The skin becomes dry and wrinkled, the subcutaneous fatty tissue disappears, and
the infant assumes the appearance of ah "old man".
3. Constipation: Motions are few and infrequent. The stools passed are small and
hard.

Mohammed 68
 Treatment

1. Nutritional support:
a) Complementary or supplementary feeding for scanty breast milk.
b) Proper preparation of infant formula regarding the volume and the strength of
milk. Correction of any difficulty in feeding .
c) Good nursing.
d) Correcting deficiencies of vitamins and /or minerals.
e) Instructing the mother in the art and practice of infant feeding.
2. Specific management: It is indicated in eases of systemic disease of the infant.

Overfeeding

Etiology: Because neither breast milk nor formulas contain either excessive fat or
excessive carbohydrate, overfeeding usually results from supplementation.
4) Diets too high in fats: They also lead to distension and abdominal discomfort due to
delay in gastric emptying and malabsorption of fat in infant s gut.
5) Diets too high in carbohydrates (pudding and dessert): They also lead to distension
and abdominal discomfort due to undue fermentation in the intestine.
6) Some bottle-fed infants: Overfeeding may occur as a result of:
1) Large volume of feeds.
2) Too frequent feedings.
3) Highly concentrated formula with high caloric value.

Mohammed 69
 Clinical manifestations

1. Behavior: Overfed infants are excessively sweated and cry continuously between feeds
(colic).
2. Overweight: It is a cardinal sign of overfeeding.
3. Gastrointestinal troubles
 Vomiting: It may occur after each feed.
 Diarrhea: Motions are frequent and stools are loose and bulky.
 Abdominal distention and colic.

Treatment

1. Avoid pudding and desserts as they provide high calories.

2. Bottle-fed infants:
a) Feeding infants with normal concentration of milk.
b) Adequate volume of milk for age.
c) Proper spacing between feeds (four-hourly feeding).

Regurgitation and Vomiting

Regurgitation: It refers to the return of small volume of swallowed food during or
shortly after eating. Within limits, regurgitation is a natural occurrence, especially during
the first several months of life.
It can be reduced to a negligible amount by adequate eructation of swallowed air, by
gentle handling, and by placing the infant on the right side immediately after eating with
the head not lower than the rest of the body.
Vomiting: It is the more complete emptying of the stomach. Causes are many and should
be investigated.

Constipation
Definition: Infrequent passage of stools >36 hr and the stools are small and hard.
Common causes :
a) Underfeeding.
b) Anal fissures or cracks.

Mohammed 70
 c) Aganglionic megacolon.

Rectal examination should be performed.

Treatment

1. Diet:
 The first few months of life: Increase the amount of fluid, and also sugar in the
formula.
 At 4th mo of age onwards: Cereals, fruits, and vegetables are source of fiber,
facilitating the passage of stools.
2. Suppositories and enemas: They should never be more than temporary measures.
3. Laxatives: They should be reserved for unresponsive or severe constipation.

Mohammed 71
 Abdominal Colic

Definition: colic is a symptom complex of paroxysmal abdominal pain.

Common causes:
1. Over feeding.
2. Supplement with high carbohydrate content.
3. Hunger.
4. Irregular feeding.
5. Failure of eructation of swallowed air.
6. Intestinal allergy.
7. Intestinal obstruction (intussusceptions, strangulated hernia),

Clinical manifestations:
 It usually occurs in infants younger than 3 mo of age.
 Attacks commonly occur late in the afternoon or evening. The attack usually begins
suddenly with a loud, more or less continuous cry.
 The face may be flushed, or there may be circumoral pallor.
 The abdomen is usually distended and tense.
 The legs are usually drawn up on the abdomen.
 The feet are often cold, and the hands are usually clenched.
 The attack may persist for several hours and may not terminate until the infant is
completely exhausted.
 Careful physical examination is important to eliminate the possibility of intestinal
obstruction.

Prevention
Prevention of attacks can be accomplished by improving feeding techniques, including:
1. Eructation of swallowed air.
2. Identifying possibly allergenic foods in the infant's .
3. Nursing mother’s diet.
4. Avoiding underfeeding or overfeeding.

Mohammed 72
 Management

1) Positioning :

Holding the infant prone across the lap or on a hot water bottle or heating pad.
Passage of flatus or fecal material spontaneously or with expulsion of suppository
sometimes affords relief.
2) Carminative and sedative medicines: They may be required to terminate the attack

Mohammed 73
 Nutritional Disorders
Nutritional disorders include:
1. Protein-Energy Malnutrition (PEM).
2. Vitamins and minerals deficiencies.
3. Obesity.

Protein-Energy Malnutrition (PEM)

Definition: PEM is the term applied to describe a group of related nutritional diseases
specific for infants and young children characterized by protein and energy deficiency but
having variable clinical and biochemical presentations.
Classification of Protein-Energy Malnutrition
5. Kwashiorkor (edematous PEM).
6. Marasmus (nonedematous PEM).
7. Marasmic kwashiorkor: Has features of both disorders.

Kwashiorkor (KWO)
(Red Boy)

Definition: Kwashiorkor is a protein energy malnutrition syndrome resulting primarily

from inadequate protein intake, particularly those of the high biological value, with
normal or almost normal total caloric intake in the form of excess carbohydrates.

Etiology
1) Dietary causes
 KWO affects the first baby when the next is born, usually during the weaning and
post- weaning phases of life i.e., age 1-2 years. This is because the newborn baby is
given the breast while the 1st infant is given a milk free - protein source, high-
carbohydrate diet in the form of rice, potatoes, and sweetened fluids (the cheapest
foods).
 KWO can affect 1st or next born babies as early as the first few months of life. It is not
related to the delivery of the 2nd baby, it is rather the result of bad dietary habits since
early life due to poverty and/or ignorance.

Mohammed 74
 2) Post-infectious causes: KWO may be precipitated by an attack of infective
gastroenteritis or measles enterocolitis. This is because:
 Associated anorexia.
Impairment of absorption.

 Prolonged dietary restrictions; restriction of proteins and giving carbohydrates
(constipating foods) as a therapeutic measure for diarrhea.
 Increased tissue catabolism induced by infections and fever.
3) Maternal deprivation syndrome: Separation of the infant or sudden displacement of
the infant from the breast due to birth of the next infant may lead to anorexia and
kwashiorkor.

Pathology
1. Fatly liver: It is a constant pathological finding, fatty liver develops secondary to
lipogenesis due to excess carbohydrate intake.

The size of the individual liver cell is not necessarily enlarged by fatty infiltration
because of the marked depletion of its protein content. Therefore, fatty infiltration of
the liver is not always associated with hepatomegaly.
2. Atrophy of the intestinal villi and pancreatic acini: This accounts for deficiency of
intestinal and pancreatic digestive enzymes resulting in a state of malabsorption.
3. Generalized muscle wasting: It is caused by protein depletion.
4. Excess subcutaneous fat: It is caused by excess carbohydrate intake.

Clinical manifestations:
VII. Constant manifestations:
1) Growth failure.
2) Generalized edema.
3) Mental changes.
4) Diminished muscle-to-fat ratio.
VIII. Variable manifestations:
1) Scalp hair changes.
2) Skin changes.
3) Hepatomegaly.
4) Anemia.
5) Vitamin deficiencies.
6) Gastrointestinal manifestations.

Mohammed 75
 7) Associated infections.

Constant manifestations

7) Growth failure: It is evidenced by

1) Under stature: The length of the infant is less than the5lh percentile for age.
2) Underweight: This feature is often masked by edema and excess subcutaneous fat.
8) Generalized edema
Site: It starts at the dorsum of hands and feet, and spreads centrally to involve the legs,
arms, and face. In severe cases, the whole body is edematous. However, ascites never
occurs in uncomplicated KWO.
Causes
1) Hypoalbuminemia: It is the major cause. Edema tends to occur when the serum
albumin level is less than 2.5 g% and the total plasma protein is less than 4.5 g%.
2) Increased activity of ant diuretic hormone: This is due to stimulation of the
baroreceptors of the hypothalamus by diminished plasma osmotic pressure.
3) Increased activity of aldosterone: Diminished plasma volume reduces the renal
blood Flow, which in turn, stimulates the juxtaglomerular apparatus to secrete more
renin.
Renin converts angiotensinogen to angiotensin which stimulates the suprarenal
cortex to secrete more aldosterone, causing water and salt retention.
9) Mental changes :
a) Anorexia(which will interfere with the nutritional management).
b) Apathy. ‫ﻓﺎﺗﺮ اﻟﺸﻌﻮر‬
c) Misery. ‫ ﻣﺜﯿﺮ ﻟﻠﺸﻔﻘﺔ‬،‫ﺑﺎﺋﺲ‬
d) Peevishness. ‫ﺳﺮﯾﻊ اﻟﻐﻀﺐ‬
e) Disinterest to the surroundings.
Causes: The cause is uncertain. Possible causes include.
1. Maternal deprivation.
2. Hypothyroid state: It is confirmed in KWO patients.
3. Disturbed amino acid metabolism: Diminished serotonin (a neurotransmitter)
activity due to disturbed tryptophan metabolism.
4. Niacin deficiency.
Mental changes are reversible with correction of the protein malnutrition.

