Neonatal thyrotoxicosis is not a rare disease, as a recent review listed 22 reported cases (2). Cardiac failure is a frequent complication, occurring in at least 7 of the 22 cases and perhaps in 3 others. The following case is reported to acquaint the radiologist with thyrotoxicosis as a cause of cardiac failure in infancy. Case Report R. H., a Negro girl, was born at term with no abnormalities noted. She was discharged at three days of age with her mother. At eight days of age the sudden onset of respiratory distress was noted, followed by cyanosis. The patient was admitted to the University of Arkansas Medical Center the same day. The mother had been seen as an out-patient eleven months before with a history of weight loss, nervousness, and easy fatigability. Exophthalmos was not present. The protein-bound iodine was 15.5 μg per 100 ml. She was treated with 6.94 mCi 131I and propylthiouracil 150 mg t.i.d. Response was good, and she was maintained on propylthiouracil and Cytomel. At the time of delivery she was euthyroid. On admission, the infant was cyanotic with a pulse rate of 200 per minute and a respiratory rate of 60 per minute. No cardiac murmurs were heard. The liver was palpable 6 cm below the costal margin and firm. Thyroid enlargement was not noted, nor was exophthalmos present. Radiographic findings are illustrated in Figure 1. A diagnosis of cardiac failure of unknown cause was made. The history of maternal thyrotoxicosis was not known at that time. Digitalis was given without effect. The infant died twelve hours after admission. At necropsy, the thyroid gland was markedly enlarged, weighing approximately 12 g. The microscopic findings were those of thyrotoxicosis. Cardiac enlargement and passive congestion of the liver were present. The lungs were poorly aerated with a foamy pink fluid on cut surface. No other abnormalities were found. The final diagnosis was neonatal thyrotoxicosis with cardiac failure. Discussion Thyrotoxicosis in the adult is associated in some instances with a high level of long-acting thyroid stimulating hormone (LATS) (6, 7). Abnormally high levels of LATS may persist even though the thyrotoxicosis is well controlled. In the pregnant woman, this hormone crosses the placental barrier and stimulates the infant's thyroid gland. Symptoms of neonatal thyrotoxicosis are usually present at birth, but if the mother received antithyroid drugs during pregnancy, the infant's thyroid may be suppressed until the antithyroid medication is degraded (5). Therefore, the appearance of neonatal thyrotoxicosis may be delayed for several days, as in our patient. Thyrotoxicosis persists in the infant until the level of LATS decreases to a normal level, usually a period of three to six weeks. Clinically the infant with thyrotoxicosis is hyperactive and irritable. The pulse and respiratory rates are increased. Periorbital edema and exophthalmos are often present (2).