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Organized labor is having a moment. Medicine has not been immune. In recent months, 75,000 Kaiser healthcare workers went on strike, and that was just one of 26 healthcare worker strikes in 2023. One of the biggest changes for medicine, though, is a significant uptick in the unionization of trainees. As of December 2023, the Committee of Interns and Residents, or CIR, the largest U.S. union for house staff, represented 31,000 trainees, almost double what it was just four years ago. But trainee unionization has been controversial. Some medical educators fear that it detracts from the nobility of the profession or drives a wedge between trainees and educators. Trainees often feel voiceless and undervalued, but also scared that a pro-union stance will hurt their career prospects. Meanwhile, trainees who don't support unions may fear being ostracized by their peers. I'm Lisa Rosenbaum, and this is Not Otherwise Specified from the New England Journal of Medicine. So why do trainees feel the need to unionize? What can unions do for their members, and what can't they do? And why have these questions become so hard to discuss? To try to answer these questions, I first spoke with two trainees with different views on unionization. Philip Sossenheimer is a palliative care fellow at Stanford where he led trainee unionization efforts. David Bernstein is an orthopedic surgery resident at Harvard's Combined Orthopedic Surgery Program. It's part of Mass General Brigham, or MGB. During MGB's unionization campaign, David wrote an article for Stat News advocating for pausing the campaign. I should add that I am an employee of MGB, and I also did my residency at Massachusetts General Hospital. Trainees at both Stanford and MGB have since voted to unionize. I started by asking Philip why unionization is happening now, and what are the problems driving trainees to unionize? You know, I think everybody that I talk to agrees that there's a problem with medical training. Even people who are opposed to unionization as the solution recognize that burnout is high among medical residents. Medical residents feel overworked. We feel underpaid. We feel that we're not receiving the value for the work that we're putting into the institutions and the huge sacrifices that we make to get to the places that we are. And my worry is that it's keeping people away from medicine and that we're starting to see a shift nationally where our profession is losing ground. And it's starting from the bottom with trainees. So what do you think is driving the burnout among trainees? And can unions help? I think that people feel disengaged. They feel like they don't have control over their work, right? I remember during the pandemic, many of us getting jeopardized to COVID wards. And that trend continues. I think a lot of folks feel like they're basically a warm body with an NPI and that they can be slotted in like any other person can be slotted into this equation to solve the staffing needs of the hospital. We have very little control over our working conditions. And that's an area where a union could potentially help. People are also burnt out because they have low wages and they're in the community trying to pay rent, trying to afford child care, and they're having trouble making ends meet. And that's another area where unions can help. People are burnt out because they look at the landscape of American health care and they see patients who are uninsured, patients who have to go home and not be able to afford the medications that they prescribe. They have to fight with insurance companies. And I'll be honest and say that's not an issue that a resident and fellows union can solve single-handedly, right? Those are bigger issues. What does excite me about the movement that's building, however, is that collective action among physicians could potentially address those solutions. And having a large body of residents and fellows who are organized under the same organization, you know, almost a third of residents and fellows now are unionized with CIR. Now we're talking about the potential for larger scale change and for, you know, conversations to actually happen with the ACGME on a larger scale. My individual house staff union at Stanford Hospital can't address the, you know, the structural issues that exist with the ACGME and the match process, nor can we address the structural issues that exist with American healthcare. So one union alone can't solve this problem, but it doesn't need to, right? If my union can get me better pay, if it can get me better vacation, if it can get me slightly better benefits, that's going to go some amount of way to solving my issues. It's certainly going to make my day-to-day life better. And if we can build a movement that incorporates not just a third of house staff, but imagine if 50% of house staff were And David, what are some of your concerns? Ultimately, the power of a union, whether we want to acknowledge it or not, is the ability to walk away and to strike for something, for something that we believe in, for something that we really want to make a difference. And when we saw that happen in the UK, for example, thousands and thousands of patients had their appointments and surgeries delayed, up to 350,000 patients. A lot of this comes with predicted consequences and not predicted consequences. A lot of what we have to think about, I think, in a more granular way is what are we after at its core? Because that was at the core of a lot of the MGB issues that I had a challenge with. I wanted to know what did residents want? If it was a seat at the table, that was perfectly fine with me. You can't walk in and say, we want better working conditions, because the answer you're going to get is, what does that mean? Yeah, I appreciate that perspective, David. And like I have told everybody who I've ever worked with, you know, unions are not going to be the only solution to the problem of American health care, nor are they going to be the only solution to your burnout. What I can say, and the only thing that I promise people is that I will stand with you to try to advocate on your behalf. That's the only thing that we can do. And that's what unions are, right? A union is just the name that we have for federally protected collective action in the workplace. My question is, you know, what's the alternative, right? We have right here a structure that's been tested, that's been used in other workforces, that's been shown in well-studied economic literature to have a positive impact on working conditions. And we can be very specific about what we mean with working conditions, which we are as we're bargaining, right? It means better parental leave. It means lactation accommodations for women. It means getting the vaccine, you know, the COVID vaccine, which was the first collective action that we took as a union, basically, at Stanford. And so I don't think it's the case, at least in my experience at Stanford, that we're promising pie-in-the-sky dreams, right? And as to the point of how the union is going to accomplish these goals and the threat of strike, right, strikes are a last resort. And just like we have the ability to negotiate without walking out of the workplace, you know, there are many steps that we can take before striking. We have engaged our political allies to pressure the CEO at Stanford Hospital to try to work with us. We write op-eds in the Stanford Daily. We write pieces that have been published in JAMA. We try to pressure people in the public. There are many ways that you can leverage your group solidarity without needing to go on strike. And if what you're saying is the only way that we can affect positive change within the workplace is through a strike, then the union would be the only way to go because the implication would be that there's no other effective means of advocacy, which just isn't true. If you look at the literature on strikes within healthcare, it's not even clear that there is an increase in morbidity or mortality for patients during that time. What we're talking about are theoretical patient harm over the real harms that we know are happening to resident fellows daily and the burnout that we know affects the quality of the patient care that we deliver. Again, I think that we should be doing something to accomplish something exactly as you had mentioned that benefits us and our patients. How that comes about, I think, can come about in a number of ways.
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Because in my opinion, having a seat at the table is important, but really having what I need to be the best physician I can be, to deliver the best care possible to my patients, to learn what I need to learn in order to operate safely and well, that's what I really care about, not necessarily for a limited short period of time having a seat at the table. When David argued in his Stott News op-ed that the MGB unionization effort be paused, he knew he was going to hear opposition, which he warned his physician wife about prior to publication. And it's funny because those comments and those discussions with my wife still ring true because I still continue to get threats on social media or via email or telling me that I must be one of the worst doctors that will ever exist. Things that I think are not inherent to why people want to unionize to begin with. Okay, so Philip, what was your experience like during the Stanford unionization campaign? You know, during our negotiations with Stanford, they were pretty clear at the bargaining table that they could afford to pay us more. They were explicit about it, you know. And the reason that they give for not wanting to pay us more is because we receive tuition-free education. Are we learning in residency? Absolutely. But we've conceived of a model in our graduate medical education that for whatever reason, needing to learn something or being a learner means that you should not be paid a living wage or that you should not be reimbursed for the value that you generate for the hospital. In addition to worrying about strikes, I also heard some people express concern that unions could negatively impact trainee education. So I asked Philip and David what they thought about this concern. David Bernstein. As someone who's going to do surgery on people, I want to operate as much as possible in order to learn the skills to take on the responsibility of being in the operating room and providing care in that manner. And I think that's a real concern that needs a discussion because I don't think that there's going to be a simple answer to that problem. A lot of the benefits or proposed benefits of a union don't tackle the underlying medical education concerns and the pipeline, listen, work hours, don't touch them because we need to get our cases. And so we're not touching them. And in fact, there hasn't been a single CIR negotiated contract at a hospital that has surgeons that reduces the work hour. This topic has been extremely difficult to talk about. And I want to understand from the two of you why you think that is. In my experience talking to other trainees, there are people are afraid for repercussions for their careers. People are worried that if they speak out in favor of unionization, that they're going to be passed over for job opportunities. This is something that I worry about. You know, if you Google my name, you're going to see that I'm a union advocate. And so when I'm applying for jobs, I worry that HR is going to look at that and say, listen, we don't want this guy here. I think it's partly what Philip mentioned and partly the era, unfortunately, we live in. We're in a moment in history where if you disagree with me, it's not viewed as you disagree with me. It's viewed as you're the other, that you're this kind of evil person who may or may not have what I think is the best interest of a patient in this situation or another objective in mind. And because of that, we're opposed and we're opposed more than just on an idea, but on our ethics and on our morals, just because we disagree on a topic. The good versus evil nature of the union debate has been hard for those trainees really trying to understand both the risks and benefits of training unionization. But it's also been hard on educational leaders. In the second half of this episode, we're going to talk to Dr. Jay Vias, an immunologist and infectious disease doctor who also directed Massachusetts General Hospital's internal medicine residency program for the last nine years. Though Jay recently decided to step down, he was still the program director during the resident's recent campaign and vote to unionize. So I started out by asking Jay about what he perceived to be the biggest changes in medical education in the last nine years. There were really a number of changes. The most important, I think, had to do with the compression of time on the clinical services. You know, when I trained, we just weren't as busy. The patients weren't as sick. And now as I watched and worked with my residents as they were training, these are incredibly sick patients that get admitted to the hospital. The turnover is incredible in terms of the length of stay being shortened. Therefore, there's an increased amount of churn. You know, when I trained, discharging a patient was a relatively straightforward and pretty lean process. Now, transitioning care to another facility, transitioning safe care to home, requires about as much work as it does for an admission. And I'm just focused right now on the inpatient setting, but there's equal challenges on the outpatient setting as well. So what I noticed was that we're training individuals in a very complicated medical landscape, oftentimes where the real resources that could really make a difference are oftentimes are in short supply or simply non-existent. And resident panels differ from attending panels significantly. And many of those have those types of needs that our system is oftentimes not optimally set up to do. So are these the factors that drove trainees to unionize? You know, the COVID pandemic put into sharp relief, you know, the role that residents and trainees had in the response to COVID. But I actually think if you look back, you'll see that there were seeds of discontent that were there for a longer period of time. And I think it goes back to thinking about who are our medical students and our trainees and what is the path that they've taken when they get to graduate medical education. And I'll take you back to college where many of them have spent a significant amount of time in college trying to perfect a perfect GPA, a perfect MCAT. Many of them have taken a gap year to get requisite research experience to get into a good medical school. They will work hard in medical school, continue to do scholastic work, engage in what I will say sometimes is this process to ensure that they get into a competitive residency. And that oftentimes may require extra time and effort to be able to do that. All the meantime, paying a significant amount of tuition debt, which puts them deeper and deeper into financial holes at a time when most of their cohorts in college have started to get a job and have started to put money into retirement and have started to think about what work and outside of work balance would look like in terms of their life choices. And so they're continuing to work in those spaces. And then they come to internship. So when they come to me, they're going to now start working 80 hours a week, oftentimes taking call, caring for some of the sickest patients, as we just described. And now they're looking for support and they're looking for some sense that there is opportunities for recognition of the work that they're doing in that area. And I think, you know, historically, the grand bargain that my generation had was that there was delayed gratification. Do the hard work now, you'll get rewarded after you finish the training process. And I think one of the byproducts that evaporated after COVID was this concept of delayed gratification. I think people recognize that time is short. There is a feeling like there's a significant amount of uncertainty in the world. I'll leave that as kind of a meta feeling that's out there. And that they need to be able to spend time that feels right in the right spaces. So if they're in an educational institution or educational environment, they want to feel like that they're getting the best education. If they're working hard to take care of those patients, they don't want to be doing things that have low yield in terms of those. And so they're insisting on a number of things that I think are actually aligned with, you know, I think the way many people think now, you know, post-pandemic in terms of the things that they would like to be able to see. But those oftentimes from a program director point of view, we didn't have the levers of power to fix those. And I think that there was a growing realization amongst residents that program directors, even though they served as the direct supervisor of trainees in the graduate medical education space, lack the agency to make the types of meaningful changes that they were looking for, whether that be in compensation, whether that be in benefits, whether that be in restructuring the workplace to prioritize education and enhance patient safety and enhance patient experience. So I think the lever that they felt was most important to pull there was to be able to have the opportunity to have a voice at the proverbial table.
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And so we want to be able to do that through unionization. And so I don't think unionization was the first lever, but rather the ultimate lever that was pulled to try to affect these types of changes. And so how did you respond to them when they came to you saying that we are organizing to vote to unionize? I think to be an effective program director, you have to journey with your residents through both those good times and bad times. And that requires a bit of vulnerability on the residents and real support, I think, by the program director as well as the faculty. When I say the program director, you should always include the incredible dedicated educational faculty that support the residency program. You know, I had wanted to make sure that that relationship, which is built on trust and that has vulnerability shown by the trainees in those situations, that wasn't, there wasn't an opportunity for there to be kind of, at least between the program directors and the trainees and us versus them philosophy. I think that becomes incredibly corrosive. And while I recognize and fully acknowledge that I am part of the leadership of the institution as serving as that program director, you know, I personally felt very sad that we had reached this point because I felt like if we could not, it felt like a personal failing to me that I wasn't able to advocate strongly enough for the trainees that they had to use unionization as the mechanism by which they felt that that change was effective. And it wasn't a lack of effort on my part. It was a lack of being effective in that voice to be able to affect the type of change that was necessary. And, you know, so I had my own personal feelings about that. But, you know, when it came to being pro-union or anti-union, I was neither pro-union. I was not anti-union. I've always been pro-resident, and I've always been pro-residency program. I love my residents, and I love my residency program. Those things will never change. I tried as many times as I could to remind the health system as we moved forward through these processes that this isn't an us versus them because, quite frankly, they are our future colleagues, and we need to treat them as our future colleagues. And sometimes I worried that that got lost in the translation in what became a relatively bitter fight for whether the trainees would choose to unionize or not. I come from a science background, and so I spend a lot of time thinking and weighing evidence and trying to determine whether we have enough evidence to formulate whether a hypothesis is true or not. And I love that exercise, but that process, which is so familiar to me, was not really available in this discussion of unionization simply because we just didn't have the forum by which we could have that type of open conversation. I think it would be helpful to hear a little bit more about what happened when you attempted to have an open and honest forum to talk about the unionization process and some potential pros and cons, benefits and risks, weighing the evidence, however you want to think about it, with your house staff. I've always had and strive to have an open and honest relationship with my residents. I felt that that was the only way to lead in that way. And so early in this process, I had intended to have a noon conference to really speak about the union efforts. And again, in that meeting, I had made efforts to do it the way I, frame it the way I saw it to be important. What were the pros? What were the cons? What are the things that I worried about and the like? It was a well-attended meeting, probably the best-attended noon conference we've had all year. I think that, unfortunately, what was a nuanced conversation got eventually framed up in ways that didn't really reflect the reality of a nuanced conversation when comments were made in social media platforms, including Reddit and Twitter, which painted a strongly different picture, you know, for those things. Just to be clear, Jay was accused on social media, and specifically Reddit, where a lot of students go to seek information about training programs, of being a union buster. Obviously, the result of the social media posts, you know, kind of prevented further open conversations like that, which, you know, I have to say I lamented. This is sort of the one of the root ills of our society, I think, is that I don't know if it's because of social media. I don't know if it's because we're so polarized in other ways. But the opportunities to have nuanced dialogue about complex topics are few and far between. So people did yearn, individuals did yearn to have those types of conversations at that level. Many times I would have those individual conversations with individuals. But, you know, I worry that, you know, sometimes when we fear having those larger conversations in larger rooms, that sometimes that might be a reflection of a lack of trust and whether someone is operating off a specific agenda. I think that there were some people who worried that, you know, being a program director and serving, you know, in a leadership role, by definition, put me on the anti-union platform. And if people got that impression, they didn't really spend any time talking to me about it or hearing what I was saying. But I think they felt that that was largely where program directors were landing. And a lot of it had to do with, you know, I think a lot of program directors, you know, who kind of grew up in education really felt that it was very important and that they do what the health system wanted simply because they've reached the pinnacle of their career being a program director. And there's some element of, you know, I worry about my job security if I'm not really kind of pleasing the people who I report to. When I came on to do, serve as the Red Sea program director, I was already a full-time, I already had a full-time job being a basic science investigator in the Division of Infectious Disease. And so I always operated under having essentially two jobs. And so for me, it was very easy because I only acted how I thought what I felt was right to do and always welcomed the opportunity to go back to my lab full time should anybody be worried that I was doing the job in the wrong way. And so that gave me a level of freedom that I think most other program directors didn't have. I knew from having spoken with Jay previously that one of the issues that became contentious at this forum were snacks for trainees. Every week, Jay filled his office with snacks so that food would be available to residents at all hours. But before we get into the fraught snack discussion, I asked Jay to explain what the snacks represented to him in the first place. The snacks were always a means to an end, right? The opportunity to be able to spend a little bit of time with the residents. And I left my door open at night, and so people could come in and get a snack at 7 p.m. or 3 a.m. or whatever time of the night. It wasn't uncommon that I would come back to my office in the morning and I would have a sticky note on my desk and said, you know, I've had a really bad night with some really terrible complications of some patients and I just needed five minutes and just a break. And I came to your office and I grabbed a snack. And, you know, thank you so much. You know, for me, those were really meaningful notes. I still have them. And, you know, for me, they always represented what I thought was being able to see our residents, right, for what they do. I'm Indian. I grew up in a very kind of a somewhat traditional Indian household. Food was a currency of love, as it is in many cultures. And so for me, the idea that you would withhold food was the equivalent of withholding love, and it just didn't make a whole lot of sense to me. Ultimately, I do think that, you know, there was, even after the union vote did occur, there was, you know, a decision that was made by leadership to remove the food. Even though the snacks for Jay were a gesture of love, my sense is that the forum he held, he ran into a shoot the messenger problem. One thing that often happens when trainees unionize at any institution is that benefits become equalized between programs. In some ways, that's good. For instance, all the trainees may get a higher salary or better benefits. But for programs that had traditionally gotten extra perks, and I can say from having been an MGH medicine resident that we got a lot of perks, there's also a risk of losing things like nice lunches or 24-7 snack availability. And in the end, the snacks did get cut. But I wanted to understand from Jay why pointing out this risk before the vote to unionize wasn't well received.
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And one of those things I did mention was that there would be limitations on those things. And so if we were to simply divide the world of programs into the haves and the have-nots, the Department of Medicine and MGH was clearly one of the ones that had. And I worried that in this effort to kind of make everything the same, what would end up having to happen would be that, you know, things would have to be taken away. And I worried out loud that that was going to happen. And a specific example that I used were these snacks. I've already measured, and you can do the calculations, but, you know, we're in excess of $50,000 a year in M&Ms and popcorn, right? And you can imagine that that's something that's going to be ripe to be removed. And so I use that as an example, you know, in that area. And so, yes, I think people did respond to that. If people saw, you know, again, I want to say there was a small minority of individuals who may have seen the snacks, you a transactional thing, that I just brought in snacks. But I think the point I was trying to make really was that I, as the program director, enjoyed a significant amount of autonomy. And if I thought there were important things that we needed to do to add to the residency program to enhance the resident experience. I recognize that that would likely come to a halt, and I wanted to express my concern to the residents in that meeting. It's ironic to me that, as you said at the outset, part of what was going on before the decision to unionize was that the residents had recognized that you, JVS, don't necessarily have the agency to move every lever at the level of the institution to get them what they want, and that part of the consequence of the unionization is actually taking away even more of your autonomy to advocate for them. And I think that that's an important thing for us to recognize, again, because it's very hard to talk about whether unions have any unintended consequences because the discourse is so fraught that they might. Yeah, and I think that that's one of the things when you're having a conversation where you want to have a nuanced conversation, there's going to be pros and cons of everything. And I believe that medical trainees are very well versed in that concept based on how they practice medicine every day. And so, again, I think the ability to be able to kind of see what are those trade-offs and what are those unintended consequences that come up would have benefited from a broader discussion, but it didn't take place with the faculty or it didn't take place with faculty and residents. I do want to ask you one more question because it's something you said to me when we talked, which is that some of the most gifted educators don't want to get in this game anymore. And I, you know, I've heard that from a lot of educators, honestly, that for some reason, lots of reasons, complex reasons, it's become a lot harder to be an educator in addition to like all of the hard things that come along with trying to train people. And I'm wondering what you think that's all about. It's more than one reason. But, you know, I think the, you know, training, first of all, being an excellent teacher for medical students, for residents, for fellows, that's hard work. But, you know, there's the increased challenges that are faced in a complicated inpatient setting, the fast pace that is required for ambulatory medicine, the increased demands to do more with less, the lack of recognition by academic medical centers on how to promote excellent educators, and then lack of how you value education in an RVU or compensation-based mechanisms pose real challenges to how we're going to educate the next generation. And there are really important challenges here that we need to be working on. Unionization adds to some of that. And I hope that for many people who are thinking and contemplating a career in medical education, that they recognize that that is an incredible and important role. We all play an important role. I'm very interested for a significant amount of self-interest. I anticipate that in the future years, I'm going to grow older and I'm going to need medical care. And I want to be cared for by really great physicians. And that's what I think we all, as humans, want to be able to do. We recognize that, you know, as much as AI sounds wonderful, at the end of the day, if someone needs to be told that they have cancer, it's not going to come from a computer. It's going to come from a human being who's going to walk and journey with that patient through the journey that is known as cancer. And we need to be able to make sure that that human experience is accompanied by people who are incredible. And to take people, you know, we still have incredible numbers of people who want to go into medicine. Look at how many people apply for medical seats in the United States. We have a number of people who want to come into this noble profession. And so we need great teachers. We have great talent in our pipeline. We need great teachers to be able to do that. And I worry that a lot of the things that I just mentioned will continue to dissuade people from a career in medical education because I think that it is both noble, it's necessary, and it's become increasingly complicated. And so I don't have a great solution to it, but I know that there is that need, and we need to be able to make sure that we still retain the very best there. I agree, which is why the rise of training unions has always seemed to me like a tip of the iceberg phenomenon. What bubbles up to the surface are tangible problems unions might be able to solve, like inadequate salaries and benefits. But underneath, we have so many layers of existential problems. Some, like medicine's corporatization, are coming from within the profession. But others, like evolving cultural norms around work and generational change, are coming from outside. Up next on Not Otherwise Specified, we're going to examine some of those generational shifts and the role they're playing in our training environments. The tensions run the gamut. Some will be that new employees are not just willing to fall in line and do what a boss tells them to do. When older generations were entering the workplace, the norm was suck it up. You know, you got to do what they tell you to do. You got to pay your dues. This generation does not necessarily see that that is the case. So sometimes they will feel like they know better. And the reality is sometimes they do know a better way to get something done because they are more adept often at using the tools of today. That can create a frustration where they do have something to contribute, but an older person is going to say, but that's not how we do it here. I'm Lisa Rosenbaum, and this is not otherwise specified from the New England Journal of Medicine. I'd like to thank our editor, Deborah Molina, our senior producer, Mary Rose Madden, and Blue Dot Sessions for the music. Thanks for listening. We're taking a brief pause next week, but we'll be back on March 6th. Until then. you
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I'm very pleased to be joined by Vikram Patel, one of the lead authors on the China-India Mental Health Alliance series. Hello, Vikram. Hi, Niall. So, the first question I have is, why this series and why now? Well, India and China together represent more than a third of the world's population, and I think both countries are at a remarkable stage of their epidemiological and demographic transition. They're also seeing a remarkable amount of social change. They're seeing a remarkable amount of new energy in investing in public health. And it just seemed to me for all these reasons that this was a great opportunity to see how these two giants, neighbors in Asia, were addressing the burden of mental health problems and what lessons could be learned, not only for these two countries, but indeed for other low and middle income countries as well. And also countries which are undergoing massive economic change. Absolutely. Indeed, most of the low and middle income world is seeing the sorts of social change. In some respects, India and China, being middle income countries, are somewhat more advanced in the stage of social change, but certainly where these two countries are today is where many of the less-resourced countries will be in a few years from now. And that brings with it opportunities. It also brings with it challenges. So let's start off by talking about some of the challenges that these changes are bringing. Well, I think the social change is accompanied by, obviously in the way families organize themselves. For example, because of urbanization, there are a range of new social determinants or an increased prevalence of certain social determinants that might affect a person's mental health. So these are some of the challenges that might explain, for example, the increasing rates of suicides that we see in young people in India and that we did see in China. But as the series will show, there have been changes in China in terms of these rates falling in recent years, whereas in India, of course, they've continued to rise. In this business of suicide rates in India, I know that it is an area of concern. And yet the pattern, the demographics are very different to what, say, European or North American suicide researchers. That's correct. Certainly the suicide paper will shed a lot more light on that. I personally think that the bigger area of difference between India and China is the investment that China has made in the last decade or a bit in its public health care system. In many ways, it has rolled out what I consider the largest publicly financed mental health care program in the developing world and possibly the world, with several million people registered now in what's called the 686 program. By contrast, India has a fairly abysmal performance in terms of not just the public financing, but more importantly, the implementation of the public mental health care system. So I think there's certainly a very significant difference between these two countries in the success they've had in achieving publicly funded coverage of mental health care. And I think India could learn quite a lot from China in that regard. Could you give me any idea of the sort of scale of treatment gap that we're talking about in India? In the paper that I lead, we've actually done a systematic review of the treatment gap. And I think the key pictures, the key findings that emerge from that is that the treatment gaps are very large for the common mental disorders, such as depressive and anxiety disorders, and also for substance use use disorders such as alcohol use disorders. They tend to be smaller, not surprising, for the serious mental disorders because those are obviously more frequently noticed. The other important finding is very large inequities in coverage comparing rural and urban areas. Again, it's not terribly surprising, but now we can show this by the systematic review. Also, we can see very little evidence of the measurement of treatment gap for certain groups of people, for example, children, in whom we have almost no literature, no research evidence on the size of the treatment gap. My guess is it's pretty large. So what are the... OK, number one priority is more money, clearly, but what would the other priorities be in enabling India to meet this challenge? I think we need very strong technical leadership. We need leadership by public mental health professionals working within government. These are the kinds of people who have the necessary skill set to design, to organize, to build capacity and to monitor public mental health programmes. At the moment, the problem in India is that most public mental health care programmes are being implemented through departments of psychiatry in medical schools. And whereas these are perfectly reasonable places for providing specialised care, these are not necessarily the right platforms for organising a public mental health care system. I know that in the UK and in the USA, in other countries in recent years, mental health has become far more part of the public discourse with anti-stigma campaigns, with films and dramas and documentaries coming out, it seems, every week on the topic, which is, of course, welcome. In India, is there a similar level of public discourse about mental health issues? Certainly. You know, in the last 20 years that I've been working in India, I've seen a dramatic shift in the discourse on mental health. Just in terms of volume, it has increased dramatically. Almost every magazine or many television programs will have themes related to mental health and mental illness. And it has to be said, it's dealt with in a very compassionate, in a very sensitive, and in a very non-stigmatizing way. So I think this is all very positive. What has happened, therefore, is a much greater awareness about mental health problems. Although that doesn't necessarily mean people use biomedical concepts, but they do recognize these as health issues. What's missing now is the actual supply of effective interventions in community-oriented platforms. And it sounds, though, as if we're getting some momentum building towards that. How can India and China help each other in harnessing this momentum and promoting change that sounds so badly needed? Well, I think both countries face very similar challenges in terms of the large population and therefore the large numbers of people affected by mental health problems and need of care, the lack of appropriate community care arrangements in both countries and the rapidly changing family systems that are used to traditional care for people with particularly serious and enduring mental health problems. So I think if academics, public health academics, policymakers, and relevant stakeholders in the community in both countries were able to come together, share experiences from various demonstration projects or pilots showing how these challenges could be addressed, I think there's a real prospect for learning on an exponential scale. So let's hope that this series of papers marks the start of a beautiful friendship. Well, you know what? I think this is one of the rare examples of academics on, you know, in these two countries which share such a long land border but could easily be living in different continents. It's one of the rare examples I know of, of academics from these two countries collaborating in this way and leading to this series of papers in The Lancet and The Lancet Psychiatry. And we look forward to much more in future. Thank you very much, Niall. Vikram Patel, thank you very much. For the second half of this podcast, I'm going to hear from one of the other driving forces of the China-India and why now? global mental health because of the sustainable goals. I think that not thinking about China and India, you're missing a huge part of the world. Also, China and India are, in some senses, very different countries in that India is the largest democracy, China is the largest communist country, and yet they're both on a very rapid developmental trajectory. And as they are, the health is improving, and so there's increasing concerns about mental health and mental well-being. So you picked up on something very interesting there, which is that these countries have very different histories and very different political systems. But nevertheless, from what I've seen in the series and from talking to you previously and talking to Vikram, they seem to also have some challenges in common and possibly some solutions in common. Challenges, yes. Solutions, we're still working on them. I think one of the challenges is that they're such large countries, there's huge diversity around the country. Now, China has 33 provinces, you include Hong Kong and Macau. And a recent publication in The Lancet showed that, for example, suicide rates around these 33 provinces varied by tenfold. Previous work in India has shown that suicide rates around the 26 states in India vary by ten to twentyfold. And so, yes, they're huge and they're developing and urbanizing very rapidly, but there's still a huge range of diversity within the countries. And that's true for both of the countries. And how do you get a national plan and how do you implement it at local levels where things are so different at local levels is a common problem that they face.
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Now, clearly, of course, within the countries, there's huge amounts of diversity. But I think the other thing for maybe readers in Britain, other European countries in the US to get their heads around, is that the sort of pattern of suicide, the demographics, they seem to be very different in China and in India. If you look over the last 20 years, the Chinese rates, and this is from the World Suicide Report that came out a year and a half ago, have dropped by 50 to 60 percent, an amazing number, whereas the rates in India have gone up maybe 20 to 30 percent. So even though they're both developing, both urbanizing, the rates are going in the opposite direction. And the question is why, and the simple answer is we don't know, and we're certainly trying to figure it out. And the pattern as well, I mean, that must be related to the shift from rural to urban life. Yeah, for example, China has gone for over the last 20 years from 20% urban to 50% urban. That means there's 300 million people less who have daily access to pesticide, which is the most common method of. But I guess this fits into the overall pattern that urbanization brings benefits, but it also brings maybe disruptions. Yeah, well, you know, there's obviously different views on this. One sense is that, you know, with the breakdown of the strong family bonds, family connections that occur in rural areas where people live together and families often extended families as the young people especially go to the city, that leaves the elderly and sometimes the children or the grandchildren in the rural areas who don't have the kind of support they have. But on the other hand, these people, you know, it also is related to hope and the sense of a future. And so it really is a mix. And there's benefits, as you say, some downsides as well. And certainly in some areas, urban, rural residents who move to cities live in kind of ghettos. And so their living conditions and the conditions, education for the kids is problematic. But it's very much mixed. I think in China, at least, I can speak about China a little bit better. There's a continuing sense of hope. People still think, despite the increased gap between the rich and the poor, their kids have a better chance at life and getting ahead than they do. And so there's a sense that things are progressing in the community at large. And that sense of hope, I think, is the positive sense that not only for suicide reduction, but also mental health reduction. The one side that is clearly negative, that the rates I think really are going up, is in substance abuse. As people have more money, they're more likely to drink. And some young groups in some parts of the country, at least in China, there's also increased rates of drug abuse. And even if any society improves economically and socially for the individuals within it, there will, in my view, still be some people who have often very severe mental illnesses. And then the question arises of treatment provision. I'm particularly interested in the long history, really, of mental health law in China. It's taken us a very, very long time, 27 years of kind of draft after draft, draft before it finally got improved. And it just, I think it's part of the international movement, you know, the WHO and the United Nations have now put a lot of emphasis on mental health. The WHO had its first global mental health plan two years ago, and China kind of is on board with that. And so that's finally moved us ahead in the law. Like everywhere, mental health laws are pieces of paper until people actually enact them. And the law is idealistic in many ways. It talks about reducing stigma, which, of course, we've been trying to do for many, many decades. Probably the most controversial or difficult to implement element is moving from an involuntary hospitalization program to a voluntary hospitalization program. Because typically in China, the family makes all the decisions. And that's part of the family culture and the communal versus individualistic approach to culture. And so moving from that to have individuals make the decision about when they go in and when they come out of hospital is a major step that's in the law, though I think it's going to be a while before it's actually implemented. And let's talk about that issue of stigma. When I spoke to Vikram, he felt that in India there have been really great strides against that. Is there a similar situation in China? It varies. Urban and rural differences. The urban areas have more contact with the West and sort of, you know, Western movies and things that sort of normalize some of the behaviors we think of mental illness. In the rural areas, people think of mental illness as psychosis, depression, alcohol abuse, dementia. Those just aren't on the, they're not considered mental illness. They're considered social problems. And so they say it's a stigmatized, yes, suicide and other things. Serious mental illness is heavily stigmatized still. There's some attempt to decrease it, and I think we've had some success. But one of the issues is that a lot of the things that we as professionals identify as mental illness aren't considered mental illness by many people, at least in rural communities. And one of the issues which Lancet Psychiatry has covered in the past and is indeed covered in this set of papers is the idea of using complementary medicine, what we call alternative forms of care, to really help to scale up mental health services. Yeah, I think, you know, in China we have traditional Chinese medicine, which is about a third of the entire medical system is traditional Chinese medicine. And, of course, in India, you have Ayurvedic medicine, you have yogis, you have others. For China and India, one of the big changes, differences that Vikram and I have talked about a couple of times is in India, there's other people. I mean, we're worried mostly about the rural areas now. There's other people who can be kind of health aides and fill out some of the other roles where you don't really need psychiatrists, but you need social support for people of mental illnesses. In China, you have your village doctor, but he or she, usually he or she, has a huge range of other responsibilities. So they have very limited energy to place on mental illness because they have to do diabetes, have to do hypertension, have to do everything else. And we don't have the kind of health aid sort of people in the rural areas. And bringing the TC, the traditional Chinese medicine people into providing more mental health services, I think is a fine idea, but it's not going to, it's really not, at least in the real rural areas, it's not going to, we don't have enough of those personnel anyway. We got to, and the idea is how can we mobilize other types of personnel because you don't really have in rural areas, we don't have enough of those personnel anyway. And the idea is how can we mobilize other types of personnel, because you don't really have in rural areas social workers and things like this, that in India they have a little better coverage. They have NGOs in rural areas, and China has very few NGOs. And so mobilizing additional manpower in rural China is, I think, our major challenge to upgrade overall mental health services. Any possibility that technology would help with this process? Well, we've looked at, you know, M-medicine and, you know, cell phones, because cell phone penetration is reasonably good. Of course, in the real poor areas, people don't have cell phones or certainly don't have apps on phones and things. But it's a possibility. I want to see it before I can believe it, frankly, because we've done stuff with schizophrenics to try and get them to take their medication and things, and it hasn't been that successful. So it sounds nice, but can it really work? I think we need a lot more work to demonstrate whether or not it can be an effective alternative having people on the ground. One of the main problems in China is that with the great improvement in health, people are living a lot longer, and with the one child per family policy, they have fewer kids to support them, and so we're having a very rapid increase in the rates of dementia. And, you know, cell phones and things like that aren't going to help for the large increasing numbers of people with dementia. You need carers on the ground, especially as people get at the terminal end of dementia when they really need high quality nursing care. And where are we going to get the manpower to provide that? That's the question that I lose sleep over because I don't, I can't see a trajectory that's actually going to get us that kind of manpower.
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But it's scary thinking of how much social resources are going to have to be committed to deal with this tidal wave of dementia that's sort of hitting us already. So without wanting to make you lose any more sleep, I wonder if we could conclude by talking about where you'd like to see mental health care in China in that just came out. I would like to see at least part-time, if not full-time, psychiatrists in county-level hospitals who could actually monitor care provision and rehabilitation services in the more rural areas. We just don't have enough coverage at the county level. You've got the big city hospitals, some areas, and the richer rural areas, you might have a hospital, but there's just the idea of having a three-tier system where you have the county, you have the village, the county, and the township and the county, and maybe the urban area just isn't there yet. And getting manpower in the county level general hospitals to at least provide outpatient services and monitor and diagnose people and sort of follow up on services is very essential. That's one area. The other areas that are underserved now, I think that really need resources, I'm very concerned about dementia. I'm very concerned about the lack of extensive services for children. And substance abuse, particularly alcohol, is a problem that nobody sees as a problem. And it looks to me like it's a big problem that's getting bigger, and it's not seen as a mental health problem by, you know, hardly anybody. And I think that's something that needs to change. So some hard work ahead, but also a bit of hope there. Certainly. I've been here 30 years and things are much, much better. I mean, it's exciting to do the work now because the law has happened and the government's putting resources into it. So there's definitely a lot of hope in terms of our opportunity to improve services to people who need them. Michael Phillips, thank you very much. Thank you. And you can access the China-India Mental Health Alliance papers on thelancet.com. Meanwhile, thank you very much for downloading and listening to this podcast, and I hope that you'll join us again next time. Goodbye.
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Welcome to the New England Journal of Medicine summary for the week of December 5, 2013. I'm Dr. Lisa Johnson. This week, we feature articles on APOL1 risk variants, race, and chronic kidney disease, targeted temperature management for cardiac arrest, bivalorudin during transport for primary PCI, and fertility treatments and multiple births, review articles on global maternal, newborn, and child health, and on mitochondrial dynamics in human diseases, a clinical problem-solving article describing a shocking development, and perspective articles on how early obesity prevention should start, on adding value to relative value units, and on assessing participant-centered research outcomes. APOL1 Risk Variance, Race, and Progression of Chronic Kidney Disease by Afshin Parsa from the University of Maryland School of Medicine, Baltimore. In two studies, the authors examined the effects of variance in the gene-encoding apolipoprotein L1, ApoL1, on the progression of chronic kidney disease. In the first study, involving 693 black patients with chronic kidney disease, the primary outcome, which was a composite of end-stage renal disease or a doubling of the serum creatinine level, occurred in 58.1% of the patients in the APO-L1 high-risk group and in 36.6% of those in the APO-L1 low-risk group. There was no interaction between APO-L1 status and trial interventions or the presence of baseline proteinuria. In the second study, involving 2,955 white and black patients with chronic kidney disease, black patients in the APO-L1 high-risk group had a more rapid decline in the EGFR and a higher risk of the composite renal outcome than did white patients, among those with diabetes and those without diabetes. Renal risk variants in APO-L1 were associated with the higher rates of end-stage renal disease and progression of chronic kidney disease that were observed in black patients as compared with white patients, regardless of diabetes status. Winfred Williams from Massachusetts General Hospital, Boston, writes in an editorial that, certainly, all racial disparities in kidney health are not attributable to APO-L1 variation. Differences in the hypertensive phenotype and in mineral metabolism remain to be explained, and we should not dismiss the role of socioeconomic factors, referral patterns, and access to the best practices for renal replacement therapy. Regardless of the genetic and biologic underpinnings of the initiation and progression of kidney disease, lower rates of kidney transplantation among black patients, for example, remains a large challenge. Still, the first step in alleviating a problem is to understand it. Increasing evidence supports a major role of one gene, APOL1, in disparities in kidney health and disease and represents a large advance in combating renal disease among Black patients. Targeted Temperature Management at 33°C vs. 36°C After Cardiac Arrest by Niklas Nielsen from the Helsingborg Hospital, Sweden Unconscious survivors of out-of-hospital cardiac arrest have a high risk of death or poor neurologic function. Therapeutic hypothermia is recommended by international guidelines, but the target temperature associated with the best outcome is unknown. In this trial, 950 patients who had been resuscitated from out-of-hospital cardiac arrest were randomly assigned to targeted temperature management at either 33 degrees Celsius or 36 degrees Celsius. At the end of the trial, 50% of the patients in the 33 degrees Celsius group had died, as compared with 48% of the patients in the 36 degrees Celsius group. At the 180-day follow-up, 54% of the patients in the 33°C group had died or had poor neurologic function according to the Cerebral Performance Category scale, as compared with 52% of patients in the 36°C group. In the analysis using the modified Rankin scale, the comparable rate was 52% in both groups. In unconscious survivors of out-of-hospital cardiac arrest of presumed cardiac cause, hypothermia at a targeted temperature of 33 degrees Celsius did not confer a benefit as compared with a targeted temperature of 36 degrees Celsius. In an editorial, John Rittenberger from the University of Pittsburgh, Pennsylvania, writes that perhaps the most important message to take from this trial is that modern, aggressive care that includes attention to temperature works, making survival more likely than death when a patient is hospitalized after CPR. In contrast to a decade ago, one-half instead of one-third of patients with return of spontaneous circulation after CPR can expect to survive hospitalization. Few medical situations have enjoyed such absolute improvement over the same time period. Future studies can continue to refine protocols, define subgroups that benefit from individual therapies, and clarify how to best adjust temperature or other interventions to each patient's illness. By Val Arudin, started during emergency transport for primary PCI. By Philippe-Gabriel St Steg from the Hôpital Bichat, Paris, France. In a randomized trial, 2,218 patients with ST-segment elevation myocardial infarction were assigned to pre-hospital treatment with either bivalirudin or heparin with optional glycoprotein 2B3A inhibitors. Bivalirudin, as compared with the control intervention, reduced the risk of the primary outcome, which was a composite of death or major bleeding not associated with coronary artery bypass grafting, CABG, 5.1% versus 8.5%, and the principal secondary outcome, which was a composite of death, reinfarction, or non-cabbage major bleeding, 6.6% vs. 9.2%. Bivalirudin also reduced the risk of major bleeding, 2.6% vs. 6%. The risk of acute stent thrombosis was higher with bivalirudin, 1.1% vs. 0.2%. Results were consistent across subgroups of patients. By Valorudin, started during transport for primary PCI, improved 30-day clinical outcomes with a reduction in major bleeding, but with an increase in acute stent thrombosis. Shamir Mehta from McMaster University, Hamilton, Canada, asks in an editorial whether the trade-off of reduced procedural bleeding is worth the increased risk of acute stent thrombosis. This depends on the relative incidence of major bleeding versus that of stent thrombosis and the association between these events and subsequent mortality and morbidity. Few observers would dispute that stent thrombosis is a serious, albeit infrequent, event that results in either reinfarction or death in most cases. On the other hand, major bleeding occurs more frequently, but varies widely in severity, depending on how the term is defined. Severe bleeding is prognostically more important, but far less frequent than less serious bleeding, which has little or no long-term importance. Thus, it is critical that clinicians weigh the relative importance of these events before selecting an antithrombotic strategy for their patients. Fertility Treatments and Multiple Births in the United States by Aniket Kulkarni from the Centers for Disease Control and Prevention, Atlanta, Georgia. The authors conducted a longitudinal analysis to determine the trends in and magnitude of the contribution of fertility treatments to multiple births. The authors estimated that by 2011, a total of 36% of twin births and 77% of triplet and higher-order births resulted from conception assisted by fertility treatments. The observed incidence of twin births increased by a factor of 1.9 from 1971 to 2009. The incidence of triplet and higher-order births increased by a factor of 6.7 from 1971 to 1998 and decreased by 29% from 1998 to 2011. This decrease coincided with a 70% reduction in the transfer of three or more embryos during in vitro fertilization, IVF, and a 33% decrease in the proportion of triplet and higher-order births attributable to IVF. Over the past four decades, the increased use of fertility treatments in the United States has been associated with a substantial rise in the rate of multiple births. The rate of triplet and higher-order births has declined over the past decade in the context of a reduction in the transfer of three or more embryos during IVF. Global Maternal, Newborn, and Child Health So Near and Yet So Far A Global Health article by Zulfikar Buta from the SickKids Center for Global Child Health, Toronto, Canada. A little more than 13 years ago, world leaders assembled in New York to sign the Millennium Declaration to address some of the greatest moral dilemmas of our times. Unequal global health, poverty, and inequities in development, and to establish a set of interrelated goals and targets to be met by 2015. Key goals included the Millennium Development Goal, MDG 4, targeting a reduction in mortality among children younger than five years of age by two-thirds, and MDG 5 targeting a reduction in maternal mortality by three-quarters. With less than three years to go, these two MDGs are seriously off-target for many countries.
