Вы находитесь на странице: 1из 16

1

Nutrition
























2

Nutritional requirements of infants & children:
1-Calories: -in the 1
st
yr: 90-110 kcal/kg/day.
-in the 2
nd
yr: 70 kcal/kg/day. -at puberty: 50 kcal/kg/day are needed.
2-Water: -in the 1
st
yr: 120-150 ml/kg/day. -in the 2
nd
yr: 90-100 mg/kg/day.
3-Proteins:
-daily needs: 2-3 gm/kg/day proteins of high biological value to supply amino acids required
for growth & metabolic processes.
-should provide about 15% of total caloric intake. -each 1 gm proteins 4 Kcal.
4-Fats:
-should provide about 30-35% of total caloric intake. -each 1 gm fats 9 Kcal.
-value: polyunsaturated fatty acids as linolenic acid are essential for skin health
& brain development (essential FAs cant be formed by the body).
5-Carbohydrates:
-should provide about 50-55% of total caloric intake. -1 gm CHO 4 Kcal.
-can be synthesized from fats or proteins.
6-Vitamins:
-value: essential to maintain good health,
many vitamins act as co-enzymes in metabolic processes.
Vitamin Daily requirements
A 1500 U
B1 0.5 mg
B2 0.5 mg for infants, 1 mg for children
B6 0.6 mg
B7 5 mg
Folic acid 50 ug
B12 0.5 ug
C 30 mg for infants, 50 mg for children
D 500 U for full terms, 1500 U for premature
E 5 mg
K 5 ug for infants, 15 ug for children
7-Minerals:
-value: as vitamins.
-the main extracellular minerals are Na & Cl, the main intracellular minerals are K, Mg, P.
-Ca & P are the main minerals of the skeleton.
Minerals Calcium Phosphorus Iron Zinc Iodine Selenium
Infants 500 mg 300 15 mg 5 mg 50 ug 10 ug
Children 800 mg 900 15 mg 10 mg 150 ug 20 ug
Infant feeding
Initiation: soon after birth or within 1-4 hrs to:
1-maintain normal metabolism. 2-promote maternal-infant bonding.
3-prevent dehydration fever. 4- risk of hypoglycemia, hyperkalemia, Hyperbilirubinemia.
Types:
1-Breast feeding. 2-Artificial feeding.
3-Mixed feeding: may be:
a-complementary feeding: mother completes one or more of breast feeds by formula given
just after the breast.
3

b-supplementary feeding: mother replaces one or more of breast feeds by formula e.g. when
mother is exhausted or breast milk is scanty.
Exclusive breast feeding:
-Def: no foods or drinks other than breast milk are given to the baby.
no pacifiers, no artificial teats are given.
-Duration: it should continue during the 1
st
4-6 months of age
then continue with other foods up to 2 yrs.
Breast feeding
Advantages:
A-To the infant:
1-Supply proper nutrients to the infant when mothers diet is sufficient & balanced.
2-Easily digestible due to low content of casein.
3-Less allergy & intolerance. 4-Always available at proper temperature.
5-Fresh & free of contaminating bacteria.
6-Human milk contains bacterial & viral antibodies.
7-Contains secretory IgA that prevents micro-organisms from adhering to intestinal mucosa.
8-Contains macrophages that can synthesize complement, lysozyme & lactoferrin enhance
infant immunity.
9-A source of lactoferrin inhibits growth of E.coli in the intestine.
10-Stool of breastfed infant has lower pH than that of cow milk-fed infant
inhibits bacterial growth.
11-Contains lipase digests fat, kills G.lamblia & E.histolytica.
12-Passive transfer of T-cell immunity.
13-It contains pre-biotic: non-digestible food ingredients that may stimulate growth & activity
of certain beneficial bacteria in the colon.
14-It contains pro-biotic: live beneficial micro-organisms.
B-For the mother:
1-Helps uterus involution. 2-Less effort, no time for preparation.
3-The cheapest food. 4-Lowers the incidence of cancer breast.
5-Helps mother to return to pre-pregnancy weight sooner.
6-Psychogeneic advantages of breast feeding for both mother & infant.
Management of breast feeding:
1-Instructions given to mother during pregnancy:
-wash your breasts with water. -keep the nipple clean. -check for flat or inverted nipples.
2-After delivery:
-start breast feeding soon after birth or within 1-4 hrs.
-breast feeding every 2-3 hrs, 20-30 min each.
-avoid giving bottles or pacifiers in these early weeks.
-rooming in is preferred so you can feed when baby seems hungry.
-make sure you are holding baby correctly.
Technique of breast feeding:
1-Holding the baby:
-mother should sit well supported & comfortable.
-baby should be semi-upright. -turn your babys whole body toward you.
-bring your babys chest close to your chest.
-nipples should be right at babys mouth. -pillow on your lap for support your arm.
4

