IV to PO Switches

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Sparda29

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My hospital has a policy that allows pharmacists to initiate IV to PO switches on certain drugs without a prescriber's approval. For example, Levaquin, Cipro, Protonix, Diflucan, and Azithromcyin.

To the more experienced pharmacists out there, what would go into your decision to switch a patient from IV to PO other than WBC counts (for infections), dietary orders (NPO, puree diet, regular diet), and general clinical stability. One problem at my hospital is that we don't have an EMR (we will in a few months) so I'm not able to read any nursing notes or physician evaluations on the patients.

Like if a patient is admitted 2 days ago, and the WBC count is down to normal levels today and they are eating food, would you make the switch, or wait for at least 5-6 days? What if they are still in the ICU/CCU?

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We do this at our hospital too. It will become much easier once you get an eMAR. At our hospital there is an eMAR so these may not all apply to you.

1. I never switch a critical care patient (ICU) to PO
2. I never switch a patient with an ID consult

3. Confirm oral diet
4. Confirm no N/V by looking at administration/orders of Zofran, Reglan, Phenergan, etc.
5. Confirm temperature <100F
6. Confirm patient has been on IV antibiotic for 48hours

7. If the above are confirmed, then I switch.
 
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Clinda is a weird one since the IV dose is higher than PO. Only drug I can think of that goes that way.
 
Clinda is a weird one since the IV dose is higher than PO. Only drug I can think of that goes that way.

Your sig is messed up. "And if you let them, they'll tell it you"

I think it should be "And if you let them, they'll tell it TO you."
 
I never worked at a place where we could do switches without physician orders, but we could certainly suggest it. Half the time, by the time we could get to the chart (this was pre-eMAR), the doctor would have changed something, or even discharged the patient. 😳
 
Tell me how it goes when you convert a patient 1:1 from 900mg of clinda.
SMH...this has fully convinced me of the benefits of pharmacy postgraduate education.

all joking aside though this does illustrate how backwards it is working without EMR/EMAR.

Sparda have you considered maybe looking at a paper chart or even better, talking with the RN so everyone's on board before you start switching? If anything the RN probably has more clout with the MDs in terms of IV to PO switching.
 
So why is the PO dose lower than IV?

im guessing in this case the high iv and low po dose is not related to po bioavailability. IV clinda is only used in severe infection. that said severe infection requires higher doses. whereas the lower po dose is use for common infection, and because of its high bioavailability it's lower dose is used. also b/c of higher chances of clostridium infection a higher po dose is not advisable.
 
im guessing in this case the high iv and low po dose is not related to po bioavailability. IV clinda is only used in severe infection. that said severe infection requires higher doses. whereas the lower po dose is use for common infection, and because of its high bioavailability it's lower dose is used. also b/c of higher chances of clostridium infection a higher po dose is not advisable.

I guess the part about the severe infection could be true, but not the real reason. We don't use lower doses of other antibiotics that are available IV and PO, even though one could argue that PO antibiotics are generally used for less severe infections. And would you think the risk of C. diff is tied to route of administration?

Sparda, any input?
 
I guess the part about the severe infection could be true, but not the real reason. We don't use lower doses of other antibiotics that are available IV and PO, even though one could argue that PO antibiotics are generally used for less severe infections. And would you think the risk of C. diff is tied to route of administration?

Sparda, any input?

I've been trying to find an answer for that but nothing. I'm thinking something to do with kinetics.
 
I guess the part about the severe infection could be true, but not the real reason. We don't use lower doses of other antibiotics that are available IV and PO, even though one could argue that PO antibiotics are generally used for less severe infections. And would you think the risk of C. diff is tied to route of administration?

Sparda, any input?

I think I know. But maybe I will PM you my proposed answer so I don't ruin it for the students.
 
imagine if we had an antibiotic with an oral option that was 100% bioavailable and 45% less costly than its IV version? imagine. we would still keep picc lines in and infuse vanc for those with poor payer coverage and send those with commercial pay to our ID's infusion suite for dapto. you bet your ass we would.
 
And would you think the risk of C. diff is tied to route of administration?

why would it not? C. dif => severe diarrhea. this would be in the colon via po route?
prolonged use of abx or high doses should play a factor.
 
why would it not? C. dif => severe diarrhea. this would be in the colon via po route?
prolonged use of abx or high doses should play a factor.

It's not tied to route of administration...lots of iv drugs reach the gut , iv clinda included, and can predispose the patient to c dif. I see it a lot with the use of Zosyn.

Also PPIs can increase the risk and it really doesn't matter IV or po
 
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It's not tied to route of administration...lots of iv drugs reach the gut , iv clinda included, and can predispose the patient to c dif. I see it a lot with the use of Zosyn.

Also PPIs can increase the risk and it really doesn't matter IV or po
I was recently at a talk about antibiotic heterogeneity, and the speaker felt that the 3rd gen cephalosporins were the biggest culprit, especially ceftazidime. Certainly any abx that can kill gut flora can be a factor.
 
why would it not? C. dif => severe diarrhea. this would be in the colon via po route?
prolonged use of abx or high doses should play a factor.

The route of administration makes no difference...about 2/3rds of a dose of clindamycin (regardless of route) is going to be eliminated in the stool. Goes back to your basic ADME principles.

And sorry I forgot about the punchline on this - GI intolerance is the main reason the PO dose is lower. If you look back at the old HIV-OI (toxo, PCP, etc.) that looked at oral clindamycin as an alternative for sulfa-intolerant patients, the dose-limiting toxicity was (and still is) adverse GI events. Anywhere from ~15% to 30% of patients couldn't tolerate the doses required for treatment (600mg PO at a time). You can imagine that the rate would be much higher for the 900mg doses.
 
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