bubble_chart Overview

Hyperthyroidism is a common endocrine disorder caused by excessive secretion of thyroid hormones. Women with hyperthyroidism often experience menstrual disturbances, reduced flow, or amenorrhea, leading to decreased fertility. However, pregnancy still occurs in some women with hyperthyroidism, whether treated or untreated, with an incidence rate of approximately 1 in 1,000 to 2,500 pregnancies. During pregnancy, hyperthyroidism is most commonly caused by Graves' disease, an autoimmune condition often triggered by psychological stress, characterized by diffuse goiter and exophthalmos.

bubble_chart Clinical Manifestations

A normal pregnancy, due to changes in maternal thyroid morphology and function, exhibits many clinical manifestations similar to hyperthyroidism, such as tachycardia, increased cardiac output, thyroid enlargement, warm skin, profuse sweating, heat intolerance, and hyperphagia, which are common in both pregnancy and hyperthyroidism.

Grade I hyperthyroidism has no significant impact on pregnancy, but moderate and grade III hyperthyroidism, as well as uncontrolled symptoms, are associated with increased rates of late abortion, pregnancy-induced hypertension, premature labor, full-term small-for-gestational-age infants, and perinatal mortality. The reasons for hyperthyroidism's impact on pregnancy remain unclear, possibly due to excessive consumption of nutritional elements by hyperthyroidism and the high incidence of pregnancy-induced hypertension, which affects placental function.

During pregnancy, due to the placental barrier, only small amounts of T₃ and T₄ can cross the placenta, thus not causing neonatal hyperthyroidism. Pregnancy generally has little effect on hyperthyroidism, and antagonism during pregnancy often leads to varying degrees of alleviation of hyperthyroidism symptoms. However, pregnancy combined with grade III hyperthyroidism can exacerbate the existing cardiac burden in hyperthyroidism patients due to the added strain on the heart during pregnancy. In rare cases, childbirth, postpartum bleeding, or infection may trigger a thyroid storm.

bubble_chart Diagnosis

Normal pregnancy, due to changes in maternal thyroid morphology and function, exhibits clinical manifestations similar to hyperthyroidism in many aspects, such as tachycardia, increased cardiac output, thyroid enlargement, warm skin, profuse sweating, heat intolerance, and hyperphagia, which are common in both pregnancy and hyperthyroidism. This makes the diagnosis of hyperthyroidism complicating pregnancy somewhat challenging. When symptoms and signs of hyperthyroidism are detected during prenatal check-ups, further thyroid function tests should be conducted to confirm the diagnosis. The diagnostic criteria for hyperthyroidism during pregnancy are as follows: presence of hypermetabolic symptoms, serum total thyroxine (TT₄) ≥ 180.6 nmol/L (14 μg/dL), total triiodothyronine (TT₃) ≥ 3.54 nmol/L (230 ng/dL), and free thyroxine index (FT₄I) ≥ 12.8. The severity of hyperthyroidism is classified as grade I when the highest level of TT₄ is <1.4 times the upper limit of normal; grade II when it is >1.4 times the upper limit of normal; and grade III when there is a crisis, thyrotoxic heart disease, heart failure, myopathy, or other complications.

bubble_chart Treatment Measures

(1) Pre-pregnancy: Due to the adverse effects of hyperthyroidism on the fetus, if hyperthyroidism is diagnosed, it is advisable to wait 1–3 years after the condition stabilizes before conceiving. Contraceptive measures should be taken during medication (antithyroid drugs or radioactive iodine), and pregnancy should be avoided.

(2) Management during pregnancy

1) Pregnant women with hyperthyroidism should be examined and followed up in a high-risk outpatient clinic. Attention should be paid to the intrauterine growth rate of the fetus, and hypertensive disorders of pregnancy should be actively controlled.

2) Grade I hyperthyroidism can be tolerated during pregnancy, so mild cases generally do not require antithyroid drug treatment, as these drugs can cross the placenta and affect fetal thyroid function. However, severe cases should still be treated with antithyroid drugs. During the middle and late stages (third trimester) of pregnancy, the dose of antithyroid drugs should not be excessive. Generally, the maternal blood TT₄ level should not exceed 1.4 times the upper limit of normal, meaning mild hyperthyroidism (Grade I) is acceptable. Antithyroid drugs should only be used when levels exceed 1.4 times the upper limit. Among antithyroid drugs, propylthiouracil (PTU) not only blocks thyroid hormone synthesis but also inhibits the peripheral conversion of T₄ to the active T₃, leading to a rapid decline in serum T₃ levels. The usual dose of PTU is 150–300 mg/d, or methimazole 15–30 mg/d. After hyperthyroidism is controlled, the dose can be gradually reduced. Medication should be discontinued or minimized to the lowest effective dose 2–3 weeks before the expected due date. If PTU is kept below 200 mg/d or methimazole below 20 mg/d, the likelihood of fetal goiter is extremely low. There is debate over whether thyroid hormone should be added during antithyroid drug treatment. Since thyroid hormone does not easily cross the placenta, its use may increase the required dose of antithyroid drugs. However, combination therapy can counteract hypothyroidism caused by antithyroid drugs and prevent fetal hypothyroidism or goiter.

