Get help with your application
Use all the free resources available to you from SDN: articles, guides, expert advising, forums discussions, and school research.
I've talked to ER docs who like to use it because they can just give them an IM dose and then discharge them. I've never used it, probably won't. I've used CIWA or our hospital's scale with Librium or Ativan depending on liver function. Our academic hospital uses a benzo-sparing protocol (Gabapentin + Clonidine scheduled, Ativan as a back-up). I've never had anyone seize or go into DTs, but have needed to give supplemental benzos PRN for some of the more severe patients.
Never used phenobarbital.
Haven't ever found a reason why, nor anything that offers superiority for its use.
Benzos work and get the job done.
Haven't ever found a reason why, nor anything that offers superiority for its use.
Benzos work and get the job done.
Advertisement - Members don't see this ad
D
deleted1100659
Awesome, I thought at first possibly I was missing something. I typically do ciwa for mild-moderate and if significant hx of DT/higher risk, long acting benzo taper. Ive never been to keen on using phenobarb and was just making sure I wasnt missing something
Agreed. I never use clonidine in EtOH.
You want to know if vitals are spiking.
You want to know if vitals are spiking.
In residency we would start with librium taper. For the 5% that would still have significant withdrawal symptoms, we would switch to phenobarbital and get very good control of withdrawal. For benzo detox we also used phenobarbital with good effect. It works well, it just has higher side effect burden than benzos.
In medical school, they would use phenobarbital for alcohol first line and from what I remember, there was a high rate of falls on the unit.
In medical school, they would use phenobarbital for alcohol first line and from what I remember, there was a high rate of falls on the unit.
This is correct clonidine is for opiate withdrawal to help with sympathetic symptoms as they are not deadly but you want to see those symptoms in alcohol withdrawal because if you mask them you might underdose the benzo and the patient can seize
Why not just use sublingual suboxone? Or are you just trying to treat withdrawal?
Also agree with gabapentin plus symptom-triggered benzo with an AWS like CIWA or alternatively librium taper. I've never use clonidine for alcohol withdrawal, but certainly have for opioid withdrawal.
You can microdose buprenorphine even with use overlap, and you should use microinduction if there are suspicions for fentanyl use/contamination. We have an in-house protocol, but there are a few studies with examples out there.
I suppose another way is clonidine and an induction to essentially pretreat for precipitation of withdrawal, which I've heard of, but never done because it wasn't really ever necessary.
You can microdose buprenorphine even with use overlap, and you should use microinduction if there are suspicions for fentanyl use/contamination. We have an in-house protocol, but there are a few studies with examples out there.
I suppose another way is clonidine and an induction to essentially pretreat for precipitation of withdrawal, which I've heard of, but never done because it wasn't really ever necessary.
This is what we do. Our microdosing usually starts at 0.5 mg, so 1/4 of a 2 mg film works well. Harder to do 1/4 of a SL tab, but I've seen people do it as well.
I don't like scheduling Clonidine, but I do use it as a PRN adjunct for withdrawal to prevent dangerous elevations in BP. There is plenty of data on protocols where it is scheduled though. Maldonado has done extensive research on benzo-sparing algorithms, and our academic hospital basically adopted one of his. Here's a link to some of his work with algorithms:
ClinicalKey
www.clinicalkey.com
It's also a common adjunct treatment for alcohol withdrawal and considered second or third line (depending on source) for EtOH withdrawal if benzos can't be used. If you're doing CIWA and the patient is scoring 0 for everything but HTN, what are you going to do? Give more benzo or just keep the HTN to a non-lethal level? If the withdrawal is severe enough to be a legit seizure risk, 0.2mg of Clonidine is not going to be enough to mask severe withdrawal symptoms. The seizure risk is typically the highest early on and you'll know pretty quickly what their actual risk is if you do a PAWSS or CIWA.
That being said, I would never use Clonidine alone. For severe withdrawal I'm going straight to Benzos and will not play around with Neurontin. Our academic center uses high dose gabapentin +Clonidine on a 7 day taper as first line though. Doses are often adjusted depending on presenting symptoms and if they want to leave AMA. Ativan is only used if they're still scoring high on AWSS despite benzo-sparing protocol. From one of our previous resident's QI projects, there was no increase in seizures after switching to that protocol.