Mohammed 76
 10) Diminished muscle-to-fat ratio
This is due to the combination of two factors
1. Generalized muscular atrophy (wasting): It is caused by the marked protein
depletion. It is best demonstrated by palpating the biceps and deltoid muscles.
2. Excessive amount of subcutaneous fat: It is caused by excessive carbohydrate intake.
It is well evidenced by the characteristic moon face of KWO patients..
Variable manifestations.
1) Scalp hair changes
5. Color: In dark-haired children, hair gets lighter by time. It changes from the black
to the dark brown, gray, red or orange, and ultimately the yellow color.
During recovery, the hair color becomes darker in the proximal areas than in the
distal ones resulting in the characteristic flag appearance of the scalp hair.
6. Texture: Soft and easily broken down.
7. Attachment: Easily epilated (detached).
8. Distribution: Sparse (you can see the scalp).
The pathogenesis of hair changes is not exactly known. It may be due to:
 Deficiency of the sulphur-containing amino acids; cysteine and cystine.

 Deficiency of cupper with subsequent disturbance of melanin synthesis.

2) Skin changes
Various types of skin changes may occur; hyper pigmentation, hypo pigmentation of
other areas, cracking and fissuring, or ulceration and secondary infection.
Site: The skin lesions are most marked over the buttocks, perineum, inguinal regions,
and backs of the thigh.
Pathogenesis: The cause is exactly known. It may be due to:
 Vitamin deficiency (vitamin A and C or niacin).

 Disturbed amino acid metabolism (tryptophan , nicotine amide ).

3) Hepatomegaly
 Hepatomegaly is a variable manifestation of KWO. This is in contrast to fatty

infiltration which is a constant pathologic finding.

 Hepatomegaly is caused by fatty infiltration and increased glycogen content in the
liver cells.
 Marked protein depletion makes hepatomegaly may or may not present in every case
of KWO.

Mohammed 77
 4) Anemia
Various types of anemia are present
 Microcytic hypochromic anemia due to associated iron deficiency.
 Megaloblastic anemia due to associated folic acid or vitamin B12 deficiency.
 Normocytic normochromic anemia due to protein deficiency,(intestinal infestations).
5) Vitamin deficiencies
 Vitamin (A) deficiency:

- Keratomalacia, It is the advanced stage of Xerox ophthalmic and consist of softening,

necrosis and ulceration of the cornea (Irreversible).
- Conjunctivitis.
- Xerophthalamia.
- Blindness.
- Skin changes.
- Faulty epiphyseal bone formation.
- Defective tooth enamel.
- Impaired resistance to infection.
 Vitamin (B1) deficiency (Beriberi):
- Anorexia.
- Fatigue.
- Constipation.
- Insomnia.
- Heart failure.
- Tachycardia.
 Vitamin (B2) deficiency (ariboflavinosis):
- Cheilosis.
- Corneal vascularization.
- Burning and itching of eyes.
- Photophobia.
 Vitamin (B6) deficiency:
- Irritability.
- Convulsions.
- Peripheral neuritis.
- Hyper acusis (Abnormal of acuteness of the since of hearing).
 Niacin deficiency (pellagra): (3Ds)
- Mental changes(Dementia).

Mohammed 78
 - Dermatitis.
- Diarrhea.
 Folic acid and vitamin (B12) deficiency: Megaloblastic anemia.
 Vitamin (C) deficiency: Scurvy and poor wound healing.
 Vitamin( D) deficiency:
- Infantile tetany and rickets.
- Clinical rickets is not common in KWO because of the retarded rate of growth
(rickets is a disease of growing bones).
 Vitamin (E) deficiency:
- Red blood cell hemolysis.
- Ataxia.
- Opthalmoplegia.
- A reflexia.
 Vitamin (K) deficiency: Coagulopathy leading to hemorrhagic manifestations.

6) Gastrointestinal manifestations
1. Anorexia: It is a constant manifestation caused by mental changes or associated
infections.
2. Vomiting: It is often present due to associated infection.
3. Loose stool and diarrhea: They are frequently present caused by malabsorption
(deficiency of pancreatic enzymes and atrophy of the intestinal villi) or associated
gastroenteritis.
4. Abdominal distension: It is due to hypotonia of the abdominal muscles,
malabsorption, and hypokalemia due to associated gastroenteritis.
7) Associated infections
 Protein deficiency leads to immunodeficiency.

 Any infection may be present; pulmonary, gastroenteritis, skin infections, and

others.

Laboratory investigations

1. Protein metabolism:
 The serum albumin level is markedly diminished (<2.5 g%), the total plasma
proteins is reduced (<4.5 g%).
 All individual aminoacids are reduced.

Mohammed 79
  The transferrin (iron binding protein), thyroxin binding proteins, and
ceruloplasmm (cupper binding protein) are reduced.

2. Fat metabolism: Hyper epidemic is often found. It is usually due to formation of large
amounts of fats from the excess carbohydrates ingested.
3. Carbohydrate metabolism: Hypoglycemia is often present despite the excess intake of
sugar by KWO patients.
The causes may be related to:
 Enhanced glycogenesis (accelerated formation of glycogen by the liver).
 Impaired glycogenolysis (inhibition of breakdown of glycogen to glucose).
 Increased insulin production (probably induced by the initial high blood
glucose level).
 Diminished activity of insulin antagonists (growth hormone, glucocorticoids,
and glucagon; their production need aminoacids).

4. Water, electrolytes, and mineral metabolism

 The total body water is increased due to increased aldosterone activity.
 Dilutional hyponatremia: It is present despite the total body sodium is
increased.
 Hypokalemia: It is due to hyperactivity of aldosterone and loss of potassium
via vomitus and diarrhea.
 Serum iron, magnesium, zinc, and copper serum levels are reduced.

5. Blood picture: Anemia (various types of anemia) and leukocytosis (infections).

Complications of KWO
1. Recurrent infections: Bronchopneumonia, gastroenteritis, and skin infections are
particularly important. The skin lesions and edema of the subcutaneous tissues
predispose to skin infections.
2. Heart failure: It is caused either by vitamin B1 deficiency, protein depletion,
septicemia, or marked anemia.
3. Hypoglycemia and hypothermia.

Differential diagnosis of generalized edema

1. Nutritional causes: KWO or marasmic KWO. It affects certain age group (during
the first 2 years).

Mohammed 80
 2. Renal causes: Nephrotic syndrome and renal failure.
3. Cardiac causes: Congestive heart failure due to congenital or rheumatic heart
disease associated with tricuspid valve incompetence.
4. Hepatic causes: Liver cell failure with hypoalbuminemia.
5. Allergic causes: There is a history of food or drug intake to whom the patient is
sensitive.

Marasmus (A threPsia or In fan tile Atrophy)

Definition : Marasmus is PEM resulting primarily from inadequate energy intake

(carbohydrates and fats). Marasmus is characterized principally by progressive loss
of weight.
Pathogenesis: In the face of inadequate energy intakes, activity and energy expenditure
decrease and fat stores are mobilized to meet the ingoing energy requirement. Once
these stores are depleted, protein catabolism must provide the ongoing substrates
for maintaining basal metabolism.
Etiology
(causes of failure to thrive or failure to gain weight)
I. Nutritional marasmus.
II. Non- Nutritional marasmus.
I. Nutritional marasmus (more common in developing countries)
It is a chronic state of under nutrition resulting from depletion of the various
constituents of the diet (protein, fats, and carbohydrates) as well as the energy intake.
1) Dietary causes
 Quantitative errors: Underfeeding due to such causes as scanty breast milk and lack
of complementary or supplementary infant formula feeding due to poverty.
 Qualitative errors: Diluted infant formula due to ignorance of the mother.
 Nursing errors:
- Irregular feeding.
- Failure of eructation of swallowed air.
- Tight abdominal binders after meals leading to loss of most of the amount of milk
received through vomiting.
2) Recurrent gastroenteritis
It can lead to marsmus because of
 Associated anorexia.

Mohammed 81
  Increased loss in vomitus and diarrhea fluids
 Impairment of absorption.
 Increased tissue catabolism induced by infections and fever.

