NUTRITION

Protein Energy Malnutrition (PEM)

Etiology:
1. An inadequate intake of food both in quantity and quality
2. Severe or frequent Infections like:
Diarrhoea
Respiratory Infections
Measles
Intestinal worm infestation
3. Deficient Breat feeding and weaning:
4. Malabsorption states
5. Immunodeficiency states (HIV)
Syndromal Classification
1. Kwashiorkor
2. Nutritional Marasmus
3. Marasmic Kwashiorkor
4. Pre kwashiorkor
5. Nutritional Dwarfing
6. Under-weight
IAP classification: It is based on percentage of weight for age
Nutritional
Percentage of standard weight
Grade
for age
Normal
> 80%
Grade 1
71 80%
Grade 2
61 70%
Grade 3
51 60%
Grade 4
Less than 50%
Wellcome Trust Classification (1969)
Weight between 80 and 60% of expected by Harvard Std
With oedema
Kwashiorkor
Without oedema
Undernutrition
Weight below 60% of expected
With oedema
Marasmic Kwashiorkor
Without oedema
Nutritional Kwashiorkor
Weight-for-Height and Height-for-Age Classification (Waterlow)
Stunting
Wasting
Nutritional status
(% of height/age)
(% of weight/height)
Normal
>95%
>90%
Mildly impaired
87.5 95%
80 90%
Moderately impaired
80 87%
70 80%
Severely impaired
<80%
<70%
Arnold classification (1969) Based on MAC
Nutritional status
Mid-upper Arm Circumference
Normal/Satisfactory
>13.5 cm
Mild to moderate malnutrition
12.5 13.5 cam
Severe malnutrition
<12.5cm
Gomez classification: It is based on weight retardation using Harvard std.
Normal nutritional status
Between 90 and 110%

1st degree, mild malnutrition

2nd degree, moderate malnutrition
3rd degree, severe malnutrition
Clinical features of PEM
Features
Marasmus
Clinical
Muscle
Obvious
wasting
Fat wasting
Severe loss of
subcutaneous fat
Edema
None
Weight for
height
Mental
changes
Appetite
Diarrhea
Skin changes

Very low

Hair changes
Hepatic
enlargement

Seldom
None

Sometimes quiet and

apathetic
Usually good
Often
Usually none

Between 75 and 89%

Between 60 and 74%
Under 60%

Kwashiorkor
Sometimes hidden by edema and fat
Fat often retained but not firm
Present in lower leg and usually in
face and lower arms
Low but may be masked by edema
Irritable, moaning, apathetic
Poor
Often
Diffuse pigmentation, sometimes
flaky paint dermatosis
Sparse, easily pulled out
Sometimes due to accumulation of
fat

Diagnosis of Malnutrition:
Nutritional anthropometry:
This is a valuable index of assessment of nutritional status. 2/3 of children with
PEM does not present with clinical signs but are diagnosed by anthropometry.
1. Weight for age:
Most sensitive method when recorded serially. A decrease in weight
gain / loss in weight can be seen within 1 month. It indicates
wasting.
2. Height for age:
Compares the child's height with the expected height for the age.
This would detect stunting.
3. Weight for height:
This compares a child's weight with the expected weight of the
same height. It is useful for differentiating between acute and
chronic malnutrition.
4. Mid upper arm circumference (MUAC):
Normal MUAC for a child between 1-5 years of age is greater than
13.5 cm. If the MUAC is 12.5-13.5, the child has mild to moderate
malnutrition and if it is less than 12.5 cm it is suggestive of severe
malnutrition. This is useful for screening a large number of children
but less useful in long term growth monitoring.
5. Chest/ Head circumference
In PEM, chest circumference is less than Head circumference even after
2 years of age.

6. Body mass index: BMI is calculated as weight in Kg/height in M; E.g.

a 6 year old girl with BMI of 21 is overweight whereas 16 year old girl
with BMI 21 is just above the 50th percentile
7. The most important measurement for malnutrition is the
growth curve: weight for age is plotted as percentiles curves and
growth is monitored over a period of time; it is also called road to
health chart
Early detection of PEM:
1. Growth Chart:
a. The first indicator of PEM is underweight for age.
b. The most practical method to detect this is to maintain
growth charts.
c. Flattenning of growth curve is the earliest sign.
2. MAC of between 125mm (12.5cm) and 135mm (13.5cm), YELLOW
COLOUR, indicates that the child is at risk for acute malnutrition
Marasmus features:
1. It results from inadequate intake of energy or both energy and proteins
2. Usual age is less than 1 year infants who are breastfeeding when the
amount of milk is markedly reduced and those who are artificially fed
3. It is a form adaptation syndrome to chronic underlnutrition; hence it is a
non oedematous form
4. Clinical:
1. There is severe wasting skin becoming wrinkled and loose
2. Buccal pad of fat is lost giving a wise mans appearance
3. Infant have constipation or starvation diarrhoea
4. Flat or distended abdomen with visible peristalsis
5. Subnormal temperature and low pulse
Kwashirokor features:
1. Lethargy, apathy, irritability are the initial features
2. Muscle wasting and edema
3. Hepatomegaly
4. Skin:
a. Depigmentataion
b. Dry and crackling: flaky paint and paddy field dermatitis
5. Hair signs:
a. Easy pluckability
b. Brownish
c. Flag sign
6. Theories of Causes of edema:
a. Reduced albumin synthesis
b. Aflatoxin poisoning
c. Impaired renal function
d. Decreaed Na- K ATPase acivity
e. Increased free radicals; methionine levels are low which is a
precursor of glutathione an antioxidant
Management of PEM:
Management of mild to moderate PEM: This is managed at home
1. Recommendations:
1. Energy 120-150 kcal/kg/day
2. Protein 2-3 gm/kg/day
3. Foods advocated:

