PE/DVT discussion

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EM2BE

EM2BE

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I've seen many ways of practice, and I'm curious as to what you guys do in the real world. If you suspect DVT / PE, how do you go about it?

I've seen:
1. US of LE - if positive, treat and don't worry about CTA and treat as PE if pt is short of breath
2. US of LE and CTA - with the reason that they are to be on coumadin/lovenox longer for PE than DVT
3. Just CTA (even if LE is swollen) - If positive, then treat, and if negative, then go for the US

I know the treatment with lovenox is becoming more common than it used to be (replacing heparin for bridging and sometimes instead of coumadin). This can be another discussion I'm open to hearing about.

All our DVTs / PEs pretty much get admitted. A few times they have gone home with Lovenox prescription, but this was for DVT or smaller PEs and making sure they have the resources available.
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US first. If positive, stop there. No need for the risks of damaging kidneys and ionizing radiation.

Especially if they're pregnant.
 
PE pays more by most insurers with DRG payments, so we always CTA. You can't admit with the diagnosis of PE with someone with chest pain/shortness of breath with only a positive DVT ultrasound. Yes, we all know it's a PE, but you'll be defending yourself in an audit and you won't have a leg to stand on (no pun intended). Many insurers are resisting payment for inpatient treatment of DVT's anyhow.

If their leg is swollen or painful, then I'll ultrasound if the CTA is negative.
 
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southerndoc said:
PE pays more by most insurers with DRG payments, so we always CTA. You can't admit with the diagnosis of PE with someone with chest pain/shortness of breath with only a positive DVT ultrasound. Yes, we all know it's a PE, but you'll be defending yourself in an audit and you won't have a leg to stand on (no pun intended). Many insurers are resisting payment for inpatient treatment of DVT's anyhow.

If their leg is swollen or painful, then I'll ultrasound if the CTA is negative.
Click to expand...

Same here
 
southerndoc said:
PE pays more by most insurers with DRG payments, so we always CTA. You can't admit with the diagnosis of PE with someone with chest pain/shortness of breath with only a positive DVT ultrasound. Yes, we all know it's a PE, but you'll be defending yourself in an audit and you won't have a leg to stand on (no pun intended). Many insurers are resisting payment for inpatient treatment of DVT's anyhow.

If their leg is swollen or painful, then I'll ultrasound if the CTA is negative.
Click to expand...

Depends on presenting symptoms.

if its CP/dyspnea, etc.. CT chest or V/Q them. If negative and the legs are swollen, doppler them.

If the complaint is only the legs, just doppler. If theyre positive treat, no CT. they all get 6months of pradaxa or warfarin anyway.

*I do CT the pts who are high risk for bleed ing events that come back with positive dopplers. reason being, If they do not already have a PE, and i do not think they are going to be an anticoaguation candidate, I have CTS put a filter in before discharge so the untreated DVT does not become a PE. if they already have the PE, their is no benefit to the filter. i do this in particular with the oncology pts who come in with DVTs as their clot risk is so high.
 
1. Realize that not all PE's arise from the legs. If I'm looking for a PE, I look for a PE, if I'm looking for a DVT, I look for a DVT. If I supsect both, I look for both.

2. I was always under the impression that filters were coagulopathic niduses after a period of years. though I guess that's why some IR guys now have a drive to use the newer removable filters.
 
Agree with Rendar, keep it simple.


First you need to drill down on what you are looking for, DVT or PE? It's two different work ups and decision pathways. Don't even combine the pathways in your head, unless they have symptoms of both.

A patient usually presents with symptoms of one or the other, not often both.

First ask yourself, "Does this patient have signs or symptoms of a PE?" If so, go after the PE. Rule it out. If they have a PE on CT, then you treat it. You are done. At that point, the presence or absence of a DVT is irrelevant. The treatment doesn't change. If your CTA is negative, and they are there for CP/SOB, why would you even think about DVT, unless there were symptoms, OR you have some reason to suspect a false negative PE study (poor bolus, low CT quality, only can do VQ, etc)?

If they present with leg pain/swelling, why jump immediately to "rule out PE"? Check their leg, if it's negative, you are done, and you don't have to worry about PE because they are there for leg pain, not CP/SOB/hypoxia.

