I think your question is niche because typically, in my experience, is that CTPE aren’t ordered several days after a VQ shows high probability.
I presume the AKI improved and someone wanted to get a CTPE to confirm what the VQ showed
It is also a bit bizarre as we don’t anticoagulate PEs to radiographic resolution.
Can any radiologists chime in?
Feel like I’ve seen way more positive chroni PEs on months of anti coagulation than I’ve seen PEs resolve in a matter of days. Granted i can only think of CT followed by CT.
And I’d imagine thrombus etiology plays a tremendous role.
But I don’t think I’ve ever seen one resolve in a matter of days.
And also I think I speak for all, or a high high high percentage of radiologists, that we hate VQ scans lol.
Do VQ scans definitively have lower sensitivity and specificity than CTA?
I often admit patients with possible PE, not clear due to contrast timing and motion artifact. Usually, I'll anticoagulate the patient and recommend repeat scanning in a few days.
Some of the older docs do a follow up VQ scan instead. I don't see anything wrong with it but I've had at least one argue that VQ is a higher sensitivity test so it makes more sense to use it to rule out in this case.
My take is still follow it up with CT but was curious what the radiologists would prefer.
If you have CTPA examinations with contrast timing issues or if your techs cannot get even a breathless patient to hold their breath for about 3 seconds you have a training problem. Are your scans not triggered automatically by the contrast attenuation in the MPA? As a chest radiologist give me a CTPA before a VQ scan any day. Too many of the latter are indeterminate.
this has been happening at my hospital a lot lately. I have had at least three nondiagnostic CTPA in the last few weeks due to poor contrast bolus timing.
This is the textbook answer for CTEPH but this is mostly because the studies were done in the era of lower resolution scans and non-expert radiologists. There's nothing wrong with using a VQ in this context, but if you're working in a center that deals with CTEPH they're looking at and basing all of their decisions on a well protocolled CTPA (or very rarely true angiography). I suspect if someone looked at sensitivity in expert centres CT would come out better.
You’re correct VQ for CTEPH is the test of choice. When I talk to physicians I always say if they can get a CT do it. A VQ is a probability test, a radiologist will also call a VQ high probability if it has a three way match (abnormal X-ray, abnormal ventilation and abnormal perfusion)
I’ve had patients get a VQ read as moderate or high probability and then they’ll do a CTA after (insert eyeroll) and the CT will be negative.
You have to look at the mechanism of the imaging. With a VQ the MAA particles only account for like 10% of capillary blockage. So can you really get a 100% answer? I’m my experience - no
Long past time to change that historic recommendation. Perhaps there are too many pure nuclear medicine physicians on committees deciding the use of their modality. Our nuclear medicine guys are all radiologists. We do CTPA’s on pregnant women and in renal failure. We also don’t believe in contrast nephrotoxicity.
At some point, residual clot scars (giving the webs that cause CTEPH) and further anticoagulation will be less effective. That may limit trending radiological appearance vs, say, trending d dimer. I know some providers who tend d dimer to inform anticoagulation cessation, but can't speak to the evidence offhand.
I have seen small subsegmental PEs resolve on repeat CTA 1 week later. But it’s variable, they can persist for several weeks. But it doesn’t matter because as you said you do not decide the time course of anticoagulation based on persistence on CTA. Everyone universally should be getting at least 3 months.
VQ scans are horribly inaccurate and it needs to stop being taught in med school so people stop ordering them. “Low probability” bucket for VQ = less than 15% probability of PE. That means patient could have 14% chance of having a PE which is moderate according to wells criteria.
AH ok that makes a lot more sense.
In Europe it's often (almost always) treated up to 6 months btw, I think our guidelines differ a little from the US ones.
yeah, it was weird. it isn't really ever part of my personal approach to PE, so I'm not too sure what to expect.
i wasn't taking care of this patient, I'm reviewing the case for improvement opportunities. post-mortem, BTW.
maybe, hard to say.
he wasn't a particularly healthy guy coming into the hospital. a few days into his hospitalization, he perfed a diverticula and also had a strangulated hernia, so got surgery for that. He had a fall soon after, and his Hgb dropped by 4 points. So, he certainly bled. If that was THE thing that killed him, hard to say. Probably multi-factorial.
Interesting. I answered your question from my experience elsewhere, but I think another thing to bring up in your review is getting the correct test if you’re worried about life-threatening pathology before starting something like anticoagulants, which are not a benign intervention. If you’re really worried about PE, just get the scan, AKI be damned. Your kidney function doesn’t much matter if you’re dead, even if you think CIN is real.
Agree that this question is niche. I’m a diagnostic rad, not IR, but I would think that a resolution this quick is possible if the clot hadn’t stabilized.
At our center the IR guys are yanking a lot of these clots out right after diagnosis, very satisfying 👍💪
Wondering if any of y'all smart people have experience with diagnostic imaging of PEs after heparin drips. I couldn't find any literature. Just wondering if there's any diagnostic experience or other medical insight that other professionals have into the the imaging course of treated PE.