1. Double or triple mixes of cereals and pulses like dal, rice,

khichdi, seasonal green leafy vegetables, root vegetables, sugar,
jaggery, milk, milk products and nuts like groundnuts.
2. Oil / ghee or butter is added to increase calories.
3. Frequent small feeds with calories and proteins distributed
proportionately are encouraged.
4. Zinc supplements
5. Miscellaneous:
1. Parents should be educated regarding the hygienic way of
preparing and handling food; personal hygiene and importance
of safe and clean drinking water.
2. Basic advice regarding ORS (oral rehydration solution)use for
diarrhoea, vitamin supplements, treatment of infections and
infestations should be given
3. Child must be immunized as per schedule.
Severe PEM: Hospital Management: (Severe acute malnutritionSAM)
1. Resuscitation : 6 - 24 hours
2. Acute Phase : 1 day - 1 week
3. Rehabilitation : 2nd - 3rd weeks
1) Resuscitation (Treatment of Complications):
Dehydration:
Assessment: Fluid and sodium given should not exceed 75% of
allowances calculated on the basis of weight.
Hypothermia: The child is kept warm
Hypoglycemia:
Blood sugar of less than 50 mg/dl; more common in Marasmus; 1-2
ml/kg of 10% dextrose as bolus; then maintenance with 10%
dextrose and saline over 24 hours.
Infection:
Broad-spectrum antibiotics are given.
Anemia:
5-10ml/kg of packed red blood cells is transfused if hemoglobin is
less than 5 mg/dl.
Xerophthalmia:
If child is > 1 year or > 10 kg, vitamin A 100,000 units are given IM
on days 1, 2 and 28.
If child is less than 1year or less than 10 kg, 1/2 the above dose is
given.
Congestive Cardiac Failure:
It is common after day 3 of the acute phase usually in Kwashiorkor.
Oxygen and Diuretics must be given.
Hypomagnesemia:
It is corrected with 1 ml of magnesium sulfate given IM every 12
hours for 1-3 days.
Hypocalcemia: It is corrected with 1-2 ml/kg of calcium gluconate IV.
2) Dietary Management:
Rule 1:

1. Calculations are to be based on actual weight (not the expected

weight).
2. Initially 80 cal/kg/day and 0.7 gm/kg/day of protein.
Rule 2:
Offer small feeds at frequent intervals (to avoid vomiting,
hypoglycemia and hypothermia).
Rule 3:
1. Step up intake gradually to 100 kcal/kg/day and 1 gm/kg/day of
protein.
2. Intragastric / NG tube feeding or total parenteral nutrition may
be required.
3. Fluid volume: 120 ml/kg/day.
High Energy Feeding:
1. After the initial phase, Protein: 1.5 - 2 gm/kg/day and calorie to
150 - 180 kcal/kg/day.
2. Semisolids and solids are increased.
3) Rehabilitation:
a. Cereals, pulses and vegetables, Bengal gram, groundnuts and
green leafy vegetables are added.
b. Oils, sugar, fruit and vitamins and minerals are also added.
Recovery And Follow Up:
1. Recovery is assessed by:
1. Improvement of general condition, alertness and smile.
2. Return of appetite.
3. Gain in weight of 50-70 gms/day.
4. Disappearance of edema (7-10 days) and hepatomegaly.
5. Rise in serum albumin over the first 2 weeks of therapy
6. Recovery is complete when the child reaches his/her standard
weight, which usually takes 6-8 weeks.
Complications of PEM:
Early Complications of PEM:
1. Infections
Common: ARI, Diarrhea, TB, helminthiasis
Severe Gram ye sepsis, septic shock, DIC
Opportunistic Candidiasis
2. Hypothermia
3. Metabolic

i. Hypoglycemia
ii. Hypocalcaemia
iii. Hypomagnesemia
iv. Dehydration
v. Hypokalemia
vi. Hypernatremia
4. Lactose intolerance
5. Severe anemia & other nutrient deficiencies eg.Pellagra; Vit.A
deficiency
6. Congestive cardiac failure
7. Late (Recovery) complications:
Diarrhea (lactose intolerance)
CCF (high protein & solute diet)
Unmasking of subclinical vit/mineral deficiencies
8. Nutrition Recovery syndromes:
a. The refeeding syndrome is a potentially lethal complication of
refeeding in patients who are severely malnourished from whatever
cause.
b. Salt and water retention leading to oedema and heart failure,
c. Hypokalaemia due to rapid cellular uptake of potassium
d. Hypophosphataemia due to increased phosphorylation of glucose,
e. Rapid depletion of thiamine, a cofactor in glycolysis, leading to
wernickes encephalopathy and cardiomyopathy,
f. Hypomagnesaemia due to cellular uptake of this mineral.
g. Kahns recovery syndrome is characterized by sudden onset of
tremors and encephalopathy, due to unmasked deficiency of
gamma aminobutyic acid (gaba)
h. Gomez recovery syndrome is characterized by progressive
abdominal distension, ascites, hepatomegaly and diarrhea, due to
secondary malabsurption and hypokalemia.
i.

Management:

i.

Monitoring of plasma glucose, sodium, potassium, phosphate,

and magnesium before and during refeeding.

ii.

