Prone Positioning for ARDS

I am a huge fan of proning patients who are in ARDS. At one point or another I'll cover the data behind proning like the PROSEVA trial (no time today or until at least June). There are a variety of ways to prone patients which reflect the disposable income of the facilities where you work and train. At the 3 institutions were I have worked and the others where I have done moonlighting shifts, we've all used some good ol' fashioned muscles and coordination.

The PDF quoted and linked here was published in December 2019 and is usually very key during flu season. I am not going to comment about the coronavirus but these patients are developing an ARDS-like syndrome where proning may work. I haven't seen any data, though. That being said, having the ability to prone patients and do it well could potentially save lives.

In the paper, they cover pretty much everything I would want them to in a document like this that's beneficial to all. They even discuss chest compressions and defibrillation in these patients, something we all fear.

The PDF is completely free and a direct link. I need to find out the citation for this bad boy. The authors did a great job and a big hat tip to them. There's a really nice safety checklist and nursing checklist included. 

How do you all prone at your institution?

Do you not prone at your shop because of fear of the tube coming out?

Have you ever had to perform CPR on a proned patient?




Link to FULL FREE GUIDELINES


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Norepinephrine versus Epinephrine for Cardiogenic Shock caused by a Myocardial Infarction

This is one sexy pilot study. The authors here decided to take a look at norepinephrine (NE) versus epinephrine in patients with cardiogenic shock s/p MI. They didn't use dopamine as they had noted an article that I have reference here where I discussed how dopamine actually increases mortality in cardiogenic shock compared to NE. 

The rationale why the authors went to NE was because data has shown that the myocardium may have a more favorable effect on myocardial O2 consumption. Epi was believed to cause more deleterious effects. Ultimately, though, none of this had been proven in a trial. Well, here is the trial. 

Over the course of 5 years they included 57 patients. See why I have such respect for these folks who do trials? I have no idea where I am going to be in 5 weeks, let alone 5 years. They measures a ton of parameters and did their statistical jumping jacks that I will not bore you with (but the article is entirely free for those curious minds out there). 

Ultimately, what we are about is how the patients did. With regards to their MAP, CI, and SVI, they were the same. As one would expect, the HR for the patients on epi was higher. Also expected, as epi hits more of the beta receptors, there was an increase in lactate in these patients (which doesn't mean they need more fluids).  

There was an early termination of the study, though, as 37% of the patients on epi went into refractory shock while just 7% of the patients on NE did the same (p=0.008). 

The authors acknowledge that it is a small trial but they were able to see a clear difference between the two groups. There are numerous other limitations to the study as well that they acknowledged.

When your patients are in cardiogenic shock, how do you all use your vasopressors/inotropes?

-EJ

Levy BC, Clere-Jehl R, Legras A, et al. Epinephrine versus norepinephrine in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2018;72:173–82.

Link to Abstract

Link to FULL FREE Article



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Renal dose Dopamine, taking down a myth.

When one looks at the dates where the publications disproved "renal dose dopamine", you see three articles published in 2000, 2003, and 2004. It's 2020 and this has not yet been put to bed. Now, I’m all worked up about this because I’ve had clinicians tell me that it absolutely works. I saw it in residency, fellowship, and now in private practice. I’m sure some of you see it at your institutions, too.
There’s data that it improves urine output transiently but no data that it improves renal outcomes in critically ill patients. No changes in creatinine. No changes in renal replacement therapy rates. In fact, that whole discussion has been put to bed so much that there haven’t been any comments made on it over the last 15 years. No further trials attempting to prove it works. Is that why we’re still seeing it? Well, it’s time to bring the arguments against renal dose dopamine, or even using dopamine altogether back into the fray.
The data about it being beneficial was from the 60’s in animal and healthy human studies. The latest studies, however, say it doesn’t work and in fact may be harmful. I have attached some of my preliminary slides from my Vasopressors in 2020 lecture. These are some of my preliminary slides. More info will come from me directly as I present these but it should provide you with an idea of why we should rarely see dopamine in our ICU's anymore. 
Do you still all use dopamine? If so, what for?
I used to use it during codes as it was already packaged in the code carts. We have since gotten rid of these and my badass pharmacy colleagues prep me levophed drips within seconds. 

