Common Known Triggers of Thyroid Storm :
Withdrawal of anti-thyroid drug therapy
Iodide compound intake or radioiodine (I131 or I123) therapy in patients with Graves’ disease or autonomously functioning thyroid nodules
Major surgery, particularly thyroidectomy
Trauma, especially in the neck area
Systemic infections
Pregnancy/parturition
Diabetic ketoacidosis
Severe emotional stress
Cerebrovascular disease
Pulmonary thromboembolism
Intense exercise
Use of tyrosine-kinase inhibitors (particularly sorafenib)
Minor surgery (such as extraction of teeth)
Presentation
In many cases thyroid storm presents as multi-organ failure with the constellation of symptoms resembling an exaggeration of the usual symptoms of hyperthyroidism [7, 8]. The organs mainly affected by excess thyroid hormone are the heart, nervous system, gastrointestinal tract, and the liver [9–12]. Cardiovascular symptoms include atrial tachycardia to rates that can exceed 140 beats/min, congestive heart failure, and atrial fibrillation. Hypotension, ventricular tachycardia, arrhythmia, and death from cardiovascular collapse can also occur [13]. Fever is a frequent event, and hyperpyrexia of 104 °F to 106 °F is common. Altered mental status with agitation, anxiety, delirium, psychosis, stupor, or coma is often encountered and considered by many experts to be integral to the diagnosis [14]. Severe nausea, abdominal pain, vomiting, diarrhea, or hepatic failure with jaundice may occur [15]. Physical examination may show warm and moist skin, hand tremor, lid lag, goiter, and ophthalmopathy (in the occurrence of Graves’ disease) [15]. Clinicians should be aware that clinical symptomatology can pose difficulties in distinguishing thyroid storm from other medical emergencies, such as neuroleptic malignant syndrome, malignant hyperthermia, and pheochromocytoma [7].
Diagnosis
In critically ill patients the diagnosis of thyroid storm is essentially a clinical one with laboratory tests of thyroid function being confirmatory in the appropriate setting [14]. Clinicians may base the diagnosis of thyroid storm on several factors, which include a history of thyroid disease and potential triggering factors, typical signs and symptoms, and serum free T3 and free T4 concentrations exceeding the normal reference range and suppression of TSH levels [16]. In all patients with suspected thyroid storm, thyroid function tests (TSH, free T4, and free T3) should be assessed. Because hormone levels in thyroid storm patients are generally not higher than in patients with uncomplicated overt hyperthyroidism, the degree of hyperthyroidism is not a diagnostic criterion [17]. The clinical findings in suspected patients are frequently associated with elevation of serum bilirubin and transaminase levels, hyperglycemia, low total cholesterol values, leukocytosis or leukopenia, and electrolyte imbalances [18]. Hyperglycemia is due to a catecholamine-induced inhibition of insulin release and increased glycogenolysis. Hypercalcemia may be secondary to hemoconcentration and enhanced bone resorption [17]. Radioiodine uptake is not necessary for the diagnosis in suspected patients, and treatment should not be delayed for scanning in patients with clinical manifestations compatible with thyroid storm [15].
Treatment
Treating thyroid storm generally follows the same principles as treating those with uncomplicated hyperthyroidism, except that the medications are given more frequently and in higher doses [15]. Because the mortality rate of thyroid storm can be substantial, full support of the patient in an intensive care unit is considered essential [3, 5]. The specific principles of thyroid storm treatment are based upon case studies and clinical experience [15]. In addition to specific therapy directed against the thyroid, supportive therapy (e.g., supplemental oxygen, intubation and mechanical ventilation, fluid resuscitation, electrolyte correction) and recognition and treatment of precipitating factors are crucial components in optimizing the final outcome [15].
In general the therapeutic regimen typically relies on the following medications, with a recommended medication dosing guide shown below in Table 48.2.
