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Letter to the Editor

Letter to the Editor: “Management of acute endosulfan poisoning in an organophosphate poisoning clinic”

, M.D., , M.D., , M.D., , M.D., , M.D. & , M.D.
Pages 563-564 | Published online: 07 Oct 2008

Management of acute endosulfan poisoning in an organophosphate poisoning clinic

To the Editor:

Endosulfan has a high toxicity consistent with other members of the family of chlorinated hydrocarbon insecticides (Citation1), and may be absorbed via skin, inhalation, and the gastrointestinal system for the purpose of suicide or by accident (Citation2–4). Characteristic clinical signs are seizures, nausea, vomiting, abdominal discomfort, headache, agitation, hyperactivity, in-coordination, confusion, dizziness, and myoclonus (Citation3–6).

Cases

Six cases were admitted into our hospital due to nausea, vomiting, and dizziness after eating a dessert containing flour, sugar, and oil. According to information acquired from patients' relatives, 27 of 50 affected patients were sent to a tertiary centre. Six of 27 were brought to our service, but 21 were sent to another service. It was learned that four patients had grand mal type convulsions and that three of them died.

Upon physical examination, five patients were observed to be confused with miotic pupils and hyperactive bowel sounds. Severe bradycardia was observed in one patient. One patient had a seizure that was unresponsive to diazepam and phenytoin treatment. Respiratory arrest occurred and the patient responded to cardiopulmonary resuscitation and was placed on mechanical ventilation. Approximately six hours later the patient was extubated. Cranial tomography was normal and no further convulsions were noted. Demographic features of the patients and findings of physical examinations are summarized in .

Table 1. Demographic features of the patients and findings upon physical examination

Upon laboratory examination, white blood cell count, glucose, aminotransferases, and LDH levels were high. Abnormal electrocardiographic findings consisting of sinus bradycardia and ST-T changes were observed in two patients. The laboratory results are summarized in .

Table 2. The laboratory results of the patients

Atropine and pralidoxime had been administered to five patients. After eight hours of observation, consciousness of all of the cases had become clear. Food analysis for toxic substances, reported two days later, revealed endosulfan. All patients were followed for five days prior to discharge.

Discussion

Toxic quantities of endosulfan have been taken in via the gastrointestinal system route predominantly following the consumption of contaminated food (Citation2–4,Citation7). The reason for poisoning in this outbreak was consumption of sweets which were made from flour contaminated with liquid endosulfan. Symptoms began nearly one-half to one hour following consumption.

Venkateswarlu et al. reported 44 individuals who consumed food accidentally contaminated by endosulfan in a rural area. Nausea and vomiting had been seen in 43 patients, emotional changes in 72%, seizure in 50%, stupefaction in 18%, peevishness in 9%, and diarrhea in 6.8% (Citation4).

Endosulfan-induced seizures should be controlled with a benzodiazepine, followed by phenobarbital if needed (Citation3,Citation6,Citation8). Our patients' seizures failed to respond to diazepam and diphenylhydantoin treatment, resulting in respiratory arrest and intubation. Atropine and pralidoxime treatment was administered to five cases due to suspected muscarinic symptoms such as nausea, vomiting, miosis, leading to suspicion of organophosphate or carbamate insecticide poisoning. Following atropine and pralidoxime, their state of conscious appeared to improve, confusion resolved, and miosis was decreased.

Acute endosulfan poisoning due to gastrointestinal exposure is rarely seen. In these patients, clinical effects span a wide range from uncomplicated gastrointestinal symptoms such as nausea and vomiting to convulsions or death, presumably related to dose. In the acute endosulfan poisoning patients who have predominant muscarinic symptoms such as miosis, the use of atropine and pralidoxime might be beneficial.

References

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  • Boereboom FT, van Dijk A, van Zoonen P, Meulenbelt J. Nonaccidental endosulfan intoxication: A case report with toxicokinetic calculations and tissue concentrations. J Toxicol Clin Toxicol 1998; 36(4)345–52
  • Oktay C, Goksu E, Bozdemir N, Soyuncu S. Unintentional toxicity due to endosulfan: A case report of two patients and characteristics of endosulfan toxicity. Vet Hum Toxicol 2003; 45(6)318–20
  • Venkateswarlu K, Suryarao K, Srinivas V, Sivaprakash N, Jagannadharao NR, Mythilai A. Endosulfan poisoning - A clinical profile. J Assoc Physicians India 2000; 48: 323–5
  • Chugh SN, Dhawan R, Agrawal N, Mahajan SK. Endosulfan poisoning in Northern India: A report of 18 cases. Int J Clin Pharmacol Ther 1998; 36: 474–7
  • Kutluhan S, Akhan G, Gultekin F, Kurdoglu E. Three cases of recurrent epileptic seizures caused by Endosulfan. Neurol India 2003; 51(1)102–3
  • Brandt VA, Moon S, Ehlers J, Methner MM, Struttmann T. Exposure to endosulfan in farmers: Two case studies. Am J Ind Med 2001; 39(6)643–9
  • Dewan A, Bhatnagar VK, Mathur ML, Chakma T, Kashyap R, Sadhu HG, Sinha SN, Saiyed HN. Repeated episodes of endosulfan poisoning. J Toxicol Clin Toxicol 2004; 42(4)363–9

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