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3. Lecture notes on Pediatric Nutrition & Nutritional Disorders1
.
S. no. Contents
Introduction
3.1 Breast – feeding
3.1.1 Colostrum.
3.1.2 Baby Friendly Hospital Initiatives (BFHI)
3.1.3 Complimentary Feeding (Weaning)
3.1.4 Tropic feeding.
3.1.5 Fore milk.
3.1.6 Hind milk.
3.2 Carbohydrates
3.2.1 Types.
3.2.2 Clinical features.
3.3 Proteins
3.4 Lipids.
3.5 Normal nutritional requirement (RDA)
3.6 Maintenance fluid & Electrolyte requirements.
3.7 Vitamin A (Fat soluble vitamin)
3.7.1 Functions
3.7.2 Sources.
3.7.3 Daily Requirements.
3.7.4 Vitamin A Deficiency.
3.7.5 Clinical features.
3.7.6 Treatment.
3.7.7 Prophylaxis.
3.7.8 Hyper Vitaminosis A
3.8 Vitamin B Complex
3.8.1 Deficiency Diseases.
3.8.2 Beri – Beri
3.8.2.1 Clinical features.
3.8.2.2 Treatment.
3.9 Pellagra
3.9.1 Pyridoxine (B6)
3.10 Scurvy
3.10.1 Clinical features.
3.10.2 Diagnosis.
3.10.3 Treatment.
3.11 Vitamin D (Calciferol)
3.11.1 Rickets
3.11.1.1 Definition.
3.11.1.2 Causes.
3.11.1.3 Pathophysiology.
3.11.1.4 Clinical features
3.11.1.5 Diagnosis.
3.11.1.6 Healing Rickets – X Ray findings.
3.11.1.7 Treatment
3.11.1.8 Refractory Rickets (Resistant Rickets)
3.12 Vitamin E
3.13 Vitamin K
3.14 Trace Elements
3.14.1 Zinc.
3.14.2 Copper
3.15 Protein Energy Malnutrition (PEM)
3.15.1 Marasmus.
3.15.2 Kwashiorkor.
3.15.3 Management of PEM.
3.15.4 Complications of PEM.
3.15.5 Prevention of PEM
3.15.6 Antioxidants.
Introduction:
→ Individual nutritional requirements vary with genetic, metabolic differences as well as with
growing age from infancy to adulthood.
→ Fast growth of infants during 1st
year of life (i.e. A 3-fold increase in weight and1½ fold increase
in height) and continued growth from 1st
year of age to adolescent imposes unique nutritional
needs.
→ Nutrition helps to:
1. Prevent illnesses.
2. To develop physical and mental potential.
3. Provide reserve for stress.
→ Energy requirement of body is met from:
1. Carbohydrates – 55 – 60%.
2. Protein – 15 to 20%
3. Fats – 20 to 30%
→ Approximately energy expenditure is as follows:
1. Metabolism – 50%
2. Growth 12%
3. Physical activity 25%
4. Fecal loss 8%
5. Thematic effect.
→ RDA: Recommended daily allowances of specific nutrient is the intake of that nutrient deemed to
meet the requirement for that nutrient by most members of the population.
3.1. Breastfeeding:
1. Breast milk is an ideal form of infant feeding.
2. There should be exclusive breast feeding up to 6 months of age and it should be continued
till 2yrs of age.
3. Feeding should be started as soon as possible after birth of an infant. In normal delivery –
within ½hr. And in caesarian delivery – within 4hrs.
4. Initially for few months demand feeding as and when child demands it should be given.
Timely feeding can also be given i.e 2-4 hrs.
5. Exclusive breast feeding:
a) Only breast-feeding milk is given for first 6months of life.
b) No other food or drink not even top milk, water.
6. Recommended nutrient to breast fed infants:
a) Fluoride – 10μgm / day.
b) Vitamin K 1mg at birth.
c) Vitamin D if infant is not exposed to sunlight or in dark colored infant.
7. Composition of breast milk (per 100ml)
S.
no.
Nutrients Human milk Cow’s milk
1 Protein 1.1gm 3 gm
2 Lactose 7gm 4.5 gm
3 Fat 4.5gm 4.5gm
4 EFA 13% 2%
5 Ash/minerals 0.25gm 7.5gm
6 Calcium phosphate ratio 2:1 <2:1
7 Sodium 0.7mEq 2.2mEq
8 Vitamin K 15mEq 60mEq
• Advantages of breast milk feeding.
1. Always readily available at proper temperature and needs no time for
preparation.
2. It is fresh and free from bacterial contamination.
3. Nutritional advantages:
a) It contains all the nutrients that a baby needs in the first 6months of life for
growth & development except fluoride.
b) Lower content of protein (1.1mg%) in breast milk causes lower solute load on
premature kidneys.
c) Whey protein: Caseinogen ratio in breast milk is 60:40. Easily digested
lactalbumin is more so; less allergic. Cow’s milk contains more casein, which
is less digestible.
d) Amino acids of breast milk are better for brain development Glutamic acid
is maximum.
e) Human B casomorphin is CNS growth factor.
f) Higher PUFA promotes brain growth & myelination.
g) Higher PUFA prevents atherosclerosis in later life.
h) Active lipase in breast milk promotes digestion of fats.
i) It has low sodium and mineral content.
j) Ca: P ratio is 2:1 so prevents neonatal hypoglycemia & tetany.
k) Iron in breast milk is low but well absorbed so prevents iron deficiency anemia.
l) It also prevents deficiency of vitamin A, B, C, D.
m) Human milk is sweetest – high content of lactose.
4. Anti – infective properties:
a) High secretary IgA, IgM.
b) Macrophages in Human milk synthesize compliment lysozyme and
lactoferrin.
c) It contains bacterial and viral antibodies which provide local GIT immunity
against the organism entering through this route especially against diarrhea.
d) There is a passive transfer of T cell immunity also.
e) It contains anti staphylococcal factors.
f) Human milk contains bile salts stimulated lipase which kills giardia lamblia
and Entamoeba histolytica.
g) Lower PH of stool breast feed infant is thought to favor intestinal flora mainly.
Bifidus and Lactobacilli which protect against E coli infection.
h) Lactoferrin in breast milk is 1/3 saturated so iron is not available for the growth
of E. coli.
i) PABA protects against malaria.
j) Recovery from infection is faster in breast feed infants.
k) Less chances of respiratory infection and septicemia.
5. Higher IQ level of breast feed infants.
6. Prevents future diseases like obesity, hypertension, coronary artery diseases,
diabetes, asthma, inflammatory bowel disease, Hodgkin’s lymphoma, sudden
infant death syndrome.
7. Protects from allergy as secretary IgA inhibits absorption of macromolecular of
protein.
8. Physiological adaptation for preterm infant as human milk contains more energy
protein, fats, Na, Zn, anti-infective factors and macrophages, lower lactose.
9. Bioactive factors like nucleotides enzymes, hormones, growth factors and
probiotics.
10. Polyamines like spermine, spermidine, and putresin. They promote cell growth
and differentiation in tissue.
• Maternal Advantages:
1) Emotional bonding satisfying experience for mother and infant.
2) Time saving for mother.
3) Economic factor.
4) Lactation suppresses ovulation so protects against pregnancy during first few
months.
5) Lower risk of breast and ovarian cancer.
• Viruses which are excreted in breast milk:
1) AIDS virus (HIV).
2) Cytomegalovirus.
3) Human T cell lymphotropic virus type I.
4) Hepatitis B.
5) Herplex simplex.
6) Rubella.
• Contraindication:
1) Mother on anti-cancer, anti-thyroid drug and lithium.
2) Galactosemia, phenylketonuria, in infant.
3) HIV in mother is relative contraindication.
4) Severe neurosis, psychosis in mother.
3.1.1. Colostrum:
3.1.1.1 Definition: It is a viscous lemon-yellow colored secretion from the breast.
Secreted from late third trimester till the first five days after birth. Amount 40 – 60
ml/day.
3.1.1.2 Composition:
S.
No.
Contents Colostrum Breast milk
1 Protein 8.6% 1.1%
2 Fat 2.3% 4.5%
3 Carbohydrates 3.2% 7.0%
4 Minerals High Low
3.1.1.3 Characteristics of colostrum:
1) Alkaline in reaction.
2) High mineral content.
3) High protein content.
4) Low carbohydrate & fat.
5) High vitamin A, D, E.
6) Low vitamins B, C, K.
7) High immunoglobulins.
8) Cellular concentration is high.
3.1.1.4 Advantages:
1) Gives higher immunity.
2) It has laxative action because of large fat globules.
3) First immunization of neonate.
3.1.2. Baby friendly hospital initiative (BFHI): It is started in 1992 by WHO and UNICEF,
aim to have a promotion of breast feeding.
Steps: Ten steps.
1. Have a written breastfeeding policy.
2. Train all health care staff.
3. Inform all pregnant women the benefits and management of breastfeeding.
4. Help mother to initiate breastfeeding within ½hr of birth.
5. Show mothers how to breast feed, how to maintain lactation.
6. Give newborn infant exclusive breast feeding.
7. Practices Rooming in allow mothers and infants to remain together 24
hours/day.
8. Encourage breastfeeding on demand.
9. No soothers, artificial teats or pacifiers to breast feed infant.
10. Foster breast feeding support group refer to them on discharge.
3.1.3. Complimentary feeding (Weaning):
1. Definition: Addition of other foods in addition to breast milk.
2. Age of introduction – 6months onwards.
3. Initially start top milk preferably cow’s milk along with the dal, water, soups or
fruit juices.
• Gradually shift from liquid diet to semisolid diet like khichadi, Dalia, mashed
potato, mashed rice.
• As the age increases gradually adds solid foods made from cereals, pulses,
vegetables, ages, mashed banana and suji.
4. Precaution:
1) Prepare hygienically.
2) Start with small quantity once daily gradually increase to 3times.
3) Freshly prepared food should be given.
3.1.4. Tropic feeds:
Definition: Small amount of expressed breast milk 1-3ml feed to preterm new born.
Advantages:
1. Helps in maturation of:
i. Intestinal mucosa.
ii. Intestinal enzymes.
iii. Gut motility.
2. Prevents necrotizing enterocolitis.
3. Decrease need for parental nutrition.
4. Less chances of sepsis.
5. Shortened hospital stay.
3.1.5. Fore milk:
Definition: Milk secreted at the start of feeding.
1. It is watery, rich in proteins, lactose, vitamins, minerals and water.
2. Satisfy Baby’s thirst.
3.1.6. Hind milk:
Definition: Milk secreted at the end of the feeding.
1. It is rich in fat so, provides more energy.
2. Satisfy Baby’s hunger.
3.2. Carbohydrates.
1. Average daily energy provided from carbohydrates is 55 – 60%
2. 1gm of carbohydrate gives 4K calories.
3. Carbohydrate from food are converted into end product glucose, which is absorbed
and stored as glycogen mainly in liver and muscles.
3.2.1. Types:
• Sucrose is most cariogenic agent.
• Sweetened beverages given through bottle throughout night are cariogenic.
• Sticky candles retained orally for long period are cariogenic.
3.2.2. Clinical features:
Cavitation’s of occlusal surface of teeth or contact surface between teeth.
1. Treatment:
a) Dental treatment by using:
 Silver amalgam.
 Plastic composite restoration.
 Stainless steel crown.
 If caries involves dental pulp pulpotomy or pulpectomy.
 Analgesics for pain.
 Oral antibiotics for infections:
o Penicillin.
o Clindamycin.
o Erythromycin.
 Parenteral antibiotics for complications like vital areas infection
b) Prevention:
1. Fluoride:
a) Fluoride content of water supply to 1ppm.
b) Dietary fluorides supplementation.
2. Oral hygiene:
a) Daily brushing.
b) Brushing with fluoridated toothpaste.
3. Diet:
a) Decreasing ingestion of sugar.
b) Discourage sweetened beverage in bottle at night.
c) Reduce sugar containing snacks between meals
4. Dental sealants:
C) Complications:
a) Pulpitis.
b) Dental Abscess.
c) Sepsis.
d) Facial space infection.
e) Disruption of normal development of the successor permanent teeth.
3.3. Proteins:
1. They constitute 20% of body weight.
2. 1gm proteins provides 4K calories.
3. Proteins are made up of 20 amino acids in various combinations.
4. Amino acids are of two types:
a) Essential amino acids: these are those amino acids, which are not synthesized in
body and are to b supplied to body through food. They are for adult – Leucine,
Isoleucine, valine, threonine, methionine, phenylalanine, tryptophan, lysine and
histidine. In addition, cystine, tyrosine, arginine and taurine for LBW. Infants and
children. Human milk contains all essential amino acids in adequate amount.
b) Non-essential amino acids: Amino acids which are synthesized in body.
5. Reference proteins: Egg protein is considered as reference protein as it is complete, well
digested protein.
6. Complete protein: A complete protein contains all essential amino acids in relatively same
amount as human require for maintenance of good and optimal growth.
7. Proteins of animal origin have higher content of essential amino acids.
8. Proteins of vegetable origin are often biologically in complete as they lack one or other
essential amino acids.
9. Combination of vegetable foods can provide complete protein.
10. Protein of rice and potato are good vegetable protein.
3.4. Lipids:
1. Lipids provides about 25 – 30% of calories (3% from essential fatty acids).
2. There are three types of Lipids:
a) Triglycerides 95%.
b) Phospholipid (Lecithin).
c) Sterols (Cholesterol).
3. Triglycerides are of two types:
a) Saturated triglycerides.
b) Unsaturated triglycerides
4. PUFA (Polyunsaturated fatty acids) are important for body.
Two important PUFA for body are:
a) Omega 6 fatty acids
i. Linoleic acids.
ii. Arachidonic acids
b) Omega 3 fatty acids
i. Linoleic acids.
ii. Eicosapentanoic acid.
iii. Docosahexaenoic acid
5. Essential fatty acids.
6. Sources: Vegetable source, nut, seeds.
7. Functions:
a) Sources of energy 25-30%.
b) Provide insulation to the body.
c) Carrier for fat soluble vitamin.
d) Precursor of prostaglandins.
e) Important component of cell membrane.
f) Omega 3 fatty acids lower blood cholesterol and triglycerides.
g) Omega 3 fatty acids serve as a raw material for:
• Prostaglandins.
• Thromboxane.
• Leukotrienes.
h) Omega 3 fatty acids regulate:
• Blood pressure.
• Immune response.
• Inflammatory response to injury and infections.
8. Deficiency diseases:
1) Growth retardation.
2) Reproductive failure.
3) Skin disorders (decrease omega 3 fatty acids)
4) Predisposes to infection.
5) Decrease myocardial contractibility.
6) Hemolysis.
7) Renal hypertension.
3.5. Normal Nutritional requirement (RDA):
S.
No.
Calorie Daily Requirement
1 0-3 months 120/kg
2 3-6 months 115/kg
3 6-9 months 110/kg
4 9-12 months 105/kg
OR
1 Under 1yr 110Kcal/kg
2 1-3Yrs. 100Kcal/kg
3 4-6 Yrs. 90Kcal/kg.
4 7-9 Yrs. 80Kcal/kg.
5 10-12 Yrs. 70Kcal/kg.
6 13-15 Yrs. 60Kcal/kg.
7 16-18 Yrs. 50Kcal/kg.
8 Adult 40Kcal/kg.
OR
1000 calories at – 1yr. Increase by 125 calories for each year after
1yr.
Protein Requirement
1 0-3 months 2.3 gm/kg.
2 1-3 months 1.8gm/kg
3 4-6 yrs. 1.5gm/kg.