Debaveye, Y., and Van den Berghe, G.: “Is There Still a Place for Dopamine in the Modern Intensive Care Unit?” Anesthesia and Analgesia. 98(2):461–468, February 2004.

Link to FREE PDF

Holmes, C., and Walley, K.: “Bad Medicine: Low-Dose Dopamine in the ICU,” Chest. 123(4):1266–1275, April 2003.

Link to CHEST Article

Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial: Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 2000; 356: 2139–2143

Link to NOT FREE Lancet Article

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Cardiac Arrest Survival Statistics

We’re getting better with our management of out of hospital cardiac arrest via quality bystander CPR. The majority of this credit should go to the organizations such as the AHA who puts together programs taught by firefighters, paramedics and EMT’s (forgive me if I screw up the semantics) to health care personnel and the lay public which empower those attendees to save lives with their training.

No matter how you look at it, the numbers are still pretty bad, but they’re getting better. 8.8% of cardiac arrest patients lived to be discharged from the hospital. Some nuisances behind those numbers include no quality of life being discussed, nor a breakdown of the etiology behind the arrests by subgroups. Nonetheless, the authors did a great job of compiling data from many different studies to give us an idea of what we can expect when our patients roll into our emergency departments and ICUs. 

Only 22% survive long enough to be admitted to the hospital.
In the last decade we’ve improved the survival to hospital discharge and 1 year survival. We should all pat ourselves on the back to some extent bc were the ones who do and will take care of these patients. I know that we sometimes prolong death, but we’ve all had some big wins that have given us purpose and made our hearts full with satisfaction for what we’re trained to do. A hat tip to the authors.

-EJ

Yan, S., Gan, Y., Jiang, N. et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis. Crit Care 24, 61 (2020). https://doi.org/10.1186/s13054-020-2773-2

Link to FULL FREE Article

Link to Abstract

Yan, S., Gan, Y., Jiang, N. et al. The global survival rate among adult out-of-hospital cardiac arrest patients who received cardiopulmonary resuscitation: a systematic review and meta-analysis. Crit Care 24, 61 (2020). https://doi.org/10.1186/s13054-020-2773-2

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Dopamine doesn’t belong in the ICU anymore

Link to FREE FULL ARTICLE and PDF

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Blood Pressure Measurements: Arterial Line vs Oscillometric Cuffs

We all do this every single day. We measure target many of our interventions in the critically ill patients to blood pressure. Whether it’s fluids, vasopressors, or blood pressure lowering agents, we obsess over these parameters. We feel warm and fuzzy if it’s okay. But are we using the right tool to find out these numbers?

I’ve always harped on arterial lines, although invasive, being the most reliable method of evaluating the blood pressure in our patients. If someone is critically ill on jet fuel, they’re getting an a-line. This is a fun study where they compared the oscillometric BP cuffs to a-lines in 736 patients.

When you look at the mean differences they obtained, the numbers weren’t too bad.
Systolic: 0.8mmHg
Diastolic: -2.9mmHg
Mean Arterial pressure: -1mmHg

This wouldn’t drive any of us crazy, right? We’d be cool with these differences if it avoids invasive (painful) interventions on our patients. But wait, there’s more. There was a large amount of variability which could lead to additional interventions.
Systolic: ± 15.7mmHg
Diastolic: ± 11mmHg
MAP: ± 10.2mmHg

The article goes as far as to say that BP cuffs would not pass the Association for the Advancement of Medical Instrumentation standards. There’s no data as to how this changes outcomes.

This was a post hoc analysis (after the fact). This shouldn’t be too challenging to accomplish a prospective study looking at this in our critically ill patients. We have many patients who have a BP cuffs and an a-line in place. Why not just record cuff pressures every 15 minutes and obtain some data? Obviously it’s more complicated than that.

A hat tip to the authors.

T. Kaufmann, E.G.M. Cox, R. Wiersema, et al., Non-invasive oscillometric versus invasive arterial blood pressure measurements in critically ill patients: A post hoc analysis of a prospective observational study, Journal of Critical Care(2019)

Link to full article (not free)

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Oscillometric devices vs Arterial lines. New data.

Why is it important to stay up to date? There’s a pendulum in medicine but there’s a time when the pendulum swing is going to bite you in the butt and you’re going to be wrong. Seems like I’m wrong.

