thyroid storm

thyrotoxic crisis

A life-threatening, multisystem decompensation of thyrotoxicosis characterised by hyperpyrexia, cardiovascular instability, and CNS dysfunction. Mortality is 10–30% despite treatment.

pathophysiology

• mechanism: acute loss of homeostasis in a thyrotoxic patient.
• key concept: serum T4/T3 levels are not necessarily higher than in uncomplicated thyrotoxicosis. diagnosis is defined by end-organ decompensation, not the absolute hormone level.
• common precipitants: sepsis, surgery, trauma, iodine load (CT contrast, amiodarone), abrupt cessation of antithyroid drugs (ATDs), parturition.

diagnosis

diagnosis is clinical. do not wait for lab confirmation to treat.

burch-wartofsky point scale (BWPS)

a score $\ge$ 45 is highly suggestive of storm. a score of 25–44 suggests impending storm.

System	Clinical Features
Thermoregulatory	Temperature is key (Score increases per 0.5°C). High fever ($>39.5^{\circ }$C) is a hallmark.
Central Nervous System	Mild (agitation) $\to$ Moderate (delirium/psychosis) $\to$ Severe (coma/seizures).
Gastrointestinal	Diarrhoea, nausea/vomiting, abdominal pain $\to$ Unexplained Jaundice (severe).
Cardiovascular	Tachycardia (score increases >99 bpm). Atrial Fibrillation. Congestive Heart Failure (pedal oedema $\to$ pulmonary oedema).
Precipitant History	Known precipitant adds points.

management

treatment requires a multimodal attack on the thyroid axis. order of administration is important.

1. block adrenergic effects

• Drug: Propranolol 60–80 mg PO q4–6h (or IV Esmolol if unstable).
• Mechanism: $\beta$-blockade controls heart rate and high doses inhibit peripheral conversion of T4 $\to$ T3.
• Caution: Monitor haemodynamics closely in decompensated heart failure (though often the failure is rate-related and requires blockade).

2. block synthesis (thionamides)

• Drug: Propylthiouracil (PTU) 500–1000 mg loading dose, then 250 mg PO q4h.
• Mechanism: Inhibits TPO (new synthesis) and inhibits peripheral conversion of T4 $\to$ T3.
• Note: PTU is preferred over Methimazole in storm for its peripheral conversion effect. If PTU unavailable, use Methimazole 20–40 mg q4-6h.

3. block release (inorganic iodine)

• Drug: SSKI (5 drops PO q6h) or Lugol’s Iodine (10 drops PO q8h).
• Mechanism: Wolff-Chaikoff effect (acutely inhibits hormone release).

the iodine timing trap

Iodine MUST be given at least 1 hour AFTER the thionamide (PTU/MMI).

• Reason: If iodine is given before the gland is blocked, the iodine load will be used as substrate to synthesize more thyroid hormone (Jod-Basedow effect), worsening the storm.

4. block conversion & support (corticosteroids)

• Drug: Hydrocortisone 300 mg IV load, then 100 mg q8h (or Dexamethasone).
• Mechanism: Inhibits peripheral T4 $\to$ T3 conversion and treats potential relative adrenal insufficiency.

5. supportive care & clearance

• Cholestyramine: 4g PO qid. Sequesters thyroid hormone in the gut (blocks enterohepatic recycling).
• Cooling: Acetaminophen (Paracetamol) and cooling blankets.
• Precipitant: Aggressively treat the underlying cause (e.g., broad-spectrum antibiotics for sepsis).

caution: aspirin

Avoid Salicylates; ASA displaces T4 from thyroid-binding globulin (TBG), transiently increasing free T4 levels. Use acetaminophen instead.

definitive management

If patient deteriorates despite maximal medical therapy (24–48h):

• Plasmapheresis: To remove circulating hormone/cytokines.
• Emergency Thyroidectomy: High risk, but may be life-saving.