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  1. 2 points
    Attached are some very recent articles referencing the use of buprenorphine for pain. They are at the expert opinion level but from reputable sources. Also, some text referencing buprenorphine for pain in the Official Disability Guidelines and the HHS Pain Management Task Force Report ====================================================== ODG Pain (updated 7/26/2019) Buprenorphine for chronic pain Recommended as an option for treatment of chronic pain (consensus based) in selected patients (not first-line for all patients). See also Buprenorphine for treatment of opioid dependence. Suggested populations: (1) Patients with a hyperalgesic component to pain; (2) Patients with centrally mediated pain; (3) Patients with neuropathic pain; (4) Patients at high-risk of non-adherence with standard opioid maintenance; (5) For analgesia in patients who have previously been detoxified from other high-dose opioids. Use for pain with formulations other than Butrans is off-label. Due to complexity of induction and treatment the drug should be reserved for use by clinicians with experience. Drug description: Buprenorphine is a schedule-III controlled substance. Its mechanism of action is complex, involving four different opioid receptors at central and peripheral sites. It is primarily classified as a partial mu-agonist and kappa antagonist. It blocks effects of subsequently administered opioid agonists. Proposed advantages of treatment: (1) An apparent antihyperalgesic effect (partially due to the effect at the kappa-receptor); (2) Ability to suppress opioid withdrawal; (3) Indications of safety for use in patients with renal impairment. There appears to be a ceiling effect for respiratory depression. (Johnson, 2005) (Kopper-t, 2005) (Pergolizzi, 2008) (Malinoff, 2005) (Landau, 2007) (Kress, 2008) (Heit, 2008) (Helm, 2008) (Silverman, 2009) (Pergolizzi, 2010) (Lee, 2011) (Rosenblum, 2012) (Daitch, 2012) (Colson, 2012) See also Opioid hyperalgesia. Treatment of chronic pain: A waiver is not required for the off-label use of sublingual buprenorphine for the treatment of pain. An X should NOT be put before the DEA number. It is recommended that the words, Chronic Pain Patient and Off-Label Use be written on the prescription. The most common use of buprenorphine formulations other than Butrans (such as Suboxone) for the treatment of chronic pain is for individuals who have a history of opioid addiction. Use in opioid-experienced patient: There is the potential for buprenorphine to precipitate withdrawal in opioid-experienced patients. ======================================================== PAIN MANAGEMENT BEST PRACTICES INTER-AGENCY TASK FORCE REPORT Updates, Gaps, Inconsistencies, and Recommendations PAIN MANAGEMENT FINAL REPORT Buprenorphine, an opioid medication that the FDA has approved for clinical use, is a partial agonist at the mu opioid receptor and therefore has a reduced potential for respiratory depression; it is thus safer than full agonists such as morphine, hydrocodone, and oxycodone.120,121 Buprenorphine also acts as an antagonist at the kappa receptor, an effect shown in experimental studies to reduce anxiety, depression, and the unpleasantness of opioid withdrawal. Buprenorphine is widely used and encouraged for treating patients with OUD and is approved for the treatment of pain. In some states, there is a significant challenge, however, for prescribing clinicians to get authorization for using buprenorphine for chronic pain management (see Section 2.2: Medication, Gap 4 and Recommendations). GAP 4: Barriers include lack of coverage and reimbursement for buprenorphine as well as the lack of education and training on the proper usage of buprenorphine. There has been a lack of access to buprenorphine treatment for chronic pain.143 • RECOMMENDATION 4A: Make buprenorphine treatment for chronic pain available for specific groups of patients, and include buprenorphine in third-party payer and hospital formularies. • RECOMMENDATION 4B: Encourage CMS and private payers to provide coverage and reimbursement for buprenorphine treatment, both for OUD and for chronic pain. Encourage primary use of buprenorphine rather than use only after failure of standard mu agonist opioids such as hydrocodone or fentanyl, if clinically indicated. • RECOMMENDATION 4C: Encourage clinical trials using buprenorphine