Silent PE

[Groove]

Should we look for silent pulmonary embolism in patients with deep venous thrombosis? - PMC

Asymptomatic or silent pulmonary embolism (S-PE) in patients with deep vein thrombosis has been the focus of numerous publications with the objective of determining the incidence of S-PE and assessing whether its existence has any clinical or ...

www.ncbi.nlm.nih.gov

Anybody else find themselves scanning your DVT patients for PE more frequently after the publishing of all this literature touting the high percentage of silent PEs with concomitant DVTs?

Some of these numbers are crazy. 32%-66% in some of these studies. I doubt the clinical relevance. Most of these pt's are asymptomatic from the PE and are on proper anti-coagulation for the DVT and would probably be fine regardless. But then you are left with the medicolegal aspect of the case. If you discharge the pt with a DVT and you didn't scan their chest, you're left knowing that at least 50% of them probably have a concomitant PE. The thing that bugs me is that you are gambling that they won't have a complication from the PE. Because if they do...and they get diagnosed with PE, that's an easy lawsuit and possibly bad for the pt. It's a sad way to look at these cases, but damned if you do (probably leading to unnecessary hospital admission unless you PESI them home) and damned if you don't (miss the PE).

So, I find myself scanning more and more of these peeps and finding an inordinate amount of PEs that lead to hospital admission for a day and then they get sent back home which really begs the question....are we doing anything for the pt by over vigilant scanning when they aren't really having any cardiopulmonary complaints?

Case in point, I just admitted a young pt in her 30s last week with no medical problems who recently had foot surgery. She developed clinical signs of DVT and was in our ER and dx with DVT by one of our docs and sent home on eliquis. Her PCP sends her back for a repeat US 3 days later (wtf?) and I see her and start grilling her about cardiopulmonary complaints. Af first, she denies any but I'm so merciless that finally she's like "Ok..ok...I dunno doc, maybe I'm a little dyspneic when I lie down at night time? It's very mild though". Which leads to my "Aha!" CTA which showed segmental and subsegmental PE's on the right. These weren't small ones either. So, she gets admitted....seen by a couple of docs, placed back on her eliquis and sent home a day or two later, with the exact same prescription she was given the first time.

I guess I could not scan these people, but some of these studies are ridiculous. It's like flipping a coin as to which ones are going to have PEs or not.

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[Zebra Hunter]

Treatment doesn’t change because you find the small or moderate size PE on the unnecessary CTA. I just assume every DVT patient I discharge has a small PE. I’ve discharged several patients with PEs before, so I have very little anxiety about doing this. I’d be shocked if anyone has ever been successfully sued for discharging a pt with a DVT and no cardiopulmonary symptoms and normal VS, who eventually died from a PE.

 

[NITRAS]

..nvm

 

[Druggernaut]

I don't scan them. Even if it's there, they'll have a low PESI or Hestia score and I'd still discharge them on anticoagulation.

 

[KGflyboy]

I don't scan them. Even if I did, I still discharge home people with low pestia. So for me the management is the same with or without the scan.

I'm more confused about the repeat ultrasound. Did you ask why she needed it? Are you sure the PCP really sent her in for that? I get people "sent in" all the time who really only called the clerk at the office or a telenurse and were told to come in. When I call their doc, he or she inevitably has no knowledge of the patient getting told to come to the ED.

For me, that second visit would have resulted in no US for sure and likely no CT. Although if it was daytime I probably would have called the PCP before sending her home.

 

[Groove]

I don't scan them. Even if I did, I still discharge home people with low pestia. So for me the management is the same with or without the scan.

I'm more confused about the repeat ultrasound. Did you ask why she needed it? Are you sure the PCP really sent her in for that? I get people "sent in" all the time who really only called the clerk at the office or a telenurse and were told to come in. When I call their doc, he or she inevitably has no knowledge of the patient getting told to come to the ED.

For me, that second visit would have resulted in no US for sure and likely no CT. Although if it was daytime I probably would have called the PCP before sending her home.

The pt had shown back up in his office c/o continued leg pain and he was paranoid the "eliquis wasn't working" (3 days of tx mind you) and wanted to see if there had been any propogation of the clot. He wanted the ultrasound repeated (original had been doing at an outpatient radiology clinic), the pt placed on a heparin drip and he wanted our CV surgeon consulted for the DVT (femoral occlusive, non occlusive popliteal, no clot proximal in the iliac or iliofemoral). I asked him why he wanted it repeated after only 3 days of treatment and why on earth he would want a CV surgeon consulted for this particular DVT. He said her leg felt "cool". (2+ pulses) Some of these guys are ancient, but they bring the hospital business and they throw monster hissy fits if you "mismanage" one of their patients. So...I repeated the US, placed her on heparin and admitted her. CV got consulted for the "DVT" though I didn't call them. The CTA was just something I added. It's not worth arguing with some of these guys. If you send them out, they're just going to send them right back in and call the CMO. In this particular case, CV saw her, said "Yep, she's got a DVT alright. Eliquis should work fine. Signing off." He consulted pulmonary for the PE. Pulmonary saw her "Yep, she's got a PE alright. Eliquis should work fine. Signing off." Then he subsequently discharged her a day or two later, back on eliquis.