Before refeeding correction of electrolyte imbalances, vitamin

and trace-element deficiencies

iii.

Volume restored gradually over12 to 24 hours.

iv. A gradual increase in calories and proteins

v.

Thiamine should be given 30 minutes before refeeding,

Prognosis:
Mortality 10-30%
PEM may rcecur as socioeconomic conditions remains the same.
Long term sequelae: Irreversible stunting and mental impairment.
Preventive Measures:
1. Promotion of breast-feeding.
2. Development of low cost weaning food:
3. The child should be made to eat more food at frequent intervals.
4. Nutrition education: Promotion of correct feeding practices.
5. Home Economics
6. Family planning and spacing of births
7. Family environment: tender loving care(TLC)
8. Food fortification
9. Immunization
10.Early diagnosis of any lag in growth.
11.Early diagnosis and treatment of infections and diarrhoea.
12.Development of supplementary feeding programmes during
epidemics.
13.Deworming of heavily infested children.
WEANING FOOD
(Complementary feeding)
1. Definition:
a. Introduction of traditional family diet to an infant after 6 mo of age
who is so far depenadant on breastfeeding
2. Rationale:
a. By the age of 6 months, birth weight is doubled and child is
becoming more active.
b. Exclusive breastfeeding is no longer sufficient
c. To supply Iron which is insufficient in breastmilk
d. Infant is developmentally ready for other foods
e. The digestive system is mature to digest the starch, protein and fat
in a non-milk diet.
f. Oral cavity has developed to handle semi-solid food
3. Important Principles for Weaning
a. Avoid foods with high allergenic potential (eg. cow's milk, eggs, fish,
nuts, soybeans).

b. Iron-containing foods (meat, iron-supplemented cereals) are

required.
c. Zinc intake should be encouraged with foods such as meat, dairy
products, wheat, and rice.
d. Phytates ntake should be low to enhance mineral absorption.
Grains, legumes, nuts & seeds contain phytates.
e. Breast milk should continue to 12 mo; formula or cow's milk is then
substituted.
f. Give no more than 24 oz/day of cow's milk.
g. Give no more than 46 oz/day of fruit juices.
4. Feedings:
a. Beginning at 6 months, an infant can eat mashed or semi-solid foods.
b. By 8 months most infants can also eat finger foods.
c. By 12 months, children can eat the same food as consumed by the
family
5. Good complementary foods are:
a. Rich in energy, protein and micronutrients (particularly iron, zinc,
calcium, vitamin A, vitamin C and folate);
b. Not spicy or salty;
c. Easy for the child to eat;
d. Liked by the child;
e. Locally available and affordable
6. Five keys to safer food
a. Keep clean
b. Separate raw and cooked
c. Cook thoroughly
d. Keep food at safe temperatures
e. Use safe water and raw materials
Nutritional advice for 1 year child:
Childs expected weight is 10 kg; actual weight is 7 kg; Gr II malnutrition
(IAP)
Nutrition requirement is calculated for expected weight and the
recommended diet is slowly stepped up to this level as per tolerance of
the child
Calories:
10x100= 1000
Proteins:
2x10=20 gm
Diet plan for 1 year old child:
Calories
Protein
Early Morning:
100 ml of milk
60
3
Breakfast:
1 idli
50
2
Dhall 3 tsp
30
1.5
Ghee/oil 1 tsp
40
-

Noon

2 biscuits
100 ml milk

40
60

Lunch:

cup rice
Dhall 3 tsp

30

1
3
85

2
1.5

Evening:

Night:

Total
Breast milk:

Ghee/oil 1 tsp

40

egg or 1 vada
100 ml milk
1 banana

40

cup rice
Dhall 3 tsp
Ghee/oil 1 tsp

60
40`

3
-

85
30

2
1.5

730
Not included

40

23
>270 calories

BREAST FEEDING
Colostrum and mature milk
1. Secreted in the first 23 days after delivery. about 4050 ml on the first
day
2. Colostrum is rich in:
1. white cells and
2. antibodies, especially Ig A,
3. larger percentage of protein,minerals and fat-soluble
vitamins(A,E and K)
3. Colostrum is a baby's first immunization against many bacteria
and viruses
4. Colostrum is laxative, and helps the baby to pass meconium
Mature milk types:
1. On the third day, an infant is normally taking about 300400 ml per 24
hours, and on the fifth day 500800 ml.
2. From day 7 to 14, the milk is called transitional, and after 2 weeks it is
called mature milk.
3. Foremilk is the milk that is produced early in a feed. It provides:
a. Plenty of protein,
b. Lactose, other nutrients and
c. Water.
4. Hindmilk is the milk that is produced later in a feed.
a. Contains more fat.
b. Provides much of the energy
c. Satiety
d. Sleep
5. Preterm milk
1. Preterm breast milk, has more protein,
2. Higher levels of some minerals including iron,
3. More immune properties than mature milk,
Four key points for attachment (latching):
1. Baby chin touching the breast
2. Nipple and lower areola inside the mouth
3. some upper areola visible
4. Lowe lip turned outside

Four key points for good position

1. The babys head and body should be in a straight line
2. His face should face the breast, with his nose opposite the nipple
3. His mother should hold his body close to hers
4. Mother should support his bottom, and not shoulders and head
Reliable Signs of NOT ENOUGH MILK :
1. Almost all mothers can produce enough breastmilk for one or even two
babies, provided the baby suckles effectively and breastfeeds as often
as he wantsthe amount of milk the breasts produce is determined by
the amount that the baby takes, and increases when the baby takes
more
2. Possible signs of not enough milk are:
a. Poor weight gain (<500gm/month)
b. Passing small amount of urine (<6times/day= wetness test)
c. Concentrated urine
d. Hard stools
e. Frequent crying?
f.