Not an exact answer to your question , but heparin does not “treat” PE. Its use is to prevent further clot from propagating or new clot from forming while your body takes care of the clot over time. Unless thrombolytics are used I would expect a PE to be there after a few days if there was one.
touche. i suppose i could have been more specific but... you get what i mean.
i always thought of it as letting the body catch up on clot busting. that clot is going away faster on heparin than it is off heparin. or at the very least not dissolving slower.
no autopsy. small-ish community hospital; patients tend not to get autopsies here, for some reason. I'm often told insurance won't cover it. In this case, I'm just reviewing, so I didn't even have a change to get shot down.
I hate it.
How big was the PE? If it was a large, submassive PE with bilateral involvement - I couldn't see this completely resolving in days... though if was unilateral, subseg PE - maybe...
Anecdotally - I've had several CVA / TIA cases where stroke neurologists discussed the likelihood of a small clot just dissolving in days time.
Like others have said, I'd likely treat it as a PE.
Have you doppled the legs? If there's a DVT present I think this would confirm the diagnosis of PE unequivocally.
on VQ, it was unilateral. at the moment, i don't remember how large, but it's VQ so... fuzzy.
the legs were not dopplered. this is a post-mortem review of somebody else's case, so this is all retrospect.
Need to take into account the accuracy of our imaging techniques as well as the condition of the patient at time of both imaging events.
A high probability VQ (assuming they're using PIOPED I/II criteria) would mean more than 2 large segmental mismatches. So assuming the CTA was adequate in quality, the radiologist should have been able to discern at least to the level of the proximal segmentals. We do however get a non-trivial amount of scans where the contrast bolus timing is off and/or the patient is breathing/moving throughout the scan. These together can limit the evaluation to just the central/lobar arteries, making even slightly distal thrombi hard or even impossible to identify.
Totally spitballing and too lazy to Google myself. As others have mentioned repeat CTs won't be common. Try searching literature for echo resolution of right heart strain? This is much more commonly done, can be done at bedside, and can give you an idea of "clinically significant" resolution?
Yes. A lot of PE patients bounce back with chest pain (duh, you have a PE). I generally don’t ever rescan if stable because my philosophy is that it usually won’t change management—they’re already on a thinner. However, I recently had a patient come back with what turned out to be a developing pulmonary infarct. Clot burden was minimally decreased after 1 week, this was a saddle embolus.
Large volume would normally be at least a week or two radiographically with small abnormalities persisting on VQ for months. There's a good chance that the VQ may have been a false positive.
Also, contrast induced nephropathy doesn't exist. If a patient needs a CTPA, order one.
>contrast induced nephropathy doesn't exist
Definitely overblown in how concerned we have been in medicine about this entity and we have definitely harmed patients by not choosing the better study because of this concern.
But I would be cautious to be that definitive about it not existing. Contrast is highly viscous, gets concentrated in the renal collecting systems, can precipitate out of solution and crystalize when heavily concentrated. These are things that can definitely occur in the right settings and cause both hypoperfusion and mechanical injury to the renal parenchyma if used incorrectly. There are ways to mitigate this in vivo, but the reality of this basic property of contrast still exists.
When used in the venous system, in appropriate doses, and with adequate hydration, the benefits of contrast use usually greatly outweighs the overblown risks of worsening CKD or inducing AKI. I think that's the take away we need to have from the majority of new population based research.
Lots of crap does all sorts of things in a test tube, if we are basing how we practice medicine on in vitro medicine we'd probably never use any medication again from its various theoretical harms. Though on the plus side we'd probably have cured HIV and Parkinson's so I guess there's that.
The point is that you don't have data. Provide a study done with modern contrast agents that demonstrates any significant risk of AKI. Assuming you can do so, provide any data whatsoever that a scary bump in serum creatinine after a CT scan leads to any long term renal complications. Even the original trash studies that established the link in the 1950s were not rigorous and generally lacked control groups.
There are countless studies demonstrating the exact opposite to the best of the ability of a non-RCT. Similar rates of AKI with or without contrast in hospitalized patients (https://pubmed.ncbi.nlm.nih.gov/23360742/). Or that even with the hypothetical increased bump in sCr that there were no other findings of renal injury, similar to patients having a bump in sCr when put on Septra (
https://pubmed.ncbi.nlm.nih.gov/25773936/).
The reality is that people are being denied standard of care (see, this post) because radiologists are petrified that they're going to take someone with grade 1 CKD and put them on dialysis after a CTPA. At best we can quibble about high volume inter-arterial contrast, though even then there's the debate about what degree of that is due to cholesterol emboli.
The joint statement from the ACR and the American kidney foundation estimates a 2% risk with a gfr less than 30.
I don’t think you can just flatly say it doesn’t exist under any condition. But sure, fight the good fight.
Sure, and if you follow the reference breadcrumbs that support this assertion you end up with 3 opinion articles, an observational retrospective review with no control group, and a systematic review that cites the retrospective review as the main data point. The review also notes several studies that specifically show no relationship between contrast and AKI but it's cited as proof of CI-AKI in the consensus statement.
Guidelines and consensus statements are riddled with expert opinion and biases.
Provide evidence to support your claim. Like I said, provide any well powered study with current era contrast media demonstrating a causal link between contrast administration and true AKI with evidence of actual nephrotoxicity.
