Tapering off Buprenorphine or Suboxone, Pt 2

In the last post we discussed some of the misconceptions about tapering off opioids. Today we will discuss a couple basic principles, and then describe the approach I recommend for my patients tapering off buprenorphine.
Opioids act at receptors that normally bind endorphins, which are released by neurons in response to a range of stimuli including trauma and rewarding behaviors such as eating a good meal or using addictive drugs. Endorphin pathways elevate mood, reduce sensation of pain, and impact urine production, immune function, intestinal motility, and other bodily functions. Endorphin pathways have a certain baseline activity or ‘opioid tone’ that is directly related to opioid tolerance. When opioid stimulation is greater than one’s tolerance, opioid tone is increased. When opioid stimulation drops below one’s tolerance, opioid tone is reduced, causing withdrawal symptoms.

The goal of any taper off opioids is to recover original or native opioid tolerance. Some people focus on getting rid of the opioid, and even use substances or behaviors to ‘flush buprenorphine from the body’. Products marketed as detox agents have minimal impact on the clearance of buprenorphine or other substances. And even if they could increase the rate of clearance, they would only make detox harder by increasing the severity of withdrawal symptoms. The relatively slow metabolism and clearance of buprenorphine provides a cushion by slowing the loss of opioid tone.

Prolonged use of any opioid changes opioid receptors. The changes are not fully understood but include a decrease in number of receptors and changes in binding properties that reduce receptor sensitivity to opioids, including endogenous opioids (endorphins). Recovery from a state of tolerance takes 2-3 months, and is initiated by reduced opioid tone. Withdrawal symptoms reflect the reduced opioid tone that provokes eventual recovery of native tolerance.

Recovery of native tolerance is the rate-limiting step when tapering off any opioid, including buprenorphine. When the dose of buprenorphine is reduced, the amount of buprenorphine at opioid receptors decreases over the next 5 days and then stabilizes at a lower level. In response, opioid tone (the summation of current flow through opioid receptors) drops below normal. If the dose of buprenorphine is maintained at that level, opioid tone will recover to normal in about 2-3 months. If buprenorphine is suddenly and completely discontinued, opioid tone will decrease to very low levels and cause severe withdrawal that lasts for 2-3 months. If buprenorphine dose decreases more slowly, opioid tone will decrease more slowly, lessening the severity of withdrawal. But it still takes 2-3 months for opioid tone to return to normal. So for any taper, patients must decide whether to decrease their dose quickly and be done in 2-3 months, at the cost of greater withdrawal, or instead to taper more slowly to reduce the severity of withdrawal.

The relationship between buprenorphine dose and opioid activity is linear up to about 2-6 mg. Beyond that point further increases in dose have less impact on opioid tone. The reverse occurs when tapering, so that opioid tone decreases only slightly as dose is reduced from 16 mg per day to 4 mg per day. The non-linear dose/response relationship allows for rapid decreases in dose early in the taper process with limited or no physical withdrawal symptoms. Since the early challenge is mostly psychological, I use the early part of a taper to help assess whether a patient is truly ready to take on the tapering process.

I like to have patients lead the way in tapering off buprenorphine. I’ve found that if I lead and reduce the amount of prescribed buprenorphine for the next month, patients often fail to make reductions and end up out of medication before the end of the month. So instead I ask patients to tell me when they are certain that they are ready to stay at the lower dose.
During a taper, I recommend dosing buprenorphine twice per day. Patients start by removing 2 mg from the evening dose. After at least two weeks 2 mg can be removed from the morning dose. This sequence is repeated at intervals of at least 2 weeks until the total dose is 4 mg per day. In my experience patients who get to that point are usually in a good mental position to begin the second, more difficult part of the taper.

