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