I use it as a PRN adjunct for Gabapentin or benzo tapers. I'm yet to have a patient I've given Clonidine to seize during withdrawal. Prophylaxis is obviously the ideal goal, but I think it's pretty obvious when treatment needs to be initiated if patients are being monitored appropriately. Clonidine use is also correlated with far greater reduction in anxiety during withdrawal than treatment with benzodiazepines, and there's quite a few smaller studies that have shown that.
Advertisement - Members don't see this ad
I use phenobarb very occasionally for benzo withdrawal, but we prefer to keep our alcohol protocols simple.
We switched to a phenobarb taper for moderate to severe risk patients about 3 years ago, but still do CIWA + Ativan for lower risk patients unless things start to go south early on. The phenobarb protocol is super straightforward and honestly easier than straight CIWA + benzo. Both medicine and our addiction service have gathered a lot of data since implementing a phenobarb protocol and the number of transfers to the ICU for complicated withdrawal, length of stay for ETOH withdrawal patients, and number of EtOH withdrawal patients leaving AMA have all gone down a fair amount. The biggest issue I can think of off the top of my head with phenobarb is precipitated withdrawal in patients on methadone. Medicine usually initiates phenobarb before consulting us which has been the case the handful of time this has occurred. For what it’s worth, the handful of patients I’ve talked to that have gone through both benzo and phenobarb managed withdrawal have preferred phenobarb, which may speak our observation of a decrease in patients leaving AMA with phenobarb - but again, that’s merely an observation.
The point of microinduction is to start bup alongside a full agonist to ease the transition to buprenorphine and not require mild-moderate withdrawal symptoms before you start opiate substitution, a period in which we see a lot of patient drop-off. Fentanyl also sticks around in the system longer (in subq tissue) so standard induction protocols are becoming harder when so many street opiates are being cut with random amounts of fentanyul. There aren't any prospective studies on different induction protocols (yet) or studies comparing microinduction to standard induction, however, there are many case series that are useful to look at. Here's a recent review.
Microinduction of Buprenorphine/Naloxone: A Review of the Literature - PubMed
This manuscript provides a review of the existing literature to help clinicians better understand the approaches to microdosing of buprenorphine in various clinical settings and populations. (Am J Addict 2020;00:00-00).
pubmed.ncbi.nlm.nih.gov
butrans is really expensive so hard to do outside of inpatient settings, for the most part. buccal buprenorphine is cheaper but technically is only for chronic pain, so depends on the patient/how willing your system is to play ball. The advantage of butrans or buccal buprenorphine is you can start with much lower doses than regular suboxone. outside of the US suboxone is available in smaller increments (e.g 0.2mg) so it's easier to do a microinduction. In the systems I work in, for outpatient microinduction we have to instruct patients to cut a 2mg film into quarters, which is hard. Also I have no idea if buprenorhpnie is equally distributed across the strip, so it's a much less precise way to do a microinduction.
Our ED docs also seem to like pheobarb for severe withdrawal symptoms, as does our hospitalist service. I agree that it doesn’t generally seem to be necessary as BZDs are more than sufficient.
How do you approach patients taking large oral doses of fentanyl? One patient last week said he takes 20 tablets per day (who knows what's really in those illicit tablets). I'm familiar with prescribing Suboxone for people using other opiates, but that is a lot.
Suboxone still for fentanyl. Same thing, mild/moderate withdrawal first, do induction.
Same for kratom.
In theory fentanyl binds to the Mu receptor more tightly than suboxone, you could potentially just start the suboxone [without microdosing], without the withdrawal state, and have the person stop the fentanyl. I've never done it, only heard it alluded to and don't think its anywhere near a standard of care (yet?).
Same for kratom.
In theory fentanyl binds to the Mu receptor more tightly than suboxone, you could potentially just start the suboxone [without microdosing], without the withdrawal state, and have the person stop the fentanyl. I've never done it, only heard it alluded to and don't think its anywhere near a standard of care (yet?).
you'd probably induce withdrawal if you just start 8 or 16 of suboxone on someone who is also taking a full agonist. bup has a higher binding affinity than fentanyl.
When did that change, where Bupe bound tighter than fentanyl?
Fentanyl is lipophilic, resulting in distribution to the peripheral tissues in a manner that is not dose dependent and leak back into circulation in somewhat random fashion over a long period of time. This is why we are seeing more precipitated withdrawals with buprenorphine inductions in an era of fentanyl laced street opiates - mild/moderate COWS scores are less specific in telling us who is physiologically ready to be induced.