It's usually one or the other. Think presenting complaint. Yes, the patho-physiology is tied together, but clinically it's almost always one or the other. If the presenting complaint is CP/SOB and leg pain/swelling, then you check both (starting with chest) then legs if negative.

As far as the OP and discharging "smaller" PEs: Personally, I've never, ever, sent home a PE. Ever. Even if they are already therapeutic on Coumadin. I don't care how small it is, how perfect their sat is, how good their follow up is. No way. This is the reason:

"Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% die subsequently from recurrent embolism. "

http://emedicine.medscape.com/article/300901-overview#7

PE has a high mortality rate. Period. Of all the BS we admit for no good reason, a disease with a mortality of 10-30% deserves admit. Being anti-coagulated is completely irrelevant. Anti-coagulation does not dissolve the clot. Anti-coagulation does not make the source clot that likely is still there, wherever it is, any less likely to break off more pieces and throw further clots and give you that 30% risk of death from subsequent PE. I don't care if they got discharged yesterday after a full PE admit and anti coagulation. If they are back in the ED with symptoms, they threw another clot and they are back in that 10-30% mortality category, until proven otherwise. Admit.

It's equivalent to an unstable angina or nstemi patient. You have a significant mortality rate even with appropriate treatment. If you had an USA or nstemi patient and cards told you, "I know him well. He's not a candidate for CABG or cath anymore. I'm not going to cath him no matter what. Just give him ASA, lopressor, lovenox, an ACE and send him home. Have him continue the lovenox at home and I'll see him in a week," would you be comfortable sending that patient home?

No. If you practice long enough, consultants will come up with stuff like this, "It's a tiny PE. Send him home on lovenox. Admitting him won't change anything."

Yeah, right.
 
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Birdstrike said:
Agree with Rendar, keep it simple.


First you need to drill down on what you are looking for, DVT or PE? It's two different work ups and decision pathways. Don't even combine the pathways in your head, unless they have symptoms of both.

A patient usually presents with symptoms of one or the other, not often both.

First ask yourself, "Does this patient have signs or symptoms of a PE?" If so, go after the PE. Rule it out. If they have a PE on CT, then you treat it. You are done. At that point, the presence or absence of a DVT is irrelevant. The treatment doesn't change. If your CTA is negative, and they are there for CP/SOB, why would you even think about DVT, unless there were symptoms, OR you have some reason to suspect a false negative PE study (poor bolus, low CT quality, only can do VQ, etc)?

If they present with leg pain/swelling, why jump immediately to "rule out PE"? Check their leg, if it's negative, you are done, and you don't have to worry about PE because they are there for leg pain, not CP/SOB/hypoxia.

It's usually one or the other. Think presenting complaint. Yes, the patho-physiology is tied together, but clinically it's almost always one or the other. If the presenting complaint is CP/SOB and leg pain/swelling, then you check both (starting with chest) then legs if negative.

As far as the OP and discharging "smaller" PEs: Personally, I've never, ever, sent home a PE. Ever. Even if they are already therapeutic on Coumadin. I don't care how small it is, how perfect their sat is, how good their follow up is. No way. This is the reason:

"Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% die subsequently from recurrent embolism. "

http://emedicine.medscape.com/article/300901-overview#7

PE has a high mortality rate. Period. Of all the BS we admit for no good reason, a disease with a mortality of 10-30% deserves admit. Being anti-coagulated is completely irrelevant. Anti-coagulation does not dissolve the clot. Anti-coagulation does not make the source clot that likely is still there, wherever it is, any less likely to break off more pieces and throw further clots and give you that 30% risk of death from subsequent PE. I don't care if they got discharged yesterday after a full PE admit and anti coagulation. If they are back in the ED with symptoms, they threw another clot and they are back in that 10-30% mortality category, until proven otherwise. Admit.

It's equivalent to an unstable angina or nstemi patient. You have a significant mortality rate even with appropriate treatment. If you had an USA or nstemi patient and cards told you, "I know him well. He's not a candidate for CABG or cath anymore. I'm not going to cath him no matter what. Just give him ASA, lopressor, lovenox, an ACE and send him home. Have him continue the lovenox at home and I'll see him in a week," would you be comfortable sending that patient home?

No. If you practice long enough, consultants will come up with stuff like this, "It's a tiny PE. Send him home on lovenox. Admitting him won't change anything."

