A 62-year-old black nursing home resident was transported to the hospital emergency department with fever of 102°F, new-onset atrial fibrillation (A-fib), and dementia. His medical history was significant for hypertension and multiple strokes.
His inpatient work-up for A-fib and dementia revealed a thyroid-stimulating hormone (TSH) level below 0.005 µIU/mL (normal range, 0.3 to 3.0 µIU/mL). Results of thyroid function testing (TFT) revealed a triiodothyronine (T3) level within normal range but a free thyroxine (T4) level of 2.9 ng/dL (normal range, 0.7 to 1.5 ng/dL) and a total T4 of 17.8 µg/dL (normal, 4.5 to 12.0 µg/dL). The abnormal TSH and T4 levels were considered suggestive of a thyrotoxic state, warranting an endocrinology consult. Cardiology was consulted regarding new-onset A-fib.
During history taking, the patient denied any shortness of breath, cough, palpitations, heat intolerance, anxiety, tremors, insomnia, dysphagia, diarrhea, dysuria, weight loss, or recent ingestion of iodine-containing medications or supplements.
On examination, the patient was febrile, with a blood pressure of 106/71 mm Hg; pulse, 74 beats/min; respiratory rate, 20 breaths/min; and O2 saturation, 98% to 99% on room air. ECG showed a normal sinus rhythm and a ventricular rate of 64 beats/min.
The patient's weight was 58.9 kg, and his height, 63" (BMI, 22.8). The patient had no skin changes, and his mucous membranes were slightly moist. The patient's head was atraumatic and normocephalic. His extraocular movements were intact, and his pupils were equal, round, and reactive to light, with nonicteric sclera. There was no proptosis or ophthalmoplegia. The patient's neck was supple, with no jugular venous distension, tracheal deviation, or thyromegaly.
The cardiovascular exam revealed an irregular heartbeat, and repeat ECG showed A-fib with a ventricular rate of 151 beats/min (see Figure 1). The patient's chest was clear, with no wheezing or rhonchi. The abdomen was soft and slightly obese, and bowel sounds were present. The neurologic examination revealed no hyperreflexia. The patient's mental status was altered at times and he was alert, awake, and oriented to others. His speech was slightly slow, and some left-sided weakness was noted.
As recommended during the endocrinology consult, the patient underwent an I-123 sodium iodide thyroid scan, which showed faint uptake at the base of the neck, slightly to the left of midline; and a 24-hour radioactive iodide uptake (RAIU), which measured 2.8% (normal range, 8% to 35%).
The patient's chest X-ray showed a right tracheal deviation not previously noted on physical examination (see Figure 2); the possible cause of a thyroid mass was considered. Subsequent ultrasonography of the thyroid revealed generally normal dimensions and parenchymal echogenicity. However, a large complex mass was detected, arising from the inferior pole of the thyroid and displacing the trachea toward the right (see Figure 3). According to the radiologist's notes, the mass contained both solid and cystic elements, scattered calcifications, and foci of flow on color Doppler. It measured about 6 cm in the largest (transverse) dimension. A 2.0-mm nodule was noted in the isthmus, slightly to the right of midline, consistent with multinodular goiter.
Following the cardiology consult, a diltiazem drip was initiated, but the patient was later optimized on flecainide for rhythm control and metoprolol for rate control. He was also initially anticoagulated using a heparin drip and bridged to warfarin, with target international normalized ratio (INR) between 2.0 and 3.0. Echocardiography revealed normal systolic function with ejection fraction of 55%, left ventricular hypertrophy, pulmonary artery systolic pressure of 35 mm Hg, and no pericardial effusions or valvular disease.
Regarding the patient's unexplained fever, results of chest imaging were negative for signs of pneumonia or atelectasis, which might have suggested a pulmonary cause. Urinalysis results were normal. Complete blood count showed no leukocytosis. The patient's fever subsided within 48 hours.
The differential diagnosis included Graves' disease, toxic multinodular goiter, Jod-Basedow syndrome, and subacute thyroiditis.
Graves' disease, an autoimmune disease with an unknown trigger, is the most common cause of hyperthyroidism. In affected patients, the thyroid gland overproduces thyroid hormones, leading to thyrotoxicosis. Thyrotoxicosis can result in multiple clinical signs and symptoms, including Graves' ophthalmopathy, pretibial myxedema, and goiter; TFT results typically include elevated T3 and T4 and low TSH.1-5 In the case patient (who had no history of thyroid disease, nor clinical signs or symptoms of Graves' disease), low uptake of iodine on thyroid scan precluded this diagnosis.
Toxic multinodular goiter, the second most common cause of hyperthyroidism, can be responsible for A-fib, tachycardia, and congestive heart failure.6,7 Iodine deficiency causes enlargement of the thyroid gland, where numerous nodules can develop, as seen in the case patient. These nodules can function independently, sometimes producing excess thyroid hormone; this leads to hyperplasia of the thyroid gland, resulting in a nontoxic multinodular goiter. From this goiter, a toxic multinodular goiter can emerge insidiously. However, in this condition, RAIU typically exceeds 30%; in the case patient, low 24-hour RAIU (2.8%) and the absence of functioning nodules on scanning made it possible to rule out this diagnosis.