2-The baby is hungry when:
-sucking on their hands. -rooting (opening mouth wide searching for milk). -fussing.
3-Let-down or milk-ejection reflex:
-sucking or psychological stimuli associated with nursing oxytocin secretion from posterior
pituitary contraction of myo-epithelial cells surrounding breast alveoli squeezing milk into
larger ducts to be available to sucking infant.
Establishing & maintaining milk supply:
1-Regular & complete emptying of breasts is the main stimulus to milk secretion.
2-Breast secretions are decreased by fatigue, worry & unhappiness.
3-Both breasts should be used at each feeding in the early wks then breasts can be alternated.
4-During the 1
st
month, breast feeds are given on demand (every 2 hrs)
5-During the following months: breast feeding every 3-4 hrs
6-Milk supply is sufficient & adequate if:
-number of breastfeeds: 8-12/24 hrs.
-baby is satisfied after feeding. -sleeps 2-4 hrs after feed.
-adequate weight gain (about 100 gm every 4 days during the 1
st
4 months).
-at least six wet diapers & 2 soft stools/24 hrs.
Contraindications of breast feeding:
A-Maternal causes:
1-Infectious diseases as active TB & AIDS.
2-Chronic cachectic conditions as cancer, congestive HF & uncontrolled DM.
3-Neuropsychiatric conditions: epilepsy, psychosis.
4-Breast conditions as cancer breast.
5-Pregnancy after 1
st
trimester.
6-Temporary causes: acute maternal illness, fissured nipples,
mastitis, abscess, engorged breast.
B-Infant causes:
1-Metabolic diseases as galactosemia & PKU.
2-Congenital anomalies as complete cleft palate.
3-Temporary causes as thrush Stomatitis & cleft lip.
Colostrum
Def: secretion of breasts during the latter part of pregnancy & for 2-4 days after delivery.
Characteristics:
1-Color: deep lemon yellow. 2-Reaction: more alkaline than mature breast milk.
3-Specific gravity: 1040-1060 (mature 1030).
4-Daily secretion: 10-40 ml.
5-Components:
-more proteins, more minerals, more immunologic factors than mature breast milk.
-less CHO & fats.
6-Fate: it is followed by transitional form of milk that gradually assumes characters of mature
breast milk by the 3
rd
- 4
th
week.
N.B. difference between mature human milk & cow/buffalo milk: table p.47




5

Artificial feeding
Aim: supply modified animal milk as a substitute to breast feeding.
Indications:
1-Contraindications of breast feeding. 2-Death or absence of the mother.
3-Institutes. 4- of breast milk. 5-Twins.
The main problems in animal milk:
1-Formation of tough curd due to excessive casein.
2-High fat content with bigger fat globules, higher content of volatile fatty acids
& less essential fatty acids.
3-High mineral content. 4-Low iron content.
Humanization of animal milk:
-Def: modification of fresh animal milk making it more suitable to infants & nearer to
composition of human milk.
-Steps: 1-Dilution: by mixing cow milk & water (2 : 1), buffalo milk & water (1 : 1).
2-Adding: 5 gm sugar to each 100 ml of the mixture.
3-Boiling: for 15 min for modification of casein & sterilization.
Disadvantages of artificial feeding:
1-Malnutrition: due to errors in milk preparation.
2-Contamination: with high incidence of diarrhea & its related complications.
3- incidence of bacterial & viral infections.
4-Intolerance & allergy. 5-High expenses. 6-Loss of Psychological benefit of breast feeding.
Advantages of artificial feeding:
-The ability to produce especially modified formulas for medical conditions
as PKU, galactosemia & lactose intolerance.
Milks used in formulas:
I-Dried powdered milk:
1-Dried humanized milk:
-composition: nearly identical to human milk in amount of proteins, CHO, fats,
vitamins & minerals.
-supplementation with extra iron, vitamin C & vitamin D
-recently, essential FAs, lactose, amino acid content of these milks
have been made very close to human milk.
-However, breastfed infants show better growth results.
2-Dried follow-on milks:
-are used after the age of 6 months. -higher protein content than humanized milk (2.5 gm/dl).
-usually supplemented with iron to prevent iron deficiency anemia.
3-Dried premature infant milk:
-used in LBW infants (below 2000 gm). -provide higher calories (80 Kcal/oz).
-contains more Na & minerals to compensate for higher urinary loss of solutes
in premature infants.
4-Dried whole (full cream) milk:
-fat content adjusted to 3.5 %. -used after the 1
st
year of life.
II-Fluid milks:
1-Raw cow milk:
-shouldnt be used for infant feeding except after humanized.
-forms large curd in stomach. -slowly digested.
6

