Ciguatera Poisoning

Ciguatera is the commonest marine biotoxin illness worldwide, with tens of thousands of cases yearly in tropical and subtropical waters (the Caribbean, Pacific and Indian Oceans, including the East African coast).

Ciguatoxins are produced by Gambierdiscus dinoflagellates growing on dead coral, and are concentrated up the food chain in large predatory reef fish: barracuda, grouper, red snapper, amberjack, moray eel, Spanish mackerel and parrotfish. The toxin is heat stable, odorless and tasteless, so cooking and appearance do not help. Toxin levels are highest in the head, viscera and roe, and in older, larger fish.

Ciguatoxins bind site 5 of voltage-gated sodium channels and hold them open. This causes spontaneous nerve firing, nerve edema and the characteristic cold allodynia. The illness has an onset of 1 to 6 hours (up to 48 hours), gastrointestinal symptoms first, then neurological and cardiovascular features. Most patients improve within days to weeks, but about 20% have fatigue, pruritus and paresthesia for months or years. Symptoms can relapse after eating fish, nuts, caffeine or alcohol. Deaths are under 0.1% and result from circulatory collapse.

• Gastrointestinal: nausea, vomiting, profuse watery diarrhea and cramps, within hours
• Neurological: perioral numbness, paresthesia of hands and feet, intense pruritus, metallic taste, myalgia, arthralgia, tooth pain, ataxia and vertigo
• Cold allodynia: cold objects feel burning or like an electric shock, which is distinctive
• Cardiovascular: bradycardia, atrioventricular block, hypotension and, rarely, shock
• Red flags: heart rate under 40 beats a minute, hypotension, respiratory weakness, coma and relapses after minimal triggers

1. Clinical diagnosis from a meal of reef fish and the typical neurological features, particularly cold allodynia.
2. ECG and continuous monitoring for bradycardia and conduction block.
3. Electrolytes, creatinine and creatine kinase to assess dehydration and muscle injury.
4. Ciguatoxin assay of leftover fish by public health laboratories (liquid chromatography with mass spectrometry), not required for treatment.
5. Cases in clusters should be reported.

Differentials: scombroid poisoning, paralytic shellfish poisoning, tetrodotoxin poisoning, organophosphate poisoning, Guillain-Barre syndrome, hypocalcemia, viral gastroenteritis.

Treatment is supportive, and no antidote exists.

1. Fluids and electrolytes: IV crystalloid 20 mL/kg for dehydration, and correction of potassium and magnesium.
2. Antiemetics and antidiarrheals: ondansetron 4 to 8 mg IV (children 0.15 mg/kg) for vomiting.
3. Cardiovascular care: atropine 0.5 to 1 mg IV for symptomatic bradycardia (children 0.02 mg/kg, minimum 0.1 mg), repeated every 3 to 5 minutes up to 3 mg. Dopamine 5 to 20 micrograms/kg/min for hypotension that persists after fluids.
4. Mannitol: 1 g/kg of 20% solution IV over 30 to 45 minutes in the first 48 to 72 hours for severe neurological symptoms. Evidence is limited. Give it only after rehydration, and avoid it in renal failure and heart failure, while monitoring sodium and osmolality.
5. Neuropathic pain and pruritus:
   • Amitriptyline 25 mg orally at night, increasing to 25 mg twice daily (avoid in cardiac conduction disease and glaucoma).
   • Gabapentin 300 mg orally at night, increasing to 900 to 1800 mg daily in divided doses.
   • Hydroxyzine 25 mg orally three times daily for itch.
6. Avoid triggers for at least 3 to 6 months: fish, shellfish, nuts, alcohol and caffeine.
7. Observation: at least 24 hours for any patient with bradycardia, hypotension or marked symptoms.

Follow-up for chronic symptoms at 2 weeks and 3 months. Counsel patients to avoid large predatory reef fish and fish heads, liver and roe, and about the risk of recurrence and of transmission through breast milk.