Thyroid storm

(Redirected from Thyroid Storm)


  • Mortality
    • Without treatment: 80-100%
    • With treatment: 15-50%
  • Difference between severe thyrotoxicosis and thyroid storm is clinical diagnosis[1]
    • Must empirically treat before TFTs back from lab
    • Thyroid storm will present with classic triad and history of hyperthyroid with precipitant


  • Longstanding untreated hyperthyroidism
  • Infection
  • Trauma
  • Recent thyroid manipulation (physical or surgical)
  • Burns
  • Surgery
  • DKA
  • Withdrawal of thyroid medication
  • Lithium withdrawal
  • Iodine administration
  • MI
  • CVA
  • PE
  • Interferon treatment
  • Recent parturition
  • Molar Pregnancy
  • Hypoglycemia
  • Exposure to iodine (or iodinated contrast)

Clinical Features

Classic Triad

Apathetic Hyperthyroidism

  • Strikingly different rare form, dominated by depressed mental status, cardiac complications[2]
  • Treatment with antithyroid therapy is still mainstay
  • More common in elderly patients [3]

Differential Diagnosis

Wide Pulse Pressure



  • Chemistry (creatinine may be low or High Ca)
  • CBC (may have Thrombocytopenia)
  • LFTs (using PTU vs. methimazole, see below)
  • TSH/Free T3/T4
  • Cortisol level (rule-out concurrent adrenal insufficiency)
  • ECG
  • Rule-out infection:

Burch & Wartofsky Diagnostic Criteria

Category Points
Thermoregulatory dysfunction (°F)
Tmax= 99-99.9 5
Tmax= 100-100.9 10
Tmax= 101-101.9 15
Tmax= 102-102.9 20
Tmax= 103-103.9 25
Tmax= 104 30
Central nervous system effects
Mild (Agitation) 10
Moderate (delirium, psychosis, extreme lethargy) 20
Severe (seizure, coma) 30
Gastrointestinal-hepatic dysfunction
Moderate (diarrhea, nausea and vomiting, abdominal pain) 10
Severe (unexplained jaundice) 20
Cardiovascular dysfunction (tachycardia)
HR= 99-109 5
HR= 110-119 10
HR= 120-129 15
HR= 130-139 20
HR= 140 25
Congestive Heart Failure
Mild (pedal edema) 5
Moderate (bibasilar rales) 10
Severe (pulmonary edema, A. fib) 15
Precipitant history
Negative 0
Positive 10


  • >45 = Highly suggestive of thyroid storm
  • 25-44 = Suggestive of impending storm
  • <25 = Unlikely to represent storm


Identify precipitant (i.e. med noncompliance, DKA, infection). When in doubt of diagnosis, the EP should treat given the high mortality rate, as a few doses of anti-thyroid medication are unlikely to harm euthyroid patient[6]

Supportive care

  1. Fever
    • Do not aggressively cool as this can lead to vasoconstriction[7]
    • Careful cooling measures (ice packs & cooling blankets)
    • Acetaminophen (avoid aspirin or NSAIDS because they displace thyroid hormone from TBG)
  2. Dehydration/hypoglycemia
    • D5NS (most patients have depleted glycogen stores)
    • Crackles in lungs are likely high output HF, NOT fluid overload
  3. Cardiac decompensation (CHF, A-fib)
    • Rate control, inotropes, diuretics as needed (short acting always better)
  4. Agitation
    • Benzodiazepines are the preferred agent

Treat Increased Adrenergic Tone

  • Propranolol PO 60-80 mg q4hr (if can tolerate PO, no PR form)
  • Propranolol IV 1-2mg over 10 min; if tolerates then 1-2mg boluses q15 minutes until HR <100[8]
    • Followed by drip at dose required for heart rate control (3-5mg/hr)
    • Relative contraindications are same as for other medical conditions (e.g. CHF, Reactive Airway Disease, see alternative therapies)
    • In addition to decreasing peripheral conversion, propranolol will improve tremor, hyperpyrexia, and agitation
  • Esmolol 250-500mcg/kg loading dose, then 50-100mcg/kg/min[9]
    • B1 selective so can be used with active CHF, asthma, etc; but does not perform other benefits of propranolol