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As we celebrate the fact that the annual number of deaths among children younger than five years of age has fallen to 6.6 million, which is a 48% reduction from the 12.6 million deaths in 1990, despite an increased number of births in many high-burden countries during the same period, the sobering realization is that even in countries that will reach their MDG4 and 5 targets, many will still have high numbers of deaths with much scope for improvement. Mitochondrial Dynamics, Mitochondrial Fission and Fusion in Human Diseases, a review article by Stephen Archer from Queen's University, Kingston, Canada. Mitochondria are mobile organelles that exist in dynamic networks. They continuously join by the process of fusion and divide by the process of fission. Mitochondria are derived from eubacterial endosymbionts that are capable of aerobic respiration. Disorders of mitochondrial structure are just emerging as mechanisms of disease. Although some disorders of mitochondrial dynamics result from monogenic mutation, most reflect changes in the function or activity of fission and fusion mediators triggered by changes in the cellular milieu. There is an emerging recognition that disordered mitochondrial dynamics contribute to the pathogenesis of complex diseases that are not classically considered to involve mitochondria. These diseases include cancer, cardiovascular disease, and neurodegenerative diseases. Recent identification of the molecular mediators of mitochondrial dynamics and recognition of their post-translational regulation by an extensive network of kinases, phosphatases, and ubiquitination mediators offer a new understanding of cell biology and novel therapeutic targets. Fission and fusion fine-tune fundamental cellular processes such as calcium homeostasis and the generation of ATP and reactive oxygen species and consequently have important roles in cell cycle progression, apoptosis, mitophagy, and oxygen sensing. rhinorrhea, followed by two days of vomiting, diarrhea, and abdominal pain. The patient was brought to an urgent care center for evaluation. At that time, she reported abdominal pain related to emesis, but said she had no dyspnea, chest pain, fever, or chills. On examination, the pulse was 130 beats per minute, and systolic blood pressure ranged from 60 to 70 millimeters mercury. Emergency medical services were called, and two liters of normal saline were administered while the patient was being transported to the emergency department of a local hospital. On arrival, the oral temperature was 34.7 degrees Celsius, pulse 126 beats per minute, blood pressure 99 over 52 millimeters mercury, respiratory rate 18 breaths per minute, and oxygen saturation 100% while she was breathing ambient air. Cardiac examination revealed irregular tachycardia without extra heart sounds. This patient contracted an acute influenza-like illness, along with members of her family. While the others recovered, her condition rapidly deteriorated. In a young person with a febrile illness and severe hypotension, the differential diagnosis is broad and must be addressed quickly, given the potentially catastrophic consequences. Any diagnostic evaluation must proceed in tandem with appropriate life-saving measures that include hemodynamic support. How early should obesity prevention start? A perspective article by Matthew Gilman from Harvard Medical School, Boston. Overweight or obese women are likely to gain excessive weight during pregnancy. This increases their risk of disease and potentially causes higher adiposity in their offspring, who may grow up to perpetuate the intergenerational cycle of obesity and chronic disease. It is time to interrupt this vicious cycle. Once obesity is present, it is challenging to treat because of multiple physiological, behavioral, and cultural feedback loops. The good news is that the prenatal period and the first postnatal year hold critical clues that may lead to interventions to reduce obesity. After birth, rapid weight gain in the first three to six months of life is a potent predictor of later obesity and cardiometabolic risk. Emerging risk factors for obesity include exposure to endocrine disruptors, which appear to do the most damage during times of maximum developmental plasticity, and the gut microbiota. Given obesity's numerous developmental determinants, it is logical that effective prevention would target multiple modifiable factors. In combination, two well-studied prenatal risk factors, excessive gestational weight gain and maternal smoking during pregnancy, and two postnatal factors, fewer months of breastfeeding and a shorter duration of daily sleep during infancy, are associated with wide variation in childhood obesity. Observational data raise the possibility that avoiding some or all of these risk factors could substantially reduce the proportion of childhood obesity. Adding Value to Relative Value Units A perspective article by Eric Stecker from the Oregon Health and Science University, Portland. Many important physician activities are not measurable by means of the current Relative Value Unit, RVU, system. A reconfigured RVU system could evolve into the best method for accounting for physician services in new value-based delivery and payment systems. Ideally, physicians' work would be reimbursed on the basis of metrics that signal whether their clinical services efficiently improve patient outcomes and that use effective clinical risk adjustment. An improved RVU formulation for physicians' work could be developed that reflects clinical value by weighting activities according to whether they demonstrably improve patient outcomes. Physician work RVUs are currently based on the relative levels of perceived time, skill, and intensity associated with clinical activities, but value-based elements could be emphasized to align physicians' work efforts with high-value clinical services. Across the board, RVU levels for cognitive clinical work could be increased and those for procedural work could be decreased to create incentives for primary care services. RVU levels could also be increased substantially for high-value clinical activities undertaken by either specialists or generalists. Activities linked to RVUs could be more broadly defined to include team-based and supervisory clinical activities as well. Assessing Participant-Centered Outcomes to Improve Clinical Research, a perspective article by Rhonda Coast from Rockefeller University, New York. The value of patient-centered outcome measures for improving care is now well established. In contrast, research participants' perspectives on aspects of their research experiences, such as whether the informed consent process prepared them for participation, are rarely examined. These authors developed and validated a standardized research participant perception survey. The survey was deployed to 18,890 research participants at 15 U.S.-based clinical research centers. In aggregate, 73 percent of participants rated their overall research experience very highly, at 9 or 10 on a 10-point scale. Similarly, 66% said they would definitely recommend research participation to friends or family members. Participants were more likely to rate their overall experiences very highly when they trusted the investigators and nurses, felt that investigators and nurses treated them with respect, listened to them, and gave them understandable answers to their questions, and could meet with the principal investigator as much as they wanted. A majority of participants indicated that they did not feel pressure from research staff to join the study, 94%, and believed that the consent form covered the study's risks, 81%. One striking finding was that most participants The images in clinical medicine features an obese 50-year-old man with no known medical history who presented with a necrotizing infection of his right foot that had begun 10 days previously. He attributed the lesions to wearing new shoes. He was found to have diabetes, glycated hemoglobin level 10.5%, with peripheral neuropathy. The patient had photographed the lesion twice daily, thinking it would heal spontaneously. The preoperative photographs show erythema on day 1, blisters day 3, a necrotizing abscess day 6, and wound infection requiring surgery day 10. The patient underwent operative debridement and was treated with antibiotic agents for three weeks. The infection resolved with no recurrence or sequelae during three years of follow-up. Diabetic foot infection may evolve rapidly, especially in patients with neuropathy. A 14-year-old girl presented to the emergency department after a car accident. She had been wearing a lap-shoulder seat belt. She had severe back pain but had normal strength and sensation of touch in her legs. She reported no paresthesias. Palpation of the lumbar spine revealed prominence of the spinous process of the first lumbar vertebra and an increased gap between the first and second lumbar spinous processes, findings that aroused suspicion of a flexion-distraction injury. CT revealed disruption of the ligaments in the posterior column and the middle column, as well as disruption of the L1-L2 intervertebral disc in the anterior column. There were also fractures of the anterosuperior aspects of L1 and L2 and dislocation of the L1-L2 facet joints. These fractures are characterized by violent flexion with all elements posterior to the axis of rotation submitted to distraction forces. The fractures are unstable and require surgical treatment. The patient underwent T12 to L2 fusion and was pain-free four months after surgery. This concludes the summary of the December 5th issue of the New England Journal of Medicine. We're interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at NEJM.org. Thank you for listening.
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Hello and welcome to the podcast for the September 2009 issue of The Lancet Oncology. Richard Lane here and I'm joined this month by TLO's editor David Collingridge to discuss some of the issue highlights. David, let's start with a study actually looking at two trials concerning the treatment of prostate cancer. Just before we actually go into the details of the study, can you just give us some background here and remind us how prostate cancer is generally managed these days? Well treatment of prostate cancer depends on the type and extent of disease and the options run the full spectrum of modalities typically associated with cancer management from simple watch and wait strategies for very small localised lesions through to surgery, hormonal treatment, chemotherapy and radiotherapy. The precise combination and constitution of these latter options again really depends on the stage of disease. And David these trials investigate the efficacy of a bisphosphonate, the one in question here being sodium clodronate. What do we know about this agent? Well sodium clodronate was one of the first generation bisphosphonates. We know that bisphosphonates have a role in bone demineralisation and they can prevent fractures and it's thought they also have an anti-tumor property by modifying tumor growth factors, adhesion to tumor cells to the bone matrix and also modifying tumor cell apoptosis. As a result bisphosphimates are already well established in the management of multiple myeloma and breast cancer. So given prostate cancer is characterized by osteoblastic metases, the combined analysis of these two trials we're publishing this month tries to ascertain whether bisphosphonates might have a role in this setting also. And David, go on and briefly just summarise the design of these two trials. In these two British trials, sponsored by the MRC, 311 men with metastatic disease were recruited into the trial designated PR05, and 508 men with non-metastatic disease were recruited into trial PR04. In both trials, men were randomised to receive 2,080 mg of sodium clodronate or placebo for up to three years for metastatic disease and up to five years for non-metastatic disease. This new analysis looks at the long-term follow-up, a median of 11.5 years, within these trials. The results, David, there seems to be a clear distinction here between the results for metastatic disease compared with that of local disease. Yes, that's right. These long-term data highlight an important distinction and help delineate who should be prescribed sodium chlodronate. The results show a significant overall survival benefit for men with metastatic disease at presentation equating to a 30% survival at 5 years and a 17% survival at 10 years compared with just 21% and 9% respectively in the placebo groups. Among patients with non-metastatic disease there is no evidence of benefit as indicated by the hazard ratio of 1.12. The authors also present a number of exploratory interaction analyses for both trials, but the results, while suggesting a few nuances, do not materially affect these top-line take-home messages. What's your and the authors' possible explanation of the difference between these two results? As I've just hinted at, these interaction analyses highlight a few nuances that give us some clues to these differences. So, for example, among men with metastatic disease, there were biochemical differences, such as raised alkaline phosphatase and creatinine, which are thought to affect osteoblastic activity and the pharmacokinetics of bisphosphate excretion. So it seems there are biological factors related to the development and progression of bone metastases that affect treatment response. And David, next steps, the usual question really, do we need more research to confirm these findings in larger studies or are there implications for clinical management straight away do you think? The data here support the use of bisphosphamides within the management strategy for metastatic prostate cancer and equally they suggest these agents probably shouldn't be used for men with localised disease. The next steps now are to ascertain whether the next generation of bisphosphamides, which are far more potent than sodium clodronate, can improve outcomes further, and whether various other combinations of chemotherapy can be added into the mix. A number of trials are ongoing to look at these issues, the MRC-sponsored STAMPEDE trial being one of the most ambitious. Moving on David to a randomised trial called PASSION-P and this concerns women with early stage breast cancer undergoing a sentinel lymph node mapping and biopsy. Give us some background here please. Well lymph node mapping and biopsy simply means identifying where the lymph nodes reside anatomically so that several can be resected for pathology. Biopsies are done to determine the stage of disease and as we all know accurate staging in any cancer is important to deciding on the most appropriate treatment options and often gives us some clues on prognosis too. For identifying nodes in patients with breast cancer radiolabel colloids or blue dye is usually injected to visualize the location of the nodes for subsequent resection. Now site of injection is contentious. Different practices exist ranging from peritumoral to interparenchymal, subdermal, dermal and intertumoral injection. This procedure is associated with pain so just to clarify the clear objectives of the current study. Yes that's right there's been very little research looking into pain associated with lymphatic mapping but given this procedure is an important component in disease, it's very important to consider patient comfort in all aspects of their care, including diagnostic procedures. In this American study, 140 patients were randomized to one of four different groups. The groups include a control of topical 4% lidocaine cream plus technetium sulfa colloid, and three study groups of topical placebo cream plus injection of technetium sulfur colloid contained neither sodium bicarbonate 1% lidocaine or sodium bicarbonate plus 1% lidocaine. The primary endpoint was patient reported pain immediately after colloid injection using two different pain scoring systems. The results seem clear based on as you say these two different pain scores. Can you just discuss those results and also the chemistry behind the way different results were observed here? The mean pain scores on both scales were significantly improved for patients who received the colloid injection with 1% lidocaine, with or without sodium bicarbonate. The reason for adding the bicarbonate to the various study groups was to adjust the pH of the injection fluid because there's some evidence that buffering improves patient comfort. However, this study showed no significant benefit to altering the pH of the injection solution. And actually, it was simply the mode of delivery of the local anaesthetic, either topical or subdermal injection, that clearly had the greater influence on patient pain. And David, the implications of these results, is there enough evidence from this to again to auto-clinically practice at centres who can offer procedures like this? is reasonable in the suggestion that centres should now consider administering sub-areola injections of radioisotope colloid in 4ml quantities containing 1% lidocaine to improve patient comfort. And moving on to a slightly lighter issue, if you like, but still important. Back in 1823, when Thomas Wackley founded The Lancet, the weekly journal, he used a column to debunk some of what he considered the nonsense that was being propagated by parts of the medical profession, often concerning homeopathic remedies. And in a kind of similar way, you're introducing a new column into the last oncology, David. Tell us more. Well, complementary and alternative medicines are used widely these days, and use among cancer patients is alarmingly quite high. And often there is very little evidence to support their use, but mass media coverage, lazy journalism, biased reporting and pseudoscience have all allowed these practices to creep into the public's consciousness as valuable medical practices. Somewhat disturbing is the fact that such thinking isn't just limited to lay people. There are a number of supporters among well-educated people who really should know better. With this in mind, it's remarkable that such debates have been ongoing among the pages of the Lancet back to its earliest issues in 1823, and yet here we are nearly 200 years later and the debate still rages on. In those inaugural issues, Thomas Wackley ran a regular column, as you mentioned, called Quack Medicines, to expose the truth behind popular alternative medicines of the day. We decided it would be a timely homage, if you like, to the Lancet's founder, to re and the first column you have is authored by Ben Goldacre, who people may well know in the United Kingdom for his column in the Guardian newspaper about bad science. Just briefly mention the sort of issues he's dealing with in this first column. Well, we were delighted Ben Goldake had found time to write for us, given the popularity of his pieces in the Guardian.
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The article covers the contrasting reports on red wine and alcohol consumption, consumption of various food types, and lifestyle choices. And finally, the piece champions the use of meta-analyses and systematic reviews, with the inference that these types of reports are perhaps a much better source of reliable information, especially for the popular press, because they're less susceptible to large swings in recommendations and conclusions. I guess I just wonder, as I probably would have done in 1823 if I'd been around, isn't there just a slight danger that we're preaching to the converted here? Maybe differently in 1823, but surely in 2009. Do we need to be telling educated, informed readers of the Lancet Oncology about this sort of thing? Well, to be honest, Richard, I'm not sure we are preaching to the converted. There are a number of complementary medicines, for example, where the evidence base is far from conclusive. It's all rather contentious, and even amongst oncologists, opinion is divided. These columns will allow us an opportunity to re-examine some of the evidence and reopen debate. And to help general public. It's a perennial issue. Thanks for that, David. And let's just quickly finish off with the leader, which I see is calling for sunbeds to be banned. Why is that? Well, last month we published a short summary from the recent IARC monograph meeting in Lyon, France, in which the previous rating for ultraviolet-emitting tanning devices was upgraded to the highest risk category available, namely, on the basis of all relevant evidence to date, these devices are officially carcinogenic to humans. The underlying meta-analysis that led to this conclusion showed a startling 75% increase in the risk of melanoma among people who began tanning regularly before the age of 30. Now, given generally agents in this highest risk category are either banned or heavily regulated to reduce risk, and given there are good alternatives to sunbeds such as various lotions and sprays that can achieve the same or similar body image, can we ethically condone the use of such devices in the name of, well, vanity? I don't think we can. And I'm sure the time must have now come to see tanning saloons and sunbeds removed from our streets and homes. Yeah, it's difficult to disagree with that, David. I just want to check that we're also not saying that any exposure to sunlight, which is obviously different to a sunbed, but obviously it's still potentially carcinogenic, is not something that we're talking about about here there's still a way that you can go away on holiday protect yourself against the sun but still come back with a with a healthy color is that right absolutely a little bit of sun is of course good for you but this is rather different from being fried at close range on a sunbed provided you limit your exposure it's all about everything in moderation don't spend large amounts of time in the sun without a high factor sun cream and especially seek the shade around noon when the sun is at its hottest. The Cancer Council Australia have long promoted a brilliant slogan to bear in mind when anyone's on holiday really, slip, slop, slap, which stands for slip on a shirt, slop on the sun cream and slap on a hat. Great, Well, I'm heading off to the Mediterranean in about 10 days time. So I will slip, slop, slap. And I hope listeners are going to do so as well whenever they go into hot, sunny areas. But anyway, many thanks, David. Those are some of the highlights from the September issue of the Lancet Oncology. Thank you all very much for listening and we'll see you next month.
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Hey folks, just a quick reminder that this episode is not meant to be used for medical advice, just good old-fashioned education. All patient information has been modified to protect their identity and the views expressed in our podcast do not necessarily reflect the opinion of our employers. Welcome back Clinical Problem Solvers. We are here again for a schema episode. How's everyone doing today? Can't complain. Doing great. Well, I'm doing better since I can see Jack Penner's mustache. It is epic, full, very Tom Selleck-y. It's wonderful. I had high hopes that the mustache was not going to be referenced on the recording, and there they go. We had this entire conversation about how this needs to be now a visual platform because of that mustache. Well, moving on to the case. I'm very excited that we have an awesome case for everybody today. Are we ready to get started? Let's do it. For the audience, just as a reminder, these schema episodes are an opportunity for us to review some of the core clinical problem solvers schemas through the lens of a clinical case. So none of us are actually blinded to the case, but we're going to be using the case as a mechanism to discuss some of the schemas, which you can find on our website. The schemas that we're going to discuss today are jaundice and lung nodules. You may remember a former schema episode in which we also examined the schema for jaundice. We are going to look at it through a different lens today, which you will see unfold in the case. And we are revisiting the jaundice schema because not only is it one of the most fun ones to think through, but it is also one of the core problems that we see in internal medicine. So get ready for jaundice round two, as well as an approach to lung nodules. And I will get us started with the first aliquot here. So this case is a 67-year-old man who presented to the emergency department with one week of progressive jaundice. For the last four to six weeks, he has had intermittent episodes of dull, achy abdominal pain, and often, but not always, the pain came following a meal. All right, so let's get started. Let's first talk about jaundice. So whenever I like to think about jaundice, I like to break it into two buckets. The first being indirect, which is unconjugated bilirubin, and the second being direct, which is conjugated. Now, once I break them into these two buckets, I first like to review the life-threatening causes of each first, because there are no misdiagnoses. You don't want to forget about these and you want to rule these out first or at least be thinking of them first, just to make sure you're not dealing with a life-threatening cause of jaundice. And so in the indirect bucket, our life-threatening cause is going to be hemolysis. And so whenever you see an elevated, indirect, unconjugated bilirubin, take a quick look at the CBC and make sure you're not having an anemia, thrombocytopenia. Don't need to go ahead and check a peripheral smear. After that, in the indirect bucket, some less common causes. So you can have some drugs can cause an indirect hyperbilirubinemia, a hematoma, and then some rare genetic causes with Gilbert's being the most common. Next, let's move into our next bucket of direct conjugated elevated bilirubin. And this bucket, I like to break into two separate sections after that. So intrahepatic, so that within the liver, so your biliary tree within the liver. And this mainly involves your infiltrated diseases, a viral hepatitis, some drugs, and then cirrhosis. And then you move into your extra hepatic biliary tree, which can lead to elevated conjugated bilirubin. And for that, I like to think about three different types. So you can either have a problem in the lumen itself causing obstruction. You can have a stricture affecting the biliary tree itself and the wall, or there you can have an external cause of obstruction, something that is pressing on the outside of the biliary tree causing obstruction. Is there anything better than learning about jaundice from the future Boss Lady GI fellow? That was awesome. Thanks, Lindsay. Yeah, so this patient's coming in with jaundice. And let's think a little bit about the other aspect of this case, abdominal pain, mostly what it seems like a postprandial pain that this patient is experiencing. And the fact that this kind of a background of the abdominal pain is going on for like subacutely for a while, it's making me a little bit worried that we're dealing with like maybe more of a subacute nature and that this jaundice is not like acutely coming out of nowhere. So we love our Venn diagrams. So right now I'm thinking about the Venn diagram of postprandial, abdominal pain, and jaundice. But first, let's just talk about postprandial pain because it's kind of cool. And then I'm going to leave the overlap to the one and only Dr. Dan Minter to talk a little bit more about. So let's focus on postprandial pain for a little bit. When I think about postprandial pain, I think basically there's a stress test for the systems that needs to help us digest food in the GI tract. So what that could be, it could be the lumen of the GI tract, it could be the vasculature that requires to bring more blood in to help us digest food. It can be the problem with the biliary tract or the pancreas. So in the lumen itself, if a patient has a peptic ulcer disease, gastroparesis, or any external compression of that lumen, it can cause pain. And sometimes with external compression, you can get early satiety as well. Vascular one is an important one to remember because mesenteric schema falls into that category, is that if you have a lot of atherosclerotic disease in the vessels of the GI tract, then when you're eating and trying to digest food, you can get basically angina of the GI tract. Biliary colic and also chronic pancreatitis are the two other things to think about as well when you're thinking about postprandial pain. So think lumen, vessels, biliary, tree, and pancreas. Okay, Dan, what are your thoughts about the overlap of abdominal pain and jaundice? So when we're examining a patient who has postprandial abdominal pain and jaundice, we can look for areas in which those two symptom complexes overlap. And then by virtue of doing that, gain an added layer of specificity. So we can go crossing out the different causes of those specifics that are perhaps not in that sort of dual shaded area of the Venn diagram. So when we think about jaundice, we're thinking prehepatic, intrapatic, posthepatic, with then posthepatic being the sort of like focus on the biliary tree. And then as Charmaine mentioned, when we think about postprandial abdominal pain, then we're going to be again thinking about luminal structures of the digestive tract, vascular structures, the biliary system, and then the pancreas. So where is the element of overlap that most adequately fits this series of Venn diagrams? I'm really going to hone in on the biliary tract. So causes of postprandial biliary abdominal pain really make me think about cholecystitis with a caveat that cholecystitis in itself doesn't tend to cause jaundice, but perhaps if a gallstone is a little bit further down into the caudal duct, or if you have something called Moritzi syndrome, where a gallstone within the neck of the cystic duct then externally compresses the common bile duct. Also with the pancreas, if you have some sort of chronic pancreatic process that is causing a stricturing of the common bile duct, that could also lead to jaundice. And we oftentimes refer to like painless jaundice in patients who have a pancreatic head mass. So, you know, that's all to say that this overlap could potentially give us, you know, sort of a leg up on advancing our diagnostic thinking in this case. It may not be true that both of these symptoms are caused by the same pathology, but if they are, then we've just advanced our thinking a little bit by at least paying more than passing tribute to diseases of the biliary system in the pancreas. Dan, it is not too late to switch from ID to GI. Come on. He did say Moritzu syndrome. So I feel like that is a valid point.
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I like Dan Minter even more now than I thought I could. Well, there's a lot of biliary pathogens, you know, those flukes and whatnot. Oh, this is bringing me a huge smile. Let me give you the next aliquot of the case. So the patient's past medical history included hypertension, hyperlipidemia, and a recent diagnosis of diabetes three months prior. He took lisinopril, Atorvastatin, and Metformin as his medications. Review of systems included a 12-pound weight loss over the last six months, a chronic cough that had developed over a similar timeframe, as well as progressive exertional dyspnea. He had a 12-pack year smoking history and had quit about 30 years prior. He consumed one to two alcoholic beverages per week and lived in the Central Valley of Northern California. On exam, he was afebrile with stable vital signs. Exam was notable for icteric sclera and jaundiced skin. He had mild epigastric tenderness to palpation, and there were no stigmata of portal hypertension or hyperestrogenism. He also had no bruises. Labs were notable for an anemia to 10.2. This is a drop from a normal hemoglobin one year prior, as well as an AST of 25, an ALT of 33, an ALKFOS of 328, and a T-billy of 5.8, which was fractionated to reveal a D-billy of 3.6. A chest x-ray demonstrated scattered nodular opacities throughout the bilateral lung fields. Well, since Lindsay is going to be our resident GI fellow pretty soon, maybe I'll leave the discussion of jaundice to her and I'll kind of focus on some of the other features of this case that have come out, including the weight loss and the pulmonary symptoms. So, you know, basically at this point, we've taken what was something of a more isolated case of jaundice and now are expanding our thought process based on these other symptoms. Weight loss, you know, the way I think about that is I'm a simple person. So I think, you know, you're not getting enough calories in or you're using too many calories. And if you're not getting enough calories in, maybe it's that you're not eating or you're not absorbing. And then if you have too many calories out, it's either, you know, something inflammatory, like an infection, some other inflammatory disease or potentially malignancy. So, you know, that's all to say that, you know, now that we have this degree of relatively well-documented weight loss over the past six months, that raises my level of concern for some serious systemic process. And then also makes me sort of think about, you know, is it a calories in or calories out problem? I'm sure we'll touch on that a little bit more in the case as it comes up. What to do with the lung findings. So this patient not only is experiencing jaundice, but they're also experiencing some cough and shortness of breath and some sort of symptom complexes that refer us to the lung. So, you know, that there's one sort of major helpful action in this case is to move us away from the biliary system as we were sort of beginning to focus in on a little bit more and wonder if this is some process that is, you know, systemic and is truly having sort of primary focus within the thorax as well as within the abdomen. Or, you know, if we're going to draw sort of causal arrows, is something abdomen, the primary process, causing pulmonary findings or the other way around? The objective data that we have at this point is that the chest x-ray demonstrates, quote unquote, scattered nodular opacities in the bilateral lung fields. So that adds a degree of specificity. This is something that we can't ignore at this point and makes me more and more worried about some intrathoracic process. So what are these opacities? As a general rule, pulmonary opacities could be something that's within the alveolar space. That could be pus, water, blood. It could be something within the interstitium, or it could be a sort of tissue-based mass. So if these are pulmonary metastases or primary pulmonary cancer or something like that. Just because I can't help myself, One thing I'll say is that, you know, for those of you who don't practice in Arizona or California, the Central Valley is a buzzword for us for coccidioidomycosis, which is a dimorphic fungal pathogen that we think a lot about here in California. So I'm not sure if that's going to be related to this case. I would be jumping up and down if it was, but I'm holding my excitement. Awesome. Now, as Dan said, I'm going to try to focus on some of the liver lab just as to refresh. So your AST was 25, ALT is 33, ALT-FOS 328, a T-billy 5.8 with a D-billy of 3.6. So how does that help us make progress in our case? So whenever I'm looking at liver labs, I'm trying to characterize them as cholestatic or hepatocellular. And cholestatic liver picture will show an elevated outfoss and an elevated direct bilirubin, whereas a hepatocellular liver injury will show more of an elevated AST and ALT out of proportion to the other two. And so with this patient's lab specifically, you're seeing that really elevated out cost and debilly, which is out of proportion to the normal AST, ALT. And so that puts us in that bucket of cholestatic liver injury. And so then when I think about cholestatic liver injury, I'm thinking about the biliary tree or something either internally in the biliary tree or something externally pressing on the biliary tree causing obstruction. Now that can be from the gallbladder. It can be from the small intestine. It can be from lymph nodes. It can be from the pancreatic head. So anything around that area that can cause obstruction can cause this picture. And, you know, what diagnostic step is next whenever you are thinking about a cholestatic liver injury? There are so many imaging modalities that you can choose to try to investigate this. And so you have an ultrasound, a CT with contrast, an MRI or MRCP that looks specifically at the biliary tree, or you can go straight to GI and ask them for an ERCP or an EUS. An ERCP is endoscopic retrograde cholangiopancreatography. Say it three times fast. I never try to say that. It's mostly because I don't know what it stands for. And then an EUS is an endoscopic ultrasound. And so basically go in with an endoscope and ultrasound the area that you're concerned about. And so really when you're trying to decide between any of those imaging modalities, you're trying to figure out how urgent you need your image, the availability of the imaging modality. And if there's anything else that the patient may have that you want to investigate that may make you want to pick one imaging study over the other. And so ultrasound is really great for the biliary tree. If you're just wanting to look at the biliary tree to see if there's any biliary dilation. A CT is great if you're wanting to look at maybe something else. So this patient has pulmonary nodules, they have biliary involvement. So if you're wanting to give this patient one study that may capture both, that may be better. An MRCP specifically looks at just the biliary tree. And it's actually better at picking up PSC and stuff that may be not a stone. And then, of course, if you're concerned about cholangitis, you may want to just go ahead and call GI for that ERCP. So since this patient has also has pulmonary triming, you may consider just going ahead and doing one study so you can try to capture both. And if you're not able to find the biliary findings on that CT, an ultrasound or MRCP can be more sensitive. Absolutely awesome discussion team. As requested by Dr. Shipley, CT of the chest, abdomen, and pelvis revealed multiple randomly distributed pulmonary nodules, some of which had central cavitation. The abdominal and pelvic portions of the CT scan showed dilation of the common bile duct up to 1.5 centimeters and no discrete stones, masses, or lymphadenopathy. All right. Who am I to get in the way of pulmonary nodules on ID fellows? So I'll leave that up to Dan and then focus with Lindsay's permission under the common bile duct dilation, which kind of makes me think about the extrahepatic ideologies of the jaundice that Lindsay laid out for us in the beginning of the case.
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And in terms of the lumen, you know, we can think about stone, sludge, biliary cast, and I have to say parasites because of that. What can happen within the walls? And the wall pathology usually leads to strictures, cancers in the form of cholangiocarcinoma, trauma, ischemic injury, and autoimmune diseases such as primary sclerosis and cholangitis. And are we really super solvers if I don't mention IgG4 disease? Yep, IgG4 disease can do it too. There are more rare causes of stricture, such as infectious processes like A-cholangiopathy and influx of processes such as mastocytosis, amyloid, but quite rare. So I would always focus my cognitive energy on the most common causes. Lastly, the external compression. So thinking about the environment that the common bile duct, this floppy tube sits in. So cancers of the pancreas and filaria of water and adenal pathologies and cancers can lead to external compression. And so those really big lymph nodes that can surround that biliary duct. Awesome, Sharmin. Thank you so much for walking us through that. And now that we have this comprehensive understanding of what potential processes can cause an extrahepatic biliary obstruction, to move our own reasoning process forward, we can start to think about how we take this list of potential etiologies and prioritize them in terms of what is more and less likely. And so if we think about rooting ourselves in the epidemiology of the causes of extrahepatic biliary obstruction, far and away the most common underlying etiology is going to be gallstone disease. Often, but not always, we'll be able to see gallstone disease on the CT scan. And so the absence of this finding here, while it certainly doesn't rule out that there is potentially a stone obstructing the common bile duct, it makes us start to expand our differential diagnosis to include some of the other disease mechanisms that Charmaine mentioned. If we go back to the reasoning that Dan and Lindsay and Charmaine shared with us earlier in the case, we can start to see an underlying process such as malignancy rising higher and higher, right? We have multiple foci of disease and multiple organs of the body. We have a subacute syndrome of systemic inflammation in somebody who is a bit elderly. And so we can see malignancy starting to work its way up the case. But, right, if we're going to actually test this hypothesis, what we're going to need in the absence of a definitive understanding of the etiology of the obstruction on CT scan is to get a look inside and around the biliary tree. And this is where the assistance of our GI colleagues or the hepatobiliary team can be quite helpful because they have the skills necessary to perform an ERCP. What an ERCP can help us do in this case is be not only diagnostic, but also therapeutic. The ERCP can give us a look at the biliary tree. Do we see a stone there that the CT scan didn't pick up? Or do we see another explanation for the extrahepatic biliary obstruction? And then the ERCP also gives us an opportunity to deploy a therapeutic intervention to relieve the obstruction in and of itself. So it's an incredibly effective, both diagnostic and therapeutic intervention that we can potentially get in one fell swoop. Other things that we can do during an ERCP procedure would be to take more diagnostic sampling, for example, tissues or acquiring the stone if we wanted to send it off for further analysis. Beautiful, Jack. I kind of think that your discussion of epidemiology was put in there in part to just dissuade me from thinking about liver flukes and all the other wonderful parasites. It was not a fluke. I'm dying on the inside. Okay. Well, yeah. Charmaine wanted me to talk about pulmonary nodules as the other part of this case, which is really interesting based on the CT scan. So if you're near a computer, I'd suggest that you go to the CP solvers website and look at the lung nodule schema. Basically, there are three main buckets of diffuse pulmonary nodules. This is in contrast to like the solitary pulmonary nodule that you might see in another context. So this is if you have multiple sort of small pulmonary nodules throughout the lungs. And these are all in reference to the pulmonary lobule, which is the smallest divisible component of the lung parenchyma. And so what that really is, is it's a sort of unit of lung parenchyma that's surrounded by lymphatics, almost in like a hexagonal sort of structure, into which run a main airway, or into which run an airway and then a blood vessel. These are also covered with sort of capillaries. So there's blood flow throughout the entirety of the pulmonary lobule. So with respect to the pulmonary lobule, there are central lobular, randomly distributed and perilymphatic forms of nodules. Let's start with central lobular nodules. These are nodules that are in the center of the pulmonary lobule. And how do you get to the center of the pulmonary lobule? The most common way is through the airway. So these tend to be airway-centric diseases. As an infectious diseases fellow, this is, you know, kind of what we tend to see most of the time is central lobular nodules more reflective of airway spread of infection. The infections that you can see can be viral, bacterial, mycobacterial, or fungal. There are also non-infectious causes like aspiration or hypersensitivity to pneumonitis or even the spread of an endobronchial tumor. But one tip off for central lobular nodules is if you look at the part of the lung abutting the pleura is there shouldn't be any nodules actually touching the pleural space. If we move on to randomly distributed nodules, these are nodules that have no relationship to the pulmonary lobule. And how do you get random distribution of things? It's wherever blood goes, a nodule might show up. So these are things that tend to be transmitted by the blood, like hematogenous infections, like miliary TB or miliary fungal infection, or potentially the transmission of a hematogenous malignancy. So you get metastatic disease. They just sort of randomly distributed throughout the lung parenchyma. So this would be a relatively good sort of picture for somebody who has hematogenous distribution of solid tumor metastases. The last major category, like I said, is perilymphatic nodules. And these, if you think about like the sort of hexagonal-ish pentagonal structure of the pulmonary lobule, these are around the edges of that where the lymphatics really serve to drain the lymph from the pulmonary system. So these can occur most commonly in inflammatory diseases like sarcoidosis or pneumoconiosis like silicosis. Or you can also see them in malignant diseases like lymphangitic carcinomatosis, where you just really have kind of a buildup of stuff around the outside of the pulmonary lobule. So again, to summarize, central lobular, randomly distributed or perilymphatic, central lobular being airway, randomly distributed being more through just kind of hematogenous system dissemination, and then perilymphatic really sort of focusing in on those lymphatic channels around the outside of the pulmonary lobule. Boom. Boom, indeed. All right. So given what Dan has told us about pulmonary nodules, it seems like this, the distribution of the nodules for this patient are, are random. And so that makes us fall into that bucket of hematogenous spread. And whenever we think about hematogenous spread, exactly what Dan was saying, we're prioritizing malignancy, especially in this patient who is having weight loss and postprandial pain, cholestatic picture, liver injury. And so I think making sure we're not dealing with an infection and making sure we're not dealing with two different things, but also realizing that given that this is a random distribution with hematogenous spread, that this could definitely be a malignancy coming from somewhere in the biliary tree. So to give you all the conclusion of this case, after this excellent discussion, blood cultures, toxidioides, immunodiffusion, and complement fixation were both negative. Patient also underwent sputum testing and an AFB smear culture and MTB-PCR were also all negative. Patient ultimately underwent ERCP and endoscopic ultrasound, which demonstrated a four centimeter pancreatic head mass and a distal bile duct stricture. A biliary stent was placed and biopsies of the mass were taken. Biopsies of both the pancreatic head mass and of one of the lung nodules revealed pancreatic adenocarcinoma. And the patient was discharged home with plans to follow up with oncology for initiation of systemic chemotherapy.
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And the fact that these lesions were cavitating also, I learned, was atypical of a pancreatic adenocarcinoma. And so there was some diagnostic uncertainty over whether if we found what was the underlying etiology of the extrahepatic balearial obstruction, whether or not it would definitively explain the pulmonary nodules in this case. For those of you who are wondering, why did they take two biopsies? So team, we'd love to hear your reflections on this case or any other thoughts overall on the topics that we covered today. I will say the last that I heard that this patient is overall doing well, despite what is a very, very sad and very sobering diagnosis overall. Yeah, thank you so much for sharing, Jack. And, you know, I love talking about like jaundice in abstract. And I think a lot of patients that we take care of, unfortunately, I don't like it in real life as much because it turns into usually often like these really terrible pancreatic cancer diagnoses that comes with it a lot of like suffering and poor prognosis. It's still important to talk about, to learn from and to reflect on. And did the abdominal pain get better, Jack, by the way? Fortunately, it didn't change much after the biliar obstruction was intervened upon. Yeah. And that's another reason to kind of like circle back to our one diagram is that our job is not done yet. I think it's also easy to contribute the abdominal pain to this terrible cancer and also making sure that there's no other ideology that we can help this patient with. Yeah, 100%. Couldn't have said it better. And there are some patients if they have, you know, pancreatic, if we do find that the pancreatic cancer is causing a lot of the pain, they can go back and do a celiac plexus block for these patients, which helps a lot. It's more of a palliative procedure, but it can help tremendously with pain in that area. That's such a great point, Lindsay. And one of the reasons I love being a doctor because our job is never done. There's always there's so many tools that we have, whether it's, you know, a diagnosis, treatment or palliative, you know, at the end of the day, it's all done in the service to make sure patients have a good quality of life and be able to help them, whether it's with pain or getting answers. So, you know, we got a pretty awesome job. One of my reflections is it's so much fun to learn from everybody's sort of specific area of interest and Lindsay and Charmaine, you know, just amazing pearls and stuff. So really, really appreciated learning from both of you on this case. And thanks, Jack, again, for presenting and rocking that mustache. It was my absolute pleasure. Thank you all for joining us today for another installment of our Schema episode series. We hope you have a great rest of the day and thanks again for tuning in.
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Welcome to the New England Journal of Medicine summary for the week of February 28, 2013. I'm Dr. Michael Bierer. This week's issue features articles on high-frequency oscillation for ARDS, on dancitron and risk of adverse fetal outcomes, and an artificial pancreas versus sensor-augmented pump, review articles on idiopathic scoliosis in adolescents, and on clonality and cancer, a case report of a woman with long-standing thoracic pain and incontinence, and perspective articles on open access. With this issue, we feature new clinical decisions on medicinal use of marijuana. Currently, 18 states allow the medicinal use of marijuana, but it remains controversial among physicians. This Clinical Decisions presents both University of Toronto, Canada. In this trial, high-frequency oscillatory ventilation was compared with conventional ventilation with a lung protective protocol in patients with new-onset moderate-to-severe acute respiratory distress syndrome, ARDS. The study was stopped early. In-hospital mortality was 47% in the high-frequency oscillatory ventilation group as compared with 35% in the control group. Patients in the high-frequency oscillation group received higher doses of midazolam than did patients in the control group, and more patients in the high-frequency oscillation group than in the control group received neuromuscular blockers. In addition, more patients in the high-frequency oscillation group received vasoactive drugs and received them for a longer period than did patients in the control group. In adults with moderate to severe ARDS, early application of high-frequency oscillation as compared with a ventilation strategy of low tidal volume and high positive end-expiratory pressure does not reduce and may increase in-hospital mortality. High-Frequency Oscillation for Acute Respiratory Distress Syndromeemia accompanying the acute respiratory distress syndrome. This trial compared high-frequency oscillatory ventilation with conventional ventilation. There was no significant between-group difference in the primary outcome of all-cause mortality at 30 days, which occurred in 41.7% of patients in the high-frequency oscillation group and in 41.1% of patients in the conventional ventilation group. After adjustment for study center, sex, score on the acute physiology and chronic health evaluation, APACHE-2, and the initial PaO2 to FiO2 ratio, the odds ratio for survival in the conventional ventilation group was 1.03. The use of high-frequency oscillation had no significant effect on 30-day mortality in patients undergoing mechanical ventilation for ARDS. Atul Malhotra from Brigham and Women's Hospital Boston writes in an editorial that these data might suggest that high-frequency oscillation as applied in these trials is not an advance. However, one could argue that it is not high-frequency oscillation itself, but the oscillation protocols studied in these trials that were ineffective, and perhaps worse than usual care. Second, patient selection may be an important factor. Some patients have recruitable lung, that is, lung tissue in which alveolar air volume is increased with small increases in airway pressure, whereas others have non-recrutable lung. Indexes of recruitability may help to define which patients may benefit from high mean airway pressures and which patients are likely to suffer deleterious effects without major lung protection. Third, currently recommended strategies that use low tidal volumes may have effectively minimized mechanical stress on the lung, and further improvements in outcomes are likely to occur only through improved understanding of the heterogeneous ARDS phenotype and its underlying biologic characteristics. On danetron in Pregnancy and Risk of Adverse Fetal Outcomes by Bjorn Pasternak from Staten Serum Institute, Copenhagen, Denmark. Ondansetron is frequently used to treat nausea and vomiting during pregnancy. This historical cohort study investigated whether receipt of ondansetron during pregnancy was associated with significantly increased risk of spontaneous abortion, which occurred in 1.1% of exposed women and 3.7% of unexposed women during gestational weeks 7 to 12, and in 1% and 2.1% respectively during weeks 13 to 22. Ondansetron also conferred preterm delivery, 6.2% and 5.2%, delivery of a low birth weight infant, 4.1% and 3.7%, or delivery of a small for gestational age infant, 10.4% and 9.2%. Ondansetron taken during pregnancy was not associated with a significantly increased risk of adverse fetal outcomes. Nocturnal Glucose Control with an Artificial Pancreas at a Diabetes Camp by Moshe Philipp from the Schneider Children's Medical Center of Israel, Petah Tikva. This randomized crossover trial compared an artificial pancreas system with a nights when the sensor-augmented insulin pump was used, there were significantly fewer episodes of nighttime glucose levels below 63 mg per deciliter, 7 versus 22, and significantly shorter periods when glucose levels were below 60 mg per deciliter. Median values for the individual mean overnight glucose levels were 126 mg per deciliter with the artificial pancreas and 140 mg per deciliter with the sensor-augmented pump. Patients at a diabetes camp who were treated with an artificial pancreas system had less nocturnal hypoglycemia and tighter glucose control than when they were treated with a sensor-augmented insulin pump. Idiopathic scoliosis in adolescence, a clinical practice article by M. Timothy Horesco from Boston Children's Hospital. Scoliosis is the most common deformity of the spine. The diagnosis of scoliosis is suspected on the basis of physical examination and is confirmed by radiography performed while the patient is in a standing position that reveals spinal curvature of 10 degrees or greater. Idiopathic scoliosis is present in 2% of adolescents. Adolescents with scoliosis should have a thorough physical examination to rule out hereditary connective tissue disorders such as Marfan syndrome, neurofibromatosis, or neurologic conditions. Most adolescents with non-progressive idiopathic scoliosis can be seen by a primary care physician and do not require active treatment. Bracing is commonly recommended in patients with an immature skeleton with curve progression of 25 to 45 degrees, but data to support this approach are observational and inconsistent. A randomized trial comparing bracing with observation for idiopathic scoliosis is currently in progress. Surgical treatment is recommended in patients with an immature skeleton who have progressive scoliosis greater than 45 degrees. Listen to the full text of this article at NEJM.org. The Implications of Clonal Genome Evolution for Cancer Medicine, a review article by Samuel Aparicio from the British Columbia Cancer Research Center, Vancouver, Canada. The concept of clonal structure and evolution in cancers was elegantly synthesized in 1976, and it crystallized many prior observations of chromosomal heterogeneity during tumor evolution. Central to these ideas is the notion of a clone, a group of cells related to each other by descent from a unitary origin. Clonal relationships among cells arise when selection operates on individual dividing cells to confer a survival advantage or disadvantage. Within the next five years, international efforts may characterize the distribution of clonally dominant somatic mutations, those present in the majority of cells within a cancer, in more than 21,000 cancers of diverse types. A reduction in costs and improvements in technology have placed the sequencing of patients' tumors within practical reach. Preliminary results suggest that full characterization Thank you. focused on the implications and opportunities afforded by the realization that cancers are composed of cellular clones. The notion that most cancers are ecosystems of evolving clones has implications for clinical application. The authors review these, with particular focus on epithelial cancers. This review article discusses how methods to detect tumor cell clonality may come to inform clinical practice. A 77-year-old woman with long-standing unilateral thoracic pain and incontinence, a case record of the Massachusetts General Hospital by Ann Louise Oaklander and colleagues. A 77-year-old woman sought neurosurgical and neurologic consultation because of a long history of left thoracic pain. The patient had had constant pain under her left breast for as long as she could remember, probably since adolescence, which worsened over time and spread horizontally to involve a band on the entire left side of the chest. The cause for this patient's chest pain had been investigated over decades, and no cause or effective treatment had been found. She had undergone extensive cardiac and pulmonary testing, but the lack of other cardiac or pulmonary signs or symptoms made these unlikely sources of her chest pain. The current complete neurologic examination was normal. Review of imaging studies revealed multiple perineurial cysts in the thoracic spine. The cysts were the most likely cause of her pain because they were located at the same thoracic level as the pain and because there were no other potential causes. Symptomatic perineurial cysts, such as those described by Tarlov, have been reported for more than 70 years. However, most physicians are either unaware of the existence of Tarlov cysts or believe that they do not cause symptoms.
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For the sake of inquiry and knowledge, the inevitability of open access, a perspective article by Anne Walpert from MIT Libraries, Cambridge, Massachusetts. It's difficult to have a measured conversation about open access, Thank you. will undermine the viability of scholarly journal publishing disagree sharply with those who believe that only open access can expedite research advances and ensure the availability of that same scholarly literature. The system that produces, evaluates, and distributes scholarly research results is complex and interdependent. In a system this interdependent, destabilization at any one point perturbs critically important relationships. The extent to which access to knowledge is constrained and controlled by publishers' business models is at the heart of the discontent researchers have for the current journal publishing system. Yet, producing high-quality, peer-reviewed articles has a cost. However, many stakeholders in the scholarly communication system have cause to seek broader access to information and are experimenting with more open, Internet-based alternatives to traditional publishing. Although the transition to open access won't be easy or inexpensive, it is inevitable. Open, but not free. Publishing in the 21st Century, a perspective article by Martin Frank from the American Physiological Society, Bethesda, Maryland. Online dissemination served as the impetus for the open access movement and the call for free dissemination of the information contained in journals. There is, however, a cost associated with this openness, a cost that may reduce the funds available for research. Open access now comes in two flavors, gold and green. Gold open access provides immediate free access to the literature. Thank you. repository, such as PubMed Central. PubMed Central diverts approximately $4 million from the NIH budget in order to collect, process, and convert NIH-funded manuscripts into PubMed Central's archival format. Funding agencies are encouraging or requiring their grantees to publish in gold open access journals, allowing them to pay their author fees with money from their research grants or funds allocated by the agency. Assuming that all articles had to be published with gold open access, Harvard Medical School would have to pay $13.5 million at $1,350 per article to publish the 10,000 articles authored by its faculty in 2010, considerably more than the $3.75 million that was in its serials acquisition budget that year. Should we be diverting funds from research in order to fund open access publishing? Creative Commons and the Openness of Open Access, a perspective article by Michael Carroll from American University, Washington, D.C. Copyright law supplies the baseline terms of use for almost all information on the Internet. Copyright owners, seeking to grant permission to everyone, have issued public licenses broadening the range of permitted uses subject to certain conditions. Creative Commons licenses are the most widely used of these public licenses for all kinds of copyrighted works except software. As part of the open access movement and with the mission of expanding the terms of use for increasingly accessible information, Creative Commons has produced six copyright licenses that permit a range of uses beyond fair use, subject to certain conditions. The four conditions are combined into six permutations reflecting the types of copyright restrictions that people who otherwise choose to share their works for free might like to retain. The licenses, designed to allow all uses except those prohibited by a specified condition, have been adopted by a variety of institutional and individual copyright owners. The Downside of Open Access Publishing, a perspective article by Charlotte Hoogue from the Journal of the Norwegian Medical Association, Oslo, Norway. The open access model in which authors pay to have their work published offers an alternative way of financing quality control in scholarly publishing. But it also opens up opportunities for unscrupulous online vanity presses to exploit authors for profit. Jeffrey Beal, an academic librarian at the University of Colorado, Denver, who is interested in scholarly open access publishing, calls its more questionable incarnations predatory. Whether it's fair to classify all these journals and publishers as predatory is an open question. Some of the publishers are intentionally misleading, naming non-existent people as their editors and editorial board members and claiming ownership of articles that they have plagiarized from other publications. Other journals and publishers may be real, though it's obvious that the people running them are not very professional, and some of the publications may have been created simply because it seemed like a clever business scheme to collect author fees of several hundred dollars apiece to post papers in a journal-like layout at a fraction of the traditional price. Viewed in some lights, such enterprises may not be unethical. Thousands of researchers worldwide need to publish, and not all of them can do so in the highest-ranked journals. But it is surely problematic for journals and publishers to pretend to be something they aren't, misleading authors, readers, and the scientific community at large. The images in Clinical Medicine features a 56-year-old woman who had undergone bilateral lung transplantation for chronic obstructive pulmonary disease and who was found to have fine crystals in the inner retina in the macula of each eye, although she was asymptomatic. The crystals were consistent with talc retinopathy, and a remote history of long-term intravenous drug use was confirmed. Talc is an inert filler in methylphenidate hydrochloride tablets, which are crushed for intravenous drug use. The talc is then unknowingly injected intravenously. Talc particles are usually fine and are distributed intravascularly and extravascularly in the retina in patients who chronically use intravenous drugs and in whom right-to-left cardiopulmonary shunting occurs through collateral vessels that may develop around sites of pulmonary infarction. However, in a patient with a patent form in ovale, larger particles may cause retinal artery occlusions and severe vision loss. Review of this patient's previous lung biopsy specimens revealed interstitial epithelioid granulomas with foreign bodies, giant cells, and abundant polarizable crystalline material typical of talc. The talc particles, although perhaps not the primary cause of the respiratory failure, most likely contributed to chronic lung inflammation and exacerbated the patient's condition. A 62-year-old woman presented for a routine dental examination. During the examination, she was asked about the increased tissue on the lingual surface of her lower jaw. The patient reported that the mass had been growing slowly for years and that several family members had similar growths. On examination, four hard sessile nodules were noted on the lingual surface with normal overlying mucosa. Exostoses are localized benign bony protrusions. The most common oral exostoses are torus palatinus and torus mandibularis, which do not have cartilage involvement, owing to their anatomical location. There are many reasons for the development of exostoses, including genetic and environmental causes. They are generally asymptomatic. Removal of oral exostoses may be indicated before prosthetic rehabilitation or if complications from chronic trauma develop. This concludes the summary of the February 28th issue of the New England Journal of Medicine. We are interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at nejm.org. Thank you for listening.