Most people will be able to continue working when opioid dose is reduced by 5% or less every 2 weeks, or 10% every month. That number is a good general guideline when deciding how fast to taper. Suboxone film makes tapering relatively easy. Patients purchase a weekly med organizer, and start the week by opening and stacking 7 films. A scissors or razor is used to cut a millimeter from the end of the stack, and one film is placed in each compartment of the organizer for that day’s dose. When the patient is comfortable with that dose, slightly more is removed for the next week. The process continues every 2-4 weeks, eventually changing to the 2 mg films. I recommend that patients continue tapering until the dose is 300 micrograms (0.3 mg) per day or less before stopping buprenorphine completely. It is fairly easy to guesstimate where to cut the film in order to reduce by 10%; just measure half, then half of that, then half of that.

Buprenorphine tablets, of course, are much harder to divide. Zubsolv did people a favor by coming out with a range of doses, and hopefully other brand and generic manufacturers will eventually follow suit. For now I usually have patients use the tablets to taper as far as possible, using the 2 mg tablets in the lower dose range, and then pay the extra cost for the film for the final month or so. A 12 mg film can be divided into 24 half-milligram pieces without too much effort, so the cost doesn’t have to be prohibitive.

I have had many patients taper successfully off buprenorphine. Fear is common and normal for a number of reasons, but the fear usually gives way to a sense of confidence and optimism when a taper is done correctly.
Things to keep in mind:

  • Be patient. Tapering by too much, or too quickly, causes withdrawal symptoms that lead to ‘yo-yos’ in dose.
  • Buprenorphine products are very potent. A sliver of Suboxone Film may contain enough buprenorphine to harm or kill an animal or small child. Take care to divide the medication in a well-lit setting, and clean up very carefully.
  • Buprenorphine is used to treat pain in microgram doses. If you jump from 1 mg, you will have considerable withdrawal symptoms.
  • If you are still running out of medication early, it is not time to taper off the medication.
  • People on buprenorphine for a year or less have rates of relapse over 90%. In my experience patients are more successful tapering off buprenorphine if they have been on the medication for 2-5 years or more.
  • If you struggle in tapering down to 8 mg, consider going back to your stable dose, waiting 6 months, and trying again.
  • People addicted to opioids often substitute other drugs for their drug of choice. Do not start a new addictive substance in order to get off buprenorphine.

Good luck!

Tapering Off Buprenorphine or Suboxone pt. 1

Many patients taking buprenorphine live in fear of a dark world around the corner where they will have to taper off the medication. They see horror stories on YouTube posted by people who, for some reason, abruptly stopped the medication and kept a video log of their experiences. My own patients sometimes ask, nervously, if I plan to retire some day. Some have asked what they should do if I ever, say, drop dead.

It needn’t be all that bad. Yes, sudden discontinuation of a typical dose of buprenorphine will result in withdrawal symptoms. But if you taper correctly, your body will slowly reset your tolerance without putting you through the wringer. In this post I’ll describe my typical approach to helping a person through that process. But first we should correct some of the misconceptions about buprenorphine and opioid dependence.

It does NOT get harder and harder to stop buprenorphine the longer you take the medication. I have heard that idea over and over in one form or another, and I presume it comes from the experience people have with active addiction where use tends to grow with time, and other facets of life gradually fade away. But the opposite occurs in patients treated with maintenance agents like buprenorphine or methadone, where use of the medication does not trigger a reward or relieve the ‘punishment’ of withdrawal. The conditioning that occurred during active addiction is slowly extinguished, and most people gradually lose the desire to use opioids. I’ve witnessed this process literally hundreds of times over the past 12 years in patients on buprenorphine or methadone. Patients of successful treatment also develop interests and accomplishments that help them avoid returning to opioids. And after a few years away from ‘using friends’, people no longer see themselves as part of the using scene. Patients get to a point where they have too much to lose to get close to that world again.

Opioid withdrawal has physical and psychological dimensions. During short-term detoxes, minor physical symptoms trigger fears that magnify the perception of those symptoms. A bead of sweat on the neck signals that hot flashes, diarrhea, and depression are on the way. Patients who have been away from the cycle of using and withdrawal don’t seem to have as many emotions about their physical symptoms. I see the change very clearly in methadone-assisted treatment, where the minor withdrawal at the end of the day is a big deal to people starting treatment, but a minor inconvenience in patients tapering off methadone after several years of treatment.

