Life-threatening hyperthyroidism with multisystem decompensation; mortality 10-30%.
Also known as: thyroid storm, thyrotoxic crisis, thyrotoxic storm
Overview
Severe, life-threatening exacerbation of thyrotoxicosis characterized by hyperpyrexia, marked tachycardia, CNS dysfunction, and multi-organ decompensation. Clinical diagnosis (Burch-Wartofsky Point Scale) — do not wait for thyroid function tests to act.
Epidemiology
Uncommon (<10% of hospitalized thyrotoxic patients), but mortality 10-30%. Most cases occur in patients with known or unrecognized Graves disease or toxic nodular goiter. Often precipitated by an identifiable trigger.
Try two board-style Thyroid Storm questions
Real questions from the FirstPassPA bank, with the full explanation. Pick an answer — no signup, no email.
Question 1EndocrineMedium
A 38-year-old woman with poorly controlled Graves disease presents to the emergency department two days after stopping her methimazole because of nausea. She is confused and agitated. Temperature is 40.2°C (104.4°F), heart rate is 152/min and irregularly irregular, and blood pressure is 148/82 mm Hg. Examination shows drenching diaphoresis, a diffusely enlarged thyroid with a bruit, and bilateral exophthalmos. Her Burch-Wartofsky score is 60. Which of the following best supports the diagnosis?
ASuppressed TSH with low free T4 and low free T3
BSuppressed TSH with high free T4 and free T3
CElevated TSH with high free T4 and free T3
DElevated total T4 with normal free T4 and TSH
Reveal answer & full explanation
Correct answer: B — Suppressed TSH with high free T4 and free T3
ASuppressed TSH with low free T4 and low free T3
BSuppressed TSH with high free T4 and free T3✓
CElevated TSH with high free T4 and free T3
DElevated total T4 with normal free T4 and TSH
Why Suppressed TSH with high free T4 and free T3 is correct
Thyroid storm is a severe exacerbation of thyrotoxicosis; the underlying biochemistry is primary hyperthyroidism, so the pituitary suppresses TSH while free T4 and free T3 are elevated.
In Graves disease the gland autonomously overproduces hormone (TSH-receptor antibody driven), giving a suppressed TSH with high free hormone levels, the pattern that confirms the thyrotoxic state behind the crisis.
Per the American Thyroid Association, storm remains a CLINICAL diagnosis (Burch-Wartofsky Point Scale >=45 is highly suggestive); labs confirm thyrotoxicosis but treatment should never be delayed waiting for them.
Why the others are wrong
Elevated TSH with high free T4 and free T3: this is the pattern of a TSH-secreting pituitary adenoma or thyroid hormone resistance, a rare central cause, not the Graves-driven primary hyperthyroidism producing storm.
Suppressed TSH with low free T4 and low free T3: suppressed TSH with low free hormones reflects central hypothyroidism, the opposite metabolic state from a hypermetabolic crisis.
Elevated total T4 with normal free T4 and TSH: an isolated high total T4 with normal free T4 and normal TSH indicates increased thyroid-binding globulin (pregnancy, estrogen), a euthyroid lab artifact rather than true thyrotoxicosis.
Question 2EndocrineMedium
A 34-year-old woman with poorly controlled Graves disease who stopped her methimazole two weeks ago is brought to the emergency department after a febrile illness. She is agitated and disoriented. Temperature is 40.4°C (104.7°F), heart rate is 168/min and irregular, and blood pressure is 158/92 mm Hg. She has a diffuse goiter with a bruit, exophthalmos, and drenching diaphoresis. Free T4 and free T3 are markedly elevated and TSH is undetectable. The clinical picture is consistent with thyroid storm. Which of the following best explains her hyperpyrexia, tachyarrhythmia, and CNS hyperactivity?
AIncreased adrenergic receptor sensitivity to circulating thyroid hormone
BAutonomous catecholamine secretion from an adrenal medullary tumor mass
CAutoantibody stimulation of TSH receptors located on the adrenal cortex
DReduced peripheral conversion of thyroxine to its inactive reverse T3 form
Reveal answer & full explanation
Correct answer: A — Increased adrenergic receptor sensitivity to circulating thyroid hormone
AIncreased adrenergic receptor sensitivity to circulating thyroid hormone✓
BAutonomous catecholamine secretion from an adrenal medullary tumor mass
CAutoantibody stimulation of TSH receptors located on the adrenal cortex
DReduced peripheral conversion of thyroxine to its inactive reverse T3 form
Why Increased adrenergic receptor sensitivity to circulating thyroid hormone is correct
In thyroid storm an acute rise in free thyroid hormone is amplified by increased tissue responsiveness, including upregulated/sensitized beta-adrenergic receptors, producing a hypermetabolic crisis.
This heightened adrenergic activity drives the hyperpyrexia, marked sinus tachycardia and atrial fibrillation, and CNS hyperactivity, while a precipitating stressor (here infection plus thionamide discontinuation) tips the patient into decompensation.
It is also why beta-blockade with propranolol is first-line, because it blunts the adrenergic effects and, at high doses, slows peripheral T4-to-T3 conversion.
Why the others are wrong
Autonomous catecholamine secretion from an adrenal medullary tumor describes pheochromocytoma, which causes episodic hypertension, headache, and sweating but not a suppressed TSH with a goiter, bruit, and exophthalmos.
Autoantibody stimulation of TSH receptors located on the adrenal cortex misplaces the target; Graves antibodies stimulate TSH receptors on the thyroid, and the adrenal cortex is not the driver of the crisis.
Reduced peripheral conversion of thyroxine to its inactive reverse T3 form is not the mechanism; storm reflects excess active T3 and heightened tissue responsiveness, not altered handling of metabolically inactive reverse T3.
🔒 Free preview limit reached
Keep reading — start your free trial
You've read your 2 free diagnosis previews. Create your free account to unlock the full Thyroid Storm outline — plus all 514 diagnoses, 6,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
ORDER MATTERS: beta-blocker first, then thionamide, then iodine AT LEAST 1 hour later (iodine before thionamide can fuel synthesis), then steroids.
PTU > methimazole in storm because PTU blocks peripheral T4→T3 conversion.
Acetaminophen for fever — never aspirin, which displaces thyroid hormone from binding proteins and worsens the crisis.
Burch-Wartofsky ≥45 = highly likely storm. Don't wait for TFTs to start treatment.
Look for the precipitant — infection is the most common trigger and must be identified and treated.
References
ATA 2016 — 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism — Thyroid Storm section (Ross et al., Thyroid 2016)
Burch & Wartofsky 1993 — Life-Threatening Thyrotoxicosis: Thyroid Storm (Burch & Wartofsky, Endocrinol Metab Clin North Am 1993)
JTA 2016 — Japan Thyroid Association Guidelines for the Management of Thyroid Storm (Satoh et al., Endocr J 2016)
Practice Endocrinology questions on FirstPassPA
Turn this outline into retention. 6,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.