Prolonged cholinergic crisis and compartment syndrome following subcutaneous injection of an organophosphate compound for suicide attempt
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Fenthion
Organophosphate poisoning
Compartment (ship)
Fasciotomy
Organophosphate compounds are possibly the most widely-used insecticides worldwide. Organophosphate compounds cause poisoning, inhibiting acetylcholinesterase at the cholinergic synapses. Civilian casualties resulted from a terrorist attack with sarin in a Tokyo subway. Recent terrorist activities have also raised concerns that organophosphate or nerve agents may be used as a weapon of terror or mass destruction.In this study, an extraordinary type of mass poisoning was evaluated. Especially by focusing on the way of poisoning, the demographic features and clinical findings of patients were analyzed.After eating a wheat bagel, 13 patients with organophosphate poisoning were admitted to our emergency department. Seven were males and 6 were females. The mean age of the patients was 26 +/- 13.9. The mean serum acetylcholinesterase level was 2945.1+/-2648.9 U/L. Nine patients who had supportive treatment and who were given atropine and pralidoxime were hospitalized approximately 6.8+/-6.5 days. All of the patients recovered after the treatment and no deaths occurred.If organophosphate poisoning is not diagnosed and treated in time, it may be fatal. When cases of food poisoning are admitted to the hospital, attention must be taken especially if it is a mass poisoning.
Organophosphate poisoning
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Abstract: Organophosphate poisoning is a common cause of severe morbidity and mortality among patients admitted to emergency departments. Tissue damages as a consequence of organophosphate poisoning are frequently reported, but preventing this potentially severe complication has not been the subject of much research. We tested whether interleukin‐10, a cytoprotective agent, could prevent or diminish pathological signs of tissue damages caused by organophosphate poisoning. Thirty rats were divided into three equal groups (n = 10). Group 1 (sham) did not receive any agent during the experiment. Group 2 (control) received 0.8 g/kg of fenthion intraperitoneally, followed by 6 ml/kg of intraperitoneal normal saline 30 min. and 3 hr later. Group 3 (treatment) received 0.8 g/kg of fenthion intraperitoneally, followed by 2 µg/kg of interleukin‐10 intraperitoneally 30 min. and 3 hr later. All rats were killed under anaesthesia after 6 hr and tissue samples were obtained from liver, kidneys and lungs. Even organophosphate poisonings do not cause significant clinical problems; several degrees of damages could be observed in liver, kidneys and lungs. These damages could be reduced by interleukin‐10 treatment.
Fenthion
Organophosphate poisoning
Liver tissue
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A case of poisoning with a new organophosphate (fenthion) is reported in which the initial cholinergic crisis was delayed 5 days and recurred 24 days after ingestion. Psychosis was a persistent and sometimes singular manifestation. Because of the high lipid solubility of this pesticide, toxin analysis of repeated fat biopsies was an essential component of the management of this patient.
Fenthion
Organophosphate poisoning
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Unintentional poisoning is the most common challenge during the childhood age. Among them organophosphate, the commonly used insecticide is the most common agent related to poisoning in children. Organophosphate poisoning causes up to 25% of mortality worldwide. The present article discusses the case of a 3 year old child with accidental intake of organophosphate revealing the symptoms experienced by the patient and different treatment modalities employed and its outcomes. Also the article suggest the importance of follow up after organophosphate poisoning.
Organophosphate poisoning
Accidental poisoning
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Organophosphate poisoning is highly lethal as organophosphates, which are commonly found in insecticides and nerve agents, cause irreversible phosphorylation and inactivation of acetylcholinesterase (AChE), leading to neuromuscular disorders via accumulation of acetylcholine in the body. Direct interception of organophosphates in the systemic circulation thus provides a desirable strategy in treatment of the condition. Inspired by the presence of AChE on red blood cell (RBC) membranes, we explored a biomimetic nanoparticle consisting of a polymeric core surrounded by RBC membranes to serve as an anti-organophosphate agent. Through in vitro studies, we demonstrated that the biomimetic nanoparticles retain the enzymatic activity of membrane-bound AChE and are able to bind to a model organophosphate, dichlorvos, precluding its inhibitory effect on other enzymatic substrates. In a mouse model of organophosphate poisoning, the nanoparticles were shown to improve the AChE activity in the blood and markedly improved the survival of dichlorvos-challenged mice.
