Thyroid Storm (Thyrotoxic Crisis) -

🔥 Thyroid Storm (Thyrotoxic Crisis)

🔍 Definition:

Thyroid storm is a rare, life-threatening exacerbation of thyrotoxicosis, characterized by severe hypermetabolism, multisystem decompensation, and organ failure due to excessive circulating thyroid hormones.

It’s not just “high T3/T4” — it’s the systemic response that makes it dangerous.

🧠 Why It Matters in ICU:

High mortality if untreated (10–30%)
Requires prompt recognition and aggressive management
Often presents like sepsis, delirium, or cardiac failure, leading to diagnostic delay

⚡️ Etiology / Precipitating Factors

Category	Examples
Infections	Pneumonia, UTI, sepsis (most common trigger)
Surgery/Trauma	Thyroidectomy, non-thyroid surgery, trauma
Metabolic stress	DKA, MI, PE, CVA
Drug-related	Amiodarone, iodine contrast, abrupt antithyroid withdrawal
Other	Pregnancy, parturition, anesthesia

🧪 Pathophysiology (Simplified)

↑↑ Free T3 and T4
Exaggerated β-adrenergic sensitivity
Hypercatabolic state → oxygen demand ↑, heat production ↑
Multisystem organ dysfunction

🧬 Diagnostic Criteria

There’s no single definitive test. Diagnosis is clinical.

✅ Burch-Wartofsky Score (commonly used)

Clinical Feature	Points Range
Thermoregulatory dysfunction (e.g., fever)	5–30
CNS effects (delirium to coma)	10–30
GI–Hepatic dysfunction (diarrhea, jaundice)	10–20
Cardiovascular (tachycardia, CHF, AFib)	5–25
Precipitating event	10

≥45 → Thyroid Storm likely
25–44 → Imminent storm
<25 → Unlikely

🧪 Labs

Test	Findings
TSH	Suppressed (↓)
Free T3, Free T4	Elevated
CBC	May show leukocytosis
LFTs	↑ bilirubin, transaminases (cholestasis)
ECG	Sinus tachycardia, atrial fibrillation
Others	Hypercalcemia, hyperglycemia, ↑ lactate

🩺 Clinical Presentation

System	Symptoms/Signs
CNS	Agitation, delirium, psychosis, seizures, coma
CVS	Tachycardia, AFib, high-output heart failure
Thermo	Fever (>38.5–40°C), flushing
GI-Hepatic	Diarrhea, nausea, vomiting, jaundice
Respiratory	Dyspnea, possible ARDS in severe cases

💊 Management – “5-Block Strategy”

🔹 1. Inhibit Hormone Synthesis

Propylthiouracil (PTU): 500–1000 mg loading, then 250 mg q4–6h

Also blocks peripheral T4 → T3 conversion

OR Methimazole (preferred for maintenance)

🔹 2. Block Hormone Release

Iodine (e.g., Lugol’s solution or potassium iodide)

Give 1 hour after PTU
Doses: 5 drops q8h

🔹 3. Block Peripheral Effects

Beta-blockers (propranolol 60–80 mg PO q6h or IV 1 mg q10 min)

Controls HR and blocks T4 to T3 conversion
Use esmolol IV if unstable

🔹 4. Prevent Peripheral Conversion

Steroids: Hydrocortisone 100 mg IV q8h

↓ T4 to T3 conversion, treat possible adrenal insufficiency

🔹 5. Supportive Care

Cooling blankets, antipyretics (no aspirin)
IV fluids, glucose
Treat precipitating cause (e.g., antibiotics for sepsis)
Anti-arrhythmics if needed

🛑 Contraindications

Aspirin: Displaces thyroid hormone from binding proteins → worsens hyperthyroidism
Iodine before PTU: May worsen thyroid hormone release (Jod-Basedow phenomenon-explained in last)

📉 Prognosis

Factor	Impact
Early recognition	Improves survival
Delay in therapy	↑ mortality (up to 30%)
Heart failure, jaundice	Associated with poor prognosis

📚 High-Yield Points for Exams

Thyroid storm is not defined by T3/T4 levels alone → clinical diagnosis
Always treat with PTU before iodine
Burch-Wartofsky score ≥45 strongly suggests diagnosis
Commonly confused with sepsis, NMS, pheochromocytoma

🧠 Tip for Exams:

“Jod-Basedow = Iodine causes goiter to BLOW (go hyper)”
Opposite of Wolff–Chaikoff, where iodine causes a block.

Feature	Jod-Basedow Phenomenon	Wolff–Chaikoff Effect
Definition	Iodine-induced hyperthyroidism	Iodine-induced temporary inhibition of thyroid hormone synthesis
Mechanism	Autonomous thyroid tissue uses excess iodine → ↑ T3/T4	Excess iodine inhibits organification of iodide and hormone synthesis
Hormonal Effect	↑↑ T3 and T4	↓ T3 and T4
TSH Levels	Suppressed	May rise slightly due to ↓ T3/T4
Typical Patients	Multinodular goiter, latent Graves’, iodine-deficient areas	Normal individuals or those with autoimmune thyroid disease
Trigger	Iodine exposure (contrast dye, amiodarone)	Same (excess iodine intake)
Onset	Days to weeks after exposure	Immediate (within 24–48 hrs)
Duration	Persistent if not treated	Transient (escapes after ~10 days)
Clinical Presentation	Hyperthyroid symptoms	Often subclinical or mild hypothyroid symptoms
Radioiodine Uptake (RAIU)	Low (iodine-saturated gland, but still overproducing)	Low (organification block)
Management	Stop iodine, antithyroid drugs (PTU/methimazole)	Usually self-limited; rarely requires treatment
Relevance in Thyroid Storm	Giving iodine before PTU can precipitate crisis	Iodine can be therapeutic if given after PTU