פוסט זה זמין גם ב:
עברית
Written by Jason Lesnick
Thyroid storm is a high-risk, low-prevalence disease that mimics multiple other emergent diagnoses due to its most common features being fever, altered mental status, and cardiovascular dysfunction.
There’s a storm brewing in your patient’s neck
Thyroid storm (TS) is a life-threatening condition defined as exaggerated signs and symptoms of thyrotoxicosis and evidence of multi-organ decompensation. Thyrotoxicosis is simply the clinical manifestation of symptoms as the result of excess T3 and T4 in peripheral tissues.
Common causes include change in medications or non-adherence, infection, Graves’ disease, thyroid surgery, trauma, exogenous iodine exposure, medication effect (amiodarone), and everyone’s favorite – idiopathic.
The signs and symptoms of TS almost always include hyperpyrexia, cardiovascular dysfunction, and altered mental status. But because of the ubiquitous nature of thyroid receptors, common disease features can include: fever, weight loss, tachycardia, atrial or ventricular fibrillation, systolic and high output heart failure, nausea, vomiting, diarrhea, abdominal pain, hepatic injury/failure, jaundice, tremor, anxiety, agitation, delirium, hallucinations, goiter, exophthalmos, and scarring in the area of the thyroid.
Diagnosing TS can be challenging due to the variable, nonspecific presentation. Classically, T3/T4 levels will be elevated and TSH low. Often there is no difference between thyroid hormone levels in uncomplicated hyperthyroidism and TS. Thankfully, there are decision tools. The Burch-Wartofsky scale is more sensitive but less specific than the Japan Thyroid Association criteria. Guidelines recommend applying both of these scoring systems if considering TS but relying on your history and physical to make the diagnosis.
The order and timing of treatment matters. Your first two medications should include a beta blocker (if not clinically in heart failure) and a thionamide. Propranolol has traditionally been used due to its ability to inhibit peripheral conversion of T4 to T3, but esmolol is a good option as well due to its short acting nature and the risk of beta blockers precipitating cardiogenic shock in these patients. For thionamides (which inhibit thyroid peroxidase), propylthiouracil (PTU) is the drug of choice in the first trimester of pregnancy (lower teratogenicity); otherwise, methimazole is preferred, including in the second or third trimester due to fewer adverse effects (hepatotoxicity is more common with PTU), though for all-comers it may not matter which thionamide is used. Steroids will block the thyroid from releasing T4 and stop the conversion of T4 to T3 as well as protect from potential adrenal insufficiency. Hydrocortisone or dexamethasone are the recommended agents. Iodine should be given 1 hour after a thionamide to avoid it being used to produce additional thyroid hormone and to block the release of preformed T3 and T4 from thyroglobulin. Finally, cholestyramine can be given to bind thyroid hormone in the intestinal system and reduce enterohepatic absorption.
How will this change my practice?
TS is a high morbidity and mortality diagnosis that is easy to miss if you don’t consider it abd treat only for sepsis, ethanol withdrawal, or various toxidromes, which mimic TS. I personally learned from this article that cholestyramine is another treatment option for TS. Keep your differential broad and, in true EM fashion, think about the ‘worst-first’ diagnoses like thyroid storm.
Source
High risk and low prevalence diseases: Thyroid Storm. The American journal of emergency medicine vol. 69 (2023): 127-135. doi:10.1016/j.ajem.2023.03.035