4 7-9 yrs. 1.5gm/kg.
5 10-12 yrs. 1.46gm/kg
6 13-15 yrs. 1.35gm/kg
7 16-18 yrs. 1.3gm/kg
Vitamins Requirement
1 Vitamin A 1500-5000 IU (300-750μgm)
2 Vitamin C 30-50mg
3 Vitamin D 400 IU (10μgm)
4 Vitamin E 4-5 IU.
B - Complex Requirement
1 B1 0.5 to 1.5 mg
2 B2 0.5 to 2.5 mg
3 Niacin 0-20 mg.
4 B6 0.4 to 1.4 mg
5 Folic acid 25 – 1000 mcg
6 B12 1-15 mcg.
Minerals Requirement
1 Iron (Elemental) 1mg/kg/day.
2 Ca Infants 400 – 600mg
3 1-10 yr. 500mg-1gm
4 >10 yr. 1.2 to 1.5gm
5 Phosphorus 200-300 mg
6 Mg (Infants) 40-70mg
7 Iodine 0.2mg
8 Fluorine 0.5to 1.0mg
9 Zinc 0.3mg / kg
10 Na+
2mg/kg
11 K+
1.5mg/kg.
3.6. Maintenance fluid and electrolyte requirements:
• Water
At birth – 75% of body weight.
Adult – 60% of body weight
• Fluid compartments:
1. ICF: Intracellular fluid 2/3 of total body water.
2. ECF: Extracellular fluids. It comprises 1/3 of total body water:
a) Plasma.
b) Interstitial fluid.
c) Transcellular fluid.
• Electrolytes are substances capable of conducting an electric current in solution.
• Electrolyte exists in two forms:
A. Cations (Positively charged) Na+
, K+
, Ca+
, Mg+
.
B. Anions (Negatively charged) Cl--
, HCO--
3, SO --
4
• Osmolality number of osmotically active particles per 1000gm of water in a solution.
• Sodium principal cation of extracellular fluid (ECF).
Normal Sr. Na = 130to145mEq.
Daily requirement = 2to3 mEq / 100cal/day.
• Potassium: is major intracellular cation (ICS)
Normal value – 3.5 to 4.5 mEq,
Daily requirement 1to2mEq/100 calories/day.
• Acid base balance is maintained by:
1. Blood buffer system.
2. Lungs.
3. Kidney.
Acid base balance
S.
No.
Parameter Arterial blood Venous blood
1 pH 7.38 – 7.45 7.35 – 7.40.
2 pCO2 35 – 45 mm Hg 23 – 27 mm Hg
3 HCO3
--
21 – 28 mEq/L 22 – 29 mEq/L
• Blood Buffer system:
a) Bicarbonate carbonic acid buffer.
b) Hemoglobin.
c) Proteins.
d) Bicarbonate – Carbonic acid in kidney tubules.
e) Monohydrogen phosphate – dihydrogen phosphate buffer.
f) Sodium hydrogen exchange.
g) Ammonia – ammonium buffer.
• Disturbances of Acid Base status:
a) Respiratory Acidosis (pCO2 increase) Low PH characterized by increased pCO2.
b) Metabolic Acidosis (HCO3
--
) decreased. Low PH characterized by reduction in
HCO3
--
c) Respiratory Alkalosis (pCO2 decrease) High PH characterized by decrease pCO2
due to hyperventilation.
d) Metabolic Alkalosis (HCO3
--
) increased High PH characterized by increase
HCO3
—
due to hyperventilation and compensatory elevation of pCO2.
• Maintenance of fluid requirements:
S. No. Body weight Fluid/day
1 0-10kg 100ml/kg
2 11-20 kg 1000ml+50ml/kg for each
kg>10kg
3 20kg 1500ml+20ml/kg for each
kg>20kg
Maximum fluid / day = 2400ml
OR
1 1days to 1yr. 150ml/kg/day.
2 1-3 yrs. 125ml/kg/day
3 4-6 yrs. 100ml/kg/day
4 7-9 yrs. 75ml/kg/day
5 10-12 yrs 50ml/kg/day
• Protein and Calorie content in 100gm of Food Article.
S. No. Items Calorie Protein
1 Pulses 350 20
2 Soybean 430 42
3 Cereals 350 11
4 Rice 350 7
5 Groundnut 567 25
6 One biscuit 20 0.5
7 Milk (cow) 67 3
8 Banana 80 1.2
9 Apple 50 0.5
10 Jaggery 383 0.4
11 Potato 100 1.6
12 Egg (Chicken) 1egg =
50gm.
173 13.3
After one year reduces 25ml every 3yrs till 12 years.
• Maintenance of electrolyte requirements.
1 Sodium 2-3 mEq/kg/day.
2 Potassium 1-2 mEq/kg/day
• Neonatal period (full term) fluid requirement.
→ Day 1 & 2 = 60 – 80 ml/kg
→ Increase 15ml/kg/day till 7th
day of life.
3.7. Vitamin A (Fat soluble Vitamin)
3.7.1. Functions. It is necessary for:
a) Vision – Retina.
b) Maintaining epithelial tissue integrity in eye, skin, mucous membrane.
c) Immune competence.
d) Growth.
e) Retinol is necessary for spermatogenesis, integrity of testis and vaginal
epithelium.
f) Beta carotene has antioxidant property so, reduce the incidence of cancers.
3.7.2. Sources:
a) Cod liver oil, Shark liver oil, egg yolk.
b) Butter, ghee.
c) Carrots, Green leafy, Yellow vegetables.
d) Ripe mango, orange, papaya.
e) Plant sources: In the form of carotene.
f) Animal sources: in the form of retinal.
g) Provitamin A: Beta carotene. (Beta carotene is converted into retinal in
intestinal wall.)
3.7.3. Daily Requirements: 300μg to 750μg.
3.7.4. Vitamin A Deficiency: - Causes
i. Malnutrition.
ii. Malabsorption.
iii. Chronic diarrhea.
iv. Pancreatic diseases.
v. Hepatic insufficiency.
vi. Severe measles.
3.7.5. Clinical features:
1. Increased risk of infection.
2. Eye changes:
a) Night blindness is earliest clinical feature.
b) Xerophthalmia: Dry wrinkled conjunctiva.
c) Bitots spots
d) Keratomalacia
e) Perforation of cornea.
f) Fundus changes pale yellow spots along vessels and periphery.
S. no. Signs Terms
A. Primary sign
1 X 1 A Conjunctival xerosis
2 X 1 B Bitots spots
3 X 2 Corneal xerosis
4 X 3 A Corneal ulceration (<1/3
Cornea)
5 X 3 B Corneal ulceration (>1/3
Cornea)
B. Secondary sign
1 X N Night Blindness
2 X F Fundal changes
3 X S Corneal Scarring
3. Skin phrynoderma - Skin is scaly and toad like (Deficiency of essential fatty
acids).
4. More prone to respiratory infection due to squamous metaplasia of
respiratory mucosa.
5. More prone to renal and bladder calculi due to alteration of mucosa.
6. Reproductive Dysfunction due to atrophy of germinal epithelium.
7. Rarely hydrocephalus.
3.7.6. Treatment:
WHO treatment of Xerophthalmia.
1. Oral vitamin A
o First dose – 50,00 units for < 6months, 1Lakh 6months to 1yr, 2Lakhs
more than 1yr.
o Second dose – Repeat on 2nd
day.
o Third dose – After one month.
2. Parenteral Vit A can be given for night blindness or Bitots spot – 10,000 IU
daily for 14 days.
3.7.7. Prophylaxis: National Vitamin A prophylaxis program 6months to 3yrs – 2Lakhs
IU in oil base every 6months (1lakhs / ml).
3.7.8. Hypervitaminosis A:
1. Rupture of lysosomal membrane.
2. Increase ICP: Pseudotumor cerebri.
Headache, vomiting, dizziness, bulging of anterior fontanel, and papilledema.
3. Chronic intoxication: Anorexia, dry itchy skin, weight loss, painful
extremities, sparse hair, hepatosplenomegaly, hypoplastic anemia, benign
intracranial hypertension, yellow skin.
4. During pregnancy: Mother consuming large amount of oral “Retinoids” for
treating acne may lead to congenital craniofacial malformation in fetus.
5. Hyperostosis.
3.8. Vitamin B Complex: It includes
o B1 Thiamine.
o Riboflavin.
o Niacin.
o Pyridoxine B6
o Biotin.
o Folate.
o Vitamin B12
They are important constituents of Enzyme system.
Pantothenic acid, choline and inositol are not associated with deficiency syndrome
through they are necessary for normal functioning of human organism.
3.8.1. Deficiency Diseases:
S. No. Vitamins Deficiencies
1 B1 (Thiamin)Beri – Beri
2 B2 (Riboflavin) – Cheilosis, Glossitis, Keratitis,
Conjunctivitis, Corneal vascularization,
Photophobia, Seborric dermatitis.
3 Niacin Pellagra
4 B6 (Pyridoxine) – Convulsions, anemia, peripheral
neuropathy, dermatitis.
5 Biotin Dermatitis, alopecia, somnolism, hallucination,
hypotonia, hyperesthesia.
6 Folic acid Megaloblastic anemia.
7 B12 Pernicious anemia.
3.8.2. Beri-Beri: diseases caused by vitamin B deficiency. Commen in those communities
whose staple diet is polished rice. It occurs in three forms:
a) In Infants (wet Beri – Beri).
b) In older children (Dry Beri – Beri).
c) Meningitis form.
3.8.1.1. Clinical features:
A. Wet Beri – Beri (Cardiac form) Restlessness, Excessive cry, Vomiting,
Abdominal distention, Flatulence, Constipation, Insomnia, Infants develops
CHF manifestation – tachycardia, dyspnea, edema, hepatomegaly &
Cardiomegaly.
B. Dry Beri – Beri (Chronic Neurologic form) Anorexia, weight loss,
weakness, diarrhea, constipation, edema, drowsiness, apathy, ataxia,
peripheral neuritis, Cranial nerve palsies, nystagmus.
C. Meningitis form Bulging anterior fontanel, dilated pupil, head retraction,
coma, convulsions.
3.8.1.2. Treatment:
• B1 – 10mg I. V. stat.
10mg I.M. for 3days.
10mg Orally for 6weeks.
3.9. Pellagra:
1. Disease caused by niacin deficiency.
2. Commen in person whose staple diet is maize.
3. Diagnostic triad (D3
)
a) Dermatitis - exposed parts.
b) Diarrhea.
c) Dementia.
4. Treatment
a) Niacin – 50mg × 3times for 3weeks.
b) Avoid sun exposure.
3.9.1. Pyridoxine (B6)
1. Functions:
a) Helps in amino acid metabolism.
b) Converts tryptophan to niacin.
c) Helps in metabolism of essential fatty acids.
2. Sources – Whole grain,
3. Daily requirements – 0.5 to 2.5mg/day.
4. Deficiency:
a) Seizures during infancy.
b) Peripheral neuritis.
c) Dermatitis.
d) Anemia – microcytic, hypochromic.
3.10. Scurvy.
1. Definition: Disease caused by deficiency of vitamin C (ascorbic acid)
2. Pathophysiology:
a) Formation of collagen and chondroitin sulphate is impaired in vitamin C
deficiency.
b) This results in tendency to:
 Hemorrhage.
 Defective dentition.
 Loosening of teeth.
 Non-formation of Endochondral bone formation.
 Bony Trabeculae become Brittle and fracture easily.
 Periosteum loose and sub periosteal hemorrhage occur especially at the end
of femur & tibia.
c) Severe deficiency result in:
 Degeneration of skeletal muscles.
 Cardiac hypertrophy.
 Bone marrow depression.
 Adrenal atrophy.
3.10.1. Clinical features:
1. Age: Any age but unusual in Newborn period because it requires time to
develop. Usual age 6 – 24 months.
2. Vague symptoms: Irritability, tachypnoea, digestive disturbances and loss of
appetite.
3. Generalized tenderness: Particularly when infant is picked up or when diaper
is changed. Pain result in pseudo-paralysis.
4. Legs are held in frog like position.
5. Edematous swelling over shaft of legs.
6. Sub periosteal hemorrhage can be at the end of femur.
7. Apprehensive facial expression.
8. Gums: Bluish, purple, spongy swelling of mucous membrane especially over
upper incisors.
9. Scorbutic Rosary: at costochondral junction Scorbutic rosary have sharp
borders due to subluxation of sternum.
10. Bleeding tendencies:
a) Petechial hemorrhage over skin, mucous membrane, and gums.
b) Hematuria, Malena, orbital and subdural hemorrhage.
11. Low grade fever.
12. Wound healing – slow.
13. Swollen joints.
14. Follicular keratosis.
3.10.2. Diagnosis:
1. Clinical picture.
2. History of poor vitamin C intake.
3. Radiological changes:
a) Site – distal end of long bone especially knee.
b) Ground glass appearance of bone.
c) Cortex is pencil thin and epiphyseal ends of bones are sharply
outlined.
d) White line of Frenkel – irregular thick white line at metaphysis
represent zone of well calcified cartilage.
e) Epiphyseal center of ossification has ground glass appearance and
surrounded by white ring.
f) Zone of rarefaction – under the white line at metaphysis and is
considered necessary for diagnosis.
g) Spur – Lateral prolongation of white line may be present.
h) Epiphyseal separation
i) Dumb bell or club shaped bone due to calcified subperiosteal
hemorrhage, not during active phase but during healing.
4. Plasma concentration of vitamin C
5. Urinary exertion of vitamin C after a test dose.
3.10.3. Treatment:
1. Vitamin C Tab. 250mg daily for 10days. (Ascorbic acid – 100to300mg/day)
2. Diet sources: Citrus fruit and vegetables including tomatoes, cabbage, green
leafy vegetables, germinating pulses, lemon, amla and guava.
3.11. Vitamin D. (Calciferol)
1. It is a hormone.
2. Exist in two forms:
a) Vitamin D2 – Ergocalciferol (Plant origin)
b) Vitamin D3 – Cholecalciferol (produced in skin by ultraviolet radiations from
precursor 7 dehydrocholesterol)
3. Metabolism - 7 dehydrocholesterol on exposure to sunlight.
In skin – Cholecalciferol transfer to liver
In Liver Hydroxylated to 25-OH Cholecalciferol
In kidney (Renal cortex) further hydroxylation 1,25 dihydroxy cholecalciferol
(Hormone)
4. Daily requirement: 10μgm or 400IU/ day.
5. Sources:
a) Sunlight.
b) Egg, Butter, milk.
c) Liver and fish oil.
d) Fortified ghee.
3.11.1. Rickets.
3.11.1.1. Definition: It is a disease caused by deficiency of vitamin D leading to
failure of mineralization of growing bone or osteoid tissue.
3.11.1.2. Causes:
a) Inadequate intake of vitamin D.
b) In breast fed infant if infant is not exposed to sunlight or mother is not
exposed to sunlight.
c) Interference with absorption of vitamin D in steatorrhea.
d) Chronic hepatic disease.
e) Chronic renal disease.
f) Condition unbalancing calcium phosphorus homeostasis.
3.11.1.3. Pathophysiology:
1. There is defective bone growth due to suppression of normal
epiphyseal cartilage growth and calcification.
a) These changes result from deficiency of calcium and phosphorus
salt in serum.
b) Cartilage cells fail to complete their normal cycle of proliferation
and degeneration.
c) Failure of capillary penetration which occurs in patchy manner.
Result in frayed irregular epiphyses at the end of the shaft.
