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0487 Chronic Buprenorphine-Induced Central Sleep Apnea and Desaturation
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Abstract
Introduction
Individuals on opioids are found dead in bed and respiratory depression is a potential cause. In contrast to other opioids, buprenorphine, is a partial μ-opioid receptor agonist and it has been suggested to have reduced respiratory depression with a ceiling threshold. However, death has also been reported in individuals using buprenorphine; yet, it is not known if chronic use of buprenorphine causes significant respiratory depression. The purpose of this study was to determine, if chronic use of buprenorphine is associated with sleep disordered breathing
Methods
A retrospective study of 11 consecutive patients who were using buprenorphine chronically were referred for evaluation suffering from snoring and daytime sleepiness. All underwent full night polysomnography which was scored page by page by a sleep specialist, according to standard criteria set by the American Academy of Sleep medicine.
Results
Two patterns of breathing were observed First, four of the 11 patients had significant CSA with an average of 13/h of sleep. This pattern was ataxic, similar to other opioids. Those with CSA, compared to those without CSA, suffered from severe sleep apnea (AHI, 35 vs.9/ hour of sleep), which was associated with a significantly low nadir of saturation (75% vs. 87%). Second, the group without CSA, in spite of a low AHI, had significantly more sustained desaturation and were on a relatively higher dose of buprenorphine (8.7 vs.5.2 mg/day).
Conclusion
This is the first study to report chronic use of buprenorphine is associated with sleep-disordered breathing. We observed two specific patterns. A subset with CSA and most severe sleep apnea and very low saturation. Second, buprenorphine was associated with sustained nocturnal hypoxemia, potentially related to hypoventilation. These disordered breathing events could be a potential cause of buprenorphine-associated death reported in the literature.
Support (if any)
none
Title: 0487 Chronic Buprenorphine-Induced Central Sleep Apnea and Desaturation
Description:
Abstract
Introduction
Individuals on opioids are found dead in bed and respiratory depression is a potential cause.
In contrast to other opioids, buprenorphine, is a partial μ-opioid receptor agonist and it has been suggested to have reduced respiratory depression with a ceiling threshold.
However, death has also been reported in individuals using buprenorphine; yet, it is not known if chronic use of buprenorphine causes significant respiratory depression.
The purpose of this study was to determine, if chronic use of buprenorphine is associated with sleep disordered breathing
Methods
A retrospective study of 11 consecutive patients who were using buprenorphine chronically were referred for evaluation suffering from snoring and daytime sleepiness.
All underwent full night polysomnography which was scored page by page by a sleep specialist, according to standard criteria set by the American Academy of Sleep medicine.
Results
Two patterns of breathing were observed First, four of the 11 patients had significant CSA with an average of 13/h of sleep.
This pattern was ataxic, similar to other opioids.
Those with CSA, compared to those without CSA, suffered from severe sleep apnea (AHI, 35 vs.
9/ hour of sleep), which was associated with a significantly low nadir of saturation (75% vs.
87%).
Second, the group without CSA, in spite of a low AHI, had significantly more sustained desaturation and were on a relatively higher dose of buprenorphine (8.
7 vs.
5.
2 mg/day).
Conclusion
This is the first study to report chronic use of buprenorphine is associated with sleep-disordered breathing.
We observed two specific patterns.
A subset with CSA and most severe sleep apnea and very low saturation.
Second, buprenorphine was associated with sustained nocturnal hypoxemia, potentially related to hypoventilation.
These disordered breathing events could be a potential cause of buprenorphine-associated death reported in the literature.
Support (if any)
none.
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