DVTs and PEs

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BJJVP

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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 on forever. However, if you have a DVT and even mention the word chest pain, a lot of my colleagues automatically scan the chest. What they have found has surprised me. For example, I had one pt tell me that she feels funny in the chest from time to time and occasionally she gets lightheaded, but the symptoms are self limited. CT demonstrated bilateral main pulmonary artery PEs. Another pt with a below knee DVT told me that she sometimes feels sharp CP but then it goes away. CT showed multiple bilateral PEs. Take into account that these are otherwise healthy subjects with stable VS and do not appear to be in distress. The chest symptoms are usually elicited during the history taking and not even volunteered by the pts themselves. I think, for the most part, management and outcomes really don't change with the identification of the PE but there is always the sense that a PE was "missed." What is your practice here?
 
"Are you having any chest pain or shortness of breath?"
If no, no further action.
If yes, maybe further action.
Most people say no, and I'm not in the habit of asking them if they've had any abnormal sensation in the thorax in the past X months or anything else more expansive.
 
If VS are unremarkable, there is no point to scan. If they are complaining of chest symptoms or SOB, just assume they have a PE and admit for observation or dc if they are low risk for complications based on validated risk stratification tools (like Hestia criteria).
 
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.

If they have a DVT and complain of any cardiopulmonary complaint then I get an ekg, cardiac markers and spin them up. Don't be the guy who sends them home with a xarelto starter pack only to have them come back in cardiac arrest from a PE. Also, beware pre-closure bias that causes you to skip an ACS work up that you otherwise would have completed if they came in without a DVT but were still complaining of X,Y,Z cardiopulmonary complaints.

I don't cut corners with these people. High risk. It may take longer, but I sleep better at night.
 
I don't discharge PE's. I know there is the PESI score, but we haven't started doing that and quite frankly I don't think it's standard of care. I know some places do it.

A PE usually results in 6 months of anticoagulation, a DVT can be only 3 months.

Just this past week I had a girl who traveled on a cross-country flight, had right leg pain/swelling, and had a DVT. I scanned her chest because she was tachycardic (120's). No chest pain, no shortness of breath, no dizziness. She had bilateral main pulmonary artery emboli that was on the border of being a saddle embolus. When I told her the diagnosis, she then told me she had chest "pressure" when she walks.

Some people minimize things.
 
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 on forever. However, if you have a DVT and even mention the word chest pain, a lot of my colleagues automatically scan the chest. What they have found has surprised me. For example, I had one pt tell me that she feels funny in the chest from time to time and occasionally she gets lightheaded, but the symptoms are self limited. CT demonstrated bilateral main pulmonary artery PEs. Another pt with a below knee DVT told me that she sometimes feels sharp CP but then it goes away. CT showed multiple bilateral PEs. Take into account that these are otherwise healthy subjects with stable VS and do not appear to be in distress. The chest symptoms are usually elicited during the history taking and not even volunteered by the pts themselves. I think, for the most part, management and outcomes really don't change with the identification of the PE but there is always the sense that a PE was "missed." What is your practice here?

I have no uniform practice or algorithm for these patients, because treatment is the same. The only difference is dispo.

For the most part, I send DVTs home with AC unless there are extenuating circumstances (very old, very frail, poor access to health care, homeless, etc).

I have only sent home 2-3 PE's in my life and those are extenuating circumstances. I usually admit almost all of them - although to be honest I think we probably admit too many because they just end up going home after an ECHO and being put on AC. I even admit normal PE's with normal vital signs. Sometimes it's too much work to arrange for outpatient re-eval / workup. Or it's 9:00 PM.


Like so many things in life, the problem usually becomes who you are handing the patient off to. Hospitalists I work with will never accept a pt with a possible PE without a CT. They will argue, argue more, and it doesn't matter if they are put on anti-coagulation. Unless there is a hard contra-indication to getting a CT they want it done. So what's the point of arguing and winning a Pyrrhic victory? I usually get the CT and go to the next patient.
 
I don't discharge PE's. I know there is the PESI score, but we haven't started doing that and quite frankly I don't think it's standard of care. I know some places do it.

A PE usually results in 6 months of anticoagulation, a DVT can be only 3 months.