for chronic pain to better understand indication, usage, and dosage. ----------------------------------------------- 2.5.2 Patients With Chronic Pain as well as Mental Health and Substance Use Comorbidities GAPS AND RECOMMENDATIONS GAP 1: CBPs for chronic pain do not adequately address how to treat individuals with comorbid psychological health concerns. • RECOMMENDATION 1A: Screen for psychological health and SUDs in patients with acute or chronic pain, and consider early referral to behavioral health providers when clinically indicated. • RECOMMENDATION 1B: Use an integrated multidisciplinary approach that may include existing evidence-based psychological and behavioral interventions (e.g., CBT, coping skills, stress reduction, mindfulness-oriented recovery) to address chronic pain when clinically indicated. • RECOMMENDATION 1C: Refer patients to both pain and addiction specialists when OUD is suspected, and ensure an integrative approach to health care. • RECOMMENDATION 1D: Buprenorphine may be considered appropriate for pain treatment in this population when clinically indicated. • RECOMMENDATION 1E: When considering buprenorphine and other opioids, use the lowest effective dose in conjunction with non-opioid treatment modalities, with enhanced monitoring and collaboration with addiction specialists. Conduct regular reevaluation and assessment, with a treatment plan and established goals, to achieve optimal patient outcomes. Webster - Bup for Pain.pdf Yale_bup.pdf Rethinking Opioid Dose Tapering.pdf
  2. 2 points
    Matt, I do not think any of the protocols are supported by evidence so you should use it as a guideline and go with your judgement following patient's response. Some initial questions? Why is the pt on tid methadone? is it used for pain? How much time you have for transition? It can be accomplished inpatient over 3-4 days or 2-4 weeks outpatient. I would first transition to once daily dose and give it 1 week to settle. If stable, and the patient is otherwise fine to tolerate transition (eg., no opioids, no heavy Benzos/alcohol use, no active psychiatric sxs etc) you can either drop methadone to 50 and 40 at weekly intervals or just go directly to 40 mg. I would start using adjunctive medications targeting withdrawal symptoms early in the process to prevent/minimize withdrawal. Do you think that continuing methadone while you titrate BUP is clinically important? It would take at least week, and most anecdotal evidence is with short-acting agonists, not clear how this would apply to methadone. I would stop methadone, increase adjunctive meds to treat emerging symptoms, and start titrating BUP with small initial doses around 24 hours after stopping methadone, e.g. start with 0.25 mg and double every 3 hr or so until you get to 16 mg, so 48 hrs later, you will have switched the patient to BUP with little with likely little withdrawal.
  3. 1 point
    Welcome to the PCSS Forums!
  4. 1 point
    #1. Dosing of gabapentanoids should be tid or qid. Half life ~ 6 hours. There are now 2 long acting gabapentins and a long acting pregabalin formulations. These are more expensive and would probably require a prior authorization. Concerns over misuse of gabapentanoids should be managed in a similar paradigm as misuse of other medications. Urine testing would require sending to lab as I don't know of a point of care immunoassay for gabapentanoids. #2. I don't have any informed advice on the suicide issue as it relates to gabapentanoids. #3. I presented a study comparing lorazepam to gabapentin in an outpatient alcohol withdrawal study(attached). I do not believe there have been publications specifically addressing prevention of seizures in the alcohol withdrawal syndrome. Benzodiazepines remain the first line drug class in treating alcohol withdrawal. Alcohol_Withdrawal_Acute_Myrick.pdf
  5. 1 point
    Hello, This sounds like it may have been a urine gabapentin test (Quest ref range < 1000 ng/mL) versus a serum gabapentin test (result peak ranges 2.7 - 4.1 mcg/mL and 4.0 - 8.5 mcg/mL for single vs multiple doses of 900 - 1800 mg/day). If the urine specimen tested was very concentrated, this would cause a higher ng/mL result. Unless you're just looking for the unexpected/expected presence of gabapentin, a serum gabapentin test would be the better one to order for a more accurate level. I hope this is helpful to someone if not the original poster.
