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No one has 100% completely perfect answer... I certainly don't.
Somebody needs to take a screenshot of this quote.
No one has 100% completely perfect answer... I certainly don't.
I got an interesting clinical question for you wizards! (too busy to answer yours i know im lazy).. I made a hypothetical clinical case based on the question in mind, but if you like, you can skip to bottom to get to the actual clinical question.
Patient is recovering hospital from acute renal failure due to a pre-renal insult, but has CKD stage to the point where their day to day crcl is 18. For whatever reason (lets say acute hospital related infection and bacteremia develops), they will be in the hospital long term (1-2 weeks) and needing VTE prophy ( hx of vte, current sepsis/bacteremia, ie they absolutely NEED VTE prophy). Initial choice is heparin SC. They develop HIT (confirmed) and you treat successfully short term with argatroban to the appropriate APTT indicator until their platelets go back up. After the platelets normalize, what do yo udo next, since heparin , lmwh, and fondaparinux are all contraindicated.
TL;DR version
Patient has ABSOLUTE need of VTE prophy, but is in ARF , CrCl=18 , HIT develops within days of hospital admission and is confirmed and treated with argatroban. Now that platelet count is normal, what do you use for VTE prophylaxis, given that heparin, LMWH, and fondaparinux all seem like inappropriate choices?
Would you continue DTI ? Start oral anticoagulation or antiplatelet therapy short term? Go with some oddball option?
I'll answer your question with a question - what level of anticoagulation does the patient need at this point? And for how long? This is for all the young'uns out there.
I'll answer your question with a question - what level of anticoagulation does the patient need at this point? And for how long? This is for all the young'uns out there.
His case is regarding HIT, not HITT. So what you are driving at is debatable.
What do you mean by what level? ?
Prophylaxis is clearly indicated due to advanced age (forgot to put this in the case),prolonged immobility, bacteremia, and history of VTE.
For duration I would say for the duration of the hospital stay, or until infection resolves and patient is mobile. No clear indication for long term therapy.
His case is regarding HIT, not HITT. So what you are driving at is debatable.
By level I mean intensity of anticoagulation (therapeutic, prophylactic, something else).
But is there a difference in the way you treat HIT vs. HITT? What percentage of patients with HIT develop thrombosis without treatment? And in what time frame?
But is there a difference in the way you treat HIT vs. HITT? What percentage of patients with HIT develop thrombosis without treatment? And in what time frame?
Yep, the numbers you are thinking of in your head are regarding the acute timeframe regarding treatment(or lack of) with DTIs, not long-term. - why do you think CHEST has always specifically avoided this question? Because there is no clear answer at all.
Sorry, but you are barking up the wrong tree trying to pimp me with questions on this disease state.
So what is your time frame for cessation of full-dose anticoagulation? I think the literature supports a specific cutoff point, in addition to the underlying pathophysiology making sense.
Define "the literature" if you mean "the literature" as in experts or a consensus view? If so, you are sadly mistaken. You will find some articles that give a cut-off point, but it's not clearly defined or well-studied. It's arbitrary.
I would recommend 30 days of overall anticoagulation therapy (including the DTI portion), but that's somewhat arbitrary from reviews I've conducted and research I've conducted myself.
All the "literature" regarding "a specific cutoff point" is very weak evidence.
Hence the debate.
So it comes down to as you were saying, what level of anticoagulation is appropriate for the patient. Not every patient is an appropriate candidate for 30 days of anticoagulation therapy in isolated HIT.
So to answer your question - I would absolutely treat HIT differently than HITT. (duration of anticoagulation)
The "literature" isn't guideline-based, I'm referring to the few studies that have actually looked at this. My arbitrary reviews reviews have also pointed me to the 30 day cutoff - which is what I use in practice.
I disagree with the differentiation between HIT and HITT though - I believe they're one in the same (unless you're talking "Type 1" and "Type 2", but I don't think you are). The underlying pathophysiology is the same, and we have no clinical way of differentiating who will and will not progress to thrombosis.
The ultimate duration of anticoagulation depends on the underlying condition - but I wouldn't go less than 30 days in the majority of cases. To me, the risk of subsequent thrombosis is the most pressing issue.
