Just a clip.
What’s the dx?
sinus tachycardia with 3rd degree HB – taken on a call on the ward before the tech brought the EKG machine.
thought it was neat.
Just a clip.
What’s the dx?
sinus tachycardia with 3rd degree HB – taken on a call on the ward before the tech brought the EKG machine.
thought it was neat.
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?
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.
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!
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%.
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!
So I was on call last weekend and got a call from one of the internists on the ward about a potential admission who may need dialysis. She was a woman in her 60’s, diabetic, hypertensive with minimal baseline renal dysfunction, who had been admitted with a hepatic abscess due to biliary obstruction. This had been stented and a pigtail catheter had been inserted to drain the abscess. However, over the last few days, her creatinine had risen to about 500 and she was becoming oliguric. Her O2 requirements had also increased and she was now on 15 liters by nasal prongs. This had been ascribed to pleural effusion and possible pneumonia.
When I saw this lady, she was visibly dyspneic at 30 with a heart rate 115-120 and a systolic BP of about 105-110, saturating 90% on 50% face mask.
So on physical examination, she had a soft abdomen (the first thing I feel just before I put probe to skin), her skin was cool, and the CUSE revealed a large (>20mm) IVC with no respiratory variation (despite the effort). I unfortunately forgot to hit the record clip button…and the parasternal long axis and apical 4 chamber are here:
Lung views showed “A” profiles except for the right base which had a small effusion and some consolidation/atelectasis and some B lines, but not very extensive.
So further assessment revealed she was not a smoker, previously quite active and easily able to go up and down several flights of stairs. She had noted dyspnea about 3 days ago, without chest pain. There were no leg symptoms, and she had been on LMWH for dot prophylaxis. The CXR was not very impressive – in a sense that there was not enough parenchymal disease to explain pulmonary hypertension.
This is PE until proven otherwise, and I would have been comfortable without further confirmation, but with the presence of some lung disease and an intrahepatic catheter, I preferred to have 100% confirmation before initiating thrombolysis.
After CT angiogram confirming bilateral and extensive embolism, I had a thorough discussion with her and her family and they all agreed to go ahead with TPA. She was quite concerned with cardiorespiratory limitation, given that she was quite active. She was comfortable with a quoted risk of intracerebral bleeding below 2%. I used the MOPETT half-dose of 50mg.
Overnight, her HR slowed to about 100, and sats increased to 93-94%.
When I rounded on her in the morning, she said “Doc, I can breathe!” with a big grin. Her HR was 95-100, she was not on 3 litters by NPs, BP 115-120 systolic, and CUSE showed:
So we can see that even though the RV is still quite impaired, it has decreased in size and the LV is now filling better. This was about 12-13h post thrombolysis. She was able to sit up without dyspnea and mobilize to the chair. Her IVC, although it remained around 18-19 mm, had clear respiratory variation.
So…success? Who really knows. It is concievable that, with heparin alone, she might have improved similarly. It is possible. I’m not putting this up to formally support the concept of thrombolysis in “submassive” PE but more to contribute to the #FOAMed discussion regarding the “grey zone” of thrombolysis, since she was technically not in shock (eg SBP>90, lactate normal), but the degree of impairment of the RV to me and the clinical picture, 3 days post, was concerning enough to warrant thrombolysis, but importantly to stress the following:
Point 1: the importance of bedside ultrasound, especially in acute cases. Without it, over a weekend, and with a patient in renal failure, how quickly would I have ordered a CT angio? Not without some hesitation…
I won’t review the MOPETT trial, these guys did a much better job than I could hope to, so definitely listen to this if this topic is of any interest to you (and it should!!!):
Great case debates in the RAGE podcast.
Keep in mind that morbidity, not mortality, is the main thing to focus on in sub-massive embolism and the MOPETT – even though I don’t really like the term, its quite vague – benefit in embolism with shock is quite clear.
