SAT-337 - Perioperative Optimization of Severe Uncontrolled Hyperthyroidism in Graves' Disease: A Multimodal Approach to Prevent Thyroid Storm

Background
Patients with severe hyperthyroidism who require urgent thyroidectomy are at high risk of thyroid storm, a life-threatening complication with 3.6-17% mortality. The American Thyroid Association recommends achieving euthyroid status preoperatively, typically requiring 1-3 months of antithyroid therapy. However, urgent surgery sometimes precludes prolonged preparation. We report successful rapid pre-operative optimization via aggressive multimodal pharmacotherapy.

Case Presentation
A 34-year-old woman with relapsing-remitting Graves' disease developed progressive compressive symptoms from a large substernal goiter necessitating urgent thyroidectomy. Initial laboratories showed profound thyrotoxicosis with TSH 0.005 μIU/mL (normal 0.4-4.0), free T4 >7.77 ng/dL (normal 0.8-1.8), exceeding 4-fold the upper limit of normal with tremors, heat intolerance, diarrhea, and tachycardia.
Aggressive multimodal therapy was initiated that included high dose methimazole (titrated to 30 mg/day), prednisone (40 mg daily), cholestyramine (4 gm twice daily) and propranolol (10 mg twice daily). Potassium iodide was added a week prior to surgery.
Within 18 days, she achieved marked clinical improvement with normalization of heart rate (73bpm) and biochemical improvement and normal free T4 1.3 ng/dL while TSH remains suppressed < 0.01 μIU/mL.
She underwent total thyroidectomy by an experienced thyroid surgeon and anesthesia team without intraoperative instability, thyroid storm and post-operative complications. Pathology confirmed benign hyperplastic tissue consistent with multinodular goiter/Graves' disease.

Discussion and conclusion
This case demonstrates that Intensive multimodal pharmacotherapy can rapidly and safely stabilize even severe hyperthyroidism, allowing urgent thyroidectomy when standard preparation is not feasible. Targeting multiple physiologic pathways enabled rapid biochemical and clinical control, with Free T4 reduction from >7.77 ng/dL to 1.3 ng/dL within 18 days and complete resolution of thyrotoxic symptoms.
Mechanistically, methimazole blocks new thyroid hormone synthesis; glucocorticoids inhibit peripheral T4-to-T3 conversion; potassium iodide suppresses hormone release via the Wolff–Chaikoff effect and reduces thyroid gland vascularity; propranolol provides β-adrenergic blockade and additional T4-to-T3 inhibition; and cholestyramine interrupts enterohepatic recirculation of thyroid hormones.

Despite persistent TSH suppression, cardiovascular stability and normalized free T4 provided adequate surgical readiness, highlighting that clinical and biochemical euthyroidism rather than TSH normalization should guide operative timing in severe thyrotoxicosis. Successful outcomes require close multidisciplinary coordination and experienced thyroid surgery and anesthesia teams.

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