Just this past week I had a girl who traveled on a cross-country flight, had right leg pain/swelling, and had a DVT. I scanned her chest because she was tachycardic (120's). No chest pain, no shortness of breath, no dizziness. She had bilateral main pulmonary artery emboli that was on the border of being a saddle embolus. When I told her the diagnosis, she then told me she had chest "pressure" when she walks.

Some people minimize things.

I think the OP might be asking what the benefit is of getting a CT on a patient with a + DVT and chest pain, dyspnea, or HR 120? They probably have a PE. Unless there is something very peculiar about their symptoms, it's a PE until proven otherwise.

So why not just admit them w/o the CT, put them on anti-coagulation, and just go to the next patient?


Likewise I'm beginning to believe that clot burden on a CT is not overtly predictive of important patient-oriented outcomes. I've seen people with subsegmental PE's with HR 130s and saddle embolism with HR 90. I think how the body is reacting (via vital signs) to the PE is a better indicator of how dangerous it is vs what we see on CT.



This is the general problem with testing. We all love tests. We all love pictures. We want to see the PE because we think we can deliver better medical care. We want to see the perfusion deficit on myocardial perfusion studies because we can "see" the ischemia and pictures look pretty.
 
I don't discharge PE's. I know there is the PESI score, but we haven't started doing that and quite frankly I don't think it's standard of care. I know some places do it.

Although I definitely agree with the above statement. The standard of care needs to change....and this usually comes down as guidelines from our nationwide societies like ACEP. I think if ACEP says you could discharge PE with certain characteristics then we would be doing it more. Or if you worked at a place like Kaiser which is trying find ways to save money, and supports things like sending home stable PE's and their lawyers will back you up.
 
I think the incidence of silent PE in patients with DVTs is something like 20%, so I'm always surprised when other people are so surprised that a patient with a DVT has one. I just assume that one in 5 patients with a DVT that I discharge has a concomitant PE.

I don't go hunting for cardiopulmonary symptoms, but I'll scan them if they volunteer something or have VS abnormalities (far more important than symptoms, in my opinion)

I also have never discharged a (diagnosed) PE but agree that it seems appropriate in many scenarios. The problem is that even with a highly selected population, there's something like a 1% mortality rate at 90 days (unaffected by initial treatment setting).
 
So why not just admit them w/o the CT, put them on anti-coagulation, and just go to the next patient?

Admitting someone for presumed PE without any definitive diagnostic study....c'mon man, that's just sloppy. No wonder we get called "triage doctors". If I were a nocturnist taking care of the pt all night, I'd really like to know if it's a saddle PE vs an isolated sub segmental PE, regardless of vital signs. If it's a 1a.m. admit, chances are the saddle goes to the ICU or step-down whereas the sub seg goes to tele. Plus...we're not talking about an MRI, most CTAs are reasonably fast as long as you can get them over to the scanner in a timely manner (assuming they are stable).
 
Admitting someone for presumed PE without any definitive diagnostic study....c'mon man, that's just sloppy. No wonder we get called "triage doctors". If I were a nocturnist taking care of the pt all night, I'd really like to know if it's a saddle PE vs an isolated sub segmental PE, regardless of vital signs. If it's a 1a.m. admit, chances are the saddle goes to the ICU or step-down whereas the sub seg goes to tele. Plus...we're not talking about an MRI, most CTAs are reasonably fast as long as you can get them over to the scanner in a timely manner (assuming they are stable).

Right, because people like pictures. They think they can deliver better medical care if they can see the problem.

You know I'm right, and I know you're right.

This is the reason why CT scanning of PE's, which has increased markedly, has not improved patient important outcomes. At least that was true in residency 5 years ago.

I wrote above in a post, prior to the one you quoted, it's not worth fighting with the hospitalist or intensivist. And I would scan them. The only time I think I may not scan them is if they are pregnant, although I don't think I've ever diagnosed a PE in a pregnant woman. (Meaning...if they have symptoms typical of a PE, vitals to support it, + D-Dimer, and + DVT, you are done. No need to scan.) So I don't know what I would do in that case. (the Canadians would not scan them, and I listen to their podcasts all the time.)