2. Failure of osseous and cartilaginous matrix to mineralize in the zone of
preparatory calcification followed by deposition of newly formed
uncalcified osteoid.
3. Lack of mineralization in sub periosteal bone – shaft is softened so
deformities and fractures.
4. Elevated serum phosphates due to increased osteoblastic activities.
5. Serum calcium is normal due to mobilization of calcium from bone by
parathormone stimulation because less calcium is absorbed from intestine.
6. Serum alkaline phosphatase is increased.
3.11.1.4. Clinical features:
Age 6months to 2yrs.
1. Early features – irritability, restlessness, profuse sweating overhead more
during night
2. Major features:
a) Head
i. Bossing, macrocephaly with flattening of vertex (box, head)
ii. Fontanel – increased size and delayed closure.
iii. Craniotabes – softening of occipital and parietal bones
(ping pong ball feeling under pressure.)
b) Teeth – delayed dentition.
c) Thorax
i. Rachitic rosary (smooth rounded, nontender
costochondral beading)
ii. Pigeon – Chest deformity.
iii. Harrison sulcus or groove (Depression along insertion of
diaphragm into ribs)
iv. Flaring of lower ribs (violin shaped)
v. Pectus excavatum sometimes (sternum depressed)
vi. Concavity at inferior angle of scapula.
d) Spine – Scoliosis, kyphosis.
e) Limbs
i. Widening of wrist, ankle.
ii. Knock knees (Genu valgum)
iii. Bow legs (Genu varum)
f) Milestones – Delayed due to poor muscle tone and lax ligaments
g) Feet – flat feet.
h) Belly Pot belly, visceroptosis due to hypotonia.
i) Acrobatic rickets – due to laxity of ligaments limbs can be bent to
any position.
j) Constipation.
k) Rarely tetany due to decreased serum calcium.
l) Rachitic dwarfism.
m) Generalized hypotonia.
n) Recurrent respiratory infection.
3.11.1.5. Diagnosis:
1. Biochemical findings.
a) Increase alkaline phosphatase due to osteoblastic activity.
b) Serum – calcium normal.
c) Serum phosphate – decreased.
d) Decreased serum 25hydroxy vitamin D reliable index.
2. X – Ray findings (Wrist).
a) Cupping of lower end or radius and ulna.
b) Widening (Flaring, champagne glass)
c) Fraying (Rarefaction)
d) Increased distance between epiphyseal center and metaphysis.
e) Periosteal lifting.
f) Rarefaction (Prominent trabecula with poor density due to
demineralization)
g) Green stick fractures.
3.11.1.6. Healing Rickets – X – Ray findings:
1. Line of calcification at the distal end of metaphysis.
2. Zone of decreased calcification proximal to above line.
3.11.1.7. Treatment:
1. Vitamin D
a) Single dose: 6 lacs (15000gm of vitamin D) units IM stat dose.
Repeat after 4weeks. If no improvement suspects refractory rickets.
b) Daily doses: - 50to150 μ gm daily of vitamin D for 2 – 4 weeks.
Radiological healing within 2 – 4 weeks.
c) 1 – 25 dihydroxycholecalciferol – 0.5 – 2μgm.
2. Supplement calcium.
Prevention:
1. Daily requirement of vitamin D 10μgm (400IU)
2. Sun shine exposure (5min daily)
3. Diet – fish, liver oils, liver, egg, Butter milk, fortified ghee, margarine.
Hypervitaminosis D
1. Skeletal sclerosis, metastatic calcification.
2. Hypercalcemia, hypercalciuria.
3. Vomiting, constipation, anorexia.
4. Poor growth, irritability.
5. Renal failure.
6. Nephrocalcinosis.
7. Polydipsia, polyuria, dehydration.
8. Anemia.
9. Aortic valvular stenosis.
10. Hypertension.
11. Eye – corneal clouding, retinopathy.
12. Fever, irritability.
13. X – Ray changes:
a) Hyperplasia of subperiosteal bone.
b) Metastatic calcification.
c) Generalized osteoporosis.
3.11.1.8. Refractory Rickets (Resistant Rickets)
1. Definition: No response or poor response to adequate dose of vitamin
D.
2. Types:
Type I
1) Disturbed vitamin D metabolism for liver diseases.
2) Disturbed vitamin D metabolism for renal diseases.
3) Failure of target cell to respond to 1,25 dihydroxy vit D (vit D
dependent rickets)
4) Failure of kidney to form 1,25 (OH3) vitamin D called renal
dystrophy.
Type II Rickets Defective reabsorption of phosphates by renal tubules.
a) Fanconi Syndrome
b) Familia hypophosphatemic vitamin D refractory rickets.
c) Isolated phosphaturia.
d) Renal tubule acidosis.
e) Oncogenous Rickets
3. Treatment:
1) High dose of vitamin D 10,00 units.
2) Phosphates supplementation – Disodium hydrogen phosphate
13.68gm + phosphoric acid 5.9gm.
3) 1,25 (OH3) vitamin D – 1 μ gm/day (Rachatrol)
3.12. Vitamin E.
1. Functions: - It is a fat-soluble vitamin.
a) Stability of biological membrane.
b) Antioxidant.
2. Sources:
a) Gram oils of various seeds, vegetables, soybeans.
b) Green leafy vegetables.
c) Nuts.
d) Legumes.
e) Egg yolk.
3. Daily Requirements:
 0.5 mg/gm of linoleic acid.
 4 – 15mg/day.
4. Features of deficiency:
a) In prematurity.
I. Hemolytic anemia, edema, skin changes.
II. Retinopathy of prematurity.
III. Bronchopulmonary dysplasia.
IV. Intraventricular hemorrhage.
b) Impaired reproductive abilities.
c) Muscular dystrophy (Fatty types)
d) Growth retardation.
3.13. Vitamin K.
1. It is fat soluble vitamin synthesized by intestinal flora.
2. Functions:
a) Synthesis of coagulation factors II, VII, IX and X in liver.
b) Prothrombin formation.
c) Protein C, S, Z.
3. Sources:
a) Green leafy vegetables.
b) Liver, Pork.
c) Cow’s milk.
4. Forms: Three forms.
a) K1 – Naturally occurring in vegetable
b) K2 – Produced by intestine.
c) K3 – Menadiones (Synthetic)
5. Daily requirements: 12μgm
6. Deficiency diseases:
a) Hemorrhagic disease of new born.
b) Hemorrhagic manifestation in older children.
7. Causes of deficiency:
I. Premature new born
II. Oral antibiotic (Broad spectrum)
III. Chronic diarrhea.
IV. Biliary obstruction.
V. Chronic intestinal parasitosis.
8. Excessive administration causes:
a) Hemolytic anemia,
b) Hyperbilirubinemia.
c) Kernicterus.
Especially in preterm and G6 PD deficiency infants.
3.14. Trace Elements:
o These are microminerals required in small amount.
o They include iron, iodine, zinc, copper, manganese, fluorine, molybdenum, selenium,
cobalt, nickel, vanadium, silicon, arsenic.
o Deficiency or excesses can have bad effects.
o Deficiency is more commen with malabsorption and parenteral nutritional therapy.
3.14.1. Zinc:
1. Infant total zinc content = 60mg.
Adult = 1600 mg.
2. Functions:
a) Essential components of many enzymes,
b) Help in protein and RNA synthesis.
3. Sources: Nuts, Grams, Dry beans, Legumes, meat, liver, fish.
4. Daily requirements: - 200mcg.
5. Causes:
a) PEM.
b) Malabsorption.
c) Regional ileitis.
d) Rheumatoid arthritis.
e) Sickle cell anemia.
f) Achondroplasia.
g) Chronic blood loss.
h) Excessive sweating.
i) Viral hepatitis.
j) Prolonged parenteral nutrition.
6. Clinical features:
a) Growth retardation.
b) Hypogonadism.
c) Anemia.
d) Hepatosplenomegaly.
e) Adolescent nutritional dwarfing syndrome.
f) Protracted diarrhea.
g) Delayed wound healing.
h) Anorexia, failure to thrive.
i) Hypogeusia – impaired taste perception.
j) Hyperkeratotic skin.
k) Infantile tremor syndrome.
7. Treatment: 1 – 5 mg/kg of body weight.
ACRODERMATITIS ENTEROPATHICA
1. It is an autosomal recessive disorder caused by inability to absorb zinc.
2. Manifest shortly after weaning.
3. It is an inborn error of metabolism in which they are:
a) Skin changes around orifices and extremities eczematous, dry
scaly, or psoriasis.
b) Diarrhea.
c) Alopecia.
d) Atrophy of nails.
e) Failure to thrive.
4. Shows dramatic response to zinc therapy.
Dose 50mg to 150mg/day.
3.14.2. Copper:
1. It is essential for iron utilization.
2. Important for many enzymes:
a) Cytochrome oxidase.
b) Monoamine oxidase.
c) Dopamine beta hydroxylase.
d) Delta – aminolaevulinic acid dehydrogenase.
e) Ascorbic acid dehydrogenase.
f) Uricase.
g) Tyrosinase.
3. Total body content:
Infant – 14mg.
Adult – 100mg
4. Deficiency features:
a) Psychomotor retardation.
b) Hypotonia.
c) Apneic spells.
d) Pallor, sideroblastic anemia.
e) Hypopigmentation in skin and hair prominent scalp veins.
f) Osteoporosis.
g) Menkes kinky hair syndrome X – linked recessive disease.
5. Excessive accumulation – Wilson disease.
PICA
1. Definition: Chronic ingestion of non – nutritive substances (Plastic,
charcoal, clay, ash, paints and sand)
2. Age: after 2years needs investigations.
3. Causes:
a) Iron deficiency anemia.
b) Mental retardation.
c) Autism.
d) Behavior disorder.
e) Psychological neglect.
Increase risk of:
1. Lead poisoning.
2. Parasitic infection.
4. Treatment:
1. Iron therapy for iron deficiency anemia.
Dose 3to6mg/kg/day of elemental iron × 3months.
2. Deworming.
3. Psychotherapy.
3.15. Protein energy malnutrition:
1. Definition: It refers to class of clinical conditions that may result from varying degree
of protein lack of energy (calories) inadequacy.
2. Types: Broadly speaking two major clinical syndromes are widely recognized i. e.
Kwashiorkor & Nutritional marasmus.
3. Cause:
o Kwashiorkor is said to be a result from gross deficiency of protein. Through
energy deficiency is also present.
o Nutritional marasmus results from gross deficiency of energy though protein
deficiency also accompanies.
o There is overlap in the clinical picture so it is appropriate to label marasmic
kwashiorkor.
o Growth failure and poor tissue repair (due to protein lack) and energy shortage
(due to calories deficiency) is also commen to forms of PEM.
SPECTRUM OF PEM
a) Invisible PEM:
Downward curve in road to health card even it is within the road to health indicates
PEM.
b) Under weight:
 Weight 60 – 80% of expected.
 No features of PEM.
c) Nutritional dwarfing: Chronic malnutrition leads to nutritional dwarf
d) Marasmus: Essential features.
o Grade I: Loose skin fold in axilla and groin.
o Grade II: Loose skin fold in thigh and buttocks.
o Grade III: Loose skin fold in chest and abdomen.
o Grade IV: Buccal pad of fat is also wasted (Saturated fat last to be wasted)
e) Marasmic kwashiorkor: When marasmic child develops edema and he is apathetic.
f) Kwashiorkor:
1) Growth retardation.
2) Muscle wasting.
3) Psychomotor changes.
4) Edema.
4. Etiology
I. Low intake of food:
a) Poverty.
b) Social customs.
c) Infections.
d) Feeding habits.
e) Maternal deprivation.
II. Normal intake but excessive loss in stool:
a) Chronic diarrhea.
b) Malabsorption.
c) Worm infestation.
III. Normal intake, normal absorption, but not metabolized:
o Chronic diseases – CHD, Chronic renal failure.
CLASSIFICATION OF PEM
I. WHO Classification:
Features Moderate Undernutrition Severe Undernutrition
1. Generalized edema No Yes, Edematous malnutrition
2. Weight for height wasting
measurement.
Wasting 70 – 79% Severe wasting <70% of expected
3. Stunting height for age. Stunting 85 – 89% of
expected
Severe stunting <855 of expected.
II. Classification of Indian academy of pediatrics:
1. Grade I – 71 – 80% of expected weight.
2. Grade II – 60 – 71% of expected weight.
3. Grade III – 51 – 60% of expected weight.
4. Grade IV – 50% or bellow of expected weight.
If the child has edema the letter ‘K’ is placed in front of grade. If no edema
then grades without ‘K’.
III. Syndromal Classification:
1. Kwashiorkor.
2. Nutritional marasmus.
3. Marasmic kwashiorkor.
4. Pre-kwashiorkor.
5. Nutritional dwarfism.
IV. Jelliffe classification:
1. 1st
Degree = wt. between 90 and 80% of expected.
2. 2nd
Degree = wt. between 80 and 70% of expected.
3. 3rd
Degree = wt. between 70 and 60% of expected.
4. 4th
Degree = wt. Below 60% of expected.
V. Gomez Classification:
PEM is graded with reference to the weight for age as percentage of expected height
(Harvard standard)
1. 1st
Degree = wt. between 90 and 75% of expected.
2. 2nd
Degree = wt. between 75 and 60% of expected
3. 3rd
Degree = wt. bellow 60% of expected
VI. Welcome & International Classification:
A. wt. between 80 and 70% of expected.
1. With edema = kwashiorkor.
2. Without edema = undernutrition.
B. wt. Below 60% of expected
1. With edema -Marasmic kwashiorkor.
2. Without edema Nutritional marasmus.
VII. McLaren Classification:
• Mild = wt. between 90 and 80% of expected.
• Moderate = wt. between 80 and 70% of expected
• Severe = wt. bellow and 70% of expected
VIII. Waterloo Classification:
1. Acute (wasted but not stunted) = wt. for height low. (ht. for age normal)
2. Acute/chronic (wasted but not stunted) = wt. for height low. (ht. for age
normal).
3. Nutritional Dwarfs = wt. for ht. normal (wt. for age decreased).
4. Stunted not wasted = Ht. for age decreased.
IX. Arnold Classification: It is based on mid arm circumference.
Mild to moderate – MAC between 12.5 cm and 13.5 cm.
Severe – MAC under 12.5 cm.
X. Classification based on skin-fold thickness:
o Mild – 80 to 90% of expected.
o Moderate - 60 to 80% of expected.
o Severe – Under 60%.
Age Independent Anthropometrics Indices
Weight in kg.
1. Dugdale’s Indices: -------------------- × 100 = 0.88 – 0.97 (or Malnourished <0.79)
Height (cm) 1.6
Weight in kg.
2. Rao’s Indices: ------------------ × 100 = 0.15 – 0.16 (PEM< 0.14)
Height (cm2
)
Mid arm circumference (cm)
3. Kanawati Indices: ----------------------------------- = 0.32 – 0.33cm (PEM <0.25)
Head circumference (cm)
4. Mid arm circumference = >13.5 cm.
Between age 1 and 5 years (PEM < 12.5cm)
Severe Acute malnutrition (SAM)
In children between the ages of 6 and 60 months, SAM may be diagnosed on the
basis of any of the following criteria.
I. Weight/Height or weight/length < 3z score, using the WHO Growth charts.
II. Mid – Upper arm circumference (MUAC) <115 mm*
.