Does buprenorphine ‘get in your bones’? YES, of course! Bones are living tissue, so anything in the bloodstream gets in the bones. Glucose gets in your bones. Aspirin gets in your bones. But so what? When you taper off buprenorphine, the buprenorphine in your body will be metabolized and removed. It does not accumulate or stay in bones or other tissues beyond what occurs with other fat-soluble molecules.

Is buprenorphine or Suboxone ‘the hardest opioid to stop’? No. The brain keeps no record of the molecules that pushed opioid tolerance higher. The challenge during a taper is that opioid receptors have become down-regulated by opioid stimulation, resulting in reduced endorphin tone as the opioid is removed. Opioids that leave the body quickly tend to have more-intense discontinuation effects than those that leave more slowly because the latter mimics a taper, where opioid activity decreases over time. The longer half-life of buprenorphine also slightly extends the total period of withdrawal by a few days.

I’ve heard people claim that ‘heroin was much easier to stop’, and rather than tell people what they should think I’ll let them have their opinions on the issue. But that opinion is not supported by studies comparing withdrawal from different opioids. Usually the claim is followed by the comment that ‘with heroin I was fine after 4 days’ or something along that line. But it takes longer for tolerance to reset, after ANY opioid. I suspect that perception comes from the severity of early heroin withdrawal, making subsequent weeks easier by comparison. Again, the brain doesn’t care which opioid you used to take; it only cares that the opioid stimulation that was there is now gone.

In a few days I’ll share the approach I recommend to patients tapering off buprenorphine.

Buprenorphine Overdose After Naltrexone Treatment

Naltrexone induces mu-receptor hypersensitivity.  Buprenorphine’s protective ‘ceiling effect’ may not prevent overdose in patients with this ‘reverse tolerance’.

