Intrauterine Growth Restriction (IUGR)
Hypothyroidism can lead to IUGR, where the fetus does not grow at the expected rate. This is often due to placental dysfunction and insufficient thyroid hormone support for fetal development. Babies born to mothers with untreated hypothyroidism are often smaller at birth and may face physical and cognitive developmental delays.
Neurological Impairment
Thyroid hormones are vital for fetal brain development, particularly in the first trimester. If maternal thyroid hormone levels are low, the risk of cognitive impairments and developmental delays in the child increases. In the landmark Haddow study (1999), children of women with untreated hypothyroidism in pregnancy scored about 7 IQ points lower at age 7 to 9 than controls, and 19% had an IQ below 85 compared with 5% of controls. Maternal hypothyroidism itself seldom causes congenital hypothyroidism, because the fetal thyroid functions independently after the first trimester; the exceptions are severe iodine deficiency, transplacental TSH receptor-blocking antibodies, and excessive maternal antithyroid drug, each of which can leave the newborn hypothyroid and, if not detected on newborn screening and treated promptly, with permanent intellectual disability.
Neonatal Hypothyroidism
Babies born to mothers with hypothyroidism from iodine deficiency, TSH receptor-blocking antibodies, or antithyroid drug exposure may have transient or permanent neonatal hypothyroidism; routine newborn screening (TSH or T4 on the heel-stick sample at 2 to 5 days) identifies it, and prompt levothyroxine replacement prevents the neurologic damage. Untreated thyroid dysfunction in the newborn can affect feeding, growth, and overall health.
Proper management of hypothyroidism during pregnancy, including regular monitoring of thyroid hormone levels and appropriate treatment, is essential to minimize the risks to both the mother and fetus, ensuring a healthy pregnancy and positive outcomes for both.
| Risk area | Hyperthyroidism | Hypothyroidism |
|---|---|---|
| Miscarriage | Increased with poor control, especially in the first trimester | Increased with elevated TSH and untreated disease, especially in the first trimester |
| Hypertensive disease | Preeclampsia, particularly with Graves’ disease; hypertension from increased sympathetic activity and cardiac output | Gestational hypertension that can progress to preeclampsia |
| Preterm delivery | Preterm labor and birth when uncontrolled | Higher risk of preterm delivery |
| Fetal growth | IUGR from placental insufficiency | IUGR from placental dysfunction and insufficient hormone support |
| Neonatal thyroid effect | Neonatal thyrotoxicosis if TRAbs cross the placenta — fetal tachycardia, goiter, IUGR | Neonatal hypothyroidism is uncommon (iodine deficiency, blocking antibodies, antithyroid drug exposure); permanent intellectual disability if not treated promptly after newborn screening |
| Maternal crisis | Thyroid storm; heart failure from the added metabolic demand | Myxedema coma — hypothermia, altered mental status, multisystem failure |
| Hematologic and placental | — | Anemia, placental abruption, and postpartum hemorrhage |
| Medication-related | Methimazole in the first trimester linked to rare malformations such as aplasia cutis and choanal atresia | — |