III. Bipedal edema of nutritional origin.
(*
For infants below 6months, criteria (i) or (iii) or “visible severe wasting “ to be used till data on
MUAC <6 mos available)
Evolution of PEM (Five Theories)
1. Gopalan Adaptation Hypothesis:
a) Dietary background of marasmus and kwashiorkor is same.
b) Marasmus is extreme degree of adaptation to prolonged inadequacy of
proteins and energy in diet.
c) Kwashiorkor is due to adaptation failure, which follows two situations;
I. Prolongation of stress of malnutrition.
II. Sudden precipitation by fulminant infection.
2. Dietetic Hypothesis:
a) Kwashiorkor is prominently protein deficiency.
b) Marasmus is energy deficiency.
3. Golden’s Hypothesis of free Radical damage:
Kwashiorkor results from:
I. Overproduction of free radicals: Because of infection, toxins, iron etc.
II. Breakdown of protective mechanism by deficiency of vitamin A, vitamin
E, Carotene., zinc, copper, selenium, magnesium.
4. Jelliffe Hypothesis: kwashiorkor is nutritional disorder precipitated by other
factors like infection, parasitosis, emotional trauma, maternal deprivation, toxin
5. Aflatoxin contamination of food.
5. Pathology of PEM
1. Sr. albumin decreases.
2. Sr. Globulins:
a) Alfa1
globulin increases.
b) Alfa2
globulin decreases.
c) ᵦ globulin decreases.
d) Gamma globulin increase.
3. Amino acids:
Essential amino acid decrease.
4. Enzyme decrease.
5. Carbohydrates:
a) Glycogen reserve in liver and muscle are depleted.
b) Chance of hypoglycemia increases.
6. Lipids:
a) Essential fatty acids decrease
b) Sr. Lipid level variable.
7. Electrolytes:
a) Total body Na+
increases.
b) Total K+
decreases.
8. Water: Total body water increases.
9. Minerals: decreased iron, zinc, Mg+2
, Cu+2
, Ca+2
, P+2
and other trace
elements.
10. Endocrine glands: Atrophied but functions maintained.
11. Heart: Microcardia but Cardiomegaly if CHF & Anemia.
12. Liver shows fatty changes:
Raised Bilirubin – Bad prognostic sign.
13. Coagulation factors: Decreased.
14. GIT:
a) Mucosal atrophy.
b) Delayed mucosal repair.
c) Disaccharides Deficiency.
d) Ascending cholangitis.
e) Pancreatitis.
15. Immunity:
a) Decreased in chemotaxis:
1) Bacterial killing decreases.
2) Lysozymes decreases.
3) Complement decreases.
4) Interferon decreases.
b) Phagocytosis: Normal.
c) Humoral immunity:
I. Antibody production to vaccine and infections is
satisfactory.
II. Antibody production against diphtheria in impaired.
III. IgA decrease.
d) Cell mediated immunity:
1) Thymic atrophy.
2) Lymphopenia.
3) Poor cell mediated immunity.
4) M.T. Test may be negative.
5) T leper cell to T suppressor cell ration is reduced which
predispose to fungal infection.
• Biochemical changes in PEM.
1) Hypoproteinemia.
2) Hypoglycemia.
3) Plasma transferase decreases, K+
decreases.
4) Plasma triglycerides cholesterol and ᵦ lipoprotein reduce.
5) Decreased Sr. Enzyme: Esterase, Amylase, Lipase, Cholinesterase, alkaline
phosphatase.
• PEM and infection.
1) Breach in skin and mucosa can increase infection.
2) Impaired chemotaxis:
a) Decrease T lymphocyte, decrease lymphokine production.
b) Normal phagocytosis.
c) Defective candidial and bactericidal capacity.
d) Cytokine production.
3) Cell mediated immunity:
a) Thymus and thymus dependent lymphoid tissues are atrophied.
b) Delayed hypersensitivity reaction is reduced.
4) Humoral antibodies:
a) Circulating immunoglobulins are normal or elevated.
b) Secretary IgA is generally reduced.
5) Micronutritional deficiency:
Iron, zinc, copper, selenium.
6) Vitamin deficiency: A, B, C, D.
• Learning abilities and PEM.
1) Undernutrition during early part of life, I.e 6months adversely affects
development of Brain.
2) Impaired learning skills.
3) IQ level is reduced.
• PEM and GIT.
1. Atrophy of salivary glands.
2. Fatty infiltration of liver.
3. Pancreatic Atrophy.
4. Intestinal villous atrophy – Total absorptive surface is reduced, increased
goblet cell and inflammatory cells.
5. Steatorrhea.
6. Lactose malabsorption is commen.
7. Rectal prolapse is commen.
• PEM and Endocrinal system.
1. Hyperfunctioning of adrenal gland, so cortisol level is high.
2. Somatomedins level are low.
3. Insulin like growth hormone (IGF 1 and 2 is low.
4. Impaired Sr. insulin levels in kwashiorkor.
5. Growth hormone levels are high.
6. Glucagon level is high.
7. Thyroxine – normal or high in kwashiorkor but normal or low in marasmus
3.15.1. Marasmus:
1. Definition: It is a type of PEM due to deficiency of mainly energy
(calorie) through protein deficiency also exists.
2. Age: Usually below 3yrs. Of age.
3. Peak: During first year of age.
4. Clinical features:
A. Essential features:
a) Growth retardation:
1) Weight below 60% expected.
2) Subnormal height.
b) Loss of subcutaneous fat:
1) Grading according to loss of fat.
c) No edema
B. Other features:
a) Age – seen in infancy.
b) Wrinkled skin – emaciated child, loose folds of skin over gluteal and inner side
of thigh.
c) Skin dry, scaly, inelastic.
d) Hair hypopigmented
e) Abdomen distended due to wasting and hypotonia.
f) Mid are circumference – reduced.
g) Bony point – prominent.
h) Baby is alert but irritable.
i) Appetite – voracious
3.15.2. Kwashiorkor:
I. Essential features:
a) Growth Retardation: Evidenced by low weight and low height.
b) Muscle wasting: with retention of subcutaneous fat.
c) Psychomotor changes: As evidence by mental apathy, listless with no interest in
the surrounding.
d) Edema: Pitting edema due to hypoalbuminemia.
II. Other features:
a) Hair changes: Hair are sparse, light colored, thin and easily pluckable.
Flag sign – Alternate band of light and dark colored hair signifying periods of
inadequate and adequate nutrition over a prolonged period.
b) Skin changes: erythema, hyperpigmented area, desquamation, raw
hypopigmented skin lesions are more on extremities “flaky paint dermatosis”.
Kin may become dry, inelastic, mosaic in appearance, follicular keratoses, may
also be observed (Crazy pavement dermatoses)
c) Infections Diarrhea, vomiting, anorexia, tuberculosis, bronchopneumonia,
pyoderma.
d) Hepatomegaly.
e) Mineral deficiency: Anemia, potassium deficiency, magnesium and zinc
deficiency.
f) Vitamin deficiency:
i. Vitamin A deficiency is frequent and may lead to night blindness, xerosis
and keratomalacia.
ii. Vitamin B complex, C, D, E deficiency may accompany.
g) Worm infestation may be there.
h) Clubbing due to steatorrhea.
3.15.3. Ten steps of Managing of PEM:
Depending on severity of PEM it can be managed in hospital or home.
1. Mild to moderate PEM
Home based treatment or at day care center.
2. Severe PEM
Hospitalization is needed.
Basic principles in management are as follows:
I. First treat complications:
1. Dehydration by I/V fluids or ORS (Resmol)
a) It is a rehydration solution for malnutrition.
b) It contains less Na+
, more K+
more calories and minerals like Mg, Zn,
Cu.
c) With the use of Resmol ORS in malnutrition I.V. fluid requirement is
less.
d) Complications: (ORS = 1packet)
S. no. Specific content Quantity
1 Sucrose 50gms.
2 Electrolyte Mineral mixture
3 Osmolality 300mosm/L
4 Potassium chloride – 22.4g.
5 Tripotassium citrate – 81g.
6 Magnesium chloride – 76g
7 Zinc acetate – 8.2g
8 Copper sulphate – 1.4g.
9 Water – 2.5 liter.
10 Glucose – 125mEq/L
11 Na – 45mEq/L
12 K – 40 mEq/L
13 Cl – 70 mEq/L
14 Citrate – 7mEq/L
15 Mg – 3g/L
16 Zn – 0.3g/L
17 Cu 0.045g/L
2. Shock by IV fluids, broad spectrum antibiotics, blood transfusions, Presser
agents if required and O2
3. Severe Anemia by blood transfusions.
4. Bleeding disorders by blood transfusions.
5. Diselectrolytemia: correct accordingly.
6. Super infections by broad spectrum antibiotics.
7. Hypothermia: warming by warmers, covering patients with woolen or cotton.
8. CHF: Restrict fluids, slow blood transfusions 10ml/kg.
II. Find out the cause and treat it: commen causes are:
1. Under feeding/diluted milk: Prolongation of Breast milk beyond 2years;
advice pure cow’s milk.
2. Delayed weaning: Weaning at 6months of age, add cow’s milk 6months of
age.
3. Chronic infections: Find out cause and treat it especially tuberculosis,
chronic diarrhea, lactose intolerance, chronic pyogenic focus in body,
malabsorption syndrome.
III. Nutritional rehabilitation:
1. Calculate amounts of calories and proteins child is consuming.
2. Calculate amounts of calories and proteins child is required at present
age.
• Calories
 Give 65% of expected calories or start with present caloric
consumption + 20% of present caloric consumption.
 Increase calories by 10 – 15% gradually till 150 – 200 cal./kg reached.
 10% calories from proteins of high biological value.
• Proteins – 3 gm/kg at present wt.
3. Give cheap locally available foods according to age.
4. Nutritional supplementation diet:
a) Initially ORS is started followed by milk base diet, semisolids
and the solids.
b) Later oil and sugar are added to milk to make high energy
milk (100cal/ml)
c) Cereal floor is added to prepare thickened feeds.
d) Supplement cereals pulses mixture (SAT MIX) by roasting and
powdering rice, wheat and black gram and adding powdered
sugar in ratio of 1.1:1.2 it is precooked.
e) Slow traditional food items should be added.
f) Coconut oil contains medium chain triglycerides, which are
directly absorbed which are directly absorbed into portal vein.
It can be added to milk and semisolids.
g) Family pot feeding:
1) Green leafy vegetables, Seasonal fruits, roots and tuber are
recommended.
2) Cereals, pulses combinations and amylase rich food are
advised.
3) Egg, potatoes and banana are beneficial.
h) Amylase rich food: Prepared by germination of grains. It is
then sun dried roasted and powdered. It will supply amylase.
o Germination increases vitamin content.
o Wheat gives maximum amylase on processing.
o Amylase increases digestibility and reduce bulk on
cooking.
i) Lactose intolerance:
→ Continue Breastfeeding.
→ If baby is below 6months soybean milk or groundnut milk
is started.
→ Curd can be added.
→ Above 6months weaning food including cereals and
legumes should be start or lactose free milk can be given.
• Diet Regimen:
A. High energy milk provides 100 cal./ml.
B. Cereal milk: 100ml
½ glass milk, + 5gm sugar 1½ teaspoon cereal floor, provides 100cal./100ml.
C. SAT milk: ½ glass milk and 2TSF SAT milk gives 100cal./100ml.
D. Egg Flip: One egg + 1glass of milk (gives 80cal.+120cal. = 200cal.)
E. Lassi: ½ glass yogurt + 100cal.
F. Hyderabad protein energy rich mixture for home treatment of PEM
S. No. Content Quantity.
1 Roasted whole wheat 40gm
2 Roasted Bengal gram 16gm
3 Roasted Ground nut 10gm
4 Jaggery 20gm
86gm
Provides Calories – 330Kcal
Proteins – 11.3gm.
IV. Supplementations of vitamins, minerals and electrolytes:
1) Vit. A – One lac unit daily for 2consecutive days and then repeat after
15days. For severe PEM repeat every month till PEM is corrected.
2) Vit. B complex – All B complex vitamins, folic – 5mg followed by 1
mg/daily.
3) Vit. C – 100mg daily for 10days then 50mg daily.
4) Vit. D – 3lacs units IM stat dose (Inj. Architol 3.0 lac) or 10,000 units
daily.
5) Vit. E – 5to14 IU/day.
6) Vit. K – 2.5mg IM stat or oral vit. K for 3days.
7) Minerals:
a) Calcium – 800 to 1000mg/day.
b) Phosphorus – 600 to 800mg/day.
c) Iron – 3-6mg/kg/day for 3months
d) Mg sulphate – 50% solution – 2ml IM or 0.3ml/kg/day.
e) Zinc – 20mg/day.
f) Cu – 20mg or 0.1 mg/kg/day.
g) Selenium – 6 to 10mg/kg/day.
8) Electrolytes:
a) Sodium – 2 to 3mg/kg/day.
b) Potassium – 5mEq/kg/day.
V. Deworming – Mebendazole – 100mg/BD/3days.
VI. Immunization – To prevent further infection.
VII. Health education for Hygiene and Balanced diet.
VIII. Family spacing or family planning.
Phenomenon encountered during nutritional rehabilitation
1) Pseudotumor cerebri: Benign and self-limited.
2) Nutritional recovery syndrome: (Gomez syndrome)
Probable cause:
a) High protein intake during rehabilitation.
b) Endocrine disturbances.
Features: Hepatomegaly, Abdominal distention, Ascites, prominent
thoracic tricosis, Parotid swelling, Gynecomastia, Eosinophilia.
3) Encephalitis like syndrome: Drowsiness may rarely progress to
unconsciousness.
4) Kahn syndrome: Coarse tremors, Parkinsonian rigidity, Bradykinesia,
Myoclonus appear 6days after dietary therapy.
5) Rickets.
6) Anemia.
7) Micronutrient deficiency.
3.15.4. Complications of PEM:
1. Superadded infections – pneumonia, tuberculosis, septicemia, UTI.
2. Dehydration following diarrhea.
3. Lactose intolerance.
4. Electrolyte imbalance especially hypokalemia.
5. Hypothermia.
6. Hypoglycemia.
7. CHF.
8. Anemia.
9. Bleeding disorders – DIC.
3.15.5. Prevention of PEM:
1. Exclusive breast feeding for 4 – 6 months.
2. Advise weaning at 4 – 6 months.
3. Supplementary feeding.
4. Micronutrient supplementation.
5. Universal immunization.
6. Nutritional and health education.
7. Overall socio-economic development.
8. Improving sanitary conditions.
INFANTILE TREMOR SYNDROME
1. Disease of unknown etiology characterized by tremors, anemia and
regressions of milestones.
2. Etiology – Three hypothesis.
a) Nutritional.
i. Response to B12 megaloblastic anemia.
ii. Due to both folic acid and B12 deficiency.
iii. Mg+2
deficiency.
iv. Zinc deficiency probably.
b) Viral encephalitis.
c) Degenerative – Due cortical atrophy.
3. Clinical features:
a) Child is plump through underweight.
b) Apathy.
c) Hair changes – light color, sparse.
d) Skin changes – Brownish reticular pigmentation more so on dorsal
aspect of hands especially over terminal phalanges, feet, knees, ankle,
axilla, buttocks, lower abdomen, middle aspect of thigh.
e) Regression of milestone
f) Tremors.
g) Anemia – can be megaloblastic or dimorphic.
h) Tremulous cry like that of lamb (Gouts cry)
i) Face – tossing of head from side to side with saliva drooling from
mouth.
j) Hypotonia.
k) Hepatomegaly.
4. Treatment:
3.15.6. Antioxidants:
1. Definition: Antioxidants are food substances, which decrease the adverse
effects of free radicals. Free Radicals are produced in body and cause tissue
damage, e.g. Singlet oxygen, peroxide anion, hydrogen peroxide, hydroxyl
radical.
