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The Complete (but Practical) Guide to Vancomycin Dosing — tl;dr pharmacy
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June 2, 2016 · Brandon Dyson
The Complete (but
Practical) Guide to
Vancomycin Dosing
Editor's Note: She's baaaaaaacccckkk... Stephanie
Kujawski, PharmD, BCPS is back with the next
installment in her epic series: Pharmacokinetics Dosing
Wars. Up for today, we have Episode II: Attack of the
Vancomycin. It seems that our hero, Han Solo, has
contracted a nasty MRSA infection (which apparently you
can do while being frozen in carbonite).
Kidding aside, this post is massive (it weighs in at just
over 4,200 words). But if a better guide for vancomycin
dosing exists, then I am unaware of it. It's really good.
Bookmark this page and spend a few days here if you
need to. By the end of it, you'll be an expert on
vancomycin. Take it away, Steph!
Pharmacokinetics Dosing Wars
Episode II: Attack of the Vancomycin
Hello, nice to see you all
again! I guess you’re all
gluttons for punishment
for coming back for
another round of kinetics
– or perhaps you’re still
This poor Wampa just lost his
just staring deer-in-the-
arm. Whatever shall we treat
headlights at your
his pending MRSA infection
kinetics professor! Either
with?
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way, glad to see Episode I
didn’t scare you off too badly, and perchance it even
helped a little.
So today we’re going to tackle vancomycin. Or at least
attempt to. It’s a BEAST, more beastly than a Wampa!
So this is a long one. Don’t say I didn’t warn you....
Part I: Vancomycin versus Bacteria
First let’s talk a little about how vancomycin kills
bacteria. In terms of very broad categories, vancomycin
affects cell wall synthesis.
Now, sure, there are many other antibiotics that also
affect cell wall synthesis, including the beta
lactams. But vancomycin is a little different. It binds to
the D-alanyl-D-alanine subunits of the bacterial cell wall
structure, which prevents peptidoglycan polymerase
and transpeptidation reactions.
Just for comparison, remember that beta lactams bind
directly to transpeptidase (a bacterial enzyme that
cross-links the cell wall). So both vancomycin and beta
lactams prevent cross-linking in the bacterial cell wall.
They just do it at different steps of the pathway.
In normal terms. Think of the bacterial cell wall as a
house being constructed. If you've ever seen a building
project in process, you've seen what looks like a spider
web of 2x4s "framing" out the house. These 2x4s are
cross-linked to provide stability to the house. Crosslinking serves the same purpose in a bacterial cell wall.
And vancomycin binds to the structure and doesn’t let
the bacterial enzymes do their cross-linking
construction jobs.
Because the cell wall is then not fully functional, the cell
(aka the bacteria) ends up also not functioning. In most
cases, vancomycin actually KILLS the bacteria;
therefore, it is deemed bacteriocidal. However, in some
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less common cases, vancomycin only stunts the growth
of bacteria, making it bacteriostatic.
We should also pause here and make sure one thing is
clear…vancomycin inhibits cell wall synthesis....and it is
ONLY active against Gram POSITIVE bacteria!
Those sneaky Gram negatives still have a cell wall. It's
just thin and wimpy and sandwiched between two cell
membranes. Also, Gram negatives don't have the D-alaD-ala sequence in their cell walls. So vancomycin is
utterly useless against them.
However, Gram negatives still have the transpeptidase
enzyme, so beta lactams are still effective.
It should also be noted that even some Gram positive
bacteria are sneaky and have come up with ways to
resist vancomycin’s actions, such as using D-lactate in
their cell walls instead of D-alanine, which prevents
vancomycin from binding.
For more info, refer to this awesome primer on
antibiotics.
Part II: Vancomycin and
Concentrations
Alright, now that we have that vancomycin background,
we can move onto kinetics. Based on our discussion of
antibiotic kinetics in Episode I, we know that most
antibiotics act in either a time-dependent or
concentration-dependent manner.
But I’m going to throw a curveball here.
Although vancomycin historically has been classified as
a concentration-dependent antibiotic, in more recent
years, it has been informally classified as “exposure” or
“AUC-dependent”. What this means is that its killing
action is really dependent upon both the concentrations
reached in the body as well as the time that those
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reached in the body as well as the time that those
concentrations are maintained. It's kind of like a
daywalker. It's both time and concentration-dependent.
