Acrobat
MS WordPerinatologist Corner - C.E.U/C.M.E. Modules
Thyroid Disorders in Pregnancy
Sponsored by The Indian Health Service Clinical Support Center
4. Hyperthyroidism
Case Scenario
Nancy Standing Crow is a 29 y/o G2P1 at 32 weeks gestation. She is complaining of palpitations and feeling breathless and anxious. Vital signs: HR-112 at rest, BP-130/60, R-20, afebrile. The thyroid gland is about twice normal size, smooth, non-tender, without nodules. Reflexes are brisk and a fine tremor is present. You draw thyroid functions and they return as follows:
TSH: 0.01 mIU/mL (nl: 0.46-4.68)
Free T4: 7.61 ng/dL (nl: 0.78-2.19)
Should you take any action? What would be most appropriate?
Graves’ disease is the most common cause of hyperthyroidism during pregnancy. The classic signs and symptoms of tachycardia, palpitations, tremor, heat intolerance, weight loss, insomnia, and a goiter are well known. The ophthalmopathy, which occurs in about 50% of patients, is distinctive for this disorder when present. It may not be frank exophthalmos, and the subtler signs of lid lag and lid retraction should be sought.
Untreated severe maternal hyperthyroidism may be associated with preterm birth, fetal growth restriction, severe preeclampsia, and heart failure. Graves’ disease is mediated by thyroid stimulating immunoglobulins (TSI) and thyrotropin receptor blocking antibodies (TBII), autoantibodies that are present in 80-99% of patients with this disorder. TSI antibodies may cross the placenta and result in fetal hyperthyroidism in 1-5% of the infants of affected mothers, and TBII antibodies may cause fetal hypothyroidism in a similar percentage.
Fetal hyperthyroidism will usually manifest as fetal tachycardia. Fetal growth restriction and a fetal goiter may be evident on ultrasound. Some women are first diagnosed with hyperthyroidism during pregnancy, but many will present with a known history of the diagnosis, and may be under treatment or partially treated.
The most feared complication of untreated hyperthyroidism is “thyroid storm”, characterized by fever, tachycardia, hypertension, mental status changes, seizures, and heart failure. It is usually precipitated by some stressful event, such as an infection, surgery, or…labor and delivery. It may be confused with severe preeclampsia, because it is uncommon.
Treatment of hyperthyroidism
Treatment of Graves’ disease during pregnancy primarily involves the thioamides, propylthiouracil
(PTU) or methimazole.
These agents work to decrease thyroid hormone synthesis by blocking the incorporation of iodine into tyrosine, the precursor of thyroxine, and by reducing the peripheral conversion of T4 to T3, the biologically more active hormone.
The goal of therapy is to maintain the free T4 in the high normal range, using the lowest dose of the drug necessary in order to minimize the fetal effects. The thioamides cross the placenta and may suppress the fetal gland and cause fetal-neonatal hypothyroidism and, occasionally, fetal goiter. Effects of therapy can be checked 4 weeks after starting the drug and the dose adjusted accordingly.
Agranulocytosis, a rare complication of thioamide therapy, is usually heralded by fever and sore throat, and may necessitate discontinuing therapy. Thyroidectomy is an option for the occasional patient who is not a candidate for medical therapy. Beta-blockers may be used to decrease symptoms (palpitations, tremor) if necessary.
The above drugs may also be used in breast-feeding mothers, but radioactive iodine-131 therapy is contraindicated during pregnancy and breast-feeding because it will be taken up by and ablate the fetal-neonatal thyroid as well. Postpartum, women with Graves’ disease may continue PTU, but may be best served by definitive radioiodine ablation and supplemental thyroxine thereafter as necessary. “Thyroid storm” is a true emergency and requires treatment with high-dose thioamides, iodide, steroids, and the specific cardiac drugs needed to address heart failure and arrhythmias.