2. Role of Antioxidants in pediatrics:
1. Kwashiorkor.
2. Rheumatoid arthritis.
3. Inflammatory bowel disease.
4. Hepatic disorders.
5. Cancers.
6. Neonatal disorders:
a) Retinopathy of prematurity.
b) Hypoxic ischemic encephalopathy.
c) Necrotizing enterocolitis.
d) Bronchopulmonary dysplasia.
References:
1. Parthasarathy, K Nedunchalian, Gowri Shankar HC, Textbook of Balram chowdhary’s Pediatrics Lecture
notes, PEE PEE Publication, 2nd edition, Pg no. 222 – 236.

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Pediatric nutrition &amp; disorders

  • 1. 3. Lecture notes on Pediatric Nutrition & Nutritional Disorders1 . S. no. Contents Introduction 3.1 Breast – feeding 3.1.1 Colostrum. 3.1.2 Baby Friendly Hospital Initiatives (BFHI) 3.1.3 Complimentary Feeding (Weaning) 3.1.4 Tropic feeding. 3.1.5 Fore milk. 3.1.6 Hind milk. 3.2 Carbohydrates 3.2.1 Types. 3.2.2 Clinical features. 3.3 Proteins 3.4 Lipids. 3.5 Normal nutritional requirement (RDA) 3.6 Maintenance fluid & Electrolyte requirements. 3.7 Vitamin A (Fat soluble vitamin) 3.7.1 Functions 3.7.2 Sources. 3.7.3 Daily Requirements. 3.7.4 Vitamin A Deficiency. 3.7.5 Clinical features. 3.7.6 Treatment. 3.7.7 Prophylaxis. 3.7.8 Hyper Vitaminosis A 3.8 Vitamin B Complex 3.8.1 Deficiency Diseases. 3.8.2 Beri – Beri 3.8.2.1 Clinical features. 3.8.2.2 Treatment. 3.9 Pellagra 3.9.1 Pyridoxine (B6) 3.10 Scurvy 3.10.1 Clinical features. 3.10.2 Diagnosis. 3.10.3 Treatment. 3.11 Vitamin D (Calciferol) 3.11.1 Rickets 3.11.1.1 Definition. 3.11.1.2 Causes. 3.11.1.3 Pathophysiology. 3.11.1.4 Clinical features 3.11.1.5 Diagnosis. 3.11.1.6 Healing Rickets – X Ray findings.
  • 2. 3.11.1.7 Treatment 3.11.1.8 Refractory Rickets (Resistant Rickets) 3.12 Vitamin E 3.13 Vitamin K 3.14 Trace Elements 3.14.1 Zinc. 3.14.2 Copper 3.15 Protein Energy Malnutrition (PEM) 3.15.1 Marasmus. 3.15.2 Kwashiorkor. 3.15.3 Management of PEM. 3.15.4 Complications of PEM. 3.15.5 Prevention of PEM 3.15.6 Antioxidants.
  • 3. Introduction: → Individual nutritional requirements vary with genetic, metabolic differences as well as with growing age from infancy to adulthood. → Fast growth of infants during 1st year of life (i.e. A 3-fold increase in weight and1½ fold increase in height) and continued growth from 1st year of age to adolescent imposes unique nutritional needs. → Nutrition helps to: 1. Prevent illnesses. 2. To develop physical and mental potential. 3. Provide reserve for stress. → Energy requirement of body is met from: 1. Carbohydrates – 55 – 60%. 2. Protein – 15 to 20% 3. Fats – 20 to 30% → Approximately energy expenditure is as follows: 1. Metabolism – 50% 2. Growth 12% 3. Physical activity 25% 4. Fecal loss 8% 5. Thematic effect. → RDA: Recommended daily allowances of specific nutrient is the intake of that nutrient deemed to meet the requirement for that nutrient by most members of the population.
  • 4. 3.1. Breastfeeding: 1. Breast milk is an ideal form of infant feeding. 2. There should be exclusive breast feeding up to 6 months of age and it should be continued till 2yrs of age. 3. Feeding should be started as soon as possible after birth of an infant. In normal delivery – within ½hr. And in caesarian delivery – within 4hrs. 4. Initially for few months demand feeding as and when child demands it should be given. Timely feeding can also be given i.e 2-4 hrs. 5. Exclusive breast feeding: a) Only breast-feeding milk is given for first 6months of life. b) No other food or drink not even top milk, water. 6. Recommended nutrient to breast fed infants: a) Fluoride – 10μgm / day. b) Vitamin K 1mg at birth. c) Vitamin D if infant is not exposed to sunlight or in dark colored infant. 7. Composition of breast milk (per 100ml) S. no. Nutrients Human milk Cow’s milk 1 Protein 1.1gm 3 gm 2 Lactose 7gm 4.5 gm 3 Fat 4.5gm 4.5gm 4 EFA 13% 2% 5 Ash/minerals 0.25gm 7.5gm 6 Calcium phosphate ratio 2:1 <2:1 7 Sodium 0.7mEq 2.2mEq 8 Vitamin K 15mEq 60mEq • Advantages of breast milk feeding. 1. Always readily available at proper temperature and needs no time for preparation. 2. It is fresh and free from bacterial contamination. 3. Nutritional advantages: a) It contains all the nutrients that a baby needs in the first 6months of life for growth & development except fluoride. b) Lower content of protein (1.1mg%) in breast milk causes lower solute load on premature kidneys. c) Whey protein: Caseinogen ratio in breast milk is 60:40. Easily digested lactalbumin is more so; less allergic. Cow’s milk contains more casein, which is less digestible. d) Amino acids of breast milk are better for brain development Glutamic acid is maximum. e) Human B casomorphin is CNS growth factor. f) Higher PUFA promotes brain growth & myelination. g) Higher PUFA prevents atherosclerosis in later life. h) Active lipase in breast milk promotes digestion of fats. i) It has low sodium and mineral content. j) Ca: P ratio is 2:1 so prevents neonatal hypoglycemia & tetany. k) Iron in breast milk is low but well absorbed so prevents iron deficiency anemia. l) It also prevents deficiency of vitamin A, B, C, D. m) Human milk is sweetest – high content of lactose.
  • 5. 4. Anti – infective properties: a) High secretary IgA, IgM. b) Macrophages in Human milk synthesize compliment lysozyme and lactoferrin. c) It contains bacterial and viral antibodies which provide local GIT immunity against the organism entering through this route especially against diarrhea. d) There is a passive transfer of T cell immunity also. e) It contains anti staphylococcal factors. f) Human milk contains bile salts stimulated lipase which kills giardia lamblia and Entamoeba histolytica. g) Lower PH of stool breast feed infant is thought to favor intestinal flora mainly. Bifidus and Lactobacilli which protect against E coli infection. h) Lactoferrin in breast milk is 1/3 saturated so iron is not available for the growth of E. coli. i) PABA protects against malaria. j) Recovery from infection is faster in breast feed infants. k) Less chances of respiratory infection and septicemia. 5. Higher IQ level of breast feed infants. 6. Prevents future diseases like obesity, hypertension, coronary artery diseases, diabetes, asthma, inflammatory bowel disease, Hodgkin’s lymphoma, sudden infant death syndrome. 7. Protects from allergy as secretary IgA inhibits absorption of macromolecular of protein. 8. Physiological adaptation for preterm infant as human milk contains more energy protein, fats, Na, Zn, anti-infective factors and macrophages, lower lactose. 9. Bioactive factors like nucleotides enzymes, hormones, growth factors and probiotics. 10. Polyamines like spermine, spermidine, and putresin. They promote cell growth and differentiation in tissue. • Maternal Advantages: 1) Emotional bonding satisfying experience for mother and infant. 2) Time saving for mother. 3) Economic factor. 4) Lactation suppresses ovulation so protects against pregnancy during first few months. 5) Lower risk of breast and ovarian cancer. • Viruses which are excreted in breast milk: 1) AIDS virus (HIV). 2) Cytomegalovirus. 3) Human T cell lymphotropic virus type I. 4) Hepatitis B. 5) Herplex simplex. 6) Rubella. • Contraindication: 1) Mother on anti-cancer, anti-thyroid drug and lithium. 2) Galactosemia, phenylketonuria, in infant. 3) HIV in mother is relative contraindication. 4) Severe neurosis, psychosis in mother.
  • 6. 3.1.1. Colostrum: 3.1.1.1 Definition: It is a viscous lemon-yellow colored secretion from the breast. Secreted from late third trimester till the first five days after birth. Amount 40 – 60 ml/day. 3.1.1.2 Composition: S. No. Contents Colostrum Breast milk 1 Protein 8.6% 1.1% 2 Fat 2.3% 4.5% 3 Carbohydrates 3.2% 7.0% 4 Minerals High Low 3.1.1.3 Characteristics of colostrum: 1) Alkaline in reaction. 2) High mineral content. 3) High protein content. 4) Low carbohydrate & fat. 5) High vitamin A, D, E. 6) Low vitamins B, C, K. 7) High immunoglobulins. 8) Cellular concentration is high. 3.1.1.4 Advantages: 1) Gives higher immunity. 2) It has laxative action because of large fat globules. 3) First immunization of neonate. 3.1.2. Baby friendly hospital initiative (BFHI): It is started in 1992 by WHO and UNICEF, aim to have a promotion of breast feeding. Steps: Ten steps. 1. Have a written breastfeeding policy. 2. Train all health care staff. 3. Inform all pregnant women the benefits and management of breastfeeding. 4. Help mother to initiate breastfeeding within ½hr of birth. 5. Show mothers how to breast feed, how to maintain lactation. 6. Give newborn infant exclusive breast feeding. 7. Practices Rooming in allow mothers and infants to remain together 24 hours/day. 8. Encourage breastfeeding on demand. 9. No soothers, artificial teats or pacifiers to breast feed infant. 10. Foster breast feeding support group refer to them on discharge. 3.1.3. Complimentary feeding (Weaning): 1. Definition: Addition of other foods in addition to breast milk. 2. Age of introduction – 6months onwards. 3. Initially start top milk preferably cow’s milk along with the dal, water, soups or fruit juices. • Gradually shift from liquid diet to semisolid diet like khichadi, Dalia, mashed potato, mashed rice. • As the age increases gradually adds solid foods made from cereals, pulses, vegetables, ages, mashed banana and suji. 4. Precaution:
  • 7. 1) Prepare hygienically. 2) Start with small quantity once daily gradually increase to 3times. 3) Freshly prepared food should be given. 3.1.4. Tropic feeds: Definition: Small amount of expressed breast milk 1-3ml feed to preterm new born. Advantages: 1. Helps in maturation of: i. Intestinal mucosa. ii. Intestinal enzymes. iii. Gut motility. 2. Prevents necrotizing enterocolitis. 3. Decrease need for parental nutrition. 4. Less chances of sepsis. 5. Shortened hospital stay. 3.1.5. Fore milk: Definition: Milk secreted at the start of feeding. 1. It is watery, rich in proteins, lactose, vitamins, minerals and water. 2. Satisfy Baby’s thirst. 3.1.6. Hind milk: Definition: Milk secreted at the end of the feeding. 1. It is rich in fat so, provides more energy. 2. Satisfy Baby’s hunger.
  • 8. 3.2. Carbohydrates. 1. Average daily energy provided from carbohydrates is 55 – 60% 2. 1gm of carbohydrate gives 4K calories. 3. Carbohydrate from food are converted into end product glucose, which is absorbed and stored as glycogen mainly in liver and muscles. 3.2.1. Types: • Sucrose is most cariogenic agent. • Sweetened beverages given through bottle throughout night are cariogenic. • Sticky candles retained orally for long period are cariogenic. 3.2.2. Clinical features: Cavitation’s of occlusal surface of teeth or contact surface between teeth. 1. Treatment: a) Dental treatment by using:  Silver amalgam.  Plastic composite restoration.  Stainless steel crown.  If caries involves dental pulp pulpotomy or pulpectomy.  Analgesics for pain.  Oral antibiotics for infections: o Penicillin. o Clindamycin. o Erythromycin.  Parenteral antibiotics for complications like vital areas infection b) Prevention: 1. Fluoride: a) Fluoride content of water supply to 1ppm. b) Dietary fluorides supplementation. 2. Oral hygiene: a) Daily brushing. b) Brushing with fluoridated toothpaste. 3. Diet: a) Decreasing ingestion of sugar. b) Discourage sweetened beverage in bottle at night. c) Reduce sugar containing snacks between meals 4. Dental sealants: C) Complications: a) Pulpitis. b) Dental Abscess. c) Sepsis. d) Facial space infection. e) Disruption of normal development of the successor permanent teeth.
  • 9. 3.3. Proteins: 1. They constitute 20% of body weight. 2. 1gm proteins provides 4K calories. 3. Proteins are made up of 20 amino acids in various combinations. 4. Amino acids are of two types: a) Essential amino acids: these are those amino acids, which are not synthesized in body and are to b supplied to body through food. They are for adult – Leucine, Isoleucine, valine, threonine, methionine, phenylalanine, tryptophan, lysine and histidine. In addition, cystine, tyrosine, arginine and taurine for LBW. Infants and children. Human milk contains all essential amino acids in adequate amount. b) Non-essential amino acids: Amino acids which are synthesized in body. 5. Reference proteins: Egg protein is considered as reference protein as it is complete, well digested protein. 6. Complete protein: A complete protein contains all essential amino acids in relatively same amount as human require for maintenance of good and optimal growth. 7. Proteins of animal origin have higher content of essential amino acids. 8. Proteins of vegetable origin are often biologically in complete as they lack one or other essential amino acids. 9. Combination of vegetable foods can provide complete protein. 10. Protein of rice and potato are good vegetable protein.
  • 10. 3.4. Lipids: 1. Lipids provides about 25 – 30% of calories (3% from essential fatty acids). 2. There are three types of Lipids: a) Triglycerides 95%. b) Phospholipid (Lecithin). c) Sterols (Cholesterol). 3. Triglycerides are of two types: a) Saturated triglycerides. b) Unsaturated triglycerides 4. PUFA (Polyunsaturated fatty acids) are important for body. Two important PUFA for body are: a) Omega 6 fatty acids i. Linoleic acids. ii. Arachidonic acids b) Omega 3 fatty acids i. Linoleic acids. ii. Eicosapentanoic acid. iii. Docosahexaenoic acid 5. Essential fatty acids. 6. Sources: Vegetable source, nut, seeds. 7. Functions: a) Sources of energy 25-30%. b) Provide insulation to the body. c) Carrier for fat soluble vitamin. d) Precursor of prostaglandins. e) Important component of cell membrane. f) Omega 3 fatty acids lower blood cholesterol and triglycerides. g) Omega 3 fatty acids serve as a raw material for: • Prostaglandins. • Thromboxane. • Leukotrienes. h) Omega 3 fatty acids regulate: • Blood pressure. • Immune response. • Inflammatory response to injury and infections. 8. Deficiency diseases: 1) Growth retardation. 2) Reproductive failure. 3) Skin disorders (decrease omega 3 fatty acids) 4) Predisposes to infection. 5) Decrease myocardial contractibility. 6) Hemolysis. 7) Renal hypertension.