I have an extremely popular post and YouTube video regarding how oscillometric devices are correct with regards to their MAP but not their SBP and DBP. I hadn’t found any studies to validate how the SBP and DBP applied. Now we have data. And I may have to eat my words. I’m cool with that, though. This study was published earlier today. I cannot get my hands on it to take it apart, but the data is compelling. They did some fancy statistics that I can’t admit to understand including Bland-Altman and error grid analyses. Although the averages seem to be close, the variations are as follows:
SAP 0.8 mmHg (±15.7 mmHg, −30.2 to 31.7 mmHg)
DAP −2.9 mmHg (±11.0 mmHg, −24.5 to 18.6 mmHg)
MAP −1.0 mmHg (±10.2 mmHg, −21.0 to 18.9 mmHg)

The interesting part is that the ICU is a world of details and although the differences were small. The variation between the two, radial arterial line and oscillometric cuff, was enough though to cause additional treatment changes in more than 20% of patients.

I despise reading abstracts and coming to conclusions but at this point I have no choice. Maybe tomorrow I’ll be able to take this apart entirely.

Link to abstract

EJ

Kaufmann T, Cox EGM, Wiersema R, et al. Non-invasive oscillometric versus invasive arterial blood pressure measurements in critically ill patients: A post hoc analysis of a prospective observational study [published online ahead of print, 2020 Feb 22]. J Crit Care. 2020;57:118–123. doi:10.1016/j.jcrc.2020.02.013

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Guidelines for Pain, Agitation/Sedation, Delirium in the ICU

I am currently working on a lecture where I discuss reducing the utilization of opioids in the ICU for our critically ill patients. The sources of pain are plentiful, unfortunately. Truth is, opioids are the best option for our patients at the time of this writing but we also need to work hard to try to minimize the exposure to this family of medications via alternatives. Which alternatives might you ask? In particular, I have taken deep dives into the utilization of ketamine, magnesium, gabapentin/pregabalin, NSAIDS, nefopam, acetaminophen, dexmedetomidine, as well as regional blocks performed by our anesthesia colleagues. 

The PADIS (pain, agitation/sedation, delirium, immobility, and sleep disruption) guidelines linked here, and are completely FREE to download, provide some direction as to how to better take care of our patients. When I write these lectures, and this may seem counterintuitive to some, I leave the guidelines for last and attempt to read everything under the sun on the topic so that it does not cloud my interpretation. I had read these guidelines in 2018 when they initially came out but now I have even more respect for the section on pain management bc the quality of the studies just aren't as good as we want them to be. Hence the "very low quality of evidence" tied to many of the recommendations made. I surprised that they even made a dosing recommendation for ketamine as the dosing behind most of the articles are pretty scattered.  

These guidelines are a monumental undertaking and I send a definite hat tip to the authors.

Devlin JW, Skrobik Y, Gélinas C, et al. Clinical practice guidelines for the prevention and management of pain, agitation/sedation, delirium, immobility, and sleep disruption in adult patients in the ICU. Crit Care Med 2018;46:e825–e873.

-EJ

Link to FULL FREE Article



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Early Vasopressors in Septic Shock?

This is a question that is often asked. Do we give fluids until the patient no longer "responds to fluids" or start vasopressors early?

Here's my bias: I dislike arbitrarily pounding patients with fluids. It causes harm. We know this.

I don't know what people who aren't doing advanced hemodynamic monitoring of some sort mean when they say "they respond to fluids". "I gave a liter of fluids and the BP got better" for 30 minutes is not a determinant of fluid responsiveness. Remember, I've cited here before that critically ill patients extravasate 80% of that liter of fluids within one hour. What did you really do outside of feeling like you did something? The authors used PPV, SVV, echo with VTI combined with PLR, end-expiratory occlusion maneuvers, and capillary refill time. Did I mention that these authors are legends in the field? Well, they are.

In my opinion, providing pressors early provides a safety net of sorts to the organs to make sure they're being perfused. You've seen it often in your ED and ICU. Patient comes in sick. They're hypotensive, they get their 30cc/kg and their BP gets "better". The cuff cycles again 15 minutes later and their BP is now 60/30. How long did those organs go under-perfused? Minutes matter. We NEED to get better at this. After all, we are supposed to be the biggest badasses in medicine, yet we often shrug our shoulders and react when it's ugly instead of preemptively fixing the issues.

