Antibiotic infusion rate

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Colba55o

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Perhaps I need to post this in the pharmacy forum but thought I might try here first.

Are there any guidelines out there re: the rate at which the antibiotics we give for surgical prophylaxis may be safely given?

During residency, we routinely pushed 1-2g Ancef within 30 minutes before incision time. Now in my practice, the pre-op RNs mix it up for us as "IV piggybacks" and all the nurses think it must be given over 30 minutes.
The only antibiotic I routinely give slowly is Vanco and I believe Cipro or flagyl if it has instructions to do so on the bag. However with Invanz and clinda, I usually give them over 5-10 minutes at the longest. I had a CRNA tell me today that giving Gentamicin too quickly can cause deafness. :rolleyes:

Anecdotal "this is what I do" responses are appreciated, but really looking for literature out there, if it exists

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I had a CRNA tell me today that giving Gentamicin too quickly can cause deafness. :rolleyes:

Sorry to dilute your thread but I'm curious -- is this not the case? I recently read a book (the brain that changes itself) in which a patient experienced ototoxicity from gentamicin. I also remember a retired NICU RN in my family telling me how they used to push gentamicin fast in neonates, not knowing its effects on hearing. Just curious, thanks...
 
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Based on a the peak and trough which are directly proportional to amount infused, it would make sense if you gave it at a faster rate, you would surpass the the therapeutic peak and enter into the toxic range for the Peak. Which states is about >10-12mcg/mL which are shown to induce nephro/ototoxcity at that concentration.

http://www.ncbi.nlm.nih.gov/m/pubmed/23557866/

But then again I posted a study that was done on newborns you might find interesting.
 
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I am aware of the risk of ototoxicity with aminoglycosides. However I have not heard of a causal relationship between rate of administration and ototoxicity. Also I don't really do a lot of peds and never work with newborns.
 
I am aware of the risk of ototoxicity with aminoglycosides. However I have not heard of a causal relationship between rate of administration and ototoxicity. Also I don't really do a lot of peds and never work with newborns.

i was taught to just run it in over 15 min because of risk of ototoxicity. all the profs said the same thing. worsened risk in renal pts. is it really worth it to push? I agree it's probably unlikely, but why risk it. I wouldn't want someone to rapid IVP it into me just b/c they felt like it.
 
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Bump. Still looking for that literature...
 
If it's in a little bag, like gent, vanco, clinda; to make people feel happy and infuse it over a hour, get a mircrodripper (60gtt/ml) and set the drip rate to (mls in the bag)/min.

100cc bag is 100 drips/min.
 
By the way, this is a great question and I wish I knew the answer.

Unfortunately, if I am unfamiliar with the antibiotic (which basically is all of them except maybe four), I'm going to do my best to follow the pharmacy recommendations because of those case reports with clinda.
 
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I was in a case today (CA-1) and I started infusing the Metronidazole very slowly to match the rate of an hour as stated on the pharmacy label. My attending turned around and said "what are you doing?" I told him I was infusing it slowly per pharmacy's recs and that I believed it should be infused slowly like clinda or even vanc. He basically called me stupid and opened up the IV fully. Then I turned around and proceeded to open the ancef full flush even though the package said over 30 minutes ;):shrug:
 
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DO NOT bolus clindamycin quickly.

There are case reports of cardiac deaths from this.

This. Those of us in the military are familiar with a case from Walter Reed where a young lady died undergoing a routine breast surgery.

Otherwise, Ancef can be pushed. Vanc slowly

The other thing to keep in mind is that the data and even the SCIP measures show that the infusion needs to be STARTED within 2 hrs of cut time. The only time it needs to be completely in is in the case of tournequit use in which the infusion should be completed prior to tournequit up.
 
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Never heard of a cardiac arrest post clindamycin, i usually give it pretty quickly (less than 1min)...mechanism?

You can bolus vanc if you block histamine receptors ( per sdn, never tried it myself).
 
This. Those of us in the military are familiar with a case from Walter Reed where a young lady died undergoing a routine breast surgery.