-easily contaminated with pathogenic organisms.
2-Pasteurized milk:
-pasteurization: heating milk to 65c for 20 min then rapid cooling to 10c.
-benefits: a-destroys most of pathogenic bacteria.
b-modification of casein formation of smaller less tough curd in the stomach.
-pasteurized milk shouldnt be boiled for infant feeding.
3-Evaporated milk:
-unopened cans can be kept for months without refrigeration.
-softer casein curd produced in stomach.
-homogenization of fat smaller curd formation.
-less allergenic than fresh milk.
4-Condensed milk:
-sweetened with CHO content of about 60%. -readily digestible.
-only used for short periods when high-calorie diet is required.
5-Goats milk:
-used in many countries including rural Egypt.
-can be used to manage cow milk allergies. -contains less Na, more unsaturated FAs.
-Its fat is more digestible, its curd has lower tension than that of cow milk.
-low in folic acid, so if used alone megaloblastic anemia due to folic acid deficiency.
-susceptible to contamination by brucella species.
Modified milks for disease states:
1-Lactose-free milk: for cases of galactosemia or lactose intolerance.
2-Phenylalanine-low milk: for cases of PKU.
3-Low calcium milk: for cases of hypercalcemia.
4-Soya milks: for cow milk protein allergy.
5-Milk protein: powdered protein used to protein content of some formulas
in premature or debilitated infants or in cases of diarrhea.
6-Elemental formula:
-prepared from purified chemical elements (free glucose, amino acids, essential FAs).
-uses: a-children with malabsorption due to 1ry disease or extensive small bowel resection.
b-severe persistent diarrhea, inflammatory bowel disease, short bowel syndrome.
N.B. technique of artificial feeding: p.52
Underfeeding
Def: -infant receives insufficient amount of milk.
-if continues untreated frank malnutrition.
C/P:
A-Symptoms:
1-Restlessness & excessive crying. 2-Lack of comfortable sleeping without apparent cause.
3-Failure to gain weight adequately. 4-Constipation with small hard infrequent stools.
5-Starvation diarrhea may occur (infant may pass frequent small loose greenish stools).
6-Vomiting: due to excessive swallowing of air from empty breast.
7-Colic: when swallowed air reaches the intestine.
B-Signs:
1-Poor weight gain or weight loss. 2-Skin: dry, wrinkled with disappearance of SC tissue.
3-Signs of dehydration may present (see diarrhea).
4-Deficiency of vitamins A, B, C, D & iron may occur.
7