Turns out that very early vasopressors were beneficial to the patients. The definitions of the two groups are defined on my slides. The outcomes are also defined there for the sake of not taking up too much space.

This could be practice changing data. I personally start vasopressors really early in my practice. Some may say, let's wait for a prospective randomized clinical trial before putting this into practice. To those people I say, there's no harm in this. Also, you can't blind the physicians so when that study comes out positive some will say "oh but the physicians weren't blinded". Research. Sigh.

A hat tip to the authors. This article was published yesterday. How's that for cutting edge?

-EJ

Ospina-Tascón, G.A., Hernandez, G., Alvarez, I. et al. Effects of very early start of norepinephrine in patients with septic shock: a propensity score-based analysis. Crit Care 24, 52 (2020).



Link to Abstract

Link to FULL FREE PDF



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Weaning Order of Norepinephrine and Vasopressin in Septic Shock Patients

This is a post for all my Critical Care Nurses out there! Please tag and share with your friends and colleagues. When you have a patient in shock on norepinephrine and vasopressin and has turned the corner, which vasopressor do you turn off first: norepinephrine or vasopressin? From my hard digging through the internets I have only found three studies which touch on this topic. Also, this seems like a pretty simple RCT that I could actually do at my shop. Anyone interested in joining in on the fun to make it multi-centered? These slides to some extent will be featured in my Hawaii and Portland lectures later this year. Seems like I'll be heading to Brooklyn and Indian Wells, CA in 2021.

Here's what the data says. Spoiler alert: there's no 100% correct answer.

2010: Bauer, et al. did a retrospective study where the team found that patients did better if the NE was weaned first and the vasopressin was weaned second.

2017: Hammond, et al. also performed a retrospective study which found similar results: patients did better if they weaned off the NE first. So far so good for weaning off NE first.

2018: Jeon, et al. just had to throw a wrench into everything. This was a prospective randomized trial where the results were the exact opposite of the other two. Ugh. Those of you who have been hanging out with me long enough may recognize that I covered this study in March of 2019 when the page was just getting ramped up.

Well what's the right answer? I guess we just don't know. Dealers choice. The randomized trial should hold more of an answer due to it being higher on the scale of evidence. The studies are small, hence me considering on doing a trial on this since ultimately it's not going to cause any harm and I really don't have a bias. What do you think?

-EJ

Link to Article (not free)

Bauer S, Aloi J, Ahrens C, Yeh J, Culver D, Reddy A. Discontinuation of vasopressin before norepinephrine increases the incidence of hypotension in patients recovering from septic shock: a retrospective cohort study. J Crit Care. 2010;25(2):362.e7-362. e11.

Link to Article (not free)

Hammond DA, McCain K, Painter JT, Clem OA, Cullen J, Brotherton AL, Chopra D, Meena N. Discontinuation of vasopressin before norepinephrine in the recovery phase of septic shock. J Intensive Care Med. 2017:885066617714209

Link to Full FREE PDF

Jeon K, Song JU, Chung CR, Yang JH, Suh GY (2018) Incidence of hypotension according to the discontinuation order of vasopressors in the management of septic shock: a prospective randomized trial (DOVSS). Crit Care 22(1):131

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Dexamethasone in ARDS

This is a big impactful study. I'm happy it came out, really happy. To start off a big hat tip to my colleagues in España who put this together. ARDS sucks. It's a b-word to treat and patients spend a frustratingly long time to come off of the vent. Mortality rates are high. Morbidity rates are through the roof. Cost burden to the healthcare system is insane. The repercussions are unquantifiable. Many of these people never even return to work.

In my practice, when I have a patient with ARDS, I make sure to treat the underlying cause, protect their lungs with the vent, keep them as dry as humanly possible, and provide them with 4 days of vitamin C, hydrocortisone, and thiamine. The CITRIS-ALI study providing vitamin C showed a decrease in mortality in this population, less time in the ICU, and less time in the hospital (albeit with many caveats to that study). There's bench research that shows how vitamin C and corticosteroids are synergistic in preventing and repairing lipopolysaccharide-induced pulmonary endothelial barrier dysfunction. But we never had good data regarding giving these patients steroids to begin with. In theory it made sense, but we needed more help. We were simply doing our best and shrugging our shoulders in many of these cases.

