NEJM: The Septic Shock Issue…groundbreaking or same old same old? #FOAMed, #FOAMcc

Ok, so it was pretty cool to see an NEJM issue basically dedicated to septic shock management, I must admit. But let’s dig a little deeper, shall we?

So here is where they are: http://www.nejm.org, and fully available for now.

I won’t go through all the details and numbers, after all they are in the papers, so let’s just analyze them from two principles:

a. the N=1 principle – how was therapy individualized?

and

b. was there any integrated monitoring of the therapeutic goals?

…and we’ll conclude by looking at the potential practice-changing potential of each of these studies.

So first of all,

High vs Low BP Target in Septic Shock, by Asfar et al.

So basically a negative study except for two findings, the increased incidence of afib in the high target group and the decreased need for renal replacement therapy among chronic hypertensives in the high target group.

so N=1 is not really revealed:

“Refractoriness to fluid resuscitation was defined as a lack of response to the administration of 30 ml of normal saline per kilogram of body weight or of colloids or was determined according to a clinician’s assessment of inadequate hemodynamic results on the basis of values obtained during right-heart catheterization, pulse-pressure measurement, stroke-volume measurement, or echocardiography (although study investigators did not record the values for these variables).”

So lets just hope that the variability evens itself out between the groups, since we don’t really know. The numbers don’t really tell the tale, because the average fluids received (10 liters over 5 days) could mean one patient got 15 and one got 5 – although let’s trust they followed the French Fluid Resus protocol…

So the atrial fibrillation makes total sense – more B agonism should result in that, and the decreased renal failure also does.

As the authors note, the actual BP averages were higher than planned. For those of us practicing critical care, we know most nurses titrating prefer having a little bit of extra BP – even when I prescribe MAP 65, I usually see the 70 or so unless I make a point to tell them. Understandable. They also note the underpowered-ness of their own study, but I think it is still worth looking at their results.

So…bottom line?  I think it’s a great study for a couple of reasons.

The first is to remind us to pay a little more N=1 attention to the chronic hypertensives, and that it is probably worth aiming for slightly higher MAPs.

The second, debunking the myth of “levophed, leave’em dead” (which I heard throughout residency at McGill), and the concept of doing everything (ie juicing patient into a michelin man) in order to avoid the “dreaded and dangerous” vasopressors. So really I think an alternative way to conclude this study is that it isn’t harmful to have higher doses of vasopressors. I think this is actually a really good study on which to base assessment of more aggressive vasopressor support vs fluid resuscitation, in the right patients.

It would have been interesting to have echo data on those who developed a fib – were they patients who had normal to hyperdynamic LVs who in truth did not need B agonism at all and would have been fine with phenylephrine?  Perhaps…

Cool. I like it.

Next:

Albumin Replacement in Patients with Severe Sepsis or Septic Shock, by Caironi et al. The ALBIOS study (a Gattinoni crew)

So basically showed no difference, so pretty much a solid italian remake of the SAFE study in a sense, confirming that albumin is indeed safe overall, and may be better in those with shock.  As the authors note, mortality was low, organ failure was low, so study power a little low as well. Note the mean lactates in the 2’s at baseline. The albumin levels of the crytalloid only gorup were also not that low, low to mid 20’s, whereas I often see 15-20 range in my patients, especially if I inherit them after a few days, as I do use albumin myself a fair bit. They also used a target albumin level, not albumin as a resuscitation fluid purely.

In my mind the benefit of albumin would be greatest in those with significant capillary leak, particularly those with intra-abdominal and pulmonary pathology. It would have been nice to see a subgroup analysis where extravascular lung water was looked at (especially coming from a Gattinoni crew!).

Another interesting thing would have been to know the infusion time of the albumin, since animal data tells us that a 3hr infusion decreases extravasation and improves vascular filling vs shorter infusion times. I routinely insist on 3hr infusion per unit, which sometimes results in 9-12hr infusions, almost albumin drips!

Bottom line?

