Neonatal Efects. Normally, cord blood calcium levels are higher than maternal levels (Chap. 7, p. 139). With maternal hyperparathyroidism, abnormally elevated maternal and thus fetal levels further suppress fetal parathyroid function. Because of this, newborn calcium levels rapidly drop after birth, and 15 to 25 percent of these neonates develop severe hypocalcemia with or without tetany (Molitch, 2000). Neonatal hypoparathyroidism caused by maternal hyperparathyroidism is usually transient and is treated with calcium and 1,25-dihydroxyvitamin D3 (calcitriol). he latter will not be efective in preterm infants, however, because the intestinal vitamin D receptor is not suiciently expressed (Kovacs, 2011) . Neonatal tetany or seizures should stimulate an evaluation for maternal hyperparathyroidism (Beattie, 2000; Ip, 2003).
The most common cause of hypocalcemia is hypoparathyroidism that usually follows parathyroid or thyroid surgery. Hypoparathyroidism is estimated to follow up to 7 percent of total thyroidectomies (Shoback, 2008). It is characterized by facial muscle spasms, muscle cramps, and paresthesias of the lips, tongue, fingers, and feet. This can progress to tetany and seizures (Potts, 2015). Chronically, hypocalcemic pregnant women may also have a fetus with skeletal demineralization resulting in multiple bone fractures in the neonatal period (Alikasifoglu, 2005).
Maternal treatment includes calcitriol, dihydrotachysterol, or large vitamin D doses of 50,000 to 150,000 U/d; calcium gluconate or calcium lactate in doses of 3 to 5 g/d; and a lowphosphate diet. Fetal risks from large doses of vitamin D have not been established. During treatment, the therapeutic challenge in women with known hypoparathyroidism is management of blood calcium levels. It is possible that the greater calcium absorption typical of pregnancy will result in lower calcium requirements or that the fetal demand for calcium will result in greater need. he goal during pregnancy is to maintain a corrected calcium level in the low normal range.
In most gravidas, even with their remarkably increased calcium requirements, it is uncertain whether pregnancy causes osteopenia (Kaur, 2003; To, 2003). In one study of200 pregnant women in which bone mass was measured, Kraemer and colleagues (2011) demonstrated a decline in bone density during pregnancy. Women who breastfed, carried twin pregnancies, or had a low body mass index were at higher risk of bone loss. From their review, Thomas and Weisman (2006) cite a 3-to 4-percent average reduction in bone mineral density during pregnancy. Lactation also represents a period of negative calcium balance that is corrected through maternal skeletal resorption. Feigenberg and coworkers (2008) found cortical bone mass reductions using ultrasound in young primiparas in the puerperium compared with nulligravid controls. Rarely, some women develop idiopathic osteoporosis while pregnant or lactating (Hellmeyer, 2007).