TCD in the ED? A discussion with Jeff Scott. #FOAMed #FOAMer #FOAMcc

So a couple weeks ago I had the chance to sit in sunny Florida with Jeff Scott (@jsemccm), an ED-intensivist who runs the ED at Jackson South in Miami as well as rounding in the ICU at Jackson Memorial.

His group recently published an awesome article on TCD that pretty much made me realize I have to up my TCD game to the next level.

Here it is (unfortunately walled…)

And here is our discussion:

So there clearly is more to be done with TCD than I have been doing, and maybe it really has a place in the ED. I don’t work first line in the ED so initial stroke patients I only see if they deteriorate, but the idea of visualizing perfusion – or reperfusion – is really interesting.

So if you want to meet Jeff and have him teach you some POCUS TCD, don’t miss H&R2019 which is just around the corner. There aren’t many spots left! Jeff will be running a TCD workshop along with Rob Chen (@ottawaheartrob) which I’m really looking forward to!

Love to hear from anyone pushing the envelope of TCD (or any POCUS application). I believe we are only scratching the surface of what we can do with POCUS, and much study, based on front-line clinicians taking bold strides ahead to see what can be done.






Bedside Ultrasound & Intracavitary Thrombolysis: Using the Ajmo sign. #FOAMed, #FOAMcc, #FOAMus

So as a follow up to a recent post about intra-abdominal thrombolysis, here is a little pearl from a colleague and fellow ICU physician, Dr. Ian Ajmo.

The Ajmo sign refers to the visualization of injected contrast in a fluid cavity, used to confirm proper position of a drainage catheter in an effusion or ascites.

In the case of a separated effusion, it is often difficult to determine if the septations are truly divisive of the fluid, or just a network of membranes that remain communication and that a single catheter can drain. I have seen both cases with similar echo graphic appearance.

However, the Ajmo sign can be used to determine of the catheter is likely to drain the bulk of the collections, or if the use of thrombolytics should be considered:


In this case, we can see that the agitated saline fills only one of the cavities with little or no spillover into adjacent pockets of pleural fluid. This is a case where thrombolytics can be considered. Hence, this consideration can be done early using bedside ultrasound, rather than follow up CT scans (notoriously poor at seeing fine separations).




Intra-abdominal thrombolysis for septated SBP: a case. #FOAMed, #FOAMcc

So we had an interesting case this week of an alcoholic cirrhotic fellow in his 60’s who was admitted with SBP, septic and in respiratory failure. A pigtail had been inserted (RLQ) a few days ago successfully draining 3 litres of cloudy ascites which grew morganella and e.coli. Obviously he was treated with antibiotics.

When I took him over on a monday morning he was hemodynamically stable but with a distended and tense abdomen. A quick look with bedside ultrasound revealed significant but highly septated ascites, and the pigtail had been draining little in the last 24 hours.


We decided to insert a second pigtail in this area, which immediately drained only 30-40 cc, and decided to use TPA to loosen things up a bit (we used 2mg TPA in each pigtail).  In the following 12 hours, the original pigtail drained 700 cloudy cc’s and the new one, 1,000 cc’s. We repeated the TPA for two more doses but little more came out. No bleeding, and he was on prophylactic anticoagulation.

Just thought I’d put the case out there to add to the intra-abdominal thrombolysis data, which is substantially less than the pleural, and, as usual, to show how routine use of bedside ultrasound reveals things you’d either never otherwise see (loculations on CT???  Naaaah.), be guessing about, or have to wait and move your patient to CT.







Here is a nice little review on lysis: sir04264

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!


PS for awesome talks by amazing speakers, don’t forget to register for CCUS 2015!!! For more info: and register at!






An Update on Pulmonary Embolism: NEJM’s PIETHO Study…what’s the verdict? #FOAMed, #FOAMcc

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.