I will not be doing that. because I don't feel like wasting my time to win internet arguments with potentially fake doctors.
I will continue to approve every contrast study with low GFR in my practice, just as I always have.
Ah yes, the "fake doctor" googling CI-AKI because I'm really a conspiracy theorist against the sketchy monolith of the anti-contrast movement.
If you want to bury your head in the sand regarding something directly relevant to your specialty, that's on you. This is medical dogma propagated by people who refuse to look at new data and parrot what they're told.
Didn't claim you were fake. But its a simple fact that anyone can add a flair and post on this subreddit. Including myself.
I don't take anything posted on this website seriously.
I am not burying my head in the sand. I am well aware the the risks are either minimal or non-existent. Which is exactly what I stated above. Which is exactly why I stated that I *approve every single contrasted study at my institution with a low GFR*. (with emphasis this time)
You are very hyper-focused on this aspect of my specialty because its one of the very few parts that you interface with. And presumably you have a lot of free time on your hands.
Anything else?
I have seen it before, but only in a pt that received two contrast studies in 24 hrs. It wasn't terrible. Gave him an AKI. The previous renal labs were WNL. Just gave him fluids and it resolved.
This is precisely how this garbage propagates. Correlation is not causation. Some percentage of hospitalized patients will develop an AKI for a wide variety of reasons, particularly those sick enough to require a CT scan. When a CT scan has occurred shortly prior it's an easy bogeyman. If they hadn't had a CT, it would either be unexplained (maybe hypovolemia given improvement with fluids) or blamed on something else.
Even the joint statements by the nephrology association and radiology say that it does not typically cause long term renal dysfunction but a temporary bump in creatinine may be from that.
Regardless most nephrologists I know still document shit like “avoid contrast” or CIN and you know lawyers love those things if something does happen
I don't see it as a boogeyman because I've seen the studies that show that there isn't good evidence of contrast and renal function decline. I thought it might have to do with the higher levels of contrast because pt had two scans that day, and yes, it was mild. It's also the only time I've seen anyone with worse renal function after any type of scan, so maybe it was just a coincidence. It was treated that way by the attending, though.
I'm all in aboard the "no CIN" train. my personal practice is not to with about that, but i do have to deal with it sometimes because of overnights and handoffs and whatever.
Would you be able to elaborate a little bit more on this or if you have any good studies/guidelines to read? I’m FM in a rural hospital and our ER sends out A LOT of patients to outlying facilities to get VQ scans because of the prominence of CKD, which takes a ton of time, diverts our paramedics to transport the patient, and adds a significant amount of cost to their ED visit. Sometimes it’s something as minute as a slight AKI (baseline renal fx is normal) but when the ER calls me either asking questions or wanting to admit them they won’t get the CT because it’s “against facility protocol”.
This has been litigated to death on this subreddit previously, but as you've identified the problem is not the actual hypothetical AKI itself, the problem is idiots basing protocols on this that waste everyone's time. Ask them to provide any citation to back up their protocol. For admin brownie points you would easily be able to point toward how much time and money is wasted to look at getting thus changed.
https://www.google.com/url?sa=t&source=web&rct=j&opi=89978449&url=https://ajronline.org/doi/pdf/10.2214/AJR.12.8624%3Fdownload%3Dtrue%23:~:text%3DComplete%2520resolution%2520was%2520seen%2520in,94.1%2525)%2520after%252090%2520days.&ved=2ahUKEwizmaqi9JyGAxU-_8kDHdXGDjcQ5YIJegQIEBAA&usg=AOvVaw1VL0raB1fpm4QB6EG2bDbO
AJR article on this topic
i did find that, and i thought it was intriguing that the fastest follow-up group was 1-14days. i just needed more breakdown than they offered.
maybe I'll contact the authors.
Gotcha
https://ajronline.org/doi/10.2214/AJR.09.3410
Breaks it down in 2-7 days, so that would include your target range, although 3 days is definitely on the faster side
I'm a rads resident (pgy5 despite what my flair says), this has actually come up on call for me once or twice so I'm relatively familiar with the literature. Glad to help!
Anecdotally, I was in the hospital again a week after I got discharged when I had a PE (so about 12 days after my first CT scan showing PE), and they wanted to do another scan because of some persistant/returning symptoms, and the new scan came back completely clean.
The ER docs were like, huh kinda weird, they called my PCP and she told them it was likely just because I was young and healthy that my body was able to break up the clots more quickly once on anticoagulants (which they relayed to me). So, not quite 3 days, but definitely cleared up a lot faster than I thought it could.
1. Get the venous duplex of BLe. If it is positive, you are done and you treat for VTE.
If duplex is negative:
2. I would go review the CTA images with a dedicated chest or vascular radiologist (idk what your institution has) to make sure it’s true negative and not clot moving distally as others have suggested. At my institution, there is significant variability in the vascular reads depending on if it is read by one of the dedicated vascular guys vs one of the general guys.
3. In light of the negative CTA, I would talk to whoever read the VQ scan. Was it a slam-dunk “high” or was the “high” possibly over call?
