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Organophosphate Pesticide Poisoning. Bishan Rajapakse MBChB Otago Emergency Medicine Advanced Trainee, MPhil Student (ANU), South Asian Clinical Toxicology Research Collaboration Sri Lanka. The Case…. Picture yourself in Anuradhapura hospital Sri Lanka – ED/ Medical SHO

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organophosphate pesticide poisoning

OrganophosphatePesticidePoisoning

Bishan Rajapakse

MBChB Otago

Emergency Medicine Advanced Trainee, MPhil Student (ANU),

South Asian Clinical Toxicology Research Collaboration

Sri Lanka

the case
The Case….
  • Picture yourself in Anuradhapura hospital Sri Lanka – ED/ Medical SHO
  • Ward 6 , teaming with patients….
  • Charge Sister tells you there is a sick patient
    • 36yo F
    • Taken 100mls of Dimethoate after a domestic argument
  • There’s nowhere to run, or hide…. So you see the patient – what do you do?
organophosphate poisoning in sri lanka
Organophosphate Poisoning in Sri Lanka
  • Organophosphate pesticide (OP) poisoning kills 300,000 worldwide
    • In Sri Lanka these are mostly impulsive deliberate self-poisoning in young people
organophosphate poisoning in sri lanka5
Organophosphate Poisoning in Sri Lanka
  • Case Fatality rates (CFR)
    • 10-20% for most
    • 50-70% for some OP’s
  • In west CFR
    • 0.3% from all poisons
  • Multifactorial
    • Toxicity of OP’s
    • Patient transport
    • Lack of resources
    • Training
  • Although less common OP Poisoning is still a problem in West
    • Occupational exposure
    • Threat of Chemical warfare
simplified acute op toxicity
Simplified Acute OP Toxicity
  • Inactivation of acetylcholinesterase enzyme

Organophosphate

pharmacology of cholinomimetics according to katzung
Pharmacology of Cholinomimetics according to Katzung
  • Structure
      • Simple Alcohols eg edrophonium
      • Carbamates Eg Neostigmine and Physostigmine (tertiary)
      • Organophosphates eg Parathion
clinical syndrome

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Respiratory failure

+ Death

Clinical Syndrome
  • Clinical Syndrome
  • Acute Cholinergic:
    • Central
    • Peripheral Muscarinic
    • Peripheral Nicotinic
  • Intermediate Syndrome
  • OPIDN: Delayed peripheral neuropathy
  • Neurocognitive dysfunction
cholinergic effects
Cholinergic Effects
  • D iarrhoea
  • U rination
  • M iosis
  • B radycardia, Bronchorrhoea, Bronchospasm
  • E mesis
  • L acrimation
  • S alivation
nicotinic effects
Nicotinic Effects
  • Respiratory difficulty
    • respiratory arrest
    • diaphragmatic weakness
  • Muscle Weakness
    • fasiculations
    • clonus
    • tremor
  • Stimulation of sympathetic nervous system
    • Mydriasis, hypertension, tachycardia
    • re-entrant dysrhythmias
    • cardiorespiratory arrest
cns effects
CNS effects
  • Malaise
  • Memory loss
  • Confusion
  • Disorientation
  • Delirium
  • Seizures
  • Respiratory centre depression or dysfunction
  • Coma
intermediate syndrome
Intermediate Syndrome
  • Delayed Respiratory Failure
    • Proximal muscle weakness and cranial nerve lesions
    • Typically 1-4 days after cholinergic crisis has resolved
  • Prolonged Effects on Nicotinic receptors
  • Primary motor end plate degeneration
  • Clinical importance
    • Delayed respiratory failure leads to death if not aware of it or prepared for it
  • Wadia et. al 1974 :Type II Paralysis, Senanayake and Karalliedde 1987
chronic effects
Chronic Effects
  • Organophosphate induced delayed neuropathy (OPIDN)
      • 1-3weeks
      • Peripheral neuropathy
      • Axonopathy due to Neuropathy Target Esterases (NTE)
  • Chronic organophosphate induced neuropsychiatric disorder (COPIND)
management
Management

The priorities in management are to:

