Chapter 1: NUTRITION AND Nutritional DISORDERS

Intended learning outcomes: by the end of this chapter the student should be able to:
1- Know the components of breast milk and the biological value of each component
2- Recognize the advantages and recent trends in practice of breast feeding.
3- Diagnose the difficulties in breast feeding
4- Know indications and types of artificial feeding.
5- Practice the recent trends in weaning.
6- Knows description, diagnosis, prevention and management of malnutrition.
7- Identify rickets and its different causes with their appropriate therapies.
8- List the causes and presentations of hypervitaminosis D and tetany
Prof Ihab Khairy and Prof May Nassar
BREAST FEEDING
• Breastfeeding is the most natural and safe way to feed infants. It provides a unique
combination of proteins, lipids, carbohydrates, minerals, vitamins, enzymes and living
cells, as well as immunological, psychological and economic benefits.
• Exclusive breast feeding is recommended as the best feeding for infants up to six
months and should be started as soon as possible. It is a cheap, sterile and ready-made
form of nutrition for children. Total duration is up to 24 months.

I- Stages of human milk production

• Colostrum: starts within 3rd trimester till 3-5 days after delivery
• Transitional milk: 3-5 days up to 2-3 weeks
• Established milk: within 2-3 weeks
Normal range in milk volume
• Volume increases rapidly in the first 2-3 days after birth, and then more slowly to an
average of about 750-800 ml/day
• Range of normal milk intake of exclusively breastfed infants is wide: 550-1200
ml/day
Physiological regulation of milk volume
• Endocrine: Infant suckling causes neural loop in hypothalamus
› Anterior pituitary: prolactin and other hormones for maintenance of lactation
› Posterior pituitary: Oxytocin for milk ejection reflex
• Autocrine: In each breast, emptying accelerates milk synthesis
II- Composition of breast milk:
Colostrum:
• It is the milk secreted from the last trimester of pregnancy till the 1st week
postnatally
• It is yellowish and sticky
 • Colostrum differs from mature milk because it contains:
- More protein.
- Much more immunoglobulins A and lactoferrin and also white blood cells
which are important for the baby's defense against dangerous neonatal
infection.
- Less fat and lactose.
- Higher level of VA.
- More sodium and Zinc.
- More intestinal growth factors.

Mature human milk

Proteins: 0.9-1-2 gm%
• Whey and casein: Approximately 70 percent of the proteins in human milk are in
the soluble whey fraction and 30 percent in the insoluble casein
• Whey proteins form a softer curd, more easily digested with faster gastric
emptying. In breast milk, the main component of whey protein is α -lactalbumin
which has better amino acid profile
• It is different from cow’s milk protein (table 1)

Table 1: Cow’s milk and breast milk protein differences

Protein Human Milk Cow’s Milk
Quantity Low (high Quality) 3-4X Higher
Type Whey predominant whey/casein ratio 23/77 = Casein predominant
with more α- β-lactoglobulin (highly allergic)
Lactalbumin
Digestibility Curds soft, easy to Curds rubbery, harder to digest
digest
Brain and Eye Taurine present Taurine absent
development Tryptophan high Tryptophan low
Bioactive proteins Present Present

What is α -Lactalbumin?
• A whey protein that is higher in breast milk than infant formulas
• Plays a role in lactose synthesis in the mammary gland
• Rich source of tryptophan (serotonin precursor) and other essential amino acids
• It has shown positive benefits in GI tolerability
 • Partial digestion in gut produces bioactive peptides (Anti-microbial and Stimulants
for immune system)
Consequences of excessive protein intake in early life:
• Metabolic stress
• Increased renal solute load
• Altered water balance
• Insulinogenic
• Programming towards obesity?
Fat: 3.5 gm%
• About half the energy in the human breast milk comes from fat.
• The first milk flow is called "Fore milk". It has a fat content of 1-2% and looks
thin. The later milk called "hind milk" may contain 3-4 times more fat.
• It contains lipase enzyme.
• Contains less volatile fatty acids and contains all essential fatty acids and LC-
PUFA.
Lactose: 7.1 gm%
• It is the only milk carbohydrate. It provides energy and is converted to lactic acid
in the intestines. It is the source of galactose.
Minerals:
• Calcium is easily absorbed and satisfies baby's needs.
• Small amount of iron is contained but 75% is absorbed.
Vitamins:
• When mother's diet is adequate all the vitamins will be sufficient during the first
four to six months.

Are vitamin-mineral supplements needed during the period of exclusive

breastfeeding?
• Human milk is ordinarily a complete source of nutrients for exclusively breastfed
infants
• Nutrients of special concern:
› Vitamin D: 200 IU/d beginning since birth in exclusively breast fed infants
› Vitamin B12: if mother is complete vegetarian
› Vitamin K: all newborns should get one dose
› Iron: if not exclusively breastfed, or by 6 m, a good source of iron is needed.
Low birth weight infants need Fe beginning at 1-2 m.
› Fluoride: recommended if water content low
 Bioactive factors: factors present in breast milk and found to have biologically active
functions and role in child health & development including immune and non-immune
protection, anti-inflammation and growth. (table 2)
Table 2: Bioactive factors in breast milk
Immunoglobulins • Ig A, G, M acting at mucosal sites, work synergistically against
microorganisms.
Lysozymes • Bacterial lysis
• Immuno-modulating activity
• Anti-adhesive against GIT & respiratory pathogens
Lactoferrin (100- • Iron chelator: Bacteriostatic
300 mg/dl) • Antiviral: interfering with virus adhesion.
• Immuno-modulating activity: ↓ release of IL1, IL2, IL6, TNF and
stimulates NKC.
• Anti-adhesive for E-coli.
Oligoconjugates • Oligoconjugates are present in milk fat globule membrane acting as
& ligands for microorganisms, viruses and their toxins.
oligosaccharides • Oligosaccharides: protect against heat stable E-coli Enterotoxins, V.
Cholera, H. influenza & S. Pneumonae.
• Lactadherin: against Rota virus
• Glycosaminoglycans: inhibit binding of HIV to CD4 receptors.
Breast milk • Digestive product of core triglycerides has a detergent like lytic action,
lipids: disrupting lipid bilayer hence, inactivates enveloped virus, G +ve and G
-ve bacteria, fungi & protozoa.
• Membrane Glycoconjugates
Immunomodulati • These affect the development of the newborn's immune system. Among
ng Agents these are cytokines defined as pleuripotent polypeptide that act as
autocrine / paracrine fashion by binding to specific cellular receptors
e.g. ILs & TNF.
Anti- • Inhibit inflammatory mediators e.g. α1antitrypsin, α1chemotrypsin.
inflammatory • Scavenge O2 radicals e.g. vitamins A, C, E
Component • Degrade H2O2 e.g. catalase
• Cytoprotective e.g. PGE1, E2
Nucleotides in • Enhance intestinal repair after injury and potentiates immune response
Breast Milk to certain vaccines. They also promote growth of [Link] which is
known to suppress the growth of enteropathogens.
Cells in Breast • Human milk leukocytes remain active in neonatal intestine and possibly
Milk migrate to other tissues.
 • PNL, Lymphocytes help in microbial phagocytosis and production of
lymphokines and cytokines.
Enzymes in • Besides providing the infant better digestive potentials, some enzymes
Breast Milk are involved in protective function as lysozymes, peroxides, catalase
and glutathione peroxidase.
Prebiotics and • Probiotics = live microorganisms which confer health benefits on the
probiotics host
• Prebiotics = Food ingredients (resistant CHO, fibers) refractory to host
digestion that reach the colon providing a dietary modulation to the gut
microbiota
Hormones & • Some hormones may be the product of local mammary synthesis,
Growth factors transfer from the maternal circulation, or a combination of mammary
modification of blood born hormones.
• Effect can be either immediate (during breast feeding) or delayed by
transfer of milk born hormones during critical period of development.
• Prolactin: enhances development of B&T lymphocytes, NKC activity.
Also affects short and long-term neuro-behaviour.
• Cortisol & Thyroxin: promotes maturation of newborn's intestine.
• Insulin & Growth Factors: development of intestinal defense
mechanism.
• EGF & TGF-α: GIT growth.
Bifidus factor • A carbohydrate that contains nitrogen.
• Function: Stimulates growth of bifidobacteria which helps in:
▪ Inhibition of colonization of pathogens either directly or indirectly
through production of acetic acid
▪ Vitamin k production and increase absorption of ca ,mg and fe
Natural • Protects the body’s immune system, may have immune-enhancing
Carotenoids effects and protects against harmful effects of free radicals.
III- Benefits of breast feeding
A-Benefits of BF for infants:
a)Nutritional benefits:
➢ The most suitable nutrient as it has ideal biochemical composition.
➢ Has more nutritional value than any other food for infants in the first six months of
life.
➢ Contains all the water a baby needs, even in hot climates (Breast milk is 80%
water).
 b) Growth: Exclusively breast fed infants achieve an optimal growth pattern for the
first six months. They will continue to grow well if supplementation with other
foods begins at this time.
c) Immunity: Exclusively breast fed infants have less risk of diarrhea, respiratory
and skin infections and allergies
d) Dental development and protection: Muscles used for breast feeding favors
normal facial development. Breast feeding prevents malocclusion which occurs
more commonly with bottle feeding.
e) Psychosocial issues: Frequent skin-to-skin contact, attention and interacting with
the mother, stimulate psychomotor and social development. The lipid in human
milk foster mental and intellectual development.
f) Other issues: Breast feeding reduces the risk of GI disorders and decreases the
incidence of SIDS.
B- Maternal benefits of BF:
a) Prevention of post-partum hemorrhage
b) Uterine involution
c) Birth spacing
d) Lactation amenorrhea prevents iron loss.
e) Reduces the risk of breast and ovarian cancer
f) Fosters a strong bond between mother and infant.
C- Benefits of BF for the family and community:
a) Inexpensive
b) Decrease cost of Medical consultation.
c) Reduces work absenteeism
d) Acts as a contraceptive method
IV-Preparation for breast feeding
Preparation during pregnancy:
• Mother should: Eat a well-balanced diet which builds up body reserve.
• Check that nipples are prominent enough to breast feed in the last trimester.
Preparation at the time of delivery:
Anesthesia, strong sedation, prolonged labour, surgical intervention and other sources of
stress may affect initiation of breast feeding.
Preparation after delivery:
• Encouraging skin to skin contact between mother's and baby immediately after
birth permitting the infant to suck at the breast.
• Keeps the baby next to the mother (Rooming in) after delivery as she can
immediately respond to his demand for breast feeding.
V- How to breast feed?
BF should start as soon after delivery as possible (within half an hour) in order not to lose
the initial milk (colostrum) and to initial bonding.
Frequency of breast feeding
1- On demand feeding:
- The babies should be fed on demand, without any fixed time to let the baby decide
how often he wants to fed. This will probably be very often during 1st week of life.
- From the second week of life, most babies begin to demand less, and gradually settle
down to a routine in which the baby suckles about 7-10 times in 24 hours.
- Consider baby's individual needs, look at baby's signals for breast feeding (crying).
2-Regular feeding: Feeding every 2,3 or 4 hours (not recommended).
Positioning
• Infant’s neck is straight or bent slightly back.
• Infant’s body is turned towards the mother.
• Infant’s body is close to mother’s body.
• Infant’s whole body supported.
Duration of each feed:
The baby gets enough milk if he is allowed to decide how long and how often a feed
should be.
Babies who suck correctly take 5-10 minutes to suck most of the milk from a breast.
Feeding from the two breasts
The baby should feed from one breast and then be offered the other breast in alternating
manner.
Determining adequacy of Milk supply:
The infant is satisfied after each nursing period, sleeps 2-4 hrs, passing stools and gains
weight adequately.
Why the milk supply decreases?
1. The mother goes on the birth control pill
2. The mother is pregnant
3. Maternal medications other than hormones
4. Maternal illness or stress
5. An emotional "shock “
6. Feeding one breast only at each feeding
7. Using bottles more than occasionally

