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Saturday, March 9, 2019

EM Chief Hired Only Men for 16 Years

BY RUTH SORELLE, MPH

It began with a short-lived post on a closed Facebook page for female physicians about a year ago.

The post revealed one of Toronto's worst-kept secrets, that Marko Duic, MD, then the chief of emergency medicine at Southlake Regional Health Centre in Toronto, had hired no female EPs during his tenure there or before that at Toronto's St. Joseph's Health Centre, a period of 16 years. The post attracted considerable attention before it was taken down, according to The Globe and Mail, the Canadian newspaper that published an article about Dr. Duic on Dec. 16.

That newspaper article led Southlake to start an independent review of ED hiring and prompted Dr. Duic to resign on Jan. 31 before the assessment was complete.

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When Dr. Duic took over each ED, he created a floating schedule giving emergency physicians more choice and control. (http://bit.ly/2T9kZUF.) Doctors were asked to come in early and perhaps stay late when volume was high, and they were asked to check vital signs in the waiting room. This decreased waits and resulted in the hospitals collecting Ministry of Health performance bonuses that, according to The Globe and Mail, amounted to $2.5 million in 2017-2018. He describes himself as an emergency patient flow advisor on his LinkedIn page.

The spotlight on Dr. Duic's hiring practices came after eight female physicians decided to demand a change. After considerable discussion, they informally surveyed 28 similar emergency departments in Ontario or nearby, finding that 34 percent of the emergency physicians in those departments were women while Southlake had no female EPs among its 31 doctors.

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They asked Danny Kastner, a Toronto attorney, to file a complaint and request an independent investigation into Dr. Duic's actions in March 2018. A copy of that complaint was given to Emergency Medicine News by an anonymous source.

Fear of Being Blackballed
Mr. Kastner said his clients do not want their identities revealed because they feared the power that Dr. Duic still wields. Even when promised anonymity, they said they were afraid they would be blackballed in the emergency medicine community.

Mr. Kastner's March 9, 2018, letter, however, noted that Dr. Duic appeared to have hired only male physicians in his role first as the chief of emergency medicine at St. Joseph's (2002-2011) and then at Southlake (2011-2019). They wrote that the leaders of Southlake Regional Health Centre, the University of Toronto Royal College, and its faculty of medicine and program directors have oversight responsibility for Dr. Duic and the trainee programs for which he has responsibility.

"…Dr. Duic appears to have engaged in a deliberate and long-standing practice of refusing to hire or work with women physicians. The institutions at which Dr. Duic has worked, including Southlake and U of T [University of Toronto], appear to have tolerated this," the women wrote.

They asked Southlake and the University of Toronto to coordinate an independent investigation to determine if their concerns were valid, to remove Dr. Duic from hiring processes in the interim, and to suspend all university rotations at Southlake until the investigation was completed and a nondiscriminatory learning environment was assured.

The letter alludes to several accounts of Dr. Duic refusing to hire women in his department. "Almost immediately after Dr. Duic ceased his role in hiring, the number of women in the Emergency Department increased dramatically. Since 2016 a total of 13 women have been hired, taking the Emergency Department from nearly all male to roughly 30 percent female in less than two years," according to the letter.

'No Evidence'
According to The Globe and Mail article, both institutions responded to Mr. Kastner that they had conducted internal investigations that did not find evidence of discrimination. (Dec. 16, 2018; https://tgam.ca/2Xhhjzx.) The institutions first told Mr. Kastner and his clients that they saw no need for an independent investigation and that their internal investigation was sufficient.

Southlake's chief of staff, Steven Beatty, MD, wrote Mr. Kastner in April 2018 to say "the only evidence that Southlake has engaged in discriminating practices is the absence of female emergency physicians currently providing care in the emergency department at Southlake," according to The Globe and Mail. He said other types of diversity, such as sexual orientation, race, and age, should be considered. The Globe and Mail reported that Dr. Beatty provided data that showed that Dr. Duic supervised 25 male and no female trainees from April 2011 to April 2015.

An open letter and petition from the group Canadian Women in Medicine noted that the internal investigation consisted of "reviewing years of evaluations from trainees who completed rotations at the St. Joseph's and Southlake emergency departments for any suggestion of gender discrimination or equity issue." Trevor Young, MD, the dean of the faculty of medicine, said the lack of specific complaints from Dr. Duic's trainees about sexism raised no equity concerns about the clinical learning environment at the Southlake Emergency Department. (http://bit.ly/2SdqZHy.)

