ICU

February 12, 2014

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.

thanks!

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.

February 11, 2014

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!

 

Philippe

January 28, 2014

Pleural effusion in the sick patient (Part 1of 3): Don’t miss it!!! #FOAMed, #FOAMcc

This, in my opinion, is an under-recognized problem when bedside ultrasound is NOT a routine part of examination of critically ill patients. I’m happy to say that as many of my colleagues have been picking up probes, it is somewhat less of an issue now, whereas a couple of years ago I’d often put in 4 or 5 pigtail catheters on day 1 of taking over the ICU.

The first and foremost reason for this is that the portable supine ICU CXR sucks at picking up the small to moderate to, yes, even the large pleural effusion.  Largely owing to the fact that many of our patients have some lung parenchymal abnormalities and to the recumbent position that causes a layering of the effusion, it is often difficult to properly assess the size of a pleural effusion.  Radiologists will usually report the presence of a probable effusion, but quantification is difficult, and physicians not performing routing bedside sonography will often realize the presence of a submassive effusion only on CT scan – after all it isn’t like you can turn and rotate your patient to percuss the shifting dullness, can you?  Not very practical.

So the following can often be seen:

pleural effusion

this is fairly large, or you might see:

pleural effusion and pneumonia

So the obvious and critical question is: when is it necessary to drain?

There are two elements to this question:

a) for diagnostic purposes: unless the diagnosis is clear (eg CHF, post-resuscitation “michelin man” patient, etc) a new effusion should be tapped.  Panapneumonic effusions, in particular, warrant ruling out empyema unless there is a compelling reason not to.  For diagnostic purposes a 22g needle usually does the trick unless you have frank pus – which generally shows up differently on ultrasound.

b) for therapeutic purposes: effusions are space occupying lesions which compress the lung and result in a variable degree of respiratory compromise, depending on chest wall and diaphragmatic compliance, as well as effusion volume.  The clinical effect is highly variable due to the above as well as the degree of parenchymal lung disease and the degree of PEEP.  In the ICU or ED, a simple way to think about it is that if your patient is in respiratory failure and has a large effusion, chances are that draining it will improve things.  It gets a little more controversial and complicated if you have a patient who is mildly dyspneic with a moderate sized effusion.

Here are a few clinical scenarios I like:

Mr. A is a 65 year old man with CHF, intubated, with large bilateral effusions. He has been aggressively diuresed to the point of his IVC being less than 5mm in diameter.  He has not been able to wean in the last 48 h.

Yes, I definitely drain this fellow. Been there and done that time and time again.  The pleural effusions are essentially the last to resolve (being the most “distal” to the circulation – vs the alveolar tissue itself) and hence can lag and cost a few more days or more of ventilation).

Mr. B is a 47 year old man with pneumonia, breathing spontaneously with a moderate (maybe 500ml) effusion. It appears free flowing and clear, he is afebrile with an improving white count, and mildly dyspneic.

Nah, I skip on this one.  If fever and WBC recur, I do a diagnostic tap to r/o empyema.

Mrs. C is intubated on PEEP 18 FiO2 85% for ARDS due to pancreatitis. She has some degree of intraabdominal hypertension (IAP 18) and has bilateral moderate pleural effusions, maybe 400-500ml.

Yup. She can physiologically benefit from decreased intra-thoracic pressure, both from the ventilatory and the intra-abdominal pressure standpoint (Remember the diaphragm is not a rigid structure so that IAP and ITP are very similar in most cases).

So is there any evidence for this?  Some. And that’s for part 2, coming within the next days. Part three will explain and show my procedure of choice for drainage.

Thanks!

love to hear what other guys’ practices are!   Apparently only about 15% of ICU guys “routinely” drain effusions.

