Thanks to @icerman_ex’s sharp eye, just finished reading @EMNerd’s awesome post on bedside ultrasound (http://t.co/y1B5G9RBIv).   I think it casts the right light on bedside ultrasound, and as usual in spectacular prose that is the only #FOAM I know that discusses science so artfully.

There are a couple of things I’d like to add, for those who may be interested.  And, as a disclaimer, I am heavily, heavily biased towards the widespread use of bedside ultrasound. It is a revolution in medicine, undoubtedly the biggest one of the last decades, but, as with any revolution, blood will be shed, and it’s only when the dust settles that our science will be better.

First of all, everyone should understand that due to bedside ultrasound coming into its own in the era of evidence-based medicine, it is being asked to jump through hoops like no other tool has been. Try looking for a randomized trial on the use of the stethoscope… So it is important to keep this in mind as the fine tuning takes place, rather than try to blindly adopt it or toss it out with every new study that comes out.

As Rory points out, the issue isn’t one of accuracy per se, rather than the clinical interpretation of that accuracy – that is, the clinician being able to tune out the noise, just like one would parts of the history or physical that are irrelevant or misleading. The failure to do so will lead to unnecessary interventions or testing.

Another point is that the second generation of bedside sonographers are not inherently the same as the first, who took up the probes to answer clinical questions and created the protocols and algorithms – as always, much kudos to Daniel Lichtenstein, “le premier des pioneers” – whereas the second generation will be a very mixed bag, many of which will carry bedside ultrasound and push it farther, but also many others who will apply what they have learnt without necessarily the same framework.  If you look at the history of medical developments, initial wonders often have subsequent setbacks, until training and practice are fine tuned – take the history of laparoscopic surgery, for instance.

The key point in all this is that proper clinical integration is necessary, and that trainees have to be well mentored by those who do use the tool in a daily fashion, and finally – as always – some good studies in a number of clinical scenarios, so as not to have (only) a pixelated view of the patient.

 

cheers!

 

Philippe

 

Jon-Emile says…

Wonderful post:

You know my position on inspiratory IVC collapse [http://pulmccm.org/main/2014/critical-care-review/inspiratory-collapse-inferior-vena-cava-telling-us/]

My problem with the Kenji trial is that is certainly does not [and cannot] tell us if seeing IVC collapse means that a patient will augment their cardiac output in response to a fluid bolus. What their trial tells us is that using less fluids and more pressors in shocked patients probably improves outcomes … but i think few of us doubt that currently [especially in light of the PROCESS trial last spring]. Instead [and i say this facetiously of course] they could have used a random number generator that was weighted to giving less fluids and more pressors instead of bedside ultrasound … and they probably would have received similar results.

It is hard for me to imagine a physiological scenario whereby a patient has a fixed and dilated IVC on ultrasound with respiration [spontaneous, triggered, or passive] but could still be fluid responsive. So when I see a fixed, dilated IVC, I feel fairly confident that fluids should stop [again this does not tell me about the patient’s volume status, as a patient could have a very plump IVC and be volume deplete].

But this physiology is not new and was published by Magder in the early 90s [invariant right atrial pressures with respiration predicted fluid non-responsiveness very well] and also by Pinsky in the early 90s when he found that in post surgical patients that right atrial distending pressure is dissociated from right ventricular end-diastolic volume. Which means that when you see right heart congestion, you have probably already reached cor pulmonale.

The true challenge is IVC collapse … it is affected by many conflicting variables [as you know]; there is probably a good portion of patients who have IVC collapse [especially those on PEEP, triggering the ventilator] who are actually fluid non-responders, yet we push them closer and closer to cor pulmonale needlessly … so until someone finds a better non-invasive physiological solution …

as EM Nerd, so aptly puts it …

“In medicine we frequently propagate half-truths and unsubstantiated certainties.”

Thanks for the post space,
Jon-Emile

 

Excellent points!

Thanks!

 

Philippe