Pharmacologic Management of Pain, Including Opioid and Non-Opioid Therapy
Match the drug to the mechanism and the patient
Non-opioid therapy is foundational. Acetaminophen is useful but has a ceiling and hepatotoxicity risk with excess alcohol or liver disease. NSAIDs relieve inflammatory and nociceptive pain but carry gastrointestinal, renal, and cardiovascular risk; avoid in CKD, heart failure, and after GI bleeding, and use topical NSAIDs for localized osteoarthritis when oral risk is high. Duloxetine and other SNRIs treat neuropathic and centralized pain and improve function; gabapentinoids help neuropathic pain but require renal dose adjustment and carry misuse and sedation risk. Tricyclics are effective at low doses but anticholinergic and cardiac effects limit use in older adults. Opioids have a narrow role in chronic noncancer pain: select patients, set functional goals, use the lowest effective dose, co-prescribe naloxone, check the PDMP, and reassess. Buprenorphine is a reasonable option and a treatment for opioid use disorder.
Traps are common: using meperidine for chronic pain (neurotoxic metabolite), codeine or tramadol without considering CYP2D6 variability and serotonergic risk, combining opioids with benzodiazepines, and escalating opioids for sedation or dysphoria rather than function. Distinguish tolerance (needing more for effect) from opioid-induced hyperalgesia (worsening pain with escalation) and from addiction (compulsive use despite harm). Withdrawal is not addiction.
Worked example: a 72-year-old with stage 4 CKD and knee osteoarthritis. Avoid oral NSAIDs; start acetaminophen and topical diclofenac; consider duloxetine; if gabapentin is used, reduce the dose for renal function; avoid codeine and morphine metabolites.
Rule of thumb: start low, go slow, and titrate to function - not to a zero pain score.