  6. 1 point
    Yes Matt, I missed that it is for a pain patient, I assume everything is OUD 🙂 Your diagram/handout looks great, and is consistent with the concept/published anecdotal evidence. However there is likely to be individual variability so that the protocol should emphasize flexibility and the possibility that there will be some withdrawal during the transision. Why do you think that for higher MED you would need higher dose patch? I would be tempted to stay with the lower dose for all cases, or go lower dose day 1-2 and then switch to higher one? Also, I would also start slower on Day the with 1mg and go up only if you confirm the tolerability. In any case this is really to be worked out depending on the patient response but it would be great to publish a larger case series with the method
  7. 1 point
    Buprenorphine is a very strong pain medicine. People with OUD tend to have much higher dosage needs than those with chronic pain without OUD. In my opinion, Bupe is a safer opioid for the majority of chronic pain patients on opioids (but it's still an opioid so don't give it to opioid naive pain patients). It's difficult to come up with conversions between the forms. See this table from Gudin's Pain Ther https://doi.org/10.1007/s40122-019-00143-6 A Butrans 20mcg/hour patch is 1/4 of a 2mg buprenorphine for total mg, but how much is absorbed is confusing, and there are case reports of transitioning people on staggering doses of opioids using just a 20mcg/hr patch so it's deceivingly powerful. See Saal & Lee's case series on using Butrans to start patients on bupe from full agonists. https://doi.org/10.7812/TPP/19.124 I'd suggest only using Butrans as a bridge from full agonists to sublingual bupe (because buccal bupe FDA approved for pain is not obtainable for many patients) for those in the MED 30-120 range. though expert opinion and case series is the best evidence we have for this now
  8. 1 point
    A related clinical situation would be that of a low-dose chronic pain patient who has tested positive for an substance such as THC or non-prescribed medication and has been deemed to be too high risk to continue chronic pain management with traditional opioids. The risk may be to the patient or to the prescriber. This recent article Understanding Buprenorphine for Use in Chronic Pain: Expert Opinion includes the following as possible reasons one could consider the use of buprenorphine for pain. Concern from health care providers regarding prescription of a Schedule II opioid due to risk of addiction, misuse, and/or overdose death A patient is receiving immediate-release treatment and would benefit from a longer-acting analgesic with a relatively favorable safety profile and Schedule III classification It would not be unusual for a patient to minimize any difficulties they may be having with their short-acting opioid regimen and for family and friends to be more aware of the behavioral problems. I would suspect that there is more of a problem than what the patient is willing to admit to given that they agreed to see you. A longer-acting analgesic may reduce the problems seen with the highs and lows of opioid effect such as cognitive efffects immediately after dosing and the relative withdrawal feeling prior to the next dose. In this instance, due to the low daily dose, the buprenorphine formulations typically used for pain, Butrans or Belbuca, may be more appropriate as a patient on 22.5 MME/day would likely require less than 2mg of buprenorphine SL per day.
  9. 1 point
    The usual rules would apply, in that the patient has to be off of all full agonists for a sufficient period of time to have withdrawal symptoms. This varies among patients, and certainly in an elderly patient, presumably with slower metabolism the wait time may be longer. I would most certainly initiate at low dose and go slowly. My question is what the clinical circumstances are that suggest that there is a problem with the fairly modest dose of morphine ER (40 mg daily). Is the patient being solely treated for pain? Is there an actual opiate use disorder? Is the patient offering the desire to get off of the morphine? If the latter is the case it may be more practical (and avoid withdrawal induction issues) to slowly taper the morphine itself. Dr. Shore
  10. 1 point
  11. 1 point
    Hi Anthony, Whether NPs need to be supervised by a X-waivered physician actually depends on which state you practice within. In CA, the CPCA (http://www.cpca.org/CPCA/CPCA/HEALTH_CENTER_RESOURCES/Value_Based_Care/Behavioral_Health.aspx) has provided the following guidance, which is attached: If you need to find X-waivered providers in your state, you can apply to the PCSS mentorship program to be matched with a waivered provider who may be able to assist with identifying a physician in your area who could assist. Otherwise, you can check out the SAMHSA provider locator website to see if you recognize any providers: http://www.samhsa.gov/medication-assisted-treatment/practitioner-program-data/treatment-practitioner-locator. CA also has a state specific list of providers here: http://choosemat.org MAT FAQ_Final_11.20(1).pdf