A new patient described his recent history of respiratory failure several days into buprenorphine treatment.  He was told by his doctors that he experienced an allergic reaction to Suboxone. The rarity of buprenorphine or naloxone allergy led me to look deeper into his history, and my conclusion differs from what he was told by his last treatment team.
The patient, a man in his mid-50s, has a history of significant opioid use over the past 20 years.  He used a variety of opioid agonists over the past year, mostly prescription opioids, with an average daily dose greater than 200 mg of oxycodone per day.
Three months ago he went through hospitalization and detox, and after a week he was discharged on oral naltrexone.  He sought further treatment at a different institution that offered buprenorphine.  He was told to stop the naltrexone two weeks before induction with buprenorphine.
He avoided all opioids for that two weeks, and then started buprenorphine, 2 mg twice per day as directed by his physician.  The patient became progressively sleepier after each dose of buprenorphine, and after 24 hours could barely maintain wakefulness.  His complaints resulted in his admission to the hospital intensive care unit.
In the ICU he had a rocky course that included several episodes of apnea, hypoxemia and bradycardia.  The patient does not currently have the records from the hospitalization, so the course of events is based only on his recollections from several weeks ago.  He blacked out several times, and was told by doctors and nurses that his ‘heart stopped on the monitor’ during those times.  He says that his oxygen level was very low at those times according to the monitors, and according to what he was told.
After the episodes when he lost consciousness, he was told that since his heart stopped he needed emergency implantation of a pacemaker.  He said that a short time later those concerns were dropped, and no pacemaker was inserted.  He was discharged from the hospital in good condition after several days.  Follow-up with a cardiologist was not deemed necessary. He was told by his hospital physician that the episodes of lost consciousness were caused by an allergic reaction to Suboxone.  He had no rash or pruritus (itching).
I’m writing about this patient’s care in the form of a ‘case report’.  The patient does not have access to his records.  If he did, I would review them and write a formal case report for publication.  Since I’m relying on the patient’s perceptions and memories, I’ll use this blog.  I will say that I have no axe to grind, and my purpose in sharing this case is to help people avoid a similar situation.  And, of course, to keep readers of this blog entertained!
As the patient shared his story, I assumed that he had an opioid tolerance well-below the ceiling actions of buprenorphine.  When I mentioned my hypothesis, the patient smiled, and told me he had been using over 200 mg of oxycodone each day, blowing that theory to pieces.
But I returned to the same theory when he said that he followed the doctor’s orders very closely, including avoiding opioids completely for two weeks before induction.  I wondered, could a 2-week interval of abstinence lower tolerance so dramatically that buprenorphine resulted in overdose? Then the patient mentioned, in an offhanded way, that ‘he even stopped the naltrexone’.
I’ve written about the increased incidence of opioid overdose following treatment with naltrexone, a risk that is unreported and largely unknown beyond brief reports from Australia cited in the linked post.   Opioid antagonists, including naltrexone (the drug that makes up Vivitrol injections), induce ‘reverse tolerance’ in mu opioid receptors to cause a heightened response, and heightened respiratory depression, from subsequent exposure to opioid agonists.  Anyone close to the field of opioid dependence notices the increased frequency of overdose in patients newly released from confinement, whether in jail or in abstinence-based treatment.  The increased risk of death after a period of abstinence is related to the resetting of tolerance during abstinence.  A return to ‘normal’ use creates significant risk of overdose.
That risk is multiplied if the period of abstinence includes treatment with naltrexone.   Imagine a person who is using six ‘30s’ of oxycodone—180 mg—every 24 hours.  If that person waits a week and then goes on naltrexone, tolerance drops to zero and then to negative levels.  After a couple of weeks on naltrexone, a tablet of Vicodin has the potency of a tablet of Percocet.  That 180 mg of oxycodone now has the potency to cause respiratory arrest and death.
Buprenorphine is a partial agonist with a ceiling effect that prevents overdose in almost all patients who have even small degrees of opioid tolerance.   Almost all deaths from buprenorphine occur in people with limited or no tolerance to opioids.  In the presence of inverse or negative tolerance, the ceiling on buprenorphine’s opioid effect has less protective value.  Such was the case in the patient who is the subject of this discussion.
So what would have been a better plan?  Buprenorphine induction is always more dangerous in patients with low opioid tolerance, so careful patient selection will mitigate that risk.  In patients with low tolerance, reducing the starting dose buprenorphine to low-milligram levels does little to reduce the risk of respiratory depression because of the ceiling effect, which reflects the minimal difference in strength between 2 or 16 mg of buprenorphine.   Much lower doses of buprenorphine, on the order of 0.5-1 mg, are required to reduce risk of respiratory depression and overdose in patients with inverse tolerance to mu opioid agonists.
A second option would be to continue naltrexone through the induction process, and afterward gradually reduce the dose of naltrexone over a week or two.  As the block from naltrexone decreases, buprenorphine bound to mu receptors would gradually increase, allowing opioid tolerance to grow more slowly.  Precipitated withdrawal would not be a problem, as PW occurs when bound agonist is suddenly displaced by buprenorphine—  not when antagonists are displaced by agonists or partial agonists like buprenorphine.
Thankfully, the patient is now doing well, with no lingering problems caused by his course of treatment.  But the incident also relates to another common problem, i.e. the erroneous blaming of symptoms on medication ‘allergies’.  In an era of electronic medical records, that mistake often removes, permanently, a patient’s access to medication that may someday be helpful—and in the case of buprenorphine, irreplaceable.

Cannabinoid Hyperemesis: How Rare?

I recently read a CBS news story about CHS, or Cannabinoid Hyperemesis Syndrome, describing a 100% increase in cases in Colorado since the legalization of marijuana there. A search for ‘THC’ and ‘CHS’ pulls stories from a range of sources including High Times, Wikipedia, Fusion.net, and Current Psychiatry. A broader search reveals articles calling the disorder ‘fake news‘.