Otherwise, Ancef can be pushed. Vanc slowly

The other thing to keep in mind is that the data and even the SCIP measures show that the infusion needs to be STARTED within 2 hrs of cut time. The only time it needs to be completely in is in the case of tournequit use in which the infusion should be completed prior to tournequit up.
That case, and a similar one at Children's were still being used as cautionary tales when I was there. Everyone involved with the Reed one got screwed.

Then, we go to WHC, where they put vanc on a micro dripper, and used it as an anti-hypertensive for off-pump cases, if needed.

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I can't find the case report itself. just bunch of titles/headlines. In the Reed case, how did they decide its the clindamycin. Did the anesthesiologist only give clindamycin in the OR..? Weird to give clindamycin as the first medication. I guess once the reports out there, it's hard to defend against it. But when clindamycin is used millions of time a year in the OR, and i feel like most anesthesiologists do not run clindamycin over 30 mins, but we had like 2 claimed cardiac arrests? does that mean anything when the risk is like .000001%. clinically? That risk is probably lower than congenital heart disease/prolonged qt, and go into cardiac arrest because of that
 
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That case, and a similar one at Children's were still being used as cautionary tales when I was there. Everyone involved with the Reed one got screwed.

Then, we go to WHC, where they put vanc on a micro dripper, and used it as an anti-hypertensive for off-pump cases, if needed.

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That's like the Co2 tank and the newborn at Tripler now. Hear about it at every lecture regarding tank specs etc etc.
 
Ancef/cefoxitin get IV pushed. Basically everything else comes in a bag, so hang it to gravity, open the roller clamp halfway and drip it in. I don't really understand what the issue here is, this is classic mental masturbation.

If we followed the package inserts for all of our drugs we couldn't even induce with propofol and we'd spend 20minutes administering drugs like ATIII etc. Now I'm not advocating IV pushing everything, but literally every drug insert says intermittent bolus if not infusion over 10-60minutes.
 
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I have accidentally (when i was an inexperienced CA-1) let the gent run in a 16 G IV. pt was not deaf when he denied nausea or pain at the end of the case.

I have also done the same to clinda before. No cardiac death. (I really question the validity of 1 case report to link causation of clinda to cardiac death, wtf is cardiac death??? how do we know it's not an anaphylaxis reaction so it was poor recognition and it really didn't matter how much clinda you gave)

I realize that is horrible science and pretty result oriented, but it got me thinking:

The gent side effect makes no sense to me: As we routinely infuse 500mg in 100cc bags of gent for a lot of hardware infections etc. If you gave that 100cc bag over 20 mins (most of the time it's over 10), you are literally giving all 100mg (standard prophy dose for just normal stuff) over 4 mins (or 2 mins if youre being realistic). i just don't see the blood concentration or the diffusion rate to the ears to be THAT fast to be causing ototoxicity. I also recall reading sometime in my medical career that the gent ototoxicity is over chronic use rather than 1 time dosing.

I would love to be proven wrong, as I really don't have that strong of an opinion on this. In fact i still infuse both drugs slowly, but the above is always on the back of my mind.
 
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DO NOT bolus clindamycin quickly.

There are case reports of cardiac deaths from this.

This. Those of us in the military are familiar with a case from Walter Reed where a young lady died undergoing a routine breast surgery.

Otherwise, Ancef can be pushed. Vanc slowly

The other thing to keep in mind is that the data and even the SCIP measures show that the infusion needs to be STARTED within 2 hrs of cut time. The only time it needs to be completely in is in the case of tournequit use in which the infusion should be completed prior to tournequit up.

please kindly link us the articles
 
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I don't know how clindamycin produces hypotension and cardiac arrest, but, since it produces muscle weakness in the skeletal muscle, I wouldn't be surprised if it's a similar mechanism (possibly by messing up some electrolytes, e.g. K+).

The fact that a drug produces life-threatening side-effects only in certain patients shouldn't make anybody just ignore them (especially when we don't know who those patients are, as with clinda). For example, one will not get torsades after haldol in most patients, but one should still check the QTc before giving it. To me, any drug that can kill or seriously harm a patient should be treated with respect and vigilance. Just because one can (e.g. bolus it) doesn't mean one should. Would one risk it if the patient were one's mother?

The cowboy or cavalier attitude in regard to certain drugs suggests that one doesn't know or doesn't care. At least to juries. First do no harm.