Ok, so let’s get to the PIETHO. 1000 patients, TPA+heparin vs heparin alone in normotensive but intermediate risk patients. So, first question is how was that risk defined?  Patients needed to have echocardiographic/CT signs of RV dysfunction AND a positive troponin. Interestingly enough, onset of symptoms was up to 15 days before randomization…not exactly early treatment, and unfortunately there is no information about the actual time to thrombolysis or subgrouping.  The results were as one could imagine. The combined endpoint of death or hemodynamic decompensation was 2.6% in the thrombolytic group vs 5.6% in the anticoagulation.  I’m not a fan of combined endpoints. Hemorrhagic stroke was 2.0% vs 0.2%. Their conclusion? Exercise caution. Hmmm…not much of a step forward. Basically tells us what we know. It helps the hemodynamics, but you can bleed. They do re-affirm that bleeding is more likely in the over-75.


What do we REALLY need to figure out? 

1. echographic risk stratification – at least into moderate and severe RV dysfunction.

2. longer term outcomes (hopefully PIETHO has a follow-up study in the pipeline, since they had good numbers).

3. a point-of-care study – time is of the essence, and may have an impact on dosage. IMHO thrombolysis should be done within a few hours of presentation at most.

4. further dosage data – 1/2? 1/3? 1/4? small boluses q1h until RV function improves?

I wish I could do it, but community hospitals don’t have the ideal setup, nor do I have a research team that can handle something of this scale. But surely someone can!


Bottom line?

It won’t change my practice. I will continue to offer thrombolysis in select cases, especially the younger patients, who obviously have a lower risk of bleeding, and stand to benefit the most, as pulmonary hypertension  can be crippling. I know I’d take the risk of bleeding when I see 50% dyspnea/exercise intolerance two years down the road…

Finally, bedside ultrasound to anyone with dyspnea/hypoxia should be a standard of care for every acute care physician. No ifs, ands or buts, no exception. Waiting for a CT angio or formal (read daytime hours) echocardiogram is, to me, unacceptable. If you, a friend or family member were in that ER bed, would you trust a physical examination and a CXR to rule out the need for an immediate intervention? I wouldn’t, not my own, and not even Dr. Bates’, Dr. DeGowin’s or Dr. Sapira’s, or all three combined.





Kline JA, Steuerwald MT, Marchick MR, Hernandez-Nino J, Rose GA. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest 2009;136:1202e1210.

Guy Meyer, M.D., Eric Vicaut, M.D., Thierry Danays, M.D., Giancarlo Agnelli, M.D., Cecilia Becattini, M.D., Jan Beyer-Westendorf, M.D., Erich Bluhmki, M.D., Ph.D., Helene Bouvaist, M.D., Benjamin Brenner, M.D., Francis Couturaud, M.D., Ph.D., Claudia Dellas, M.D., Klaus Empen, M.D., Ana Franca, M.D., Nazzareno Galiè, M.D., Annette Geibel, M.D., Samuel Z. Goldhaber, M.D., David Jimenez, M.D., Ph.D., Matija Kozak, M.D., Christian Kupatt, M.D., Nils Kucher, M.D., Irene M. Lang, M.D., Mareike Lankeit, M.D., Nicolas Meneveau, M.D., Ph.D., Gerard Pacouret, M.D., Massimiliano Palazzini, M.D., Antoniu Petris, M.D., Ph.D., Piotr Pruszczyk, M.D., Matteo Rugolotto, M.D., Aldo Salvi, M.D., Sebastian Schellong, M.D., Mustapha Sebbane, M.D., Bozena Sobkowicz, M.D., Branislav S. Stefanovic, M.D., Ph.D., Holger Thiele, M.D., Adam Torbicki, M.D., Franck Verschuren, M.D., Ph.D., and Stavros V. Konstantinides, M.D., for the PEITHO Investigators*, Fibrinolysis for Patients with Intermediate- Risk Pulmonary Embolism, N Engl J Med 2014;370:1402-11.

Mohsen Sharifi, MDa,b,*, Curt Bay, PhDb, Laura Skrocki, DOa, Farnoosh Rahimi, MDa, and Mahshid Mehdipour, DMDa,b, “MOPETT” Investigators, Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT” Trial), Am J Cardiol 2012