Abstract
Opioid-induced hyperalgesia (OIH) occurs when opioids paradoxically enhance the pain they are prescribed to ameliorate. To address a lack of perioperative awareness, we present an educational review of clinically relevant aspects of the disorder. Although the mechanisms of OIH are thought to primarily involve medullary descending pathways, it is likely multifactorial with several relevant therapeutic targets. We provide a suggested clinical definition and directions for clinical differentiation of OIH from other diagnoses, as this may be confusing but is germane to appropriate management. Finally, we discuss prevention including patient education and analgesic management choices. As prevention may serve as the best treatment, patient risk factors, opioid mitigation, and both pharmacologic and non-pharmacologic strategies are discussed.
Lay abstract
Opioid-induced hyperalgesia (OIH) occurs when opioid medications worsen rather than decrease pain. We present an educational review of the disorder. Although mechanisms of OIH are thought to primarily start in the brain or brainstem before traveling through the spinal cord to the area of pain in the body, there are likely many causes. We provide a suggested clinical definition and a pathway for clinical differentiation of OIH from other diagnoses to help with management. Finally, we discuss prevention including patient education and medication management choices. As prevention may serve as the best treatment, patient risk factors for OIH, decreased opioid use, and both medication and non-medication strategies are discussed.
Tweetable abstract
Opioid-induced hyperalgesia occurs when opioids worsen pain. Our review provides a clinical definition and pathway for differentiation from other diagnoses. Screening, patient education, and medication management choices offer opportunities for prevention.
Author contributions
SH Wilson, KM Hellman, and A Chandrakantan participated in the manuscript design. SH Wilson, KM Hellman, D James, AC Adler, and A Chandrakantan participated in manuscript creation. All authors contributed to literature search and interpretation, and manuscript drafting and revision. All authors have approved the final manuscript and agree to be accountable for the integrity of the article.
Acknowledgments
We would like to thank S Darnell for her editorial assistance.
Financial & competing interests disclosure
KM Hellman is supported by NIH grant R01HD098193. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.