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KEY POINTS
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Key Points

  • Goiter in the fetus, a rare condition, can occur as part of a hypothyroid, hyperthyroid, or euthyroid state.

  • Hypothyroid fetal goiter may be secondary to transplacental passage of antithyroid medication, iodine deficiency, iodine intoxication, transplacental passage of antithyroid antibodies, congenital metabolic disorders of thyroid hormone synthesis, or hypothalamic-pituitary hypothyroidism.

  • Congenital hypothyroidism is a serious condition, which if not treated in the first 3 months of life is likely to result in irreversible mental retardation.

  • Hyperthyroid fetal goiter is most often caused by transplacental passage of a thyroid-stimulating IgG antibody from the mother. Such antibodies are present in approximately 95% of women with Graves disease.

  • Thyroid-stimulating antibody levels in Graves disease may not reflect maternal thyroid status because they are detectable in women who are clinically hyperthyroid, euthyroid, or hypothyroid.

  • The typical sonographic appearance of a fetal goiter is a symmetric, homogenous mass in the anterior neck, with an echogenic consistency, and with some lobulation.

  • The diagnosis of fetal goiter is rarely made prior to 24 weeks’ gestation. The fetal neck may be hyperextended and the trachea and esophagus may become compressed or displaced resulting in polyhydramnios.

  • It is extremely important to thoroughly evaluate and treat a fetal goiter.

  • Because ultrasound methods of differentiating between hypothyroidism and hyperthyroidism may not be reliable, fetal cord blood sampling may be required. Amniotic fluid thyroid hormone values may not be reliable.

  • If fetal hypothyroidism is diagnosed, intra-amniotic injection with levothyroxine will be required.

  • Little information is available to guide patient counseling regarding the antenatal natural history of fetal goiter. The clinical course will depend on whether or not the fetus is hyperthyroid, euthyroid, or hypothyroid.

  • Serial sonographic surveillance is suggested due to the fact that fetal goiter may be associated with polyhydramnios, intrauterine growth restriction, hydrops, and intrauterine fetal demise.

  • A neonatologist should be present in the delivery room because problems securing an airway may be encountered. In the most severe cases of fetal goiter, the ex utero intrapartum treatment (EXIT) procedure may be needed to maximize the ability to promptly secure an airway at delivery.

  • There is little data available to counsel patients on the long-term prognosis of antenatal fetal goiter.

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CONDITION
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Fetal goiter, or thyromegaly, is a diffuse enlargement of the fetal thyroid gland. Goiter in the fetus can occur as part of a hypothyroid, hyperthyroid, or euthyroid state. Hypothyroid fetal goiters are more common than those associated with either the hyperthyroid or euthyroid states.

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Goiter associated with fetal hypothyroidism can be caused by transplacental passage of antithyroid medications being used by a mother with hyperthyroidism, iodine deficiency, iodine intoxication, transplacental passage of antithyroid antibodies, congenital metabolic disorders of thyroid hormone synthesis, or hypothalamic-pituitary hypothroidism (Weiner et al., 1980; Romero et al., 1988; Noia et al., 1992; Soliman et al., 1994; Van Loon et al., 1995; Bruner and Dellinger, 1997; Vicens-Calvet et al., 1998...

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