The women's group took issue with those findings drawn from teaching evaluations by the 25 men Dr. Duic supervised at that time. They called the investigation incomplete, and asked: "How can this reasonably be considered a sensitive test for gender discrimination in the department?"

Once The Globe and Mail reporter started investigating the claims this past October, Southlake hired a female emergency physician as well as an outside firm to conduct an independent investigation. Mr. Kastner said he was told the investigation is ongoing, and hopes its results will be made public.

Petition Posted
Canadian Women in Medicine's petition about the issue has recorded at least 450 signatures so far. (https://canadianwim.ca/.) Setareh Ziai, MD, the president of the organization, said Dr. Duic was also reported to have resisted supervising female medical students and residents. "Canadian Women in Medicine has heard [this] from many members of our organization, who themselves were aware of Dr. Duic's reputation or rotated as trainees through one of the emergency departments where Dr. Duic was chief," she said. "[W]e are disappointed with the University of Toronto's inaction on this issue. This conduct is completely unacceptable and unethical. He continues in his clinical role as an emergency physician and maintains his faculty appointment at the University of Toronto. This means that he continues to teach medical trainees who are sent to rotate through his department."

Dr. Ziai said CWIM also has strong concerns about the clinical learning environment in the Southlake ED. "We don't see that an all-male environment where there is an ongoing investigation into a leader's misogyny can reasonably provide an equitable learning experience for female trainees. We are also concerned about the messages that male trainees may be receiving in this 'learning' environment," she wrote to EMN in an email.

A spokesperson for the faculty of medicine at the University of Toronto wrote to EMN in an email that the faculty has contractual agreements with its hospitals, each of which is an independent organization governed by its own board. "The University has no approval authority over hospital hiring decisions, nor does it comment on personnel matters," she wrote.

A spokeswoman for Southlake did not respond to a query from EMN about this article.

Dr. Duic responded to EMN's request for an interview with an email that stated: "I made the decision [to] step down as Chief of the Emergency Department as of January 31, 2019. My sole focus now is my full-time clinical duties, supporting hospital leadership and my emergency colleagues. Working as the Chief of Emergency Medicine at Southlake Hospital was one of the most rewarding experiences of my professional career. I worked with an outstanding team, and am proud of our collective accomplishments. The positive changes we made together were considerable and established a legacy of innovation and efficiency, resulting in some of the best waiting times in the Province of Ontario. The key to our success has been our intense and unwavering commitment to the people we serve: our patients and the community."

He did not respond to questions about his hiring or educational practices.

Ms. SoRelle has been a medical and science writer for more than 40 years, previously at the University of Texas MD Anderson Cancer Center, the Houston Chronicle, and Baylor College of Medicine. She has received more than 60 awards, including the Texas Human Rights Foundation Award. She has been a contributor to EMN for more than 20 years.

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Wednesday, March 6, 2019

Don't Be Fooled by New Study: 
Tamiflu Still Pretty Worthless for H1N1

BY DAN RUNDE, MD

It's possible that the Tamiflu pandemonium may be peaking for most emergency and primary care physicians because the dubious benefits of oseltamivir have now been well documented, discussed, and disseminated. (See box.) But there's also a new kid on the block (baloxavir marboxil, AKA Xofluza) that is all too likely to be jammed down our collective throats, displacing its controversial cousin.

That said, it seems we never go too long before another article comes along touting the life-saving properties of this wonder drug. It's not that the medicine doesn't work, its proponents claim, it's that we're giving it to the wrong population or with the wrong timing or in the wrong amount. We end up with endless speculation on how the mechanism of action for this medication might be more or less effective against various subtypes of influenza, despite the fact that the authors of the definite Cochrane Review about this subject have written that "the influenza virus-specific mechanism of action proposed by the producers does not fit the clinical evidence." (Cochrane Database Syst Rev 2014 Apr 10;[4]:CD008965; http://bit.ly/2Hdwgx5.)

