Organophosphate poisoning

Organophosphate poisoning


  • Organophosphate compounds can be commonly found in insecticides and are associated with systemic illness.
  • Mortality is higher in developing countries where organophosphate pesticides are more commonly available.
  • Organophosphorus poisoning can result from occupational, accidental, or intentional exposure.
  • Its use as a suicidal agent is frequent.
  • The primary cause of death in acute organophosphate poisoning is bradyasystolic arrest from respiratory failure.


Organophosphate compounds bind irreversibly to acetylcholinesterase inactivating the enzyme through the process of phosphorylation and acetylcholine at nerve synapses and neuromuscular junctions. Thus, it results in overstimulation of acetylcholine receptors.

Clinical presentation

Here are a few mnemonics for the Muscarinic Effects of Cholinesterase Inhibition: SLUDGE, DUMBELS, and Killer B’s (Figure 1 & 2).

Killer B's
  • Out of four distinct syndromes that can occur from organophosphate poisoning, the first two are clinically important in emergency setting 1. Acute poisoning, 2.intermediate syndrome, 3.chronic toxicity, and 4.organophosphate induced delayed neuropathy. Of these syndromes, the intermediate syndrome is the most feared one as it presents with paralysis of the neck’s flexor muscles, muscles innervated by the cranial nerves, proximal limb muscles, and respiratory muscles. It occurs up to 40% of poisonings within 1 to 5 days of initial symptoms.
  • Acute organophosphate poisoning can present with differing severities. Mild poisonings generally present with symptoms like lightheadedness, nausea, headache, dyspnea, lacrimation, rhinorrhea, salivation, and diaphoresis while moderate poisonings cause autonomic instability, confusion, vomiting, muscle spasms, bronchorrhea and bronchospasm. Coma, seizures, flaccid paralysis, urinary and fecal incontinence, and respiratory arrest may occur in the course of severe poisonings.
  • Diagnosis is based on history (people may bring bottles/substance itself) in the presence of a suggestive toxidrome. Cholinesterase assays and reference laboratory testing for specific compounds may confirm the diagnosis but take time and have limitations. Treatment should be started without delay based on the clinical findings.
  • Miosis (papillary constriction) and muscle fasciculation are the most reliable signs of organophosphate toxicity and help in diagnosis.


  • The first step of the treatment is decontamination. Healthcare workers must wear protective equipment to avoid secondary poisoning. The patient should be decontaminated with ample water and soap preferably before arriving in a hospital or once stable. Water should be disposed of as hazardous waste.
  • In addition to decontamination, treatment consists of airway control, intensive respiratory support, general supportive measures, prevention of absorption, and the administration of antidotes.
  • The patient should be monitored continuously and provided 100% oxygen. Gastric lavage and activated charcoal are not recommended.
  • A non-depolarizing agent should be used when the neuromuscular blockade is needed during intubation since succinylcholine is metabolized by plasma butyrylcholinesterase, and therefore, may prolong paralysis.
  • The specific agents are atropine and Atropine can be given repeatedly every 5 minutes until tracheobronchial secretions attenuate (1-3 mg IV in adults or 0.01-0.04 mg/kg IV in children – never <0.1 mg per dose). Then, a continuous infusion should be started to maintain the anticholinergic state (0.4-4 mg/h in adults).
  • Pralidoxime is the single most important treatment for the nicotinic effect of organophosphate poisoning and is life-saving for intermediate syndrome if used within 48 hours (First dose: 1-2 g in adults or 20-40 mg/kg – up to 1 g – in children, mixed with NS and infused over 5-10 min, continuous infusion: 500 mg/h in adults or 5-10 mg/kg/h in children)
  • Seizures can be treated with benzodiazepines.

Disposition and follow-up

  • Minimal exposures may require only decontamination and 6 to 8 hours of observation in the ED to detect delayed effects.
  • Admission to the intensive care unit is necessary for significant poisonings.
  • Most patients respond to pralidoxime therapy with an increase in acetylcholinesterase levels within 48 hours.
  • The endpoint of therapy is the absence of signs and symptoms after withholding pralidoxime therapy.
  • Death from organophosphate poisoning usually occurs in 24 hours in untreated patients, usually from respiratory failure secondary to paralysis of respiratory muscles, neurologic depression, or bronchorrhea.

References and Further Reading

  1. Burillo-Putze, G. & Xarau S. N. “Pesticides. Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, editors. Tintinalli’s emergency medicine: a comprehensive study guide 8th ed.” (2016): 1318-25.
  2. Katz K. D. & Brooks D. E. “Organophosphate Toxicity Treatment & Management” Medscape, Dec 31, 2020, Accessed Feb 05, 2021.
Cite this article as: Temesgen Beyene, Ethiopia, "Organophosphate poisoning," in International Emergency Medicine Education Project, March 29, 2021,, date accessed: December 2, 2023

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