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EMERGENCY

Organophosphate Poisoning

Moderate EvidenceUpdated: 2024-12-21

On This Page

Red Flags

  • SLUDGE/BBB symptoms
  • Miosis
  • Bradycardia
  • Respiratory distress
  • Reduced consciousness
  • History of pesticide exposure
Overview

Organophosphate Poisoning

Topic Overview

Summary

Organophosphate (OP) poisoning results from exposure to pesticides (agricultural) or nerve agents (chemical warfare). OPs irreversibly inhibit acetylcholinesterase, causing excess acetylcholine accumulation at muscarinic and nicotinic receptors. This produces the classic SLUDGE/BBB syndrome (salivation, lacrimation, urination, defaecation, GI upset, emesis / bronchospasm, bradycardia, bronchorrhoea). Treatment is atropine (muscarinic blockade), pralidoxime (oxime — reactivates AChE), and supportive care including ventilation.

Key Facts

  • Mechanism: Irreversible acetylcholinesterase inhibition → cholinergic crisis
  • SLUDGE: Salivation, Lacrimation, Urination, Defaecation, GI upset, Emesis
  • BBB: Bronchospasm, Bradycardia, Bronchorrhoea
  • Nicotinic effects: Muscle fasciculations, weakness, paralysis
  • CNS effects: Agitation, seizures, coma
  • Treatment: Atropine (high doses) + Pralidoxime + supportive care

Clinical Pearls

"SLUDGE + miosis + bradycardia = cholinergic toxidrome = OP poisoning"

Atropine doses in OP poisoning are MUCH higher than standard doses — titrate to dry secretions

Pralidoxime must be given early (before "ageing" of enzyme-OP complex)

Why This Matters Clinically

OP poisoning is a common cause of death from poisoning in agricultural regions. Rapid recognition and aggressive atropinisation saves lives. Delayed treatment leads to respiratory failure and death.


Visual Summary

Visual assets to be added:

  • SLUDGE/BBB mnemonic diagram
  • Cholinesterase inhibition mechanism
  • Atropine titration algorithm
  • OP poisoning management flowchart

Epidemiology

Incidence

  • Over 3 million poisoning cases/year globally
  • Over 200,000 deaths/year (mostly in Asia, Africa)
  • Common in agricultural communities

Demographics

  • Agricultural workers (occupational exposure)
  • Rural areas (developing countries)
  • Intentional self-harm (suicide attempt)

Sources

TypeExamples
Agricultural pesticidesParathion, malathion, chlorpyrifos
Nerve agentsSarin, VX, novichok (chemical warfare)
DomesticHousehold insecticides (rare severe toxicity)

Pathophysiology

Mechanism

  1. OP binds and inhibits acetylcholinesterase (AChE)
  2. Acetylcholine accumulates at synapses
  3. Overstimulation of muscarinic, nicotinic, and CNS receptors
  4. "Ageing" — OP-enzyme bond becomes irreversible over time

Receptor Effects

ReceptorLocationEffects
MuscarinicParasympathetic (smooth muscle, glands)SLUDGE, miosis, bradycardia, bronchospasm
Nicotinic (NMJ)Skeletal muscleFasciculations, weakness, paralysis
Nicotinic (ganglia)ANS gangliaTachycardia, hypertension (can confuse picture)
CNSBrainAgitation, confusion, seizures, coma

"Ageing"

  • OP-enzyme bond undergoes chemical change
  • Becomes irreversible after hours-days (depending on OP)
  • Pralidoxime only effective before ageing

Clinical Presentation

Muscarinic Effects — SLUDGE/BBB

MnemonicSymptom
SSalivation
LLacrimation
UUrination
DDefaecation/Diarrhoea
GGI upset
EEmesis
BBronchospasm
BBradycardia
BBronchorrhoea (excessive secretions)

Nicotinic Effects

CNS Effects

Examination Findings

Red Flags

FindingSignificance
Respiratory failureLife-threatening; needs intubation
Severe bronchorrhoeaAtropine urgently needed
Coma/seizuresSevere toxicity
Fasciculations + weaknessNicotinic; may need pralidoxime

Muscle fasciculations
Common presentation.
Weakness
Common presentation.
Paralysis (including respiratory muscles)
Common presentation.
Tachycardia (ganglionic)
Common presentation.
Clinical Examination

Vital Signs

  • Bradycardia (muscarinic) or tachycardia (nicotinic)
  • Hypotension or hypertension
  • Tachypnoea

Eyes

  • Miosis (pinpoint pupils)
  • Lacrimation

Respiratory

  • Bronchospasm
  • Copious secretions
  • Respiratory failure

Neurological

  • Fasciculations
  • Weakness
  • Altered consciousness
  • Seizures

Skin

  • Sweating
  • Odour of pesticide (garlic-like in some OPs)

Investigations

Clinical Diagnosis

  • Primarily clinical (history + cholinergic syndrome)