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The newest entry in the saga to find the elusive One True Cohort for Tamiflu is an article by Lytras, et al., a retrospective cohort of 1330 very sick patients admitted to Grecian ICUs over eight flu seasons starting in 2010. (Clin Infect Dis 2019 Feb 7. doi: 10.1093/cid/ciz101.) By very sick, I mean very sick: All the patients were intubated, had laboratory-confirmed influenza, and were treated with oseltamivir. Nearly half (46.8%) of the patients in this study died in the ICU. This publication has generated some pro-oseltamivir headlines, so it's probably worth taking a look at the results for patients treated early (48 hours or less from symptom onset ) or late (48 hours or more after symptoms):

  • Death in the ICU (primary outcome): No difference
  • Death in the ICU for A type H1N1 strain: No difference
  • Death in the ICU for A type H3N2 strain: No difference
  • Death in the ICU for B type influenza: No difference (obviously)
  • Increased cause-specific hazard for discharge for A type H3N2 strain: csHR 1.89, 95% CrI 1.33-2.70

The first (and second and third) time I looked at those results, I thought, "Well, that looks like another swing and a miss for Tamiflu." The authors, however, arrived at a slightly different conclusion: "[I]n the absence of randomized trials, our study provides strong and important new evidence about oseltamivir use in critically ill influenza patients."

The Bottom Line
I turned to a colleague to seek some clarity. Brett Faine, PharmD, an emergency medicine clinical pharmacy specialist and an assistant professor of pharmacy practice and science at the University of Iowa College of Pharmacy, has a passion for evidence-based clinical practice and, in a related development, a long-standing skepticism of oseltamivir and the way it has been marketed and recommended around the world. My first question to him was whether I was alone in my confusion about the conclusions from this paper. "No, I think it's important to note that this was a negative study," he said. "There was no difference in the primary outcome. Period. Overall, early oseltamivir didn't appear to save any lives, even in this very sick cohort."

How did we go from there to a recommendation to keep giving Tamiflu to critically ill patients? "They are basing this entirely on a finding from a subgroup analysis [only 20.8% of patients], which found that fewer patients with the A/H3N2 subtype died in the early oseltamivir group [33.7% vs 48.4% respectively, p=0.029]," Dr. Faine said.

Were patients at less risk of dying in the ICU if they got early Tamiflu and had H3N2? "No," he said. "Actually there was no difference in deaths in the ICU for these patients. The benefit was entirely driven by an increase in the number of patients in this group who were discharged from the ICU."

I'm still confused, so I asked him to explain it once more. "The cumulative hazard analysis revealed that among the A/H3N2 patients, the hazard of death was no different, but the hazard of ICU discharge, a good thing in this case, was significantly increased," he said. "The authors argue that the instantaneous risk of dying is not [affected] by Tamiflu but that the hazard of discharge from ICU translated into lower mortality. They discuss that this is likely due to the mechanism of action—inhibition of viral replication and neuraminidase, but I would just note that the Cochrane authors call into question whether oseltamivir even works this way at all."

Are there other reasons to be skeptical of these findings? "Where to start?" Dr. Faine said. "It was a negative study with a positive subgroup analysis. The study is limited based on the usual stuff that plagues observational studies, but also the fact that we do not have information on dosage or duration, so we have no idea how much of the medicine was given, for how long, or if it was discontinued. We also get no data on adverse events. It took a lot of statistical massaging to come to the conclusion that Tamiflu was effective in A/H3N2. And we have no data on overall mortality in these patients. We have no idea what happened to them once they left the ICU, no data on hospital discharge, inpatient mortality, or survival at any time post-discharge."

Bottom line? "In my opinion," Dr. Faine said, "the conclusions made in this article, specifically that we give Tamiflu to all sick influenza patients, is not supported by the study findings."

To his credit, Theodore Lytras, MD, PhD, also acknowledged some room for doubt in an interview on the topic. "We would not describe the results of our study—or any single study, no matter how well-designed and analyzed—as a basis for 'firm conclusions,'" he said. "[W]e believe our results will need to be replicated in further studies, ideally randomized." (MD Feb. 22, 2019; http://bit.ly/2EntfXR.)

We should remember that almost all of the literature purporting that oseltamivir decreases mortality has been related to H1N1, and if there's one thing that this study makes abundantly clear, it's that Tamiflu appears pretty worthless for the H1N1 cohort.

Dr. Runde is the assistant residency director and an assistant professor of emergency medicine at the University of Iowa Hospitals and Clinics, where he serves as co-director for the associate fellowship in medical education. He creates content for and is a member of the editorial board for www.TheNNT.com, and is a content contributor for www.MDCalc.com. Follow him on Twitter@Runde_MC, and read his past articles at http://bit.ly/EMN-MythsinEM.


Read Dr. Runde's first article, "Still Prescribing Oseltamivir?" at http://bit.ly/JustSayNoToTamiflu.


