3-Quinuclidinyl Benzilate Poisoning Clinical Presentation

  • Author: Christopher P Holstege, MD; Chief Editor: Robert G Darling, MD, FACEP   more...
 
Updated: Mar 16, 2010
 

History

  • An event involving QNB probably would create confusion, panic, multiple seriously ill or dead victims, and a major emergency medical service, police, and/or military response.
    • Large numbers of casualties would overwhelm any community's emergency response.
    • Chaos appropriately would describe events following such an event.
    • In the early phases of an emergency response, the toxin's identification would be unknown, and the history would be misleading and inaccurate.
  • Physical examination is the key to diagnosing the causative agent.
Next

Physical

After exposure to QNB, the physical examination is consistent with an anticholinergic syndrome. Characteristics of the anticholinergic syndrome have long been taught using the old medical adage, "dry as a bone, blind as a bat, red as a beet, hot as a hare, and mad as a hatter."

  • Central nervous system
    • Depending on the dose and time postexposure, a number of CNS effects may manifest. Restlessness, apprehension, abnormal speech, confusion, agitation, tremor, picking movements, ataxia, stupor, and coma are described.
    • Hallucinations are prominent, and they may be benign, entertaining, or terrifying to the patient experiencing them. Exposed patients may have conversations with hallucinated figures, and/or they may misidentify persons they typically know well.
    • Simple tasks typically performed well by the exposed person may become difficult. Motor coordination, perception, cognition, and new memory formation are altered as CNS muscarinic receptors are inhibited.
  • Peripheral nervous system
    • Eye: Mydriasis resulting in photophobia is expected. Impairment of near vision occurs because of loss of accommodation and reduced depth of field secondary to ciliary muscle paralysis and pupillary enlargement. If QNB is splashed into the eye, conjunctival injection and eye pain also occur.
    • Cardiovascular system: Tachycardia is a prominent feature of QNB exposure. Heart rates may be rapid but rarely exceed 150 beats per minute. Exacerbated heart rate responses to exertion also are expected. Systolic and diastolic blood pressure may show moderate elevation. A decrease in capillary tone may cause skin flushing.
    • Gastrointestinal: Intestinal motility slows, and secretions from the stomach, pancreas, and gallbladder decrease. Nausea and vomiting may occur. Decreased or absent bowel sounds are noted on examination.
    • Respiratory: All glandular cells become inhibited, and dry mucus membranes of the mouth and throat are noted. Speech may decrease to a whisper. Breath of the exposed patient may develop a foul odor.
    • Skin: Inhibition of sweating results in dry skin. Place hands directly into the axilla of the exposed patient and note the absence of moisture. Red flushed skin also may occur.
    • Urinary: Urination is difficult or impossible. Subsequent urinary retention may occur, and an enlarged bladder may be palpable on examination.
    • Temperature: The exposed patient's temperature may become elevated from the inability to sweat and dissipate heat. In warm climates such as the desert, this may result in marked hyperthermia.
Previous
Next

Causes

Human QNB exposures rarely are reported. Potential causes of exposure to this agent are a laboratory accident, a terrorist event, or a military conflict.

Previous
Proceed to Differential Diagnoses
 
 
Contributor Information and Disclosures
Author

Christopher P Holstege, MD  Associate Professor of Emergency Medicine and Pediatrics, University of Virginia; Director, Division of Medical Toxicology, Center of Clinical Toxicology; Medical Director, Blue Ridge Poison Ctr, Associate Medical Toxicology Fellowship Director, VA Dept of Health

Christopher P Holstege, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, European Association of Poisons Centres and Clinical Toxicologists, Medical Society of Virginia, Society for Academic Emergency Medicine, Society of Toxicology, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Jennifer S Boyle, MD, PharmD  Fellow in Toxicology, University of Virginia Health System

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  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Rick Kulkarni, MD 

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. Hay A. Surviving the impossible: the long march from Srebrenica. An investigation of the possible use of chemical warfare agents. Med Confl Surviv. Apr-Jun 1998;14(2):120-55. [Medline].

  2. US Army Center for Health Promotion and Preventive Medicine. Psychodelic Agent 3 - Quinuclidinyl Benzilate (BZ). The Deputy for Technical Services' Publication: Detailed Chemical Facts Sheets. 1998;[Full Text].

  3. Byrd GD, Paule RC, Sander LC, et al. Determination of 3-quinuclidinyl benzilate (QNB) and its major metabolites in urine by isotope dilution gas chromatography/mass spectrometry. J Anal Toxicol. May-Jun 1992;16(3):182-7. [Medline].

  4. Gibson RE, Rzeszotarski WJ, Jagoda EM, et al. [125I] 3-quinuclidinyl 4-iodobenzilate: a high affinity, high specific activity radioligand for the M1 and M2-acetylcholine receptors. Life Sci. Jun 4 1984;34(23):2287-96. [Medline].

  5. Glendenning KK. Distribution of muscimol, QNB, and 5HT binding in the vertebrate diencephalon: a comparative study of eight mammals and three non-mammals. Microsc Res Tech. Oct 15 2003;62(3):247-61. [Medline].

  6. Hiramatsu Y, Eckelman WC, Baum BJ. Interaction of iodinated quinuclidinyl benzilate enantiomers with M3 muscarinic receptors. Life Sci. 1994;54(23):1777-83. [Medline].

  7. Holstege CP, Bechtel LK, Reilly TH, Wispelwey BP, Dobmeier SG. Unusual but potential agents of terrorists. Emerg Med Clin North Am. May 2007;25(2):549-66; abstract xi. [Medline].

  8. Hull LA, Rosenblatt DH, Epstein J. 3-Quinuclidinyl benzilate hydrolysis in dilute aqueous solution. J Pharm Sci. Jul 1979;68(7):856-9. [Medline].

  9. J R Army Med Corps. Chemical casualties. Centrally acting incapacitants. J R Army Med Corps. Dec 2002;148(4):388-91. [Medline].

  10. Ketchum JS, Sidell FR. Incapacitating agents. In: Textbook of Military Medicine. 1997:287-305.

  11. McDonough JH Jr, Shih TM. A study of the N-methyl-D-aspartate antagonistic properties of anticholinergic drugs. Pharmacol Biochem Behav. Jun-Jul 1995;51(2-3):249-53. [Medline].

  12. Sorger D, Kampfer I, Schliebs R. Iodo-QNB cortical binding and brain perfusion: effects of a cholinergic basal forebrain lesion in the rat. Nucl Med Biol. Jan 1999;26(1):9-16. [Medline].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.