Philippe

COMMENTS

Hi Philippe,
I am very happy to read your post tonight, bacause I am part of that 15% and luckily most of my colleagues are in the same group. I agree in particular when you say that pleural effusions are the last to resolve, being the most “distal” to the circulation. I often find patients, at a certain point during their ICU stay, be not only like a “michelin man” but also (and at the same time!) hypovolemic. I call this situation, when I try to explain it to residents, “empty in full” (maybe in english it doesn’t sound as good as in italian): we are trying with diuretics and some fluid restriction to manage those extravascular fluids that prevent weaning from mechanical ventilation, but often we get the only effect of causing renal failure rather than eliminating pleural effusions. In this case the only way is to drain.
Another important point is that bedside chest x-ray is absolutely useless when you have to discriminate between pleural effusion and parenchimal consolidation, both of them often coexisting in ICU patients.
In our routine we use 14-gauge single lumen CVCs, inserted with Seldinger technique and ultrasound assisted procedure, effective in 95% of the effusions and less invasive than a pleurocath (that we use most of the times for pneumothorax) or a real chest tube, which I keep for blood or traumatic pneumothorax.
Greetings from Italy,
Marco

 

Glad to hear it Marco!  I started with CVCs as well before we were able to find inexpensive pigtails – email me for info if you want I don’t want to “brand” these things!  They are actually really good because I found CVCs would often occlude. Patient comfort with either is so much more than chest tubes. 

Great point about the “michelin man” who is very “wet” but intravascularly dry, which we see commonly post acute phase of critical illness, especially when physicians are so keen to use crystalloids.

thanks for reading!

 

Philippe

January 15, 2014

Bedside Ultrasound Clip Quiz #7: Discussion #FOAMed, #FOAMcc

So here is the clip again.  This is a transverse epigastric view with the IVC in short axis and the hepatic veins (bunny ears) draining into it.  We can see bright hyperechoic material moving up and down, which are air bubbles.  Note that this is air in the hepatic veins and NOT the portal veins, which can be “relatively” common due to ischemic bowel and a few unusual causes.

Air in the systemic hepatic circulation is quite unusual.  Obviously, air anywhere in the circulation implies a breach of vascular integrity somewhere – in the case of portal venous air, the breach is in the bowel microvasculature as the bowel breaks down. In the case of air in the hepatic veins, we are looking at air coming from (a) the lower body vasculature, so in the absence of trauma the most likely cause is iatrogenic from a femoral line, or (b) the upper body vasculature if associated with tricuspid regurgitation (iatrogenic or lung vascular injury coupled with positive pressure ventilation).

Here is an article discussing hepatic vein air.

533.full

Their clinical point is important to note – you have to investigate to get an idea of the amount of air and the possible source.

So this patient was transferred to my ICU from a smaller centre for more aggressive care. He was in profound septic shock felt to be pulmonary in aetiology, on levo/vaso/epi and dobutamine, ventilated on 100% with PEEP 16. My basic CUSE (critical ultrasound examination) done on essentially every critical care patient revealed this rapidly and, concerned that air embolism had occurred (femoral line was in situ at arrival), I scanned him.

Here is the CT:

photo-8 copy

 

photo-7 copy

You can see a small sliver of air in the IVC, and none was noted in the liver or in the heart (which was what I wanted to r/o). Now of course ultrasound is much more sensitive than CT for identifying small air bubbles (a CT image is a composite of several slices so a small bubble is lost) but when he returned form CT and I scanned him again, the hepatic veins no longer had air, but the IVC was full of air below the liver (as in the CT), so I think moving the patient had relocated the air.

More to come on the clinical story and investigations of this particular case, which is still ongoing.

thanks for looking!

 

Philippe

December 10, 2013

The Glycocalyx: an overview for the clinician. #FOAMed, #FOAMcc

Ok, so I’d had a couple of glimpses at articles in the past few years which referred to the glycocalyx, but, in truth, I tend to read most of the “bench” studies a little, well…quickly.  So basically, when I listened to Paul’s (Marik) recent lecture at Scott’s (Weingart, emcrit.org) New York Sepsis Collaborative, I started to dig a little…and whoa! And then of course, then now-famous expose by John (Doe?) on EmCrit continued to convince me that this is definitely something I need to pay attention to! Its not like there hasn’t already been a high level of scrutiny of the glycocalyx in the field of sepsis.  Google it. Its like a whole new world. It just hasn’t yet translated into an effective therapy, but nor has it seemed to spread into general awareness, and it seems like it’s high time it does, since it is the interface between the blood and the body – a “blood-body barrier” of sorts.

