🔥 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 |