Maternal vitamin D insufficiency is not uncommon. Infants born to mothers who are deficient in vitamin D and or calcium, usually due to cultural modifications in their diets or clothing habits, and in addition are breastfed, are at risk of developing vitamin D deficiency and hypocalcaemia. We present a case of neonatal hypocalcaemic seizures secondary to vitamin D deficiency.Rickets in children resulting from vitamin D deficiency is well documented. It is also becoming clear that there is a positive correlation between maternal vitamin D status during pregnancy and lactation and the development of rickets both in infancy and childhood. The correlation between maternal vitamin D, neonatal vitamin D and hypocalcaemia is not well documented.
IntroductionOver 80% of very preterm (<32 weeks) and very low birthweight (<1500 g) infants will have either typical development (TD) or mild developmental delay (MDD) in multiple domains. As differentiation between TD and MDD can be difficult, infants with MDD often miss opportunities for intervention. For many clinicians, the ongoing challenge is early detection of MDD without over servicing the population. This study aims to: (1) identify early clinical biomarkers for use in this population to predict and differentiate between TD and MDD at 24 months corrected age. (2) Determine the extent to which family and caregiver factors will contribute to neurodevelopmental and behavioural outcomes.Methods and analysisParticipants will be a prospective cohort of 90 infants (<32 weeks and/or <1500 g). Between 34 weeks gestational age and 16 weeks post-term, infants will have a series of 5 neurological, neuromotor, neurobehavioural and perceptual assessments including General Movement Assessment at preterm, writhing and fidgety age. Primary caregivers will complete questionnaires to identify social risk, maternal depression and family strain. Extensive perinatal data will be collected from the medical record. At 24 months, corrected age (c.a) infants will be assessed using standardised tools including the Bayley Scales of Infant and Toddler Development—Third Edition (Bayley III). Longitudinal trajectories of early assessment findings will be examined to determine any predictive relationship with motor and cognitive outcomes at 24 months c.a. Published data of a cohort of Australian children assessed with the Bayley III at 24 months c.a will provide a reference group of term-born controls.EthicsEthical approval has been obtained from the Queensland Children's Health Services Human Research Ethics Committee (HREC/13/QRCH/66), the University of Queensland (2013001019) and the Sunshine Coast Hospital and Health Service, SC-Research Governance (SSA/13/QNB/66). Publication of all study outcomes will be in peer-reviewed journals.Trial registration numberACTRN12614000480684; Pre-results.
Aim: This study aimed to identify early clinical biomarkers from birth to 16 weeks corrected age to predict typical outcome and developmental delay in infants born very preterm or with very low birthweight. Method:A prospective cohort of infants on the Sunshine Coast, Australia, was assessed using the Premie-Neuro Examination, the General Movement Assessment (GMA), the Alberta Infant Motor Scale, and the Infant Sensory Profile 2. At 24 months corrected age, delay was identified using the Bayley Scales of Infant and Toddler Development, Third Edition (Bayley-III) and Neurosensory Motor Developmental Assessment (NSMDA).Results: One hundred and four infants were recruited; 79 completed outcome assessments (43 females, 36 males; mean gestational age 30 weeks [SD 1 week 6 days], mean birthweight 1346 g [SD 323]). The incidence of developmental delay (motor or cognitive) was 6.3%. Suboptimal quality of fidgety general movements (temporal organization) at 16 weeks corrected age demonstrated the best predictive accuracy
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