So, if you think of your time-concentration curves,
exposure is graphically represented by the AUC.
All of the drawings on this post are original artwork by Stephanie
Kujawski, PharmD, BCPS. Please contact Stephanie if you are
inspired and would like reprints to hang in your house.
So as pharmacists we must pay close attention to the
concentrations we are achieving in the body in order to
ensure we are adequately treating an infection. These
days, with resistance rates what they are, we usually
want to target trough levels of 15-20 mcg/mL.
Sometimes we might let those trough levels range a
little lower to 10-15 mcg/mL for a cellulitis indication.
If you just think "shoot for 15 mcg/ml," you'll generally
be right either way. But as you learn and practice, you’ll
find there are times that targeting a more specific range,
like 18-20 mcg/mL for that meningitis patient, is
important!
Let's take the idea of following concentrations a step
further. This means we have to be able to predict how a
drug enters and distributes through the body and how it
leaves or is cleared from the body.
To illustrate, let's use our shopping and closet analogy
from Episode I. Let’s say your roommate is fed up and
has imposed a clothes limit on your exploding closet
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has imposed a clothes limit on your exploding closet.
You are only allowed to have 50-60 items in the closet
at any given time. (I'm not sure how you got into such
an agreement with your roommate, but you probably
should have had a lawyer look at the paperwork before
you signed off on it.)
Regardless, now you’re going to have to keep track of
how many items you’re buying versus how many items
your friends are willing to take off your hands.
As long as you keep these balanced, your closet will
stay in check. But if either your buying or your friends’
willingness to take your stuff changes, then your closet
may either explode again or you won’t have anything to
wear!
And don't noooobody wanna see that birthday suit.
You've seen similar "in versus out" analogies in your
calculus classes. Bathtubs filling with water while the
drain is open. The amount of your income versus your
expenses. The point is, to treat an infection we have to
balance the amount of vancomycin going into the body
with the amount leaving.
If we have too much vancomycin going in, toxicity will
follow (won't somebody please think of the poor
kidneys!?). If we have too little vancomycin going in, the
infection will worsen and spread.
Part III: Distribution of Vancomycin
Doses
Let’s begin by tackling the intake end of things by trying
to predict how vancomycin behaves when administered
to a patient.
We need to consider a few pieces when trying to predict
a drug's distribution....
1. Is the drug highly protein bound?
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2. Is it such a large molecule that its size may
affect its ability to travel certain places in the
body?
In the case of vancomycin, it has a wide range of
reported protein binding - anywhere between 10-50%. It
is also quite a large molecule with a molecular weight
of over 1400 Da.
Just for comparison, another commonly used
intravenous antibiotic, the beta lactam cefazolin, only
has a molecular weight of just over 450 Da.
So you can imagine how vancomycin might get a little
"distracted" on its travels through the body. It's semisocial with other proteins. And it's just too large to fit
through some of the doorways in the body.
That being said, it still distributes quite well out of the
blood and into tissues. This is why we can use it to treat
such a variety of infections, from bacteremia to
osteomyelitis. Its ability to treat meningeal infections is
a little more dependent on the degree of inflammation
present.
Remember that the Blood Brain Barrier (BBB) is
supposed to be an impenetrable fortress that prevents
things from getting into the CNS. However, with
meningitis, inflammation causes the BBB to open up a
bit. That inflammation is what allows a large molecule
such as vancomycin to pass through and get into the
CNS.
Ironic, isn’t it, that the infection itself is what allows us
to use a certain antibiotic to treat it?!? As the group "Lit"
once told us, "Sometimes it seems to me I am my own
worst enemy..."
So, anyways, you have a patient who needs vancomycin,
and you start administering doses. Each vancomycin
dose goes through a process where it is administered
intravenously, which causes the serum level to increase.
Then the vancomycin is distributed out of the blood
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and into the tissues. The blood and the tissues reach a
sort of equilibrium. Finally, it is eliminated from the
body, which is done largely via the kidneys.
At first, the body is going to be like, whoa, what is this
new stuff you’re pouring into me! So you have to fill the
tank, per se. But as you start regularly administering
more doses, each one is being eliminated as the next
one is coming in. Eventually you reach what is called
steady state.
This is the time period when serum levels are pretty
constant from dose to dose, meaning each peak and
trough you obtain with each individual dose should be
pretty similar to the ones obtained with the last dose.