Diagnosis:
1-Clinical: symptoms & signs of underfeeding.
2-Test weighing: average weight gain of about 100 gm every 4 days
during the first 4 months of life is considered adequate.
3-Test feed:
-infant is weighed just before & just after feed without changing clothes.
-the difference represents the amount of milk taken.
-better done for 3 days and average is taken.
-adequate milk intake without corresponding wt gain indicates underfeeding due to
malabsorption or systemic disease & investigations should be done to detect the cause.
TTT:
1-Increasing fluid & caloric intake: by complementary or supplementary feeds.
2-Correction of vitamins & minerals deficiencies.
3-Teaching the mother the ideal method of infant feeding.
4-Management of underlying cause if detected.
Overfeeding
Causes: may occur in hot weather due to excessive thirst satisfied by more breast or formula
feeding, usually leads to obesity.
C/P:
1-Overweight. 2-Regurgitation & vomiting. 3-Discomfort & abdominal distension.
4-Diarrhea.
Types: overfeeding may be quantitative or qualitative:
1-Diets too high in fat: delay gastric emptying, abdominal distension & discomfort
may cause excessive wt gain.
2-Diets too high in CHO: undue fermentation in the intestine distension & flatulence
too rapid wt gain.
3-Such diets may be deficient in essential protein, vitamins & minerals.
Diagnosis: 1-Test weighing. 2-Test feeds.
TTT:
1-Increasing intervals between feeds. 2-Giving baby low calorie fluids in-between feeds.
3-Strict follow-up of body wt gain to make necessary changes in caloric intake.
Weaning
Def: -is to accustom infant or child to take food materials other than milk.
-not recommended before the age of 4-6 months.
Indications of sudden weaning:
1-Death of the mother. 2-Serious illness of the mother. 3-Pregnancy (after the 4
th
mo).
Aim of weaning:
1-Supply sufficient nutrients in which milk is deficient as iron, vitamin B1, vitamin D.
2-Train GIT to digest starch & more solid foods.
3-Educate the child independence by using cup or spoon.
4-Cover the extra needs of calories (infant cant tolerate > 1 liter of milk/day).
General rules of weaning:
1-Dont start weaning in very hot or very cold weather.
2-Dont start weaning during illness, early convalescence or just after vaccination.
3-Start by one type of food at a time, given every day till baby becomes accustomed to it.
8

4-Dont add new type of food before 1-2 wks.
5-New food is started once a day in a diluted small amount, then gradually according to
babys tolerance & appetite.
6-Stop the new food if persistently disliked by the baby or if allergy or diarrhea occurs.
7-Baby cant yet swallow efficiently food is frequently pushed out by the tongue
(this is not a dislike).
Sequence of food introduction:
Age Introduced food
The end of 4
th
mo Milk products as yoghurt - mashed fruits & fruit juices.
4
th
-6
th
months Cereals, potatoes, biscuits - strained cooked fruits - raw ripe mashed banana.
The end of 6
th
mo Egg yolk (hard-cooked with little salt).
The end of 7
th
mo Vegetables (supply iron, minerals, vitamin B complex).
The end of 8
th
mo Meats, liver well-cooked & ground with rice & vegetables.
9
th
- 12
th
months -other foods as poultry, fish, egg white (with precaution).
-gradual amount of previously introduced foods.
Malnutrition
Causes:
1-Improper or inadequate food intake:
-insufficient food supply. -poor dietary habits. -emotional factors.
2-Inadequate food absorption.
3-Increased food requirements:
-stress. -disease. -antibiotic TTT.
-catabolic or anabolic drugs. -certain metabolic abnormalities.
Diagnosis:
1-Accurate dietary history.
2-Deviations from average height, weight, head circumference for childs age.
3-Past rates of growth. 4-Measurements of mid-arm circumference & skin fold thickness.
5-Other tests:
a-Muscle mass: calculated as follows
mid-arm muscle circumference = mid-arm circumference - (skin fold thickness x 3.14)
b-Lean body mass: estimated from 24-hr creatinine excretion.
c-Protein reserves: assessed from serum albumin & total proteins.
d-Rapid turnover proteins: as transferrin, pre-albumin for evaluation of response to TTT.
e-serum levels of essential & non-essential amino acids.
Classifications:
1-Waterlow classification:
Grade Acute malnutrition (wasting) Chronic malnutrition (stunting)
% weight for height % height for age
Normal > 90% > 95%
I (mild) 80-90 % 90-95%
II (moderate) 70-80% 85-90%
III (severe) < 70% < 85%
-% weight for height: (actual childs weight/50
th
percentile of weight for his height) x 100.
-% height for age: (actual childs height/50
th
percentile of height for his age) x 100.
2-Wellcome classification: (wt in relation to age)