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Hey folks, just a quick reminder that this episode is not meant to be used for medical advice, just good old-fashioned education. All patient information has been modified to protect their identity and the views expressed in our podcast do not necessarily reflect the opinion of our employers. Welcome back, family. It is great to be back for another episode of Queer Rounds, a podcast series that looks to highlight the reality of gender and sexual diverse communities in healthcare and how transphobia and homophobia are important causes of health disparities. This is the first episode of our first season titled LGBTQI plus health 101. Today we will cover terminology and concepts. Joining me today are my two lovely co-hosts, Gabriel and Brody. Hi! Hi family, excited to be back with you. Hello y'all, excited for today's episode. Being comfortable with terminology about gender and sexuality is key to improving our patient care. Couldn't agree more, Bernie. It is incredible how only respecting someone's identity or sexual orientation can go far to create a safe space within our practice. We would like to begin by saying that by no means a list of terms we will search today is exhaustive. You know, language involves with time and definition that may be of widespread use today, may be obsolete a decade from now. This is also true of geographical location. The same terms are not used in South America compared to Europe or Asia. Even within a country or a region, there are multitudes of terms that are unique to specific communities, and we should acknowledge that. That's totally true. So let's begin with the basics. What does LGBTQI plus stand for? It is an acronym that covers diverse groups with respect to their gender identity and their sexual orientation. The L stands for lesbian, the G for gay, the T for trans, the Q for queer, the I for intersex, and the A for asexual. The plus sign is usually added at the end to include all the terms that exist. We should acknowledge that gender and sexuality is a spectrum. So in reality, it would be impossible to have every individual identity and orientation in an acronym. Before we explore what each term means, let's talk about the difference between gender and sex. Yes, you're very right, Vali. This is a point of confusion for a lot of people. We define gender as a socially constructed set of ways that people understand and express themselves along the continuum of masculinity, femininity, both or neither. Sex is different from gender and refers to the biological distinctions that exist between male, female, and intersex with respect to specific genes, sex chromosomes, and or reproductive anatomy. Based on these biological distinctions, most infants are assigned a sex at birth according to the binary framework of male or female. Over to you, Vali. Thank you, Brody. It is key to point out that even though gender and sex are different concepts, they have in common that neither are binary. This means that the idea that there's only two sexes, male or female, is not scientifically or medically accurate. Intersex people exist and have always existed. There are people whose reproductive or sexual anatomy doesn't fit the typical definitions of male or female. For example, a person may be born appearing to be female on the outside, but having mostly male typical anatomy on the inside. Or a person may be born with genitals that seem to be in between the usual male and female types. For example, a girl may be born with a noticeable large clitoris or lacking a vaginal opening, or a boy may be born with a notably small penis or with a scrotum that is divided so that it has formed more like labia. The bottom line of what I'm trying to say is that neither sex nor gender are binary. They're in a spectrum. So next time you hear someone say they're only two sexes, you can confidently say no, they are not. Right, vale. And most people are designated as sex when they are born based on their external genitalia. However, in most of the societies, what is considered maleness or femaleness are associated with not only physical, but cultural, behavioral, and psychological characteristics, as well as the expectations about their roles as male and female. People often play in a certain community. In the bottom line, let's not pretend that we check all the chromosomes or genitalia and we do a very complex molecular study in every person that we met. We only question someone's sex when they don't fit our cultural expectations of what male and female should be. That's so true. For some people, the cultural expectations associated with their sex assigned at birth align with their gender identity. For example, for someone assigned male at birth may identify as a man and with the cultural and social expectations for men in their society. For others, like myself, the cultural expectations associated with their sex assigned at birth do not align with their gender identity. For example, someone assigned at female at birth may not identify as a woman or with the cultural and social expectations for women in the society. Let's discuss some of these terms that can be used to describe someone's gender, gender identity, and gender expression. Let's start with the term cisgender. It refers or is used to describe someone whose current gender identity aligns with the sex they were assigned at birth. For example, I am cisgender, I'm a cisgender woman, which means they assigned me the female sex when I was born. And growing up, I found out that I identify as a woman as well. So these two moments align for me. And following up, someone who is transgender or trans is an individual whose gender identity does not align with the sex they were assigned at birth. Let's put example of John. He's a transgender man, which means he was assigned a female sex when he was born, but identifies as a man. Now, let's make something very clear. Even though we use transgender and cisgender to differentiate two types of individuals, trans women are women, period, and trans men are men, period. Cisgender women are not more women than trans women because they were assigned female at birth. The same goes for men. If someone identifies as a man or a woman, this is a self-identification independent of what anyone assigned them to be. It is based on what is important to them as an individual, including gender roles, behavior, expression, identity, and or physiology. Period, Vale. And you also may have heard terms such as transsexual or, for example, very much common in Latin communities, the term travesty, to refer to trans people. However, these terms are outdated and they can be hurtful because they were used to differentiate trans people who had undergone gender confirmation surgery. That is incredibly invasive. Like, no one is asking you about your gender laws when you meet them. So please don't use them unless a person refers to themselves like that. Thank you for mentioning that, Gabriel. We should emphasize the fact that we should listen to how the person refers to themselves and respect that. Now let's talk about being non-binary, a term used to describe someone who identifies their gender outside the binary of man and woman, either because they identify as both masculine and feminine, or because they identify as neither masculine or feminine, or because they identify in a way that does not conform with the normative views of sex and gender in their culture and historical period. Related terms are genderqueer, gender nonconforming. In my experience of being nonconforming myself, there are times when I feel to be a man, woman, both or none. To me, it's fluid, amorphous, and there is no single box that I put myself in. Thank you for sharing that, Brody. There are also people who identify as a gender, which means that they don't identify with any particular gender. A term that you will hear most likely, especially if you're a health provider, is the term transition. Transition is the process of shifting towards a gender role different from that typically associated with the one sex assigned at birth, which can include social transitions, such as assuming a new name, pronouns, and clothing, and or medical transition, such as hormone therapy or surgery. The transition process is very specific to each person. We as health providers shouldn't expect all our trans and non-binary patients to want to undergo medical transition necessarily. The fact that someone decides they don't need surgeries or to be in a long-term hormonal replacement therapy doesn't make them less trans or not does mean their transition is incomplete. Transition looks different in everyone. This is so true and gender expression grows from person to person. One way gender is expressed is through the use of pronouns. Thank you for bringing that up. I would like to say also that assuming someone's pronouns, even if correct, can be harmful. And it's something that actually has happened to me. I assumed someone's pronouns and turned out to be incorrect.
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So we would like to suggest to you, our listener, that in the setting of meeting a patient, it's not, or really anyone, it's not really the way to start building trust with them by assuming their gender and their pronouns. You don't want to start by that. And so we suggest you offer your pronouns. That way, the person can know that if they feel comfortable to share with you, they will, they can. Of course, you also need to have in mind that when someone shares their pronouns and they do not fit the binary or the expectations that you have on them because of how they look, well, that's also like out in them. So that takes a lot of bravery. That's a very nice advice, Vale. Thank you for that. Okay, let's take a deep breath. We have now covered the basics on gender, the difference with sex, and tried to describe gender identity. For now, we discussed what is asexual, cisgender, transgender, agender, and gender nonconforming. And one piece of advice is that it is best to practice to ask patients how to refer to themselves and to mirror their language. That's very, very true, Ariel. To mirror the language that people use, it's the best way to not make a mistake. And another advice that I would like to share is that I wouldn't suggest people to ask about sex assigned at birth. At least it is extremely necessary, which I think, I don't know, I couldn't come up with a scenario which was extremely necessary. Because if someone tells you, I am a trans woman, your next question shouldn't be, oh, so you were born a man. Because on a way, that's like implicit in them telling you they are trans women or a trans woman and so saying something like you were born a man can be harmful and you really don't want to put a person in an awkward spot referring to them with a gender they don't identify with right love the love those points Another point that I'm just going to make in passing is that asking somebody about their pronouns, I think the first step is to share your own pronouns. That fosters that confidence and interaction that makes them come up with their pronouns. And I think that's how we can not assume, but just ask by sharing our own pronouns. So now that we have covered gender, let's talk about sexual orientation. This is a critical point, as it's one of the most common mistakes I hear people make. Gender and identity and sexual orientation are not the same. Sexual orientation is how a person describes a gender or genders of people they're attracted to sexually or romantically. Gender refers to someone's identity, how they are identified. Sexual orientation is who they like. Let's explore some terms that are used to describe someone's sexual orientation. Let's start with heterosexual. This is a term used to describe someone who is mostly or exclusively attracted to partners of a different gender than their own. The colloquial term used to refer to heterosexual people is as straight. On the other hand, gay is a term used to describe a person attracted mostly or exclusively to someone of their same gender. For example, I am gay. Some people still use the term homosexual to refer to gay people. But, you know, that's like a mouthful and it sounds very serious. So I don't think it's very used within the community. You may have also found yourself confused when I said that I was gay because it is a term used more often by gay men. And gay women can refer to themselves as gay, but another term used is as lesbians. So basically to refer to women who love other women or identify as part of the lesbian community. Nice. Now let's talk about being bisexual. It's a term used to describe a person who is attracted to partners of their same gender and partners of different genders to their own. You may be like, wait, what? I thought gender is not binary. So how come is it called bisexuality? That's a great point. And that's why in practice bisexual is used more or less synonymously with the term pansexual. Yes. And moving on, we have to queue for queer. And what does queer mean? It is in the title of the series, and that is because it used to refer to people who are neither cisgender nor heterosexual. And it functions as a unifying umbrella term inclusive of everyone in the LGBTQ plus community. We reclaim this term after its historical use as a pejorative slur. Finally, let's talk about being asexual. This is a term used to describe a person who experiences little or no sexual attraction. A related term is aromantic, which refers to someone who experiences little or no romantic attraction. Individuals may identify with both or neither of these terms. Importantly, asexual and aromantic people may still pursue sexual and or aromantic relationships for a variety of reasons, and they should still be screened with a full sexual history like any other patient. Wow, what a ride. We have covered a lot today. We would like to finish with emphasizing this. Gender identity and sexual orientation are not the same. This means that some people can be cisgender and gay, some people can be trans and straight, or some people can be gender non-binary and pansexual. They are two different things. The second point is that most of these terms are adjectives, not nouns, which means that you don't call someone a transgender. You say they are transgender. You don't call someone a gay. You say they are gay. Pretty straightforward, right? That was a very much intended pun. So please congratulate me for making that joke. Yeah, thank much vali that was a very awesome point and it was really great to cover terminology with you today we hope you are more comfortable using these terms and don't worry if you make a mistake we all do but give your best effort to learn respect and practice empathy to To finish this episode, let's share our faves. This space is to highlight someone or something that is inspiring us right now. I would like to recommend my favorite book of all time, which is called Las Malas or Bad Girls by author Camila Cesavillada. It is simply beautiful. I cannot recommend it enough. It is about a group of trans women doing sex work in Argentina. It's very poetic, very raw. I really, really recommend everyone should read it. The mic is all yours, Gabriel. Well, my fave for this episode, continuing with the line of Latin, LGBTQ+, arts, literature, and movies, is one of my, I would say, one of my favorite gay movies, and it's called, in Spanish, Contra Corriente, or in English, Undertow. It's a 2009 Peruvian film and it was the Peruvian entry for the face for a movie in Oscars 2010. And the story it's about a secret romance of a local Peruvian fisherman and a photographer. And what I really like about this movie is that it's very organic, very fresh, and portrays pretty well the vision of the Peruvian community at that time of a gay relationship. I feel like if I keep continuing telling you about the movie, I will make a spoiler at some point, but, oh my God, the ending was quite bittersweet and I couldn't recommend it more. Well, I think it's only fair that I share my favorite now, but it's, okay, so what I'm watching queer right now, so I've been catching up a lot of Queer Eye, obviously every queer person sees that, and I have also been following, I just ordered Jonathan Van Ness's book. So I'm looking forward to reading that. And I recommend that to the people who are listening to this. And obviously you need to go to watch Queer Eye, right? But that's what I recommend at this point. So it was amazing to hang out with all you today. And we'll see you in the next episode of Queer Rounds. Happy Pride!
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Welcome to the New England Journal of Medicine audio summary for the week of February 24, 2011. I'm Dr. Lisa Johnson. This week's issue features articles on environmental microorganisms and childhood asthma, heterogeneity of hemoglobin H disease, BMI and risk of death in Asians, perilipin deficiency and lipodystrophy, and melanoma and resistance to BRAF inhibitor, a review article on point-of-care ultrasonography, a case report of Thank you. and on residents, workers, or students in the law's eyes. This week at NEJM.org, we feature a new video in clinical medicine. This video demonstrates the placement of intraosseous catheters in children and reviews the indications, contraindications, placement techniques, and potential complications. Both manual insertion and insertion with the use of a power-assisted device are shown. Exposure to Environmental Microorganisms and Childhood Asthma by Markus Ege from University Children's Hospital, Munich, Germany Children who grow up in environments that afford them a wide range of microbial exposures, such as traditional farms, are protected from childhood asthma and atopy. These authors assessed the prevalence of asthma and atopy among children living on farms and among other children living in the same areas. The reference group measured the diversity of the microbial exposure in both groups and related the diversity of exposure to asthma and atopy. In both studies, children who lived on farms had lower prevalences of asthma and atopy and were exposed to a greater variety of environmental microorganisms than the children in the reference group. In turn, diversity of microbial exposure was inversely related to the risk of asthma. Odds ratio for the first study, 0.62. Odds ratio for the second, 0.86. In addition, the presence of certain more circumscribed exposures was also inversely related to the risk of asthma. This included exposure to species in the fungal taxon Urodium and to a variety of bacterial species, including Listeria monocyt Wisconsin School of Medicine and Public more than doubled, and although the treatments used to control asthma have improved greatly, there has been little progress in prevention. Identification of the association between exposure to an environment rich in non-pathogenic microbes and reduced risk of asthma offers hope that this and other new conceptual breakthroughs will lead to novel preventive strategies. These findings also raise additional questions about the possible mechanisms through which the nature and range of microbial exposure may alter the developmental biology of the lung and immune system. Resolving these questions is of critical importance if we are to bring the substantial health benefits of being raised on a farm to those who are not. Early diagnosis during newborn screening or infancy has enabled the observation of the natural history of hemoglobin H disease, a subtype of alpha thalassemia. Hemoglobin H disease can result from deletion of three alpha globin genes or deletion of two such genes with a point mutation in the third, as is seen in patients with hemoglobin H constant spring. Nearly all the clinical manifestations occur in patients with hemoglobin H constant spring. Patients with H constant spring have a significant growth delay, require intermittent blood transfusions, have iron overload in the first decade of life, and have a good response to splenectomy. A similar drop in hemoglobin during infection does not occur in patients with hemoglobin H disease, and blood transfusion appears to be unnecessary in the management of this disorder. H-constant spring should be recognized as a distinct thalassemia syndrome with a high risk of life-threatening anemia during febrile illnesses. Many patients with these disorders had mixed ethnic backgrounds, which highlights the need for extended newborn screening in populations that are traditionally considered to be at low risk for hemoglobin H disease. Edward Benz, Jr., from the Dana-Farber Cancer Institute, Boston, writes in an editorial that, among the most common single-gene disorders in humans, thalassemias are a cause of substantial morbidity and mortality in Asia and the Mediterranean Basin. Symptomatic thalassemia has historically been an uncommon illness in the United States. However, as these authors report, a moderately severe symptomatic form of alpha-thalassemia, hemoglobin H disease, is being encountered with increasing frequency as Asian migration increases to the west coast of the United States. Moreover, hemoglobin constant spring disease appears to account disproportionately for the burden of symptomatic disease. These results highlight the dynamically changing effect of globalization on public health, as genetic disorders indigenous to specific populations become more common in the countries to which they migrate and make a strong case for newborn screening for alpha-thalassemia, at least in states with a substantial increase in their Asian populations. body mass index, BMI, and risk of death in more than 1.1 million people from 19 cohorts in Asia after a mean follow-up of 9.2 years. In the cohorts of East Asians, including Chinese, Japanese, and Koreans, the lowest risk of death was seen among persons with a BMI in the range of 22.6 to 27.5. The risk was elevated among persons with BMI levels either higher or lower than that range, by a factor of up to 1.5 among those with a BMI of more than 35.0, and by a factor of 2.8 among those with a BMI of 15.0 or less. A similar U-shaped association was seen between BMI and the risks of death from cancer, from cardiovascular diseases, and from other causes. In the cohorts comprising Indians and Bangladeshis, the risks of death from any cause and from causes other than cancer or cardiovascular disease were increased among persons with a BMI of 20.0 or less, as compared with those with a BMI of 22.6 to 25.0, whereas there was no excess risk of either death from any cause or cause-specific death associated with a high BMI. Underweight was associated with a substantially increased risk of death in all Asian populations. The excess risk of death associated with a high BMI, however, was seeny from the British Columbia Center for Disease Control, Vancouver. Over a three-year period, a total of 41 cases of tuberculosis were diagnosed in a British Columbia community struggling with the challenges of alcoholism, drug use, and transient housing arrangements. Because of the recognized limitations of contact tracing, field epidemiologists used social network analysis early in the outbreak. Whole genome data revealed two genetically distinct lineages of M. tuberculosis with identical genotypes, suggesting two concomitant outbreaks. Integration of social network and phylogenetic analyses revealed several transmission events, including those involving super-spreaders. Both lineages descended from a common ancestor and had been detected in the community before the outbreak, suggesting a social rather than genetic trigger. Further epidemiologic investigation revealed that the onset of the outbreak coincided with a recorded increase in crack cocaine use in the community. These authors show that a socio-environmental factor most likely increased crack cocaine use triggered the simultaneous expansion of two extant lineages of M. tuberculosis that was sustained by key members of a high-risk social network. Genotyping and contact tracing alone The adipocyte lipid droplet is now recognized as a dynamic cell organelle. Perilipin is the most abundant adipocyte-specific protein that coats lipid droplets, and it is required for optimal lipid incorporation and release from the droplet. These authors identified two heterozygous frame-shift mutations in the perilipin gene, PLIN1, in three families with partial lipodystrophy, severe dyslipidemia, and insulin-resistant diabetes. Subcutaneous fat from the patients was characterized by smaller-than-normal adipocytes, macrophage infiltration, and fibrosis. In contrast to wild-type perilipin, mutant forms of the protein failed to increase triglyceride accumulation when expressed heterologously in pre-adipocytes. These findings define a novel dominant form of inherited lipodystrophy and highlight the serious metabolic consequences of a primary defect in the formation of lipid droplets in adipose tissue. Point-of-Care Ultrasonography, a review article by Christopher Moore from Yale University School of Medicine, New Haven, Connecticut. recorded by a sonographer and interpreted later, allowing findings to be directly correlated with the patient's presenting signs and symptoms. Point-of-care ultrasonography is easily repeatable if the patient's condition changes. The concept of a focused, limited, or goal-directed examination is important in point-of-care ultrasonography. Point-of-care ultrasonography may involve the use of a series of focused ultrasonographic exam with examples and discussions of its use. A 77-year-old man with dyspnea, weakness, and diaphoresis. A case record of the Massachusetts General Hospital by Atha Sibris and colleagues. A 77-year-old man was admitted to the hospital in mid-spring because of increasing dyspnea, weakness, and diaphoresis. Three days before admission, weakness, loss of appetite, fatigue, and diarrhea developed, followed by progressive shortness of breath. On the morning of admission, he awoke with dyspnea, which was worse when he was lying flat. He was taken to the emergency room.
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There are many causes of septic shock that are consistent with his presentation, so the physicians needed a way to limit and focus their differential diagnosis. The immune status of the patient is an important consideration. No overt immunosuppression is evident, but his advanced age confers a relatively immunosuppressed state. Immunosenescence, a decline in immune system function with age, is increasingly well characterized and affects both innate and adaptive immunity. Immunosenescence may predispose the elderly to more frequent and more severe infections than the non-elderly. And when we cross a list of infections in the elderly with a list of causes of septic shock, keeping in mind this patient's presentation, the physicians believed they could limit their discussion to five infectious processes, pneumonia, infective endocarditis, infectious diarrhea, bacteremia, and tick-borne illnesses. Resistance to BRAF Inhibition in Melanomas, a Clinical Implications of Basic Research article by David Solett from Memorial Sloan Kettering Cancer Center, New York. Approximately 50% of melanomas contain a mutation in the gene that encodes the RAF family member, BRAF, a protein kinase that phosphorylates the MEK protein and activates the ERK signaling pathway. This mutation, which in most cases is a substitution of glutamic acid for valine at position 600 of the protein, activates and deregulates the kinase activity of BRAF. Selective inhibitors of RAF, such as PLX4032, have remarkable clinical activity in patients with melanomas that contain the V600E mutation in BRAF. However, as has been the pattern for other inhibitors of oncogenic kinases, responses to PLX4032 are often profound but temporary. Two recent studies discussed in this article shed light on some of the mechanisms that may underlie resistance to RAF inhibitors and thus suggest new strategies to treat patients with melanomas carrying the BRAF V600E mutation in whom resistance to PLX4032 develops. Transforming Graduate Medical Education to Improve Healthcare Value A perspective article by Glenn Hackbarth from the Medicare Payment Advisory Commission, Washington, D.C. To ensure that health care will be affordable for future generations and appropriate for our burgeoning geriatric population, its delivery and organization must change. Physicians should be in the vanguard of this change, and transforming medical education will be instrumental in preparing tomorrow's physicians to lead the way. To provide high-value care, physicians will need skills in such domains as quality improvement, cost-aware practice, and care coordination. Medicare invested $9.5 billion in Graduate Medical Education, GME, in 2009. It is the single largest payer for GME, but it establishes minimal accountability for achieving education and training goals. MedPAC has therefore recommended that Congress authorize Medicare to use this financial leverage to catalyze more rapid GME reform by linking some funding to programs' performance on relevant measures. Advancing Medical Education by Teaching Health Policy A perspective article by Mitesh Patel from the Hospital of the University of Pennsylvania, Philadelphia. Standards for health policy curricula in medical education are long overdue. Matters affected by health policy ultimately affect patient care, and physicians need the skills to address them. Training must begin with the building of foundational knowledge and analytic skills during medical school, and perhaps even as early as pre-medical education through courses in public health or public policy. Continue with further instruction, dialogue, and application during residency training, and include reinforcement during clinical practice. These authors propose a focus on four domains, health care systems and principles, health care quality and safety, value and equity, and health politics and law. They represent a foundation of core principles on which we might build as we advance health policy education in the United States. A perspective article by Aaron Kesselheim Foundation for Medical Education and Research et al. v. United States, the Supreme Court added its weighty voice to the question of whether residents are workers or students. Mayo in Minnesota offered both functional and structural reasons why House officers should legally be considered students. In defense of the Treasury regulation declaring residents to be employees, government lawyers pointed to residents' vast patient care responsibilities, which absorb 85 to 90 percent of their time and take precedence over educational conferences. At stake in Mayo v. United States were substantial financial implications for academic medical centers and their house staff. The taxes at issue amount to about $700 million per year for U.S. hospitals and academic medical centers. The Supreme Court ruled in an 8-0 decision that the Treasury regulation making residents categorically ineligible for the student exemption was a perfectly sensible way of distinguishing education from service for the purposes of the tax code. Chief Justice John Roberts wrote that residents could reasonably be construed as the kind of workers that Congress intended to both contribute to and benefit from the Social Security system. The images in clinical medicine features a 40-year-old Korean woman who had been immobilized in bed for several weeks while recovering from tuberculous meningitis and who reported having pain in her right hip. Her right leg was externally rotated and flexed. CT showed a well-defined calcified mass within the gluteus minimus muscle, with bony trabeculation and cortex formation. Myositis ossificans, also known as heterotopic ossification, refers to the deposition of extraskeletal bone within soft tissue. Although the condition sometimes occurs spontaneously, it often is the result of trauma, surgery, burns, or neurologic injury. The calcification typically occurs within two to six weeks after injury. Also featured in the images in clinical medicine is a 55-year-old woman with hypertension who presented with a one-day history of periorbital discomfort, inferior chemosis, and conjunctival injection of the left eye. Examination of the left eye revealed a visual acuity of 2060, a relative afferent pupillary defect, exophthalmos, with 6 mm of protrusion, and an elevated intraocular pressure, 48 mmHg. CT of the orbit showed a dilated left superior ophthalmic vein, suggesting the presence of a carotid cavernous sinus fistula. Angiography confirmed that the internal carotid artery was connected to the cavernous sinus by a large fistula. Dilatation of the superior ophthalmic vein is a key feature of this condition and results from the transmission of arterial pressures to the venous system. This concludes the summary of the February 24th issue of the New England Journal of Medicine. We're interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at NEJM.org. Thank you for listening.
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Welcome to Intention to Treat from the New England Journal of Medicine. I'm Rachel Gottbaum. For decades, scientists have tried to find effective ways to treat Alzheimer's disease, with very little success. But that could be changing. New medications may help slow the progression of the disease, and new diagnostic tools could help predict who might need treatment before their symptoms even start. My name is Heidi Levitt, and my husband, Charlie Hess, was diagnosed with what we think is early onset Alzheimer's when he was 57 years old. It was in 2019. So his work is extremely particular in terms of details. And he probably was having trouble with the details for quite a while. Charlie's saying, I'm feeling foggy. And he's watched me navigate with my own mom when I've sent her to a geriatric psychiatrist to get another assessment on what's going on with her cognitively. And he says, maybe I should see that person too. And he goes in for this exam, which is like having an SAT and you're 10 years old and it's college level. Like, it's terrible. It's three hours long. And if you ask him, it was the worst day of his life. What the psychiatrist said to us was the test showed problems across the board on cognitive function, like, you know, from the point of view of being visual spatial to the point of view of vocabulary to comprehension to following story, Like everything across the board was off. I said, tell me what is going to happen. And she says, I think because he's young, it can be a lot more aggressive. And then in three years, cognitive abilities will hugely decline. She said it was bad and it was going to get worse and offered me little to no solace. Then I said, look, we need to get scans and at least like confirm what's coming out on this exam. So we started with a study that was really more diagnostic study where we had to do a series of MRIs and we were able to get the amyloid PET scan to confirm the amyloid. So his symptoms started already where he was always feeling somewhat left out of a conversation, then became the executive function, having trouble making coffee. Now it's gotten to the point where he doesn't make the coffee at all. He can't turn on the TV. He can't get dressed by himself. I mean, everybody will say, oh, he looks great. He's taking great pictures because all he does every day is go out and take pictures and post it on his Instagram because he's an artist. You can't see this disease, right? Easily. Until what you see in the media is end stages of people who don't recognize someone or are drooling. But you're not seeing the years of loss. So it's not like you wake up the next morning and suddenly you can't do this. I think that's very hard to understand the pace of this disease. I was offered a drug that they felt it's showing great improvement to take away the amyloid plaque, which will then lead to possibly preserving him longer. And I get a call saying, your name was on the list. And we really want you to tell us if you want to try this drug, because there's a waiting list of 20 people. And if you can tell me, yes, I can get you in it. And if you don't tell me by tomorrow, the spot is gone. I said to Charlie, do you want to do this? And he said, no, we don't know that it's really going to work. And we said, no. I was skeptical about this new drug because there was not enough data that corroborated that it was going to change the course of his disease or stop it. It's not like they're offering me a cure. It's not like somebody saying, take this and it goes away. Nobody has said that. They're saying that this is going to help delay the disease progression. And if you look at the numbers, it's not high enough to take that risk. I feel like there's so much pressure because there has been absolutely nothing out there to delay, to treat, to cure. Just offering people something on the off chance that it will work, rather than finding something that works, is selling hope. My name is Carol Balmer. My husband, Jim, has been diagnosed with Alzheimer's disease. I started recording symptoms, things that I found unusual back in 2013, but it was not until 2017 that he was officially diagnosed. At that time, his condition was called mild cognitive dysfunction. Jim was doing peculiar things. He would lose his way to the shopping mall where we'd been hundreds of times and take the wrong turn. He would drive sometimes at 95 miles an hour on the interstate instead of the 75 that was allowed and not notice. He would miss the turn to our house, but then would catch it when he'd gone a block or so too far. These things began to be more and more troubling. And he had an event where he failed to recognize himself in a photograph just a couple days after the photograph had been taken. That troubled him, and he told his physician about it, and the physician did a screening test. Jim was eager from the very beginning to be part of this monoclonal antibody trial because it seemed so promising. We discussed the possibility of the side effects, but he didn't really care about the side effects. Even if he died in the study, he said, you know, you got to die of something. It would be great if he got the benefit of this medication. But the main thing was that he could help others. Jim's enrolled in the Trailblazer 2 trial that's testing one of the monoclonal antibodies, Donanumab, against placebo. So Jim's decline seemed very slow for a long time, and I hope it was from the drug, but maybe that was the pace of change that he was destined to have anyway. So because of the blinding, there's no way of knowing. Jim's functioning has declined quite a bit over the last several months. So Jim's short-term memory right now is non-existent. His memories go back in his early childhood, but not even his later childhood. We know that the next stages of this disease are terrible, but we're relieved and grateful and excited that he's hadling. She's director of the Center for Neuros Research Institute at the University of California, Santa Barbara. And also Dr. Risa Sperling. She's director of the Center for Alzheimer's Research and Treatment at Brigham and Women's Hospital in Boston. So Dr. Sperling, I'd like to start with you. We've just heard from two families who have very different perspectives on the new monoclonal antibodies for Alzheimer's. What can you tell us about the status of these treatments? We now have two monoclonal antibodies that are targeting different forms of amyloid in the brain and two phase three trials have been positive. One of those drugs is already approved, lakenamab, and one I think is likely to be approved over the next few months. We've had medications that have rid patients of amyloid without any result. So what's different here, Dr. Sperling? I think previous antibodies actually have not fully decreased amyloid sufficiently in the brain. There seems to be a relationship with how much amyloid do you lower and how quickly you do it and how many people you get down below some point. So I think number one is we've learned we have to be pretty aggressive with amyloid removal. Number two is that we're in earlier populations than we were before. And we've seen multiple times now that there's probably a point at which when there's a lot of tau in the brain that I think it's less clear that amyloid therapeutics, in isolation anyway, are sufficient to really bend the curve. And then third, I'll say we haven't hit the home run yet. We can see very consistently across these trials that we can bend the curve with very aggressive amyloid if we start early enough. But of course, we all want to find a way that we really stop decline, where we ultimately keep people stable or one day make them better. So Dr. Kosick, how do you see these medications? Do you see them as a breakthrough? My feeling about these anti-amyloid drugs is that they have bent the curve. There's no doubt about that. I suppose if I had to sum up my feeling about this is how we want to calibrate our enthusiasm because we really don't want to create false expectations. We have to make sure that our patients understand what's been accomplished here. And there's still a long ways to go.
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So what does moving the curve actually mean for patients? What it means for the patient, if we interpret the data literally, it means that they deviated from the control curve according to some neuropsychological tests. And what is hotly debated, do those changes in the neuropsychological parameters, are they discernible by family members? You know, if they are able to do things like spell world backwards or, you know, do some of the things that we measure neuropsychologically, is that going to translate into improved quality of life, lifestyle, all of that? And we just don't have those answers yet. And what about the significance in the realm of research? On the research side, there's no doubt that these medications have an effect on amyloid accumulation in the brain. And that's what part of the breakthrough was all about. And what about tau, which clearly has a role in this disease? Where does that fit in in this approach? We know that we all harbor some tangles in the brain, some neurofibrillary tangles. And with the deposition of amyloid, that pool of tangles gets released and begins to spread through the brain. And since tau tangles are a major driver of the disease, and we know from the second trial, the DENAMIMAB study, that the drug didn't have very much effect on the tau PET imaging, that we really have to be able to say that the impact of this has to be moderated because it only affected one portion of the disease. And you've found in your genetic work clues that a lot of amyloid in the brain does not always translate into developing Alzheimer's disease. We do know from at least one patient, the woman who had the Christchurch variant with APOE, the mutation that will cause early onset Alzheimer's disease at age 45 or 50. She had a head full of amyloid, very few tangles, and did not have very much dementia. She did not have the disease. And when she had a tau PET scan, she had very minimal findings of the tau PET. So that's one case. It's a decoupling, but I do think we have to take that into our consideration here. So Dr. Sperling, what does this mean for the research if having amyloid in the brain doesn't always lead to Alzheimer's. So we've known for a long time that amyloid is necessary, but not sufficient to cause Alzheimer's dementia. So what we've learned more recently is that in the setting of amyloid, tau begins to spread throughout the brain and that is occurring as people start to develop symptoms. So the amyloid occasionally is there for more than a decade before you get this where the tau suddenly explodes out of the deep parts of the brain and the medial temporal lobe and goes around the rest of the brain. And that's very commonly associated with a rapid cognitive decline. So I very much agree that you need both amyloid and tau to get to Alzheimer's dementia. The majority of people who have a lot of amyloid in their brain do show decline over time, and that is associated with tau spreading. And we don't fully understand that relationship. I'll even go so far as to say I'm not sure it's amyloid causing it or whether there's an association between these. Perhaps it's a process that's upstream of both amyloid and tau. You know, people have cholesterol building up for years and decades before they get a heart attack or a stroke. And many people with high cholesterol never have a stroke or a heart attack. And I think the same is true with amyloid. I think if you lower amyloid early enough, you are likely to affect tau. And I think that will help slow symptoms. So I think amyloid is a crucial player, but it's not the only player. And we're starting the first combination trial of amyloid and tau where we will look at multiple tau therapies alone and in combination with amyloid because just like cancer, heart disease, diabetes, when people have symptoms, you're going to need more than one approach. So that's what I want to talk about is this path. Some people say we've put our eggs in the anti-amyloid basket and we've taken oxygen out of the other research. Dr. Kosick, what other research do we need to do? We have taken the approach of antibodies to the amyloid. That's been like close to 30 years or so. And I really do believe that for a large portion of that time, it was somewhat unfortunate that other directions were not given as much attention. That has changed where the NIH budget, if you look at the breakdown of that budget, there is a fair amount of funds going to projects that are not solely focused on a single hypothesis. Just as Risa said, we're probably going to need more than one drug. So what are those drugs going to be? And that's, I think, where the research direction is now going. So we think of Alzheimer's as a triad of conditions, the amyloid, the tau, and inflammation. The other two limbs of the triad are now getting much more attention, and I think that's where the next breakthroughs are going to come. Dr. Kosick, you work in genetics. Talk about some of the things that you've learned and how it might help us towards finding treatments. People that I've been interested in are those with early onset Alzheimer's that have mutations leading to the disease. So I've always thought of that as a more pure form of Alzheimer's disease because they're getting it at a relatively young age. I really think that when people begin to get Alzheimer's well into their 80s and their 90s, there are many, many comorbidities, not the least of which is some vascular disease too. None of the therapies we're currently thinking about are addressing the comorbidities, copathologies actually. What we are also beginning to appreciate, these copathologies don't just exist in the oldest old, but there are even in the Alzheimer brain of younger people, even in the patients I study from very early onset that I always thought of as pure Alzheimer's, they will often have synuclein depositions in a protein that deposits in the brain that we usually associate with Parkinson's disease, but it shows up in Alzheimer's too for reasons we don't fully understand. They will also have some degree of vascular problems. So since our therapies are really targeted toward amyloid, there's a lot of the co-pathologies that are not being treated. And I think that is one area where we sort of fall short a little bit. And in my view, one of the things that has held us up a little in the Alzheimer's field is that we haven't paid enough attention to the underlying direct problem. The answer in cancer was a cell biological answer. We learned how cells proliferate. The question in Alzheimer's isn't why cells proliferate, but why they die. We don't know that. And that's a cell biological question. We need to learn how cells die. And that's why I think a part of the delay here has been not enough attention to the underlying fundamental cell biology of the problem. I want to switch gears to diagnosis and new tests coming online. How do we diagnose Alzheimer's? So I think we do now diagnose Alzheimer's disease as at a minimum the presence of amyloid and that it's increasing certainty that it is Alzheimer's disease if we also have a marker of tau. The newest blood tests we have, which are actually markers of tau, tell us mostly about how much amyloid buildup there is in the brain, but they also tell us that the amyloid is bothering the tau. And some of these high accuracy measures of what we call phosphorylated tau, particularly p-tau-217, is a great marker of amyloid and a pretty good marker of tau. And I think tell us that the underlying pathology is Alzheimer's disease. I think the biomarkers have been a genuine advance. That is where we've really made some inroads. And the fluid biomarkers that Reese is talking about, potentially just around the corner, blood tests that measure phospho-tau-217 and the microtubule binding region of tau look really, really interesting. What we have to learn is how to use them, because exactly how much earlier are they going to predict? How are they going to show us progression and dynamic range? There are so many interesting questions that are going to open the door for the use of these biomarkers. And that's where I think one of our biggest advances has been. So how do we diagnose early onset? How do we diagnose if people come in and they have amyloid in their brain, but they don't have any issues? How do we handle this? Well, I think that's when we should diagnose and treat Alzheimer's disease, just like we do most other diseases where we find it in the asymptomatic stage. I think we have to risk stratify.
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Because the more amyloid you have, the much more likely that you have some tau. And again, these blood tests can tell us whether the amyloid's bothering the tau. So I envision that eventually we will be at a point where we will offer this as a blood test to everybody who's entering the age of risk in the same way we measure cholesterol. But we shouldn't do that until we know that treating at that stage of disease can really make a difference. And that's what these clinical trials like the AHEAD study are really focused on. People who don't yet have symptoms do have amyloid buildup and early tau and trying to say, can we prevent cognitive impairment and dementia? So there's concerns about these new blood tests. There's now at-home versions of these tests for Alzheimer's disease. How do we know how accurate they really are? There's no doubt that this has to be regulated. You know, having home tests that are just coming out from somebody who's a cowboy trying to make money from this is not the way to do it. They must be regulated. And if they are, we really have a great opportunity here. Because as Risa pointed out, the turning point here, the danger, is when the amyloid has deposited to the extent that the tau explosion occurs. Once the tau explosion occurs, then I think we have some problems on our hands and that the anti-amyloid drugs are not going to be as effective. And some of the people that may look like in these current trials, they're responding less well, may have already had a tau explosion. So I think if we are able to treat very, very early while the tau is still quiescent, then that's worth studying. And that's what the biomarkers promise us. Where are we now and where do we need to go in your view? I think everybody would agree that there's more to Alzheimer's than amyloid and tau as well, you know, the inflammation side. And the search for individuals who have mutations but escape the disease, those pathways are really another way for us to learn about therapeutics. I think we have some very interesting clues that have come to light with the approval of these drugs. But I would say this is one more step in a very long process. Dr. Sperling? I think we have seen that lowering amyloid dramatically can bend the curve of decline. And there's two pathways from here for me. One is that we go earlier if we're going after amyloid because we want to go before there's tau spreading throughout the brain. I think that's very clear. And two, that if we're at a later stage of disease, we do amyloid and tau and trying to save the neurons, neuroprotection, inflammation, multiple avenues that would help the neurons be more resilient to the pathology. But I do think this is a really important moment where we can make a difference. It's not enough of a difference. And we have to be cautious that we're not there yet. But we also have to step back and say, it took us a quarter of a century to get here. How do we accelerate so it doesn't take us a quarter of century to get the next breakthrough and make a bigger difference in people's lives? Thank you both so very much. Thank you. Thank you very much. Dr. Kenneth Kosick is a professor of neuroscience at the University of California, Santa Barbara, and Dr. Risa Sperling is a professor of neurology are a viable substitute. But are we ready for human trials? We've demonstrated that the pig kidneys worked right away, made tons of urine. The serum creatinine dropped to normal and maintained that for seven days. And I can tell you as a transplanter, when a kidney performs that well out of the gate, you're looking good. That's next time on Intention to Treat from the New England Journal of Medicine. I'm Rachel Gottbaum.
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This is the New England Journal of Medicine audio summary. The full text of all articles is available to personal subscribers on our website. We offer discounts on personal subscriptions to residents and students. Go to NEJM.org and click on subscribe. Welcome to the New England Journal of Medicine audio summary for the week of November 23, 2006. I'm Dr. Michael Bierer. This week's issue features articles on avian influenza Thank you. Review articles on educational strategies to promote clinical diagnostic reasoning and on the asthma epidemic. A case report of a pregnant woman with new hypertension and perspective articles on burying the evidence of adverse drug effects and on aprotonin and the absence of transparency in observational studies of drug safety. Avian Influenza A H5N1 Infection in Eastern Turkey in 2006 by Ahmet Faik Onur from the Üzüncü Yıl University in Van, Turkey An outbreak of H5N1 was detected in poultry in eastern Turkey from December 27, 2005 through January 26, 2006, and the outbreak was followed by infection in humans. The human outbreak was concentrated in a small geographic area. H5N1 infection was diagnosed in 12 patients, eight of whom were followed at a hospital in Vann. These investigators report the clinical, epidemiologic, and radiologic features and history of exposure of the eight patients with H5N1 infection cared for at the center in Van. The patients were 5 to 15 years of age, and all eight had a history of close contact with diseased or dead chickens. The mean time between exposure and the onset of illness was five days. All the patients had fever, and seven had clinical and radiologic evidence of pneumonia at presentation. Four patients died. Results of enzyme-linked immunosorbent assay and rapid influenza tests were negative in all patients, and the diagnosis was made by means of a polymerase chain reaction assay. An important observation in this case series is that the results of initial diagnostic testing for H5N1 were negative in many of the patients. Because of the difficulties in detecting H5N1 infection, repeated testing from nasopharyngeal swabs or deep tracheal aspiration samples in patients who are strongly suspected of having H5N1 infection should be performed. The Indonesian cluster of H5N1 Virus Infection in 2005 by Ayn Yoman Kandun from the Ministry of Health in Jakarta, Indonesia. Since 2003, H5N1 outbreaks in poultry have occurred throughout Indonesia. Indonesia's first human H5N1 case was confirmed in July 2005, and three clusters were noted among H5N1 cases through October 2005. This report describes the epidemiologic, clinical, and virologic findings of the three H5N1 case clusters. Severe disease occurred, including deaths in two clusters. Mild illness in children was documented in two clusters. Severe disease occurred, including deaths, in two clusters. Mild illness in children was documented in two clusters. The median age of the eight patients was 8.5 years. Four patients required mechanical ventilation, and the overall proportion of deaths was 50%. In each cluster, patients with H5N1 virus infection were family members, and most lived in the same home. In two clusters, the source of H5N1 virus infection in the index patient was not determined. Virus isolates were available for two clusters, and molecular sequence analyses determined that the isolates were clade 2 H5N1 viruses of avian origin. These findings and other reports from Hong Kong, Vietnam, Thailand, China, Azerbaijan, and Turkey raise questions as to whether genetic or other factors may predispose some persons to H5N1 virus infection or to severe disease. Further research is needed to understand the role of mild cases in the epidemiology of this disease and whether genetic, behavioral, immunologic, and environmental factors may contribute to case clustering of H5N1 virus infection. H5N1 Influenza, Continuing Evolution and Spread, a perspective article by Robert Webster and Elena Gavorkova from St. Jude Children's Research Hospital in Memphis, Tennessee. Thank you. The bad news is that these clades and the subclades probably differ sufficiently in their antigenic structure to warrant the preparation of different vaccines. The continuing evolution of H5N1 viruses and the clusters of human infections in Indonesia and Turkey raise important questions. First, can the source of H5N1 be eliminated? And second, is the increasing number of clusters of human infection an indicator of evolution toward consistent human-to-human transmission? Clearly, we must prepare for the possibility of an influenza pandemic. If H5N1 influenza achieves pandemic status in humans, and we have no way to know whether it will, the results could be catastrophic. Fetal Pulse Oximetry by Stephen Bloom from the University of Texas Southwestern Medical Center in Dallas. Knowledge of fetal oxygen saturation as an adjunct to electronic fetal monitoring may be associated with a significant change in the rate of cesarean deliveries or the infant's condition at birth. In May 2000, the FDA granted conditional approval of the OxyFirst fetal oxygen saturation monitoring system for use as an adjunct to electronic fetal monitoring. This new technology was designed to improve knowledge of the fetal condition by continuously measuring fetal oxygen saturation in the presence of a non-reassuring fetal heart rate pattern. Thank you. at birth between women whose clinicians were made aware of the oximetry results and women whose clinicians were not. These findings do not support the use of fetal pulse oximetry in women in labor. In an editorial, Michael Green from the Massachusetts General Hospital in Boston writes that more than 30 years ago, the new technology of electronic fetal heart rate monitoring was introduced with the noble aspiration to eliminate cerebral palsy. After 25 years of use, electronic fetal heart rate monitoring was associated with an unchanged rate of cerebral palsy in term infants, but a soaring rate of cesarean deliveries. We now find ourselves in the far less noble position of seeking new technology to mitigate the unintended and undesirable consequences of our last ineffective, but nonetheless persistent, technologic innovation. Vivala Rudin for Patients with Acute Coronary Syndromes, by Greg Stone, from the Columbia University Medical Center in New York. Current guidelines for patients with moderate or high-risk acute coronary syndromes recommend an early invasive approach with Thank you. This study, in over 13,000 patients, evaluated the role of thrombin-specific anticoagulation with bivalirudin. Patients with acute coronary syndromes undergoing an early invasive approach were randomly assigned to treatment with heparin plus a glycoprotein 2b3a inhibitor, bivalirudin plus a glycoprotein 2b3a inhibitor, or bivalirudin alone. Rates of ischemic events at 30 days were similar for all three groups, whereas major bleeding was significantly reduced in the group receiving bivalirudin alone. The trial suggests that bivalirudin monotherapy may be similar in efficacy to standard therapy, although bivalirudin monotherapy is associated with a reduced risk of bleeding. Pretreatment with a thionopyridine seems to be necessary if bivalorudin monotherapy is used. Educational Strategies to Promote Clinical Diagnostic Reasoning, a medical education article by Judith Bowen from the Oregon Health and Science University in Portland. Clinical teachers must diagnose both the patient's clinical problem and the learner's ability and skill. The first step in diagnostic reasoning, which is based on knowledge, experience, and other important contextual factors, is always data acquisition. Another early step is the creation of the mental abstraction or problem representation. Other key elements of clinical diagnostic reasoning include the generation of a hypothesis, the search for and selection of an illness script, and making a diagnosis. As learners listen to patients' stories, learn to transform these stories into case presentations, develop their own illness scripts, and learn to reason about clinical information, teachers can use case-specific instructional strategies to help learners strengthen their skills. This article considers how doctors learn to reason in the clinical environment and recommends practical approaches that clinical teachers can use to promote the development of strong diagnostic reasoning skills in their students. For more information, visit NEJM.org slash features. that the prevalence of asthma is still rising in developed countries. Primary prevention strategies to combat the asthma epidemic are therefore urgently sought, but they must be based on a sound understanding of the various determinants of the onset of asthma. However, the disparity and heterogeneity of findings in the asthma literature are daunting, reflecting the complex nature of the illness. This review surveys the data on the increase in the prevalence of asthma in recent decades and finds evidence of a plateau in many Western countries. The authors examine the evidence of possible causal relations to factors such as air pollution, obesity, diet, and exposure to infections, antibiotics, and allergens, including exposure at very young ages. The most strongly supported preventive measure is the avoidance of passive and active exposure to smoke.