Most articles about CHS describe the condition as rare, but becoming less rare as the legalization movement takes root and grows. The syndrome occurs in heavy, long-time users of marijuana who first notice reduced appetite, mild nausea, and sometimes weight loss. Those symptoms, and the symptoms that follow, are relieved by smoking marijuana, leading those with the condition to become heavier users who come to see marijuana as beneficial to their health.

Over time the symptoms worsen to include paroxysms of severe abdominal pain, nausea, and vomiting. Patients often seek help from a number of health practitioners, including alternative health treatments. Tests come up negative, and patients continue to turn to marijuana to treat the symptoms– along with hot baths and showers, which for some reason make the pain and nausea more-tolerable.

Since we live in an era of social media I’ll point out that I have no strong feelings toward marijuana. I don’t kick people off buprenorphine products for testing positive for THC, as it makes little sense to stop treating a potentially fatal disease because the patient smokes pot. I doubt doctors would withhold cancer treatment because of marijuana use either. I’m describing my observations only to get the word out about something that doctors are missing. Over the past 2-3 years I’ve had several patients with symptoms identical to those described in stories about CHS, so I suspect the condition is more common than thought.

The Current Psychiatry article describes possible mechanisms for symptoms of CHS. The nausea and vomiting may be caused by accumulation of cannabinoids in the lipid tissue of the gut, causing activation of the CB1 receptor in the intestine to override the anti-emetic effects of CB1 activation in the hypothalamus. Activation of CB1 receptors in the gut slows peristalsis (the motion of the intestines that propels food forward) and dilates the blood vessels to the intestinal system. Hot baths and showers may provide relief by dilating blood vessels in the skin and redirecting blood flow away from the gut. Other possible causes relate to the effects of specific cannabinoids, or perhaps herbicides or pesticides.
One of my patients had classic symptoms of CHS for several years. A year ago I had not yet heard of the condition, but noticed that he repeatedly talked about marijuana being a ‘wonder drug’ for disabling stomach pain and nausea, even as he lost weight and his general health deteriorated. When I asked if he considered that marijuana may actually be harming his health he became angry and defensive, and never returned for follow-up.

Another patient talked about his spouse’s health problems, hoping I would have ideas about the cause of her symptoms that weren’t found through visits to many specialists. Marijuana wasn’t even part of the discussion as he described her severe pain and nausea over the past year that caused her to go to the ER several times each month. At his last appointment, armed with new knowledge about CHS, I asked him if his wife smoked marijuana.

He said that she not only smoked it, she recently got her ‘medical marijuana’ card because smoking was the only thing that relieved her nausea. I asked if she ever felt better after a shower, and he said “oh my gosh, she is in the shower for three hours or more every day with the hot water turned up!”

The big question, of course, will be whether people with similar symptoms will try going without pot for a month, the length of time required for symptoms to fade, and whether clearing their systems of THC actually relieves their symptoms. But other heavy marijuana users with pain and nausea should read up on CHS, and consider a trial off THC. One month without pot isn’t going to kill you.

Post-op Pain on Suboxone

Many patients on Suboxone or buprenorphine eventually require pain treatment, just like people who aren’t on buprenorphine products. I’ve written about post-op pain control several times, but I continue to get emails from patients who haven’t seen my comments and who view an upcoming surgery with the same fear experienced by patients before the early 1900’s, when the OR was correctly seen as a horror-chamber.
These patients are often torn between following the treatment plan vs. doing what they have learned may work better. In all cases, I tell patients that they cannot act in ways counter to what their physician prescribes. But I often support their intent to ask their doctors to clarify or modify their treatment plans.

Patients write about ‘the look’– the way doctors, nurses, and pharmacists react when patients ask about pain control. As a recovering addict myself, I know what they are referring to. Doctors encourage other patients to discuss concerns about pain control, and as long as they have no piercing or tattoos, patients will usually be comforted with assurances that their doctors will take their pain seriously. But people on buprenorphine often see their doctors roll their eyes, or even say that the opposite is true– that if they have pain, they had better not bother the doctor about it! Doctors who act that way are asses, of course, and I urge patients to avoid them if possible. This post is not for those doctors, as they are not likely to ‘get it’ after reading the comments of another doctor— if they would ever read them in the first place!