Steady state is generally achieved in five half lives or,
alternately, after about 4 consistent doses of a
medication.
For those of you who don't remember your biochemistry classes, [ ] =
concentration.
Steady state depends on a number of things. But in the
case of vancomycin, because of its renal elimination,
we’re looking for consistency in renal function in order
to achieve this shining mecca of drug administration.
When the renal function changes abruptly, we may lose
steady state.
So whatever calculations we do at a particular level of
renal function are only applicable if the renal function
t
th
B t ’
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i
t t
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di t d
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stays the same. But we’re going to try to predict drug
action anyway.
In pharmacy land, we use the term volume of
distribution (VD) to describe how a drug distributes
through the fluid and tissues in a person’s body. We
figured out the VD from population kinetic studies, in
which vancomycin was administered to a bunch of
people and then blood concentrations were measured
and compared to the doses given. Using that info, a
generally accepted VD for vancomycin is 0.7 L/kg.
And because vancomycin (somehow) distributes quite
well into most tissues, we usually use a person’s total
body weight to calculate this (rather than ideal or
adjusted body weight). Ideal and adjusted body weight
might not take into account all of a person’s muscle or
adipose tissues that are exposed to vancomycin.
So in general, remember actual (aka total) body weight
and a volume of distribution of 0.7 L/kg using that total
body weight.
Vancomycin Volume of Distribution (VD) = 0.7 L/kg
CAVEAT #1: Some institutions practice slightly
differently regarding which weight to use for obese
patients requiring vancomycin. While total body weight
is generally good for most patients, it might lead to
problems in morbidly obese patients. So some
pharmacists will use adjusted body weight in these
cases.
The thought behind this is that using total body weight
will eventually lead to accumulation and overshooting
our target serum levels. Basically, the empty tissues
soak up the vancomycin and then when they’re all good
and saturated, the high doses of the drug don’t really
have anywhere else to go.
They accumulate until you end up with super high
trough levels and renal injury. So for people who are
~150 kg and upwards, you may want to consider using
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p
,y
y
g
an adjusted body weight.
CAVEAT #2: For the same reasons as above, some
pharmacists will also use an empirically lowered
volume of distribution in their calculations for morbidly
obese patients. So instead of using 0.7 L/kg, they might
do 0.6 or 0.5 for people that are very large. This may
help to prevent overshooting levels.
This is in no way actually a proven practice, but we’re
estimating all around anyway…
So let’s practice! Meet
HS. He’s a smooth 40
YOM with a penchant for
flying and leather vests.
He’s a trim, fit 6 feet tall,
80 kg person.
What is his vancomycin
volume of distribution?
Well, 0.7 L/kg * 80 kg =
56 L.
Part IV:
Image
Vancomycin's First Order Elimination
So now that we know how vancomycin distributes
throughout the body, we need to examine the other end
of things - how vancomycin is cleared from the body.
Do you remember from Pharmacokinetics Dosing Wars:
Episode I when we talked about first order kinetics?
When a constant proportion of drug is eliminated over a
period of time (rather than a constant amount)?
Good, because vancomycin kinetics are described by
first order (or linear) processes.
Think back to your high school algebra class. You
probably learned about something called decay.
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Described by the equation A = Pert.
You probably learned it in reference to radioactive
materials (where your math teacher wanted you to find
out how old some rock was by how much radioactive
carbon was left in it).
It's exactly the same equation for first order drug
elimination.
The A is your C2 (or for simplicity’s sake, your trough),
the P is your C1 (or your peak), r is your ke (your
elimination rate constant that describes how fast the
drug is going away), and t is still t (the amount of time
that has passed between C1 and C2).
And so, in pharmacy, first order elimination is described
by the equation C2 = C1eket, where ke is intrinsically
negative since it is elimination. This equation is
graphically represented on our normal timeconcentration curve as such:
Now let’s take just the elimination portion of that curve
and take the ln (natural log) of each data point. That
results in a figure that looks like this:
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See how the elimination line becomes linear instead of
curved?? And the slope (aka the ke) is constant?? Well
that fits right in with our first order kinetics! A constant
rate of elimination!
Alright, so we talked about weight and volume of
distribution for the intake portion of vancomycin
dosing. Now we’re going to talk about how to find the ke
to help describe elimination.
