Agent 15 Poisoning Clinical Presentation

  • Author: Geoffrey M Fitzgerald, MD; Chief Editor: Robert G Darling, MD, FACEP   more...
 
Updated: Mar 13, 2012
 

History

  • The patient may complain of dry mouth, a hot feeling, or blurred vision.
  • Changes in mental status produced by incapacitating agents may leave some patients delirious to the point that they fail to or are unable to report symptoms.
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Physical

Remarkably little variation exists among individuals when anticholinergics are administered.

  • Following exposure, typically a latent period of 30 minutes to 24 hours occurs before signs and symptoms appear.
  • Anticholinergic toxicity caused by BZ or Agent 15 can last up to 3-4 days, depending on the amount of drug absorbed.
  • Peripheral effects usually precede CNS effects and can be summarized by the mnemonic "dry as a bone, hot as Hades, red as a beet, and blind as a bat."
    • "Dry as a bone" results from decreased glandular secretions in the oral pharynx, GI tract, and eccrine and apocrine glands. Urinary retention also is common.
    • "Hot as Hades" refers to hyperthermia caused by decreased sweating.
    • The body attempts to maintain thermoregulation via compensatory cutaneous vasodilatation, hence "red as a beet."
    • Decreased cholinergic stimulation of the pupillary sphincter muscle causes mydriasis. Anticholinergic effects on the ciliary muscles inhibit accommodation, hence "blind as a bat."
    • Anticholinergic effects on the heart produce tachycardia. This occasionally is preceded by a bradycardia that results from anticholinergic effects in the brain stem.
  • The CNS effects of BZ and Agent 15 make them effective incapacitants.
    • Patients receiving these agents react with mental status changes ("mad as a hatter") in a dose-dependent fashion.
    • After a latent period and following the appearance of the peripheral effects, the casualty's mental status begins to fluctuate between a relatively conscious state and frank delirium.
    • Level of consciousness can range from drowsiness to coma.
    • Disorientation to time and place, decreased social restraint with inappropriate behavior, and decreased short-term memory are common.
    • Speech becomes slurred and indistinct.
    • Poor coordination leads to ataxia and agraphia.
    • Anticholinergic toxicity can produce vivid and realistic hallucinations that tend to decrease in size over time. For example, a polar bear may be replaced by a smaller animal such as a rabbit as the toxidrome clears.
    • When multiple victims of anticholinergic toxicity interact, they may play off each other's delirium. An example is 2 victims playing tennis with imaginary racquets. Another term for this shared hallucination is "folie a deux."
    • Phantom behaviors such as plucking or picking at one's clothes (ie, wool gathering) often were observed in Army test subjects who received BZ.
    • As the BZ victim's delirium clears, paranoid tendencies are not uncommon.
  • Of final note on the examination is an increase in deep tendon reflexes. Anticholinergic effects on the Renshaw interneurons in the spinal cord cause hyperreflexia.
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Causes

  • Consider any cause of delirium. Psychiatric disorders such as anxiety reaction also are in the differential diagnosis.
  • The presence of peripheral anticholinergic signs suggests another source of anticholinergic such as scopolamine,[1] atropine, jimsonweed, or other anticholinergic source exposure.
  • Usually, 6-7 MARK-1 Autoinjectors (ie, 12-14 mg of IM atropine) are needed to cause a significant degree of confusion.
  • Nerve agent poisoning can be differentiated by its hyperstimulation of glands.
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Contributor Information and Disclosures
Author

Geoffrey M Fitzgerald, MD  Consulting Staff, Concord Emergency Medical Associates

Disclosure: Nothing to disclose.

Coauthor(s)

David P Sole, DO, FACEP  Associate Director of Emergency Medical Service Programs, Clinical Assistant Professor of Surgery (Emergency Medicine), Department of Emergency Medicine & Residency Program, Geisinger Medical Center

David P Sole, DO, FACEP is a member of the following medical societies: American College of Emergency Physicians and National Association of EMS Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Suzanne White, MD  Medical Director, Regional Poison Control Center at Children's Hospital, Program Director of Medical Toxicology, Associate Professor, Departments of Emergency Medicine and Pediatrics, Wayne State University School of Medicine

Suzanne White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Clinical Toxicology, American College of Epidemiology, American College of Medical Toxicology, American Medical Association, and Michigan State Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Robert G Darling, MD, FACEP  Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

References
  1. Goldfrank L, Flomenbaum N, Lewin N, et al. Anticholinergic poisoning. J Toxicol Clin Toxicol. Mar 1982;19(1):17-25. [Medline].

  2. Bowen TE. Emergency War Surgery. Revisionist Press; 1988:93-94.

  3. Burns MJ, Linden CH, Graudins A, et al. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. Apr 2000;35(4):374-81. [Medline].

  4. Goldfrank LR, Flomenbaum NE. Goldfrank's Toxicologic Emergencies. Appleton & Lange; 1998.

  5. Ketchum JS, Sidell FR. Incapacitating agents. In: Textbook of Military Medicine, Warfare, Weaponry and the Casualty: Medical Aspects of Chemical and Biological Warfare. United States Government Printing Office; 1997:287-306.

  6. Schneir AB, Offerman SR, Ly BT, Davis JM, Baldwin RT, Williams SR, et al. Complications of diagnostic physostigmine administration to emergency department patients. Ann Emerg Med. Jul 2003;42(1):14-9. [Medline].

  7. Shannon M. Toxicology reviews: physostigmine. Pediatr Emerg Care. Jun 1998;14(3):224-6. [Medline].

  8. Tintinalli JE. Anticholinergic toxicity. In: Emergency Medicine: A Comprehensive Study Guide. McGraw Hill; 2000:1182-1185.

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