We know from clinical experience that bupe readily displaces fentanyl from the mu receptor because fentanyl-dependent people who take bupe too soon precipitate withdrawal. When a person is on a ceiling dose of bupe, most of the effects of fentanyl are blocked or blunted because fentanyl does not readily displace bupe.
As to your specific question, bup has a lower ki (higher binding affinity) than fentanyl. There may be fentanyl analogues that bind more tightly than bup, but the average binding affinity for bup is higher than the average binding affinity for fentanyl.
So, with this in mind, how do you treat fentanyl dependence? Start with low dose suboxone that will not necessarily reduce opioid cravings?Fentanyl is lipophilic, resulting in distribution to the peripheral tissues in a manner that is not dose dependent and leak back into circulation in somewhat random fashion over a long period of time. This is why we are seeing more precipitated withdrawals with buprenorphine inductions in an era of fentanyl laced street opiates - mild/moderate COWS scores are less specific in telling us who is physiologically ready to be induced.
We know from clinical experience that bupe readily displaces fentanyl from the mu receptor because fentanyl-dependent people who take bupe too soon precipitate withdrawal. When a person is on a ceiling dose of bupe, most of the effects of fentanyl are blocked or blunted because fentanyl does not readily displace bupe.
As to your specific question, bup has a lower ki (higher binding affinity) than fentanyl. There may be fentanyl analogues that bind more tightly than bup, but the average binding affinity for bup is higher than the average binding affinity for fentanyl.
the complication with fentanyl is with the initial induction of buprenorphine and a higher risk of induced withdrawal than we see with other opiates. once you are past this induction stage, treatment outcomes are no different than with other opiates afaik and you would still aim for a blocking dose of suboxone - e.g somewhere around 16mg give or take.
as far as the decision to do a microinduction vs. standard induction, I don't know of any good data suggesting one approach over the other. There's a trial in Vancouver that should hopefully have some good data in the next year or so. Clinical characteristics that might point you towards a microinduction protocol might be repeated failure of a standard induction protocol b/c of induced withdrawal, difficulty tolerating the build up to mild-moderate withdrawal needed for a standard induction.
there is always methadone, of course, if your patient can tolerate the logistics required.
also bear in mind many of the microinduction protocols simultaneously dose increasing (tiny) amounts of bupe while continuing a full agonist. by slowly building up bupe, you minimize the amount of full agonist you are shoving off the opiate receptors and hopefully minimize any withdrawal. once you build up to a reasonable dose of bupe, e.g 8 or 12mg/day, you can just discontinue the full agonist with less concern about withdrawal. the paper I linked a few posts above has details about various things people have tried.
Our protocol in residency was really thorough. Started with a lorazepam dose roughly equivalent to prior alcohol use. Doc assessed for withdrawal signs. Was primarily a standing/scheduled lorazepam taper. Nurses have notorious variability in CIWA scoring and pts will also game that at times. Then can convert to librium/valium when down to a relatively low lorazepam dose and ready to move on to lower levels of care.
What's the conversion from alcohol to lorazepam?
Advertisement - Members don't see this ad
The point of microinduction is to start bup alongside a full agonist to ease the transition to buprenorphine and not require mild-moderate withdrawal symptoms before you start opiate substitution, a period in which we see a lot of patient drop-off. Fentanyl also sticks around in the system longer (in subq tissue) so standard induction protocols are becoming harder when so many street opiates are being cut with random amounts of fentanyul. There aren't any prospective studies on different induction protocols (yet) or studies comparing microinduction to standard induction, however, there are many case series that are useful to look at. Here's a recent review.
Microinduction of Buprenorphine/Naloxone: A Review of the Literature - PubMed
This manuscript provides a review of the existing literature to help clinicians better understand the approaches to microdosing of buprenorphine in various clinical settings and populations. (Am J Addict 2020;00:00-00).
butrans is really expensive so hard to do outside of inpatient settings, for the most part. buccal buprenorphine is cheaper but technically is only for chronic pain, so depends on the patient/how willing your system is to play ball. The advantage of butrans or buccal buprenorphine is you can start with much lower doses than regular suboxone. outside of the US suboxone is available in smaller increments (e.g 0.2mg) so it's easier to do a microinduction. In the systems I work in, for outpatient microinduction we have to instruct patients to cut a 2mg film into quarters, which is hard. Also I have no idea if buprenorhpnie is equally distributed across the strip, so it's a much less precise way to do a microinduction.