Again, based on population kinetics, it has been
determined that we can estimate ke with the equation
0.00083*CrCl + 0.0044.
Vancomycin ke = 0.00083CrCl + 0.0044
Where did that come from? From the same place we
estimated VD earlier. Basically, investigators again gave
vancomycin to a whole bunch of people. They
measured peak and trough levels. They calculated the
ke from our friend C2 = C1eket. And then they plotted ke
versus CrCl (calculated according to Cockcroft Gault).
From this, they were able to determine the line of best
fit in the format y=mx + b.
And voila, you have ke=0.00083*CrCl + 0.0044!
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From the ke, it is pretty easy to find the patient’s half life.
What is half life, you say? It’s the time it takes for the
concentration of the drug to decrease by 50% in the
body.
For first order drugs, the easy way to find half life is to
divide 0.693 by ke. Graphically, half life looks like this:
CAVEAT #3: Finding k e is pretty straightforward. Plug in
the CrCl and chug the math for k e . The tricky part is in
finding CrCl! Of course, Cockcroft Gault is supposed to
be straightforward…for more info on this lie, see our
post on Kidney Beans Part 1.
Plug in the patient’s age, ideal body weight, and serum
creatinine, adjust for gender, and math away!
However, it’s a little more difficult when you have a little
old 95 year old lady who only weighs 45 kg and doesn't
have much muscle mass. Her SCr of 0.3 and calculated
CrCl of 80 ml/min are probably more fitting for her 40
year old grandson than for her.
So you may have to fudge some numbers here and
there. Yes, I said you may have to fudge some numbers
(#gasp!). Perhaps you round her serum creatinine to
0.8…or 0.9…or 1 for the purposes of calculation to get a
more reasonable renal estimate.
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CAVEAT #4: In another scenario, what if you have the
obese 260kg person? Are you going to use ideal body
weight to calculate CrCl? Or would adjusted body
weight be more appropriate since that patient has more
tissue (some of which is bound to produce creatinine)??
There is no consensus on the best practice for these
situations. We just know doing the black and white
calculation may not be the most accurate.
So for our patient HS, if his serum creatinine is 0.8, what
is his CrCl? Remember he’s a trim 80kg, 6 feet tall, 40
year old.
So, first, his ideal body weight has to be calculated:
Then, Cockcroft Gault can be employed:
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Now, we have HS’s CrCl, so what is his ke based on our
population estimate equation?
Ok, so at this point, we have the patient’s total body
weight, as well as population estimations for volume of
distribution, CrCl, and ke. It is FINALLY time to calculate
a vancomycin dose.
I promised it would come, right?!
Part V: The Vancomycin Dosing Process
Some institutions believe in giving every patient a
loading dose of vancomycin. The thought is that
because you’re starting from scratch, you want to fill the
tank to achieve target trough levels more quickly.
If you are going to load, you will usually use the patient’s
actual body weight…whether or not they’re obese.
Remember, you’re starting from nothing. That being
said, most places cap a single vancomycin dose at
either 2000 or 2500 mg.
Other institutions do not load unless a patient is septic.
The thought is to prevent overshooting and causing
renal injury.
You will just have to get a feel for your institution’s
practices and also which patients are more critical. In
general, if you are going to load, it’s a 20-25 mg/kg
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yThe Complete
g (butg Practical) Guide to Vancomycin Dosing
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g
dose.
Regardless of loading dose, you are going to need to
figure out a vancomycin maintenance dose. There are
two pieces to figure out with every vancomycin regimen:
Dose
Interval
It's a bit of "guess and check" to determine how a given
dose is going to behave in a particular patient. We
figure this out by using derivations of our trusty first
order equation.
We need to estimate what a particular regimen’s peak is
going to be at steady state so that then we can
calculate an estimated trough at steady state…
Which hopefully will be between our goal of 15-20
mcg/mL.
So first, let’s estimate the dose we want to give. In
general, a good place to start is 15-20 mg/kg. Then
round your dose to the nearest 250mg (technicians
won’t particularly like having to draw up a dose of 1289
mg…just go ahead and make that 1250mg).
Next, let’s determine an interval to give this dose. Here
are some general rules to start with:
q8h for CrCl > 100
q12h for CrCl 60-100
q24h for CrCl < 60
(Hemodialysis is another beast that we won’t
address here...you’re probably already bleary eyed.)
So for HS, we get a range of doses of 1200-1600 mg.
