The topic of post-op pain control on buprenorphine is important enough to get top billing
Many thanks to Dr. J Walsh in Seattle for the following post:
I am a physician in Seattle. In two c-section cases we have found that high affinity opiates (fentanyl or hydromorphone) delivered by PCA can provide adequate anesthesia even while sublingual buprenorphine is continued.
To clarify, patients taking Suboxone, Subutex, or any other form of buprenorphine face a problem when they need pain control, particularly if the need is acute– after injury or surgery. Buprenorphine is a ‘partial agonist’ at the mu opiate receptor; it has a ‘ceiling’ to its effects, so that increases in dose of buprenorphine will not provide increased analgesia. This is great for addiction treatment, as the addict has no reason to take extra buprenorphine. But buprenorphine not only won’t be more effective in higher doses– it also prevents other pain medications from working. Again, this is a positive when it comes to treating addiction, as the addict will find oxycontin to be a complete waste of money (of course, it always WAS a waste of money!). But for a person who just had his/her belly cut open, a bit of oxycodone can be quite valuable!
Several of my patients on buprenorphine have had surgeries for one thing or another. My general procedure is to augment the pain medication used after surgery. The receptor blockade from buprenorphine is ‘competetive’, meaning that it can be overcome by using very high doses of potent narcotics. I strongly recommend avoiding doing this on your own; people die from overdose every day, and trying to overcome the block from an opiate antagonist is asking for big trouble. A small miscalculation can easily kill a person. So when patients on buprenorphine need post-op pain control, they are usually put in the ICU where their resperation and other vitals can be monitored, particularly by using something called ‘pulse-oximetry’.
I have had patients use morphine in high doses to get pain relief; this writer reports success using high-potency opiates (he mentions fentanyl, the product in the skin patch ‘duragesic’ and a common anesthetic medication, and hydromorphone, AKA Dilaudid) by PCA– Patient Controlled Analgesia. With PCA patients are usually given a constant infusion of narcotic and also have a button to push that provides a ‘boost’ injection on demand– with a ‘lock-out interval’ to prevent getting too much medication from pushing quickly and repeatedly.
Fentanyl and other high-potency narcotics are not used by nurses as often as are morphine and (unfortunately) Demerol. (Demerol is slowly being removed from many hospital formularies because of the toxicity of its principle breakdown product, normeperidine). The high-potency opiates are more dangerous when given intravenously primarily because of their high solubility in lipids, or fatty material. This solubility allows them to cross the ‘blood brain barrier’ much more quickly then water-soluble drugs like morphine, so that the effect is almost instantaneous– equal to one ‘arm to brain circulation time’, as we said back in the anesthesia days. This causes in instantaneous shift in the response of the respiratory rate to carbon dioxide, causing the patient to completely stop breathing until the carbon dioxide level increases to the new threshold required to stimulate breathing. During this pause in breathing, the patient’s oxygen level can drop to levels low enough to trigger a fatal arrhythmia– killing the patient. This sequence, by the way, is ‘overdose in a nutshell’. The water-soluble opiates like morphine, on the other hand, enter the brain more slowly– over 5-15 minutes, even when injected intravenously. The shift in the breathing response occurs more slowly, so the patient SLOWS his/her breathing, rather than just stopping– allowing the carbon dioxide level to increase without having the oxygen level fall as dramatically.
The competetive interactions of molecules at the receptor are much more complicated than visualized in the simple drawings that are used to teach introductory neurochemistry. Parts of receptors may be more accessible to one part of a stimulating chemical than to other parts of the same chemical. Perhaps some parts of the opiate receptor are shielded by other receptor structures. Or perhaps more lipid-soluble drugs have access to parts of the receptor that more water-soluble drugs do not. I’m just ‘hypothesizing’ here– much more is known about opiate receptors than was known back in the 1980’s when I was doing basic science research, and there are many people out there who will have more accurate ideas of what might be going on. But the point is that in at least one person’s experience, the high-potency opiates, given by PCA, were useful in providing analgesia for people taking buprenorphine.
Thanks again, Dr, for your comments.