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A 35-year-old pregnant woman was admitted to the hospital at 19 weeks and 6 days of gestation because of the recent onset of hypertension and diabetes. She had recently had polyuria and polydipsia and increased facial puffiness. During her first pregnancy, she had had gestational diabetes. On physical examination, the patient's blood pressure was 180 over 100 millimeters mercury. She was treated with labetalol, nifedipine, and insulin, and both the blood glucose levels and the blood pressure fell. The patient was discharged on the third hospital day. One week later, the patient was seen in the neuroendocrine clinic. A repeated 24-hour urinary cortisol measurement showed that the level was 1,865 micrograms. Serum electrolytes were normal, except for a potassium level of 2.6 millimoles per liter. In a patient with newly diagnosed chronic hypertension, the major question is whether it is essential hypertension or associated with another condition. A search for a secondary cause in a case such as this is mandatory. In this patient, the presence of hypokalemia increased the suspicion that the problem was secondary hypertension. Additional laboratory testing and a diagnostic procedure were performed. Stress, Aging, and Neurodegenerative Disease, a Clinical Implications of Basic Research article by Richard Morimoto from Northwestern University in Evanston, Illinois. Aging and stress, when paired, can profoundly affect the quality of life. When events go awry, molecular processes take place that, over time, can lead to neurodegenerative disease. At the root of the problem is a fundamental process, protein folding. When proteins misfold, they can acquire alternative proteotoxic states that seed a cascade of deleterious molecular events, resulting in cellular dysfunction. When these events occur in neurons, the consequences can be devastating. A recent study shows that cellular degeneration in diseases of protein conformation is unlikely to be caused by a single defect. Instead, it is likely to be the net consequence of cumulative insults to the quality control of protein folding, resulting in deleterious effects on multiple cellular processes. Dangerous Deception, Burying the Evidence of Adverse Drug Effects, a prospective article by Jerry Avorn from Brigham and Women's Hospital in Boston. On September 30, 2006, a front-page article in the New York Times reported that the FDA had issued a warning that the antifibrinolytic drug aprotonin, widely used to reduce perioperative bleeding in patients undergoing cardiac surgery, could cause renal failure, congestive heart failure, stroke, and death. What put aprotonin on the front page was the revelation that its manufacturer, Bayer, had hired a private contract research organization to perform its own large observational study of postoperative complications in patients given the drug. The analysis showed that patients who received aprotonin had higher mortality rates and substantially more renal damage than those given other treatments. But neither Bayer nor its contractor had provided the report to the FDA or even acknowledged its existence before the meeting. Many aspects of the aprotonin saga are familiar to observers of the drug evaluation process. A product is approved because it is more effective than placebo, worries emerge about its safety, few or no adequately powered controlled trials are conducted to address these issues, and payers spend huge sums on the drug, despite the dearth of evidence that it is better than older, cheaper agents. Observational Studies of Drug Safety, Aprotinin and the Absence of Transparency, a perspective article by William Hyatt from the University of Colorado School of Medicine in Denver. Thank you. to approval, nor the numerous randomized controlled trials conducted after approval, identified an association between deprotonin and any short-term increase in the risk of death or non-fatal cardiovascular events or any serious renal toxic effects, except for a transient increase in the serum creatinine concentration. However, in early 2006, two observational studies were published that raised serious concerns about the drug's safety. The recent discussions of Thank you. of using a transparent and open process when reviewing such data. This week's images in clinical medicine features a 38-year-old man with chronic total occlusion of the proximal part of the left anterior descending coronary artery, or LAD, clinically insignificant atherosclerotic plaque in the right coronary artery, and collateral circulation to the distal portion of the LAD. Treatment with a beta blocker was begun. CT showed tight bifocal stenosis in the first segment of the right coronary artery. Coronary artery spasm was suspected, and a multi-slice CT was repeated with the use of intravenous isosorbide dinitrate as a vasodilator and showed no stenosis in the right coronary artery. Squamous cell carcinoma with pericardial metastases is also featured in the images in clinical medicine. This concludes the summary of the November 23rd issue of the New England Journal of Medicine. We are interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at NEJM.org. To see the complete text, as well as any accompanying charts, figures, animations, or videos from any of these articles, please visit our website at NEJM.org. Join us again next week.
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Welcome to the latest episode of the In Conversation with E-Clinical Medicine podcast. My name is Ari, I am Deputy Editor at E-Clinical Medicine. Each month we will be interviewing the author of a paper published in our journal, giving them an opportunity to provide a deeper discussion of the research. I'm here today with Dr. James Kite to talk about his recent review on the influence and effects of media-based stigmatization. Dr. Kite is a lecturer in disease prevention and health promotion in the Sydney School of Public Health at the University of Sydney in Australia, and his research focuses on the use of mass media and social media for public health communication. James, thank you for joining us and welcome to the podcast. It's good to be here. So can you please introduce the listeners to your study and describe the main aims and your key findings? Yeah, so what we've done is a systematic review of the scientific literature around weight stigma in the media. And we're particularly interested in how common weight stigma is, what its effects are, and what we can do about it. And what we found, we've included 113 papers in the end, and what we found was essentially that most of the focus of all the papers is on the presence of stigma in media content and what the impact of that stigma is. And that's especially about how exposure to stigmatising content shapes the attitudes and beliefs of people of all sizes. We found that across all types of media, so news media, entertainment media, social media, and even public health campaigns. We also found that it's particularly harmful. So one of the really important findings was that media content just seemed to be perpetuating the idea that obesity is an individual problem and that fatness is inherently a bad thing. And what the media content is really doing, it's overlooking and it's downplaying the influence of other causes, so biological and environmental causes, things like the high availability and low cost of unhealthy foods. And we also found that very few studies are actually looking into ways to address stigma in the media. So we're really trying to push for a bit of a shift away from just sort of cataloging what's in the media, what stigmatizing content is there and whether it's bad. We kind of know that, yes, it's there and yes, it's bad. We now really need to be sort of switching focus and thinking about what do we actually do to address it. Thank you. And can you explain how you became interested in this topic and its relevance. Yeah, so the research group I'm a part of at the University of Sydney is the Prevention Research Collaboration and we really specialise in research and evaluation of efforts to address overweight and obesity. And there's another group, the Obesity Collective, which is an advocacy group in Australia, and they approached one of our members and asked us to conduct this review to inform their work around reducing stigma. And then once we've actually conducted this review, they've already been using the findings to help them in developing a pilot campaign that aims to highlight the harms of weight stigma, which is, as I said, is something a bit new because there's not a lot of efforts out there, or at least not a lot of published efforts on what we can do about weight stigma in the media. Thank you. And I think several studies suggested that having obesity increases the risk of severe illnesses from COVID. And I was wondering, have you found any evidence that stigma towards people with obesity has been exacerbated somehow during the COVID pandemic in your study? So there wasn't a lot of papers that looked at whether weight stigma had increased or changed at all during the pandemic. There was one study, a US-based study, that did find there was an increase in exposure to stigmatising content on social media and that this had led to an increase in body dissatisfaction among adolescents. But we can't take much from that. It is just one study. We also did find another review paper that noted that it was really quite too early to be really getting a full understanding of the effects of the pandemic on weight stigma. Okay, thank you. So maybe an area to further explore for future studies? Yeah, definitely. It would certainly be an interesting area to get into a bit more. Thank you. And my last question would be, what sort of interventions in terms of health messaging via mass media or other public health messaging could be useful in your view to decrease weight stigma and improve outcomes for people living with obesity? And in this context, do you think that perhaps more awareness would make a difference or what else would you suggest? and content does to people with overweight and obesity. And that was one of the things with the Obesity Collective campaign is around sort of challenging that idea. As I mentioned, there was really very few studies that were explicitly about trying to address weight stigma through media. The few ones that were there, education was their focus. So one study created a film for trainee health professionals, and another one created a video aimed at children. And both of those found some positive findings that they could make a difference to reducing weight stigma. But it is only those two studies in those two particular contexts. There was a bit of experimental evidence around public health messages, and what they found was that the messages that challenge weight stigma and promote body positivity, they do have a potential benefit in addressing stigma and improving well-being of people of all sizes, which is a really positive thing because when we're running these public health campaigns, we're trying to do good. So it's a bit disconcerting that we were finding that stigmatising messages were present in a lot of public health campaigns. So we should really be leading this as public health people. We should really be pushing against weight stigma. So this is an important finding around that we can actually create messages that challenge weight stigma and really help in that way. Thank you so much. Maybe have the last question that is a bit related to what we touch on now, but what do you think future studies should address in the field? Yeah, so that there definitely needs to be more evaluation of efforts to challenge weight stigma and what that should look like in reducing that weight stigma through media. So anything that's going to help us understand what should our public health campaigns look like? What sorts of policy changes do we need to make? So there's some discussion in the literature about should we change guidelines to help out news media in how they report around weight and issues related to weight. Thank you. Thank you very much, James, for being with us today and congratulations on your publication. Thank you. Indeed, there is increased research demonstrating the complexity of obesity and also the negative impact of stigma in healthcare. Dr. Skye's manuscript will be featured in a collection focused on obesity and healthcare for which we are currently accepting submissions. The collection welcomes research articles exploring innovation in obesity healthcare delivery, treatments, and the necessity to address stigma and develop weight-inclusive environments. Thank you and have a lovely day.
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Welcome, my name is Devine. This is episode 494 of the Devine Intervention Podcast. In today's podcast, we're going to be examining thalassemia. It's a high-yield topic, frequently tested on all the USMLEs, so I just want to make sure that you kind of have it down. So, typically, let's start off with a question. So, what if they give you a question about a 10-year-old child? They tell you that this child looks pale. His parents are bringing him to the office because he looks pale. And that he has been having chronic right and left upper quadrant pain. And they tell you that he has abnormal contours to his face. And they give you a bunch of labs. You notice that the hemoglobin is pretty low. I'd say it's like 6. And you notice that, well, it's not just low, but the MCV is less than 80. So it's a microcylic anemia. And then you're told that the serum ferritin is pretty elevated. When you see something like this, and you're told that it has required many blood transfusions in the past, when you see something like this, what should you be thinking of? I hope you're thinking about some kind of thalassemia. So in this short podcast, let's go ahead and break down thalassemias. Again, they're pretty important disorders to know and understand. But basically, we know that thalassemia, they affect a ton of people, actually. About 280 million people worldwide have thalassemia. And to understand thalassemia, you've got to go back to hemoglobin. Hemoglobin is the thing that helps us carry oxygen in our bodies. And as we know, there are two major types, right? I mean, there are two major globing chains in hemoglobin. Okay, let's maybe even go a little further down. So hemoglobin is made of heme and globin, right? And we know that heme is made in a certain pathway that I would imagine you've learned in biochemistry that has an ALA synthase as the read-limiting enzyme. And then globin is just made, you know. And those globins, we have a bunch of them, but the big ones are alpha globin and beta globin, right? So as you've learned, I've discussed this in previous podcasts before, but whenever you have anything that messes up your synthesis of hemoglobin, you're going to have thalassemia. So if you have anything that messes up heme synthesis, like lead poisoning, that's going to cause you to have microcytic anemia. Or you have something that messes up globin synthesis, like thalassemia, that's going to cause microcytic anemia. Or again, remember, heme is iron plus protoporphyrin. So if you mess up, if you don't have enough iron, you're also going to cause microcytic anemia or again remember heme is iron plus protoporphyrin so if you mess up if you don't have enough iron you're also going to have microcytic anemia for those reasons so there are many causes of microcytic anemia the big ones on exams iron deficiency lead poisoning so iron deficiency lead poisoning thalassemias right you're going to see mVs under 80 for those cases. So since we know that normal hemoglobin contains alpha globin and beta globin, that can then begin to tell us what the two kinds of thalassemias are. And really, the two kinds of thalassemias are pretty straightforward. There's the alpha thalassemia, there's the beta thalassemia. I think for purposes of ease, we're going to start off with the beta thalassemia first. But the critical thing to know is that all the thalassemias are inherited in an autosomal recessive fashion. With the beta thalassemia, we have two genes that code for beta globin. Literally two genes. We pretty much have like one on each chromosome. In this case, there's going to be chromosome 11 actually. So that's a high-yield thing to just come into memory especially for the step one folks i don't know the whole chromosome 11 business so chromosome 11 uh the one you the copy you have from your dad you have one beta globin gene on that the one from your mom you have one beta globin gene on that so if you have those things normal then it's not a big deal but if you lose one if you have a mutation in one then you're gonna have beta thalassemia minor and then you may be like wow divine that must be so bad no it's not really that bad it's really not because at least you have one beta globin gene that's still helping you produce so you you're going to be getting enough beta-globins. But if you lose two, so usually people would have lost one. They don't have many significant problems. They have like a mild anemia. And on a blood spurt, you're going to see like target cells and whatnot. But whatever. But if you lose both, then you can potentially see how that can be a problem. You literally have no beta-globins whatsoever. Now, if you don't have beta-globins whatsoever, that's problematic. You may be like, Devine, why is that problematic? Well, let me explain. First, normal hemoglobin is alpha-2, beta-2. If you don't have any beta-globins, you literally cannot form normal hemoglobin, which we call hemoglobin A. So one kind of hemoglobin that will really rise up in these people is hemoglobin A2. Hemoglobin A2 in normal individuals is about 2.5 to 3% roughly of their hemoglobin. That's alpha 2 and delta 2. Notice it does not have beta globin chains in it. So since it doesn't require beta globin chains in it and your body is kind of struggling with having beta globin chains your hemoglobin e2 is gonna go up and what other hemoglobin will go up in beta thalassemia i would hope you're also seeing divine hemoglobin f hemoglobin f is alpha 2 gamma 2 alpha 2 gamma 2 right that does not have beta globin chains in it. So the person is going to be pretty, pretty good. So how can you differentiate between beta thalassemia minor, which is where you lose one gene, and beta thal major, which is where you lose both genes? Simple. Again, you don't have to memorize any of these things. Just try to understand. I'm going to try to go slowly so you can understand it. But in beta thal minor, you're still going to have some hemoglobin A, because at least you're making some beta-globin you're gonna have some hemoglobin a although it will be reduced compared to the normal adult you're gonna have an increase in your hemoglobin f that's alpha 2 gamma 2 right because that doesn't have beta-globin chains in it you're gonna have an increase in your hemoglobin a2 that's alpha 2 delta 2 right and again those people are going to have like minor anemia they may be completely symptomatic now if a person has beta thal major where they literally have no beta globines at all they will have no hemoglobin a at all because they have literally no beta globing they have you have no hemoglobin a at all right that's very important to understand that's a very critical difference from beta thal minor they'll have no hemoglobin a because hemoglobin a is alpha 2 beta 2. if you ain't got beta chains you're not going to have any hemoglobin a they're going to have an increase in their hemoglobin a2 right so alpha 2 delta 2 they're going to have an increase their hemoglobin f alpha 2 gamma 2 it's very important to keep in mind and those people tend to have pretty significant anemia pretty significant anemia now how do we okay i guess i'll talk about treatment of thalassemia in general in a bit but i want to deal with the molecular basis of both and then we'll kind of go from there. So again, remember hemoglobin, I mean, beta thalassemia, it's a chromosome 11 issue. Now let's go into alpha thalassemia. Alpha thalassemia is also a hormone recessive, but this is more of a chromosome 16 problem. So here you have four genes. Four genes. Four genes. Four genes. You have two on each chromosome from your parents.
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Now, since you have four genes, you can already begin to see that, oh, there's more disease permutations. Now, what are the disease permutations to know? Well, number one is, let's say you lose one alpha, let's say you lose one alpha globin chain. If you lose one alpha globin chain, it's not a big deal. You're going to pretty much be asymptomatic. If you lose two, honestly, for the most part, you're also going to be asymptomatic as well. Yeah, you may have a mild anemia, but it's not a big deal. You literally still have 50% of your genes kind of working for you. I almost like to think of that as like the, you're like, oh, I've lost 50, because remember, beta thalminer, you've lost 50% of your beta globins, right? So you've lost 50% of your alphas, it's not a big deal. The only thing I'll say to know about these alpha business, I mean, this losing two genes business, is especially on the USMLE step one exam, they love to see if you can epidemiologically tell the cis from the trans problem. So remember I said that you have two on your dad's chromosome 16 and two on your mom's chromosome 16. If you knock out both on one chromosome, let's say you lose all two from dad or you lose all two from mom, that's a cis deletion. It's actually pretty high yield to know that's pretty common in in asians it's pretty common in asians pretty common in asians and then the trans deletion is where you lose one from dad's chromosome and one from mom's chromosome that's tend to be found more in africans the thing is if you compare both again i wouldn't worry too much about the prognosis of both but in in general, if you have the cis deletion, it tends to be a bigger issue than the trans deletion. But again, not a big deal. So again, don't sweat it with regards to the difference in prognosis. Cis trans is largely the same. If you have a 2G deletion, it's not a big deal. Now, the most critical thing to know about the cis versus the trans is that for cis, we tend to find it more in Asians. Trans, we tend to find it more in Africans. That's it. Just leave it at that, okay? Just leave it at that. Okay, so now, what if you have a three-gene deletion? Okay, so that's where things start getting interesting because when you have a three-g gene deletion, you've pretty much lost 75% of your genes, right? So that's problematic. Now for these people, you know, they're still going to be making, you know, hemoglobin A, alpha 2, beta 2, but it will be vastly decreased. They'll still be making hemoglobin A2, alpha 2, delta 2, but again, it's going to be vastly decreased because they have a shortage of hemoglobins. They're still going to be making hemoglobin F, alpha 2, gamma 2, but again, that's going to be vastly decreased. But one thing to kind of keep in mind when you have this problem is when you have these three alpha-regined lesions, since you have very few alphas and you have way more betas, the thing that's going to happen is that the betas are going to start pairing up with each other. So you'll have something like beta-4. Beta-4 is what's known as hemoglobin H. Hemoglobin H. Hemoglobin H is literally beta-4. That's why sometimes when you've lost all three alpha-globin chains, we call it hemoglobin H disease, hemoglobin H disease, these people tend to require a lot of transfusions. They tend to be more symptomatic. And one thing I'm going to say is that people that have this alpha-thalassemia, especially people that have hemoglobin H disease, you may actually see, so you'll see target cells like you see for thalassemias. It's going to be a microcylic anemia. But you may actually see Heinz bodies as well, right? You may actually see Heinz bodies. So this hemoglobin H that precipitates within the red cell can form a Heinz body. So just be careful. Heinz bodies are not only found in G6PD deficiency. You certainly can find them in thalassemia, especially like the alpha-thalassemia, just FYI, especially the more severe forms of alpha-thalassemia. And then obviously the one that's the worst of the worst of the worst is going to be where you've lost all four genes. When you've lost all four genes, that's really bad. So when you've lost all four genes, you literally have no alpha chains. Literally none. So are you going to be able to make hemoglobin A? No. That's alpha-2 beta-2. You don't have it. Are you going to be able to make hemoglobin A2? No. That's alpha 2 delta 2. You literally have no alpha globin chains. Are you going to be able to make hemoglobin F? No. Alpha 2 gamma 2, right? You literally don't have any alpha chains, right? So what are the options you have? Well, people that have the 4-gene deletion 1, they can have a hemoglobin H, right? Because again, remember, hemoglobin H is beta 4. They have no alpha, but they have betas, so they can make beta 4. That's hemoglobin H, right? So again, these people can also have Heinz bodies. But think about things from a more in utero perspective. From more in utero perspective, right? In utero, you need alpha 2 gamma 2 hemoglobin F. They have no alpha, so they're going to be able to make hemoglobin F at all. So those gammas, since there's a ton of it while you're in utero, the gammas are going to start pairing up with each other. They're going to form gamma 4. Gamma 4, that's hemoglobin BART. That's hemoglobin BART. Hemoglobin BART is not very compatible with life. So many of these kids are either going to die in utero or right after they are born, they're going to be dead. That's the critical thing to know about hemoglobin BART. So if you see a child that has thalassemia and they die in utero or they die just right after birth, they have the four gene deletion from an alpha-globin perspective. So again, oh divine, how can I differentiate between the three gene deletion and the four gene deletion for alpha-thalassemia? Simple. In alpha-thalassemia, the one where you've lost all 3 genes, you're going to have a decrease in hemoglobin A, decrease in hemoglobin A2, decrease in hemoglobin F, and an increase in hemoglobin H. But for those that have the 4-gene deletion, they're going to have no hemoglobin A, no hemoglobin A2, no hemoglobin F. They'll have hemoglobin h and they will have a hemoglobin bars right that's the gamma gamma form okay so i guess the big thing is if a person has a thalassemia how may you make the diagnosis if you suspect thalassemia the very first thing you're going to do is you're going to do a complete blood count uh that's many times going to be the right answer on the usml you're going to get a complete blood count and after you get that complete blood count um you know you times going to be the right answer on the USMLEs. You're going to get a complete blood count. And many times it's good to get a peripheral blood smear as well. While you're doing that complete blood count, you'll see the target cells. Again, if you see those Heinz bodies, that should tell you that, oh, wait, I'm probably dealing with alpha thalassemia, where these folks have lost three or four of those genes. But then after that, you're going to do some more specific testing. You're going to do hemoglobin electrophoresis. Hemoglobin electrophoresis is something we tend to do more for beta thalassemia than for alpha thalassemia. Hemoglobin electrophoresis is just something that's done more for beta than alpha. So I would not think of it as a way you want to diagnose alpha thalassemia on your exams.
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So some of you may wonder, Divine, what are some of the symptoms a person may see when they have these thalassemias? They can actually see a bunch of symptoms, right? So one, you may notice that they have these chipmunk faces. You may wonder, Divine, what's the mechanism there? They may have chipmunk faces. They may have hepatomegaly. They may have splenomegaly. They may have all those bone pain, brittle bones. Well, what causes that? Well, the thing that causes that that you want to know for your exams is extramedullary hematopoiesis. Extramedullary hematopoiesis. Right? Because these red blood cells are pretty defective that are made, so your body just destroys them quick. So you're always making as much hemoglobin as possible. As much hemoglobin as possible, as much hemoglobin as possible, as much red cells as possible. So you're not going to just leave it to the bone marrow. You're going to make it in any other place you can make red cells so you can keep up with the demand. So you're going to make it in the spleen, you're going to make it in the liver, you're going to make it in your bones, right? That's why they'll have like that, those chipmunk faces, they'll have the hepatomegaly, they'll have the splenomegaly. And also, another thing that stimulates these people's red cell production, believe it or not, is that when you have these anemias, the oxygen carrying capacity of your blood literally plummets. Because remember, hemoglobin is like the bus that carries oxygen around in your body. If your oxygen carrying capacity plummets, then your tissues are going to be hypoxic. That's going to cause your kidneys to make a ton of EPO. So EPO is going to keep grinding, stimulating a ton of red blood cell production, right? So those are the two, part of the two reasons why they may have, you know, all this extra-metalluric hematopoiesis. It's actually pretty high yield to know. And again, hepatomegaly, splenomegaly because of extra-metalluric hematopoiesis. Although one of the big reasons they get this splenomegaly business is that over time, because the spleen is just destroying, because the spleen, I like to think of it as like the quality control red blood cell region in the body. So it looks at red blood cells. Do they look quality? Do they not look quality? If they don't look quality, it's going to destroy them. And that's certainly going to cause problems. So just something you want to keep at the back of your mind, for example. So that's why they may have hepatomegaly. That's why they may have spleenomegaly. And the thing is, since they are making so many red cells all the time, their bone marrow just expands. So it's almost like your bone marrow has bone and marrow. But if the marrow part, because you're making so many red cells all the time, right, their bone marrow just expands. So it's almost like your bone marrow has like bone and marrow. But if the marrow part, because you're making so many red cells, just sticks over the whole apparatus, then the bone is going to be less and less and less. So this will have brittle bones. They have a pretty high risk of osteoporosis. That's an association you certainly want to know for your exams. And then another association you want to know is you want to, if they tell you that, well, you see like crud upper cauldron pain and fever in one of these folks, it's because they have cholecystitis. Why? What's the mechanism there? Well, again, think about it. You're always breaking down red cells, always breaking down red cells. That's going to make a ton of indirect bilirubin. As you make a ton of indirect bilirubin, you're going to start making a lot of all these bilirubin gallstones. So these people have a very high risk of these bilirubin-related issues like cholecystitis, cholelithiasis, biliary colic, and things like that. And you may say, Devine, you know, you said that the one that tends to kill people in utero or they die right after birth is when you have the 4-alpha gene deletion, 4-alpha thalassemia. Yes, that's absolutely the big one because they can have hydrops fatalis. And many people always struggle like, Devine, what in the world do you mean by hydrops fatalis? Well, let me explain. Let me explain. So say, for example, you have the alpha, the 4-alpha gene deletion, right? So you don't have any hemoglobin A, no hemoglobin A2, no hemoglobin F. Hemoglobin F is like the big, big, big hemoglobin we need in utero. But you don't have hemoglobin F at all. So you're going to start doing these gamma-4s, hemoglobin BARTs. Now, why do you think that hemoglobin BARTs is bad? Well, think about it. You already know this from your studies that hemoglobin F has a higher affinity for oxygen compared to regular hemoglobin compared to regular adult hemoglobin A it has a higher affinity for oxygen right if you have a high affinity for oxygen are you going to be delivering oxygen to the tissues no you're not going to be doing any of that now think about this then imagine you have hemoglobin BART hemoglobin BART does not just have two gamma because remember phthalo hemoglobin is two alpha two two gammas no now you don't have two alphas two gammas you have four gammas that has an even higher oxygen affinity than hemoglobin f right literally hemoglobin barts has super super high affinity for oxygen compared to hemoglobin f and also hemoglobin barts that beta 4 also has a super super high affinity for oxygen compared to hemoglobin F. So you have a bunch of the predominant hemoglobins in this fetus, or hemoglobins that have a high affinity for oxygen. So since they have such a high affinity for oxygen, they're not going to be releasing oxygen to the fetal tissues. So there's going to be a lot of fetal hypoxia. There's going to be a lot of fetal hypoxia. And that fetal hypoxia, what do you think it's going to do? Well, it's going to do one big thing. It's going to put your heart under pressure because the tissues in the fetus are telling the fetal heart, we want oxygen, we want oxygen, we want oxygen. The fetal heart is like, okay, fine. I'm going to make the blood go around the body more often. If the blood goes around the body more often, that will probably help. So the blood starts going around the body more often because again, your oxygen carrying capacity in your blood is low. So your heart is always pumping, pumping, pumping hard, pumping, pumping, pumping hard. If your heart is always working that hard, one day it's going to fail. That's literally what's called high output heart failure. Because remember, your heart is a muscle, right? So you have heart failure because your heart is working at chronically elevated cardiac output. That's literally what upward heart failure is over time the heart will fail when the heart fails you're going to have a build up right or fluid in the lungs the right heart will then fail and then you're going to have a build up of fluid in the body right you're literally having a an increase in hydrostatic pressure within the body that's going to cause hydrops vitalis high drops right means you're hydropic that's fluid hydrops vitalis in the fetus now another mechanism to cause hydrops fetalis. Hydrops, right? Means you're hydropic. That's fluid. Hydrops fetalis in the fetus. Now, another mechanism behind the hydrops fetalis that, again, many people do not kind of give credit for is this, right? So, again, remember I said that one of the things that happens in thalassemias is you have like extramedullary hematopoiesis. Yeah, absolutely. You have extramedullary hematopoiesis just to keep up with the constant making of red cells. And, again, I've discussed the reasons why you may need to keep making these red blood cells. So since the liver becomes a site of extramedullary hematopoiesis, the liver is like struggling.
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So think about it this way. If your attention is divided, then things you're supposed to give very good responsibility to, time and attention to, you don't. So one of the things the liver does not give as much time and attention to when it's so preoccupied with making red cells in extramedullary hematopoiesis is albumin. Your liver stops making adequate amounts of albumin. Do you see my story there? If you're not making adequate amounts of albumin, surprise, surprise, guess what's going to happen to you? You're going to have a decrease in oncotic pressure in your vascular tree. And if you have that decrease in oncotic pressure, you're not going to be keeping fluid within your vascular tree. You're going to have more fluid extravasation because of that decrease in oncotic pressure. That's going to cause you to become edematous. So again, the two mechanisms behind hydrospitalis, one is a decrease in oncotic pressure and an increase in hydrostatic pressure. I've kind of targeted those two mechanisms. Honestly, like the more I talk in this podcast, the more I'm like, wait, this podcast is actually pretty nice because there's a lot of mechanistic things that you can learn. Honestly, I love hematology for this reason. Most things can be reasoned out through mechanisms. But anyhow, let's keep going. So hopefully you understand the two major types of thalassemias. You know, the one thing I'll comment on is, before I talk about treatment, the one thing I'll comment on is this beta-thal in intermedia. You know, some resources kind of stress it. I wouldn't worry too much about it if I were you, honestly. But the big thing about that is that those people have compound heterozygote so they don't have the situation where wow both beta globin genes are completely trashed no it's like both beta globin genes have like partial functions so these people are kind of like intermediate they're kind of in the middle they are compound header heterozygotes again i don't sweat too much about about that if i were you right so again remember you have thalassemias, you're going to see target cells on the blood smear. When you have that 3 or 4 alpha globin gene deletion, you're going to see Heinz bodies as well. And this one is going to have a microcytica anemia. So the MCV is going to be less than 80, right? And again, remember, this one can develop jaundice because of an increase in indirability. And obviously, because their red cells just keep getting broken, right? Again, that's going to cause that indirect hyperbilirubinemia. So how in the world do we treat these people? Well, the thing is, if they're asymptomatic, you don't have to do anything. But if they have symptoms, they're going to need blood transfusions. You're going to need blood transfusions. But think about it. When you're giving a person a blood transfusion, you're literally giving them iron. Blood, literally one of the biggest components is iron. So you're giving them not just blood, but you're giving them a ton of iron. That iron can begin to cause iron overload, right? And iron loves to deposit in people's like levers and damage it. Think of like hemochromatosis, right? You can develop liver failure. You can develop pancreatic failure, right? Because the iron, fentanyl reaction, free radical production, damage your pancreas. You can also damage these people's pituitary glands. So that can cause all these problems. You can have iron overload. So many times, people that have thalassemias, in addition to the blood transfusions, you're going to be put on ion chelator therapy. So something like deferoxamine or deferocerox or deferiprone. Deferoxamine is spelled D-E-F-E-R-O-X-A-M-I-I-N-E. That's an amine. I probably remember that from old camp. Anyway, deferocerox, right? Deferocerox is spelled D-E-F-E-R-A-S-I-R-O-X, deferocerox. And then deferiprone is spelled D-E-F-E-R-I, then prone, P-R-O-N-E, you know, like being prone to something, right? So you're going to use those iron chelators so that they don't develop iron overload. And then if those things are not controlling their symptoms, in addition to that, one thing you can use is hydroxyurea. Hydroxyurea is actually pretty helpful in thalassemia because what does it do? It jacks up your hemoglobin F. It jacks up your hemoglobin F. Having more hemoglobin F is very helpful in people that have alpha thalassemia or beta thalassemia, right? Raise those people's hemoglobin F. Raise their hemoglobin F. It's going to be very helpful for those folks. It's going to be extremely helpful for those folks. Extremely, extremely, extremely helpful for those folks. Okay, so something you want to keep at the back of your mind for your test. test and also this book should also get folate supplementation uh because again the their red cells they just use them up so quickly so they are always like in red blood cell production mode remember you have only about three months worth of folate in the body right but this book they just use up their folate so quick so they need consistent folate supplementation and then if you see like this massive precipitous drop in a thalassemia patient, you see a massive precipitous drop in their hemoglobin, they have disacute anemia, and they tell you that, oh, they had like a viral URI recently. Think of a parvo B19 aplastic crisis, a parvo B19 aplastic crisis. And then remember, one method you may use potentially to cure thalassemia is to do a bone marrow transplant. It actually works pretty well if you can find the right match, right? You can do a bone marrow transplant. And then I think one final thing I want to say is that people that have, actually maybe two final things. You tend to find thalassemias in people from the following countries on the exam. People from Greece, people from Italy, Middle Eastern populations, South Asian populations, and Africans, right? Sometimes they can also put this in Turkish people. But again, just kind of keep that at the back of your mind as you're studying. And remember, it also kind of comes having thalassemia, especially like the more minor ones, like the beta and alpha thalaminers, kind of reduces your, has some protection against malaria. So that's something that may be helpful to you to keep in mind. Okay, I think I'm going to go ahead and stop here. Again, I know this may be called a phallicemia podcast, but man, have we talked about a lot of different mechanisms. So this is actually a pretty clutch podcast to know about. So I'm going to stop here. Again, I offer review classes for step one. I have a 25-hour class coming up in early January. And then for step one to step three, I offer a two-and-a-half-hour MBME test-taking class, a four-hour biostats class, a five-hour social sciences, quality improvement, ethics and communications and healthcare systems class. And then for step two, step three itself and shelf exams, I have a 20-hour step two class, a step two, step three class. And then I have a one, that's actually coming up about two weeks from now. These other classes I said, the two and a half hour MBME test taking class, that's actually taking place next week. So if you're interested, just shoot me an email. And then I also have a 100 hour super comprehensive step two, step three review. It's going to be taking place in May of 2024. If you're interested in any of them, just shoot me an email. I also offer one-on-one tutoring for all the USMLE exams and med school exams. And then I have these podcasts on Apple, Google, and Spotify. I have a YouTube channel, Divine Intervention USMLE Podcasts and Videos. And then I have another website called DivineInterventionLifeLessons.com. Every week, I try to post like two podcasts where from a biblical perspective, I try to address a life lesson. And there's actually an Apple podcast associated with that. But again, thank you for listening to me today. Have a wonderful rest of your day. God bless you. I'll see you next time. Bye for now.
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Hello there and welcome to the May edition of the Lancet HIV podcast. I'm the journal's editor, Peter Hayward. This month, I'm delighted to be joined by Adam Castillejo, who is at the centre of an article published recently online and included in the May issue of the Lancet HIV. Adam, also known as the London patient, is the second person ever to have been cured of HIV after a stem cell transplant. I'm going to be speaking to Adam about his remarkable story. Hi Adam, thank you for joining me. Hi Peter, thank you for having me. My pleasure. When you were first diagnosed with HIV, how did you feel at that point living with HIV? Did you find acceptance when you revealed to people that you were living with HIV? So, do you mean when I was diagnosed? When I was diagnosed back in the 90s? Yes. I was diagnosed in 2003. We just live in the 90s. And the 90s was a very turbulent time for the HIV crusade, as we say. So, in the 90s, it still was a death sentence. We just came out from the 80s. And in the 90s, it's still, it was a death sentence. We just came out from the 80s and in the 90s, it was just a progression from the 80s. So when we turn to the 90s, it's still, you fear as an ultimate diagnosis. And from my, how I felt, for me, it was like a death sentence because, you know, it was very close to the 90s to be told you can live a healthy life for the next 10 years. And we hope you can live to more 20 years. So that was a very challenging, overwhelming experience. It's a death sentence when somebody gives you that at that time. Nowadays, it's a very different outlook. I think people now have better treatment, threat of viral medication, and better outlook to life. You can live a healthy life and, you know, normal life, bracket, normal. But in the early 90s, it was a very different picture. We weren't just coming out from the night. And in my case, I felt, you know, three men were well, I thought I was going to die. There's not much hope I'm going to die anytime soon because you still have the reference for the A pandemic when people had diagnosed you would die quite soon. So it was a very scary time for me. And I was lucky enough to have a partner at the time we accept me no matter what and they embrace me and that was one of the key factors for me to kind of endure and say oh I can let's be happy let's embrace my life and let's do the best I can do let's be healthy prior to that I was already like anybody in their 20s you know a healthy person you know a healthy guy young man working sports training you know like I've always been very active through my life so I like sports cycling running swimming so I've always been a very. So for me, it was kind of reinforcing me at that time, reinforced my belief to live a healthy life. Right. Was that easy to do after you got the diagnosis of HIV? I mean, obviously that was a shock, but once you'd accepted the reality of having HIV, did you find it sort of easy to, were you able to maintain your activity and your sportiness and your training and all that? Yeah, I think when that happened, it's like you have to grieve that diagnosis. You have a period of grief and then you move on from that, the acceptance of your diagnose i think that's very important a lot of people struggle with that and in that time in the early 90s it was still as i said before it was still the 90s it was very difficult even for the medical doctors and nurses and the care workers still telling you reinforcing and and giving you that hope. They were very cautious about how hopeful they want to be. They want to be very kind to you, but they were kind of the facts. You know, the Spentex in your life spans 10 years or maximum 20 years. And that's a wonderful life to live. So that was kind of the outlook when I was diagnosed. So, and I said to myself, well, it took a while, I have to be honest. If it's something you don't just recover instant, it took quite a while for me to recover and to accept my diagnosis. And then later on, I said, well, I can't let this to damper my spirit. And that reinforced me to eat well, continue to live my life, to live to the fullest. I think that was important to do at that time. Not everyone can do that. I was very lucky enough to have all the medications and all the things available here in London, which all the people around the world, they are not that lucky or they have that privilege because sometimes I feel like we here in Europe, we have privilege compared to all the parts of the world. We don't have the same amount of resources to get medications. To live a healthy life, you have to go into medications to help, you know, to maintain your life. I think that was something which had been progressing through the years compared to when I was diagnosed. I think it was more tragic and more horror when I was diagnosed, when you were diagnosed today. It felt a bit different. It's a huge... Yeah, certainly there's. The treatments are better now and access around the world is, while definitely not perfect, greatly improved. So obviously you've been living with HIV for a while and then you were diagnosed with another very serious disease. Can you tell us about that and how that affected you? Before the diet I was, again, what I say, I live a healthy lifestyle. You know, working, training, I always be very cautious about my well-being. The training, I really look after myself and eat well. Because as a chef myself, it was unable to kind of eat well I keep training I keep looking up and then that happens unfortunately I have to kind of relieve relieving the the death sentence I have one I have the HIV it was kind of similar but this time you have a more a more immediate effect. You can die really quickly compared to when I have the HIV diagnosed, when you can die quickly too, but you had an outlook about 10 or 20 years. This time around, you can die in very short periods of time because a cancer patient can die very quickly. So people die two or three days after being diagnosed so it's a very scary place to be I felt wow I couldn't believe it that this was happening to me what have I done I questioned myself and thinking what have I done wrong to deserve this again? It's just like, and I felt, well, Adam, is this what you need to go through? You go through and let's face it head on. And that's what I did. But it was kind of relieving all the emotion. But at the same time, you feel numb because it's a very scary scenario. And you have to, and again, because I think when you have the HIV, you are apprehensive about all the HIV treatment. And then you go apprehensive when you have the chemotherapy treatment. And you don't know what is going to happen. You don't know the side effects. You have no idea. It's a lot of uncertainty when you embark on it. But I have kind of that spirit, sadly, from the HIV early in the notice. So I'm able to navigate better that aspect. But it was very scary. I was petrified to die like anybody who has an OECD. It's a very scary situation. It's extremely overwhelming. You're thinking, my God, I'm going to die. And the diagnosis, it was acute myeloid leukemia, was it? No, I did not have leukemia. I have a state lymphoma. Okay. It's a blood cancer. I think that was one of the things people still confuse between me and Timothy Brown. Timothy has leukemia and I have lymphoma. They're both blood cancers. Oh yeah, so you have Hodgkin's lymphoma. Yeah, it's stage four. Yeah. So you were diagnosed at stage four Hodgkin's lymphoma. Yes, correct. So yeah, so that must have been... Yeah, it's extremely overwhelming because, you know, people think it's stage one, it's stage two, it's stage three, but mine was straight to stage four. So it was, suddenly I become very ill, very ill. And I thought I was going to die. But it seems like... Because I was extremely ill.
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Yeah. Back when I was my diagnosis. I was, it was touch and go, if we can say. I felt like I was going to die. But then once you began treatment for the Hodgkin's lymphoma, you suggested it before that perhaps the experience with HIV had given you some sort of resilience and ability to sort of cope with the treatment. Yes, it gave you some resilience, but it was a a very different topic i think you have the hiv you have medication and you have control you regularly control yourself uh checkups but with cancer you are have no control whatsoever the narrative is a very different one but at the same time you are overwhelmed by what you have to endure compared when you had an HIV diagnosis. It's a very different prospect. So then down the line, you're receiving treatment for... You're receiving treatment, but how did you come to be involved in the attempt to cure your HIV? It is important to remind everyone to get involved with this. It happened in a very many years on the line. So I was around 2011. We're talking about in 2015. So we're talking about several years. I had to endure chemotherapy regimes, disappointing results, and having people think they don't realize that there was something that is important for me to emphasize and clarify. From 2011 to 2015, I was enduring, on a regular basis, chemotherapy regimes. Endure month after month, year after year, nonstop chemotherapy regimes. I had to face the reality of my mortality. It was nothing I came across in 2015, but my will to not to give up in life. You have to remember a lot of people who have currently suffered from cancer who are HIV patients, a lot of treatments are not available to them because there's not a lot of medical expertise how to deal with cases. You have to bear in mind, when you have a cancer diagnosis and you are HIV, you have to make sure your retroviral medication doesn't interact with your chemotherapy regime to be able to be efficient to cure your cancer. So that's very complex, and people need to be aware that it's a very complex task. For any medical clinician in the HIV world and the cancer world, that's a very complex way to go. In my case, I have been fortunate to have Professor Simon Edwards, who was able to liaise with my medical team for oncology and hematology to liaise how to be efficient with my rectal viral medication, which was changing, ever changing. As my cancer, it was becoming more aggressive and the chemotherapy, it was not working. It was important to change, constant change or rectal power medications to work with that. It's a very complex situation. It didn't have to be very unlikely that when I was involved, I think that was an effort, a personal effort to find somebody willing to take that risk to have some hope because I was being a very hopeful person but at the same time very skeptical and critical about things so at the time when I was given a terminal diagnosis in 2015 I decided to look elsewhere and to see all the avenues and opportunities not only in the the UK, around the world, to see what can be done. I was just deciding to take the lead in my case and thinking I need to take some ownership and more control of it to see what else I can be done with my life because I didn't want to die in a hospice, just resigning to a hospice palliative care. I'd rather die fighting that bad. But that was an effort from my support network who were willing to help me to find different medical teams across London and across the world who were willing even to consider as a second opinion what can be do in my case. And I was very fortunate enough to find Dr. The Consultant Ian Gabriel. He was willing to take the risk on my case. Bearing in mind, it's very complex and people need to understand it. Not every clinician will take the risk to have a transplant. And I was fortunate enough to have a wonderful medical team and have a Hammersmith Hospital in London to able to give me that second chance. And it turned out it was another opportunity because they're working in the field of cancer and HIV. And they knew the Timothy case and I was always hoping and I was always aware of some other people behind me and in front of Timothy after Timothy has passed away he has to be successful I was aware of that but the main thing it was to cure my cancer and I always knew for the very beginning about that I could have a CCFI mutation. And that was something I was really willing to take, no doubt. That was my only option. My other option, it was going to hospice. So after I got involved, you know, in the beginning, I was not fully aware of the stance of what I was going to become and what I was going to be involved. And then I started to, and then the doctors are telling me, explaining to me what's going to happen and how wonderful this opportunity is. But always remain cautious about expectations. One of the things, you have to be cautious about expectations because if you expect too high if you fail unless you are more skeptical and more pragmatic in your approach then you can reach that that hope right so it sounds like at the time of you coming up to your stem cell transplant you were very you were very aware and very well informed about the possibilities, what the different outcomes of the procedure could be. Was it, for you, a scary or a hopeful time? As I say, I mean, to have an 80% chance of dying, that's a high, high percentage. I was petrified scared but at the same time I have no other option and I have to embrace it once again that's one of the things I always unable to kind of head on and embrace it doesn't mean I'm scared and petrified and terrified of the outcome, but at least I try. If I die, as I say to myself, at least you die trying. And that was my spirit saying to me, just try and hope for the best. But it was a very overwhelming experience for not only for me, I think for my family and my friends, they hoped the best for me. And they have seen me for so many years struggle with cancer. They want to be happy for me. They want to do the best for me. They want everything to be successful. But we've been so disappointed throughout the year. We know we have to remain skeptical and cautious. Yeah. I mean, there must have been sort of such a huge mixture of emotions for you and your loved ones at that time. You know, it's hard to comprehend for someone who's not been through that and so obviously you have the procedure and you knew about the possibilities the procedure the procedure went seemed to work from the obviously work from the point of view of treating the cancer yeah um correct how did you feel obviously that's a massive relief to you. And as you said, the main point in the procedure was to cure the cancer. How did you then feel as time went on and you were having follow up and it seemed that the HIV had gone as well. Yeah. So it's important to clarify when I have a transplant, I think we were, I was fully aware and it was a big part of the transplant, how to do the HIV part as well. So we don't think it was just to have a transplant and we forgot about the HIV. No, it was, and that was together. So I have a team of doctors working around the club to find out what medication I should have to take, how I'm able to take the medication, because it was very important for me to maintain the continuity to take the retroviral medication throughout my transplant. A very challenging way to do it. I recall one of the lead doctors and one of the hospitals he came and said oh my oh my god i never think somebody's so how important you must be i have 40 more than 14 clinicians and pharmacists talking about your medication it's very overwhelming i said it's a pleasure to meet you and i was kind of that's what i tell you it was behind the scenes um the hiv was working beside the transplant and i was always fully aware of or i have to the the importance to maintain to take my medication that was really important for everyone around me and the responsibility to science because for that point even i knew i had a transplant but i knew my responsibility to science. I want this to work. And I'm thinking, if I can't get cured at once, I can't get cured at the other one. Why not? Why should I jeopardize that prospect? So I understood my responsibility to the scientific community and to myself as well. I think that was a chance for me to get cured. And saying that, I don't want to ever people think I was fortunate, I was lucky enough. No, I was in the right place at the right time.