Point 2: Equally interesting to me was the fact that the renal failure improved. In fact, overnight following thrombolysis, she had a urine output (without diuretic) over a litre, and over the next few days her creatinine normalized and renal replacement therapy was not needed. Interesting, since she even got a good blast of toxic dye with the CT. Some will feel that it is the improvement in CO that improved renal function, and this may be partly true, but in view of the lack of “systemic shock,” I think that venous decompression resolved the congestive renal failure, which I think was the main cause of her ARF. I posted about this topic a few months ago, so for more on this see:
so thanks for reading and love to hear anyone’s opinion!
QUESTION. IF SOMEONE DOES NOT HAVE A PALPABLE PULSE BUT HAS CARDIAC ACTIVITY ON THE ECHO AND RATE IS 90 AND BP IS 50. DO YOU CONSIDER THIS PEA AND INITIATE CPR?
Great question! There is a whole grey area in “PEA” and management is unclear. I don’t think there is a single answer to that, but physiologically and without further information about RV/LV, I would say your patient needs vasopressor/inotrope support, so I would probably give a small bolus of epi (maybe 100ug) and start an infusion. If I see little reaction (eg HR/BP doesn’t pick up in 30 seconds, I would probably give a short cycle of CPR to get the epi back to the heart. Of course, hopefully there is a reversible cause (MI/PE), that can be addressed.
So a few months ago I posted about central line insertion and my concerns about the current standardization of care of ultrasound guidance:
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.
…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!
This year, as part of the pre-congress courses being held prior to the main symposium (may 10th and 11th), we are introducing a half-day symposium entitled: “The Educators‘ Symposium: How to integrate Bedside Ultrasound into Ungergraduate and Graduate Programs,” coordinated by Dr. Catherine Nix of the University of Toronto who has been the driving force behind U of T’s implementation of an ultrasound program for undergraduates.
Here is the preliminary programme, really good stuff for anyone involved in education, whether at the institutional level or even at the departmental level.
program subject to (minor) changes…
Attendants may register for this independently or as part of the whole symposium. You can register at:
Stay tuned for more updates, and the final programme of the main conference should be out by next week. Guess what, it’ll be a great place to meet @criticalcarenow, @bedsidesono, @EGLS_JFandMax, @nobleultrasound, and many more not yet deep into the #FOAMed or twitter-verse, but soon to be.
See you there!
“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:
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!
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.
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.
First of all, congratulations to all who are picking up a probe and working to add it to their diagnostic and therapeutic armamentarium. It will serve you – but more importantly, your patients – for the rest of your career.
I would like to caution you, however, in remembering that this, unlike knowledge, is a skill. More than half the challenge is in image acquisition, and this requires practice. Practice, practice, practice. You can’t just reach for the probe in that one patient during your shift in whom you really want to have an idea of his or her cardiac function or volume status, then try to remember how to do it. That’s a road to early discouragement and worse, never developing the skill or the necessary confidence.
Especially early on, scan everyone you can, including yourself. You make a very patient patient.
If you’re not a fortunate medical student whose school is one of the pioneering ones with an undergraduate programme, take every course you can. Make friends with ultrasound tech and spend some lunch hours watching some of their exams. Pin (4 point restraints preferably) a colleague to a gurney when a machine is available.
Once you can reliably acquire images, start making clinical calls on the extremes: the tiny or the huge IVC, the hyperdynamic and the minimally moving ventricle, etc… and as your skills and experience grow, work your way towards the middle.
The last thing we need, as a bedside sonographer community, is to have the current trainees, which really represent the first generation (as most of the educators out there today are largely self-taught, or at least devised their own unique programs), misuse this amazing tool. We are under scrutiny, as it is a novel application (of an old technology), and cannot afford mistakes, lest roadblocks re-appear.
So practice, practice, practice, and if you’re not sure, get another opinion or another diagnostic modality!
So your intubated patient has developed abdominal distension and residuals are 250. You scan the LUQ:
what do you see? what should you do?
You have gastric distension with at least a liter of fluid in there. Put in an OG, hold feeds, assess the rest of the abdomen to r/o bowel obstruction, consider motility agents and look for a reason behind the ileus or obstruction.
the best is yet to come.
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