We now have way too many treatment options for sub-massive and massive pulmonary embolism (PE) patients who aren't coding in front of you. How do you decide which one is right for your patient? To help answer this question, I am joined today by Oren Friedman, pulmonary critical care doc and one of the members of the Cornell PEAC team.
Cornell Pulmonary Embolism (PE) Advanced Care Team (PEAC), aka the CLOT Team
Oren Friedman MD, Pulm Crit Care; James Horowitz MD, Cardiology; Arash Salemi MD, Cardiac Surgery; Akhilesh Sista MD, Interventional Radiology
You can shoot the team an email: peadvancedcare at gmail dot com
Who Should We Treat?
Wood 2002 PE Mortality Curve
30% normotensive patients have RVD; 10% progressed to shock; 5% in hospital mortality[cite]10859287[/cite]
The Better Risk Categories for Pulmonary Embolism
Well and Stable Sub-Massive
Full dose tenecteplase with concurrent heparin
Death or hemodynamic decompensation occurred in 2.6% of the tenecteplase group as compared with 5.6% of the placebo group
Extracranial bleeding occurred in 32 patients (6.3%) in the tenecteplase group and 6 patients (1.2%) in the placebo group (P<0.001)
Intracranial Bleed 10 patients (2%) in the tenecteplase group and 1 patient (0.2%) in the placebo group (P=0.003)
Also see my bud, Salim Rezaie's post on PEITHO and Konstantinides' prior study [cite]12374874[/cite]
Ryan Radecki made some great observations in his post on PEITHO
The criteria for myocardial injury was a troponin I >0.06 ?g/L or troponin T >0.01 ?g/L. These may be relatively inclusive thresholds.
Not all placebo patients developing hemodynamic collapse received subsequent thrombolysis; likewise, almost half of those who received open-label thrombolysis had no hemodynamic collapse.
Half the deaths in the placebo arm were “sudden unexplained” or “other”, compared with bleeding or stroke complications in the thromboysis arm.
Jeff Kline's trial was stopped midway through due to an institution change. Complicated primary endpoint with promising, but unusable results [cite]24484241[/cite]
For the scoop on this one see the Bottom Line Review post on TOPCOAT
Half-dose alteplase led to a marked reduction in pulmonary hypertension without sig. complications
Sharifi M et al. Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT trial). (J Cardiol 2013; 111: 273)
See this prior EMCrit Wee as well on MOPPETT
Update: This meta-analysis states that the half-dose may be appropriate, effective, and safe [cite source='pubmed']24412030[/cite]
Chatterjee et al. have the most current meta-analysis on this topic (JAMA. 2014;311(23):2414-2421)
See the Bottom Line Review post on this study
Nakamura just published another MA this week; see Rory Spiegel's take on the two here
Is it just in the Oldies?
Markedly lower risk in <75 y/o in PEITHO and <65 in the Meta-Analysis
The Treatment Options
tried and true. but even if some degree of resolution of presenting severe symptoms, there is the question of long-term consequences of leaving a large clot burden--namely, loss of exercise tolerance due to chronic pulmonary hypertension
With either full or half-dose alteplase or full-dose tenecteplase
Catheter-Based Intra-Arterial Thombolytic Infusion
Angiography guided placement of pulmonary artery catheters allowing a 24-hour infusion of low dose tPA. [cite]19875060[/cite]
A newer therapy is the EKOS catheter. This uses ultrasound to continuously break up the clot during the IA Thrombolysis. Many of us wonder if this is any better than standard catheter-based therapy. [cite]24226805[/cite], [cite]23601295[/cite] See the PulmCCM Post on the Circulation RCT of EKOS
Interventional Mechanical Clot Disruption