Practice Guidelines

ACOG Practice Bulletin on Thyroid Disease

in Pregnancy

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Barrett M. Schroeder
Am Fam Physician. 2002 May 15;65(10):2158-2162.
The Committee on Practice BulletinsObstetrics of the American College of Obstetricians and
Gynecologists (ACOG) has developed a practice guideline on thyroid disease in pregnancy.
ACOG Practice Bulletin No. 32 appears in the November 2001 issue of Obstetrics and
Gynecology.
The ACOG guideline discusses changes in thyroid function during pregnancy, hyperthyroidism,
hypothyroidism, and clinical considerations; and provides recommendations. The following
information is a summary of the ACOG practice bulletin.

Thyroid Function During Pregnancy

Normal pregnancy, hyperthyroidism, and hypothyroidism affect thyroid function test results (see
accompanying table). In pregnancy, the values influenced by the serum thyroid binding hormone
level (i.e., total thyroxine, total triiodothyronine, and resin triiodothyronine uptake) change
significantly.

Plasma iodide levels decrease as a result of fetal iodide use and increased maternal renal
clearance. In about 15 percent of pregnant women, these lower iodide levels are associated with
a noticeable increase in thyroid gland size.

Hyperthyroidism
Thyrotoxicosis is a clinical and biochemical state resulting from excess production of and
exposure to thyroid hormone because of any etiology. Hyperthyroidism, which occurs in 0.2
percent of pregnancies, is thyrotoxicosis resulting from hyperfunction of the thyroid gland. The
many signs and symptoms of hyperthyroidism include tremors, nervousness, insomnia, excessive
sweating, heat intolerance, tachycardia, hypertension, and goiter.
Graves' disease is responsible for 95 percent of hyperthyroidism cases in pregnancy. Distinctive
ophthalmic signs include eyelid lag or retraction; dermal signs include localized and pretibial
myxedema. The diagnosis of this disease is generally based on an elevated free thyroxine (FT4)
level or free thyroxine index (FTI), with suppression of thyroid-stimulating hormone (TSH) in
the absence of thyroid mass or nodular goiter.
Thyroid storm, a rare condition affecting 1 percent of pregnant women with hyperthyroidism, is
characterized by severe, acute exacerbation of the signs and symptoms of hyperthyroidism.
Thyroid storm is a medical emergency.
Unless hyperthyroidism is treated adequately, pregnant women are at increased risk for severe
preeclampsia, preterm delivery, heart failure, and, possibly, miscarriage. Low birth weight in
neonates also can occur.
Graves' disease and its treatment (thioamides) increase fetal and neonatal risks. Fetal
thyrotoxicosis needs to be considered in women who have a history of Graves' disease; if this
condition is diagnosed, appropriate consultation should be sought. Because of antibodies that
cross the placenta, the possibility of neonatal immune-mediated hypothyroidism or
hyperthyroidism is an additional concern.
View/Print Table
Changes in Thyroid Function Test Results in Normal Pregnancy and in Thyroid Disease
Maternal status TSH
Pregnancy

FT4

FTI

TT4

TT3

No change No change No change Increase Increase

RT3U
Decrease

Hyperthyroidism Decrease

Increase

Increase

Increase Increase or no change Decrease

Hypothyroidism Increase

Decrease

Decrease

Decrease Decrease or no change Increase

Maternal status TSH

FT4

FTI

TT4

TT3

RT3U

TSH = thyroid-stimulating hormone; FT4 = free thyroxine; FTI = free thyroxine index; TT4 =
total thyroxine; TT3 = total triiodothyronine; RT3U = resin triiodothyronine uptake.
Reprinted with permission from ACOG Practice Bulletin. Clinical management guidelines for
obstetrician-gynecologists. No. 32, November 2001. Thyroid disease in pregnancy. Obstet
Gynecol 2001;98(5 pt 1):8798.

Hypothyroidism
Hypothyroidism is usually caused by a primary thyroid abnormality, although a few cases are
caused by hypothalamic dysfunction. In pregnant or postpartum women, the most common
causes are chronic thyroiditis or chronic autoimmune thyroiditis (Hashimoto's disease), subacute
thyroiditis, radioactive iodine therapy, thyroidectomy, and iodine deficiency. Hashimoto's disease
is the most frequent cause in industrialized nations; worldwide, iodine deficiency is the most
common cause.
Signs and symptoms of hypothyroidism include fatigue, muscle cramps, constipation, cold
intolerance, hair loss, and others. With progression of the disorder, voice changes, weight gain,
intellectual slowness, and insomnia can occur. Untreated hypothyroidism progresses to
myxedema and myxedema coma. Presentation of advanced hypothyroidism in pregnancy is
unusual. Subclinical hypothyroidism is identified by an elevated TSH level in a pregnant woman
without symptoms.
Untreated maternal hypothyroidism increases the risk of preeclampsia. Whether subclinical
hypothyroidism increases this risk is uncertain. Inadequate treatment of hypothyroidism is
associated with low birth weight in neonates. Maternal hypothyroidism from iron deficiency
increases the risk of congenital cretinism (growth failure, mental retardation, other
neuropsychologic defects). Iodine therapy in the first and second trimesters significantly reduces
neurologic abnormalities associated with this disorder.
Cretinism also occurs with untreated congenital hypothyroidism. Newborn screening for
congenital hypothyroidism is offered throughout the United States. Treatment in the first several
weeks of life can result in nearly normal intelligence and growth.