Enter the DEXA-ARDS trial. They randomized patients with moderate to severe ARDS to either get dexamethasone or placebo. Note that they give the first dose immediately after randomization, something that they waited 12+ hours to do in the VITAMINS trial. I digress. Not bitter. Okay I'm bitter. Nonetheless, the pts who got steroids did better. They came off the vent quicker and had fewer deaths. Both statistically significant. One of the key takeaways regarding the vent free days is that we start thinking to trach pts around day 10-14. The dexamethasone group got off the vent around day 14. The control group around day 20. How many trachs were spared and the morbidity that comes with that? It's not specified in the article but I'm curious. Another key piece is the fact that there was no increase in side effects of the steroids.

Ultimately this trial is changing my practice. I was perhaps stopping steroids too early in the past.

-EJ



Villar J, Ferrando C, Martínez D et al. Dexamethasone treatment for acute respiratory distress syndrome: a mutlicentre, randomised controlled trial. Lancet Respir Med. 2020; (published online Feb 7.)

Link to Article (NOT FREE boooooo!)

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Non-Invasive Ventilation Algorithm

Not every patient reads the textbook, but you and I have to know where to start when managing our patients who have hypercapnic respiratory failure that we want to treat with non-invasive ventilation (or what you and I frequently call BiPAP). This algorithm is taken from the British Thoracic Society/Intensive Care Society Acute Hypercapnic Respiratory Failure Guidelines that were published in 2017. Fortunately, they are free for you to download your own copy and put it up on your wall. 

This guideline recommends starting with an EPAP of 3. If I'm honest, everywhere I've been and the way I've been trained is to start at 5. Also, they recommend uptitrating the IPAP up to 20-30. In my practice, once I start kissing 20, I start thinking very seriously about intubating the patient. 

For those who are unfamiliar with the kilopascal units (as I certainly was), the equivalent PCO2 is 48.75mmHg. Note that you need to have acidosis and hypercapnia in COPD exacerbations to have any benefit from NIV. 

A hat tip to the authors. 

Davidson AC, Banham S, Elliott M et al. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016;71 (Suppl 2):ii1–35.

-EJ






Link to Article with FULL FREE Algorithm

Ghosh D, Elliott MW. Acute non-invasive ventilation - getting it right on the acute medical take. Clin Med (Lond). 2019;19(3):237–242.



Link to the FREE FULL Guidelines

Davidson AC, Banham S, Elliott M et al. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016;71 (Suppl 2):ii1–35.

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Cortisol Levels: Check prior to SDS in Septic Shock?

Your patient is in septic shock. They've gotten the correct source control, antibiotics, fluids, vasopressors. They remain hypotensive. Getting worse, actually. Could they have relative adrenal insufficiency or one of these fancy-termed conditions such as "critical illness-related corticosteroid insufficiency" (CIRCI)?

Should you check a cortisol level to find out or just start stress dose steroids?

In my practice, I do not check cortisol levels. No need to stick the patient for more blood. No need to waste any additional money for lab tests. No need to delay care in waiting for a lab result. Once the norepinephrine dose starts creeping up, I order stress dose steroids (as well as vitamin c and thiamine at the time of this writing). This is all my medical opinion and not advice, in case you didn't know.

The most recent trials on stress dose steroids do not check cortisol levels, so why should you? I tried to dig deeper into this point as I cannot get others to stop checking random cortisol levels on their critically ill patients. But why? There's no diagnostic consensus about the appropriate cortisol level for patients in septic shock. In addition to that, there's data that states that "both cortisol and synthetic ACTH challenge assays are unreliable in critically ill patients". So then why do we keep doing it?

Is there something out there that I don't know and you all can provide me with insight on? I'm looking for help on this.

A hat tip to the author. 

Reddy, Pramod. Diagnosis and Management of Adrenal Insufficiency in Hospitalized Patients. American Journal of Therapeutics, 2019. E-pub ahead of print.

Link to Article

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Probiotics in ICU: UPDATED

It certainly got me thinking when several people messaged and commented to me regarding their hospitals not allowing probiotics on their ICU patients. I decided to take a little bit of time to see if this was an old habit that just doesn't die, you know, a resistance to change, or if it's something substantiated by data. 

At first I didn't find anything to substantiate the claims. Key words were "at first". Now I understand what they're talking about and I even more appreciate the fund of knowledge that this page brings to the medical community. 