VI-Special problems during breast feeding

1- Problems of the breast:
Fissures of the nipple
• Usually cause severe pain during suckling and oozing of blood swallowed by the
baby.
• Treatment
→ Continue nursing from the affected breast or complete regular evacuation to avoid
engorgement and the use of local antiseptic and local anesthetic
→ Avoided by following the cleanliness and washing the nipple by water before and
after lactation.
Retracted nipple:
• Minor degree of retracted nipples could be managed by frequent traction of the
nipples or by early frequent suckling by the baby.
• Severe degree could be managed by:
→ Expression of B.M. and to be given by bottle or syringe.
→ Nipples Shields can be very useful to help with early breast feeding problems.
Breast engorgement: It leads to enlarged, firm and tender breast
• Avoided by early frequent suckling and complete regular evacuation of the breasts.
• Treatment by cold fomentation and coupled regular evaluation of the breasts.
Mastitis:
• Usually results from the presence of engorgement and fissures.
• The breasts are enlarged hot, firm, red, tender plus the presence of high fever.
• Treatment is by hot fomentation and complete regular evacuation and antibiotics.
• Breast feeding is avoided till the subsidence of mastitis.
Breast Abscess: Treated as mastitis and early evacuation of the abscess.
Cancer breast: Lactation should be avoided and the baby will be given artificial milk.
Scanty Breast milk:
• This could be avoided by:
→ Early frequent suckling,
→ Good Maternal nutrition especially fluid intake.
→ Intake of lactagogue
• Treatment is by supplementary or complimentary feeding.
2- Maternal infection:
HIV
In developing countries, where mortality from malnutrition is higher than mortality from
HIV, mothers can continue breast feeding for 3 – 7 months. In developed countries,
where morality is low and therapy is available, bottle feeding is recommended
Herpes Simplex Virus
Woman with herpetic lesion on her breasts should refrain from BF and active lesion
should be covered.
In absence of breast lesions, mothers can continue BF while receiving acyclovir therapy
accompanied by hand washing, covering other lesions and avoiding kissing with oral
lesions.
Hepatitis A
• Transmission via BM has been implicated but no data exist on the frequency of
isolating HAV from BM.
• If the mother has HAV, BF is permitted and gamma globulin is given to the infant.
Hepatitis B
• Hepatitis B sAg is found in BM but there is no evidence that BF increases the rate of
HBV infection in infants so there is no contraindication for breast feeding.
• Newborns delivered to HBs Ag +ve mother should immediately receive Hepatitis B
Specific Ig and active immunization at accelerated schedule of vaccination 0, 1, 2
months.
Hepatitis C
• Although HCV can be found in BM, infection through BF appears to be infrequent.
• Breast feeding with maternal HCV is a controversial topic. However, benefits to
infant’s health relative to the potential risk for HCV infection favour continued breast
feeding.
Acute infection of the mother
• May contraindicate BF if the infant doesn't have the same infection; otherwise, there
is no need to stop nursing unless the condition of either necessitate it. The breast may
be emptied and the milk given to the infant.
• Maternal septicemia, typhoid fever and Malaria are contraindication to breast feeding.
Maternal TB
• If the mother has suspected TB at the time of delivery, the newborn should be
separated from the mother until chest radiograph is taken.
• If chest x-ray is abnormal separation should be maintained till the mother has been
thoroughly evaluated including sputum examination.
• If the history, examination, sputum analysis and evaluation of the radiograph show no
active TB, the infant is at low risk and the mother should receive care and follow up.
• If radiograph and sputum analysis show evidence of current TB disease INH therapy
for newborn, this can avoid separation for infant and the mother.
• Separation only if the mother is ill enough to require hospitalization.
• INH treatment of the infant is continued till sputum of the mother has been negative
for 3 months at this time tuberculin test for the child: if +ve then INH is continued 9-
12 months and if -ve INH is discontinued.
3- Maternal epilepsy: Lactation should be avoided if it leads to precipitation of the
epileptic fits or if the anticonvulsant used is secreted in BM and can lead to side effects
e.g. tegretol.
4- Maternal Malignancy: B.F. is avoided due chronic ill health and the intake of
cytotoxics.
5- Twin delivery: In this case we can use either complementary or supplementary
feeding.
6- Other maternal problems:
• Resumption of menstruation This should not discontinue nursing, although
temporary behavior changes of mother may call for reassurance.
• Pregnancy It doesn't necessitate immediate cessation of nursing.
7- Problems of the newborn:
a) Painful mouth
b) Cleft lip or palate
c) Respiratory distress
d) weak suckling power
VII- Contraindications and controversies in Breast feeding
Temporary contraindications (no breast feeding for specified period of time)
• Infant infections- oral herpes simplex
• Maternal infections.
Conditions in which breast feeding is not contraindicated.
• Mastitis, Hepatitis A, B and C
• Neonatal jaundice
Absolute contraindication
• IEM
• Maternal intake of inevitable drugs

ARTIFICIAL FEEDING
Infant formula
Product intended for use by infants that simulates human milk or is suitable as a complete
or partial substitute for human milk
Indications
• Infants should receive specialized formula if they have inborn errors of
metabolism
• Classic galactosemia: galactose-free (lactose free) formula.
• Maple syrup urine disease: formula free of leucine, isoleucine and valine.
• Phenylketonuria: phenylalanine-free formula.
• Infants who may need other food in addition to breast milk for a limited period
• VLBW (birth weight <1500 g)
• Newborn infants who are at risk of hypoglycemia &fails to respond to optimal
breastfeeding (significant intrapartum hypoxic/ ischemic stress, those who are ill
and those whose mothers are diabetic)
• Maternal conditions that may justify temporary avoidance of breastfeeding
• Severe illness that prevents a mother from BF for example sepsis.
• Maternal medication:
— Sedating drugs, anti-epileptic drugs and opioids
— Radioactive iodine-131 – resume breastfeeding after two months
— Excessive use of topical iodine or iodophors (e.g. povidone-iodine), especially
on open wounds or mucous membranes, can result in thyroid suppression or
electrolyte abnormalities in the breastfed infant
— Cytotoxic chemotherapy
— Substance abuse
• Maternal conditions that may justify permanent avoidance of breastfeeding
HIV infection: if replacement feeding is acceptable, feasible, affordable, sustainable
and safe

Types of Artificial Feeding

A) Adapted (humanized) formula: nutrients are close to those of human milk.
Modifications done:
• Protein is small to give fine curd.
• vegetable fats are added to increase content of essential FA
• Minerals are lowered but with iron fortification
• Some types fortified with vitamins and or biogenic factors
• Examples: Aptamil 1- Bebelac 1– Nan1- S26 gold- Similac

Composition of adapted formula compared to breast milk

Breast milk Standard formula
Calories/ 100 ml 67 67
Protein (gm/dl) (% of calories) 1.1 (6%) 1.5 (9%)
• Whey/ casein ratio 70/30 Mostly 60/40 (NAN 70/30)
Fat (gm/dl) (% of calories) 3.5 (55%) 3.6 (50%)
CHO (gm/dl) (% of calories) 7.1 (40%) 7.2 (41%)
• Source Lactose Lactose
Minerals • Ca (mg/L) 290 420-550
• P (mg/L) 140 280-390
• Na (mEq/L) 8.0 1.5-8.5
• Vitamin D (IU) Variable 400
Osmolarity (mosm/L) 273 300
Renal free solute load (mosm/L) 75 100-126
B) follow-on formula from 6-24 months with higher iron and protein
C) Special formula which benefits infants in certain medical conditions as GERD, allergy
to cow milk and some surgical and systemic medical conditions. They serve as an integral
part in disease management.