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Wednesday, February 20, 2019

In Honor of the Clot (Consider the Lobster)

BY MICHELLE JOHNSTON, MBBS

David Foster Wallace wrote novels that were dense and impenetrable, but his essays were breezy, and they sparkled with wit and wisdom. One of my favorites was called "Consider the Lobster," commissioned by Gourmet Traveler, about the Maine Lobster Festival. (August 2004; http://bit.ly/2BYyoo1.) He wrote so well, so beautifully, that you could see the sunshine dancing on the yachty harbor, you could just about taste the melted butter from the freshly cooked lobster, smell the spritz of the lemon.

SR lobster.jpg

But then, fairly quickly, the essay turned, morphing into something darker, and we were shown Disneyland-grade queues of sweating, overweight people who were watching live lobsters being plunged into a boiling pot in front of them. The essay turned out to be about rather different things: Is it right and moral to boil sentient creatures alive for our own gluttonous pleasure? Do these simple animals feel pain? But as interesting as these neurobiological arguments are, really what I want is for you to hold two things in your head. One is that sometimes the main learning points of an essay or talk are hidden off in the shadows, in the periphery, and two, the image of a lobster.

But let's get clinical. I am the consultant on duty, and it's close to midnight. I get a phone call from a hospital about 60 km away. They've got a 72-year-old farmer who has had a big anterior infarct. Quite rightly, because of the time and the distance, they have thrombolized him. His chest pain is settling, his ST segments are coming down, and they want to send him to us. I say, we'd love to have him. Several minutes later, I get another phone call, quite panicked, and the unwelcome has happened: massive hematemesis.

Say what you like about us emergency physicians, but when things become unexpected and messy, that is our bread and butter. I say, I know how to reverse this. Not much works, but what you should do is throw the kitchen sink at him. Unfortunately, they only have the tepid water of the kitchen sink (FFP), but I say just get him on his way, and we'll be ready. Don't you worry; it will all be good.

Hold the Sink
While I'm waiting for this patient, I look at his name, and I realize he is a very dear old friend of mine. I don't know about you, but when you know someone, you start to second-guess yourself. Throwing the kitchen sink aat him now sounds terrible. Do I really know what the best treatment is? Am I going to make him reclot again if I start pouring stuff in? I don't know the answers as well as I thought I did. So I'm madly googling, looking for guidelines, and I come up with…nothing.

So I ring the hematologist on call for his advice, and he says, ring the emergency physician, and I say, that's me. The patient is suddenly on our doorstop, doing a bit poorly, but luckily, he does fine.

Afterwards, I thought this is not good. This is a big knowledge hole; reversing the effects of thrombolysis. So I did a very scientific study—all the researchers would be proud of me—I asked a hematologist, a neurologist, a respiratory physician, a cardiologist, an intensivist, and an emergency physician, "How do you reverse thrombolysis?" They all came up with the same thing: Throw the kitchen sink at them. Throw all the products at them, and good luck to you. Not much works.

I'm not happy here. All I'm left with is a big fat pile of questions. So I read and read, and I performed a literature review, some of which I'll present here. The thing is, the more I read, the more I realized that not only do we not know how to reverse the effects of thrombolysis, we hardly even know how tPA works. And not only that, we hardly even understand the coagulation-fibrinolysis system.

About this time I go to the museum under the pretense of taking my 12-year-old son, but it's really because I love dinosaurs. There, next to the T-Rex bones, is a plaque that says, "On this bone is evidence of clot." I thought, whoa! Two hundred million years ago, we were clotting. I had never considered how old this whole clotting system is. How far back am I going to have to go to really understand coagulation so I can return and understand what we do to it now? As Carl Sagan said, "If you wish to bake an apple pie from scratch, you must first invent the universe."

Understanding Clotting and tPA
I had to learn about how clotting evolved. What I discovered, what's fascinating about the evolution of clotting, is that it is held up, along with the human eye, by creationists as an example that evolution cannot possibly exist because it is an example of something called irreducible complexity, meaning a biological system so complex that if you take away one part, the whole system can't work. It couldn't just evolve, piecemeal, over time.

This, of course, is completely bollocks, and lots of wonderful bits of evidence show us how clotting and fibrinolysis evolved. One of the great pieces of evidence comes back to our old mate, the lobster, who is a very, very distant archeological relative of ours. He has managed to evolve his very own fibrinogen, which works exactly the same but has come from a very different protein called vitellogenin, a yolk protein, which is very cool.

This is how we teach the clotting-fibrinolysis connection; this is how we all learn it in med school. (See diagram.)

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The preposterously oversimplified diagram of the Coagulation Minuet.

