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Ciguatera (a variety of fresh fish poisoning) (A Case Report) Ujjwala G Rege, GH Tilve, IA Juvale, VV Jayakar, KG NairDepartment of Medicine, Seth G. S. Medical College, and K.E.M. Hospital, Parel.. Bombay-400 012, India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 574161
A case of fresh fish poisoning, most probably ciguatera, is reported. A brief review of the literature is presented.
Peter Martyr of Anghera (1457-1526), the first historian of America had recorded in his book that was first published in 1571, the earliest remarks on ciguatoxic fishes in America. [1] Four centuries have turned their cycles after that and still ciguatera persists to be an enigma. Not only that, fresh fish poisoning is an entity that we do not even suspect in our food poisoning patients. We report here a case of fresh fish poisoning presenting with a combination of gastrointestinal and neurological manifestations.
A 22 year old male got admitted with his two brothers and one sister on the 24th of August, 1.978, with vomiting and diarrhoea since morning. They had not eaten anything that day. On the previous morning all of them had eaten fresh fish, cooked at home. Even the parents had eaten the same food. The next morning, the four children developed diarrhoea and vomiting that did not respond till evening. Hence, they were brought to the hospital at 8.40 P. M. On admission, they had tachycardia and mild fever but no dehydration or any neurological signs. They were given injection prochlorperazine along with other symptomatic treatment. By 12.00 midnight two of them developed very high fever that could not be recorded by the clinical thermometer. Their blood pressure dropped and became unrecordable and the pupils became pinpoint. The patient was the only one to worsen still further. He developed faccidity, absent reflexes and lost consciousness. His blood was sent for culture and then he was given broad spectrum antibiotics along with parenteral fluids. Endotracheal intubation was performed in anticipation of respiratory paralysis. By next morning, his blood pressure returned to normal; central venous pressure came upto 7 cms. of water from 3 cms. of water and he became afebrile. By evening he regained consciousness and the endotracheal tube was removed. But on the next day, i.e. on 26-8-1978, he started running high fever .again and developed profuse haematuria, subconjunctival haemorrhage and paralysis of the horizontal and downward gaze. His bleeding and clotting time were normal. The antibiotics, now, were changed to Gentamicin-Ampicillin combination. Intravenous fluids with round, the clock sodabicarb were continued. On 27- j1978, he developed oliguria, gastrointestinal bleeding, neck stiffness and became semiconscious. His abdomen got more and more distended gradually. By evening it was boardlike with absent peristalsis. Within half an hour, he started gasping and expired. On postmortem examination all his organs showed acute congestion. Both kidneys showed patchy areas of necrosis. The gastrointestinal tract showed marked mucosal congestion with tiny ulcerations in the small intestine. Submucous patches of haemorrhages were seen. The entire G.I. tract was markedly distended with gas. There were no signs of peritonitis.
The clinical and postmortem findings of our case made us think in terms of botulism and also of septicaemia with consumptive coagulopathy. But many findings did not f t in either group. Patients affected with botulism remain mentally clear and usually have fixed, dilated pupils, retention of urine, with preserved deep tendon jerks. Our patient had constricted, pinpoint pupils, absent deep jerks and no retention of urine. He had lost consciousness on the first and the last day. Though we could not rule out consumptive coagulopathy we would have got to think of some neurotoxic agent in addition to septicaemia with disseminated intravascular coagulation. And even if we accepted this dual pathology the most important fact in the history would not fit in both. The family had consumed a fresh fish that was just cooked, and that too, at home. This made us search for other types of fish poisoning, especially, fresh fish poisoning. There are many varieties of sea fish that are inherently poisonous. The toxins are acquired from the organisms like algae or dianoflagellates on which they feed. The variety into which our jigsaw puzzle fitted best was ciguatera (cigua = toxic snail, in Spanish). This can be acquired from a large number of species, about 300 in all. These include some common varieties of edible fish available on Bombay coast like Herring (Bhingi), Salmon (Raos), Anchovie (Kati), Sardine (Tarli), Snappers (Tamboshi). Groupers (Hekru), Swordfish (Tadmasa). [2] The toxin is thought to originate in the blue green algae in the food chain of these fish. The toxin accumulates in the tissues and is excreted very slowly. Poisoning of this type is difficult to prevent because the toxin is stable to heat, cold and drying and the taste and small of the fish are unaffected. The toxicity is extremely variable. The geographical distribution is spotty and variable. But these fish are usually associated with coral reefs and island environment. At any coastal region, a poisonous fish population may suddenly develop, following natural calamities like earthquake, hurricane, etc. or may follow man made catastrophies. The symptoms and signs of poisoning develop upto 30 hours after ingestion of the fish. In a single group of people who have ingested the fish, one person may get just mild gastrointestinal upset while another may go into respiratory paralysis and succumb. Relapses and remissions are known. The early picture is that of nausea, vomiting, watery diarrhoea and abdominal cramps. Later on, neurological manifestations set in. These are paraesthesiae, myalgia, hyperpyrexia of central origin, neurogenic shock, various cranial nerve palsies, respiratory paralysis, depressed deep jerks, abnormal superficial reflexes, and paradoxical sensory disturbances. Death is usually due to respiratory paralysis. Post mortem examination shows acute visceral congestion with occasional haemorrhages. No significant micropathological data has been recorded so far. Pharmacology of ciguatoxin has been studied, though not completely. At least one component of ciguatoxin acts as an irreversible cholinesterase inhibitor. [3],[4],[5] Some other components, when mixed with human and animal blood, prevented coagulation. [2] The treatment so far is largely symptomatic. Indigenous therapies like juices from the leaves of Pithecellobium (Vilayati Chinch) and Passiflora (Krishnakamal) and the sap of Euphorbia (Tidhari Nivdung) are still given in sporadic cases. Intravenous calcium and Pralidoxime have been tried. Edrophonium has been given successfully in one case. But no systematic, controlled study has been carried out so far. Rest, quiet and cautious sedation are advocated along with mechanical respiratory aid, when needed. The measures to prevent such a disastrous disease are very few. The viscera of any fish should never be eaten. If any fish like snappers or groupers is found to be unusually large, it should not. be Most of the ciguatera outbreaks occur in scattered, underdeveloped, insular areas, having limited public health facilities. The disease is not generally reported to international health authorities. Hence there are no reliable public health records on the subject, in any part of the world. In the case of our patient, we learnt the lesson too late to investigate effectively and to prove ciguatera beyond doubt. But this case report is meant to work as a mere bell on the 'Inchcape Rock' of fresh fish poisoning. We hope it will serve this purpose properly.
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