But honestly I just don't care anymore if it's a saddle PE or subsegmental. I mean the truth I care about vital signs, duration of symptoms. We all know that if a PE is going to kill you, it's going to happen in < 24 hours.
 
Don't be the guy who sends them home with a xarelto starter pack only to have them come back in cardiac arrest from a PE.
Don't get me wrong. I agree with you to a certain extent.
But we have not moved the needle on PE mortality at all. They die at the same rate if we anticoagulate them or not. Admit them or not. Because the lungs filter out all the ones we shouldn't care about, and the ones we do care about will kill them dead before we can treat them. I'm not going to lose any sleep regardless.
 
Admitting someone for presumed PE without any definitive diagnostic study....c'mon man, that's just sloppy. No wonder we get called "triage doctors". If I were a nocturnist taking care of the pt all night, I'd really like to know if it's a saddle PE vs an isolated sub segmental PE, regardless of vital signs. If it's a 1a.m. admit, chances are the saddle goes to the ICU or step-down whereas the sub seg goes to tele. Plus...we're not talking about an MRI, most CTAs are reasonably fast as long as you can get them over to the scanner in a timely manner (assuming they are stable).
I don't always order every possible relevant diagnostic test before admission, especially if it doesn't change initial management. And with normal vital signs, no hospitalist I know puts them in the ICU.
 
ER PA here. Interesting topic and I liked reading all the responses. Here’s my take on some of these ideas.

I have never blown off chest pain in a patient with a known DVT. If they have any cardiopulmonary symptoms, unless they’ve been going on forever or unless it’s clearly related to something minor (i.e. “cold symptoms”) they’re getting a CT angiogram. I have seen enough patients with significant pulmonary emboli who made a mere “by the way...” mention of a cardiopulmonary symptom. I had a 30 year old with a DVT who said he had “chest pain for a minute last night that went away completely” without dyspnea, cough, dizziness, etc. And he had bilateral pulmonary emboli. There was another kid I saw with Down’s syndrome who had a known DVT that the primary doc was “treating” with a half dose of Xarelto “because the doc said he wanted to start slow and gradual with the Xarelto” who just had a cough and I scanned him and he also had bilateral pulmonary emboli. It’s easy to take these symptoms seriously when ONE IN THREE patients with DVT have a concomitant PE.

When I have a patient with a DVT and he’s got chest pain and dyspnea, tachycardia, hypoxia, etc. and all signs are pointing to PE - I would still have to scan the chest in my facility (I probably wouldn’t and would go ahead and just treat if there was a compelling reason not to scan like pregnancy). Our hospitalists would rip me a new one if I admitted without the confirmatory test.

Last thing - I’ve never sent a patient with a PE home. Can’t bring myself to do it and I’ve never had an attending encourage me to do so either
 
Most of the US is still behind the curve on low risk PE discharge, although many large institutions are moving towards it. Most of the current existing evidence supports very low mortality using stratification tools such as PESI. I also haven't been able to find any compelling evidence that clot burden in isolation has any true patient-related outcome changes.

Unfortunately, I currently put patient in Obs because my current hospital local practice pattern is to Obs pretty much everyone and they love to peer review everything. So, I acknowledge that I obs my PE patient for my own benefit, with the understanding they receive 0 benefit and are exposed to additional costs, at least until our local practice environment catches up.
 
Most of the US is still behind the curve on low risk PE discharge, although many large institutions are moving towards it. Most of the current existing evidence supports very low mortality using stratification tools such as PESI. I also haven't been able to find any compelling evidence that clot burden in isolation has any true patient-related outcome changes.

Unfortunately, I currently put patient in Obs because my current hospital local practice pattern is to Obs pretty much everyone and they love to peer review everything. So, I acknowledge that I obs my PE patient for my own benefit, with the understanding they receive 0 benefit and are exposed to additional costs, at least until our local practice environment catches up.
Most of the US is still behind the curve on meaningful tort reform.
 
Someday I want to see a study on totally asymptomatic people in v large numbers to find out how many have a small subsegmental PE that never would have come to attention otherwise. It has to happen not infrequently, if my somatic symptom disorder/anxiety/q48h chest pain x years chest pain experiences are representative.
 
