FETAL GOITER (9-15) |
Antenatal diagnosis is essential as timely recognition and treatment is essential to achieve normal growth and neurological development. Untreated fetal hypothyroidism may result in mental retardation, language, motor and spatial problems, growth retardation, congenital heart block and delayed skeletal maturation.
A large fetal thyroid gland may also result in fetal malposition due to hyperextension of the neck, tracheal obstruction, esophageal compression and polyhydramnios, neonatal asphyxia and death.
RISK FACTORS FOR FETAL GOITER
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Risk factors for fetal goiter (goiter in the fetus may be due to either hypothyroidism or hyperthyroidism):
1. Previous medical therapy for hyperthyroidism.
2. Previous high dose irradiation of the neck.
3. Thyroid autoimmune disease (thyroiditis).
4. Family history of thyroid disease.
5. Treatment with amiodarone.
6. Type I maternal diabetes mellitus.
7. Hypopituitarism.
FETAL HYPOTHYROIDISM
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Transient fetal hypothyroidism is most frequently associated with maternal ingestion of anti-thyroid drugs (propylthiouracil –PTU; carbimazol; I-131 in pregnant women).
FETAL HYPERTHYROIDISM
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Fetal Hyperthyroidism is usually secondary to maternal autoimmune disease. In Graves disease the mother produces several IgG thyroid stimulating immunoglobulins which can cross the placenta and cause fetal hyperthyroidism. Fetal tachycardia is usually the first sign of fetal hyperthyroidism, usually arising after the 25th week of gestation. Sustained fetal tachycardia can result in high output cardiac failure.
ULTRASOUND
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REFERENCES
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