notes about rickets .

1. RICKETSRICKETS
HYPERVITAMINOSIS DHYPERVITAMINOSIS D
SPASMOPHILIASPASMOPHILIA

2. Plan of the lecturePlan of the lecture
 1. Definition of Rickets1. Definition of Rickets
 2. Biological activity of VitD metabolites2. Biological activity of VitD metabolites
 3. Exogene and endogene reasons of Vit D3. Exogene and endogene reasons of Vit D
deficienciesdeficiencies
 4. Rickets classification4. Rickets classification
 5. Changes of skeleton in rickets5. Changes of skeleton in rickets
 6. Treatment fnd prevention of rickets6. Treatment fnd prevention of rickets
 7. Hypervitaminosis D7. Hypervitaminosis D
 8. Spasmophilia8. Spasmophilia

3. Rickets is the disease of growingRickets is the disease of growing
organism characterized byorganism characterized by
metabolism impairment,metabolism impairment,
especially of phosphorus-calciumespecially of phosphorus-calcium
content abnormality that leads forcontent abnormality that leads for
bone formation, bone growthsbone formation, bone growths
mineralization failure.mineralization failure.

4. Necessity of Vit DNecessity of Vit D
 Vit D activity is measured in IU. One IU containsVit D activity is measured in IU. One IU contains
0,025 mcg of Vit D. 400 IU contain 10 mcg of Vit D0,025 mcg of Vit D. 400 IU contain 10 mcg of Vit D
Age ofAge of
childchild
0-12 mo0-12 mo 1-31-3
yearsyears
oldold
3-73-7
yearsyears
oldold
7-107-10
yearsyears
oldold
11-1711-17
yearsyears
oldold
Vit DVit D
(mcg)(mcg) 1010 1010 2,52,5 2,52,5 2,52,5

5. Biological activity of VitDBiological activity of VitD
metabolitesmetabolites
 Enhancing of intestine Ca absorbtionEnhancing of intestine Ca absorbtion
 Active Ca and P reabsorbtion in kidneyActive Ca and P reabsorbtion in kidney
 Mineralization of cartilages and boneMineralization of cartilages and bone
formationformation
 Bone collagen and bone proteins synthesisBone collagen and bone proteins synthesis
activation ( osteocalcin, osteopontine)activation ( osteocalcin, osteopontine)
 Bone resorbtion stimulationBone resorbtion stimulation
 Immune response modulation,Immune response modulation,
phagocytosis activationphagocytosis activation

6. Vit D deficiency consequencesVit D deficiency consequences
OrgansOrgans Deficiency consequencesDeficiency consequences
Bones and bone marrowBones and bone marrow Osteoporosis, osteomalacia, myelofibrosis,Osteoporosis, osteomalacia, myelofibrosis,
anemia, myeloid dysplasiaanemia, myeloid dysplasia
GutGut Ca, P absorbtion retardation, hepatolienalCa, P absorbtion retardation, hepatolienal
syndrome, dyskinesia of gutsyndrome, dyskinesia of gut
Lymphoid systemLymphoid system Immunity suppression, interleukin 1, 2,Immunity suppression, interleukin 1, 2,
phagocytosis, interferon productionphagocytosis, interferon production
decreasing. Realise predisposing to atopydecreasing. Realise predisposing to atopy
and allergyand allergy
Muscular systemMuscular system Muscular hypotonia, seizures ( tetany)Muscular hypotonia, seizures ( tetany)

7. Rickets predisposing factorsRickets predisposing factors
Mother’sMother’s Child’sChild’s
-Mother’s age <17 and> 35-Mother’s age <17 and> 35
years oldyears old
-Toxicosis during pregnancy-Toxicosis during pregnancy
- Extragenecologic- Extragenecologic
pathology (metabolismpathology (metabolism
abnormality, chronic kidney,abnormality, chronic kidney,
gut diseases)gut diseases)
- Defects of feeding during- Defects of feeding during
pregnancy and breastpregnancy and breast
feeding (deficiency offeeding (deficiency of
proteins, Ca, P, Vit D,Vit B)proteins, Ca, P, Vit D,Vit B)
- Lack of insolation,- Lack of insolation,
hypodynamiahypodynamia
-Complicated delivery-Complicated delivery
- Poor social- economic- Poor social- economic
conditionsconditions
--Time of birth (childrenTime of birth (children
delivered in fall or winter )delivered in fall or winter )
-Prematurity,-Prematurity,
morphofunctionalmorphofunctional
immaturityimmaturity
-Birth weight more 4 kg-Birth weight more 4 kg
-Quick weight gaining-Quick weight gaining
during first 3 moduring first 3 mo
-Early weaning-Early weaning
- Rare outdoor staying- Rare outdoor staying
-Diseases of skin, liver,-Diseases of skin, liver,
kidney, malabsorbtionkidney, malabsorbtion
syndromesyndrome
-Frequent respiratory-Frequent respiratory
infectioninfection
-Anticonvulsant drugs-Anticonvulsant drugs