Someday I want to see a study on totally asymptomatic people in v large numbers to find out how many have a small subsegmental PE that never would have come to attention otherwise. It has to happen not infrequently, if my somatic symptom disorder/anxiety/q48h chest pain x years chest pain experiences are representative.

I have no science to back this up, but my experience is the same.
 
Someday I want to see a study on totally asymptomatic people in v large numbers to find out how many have a small subsegmental PE that never would have come to attention otherwise. It has to happen not infrequently, if my somatic symptom disorder/anxiety/q48h chest pain x years chest pain experiences are representative.
I read it somewhere, some long time ago, and can't find it again, but it was that, on autopsy, 25% of bodies have clinically noticeable pulmonary emboli, that did NOT contribute to the person's death.

So, that quick, sharp pain? Yeah, maybe, lungs doing what they do!
 
A lot of patients (some studies quote 40%) with proximal dvts have PEs as well. If you aren’t scanning all your DVTs I can almost guarantee you sent a PE home at some point in time. No biggie though cause you started anticoagulation I’m sure.

I do the following:

All patients with dvt and abnormal vitals/elevated troponin or patients requiring oxygen get CTA and admitted.

If a patient is perfectly normal and has no complaints of chest pain or SOB I look at the ultrasound. If you have a small isolated DVT I discuss inpatient/outpatient with patient and usually they just want to be anticoagulated and DC. I do not scan these patients.

If the patient is perfectly normal with no chest pain or SOB and normal vitals, but the patient has a LARGE very proximal dvt I admit these patients. These are the ones that break off and kill you. They also very likely have a PE already.

I also send small stable PEs home quite frequently so long as they don’t have a huge swollen leg full of clot ready to go on the IVC expressway.
 
HAHA
this debate, if it's a debate, kind of reminds how some docs approach minor blunt head trauma. Some go by the guidelines, and if the CT Head rules (Canada or Nexus or whatever) say scan they do....if they say don't scan they dont...others just scan no matter what.

What's great about these rules, that I like, is they freely admit that you might be sending home someone with a tiny brain bleed but that's OK....they 99.9% do just fine.

Here's a theoretical question: How would you guys approach with PE's change if all you got was a radiologist who wrote "There is a acute pulmonary embolism" and did not describe where it is, whether proximal or distal, etc. It's just a "yes there is one" or "no there is not one."?

My guess is we would use a history, vitals signs, and physical and make a decision about what to do. The decision to go to the ICU or whatever would be based on the H&P (which is what we should be doing anyway).
 
Don't get me wrong. I agree with you to a certain extent.
But we have not moved the needle on PE mortality at all. They die at the same rate if we anticoagulate them or not. Admit them or not. Because the lungs filter out all the ones we shouldn't care about, and the ones we do care about will kill them dead before we can treat them. I'm not going to lose any sleep regardless.

Surely you don't believe a large proximal PE has the same mortality treated vs untreated? Regardless, I'm not even arguing about any of that. In my post, I'm not talking about mortality, treatment, p-values, etc.. I'm talking about missing a diagnosis carrying a statistically significant mortality risk where there was no CDR employed to risk stratify the pt because the physician simply didn't know about it. Regardless of what you believe, good luck defending that one or explaining why the CTA wasn't "really indicated" to the family or trying to retrospectively apply a CDR on a condition that wasn't thought to exist. I know where you're coming from but that isn't what I'm talking about... I'm talking about missing a diagnosis that likely resulted in cardiac arrest and/or death. Surely I'm not the only person that has seen these in the ED. There's a lot of things we can miss in the ED, but I wouldn't recommend starting with PEs.

I don't always order every possible relevant diagnostic test before admission, especially if it doesn't change initial management. And with normal vital signs, no hospitalist I know puts them in the ICU.

Smart ones are worried about occult cardiac compromise such as RV strain and/or ventricular thrombus or some other condition that would accelerate consideration of more invasive strategies such as CDT, etc... If it's a saddle and 1:6 nursing on a busy night with a sole nocturnist...some would feel better with the pt in a closely monitored setting pending a cardiac echo, etc. to rule out any of the above prior to placing on telemetry when he/she knows they can't get to them in the next couple of hours due to multiple admissions. I can't really argue with their logic and think it's a perfectly reasonable request.
 
