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. Have you found similar results with those or other pain medications?
To provide some background, 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!
Many of my buprenorphine patients have had surgeries for one thing or another. My approach is to increase the dose pain medication used after surgery by about two- or three-fold. The receptor blockade from buprenorphine is ‘competetive’, meaning that it can be overcome by using high doses of potent narcotics.
I strongly recommend that patients on buprenorphine avoid increasing the dose of any pain medication beyond their doctor’s recommendations, as many 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. Buprenorphine patients who need intensive post-op pain control are usually put in the ICU where their resperation and other vitals can be monitored using pulse-oximetry and other devices.
I have had patients use morphine or oxycodone 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 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.
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 receptors are much more complicated than visualized in the simple drawings 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 suspect that over time, we will develop protocols for dealing with post-operative pain in buprenorphine patients.
Thanks again, Dr, for your comments.