Metabolic bone disease

Metabolic bone disease

Also known as osteopenia of prematurity, the incidence is 32–90% in pre-term infants (mostly ELBW).

Cause

Chronic substrate deficiency—usually phosphate, rarely calcium or vita-min D. Risk is increased if:

• prolonged PN;
• breastfed (low in phosphate);
• chronic diuretic treatment.

Presentation

• Bone mineral biochemical derangement (see b Investigations); measure serum Ca2⁺, PO₄^3-and alkaline phosphatase weekly in all infants under 33wks gestation.
• ‘falls’ Linear growth.
• Rib or distal long bone fractures.

Investigations

• Biochemistry: PO₄^3-<1.2mmol/L; Ca²⁺ >2.7mmol/L; alkaline phosphatase >1000IU/L.
• Bone X-ray: osteoporosis, features of rickets, fractures.
• Urine Ca²⁺/PO₄^3-ratio >1 after 3wks of age (high renal PO₄^3- reabsorption).

Treatment

• Oral PO₄^3-1mmol/kg/day supplement if milk fed.
• Increase TPN Ca²⁺and PO₄^3- (consult pharmacist).

Prevention

In infants <2kg or <33wks gestation:

• Supplement breast milk with oral PO₄^3-1mmol/kg/day (not required if fed preterm formula as already contains added PO₄^3- );
• Oral vitamin D 400IU/day;
• Ensure TPN contains Ca²⁺2mmol/kg/day and PO₄^3- 2.5mmol/kg/day (organic phosphate solution avoids mineral precipitation);
• 10min/day of passive exercise appears beneficial.

Prognosis

Stature is reduced at age 18mths. Bone mineralization and fracture risk appear to be normal by 2yrs