Untreated fetal thyrotoxicosis may present with goiter, tachycardia, growth restriction, hydramnios, accelerated bone maturation, and even heart failure and hydrops (Huel, 2009; Peleg, 2002). The cause is usually maternal Graves disease with transplacental passage ofIgG thyroid-stimulating immunoglobulins. Fetal blood sampling may confirm the diagnosis (Duncombe, 2001; Heckel, 1997; Srisupundit, 2008). Conirmed fetal thyrotoxicosis is followed by maternal antithyroid treatment. During this, if the mother develops hypothyroidism, she is given supplementalilevothyroxine (Hui, 2011).
In a woman receiving medication for Graves disease, transplacental passage of methimazole or propylthiouracil may cause etal hypothyroidism (Bliddal, 2011 a). Other potential causes of fetal hypothyroidism resulting in goiter include transplacental passage of thyroid peroxidase antibodies, fetal thyroid dyshormonogenesis, and maternal overconsumption of iodine supple ments (Agrawal, 2002; Overcash, 2016).
Goitrous hypothyroidism may lead to hydramnios, neck hyperextension, and delayed bone maturation. If the mother is receiving antithyroid medication, discontinuation is generally recommended, along with intraamnionic levothyroxine injection. Numerous case reports describe intraamnionic levothyroxine treatment. However, optimal dosage and frequency have not been established, and reported dosages range from 50 to 800 �g every 1 to 4 weeks (Abuhamad, 1995; Bliddal, 2011b; Ribault, 2009) .
Also called maternaletal surgery, these procedures are ofered for selected congenital abnormalities in which the likelihood of fetal deterioration is so great that delaying treatment until after delivery would risk fetal death or substantially greater postnatal morbidity. Open fetal surgef) is a highly specialized intervention performed at relatively few centers in the United States and for only a few fetal conditions. Criteria for consideration of fetal surgery are listed in Table 16-1. In many cases, data regarding the safety and eicacy of these procedures are limited.
TABLE 16-1. Guiding Principles for Fetal Surgical Procedures
Accurate prenatal diagnosis for the defect is available, with staging if applicable
The defect appears isolated, with no evidence of other abnormality or underlying genetic syndrome that would significantly worsen survival or quality of life
The defect results in a high likelihood of death or irreversible organ destruction, and postnatal therapy is inadequate The procedure is technically feaSible, and a multidisciplinary team is in agreement regarding the treatment plan Maternal risks from the procedure are well documented and considered acceptable
There is comprehensive parental counseling It is recommended that there be an animal model for the defect and procedure
Data from Deprest, 201s0; Harrison, 1982; Vrecenak, 2013; Walsh, 201s1.
TABLE 16-2. Selected Fetal Abnormalities Amenable to Fetal Surgery
Twin-twin transfusion: laser of placental anastomoses Diaphragmatic hernia: fetal endoscopic tracheal occlusion
Posterior urethral valves: cystoscopic laser Congenital high airway obstruction: vocal cord laser Amnionic band release
Posterior-urethral valves/bladder outlet obstruction Pleural effusion: chylothorax or sequestration Dominant cyst in CCAM
Twin-reversed arterial perfusion (TRAP) sequence Monochorionic twins with severe anomaly in 1 twin Chorioangioma
Aortic or pulmonic valvuloplasty for stenosis Atrial septostomy for hypoplastic left heart with