Organophosphate Poisoning Summary

Pathophysiology

  • Inhibition of acetylcholinesterase
  • Excess acetylcholine at synapses
  • Affects parasympathetic, sympathetic, CNS, and neuromuscular sites

Key Clinical Features

  • DUMBELS: Diarrhea, Urination, Miosis, Bronchorrhea, Emesis, Lacrimation, Salivation
  • Fasciculations
  • Pinpoint pupils
  • Respiratory distress
  • Altered mental status

Diagnostic Approach

  • Therapeutic atropine trial (1-2 mg IV)
  • Plasma cholinesterase levels
  • Clinical presentation
  • History of exposure

Emergency Management

  • Atropine: 2 mg IV, double every 5 min until secretions controlled
  • Decontamination: Immediate clothing removal + dry decontamination
  • Pralidoxime: For severe poisoning (controversial)
  • Airway management and ventilation

Investigations

  • Cholinesterase activity
  • ABG for respiratory failure
  • CXR for aspiration pneumonia
  • ECG for QT prolongation

Decontamination Protocol

  • Remove clothing immediately (within 15-20 min)
  • Dry decontamination first
  • Avoid water initially (wash-in effect)
  • Protect healthcare staff

Complications

  • Respiratory failure
  • Aspiration pneumonia
  • Seizures
  • Delayed neuropathy
  • Intermediate syndrome

Organophosphate Poisoning

Life-threatening poisoning from pesticides or nerve agents requiring immediate intervention

Overview

Poisoning occurs after dermal, respiratory, or oral exposure to either organophosphate pesticides (e.g. chlorpyrifos, dimethoate, malathion, parathion) or nerve agents (e.g. tabun, sarin), causing inhibition of acetylcholinesterase at nerve synapses.

Medical Emergency: Organophosphate poisoning is life-threatening and requires immediate aggressive management. Treatment should not be delayed for confirmatory testing.

Pathophysiology

Organophosphates are used as pesticides in a wide range of settings including agricultural spraying, domestic baits and sprays, termite treatments, and lice and tick products. They may also be used as chemical weapon nerve agents; however, these are different from pesticides in that they have been specifically selected for their unfavourable characteristics.

Mechanism of Action

Primary Mechanism

  • Inhibition of neuronal acetylcholinesterase (AChE)
  • Leads to excessive acetylcholine accumulation
  • Affects multiple sites throughout the body

Systemic Effects

  • Parasympathetic: Excessive secretions, bronchospasm, diarrhea, pinpoint pupils
  • Sympathetic: Hypertension, tachycardia
  • CNS: Seizures, respiratory failure
  • Neuromuscular: Fasciculations, weakness

Time Course

Phase Timing Features
Acute Cholinergic Minutes to hours DUMBELS symptoms, fasciculations, respiratory distress
Intermediate Syndrome 24-96 hours Proximal muscle weakness, respiratory muscle paralysis
Delayed Neuropathy 1-3 weeks Distal sensorimotor neuropathy, permanent disability

Clinical Features

In most cases, diagnosis is based on a history of exposure with characteristic signs of cholinergic excess. A therapeutic trial of atropine should be ordered in all suspected cases or if diagnosis is in doubt, as this is a quick and safe way to confirm diagnosis.

Presentation Spectrum

Mild Exposure

  • Influenza-like syndrome
  • Fatigue, runny nose, headache
  • Dizziness, anorexia, sweating
  • Diarrhea, muscle weakness
  • Nausea and vomiting
  • Visual disturbances, blurred vision

Moderate Exposure

  • All mild symptoms plus:
  • Fasciculations (periorbital, chest, legs)
  • Excessive secretions
  • Pinpoint pupils
  • Bronchospasm, bronchorrhea
  • Incontinence

Severe Exposure

  • All moderate symptoms plus:
  • Seizures
  • Respiratory failure
  • Coma
  • Cardiovascular collapse
  • Hypothermia

DUMBELS Mnemonic

Cholinergic Features

  • D - Diarrhea
  • U - Urination
  • M - Miosis (pinpoint pupils)
  • B - Bronchorrhea
  • E - Emesis
  • L - Lacrimation
  • S - Salivation

