Studies

Deng et al. 1991: 30 cases. Identification: TTX in the remains of the meal; 1 fatality.

Case reports

Australia
Tibbals 1988: 1 case. Identification: Tetractenas glaber.
Hawaii
Sims and Ostman 1986: 1 case. Identification: Diodon hystrix.
Malaysia
Lyn 1985: 4 cases. Identification: description by the patient; 1 fatality.
Taiwan
Hwang et al. 1989: 2 cases. Identification: TTX in the remains of the meal; 1 fatality.
Thailand
Laobhripatr et al. 1990: 6 cases. Identification: freshwater Puffer Tetraodon fangi.
Japan
Oda et al. 1989: 1 case. Identification: Fugu poecilonotus.
Tsunenari et al. 1980: 3 cases. Identification: description by the patient, mouse assay; 1 fatality.

Signs & symptoms

Neurological effects

Paralysis of the skeletal musculature including the respiratory musculature, with dyspnoea and respiratory failure, cranial nerve deficits, ataxia, paraesthesias of the lips, the tongue and the oropharynx, paraesthesias of the (distal) extremities; dilated pupils, sweating; vomiting; cerebral seizures with high doses (primary/secondary hypoxic?).

Time interval between ingestion and onset of symptoms: 10–45 min, maximum of a few hours (Bower et al. 1981).

Cardiac effects

Arterial hypotension, arrhythmias, bradycardia, tachycardia, AV conduction defects.

Time interval between ingestion and onset of symptoms: 10–45 min, maximum of a few hours (Bower et al. 1981).

Other signs & symptoms

Arterial hypotension 8/30, mean blood pressure 192/110 mmHg, 1 of these 8 patients died as the result of acute pulmonary oedema. All of the surviving patients already had mild hypertonicity before the poisoning (7/8, TTX appears to cause dramatic blood pressure increases in persons with pre-existing hypertension), headache (Deng et al. 1991).

Morbidity

If a patient survives the first 24 hours, the prognosis is good. The symptoms of poisoning generally disappear within a period of days (Bower et al. 1981).

Case fatality rate

Mortality rate from TTX poisoning 372/1,015 (36.7%) (Tsunenari et al. 1980). Causes of death are respiratory paralysis and cardiovascular failure. Death can occur very rapidly. The minimum time reported between ingestion and death is 17 min (Halstead 1988).

Laboratory and physical investigations

1. Detection of toxin

• Detection of TTX in remains of fish tissue using thin-layer and high-performance liquid chromatography.
• Detection of TTX in blood and urine using gas chromatography (Suenaga and Kotoku 1980).

2. Electrophysiological investigations

Electrophysiological findings indicate that TTX blocks the Na channels on myelinised nerves and thus impairs nerve conduction. TTX and saxitoxin have the same mechanism of action, with the difference that saxitoxin has a weaker action (Kao 1972, Oda et al. 1989, Long et al. 1990).

First aid

Gastric lavage with a 2% sodium bicarbonate solution. Instillation of activated charcoal (Sims and Ostman 1986).

Treatment (symptomatic)

1. Oxygen, endotracheal intubation, artificial respiration (Sims and Ostman 1986, Tibballs 1988).
2. Plasma expansion (physiological salt solution etc.) for arterial hypotension (Sims and Ostman 1986, Tibballs 1988).
3. Atropine for bradycardia; possibly temporary pacemaker (Sims and Ostman 1986, Tibballs 1988).
4. If 2. and 3. are unsuccessful, i.e. persistent hypotension and reduced cardiac output, catecholamine i.v., dopamine i.v. (microdrip) (Sims and Ostman 1986, Tibballs 1988).
5. In the case of pre-existing hypertension, it appears that hypertensive crises are possible, which require antihypertensive treatment in order to avoid serious complications (Deng et al. 1991).
6. Acetylcholinesterase inhibitors: efficacy observed (Chew et al. 1984), not observed (Lyn 1985, Tibballs 1988). An experimental electromyographic study is necessary to resolve this controversy (Tibballs 1988).

Treatment (specific)

A specific antagonist has not yet been developed.