Yeah, right.
Click to expand...

I'm quoting this one for posterity. You are absolutely right. How many times on SDN have the cowboys/minimalists said "doppler the legs - if negative, there's no PE"? I shudder (minimally, but I do) when I think of how this pathway can play out.

They are both clots - but, just like a fire, where is important. In a forest or in a field? OK, bad enough. However, what about a fire in your house? In a bedroom? Different story.
 
Birdstrike said:
Agree with Rendar, keep it simple.


First you need to drill down on what you are looking for, DVT or PE? It's two different work ups and decision pathways. Don't even combine the pathways in your head, unless they have symptoms of both.

A patient usually presents with symptoms of one or the other, not often both.

First ask yourself, "Does this patient have signs or symptoms of a PE?" If so, go after the PE. Rule it out. If they have a PE on CT, then you treat it. You are done. At that point, the presence or absence of a DVT is irrelevant. The treatment doesn't change. If your CTA is negative, and they are there for CP/SOB, why would you even think about DVT, unless there were symptoms, OR you have some reason to suspect a false negative PE study (poor bolus, low CT quality, only can do VQ, etc)?

If they present with leg pain/swelling, why jump immediately to "rule out PE"? Check their leg, if it's negative, you are done, and you don't have to worry about PE because they are there for leg pain, not CP/SOB/hypoxia.

It's usually one or the other. Think presenting complaint. Yes, the patho-physiology is tied together, but clinically it's almost always one or the other. If the presenting complaint is CP/SOB and leg pain/swelling, then you check both (starting with chest) then legs if negative.

As far as the OP and discharging "smaller" PEs: Personally, I've never, ever, sent home a PE. Ever. Even if they are already therapeutic on Coumadin. I don't care how small it is, how perfect their sat is, how good their follow up is. No way. This is the reason:

"Approximately 10% of patients who develop pulmonary embolism die within the first hour, and 30% die subsequently from recurrent embolism. "

http://emedicine.medscape.com/article/300901-overview#7

PE has a high mortality rate. Period. Of all the BS we admit for no good reason, a disease with a mortality of 10-30% deserves admit. Being anti-coagulated is completely irrelevant. Anti-coagulation does not dissolve the clot. Anti-coagulation does not make the source clot that likely is still there, wherever it is, any less likely to break off more pieces and throw further clots and give you that 30% risk of death from subsequent PE. I don't care if they got discharged yesterday after a full PE admit and anti coagulation. If they are back in the ED with symptoms, they threw another clot and they are back in that 10-30% mortality category, until proven otherwise. Admit.

It's equivalent to an unstable angina or nstemi patient. You have a significant mortality rate even with appropriate treatment. If you had an USA or nstemi patient and cards told you, "I know him well. He's not a candidate for CABG or cath anymore. I'm not going to cath him no matter what. Just give him ASA, lopressor, lovenox, an ACE and send him home. Have him continue the lovenox at home and I'll see him in a week," would you be comfortable sending that patient home?

No. If you practice long enough, consultants will come up with stuff like this, "It's a tiny PE. Send him home on lovenox. Admitting him won't change anything."

Yeah, right.
Click to expand...

I agree with about 90% of this post. I don't know why people feel like they need to r/o a venous clot anywhere if you have clear localizing symptoms. The only exception I could see would be in a pregnant patient where you're hoping the doppler is going to find clot to save the CT, but in practice I usually will just throw a dimer at them and if it's positive they get scanned (in the absence of unilateral leg swelling). I categorically reject the idea that chest pain + pos. dimer +neg. CT = order dopplers.

The mortality figures you're quoting are ridiculously high. They're probably accurate from back when all we were picking up were saddle and main PA clots, but the majority of PEs I'm diagnosing these days are segmental or subsegmental with nl biomarkers and no evidence of right heart strain. I don't think anyone has published on this, but I'd be suprised if the mortality from those is higher than a percent or two. My guess is that the morality numbers are also going to reflect a bias in the patient population that gets diagnosed with PEs as a significant number are going to be critically ill or have a terminal disease (especially CA) that is going to lead to an artificially high mortality because of patients dying with PE not because of PE.

