Bedside Ultrasound Quiz Part 2: A 50 yr old man with dyspnea, acidosis, hepatitis and leg edema. #FOAMed, #FOAMer, #FOAMus

So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.

So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED.  I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis.  He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.

So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.

Bottom Line:

I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.”  This would have been the polar opposite of the necessary treatment.

The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued.  Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”

The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…

Love to hear anyone’s thoughts!

 

Cheers

Philippe

Bedside Ultrasound Case: Control the source. #POCUS #FOAMed, #FOAMcc, #FOAMus

So this morning a 65yr old man with shock and respiratory failure was admitted to the ICU, hypotensive on levophed and vasopressin, with a lactate over 10.

So, as usual, my first reflex was to reach for the probe to assess hemodynamics. He had been well resuscitated by a colleague, and the IVC was essentially normal, somewhere around 15 mm and still with some respiratory variation. However, scanning thru the liver, my colleague had noted a large hepatic lesion, which on CT scan (non-infused since patient had acute renal failure) the two radiologists argued whether it was solid, vascular or fluid filled.

image

Having the advantage of dynamic ultrasound, you can tell that there is some fluid motion within the structure, very suggestive of an abcess, especially in the context of severe septic shock:

So the next step was source control:

 

Pretty nasty. Pardon my french!

We got over 1.5 L of exceedingly foul pus.

imageimage

Within a couple of hours the lactate dropped to 3 and the levophed was down by more than half.

I think this case illustrates once again, the power of POCUS in the hands of clinicians.  While I am certain that the diagnosis would have been made without POCUS, it probably would have taken additional time as the radiologists themselves were debating its nature, and without POCUS, bedside drainage in the ICU would have been out of the question. That liter might still be in there tonight…

For those interested in how to integrate POCUS in their daily rounds, I think I put together a fair bit of clinical know-how and tips in this little handbook.

 

Cheers!

 

Philippe

Fluids in Sepsis: An EmCrit Webinar! #FOAMed, #FOAMcc

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So a few weeks ago Scott (@EmCrit) asked me to be part of a pretty cool webinar organized by the Greater New York Hospital Association about fluids in sepsis. The gang consisted of David Gaiesky, Emmanuel Rivers and moderated by Scott himself. And for some obscure reason, he asked me to be part of it – much to my honour (terror, also), naturally.  It was only afterwards that he told me it was to help stir the pot and be controversial, challenge the “old school” etc… He seemed to have overlooked that I am Canadian, and inherently and perhaps overly polite and considerate – at least live and in “person”!

We talk about a bunch of stuff around fluids, which, how much, how to assess, etc.

Anyhow, I hope I got a few ideas across, but it was really cool to hear that these gurus do use ultrasound – don’t necessarily strictly adhere to, for instance, EGDT, and also advocate that guidelines are guidelines and not necessarily gold standards.

Here is the link to the webinar for those interested:

 

https://t.co/dbL03Vuqlj

 

And here is the figure for the section where I refer to fluid responsiveness/tolerance:

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I further talk about this in a previous post here.

Scott and I also recorded a debrief which should be coming up in the next weeks on EmCrit – link to follow!

cheers!

 

Philippe

CCUS Institute Bedside Ultrasound Mini-Fellowships. #POCUS #CME

The personalized CCUS Institute’s Mini-Fellowships (CME-eligible) are focused on bedside ultrasound and designed to take clinicians with some degree of proficiency in basic ultrasound to a whole other level. The opportunity to follow a seasoned clinical ER/ICU sonographer and see actual cases, learn the clinical integration of ultrasound data into decision-making is a unique one, outside of a handful of residency programs whose faculty includes experienced bedside sonographers. Basic how-to courses are great, and certainly the first step for those clinicians adding ultrasound to their armamentarium, but what we have seen, sadly, is after initial enthusiasm, many don’t really pick up the probe because the confidence to “make the call” simply isn’t there. Yet.

In a sense, it’s almost as if, as medical students, we’d read Bates, practiced physical exam on each (more or less normal ) other, and were then set out to make diagnoses and treat without having residents and attendings around to confirm our findings a few times, until we got the hang of it. Hmm. That would be rough.

Some physicians are fortunate enough to practice in a center where there are a few “veterans” of bedside ultrasound and can gain some acumen that way, but others may be the ones spearheading their institution into the 21st century, and it is from the comments of several of those, attending the CCUS Symposium (2008-2014 – perhaps a return in 2017) asking for the possibility of shadowing some of us, that the Mini-Fellowships came to be.