8. Exogene reasons of Vit DExogene reasons of Vit D
deficienciesdeficiencies
 Lack of Vit D consumption with food.Lack of Vit D consumption with food.
Poor containing of products in diet that arePoor containing of products in diet that are
rich in VitD ( yolk, fish, oil, milk, butter,rich in VitD ( yolk, fish, oil, milk, butter,
liver)liver)
 Deficiency of insolation and rare outdoorsDeficiency of insolation and rare outdoors
walks that leads to poor production of Vitwalks that leads to poor production of Vit
D in skin under influence of sun beamsD in skin under influence of sun beams
(UV spectrum 280-310 nm)(UV spectrum 280-310 nm)
 Inproper intake of phosphates and Ca withInproper intake of phosphates and Ca with
foodfood

9. Endogene reasons of Vit DEndogene reasons of Vit D
deficiencydeficiency
 Malabsorption of Vit D in intestineMalabsorption of Vit D in intestine
 Hydroxylation of Vit D precursors impairmentHydroxylation of Vit D precursors impairment
into active metabolites in liver, kidneys due tointo active metabolites in liver, kidneys due to
chronic diseases of theses organschronic diseases of theses organs
 Genetic or inherited abnormalities of Vit DGenetic or inherited abnormalities of Vit D
synthesizing processsynthesizing process
 Outstanding loosing of Ca and P by kidneys intoOutstanding loosing of Ca and P by kidneys into
urine or impairment of bone absorption of Caurine or impairment of bone absorption of Ca
and P.and P.
 Absence or degradation of Vit D receptorsAbsence or degradation of Vit D receptors
functional activity.functional activity.

10. Risk group of Vit D deficiencyRisk group of Vit D deficiency
 Premature children with low body weightPremature children with low body weight
 Neonates with signs of immaturityNeonates with signs of immaturity
 Malabsorbtion syndrome ( celiac disease, foodMalabsorbtion syndrome ( celiac disease, food
allergy, exudative enteropathy)allergy, exudative enteropathy)
 Convulsions that demand specific therapyConvulsions that demand specific therapy
(anticonvulsants)(anticonvulsants)
 Decreasing of motion activity ( paresis, paralysis,Decreasing of motion activity ( paresis, paralysis,
prolonged immobilization)prolonged immobilization)
 Chronic pathology of liver, bile ductsChronic pathology of liver, bile ducts
 Frequent respiratory pathologyFrequent respiratory pathology
 Children fed by nonadapted formulaChildren fed by nonadapted formula
 Abused by inherited abnormalities of Ca-PAbused by inherited abnormalities of Ca-P
metabolismmetabolism
 Twins or neonates from pregnancies with shortTwins or neonates from pregnancies with short
period between them.period between them.

11. Rickets classificationRickets classification
DegreesDegrees Disease periodDisease period Disease courseDisease course
1-st mild1-st mild
2-nd moderate2-nd moderate
3-d severe3-d severe
InitialInitial
Clinically obviousClinically obvious
(swing) period(swing) period
ReconvalescenceReconvalescence
ResidualResidual
AcuteAcute
SubacuteSubacute
RecurrentRecurrent

12. Criteria of rickets’ severityCriteria of rickets’ severity
 !-st degree rickets is characterized predominantly by!-st degree rickets is characterized predominantly by
neuro-muscular abnormalities and minimalneuro-muscular abnormalities and minimal
disturbances of bone formation (craniotabes, occiputdisturbances of bone formation (craniotabes, occiput
flattening, minimal tissue signs in growing zones offlattening, minimal tissue signs in growing zones of
metaphysicmetaphysic
 2-nd degree rickets ( moderate) – beside neuro-2-nd degree rickets ( moderate) – beside neuro-
muscular dystonia bone deformities of sculp, chestmuscular dystonia bone deformities of sculp, chest
and limbs are present, moderate functional changes ofand limbs are present, moderate functional changes of
inner organsinner organs
 3-d degree rickets (severe) – prominent bone and3-d degree rickets (severe) – prominent bone and
muscular abnormalities, articular hypermobility, staticmuscular abnormalities, articular hypermobility, static
and locomotor function retardation, impairment ofand locomotor function retardation, impairment of
inner organs function due to acidosis and concomitantinner organs function due to acidosis and concomitant
microvasculaturemicrovasculature changeschanges