Complementary feeding (weaning)

Definition
A process that starts when BM is no longer sufficient to meet the nutritional requirements
of infants, and therefore other foods and liquids are needed along with BM to close the
energy gap.
Timing by 6 months of age, Why?
• BM is unable to meet the infant’s recommended energy & nutrient intake leading to
energy gap and micronutrient gap
• Lower micronutrient stores: Breast milk provides little iron & vitamin D & in the later
stages, Zn & Cu concentrations in milk begin to fall.
• Mature digestive and absorptive capacity
• Teeth eruption, and the infant is more active and beginning to explore his or her
surroundings
• Infant showed appropriate development (neck support, decreased extrusion reflex)

Guiding principles for complementary feeding of the breastfed child

1. Practice exclusive breastfeeding from birth to 6 months of age, and introduce
complementary foods at 6 months of age while continuing to breastfeed.
2. Continue frequent, on-demand breastfeeding until 2 years
 3. Practice responsive feeding, applying the principles of psychosocial care.
4. Practice good hygiene and proper food handling.
5. Start at 6 months of age with small amounts of food and increase the quantity as the
child gets older, while maintaining frequent breastfeeding.
6. Gradually increase food consistency and variety as the infant grows older.
7. Increase the number of complementary foods as the child gets older.
8. Feed a variety of nutrient-rich foods to ensure that all nutrient needs are met.
9. Use fortified complementary foods or vitamin-mineral supplements as needed
10. Increase fluid intake during illness, including more frequent breastfeeding

Important Principles for complementary feeding:

• Avoid foods with high allergenic potential (cow's milk, egg white, fish, nuts).
• Introduce 1 food at a time, space new food by at least 3–4 days to monitor for adverse
effects
• At the proper age, encourage a cup rather than a bottle.
• Energy density should exceed that of breast milk (at least 0.8 kcal per gram)
• Iron-containing foods (meat, iron-supplemented cereals) are required.
• Zinc intake should be given (meat, dairy products, wheat, and rice).
• Phytate intake should be low to enhance mineral absorption.
• Fluids other than breast milk, formula, and water should be discouraged. Give no more
than 180 ml of fruit juices. No soda.

Considerations about delivery of adequate amounts of nutrients table

1- The amount that a child can eat at one meal depends on the capacity or size of the
child’s stomach which is usually 30 ml per kg.
2- Type of food
The basic ingredients should contain at least 4 out of 8 groups (in specific amounts)
for diversity.
• Staples: cereals, roots and starchy fruits that consist mainly of carbohydrate
and provide energy but contain very little protein.
• Foods from animals or fish are good sources of protein, iron and zinc. Liver
also provides vitamin A and folate.
• Egg yolk is a good source of protein and should be introduced in a stepwise
fashion to both breast-fed and formula-fed infants
 • Dairy products, such as milk, cheese and yoghurt, are useful sources of
calcium, protein, energy and B vitamins (Fresh cow milk isn`t recommended
before 1 year)
• Pulses, peas, beans and lentils are good sources of protein, and some iron.
• Orange-coloured fruits and vegetables as carrot, pumpkin, mango, and dark-
green leaves such as spinach, are rich in carotene and vitamin C.
• Other vegetables and fruits.
• Fats and oils are concentrated sources of energy and contain certain essential
fatty acids that children need to grow.
3- Sugar is a concentrated source of energy, but it has no other nutrients. It can
damage children’s teeth, and lead to overweight and obesity
4- Tea and coffee interfere with iron absorption and has caffeine thus thay are not
recommended
5- There are no controlled studies that show that restrictive diets have an allergy-
preventing effect
6- Home-prepared foods are preferred but manufactured complementary or
replacement foods can be also used. The latter are more convenient for mothers,
and many contain supplemental nutrients (iron) and are available in different
consistencies to match the infant's ability to tolerate larger size particles. They
should be age appropriate and free from any preservatives or added sugar.

How to judge the success of weaning

1- Dietary history for starting in the right time by the right foods in the right
amounts and consistency.
2- Proper infant growth judged by plotting his anthropometric measurements
against the growth charts by his pediatrician

Problems of weaning period (starting early or late and not following the guidelines can
cause hazards)
1. Gastroenteritis due to unhygienic conditions
2. Malnutrition due to faulty weaning
3. Food intolerance or allergic disorders may be caused by some food ingredients
4. Obesity and risk for atherosclerosis with excess salts and calories.
5. Manifestations of hypo or hypervitaminosis.
6. Early cessation of breast-feeding may lead to an early return of fertility and undesirable
early pregnancy.
 Nutritional Disorders
Assessment of nutritional status
• Nutritional assessment is the evaluation of an individual’s nutritional status &
requirements. It can detect under or malnutrition.
• There are 5 principle approaches to nutritional assessment: Dietary, clinical,
anthropometric, biochemical & immunological.
[Link] assessment: Assessment of the quantity and quality of food consumed in
comparison with the individual needs according to age and sex.
[Link] assessment:
a. Good history taking.
b. Thorough clinical examination to:
*Detect signs of macro & micronutrient deficiency.
*Determine the type & degree of nutritional disorder.
*Detect physical findings of associated conditions.
*Determine specific deficiencies & complications.
3. Anthropometric nutritional assessment:
Weight for age (W.F.A.):
• A low WFA (less than 5th centile of the reference population) is a good index for
acute and chronic illnesses.
• Presence of a flat (Plateau) curve is an alarm sign of nutritional disorder
Height for age: (H.F.A.):
• A low HFA (less than 5th centile of the reference population) indicates stunting that
occurs due to chronic malnutrition.
Weight for height: (W.F.H.):
• Low WFH index indicates wasting due to acute severe growth retardation.
• WFH is the optimal anthropometric index to assess childhood malnutrition.
Mid-arm circumference:
Skin fold thickness: It is an indicator of SC fat which indicates fat reserve and is a good
indicator for obesity
Head circumference
[Link] nutritional assessment:
Serum albumin: Low serum albumin can be an indicator of inadequate protein intake
Essential amino acids: In long term PEM the level of essential amino acids will fall
starting by the branched amino acids; leucine, isoleucine and valine.
Serum transferrin: Indicates protein depletion before serum albumin changes.
Serum prealbumin: Half-life 48 hours. It is the first blood protein to be significantly
decreased as a result of borderline malnutrition.
Serum fibronectin: It is a glycoprotein of short half-life (9hours).
Serum somatomedin C: Half-life 2hours. Normalizes within 3 to 5 days of therapy.
[Link] assessment:
• Immunocompetence is a sensitive index of the nutritional status.
• Alteration in immune response may precede any decrease in the rate of weight gain &
is seen in varying degrees even in children with marginal malnutrition.
Abnormal nutrition
Under nutrition: Undernutrition is primarily an inadequate intake of dietary energy,
with or without deficiency of any specific nutrient. It includes stunting, wasting,
nutritional oedema
Malnutrition: refers to all deviations from adequate nutrition, including undernutrition
and overnutrition, resulting from imbalance of food intake relative to need and/or disease.
Malnutrition also encompasses specific deficiencies or excesses of essential nutrients
such as vitamins and minerals.
Decrease in vitamin D (rickets). Decrease in proteins (KWO).
Decrease in iron (iron deficiency anemia). Excess calories (obesity).
Underweight: refers to low weight-for-age. This concept does not distinguish between
wasting and stunting as it does not indicate if the deficit is in weight (with normal height)
or in height itself
Acute Malnutrition :results from severe nutritional restriction. It can present in the form
of wasting or kwashiorkor. Acute malnutrition is measured as either moderate (MAM) or
severe (SAM). KWO is considered SAM
The diagnosis of acute malnutrition can be done in different ways:
• Weight for height (W/H): using WHO Growth Standards (Z-scores).
• Middle Upper Arm Circumference (MUAC):
• Bilateral Oedema: bilateral pitting oedema, for identification of Kwashiorkor and
Marasmic kwashiorkor.
• Severe Wasting and other clinical signs of SAM and its complications
Pathophysiology of Severe Acute Malnutrition
Severe acute malnutrition can result in profound metabolic, physiological and anatomical
changes.
Reductive adaptation is the physiological response of the body to undernutrition i.e.
systems slowing down to survive on limited macro and micro-nutrient intake. Every organ
and system is involved in reductive adaptation.
Protein energy undernutrition (PEU)
Protein energy undernutrition is a spectrum of conditions due to varying proportions of
proteins deficiencies with decreased caloric intake.
Classification of PEM: Classification based on weight and edema e.g. Wellcome
Wellcome classification: based on the deficit of body weight and edema.
Body Weight Edema No Edema
60-80% KWO Simple Under Nutrition
>60% M. KWO Marasmus
Protein energy malnutrition include:
1. Marasmus 2. KWO. 3. Marasmic KWO.
4. Pre KWO 5. Nutritional oedema.