ETA: In response to your Devil's advocacy - I'm not supporting 3 - 6 months of anticoagulation by any means, unless the underlying condition (e.g., non-provoked PE) would support that duration. In this patient, I would probably acutely treat for 30 days and then switch to prophylaxis if warranted. And malpractice lawyers would have a field day in either event if they really wanted to, so they wouldn't sway me one way or another.
See my post, I didn't say guidelines, I say strong evidence. It's not out there. Trust me.
You are contradicting yourself. You are saying you would treat HIT for 30 days. You should be treating HITT for longer than that.
You said expert consensus, which to me means guidelines.
And I am not contradicting myself. What I was getting at was the treatment of HIT in and of itself, which requires therapeutic anticoagulation for a period of time beyond the acute platelet recovery (my 30 day cutoff). Thrombosis should be treated as such, although the guidelines do not have a clear duration - however, it's probably reasonable to treat as a provoked VTE in that case. So yes, perhaps beyond 30 days.
Sorry, when I did my edit, I added the "good" evidence part. There isn't any.
Not to get all semantics here, in a way you disagree with my differentiation of HIT and HITT, but you then say they same things I do regarding duration of treatment - hence you are differentiating too.
Coagulopathies, mechanical ventilation
That is true - I think where I disagreed was during the initial treatment phase (not withstanding the thrombosis part). I think every patient requires a minimum duration of full anticoagulation, regardless of platelet recovery. And that is what I often see missed - platelets bounce back, switch to prophylaxis. Which I don't think is appropriate.
My apologies for the misunderstanding.
QUESTION FOR 4/19
In which patients is stress ulcer prophylaxis actually indicated? Our medical interns can never get this right.
Personally, in most cases, I agree with you, but you do realize we could very well be "wrong."
And even that said as to what I have been alluding to, I don't think every isolated HIT patient is warranted the risk of even 30 days of warfarin. The patient scenario presented gives a couple of factors that make warfarin a little tricky. (i.e. increased bleeding risk)
Cook's criteria, and what I believe also.
However, there is at least one disease state outside of those that is a quality measure that you add SUP.
It's not an easy answer to find, but will be impressed if someone does.
Follow-up question - do PPI increase or decrease your risk of VAP?
There were a few missing in there, I thought.
>>>Numerous randomized trials, using different doses
and various study populations, have provided controversial results
on the benefits of specific stress bleeding prophylaxis agents
in relation to the increased risk of VAP.
LOL I told you those guidelines were a page turner
EDIT:
Stress bleeding prophylaxis, transfusion, and hyperglycemia.
1. Comparative data from randomized trials suggest a trend
toward reduced VAP with sucralfate, but there is a slightly
higher rate of clinically significant gastric bleeding, compared
with H2 antagonists. If needed, stress bleeding prophylaxis
with either H2 antagonists or sucralfate is acceptable
(Level I).
So much for question of the day.
So much for question of the day.
A new thread for each question would make it easier to follow. Just saying.
I vote to have a separate pharmacy forum for healthcare system practice.
Then we would need one for CVS vs. Walgreens (...and PBMs too) ...
BTW - back on hyponatremia.
IV conivaptan is an option.
The vaptans also run the risk of overcorrection.
In acutely symptomatic situations (i.e. seizures/coma) yes, the use of hypertonic saline is absolutely justified in those cases.
However, you do NOT want to correct it to normal in the next 48 hours. .
We don't load vanco! All dosing is based on a hospital nomogram targeting a 10-15 trough for all indications. I wasn't a believer at first, but I think the literature that has come out in the last year, year and a half really fails to support higher troughs at this point.
SInce you are really working at this - I'll throw you a bone, start looking for the outcomes of "ventilator bundles" and the components.
. To be more specific, how fast is too fast? (i.e. how much of a rise is safe in 24hrs, 48 hrs) Sometimes in that timeframe, you can actually hit the "normal" range in 48 hours and still be safe depending on where you started.
Renal Impairment and Anticoagulant DosingI got an interesting clinical question for you wizards! (too busy to answer yours i know im lazy).. I made a hypothetical clinical case based on the question in mind, but if you like, you can skip to bottom to get to the actual clinical question.
