Epidemiology & Risk Factors

Acute, life-threatening hypermetabolic state caused by severe thyrotoxicosis.
Precipitating factors: Acute stressors (e.g., infection, trauma, surgery, childbirth, acute coronary syndrome) in a pt w/ undiagnosed or poorly controlled hyperthyroidism.
Other triggers: Radioiodine therapy, iodinated contrast administration, sudden cessation of antithyroid drugs (ATDs).
Underlying etiology: Most commonly Graves’ disease, but can occur w/ toxic multinodular goiter or toxic adenoma.

Clinical Features

Hyperpyrexia: High fever (typically >104°F/40°C), profuse sweating.
Cardiovascular: Severe tachycardia (often >140 bpm, out of proportion to fever), atrial fibrillation (AFib) w/ rapid ventricular response, high-output congestive heart failure (CHF), hypotensive shock. c
Central Nervous System: Extreme agitation, delirium, psychosis, seizure, coma.
Gastrointestinal: Nausea, vomiting, diarrhea, abdominal pain, jaundice (indicates severe hepatic congestion/dysfunction).
Thyrotoxic signs: Goiter, ophthalmopathy (lid lag, exophthalmos in Graves’), fine tremors, warm/moist skin.

Initial: Clinical diagnosis utilizing the Burch-Wartofsky Point Scale (evaluates thermoregulatory dysfunction, CNS effects, GI/hepatic dysfunction, CV dysfunction, CHF, AFib, and precipitant history). Do not delay treatment while waiting for lab confirmation.
Key Labs:
- Thyroid Panel: Suppressed TSH, elevated free T3 and T4 (levels may not differ significantly from uncomplicated thyrotoxicosis; severity is clinical).
- CBC: Leukocytosis (even in the absence of infection).
- LFTs: Mildly elevated AST/ALT, elevated bilirubin.
Electrocardiogram (ECG): Sinus tachycardia, AFib, atrial flutter.

Sepsis / Septic Shock: Diff by absence of thyrotoxic stigmata (e.g., goiter, exophthalmos) and negative thyroid panels; localized infectious focus usually present.
Pheochromocytoma Crisis: Diff by paroxysmal HTN/headache, lack of hyperpyrexia (usually), elevated urinary/plasma metanephrines.
Malignant Hyperthermia: Diff by exposure to volatile anesthetics/succinylcholine, muscle rigidity (masseter spasm), respiratory/metabolic acidosis.
Neuroleptic Malignant Syndrome (NMS): Diff by exposure to antipsychotics, “lead-pipe” rigidity, elevated CK.
Serotonin Syndrome: Diff by exposure to serotonergic agents, neuromuscular irritability (clonus, hyperreflexia).

Hemodynamic Control & Peripheral Conversion Blockade:
- Beta-blocker: Propranolol (IV or PO) to control tachycardia/arrhythmia and inhibit peripheral T4-to-T3 conversion. Esmolol is an alternative.
Inhibition of Thyroid Hormone Synthesis:
- Propylthiouracil (PTU) (preferred over Methimazole): Blocks new hormone synthesis and inhibits peripheral conversion of T4 to T3. Administer before iodine.
Inhibition of Thyroid Hormone Release:
- Iodine (SSKI or Lugol’s solution): Must administer at least 1 hour after ATD/PTU therapy to prevent the thyroid from using the iodine as substrate to synthesize more hormone (Wolff-Chaikoff effect).
Inhibition of Peripheral Conversion & Adrenal Support:
- Glucocorticoids (Hydrocortisone or Dexamethasone): Decreases peripheral T4-to-T3 conversion and treats potential relative adrenal insufficiency.
Supportive Care:
- Aggressive cooling w/ ice packs/cooling blankets.
- Acetaminophen for fever (avoid aspirin/salicylates as they displace thyroid hormone from TBG, worsening thyrotoxicosis).
- IVF (crystalloids w/ dextrose to replenish glycogen stores).
- Identify and treat the precipitating cause (e.g., empiric Abx for infection).

Cardiovascular collapse, cardiogenic shock, and death (mortality rate up to 10-30%).
Arrhythmias (refractory AFib, ventricular tachycardia).
Hepatic failure.
Miscarriage or fetal demise in pregnant pts.

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