ICCBH2015 Poster Presentations (1) (201 abstracts)
1Royal Childrens Hospital, Melbourne, Victoria, Australia; 2Deparment of Paediatrics, Dandenong Hospital, Melbourne, Victoria, Australia; 3Department of Neonatology, Monash Childrens, Melbourne, Victoria, Australia; 4Department of Endocrinology and Diabetes, Monash Childrens, Melbourne, Victoria, Australia; 5Murdoch Childrens Research Institute, Melbourne, Victoria, Australia.
Metabolic bone disease (MBD) of prematurity is a well-recognized complication of preterm birth. Yet there is limited evidence for the optimal assessment, monitoring, and subsequent bone health management.
Retrospective audit of 171 infants born <32 weeks gestation between November 2012 and January 2014 at three Monash Health neonatal units (Melbourne, Australia) was undertaken. Infants had mean gestational age (GA) 28.6±2.1 weeks and birth weight (BW) 1190±374 g. Identified MBD risk factors include intrauterine growth retardation (IUGR; n=33, 19.3%), maternal pre-eclampsia (n=17, 9.9%), necrotising enterocolitis (NEC; n=9, 5.4%), and medication exposure: methylxanthines (94.2%; mean 54.8days), diuretics (38.6%; mean 49.2days) and glucocorticoids (5.3%; mean 35days). Infants received an average 19.8 days of total parenteral nutrition (TPN), with majority on fortified expressed breastmilk once enteral feeding established.
84.8% infants had initial MBD screen (mean age 36.3 days) with only 45% of the total cohort having repeated monitoring (mean age 71.9 days). 14.2% had alkaline phosphatase (ALP) levels >500 U/I initially, reducing to 10.1% on follow-up. All infants received at least vitamin D 400 units/day. 25.1% (n=43) commenced phosphate supplements (mean 46.3 days) and 19.9% (n=34) commenced calcium supplements (mean 31 days).
Average birth length was 37.7±5 cm with evidence of slowing growth velocity compared to reference charts (mean follow-up length 51.8±9.5 cm at mean age 118.6 days). Fractures identified from clinical documentation include birth trauma related fractures (n=2), suspected non-accidental injury diagnosed post-discharge (n=2), and one infant with multiple MBD risk factors. Rate of fractures may be underestimated given that radiological evidence was not included in this audit.
Comparing phosphate-treated and untreated groups revealed significant difference (P<0.001) for GA and BW: 26.7±1.7 weeks, 918±272 g for treated vs 29.2±1.9 weeks, 1283±359 g for untreated. In the phosphate-treated group, both mean ALP (pre-treatment 467±204 U/l and post-treatment 342±221 U/l, P≤0.01) and mean phosphate levels improved (1.8±0.4 mmol/l vs 2.2±1.0 mmol/l, P<0.01). Linear growth difference between phosphate-treated (n=10) and untreated (n=24) was insignificant at >6 months age (P=0.13), although this may reflect limited data.
Further evaluation is anticipated to improve MBD understanding in this high-risk cohort particularly given morbidity associated with occult fractures. Simplifying the MBD protocol to key components (ALP and phosphate) would allow for more cost-effective surveillance.
Disclosure
The authors declared no competing interests.