TR Pearl: Thyroid Storm Management

  • Endocrine emergency: severe clinical manifestations of thyrotoxicosis
  • Mortality rate of thyroid storm is 10-30%
  • Often precipitated in patients with hx of hyperthyroidism by an acute event such as surgery (thyroid or non-thyroidal surgery), trauma, infection, acute iodine load (including amiodarone), or parturition 
  • Risk factor includes irregular use or discontinuation of antithyroid drugs 

Diagnosing Thyroid Storm

  • The distinction between severe thyrotoxicosis and thyroid storm is a clinical one
  • Degree of thyroid hormone excess is typically not more profound than that seen in patients with uncomplicated thyrotoxicosis!!! In other words, degree of hyperthyroidism on thyroid labs do not predict severity of thyrotoxicosis.
  • In severe thyrotoxicosis, in addition to other hallmark signs of hyperthyroidism, patients may have N/V/D, abd pain, liver failure (and subsequent jaundice).
  • More hallmark signs of thyroid storm as opposed to severe thyrotoxicosis are:
  1. Severe tachycardia above 140bpm and/or Afib, CHF, cardiovascular collapse
  2. Hyperpyrexia to 104-106F
  3. CNS component including agitation, anxiety, delirium, psychosis, stupor or coma (CNS component considered by many to be essential to the diagnosis)
  • No well established criteria, but Burch Wartofsky point scale on MD Calc can help distinguish severe thyrotoxicosis from thyroid storm
    • High sensitivity, low specificity 


Things to keep in mind

  1. ICU dispo
  2. While treating, continue to identify and treat the precipitating factor
  3. Fluid status is individualized to the patient — some require fluids, some require diuresis
  4. Medication requirements might be high 2/2 increased drug metabolism 2/2 hyperthyroidism
  5. Treat hyperpyrexia aggressively: Acetaminophen should be used instead of aspirin since the latter can increase serum free T4 and T3 concentrations by interfering with their protein binding. Use external cooling methods as necessary

For patients in thyroid storm or impending storm

  1. Beta blocker – Propranolol preferred.
    • Goal: reduce HR and BP
    • Mechanism: mitigates adrenergic surge to improve symptoms. In addition, at high doses it inhibits the conversion of T4 to T3
    • PO Dose:  60 to 80 mg q4-6 hr, titrated to achieve rate control while ensuring blood pressure remains stable.
    • IV dose: 0.5 to 1 mg over 10 minutes followed by 1 to 2 mg over 10 minutes q2-3 hr.
    • Considerations:
      • If concern for severe asthma/COPD, can use cardioselective beta blocker such as metoprolol. If beta blocker contraindicated in these patients, use CCB.
      • Contraindicated in patients with acute decompensated heart failure (may block the adrenergic surge that is maintaining CO). If unsure if patient can tolerate beta blocker from a HF perspective, in Japan, they use esmolol since it is more easily titratable. For esmolol, loading dose of 250 to 500 mcg/kg, followed by an infusion at 50 to 100 mcg/kg per minute OR a loading dose of 1 mg/kg over 30 seconds followed by approximately 150 mcg/kg/minute
  2. Thionamide – PTU preferred.
  1. Mechanism: block de novo thyroid hormone synthesis within one to two hours after administration (no effect on release of preformed hormone)
  2. PTU Dose: 200 to 250 mg every four hours; Not necessary to give a loading dose, but can give a loading dose of 500 to 1000mg
  3. Methimazole Dose: 20 mg orally every four to six hours
  4. Considerations:
    • Propylthiouracil preferred in storm. 
    • As compared to methimazole, PTU is more effective over the first 24 hours, which is why it is preferred in thyroid storm.
    • In severe thyrotoxicosis (but not life threatening storm), methimazole is preferred because methimazole has a longer duration of action and, after weeks of treatment, results in more rapid normalization of serum T3 compared with PTU. Also has less hepatotoxicity. 
    • Both PTU and Methimazole can be given via NGT. 
  5. If a patient cannot tolerate thionamides 2/2 hepatotoxicity or agranulocytosis or other reason:
    • Patient needs urgent thyroidectomy. 
    • Can use bile acid sequestrants aka cholestyramine (4g PO QID) to reduce enterohepatic circulation of thyroid hormone
      1. Since cholestyramine can interfere with the absorption of oral medications, other drugs given orally should be given two hours before or two hours after cholestyramine administration 
  6. Iodine – Saturated solution of potassium iodide (SSKI) or Lugol’s solution
  1. Administered 1 hour after first dose of thionamide administration!!! Important, earlier administration may precipitate increased production of thyroid and worsening of storm. 
  2. Mechanism:  blocks the release of T4 and T3 from the gland within hours
  3. Needs to be diluted in 240 mL or more of beverage or taken with food
  4. SSKI:  5 drops (50 mg iodide/drop [0.05 mL]) PO q6hr
  5. Lugol’s solution: 10 drops (6.25 mg iodide/iodine per drop [0.05 mL]) PO TID
    • 10 drops of Lugol’s solution can also be directly added to intravenous fluids
  6. Can also be given rectally

If thyroid storm for sure, add glucocorticoids. They reduce T4 to T3 conversion.

  • Hydrocortisone 300 mg loading dose, then hydrocortisone, 100 mg IV q8h

Other treatment considerations: 

  • Cholestyramine
  • Plasmapheresis when other therapies unsuccessful for patients who cannot tolerate thionamides and in patients who are being prepared for urgent thyroidectomy
  • Consider lithium
June 2024