Vancomycin max daily dose

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I'm not a pharmacy student yet but I'm curious...

What is your trough, dose, and frequency? And is the patient obese?
 
I'm looking for a maximum daily dose for vanc.

I've always gone by 4g max daily, but some patients in the hospital are not getting the trough levels I want even at that dose.


What is your frequency??? I have seen doses greater than 4gm / day. The patients were morbidly obese w/ decent renal function. Not sure of a max dose, someone with more experience can chime in.
 
I ask because I've read somewhere that > 4g daily is associated with nephrotoxicity.
 
the prudent decision seems to be to supplement with another antibiotic, not exceed the max recommended vanco dose and run the risk of irreversibly damaging renal tubules
 
Do what it takes to get the trough over 10 or 15 (whatever the dx)...nephrotoxicity isn't as much of a concern w/ vanc as originally thought...drug effects are dependent on plasma concentation...just don't give it with AGs...make sure they did labs 30 min before the 4th dose, too...
 
vanco is not about max dose. its not apap. vanco is not as nephrotoxic and its certainly reversible. however, ototoxicity is associated with very high peak above 50ug per mil. in order to attain that kind of peak, it requires a loading dose of almost 40mg per kg.
its critical to get the trough maintained between 10 to 20 and not fall below it as auc over mic neds to be about 400 in order to keep mrsa in check in pneumonia.

instead of looking at daily total max dose, you need to look at concentration in vivo to minimize toxicity while maintaining efficacy.
 
vanco is not about max dose. its not apap. vanco is not as nephrotoxic and its certainly reversible. however, ototoxicity is associated with very high peak above 50ug per mil. in order to attain that kind of peak, it requires a loading dose of almost 40mg per kg.
its critical to get the trough maintained between 10 to 20 and not fall below it as auc over mic neds to be about 400 in order to keep mrsa in check in pneumonia.

instead of looking at daily total max dose, you need to look at concentration in vivo to minimize toxicity while maintaining efficacy.

+1 well said
 
Thanks guys.

A lot of the vanc patients are on 1g q 6hr but they are still not getting above 10 and we'd like to see about 15-16. They are a little on the heavy side so they probably might be 3rd spacing. I am also concerned about ototoxicity as well.
 
Thanks guys.

A lot of the vanc patients are on 1g q 6hr but they are still not getting above 10 and we'd like to see about 15-16. They are a little on the heavy side so they probably might be 3rd spacing. I am also concerned about ototoxicity as well.

q6h? I bet the nurses love you.
 
Thanks guys.

A lot of the vanc patients are on 1g q 6hr but they are still not getting above 10 and we'd like to see about 15-16. They are a little on the heavy side so they probably might be 3rd spacing. I am also concerned about ototoxicity as well.
why the hell do you worry bout oto when you cant even get to therapeutic trough????
id be more worried bout treatment failure and killing the pt.
 
what lawnmower boy said.....

i've had to go as high as 2 q 6 to get there (i know i know basically a CI but you do what you have to do)
 
Do what it takes to get the trough over 10 or 15 (whatever the dx)...nephrotoxicity isn't as much of a concern w/ vanc as originally thought...drug effects are dependent on plasma concentation...just don't give it with AGs...make sure they did labs 30 min before the 4th dose, too...

Agreed in general, but I think you do have to be concerned with the higher doses.

The paper by Tom Lodise in AAC found a pretty strong correlation between nephrotoxicity with vancomycin doses >4g/day, especially if the patients treated were obese (somewhere around 100kg, can't remember the cutoff). There's also limited data showing that troughs >15 are associated with nephrotoxicity, but it's much harder to interpret the validity of those results.

You also have to look at the MIC of the staph...if it's 2 or more, vanco might be a lost cause anyways.
 
Agreed in general, but I think you do have to be concerned with the higher doses.

The paper by Tom Lodise in AAC found a pretty strong correlation between nephrotoxicity with vancomycin doses >4g/day, especially if the patients treated were obese (somewhere around 100kg, can't remember the cutoff). There's also limited data showing that troughs >15 are associated with nephrotoxicity, but it's much harder to interpret the validity of those results.

You also have to look at the MIC of the staph...if it's 2 or more, vanco might be a lost cause anyways.

actually if mic is 1 and above in pneumonia, trough of 15 wont attaint sufficient concentration in epithelial lining fluid where mrsa typically resides. there is however a recent nonpublished study showing a strong correlation of treatment success and intial trugh over 15.
 
actually if mic is 1 and above in pneumonia, trough of 15 wont attaint sufficient concentration in epithelial lining fluid where mrsa typically resides. there is however a recent nonpublished study showing a strong correlation of treatment success and intial trugh over 15.

That is true...then we get to switch to Zyvox!
 
as far as obese patients, i like to use the dosing weight not ibw or abw but ibw plus 40 percent of difference between ibw and abw. controversial i know
 
You also have to look at the MIC of the staph...if it's 2 or more, vanco might be a lost cause anyways.