My understanding from the clinical pharmacists is that the initial SL films used to have much bigger spots of buprenorphine, making cutting them a lot more difficult from a consistency standpoint. Supposedly this has changed over the last couple years to much smaller dot spread more evenly throughout the film.
Our microinduction protocol involve cutting the films into quarters, and anecdotally, this seems to work pretty well even with fentanyl onboard.
You treat it the same way you would any opioid dependence, but the primary difference is in the induction process. Ours is about 7-12 days long. Its not too far off from the modified Bernese method.
The article below describes one protocol that is similar to what we use, but our Suboxone ramp up is a little more aggressive.
Buprenorphine Microdose Induction for the Management of Prescription Opioid Dependence
Prescription opioid dependence remains a major source of morbidity and mortality in the United States. Patients previously on high-dose opioids may poorly tolerate opioid tapers. Current guidelines support the use of buprenorphine therapy in opioid-tapering protocols, even among patients without...
EDIT: Here's another proposed example: Buprenorphine–naloxone “microdosing”: an alternative induction approach for the treatment of opioid use disorder in the wake of North America’s increasingly potent illicit drug market
Last edited:
D
deleted1100659
Is anyone doing detox on an outpatient setting for alcohol? Makes me a bit nervous to do that, I usually tend to prefer they do it at the CSU/detox center
It depends. I prefer they come in most of the time honestly, but I also use the following calculator if they are really insistent on not:
Prediction of Alcohol Withdrawal Severity Scale - MDCalc - 4 or more, absolutely not. <2 probably OK.
Honestly though, most of the time its been either admission, counseling on gradual reduction (rarely successful), or I've just had people start naltrexone, watch them cut alcohol intake down on their own and then go from there (sometimes successful).
D
deleted1100659
yea the hard part is, even with education theyre going to stop on their own cold turkey or just keep drinking the same, i feel like the majority arent able to gradually cut back unfortunately. Also I get a lot of people on multiple substances with alcohol so I usually strongly recommend inpatient detox, most of my patients tend to already under report what they're using.
Nearly every day. Only the heaviest alcohol users who have a history of DTs are admitted to inpatient.
D
deleted1100659
I suppose my concern is having a trustworthy family member to be there with the patient during the process and I get nervous at the idea of giving them a benzo but not doing any monitoring/check in in regards to sx/vitals/etc. Most of the ones with alcohol use d/o that I see are already on multiple substances as it is so the accountability isnt super high. Also my patients arent the best historians..
Last edited by a moderator:
Great thread.
My understanding is opioid withdrawal is absolutely miserable but not deadly. Listened to this psychiatrist on NPR a short while ago and she referenced it sometimes being deadly. In 'Dopamine Nation,' Overabundance Keeps Us Craving More
Can opioid withdrawal prompt autonomic instability or something, such that someone dies? Do any of you ever see death in opioid withdrawal (apart from seeking relief via more opioids and subsequently overdosing).
Our clinic nurse does CIWA assessment and vitals and re-checks the patient after half an hour, similar to suboxone induction. Then they go home with their limited supply of your withdrawal prevention drugs of choice and come back the next morning for a week. We try to enroll them in our dual diagnosis partial hospitalization program.
A partial program with spots and the ability to see people every day would probably make this much more manageable. Good on you for having those options available to your patients!
I think this is reasonable. Have done outpatient alcohol detox, but it’s not usually my first preference if the patient is consuming large amounts. The risk is precipitating a withdrawal event without being able to monitor, so a depending on amount consumed a gradual reduction is usually the first step as opposed to initiating benzo regimes. There’s also the risk that the patient doesn’t stop drinking and doubles up on benzos which goes to your point about trust.
I think when I started private practice I did sometimes do this, as I could get patients back into see me within the next week. However, the way things are now I don’t have that capacity and prefer the admission option to manage things more aggressively.
D
deleted1100659
ahhh ok, that makes sense.
I suppose it ultimately comes down to resources at your clinic. One thing is we do have an affiliated CSU that does detox so ultimately I just try to get them there. My facility is sliding scale payments so they dont incur a huge bill regardless
