Conditions · Emergency medicine and toxicology

Organophosphate and carbamate poisoning !

Poisoning by common insecticides that block an enzyme in nerves, flooding the body with acetylcholine. It can stop breathing and is often intentional.

Updated 2026-11-01

Structures involved

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Why it happens

What it is

Poisoning by insecticides that inhibit acetylcholinesterase, so acetylcholine builds up at nerve endings and produces the cholinergic toxidrome. Organophosphates bind the enzyme almost permanently; carbamates bind reversibly and usually cause shorter illness.

Who gets it

Pesticide self-poisoning is a major cause of suicide deaths in rural low- and middle-income countries. In Colombian surveillance (INS, 2008–2015), insecticides were the pesticides most often involved, mainly organophosphates and carbamates; most cases were men of working age, and more than half had suicidal intent.

Causes

Intentional ingestion (self-harm) of agricultural insecticides
Occupational exposure through skin or inhalation during spraying or mixing
Accidental ingestion by children or from food or containers contaminated with pesticide
Nerve agents act by the same mechanism

Risk factors

Agricultural work and easy access to pesticides at home
Depression, alcohol use and previous self-harm
Spraying without protective equipment
Storing pesticides in unlabelled drink bottles

Pathophysiology

Inhibited acetylcholinesterase cannot break down acetylcholine, which overstimulates muscarinic receptors (glands, smooth muscle, heart), nicotinic receptors (skeletal muscle, autonomic ganglia) and the central nervous system. Organophosphate-enzyme complexes undergo 'ageing', after which oximes can no longer reactivate the enzyme. Death usually comes from respiratory failure caused by bronchorrhoea, bronchospasm, respiratory muscle weakness and central depression.

Classification

Acute cholinergic crisis (minutes to hours)
Intermediate syndrome (about 1–4 days): weakness of neck flexors, proximal limb and respiratory muscles
Organophosphate-induced delayed polyneuropathy (weeks later)

Symptoms and signs

Muscarinic: salivation, tearing, sweating, bronchorrhoea, wheeze, vomiting, diarrhoea, urinary incontinence
Miosis (pinpoint pupils) and blurred vision
Bradycardia and hypotension (tachycardia can also occur from nicotinic effects)
Nicotinic: muscle fasciculations, cramps and weakness progressing to paralysis
Central: anxiety, confusion, seizures and coma
Garlic- or solvent-like smell of the breath or clothing

Diagnosis

Clinical: Diagnosis is clinical: exposure history (container, smell) plus the cholinergic toxidrome; improvement with antimuscarinic treatment supports it. Treatment never waits for laboratory confirmation.
Tests: Red blood cell acetylcholinesterase (more specific) and plasma butyrylcholinesterase activity; arterial blood gases, glucose, electrolytes, ECG for bradycardia and QT prolongation, and screening for co-ingestants such as alcohol.
Imaging: Chest X-ray for aspiration pneumonia or pulmonary oedema.

Differential diagnosis

Opioid overdose (miosis and coma, but dry secretions)
Nicotine or cholinergic mushroom poisoning
Paraquat or other pesticide poisoning
Acute asthma or pulmonary oedema
Guillain-Barré syndrome or myasthenic crisis for the later weakness

Goal of treatment

Secure breathing, reverse muscarinic effects until the chest is dry, reactivate acetylcholinesterase when possible, stop seizures, limit further absorption and protect staff.

Treatment

Acute: Staff wear protective equipment; contaminated clothing is removed and skin washed with soap and water. Airway and breathing are supported, with early intubation when needed (succinylcholine is avoided because its action is prolonged).
Medical: Atropine (an antimuscarinic) given intravenously and repeated, titrated to clear bronchial secretions, adequate heart rate and blood pressure, not to pupil size.
Medical: Oximes such as pralidoxime may reactivate the enzyme in organophosphate poisoning if started before ageing; benzodiazepines for seizures and agitation.
Follow-up: Close monitoring of secretions, oxygen saturation, neck-flexion strength and ventilation for several days because of the intermediate syndrome; psychiatric assessment after intentional poisoning.

Drugs for this condition

Atropine

Complications

Respiratory failure and aspiration pneumonia
Intermediate syndrome needing prolonged ventilation
Arrhythmias including QT prolongation
Delayed polyneuropathy
Atropine excess (agitation, hyperthermia, tachycardia)
Death, especially after large intentional ingestions

Prognosis

Mortality depends on the compound, amount and speed of care; it is highest in intentional ingestions of highly toxic organophosphates. Carbamate poisoning is usually shorter. Survivors may have weakness or neuropathy for weeks.

Prevention

Restricting highly hazardous pesticides and safe, locked storage
Protective equipment and training for agricultural workers
Detection and treatment of depression and suicide risk in rural communities

Test yourself

Think of the answer, then tap the question to see it.

What enzyme do organophosphates and carbamates inhibit?

Acetylcholinesterase, causing acetylcholine to accumulate at muscarinic, nicotinic and central synapses.

What is the clinical endpoint for titrating atropine in organophosphate poisoning?

Drying of bronchial secretions with clear lungs and adequate heart rate and blood pressure, not pupil size.

Why are oximes given early in organophosphate poisoning?

They reactivate acetylcholinesterase only before the enzyme-poison complex 'ages' and becomes permanent.

What is the intermediate syndrome?

Weakness of neck flexors, proximal limb and respiratory muscles 1–4 days after exposure, which can cause late respiratory failure.

Which nursing priority protects staff when receiving a pesticide-poisoned patient?

Personal protective equipment and decontamination: removing clothing and washing the skin before or during resuscitation.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Insecticide poisoning (MedlinePlus, US National Library of Medicine, 2026); Comportamiento epidemiológico de los casos de intoxicaciones por plaguicidas en Colombia, 2008 - 2015 (Instituto Nacional de Salud (Colombia), Informe Quincenal Epidemiológico Nacional (IQEN), 2017).

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Main bronchi highlighted on the Durgical 3D model