I’m writing for the doctors who are open to hearing about new ways to help their patients. I intend to use this post, going forward, to answer the emails from patients about this topic If you are a physician who received this from a patient, please consider my comments– as I have found the approach described below far more helpful for surgical patients on buprenorphine products than the alternatives described elsewhere. There was an NIH consensus paper a few years ago for example that described several alternatives, but mostly focused on discontinuing buprenorphine before surgery, then restarting buprenorphine at some point through a standard induction that includes 24 hours of withdrawal in patients already weakened by surgery. Standard doses of opioid agonists were recommended for pain. That approach was also described in a flashy article in one of the throw-away journals a month or two ago (i.e. Autumn of 2015).

There are so many problems with that approach:

  • Patients forced to stop buprenorphine before surgery and enter surgery dehydrated and weakened (IF they even managed to stop, as many patients end up staying on buprenorphine covertly– NOT a good situation for surgery.)
  • Buprenorphine discontinuation not an option for emergency surgeries;
  • Constant opioid levels are necessary to avoid withdrawal, before even considering pain control;
  • Buprenorphine is erroneously considered gone, when the long half-life actually assures that buprenorphine is still present;
  • Patients fret and argue over pain control every time the nurses change shifts;
  • Buprenorphine re-induction at some point after surgery, requiring patients to go through withdrawal symptoms;
  • Agonist treatment alone causes tolerance to rise very rapidly, requiring high doses of narcotic at hospital discharge;
  • An increased risk of overdose from narcotic pain medication in patients off buprenorphine;
  • And many other reasons. Using the ‘discontinuation’ approach, patients end up on a Hellish roller-coaster ride where pain is grossly under-treated and withdrawal symptoms are only 4 hours away, day after day.

I’ve read emails from people whose buprenorphine doctors recommended taking more buprenorphine for post-op pain, or dosing more often. I’ve read about suggestions to use Tramadol for pain after major surgery(!)
Earlier today I sent a letter in response to a woman who is planning a series of painful procedures. I’ll share that letter to spare myself some time:

Dear A,

You’ve been through enough misery, and I hope you convince your physician to consider a different approach to your pain. I’ve had patients on buprenorphine go through many surgeries including thoracotomy, nephrectomy, open cholecystectomy, total knee replacement, and rotator cuff repair– all very painful surgeries. My experience as an anesthesiologist piques my interest in post-op pain control.

My favored approach is very simple. Maintain buprenorphine, and use oxycodone or other agonists to out-compete buprenorphine at the mu receptor as needed for pain relief. The benefits of the approach are obvious once the prescriber opens his/her mind to the realities of ligand competition. There is no need to go through withdrawal, no need for ‘comfort meds’ to tolerate the withdrawal, and no need to enter surgery in an already-weakened state. As you know, even minor withdrawal causes people to feel very depressed, lose their appetites, stop sleeping…. is that really any way to go into surgery?

As an aside, buprenorphine alone does not provide ‘real’ pain control in patients who take chronic buprenorphine. Yes, buprenorphine seems to reduce pain in people with minor pain issues. But it is of no use for the pain of major surgery. Of course in theory, why would buprenorphine treat chronic pain in patients with complete mu tolerance to a medication with a ceiling effect?

A few years ago, an NIH consensus paper described a few approaches to acute pain in patients on buprenorphine. I don’t know who was on that panel, but the paper suggested stopping buprenorphine for several days before surgery and then using agonists. The panel mentioned the approach that I favor near the end of the paper. I also described my favored approach at an annual meeting of ASAM, in a talk that was very-well received. I was optimistic that the discussion would open enough minds among prescribers to follow the neurochemistry, instead of focusing on the misplaced fear of combining an agonist and a partial agonist. There are other papers out there– and book chapters– about the effects gained by combining an agonist with a partial agonist. You can find my ASAM slides at www.slideshare.net by searching for ‘junig’ and ‘uncoupling analgesia’.
The ‘uncoupling’ part BTW is what makes my favored approach so valuable, but that gets into the area of chronic pain, which is not entirely relevant to this discussion. In short, opioid analgesia has always been limited by tolerance and dependence. I believe that those limits can be removed by combining mu receptor agonists with partial agonists, allowing for pain relief from agonists while partial-agonists prevent euphoria and anchor tolerance at a lower level.