So here we go, a crash course on the glycocalyx for the clinician in the trenches…

The existence of an acellular layer lining the endothelium was described by Luft some 40 years ago (1), and in the last decade has come under scrutiny for its role in various pathophysiological states, which seems to be quite exhaustive. This has not yet translated into diagnostic or therapeutic interventions, but it seems its properties, or at least those we are currently aware of, should be kept in mind when we are faced with therapeutic choices given that some of these may have an effect on the glycocalyx.

Its existence was deduced due to the lower capillary hematocrit – meaning that the hematocrit in the capillaries, adjusted for the luminal volume, is lower than that of the large or medium vessels, implying an area where there are no red cells. This was confirmed by electron microscopy and found to be a gel-like epithelial lining which acts as an interface between the blood and the endothelial cells, of a thickness of about 0.5 um at the level of tha capillaries, and thicker in the larger vessels.

So what is it made of? Its is essentially a meshwork of glycoproteins and proteoglycans, anchored to the epithelial cells, in which many soluble molecules are enmeshed. It is important to note that there is a dynamic equilibrium between this layer and the adjacent flowing blood, which will affect the thickness and composition of the glycocalyx. The layer seems to be vulnerable to both enzymatic degradation as well as to shear forces, in variable degrees. Enzymatic removal of components seems to radically alter properties, pointing to a strong synergistic effect of the various components. It is a constantly shedding and regenerating structure.

glycocalyx em pic

EM view of the glycocalyx (reproduced with authors’ permission from Reitsma et al.)

glycocalix pic2

(reproduced with authors’ permission from Reitsma et al.)

Major components:

– Proteoglycans (protein core with chains of glycosaminoglycans) are the “backbone” of the glycocalyx, and consist of syndecans, glipicans, mimecan, perlecans and biglycans.

– Glycosaminoglycans (linear disaccharide polymers of a uronic acid and a hexosamine) are predominantly heparan sulfate (50-90%), then dermatan sulfate, chondroitin sulfate, keratan sulfate and hyaluronan (or hyaluronic acid).

– Glycoproteins are also part of the “backbone” structure and the main types are the endothelial cell adhesion molecules ( -cams, which are selectins, integrins and immunoglobulins) and components of the fibrin/coagulation system.  E- and P-selectins as well as others are involved in leukocyte-endothelial interaction and diapedesis, an important aspect of local inflammation.

– Soluble components are also embedded in the glycocalyx such as proteins and soluble proteoglycans and are important in preserving the charge of the layer and play critical roles in functionality.

Function of the glycocalyx (as far as we know…)

a. gatekeeper

It is a key determinant of vascular permeability. Partial enzymatic removal without damage to the endothelial cells themselves result in a radical change in permeability in aminal models. Charge, size and steric hindrance affect permeability. The glycocalyx has a highly net negative charge towards the bloodstream – neutralizing this induces an increase in cellular albumin uptake.

Weinbaum introduced a new model integrating the glycocalyx in the classical (but now outdated and disproven) Starling model of microvascular fluid exchange. The revised Starling principle stresses the importance of an intact glycocalyx.

Its role with cellular elements is interesting, as it contains key elements for interaction (-CAMs) but at the same time physically prevents direct interaction between cells (WBC, RBC, plt) and the endothelium. This clearly points to a pivotal role in controlling the interaction. Damage by various methods consistently shows increased neutrophil-endothelial interaction (often termed “leukocyte rolling”). It isn’t much of a stretch to see how the glycocalyx will thus be involved in the control of local inflammation.

b. mechanotransduction

The glycocalyx provides mechanical protection from shear stress to the endothelium.  Increased shear leads to upregulation of synthesis, and correspondingly, thicker glycocalyx is found in high shear areas.

c. microenvironment

Receptor binding, local growth and repair, and vasculoprotection. For instance, ATIII is bound to the glycocalyx (inhibits procoagulants), as well as superoxide dismutase, key in reducing oxidative stress and maintaining MO availability.