Regarding boluses, unless I have to, I give a number of drugs in small aliquots, especially the first dose. One never knows when somebody has made a mistake while preparing or labeling the drug. It may take a few minutes longer, but that's what I am there for. You can always give more, but you can seldom take it back.
 
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Here is a Washington Post article I found quickly that talks about it. A lot of the hub bub deals with the ensuing events, but the supposed inviting event was the bolus of 900 of clinda. And I misspoke. It was a neck cyst, not a breast surgery.


Army Doctor Today Faces Charges in Girl's Death

This article is just weird. He gave clindamycin, supposedly UNdiluted, over 1-2 MINUTES. Then , the girls BP and HR fell. This would very well be anaphylaxis. Then the resident gave some drug that didn't make her pressure go up, but did increase her HR. Then he gave esmolol for her HR when there was no pressure.

Sounds weird, and probably poorly managed. But im guessing some details were left out. Most importantly what did he give that made the HR go up. Was it atropine or the like , or was it something like epi.
 
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This article is just weird. He gave clindamycin, supposedly UNdiluted, over 1-2 MINUTES. Then , the girls BP and HR fell. This would very well be anaphylaxis. Then the resident gave some drug that didn't make her pressure go up, but did increase her HR. Then he gave esmolol for her HR when there was no pressure.

Sounds weird, and probably poorly managed. But im guessing some details were left out

That and the story is being reported/relayed by individuals presumably with zero medical training.
 
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How did they decide that the infusion rate of clindamycin was the culprit? There are multiple reports of clindamycin causing cardiac arrest even when it is infused slowly. In fact there are multiple reports of cefazolin causing cardiac arrest too. Who really knows the cause in these cases. I'm not convinced that rapid infusion of clindamycin caused the cardiac arrest in this or any other cases. Especially in the setting of general anesthesia, there are much more likely causes including anesthetic overdose or airway issues and hypoxemia.
 
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The fact that a drug produces life-threatening side-effects only in certain patients shouldn't make anybody just ignore them (especially when we don't know who those patients are, as with clinda). For example, one will not get torsades after haldol in most patients, but one should still check the QTc before giving it. To me, any drug that can kill or seriously harm a patient should be treated with respect and vigilance. Just because one can (e.g. bolus it) doesn't mean one should. Would one risk it if the patient were one's mother?

I am sure this is generalized enough and worded well enough that no one will disagree with this.

However, that's not the point. As i understand it: we are still in the prelim stages of trying to determine whether or not the drug ACTUALLY produces a life threatening side-effects. As mentioned above, 1 barely reliable source is saying clinda was the culprit. That is LITERALLY the extent of our knowledge.

Also 0 sources have been produced that showed gent caused ototoxicity with rapid infusion.
 
I am sure this is generalized enough and worded well enough that no one will disagree with this.

However, that's not the point. As i understand it: we are still in the prelim stages of trying to determine whether or not the drug ACTUALLY produces a life threatening side-effects. As mentioned above, 1 barely reliable source is saying clinda was the culprit. That is LITERALLY the extent of our knowledge.

Also 0 sources have been produced that showed gent caused ototoxicity with rapid infusion.
The way I see it, this is like with anaphylaxis to a penicillin: it's just not worth the risk of even trying a cephalosporin.

With major adverse effects, even if there is just one case report, why risk it, especially if it's as easy as infusing instead of bolusing the drug? First do no harm.
 
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The way I see it, this is like with anaphylaxis to a penicillin: it's just not worth the risk of even trying a cephalosporin.

With major adverse effects, even if there is just one case report, why risk it, especially if it's as easy as infusing instead of bolusing the drug? First do no harm.

But there's case reports of clindamycin associated cardiac arrest with bolus, infusion, and unspecified infusion rate. Why do people assume bolus is worse? Maybe it needs a black box warning. Jk
 
The way I see it, this is like with anaphylaxis to a penicillin: it's just not worth the risk of even trying a cephalosporin.

With major adverse effects, even if there is just one case report, why risk it, especially if it's as easy as infusing instead of bolusing the drug? First do no harm.