Kwashiorkor
Definition:
• It is an acute protein energy undernutrition resulting from severe deficiency of proteins
(mainly high biological values protein), in the presence of excess CHO intake, in
addition to manifestations of minerals and vitamins deficiencies.
• It is getting uncommon in Egypt nowadays.
• It is the most serious form of malnutrition especially in the developing countries.
Etiology
Primary KWO: It is a result of sudden faulty weaning with deficiency of proteins. Poverty
and ignorance are the underlying causes, but the interaction of nutrition and infections
plays the most important role.
Secondary KWO:
Results from other diseases, which are usually predisposing factors:
1- Acute severe gastroenteritis. 2- Post enterocolitis.
3- Whooping cough. 4- Measles.
5- Parasitic infestations e.g. giardiasis.
Epidemiology: KWO is common in low social class especially with bad sanitation.
Age: From 6 months to 3 yrs
Clinical picture
• Early clinical picture is vague but do include lethargy, apathy or irritability.
• It is an acute disease within 1 or 2 wks.
• When well advanced features are divided into 2 groups:
Constant features: Variable features:
Growth retardation. Ectodermal changes.
Edema. GI manifestations.
Muscle wasting + some retention of SC fat. Anemia.
 Mental changes. Vitamins & mineral deficiencies.
Associated infections
Constant features:
1. Growth retardation
• It is always present and is best detected by failure to gain weight (flat weight curve) or
loss of weight on serial measurements.
• The deficit in height is less in KWO than in marasmus & marasmic KWO.
• Loss of weight may be partially masked by edema and amount of subcutaneous fat.
2. Edema
• Pitting soft painless bilateral edema is the main clinical feature of KWO on which the
diagnosis is based. It starts in the dorsum of the hands and feet, spreading to affect the
legs to the mid-thighs, in late cases the eye lids are affected. Nearly almost always there
is no ascitis.
Edema is coded in the following way:
• edema in both feet: +
• edema in both feet plus legs: + +
• edema in both feet, legs and hands or face: + + +
Causal factors of edema
• Hypoalbuminemia (Serum albumin less than 2.5 gm %).
• Other factors as Na retention with hyperaldosteronism, increased release of ADH,
increased capillary permeability, kidneys malfunction and thiamine deficiency.
3. Muscle wasting & decreased Muscle/Fat ratio: The muscles are wasted and flabby.
This is demonstrated by palpating the biceps and the triceps and by measuring the left
middle arm circumference. Subcutaneous fat is preserved or increased because of the
relative caloric excess leading to carbohydrate facies (moon face baby).
4. Mental changes: Children with KWO manifest striking behavioural symptoms:
• Apathy, inactivity, misery, anorexia and lack of interest in the surrounding.
• The look of the child’s eyes has been described as the “radar gaze” focusing not in
the immediate surroundings but on the infinity.
These changes are due to:
Maternal deprivation or deficiency of aromatic amino acids, EFAs, nicotinic acid, thyroxin,
trace elements or serotonin.
Variable features:
1. Ectodermal changes
A- Hair changes:
• Color: progressive lightening from black to brown, light red then yellow.
 • Flag sign: There is alternating bands of normal color and light color in the same hair
under the microscope (it signifies multiple relapses).
• Character: dry, coarse, lustreless, brittle and easily detached.
• Distribution: sparse.
Causes: decrease of melanin, deficiency of vitamin A, nicotinic acid or EFA.

B- Skin changes:
• Skin changes are called “flaky paint” dermatosis.
• Erythema followed by hyperpigmentation appears in pressure areas (buttocks and
back) but not in those exposed to sunlight in contrast to the situation in pellagra.
• Desquamation then occurs, leading to a hypopigmented area surrounded by a
hyperpigmented margin.
• Fissuring, crackling and ulceration may occur leading to 2ry infection that may reach
up to gangrene. Skin infections are more in KWO than marasmus due to edema and
skin fissuring
Causes: deficiency of EFA, EAA, nicotinic acid, zinc and/or vitamin A.

2. Gastro-intestinal manifestations:
Hepatomegaly:
• Fatty infiltration is essential in KWO but hepatomegaly is not constant.
• No cirrhosis as it is an acute illness.
Anorexia and vomiting: Due to: 1. Mental changes. 2. GI infections.
Diarrhea:
• Usually starts as an acute episode, then turn to become chronic or remittent.
• Diarrhea may be either infectious or due to maldigestion and malabsorption.
Abdominal distension due to: Hypokalemia up to paralytic ileus, weak abdominal
muscles, toxic ileus due to infections or malabsorption with fermentation.

3. Anemia: Is a frequent feature of KWO due to:

• Iron and cupper deficiency Microcytic, hypochromic.
• Vitamin B12 and folate deficiency megaloblastic anemia.
• Protein deficiency normocytic, normochromic anemia
• Repeated infections bone marrow depression.
• Severe infections hemolysis or DIC.

4. Associated vitamins and minerals deficiencies:

A. Vitamin A: Its deficiency is very common in KWO due to decrease of:
• Intake. • β carotene in the liver.
• Zinc deficiency. • Decrease carrier proteins.
Manifestations:
• Eye: Xerophthalmia, bitot spots, keratomalacia, corneal ulcers ending in
endophthalmitis and blindness.
• Skin: hyperkeratosis.
• Mouth: stomatitis.
• Respiratory tract: repeated infections due to weakness of epithelial lining.
[Link] B2: Angular stomatitis, cheilosis, glossitis, corneal vascularization.
C. Vitamin D: Atrophic rickets.
D. Vitamin C: Scurvy.
E. Nicotinic acid: Pellagra.
F. Cupper: Anemia, hair and mental changes.
G. Zinc: Hair, mental and skin changes.

5. Associated infections:It occurs due to:

A. Atrophy of the thymus: leading to cell mediated immune deficiency
B. Deficiency of complement.
C. Deficiency of phagocytes. Due to deficiency of Zinc and proteins
D. Vitamin A deficiency.
E. Edema and skin fissuring.
F. Bad hygienic conditions.
The common sites of infections are:
*GIT (gastroenteritis). *Respiratory tract (Pneumonia).
*Skin and mouth (monilia). *Urinary tract.
The common organisms are:
Gram negative organisms, encapsulated organisms, fungal especially monilia.

Complications
1- Intercurrent infections.
2- Dehydration, acid-base disturbance, electrolytes imbalance, and shock
3- Hypothermia: Uncommon in KWO compared to marasmus, it is due to:
a. Severe dehydration and shock. b. Electrolytes disturbances.
c. Impaired shivering due to muscle wasting d. Hypoglycemic attacks.
e. Impaired thermoregulatory mechanisms. . f. Septicemic shock.
4- Hypoglycemia: Patients are liable to develop fasting hypoglycemia
5- Bleeding tendencies and purpura: This is a grave and bad prognostic sign. This is due
to DIC and Fragile blood vessels.
6- Heart failure: due to:
a. Degenerative changes in the cardiac muscles. d- Anemic heart failure.
b. Toxic myocarditis 2ry to infections. e- Volume overload.
c. Arrythmia (hypokalemia).
7- Metabolic complications:
a. Hypocalcemia. d. Hyponatremia
b. Hypokalemia. e. Hypomagnesemia.
c. Renal failure due to dehydration. f. Hepatic failure.

Investigations
1. Plasma proteins:
a. Decreased total serum proteins. b. Decreased serum albumin <2.5gm%1.
c. Decreased carrier proteins (ceruloplasmin, transferrin, TBG).
2. Disturbed fat metabolism:
a. Increased free fatty acids b. Decreased serum cholesterol.
3. Disturbed carbohydrates metabolism:
a. Fasting hypoglycemia. b. Disturbed oral glucose tolerance curve.
4. Serum enzymes: All are decreased except :
a. Alkaline phospahatase (atrophic rickets). b. Liver transaminases may increase.
5. Hematological findings: (Anemia, Leucocytosis and High ESR).
6. Water and electrolytes:
• Sodium: Increase total body Na. + Decrease serum Na (dilutional).
• Potassium: decrease total body K and serum K.
• Decrease of serum Cu, Mg, Zn, P.
• Decrease protein bound Ca but with normal ionized Ca.
7. Stool analysis:
8. Urine analysis:
a. Decrease urinary urea. b. Search for pus cells and do urine culture.
9. Investigations for the cause.
Differential diagnosis
a. From other causes of generalised edema.
1- Cardiac 2- Hepatic 3- Renal 4- Angioedema
b. From other causes of dermatitis.

