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Screening Infants at Risk for Fractures — Infants < 1 yr at Risk for Metabolic Bone Disease, Osteopenia and Fractures — Clinical Pathway: Inpatient

Screening Infants and Children at Risk for Fractures Clinical Pathway — Inpatient

Infants < 12 mos at Risk for Metabolic Bone Disease, Osteopenia and Fractures

  • Infants with the following conditions or treatments are at high risk for metabolic bone
    disease/osteopenia of prematurity and associated fractures
  • Screen infants if any of the following conditions are present
  • Initiate therapeutic and nutritional interventions as soon as possible to help prevent fractures
Condition/Treatment Rationale
Parenteral Nutrition (PN) > 4 wks Difficult/nearly impossible to provide adequate mineral intake from PN regimens to mimic intrauterine bone mineral accretion rates.
Preterm Infants on Unfortified
Breast Milk Term formula
Unfortified human milk and term formulas are inadequate to meet the preterm infant's nutritional needs and are especially lacking in nutrients essential for bone health (e.g., calcium, phosphorus, vitamin D, zinc).
Small for Gestational Age (SGA)
Intrauterine Growth Restriction (IUGR)
Factors contributing to SGA and/or IUGR (e.g., placental insufficiency) may impact bone health, including reduced bone mineral density.
Conjugated Bilirubin
> 2 mg/dL for 2 consecutive weeks
Malabsorption of nutrients caused by decreased bile flow may contribute to metabolic bone disease.
Surgical Necrotizing Enterocolitis (NEC)
Malabsorption (functional vs. anatomical)
Short Bowel Syndrome (SBS)
  • Infants with SBS are at risk for malabsorption of nutrients caused by altered GI function, which may contribute to metabolic bone disease.
  • Due to NEC or SBS, these infants are often on prolonged parenteral nutrition. See PN rationale.
Osteopenia or “Gracile Bones” on X-ray Indicates reduced bone mineral density.
Birth Weight
< 1,000 g or Gestational Age < 28 wks
Majority of fetal bone mineral accretion occurs during the 3rd trimester and peaks at 36 to 38 wks of gestation.
High-Risk Medications
  • Prostaglandins
  • Methylxanthines
  • Phenobarbital
  • Prolonged Remodulin (Treprostinil)
  • Prolonged Heparin Infusions
  • Steroids or loop diuretic use for 2 wks
  • Prostaglandin (Alprostadil) and prostacyclin (Treprostinil) use has been shown to increase osteoclast formation and increase bone resorption. 2,4,6,7
  • Methylxanthines, such as caffeine and theophylline, increase calcium and phosphorus excretion, leading to irregularity in calcium homeostasis. 1,4,10
  • Phenobarbital, well as other enzyme-inducing anti-epileptic medications, increase the metabolism of vitamin D, thus decreasing vitamin D concentrations and altering calcium absorption. 9
  • Heparin may potentiate osteoclast activity as well as decrease osteoblast activity and vitamin D metabolism. 9
  • Loop diuretics cause loss of electrolytes, such as sodium and calcium, through the kidneys that are needed for optimal calcium absorption. 5
  • Steroids impact calcium homeostasis, hormones, and inhibit bone formation, thus increasing the risk of bone disease. 8,9
Diagnoses
  • Chronic lung disease (CLD)
  • Arthrogryposis
  • Myelomeningocele (MMC)
  • Infants with CLD often have history of exposure to long-term PN and/or medications that contribute to drug-induced osteopathy.
  • Arthrogryposis is generally thought to occur as a result of decreased fetal movements.11 In addition, the diagnoses has the potential for contractures. Fractures can result if a caregiver is trying to force movement in a joint with a contracture.
  • Osteoporosis has been described in infants with MMC. High-level neurological involvement (thoracic or L1) and intermediate level (L3), and significant contractures are associated with fractures in the neonatal period.12

 

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