The benefit of knowing what the truth is and having a good intellectual discussion without trolls can be beneficial regardless of whether or not you "risk it" in actual practice, some say that might be what separates us from CRNAs. Also, for what it's worth, i'm still not convinced there is actually a "major adverse effect".

But it's kinda funny that you mention the cephalosporin comment, it is precisely because you're NOT RISKING the cephalosporins that led us to the discussion of benefit/risks of clinda and gent infusions.
 
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I've just been enlightened!
For the next bull.s pen allergic patient (99.9%) i'll tell them that i can't give a cephalosporin because of the bs risk of cross allergy and that i can't give them clindamycin because there are news reports of cardiac death, and a risk of going deaf from genta so i'll give them nothing and my day will be easier.
 
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I've just been enlightened!
For the next bull.s pen allergic patient (99.9%) i'll tell them that i can't give a cephalosporin because of the bs risk of cross allergy and that i can't give them clindamycin because there are news reports of cardiac death, and a risk of going deaf from genta so i'll give them nothing and my day will be easier.

linezolid?
 
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Lets just ertapenem everyone.
lol I just got burned by my fellow/staff on rounds for a septic sicu pt. We had them on ertapenem for a perfed bowel and the hospital policy is that we need to get an ID consult for use greater than 72 hours. They wanted to switch to zosyn and I was arguing for just giving ID a call and keeping it going. I was under the impression (wrongly) that it's bad to switch antibiotics mid treatment for pan sensitive bugs, so I wanted to stick with ertapenem. So after I got drilled, low and behold two days later, the pt is back on ertapenem after they got sicker. I know that's only tangentially related, but I just wanted to share the story.
 
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lol I just got burned by my fellow/staff on rounds for a septic sicu pt. We had them on ertapenem for a perfed bowel and the hospital policy is that we need to get an ID consult for use greater than 72 hours. They wanted to switch to zosyn and I was arguing for just giving ID a call and keeping it going. I was under the impression (wrongly) that it's bad to switch antibiotics mid treatment for pan sensitive bugs, so I wanted to stick with ertapenem. So after I got drilled, low and behold two days later, the pt is back on ertapenem after they got sicker. I know that's only tangentially related, but I just wanted to share the story.

yea always narrow down. zosyn is still a big gun. probably shouldve switched to ampicillin
 
lol I just got burned by my fellow/staff on rounds for a septic sicu pt. We had them on ertapenem for a perfed bowel and the hospital policy is that we need to get an ID consult for use greater than 72 hours. They wanted to switch to zosyn and I was arguing for just giving ID a call and keeping it going. I was under the impression (wrongly) that it's bad to switch antibiotics mid treatment for pan sensitive bugs, so I wanted to stick with ertapenem. So after I got drilled, low and behold two days later, the pt is back on ertapenem after they got sicker. I know that's only tangentially related, but I just wanted to share the story.

We gotta be good stewards of ABx. but the true lesson here for me is to not be result oriented, i think switching is still the right move.


yea always narrow down. zosyn is still a big gun. probably shouldve switched to ampicillin

Does amp cover gram - from the bowel?

to me, zosyn (grame + and gram -) is much more broad than ertapenem (ESBL gram -), am i wrong?


Can we plz get back to the goal? verify/debunk that clinda infusion rate causes cardiac death and gent causes deafness?
 
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We gotta be good stewards of ABx. but the true lesson here for me is to not be result oriented, i think switching is still the right move.




Does amp cover gram - from the bowel?

to me, zosyn (grame + and gram -) is much more broad than ertapenem (ESBL gram -), am i wrong?


Can we plz get back to the goal? verify/debunk that clinda infusion rate causes cardiac death and gent causes deafness?

ertapenem covers everything pretty much.
ampicillin covers gram negatives some. i just randomly threw it out there as an example
 
lol I just got burned by my fellow/staff on rounds for a septic sicu pt. We had them on ertapenem for a perfed bowel and the hospital policy is that we need to get an ID consult for use greater than 72 hours. They wanted to switch to zosyn and I was arguing for just giving ID a call and keeping it going. I was under the impression (wrongly) that it's bad to switch antibiotics mid treatment for pan sensitive bugs, so I wanted to stick with ertapenem. So after I got drilled, low and behold two days later, the pt is back on ertapenem after they got sicker. I know that's only tangentially related, but I just wanted to share the story.