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It's not to be privileged. It's a privilege to be in this position right now. But at that time, I was in the right place at the right time. So it's important for that. So throughout, and going back to one of your questions about the process, after the transplant, we were in a constant monitor to this day, and a continuing monitor in a very regular basis to check that. After a year, when we decided to consider the possibility to stop medication that was a very how can I say it's a situation in reverse from my diagnosis because I was specifying to be once and get HIV positive you are thinking in reverse my God, I'm going to be from HIV positive to HIV negative. Obviously, any human being would be a desire to get cured. And that anybody can tell that desire to be cured. And at that point, when I was aware we have to take medication and that we have to embark in the journey of not taking medication and the constant monitor to realize if this actually worked on that aspect of the HIV. And the CCFI mutation worked effectively. It was very scary. And I decided to, and I have very very important I decided to take the medication on my birthday on a very symbolic day to stop medication because I thought it's something I want to give to myself and one better present to myself is to stop medication on my birthday and I did that and then we embarked in the situation when they stopped medication a month, a week later, negative. The next four nights, negative. A month, negative. And the time goes. Obviously, we both, the medical team and myself and I, we were cautious. We were happy but remained cautious because of the failings in the past. So we were very cautious. And I think managing expectation is very important at that stage. I think when the time passed, six months, then a year, then we started looking more positive. And we kind of realized, oh, we had something good going on. But it took several, it was no instant. I think we were, the medical team and I would be very, very positive. We've always been very looking at the positive outlook, but always being cautious. Yeah, no, absolutely. Does each subsequent follow-up when you're off treatment, so obviously, you know, it's now been well over two years. Maybe three, I'm happy. Is it three years? Yeah it's going to be any three years we have more than 30 yeah more than 30. Yeah yes actually yeah of course yeah so well we're now getting you know you're approaching three years of treatment. What is the feeling like at each follow-up when you receive the news that there's still no detectable HIV? I think it was a very, as I say, early stage. It was the first time, the first month, the first several months. I was very apprehensive every time we did the test. Professor Gupta designed a new machine in Cambridge University to actually find out the authenticity and the effectiveness of the HIV test. And yeah, obviously we were very cautious and very excited and I was very apprehensive every time. But then it eased away every time it was negative, negative, negative it's nothing but you start believing oh this is a positive way and this is looking good building my expectations in later on yeah i think with that building the expectations slowly yeah slowly step by step and then after year, we realized we are in a good place. And then it was about, well, the London patient and then going to last year at Croix. That's when I started understanding more the relevance and the importance of how the new steps of this journey will be. Because I've always, my medical team is always the main focus is about my well-being and my welfare and make sure physically and mentally I'm well enough to embrace after all I have a transplant and any transplant can tell you it's a very challenging way of living you have to live a post-transplant life which remains you have to be cautious you have to obviously try to visualize the best you can enjoy life but you always have to remember you have a transplant so that's always it's in the back of your mind and as i say after a year and then when we are approaching last year but croit i start asking myself where is all the i become more and more think that the time goes, I become more and more involved in my case, in my care and understanding the ins and outs about the treatment, about what had been happening, not only for the medical perspective, but then I say with Timothy, but the other side, for the patient perspective. And I think after a year, and then I start asking questions about how we're going to go to cure. And I think, as you know, cure in the medical world is a very emotional world. Yeah. It has people, the clinicians around the world don't tend to like to use the word cure. I think beginning, we were using functional cure. Yeah. And I think that was a more cautious way to define cure. And I think now we are more into a different stage. We call it now operational cure. So that's important for me to have the knowledge. And I think now I am more aware of what's happening. And I continue to work with Professor Guter. I volunteer myself to do research. So I donate blood to different research in gene therapy. And I think that they're important to continue helping the scientific community. And I want to do that. And I feel, once again, responsibility to the science and to the millions of people around the world who are living and fear of HIV. And as well to be a voice for the people who are not with us. So I feel very passionate about that. I thought I'd just ask you about your decision to reveal your identity and what prompted that, if that's okay. Yeah, I think that beginning in 2015 when I was given this amazing opportunity to have cured my cancer but as well my HIV. That's when the London patient kind of born at that time I felt at the time I was going to have to concentrate on my health because cancer I was in danger to die so I think my main focus at that time it was concentrating on my cancer I think all my medical teams they were very exciting at the same time for me I was a very exciting prospect to I could never imagine in my lifetime will ever endure or imagine to be cured or HIV because what we're living for the last decade so I embarked on this journey at that time but I think my concentration at that period it was about my recuperation to go through my transplant but after the transplant and I think seemed to go well relatively well I started understanding the relevance and the importance of my story and what it means to people all around the world and I understood this story is just beyond me. It would be very selfish of me not to tell my story to people and give hope. I think that's one of the things that resonated with me. It was I need to give hope to people. It's a possibility. Obviously, we need to be very clear about the way I was cured. That stuff, it cannot be replicated easily, feasible, and costly. And it's highly risky. And this has to only be taken when you have a cancer diagnosed. And your only way is having a transplant. So at that time, I thought, well, I believe this is very difficult for people. And I see a lot of people struggle mentally and physically about the HIV diagnosis. For me, it would be important, and I feel very humbled to be in this position. And I felt that it would be selfish, once again, of me not to reveal my story and to tell people, yes, it's a hope and it's a lie in the end of the tunnel. That's great, thank you. It's very difficult. It's not something I took time for me to think about and it was something I had to consider because I had to see the pros and cons. And did you, when you were thinking about revealing your identity, did you consider what Timothy Brown had gone through as well, the Berlin patient? What happened to Timothy Brown is my blueprint, basically. I mean, I only can be a referrer and I only can have reference to him. So for me, it was start to understand his journey from my perspective, you know, to how it can be related to it and understanding the difficulties he experienced throughout his coming out, as people tend to call it, and to reveal the identity. I think it was a blueprint for me to understand and I tried to get some advice and guidance from him because I was the only person I can relate to. Yeah. So you did speak to him about it? Yes, I did. I did. For several months, we engaged in conversations to kind of him to let me know and for me to have an understanding because bearing in mind, we are two strangers.
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And for him, I think that was very special. That bond, that instant bond we have. Yeah, to go from being the only person in the world to then having someone who's shared that experience must be, you know. Yeah, and that's a very special and unique bone we have. Yeah. And we value and share that. And we continue talking and we're still in touch and we're still, I think, this brotherhood because I think he recall, I recall when he say, welcome to the family. Hello, big hug to my brother. I thought that was very, very kind. And that was really special to me. And it meant a lot to me. Not to feel alone. Because for him, as you say, for him to be alone for so long time, to find somebody who can actually relate. Because he couldn't relate to anyone. I've been fortunate enough to able to relate to someone. So for me, I was kind of supporting and say, I understand where you're coming from and nobody else could. So the way he could actually feel, oh, somebody can relate to me as well. So it's very special for me. Yeah. Yeah. So that is, I mean, one of the things that you've done over the past few months and particularly since you're coming out, to use that phrase, is that you've embraced, you've really sort of embraced your position as an advocate. And I just wonder, what is the message that you would most like to use your platform to convey? You know you mentioned about advocates and people tend to go and say advocate or activist. I prefer to use the word ambassador of hope because that gave me more, it amplified my message to give hope for people with cancer because I always have to remember I'm in this position because of my cancer treatment and I cannot let that to be diminished by any mean or form and I think I would like to advocate many causes but I prefer to use the ambassador of hope because I give me more I can amplify my message because I think that what I want to do is give it hope. And obviously, I want to advocate to many causes, not only for the HIV world, I'm going to do other cancer world. And one of the things where people seem to miss out on what happened is your mental health. And it's very important to look after your mental health because that's a key factor in your well-being during both cancer or HIV. Your well-being is a major factor. And I think that's what I want to, not only you being an advocate, I want to amplify and broaden my horizons to have a wider approach. And I sympathize and empathize with a lot of people, no matter your gender, colour, race, that's what I want to do. And I feel, once again, very passionate and that's what I want to do. Well, thank you, Adam. It's been absolutely fascinating and inspiring and, yeah, humbling to speak to you today. I think, you know, I think this is going to be of great interest to our readers and I'm really grateful for your participation in this recording today. The pleasure is mine, Peter. I think I'm very honoured you asking me to do this interview and I think it's important to raise awareness and give hope and I think people relate. For me, it's very important people relate to me and feel like you're not alone in this journey. You don't feel alone. And the way I feel, the scare, sadness, happiness, that rollercoaster of emotions is normal. It happens to everybody, anybody who is dealing with this right now. Yeah. You know very well how challenging it it is and it's still a lot of discrimination and stigma attached. Because something before I finish, I think it's important for you to know when you have HIV, you have people, you have discrimination. But when you have cancer, you have kindness. And that's something I want to readdress the balance of that. I think that's one of the things I want to. Very passionate, once again. I'm very keen to rebalance that, to make sure people want, you have HIV, have compassion for you too, the same way people have compassion when you have cancer. Thank you so much for talking to us. And, you know, your message of hope is certainly one that we can all use in this current time as well. So, yeah, thank you so much. Yeah, during coronavirus, it's important to be united. Myself, which I am in self-isolation, I'm keeping myself safe, follow the UK guidelines. It's important at this time, we are all together and we need to be united and help each other. I think it's important to help each other, talk to one another and don't be afraid to ask for help. Don't be afraid to show emotion. Don't be afraid to ask. I think at this current time during coronavirus pandemic, it's important to feel love, to feel care and to don't feel alone in this world. We're all here together and thank you for having me. Thank you so much, Adam.
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From the JAMA Network, this is Conversations with Dr. Bauchner, interviews featuring researchers and thinkers in healthcare about their publications in the latest issue of JAMA. Hello and welcome to Conversations with Dr. Bauchner. Once again, it is Howard Bauchner, Editor-in-Chief of JAMA. Last Monday, JAMA published two research letters, three viewpoints, and two editorials. In some regards, to summarize where we are with respect to the COVID-19 pandemic, six of those articles will be in today's issue of JAMA in the print issue and once again on our website live. I am pleased to be joined by authors of the three viewpoints, Lisa Cooper, David Cutler, and Charlie Marmar. But before I begin with the interviews and the introductions, I just wanted to remind people of the other four articles that were the basis or also accompanied these three viewpoints. There was a research letter by Zeke Emanuel and colleagues entitled COVID-19 in Excess All-Cause Mortality in the U.S. in 18 Comparison Countries, in which the data are overwhelmingly clear that the U.S. has performed less well than virtually every other country in the world with a similar economic base. And we've done poorly at the beginning of the pandemic, the middle of the pandemic, and more recently. Steve Wolf published his second research letter entitled, Excess Deaths from COVID-19 and Other Causes, March through July. The most current estimates suggest that by January 1, 2021, the U.S. will have had more than 400,000 excess deaths related to this pandemic. It's quite possible that by the end of this year, that number will approach 500,000 deaths, exceeding the number of dead from World War II. These two research letters were accompanied by two editorials, one by Harvey Feinberg, a former head of the National Academy of Medicine, the toll of COVID-19, and then one by Phil Fontana Rosa and me entitled Excess Deaths in a Great Pandemic of 2020. Welcome, Charlie, Lisa, and David. David, you're the Otto Eckstein Professor of Applied Economics at Harvard. The title of your viewpoint was the COVID-19 pandemic and the $16 trillion virus. First, can you say something about your co-author and can you tell us what $16 trillion means? So thank you, Howard, for having me and for the questions and for your help with the publication process. My co-author is Lawrence Summers. He's a Charles Elliott University professor at Harvard. He's also a former secretary of the treasury. He's a mentor of mine, actually, so I've known him for quite a long time. We were interested in calculating the cost of COVID economically, and there are two parts to that. One is the lost output, that is, people are not at work, so they're not producing things. For that, we took estimates from what the Congressional Budget Office says will likely be the trend in output for the next decade. And that's about $8 trillion of lost output for the next decade. And I'll come back a little bit to output these in perspective for you in a second. But that's about $8 trillion over the next decade. But of course, that's not the only consequence. The fact that some people have died, many people have died, many more under current forecasts will. Some people will have their long-term health impaired. People are suffering very high rates of anxiety and depression. About 40% of Americans report feelings of anxiety and depression. So what we do in this second part, the first half of it roughly is the $8 trillion from lost output. The second part is saying, what is the economic value of the health loss? And there we use a very familiar technique, which is called valuing statistical lives. That is, how much do we typically pay to reduce things like risks from automobile deaths, or how much more do you have to pay people to work in riskier jobs, we use that to then add up the costs of the premature mortality, the morbidity from survivors with severe complications, and the mental health impairments that people are experiencing. Those are two reasonably conservative assumptions that there are deaths for another year, but none after that, and that the deaths for the next year stay at the relatively low level of a few weeks ago. So that's the other $8 trillion. How do you think about $16 trillion? You know, it's obviously a very high number. To put it in perspective, it's roughly about $200,000 for a family of four. So that's roughly what the loss is. Now, it's not all economic loss in terms of lost income. Because, for example, when a family member passes away, that is an economic loss, but it's not lost income. But on the other hand, the point of the economy is not to accumulate sheets of paper with little number signs on them and numbers after them. It's to enjoy life. And so it's that lack of enjoyment, the sort of lost enjoyment of life that people are experiencing in their lives that's really going on. We give a couple of markers. So one marker is it's roughly four times what the Great Recession cost. It's roughly twice what we spent on all the wars in the Middle East since 9-11. And it's roughly 50 years of what people estimate will be the cost of climate change to the U.S. Thanks, David. I have many questions, but I want to make sure I get to Lisa and Charlie, and then we'll come back. Lisa Cooper is the Bloomberg Distinguished Professor at Johns Hopkins with appointments in the School of Public Health and Medicine. Lisa, this is the second piece you've written for us this year. The title of this viewpoint is Excess Deaths from COVID-19, Community Bereavement and Restorative Justice for Communities of Color. A remarkably painful year for the United States, for the world, and particularly for individuals from Black, Latinx, and Indigenous populations in the United States. Your co-author, once again, is David Williams. So could you say something about David? And then eight months in to the pandemic, how are you thinking about this vis-a-vis communities of color? renowned sociologist and public health scholar. And so David and I have been colleagues for many years. So it's been a great collaboration between him, you know, a preeminent social scientist and me, a clinician and also a public health and social scientist. So it was a difficult piece to write. I'll just be honest with you. It was one of the most painful things I've written this year and, of course, over the course of my career. And really, it's because it's so sobering, the fact that our country is going through this. But on top of that, we know that communities of color have borne the burden of excess deaths for centuries. And so, you know, one of the things we looked at was the excess deaths that were reported between 1900 and 1999. And it was close to 8 million excess deaths that were predicted in the African American community alone during that time period. And sort of the lack of progress that we've made on this issue, even though the health of the country has improved overall, that people of color continue to die at much higher rates than their white counterparts. And so this pandemic has actually made things even worse. Some of the estimates now are that the death rates from COVID-19 are about three times higher in African Americans, Latinos, and indigenous groups across the country. So the first thing is to basically, I think, to accept that this is going on and acknowledge that it is going on. And it is part of a legacy of social injustice, social and economic injustice that has gone on for a long time in this country. And the pandemic has just magnified that. But one way to do that is for us to deal with this, to first acknowledge it and then begin to think about how we can put in place a plan to restore health and wholeness, not only to the entire country, but particularly to these communities that have lost so much. You know, so we've seen these excess rates of chronic conditions for a long time that we know are in part due to behavioral choices. But we also know that those allow them to become gainfully employed, to environments that are safe from crime and environmental toxins, access to healthy food. You know, a lot of that has been shaped by our policies and practices that have led to this sort of segregation of people of different racial and ethnic groups into different communities and then sort of the systematic disinvestment economically in those communities. So we have that. We've seen higher rates of diabetes, heart disease, asthma. We have people who are already suffering from lack of access to health care as well in these communities.
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And then when you add to that to all the police violence against these communities that has happened during this time as well, which has had a profound effect on the mental health of African Americans. Lots of data now showing that violence against unarmed people of color actually leads to four and a half extra mental health days lost in those communities that we don't actually see among whites, even though I'm sure everyone is negatively impacted by what's going on, but it's just magnified in communities of color. And then the excess deaths leads to people in those communities losing family members at much younger ages in producing what we know as community bereavement right now. So we're going to have a steep climb to bring some of these communities out of where we are right now. A lot of focus on mental health and on access to primary care and on addressing sort of these broader societal issues. Lisa, two years ago, we published a piece from Otis Bradley called Cancer Justice. And Otis talked about we need no new technology to collapse the screening rates for black Americans for colorectal cancer, prostate cancer, and mammography. Certain communities have done it. We haven't done it nationally. But these are three diseases that are usually changed if people are appropriately screened. Do you think it will be different this time? Do you think something is fundamentally different so that in 2022, 2023, 2024, we won't look back and we'll say another lost opportunity or lack of progress? Do you think it will be different this time, Lisa? Well, you know, I certainly hope so. You know, in order to do the kind of work that I do, I think I have to be an optimist. And so to me, I think one thing that feels different this time is just a greater recognition among people outside of these communities of how severe this problem because of the inequities we have. We actually, our population and our morbidity and mortality in this country from many diseases that are treatable look like a country that's a developing country. And that's in large part because we don't really invest in our safety net and our social services in this country. and we don't protect the most vulnerable in our society. And I think it's really manifested in this COVID pandemic. And now, because so many people have been affected by it, we can see how interconnected we are. And hopefully, we won't forget about that when this moment passes. Charles Marmar, Charlie is a Lucius Littauer Professor of Psychiatry at NYU. We gave Charlie all of the U.S. mental health to talk about. The title of his viewpoint is Mental Health Disorders Related to COVID-19 Related Deaths. Charlie and his co-authors, Charlie particularly is a world-renowned expert in post-traumatic stress disorder. Charlie, can you say something about your two co-authors and then talk about what you and they have written about with respect to this viewpoint? With pleasure, Howard. But let me just start by thanking, first of all, thank you for welcoming us to this conversation and to the JAMA pieces. And I would say also perhaps more deeply, Howard, thank you and JAMA for your leadership in conveying accurate and timely information about COVID. We live in an age of profound disinformation. And I think JAMA, perhaps more than any other medical journal internationally, has been an antidote to fake news in this area. It's been profoundly important. So I wanted to just start by thanking you and the journal for that. With respect to my co-authors, I have an enormous pleasure and privilege to have a wonderful faculty at NYU. And Naomi Simon, who is my vice chair for faculty development in the Department of Psychiatry at NYU, is an internationally recognized leader in the understanding of normal and complicated or pathological bereavement, which is the central focus of our article. And Glenn Sachs, who is a professor at NYU and previous chair of the Child Psychiatry Department here, is a renowned expert in childhood trauma. So just very privileged to work in such an enriched environment and to have such wonderful colleagues. Now, with respect to the topic on hand, the impact of COVID, there are two very broad dimensions to the impact of COVID on the mental and emotional health of Americans and perhaps all citizens of the world. The first is more narrowly defined and was more the subject of our article, which is the large number of deaths which have profoundly impacted American families. So just by rough estimate, the numbers that we understand are at least actually 300,000. As you mentioned, perhaps soon more than 400,000 deaths can be directly or indirectly attributed to COVID. We know from previous research that for each death in a family, given average family network sizes, on average nine people are profoundly impacted by that loss in terms of their personal grief, mourning, and risk for psychiatric complication. So alone from the 300,000, 400,000 deaths, we have three to four million Americans who are recently bereft, and that's over a relatively brief period of six or seven months. So it's unprecedented, even compared to times of war. Second, among those who do experience a family loss of a beloved grandparent, parent, sibling, child, or other close family member, we know that roughly one in ten will experience an abnormal, prolonged, pathological form of grief called PG, prolonged grief, which is characterized by persistent, unremitting, painful experiences of the loss, inability to accept the reality of the loss, constant yearning, searching, and pining for the person who has died, inability to restore a sense of hope and optimism for going forward in life, loss of energy and pleasure, feelings of depression, and increased use of alcohol and drugs, and unfortunately, increased suicidal thoughts and suicidal intentions. So that's 10% of 3 to 4 million people. So that is an epidemic of pathological grief, which is a downstream consequence of the pandemic. And this is a worldwide phenomenon. So it's very profound. Now, the second dimension to this problem is one that David Cutler alluded to, which is that setting aside for a moment those most profoundly affected by losing someone close to them, whether we have or have not lost a family member, we are all affected by the stress and uncertainty and ambiguity of COVID. Economic uncertainty, social uncertainty, social unrest, worries about our health, worries about protecting the health of our parents and our children. The list goes on and on. So there is a second kind of psychological epidemic, which is one of anxiety, depression, and difficult to manage uncertainty, complicated by the fact that it will take an uncertain amount of time to have a safe and effective vaccine and safe and effective and well-confirmed treatments for the disease. So taken all together, 30 to 40% of the general population are burdened with stress, anxiety, and depression, and a subgroup of three to four million Americans are deeply burdened by loss, and some of those quite severely. I'm also happy, Howard, to talk about what we can do on a more optimistic note very briefly. We adopt a three-point approach, which is education, treatment in primary care, and specialty care. But that's the scale of the problem. We'll come back to the treatment. I'd like to depart some optimism. David, how does the $16 trillion relate to what Lisa just talked about? Disenfranchisement of an entire community for centuries manifest acutely, once again, acutely during this pandemic. You're the applied economics. So you must think about this in terms of human beings, not just theoretical economics. What's the $16 trillion mean vis-a-vis what Lisa just talked about? Actually, what Lisa talked about is quite relevant here in the sense that the lost output, the lost value to society of having historical levels of segregation and historical levels of inequality are really just immense. So, for example, the consequences of people not their full lives, or people not being able to live to their fullest extent, those are very big numbers. And people have often done these calculations about, you know, for example, if women are paid 79 cents on the dollar for men, what is the output that we're not having, because women are not earning those 21 cents that men are. And one could do the same thing for racial and ethnic minorities, Blacks and Hispanics and other minority groups. And the numbers would be immense as well. You sort of pick it up in things like people who don't go on to do the kinds of things that they would want to do in life, or people who are shut out of institutions that they ought not to be shut out of. So those are really very big costs that in some ways, with the specifics on the $16 trillion, we did not allocate it by group because we just calculated the national number. But surely that number is greater per person in lower SES groups and racial minority groups because the economic loss is greater there as well as the health loss.
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The estimates from the Congressional Budget Office are that for the next decade, we will not reach the level of economic output that we would have absent COVID-19. So that's a very big period of time. It will depend a lot on actions that we take both as a society and as a government. So if we do nothing now, nothing to address the virus, nothing to address the fact that people are still out of work, then things will stop their upward trajectory and go back down and get worse. On the other hand, if we do things to both address the path of the virus, Larry Summers and I call for devoting at least 5% of any new bill passed to testing, so that once you test people, they can isolate and then you can stop the spread of the virus. So if we can support those people, then we can get the economy going better again. The worry is that we will be held up by paralysis and that will make any recovery be less rapid and that we won't get the virus under control. And that's going to make everybody be fearful about going back to work. Lisa, when you hear Charlie talk about bereavement, nine affected people for each death, and you already mentioned when you talked that there's emerging data about the mental health within particularly black communities. I've seen some of the data. How do you think about it vis-a-vis Charlie's comments about bereavement, mental health needs, post-traumatic stress disorder? I think it just makes the case even more strongly that we have to work on equity because I think when a group has been disproportionately impacted, so we're talking about how everyone across the country has been impacted. We're talking about families that have lost loved ones. But when you think about the scope of it, the number of families and the number of people in communities of color that are affected is much greater proportionately. So you're talking about people who many of them were already probably in a precarious position because of the inequities in our society. So many of them were already living economically on the edge, struggling with getting their basic needs met, making sure they actually had health care and all of that. And now they've sort of been pushed off the ledge. And so it's even more profound at this point in time. So we're going to need to do some of the restorative things that we're talking about for everyone, but we're really going to need to pay particular attention to those groups that have been hardest hit. So I think it just really makes the case for the fact that we have an overwhelming problem here, but also the fact that if we try to take a one size fits all approach, that we may not get the result we're aiming for, because there are certainly certain groups that are going to need more to get back on track. And a lot of these communities didn't have, for example, the family wealth that could serve as a cushion at a time like this,, again, of these sort of years and years of economic inequality that have sort of prevented people from building up that kind of a safety net for a crisis like this. If I put you in charge of equity for the country, you don't have quite a blank check, but you have a lot of money to spend, some of that $16 trillion that David mentioned. How would you start, Lisa? You know, I'm just thinking about the interventions that have been shown to have an effect, you know, on health. And the ones that are actually most promising are on early childhood development and education and on income inequality. So providing a living wage to people who are young adults. And so I think I would start with those two areas with really focusing in on young children and their development and investing in education. And then in making sure people have a living wage because then they can afford to pay for safe housing. Affordable housing would be part of that, but I think income inequality and early childhood education would be where I would focus. And then, of course, on universal coverage for health care. Well, I am a pediatrician, so whenever anyone mentions early education, I'm always very supportive. But this issue about income inequality, it's amazing that we're stuck on discussing a minimum wage of $15 an hour. In many cities, that keeps you below the poverty line and you can't get housing. I just can't understand why, unlike most other countries, we somehow can't move that, not in everywhere in the country, but in certain areas to $20 or $25 an hour to give people living wages. I just don't need to see the wealthy get wealthier. That's just not, to me, the future of the country. Charlie, you know we're facing a mental health pandemic. And my Lord, no one really knows what's going to happen over the next six to eight to 10 weeks. The number of new cases over the last two weeks have been very, very discouraging. Back up into the 50, 60, 70,000 range, deaths have remained below 1,000, but still concerning. How do we prepare for the coming mental health pandemic or the one that's already here but has not yet surfaced in terms of requests for more help? What is it that we need to do going into 2021? I think we need to take a three-pronged approach. The first is, and this podcast is a beautiful example of that, we need at the base of the pyramid, we need a broad, honest, open dialogue with the American people and in the international community about what the nature of the problems are, what the risks are, how to recognize when you're managing or not managing the stress, anxiety, and depression related to this ongoing pandemic threat, and where to find resources. So that's the first approach is education at the deepest level, real, accurate, timely, honest information, which gets to all communities, including the black and Latinx and indigenous communities and others. Second level of approach, and it's important to remind our listeners, Howard, because this is largely a medical audience, that the front line for mental health is not psychiatry and medicine. It never has been. It's pediatrics and primary care. 70% of all children, adolescents, and adults with psychiatric difficulties are managed in pediatrics and primary care. So it's very important for our family doctors to be educated about the nature of normal and pathological grief, normal and traumatic stress, alcohol and drug misuse, and suicidal risk, because that is where the initial safety net is. And then finally, for the subset of people, which is a more of a minority, who maybe had psychiatric vulnerabilities or illnesses pre-COVID and then have had them complicated. Someone who has had a history of bipolar disorder and now has lost a family member, they're at much greater risk. And those usually require tertiary specialized child, adolescent, and adult psychiatric care with a sophisticated psychotherapy, pharmacotherapy, and other approaches. So that's how we think about it. But it's very important to remind our listeners that for the majority of people, the approach is education and family medicine. Those are the front lines to manage the psychiatric crisis. David, so unemployment is way up. I'm assuming that the number of uninsured is going to approach 35 or 40 million at some point, unless we do something. State budgets are in shambles. I actually think they'll manage this year because of rainy day funds and some manipulation probably of their budgets. 2021, that will not be true because the rainy day funds will have been spent and they won't be able to keep pushing payments into the future. And because states spend so much on Medicaid, that will become an issue in 2021. 30%, 35% of state budgets go to Medicaid. Is there enough money to borrow? Can we borrow enough money? Or do economists then get worried that we have too big a deficit? This always drives me a little crazy, because sometimes we seem like we can spend an ungodly sum of money. And then other times I hear about deficits and I can't figure it out. At the moment, we can borrow. If you look at the people with money in the world, they're willing to lend it to the U.S. government that is for essentially no interest. They're looking for a safe place to put the money. So there's no problem at the moment in our fiscal capacity to borrow. Interest rates are and remain very low. At some point, debt has to be paid back. And so a big issue will be how do we go about doing that? My guess is that what we're going to start to see next year are calls for austerity. We need austerity in Medicare funds, and we need austerity in Medicaid funds, and we need austerity in funds for low-income populations, and so on. And I think partly that will be true worry about how much debt we can afford, and partly that will be, depending on who's the president and the makeup of the Congress, an attempt to try and avoid any new spending.
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I'm not an MD, but it's a little bit like at some times you have to treat the patient with something that's too much for the long term because you have to get them over the short term health impairment. Lisa, I want to give you the final word. It's been a painful search for equity in the United States in health care and in society in general. It's been elusive for centuries. It's just been elusive. Are you optimistic that it will be different this time? I have to be. There are days when I wake up and wonder whether I've actually lost it and whether I'm living in a fantasy by believing this, but I have to believe that. I do think that we're going to have to get creative about this. I think there's a lot of fear circulating among people that somehow if one group of people get something, that means the other group is going to suffer more. And I think there's a lot of fear about that. I think everyone's sort of in defense mode right now. And I think one thing that will help us is to really understand that we are all in this together and no one's going to succeed unless we all do. And I think that's the thinking that needs to shift in our society away from this sort of us against them and this group against that group to really thinking about the fact that in order for us to all succeed and get better, we have to work together. And it may mean that, you know, it's a give and take. It's like, as if, like, if it was your immediate family, would you basically starve one of your children because, you know, you were afraid that you wouldn't get something to eat? Or would you try to make the best of what you had? And, and would you make sure that everyone had a chance, especially the person or the groups that had been left behind for whatever reason, which we know that there are many reasons. But I think if we can get a shift in attitudes around that, like we are in this storm, we're not all in the same boat, but we're all in the same storm. And that in order for any of us to actually succeed, we all have to succeed. We can't leave anyone out. entitled The COVID-19 Pandemic and the $16 Trillion Virus. Naomi Simon at Glenn Sachs and Charles Marmar have written a viewpoint entitled Mental Health Disorders Related COVID-19 Related Deaths. Lisa Cooper and David Williams have written a viewpoint Excess Deaths from COVID-19 Community Bereavement and Restorative Justice for Communities of Color. And I really want to acknowledge Harvey Feinberg, former president of the National Academy of Medicine, who's written an editorial that has summarized the toll of the COVID-19 pandemic. He's talked about the two research letters that I mentioned earlier, as well as these three viewpoints. Charlie, David, Lisa, thank you so much for joining me today. And please stay healthy. Thanks so much. Thank you. Thank you so much. For more podcasts, visit us at jamanetworkaudio.com. You can subscribe to our podcasts on Stitcher and Apple Podcasts.
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Welcome to Intention to Treat from the New England Journal of Medicine. I'm Rachel Gottbaum. Today, part two of our examination of the journal's racist history and what we can learn now. There are still such deep legacies from the past in our present practices. And it's the past that's Historical Injustice series. And also with us again is Dr. David Jones. He's a professor of the culture of medicine at Harvard and an editor of the series. Let's start by talking about the era after World War II. This is a period when the New England Journal of Medicine becomes a central publication, not only for doctors, but also policymakers and researchers. And it's a time when health care really begins to be centered at hospitals. But it's also a time of segregation. Well, remember, this is the era of Jim Crow. And so many hospitals, even in places like New York City, which is not a Jim Crow state, are still segregated. But in the South, there was absolute segregation between white wards and black wards, between nurse training schools at Grady Hospital in Atlanta. The black nurses were trained on one side of the huge hospital complex. White nurses were trained on the other side of this hospital complex. They never saw each other. White and Black nurses did not treat the same patients at all. This building is shaped in a way that as a White person, you could graduate from Grady Hospital Nursing School and never see a Black patient. Rigid segregation meant that in many places throughout the American South, and not just the South, Black people simply had no access to hospitals because the funding of hospitals, certainly post-World War II, required enormous amounts of money, both federal money and philanthropic funds. The Black community didn't have generations of very, very wealthy people who could provide funds to hospitals. And so therefore, access to hospitals was profoundly inadequate for African-Americans. And it wasn't until the federal government moved in to say that those hospitals who will receive federal funds must desegregate. And it was only then, when hospitals faced losing high levels of federal funding, that those hospitals did desegregate, and we have more or less some of the situation we see today. I would say still not completely fully integrated in many respects, but at least far, far better than what happened in the early post-World War II period. Just to emphasize the point that Professor Hammons had been making, the federal government's policy immediately after World War II was a segregationist policy. So in 1946, Congress passes the Hill-Burton Act, which makes large amounts of federal funding available for hospitals. And in a concession to Southern Democrats, the Hill-Burton Act allowed that money to be spent on hospitals that were segregated. And so the federal government is actively financing the creation of segregated hospitals, 1940s, 1950s. And it's only with the passage of Medicare in 1965 that you see hospitals were given a choice. If you want federal funding, then you have to desegregate, at least in principle. In practice, it remains a question. And of course, in this same period when hospitals were largely segregated, doctors continued to approach research and medicine with a lot of internalized notions of race. How did this evolve as medicine evolved? Over the course of the 20th century, the kinds of diseases that are common in society start to shift. And so you see rising concern about problems like cancer, heart disease, diabetes, substance use. You still see the same patterns of racial thought and medical theory and practice. Doctors would actively look for differences in the incidence and prevalence of disease between different racial groups and then give explanations that foregrounded these biological genetic notions of race. And so one of the famous examples of this is what happened with a group who at the time were referred to the Pima Indians in Arizona, now that the preferred term is the Akmul Odom community. And a series of studies were done in the 1950s and the 1960s that led medical researchers to conclude that this group had the highest prevalence of diabetes seen anywhere in the world. And so first they start talking about Pima diabetes as if it's a distinct phenomena. And the interpretation is there must be something inherent to this group of humans, such that they get more diabetes than anyone else in the world. And so NIH got interested, and there was a research study that was established that ran for decades. And the real hope was that they would find the genes that determined who did or did not get diabetes. And decades later, you know, fast forward to the early 2000s, and they still hadn't found the genes that would explain diabetes in this community. And two interesting things had happened in the meantime. One was the recognition that all humans are really susceptible to diabetes. And the ways in which the Pima had seemed distinctive in the 1950s and 1960s were not so true by the 2000s. There were lots of people who had really high rates of diabetes, and they were no longer the group that had the highest rate of diabetes. But the most interesting observations came from outside the medical profession, really from anthropologists, who said, hold on here. You geneticists totally misunderstand what's going on. This community of people is not one community who lives in Arizona. This was a community of people who moved freely across what's now the U.S.-Mexican border for centuries. And so the people you are seeing in Arizona have close relatives on the other side of the border. So let's look at them too. And if you look at the members of this community who are living in Mexico, they did not have high rates of diabetes. And so if you have genetically the same group of people that's been split in half, and half of them have lots of diabetes, and half of them don't, it's really hard to make a case that this population is genetically predisposed to diabetes. But that's what the American researchers had done for decades. The ways in which the questions, the research questions that the scientists were engaged in trying to answer, which were based on a fundamental flaw at the very beginning of it, that they understood who these people were, and they did not understand who these people were. And they did not understand how these people were connected to other people in more or less the same region. And those things took backseat to how they went about their research, whether or not it was rigorous or robust or whatever. But the fundamental premise was, we know who these people are, and we understand their cultures and their lived experiences, which they did not. And so one of the things that's so interesting about the diabetes case is because so much had been written about this group for so long, it still circulates in the medical literature. So there was a study that was published a couple years ago in the New England England Journal of Medicine based on analysis of the medical curricula at University of Pennsylvania. In at least one class, the professor continued to talk about Pima diabetes as an example of a genetic cause of a disease in a minority community. So the idea continues to circulate even after the evidence base for it has collapsed. So that pattern of thinking continues, but the response to it has evolved. So tell us what you found. So there was a very interesting article that gets published in the New England Journal of Medicine in 1990 from researchers from the Department of Health in Arkansas, that if you look at white people and black people who are admitted to these nursing homes who don't have tuberculosis, and if you follow them over time, the black nursing home residents were more likely to acquire tuberculosis than the white people were. And the conclusion of this article was that this proves that black people really are more susceptible to tuberculosis. And that's the article that gets published by the New England Journal of Medicine. Well, by the 1990s, when you publish that kind of thing, you're going to get pushback. And so the journal published a series of really angry letters to the editor. And there were many critiques that were suggested of this finding, but the most basic one was, just because these people are in the same nursing home doesn't mean that they're being treated equally. It was very easy to imagine that if you were in a nursing home in Arkansas, in a publicly funded nursing home in 1990, maybe the Black and white patients weren't actually treated in the same way. Or at the time of admission, maybe the health status was different. Maybe on arrival, their health status was compromised. Not because of some genetic liability, but because they had lived their lives in a racist society. And that's why their health was compromised. And that's why they were getting tuberculosis at higher rates. And one of the letter writers really put a fine point on this. And they said, well, look, if you focus on these inherent differences, you're robbing us of the desire to intervene.
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So let's go forth and fix this. That is a much more valuable approach to take. Where if you say, as had been said by this point for 180 years, well, of course, there's more tuberculosis in Black people. That's what we've always seen. There's nothing to be done about that. That really takes the doctors, the nursing home executives off the hook for doing anything about this problem. So there are real consequences to that kind of racialized interpretation of the data. So obviously there's a lot more awareness of how flawed these genetic and racialized theories were. And yet, as you point out, they continue to circulate. So what needs to happen? If you really want to change how doctors think, you need to have a deliberate research policy. You need to think, okay, how can we generate evidence that's really going to undermine that faith? And you do see very good examples of that. And so one of my favorite ones is this article published in the New England Journal of Medicine in 1997 about birth weight. And so researchers had recognized for decades that if you look at births in the United States to black women or white women, the babies born to black women tended to have lower birth weight. That's seen as a sign that something has gone wrong. And given habits of American medical thought, many people assume that, well, there must be a genetic cause of that. We know that Black people and white people are different. There must be something wrong with these Black mothers, and it must be genetic. And so these two researchers came up with a very clever study design. They're like, okay, let's do this. Let's look at children born to white women who had been born in the United States, to Black women who had been born in the United States, and then to black women who had been born in Africa and had recently immigrated to the United States. And so if the genetic explanation is true, there's something about African ancestry that gives low birth weight, then you should see those three populations line up in a row with the healthiest birth weights in white people, low birth weights in African-American mothers, and even lower birth rates in these African-born because they're the ones who are most purely genetically African. So what did they find? It turns out that the birth weights of U.S.-born white women and African-born Black women were pretty similar. And that finding really drops a bomb on the idea that this could possibly be genetic. If it were about genetics, the African-born women would be having the worst pregnancy outcomes. And the ways in which that was theorized has so many issues in it. Number one, you know, the African-born women. Africa is the most genetically diverse continent on the planet. So there's a whole lot of issues going on there. And some people want to study the African genome project. There's no African genome. There will be multiple genomes, multiple contributions to what constitutes the human genome from across the continent. And then, of course, we also use something called the white group that is never interrogated. So what constitutes the white group? What are the multiple ancestries from the people that we throw willy-nilly into something called white? And so this kind of result shows us that our perspective on racial differences blinded us to fundamental questions that should be asked. And so we can't settle for these default notions that have long, uninterrogated histories as we do our work today. We have to ask these questions. What populations are we talking about? How do we define those populations? Are those definitions based on very serious analyses that include a host of things that in many strictly medical settings are not considered? Culture, environment, work, education, socioeconomic status, all these kinds of things that play a role in what we're seeing. And then do more careful work to try to discover the pathological and physiological issues of disease that we want to really understand. And that ultimately our goal is to relieve human suffering, but we aren't doing it unless we take this much more seriously. So Dr. Jones, what's your view on what we can learn moving forward? And the fact that doctors care about this, you know, would just suggest that everyone else should care about this as well. And I've heard this from medical students at Harvard Medical School. It can be exhausting to be a Black or Hispanic or Indigenous medical student in a medical school in the United States in 2024, because when they're taught about health disparities, they're exposed to a litany of ways in which their people are sicker than everyone else. The black people have higher rates of this. Black people have higher rates of this. And then to the extent that a whole bunch of sort of old racist ideas continue to circulate. Black people have thicker skin. Black people are less sensitive to pain. The Pima diabetes is a true genetic problem. All of the signaling that medicine does by perpetuating these beliefs is toxic to society in general. It's toxic to future physicians who are trying to train in medicine. And so if we can figure out better ways to engage with difference, to write about difference, better ways to publish articles that take up questions of human difference, it has the potential to have an impact on medicine and society in many, many different ways. So Professor Hammonds, in conclusion, does this examination the journal is undertaking matter? Does this history matter? I think the history matters because there are still such deep legacies from the past in our present practices. And it's the past that's in the present that matters. And that if we don't deeply interrogate the kind of examples that David has described in detail and see the ways in which our continuing beliefs and fundamental biological differences between human groups that we have identified as racist has actually been flawed and have not led to our deeper understanding of disease and differences in disease and susceptibility and other very important medical issues that we continue to make the same mistakes when we approach trying to help relieve human suffering. That past is still active. It's not just in the past that we can forget about. We still have high rates of low birth rate among African-American women. We still have high rates of maternal morbidity among African-American women. We have a whole industry now dedicated to health disparities. But if we want to not have to continuing to deal with this issue of health disparities, then for me, it requires a reckoning of the past that says, how did we get here? And if we don't understand how we got here, we can't change the future. Thank you both so very, very much. Thank you. Thank you. It's terrific that the journal is giving these important problems the serious attention. That's Dr. David Jones, professor of the culture of medicine at Harvard University, and also Evelyn Hammonds, professor of the history of science and African American studies at Harvard. We had help from our managing editor, Deborah Molina. There's still a wide gap between doctors and their patients. We're offering patients hope that we're going to try and keep supporting them, getting any care that's really going to help them, but also helping them get ready for the final stage of their life. If they're well prepared for it, I think that's one of the best things we can do for our patients. That's next time on Intention to Treat from the New England Journal of Medicine. I'm Rachel Gottman.
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Hello out there. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, the Journal of the American Medical Association. And this week I will tell you about the December 19, 2007 issue of JAMA. And as always, I'll begin with the art cover. And the art on the cover this week is one of my very favorites. It's a painting by Pierre-Auguste Renoir, who lived from 1841 to 1919, and it's the painting of two girls at the piano. Of course, it's French, and it was painted in 1892. The first article deals with imaging of suspected pulmonary embolism. Computed tomographic pulmonary angiography, that's CTPA, is an alternative to ventilation perfusion or VQ lung scanning to evaluate patients with suspected pulmonary embolism. But whether CTPA is as reliable and safe as is VQ scanning for the initial patient evaluation is not clear. So to examine this question, Dr. David Anderson from the Health Science Center in Halifax, Nova Scotia, Canada, and his colleagues randomly assigned patients with symptoms or signs associated with a high pretest probability of an acute pulmonary embolism to either CTPA or VQ scanning. Now, patients in whom pulmonary embolism was excluded by either procedure did not receive antithrombotic therapy, and the patients were followed up for three months to assess subsequent development of symptomatic pulmonary embolism or proximal deep vein thrombosis. The authors found that CTPA was not inferior to VQ scanning in ruling out pulmonary embolism. However, more patients were diagnosed with pulmonary embolism using CTPA. In an editorial, Dr. Jeffrey Glasroth from Northwestern University School of Medicine discusses the clinical implications of the study findings and issues for further investigation. The second article deals with false positive cardiac catheterization. Rapid activation of the cardiac catheterization laboratory based on an assessment of the initial diagnostic electrocardiogram by the emergency department physician can reduce door-to-balloon times in patients with ST segment elevation myocardial infarction, or STEMI. However, rapid catheterization laboratory activation may result in some patients undergoing angiography who do not need acute reperfusion therapy. These are so-called false positives. To determine the prevalence of false positive catheterization-laboratory activation, defined as no culprit coronary artery, no significant coronary artery disease, or negative cardiac biomarker results. Dr. David Larson from the Minneapolis Heart Institute and his colleagues reviewed regional registry data from 1,335 patients with suspected STEMI who had undergone angiography. The authors found that the frequency of false positive catheterization laboratory activation was common, ranging from 9.2% to 14%, depending on the definition used. In an editorial, Dr. Frederick Massoudi from the Denver Health Science Center discusses the need to assess both the positive and negative consequences of quality improvement efforts. The third article deals with risk of incident vertebral fractures in older women. Women with low bone mineral density, BMD, and prevalent vertebral fractures are at increased risk of incident vertebral fractures, but the absolute risk of fractures over the long term is not known. Therefore, Professor Jane Cawley from the University of Pittsburgh Department of Epidemiology and her colleagues analyzed data from the longitudinal study of osteoporotic fractures Thank you. 2,680 women who attended the 15th year visit and who had a mean age at baseline of 68.8 years, the authors found that women with the prevalent vertebral fracture and osteoporosis by BMD had an absolute risk of incident vertebral fracture of 56%. Among women without prevalent vertebral fractures and it deals with catheter ablation of supraventricular arrhythmias. It is a Grand Rounds from the Johns Hopkins University School of Medicine, and the Grand Rounds was presented by Dr. Joseph Marine. The discussion involves the symptoms, pathophysiology, and catheter ablation treatment of supraventricular arrhythmias. The JAMA patient page has information for your patients about atrial fibrillation. In this issue, we have three commentaries. The first deals with lethal injection and physicians, state law versus medical ethics, and is presented by Mr. Lee Black from the American Medical Association. The second commentary is nonpayment for harms resulting from medical care, catheter association. Thank you. What is different about the market for health care? And it's written by Mr. David Wells and Drs. Joe Ross and Alan Detsky from the University of Toronto in Canada. We also have a call for papers in this issue, the 2008 theme issue on violence and human rights. The call is presented by Drs. Thomas Cole and Ms. Annette Flanagan, both who are editors of JAMA. The medical news and perspectives, community-based efforts to curb obesity are enlisting schools, businesses, families, restaurants, grocery stores, and local government to play a role in encouraging healthful behaviors. Researchers address childhood obesity through community-based programs. A seven-country survey of patients shows that U.S. adults are most unhappy with the health care. Hmm, now there's news. Broccoli extract may help reduce UV skin damage. I still don't like broccoli. Research law address veteran suicide. And in the world in medicine, caffeine for preemies, HIV vaccine concerns, chikungunya virus, and from the Centers for Disease Control and Prevention, acute respiratory disease syndrome in persons with tick-borne relapsing fever in three states from 2004 to 2005, and finally, reported HIV status of tuberculosis patients in the United States from 1993 through 2005. We have our special literatum in the book reviews. We have these periodically in JAMA. And this one deals with exploring the dangerous trades with Dr. Alice Hamilton. And it's written by Dr. Howard Markell, who is from the University of Michigan School of Medicine. And those of you who don't know who Dr. Alice Hamilton is really need to read this. And finally, we have A Peace of My Mind, written by Dr. Scott Williams from the Walter Reed Army Medical Center. And I'll give you one quote from what he titled Giving Back. I have never been particularly close to my father, but the process of sharing an organ with him changed our relationship dramatically. And for those of you interested in the reader's respond, how would you manage a 39-year-old man with erythema and swelling of a finger? Go to www.jama.com to read the case and submit your response make this podcast more educational or interesting to you. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, speaking to you from beautiful downtown Chicago, where the wind is blowing mightily, but the patients are always our top priority.
