How is this not a PE?

[leviathan]

Saw this patient on call. A heavy smoker with AECOPD being worked up for malignancy suddenly develops chest pain, shortness of breath, going from 90% sats on room air now requiring 100% fio2 to keep her in the high 80s. Breath sounds clear, CXR is clear except for a suspicious nodule. High sensitivty trop comes back at 500, then 800 (20 on admission). A new RBBB is found on ECG which was not there 2 days before, no ST-T changes.

According to another resident, the attending stopped the heparin I had started, saying it was not a PE or NSTEMI and that the troponin rise was from COPD exacerbation.

Does that make sense? I would not second guess my decision to start heparin on call, no matter what, but is there anything anyone can think of which would point you away from this diagnosis the next morning?

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[Bostonredsox]

Why would they stop the heparin prior to the chest ct? Your description generates a high enough wells score to anticoagulate until you get definitive diagnosis/exclusion from imaging.

 

[dotcb]

Sounds like an outlier attending. Continuing the heparin would've been appropriate unless in their opinion this was worsening of a COPD exacerbation w/ demand ischemia. I think most would've continued heparin. What did the CT show?

 

[Hernandez]

Sounds like an outlier attending. Continuing the heparin would've been appropriate unless in their opinion this was worsening of a COPD exacerbation w/ demand ischemia. I think most would've continued heparin. What did the CT show?

http://www.ncbi.nlm.nih.gov/pubmed/18812453

 

[leviathan]

CT angiogram was never done because of the patient's creatinine. I just can't understand what else could cause a troponin rise that significant with ECG evidence of R heart strain AND significantly higher oxygen requirements when the chest was clear to auscultation and CXR looked clear as well. This attending is supposed to be very smart, and something must have made him change his mind the next morning. I can't figure out what that could have been, though. Would love to ask him myself but he's gone for the next month.

 

[Bostonredsox]

Did the pt end up getting a v/q once the respiratory status had improved?

 

[VentdependenT]

Hopefully the pt wont drop dead from obstructive shock in the next month

 

[leviathan]

Did the pt end up getting a v/q once the respiratory status had improved?

I don't think so. I stopped by to check on him over the next few days and he seemed to be doing much better, back on just 3LPM nasal prongs. Seems like the staff made the right call, but again, I wish I knew what his rationale could have possibly been. Even if it was not a PE, the only other option I can think of is NSTEM with that troponin bump, but not sure how that would drop his sats so much without developing flash pulmonary edema.

 

[Bostonredsox]

I don't think so. I stopped by to check on him over the next few days and he seemed to be doing much better, back on just 3LPM nasal prongs. Seems like the staff made the right call, but again, I wish I knew what his rationale could have possibly been. Even if it was not a PE, the only other option I can think of is NSTEM with that troponin bump, but not sure how that would drop his sats so much without developing flash pulmonary edema.

Him looking ok doesn't mean they were right. Unless he has had a v/q or ct angio, a PE has still not been excluded. Even though he is high risk for PE so it doesn't apply, did he by chance have a dimer drawn?

 

[TrustMe]

Did he get TTE to look at RV? If RV dilation or decreased function > PE. If global hypokinesis or RWMA > MI.

 

[jdh71]

Hopefully the pt wont drop dead from obstructive shock in the next month

gomers don't die son, they go to ground

you should know that by now and I am disappoint

 

[NontradICUdoc]

I am not t sure hat a VQ would really be helpful if the patient has bad COPD, it may, at baseline, come back with anything other than low probability. Was a bedside echo performed to see if there were any new wall motion abnormalities of the RV, increase in RV pressure, or septal motion changes?

If the patient's Cr was elevated what about nephro consult which they usually say to fluid bolus the patient and continue with fluid management for about 24 hours.....

 

[jdh71]

CT angiogram was never done because of the patient's creatinine. I just can't understand what else could cause a troponin rise that significant with ECG evidence of R heart strain AND significantly higher oxygen requirements when the chest was clear to auscultation and CXR looked clear as well. This attending is supposed to be very smart, and something must have made him change his mind the next morning. I can't figure out what that could have been, though. Would love to ask him myself but he's gone for the next month.

If you've got a bad COPDer of the emphysematous type with plenty of loss of capillary surface area, who has a bad exacerbation, you can limit the ventilation enough in the areas that are still working that you get hypoxic at rest. You get that hypoxic with the PA vasoconstriction and you could get enough strain on the heart, especially a heart that may not be great at baseline, to bump your trops, especially given the forward feeding hypoxic spiral of crap that is the straining and hypoxic RV.

I guess maybe some of this is a matter of style, but I think I would have ran heparin on this guy too until I had more information to feel better about there not being a PE - at minimum a LE U/S.

 

[Hernandez]

http://www.ncbi.nlm.nih.gov/pubmed/18812453

I case you guys glazed over this. You should have this in the back of your head

 

[jdh71]

I case you guys glazed over this. You should have this in the back of your head

I presented that paper in conference when it came out back in residency.

It's interesting but do you really think every AECOPD needs a CT of the chest for PE? 1/3 is a big number and I'd think if you really believed the meta analysis that we should be getting scans on all our AECOPD.

 

[Hernandez]

I presented that paper in conference when it came out back in residency.

