PE Prognostication (part 3): Dr Senthi Strikes Back
To CT, or not to CT: that is the question:
Whether ’tis nobler in the lungs to suffer
The risks and harms of outrageous investigation
Or to take up probes against DVTs of troubles,
And by sonography end them? To die: to bleed;
No more; and by our tweets to say we end
The head-ache and the thousand natural clots.
(not quite Shakespeare, not quite Hamlet!)
At last – the light at the end of the tunnel! The final installment in the epic PE Prognostication series from Dr Anand Senthi ( @DrSenthi ).
In the first podcast we looked a the history of PE in the literature from the 1960s through to the modern era of Clinical decision rules, D-Dimers, multidetector CTPAs and arrived at today – how do we currently approach the patient with a possible PE. And then we talked about what it means – in the low risk groups what do we know about the treatment of these patients with small, stable PEs?
In part 2 we took a look at Anand’s proposed algorithm – and it was controversial to say the least. The main differences were:
- using a higher “test threshold” for CTPA. Somewhere above 4.8%
- Using the sPESI score to prognosticate prior to subsequent investigation in order to define a subset of patients whom are potentially going to derive nett harm from the CTPA and subsequent risk of false positivity and uneccessary treatment.
- Coming to terms with the concept that anticoagulation may not really be making a big difference to outcomes in simple, haemodynamically stable, small PEs
Then we had a great audio comment from Dr Scott Weingart ( @emcrit ) – he raised a lot of great points – VTE recurrence risk, Well’s, test thresholds, contrast-risk, ECHO and leg US. This is great pre-publication peer review.
In this final episode
- Anand responds to Dr Weingart’s comments, it is not always a #FOAMed love in !
- we integrate ED-bedside DVT US into the mix with the assistance of Dr Matt Dawson ( @ultrasoundpod ),
- we discuss the refined version of Anand’s algorithm.
- We look at the ethics of doing a RCT in the current atmosphere
- we discuss what such a trial (or trials) might look like
- Anand invites you all to get involved
***WARNING: this is a long podcast! 1 hour! But it could be broken into 2 parts – listen firstly to Anand’s response to Scott, then the rest – makes it a bit easier on the brain.
DIRECT DOWNLOAD HERE
As a special bonus there is a 5 minute literature review by Dr Matt Dawson ( ultrasoundpodcast.com ) on the utility of ED-physician performed DVT US. Short summary: you can do it with good accuracy! DOWNLOAD by Clicking here to learn what bedside US, driving a car and ‘horizontal folk-dancing’ all have in common. Wisdom from the South!
I have really enjoyed going through this process with Anand and seeing the FOAM peer review work as we know it can. I hope that this is the start of a great thing – maybe a trial or two into the previously uncertain area of the low-risk, stable PE patients. PLease, if you are interested in this type of research, or just have questions – get in touch with Anand – either via the comments or on Twitter.
Thanks for listening
Casey
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About The Author
Casey Parker
I am a GP working in Broome, NW of Western Australia. I work as a hospital DMO (District Med Officer) doing Emergency, Anaesthestics, some Obstetrics and a lot of miscellaneous primary care. Also on the web as @broomedocs | + Casey Parker | Contact
I would be happy to debate in real time with moderation. I will leave aside all the slight misstatements of my points, b/c overall I agree with the thrust of this as I have done since the outset.
The one point that needs to be made is the weird ommission of the fact that the risk of recurrent thromboembolism was IN PTS ON ANTICOAGULATION in the PESI data and in the the other data I have seen. You can’t roll that data into an algorithm that sends pt home without anticoagulation. We know anti-coag is shite for the existing PE, where it is actually useful is in preventing clots.
Yes, agree.
I did make that point in part 2 – sPESI data: hard to compare treated vs. non-treated VTE outcome data.
One would have to make assumptions about the effect of AC in order to make any statement about prognosis
What we really need is the trial of AC – to quantify the benefit or harm it may have on the low risk pts.
Apologies for any misquotation. Best done in real time to be fair.
C
thanks Scot, but yes no omission. Made it clear that sPESI mortality was in treated patients. However it will almost certainly risk stratify any group to a lower risk cohort WITHIN that group, as it appears to be the most powerful prognostic risk stratification tool available.
So my contention is that
– Wells <2 are below TT. You can stop there.
– Wanna be more conservative? Add bedside U/S – negative, you can stop there.
