EMA Cited · Endocrine · Critical care

Thyroid storm

Updated Oct 31, 2026Adults · ED management9 sources · 7 checked in PubMed2 figuresETA/BTA/SfE consensus 2026

Bottom line

It is a clinical diagnosis. No hormone level separates storm from severe thyrotoxicosis. The Burch–Wartofsky score and the Japanese criteria help, but neither has been validated against a gold standard.¹
Altered mental status is the red flag. It was the one feature that set clinically diagnosed storm apart from thyrotoxic patients who merely met the score cutoffs.⁵
Four drugs, in order: beta-blocker, high-dose antithyroid drug, hydrocortisone, then iodine at least 1 hour after the antithyroid drug.¹
Beta-blockers can cause collapse in heart failure or shock. Use cautious doses or titratable IV esmolol, and get an echo early.¹
It still kills. In-ICU mortality was 17% in a French cohort, and cardiogenic shock in the first 48 hours carried odds of death of 9.43.⁴ US storm admissions had a 12-fold higher mortality than thyrotoxicosis without storm.³

Recognize

Cardinal features: fever, usually above 38.5 °C (101.3 °F); tachycardia out of proportion to the fever; arrhythmia, especially atrial fibrillation; heart failure and pulmonary edema; altered mental status; and gut dysfunction.¹
Underlying cause: usually Graves' disease; also toxic multinodular goitre and, less often, thyroiditis.¹ In a French ICU cohort, amiodarone-associated thyrotoxicosis was the commonest cause (33%), and hyperthyroidism was unknown before admission in 32%.⁴
Triggers: infection, surgery, trauma, myocardial infarction, stroke, childbirth, DKA, iodinated contrast, and stopping antithyroid drugs.¹ LITFL adds amiodarone, salicylates and burns, and notes that post-operative storm typically appears 6–24 hours after surgery.⁹
Older patients may look apathetic, with little tachycardia or agitation. Check thyroid function even when the picture isn't classic.¹
Disseminated intravascular coagulation is a recognized complication. Suspect it with unexplained bleeding or bruising.¹
Common look-alikes: sepsis, meningitis or encephalitis, heatstroke, sympathomimetic toxicity, neuroleptic malignant syndrome, hypertensive encephalopathy.¹

Burch–Wartofsky item	Points
Temperature
38–38.5 °C / 38.6–39 / 39.1–39.5 / 39.6–40 / 40.1–40.6 / > 40.6	5 / 10 / 15 / 20 / 25 / 30
Central nervous system
Agitation / delirium, psychosis or extreme lethargy / seizure or coma	10 / 20 / 30
Gut and liver
Diarrhea, abdominal pain, nausea or vomiting / jaundice	10 / 20
Heart
Heart rate 90–109 / 110–119 / 120–129 / 130–139 / ≥ 140	5 / 10 / 15 / 20 / 25
Heart failure: pedal edema / bibasilar rales / pulmonary edema	5 / 10 / 15
Atrial fibrillation	10
Precipitating event
Present	10
Total
< 25 unlikely · 25–44 impending storm · ≥ 45 highly suggestive

Scores from the 2026 consensus.¹ The Japanese (JTA/JES) criteria require raised free T4 or T3. Definite storm is any CNS feature plus one other (fever ≥ 38 °C, heart rate ≥ 130, heart failure, gut or liver dysfunction), or three of the others without CNS change. Suspected storm is two of the others.^1,2 Burch–Wartofsky can overcall storm in sepsis and other ICU illness; the Japanese criteria can miss early cases.¹

Score 25–44

The consensus advises that the decision to start full storm treatment at a score of 25–44 be made by an experienced clinician or intensivist together with an endocrinologist.¹

First steps

Monitored bed. Manage in high-dependency or intensive care, and involve critical care early. Tell the surgeons in case thyroidectomy is needed.¹
Supportive care: cooling, acetaminophen, IV fluids, close glucose checks, and thiamine. Avoid aspirin, which raises free thyroid hormone.¹
Tests: free T4 and T3, ECG, chest X-ray, and a pregnancy test in anyone who could be pregnant.¹
Beta-blocker, unless heart failure or shock makes it dangerous (see below).¹
High-dose antithyroid drug, then hydrocortisone.¹
Iodine at least 1 hour after the antithyroid drug.¹
Treat the trigger aggressively, for example antibiotics for infection.¹