No milk comes out when the mother expresses

g. Breasts did not enlarge (during pregnancy)

h. Milk did not "come in" (after delivery)
Reasons for not enough milk
1. Delayed initiation of breastfeeding
2. Poor attachment
3. Infrequent feeds-8 upto 8 weeks; 6 upto 6 months
4. Short feeds
5. Using bottles or pacifiers
6. Giving other foods or drinks
7. Stressed mother
8. Sick mother
9. Oral pill ; pregnancy
10.Sick baby
Lactation management of not enough milk:
1. Help the mother practically
2. Sit quietly and privately or with a supportive friend.
3. Hold her baby with skin to skin contact if possible
4. Take a warm soothing drink
5. Stimulate her nipples
6. Massage or stroke the breasts lightly
7. Ask a helper to rub her back
Breastfeeding &Working Mother
1. If working mother she should take maternity leave
2. xpress milk before leaving for work and somebody can feed using
paladai
3. Reverse the feeding pattern

Maternal Nutrition during Breastfeeding

1. The average increase in calories to support breastfeeding is 750
calories/day
2. Recommendations are to eat an additional 500 calories/day and let
fat reserves accumulated during pregnancy provide the rest
3. Fluid
1. Fluid needs increase with breastfeeding
2. Women need to drink 8 to 12 cups of fluid/day to prevent
dehydration and milk production
Duration of breastfeeding:
Exclusive breastfeeding for 6 months
Continue breastfeeding for 2 years with supplementary feeding
(home food)

Breast milk contents

1. Vitamins/minerals:
1. Breast milk normally contains sufficient vitamins for an infant
2. Vitamin D also reflects its level in mother.
3. The vitamin K content of human milk also is low

2.

3.

4.

5.

6.

7.

4. Iron and zinc are present in relatively low concentration, but their
bioavailability and absorption is high.
Anti-infective factors:
a. Immunoglobulin A, coats the intestinal mucosa
b. White blood cells kill micro-organisms;
c. Whey proteins (lysozyme and lactoferrin) can kill bacteria, viruses and
fungi;
d. Oligosacccharides prevent bacteria from attaching to mucosal surfaces.
Other bioactive factors
1. Bile-salt stimulated lipase facilitates the complete digestion of fat
2. Epidermal growth factor stimulates maturation of the lining of the infants
intestine
Fat:
1. Breast milk contains about 3.5 g of fat per 100 ml.
2. Breast-milk fat contains long chain polyunsaturated fatty acids
(docosahexaenoic acid or DHA, and arachidonic acid or ARA) which are
important for the neurological development of a child.
Carbohydrate:
a. Breast milk contains about 7 g of lactose per 100 ml,
b. Oligosaccharides provide important protection against infection
Protein:
a. The concentration of protein in breast milk is 0.9 g per 100 ml
b. Breast milk contains less of the protein casein,
c. Among the whey, or soluble proteins, human milk contains more alphalactalbumin;
Antibodies:

1. Immunoglobulin A prevents bacteria from entering the cells;

2. Maternal live white blood cells in intestine of baby can kill microorganisms;
3. Whey proteins (lysozyme and lactoferrin) can kill bacteria, viruses and
fungi;
4. Oligosacccharides prevent bacteria from attaching to mucosal surfaces
Exclusive breast feeding
Definition:
Exclusive breastfeeding means that an infant receives only breast milk from his
or her mother or a wet nurse, or expressed breast milk, and no other liquids or
solids, not even water, with the exception of oral rehydration solution, drops or
syrups consisting of vitamins, minerals supplements or medicines
ADVANTAGES OF BREAST MILK-For baby:
1. Natural food available at the proper temperature and requires no
preparation time.
2. It is fresh and free of contaminating bacteria,
3. Has the protective effects of breast milk against enteric and other
pathogens
4. Free from allergy which may cause diarrhea, intestinal bleeding, occult
melena, "spitting up," colic, and atopic eczema.
5. Secretory IgA prevents microorganisms from adhering to the intestinal
mucosa.
6. It also contains substances that inhibit growth of many common viruses.
7. Antibodies provide lower incidence of diarrhea, otitis media, pneumonia,
bacteremia, and meningitis
8. Macrophages in human milk may synthesize complement, lysozyme, and
lactoferrin.
9. Lactoferrin has an inhibitory effect on the growth of Escherichia coli in the
intestine.
10. The lower pH of the stool protects against infections
11. Bile salt-stimulated lipase kills Giardia lamblia and Entamoeba histolytica.
12. passive transfer of T-cell immunity against TB
13. Less chances for asthma and other atopic conditions, type 1 diabetes,
celiac disease, ulcerative colitis and Crohn disease and childhood
leukaemia.
14. obesity in later childhood and adolescence is less common among
breastfed children
15. Less chances for increased blood pressure, altered blood cholesterol
levels and atherosclerosis in later adulthood.
16. Increased duration of breastfeeding has been associated with greater
intelligence in late childhood and adulthood, which may affect the
individuals ability to contribute to society.
For Mother:
1. The psychologic advantages of breast-feeding; a feeling of being
essential and a sense of accomplishment
2. The risk of postpartum haemorrhage may be reduced by breastfeeding
immediately after delivery