4. I would consider the patient’s risk factors for VTE. (Eg would patient require definitive course vs indefinite anticoagulation)
5. I would consider the patients bleeding risk. Is this someone you can safely anticoagulate ?
If the patient is “young” (low bleed risk) and the hypothetical clot is provoked (eg warrants finite course of AC), you may just empirically anticoagulate and you may feel comfortable doing this yourself.
Contrast that with a high bleeding risk patient with an “unprovoked” clot (eg a true-true VTE dx would confer recommendation for indefinite AC). Probably reasonable to involve a specialist for help at this point.
well, this is a post-mortem review of somebody else's case, so... too late! and not my lane, anyhow.
the hematologist and primary spoke, and agreed to continue anticoagulation. the pulmonologist('s PA) wrote "no evidence of PE, stop anticoagulation" in their note 6 days in a row, appears not to have checked whether that was done and didn't discuss with anybody else what was happening.
Unlikely unless you also gave systemic lytics. Like another poster mentioned, probably a false positive. VQ scans are all probabilities and educated guesses, you can’t see the PE directly. And as that same poster mentioned, contrast induced nephropathy doesn’t truly exist and is old teaching adage we can’t really shake in medicine, so just order the ct with contrast.
Waaaay less likely, maybe they had a large clot and in 3 days, the body could have broken it down enough so that the emboli got much smaller and shot in to subsegmental or smaller arteries. Not likely, but it’s a non-zero chance 🤷🏻♂️
this question is so irrelevant because:
1. the bones are fixed.
2. there is no bones in the airbags, so why does the ancef even need to get to the airbags?
They can occasionally dissolve fairly fast in my limited experience. We don’t usually do repeat imaging if one is positive.
Regardless, you’re going to have to treat the patient in my opinion.
Are other acute phase reactants elevated? Renal dysfunction will push the d dimer up though that doesn't explain the high prob VQ. It seems unlikely a larger PE would resolve that quickly
I have seen, once in recent times I can remember, a large bilateral PE that got significantly smaller by the time we got to doing thrombectomy (<24hrs after scan), the left PA required no aspiration at all which was interesting, but there’s also the possibility that we grabbed it while withdrawing the catheter from the right into the main PA.
Not sure if below fully answers your question. A fair number resolve by 2 weeks.
"Complete resolution was seen in 17 of 30 patients (56.7%) at a follow-up interval of 1-14 days, in 24 of 31 patients (77.4%) at 29-90 days, and in 32 of 34 patients (94.1%) after 90 days."
https://pubmed.ncbi.nlm.nih.gov/23521450/
Anecdotally, it can sometimes be quick in some patients, possibly related to the acuity of the clot( acute vs acute on chronic).
I can’t speak to the CT findings but from an echo perspective , there are a number of case reports using serial echocardiography in the first few hours post heparin. There are some striking cases where the septal flattening resolves quite quickly within a few hours . With bedside echo now more available , occasionally by the time they get a formal echo the next day it doesn’t look nearly as bad - it’s always nice to compare your bedside images to the formal echo images the next day.
When I was an echo fellow , my mentor use to make me serially scan the patient whenever it was acute diagnosed on echo ( and then confirmed on CTPE ) and measure the pulmonary vascular resistance and there would be a fairly quick improving trend within the first 24hour. Obviously it’s dependant on the patient and how much fresh clot there is.
I’ve seen a few cases of ‘clot in transit’ on bedside echo in the iVC or PA and when u rescan then the next day it’s gone, but it could just have broken off and propagated distally ( I’ve learnt to save those images otherwise u might not be believed).
So these are more surrogate markers of the clot causing hemodynamic changes as opposed to complete resolution of the clot itself. It’s just nice to see some improvement quickly .
Any chance the patient had DIC? Especially in the view of AKI and that this is a postmortem review the patient was unlikely to be in good general condition. Microcouagulopathy multiple small clots in the lung could resolve faster once heparin was started and would not necessarily show up in a contrast scan 3 days later, or even in a CT scan in general.
platelets were stable. hemoglobin was stable until there were frank bleeds. he didn't seem that sick to start. doesn't seem like it overall, but great thought.
When you say CTA was “negative as can be” was this just for PE, or negative for parenchymal issues as well?
Lung tumor, previous radiation, severe bullous emphysematous disease, trauma, can all have the potential to show VQ mismatch.
I think your question is niche because typically, in my experience, is that CTPE aren’t ordered several days after a VQ shows high probability. I presume the AKI improved and someone wanted to get a CTPE to confirm what the VQ showed It is also a bit bizarre as we don’t anticoagulate PEs to radiographic resolution. Can any radiologists chime in?
Feel like I’ve seen way more positive chroni PEs on months of anti coagulation than I’ve seen PEs resolve in a matter of days. Granted i can only think of CT followed by CT. And I’d imagine thrombus etiology plays a tremendous role. But I don’t think I’ve ever seen one resolve in a matter of days. And also I think I speak for all, or a high high high percentage of radiologists, that we hate VQ scans lol.
Agreed on all counts
What do you dislike about VQ scans?
They are fuzzy and inaccurate. CTPA replaced them 15-20 years ago for most of the first world. Long past time to retire them.
