Bedside Ultrasound Quiz Part 1: a 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So last night, an interesting call from the ED about a 50 year old man who presented with a 3 week history of increasing dyspnea, leg edema, temp of 39,  a lactate of 3.9, an INR of 1.7, elevated LFTs and a WBC of 18, but a BP of 130/75.

Fortunately, I was dealing with a saavy ER doc with some POCUS capabilities, so he also told me he saw a pretty big IVC and he was a bit leery about giving fluids, though this looked like pretty severe sepsis with 3 or 4 affected organ systems…

So I asked him to hold fluids until I got there. Here is what POCUS found:

He revealed a past history of untreated hypertention, and a flu-like illness 3-4weeks ago.

What’s the diagnosis (-es) and management?

Answers & Clinical evolution in part 2 tomorrow!

 

cheers

 

Philippe

 

 

 

 

 

 

 

 

Hepatic Portal Venous Gas (HPVG): a Less Ominous Sign than We Thought? A Case of HPVG associated with massive PE… #FOAMed, #FOAMcc

So a few years ago I had a patient in the ICU, post op for some abdominal surgery, and, using POCUS, I detected a hyper echoic area in the liver, in a wedge shape.  I scanned the patient and, lo and behold, there was a matching area of air-filled hepatic venous sinuses on CT scan. Well, my surgical colleague and I were very concerned and proceeded to inform the patient he would be needing exploratory surgery for what was likely ischémie bowel. He essentially – though in more polite words – told us we were idiots and that his belly felt fine and he didn’t think surgery would be needed at all.

His belly did feel fine. So were his labs. So we worried, but, given this whole thing about free will and consent, etc, couldn’t very well force him into what we felt was necessary surgery.

The next day he was fine. On POCUS, the area of air had shrunk. The next day, it was gone altogether.

We thanked him for his keen clinical acumen and for teaching us a good lesson.

However, we were a bit perplexed, because traditional teaching equated portal venous air with a severe bowel disorder, usually ischemic or inflammatory, with exceedingly high mortality. At least that is what we had been fed. We are both grads of 1999. Hmmm…

So over the next few years we saw a few of these cases, sometimes bad, sometimes not, and a review of the literature (see below)  showed an interesting evolution of the disease. Described in the 1950’s on plain films, hepatic air was a bad omen indeed, with mortality in the 75-90% range. In the CT era, the mortality started to “drop” to the 35-60% range. Now you can find quite a few reports of “surprisingly” good outcomes with conservative management. So this evolution doesn’t represent a change in severity so much as the technological capability to detect smaller and smaller amounts of air in the venous system – just increased sensitivity. And now, with POCUS – ultrasound is the most sensitive detector of air in a vascular tree – the associated mortality is likely to take another drop, not only because of our ability to detect very small amounts of air, but also because we are actually looking at the area, and also in a wider range of patient’ pathologies that those commonly associated with HPVG.

 

Clinical Case: HPVG and PE!

So a couple weeks ago I saw a patient in the ED who’d recently broken an ankle, had her foot put in a boot and managed conservatively and came back dyspneic and tachycardic. Here are a couple of clips:

As always, I start with the IVC:

Big & fixed.

Hepatic veins:

Biphasic flow.

Femoral veins:

So here the source of the problem is pretty clear, a large common femoral DVT.

She wasn’t very echogenic so I don’t have great clips of the heart but she had a dilated and hypocontractile RV with a McConnell’s sign (preserved apical contraction), small and hyper dynamic LV with septal flattening.

Now here is where it gets interesting, the portal vein:

You can clearly see bubbles traveling up the portal vein. Ominous, or not?

So clinically, her abdomen was normal, she had no abdominal symptomatology at all…

 

Pathophysiological musings:

So the severe RV obstruction resulted in significant venous congestion. Additionally, the decreased cardiac output – as manifested by a lactate of 4 and mild tachycardia/hypotension (110 HR, BP sys 90’s) was clear.

The etiology of HPVG in the literature isn’t clear – mucosal disruption, bacterial gas are all mentioned but as far as I could find, no definitive answer.

Is it possible that there is a “normal” inward leak of mucosal gas that is normally fully dissolved in the venous bloodstream, but that, in cases of low flow and/or venous congestion, the dissolution capacity (per unit time) decreases, and that gas comes out of solution?  Alternately, those who have increased intraluminal pressure (gastric distension, etc), the increased transmembrane gas driving pressure may overload an adequate blood flow…

This would explain the benign course of many patients, particularily those with gastric dilation.

