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Organophosphate Poisoning (organophosphate + poisoning)

Distribution by Scientific Domains

Medical Sciences	83%

Selected Abstracts

Early Death Due to Severe Organophosphate Poisoning Is a Centrally Mediated Process

ACADEMIC EMERGENCY MEDICINE, Issue 4 2003
Steven B. Bird MD
Objective: To distinguish whether early death from severe organophosphate (OP) poisoning with dichlorvos is mediated through peripheral or central nervous system (CNS) actions. Methods: Wistar rats (n= 72) were randomized to pretreatment with either: normal saline (controls), peripheral anticholinergics (glycopyrrolate [low, medium, or high dose] or nebulized ipratropium bromide), or CNS + peripherally acting anticholinergics (diphenhydramine, nebulized atropine, or injected atropine). All treatments were given prior to a subcutaneous injection of 25 mg/kg dichlorvos (n= 8 per group). Survival was assessed at 10 minutes (early death) and 24 hours (delayed death). Kaplan-Meier (95% confidence intervals [95% CIs]) and chi-squared analysis was then performed to determine differences between treatments. Results: Regardless of treatment, all animals exhibited profound nicotinic effects (fasciculations) without obvious seizures within 2 minutes of poisoning. In rats pretreated with peripherally acting agents, the fasciculations were rapidly followed by reduced motor activity, sedation, and death. Mortality at 10 minutes for saline controls, glycopyrrolate, and ipratropium was 88%, 96%, and 100%, respectively. The single control animal surviving beyond 10 minutes went on to develop peripheral cholinergic manifestations, including hypersalivation, urination, and defecation. Only one of 24 animals treated with injected atropine, nebulized atropine, or diphenhydramine died during the early phase of poisoning; all others survived to 24 hours (p < 0.01). Conclusions: Death in acute, severe OP poisoning is prevented by pretreatment with anticholinergic agents that cross the blood,brain barrier, but not by agents with only peripheral actions. Early death due to OP poisoning appears to be a centrally mediated process. [source]

Diphenhydramine as a Protective Agent in a Rat Model of Acute, Lethal Organophosphate Poisoning

ACADEMIC EMERGENCY MEDICINE, Issue 12 2002
Steven B. Bird MD
Objective: To evaluate the effects of diphenhydramine chloride (DPH) on mortality in a rat model of acute, severe organophosphate poisoning (OP).Methods: Wistar rats (n = 40) were randomized to pretreatment with either normal saline (controls), 5 mg/kg atropine, 3 mg/kg DPH, 15 mg/kg DPH, or 30 mg/kg DPH given as a single intramuscular injection 5 minutes prior to a subcutaneous injection of 25 mg/kg dichlorvos (n = 8 per group). The primary endpoint was 10-minute survival. Survival at 24 hours was a secondary endpoint. Comparison of survival rates between groups was carried out by ANOVA and the Student-Newman-Keuls test. Results: Dichlorvos exposure resulted in profound fasciculations within 2 minutes of injection in all cohorts. In controls, fasciculations were followed by respiratory arrest within 10 minutes (0% survival). The rats receiving atropine pre-treatment exhibited similar fasciculations (nicotinic effects) without subsequent respiratory arrest, resulting in a significant improvement in survival (88%, p < 0.001). The DPH-treated rats exhibited a significant dose-dependent reduction in mortality, with the 3 mg/kg, 15 mg/kg, and 30 mg/kg groups demonstrating 0%, 25%, and 100% survival, respectively. There was no additional mortality between 10 minutes and 24 hours in any group. There was no significant difference in survival between the high-dose DPH and the atropine groups. Conclusions: Diphenhydramine chloride significantly reduced mortality in rats with acute, severe dichlorvos exposure. [source]

Pretreating Rats with Parenteral Ophthalmic Antimuscarinic Agents Decreases Mortality from Lethal Organophosphate Poisoning

ACADEMIC EMERGENCY MEDICINE, Issue 4 2007
Sean M. Bryant MD
No abstract is available for this article. [source]

Organophosphate poisoning complicated by a tachyarrhythmia and acute respiratory distress syndrome in a child

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5 2002
L Nel
Abstract: A 9-year-old child presented with documented organophosphate insecticide poisoning. His course was initially complicated by a tachyarrhythmia with QT-interval prolongation that responded promptly to intravenous magnesium. However, following partial recovery, he developed progressive acute respiratory distress syndrome characterized by irreversible fibrosis and obliteration of the lung parenchyma. [source]

Diphenhydramine as a Protective Agent in a Rat Model of Acute, Lethal Organophosphate Poisoning

Weak inhibitors protect cholinesterases from strong inhibitors (paraoxon): in vitro effect of tiapride