  12. 1 point
    I didn’t find a specific requirement under the original DATA 2000 legislation regarding coverage, but below included more recent guidance from SAMHSA. SAMHSA’s Treatment Improvement Protocol (TIP 63), Medications for Opioid Use Disorders (2018), states: “On-call services and backup during absences should be available either directly or through contracts or cooperative agreements with other local providers with waivers. Qualified medical staff can offer routine medical and psychiatric coverage even without a buprenorphine waiver.” In some instances, having a local contract or cooperative agreement with a waivered clinician might not be feasible, such as in smaller practices or potentially rural settings such as yours. Local urgent care or emergency departments might suffice, even if direct linkage to a waivered prescriber would be preferable. Such interpretation is supported by SAMHSA’s recent regulation for defining Qualified Practice Setting when setting regulations that allow an increase in the prescribing limit to 275 patients: https://www.deadiversion.usdoj.gov/pubs/docs/SAMHSA_Regulations_275.pdf: "Subpart F—Qualified Practice Setting (§ 8.615) HHS proposed § 8.615 to describe the necessary elements of a qualified practice setting, which can include practices with as few as one waivered provider as long as these criteria are met, and can include both private practices and community-based clinics. Necessary elements of a qualified practice setting would include: (1) The ability to offer patients professional coverage for medical emergencies during hours when the practitioner’s practice is closed; this does not need to involve another waivered practitioner, only that coverage be available for patients experiencing an emergency even when the office is closed." A discussion with a regional mentor could be beneficial for strategizing about your behavioral health program. Perhaps there would be a way to integrate into the existing system and develop a shared after-hours coverage plan.
  13. 1 point
    From the clinical description you provide, this patient should now be considered a pain patient with a history of OUD. Hospice and palliative care patients have always been excluded from the standard guidelines such as the CDC guidelines I would recommend stopping the buprenorphine (switching formulations will not result in better pain management) and starting full opioid agonist therapy for end of life pain management. If you are comfortable with using methadone for pain, I would agree it is an excellent choice. You do not need to taper the Bupe prior to starting the methadone--there is often confusion about precipitated withdrawal in this scenario--but precipitated withdrawal only occurs in the other direction--adding Bupe to someone on regular full opioid agonist analgesics. Since the Bupe has a higher affinity and slower dissociation from the mu receptor than methadone, it will temporarily block the full effect of methadone. As the Bupe is metabolized and excreted the methadone will have increasing efficacy.. With methadone it is always judicious to start low and titrate up slowly. You could also consider adding a high potency short acting opioid, such as hydromorphone, to manage the pain until you reach adequate doses of methadone. The methadone should be dosed either QID or Q6H to maximize analgesic benefit.
  14. 1 point
    Obviously sleep is important for all human beings, and there are many causes for sleep disruption that can affect patients with opioid use disorder beyond opioid withdrawal effects on sleep. If all other withdrawal symptoms have resolved, and insomnia remains an issue, it makes sense to consider other potential treatments for insomnia because an increase in morning methadone dose is unlikely to address the insomnia. The optimum treatment is cognitive-behavioral therapy for insomnia (CBT-I) which can be delivered by a therapist or accessed online. If pharmacologic interventions are being considered, it is obviously best to avoid benzodiazepines and Z-drugs such as zolpidem. Other alternatives include melatonin, orexin receptor antagonists like suvorexant, trazodone, and hydroxyzine among others. If a patient is on a "high" dose of methadone and still having withdrawal symptoms, this situation is one that calls for obtaining peak and trough methadone serum levels to determine if the patient is a rapid metabolizer. The peak level is obtained 3-4 hours after the methadone dose, and the trough level is obtained just prior to receiving the methadone 24 hours after the last dose. If the peak to trough ratio is greater than 2, the patient is likely and rapid metabolizer and may require split dosing in order to stabilize. We do not have enough information about methadone and sleep to answer that question with certainty. We do know that all human brains undergo important repair functions during sleep so it makes sense that the same idea applies to patients receiving methadone.
