CBRNE - Opioids/Benzodiazepines Poisoning Clinical Presentation

Updated: Oct 21, 2021
  • Author: Christopher P Holstege, MD; Chief Editor: Zygmunt F Dembek, PhD, MS, MPH, LHD  more...
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Presentation

History

An event involving an opioid or benzodiazepine aerosolized incapacitating agent is likely to create confusion and panic, cause multiple serious injuries or fatalities, and necessitate a major emergency medical service, police, and/or military response.

  • Large numbers of casualties could overwhelm any community's emergency response services.
  • Chaos might occur following such an event.
  • In the early phases of an emergency response, the agent would probably be unknown, and the history might be misleading and inaccurate.
  • Physical examination is the key to identifying the causative agent.
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Physical Examination

Following exposure to an aerosolized opioid or benzodiazepine incapacitating agent, the presentation would be a syndrome consistent with opioid or benzodiazepine toxicity, respectively. These syndromes can vary depending on the opioid or benzodiazepine agent used. In addition, findings may vary depending on the patient's preexisting medical problems, the treatment(s) provided by first responders, and the potential complications of the intoxication. For example, if hypoxic brain injury occurs, the patient may have fixed dilated pupils rather than the miosis that is characteristic of an opioid syndrome.

In opioid intoxication, the following features may be present:

  • Central nervous system depression manifesting as fatigue, somnolence, ataxia, and/or coma.

  • Miosis -  Of note, intoxication with the opioids meperidine and propoxyphene (withdrawn from the US market) does not typically cause miosis, and normal pupillary size is regularly maintained; however, neither of these agents have been associated with aerosolization. Miosis may be limited by preexisting medical conditions such as a history of previous cataract surgery. Mydriasis may occur in patients with severe toxicity because of anoxic brain injury.

  • Cardiovascular manifestations of opioid toxicity may include hypotension secondary to arteriolar and venous dilation. Both tachycardia (secondary to hypotension or hypoxia) and bradycardia (secondary to a reduction of direct central nervous system stimulation) may be observed. If hypoventilation becomes prominent, hypoxia-induced cardiac arrhythmias may occur.

In benzodiazepine intoxication, the following features may be present:

  • Respiratory depression manifesting as hypoventilation, apnea, and airway occlusion
  • Central nervous system depression manifesting as drowsiness, somnolence, ataxia, nystagmus, and/or coma
  • Cardiovascular manifestations, including hypotension, tachycardia, bradycardia, and hypoxia-induced cardiac arrhythmias
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