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  • Dr Eanna Mac Suibhne

THOMBOLYSIS FOR PULMONARY EMBOLISM

Updated: Nov 3, 2023

Dr Eanna Mac Suibhne Emergency Registrar

Peer review: Dr David McCreary


THE CASE

Gerard is a 55-year-old gentleman who has presented to your ED with a collapse episode while at home. It was an unwitnessed event but he reports it to be like a fainting episode. He slowly picked himself up and called an ambulance because he didn’t feel right. Recently, he reports having some chest pain and has become more short of breath on exertion in the past week. Gerard thought he was getting back to his old self after he underwent an ORIF of his tibia 5 weeks ago having fallen off some scaffolding at work. As you sit there with Gerard, you note that he is quite pale and sweaty, not entirely comfortable. His blood pressure reads a systolic of 95mmhg and has had a persistent tachycardia of 115 bpm since arriving in the department. The nurse hands you an ECG which shows a RBBB, which is new for Gerard since his pre-op ECG 5 weeks previously. An i-Stat troponin has come back elevated above the reference range.


NO MARKS FOR GUESSING THE DIAGNOSIS HERE…BUT WHAT ARE WE GOING TO DO ABOUT IT? DO YOU ANTICOAGULATE OR DO YOU PULL OUT THE BIG-GUNS AND THROMBOLYSE THIS CHAP?


WHEN DO YOU PUSH THE BUTTON FOR THROMBOLYSIS IN PE?

If you were to go with current literature basically it would suggest you should thrombolyse a massive PE and after that, well, the evidence is sketchy. About 10% of patients diagnosed with acute PE die within the first three months of diagnosis<1>, so getting the correct treatment to the correct patient is important. The difficult decision relates to a particular subset of patients who have maintained hemodynamic stability yet have signs of RV dysfunction and who could potentially deteriorate. What to do?


When it comes to this topic it all seems to hinge on definitions and so let’s start with the question:


WHAT’S THE DIFFERENCE BETWEEN A MASSIVE AND A SUBMASSIVE PE?


MASSIVE PE

Let’s first talk about massive PE, as there is little argument in the literature that thrombolysis is the appropriate treatment here. To be labelled with this ominous tag, a PE must satisfy certain criteria, which vary depending on where you are looking.


The definition had originally relied on anatomical criteria, those being occlusion of two or more lobar arteries or more than 50% occlusion of pulmonary vasculature. This view, however, has evolved to incorporate a patient’s hemodynamic status. A succinct definition is provided by the AHA:


An acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

‘Shock secondary to another cause’; this point should not be skimmed over. Are you sure your patient is not hypotensive for another reason that you haven’t considered, e.g. sepsis, hypovolemia, arrhythmia, LV dysfunction etc?<2>


Approaches to help you consider this would be:

  1. Assess the clot burden on CT. For a PE to be the perpetrator of a patient’s compromised hemodynamics, there should be at least moderate to large clot burden on the CT. Patients who are hemodynamically unstable with a small amount of clot - it’s probably not going to be the PE that is causing the instability.

  2. Get your probe out. If the IVC and RV aren’t dilated, consider reassessing if it’s the PE that is causing the shock.

In patients with massive PE, systemic thrombolytic therapy has been shown to reduce mortality<3>, decrease the risk of developing chronic thromboembolic pulmonary hypertension and improve quality of life<4> <5>.


The Alfred guideline, summarised in the flow chart below, supports thrombolysis in the massive PE patient cohort in the context of no contraindications for its administration.