I think the future of medicine is to not stick people in the hospital simply as a CYA, but the medicolegal climate needs to change first. Especially in non-teaching hospitals, the chances that a tele patient that is admitted with a hemodynamically insignicant PE and throws another massive PE that is recognized by nursing staff and the attending succeeds in getting vascular or IR to do thrombolysis in time to prevent the patient from coding is going to be almost zero. That being said I've never sent a PE home(unless it's a known PE that hasn't changed in size from prior scan with pt therapeutic on anti-coagulation) and won't without an ACEP guideline change specifically stating conditions for which it's safe to do so.
 
Arcan57 said:
I agree with about 90% of this post. I don't know why people feel like they need to r/o a venous clot anywhere if you have clear localizing symptoms. The only exception I could see would be in a pregnant patient where you're hoping the doppler is going to find clot to save the CT, but in practice I usually will just throw a dimer at them and if it's positive they get scanned (in the absence of unilateral leg swelling). I categorically reject the idea that chest pain + pos. dimer +neg. CT = order dopplers.

The mortality figures you're quoting are ridiculously high. They're probably accurate from back when all we were picking up were saddle and main PA clots, but the majority of PEs I'm diagnosing these days are segmental or subsegmental with nl biomarkers and no evidence of right heart strain. I don't think anyone has published on this, but I'd be suprised if the mortality from those is higher than a percent or two. My guess is that the morality numbers are also going to reflect a bias in the patient population that gets diagnosed with PEs as a significant number are going to be critically ill or have a terminal disease (especially CA) that is going to lead to an artificially high mortality because of patients dying with PE not because of PE.

I think the future of medicine is to not stick people in the hospital simply as a CYA, but the medicolegal climate needs to change first. Especially in non-teaching hospitals, the chances that a tele patient that is admitted with a hemodynamically insignicant PE and throws another massive PE that is recognized by nursing staff and the attending succeeds in getting vascular or IR to do thrombolysis in time to prevent the patient from coding is going to be almost zero. That being said I've never sent a PE home(unless it's a known PE that hasn't changed in size from prior scan with pt therapeutic on anti-coagulation) and won't without an ACEP guideline change specifically stating conditions for which it's safe to do so.
Click to expand...

Don't forget a lot of PEs are missed and/or diagnosed at autopsy. People drop dead or die in their sleep and never present to an ED. Those are included in the numbers, not just the ones that get optimal treatment. So the numbers I quoted may well be that high. OTOH, is it possible that PE mortality has dropped some since high-res ct's, d-dimers, and more aggressive detection and treatment?

Possibly, but doesn't that only argue for more aggressive detection and treatment?
 
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This makes me think of a case I had the other day.

50s male with h/o several PEs. Comes in with tachycardia into the 110s and mild SOB. Otherwise hemodynamically stable. Cardiac workup and chest xray negative. He is on lifelong Warfarin and his INR is actually supratherapeutic at 4.0

Would you scan? We opted not to because he is already anticoagulated. Admitted him for obs.
 
UnderwaterDoc said:
This makes me think of a case I had the other day.

50s male with h/o several PEs. Comes in with tachycardia into the 110s and mild SOB. Otherwise hemodynamically stable. Cardiac workup and chest xray negative. He is on lifelong Warfarin and his INR is actually supratherapeutic at 4.0

Would you scan? We opted not to because he is already anticoagulated. Admitted him for obs.
Click to expand...

Are there any other explanations for his tachycardia and dyspnea? Is he in pulmonary edema? Pneumonia? simple URI? If he has no clear obvious answer then yes I would scan him. His wells is >4 just on the limited data you showed me and there are plenty of coumadin failures.

About a month ago I got called by ed doc for "expanding DVT already on coumadin for DVT" INR was 2.7 Wanted to send him home but pt had alot of leg pain so asked me for consult. Not only did he have extensive DVT in popliteal, sup fem, ant tibial on coumadin....he had no dopplerable pulses in the fem/pop/doraslis pedis in that leg. Went to emergent angio that night, got bypassed then multiple embolectomies after he clotted the grafts eventually an an AKA, complete renal failure, septic shock--> death. This is an extreme case and he had arterial and venous clots, but what it shows is that hypercoagulable patients can fail coumadin therapy even if theraputic and compliant. IF the wells is high and you dont have another answer....rule out a clot.

And I agree with Birdstrike, I will never ever give you **** for calling me with a PE or DVT regardless of the timeframe or anticoagluation status. Do not send them home.
 
