Bedside Ultrasound Case Debate Part 2: To lyse or not to lyse… #FOAMed, #FOAMcc, #FOAMus

If you haven’t read Part 1, get the story and the cool clips here first:


So the polls are in!  So far at least, 58% of you would blast away with full dose lytics, 26% with MOPETT-style half-dose, 10% content with heparin, and 5% would go for a PA catheter directed lysis.

So 90% would lyse this patient.  I’m glad to hear that, because in my opinion, more patients should be lysed than I see being done around me.

What did I do?  I went for the half-dose lytics, with an excellent result. Within a few hours she was much less dyspneic, BP was up to 110-120 systolic, and though RV dysfunction persisted, it was mostly resolved by the next day.  I think it is important to note that I had a long chat with her, explaining the risk of intracerebral hemorrhage, which I quoted as being less than 2%.  She opted for thrombolysis with the idea of averting cardiopulmonary limitation given her active lifestyle.

I think the physiological rationale for half-dose lytics is good, since, unlike when used for arterial lysis (coronary or cerebral) the entire dose will pass through the lungs. One could argue that the clot burden is larger,  but the resolution seen in MOPETT and in the dozen or so cases I’ve lysed (no intracerebral bleeds yet), rapid resolution of RV dysfunction supports a sufficient response.  I’ve yet to give – but am ready and willing – a “rescue” top-up 2nd half dose if the first hasn’t worked.

I think the other important point in this case is the importance of bedside ultrasound in the assessment of all shock patients. Although I have no doubt whatsoever that my competent colleague would have come to the diagnosis of PE, it may have been minutes to hours later, possibly after having to begin pressors for a lack of response to fluids.  I won’t hypothesize what might have happened in that time. Maybe nothing, maybe not.

She went home a few days later.

This is why the blind administration of fluid resuscitation is a growing pet peeve of mine.  Two litres in sepsis? Ok, probably, but not every shock is sepsis…  I think that in 2014, going on 2015, with virtually all ERs and ICUs equipped with an ultrasound, there is no place for the empiric bolus. It takes all of 5 seconds to look at an IVC, and another 15 to get an idea of cardiac function in most patients. Like a famous corporation says:

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Opinions, rants and rotten tomatoes welcome!





Bedside Ultrasound Case Debate Part 1: A Poll ! #FOAMed, #FOAMcc, #FOAMus

So I’m walking to the ED to reassess a COPD’er that was on BiPAP, and one of the ED docs sees me in passing and says – “I might have a case for you, she’s on her 3rd litre and still a bit hypotensive…I’ll let you know.”  So I re-route and decide to take a look right away, because I’m never fond of shock NYD.

So here is this woman in her 50’s, BP is 93/67, RR 22 and moderately dyspneic. She has been increasingly so for a few days without infectious symptoms. The X-ray is clear and her labs unremarkable aside from a lactate at 3.3 mmol/l.  She is moderately overweight but quite active. Non=smoker without any cardiorespiratory known illness and on no medications.

Here is what we see on ultrasound-enchanced physical examination:

So, what do you see?

In the first clip, we see a large, dilated IVC with little variation – despite the dyspnea, making it a more significant finding – according to the Effort-Variation Index (   This automatically implies there will be some pathology (unless iatrogenically very volume loaded) to be found downstream.

In the second clip, you have a hyperdynamic and underfilled LV and a dilated, poorly contractile RV.  In the absence of cardiopulmonary disease and in an active patient, this is highly suggestive of an acute process, namely pulmonary embolism.

On further questioning she had done a new yoga stretching class as a possible endothelial-damaging process.

So what did I do? Get a STAT angioscan:


What would you do next?


I’ll tell you what I did tomorrow, and hopefully have some good bloody arguments!


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“Doc, I can breathe!” – Thrombolysis in PE…a case discussion. #FOAMed, #FOAMcc

So I was on call last weekend and got a call from one of the internists on the ward about a potential admission who may need dialysis.   She was a woman in her 60’s, diabetic, hypertensive with minimal baseline renal dysfunction, who had been admitted with a hepatic abscess due to biliary obstruction. This had been stented and a pigtail catheter had been inserted to drain the abscess.  However, over the last few days, her creatinine had risen to about 500 and she was becoming oliguric.  Her O2 requirements had also increased and she was now on 15 liters by nasal prongs. This had been ascribed to pleural effusion and possible pneumonia.