3. the risk of breast and ovarian cancer is less among women who

breastfed
4. Breastfeeding mother tends to develop less obscity
5. Exclusive breastfeeding can delay the return of fertility - Lactation

amenorrhea
For Family:
1. The cost of rearing a child by buying formula or cows milk is reduced
2. The cost of frequent visits to hospital is reduced due to less incidence

of illnesses
3. Lactation amenorrhea helps planning the family size in the first year
4. Infanticide is unknown if mother starts breastfeeding and develops

bonding
Ten steps to successful breast feeding in health facilities:
1. Have a written breastfeeding policy that is routinely communicated
to all health care staff.
2. Train all health care staff in skills necessary to implement this policy.
3. Inform all pregnant women about the benefits and management of
breastfeeding.
4. Help mothers initiate breastfeeding within one half-hour of birth.
5. Show mothers how to breastfeed and maintain lactation, even if
they should be separated from their infants.
6. Give newborn infants no food or drink other than breastmilk, unless
medically indicated.
7. Practice rooming in - that is, allow mothers and infants to remain
together 24 hours a day.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or pacifiers (also called dummies or soothers)
to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer
mothers to them on discharge from the hospital or clinic.

VITAMINS
Vitamin A
Introduction
1.

Vitamin A is made up of a family of compounds called the retinoids

2. There are essentially 3 natural forms of vitamin A:

1. Retinols: most active form and is mostly found in animal sources of
food.

2. Beta carotenes: provitamin A, is the plant source of retinol;

provides twice the vitamin A activity
3. Carotenoids: exist in a free alcohol or in a fatty acyl-ester form. -,
-, and carotenes; and -cryptoxanthins
Absorption:
1. It is a fat soluble vitamin
2. Bile is necessary for for its absorption in intestines
3. Stored in liver
4. Released from the liver into the circulation as retinol bound to retinolbinding protein (RBP), which binds to the thyroid hormone transport
protein, transthyretin; this complex delivers retinol (as well as the thyroid
hormone) to tissues.
Derivatives of Vit.A
1. All-trans-retinol, the alcohol form is the regular Vit.A; is present only in
animal tissues;
2. Retinyl palmitate: The storage form
3. Retinal: the aldehyde form; functions in vision; enables rhodopsin to
mediate vision
4. Retinoic acid: The physiologically most important acid derivative,
functions at the gene level as a ligand for specific nuclear transcription
factors; thus, regulate many genes involved in fundamental biologic
activities of the cell; is not reversible to other forms
Functions :
1. Genomic role: retinoic acid regulates cell division, cell death, and cell
differentiation
2.

physiologic role: reproduction, growth, embryonic and fetal development,

and bone development, respiratory, gastrointestinal, hematopoietic, and
immune functions.

3. Vision: retinal, is the prosthetic group on both visual proteins. low-intensity

light isomerizes 11-cis retinal, to all-trans- retinal resulting in visual
sensation

4. Epithelium: Maintains the integrity of epithelium of skin, conjunctiva,

cornea, urinary tract, vagina, pancreatic and salivary ducts
Deficiency manifestations:
1. keratinizing mataplasia of epithelium
2. Incresaed incidences of diarrhea and respiratory infections
3. bronchial obstruction-bronchiectasis
4. UTI
5. Dry scaly skin
6. Cystitis- hematuria and pyuria
7. Growth retardation due to recurrent infections
8. Anemia, apathy, mental retardation
9. Increased intracranial pressure with & pressure on the optic nerve.
Risk factors for Vit.A deficiency:
1. Children with measles, respiratory disease, tuberculosis diarrhoea
2. Proteinenergy malnutrition, which interferes with the storage transport,
and utilization of the vitamin
3. Intestinal infestations and infections
4. NB born to mother with vit.A deficiency
5. Denial of Colostrum and early breast milk which are concentrated sources
of vitamin A .
6. Bottle-fed children are often at even greater disadvantage
7. patients with chronic malabsorption
Epidemiology of Vit.A deficiency:
1. Boys are frequently at greater risk of xerophthalmia
2. Xerophthalmia may be more prevalent at certain times of the year
(measles, famine, harvest)

3.

Clustering of cases ( cultural practices)

4. 1-4 years more prone for corneal involvement

5. 2-8 years: conjunctival xerosis
Serum levels
1. vitamin A normal serum retinol levels are above 1.0 to 1.4 mol / litre.
2. Below 0.35 mol / litre is considered deficient.
WHO Classification of xerophthalmia:
1. XN -

Night blindness

2. X1A -

Conjunctival xerosis

3. Xl B -

Bitots spot

4. X2 -

Corneal xerosis

5. X3Asurface

Corneal ulceration / keratomatacia < 1/3 corneal

6. X3Bsurface

Corneal ulceraiuon / keratomalacia >1/3 corneal

7. XS -

Corneal scar

8. XE -

Xerophtbalmic fundus

Diagnosis.
1. Dark adaptation tests
2. Conjunctival impression cytology,
3. Relative dose response
4.

Levels of retinol (pure vitamin A) in the blood.

5.

