CCUS 2014 – The Ultrasound-Assisted Clinical Assessment!

If you’re thinking of coming to Montreal to beef up your clinical skills and decision making, hurry up and register, we have to cap the participants to 100 (physical restrictions of the venue) and there aren’t too many spots left!

Myself, am looking forward to learning a bunch of things: how to diagnose bowel obstruction (Vicki Noble), how Andre Denault likes to integrate hemodynamic modalities in shock, how Mike (Stone) uses ultrasound to manage CHF patients, how Haney (Mallemat) uses it to manage abdominal pain, and many more…

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Montreal, May 9-11, 2014, Santa Cabrini Hospital.

More info and registration at:


See you there!





“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.




Central line insertion: US-spotted “Blind” technique Video (HERE IT IS!) #FOAMed, #FOAMcc

My apologies, had technical issues with the video uploading so here it is in two formats:




…please let me know if there is a problem!





Central line insertion: US-spotted “Blind” technique video. #FOAMed, #FOAMcc

So a few months ago I posted about central line insertion and my concerns about the current standardization of care of ultrasound guidance:

I promised a video so finally got around to remembering to do it.  This one actually happens to be a dialysis catheter so a bit bigger, but otherwise the technique is the same. In this case I am using my standard ultrasound-spotted procedure with “blind” insertion.

So here, I spot the vein, confirm it is just lateral to the carotid, and that it collapses nicely, without thrombosis:

Now, I insert the line. A few important points to note that are not seen in the frame:

Line Insertion video:

a. my introducer needle/syringe and loaded guide wire (pulled pack and “loaded”)  are ready  and within my vision, and also nearby are the dilator and catheter.

b. note that the off hand (right hand in this line) protects the carotid and stays in place until there is venous flashback, then secures the needle position.


Note that in this particular case, I didn’t quite make a large enough incision so the dilator insertion was a little difficult – unnecessary delay, and also unfortunately lost the last few seconds as my iPhone memory was full. 

Next, I confirm position in the internal jugular vein, and verify for lung sliding to rule out and anterior/apical pneumothorax.

In me experience, the key mistake I see inexperienced operators (and sadly, some experienced ones also) make is not to have a proper setup, such that once they do find the vein with the introducer needle, their subsequent steps are not immediately ready, and in the process, the relationship between needle tip and vein is lost, resulting in an inability to thread the guidewire (often blamed on mysterious anatomical abnormalities). It is key to find the vein with the freezing/searcher needle, fix the depth/angle relationship in your mind, withdraw and reach for the introducer needle/syringe using peripheral vision so as not to break the visual fix, and reproduce this while introducing it.

This is what I try to install in students/residents rounding with me, and in fact this approach is useful for any procedure.  Not having to turn your head, reach and fiddle with things that are not ready prevents mistakes.

If you haven’t read my previous post on central line insertion, I’m not advocating agains the use of ultrasound guidance, but for the maintenance of the ability to insert blind lines if necessary.



Pleural effusion: Draining it! (Part 3 of 3) #FOAMed, #FOAMcc

Ok, so once you’ve determined you should drain a pleural effusion, your options are to insert a small catheter (CVC, pigtail, generally 8.5 to 14F) or a traditional chest tube.  CVCs/pigtails should only be inserted when (a) you have ultrasound guidance and (b) the effusion appears to be free flowing and without a great deal of echogenic contents. Why? Because to go in with a sharp needle, as the seldinger technique requires, you need to visualize a safe spot by ultrasound, and because if the effusion is complex with septations and blood/pus, it likely needs a large bore chest tube to successfully drain. For the less experienced, a traditional chest tube insertion is done using blunt dissection and exploration with a finger, such that the risk of pneumothorax is minimal (no needle).

In terms of the pigtail insertion, choose a spot using ultrasound, generally posterior to the midaxillary line to optimize drainage, then freeze, insert the guide needle then guidewire, then dilator and finally the drainage catheter.

Here is a makeshift video showing a pigtail insertion.  I will make another one more focused on the technique, as this one is a bit more focused on the ultrasound. We ca see a large effusion with a bit of atelectatic lung, and also confirm the placement of the guidewire and the pigtail catheter.

Although in this video I showed live ultrasound guidance, in most cases I prefer to pick the spot, mark the skin, and do the technique blind. It is simply faster that way. However in some cases, especially with small fluid collections, I may choose to use live ultrasound guidance.

This is actually a very practical skill to have, as otherwise pigtails are generally inserted by interventional radiology, which implies delays, and more importantly, patient transport and its inherent risks and disadvantages. So for those without experience, I would highly encourage you to seek out an experienced operator and learn this technique.