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From the JAMA Network, this is JAMA Cardiology Author Interviews, conversations with authors exploring the latest clinical research, reviews, and opinion featured in JAMA Cardiology. Welcome to this podcast from JAMA Cardiology. This is Dr. Robert Bono, Editor-in-Chief of JAMA Cardiology, and we're going to have a very interesting author interview on a very timely topic of atherosclerotic disease in people with HIV. We know this is an accelerated form of atherosclerosis. It occurs in relatively young people who may otherwise have very few risk factors for cardiovascular disease. And today we're going to be discussing an embedded sub-study of the REPRIEVE trial, which was a study of statin therapy in individuals with HIV, showing a dramatic reduction in adverse cardiovascular effects in patients randomized to butapastatin. So with me today is Dr. Michael Liu. Dr. Liu is the co-director of the Cardiovascular Imaging Research Center in Radiology at the Massachusetts General Hospital, Associate Chair of Imaging Science, and Associate Professor of Radiology at the Harvard Medical School. And importantly, he's also co-PI of the REPRIEVE trial. Welcome, Michael. Thank you, Dr. Bonnell. Great to have you here today. And also joining us is Dr. Matthew Feinstein, who wrote a very important and complimentary editorial commentary to go along with the presentation from Dr. Liu. Dr. Feinstein is Associate Professor of Medicine, Pathology, and Preventive Medicine at the Northwestern University Feinberg School of Medicine, where he is also a translational scientist investigating inflammation and cardiovascular disease. Welcome, Matt. Thanks for having me. Excited to talk about this topic. So this is really an interesting mechanistic embedded sub-study of the REPRIEVE trial that we're publishing in JAMA Cardiology. And Michael, it would be helpful perhaps for the listeners for you to first give us a kind of an overview of the REPRIEVE trial and what we learned from that important study published last year in the Newton Journal of Medicine. Sure, yeah, I'd be happy to. So REPRIEVE was a multi-center phase three randomized controlled trial enrolling 7,769 people with HIV and low to moderate risk of atherosclerotic cardiovascular disease around the world, those participants were randomized to pitavastatin and calcium, four milligrams a day, or placebo. And the main outcome of REPRIEVE was that over a median of five years, there was a 35% lower incidence of major adverse cardiovascular events, including myocardial infarction and stroke, in the pitavastatin arm compared to the placebo arm. Furthermore, that reduction was greater than what would be anticipated just based on LDL lowering alone. And, you know, the reason that's important is because we recognize that people with HIV have a higher risk of cardiovascular disease and that it develops earlier than in people without HIV. But at present, the current guidelines, at least from the ACC and HA, recognize HIV as a risk enhancer, but there are not specific recommendations for these low to intermediate risk patients, whether they should be getting a statin or not. So in November, actually, the first guideline in response to REPRIEVE came out. The British HIV Association released a recommendation that persons with HIV, age 40 and over, should be on a statin. So that's the first guideline that I'm aware of to have been based on the results of the REPRIEVE trial. And there may be more to come soon. Yeah, very nice summary. And of course, we could get more into the innards of the parent trial, Michael, but what we'd really like to get into then is the mechanistic observations you made in this pre-specified sub-study of REPRIEVE, where you're really getting at an in-close and up-front look at the coronary plaques in patients with HIV, with or without pitavastatin. So tell us more now about this really intriguing novel paper that you're publishing in JAMA Cardiology for us. Absolutely. Yeah, so the REPRIEVE mechanistic sub-study was an embedded study, including 31 sites from the United States that were also participating in REPRIve. And essentially what we did is we took 804 Reprieve participants, and these people had additional testing. They had a coronary CT scan when they enrolled in the study, and then on two years of either pitavastatin or placebo. They also had various blood measures of inflammation and immune activation taken again at a baseline at four months and then at two years. And the goal of the sub-study was to try to explain the anticipated reduction in MACE in this population. So are we seeing changes in coronary plaque, reductions in non-calcified coronary plaque? That was the primary outcome. Are reductions in non-calcified coronary plaque progression, and whether those changes in plaque were associated with reductions in inflammation and immune activation. Yeah, so the REPRIEVE trial told us that there was a striking reduction in adverse atherosclerotic events. And your study is then going to be telling us whether there are changes in plaque as well as changes in inflammatory markers that are associated with those outcomes. So I think the nidus of your study here is really important to trying to get into the really striking results you found in Reprieve. Matt, what was your take-home message from Reprieve and why you feel this is an important sub-study? Michael hit it right away, which is the effect size we saw in Reprieve was pretty substantial and honestly, I think surprising. So, based on the amount of lipid lowering we saw, specifically LDL lowering we saw in Reprieve, we would have anticipated, if we were extrapolating from historical clinical trials, we probably would have anticipated about a 15% to 20% relative risk reduction. And we saw a 35% or so relative risk reduction in reprieve in terms of risks for the cardiovascular endpoint. So, you know, the next question is why? And I think that's what's so exciting about this study, by Michael, by you, by the whole team, is that this starts to get at that question. And I think we still don't know. And certainly one of the leading hypotheses is inflammation. But then the question is, what do we mean by inflammation? Where is the inflammation happening? What is this lipid-derived inflammation? Is this, quote unquote, lipid-independent inflammation? And I mean, that's what's really fun to talk about, think about, and potentially also has implications for how we start treating inflammatory risk in particular, along with kind of lipid-related risk in both primary and secondary prevention. Great, Matt. So, Michael, then give us a little more insight into the results of your study. You know, The main result in REPRIEVE was that in these participants, the pitavastatin arm had a 7% greater reduction in non-calcified plaque volume compared to the placebo arm. And when we look at plaque regression, which we defined as plaques getting bigger or new plaques, there was a relative risk that was 33% lower in the pitavastatin arm compared to placebo. So that was the primary result of the trial. The 33% reduction in plaque progression, perhaps a coincidence that it's similar to the 35% reduction in MACE seen in the overall trial. So LDL lowered as you would expect, and it was a similar amount of lowering as in the main trial. There were also reductions in oxidized LDL, LPL, PLA2 as well. So that was, I think, the other aspect of your study that was really intriguing, Michael, in that you were not only looking at changes in plaque composition and plaque volume, focusing on non-calcified plaque, kind of the vulnerable plaques. But you've also measured both systemic markers of inflammation as well as those markers that may be more lipid-related, oxidized LDL and lipoprotein phospholipase A2, which are very inflammatory as well, kind of at the plaque level. So tell us more about the changes in the biomarkers and what they might tell us regarding the mechanisms for the changes in plaque. So yes, we did see decreases, significant decreases in oxidized LDL and LPPLA2. I think interestingly though, there was not a large decrease in high-sensitivity CRP. And I'm kind of tempering that wording a little because there was actually a little decrease. If you look at the HSR CRP levels in month 24, they were lower in the pitavastatin arm than the placebo arm, though when you look at change from baseline, there was a trend. Also, if you look at the four-month CRP, there was actually a larger decrease in CRP in the betavastatin arm at four months, but then that got attenuated out at 24 months. So why was that? We did expect to see a larger decrease in CRP.
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It was about 1.8 mg per liter, both arms, which is sort of in their intermediate range. So that may be one of the explanations why there wasn't a large decrease in HSCRP. I think one of the other interesting things with the biomarkers is that, in fact, the immune biomarkers, we did not see a significant decrease with those immune biomarkers. So at least on a systemic level, that did not seem to be the driver behind the changes in non-calcified plaque volume that we did see. Thanks, Michael. Matt, now in your editorial comments, you do make the point that there could be something special about people with HIV regarding their dysregulated immune system that may put them at higher risk of not only atherosclerosis, but the inflammatory mechanisms underlying atherosclerosis. So how do you interpret the biomarker changes relative to the changes in plaque that we saw in the sub-study? It's a really good question. And I mean, it's a fun study to interpret because, so what do we know? We know that people with HIV, even when their viremia is reasonably well controlled, and even if they haven't had a dramatic CD4 decline and have had some reasonable degree of CD4 recovery, there is still some degree of chronic immune dysregulation, which is marked by a shift in the T cell repertoire, but also a shift in a little bit more of a bias towards monocyte activation and monocyte-related inflammation, all of which you would expect to result in increased systemic markers of inflammation, which, I mean, certainly a number of observational studies in people with HIV do tend to show elevated markers of systemic inflammation, although the specific markers vary somewhat by the cohort study. So that said, we think, okay, fundamentally, people with HIV, in general, tend to have more of an inflammatory milieu than people without HIV. But then the questions are, where is the inflammation? And how is that going to be modulated by various therapies? And that's where this gets really interesting because prior to reading this paper, one would expect to see, okay, there was a 35% relative risk reduction, almost twofold higher than expected. That is probably relates to some degree to residual inflammatory risk. So I would expect to see some reduction in inflammatory biomarkers. And we didn't really see that here, which is, again, it's interesting. Then again, the caveats, I think, are a couple of fold. You can still have a reduction in atherosclerosis-relevant inflammation without necessarily seeing it in some of these biomarkers. And I think a couple of things. One is this study. This is a sub-study of the parent trial. So this was, what was it, Michael, it was about an eighth of the overall trial population. Is that about right? Yeah, it's like 800 versus 7,800. So something like that. But that said, it still seemed fairly reflective of the overall trial population. So because of that, I mean, there were the confidence intervals for some of the inflammatory markers are maybe a little bit broader. So maybe that decreases the ability to see a significant association. But for a lot of them, there wasn't a significant numerical difference either. So the question is, if inflammation is playing a role, which I think it's certainly still possible it is, you saw a reduction in non-calcified plaque volume, and you saw a really effect size. And then how could it be playing a role if we don't see that reflected in the inflammatory markers? And I think one possibility certainly is that you're seeing arterial retained lipid related inflammation that is being reduced without necessarily being reflected in systemic biomarkers. That's one possibility. Again, it's surprising. I think it's certainly fodder for more discussion and more thinking about why are we seeing this robust residual risk reduction. The other thing which was intriguing for me as more of a general cardiologist was that we all know that statin therapy can increase the amount of calcified plaque. And so what was interesting was that the reduction and lack of progression of non-calcified plaque was not associated with an increase in the calcified plaque in the treated group compared to the control group. And so what it appears to show us is that betavastatin was reducing the amount of non-calcified plaque and preventing the formation of new plaque, not that it was just converting the non-calcified plaque to calcification. So that's really striking also regarding the preventive aspect of this therapy in reducing the softer plaques, non-calcified plaques, and also preventing new plaques from forming. Is that an appropriate interpretation, Michael? Yeah, I think so. So I mean, certainly the reason we focused on now-calcified plaque is because we think that's the biologically active component of plaque that's more likely to rupture and cause acute events. So going into this, my thought was probably you'd see conversion of non-calcified to calcified plaque, which at least in the results we saw that was like a minor contributor. I think we'll be looking at this a little more carefully because we're humans and we have to categorize things. We define non-calcified plaque as plaque with a Hounsfield unit attenuation less than 350 and calcified over 350. But in fact, really the whole thing is a continuum. And there are plaques less than 350 that probably have some of those plaque voxels, probably have some calcification in them. They may be higher in attenuation than other parts. So there may still be more going on, even though with the strict categorical definition, we didn't see much change. Another point too, we did measure low attenuation plaque volumes. So that's plaque with an attenuation less than 30 pounds per unit. That's thought to be particularly bad. Several recent trials, like the EVAPORATE trial and Scott Hart's study, have pointed to that as particularly bad plaque. So that also did decrease. But I think perhaps there's more to look at the plaque composition. And that's really one of the great things things about CT and about this trial is that you can actually see the plaques and how they change over time. And looking at that, and also to Matt's point, one of my colleagues is an R1 to look at pericoronary inflammation, looking at the fat around the coronary arteries and seeing how does that relate to whether the plaques progress or not or get more calcified or not. I think that'll be really interesting to look at. Well, there is a great interest now in perivascular inflammation. So I think that would be a nice follow-up to this study, as well as the others that you've got planned. And that's pretty exciting, the perivascular inflammation component too, because these plaques are active from an inflammatory standpoint. And then underlying that inflammation, what does that mean? It's really an immune response to something and in a lot of cases, lipid, but also the looking at the pericoronaries and pericoronary inflammation that then that actually starts to get into some of the actual immune trafficking that's going on and sort of actively involved in kind of dynamic changes in plaque, plaque composition and plaque. I guess vulnerability is probably not exactly the right word I'm looking for here. But yeah, I mean, that's, Michael, that's really exciting. I'm really looking forward to seeing a lot more in the, both obviously in the plaque characterization, but also how that then relates to some of the pericoronary measures. I think that'll really lend a lot of insights into the biology that you can't really, you know, unfortunately, we're not really able to get direct coronary plaque immune cells too often. So I think the more we can have imaging markers that get at some of these active processes, the more insights we're going to be able to derive. A great discussion. Before we wrap up, I would like to just get a feeling from both of you. We're not going to serve as a three-person guidelines committee, but do you feel that the data we're seeing thus far from RETRIEVE and this important sub-study would indicate that we should be using statin therapy more liberally in individuals with HIV? Yeah, I'm not sure if I should comment on this because I know there's several active discussions now. Also, of course, a radiologist, I don't prescribe statins. My feeling though is that based on the data on Reprieve, it's likely that guidelines committees will support pitavastatin in people with HIV. It may be based on a different ASCVD threshold than we included in the study when you look at the number needed to treat, but I think that is coming. Okay, I think that's politically correct. Matt, what's your take on this? Yeah, I'll be maybe slightly, not less politically correct, but maybe a little more expansive. So, Michael, I agree with you.
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Will recommendations extend to statins beyond pitavastatin? And I think the answer is likely yes. Pitavastatin is more of a kind of moderate intensity statin. And I think having more flexibility to do higher intensity when needed is going to be important. And there have been a lot of studies now on statins with respect to other antiretroviral medications. And there is some caution that needs to be exercised. But increasingly, there's, you know, reasonable observational evidence that other statins like rosuvastatin and atorvastatin are also reasonably well tolerated in people with HIV. But then I think the real question is, when do we start? And how do our time horizons change? Because in the general cardiology and preventive cardiology field, so much of what we think about is 10-year risk. And a lot of that's based on the calculators we have, the observational studies that inform kind of our effect estimates of the different exposure variables that go into the calculators. But the question is in HIV, if we're seeing ASCD earlier, if we're seeing plaques begin to get a foothold at an earlier phase and then ultimately have many decades of plaque continued progression and vulnerability, how do we think about the time horizon? Do we think lifetime risk? Do we think different time thresholds than a 10-year risk threshold? Do we change our risk estimates knowing that people with HIV in general have about a 1.5-fold higher risk for ASCVD than people without HIV? I think it's a lot of challenging questions, and ultimately, a lot of it is probably going to look at potential benefit weighed against any potential harms, and then also just individualizing the discussion and really making a thoughtful risk-benefit decision that's informed by as best of a precise calculation as we can get, which I don't think our calculations are going to be perfect in people with HIV. But then also placing that in the context of polypharmacy and how do we prioritize statin therapy versus other therapies that are meant to obviously address underlying HIV, antiretroviral therapy being key, but also other components of premature inflammation in people with HIV. So I think a lot of interesting questions. My instinct would be this certainly moves the needle towards more statin therapy in people with HIV. How much more, how early, I think that still remains to be seen. Well, thank you. This has been a great discussion, Michael and Matthew, and certainly underscores that as we gain more knowledge, we also begin to ask more questions. So I'd like to thank Dr. Michael Liu, Dr. Matthew Feinstein for being with us today. And thank you also for listening to this very intriguing podcast. This episode was produced by Daniel Musisi at the JAMA Network. To follow this and other JAMA Network podcasts, please visit us online at jamanetworkaudio.com. And thank you for listening. And thanks again to Drs. Liu and Feinstein.
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Welcome to this JAMA Network author interview. I'm Dr. John Iannion, the Director for the Institute of Healthcare Policy and Innovation at the University of Michigan, and the Editor of JAMA Health Forum. And I'm Dr. Melinda Bunton, Chair of the Department of Health Policy at Vanderbilt University and the Deputy Editor of JAMA Health Forum. JAMA Health Forum is a peer-reviewed, open-access, online journal focused on health policy, healthcare systems, and population health, and one of 12 specialty journals in the JAMA Network. For more conversations like this one on health policy, subscribe to the JAMA Health Forum Editor's Summary, along with all of our JAMA Network podcasts on jamanetworkaudio.com. In this podcast, we'll be speaking with Dr. Anne Thorndyke, a physician researcher at Massachusetts General Hospital and associate professor at Harvard Medical School. Dr. Thorndyke's research focuses on individual and population-level behavioral interventions to prevent cardiometabolic disease. We'll be talking with her today about her article entitled, Assessment of the Massachusetts Flexible Services Program to Address Food and Housing Insecurity in a Medicaid Accountable Care Organization, written with colleagues at Mass General and Brigham and Women's Hospital. Welcome, Anne. Thank you so much. It's a pleasure to be here, and I look forward to our conversation. Well, we do too, because you looked at a very interesting program, and specifically the implementation of that program that was aiming to address food and housing insecurity in a Medicaid context. Can you tell us a little bit about the mixed methods approach you took in this article to bring information to bear on this topic? Sure. So we used a mixed methods approach to evaluate the early implementation of this program because we really wanted to take a deep dive into how this program was working early on to get the data out as soon as possible. So we looked at quantitative data from our health system electronic health record, as well as qualitative data from health system staff and from the Medicaid enrollees who were participating in the FLEX program. Before we talk about the data that you collected for your study, could you tell us a little bit more about the Medicaid ACO program in Massachusetts and the FLEX program for our listeners who may not be familiar with that program? So in Massachusetts, there are 17 Medicaid accountable care organizations. And with the Medicaid 1115 waiver in Massachusetts, $149 million was going to support the Flexible Services Program. Flexible Services is a program in which Medicaid provides resources to the health systems, and they directly pay for food or housing and services for some eligible patients. So it's important to keep in mind that this is not an entitlement program, that this is a program for some eligible patients. There's not enough money to go around for everybody to receive these services. That's helpful. Thanks. And what data did you collect in the course of your study? So we collected data from one Medicaid ACO, the Mass General Brigham ACO. And for this particular study, we limited it to our two largest hospitals and their affiliated community health centers, patients who are affiliated with those health systems. So the data that we collected from the electronic health record included data on social determinant of health screening, which we started in our health system for Medicaid ACO participants in 2018, as well as enrollment in the FLEX program. We got this data from the electronic health record. The other data that we collected was our qualitative data, which was directly from interviews with health system staff and patients. And can you summarize for us the main findings of your study and particularly note any that surprised you? So the quantitative data is really looking at the reach of the program. And so the first thing we looked at was how many people got screened for social determinants of health, for the food and housing insecurity, because that was really the first step in trying to link people with these services. So we looked at screening starting in 2018 through July of 2021. The FLEX program started in March of 2020. So the screening started well before the FLEX program was available. And we found that 57% of the entire Medicaid ACO population was screened at least once for food and housing insecurity. So this is less than what would have been ideal, which is that 100% of people were screened at least once. The goal was that everybody got screened at least annually, but there were a lot of reasons for why this might have happened. The other thing we looked at is the reach of the FLEX program. So what percent of people in the ACO got enrolled into FLEX? And we found that 1.6 percent of adults were enrolled into FLEX and 0.7 percent of children. A positive thing is that most people who are enrolled actually receive services. And this is different from prior programs that because the follow-up was so intensive that we were able to connect most people with their services. And that in this quantitative data, we found that those enrolled in FLEX were really representative of the overall Medicaid ACO population. As far as our implementation evaluation, looking at the adoption, the implementation factors, and some of the internal and external contextual factors, we found several challenges, which included the administrative burden of the program that is related to complex eligibility requirements and time-intensive quote-unquote paperwork, which is really clicking on the EHR, and that the staff really felt that it took about one year to make the adaptations to reduce the administrative burden for this program. There are also challenges related to health system partnerships with the community-based organizations and challenges due to the financial contracts as well as cross-sector differences in communication. The COVID-19 pandemic started in March of 2020, the same month that the program started, and this created a lot of challenges with enrollment. And then patient-reported experiences, some implementation challenges included poor access to services regarding transportation. Sometimes people felt that there was poor fit with their dietary preferences. And overall, those receiving housing services reported lower satisfaction. And just a few facilitators that actually, because I don't want this to be all negative, there were some positives that the MassHealth did provide funding for administrative staff, which was very beneficial, especially to one of our hospitals, that there was a bi-directional data sharing platform that had a few kinks, but actually over time improved communication. There are numerous adaptive strategies within the health system, and that patients did report numerous positive outcomes, particularly around the food resources. So what was the surprise? I'd say the biggest surprise was the low reach of the program. I thought going into this that we'd see more people enrolled, and maybe that was the reality of the funding, but I was surprised that it was that low. But I was also pleasantly surprised that despite there were numerous challenges for the staff, and it was a very difficult time in health care anyway, that overall the staff remained very positive about the program. There was a lot of enthusiasm. And even though it was a lot of work and burden, I think they really believed that this program was the right thing to do. And thanks for that very helpful summary of your key findings. How does your work relate to the literature on addressing health-related social needs? And does this study shed light on whether and how health insurers and accountable care organizations are equipped to address these challenges? So I think that the way that the study adds to the current literature is that this was a real-time evaluation of a policy that was going into place. And this was on purpose that we did this evaluation early because we wanted to get the data out there so that other health systems could benefit from it. I think that it sheds light demonstrating that actually this is possible. This was feasible, that despite challenges that we were able to overcome within the first year or so, that patients received the food services that they wanted. The housing services are more complicated, which we could discuss later if you want. But I think that the feasibility is important. There are many, many challenges that need to be overcome, that need to be figured out with these types of programs. But I think that I feel very encouraged that ACOs and other health insurance programs, that this is all possible. And I think that this is a great next step for doing this type of work. Great. What do you think are the key takeaways from this study for policymakers, including those outside of Massachusetts? And maybe when you answer this question, you could reflect on what you just alluded to, whether there's more evidence or better evidence on the food security side than the housing security side? Yeah, I think that what I would say for policymakers, we didn't look at the effectiveness of this program, but we looked at perceived effectiveness. And there was a perception by patients and staff that the patients were getting a benefit, particularly from the food services. And there is a benefit for some of the housing services, but we just all know that housing is a very difficult problem to address. And more people were enrolled into the food programs than the housing programs. So I'd like to emphasize that to policymakers.
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But I think that there's a lot of lessons learned from what we found in our qualitative interviews with the staff. And I'd say that good implementation of these programs requires that there is adequate funding for administration of the program. Early on, that was a large problem, that it was expected that this program was just going to be rolled out in current workflows. That couldn't happen. People are already too busy. So there does need to be administrative funding. We need better data sharing platforms between the health systems and the community organizations, a better way for the two very different sectors to communicate, and so more investment in those types of platforms. And I think we need continued investment in evaluation of these programs, figuring out how they should be implemented and adapted over time. And I really think that's an important thing to emphasize. These are going to have to be adapted based on what we learn as we go along. And at the end of our podcast interviews, we like to ask a couple of more general questions of our guest authors, and I'll pose the first one. What good advice have you received from mentors about how to be effectively involved in policy debates like the one that you're studying in Massachusetts? So I don't know if I've received advice, but I've learned some things over time, and I have observed mentors and experts in the field, as well as my collaborators. And as a researcher, I just feel very strongly that providing data and rigorous evaluation is the way that I personally can contribute. And I think other health service researchers can contribute. For policies, I think being creative in study design is really important. You often can't do a randomized controlled trial. I love doing randomized controlled trials. They're so neat. But this is not the place where you can use them. But there are a lot of other strategies, study design wise, that you can use. And I think being practical in an approach to these types of problems, meaning that you're thinking about what actually is going to benefit people, listening to the communities and the populations that are going to be affected by the policy is really important. Please talk about the biggest change in health policy that you would expect to see over the next five years? So I don't know if this is what I expect to see or what I hope to see, but I'll talk about them as the same. I think there is increasing recognition that health is determined beyond factors that are related to health care delivery. And I think that that is going to be reflected in policy. I hope. I think that the Flexible Services Program does acknowledge that, that health policy is also food policy and housing policy and these financial policies. And so I think we'll see more integration of these health and social and financial policies as we move forward. At least that's what I hope. That's a good hopeful note for us to conclude on. Thanks to our guest author, Dr. Anne Thorndyke from the Massachusetts General Hospital. To follow this and other JAMA Network podcasts, please visit us online at jamanetworkaudio.com. This episode was produced by Daniel Musisi at the JAMA Network. Thanks for listening.
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Hello out there. This is Dr. Kathy DeAngelis, Theatritor-in-Chief of JAMA, the Journal of the American Medical Association, and this week I'm going to tell you about the October 27, 2010 issue. As usual, I will start with the art on the cover, which this week features a painting by Roberto Antonio Sebastian Mata Anchoron, who lived from 1911 to 2002. It's called A Glimmer of Violence, 1958. He's French, but he was born in Chile. And unfortunately, Chile has seen too much violence in the last couple of months, but something very wonderful with the miners being saved. Now, this cover has a lot of bright oranges and black, kind of a surreal art, just right for Halloween. Now, the first article deals with sepsis and cognitive and functional impairment. In an analysis of data from a subset of participants in the Health and Retirement Study, that's a nationally representative and longitudinal survey of older community dwelling adults who had baseline assessments of cognitive and functional status and whose survey data were linked with Medicare claims information, Dr. Theodore Iwashna and colleagues found that in an incident episode of severe sepsis was independently associated with substantial and persistent new cognitive impairment and functional disability. In an editorial, Dr. Derek Angus from the University of Pittsburgh School of Medicine, who is also a contributing editor with JAMA, he discusses the longer-term consequences of sepsis and implications for patient care and research. And the JAMA patient page has information for your patients about sepsis. The second article actually was published online ahead of print. It is the clinician's corner and deals with diet and physical activity in severely obese adults. Professor Brett Goodpaster of the University of Pittsburgh School of Medicine and colleagues assessed the effects of a one-year intensive lifestyle intervention on weight and cardiometabolic risk among adults with severe obesity who were enrolled in a randomized trial that assigned participants to either 12 months of reduced calorie diet plan and prescribed moderate intensity physical activity or to the same 12-month dietary intervention with the physical activity program delayed for six months. The authors report that participants in both groups experienced clinically significant weight loss and favorable changes in cardiometabolic risk factors. In an editorial, Dr. Donna Ryan from Louisiana State University and Dr. Robert Kushner from Northwestern University School of Medicine discuss obesity treatment and the state of obesity research. And the third article, also published online ahead of print, deals with weight loss in overweight and obese women. Professor Cheryl Rock from the University of California San Diego Cancer Center and colleagues report results of a clinical trial that enrolled 442 overweight or obese women and randomly assigned them to a structured and commercial weight loss program that included prepared calorie reduced meals, physical activity recommendations, and weekly in-person one-to-one weight counseling, or to receive two individualized weight loss counseling sessions with a dietetics professional and monthly contacts. That's the usual care. The authors assessed weight loss at a two-year follow-up and found that compared with usual care, the structured commercial weight loss program was associated with greater weight loss. In an editorial, Professor Rena Wing from Brown University School of Medicine discusses commercial weight loss programs and the importance of evaluating their cost effectiveness. I might add that the commercial program used in this study involved providing the patients with the commercial plan free of charge, which meant that they actually got free food. That's not a bad deal. And the fourth article is the KRAS mutation and metastatic colorectal cancer. Cetuximab is not considered effective therapy for KRAS-mutated metastatic colorectal tumors. However, anecdotal reports suggest that a minority of patients may respond, some with long-term stabilization. Dr. Wendy Dirac from the University Hospital in Guthersburg, Belgium, and colleagues examine the association between KRAS mutation status and survival in a retrospective study of 579 patients with chemotherapy refractory metastatic colorectal cancer treated with cetumabab and found that patients with KRAS PG13D mutations had longer overall and progression-free survival than patients with other KRAS mutations. The fifth article deals with CYP2C19 genotype, clopidogrel, and PCI outcomes. The antiplatelet agent clopidogrel requires biotransformation by cytochrome P450 CYP isoenzymes, and evidence suggests that reduced function variants in CYP2C19 may be associated with diminished platelet inhibition. Dr. Jessica Mega from Harvard Medical School and colleagues analyzed patient-level data from nine studies that evaluated the CYP2C19 genotype and clinical outcomes in patients treated with clopidogrel, primarily for percutaneous coronary intervention in acute coronary syndrome, and found that carriage of even one reduced function CYP2C19 allele was associated with an increased risk of major cardiovascular events, particularly stent thrombosis. In an editorial, Drs. Valentine Fuster and Dr. Joseph Sweeney from Mount Sinai Medical Center discussed the clinical implications of the study findings. We have one commentary in this issue, this one by Dr. Robert Brook from Rand Corporation in California. The end of quality improvement movement, long live improving value. And medical news and perspectives, a move to add a test for severe combined immune deficiency to newborn screening panels nationwide may help more patients with the disorder receive early life-saving treatment. Oversight of fast-track drug approval by FDA stuck in low gear, the critics say. Reports of concussions from youth sports rise along with awareness of the problem. And the National Children's Study expands. And the Health Agencies Update, AIDS Benefits, Egg Inspections Slated, Pharmacogenetics Resources, Regulation for E-C Leanna Nguyen from Boston, Massachusetts, and I quote, you probably don't remember me, but I remember you so well. You were my first ICU admission. And that's from the Red Sox cap. And author in the room teleconference, we invite you to join Dr. Michael Steinman Wednesday, November 17th from 2 to 3 p.m. Eastern Time when he will discuss managing medications for elders with clinically complex medical conditions. And that's it for this week. Thank you very much for listening. Please let me know if you have suggestions to make this podcast more educational or interesting to you. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, speaking to you from beautiful downtown Chicago, where the wind blows mightily, but the patients are always our top priority.
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Welcome to the New England Journal of Medicine summary for the week of July 12, 2012. I'm Dr. Lisa Johnson. This week's issue features articles on MEK inhibition in BRAF-mutated melanoma, potassium channel as a target of immune response in MS, hydroxyethyl starch or ringer's acetate in severe sepsis, blockade of lymphocyte chemotaxis in GVHD, and boosting metabolism, a review article on opioid analgesic overdose, a case report of a man with fatigue, weakness, weight loss, and decreased libido, and perspective articles on redefining the physician's role in assisted dying, on sense and sensitivity, on the birth of antibiotic regret, and on Zen and the art of pediatric health maintenance. Thank you. procedures. This video demonstrates circumcision as performed with a clamp device. Improved Survival with MEK Inhibition in BRAF Mutated Melanoma by Keith Flaherty from the Massachusetts General Hospital Cancer Center, Boston. Activating mutations in serine threonine protein kinase, BRAF, are found in 50% of patients with advanced melanoma. In previous trials, MEK inhibition appeared to be promising in this population. In this study, 322 patients who had metastatic melanoma with a V600E or V600K BRAF mutation received either trimetinib, an oral selective MEK inhibitor, or chemotherapy. Median progression-free survival was 4.8 months in the trimetinib group and 1.5 months in the chemotherapy group. At 6 months, the rate of overall survival was 81% in the trimetinib group and 67% in the chemotherapy group, despite crossover. Rash, diarrhea, and peripheral edema were the most common toxic effects in the Tremetinib group. Tremetinib, as compared with chemotherapy, improved rates of progression-free and overall survival among patients who had metastatic melanoma with a BRAF V600E or V600K mutation. Edward Sovil from the University of Maryland, Baltimore, asks in an editorial, what is so special about Tremetinib as compared with other MEK inhibitors? The preclinical evaluations of Tremetinib revealed a molecule with very desirable mechanistic and pharmacologic attributes. It is an allosteric non-ATP site inhibitor that decreases both activation of MEK by BRAF and the capacity of MEK to act on downstream substrates. We need to maximize the promise of MEK inhibition by using trimetinib perhaps in combination with other pathway inhibitors to define its potential value in tumors without a BRAF mutation but with MEK activation by other routes. Potassium Channel Kier 4.1 as an Immune Target in Multiple Sclerosis by Rajneesh Srivastava from the Technische Universität, Munich, Germany. Evidence suggests that B-cells and antibodies contribute to multiple sclerosis in a subgroup of affected persons. These investigators screened serum IgG from persons with multiple sclerosis to identify antibodies that are capable of binding to brain tissue and observed specific binding of IgG to glial cells in a subgroup of patients. Serum levels of antibodies to Kier 4.1 were higher in persons with multiple sclerosis than in persons with other neurologic diseases and healthy donors. The antibody was present in 46.9% of the group that was analyzed, and it has biologic effects in vivo. Kier 4.1 is a target of the autoantibody response in a subgroup of persons with multiple sclerosis. In an editorial, Anne Cross from Washington University School of Medicine, St. Louis, writes that putting aside a priori assumptions in the search for autoantigens in multiple sclerosis, these investigators took an unbiased approach that resulted in the identification of an unexpected but plausible antigenic target. The specific role of antibodies to cure 4.1 in the pathogenesis of multiple sclerosis awaits further definition. Hydroxyethylstarch 130.4-2 vs. Ringer's acetate in severe sepsis by Anders Perner from Copenhagen University Hospital, Denmark. Hydroxyethyl starch is widely used for fluid resuscitation in intensive care units, ICUs, but its safety and efficacy have not been established in patients with severe sepsis. In this study, patients with severe sepsis were assigned to hydroxyethyl starch or Ringer's acetate. At 90 days after randomization, 201 of 398 patients, 51%, assigned to hydroxyethyl starch, had died, as compared with 172 of 400 patients, 43%, assigned to Ringer's acetate. One patient in each group had end-stage kidney failure. In the 90-day period, 22% of patients assigned to hydroxyethyl starch were treated with renal replacement therapy, versus 16% assigned to Ringer's acetate, and 10% and 6% of patients, respectively, had severe bleeding. Patients with severe sepsis assigned to fluid resuscitation with hydroxyeth-versus-host disease, GVHD, is a major barrier to successful allogeneic hematopoietic stem cell transplantation. The chemokine receptor, CCR5, appears to play a role in alloreactivity. This study tested whether CCR5 blockade with the CCR5 antagonist, Mraviroc, would be safe and limit GVHD in humans. Mraviroc-c inhibited CCR5 internalization and lymphocyte chemotaxis in vitro without impairing T-cell function or formation of hematopoietic cell colonies. In 35 patients who could be evaluated, the cumulative incidence rate of grade 2 to 4 acute GVHD was low at 14.7% on day 100 and 23.6% on day 180. Acute liver and gut GVHD were not observed before day 100 and remained uncommon before day 180, resulting in a low cumulative incidence of grade 3 or 4 GVHD on day 180, 5.9%. The one-year rate of death that was not preceded by disease relapse was 11.7%, without excessive rates of relapse or infection. Serum from patients receiving Miraviroc prevented CCR5 internalization by CCL5 and blocked T-cell chemotaxis in vitro, providing evidence of anti-chemotactic activity. In this study, inhibition of lymphocyte trafficking was a specific and potentially effective new strategy to prevent visceral acute GVHD. Management of Opioid Analgesic Overdose, a review article by Edward Boyer from the University of Massachusetts Medical Center, Worcester. Opioid analgesic overdose is a preventable and potentially lethal condition that results from prescribing practices, inadequate understanding on the patient's part of the risks of medication misuse, errors in drug administration, and pharmaceutical abuse. Three features are key to an understanding of opioid analgesic toxicity. First, opioid analgesic overdose can have life-threatening toxic effects in multiple organ systems. Second, normal pharmacokinetic properties are often disrupted during an overdose and can prolong intoxication dramatically. Third, the duration of action varies among opioid formulations, and failure to recognize such variations can lead to inappropriate treatment decisions, sometimes with lethal results. Opioid analgesic overdose encompasses a range of clinical findings. The sine qua non of opioid intoxication is respiratory depression. The presence of hypopnea or apnea, meiosis, and stupor should lead the clinician to consider the diagnosis of opioid analgesic overdose, which may be inferred from the patient's vital signs, history, and physical examination. In patients with severe respiratory depression, restoration of ventilation and oxygenation takes precedence over obtaining the history of the present illness or performing a physical examination or diagnostic testing. Naloxone, the antidote for opioid overdose, is a competitive mu-opioid receptor antagonist that reverses all signs of opioid intoxication. A 27-year-old man with fatigue, weakness, weight loss, and decreased libido. A case record of the Massachusetts General Hospital by Daniel Hunt and colleagues. A 27-year-old man with a history of obesity was seen in the endocrinology clinic at the hospital because of fatigue, myalgias, weakness, weight loss, and loss of libido. Thirteen months before presentation, the patient reported weighing 108.9 kilograms, body mass index 35.4, and began aerobic exercises two hours daily and a calorie-restricted diet, 2,400 kcals daily, resulting in a loss of 36.3 kilograms in 10 months. Two months before evaluation, arm weakness, numbness and aching in his legs, decreased libido with loss of morning erections, and a faint, lacy rash on his legs developed. He reportedly stopped aerobics, began lifting weights, and increased his caloric intake, without improvement in his symptoms. Approximately five weeks before this presentation, the patient was admitted to the hospital because of a submandibular abscess in the neck associated with dental caries. The patient reportedly stopped exercising but continued to lose weight. On examination, the patient was cachectic with bitemporal wasting. Marked abnormalities in liver function were noted, and chest imaging revealed pneumomediastinum.
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It's highly unusual for air in the mediastinum to be incidentally detected in a young man during evaluation for weakness, myalgias, weight loss, and loss of libido. Obesity and Pharmacologic Control of the Body Clock A Clinical Implications of Basic Research article by Stephen Shea from Oregon Health and Science University, Portland Knowledge of the mechanisms that govern mammalian circadian rhythm permits the molecular manipulation of these mechanisms. In mammals, a central circadian pacemaker exists in the suprachiasmatic nucleus of the hypothalamus that orchestrates the many circadian rhythms in physiological processes and behaviors. The circadian molecular clock exists in all cells in the body and consists of a positive limb and a negative limb. It is modulated by the nuclear receptor Rev-erb. Cells in the suprachiasmatic nucleus form a network of interactions, resulting in altered ion channel activity and, ultimately, neural output with a circadian rhythm. This circadian neural output then acts directly or indirectly, such as through intermediary endocrine signals, to synchronize the activities of the peripheral organs. However, peripheral cells also contain the circadian molecular clock. The authors of a recent study found that synthetic rev-herb agonists can affect clock function in the suprachiasmatic nucleus and peripheral sites and can cause weight loss in obese mice. Redefining the Physician's Role in Assisted Dying A perspective article by Julian Prokopitz from the Brigham and Women's Hospital, Boston. Terminally ill patients spend their final months making serious decisions about medical care and the disposition of their assets after death. Increasingly, they are also choosing to make decisions about the manner and timing of their death, and many are completing advanced directives to withhold life-sustaining treatment. A controversial facet of this trend toward a more self-directed dying process is the question of assisted dying, whether patients should have the option of acquiring a lethal dose of medication with the explicit intention of ending their own life. This practice is generally illegal, but there is a movement toward greater social and legal acceptance. Data from places with legal-assisted dying have allayed concerns about potential abuses and patient safety, but a lingering challenge comes from the medical establishment. Many medical professionals are uncomfortable with the idea of physicians playing an active role in ending patients' lives, and the American Medical Association and various state medical groups oppose legalization. This position is not an insurmountable barrier, however. The authors propose a system that would remove the physician from direct involvement in the process. They envision the development of a central state or federal mechanism to confirm the authenticity and eligibility of patients' requests, dispense medication, and monitor demand and use. Sense and Sensitivity Teaching Physicians to Think About Costs A perspective article by Lisa Rosenbaum, an editorial fellow at the Journal. Imagine your first medicine rotation. You present a patient admitted overnight with cough, fever, and an infiltrate on chest x-ray. After detailing a history and physical, you conclude, this is a 70-year-old man with community-acquired pneumonia. Dead silence. Perhaps, the attending finally says, but what else could this be? Your face reddens. Pulmonary embolism, you say. The resident nods. Heart failure, now you're talking. Chirk Strauss, you add. The patient does have a history of asthma. The attending smiles. How might you investigate these other possibilities, he asks. Next thing you know, the patient's lined up for a chest CT, lower extremity Doppler's, echo, and a room panel. You get honors. And so it begins. Our profession has traditionally rewarded the broadest differential diagnosis and a patient care approach that uses resources as though they were unlimited. Good care, we believe, cannot be codified in dollar signs. But with health care costs threatening to bankrupt our country, the financial implications of medical decision-making have become part of the national conversation. Some physicians now believe that considering costs as well as risks and benefits when making medical decisions serves not only the equitable distribution of services, but also the real interests of individual patients. How should that change medical education? Finland, Weinstein, and the Birth of Antibiotic Regret, a perspective article by Kent Sepkiewicz from Memorial Sloan Kettering Cancer Center, New York. In 1953, two pioneers in the field of infectious diseases, Maxwell Finland and Louis Weinstein, co-authored an article in the journal describing the numerous untoward effects caused by antibiotic chemotherapy, then a new form of treatment. With characteristic thoroughness, they gave an organ-by-organ accounting, skin reactions, hepatitis, mental status perturbation, hypersensitivity, gastroenteritis, and all the rest. In many ways, the article marked antibiotics' official fall from grace. Finland and Weinstein knew something larger was up, that for each step of progress, some new problem could and would arise. Their comments were among the first to sound the alarm about the likelihood that, ironically, antibiotics might introduce a new health monster that, pound for pound, was as bad as the misery-inducing but relatively predictable Staphs and Streps of yesteryear. In the 60 years since Finland and Weinstein's review, we have continued to worry mightily about the risk of unleashing the doomsday organism. Standing on the shoulders of giants such as Finland and Weinstein, we seem not to be celebrating the miraculous progress we have made, but wallowing in our feckless ineptitude. In doing so, we have also promoted the notion that the field of clinical medicine is far simpler than it actually is. In the daily tumult that is clinical care, antibiotics have bailed us all out countless times. Zen and the Art of Pediatric Health Maintenance, a perspective article by Perry Klass from New York University, New York. Dr. Klass was on a secluded Caribbean beach, floating on her back under a postcard sky, rolling in the gentle swells, and praying, Please, next time let me pay attention. Don't let me do this again. Before she left for vacation, she had seen a baby whose mother was taking him to Haiti, and Dr. Klass had conscientiously followed the Yellow Book anti-malarial recommendation to give him prophylactic chloroquine. The baby was on digoxin because of a congenital cardiac defect, but he was feeding and growing well. So Dr. Klass made sure his mother had enough ditch for the trip, recommended that she identify a pediatrician in Haiti to call with any problems, and quickly reviewed the signs of heart failure. Here's what she didn't do. She didn't say to herself, gee, I don't take care of many babies on gejoxin, so maybe I should check whether there are potential interactions with chloroquine. Instead, a day or two later, it occurred to her to wonder. And she read that chloroquine might increase the blood digoxin levels. The combination was not recommended and could be dangerous. She remembers feeling in the pit of her stomach, oh no, I didn't pay attention. I did something dumb. She couldn't reach the mother, and she went on vacation. Clinical medicine makes you worry, and a good thing, too. When routine care gets too routine, a physician may end up not completely there, in the exam room. Can we learn to be truly in the moment during visits, to still ourselves, concentrate our minds, pay attention. The images in clinical medicine features a 69-year-old man who presented for evaluation of an unusual color and decreased mobility on the right side of his tongue. The patient had undergone radical dissection of the right side of the neck seven years earlier for a malignant tumor of the right tonsil. Intraoral examination of the patient revealed hemiatrophy of the tongue on the right side and the inability to completely deviate the tongue toward the left side of the mouth on protrusion. A CT scan showed atrophy of the right side of the tongue with fatty infiltration. The hypoglossal nerve, cranial nerve 12, supplies motor innervation to the muscles of the tongue. Damage to the hypoglossal nucleus or hypoglossal nerve can cause denervation atrophy of the tongue, as seen in this patient. During radical neck dissection, the cranial and cervical nerves are at risk for injury. A 43-year-old woman presented to the hospital after five days of itchy, diffusely distributed evanescent lesions. Ductal carcinoma of the breast had been diagnosed 11 years earlier. Despite breast-conserving surgery, radiation, and several rounds of chemotherapy, metastatic disease to the liver and bone had developed. Physical examination revealed diffuse, large, edematous plaques that were yellow with an erythematous edge. Blood testing revealed that the patient had hyperbilirubinemia and elevated aminotransferase levels. A skin biopsy specimen revealed edema, and Hall's staining of the specimen for bilirubin revealed focal deposits of olive green crystals. Yellow urticaria was diagnosed.
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This concludes the summary of the July 12 issue of the New England Journal of Medicine. We're interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at NEJM.org. Thank you for listening.
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Hello, this is Aaron Van Dorn from the Lentz New York office. Today I'm speaking with Dr. Rodrigo Hasbun from the University of Texas Science Center in Houston, where we discuss research into bacterial meningitis in the United States. Dr. Hasbun, how did you gather the data for your study of the epidemiology of bacterial meningitis? Well, it's based on a national inpatient sample database that is part of the Healthcare Cost and Utilization Project. It's a free online database that's accessible to anybody to provide studies based on ICD-9 codes. Can you summarize your findings on the incidence of inpatient mortality for the most important causes of bacterial meningitis? Well, we analyzed the epidemiology of not only three community-acquired pathogens, the most important ones, pneumococcus, meningococcus, and H. influenza, but also we looked at the prevalence of two common nosocomial meningitis pathogens, gram-negative meningitis and staphylococcus meningitis. And what we learned from our study is that pneumococcal meningitis is still the most prevalent meningitis pathogens, but the incidence has steadily dropped since 1997 to 2010. And that is, you can see that correlated with the introduction of PCV7 in the year 2000 as well. There's a significant drop after that introduction. There's also been a decrease in the incidence of Neisseria meningitidis after the introduction of MCV4, the conjugate meningococcal vaccine. Now, at the end of the study period in 2010, the incidence of Haemophilus influenzae is lower than the nosocomial meningitis pathogen SAF in gram-negative meningitis. There's also been a decrease in mortality that we saw in patients with pneumococcal meningitis. And this is associated, at least temporarily correlated, with the introduction of the recommendations of adjunctive dexamethasone. We cannot really know how many patients in the study were treated with steroids. So this is just an association study, but it's a very striking decrease that we have documented in the mortality of the most common meningitis pathogen, strep pneumo. And speaking of the vaccines that you mentioned earlier, why do you think hospital admissions for bacterial meningitis were declining even before the introduction of PCV7 and MCV4 vaccines? You know, it's unclear. Database is very limited in the content of the data that we have. We saw a decrease of patients being discharged with home health, and that's possibly due to, you know, there's decreased neurological morbidity after the introduction of steroids. But again, all this is just very difficult to address in analyzing a database where there's not a lot of specific comprehensive clinical data on the patient. What effect do you think the recommendation for the use of adjunctive dexamethasone had on the mortality from pneumococcal meningitis? Again, in the Netherlands, they were able to clearly demonstrate a decrease in the mortality of pneumococcal meningitis after the introduction of steroids. In their study, they were able to document the degree of how much steroid use was being given to those patients before and after the recommendations by the IBSA guidelines. In our study, we don't have that data, but we're seeing similar results in regards to a decrease in mortality after the introduction of adjunctive dexamethasone. So this is encouraging because streptococcus pneumoniae, not only being the leading pathogen of bacterial meningitis, is also the leading pathogen of adverse outcomes, including death and neurological disability. So this is great news that we're finally seeing a decrease in mortality in patients with pneumococcal meningitis. And is there anything else our listeners should know about bacterial meningitis? Yes. There's basically two types that were analyzed in our study. The three most common community-acquired pathogens and the two most common nosocomial-acquired pathogens. And this is in distinction to similar studies done from the UK and Wales where community-acquired meningitis was the most important pathogen being analyzed in their studies. In our study, we were able to look at other pathogens as well and see how those are also affecting patients in the United States. Well, thank you very much for your time. Really appreciate it. Thank you so much, Aaron.