 

Clinical course:

Based on hemodynamics, tachypnea and, to some degree, venous congestion, I decided to thrombolyse her using 1/2 dose lytics. Within a couple of hours her HR decreased to the 90’s and BP rose to 110 systolic.  Echographically, however, the IVC/RV findings remained similar, but the HPVG decreased. By the next day, HPVG was altogether gone, lactate had resolved and dyspnea was significantly better.

 

Take Home Message:

HPVG, although not quite as poor a prognostic sign as once thought, nonetheless warrants concern and investigation, even if the abdominal exam is entirely normal and without symptomatology, as correction of an underlying cause of “benign” HPVG (whether low-flow or bowel distension) would still need to be addressed.

In the meantime, I suspect that, reported or not, this has been noted by other POCUS enthusiasts, since we are now looking more frequently at this area, and are dealing with patients with low-flow states, congestion, bowel obstruction/ileus or more than one of these.

Hopefully some investigators will take a look at this phenomenon and delineate the pathophysiological mechanism!

Love to hear of your experience with this.

cheers!

 

Philippe

For those interested in POCUS, see here for a quick read primer on clinical applications of POCUS.

 

HPVG Review article 2009:

wjg-15-3585

 

Transpulmonary Pressure (Ptp)-Guided Ventilation: A Case. #FOAMed, #FOAMcc

So in my last post I quickly reviewed the basics of Ptp-guided ventilation. So here is a case. We had a woman in her 60’s admitted with bilateral pneumonia, intubated and ventilated. She is morbidly obese and diabetic. Despite antibiotics and usual care, she was getting progressively worse, and was labelled “ARDS.”  POCUS showed she was not in terrible venous congestion, and she had been digressed to a relatively normal IVC. Slowly her ventilator settings crept up to a PEEP of 14 and FiO2 of 100%. As the plateau pressures were approaching 35, we were getting a little antsy, so decided to put in the esophageal balloon and get a better grip as to what was going on.

Here are her original readings:

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So here we can see that her Pes in expiration is around 23. With a PEEP at 15, that gives us a Pep (exp) of -8. That likely represents a fair bit of atelectasis/derecruitment. Here are some measurements:

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Her dynamic compliance is 21, and static 24. Not too great. Her PV loops are interesting, certainly not showing any over distension (the penguin beak look), and, as Jon Emile Kenny (@heart_lung) cleverly explains about the Pop tracing:

“On this patient, the stress index appears to be low, which is somewhat consistent with your Ptp tracing. there is a terminal fall in the Ptp [wave looks like an upside down U] which suggests terminal airway recruitment; that is, during the terminal portion of the breath, the Ptp is falling with equivalent volume delivered [again only works with square-wave/constant flow]. in other words, if [at the end of the breath] less Ptp is needed to accommodate equivalent flow/volume, there is terminal increase in compliance/decrease in elastance – or lung units are recruitedSo these numbers suggest that there is extrinsic compression of the lung, due to chest wall weight and abdominal pressure. This makes the airway pressure (Paw) not representative of alveolar stretch, and hence not a good guide of ventilation. The PEEP, despite being fairly high, is below the level needed to prevent atelectasis.”

Indeed Jon, that appears to be the case.

So we started to raise the PEEP, trying to get the Ptp (exp) closer to zero:

 

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So we can see that our Ptp (exp) is approaching zero, and the PV loops suggest there is still no over distension. In fact, the compliance, as Jon had predicted, improves slightly. The plateau pressures are up into the mid 40’s which, without a balloon, would be pretty concerning. But the Ptp (insp) is less worrisome, in the mid 20’s, about at the limit we’d like.

At this point, still seeing that increasing compliance, we continue raising the PEEP to 23, and actually see the plateau pressures start to drop, consistent with having recruited lung. Now the Ptp (insp) is 23, and the compliances have increased.

 

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We thus leave things as is, and by the next morning, we are down to 30% FiO2. Here are the before and after CXRs:

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So a fair bit of her “ARDS” was actually atelectasis related to obesity and increased intra-abdominal pressure, and that what seems like exceedingly high PEEP is actually just enough to prevent atelectasis.

