Poisoning with the neurotoxin tetrodotoxin (TTX) occurs after ingestion of various species of puffer fish (see the image below).
View Image | Puffer fish. |
The flesh of the puffer fish (ie, fugu) is considered a delicacy in Japan. It is prepared by chefs specially trained and certified by the government to prepare the flesh free of the toxic liver, gonads, and skin. Despite these precautions, many cases of tetrodotoxin poisoning are reported each year in patients ingesting fugu.
Poisonings usually occur after eating fish caught and prepared by uncertified handlers.
The toxic dose is not clear because puffer fish have different concentrations of tetrodotoxin. A dose of 1-2 mg of purified toxin can be lethal. Reported cases from the Centers for Disease Control and Prevention (CDC) have documented toxicity with ingestion of as little as 1.4 ounces of puffer fish.
Tetrodotoxin also is found in the the following:
Detection of tetrodotoxins in European bivalve shellfish in the United Kingdom along the English Channel has been reported, although concentrations were low in comparison to published minimum lethal doses for humans.[2]
Puffer fish contain the potent neurotoxin tetrodotoxin. TTX is thought to be synthesized by a bacterial or dinoflagellate species associated with the puffer fish.[3, 4]
The toxin is concentrated in the liver, gonads, and skin. The level of toxicity is seasonal, and, in Japan, fugu is served only from October through March.
Tetrodotoxin is a heat-stable (except in alkaline environments) and water-soluble nonprotein.
It is a heterocyclic, small, organic molecule that acts directly on the electrically active sodium channel in nerve tissue (see the image below).
View Image | Chemical structure of tetrodotoxin. |
Tetrodotoxin blocks diffusion of sodium through the sodium channel, thus preventing depolarization and propagation of action potentials in nerve cells.
All of the observed toxicity is secondary to blockade of the action potential. Tetrodotoxin acts on the central and the peripheral nervous systems (ie, autonomic, motor, sensory nerves).
Tetrodotoxin also stimulates the chemoreceptor trigger zone in the medulla oblongata and depresses the respiratory and vasomotor centers in that area.
Recent study using tetrodotoxin therapeutically shows that tetrodotoxin used in conjunction with bupivacaine prolonged the local anesthetic effect.[5] If tetrodotoxin begins to be used clinically, the incidence of toxicity may increase.
United States
Reports of tetrodotoxin poisoning are rare in the United States. A 1996 report documents three cases of tetrodotoxin toxicity from persons who ingested contaminated fugu imported by a coworker from Japan.[6] A 2014 report describes two patients in Minneapolis, Minnesota, who developed tetrodotoxin poisoning after consuming dried puffer fish purchased during a recent visit to New York City; the patients noted that two friends who consumed the same fish had similar but milder symptoms and had not sought care.[7]
International
Despite the careful training and certification of fugu chefs in Japan, cases of mortality and morbidity from puffer fish ingestion continue to be reported. Estimates vary, but up to 50 deaths may occur each year from tetrodotoxin poisoning in Japan.
Mortality rates are difficult to calculate, but estimates of mortality approach 50%, even with modern supportive medical care. Patients who live through the acute intoxication (ie, first 24 h) usually recover without residual deficits. Recovery takes days to occur.
No known racial predilection exists. However, the poisoning is more common in Japanese people because of their dietary preferences for fugu.
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Prehospital care includes the following:
Emergency department (ED) management includes the following:
No drug has been shown to reverse the effects of tetrodotoxin poisoning. Treatment is symptomatic. Specific drug efficacy has only been documented anecdotally.
Anticholinesterase drugs (eg, neostigmine) have been proposed as a treatment option but have not been tested adequately.[9]
Clinical Context: Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
For maximum effect, administer within 30 min of ingesting poison. Generally mixed and given with a cathartic (eg, 70% sorbitol), except in young pediatric patients in whom electrolyte disturbances may be of concern.
Empirically used to minimize systemic absorption of the toxin. May only benefit if administered within 1-2 h of ingestion.
Clinical Context: Although not clinically proven, neostigmine has been used anecdotally to restore motor strength. Inhibits destruction of acetylcholine by acetylcholinesterase, which facilitates transmission of impulses across myoneural junction.
Repeat doses based on patient's response.
May be useful in reversing the neurological complications of the venom; however, they should not be a substitute for airway management.
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For patient education information, see the First Aid and Injuries Center, as well as Food Poisoning and Activated Charcoal.