13. Criteria of rickets’ courseCriteria of rickets’ course
 Acute course – prompt development of allAcute course – prompt development of all
symptoms, clear neurologic and vegetativesymptoms, clear neurologic and vegetative
disorders, significant hypophosphatemia, high leveldisorders, significant hypophosphatemia, high level
of alkaline phosphatase, osteomalacia symptomsof alkaline phosphatase, osteomalacia symptoms
prevelanceprevelance
 Subacute course –moderate and vague neurologicSubacute course –moderate and vague neurologic
and vegetative abnormalities, not significantand vegetative abnormalities, not significant
biochemical changes, osteoid hyperplasiabiochemical changes, osteoid hyperplasia
predominancepredominance
 Recurrent course – typical periods of exacerbationRecurrent course – typical periods of exacerbation
and remission with residual signs. X-ray reveals inand remission with residual signs. X-ray reveals in
methaphysis several calcification linesmethaphysis several calcification lines

14. Criteria of rickets periodCriteria of rickets period
 Initial period – signs of disease can be seen in 2-3Initial period – signs of disease can be seen in 2-3
mo old child 9 in premature children at the end ofmo old child 9 in premature children at the end of
first mo). Behavior of child changes. He becomesfirst mo). Behavior of child changes. He becomes
irritated, jerky. Neuro-vegetative symptomsirritated, jerky. Neuro-vegetative symptoms
become visible. Ca level is slightly elevated orbecome visible. Ca level is slightly elevated or
normal ( N-2,37-2,62 mmols/l), P level isnormal ( N-2,37-2,62 mmols/l), P level is
decreased (N- 1,45-1,77 mmols/l), alkalinedecreased (N- 1,45-1,77 mmols/l), alkaline
phosphatase is slightly elevated, acidosis isphosphatase is slightly elevated, acidosis is
present, hyperphosphateuria, hyperaminoaciduriapresent, hyperphosphateuria, hyperaminoaciduria
can be find. Initial period elongation in ricketscan be find. Initial period elongation in rickets
acute course can be 2-6 weeks, in subacute courseacute course can be 2-6 weeks, in subacute course
– 2-3 month– 2-3 month

15. Criteria of rickets periodCriteria of rickets period
 Swing periodSwing period ( clinically obvious) (6 mo of( clinically obvious) (6 mo of
life) – is characterized by more prominentlife) – is characterized by more prominent
neuro-muscular and vegetative disorders,neuro-muscular and vegetative disorders,
retrardation of psychomotor and somaticretrardation of psychomotor and somatic
development, visible skeletal disordersdevelopment, visible skeletal disorders
especially in growing zones of bones.especially in growing zones of bones.
Hypophosphatemia become obvious,Hypophosphatemia become obvious,
moderate hypocalcaemia, elevated level ofmoderate hypocalcaemia, elevated level of
alkaline phosphatasealkaline phosphatase

16. Criteria of rickets periodCriteria of rickets period
 Reconvalescence period – condition improves,Reconvalescence period – condition improves,
neurologic ad vegetative disorders disappear, staticneurologic ad vegetative disorders disappear, static
function improves, new reflexes appear but muscularfunction improves, new reflexes appear but muscular
hypotonia and skeletal deformities can be present forhypotonia and skeletal deformities can be present for
long time. The levels of Ca, P, alkaline phosphataselong time. The levels of Ca, P, alkaline phosphatase
normalizenormalize
 Residual period – all reversible changes in skeletonResidual period – all reversible changes in skeleton
disappear ( muscular hypotonia, joint and ligamentdisappear ( muscular hypotonia, joint and ligament
dysfunction) biochemical indexes normalize, butdysfunction) biochemical indexes normalize, but
nonreversible changes of skeleton are presentnonreversible changes of skeleton are present
(deformities, osteoid hyperplasia symptoms).(deformities, osteoid hyperplasia symptoms).