Part of the problem is that d/c'ing PEs from the ED is not that common where I'm at and def not regional standard. I'm very familiar with PESI and have on rare occasion discharged low PESI pt's with good follow up but it's still not that common where I'm at. We also have a great deal of uninsured, medically complicated, poor follow up patients who either can't afford the drugs or get lost to follow up and need the usual case management assistance. I'm kind of jealous of some of you in areas where this is common practice. I think I've discharged exactly one PE from the ED in the past 2 years.

 

[Zebra Hunter]

We also have a great deal of uninsured, medically complicated, poor follow up patients who either can't afford the drugs or get lost to follow up and need the usual case management assistance.

This is why I advise my residents to use both the Hestia criteria and PESI when documenting, as the latter does not take into account social support, and the former does not take into account chronic cardiopulmonary co-morbidities.

 

[KGflyboy]

The pt had shown back up in his office c/o continued leg pain and he was paranoid the "eliquis wasn't working" (3 days of tx mind you) and wanted to see if there had been any propogation of the clot. He wanted the ultrasound repeated (original had been doing at an outpatient radiology clinic), the pt placed on a heparin drip and he wanted our CV surgeon consulted for the DVT (femoral occlusive, non occlusive popliteal, no clot proximal in the iliac or iliofemoral). I asked him why he wanted it repeated after only 3 days of treatment and why on earth he would want a CV surgeon consulted for this particular DVT. He said her leg felt "cool". (2+ pulses) Some of these guys are ancient, but they bring the hospital business and they throw monster hissy fits if you "mismanage" one of their patients. So...I repeated the US, placed her on heparin and admitted her. CV got consulted for the "DVT" though I didn't call them. The CTA was just something I added. It's not worth arguing with some of these guys. If you send them out, they're just going to send them right back in and call the CMO. In this particular case, CV saw her, said "Yep, she's got a DVT alright. Eliquis should work fine. Signing off." He consulted pulmonary for the PE. Pulmonary saw her "Yep, she's got a PE alright. Eliquis should work fine. Signing off." Then he subsequently discharged her a day or two later, back on eliquis.

Part of the problem is that d/c'ing PEs is not that common where I'm at and def not regional standard. I'm very familiar with PESI and have on rare occasion discharged low PESI pt's with good follow up but it's still not that common where I'm at. We also have a great deal of uninsured, medically complicated, poor follow up patients who either can't afford the drugs or get lost to follow up and need the usual case management assistance.

I hear ya. I really like that my location just doesn't admit PEs anymore. Sometimes I get pushback when I do admit, which is usually for a small amount of right heart strain on CT.

My mind is blown right now that CV saw this patient. The way people in different locations varies so much. I can barely get consults from CV when needed. I can't imagine the type of pushback CV would give me or a hospitalist for consulting on this DVT.

 

[deleted245139]

I don't reflex spin them esp if asx...
I will say, I use caution in NOAC with malignancy.... Anecdotally I've seen a ton of recent dvt dx on a NOAC with malignancy that subsequently propagate and embolize.

 

[bravotwozero]

Yeah for me to discharge a patient with Stable PE would require a lot of moving parts to align. The patient has to have good follow up, the PCP has to agree with the plan, and the insurance company should cover the eliquis. This doesn’t always happen and I work in a place with insured patients who have PCPs. Can’t say I have ever discharged someone with a PCP.


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[TheSingularity]

I quit a place with this culture. Stupid PCPs calling in all their stupid ass nonsense, demanding consults and such. I think cause they all admit their own patients and the patients have good insurance (follow the money).

My favorite was PCP sends in asymptomatic patient with known PE from CTA a couple weeks ago for repeat CTA to "see if clot resolving."