Now, this is ridiculously, preposterously oversimplified. Really it is much more of a swirling concatenation of these elements, and so much more. It is so complex; it is not just those proteases that we all learned about, those nice cascades, it is cellular, it is endothelial, there are amplifications, dampenings, there are positive feedback loops, negative feedback loops. The clotting cascade has effects on almost countless other cascades in the body. It is so utterly complex.

Into it we bring this: recombinant tPA, very similar to our endogenous tPA. You all remember how tPA works. It activates plasminogen to form plasmin, and plasmin dissolves the ropey fibrin around the clot, usually in about three to six days, and the clot goes away. But if you actually asked tPA, it would be highly insulted that it was given this name because tPA is what is known as a highly pleiotropic molecule, meaning it has many, many, many functions, including stimulating these matrix metalloproteinases, which cause breakdown of the blood-brain barrier, and extracellular proteolysis. It causes vasoconstriction. It has many effects on exocytotoxic transmission, and it has an extensive role in neuronal remodeling in embryos and in later life. And we have no idea what role all of these things play in us because we are only finding them out in animal models.

The Elephant
Let's try to understand that whole clotting-fibrinolysis web a little bit better by thinking about it as a regency dance. In a normal situation, it is a very cultured and genteel situation, and things happen at the right time. We clot, and in three to six days, tPA comes in, bows, does its bit, and leaves. That's how it should work. But when we give tPA, basically we pour this souped-up, narcissistic-brute-on steroids, this recombinant tPA, and things go to hell in a handbasket. Everything happens at once. I was taught that tPA was fibrin-specific, but that is mildly rubbish too. It is fibrin-selective but not -specific, so you get this interesting thing called early fibrinogen degradation coagulopathy, fairly newly coined and fascinating. The whole clotting system, that massive Van Gogh swirl of things has to try to catch up once you've done this.

But I've been skirting around the elephant in the room, which is, using tPA in stroke. If it weren't for the cerebral hemorrhages we cause by giving thrombolysis, we wouldn't care that tPA doesn't do much for strokes. We are causing this horrendous complication, however. Six to eight percent get cerebral hemorrhages, and there is no coming back from it. It is terrible. That may not sound like a lot, but if it's something you've done, an iatrogenic injury, then those numbers are much more important.

To argue with myself for a moment, we don't actually know it's the tPA that's causing these patients to have the intracranial hemorrhages. We know when we reperfuse anoxic brain, it's highly at risk for bleeding anyway, and we know that mechanical thrombectomies cause almost as many intracranial hemorrhages without the tPA. We don't know how much tPA badness is going on. But we sure know we need to attempt to reverse the effects of thrombolysis if there is a bleed.

Let me briefly summarize the evidence we do have about reversing the effects of thrombolysis. One, we don't really know the extent of what tPA is doing. Two, it seems the patients who have the greatest drop in their fibrinogen level after tPA are the ones who bleed, and this is the only solid piece of evidence we've got. We don't know if it's causal or correlative, but that's what we've got. It's not the nadir of the fibrinogen level; it's the biggest drop. Three, when we look at all the retrospective and observational studies to see who does what to try to reverse the effects of thrombolysis in intracranial hemorrhage, it's a dog's breakfast. Everyone is doing something different, and there is no consensus at all. And, four, there is no single agent that seems to make a difference.

Reversing Thrombolysis
What is in our guidelines? The best chance we have, based on simple biologic plausibility, is cryoprecipitate. We in the colonies don't get the lovely fibrinogen concentrate, so we get this martini of fibrinogen, fibronectin, factor XIII, factor VIII, von Willebrand factor, and a few other secret ingredients. (Update: We do now. Will it make any difference? Who knows?) They both have fibrinogen, however, and the consensus is that if your fibrinogen is low with a bleed, give the stuff.

Tranexamic acid, you all remember, is a lysine analogue and stops fibrinogen from being activated. Brilliant drug in certain circumstances. But, in post-thrombolysis hemorrhage, fibrinogen has already been activated—the drug has been and gone—if we're trying to reverse thrombolysis, it probably doesn't have much role at all except that it sounds like a good idea. We often revert back to that academically cachectic argument: Well, it doesn't cost very much, it doesn't do much harm, let's just give it anyway.

Using platelets, surprisingly, has a reasonable biologic rationale. There is a complex way that platelets become activated and grow dysfunctional after tPA because of all the downstream effects. Having said that, of course, the PATCH trial found that antiplatelet agents don't make a difference in intracranial hemorrhage anyway. (Lancet 2016;387[10038]:2605.)

