Paralysis after treatment for thyrotoxicosis.

Accepted 27 June 1996 A 41-year-old man was evaluated in February 1994 for weight loss, tremor, tachycardia and goiter. Thyroid function tests and a thyroid scan were consistent with the diagnosis of Graves' disease and he was treated with propylthiouracil (300 mg/day). Two months later, the patient presented to the emergency room with a flaccid paralysis of all extremeties. At night he had experienced tingling in his legs followed by weakness that ascended to his arms. At the time of admission he was able to move only head and neck. He denied shortness of breath, dysphagia, diplopia or any symptoms suggestive of hyperthyroidism. Except for propylthiouracil he had not used other medication, drugs, alcohol or licorice. The patient was an engineer who had taken refuge from Iraq where he had been in political imprisonment for several years. He had been in The Netherlands for eight months. He was unaware of any family members with neurologic or thyroid disease. On physical examination he had a temperature of 37.2°C, a pulse rate of 85 beats/ min and a blood pressure of 100/70 mmHg. There was a diffusely enlarged thyroid gland. Neurologic examination demonstrated an alert and well oriented patient with a flaccid quadriplegia. Deep tendon reflexes were absent and there was no sensory impairment. Results of investigations at admission are listed in box 1. The patient was admitted to the intensive care unit where potassium was administered. Seven hours after admission his paralysis had disappeared completely and his serum potassium had normalised to 4.4 mmol/l. Because of intractable itch propylthiouracil was replaced by thiamizole 30 mg daily. Four days later, after KCI supplementation was discontinued, he again experienced severe weakness in all limbs on awakening. The potassium level had dropped to 2.9 mmol/l. After supplementation of KC1, both the hypokalaemia and the paralysis disappeared again with a few hours.