The pt had shown back up in his office c/o continued leg pain and he was paranoid the "eliquis wasn't working" (3 days of tx mind you) and wanted to see if there had been any propogation of the clot. He wanted the ultrasound repeated (original had been doing at an outpatient radiology clinic), the pt placed on a heparin drip and he wanted our CV surgeon consulted for the DVT (femoral occlusive, non occlusive popliteal, no clot proximal in the iliac or iliofemoral). I asked him why he wanted it repeated after only 3 days of treatment and why on earth he would want a CV surgeon consulted for this particular DVT. He said her leg felt "cool". (2+ pulses) Some of these guys are ancient, but they bring the hospital business and they throw monster hissy fits if you "mismanage" one of their patients. So...I repeated the US, placed her on heparin and admitted her. CV got consulted for the "DVT" though I didn't call them. The CTA was just something I added. It's not worth arguing with some of these guys. If you send them out, they're just going to send them right back in and call the CMO. In this particular case, CV saw her, said "Yep, she's got a DVT alright. Eliquis should work fine. Signing off." He consulted pulmonary for the PE. Pulmonary saw her "Yep, she's got a PE alright. Eliquis should work fine. Signing off." Then he subsequently discharged her a day or two later, back on eliquis.

Part of the problem is that d/c'ing PEs from the ED is not that common where I'm at and def not regional standard. I'm very familiar with PESI and have on rare occasion discharged low PESI pt's with good follow up but it's still not that common where I'm at. We also have a great deal of uninsured, medically complicated, poor follow up patients who either can't afford the drugs or get lost to follow up and need the usual case management assistance. I'm kind of jealous of some of you in areas where this is common practice. I think I've discharged exactly one PE from the ED in the past 2 years.

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[KGflyboy]

Yeah for me to discharge a patient with Stable PE would require a lot of moving parts to align. The patient has to have good follow up, the PCP has to agree with the plan, and the insurance company should cover the eliquis. This doesn’t always happen and I work in a place with insured patients who have PCPs. Can’t say I have ever discharged someone with a PCP.


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I give 30 day started packs to everybody I discharge. It gets them a 30 day supply of anticoagulation for free. Their PCP can switch them to warfarin if needed for insurance reasons, but that's rare. Insurance covers NOACs most of the time these days.

I don't have many patients without a PCP, so the follow up part is super easy. Sometimes I call the PCP to ensure they have close follow up, but I'm starting to wonder if I even need to go that far. The PCPs just expect us to discharge PEs home with a NOAC at this point because it has been done that way for so long here. Anything else would raise eyebrows.

When you admit people for stable PE without right heart strain... What does the hospitalist do typically? Is there any specific treatment or evaluation that happens in the hospital?

If I admit those patients, the hospitalist will start a NOAC and discharge with PCP follow up, usually after asking me why I didn't just do that myself.

 

[bravotwozero]

I had a patient with a post operative DVT that I sent home with a script for elliquis once (didn't have starter packs at the time). Spoke with their PCP and ortho, both ok'd the plan and agreed to see patient in their office.

3 hours later, patient returns to the ED because insurance wouldn't approve it. I guess the @sshats thought a hospital stay would be cheaper...

If I'm admitting a stable PE, and the hospitalist asked me why, it would be for precisely those reasons, like 'the patient's insurer is a *****', or 'no follow up with this dude could be arranged, so tag you're it'...

 

[thegenius]

The pt had shown back up in his office c/o continued leg pain and he was paranoid the "eliquis wasn't working" (3 days of tx mind you) and wanted to see if there had been any propogation of the clot. He wanted the ultrasound repeated (original had been doing at an outpatient radiology clinic), the pt placed on a heparin drip and he wanted our CV surgeon consulted for the DVT (femoral occlusive, non occlusive popliteal, no clot proximal in the iliac or iliofemoral). I asked him why he wanted it repeated after only 3 days of treatment and why on earth he would want a CV surgeon consulted for this particular DVT. He said her leg felt "cool". (2+ pulses) Some of these guys are ancient, but they bring the hospital business and they throw monster hissy fits if you "mismanage" one of their patients. So...I repeated the US, placed her on heparin and admitted her. CV got consulted for the "DVT" though I didn't call them. The CTA was just something I added. It's not worth arguing with some of these guys. If you send them out, they're just going to send them right back in and call the CMO. In this particular case, CV saw her, said "Yep, she's got a DVT alright. Eliquis should work fine. Signing off." He consulted pulmonary for the PE. Pulmonary saw her "Yep, she's got a PE alright. Eliquis should work fine. Signing off." Then he subsequently discharged her a day or two later, back on eliquis.

Well that's bad medicine for a variety of reasons. And not on your part. You tried to do good medicine, and the system didn't let you.

I look at DVT with possible PE like this.

If you come in with unilateral leg swelling, and have no thoracic symptoms and normal vitals, and your ultrasound is negative.....do you scan their chest to see if they HAD a DVT that broke off and went to their lungs? Probably not. I don't.