Riddle me this big ballers, how many of you are admitting "PE" on your admitting diagnosis without a CTA. I'm not talking about hemodynamically unstable and headed to the ICU. I'm talking "Hey, I got a PE in room 5 because I'm just THAT GOOD and started them on heparin, get a CTA IF YOU WANNA." click..BAMM. Just like that. LOL, I call some BS. Either that or you have your hospitalists and intensivists seriously trained... :laugh:
 
Surely you don't believe a large proximal PE has the same mortality treated vs untreated? Regardless, I'm not even arguing about any of that.

It very well could be that predictors of mortality with acute PE has nothing to do with saddle, subsegmental, etc. The PESI does not use clot burden to determine mortality.
 
Someday I want to see a study on totally asymptomatic people in v large numbers to find out how many have a small subsegmental PE that never would have come to attention otherwise. It has to happen not infrequently, if my somatic symptom disorder/anxiety/q48h chest pain x years chest pain experiences are representative.

Of course current recommendations are to not anticoagulate subsegmental PEs.
 
Riddle me this big ballers, how many of you are admitting "PE" on your admitting diagnosis without a CTA. I'm not talking about hemodynamically unstable and headed to the ICU. I'm talking "Hey, I got a PE in room 5 because I'm just THAT GOOD and started them on heparin, get a CTA IF YOU WANNA." click..BAMM. Just like that. LOL, I call some BS. Either that or you have your hospitalists and intensivists seriously trained... :laugh:

EVERY SINGLE ONE! LOL :scared:
 
I missed a big ass PE once. Pt died three days later.

Pt was elderly, was just in the hospital for about a month and had a lap abdominal surgery that was complicated by numerous intra-abdominal abscesses. Had a few post-op laparotomies to get rid of those abscesses too. She finally got healthy enough and was sent to a SNF.

She returned 1 week later when I saw her in the ED and was complaining of a bunch of things: chest pain, dyspnea, abdominal pain, incisional pain, etc. Had a temp of 101.5, HR was like 145 and it was aflutter. Her abdomen was tender. For some reason I didn't think much of her CP/Dyspnea complaint. Her labs were all wacky, she was septic, and I scanned her abdomen and there was yet another abscess. So i admitted her with IVF, Abx, and she went back to the ICU.

I got a call from the ICU doc 30 minutes later and he said "did you scan her for a PE?" I said why? He said "the EKG shows a new RBBB." I looked at the EKG and it indeed showed an RBBB, but it also showed new aflutter. I remember saying I chalked up her EKG findings to sepsis. The ICU doc ordered dopplers of her legs which were + DVT and he started heparin. The CT the next day (as she just got a CT Abd w/ IV contrast from me) showed PE.

Pt died 3 days later from probably a number of things, the PE being one of them.

I was pretty upset about this case...I try hard not to miss things like PE especially when people could have them and could hurt them. But I also remember that the intensivist started heparin a mere 3 hours after I would have had I scanned her for a DVT / PE. So there was just a 3 hr delay with the definitive treatment and the pt died 3 days later anyways. So I didn't feel all that bad about missing it.
 
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Really? Can you post the link?

"Whether to Anticoagulate Subsegmental PE
∗19. In patients with subsegmental PE (no involvement of more proximal pulmonary arteries) and no proximal DVT in the legs who have a (i) low risk for recurrent VTE (see text), we suggest clinical surveillance over anticoagulation (Grade 2C) or (ii) high risk for recurrent VTE (see text), we suggest anticoagulation over clinical surveillance (Grade 2C).

Remarks: Ultrasound (US) imaging of the deep veins of both legs should be done to exclude proximal DVT. Clinical surveillance can be supplemented by serial US imaging of the proximal deep veins of both legs to detect evolving DVT (see text). Patients and physicians are more likely to opt for clinical surveillance over anticoagulation if there is good cardiopulmonary reserve or a high risk of bleeding."

Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report.[URL='https://www-sciencedirect-com.ezproxylocal.library.nova.edu/science/journal/00123692/149/2'] Volume 149, Issue 2, February 2016, Pages 315-352

Basically the gist of the recommendation is that a large portion of "subsegmental" PEs are actually artifact and not a PE... and the PEs that do exist are low risk to begin with.
[/URL]
 
Surely you don't believe a large proximal PE has the same mortality treated vs untreated?
It's not religion. I don't believe in anything.
The data, on the other hand, demonstrate that there is no difference in mortality. It's a lethal condition. We wave our hands a lot, and they still die. Submassive PE is also wanting for treatment. We kill people with thrombolytics for that.
Management of massive and nonmassive pulmonary embolism
 
Riddle me this big ballers, how many of you are admitting "PE" on your admitting diagnosis without a CTA. I'm not talking about hemodynamically unstable and headed to the ICU. I'm talking "Hey, I got a PE in room 5 because I'm just THAT GOOD and started them on heparin, get a CTA IF YOU WANNA." click..BAMM. Just like that. LOL, I call some BS. Either that or you have your hospitalists and intensivists seriously trained...
No, but I'm sure I've admitted ACS on heparin that ends of being PE.
 
I missed a big ass PE once. Pt died three days later.

Pt was elderly, was just in the hospital for about a month and had a lap abdominal surgery that was complicated by numerous intra-abdominal abscesses. Had a few post-op laparotomies to get rid of those abscesses too. She finally got healthy enough and was sent to a SNF.

She returned 1 week later when I saw her in the ED and was complaining of a bunch of things: chest pain, dyspnea, abdominal pain, incisional pain, etc. Had a temp of 101.5, HR was like 145 and it was aflutter. Her abdomen was tender. For some reason I didn't think much of her CP/Dyspnea complaint. Her labs were all wacky, she was septic, and I scanned her abdomen and there was yet another abscess. So i admitted her with IVF and she went back to the ICU.

I got a call from the ICU doc 30 minutes later and he said "did you scan her for a PE?" I said why? He said "the EKG shows a new RBBB." I looked at the EKG and it indeed showed an RBBB, but it also showed new aflutter. I remember saying I chalked up her EKG findings to sepsis. The ICU doc ordered dopplers of her legs which were + DVT and he started heparin. The CT the next day (as she just got a CT Abd w/ IV contrast from me) showed PE.

Pt died 3 days later from probably a number of things, the PE being one of them.

I was pretty upset about this case...I try hard not to miss things like PE especially when people could have them and could hurt them. But I also remember that the intensivist started heparin a mere 3 hours after I would have had I scanned her for a DVT / PE. So there was just a 3 hr delay with the definitive treatment and the pt died 3 days later anyways. So I didn't feel all that bad about missing it.
The key takeaway is that you provided appropriate and timely care to a critically ill patient, started appropriate therapy for what you thought was the underlying diagnosis, and made the appropriate disposition at which point someone else continued care and added additional diagnostics and therapeutics.
 
Riddle me this big ballers, how many of you are admitting "PE" on your admitting diagnosis without a CTA. I'm not talking about hemodynamically unstable and headed to the ICU. I'm talking "Hey, I got a PE in room 5 because I'm just THAT GOOD and started them on heparin, get a CTA IF YOU WANNA." click..BAMM. Just like that. LOL, I call some BS. Either that or you have your hospitalists and intensivists seriously trained... :laugh:

I've done this, but it's always been in the context of extenuating circumstances: Consider a patient with an acute kidney injury and a reported contrast reaction (neither of which I actually care about, but my Rads department does) who comes in with a good story while the VQ tech is at home for the night, and they have a positive duplex.

So, I don't do it cuz I'm a baller (tho I am:meh:), but I have done it...
 
I think the management of PEs varies greatly by region. Where I trained we sent home pretty much all low risk PEs (low PESI score and clinical gestalt). I still do the same. Many colleagues don't. I can't really see how a hospitalization will benefit them.

I have sent home a "PE" without a CTA. The patient had a history of hypercoagubility, wasn't taking anticoagulants, was taking hCG (that she bought on the internet). Was there for an incidental complaint, noted one month shortness of breath on ROS, had a positive d-dimer and an echo without right heart strain -> stop hCG and re-start your anticoagulant.
 