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Hello, welcome to a podcast for The Lancet Oncology, which forms part of our March 2019 issue. I'm Gavin Cleaver, and I'm delighted to be joined on the phone today by Bianca Herben to talk about her recent work with the SIOP Radiotherapy Working Group. Dr. Herben, thank you so much for your time today. No thanks at all. Please could you give us a little bit of background to the SIOP Radiotherapy Working Group, and then maybe go on to talk about why it was particularly important, in opinion to investigate vertebral radiotherapy dose for children. Well the SILP is short for the European Society for Pediatric Oncology and the radiotherapy working group is an international group of pediatric radiation oncologists from Europe. They aim to include as many European countries as possible, and they want to train and unify radiotherapy policies across the field. And I just felt that this is especially important since there are great differences between countries in survival of pediatric cancer as well as long-term side effects. And the goal is to equalize and improve those health outcomes. And the radiotherapy working group organizes meetings, workshops, teaching courses, and they provide peer recommendations to guide optimization of radiotherapy protocols. And this is mostly done because the field of radiotherapy is becoming more and more complex because of new radiotherapy modalities and techniques, but also because there are more and more findings in molecular biology of pediatric cancers, as well as differences in systemic treatments. So the field is constantly moving, and it's important for pediatric radiation oncologists to stay on top of all those developments, in essence to increase chances and quality of life for their patients. And there are about 250 pediatric radiotherapy centers across Europe, so equalizing therapy strategies is, well, to say the least, not the easiest task. And the particular task force on vertebral radiotherapy was formed because we discovered that even very experienced radiation oncologists had different approaches to radiotherapy of spinal volumes in growing children. So they all knew that inhomogeneous radiotherapy could cause skewed growth of vertebrae and development and functional problems such as scoliosis. And they all had taken away certain ideas from literature as well as their own experiences, of course, and they had worked with that for years. And in the past, when using 2D and 3D radiotherapy planning, there was not much to work with because you had the inherent features of radiotherapy beams that you had to accept, and there was only minimal room to individualize or adapt your radiotherapy doses. But nowadays, you can use intensity-modulated proton therapy or proton therapy, and it gives you a lot of freedom to really regulate your dose over any tissue volume but that also means that you can give a really sharp dose fall off over vertebrae and potentially cause more growth problems if you're not careful if you don't think about that so to explore different approaches and local practices concerning radiotherapy over spinal volumes, we sent out a survey with multiple questions to different centers, and we asked about what dose could cause bones to stop growing, what gradients they believed would skew growth, what age cut-offs they would use if they thought there was a difference between sexes, so if boys would have different effects than girls, et cetera. And we found that the answers to that survey were really variable. So we knew that it would be good to come to a more broadly accepted peer consensus, and we would like to base that on a literature review. And everybody in the group felt that it was a really important subject to tackle simply because none of the specialists had the definite answers to the problem of vertebral radiotherapy. And I'm very pleased that in the end people from 35 centers across Europe worked together in parts of the project and 32 representatives from 27 centers in 11 countries from Europe worked on the final manuscript. What we did was we made an interview of the literature and then we organized a workshop and through much discussion developed a consensus that is now published. And based on current knowledge, working with information mostly from old techniques, this is, we think, what we know and can advise to our view. But we mostly view these guidelines as a starting point from which to work out new studies and through that come to new and better validated understanding of radiotherapy effects on vertebral growth. Yeah, so important to develop a consensus in these areas. Tell us then about some of the key recommendations that came out of your paper and the literature review, especially with respect to a homogenous radiotherapy dose, which is very interesting. So after doing a review on normal spinal development and literature on radiotherapy effects of the vertebral growth. We also looked at how to establish the end of the most important growth for a child, and we deemed that the end of the acceleration phase of the pubertal growth spurt. And with all that information, we summed up the five most influential factors on development aberrations. And those factors are partially interrelated, but we deemed age at which a tumor presents, and of course the child is treated very important. The total radiotherapy dose that is given, but also radiotherapy dose in homogeneities over the vertebrae, and the location of primary ossification centers and growth plates of the vertebrae. That is where radiotherapy exerts most of its effect. And also we found the number of vertebrae that are irradiated of importance. But I think we start the guideline with an important message, and that is to keep thinking for yourself when you are prescribing a dose. So if a very important organ is at risk near the vertebrae, you may want to accept more inhomogeneity over the adjacent vertebrae than when there's no special consequence of giving a bit more pyrovertebral dose. To give an example, if a child only has one kidney left after nephrectomy for a Wilms tumor, you will design your radiotherapy plan to put an acceptable risk on that kidney and then you see what you can do to put least strain on the vertebrae. So overall, we recommend to keep the radiotherapy dose homogeneous in all directions of the vertebrae that are within your treatment field if you can do this. If not, convenient because there are other tissues at risk near the vertebrae that need sparing. We are given advice on what kind of limits may be acceptable to invoke only minor changes of the vertebrae when the child grows. So in general, we state that there's a dose effect per gray given, and at any dose level, there's a more pronounced effect at a younger treatment age. So for example, under the age of two, there's a substantial impact on vertebral growth even at doses below 10 grades. But between two and six, that starts at doses of about 15 grades. And when a child is six up to the end of the puberal growth, that is about 35 grades. So big differences there. And we found that after the end of the acceleration phase during puberty, radiotherapy will have only very insignificant effects because the growth has almost stopped, so we have more liberty to have inhomogeneous doses from that age onward. We recommend to assess the end-of-growth acceleration for teenagers between about 10 and 16, and we recommend to use the Risser criteria and the Silver-Grain criteria, and they use x-rays of pelvis and the elbow. And we have added an appendix to the paper to explain how to approach these classifications. So then we come to the radiotherapy gradients that may be acceptable. So if you need to accept those gradients, we deem gradients that are given in the left-right direction as most detrimental, but also posterior-anterior gradients, especially for partial spine radiotherapy, can cause scoliosis, for example. We advise to accept steep gradients in the cranial caudal direction. And then in the paper, we proceed to give some direction to what gradients to accept in those different directions for different age groups and different prescription doses. If you irradiate a paravertebral target in the thoracic region, we advise that, of course, if possible, without compromising your target, you limit the number of vertebrae to seven, especially in children under the age of six and if you give doses above 20 grades. Because if you cause too much growth stunting for the thoracic vertebrae, you can cause underdevelopment of the thoracic cage and potentially induce respiratory problems later in life. But this is more of a tricky recommendation because there's not a specific guidance for this in the literature. Okay. So the recommendations that you put forward arising from the framework, they're quite open-ended, so they can be revised as more data become available. So what research is needed from here on in, and what's expected in this setting that might change or adapt these recommendations, do you think? Well, we do get some suggestions about this in the paper. First of all, we feel that there's a definite need for more high quality and preferably multi-institutional research on this subject.
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So potential designs for such future studies could focus on several aspects of vertebral growth development. You could use a retrospective multicenter setting to gather big data from patients who were irradiated on the spinal axis and who have received high-quality imaging during their follow-up. And you could analyze those data to develop prediction models. So in parallel, going forward with the recommendations that we put out in this paper, you can gather new data from patients treated with IMRT techniques to be collected, and then you can validate and refine the prediction models that you came up with from the retrospective studies. And then you can correct the guideline when that is indicated. And in addition, you can also see if vertebral growth disturbances need to be correlated with functional outcomes. So some growth disturbances can be objectified, but maybe the child or the adult will not have many problems because of that skewed growth. But you can organize that through multidisciplinary-related effects of patient clinics or scoliosis clinics, and you can involve orthopedic surgeons, rehabilitation specialists, and through that you can get a validated and more precise view of the problems and then re-evaluate how to organize your radiotherapy to prevent these as much as possible. Well, it's really important that guidelines were standardized in this area, and you can read Dr. Herben's work and her colleagues' work, online now at thelancet.com and you can read it in our March 2019 issue of the Lancet Oncology. Dr. Bianca Herbin thank you so much for your time today. Well thank you for the opportunity to present our work.
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I'm Stephen Morrissey, managing editor of the New England Journal of Medicine, and I'm talking with Arthur Kellerman, a policy analyst at RAND and an emergency medicine physician. Dr. Kellerman has co-authored a perspective article on lessons from the Boston response to the Marathon bombing. Dr. Kellerman, in your article, you point out that there were a number of factors that were not under the control of Boston's medical responders, but that favored the provision of rapid and effective care for the victims of that bombing. Which factors do you think were most critical? Well, in terms of event severity, as terrible as the bombings were, they could have been much worse. The devices were relatively crude and of relatively low yield compared to those that are often detonated in the Middle East. So the magnitude of the blast reduced the casualty count as high as it still was. It could have been a lot worse. And the other important factor were that the devices were placed out of doors. There's now ample evidence that when bombings are carried out in a closed space, inside a building, a subway tunnel, a bus, a train, the walls of the structure amplify and reverberate the blast and create more severe injuries. In terms of response, there were a number of factors that played into the favor of the rescuers. It was race day. There were pre-positioned fire, police, and EMS personnel. Boston's bystanders responded with class. Instead of going crazy and racing everywhere, many of them pivoted almost moments after the blast and began rendering assistance. EMS in Boston has long performed well. They did an excellent job of routing and distributing casualties. Because it was Boston and given the location of the attack, it was in the center of a complex with rich resources in terms of trauma centers relative to many cities and certainly more rural areas. It was 3 p.m., so you had the day shift and the evening shift physically in the hospital at the moment of the blast. And the city and the hospitals had done a good job of preparing. But the timing, the nature of the devices, their placement, and the fact that you had pre-positioned resources all acted in favor of the rescuers and ultimately gave the victims a much better shot at survival and helped attribute a remarkably low fatality count for such an event. You speculated that since it was a holiday, the city's operating rooms probably weren't running at full capacity. But in fact, prospective authors from the Boston hospitals indicate that the ORs were booked and most emergency departments were also full. So was the key that they had capacity on the hospital wards or, in the case of psychiatric patients, that there were other hospitals to which they could be moved so that the EDs and the ORs could be emptied quickly to make room for the bombing victims? The most important aspect is being able to rapidly open up your emergency apartment, your operating rooms, and within a matter of hours, your critical care units. And those tend to be the most bottlenecked locations in any hospital at any point in time. So one of the factors that I think really is a tribute to Boston's hospitals were how quickly they grasped the nature of the event and how aggressively they moved to clear their emergency departments for incoming casualties and to get operating room space opened. If they had not made that decisive action, it would have been a much more difficult situation for them. So that decisive action is critical. Often the most important decisions, particularly in a sudden event like a bombing, are made before the first victim comes in the door. And my hat's off to Boston's hospitals in this case. In that regard, you clarified that Boston had planned carefully and had drilled repeatedly for such an event well before it happened. Can you walk us through some of the key elements of that kind of planning? Well, the first thing to understand, and very importantly, are that terrorist bombings, tornadoes, earthquakes, other sudden what I call kinetic events are both qualitatively and quantitatively different than many of the disasters that hospitals drill or prepare for. When you have a flood, a hurricane, an epidemic, you have warning it's coming, you have an opportunity to prepare, you can sort of pre-position, and the event typically ramps up over hours or in some cases even days. But in these events, like the Boston bombing, it is a sudden surprise. You have no time to prepare a ramp up. You may have just a few minutes before the first casualties roll in the door. So the most critical actions in many instances are in that lull before the storm. When the scene is chaotic, units are responding, the casualty count is often highly inaccurate and may be wildly inflated or undercounted. That's when you have to be moving as aggressively and decisively as when you're fully engaged. That's an important premise that drills that are properly designed teach and that staff who take drills seriously can master and be much better when the time comes. You want to be responding from muscle memory, not searching for a manual and trying to find if it's on page 25 or page 48. There were a number of critical steps that were taken, and these were described in short form in an essay that my co-author, Dr. Kobe Pellig of Tel Aviv University and I wrote a few years ago, and it's cited in the Perspective article. But a far more authoritative source, and one I'd recommend all of your listeners pull up on the web, is a CDC monograph entitled, In a Moment's Notice, Surge Capacity for Terrorist Bombings. It walks through ER, operating room, blood bank, radiology, other logistical issues that hospitals need to consider and that EMS needs to consider to prepare for these events. It's very easy to find and download off the CDC's website. Something the Israelis learned years ago and we would do well to study is that if you practice and become really good at managing a bombing, the core skills that you need to do that, the decision-making, the preparation, the decisive action, will serve you in good stead for any disaster that you might have to encounter. And in this era of terrorism, it's quite likely that hospitals will deal with a terrorist bombing and never have to contend with the far more exotic WMD-type events that we spent much of the last decade preparing for. So the basics matter, and doing them well matters, and good disaster plans emphasize that fact. One of those basics might be teamwork, which was clearly essential in this response, both within hospitals and in the overall emergency response system. What sorts of preparation should be made across institutions to ensure that teams can form quickly and then collaborate effectively? Teamwork is absolutely critical. You can't get through a busy night in an emergency room or an OR as a cowboy or a cowgirl, you certainly can't do it in a mass casualty event. Disaster plans should ideally be straightforward, simple, clear, and very easy to follow. I've often said that the likelihood that a disaster plan in a hospital will work is inversely related to the thickness of the document. The more complicated, the more tabs it has, the less likely anyone will read it, understand it, or even refer to it when the time comes. Basic elements should form the foundation, and people should practice together, not just within their typical group or tribe, surgeons with surgeons, nurses with nurses, but across disciplines and across units. The best drills are actually smaller real-world events. We often don't pay enough attention to handling how we responded to a three-vehicle car crash, for example, how we responded to a bus crash that turned out to be a minor event rather than a major event. It's those no-notice instances when we are called to go beyond the normal trauma response or the normal emergency response that really begin to stress the staff but also emphasize how well they're working together. And so those natural exercises can be very helpful. Scripted events, which are the typical approach most American hospitals take, are certainly better than nothing, but they tend to be dress rehearsals. Everyone has plenty of time to prepare. The most senior or the leadership people are all pre-positioned with time off from their workday. A far better approach is to plan and to use no-notice exercises. My colleagues at RAND recently devised a prototype no-notice exercise that actually doesn't disrupt hospital operations but can challenge your emergency operations center, your incident commanders, key decision makers, and be over and done and documented in less than two hours. That prototype has been completed. We've pilot tested it in several major trauma centers around the country and have had initial discussions with Joint Commission about refining it and hopefully offering it to America's hospitals. I can tell you from having participated in these pilot developments, it is a totally different experience than a typical dress rehearsal drill and something every American hospital should consider and regularly use. In their perspective article about the response at Brigham and Women's Hospital, Goralnik and Gates also point to the specific experience of several individuals in the hospital, for example, in Haiti after the 2010 earthquake.
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It's certainly helpful. Veterans typically respond better than rookies in any situation because they've worked under stress before. They have some background or perspective on the event. But I think perhaps more helpful over time, probably in Boston and certainly in the country, is the collective sharing of experience and lessons learned as our veteran military health personnel, the doctors, the nurses, the technicians, the medics, and others returned to the United States from experience in Iraq and Afghanistan. Their collective knowledge of not just how to handle bombing victims, but multi-casualty events, the surgical techniques that were developed, such as damage control surgery and the greater use of external fixation in severely complex orthopedic cases, the use of tourniquets in pre-hospital settings. A number of remarkable innovations that the military health system has championed out of necessity in the past 12, 13 years are ultimately going to advance emergency and trauma and disaster care in this country every bit as decisively as our battlefield experience in Vietnam and in Korea did for earlier generations. So I think it's that collective expertise being brought home that really will make a difference over time. A third perspective article laments the fact that U.S. health departments, hospitals, EMS systems are facing severe budget constraints, owing in great part to cuts in federal funding. And those constraints will undermine planning, training, practice activities. Do you see this as a serious problem now? It's an enormous problem, and it's been getting worse for years. Ironically, even when we had that flood of federal funding after September 11th, much of those resources were tightly earmarked and dedicated to WMD and particularly to bioterrorism. Local health departments and preparedness planners weren't allowed to use the money to do broad-level preparedness. They had to keep it very tightly focused in programmatic areas. So in some respects, while it clearly helped, it didn't help as much as it might have. But now we're seeing a rapid erosion of core funding for public health, core funding for EMS, and even core funding for hospitals, emergency and trauma care operations. And I equate this to pulling planks out of a bridge. You can get away with it for a while. People can compensate for a while. But if you hollow the structure out to a critical point and then put it under a load, the entire apparatus can collapse. And all that will come out of that is grief and calamity. It's equally dangerous to think that the daily business of hospital operations, keeping a hospital going, is more important than having that capacity for a major challenge. That's why too many hospitals allow their emergency departments to get gridlocked and bottlenecked with admitted patients because they're more concerned about keeping the high reimbursement, high margin elective cases flowing smoothly, and they're willing to back up the emergency rooms admitted cases to allow those electives to get in ahead of them. Too many hospital boards put the purchase of a surgical robot or a new scanner higher on their capital list than they do a reliable and well-positioned generator. And that can create real problems for an entire community in a major event. So that preparedness really does have to be seen as part of the fundamental mission of any hospital in its relationship to the community and its role as part of our nation's health security. And perhaps the third threat, which is hard to imagine in light of, number one, funding cuts, and number two, the daily demand, is complacency. I know too many hospital administrators that have blandly assured me over the years, don't worry about a crowded ER. Don't worry about the fact that all our hours are full. Don't worry that every ICU bed is occupied. If we're challenged, my doctors and my nurses will rise to the occasion. That's total nonsense. You can't under-resource your medical staff. You can't under-prepare your medical staff and then expect that they will instantly, on no notice, in the heat of the moment, perhaps at 2 o'clock a.m. rather than 3 p.m., figure out what to do. That's a very dangerous and misleading assumption. We have to give our medical staffs, our EMS providers, and the key people who are involved in preparedness at the community level sufficient resources to do their jobs and sufficient opportunities to hone and refine their skills. You're not going to get a second chance. You write, in fact, that hospitals need to weave the threads of preparedness into their daily routine. So what exactly would that entail? There are several values that we really have to mainstream, I believe, in hospital operations. First, as you discussed earlier, is the focus on teamwork. The Red Sox didn't win the World Series because they just showed up or it was their turn. They practiced, they picked good personnel, they worked as a team, and they focused on results. Another key value in hospitals is understanding the critical importance of patient flow. Everybody should be moving to that system as efficiently and as effectively as possible. If a patient is discharged out of an inpatient bed and the floor nurse doesn't call housekeeping for two or three hours because it's getting close to the end of shift, and then housekeeping comes and cleans the bed and the next nurse doesn't call housekeeping for two or three hours because it's getting close to the end of shift. And then housekeeping comes and cleans the bed and the next nurse doesn't call because she thinks or he thinks that if it's, you know, another hour or two, it'll be the next shift's problem after that. Admissions are backing up in the emergency department. It's inexcusable that there are hospitals in America today that will have admitted patients in hallways of their ERs, in trauma bays, in exam rooms, and have empty inpatient beds upstairs because they simply aren't focusing adequately on patient flow. The same is true when you're considering how to balance electives, how you schedule your operating room cases. We can manage America's hospital resources far more efficiently and effectively than we do today. And there are tracking systems and computer algorithms and other tools that allow hospital administrators, chiefs of service, and physician and nursing leadership to do that. A third issue is being aware of your resources. How many beds do you have right now? How many spare generators? What is the diversion status of hospitals in the community? It should be zero all the time. Are we adequately prepared? How did we do on the last drill? How did we do when we ran a no-notice drill? And ultimately, accountability. Again, I look to a country like Israel that has had to deal with more of these events, quantitatively and qualitatively, than the United States, fortunately, to date. They take a very no-nonsense approach to this. They have the medical staff of one hospital stage the drill in another hospital. They expect their hospitals to regularly share and report their critical care capacity, backup supplies, and how crowded or uncrowded their emergency departments do. The last part of a hospital that they will allow to back up and get congested with patients are their ERs. That tends to be the first unit of an American hospital that gets congested. These are very doable things. Remember, as much as we complain about how under-resourced we are in health care, we are using 18% of the nation's GDP and over $2.7 trillion a year. So this is not about lack of resources. It's about prioritization and choices. And we should prioritize life and death care and preparedness for threats to a community and to our nation higher than we currently do today. So what should other U.S. cities, perhaps without Boston's facilities, do to be prepared for these kinds of mass casualty events? Well, the first thing they can do is not say, wow, Boston did pretty well. I'm sure we will, too. Boston's success, the astonishingly low fatality count in this case, the swift evacuation of casualties, the way that they were distributed to different trauma centers so that no single hospital was overwhelmed with casualties, that wasn't happenstance. That was done because of thoughtful preparation, practice, and a commitment at a community level and at a service level to doing the right thing in the right way. Other hospitals can learn from that, can learn from Boston's success. They can and should monitor their surge capacity on a regular, continuous basis. They should be aware of emergency department crowding. I think it's interesting that Massachusetts a few years ago said, basically, we're not going to let people divert ambulances anymore. You have to be able to deal with incoming ambulances, and I think that has helped Boston to do a better job. Hospitals and communities need to be more serious about supporting their local EMS providers and giving them the opportunity to do drills and practice. And all of us throughout this country, urban communities and suburban and rural towns, need to do more to recognize how important bystanders are.
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It's your neighbor or you who will be the first responder. And so basic first aid skills, basic knowledge of what to do, I think should be an important part of citizenship in this country for all of us. And I think that the citizens of the race, the people who came back, stopped running, turned around, and returned to the scene, were also fundamental to Boston's response. And then finally, sound plans, simply drawn, clearly communicated, and regularly practiced really make the difference, including, ideally, no-notice exercises. We do that, and it doesn't take a whole lot of time and effort. It can make all the difference. We should all hope that we will never have to have a response like we did in Boston. I was in Atlanta the night of Olympic Park. I know how surprising that can be and how challenging those moments can be. But every community in America needs to be prepared to be a Boston. Thank you, Dr. Kellerman.
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This debate is not about health versus wealth. It's not an either-or. It's not mutually exclusive. What we're trying to argue is that they are intertwined and that wealth cannot be pursued as an end in itself, which I think we have seen to date. But rather the question facing us is wealth for what purpose? And we hold that wealth without health is ultimately meaningless. the 21st. The trade and health series covers a wide range of issues particularly relevant at this time of global economic crisis. Fundamentally it shows how inextricably linked health is to trade and how up until now the balance of power has definitely been with trade and not with health. Let's return to the press conference and hear from Dr Richard Horton, the Lancet's editor. Welcome this morning to an on-the-record press briefing about a series of papers that we're launching today on the relationship between trade and health. On Monday this week in Geneva at the World Health Organization, before the executive board meeting, a high-level consultation took place with member states of WHO about the impact of the global financial crisis on health across the world. The message from that meeting was that we should prepare for the worst, that the impact of the financial crisis on health is going to be deep and severe, plunging millions of people into poverty. An absolutely critical dimension of this financial crisis is the evolution of the relationship between trade and health. The projections from the World Bank are that world trade will diminish something like 2.5% over the course of the next 12 months, adding to the burden of poverty in low and middle income countries. The series that we're going to spend the next 20 minutes or so talking about outlines the contours of the relationship between trade and health, the crisis that we are facing in that relationship, and identify some of the actions that can ameliorate that crisis and put us into a better position where health is taken more seriously. In all, there are six papers in the series with some linked comments as well. Paper six, the final paper in the series, is a serious call to action which crystallizes the key messages emerging from the series. So if you read one paper, do read that one. But for the rest of this podcast, we're going to listen to a very lively and engaging debate that took place at the press conference between attending journalists and the two authors present at the launch, Dr. Kelly Lee and Professor Richard Smith from the London School of Hygiene and Tropical Medicine. You'll also hear again from The Lancet's editor, Dr. Richard Horton, and from Dr. Rona MacDonald of The Lancet, who coordinated the series. It's Michael Kahn with Reuters. I guess there's a lot of stuff here. You talk about the key messages, and this is partly what the Millennium Goals are about. Are you calling for something different here? I know you mentioned the WHO saying they should have more teeth. I'm just wondering what's the main think that sort of the link between health and wealth that people are... seems to me is pretty well established. So what's kind of new here or the main message or what you're trying to... you know, needs to be done aside from what's already happening with the Millennium Goals? And, you know, there's obviously commitment from governments that way. Excellent question question. Obviously the Millennium Development Goals and what we're saying are very closely related. What we've tried to do is focus down on health. Obviously health is a key part of the MDGs but there are clear problems with the MDGs in terms of achieving the health goals within a larger development agenda. What we've tried to do is obviously focus down on health, the kind of weaknesses that we see in terms of the health voice, in terms of specifically trade. But it is part of a larger agenda. What we've tried to do, I guess, is boil it down to some really specific issues that we're facing in terms of the global economy. So I suppose it's, you know, they are related and I agree with what you're saying. I think the key point of this series for me is that it's arguing that there are forces outside of the health sector that are undermining concerted efforts to improve the health and well-being of the global population. And that these forces, of which trade is one of the most important, are insufficiently recognised. And so what we are doing is putting trade ahead of the health and wellbeing of the most vulnerable peoples of the world. Now that is happening, has been happening, even without a global financial crisis. And what we're going to see with the next 12 months is an acceleration of poverty, an increase in mortality, particularly amongst women and children who are going to be hit hardest. We're seeing a humanitarian crisis emerging, not just a financial crisis. And the imbalance in global institutions, the fact that WTO is so much more muscular than WHO, is going to stop any efforts to protect the health and well-being of these vulnerable peoples. So for me, that's the core message of the series. Absolutely right. There's so much information in this series and as outlined in the first five papers but what paper six does is it builds on all that and it comes up with some key messages and some specific recommendations around each. So these three key messages are that we need to strengthen the evidence on the trade and health links, that we need to build trade and health engagement and capacity and what I think the most important one is asserting health goals and trade policy. In the last paper, it looks at all the main players in trade and health, for example, WHO, WTO, but also the World Bank and others, and it gives specific recommendations in each of these key areas. So we are trying to be quite specific rather than just unload all this information. Linda Geddes from New Scientist. I was just going to ask if you could give us any concrete examples of how you think the economic downturn is likely to impact health in developing countries and in developed countries as well. The high-level consultation that took place on Monday was very specific about this. We know from past economic crises that we're going to see reductions in health expenditure in lower middle income countries, reductions in foreign direct investment, likely reductions in overseas aid, reductions in remittances, and overall low growth. Those forces are going to plunge millions more people into poverty. They're going to force people to turn to the public sector more at a time when there's less money going into the public sector. And the consequences are going to be born particularly for women and children. In past economic downturns, infant mortality has gone up, nutrition has worsened, maternal mortality has gone up. And so that is why the conclusion has to be that we're on the edge of this humanitarian crisis, not only a financial crisis. And if we think the situation is bad now, over the next 12 months, for health, it's going to get a lot worse. We've barely begun to see the impact on health, as we've seen the impact already on markets. So there is an imperative for donors to keep their promises, which they've made in past years, and for countries to focus very much on protecting essential services for the most vulnerable people. And the contribution that this series makes to that is to show the massive imbalance in power between those institutions which are there to protect health, like WHO, and those institutions which, although they claim to have an interest more broadly than trade, actually undermine efforts to protect health. Sarah Bursley from The Guardian. A lot of this is very political, obviously, and you're going to have to get the political leaders on board to do anything about it one would have thought but there are institutions like the WTO where the fight has been going on and and their campaigners have tried to to get changes to the TRIPS agreement I'm wondering whether it isn't still possible to do things do you think that it's a write-off really that you can't get reform through WTO and you have to somehow do things differently no I don't I don't think it's a write-off at all. It's a question of the balance, as Richard has said. And we say in the paper that WTO has certain abilities with respect to observation and intervention in WHO, for example, but those aren't reciprocated. We have imbalance in terms of regulations or frameworks, so WTO is a very legalistic, hard-edged, enforceable framework and WHO is a very normative, much more softer framework. So in a sense where WHO may suggest what should be done, WTO can say what will be done, because they have got the power to do that. Having said that, there's been a lot of dialogue between those two organisations and others in health with WTO, but that has tended to be largely informal, and in that case, of of course the health input there is still very clearly acknowledged by everybody to be kind of the poor relation in the deal.
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Why shouldn't issues around trips, trade issues, liberalisation, globalisation more generally be part of an MBBS undergraduate programme? So we could take it through all levels to make sure that we generate enthusiasm and understanding and interest and ability for the health profession to get their voice heard more clearly in existing structures and then it's a separate issue as to whether we wish to fight for some different ones or not. Sarah, to answer your specific question about TRIPS, I mean I'm very aware of all the campaign against TRIPS but I think even those campaigning against it have realised now that it is here to stay and so what they're trying to do now that's more effective is to what are the areas that we can manoeuvre within TRIPS and so things like the Intergovernmental Working Group and WHO has been set up to actually look within the TRIPS framework how we can move things forward so things like the patent pool for example has been advocated along with medical prizes, etc. So within the TRIPS framework, I think now NGOs are putting their efforts around that because it looks like it's not going to budge. But I think another really important point is that despite WTO and its really rigid rules, even when governments stick to the rules, they can be penalised. And in this series, we've got a very strong comment from the former Health Minister of Thailand, who, as you may remember, was responsible for commissioning the compulsory licences for HIV drugs. And yet, Thailand was absolutely vilified by the international community for doing this, especially by the US. Yet, within TRIP's, it was in the right to do so because HIV-AIDS is an emergency within Thailand. And yet when you consider that the first ever, because TRIPS flexibilities is very complex, the first ever compulsory licence was for making bird flu vaccines in the West, but somehow that was acceptable, yet within Thailand for this it wasn't. So I think that just shows that even within the rigid rules of WTO, it's still all about the balance of power and who has it and who hasn't got it. Jeremy Lawrence, Independent. We've heard about the global downturn, but the other message of this series seems to be the upturn in health tourism. I just wondered if I could ask Richard Smith a bit more about that, particularly the impact in the UK. You mentioned 100,000 patients going abroad, which sounds like an astonishingly large number given we have an NHS here. Yes, we do have an NHS here. I mean, the issue with the health tourism really is more about its potential, I think. I mean, you were saying that 100,000 sounds like a lot, but of course of the entire population of the UK, which is all covered by the NHS, it's a very tiny fraction. Is that a cosmetic surgery? A substantial amount is cosmetic surgery, but it's not wholly cosmetic. What does the figure come from? What does the figure? removal, knee operations, those kind of things. Although there's substantial advertising for organ replacement, for example, in many countries, and just a very quick search of the internet, googling some of this stuff. It's cheaper, it's available. If, for example, you're on a waiting list, then the issue is about your time. If you wish to have this procedure very quickly, then your only option is to get out of that system and to go private. And then your options, of course, are to go private in your domestic circumstance, so for example, here in the UK, versus go overseas for that. Then you get into issues of relative price, and then you get into issues of the package as well. I mean, it's called health tourism because there is also an element of tourism in there, and a lot of the companies which offer these procedures offer you a package. So in week one, you will have a procedure, etc., but they sell to you very much the institution you will have the procedure in. It's a very hotel-like institution anyway, and then after that, of course, you remain on for a week to convalesce, but in a very conducive and pleasurable environment. And that's very deliberately sold in that way. A lot of the health tourists are regional as well. So within Asia, people will move around between countries. To an extent, you could say that that could happen more in the UK. Within Europe, why can't people move, or maybe people will be moving more to other countries? The issue around its expansion is, as I said, this insurance portability, whether that's private or whether that's, for our circumstance, particularly the NHS, it's public insurance, whether that will cover you to go overseas. And the releasing of that will generate a much higher level of trade. Then of course you move on to whether that is desirable or not and actually is it much more efficient for the NHS to be seeking to export some of its patients than seek to treat them domestically or not is an interesting question. Olivia Roberts from the British Medical Association and I wanted to get the panel's view on some UK-centred initiatives and going back to the comment about health professionals and I know that's something you Richard picked up on in your comments as well. We're working with the NHS on the concept of fair trade in the NHS so using health trade to impact on the health in other countries. The NHS purchases £4 billion worth annually, surgical instruments manufactured in Pakistan, used in NHS organisations. What is their view on the feasibility of this kind of policy coherence, so linking different government departments in this way? Is this a model they would recommend being rolled out? What are their views on that? What's the UK policy view on this? What's your view? What's quite an interesting example with that is, I'm afraid I'm going to have to move straight into Thailand again, but they established an intergovernmental committee which deliberately brought together stakeholders through health and those involved in trade and finance together to explore particular areas which were relevant to both and to seek to pursue, as in a sense Kelly said, their health and wealth together and to try to get to the bottom of where the synergies may lie between those various stakeholders around issues, as you said, about importation of products, for example. So I've picked pharmaceuticals, but lots of goods are imported and exported in and out of the UK. So that would be, in a sense, a quite obvious institution to replicate across many countries, developing and developed, as a first step to getting health further on the agenda, but also to potentially improve the trade situation as well, is to get those people talking together and making decisions together and creating some policy coherence within domestic policy, let alone on international policy. So can I just add to that, Oliver, as I'm sure you know, the UK global health strategy was launched last year, which is actually an amazing document and I think we should pay much more attention to it, where it's a government-wide strategy and it's signed off by the Prime Minister and it sets out what the UK is going to do in global health, but includes things like trade. There's a whole chapter on trade, and it includes things like trips, for example. And it also has this amazing set of ten principles. The first is which first do no harm. And it's quite strong, and it gives some specific recommendations, and it's going to be evaluated after five years. And one of the first recommendations in the trade one was to actually look at the fair trading in health instruments, for example, because it is quite shocking the way that the NHS uses instruments that are being made by people who are clearly exploited in other countries, especially Pakistan. And so I think the initiative that you're mentioning there and that the BMA is helping to lead on is a really good one. But I see a lot of what is said here in the series is actually rather surprisingly reflected in this UK global health strategy. And the thing is whether we can hold our government to account for all the things that it says. Because again, it has been quite specific in these recommendations, but it looks like the UK government is saying almost the same things as we're saying in our series. It's Judith from the Spanish news agency EFE. I just wanted to clarify in the conclusions of your series, what exactly are you calling for now? I know that these are the key messages, but are you asking governments to take more interest in health and put it before trade and profit? Or how are you going to put pressure for the change of the structures that is so vital to achieve the goals that you want? Because if we go out here and write it, nobody reads it, it's going to stay the same way tomorrow. So what exactly do you want, would you like to see done? We'd like to see done everything that we recommend in paper six. These are the key messages.
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I think the overall messages are that the health profession needs to become involved and engaged in this. National health is not national health anymore, it's international health. Whether you're on the developing country end or the developed country end, it's international health. And you need to be aware of the international context, and in particular the international context is very driven by trade and trade liberalisation, and we've got a particularly pressing context at the moment of the financial crisis. But irrespective of that, the international context is the context in which national health plays now, whether you like it or not. So there needs to be greater engagement by the health profession, from individual doctors and nurses through to the administrative structures in the NHS, people who do purchasing, for example, of these goods, the policy makers, all the way through to the minister and prime minister and beyond. And again, on the regional level, the EU, again, has a great impact and has certain policies around trips and the bilateral trade, for example. So, again, doing that. So I think my underlying message is, and why it's in the Lancet, we haven't published this in the Economic Journal or anything, this is in the Lancet for a reason, it's for the health audience to become sensitised to this and hopefully more inspired by it as well. And just ultimately I think beyond the health sector that we need to convince trade people that health matters. I just want to reiterate what Richard and myself said in the comment that opens the series and that's again very much the engagement of medical professionals in this because you're right, trade is such a political issue, but when you look at the whole health as a foreign policy agenda and look at health as an outcome, who are better advocates for health than the medical profession who are just really advocating for health? And I think if we can all band together and drive it forward, and Richard and I finished this comment by saying that we want to do more, and we do, and we're holding various discussions with other people on how we can move this forward. But I think if the health professionals, especially the medical profession, get together on this, it could be a very powerful advocate. Those final remarks from Dr Rona MacDonald, coordinator of the Lancet series on trade and health. Many thanks for listening. See you next time.
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Hey everyone, I hope that you are staying safe in the midst of pandemic world. I wanted to let you know that tonight we will be doing another live show on Twitter, a curbside quiz show with Hannah R. Abrams as host and me facing off against Chris the Chew Man Chew in a Curbsiders trivia. We hope that you'll join us tonight at 8 30 p.m eastern time on Twitter and Periscope. So we'll use that to sync this. Masterfully timed as ever. Paul, we're back. We just clapped to sync up here. We're ready to do the show tonight. Paul, I'm going to take that again. So, Paul, we're back. We are ready to do the show tonight. This is the Curbsiders. Tonight, we're going to be, it's a little bit meta. We're going to be talking about how to create a medical podcast, or as Paul pointed out to me, it's really any podcast. There's not much specific to medicine here. So, Paul, before we tell them a little bit more about the show, can you tell them what we normally do on this show? Yeah, so normally we are the Internal Medicine Podcast. We bring you expert interviews to bring you clinical pearls and practice changing knowledge. But it turns out that tonight we're calling ourselves the experts, which never feels quite right. But as you alluded to, we're now at sort of a weird time in history where there's going to be a whole lot of thirst for creating content that can be sort of parsed out asynchronously. And so we're hoping to contribute to that and make things a little bit easier for you guys. But Matt, you'll talk us more through it. Yeah, that's right, Paul. The other thing unusual about tonight is we're going to try this as a video as well. So you'll be able to actually see us as we're recording and we'll see how that goes. But this podcast is, you know, we're in the middle of a pandemic here. Medical schools have pretty much sent their students home and we are trying to, I know a lot of people are trying to move to online curriculums and less groups of people huddled together in a room getting coronavirus. So here we go. So kind of the goal here is to give you, develop a framework for how you can approach podcasting from the conceptual, of the actual ideas of what your podcast is going to be, all the way up through the equipment and a little bit on the editing of the podcast. So Paul, let's get into it. Let's start it off here. So we have this document that you should be able to see in our screen share if the technology works. It says, How to Create a Medical Podcast, Tales from the Curbside. That's the title of this episode. And some of the random pearls, maybe Paul, I'll read the first few and you can read the second few, but we have some random pearls that we really want to make sure we don't forget to say them. So the first one is, I cannot stress this enough, clear audio is key. I have, even within the past week, turned off podcasts because their audio was not clear. There was horrible background noise or echo. And one of the ways to do that, it took us a long time to figure this out, but we just, we sort of demand or recommend, strongly recommend that all our guests at least purchase a USB headset with microphone. It's very easy to set up. It provides at least a certain level of sound quality. And usually there's not a lot of echo. So that right there will set your podcast apart if you ensure that you're getting good audio. And there's only so much you can do in post-production to fix things. I feel like once you hear someone record with the iPhone earbuds and you know what that sounds like, then you can't unhear it ever again. So any other podcast or any recording you hear someone's recorded like that, you just you recognize it right away. And it just it makes a real difference to actually have just the bare minimum decent, not terribly expensive equipment. I'm sure there's some wireless headset and mics that work, but we have not yet found it. So we do not recommend a wireless or Bluetooth headset or mic for podcast recording. So get something with a wire, at least for the time being. We do recommend that before you ever put out an episode that people are going to hear or see, that you probably just do a couple practice runs and only show them to friends and family, if that, and then throw them away. They probably won't be very good if our experience is anything. And another thing is that all the stuff that's in this document that we're talking through and that we've learned, it was available online. There's great resources on YouTube. There's blog posts, and you can really piece this all together yourself. We've tried to do a lot of the heavy lifting there, but you can pretty much teach yourself a lot of this stuff, and a lot of it's just trial and error. Other advice that we typically hand out to listeners, and one that makes me laugh especially, is just limiting yourself to one standard drink, whether it's your beer or glass of wine before recording. If you have two, you might get a little bit too loose. And if you have three, it's just a recipe for disaster. So a fun assignment for you as a longtime Curbsiders fan would be go back and listen to older episodes and see if you can find the ones where we learned that lesson. Because you could probably pick it out. We do recommend making professional show notes that have your learning objectives, your summaries of key points, include conflicts of interest, which is a quality measure, I think, of really good podcasts, especially for medical podcasts. Visual aids, links from the show. These things are all useful. I would add to that, and I'm not sure how you feel about this, Matt. You know, you guys are looking at an example of something that looks a lot like the script that we use. So preparation is also key, too. So you can't just sort of turn on the microphone and sort of roll out. So actually have an idea of what you're going to say before you say it. And that will save you tons of time in the back end. Right. Yeah. For like an actual learning podcast, I don't think it works to just turn on the mics for three hours and talk. I think maybe Joe Rogan does something like that, or at least he wants you to think that. But I don't think it works for a medical podcast where people are hoping to gain some sort of concrete takeaway from it. Until we do our ayahuasca episode. And then the last one is don't forget to press record. That's happened to me multiple times, but usually I've been recording in multiple different ways. So I have a recorder where I actually have to press record and then there's a button within the software. And so I'm recording both a hardware and software copy of all our shows. And then depending on what software you use, you and your co-hosts can each record everybody. That way you have a lot of redundancy and you don't lose like an hour's worth of material. So let's move on to the first part of this, which is really if you are going to make a podcast, I think one of the first things you need to do is figure out what is that going to be? Who is it for? Is it an internal podcast or is it something like ours where you're going to be putting it out to an international, at least national or international audience? And you want to just kind of figure out like, who is this for? What is my ideal listener? In the case of the Curbsiders, we were our own ideal listeners, which made it easy to figure out what kind of shows we should be making. Paul, what do you think is important to highlight here? I know you've helped a couple people start their own shows. No, I think you covered the important points. Again, it's not going back and just clicking the record button because you're a wonderful person with things to say. We assume that's the case, but I think really clearly defining what it is you're trying to communicate, who you're trying to communicate it to, and then what the actual purpose of the show is. I think it's even helpful, and again, I'll leave it to you to correct me if I'm wrong, but to even sort of craft a mission statement, like what are you specifically trying to accomplish when you put this out into the world? And I think that will sort of help shape the show and make your early experiments move a little bit more quickly. Yeah, I think that's absolutely true.
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And you make sure, like, did I hit my learning objectives in the talk? You plan those ahead of time. Otherwise, you might get lucky, but probably you won't. Probably not. Yeah. So our mission statement is supercharge your learning and enhance your practice with this internal medicine podcast featuring board certified internists as they interview the experts to bring you clinical pearls, practice changing knowledge, and bad puns. And I think we've delivered on that, Paul. I hope to say that anyway. right away and says what it's supposed to be, whether or not you agree with that. But that is pretty much what our mission statement is. And depending on, I think we can kind of skip over the logo stuff. If you are going to be putting something out on iTunes and into the public, you should be making a logo and kind of thinking about the show aesthetic. And there is a great free website that we use. And this is also great for just making infographics and figures. It's called canva.com. We don't get paid anything for saying that, but if they would like to advertise on the show, we would love it. But we make, we use it to make infographics and cover art and it's, it's free for most, the most of the basic features. And really intuitive. Even, even I land to track down. So you got to really think about, do you have time to do this? In our case, we, I mean, we sort of have built this into our schedules over the past four and a half years. And then we also enlisted this team of volunteers who are amazing and they kind of work. They kind of work when they have time. So each person will be involved with three or four shows a year and we have 20-ish people. So it sort of just works out where people are always working on projects and we have a show every week. The other things that you can see, well, oh, and if you're watching on the video, you can see the, this picture just cracks me up, Paul. This is the Green Bay Packers coaching staff. I want to say it's the 1990s. And this picture was like the Green Bay Packers staff. And they used to show it on ESPN. And at the time, there was one head coach and a bunch of assistant coaches. And a bunch of those assistant coaches eventually went off to become head coaches themselves. And that's not the funny part of this. The funny part is that the whole curbsiders team photoshopped poorly onto this. And we're all wearing khakis and polo shirts and white shoes, which just looks great. So I think to have one person who has not ultimate ownership, but at least a leader who's kind of driving things forward, who can kind of make sure the rest of the team is working appropriately is a really helpful thing to have. Because I think if you have just sort of general diffused shared accountability, I don't think you're going to be able to move as consistently forward as you can if you have one person who's sort of consistently driving things. So if you can agree upon someone to do that, I would recommend that if you can. That is true. You need somebody that is going to be essentially your showrunner. And when you hear people talking about like TV shows, the showrunner for the TV show is the person who's keeping tracks of episodes and storylines and sort of steering the ship from a high level. And that is definitely something that you need to have someone that consistently has the time to do that. I think it's harder to do it the other way where people are just coming in and out and no one's really a consistent presence. I think we can probably skip over the frequency. I can just say that for us, the time that we found that, that works to record is on weeknights. We try to keep weekends sacred. Right now we're in a pandemic. So like every day feels the same when you're, when you're stuck at home, at least for me right now. But the, we, we try to do Monday through Thursday after 8 PM Eastern time, because at that time kids are in bed. Most notes are done-ish for the day, and people are home. So we record on weeknights. That's what works for us. But maybe depending on what kind of podcast you're doing, you might find another time to record. And if you're going to put out a podcast weekly, you got to record at least once a week on average and so forth. We can probably just briefly touch on this, Paul, the business finance and legal stuff. Did you have any like? No, I think the broad message and you and I'll defer to your expertise as per use. But I think that the big thing to consider is as you're creating this, and if you're creating with a team is to think about intellectual property, and who's going to have ownership of the idea behind it, and how are you going to make sure that's actually the case and make sure you discuss that and are explicit about it ahead of time. And if you're affiliated with an institution, it'd be helpful to actually talk this over your institution as to who's going to own this finished product now and then in perpetuity too. So I, you know, the other business stuff, I think, you know, depending on how big it gets, we'll all be useful, but I think just broadly, so feelings don't get hurt or you don't get in trouble just talking about who owns the intellectual content that you're putting out into the world. And this mainly comes in play when you leave your institution, because if you created something while you were there and then you want to leave and bring it with you elsewhere, that you will run into issues there. And there are horror stories out there. I don't want to get into specifics, but that's why it's worth finding out what the intellectual property policies are at your institution. And then you'll probably need to retain counsel, if that's the right way to say it, and try to have something put into your contract so that you can do that and make sure that you keep ownership of it. Now moving on to the equipment. So let's just say at this point, we've decided we want to make a podcast. Let's say it's going to replace our morning report and it's for the medical residents at our internal medicine program. It's going to be done by the chief residents and the residents are going to take turns appearing on the podcast with maybe a subspecialist. And now we have to decide what we're going to use to record. The first thing to start off with is the microphones. So you could use the USB headsets that I talked about. But I think if you're going to be consistently hosting a podcast, the entry-level microphone that we recommend is an Audio-Technica microphone. And it is the AT205 USB cardioid mic or the ATR2100 USB cardioid mic. And the reason I like this mic is because it has two different types of connectors on it. So you can either, you can kind of plug in a traditional microphone cord to it, but you can also just plug in a USB cord and plug it directly into your laptop and start recording. And it has really good sound, pretty similar to the $100 Shure stage microphone that you probably always see people holding at rock concerts. Yeah. At rock and roll shows, you know, like the kids like, sure. The kids like rock and roll. Rock and roll is that's hip right paul it's here to stay as someone famously said yeah so the the xlr is a type that's that's a microphone cable it's this kind of fat round cable it has a male and female end that plugs into the microphone and then usually plugs into some sort of uh recording device um if you want use that type of microphone with a laptop, then you're going to need some sort of interface that you plug from the microphone into the interface, and then the interface will connect with USB to the laptop. So it's a little bit of an extra step, and that's why I don't recommend it for people that are just starting off. In theory, you could just start off with just a laptop and a USB microphone and talk to your friend with a laptop and a USB microphone when they're at their house and you could record a podcast that's say a couple people are going to get together and record something at least six feet apart in the modern era, you can get this Zoom H4 recorder, which allows you to plug in two microphones via this XLR cable I was just talking about. And two people can talk to each other there. It's nice. It lets you see how loud the sound is for each person and you can adjust their levels. And it records them each on separate tracks, which makes it very easy to edit in the end.