We are so damn scared about PE's in this country. The PESI score is good. Kaiser discharges low risk PE's on a regular basis. If you start treatment for a PE or DVT, and they die, it's hard to say you didn't meet standard of care.

 

[thegenius]

I suspect the approach to stable, low risk PE's will generally go the same way we are now approaching low risk chest pain....--> discharged from the ED.

Slowly we are seeing a change in low risk chest pain, you rule them out and send them home. No stress tests, and they don't get admitted. It's a slow change and might take 10 years, but its going to happen.

Kaiser is starting to do this.

 

[Brigade4Radiant]

With all the stuff we do for PE's mortality hasn't changed.

I also tell my patient's warfarin is actually the most expensive anticoagulant when you factor in the blood checks and then the stays in the hospital when it becomes subtheraputic.

 

[RuralEDDoc]

I do a few shifts a month for kaiser.
Low risk PEs go home.
Low and intermediate chest pain goes home. High risk gets a real stress test or cath and goes home.
Simple, cost effective, patient centric medicine. Patients don’t really want a rule out and 23 hour stay for GERD.
At my non kaiser sites, well, a lot of those patients are getting “observed”, whatever that horse**** loosy goosey nonsense means for patients with a symptom but no evidence of disease.

 

[southerndoc]

I've scanned a few that had +DVT on ultrasounds ordered by the screening APP. They had a HR of 130, sat of 92%, etc. All had some sort of abnormal vital sign that made me think they had a PE, and all of them had a fairly large PE. If they have a normal sat, not tachypneic, not persistently tachycardic (I mean 110+ not like 101-103 bpm), etc., then they have a higher chance of having a larger PE.

 

[thegenius]

If you have a DVT and abnormal vital signs and thoracic complaints, then you have a PE. If it smells like PE, walks like a PE, and farts like a PE it's a PE. We should just be treating it. I don't know what the advantage is of doing a CT PE to verify what you already know, unless you are going to catheter directed lysis of the clot.

What are you going to do if the clot is in 1 lobe, 2 lobes, in 2 segmental arteries, 1 segmental + left main, or 5 segmental arteries.
Since when did looking at radiographic pictures alter the outcome of those who have a PE (unless you plan on doing CT surgery to remove the clot, or catheter-directed lysis). The only times I would see getting a CT is beneficial is if you plan on doing an intervention OR if the patient becomes markedly more ill and has hypotension or requires pressors. (This is thankfully not all that often.)

This is one of the problems in our health care system. We have a test that shows us nice, pretty pictures and we order it. Then what do we do? The same thing we always do. Give heparin

Reminds me of a stroke pt I admitted a few years ago. The inpatient team ordered an MRA of the neck, CTA of the neck and carotid ultrasounds of the neck. They all said no stenosis. What is the purpose in that? If I were an insurance provider I wouldn't pay for that nonsense.

I should invest in all companies that make products to help you "look" in a patient more than what we already do. Because we are going to use it. Would make a lot of money

 

[DrGasPasser]

I've scanned a few that had +DVT on ultrasounds ordered by the screening APP. They had a HR of 130, sat of 92%, etc. All had some sort of abnormal vital sign that made me think they had a PE, and all of them had a fairly large PE. If they have a normal sat, not tachypneic, not persistently tachycardic (I mean 110+ not like 101-103 bpm), etc., then they have a higher chance of having a larger PE.

I think you are being very reasonable. Patients with jacked-up vitals like you describe are the ones that I want to see if they have evidence of right heart strain such as elevated biomarkers or RV/LV > 1. I have a low threshold for consulting our interventional group for these patients to consider EKOS or other catheter directed therapies depending on the appearance of the clot burden. Otherwise, I see no need to CTA patients with DVTs and reasonable vitals.

I suspect that the management of patients with submissive PE will be getting more complex over the next decade. Some of the big names in the field of VTE management are looking at an adaptive trial designed to find the ideal dose of TPA to be used in submissive PE that improves outcomes while minimizing bleeding risk.

 

[southerndoc]

People who have submassive PE's that aren't treated with thrombolytics have poor functional capacity from their pulmonary hypertension 5-10 years down the road.

 

[DrGasPasser]

I’m not sure that at I completely buy the argument at systemic thrombolysis improves functional outcomes in submassive PE. While there was a reduction in PHTN in the MOPETT trial, and TOPCOAT showed a non-significant trend toward improved function with a small sample size, PEITHO did not show improved functional outcomes with full dose tenectaplase. PEITHO was much bigger although the F/U was shorter (30 vs 90 days I think). The problem is that full dose tenectaplase with heparin carried a 2% ICH rate that essentially erased the mortality benefit in PEITHO.

