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Hypocalcemia - and Hypomagnesemia
Hypocalcemia - and Hypomagnesemia
Hypocalcemia - and Hypomagnesemia
During fetal life, calcium is transferred by active transport across the placenta. The fetus, especially during the third trimester, has low parathyroid
hormone (PTH) due to the relatively high serum calcium levels. At birth, with the abrupt end of maternal calcium transfer, infant parathyroid hormone
levels rise to compensate for decreasing serum calcium. In the IDM, parathyroid hormone levels and endorgan sensitivity to PTH are lower than age
matched controls during the first 4 days after birth. Additionally, PTH secretion may be hampered by hypomagnesemia, even in the setting of
hypocalcemia. Hypocalcemia can be magnified if the IDM is born prematurely or suffers from perinatal depression. Persistently high levels of calcitonin
and alterations in vitamin D metabolism may also play a role.
Hypomagnesemia occurs in up to one third of IDMs. Neonatal magnesium levels correspond to the mother’s levels as well as to maternal insulin
requirements.20 Mothers with advanced diabetes and renal insufficiency may have significant renal losses of magnesium, which contribute to low
placental transfer of this electrolyte.
Total and ionized serum calcium should be measured at least daily during the first 72 to 96 hours of life. Daily calcium requirements are 100 to 200
mg/kg, and IDMs may require up to 3 times that amount. Symptomatic infants should be treated with 10% calcium gluconate given intravenously under
careful monitoring because of the risk of arrhythmias and intravenous infiltrates. Daily maintenance therapy can be considered on the basis of feeding
status and laboratory value trends. It should be noted that if a hypocalcemic infant is also hypomagnesemic, calcium therapy is futile unless
magnesium levels are replete.