Block New Hormone Synthesis[10]

Thionamides are the main class of medications which prevent new hormone synthesis by inhibiting the iodination of tyrosine residues by thyroid peroxidase (TPO) enzymes. Propylthiouracil (PTU) is prefered over methimazole because it will also bock T4→T3 conversion

  1. PTU 600-1000mg PO or PR followed by 200-250mg q4hr
    • Note black box warning of hepatotoxicity so check LFTs prior
    • Avoid in patients with significant liver disease; use methimazole instead
  2. Methimazole 20-25mg q4hr
    • Longer acting than PTU
    • Should be avoided in pregnancy by classic teaching (freely crosses placenta, birth defects)
  3. Potassium iodide (SSKI)
    • Give 1hr after PTU to prevent increased hormone production (Jod-Basedow effect)[11]
    • Block hormone release: (Wolff-Chaikoff effect) only after hormone synthesis is inhibited. Iodine concentration leads to transient decrease of T3/T4
    • 5 drops (0.25 mL or 250mg) orally every 6 hours
    • Avoid potassium iodide if patient is on amiodarone
    • Can substitute radiocontrast dyes (Iopanoic acid, ipodate and iopanoate), PO Lugol solution, OR IV sodium iodide [12]
  4. Lithium carbonate[13]
    • Consider if iodine allergic
    • Lithium carbonate 300mg PO q8hr
    • Lithium inhibits thyroid hormone release from the gland and reduces iodination of tyrosine residues, but its use is complicated by the toxicity that can ensue.
  5. Lugol’s Solution 8 drops PO q 6 (alternative iodine source)
  6. Sodium Iodide 0.5mg IV Q 12 hours (alternative iodine source)

Adrenal Insufficiency Treatment

Often there may be associated adrenal insufficiency (also blocks T4>T3)


  • For recalcitrant thyroid storm, with remaining cardiac and neurologic symptoms
  • Especially in the case of fulminant liver failure, in which anti-thyroid drugs are contraindicated[15]
  • Repeat sessions until TFTs normalize
  • Removes cytokines, auto-antibodies, thyroid hormones, thyroid hormone bound proteins


  • Admission to ICU

See Also

External Links


  1. Nayak B1, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. 2006 Dec;35(4):663-86, vii.
  2. Parker KI et al. A case of apathetic thyroid storm with resultant hyperthyroidism-induced hypercalcemia. Am J Med Sci. 2013 Oct;346(4):338-40.
  3. Poudel RR et al. Apathetic thyrotoxicosis presenting with diabetes mellitus. J Community Hosp Intern Med Perspect. 2014 4(5).
  4. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am. 1993 Jun;22(2):263-77
  5. Bahn chair RS, Burch HB, Cooper DS, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. 2011;21(6):593-646.
  6. LoPresti J. A New Look at Thyroid Emergencies Part II: Handling Thyroid Storm.
  7. Chiha, Maguy, Shanika Samarasinghe, and Adam S Kabaker. 2013. Thyroid storm: an updated review. Journal of intensive care medicine, no. 3.
  8. EMCrit - Thryoid Storm (149)
  9. Brunette DD, Rothong C. Emergency department management of thyrotoxic crisis with esmolol. Am J Emerg Med. 1991;9(3):232-4.
  10. Doses based on American Association of Clinical Endocrinologists recommendations
  11. Chiha M. et al Thyroid storm: an updated review. J Intensive Care Med. 2015 Mar;30(3):131-40.
  12. Weingart, Scott. EMCRIT Thyroid Storm Show Notes.
  13. Carroll R, Matfin G. Endocrine and metabolic emergencies: thyroid storm. Ther Adv Endocrinol Metab. 2010 Jun; 1(3): 139–145. Full Text
  14. Muller C et al. Role of plasma exchange in the thyroid storm. Ther Apher Dial. 2011 Dec;15(6):522-31.
  15. Garg N et al. CALMING THE STORM - ROLE OF PLASMAPHERESIS IN THYROTOXIC CRISES. The Endocrine Society's 95th Annual Meeting and Expo, June 15–18, 2013 - San Francisco.


Ross Donaldson