I think the big question is can we have our cake and eat it too with reduced dose systemic TPA - reduce the 2-5% of submassive PEs that progress to PEA, improve functional outcomes, AND keep ICH rate less than 1%. That study is being designed as I type this. I suspect that it will be 25-50 mg of TPA infused over 2 hours with either simultaneous LMWH, or unfractionated heparin held until a couple of hours after the TPA infusion.

In the meantime catheter directed thrombolysis is an expensive alternative but with very little robust data. Interestingly, there is also a trial looking at CDT vs low dose systemic TPA for submassive PE that will finish enrolling in 2 years.

Like I said, the PE landscape is about to become a whole lot more complex. My real concern is that we are about to dump a bunch of money into things like PE response teams, CDT, and TPA to change outcomes around the slimmest of margins of a very rare disease.

 

[Zebra Hunter]

Speaking of treating submassive PEs. Do we have ANY evidence that EKOS actually works? All I have ever seen is the SEATTLE II trial which had no control group, so it is basically a case series. Despite this, I see everyone here and on EMDocs talking about it like it is standard of care, and have my partners immediately paging IR or vascular for these non-massive PEs. Seems questionable at this point.

 

[southerndoc]

There really isn't much evidence to support EKOS as far as I know. We have a PE Response Team (PERT) that use EKOS frequently. We get so many PE's it's unbelievable (saw 2 yesterday, one bilateral the other not that big).

Regarding ICH with tenecteplase, well yea. That's a given. Tenecteplase is there only for the nurses. One dose instead of an infusion. Alteplase has much lower ICH rates. Tenecteplase hasn't shown to be superior to alteplase unless I've fallen behind on the literature.

 

[DrGasPasser]

There really isn't much evidence to support EKOS as far as I know. We have a PE Response Team (PERT) that use EKOS frequently. We get so many PE's it's unbelievable (saw 2 yesterday, one bilateral the other not that big).

Regarding ICH with tenecteplase, well yea. That's a given. Tenecteplase is there only for the nurses. One dose instead of an infusion. Alteplase has much lower ICH rates. Tenecteplase hasn't shown to be superior to alteplase unless I've fallen behind on the literature.

I agree that EKOS probably has identical outcomes to other forms of CDT.

On the other hand, Tenecteplase and Alteplase have very similar safety profiles (including bleeding risk) in PE, ACS, and stroke:

Safety and efficacy of tenecteplase versus alteplase in acute coronary syndrome: a systematic review and meta-analysis of randomized trials - PMC

Alteplase and tenecteplase are two widely used thrombolytic agents and are both approved for the treatment of acute myocardial infarction. These two molecules have increased fibrin specificity compared with older thrombolytics but distinct ...

www.ncbi.nlm.nih.gov

Tenecteplase versus Alteplase for the Management of Acute Ischemic Stroke in a Low-income Country–Nepal: Cost, Efficacy, and Safety - PMC

Intravenous alteplase is the only approved treatment for acute ischemic stroke. Tenecteplase, a genetically engineered, mutant tissue plasminogen activator, is an alternative thrombolytic agent. The economic feasibility of stroke treatment has been ...

www.ncbi.nlm.nih.gov

https://www.nejm.org/doi/full/10.1056/NEJMoa1716405

 

[southerndoc]

Where's the comparison for PE?

My dog likes apples, but hates bananas. Does that mean that monkeys would prefer apples?

 

[DrGasPasser]

Where's the comparison for PE?

My dog likes apples, but hates bananas. Does that mean that monkeys would prefer apples?

To the best of my knowledge, there has never been a head to head study of tenecteplase vs TPA in PE. However, the studies that have looked at alteplase and tenecteplase individually for PE (and just about every other condition where lyrics are given) have shown similar efficacy and safety when account for equivalent dosing. This is not all that surprising since tenecteplase is essentially an engineered form of TPA with greater fibrin specificity and a longer t1/2.

My point being, I’m not sure where you are seeing more ICH with tenecteplase.

 

[SamtheWise]

We're all probably sitting here with silent sub segmental PEs in our lungs arguing about lytics, while there's hundreds of thousands of people in the US getting in a car or riding a bike or getting drunk while taking their useless eliquis we gave them for their subsegmental PEs.

 

[deleted109597]

We're all probably sitting here with silent sub segmental PEs in our lungs arguing about lytics, while there's hundreds of thousands of people in the US getting in a car or riding a bike or getting drunk while taking their useless eliquis we gave them for their subsegmental PEs.

We absolutely know this based on autopsy data. Just like the BS "syncope" study that made us look for PEs because so many people have them.

