Chest pain in PE

[KiloAxe]

Hey guys, I've had a couple cases recently with patient who has known PE presenting with their 'PE' chest pain and I wanted to see what others typically do in these cases. To give an example. 40 yo with recent diagnosis of PE, on Coumadin, returning to ED with pleuritic chest pain. INR therapeutic. Hemodynamically stable, EKG looks unchanged, and satting >95%. I am typically of the mindset that there is not really a benefit to reimaging as the patient is already anticoagulated and management would be unlikely to change so I don't typically do any further workup. The flip side of the argument is that if he is continuing to throw clots while on anti coagulation, do we need to know this and consider IVC filter placement (FYI no DVT found on ultrasound at time of diagnosis)?

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[xaelia]

One pathway I might consider in these folks who are anticoagulated, but in which I still suspect new clot, is to evaluate their total fractional obstruction of the pulmonary tree. We're starting to see some evidence that lytics – probably half-dose lytics –*may have a role in treating submassive/significant clot burden to decrease the incidence of subsequent pulmonary hypertension.

That said, I wouldn't do a test unless I expected it to change treatment in such a fashion as to improve outcomes.

 

[dotcb]

Depending on the case details, I'd consider other diagnoses such as ACS, pericarditis, etc, but I would be unlikely to repeat the PE workup or make changes in its management plan.

 

[WilcoWorld]

When known PE's come in with chest pain I ask myself 3 questions:
1) Is this CP due to the PE?
2) Is their INR therapeutic?
3) Are there any signs of increased clot burden (tachycardia, hypoxia, hypotension, worsening dyspnea, syncope, tachypnea, ECG changes, troponin leak)?

If they're stable and adequately anti coagulated, I treat their pain with pain medication and discharge without reimaging.

 

[gutonc]

When known PE's come in with chest pain I ask myself 3 questions:
1) Is this CP due to the PE?
2) Is their INR therapeutic?
3) Are there any signs of increased clot burden (tachycardia, hypoxia, hypotension, worsening dyspnea, syncope, tachypnea, ECG changes, troponin leak)?

If they're stable and adequately anti coagulated, I treat their pain with pain medication and discharge without reimaging.

As the hematologist who will have to take this call from you (or see them in clinic in the next day or two when their PCP s***s a brick about having to deal with this), I completely support this approach.

 

[dotcb]

I agree.

Just for the spirit of debate, how would it change your management if their INR was 1.2? 1.8?

Take the coumadin as you were directed to? Close F/U? Re-bridge w/ LMWH?

Personally, if I feel comfortable with 1 & 3, #2 is less important and wouldn't make me re-image them.

When known PE's come in with chest pain I ask myself 3 questions:
1) Is this CP due to the PE?
2) Is their INR therapeutic?
3) Are there any signs of increased clot burden (tachycardia, hypoxia, hypotension, worsening dyspnea, syncope, tachypnea, ECG changes, troponin leak)?

If they're stable and adequately anti coagulated, I treat their pain with pain medication and discharge without reimaging.

 

[WilcoWorld]

I agree.

Just for the spirit of debate, how would it change your management if their INR was 1.2? 1.8?

Take the coumadin as you were directed to? Close F/U? Re-bridge w/ LMWH?

Personally, if I feel comfortable with 1 & 3, #2 is less important and wouldn't make me re-image them.

I wouldn't reimage solely because of a subtheraputic INR. I mentioned that because a subtheraputic INR would suggest that their coumadin dosing requires adjustment (or perhaps their compliance requires adjustment). As for bridging, if they've been off of meds for a week and the INR = 1.0, it may be worth it. If they've been taking their meds and the INR is 1.6, then they probably don't need bridging. If I'm in doubt, I'll give gutonc a ring...

 

[gutonc]

I wouldn't reimage solely because of a subtheraputic INR. I mentioned that because a subtheraputic INR would suggest that their coumadin dosing requires adjustment (or perhaps their compliance requires adjustment). As for bridging, if they've been off of meds for a week and the INR = 1.0, it may be worth it. If they've been taking their meds and the INR is 1.6, then they probably don't need bridging. If I'm in doubt, I'll give gutonc a ring...

And I'll take that call. Honestly, it will take me 5 minutes to deal with it and I'd rather do it then than curse your name when he shows up in clinic all messed up one way or another.

I assumed the sub-therapeutic INR was more for determining management than diagnosis. Recent PE w/ recurrent/continued CP and sub-therapeutic INR (and no evidence of other cardiovascular badness)? No s**t Batman. Lovenox 'em, double the coumadin dose and have them see me or AC clinic in 48h.

IMHO it would also depend on how "recent" the PE dx was. 1 week ago? 1 month ago?

 

[GeneralVeers]

For liability and patient satisfaction/widget reasons I just re-scan them. I tell them it's to "make sure the PE Isn't bigger".

It's simple, no thought involved for me, makes the patient happy, and I don't have to worry about someone second-guessing my management if they have a bad outcome.

Welcome to modern medicine.

 

[Apollyon]

One pathway I might consider in these folks who are anticoagulated, but in which I still suspect new clot, is to evaluate their total fractional obstruction of the pulmonary tree. We're starting to see some evidence that lytics – probably half-dose lytics –*may have a role in treating submassive/significant clot burden to decrease the incidence of subsequent pulmonary hypertension.

That said, I wouldn't do a test unless I expected it to change treatment in such a fashion as to improve outcomes.

As is common, I don't completely follow your line of thought (which is likely all my own fault). Are you saying that you would rescan if - prior to imaging - you were considering lysing the patient? I mean, you say two things: "evaluate the tree" and "not do a test that won't change anything", but you also say the evidence is not strong for lytics. Or am I reading too much into that? I hope that what I've written outlines my confusion.

 

[xaelia]

As is common, I don't completely follow your line of thought (which is likely all my own fault).

Hah - hardly your fault when I'm vague and non-specific.

I'm pretty much in agreement with WilcoWorld – does a change in physiology possibly reflect significantly increased clot burden? And, since I'd probably offer someone with physiologic derangement half-dose lytics, that's when I'd go ahead and rescan them.

 

[Birdstrike]

It all comes down to whether this is the same pain from the old clot or a new clot. It's obviously hard to determine. Err on the side of safety. Assume it's a new clot until proven, otherwise. Obviously, if they're throwing new clots despite anticoagulant, something is seriously wrong.

Is the pain worse?
Is it different in character?
Is it in a different lung?
Is the anti-coagulation sub-optimal?
Have the vital signs changed?
If nothing has changed, why did they choose today to come to the ED, all of a sudden? (Big red flag right there.)
Does a new scan show higher clot burden?
If not, can a repeat scan necessarily rule out increased clot burden?

If the patient is throwing new clot, their morbidity and mortality will be significantly higher, no? It's a hard thing to rule out. Just because the hospitalist isn't excited about another admission doesn't necessarily mean the patient isn't sick.

It's much like someone who is on ASA, plavix, has horrendous coronary disease and often has angina, despite a recent cath where nothing was stented. A recent cath where nothing was stentsble doesn't mean there heart is perfect and un-infarctable. It could mean the exact opposite.

These cases are tough. They require something you can't find in a book. It's called,

Clinical Judgement.