Please note that some guidelines may be past their review date. The review process is currently paused. It is recommended that you also refer to more contemporaneous evidence.
Risk factors for maternal vitamin D deficiency include:
- dark-skinned women, including Asian women
- women who spend a lot of time indoors and who 'cover up'
- limited sunlight exposure: cold climate, short winter days, indoor occupation, need for protective clothing.
Diagnosis of vitamin D deficiency in the mother
- Serum 25-OHD concentration is the best indicator of vitamin D status.
- The normal adult concentration is > 50 nmol/L, although several sources use > 75 nmol/L for pregnant women.
Definition of deficiency
Vitamin D deficiency is defined as:
- mild (serum 25-OHD 25-50 nmol/L)
- moderate (serum 25-OHD 12.5-25 nmol/L)
- severe (serum 25-OHD < 12.5 nmol/L).
Antenatal management of the mother
Depending on the vitamin D level, supplementation should be commenced and continued throughout pregnancy and lactation. A maternal dose of at least 1,000 U/d of cholecalciferol should be adequate for mild deficiency, but a higher dose will be appropriate for women with moderate to severe deficiency.
Note: Most pregnancy and BF multivitamins do not contain 1,000 units/dose; for example, Elevit and Blackmore's pregnancy and BF Gold both contain only 500 units/day of cholecalciferol when taken at the recommended dose. If a pregnant woman is vitamin D deficient, a vitamin D supplement in addition to the standard pregnancy multivitamin preparation will therefore be required.
Signs of vitamin D deficiency in newborns
Signs of vitamin D deficiency include:
- most are asymptomatic
- craniotabes (softening of skull bones)
- other osseous signs (such as rickets) are not seen in the newborn but classical signs in the older infant include broadening of the metaphyses, bowing of the long bones once weight bearing and the rachitic rosary (prominent chostochondral joints)
- hypocalcaemic seizures.
Postnatal management of an infant at risk of vitamin D deficiency
These at risk infants include:
- babies born at < 37 weeks' gestation
- babies with birth weight < 2 kg
- dark-skinned babies, even if maternal vitamin D levels were normal in pregnancy
- babies of mothers with known vitamin D deficiency in pregnancy
- babies of untreated mothers who had been at risk of vitamin D deficiency in pregnancy.
Asymptomatic infants at risk for vitamin D deficiency should routinely be started on a vitamin D supplement in the first days of life.
Management of symptomatic hypocalcaemia
Hypocalcaemia with seizures
Administer 10 per cent diluted calcium gluconate 0.5 mL/kg (maximum 20 mL) IV over 30-60 minutes (1 mL of 10 per cent calcium gluconate contains 0.2 mmol of calcium).
Hypocalcaemia and no seizures
Administer 40-80 mg/kg/day (1-2 mmol/kg/day) of oral calcium gluconate in four to six divided doses and Calcitriol 50-100 ng/kg/day orally in two to three doses until serum calcium level is > 2.1 mmol/L.
Preparations for vitamin D supplementation
- OsteVit-D (0.1 mL daily - equivalent to 500 units cholecalciferol/dose), or
- Pentavite (0.45 mL daily - equivalent to 400 units cholecalciferol/dose)
This dose is a physiological dose and the potential for hypervitaminosis D is negligible.
Note: Do not use Pentavite with Iron, as this contains about 1/20th the amount of vitamin D per millilitre.
The supplement is commenced as soon as tolerating feeds after birth and continued for the first 12 months of life. Vitamin D supplementation is not required in infants that are fully formula fed.
Stoss therapy (high-dose vitamin D therapy)
- High-dose vitamin D therapy (Stoss therapy) can be considered in patients with poor compliance, recalcitrant vitamin D deficiency or vitamin D deficient rickets.
- There are many stoss regimens with doses ranging from 100,000 to 600,000 units given as single or divided doses.
- There is currently no consensus on the most effective and safest regimen and until this is studied further, a conservative approach is recommended.
Further comments
If a mother was identified as at risk and treated for vitamin D deficiency in early pregnancy, the infant should be commenced on a vitamin D supplement (at least 400 IU/d), regardless of subsequent maternal levels. There is no role for a vitamin D assay in the infant at any stage, unless there are overt symptoms of hypocalcaemia (seizures) or rickets.
If a mother is at risk of vitamin D deficiency, but did not have screening, or was not adherent with vitamin D supplementation in pregnancy, the management is the same as above. A vitamin D assay in the baby is generally not required, as it is unlikely to change management and as the assay is not a good reflection of vitamin D stores. The exception would be if the maternal levels reflect severe deficiency (< 10 nmol/l), which puts the infant at significant risk of hypocalcaemia and osteopenia. The management of such cases should be discussed with a paediatrician/paediatric endocrinologist. The mother's low vitamin D should be treated postnatally in its own right.
It is not necessary to initiate vitamin D supplementation in an otherwise healthy term newborn, with no infant or maternal risk factors, on the basis of not having a vitamin D level for the mother.
All parents should receive information about vitamin D and the importance of adhering to suggested supplementation. Just like immunisation, the topic should be discussed antenatally, during the birthing admission, as part of the discharge check and at the six-week review.
More information
References
- Wagner CL et al. (AmericanAcademy of Pediatrics). Prevention of rickets and Vitamin D deficiency in infants, children and adolescents. Pediatrics 2008;122:1142-52
- Munns C et al. Position statement: Prevention and treatment of infant and childhood Vitamin D deficiency in Australia and New Zealand: a consensus statement. Med J Aust 2006;185:268-72
- Mason RS, Diamond TH (Editorials). Vitamin D deficiency and multicultural Australia. Med J Aust 2001;175:236-7
- Grover SR, Morley R. Vitamin D deficiency in veiled or dark-skinned pregnant women. Med J Aust 2001;175:251-2
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Version history
First published: August 2014
Review by: August 2017