When I saw this lady, she was visibly dyspneic at 30 with a heart rate 115-120 and a systolic BP of about 105-110, saturating 90% on 50% face mask.

So on physical examination, she had a soft abdomen (the first thing I feel just before I put probe to skin), her skin was cool, and the CUSE revealed a large (>20mm) IVC with no respiratory variation (despite the effort).  I unfortunately forgot to hit the record clip button…and the parasternal long axis and apical 4 chamber are here:

Lung views showed “A” profiles except for the right base which had a small effusion and some consolidation/atelectasis and some B lines, but not very extensive.

So further assessment revealed she was not a smoker, previously quite active and easily able to go up and down several flights of stairs.  She had noted dyspnea about 3 days ago, without chest pain. There were no leg symptoms, and she had been on LMWH for dot prophylaxis.  The CXR was not very impressive – in a sense that there was not enough parenchymal disease to explain pulmonary hypertension.

This is PE until proven otherwise, and I would have been comfortable without further confirmation, but with the presence of some lung disease and an intrahepatic catheter, I preferred to have 100% confirmation before initiating thrombolysis.

After CT angiogram confirming bilateral and extensive embolism, I had a thorough discussion with her and her family and they all agreed to go ahead with TPA.  She was quite concerned with cardiorespiratory limitation, given that she was quite active. She was comfortable with a quoted risk of intracerebral bleeding below 2%. I used the MOPETT half-dose of 50mg.

Overnight, her HR slowed to about 100, and sats increased to 93-94%.

When I rounded on her in the morning, she said “Doc, I can breathe!” with a big grin. Her HR was 95-100, she was not on 3 litters by NPs, BP 115-120 systolic, and CUSE showed:

So we can see that even though the RV is still quite impaired, it has decreased in size and the LV is now filling better. This was about 12-13h post thrombolysis. She was able to sit up without dyspnea and mobilize to the chair. Her IVC, although it remained around 18-19 mm, had clear respiratory variation.

So…success? Who really knows. It is concievable that, with heparin alone, she might have improved similarly. It is possible. I’m not putting this up to formally support the concept of thrombolysis in “submassive” PE but more to contribute to the #FOAMed discussion regarding the “grey zone” of thrombolysis, since she was technically not in shock (eg SBP>90, lactate normal), but the degree of impairment of the RV to me and the clinical picture, 3 days post, was concerning enough to warrant thrombolysis, but importantly to stress the following:

Point 1: the importance of bedside ultrasound, especially in acute cases.  Without it, over a weekend, and with a patient in renal failure, how quickly would I have ordered a CT angio?  Not without some hesitation…

I won’t review the MOPETT trial, these guys did a much better job than I could hope to, so definitely listen to this if this topic is of any interest to you (and it should!!!):

Great case debates in the RAGE podcast.

Keep in mind that morbidity, not mortality, is the main thing to focus on in sub-massive embolism and the MOPETT – even though I don’t really like the term, its quite vague – benefit in embolism with shock is quite clear.

Point 2: Equally interesting to me was the fact that the renal failure improved. In fact, overnight following thrombolysis, she had a urine output (without diuretic) over a litre, and over the next few days her creatinine normalized and renal replacement therapy was not needed.  Interesting, since she even got a good blast of toxic dye with the CT.  Some will feel that it is the improvement in CO that improved renal function, and this may be partly true, but in view of the lack of “systemic shock,” I think that venous decompression resolved the congestive renal failure, which I think was the main cause of her ARF. I posted about this topic a few months ago, so for more on this see:

so thanks for reading and love to hear anyone’s opinion!





Great question!  There is a whole grey area in “PEA” and management is unclear. I don’t think there is a single answer to that, but physiologically and without further information about RV/LV, I would say your patient needs vasopressor/inotrope support, so I would probably give a small bolus of epi (maybe 100ug) and start an infusion. If I see little reaction (eg HR/BP doesn’t pick up in 30 seconds, I would probably give a short cycle of CPR to get the epi back to the heart.   Of course, hopefully there is a reversible cause (MI/PE), that can be addressed.