3-Quinuclidinyl Benzilate Poisoning Medication

Updated: Feb 22, 2021
  • Author: Christopher P Holstege, MD; Chief Editor: Duane C Caneva, MD, MSc  more...
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Medication Summary

No specific antidote has been found to reverse the action of QNB definitively. Peripherally acting anticholinesterase drugs that do not cross the blood-brain barrier (eg, pyridostigmine, neostigmine, pilocarpine) are ineffective against the central effects of QNB. [2]

Physostigmine does cross the blood-brain barrier and can be used to reverse the effects of anticholinergic agents. Use of physostigmine in QNB poisoning has been studied. [3]  However, its efficacy in QNB intoxication and its adverse effect potential have not been delineated definitively. A number of other compounds have been considered for treatment, including 7-methoxytacrine, which was one of the most widely investigated potential antidotes for QNB. [2]  

Supportive care is the mainstay of therapy. The patient is at risk for injuries from erratic, agitated behavior. QNB casualties may act on their delusions, so they must be kept safe from harming themselves or others. [2]  If the exposed patient is markedly agitated, consider administration of a benzodiazepine to calm. 

QNB poisoned patients are also at risk for hyperthermia, especially in hot and/or humid environments.  This significant complication arises due to the suppression of the ability to secrete sweat, which, along with agitation and warm ambient temperatures, can give rise to fatal hyperthermia. [3] Management of heat stress assumes a high priority in patients poisoned with QNB, including appropriate rehydration. 




Class Summary

Consider in patients sustaining exposure to QNB and presenting with marked agitation.

Diazepam (Valium, Diastat)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Induces sedation and helps cease seizure activity.


Antidote, anticholinergic agents

Class Summary

These agents prolong the central and peripheral effects of acetylcholine.


Inhibits destruction of acetylcholine by acetylcholinesterase, which facilitates transmission of impulses across myoneural junction.