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Rickets of premature infants induced by calcium deficiency. A case report

J R Tsai1, P H Yang

  • 1Division of Neonatology, Chang Gung Children's Hospital, Taipei, Taiwan, R.O.C.

Changgeng Yi Xue Za Zhi
|June 1, 1997
PubMed

Insights

Rickets of prematurity, often due to calcium and phosphorus deficiency, can occur in premature infants receiving prolonged total parenteral nutrition (TPN). Supplementing TPN with calcium can heal fractures and lower alkaline phosphatase levels, indicating recovery.

Area of Science:

  • Neonatalogy
  • Pediatric Nutrition
  • Pediatric Orthopedics

Background:

  • Rickets of prematurity is a significant concern in neonatal intensive care units.
  • Unlike childhood rickets (often vitamin D deficient), premature infant rickets is primarily linked to calcium and phosphorus imbalances.
  • Necrotizing enterocolitis sequelae can necessitate prolonged total parenteral nutrition (TPN) in premature infants.

Observation:

  • A premature infant with necrotizing enterocolitis complications required extended TPN and developed a ricketic fracture.
  • High calcium-fortified TPN was administered to address the fracture.
  • Following supplementation, the ricketic fracture showed signs of healing, and serum alkaline phosphatase levels decreased.

Findings:

  • Serum calcium and phosphorus levels serve as valuable predictors for rickets development.
  • Monitoring alkaline phosphatase levels alongside radiography is crucial for early detection in high-risk premature infants.
  • Extended TPN in premature infants requires higher calcium and phosphorus concentrations compared to older children.

Implications:

  • Early identification and management of mineral deficiencies are critical for premature infants on TPN.
  • Optimized TPN formulations are essential to prevent and treat rickets of prematurity.
  • This case highlights the importance of tailored nutritional support in vulnerable neonatal populations.

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