Intensive-care unit

October 28, 2016

Bedside Ultrasound Case: Control the source. #POCUS #FOAMed, #FOAMcc, #FOAMus

So this morning a 65yr old man with shock and respiratory failure was admitted to the ICU, hypotensive on levophed and vasopressin, with a lactate over 10.

So, as usual, my first reflex was to reach for the probe to assess hemodynamics. He had been well resuscitated by a colleague, and the IVC was essentially normal, somewhere around 15 mm and still with some respiratory variation. However, scanning thru the liver, my colleague had noted a large hepatic lesion, which on CT scan (non-infused since patient had acute renal failure) the two radiologists argued whether it was solid, vascular or fluid filled.

image

Having the advantage of dynamic ultrasound, you can tell that there is some fluid motion within the structure, very suggestive of an abcess, especially in the context of severe septic shock:

So the next step was source control:

 

Pretty nasty. Pardon my french!

We got over 1.5 L of exceedingly foul pus.

imageimage

Within a couple of hours the lactate dropped to 3 and the levophed was down by more than half.

I think this case illustrates once again, the power of POCUS in the hands of clinicians.  While I am certain that the diagnosis would have been made without POCUS, it probably would have taken additional time as the radiologists themselves were debating its nature, and without POCUS, bedside drainage in the ICU would have been out of the question. That liter might still be in there tonight…

For those interested in how to integrate POCUS in their daily rounds, I think I put together a fair bit of clinical know-how and tips in this little handbook.

 

Cheers!

 

Philippe

October 28, 2016

Bedside Ultrasound: a primer for clinical integration. #POCUS

screen-shot-2016-10-28-at-1-11-48-am

So I had a lot of people ask me over the years to put to paper (or screen) a POCUS book, but I figured there were so many good ones out there, like my original Bible, General Ultrasound in the Critically Ill by my good friend Daniel Lichtenstein, or Vicky & Bret’s book, Emergency and Critical Care Ultrasound, that I would be trying to re-invent the wheel, and probably not doing as good a job.

But then I remembered Dubin’s EKG book, the kind of book you could almost read in a single sitting, and certainly over a few days, and get a decent grasp of the concepts and actually have some skill at the end of it.  So I figured maybe I could put together something like that for POCUS from the standpoint of clinical integration. Not so much a protocol, but how you fit your findings together in clinical syndromes, and inserting as many tips and pearls as possible.

It’s a light read, it’s irreverent, it’s kinda like #FOAM. So I hope I did a decent enough job, and I was pretty happy with the comments from a couple of respected colleagues:

Philippe has created a fantastic real-time reference for the busy practicing clinician who wishes to adopt point of care ultrasound into their working cinical armamentarium. The strength of this work is it’s immediate applicability to the clinical scenario. Dr. Rola’s extensive experience in clinical practice and teaching shines through with a concise and clinically minded approach to each scanning modality. The work is greatly enriched by many practical tips and tricks and that are often missing from larger, more formal texts. The sum of these “truths” is an important part of what transforms a clinician to an expert in the field. A final unique feature of this resource is it’s focus on integration. In Philippe’s mind, findings of differing ultrasound modalities are blended together with the patient’s clinical picture to derive a true ultrasound enhanced understanding of the patient’s pathophysiology. With characteristic plain language and descriptions, the book succeeds in taking the reader closer to that vision.

Dr. Edgar Hockmann, MD, FRCP

Dr. Rola has created the ideal compendium for contemporary healthcare professionals. Bedside Ultrasound: a primer for clinical integration concisely and intuitively describes the essentials of examining a patient in the 21st century. The guide is both unique and useful because it speaks to all levels of training for all professionals caring for patients within multiple hospital environments – the emergency department, general medical ward, operating room and intensive care unit. Dr. Rola’s succinct account of ultrasound examination leads the reader through a patient’s anatomical and physiological underpinnings using the ultrasound probe as his guide; it is a resource to be found in the pocket – virtual or otherwise – of all those interested in the future of the physical exam.

Jon-Emile Kenny M.D.

The first print run just got off the press, is on Amazon here, as is our casebook, and on our website http://www.ccusinstitute.org. The iPad version is available on iTunes here! Please give me feedback as it is important, so that the second edition just gets better!

cheers!

Philippe

July 13, 2016

The NYC Tracks with Jon-Emile part 2: a discussion on congestion, pulmonary and otherwise. #FOAMed, #FOAMcc, #FOAMus

So here is our second discussion, where we delve a bit into diuretic physiology, the issue of organ congestion, the myth of the “low-flow” acute renal failure associated with CHF (see earlier post), and a couple other things including a great way to determine if a patient isn’t respecting the low salt diet prescription!

I meant to, but forgot to discuss with Jon what I think is an important end-point in CHF management: the IVC. Yes, it is useful not just to make the diagnosis of congestion, but also target normalization of IVC physiology prior to discharge. It just makes common sense. If you decongest a patient just enough to get them off O2 and send them home, they bounce back a lot quicker than if you make sure you’re given them some intravascular leeway.  How do you determine this? Simple enough, make sure your IVC is down at least to below 20mm, and has recovered the classic acxvy and respiratory variation. I personally try to get into the 8-12 mm range, but that’s arbitrary. Here is some good data for 20mm:

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Without further due, here is the NYS Track 2:

 

Please share your thoughts!