Organophosphate poisoning
Dichlorvos
Detoxification
Cholinesterase
Paraoxon
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Introduction: Organophosphate compounds are used as insecticides, nerve gases, ophthalmic agents, and antihelmintics.The primary mechanism of action of organophosphate pesticides is inhibition of acetylcholinesterase (AChE). However Pralidoxim has been introduced as organophosphate `s antidote but recent studies establish that pralidoxim has unclear benefit in treatment of organophosphate poisoning.We explain two cases of organophosphate poisoning that they treaeted well without pralidoxim. The first case was a 36-years old man with history of organophosphates poisoning. He was under mechanical ventilation. Atropine was initiated due to muscarinic signs such as salivation, bronchorrhea and auscultation of alveolar rhales. On admission day, the pseudocholine esterase level was 235 unit per liter. Pralidoxime was not available, so we did not use it for management of this patient.The patient was discharged when he was in free symptom completely on the 22 th day. The second case was a 23 years old woman with the history of deliberate self poisoning with organophosphate compounds. Atropine was started and she was under mechanical. However, pralidoxim was not available. The pseudocholine esterase level was 1690 unit per liter on the first day which dropped to 952 unit per liter on the 2 nd day. After 9 days the discharged from the hospital. Discussion: Pralidoxim has been introduced as organophosphate`s antidote, on the other hand, it has benefit in organophosphate poisoning theoretically, but patients can be treated without it. Key words: Organophosphate, Poisoning, Pralidoxim
Organophosphate poisoning
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Pralidoxime
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Organophosphates are chemicals commonly used as pesticides and work to inhibit acetylcholinesterase, leading to acetylcholine build up at muscarinic and nicotinic receptors throughout the body. Poisonings are often seen as small volume, chronic cases due to agricultural exposures, but can present as suicide attempts via organophosphate ingestion. Organophosphate poisonings, particularly when large volumes are ingested, require rapid and robust initiation of treatment. We present a case highlighting the appropriate management of profound organophosphate toxicity. We present a case of a 40-year-old female brought in by ambulance after purposefully ingesting two bottles of 100mL dichlorvos (DDVP), one of the largest volume organophosphate ingestions documented in the literature. She presented with severe salivation, diaphoresis and encephalopathy and was then intubated, requiring mechanical ventilation. She received multiple days of intensive care as she was treated with atropine, pralidoxime, intravenous fluids and vasopressors.
Pralidoxime
Organophosphate poisoning
Dichlorvos
Cholinesterase
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In the last several decades, exposure to pesticides has become a concern to environmental and human health. Many pesticides are environmentally persistent and are characterized by varying degrees of toxicity and adverse effects, including DNA damage. The present study was undertaken to evaluate the genotoxic potential of organophosphate pesticide fenthion in Wistar rats, as assessed by the comet assay. Adult male Wistar rats were treated with a solution of fenthion at a concentration of 40 mg/kg/day, administered intraperitoneally for 18 consecutive days. Rats were killed 24 hours after the last pesticide administration, and the comet assay was performed in peripheral blood cells. The comet assay results revealed that the damage index (19.29 ± 3.59 vs. 7.80 ± 2.25) and the damage frequency (17.00 ± 3.46 vs. 7.5 ± 2.46) found in fenthion-treated rats were significantly higher than those found in the control group (p = 0.001 and p = 0.0006, respectively). The results show that fenthion affects the DNA integrity of rat cells and may induce DNA damage in exposed organisms.
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Prolongation of the prothrombin time owing to a transient reduction in factor VII activity is described in a 14-month-old child with organophosphate poisoning. Correction after vitamin K administration suggested an organophosphate-related effect on vitamin K-dependent factor VII activity. Historically, coagulation screening has not been routinely recommended after organophosphate intoxications. We suggest, however, that routine screening in such patients may be important. A brief review of organophosphate poisoning and the unique features of our case are presented.
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Prothrombin time
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Organophosphate poisoning
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