Cholinesterase Levels

TestNotes
Plasma (butyryl) cholinesteraseRapidly available; correlates with exposure
RBC (acetyl) cholinesteraseMore specific for tissue AChE; slower turnaround

Other Tests

TestPurpose
ABGRespiratory failure assessment
ECGArrhythmias (QT prolongation)
U&E, glucoseBaseline
CXRAspiration, pulmonary oedema

Classification & Staging

By Severity

SeverityFeatures
MildMiosis, excessive secretions, no respiratory compromise
ModerateSLUDGE, fasciculations, mild respiratory distress
SevereRespiratory failure, coma, seizures, cardiovascular collapse

By Agent Type

  • Agricultural pesticides (common, variable toxicity)
  • Nerve agents (highly toxic, rapid onset)

Management

Immediate Resuscitation

ActionDetails
DecontaminationRemove clothing, wash skin with soap and water; protect staff (PPE)
AirwaySuction secretions; intubate early if needed
OxygenHigh flow
IV accessLarge bore

Atropine — Muscarinic Blockade

DosingDetails
Initial dose1-3 mg IV (adults); 0.05 mg/kg (children)
RepeatDouble dose every 5 minutes if no response
EndpointClear chest (dry secretions), HR over 80
MaintenanceInfusion may be needed (0.02-0.08 mg/kg/hr)

Key point: Atropine doses are MUCH higher than usual — may need tens of milligrams

Pralidoxime (Oxime) — AChE Reactivation

DosingDetails
Loading30 mg/kg IV over 20 minutes (max 2g)
Maintenance8-10 mg/kg/hr infusion
DurationContinue for 24-48 hours or until clinically improved

Key point: Most effective if given early (before "ageing"); continue even if late

Other Treatments

TreatmentIndication
BenzodiazepinesSeizures (diazepam, lorazepam)
Avoid succinylcholineProlonged paralysis
Avoid morphine, theophyllineWorsen toxicity
Gastric lavageOnly if very recent ingestion, protected airway
Activated charcoalOnly if within 1 hour

ICU Care

  • Mechanical ventilation if needed
  • Prolonged monitoring (intermediate syndrome may occur days later)

Intermediate Syndrome

  • Occurs 1-4 days after exposure
  • Weakness of respiratory muscles, proximal limbs, neck flexors
  • May need prolonged ventilation

Complications

Acute

  • Respiratory failure
  • Aspiration pneumonia
  • Arrhythmias
  • Seizures
  • Death

Delayed

  • Intermediate syndrome (paralysis days after exposure)
  • Organophosphate-induced delayed neuropathy (OPIDN) — rare

Prognosis & Outcomes

Prognosis

  • Mortality 10-20% with treatment (higher without)
  • Survival depends on early treatment

Factors Affecting Outcome

  • Type and dose of OP
  • Time to treatment
  • Access to ICU care
  • Aspiration/respiratory failure

Evidence & Guidelines

Key Guidelines

  1. WHO Clinical Management of Acute Pesticide Intoxication
  2. TOXBASE (UK National Poisons Information Service)

Key Evidence

  • Atropine is life-saving
  • Role of pralidoxime is debated but recommended in severe cases

Patient & Family Information

What is Organophosphate Poisoning?

Organophosphate poisoning happens when someone is exposed to pesticides or chemicals that affect the nerves. This can happen by swallowing, breathing in, or skin contact.

Symptoms

  • Too much saliva, tears, and sweat
  • Difficulty breathing
  • Muscle twitching
  • Confusion or unconsciousness

Treatment

  • Emergency treatment with specific antidotes
  • May need help breathing with a machine

Prevention

  • Use protective equipment when handling pesticides
  • Store pesticides safely away from children

Resources

  • TOXBASE
  • WHO Pesticide Safety

References

Primary Guidelines

  1. Eddleston M, et al. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597-607. PMID: 17706760

Key Reviews

  1. Jokanovic M, Kosanovic M. Neurotoxic effects in patients poisoned with organophosphorus pesticides. Environ Toxicol Pharmacol. 2010;29(3):195-201. PMID: 21787591
  2. Peter JV, et al. Oximes in organophosphate poisoning. Clin Toxicol. 2007;45(3):312-317. PMID: 17453878

Last updated: 2024-12-21

At a Glance

EvidenceModerate
Last Updated2024-12-21
Emergency Protocol

Red Flags

  • SLUDGE/BBB symptoms
  • Miosis
  • Bradycardia
  • Respiratory distress
  • Reduced consciousness
  • History of pesticide exposure

Clinical Pearls

  • "SLUDGE + miosis + bradycardia = cholinergic toxidrome = OP poisoning"
  • Atropine doses in OP poisoning are MUCH higher than standard doses — titrate to dry secretions
  • Pralidoxime must be given early (before "ageing" of enzyme-OP complex)
  • **Visual assets to be added:**
  • - SLUDGE/BBB mnemonic diagram

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines