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Neurotoxicology
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Sean D. McCann, Trevonne M. Thompson
Treatment of OP poisoning should include careful decontamination of the patient since many OP agents have the potential to contaminate health care providers who care for exposed patients. Pharmacologic therapy consists of atropine, an antagonist of the muscarinic ACh receptor. Administration of atropine should be titrated to the reduction of bronchial secretions, and large doses may be needed, totaling hundreds of grams in some severely poisoned patients. Oximes are compounds that react with and bind to OP agents with higher affinity than the binding between OPs and AChE, and are used to reverse OP-mediated inactivation of the enzyme as well as prevent formation of a permanent covalent bond between the OP and AChE, a process referred to as “ageing.” Different OPs age at different speeds, some occurring within minutes, in which case oximes will be of little benefit. However, the specific OP agent is usually unknown at the time of patient presentation, so empiric therapy with oximes is typically indicated. Pralidoxime is the most commonly used oxime in the United States, though others are used internationally. Severe poisoning can progress to seizures which can be treated with BZD (diazepam is classically cited, but any immediately available BZD can be used) in addition to continued treatment with atropine and general supportive care. The etiology of OP-induced seizures is not well described and may be due to hypoxia.
Toxicology
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
Give pralidoxime 2 g (30 mg/kg) i.v. over 15 min and then 500 mg/h for at least 24 h, in all moderate-to-severe cases (except for carbamate poisoning). Monitor serial plasma or red cell cholinesterase levels and look for signs of clinical improvement before ceasing treatment.
Chemical injuries
Published in Jan de Boer, Marcel Dubouloz, Handbook of Disaster Medicine, 2020
The treatment of organophosphate poisoning requires removal of casualties from fumes and spills; decontamination should be performed after administration of antidotes and life-support measures. Atropine blocks the muscarinic and central manifestations and oximes counteract the nicotinic effects and some muscarinic effects10,13,21,23. Pralidoxime promotes the reactivation of acetylcholinesterase activity1. Anticonvulsants such as diazepam also may be needed to treat seizure activity in the poisoned casualties.
Polyethyleneglycol-serine nanoparticles as a novel antidote for organophosphate poisoning: synthesis, characterization, in vitro and in vivo studies
Published in Drug and Chemical Toxicology, 2023
Pedram Ebrahimnejad, Ali Davoodi, Hamid Irannejad, Javad Akhtari, Hamidreza Mohammadi
Currently, management of OP poisoning is still difficult and challenging (Eddleston 2019). In our study, the percentage of surviving of mice after administration of DZ was significantly increased (approximately 25%) in the groups treated with PEG-NPs. Atropine, a standard and the primary antidot for OPs treatment, was used in the 1940s. However, in spite of its approval, there is no universal guideline on its dosing and administration. Under-dosing can postponement the optimum atropinization, causing death because of hypoxia, hypotension and central respiratory depression. On the other hand, atropine overdosing leads to excessive anticholinergic toxicity, which can be lethal in severe cases (Pang et al.2015). Also, oximes are used as a distinctive class of anti-organophosphorus countermeasures, where they remove attached OP from inhibited AChE to reactivate its activity. However, the effectiveness of oximes therapy in OPs poisoning is still under debate. Despite extensive research and improvement, there is no single, broad-spectrum and appropriate oxime as an effective antidote in the management of all OPs agents poisoning (Worek et al.2016). Hence, according to previous studies, we used of pralidoxime (40 mg/kg) for evaluation of the effectiveness of standard therapy and different treatments (Satar et al.2008, Kose et al.2010, Siqueira et al.2019, Jung et al.2020). This study revealed that PEG-NPs (especially at doses of 200 and 400 mg/kg) have equal or more effectiveness than pralidoxime.
Changes of attention-related brain activity over 6 months after acute organophosphate pesticide poisoning: a prospective follow-up study
Published in Clinical Toxicology, 2022
Tharaka L. Dassanayake, Vajira S. Weerasinghe, Indika B. Gawarammana, Nicholas A. Buckley
All patients were admitted under the care of a specialist physician. All OP-group participants underwent a neurological examination and RBC-AChE measurement on admission. The patients were monitored frequently during the first few hours following the initial clinical assessment, and thereafter at least twice a day by the ward doctors. OP-poisoned patients were managed according to standard protocols [30], atropine dosing and timing being determined by the need of each patient. Pralidoxime was administered to some of those patients. Patients with paracetamol toxicity, when indicated, were treated with N-acetylcysteine. All patients were seen, and if necessary were managed by a psychiatrist. We also recorded demographic information, circumstantial evidence related to the episode of poisoning, clinical data and laboratory investigation findings. On discharge, the participants were given an appointment for the first (post-discharge) electrophysiological assessment.
Acute phenthoate self-poisoning: a prospective case series
Published in Clinical Toxicology, 2022
Lekaashree Rambabu, Fahim Mohamed, Jeevan Dhanarisi, Indika Gawarammana, Jacques Raubenheimer, Lorraine Mackenzie, Michael S. Roberts, Nicholas Buckley, Michael Eddleston
Six patients received pralidoxime, of which five showed modestly increased AChE activity after treatment. For four patients with detectable AChE activity at baseline (Figure 3), in vivo AChE activity increased in the first hour by a median of 50 (IQR 22 − 165.5, range 5–188) mU/µmol Hb. The fifth who presented after 14.6 h showed an increase from zero to 39 mU/µmol Hb in the first hour after administration; the sixth who presented after 3.6 h showed no increase (6 mU/µmol Hb to zero). This rapid effect (too fast for ageing) may be due to changes to the phenthoate in the bottle, before ingestion. Such reactions have been noted with dimethoate, forming isodimethoate, which can result in intractable AChE inhibition [28]. AChE reactivation was poorly maintained at 12 h. There was a modest increase in BuChE activity (median increase of 272 [IQR 8.1–1519] mU/ml) in five of six patients receiving pralidoxime (Figure 3). The AChE activity in those who didn’t received pralidoxime decreased by 8 mU/µmol Hb (4.6% from baseline) in the first patient, and increased by 13 mU/µmol Hb (25.7% from baseline) in the second patient.