Clinical implications…

Now this is the real question.  I think that the first step is acknowledging the presence and importance of the glycocalyx, and trying to discern which of our interventions may have an impact.  It is quite clear that enzymes, cytokines and ischemia/reperfusion all damage the glycocalyx and result in increased cellular interaction and permeability. In a way this can explain the entire “SIRS” spectrum with diffuse damage resulting from an insult that may or may not be infectious in origin. Obviously, we know to avoid anything that might cause the above.

I think we can divide our interventions into two types:

a. those that inherently disrupt the glycocalyx –

b. those that secondarily disrupt it via another mediator – eg over-resuscitation and ANP/BNP (John’s “evil twins”) elevation causing breakdown.

Here are some interesting facts, in no particular order of importance:

a. in acute hyperglycemia and in type I diabetes, there is significant loss of glycocalyx volume.

Nieuwdorp M, van Haeften TW, Gouverneur MC, Mooij HL, van Lieshout MH, Levi M, Meijers JC, Holleman F, Hoekstra JB, Vink H, Kastelein JJ, Stroes ES (2006) Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo. Diabetes 55:480–486.

Nieuwdorp M, Mooij HL, Kroon J, Atasever B, Spaan JA, Ince C, Holleman F, Diamant M, Heine RJ, Hoekstra JB, Kastelein JJ, Stroes ES, Vink H (2006) Endothelial glycocalyx damage coincides with microalbuminuria in type 1 diabetes. Diabetes 55:1127–1132

b. high fat/high cholesterol diet and high LDL levels disrupt the glycocalyx. The co-infusion of superoxide dysmutase and catalase with ox-LDL abolishes the glycocalyx shedding found with ox-LDL infusion only. (not exactly a big surprise, but certainly brings up a therapeutic possibility in acute coronary events, especially NSTEMIs…)

Vink H, Constantinescu AA, Spaan JA (2000) Oxidized lipoproteins degrade the endothelial surface layer: implications for platelet–endothelial cell adhesion. Circulation 101:1500–1502

van den Berg BM, Spaan JA, Rolf TM, Vink H (2006) Atherogenic region and diet diminish glycocalyx dimension and increase intima-to-media ratios at murine carotid artery bifurcation. Am J Physiol Heart Circ Physiol 290:H915–H920

c. hydrocortisone and antithrombin prevent TNF-a induced shedding of the glycocalyx. (we never really knew how steroids help in sepsis; ATIII trials failed, but were they designed with glycocalyx-sparing in mind…?)

Daniel Chappell MD, Klaus Hofmann-Kiefer, Matthias Jacob, Markus Rehm, Josef Briegel, Ulrich Welsch, Peter Conzen, Bernhard F. Becker TNF-α induced shedding of the endothelial glycocalyx is prevented by hydrocortisone and antithrombin Basic Research in Cardiology, January 2009, Volume 104, Issue 1, pp 78-89

 d. endotoxemia damages the pulmonary vascular endothelium and results in ALI (now the neutrophils can attach and activate inflammation…)

Eric P Schmidt, Yimu Yang, William J Janssen, Aneta Gandjeva, Mario J Perez, Lea Barthel, Rachel L Zemans, Joel C Bowman, Dan E Koyanagi, Zulma X Yunt, Lynelle P Smith, Sara S Cheng, Katherine H Overdier, Kathy R Thompson, Mark W Geraci, Ivor S Douglas, David B Pearse & Rubin M Tuder The pulmonary endothelial glycocalyx regulates neutrophil adhesion and lung injury during experimental sepsis, Nature Medicine 18,1217–1223 (2012)

e. sepsis and major abdominal surgery damage the glycocalyx (a good example of common pathway pathophysiology…)

Jochen Steppan, M.D., Stefan Hofer, M.D., Benjamin Funke, M.D., Thorsten Brenner, M.D., Michael Henrich, M.D., Ph.D., Eike Martin, M.D.,Jürgen Weitz, M.D., Ursula Hofmann, M.D., Markus A. Weigand, M.D.Sepsis and Major Abdominal Surgery Lead to Flaking of the Endothelial Glycocalix Journal of Surgical Research Volume 165, Issue 1 ,Pages 136-141, January 2011

f. molecules (eg Slit2N,  good old aPC) that enhance or preserve barrier function have shown some success in animal models. (the key might be to using a bunch of them at once, not one of them vs placebo)

