Search

Background: Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well-known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure., Case Reports: Both cases developed life-threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x-ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post-ingestion. Post-mortem endosulfan levels in different organs were determined., Conclusion: Endosulfan is a highly toxic organochlorine insecticide that produces well-known neurological symptoms of tonic-clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. Life-threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.

Introduction: A number of families in a rural area of Jabalpur District (Madhya Pradesh), India, were affected by repeated episodes of convulsive illness over a period of three weeks. The aim of this investigation was to determine the cause of the illness., Methods: The investigation included a house-to-house survey, interviews of affected families, discussions with treating physicians, and examination of hospital records. Endosulfan poisoning was suspected as many villagers were using empty pesticide containers for food storage. To confirm this, our team collected blood and food samples, which were transported to the laboratory and analyzed with GC-ECD., Results: Thirty-six persons of all age groups had illness of varying severity over a period of three weeks. In the first week, due to superstitions and lack of treatment, three children died. In the second week, symptomatic treatment of affected persons in a district hospital led to recovery but recurrence of convulsive episodes occurred after the return home. In the third week, 10 people were again hospitalized in a teaching hospital. Investigations carried out in this hospital ruled out infective etiology but no facilities were available for chemical analysis. All persons responded to symptomatic treatment. The blood and food samples analyzed by our team showed presence of endosulfan, which was confirmed by GCMS. One of the food items (Laddu) prepared from wheat flour was found to contain 676 ppm of alpha-endosulfan., Conclusions: Contamination of wheat grains or flour with endosulfan and its consumption over a period of time was the most likely cause of repeated episodes of convulsions, but the exact reason for this contamination could not be determined. This report highlights the unsafe disposal of pesticide containers by illiterate farm workers, superstitions leading to delay in treatment, and susceptibility of children to endosulfan.

Case Report: A case of nonaccidental endosulfan intoxication in a previously healthy 43-year-old male patient is reported. On admission, the patient had few symptoms, but refractory seizures began 1 hour after ingestion. The patient died on the fourth day after admission showing clinical signs of cerebral herniation confirmed at autopsy. Blood, urine, and tissue samples were analyzed for alpha-endosulfan, beta-endosulfan, and endosulfan sulfate by capillary gas chromatography with electron capture detection. Concentration versus time data for endosulfan were fitted using the program MW/Pharm, assuming complete bioavailability although it is recognized that the bioavailability of endosulfan after ingestion may have been low and the calculated clearance was primarily due to redistribution. Hemoperfusion was shown to be ineffective.

Objective: We report the first case of intravenous self-poisoning with Thiodan (30% endosulfan in xylene)., Case Report: A 28-year-old woman with a past history of epilepsy presented with refractory grand mal seizures after injecting 1 mL of Thiodan intravenously. She developed liver dysfunction, proximal myopathy secondary to rhabdomyolysis and renal failure., Interventions and Outcomes: The seizures were terminated with midazolam and thiopentone. Mechanical ventilation was required for nine days. Renal and liver dysfunction resolved with supportive measures only. Hemodialysis was not required. Pulmonary complications and neurological sequelae were minimal with the patient making a full recovery over three months., Conclusion: The intravenous adminis-tration of a small dose of endosulfan in xylene caused the rapid onset of severe grand mal seizures. The absence of pulmonary edema in this case suggests aspiration to be the cause of pulmonary toxicity due to oral endosulfan poisoning.

Endosulphan is a chlorinated hydrocarbon insecticide with potential toxicity for the respiratory and central nervous systems. Renal toxicity has been rarely reported. We describe a man who developed renal failure due to acute tubular necrosis following a suicidal attempt with endosulphan in the absence of significant hypotension or sepsis.

The authors report six patients with acute endosulfan intoxication. The symptoms of nausea, vomiting, headache, and dizziness began 2.7 +/- 0.5 h after ingestion; in four cases the patients had been hospitalized but were asymptomatic. All had severe metabolic acidosis with high anion gap and hyperglycemia; five of six had decreased blood platelets. Three patients had pulmonary aspiration, and five required mechanical ventilation. The one fatality followed acute renal failure, disseminated intravascular coagulation, thrombi in the pulmonary arteries and aorta, and cardiogenic shock. In this patient the blood endosulfan was 2.85 mg/L versus a mean of 0.48 mg/L in the survivors.

The clinical course following endosulfan ingestion in a suicidal attempt is described. The clinical picture comprised three stages: the acute cardiac and convulsive stage followed by subacute pulmonary and convulsive stage and finally the slow recovery stage. This is the first known survivor of endosulfan ingestion.