1
Serum albumin < 2.85gm % but > 2.5 gm% and decreased serum prealbumin are indicative of preclinical
malnutrition.
1. Napkin dermatitis:
• Ammoniacal dermatitis2
• Prolonged soiling excoriation.
• Monilial infection.
• Overfeeding.
• Rough clothes.
• Acidic diarrhea.
• Contact and allergic dermatitis.
2. Infantile pellagra: In sun exposed areas and over bony prominences.
3. Hartnup disease3
4. Acrodermatitis enteropathica4

Prevention of PEM (by social community based program GOBI FFF)

- Growth monitoring.
- Use of ORT
- Breast feeding up to 2 yrs.
- Expaned program of immunization
- Female education.
- Provision of good supply of food.
- Family planning.

Management of PEM:
WHO divides the management of malnutrition into 3 phases:
I-Initial treatment. II- Rehabilitation. III- Follow-up.
I- Initial treatment:
[Link]
[Link] treatment:
1-Management of shock by: Antishock measures.
2- Correction of dehydration, electrolytes disturbances & acid base imbalance.
3-Hypothermia: Warm the infant using mother’s body, cover with a warmed blanket.
4-Treatment of hypoglycemia:

2
The most common: It is due to continuous soiling of the infant with urine bacterial splitting of urea
production of ammonia irritation and excoriation of the skin.
3
It is an autosomal recessive defective intestinal transport of tryptophan leading to niacin deficiency with pellagra
like manifestations.
4
An AR disorder characterized by defective absorption of Zn leading to chronic diarrhea dermatosis, nail
dystrophy and stomatitis.
 • If the patient is able to drink give 50ml of 10% glucose by mouth.
• If the patient is unconscious give 5ml/kg of 10% glucose IV followed by oral glucose.
5-Treatment of infections: antibiotics, better according to culture & sensitivity.
6-Blood or plasma transfusion: if indicated
7-Multiple amino acids solution.
3. Dietetic management
Route of administration:
Enteral Parenteral
Oral NG Gavage: Indicated in: By TPN : Indicated in:
By bottle, Cup & ➢ Severe stomatitis ➢ contraindications to entral feeding
spoon or dropper ➢ Frequent vomiting (ileus toxic & paralytic, GIT
➢ To complete oral hemorrhage)
feeding ➢ Persistent vomiting
➢ Failure of oral feeding ➢ Failure of enteral feeding
➢ Cleft lip & palate
Frequency:
Small feeds from 6-12 feeding per day depending on the patient’s age and general
condition. This frequent feeding of small volumes prevents vomiting and hypoglycemia.
Amount:
• It is important begin feeding with a diet that is low in protein, fat and sodium and high
in carbohydrates.
• During this initial stage we should start with 100cal/kg/24 hours calculated midway
between the actual and the expected weight. Proceed gradually.
• Total amount of milk/24 hrs=total caloric needs/dayx100/67
• During initial phase, we start to give proteins as 0.9 gm/kg/day and gradually
increasing the amount to avoid refeeding syndrome.
Type:
• Non weaned infants:
➢ Breast milk.
➢ Artificial as follows (if breast milk is scanty or not available):
➢ Patients with lactose intolerance ➢ Patients without lactose intolerance are
lactose free milk for 2 weeks, then given adapted milk
adapted milk.
• Weaned infants:
➢ Adequate balanced diet according to nutritional table.
➢ Start by light diet as yogurt, vegetable soup, cereals, and minced meat.
IV. Adjuvant treatment
• Adequate amount of vitamins and minerals:
-Either orally or parenteral.
-The most important is to give vitamin A as 50.000 IU / day orally on day 1.
-Vitamin K, thiamine, vit.D and folic acid are also recommended.
• Zinc sulphate orally (2mg/kg/day) and zinc oxide ointment locally.
• Treatment of moniliasis:
-Oral moniliasis Mycostatin drops and gentian violet paint.
-Skin moniliasis Nystatin cream and gentian violet paint.
• Treatment of the cause.
• Expected hospitalization is 1-2 weeks.
• On discharge advices: (Cleanliness, High protein foods and Follow-up visits).
Complications during treatment
• Transient increase in ICT due to fluid overload.
• Diarrhea due to carbohydrate or cow’s milk intolerance.
• Refeeding syndrome
• Hypokalemia, which is aggravated by IV glucose.

II. Rehabilitation:
• The initial phase of treatment ends when the child becomes hungry, and is now ready
to begin the rehabilitation phase. This usually occurs after 1 week.
• The aim of this phase is to achieve rapid catch up growth which requires high calories
(150cal/k/day + high protein intake (4gm/klday).
• This phase takes from 2-6 weeks until attaining 90% of expected weight for height.
III. Follow-up:
• As the risk of relapse is greatest soon after discharge the child should be seen after 1
week, 2 weeks, 1 month, 3 months and 6 months.
• At each visit, ask the mother about the child’s health, feeding and play activities.
• The child should be examined, weighed and measured and the results recorded.

Prognosis
1-Early prognosis (mortality): Depends on:
a. Age: Young age bad prognosis.
b. Cause: Irreversible cause bad prognosis.
c. Presence of complications: Bad prognosis.
d. Treatment: Early treatment good prognosis.
2-Late prognosis (morbidity):
 a. Growth: with early efficient treatment, the growth is almost normal.
b. Mentality: Defective intellectual development was found in malnourished children.
c. Liver cirrhosis usually doesn’t occur as the disease runs an acute course.
Mortality is high in infants with KWO especially with faulty management.

Marasmus
• Is a state of under nutrition resulting from prolonged deficiency of caloric intake as
well as deficiency of different food stuff.
• It is characterized by progressive loss of weight reaching below 60% of normal.
Causes:
I- Dietary: (It is the most common in Egypt). It is due to eating very little of otherwise
well balanced diet i.e. deficiency of all food components. It is due to:
1-Causes in milk-fed baby:
Quantitative (Breast fed & artificially fed):
*Scanty breast milk. *Delayed weaning.
*Small amount of feed. *Decreased frequency.
Qualitative (only in artificial fed):
*Diluted formula. *Cow milk allergy.
Feeding difficulties:
*Breast feeding (both baby and mother). *Artificial feeding (baby only).
2-Causes in weaned infant: Failure to maintain a well balanced diet.
II- Non dietary :( Secondary marasmus)5
Infections
*GE: the commonest, only if prolonged. *Chronic chest infections & TB.
*Chronic suppurative otitis media. *UTI.
*Congenital infections.
GIT causes:
*Congenital: cleft lip – cleft palate – congenital pyloric stenosis.
*Malabsorption syndromes.
Chronic systemic disorders:
*Cardiac: -Congenital heart diseases. -Intractable heart failure.
*Renal: -Renal tubular acidosis. -Obstructive uropathy and RF.
*Neurological.
*Hepatic cirrhosis.
*Congenital lung cysts.

5
If happened in childhood, usually it is called failure to thrive.
Metabolic disorders: e.g. Glycogen storage diseases – Galactosemia – PKU.
Endocrinal disorders: e.g. Juvenile D.M. – thyrotoxicosis.
Chromosomal anomalies due to: MR or associated with congenital anomalies.
Prematurity: due to Weak suckling + -Maldigestion and malabsorption
Clinical picture:
Onset is gradual with age between 6ms – 3yrs
1-Growth retardation:
• Starts as failure to gain weight, then loss of weight (body weight is less than 60%).
2-Loss of subcutaneous fat:
Marasmus is classified into 3 degrees according to loss of S. C. fat (figure 2):
1st degree: loss of S. C. fat from anterior abdominal wall.
2nd degree: loss of S. C. fat from over the limbs, trunk and buttocks redundant skin
3rd degree: loss of buccal pad of fat (SENILE face), he appears as skin over bone
3-Decreased muscle bulk:
• It is evident by decreased mid-arm circumference.
• Muscle wasting Stick like limbs.
4-Skin manifestation:
• Loss of skin elasticity.
• Skin is thrown into multiple folds especially in the groin.
• We can’t depend on loss of skin elasticity as sign of dehydration in marasmus.
5-Abdomen:
• Scaphoid abdomen: due to thin abdominal muscles.
• Visible peristalsis: due to thin abdominal muscles.
6-Irritability: due to hunger pain.
7-Hypothermia:
• Decreased caloric intake.
• Loss of S.C. fat with increased heat loss.
• Decreased muscle bulk with impaired shivering.
• Dehydration and electrolyte imbalance.
• Septicemic shock.
8-GI manifestations.
• Constipation: Due to decreased food intake.
• Starvation stools: Which are small in amount, greenish in color and loose in
consistency. It is formed of mucus & cellular debris.
• Diarrhea: Causes as kwo.
9-CVS:
 • Weak and slow pulse (unless with dehydration where the pulse is weak and rapid).
• Peripheral circulatory failure in the end stage.
10-Respiratory system:
• Shallow respiration due to weak respiratory muscles.
• Repeated chest infections.
11-Other vitamin and mineral deficiency: as KWASHIORKOR
12-Infection: as KWO
Complications:
1-Dehydration, electrolyte imbalance, acid-base disturbances and shock.
2-Marasmic kwashiorkor: if the patient is fed on CHO diet with deficient proteins.
3-Infections: GE – chest infection – UTI –moniliasis.
4-Purpura: it is a bad prognostic sign;
It is due to:
-Loss of subcutaneous support of blood vessels.
-DIC: from severe dehydration and fulminant infections.
5-Bleeding tendency.
6-Hypothermia.
7-Fasting hypoglycemia: due to lack of glycogen storage in the liver.
Investigations:
1. Blood picture: As KWO
2. Chemistry:
*Slight hypoproteinemia.
*increased immunoglobulins due to infection.
*Fasting hypoglycemia.
*Serum electrolytes may be disturbed due to GE and dehydration.
3. Urine examination:
*Ketonuria due to starvation ketosis.
*Increased urea due to hypercatabolic state.
*Urine culture & sensitivity (UTI may be a cause or a result).
4. Stool examination: *Parasites. *Steatorrhea. *Malabsorption.
5. Investigations for TB (with positive FH): *tuberculin test. *X rays. PCR test
Management:
1- Treatment of the cause.
2- Hospitalization in complicated cases.
3- Blood or plasma transfusion is not a routine rule (revised rules in hematology).
4- Emergency control of:
-Dehydration and shock. -Infections.
 -Hypothermia. -Hypoglycemia.
5- Vitamins and minerals especially B and C.
6- Dietetic management:
Amount: as KWO. In first degree marasmus, calculate milk according to the expected
weight.
In the second and third degree marasmus we calculate the amount midway between actual
and expected weight then gradually increase the amount according to gain of weight and
tolerance.
Frequency: every 2 hours.
Type of diet and Adjuvant therapy: as KWO
Prognosis: Depends on:
*Degree: bad in severe cases. *Age: worse in younger age.
*Infections: bad prognosis. *Cause: whether reversible or not.
Marasmic kwashiorkor
Causes:
*Marasmus marasmic kwashiorkor in presence of protein deficient diet.
*Diet deficient in calories with more deficiency of proteins.
Clinical picture:
*Loss of subcutaneous fat. *decreased Wt (> 40 % loss of body weight).
*Lack of moon face of kwashiorkor. *Edema.
*With or without skin and hair changes.
Treatment: *As kwashiorkor.