UnderwaterDoc said:
This makes me think of a case I had the other day.

50s male with h/o several PEs. Comes in with tachycardia into the 110s and mild SOB. Otherwise hemodynamically stable. Cardiac workup and chest xray negative. He is on lifelong Warfarin and his INR is actually supratherapeutic at 4.0

Would you scan? We opted not to because he is already anticoagulated. Admitted him for obs.
Click to expand...

I've seen a few supra therapeutic with a new PE. They got filters to prevent further issues.
 
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I'd only scan if you think you may need thrombolytics (pt is developing hypotension)
 
UnderwaterDoc said:
This makes me think of a case I had the other day.

50s male with h/o several PEs. Comes in with tachycardia into the 110s and mild SOB. Otherwise hemodynamically stable. Cardiac workup and chest xray negative. He is on lifelong Warfarin and his INR is actually supratherapeutic at 4.0

Would you scan? We opted not to because he is already anticoagulated. Admitted him for obs.
Click to expand...

There is a small (probably in the 1-3% range at the most but don't quote me on that) portion of patients who have recurrent thromboses on coumadin, even with therapeutic INRs.

In the scenario you describe, he deserves a repeat scan...sometime. He's hemodynamically stable so it's not a rush. Either you do it in the ED (which if I talked to you on phone I would ask for simply because it would happen much faster that way...I'd still admit him regardless of the outcome), or they do it on the floor, or his PCP or cardiologist or hematologist does it as an outpatient. But it probably needs doing.

I'm not in any way arguing with your management of this case, just pointing out that a "therapeutic" INR doesn't mean "can't throw a clot." There's good evidence that even compliant patients have therapeutic INRs <75% of the time due to all the hassles inherent in coumadin anticoagulation. My institution has actually gone to making rivaroxaban the formulary first-line therapy for median/long-term anticoagulation for this reason (of course...the data on direct Xa inhibitor failures remains to be seen).
 
Agree with Rendar5- keep it simple,

But recently I had a patient with both. I actually thought my workup would be negative. dizziness, tachypnea that resolved (about 3 min) oh, and doc my leg hurt last night. near normal vs (HR in 90's)

So, I did a venous doppler and a dimer. ++++++ to both. (planned to stop if negative!) Got the CTA Saddle embolus with evidence of R heart strain. candidate for thrombolysis

(did y'all see this?: MOPETT trial - 1/2 dose tPA vs standard care - 41%ARR PHTN at 28 months in thrombolysis group)
 
Zanegray said:
Agree with Rendar5- keep it simple,

But recently I had a patient with both. I actually thought my workup would be negative. dizziness, tachypnea that resolved (about 3 min) oh, and doc my leg hurt last night. near normal vs (HR in 90's)

So, I did a venous doppler and a dimer. ++++++ to both. (planned to stop if negative!) Got the CTA Saddle embolus with evidence of R heart strain. candidate for thrombolysis

(did y'all see this?: MOPETT trial - 1/2 dose tPA vs standard care - 41%ARR PHTN at 28 months in thrombolysis group)
Click to expand...

curious to see if those results become standard still. definitely interesting to expand thrombolysis to submassive PE's by reducing the risk side of the risk:benefit equation.
 
Chest xray was clear, no signs of failure or dissection. Bedside cardiac US was negative for effusion or right sided strain. No clear infectious etiology.

As Rendar said, this guy did not need thrombolytics, therefore we did not scan. My argument is not the fact that they cannot throw a new clot but the fact that we would do nothing different in the ED even if he did have newer clot burden (again, assuming hemodynamic stability, intact peripheral pulses, etc).

I do agree with gutonc that likely a CT is in his future, just not emergently.
 
I think I might scan but hard to tell--was listening to a podcast with Jeff Kline and he addressed this issue (might have been on emcrit but not sure)

Basically, he said his theory is that a lot of patients feel somewhat abnormal and end up increasing their coumadin dose as a response. His premise is that they were likely subtherapeutic when devoloping the clot but present to the ED supratherapeutic because of self-dosing.

Not sure if it's valid or not, but has given me pause when thinking about the patient presenting with PE symptoms who's already anticoagulated . . .
 
