MEDICI OMNES DUCIENS - EX FLAMMIS RESURGE

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Pediatrics
Nutritional Disorders II
Marie Clare V. Robles, MD

There is no hard and fast rule for the age of administering

Vitamin A, but for the Government programs, the cut-off age
is 5 years old and below (Patak Pinoy Programs).

* italized notes are must knows!

3 Vitamins deficiency advocated by the WHO because they

are the most common worldwide:
Vitamin A,
Iodine defiency,
Iron Deficiency (Iron is associated with poor
mental performance as well as Iodine

Fat Soluble Vitamins: ADEK

Vitamin A
Active forms are retinol, retinaldehyde and retinoic acid
Plants synthesize the more complex carotenoids which are
cleaved to retinol by most animals and stored in the liver as
retinyl palmitate
Betacarotene- Vitamin A found in plants
N retinol plasma values: 15-30 mcg/dl in infants & 30-90
mcg/dl in adults
Vitamin A (Retinol) Deficiency
Functions:
1. Eye component: Retinal is the prosthetic group of
photosensitive pigment in both rods (rhodopsin) & cones
(iodopsin) of the eyes, major difference lies in the nature of
protein bound
*for night adaptation that is why the earliest symptom is
nyctalopia or night blindness, how is it found? They always
bump into things at night.
2.
3.

Clinical Manifestations of Hypovitaminosis A

A. Eye signs & symptoms (according to appearance)
1. An early symptom is nyctalopia or night blindness
later photophobia then insensitivity to pain
st
2. 1 clinical sign is xerosis conjunctivae-lack of luster
in the eyes, associated with dry eyes
3. Bitots spots
4. Corneal xerosis or xeropthalmia-opacity; later
stage
5. Corneal ulcers or keratomalacia (last stage- semi
blind)
6. Blindness
B. Skin signs: xerosis of the skin & follicular hyperkeratosis or
phrynoderma

Needed in lysosomal membrane stability

Plays a role in keratinization. cornification, bone
development & cell growth & reproduction

Remember that in hypovitaminosis A, it is not only the eyes

that is affected but also you have skin manifestations.
Treatment: Vitamin A, WHO recommendation: give today,
tomorrow and 4 weeks after (3 doses)

*If you are asked, Which is the Vitamin important for

recurrent cough and colds (Pneumonia)?It should be Vitamin
A, because you need it for reepithelialization. So, its not only
for the eyes but also for the skin.

Case: 2 y/o with night blindness, Give 200,000 UI today,

tomorrow & 4 weeks after.
Case: Malnourished, poor weight, stunted, poor diet. Just
Give a single dose as long as there are still no manifestations
of hypovitaminosis A.

In diarrhea, which Vitamin would have an effect?Vitamin A,

but we dont normally give it because it is a fat soluble
vitamin, therefore we are afraid of toxicity.
However, if you read protocols,if you have patients with
measles, you are given a case, a child has measles, which
Vitamin will be given? Vitamin A, why Vitamin A? because it
helps in the reepithelialization of your cells. Thats why if you
have pimples, it should not be Vitamin C, it should be
Vitamin A, however, it is not practiced right and left because
of toxicity.
Dose of Vitamin A aged 6 months old to 1 year old; seldom
do you give Vitamin A to children less than 6 months old
unless in mothers with deficiency therefore we have fetal
deficiency. We give it to

6 months to 1 year: 50,000 IU

1 -2 years old: 100,000 IU
2+ years old: 200,000 IU
Prophylaxis: give it only as a single dose
Interval: every 6 months

Healthy individuals: give as prophylaxis. 4 weeks interval.

Give today, tomorrow and 1 month after.
Hypervitaminosis A
Acute Intoxication:
Results when excessively large single doses 300,000 IU
ingested
Infants: nausea, vomiting, drowsiness or irritability with
signs of increased ICP

Chronic Intoxication:
Results when 50,000 IU/day ingested for several weeks or
months
If you are giving Vitamin A, make sure that in the past six
months, the patients has not received Vitamin A before giving
another dose to reduce risk of toxicity due to errors.If you are
unsure when the last dose was given, just give as a prophylaxis
(1 dose).