They were still right and you were wrong. Just because the patient got worse doesnt mean it had to do with deescalation of the antibiotic.
 
They were still right and you were wrong. Just because the patient got worse doesnt mean it had to do with deescalation of the antibiotic.
I know, I'm just a little butthurt that they demolished me on rounds and we've come back full circle to where we were before.
 
If you google the book "Avoiding Common Anesthesia Errors" you can read chapter 42 starting on page 176 for free entitled "Be aware of the drugs that require slow intravenous administration".
They don't provide resources but a few of their annectodal stories were enough to convert me from a slammer to a slow pusher.
 
Well played with the comment above!

Also do you really think slow pushing it vs slamming it is any different as far as concentration in the blood after you give it? And the brief transient concentration that is higher makes a difference in these "sudden cardiac death" or anaphylaxis situations?
 
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I bet the wife has been much happier since you made the change.

Hah! Nice


Also do you really think slow pushing it vs slamming it is any different as far as concentration in the blood after you give it? And the brief transient concentration that is higher makes a difference in these "sudden cardiac death" or anaphylaxis situations?[/QUOTE]

To illiterate, I do a lot of peds. For a give dose of Clindamycin I'll dilute it in a 20 cc syringe and give a little here and a little there as I'm getting the little fella/gal settled in.

I have the same method when I have to give a int. dose of Protamine and have seen the hypotension when I get too eager.

Yes, I realize that Protamine and antibiotics are different but it gives me peace of mind and doesn't slow me down in the least.

If I ever have you as a patient I'll be happy slam in some clinda with a gent chaser before you're off to sleep and we can see what happens. It'll be a hoot.
 
If I ever have you as a patient I'll be happy slam in some clinda with a gent chaser before you're off to sleep and we can see what happens. It'll be a hoot.

I realize the way i phrased the question might have been interpreted as an ad hominem attack. I did not mean You (@swap gas) personally, and i will try to phrase it better in the future to avoid offending anyone.

However, i believe the point still stands in peds. the dose you give is lower. Even with a smaller volume of distribution (higher in terms of cc/kg), the concentration will be comparable to adults.

Furthermore, I guess not everyone agrees that it is assumed the pt is asleep under GA. But please interpret my basic setting as someone who is under general anesthesia.
I make it a point to slowly drip cefazolin for c-section awake patients.

Again, the reason i bring this up is to really have a good philosophic discussion about this topic. does how fast the antibiotic go in matter given its elimination is slow (and negligible) and the concentration is going to be the same in a few cardiac cycles regardless of how fast it goes in? . Literature certainly says it does not matter in anaphylaxis or anaphylactoid reactions. Does it matter in the "cardiac deaths"?
 
I realize the way i phrased the question might have been interpreted as an ad hominem attack. I did not mean You (@swap gas) personally, and i will try to phrase it better in the future to avoid offending anyone.

However, i believe the point still stands in peds. the dose you give is lower. Even with a smaller volume of distribution (higher in terms of cc/kg), the concentration will be comparable to adults.

Furthermore, I guess not everyone agrees that it is assumed the pt is asleep under GA. But please interpret my basic setting as someone who is under general anesthesia.
I make it a point to slowly drip cefazolin for c-section awake patients.

Again, the reason i bring this up is to really have a good philosophic discussion about this topic. does how fast the antibiotic go in matter given its elimination is slow (and negligible) and the concentration is going to be the same in a few cardiac cycles regardless of how fast it goes in? . Literature certainly says it does not matter in anaphylaxis or anaphylactoid reactions. Does it matter in the "cardiac deaths"?

I was just having fun with you. I agree with you regarding anaphylaxis, rate of infusion would not have any influence. I'm referring to Clindas case reports of profound/refractory hypotension. I have no idea what the mechanism is or how real/rare it is. As FFP stated, it causes muscle weakness and so for me, it's conceivable that those anecdotes could have some merit.

If I push 100 mcg of phenylephrine I would expect more of a response than if I diluted it and peppered it in over the course of 10 mins. Maybe it's voodoo when it comes to Clinda but I've heard about it enough times that I'm happy to water it down.
 
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