Buprenorphine/Naloxone Toxicity Clinical Presentation

Updated: Dec 29, 2015
  • Author: Timothy J Wiegand, MD; Chief Editor: Asim Tarabar, MD  more...
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Presentation

History

See the list below:

  • Pertinent history may be obtained from bystanders, family, friends, or EMS providers. Pill bottles, drug paraphernalia, or eyewitness accounts may assist in the diagnosis.
  • Ingestion time, quantity, and co-ingestants are important aspects of the history and should be ascertained.
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Physical

The clinical effects of the Suboxone preparation depend substantially upon individual patient characteristics and will vary depending on whether the patient is opioid naive, tolerant or dependent, a special vulnerable population (eg, a toddler, a patient with lung disease such as COPD, or dependent on opioids). Clinical effects also vary based on the route of administration of buprenorphine/naloxone combinations and whether the patient has other opioids in his or her system when Suboxone was ingested.

In children younger than 6 years, the most common clinical effects include the following:

  • Lethargy
  • Vomiting
  • Miosis
  • Respiratory depression
  • Agitation
  • Coma

In one retrospective review of 86 children younger than 6 years with exposures to buprenorphine, 54 children were found to develop toxicity. The mean time to onset of clinical effect was 64.2 minutes (range, 20 min to 3 h). Fifty-nine percent of the children experienced clinical effects that lasted between 2 and 8 hours, and 26% of children experienced clinical effects of up to 24 hours in duration. [9] The mean duration of clinical effects in this review is illustrated in the chart below:

Duration of clinical effects in pediatric Suboxone Duration of clinical effects in pediatric Suboxone exposure. Adapted from Pediatrics. Apr 2008;121(4):e782-6.

Specific toxicity:

  • The respiratory effort frequently is impaired in opiate intoxication. Both bradypnea and hypopnea are observed. Rates as slow as 4-6 breaths per minute often are observed with moderate-to-severe intoxication. The body retains the hypoxic drive to breathe but may be overridden by the CNS sedative effects of a severe overdose.
  • Mild peripheral vasodilation may occur and result in orthostatic hypotension. However, persistent or severe hypotension should raise the suspicion of co-ingestants and prompt reevaluation.
  • Opioids prolong GI transit times, possibly causing delayed and prolonged absorption. Initial tendencies for nausea and emesis are transient.
  • Pink frothy sputum, dyspnea, hypoxia, and bronchospasm strongly suggest acute lung injury (ALI).
  • Cardiovascular effects, as well as other clinical findings (ie, sedation, nausea, vomiting, dizziness, sweating, headache) may be similar to full opiate agonists such as morphine. [7]
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Causes

See the list below:

  • Intentional ingestions in attempted suicide
  • Unintentional exposure (illicit or diverted Suboxone source)
  • Unintentional pediatric exposure to Suboxone
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