  • 11. 3.5. Normal Nutritional requirement (RDA): S. No. Calorie Daily Requirement 1 0-3 months 120/kg 2 3-6 months 115/kg 3 6-9 months 110/kg 4 9-12 months 105/kg OR 1 Under 1yr 110Kcal/kg 2 1-3Yrs. 100Kcal/kg 3 4-6 Yrs. 90Kcal/kg. 4 7-9 Yrs. 80Kcal/kg. 5 10-12 Yrs. 70Kcal/kg. 6 13-15 Yrs. 60Kcal/kg. 7 16-18 Yrs. 50Kcal/kg. 8 Adult 40Kcal/kg. OR 1000 calories at – 1yr. Increase by 125 calories for each year after 1yr. Protein Requirement 1 0-3 months 2.3 gm/kg. 2 1-3 months 1.8gm/kg 3 4-6 yrs. 1.5gm/kg. 4 7-9 yrs. 1.5gm/kg. 5 10-12 yrs. 1.46gm/kg 6 13-15 yrs. 1.35gm/kg 7 16-18 yrs. 1.3gm/kg Vitamins Requirement 1 Vitamin A 1500-5000 IU (300-750μgm) 2 Vitamin C 30-50mg 3 Vitamin D 400 IU (10μgm) 4 Vitamin E 4-5 IU. B - Complex Requirement 1 B1 0.5 to 1.5 mg 2 B2 0.5 to 2.5 mg 3 Niacin 0-20 mg. 4 B6 0.4 to 1.4 mg 5 Folic acid 25 – 1000 mcg 6 B12 1-15 mcg. Minerals Requirement 1 Iron (Elemental) 1mg/kg/day. 2 Ca Infants 400 – 600mg 3 1-10 yr. 500mg-1gm 4 >10 yr. 1.2 to 1.5gm 5 Phosphorus 200-300 mg 6 Mg (Infants) 40-70mg 7 Iodine 0.2mg 8 Fluorine 0.5to 1.0mg 9 Zinc 0.3mg / kg 10 Na+ 2mg/kg 11 K+ 1.5mg/kg.
  • 12. 3.6. Maintenance fluid and electrolyte requirements: • Water At birth – 75% of body weight. Adult – 60% of body weight • Fluid compartments: 1. ICF: Intracellular fluid 2/3 of total body water. 2. ECF: Extracellular fluids. It comprises 1/3 of total body water: a) Plasma. b) Interstitial fluid. c) Transcellular fluid. • Electrolytes are substances capable of conducting an electric current in solution. • Electrolyte exists in two forms: A. Cations (Positively charged) Na+ , K+ , Ca+ , Mg+ . B. Anions (Negatively charged) Cl-- , HCO-- 3, SO -- 4 • Osmolality number of osmotically active particles per 1000gm of water in a solution. • Sodium principal cation of extracellular fluid (ECF). Normal Sr. Na = 130to145mEq. Daily requirement = 2to3 mEq / 100cal/day. • Potassium: is major intracellular cation (ICS) Normal value – 3.5 to 4.5 mEq, Daily requirement 1to2mEq/100 calories/day. • Acid base balance is maintained by: 1. Blood buffer system. 2. Lungs. 3. Kidney. Acid base balance S. No. Parameter Arterial blood Venous blood 1 pH 7.38 – 7.45 7.35 – 7.40. 2 pCO2 35 – 45 mm Hg 23 – 27 mm Hg 3 HCO3 -- 21 – 28 mEq/L 22 – 29 mEq/L • Blood Buffer system: a) Bicarbonate carbonic acid buffer. b) Hemoglobin. c) Proteins. d) Bicarbonate – Carbonic acid in kidney tubules. e) Monohydrogen phosphate – dihydrogen phosphate buffer. f) Sodium hydrogen exchange. g) Ammonia – ammonium buffer. • Disturbances of Acid Base status: a) Respiratory Acidosis (pCO2 increase) Low PH characterized by increased pCO2. b) Metabolic Acidosis (HCO3 -- ) decreased. Low PH characterized by reduction in HCO3 -- c) Respiratory Alkalosis (pCO2 decrease) High PH characterized by decrease pCO2 due to hyperventilation. d) Metabolic Alkalosis (HCO3 -- ) increased High PH characterized by increase HCO3 — due to hyperventilation and compensatory elevation of pCO2.
  • 13. • Maintenance of fluid requirements: S. No. Body weight Fluid/day 1 0-10kg 100ml/kg 2 11-20 kg 1000ml+50ml/kg for each kg>10kg 3 20kg 1500ml+20ml/kg for each kg>20kg Maximum fluid / day = 2400ml OR 1 1days to 1yr. 150ml/kg/day. 2 1-3 yrs. 125ml/kg/day 3 4-6 yrs. 100ml/kg/day 4 7-9 yrs. 75ml/kg/day 5 10-12 yrs 50ml/kg/day • Protein and Calorie content in 100gm of Food Article. S. No. Items Calorie Protein 1 Pulses 350 20 2 Soybean 430 42 3 Cereals 350 11 4 Rice 350 7 5 Groundnut 567 25 6 One biscuit 20 0.5 7 Milk (cow) 67 3 8 Banana 80 1.2 9 Apple 50 0.5 10 Jaggery 383 0.4 11 Potato 100 1.6 12 Egg (Chicken) 1egg = 50gm. 173 13.3 After one year reduces 25ml every 3yrs till 12 years. • Maintenance of electrolyte requirements. 1 Sodium 2-3 mEq/kg/day. 2 Potassium 1-2 mEq/kg/day • Neonatal period (full term) fluid requirement. → Day 1 & 2 = 60 – 80 ml/kg → Increase 15ml/kg/day till 7th day of life.
  • 14. 3.7. Vitamin A (Fat soluble Vitamin) 3.7.1. Functions. It is necessary for: a) Vision – Retina. b) Maintaining epithelial tissue integrity in eye, skin, mucous membrane. c) Immune competence. d) Growth. e) Retinol is necessary for spermatogenesis, integrity of testis and vaginal epithelium. f) Beta carotene has antioxidant property so, reduce the incidence of cancers. 3.7.2. Sources: a) Cod liver oil, Shark liver oil, egg yolk. b) Butter, ghee. c) Carrots, Green leafy, Yellow vegetables. d) Ripe mango, orange, papaya. e) Plant sources: In the form of carotene. f) Animal sources: in the form of retinal. g) Provitamin A: Beta carotene. (Beta carotene is converted into retinal in intestinal wall.) 3.7.3. Daily Requirements: 300μg to 750μg. 3.7.4. Vitamin A Deficiency: - Causes i. Malnutrition. ii. Malabsorption. iii. Chronic diarrhea. iv. Pancreatic diseases. v. Hepatic insufficiency. vi. Severe measles. 3.7.5. Clinical features: 1. Increased risk of infection. 2. Eye changes: a) Night blindness is earliest clinical feature. b) Xerophthalmia: Dry wrinkled conjunctiva. c) Bitots spots d) Keratomalacia e) Perforation of cornea. f) Fundus changes pale yellow spots along vessels and periphery. S. no. Signs Terms A. Primary sign 1 X 1 A Conjunctival xerosis 2 X 1 B Bitots spots 3 X 2 Corneal xerosis 4 X 3 A Corneal ulceration (<1/3 Cornea) 5 X 3 B Corneal ulceration (>1/3 Cornea) B. Secondary sign 1 X N Night Blindness 2 X F Fundal changes 3 X S Corneal Scarring
  • 15. 3. Skin phrynoderma - Skin is scaly and toad like (Deficiency of essential fatty acids). 4. More prone to respiratory infection due to squamous metaplasia of respiratory mucosa. 5. More prone to renal and bladder calculi due to alteration of mucosa. 6. Reproductive Dysfunction due to atrophy of germinal epithelium. 7. Rarely hydrocephalus. 3.7.6. Treatment: WHO treatment of Xerophthalmia. 1. Oral vitamin A o First dose – 50,00 units for < 6months, 1Lakh 6months to 1yr, 2Lakhs more than 1yr. o Second dose – Repeat on 2nd day. o Third dose – After one month. 2. Parenteral Vit A can be given for night blindness or Bitots spot – 10,000 IU daily for 14 days. 3.7.7. Prophylaxis: National Vitamin A prophylaxis program 6months to 3yrs – 2Lakhs IU in oil base every 6months (1lakhs / ml). 3.7.8. Hypervitaminosis A: 1. Rupture of lysosomal membrane. 2. Increase ICP: Pseudotumor cerebri. Headache, vomiting, dizziness, bulging of anterior fontanel, and papilledema. 3. Chronic intoxication: Anorexia, dry itchy skin, weight loss, painful extremities, sparse hair, hepatosplenomegaly, hypoplastic anemia, benign intracranial hypertension, yellow skin. 4. During pregnancy: Mother consuming large amount of oral “Retinoids” for treating acne may lead to congenital craniofacial malformation in fetus. 5. Hyperostosis.
  • 16. 3.8. Vitamin B Complex: It includes o B1 Thiamine. o Riboflavin. o Niacin. o Pyridoxine B6 o Biotin. o Folate. o Vitamin B12 They are important constituents of Enzyme system. Pantothenic acid, choline and inositol are not associated with deficiency syndrome through they are necessary for normal functioning of human organism. 3.8.1. Deficiency Diseases: S. No. Vitamins Deficiencies 1 B1 (Thiamin)Beri – Beri 2 B2 (Riboflavin) – Cheilosis, Glossitis, Keratitis, Conjunctivitis, Corneal vascularization, Photophobia, Seborric dermatitis. 3 Niacin Pellagra 4 B6 (Pyridoxine) – Convulsions, anemia, peripheral neuropathy, dermatitis. 5 Biotin Dermatitis, alopecia, somnolism, hallucination, hypotonia, hyperesthesia. 6 Folic acid Megaloblastic anemia. 7 B12 Pernicious anemia. 3.8.2. Beri-Beri: diseases caused by vitamin B deficiency. Commen in those communities whose staple diet is polished rice. It occurs in three forms: a) In Infants (wet Beri – Beri). b) In older children (Dry Beri – Beri). c) Meningitis form. 3.8.1.1. Clinical features: A. Wet Beri – Beri (Cardiac form) Restlessness, Excessive cry, Vomiting, Abdominal distention, Flatulence, Constipation, Insomnia, Infants develops CHF manifestation – tachycardia, dyspnea, edema, hepatomegaly & Cardiomegaly. B. Dry Beri – Beri (Chronic Neurologic form) Anorexia, weight loss, weakness, diarrhea, constipation, edema, drowsiness, apathy, ataxia, peripheral neuritis, Cranial nerve palsies, nystagmus. C. Meningitis form Bulging anterior fontanel, dilated pupil, head retraction, coma, convulsions. 3.8.1.2. Treatment: • B1 – 10mg I. V. stat. 10mg I.M. for 3days. 10mg Orally for 6weeks.
  • 17. 3.9. Pellagra: 1. Disease caused by niacin deficiency. 2. Commen in person whose staple diet is maize. 3. Diagnostic triad (D3 ) a) Dermatitis - exposed parts. b) Diarrhea. c) Dementia. 4. Treatment a) Niacin – 50mg × 3times for 3weeks. b) Avoid sun exposure. 3.9.1. Pyridoxine (B6) 1. Functions: a) Helps in amino acid metabolism. b) Converts tryptophan to niacin. c) Helps in metabolism of essential fatty acids. 2. Sources – Whole grain, 3. Daily requirements – 0.5 to 2.5mg/day. 4. Deficiency: a) Seizures during infancy. b) Peripheral neuritis. c) Dermatitis. d) Anemia – microcytic, hypochromic.
  • 18. 3.10. Scurvy. 1. Definition: Disease caused by deficiency of vitamin C (ascorbic acid) 2. Pathophysiology: a) Formation of collagen and chondroitin sulphate is impaired in vitamin C deficiency. b) This results in tendency to:  Hemorrhage.  Defective dentition.  Loosening of teeth.  Non-formation of Endochondral bone formation.  Bony Trabeculae become Brittle and fracture easily.  Periosteum loose and sub periosteal hemorrhage occur especially at the end of femur & tibia. c) Severe deficiency result in:  Degeneration of skeletal muscles.  Cardiac hypertrophy.  Bone marrow depression.  Adrenal atrophy. 3.10.1. Clinical features: 1. Age: Any age but unusual in Newborn period because it requires time to develop. Usual age 6 – 24 months. 2. Vague symptoms: Irritability, tachypnoea, digestive disturbances and loss of appetite. 3. Generalized tenderness: Particularly when infant is picked up or when diaper is changed. Pain result in pseudo-paralysis. 4. Legs are held in frog like position. 5. Edematous swelling over shaft of legs. 6. Sub periosteal hemorrhage can be at the end of femur. 7. Apprehensive facial expression. 8. Gums: Bluish, purple, spongy swelling of mucous membrane especially over upper incisors. 9. Scorbutic Rosary: at costochondral junction Scorbutic rosary have sharp borders due to subluxation of sternum. 10. Bleeding tendencies: a) Petechial hemorrhage over skin, mucous membrane, and gums. b) Hematuria, Malena, orbital and subdural hemorrhage. 11. Low grade fever. 12. Wound healing – slow. 13. Swollen joints. 14. Follicular keratosis. 3.10.2. Diagnosis: 1. Clinical picture. 2. History of poor vitamin C intake. 3. Radiological changes: a) Site – distal end of long bone especially knee. b) Ground glass appearance of bone. c) Cortex is pencil thin and epiphyseal ends of bones are sharply outlined.
  • 19. d) White line of Frenkel – irregular thick white line at metaphysis represent zone of well calcified cartilage. e) Epiphyseal center of ossification has ground glass appearance and surrounded by white ring. f) Zone of rarefaction – under the white line at metaphysis and is considered necessary for diagnosis. g) Spur – Lateral prolongation of white line may be present. h) Epiphyseal separation i) Dumb bell or club shaped bone due to calcified subperiosteal hemorrhage, not during active phase but during healing. 4. Plasma concentration of vitamin C 5. Urinary exertion of vitamin C after a test dose. 3.10.3. Treatment: 1. Vitamin C Tab. 250mg daily for 10days. (Ascorbic acid – 100to300mg/day) 2. Diet sources: Citrus fruit and vegetables including tomatoes, cabbage, green leafy vegetables, germinating pulses, lemon, amla and guava.
  • 20. 3.11. Vitamin D. (Calciferol) 1. It is a hormone. 2. Exist in two forms: a) Vitamin D2 – Ergocalciferol (Plant origin) b) Vitamin D3 – Cholecalciferol (produced in skin by ultraviolet radiations from precursor 7 dehydrocholesterol) 3. Metabolism - 7 dehydrocholesterol on exposure to sunlight. In skin – Cholecalciferol transfer to liver In Liver Hydroxylated to 25-OH Cholecalciferol In kidney (Renal cortex) further hydroxylation 1,25 dihydroxy cholecalciferol (Hormone) 4. Daily requirement: 10μgm or 400IU/ day. 5. Sources: a) Sunlight. b) Egg, Butter, milk. c) Liver and fish oil. d) Fortified ghee. 3.11.1. Rickets. 3.11.1.1. Definition: It is a disease caused by deficiency of vitamin D leading to failure of mineralization of growing bone or osteoid tissue. 3.11.1.2. Causes: a) Inadequate intake of vitamin D. b) In breast fed infant if infant is not exposed to sunlight or mother is not exposed to sunlight. c) Interference with absorption of vitamin D in steatorrhea. d) Chronic hepatic disease. e) Chronic renal disease. f) Condition unbalancing calcium phosphorus homeostasis. 3.11.1.3. Pathophysiology: 1. There is defective bone growth due to suppression of normal epiphyseal cartilage growth and calcification. a) These changes result from deficiency of calcium and phosphorus salt in serum. b) Cartilage cells fail to complete their normal cycle of proliferation and degeneration. c) Failure of capillary penetration which occurs in patchy manner. Result in frayed irregular epiphyses at the end of the shaft. 2. Failure of osseous and cartilaginous matrix to mineralize in the zone of preparatory calcification followed by deposition of newly formed uncalcified osteoid. 3. Lack of mineralization in sub periosteal bone – shaft is softened so deformities and fractures. 4. Elevated serum phosphates due to increased osteoblastic activities. 5. Serum calcium is normal due to mobilization of calcium from bone by parathormone stimulation because less calcium is absorbed from intestine. 6. Serum alkaline phosphatase is increased.