The exact mechanism, whether translocation from the gut, contamination with a central line, or something else is unknown. What is known is that 1.1% (6 of 522) of the patients at this facility who received probiotics developed a bacteremia related to the probiotic agent. That's not a large number but at the same time a large number in my opinion. I'll stress again, my opinion, not medical advice. I do not want to cause harm to my ICU patients. For those wondering, these patients were not severely immunocompromised nor did they have bowel disintegrity. 

I will wait until more data comes out before I start implementing this in my practice. As always, I appreciate the insight that you all provide. 

A hat tip to the authors. 

-EJ

Yelin, I.; Flett, K.B.; Merakou, C.; Mehrotra, P.; Stam, J.; Snesrud, E.; Hinkle, M.; Lesho, E.; McGann, P.; McAdam, A.J.; et al. Genomic and epidemiological evidence of bacterial transmission from probiotic capsule to blood in ICU patients. Nat. Med. 2019, 25, 1728–1732.

Link to the Article

Yelin, I.; Flett, K.B.; Merakou, C.; Mehrotra, P.; Stam, J.; Snesrud, E.; Hinkle, M.; Lesho, E.; McGann, P.; McAdam, A.J.; et al. Genomic and epidemiological evidence of bacterial transmission from probiotic capsule to blood in ICU patients. Nat. Med. 2019, 25, 1728–1732.

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Probiotics in the ICU

ADDENDUM: I have found new data regarding probiotics leading to bacteremia that was published HERE. This changes my take on prior research. 

Here's something I'm fairly certain we (meaning your team and mine) do not do in our practice that perhaps we should give some more consideration to: providing probiotics for our patients.

There's much we don't know regarding the microbiome. It completely fascinates me. Immediately upon arrival to the ICU, damage is done to the microbiome in our intestines via stress, shock, antibiotics, etc. Bad bugs take over where the good bugs used to live. How do we get those good bugs to come back? Could providing good bugs (probiotics) help get our patients better faster?

The following slides are some of my preliminary slides for my "ICU Nutrition and Gut Health" lecture. I was a bit too excited to share to wait until they were complete.

The 2016 ASPEN guidelines state that they cannot make a recommendation regarding using them routinely. I'm curious as to whether the 2020 guidelines (coming out next month) will state the same. I have cited articles where probiotics improve antibiotic associated diarrhea, two meta-analyses where they show benefit for ventilator associated pneumonias, a meta-analysis where the show decreased overall infections, and how they help to reduce the development of C.diff.

Now, if one were to think that probiotics were a cure to everything, that person would be wrong. There will likely never be a one-treatment to cure all the ailments in critical care. But if we can keep adding tools to our tool belts as more data comes out, then we will better be able to care for our patients and improve outcomes.

A hat tip to all the authors.

-EJ

Link to Article

McClave SA, Taylor BE, Martindale RG, et al; Society of Critical Care Medicine; American Society for Parenteral and Enteral Nutrition: Guidelines for the provision and assessment of nutrition support therapy in the adult critically Ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr 2016; 40:159–211

Link to Article

Hempel, S. et al. Probiotics for the prevention and treatment of antibiotic-associated diarrhea: a systematic review and meta-analysis. JAMA 307, 1959–1969 (2012).

Link to Article

Weng, H.; Li, J.G.; Mao, Z.; Feng, Y.; Wang, C.Y.; Ren, X.Q.; Zeng, X.T. Probiotics for preventing ventilator-associated pneumonia in mechanically ventilated patients: A meta-analysis with trial sequential analysis. Front. Pharmacol. 2017, 8, 717.

Link to Article

Manzanares, W., Lemieux, M., Langlois, P.L. et al. Probiotic and synbiotic therapy in critical illness: a systematic review and meta-analysis. Crit Care 20, 262 (2016).

Link to Article

Goldenberg JZ, Yap C, Lytvyn L, Lo CKF, Beardsley J, Mertz D, Johnston BC. Probiotics for the prevention of Clostridium difficile‐associated diarrhea in adults and children. Cochrane Database of Systematic Reviews 2017, Issue 12. Art. No.: CD006095.

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Nutrition in Critical Illness

I’m writing a lecture on Nutrition for the ICU patient population. It’s been quite tough to find substantial data because of the many nuances and the vast heterogeneity of the patient population. That being said, this review article came out a few days ago and it provides a guide of sorts to provide our patients with nutrition during their different phases in the ICU. My understanding is that the ASPEN group shall be meeting towards the end of March. I am looking forward to whatever guidance they can provide so I can better care for my patients.

