Which benzo equiv chart?

[jumpingcactus]

Trying to figure out which benzo equiv chart is best to use when converting benzos for taper. I'm seeing such a difference between equiv benzo doses. Some charts show alprazolam 1:1 with clonazepam and some show 0.5 alprazolam to 0.25 clonazepam. What resource do you use?

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[OldPsychDoc]

Trying to figure out which benzo equiv chart is best to use when converting benzos for taper. I'm seeing such a difference between equiv benzo doses. Some charts show alprazolam 1:1 with clonazepam and some show 0.5 alprazolam to 0.25 clonazepam. What resource do you use?

Because of the difference in half-life, I think a conversion chart is only going to be a guideline, at best. If you're looking a total daily dose for taper, well, yeah, I'd rather see my patient on 2 mg of clonazepam instead of 4 of alprazolam, and 4 of clonazepam would start far too high. If you're looking at subjective anxiolytic effect, you probably need the higher dose of clonazepam because the onset is slower than alprazolam, so it may be closer to 1:1.

 

[whopper]

Because of the difference in half-life, I think a conversion chart is only going to be a guideline, at best

Very much agree.

For defensive purposes (and I mean that in a sense where you are doing the best to protect your patient in addition to yourself, not just yourself), use a benzo equivalence chart that is accepted by recognizable authorities (E.g. Kaplan and Sadock). Another thing is if the person is in inpatient, still have PRNs available to the patients only if they meet a specific criteria of withdrawal symptoms.

E.g. an attending I had in residency had the following (Librium PRN for 3 of the following : 1)T >100 2) SysBP>150 3)DiastolicBP>100 4) HR>100 5) diaphoresis 6)tremor 7) Nausea OR vomiting

As was said above, charts are just guidelines. They are effective most of the time, but there are sometimes exceptions. I remember a few patients on a CIWA scale still have a seizure.

Remember, if there's just a 1% chance of something occurring once a day, after 100 days, the odds of that 1% chance occurring at least once is not slim.

 

[jumpingcactus]

Thanks!

 

[billypilgrim37]

Remember, if there's just a 1% chance of something occurring once a day, after 100 days, the odds of that 1% chance occurring at least once is not slim.

Particularly, it is approximately 63%.

 

[Speculatrix]

Because of the difference in half-life, I think a conversion chart is only going to be a guideline, at best. If you're looking a total daily dose for taper, well, yeah, I'd rather see my patient on 2 mg of clonazepam instead of 4 of alprazolam, and 4 of clonazepam would start far too high. If you're looking at subjective anxiolytic effect, you probably need the higher dose of clonazepam because the onset is slower than alprazolam, so it may be closer to 1:1.

How much does the ODT preparation of clonazepam obviate the slower onset as compared to alprazolam? (or does it?) I feel you could get away with a lower dosage ODT than just the regular PO if you were looking at subjective anxiolytic effect?

 

[billypilgrim37]

How much does the ODT preparation of clonazepam obviate the slower onset as compared to alprazolam? (or does it?) I feel you could get away with a lower dosage ODT than just the regular PO if you were looking at subjective anxiolytic effect?

The time of onset is limited by the lipophilicity and rate of crossing the blood brain barrier, not GI absorption.

 

[Speculatrix]

The time of onset is limited by the lipophilicity and rate of crossing the blood brain barrier, not GI absorption.

Doh. I feel stupid. That's an excellent point, thank you. So when would you consider prescribing the ODT form over the regular PO? Other than just psychological feeling "working faster". Another dumb question, but does this apply to Niravam as well, the ODT form of alprazolam?

 

[billypilgrim37]

The only reasons I could think would be for a) mechanical reasons, people/little kids that can't swallow pills, etc., or b) for compliance, as it's much more difficult to "cheek" an ODT than a pill. I've never used a benzo ODT. Use M-tabs and Zydis more frequently.

 

[OldPsychDoc]

The only reasons I could think would be for a) mechanical reasons, people/little kids that can't swallow pills, etc., or b) for compliance, as it's much more difficult to "cheek" an ODT than a pill. I've never used a benzo ODT. Use M-tabs and Zydis more frequently.

you left out c) to get a buzz on faster...

 

[billypilgrim37]

you left out c) to get a buzz on faster...

Does that seem to really work? I mean, I could imagine people might "think" it would, but my understanding is that the onset wasn't actually much different at all.

 

[Regnvejr]

Does that seem to really work? I mean, I could imagine people might "think" it would, but my understanding is that the onset wasn't actually much different at all.