Prekwashiorkor
It is early stage of clinical kwashiorkor with the following manifestations:
- Decreased body weight. - Mental changes.
- Hair changes and may be skin changes. - No edema.
Nutritional edema
Edema due to hypoproteinemia which is caused by decrease protein intake.

Obesity in children
Childhood obesity is a condition where excess body fat negatively affects a child's
health or wellbeing. The diagnosis of obesity is based on BMI. The term overweight
rather than obese is often used in children as it is less stigmatizing.
Diagnosis:
Body mass index (BMI) is acceptable standard measure for determining obesity for
children two years of age and older. The normal range for BMI in children varies with
age and sex.
BMI = Weight in kilograms / (Height in meters)2
• Overweight – BMI between the 85th and 95th percentile for age and sex.
• Obesity – BMI ≥95th percentile for age and sex.
• Morbid obesity – BMI ≥120% for age and sex, or a BMI ≥35, or BMI z-score
≥2.33.
"Overweight" technically refers to an excess of body weight, whereas "obesity" refers to
an excess of fat.
Etiology
• Environmental factors
a) Increasing in glycemic index of b) Sugar-containing beverages
foods
c) Larger portion sizes for prepared d) Fast food service,
foods
e) Diminishing family presence at f) Decreasing structured physical
meals, activity,
g) Shortened sleep duration, h) Television viewing,
i) Medications as some psychoactive
drugs
• Genetic factors play a permissive role and interact with environmental factors to
produce obesity. Studies suggest that heritable factors are responsible for 30 to
50 percent of the variation in adiposity.
A few specific syndromes and single-gene defects which are linked to obesity in
childhood
a. Prader-Willi syndrome b. Pseudohypoparathyroidism
c. Down syndrome d. Turner syndrome
e. Laurence-Moon-Biedl (Bardet-
Biedl) syndrome
• Endocrine causes of obesity are identified in less than 1 percent of children and
adolescents with obesity. Most children with these problems have short stature
and/or hypogonadism eg (hypothyroidism, cushing syndrome, growth hormone
deficiency)
Metabolic programming refers to the concept that environmental and nutritional
influences during critical periods in development, particularly during first one thousand
days, can have permanent effects on an individual's predisposition to obesity and
metabolic disease
Complications
• Type 2 diabetes • Hypertension
• Hyperlipidemia • Pseudotumor cerebri.
• Fatty liver (NAFLD) is common • Cholecystitis
• Gynecomastia, • Sleep apnea and sleep-disordered
breathing
• Orthopedics (Slipped femoral
epiphysis and Bow legs)

Management
The initial management of overweight and obesity is lifestyle intervention, a combination
of diet, exercise, and behavioral modification. This combination can produce weight
losses of up to 10 percent
For children and adolescents who are overweight or mildly obese, the goal of maintaining
current body weight is appropriate, because this will lead to a decrease in BMI as the
child grows taller. If the child is in a phase of rapid linear growth, merely slowing weight
gain is more realistic and often improves weight status.
At higher degrees of obesity (BMI substantially above the 95th percentile), gradual weight
loss is safe and appropriate, depending on the child’s age and degree of obesity.
Prevention Messages: 5-3-2-1-0
• 5 or more servings of fruits and vegetables daily
• 3 structured meals daily—eat breakfast, less fast food, and more meals prepared at
home
• 2 hours or less of TV or video games daily
• 1 hour or more of moderate to vigorous physical activity daily
• 0: Limit sugar-sweetened beverages to “almost none
Dietary goals
• Limiting consumption of sugar-sweetened beverages, including juice
• Encouraging a diet with ample servings of vegetables and fruits
• Limiting eating at restaurants, particularly fast-food restaurants
• Limiting portion size
Activity goals
• Encouraging moderate to vigorous physical activity for one or more hours daily .
 • Limiting television and other screen time – no screen time for children under two
years of age; less than two hours daily after age two
Medications
• Orlistat >12 years inhibit lipase enzyme in GIT

Rickets AND VITAMIN D

• Rickets is a primary disturbance of calcium and phosphorus metabolism that results
in failure of mineralization of growing bone.
• Osteomalacia is failure of mineralization of mature bone.
• Osteoporosis is equal loss of bone volume and minerals (e.g. with steroid therapy).
Vitamin D (revise your biochemistry and physiology courses)
Requirement of vitamin D
Infants and children 400 IU/day
LBW, pregnant & lactating mothers 800 – 1000 IU/day
Classification of Rickets
VITAMIN D DISORDERS
1. Nutritional or Congenital vitamin D deficiency
2. Secondary vitamin D deficiency as Malabsorption, Increased degradation or
Decreased liver 25-hydroxylase
3. Vitamin D–dependent rickets type 1
4. Vitamin D–dependent rickets type 2
5. Chronic renal failure
CALCIUM DEFICIENCY
1. Low intake: Diet or Premature infants (rickets of prematurity)
2. Malabsorption: Primary disease or Dietary inhibitors of calcium absorption
PHOSPHORUS DEFICIENCY
Inadequate intake: Premature infants (rickets of prematurity) or Aluminum-containing
antacids
RENAL LOSSES:
1. X-linked and AD hypophosphatemic rickets
2. Hereditary hypophosphatemic rickets with hypercalciuria
3. Fanconi syndrome
[Link] renal tubular acidosis