FIG 1 · Decision flowCited

Suspect storm: thyrotoxicosis with fever, disproportionate tachycardia, AF, heart failure, altered mental status, or gut or liver dysfunction. Score it, but treat on clinical judgement.¹
Monitored bed and supportive care: cooling, acetaminophen (not aspirin), IV fluids, glucose checks, pregnancy test; treat the trigger.¹
Hypotension, heart failure or cardiogenic shock?
Yes
IV esmolol, cautiously: 500 µg/kg over 1 min, then up to 200 µg/kg/min. It can be stopped quickly.¹
Get an echo early. Beta-blockade can remove the adrenergic support these patients depend on.¹
No
Propranolol 60–80 mg PO every 4 h, or IV if vomiting or unstable. If beta-blockers are contraindicated, diltiazem 60–90 mg PO every 6 h.¹
Antithyroid drug: methimazole 60–80 mg/day, or PTU 500–1,000 mg load then 250 mg every 4 h. Methimazole if liver tests are over 3× normal; PTU in the first trimester.^1,8
Hydrocortisone 100 mg IV, then 50 mg four times a day.¹
At least 1 hour after the antithyroid drug, iodine: Lugol's 8 drops or SSKI 5 drops four times a day, diluted. Unlikely to help in thyroiditis.¹
Not stabilizing within 24–48 hours?
Yes
Check doses, absorption and the trigger. Add cholestyramine; consider plasma exchange, thyroidectomy, or VA-ECMO for cardiogenic shock.¹
Improving
Once stable: continue the beta-blocker and antithyroid drug, stop iodine when hormone levels are controlled, and plan definitive treatment.¹

FIG 1Thyroid storm in the ED. Drawn for this page from the 2026 European Thyroid Association, British Thyroid Association and Society for Endocrinology consensus, and the propylthiouracil label. Each box carries its own citations.^1,8

Treatment

Drug	Adult dose	Notes
1 · Block adrenergic effects
Propranolol PO	60–80 mg every 4 h	High doses also reduce T4-to-T3 conversion.¹
Propranolol IV	1–3 mg at up to 1 mg/min; repeat once after 2 min; infusion 2–3 mg/h	For vomiting, agitation or instability.¹
Esmolol IV	500 µg/kg over 1 min, then 0–200 µg/kg/min	Preferred with cardiomyopathy, hypotension or evolving shock; short half-life.¹
Diltiazem	60–90 mg PO every 6 h; can be given IV	If beta-blockers are contraindicated, such as asthma.¹
2 · Stop new hormone synthesis
Methimazole	60–80 mg/day	Prefer if liver tests are over 3× normal. Lower to 30 mg/day as soon as practical.¹
Propylthiouracil (PTU)	500–1,000 mg load (PO, NG or PR), then 250 mg every 4 h	Also blocks T4-to-T3 conversion. Boxed warning for severe liver injury; may be preferred in the first trimester. Lower to 400 mg/day as soon as practical.^1,8
3 · Reduce conversion
Hydrocortisone IV	100 mg, then 50 mg four times a day	Stop once stable if adrenal insufficiency is not suspected.¹
4 · Block hormone release (≥ 1 h after the antithyroid drug)
Lugol's iodine	8 drops four times a day, diluted	Stop once stable. Delays radioiodine for at least 2–3 months.¹
SSKI (potassium iodide)	5 drops four times a day, diluted	Unlikely to help in destructive thyroiditis.¹
Adjuncts
Cholestyramine	4 g three times a day	Off-label; increases hormone clearance.¹
Lithium	Specialist advice only	Toxicity is a concern.¹

Unreviewed doses. Verify against the current label and your institution's protocol before giving anything.

FIG 2The order matters. Drawn for this page from the 2026 consensus. Iodine given before the antithyroid drug can worsen thyrotoxicosis, so it waits at least an hour.¹ Times show when each drug starts, not how fast it works.

Sources disagree

Doses differ between sources. Hydrocortisone: 100 mg then 50 mg four times a day in the consensus¹, but 300 mg then 100 mg every 8 hours on LITFL.⁹ Iodine: Lugol's 8 drops four times a day in the consensus¹, 10 drops every 6–8 hours on LITFL.⁹ This page uses the consensus doses.

PTU or methimazole?