Mini-Fellowship Structure

Montreal Mini-Fellowship: Participants shadow one of our instructors (ICU attending) during the regular working days and discuss the cases and ultrasound-relevant aspect of each case (more often than not the case in entirety), and are able to practice their ultrasound skills. The duration is flexible although we generally suggest a minimum of two or three days. Each day would usually be about 6-8 hours, some may be more.

Toronto Mini-Fellowship: Participants get a dedicated and highly experienced preceptor (Dr. Edgar Hockmann) who is not on clinical service but with access to the ICU patients, and will provide a structured and dynamic session adapted to the participant’s needs and abilities.

The case exposure will be mainly ICU as well as ER and ward patients. The focus will be on acute care issues. After two days, participants who had a basic ability in ultrasound should be fairly comfortable with assessing volume status, cardiac function, perform lung ultrasound, be able to identify and assess intrathoracic and intr-abdominal fluid collections, assess the kidneys, bladder and gall bladder, measure optic nerve sheath, assess carotid flow and some may have exposure to trans-cranial doppler. The focus may be shifted depending on a participant’s interest.

This takes place in Montreal, Quebec or Toronto, Ontario, Canada.

Participants will have the opportunity to work with handhelds, midrange and high-end ultrasound devices.

Space is limited as we can generally only accommodate 1-3 participants per month.

 

CME

This activity qualifies for 25 Section 2 credits and 2 hours per day of Section 3 credits under the Royal College of Physicians and Surgeons of Canada (equivalence given to AMA CME credits).

 

Bonus!

Upcoming participants will also receive a copy of the forthcoming handbook:

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Requirements 

Please have basic experience in bedside ultrasound. We don’t want to teach you about depth and gain. We’re happy to fine tune your views but not to introduce you to the main cardiac views. It would just be wasting your clinical time. We’re here to show you how to assess pathology and integrate your findings into clinical decision-making. Take the basic group course to learn the views, or be self-taught from youtube/iphone and practicing on your patients. You don’t have to be great, but to get the most out of this experience it shouldn’t be your first time holding a probe.

Registration

email me at philipperola@gmail.com or reach out on twitter @ThinkingCC

Tuition

Montreal Mini-Fellowships: 500$ CAN / 400$ USD per day for 1 physician, 425$ CAN / 350$ USD per day for 2, and 350$ CAN / 300$ USD for 3 physicians (maximum)

Toronto Mini-Fellowships: 800$ per half day (4h).

100% refundable until you start. Even if you don’t show up. Really. We’re not in it for the business. We get to go home earlier if you don’t come.

Testimonials:

« I have had the chance to participate in a shadowing experience with Dr Rola at the Scarborough General Hospital ICU during two days in 2013. As a general internist and assistant program director, this experience really opened my eyes regarding the use of bedside ultrasound in general internal medicine and for IM residents. I think I would have benefited more of this experience if I had done more training previously, and I encourage future participants to do so. However, I came back from this experience with a very clear idea of the benefit of CUSE for my patients and for our residency training program. I really saw how ultrasound was used ‘in action’, in a much more realistic way than what is usually shown in CPD meetings. I also saw its limitations and the skills I needed to develop to generate good images (not something you can learn over the weekend!). Since then, I participated in formal trainings and licensing activities (more than 250 supervised US on acute care patients) and now practice bedside ultrasound autonomously. We now offer a bedside ultrasound training for our residents with the help of the emergency medicine department and an ultrasound-guided procedural simulation lab. Nothing in CPD has improved my practice and benefited the health of my patients as much as bedside ultrasound training. »

Alexandre Lafleur, MD, MSc (Ed.), FRCPC
Spécialiste en médecine interne
CHU de Québec – CHUL
alexandre.lafleur.1@ulaval.ca

“Thank you very much for the exposure and teaching offered via the CCUS “Mini-Fellowship.”  These few days allowed me to enormously improve my mastery of bedside ultrasound in clinical decision-making in critical care. I recommend the experience to clinicians already having experience in bedside ultrasound, but who feel they could benefit from the expertise of an instructor to attain a level beyond basic courses and available textbooks.”