– Wanna be more conservative? Add sPESI=0, you can stop there.
Again sPESI, merely risk stratifying WITHIN this Wells <2, U/S negative group. Not making any claims re actually definitive mortality.
I should add that it is likely that almost all of the Wells <2 group would probably have the relatively normal vitals defined in sPESI=0 group. So by adding sPESI=0 to the algorithm you are probably only additionally removing patients with certain prognostically relevant comorbidities from the exclusion group (i.e cancer, heart failure and COPD). The rationale for NOT excluding these guys from investigation would be that they are more likely to have a worse prognosis if they had a PE v's the rest of the exclusion group.
thanks guys!
I lost my wifi so only on 3 G connection. So yet to listen to podcast but wanted to take up Scott’s salient point.
if you cannot make any claims regarding definitive mortality and declare your use of data outside of its original study population
I do not think you can ethically run the trial you want.
And you certainly cannot claim improved safety in such a trial over current standards of care.
You might be right. But I dont think you are going to be able to prove it.
Hi Minh
A blogger without wifi! – you poor lost soul. You must be in Mt Isa ?
Anand makes a long and detailed argument around the ethics of a RCT in the proposed Wells < 2, sPESI = 0 subgroup of patients. Have alisten when your connection is back up and let us know if you think he makes the case... Coffee next week, in Cairns for BCC - my shout. Casey
Very much enjoyed the podcast, thanks guys.
I think we would overstep ourselves suggesting that the standard of care can be changed based on current data though. There is some evidence of harm in current practice, which provides the equipoise for a trial, but we have effectively no idea of its benefits! AC does seem to prevent some thromboembolic problems in some populations, but we don’t know the benefit/not in this group – hence need the trial.
Anand’s 3-armed trial of AC vs aspirin vs placebo would be a good start in finding the unknown benefit (?) of AC.This could then inform our test threshold calculations. My suggestion on twitter of trialling the entire process was based on experience in other fields (eg chest pain units) which suggests that benefits/harms of systems are not always the sum of their parts.
halfway through listening to podcast. thanks guys!
Had to stop to make this rebuttable comment in regard to “where are all these contrast induced renal failure cases?” and Anand’s response :”you probably encountered them without realising it”
Yes I have seen lots of renal failure of new onset. I have always looked for a cause and this includes Hx of recent IV contrast. I am sure both of you have done and would do the same.
It costs nothing to take a decent history or review the notes.
I have yet to come across a conclusive case of contrast induced renal failure /death.
I do not deny such cases must exist.
the point of arguement is whether such a thing occurs frequently enough to weigh into the risk/benefit process for ordering CTPA.
And my point is to understand what the real world clinical experiences of peer clinicians dealing with this issue is. Hence my question : how many actual or suspected cases of contrast induced renal failure/death have any of you come across?
You cite 1 prospective observational, uncontrolled study to support your claims yet dismiss 2013 recent reviews/meta-analyses in a radiology journal!
If you dont agree on the evidence then at least look to your own clinical experience!
Just finished the podcast. thanks to Anand and you Casey.
Its a novel concept that still needs more proof/support.
There is a vein of inconsistent logic that I wanted to raise again.
Let me start backwards.
Anand you conclude the podcast saying we do not need to wait for more proof. We should just be making the decision now based on your concept because it makes sense and there is sufficient evidence already of some harm to our current practice. You cite cricoid pressure as example.
The inconsistency is that just before you had a mild rant about that, you clearly declared that peers should not follow/adopt your concept until it gets journal peer reviewed published.
You cant have it both ways. I suspect you want to adopt into real clinical practice your approach but even you are worried about something going wrong and you get left holding the baby!
Secondly the use of cricoid pressure controversy as a prime example whilst sounding similar is in fact quite the opposite! I know you tried to use analogy of dissection before without much success, and using CP as example is no better. Crcioid pressure is part of emergency RSI which is something that usually patients cannot consent for and the doctor is doing things as part of resuscitation. The success of getting the tube in as well as preventing aspiration is critical to safety of the patient in ONE point in time. This is unlike low risk PE patients who have risk over at least 3 weeks period of time ( by your own admission)
Also the next point I contend is your claim that we must have missed cases of contrast induced renal failure..”because we just were not thinking about it”. That may or not may be true but is a huge assumption on your part. IN good faith I cannot recall a single proven case of contrast induced renal failure/death in my 18 yrs of clinical practice so far!. Yet I have seen/know about 5 fatal PEs, 2 of which were recurrent PEs that were missed on initial presentation.
