Organophosphate Poisoning
Description
Organophosphate (OP) poisoning occurs due to ingestion, inhalation, or dermal exposure to organophosphate compounds, which are commonly used as pesticides, insecticides, or nerve agents. Exposure can be:
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Intentional: Parasuicide, self-harm
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Accidental: Farmers, pesticide handlers
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Homicidal or warfare-related
Organophosphates irreversibly inhibit acetylcholinesterase, leading to excessive acetylcholine accumulation at muscarinic, nicotinic, and central nervous system receptors, resulting in a cholinergic crisis.
Carbamates, in contrast, inhibit acetylcholinesterase reversibly and usually cause a shorter duration of toxicity.
Common Sources
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Agricultural insecticides, herbicides, fungicides
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Fertilizers
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Livestock dipping agents
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Shampoos for lice
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Nerve agents (warfare)
Pathophysiology
Excess acetylcholine stimulates:
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Muscarinic receptors: bronchorrhea, bradycardia, miosis, vomiting, salivation, urination, lacrimation
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Nicotinic receptors: muscle fasciculations, weakness, paralysis, hypertension, tachycardia
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CNS effects: confusion, agitation, seizures, coma
Signs and Symptoms
Muscarinic (DUMBBBELS)
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Diarrhea
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Urination
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Miosis (constricted pupils)
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Bronchorrhea
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Bradycardia
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Bronchospasm
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Emesis (vomiting)
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Lacrimation
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Salivation
Nicotinic
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Muscle fasciculations
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Weakness or paralysis
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Tachycardia
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Hypertension
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Anxiety, seizures, coma
CNS / Other
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Confusion, agitation, altered mental status
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Hypoglycemia
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Hypotension
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Type 2 respiratory failure (hypercapnic)
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Intermediate syndrome (proximal muscle weakness, neck flexor weakness, respiratory compromise after 24–96 hours)
Investigations
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Baseline labs: FBC, U&Es, creatinine, LFTs, RBS
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Toxicology: Blood and urine organophosphate levels
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Enzyme assays: Serum or red-cell cholinesterase activity
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ABG: Evaluate respiratory compromise and acid-base status
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Other supportive investigations as clinically indicated
Management
1. Airway and Breathing
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Ensure airway patency
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Oxygen therapy and escalation as needed
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Suction secretions if present
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Mechanical ventilation if respiratory failure
2. Circulation
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Insert 2 large-bore IV lines
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Obtain blood for investigations
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Administer crystalloids for resuscitation and maintenance
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Monitor BP, HR, perfusion
3. Disability / Neurologic Status
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Assess GCS
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Monitor for seizures (manage per seizure protocol)
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Correct hypoglycemia
4. Decontamination
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Remove contaminated clothing
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Wash skin thoroughly with soap and water
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Eye irrigation if ocular exposure
5. Antidotal Therapy
a. Atropine (Muscarinic Antagonist)
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Initial dose: 1–2 mg IV, double every 5 minutes until atropinization endpoint (clearing of bronchial secretions, improvement of oxygenation, resolution of bronchospasm)
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Maintenance infusion: 20% of total atropinization dose over 24 hours
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Monitor for atropine toxicity: confusion, extreme tachycardia, blurred vision, fever, ileus, urinary retention
b. Pralidoxime (2-PAM, Cholinesterase Reactivator)
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Loading dose: 30 mg/kg IV over 20 minutes
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Continuous infusion: 8 mg/kg/hour (max 12 g/day)
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Effective mainly if given early (before “aging” of acetylcholinesterase)
6. Supportive Care
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Mechanical ventilation for respiratory failure
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Correct electrolyte imbalances
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Treat secondary infections (aspiration pneumonia)
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Monitor urine output
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ICU / HDU admission often required
Complications
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Aspiration pneumonitis or pneumonia
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Hypoxic organ injury
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Shock
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Intermediate syndrome (muscle weakness, respiratory compromise)
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Organophosphate-induced delayed polyneuropathy (OPIDP)
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Chronic organophosphate-induced neuropsychiatric disorder (COPIND)
Referral Criteria
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All cases of acute poisoning, even asymptomatic exposures
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Type 2 respiratory failure requiring mechanical ventilation
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Intermediate syndrome
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Persistent cholinergic symptoms despite antidotal therapy
Key Points
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Early recognition and rapid initiation of antidotes (atropine + pralidoxime) save lives.
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Supportive care, especially for airway and respiratory failure, is critical.
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Continuous monitoring in ICU is required for at least 24 hours, often longer.
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Consider psychosocial evaluation for intentional ingestion cases.