Let’s choose 1250mg to start. Based on his CrCl, we
would choose an initial dosing interval of q8h.
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Now that we have our dose and interval, we need to see
what it’s going to do in our particular patient. It’s time to
plug and chug our data into the estimated steady state
peak equation. We need the dose, infusion time (usually
no faster than 15 mg/min), ke, volume of distribution,
and interval.
Of note....
Even though there’s no “target” peak, per se,
vancomycin toxicity is associated with supratherapeutic
troughs. We usually shoot for peaks < 45 mcg/mL. Any
higher and you’re not going to get the troughs you want.
Now that we have our estimated steady state peak, let’s
get the estimated steady state trough using our
equation.
If your trough is not within the desired range of 15-20
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you t oug
s ot
t
t e des ed a ge o
5 0
mcg/mL, you have a decision to make. Do you change
the dose? Or do you change the interval?
A good rule of thumb is that if you are just slightly off
from the goal trough level, try changing your dose first.
If you are drastically off (i.e. estimating troughs of 27…
33 mcg/mL), you’re going to have to change the
interval. You won't be able to change the dose enough
to get that into range!
Once you have a regimen that is meeting your desired
trough goals, it’s time to move forward! If you didn’t load
your patient, go ahead and recommend/enter your
maintenance dose.
If you did happen to give a load, you need to determine
when to start your maintenance dose after the load
finishes.
This can be done using our trusty first order equation.
C2 = C1eket
C2 is the serum concentration at which we want to
redose the patient. In most cases, it's going to be 15
mcg/mL. C1 is the peak concentration obtained from
the load (which is the loading dose divided by the
estimated volume of distribution (LD / VD) since we’re
starting giving the load to an empty tank).
You have an estimated ke, and you need to solve for t.
Remember, we’re trying to find how long after the
loading dose FINISHES we have to wait to give the first
maintenance dose (so the count starts at the end of the
infusion).
Solve for t and voila, you have your time to wait! Enter
your dose, and you’re golden!
Part VI: Vancomycin Levels and
Adjustments
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After you get your dose going, it’s up to the medical
team’s and your discretion as to if and when to check a
vancomycin level. If the patient is clinically improving
and their renal function is stable, you might get away
without checking one. If vancomycin isn’t expected to
continue very long (greater than a few days), maybe you
don’t need to spend the money on the level.
IF, however, the patient is not improving, their renal
function tanks, or they’re going to be on an extended
course, (especially if it’s the little old lady or the
morbidly obese patient from earlier), perhaps THEN you
want to check a level.
If you do check a level, try to get one at steady state.
Troughs should be drawn about 30 minutes prior to the
next dose.
Quick side note. ALWAYS make sure the trough was
drawn at the correct time before reacting to it. It's
very common to see low or high troughs just
because they were drawn inappropriately. The first
question to ask when looking at a trough is, "Was this
drawn at the right time?"
If your trough is only slightly off from goal range, no
problem. Remember vancomycin has LINEAR kinetics!
Changes in dose should produce proportional changes
in serum level, as long as the dosing interval remains
constant.
So a simple proportion is often all that is required to
find your new regimen.
Let’s pretend HS’s appropriately timed vancomycin
steady state trough on 1250mg q8h returned at 12.5
mcg/mL. And let's say you’re trying to keep his troughs
between 15 and 20 mcg/mL. Since it’s just a little off,
let’s do the proportion method:
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The trickier case is when your trough level is way off
goal. Just changing the dose may not be adequate to
achieve the trough you want. So you’re going to have to
change the interval…which means cycling back through
the guess and check calculations.
The advantage of having a patient specific drug level is
that then you can calculate a patient specific ke to use
in the equations (rather than just a population based ke
from the equation).
We get to use the same trusty equation (see a
pattern???).
C2 = C1eket
Your C2 is the trough you obtained. The C1 is your peak
steady state concentration (which can roughly be
calculated by dose divided by volume of distribution,
plus your trough!)
D/VD + Trough = C1
It’s the same idea as the estimation of your loading
dose peak, except now you’re not starting from scratch.
You’re starting from your steady state trough level.