  • 21. 3.11.1.4. Clinical features: Age 6months to 2yrs. 1. Early features – irritability, restlessness, profuse sweating overhead more during night 2. Major features: a) Head i. Bossing, macrocephaly with flattening of vertex (box, head) ii. Fontanel – increased size and delayed closure. iii. Craniotabes – softening of occipital and parietal bones (ping pong ball feeling under pressure.) b) Teeth – delayed dentition. c) Thorax i. Rachitic rosary (smooth rounded, nontender costochondral beading) ii. Pigeon – Chest deformity. iii. Harrison sulcus or groove (Depression along insertion of diaphragm into ribs) iv. Flaring of lower ribs (violin shaped) v. Pectus excavatum sometimes (sternum depressed) vi. Concavity at inferior angle of scapula. d) Spine – Scoliosis, kyphosis. e) Limbs i. Widening of wrist, ankle. ii. Knock knees (Genu valgum) iii. Bow legs (Genu varum) f) Milestones – Delayed due to poor muscle tone and lax ligaments g) Feet – flat feet. h) Belly Pot belly, visceroptosis due to hypotonia. i) Acrobatic rickets – due to laxity of ligaments limbs can be bent to any position. j) Constipation. k) Rarely tetany due to decreased serum calcium. l) Rachitic dwarfism. m) Generalized hypotonia. n) Recurrent respiratory infection. 3.11.1.5. Diagnosis: 1. Biochemical findings. a) Increase alkaline phosphatase due to osteoblastic activity. b) Serum – calcium normal. c) Serum phosphate – decreased. d) Decreased serum 25hydroxy vitamin D reliable index. 2. X – Ray findings (Wrist). a) Cupping of lower end or radius and ulna. b) Widening (Flaring, champagne glass) c) Fraying (Rarefaction) d) Increased distance between epiphyseal center and metaphysis. e) Periosteal lifting. f) Rarefaction (Prominent trabecula with poor density due to demineralization)
  • 22. g) Green stick fractures. 3.11.1.6. Healing Rickets – X – Ray findings: 1. Line of calcification at the distal end of metaphysis. 2. Zone of decreased calcification proximal to above line. 3.11.1.7. Treatment: 1. Vitamin D a) Single dose: 6 lacs (15000gm of vitamin D) units IM stat dose. Repeat after 4weeks. If no improvement suspects refractory rickets. b) Daily doses: - 50to150 μ gm daily of vitamin D for 2 – 4 weeks. Radiological healing within 2 – 4 weeks. c) 1 – 25 dihydroxycholecalciferol – 0.5 – 2μgm. 2. Supplement calcium. Prevention: 1. Daily requirement of vitamin D 10μgm (400IU) 2. Sun shine exposure (5min daily) 3. Diet – fish, liver oils, liver, egg, Butter milk, fortified ghee, margarine. Hypervitaminosis D 1. Skeletal sclerosis, metastatic calcification. 2. Hypercalcemia, hypercalciuria. 3. Vomiting, constipation, anorexia. 4. Poor growth, irritability. 5. Renal failure. 6. Nephrocalcinosis. 7. Polydipsia, polyuria, dehydration. 8. Anemia. 9. Aortic valvular stenosis. 10. Hypertension. 11. Eye – corneal clouding, retinopathy. 12. Fever, irritability. 13. X – Ray changes: a) Hyperplasia of subperiosteal bone. b) Metastatic calcification. c) Generalized osteoporosis. 3.11.1.8. Refractory Rickets (Resistant Rickets) 1. Definition: No response or poor response to adequate dose of vitamin D. 2. Types: Type I 1) Disturbed vitamin D metabolism for liver diseases. 2) Disturbed vitamin D metabolism for renal diseases. 3) Failure of target cell to respond to 1,25 dihydroxy vit D (vit D dependent rickets) 4) Failure of kidney to form 1,25 (OH3) vitamin D called renal dystrophy. Type II Rickets Defective reabsorption of phosphates by renal tubules. a) Fanconi Syndrome b) Familia hypophosphatemic vitamin D refractory rickets. c) Isolated phosphaturia. d) Renal tubule acidosis.
  • 23. e) Oncogenous Rickets 3. Treatment: 1) High dose of vitamin D 10,00 units. 2) Phosphates supplementation – Disodium hydrogen phosphate 13.68gm + phosphoric acid 5.9gm. 3) 1,25 (OH3) vitamin D – 1 μ gm/day (Rachatrol)
  • 24. 3.12. Vitamin E. 1. Functions: - It is a fat-soluble vitamin. a) Stability of biological membrane. b) Antioxidant. 2. Sources: a) Gram oils of various seeds, vegetables, soybeans. b) Green leafy vegetables. c) Nuts. d) Legumes. e) Egg yolk. 3. Daily Requirements:  0.5 mg/gm of linoleic acid.  4 – 15mg/day. 4. Features of deficiency: a) In prematurity. I. Hemolytic anemia, edema, skin changes. II. Retinopathy of prematurity. III. Bronchopulmonary dysplasia. IV. Intraventricular hemorrhage. b) Impaired reproductive abilities. c) Muscular dystrophy (Fatty types) d) Growth retardation.
  • 25. 3.13. Vitamin K. 1. It is fat soluble vitamin synthesized by intestinal flora. 2. Functions: a) Synthesis of coagulation factors II, VII, IX and X in liver. b) Prothrombin formation. c) Protein C, S, Z. 3. Sources: a) Green leafy vegetables. b) Liver, Pork. c) Cow’s milk. 4. Forms: Three forms. a) K1 – Naturally occurring in vegetable b) K2 – Produced by intestine. c) K3 – Menadiones (Synthetic) 5. Daily requirements: 12μgm 6. Deficiency diseases: a) Hemorrhagic disease of new born. b) Hemorrhagic manifestation in older children. 7. Causes of deficiency: I. Premature new born II. Oral antibiotic (Broad spectrum) III. Chronic diarrhea. IV. Biliary obstruction. V. Chronic intestinal parasitosis. 8. Excessive administration causes: a) Hemolytic anemia, b) Hyperbilirubinemia. c) Kernicterus. Especially in preterm and G6 PD deficiency infants.
  • 26. 3.14. Trace Elements: o These are microminerals required in small amount. o They include iron, iodine, zinc, copper, manganese, fluorine, molybdenum, selenium, cobalt, nickel, vanadium, silicon, arsenic. o Deficiency or excesses can have bad effects. o Deficiency is more commen with malabsorption and parenteral nutritional therapy. 3.14.1. Zinc: 1. Infant total zinc content = 60mg. Adult = 1600 mg. 2. Functions: a) Essential components of many enzymes, b) Help in protein and RNA synthesis. 3. Sources: Nuts, Grams, Dry beans, Legumes, meat, liver, fish. 4. Daily requirements: - 200mcg. 5. Causes: a) PEM. b) Malabsorption. c) Regional ileitis. d) Rheumatoid arthritis. e) Sickle cell anemia. f) Achondroplasia. g) Chronic blood loss. h) Excessive sweating. i) Viral hepatitis. j) Prolonged parenteral nutrition. 6. Clinical features: a) Growth retardation. b) Hypogonadism. c) Anemia. d) Hepatosplenomegaly. e) Adolescent nutritional dwarfing syndrome. f) Protracted diarrhea. g) Delayed wound healing. h) Anorexia, failure to thrive. i) Hypogeusia – impaired taste perception. j) Hyperkeratotic skin. k) Infantile tremor syndrome. 7. Treatment: 1 – 5 mg/kg of body weight. ACRODERMATITIS ENTEROPATHICA 1. It is an autosomal recessive disorder caused by inability to absorb zinc. 2. Manifest shortly after weaning. 3. It is an inborn error of metabolism in which they are: a) Skin changes around orifices and extremities eczematous, dry scaly, or psoriasis. b) Diarrhea. c) Alopecia. d) Atrophy of nails. e) Failure to thrive. 4. Shows dramatic response to zinc therapy.
  • 27. Dose 50mg to 150mg/day. 3.14.2. Copper: 1. It is essential for iron utilization. 2. Important for many enzymes: a) Cytochrome oxidase. b) Monoamine oxidase. c) Dopamine beta hydroxylase. d) Delta – aminolaevulinic acid dehydrogenase. e) Ascorbic acid dehydrogenase. f) Uricase. g) Tyrosinase. 3. Total body content: Infant – 14mg. Adult – 100mg 4. Deficiency features: a) Psychomotor retardation. b) Hypotonia. c) Apneic spells. d) Pallor, sideroblastic anemia. e) Hypopigmentation in skin and hair prominent scalp veins. f) Osteoporosis. g) Menkes kinky hair syndrome X – linked recessive disease. 5. Excessive accumulation – Wilson disease. PICA 1. Definition: Chronic ingestion of non – nutritive substances (Plastic, charcoal, clay, ash, paints and sand) 2. Age: after 2years needs investigations. 3. Causes: a) Iron deficiency anemia. b) Mental retardation. c) Autism. d) Behavior disorder. e) Psychological neglect. Increase risk of: 1. Lead poisoning. 2. Parasitic infection. 4. Treatment: 1. Iron therapy for iron deficiency anemia. Dose 3to6mg/kg/day of elemental iron × 3months. 2. Deworming. 3. Psychotherapy.
  • 28. 3.15. Protein energy malnutrition: 1. Definition: It refers to class of clinical conditions that may result from varying degree of protein lack of energy (calories) inadequacy. 2. Types: Broadly speaking two major clinical syndromes are widely recognized i. e. Kwashiorkor & Nutritional marasmus. 3. Cause: o Kwashiorkor is said to be a result from gross deficiency of protein. Through energy deficiency is also present. o Nutritional marasmus results from gross deficiency of energy though protein deficiency also accompanies. o There is overlap in the clinical picture so it is appropriate to label marasmic kwashiorkor. o Growth failure and poor tissue repair (due to protein lack) and energy shortage (due to calories deficiency) is also commen to forms of PEM. SPECTRUM OF PEM a) Invisible PEM: Downward curve in road to health card even it is within the road to health indicates PEM. b) Under weight:  Weight 60 – 80% of expected.  No features of PEM. c) Nutritional dwarfing: Chronic malnutrition leads to nutritional dwarf d) Marasmus: Essential features. o Grade I: Loose skin fold in axilla and groin. o Grade II: Loose skin fold in thigh and buttocks. o Grade III: Loose skin fold in chest and abdomen. o Grade IV: Buccal pad of fat is also wasted (Saturated fat last to be wasted) e) Marasmic kwashiorkor: When marasmic child develops edema and he is apathetic. f) Kwashiorkor: 1) Growth retardation. 2) Muscle wasting. 3) Psychomotor changes. 4) Edema. 4. Etiology I. Low intake of food: a) Poverty. b) Social customs. c) Infections. d) Feeding habits. e) Maternal deprivation. II. Normal intake but excessive loss in stool: a) Chronic diarrhea. b) Malabsorption. c) Worm infestation. III. Normal intake, normal absorption, but not metabolized: o Chronic diseases – CHD, Chronic renal failure. CLASSIFICATION OF PEM I. WHO Classification:
  • 29. Features Moderate Undernutrition Severe Undernutrition 1. Generalized edema No Yes, Edematous malnutrition 2. Weight for height wasting measurement. Wasting 70 – 79% Severe wasting <70% of expected 3. Stunting height for age. Stunting 85 – 89% of expected Severe stunting <855 of expected. II. Classification of Indian academy of pediatrics: 1. Grade I – 71 – 80% of expected weight. 2. Grade II – 60 – 71% of expected weight. 3. Grade III – 51 – 60% of expected weight. 4. Grade IV – 50% or bellow of expected weight. If the child has edema the letter ‘K’ is placed in front of grade. If no edema then grades without ‘K’. III. Syndromal Classification: 1. Kwashiorkor. 2. Nutritional marasmus. 3. Marasmic kwashiorkor. 4. Pre-kwashiorkor. 5. Nutritional dwarfism. IV. Jelliffe classification: 1. 1st Degree = wt. between 90 and 80% of expected. 2. 2nd Degree = wt. between 80 and 70% of expected. 3. 3rd Degree = wt. between 70 and 60% of expected. 4. 4th Degree = wt. Below 60% of expected. V. Gomez Classification: PEM is graded with reference to the weight for age as percentage of expected height (Harvard standard) 1. 1st Degree = wt. between 90 and 75% of expected. 2. 2nd Degree = wt. between 75 and 60% of expected 3. 3rd Degree = wt. bellow 60% of expected VI. Welcome & International Classification: A. wt. between 80 and 70% of expected. 1. With edema = kwashiorkor. 2. Without edema = undernutrition. B. wt. Below 60% of expected 1. With edema -Marasmic kwashiorkor. 2. Without edema Nutritional marasmus. VII. McLaren Classification: • Mild = wt. between 90 and 80% of expected. • Moderate = wt. between 80 and 70% of expected • Severe = wt. bellow and 70% of expected VIII. Waterloo Classification: 1. Acute (wasted but not stunted) = wt. for height low. (ht. for age normal) 2. Acute/chronic (wasted but not stunted) = wt. for height low. (ht. for age normal). 3. Nutritional Dwarfs = wt. for ht. normal (wt. for age decreased). 4. Stunted not wasted = Ht. for age decreased. IX. Arnold Classification: It is based on mid arm circumference. Mild to moderate – MAC between 12.5 cm and 13.5 cm.
  • 30. Severe – MAC under 12.5 cm. X. Classification based on skin-fold thickness: o Mild – 80 to 90% of expected. o Moderate - 60 to 80% of expected. o Severe – Under 60%. Age Independent Anthropometrics Indices Weight in kg. 1. Dugdale’s Indices: -------------------- × 100 = 0.88 – 0.97 (or Malnourished <0.79) Height (cm) 1.6 Weight in kg. 2. Rao’s Indices: ------------------ × 100 = 0.15 – 0.16 (PEM< 0.14) Height (cm2 ) Mid arm circumference (cm) 3. Kanawati Indices: ----------------------------------- = 0.32 – 0.33cm (PEM <0.25) Head circumference (cm) 4. Mid arm circumference = >13.5 cm. Between age 1 and 5 years (PEM < 12.5cm) Severe Acute malnutrition (SAM) In children between the ages of 6 and 60 months, SAM may be diagnosed on the basis of any of the following criteria. I. Weight/Height or weight/length < 3z score, using the WHO Growth charts. II. Mid – Upper arm circumference (MUAC) <115 mm* . III. Bipedal edema of nutritional origin. (* For infants below 6months, criteria (i) or (iii) or “visible severe wasting “ to be used till data on MUAC <6 mos available) Evolution of PEM (Five Theories) 1. Gopalan Adaptation Hypothesis: a) Dietary background of marasmus and kwashiorkor is same. b) Marasmus is extreme degree of adaptation to prolonged inadequacy of proteins and energy in diet. c) Kwashiorkor is due to adaptation failure, which follows two situations; I. Prolongation of stress of malnutrition. II. Sudden precipitation by fulminant infection. 2. Dietetic Hypothesis: a) Kwashiorkor is prominently protein deficiency. b) Marasmus is energy deficiency. 3. Golden’s Hypothesis of free Radical damage: Kwashiorkor results from: I. Overproduction of free radicals: Because of infection, toxins, iron etc.