JOURNAL OF APPLIED TOXICOLOGY, Issue 6 2005
G. A. Petroianu
Abstract Weak and reversible inhibitors of cholinesterases, when administered before potent organophosphorus inhibitors (pretreatment), have the ability, to a certain extent, to protect enzymes from inhibition. Such a protective effect was demonstrated in vitro for metoclopramide and ranitidine. The putative mode of protective action of these substances is, when administered in excess, competition for the active site of the enzyme with the more potent organophosphate. The present paper presents results using another benzamide with weak cholinesterase inhibitory properties: tiapride (TIA). The purpose of the study was to quantify in vitro the extent that TIA conferred protection, using paraoxon (POX) as an inhibitor, and to compare the results with existing data obtained using TIA as a protective agent against dichlorvos (DDVP). POX is a highly toxic non-neuropathic organophosphate. While the use of parathion (the inactive prodrug which is metabolically converted to POX) has been restricted in most countries, the organophosphate is still responsible for a large number of accidental or suicidal exposures. DDVP is a moderately toxic, non-neuropathic organophosphate. Red blood cell (RBC) acetylcholinesterase (AChE) activities in whole blood and butyrylcholinesterase (BChE) activities in human plasma were measured photometrically in the presence of different POX and TIA concentrations and the IC50 was calculated. Determinations were repeated in the presence of increasing TIA concentrations. The IC50 of POX increases with the TIA concentration in a linear manner. The protective effect of tiapride on cholinesterase could be of practical relevance in the pretreatment of organophosphate poisoning. It is concluded that in vivo testing of TIA as an organophosphate protective agent is warranted. Copyright © 2005 John Wiley & Sons, Ltd. [source]

The recognition and treatment of the intermediate syndrome of organophosphate poisoning in a dog

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 1 2003
K Hopper BVSc
[source]

Perioperative care of children with nerve agent intoxication

PEDIATRIC ANESTHESIA, Issue 6 2001
Ron Ben Abraham MD
Nerve agents (NA) present a major threat to civilian populations. When a ballistic system is used for spreading poison, multiple trauma, as well as toxic trauma could be caused. Children are more susceptible, due to their smaller physiological reserve. Urgent surgical intervention for combined intoxication in the multiple-traumatized child could be a tremendous task in view of the background of physiological instability. Nerve agents affect the autonomic, as well as the central nervous system, leading occasionally to unexpected interactions with agents normally used for resuscitation. This can cause additional instability, and possibly systemic collapse. This review presents and emphasizes points concerning treatment of a child who suffers from combined multiple and toxic traumas. The review is based on scant knowledge of a database of similar cases of pesticide organophosphate poisoning in children since these compounds are alike. We also extrapolated data from reports concerning episodic civilian exposure to NA. [source]

Central anticholinergic syndrome secondary to atropine treatment of organophosphate poisoning,

PSYCHOGERIATRICS, Issue 3 2006
AN EROL, Demet DO
Abstract Anticholinergic syndrome is a common phenomenon because of the frequent administration of atropine in organophosphate poisoning. This diagnosis should be considered in patients with altered mental state following therapy with atropine. We report a case of delirium 48 h after atropine treatment for organophosphate poisoning. [source]

Characterization of early plasma concentrations of midazolam in pigs after administration by an autoinjector

BIOPHARMACEUTICS AND DRUG DISPOSITION, Issue 7 2004
Aharon Levy
Abstract The treatment of organophosphate-induced poisoning is based mainly on atropine and an oxime. Prompt anticonvulsive intervention is usually also required to terminate the ensuing seizure activity and to prevent delayed permanent brain damage. Midazolam, a water-soluble benzodiazepine agonist, has the advantage of rapid absorption following intramuscular administration. In mass casualty situations, the availability of an autoinjector, filled with midazolam, might be a further advantage. In the present study, the plasma pharmacokinetics of midazolam after administration by an autoinjector was compared with conventional intramuscular (i.m.) administration in two groups of four pigs each. During the first 15 min after injection, significantly higher plasma concentrations of midazolam were detected following autoinjector administration, compared with the i.m. injection. The physiological reflection of the accelerated midazolam absorption was a marked reduction in the time interval required for muscle relaxation, induced by midazolam. It is concluded that a midazolam autoinjector might be helpful in the mass casualty scenario following organophosphate poisoning. Copyright © 2004 John Wiley & Sons, Ltd. [source]

Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats

CELL BIOCHEMISTRY AND FUNCTION, Issue 7 2008
N. Gunay
Abstract This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30,mg,kg,1 i.p.), 1 and 10,mg,kg,1 Y-27632,+,dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats. Copyright © 2008 John Wiley & Sons, Ltd. [source]