It's interesting but do you really think every AECOPD needs a CT of the chest for PE? 1/3 is a big number and I'd think if you really believed the meta analysis that we should be getting scans on all our AECOPD.

I don't fully believe it the numbers but one of the main papers it uses is a decent study, but I will scan my COPD PTs who seem to have higher o2 requirements than I'd expect and if they don't have much sputum production increase I have a lower threshold. That being said, many of these PEs do fall into the single sub-segmental category, so then what so we do with them?

 

[jdh71]

I don't fully believe it the numbers but one of the main papers it uses is a decent study, but I will scan my COPD PTs who seem to have higher o2 requirements than I'd expect and if they don't have much sputum production increase I have a lower threshold. That being said, many of these PEs do fall into the single sub-segmental category, so then what so we do with them?

Exactly, which is what we all kind of do, allow our experience to guide when and when it's probably not a PE in this kind of a scenario. One of our staff in residency started getting CT PE's on all AECOPD patients after this study came out and our division chief had to sit him down and be like, "stop that".

 

[leviathan]

I am not t sure hat a VQ would really be helpful if the patient has bad COPD, it may, at baseline, come back with anything other than low probability. Was a bedside echo performed to see if there were any new wall motion abnormalities of the RV, increase in RV pressure, or septal motion changes?

If the patient's Cr was elevated what about nephro consult which they usually say to fluid bolus the patient and continue with fluid management for about 24 hours.....

That's one thing that I'm kicking myself for not doing (getting the echo). I think my mindset at the time at 3am was that this was definitely a PE that I was already treating appropriately, so I didn't think there was any need to do anything further. tPA would have been the only extra therapy and you could consider this a submassive PE with the trop increase and RBBB, but my understanding is that the evidence for that is weak. Anyway, if I could go back I definitely would have got an echo just to get further info, since I didnt go for the CT.

If you've got a bad COPDer of the emphysematous type with plenty of loss of capillary surface area, who has a bad exacerbation, you can limit the ventilation enough in the areas that are still working that you get hypoxic at rest. You get that hypoxic with the PA vasoconstriction and you could get enough strain on the heart, especially a heart that may not be great at baseline, to bump your trops, especially given the forward feeding hypoxic spiral of crap that is the straining and hypoxic RV.

I guess maybe some of this is a matter of style, but I think I would have ran heparin on this guy too until I had more information to feel better about there not being a PE - at minimum a LE U/S.

That's a good explanation and makes sense to me re: the trop rise and new RBBB. I forgot that I had actually got an ECG the first time I saw him which was normal, and it wasnt until later in the night I did a repeat ECG which showed the block.

The only thing I didn't mention is he was already in the hospital for several days for his AECOPD, and had been doing well until the evening I was paged about him. So what would make him suddenly have a second exacerbation while already being on steroids+abx+your usual treatment.

 

[souljah1]

That's one thing that I'm kicking myself for not doing (getting the echo). I think my mindset at the time at 3am was that this was definitely a PE that I was already treating appropriately, so I didn't think there was any need to do anything further. tPA would have been the only extra therapy and you could consider this a submassive PE with the trop increase and RBBB, but my understanding is that the evidence for that is weak. Anyway, if I could go back I definitely would have got an echo just to get further info, since I didnt go for the CT.


That's a good explanation and makes sense to me re: the trop rise and new RBBB. I forgot that I had actually got an ECG the first time I saw him which was normal, and it wasnt until later in the night I did a repeat ECG which showed the block.

The only thing I didn't mention is he was already in the hospital for several days for his AECOPD, and had been doing well until the evening I was paged about him. So what would make him suddenly have a second exacerbation while already being on steroids+abx+your usual treatment.

How about the possibility that the initial COPD exacerbation was due to a PE and the second exacerbation was due to another one?

You kind of describe shunt physiology above, which rarely happens in PE. usually you see hemodynamic compromise before you see severe hypoxemia, though you can see shunt physiology with a R to L shunt through a PFO due to acute PH.

I would have kept heparin on and hunted for clot. Little downside.

 

[VentdependenT]

I don't fully believe it the numbers but one of the main papers it uses is a decent study, but I will scan my COPD PTs who seem to have higher o2 requirements than I'd expect and if they don't have much sputum production increase I have a lower threshold. That being said, many of these PEs do fall into the single sub-segmental category, so then what so we do with them?

Treat em. Its the next one that gets em.

 

[VentdependenT]

gomers don't die son, they go to ground

you should know that by now and I am disappoint

I still refuse to read that. I was so jaded at one point in my career (>4 yrs ago) that I didnt need any more fuel.

However, that statement is correct.

 

[deleted6669]

I case you guys glazed over this. You should have this in the back of your head

Thank you for posting this. I was not aware of this study.

 

[Hernandez]

Treat em. Its the next one that gets em.

Show me the data.......

 

[slycaper]

Maybe the attending had dissection in his differential and wanted a CXR prior to AC

 

[Bostonredsox]

Maybe the attending had dissection in his differential and wanted a CXR prior to AC

cxr is not sensitive nor specific enough to exclude a dissection prior to starting AC for a presumed PE. CTA timed for the aorta or a TEE are the only ways to exclude the diessection if you are truly worried about it.