Acute gastroenteritis does not lead to marasmus, but it causes temporary arrest of weight
gain or temporary weight loss which is followed by catch-up growth during recovery
period.
II. Non-nutritional marasmus (more common in developed countries)
1) Chronic infections
 Chronic non-specific infections: Chronic osteomyelitis, chronic pyelonephritis,..etc.
 Chronic specific infections: Tuberculosis, Syphilis,...etc.
2) Systemic diseases
 Gastrointestinal diseases: Hare lip, cleft palate, congenital hypertrophic pyloric stenosis,
malabsorption conditions, chronic liver diseases,...etc.
 Respiratory diseases: Chronic suppurative lung diseases as lung abscess,
bronchiectasis, and chronic empyema.
 Cardiac diseases: Congenital heart diseases particularly the cyanotic group (chronic
hypoxemia) and rheumatic heart diseases.
 Renal diseases: Chronic obstructive uropathy and renal failure.
 Metabolic diseases: Various inborn errors of metabolism as galactosemia.
 Neurological diseases: Cerebral palsy.

Pathology
1. Loss of subcutaneous fat.
2. Generalized muscle atrophy.
Clinical manifestations
1. Loss of weight
Marasmus is described when the weight is less than the 5th percentile for age.
According to the degree of weight loss, marasmus is recognized as
a) Mild marasmus: The weight is 75-90% of the average value (50'h percentile).
b) Moderate marasmus: The weight is 60-74% of the average value (50th percentile).
c) Severe marasmus: The weight is <60% of the average value (50tn percentile ).

Mohammed 82
 2. Loss of subcutaneous fat
According to the extent of fat loss, marasmus is recognized as
- First decree: loss of Fat over axilea.
- Second degree marasmus: Loss of subcutaneous fat of the abdominal wall.
- Third degree marasmus: Loss of subcutaneous fat over the limbs and inguinal area.
- Fourth degree marasmus: Loss of fat from the sucking pads of the cheeks, leading to the
typical senile face.(it takes time, to disappear ).
- The skin loses turgor and becomes thin, redundant, and wrinkled; more marked on the
medial aspects of the thighs and buttocks.
- Loss of subcutaneous fat of the chest wall makes the normal costo-chondral junctions
abnormally visible. This should not be mistaken as rickets manifestation (rickets is not
common due to retarded rate of growth in marasmic patients and rickets is a disease of
growing bones).
3. Generalized muscle wasting
- It involves the whole body musculature with resultant hypotonia.
- The abdomen may be distended (hypotonia of the abdominal muscles) with the intestinal
pattern readily visible (loss of subcutaneous fat over the abdomen).
4. Gastrointestinal manifestations
The infants are usually constipated but may develop diarrhea(malabsorption) with frequent
stools containing mucus.
5. Vital signs
Hypothermia and slow pulse are common.

Mohammed 83
 Laboratory investigations

1) Protein metabolism:
 The albumin and total plasma proteins levels are not markedly reduced because of the
adaptive responses to inadequate energy and or protein intakes; tissue protein
catabolism pours proteins in the plasma and provides the ongoing substrates for
maintaining basal metabolism.
 It has been proposed that giving excess carbohydrate (without sufficient protein
intake; to a child with clinical marasmus reverses the adaptive responses to low
protein intake, and eventually albumin synthesis decreases, resulting in
hypoalbuminemia with edema (marasmic KWO).
2) Anemia and leukocytosis are usually present.

Complications and causes of death

Recurrent infections: Bronchopneumonia and gastroenteritis are common
and are usually the terminal events in most cases.
Skin infections are not as common as in KWO because of the absence of skin lesions and
of edema of the subcutaneous tissues.

Marasmic Kwashiorkor
Definition: It is a combination of energy deficiency (marasmus) and protein malnutrition
(KWO).
Etiology
1. Feeding a marasmic infant with a high-carbohydrate, low-protein diet.
2. Restriction of caloric intake (carbohydrates) in a KWO patient.
Clinical manifestations
There is a combination of growth failure and loss of subcutaneous fat: the
manifestations of marasmus, plus edema and hair changes characteristic of KWO.
Prevention of PEM
1. Prolongation of breast feeding: In the developing countries, breast feeding may be
prolonged up to 2 years of age to avoid the sudden switch from a good source of
protein supply to carbohydrate sources (the cheapest foods).
2. improving standard of living with spread of education and improving the hygienic
facilities.

Mohammed 84
 3. Improving food supplies with special attention to protein food of animal and fish
sources. Economic aspect should be considered in the developing countries.
The use of vegetable protein (the cereals mixtures)could supply the essential amino
acids.

Management of PEM

1. Hospitalization: All moderate or severe PEM patients should be hospitalized.

2. Maternal education (treatment of the cause): This is crucial for continued effective
treatment as well as prevention of additional episodes.
The usual approach to treatment of PEM includes three phases
1. First phase (24-48 hr) is the stabilization phase
 Correction of dehydration, if present, by oral or intravenous routes. Human plasma
(10 mL/ kg) can be used in case of shock.
 Antibiotic therapy is initiated to control infection.
2. Second phase (an additional week or 10 days)
 Continued antibiotic therapy with appropriate changes if the initial combination was
not effective.
 Initial diet administration:
Introduction of a diet to provide maintenance requirements of energy and protein
(~75 cal/ kg/ 24 hr and ~1 g/ kg/ 24 hr).
 Lactose-free milks may be initially given, followed by humanized milks.
If the infant is unable to take the feedings from a cup or bottle, administration of feeding by
nasogastric tube is preferred.
 Adequate electrolytes and vitamins (particularly vitamin A and vitamin B complex).
3. Third phase
 The child is becoming more interested in his or her surroundings, and his or her
appetite is returning. The infections are usually under control.
 Recovery diet administration: A diet provide up to 150 kcal/ kg/ 24 hr and 4 g/ kg/ 24 of
protein. After adjustment to this diet, the child can be fed ad labium; when intakes of both
energy and protein can be significant.
 Iron therapy: It is usually not started until this final phase of treatment so as to prevent
binding of iron to already limited stores of transferring.
«The free iron may interfere with the protein’s host defense mechanisms and it may
exacerbate oxidant damage, precipitating marasmic KWO in a child with clinical
marasmus.

Mohammed 85
  Blood transfusion: It is indicated at a dosage of 15-20 mL/ kg, in cases of anemia,
serious infections, or bleeding tendency.

Vitamins and Minerals Deficiencies

Rickets

Definition:
 Rickets is a systemic metabolic disease resulting from::
1. Pathologically by defective mineralization of bones.
2. Clinically by various:
- Skeletal.
- Muscular.
- Neurological manifestations.
 Rickets is found only in growing infants and children before fusion of the epiphyses.

Bone growth
1) Hormonal control of bone growth.
Bone growth occurs in children by the process of calcification of the cartilage cells
present at the ends of bone.
a) Vitamin D/parathyroid hormone: The main function of vitamin D in the presence
of parathormone is to maintain the extracellular calcium and phosphate
concentrations at appropriate levels to permit mineralization.
b) Other hormones:
1. Growth hormone.
2. Thyroid hormones.
3. Insulin .
4. During the pubertal growth spurt, sex hormones (androgens and estrogens)
appear to regulate the growth and mineralization of cartilage.
5. Supraphysiologic concentrations of glucocorticoids impair cartilage
function and bone growth and augment bone resorption.
2) Minerals (calcium and phosphate)
Mineral deficiency prevents the normal process of bone mineral deposition.. If
mineral deficiency occurs despite adequate vitamin D stores, bone growth slows and
bone age is retarded—rickets occurs.
Types of rickets

Mohammed 86
 Because both calcium and phosphorus ions constitute bone mineral, the
insufficiency of either type in the extracellular fluid that bathes the mineralizing
surface of bone results.
1) Calcium-deficient rickets with secondary hyperparathyroidism due to vitamin D
deficiency: It is much more common than other forms of rickets. It affects infants as
early as the age of 2 months to the age of 2 years. It is rare later in childhood. It
responds to ordinary therapeutic doses of vitamin D.
2) Phosphate-deficient rickets with no secondary hyperparathyroidism (vitamin D-
resistant rickets):
The vitamin D- refractory rickets is rare and affects infants and children at any age. It
does not respond at all to the therapeutic doses of vitamin D, Massive doses of vitamin D
in an attempt to treat these disorders will lead to hypervitaminosis D, hypercalcemia,
nephrocalcinosis, and permanent renal damage.
3) End-organ resistance to 1,25 dihydroxy-cholecalciferol.
Vitamin D metabolism
Definition: Vitamin D is a fat-soluble vitamin. It is responsible for regulation of calcium
phosphorus metabolism and mineralization of bones and teeth.
Forms of vitamin D – Two forms of vitamin D:
 Vitamin D2: Calcifero of plant origin , produced by irradiation of plant ergo sterol.