N. R. London, W. Zhu, F. A. Bozza, M. C. Smith, D. M. Greif, L. K. Sorensen, L. Chen, Y. Kaminoh, A. C. Chan, S. F. Passi, C. W. Day, D. L. Barnard, G. A. Zimmerman, M. A. Krasnow, D. Y. Li, Targeting Robo4-dependent Slit signaling to survive the cytokine storm in sepsis and infl uenza. Sci. Transl. Med. 2, 23ra19 (2010).

…and this is just the tip of the iceberg. Seriously, google it…

Conclusion:

For now, it is difficult to make any hard recommendations, but it has certainly made me pause to regroup and re-strategize. I think the critical thing is to reframe our thinking and redesign our approach to be a glycocalyx-sparing therapy.

In sepsis therapy, so many molecules have failed, but little emphasis so far has been on targeting the glycocalyx, and in all likelihood, the key is not in finding the “magic bullet” but rather using multiple interventions to bolster it. One could think of this as the sepsis “chain-of-survival”, and now that we can see the complexity of the glycocalyx, it is easy to understand how no one therapy, even if it did do its job, would succeed in preventing the degradation of the other links in the chain, and fail.  In all likelihood, a successful strategy will probably involve the following:

1. fancy molecules to prevent glycocalyx damage.

2. fluid choices which are glycocalyx-friendly.

3. fluid in just the right amount (not by macro/volume-responsiveness but by micro/glycocalyx management).

4. rapid diagnosis/abx/source control, etc, all the good stuff we know about.

5. preventing hyperglycemia.

A trial like that would be a monumental undertaking. I can only hope someone does it.

My next step, as a guy in the bedside trenches and not at the bench, after gaining a modicum of understanding on the topic, will be to delve deeper into the effects of currently available fluids on the glycocalyx.  Look for a post on that in the next weeks.  As a starter, everyone should review Woodcock & Woodcock’s excellent clinical review.

And if anyone has any amazing information to share, please do!!! That’s what #FOAMed is for!!!

Suggested viewing/reading:

Woodcock and Woodcock, BJA 2012,  http://bja.oxfordjournals.org/content/early/2012/01/29/bja.aer515.full.pdf+html

Broken Barriers: A New Take on Sepsis Pathogenesis Neil M. Goldenberg,1* Benjamin E. Steinberg,1* Arthur S. Slutsky,2,3,4 Warren L. Lee2,4 Science Translational Medicine, 22 June 2011 Vol 3 Issue 88 88ps25

Click to access Science_Translational_Medicine_2011_Pathogenesis_of_Sepsis.pdf

a great article on understanding the glycocalyx in sepsis by a U of T gang!

emcrit:

http://emcrit.org/blogpost/best-fluids-comment-ever/

http://emcrit.org/podcasts/fluids-severe-sepsis/

http://emcrit.org/podcasts/paul-marik-fluids-sepsis/

all must-listen/watch material!

other refs.

Luft JH (1966) Fine structures of capillary and endocapillary layer as revealed by ruthenium red. Fed Proc 25:1773-1783

Reitsma et al, The endothelial glycocalyx: composition, functions, and visualization, Eur J Physiol (2007) 454:345–359

Zhang X, Adamson RH, Curry FR, Weinbaum S (2006) A 1-D model to explore the effects of tissue loading and tissue concentration gradients in the revised Starling principle. Am J Physiol Heart Circ Physiol 291:H2950–H2964

November 30, 2013

Bedside Ultrasound Clip Quiz #4 – #FOAMed, #FOAMcc

So you’ve been doing ACLS for a few minutes in the ED on an elderly male who collapsed at a bus stop and shocked out of VF on the scene by EMS, and when you do a 3 second pause to assess the heart, just after an epi got flushed, this is what you see in the subxiphoid view:

 

Is this a case of tamponade?