Resuscitation

Atropinisation of symptomatic patients

Decontamination

Other Treatments - Oximes

antidotes

? Dose

  • ? Duration
  • ? Effectiveness
Antidotes
  • Atropine
  • Oximes
    • Expensive
  • Does treatment affect outcome
    • Intermediate Syndrome?
    • OPIDN?
does the patient need atropine
Does the patient need atropine?
  • How much and for how long
scheme of atropinization endpoints to be reached

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Scheme of atropinization (endpoints to be reached)
  • Eddleston M, Buckley NA, Mohamed F, Senarathna L, Hittarage A, Dissanayake W, Azhar S, Sheriff MHR, Dawson AH. Speed of initial atropinisation in significant organophosphorus pesticide poisoning - a comparison of recommended regimens. Journal of Toxicology – Clinical Toxicology 2004;6:865-875.
atropine
Atropine
  • Loading
    • Doubling dose regime e.g. 2 4 8 16 mgs every 5 minutes
  • Maintenance
    • Continuous infusion < 3mg/hr
    • 10-20% of loading dose/hour
  • Endpoints
    • Clear chest on auscultation with no wheeze
    • Heart rate >80 beats/min
  • Withdrawal
    • Atropine toxicity
    • Clinical Improvement
what if you give too much atropine
What if you give too much Atropine ?
  • Anticholinergic Syndrome:
    • Hot as hell
    • Blind as a bat
    • Red as a beet
    • Dry as a bone
    • Mad as a hatter
  • A sensitive indicator for ingestion, but poor predictor for toxicity.
  • Full syndrome is rare
our decision should depend on a risk benefit analysis
Our Decision should depend on a risk/benefit analysis
  • Nothing
  • Emesis
  • Gastric Lavage
  • Activated Charcoal
  • Whole bowel irrigation
risk of intervention
Risk of Intervention
  • Aspiration
    • Impaired GCS + Unprotected Airway
      • Emesis, Lavage, Charcoal (worse with cathartics)
  • Trauma
    • Oesphageal Injury
      • Emesis, Lavage, Charcoal
  • Electrolyte Abnormalities
      • Forced Emesis, Cathartics
  • Cardiac Arrest
    • Toxin induced bradycardia + Vagal Tone
      • Induced emesis, Lavage
  • Cost
summary of experimental evidence
Summary of Experimental Evidence
  • Ideal settings
  • Little benefit in outcomes after 1 hour
  • Activated Charcoal is equivalent or better than emesis or lavage
      • Position statement: single-dose activated charcoal. J Toxicol Clin Toxicol 1997;35:721-41.
      • Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. J Toxicol Clin Toxicol 1999;37:731-51.
oximes
Oximes
  • Ineffective in some situations
    • Ageing
    • Variation between organophosphates
  • Effective protocols not established
    • Variation in use
      • Zero – 24 grams a day
  • Expensive
      • USA $30-600 / gram
      • India $6- 9 / gram
      • Sri Lanka 55 cents / gram
  • Unlikely to address Non-ACh effects
alternate sites for antidotes
Alternate sites for antidotes
  • Protect AChE
  • Supply AChE
  • Reduce ACh
  • Protect ACh Receptor
  • Reduce OP Load
  • Multiple Mechanisms
other treatments under investigation
Other Treatments under investigation
  • Magnesium
      • Reduces acetylcholine release
      • Blockage pre-synaptic calcium channels
      • Limited human studies
  • Clonidine
      • Decrease the presynaptic synthesis and release of acetylcholine.
      • Central nervous system > peripheral cholinergic synapses
  • Diazepam
      • Diazepam reduces respiratory failure (rats) and cognitive deficit (primates)
      • Postulate “uncoordinated stimulation of the respiratory centres decreases phrenic nerve output”.
the case30
The Case….
  • Picture yourself in Anuradhapura hospital Sri Lanka – ED/ Medical SHO
  • Ward 6 , teaming with patients….
  • Charge Sister tells you there is a sick patient
    • 36yo F
    • Taken 100mls of Dimethoate after a domestic argument
  • There’s nowhere to run, or hide…. So you see the patient – what do you do?
summary
Summary
  • OP’s are Indirect Cholinomimetic
    • Block AChE, prolonged duration of ACh in synapse
  • Effects
    • Muscarinic, Nicotinic, CNS
    • Respiratory failure and Death result from this
  • Treatment
    • ABC’s, Atropine, Decontaminate, Oximes
  • Important also in West