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Q1: What is the diagnosis and how frequently is this condition encountered?
The patient had developed thyroid storm secondary to radioiodine therapy. Thyroid storm is a rare, life threatening complication of hyperthyroidism with an incidence of 1%–2% in hospitalised patients with hyperthyroidism, although it has a high mortality of around 15%.1 The incidence of the thyroid storm after RAI is variable because of variations in the regimens of RAI, in patient selection, and in the use of thyrostatic medications before and after RAI. The overall incidence is low and in one series only one patient out of 525 patients treated with 550 MBq RAI developed thyroid storm.23 The risk of thyroid storm after RAI treatment is difficult to predict in an individual patient but appears to be higher in patients with severe hyperthyroidism, in older patients, and in the presence of cardiovascular and cerebrovascular disease.2
Q2: What is the mechanism and what are the criteria for diagnosis of this condition?
The mechanism of thyroid storm is either a reduction in levels of binding proteins or the release of preformed thyroid hormones. Examples of the former include postoperative state or a major systemic illness; the latter is encountered as a result of injury to the follicular cells after RAI treatment or even after vigorous manipulation of the thyroid gland. Other precipitating factors include radiation, diabetic ketoacidosis, toxaemia of pregnancy, and parturition. Diagnosis is entirely based on typical clinical features in an appropriate setting. Important clinical manifestations include vomiting, diarrhoea, pyrexia, tachycardia, atrial fibrillation, cardiac failure, and neurological manifestations including agitation, delirium, seizures and coma, although not all classical features are essential for the diagnosis.2 Suppressed thyroid stimulating hormone and raised thyroid hormone levels support the diagnosis but the degree of elevation of the latter is not always exceptional.
Q3: How is this condition managed and how can one prevent it?
Management of thyroid storm precipitated by RAI therapy is along similar lines as that of thyroid storm caused by any other precipitant. Thyroid storm should preferably be managed in conjunction with an endocrinologist and management includes the administration of Lugol’s iodine, high dose propylthiouracil, corticosteroids, and supportive measures. There are no specific recommendations for prevention of thyroid storm after RAI, although, in high risk patients, prior hospitalisation,45 rendering patients euthyroid,6 and use of antithyroid drugs after RAI therapy have been recommended.7 Our patient developed thyroid storm even though she had been rendered euthyroid before RAI therapy and did not have any associated comorbidity. After recovery from thyroid storm, carbimazole was continued till May 1994 for persistent hyperthyroidism when RAI was readministered at a very high dose of 1110 MBq in view of an isotope uptake study showing an extremely high radioiodine turnover. On this occasion she was hospitalised before the administration of RAI therapy and carbimazole was recommenced five days after RAI. There was no recurrence of thyroid storm and three months later the patient became hypothyroid, requiring thyroxine replacement. It is likely that thyroid storm was successfully prevented by early reintroduction of carbimazole after the RAI treatment.
Thyroid storm secondary to radioiodine therapy.