As has been discussed in a previous post, patients with sub-massive PE (hypoxic, tachycardic, some troponin rise, etc…but no hypotension) remain in a grey zone, which is, to me , a dubious situation at best – their mortality can be up to 15%, morbidity likely more. Everyone agrees the low-risk patients don’t need thrombolysis, and everyone pretty much agrees that the patient in shock needs it. There is data out there suggesting that some patients clearly benefit from thrombolysis despite not being in shock, in good part relating to avoiding chronic pulmonary hypertension and its consequences.

The issue for many clinicians is that they have a “stable” patient in front of them, and they are considering giving them a drug that can potentially give them a bleed in the head and leave them dead or crippled. Many shy away from this. Part of this is cultural, because the same docs probably wouldn’t hesitate giving the drug to a lateral or posterior MI, which is not likely to kill you, or even leave you a cardiac cripple (just to be clear, I’m not advocating against thrombolysis in these cases, just trying to find a parallel), but since the AHA guidelines say to do it and everyone else does it, there’s no trepidation. It is the standard of care. For most of us acute care clinicians who do not do outpatient medicine, if the patient survives and gets discharged home, chalk one up in the win column. But, as has become clear in recent years with the post-critical illness syndromes, morbidity can be just as important as mortality, especially in the younger patients. Kline et al (Chest, 2009) showed how almost 50% of “submassive PE” patients treated with anticoagulation alone had dyspnea or exercise intolerance at 6 months. They only had a 15% improvement in their pulmonary artery pressures (mean 45 mmhg).

What are the real risks? Pooling the data together gives a value around 2% with a spread between 0.8% and 8%, more or less. This represents each patient’s inherent risk of bleeding, as well as some of the inconsistencies with post-thrombolysis anticoagulation (safest to aim for 1.5-2 x PTT baseline in the first 48h).

The MOPETT trial which, as a #FOAMite you have certainly come across, showed that a half-dose of TPA was highly effective, and they felt it might be possible to go lower. The physiological beauty in that is that, unlike other sites we thrombolyse with full dose TPA, the lungs get 100% of the TPA (coronary artery gets maybe 5%, brain gets 15%). Mind you, of course, the culprit clot/artery obviously doesn’t get 100%, but much, much more (if we figure that you need about 50% vascular area occlusion to cause RV dysfunction) TPA per “clot” than other pathologies. One can argue that anatomically, there is a greater clot burden than coronary or arterial thrombolysis, which may offset this somewhat. However, the date was quite clear in this trial that the therapy was effective, and the bleeding was none.

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