17. Changes of skeleton in ricketsChanges of skeleton in rickets
Part of skeletonPart of skeleton Bone deformitiesBone deformities
Bone deformitiesBone deformities Craniotabes (in young infants pressure overCraniotabes (in young infants pressure over
the soft membranous bones of the skull is feltthe soft membranous bones of the skull is felt
like ping-pong ball)like ping-pong ball)
Skull deformities(bossing of frontal andSkull deformities(bossing of frontal and
parietal bones, delayed eruption of primaryparietal bones, delayed eruption of primary
teeth, defects of teeth enamel, inclination toteeth, defects of teeth enamel, inclination to
cariescaries
Large anterior fontanel with delayed closureLarge anterior fontanel with delayed closure
ChestChest Clavicular deformities, rachitic rosariesClavicular deformities, rachitic rosaries
Wide low aperture, narrowing of theWide low aperture, narrowing of the
chest from the sides –“pigeon breast”,chest from the sides –“pigeon breast”,
sternum project forwardsternum project forward
Navicular depression on the lateral sideNavicular depression on the lateral side
of chestof chest

18. Changes of skeleton in ricketsChanges of skeleton in rickets
Upper limbsUpper limbs Deviation of humerus and armsDeviation of humerus and arms
Joint deformities: “bracelet” (bossing inJoint deformities: “bracelet” (bossing in
radiocarpal joints), “pearl fibers” (bossingradiocarpal joints), “pearl fibers” (bossing
in fingers distal part)in fingers distal part)
ColumnColumn Scoliosis, kyphosis or lordosisScoliosis, kyphosis or lordosis
PelvisPelvis Flat pelvis, narrow low aperture of pelvisFlat pelvis, narrow low aperture of pelvis
Lower limbsLower limbs Anterior bowing of legs, knock knee, coaxAnterior bowing of legs, knock knee, coax
veravera

19. Main treatment goalMain treatment goal
 Restoration of Ca-P metabolismRestoration of Ca-P metabolism
 Normalizing of peroxydative process inNormalizing of peroxydative process in
lipidslipids
 Elimination of metabolic acidosis andElimination of metabolic acidosis and
hypokaliemiahypokaliemia
 Elimination of VitD deficiencyElimination of VitD deficiency

20. Treatment must includeTreatment must include
 Proper regimen for child. Infant mustProper regimen for child. Infant must
spend not less than 2-3 hours outdoors,spend not less than 2-3 hours outdoors,
room of child must be aired.room of child must be aired.
 Proper feeding. Diet must contain productsProper feeding. Diet must contain products
rich in vit D and mustn’t be overloaded byrich in vit D and mustn’t be overloaded by
wheat or semolina porridge because itwheat or semolina porridge because it
absorb Ca and P and decrease itabsorb Ca and P and decrease it
penetration through intestinepenetration through intestine
 Medication with vit DMedication with vit D
 Hygienic bathing, massage, physicalHygienic bathing, massage, physical
exercisesexercises

21. Antinatal nonspecific prevention ofAntinatal nonspecific prevention of
ricketsrickets
Pregnant woman must spend outdoors not less thanPregnant woman must spend outdoors not less than
2-4 hours every day, must be active, get proper diet2-4 hours every day, must be active, get proper diet
with high containing of vit D and C and otherwith high containing of vit D and C and other
micro and macro nutrients, proteinsmicro and macro nutrients, proteins
Specific antenatal prophylaxis : Pregnant womanSpecific antenatal prophylaxis : Pregnant woman
must take vit D 400-500 IU daily from 28-32 weekmust take vit D 400-500 IU daily from 28-32 week
of pregnancy beside summer month. If woman hasof pregnancy beside summer month. If woman has
chronic nephropathy or another extragenitalchronic nephropathy or another extragenital
pathology like diabetus mellitus, rheumatic fever,pathology like diabetus mellitus, rheumatic fever,
hypertension dosage of vit D increases to 1000-1500hypertension dosage of vit D increases to 1000-1500
IU daily for 8 weeks. Another way can beIU daily for 8 weeks. Another way can be
performed UV radiation of skin.performed UV radiation of skin.

22. Postnatal nonspecific preventivePostnatal nonspecific preventive
effortsefforts
 Consist of performing everyday massagesConsist of performing everyday massages
and exercises, walking outdoors, bathing,and exercises, walking outdoors, bathing,
proper feeding ( breast feeding is preferable.proper feeding ( breast feeding is preferable.
In the case of hypogalactia –proper formulaIn the case of hypogalactia –proper formula
feeding must substitute breast milk)feeding must substitute breast milk)
Mother’s breast milk contain the mostMother’s breast milk contain the most
suitable quantity of Ca and P in mostsuitable quantity of Ca and P in most
rational rate of these electrolytes to berational rate of these electrolytes to be
absorbed in gut.absorbed in gut.