OTOH, at least we have decreased mortality from PE finally.

 

[SamtheWise]

We absolutely know this based on autopsy data. Just like the BS "syncope" study that made us look for PEs because so many people have them.

OTOH, at least we have decreased mortality from PE finally.

My kingdom for an RCT comparing mortality from sub-segmentals on AC to sub-segmentals on no AC.

I remember when that wretched NEJM article came out, as if millions of ED doctors suddenly cried out in terror and were suddenly silenced.

 

[Apollyon]

We're all probably sitting here with silent sub segmental PEs in our lungs arguing about lytics, while there's hundreds of thousands of people in the US getting in a car or riding a bike or getting drunk while taking their useless eliquis we gave them for their subsegmental PEs.

Please expand on why apixiban is "useless".

 

[Brigade4Radiant]

Please expand on why apixiban is "useless".

it hasn’t decreased mortality of PE

 

[Apollyon]

it hasn’t decreased mortality of PE

Granted, I haven't read all studies, but I thought it had, compared to warfarin. I'm happy to be wrong.

 

[ShockIndex]

Granted, I haven't read all studies, but I thought it had, compared to warfarin. I'm happy to be wrong.

I suspect that people are referring to the paucity of direct data showing a mortality benefit to anticoagulation for PE. That is to say, there is very little (if any) large, RCT data comparing anticoagulation to placebo, and there never will be as such trials would be unethical. For example, here is an example of the data from the ‘60s that is the foundation for our current approach: https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S0140673660922996/first-page-pdf

It’s largely case series and small non-blinded studies.

On the other hand, there is a plenty of quality indirect evidence suggesting that anticoagulation is absolutely beneficial for the vast majority patients with VTE. Moreover, the overall trend in decreasing mortality from VTE over the past 30 years is probably multifactorial (better prevention, diagnostics, and therapeutics).

Finally, there is reasonable evidence that oral direct FXa inhibitors are non-inferior to warfarin at preventing death, and may have lower major bleeding risks. If anyone thinks that they are worthless, then I’m curious to hear what they would want to be treated with for their own PE...nothing?

 

[KGflyboy]

I suspect that people are referring to the paucity of direct data showing a mortality benefit to anticoagulation for PE. That is to say, there is very little (if any) large, RCT data comparing anticoagulation to placebo, and there never will be as such trials would be unethical. For example, here is an example of the data from the ‘60s that is the foundation for our current approach: https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S0140673660922996/first-page-pdf

It’s largely case series and small non-blinded studies.

On the other hand, there is a plenty of quality indirect evidence suggesting that anticoagulation is absolutely beneficial for the vast majority patients with VTE. Moreover, the overall trend in decreasing mortality from VTE over the past 30 years is probably multifactorial (better prevention, diagnostics, and therapeutics).

Finally, there is reasonable evidence that oral direct FXa inhibitors are non-inferior to warfarin at preventing death, and may have lower major bleeding risks. If anyone thinks that they are worthless, then I’m curious to hear what they would want to be treated with for their own PE...nothing?

I would gladly not be anticoagulated for a subsegmental PE.

I bet many of us have already had subsegmental PEs and never knew. I think we need to find a way to identify high risk vs low risk PEs. Until that happens, there is no evidence to suggest we are doing more good than harm anticoagulating all of these tiny PEs as far as I know.

 

[ShockIndex]

I would gladly not be anticoagulated for a subsegmental PE.

I bet many of us have already had subsegmental PEs and never knew. I think we need to find a way to identify high risk vs low risk PEs. Until that happens, there is no evidence to suggest we are doing more good than harm anticoagulating all of these tiny PEs as far as I know.

I’d gladly not be anticoagulated for a subsegmental PE if I were at low-risk for a recurrence. On the other hand, I’ll take my chances with a NOAC if I have a reason to throw another clot. Those are the guidelines from CHEST based on level 2c evidence. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. - PubMed - NCBI

That is to say, I think there is a much better case to be made for getting Dopplers on patients with subsegmental PEs to determine if anticoagulation can be avoided rather than getting CTAs on most DVTs where we know that anticoagulation cannot be avoided.

Also, my statement that you quoted was not referring to subsegmental PEs - the evidence for anticoagulating ALL clots is surprisingly retrospective.