Scroll below!

 

 

 

 

 

 

 

 

Nope!  There’s no pericardial effusion, and the atria are huge!  What you do see is microbubbles from the flushed IV medication in the RA and RV, and severe LV dysfunction.   The severe LA dilation suggests at least a component of chronic overload (also supported by significant leg edema in this case). Note that you can have severe LV dysfunction (post-resuscitation myocardial dysfunction or PRMD) after cardiac arrest of ANY etiology and does not necessarily imply pre-existing LV dysfunction or predict eventual LV function.

 

 

 

 

November 27, 2013

A Paradigm shift: re-thinking sepsis, and maybe shock in general… #FOAMed, #FOAMcc

Thomas Kuhn, physicist and philosopher, in his groundbreaking and science changing text, The Structure of Scientific Revolutions, states that:

“Successive transition from one paradigm to another via revolution is the usual developmental pattern of a mature science.”

In other words, a science has growing pains and is bound to have a fair bit of debate and controversy, until a new paradigm becomes dominant.  I think that there is a current – in part prompted by the power of socio-professional media which has allowed minds to connect and knowledge to spread – that will see many of the things that are now “Standard of Care” out the door.

So first of all, the following are must-listens, the first a lecture by Paul Marik, whom I have had the chance to collaborate with in the last years and respect greatly, on knowledge, experience, and even more on his refusal to take anything for granted and being in a seemingly-constant quest for the improvement of medicine.

The second link is Scott Weingart’s take on it, which I think is equally awesome.

I think Paul is pushing the envelope in an essential way, and Scott does a fantastic job of seeing or putting it in perspective. Enjoy:

http://emcrit.org/podcasts/paul-marik-fluids-sepsis/

EMCrit 112 – A Response to the Marik Sepsis Fluids Lecture

My (very) humble opinion on this is a rather simple, almost philosophical one:  why are we seemingly obsessed with treating a predominantly vasodilatory pathology with large amounts of volume?  I’ve said this in previous posts and podcasts, but this, in my opinion, is largely cultural and dogmatic. “Levophed – Leave’em dead” is something I heard as a student and resident, and came to take for granted that I should give lots of fluid in hopes of avoiding pressors… But there’s no evidence at all to support this.  The common behavior of waiting until someone has clearly failed volume resuscitation before starting pressors befuddles me (think how long it takes to get two liters of fluid in most ERs…).  If I was in that bed, I’d much rather spend an hour a bit “hypertensive” (eg with a MAP above 70) than a bit hypotensive while awaiting final confirmation that I do, in fact, need pressors.

I strongly suspect that it’s just a matter of improving vascular tone, giving some volume (which may be that 3 liter mark), and ensuring that the microcirculation/glycocalyx is as undisturbed as possible. Now when I say it may be the 3 liters, I firmly believe this will not apply to everyone, and that it will be 1 liter in some, and 4 in others, and that a recipe approach will be better than nothing, but likely harm some.

I think that blind (eg no echo assessment) of shock is absurd, and for anyone to propose an algorithm that does not include point-of-care ultrasound is only acceptable if they are in the process of acquiring the skill with the intention of modifying their approach in the very near future.

The whole microcirculation/glycocalyx is absolutely fascinating stuff, and undoubtedly will come under scrutiny in the next few years, and it is definitely something I will focus on in upcoming posts & podcasts. Our resuscitation has been macro-focused, and certainly it is time to take a look at the little guys, who might turn out to have most of the answers. For instance, there is some remarkable data on HDAC inhibitors (common valproic acid) and their salutatory effects in a number of acute conditions such as hemorrhagic shock (Dr. Alam) which have nothing to do with macro-resuscitation, and everything to do with cell signaling and apoptosis. Hmmm…

please share your thoughts!