9

Wt % of normal 60-80% 60-80% 60% or less 60% or less
Edema Absent Present Absent Present
Type of PEM Underweight KWO Marasmus Marasmic KWO
Kwashiorkor (KWO)
Def: -clinical syndrome resulting from severe protein deficiency.
-patient depends mainly on CHO in his caloric intake.
-occurs from 6
th
month to 3 yrs of age usually after weaning from breast.
C/P:
I-Early: vague manifestations as apathy, lethargy, irritability.
II-Advanced cases:
A-Constant signs:
1-Growth failure: detected by suitable anthropometric measurements.
2-Edema: -usually develops early & may mask growth failure.
-causes: 1- plasma proteins. 2-Salt retention due to activation of renin-angiotensin system.
3-water retention due to hepatic degradation of ADH.
3-Muscle wasting: with preservation of some SC fat
-muscles: weak, thin, atrophic due to hypoproteinemia.
-hypotonia & delayed motor development.
-occasionally: amount of SC fat due to CHO intake.
4-Psychomotor changes:
-apathy, lethargy, indifference to surrounding & food.
-miserable look, peevish cry, marked anorexia.
-cause: deficiency of amino acids (esp. tryptophan) & serotonin.
B-Usual signs:
1-Dermayosis (dermatitis): is common
-erythema followed by skin darkening, appears in irritated areas
not in those exposed to sunlight.
-dyspigmentation or hypopigmentation may occur in these areas after desquamation.
-cause: may be of essential FAs, vitamin A & amino acids as tryptophan.
2-Hair:
-thin sparse with loss of luster, easily picked patchy baldness.
-sometimes dyspigmentation flag sign (streaks of red hair alternating with darker hair) due to
periodic changes in protein intake.
-coarse hair texture in chronic disease.
-cause: may be of sulfur-containing amino acids as riboflavin.
3-Liver:
-hepatomegaly due to fatty infiltration. -when neglected steatohepatitis or cirrhosis.
4-Renal functions: sometimes especially renal plasma flow & GFR.
5-Heart: small in early cases, enlarged in late cases.
6-Anemia: microcytic, macrocytic or normocytic anemia
-cause: 1-multiple of proteins, iron, folic acid, vitamin B12, vitamin B6, zinc, copper.
2-chronic infections.
7-Secondary immune : demonstrated by
-low concentration of Igs. - total lymphocyte count < 1500/mm3.
-anergy to skin test antigens.
8-Infections & parasitic infestations: common anorexia, vomiting, continuous diarrhea.
10

9-Secondary vitamin & mineral deficiency: as vitamins A, C, D.
Lab investigations:
1-Decreased serum levels of the following:
- serum albumin (CCC). - blood glucose (impaired glucose tolerance may occur).
- serum K+ & Mg+. - serum cholesterol.
-enzymes: amylase, cholinesterase, transaminase, lipase, phosphatase.
2-Ketonuria: common in the early stage.
3-Anemia: microcytic, macrocytic or normocytic.
4-Delayed bone growth in severe cases.
5-Growth hormone secretion may (stress response).
DD: from other causes of
1-Generalized edema. 2-Chronic infections. 3-Conditions with impaired protein synthesis.
4-Diseases with proteins loss in urine or stool.
Bad prognostic factors:
1-Severe wt loss. 2-Presence of dehydration. 3-Marked hepatomegaly.
4-Disturbed consciousness. 5-Hypothermia. 6-Skin hemorrhage.
Marasmus
Causes:
1-Nutritional marasmus: of dietary origin
-diet contains insufficient quantity of total calories but balanced qualitatively.
-e.g. infant exclusively breast-fed for prolonged period without food supplementation.
2-Non-nutritional marasmus:
-chronic infections as TB. -metabolic disorders as DM. -endocrinopathies: as thyrotoxicosis.
-local GIT disease or malformations. -malabsorption syndromes as cystic fibrosis.
-chronic heart disease as CHF. -chronic renal disease as uremia.
-CNS disorders as cerebral palsy.
C/P:
A-Constant signs:
1-Growth failure: early there is failure to gain wt, then wt loss & finally emaciation.
2-Loss of subcutaneous fat:
-occurs gradually: anterior abdominal wall thighs buttocks & shoulders
face except sucking pads of cheeks.
-may show senile face.
3-Muscle wasting: -atrophy of muscles with hypotonia.
-abdomen may be flat or scaphoid with visible peristalsis.
B-Usual signs:
1-Vitamin deficiency: e.g. angular Stomatitis, keratomalacia.
2-Hypothermia, bradycardia & basal metabolic rate.
3-At first: infant may be fretful, later on: becomes listless with poor appetite.
4-GIT disorders:
-constipation. -starvation diarrhea with small frequent stools containing mucus.
C-Bad prognostic factors:
1-severe wt loss. 2-younger age. 3-associated infection. 4-persistent irremovable cause.