FFP? This is weak tea. There are just not enough factors in there to make a difference at all.

What about prothrombinex? We have three-factor prothrombinex; a lot of places have four factors. We've got II, IX, and X. But, when you think about it, the factors are blameless in post-thrombolysis bleeding. They have done nothing. They are not depleted at all. We have given tPA at the other end of the clotting dance, and that is where the mischief is occurring, at the fibrinolysis end. You can also soup up the protease cascade with factors, give so many inappropriate numbers of prothrombins, that you can make patients clot in all of the unhappy places that people don't want to clot.

We have to ask the singular question in biology. Do I know an incredible amount or do I know absolutely nothing? I'm not sure here.

The future in thrombolysis in strokes is that we won't be looking for agents that reverse thrombolysis better. We'll be looking for agents that are actually able to remove the clot from the stroked out area without causing bleeding and having the problems with reperfusion.

Why did I tell you about evolution? I figure medicine isn't much without a whole lot of wonder, and it's all about the future. To quote another David to finish, "David Bowie: Tomorrow belongs to those who hear it coming."

Dr. Johnston is a board-certified emergency physician, thus the same as you but with a weird accent. She works in a trauma center situated down the unfashionable end of Perth, Western Australia. She is exceptionally skilled in the avoidance of meetings, as well as being very keen on teaching and getting her hands (very) dirty with clinical care. Any time left over is spent writing odd fiction. This leaves no time for domestic duties, at which she is an abject failure. She is the author of the novel Dustfall, available on her website, http://michellejohnston.com.au/. She also contributes regularly to the blog, Life in the Fast Lane, https://lifeinthefastlane.com. Follow her on Twitter @Eleytherius.

This article was gleaned from a lecture Dr. Johnston gave at DAS SMACC. Watch a video of it and view the accompanying slides at http://bit.ly/2H09QAP.

Dr. Johnston's New Column!
We are excited to announce that Dr. Johnston will begin writing a monthly column for Emergency Medicine News. Look for "What Lies Beneath" in April!


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Friday, February 15, 2019

AAEM Opposes NP and PA Independent Practice

BY ANDY MAYER, MD

Talk to any emergency medicine resident, and you'll hear how the incredible burden of student loans looms over them. They calculate the percentage of their future salaries that will be dedicated to repaying these loans, but say the upside is that they expect to have a lucrative job waiting for them.

Residents have delayed their gratification for so long that these loans are just another expected and painful hurdle, but now they face a new and scarier concern, that the golden ring of a secure, lucrative job is no longer certain. What role will they have in the emergency department? Will all advanced practice providers (APPs) with doctorates be called doctors and work independently without physician supervision, limiting the "need" for those expensive and pesky physicians?

It is predicted that the number of APPs will increase by more than a third in the next decade. (Bureau of Labor Statistics, April 13, 2018; http://bit.ly/2RUqnGt.) The evolving relationship between emergency physicians and APPs cannot be ignored.

Emergency physicians need to take a stand on this trend if they want to have any impact on the outcome. If money is the reason for the developing role of APPs in EDs, then insurance companies, government agencies, and corporate management groups will devalue board-certified emergency physicians in the workforce in favor of a less expensive option. The bottom line is that this decision will be easy if the dollar is the major determining factor, especially if physicians are out-lobbied.

Various posts and programs by corporate management groups show where this is going. One by Envision on May 18, 2017, stated, "A new program is empowering emergency department advanced practice providers (APPs) to practice at the top of their license…." (http://bit.ly/2Gh7hsO.) This post stated that the goal of the company's APP Skills, Training, Experience, and Professional Credential (STEP) program is to "prepare APPs to become expert emergency medicine caregivers."

Another example comes from Apollo MD's website: "Apollo MD is proud to offer rewarding practice opportunities for our Advanced Practice Clinicians who serve as vital members of our team. We support our APCs practicing at the top of their licenses…." (http://bit.ly/2Btuvb4.)

Are they supporting independent practice for all of their APPs? What is the top of an APP license? My license enables me to practice as a physician. My credentials and rigorous training enable me to practice as a board-certified emergency physician. The same cannot be said for any APP license.

What about nurse practitioners? A report from the relatively new organization, the American Academy of Emergency Nurse Practitioners (AAENP), stated that 62 percent of emergency departments were using APPs as of 2016, up from only 23 percent in 2010. (April 2018; http://bit.ly/2E0O4JA.) AAENP helped create a national board certification exam for nurse practitioners in emergency care, and they reported a rapidly increasing number of graduate-level programs in emergency care; four new programs opened last year alone. This document also stated that AAENP now represents almost 800 ENPs and "is endorsed and supported by the American College of Emergency Physicians and the American College of Osteopathic Emergency Physicians in its mission to promote high quality, evidence-based practice for nurse practitioners providing emergency care for patients of all ages and acuities in collaboration with an interdisciplinary team."