 

Love to hear from others who use the technology, or just interested!

cheers

 

Philippe

 

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.

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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

MOPOCUS: A great synopsis by Ha & Toh. #FOAMed, #FOAMcc, #FOAMus

Just came across this review and figured I should share. The authors make a great synopsis and review of POCUS in acute illness:

MOPOCUS Review by Ha &To

The only thing I would add to this is a more physiological way to assess the IVC, which I’ve blogged about here.  Sadly, I’ve heard a few people stating how they didn’t want to get into the dogma of IVC ultrasound, that it wasn’t reliable, etc.  The IVC doesn’t lie. It’s just not a recipe. The IVC findings have to be integrated into the rest of the echo graphic and clinical examination.  Trying to use it as a single value is akin to using serum Na+ as a diagnostic test for volume. It works only sometimes.

Please spread among the POCUS non-believers. We’ll convert them, slowly but surely. But the sooner, the better for the patients. Again, there’s no excuse to practice acute care without ultrasound. It’s not right. I’m not saying every probe-toting MD is better than one without, but everyone would up their game by adding POCUS, once past the learning curve!

cheers!

 

Philippe

Tom Woodcock: The Revised Starling Principle and The Glycocalyx! #FOAMed, #FOAMcc

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So today, I had the chance of having a private tutorial with Dr. Thomas Woodcock (@thomaswoodcock) about the glycocalyx and the revised Starling principles.  For anyone interested in fluid resuscitation, this is an area you have to delve into. The basic principles we all learned (which are still being taught) are basically the physiological equivalent of the stick man we all started drawing as toddlers: overly simplified and far from an accurate representation of reality.

Now my first disclaimer is that I have been a colloid supporter for many years. My physiological logic for that had been to minimize the crystalloid spillover into inflamed/septic areas, particularly the lungs and abdomen, when those are the septic sources. However, I was likely misled by my education and lack of knowledge about the endothelium.

So I stumbled upon the whole glycocalyx thing a couple years ago, and this prompted me to try more enteral fluids – the only way fluids normally ever enter the vasculature – but little else. Aware that it’s there, but unsure what to do about it.

Now a year and a half ago, Andre Denault, my closest thing to a mentor, casually dropped the line to me about albumin not working. “Don’t use it. It doesn’t act the way we think it does.”  But it was a brief chat, and I didn’t get to pick his brain about it.  Just a few weeks ago, I discuss with Jon Emile (Kenny), and he’s coming to the same conclusion.  Damn. I’m finding it a bit harder to hang on to my albumin use, which is beginning to look a bit dogmatic and religious.

Here is Jon-Emile’s take on it – a must-read.

Here is Tom Woodcock’s site and article – another must-read.

And here is my discussion (in two parts) with Tom (to skip the silence, skip forward to about 30 seconds into each – sorry my editing skills are limited!)

 

Bottom line?

Probably stick to isotonic crystalloids, and some hypertonics.

 

Love to hear some thoughts!

Cheers

 

Philippe

 

 

The NYC Tracks with Jon-Emile: The Glycocalyx – The Next Frontier. #FOAMed, #FOAMcc

I was really psyched when Jon-Emile mentioned he would like to talk about the glycocalyx.  I first blogged about it here, basically when I stumbled on the extensive literature on this huge organ we have been completely ignoring in terms of physiology and therapeutics. It lines our entire endothelium, which is where most of our therapeutic interventions go, and we only heard of it in passing, possibly in histology class as med 1’s.   Hmmm.  Anyhow, here, Jon-Emile and I talk about it a little, discuss possible clinical implications, but more importantly Jon mentions the relatively new blog of Dr. Thomas Woodcock (@thomaswoodcock), http://www.fluidtherapy.org, who is one of the pioneer clinicians who have studied the glycocalyx, and who is now trying to bridge the bench to the bedside.

I’ve been fortunate enough to get in touch with him and we’re planning to record some discussions soon.

So, in my view, the glycocalyx is a formidable force we have been ignoring, and have been damaging often with our interventions. I’m hoping to see some developments allowing glycocalyx assessment outside of the labs in order to give us the tools to reassess every fluid in terms of the relative damage it does to what is essentially the gatekeeper between the blood and the tissues.

Love to hear some comments!

Here is the chat with Jon:

 

cheers

 

Philippe