11

Marasmic kwashiorkor
-The worst prognosis among syndromes of PEM.
-Cause: diets poor in total calories + acute deprivation or demands of proteins e.g. attack of
gastroenteritis or febrile illness.
-C/P: 1-Signs of marasmus. 2-generalized edema, psychomotor changes of KWO.
Complications of PEM: 2, 3 failure, GIPS
1-Hypothermia. 2-Hypoglycemia.
3-Heart failure. 4-Renal failure. 5-Hepatic failure.
6-Gastroenteritis, dehydration, electrolyte disturbance.
7-Infections as bronchopneumonia, meningitis.
8-Purpura. 9-Sudden death.
Prevention of PEM:
1-Encouragement of breast feeding.
2-Adequate dietary instructions & food distribution.
3-Avoid bad dietary habits as food withdrawal during diarrhea.
4-Immunization against infectious diseases.
5-Early detection & TTT of PEM cases.
TTT of PEM:
1-Hospitalization for advanced cases.
2-Immediate management of any acute problems: e.g.
-severe persistent diarrhea. -dehydration. -shock. -severe anemia. -renal failure.
-vitamin A . -hypoglycemia. -hypothermia.
-infections (using effective parenteral antibiotics for 5-10 days).
3-Dietetic TTT:
-breastfed infant should be well-nursed.
-after correction of dehydration:
a-start oral feeding with small frequent diluted milk.
b-over the next 5 days, gradually volume & frequency of feeds.
c-by the 6
th
- 8
th
day: 150 ml/kg/24 hrs should be given in 6 feeds.
-avoid giving high calorie & high protein diets too early & rapidly
for fear of re-feeding syndrome (hepatomegaly, abdominal distension & encephalopathy).
-cows milk should be made with 50 gm sugar/L.
-vegetable fat is better absorbed than cows milk fat.
-gradually add semisolid & solid foods guided by patient tolerance & general condition.
4-Symptomatic TTT:
-proper TTT of infections (bacterial or parasitic) & diarrhea.
-TTT of dermatosis (gentian violet 2%, antibiotic or antifungal creams).
-vitamins & minerals replacement (esp. vitamins A, B, D & K+, Mg+).
-iron & folic acid to correct anemia.
N.B. signs of improvement: -sense of well-being. -improvement of appetite.
-disappearance of edema. -progressive in body weight.
-healing of skin lesions. -cure of infections.
-normalization of serum proteins esp. albumin.
N.B. vitamin & see the table.


12

Rickets
Def: defective mineralization of growing bones due to vitamin D deficiency
or abnormal metabolism
Vitamin D:
1-Sources: -diets as fats & oils. -vitamin D supplements.
-UV sun rays effect on 7-dehydrocholesterol in skin.
2-Types: 1-Vitamin D2 of plant origin. 2-Vitamin D3 of animal origin & formed by human skin.
3-Metabolism:
a-absorption from the gut or formation in skin.
b-activation: -hydroxylation in the liver to 25-hydroxy vitamin D.
-hydroxylation in the kidney to 1,25 dihydroxy vitamin D (active form).
4-Actions:
-in the intestine: absorption of Ca & P. -in the kidney: re-absorption of Ca & P.
-in the bone: stimulates bone mineralization.
Growth plate in normal bone:
1-Zone of resting cartilage: one layer of cells.
2-Zone of proliferating cartilage: regular columns of cells originating from resting layer.
3-Zone of degeneration: cells become swollen with glycogen, glycolytic enzymes,
alkaline phosphatase with Ca deposition in the matrix.
4-Zone of ossification: blood vessels invade developing bone ossification & remodeling
mature bone.
Pathologic changes in rickets:
1-Zone of proliferation: increases & becomes very vascular enlargement of metaphyseal area
invades adjacent zone of degeneration.
2-Zone of degeneration:
-fails to mineralize excessive formation of new osteoid tissue.
-osteoid tissue is soft so under pressure, bulging & deformity of metaphyseal area
of long bones occur (flaring of ends of long bones rachitic rosary).
3-In the shaft: -bone resorption occurs.
-new osteoid is formed around the shaft from the periosteum.
4-During healing of rickets:
-appearance of new line of calcified bone (line of provisional calcification) at the end
of zone of degeneration.
-the area between it & the shaft is gradually filled with normal density bone.
Radiologic changes:
1-Active rickets:
-distal ends of long bones appear flared, frayed & cupped.
-distance between distal ends of radius & metacarpal bones appears wider than normal as it is
filled with osteoid tissue.
-diaphysis appears rarefied, may show double contour or deformity.
2-Healing rickets: 2-3 wks after successful TTT
-appearance of line of provisional calcification at the end of metaphysis.
-osteoid in-between this line & diaphysis gradually ossifies.
3-Healed rickets:
-bone density returns to normal.
-slight cupping remains as a stigma of previous rickets.
13