 

cheers

 

Philippe

May 31, 2016

Fluids in Sepsis: An EmCrit Webinar! #FOAMed, #FOAMcc

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So a few weeks ago Scott (@EmCrit) asked me to be part of a pretty cool webinar organized by the Greater New York Hospital Association about fluids in sepsis. The gang consisted of David Gaiesky, Emmanuel Rivers and moderated by Scott himself. And for some obscure reason, he asked me to be part of it – much to my honour (terror, also), naturally.  It was only afterwards that he told me it was to help stir the pot and be controversial, challenge the “old school” etc… He seemed to have overlooked that I am Canadian, and inherently and perhaps overly polite and considerate – at least live and in “person”!

We talk about a bunch of stuff around fluids, which, how much, how to assess, etc.

Anyhow, I hope I got a few ideas across, but it was really cool to hear that these gurus do use ultrasound – don’t necessarily strictly adhere to, for instance, EGDT, and also advocate that guidelines are guidelines and not necessarily gold standards.

Here is the link to the webinar for those interested:

 

https://t.co/dbL03Vuqlj

 

And here is the figure for the section where I refer to fluid responsiveness/tolerance:

Screen Shot 2016-02-21 at 9.25.50 AM

I further talk about this in a previous post here.

Scott and I also recorded a debrief which should be coming up in the next weeks on EmCrit – link to follow!

cheers!

 

Philippe

April 8, 2016

Bedside US Procedure: Pericardial drainage – Pearls! #FOAMed, #FOAMcc, #FOAMus

So here is a video of a pericardial drain placement for pre-tamponade in a 33 yr old man, presumptively for a viral pericarditis (cultures and cytology pending).  In this case, the approach was subxiphoid, because this offered a large pocket of fluid with little or no risk of hitting the RV. The apical approach would have been more risky. Due to technical issues, the video only starts once the guide wire is already in place, but there are a couple of teaching points worth sharing nonetheless.

First, it is useful to confirm guide wire placement prior to dilating. Secondly, in cases such as this where the distance to the pericardium is more than a couple of centimetres (it was about 6 cm here), it is nice to be able to confirm under real-time that the dilator is indeed in the intended area. Because the guide wire is highly echogenic, and the dilator is not, one can see the proximal part of the guide wire “disappear” which indicates that the dilator has covered it, now visibly in the effusion. Once the pigtail is  inserted over the guide wire, final confirmation can be obtained by injecting back thru the pigtail and seeing echogenic material (due to minute amounts of air) appear in the pericardium. This is known as the Ajmo sign.

Cheers!

 

Philippe

March 19, 2016

Cerebral & Somatic NIRS (Near InfraRed Spectroscopy) in shock states: tailoring therapy. (PART 1) #FOAMed, #FOAMcc

So I’d mentioned using NIRS to monitor and tailor therapy a few months ago, and promised a more in-depth discussion to come, so here we go.

For this not familiar with the technology or the concept, NIRS measures tissue saturation, predominantly venous. Hence physiologically it is akin to central/mixed venous gases, but localized. Cerebral NIRS found its foothold in the OR with carotid and cardiac surgery, but its use is now expanding. Given typical knowledge translation time of a decade, it should end up joining ETCO2 as a routine vital in monitored units, but probably not soon enough.

So in our unit at Santa Cabrini Hospital in Montreal, we’ve had this technology for about a year (the INVOS system), and have been studying its uses. In this time, three applications have stood out:

  1. Finding the “Sweet Spot” for vasopressors.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate.
  3. Cardiac arrest: CPR adequacy, prognostication and detecting ROSC.

 

  1. Finding the “Sweet Spot” – I think (hope) that anyone reading this with professional interest understands that pressure does not necessarily equal perfusion.  With that in mind, adjusting vasopressors to a pressure makes little sense, and represents at best a guesstimate of perfusion, which is what we really are after. We can all agree, however, that a certain minimum pressure is required, but whether that is 65, 55 or 45 MAP no one can say for sure.  So the way I like to use it is to establish a baseline and watch the direction of the tissue saturation with vasopressor therapy. If the saturation begins to drop off, we may have reached a point at which excessive vasoconstriction is worsening tissue perfusion, and that inflexion point may represent the upper beneficial limit of the vasopressor – this may happen to be under 60 or 65 of MAP.  However, it is key to understand that this inflexion point is reflective of the current state of hemodynamics, such that a change in volume status or cardiac output, in one direction or the other, would likely change the position of this physiological point.  For example,  a volume depleted patient may reach a decreasing tissue saturation point at 55 MAP, but, once volume replete, may reach a higher MAP of 65 or above before a drop in saturation is seen.  Conversely, a patient whose best tissue saturations were around 65 MAP who suffers an MI and sudden drop in cardiac output may now see his perfusion compromised at that same MAP, which would now be achieved with a greater vasoconstriction, less cardiac output and consequently, poorer flow… I posted a case discussion which illustrates this.
  2. Confirmation that therapeutic interventions are hemodynamically appropriate – I feel this is really important. When a patient’s life is literally on the line, and knowing that our interventions are seldom without potential nefarious side effects, it is poor medicine to be introducing a therapy without having some form of monitoring – preferably multiple – that we are headed in the right direction, or at least not making things worse. Of course, we already do this – with BP, sat, lactate, CCO, ultrasound, ETCO2 – but I think using a realtime measure of tissue saturation adds to this. It is also my firm opinion that integrated, multimodality monitoring is necessary – at least until someone develops some form of mitochondrial monitoring which tells us that the cytoenergetics are sufficient to survive. Until then we are stuck with surrogate markers and many of them (e.g. lactate) are the result of complex processes that preclude them being a simple indicator of perfusion adequacy. For instance, when giving a fluid bolus/infusion – after having determined that the patient is likely fluid responsive AND tolerant – one should expect to see an increase in ETCO2 (other parameters being constant), an increase in CO, an increase in NIRS values. The absence of such response should make one reconsider the intervention, because without benefit, we are left only with side effects.