 

[Groove]

I had foot surgery a couple years ago and am almost positive I had a PE. Very pleuritic chest pain on the right and was mildly dyspneic for a couple weeks. The dyspnea improved but the chest pain persisted for....hell, it must have gone on for 4-5 weeks or so, at least. Finally cleared up. I wouldn't have taken a NOAC if someone offered it to me. I made the mistake of mentioning it to the orthopod during f/u and was laughing about it and saw him grimace as he was typing the note. I go "Ahhh, my bad. You know what? Why don't you leave that part out of the note?" He nods and goes "Groove, my hearing is a little bit off today and I had a hard time making that last part out. Let's start over. How's the foot?" LOL

Our medicine guys are all over the map in their practice patterns where I'm at. We have some hyper aggressive guys who want to d/c them from the ED (which I'll admit is a pattern that is nearing critical mass for more widespread adoption in the future), but I never know... I've got a young, healthy girl in her early 20s that one of my NP's dx with PE other day who presented with a CC of dyspnea. No risk factors, none. Normal Vitals. Wells and PERC neg. Completely normal exam. She obtained a dimer for some reason and it was marginally positive, in fact...depending on your hospital, it might have been negative where you are at, but our upper limit is 0.47. Her dimer was 0.49. The NP got a CTA and there was a RLL segmental PE. PT had poor f/u and couldn't afford medications so I took over and talked to the hospitalist who requested admission. I check back a couple days later expecting a case management consult and quick discharge and they have a hematology consult placed and she's still in the hospital 3 days later.

 

[ShockIndex]

I check back a couple days later expecting a case management consult and quick discharge and they have a hematology consult placed and she's still in the hospital 3 days later.

You can absolutely find case reports of decision rules failing. You will also find a lot more than just case reports of clinicians practicing expensive, overly conservative, defensive medicine. In fact, that is probably endemic.

 

[KGflyboy]

I’d gladly not be anticoagulated for a subsegmental PE if I were at low-risk for a recurrence. On the other hand, I’ll take my chances with a NOAC if I have a reason to throw another clot. Those are the guidelines from CHEST based on level 2c evidence. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. - PubMed - NCBI

That is to say, I think there is a much better case to be made for getting Dopplers on patients with subsegmental PEs to determine if anticoagulation can be avoided rather than getting CTAs on most DVTs where we know that anticoagulation cannot be avoided.

Also, my statement that you quoted was not referring to subsegmental PEs - the evidence for anticoagulating ALL clots is surprisingly retrospective.

I think we are on the same page. We are aware of the guidelines and standard of care. And I think a large minority of ED docs recognize there probably isn't much benefit of anticoagulating the real small PEs, but we do it because we do t have any evidence or guidelines telling us not to.

I would like to see someone study an approach similar to what you suggested.

If someone has a subsegmental PE, and a LE US is negative, perhaps those are ideal candidates to skip anticoagulation. But I don't see that happening any time soon.

 

[deleted547339]

If someone has a DVT, they, almost by definition, have a PE if you had a scanner good enough. I always ask my DVTs about DOE, CP, hemoptysis and document as such. If not, it’s not significant and doesn’t need further work up. I’d argue a trop, BNP and echo have a lot more prognostic effect than a CTA if you have know dvt and sx if a PE.

 

[thegenius]

I would gladly not be anticoagulated for a subsegmental PE.

I bet many of us have already had subsegmental PEs and never knew. I think we need to find a way to identify high risk vs low risk PEs. Until that happens, there is no evidence to suggest we are doing more good than harm anticoagulating all of these tiny PEs as far as I know.

Most of us probably wouldn't admit ourselves to the local ED if we had mild or moderate pleuritic chest pain. I've had it a few times...goes away after less than a day. Even purposely checked my HR once - was 90. Probably nothing.

PE risk stratification tools already exist:
Pulmonary Embolism Severity Index (PESI) - Pulmonary Embolism Severity Index (PESI) - MDCalc
Simplified Pulmonary Embolism Severity Index (sPESI) - Simplified PESI (Pulmonary Embolism Severity Index) - MDCalc
Hestia - Hestia Criteria for Outpatient Pulmonary Embolism Treatment - MDCalc

 

[thegenius]

I had foot surgery a couple years ago and am almost positive I had a PE. Very pleuritic chest pain on the right and was mildly dyspneic for a couple weeks. The dyspnea improved but the chest pain persisted for....hell, it must have gone on for 4-5 weeks or so, at least. Finally cleared up. I wouldn't have taken a NOAC if someone offered it to me. I made the mistake of mentioning it to the orthopod during f/u and was laughing about it and saw him grimace as he was typing the note. I go "Ahhh, my bad. You know what? Why don't you leave that part out of the note?" He nods and goes "Groove, my hearing is a little bit off today and I had a hard time making that last part out. Let's start over. How's the foot?" LOL

