7. CAUSES OF RICKETS:
• NUTRITIONALVITDDEFICIENCY:
Most common causeof ricketsglobally.
Etiology:
Most common in infancy: Duetopoor intake +inadequate cutaneous synthesis.
Transplacentaltransport of vitamin D,mostly 25-D,providesvitaminDfor 1st 2month of life unlessthere issevere
maternal vitamin Ddeficiency.
Breast-fed infants, becauseof low vitamin Dcontent of breastmilk, rely on cutaneous synthesisor vitamin
supplements.
Infants who receive formula receive adequate vitaminD,even without cutaneoussynthesis.
8. CAUSES OF RICKETS:
• NUTRITIONALVITDDEFICIENCY:
Most common causeof ricketsglobally.
Etiology:
Cutaneoussynthesisislimited by ineffective winter sun;andby increasedskinpigmentation.
Mothers may have same risk factors decreased maternal vitamin D reduced vitamin D in breast milk + less
transplacental deliveryof vitamin D.
Unconventional dietary practices, suchasvegandiets that use unfortified soymilk or ricemilk.
9. • NUTRITIONALVITDDEFICIENCY:
DIAGNOSIS:
• History of poor vitamin Dintake & risk factorsfor decreased cutaneoussynthesis.
• Radiographicchangesconsistent with rickets.
• Laboratory findings.
• Normal PTHlevel almost never occurswith vitamin Ddeficiency and suggestsaprimary phosphatedisorder.
• Calciumdeficiency mayoccur with or without vitaminDdeficiency.
• Anormal level of 25-Dandadietary history ofpoor calcium intake support adiagnosisof isolated calcium
deficiency.
CAUSES OF RICKETS:
10. CAUSES OF RICKETS:
• NUTRITIONALVITDDEFICIENCY:
• Treatment:
2 strategies for vitamin D adminstration:
Stosstherapy:
300,000–600,000 IU of vitamin Doral or IMas2–4 dosesover 1 day.
Becausedoses are observed, stoss therapy is ideal where adherence to therapy is questionable.
Alternative:
Daily, high-dose vitamin D,with dosesrangingfrom 2,000–5,000 IU/day over 4–6wk.
Either strategy should be followed by daily vitamin Dintake of400 IU/day, typically given asa
multivitamin.
Ensureadequate dietary calcium & phosphorus; (milk, formula, and other dairyproducts)
13. CAUSES OF RICKETS:
CALCIUMDEFICIENCY:
CAUSES:
• After weaning/ early weaning.
• Lowcalcium content in diet. (<200mg/day)
• Grains&greenleafy vegetables high in phytate, oxalate, and phosphate decreaseabsorption of dietarycalcium.
• In children gettingIVnutrition without adequatecalcium.
• Malabsorption ofcalcium:
-in celiacdisease,
-intestinal abetalipoproteinemia,and
-after small bowelresection.
14. CAUSES OF RICKETS:
CALCIUMDEFICIENCY:
Treatment.
• Calciumsupplement (350–1,000 mg/day of elementalcalcium).
• Vitamin Dsupplementation if concurrent vitaminDdeficiency.
• Prevention:
-Discourageearly cessationof breast-feeding.
-Increase dietary sourcesof calcium.
20. • Transferof calciumand phosphorus from mother to fetus occurs throughout pregnancy, but 80%
occursduring the 3rdtrimester.
• Premature birth interrupts this process sorickets develop.
• Most casesof ricketsof prematurity occurin birthweight <1,000g.
• More likely to develop in infants with lower birthweight and younger gestationalage.
• Rickets occurs because unsupplemented breast milk and standard infant formula do not contain
enough calcium and phosphorus to supply the needsof the prematureinfant.
Rickets of Prematurity
PATHOGENISIS