23. Specific preventive activitySpecific preventive activity
For full term children with natural feeding vit D is proposed fromFor full term children with natural feeding vit D is proposed from
3-4 week after birth in fall, winter period in daily dosage 400-3-4 week after birth in fall, winter period in daily dosage 400-
500 IU. If child was born in spring or summer you needn’t500 IU. If child was born in spring or summer you needn’t
prescribe vit D.prescribe vit D.
Premature neonates with 1 degree of immaturity are prescribed vitPremature neonates with 1 degree of immaturity are prescribed vit
D 500-1000 IU from 10-14 day old for 2 mo with 2 mo intervals.D 500-1000 IU from 10-14 day old for 2 mo with 2 mo intervals.
Premature neonates with 2-3 degree of immaturity must get 1000-Premature neonates with 2-3 degree of immaturity must get 1000-
2000IU of vit D from 10-20 day old daily for 1 year, except2000IU of vit D from 10-20 day old daily for 1 year, except
summer months. When they get 1 year dosage of vit D must besummer months. When they get 1 year dosage of vit D must be
500-1000 IU daily. You must also add treatment with500-1000 IU daily. You must also add treatment with
medications of Ca and P. UV radiation can be prescribed 1-2medications of Ca and P. UV radiation can be prescribed 1-2
times per year. Course consist of 10-12 radiations starting fromtimes per year. Course consist of 10-12 radiations starting from
1/8 biodosages of UV with steady elevation to 1,5 – 2 biolog.1/8 biodosages of UV with steady elevation to 1,5 – 2 biolog.
dosages.dosages.

24. Rickets’ treatmentRickets’ treatment
 Prescribing specific treatment you must take intoPrescribing specific treatment you must take into
account period and course of disease. Daily dosageaccount period and course of disease. Daily dosage
differs from 2000to 5000 IU for 30-45 days. Afterdiffers from 2000to 5000 IU for 30-45 days. After
gaining therapeutic effect child is proposedgaining therapeutic effect child is proposed
preventive dosage (500IU) daily for 3 years.preventive dosage (500IU) daily for 3 years.
 Such medications can be usedSuch medications can be used
 Videchol (0,125% oil solution of cholecalciferolumVidechol (0,125% oil solution of cholecalciferolum
(D3). 1 ml of solution contain 25000 IU, 1 drop –(D3). 1 ml of solution contain 25000 IU, 1 drop –
500IU.500IU.
 Vit D2 ( 0,125% oil solution of ergocalciferoli; 1 ml ofVit D2 ( 0,125% oil solution of ergocalciferoli; 1 ml of
it contain 50 000IU, 1 drop-1000 IUit contain 50 000IU, 1 drop-1000 IU
 AQUADETRIM water solution of vit D3 1 dropAQUADETRIM water solution of vit D3 1 drop
contain 500 IUcontain 500 IU

25. Main biological functions of Ca inMain biological functions of Ca in
organismorganism
 Mineralization of bones and formation of skeletonMineralization of bones and formation of skeleton
 Generate electrical potential of cellGenerate electrical potential of cell
 Regulate activity of cells, biologically activeRegulate activity of cells, biologically active
substancesubstance
 Take part in integrity of organism functionTake part in integrity of organism function
 Maintain normal neuro-muscular excitability andMaintain normal neuro-muscular excitability and
contractilitycontractility
 Maintain homeostasisMaintain homeostasis
 Activate big quantity of enzymes and biologicallyActivate big quantity of enzymes and biologically
active substanceactive substance

26. Food and products that contain CaFood and products that contain Ca
Quantity of CaQuantity of Ca
(mg/100g)(mg/100g)
ProductsProducts
Plenty ( >100)Plenty ( >100) Cheese, milk, kefir, cottage cheese, pod, parsle.Cheese, milk, kefir, cottage cheese, pod, parsle.
spring onionspring onion
Big quantity (51-Big quantity (51-
100)100)
Sour cream, eggs, buckwheat, oatmeal, pea,Sour cream, eggs, buckwheat, oatmeal, pea,
carrot, horse mackerel, herring, caviarcarrot, horse mackerel, herring, caviar
Moderate (25-50)Moderate (25-50) Butter, perch, cod, millet. Cabbage, reddish,Butter, perch, cod, millet. Cabbage, reddish,
beet, apricot, cherry, plums grapes, oranges,beet, apricot, cherry, plums grapes, oranges,
strawberrystrawberry
Lack ( less than 25)Lack ( less than 25) Meat products, semolina, macaroni, potato,Meat products, semolina, macaroni, potato,
cucumber, tomato, water melon, apple, pearscucumber, tomato, water melon, apple, pears