Fortunately this article is free! A hat tip for the authors.

Lambell, K.J., Tatucu-Babet, O.A., Chapple, L. et al. Nutrition therapy in critical illness: a review of the literature for clinicians. Crit Care 24, 35 (2020).

Link to article

Link to FREE PDF

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

Lactate Levels cannot be corrected by Giving More Oxygen

I have covered lactate quite thoroughly over the last couple weeks but I still receive comments and questions from followers talking about oxygen deficiency to the cell causing elevated lactate and lactic acidosis. They ask "why don't you just increase the O2 that you're providing to the patient to help the cells out"? This question is not out of line with traditional thinking behind lactic acidosis being the byproduct of "tissue hypoxia" which I hope at this point you understand is NOT the cause of elevated lactate levels in septic shock patients (see many other posts for further details).

This study published in JAMA in 1993. The three key findings of their work include:

1. Critical O2 delivery was identified and is considerably lower than previously estimated. Increasing O2 delivery to supra-normal levels in critically ill patients in the hope of increasing O2 consumption may be inappropriate.

2. Sepsis was not associated with an increased critical O2 delivery

3. The increased concentration of arterial lactate at baseline was not associated with global tissue hypoxia, suggesting that lactate may not be a specific marker of tissue hypoxia in critically ill patients.

Hope this helps! A hat tip to the authors!

- EJ



Link to Article

Ronco JJ, Fenwick JC, Tweeddale MG, et al. Identification of the Critical Oxygen Delivery for Anaerobic Metabolism in Critically III Septic and Nonseptic Humans. JAMA. 1993;270(14):1724–1730.

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.

Can We Use Something Other Than Lactate To Guide Resuscitation?

Nurses: you see those orders. q1, q2, q4h lactates to help guide resuscitation in septic shock. You have to drop what you're doing and draw labs. Hopefully, if the patient is sick enough to need the labs, they have a central line. Hold off of titrating drips, hold off on the ever important charting you are required to do, let's trend lactates which I have previously discussed the utility of (or lack of utility). Along the way we contribute to iatrogenic anemia, spend a bunch of lab money, etc.

What if there was another option? Well, the ANDROMEDA-SHOCK trial proves that you can intelligently resuscitate patients without checking lactate levels. What they did was randomize >400pts to either have their resuscitation guided by lactate or this nifty little trick called Capillary Refill Time.

One of my favorite parts of the trial wasn't even the CRT vs. lactate component but their algorithm to determine fluid responsiveness which is a major interest of mine. I am not a fan of arbitrarily giving a pt liter after liter of fluid to "clear lactate" or improve the blood pressure. That just does not work and my body of work has data to prove that. I digress. Sometimes you need to read the supplementary materials in these articles as their algorithm was hidden in there.

Standard of care by CMS (the body that pays the hospitals and therefore us in the US) has mandated checking lactates despite no good evidence that trending it does much. This study shows that checking CRT is AT LEAST as good as checking lactate levels. The mortality was not statistically significant (p=0.06) but I wonder what would've happened if they would've had an additional 200pts in the trial. The CRT group had 34.9% mortality vs 43.4% in the lactate group. The CRT group also had fewer organ failures (p=0.045). Other fun facts include the fact that the lactate group received more fluids in the first 8h (p=0.01) but not overall. I don't know what to make of this.

All in all, even with its limitations, I feel this is a solid study. I really like it. I do not use CRT in my practice but I may be asking for a microscope slide to keep in my pocket in the upcoming weeks.

A hat tip to the authors

Hernandez G, Ospina‐Tascon GA, Damiani LP, Estenssoro E, Dubin A, Hurtado J, et al. Effect of a resuscitation strategy targeting peripheral perfusion status vs serum lactate levels on 28‐day mortality among patients with septic shock: the ANDROMEDA‐SHOCK randomized clinical trial. JAMA. 2019;321(7):654–64.

- EJ




Link to FULL FREE ARTICLE

Although great care has been taken to ensure that the information in this post is accurate, eddyjoemd, LLC shall not be held responsible or in any way liable for the continued accuracy of the information, or for any errors, omissions or inaccuracies, or for any consequences arising therefrom.