How slippery of a slope is this to you? Nurse practitioners of the future will have a doctorate of nursing practice and be "board-certified!" Are they the board-certified emergency doctors of the future?

What about the workforce shortage we hear so much about? Do we really need all of these APPs in our EDs? Does anyone else notice the number of emergency physician residencies popping up each year? There is increasingly rapid growth in the number of these new programs, especially those run by corporate management groups. CMGs running residency programs is certainly questionable and is not the subject of this essay, but is the sky really falling? Will there not be enough ABEM/ABOEM emergency physicians available?

This is the real question that needs to be objectively studied. Mark Reiter, MD, a past president of the American Academy of Emergency Medicine (AAEM), has studied this and said if there is really a significant shortage, the question is where APPs would be most helpful. The job market is always tight in areas where people want to live, and many opportunities are available in less desirable areas. Do we have a shortage or just a distribution problem?

AAEM remains committed to our core and founding beliefs and values, and has taken a clear stand on this issue. We believe every patient should have unencumbered access to quality emergency care provided by a specialist in emergency medicine, which means certification by ABEM or AOBEM. AAEM does see a role for APPs in EDs but with a clearly defined and supervised role as part of a physician-led team. Because of these values, the AAEM board of directors decided to eliminate the allied health category of AAEM membership. The academy is a physician organization for ABEM/ABOEM physicians.

I ask you to review these guidelines carefully. (http://bit.ly/2Sj69Lz.) Our profession faces many significant challenges in the near future, and the expanding role of APPs is high on this list. Please advocate for what you believe, and please consider commenting on this vital matter with a letter to the editor.

Dr. Mayer is the president and medical director of the West Jefferson Emergency Physicians Group, a single-hospital democratic group, in Marrero, LA. He is also the editor of AAEM's newsletter, Common Sense.

Read more below about why AAEM decided to dissolve its allied health membership category for nurse practitioners and physician assistants.



Why Did AAEM Take a Stand Against APP Independent Practice?

BY THE AAEM APP TASK FORCE

Physician members of the American Academy of Emergency Medicine have voiced concerns about the use of advanced practice providers (APPs) in the emergency department and their push for independent practice without the supervision or even availability of a physician. The task force spent hours discussing the issues, comparing the education of physician assistants, nurse practitioners, and board-certified emergency physicians, speaking to physicians about their concerns, and examining the literature. (J Emerg Med 2004;26[3]:279; Acad Emerg Med 2002;9[12]:1452; J Emerg Med 1999;17[3]:427; Acad Emerg Med 1998;5[3]:247; Ann Emerg Med 1992;21[5]:528.)

Most emergency physicians have worked with APPs and appreciate that they are talented clinicians who improve emergency department flow, efficiency, and quality of care under the guidance of the emergency physician-led team. Many emergency physicians are aware of situations that place APPs in clinical environments that are beyond their capabilities, level of training, and even scope of practice. This is not the quality of care our emergency patients deserve.

There is a vast difference in the clinical training of APPs compared with EPs. Some APP training programs require only 500 hours of unregulated, supervised clinical experience before graduating, while physicians must complete approximately 4000 hours of clinical experience during medical school and an additional 8500 hours of highly regulated and supervised training as an emergency medicine resident before entering independent clinical practice. (J Emerg Med 2015;48[4]:474.)

APPs do have a valuable role in many emergency departments, but their skills should be used as part of a team led by an ABEM/AOBEM emergency physician. APPs as members of that team should fill a role clearly defined by the emergency physicians in that department which professionally stimulates the APP and results in quality care. The cost of employment is lower for APPs than for EPs. As increasing patient volume drives increased need for coverage, the potential for increased profits grows if APPs replace EPs. The delivery of safe, expert physician-led care to every patient must be the primary factor when making staffing decisions, not profit.

The physicians staffing an emergency department are best capable of determining the needs of their department. Physicians should not be told by management that they must use APPs who have been hired for them. Rather, they should decide how many APPs they need and hire only those candidates who have the expertise and personality to mesh well with the culture of their emergency department team.