Mathieu Brunet, MD, GP/ER/ICU, Magdalen Islands, Quebec, Canada

“The CCUS Mini Fellowship In House training is very essential in to experience the echo skills that we get from the courses,being supervised in ICU will offer the chance to be corrected and get real live practice/exposure by being at the bedside and learn what is priority in echo for the best of patient care. The in-house experience is very helpful, practical, I recommend this training to any physician involved in ER, ICU, CCU, Anesthesia and rapid response team.”

Joe Choufani, MD, Internal Medicine/Cardiology, St-Lawrence Health Association, NY

“Thanks for everything. I really appreciate you sharing your vast fund of knowledge with me.”

Sean Sue, MD, ER, Philadelphia

CME

So, great news, finally went thru the CME process and lo and behold, the Mini-Fellowships qualify for 25 Section 2 credits (regardless of the length) and 3 hours of Section 3 credits (per day of fellowship). For you americans:

Through an agreement between the Royal College of Physicians and Surgeons of Canada and the American Medical Association, physicians may convert Royal College MOC credits to AMA PRA Category 1 Credits™., #CME

NIRS-Assisted Resuscitation: Following the N=1 Principle. (Part 1) #FOAMed #FOAMcc #NIRS

So for anyone who has been reading any of my stuff, you know that I believe we best serve our patients by using the information in good evidence and blending it with bedside assessment (ultrasound being an integral part of physical examination) and physiology to come up with the best therapeutic approach to the one patient we are treating.  Contrast that to the blinded and naive belief that one protocol from one study is the best thing for all patients suffering from disease X.

So I am constantly looking for a way to fine tune resuscitation to the individual patient, given his/her particular cardiovascular function, volume tolerance (not just volume responsiveness), vasopressor tolerance (blue fingers probably mean blue livers and kidneys to some degree) and metabolic reactions.

One of my friends and mentors is Dr. Andre Denault. Absolutely incredible guy who is a complete triple threat of academia (internist/intensivist/anaesthetist massively published), experience and raw neuronal power. Throw in open-mindedness and humility (he actually once picked my brain about abdominal compartment syndrome pressure monitoring) and you have a lethal package. So after killing off the filed of intraoperative/critical care TEE (yes the leading textbook is his), he’s plunged into NIRS spectroscopy and is now dragging it from the OR to the ICU, and so in the last few years he’s put me on this trail with anecdotes and his (unpublished yet but coming) findings.

So a quick few words about NIRS (Near InfraRed Spectroscopy). The technology looks at hemoglobin saturation, and does so in a predominantly venous way. Hence this behaves similarly to a central or mixed venous gas, except at the local tissue level. A gross normal is >70% but this has to be interpreted in clinical context, along with the knowledge of simultaneous arterial saturation. Hence lower values (assuming normal arterial sats) will mean one of two things: increased demand or decreased supply. The demand issue is a clinical one. What we are looking for using this type of monitoring is decreased supply, e.g. cardiac output that is inadequate for current demands.

The information gleaned from our discussions was enough to make me get some loaner time with some devices, and that was enough to have a few clinical cases pique my interest.

Here is one:

In the ICU at Scarborough General in Toronto, I admit a lady with urosepsis on a stone-obstructed hydronephrosis. We get urology to slip in a double J, but she is still very norepinephrine-dependant. She isn’t intubated, lactate about 5 and on high doses of norepi to maintain MAP 60-65. Extremities are cold and mottled and there is mottling up to the thighs. She is awake and communicating. Over the next hour or so lactate rises to 5.5. I’m not liking this.

I put on the NIRS monitor with a cerebral lead and one on the thigh. They both read in the 50’s, somewhat suboptimal.

Bedside US reveals a good sized IVC with little variation. She’s well filled. Her LVEF is 50-60%, her RV is dynamic and with a normal RV/LV ratio. The hydronephrosis is improved on the affected side.

So I have a patient who’s adequately preloaded, without obstructive or systolic failure, who is on very high doses of norepinephrine with a rising lactate, despite source control and antibiotics. However, she doesn’t “look” that bad aside from the cold and blueish extremities…

So I decrease the norepinephrine. Systolic BP drops to 80…but…cerebral NIRS and tissue NIRS rise…now in the high 50’s. Patient remains awake and communicating. Drop norepinephrine some more. Systolic 75. Cerebral NIRS 62%, tissue 61%. Systolic 70. Cerebral 59%, tissue 57%. Back up to 75%. NIRS back up.  I finally settle on 75-80 systolic. NIRS settles in low 60’s. An hour later, lactate is 4, two hours later 2.5, then normalizes. Over that time span, the mottling gradually resolves and the urine output picks up. By the next morning she is off norepinephrine, and her BP sits around systolic 85-90 on its own. Turns out her usual BP is in the low 100’s.