thanks

Philippe

November 18, 2013

Enough with the “Normal” Saline!!!!! #FOAMed, #FOAMcc

Enough with the “Normal” Saline!
So its been about a year since a JAMA article (http://jama.jamanetwork.com/article.aspx?articleid=1383234) finally showed that the downside of 0.9% saline isn’t just theoretical, but has some associated clinical morbidity (bad for the kidneys!).  Sadly enough, it still seems to be the routine fluid used for boluses. Whether the ER, hospitalist or intensivist, residents, students…it seems people are reluctant to let go.
Today, rounding in the ICU, I was changing an order for a bolus from another doc from NS to RL, and a nurse asked me why.  I gave her a capsule summary and she was in disbelief.  “Come on Phil, they wouldn’t call it normal saline if it wasn’t!”
I’m an internist by training, so naturally I grew up using NS, since that’s what all the attendings and residents used around me.  Ringer‘s was the stuff the surgeons used, so well, I guess it had to be wrong…no?
So forward to 2001 and John Kellum‘s lecture on acid-base I’ve previously mentioned, and my exploring Stewart’s Physicochemical Approach, and wait, I look at the back of a bag of NS, and find out, much to my dismay, that the stuff I’ve been using like holy water has a pH of 5.6.  And who have I been giving liters and liters of this stuff to?  Yup, mostly patients with acidosis. Hmmm. Interesting. So although I don’t necessarily advocate correcting metabolic acidosis for the sake of doing so (see my previous post on bicarb), I’m not a proponent of worsening acidosis either, even if by another mechanism.
I think there are a number of factors that have resulted in this situation.  For starters, there is the issue of false advertising – the “normal saline” monicker has been influencing subliminal thought for decades (think Malcolm Gladwell thin-slicing), making physicians feel they are giving and inherently “good” substance.  Then there’s the whole tribalism thing with the surgeons vs non-surgeons making all the non-surgeons polarize away from RL (not that RL is perfect, just a bit better, and certainly closer to “normal”). Finally, there’s this sad, sad factor that makes people, even (or maybe even more) smart people reluctant to accept that they have been doing something wrong (or, for those who are offended right now, not ideal) for a long time (I sure was) and prefer to fight it and rationalize it for a few more years until, eventually, the evidence becomes overwhelming or the changing of the guard has fully taken place.
I think what we should be hanging on to is not a drug or a fluid but rather what we learned in the first couple of years of med school: physiology.  Now mind you, at that point we (or most of us) didn’t have a clue how to use it for anything more that answering multiple choice questions, but at some point, we have to go back to it and realize that is what we should be basing our assessment of our therapeutic acts and decisions.
So…if I have a situation where I am low on chloride, I might want to use NS. But otherwise, let try to give something whose composition is a bit closer to our own than NS is.  So, for my students and residents, don’t let me see you prescribing boluses of NS.  If you really, really need to, wait until your next rotation please.
thanks!
Philippe
ps for a great review of the original aritcle, please see Matt’s on PulmCCM at :
Reply:  by Marco Vergano
Totally agree!
I have been struggling for years with the bad habit of some of my colleagues prescribing NS as the most harmless and physiologic replacement fluid. Here in Italy we don’t have such a clear separation between internists and surgeons about NS/RL choice: the bad habit of easily prescribing NS is ubiquitous.
Given the results you mentioned about the increased incidence of renal failure with NS, I am wondering if the ban on ALL starch solutions would have been necessary after the introduction of new balanced starch/electrolyte solutions.
What I really don’t like about RL is that it’s not only hypotonic, but also low in sodium. In our ICU we often have many ‘neuro’ patients (trauma or vascular) and sodium variations become a major issue. Also I prefer Ringer’s acetate over lactate on most of the patients who struggle to ‘manage’ their own lactate.
So my favorite solution remains our good old “Elettrolitica reidratante III” (very similar to Plasma-lyte).
November 14, 2013

Bedside Ultrasound: The Sluggish IVC – something to look for… #FOAMed, #FOAMcc

So take a look at this:

I’m sure most experienced bedside sonographers come across this all the time.  For those who are starting out, and until now have just been looking at size and variation, take a second to look at the flow.  You can actually see the flow stop and start, which tells you your cardiac output is bad.  It could be bad because of the RV, the LV, the pericardium, the tension pneumothorax, anything, but it’s bad.  So just in case you were only gonna look at the IVC, keep looking! You will find something abnormal downstream, perhaps that you can do something about (not fluids, though).