I like it. Reinforces that albumin is safe, so makes me even more comfortable in using it in the patients where my N=1 analysis tells me to be wary of third-spacing. Also the fact that they used 20% – in Canada we have 100cc bottles of 25% for the most part – is nice, since the SAFE data used 4%.

Next!

A Randomized Trial of Protocol-Based Care for Early Septic Shock – The ProCESS Trial.

So right off that bat my allergy to protocols flares up, so I’ll try to remain impartial. It just goes against the N=1 principle. The absolutely awesome thing about protocols is that it primes the team/system to react – so clearly protocols are better than no-protocol-at-all, but strict adherence would clearly not fit everyone, so that some built-in flexibility should be present.

This being said, the ProCESS study is really interesting, for a number of reasons. They have three groups, and compare basically (1) Rivers’ EGDT to (2) their own protocol (see the S2 appendix online) which gives a little more flexibility and (3) “usual care”.  Net result is that all are pretty equal, no change in mortality. As the authors note, their mortality was low, so again may not have been able to detect a difference.

So, what does this mean. To me it’s a little worrisome because I doubt that the “usual care” represents the true usual care found in EDs/ICUs all over the world, so I am concerned that many docs will use this as a reason to justify not changing their practice, similarly to many I’ve heard say they don’t need to cool anymore after the TTM trial. Human nature for some I guess.

Bottom line? You don’t have to follow EGDT if you’re conscientious and reassessing your patient frequently and have done all the other good things (abx, source control, etc). I think that’s really important because giving blood (see my post about S1P) to those with hb > 70 and giving dobutamine to patients with potentially normal or hyper dynamic LVs never made physiological sense to me, and the problem with a multi intervention study such as EGDT is that you can’t tease out the good from the bad or the neutral. Again, studies such as EGDT are pivotal in changing practice and raising awareness, so this is not a knock against a necessary study, just to highlight the point that each study is a step along the way of refining our resuscitation, and the important thing is to move on. In fact, the reason that this is a negative study is probably due to the improvement in “usual care” that EGDT brought along.

Conclusion: No new ground broken, but these studies do make me feel more confident and validated in continuing to not do certain things (strict EGDT) and  doing others (albumin and earlier use of vasopressors).

Kudos to all investigators.

 

let me know what you think!

 

P

 

Central line insertion: US-spotted “Blind” technique Video (HERE IT IS!) #FOAMed, #FOAMcc

My apologies, had technical issues with the video uploading so here it is in two formats:

 

 

 

…please let me know if there is a problem!

 

thanks

 

Philippe

Central line insertion: US-spotted “Blind” technique video. #FOAMed, #FOAMcc

So a few months ago I posted about central line insertion and my concerns about the current standardization of care of ultrasound guidance:

https://thinkingcriticalcare.com/2013/10/21/ultrasound-guided-central-venous-catheter-insertion-standard-of-care-or-preventing-procedural-skills-foamed-foamcc

I promised a video so finally got around to remembering to do it.  This one actually happens to be a dialysis catheter so a bit bigger, but otherwise the technique is the same. In this case I am using my standard ultrasound-spotted procedure with “blind” insertion.

So here, I spot the vein, confirm it is just lateral to the carotid, and that it collapses nicely, without thrombosis:

Now, I insert the line. A few important points to note that are not seen in the frame:

Line Insertion video:

a. my introducer needle/syringe and loaded guide wire (pulled pack and “loaded”)  are ready  and within my vision, and also nearby are the dilator and catheter.

b. note that the off hand (right hand in this line) protects the carotid and stays in place until there is venous flashback, then secures the needle position.

 

Note that in this particular case, I didn’t quite make a large enough incision so the dilator insertion was a little difficult – unnecessary delay, and also unfortunately lost the last few seconds as my iPhone memory was full. 

Next, I confirm position in the internal jugular vein, and verify for lung sliding to rule out and anterior/apical pneumothorax.

