Dr. Cormier comments:
“I could be wrong.. but the IVC is blown with poor variability. RV is dilated and there seems to be an echogenic mass abiding the RV wall. Could it be thrombus? In the setting of hypotension, a massive PE would be high on my list.”
Great work! I agree. But let’s break it down in a bit more detail for those who aren’t as ultrasound-saavy as Maxime.
The IVC is blown – indeed, it is dilated to upper range (>20mm), and more importantly shows little variation (for more on this see this past post ) which tells us we should expect to find a downstream abnormality explaining this (massive iatrogenic over-resuscitation or renal failure with volume overload being the exceptions).
RV is dilated – indeed, the ratio is above 1.5 to 1 to the LV, and you can see that the LV is small and hyper dynamic.
An echogenic mass – right again. One can clearly see a complex mass coming in and out of plane inside the RV cavity. Importantly, is is moving very asynchronously with the RV tissue.
Clinical Course: So here is where it gets interesting. Based on this finding (a great pick up by Dr. St-Arnaud as the ICU consultant in the ER) she was started on heparin, but not lysed as the hemodynamics had recovered by the time he saw her.
I inherited her the next day in the ICU, and in the afternoon, she developed some decreased LOC with elevated pCO2, which may in part have been triggered by sedation. Concerned she may have embolized the rest,I came back to the ICU after hours to do a pulmonary angioscan with the intention of likely thrombolysing her. To my surprise, this turned out to be negative… She progressively woke up and aside from some tachycardia, remained relatively stable. Her CXR (and parenchyma on CT) was clear. Over the next two days, the RV masses became more difficult to see, and the RV to LV ratios recovered. By day 4 her echo was essentially normal, her PCO2 normalized and no longer required supplemental O2. All this while being on IV heparin.
So it remains a bit unclear. The negative angioscan does essentially rule out significant embolism being in the vasculature at the time of the scan, however doesn’t rule out the possibility of embolic material having been lysed by the heparin (it was done more than 36 hours into heparin treatment). This brings up the interesting possibility that much of the pulmonary hypertension noted may have been due to mediator release by the RV clot… For a great discussion on PE hemodynamics see Oren Friedman’s lecture on EMCrit here:
A few days later, she got a cardiac MRI, which was read as normal, aside from a central papillary muscle in the RV, which some attributed as the finding in the ultrasound (although at this time it was no longer seen in the RV by ultrasound!). On the basis of this and the negative angioscan, anticoagulation was stopped.
When I re-inherited the ICU a few days later, I was uneasy about this management course, and, after discussion with the cardiologist – who had seen the initial echo findings himself, restarted anticoagulation.
So I’d love to hear some comments!