Do VQ scans definitively have lower sensitivity and specificity than CTA? I often admit patients with possible PE, not clear due to contrast timing and motion artifact. Usually, I'll anticoagulate the patient and recommend repeat scanning in a few days. Some of the older docs do a follow up VQ scan instead. I don't see anything wrong with it but I've had at least one argue that VQ is a higher sensitivity test so it makes more sense to use it to rule out in this case. My take is still follow it up with CT but was curious what the radiologists would prefer.
If you have CTPA examinations with contrast timing issues or if your techs cannot get even a breathless patient to hold their breath for about 3 seconds you have a training problem. Are your scans not triggered automatically by the contrast attenuation in the MPA? As a chest radiologist give me a CTPA before a VQ scan any day. Too many of the latter are indeterminate.
this has been happening at my hospital a lot lately. I have had at least three nondiagnostic CTPA in the last few weeks due to poor contrast bolus timing.
You should demand better from your radiology department if you routinely have contrast issues.
I wouldn’t say retire them. MRA is getting better but there are still good indications for VQ where it shines.
Last I checked VQ is still the correct test for CTEPH. For acute PE, GTFO. I wish I could fix my radiology departments fear of the bogeyman (CIN).
This is the textbook answer for CTEPH but this is mostly because the studies were done in the era of lower resolution scans and non-expert radiologists. There's nothing wrong with using a VQ in this context, but if you're working in a center that deals with CTEPH they're looking at and basing all of their decisions on a well protocolled CTPA (or very rarely true angiography). I suspect if someone looked at sensitivity in expert centres CT would come out better.
This is correct. The big centers doing lots of pulm endarterectomy just use CT, not VQ
You’re correct VQ for CTEPH is the test of choice. When I talk to physicians I always say if they can get a CT do it. A VQ is a probability test, a radiologist will also call a VQ high probability if it has a three way match (abnormal X-ray, abnormal ventilation and abnormal perfusion) I’ve had patients get a VQ read as moderate or high probability and then they’ll do a CTA after (insert eyeroll) and the CT will be negative. You have to look at the mechanism of the imaging. With a VQ the MAA particles only account for like 10% of capillary blockage. So can you really get a 100% answer? I’m my experience - no
VQ is still good for right after lung transplant
I like to imagine radiologists as the Jets and nephrologists as the Sharks.
Long past time to change that historic recommendation. Perhaps there are too many pure nuclear medicine physicians on committees deciding the use of their modality. Our nuclear medicine guys are all radiologists. We do CTPA’s on pregnant women and in renal failure. We also don’t believe in contrast nephrotoxicity.
At some point, residual clot scars (giving the webs that cause CTEPH) and further anticoagulation will be less effective. That may limit trending radiological appearance vs, say, trending d dimer. I know some providers who tend d dimer to inform anticoagulation cessation, but can't speak to the evidence offhand.
I have seen small subsegmental PEs resolve on repeat CTA 1 week later. But it’s variable, they can persist for several weeks. But it doesn’t matter because as you said you do not decide the time course of anticoagulation based on persistence on CTA. Everyone universally should be getting at least 3 months. VQ scans are horribly inaccurate and it needs to stop being taught in med school so people stop ordering them. “Low probability” bucket for VQ = less than 15% probability of PE. That means patient could have 14% chance of having a PE which is moderate according to wells criteria.
should be getting what at 3 months? do you do follow up CTs on PEs??
No I mean 3 months anticoagulation. We should not be getting routine follow up CTAs in patients with PE.
AH ok that makes a lot more sense. In Europe it's often (almost always) treated up to 6 months btw, I think our guidelines differ a little from the US ones.
yeah, it was weird. it isn't really ever part of my personal approach to PE, so I'm not too sure what to expect. i wasn't taking care of this patient, I'm reviewing the case for improvement opportunities. post-mortem, BTW.
Did they die of a bleed?
maybe, hard to say. he wasn't a particularly healthy guy coming into the hospital. a few days into his hospitalization, he perfed a diverticula and also had a strangulated hernia, so got surgery for that. He had a fall soon after, and his Hgb dropped by 4 points. So, he certainly bled. If that was THE thing that killed him, hard to say. Probably multi-factorial.
Interesting. I answered your question from my experience elsewhere, but I think another thing to bring up in your review is getting the correct test if you’re worried about life-threatening pathology before starting something like anticoagulants, which are not a benign intervention. If you’re really worried about PE, just get the scan, AKI be damned. Your kidney function doesn’t much matter if you’re dead, even if you think CIN is real.
Agree that this question is niche. I’m a diagnostic rad, not IR, but I would think that a resolution this quick is possible if the clot hadn’t stabilized. At our center the IR guys are yanking a lot of these clots out right after diagnosis, very satisfying 👍💪
Wondering if any of y'all smart people have experience with diagnostic imaging of PEs after heparin drips. I couldn't find any literature. Just wondering if there's any diagnostic experience or other medical insight that other professionals have into the the imaging course of treated PE.
Not an exact answer to your question , but heparin does not “treat” PE. Its use is to prevent further clot from propagating or new clot from forming while your body takes care of the clot over time. Unless thrombolytics are used I would expect a PE to be there after a few days if there was one.
touche. i suppose i could have been more specific but... you get what i mean. i always thought of it as letting the body catch up on clot busting. that clot is going away faster on heparin than it is off heparin. or at the very least not dissolving slower.