  • 31. II. Breakdown of protective mechanism by deficiency of vitamin A, vitamin E, Carotene., zinc, copper, selenium, magnesium. 4. Jelliffe Hypothesis: kwashiorkor is nutritional disorder precipitated by other factors like infection, parasitosis, emotional trauma, maternal deprivation, toxin 5. Aflatoxin contamination of food. 5. Pathology of PEM 1. Sr. albumin decreases. 2. Sr. Globulins: a) Alfa1 globulin increases. b) Alfa2 globulin decreases. c) ᵦ globulin decreases. d) Gamma globulin increase. 3. Amino acids: Essential amino acid decrease. 4. Enzyme decrease. 5. Carbohydrates: a) Glycogen reserve in liver and muscle are depleted. b) Chance of hypoglycemia increases. 6. Lipids: a) Essential fatty acids decrease b) Sr. Lipid level variable. 7. Electrolytes: a) Total body Na+ increases. b) Total K+ decreases. 8. Water: Total body water increases. 9. Minerals: decreased iron, zinc, Mg+2 , Cu+2 , Ca+2 , P+2 and other trace elements. 10. Endocrine glands: Atrophied but functions maintained. 11. Heart: Microcardia but Cardiomegaly if CHF & Anemia. 12. Liver shows fatty changes: Raised Bilirubin – Bad prognostic sign. 13. Coagulation factors: Decreased. 14. GIT: a) Mucosal atrophy. b) Delayed mucosal repair. c) Disaccharides Deficiency. d) Ascending cholangitis. e) Pancreatitis. 15. Immunity: a) Decreased in chemotaxis: 1) Bacterial killing decreases. 2) Lysozymes decreases. 3) Complement decreases. 4) Interferon decreases. b) Phagocytosis: Normal. c) Humoral immunity: I. Antibody production to vaccine and infections is satisfactory. II. Antibody production against diphtheria in impaired.
  • 32. III. IgA decrease. d) Cell mediated immunity: 1) Thymic atrophy. 2) Lymphopenia. 3) Poor cell mediated immunity. 4) M.T. Test may be negative. 5) T leper cell to T suppressor cell ration is reduced which predispose to fungal infection. • Biochemical changes in PEM. 1) Hypoproteinemia. 2) Hypoglycemia. 3) Plasma transferase decreases, K+ decreases. 4) Plasma triglycerides cholesterol and ᵦ lipoprotein reduce. 5) Decreased Sr. Enzyme: Esterase, Amylase, Lipase, Cholinesterase, alkaline phosphatase. • PEM and infection. 1) Breach in skin and mucosa can increase infection. 2) Impaired chemotaxis: a) Decrease T lymphocyte, decrease lymphokine production. b) Normal phagocytosis. c) Defective candidial and bactericidal capacity. d) Cytokine production. 3) Cell mediated immunity: a) Thymus and thymus dependent lymphoid tissues are atrophied. b) Delayed hypersensitivity reaction is reduced. 4) Humoral antibodies: a) Circulating immunoglobulins are normal or elevated. b) Secretary IgA is generally reduced. 5) Micronutritional deficiency: Iron, zinc, copper, selenium. 6) Vitamin deficiency: A, B, C, D. • Learning abilities and PEM. 1) Undernutrition during early part of life, I.e 6months adversely affects development of Brain. 2) Impaired learning skills. 3) IQ level is reduced. • PEM and GIT. 1. Atrophy of salivary glands. 2. Fatty infiltration of liver. 3. Pancreatic Atrophy. 4. Intestinal villous atrophy – Total absorptive surface is reduced, increased goblet cell and inflammatory cells. 5. Steatorrhea. 6. Lactose malabsorption is commen. 7. Rectal prolapse is commen. • PEM and Endocrinal system. 1. Hyperfunctioning of adrenal gland, so cortisol level is high. 2. Somatomedins level are low. 3. Insulin like growth hormone (IGF 1 and 2 is low.
  • 33. 4. Impaired Sr. insulin levels in kwashiorkor. 5. Growth hormone levels are high. 6. Glucagon level is high. 7. Thyroxine – normal or high in kwashiorkor but normal or low in marasmus 3.15.1. Marasmus: 1. Definition: It is a type of PEM due to deficiency of mainly energy (calorie) through protein deficiency also exists. 2. Age: Usually below 3yrs. Of age. 3. Peak: During first year of age. 4. Clinical features: A. Essential features: a) Growth retardation: 1) Weight below 60% expected. 2) Subnormal height. b) Loss of subcutaneous fat: 1) Grading according to loss of fat. c) No edema B. Other features: a) Age – seen in infancy. b) Wrinkled skin – emaciated child, loose folds of skin over gluteal and inner side of thigh. c) Skin dry, scaly, inelastic. d) Hair hypopigmented e) Abdomen distended due to wasting and hypotonia. f) Mid are circumference – reduced. g) Bony point – prominent. h) Baby is alert but irritable. i) Appetite – voracious 3.15.2. Kwashiorkor: I. Essential features: a) Growth Retardation: Evidenced by low weight and low height. b) Muscle wasting: with retention of subcutaneous fat. c) Psychomotor changes: As evidence by mental apathy, listless with no interest in the surrounding. d) Edema: Pitting edema due to hypoalbuminemia. II. Other features: a) Hair changes: Hair are sparse, light colored, thin and easily pluckable. Flag sign – Alternate band of light and dark colored hair signifying periods of inadequate and adequate nutrition over a prolonged period. b) Skin changes: erythema, hyperpigmented area, desquamation, raw hypopigmented skin lesions are more on extremities “flaky paint dermatosis”. Kin may become dry, inelastic, mosaic in appearance, follicular keratoses, may also be observed (Crazy pavement dermatoses) c) Infections Diarrhea, vomiting, anorexia, tuberculosis, bronchopneumonia, pyoderma. d) Hepatomegaly. e) Mineral deficiency: Anemia, potassium deficiency, magnesium and zinc deficiency. f) Vitamin deficiency:
  • 34. i. Vitamin A deficiency is frequent and may lead to night blindness, xerosis and keratomalacia. ii. Vitamin B complex, C, D, E deficiency may accompany. g) Worm infestation may be there. h) Clubbing due to steatorrhea. 3.15.3. Ten steps of Managing of PEM: Depending on severity of PEM it can be managed in hospital or home. 1. Mild to moderate PEM Home based treatment or at day care center. 2. Severe PEM Hospitalization is needed. Basic principles in management are as follows: I. First treat complications: 1. Dehydration by I/V fluids or ORS (Resmol) a) It is a rehydration solution for malnutrition. b) It contains less Na+ , more K+ more calories and minerals like Mg, Zn, Cu. c) With the use of Resmol ORS in malnutrition I.V. fluid requirement is less. d) Complications: (ORS = 1packet) S. no. Specific content Quantity 1 Sucrose 50gms. 2 Electrolyte Mineral mixture 3 Osmolality 300mosm/L 4 Potassium chloride – 22.4g. 5 Tripotassium citrate – 81g. 6 Magnesium chloride – 76g 7 Zinc acetate – 8.2g 8 Copper sulphate – 1.4g. 9 Water – 2.5 liter. 10 Glucose – 125mEq/L 11 Na – 45mEq/L 12 K – 40 mEq/L 13 Cl – 70 mEq/L 14 Citrate – 7mEq/L 15 Mg – 3g/L 16 Zn – 0.3g/L 17 Cu 0.045g/L 2. Shock by IV fluids, broad spectrum antibiotics, blood transfusions, Presser agents if required and O2 3. Severe Anemia by blood transfusions. 4. Bleeding disorders by blood transfusions. 5. Diselectrolytemia: correct accordingly. 6. Super infections by broad spectrum antibiotics. 7. Hypothermia: warming by warmers, covering patients with woolen or cotton. 8. CHF: Restrict fluids, slow blood transfusions 10ml/kg. II. Find out the cause and treat it: commen causes are: 1. Under feeding/diluted milk: Prolongation of Breast milk beyond 2years; advice pure cow’s milk.
  • 35. 2. Delayed weaning: Weaning at 6months of age, add cow’s milk 6months of age. 3. Chronic infections: Find out cause and treat it especially tuberculosis, chronic diarrhea, lactose intolerance, chronic pyogenic focus in body, malabsorption syndrome. III. Nutritional rehabilitation: 1. Calculate amounts of calories and proteins child is consuming. 2. Calculate amounts of calories and proteins child is required at present age. • Calories  Give 65% of expected calories or start with present caloric consumption + 20% of present caloric consumption.  Increase calories by 10 – 15% gradually till 150 – 200 cal./kg reached.  10% calories from proteins of high biological value. • Proteins – 3 gm/kg at present wt. 3. Give cheap locally available foods according to age. 4. Nutritional supplementation diet: a) Initially ORS is started followed by milk base diet, semisolids and the solids. b) Later oil and sugar are added to milk to make high energy milk (100cal/ml) c) Cereal floor is added to prepare thickened feeds. d) Supplement cereals pulses mixture (SAT MIX) by roasting and powdering rice, wheat and black gram and adding powdered sugar in ratio of 1.1:1.2 it is precooked. e) Slow traditional food items should be added. f) Coconut oil contains medium chain triglycerides, which are directly absorbed which are directly absorbed into portal vein. It can be added to milk and semisolids. g) Family pot feeding: 1) Green leafy vegetables, Seasonal fruits, roots and tuber are recommended. 2) Cereals, pulses combinations and amylase rich food are advised. 3) Egg, potatoes and banana are beneficial. h) Amylase rich food: Prepared by germination of grains. It is then sun dried roasted and powdered. It will supply amylase. o Germination increases vitamin content. o Wheat gives maximum amylase on processing. o Amylase increases digestibility and reduce bulk on cooking. i) Lactose intolerance: → Continue Breastfeeding. → If baby is below 6months soybean milk or groundnut milk is started. → Curd can be added. → Above 6months weaning food including cereals and legumes should be start or lactose free milk can be given.
  • 36. • Diet Regimen: A. High energy milk provides 100 cal./ml. B. Cereal milk: 100ml ½ glass milk, + 5gm sugar 1½ teaspoon cereal floor, provides 100cal./100ml. C. SAT milk: ½ glass milk and 2TSF SAT milk gives 100cal./100ml. D. Egg Flip: One egg + 1glass of milk (gives 80cal.+120cal. = 200cal.) E. Lassi: ½ glass yogurt + 100cal. F. Hyderabad protein energy rich mixture for home treatment of PEM S. No. Content Quantity. 1 Roasted whole wheat 40gm 2 Roasted Bengal gram 16gm 3 Roasted Ground nut 10gm 4 Jaggery 20gm 86gm Provides Calories – 330Kcal Proteins – 11.3gm. IV. Supplementations of vitamins, minerals and electrolytes: 1) Vit. A – One lac unit daily for 2consecutive days and then repeat after 15days. For severe PEM repeat every month till PEM is corrected. 2) Vit. B complex – All B complex vitamins, folic – 5mg followed by 1 mg/daily. 3) Vit. C – 100mg daily for 10days then 50mg daily. 4) Vit. D – 3lacs units IM stat dose (Inj. Architol 3.0 lac) or 10,000 units daily. 5) Vit. E – 5to14 IU/day. 6) Vit. K – 2.5mg IM stat or oral vit. K for 3days. 7) Minerals: a) Calcium – 800 to 1000mg/day. b) Phosphorus – 600 to 800mg/day. c) Iron – 3-6mg/kg/day for 3months d) Mg sulphate – 50% solution – 2ml IM or 0.3ml/kg/day. e) Zinc – 20mg/day. f) Cu – 20mg or 0.1 mg/kg/day. g) Selenium – 6 to 10mg/kg/day. 8) Electrolytes: a) Sodium – 2 to 3mg/kg/day. b) Potassium – 5mEq/kg/day. V. Deworming – Mebendazole – 100mg/BD/3days. VI. Immunization – To prevent further infection. VII. Health education for Hygiene and Balanced diet. VIII. Family spacing or family planning. Phenomenon encountered during nutritional rehabilitation 1) Pseudotumor cerebri: Benign and self-limited. 2) Nutritional recovery syndrome: (Gomez syndrome) Probable cause: a) High protein intake during rehabilitation. b) Endocrine disturbances. Features: Hepatomegaly, Abdominal distention, Ascites, prominent thoracic tricosis, Parotid swelling, Gynecomastia, Eosinophilia.
  • 37. 3) Encephalitis like syndrome: Drowsiness may rarely progress to unconsciousness. 4) Kahn syndrome: Coarse tremors, Parkinsonian rigidity, Bradykinesia, Myoclonus appear 6days after dietary therapy. 5) Rickets. 6) Anemia. 7) Micronutrient deficiency. 3.15.4. Complications of PEM: 1. Superadded infections – pneumonia, tuberculosis, septicemia, UTI. 2. Dehydration following diarrhea. 3. Lactose intolerance. 4. Electrolyte imbalance especially hypokalemia. 5. Hypothermia. 6. Hypoglycemia. 7. CHF. 8. Anemia. 9. Bleeding disorders – DIC. 3.15.5. Prevention of PEM: 1. Exclusive breast feeding for 4 – 6 months. 2. Advise weaning at 4 – 6 months. 3. Supplementary feeding. 4. Micronutrient supplementation. 5. Universal immunization. 6. Nutritional and health education. 7. Overall socio-economic development. 8. Improving sanitary conditions. INFANTILE TREMOR SYNDROME 1. Disease of unknown etiology characterized by tremors, anemia and regressions of milestones. 2. Etiology – Three hypothesis. a) Nutritional. i. Response to B12 megaloblastic anemia. ii. Due to both folic acid and B12 deficiency. iii. Mg+2 deficiency. iv. Zinc deficiency probably. b) Viral encephalitis. c) Degenerative – Due cortical atrophy. 3. Clinical features: a) Child is plump through underweight. b) Apathy. c) Hair changes – light color, sparse. d) Skin changes – Brownish reticular pigmentation more so on dorsal aspect of hands especially over terminal phalanges, feet, knees, ankle, axilla, buttocks, lower abdomen, middle aspect of thigh. e) Regression of milestone f) Tremors. g) Anemia – can be megaloblastic or dimorphic. h) Tremulous cry like that of lamb (Gouts cry)
  • 38. i) Face – tossing of head from side to side with saliva drooling from mouth. j) Hypotonia. k) Hepatomegaly. 4. Treatment: 3.15.6. Antioxidants: 1. Definition: Antioxidants are food substances, which decrease the adverse effects of free radicals. Free Radicals are produced in body and cause tissue damage, e.g. Singlet oxygen, peroxide anion, hydrogen peroxide, hydroxyl radical. 2. Role of Antioxidants in pediatrics: 1. Kwashiorkor. 2. Rheumatoid arthritis. 3. Inflammatory bowel disease. 4. Hepatic disorders. 5. Cancers. 6. Neonatal disorders: a) Retinopathy of prematurity. b) Hypoxic ischemic encephalopathy. c) Necrotizing enterocolitis. d) Bronchopulmonary dysplasia. References: 1. Parthasarathy, K Nedunchalian, Gowri Shankar HC, Textbook of Balram chowdhary’s Pediatrics Lecture notes, PEE PEE Publication, 2nd edition, Pg no. 222 – 236.