- Women in her 60's with PMH of Breast cancer stage 1A currently in remission presented with 1 day history of dyspnea on exertion, dizziness on exertion. She was functionally active prior to the onset of these symptoms. No Hypoxemia and no hemodynamic compromise.
- CT PE study revealed extensive bilateral PE with occlusive segmental and sub-segmental emboli (Saddle embolus). Troponin was elevated at 0.9, BNP 600's. (no known cardiac history). STAT ECHO showed mildly enlarged RV, with normal RV and LV function. BLE venous dopplers revealed extensive DVT in both lower extremities.
- This is probably the largest PE that I have seen on a CT scan so far.
- What would you do now?
- Does this patient have a massive or submassive PE?
- Does she have right heart strain? What is right heart strain?
- Do you give tPA or heparin only?
- Is there a role for Interventional radiology in this case?
- This is a stable patient (normal hemodynamics, no hypoxemia) with evidence of right heart strain.
- The patient has an acute unprovoked submassive / intermediate PE
- No indication for tPA in this patient.
- Patient received heparin only.
- No role for IR in this case.
* Difference between Massive vs Sub-massive PE?
- Massive PE: Acute PE with sustained hypotension (SBP <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LV dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).
- Submassive PE: Acute PE without systemic hypotension (SBP >90 mm Hg) but with either RV dysfunction or myocardial necrosis.
- RV dysfunction means the presence of at least 1 of the following:
- RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
- RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
- Elevation of BNP (>90 pg/mL)
- Elevation of N-terminal pro-BNP (>500 pg/mL); or
- Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)
- Myocardial necrosis is defined as either of the following:
- Elevation of troponin I (>0.4 ng/mL) or
- Elevation of troponin T (>0.1 ng/mL)
- Size of PE is not the only variable that dictates whether PE is massive vs submassive. It is a constellation of the above mentioned findings that dictate if a PE is massive vs submassive.
* Who gets tPA?
- Patients with massive PE (above mentioned criteria) and no contraindications to tPA.
- For most patients with acute PE who do not have hemodynamic compromise, tPA is NOT recommended. Treat with heparin only. Acute PE with right ventricle (RV) dysfunction constitutes a spectrum of severity and more data are needed before thrombolytics can be routinely administered in this population of patients. However, thrombolysis may be considered on a case-by-case basis when the benefits are assessed by the clinician to outweigh the risk of hemorrhage.
* Do we consult interventional radiology?
- In unstable PE patients, once it is decided that thrombolytic therapy is warranted, evidence suggests that tPA be administered by a peripheral venous catheter, rather than a pulmonary arterial catheter. So no absolute indication to call IR right away.
- In sub-massive PE patients, if the clinician decides to give tPA, the optimal method of administering tPA is unknown. If tPA is to be administered in acute PE with RV dysfunction, a discussion between IR and an intensivist is required to decide the preferable route based on the local expertise.
I recently wondered aloud why we don't have tPA in the 'crash carts' specifically for Massive PEs. I'm sure the high price-tag (somewhere around $6000/bottle), and if I'm not mistaken, a tendency to denature if not stored at the appropriate temperature, factor into this decision. With that said, I'm confident that some good could come of it if the aforementioned issues could be mitigated.ReplyDelete