In 1,383 US ICU patients with thyroid storm, in-hospital death was 8.5% with PTU and 6.3% with methimazole. The adjusted difference was not significant, and adverse events were similar.⁶ The consensus treats the two as equivalent options.¹ The PTU label carries a boxed warning for severe liver injury, including liver failure needing transplant.⁸

Beta-blockers and the failing heart

Beta-blockade remains a cornerstone, but it can precipitate collapse in thyrotoxic cardiomyopathy or shock. Use cautious low initial doses or esmolol, and consider invasive monitoring.¹
Retrospective data suggested higher mortality with propranolol than beta1-selective drugs in heart failure; a larger cohort found no difference. The consensus picks the drug by patient and local availability.¹

Watch potassium after steroids. High-dose glucocorticoids can trigger thyrotoxic periodic paralysis, especially in young Asian or Hispanic men.¹
Sedation: chlorpromazine 50–100 mg IM can be considered; it also lowers temperature.¹
Atrial fibrillation: decide on anticoagulation by usual stroke and bleeding risk. Many patients return to sinus rhythm once euthyroid.¹

Not improving

Expect improvement within 24–72 hours. Follow temperature, heart rate, blood pressure, mental status and gut function. Don't use TSH to judge early response.¹
No improvement by 24–48 hours: check doses and absorption, the timing of iodine, and the trigger, and look for cardiomyopathy.¹
Rescue options: therapeutic plasma exchange; emergency thyroidectomy in specialist centers; VA-ECMO for refractory cardiogenic shock.¹ LITFL suggests plasma exchange if there is no improvement after 24–48 hours of maximal therapy.⁹

Disposition

ICU for vasopressors, reduced consciousness, ventilatory support, heart failure, cardiogenic shock or significant arrhythmia, multi-organ dysfunction, or deterioration despite treatment.¹
Everyone else with suspected storm: a high-dependency bed with endocrinology involved.¹
Pregnancy: rare but high-risk; involve obstetrics and neonatology early.¹
Before discharge: plan definitive treatment, usually thyroidectomy or radioiodine.¹

Pitfalls

Giving iodine before the antithyroid drug.^1,9
Treating fever with aspirin.¹
Full-dose propranolol in a patient with cardiogenic shock or thyrotoxic cardiomyopathy.¹
Waiting for a hormone level to make the diagnosis. Levels overlap with uncomplicated thyrotoxicosis.^1,2
Calling it sepsis, or calling sepsis storm. Fever and tachycardia drive both.¹
Missing apathetic storm in an older patient.¹

How strong is the evidence?

Storm is rare: 0.57–0.76 cases per 100,000 US people a year, and 16.2% of thyrotoxicosis admissions.³ The consensus did not grade its evidence, because the data are mainly observational.¹ The PTU-versus-methimazole comparison is a large observational cohort, not a trial.⁶ In a Japanese prospective registry, 30-day mortality was 5.5%. Among sicker patients (APACHE II ≥ 12), it was 4.7% when the Japanese guideline was followed and 50% when it wasn't.⁷

On-shift teaching

Questions to ask a learner at the bedside. Tap a question to see the answer. Every answer uses facts cited above.

Q1Can thyroid function tests tell you whether a thyrotoxic patient is in storm?

No. Hormone levels overlap between storm and uncomplicated thyrotoxicosis. It is a clinical diagnosis, helped by the Burch–Wartofsky score or the Japanese criteria.^1,2

Q2Which clinical feature best set real storm apart from thyrotoxic patients who simply met the score cutoff?

Altered mental status (central nervous system dysfunction).⁵

Q3Why wait an hour after the antithyroid drug before giving iodine?

Iodine given first can worsen thyrotoxicosis, depending on the cause. Block new synthesis first, then give iodine at least 1 hour later.¹

Q4A patient in storm is hypotensive with a poor ejection fraction. How do you control the rate?

Cautiously, with titratable IV esmolol (500 µg/kg over 1 min, then up to 200 µg/kg/min), because beta-blockade can cause collapse. Get an echo early.¹

Q5PTU or methimazole?

In 1,383 ICU patients, mortality did not differ significantly (8.5% vs 6.3%).⁶ Choose methimazole if liver tests are over 3× normal; PTU may be preferred in the first trimester.^1,8

Q6Why is acetaminophen preferred over aspirin for fever?

Aspirin displaces thyroid hormone from binding proteins, raising free T4 and T3.¹

References

Evidence base

What this page is built on

9 sources, cited 84 times. Dots are sources, filled by how far each was read; stronger color means a larger share of the citations. Tap a tier to see its sources.

Read in full · 3Abstract read · 6Record only · 0Link checked · 0

Checked by the writer, not a physician. The dots show how each source was read, not that anyone has confirmed the claims.

Not for clinical use

AI-generated draft. Not reviewed by a physician. This page is for education only and may contain errors, including in doses. Do not use it to diagnose, treat or make decisions about any patient. Rely on your own clinical judgment, your institution's protocols and current drug labeling. Reading this page does not create a physician-patient relationship. Full terms