You know t to be the time between peak and trough on
the same dosing interval. Then solve for ke. (And
sneaky tip…now you can back calculate an estimate of
CrCl using your population kinetics ke equation. It's not
100% accurate, but it's a more patient-specific
estimate). (see below figure)
So let’s say HS’s steady state trough from a regimen of
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So let s say HS s steady state trough from a regimen of
1250mg q8h returned at 26.5 mcg/mL (#eek!). His last
dose prior to the level was infused over 2 hours starting
at 1200. And the level was drawn appropriately at 1930.
What is HS’s ke? What should his new dose be?
Let’s start by representing the problem graphically.
This is a figure that shows one dose of the vancomycin.
Specifically the dose right before the level was drawn.
We see the start of the infusion at 1200 (yes, of course
we know that, since we are at steady state, the starting
concentration isn’t zero, but bear with my chart drawing
skills).
The dose infuses over 2 hours until 1400, at which point
we know there’s a C1 peak. But we don’t know what that
is since we don’t actually check vancomycin peaks.
Then, we know there are 5.5 h in between the end of the
infusion and when the level was drawn.
And we have our unknown ke....
So essentially we have an equation at this point with 2
unknowns, C1 and ke, where, remember ke is inherently
negative since it’s elimination:
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Now, you can’t find ke at this point…but you can get rid
of one unknown by estimating C1.
Remember when we were trying to figure out how long
after our loading dose to wait to give the first
maintenance dose? Remember we said concentration is
dose divided by volume to get our initial C1 for the load?
Well this is a similar situation, except instead of starting
from scratch as we did for the load, we’re at steady
state with a trough of 26.5. So our steady state peak
concentration should be our dose divided by volume of
distribution added to our trough level.
Cpeak(ss) = Dose/VD + Trough
Visually:
So, once we find C1, we’re only left with ke as an
unknown in our trusty equation. And we can solve for a
patient-specific (rather than a population estimate) ke!
See here:
https://www.tldrpharmacy.com/content/complete-guide-to-vancomycin-dosing
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Yay! So, now that we have HS’s specific ke, sometimes
it’s handy to back calculate a CrCl using our original ke =
0.00083 * CrCl + 0.0044 equation.
Yes, I know we’re using a population equation to back
calculate a patient-specific estimate, but this is still an
estimate more specific to your patient than Cockcroft
Gault.
If we do this for HS, we get an estimated CrCl of 128
ml/min, which isn’t too far off from our earlier estimate
of 135 ml/min. However, for some reason he doesn’t
seem to be clearing the vancomycin like we thought he
would. We know this because of his supratherapeutic
trough!
But now, armed with his specific ke, we can decide on a
new dosing regimen. Using our steady state estimation
equations we can get back within our goal trough range
of 15-20 mcg/mL.
This is the same guess and check process we used
with the initial regimen, just now with a patient-specific
ke.
So once you come up with a reasonable new regimen
that meets our goal level criteria, you have to decide
how long you are going to wait before starting said
regimen.
We know we need to let the patient’s blood levels wash
down a little bit since his trough is 26.5. But the
question is how long?
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question is how long?
Well, guess what (spoiler alert)? We’re going to use our
same trusty equation to find this out.
C2 = C1eket (you will learn this equation by the time I'm
through with you ;) )
Just like our load, we want to wait until the serum level
washes down to about 15 mcg/mL (C2) from the
current level of 26.5 mcg/mL (C1). We know our ke for
our patient (0.111/h), and we need to solve for t.
Once you have t, you know when to resume therapy with
your new maintenance dose!
Part VII: Just Kidding
Ok, breathe!!! In a nutshell, that is how we dose, monitor,
and adjust vancomycin therapy. Take a moment to sit
back and consider all of the estimations...on
estimations...on estimations. It's crazy, isn't it?! Hence,
the importance of knowing when to check serum levels
to get a true answer.
On that note, happy trails practicing your vancomycin! It
takes time, but eventually you’ll see all the ways that the
one trusty equation is the Chewbacca to your Han Solo.
You'll also learn how to navigate the gray areas of
obesity, renal dysfunction, and when to check levels, but
never hesitate to bounce your plan off of someone with
more experience.
Remember: C2 = C1eket
If you made it through this entire post, you legitimately
deserve a medal. No, but really. I’ll recommend you to
the Resistance for recognition by Leia.
And FYI, Episode III: Revenge of the Aminoglycosides is
available for more kinetics fun!
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The Complete (but Practical) Guide to Vancomycin Dosing — tl;dr pharmacy
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