My approach is to reduce buprenorphine to about 4 mg per day. Higher doses in my experience get in the way of pain control. I then treat post-op pain as I would in any patient, but using 4 times more agonist (warning– see * below). I typically prescribe oxycodone, 15 mg tabs,* and direct patients to take one tab every 4 hours as needed. When patients no-longer needs narcotic analgesia, I stop the agonist and have them resume their regular doses of buprenorphine. That’s it. No tapering, and no withdrawal… just treating patients as I would any other patients, but realizing that mu receptors are competitively blocked, and effective doses of oxycodone must out-compete buprenorphine.

Dilaudid or fentanyl are not necessary. You could approach post-op pain in a very elegant way in a hospital using sublingual buprenorphine, fentanyl infusion, and PCA, but that gets a bit complicated. Oxycodone works fine. In rare cases my patients required higher doses of oxycodone, but I’ve never had reason to use more than 30 mg. Oxycodone is typically used every 4 hours. My buprenorphine patients have found good pain relief from total daily doses of 60-120 mg of oxycodone. The patients who went to a hospital where I couldn’t control their analgesia, who were told to stop buprenorphine, ended up on much higher doses of oxycodone at discharge.

Advantages of Combined Approach:

There are many advantages to maintaining buprenorphine throughout the perioperative period. The entire process is much simpler, and the patient’s experience is better because there is no euphoria, and no warm rush from oxycodone to rekindle addiction. The pain is relieved, but the reinforcing effects of oxycodone are eliminated. I assume the that the limits on mu effects by buprenorphine are like a ‘governor’ that limits the speed of fleet vehicles. You can get only so much opioid effect in the presence of buprenorphine, and not enough to cause a ‘high.’

The combined approach also prevents tolerance, which is a greater issue with chronic pain than with post-operative pain. Buprenorphine anchors tolerance at the level yielded by the ceiling effect, allowing agonist effects to continue over time. I’ve treated people with the combination of buprenorphine and oxycodone for over 2 years, and the combination continues to work as well as it did on the first day.

Some prescribers and pharmacists worry about ‘precipitated withdrawal’, but that is not an issue as long as buprenorphine is continued every day. The only way to precipitate withdrawal would be to stop buprenorphine for at least a few days, boost tolerance higher with an agonist, and then give buprenorphine– which would ‘yank’ tolerance back down again. Patients who stay on buprenorphine can add agonists without fear of precipitated withdrawal.

I’ve convinced a few doctors to try this approach, and I’ve received a number of positive reports about the approach. I’ve described the idea to several pharmaceutical companies as an approach that would revolutionize pain treatment. Can you imagine pain relief without addiction, without tolerance, and without euphoria? I realize that the large number of deaths caused by opioid overdose limits interest in opioid analgesia. But I suspect that a product that combines buprenorphine and an agonist would go a long way to reducing opioid dependence, providing that the two medications were irreversibly bonded together in a combination product. I have some thoughts about how to do that… but that’s for another day.

It is NEVER safe to prescribe one’s self opioids or other controlled substances, so this discussion is intended to provoke discussion between patients and their doctors. Patients must realize that there are many things that go into decisions about post-operative analgesia, and NO approach is the right approach for everyone. Any individual patient may have features to his/her history that make the combination approach inappropriate, or even dangerous.

*Doses described in this post are intended as approximations for consideration by trained and licensed medical professionals. Doses described may not be safe in some patients, including patients at the extremes of age, patients with respiratory or other chronic illness, patients with central nervous system disorders, or patients on other respiratory depressant medications.

NEVER use opioids except as directed by your own physician.