3) Since antithyroid drugs rapidly cross the placenta and affect fetal thyroid function, some advocate subtotal thyroidectomy after antithyroid drug treatment, with good results. However, the general consensus is to avoid thyroidectomy during pregnancy due to the increased surgical difficulty, higher risks of maternal hypothyroidism, hypoparathyroidism, and recurrent laryngeal nerve injury, as well as the potential for late abortion and premature labor.

4) The use of β-blockers such as propranolol (10–20 mg, three times daily). Propranolol is an effective treatment for pregnant women with hyperthyroidism, alleviating systemic symptoms caused by excessive thyroid hormone. It acts quickly and is effective for thyroid crisis and rapid preoperative preparation for emergency thyroid surgery. However, β-blockers can trigger acute heart failure in early heart failure or metabolic acidosis and may cause severe hypotension under general anesthesia. Long-term use of propranolol can increase uterine muscle tension, impair placental development, and lead to intrauterine growth restriction. Therefore, it should not be the first-line treatment for hyperthyroidism during pregnancy.

5) Obstetric management: With proper treatment, pregnancy complicated by hyperthyroidism can proceed to term, with vaginal delivery and a live birth. Hyperthyroidism is not an indication for cesarean section. However, pregnancy with Grade III hyperthyroidism is associated with higher rates of premature labor and perinatal mortality, as well as possible intrauterine growth restriction. Thus, close monitoring and control of hyperthyroidism during pregnancy are essential, along with regular follow-up of fetal-placental function and prevention of premature labor.

6) Management during the puerperium: Postpartum hyperthyroidism has a tendency to recur, so the dose of antithyroid drugs should be increased after delivery. Regarding the issue of postpartum breastfeeding, although antithyroid drugs can affect the infant's thyroid function through breast milk, we believe that the decision to breastfeed should be based on the severity of the mother's condition and the dose of antithyroid medication being taken.

7) Management of thyroid storm: Uncontrolled hyperthyroidism during pregnancy, discontinuation of antithyroid drugs, obstetric surgery, postpartum infections, and postpartum bleeding can trigger thyroid storm. If left untreated, it may lead to high fever, tachycardia, heart failure, loss of vitality, and unconsciousness. Treatment involves administering large doses of antithyroid drugs, such as propylthiouracil or methylthiouracil, 100–200 mg every 6 hours orally; or methimazole or carbimazole, 10–20 mg every 6 hours orally. For unconscious patients unable to take oral medication, administer via nasogastric tube. Give compound iodine solution orally, approximately 30 drops daily. Propranolol, 20–40 mg every 4–6 hours orally, or 0.5–1 mg intravenously, with attention to cardiac function. Reserpine, 1–2 mg intramuscularly every 6 hours. Hydrocortisone, 200–400 mg daily via intravenous drip; also administer broad-spectrum antibiotics, oxygen therapy, cold compresses, sedatives, and antipyretics, and correct typical edema, electrolyte imbalances, and heart failure.

8) Neonatal management: For newborns delivered by hyperthyroid mothers, monitor for hypothyroidism, goiter, or hyperthyroidism, and perform thyroid function tests.

Maternal TSH, T₄, and T₃ rarely cross the placental barrier, but long-acting thyroid stimulator (LATS) easily crosses it. Thus, infants of hyperthyroid mothers may develop neonatal hyperthyroidism, presenting with prominent exophthalmos and signs of hyperthyroidism. Measurement of T₄ and TSH levels in umbilical blood can assess neonatal thyroid function. Neonatal hyperthyroidism may appear immediately after birth or after 1 week. Treatment includes methimazole, 0.5–1 mg/kg daily, or propylthiouracil, 5–10 mg/kg daily, divided doses, plus compound iodine solution, 1 drop three times daily. For heart failure, administer digitalis; for agitation, use sedatives.

Newborns of mothers who took antithyroid drugs during pregnancy may develop transient hypothyroidism and should be monitored closely.