Thyroid storm (thyrotoxic storm, thyrotoxic crisis) is a rare life-threatening emergency that, despite of medical progress, remains a diagnostic and therapeutic challenge. It is generally observed among patients with Graves’ disease, but also with nodular goiter. Early detection of hyperthyroidism, due to increased availability of thyroid function tests and improved preoperative thyroid surgery management has led to marked reduction in the number of thyroid storm cases. The accurate incidence of thyroid storm is difficult to determine due to the variability in diagnostic criteria. Only 1-2% of hyperthyroid cases manifest as thyroid storm but the mortality ranges from 20 to 30%, despite treatment used. Thyroid storm occurs rapidly in hours or progressively in few days. Its most common precipitating cause is non-compliance with prescribed anti-thyroid treatment. Other precipitating factors include infection, radioiodine therapy (that happened to our patient), withdrawal of anti-thyroid drugs, trauma, cerebrovascular events, diabetic ketoacidosis, toxemia of pregnancy and severe emotional stress (1-7).

57-year old woman was admitted to our clinic in August 2014, due to 6-day continuous fever up to 41°C, without any response to treatment with antipyretics (ibuprophen and metamizole) and antibiotic (cefuroxime) given for 4 days prior to the admission. The fever was accompanied by general weakness, dizziness and tremors occurring periodically. Patient denied any signs of infection, diarrhea, abdominal pain, profuse sweating, heat intolerance, irritability and loss of weight. At admission patient was in average general condition, conscious, with preserved verbal contact, periodically confused, febrile (41^oC), with blood pressure of 160/90 mmHg, regular heart rate 110/min, skin of fine texture, dry, velvet and gleaming. Periodical muscle tremor was observed. Lung auscultation was correct, abdomen physical examination presented no deviation, and there were no signs of peripheral edema. The laboratory tests revealed leukocytosis with neutrophilia, without anemia or thrombocytopenia, normal inflammatory parameters (CRP – 1.9 mg/L, ESR – 11 mm/hr, procalcytonin concentration within normal range). Deviations in lab tests found at the admission were: slightly elevated liver enzymes (GOT > GPT) without features of cholestasis, elevated creatine kinase (CK – 2610 U/L), lactate dehydrogenase (LDH – 476 U/L), hyponatremia (125 mmol/L), hypokalemia (2.6 mmol/L) and hyperglycemia. Serum TSH concentration was slightly decreased (0.13 μIU/mL, n: 0.55-4.78). Chest X-ray revealed no pathology and abdominal USG showed the deposit in the gall bladder without other irregularities.

The infectious causes of the fever, such as urinary, pulmonary and gastrointestinal tract infections, hepatitis caused by EBV, CMV, HBV, HCV, HIV infections and endocarditis were firstly excluded. Blood and sputum cultures were negative. The other suspected causes of high fever as cancer, autoimmune diseases, and neuroinfection were also excluded. Contrast-enhanced CT scans of the chest, abdomen and pelvis revealed neither abscessus nor neoplasm. A check for wide panel of antibodies allowed to exclude autoimmune disorders of connective tissue. Because of permanent, idiopathic high fever, without any significant reaction to antipyretics, and periodic impaired conciousness it was decided to use glucocorticosteroid therapy. Methylprednisolone was given intravenously at a dose of 1,000 mg daily for 3 days, followed by therapy with oral prednisolone.