Examination Findings

System Findings
Ocular Pinpoint pupils, lacrimation, blurred vision
Respiratory Bronchorrhea, bronchospasm, crackles/rhonchi, respiratory distress
Neurological Fasciculations, increased then decreased reflexes, seizures, coma
Gastrointestinal Salivation, nausea, vomiting, diarrhea, incontinence
Cardiovascular Variable: bradycardia/tachycardia, hypotension/hypertension
Other Distinctive solvent odor, hypothermia, diaphoresis

Investigations

Diagnostic Approach

Therapeutic Atropine Trial

  • 1-2 mg IV atropine as diagnostic test
  • Positive test: No anticholinergic effects seen
  • Negative test: Dry skin, tachycardia, dilated pupils
  • Quickest and most reliable bedside test

Laboratory Tests

  • Plasma cholinesterase (pseudocholinesterase)
  • RBC acetylcholinesterase (more specific)
  • Both typically depressed in poisoning
  • Not reliable for severity assessment

Additional Investigations

Investigation Purpose Findings
Arterial Blood Gas Respiratory failure monitoring Hypoxemia, respiratory acidosis
Chest X-ray Aspiration pneumonia detection Infiltrates, pulmonary edema
ECG Cardiac monitoring QT prolongation, arrhythmias
Basic Metabolic Panel Metabolic status Metabolic acidosis, electrolyte imbalances

Emergency Management

Critical: All patients with suspected significant exposure should be treated presumptively, as treatment needs to be started before test results are returned.

Initial Resuscitation

ABCDE Approach
  1. Airway: Intubation if decreased consciousness or excessive secretions
  2. Breathing: Oxygen, ventilation support, monitor for respiratory failure
  3. Circulation: IV access, fluids, atropine administration
  4. Disability: Neurological assessment, seizure control
  5. Exposure: Decontamination, temperature management

Specific Antidotes

Atropine

  • Initial dose: 2 mg IV
  • Subsequent doses: Double every 5 minutes (4 mg, 8 mg, 16 mg...)
  • Endpoint: Secretions controlled, chest clear
  • Mechanism: Competitive muscarinic antagonist
  • No maximum dose - titrate to effect

Pralidoxime

  • Dose: 30 mg/kg IV loading, then 8 mg/kg/hr infusion
  • Mechanism: Reactivates non-aged AChE-OP complexes
  • Limitations: Ineffective for rapidly aging complexes
  • Evidence: Conflicting, use in severe cases
  • Give within 24-48 hours for maximum effect

Decontamination Protocol

Healthcare Worker Protection: Use appropriate PPE (gloves, gown, eye protection, respiratory protection) during decontamination.

Decontamination Steps
  1. Immediate clothing removal (within 15-20 minutes)
  2. Dry decontamination: Use absorbent materials to blot skin
  3. Start at head/face and work downward
  4. Avoid water initially (prevents wash-in effect)
  5. Wet decontamination only after dry process for hair if contaminated
  6. Double-bag contaminated clothing and materials

Supportive Care

Complication Management
Respiratory Failure Mechanical ventilation, frequent suctioning
Seizures Benzodiazepines (lorazepam, diazepam)
Bronchospasm Bronchodilators (nebulized ipratropium/salbutamol)
Hypotension IV fluids, vasopressors if needed
Arrhythmias Cardiac monitoring, antiarrhythmics

Complications and Prognosis

Acute Complications

Immediate

  • Respiratory failure
  • Aspiration pneumonia
  • Cardiovascular collapse
  • Status epilepticus
  • Cardiac arrest

Delayed

  • Intermediate syndrome (24-96 hours)
  • Organophosphate-induced delayed neuropathy (1-3 weeks)
  • Chronic neurological sequelae
  • Psychological effects

Prognostic Factors

  • Poor prognosis: Coma on admission, respiratory failure, hypotension, need for large atropine doses
  • Better prognosis: Early presentation, rapid decontamination, prompt atropinization
  • Mortality ranges from 10-40% depending on severity and timeliness of treatment

Long-term Follow-up

  • Monitor for delayed neuropathy (weeks after exposure)
  • Psychological support for intentional ingestions
  • Occupational health referral for occupational exposures
  • Regular neurological assessments