This presentation explains about epidemiology of organophosphate poisoning, the toxic mechanism and pathophysiological basis of clinical features. It briefly outlines diagnosis in an emergency situation and management.
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Added: Apr 28, 2023
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Organophosphate poisoning Dr ktd priyadarshani Registrar in emergency medicine Teaching hospital- Peradeniya 2023/03/24
scope Overview Toxic mechanism Clinical features Diagnosis Management
overview Important clinical problem in rural Asia Mostly self ingestion in young adults Case fatality rate 10-30% for most Ops self poisoning kills 150, 000 every year world wide – 20% of suicide* Fall in deaths 260,000 to 150,000 with tighter regulation *Case fatality of agricultural pesticides after self-poisoning in Sri Lanka: a prospective cohort study Buckley, Nicholas A et al. 2021 The Lancet Global Health, Volume 9, Issue 6, e854 - e862
Acute effects Most within 8 hrs all with in 24 hrs Local irritation of skin and respiratory tract without evidence of sysytemic absorption Mild to moderate- combinations Severe- nicotinic features first- time depend on route and dose Tintinali emergency medicine 9E
Intermediate syndrome Delayed 1-5 days In 40% of patients following ingestion Clinical features- paralysis of neck muscles, muscles innervated by cranial nerves, proximal limb muscles, respiratory muscles paralysis Absent symptoms and signs of cholinergic excess Electromyography Prevention Aggressive early antidote therapy and supportive therapy
Op induced delayed neuropathy (OPIDN) Chronic toxicity- agricultural Symmetrical sensorimotor axonopathy Begin with leg crams and ascend- mimic GBS
Chronic op-induced neuropsychiatric disorder ( copind ) Cognitive dysfunction, impaired memory, mood changes, autonomic dysfunction, peripheral neuropathy and extrapyramidal signs Chronic fatigue syndrome and multiple chemical sensitivity Children are at greater risk Small body size Lower baseline level of cholinesterase activity BDZ may help if given during acute poisoning
management Peter, John Victor & Moran, J & Pichamuthu , Kishore & Chacko, Binila . (2008). Adjuncts and Alternatives to Oxime Therapy in Organophosphate Poisoning—is There Evidence of Benefit in Human Poisoning? A Review. Anaesthesia and intensive care. 36. 339-50. 10.1177/0310057X0803600305.
Supportive care and monitoring Monitor Cardiac monitor Pulse oximeter 100% oxygen NRBM Seizure- IV benzodiazepine AVOID Sux Ester anesthetics Beta blockers
investigations Plasma butyryl cholinesterase level/ red cell cholinesterase level Markers of AchE activity at the synaptic junction Not reliable due to Baseline varies degree of inhibition needed to produce symptomatic illness also variable
Look for Hypo/hyperglycemias Leukocytosis Abnormal liver function Evidence of pancreatitis Chest x-ray- Pulmonary edema, aspiration ECG- torsade pointes, VT, VF, ST segment changes, peaked T waves, AV block, Prolonged QT
decontamination Protective clothing must be worn to prevent secondary poisoning of healthcare workers. Handle and dispose of all clothes as hazardous waste. Wash patient with soap and water. Handle and dispose of water runoff as hazardous waste Gastric lavage- no proven benefit Given with in 2 hrs
Enhanced elimination Activated charcoal- no proven benefit Hemodialysis, hemofiltration and hemoperfusion- no proven value
Antidote- atropine Competitive antagonist of Ach at central and peripheral muscarinic receptors Initial bolus depending on symptoms 1.2-3 mg IV in adult 0.05 mg/kg IV in pediatric No IV access- 2-6 mg IM Absence of anticholinergic symptoms after initial dose- confirms OP poisoning Double dose every 5 min Check for end points Continuous infusion of 10-20% per hour of initial dose to achieve adequate atropinization (0.4-4 mg/ hr IV in adult)
KUO for atropine toxicity Absent bowel sounds Hyperthermia delirium Tachycardia is not a contraindication for atropine if other features suggest under atropinisation Pupil dilatation is sometimes delayed and other parameters usually improve much more rapidly Atropine reduces bronchorrhea , but does not reverse muscle weakness. Recurrence of toxicity with fat soluble Ops for weeks- need continuous atropine infusion Febrile patient- Sedate if agitated- IV diazepam 10mg Active cooling
Pralidoxime Give as soon as possible- 24-48 hr after exposure 30 mg/kg IV in adults 30mg/kg up to 1g in children Mix with NS and infused over 5-10 min Continuous infusion 8 mg/kg per hour for 24-48 hrs End points Atropine has not been needed for 12-24 h Patient is extubated No evidence about reduce mortality or complication rate- Not recommended for asymptomatic pts Carbamate exposure with minimal symptoms
disposition Minimal exposure Decontamination Observe 6-8 hrs Avoid re-exposure- cumulative toxicity Significant poisoning Admit Symptomatic recovery 10 days if toxins are fat soluble Pralidoxime infusion – assess 24 hr after stopping Follow up for intermediate or delayed syndromes
References Management of poisoning 4 th edition- prof Ravindra Fernando Tinitnali Emergency Medicine 9 th Edition Case fatality of agricultural pesticides after self-poisoning in Sri Lanka: a prospective cohort study Buckley, Nicholas A et al. 2021 The Lancet Global Health, Volume 9, Issue 6, e854 - e862 Peter, John Victor & Moran, J & Pichamuthu , Kishore & Chacko, Binila . (2008). Adjuncts and Alternatives to Oxime Therapy in Organophosphate Poisoning—is There Evidence of Benefit in Human Poisoning? A Review. Anaesthesia and intensive care. 36. 339-50. 10.1177/0310057X0803600305. Giyanwani P, Zubair U, Salam O, et al. (September 03, 2017) Respiratory Failure Following Organophosphate Poisoning: A Literature Review . Cureus 9(9): e1651. doi:10.7759/cureus.1651 Umakanth M. Intermediate Syndrome Following Organophosphate Poisoning; Review Article. Asia Pac J Med Toxicol 2019;8:19-24. Kharel H, Pokhrel N B, Ghimire R, et al. (March 04, 2020) The Efficacy of Pralidoxime in the Treatment of Organophosphate Poisoning in Humans: A Systematic Review and Meta-analysis of Randomized Trials. Cureus 12(3): e7174. doi:10.7759/cureus.7174