Therefore, in DOH programs, when giving Vitamin A

capsules ask when was the last dose given.
Available preparation: 25,000 IU & 50,000 IU, if you need
100,000 IU, give it at one sitting. It means that if the
available preparation is 50,000 IU, you give 2 capsules. Prick
the capsule (gel form) and let the contents drop to the childs
mouth. If you are giving the one in the (health) center, what
is the preparation? 200,000 IU, how do you give it? Just give
2 drops (equivalent to 100,000 IU).
Government programs are must know because they are
always asked in the board exams.

Vomiting is a sign of increased ICP

Adults: drowsiness, irritability, headache & vomiting
Serum vitamin A values= 200-1000 IU/dl (N: 50-100 IU/dl)

Signs & symptoms in infants:

a. Early are anorexia, pruritus, irritability, tender swollen
bones with motion
limitation
b. Alopecia,
seborrhea, cheilosis
& peeling of palms
& soles
c. Hepatomegaly &

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hypercalcemia observed
Craniotabes & hyperostosis of long bones (differentiate
from Caffeys disease)
Elevated serum Vitamin A levels confirms diagnosis
Reversible manifestations when Vitamin A discontinued
d.

Vitamin D
90% as Vitamin D3, cholecalciferol produced in the skin by
UV irradiation of 7- dehydrocholesterol (predominantly
animal sterol)blood25 hydroxylation to calcidiol in liver
+ PTHdi-hydroxylation in kidney to calcitriol 1,25 (OH) 2cholecalciferol
1,25-dihydroxycholecalciferol is most active form of Vitamin
D
Vitamin D2, calciferol, is taken orally from plants then
irradiated as above
Animal derived Vitamin D3, cholecalciferol and Vitamin D2
(in plants) activated ergosterol are biologically equal

3.

4.

Almost all bones are affected. There is also

delayed teeth eruption.
5.

If you are asked in the exam when the best time to is for the
baby for sunlight exposure to get Vitamin D, answer,
between 10am- 2pm. 10 am is the peak. However, maybe
this may only be applicable in non-tropical countries.
Vitamin D (Cholecalciferol) Deficiency
Functions: Vitamin D enhances the absorption of calcium from the
gut, removal of calcium from the bone and phosphate reabsorption in
the kidney.
Etiology:
st
nd
Florid rickets appears toward the end of the 1 year to 2
year of life
Lack in the diet or lack of sunlight exposure
Rapid growth as in prematures & adolescents
Disorders of absorption such as celiac disease, steatorrhea
or cystic fibrosis
In children with hepatic disease
Maternal malnutrition
Clinical Manifestations of Hypovitaminosis D
A. Rickets: deficient calcification or softening bones in a
growing child resulting in deformation of bones
1.

Head manifestations
a. Craniotabes: Thinning of skull outer
table detected by pressing firmly over
occiput or posterior parietal bones &
feeling a ping-pong ball sensation, may
st
disappear before end of 1 year but
rickets continues resulting in flattening
& at times permanent head asymmetry
b. Anterior fontanel larger & closure
delayed
c. Caput quadratum: Box-like head due to
thickened & prominent central parts of
the parietal & frontal bones
Scurvy is more in the mouth and ribs (most usually
the ribs) but rickets manifest with cartilage
problem. Vit.C deficiency has associated bleeding
problems and scorbutic bead with chest
depression. Both scorbutic and rosary rachitic
beads occur in costochondral junctions but in
rachitic it is usually have widening and elevated
thorax(palpable), and Harrisons groove. The long
bones and the cranial bones are also affected as
opposed to scurvy which usually affects just the
ribs.

2.

Thorax signs

a. Palpable enlargement of the

costochondral junctions called the
rachitic rosary
b. Flattened sides of the thorax with
posterior longitudinal grooves
c. Pigeon-breast deformity
d. Harrison groove
Spinal column signs
a. Scoliosis commo
b. Kyphosis when sitting
c. Lordosis in the erect position
.

B.

C.