Patient is recovering hospital from acute renal failure due to a pre-renal insult, but has CKD stage to the point where their day to day crcl is 18. For whatever reason (lets say acute hospital related infection and bacteremia develops), they will be in the hospital long term (1-2 weeks) and needing VTE prophy ( hx of vte, current sepsis/bacteremia, ie they absolutely NEED VTE prophy). Initial choice is heparin SC. They develop HIT (confirmed) and you treat successfully short term with argatroban to the appropriate APTT indicator until their platelets go back up. After the platelets normalize, what do yo udo next, since heparin , lmwh, and fondaparinux are all contraindicated.
TL;DR version
Patient has ABSOLUTE need of VTE prophy, but is in ARF , CrCl=18 , HIT develops within days of hospital admission and is confirmed and treated with argatroban. Now that platelet count is normal, what do you use for VTE prophylaxis, given that heparin, LMWH, and fondaparinux all seem like inappropriate choices?
Would you continue DTI (and break the bank?) ? Start oral anticoagulation or antiplatelet therapy short term? Go with some oddball option? Do you risk renal dosing of fonda?
Im intersted in knowing what you guys think would be the most effective real world option based on the costs and overall likelyhood of efficacy. Personally I would probably pick warfarin on gut instinct alone, but am unsure if this is effective for VTE prophy. (edit.. looked up some articles, warfarin is good VTE prophylaxis .. and is still my top choice pick, but is it the best for this patient?)
How about the link to c. Diff? What to do what to do...
Hmm, was it 10 mEq/L/day?
Renal Impairment and Anticoagulant Dosing
1.4.6. We recommend that renal function be considered when making decisions about the use and/or the dose of LMWH, fondaparinux, and other antithrombotic drugs that are cleared by the kidneys, particularly in elderly patients, patients with diabetes mellitus, and those at high risk for bleeding (Grade 1A). Depending on the circumstances, we recommend one of the following options in this situation: avoiding the use of an anticoagulant that bioaccumulates in the presence of renal impairment, using a lower dose of the agent, or monitoring the drug level or its anticoagulant effect (Grade 1B).
http://chestjournal.chestpubs.org/content/133/6_suppl/381S.full
circa 2008
Does anyone else have a Zosyn continuous infusion protocol?
I got an interesting clinical question for you wizards! (too busy to answer yours i know im lazy).. I made a hypothetical clinical case based on the question in mind, but if you like, you can skip to bottom to get to the actual clinical question.
Patient is recovering hospital from acute renal failure due to a pre-renal insult, but has CKD stage to the point where their day to day crcl is 18. For whatever reason (lets say acute hospital related infection and bacteremia develops), they will be in the hospital long term (1-2 weeks) and needing VTE prophy ( hx of vte, current sepsis/bacteremia, ie they absolutely NEED VTE prophy). Initial choice is heparin SC. They develop HIT (confirmed) and you treat successfully short term with argatroban to the appropriate APTT indicator until their platelets go back up. After the platelets normalize, what do yo udo next, since heparin , lmwh, and fondaparinux are all contraindicated.
TL;DR version
Patient has ABSOLUTE need of VTE prophy, but is in ARF , CrCl=18 , HIT develops within days of hospital admission and is confirmed and treated with argatroban. Now that platelet count is normal, what do you use for VTE prophylaxis, given that heparin, LMWH, and fondaparinux all seem like inappropriate choices?
Would you continue DTI (and break the bank?) ? Start oral anticoagulation or antiplatelet therapy short term? Go with some oddball option? Do you risk renal dosing of fonda?
Im intersted in knowing what you guys think would be the most effective real world option based on the costs and overall likelyhood of efficacy. Personally I would probably pick warfarin on gut instinct alone, but am unsure if this is effective for VTE prophy. (edit.. looked up some articles, warfarin is good VTE prophylaxis .. and is still my top choice pick, but is it the best for this patient?)
is arixtra ci?
That is technically correct...the best kind of correct.
And what about the cost?Newer drugs are a good option here. I would continue with argatroban because (from the info we have) the patient is tolerating it at this point. Not best choice for short term therapy. Lovenox could be TRIED as it is not certain that HIT will reappear with it and risk in general is lower, but I think argatroban is more appropriate in this patient.
I thought he said abcdefg?That is technically correct...the best kind of correct. But you could counter that one could monitor antiXa levels.
And what about the cost?
I thought he said abcdefg?
No cqod 4/21?
No cqod 4/21?
Clinical every other day?