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Introduction Graves’ disease is an autoimmune disorder causing hyperthyroidism through antibodies that stimulate levothyroxine (T4) and triiodothyronine (T3) production.1 It typically presents with palpitations, weight loss, tremors, and sweating.2 While thyroid storm is a rare complication of Graves’ disease, its occurrence as the first clinical manifestation is exceptionally uncommon.3 Therefore, a detailed history, thorough examination and holistic approach are essential for diagnosis, management, and follow-up.2 Case A 62-year-old woman with a background of hypertension, T2DM, COPD, OSA, and HF presented with acute-onset confusion, shortness of breath, chest and abdominal pain, and vomiting. Examination revealed GCS 14/15, hypoxia and signs of decompensated cardiac failure. ABG on 4 L of oxygen demonstrated T1RF. Chest radiography showed features consistent with pulmonary oedema (Figure 1). Blood investigations revealed AKI-1 and an elevated BNP (Table 1). CT of the head and abdomen/pelvis were unremarkable. The patient was transferred to the critical care unit in view of multi-system involvement. A thyroid function test demonstrated a hyperthyroid picture (Table 1). The Burch–Warsofsky Point Scale score was 80, highly suggestive of thyroid storm. Thyroid ultrasonography demonstrated features of thyroiditis (Figure 2). ECHO showed preserved EF. The patient was started on carbimazole, intravenous hydrocortisone, and beta-blocker. The patient’s symptoms improved clinically, and repeat thyroid function tests on day 6 showed biochemical improvement, with positive TSH receptor antibodies (Table 2). The patient continued to improve and was discharged after two weeks with a plan for repeat thyroid function testing in two weeks and follow-up in endocrinology and arrhythmia clinics. Conclusion This case illustrates the rare occurrence of thyroid storm as the initial presentation of Graves’ disease and underscores the critical importance of timely diagnosis and appropriate management in the intensive care setting due to the high mortality rate of this endocrine emergency.Figure 1Left pleural effusion and B/L prominent vascular markings.Figure 2Enlarged thyroid gland with increased vascularity.Table 1Blood tests11/8/256/8/25ReferenceTSH<0.02<0.020.3-4.8 mIU/LFree T34.17.94.2-6.9 pmol/LFree T412.4527.7-20.6 pmol/LTSH receptor antibody3850.0-0.9 IU/LBNP26920.0-99 pg/mL
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Dalili et al. (2026) studied this question.
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