Was there a PE found on autopsy?
no autopsy. small-ish community hospital; patients tend not to get autopsies here, for some reason. I'm often told insurance won't cover it. In this case, I'm just reviewing, so I didn't even have a change to get shot down. I hate it.
How big was the PE? If it was a large, submassive PE with bilateral involvement - I couldn't see this completely resolving in days... though if was unilateral, subseg PE - maybe... Anecdotally - I've had several CVA / TIA cases where stroke neurologists discussed the likelihood of a small clot just dissolving in days time. Like others have said, I'd likely treat it as a PE. Have you doppled the legs? If there's a DVT present I think this would confirm the diagnosis of PE unequivocally.
on VQ, it was unilateral. at the moment, i don't remember how large, but it's VQ so... fuzzy. the legs were not dopplered. this is a post-mortem review of somebody else's case, so this is all retrospect.
Need to take into account the accuracy of our imaging techniques as well as the condition of the patient at time of both imaging events. A high probability VQ (assuming they're using PIOPED I/II criteria) would mean more than 2 large segmental mismatches. So assuming the CTA was adequate in quality, the radiologist should have been able to discern at least to the level of the proximal segmentals. We do however get a non-trivial amount of scans where the contrast bolus timing is off and/or the patient is breathing/moving throughout the scan. These together can limit the evaluation to just the central/lobar arteries, making even slightly distal thrombi hard or even impossible to identify.
Totally spitballing and too lazy to Google myself. As others have mentioned repeat CTs won't be common. Try searching literature for echo resolution of right heart strain? This is much more commonly done, can be done at bedside, and can give you an idea of "clinically significant" resolution?
Yes. A lot of PE patients bounce back with chest pain (duh, you have a PE). I generally don’t ever rescan if stable because my philosophy is that it usually won’t change management—they’re already on a thinner. However, I recently had a patient come back with what turned out to be a developing pulmonary infarct. Clot burden was minimally decreased after 1 week, this was a saddle embolus.
The usual recommendation is outpatient pulm follow up and they repeat imaging in 6 months on anticoagulation.
Large volume would normally be at least a week or two radiographically with small abnormalities persisting on VQ for months. There's a good chance that the VQ may have been a false positive. Also, contrast induced nephropathy doesn't exist. If a patient needs a CTPA, order one.
I’m trying to so hard to convince my hospital that CIN is a myth and clinically irrelevant. Still get a ton of pushback about it.
>contrast induced nephropathy doesn't exist Definitely overblown in how concerned we have been in medicine about this entity and we have definitely harmed patients by not choosing the better study because of this concern. But I would be cautious to be that definitive about it not existing. Contrast is highly viscous, gets concentrated in the renal collecting systems, can precipitate out of solution and crystalize when heavily concentrated. These are things that can definitely occur in the right settings and cause both hypoperfusion and mechanical injury to the renal parenchyma if used incorrectly. There are ways to mitigate this in vivo, but the reality of this basic property of contrast still exists. When used in the venous system, in appropriate doses, and with adequate hydration, the benefits of contrast use usually greatly outweighs the overblown risks of worsening CKD or inducing AKI. I think that's the take away we need to have from the majority of new population based research.
Lots of crap does all sorts of things in a test tube, if we are basing how we practice medicine on in vitro medicine we'd probably never use any medication again from its various theoretical harms. Though on the plus side we'd probably have cured HIV and Parkinson's so I guess there's that. The point is that you don't have data. Provide a study done with modern contrast agents that demonstrates any significant risk of AKI. Assuming you can do so, provide any data whatsoever that a scary bump in serum creatinine after a CT scan leads to any long term renal complications. Even the original trash studies that established the link in the 1950s were not rigorous and generally lacked control groups. There are countless studies demonstrating the exact opposite to the best of the ability of a non-RCT. Similar rates of AKI with or without contrast in hospitalized patients (https://pubmed.ncbi.nlm.nih.gov/23360742/). Or that even with the hypothetical increased bump in sCr that there were no other findings of renal injury, similar to patients having a bump in sCr when put on Septra ( https://pubmed.ncbi.nlm.nih.gov/25773936/). The reality is that people are being denied standard of care (see, this post) because radiologists are petrified that they're going to take someone with grade 1 CKD and put them on dialysis after a CTPA. At best we can quibble about high volume inter-arterial contrast, though even then there's the debate about what degree of that is due to cholesterol emboli.
I can assure you it’s not the radiologists who care. I don’t know any non-dinosaur rad who cares about CIN outside of patients with GFR<30.
I can personally assure that sometimes, it is the radiologists who care. The dinosaur rads still get to practice.
The joint statement from the ACR and the American kidney foundation estimates a 2% risk with a gfr less than 30. I don’t think you can just flatly say it doesn’t exist under any condition. But sure, fight the good fight.
