Hyperthyroidism may occur in up to 0.2% of pregnancies. It is the second most
common endocrinopathy in pregnancy after diabetes.
Preexisting disease may worsen in the 1st trimester and ease in the last 2
Pregnant patients may normally have symptoms that are similar to
hyperthyroidism. These include: heat intolerance, nervousness, and
hyperdynamic circulation. Weight loss and tachycardia that is unchanged with
Valsalva maneuver should raise the index of suspicion toward hyperthyroidism.
Also look for eye signs, thyromegaly, frequent stools, and myopathy.
This occurs in 2 out of every 1000 pregnancies. Hyperthyroidism can manifest
as hyperemesis gravidarum. Also approximately half of pregnant women with
hyperemesis gravidarum will show increased free T4 levels and an undetectable
or suppressed TSH (TSH level is almost always less than 2.5 mU/ml in
hyperemesis gravidarum). A lesser number of patients will have elevated free
T3 levels. High levels of HCG appear to stimulate the thyroid. Generally, thyroid
levels return to normal by a month after resolution of the hyperemesis (i.e., by
about 18 weeks) without specific treatment of the hyperthyroidism. Other
hyperthyroid symptoms are usually absent. If symptoms persist beyond 20
weeks, if the patient is positive for TSIg, or if symptoms of hyperthyroidism
predate the pregnancy, then the patient is likely to be truly hyperthyroid.
Some patients with a hydatidiform mole will have a syndrome of hyperthyroidism
without other autoimmune phenomena. Trophoblastic disease occurs in 1 out of
1500 pregnancies. Clinical symptoms range from none to severe thyrotoxicosis
with thyroid storm.
This is an autoimmune disorder in which antibodies to the TSH receptor cause
hyperthyroidism. It is important to treat the maternal hyperthyroidism without
inducing fetal hypothyroidism. Furthermore, the fetus must be evaluated for
hyperthyroidism. In patients who have not been treated prior to pregnancy,
Graves disease is usually worse in the first half of pregnancy and then improves
because of the relatively immunosuppressed nature of pregnancy. Postpartum,
Graves disease tends to worsen because of the return of relative
immunocompetence. In these patients, thyroid function tests should be ordered
every 4 weeks until the hyperthyroidism improves. The free T4 level is best to
monitor these patients as TSH levels may remain in the suppressed range.
Medication adjustments, therefore, should not be based on the TSH level. This
can be planned by adding a line on the Flow Sheet and circling appropriate
boxes plus adding a note on section 33: e.g., follow thyroid.
The necessary tests include a serum free T4, total or free T3, TSH, and antibody
studies. The diagnosis is difficult in the 1st trimester because T4 levels can be
high and TSH levels can be low-normal (TSH can be suppressed in 15% of
patients). If the free T4 level is high and the TSH is <0.05, the mother is likely to
be hyperthyroid. A level of thyroid-stimulating antibodies greater than 300% is
highly suggestive of Graves disease, although TSIg may be normal in Graves
disease. Radioiodine uptake and thyroid scans are absolutely contraindicated in
pregnancy as they may be harmful to the fetus.
Initiate treatment along with consultant. Beta blockers can be used to control
symptoms (see Section C1 Cardiac Medications, page 264.00 for additional
discussion of these drugs). Consultant may recommend starting drugs such as
propranolol at 20 mg PO q6H. After symptomatic control with beta-blocker,
antithyroid drugs are preferred as definitive treatment for patients requiring it.
Hyperthyroidism diagnosed during pregnancy often does not require definitive
treatment when it is mild; spontaneous resolution may occur. (9)
See Section C1 Cardiac Medications, page 264.00 for discussion. Use of drugs
for acute management should be relatively safe. Review chronic use with your
consultant. Chronic use of beta-blockers has been associated with IUGR, small
placenta, postnatal hypoglycemia, bradycardia, and increased fetal loss.
1. Rule out anemia, infection, and preeclampsia as precipitating causes.
2. Cardiac and fetal monitoring of viable fetus.
3. Supplemental oxygen and IV hydration.
4. Acetaminophen for fever and a cooling blanket if needed.
5. IV propranolol at 1 mg/min q 10-15 minutes up to 10 mg.
6. If congestive heart failure is present, pre-treatment with digoxin should be
considered prior to giving propranolol. Add diuretics if needed.
7. Dexamethasone 10 mg IV.
8. Propylthiouracil (PTU) can be given at a dose of 900-1200 mg loading dose
PO or by NG tube.
9. Sodium iodide can be given 1 hour after the PTU at a dose of 1 g.
Because of the life threatening nature of the condition, items 8 and 9 above are
given to the mother despite potential risks to the fetal thyroid. The risks are
discussed in the next paragraph.
Iodine 131 and inorganic iodides are contraindicated since they will lead to
congenital hypothyroidism. Subtotal thyroidectomy can be attempted in the 2 nd
trimester after the patient has been rendered euthyroid with antithyroid drugs. A
second option is to treat purely with antithyroid medications (propylthiouracil or
Antithyroid drugs cross the placenta and may lead to transient fetal goiter or
hypothyroidism approximately 1-5% of the time. This can generally be prevented
if doses are kept low during the 3rd trimester. Propylthiouracil does not cross the
placenta as well as methimazole does. Compliance is usually better with
methimazole as it only needs to be dosed once or twice per day. Methimazole,
however, has been associated with the congenital condition aplasia cutis.