I have seen this disappear and clear up with – when possible – correction of the problem, back to the normally anechoic IVC we usually see.

thanks!

Philippe

ps note there is also a mirror artifact in the right lower portion of the field, making it look as though there are two beating hearts.

November 8, 2013

Beta-blockers in Sepsis? Interesting… #FOAMed, #FOAMcc

Very interesting article in JAMA: http://jama.jamanetwork.com/article.aspx?articleID=1752246

I’m curious as to whether this has been generating interest in the cc community.  I think it is one of those articles that – at least conceptually – shines light in an area we don’t spend much time reflecting on.

I know that as an IM resident, and a CC fellow, my understanding of vasopressor therapy was pretty basic: squeeze the vessels to bring up the pressure, and hope you don’t squeeze so hard the fingers and toes fall off. In truth, no one ever really pointed out that to some degree or other, the same process killing off the fingers is probably happening to a varying degree in all organs. But maybe I just nodded off and missed it.

Since then, however, I’ve had some time to  re-examine things, and my practice has slowly been evolving.  For one thing, bedside ultrasound allows a really good assessment of inotropy, so I started to ask myself why I was giving b-agonists to patients who clearly didn’t need any help with contractility (e.g. normal, and even more so, hyperdynamic RVs and LVs).  After all, I’m putting them at risk for arrhythmias, or at least tachycardia. So whereas levophed (norepinephrine) remains my reflex pressor, I routinely shift to phenylephrine when faced with arrhythmias (most commonly fast atrial fibrillation) or tachycardia (beyond 110-120) once adequate volume resuscitation has been done.  Why 110-120?  Its an absolute guess. Somewhat educated – or I try to convince myself of that – in figuring that at some point, the increased CO via HR will be offset by decreased filling time, and with the weak but recurring data showing an association between tachycardia over 90-100 and poor outcome.

So this study – counterintuitive as it may sound to some – is really about blunting the potentially unwanted effects of b-agonists.  They randomised 336 patients to IV esmolol to a HR <95 vs a control group of standard care. They found a reduced mortality of 60%… Obviously the massive benefit should be taken with a healthy dose of skepticism, but even just the fact that they didn’t make patients worse is very, very significant.

Read the paper. They do a great job of reviewing the concept and it’s worth going over their protocol.

Physiologically, we know that catecholamines can cause stress cardiomyopathy.  The question is, when cardiomyopathy is noted, how often do we think this is related to therapy?  More often, we figure it’s the disease process – septic cardiomyopathy. At the bedside, this is impossible to differentiate.

The concept of lusitropy – active relaxation – and its contribution to cardiac output – is often overlooked, and can be affected by catecholamines. In fact it can be the most important factor related to preload, despite getting much less attention than volume loading. Remember that preload is not a pressure (especially not a CVP!!!), but a volume, and physiologically it is the degree of myocardial stretch. The ventricle is not passive, and its compliance is highly related to the active relaxation phase. Fluids will not affect this.

In addition, the decreased filling time by tachycardia can also decrease output.

Fantastic study, even if only to open the door.  I would have liked (in typical N=1 fashion and as a bedside sonographer) to see a quick echo prior to initiation, and seeing if there would have been an association with baseline RV/LV function and response/outcome to esmolol. Intuitively and physiologically, it would seem that the hyperdynamic RVs and LVs would have benefitted most, since they didn’t need beta agonism to start with – but I can also entertain that those would be unaffected and that the worse ventricles could have been worsened by stress cardiomyopathy… So a critical question in my opinion.

So…bottom line?  Is this practice-changing? It might be.  For me, I might start looking at RV/LV and opting for a quicker conversion to neosynephrine if I see a hyperdynamic state or lowering my HR threshold to do so…100? 105? – maybe just a shift rather than a change in practice. I’m not sure I’ll start esmolol infusions yet, but it will be at the back of my mind and I might, given the right set of circumstances. What I would like to see is reproducibility, and if it does happen, I would be happy to get HR’s under 95.

Love to hear what anyone else has to say!

 

 

Philippe