If it's 2 or more we've left the MRSA reservation and have entered VISA-land, so to say 'might' be a lost cause is an understatement
 
so evidently prazi is the only one on sdn rx now that i can have a decent pharamaco tx dialogue with since wvu graduated, i dont think hes reading as much or reading anything pertinent. shame..and im not even a clinical pharmacist per se.
 
If it's 2 or more we've left the MRSA reservation and have entered VISA-land, so to say 'might' be a lost cause is an understatement

I've always wondered about this actually...why does CLSI set the standards for VRSA so high? Is it the different resistance mechanisms/genotypes at play among the hVISA/VISA/VRSA strains, or is that the near-impossibility of treating VISA strains with vanco was only recently realized?
 
i would try bactrim or rifampin... and gasp synercid.

just dont say tygacil or dapto for pneumonia.
 
I've always wondered about this actually...why does CLSI set the standards for VRSA so high? Is it the different resistance mechanisms/genotypes at play among the hVISA/VISA/VRSA strains, or is that the near-impossibility of treating VISA strains with vanco was only recently realized?

Dunno, ask lawnmower boy, he's the only one who knows anything.
 
i would try bactrim or rifampin... and gasp synercid.

just dont say tygacil or dapto for pneumonia.


if sensitive to bactrim....

rifampin monotherapy? :laugh: <---(that's the face of the MRSA/VISA you speak of


might get by with tigecycline if not bacteremic (which Staph PNA is fairly uncommon)

EDIT: syncerid response rates to MRSA pna sux a lot too btw
 
so evidently prazi is the only one on sdn rx now that i can have a decent pharamaco tx dialogue with since wvu graduated, i dont think hes reading as much or reading anything pertinent. shame..and im not even a clinical pharmacist per se.

Well, shucks. I don't know what to say.

i would try bactrim or rifampin... and gasp synercid.

just dont say tygacil or dapto for pneumonia.

No quinolone (if susceptible)?
 
No quinolone (if susceptible)?

If the very unlikely event it was then yes, but that's going to be rare. If CA-MRSA, a slightly better chance (and then clinda might be an option as well)
 
You can't use tygacil for MRSA pneumonia dummy.... look at the package insert under "Warnings."


:laugh::laugh:

Looks like someone should delve a little into the primary literature and re-read my statement.

(hint I gave the disclaimer)
 
Rifampin plus vanco, yo. I journal clubbed it.
 
I admire the dialogue between you two...hopefully around the P2 -P3 stage of my pharm education I can jump right into a conversation such as this!
 
:laugh::laugh:

Looks like someone should delve a little into the primary literature and re-read my statement.

(hint I gave the disclaimer)


There lies your problem. You belive primary literature is it. The issue is, the halted pneumonia trial with Tygacil is where you will find the answers to why you can't use tygacil for typical pneumonia yet wyeth/pfizer will never publish it. Also look at why tygacil never received approval in Europe for CAP.

Also understand the pathophysiology of pneumonia and see where different pathogens reside.

Instead of spoon feeding you the answer, why don't I let you figure it out.

This has nothing to do with bacteremia.
 
one more thing...understand tyacil's pharmacodynamics and kinetics...
 
It was an interesting study, but not practice-changing by any means.


Not practice changing yet a valuable information which many prescribers don't practice...but should use as an option.
 
There lies your problem. You belive primary literature is it. The issue is, the halted pneumonia trial with Tygacil is where you will find the answers to why you can't use tygacil for typical pneumonia yet wyeth/pfizer will never publish it. Also look at why tygacil never received approval in Europe for CAP.

Also understand the pathophysiology of pneumonia and see where different pathogens reside.

Instead of spoon feeding you the answer, why don't I let you figure it out.

This has nothing to do with bacteremia.


You mean the one where it was compared to imipenem and if/when pseudomonas was a concern the tigecycline arm was given the mighty aztreonam and if MRSA was a concern the imipenem arm was given vanco?

And bacteremia does play a huge role as usually the serum levels of tigecycline is below most gm- MICs and usually only the peak level is above the MIC for gm+.

EDIT: would never use tigecycline in a real patient unless no other option and while it seems like i'm "defending" tigecycline, I'm not like a employee of wyeth or pfizer or whoever owns it now, just speaking in the hypothetical realm of SDN.
 
so evidently prazi is the only one on sdn rx now that i can have a decent pharamaco tx dialogue with since wvu graduated, i dont think hes reading as much or reading anything pertinent. shame..and im not even a clinical pharmacist per se.

oh, I read...just more interesting topics...metabolism...opiate receptor dynamics...endocannabinoids...antibiotics are boring...see bug...kill bug...be annoyed by hqaving to do kinetics...

The reason so many pharmacists like it and think it's "neat" is because it is so simple to understand. I'll say it. ID is paper tiger material.
 
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Not practice changing yet a valuable information which many prescribers don't practice...but should use as an option.

debatable.........

the only outcome that showed a difference was "clinical cure" which had to include a >50% improvement by Xray reading....

why debatable?

It's an open-label study and any % improvement in an Xray reading is going to be subjective and variable. Were the Xrays read by the same people? were the people who read the xrays the investigators (and hence by showing a "difference" are more likely to get published and their name out there)
 
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