Clinical Considerations and ACOG Recommendations

What laboratory tests for thyroid disease are used in pregnant women? TSH testing (now
performed using monoclonal antibodies) is the recommended initial test for screening and
evaluating patients with symptomatic disease. TSH and FT4 or FTI testing should be performed

in pregnant women with suspected hyperthyroidism or hypothyroidism. The thyrotropinreleasing hormone level is another test of thyroid function. The clinical usefulness of various
antibody tests depends on the individual situation.
What medications are used to treat hyperthyroidism and hypothyroidism in pregnancy?
Hyperthyroidism in pregnant women is treated with a thioamide (propylthiouracil or
methimazole). Recent studies have found no significant differences between propylthiouracil and
methimazole in mean FT4 or TSH levels in newborn cord-blood samples, as well as no cases of
aplasia cutis and similar rates of fetal anomalies for both agents. Women treated with
propylthiouracil or methimazole can breastfeed safely.
The goal is to maintain FT4 or FTI in the high-normal range using the lowest possible thioamide
dosage. Measuring the FT4 or FTI every two to four weeks can be helpful. Until thioamide
therapy reduces thyroid hormone levels, a beta blocker (e.g., propranolol) can be used to reduce
symptoms.
Agranulocytosis, a side effect of thioamides, usually presents with sore throat and fever. If these
symptoms develop, a complete blood cell count should be obtained, and the thioamide should be
discontinued. Other side effects include hepatitis, vasculitis, and thrombocytopenia.
Although suppression of fetal and neonatal thyroid function can occur with thioamide therapy for
Graves' disease, it is usually transient, and treatment is rarely required. Fetuses of women with
Graves' disease should be monitored for normal heart rate and appropriate growth; unless
problems are detected, ultrasound screening for fetal goiter is not necessary. The newborn's
physician needs to be aware that the mother has Graves' disease because of the associated risk of
neonatal thyroid dysfunction.
Thyroidectomy should be reserved for women who do not respond to thioamide therapy.
Treatment with iodine 131 (I-131) is contraindicated in pregnant women. Fetal thyroid is
unlikely to have been ablated if inadvertent exposure to this agent occurred before 10 weeks of
gestation. If exposure occurred after this time, the woman needs to consider the risk of induced
congenital hypothyroidism and whether pregnancy should be continued. Women should not
breastfeed for four months after treatment with I-131.
Hypothyroidism in pregnant women is treated with levothyroxine in a sufficient dosage to return
the TSH level to normal. The dosage should be adjusted every four weeks until the TSH level is
stable. Checking the TSH level every trimester is advised.
What thyroid function changes occur with hyperemesis gravidarum? Nausea and vomiting of
pregnancy is associated with biochemical hyperthyroidism (undetectable TSH level, elevated
FTI, or both). The condition is rarely associated with clinical hyperthyroidism, and no treatment
is usually required. Routine thyroid testing is not recommended unless other signs of
hyperthyroidism are present.
How is thyroid storm diagnosed and treated in pregnancy? This extreme hypermetabolic state is
associated with a high risk of maternal heart failure. Diagnosis is based on a combination of

signs and symptoms: fever, tachycardia out of proportion to the fever, altered mental status
(nervousness, restlessness, confusion, seizures), vomiting, diarrhea, and cardiac arrhythmia. An
inciting event (e.g., surgery, infection, labor, delivery) may be identified. Untreated thyroid storm
can result in shock, stupor, and coma. Serum-free triiodothyronine (FT3), FT4, and TSH levels
help confirm the diagnosis, but treatment should not be delayed for test results.
A standard series of drugs is used to treat thyroid storm: propylthiouracil or methimazole;
saturated solution of potassium iodide or sodium iodide (alternatives: Lugol's solution, lithium);
dexamethasone (and with a history of severe bronchospasm: reserpine, guanethidine, diltiazem);
and phenobarbital. General supportive measures, such as oxygen, antipyretics, and appropriate
monitoring, are also important. The perceived underlying cause of thyroid storm should be
treated.
Depending on gestational age, fetal status should be evaluated with ultrasound examination,
nonstress testing, or a biophysical profile. Unless deemed necessary, delivery during thyroid
storm should be avoided.
How should thyroid cancer be managed during pregnancy? All thyroid nodules should be
evaluated; up to 40 percent are found to be malignant. Thyroid cancer is treated with
thyroidectomy and radiation (i.e., I-131). Thyroidectomy can be performed, preferably during the
second trimester, but radiation therapy should not be administered until after the pregnancy.
Management options for thyroid cancer are termination of the pregnancy followed by full
treatment, treatment during pregnancy, and preterm or term delivery followed by full treatment.
Gestational age and tumor characteristics affect the management choice. Women should not
breastfeed for four months after I-131 treatment.
How is postpartum thyroiditis diagnosed and treated? Postpartum thyroiditis is diagnosed by new
onset of an abnormal TSH level, abnormal FT4 level, or both. Antibody testing may be useful in
confirming the diagnosis. Whether postpartum thyroiditis requires treatment is less clear.
TSH and FT4 levels should be evaluated in women who develop a goiter during pregnancy or
after delivery. Evaluation may also be appropriate for women who develop post-partum
symptoms of hyperthyroidism or hypothyroidism. Evaluation depends on the physician's
judgment, as some of these symptoms are common in the postpartum period. Whether treatment
is needed depends on the severity of the abnormality and symptoms. The risk of permanent
hypothyroidism is greatest in women with the highest levels of TSH and antithyroid peroxidase
antibodies.
Which pregnant women should be screened for thyroid dysfunction? Screening is appropriate in
pregnant women with symptoms of thyroid disease or a history of thyroid disease. Thyroid
nodules or goiter should be evaluated.
Available data support a possible association between maternal hypothyroidism and decrements
in some neuropsychologic tests in their children. However, further testing is needed to document
validity and provide evidence of treatment efficacy. According to ACOG, it is premature to
recommend universal hypothyroidism screening in pregnant women.