LOL, I knew it.... Big Ballers! Now I know how you guys walk into every shift:



Which go something like this....

8Us7Bl2.gif
 
It's not religion. I don't believe in anything.
The data, on the other hand, demonstrate that there is no difference in mortality. It's a lethal condition. We wave our hands a lot, and they still die. Submassive PE is also wanting for treatment. We kill people with thrombolytics for that.
Management of massive and nonmassive pulmonary embolism

"The data demonstrates there is no difference in mortality." Be specific, I have no idea what point you're arguing. Are you arguing that a large proximal occlusive PE has the same mortality as any other PE regardless of treatment and therefore we shouldn't care as much about diagnosing them with PE and/or admitting them for anticoagulation? (You do realize you posted an article arguing for a causal link between PE with RV dysfunction and mortality, yet you seem to imply that it would be illogical to assume that proximal location and/or clot burden would have any direct effect on RV dysfunction and/or mortality...which seems completely illogical to me.)

So, you disagree with this one?

Early Anticoagulation Is Associated With Reduced Mortality for Acute Pulmonary Embolism

What about uptodate, you disagree with them too?

Morbidity and mortality — Prognosis from pulmonary embolism (PE) is variable. Accurate estimates have been limited by data that are mostly derived from older studies, registries, and hospital discharge records collected from heterogeneous populations of patients. As an example, a patient with a single, asymptomatic, subsegmental pulmonary embolism (SSPE) likely has a different prognosis than a patient with massive PE and shock. However, in general, if left untreated, PE is associated with an overall mortality of up to 30 percent compared with 2 to 11 percent in those treated with anticoagulation [1,4,43,83-89]. PE-related mortality may be decreasing with reported rates falling from 3.3 percent (2001 to 2005) to 1.8 percent (2010 to 2013) in one study and from 17 to 10 percent in another study [89,90].

Supporting citations:
UpToDate


I'm not sure what you're arguing. If you're arguing that mortality remains the same for all PEs regardless of treatment and therefore we shouldn't care as much about diagnosing or treating them....well that's just not supported consensually in the overwhelming body of literature, nor is that standard of care in our specialty or any others at the moment. I hope you're not referencing to Mel Herberts old article from the early 2000s.
 
LOL, I knew it.... Big Ballers! Now I know how you guys walk into every shift:

Which go something like this....

Do you think it is never appropriate to make a significant diagnosis without getting a confirmatory test?

I'm not advocating for being cavalier, I'm saying that sometimes the context makes it such that getting the CTA is unlikely to add anything but radiation and expense to the patient's management.

You do realize that skipping the CTA in a pregnant patient with chest pain and a + DVT study is the (ACOG/ACEP/Chest) society recommended approach, right?

Now, if you'll excuse me - I need to go shine up the rims on my Toyota.
 
Actually, I disagree with Uptodate a lot. They interpret studies incorrectly, and there's a lot of bias. If you don't read the articles, you can miss it, as they often don't explicitly say it. That's not to say that they're always or even frequently wrong. But the same problems a lot of people have with #FOAM is much worse with Uptodate, as people aren't critiquing them as regularly.
Uptodate is like wikipedia to me. I used to look at it, but now I look to other sources.
The paper they're quoting?
Early Anticoagulation Is Associated With Reduced Mortality for Acute Pulmonary Embolism
It only follows 400 patients. It doesn't compare no anticoagulation to anticoagulation. It only discusses the timing of the anticoagulation.
It also talks about guidelines, one of which is the Herbert paper you apparently don't like.
It then goes to papers written in 76, 75, 60, 59, and finally a 2006 Jeff Kline paper that is about pre-test probability.

https://www.ajpmonline.org/article/S0749-3797(09)00946-5/fulltext
https://www.atsjournals.org/doi/full/10.1164/rccm.200907-1141OC

Again, I'm not sure what you're railing against here. Nowhere am I saying not to treat them. You absolutely should. You just just recognize that it isn't doing much.
 
