Situation: A 34-year-old woman with Graves disease is admitted for total thyroidectomy because a large goiter makes swallowing difficult. She has taken methimazole for 3 months, and potassium iodide solution was added 9 days ago. She has no known drug allergies. On admission she said she had missed about half of her methimazole doses over the past month. On the first postoperative day she becomes restless and confused and vomits twice. Her temperature is 39.6 °C (103.3 °F), heart rate 152 beats/min and irregular, and white blood cell count 13.5 × 10⁹/L (4.5–11.0). Her muscles are not rigid, and the incision is clean and dry. Which condition do these findings MOST suggest?

Missed antithyroid doses mean she was probably not euthyroid at surgery, and surgery in such a client can trigger thyroid storm, a hypermetabolic crisis with high fever, marked tachycardia or atrial fibrillation, vomiting, and agitation or delirium. A raised white cell count is common after surgery and in thyroid storm, so it does not establish sepsis, which is unlikely on the first day with a clean incision. Malignant hyperthermia occurs during or soon after anesthesia with muscle rigidity.

Clinical picture A 34-year-old woman with Graves disease undergoes total thyroidectomy for a large goiter causing dysphagia. She was treated with methimazole for 3 months and potassium iodide for 9 days, but she missed about half of her methimazole doses in the past month. On postoperative day 1, she develops restlessness, confusion, vomiting, a temperature of 39.6 °C (103.3 °F), an irregular heart rate of 152 beats/min, and a white blood cell count of 13.5 × 10⁹/L. The incision is clean and dry, and there is no muscle rigidity.

Why this is thyroid storm The most likely diagnosis is thyroid storm, a life-threatening hypermetabolic crisis caused by severe thyrotoxicosis with multiorgan decompensation ^[1][3]. The key clue is that the patient was not euthyroid at the time of surgery because she missed about half of her methimazole doses over the preceding month. Abrupt discontinuation or inconsistent use of antithyroid medication is a recognized precipitant of thyroid storm, and surgery itself is another well-documented trigger ^[1]. When thyroid surgery is performed in a patient with poorly controlled hyperthyroidism, manipulation of the gland can release large amounts of preformed thyroid hormone into the circulation, precipitating a crisis.

The clinical findings fit the classic presentation. Thyroid storm is characterized by hyperthermia, tachyarrhythmia—including atrial fibrillation, which explains the irregular pulse—vomiting, and central nervous system disturbance such as agitation, confusion, or delirium ^[1][4]. The combination of high fever, marked tachycardia, gastrointestinal symptoms, and altered mental status in the immediate postoperative period after thyroid surgery strongly points to thyroid storm rather than a localized surgical complication.

Why the other options are less likely Acute hypocalcemia can occur after total thyroidectomy if the parathyroid glands are devascularized or inadvertently removed. It typically presents with neuromuscular irritability—perioral or acral paresthesias, carpopedal spasm, positive Chvostek or Trousseau sign, and in severe cases laryngospasm or seizures. This patient has no muscle rigidity, tetany, or paresthesias, and hypocalcemia does not explain the high fever, tachycardia, vomiting, or confusion.

Malignant hyperthermia is a pharmacogenetic disorder triggered by volatile inhalational anesthetics or succinylcholine. It classically occurs during or shortly after anesthesia and is marked by hyperthermia, tachycardia, hypercapnia, and generalized muscle rigidity. The absence of muscle rigidity and the onset on postoperative day 1—rather than intraoperatively or in the immediate recovery period—make malignant hyperthermia unlikely.

Early wound sepsis is not supported by the findings. The incision is clean and dry, with no erythema, purulence, or local signs of infection. Although the white blood cell count is elevated at 13.5 × 10⁹/L, leukocytosis is a nonspecific finding that commonly occurs after surgery as part of the stress response and is also seen in thyroid storm ^[1]. Sepsis on the first postoperative day with a clean incision would be unusual, and the constellation of hyperthermia, tachyarrhythmia, vomiting, and delirium is better explained by the hypermetabolic crisis.

Pathophysiology and clinical reasoning In Graves disease, circulating thyroid-stimulating immunoglobulins continuously activate the TSH receptor, driving excess synthesis and release of thyroxine (T4) and triiodothyronine (T3). Methimazole blocks new hormone synthesis by inhibiting thyroid peroxidase, but it does not remove hormone already stored in the gland. Potassium iodide acutely inhibits hormone release and reduces gland vascularity, which is why it is given preoperatively. However, missed methimazole doses over the preceding month mean hormone synthesis was not adequately suppressed, and the gland remained loaded with preformed hormone. Surgical manipulation then released a large bolus of T4 and T3 into the circulation, overwhelming the body’s compensatory mechanisms and producing the exaggerated adrenergic and metabolic response seen in thyroid storm ^[1].

Diagnosis of thyroid storm is clinical, supported by scoring systems such as the Burch-Wartofsky score and the Japanese Thyroid Association criteria, which weigh temperature, central nervous system effects, gastrointestinal-hepatic dysfunction, heart rate, heart failure, and the presence of a precipitating event ^[3]. Laboratory findings typically show suppressed TSH (