From the Guidelines
Thyroid storm is a life-threatening medical emergency that requires immediate treatment with beta-blockers, thionamides, iodine solution, and glucocorticoids to control thyroid hormone effects and address the underlying cause. The treatment begins with beta-blockers like propranolol (60-80 mg orally every 4-6 hours) to control cardiovascular symptoms, as it is the most widely studied nonselective beta-blocker for this condition 1.
Treatment Approach
- Beta-blockers: propranolol is the preferred choice due to its ability to inhibit the peripheral conversion of T4 to T3, in addition to controlling heart rate and tremor 1.
- Thionamides: methimazole (20-25 mg orally every 6 hours) is used to block new thyroid hormone synthesis.
- Iodine solution: SSKI 5 drops orally every 6 hours or Lugol's solution should be administered one hour after starting thionamides to block thyroid hormone release.
- Glucocorticoids: hydrocortisone (100 mg intravenously every 8 hours) helps reduce T4 to T3 conversion and treat potential adrenal insufficiency.
Supportive Care
- Fever management with acetaminophen
- Aggressive fluid resuscitation
- Treatment of the precipitating factor (infection, trauma, surgery, etc.)
- Patients require ICU admission with continuous cardiac monitoring, as thyroid storm can lead to cardiac failure, arrhythmias, or multi-organ dysfunction without prompt treatment 1.
The choice of treatment should prioritize reducing morbidity, mortality, and improving quality of life, and the most recent and highest quality study should guide the decision-making process 1. In this case, the use of propranolol as a beta-blocker is supported by the most recent evidence 1, making it the preferred choice for treating thyroid storm.
From the FDA Drug Label
Propylthiouracil inhibits the conversion of thyroxine to triiodothyronine in peripheral tissues and may therefore be an effective treatment for thyroid storm. The treatment for thyroid storm (thyrotoxic crisis) may include propylthiouracil (PO), as it inhibits the conversion of thyroxine to triiodothyronine in peripheral tissues, making it a potentially effective treatment option 2.
- Key points:
- Propylthiouracil inhibits thyroid hormone synthesis
- It does not inactivate existing thyroid hormones
- It may be effective in treating thyroid storm by inhibiting thyroxine to triiodothyronine conversion
From the Research
Treatment Overview
The treatment for thyroid storm (thyrotoxic crisis) typically involves a combination of medications and supportive care. The goals of treatment are to:
- Reduce the production of thyroid hormones
- Block the peripheral effects of thyroid hormones
- Manage systemic complications
Medications
Some of the medications used to treat thyroid storm include:
- Propranolol to inhibit the catecholamine-mediated peripheral effects of circulating thyronines 3
- Propylthiouracil to inhibit thyroid hormone synthesis and peripheral conversion of thyroxine to triiodothyronine (T3) 3, 4, 5
- Methimazole as an alternative to propylthiouracil for inhibiting thyroid hormone synthesis 4, 5
- Iodine to block the glandular release of thyroid hormones 3
- Dexamethasone for general supportive therapy 3
Therapeutic Plasma Exchange
Therapeutic plasma exchange (TPE) may be considered for patients who cannot tolerate or fail pharmacotherapy, especially if they cannot undergo thyroidectomy 4. TPE can remove T3 and T4 bound to albumin, autoantibodies, catecholamines, and cytokines.
Surgical Intervention
Early thyroidectomy should be considered as the treatment of choice if medical treatment fails to result in clinical improvement 6.
Important Considerations
- Caution should be exercised when using long-acting β-blocking agents in patients with underlying thyrocardiac disease, as they may cause circulatory failure 7.
- Ultra-short-acting β-blockers may be a suitable alternative in this subset of patients 7.
- Current guidelines recommending propylthiouracil over methimazole for treatment of thyroid storm may merit reevaluation, as no significant differences were found in mortality or adverse events between the two treatment groups 5.