Rendar5 said:
I'd only scan if you think you may need thrombolytics (pt is developing hypotension)
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If i were an ER doc, I'd scan if I thought he could be a discharge home if negative, or let the admitting team decide if they want to scan, as frankly a new PE while therapeutic on Coumadin would likey be changed to either life long lovenox or something else. And yes, clots can happen despite Coumadin.
 
Hernandez said:
If i were an ER doc, I'd scan if I thought he could be a discharge home if negative, or let the admitting team decide if they want to scan, as frankly a new PE while therapeutic on Coumadin would likey be changed to either life long lovenox or something else. And yes, clots can happen despite Coumadin.
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Although the data to my knowledge is non-inferior not superior, for these warfarin failures we are sending them out on pradaxa. May change when apixiban is out as the studies show superiority with lower bleeding risks. If they cannot afford pradaxa, they are getting lifelong 1.5mg/kg per day lovenox as Hernandez alluded to. They should be admitted to be monitored regardless of the scan as the risk is too high of a bad outcome and it allows me to get the hypercoag workup going as well.
 
Great reference ninja
Ok I'm gonna get some flak for this but here we go.
We have no evidence that I know of that anticoagulating pts with pe improves outcome vs placebo. The landmark article is from 1960's by Barrett et al and is in nice words not a scientific paper.
I specifically asked Jeff Kline and he referenced the same article and shrugged his shoulders said " it's the standard now " and didn't say whether he agreed or disagreed
Inpt dvt are a different story, ie post surgical/ortho ppx
Tpa does work.
Some people have terrible coag disorders that will clot no matter what they're on and they might need work up and probably anticoagulating for long term
We are picking up a ton of small pe and might be doing the wrong thing by "treatment" with lovenox warfarin
I do understand that medico legally there is no reason not to scan
When are young and have real objective problems. Elevated ctni or bnp or dilated right ventricle we need to discuss tpa and maybe give it. The mopett trial says this.
I'm calling it that the next lawsuits will be us NOT giving tpa for submassive PE

Thoughts?
 
thorg12 said:
Great reference ninja
Ok I'm gonna get some flak for this but here we go.
We have no evidence that I know of that anticoagulating pts with pe improves outcome vs placebo. The landmark article is from 1960's by Barrett et al and is in nice words not a scientific paper.
I specifically asked Jeff Kline and he referenced the same article and shrugged his shoulders said " it's the standard now " and didn't say whether he agreed or disagreed
Inpt dvt are a different story, ie post surgical/ortho ppx
Tpa does work.
Some people have terrible coag disorders that will clot no matter what they're on and they might need work up and probably anticoagulating for long term
We are picking up a ton of small pe and might be doing the wrong thing by "treatment" with lovenox warfarin
I do understand that medico legally there is no reason not to scan
When are young and have real objective problems. Elevated ctni or bnp or dilated right ventricle we need to discuss tpa and maybe give it. The mopett trial says this.
I'm calling it that the next lawsuits will be us NOT giving tpa for submassive PE

Thoughts?
Click to expand...

This is my understanding of the submassive PE recommendations. This is from late 2011 I believe, we did it in a journal club intern year.

Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).

Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).

From http://circ.ahajournals.org/content/123/16/1788.full

IIB, level C, not exactly saying that it is the standard of care and thus lawsuits for lack of lysing should not be a huge issue.
 
Are you guys discharging DVTs with rivaroxaban? My institution has a lot of doctors that do this and some that do not feel comfortable with it. It seems to be a case by case basis for now. Any of you at hospitals that have a protocol for outpatient management of DVTs that involve rivaroxaban?
 
Dr. Ditka said:
Are you guys discharging DVTs with rivaroxaban? My institution has a lot of doctors that do this and some that do not feel comfortable with it. It seems to be a case by case basis for now. Any of you at hospitals that have a protocol for outpatient management of DVTs that involve rivaroxaban?
Click to expand...

Personally no. I have to have good reason to not use Coumadin or lovenox bridge to heparin. I've seen several bad bleeds on these new meds that you can't reverse .
 
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Hernandez said:
Personally no. I have to have good reason to not use Coumadin or lovenox bridge to heparin. I've seen several bad bleeds on these new meds that you can't reverse .
Click to expand...

:thumbup:

I know it's a bit of a selection bias with us, but I'd NEVER send someone out who was old with multiple morbiditiess that I expected to anticoagulate for more than a 3-6 month window.