You cite one uncontrolled prospective study of CTPA showing contrast induced renal failure with assoc mortality..versus..recent reviews/meta-analyses by Radiology journal showing no increased risk.
IF there is that level of controversy or dispute between the actual rates of harm, then I see no problem in asking peers what their ACTUAL clinical experience of this condition is!
Also you still have not adequately addressed the question of whether you regard DVT/PE as the same entity or separate. I infer with your addition of leg USS that you consider a DVT and PE are worse cause you would Rx someone with both whereas someone with a PE but no DVT you would consider for observation only? DVT/PE do worse than PE which does worse than DVT alone. 3 month studies backup this claim http://www.ncbi.nlm.nih.gov/pubmed/16855358
I see no reason to differentiate them as if you would Rx a DVT, why would you not Rx if PE alone, if we know it does worse than DVT.
I dont mind at all Anand if you want to make clinical decisions based on your own ideas /concepts/interpretations of the existing evidence and standard of care. Thats between you and the patient. Scott and I are just expressing our views that its not clear cut as you contend it is and that readers need to be mindful that what you propose is not current standard of care and ask you to be mindful of our perception of some illogical arguements you make.
I think the 3 stage process of publicly proposing this concept is reasonable and respect that you think we can do better for our patients.
Minh, thanks for considering these podcasts and providing your feedback.
I feel though we are largely rehashing old ground and that we will need to agree to disagree but just in case, I will respond again:
1. Your perception that my arguments are illogical does not make them illogical, however I am extremely mindful of your perception. Please rest assured, you need not be concerned about any lack of awareness on my part.
2. I have made it very clear that my approach differs from the standard of care. In fact I have made it very clear that the so called “standard of care” is the very problem that needs to be addressed and rejected at a minimum in a select group of patients I define.
3. Re Cricoid – the urgency of the situation does not affect the relevancy of the comparison. When performing urgent intubation one needs to apply what they believe is in the best interest of the patient and the inability of the patient to consent does not change this requirement. The point of the comparison is that where the “status quo” has on review of the old and new evidence to found to be without a firm evidence base of benefit but with evidence of harm, it can be rejected. I advocate the same is true for our approach to low risk PE patients. The “urgency” of Cricoid does not make it “the opposite” as you say. The only aspect of interest in bringing up the urgency of Cricoid is that it is worth noting as you suggest that the PE patient have time to be consented regarding your decision. This supports my contention that the onus is on the doctor where there is uncertainty of harm/benefit to involve the patient in the decision making process and obtain informed consent to proceed/not proceed with a harmful investigative pathway. This is not happening in the “standard of care”. One can’t obtain true informed consent in this area without some appreciation of the relevant data.
4. It is inconceivable that any sane doctor would be likely to attribute any case of renal failure to contrast when the prevailing belief at the time was that the risk of contrast induced renal failure was essentially zero. This would be be nonsensical – one could only attribute blame, based on the probability weighted risk factors that were present in your mind at the time. That’s how the diagnostic process works. With respect, I have no confidence in your ability to retrospectively recollect anecdotes of contrast induced renal failure for this reason, just like I have no confidence in my ability or any doctor’s ability to detect this in a retrospective anecdotal fashion. Only when carefully and prospectively following up patients would we be able to detect this. I’ve explained this as best I could on the podcast. I therefore think such anecdotal recollections are utterly meaningless and unhelpful. With knowledge of the new data, if you were to go back through your career and carefully evaluate each renal failure patient chasing their entire public and private medical record to ascertain possible temporal relationships, then your anecdotes would be a bit more interesting. Even then they would be far less interesting then the best prospective analysis I’m aware of.
5. There is absolutely no contradiction or inconsistency in my suggestion that docs should feel free to wait until my article completes it’s 3rd stage of peer review before considering adopting the approach. I was merely supporting Scott’s valid point that to change practice they may wish to be happy that the data has had it’s appropriate peer review. Alternatively they could spend an enormous amount of time researching the area themselves and form their own conclusions based on that.
6. No one is disputing that patients with PE who have DVT are likely to have a worse clinical outcome than PE alone. You have misinterpreted the addition to the algorithm if you believe that patients with PE +DVT get treated while patients with PE only get observed.
