Management of Hyperemesis Gravidarum with Biochemical Hyperthyroidism

Do Not Treat the Biochemical Hyperthyroidism with Antithyroid Drugs

In first-trimester pregnant women with hyperemesis gravidarum and biochemical hyperthyroidism (elevated free T4/T3, suppressed TSH) but no overt hyperthyroid symptoms, antithyroid drugs are NOT indicated because this represents transient gestational thyrotoxicosis that resolves spontaneously with treatment of the hyperemesis itself. 1, 2

Core Management Strategy: Supportive Care Only

Fluid Resuscitation and Electrolyte Correction

Initiate aggressive intravenous rehydration to correct dehydration and restore intravascular volume 1
Correct electrolyte abnormalities, which occur in 59% of hyperthyroid hyperemesis patients versus 21% of euthyroid patients 3
Monitor and replace potassium, sodium, and chloride as needed based on laboratory values 1

Thiamine Supplementation (Critical)

Administer thiamine supplementation to prevent Wernicke's encephalopathy—this is mandatory in all hyperemesis cases with significant weight loss and prolonged vomiting 1
Give thiamine 100 mg IV or IM daily until oral intake resumes 1

Anti-emetic Therapy

Use ondansetron, metoclopramide, or promethazine as first-line anti-emetics with favorable pregnancy safety profiles 1
Oral prednisolone has no proven benefit; intravenous corticosteroids show conflicting data but can be considered for severe refractory disease 1

Beta-Blocker Use: Only for Symptomatic Hyperthyroidism

When Beta-Blockers Are Indicated

Use propranolol temporarily only if the patient develops overt hyperthyroid symptoms: tachycardia out of proportion to dehydration, tremor, heat intolerance, or anxiety 2, 4
Beta-blockers control symptoms while awaiting spontaneous resolution of the biochemical abnormalities 2

When Beta-Blockers Are NOT Needed

In asymptomatic patients with only biochemical hyperthyroidism (the scenario described), beta-blockers are unnecessary 1, 2
The biochemical abnormalities alone do not warrant beta-blocker therapy 1

Antithyroid Drugs: When NOT to Use Them

Transient Gestational Thyrotoxicosis Does Not Require Antithyroid Drugs

Biochemical hyperthyroidism associated with hyperemesis gravidarum is caused by hCG-mediated thyroid stimulation, not Graves' disease 5, 3
This condition is self-limited and resolves by 18 weeks' gestation as hCG levels decline 3
Antithyroid drugs do not improve nausea and vomiting—one case series showed persistent hyperemesis despite normalization of thyroid function with methimazole suppositories 6
Treatment of hyperemesis (hydration, anti-emetics) leads to spontaneous resolution of both vomiting and thyroid abnormalities within days to weeks 6, 3

Distinguishing Transient Thyrotoxicosis from Graves' Disease

Transient thyrotoxicosis: No goiter, no ophthalmopathy, no thyroid bruit, negative TSH receptor antibodies, resolves with hyperemesis treatment 5, 7, 3
Graves' disease: Goiter present, possible ophthalmopathy (proptosis, lid lag), thyroid bruit, positive TSH receptor antibodies, requires antithyroid drugs 2, 5
If clinical or immunological features of Graves' disease are present, treat with propylthiouracil (PTU) in the first trimester, then switch to methimazole for the second and third trimesters 2, 8

Monitoring Strategy

Thyroid Function Tests

Recheck TSH and free T4 every 2-4 weeks to confirm spontaneous resolution 2, 3
Thyroid function normalizes within several weeks as hyperemesis improves 3
If thyroid abnormalities persist beyond 18 weeks or worsen, reconsider the diagnosis and evaluate for Graves' disease 5, 3

Liver Enzymes

Check liver enzymes (AST, ALT) at presentation, as 59% of hyperthyroid hyperemesis patients have elevated transaminases versus 18% of euthyroid patients 3
Liver abnormalities typically resolve with hydration and resolution of vomiting 1
Persistent liver chemistry abnormalities despite symptom resolution should prompt investigation for another etiology 1

Fetal Monitoring

Monitor fetal heart rate and growth, though routine ultrasound screening for fetal goiter is not necessary unless problems are detected 1, 2

Common Pitfalls to Avoid

Do Not Initiate Antithyroid Drugs Based on Biochemistry Alone

The most critical error is treating biochemical hyperthyroidism in hyperemesis gravidarum with antithyroid drugs when no clinical hyperthyroidism exists 1, 6, 7
Antithyroid drugs expose the patient to unnecessary risks (agranulocytosis, hepatotoxicity) without improving outcomes 8, 7
One study showed that 4 of 11 patients with hyperemesis and elevated free T4 were treated with antithyroid drugs, but only 3 of these 4 had other signs of hyperthyroidism—the fourth likely had transient thyrotoxicosis and did not require treatment 9

Do Not Overlook True Graves' Disease

If the patient has a goiter, ophthalmopathy, or persistent hyperthyroidism beyond 18 weeks, this is Graves' disease requiring antithyroid drugs 2, 5
Untreated Graves' disease in pregnancy increases risks of severe preeclampsia, preterm delivery, heart failure, miscarriage, and low birth weight 2, 5

Do Not Forget Thiamine

Failure to administer thiamine in severe hyperemesis with weight loss >5% can result in Wernicke's encephalopathy, a preventable neurological catastrophe 1

Expected Clinical Course

Resolution Timeline

With supportive care (hydration, anti-emetics, thiamine), hyperemesis typically improves within 1-2 weeks 1, 3
Biochemical hyperthyroidism resolves within several weeks as hCG levels decline and hyperemesis improves 6, 3
Both elevated thyroid function and nausea/vomiting resolve within 3 days after delivery if hyperemesis persists throughout pregnancy 6

Prognosis

Hyperemesis gravidarum is not usually associated with major adverse maternal or fetal outcomes when appropriately managed 1
Low birth weight and premature delivery have been associated with severe hyperemesis, though long-term health effects are unknown 1
Recurrence is high with subsequent pregnancies 1

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