Clinical Management of Acute OP Pesticide Poisoning



Organophosphorus pesticide (OP) poisoning is a worldwide problem. OPs inhibit various enzymes, in particular acetylcholinesterase (AChE) which is considered the key action that induces the clinical features of OP poisoning known as acute cholinergic syndrome. Multisystem clinical features are noted with most cases of OP poisoning but the manifestations can differ between individual OP compounds. Proper medical treatment follows an initial diagnosis, which in turn requires a high index of suspicion. If required, OP exposure can be confirmed by quantifying the blood or plasma cholinesterase activity. Standard resuscitation and supportive care is essential in the management of the exposed patient. This is accompanied by rapid administration and dose titration of antagonists of muscarinic cholinergic receptors (anti-muscarinics, notably atropine). A detailed risk assessment should be conducted so that adverse outcomes can be anticipated and treated, where possible. The risk of secondary poisoning in staff providing health care to patients is anticipated to be low if standard precautions are exercised. Other treatments are available but their role is more controversial; indeed, use varies across the world. For example, oximes such as pralidoxime and obidoxime appear to have the ability to reverse AChE inhibition in patients. However, clinical trials have yielded conflicting results (both benefit and harm), so their role in routine clinical practice is not confirmed. The role of oximes and other treatments such as magnesium, bicarbonate, clonidine, nicotinic antagonists, and extracorporeal blood purification modalities are the areas of research interest. Careful monitoring and development of a discharge plan are also necessary to optimise outcomes.


Organophosphorus Organophosphate Pesticide Poisoning Cholinesterase AChE Mortality Atropine Pralidoxime Obidoxime Clonidine Magnesium Bicarbonate Developing country Acetylcholinesterase–inhibition Acetylcholinesterase- reactivation Activated charcoal Acute cholinergic syndrome Acute cholinergic syndrome or crisis Acute Physiology and Chronic Health Evaluation (APACHE) Ageing Alcohol- ethanol Alkalinisation Anticholinergic medicines Antidotes Arrhythmias Aspiration pneumonitis and pneumonia Atropine- antidote Atropine- diagnostic test Autonomic nervous system Benzodiazepines Bicarbonate Bioscavengers Bradycardia Bronchorrhoea Bronchospasm Butyrylcholinesterase Carbamate Case fatality- acute poisoning Catecholamine Chlorpyrifos Clinical scoring tools Clonidine Coformulants Concentration- OP in plasma Concentration- OP in the product Cyclohexanone CYP450 Decontamination- dermal Decontamination- gastrointestinal Diagnosis-acute poisoning Diaphoresis Diarrhoea Diazepam Diazinon Differential diagnosis-acute poisoning Dimethoate DUMBELS Electrophysiology- peripheral Emesis-forced (treatment) Emesis-symptom Enhanced elimination Epidemiology- acute poisoning Erythrocyte cholinesterase Ethanol-alcohol European Association of Poison Control Centres and Clinical Toxicologists Exposure-amount Exposure-dermal  Exposure-inhalation Exposure-oral Extracorporeal blood purification Fasciculations Fenthion Formulation-concentration and solvent Fresh frozen plasma Gastric lavage Glasgow Coma Score Glycopyrrolate Haemodialysis Healthcare workers- protection HI-6 Hyoscine Hypertension Hypotension Intentional self-poisoning Intermediate Syndrome International Program on Chemical Safety (IPCS) IPCS (International Program on Chemical Safety) Lacrimation LD50 Magnesium Malathion Management-acute poisoning Miosis Mixing study Mydriasis Nerve conduction study Neuropathy target esterase Nicotinic antagonists Obidoxime OP-diethyl OP-dimethyl OP-induced delayed polyneuropathy OP-induced neuropsychiatric Outcomes- age Oxime therapy-ageing Oxime therapy-clinical endpoints Oxime therapy- clinical evidence Oxime therapy- principles Oxime- dose-equivalents Oxon Pancuronium Paralysis Paraoxonase Pesticide Phosphoryl-oxime compound (POX) Pilocarpine Plasma cholinesterase Pralidoxime Prognosis- acute poisoning Profenofos Pseudocholinesterase Randomised controlled trials RBC cholinesterase Regulations Respiratory failure Resuscitation Risk Assessment- acute poisoning Salivation Secondary contamination Seizures Simplified Acute Physiology Score (SAPS) Solvent Spirometry Succinyl choline Suxamethonium Tachycardia Thion Toxicogenomics Urination WHO- classification 


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Copyright information

© Springer-Verlag London 2014

Authors and Affiliations

  1. 1.Burns, Trauma and Critical Care Research CentreRoyal Brisbane and Women’s Hospital, University of QueenslandSt LuciaAustralia
  2. 2.Department of Renal MedicineAddenbrooke’s HospitalCambridgeUK
  3. 3.Department of Drug HealthRoyal Prince Alfred HospitalSydneyAustralia

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