Clinical Case 057: big PE, now what?

This is a pulmonary embolism case – but I promise – not another diagnostic case.  That territory has been well covered by all the big names in blogging over the past 12 months.

This case is about decision-making after the diagnosis is made. Risk stratification and the evidence as it stands in 2012…

60 year old man, recently retired and on holidays in sunny Broome. Usually fit and healthy.  Presented with chest pain, had a typical S, Q3, T3 pattern on the ECG, hypoxia on oxygen and a positive D-Dimer.  He remained normotensive throughout, with a tachycardia of 110 in SR.  So he got a CTPA… (there are 3 slices to see if you click the arrows)

axial

CTPA cor

Coronal

OK, so the diagnosis is easy – he has PE (s).  But now what?

Do we simply commence anticoagulation admit him and hope he doesn’t get really sick?  Or should we look a little further and consider more aggressive therapy such as thrombolysis, or even referral for embolectomy?

These are tough questions – an not some we have to ponder often as most of the PEs we see are smaller, and don’t cause much in the way of cardiac dysfunction.

So how do we decide when we should be going for a more aggressive option – and what should we tell the patient in this scenario?

There has been a lot of research coming out in the last 2 – 3 years a lot by Dr Kline in the US – and some new guidelines have been produced based on the studies.

The basic strategy here is to try and stratify the patient with PE into groups – kind of how we do with ACS, the different risk groups get a different management plan.

So how do we do this?  There are a few criteria:

  • Blood pressure / shock – patients with low BP (less than 90 systolic for >15 minutes) are called MASSIVE PE
  • Those with no shock but evidence of cardiac strain eg. troponin, BNP rise, a dilated RV / increased RVP are called SUBMASSIVE PE
  • Then the others – the ones with normal cardiac markers, normal haemodynamics etc are the NOT MASSIVE PE.

Makes sense? It is a bit of odd nomenclature but that is what we call em!

The real controversy here is deciding whom to use thrombolytics upon in the SUBMASSIVE group, and who just gets heparin and watching – traditional management for most of us.

So lets go back to our case.  The CTPA is convincing – he has a big  PE(s).  But what about his other markers of severity?

This demonstrates a D-sign, the RV is at high pressure and flattening the septal wall – usually should be a round LV doughnut: Click here to viewPEECHOPSSAX

And using a super-sensitive troponin we got a small bump of 0.19.  So he has 2 factors that suggest his heart is struggling.

I asked Scott Weingart this question and he answered it on his recent Emcrit Live #2 show – Scott reckons he would take the lytics, but the evidence suggests the benefit is about improved function / exercise tolerance later – not so much about improved mortality in the short term.  the risk of a bad bleed is small – 0.5 – 0.9% depending on what you read.

The AHA published its guidelines in Circulation , March 2011. Follow this link to a nice algorithm that I think is reasonably practical and allows us to make an informed decision with the patient about risk.

There is certainly enough wiggle room in the data to mean you should discuss the pros and cons on a case by case basis.  remember you are not likely saving a life – just making the long term function better, so your baseline level of function comes into this discussion I think.

So here is my question – would you offer thrombolysis to this man in your hospital? Let me know on the comments…

Further food for thought – this retrospective analysis of “unstable PE’ patients in American Medical Journ. May 2012  appears to show all cause mortality was improved with thrombolytics in the sick end of the disease.

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