The dirty little secret of the mediations is that while they have fewer brain bleeds, when they do bleed it's so much worse. Couple of investigators at my institution are putting together a case series on this and when they presented their preliminary data to date, I was horrified.
 
Submassive --> Cath directed thrombolytics. Increasing evidence supports this, with overall mortality rates down from 3% to <1% as well as increased functional status at 6 months and decreased incidents of pulmonary hypertension. 2 trials currently in progress to study these later endpoints. Takes days to get heparin gtt to have an effect on the clots. TNK is another option if you don't have access.

Submassive for us is SBP <90 for 15 minutes or >40 drop in their normal SBP for 90 minutes, BNP>500, Trop >.1, or any evidence of right heart strain on CT or ECHO. All of these guys get thrombolytics. It's been a big discussion here between ED, IR, and ICU and this is what we've decided to do. Goal PTT 65-80.
 
fahimaz7 said:
Submassive --> Cath directed thrombolytics. Increasing evidence supports this, with overall mortality rates down from 3% to <1% as well as increased functional status at 6 months and decreased incidents of pulmonary hypertension. 2 trials currently in progress to study these later endpoints. Takes days to get heparin gtt to have an effect on the clots. TNK is another option if you don't have access.

Submassive for us is SBP <90 for 15 minutes or >40 drop in their normal SBP for 90 minutes, BNP>500, Trop >.1, or any evidence of right heart strain on CT or ECHO. All of these guys get thrombolytics. It's been a big discussion here between ED, IR, and ICU and this is what we've decided to do. Goal PTT 65-80.
Click to expand...

Hypotension doesn't make it massive for ya?
 
fahimaz7 said:
Submassive --> Cath directed thrombolytics. Increasing evidence supports this, with overall mortality rates down from 3% to <1% as well as increased functional status at 6 months and decreased incidents of pulmonary hypertension. 2 trials currently in progress to study these later endpoints. Takes days to get heparin gtt to have an effect on the clots. TNK is another option if you don't have access.

Submassive for us is SBP <90 for 15 minutes or >40 drop in their normal SBP for 90 minutes, BNP>500, Trop >.1, or any evidence of right heart strain on CT or ECHO. All of these guys get thrombolytics. It's been a big discussion here between ED, IR, and ICU and this is what we've decided to do. Goal PTT 65-80.
Click to expand...

Ditto Rendar. I have no qualms with using hypotension as a lytic criteria, but I'm not sold on using biomarkers or CT criteria.
 
Bostonredsox said:
RV dilatation/hypocontractile--> lyse. .
Click to expand...

You should be careful, you do this and have a bad outcome, you will get a crotchety old greedy fart like me who will sit on the stand and say this is not the ACCP guideline answer and there is only very limited data to support this scenario outside of an academic center or outside of a research protocol and as such you deviated from standard of care.
 
Hernandez said:
For the time being, bio markers can risk stratify for who will decompensate, but are not an indicator for lytics
Click to expand...
Agreed - while I don't lyse unless there's shock, I do alter my management for submassive PE in the following 3 ways:
1) Proactively screen for contraindications to lytics so that myself and/or the ICU doesn't need to do this as the patient is decompensating.
2) Use unfractionated heparin, so that it can be stopped if the patient needs lytics.
3) Admit to the ICU so decompensation can be picked up and acted upon promptly.
 
Can those who are against the new anticoagulants please explain why? Is it all because the difficulty of reversal? I'm not sold yet, but I am pretty attracted to the idea of discharging DVT's with nothing more than a prescription for pills and a followup appointment. Plus, it's not as if FFP works all that well for coumadin-related bleeding anyway.
 
Last edited:
WilcoWorld said:
Can those who are against the new anticoagulants please explain why? Is it all because the difficulty of reversal? I'm not sold yet, but I am pretty attracted to the idea of discharging DVT's with nothing more than a prescription for pills and a followup appointment. Plus, it's not as if FFP works all that well for coumadin-related bleeding anyway.
Click to expand...

FWIW, I've seen more bad bleeds on coumadin than the new meds, where reversal "worked" but the patient was f*&^ed anyway. Reversal's kind of a Hail Mary in these situations, no matter what drug is responsible. Last one I had to deal with was on lovenox and had a bleed so bad he herniated before EMS even got there...wouldn't have made a difference what AC he was getting.