I’m not sure how long – without the reassurance of improved tissue saturation – I would have been able to tolerate systolic BPs in the 70’s. Remember that lactate takes time to clear and urine takes time to make.

So this case reinforced my belief that not every patient’s needs are best met by an MAP of 65, and that targeting this may be harmful. It isn’t hard to imagine a scenario (which I may very well have pursued at a more junior stage) where further fluid resuscitation, coupled with insistence on a BP value may have resulted in iatrogenic fluid overload or Paul Marik’s “salt water drowning” (more commonly thought of as “ARDS”) and tissue ischemia/organ dysfunction (partly related to over-vasoconstriction) and who knows what outcome could have transpired… And very possibly, a bad outcome may have been blamed on severity of illness… Food for thought.

So one definitely possible use for NIRS is to find the “sweet spot” for the BP/vasopressor relationship.

More on NIRS in Part 2 in the next week or so.

Bedside Ultrasound-Assisted Procedure: Hepatic abcess drainage. #FOAMed, #FOAMcc

Hi,

Apologies for a long hiatus. Thought I’d share a case from last night. A 54 year old man had been admitted with e.coli sepsis complicated by portal vein thrombosis and multiple hepatic lesions a few weeks ago. A follow up scan by the hospitalist showed the following:

Yup, nasty. So our ICU Outreach service was called (we do all manners of procedures on the wards/er) and it happened to be me.

So 10pm I make my way with all the necessary gear (not much you can’t get done with ultrasound and caffeine!):

IMG_4242

Here is the clip:

So this is a synthesis of several US loops. The first ones simply show the lesion, which under US is clearly fluid – movement well seen with respiration/pulsation. Next you see the associated ascites and a quick peek at a subxiphoid view of the heart.

You then see the procedure itself, with a needle insertion (purposely jerky for visualization’s sake), and, following a 3 way stopcock connection, gradual drainage of the abcess.

IMG_4246

I chose to hand-drain it in this case to avoid possible blockage of the tube if simply left, since it was a small 8.5 french pigtail catheter (better for comfort). You can see that the access cavity was essentially obliterated. 400 ml or so drained:

IMG_4247

So technically this was very simple, however the one important teaching point is to pick an inferio-lateral approach, as an easier but more treacherous one – simple lateral – might result in going thru the pleural space because of the lateral costodiaphragmatic recess which extends quite inferiorly. So when picking the entry point, it is important to make sure it is below the diaphragmatic insertion. Otherwise the potential to seed the pleural space with abcess content is there. This would be sub-optimal.

The advantage of bedside ultrasound? Quick and easy drainage during the weekend when interventional radiology isn’t readily available.

cheers!

Philippe

The Great Septic Debate (Part 2): Resolution? #FOAMed, #FOAMcc

So, echoing my thoughts form the end of the debate, Steven adds:

Well, I didn’t expect to see my name in a headline, but I suppose it’s a hazard one should expect when they go spreading their arguments across the interwebs!

In truth, I don’t think that Dr. Lynn and I really think that much differently on these issues. We both desire for the science of sepsis to continue developing and to be better than it is. I, personally, would love to be a part of the clinical trials that use genome-based data to determine which treatment arm a patient belongs in. We both deplore any “old guard” attempting to prevent the onward march of discoveries that make our knowledge and abilities more complete. I am actually sorry that some young scientists feel intimidated and that there is anything less than civility and scientific curiosity in our community. Period.

Likewise, I would be shocked if Dr. Lynn did not at least use the observation of infection, SIRS, and organ dysfunction as physical markers of sepsis and warning signs that intervention is necessary. It will be true for a very long time that it is going to be an interaction between two human beings that initiates the diagnosis and treatment of sepsis. A physician will recognize a patient in distress by some means and start the process. For now, these findings are the best we have, and they should prompt us to intervene before the completely diagnostic test results are available. Even when we have the tricorder, something is going to trigger the doc to pull it out of a pocket and use it.