Levels of retinol-binding protein simple diagnostic procedures

TREATMENT
1. Xerophthalmia is a medical emergency carrying a high risk of corneal
destruction and blindness, and/or sepsis and death

2. concomitant treatment of underlying systemic illnesses and PEM

6. Oral administration is preferred, because it is safe, cheap, and highly
effective; 200000 IU vitamin A is administered by mouth immediately
upon diagnosis and the dose is repeated the following day; An additional
dose is commonly given 1-4 weeks later; Children less than 6 11 months
half of the oral dose
7. Intramuscular injection:
1. 100,000 IU IM water soluble retinyl palmitate when child can not
swallow Severe vomiting or malabsorption
Vit.A Requirements in normal status:
1. 1 IU is equal to 0.3 g of retinol and 0.6 g of -carotene
2. Daily requirements: Infants 500 g older children 600-1500 g
Vit.A prophylaxis program in India - 2007
1. 100000 IU at 9 months with measles immunisation
2. 200000 IU at 16-18 months, with DPT booster
3. 200000 IU every 6 months, up to the age of 5 years.
4. Thus a total of 9 mega doses are to be given from 9 months of age up to 5
years.
Dietary sources of Vit.A
1. Lightly cooked green leafy vegetables, including leaves of the drumstick
tree (moringa oleifera), the various amaranths, cassava leaves, etc,
2. Red palm oil, and coloured fruits, such as papaya and mango
3. Adding a small amount of edible oil will enhance the absorption of the bcarotene
Eye care
1. In the presence of corneal involvement, broad-spectrum antibiotic eye
ointment should be applied every 8 hours to reduce the risk of secondary
bacterial infection

2. Until the causative agent is identified, antibiotics that cover a wide range
of organisms, especially Staphylococcus and Pseudomonas, should be
chosen

Bb Preventable causes of blindness in children:

Condition
Cataract

Corneal
scarring

Associated Factors
Genetic disease
Maternal rubella
Injuries and
inflammation
Vitamin A deficiency

Prevention
Counseling
Rubella vaccine
Injury prvention

Treatment
Surgery

Vitamin A supplementation
twice a year

Measles
Neonatal conjunctivitis

Measles vaccine
Antibiotics and control of
sexually-transmitted infections
Health education

Antibiotics
Surgery for
advanced
stages

Harmful traditional eye

remedies
Trachoma

Facial cleanliness and

environmental improvement
Insecticide spraying of affected
area

Microfilaria

Onchocerciasis (river
blindness)

Refractive
error (blurred
vision)
Retinopathy
of prematurity
(ROP)

Genetics
Environmental factors

None

Oxygen therapy

Limited use of low dose oxygen

Single annual
dose of
ivermectin
Optical
correction
Follow up
examination
and optholmic
referral

HYPERVITAMINOSIS A:
1.

Toxicity can be induced in adults and children with chronic daily intakes
of 15,000 g and 6,000 g, respectively.

2. Symptoms subside rapidly on withdrawal of the vitamin.

Signs of subacute or chronic toxicity may include
1. Headache; vomiting; anorexia;
2. Dry, itchy desquamating skin;

3. Alopecia and/or coarsening of the hair;

4. Bone abnormalities; swelling of the bones; hyperostosis affecting several
long bones, especially in the middle of the shafts.
5. Enlargement of the liver and spleen;
6. Diplopia; increased intracranial pressure; irritability; stupor;
7. Desquamation of the palms and the soles of the feet is common.
8.

Hypercalcemia and/or liver cirrhosis may be present.

In young children
1.

Vomiting and bulging fontanelles.

2. Anorexia, pruritus, and a lack of weight gain.

3. Drowsiness; diplopia, papilledema, cranial nerve palsies, and
4. Other symptoms suggestive of pseudotumor cerebri.
Pregnancy
1. Severe congenital malformations occur in infants of mothers who
consumed therapeutic doses during the 1st trimester of pregnancy for
treatment of acne
2. This results in a high incidence (>20%) of spontaneous abortions and birth
defects
Excess b-carotenes (carotenemia)
1. Excessive intake of carotenoids is not associated with toxicity,
2. But may cause yellow coloration of the skin that disappears when intake is
reduced;

RICKETS
Vitamin D:
1. Two forms are important in humans:
a. Ergocalciferol (vitamin D2) synthesized by plants
b. Cholecalciferol (vitamin D3) synthesized by humans from 7dehydrocholesterol in the skin when it is exposed to ultraviolet
B (UVB) rays from sunlight.
2. Metabolism:

a.

In Liver it si converted to 25-hydroxyvitamin D (25-OH-D) by the

action of 25-hydroxylase
b. 25-OH-D undergoes a second hydroxylation in the kidney to
become 1,25-dihydroxyvitamin
3. Functions of Vit.D:
a. It is a Steroid hormone
b. Active form: 1,25-dihydroxy vitamin D3 (Calcitriol)
c. Action via intracellular receptor
d. Regulates Ca++& Phosphorus homeostasis

e.

Essential for normal absorption of calcium from the gut

4. Vit.D in diet:
a. Animal: fish, eggs, fortified milk, and cod liver oil
b. Vegetable source: mushroom
Rickets:
1. It is a disease of growing bone before fusion of the epiphyses;
2. Uncommon in PEM as their growth is restricted.
3. The mineralization of matrix at the growth plates does not occur as Ca is
not availble due to Vit D deficiency.
4. Increase in the circumference of the growth plate and the metaphysis
causes widening of the wrists and ankles.
5. General softening of the bones leads to a variety of bone deformities.
6. Osteomalacia is a disorder of mineralization of newly formed matrix in
adults
Etiology of rickets:
a. Vitamin D disorders,
b. Calcium deficiency,
c. Phosphorous deficiency, and
d. Renal causes
Classification of Rickets:
A. VITAMIN D DISORDERS
1. Vit.D deficiency:
1. Nutritional
2. Congenital
3. Secondary
4. Malabsorption
5. Increased degradation
2. Decreased liver 25-hydroxylase
3. Vitamin Ddependent rickets type 1&2
4. Chronic renal failure
B. CALCIUM DEFICIENCY
1. Premature infants (rickets of prematurity)
2. Malabsorption
3. Primary disease
4. Dietary inhibitors of calcium absorption
5. Low intake
C. PHOSPHORUS DEFICIENCY:
1. Inadequate intake
2. Premature infants (rickets of prematurity)
3. Aluminum-containing antacids