Vitamin D3: Calcifero of animal origin, produced by irradiation of 7- dehydro- cholesterol

present in skin. It is also synthesized in the human skin.
There are available as dietary supplements.

Sources
1. Dietary sources of both vitamin D2 and D3
 Food poor in vitamin D: Breast milk, fresh animal milk (less amount), cereals,
vegetables, and fruits.
 Foods rich in vitamin D: Fortified infant formula and egg yolk.
2. Vitamin D3 formation in the human skin: The provitamin form, 7-dehydro- cholesterol is
activated by direct exposure to the ultraviolet rays of sunlight, which do not pass through
ordinary window glass or dark skin of black race.
Absorption of vitamin D: Vitamin D is absorbed in the upper intestine. Its absorption
requires bile salts and fats.
Activation of vitamin D: Both vitamin D2and D3 are transferred to the liver, where they
are hydroxylated to 25-hydroxy-cholecalciferol. and then it is transferred to the renal
Mohammed 87
 cortex where it is activated to 1,25-dihydroxy-cholecalciferol (1, 25 (OH)2 D3. the active
form) by 1 a-hydroxylase enzyme. The active form is released to the blood and functions
as a hormone. Receptors of this hormone are present in the intestine, renal tubules, and
bones.
Actions of vitamin D
1. Intestinal function: It regulates the absorption of both calcium and phosphorus from
the intestine.
2. Renal function: It facilitates the reabsorption of phosphorus by the renal tubules.(in
the proximal).
3. Bone function: It regulates the deposition of calcium and phosphorus from the blood
into the bones.
Daily requirement of vitamin D
1. Normal breast-fed infants: The maintenance dose is 400 IU/ day. It should be given as
early as the 3ld mo of life because at that time the stores are decreased and the
requirements are increased. Protected infants from sunlight, dark-skinned infants, and
infants born during the winter months also should receive a supplement of 400 IU/ day
of vitamin D daily, particularly if breast-fed.
2. Pre-term and low-birth weight infants: They should receive up to 1,000 IU/ day of
vitamin D). It should be given as early as the Ist mo of life because at that time the
small stores are depleted and the requirements are increased due to rapid rate of
growth,
3. Pregnant and lactating mothers: They should receive vitamin D to supply the fetus and
infant, respectively, with sufficient vitamin D.

Calcium-Deficient Rickets
With Secondary Hyperparathyroidism
(Vitamin D-Deficiency Rickets)

Age incidence: Rickets may develop in breast-fed infants of vitamin D-deficient mothers as
early as 2 mo of age, but osseous changes of rickets can not be recognized radiographically until
several months of vitamin D deficiency; at the age of 6 mo-2 years.
Etiology
1. Lack of vitamin D
a) Dietary causes
The term rachitogenic diet is used to describe any diet which when used in infant
feeding will produce rickets.

Mohammed 88
  Foods poor in vitamin D:
1. Exclusive breast milk.
2. Fresh animal milk.
3. Cereals.
4. Vegetables.
5. Fruits.
 Foods with low content of calcium and phosphorus:
1. Breast milk.
2. Carbohydrates.
 Foods with unsuitable calcium and phosphorus ratio: Maximum calcium absorption
occurs when the ratio of calcium to phosphorus in the diet is about 2:1 (breast milk); a
lower ratio results in less calcium absorption (fresh animal milk).
 Foods with high content of calcium chelating agents: Phytates of cereals.
Calcium absorption is higher if the intestinal contents are acid and if the dietary sugar is
lactose.
b) Inadequate direct exposure to sunlight (failure of activation of provitamin D)
 Ordinary window glass prevents sunlight ultraviolet rays,
 Dark skinned infants in black race.
 Winter season.
 Excessive dust and fog.
 Ovcrclothing of the infants and keeping them indoors most of the time.
c) Congenital rickets: It develops in breast-fed infants born to vitamin D-deficient mothers as
early as 2 mo of age due to insufficient stores of vitamin D and minerals.
2. Malabsorption of vitamin D
a) Chronic recurrent diarrhea.
b) Cholestasis: The bile salts are essential for the absorption of calcium and vitamin
D.
c) Cystic fibrosis.
d) Various generalized malabsorptive disorders.
3. Hepatic diseases
Failure to secrete bile and /or failure of activation of vitamin D to 25, hydroxyl-
cholecalciferol lead to rickets.
Anticonvulsant drugs (Phenobarbital and phenytoins): They interfere with the
metabolism of vitamin D at the hepatic level.
4. Renal conditions

Mohammed 89
  Renal osteodystrophy: Decreased functional renal mass in chronic renal failure leads
to decreased la-hydroxylase activity resulting in reduction of active vitamin D &
formation and subsequent malabsorption of calcium and phosphorus from the
intestine.
 Vitamin D-dependent rickets: Mutation of the la-hydroxylase gene leads to rickets.
Clinical manifestations of calcium-deficient rickets due to vitamin D deficiency.
The clinical manifestations include :
 Constitutional manifestations.
 Skeletal manifestations.
 Muscular manifestations (hypotonia).
 Neurological manifestations (tetany).
I. Constitutional manifestations
The rachitic infants usually present with:
a) Excessive sweating with regard to winter season.
b) Baldness of the occipital hair.
c) Anorexia.
d) Constipation.
e) Irritability.
 The pathogenesis of these early manifestations is not known.
II. Skeletal manifestations
1) Skull
 Craniotabes: It is one of the early clinical signs of rickets. It is caused by thinning of the
outer table of the skull. It can be detected by a Ping-Pong sensation when pressing
firmly over the occiput or posterior parietal bones.
 Macrocephaly and asymmetry.
 Bossing at the parietal and frontal eminences due to abnormal proliferation of
cartilage at these areas, giving the head a boxlike appearance (caput quadratum).
 The anterior fontanel is larger than normal, and its closure may be delayed until after
the 2nd year of life.
 Eruption of the temporary teeth may be delayed, and there may be defects of the enamel
and extensive caries. The permanent incisors, canines, and first molars that are
calcifying during the period of vitamin D deficiency almost always have enamel defects.
2) Chest
 The rachitic rosary: Palpable enlargement of the costo-chondral junctions, often

visible, resulting from abnormal proliferation of cartilage at these areas.

Mohammed 90
  Longitudinal sulcus, lateral to Rosary.
 Harrison groove: It is a transverse groove along the lower border of the chest produced
by the pulling effect of the diaphragm on the lower ribs where it is attached.
 Pigeon breast deformity: The sternum with its adjacent cartilage appears to project
forward.(pectus carinatum).
 Flaring of lower ribs with eversion of the costal margins.
Depressed sternum (pectus excavation)Rare.
3) Spine
Kyphosis and scoliosis are often present. It is due to relaxation of the ligaments, and
hypotonia of the muscles.
These deformities can be corrected by placing the infant on his/her face on the table, fixing
the trunk at the shoulders by one hand and stretching the legs by the other hand.
This is to differentiate this condition from fixed tuberculous spine (Pott disease) which can
not be corrected.
4) Pelvis
The patients with rickets frequently have deformity of the pelyis, including the
contraction of the outlet due to forward projection of tip of the coccyx. In girls, if the
deformity becomes permanent, add to the hazards of childbirth and may necessitate
cesarean section.
5) Extremities
 Enlargement of the ends of long bones due to abnormal proliferation of cartilage cells

in the metaphysis.
 Deformities of long bones due to softening of the shafts of long bones (defective

mineralization) and the effect of the weight, stress, and fractures. Deformities
(bending) usually affect the upper limbs in crawling infants and lower limbs in
standing and walking infants in the form of bowleg (genu varum) or knock knees (genu
valgum),and (genu recurr valgum) The deformities are augmented by hypotonia of the
muscles and relaxation of the ligaments.
 Marfan sign: It is a transverse groove felt by palpation at the lower ends of long bones
of the lower limbs at the ankle area. Its pathogenesis is not exactly known, it may be
due to abnormal proliferation of cartilage at two different areas producing two
elevations with a groove in between.
 Pathological (greenstick) fractures: They may occur in the long bones due to softening
of the shafts, with minimal displacement, often with no clinical symptoms, and rapid
healing ability.

Mohammed 91
 III. Neurological manifestation
Hypocalcaemia tetany (see later).
IV. Muscular manifestations
Hypotonia of the muscles is a constant manifestation of rickets. The pathogenesis is
uncertain, but it may be related to hypophosphatemia.
Hypotonia is responsible for:.
1. Delay in motor development (sitting, standing, and walking).
2. Abdominal manifestations.
 Abdominal protrusion: It is due to various causes including hypotonia of the

abdominal wall muscles, hypotonia of the intestinal muscles, and diminished

capacity of the chest pushing the liver and spleen downwards (visceroptosis).
 Umbilical hernia: It is usually present.

