Astute triage results in a good outcome.
- Organophosphate poisoning is a life-threatening condition caused primarily by occupational exposure in agricultural environments.
- It remains a potentially fatal condition due to its capacity to cause respiratory compromise, paralysis, and excessive secretions.
- Timely identification, accurate diagnosis, and rapid implementation of appropriate treatment protocols are essential.
CRAIG BIVENS*, A 32-YEAR-OLD man with no significant past medical history, experiences acute shortness of breath, lacrimation (watery eyes), and upper extremity fasciculations (twitching) while working in a soybean field. A coworker drives him to the local ED.
History and assessment
Mr. Bivens informs Laura, the ED triage nurse, that he was working in a field recently sprayed with pesticides. Recognizing that the patient’s symptoms might connect to organophosphate poisoning, Laura isolates him, activates the hospital’s emergency response team to begin decontamination, dons PPE, and notifies the attending physician. The team decontaminates Mr. Bivens with copious amounts of water for 15 minutes.
After decontamination, Laura obtains Mr. Bivens’ vital signs: temperature 36.3° C (97.7° F), HR 50 bpm, RR 32 breaths per minute, BP 78/38 mmHg, and O2 88% on room air. She notes the patient’s worsening shortness of breath, rhinorrhea and lacrimation, and bilateral arm and leg fasciculations.
Taking action
Cardiac and continuous pulse oximetry are initiated. Further assessment notes profound shortness of breath and declining O2 saturation despite supplemental O2 at 15 L/min via non-rebreather. A STAT CBC, chemistry panel, arterial blood gas, red blood cell acetylcholinesterase (AChE), plasma butyrylcholinesterase (BChE), and plasma pseudocholinesterase (PChE) are obtained. At the direction of the ED physician, Laura administers atropine sulfate (muscarinic antagonist) 2 mg I.V. for its anticholinergic effect with pralidoxime (cholinesterase reactivator) 2 g I.V., diazepam 2 mg I.V. for fasciculations, and a 1-L 0.9% normal saline bolus. The patient’s deficient AChE, BChE, and PChE levels confirm organophosphate poisoning.
Outcome
Mr. Bivens’ respiratory status improves after treatment. He is monitored overnight in the ICU, receives two additional doses of atropine with continued improvement, is transferred to intermediate care due to risk of delayed symptoms, and is discharged after 5 days with close primary care follow-up.
Education and follow-up
Organophosphate poisoning, a potentially life-threatening condition, results primarily from unintentional occupational exposure in agricultural environments. An estimated three million poisonings per year occur worldwide.
Organophosphate substances exert toxic effects by irreversibly inhibiting acetylcholinesterase at the synaptic cleft, leading to the accumulation of acetylcholine. This causes overstimulation of nicotinic and muscarinic receptors, producing a range of cholinergic symptoms. Exposure typically occurs through dermal contact, although it can also occur via inhalation, ingestion, or injection. (See Organophosphate poisoning and next steps)
Organophosphate poisoning and next steps
The severity of organophosphate poisoning symptoms depends on the dose and duration of exposure. High-dose acute exposures can result in a mortality rate between 12% and 25%, with rates approaching 50% for patients requiring mechanical ventilation. In many such cases, patients may not survive long enough to reach definitive medical care, as symptoms can progress rapidly to life-threatening complications. Less severe cases may mimic a flu-like syndrome and not initially attributed to organophosphate exposure.
Symptoms of intermediate syndrome, a complication that arises in approximately 40% of patients 1 to 5 days after exposure, include weakness of the neck flexors, cranial nerve-innervated muscles, proximal limb muscles, and respiratory muscles. Notably, it occurs in the absence of ongoing cholinergic signs and frequently resolves within 1 to 2 weeks. Residual effects are uncommon.
Readiness aids prompt treatment
Organophosphate poisoning remains a potentially fatal condition. Laboratory results are rarely available in time to influence clinical decision-making. Therefore, timely identification, accurate diagnosis, and rapid implementation of appropriate treatment protocols are essential. In Mr. Bivens’ case, Laura’s astute triage assessment and prompt administration of antidotes contributed significantly to his recovery.
Next steps
Healthcare facilities, particularly in rural areas, should assess their readiness to respond to organophosphate poisonings by consulting with emergency management or pharmacy leadership regarding the availability and location of organophosphate antidotes. In the United States, ChemPaks from the federal antidote stockpile and emergency kits such as Mark-1 or DuoDote auto-injectors should be easily accessible for immediate use in suspected cases of organophosphate poisoning. Frontline clinical staff may benefit from routine training and drills.
*Names are fictitious
Aaron Sebach is dean and professor in the College of Nursing and Health Sciences at Wilmington University in New Castle, Delaware, and EMS Nurse Practitioner at TidalHealth in Salisbury, Maryland. Charles Dolan is vice president of clinical operations and chief safety officer at TidalHealth.
American Nurse Journal. 2026; 21(3). Doi: 10.51256/ANJ032648
References
Bereda G. Poisoning by organophosphate pesticides: A case report. Cureus. 2022;14(10):e29842. doi:10.7759/cureus.29842
Escobar D, Geib AJ. ToxCard: Acute organophosphate toxicity. emDocs. June 7, 2023. emdocs.net/toxcard-acute-organophosphate-toxicity/
Environmental Protection Agency. Chapter 5: Organophosphate insecticides. epa.gov/sites/default/files/documents/rmpp_6thed_ch5_organophosphates.pdf
Robb EL, Regina AC, Baker MB. Organophosphate toxicity. StatPearls. November 12, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470430/
Key words: organophosphate poisoning, rapid response, occupational exposure