  15. 1 point
    Hello, I am a new PMHNP working on a newly formed addiction consult team for inpatient in Massachusetts
  16. 1 point
    Full transparency - I'm not a pain expert, just a PCP with a waiver who has moved a handful of persistent pain patients over to bup. I think the MED equivalents you propose seem like a good starting point, but I've also been struck by how variable their needs are. I suspect that it just emphasizes that most patients don't fall neatly into the OUD vs. Pain bucket, but live somewhere in between. I also find that I can let patients figure out what works for them, they are pretty good about backing off if it's too much. I don't see the >90 as a limit, and actually think those are the folks where I sleep better at night knowing they are safer on bup than whatever full agonist regimen they were on, and they seem to do really well. I moved an elderly, wheelchair-bound lady off of 100mcg of Fentanyl (240 MED), and she is doing great on 2/0.5 mg Subox TID... Another lady in her 70s who had been up to 140mg oxycodone daily, self-weaned to 70mg (still 105 MED) before she transitioned over, and she is now on 4mg subox QID doing awesome, feels mentally clearer and has "100% better pain control" (her words) than she ever did on her prior regimen, even at 140mg. (and no- I didn't get either of them to those previous opiate doses ) I recognize that this is anecdotal, don't have a great evidence-based answer, but these cases highlight the variability I have run into.
  17. 1 point
    Hello mentor Matt (I'm your PCSS mentee out in Okanogan County)! That handout is great and for better or worse my brain just thinks in edits. So here's a version with my minor suggestions for further smoothing readability while maintaining the lower reading level. Sorry if this is an annoying thing to do! Your handout info is great KM suggestions_BupforChronicPainPatientHandout.docx
  18. 1 point
    Welcome to the Forums. If you would like to arrange a mentor through PCSS, please complete our form and we will match you up with one of our clinical experts: https://pcssnow.org/mentoring/find-a-mentor/
  19. 1 point
    Also, in LA County, we use the attached expected practice for smoking cessation (with variable levels of adherence from PCPs in our county system of care). Appendix B in this document has a medication summary that may be helpful. Brian Addiction Medicine - Treatment of Smoking and Tobacco-Related Product Use Expected Practice.pdf
  20. 1 point
    Yes, see attached for a handout a few of us used awhile back - I use it all the time for PCP MI trainings, and it was initially developed by Carla Marienfeld at UCSD (with a few edits my myself, Mike Flaum, and Petros Levounis). Feel free to use with attribution. I support the hypothesis that smoking cessation comfort correlates with comfort with addiction treatment in general (OUD an otherwise). UCSF has a great front-and-back summary of the smoking cessation meds: https://rxforchange.ucsf.edu/file_downloads/A9 PRODUCTS.pdf Brian MI Course Handout IPS Oct 2015.docx
  21. 1 point
    Welcome! I recommend going into each forum such as "Buprenorphine" and clicking the Follow button in the upper right corner. That way you'll get emails when new topics are posted.
  22. 1 point
    Hi my name is Jill Bryant. I am a nurse practitioner in a small clinic located in Williamsburg Ky. I have recently obtained my waiver and plan to begin a MAT program. We have a huge population of substance abuse disorder and I am looking forward to providing treatment.
  23. 1 point
    I agree that there is an association between higher doses and a greater risk of OD, but I would like to add that OD Risk is an accumulation of factors including medical and psychiatric co-morbidities, history of substance use disorder, and polypharmacy/polysubstance. In a study by Glanz and colleagues dose alone did not predict an overdose event (Glanz et al. J Gen Intern Med. 2018 Oct;33(10):1646-1653.) and many factors play a role. We have to carefully weigh the risks and benefits in patients receiving opioid medications and treat them individually. I have seen to many patients being harmed by forced and involuntary tapers and abandonment. Yes, we need to take a multimodal approach to treating chronic pain and use opioids cautiously and more appropriately, but it is complicated treating and managing risks of patients on long term opioids for chronic pain.
  24. 1 point
    Oxycodone 10 mg four times per day is 60 MME so 16-24 mg of bup per day sounds somewhat high, to me, as a target dose. There are no real established guidelines about how to transition patients from Schedule 2 opioids for pain, however, this is something that I do on a daily basis in my practice. What I would do is stop the oxycodone for 12 to 24 hours. Then bup/nalox 2mg tab or film 1/2 sl bid for two days; 1/2 sl tid for 2 days; then 1/2 sl qid after that. Target dose of 4 mg per day. My general formula for this kind of conversion is 1 mg bup for every 10 MME MINUS 30-50% for incomplete cross tolerance. Something I still have a hard time comprehending is the incredible gab between pain management dosing of buprenorphine which is usually less than 2 mg per day and dosing for OUD at up to 24 mg per day.