Transparency to Patients
We are aware of situations where EPs are expected to supervise three, four, or even five APPs while simultaneously seeing patients primarily. The reality of those situations is often that the EP has only a cursory knowledge of the patients that the APP sees and little or no time to evaluate those patients independently. If defined patients and scenarios are deemed safe for the patient to be seen by the APP with the supervising physician providing only guidance and backup, then a bill should not be sent in the physician's name. We support meaningful patient care by the physicians who are billing for it and transparency to patients. A signature in medicine implies that the signatory attests to the accuracy of the document. Without direct evaluation of the patient, how can one know the accuracy of the document?

Emergency medicine residency is a time for physicians to learn how to practice their profession. Residents should be trained by those who practice the profession in which they are seeking board certification. In a situation where APPs are practicing alongside EM residents, it is imperative to establish processes so that the training of the EM residents is not compromised. Residents need to complete a certain number of procedures to become competent. Attaining these skills should be a priority, and the residents should be the first priority to perform a procedure to become independently skilled.

It is challenging, if not impossible, for a patient to determine the role of all the people with whom they interact in the emergency department. Patients can easily be misled by non-physicians using the term doctor. They should not be expected to understand the difference between an MD or DO and a DNP or DScPAS (doctorate of science in PA studies). Patients deserve full transparency about who is caring for them, and non-physician clinicians must truthfully represent their level of training.

Throughout its history, AAEM has consistently asserted that ABEM/AOBEM certification is essential. The academy has also spoken against emergency departments staffed by non-ABEM/AOBEM physicians. Supporting the independent practice of APPs in our emergency departments is inconsistent with these core values. If APP independent practice is tolerated, a logical profit-driven next step is staffing entire emergency departments with APPs and even developing staffing companies to provide that coverage.

Our specialty owes its identity to our founders who demonstrated that the skills required to manage an emergency department expertly were unique in the house of medicine. They struggled to establish the specialty of emergency medicine and define the training required to become a specialist in emergency medicine. The independent practice of APPs has the potential to undermine all the efforts of those men and women who created the specialty of emergency medicine.

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Wednesday, February 13, 2019

Ultrasound Can Shorten Pulse Checks during CPR

BY CHRISTINE BUTTS, MD

The use of ultrasound in cardiac arrest has received some bad press over the past few years. It has been shown to prolong pulse checks and delay chest compressions. The recent REASON trial, however, demonstrated that ultrasound does have utility, at times powerfully so, in cardiac arrest. (Resuscitation 2016;109:33.)

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The CASA exam (Cardiac Arrest Sonographic Assessment) was proposed as a standardized approach in treating PEA arrest to obtain a good assessment of the heart while minimizing pauses in CPR. (Am J Emerg Med 2018;36[4]:729; http://bit.ly/2TSykxd.) The idea is to perform a stepwise assessment with each pulse check rather than a full evaluation during one pause. The goal during the first break is to assess for the presence of a pericardial effusion. The right ventricle is examined for enlargement, which may indicate a massive pulmonary embolism in the second pause. Cardiac activity is assessed during the third pause. Evaluation for pneumothorax and a FAST exam can be performed while CPR is ongoing without affecting compressions.

The CASA exam creators also offer tips to minimize delays in CPR:

n The subxiphoid approach is preferred because the sonographer can place the transducer in position before the pause, and this area is usually open during compressions.

n A predetermined clinician other than the code leader should be designated to perform the ultrasound.

n Have a verbal clock running during each pulse check to keep everyone focused on the time elapsing.

A study in Resuscitation assessed the length of pulse checks before and after implementation of the CASA protocol by evaluating videotaped resuscitations. (2018;131:69.) The average pulse check before the protocol took 19.8 seconds and 15.8 seconds after it was implemented. They also found that planning ahead for the pulse checks by getting the transducer in position beforehand saved 3.1 seconds, as did utilizing attending physicians with ultrasound fellowship training. The study design had a few methodological issues, but overall it seems that having an organized plan before pulse checks saves valuable seconds.

Recommendations from my experience? Put your probe in position early without disrupting CPR. Record a short clip and resume compressions without pausing to interpret the scan. Many machines have settings that allow you to select longer clip times. Once CPR has resumed, the clip can be scrutinized for signs of reversible causes of cardiac arrest (tamponade, PE) or subtle cardiac motion.

Dr. Butts is the director of the division of emergency ultrasound and a clinical assistant professor of emergency medicine at Louisiana State University at New Orleans. Follow her on Twitter @EMNSpeedofSound, and read her past columns at http://bit.ly/EMN-SpeedofSound.

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