VITAMIN D DEFICIENCY RICKETS

Etiology
A) Rachitogenic diet
1. Cow milk
2. Prolonged breast milk without supplementation of Vit. D.
3. Cereals rich in phytates & phosphates.
4. High dietary levels of stearic & palmitic acids which are poorly absorbed.
5. Decreased acidity (poor intake of Vit. C).
6. Increased alkalinity (e.g. excess beverages).
B) Inadequate exposure to sunlight
1. Glass windows & high buildings. 4. Cloudy and foggy weather.
2. Overwrapped infants. 5. Dark skin infants.
3. Industrialized countries with heavy pollution.
Pathology
A) Active rickets
1- At growth plate
Normally the growth plate contains 4 different zones:
a) Zone of resting cartilage formed of a single layer of cells.
b) Zone of proliferating cartilage formed of 4-6 layers of proliferating cartilage. It is
bloodless and calcium free.
c) Zone of provisional calcification (ZPC) where the chondrocytes die and calcium &
phosphate are precipitated in the matrix.
d) Zone of ossification, where osteoblasts and capillaries appear. The osteoblasts
deposit the organic bone matrix (osteoid).
In rickets, the cartilage cells fail to complete their cycle. The result is excess disorganized
proliferating cartilage, loss of ZPC & excess osteoid tissue.
2- Beneath the periosteum: There is resorption of pre-existing cortical bone with increased
osteoid tissue over the entire shaft.
B) Healing rickets: ZPC reappears but it is separated from the shaft by osteoid tissue.
C) Healed rickets: Osteoid tissue is mineralized uniting with ZPC, thus the growth plate
appears thick.
Clinical Picture
A) Early manifestations
1. Increased sweating, anorexia & irritability.
2. Craniotabes. It is abnormal softness of the skull due to reduction of mineralization
of its outer table. It is detected by pressing firmly over the occiput or posterior
parietal bones. A ping-pong ball sensation will be felt. It usually disappears before
the end of the first year.
3. Rachitic rosary. It is prominent enlargement of the costochondral junctions seen and
felt as a row of beads about the size of cherries.
4. Enlargement of wrists and ankles due to epiphyseal enlargement.
B) Advanced manifestations
I) Skeletal signs
Head
1. Frontal and parietal bossing a box-like head (caput quadratum).
2. Delayed closure of the anterior fontanelle.
3. The size of the skull is larger than normal and may remain so throughout life.
4. Delayed eruption of deciduous teeth and defects of the dental enamel and extensive
caries.
Thorax
1. Rachitic rosary.
2. Longitudinal grooves developed posterior to the rosary with flattening of sides of
chest cage.
3. Harrison sulcus: horizontal groove along the lower border of the chest
corresponding to the line of attachment of the diaphragm with flaring of the costal
margin below.
4. Thoracic deformities including pigeon chest deformity
Spinal column
1. Smooth kyphosis of the dorso-lumbar region while sitting due to laxity of spinal
muscles and ligaments. It disappears if the child is suspended from his shoulders.
Lordosis of the lumbar region may be seen while standing.
2. Mild to moderate degrees of scoliosis are common.
Pelvis
1. Narrow pelvic inlet due to forward projection of the premonitory.
2. Narrow pelvic outlet due to forward displacement of the sacrum. In the female, if
these changes become permanent, they may lead to obstructed labor.
Extremities
1. Enlargement of wrists and ankles.
 2. Marfan sign is a transverse groove that is felt over the tibia and fibula just proximal
to the ankle. It is due to disorderly deposited osteoid tissue in the centers of
ossification of the malleoli and the ends of tibia and fibula.
3. Knee deformities:genu valgum (knock knees), genu varus (bow legs) and genu
recruvatum (over extension).
Bending of soft shafts of weight bearing long bones as femur, tibia and arms as the infant
crawls.
NB: Collectively, these deformities may result in rachitic dwarfism.
II) Non skeletal signs
1. Hypotonia: this is manifested by:
a) Delay in gross motor development as sitting, standing and walking
b) Pot-belly due to weakness of abdominal muscles, gastric and intestinal walls.
Downward displacement of the liver due to deformed thoracic cage and lax
ligaments exaggerates the pot-belly.
c) Acrobatic rickets (hyperextensibility of joints & flaccidity of whole body).
2. Tetany: It is uncommon in nutritional rickets, (occur during infections or
following massive doses of vitamin D without calcium supplementation).
3. Pseudoleukemia infantum: Manifesting as rickets, anemia & splenomegaly. It is
secondary to the effects of Vit. D lack on the hemopoietic system.
Complications
1. ARI and GE. 3. Deformities and dwarfism. 5. Tetany.
2. Anemia. 4. Obstructed labor in adult life 6. Dental caries.
Laboratory investigations
1. Serum calcium is low normal (N 9-11 /ml) due to secondary hyperparathyroidism.
2. Serum phosphorus is low 1.5 – 3 mg/dl (N 4.5 – 6.5 mg/dl) as parathormone
decrease phosphate renal re-absorption.
3. Serum alkaline phosphatase activity (ALP) is high > 500 IU/L (N 145 – 200 IU/L)
due to increased osteoblastic activity. It is the first laboratory parameter to change
in rickets and last to return to normal after complete healing.
4. Serum parathormone (PTH) is high & urinary c-AMP is increased.
5. Serum 25(OH)D3 is low and serum 1,25(OH)2D3 is low (N 25 – 45 pg/ml).
6. Generalized aminoaciduria.
Radiological changes (figure 3,4 and 5 )
I) Active rickets
(1) At growth plate (wrists & ankles)
1. Loss of ZPC.
 2. The distal ends of long bones become broad, concave (cupping) and frayed in
contrast to normally sharply demarcated slightly convex ends.
3. Increased distance between ends of radius & ulna & carpal bones because the
large rachitic metaphyses which is not calcified does not appear in the x-ray.
(2) At the shaft
1. Rarefaction (decreased bone mineralization).
2. Periosteal elevation (double contour along lateral outline).
3. Greenstick fractures which are often asymptomatic and bone deformities.
II) Healing rickets: Appearance of ZPC separated from shaft by rachitic metaphysis.
III) Healed rickets: Ossification of the rachitic metaphysis which become continuous
with ZPC forming straight thick plate.

Fig (3): Active rickets Fig (4): Healing rickets Fig (5): Healed rickets
with green stick fracture (Ain Shams children’s (Ain Shams children’s
(Ain Shams children’s Hospital) Hospital)
Hospital)
Prevention
1. Adequate exposure to direct sunlight in haze free areas.
2. Adequate oral intake of vitamin D for infants and pregnant & lactating mothers.
Treatment
1. Vitamin D in daily oral dose (2000 – 6000 IU) produces healing in 2-4 weeks.
2. Alternatively Stoss therapy with a huge dose (600,000 IU) can be given IM.
3. Supplementation of calcium is necessary to avoid tetany.
Other types of rickets
1- Calcium deficiency (with secondary hyperparathyroidism)
1. Early weaning
2. Diet with low calcium content
3. Diet with high phytate, oxalate or phosphate (reliance on green leafy vegetables)
4. Children with unconventional diet (children with milk allergy)
5. Transition from breast milk or formula to juice, soda, calcium poor soy milk
6. Intravenous nutrition without adequate calcium intake
7. Calcium malabsorption (Celiac disease, abetalipoproteinemia, small bowel resection)
2- Primary phosphate deficiency (no secondary hyperparathyroidism)
1. Familial hypophosphatemia.
2. Fanconi syndromes.
• Generalized
• Cystinosis (Lignac syndrome)
• Oculo-cerebro-renal dystrophy (Lowe syndrome)
3. Renal tubulo-acidosis (type I & II).
Familial Hypophosphatemia (Vitamin D Resistant Rickets)
• This XLD disease is the commonest non nutritional form of rickets. It is due to defects in proximal
tubular reabsorption of phosphate.
• It presents with bowing of legs, waddling gait and adult height in untreated patients is 130-135 cm.
Serum phosphorus is markedly low and urinary phosphorus is large.
• Massive oral intake of phosphorus (1-4 g/day in divided doses) coupled with calcitriol.
Fanconi Syndromes
• It is due to abnormality in proximal renal tubular function
• It may be due to inborn errors of metabolism, environmental toxin or idiopathic.
• Fanconi syndrome is characterized by early onset of growth failure, rickets, vomiting, polydypsia,
polyuria and constipation. There is generalized aminoaciduria, phosphaturia and renal glycosuria with
normal serum glucose.
• Treatment is by calcitriol and oral phosphate supplementation.
Metabolic errors with Fanconi syndrome
Cystinosis (Lignac syndrome)
• Cystinosis is an AR disease presenting as Fanconi syndrome with the additional finding of abnormal
accumulation of cystine in spleen, liver, bone marrow, lymph nodes, kidneys, cornea and conjunctiva.
The infantile form ends by renal failure.
• Treatment is similar to that of primary Fanconi syndrome together with cysteamine to slow progression
of renal failure.
Oculo-cerebro-renal dystrophy (Lowe syndrome)
• It is an XLR disease. Early in life, eye affection (glaucoma followed by cataract) and mental retardation
predominate. Fanconi syndrome becomes apparent later.
Renal Tubular Acidosis (RTA): RTA is classified into
i) Proximal RTA (type II): resulting from reduced proximal tubular reabsorption of bicarbonate.
ii) Distal RTA (type I): resulting from reduced hydrogen ion secretion by distal RT.
• RTA may be sporadic or inherited. Rickets in RTA is due to dissolution of bone as calcium carbonate
in the bone serves as a buffer against metabolic acidosis.
• RTA is characterized by hypokalemic hyperchloremic metabolic acidosis. The low serum (K) is due to
exchange for Na to compensate for the lost NaHCO3. The high serum Cl is due to stimulated Cl
reabsorption to compensate for contraction of extracellular fluid volume resulting from lost NaHCO 3.
• RTA is treated by giving oral bicarbonate, phosphate and calcitriol.

3- Renal Osteodystrophy (ROD)