With the clonazepam, it really won't matter much. Time to action still lies at around 1 hr, even with ODT. If the patient is taking a long-acting benzo only for relief of acute stress, then it is pointless to use. The clinical strength of the long-acing benzos is in the prevention of the agitation, the background coverage of anxiety.

On Lorazepam, and to some extend Alprazolam, absorption through sub lingual salivary glands do make a difference. You can shut down a PTSD flashback in 7-8 min instead of 15 min. On the other hand, properly trained breathing exercises and muscle relaxation techniques can start giving relief in 30 sec. It just isn't as prolonged.

 

[whopper]

This is something I learned way better and in more depth in college as a psychology major vs being in psychiatry residency. While this was taught in residency, the reality of being overworked and tired made a lot of residents half-awake in class. Further, in residency, these things aren't tested.

The quicker the "buzz" is felt after administering a substance, the more likely it is to be addictive. It's a type of classical conditioning. The quicker the 2 stimulus and the effect, the harder it is to break the reinforcement.

Does that seem to really work? I mean, I could imagine people might "think" it would, but my understanding is that the onset wasn't actually much different at all.

From what I've read in Kaplan and Sadock, Xanax's concentration in the blood shoots up quite dramatically vs the other benzos. In fact, the book mentioned something to the effect that like I mentioned above, because it does that, it is more addictive. Further, it also mentioned that in studies, Ativan was just as effective as Xanax in treating anxiety disorders. Bottom line I got out of it, there's very little reason to prescribe Xanax if Ativan can do the same trick and it's less addicting.

 

[billypilgrim37]

From what I've read in Kaplan and Sadock, Xanax's concentration in the blood shoots up quite dramatically vs the other benzos. In fact, the book mentioned something to the effect that like I mentioned above, because it does that, it is more addictive. Further, it also mentioned that in studies, Ativan was just as effective as Xanax in treating anxiety disorders. Bottom line I got out of it, there's very little reason to prescribe Xanax if Ativan can do the same trick and it's less addicting.

Right, but we don't care about the concentration in the blood, we care about the concentration in the brain. The question remains (which Reg seems to be answering) whether the ODTs matter. As we all speculated earlier, Klonopin doesn't matter. But, for Xanax, I'm still not seeing why it would actually increase the rate of absorption and time of onset. I've always been taught that the sub-lingual absorption was essentially a fiction.

Now, Reg says it shuts down the PTSD flashback about 5-10 minutes quicker, and suggests it's b/c of SL absorption. Which means either a) psychologycally, the ODT "feels" faster, or b) there really is some expedited absorption, sub-lingual or otherwise (I would tend to expect otherwise), and that in the case of alprazolam, given that it's a big fatty jerk, the absorption approaches the rate of blood-brain barrier crossing.

 

[Regnvejr]

From what I've read in Kaplan and Sadock, Xanax's concentration in the blood shoots up quite dramatically vs the other benzos. In fact, the book mentioned something to the effect that like I mentioned above, because it does that, it is more addictive. Further, it also mentioned that in studies, Ativan was just as effective as Xanax in treating anxiety disorders. Bottom line I got out of it, there's very little reason to prescribe Xanax if Ativan can do the same trick and it's less addicting.

In addition, Xanax has a withdrawal effect that Ativan doesn't have. And it is a stronger seizure suprpessant, meaning that withdrawal from high doses xanax can cause a rebound into seizures, even if there has never been a seizure before.

 

[Regnvejr]

Right, but we don't care about the concentration in the blood, we care about the concentration in the brain. The question remains (which Reg seems to be answering) whether the ODTs matter. As we all speculated earlier, Klonopin doesn't matter. But, for Xanax, I'm still not seeing why it would actually increase the rate of absorption and time of onset. I've always been taught that the sub-lingual absorption was essentially a fiction.

Now, Reg says it shuts down the PTSD flashback about 5-10 minutes quicker, and suggests it's b/c of SL absorption. Which means either a) psychologycally, the ODT "feels" faster, or b) there really is some expedited absorption, sub-lingual or otherwise (I would tend to expect otherwise), and that in the case of alprazolam, given that it's a big fatty jerk, the absorption approaches the rate of blood-brain barrier crossing.

Also, sublingual absorbtion bypasses the gi tract and liver. Faster access for the brain. Not by a lot, but in a panic attack, 5 minutes do matter. For Clonazepam, 55 min vs 1 hr is a whopetidoo, though.

And even without ODT, sticking a regular Ativan under the tongue does give faster absorbtion. They dissolve nicely over a minute or so, even in normal formulation.