  25. 1 point
    I often print this article for patients in brochure form and hand it to patients (attached PDF). It's two sheets of paper folded in half to make a six-page booklet. https://www.verywellhealth.com/buprenorphine-for-chronic-pain-management-4156472 Using Buprenorphine for Chronic Pain Management Is buprenorphine the future of chronic pain treatment? By Naveed Saleh, MD, MS Updated May 22, 2018 At face value, the opioid crisis and chronic pain are directly opposed. Although the CDC points out that “evidence on long-term opioid therapy for chronic pain outside of end-of-life care remains limited, with insufficient evidence to determine long-term benefits versus no opioid therapy,” the fact remains that opioids are the principal intervention for the treatment of chronic pain. Although primary care providers can prescribe opioids for chronic pain, they are reluctant to do so for fear of patient overdose or dependence. Most primary care physicians find the prospect of giving patients opioids for a long period of time too stressful and quickly refer these patients to pain specialists. Despite reluctance to treat it, chronic pain is becoming increasingly frequent. In 2010, 31 percent of Americans experienced chronic pain, which is defined as pain lasting more than three to six months. Because the vast majority of people with chronic pain present to primary care physicians, it would be a breakthrough if we had some safe and effective alternative to opioids—some medication that these physicians would feel comfortable prescribing. A medication called buprenorphine may someday help fit this bill. What Is Buprenorphine? Buprenorphine belongs to a class of drugs called opioid partial agonist-antagonists. In addition to another drug which combines buprenorphine and naloxone (Suboxone), buprenorphine is used as opioid substitution therapy to treat opioid dependence (dependence on heroin or prescription narcotics). These drugs work by preventing withdrawal symptoms when a person who is dependent on opioids stops taking opioids. Buprenorphine is a semisynthetic opioid derivative of the opium alkaloid thebaine, which is found in the opium poppy (Papaver somniferum). It actually took decades for researchers to synthesize the drug, and there were many failed attempts before an English pharmaceutical company finally made it in 1966. By 1978, an intravenous formulation of buprenorphine was introduced, followed by a sublingual (applied under the tongue) iteration in 1982. In 1985, buprenorphine was introduced in the United States as an opioid analgesic. How It Works Buprenorphine has very specific mechanisms of action that make it enviable not only for treating opioid dependence but possibly chronic pain, too. First, buprenorphine has a high binding affinity for the μ-opioid receptor, which is responsible for pain relief. Moreover, buprenorphine has a slow rate of dissociation from the μ-opioid receptor, meaning that it stays attached longer to the receptor, and has prolonged effect. Second, although buprenorphine likes the μ-opioid receptor quite a bit, it acts only as a partial μ-opioid receptor agonist, which means that while buprenorphine prevents opioid withdrawal, its actions are less potent than opioids. Third, buprenorphine is a full κ-opioid receptor antagonist. Activation of the κ-opioid receptor results in the euphoric and psychotic effects of opioids. In other words, buprenorphine won’t make you “high.” Administration As mentioned earlier, naloxone is often combined with buprenorphine in the form of Suboxone. Naloxone is a short-acting, opioid receptor antagonist. When combined in low doses with buprenorphine, naloxone can counteract dangerous opioid side effects—including respiratory depression, sedation, and hypotension—without diminishing analgesia, or pain relief. Furthermore, the addition of naloxone to buprenorphine serves as a deterrent to substance abuse. According to the NIH: "Buprenorphine comes as a sublingual tablet. The combination of buprenorphine and naloxone comes as a sublingual tablet (Zubsolv) and as a sublingual film (Suboxone) to take under the tongue and as a buccal [cheek] film (Bunavail) to apply between the gum and cheek." Buprenorphine also comes in a transdermal patch, intravenous formulation, and, most recently, a sublingual spray. In December 2017, it was announced that the FDA was reviewing the new sublingual spray for treatment of acute pain. Side Effects Although not nearly as dangerous as opioids, both buprenorphine and Suboxone can have negative side effects including the following: Back pain Blurred vision Constipation Difficulty with sleep Mouth numbness Headache Stomach pain Tongue pain More serious side effects, such as difficulty breathing