Pulmonary Embolism

This month’s questions:
In patients with pulmonary embolism and evidence of right ventricular failure as a result of acute pulmonary artery hypertension:
1. How is the decision made as to whether to thrombolysis is appropriate?
2. When should surgical or mechanical thrombectomy be considered?
3. Is there a role for inotropes and if so, what is the ‘best’ strategy’?
4. Should we be using pulmonary artery vasodilators and if so, which ones?
This months article is a special report by Paul Young on the value of P-Values…..

https://journals.lww.com/em-news/Fulltext/2018/12000/Special_Report__P_Values_Have_No_Value,_but_There.4.aspx

 


A – 

In patients with pulmonary embolism and evidence of right ventricular failure as a result of acute pulmonary artery hypertension:
1. How is the decision made as to whether to thrombolysis is appropriate?
In my (modest) experience, by the medical consultant, on the phone from home, after much head-scratching, but with no particular rationale given. My take on it is that while the evidence is very far from compelling, there are likely to be some patients with submassive PE who benefit from thrombolysis – probably those with more severe presentations (who are more likely to come to our attention anyway) but with a relatively low bleeding risk (young age, no hypertension, no previous stroke). On current evidence I’d probably favour “half-dose” thrombolysis (50mg alteplase) in these selected patients.
2. When should surgical or mechanical thrombectomy be considered?
 The only evidence for catheter-directed thrombolysis/mechanical thrombolysis or surgical thrombectomy is with small numbers and non-patient-centred outcomes (or non-randomised), so would only consider in those who would otherwise have received thrombolysis (based on judgments above) but have a higher bleeding risk.
3. Is there a role for inotropes and if so, what is the ‘best’ strategy’?
I doubt that the RV can be pharmacologically cajoled into pumping better in the face of massive afterload. In terms of pressors I wonder whether we should favour vasopressin over norad for the lesser effect on PVR.
4. Should we be using pulmonary artery vasodilators and if so, which ones?
Would like to hear others’ opinions/experience on this, but physiologically I might expect that whilst it’s important for us to avoid further increases in PVR, attempting to reduce PVR won’t have much effect due to mechanical obstruction, and may worsen shunt.
To piggyback on this topic, what are people’s experiences of managing cardiac arrests where someone has decided to thrombolyse and (therefore) thinks that it’s mandatory to continue CPR for 90 mins? I’ve generally tried to inject some sense by suggesting that if we have evidence that CPR is ineffective (minimal ETCO2, worsening gases) – and we generally do – then prolonged CPR is futile.
B – 
Im not a clever ICU doctor but thought I’d share a case I had a few years back. During a trauma case a patient suffered an on table PE following inflation of a thigh tourniquet.
CTPA post op showed I think an iliac vessel thrombus that extended down into the leg, and had formed despite appropriate prophylaxis being administered in the time between her injury and her surgery.
The impact of this was predominantly seen in problems with gas exchange (hypoxia) rather than  cardiovascular instability.
Discussions at the time about subsequent management involved a risk benefit analysis of the available treatment options.
She didn’t go for mechanical thrombectomy as this apparently primarily benefits the CVS side of the problem, but can exacerbate respiratory problems by causing microemboli that can further  compromise the lungs. In this instance as oxygenation was problematic it was thought it might make things worse.
Similarly recent surgery might play a part in deciding if making the blood runny is a good idea.
This was my N=1 experience of encountering this perioperatively, as opposed to a literature review.
My reflection on this for what it’s worth is that I should have stopped the surgeon operating whilst we went through trying to stabilise the patient.
PE was high up on my list of differentials due to a simultaneous desaturation and drop in EtC02, but I went through the process of scoping the patient to exclude tube misplacement, mucus plugs etc and on table CXR too.
If we had stopped after just the skin incision it might have made drug based thrombolysis more feasible.
Similarly on table TTE didn’t go through my mind as a way of looking for right heart issues due to a PE, and if faced with the same situation again I’d recommend trying to arrange one as part of the investigation process. Quicker and easier than getting a slot for a CTPA if a patients in extremis.
Hopefully an interesting case, that others can learn from, and I’ll be on tenterhooks for any novel treatment aids that people might have that I’m blissfully unaware of.
C – 

Good Question!

1)We Had a discussion at this in PGH a few years ago. This is what I remember from doing a bit of reading then:

In High risk (hypotensive) PE. Benefits of thrombolysis outweigh benefit. In Low risk PE risk outweighs benefit.

Intermediate Risk PE: (RV pressure/overload or significant TR on Echocardiography/CT), ECG findings of R heart strain, Elevated TnI or BNP/proBNP. There is an absence of robust evidence to support thrombolysis. We Looked at the 2014 ESC Guidelines:  (https://academic.oup.com/eurheartj/article/35/43/3033/503581#125292847), and Specifically at the Recent MOPETT (https://www.thebottomline.org.uk/summaries/icm/mopett/), TOPCOAT (https://www.thebottomline.org.uk/summaries/icm/topcoat/), PEITHO (https://www.thebottomline.org.uk/summaries/icm/peitho/).

Our patient was young (40s Male), with no co-morbidities and presented with 2 episodes of syncope, one of which was on AMU. From memory his ECG just showed tachycardic, TnI was slightly elevated, Initial ECHO Showed RV:LV Ratio of just above normal (0.7ish).

I agree with Pete in that there is almost certainly a subset of patients that benefit from some form of Low Dose thrombolysis. However PEITHO showed no mortality benefit and a significant incidence of major bleeding events. MOPETT showed a reduction in PASP at 28 months, but had some significant flaws: using an older definition of moderate risk, and being underpowered to show a mortality, or other clinically significant benefit.

Our patient had LMWH and serial TnI and Echocardiography which showed resolution of his right heart strain so was discharged to ward after 48 hours.

ps. I have no experience of Inhaled Nitric Oxide for PE but super hot of the press iNOPE – Inhaled NO for Submassive PE published this month : https://www.ncbi.nlm.nih.gov/m/pubmed/30633959/, and there is a good summary on the emcrit website here : https://emcrit.org/pulmcrit/inope/

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