You are again not comparing apples with apples. We are talking about people with a 3% or less risk of PE not patients with 100% risk of PE.
You repeated contention that we treat patients who actually have disease X exactly the same as patients who have absolutely any risk of having disease X regardless of PTP is not sound and we discussed it at length already here
http://broomedocs.com/2013/09/pe-prognostication-dr-anand-senthi-part-2/
The reason for the addition of the bedside U/S algorithm was despite the fact that it was extremely low yield, the yield it did provide was:
– further risk stratifying PTP – absence of DVT would likely drop PTP by an additional 1/3 to 1/2 roughly
– further risk stratifying prognosis.
Given this low yield could be achieved at in a non toxic and rapid manner at the bedside with high accuracy, it is hard to argue against it.
thanks Anand. I agree you have an interesting concept, but some illogical aspects to it.
Simple question. Are you applying your concept in actual clinical practice right now to real patients with suspected PE? If so, is this in context of a research project? If not how are you collecting your prospective data to ensure safety?
Using your own analogy of cricoid pressure, as you cite, many ED docs have abandoned cricoid pressure already with the logic that existing evidence proves potential harm vs no real benefit. Therefore by your own logic, then adopting your new PE concept seems the “right” thing to do. I disagree but it would seem logical that you have adopted it as your “standard of care”
ON the issue of cricoid pressure, You make it out as clear cut but I point out that is not the true picture. Ask many anaesthetists and other intubators and cricoid pressure is still regarded as standard of care in RSI. Recent French ICU paper http://xa.yimg.com/kq/groups/22459940/368537338/name/Intervenções+para+redução+de+complicações+de+IOT.pdf
advocated cricoid pressure as part of improvement bundle for ICU intubation, showing some reasonable safety benefits.
And on the nature of anecdote being meaningless I regard that as unfair and unjust claim. Anecdote has always been an important part of human oral tradition and how we learn. In medical training/learning/professional development, anecdotal learning is still important even in the era of EBM.IN some ways it is even more important. during SARS, H1N1, epidemics, its was through case reporting and epidemiology that we learned key aspects of the problem. There is nothing wrong with asking an honest clinician , an honest question about their honest clnical experience.
let me frame it simpler
If a patient with suspected PE, gets to see you and you counsel them on your approach..and they ask you ” How many cases of CTPA/contrast induced renal failure and death have you seen, Doctor Anand? Also How many cases of PE death have you seen?”
whats your honest answer?
thanks for your comments Kirsty – sorry I didn’t reply earlier. I completely agree that a treatment based trial (as opposed to a trial of different investigative pathways) would be most valuable in the first instance and would provide key data to inform the test threshold. Such data may clarify the TT to such an extent that a planned ensuing trial of the investigative pathway may not be necessary.
Anand, I also would point out your comment that ED doctors would not have been thinking about contrast induced nephropathy in the past “because the prevailing belief was that the risk was zero” is false and I completely reject that assumption.
Contrast induced nephropathy has always been part of the differential diagnosis of new onset renal failure at least in the Australian medical schools and hospitals I studied and worked in!
I am not claiming this complication does NOT happen.
I am stating an honest statement that I, in good faith, have not come across a convincing case in 18 yrs.
I am stating an honest statement that I , in good faith, have come across 5 cases of fatal PE in 18 yrs.
It is not unreasonable that we honestly answer a direct question if posed by our patient!
Minh – I do not dispute your honesty. I dispute your accuracy.
Put it this way if you believed for a patient with renal failure of likely causes are:
– dehydration 50%
– medications 30%
– lots of other causes >19.9%
– contrast 1/100,000
I simply do not have any faith that docs would have properly considered contrast as a real and primary diagnostic possibility at any stage of their dealings with renal failure.
So you can honestly state what you like on this matter, but I sincerely believe it adds nothing to the debate. Again I do not dispute your honesty.
While I agree is is not unreasonable that we answer the honest questions posed by the patient we should be very careful to answer in a way that is not misleading and deceptive.
Often by saying “I’ve never seen it” we overestimate how rare a disease is because our patients don’t understand our real exposure to diseases and how statistics of rare diseases would impact on that.
