A 48-year-old man had been treated at our hospital for type 2 diabetes and Graves' disease. He was diagnosed with diabetic ketoacidosis (DKA) twice during previous visits. He was prescribed methimazole (10 mg/day) and insulin,but his drug compliance was poor. He had not visited our hospital since 3 September 1998, when his HbAlc level was 11.6% (normal 4.3-5.8) and his thyroid function tests revealed euthyroidism. He had stopped taking medication 30 December 1998, and he was admitted to our hospital on 6 January 1999, with general fatigue, a sore throat, and excessive thirst. He appeared drowsy, and he presented with Kussmaul respirations, irregular tachycardia,dry skin, injected tonsils, and a diffuse goiter, but he had no fever or exophthalmos. Laboratory studies revealed excessive urine ketone bodies, a normal peripheral white blood cell count, a plasma glucose level of 763 mg/dl,a HbAlc level of 14.6%, and a C-reactive protein level of 13.6 mg/dl (normal <0.5). Arterial blood gas analysis revealed the following: pH 7.151, Po2 120.4 mmHg, Pco2 16.7 mmHg, and HCO3 5.6 mEq/l. Electrocardiography showed atrial fibrillation with a rate of 140 beats/min, and the chest radiograph was normal. He was diagnosed with DKA and tonsillitis.

We began administering saline, insulin, antibiotics, methimazole (10 mg/day), and propranolol (30 mg/day). On 7 January he became alert and had sinus tachycardia at a rate of 110 beats/min. His temperature never exceeded 37.8°C, and his plasma glucose was under control. On 8 January, his tachycardia persisted, but he still had no fever. On admission, thyroid function tests revealed that his thyroid stimulating hormone was <0.03μU/ml (normal 0.2-3.2), his free triiodothyronine level was 14.12 pg/ml(normal 2.9-6.0), and his free thyroxine level was 6.21 ng/dl (normal 0.78-2.10). Therefore, the administration of methimazole was increased to 30 mg/day. On 9 January, he became extremely confused and agitated. Suddenly, he lapsed into a coma and cardiopulmonary arrest. An autopsy revealed that the enlarged thyroid gland had histological findings of papillary projections of follicular cells with an increased endocytosis of colloid. The focal infiltration of the neutrophils was restricted to the alveoli contiguous to the bronchi. Serratia marcescens was cultured from the sputum. These findings indicated focal bronchopneumonia that was not severe enough to have been a singular cause of death. Persistent tachycardia and increased central nervous system (CNS) activity suggested that a thyrotoxic storm participated in the cause of death, although he denied fever, sweatiness, and gastrointestinal involvement.

A thyrotoxic storm is rare, but prompt diagnosis and treatment are required. The diagnosis depends on exaggerated thyrotoxic manifestations,including high fever, marked tachycardia, gastrointestinal dysfunction, and CNS involvement varying from confusion to coma(1). DKA is one of the precipitating factors, and many patients are normothermic or hypothermic even when the condition is associated with infection(2). In some cases of thyrotoxic storm with DKA, a high fever develops after the improvement of DKA(3,4). Severely uncontrolled diabetes influences the assessment of thyrotoxicosis by falsely decreasing the blood levels of thyroxine and triiodothyronine(5). DKA may obscure thyrotoxicosis and/or infection, resulting in a fatal outcome. This case emphasizes that the possibility of thyrotoxic storm should be considered as soon as possible, even when the symptoms are not so obvious in patients with DKA.

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