D. RENAL Rickets:
1. Hypophosphatemic rickets
a. X-linked
b. Autosomal dominant
2. Overproduction of phosphatonin
3. Tumor-induced rickets
4. McCune-Albright syndrome
5. Fanconi syndrome
6.
Distal renal tubular acidosis

Nutritional Rickets:
Etiology of Nutritional rickets:
1) Transplacental: if mother has poor source of vit.D, infant may have
congenital rickets
2) Breast fed infants has less vit.D (low content)
3) Deficiency of cutaneous synthesis:
i. Lack of exposure to sunlight due to illness or cultural factors
ii. High skin pigmentation(dark color) which filters UV light
iii. Prolonged winter months
4) Unfortified formula milk
5) Phenobarbital and Phenytoin
6) Aluminum containing antacids interferes with absorption of phosphate
from gut
7) Malabsorption of vit.D occurs in:
i. Fat malabsorption (liver disorders): celiac disease and cystic
fibrosis
ii. Chronic diarrhea
iii. Giardiais
Clinical features of rickets:
1. Breast-fed infants of vitamin D-deficient mothers may develop rickets
within 2 mo, but rickets usually appears toward the end of the 1st and
during the 2nd yr of life.
2. Vitamin D-deficient rickets is rare later in childhood;
3. It is rare in PEM due to depressed growth
Cranium:
1. Craniotabes is caused by thinning of the outer table of the skull
2. The softness of the skull may result in asymmetry of the head.
3. The anterior fontanel is larger than normal, and its closure may be delayed
until after the 2nd yr of life.

4.

parietal and frontal bosses giving the head a boxlike appearance (caput
quadratum or hot cross bun appearence)

Dentition:
1. Eruption of the temporary teeth may be delayed, and there may be
defects of the enamel and extensive caries.
Chest:
1. Palpable enlargement of the costochondral junctions (the rachitic rosary)
2. The sternum with its adjacent cartilage appears to project forward-pigeon
breast deformity
3. horizontal depression in the lower chest, Harrison groove, develops along
the lower border of the chest
Pelvis: Deformity of the pelvis in girls add to the hazards of childbirth
Limbs:
1. The epiphyseal enlargement at the wrists and ankles
2. Weight bearing produces bending of the softened shafts resulting in

bowlegs or knock-knees
3. Greenstick fractures in the long bones
4.

knock-knees, overextension of the knee joints

5. tibial malleolus gives the impression of a double epiphysis (Marfan sign).

Spine:

kyphosis and scoliosis

Stature: rachitic dwarfism.

Muscle tone: hypotonia and delayed walking
Tetany: Tetany due to vitamin D deficiency occasionally accompanies rickets.
Investigations:
1. Calcium (ionized fraction) is low; becomes normal as parathyroid hormone

levels increase.
2. Calcidiol (25-hydroxy vitamin D) levels are low,
3. Serum parathyroid hormone levels are elevated;

4. Calcitriol levels maybe normal or elevated because of increased

parathyroid activity.
5. The phosphorus level is always less than 4 mg/dLlow
6. Alkaline phosphatase levels are elevated. 200 IU/dL in normal children,

increases to more than 500 IU/dL

7. Urinary cyclic AMP level is elevated
8. A generalized aminoaciduria occurs from the parathyroid activity;

aminoaciduria does not occur in familial hypophosphatemia rickets (FHR).

Phosphaturia with occasional glucosuria can occur
Imaging:
1. Anterior view of the knee reveals metaphyses with cupping and fraying
2. Along the shaft, the uncalcified osteoid causes the periosteum to appear
separated from the diaphysis giving a double contour appearance
3. Green stick fractures
Treatment of nutritional rickets:
I.
Vit.D3 oral daily 50-150 g or 1,25 dihydroxy cholecalciferol .5 to 2 g
II.
Alternatively a single dose of 15000 g (600,000 U) of Vit.D
Prevention:
I.
Adequate exposure to UV light
II.
Supplemt of 400 Iu vitD daily to breastfed infants
III.
Vit D to pregnant and lactating mother to increase the levels in NB
9.

Vitamin DDependent Rickets

Type 1 (renal 1-hydroxylase deficiency)
1. An autosomal recessive disorder, have mutations in the gene encoding
renal 1-hydroxylase, preventing conversion of 25-D into 1,25-D.
2. These patients normally present during the 1st 2 yr of life
3. May present with symptomatic hypocalcemia.
4. They have normal levels of 25-D but low levels of 1,25-D
5. Renal tubular dysfunction can cause a metabolic acidosis and generalized
aminoaciduria.
Treatment:
1. These patients respond to long-term treatment with 1,25-D (calcitriol).
Initial doses are 0.25-2 g/day, and lower doses are used once the rickets
has healed.
2. Especially during initial therapy, it is important to ensure adequate intake
of calcium.
Type 2 (defective receptor for 1,25-D)
1. Autosomal recessive
2. Mutations in the gene encoding the vitamin D receptor, preventing a
normal physiologic response to 1,25-D.
3. Levels of 1,25-D are extremely elevated
4. 50-70% of children have alopecia, which tends to be associated with a
more severe form of the disease and can range from alopecia areata to
alopecia totalis.
5. Epidermal cysts are a less common manifestation.
Treatment

1. Some patients respond to extremely high doses of vitamin D 2, 25-D or

1,25-D, especially patients without alopecia. This response is due to a
partially functional vitamin D receptor. All patients with this disorder
should be given a 3-6 mo trial of high-dose vitamin D and oral calcium.
The initial dose of 1,25-D should be 2 g/day, but some patients require
doses as high as 50-60 g/day. Calcium doses are 1,000-3,000 mg/day.
Patients who do not respond to high-dose vitamin D may be treated with
long-term intravenous calcium, with possible transition to very high dose
oral calcium supplements.
2. Treatment of patients who do not respond to vitamin D is difficult.

