Thyroid Storm With Multiorgan Dysfunction Mimicking Sepsis: Thionamide-Sparing Bridge to Delayed Carbimazole

Thyroid storm represents a critical exacerbation of thyrotoxicosis, often associated with Graves' disease, characterized by fever, gastrointestinal disturbances, neuropsychiatric manifestations, and tachyarrhythmias, closely resembling sepsis in its clinical presentation. The elevation of inflammatory biomarkers can be significant, frequently leading to delayed or missed diagnosis. Conventional treatment (beta-blockade, thionamides, iodine after thionamide, and corticosteroids) involves rapid management of adrenergic symptoms alongside inhibition of thyroid hormone synthesis and release; however, severe hepatocellular injury and coagulopathy may limit early thionamide administration, necessitating alternative "bridging" therapeutic strategies. We present the case of a 31-year-old male patient with no prior history of thyroid disease who presented with fever and vomiting for three to four days, followed by agitation and palpitations, subsequently developing atrial fibrillation with rapid ventricular response (150 beats per minute (bpm)). Laboratory investigations revealed significant hypokalemia (1.9 mmol/L), markedly elevated procalcitonin (58.1 ng/mL), and severe hepatocellular injury with coagulopathy, as evidenced by elevated aspartate aminotransferase (AST; 3740 U/L), alanine aminotransferase (ALT; 1232 U/L), and international normalized ratio (INR; 2.06). Thyroid function tests demonstrated suppressed thyroid-stimulating hormone (TSH; <0.01 mIU/L), elevated free thyroxine (free T4; >90 pmol/L), and positive thyroid-stimulating hormone receptor antibodies (TSH-receptor antibodies; 19.5), supporting a diagnosis of Graves' disease, while ultrasound and scintigraphy were consistent with the diagnosis. The diagnosis of thyroid storm was established using the Burch-Wartofsky Point Scale (BWPS; 70) and Japanese Thyroid Association (JTA) criteria. Given the hepatic dysfunction, initial management deferred thionamide therapy; treatment comprised propranolol, corticosteroids, cholestyramine, and lithium, along with supportive intensive care and empirical antibiotics. Carbimazole was initiated on day 8 following hepatic improvement, and the patient was discharged on day 12, demonstrating normal liver function and thyroid hormone levels at two-week follow-up. This case illustrates that thyroid storm can closely mimic sepsis with markedly elevated inflammatory biomarkers and may be complicated by severe hepatocellular injury. A thionamide-sparing approach, when thionamides are contraindicated (e.g., agranulocytosis, hypersensitivity reactions, or severe hepatic dysfunction), utilizing lithium and cholestyramine can effectively serve as a bridging strategy, facilitating postponement of thionamide therapy when immediate antithyroid treatment is contraindicated.