OK, so I have to admit that Dr. Lynn stung me a little with his characterization of TNF-alpha as a “biomarker”. I would rather say that TNF is one of the heavy hitters in the proteomics of sepsis, and I’ll bet that I can get him to concede that point! It stimulates receptors and causes other actions to take place, it’s synthesis and release are regulated and dysregulated; it’s more than just a marker! And I ABSOLUTELY agree that the failure of TNF-directed therapies stems from the fact that they were given both to patients who could benefit from them and patients who, with better characterization, we would have known had no chance of benefitting. The same goes for high dose corticosteroids, anti-endotoxin antibodies, IL-1 directed therapies, and coagulation based therapies. In fact, that’s what I’ve been teaching my trainees for years – if you can call bemoaning the fact that we can’t yet recognize and separate responders from non-responders teaching. We have a desperate need for understanding better, and the science MUST be encouraged. Again, period. Or full stop, for those of you who have that bent! That is, I think, Dr. Lynn’s argument in a nutshell.

I REALLY appreciate the interchange. It is healthy and necessary. The two of us are aiming at the same thing – fewer people dying from sepsis. I haven’t met Dr. Lynn (though I hope to), but I suspect that he spends more hours in his day formulating and doing the new science, while I spend more hours in my day pushing people who think that it isn’t sepsis until it’s shock and multiple organ failure to do something about it before it gets that far. Those are both important parts of the war, but in the end, it is the same war. And we are allies in it.

Steven Q Simpson

And, soon after, Lawrence reaches for that handshake:

I agree completely with Dr. Simpson. We all teach that a good history, physical, basic lab, and a high degree of vigilance for subtle signs of sepsis are pivotal. This includes the use of awareness campaigns which simplify sepsis to something easily understood and screening protocols to assure vigilance. These are great advances.

I also share Dr. Simpson’s concern about empowerment of naysayers who may use the promulgation of the imperfections of sepsis science as a reason not to move forward with early action based detection protocols.

Relevant TNF-alpga, I have to agree that it likely has a fundamental role in some phenotypes of sepsis including the sepsis-like syndrome generated in Ebola patients.

So Dr. Simpson and I probably agree on most sepsis related issues.

To explain a little further, many years ago our research team applied for an NIH grant to define the dynamic relational patterns of all the lab and vitals over time in infected patients. The reviewers did not seem to comprehend why we wanted to do that since a standard for a single unified phenotype of sepsis was already widely accepted. Yet had they realized the need for these types of complete data sets, the entire time time series matrix of vitals, lab, biomarkers, and treatment for each case would have been acquired in PROcess , ARISE, and Promise. This would have occurred if the entire field of scientists had not convinced themselves they already knew that “sepsis/septic shock ” comprised a unified phenotype, “an entity” “a single condition” “a thing or object” definable by a few static thresholds.

So this is why we say the young should call for reform ASAP of sepsis science (not sepsis awareness) and at the upcoming SCCM. Imagine a mult-center trial where these complete time matrices are generated and we define the phenotypes. We can define the phenotypic subtypes and then examine treatments in relation to these.

One might think of sepsis syndrome as analogous to the syndrome of CHF where there is systolic failure, diastolic failure, hypertensive failure, and valvular failure defined phenotypes of CHF.

Perhaps we might have sepsis with capillary membrane failure phenotype and/or, vascular muscle failure phenotype, coagulation control failure , neutrophilic control failure, TNF-alpha mediated immune control failure.

These are simply general gross simplistic considerations, Discussion points.

However the final conclusion of my original post is that, beginning at this SCCM, we must stop trying to explain away the anomalies caused by the past sepsis dogma and accept that these anomalies ARE counter instances. We must accept that we cannot rely on research which uses billing codes as data or by using retrospective controls at the same time the denominator balloons as a function of awareness.

Then we can finally assure that we do not fool ourselves because the world depends only on us. There is no back up. We must accept that we need a new surge of sepsis research ASAP, and…..in a new direction.

This, along with the effort and dedication of Dr. Simpson team, the Sepsis Alliance, and the SSC (now gathering the entire time series matrix of all the diagnostic and treatment data and not just thresholds) will produce an exciting future. If this happens, it would be great to be a young sepsis scientist in 2015.

So yes Dr. Simpson and I actually agree. We are simply fighting the war on sepsis from different fronts.

Most Respectfully
Lawrence Lynn

Thanks again Steven and Lawrence for what I think was both a really informative AND formative discussion.

Philippe