1.

2.

3.

4.

5.

6.

RENAL RICKETS
X-Linked Hypophosphatemic Rickets
a. The defective gene is on the X chromosome, but female carriers are
affected, so it is an X-linked dominant disorder.
b. The gene appears to have an indirect role in inactivating the
phosphatonin FGF-23. It leads to inhibition of phosphate
reabsorption in the proximal tubule, and phosphate excretion is
increased.
c. FGF-23 also inhibits renal 1-hydroxylase, leading to decreased
production of 1,25-D
d. These patients have rickets, but abnormalities of the lower
extremities and poor growth are the dominant features. Delayed
dentition and tooth abscesses are also common. Some patients
have hypophosphatemia and short stature without clinically evident
bone disease.
e. Patients have high renal excretion of phosphate,
hypophosphatemia, and increased alkaline phosphatase; PTH and
serum calcium levels are normal
f. Patients respond well to a combination of oral phosphorus and 1,25D (calcitriol).
Autosomal dominant hypophosphatemic rickets (ADHR):
a. It is much less common than XLH. There is incomplete penetrance
and variable age of onset
Autosomal recessive hypophosphatemic rickets:
a. It is an extremely rare disorder due to mutations in the gene
encoding dentin matrix protein 1, which results in elevated levels of
FGF-23
Hereditary hypophosphatemic rickets with hypercalciuria (HHRH):
a. It is a rare disorder that is mainly described in the Middle East. This
autosomal recessive disorder is due to mutations in the gene for a
sodium-phosphate cotransporter in the proximal tubule.
McCune-Albright syndrome:
a. It is an entity that includes the triad of polyostotic fibrous dysplasia,
hyperpigmented macules, and polyendocrinopathy. Affected
patients have inappropriately low levels of 1,25-D and elevated
levels of alkaline phosphatise.
Fanconi syndrome:

a. It is secondary to generalized dysfunction of the renal proximal

tubule. There are renal losses of phosphate, amino acids,
bicarbonate, glucose, urate, and other molecules that are normally
reabsorbed in the proximal tubule.
7. Distal renal tubular acidosis:
a. It usually manifests with failure to thrive. Patients have a metabolic
acidosis with an inability to acidify the urine appropriately.
Autosomal recessive and autosomal dominant forms. Rickets is
variable, and responds to alkali therapy
HYPERVITAMINOSIS D
Hypervitaminosis D is secondary to excessive intake of vitamin D. It may occur
with long-term high intake or with a substantial, acute ingestion. Most cases are
secondary to misuse of prescribed or over-the-counter vitamin D supplements,
but other cases have been secondary to accidental overfortification of milk,
contamination of table sugar, and inadvertent use of vitamin D supplements as
cooking oil. The recommended upper limits for long-term vitamin D intake are
1,000 IU for children younger than 1 year old and 2,000 IU for older children and
adults.
Clinical manifestations:
1) Hypotonia
2) Anorexia
3) Irritability
4) Constipation
5) Poydipsia
6) Polyuria
7) Pallor
8) Hypercalcemia and hypercaliuria
9) Metatstatic calcification
10) Aortic stenosis
11) Osteopetrosis of bones
12) Treatmnt: aluminium hyderoxide by mouth
ZINC
Functions:
Component of many enzymes and gene transcription factors; plays critical
roles in nucleic acid metabolism, protein synthesis, and gene expression;
supports membrane structure and function.
Dietary sources: Human milk, meats, shellfish, legumes, nuts, and whole-grain
cereals.
Causes of Deficiency:
1. Diets low in available zinc (high phytate), unfortified synthetic diets;
2. malabsorptive diseases (enteritis, celiac disease, cystic fibrosis);
3. excessive losses (chronic diarrhea);
4. Inborn errors of zinc metabolism (acrodermatitis enteropathica, mammary
gland zinc secretion defect).
5. Inadequate intake in breast-fed infants after age 6 mos.
6. Prematurity and low birth weight is risk factors.
Clinical Features
1. Mild: impaired growth, poor appetite, and impaired immunity.

2. Moderatesevere: mood changes, irritability, lethargy, impaired immune

function, increased susceptibility to infection; acro-orificial skin rash,
diarrhea, alopecia.
3. Response to zinc supplement is gold standard for diagnosis of deficiency;
plasma zinc levels are lowered by acute phase response.
Treatment:
1. 1 mg/kg/d of elemental zinc for 3 mo (eg, 4.5 mg/kg/day of zinc sulfate
salt), given separately from meals and iron supplements.
2. With acrodermatitis enteropathica, 3050 mg Zn 2+ per day (or more)
sustains remission.
3. WHO recommendation for Diarrhea:
a. Less than 6 mo: 10 mg OD for 14 days
b. More than 6 mo: 20 mg OD for 14 days