Extremities in children above 2 years

a. Thickened & enlarged wrists & ankles
b. Bowlegs or knock-kness as a result of the
bending of the softened shafts of the
femur, tibia & fibula (long bones)
c. Coxa vara or pronated feet
d. Greenstick fractures
e. Arm position- internal rotation
6. Muscles are poorly developed & lack tone
Osteomalacia: accumulation of uncalcified osteoid tissue in
rib joints of an adult resulting in
1. Pain in the pelvis, lower back and legs
2. Tenderness felt in the shins and in other bones
3. Waddling gate
4. Deformities afo the pelvis
5. Tetany may occur manifested by involuntary
twitching of the facial muscles or by carpopedal
spasm
6. Spontaneous fractures may be a feature
Osteomalacia should not be confused with osteoporosis, a
disease of ageing, in which decalcification is also a feature.
They are not the same.
Osteomalacia have problems with osteofication while in
osteoporosis due to aging, there is decalcification.
Osteomalacia is associated with Vitamin D deciency and not
Osteoporosis. Fractures are common in Osteomalacia due to
poor calcification (main problem in osteomalacia)

Diagnosis:
1. History & clinical observation
2. Laboratory findings:
a. Serum Ca may be normal or low but high phosphate
level
b. Serum phosphorus level below 4 mg/dl (Normal: 4.56.5 mg/dl but in rachitic infants reduced to 1.5-3.5
mg/dl even lower)
c. Serum alkaline phosphatase elevated (Normal: 5-15
Bodansky units per 100ml but elevated to 20-30 in mild
rickets & up to 60 or more in severe cases)
d. Serum 25-hydroxycholecalciferol decreased
e. Urinary cyclic AMP elevated
3. Roentgenographic changes
a. X-ray of the wrist best for early diagnosis because of
the cupping & fray of the proximal ends of ulna &
radius (poor
calcification of
bones is a problem
seen and
manifested in the
wrist. Bone age is
best manifested

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b.
c.
d.

with the wrist x-ray)

Humeral ossification center barely visualized
Shafts osteoporotic or density decreased but
trabeculae unusually prominent
Rosary beading of the sterna ends of the ribs due to
deposited uncalcified osteoid tissue becoming
compressed & bulges laterally

Case: Regularly pigeon chested is not malnourished (normal

weight, no stunting, big chest- pigeon breast, no wasting)
Finding: Normal.
Advise to parents: expose to sunlight, take vitamin D
capsule. Take calcium supplements and that the parents
should not worry.
Always look for undernutrition in specific vitamin
deficiencies because seldom do you see a specific vitamin
deficiency without undernutrion.
Differential Diagnosis:
1. Craniotabes in hydrocephalus & osteogenesis imperfect
2. Rosary at the costochondral junctions in scurvy &
chondrodystrophy
3. Epiphyseal lesions in congenital epiphyseal dysplasia,
cytomegalic inclusion disease, syphilis, rubella & copper
deficiency
4. Congenital pigeon breast deformity
5. Familial bowlegs
6. Metabolic disturbaces with osseous lesions
Complications:
1. Respiratory infections
Prognosis
1. In the tropics, usually has a tendency to heal spontaneously
2. A possibly deforming disorder
3. Not fatal but complications & intercurrent infections may
cause death
RDA: 400 IU (1 IU Vitamin D= 0.025 mcg cholecalciferol/
ergocalciferol)
Prevention:
1. Sunlight prophylaxis effective only in temperate zones
during the summer months in haze-free areas
2. Daily requirement of Vitamin D is in 1 quart of fresh whole
milk or a can of evaporated milk
3.
4. Prematures or breast-fed infants should receive
supplemental Vitamin D daily because milk is a poor source
unless fortified. Breastmilk is low in Vitamin D.
5. Vitamin D should also be administered to pregnant &
lactating mothers
Treatment:
1. Daily administration of 50-150 mcg of Vitamin D3 or 0.5-2
mcg of 1,25-dihydroxycholecalciferol will produce healing
seen on X-ray within 24 weeks
2. Vitamin D 15,000 mcg in a single dose without further
therapy for several months may be advantageous
3. After healing is complete, the dose of vitamin D should be
lowered to 20 mcg/day
4. If no healing occurs, rickets is probably resistant to Vitamin
D or non-nutritional rickets
Problems with vitamin D may be secondary to poor milk
intake.
Hypervitaminosis D
Etiology:
Excessive intakes from:
Inadvertently substituting concentrated form for dilute