In me experience, the key mistake I see inexperienced operators (and sadly, some experienced ones also) make is not to have a proper setup, such that once they do find the vein with the introducer needle, their subsequent steps are not immediately ready, and in the process, the relationship between needle tip and vein is lost, resulting in an inability to thread the guidewire (often blamed on mysterious anatomical abnormalities). It is key to find the vein with the freezing/searcher needle, fix the depth/angle relationship in your mind, withdraw and reach for the introducer needle/syringe using peripheral vision so as not to break the visual fix, and reproduce this while introducing it.

This is what I try to install in students/residents rounding with me, and in fact this approach is useful for any procedure.  Not having to turn your head, reach and fiddle with things that are not ready prevents mistakes.

If you haven’t read my previous post on central line insertion, I’m not advocating agains the use of ultrasound guidance, but for the maintenance of the ability to insert blind lines if necessary.

cheers!

Philippe

Pleural effusion in the sick patient (Part 2 of 3): Physiology & Literature! #FOAMed, #FOAMcc

So once your routine cardiopulmonary bedside ultrasound examination has revealed the presence of a significant pleural effusion, should you drain it?

I guess the first real question is actually what is a significant pleural effusion?  As you can imagine, the N=1 principle pops up again, and there is no single threshold answer (e.g.: >750ml  drained and <749ml  ignored), naturally.  So here are the main factors that impact physiologically:

1. underlying global respiratory function – eg how much reserve you have. With healthy lungs, a young adult can usually tolerate complete atelectasis of one lung or even more, which would take 2-3 liters of effusion at least. However, the more compromised gas exchange is, the less atelectasis can be tolerated.  This also encompasses the level of required ventilatory support, including the level of PEEP. Basically, the worse your lungs are, the more significant the effusion becomes.

2. thoracic compliance – which combines chest wall and abdominal pressure, since the diaphragm is thin and easily displaced.  The greater the compliance, the less atelectasis will occur as the diaphragm and chest wall will shift to accommodate some of the fluid. This is very important especially in surgical patients (or anyone with a tense abdomen).

…so there is no number.  Of course, if you take it to the extremes, I think everyone would agree that if you have 200ml,  it’s probably not worth doing, and if you have 2,000ml, it is. But in the grey zone of, say 500-1,000 ml, you have to make a call given the patient in front of you.

Now what does the literature say?

First of all, there is no large study looking at the impact of effusions in generally ill patients (ED/ICU).  There are some small, specific studies showing worse prognosis in some pathologies (eg Legionella pneumonia) but nothing that can really be extrapolated to general ED/ICU patients.

What about in ARDS? Talmor et al, (Surgery 1998, v 123) showed benefit in survival in a small study of ARDS patients.

I think the best overall study was Vignon et al (CCM 2005, v 33) who demonstrated that bedside ultrasound was much more sensitive in diagnosing pleural effusion (CXRs read as normal had as much as 1,000 ml effusions, as well as diagnoses of effusions which were actually consolidations ), but also that it was quite accurate in quantifying (inter-pleural distance >45-50mm at the base correlates with effusions >800 ml).

Usta et al (Interactive CV and thor surg, 2010 v 10) had similar results in spontaneously breathing post op patients with 45 mm (interpleural distance between diaphragm and base of lung) corresponding to about 700ml, although their range was quite wide, and they were using a somewhat impractical sitting position. They actually came up with a formula (16xdistance in mm) to estimate effusion volume.

Sikora et al (ISRN Emergency Medicine 2012) did a good review on the whole thing as well.

Sikora et al review

My empiric observations: I must have put in at least a thousand pigtails or (back in the day) CVCs in pleural effusions over the last 14 years, and my therapeutic goal has always been to drain effusions at least 750 to 1,000 mls. I have drained 350-500 ml in patients in severe respiratory failure a few times, some with apparent benefit, others without. I don’t recall regretting putting one in, but I do regret a few cases of not draining, only to have recurrent respiratory failure post-extubation. Grossly, I would say 750-1,000 or more in a patient with respiratory failure warrants drainage, but 1,000 mls in a CHF patient on nasal prongs can wait for the outcome of diuretic therapy. Of course we are talking about therapeutic and not diagnostic drainage. Under ultrasound guidance with an experienced operator, pneumothoraces should be exceedingly rare.