 Visceroptosis of the liver and spleen: The liver and spleen are palpated, due to simple
downward displacement and not due to actual enlargement. This is visceroptosis is
due to deformity of the chest, hypotonia of the abdominal wall muscles, and laxity of
the suspending ligaments.
 Constipation.

3. Spine and lower limbs deformities.

Complications of rickets
1) Recurrent chest infections, particularly bronchitis and bronchopneumonia, are frequent
and are due to.
 Chest deformity interfering with proper expansion of lungs.

 Hypotonia of respiratory muscles leading to ineffective cough reflex.

2) GIT disturbances : Constipation, G.E.

3) Bone Fractures and deformities which many lead to dwarfism.
4) Anemia (Von Jaks anemia).
5) Tetany.
6) Obstructed labor.
Causes of Tetany in Rickets (Commonest)
Hypocalcaemia occurs in rickets in the following conditions.
1. Sever cases of rickets.
2. Failure of the parathyroid gland.
3. Shock therapy with vit D (600,000Unit), if calcium was not given.
4. In primary hypocalcaemic rickets (vit-D dependent rickets).
Differential diagnosis of rickets

Mohammed 92
 1. Differential diagnosis of delayed walking: See causes in Floppy infant syndrome. In
Pediatric Neurology.
2. Differential diagnosis of muscular hypotonia includes:
1. Rickets.
2. Marasmus.
3. KWO.
4. Congenital myopathy.
5. Poliomyelitis.
6. Hypokalemic states.
3. Differential diagnosis of craniotabes:
1. Rickets.
2. Hydrocephalus.
3. Prematurity.
4. Osteogenesis imperfecta.
4. Differential diagnosis of macrocephaly and delayed closure of the anterior fontanel:
See Pediatric Neurology.
5. Differential diagnosis of rosary chest:
1. Rickets.
2. Scurvy.
3. Chondrodystrophy.
4. Marasmus
Pathogenesis: Vitamin D deficiency leads to initial hypocalcaemia which in turn
stimulates the parathyroid gland to secrete more parathormone. Calcium is mobilized
from bone to maintain normocalcemia.
Secondary hyperparathyroidism is responsible for the biochemical changes characteristic
of this type of rickets.
Biochemical changes in vitamin D deficiency rickets
I. Blood changes:
 Normocalcemia.
 Hypophosphatemia.
 Hyperphosphatasia.
1) Serum calcium (normal level is 9-11 mg/ dL): It is maintained normal
(normocalcemia) or mildly reduced,

Mohammed 93
 2) Serum inorganic phosphorus (normal level is 4.5-6.5 mg/ dL): It is markedly
reduced (hypophosphatemia). The level is always less than 4 mg/ dL as
parathormone decreases phosphorus reabsorption in the kidneys.
3) Serum alkaline phosphatase (normal level is less than 200 IU/ dL): It is markedly
elevated (hyperphosphatasia) due to increased osteoblastic activity.
4) Serum 1, 25 dihydroxy chole-calciferol level: It is reduced.
II. Urine changes
1. Phosphaturia: Parathormone decreases phosphorus reabsorption in the kidneys.
2. Generalized aminoaciduria, impaired renal acidification, and occasionally,
glucosuria are other findings due to hyperparathyroidism.
Radiology of rickets
Path Ophysiology: New bone formation is initiated by osteoblasts, which are
responsible for matrix deposition and subsequent mineralization.
Osteoblasts secrete collagen, and changes in polysaccharides, phospholipids, and
alkaline phosphatase follow_ until mineralization occurs.
However, mineralization can not occur unless adequate calcium and phosphorus are
available in the presence of parathormone and vitamin D.
Active rickets
Defective mineralization of the bones results in the cartilage cells fail to complete their
normal cycle of proliferation and degeneration and lead to:
1. Deposition of newly formed uncalcified osteoid tissues in the metaphvsis leading
to .
 Enlargement of the ends of long bones.
 Swelling of the costo-chondral junctions.
 Bossing of the frontal and parietal eminences of skull.
2. Irregular invasion of the metaphyseal area by uncertified asteroid more tissues
centrally than peripherally leading to the typical cupping (saucer-like depression),
fraying(Rarefaction) and Flaring – widening are seen in X-ray films of long
bones.
With healing
Degeneration of cartilage cells along the metaphyseal-diaphyseal border occurs and
calcification in the zone of preparatory calcification in the metaphysis takes place,
producing a line that is clearly visible on radiographs.. As healing progresses, the
osteoid tissue between the line of preparatory calcification and the diaphysis also
becomes mineralized, as well as the osteoid tissue in the cortex.

Mohammed 94
 Healed rickets
The mineralization extends to fill the whole cupping of the metaphysis.

The radiological stages

[

The radiological findings are best seen in antero-posterior view in the ankle or the wrist
areas. Three radiological stages can be recognized.
1) Active rickets Metaphyseal areas .
1. Broadening (widening) of the ends of long bones(Flaring).
2. Fraying of the metaphysis. .
3. Cupping of metaphysis.
4. Absence of the provisional line of calcification.
5. Widening of the joint spaces due to increased translucency of the epiphyseal
cartilage.

Diphyseal areas (shaft of the long bone)

1. Generalized rarefaction (osteopenia).
2. Deformity of long bones.
3. Pathological fractures, mostly greenstick type.
2) Healing rickets
1. The appearance of the provisional (preparatory) line of calcification as a dense
white transverse slightly concave line in the region of the metaphysis.
2. Calcification increases towards the diaphysis.
3) Healed rickets
1. The line of provisional calcification thickens and extends to fill the whole cupping
of the metaphysis.
2. Healing of the fractures and correction of deformities.
3. Improvement of bone calcification in all-areas and they become more dense.
Prevention of calcium-deficient rickets due to vitamin D deficiency
1. Vitamin D administration to pregnant and lactating mothers.
2. Exposure to ultraviolet light (natural or artificial).
3. Oral administration of vitamin D supplement as early as the 3rd mo of life at a
dosage of 400 IU/ day especially for exclusive breast-fed infants, dark skinned
infants, infants protected form sunlight, and infants born during the winter months.
Treatment of calcium-deficient rickets due to vitamin D deficiency

Mohammed 95
 1. Exposure to both natural sunlight and artificial light of the appropriate
wavelength.
2. Vitamin D- administration
 Oral vitamin D3: 2,000-6,000 IU/ day for 2-4 wk.
 Oral active vitamin D form (1,25 dihydroxy-cholecalciferol): 0.5-2 ug/ day for 2-4
wk.
 A single intramuscular vitamin D at a dosage of 600,000 IU.
Failure to demonstrate radiological improvement (healing) within appropriate time, the
rickets is probably resistant to vitamin D(phosphate-deficiency rickets or end-organ
resistance to 1,25 (OH)2 D3).

Diagnosis of rickets

1) History: Exclusive breast feeding for more than 6_mo without supplementation is
usually obtained.
2) Clinical manifestations: Constitutional, skeletal, muscular, and
neurologicalManifestations.
3) Biochemical changes: The biochemical changes, particularly elevated serum
alkaline phosphatase enzyme, are the earliest manifestations of rickets. They occur
long before any radiological findings or clinical manifestations appear.
4) Radiological findings: They occur long before the onset of clinical manifestations.

Renal Rickets
A- Glomerular Rickets or Renal Osteodystrophy
B - Tubular Ricket
C- Vit-D Dependent Rickets

A. Glomerular Rickets or Renal Osteodystrophy:

Bone disease is one of the main features of chronic glomerular insufficiency and
chronic renal failure. The most common causes are:
1. Chronic glomerulonephritis.
2. Chronic pyelonephritis.
3. Polycystic kidneys.
4. Chronic renal failure of any other cause.

Pathogenesis:
1. Renal parenchymal damage leads to failure of renal 1-hydroxylation of Vit-D.