27. Contraindications for Vit DContraindications for Vit D
treatmenttreatment
 Intrapartum intracranium trauma or hypoxiaIntrapartum intracranium trauma or hypoxia
 JaundiceJaundice
 Little sizes of anterior fountanella.Little sizes of anterior fountanella.
 If child is fed by adopted formula thatIf child is fed by adopted formula that
contain vit D.contain vit D.

28. Hyper-VitD treatmentHyper-VitD treatment
 Stop intake of Vit DStop intake of Vit D
 Decrease Ca intakeDecrease Ca intake
 Eliminate milk, cheese from dietEliminate milk, cheese from diet
 Plants, cereals are recommended because they fix Vit DPlants, cereals are recommended because they fix Vit D
and Ca in intestine and help eliminate itand Ca in intestine and help eliminate it
 In severe conditions is recommended IV injections ofIn severe conditions is recommended IV injections of
albumin, 5% solution of glucose, Ringer solution, Vit C.albumin, 5% solution of glucose, Ringer solution, Vit C.
Prednisone (2 mg/kg) is recommended. It can decreasePrednisone (2 mg/kg) is recommended. It can decrease
absorbtion of Ca from intestine and induce resorbtion ofabsorbtion of Ca from intestine and induce resorbtion of
Ca from bone and thus accelerate loses of thisCa from bone and thus accelerate loses of this
macroelement from organism.macroelement from organism.

29. Vit D antagonistsVit D antagonists
 Vit AVit A
 - Vit E- Vit E
 Furosemide (1 mg/kg)Furosemide (1 mg/kg)
 Myocalcic (synthetic thyrocalcitonin – 5-10Myocalcic (synthetic thyrocalcitonin – 5-10
U/kg IV)U/kg IV)

30. Medication that bind Ca in intestineMedication that bind Ca in intestine
 Cholestiramine (o,5 g/kg bid)Cholestiramine (o,5 g/kg bid)
 Almagel (50-100 mg/kg daily)Almagel (50-100 mg/kg daily)
 Trilon B (50 mg/kg daily IVTrilon B (50 mg/kg daily IV ))

31. Diagnostic approachDiagnostic approach
 Principle approach is monitoring of ionizedPrinciple approach is monitoring of ionized
Ca ( normal one is 1,1-1,4 mmols/l; inCa ( normal one is 1,1-1,4 mmols/l; in
spasmophilia less than 0,85 mmol/l)spasmophilia less than 0,85 mmol/l)
 Decreasing of common Ca level ( less thanDecreasing of common Ca level ( less than
1,75 mmols/l)1,75 mmols/l)
 ECG –elongation of QT and ST intervalsECG –elongation of QT and ST intervals
 Metabolic alkalosisMetabolic alkalosis

32. Spasmophilia treatmentSpasmophilia treatment
Latent formLatent form
 Regimen normalizationRegimen normalization
 Diet restrict of cow milk and milkfish productsDiet restrict of cow milk and milkfish products
 Ca containing medicationCa containing medication
 Necessity of Ca in infants is 50-55 mg/kg dailyNecessity of Ca in infants is 50-55 mg/kg daily
 Neonates -400mg dailyNeonates -400mg daily
 Infants – 600 mgInfants – 600 mg
 Children from 1 to 5 years old – 800-1200 mgChildren from 1 to 5 years old – 800-1200 mg
 Adolescents – 1200-15000mgAdolescents – 1200-15000mg
 Adults -1000-1200-1500 mgAdults -1000-1200-1500 mg

33. To restore Ca level can be usedTo restore Ca level can be used
 10% solution of Ca gluconates ( I ml of10% solution of Ca gluconates ( I ml of
solution contain 9 mg of CA)solution contain 9 mg of CA)
 5% sol. Of Ca gluconatis, Ca lactis5% sol. Of Ca gluconatis, Ca lactis
 To eliminate alkalosis by 10% sol. OfTo eliminate alkalosis by 10% sol. Of
ammonii chloride ( 1 teaspoon tid)ammonii chloride ( 1 teaspoon tid)