Our medicine guys are all over the map in their practice patterns where I'm at. We have some hyper aggressive guys who want to d/c them from the ED (which I'll admit is a pattern that is nearing critical mass for more widespread adoption in the future), but I never know... I've got a young, healthy girl in her early 20s that one of my NP's dx with PE other day who presented with a CC of dyspnea. No risk factors, none. Normal Vitals. Wells and PERC neg. Completely normal exam. She obtained a dimer for some reason and it was marginally positive, in fact...depending on your hospital, it might have been negative where you are at, but our upper limit is 0.47. Her dimer was 0.49. The NP got a CTA and there was a RLL segmental PE. PT had poor f/u and couldn't afford medications so I took over and talked to the hospitalist who requested admission. I check back a couple days later expecting a case management consult and quick discharge and they have a hematology consult placed and she's still in the hospital 3 days later.

Is she still admitted because she was getting physiologically worse, or they are having trouble with discharge due to social reasons or difficulty getting her meds? Doesn't really matter one way or another though. The fact that she is admitted for 3 days indicated there was no way the ER could have taken care of all those problems.

 

[thegenius]

You can absolutely find case reports of decision rules failing. You will also find a lot more than just case reports of clinicians practicing expensive, overly conservative, defensive medicine. In fact, that is probably endemic.

Just depends on why she is still admitted. If the pt is stable and they are having problem getting her OP anticoagulation, that is not a failure of the decision rule.

 

[thegenius]

All this talk about not treating small PE's is all fine and dandy in an academic conference where a bunch of ER and hematologists research doctors can debate the merits and drawbacks of doing such a thing.

However, for the standard of care to change in the American Health Care Community re: treating PE's, there has to be
1) unequivocal change in the national guidelines using words like "recommend DO NOT treat single subsegmental PE's in low risk patients" (emphasis mine), and not words like "consider not treating"
2) wait 5-10 years, maybe more, for the average community doctor to change their practice pattern.

 

[ShockIndex]

Just depends on why she is still admitted. If the pt is stable and they are having problem getting her OP anticoagulation, that is not a failure of the decision rule.

I have a couple thoughts. First, Janssen Pharma offers 30-day rivaroxiban starter packs for free. If you don’t have them in you ED Omni Cell, then your hospital pharmacy may have them. If not, then one of your partners needs to take one for the team, give the pharm rep their phone number, suffer through all of the calls letting them know about the new indications for their latest drug (that you never prescribe), and get a couple of free steak dinners so that your hospital can get the packs.

Since getting those starter packs, our social admissions for DVT and low-risk PE are way down. The patient leaves the ED with 30-days of anticoagulation in hand and social work has plenty of time to arrange charity care follow-up.

 

[Groove]

Is she still admitted because she was getting physiologically worse, or they are having trouble with discharge due to social reasons or difficulty getting her meds? Doesn't really matter one way or another though. The fact that she is admitted for 3 days indicated there was no way the ER could have taken care of all those problems.

Well, in this case it probably had more to do with the fact that the heme consult took 2 days to get done and they probably didn't need it in the first place. The main issue with her was going to be obtaining her meds and establishing f/u.

Everyone's difference in practice pattern regarding PEs is reminding me of that DVT/PE thread from earlier this year. I got tickled when people were implying they were admitting PEs without confirmatory CTAs if I'm recalling correctly.

DVTs and PEs

Whenever, I find DVTs in patients, I usually ask about chest pain, SOB, etc. What do you guys do with pts who have newly diagnosed DVTs and then complain of vague CP. I usually don't pursue the PE diagnosis if the symptoms are short lived, migratory in location on the chest, or have been going...

forums.studentdoctor.net

 

[deuist]

I have a couple thoughts. First, Janssen Pharma offers 30-day rivaroxiban starter packs for free. If you don’t have them in you ED Omni Cell, then your hospital pharmacy may have them. If not, then one of your partners needs to take one for the team, give the pharm rep their phone number, suffer through all of the calls letting them know about the new indications for their latest drug (that you never prescribe), and get a couple of free steak dinners so that your hospital can get the packs.

Since getting those starter packs, our social admissions for DVT and low-risk PE are way down. The patient leaves the ED with 30-days of anticoagulation in hand and social work has plenty of time to arrange charity care follow-up.

Tell me more about becoming a conduit...

 

[ShockIndex]

Tell me more about becoming a conduit...

If you don’t have a relationship with Jannsen, I’d see if someone on your hospital’s P&T Committee does and get them to ask for the starter packs. I was one of the MERCURY PE investigators, so I got introduced to our region’s Janssen rep since they sponsored that study. At one point, I think that Janssen had an actual program to supply hospitals with these packs for charitable purposes. I’m not sure if the actual program still exists, but I know that we have the starter packs in our ED pharmacy.