or swelling of the mouth or tongue, require immediate medical attention. Importantly, mixing buprenorphine with other drugs like benzodiazepines can be lethal. Buprenorphine for Chronic Pain In a systematic review published in December 2017, Aiyer and co-authors examined the efficacy of buprenorphine for the management of chronic pain. The researchers analyzed 25 randomized controlled trials involving five buprenorphine formulations: Intravenous buprenorphine Sublingual buprenorphine Sublingual buprenorphine/naloxone (Suboxone) Buccal buprenorphine Transdermal buprenorphine Overall, the researchers found that 14 of 25 studies suggested that buprenorphine in any formulation was effective for the treatment of chronic pain. More specifically, 10 of 15 studies showed that transdermal buprenorphine was effective, and two of three studies showed that buccal buprenorphine was effective. Only one of six studies indicated that either sublingual or intravenous buprenorphine was effective for the treatment of chronic pain. Importantly, no serious adverse effects were reported in any of the studies, which indicates that buprenorphine is safe. In 2014, Cote and co-authors published a systematic review examining the efficacy of sublingual buprenorphine for the treatment of chronic pain. Although the majority of studies they analyzed were observational and low-quality, the researchers did find that sublingual buprenorphine was effective at treating chronic pain. Notably, Cote and co-authors compiled the following list of potential benefits of buprenorphine: Increased efficacy in neuropathic pain due to its unique pharmacological profile. Ease of use in the elderly and in renal impairment due to its minimal effect on half-life and metabolites. Less immunosuppression compared with morphine and fentanyl based on very limited evidence from preclinical and clinical work. Ceiling effect for respiratory depression when used without other central nervous system depressants, perhaps because the intrinsic activity to produce analgesia may be less than that of respiratory depression. Less effect on hypogonadism, as demonstrated in maintenance therapy. Less development of tolerance, possibly through kappa receptor antagonism or opioid-receptor-like (ORL-1) agonism. Antihyperalgesic effect, perhaps due to kappa receptor antagonism or ORL-1 agonism. Antidepressant effect in patients unresponsive to conventional therapy. Interestingly, it’s hypothesized that because of its binding properties, buprenorphine may be able to help people who experience opioid-induced hyperalgesia. In an article titled “A comprehensive review of opioid-induced hyperalgesia,” Lee and co-authors opioid-induced hyperlagesia as the following: "Opioid-induced hyperalgesia (OIH) is defined as a state of nociceptive sensitization caused by exposure to opioids. The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli. The type of pain experienced might be the same as the underlying pain or might be different from the original underlying pain. OIH appears to be a distinct, definable, and characteristic phenomenon that could explain loss of opioid efficacy in some patients." Of note, nociceptive pain is the sharp pain resulting from damage to a body part. It’s hypothesized that buprenorphine has antinociceptive properties. In a 2014 article published in Anesthesiology, Chen and co-authors write the following: "Buprenorphine has been shown to reverse hyperalgesia induced by opioids through ‘buprenorphine-induced antinociception.’ Moreover, buprenorphine is a κ-receptor antagonist and can compete with the effect of spinal dynorphin, an endogenous κ-receptor agonist. Because spinal dynorphin is increased after opioid exposure and contributes to OIH, this competitive effect of buprenorphine on the κ-receptor binding site may decrease the effect of spinal dynorphin resulting in the decreased OIH." Prescribing Buprenorphine To a limited extent, in the United States, buprenorphine is already being used to treat chronic pain. Suboxone is prescribed off-label for the treatment of chronic pain. Furthermore, the transdermal buprenorphine patch is available for the treatment of severe chronic pain in the United States. However, there is no consensus opinion with regard to the efficacy of using buprenorphine for this purpose. Currently, the few studies examining the effect of buprenorphine on chronic pain are too disparate in their approaches, and are thus too difficult to compare with one another. Before the prescription of buprenorphine for the treatment of chronic pain becomes an evidence-based practice, various issues would need to be resolved. For example, current studies use a variety of pain rating scales when evaluating efficacy thus providing an