Biochemical (lab) manifestations of rickets:
1-Elevated serum alkaline phosphatase: due to hyperactivity of osteoblasts during excessive
osteoid formation (n: 5-15 Bodansky U/dl).
2- serum inorganic phosphorus (n: 4.5-6.5 mg/dl).
3- vitamin D & its metabolites.
4-Serum Ca is maintained within normal 9-11 mg/dl due to compensatory hyperactivity of
parathyroid gland.
Clinical manifestations:
-Vitamin D deficiency rickets commonly occurs at the end of the 1
st
yr & during the 2
nd
yr of life.
-Early rickets:
1-Craniotabes:
-cause: a-thinning of inner table of occipital bone under pressure of intracranial contents.
b-failure of mineralization.
-diagnosis: a-can be elicited by gentle pressure over occipital bone by both thumbs produce
a dent with crackling sensation (ping pong-ball like).
b-can be elicited from 3
rd
- 12
th
months of life.
2-Rosary:
-enlargement of costochondral junction of ribs giving the appearance of beads.
-due to excessive osteoid formation.
3-Radiological finding of active rickets (see before).
4-Rise of serum alkaline phosphatase enzyme.
-Advanced rickets:
1-Head:
-bossing of skull: skull looks like a box due to excessive proliferation of cartilage at occipital &
parietal eminences.
- head circumference. -delayed closure of anterior fontanels.
-delayed eruption of primary dentition with possible enamel hypoplasia.
2-Thorax:
-Rosary beads.
-Longitudinal sulcus: appears lateral to rosary beads due to compression of rib cage
by atmospheric pressure.
-Harrison sulcus: transverse sulcus along the lower border of costal margin due to inward
retraction of ribs at the sites of diaphragm insertion.
-Everted costal margin below Harrison sulcus.
-Forward protrusion of sternum & adjacent costal cartilages.
-Pigeon chest: chest is triangular in cross section.
3-Abdomen:
-appears protruded.
-palpable liver & spleen due to deformed chest & weak abdominal muscles.
4-Pelvis:
-narrowing of pelvic inlet by forward protrusion of sacral promontary.
-narrowing of pelvic outlet by forward projection of coccyx.
-this may affect females during labor in the future.
5-Spine: -correctable kyphosis & lordosis (esp. in the lumbar region).
-results from muscle weakness & laxity of ligaments.
6-Muscle weakness & lax ligaments: delayed motor mile stones.
14