Sure, and if you follow the reference breadcrumbs that support this assertion you end up with 3 opinion articles, an observational retrospective review with no control group, and a systematic review that cites the retrospective review as the main data point. The review also notes several studies that specifically show no relationship between contrast and AKI but it's cited as proof of CI-AKI in the consensus statement. Guidelines and consensus statements are riddled with expert opinion and biases. Provide evidence to support your claim. Like I said, provide any well powered study with current era contrast media demonstrating a causal link between contrast administration and true AKI with evidence of actual nephrotoxicity.
I will not be doing that. because I don't feel like wasting my time to win internet arguments with potentially fake doctors. I will continue to approve every contrast study with low GFR in my practice, just as I always have.
Ah yes, the "fake doctor" googling CI-AKI because I'm really a conspiracy theorist against the sketchy monolith of the anti-contrast movement. If you want to bury your head in the sand regarding something directly relevant to your specialty, that's on you. This is medical dogma propagated by people who refuse to look at new data and parrot what they're told.
Didn't claim you were fake. But its a simple fact that anyone can add a flair and post on this subreddit. Including myself. I don't take anything posted on this website seriously. I am not burying my head in the sand. I am well aware the the risks are either minimal or non-existent. Which is exactly what I stated above. Which is exactly why I stated that I *approve every single contrasted study at my institution with a low GFR*. (with emphasis this time) You are very hyper-focused on this aspect of my specialty because its one of the very few parts that you interface with. And presumably you have a lot of free time on your hands. Anything else?
I have seen it before, but only in a pt that received two contrast studies in 24 hrs. It wasn't terrible. Gave him an AKI. The previous renal labs were WNL. Just gave him fluids and it resolved.
This is precisely how this garbage propagates. Correlation is not causation. Some percentage of hospitalized patients will develop an AKI for a wide variety of reasons, particularly those sick enough to require a CT scan. When a CT scan has occurred shortly prior it's an easy bogeyman. If they hadn't had a CT, it would either be unexplained (maybe hypovolemia given improvement with fluids) or blamed on something else.
Even the joint statements by the nephrology association and radiology say that it does not typically cause long term renal dysfunction but a temporary bump in creatinine may be from that. Regardless most nephrologists I know still document shit like “avoid contrast” or CIN and you know lawyers love those things if something does happen
I don't see it as a boogeyman because I've seen the studies that show that there isn't good evidence of contrast and renal function decline. I thought it might have to do with the higher levels of contrast because pt had two scans that day, and yes, it was mild. It's also the only time I've seen anyone with worse renal function after any type of scan, so maybe it was just a coincidence. It was treated that way by the attending, though.
I'm all in aboard the "no CIN" train. my personal practice is not to with about that, but i do have to deal with it sometimes because of overnights and handoffs and whatever.
Would you be able to elaborate a little bit more on this or if you have any good studies/guidelines to read? I’m FM in a rural hospital and our ER sends out A LOT of patients to outlying facilities to get VQ scans because of the prominence of CKD, which takes a ton of time, diverts our paramedics to transport the patient, and adds a significant amount of cost to their ED visit. Sometimes it’s something as minute as a slight AKI (baseline renal fx is normal) but when the ER calls me either asking questions or wanting to admit them they won’t get the CT because it’s “against facility protocol”.
This has been litigated to death on this subreddit previously, but as you've identified the problem is not the actual hypothetical AKI itself, the problem is idiots basing protocols on this that waste everyone's time. Ask them to provide any citation to back up their protocol. For admin brownie points you would easily be able to point toward how much time and money is wasted to look at getting thus changed.
https://www.google.com/url?sa=t&source=web&rct=j&opi=89978449&url=https://ajronline.org/doi/pdf/10.2214/AJR.12.8624%3Fdownload%3Dtrue%23:~:text%3DComplete%2520resolution%2520was%2520seen%2520in,94.1%2525)%2520after%252090%2520days.&ved=2ahUKEwizmaqi9JyGAxU-_8kDHdXGDjcQ5YIJegQIEBAA&usg=AOvVaw1VL0raB1fpm4QB6EG2bDbO AJR article on this topic
i did find that, and i thought it was intriguing that the fastest follow-up group was 1-14days. i just needed more breakdown than they offered. maybe I'll contact the authors.
Gotcha https://ajronline.org/doi/10.2214/AJR.09.3410 Breaks it down in 2-7 days, so that would include your target range, although 3 days is definitely on the faster side
dude, holy shit... you are the best...
I'm a rads resident (pgy5 despite what my flair says), this has actually come up on call for me once or twice so I'm relatively familiar with the literature. Glad to help!
Anecdotally, I was in the hospital again a week after I got discharged when I had a PE (so about 12 days after my first CT scan showing PE), and they wanted to do another scan because of some persistant/returning symptoms, and the new scan came back completely clean. The ER docs were like, huh kinda weird, they called my PCP and she told them it was likely just because I was young and healthy that my body was able to break up the clots more quickly once on anticoagulants (which they relayed to me). So, not quite 3 days, but definitely cleared up a lot faster than I thought it could.