Alteration in skeletal growth in children with chronic renal failure (CRF).
Etiology & pathogenesis
1- vitamin D deficiency secondary to impaired renal synthesis of 1,25(OH)2D3.
2- secondary severe hyperparathyroidism resulting from phosphate retention
Clinical manifestations
1. Symptoms & signs of CRF in childhood + deformities (see nephrology).
2. Tetany is rare despite hypocalcemia due to metabolic acidosis.
Investigations
1. Serum P is high, serum Ca is low, ALP activity & serum PTH are very high, together with
impairment of renal function tests.
2. Radiological findings of rickets together with manifestations of osteitis fibrosa due to 2 ry
hyperparathyroidism (subperiosteal erosions of phalanges & distal clavicle).
Treatment
1. Renal transplantation is a radical treatment of ROD.
2. If this is not feasible, ROD can be managed by:
i. Control hyperphosphatemia (dietary restriction, phosphate binders and dialysis).
ii. Adequate supplementation of calcium and calcitriol.
4- Vitamin D Dependent Rickets
VDDR type I: AR disease due to deficiency of renal 1- hydroxylase. Tetany usually occurs by 3-6 month
of age and affected children develop dental enamel hypoplasia.
VDDR type II: AR disease due to end organ resistance to 1,25(OH)2D3. There is early onset of tetany and
rickets. Some children develop short stature and alopecia totalis.
5- Hypophosphatasia
• It is an AR disease secondary to deficiency of alkaline phosphatase activity.
• The congenital form is lethal. Hypophosphatasia tarda is characterized by rickets, bow legs, short stature,
hypercalcemia and increase phosphoethanolamine in urine.
HYPERVITAMINOSIS D
Hypervitaminosis D is usually iatrogenic and appears after intake of large doses of vitamin
D for 1-3 months.
Clinical manifestations
1. Irritability, pallor and weight loss.
2. Polydypsia, polyuria and dehydration.
3. Anorexia, nausea & vomiting and constipation.
4. In severe cases, metastatic calcification & nephrocalcinosis.
Treatment
1. Discontinuation of vitamin D.
2. Decrease intake of calcium by oral aluminum hydroxide.
3. In severe cases, prednisone (2 mg/kg) as glucocorticoid appears to be antagonistic
to vitamin D in calcium transport.
TETANY
Tetany is a state of hyperexcitability of central and peripheral nervous system resulting
from abnormal concentrations of ions in the fluid bathing nerve cells. These abnormalities
include hypocalcemia, hypomagnesemia and alkalosis.
Etiology
I) Hypocalcemia
A) Hypoparathyroidism
1. Early neonatal hypocalcemia (first 72 hours), infant of diabetic mother, preterms,
IUGR, perinatal asphyxia.
2. Late neonatal hypocalcemia (5–10 days): A high phosphate food as cow milk
depresses serum calcium level through the deposition of calcium in bone while the
infant parathyroid glands are not yet able to respond by increasing PTH.
3. Aplasia or hypoplasia of parathyroid e.g. DiGeorge syndrome.
4. Surgical hypoparathyroidism as a complication of thyroidectomy.
5. Infiltrative lesions as in hemosiderosis.
6. Autoimmune.
7. Familial.
B) Tetany of vitamin D deficiency
1. VD deficiency + infection or stoss therapy without supplementation of calcium.
2. VDDR type I or II.
3. Steatorrhea & severe liver disease.
II) Hypomagnesemia
1. Chronic diarrhea.
2. Exchange transfusion with citrated blood.
3. Total parenteral nutrition without sufficient Mg.
4. Nephrotoxic medication and diuretic therapy.
III) Alkalotic tetany (see gastroenterology chapter)
Clinical manifestations
Manifest tetany (serum calcium  7 mg%)
1. Brief recurrent convulsions: usual manifestation in neonates & young infants.
2. Carpopedal spasm: wrists are flexed, fingers are extended and adducted thumbs.
3. Laryngospasm: manifesting as inspiratory obstruction and a crow.
4. Sensory parathesias, numbness and tingling.
Latent tetany (serum Ca 7-9 mg%)
1. Chvostek’s sign: tapping the facial nerve anterior to the external auditory meatus
→ twitching of orbicularis oris.
2. Trousseau sign: production of ischemia of motor nerves of the arm by
sphygmomanometer calf → twitches and carpal spasm.
 3. Peroneal sign: tapping the peroneal nerve where it passes over the head of fibula
→ dorsiflexion and abduction of the foot.
4. Prolonged QT interval.
Treatment
1- Emergency treatment IVI of 10% calcium gluconate 2 ml/kg slowly while monitoring
for bradycardia.
2- For maintenance, calcium lactate, 10-12 g/day.
3- For convulsive seizures, oxygen inhalation is indicated.
4- In cases of vitamin D deficiency tetany: Vitamin D 2000 – 6000 IU/day for nutritional
rickets and calcitriol 0.25 – 1 g/day for resistant rickets.
5- For hypomagnesemia: IMI of MgSO4 0.2 ml of 50% solution.
6- For psychogenic overventilation: re-breathe into a bag to increase PCO2.

Further extracurricular readings (may help you if prepared for an

international certificate)
1- Nutrition and cancer
2- Nutrition and immunity
3- Nutrition in different system disorders
References
• WHO. Guideline: Updates on the management of severe acute malnutrition in infants and
[Link]: World Health Organization; 2013.
• WHO/UNICEF. Acceptable medical reasons for use of breast-milk substitutes. World Health
Organization, Geneva,2008.
• WHO/UNICEF. Planning Guide for national implementation of the Global Strategy for Infant
and Young Child Feeding. Geneva, World Health Organization, 2007
[Link]
• WHO, UNICEF, WFP, UN-SCN. Community-based management of severe acute malnutrition:A
joint statement. Geneva, World Health Organization, 2007
[Link]

MCQs
Choose ONE answer only :
1. Compared to breast milk, cow’s milk contains:
a) less protein
b) more lactose
c) less minerals (ash)
d) more phosphorus
e) less calcium
2. The criteria of good attachment for breast-feeding include the following EXCEPT:
a) Mother’s first finger should support the breast
b) Infant’s chin should be touching the breast
c) Infant’s mouth should be widely open
 d) Lower lip should be turned outwards
e) More areola should be visible above than below the mouth
3. In exclusively breast-fed infants, the following is true for complementary feeding EXCEPT:
a) It should not be started before the end of 6th month
b) If weight gain is not satisfactory we can start complementary feeding by the end of 4th month
c) Start by replacing one milk feed by the new foreign food
d) The new food is given gradually and in small amounts at first
4. The following associations with kwashiorkor are true EXCEPT:
a) infection is always present
b) hypothermia
c) hypoglycemia
d) low total body potassium
e) low total body sodium
5 - The best source of Iron for a 2-mo, infant of a normal mother is ;
a) Cows milk.
b) Breast milk.
b) Medicinal iron.
c) Milk adapted formula.
d) None of the above.
6 - All are indications of adequate breast milk supply except:
a) The infant appears satisfied and contented after feeding.
b) The infant sleeps about 2 hours after feeding.
c) Adequate gain in weight.
d) A negative let-down reflex.
e) Normal stools in number and consistency.
7 - An absolute contraindication to breast-feeding is:
a) Erythroblastosis fetalis.
b) Inverted nipples.
c) Mastitis.
d) Cigarette smoking.
e) Phenyl Ketonuria.
8 - The main protein in breast milk is :
a) Casein.
b) Thyroglobulin.
c) Lactoferrin.
d) Lactalbumin.
e) Gamma globulin.
9 - In adapted formula milk, the following modifications are true except:
a) Calcium/phosphorus ratio is optimized to be 2/1 as in breast milk.
b) Proteins are modified to contain less caseinogen and higher whey proteins.
c) Sodium chloride content of cow milk is increased to approximate that of breast milk.
d) The amount of proteins, carbohydrates, and fat are approximate to human milk compositions.
e) The cow milk fat is partially substituted by vegetable.
10 - All are Common causes of death in marasmus except:
a) astroenteritis and dehydration.
b) Encephalopathy.
c) Hypoglycemia.
d) Intercurrent infections.
e) Hypothermia.
11 - The following are possible features of infant overfeeding except:
a) Repeated colics and vomiting.
 b) Hyperglycemia and glucosuria.
c) Diarrhea with bulky stools.
d) Polyuria and sore buttocks.
e) Dyspnea with excessive sweating.
12 - The following anti-infective properties of breast milk are true except
a) Breast milk is naturally sterile .
b) Contains interferon producing cells.
c) Contains lactoferrin which is a bacteriostatic iron binding protein.
d) Contains antibodies of the IgA class against numerous viruses and bacteria.
e) Contains "Bifidus factor " which prevents intestinal colonization & multiplication of
Lactobacillus bifidus.
13 - Hepatomegaly in kwashiorkor is due to:
a) Biliary obstruction
b) Excessive glycogen storage
c) Fatty infiltration
d) All of the above
14- Skin changes in Kwashiorkor are due to:
a) Deficiency in trace elements
b) Deficiency in essential amino acids specially sulfur containing types
c) Deficiency in essential fatty acids
d) Vitamin deficiency specially vitamin A
e) All of the above
15 - The earliest change in growth chart in nutritional marasmus is:
a) Flat (plateau) weight curve
b) Low skin fold thickness
c) Decreased mid arm circumference
d) Decreased body length
16 - Colostrum has all of the following properties except:
a) It has a higher fat and sugar content than mature milk
b) It has a higher protein content than mature milk
c) It is richer in vitamin A, compared with mature milk
d) It contains protective antibodies
17 - All of the following statements are true EXCEPT:
a) Xerophthalmia in a 3-years old child is a sign of vitamin A deficiency.
b) Vitamin A overdose can cause raised intracranial pressure.
c) Scurvy is common in breast fed infants.
d) Vitamin D deficiency in infants can present with convulsions.
e) Babies fed on goat’s milk require supplements of folic acid.
18 - The earliest bony change in infantile rickets is:
a) Bowing of legs.
b) Green stick fractures.
c) Epiphyseal enlargement in wrists & ankles
d) Craniotabes
e) Frontal and parietal bossing
19 - Regarding breast-feeding, which statement is true?
a) Hind-milk is the sugar rich milk at the end of a breast milk feed.
b) Oxytocin is the hormone responsible for the let-down reflex.
c) Breast feeding should be stopped when breast engorgement develops.
d) Breast milk is rich in -lactoglobulin.
e) Regular feeding is the best method of lactation.
20 - Pathological changes in kwashiorkor include all except:
 a) Edema of limbs.
b) Growth retardation.
c) Fatty infiltration of the liver.
d) Generalized muscle wasting.
e) Generalized atrophy of subcutaneous fat.
Key answers
1 d 6 d 11 B 16 a
2 a 7 e 12 E 17 c
3 c 8 d 13 C 18 d
4 e 9 c 14 E 19 b
5 b 10 b 15 A 20 e