A Discussion on Fluid Management Protocols with Rory Spiegel. #FOAMed, #FOAMcc, #POCUS

 

So Rory (@EMnerd) is in the process of building a fluid resus protocol for Shock-Trauma, and asked me if we could have a chat about it, which I feel very honored for – and had a brief impostor syndrome crisis – but it’s always great to chat with people who are really bright, really physiological and after the same goal, to make patients better. Always a pleasure to chat with Rory, so here it is.

I really can’t wait to see their protocol, because I think this is a huge and complex endeavor, but has to be done.  I will try to put pen to paper (probably really pixels to a screen but that doesn’t sound as good) and put what I try to do for fluid resus on a diagram of sorts.

Love to hear comments and questions.

 

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

 

Bedside ultrasound case: Fibroids, Syncope and Dyspnea. #FOAMed, #FOAMus, #FOAMcc

So today, a 33F presented following syncope. She was mildly tachypneic wiyh a HR of 135 and BP of 130/80. I’m inserting the clip of my bedside ultrasound evaluation, as this takes place essentially simultaneously with my history-taking:

So this clip runs thru a few views, starting with an IVC long axis, showing a relatively plethoric IVC with minimal variation. This is not normal. Tells me to expect something abnormal downstream, unless someone has flooded the patient with IV fluids. The next view is the parasternal long, then short axis, showing an increased RV to LV ratio, and a small, hypercontractile LV, with septal flattening consistent with RV pressure overload, the “D” sign.  The apical 4 chamber follows with little else to add (difficult to measure TAPSE well in that segment).

So this is sure looking like pulmonary embolism, and I’m already toying with a half dose TPA, MOPETT-style, until the reveals that the cause of her starting oral contraceptives two months ago was to control heavy menses associated with large uterine fibroids… So I figure I’ll buy myself some decision time anyhow by ordering the CT angio – unless in pre-arrest, I don’t thrombolyse without formal confirmation – but I did start IV heparin on the echo findings. Here is the CT:

So this indeed confirms submissive embolism, particularly to the left PA.

Next?  I work in a community hospital, and although I’m totally comfortable thrombolysing PE, in this case, I was concerned about bleeding related to the fibroids, and I haven’t yet figured out a way to embolize bleeding vessels at the bedside, so I felt that the safest thing was to transfer her to a tertiary care center with a solid interventional radiology program. So off she went. I’ll update if anything funky was done like a catheter suction and I can get some clips.

So in terms of POCUS, I think this illustrates how speedily a diagnosis can be made, and although in this case the pre-test probability and index of suspicion was pretty high, it isn’t always!

cheers!

 

Philippe

 

For more POCUS tips, see here!

A Bedside Ultrasound Case & Poll: All Infiltrates Are Not Created Equal. #FOAMed, #FOAMcc, #FOAMus

So I get an early morning call from a really good ER guy informing me of a likely ICU admission: a young guy (30’s) with a bilateral pneumonia and fever whom he suspected might get worse before he got better. He’s given him some fluids and started ceftriaxone and azithromycin. Sounds good to me. Sold. I tell him I’ll come take a look as soon as I roll into work (we do home call).

An hour or so later I head to the ED and see a him, in bed at 30 degrees or so with nasal prongs, maybe a little tachypneic but certainly not in severe distress and not particularly toxic. The nurse informs me that his temperature was apparently 40 degrees. The CXR (I’ll try to put it up soon) shows bilateral infiltrates, more predominant in the lower two thirds of the lung fields. WBC is 14, lactate 2.3.

So this guy had been short of breath for about 2 weeks, having some cough and localized left sided pain associated with movement, cough and pressure. The cough was non-productive.  As I was getting this history (yup, generally bedside ultrasound is simultaneous with history-taking for me), this is what I see:

(parasternal long axis)

(parasternal short axis)

(right lower costal margin)

(you can see this in most of the lung fields)

He has no past medical history or notable family history, drinks occasional wine, has not traveled of late and works as an electrician. He is active and played soccer – the last time a few weeks ago. He came to the ED for dyspnea, but had still been able to go up several flights of stairs, albeit with more dyspnea than he normally would have.

 

 

 

check back tomorrow and let’s see what happens!

 

cheers!

 

Philippe

Bedside Ultrasound Case Debate Part 2: To lyse or not to lyse… #FOAMed, #FOAMcc, #FOAMus

If you haven’t read Part 1, get the story and the cool clips here first:  http://wp.me/p1avUV-ce

 

So the polls are in!  So far at least, 58% of you would blast away with full dose lytics, 26% with MOPETT-style half-dose, 10% content with heparin, and 5% would go for a PA catheter directed lysis.

So 90% would lyse this patient.  I’m glad to hear that, because in my opinion, more patients should be lysed than I see being done around me.

What did I do?  I went for the half-dose lytics, with an excellent result. Within a few hours she was much less dyspneic, BP was up to 110-120 systolic, and though RV dysfunction persisted, it was mostly resolved by the next day.  I think it is important to note that I had a long chat with her, explaining the risk of intracerebral hemorrhage, which I quoted as being less than 2%.  She opted for thrombolysis with the idea of averting cardiopulmonary limitation given her active lifestyle.

I think the physiological rationale for half-dose lytics is good, since, unlike when used for arterial lysis (coronary or cerebral) the entire dose will pass through the lungs. One could argue that the clot burden is larger,  but the resolution seen in MOPETT and in the dozen or so cases I’ve lysed (no intracerebral bleeds yet), rapid resolution of RV dysfunction supports a sufficient response.  I’ve yet to give – but am ready and willing – a “rescue” top-up 2nd half dose if the first hasn’t worked.

I think the other important point in this case is the importance of bedside ultrasound in the assessment of all shock patients. Although I have no doubt whatsoever that my competent colleague would have come to the diagnosis of PE, it may have been minutes to hours later, possibly after having to begin pressors for a lack of response to fluids.  I won’t hypothesize what might have happened in that time. Maybe nothing, maybe not.

She went home a few days later.

This is why the blind administration of fluid resuscitation is a growing pet peeve of mine.  Two litres in sepsis? Ok, probably, but not every shock is sepsis…  I think that in 2014, going on 2015, with virtually all ERs and ICUs equipped with an ultrasound, there is no place for the empiric bolus. It takes all of 5 seconds to look at an IVC, and another 15 to get an idea of cardiac function in most patients. Like a famous corporation says:

Screen Shot 2014-11-13 at 10.31.18 PM

Opinions, rants and rotten tomatoes welcome!

cheers

 

Philippe

 

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 (http://wp.me/p1avUV-9k).   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: http://wp.me/p1avUV-aU and register at www.ccusinstitute.org!

 

cheers

 

Philippe