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Parents increasing prescribed dose

Inadequately controlling dosages for children receiving
large amounts of Vitamin D for chronic
hyperphosphatemic states

Clinical Manifestations
Symptoms after 1-3 months
1. Hypotonia, anorexia, irritability, constipations,
polydypsia, polyuria & pallor
2. Dehydration usually present
3. Aortic valvular stenosis, vomiting, hypertension,
retinopathy & clouding of cornea & conjunctiva may
occur
Vitamin E (Tocopherol) Defiency
Deficiency is not common in Vit. E. It is only common in preterms
Manifestation: poor skin luster, hemolytic problems, neurologic,
muscle weakness and neurologic problems
Poor skin
1. Some have creatinuria, ceroid deposition in smooth muscle,
focal necrosis of striated muscle & muscle weakness
2. Prematures may develop hemolytic anemia at 6-10 weeks of
age
3. Increase risk of retrolental fibroplasias in prematures,retinopathy of prematurity- going blind
4. Degenerative neurologic syndrome when due to biliary
atresia
5. Increased platelet adhesiveness
6. Anemia in kwashiorkor
Prevention & Treatment:
1. RDA not known but ).7 mg/g of unsaturated fat in the diet
adequate
2. Premature infants may be given 15-25 IU/ 24 hours
3. Large oral or parenteral doses may prevent permanent
neurologic abnormalities in biliary atresia or
abetelipoprotenemia
Vitamin K
Vitamin K1, naturally occurring vitamin K, is abundant in
pork, liver, soybeans & green leafy vegetables
Intestinal microorganisms synthesize
Required for normal clotting of blood
Vitamin K-dependent clotting factors made in the lover:
prothrombin (Factor II), proconvertin (Factor VII), plasma
thromboplastin component or PTC (Factor IX) & StuartProwter factor (Factor X) factors 1972
Vitamin K Deficiency (Hypoprothrombinemia)
Clinical Manifestatios:
1. Hemorrhagic manifestations are the hallmark
2. Bleeding in the newborn from the cord or circumcision site
3. GIT bleeding, hematuria & intracranial hemorrhage more
serious
4. Anemia & shock may ensue from severe blood loss
Laboratory test: The most useful test is the 1-stage prothrombin time
test (Quick), prolongatioin indicates presumptive evidence deficiency
(Protime- PT)- diagnose
Vitamin K should be given to all newborns at the dose of 1mg IM,
though it can be given SQ or PO, but the best route is IM, 1mg in term
and 0.5mg in preterm.
Why give it to all newborns?
Because of the sterile gut, you
need the normal flora to
synthesize Vit. K and produce it.
Early in life, Vit. K deficiency is
manifested as Hemorrhagic

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Disease of the Newborn. It will manifest as bleeding from the umbilical

stump. If the umbilical stump is about to fall off, there will be blood
but usually it is minimal because it is clamped and dried off. To
recognize active bleeding, the bleeding is continuous or oozing
depending on the severity as opposed to normal, which only has few
bleeding.
Late manifestation: Acquired Prothrombic Complex Deficiency
Risk factor:
No Vitamin K at birth
Exclusive breastfeeding- Vitamin D & K, ( very low in Breastmilk)
Prolonged antibiotic use- sterilizes the gut
Prolonged NPO (nothing per orem)
Prematurity
Therapeutic dose of Vit K:. 1 mg/kg
max: 10kg
Large doses of Vitamin K should not be given Vit. K because infants
with G6PD because it precipitates hemolytic anemia, also in preterms
Micronutrients-Iron & Iodine deficiency assiated with congenital
hypothyroidism, which is the most common cause.
Iodine def- congenital hypothyroidisms, MC of mental retardation
Iron def- MC cause of iron 3-6 mg every day per month Mc secondary
to malnutrition, if the RBC is normal then give it as a prophylactic dose
(1mg/kg)
Therapeutic dose of Iron: 3-6 mg for 1 month & repeat CBC, if normal
then continue for 3 months as prophylaxis
Prophylactic dose: 1mg per kilo
Therapeutic dose per month next 3 dose as prophylactic
1 month then 3 months maintenance

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