inconsistent analysis. Pain rating scales in studies examining buprenorphine would need to be standardized. Furthermore, dosing strategies and route of administration would need to be examined for different presentations of chronic pain. If the prescription of buprenorphine for chronic pain were ever to become evidence-based, primary care physicians would ostensibly be primed for this practice. In 2000, the U.S. Drug Addiction Treatment Act made it legal for primary care physicians to provide opioid substitution therapy using Schedule III, IV, and V drugs. In 2002, the FDA approved out-patient treatment with buprenorphine, characterizing it as a Schedule III drug. All that a primary care physician needs to do to be able to prescribe buprenorphine in an out-patient setting is to complete eight hours of training. Nevertheless, few primary care providers have become eligible to prescribe buprenorphine. Although many primary care physicians would likely bristle at the suggestion, it wouldn’t be that big of a stretch to think that primary care physicians could someday treat chronic pain in the outpatient setting using buprenorphine. In addition to primary care physicians having the ability to prescribe buprenorphine, the CDC also has guidelines in place for primary care physicians to treat chronic pain with opioids. Essentially, the CDC guidelines recommend that primary care physicians prescribe opioids for chronic pain only when non-opioid treatments are not sufficient, and to prescribe opioids at the lowest dose possible. In this context, buprenorphine could essentially be considered an opioid alternative. Bup Chronic Pain.pdf
  26. 1 point
    There is a significant misuse problem with the gabapentanoids: gabapentin and pregabalin, I have attached a few papers which will take you through the issue. Most importantly: The highest rates of misuse occur in patients on methadone and buprenorphine maintenance There are now data showing overdose deaths when a gabapentanoid is combined with opioids. Above 1800mg of gabapentin, the bioavailability decreases markedly with gabapentin. There is markedly increased toxicity with any renal impairment. The patient should be weaned off the gabapentin. Abrupt cessation may result in a sedative/hypnotic type of withdrawal syndrome. A psychiatric referral should be obtained to optimize treatment for her anxiety. Withdrawal_DTs.pdf Addictive_Review_2017.pdf Edit_Stannard-2016-Addiction.pdf Opioids_ODs_2017.pdf Pharmacology_Pregabalin_Gabapentin_2010.pdf Pregabalin_Opioids_Deaths_Edit_2018.pdf Renal_Failure.pdf trends_2002_2015_JAMAI.pdf
  27. 1 point
    You have ruled out rapid metabolism of methadone with the P/T serum levels <2. 125mg of methadone is not a "particularly" high dose. although the serum levels are high. I would observe the patient at the peak level after dosing--2--3 hours after the dose, to observe for sedation. The dose can be increased carefully, allowing 4-5 days between dose increases. Hopefully you are titrating not only to subjective complaints of withdrawal, but hopefully to increased functionality. If possible, include significant others for a better idea of how the patient is doing.
  28. 1 point
    Dr. Andrew Saxon provided this response: If OUD is being treated with buprenorphine in the context of chronic pain, the buprenorphine dosage can be optimized to help with the pain. Typically, that would require a dosage of 8 mg tid or qid. For some patients with OUD and chronic pain, methadone maintenance is a better option since methadone is a full agonist. Neither of these medications have serious interactions with lithium In regard to other possibilities, although non-steroidal anti-inflammatory medications do interact with lithium, lithium is not a contraindication to their use. Since they can elevate lithium levels, one simply has to monitor the patient and obtain serum lithium levels to make sure lithium levels remain in the therapeutic range. So NSAIDS are one option and can be combined with acetaminophen for even more robust pain control. It is now fairly clear that antidepressants can be safely used in bipolar patients who are on a mood stabilizer such as lithium. Thus, tricyclic antidepressants like nortriptyline or SNRIs like duloxetine which can help with chronic back pain are another option. If the pain has a neuropathic component, gabapentenoids or baclofen are other options that can be safely used with lithium. Of course, behavioral interventions like cognitive-behavioral therapy also show benefit for chronic pain. It is understood that this form of treatment may be out of reach if there is no trained therapist available or for patients who do not have insurance.
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