Abstract Introduction Thyroid storm is a rare, life-threatening decompensation of thyrotoxicosis marked by multiorgan dysfunction and high mortality. Here we present a case of thyroid storm triggered by iodide contrast media exposure. Case Presentation A 56-year-old man with Graves' disease, heart failure with mildly reduced ejection fraction, chronic kidney disease stage 3a, atrial fibrillation, and alcohol use disorder presented with one day of dyspnea, nausea, and lightheadedness. The patient and chart review both described inconsistent methimazole (MMI) use due to cost. Less than two weeks earlier, he had undergone contrasted CT of the chest, abdomen, and pelvis; at that time TSH was 0.02 mU/L and free T4 was 2.8 ng/dL. On arrival, he was agitated, hypertensive (182/99 mmHg) and tachycardic (145 bpm). Labs showed TSH 0.01 mU/L, free T4 3 ng/dL, and free T3 7 pg/dL. Before transfer from the ED, he developed respiratory distress and hypoxia requiring intubation. Chest X-ray showed bilateral pulmonary edema; venous blood gas revealed pH 7.18, pCO2 53 mmHg, and lactate 6.4 mmol/L. He was transferred to the ICU and required vasopressor support. The Burch–Wartofsky score was 70, which is highly suggestive of thyroid storm. Given his presentation, contrast exposure, reduced renal clearance, and medication nonadherence, iodine-induced thyroid storm was suspected. He was treated with propylthiouracil, supersaturated potassium iodide (SSKI), hydrocortisone, and beta-blockade. After five days, he was extubated, transitioned to the floor, and discharged on oral MMI with endocrinology follow-up. Discussion Thyroid storm is a clinical diagnosis defined by severe thyrotoxicosis with systemic decompensation. It is commonly triggered by infection, surgery, or trauma, but very rarely by iodinated contrast media (ICM). The estimated incidence of hyperthyroidism following ICM exposure is 1%. ICM provides a large iodide load that can trigger thyrotoxicosis through the Jod-Basedow phenomenon, where excess iodine in patients with underlying thyroid disease drives thyroid hormone (TH) overproduction. The patient’s treatment in this case included thionamides to inhibit TH synthesis, immediately followed by a modest iodide load, i.e. SSKI. In contrast to ICM administration, the pairing of anti-thyroid medicines with an iodide load inhibits TH release, which represents normal physiology known as the Wolff–Chaikoff effect. Conclusion Patients with thyroid disease are vulnerable to ICM-induced thyrotoxicosis. Management of these patients may paradoxically involve further iodide administration to suppress hormone release, but only after timely administration of thionamides. Clinicians should use contrast judiciously in patients with uncontrolled hyperthyroidism or limited renal clearance. This abstract is funded by: None
Landess et al. (Fri,) studied this question.