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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
TOXIC MECHANISM
CLINICAL FEATURES
4 clinical syndromes
• Acute poisoning
• Intermediate syndrome
• Chronic toxicity
• Organophosphate induced delayed neuropathy
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.
RESUSCITATION
1. Airway
• Gentle suction
• Intubate
2. Breathing
• Oxygen
• PPV
3. Circulation
• IV access
• Fluid- fluid bolus
4. Disability
• Seizures
INTUBATION
• Indications
• Coma, Seizure, respi failure, excessive respi secretions, severe
bronchospasm
• TV <5 mL/kg, VC <15 mL/kg, apneic spells, Pa O2<60 mmHg on FiO2 >60%
• Drugs
• Non depolarizing agent (sux- prolonged paralysis)
RISK ASSESSMENT
• Agent
• Quantity absorbed
• Route – oral > dermal/ inhalation
• Additives
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
1. 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
2. Double dose every 5 min
• Check for end points
3. 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
1. Management of poisoning 4th edition- prof Ravindra Fernando
2. Tinitnali Emergency Medicine 9th Edition
3. 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
4. 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.
5. 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
6. Umakanth M. Intermediate Syndrome Following Organophosphate Poisoning; Review Article. Asia Pac J
Med Toxicol 2019;8:19-24.
7. 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
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Organo Phosphate Poisoning.pptx

  • 1. ORGANOPHOSPHATE POISONING DR KTD PRIYADARSHANI REGISTRAR IN EMERGENCY MEDICINE TEACHING HOSPITAL- PERADENIYA 2023/03/24
  • 2. SCOPE • Overview • Toxic mechanism • Clinical features • Diagnosis • Management
  • 3. 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
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  • 8. CLINICAL FEATURES 4 clinical syndromes • Acute poisoning • Intermediate syndrome • Chronic toxicity • Organophosphate induced delayed neuropathy
  • 9. 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
  • 10. 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
  • 11. OP INDUCED DELAYED NEUROPATHY (OPIDN) • Chronic toxicity- agricultural • Symmetrical sensorimotor axonopathy • Begin with leg crams and ascend- mimic GBS
  • 12. 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
  • 13. 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.
  • 14. RESUSCITATION 1. Airway • Gentle suction • Intubate 2. Breathing • Oxygen • PPV 3. Circulation • IV access • Fluid- fluid bolus 4. Disability • Seizures
  • 15. INTUBATION • Indications • Coma, Seizure, respi failure, excessive respi secretions, severe bronchospasm • TV <5 mL/kg, VC <15 mL/kg, apneic spells, Pa O2<60 mmHg on FiO2 >60% • Drugs • Non depolarizing agent (sux- prolonged paralysis)
  • 16. RISK ASSESSMENT • Agent • Quantity absorbed • Route – oral > dermal/ inhalation • Additives
  • 17. SUPPORTIVE CARE AND MONITORING • Monitor • Cardiac monitor • Pulse oximeter • 100% oxygen NRBM • Seizure- IV benzodiazepine • AVOID • Sux • Ester anesthetics • Beta blockers
  • 18. 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
  • 19. • 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
  • 20. 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
  • 21. ENHANCED ELIMINATION • Activated charcoal- no proven benefit • Hemodialysis, hemofiltration and hemoperfusion- no proven value
  • 22. ANTIDOTE- ATROPINE • Competitive antagonist of Ach at central and peripheral muscarinic receptors 1. 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 2. Double dose every 5 min • Check for end points 3. Continuous infusion of 10-20% per hour of initial dose to achieve adequate atropinization (0.4-4 mg/hr IV in adult)
  • 23. • 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
  • 24. 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
  • 25. 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
  • 26. REFERENCES 1. Management of poisoning 4th edition- prof Ravindra Fernando 2. Tinitnali Emergency Medicine 9th Edition 3. 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 4. 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. 5. 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 6. Umakanth M. Intermediate Syndrome Following Organophosphate Poisoning; Review Article. Asia Pac J Med Toxicol 2019;8:19-24. 7. 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