Mohammed 96
 2. The diminished glomerular filtration rate leads to phosphate retention and
acidosis. The hyperphosphatemia leads to 2ry hyper-parathyroidism, which leads
to bone resorption, and picture of osteitis fibrosis cystica.
3. Also acidosis increases solubilization of bone calcium salts.
Clinical Picture :
a) Manifestations of chronic renal failure usually dominate the clinical picture. There
are headache, fatigue, lethargy, anorexia, vomiting.
1. Marked growth failure and Dwarfism : due to under-nutrition, osteodystrophy,
hormonal abnormalities, medications especially steroids, and acidosis.
2. Anemia, which is progressive (look anemia of chronic renal disease).
3. Hypertension may be present.
b) Rickets, and picture of osteitis cystica.
1. There is muscle weakness.
2. bone pains.
3. bone deformities.
4. pathological fractures.
5. dental abnormalities.
Laboratory findings :
 Serum Ca : normal or decreased (no tetany due to acidosis).
 Serum PO4 : increased (in contrast to Vit-D deficiency).
 Serum Alkaline Phosphatase : increased.
 Ca X P product : elevated (in contrast to Vit-D deficiency).
 Renal function tests : increased BUN, increased serum creatinine.
 Blood examination : Anemia (caused by chronic renal disease).
 X-ray of bones : Picture of rickets + osteitis fibrosis cystica.
Treatment:
1. Treatment of the original renal condition. Dialysis may be needed.
2. Correction of acidosis : Na bicarbonate 1-3 mEq/kg/day.
3. Vit-D in high doses 2000 IU/kg/d was previously recommended Hypervitaminosis
D, with nephrocalcinosis, hypercalcemia, and renal damage occurred commonly.
4. Recently; dihydrotachysterol 20 ug/kg/d; or 1.25-(OH)2:-D3 (Calcitriol) 20-50
ng/kg/d are used.These two drugs proved to be safe and effective.
5. High Ca intake.

Mohammed 97
 6. Low P04 intake + oral administration of PO4 binders as "Aluminum hydroxide,
Aluminum carbonate gel or Ca carbonate". These bind P04 in intestinal lumen, and
help in lowering its serum level to around normal.
7. Surgical correction of deformities (corrective osteotomy) after healing.
N.B. stop Vit-D before surgery to avoid immobilization hypercalcemia.
8. Renal transplantation for treatment of renal failure, cures the bones disease, and
the metabolic abnormalities.
9. Parathyroidectomy is indicated in cases of 2ry hyper-parathyroidism refractory to
TTT (3ry).
B) Tubular Rickets :
This type results from renal tubular dysfunction. It can be further classified into :
1) Vit-D Resistant Rickets or Primary Hypophosphatemic Rickets (XL-D):
 It is an X-linked dominant disease. Both males and females are affected, but the
clinical picture is more severe in males.
 Two pathogenic mechanisms lead to rachitic bone disease :
1. Hereditary defect in tubular reabsorption of Phosphate, which
leads to phosphate loss in urine (Phosphaturia), and Hypo- phosphatemia.
2. Defective renal hydroxy lation of Vit-D at position 1, leading to a low serum
level of calcitriol (l,25-(OH)2 -D3).
This defect does not respond to the usual therapeutic doses of Vit-D, but responds
to high doses.
Clinical Picture :
- Bowing of lowerlimbs, genu varum, genu vulgum, coxa vara (due to weight bearing).
- Waddling gait.
- Short stature (Dwarfism).
- Teeth abnormalities (defective dentin), with periapical infections.
- The general condition of the patient is good.
- No tetany, weakness, rosary beads, or Harrison sulcus.
- No muscular hypotonia in spite of hypophosphatemia.
Laboratory findings :
- Serum Ca : N or slightly decreased.
- Serum PO4 : Markedly decreased with increased urinary PO4.
- Alkaline phosphatase : Increased.
- No evidence of hyper-parathyroidism.
Treatment

Mohammed 98
 The usual therapeutic doses of Vit-D are not effective.
- High phosphate intake : 0.5 - 1 gm/d in young children and 1-4 gm/d in older children,
as Na & K phosphate, orally divided every 4 hours.
- Previously, large doses of Vit-D were used, starting 25.000 iu/day, then gradual
increase of the dose by 25.000 iu every month until healing or toxicity.
- Recently, dihydrotachysterol 20 ug/kg/d or l,25-(OH)2-D , 20-50 ng/kg/d.
These drugs are less prone to cause toxic manifestations due to hypervitaminosis-D
(hypercalcemia, nephrocalcinosis & renal damage).

2- De Toni-Fanconi Syndrome :
It is a congenital or acquired (usually AR), multiple defects of the proximal renal tubules
to reabsorb the following:
- Phosphate  phosphatuvia + hypophosphatemia.
- Glucose  glucosuria without hypoglycemia.
- Amino acids  generalized aminoaciduria without hypoproteinemia
In addition, there may be :
- Potassium  hyperkaluria + hypokalemia.
- Bicarbonate  bicarbonaturia + metabolic acidosis.
Etiology:
1. Idiopathic : is the most common; either sporadic, AR, or AD in inheritance.
2. 2ry to : Renal toxins as mercury', lead, cadmium, or exposure to outdated
tetracyclines.
3. In association with certain inborn errors of metabolism as cystinosis, fructose
intolerance, galactosemia, tyrosinemia. Lowe syndrome, Wilson disease.

Clinical Picture :
- Dwarfism in addition to failure to thrive.
- Rickets; resulting from hypophosphatemia and acidosis. It does not respond to
ordinary doses of Vit-D.
- The general condition is usually bad due to acidosis & hypokalemia.
- Vomiting, polyuria, polydipsia, constipation.
- Weakness, fever with dehydration, and metabolic acidosis.
Laboratory findings :
1. Hyperchloremic metabolic acidosis .
2. Hypokalemia.
3. Hypophosphatemia.

Mohammed 99
 4. Glucosuria despite normal blood glucose level.
5. Generalized aminoaciduria.
Treatment:
In 2ry Fanconi syndrome : remove the cause as heavy metals, outdated tetracycline.
1) Vit-D : One of the following is used :

- High doses of Vit-D, starting 5.000 iu/day and gradual increase till a maximum of
2000- 4000 iu/kg/d. Most patients need at least 25.000 iu/d to heal rickets. These high
doses may produce toxicity. More recently, the following drugs are used :
- Dihydrotachysterol: starting dose of 50-100 ug/d (1mg = 120.000 iu of Vit-D).
- Calcitriol (l,25-(OH)2-D3) has been tried in TTT' with success.
2) Serum calcium : should be monitored weekly to avoid toxicity.
3) Correction of hypophosphatemia : Oral Phosphate 1-3 gm/d (neutral phosphate.)
4) Correction of acidosis and hyponatremia by alkali therapy 2-15 mEq/kg/day as :

- Na bicarbonate solution 1 ml = 1 mEq.

- Shohl solution (140 gm citric acid + 90 gm Na citrate in 1 liter H2O. 1 ml = 1 mEq of base.
- Polycitra solution (5 ml = 550 mg K citrate + 500 mg Na citrate + 334 mg citric
acid);1ml=2 mEq of base. This solution is helpful in correcting hypokalemia as well as
acidosis.
- Correction of hypokalemia by K salts 2-3 mEq/kg/day; if polycitra is not used.
3- Lignac Syndrome (Fanconi Syndrome with Cystinosis): (AR)
In addition to the manifestations of Fanconi syndrome, there is abnormal accumulation
of cystine in various tissues. These crystals are deposited in RES cells (spleen, liver, LN,
and bone marrow), in addition to renal tubules, renal parenchyma, cornea and
conjunctiva.
a) The infantile or nephropathy form of cystinosis presents with:
- Fanconi syndrome at 3-6 Mo, severe growth failure, and hypothyroidism.
- Gradual progress to renal failure develops within 10 years.
- The hair may be blond, with fair complexion (diminished pigmentation).
- Photophobia 2ry to deposits of cystine crystals in cornea.
b) The adolescent form : onset on 2nd decade of life, mild renal involvement, with very slow
progression. No growth failure.
c) The adult form (benign) : no renal disease.
Investigations :
- Slit lamp examination of cornea shows the refractile cystine crystals.

Mohammed 100
 - Measuring cysteine content in WBCs or fibroblasts.
- Lab. findings of Fanconi syndrome, or end stage renal disease.
Treatment:
- Same as lry Fanconi syndrome.
- D-Penicillamine was used to chelate cystine.
- Recently; Cysteamine : a drug which binds -SH group of cystine, showed effective in
slowing the rate of progression of the disease.
- Patients with end stage renal disease : hemodialysis and renal transplantation.
4- Infantile Renal Tubular Acidosis ; Lightwood syndrome. (AR)
The condition results from renal proximal tubular inability to acidify urine. This leads
to metabolic acidosis, hypophosphatemia, and hypokalemia.
Treatment :
1. Treatment of acidosis and hypokalemia (alkali therapy ).
2. Phosphate therapy (as in Fanconi).
3. Large doses of Vit-D.

