els are low and TSH elevated, with fetal goiter and evidence of hypothyroidism, ATD therapy is reduced and intra-amniotic T4 may be given. If maternal T4 levels high and TSH low, with fetal goiter and signs of fetal hyperthyroidism, increased doses of ATD are suggested. If the probable metabolic status of the fetus is not clear, fetal blood sampling is feasible although carrying significant risk to the fetus. Plasmapheresis to reduce maternal TRAb has been recommended, but few facts are available. Thyrotoxicosis is rare in the newborn infant and is usually associated with past or present maternal hyperthyroidism. 
Neonatal hypermetabolism usually arises from transplacental passage of TSAb. Frequently the infant is not recognized as thyrotoxic at birth, but develops symptoms of restlessness, tachycardia, poor feeding, occasionally excessive hunger, excessive weight loss, and possibly fever and diarrhea a few days after birth. The fetus converts T4 to T3 poorly in utero, but switches to normal T4 to T3 deiodination at birth. This phenomenon may normally provide a measure of protection in utero that is lost at birth, allowing the development of thyrotoxicosis in a few days.
The syndrome may persist for two to five weeks, until the effects of the maternal antibodies have disappeared. The patient may be treated with propranolol, antithyroid drugs given according to the schedule above, and iodide. The antithyroid drug can be given parenterally if necessary in saline solution after sterilization by filtration through a Millipore filter. Newborn infants with thyrotoxicosis are frequently extremely ill, and ancillary therapy, including sedation, cooling, fluids in large amounts, electrolyte replacement, and oxygen, are probably as important in management as specific therapy for the thyrotoxicosis. Propranolol is used to control the tachycardia (218.1). Because of the increased metabolism of such infants, attention to fluid balance and adequacy of nutrition are important. The patient usually survives the thyrotoxicosis, and the disease is typically self-limiting, with the euthyroid state being established in one or two months. Antithyroid medication can be gradually withdrawn at this time. Graves’ disease can also occur in the newborn because the same disturbance that is causing the disorder in the mother is also occurring independently in the child. Hollingsworth et al  have described their experience in such patients. The mothers did not necessarily have active disease during pregnancy. Graves’ disease persisted in these patients from birth far beyond the time during which TSAb of maternal origin could persist. Advanced bone age was one feature of the disorder. Behavioral disturbances were later found in some of these children at a time when they were euthyroid.
General Therapeutic Relationship of the Patient and Physician
The foregoing discussion explains several methods for specifically decreasing thyroid hormone formation. They are, in a sense, both unphysiologic and traumatic to the patient. As a good physician realizes in any problem, but especially in Graves’ disease, attention to the whole patient is mandatory. During the initial and subsequent interviews, the physician caring for a patient with Graves’ disease should recognize any psychological and physical stresses. Frequently major emotional problems come to light after the patient recognizes the sincere interest of the physician. Typically the problem involves interpersonal relationships and often is one of matrimonial friction. The upset may be deep-seated and may involve very difficult adjustments by the patient, but characteristically it is related to identifiable factors in the environment. To put it another way, the problem is not an endogenous emotional reaction but a difficult adjustment to real external problems. On the other hand, one must be aware that the emotional lability of the thyrotoxic patient may be a trial for those with whom he or she must live, as well as for the patient. Thus thyrotoxicosis itself may create interpersonal problems.
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