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Fetal goiter is defined as an enlargement of the thyroid gland that can be secondary to thyroid dysfunction, generally hypothyroidism. It can be originated by the passage of drugs such as propylthiouracil or methimazole administered to the mother to treat hyperthyroidism. It can also be the result of the transplacental passage of stimulating immunoglobulins or antibodies against the thyroid-stimulating hormone (TSH) receptor. The enlarged thyroid gland can potentially obstruct the fetal airway and/or esophagus and so polyhydramnios can be associated. In a case where there is a suspicion of an obstruction of the fetal upper airway, an ex utero intrapartum treatment (EXIT) should be considered for the moment of delivery. Other signs associated with fetal thyroid dysfunction can be observed such as fetal tachycardia, cardiac dysfunction, or abnormalities in skeletal ossification. In cases of fetal hypothyroidism, there is a higher risk for developmental delays. Fetal growth can also be impaired when there is fetal thyroid dysfunction. Fetal ultrasound (US) is the standard for its diagnosis, but magnetic resonance imaging (MRI) could be helpful to assess the extension of the enlarged gland. Both fetal hyperthyroidism and hypothyroidism can be treated prenatally, the former by administering antihyperthyroid drugs to the mother and the latter by administering levothyroxine intraamniotically. |