I like the new drugs and give them a lot. But only to my relatively healthy patients and only for short-term AC, where cost is less of an issue. I can see the draw of giving them out in the ED, as well as the wish to avoid potential liability. Everyone I see in ED f/u for new DVT/PE comes on lovenox+coumadin and I have no problem changing to a direct Xa inhibitor when I feel comfortable with it...or sticking with coumadin. I also have no problem taking a call from you guys asking if I'd be OK with Xarelto instead of Lovenox/coumadin and helping with the MDM in that case.
 
Hernandez said:
You should be careful, you do this and have a bad outcome, you will get a crotchety old greedy fart like me who will sit on the stand and say this is not the ACCP guideline answer and there is only very limited data to support this scenario outside of an academic center or outside of a research protocol and as such you deviated from standard of care.
Click to expand...

The AHA guidelines do advise "consideration" of thrombolysis for submassive PE. As you know, guidelines and literature do not determine standard of care, so that is really a separate issue. I don't think that anyone knows the answer yet for these difficult cases, but I'd check out the MOPETT trial.
 
pseudoknot said:
The AHA guidelines do advise "consideration" of thrombolysis for submassive PE. As you know, guidelines and literature do not determine standard of care, so that is really a separate issue. I don't think that anyone knows the answer yet for these difficult cases, but I'd check out the MOPETT trial.
Click to expand...

Not to mention that Boston is not an ED doc, but rather going to be one of our brothers upstairs in the ICU =p and is in fact at an academic institution, lol.
 
pseudoknot said:
The AHA guidelines do advise "consideration" of thrombolysis for submassive PE. As you know, guidelines and literature do not determine standard of care, so that is really a separate issue. I don't think that anyone knows the answer yet for these difficult cases, but I'd check out the MOPETT trial.
Click to expand...

MOPETT looks really promising but still not standard of care as mentioned. I have a discussion with the patient and am open to either approach
 
pseudoknot said:
The AHA guidelines do advise "consideration" of thrombolysis for submassive PE. As you know, guidelines and literature do not determine standard of care, so that is really a separate issue. I don't think that anyone knows the answer yet for these difficult cases, but I'd check out the MOPETT trial.
Click to expand...

I'm giving Boston a hard time because he is a new third year IM resident. He speaks with alot of confidence for one so young.
 
thanks for the support. rendar ;) i knew i could draw out hern with that response. And he's right, i am young and inexperienced and thus warrant the hard time :)

but my understanding of the data is rv dilatation or hypocontractility on echo carrys a 2b recommendation for lytics. not as strong as shock and massive pe, but 2b is decent evidence.

unless they have a GOOD reason not t lyse in the setting of a submassive, i still present the choice to the pt. but in my opinion, i would lyse them
 
Bostonredsox said:
thanks for the support. rendar ;) i knew i could draw out hern with that response. And he's right, i am young and inexperienced and thus warrant the hard time :)

but my understanding of the data is rv dilatation or hypocontractility on echo carrys a 2b recommendation for lytics. not as strong as shock and massive pe, but 2b is decent evidence.

unless they have a GOOD reason not t lyse in the setting of a submassive, i still present the choice to the pt. but in my opinion, i would lyse them
Click to expand...

Did you read the studies that the AHA guidelines based this on? I wouldn't call it "good evidence". At least not good evidence in favor of lysing submassive PE.
 
This is pre-MOPETT (as were the AHA guidelines, I believe), but a metaanalysis of lytics for submassive PE vs heparin showed:

Mortality
RR = 0.63 (95% CI = 0.32 – 1.23)
Major hemorrhage
RR = 1.76 (95% CI = 1.04 – 2.98)

Statistically significant higher bleeding, without significant mortality benefit.
 
WilcoWorld said:
This is pre-MOPETT (as were the AHA guidelines, I believe), but a metaanalysis of lytics for submassive PE vs heparin showed:

Mortality
RR = 0.63 (95% CI = 0.32 – 1.23)
Major hemorrhage
RR = 1.76 (95% CI = 1.04 – 2.98)

Statistically significant higher bleeding, without significant mortality benefit.
Click to expand...

Mortality isn't the only endpoint of interest, especially here.
 
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