Disclaimer: this description and video is for the sole intent of sharing medical knowledge and does not replace formal training. Do not try this without adequate training and/or supervision.

Pleural Effusion Podcast – physiology and clinical approach! #FOAMed, #FOAMcc

…just for those who prefer to listen rather than stare at a screen…

…and also because I had my sick toddler napping on me for two hours and typing was not an option.

Part 3 with the vid coming in the next couple days, though, apologize for the delay!



Pleural effusion in the sick patient (Part 2 of 3): Physiology & Literature! #FOAMed, #FOAMcc

So once your routine cardiopulmonary bedside ultrasound examination has revealed the presence of a significant pleural effusion, should you drain it?

I guess the first real question is actually what is a significant pleural effusion?  As you can imagine, the N=1 principle pops up again, and there is no single threshold answer (e.g.: >750ml  drained and <749ml  ignored), naturally.  So here are the main factors that impact physiologically:

1. underlying global respiratory function – eg how much reserve you have. With healthy lungs, a young adult can usually tolerate complete atelectasis of one lung or even more, which would take 2-3 liters of effusion at least. However, the more compromised gas exchange is, the less atelectasis can be tolerated.  This also encompasses the level of required ventilatory support, including the level of PEEP. Basically, the worse your lungs are, the more significant the effusion becomes.

2. thoracic compliance – which combines chest wall and abdominal pressure, since the diaphragm is thin and easily displaced.  The greater the compliance, the less atelectasis will occur as the diaphragm and chest wall will shift to accommodate some of the fluid. This is very important especially in surgical patients (or anyone with a tense abdomen).

…so there is no number.  Of course, if you take it to the extremes, I think everyone would agree that if you have 200ml,  it’s probably not worth doing, and if you have 2,000ml, it is. But in the grey zone of, say 500-1,000 ml, you have to make a call given the patient in front of you.

Now what does the literature say?

First of all, there is no large study looking at the impact of effusions in generally ill patients (ED/ICU).  There are some small, specific studies showing worse prognosis in some pathologies (eg Legionella pneumonia) but nothing that can really be extrapolated to general ED/ICU patients.

What about in ARDS? Talmor et al, (Surgery 1998, v 123) showed benefit in survival in a small study of ARDS patients.

I think the best overall study was Vignon et al (CCM 2005, v 33) who demonstrated that bedside ultrasound was much more sensitive in diagnosing pleural effusion (CXRs read as normal had as much as 1,000 ml effusions, as well as diagnoses of effusions which were actually consolidations ), but also that it was quite accurate in quantifying (inter-pleural distance >45-50mm at the base correlates with effusions >800 ml).

Usta et al (Interactive CV and thor surg, 2010 v 10) had similar results in spontaneously breathing post op patients with 45 mm (interpleural distance between diaphragm and base of lung) corresponding to about 700ml, although their range was quite wide, and they were using a somewhat impractical sitting position. They actually came up with a formula (16xdistance in mm) to estimate effusion volume.

Sikora et al (ISRN Emergency Medicine 2012) did a good review on the whole thing as well.

Sikora et al review

My empiric observations: I must have put in at least a thousand pigtails or (back in the day) CVCs in pleural effusions over the last 14 years, and my therapeutic goal has always been to drain effusions at least 750 to 1,000 mls. I have drained 350-500 ml in patients in severe respiratory failure a few times, some with apparent benefit, others without. I don’t recall regretting putting one in, but I do regret a few cases of not draining, only to have recurrent respiratory failure post-extubation. Grossly, I would say 750-1,000 or more in a patient with respiratory failure warrants drainage, but 1,000 mls in a CHF patient on nasal prongs can wait for the outcome of diuretic therapy. Of course we are talking about therapeutic and not diagnostic drainage. Under ultrasound guidance with an experienced operator, pneumothoraces should be exceedingly rare.

Bottom Line: start by examining your patient, physically and by bedside ultrasound. Understand his degree of respiratory failure and estimate the size of the effusion and the compliance of his chest.  Then you have to make the call (that’s why we’re MDs) as to whether this particular amount of pleural effusion in this particular patient is worth draining.

Next week:  how to do it video!



@shanxonline says:

Great post Phillippe and I fully agree that a global assessment is necessary before draining an effusion. With ultrasound we’ve become really good at identifying effusions, but need to understand physiology and especially chest wall/abdominal compliance to understand the physiological implications of drainage vs conservative management.