5- Lowe Syndrome : Oculo-Cerebro-Renal Syndrome: (XL-R)

It is a rare X-linked recessive disease, which presents as :
- Ocular  Congenital Cataract, Glaucoma, Buphthalmos.
- Cerebral  Mental retardation, severe hypotonia and hyporeflexia.
- Renal  Inability to acidify the urine properly + other features of Fanconi syndrome.
- Rickets is the result of acidosis and hypophosphatemia.
TTT: No specific TTT, other than supportive as in case of Fanconi syndrome.
C) Vit-D Dependent Rickets : or Primary Hypocalcemic Rickets :
It is an AR disease, which usually presents in one of the following types:
Type I: It is due to hereditary defect in renal hydroxylation of Vit-D. leading to
deficiency of 1,25-(OH)2-D3 .Both serum Ca & P are low, while alkaline phosphatase
enzyme is elevated. There is also 2ry hyper-parathyroidism.
Treatment is by high doses of Vit-D. However, the best treatment is
"1,25-(OH)2-D3" in a very small dose (1 ug/day), or Dihydrotachysterol 1 mg/day.
Type II : There is normal hydroxylation of Vit-D, but there is target organ resistance to
1,25(OH)2-D3 .There is short stature and alopecia totalis.
- Rickets may respond to very high doses of the active Vit-D "1,25-(OH)2-D3," 15-
30 ug/d.

Mohammed 101
 Hepatic Rickets
Rickets as a result of hepatic affection is usually due to one of the following :
1. Defective hydroxylation at the position 25.
2. Malabsorption of Vit-D due to absence of Bile salt from the intestine as a result of
biliary obstructive lesions.
3. Toxic Hepatic Hydroxylation : This occurs in case of anti-convulsive therapy
(Epanutin, Phenobarbitone). Both drugs induce accelerated metabolism and
catabolism of Vit-D. Hence the daily intake of Vit-D should be increased.

Celiac Rickets
This results from malabsorption of Vit-D (fat soluble). In addition, the unabsorbed fatty acids
bind Ca++ ions in the intestine forming Ca soaps, which are precipitated in the intestine,
leading to Ca malabsorption.
Treatment:
- Give water soluble Vit-D orally, or Vit-D by IM inj.
- Calcium should be given in high doses to compensate for Ca loss in stools.

Hypo-Phosphatasia

This is an autosomal recessive disease, which results from congenital absence or deficiency
of the enzyme "Alkaline Phosphatase". It leads to defective mineralization of bones.
- In severe cases it is lethal (Congenital lethal hypophosphatasia)
- In mild cases it presents as rickets, with bowing and short stature.
- Serum Ca is high (hypercalcemia), which may lead to nephrocalcinosis.
- Serum alkaline phosphatase is markedly low.
- The urine characteristically contains increased amount of phospho-ethanolamine.
Treatment:
- Infusion of plasma rich in alkaline phosphatase.
- Spontaneous improvement occurs in the mild form as the child grows.

Hyper-Parathyroidism
- In cases of primary' hyper-parathyroidism (Hyperplasia, Adenoma, or Carcinoma) there is
increased production of parathormone. The condition may resemble that of rickets, but more
commonly the picture of osteitis fibrosa cystica dominates.
- There is increased serum Ca, and increased serum alkaline phosphatase.

Mohammed 102
 - There is marked phosphaturia + hypophosphatemia.
TTT : Surgical exploration :
- If adenoma : excision is done.
- If hyperplasia : total parathyroidectomy. Post operative supplementation with Ca is essential

Tetany of Vitamin D Deficiency

(Infantile Tetany)

Definition: Tetany is a state of muscular irritability resulting from reduced serum calcium
level, the calcium ions normally exert inhibitory control on the neuromuscular junctions.
Etiology and pathogenesis
In vitamin D deficient rickets, secondary hyperparathyroidism maintains
normocalcemia via mobilization of calcium from bones.
Hypocalcemia in these patients may occur in the following conditions.
1) Prolonged untreated cases: The bone is markedly depleted of calcium.
2) Administration of massive dose of vitamin D (600,000 IU): It leads to rapid
mobilization of calcium from blood to bone.
3) Associated conditions that impair intestinal calcium absorption: Hepatic diseases.
Diagnosis
1. Clinical manifestations of rickets.
2. Clinical manifestations of tetany.
3. Biochemical findings
 Hypocalcemia: The serum calcium level is less than 9 mg/ dL (the ionized calcium is
less than 4 mg/ dL).
It is 7-9 mg/ dL in latent tetany and less than 7 mg/ dL in manifest tetany.
 Hypophosphatemia and hyperphosphatasia.

Clinical manifestations
Manifest tetany
1. Carpal spasm: The thumb is drawn into the cupped palm, the other fingers are
flexed at the metacarpo-phalangeal joints, and the wrists are flexed.
2. Pedal spasm: The ankle is extended, the sole is cupped, and the toes are flexed.

Mohammed 103
 3. Laryngeal spasm: Attacks of spasmodic closure of the glottis lead to inspiratory
high- pitched sounds.
4. Generalized convulsions: They are associated with carpo-pedal spasms.

Latent tetany: They are no clinical manifestations. The condition can be elicited by
certain provocating tests.
1. Chvosteck sign: Tapping the facial nerve anterior to the external auditory meatus
elicits a twitch of the upper lip or entire mouth due to excitation of the facial
muscles on the stimulated side.
This test is not very specific as it is positive in 10% of normal individuals without
hypocalcemia.
2. Trousseau sign: Compressing the upper arm with a sphygmomanometer cuff with a
pressure slightly above the systolic pressure for more than 3 min will result in carpal
spasm due to more hypocalcemia is present as a result of the ischemia of the motor
nerves.
The same maneuver can be applied to the lower limbs leading to pedal spasm.
3. Peroneal sign: Tapping of the peroneal nerve near the lateral malleolus in the ankle
area leads to pedal spasm.
Other causes of tetany
1. Hypomagnesemia: Adequate serum magnesium concentration is necessafy for
normal release of parathormone leading to hypocalcemia and tetany, the later
condition is not resolved by calcium administration.
2. Alkalosis: Acidosis increases the ionized calcium concentration by displacing
calcium from albumin, whereas alkalosis decreases the ionized calcium
concentration, causing tetany.
Management of hypocalcemic tetany
1. Management of convulsions
 Intravenous calcium gluconate 10% solution (1 mL contains 9 mg elemental
calcium) at a dosage of 10 mL over 5-10 min. Patients receiving intravenous
calcium should be on a cardiac monitor (bradycardia and cardiac arrest due to its
inhibitory effect on sinus; node). Monitoring of serum ionized calcium is
mandatory. Additional doses are given as necessary. Some patients require a
continuous calcium drip to maintain the desired serum calcium level.
 If no response search for the etiology and correct the alkalosis or magnesium
deficiency (mag. sulp hate 50% 0.2ML/Kg i.m injection)

Mohammed 104
 2. Maintenance management: It is started once the symptoms of hypocalcemic tetany are
resolved.
a) Oral calcium supplementation: Liquid preparations of calcium are available. The
starting dose is 50 mg/ kg/ 24 hr, usually divided into 3-4 doses. Increase the dose
of calcium according to the serum calcium level.
b) Vitamin D supplementation: It is also necessary for many conditions.

Vitamin Toxicity or Hypervitaminosis

 Hypervitaminosis D: Usually due to high doses (over 20.000 U/day for 1-3 months).
Clinical Picture : The signs & symptoms are similar to those of "Idiopathic
Hypercalcemia".
- GIT : anorexia, vomiting, constipation + weight loss.
- Kidney : polyuria, polydipsia, dehydration, renal stones, nephrocalcinosis.
- Generalized weakness and hypotonia + anemia + irritability.
- Hypercalcemia  hypercalcuria + metastatic calcifications (renal + other tissues) +
Calcific aortic stenosis.
Investigations :
- Increased serum Ca (N= 9-11 mg/dL).
- Hypercalcuria  +ve Sulkowitch test on urine.
- X-ray shows : metastatic calcifications, nephrocalcinosis & osteoporosis.
Differential diagnosis:
- Hyper-Parathyroidism.
- Idiopathic Hypercalcemia.
- Chronic renal failure.
Treatment:
A. Preventive : avoidance of high doses of Vit-D for long periods.
If necessary, monitoring of serum Ca is important.
B. Curative :
1. Stop Vit-D intake till symptoms disappear, and serum Ca becomes normal.
2. Low Ca diet.
3. Correction of dehydration.
4. Aluminum hydroxide gel orally (to decrease Ca absorption).
5. Na versinate (EDTA) to chelate Ca.
6. Cortisone in severe cases, to decrease Ca absorption from intestine.