7-Extremities:
-enlargement of metaphyseal region esp. at the wrists & ankles.
-Marfan sign: transverse groove above medial malleolus & sometimes lateral malleolus.
-deformities of long bones due to weight bearing. -greenstick fracture.
8-Rachitic dwarfism: due to spinal & lower limb deformities.
Complications:
1-Respiratory: infections or atelectasis due to chest deformities.
2-GIT: diarrhea or constipation. 3-Bone: deformities or fractures.
4-Anemia: due to chronic infections or deficiencies.
5-Tetany: in late cases due to hypocalcemia.
Prognosis:
-Usually good prognosis with: 1-exposure to sunshine in the morning or afternoon.
2-after vitamin D administration.
-Skeletal deformities: 1-usually improve with normal growth but slowly.
2-sometimes require orthopedic correction.
Prevention:
1-Exposure to UV rays of sunlight or administration of oral vitamin D.
2-Daily requirements of vitamin D:
-normal children: 400-800 U/day.
-LBW infants, PEM patients, hypothyroidism: 1000-1500 U/day (for the increased growth rate).
TTT of vitamin D rickets:
1-Oral vitamin D: 1500-5000 U/day for 6-8 weeks.
2-Shock therapy: vitamin D 600 000 U single dose IM injection or orally.
3-After 2-4 wks: if no evidence of complete healing (radiological or lab) repeat the dose.
Non vitamin D rickets
1-Vit D dependant type: dt -deficiency of renal alpha 1 hydroxylase enzyme.
-failure of end organ response to it.
2-Familial hypophosphatemic resistant rickets:
-more in girls.
-renal tubular defect excessive urinary phosphate loss.
3-Fanconi syndrome: urinary loss of P, glucose, amino acids, Hco3. 4-CRF.
5-Acquired renal tubular damage: as drugs.
6-Malabsorption syndromes :e.g. Celiac disease.
7-Anticonvulsant TTT : vitamin D metabolism.
Tetany
Def: state of neuromuscular excitability due to ionized serum Ca.
Causes : -rickets after exhaustion of parathyroid glands.
-Alkalosis.
C/P:
-Latent tetany: no clinical manifestations appear except after provocative tests.
-Manifest tetany: carpopedal spasm, laryngospasm, generalized convulsions.
TTT:
-Calcium gluconate 10%,5-10 ml, IV very slowly.
-Calcium chloride or lactate orally 1gm/day for 1 week.

15

Hypervitaminosis D
Causes: -Vitamin D intake. Hyper sensitivity to Vitamin D.
C/P:
-Weakness ,irritability. -Anorexia ,nausea, vomiting weight loss.
-Hypotonia ,constipation. -polydepsia ,polyuria ,dehydration.
-Pallor ,macrocytic anemia. -Hypercalcemia , hypercalciuria.
-Aortic stenosis . HTN. -Retinopathy, corneal clouding.
-Proteinuria and CP of renal damage (d.t. progressive nephrocalcinosis and nephrolithiasis.)
-Metastatic calcification e.g. in heart ,lungs, thyroids.
-Roentogenograms of long bones -metastatic calcification of metaphyseal area.
-generalized osteoporosis.
-calcification of soft tissues around joints.
DD:
-metastatic calcification d.t. chronic nephritis.
-Hyperparathyroidism. Idiopathic hypercalcemia.
-Dystrophic calcification ( benign physiologic condition)
Prevention:
-Careful evaluation of Vitamin. D dosage.
-Warning mother from using Vitamin d without medical consultation.
TTT:
1-stop Vitamin D intake , calcium intake.
2-Correction of dehydration and electrolyte disturbances.
3-Aluminium hydroxide gel to prevent Ca absorption.
4-Hydrocortisone. 5-Symptomatic TTT e.g. HTN , arrhythmia.
Malnutrition in children beyond infancy
Etiology: it may arises in childhood or as a continuation of malnutrition in inancy
1-Poor hygiene with chronic disease. 2-Disturbed parent-child relations.
3-Poor dietary habits as regard quantity or quality of diet.
4-Insufficient sleep, too much emotional excitement.
5-Insufficient time allotted for meals.
6-Some children eat little for fear of obesity.
7-Eating between meals e.g. snacks decreased mealtime appetite.
C/P:
1-General: fatigue, lassitude, restlessness, irritability, poor attention, poor school performance.
2-GIT: anorexia, constipation or starvation diarrhea.
3-Increased susceptibility to infections.
4-Muscles:
-weak & flabby posture of fatigue with rounded shoulders, flat chest, distended abdomen.
5-Anemia: hypochromic anemia is common.
6-Severe cases: delayed epiphyseal development, irregular dentition & delayed puberty.
Diagnosis:
1-Clinical: -accurate dietary history, history of PEM during infancy.
-thorough clinical examination.
2-Lab investigations: usually unnecessary.


16

TTT:
1-Correction of underlying psychological & physical disturbances.
2-Adequate & balanced diet quantitatively & qualitatively.
3-Vitamin concentrates.
4-If anorexia is present: -use concentrated forms of essential diets.
-fat content should be low. -offer fruit or fruit juices between meals.
5-Re-educating family about dietary habits.

Вам также может понравиться