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Pediatric Organophosphates Toxicity Treatment & Management

  • Author: William Freudenthal, MD; Chief Editor: Timothy E Corden, MD  more...
 
Updated: Sep 07, 2015
 

Medical Care

Prehospital care

Prehospital care includes the following:

  • Ensure airway support and ventilation and perform endotracheal intubation, if necessary, in patients with respiratory failure.
  • Circulatory support with intravenous (IV) access, fluids, and cardiac and pulse oximetry monitoring can facilitate safe transport.
  • Decontamination is of the utmost importance in minimizing continued exposure and to protect providers and other patients from contamination. Decontamination involves removing all of the patient's clothing and washing him or her with water and soap.
  • By describing the scene, prevalent odors, or other casualties, prehospital providers may provide important clues to the presence of exposure.

Emergency department care

Assess the patient's airway, breathing, and circulation (ABCs). Secure the airway and perform cardiovascular resuscitation if needed. Endotracheal intubation may be necessary for airway protection and ventilatory support.

If the patient's condition is stable, decontamination is the next priority. Patients who are inadequately decontaminated may expose rescue personnel and hospital staff to the toxin. Prehospital providers may also need decontamination. The dermal decontamination of exposed individuals is a priority before they enter the emergency department, where they can contaminate other patients and staff members. Gastric decontamination with activated charcoal should be performed in cases of ingestion.

Severe exposures require expeditious anticholinergic therapy. Atropine antagonizes the central and muscarinic effects by blocking these receptors. Atropine does not bind to nicotinic receptors; hence, muscular weakness, including respiratory muscle weakness, is not affected.

Anticholinergic agents should be used in doses large enough to reverse the cholinergic signs. Some authors recommend giving atropine until signs of atropinization appears. These signs include warm, dry, flushed skin; dilated pupils; and an increased heart rate.

Atropine should be used for at least 24 hours to reverse the cholinergic signs while the organophosphate is metabolized. Atropine is indicated when evidence of bronchorrhea and other secretions is present.

Pralidoxime (2-PAM) is a cholinesterase reactivator and the antidote for organophosphate poisoning. Administer 2-PAM to patients with organophosphate exposure and signs of muscle and respiratory muscle weakness. This drug primarily affects the nicotinic receptors and does not reverse the CNS effects. Administer 2-PAM as soon as possible because its effectiveness decreases with prolonged exposure due to the aging of the organophosphate-cholinesterase bond.[13] Administer 2-PAM as an IV infusion after a loading dose until signs of weakness improve.

Treat seizures that do not respond to 2-PAM with benzodiazepines. In experimental models, midazolam effectively terminates seizures caused by organophosphates; however, the efficacy of benzodiazepines decreases when these drugs are given 30 minutes or more after organophosphate exposure or seizure onset.[14]

In a child with acute, severe organophosphate poisoning that was unresponsive to standard treatments, Yesilbas and colleagues reported successful treatment with high-volume continuous venovenous hemodiafiltration and therapeutic plasma exchange combined with lipid infusion.[15]

Avoid the use of morphine, caffeine, loop diuretics, theophylline, and succinylcholine in patients with organophosphate poisoning because these drugs can increase the toxicity of the exposure.

Next

Consultations

See the list below:

  • Consult a medical toxicologist or poison control center personnel early in the course of treatment.
  • Consult a critical care specialist early in severe poisonings for ongoing care outside the emergency department.
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Contributor Information and Disclosures
Author

William Freudenthal, MD Staff Physician, Department of Emergency Medicine, St. Vincent Hospital Indianapolis, IN

William Freudenthal, MD is a member of the following medical societies: American College of Emergency Physicians, Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Coauthor(s)

Mark E Ralston, MD, MPH Staff Pediatrician, Naval Hospital Oak Harbor; Assistant Professor of Pediatrics, F Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences

Mark E Ralston, MD, MPH is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Received salary from Merck for employment.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

Michael E Mullins, MD Assistant Professor, Division of Emergency Medicine, Washington University in St Louis School of Medicine; Attending Physician, Emergency Department, Barnes-Jewish Hospital

Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians

Disclosure: Received stock ownership from Johnson & Johnson for none; Received stock ownership from Savient Pharmaceuticals for none.

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