It's not religion. I don't believe in anything.
The data, on the other hand, demonstrate that there is no difference in mortality. It's a lethal condition. We wave our hands a lot, and they still die. Submassive PE is also wanting for treatment. We kill people with thrombolytics for that.
Management of massive and nonmassive pulmonary embolism

The way I interpret your statements, makes me think you are saying there is no benefit treating acute PE with anti-coagulation. That is...if there are 200 patients with massive or sub-massive PE and you give 100 of them anti-coagulation and the other 100 placebo, the outcomes (of mortality, lets say) would be the same.

yet the article you put forth doesn't say that at all. In fact...I think it would be a very hard thing to study because it would never pass the IRB.

The most important table of that paper above is the first one. PE is a killer according to this (because I bet all 1001 of those patients were treated).

For what it's worth, I don't really believe that 8.1% of patients with RV dysfunction, no arterial hypotension died while in the hospital. that seems too high.
 

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Do you think it is never appropriate to make a significant diagnosis without getting a confirmatory test?

I'm not advocating for being cavalier, I'm saying that sometimes the context makes it such that getting the CTA is unlikely to add anything but radiation and expense to the patient's management.

You do realize that skipping the CTA in a pregnant patient with chest pain and a + DVT study is the (ACOG/ACEP/Chest) society recommended approach, right?

Now, if you'll excuse me - I need to go shine up the rims on my Toyota.

Docs love pictures...they love to look at the thing they are treating instead of just looking at the patient or vital signs. If it walks like a duck, quacks like a duck, paddles in the water like a duck, looks like every other duck in the pond, swims like a duck, poops like a duck, and tastes like a duck, why do you need DNA analysis to tell you it's a duck?
 
"The data demonstrates there is no difference in mortality." Be specific, I have no idea what point you're arguing. Are you arguing that a large proximal occlusive PE has the same mortality as any other PE regardless of treatment and therefore we shouldn't care as much about diagnosing them with PE and/or admitting them for anticoagulation? (You do realize you posted an article arguing for a causal link between PE with RV dysfunction and mortality, yet you seem to imply that it would be illogical to assume that proximal location and/or clot burden would have any direct effect on RV dysfunction and/or mortality...which seems completely illogical to me.)

You do make a point about RV dysfunction and mortality, and conceivable clot in the main pulmonary artery ought to cause more RV dysfunction than a subsegmental one.

But we have all seen stable saddles and unstable segmental PE's.

And...the PESI score which, prima facie is believable, doesn't account for RV dysfunction and clot burden on CT. It looks at important stuff like hypotension, age, co-morbidities, and others.

I said it above.....I don't think location or size of clot on CT should mean that much!
 
Of course current recommendations are to not anticoagulate subsegmental PEs.
This is going to be good news for the Munchausen folks I’ve known who OD on their warfarin once in a while to get in the hospital, when they’re not ODing on their insulin to get hypoglycemic or skipping it entirely to get DKA. I hope someone has recalculated the risk benefit ratio for the person I’m thinking of by now. It’s not a lot of cases but my observation is that if a patient is a hospital hopper who presents to different places with nonspecific chest pain every couple of days and gets a therapeutic dose of radiation from their q48-72 hour CTAs, they’re going to have a small subsegmental PE at least once. It makes physiologic sense, why shouldn’t you every once in a while get a tiny thrombus that gets stuck in a tiny vessel and causes no problems? No body system is perfect and if you’re looking continuously eventually you will find a (transient) problem with anything.

The other challenge in this area I’ve experienced are a couple people with chronic hypoxic respiratory failure of Pickwickian nature, who present every few weeks with more trouble breathing than usual. You can’t get them in any scanner so they end up empirically anticoagulated forever.
 
It doesn't compare no anticoagulation to anticoagulation. It only discusses the timing of the anticoagulation.

Of course it doesn't because nobody is trying to do that kind of research anymore. Nobody believes that "no anticoagulation" therapy is just as good as anticoagulation in PEs across the board. You only see people talking about it with small sub segmental PEs. How would you even try to design an RCT with control groups comparing placebo vs LMWH in submassive PE. Is that even ethical? I doubt that's even capable of being IRB approved. Most of our research at this point with PEs is focusing on outpatient therapies, risk stratification, etc..
 
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