Table 48.2
Medication dosing guide
*Principles of medication dosing outlined below are based upon clinical experience and case studies |
Beta-Blockers |
Propranolol: 60–80 mg PO every 4–6 h; 1–2 mg IV every 4–8 h |
Esmolol: Loading dose of 250–500 mcg/kg followed by infusion at 50–100 mcg/kg per minute |
Thionamides |
Propylthiouracil (PTU): 200 mg PO every 4 h; PTU enema (eight 50 mg tablets of PTU dissolved in 90 mL of sterile water); PTU suppository (200 mg of PTU dissolved in polyethylene glycol base) |
Methimazole: 15–20 mg PO every 4–6 h |
Iodine Solutions |
Potassium iodide-iodine (Lugol’s) solution: 10 drops (8 mg iodide/iodine per drop [0.05 mL] every 6 h |
Saturated solution of potassium iodide (SSKI): 5 drops (50 mg iodide/drop [0.05 mL] every 6 h |
*Iodine solutions can be irritating and should be diluted in 240 mL or more of beverage |
Iodinated radiocontrast agents |
Sodium ipodate: 500–1000 mg/day PO |
Iopanoic acid: 500–1000 mg/day PO |
Glucocorticoids |
Hydrocortisone: 100 mg IV every 8 h |
Lithium |
Lithium carbonate: 300 mg PO every 6–8 h |
*Renal and neurologic toxicity limit lithium utility |
Beta-Blockers
These medications are cornerstones of treatment in most patients with severe hyperthyroidism. Caution is advised when using these medications in patients with heart failure; however it is important to note that improvement in cardiac function may be seen with control of tachycardia. Propranolol is often the drug of choice because it antagonizes the increased binding of catecholamines to beta-adrenergic receptors and it reduces the peripheral deiodination of T4 to T3, the process by which the majority of T3 is created [6]. An alternative to propranolol is to utilize the short-acting beta-blocker esmolol. Esmolol use permits rapid titration of the drug to achieve the desired effect while minimizing adverse reactions [19]. In patients with severe reactive airways disease, cardioselective beta-blockers may be considered, but should be used with caution [15].
Thionamides
Thionamides block de novo thyroid hormone synthesis roughly within 1–2 h after administration. However, it is noted that these medications have no effect on the release of preformed hormone from the thyroid gland. In the United States the thionamide drugs available are propylthiouracil (PTU) and methimazole.
No consensus data exist that show patients do better clinically with one thionamide over another. Some sources suggest starting treatment for life-threatening thyroid storm with PTU since it can be administered regularly every four hours in an intensive care unit, and because PTU, but not methimazole, blocks T4 to T3 conversion [20]. However, because methimazole has a longer duration of action and is less hepatotoxic than PTU it may be preferred for severe but not life-threatening hyperthyroidism. Patients who are started on PTU in the intensive care unit should be transitioned to methimazole before discharge from the hospital.
Iodine Containing Solutions
These medications help block the release of T4 and T3 from the thyroid gland within hours and are traditionally used in the treatment of thyroid storm. Importantly, the administration of iodine should be delayed for at least one hour after thionamide administration in order to prevent the iodine from acting as substrate for new hormone synthesis [17]. Oral doses are potassium iodide-iodine (Lugol’s) solution or saturated solution of potassium iodide (SSKI). Iodine containing solutions can also be given rectally [21, 22]. Because these solutions may irritate the gastrointestinal tract, they should be diluted in 240 mL or more of beverage and taken with food. Local esophageal or duodenal mucosal injury and hemorrhage have been reported after oral administration of potassium iodide-iodine solution [23].
Glucocorticoids
Glucocorticoids reduce T4 to T3 conversion. They may also treat potentially associated adrenal insufficiency and have a direct effect on any underlying thyroid related autoimmune process [24]. Limited data suggest improved outcomes with the use of glucocorticoids for the treatment of thyroid storm [25]. Therefore, it is reasonable to consider administering hydrocortisone in patients with thyroid storm.
Patients Unable to Take a Thionamide
Some patients must discontinue thionamides because of side effects such as agranulocytosis, hepatotoxicity, or allergic reaction. In such patients who require urgent treatment of hyperthyroidism, thyroidectomy is the treatment of choice. Preoperative treatment of thyrotoxicosis is required in patients who are to undergo surgery, and this typically involves medications such as beta-blockers, glucocorticoids, and iodine containing solutions [26].
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