Mohammed 105
  Hypervitaminosis A :
A. Acute:
- Usually after ingestion of 300.000 U or more.
- Nausea, Vomiting + increased I.C. pressure, bulging fontanel, papilledema, 6th cranial
nerve palsy, giving the picture of Pseudo-tumor Cerebri
B. Chronic : Anorexia pruritus, tender swelling of bones, alopecia, craniotabes, fissuring of
angles of mouth, and desquamation of palms and soles.
X-ray  Cortical hyperostosis of bones.
 Vitamin K toxicity :
- Large doses of synthetic Vit-K leads to hyperbilirubinemia and kern-icterus in the
premature and G-6-PD deficient newborn. It is an oxidizing agent which leads to
hemolysis of RBCs.
- Vit-K1 is not toxic (the naturally occurring Vit-K).
 Nicotinic acid Toxicity : "not the amide form"
It is a vasodilator, leading to peripheral vasodilatation, flushing and pruritus within 1/2
hour from injection.
Obesity

Definition of obesity: The body mass index (BMI) exceeds the age-sex-specific 95th
percentile.
Definition of overweight: The body mass index (BMI) is between 85th and 95th
percentiles.
Etiology
I. organic obesity
1. Obesity occurs due to hormonal aberrations: Cushing syndrome and
hypothyroidism.
2. Certain genetic syndromes as Prader-Willi are rare and are associated with
defects at a single genetic locus.
II. Simple (exogenous) obesity
It is the most common type of obesity. It is reflecting complex interactions between:
1. Genetic background of the patient: In large unrelated populations, there is statistical
evidence for recessive gene effects on body size variables, including BMI, abdominal
visceral fat, relative fat pattern, and obesity. Studies have demonstrated familial

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 aggregation of obesity. Parental obesity, particularly maternal, is predictive of
childhood obesity.
2. Environmental stimuli:
 Factors that increase energy intake or those that lead to reduced energy expenditure,
ultimately lead to obesity.
 Factors increasing energy intake: Trends in food intake; plentiful and easily
accessible high-caloric food (fast foods).
 Factors reducing energy expenditure: Obesity is directly related to lack of physical
activity during hours of television viewing and computer games during the growing
years, particularly the 10-14 yr age groups.

Control of feeding
 Energy intake and energy expenditure is under the control of complex interactions
between peripheral signaling and effector systems and neuroendocrine systems
(hypothalamus-pituitary-adrenal axis).
 Leptin hormone is made in adipose tissue and acts centrally in the hypothalamus.
1. During fasting and weight loss period  low plasma concentrations of leptin and
insulin  release of orexigenic neuropeptides (that stimulate feeding) from
hypothalamus  hyperphagia  increase food intake and decrease energy
expenditure (by inhibiting sympathetic activity and other catabolic pathways).
2. During feeding and weight gain period  high plasma concentration of leptin and
insulin release of anorexipenic agents from hypothalamus (that inhibits feeding)

such as melanocyte-stimulating hormone, corticotropin releasing hormone(releasing
ACTH from pituitary gland, resulting in increased corticosteroids formation by the
suprarenal gland),and thyrotropin-releasing hormone(stimulating TSH release from
pituitary, increasing the thyroid hormones) anorexia decrease food intake and
increase energy expenditure.

Diagnosis
Obesity is diagnosed by plotting the BMI of the patient into the percentile curves and the
finding it is more than 95th percentile.
First of all, we have to differentiate between simple exogenous obesity and organic obesity.

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 Differentiation between Simple Exogenous Obesity and
Organic Obesity
Items Simple Exogenous Obesity Organic Obesity
1. Stature Normal for age or tall stature Short stature

2. Bone age Normal for age or slightly advanced Retarded bone age

3. Pubertal changes Normal at proper age Delayed

Hypothyroidism or
4. Hormonal changes Normal
hypercortisolemia may be found

Acanthosis nigricans: Many obese youth have a hypertrophic hyperpigmentation of the skin,
most commonly seen on the posterior neck and in skin creases.
Complications of obesity
1. Hypertension. 2. Hyperlipidemia and cardiovascular diseases.
3. Type 2 diabetes mellitus. 4. Respiratory disease (asthma).
5. Degenerative joint disease. 6. Depression and anxiety.
7. Infertility. 8. Cancer.

Prevention of simple exogenous obesity.

1. Nutritional education:
 Changing dietary habits. School meal programs should provide healthy choices and
avoid high-caloric beverages and snacks.
 Counsel obese parents about the risk of childhood obesity in their children, and the
parents about the' fact that breast-fed infants are less likely to develop adult obesity
than bottle-fed infants.
2. Physical education: Physical education programs should be a priority of the school.
systems, and increasing the safety of streets and playgrounds may be necessary.
3. Screening of the school-aged children for overweight to prevent obesity.

Treatment of simple exogenous obesity

1. Reduction in energy intake: Diet that is lower in carbohydrates and fats with
increasing fiber content. The goal of treatment is to achieve a 10% reduction in weight,

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 as severe caloric restriction, especially in young children, may result in an
unacceptable decrement in height velocity.
2. Increasing in energy expenditure: Any increase in physical activity is good, with
regular aerobic exercise being the goal. This should be accompanied by a decrease in
television viewing and computer games.
3. Medications: Anti-obesity drugs are not approved for prolonged use or for use in
youth, and further more, may only benefit a minority of patients.
4. Surgery.
a) Surgical therapy to reduce the volume of the stomach: It may be successful in the
long-term management.
b) Surgical therapy to remove fat (liposuction): It is not a long-term solution ,if used
alone.

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 Other Vitamin Deficiencies
The following table shows the most important sources, manifestations of deficiency, and
treatment of the different vitamins.
Name Rich sources. Manifestations of Deficiency Treatment

- Liver, Fish, Oils, Milk & - Night blindness. - 5000 U/day Oral +
Milk products, Egg yolk. - Xerophthalmia, Keratomalacia, Blindness. 25.000 U/ IM, till
Vit-A - Carotenoids from plants - Hyperkeratosis of m.m. & skin (goose recovery.
green vegetables, yellow skin). - then 5000 U/d (O).
fruits and vegetables. - Retarded growth.
- Green leafy vegetables - Hgic tendency specially in newborn, due to - 5 mg/d of Vit-K1.
Vit-K Liver. It is synthesized by deficiency of factors II, VII, IX, X. Whole blood if due to
intestinal flora. Liver disease.
Vegetable oils, Green - Hemolytic anemia in premature. - 10-20 U/d for
Vit-E leafy veg., Nuts, Legumes. - Anemia of malnutrition. preterms.
- Liver, Meat, Milk. Beriberi - 10 mg/d (O or IM).
- Whole grains, Wheat, - Early : Fatigue, Irritability, Anorexia.
Vit-B 1 Legumes. - Then : Indigestion, constipation,
Headache, Insomnia.
- Late : Polyneuritis, Heart failure.
- Milk, Cheese, Liver, - Angular stomatitis, Cheilosis, Glossitis. - 10 mg/d (Oral) +
Organ meat, Eggs, Fish. - Vascularization of cornea, Photophobia, Other Vitamins.
Vit-B2
- Whole cereals, Green, Blurred vision, Keratitis, Itching of eyes.
leafv vegetables. - Growth retardation.
- Meat, Liver, Kidney. - CNS : Convulsions, Poly-Neuropathy. - 100 mg IM for
- Whole grain, peanut, - Anemia: Hypochromic Convulsions.
Vit-B6
Soybeans. - Glossitis, Seborrhea. - 100 mg O for other
Conditions.
- Poultry, Meats, Fish, Pellagra :- Early : Fatigue, Anorexia, - 50-300 mg/d O or IM.
Eggs. Headache. + Well balanced diet.
Niacin - Whole grains, Green - Late : (4Ds): Diarrhea, Dermatitis,
vegetables. Dementia and Death.

Folic - Liver, Cheese, Cereals, - Megaloblastic anemia. - 2-5 mg/d IM then

acid Green vegetables, Nuts. orally.
- Muscles, Organ meats, - Pernicious anemia : - Megaloblastic - 1 mg/d IM for 2 wks.
Vit-B12 Fish, Egg, Milk, Cheese. anemia + SCD (Subacute Combined - Then 1 mg/month.
Degeneration).
- Yeast, Animal products, - Dermatitis, Seborrhea, Retarded growth.
Biotin Produced by intest , It is inactivated by Avidin of raw egg white.
flora.
- Citrous fruits, Tomatoes, Scurvy - 100-200 mg/d Oral or
Green - Hgic manifestations (gums). IV.
vegetables(uncooked) - Poor wound healing. - 3-4 ounces of orange
Vit-C juice.
- Subperiosteal He.
- Tender limbs.
- Susceptibility to infection.

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