Propylthiouracil is probably the better drug, if tolerated, because it lacks this
association and has only very low concentrations in the breast milk. Thyroxine at
0.1 mg/day has been reported to cause a significant reduction in postpartum
Overall therapy decisions, doses, etc. should involve OB and endocrine
Endocrinologist or internist with experience in this area, Maternal-Fetal Medicine
Under certain circumstances, consultant may recommend that the patient can be
followed up as an outpatient. Arrange prompt, definitive appointment.
Depending on choice of therapy, different clinical and lab parameters will need to
be followed. For example, patients on antithyroid drugs should have regular T4
levels checked. These can be programmed by entering T4 levels on one of the
blank lines of the Flow Sheet (e.g., blank line below 6H Vits Iron) and then
circling boxes at appropriate intervals on that line. Clinical responses (e.g.,
elimination of tachycardia) are also helpful in adjusting therapy. Weight gain
should be followed carefully. Patients with known Graves disease should
establish a euthyroid state for at least three months prior to pregnancy. If a
woman decides to have radioactive iodine prior to conception, she should wait
several months before attempting to conceive.
All newborns should be receiving routine thyroid screens at birth.
Risk to Mother
Most complications occur in patients who are either undiagnosed or
uncontrolled.(1) If untreated, these patients are at increased risk for pregnancy-
induced hypertension, premature delivery, congestive heart failure, thyroid storm,
placental abruption and infectious complications.(7) There is controversy as to
whether hyperthyroidism increases the rate of spontaneous losses.
Risk to Fetus
In fetuses of mothers with hyperthyroidism, there is an increased risk of
intrauterine growth restriction, prematurity and stillbirths. One study found a
stillbirth rate of 24% in patients with untreated hyperthyroidism and 5-7% of
treated patients.(7) In this same study, there was a premature delivery rate of
53% in untreated patients and 9-11% of treated patients. Furthermore, thyroid
storm was seen in 21% of untreated patients and 5% of treated patients. The
risk of low-birthweight babies has been correlated to the number of gestational
weeks in which the mother was hyperthyroid. The risk was lower in mothers
whose hyperthyroidism was controlled by the end of the 1 st trimester as opposed
to those that suffered from the condition throughout their pregnancy. (8)
Other authors have noted that small-for-gestational age babies are more likely in
mothers who were hyperthyroid for more than 30 weeks during pregnancy, had
Graves disease for more than 10 years, had Graves disease beginning at an age
less than 20 years, or had maternal TSIg or TSH-binding inhibitor IgG levels of
more than 30%.(9) There is also an increased risk of congenital malformations.
Risk to Newborn
In mothers whose hyperthyroidism is secondary to Graves Disease, there is an
increased risk of fetal hyperthyroidism. This includes mothers who have been
treated previously with radioactive iodine and are either using no medication or
are receiving T4 replacement. Even though the mother may be euthyroid, she
still carries autoantibodies. When TSIg crosses the placenta, the fetal thyroid
may be stimulated causing fetal hyperthyroidism. The clinician should be alert
for a previously affected sibling, fetal tachycardia or persistent maternal antibody
titers despite seemingly adequate therapy. This can be associated with infant
Add to area 31 of the Flow Sheet: e.g., hyperthyroidism. Add treatment, e.g.,
1. Davis LE, Lucas MJ, Hankins GDV, et al: Thyrotoxicosis complicating pregnancy. Am J
Obstet Gynecol 160:63, 1989.
2. Swaminathan R, Chin RK, Lao TTH, et al: Thyroid function in hyperemesis gravidarum. Acta
Endocrinol 120:155, 1989.
3. Bober SA, McGill AC, Tunbridge WMG: Thyroid function in hyperemesis gravidarum. Acta
Endocrinol 111:404, 1986.
4. Burrow GN: Thyroid function and hyperfunction during gestation. Endocr Rev 14:194, 1993.
5. Hashizume K, Ichikawa K, Nishii Y, et al: Effect of administration of thyroxine on the risk of
postpartum recurrence of. J Clin Endocrinol Metab 75:6, 1992.
6. Singer PA: Will postpartum recurrence of hyperthyroid Graves’ disease be a thing of the
past? (editorial). J Clin Endocrinol Metab 75:5A, 1992.
7. Inzucchi SE, Burrow GN: Hyperthyroidism in pregnancy. In: Bardin CW, ed. Current
Therapy in Endocrinology and Metabolism, 6 ed. St. Louis, MO: Mosby, 312-7, 1997.
8. Millar LK, Wing DA, Leung AS, et al: Low birthweight and pre-eclampsia in pregnancies
complicated by hyperthyroidism. Am J Obstet Gynecol, 84:946-9, 1994.
9. Mitsuda N, Tamaki H, Amino N, et al: Risk factors for developmental disorders in infants born
to women with Graves Disease. Obstet Gynecol, 80:359-64, 1992.