Management of Thyroid Disorders in Pregnancy

Initial Laboratory Evaluation

Screen all pregnant patients with suspected thyroid disease using serum TSH as the first‑line test; when hyper‑ or hypothyroidism is suspected, obtain both TSH and a free‑thyroxine measurement (FT4 or free thyroxine index). 3
Test for thyroid‑stimulating hormone‑receptor antibodies in women with current or prior Graves’ disease to guide management. 4

Begin levothyroxine therapy immediately after diagnosis (do not await repeat labs) to prevent first‑trimester‑related neurocognitive injury in the fetus. 1
Target a maternal TSH < 2.5 mIU/L throughout the first trimester and keep free T4 in the high‑normal range for the duration of pregnancy. 1
Increase the pre‑pregnancy levothyroxine dose by 25–50 % as soon as pregnancy is confirmed; thereafter adjust in 12.5–25 µg increments based on serial TSH values. 1
Monitor TSH every 4 weeks until a stable level is achieved, then at least once each trimester. 3
Untreated overt hypothyroidism markedly raises the risk of preeclampsia, low birth weight, placental abruption, and fetal death, and it causes permanent neurocognitive impairment in offspring. [1][4]

In pregnant women with elevated TSH and positive thyroid peroxidase antibodies, treat with levothyroxine to achieve TSH < 2.5 mIU/L in the first trimester, given the low medication risk and the potential for adverse obstetric outcomes. 1

Use propylthiouracil (PTU) as the first‑line antithyroid drug during the first trimester because it carries a lower risk of congenital malformations than methimazole; switch to methimazole in the second and third trimesters. 2
Aim for free T4 (or free thyroxine index) in the high‑normal range using the lowest effective thioamide dose. [5][2]
Check free T4/FTI every 2–4 weeks to guide dose adjustments; once euthyroid, measure TSH each trimester. [5][2]3
Monitor for agranulocytosis (fever, sore throat) with a complete blood count and discontinue the thioamide immediately if suspected; be aware of other rare adverse effects such as hepatitis, vasculitis, and thrombocytopenia. 5
Provide short‑acting β‑blockers (e.g., propranolol) for symptomatic control of tremor, tachycardia, or palpitations until thyroid hormone levels normalize. [5][2]
Inadequately treated hyperthyroidism increases the risk of severe preeclampsia, preterm delivery, maternal heart failure, miscarriage, and low birth weight. [4][5]
Graves’ disease accounts for roughly 95 % of hyperthyroidism cases in pregnancy. 4
Transplacental passage of TSH‑receptor antibodies can cause fetal thyrotoxicosis and neonatal thyroid dysfunction. [4][5]

Diagnose based on elevated free T4/FTI with suppressed TSH in the absence of a thyroid mass or nodular goiter; characteristic ocular signs (eyelid lag/retraction) and pretibial myxedema may be present. 4
Monitor fetal heart rate and growth; perform ultrasound for fetal goiter only if clinical concerns arise. 3
Notify the newborn’s care team of maternal Graves’ disease because of the risk of neonatal thyroid dysfunction. [3][2]
Transient fetal or neonatal thyroid suppression from maternal thioamide therapy usually requires no specific treatment. 5

Recognize as a medical emergency (fever, marked tachycardia, altered mental status, gastrointestinal symptoms, arrhythmia). 2
Treat promptly without waiting for labs using PTU or methimazole, inorganic iodide, dexamethasone, phenobarbital, and supportive care; avoid delivery unless absolutely necessary. 2

Biochemical hyperthyroidism associated with severe nausea/vomiting rarely needs antithyroid therapy unless overt clinical signs are present; routine thyroid testing is not recommended in isolated hyperemesis. 2

Reserve thyroidectomy for patients who fail thioamide therapy or develop severe drug intolerance (e.g., agranulocytosis, hepatotoxicity). [3][2]
If surgery is required, schedule it in the second trimester. 2

Radioactive iodine (I‑131) is strictly contraindicated throughout pregnancy because it ablates the fetal thyroid. [3][2]
If inadvertent exposure occurs after 10 weeks gestation, assess the risk of congenital hypothyroidism; women must wait at least 4 months after I‑131 therapy before initiating breastfeeding. [3][2]

Women who were treated with PTU or methimazole during pregnancy may breastfeed safely. 5

Do not postpone treatment while awaiting repeat thyroid tests; fetal harm can precede maternal symptom onset. 1
Never aim for a TSH > 2.5 mIU/L in the first trimester, as even subclinical elevations are linked to adverse pregnancy outcomes. 1
Avoid methimazole in the first trimester when PTU is available because of its higher teratogenic risk. 2
Do not use radioactive iodine during pregnancy. [3][2]
Promptly evaluate any sore throat or fever in a patient on thioamides with a complete blood count and discontinue the drug if agranulocytosis is suspected. 5