Here is a patient’s cerebral (top) and and somatic (thigh – bottom) and CO values. This patient had an RV infarct and was in shock.

IMG_7948IMG_7946

 

Following initiation of dobutamine, this is what occurred:

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Given that we cannot always predict the response to an inotrope – depending on the amount of recruitable myocardium, it is reassuring to see an improving trend. This enabled us to decrease the vasopressor dose significantly.

Note that, so far, and unless some good evidence comes out, I don’t use a goal value, and so far, I have not identified a value that is predictive of prognosis. However, downward trends usually bode very poorly. For instance, I had a severe chronic cardiomyopathy patient whose cerebral saturation was 15%!!!  But more surprisingly, she was awake, alert and hemodynamically stable. Adaptation.

Part 2 and the stuff on cardiac arrest coming soon!

Please, anyone using NIRS in shock, share your experience!

 

cheers

 

Philippe

January 29, 2016

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).

 

cheers!

Philippe

January 22, 2016

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.

IMG_7538

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.

 

Cheers!

 

 

Philippe

 

Here is a nice little review on lysis: sir04264

December 30, 2015

Bedside Ultrasound for neuro-assessment in the ICU: A Case

So a couple of days ago my colleague Ian Ajmo asks me to take a look at one of our patients for a second opinion. It’s a 75 year old male who had surgery for an incarcerated inguinal hernia during the night and was left intubated, but, despite his last sedation being during surgery (4 am), he still hasn’t woken up (11 am). He is known for a cerebellar glioblastoma but was functional living at home and had been given a one year prognosis.

So Ian was concerned, rightly so, and took the savvy initial step, after noting a GCS of 5 (some minimal reaction to pain), of looking at his optic nerve sheaths (ONS), and found them to be over 6 mm. For those unfamiliar, an optic nerve sheath dilation (ONSD) of 5.7mm (normal <4mm) generally corresponds to an ICP over 2o mmhg.

So this astute finding (as the requisition for a CT was being done) prompted me to do a little further neuro-ultrasound.  Here is the distal carotid doppler:

internal carotid

internal carotid

external carotid

external carotid

So this is done in the upper neck, just distal to the bifurcation, so while extra cranial, the internal carotid nonetheless represents a view into the relationship between arterial flow and intracranial hemodynamics. It takes virtually no experience to see the radical difference in flow between the internal and the external carotid. The EC shows a beautiful systolic peak and diastolic flow. On the other hand, the IC shows a small systolic peak, a bit of retrograde flow, and essentially minimal or no diastolic flow. That is telling us, physiologically, that the ICP elevation has radically limited diastolic flow. This isn’t good.

Next, I do trans-cranial doppler (TCD):

TCD

Now despite good visualization of brain tissue, specifically brainstem (sometimes difficult in men), I struggle to find any blood flow, and finally manage to see what looks like the basilar artery, and has very poor flow, similar to the EC, with a small systolic peak, retrograde flow  and little diastolic flow.

This right away tells us there is a massive ICP elevation explaining the lack of awakening, and a dismal prognosis.

CT:

Confirms a huge RT MCA stroke with 15mm midline shift and foci of hemorrhage.  While waiting for the CT his urine output was > 6 liter, prompting the attending to give some DDAVP and fluids to preserve hemodynamics (at least until the scan).

We withdrew therapy in view of the prognosis.

This case illustrates the usefulness and rapidity of bedside ultrasound to assess functional intracerebral dynamics, which can help diagnosing or ruling out an elevated ICP as a cause for a change in neuro status, or a “non-waking” patient, which is usually due to sedation accumulation, but now always…

 

cheers,

 

Philippe

September 10, 2015

Musings with Jon-Emile and Philippe 4: A Podcast on Pointers, Pearls and Opinions on Tough Ventilation Cases. #FOAMcc, #FOAMed

Hi, so in this little discussion, we go over some points about ventilating ARDS, obese patients, looking for optimal PEEP and other obscure physiological point that we are somehow interested in…

 

Love to hear comments and questions!

 

 

cheers

 

 

Philippe