Two cases of fetal goiter
A 27-year-old hypothyroid woman on thyroxine supplementation (75 mcg) having dichorionic diamniotic pregnancy underwent a routine antenatal ultrasound at 24 weeks of gestation, which revealed a large, butterfly shaped, uniformly echogenic solid mass (1.5 × 2.6 cm) suggestive of FG, in twin 1 [Figure and ]. The thyroid swelling was confirmed on fetal magnetic resonance imaging (MRI) which showed a 1.5 × 1.63 cm sized neck swelling. The other twin had no thyroid swelling. Cordocentesis was done and fetal free T4 values were 0.29 in twin 1 and 0.77 in twin 2. Free T3 values were 0.45 and 0.98 in twin 1 and 2, respectively. Mothers thyroid function showed a TSH of 8.3 and a free T4 of 0.6 and a very high titer of anti-thyroperoxidase (TPO) Ab (>3000). Dose of thyroxine was increased to 200 mcg and free T4 after 2 weeks was 1.4 mcg. Repeated sonography was done to monitor FG size, evidence of fetal cardiac dysfunction, delayed bone maturity and polyhydroamnios. Sonography confirmed reduction in size of goiter. Mother delivered preterm at 28 weeks and surprisingly, none of the twins had thyroid swelling, which was confirmed on fetal ultrasound. Fetal euthyroidism was confirmed on biochemical screening.\nAnterior fetal neck masses are rarely encountered during the second or third trimester of pregnancy. Ultrasound screening can reveal intrauterine FGs, along with anatomical assessment for size, volume and compression of neck structures. MRI may be done for better details.\nUsually, dyshormonogenesis is responsible for FG. Blockage of hormone biosynthesis increases fetal TSH levels, and this leads to FG. FG can lead to hyperextension of neck, polyhydroamnios, and compression of vascular structures in neck and edema. Mental and motor retardation also have been reported.[] These reasons make fetal hypothyroidism important for early diagnosis and appropriate hormone-replacement treatment.\nAn ultrasonography (USG) score is also proposed including fetal heart rate (FHR), fetal movement, Colour Doppler ultrasound (CDU) vascularity and bone maturation.[] The color Doppler indirectly indicates fetal thyroid function with the pattern of vascularity. Peripheral vascularity is suggestive of a nonfunctional hypertrophied gland, and central vascularization is suggestive of the overactive hyperfunctioning gland.\nMaternal anti-TPO, anti-Tg titers suggest transient suppression of thyroid hormone synthesis in the fetus. Maternal thyroid stimulating hormone- receptors (TSH-R), thyroid receptors antibody (TRAb) can stimulate a fetal thyroid to hypertrophy and produces goitrous hyperthyroidism.\nIf the maternal thyroid functions are in the normal range, amniotic fluid sampling for fetal TSH, FT3 and FT4 levels should be done to detect fetal hypothyroidism. If fetal hypothyroidism is diagnosed, intra-amniotic thyroxine injections (200-600 μg/week) are administered, and serial amniocenteses or preferentially cordocenteses are performed to follow the changes in the fetal thyroid metabolism.[]\nLately non-invasive techniques can be tried in cases of non-obstructing FG by just monitoring thyroid size on USG and titration of maternal thyroxine dose in case of maternal hypothyroidism.\nTo conclude, FG is a condition which can be noticed on routine ultrasonography, if carefully done. A high index of suspicion is required. Its diagnosis is important, as it is one of the treatable cause for mental and motor retardation. Fetal hypothyroidism should be thoroughly evaluated, diagnosed and immediately treated. Although in utero options for fetal hypothyroidism management are available, emphasis should be laid on non-invasive procedures with newer and better resolution techniques in ultrasonography, which are less harmful.