Further on this particular issue, if a patient asked me that particular question I would say exactly what I’m telling you – “I don’t know – I’ve seen many cases of renal failure but until the recent evidence I never really considered the contrast to be a realistic possibility as a cause, so I can’t honestly say whether or not some of the renal failures I’ve seen may have been caused by it”
If you are concerned with being honest to your patients, I’d be more concerned about being able to in good conscience state that you honestly believe that they are quite clearly above the test threshold. i.e I believe based on the best available data that the risks of helping you by investigating you for PE are greater than the risks of harming you”.
My contention that for the average patient who is Wells <2 (especially if bedside CUS neg and sPESI=0) we simply can't make that statement in good conscience.
And at the end of the day I believe that is the crux of the discussion. It is our responsibility to be confident that our patients are ABOVE the TT before we expose them to the risks of an investigation pathway. This is the essence of the "First Do No Harm" tenant of medical practice. When you stand in front of a healthy person with a very low risk of PE and mortality you need to be confident that they are above the TT before you MANDATE investigation. If you are not, you should be discussing the uncertainty about this proposition with the patient so that they can make an informed decision.
That is the essence of my entire approach. My approach does not mandate "exclusion" from investigation for anyone. It merely suggests for a certain group of patients we can no longer mandate investigation. Instead what should be mandatory is that we have a risk-benefit discussion with the patient, based on the best data available and let them decide.
thanks Anand.
I am not denying CTPA contrast induced renal badness does not exist.
I am being honest about how many cases I convincingly can claim to seen.
How many have you honestly seen? Or are you saying you NEVER considered it a possibility and therefore NEVER diagnosed it.
I agree that just because we have never seen a condition does not mean it is not important. But equally I do not want readers to think that missing PE is not important. I have my own cases as sure we all do.
You still have not answered the simple question if indeed you are already adopting your concept into current clinical practice. You can even admit if you have abandoned cricoid pressure if you want. I still advocate and apply cricoid pressure. I admit that and can explain my rationale, which is supported by many peer anaesthetists, the UK DAS guidelines and ANZCA curriculum.
I am fully aware the ED community is swinging away from CP and even one of my airway mentors Dr Levitan is totally against the use of CP. I respect him as a mentor but disagree with him on this point.
So Anand we can agree to disagree thats fine. You promised a paper published and we can wait till then.
thanks Minh,
Yes I can say I don’t recall every realistically considering CT contrast as high up on my list of diagnostic probabilities in a patient with renal failure given the data I knew in the past.
Therefore I can not say with confidence that I ever really gave it the probability weighting it deserved so I can’t say with any confidence whatsoever that I have never seen a case of contrast induced renal failure and accept there is reasonable chance I have already. I suggest this probability weighting issue would be the same for pretty much all docs.
I don’t think you need to worry at all about folks not being concerned about missed PE. EVERYBODY is overly concerned about missed PE which is exactly why we are over investigating, at least in the Anglo-Saxon derived countries with the common law legal system.
We have also seen many cases of people dying or having ICH from AC.
When we ruminate about anecdotes it creates a cognitive bias that impairs our ability to fairly weight competing probabilities in the patient’s risk management equation. We must do better than that.
I have joined the growing chorus of ED docs who have abandoned cricoid as the evidence shows harm without benefit.
Given you speak vigorously about the lack of evidence of Cricoid and yet you still practice it, suggests to me that we may never agree on the over-riding issue about when it is right to reject a status quo that lacks an evidence base. I suspect from our discussions that you are more inclined to defer to guidelines and “experts”. I am more inclined to defer to the available evidence and put less weight on guidelines and experts. Both approaches have their pro’s and con’s.
Finally yes, I am already adopting my approach with my patients which means: where they have a PTP for PE where I can’t be confident they are above the TT and therefore don’t think it is ethical to mandate their investigation, I discuss the risk and benefits of proceeding with Ix and let them decide. I am very comfortable that this is providing my patients with the best, patient centred, risk management that I can.
But yes, for now .. wait for the article. Less debates on here will give me more time to write it 🙂
ok fine. thanks for the honest answer!
next simple question
So do you now advocate all your peers adopt your approach?
Yes Minh – I advocate that where my peers are not confident that their patient’s above the TT, that they should not mandate investigation and instead have a risk-benefit discussion with the patient regarding this decision.
However I think my peers may be more confident in their knowledge of the data regarding risks and benefits I have put forward and have greater understanding of its accuracy and certainty once they have read a peer reviewed published article from me on the topic. Alternatively if they have the time to independently investigate all the data, they could form their own conclusions and factor this data into their own risk-benefit discussion now.
Sound fair and reasonable?