Core EM - Emergency Medicine Podcast

Episode 223: Thyroid Storm

May 15, 2026·9 min
Episode Description from the Publisher

Diagnosis, workup, and the four-step treatment protocol for thyroid storm. Hosts: Annaliese Elam, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid_Storm.mp3 Download Leave a Comment Tags: Critica Care, Endocrine, Thyroid Storm Show Notes I. Pathophysiology & Diagnosis Definition: Life-threatening hypermetabolic state resulting from decompensated thyrotoxicosis. Hormonal Profile: Absolute levels of total T₄/T₃ often mirror uncomplicated thyrotoxicosis; storm is driven by rapid rate of rise, increased catecholamine sensitivity, or increased free T₄/T₃ concentrations. Clinical Presentation: Hyperpyrexia (e.g., 104.2°F) Tachycardia/Arrhythmias (e.g., 155 bpm) Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism Warm, moist skin Precipitating Events: Infection, trauma, or surgery Parturition Abrupt cessation of antithyroid medications Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of Thyroid Storm 25–44: Suggestive of impending storm < 25: Storm unlikely Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness. II. Laboratory & Ancillary Findings Thyroid Panel: Characteristically low TSH with elevated free T₄ and T₃. Metabolic Abnormalities: Mild hyperglycemia (catecholamine-induced insulin inhibition) Mild hypercalcemia Elevated LFTs and leukocytosis Cardiovascular: EKG may show sinus tachycardia or atrial fibrillation with rapid ventricular response. III. Management: The Four-Step Blocking Strategy Step 1: Sympathetic Blockade (Beta Blockers) Agent of Choice: Propranolol Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃. Dosing: PO: 60–80 mg every 4–6 hours IV: 0.5–1 mg over 10 minutes Critical Pitfall: Avoid in patients with acute decompensated heart failure with systolic dysfunction; risk of cardiovascular collapse. Step 2: Inhibition of Hormone Synthesis

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