Bottom Line: start by examining your patient, physically and by bedside ultrasound. Understand his degree of respiratory failure and estimate the size of the effusion and the compliance of his chest.  Then you have to make the call (that’s why we’re MDs) as to whether this particular amount of pleural effusion in this particular patient is worth draining.

Next week:  how to do it video!

cheers!

Philippe

@shanxonline says:

Great post Phillippe and I fully agree that a global assessment is necessary before draining an effusion. With ultrasound we’ve become really good at identifying effusions, but need to understand physiology and especially chest wall/abdominal compliance to understand the physiological implications of drainage vs conservative management.

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

Bedside Ultrasound Clip Quiz #7: What is it? #FOAMed, #FOAMcc

Ok, so no history for you. Say you’re doing a general bedside ultrasound exam on someone in shock and you see this:

What am I looking at?  (HINT we’re in the RUQ)

What should I be thinking of?

Answers tomorrow.  Lets see what you guys come up with!

Philippe

rubbadoc says:  What’s air doing there?

…and indeed he is right, it is air where there should not be. Now where is it exactly? (experts, refrain from answering…)

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/

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

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

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.

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

 

NEJM Circulatory Shock Review by Vincent & DeBacker: the sweet and the not-so sweet… #FOAMed, #FOAMcc

So if anyone hasn’t read it, here it is:

Click to access Circulatory%20Shock%20-%20NEJM%202013.pdf

I read the article by critical care icons Dr. Jean-Louis Vincent and Dr. De Backer with interest  as I am always keen to find out what the cutting edge is… So here is my take on their review.

The not-so-sweet:

The inclusion of CVP in the assessment. Ouch. No evidence whatsoever. Evidence for lack of correlation to fluid responsiveness… I wonder if they themselves were cringing a little about including it, particularly form the fact that they just put high vs low rather than commit to a value, which makes me think they realize it’s a bit of a trap. (It reminds me a bit of those night-time orders I still sometimes see which say if u/o < 30 cc/hr give a bolus if CVP under 12 or lasix if over 12.  So basically depending on whether that patient’s head is elevated, or if he’s turned on one side or the other, he may go from “needing fluids” to “needing diuretics”…).

The sweet:

First of all, they obviously did an elegant job on description of shock states, and particularly of highlighting the common-ness of mixed etiology shock.

I like that they admitted that the end-point for fluid resuscitation is “difficult to define.”  Any answer other than that would really speak to non-physiological thinking, as I’ve referred to in prior posts/podcasts.

Dopamine: good job on trying to take it off the shelf for shock. As far as I’m concerned, only useful when you’ve run out of norepinephrine, although there is the odd time when you have a septic AND bradycardic patient where it could come in handy…

Bringing some focus on the microcirculation: no recommendations, but that’s appropriate since there are none to be made yet, but this is where the money is in the future, as far as I’m concerned. Once we figure out how to manage the microcirculation (we do ok with the macro circulation) we might forge ahead. But good to point the finger in that direction.

The super-sweet!

I do (not surprisingly) really, really like the fact that they included ultrasound in their assessment protocol, and emphasizing that focused echocardiography should be done as soon as possible.  Very nice. Finally.

Hopefully, this pushes mainstream ED and critical care physicians to realize they need basic bedside ultrasound skills…

 

Overall, I think it is a good review, certainly worth the read for trainees. I would like to see focus on re-examining and questioning our approach, which could spur readers to embark on research with a different angle. For instance, why do we assume that we need to fill patients to the point of no longer being fluid responsive in order to avoid vasopressors? Is there any evidence for that? Not that I know of…

But, for having put an emphasis on point-of-care ultrasound, it gets a big round of applause from me!

 

Philippe