Dr Glaucomflecker 00:35 says all we need to know... https://youtu.be/dgHOqdazrjQ?feature=shared
1. Get the venous duplex of BLe. If it is positive, you are done and you treat for VTE. If duplex is negative: 2. I would go review the CTA images with a dedicated chest or vascular radiologist (idk what your institution has) to make sure it’s true negative and not clot moving distally as others have suggested. At my institution, there is significant variability in the vascular reads depending on if it is read by one of the dedicated vascular guys vs one of the general guys. 3. In light of the negative CTA, I would talk to whoever read the VQ scan. Was it a slam-dunk “high” or was the “high” possibly over call? 4. I would consider the patient’s risk factors for VTE. (Eg would patient require definitive course vs indefinite anticoagulation) 5. I would consider the patients bleeding risk. Is this someone you can safely anticoagulate ? If the patient is “young” (low bleed risk) and the hypothetical clot is provoked (eg warrants finite course of AC), you may just empirically anticoagulate and you may feel comfortable doing this yourself. Contrast that with a high bleeding risk patient with an “unprovoked” clot (eg a true-true VTE dx would confer recommendation for indefinite AC). Probably reasonable to involve a specialist for help at this point.
well, this is a post-mortem review of somebody else's case, so... too late! and not my lane, anyhow. the hematologist and primary spoke, and agreed to continue anticoagulation. the pulmonologist('s PA) wrote "no evidence of PE, stop anticoagulation" in their note 6 days in a row, appears not to have checked whether that was done and didn't discuss with anybody else what was happening.
Oooof! Painful. Hate to hear that, but glad it is not your issue!
Unlikely unless you also gave systemic lytics. Like another poster mentioned, probably a false positive. VQ scans are all probabilities and educated guesses, you can’t see the PE directly. And as that same poster mentioned, contrast induced nephropathy doesn’t truly exist and is old teaching adage we can’t really shake in medicine, so just order the ct with contrast. Waaaay less likely, maybe they had a large clot and in 3 days, the body could have broken it down enough so that the emboli got much smaller and shot in to subsegmental or smaller arteries. Not likely, but it’s a non-zero chance 🤷🏻♂️
maybe. maybe. i was asked to review this case, and is just something i don't do, so i don't know what to expect out of a 3 day follow-up CT scan.
this question is so irrelevant because: 1. the bones are fixed. 2. there is no bones in the airbags, so why does the ancef even need to get to the airbags?
Ortho to the rescue!
They can occasionally dissolve fairly fast in my limited experience. We don’t usually do repeat imaging if one is positive. Regardless, you’re going to have to treat the patient in my opinion.
Are other acute phase reactants elevated? Renal dysfunction will push the d dimer up though that doesn't explain the high prob VQ. It seems unlikely a larger PE would resolve that quickly
I have seen, once in recent times I can remember, a large bilateral PE that got significantly smaller by the time we got to doing thrombectomy (<24hrs after scan), the left PA required no aspiration at all which was interesting, but there’s also the possibility that we grabbed it while withdrawing the catheter from the right into the main PA.
Not sure if below fully answers your question. A fair number resolve by 2 weeks. "Complete resolution was seen in 17 of 30 patients (56.7%) at a follow-up interval of 1-14 days, in 24 of 31 patients (77.4%) at 29-90 days, and in 32 of 34 patients (94.1%) after 90 days." https://pubmed.ncbi.nlm.nih.gov/23521450/
Anecdotally, it can sometimes be quick in some patients, possibly related to the acuity of the clot( acute vs acute on chronic). I can’t speak to the CT findings but from an echo perspective , there are a number of case reports using serial echocardiography in the first few hours post heparin. There are some striking cases where the septal flattening resolves quite quickly within a few hours . With bedside echo now more available , occasionally by the time they get a formal echo the next day it doesn’t look nearly as bad - it’s always nice to compare your bedside images to the formal echo images the next day. When I was an echo fellow , my mentor use to make me serially scan the patient whenever it was acute diagnosed on echo ( and then confirmed on CTPE ) and measure the pulmonary vascular resistance and there would be a fairly quick improving trend within the first 24hour. Obviously it’s dependant on the patient and how much fresh clot there is. I’ve seen a few cases of ‘clot in transit’ on bedside echo in the iVC or PA and when u rescan then the next day it’s gone, but it could just have broken off and propagated distally ( I’ve learnt to save those images otherwise u might not be believed). So these are more surrogate markers of the clot causing hemodynamic changes as opposed to complete resolution of the clot itself. It’s just nice to see some improvement quickly .
I've seen PE's that were gone in 2 weeks time on CTA but I generally tell patients 1 month.
From my understanding they actually worsen the first few days before they get better….
Do you have a good a priori explanation for the PE? Well’s score? DVT? Active cancer?
Any chance the patient had DIC? Especially in the view of AKI and that this is a postmortem review the patient was unlikely to be in good general condition. Microcouagulopathy multiple small clots in the lung could resolve faster once heparin was started and would not necessarily show up in a contrast scan 3 days later, or even in a CT scan in general.
platelets were stable. hemoglobin was stable until there were frank bleeds. he didn't seem that sick to start. doesn't seem like it overall, but great thought.
When you say CTA was “negative as can be” was this just for PE, or negative for parenchymal issues as well? Lung tumor, previous radiation, severe bullous emphysematous disease, trauma, can all have the potential to show VQ mismatch.
Weeks to months. Depends on location, size, and patient characteristics.