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And that one runs you about $330, but definitely that I would recommend that option if you're going to be doing any in-person recording. And I actually use it even recording right now. Um, I use it to record a backup of this conversation that Paul and I are having. Um, Paul, do you have any, I know you use one of the odd, like you have XLR mic, one of the Shure stage mics, and you use an audio box. If you could go back and do it again, do you think you would start off with just a plain old USB? I think probably so. I think I was trying to be fancier than what I actually am. And I think the USB will get you where you need to go without having to fuss around with an audio box. So I think I was trying, I think I overshot. That's okay. What, what kind of mic stand do you like, Paul? There's the, there's a couple of different types of mic stands. I think it's, it is important to get a mic stand, uh, because for sound quality, for sure. Yeah, I agree. And I, I, I'm assuming there's going to be some version of show notes. They'll go out that have some of these things linked in here. I like the boom mic stand. I just think it's a little bit more flexible and you're not wrestling with as many parts um which is basically just sort of a stick it's basically here for those you're watching the video i'm moving the mic up and down probably making terrible noise too yeah and i'm circling it in the video there the it's this it stands on the floor right if you're a former band or like myself and you remember what music stands look like it's like that except then there's a stick with a microphone on the end of it rather than the thing that holds the sheet music, if that helps you at all. And then I guess the other option is an adjustable microphone suspension boom, which has an armature that probably allows for a little bit more flexibility, but adjusts by like a C-clamp to whatever sort of flat surface that you're using. Yeah. And one of the things, one of the caveats with that is it can make, if you bump into it, it can make like a gong noise, which we've experienced many times. Compliments of Stuart Brigham. So we, yeah, just be aware of that. So, all right. Now this is going to, now this is going to, I drew this thing on the screen, Paul, and it's going to, let's clear this out. Clear my drawings. There. Oh, you're a pro. I'm a pro. So intuitive. Okay. So that's it. So you buy a microphone. You may or may not buy an audio box or a recorder. This thing, if you're watching the video, is called a pop filter. That's that sort of screen that you see when people are recording in a booth. It kind of, for the loud like pee noises, it kind of blocks that puff of air that comes out. What's that called, Paul? Aplosive? Is that? Aplosive, yeah. I can't remember how it's different from a tussle, but I think you're right. I think plosive. Okay. So I would recommend one of those. They're only like five bucks or something. They're not too expensive. You're not going to break the bank. And then some over the ear headphones, which like right now I'm monitoring how loud my voice sounds on the microphone and using these monitoring headphones. They can run you anywhere from like 20 to 50 bucks. You can definitely spend more if you want to. Right. I do want to emphasize the importance of those because when you're recording, if you have something coming through your computer speaker, any speaker that then gets picked up by your microphone and starts feeding back and sounds echoey and awful. So in addition to being able to monitor your own levels, you avoid this feedback loop. Okay. So let's take it from headphones. Right. So I just wanted to emphasize the point, and ironically, we just had some sound issues, that headphones, in addition to helping you monitor your own levels, also are really, really important when you record because if you try to use your computer speaker for audio as you're recording, it can then feed back into the microphone and cause echo and noise and just sound awful. So you'll also want the headphones just to cancel out extraneous noises as you're recording. Right. And I added a separate microphone here because we're trying to do the audio and video recording and it wasn't working out with the single microphone setup. The audio technical problems might have been my fault. Even after all this time, Paul, I still keep finding new ways to mess up the recording. This is going to be a shorter episode, so let's move on. As far as recording yourself goes, there are some programs. The two most basic ones that I would recommend people start off with are Audacity, which is a program for both Windows or Mac. It lets you both record yourself and edit yourself. The other one is GarageBand, which is for Mac users. And that one lets you both record. You can record directly into it with a USB mic, and you can also perform the editing within there. And it actually lets you add tracks and edit them. And so I have a screenshot here and I'll circle it. So you can see here, there are two audio tracks there. Actually, one is a voice track that says Watto. The other one is a music track. And so within the program, you can just add the tracks and you can make cuts. You can drag them around. You can stagger things. You can add in music. And this is what the software allows you to do. So first you'll record just the audio and then you can add in all these other things after the fact. And I recommend with starting with one of the free softwares. And if you have the funds, probably if you're an attending, you can probably afford to do so. And you can actually, you can probably find someone on a service like Fiverr or TaskRabbit that can actually do some editing for you. But if your podcast is going to be short, like 15 minutes or less or 30 minutes or less, and you don't really plan to have too many bells and whistles, and it's just going to be for internal release, then you could probably figure out most of the editing on your own. And we do have some videos that we link to later in the document that show you how to do the editing. Paul, you haven't really delved into this too much, but did you have any, as far as recording yourself, is there anything you wanted to let people know about Audacity, which is this program here at the top with the kind of purplish blue waveform? Not really. I like Audacity a lot because there's not a whole lot to say about it. It's pretty straightforward, it's really intuitive, and it's kind of hard to screw up for the most part. So I think it just is, you hit the record button and then you're kind of off to the races as long as you have your computer, everything plugged in where it belongs. So I think that's probably the simplest one to start out with in terms of the editing stuff. I am cheerfully and blissfully unaware of most of the details that go into that. And most of these programs, when you record an audio file, the non-compressed files are usually a .wav or a .aiff file, and they're very big files. And then you can pull those tracks into an audio recording software, make your edits, and then you kind of export them or bounce them out of that program as an mp3 or dot m4a track those are usually the the finished tracks that contain everybody's voice and any music any other mixing and mastering that you've added to it if you are going to go make be making a podcast i usually recommend especially if it's going to be something that that you're trying to put there on Apple Podcasts and Stitcher, Spotify, et cetera, that you have a website. And if you're making something for your institution, probably they can help you make an internal webpage. But if you need to purchase a domain name, I never had a cause to know what GoDaddy was until I needed to purchase a domain name. But GoDaddy.com is a place where you can buy all sorts of different domain names. And if someone already owns your domain name, you're probably going to have to pay a lot more money than if it's a domain name that is not yet owned by anybody.
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Like you probably don't want to have like three underscores in your website name. So you purchase a domain name and then I'm not really going to go into this on this podcast because this is not how to create a website. But there are websites that some that require coding like WordPress and some that don't like Squarespace or Wix. And you can look into that and decide if you want a website that's kind of out of the box or if you're going to make it yourself. When you are sending your podcast out there to the world, you need this thing called a media host. The one that we use is called LibSyn, Liberated Syndication. It's one of the ones that's been around for a long time and we've been very happy with their service, but there's a lot of other competitors out there now. And this basically is a place where you upload the finished audio files to, and then they make it very easy for you to send it to Google and Apple and Stitcher and Spotify and all the various services. Additionally, they create what's called an RSS feed for people. And that's that some of these other websites like podcast, pod catchers, like overcast and things like that will pick up the RSS feed. And and that RSS feed contains information about your show that you put in within your media host. So within Libsyn, we put in all these things about our show and our logo and our website. And then when we create a podcast episode and upload it, Libsyn sends it out to all these places so that we don't have to manually do that ourselves. So when a new episode of my favorite podcast that is almost certainly non-medical shows up on my iPhone, that is because they went through a media host that has it sort of set up that way? I just want to make sure I'm understanding correctly. Yes, the media host helped them create an RSS feed and distribute it. It's kind of a central location that you can use. You can individually try to go to all these different places, but there's so many of them. It's better to just go to a central place and then they send it out for you to all the places you want it to go. And then how do you make sure that people can find it? Because there's one podcast for every single person now and everyone has their own podcast. How do you make it sort of searchable and findable by the general public? Right. Well, that's why I think naming the podcast is important. Usually you get to name the podcast and then you get a subtitle for the podcast. So you can make sure that both the name and the subtitle have some keywords. And then the mission statement we talked about earlier, that goes into the summary about our show. So if someone searches an internal medicine podcast, the Curbsiders comes up. And these podcast episodes are actually searched the way, like the podcast websites like Apple, Spotify, they are search engines. So you need to have keywords in the title. So if you wanted to make a show about alcohol use disorder, make sure that's in your title so that if people are searching for shows about alcohol, Perfect. how to set up your recording studio. I guess the Cliff Notes version there is you want to record someplace that's got carpets and drapes and books and furniture and maybe drop ceilings. These are things that can absorb sound and prevent echo. Echo is not your friend when you're recording audio. So what has a lot of echo? Rooms with hardwood floors, lots of windows, bare walls, no furniture. Things are going to echo like crazy in there. So you need stuff that's going to dampen the sound. And you can see some pictures of my, what I like to call my podcast fort. Do you really have the shower curtains up? Those are, those are actually a painter's drapes are like painting tarps. And I do have those up. Yes, I do. Amazing. Great. Yeah. They're not up all the time. Like they kind of, you can slide them over. Sure. Otherwise it'd be crazy. Yeah. Otherwise it'd be crazy. Yeah. The kids, my kids do swing on them like Tarzan, Paul. Excellent. Yeah. And I give, uh, within the document, uh, within the handout, I give a couple of different ways that you can set up your, your hardware. So I think that's going to be too hard to conceptualize on the actual um on the actual audio version of the podcast but if you're following along on video i have uh pictures with that are kind of labeled with all the equipment so you can see where all the cords plug in and what everything is but probably paul you were telling me you thought the most useful thing to tell people about would be sort of like where we actually, how we actually do the recording at the time of the recording. Right. As we meet more and more of our listeners, I think far and away the thing that surprises people most is that we don't all record in the same location at the same time and that we are all sort of recording remotely. So I think just talking people through that process might be especially helpful if you can't be physically co-located with your co-host or your guests. Right. Yeah. So sometimes when we're at conferences, we're co-located and that makes it easy in some sense, hard in other senses, because there's a lot of echo. If you're sitting next to somebody else that's recording with you and you're not in an actual studio, you get a lot of echo between the microphones, which is more for the concern when you're editing. But the recording setup that we use most commonly is where we have the hosts, the co-hosts are all at their houses in their own home recording studio. We meet up with on either Skype or Zoom, or you can, you could use Google Hangouts and you would, you would start to record yourself. I recommend Zoom because it does have an, an, an option to record for, to record both the video and audio from the call. And it'll actually record all the participants on separate audio tracks, which makes it nice when you're going to edit things afterwards. So essentially what you do is you have everybody's in their own location and then everyone records themselves. I also record everybody within Zoom. That's really meant to be a backup and it also helps me kind of line things up after the fact, but that's really meant to be a backup. And it also helps me kind of line things up after the fact. But that's really meant to be a backup. The audio that everyone records by themselves in theory should be the best because it's not going over an internet connection. Sometimes going over an internet connection, you get some words that sort of drop out and that doesn't sound great on the final recording. So usually at the end, I have a couple different versions of a track from somebody. I have the version that I pulled that I kind of copied on my end within the software that I use to record. There's a software for Skype, a third party software you can get for Skype called Ecamm that will record anyone that you're talking to. And then in Zoom, Zoom records everybody so I just go with whatever track sounds better either the one that the person sent me that they recorded or the one that I recorded on my end, merge them all together and then you send them out and it sounds like everybody was in the same room together. with both of us on it. And so it gives, it kind of gives you that master track with everybody on it is a good way to line up all the tracks because Paul and I probably started and stopped our tracks, our local tracks at different times. So they're not going to be in perfect sync. So that's why actually before we started recording, Paul and I, we do a hand clap. So that way we, on my track and Paul's track, I find out where we both clapped and that's roughly where I should put those two parts right next to each other, and then the rest of the conversation should line up as well. So that's another tip for you. I think, Paul, as far as the other recording setup, sometimes if you have two people in one location and you're talking to a remote guest, that's another thing that we had done for a while. There was a while where Stuart was living in the same neighborhood as me and he would record at my house. And then we would talk to Paul who was in Philadelphia, plus a guest who was somewhere else. So you can have various combinations of this, but usually things sound best if you have everybody record a local copy of themselves and then merge them. But there's all different ways to kind of do this together.
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And when you open QuickTime, you just click File, New Recording, and hit the Record button. And with Voice Recorder, you just search for it in Windows and open it and click Record. Because no one's ever actually used it before, and no one knows where it is on their computer. So invariably, you have to search for it first. But those work well. Okay. And then the final part of this, we have some tutorials that we actually put out. We have a tutorial for garage band, how to both record and how to edit in garage band. And then a tutorial for audacity that tells you how to record yourself on audacity. And if you have two people recording in the same location, how to split the track so that you have one track for each of the people. So those, I don't think we have time to talk through on this episode, but editing the podcast, I would recommend if you have a Mac starting off, you can use GarageBand to do it. And then you can kind of upgrade to one of the more expensive programs like Logic Pro X is the sort of bells and whistles version of GarageBand. And that's what I use when I do editing because it has a lot of shortcuts and things that save time once you get the hang of the basic features of GarageBand. Paul, I know we only have a little bit of time left here. Is there any other stuff that you thought was really, really important about this? Gosh, I know you talk a little bit about search engine optimization, but I guess that's sort of more if you're trying to put out an external podcast and not something specific to your institution. But do you want to talk a little bit about that? I could. I could. So search engine optimization, if you are trying to make a podcast that you're going to be putting out into the world and you want people to find it outside of your own institution, search engine optimization is a way that you tag content, basically attach keywords to the content, the way that you name your files, the way that you structure your webpages. And it's so that it's able to be found in search and so that it ranks highly in search within Google. I can't say that I'm an expert on this. There are literally marketers and search engine optimization pros out there that charge businesses thousands of dollars a month to do this for them. It's a valuable service. It feels like a scam. I don't know if it's a scam, but it's definitely something that, it's definitely something I think, knowing the basics of it, if you're using a WordPress website, and I'm not sure if this plugs into Squarespace or Wix as well, but there's a program called Yoast, Y-O-A-S-T. And that basically gives me a grade at the end of like when we put it when we make the web page for the show notes of each each week, that program Yoast gives us a grade. And it says like either you did a great job or you didn't, and it'll give you some things you can change to boost your search engine optimization. But you just I mean, you're you're spending all this time making content, you want people to be able to find it. Right. And then I think the other pro tip that we may have neglected to mention is talk to me a little bit about how you sort of process things at the end. So you've edited together all the tracks and you have the final product. Is there a way to make sure everything's all kind of at the same level and sounds as good as it possibly can? Yes, because the microphones that we use are directional microphones. So they try to only pick up sound right in front of them because we're not in a professional studio. So if someone's stomping around above me, I don't want my mic to pick it up and I don't want it to pick up every little noise in the room. But that also means that if I move my head one way or another, or if I'm not as close to the mic, the sound volume will differ. And also, if you're talking to multiple co-hosts, everyone's going to have different sound settings. So there's a program called Auphonic, A-U-P-H-O-N-I-C, and that basically brings everyone's track up to the same level. And even within your own track, if there were certain times where you were not as loud as other times, it'll kind of level things out so that the audio is loud enough. And kind of getting back to our initial main points, the first point we made on this podcast was having clear audio is very important. And that is one of the ways I think you can get clear audio is after you edit the tracks, I run each track that's been edited through this Auphonic program and then merge them into a final track at the end. But I always use that. Great. So this is used, just so I'm understanding, to level individual tracks before you then re-put them back together for the final product? Yes. And then the version of the software that I have actually, I feed in for, I can feed in as many tracks at a time as I want and then it'll send them out as one final track with just all the all the voices on it and they've all been merged together in one track and they've all been leveled out but it's so that's that that is that requires a purchase to get that version but it's it's like 90 bucks or something so it's it was definitely worth the time. It definitely worth the amount of time that it saved me. So I think just to go back to, uh, for me, some of the take-home points, make sure that, uh, make sure that you're practicing the audio, try, try recording the audio, um, and, and listen back to it and see if it sounds like something you would listen to or if it just sounds like a bunch of echo or a bunch of computer fan noises. If that's the case, then try to troubleshoot things because I think your audience is really not going to put up with – they don't need NPR quality audio, but they do want to be able to understand what you're saying. And I'm sure you're going to be making great shows. So make sure that they can hear it and understand it. Uh, Paul, did you have any final things about this, how to create a podcast that you wanted to, to say? No, it's, I go forth podcast. I think one of the appealing things about it is the relatively low barrier to entry. And you really, a lot of the ways I know that Matt, you're obviously one of the main drivers behind this, but a lot of the stuff you taught yourself and there's, there's other than this excellent resource that we're just about to unleash upon you. There's lots of resources available online as to how to edit and how to record and what equipment to use. So just avail yourself of that because at the end of the day, it's not as complicated as you think. And so now you have no reason to not do it, I guess. Yeah. You just gotta, just gotta get out there. Uh, one of the other main tips, don't forget to press record and, and try to have, try to have multiple backups because equipment will fail. You will have technical difficulties. And early on, we had a lot of them and, uh, felt like quitting a lot of the time, but you'll get, you'll get through that. Um, I hope this helps you this helps you start to think about how you can move some of your content online in the midst of this pandemic that's happening. And please check out our website, the handout. We've talked through it, kind of the Cliff Notes version, but there's lots of detail in there. And send me feedback and I can kind of add to it if there's a lot of follow-up questions about any specific portions. So forward slash knowledge food to get our weekly show notes in your inbox. And we're committed to providing you with high value practice changing knowledge. But to do that, we need your feedback. So please send an email to thecurbsiders at gmail.com. A special thanks to Paul for joining me for this episode and to our social media team, Hannah R. Abrams on Twitter, Beth Garbs Garbatelli on Instagram, and Chris the Chew Man Chew on Facebook. Until next time, I've been Dr. Matthew Frank Watto. And I'd of course like to thank Stuart for composing our amazing theme music, as well as to Claire Morgan of Nautily for doing heroic work editing our audio. And just as a reminder, I remain Dr. Paul Nelson-Williams. Thank you, and goodbye. All right, goodbye.
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Hello and welcome to the Annals of Internal Medicine August 21st, 2018 podcast. I'm Dr. Christine Lane, Annals Editor-in-Chief, with highlights of what's new in Annals since our last highlights podcast. Let's begin with articles published online first on August 14th. All women should be screened annually for urinary incontinence according to new guidelines from the Women's Preventive Services Initiative. At some point, urinary incontinence infects an estimated 51% of women and can adversely affect a woman's physical, functional, and social well-being. However, many women are reluctant to discuss urinary incontinence with their health care providers, so they may endure symptoms for a long time before the issue is addressed. Researchers from Oregon Health and Science University conducted a systematic review of published studies to evaluate whether screening for urinary incontinence in women not previously diagnosed improved physical and functional outcomes. They also assessed studies on the accuracy of screening methods and potential harms. The researchers found that no studies evaluated the overall effectiveness or harms of screening. Limited evidence suggested that some screening methods that used brief questionnaires had fairly high accuracy for identifying symptoms of urinary incontinence in primary care settings. Despite the lack of direct evidence, the Women's Preventive Services Initiative asserts that screening has the potential to identify urinary incontinence in many women who silently experience its adverse effects. Because early intervention may reduce symptom progression, improve quality of life, and limit the need for more complex and costly treatment, the group recommends annual screening for women of all ages. However, the authors of an accompanying editorial from the Women's Health Research Program at Monash University in Melbourne, Victoria, Australia, argue that implementing screening in a large population without better evidence that it will yield net benefit may not be very wise. The editorialists call for a randomized trial to directly assess the benefits and harms of urinary incontinence screening in women before recommending it for all. Most cases of colorectal cancer develop from adenomas or sessile serrated polyps, and removal of these lesions is recommended. However, hyperplastic polyps, especially if small and located in the distal part of the large bowel, are not associated with subsequent development of adenomas or colorectal cancer. Therefore, they do not have to be removed to reduce cancer risk. Diagnosing and leaving these polyps would save time and expense as the annual cost of unnecessary polypectomy is estimated to be 33 million dollars in the U.S. annually. As reported in another August 14th online first article, researchers from the Digestive Disease Center at Showa University in Yokohama, Japan, compared diagnoses derived from real-time computer-assisted diagnosis with endocystopies for 791 consecutive patients undergoing colonoscopy with pathologic reading of the resected specimen. They found that the computer-assisted diagnosis system provided 93.7% negative predictive value for identification of diminutive neoplastic polyps. According to the authors, these results suggest that computer-aided colonoscopy has the potential for replacing histological assessment of diminutive colorectal polyps in the near future. Clinical guidelines have issued cautions about the use of tumor necrosis factor inhibitors in patients with a history of cancer because these drugs may have tumor-promoting effects. TNF inhibitors are widely used to treat rheumatoid arthritis, which makes treating patients with rheumatoid arthritis and a history of cancer a clinical dilemma. Researchers from the Karolinska Institute in Stockholm, Sweden, studied data from national registries in Sweden to compare cancer recurrence rates in 467 patients who had started TNF inhibitor treatment for RA after their cancer diagnosis between 2001 and 2015 versus an individually matched cohort of 2,164 patients with RA and a similar cancer history who had never been treated with the TNF inhibitors. They also compared cancer recurrence rates between the TNF inhibitor patients and an unmatched cohort of 3,826 patients who were diagnosed with RA during the same timeframe but had no history of biologic treatment before inclusion. Cancer recurrence rates were similar in all of the groups, suggesting that TNF inhibitor treatment did not increase risk for recurrent cancer. However, the authors cautioned that because several estimates had confidence intervals with upper limits around 2 or above, the clinically relevant risk for cancer recurrence could not be ruled out. Next is an interesting case report of novel treatment for a woman hospitalized with severe inhalant intoxication. Clinicians from Vanderbilt University Medical Center treated a 26-year-old woman who developed confusion, lethargy, respiratory failure, and cardiac arrest after inhaling suspected 1,2-diifluoroethane, a common ingredient in household aerosol products. Difluoroethanes are inhaled for recreational purposes sometimes, known as huffing, because they are intoxicating, inexpensive, and easily acquired. After 36 hours of standard therapy, the clinicians began salvage therapy with simultaneous infusion of dextrose, insulin, levocarnitine, and acetylcysteine, niacinamide, and fat emulsion in an attempt to restore bioenergetic and redox status. The patient showed sudden and dramatic improvement in all clinical variables, including neurologic function, ejection fraction, arrhythmias, and hemodynamic status. The authors say that they may have discovered a strategy for treating this type of inhalant intoxication, a dangerous poisoning that currently has no antidote. Because the five drug components are readily available at most hospitals and generally safe to use, the authors suggest consideration of this approach as soon as 1,2-difluoroethane intoxication is suspected. Let's move to articles published online first on August 21st. The first one reports a study that looks at gains in viral suppression in persons with HIV infections over the past two decades. Approximately 1.2 million adults in the U.S. are living with HIV, and men who have sex with men and African Americans are disproportionately affected. Achieving and maintaining HIV viral suppression is essential for optimal outcomes and prevention efforts. As such, understanding trends and predictors of viral suppression is imperative to inform public health policy. Researchers supported by the National Institutes of Health analyzed data for nearly 32,000 adults living with HIV Thank you. The researchers evaluated associated factors such as demographic characteristics and medication use. They found that overall rates of viral suppression increased significantly during the time frame from 32% in 1997 to 86% in 2015. They also found that the average interval from enrollment to suppression was shortened substantially from nine months for those initiating antiretroviral therapy between 1997 and 2000 to two months for those initiating antiretroviral therapy between 2010 and 2015. However, the gains in viral suppression were not equally distributed across populations. Younger persons and blacks were more likely to have detectable viral load. According to the researchers, these disparities warrant further research. In an accompanying editorial, Dr. Anthony Fau duration of patient experience and specific insights into patient-oriented outcome measures. Investigators are thus able to interrogate the impact of newer treatment guidelines on viral suppression, particularly with regard to the promotion of earlier initiation of antiretroviral therapy after diagnosis, end quote. Next is a brief research report that suggests that pregabalin, an anticonvulsant increasingly prescribed as an adjunct for chronic pain, is associated with an increased risk for opioid-related death when co-prescribed with opioids. Researchers from St. Michael Hospital and the University of Toronto noted that because more than one-half of Ontario residents who initiate pregabalin therapy are concurrently prescribed an opioid, determining the risk for opioid-related death among persons co-prescribed these medications has important clinical implications. The researchers identified a cohort of persons aged 15 to 105 who received publicly funded opioid prescriptions between August 1997 and December 2016. They matched case patients who died of an opioid-related cause by age, sex, and other characteristics to up to four controlled participants. After adjusting for multiple variables, the researchers concluded that concomitant exposure with opioids and pregabalin in the preceding 120 days was associated with significantly increased odds of opioid-related death compared with exposure to opioids alone. According to the researchers, these findings warrant a revision to the pregabalin package insert, which does not currently warn about the risk for serious adverse events when combined with opioids. Marijuana has been advocated by some as a treatment for pregnancy-related nausea. With the growing acceptance, accessibility, and legalization of marijuana, its use is likely to rise among pregnant women. As such, it is crucial to understand the effects of prenatal exposure. The weakness of previous studies is that they do not fully account for confounding factors. In the next article, researchers present data on the high rate of substance co-use of pregnant patients in the Kaiser Permanente Northern California health system who were universally screened for any prenatal substance use between 2009 and 2016. More than a third of the women who had a screening result positive for marijuana use also had a positive result for at least one other substance. This result highlights the importance of controlling for co-occurring prenatal substance use to accurately detect marijuana-specific health risks.
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Next is a research and reporting methods article that evaluates the association of publication status and language with treatment effects using a meta-epidemiological approach. The authors examined Cochrane reviews published between March 2011 and January 2017 with a meta-analysis of a binary outcome including three or more randomized controlled trials. For each trial, the authors identified the primary reference and evaluated whether it corresponded to a journal article or to unpublished data. They found larger treatment effects in published than unpublished trials and larger treatment effects in trials published in a language other than English than in English. The authors suggest that those conducting meta-analyses consider these findings. There is increasing recognition of the importance of social determinants of health and food insecurity is one such factor. Disruptions in food availability are associated with worse health outcomes and increased healthcare utilization. For example, inadequate healthy food is associated with poor physical and mental health and diseases such as diabetes, hypertension, and depression. A commentary published online first on August 21st discusses how clinical community partnerships can address food insecurity among high-need, high-cost Medicaid patients. Most of the articles published in the August 21st print issue were initially published online first and discussed in prior podcasts. However, some new web-only material accompanies the issue. First is Annals for Hospitalists. In addition to key points from articles that the Annals for Hospitalists editors judged to be very relevant to hospital medicine, this month's Annals for Hospitalists includes a commentary Thank you. podcast, Annals on Call, features podcast host Dr. Bob Senter interviewing Dr. Devin Kansagara about conflicting recommendations concerning blood pressure thresholds for initiating pharmacologic treatment of hypertension. Watch and listen to ConsultGuys and Annals on Call to earn CME and MOC credit. That's all for this podcast. Thanks for listening, and I hope you'll go to annals.org to take a closer look at some of the new Annals material that I've mentioned. Thanks to Beth Jenkinson, Megan Caffrey, and Andrew Langman for their technical support.
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Hello and welcome back to Sharp Scratch. You're listening to episode 102, The Social Life of Medics. This is a podcast brought to you by the BMJ, where medical students, junior doctors and expert guests come together and discuss all the things you need to know to be a good doctor, but that you might not get taught at medical school. My name's Eva Lynn and I've just finished my third year as a medical student at Lancaster University. This year I'm working at the BMJ as the editorial scholar, looking after all the content that BMJ students are producing. I'm also the new host of Sharp Scratch. Today we're joined by our panellists Charlotte and Judy. Would you like to introduce yourselves? Yeah hi everyone I'm Charlotte. Until recently I worked at the BMJ but I'm now back in medical school doing my final year at the University of Oxford and it is really nice to be back. Hi, hello, my name is Judy. I'm a fourth year medical student. I study at the University of Silesia in Poland and it's also nice to be back on this episode. So lovely to have you both back. We're also joined by our expert guest today, Christina. Christina, could you tell us a little bit about yourself? Hi, I'm Christina. I'm a final year med student at Newcastle and also a content creator. I post a bunch of tips on TikTok and Instagram, just on how to study for your exams. And also just, I guess, the side of uni that no one really talks about, the friendships, the loneliness and all that sort of stuff. Thank you so much for joining us today. Thanks for having me. So today we are going to be talking all about socialising in medical school. They say that nobody parties harder than medical students but is that really true? Long-time listeners of Sharp Scratch will remember the Freshers First socialising episode recorded in the middle of the pandemic so I'm pretty pleased and excited to be able to revisit this topic now that medical school and university life feels a little bit more normal. I thought in this episode we could talk about our own friends and Freshers Weeks, the sports and societies that we all got involved in and give a little bit of appreciation to the non-medics in our lives. So Christina, we've met before, and you told me that you actually kept your head down during Freshers' Week. Could you just tell me a little bit more about that, and why you did that, and would you do it again? To start off, no, I definitely wouldn't do it again. In Freshers' Week, I only went out like once, I think. I was honestly just so nervous coming into Freshers' Week. I always heard the stereotypical thing of like we're all in the same boat we're all you know trying to meet new friends and meet new people but I think I was just so nervous and anxious I let that get the best of me and I didn't really put myself out there um but looking back I think that wasn't unique to me everyone's probably a little bit nervous a little bit anxious so I probably should have just put myself out there but yeah yeah I had a very very different freshers week um Charlotte what was what was freshers week like at your medical school yeah I think similarly to you Eva I also had quite a different freshers week I think sometimes you do just get caught up in all the kind of craziness and hecticness of freshers and all that kind of entails um yeah maybe like a kind of rogue take but I actually enjoyed freshers week a lot I was really worried that coming to university would feel like really different to home um in a way that I couldn't cope with very well or any of those things but I actually just found the chance to kind of get involved in different things like really exciting and yeah also really nerve-wracking though Christina so I completely like completely relate to what you were saying like and I think everyone everyone was anxious and you could kind of sense the anxious energy in some of those rooms in Freshers Week. And then Judy you are you're a graduate medical student so you've had like two different freshers weeks so tell us a little bit about those like what did you get off to do you think studying like not medicine and then doing a medic freshers week were very different um so yes um in my undergrad I actually did not know what a fresh' Week was. And I feel like I kind of went in. I literally, because I was coming from Ireland, so I stalled as long as I could. So like literally the day before the lectures was when I actually arrived on campus. And I feel like I wasn't told much about Freshers' Week. I didn't really know the culture around Freshers' Week. I think we have something like we have a similar thing in Ireland, but in my final year of high school, it was never mentioned. So I did sort of miss Freshers' Week for my undergrad. I did end up making up for it because I got involved with some societies. So then I was sort of planning Freshers' Week events for like following years. So then I did get involved in like that sense. And I thought it was really fun. It was great. I didn't take like a lot of time to like enjoy everything, which I feel like I really should have for my grad. So we don't really have a Freshers Week here. I feel like I've like missed out twice now but um I like when I got here um we sort of just started lectures and I was lost and like I didn't know where I was going um but in terms of like social life it was very easy to like fall into the social like life of here because we live in student to calm like most students live in student to calm so we all just kind of met each other from that and socially it was really nice to kind of like be close to everyone. Yeah that definitely resonates with me too my university has like colleges which are like little mini universities within the university and it means that you kind of get very close to a lot of people without needing to worry about this like vast giant campus which I really liked but I also think it's it's kind of luck of the draw with who you end up living with because like in my first year house there were no medics so it made it very easy for me to meet non-medical students and then quite difficult for me to kind of get in with other medical students which I guess has its pluses and its minuses so yeah I had quite an interesting but like not dissimilar experience of the start of uni. So we've all kind of talked about socials and socialising that's what the whole episode is about so I'm kind of intrigued by what everyone's first medic social was. I know my uni has a different theme every year where we kind of plot freshers and first years against upper years in like and we do that it's always revolves around drinking like but it's always like themed so in my first year it was angels versus devils so I was a little angel and all of the upper years were devils that would kind of tempt us to the dark side and take us around all of the bars. But I really enjoyed it. I think it was a good way for me to meet upper years who like I've taken a couple of years out of medical school now. So all of the devils from that time are now doctors. And it's like terrifying to think about all of the like devil doctors running around all over the country yeah what about you guys ours was a bit different it was like it's the same theme every year I don't think it was in freshers week it was probably the week after it was like it's called cheese and wine and it's essentially like you pay I think 10 pounds or 15 pounds and you get a bottle of wine on entry and then there's like weird little cheese boards and like crackers and you're in like this club. It's super dark. And yeah, that was our first like medic social. I think it had medical students and dentistry students. So you got to mix with other people.
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At the time I was open to it, but I think now I don't know if it was my sort of thing just because it was I don't know a bit sketchy like if you saw the venue it was a bit weird um for me that we had like we planned a barbecue for freshers um for the freshers coming in um and I think it was like end of August or sometime around so the weather was really good um the barbecue it went terribly because we couldn't get the actual barbecue working so we ended up like going to kfc to like get like made food um but like in terms of like atmosphere it was really nice like i was just watching and i was like oh like i was like this is so cute like they're so excited and like they're ready for university and it was a really wholesome like feeling um and i think here um even though we don't have like an official freshers week um i saw like posters up for like speed friending i think that's the cutest thing like i'm not even a freshers and i want to go and i'm just like this is like such a this is such a nice idea like just being on different tables like getting to know people moving on like getting like people's contact details and I think it's such a it's a nice uh part of freshers week that's so wholesome I really wish we had like more of that culture I agree yeah completely I I think that sounds so much better Judy honestly so my first medic social sounds like much more similar to yours Christina and Eva um it was called dissection drinks I think that sounds so much better, Judy, honestly. So my first medic social sounds like much more similar to yours, Christina and Eva. It was called Dissection Drinks. I think it was also like in the second or third week or something. And it was, again, just like a super like boozy night. And I didn't actually drink at the time. So, yeah, like having all these socials like completely geared around like just getting hammered and making friends that way wasn't necessarily kind of in line with kind of what I wanted to be doing. My uni does like the college system as well, like Eva's and having events back in college that were kind of much more of a mix. There'd be like lots of wholesome non-drinking things and also just like hanging out with people like in your kind of corridor rather than house it was like a big a big block of rooms um and then having the like the nights out and the like parties and all of those kind of things I think that was much more balanced whereas yeah can't say I enjoy dissection drinks a great deal yeah that sounds much less wholesome I guess that's one of the good things about having a college system. It's kind of like social situations are kind of set up for you already in a way. Like you've already got a little people, a little group of people to hang out with and have your meals with and stuff. And I guess you do have that with flatmates, but it's not always the same. You might not click with them straight away or they're doing different courses. They've already got a bunch of friends at uni that they're like friends with and they're not really open to new people that's a good thing about colleges I guess I think on the point with flatmates um I think I mentioned this when I was talking to Eva like earlier um I ended up getting really really close with my flatmates based on like a game so there's this game I don't know if you've heard it uh of it it's called we're not really strangers it's like a card game oh yeah yeah and it has like all these like really cool prompts and you basically like there's like different levels like the first level would be like first impressions and then level two is like deeper connection and i feel like we learned so much about each other um and it gets quite emotional i think think by the end of the game, we were all crying and bonding over some of the questions. And we were in an all-girls flat. So it was very girly energy. Even though we were all quite different and different years and stuff, I feel like it encompasses the whole girlhood thing that you see on TikTok. And it just felt really nice. We would have like movie nights in. I helped one of the girls get ready for her first ever date. Like it was so nice. But yeah, that's kind of was my experience with flatmates. That sounds so cute, Judy. I really want to play that game now as well. That is like exactly like it's just so up my street. Like really want to play that no I love that I think that's such an important part of like starting uni like that whole first year of uni that like never gets talked about because I think like the whole discourse around it is so overcome by like drinks and like big nights and then all of the like work of uni that you actually like no one ever talks about how nice it is to just be like 18 like living independently for the first time and how much fun it is to get to like actually meet all these people like from all over the place that you would never kind of having well I don't maybe you guys would have I am from a tiny tiny village so I would have never met half of the people that I got to meet at uni had I not gone to uni and yeah I think it's just it doesn't have to be all kind of drinks and debauchery like there is definitely like a very wholesome side to it all as well. Yeah and I think like actually those are the moments you remember afterwards as well like yeah I the similarly to you Eva like the people I met in my first year I'd never would have met if I'd stayed at home. Like we're all very different. But like they're still my best friends now. And like we look back at that time of like, you know, getting to uni and within a week or two weeks, we'd kind of really tried to band together because everything was uncertain and new. But like it was so nice to just have those little moments. I think's all the like in between bits that are almost more special than yeah the you know the freshers week events or you know your first lecture or whatever and I think there's such a pressure put on people when they start you know that it's like freshers week has to be the best week ever and you have to go out every night and you have to go to every single lecture you won't do very well whereas like I don't think that's necessarily true I think there is a lot of value in like the the quieter bits like the as you say Charlotte the in-between so we've spoken quite a lot there just about how there's so much more to uni and socializing at university than the drinking and the big nights um there are also sports and societies that we can get involved with and we'll talk a lot more about those Let's get back to the show. Medical schools and university campuses have hundreds of student societies and sports teams for you to get involved with. For many, these can be a great opportunity to de-stress and to get to know people from other courses at your new university. So I wanted to ask everyone what sports and societies they got involved with. Charlotte do you want to start us off? Yeah so in my first year I found actually that everything was just so busy that although you go to Freshers' Fair and you seem to like put your name down, well at least I did like put my name down for pretty much everything, I think like you get caught up in all the like all the chaos of Freshers' Fair and you're so excited and you're putting your name on all these sheets and then you get inundated with thousands of emails but um I didn't actually have that much time to do societies um or sports properly in first year but I did go to a creative writing club quite a bit um which I think in hindsight I'm not actually sure whether that was like the right like place for me I'm not I'm not actually sure if I enjoyed it all that much sometimes which is I don't know it's kind of weird to look back on things now and you know when you just get caught up with something in the moment um but it was nice to have something completely different to medicine completely outside of college it was a whole new group of people um lots of whom weren't actually students at the university, so it wasn't like a university club, it was kind of just like a Oxford-wide thing.
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In second year, when I was a bit more kind of sure of myself and sure of what I wanted to get involved in I was on the like college welfare team and there were three of us who like supported the kind of students throughout the whole of the college and it was really really hard, it was absolutely exhausting, I failed my exams that year, I ended up in hospital with mumps that year, like it was in so many ways it was a it was a stressful time um but it was also I think where I really like found people who were like really super important to me and still are um and we work closely with the staff in the college as well um and yeah that was that was like a really comforting and like safe space and like a real community of people and I think I think if anyone is interested in like advice on joining sports and societies I think it for me it was about finding that community that might be different to the people who your friends are than seeing all the time but um yeah who just kind of offer you that different like side of things maybe I'm so sorry that it took like getting mumps and failing exams for you to find that community. That sounds so stressful. I know, that's awful. Okay, maybe I made it sound worse than it was. It was a stressful time, but I think, and it should never have been that stressful, but there was like a real like, a real like sense of bonding between the three of us who did it and helped each other get through like various stressful times, which was really nice. Yeah, I'd agree with what you said earlier, though, about like certain societies, you might join them and then realise it's not the right one for you. Like I joined, I think the civil, I joined too many and I had to kind of realize afterwards which ones do I actually want to go to and then some of the ones that I thought oh I'd enjoy this I actually went a few times and I didn't so I think that's why it's so important to just try as many as you can get all the emails in the world and then sift it down afterwards um but yeah yeah completely and also acknowledge that you actually just can't do it all like you will never be able to do it all. And it's really fun to like dabble in different things and like explore everything. But yeah, you can't, you can't pack it all in. Yeah. And it's good to try as many as you can, I think at the start, because that's when you probably have the least commitment and the least work. As the term goes on, and you've got exams and assignments, it gets a lot harder to try new things. So yeah, best at the start. Yeah start yeah I think also in first year if you really put like your everything into society and you you decide at the end of first year even before then that you don't like it I felt this real pressure like oh I've wasted first year like I've wasted this one year where I can do all this and I can never do societies again because first year's now over and I've not found anything yet but like in my second year I got involved with my college pool team like bar sports pool not like swimming pool and I loved it and I think I would I was never a sports person at school I was never like a I was so bad at PE that like I I don't think I ever passed a PE exam in my entire life, like I hated physical education. Stumbled into this college bar sports league and like really found my tribe over like hitting balls with sticks. And that was in second year, like you can keep finding what you want to do, like the whole way through uni. I think if you pick one thing or maybe two things that you really, really enjoy, like you find the time for them. You don't need to put that pressure on yourself to like always be working all the time. I think if you have to fit work around other things, it like nearly forces you to learn how to do that. Yeah, definitely. And also medicine is a a really long degree so there's like so much time to try different things like even in my so in my fifth year I got involved with the um kind of group of medics who like do a lot of fundraising and like write the medic pantomime and things like that and I met new people through that who are now really close friends again and yeah there's there's definitely no time limit it's not like you have to you're gonna meet so many new people through that who are now really close friends again. And yeah, there's definitely no time limit. It's not like you have to, you're going to meet so many new people all throughout uni. And that's another reason to take some of the pressure off first year, I think. So for me, for like getting involved in societies. So my year were like we were the pandemic year. Like we were just on the cusp of the pandemic when we started. So like by March, everything was like online. And I feel like the aspect of societies, a lot of them had to move online. And it was really, really helpful for time management for me. And then also like just in terms of like, I don't know, I think being involved in those societies really, really helped my mental health at the time because I felt like I was trapped indoors and like I wasn't really seeing people as much like face to face. And I think I was involved in a creative writing society like Charlotte as well. Except this one was run like inside of like our university and it was actually recommended by the well-being team at our university which I think is a really good technique because what it did was like a lot of people were like writing about like how they felt we would be giving like given prompts and then if you wanted to you could read it out to other people so it was kind of like sharing a lot of like emotions and ideas and stuff like that. And there was just a very supportive like network around it. And then I also got involved with the African Caribbean Society. I was vice president and I really enjoyed like the planning aspect. Like I really liked making things like happen, even though everything was online. We did like an online quiz night and I met two of my really like close friends like now, just from like that night, just because they decided to like log on. So I'm thinking, I'm like, imagine they hadn't logged on. I probably would never have met these like amazing people. So I think the social aspects of sort of joining societies, I guess it's in the name as well, is just a huge, like huge benefit as well. Yeah, absolutely. And it's really interesting what you're saying there as well about how like many, I hate calling them soft skills, but like skills that you don't get taught in your degree that you can pick up through doing like society work. Because I did, I guess, similar to Charlotte I did um media and communications for my college as well what year was I in second year maybe third and uh at the time I did it everyone was like why are you doing that like it's such a waste of time like you've got a medical degree to do and then I started this job with the BMJ and the the skills that I developed in that, I use like most days in this job. So it's not like sports and societies are completely in competition with your studies. Like they are developing life skills as well. And they're also an opportunity for you to meet people and enjoy your time at uni because it is like, yeah, medicine is long, but it's also precious time. like we're going to be doctors someday and have a lot less free time than we have at the moment so yeah I'd agree 100% with that either because to some extent I think society shouldn't really be seen as like an optional thing I think it should be not compulsory but you not only make a lot of friends and connect with people there's also a lot of skills that you learn well. I definitely agree with that. Even if it's just like extracurricular things like sports and stuff, I think there's so much that you can develop in that time that you might not think it's important now, but later on down the line, it would be like super crucial. Thank you all for your great stories about socialising at uni and about all these sports and societies that we have all got involved with. We will talk a little bit more about fitting these around our studies and how to achieve and maintain a decent work-life balance right after this short message. Welcome back to the show. So now I think it would be a good time for us to talk about work-life balance and how to practically fit all of these really important parts of the university experience in alongside our studies. Judy, did you have anything to say on this?
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So when I was working as VP for the ACS um I would try a lot to plan things around when I knew I would have a formative um or summative exam um and this would just be like a matter of like looking at the dates and knowing that okay maybe this week I'm not going to be doing as many meetings or this week we're not going to have any meetings as like at all um and then also like delegating with your um society members as well and you know if there's something that's come up like letting them know like far in advance or asking for help when you like need it um I know for our society because we were running it we had different roles but it was also a thing where if I was struggling with a specific area I would also be able to talk to someone else and they could sort of slot it or like help or fit fit things in so I that would sort of be my advice so schedule around exams and don't be afraid to sort of ask for help or ask for time off if you need it. That's amazing advice thank Thank you, Judy. Christina, you fit a lot of different things in alongside your studies, including but obviously not limited to your huge content creation for yourself and for other companies too. Do you have any kind of practical tips on how to manage your time and manage doing lots of things alongside med school? Yeah, I literally swear by using a calendar, like whether it's Google Calendar, Apple Calendar. At my med school, they give us a timetable and you can kind of like transfer it onto Apple or Google. So then that's what I do. So my Monday to Friday timetable's there. And then any time with friends, studying, like important events, appointments, I slot it in and I colour code everything. So I know like green is is studying I'm spending a lot of time studying this week or my social events are in yellow I can kind of like plan it out in advance so Monday to Sunday I know what I'm doing over the course of the week and it means that like Charlotte said earlier I can kind of like plan things in advance if I've got if I want to see friends in a few months time I can plan that out um I prefer it to to-do list because I think to-do lists I always just spend all day on one or two things and then ignore the rest but then putting it in my calendar means everything will get done. So that that advice is really useful and practical I honestly wish I could be a calendar person I think I really need to get on to that like when I get back to medical school so I thought like kind of tangentially linked to that then like managing your time around your studies and kind of important life events kind of links into staying in touch with these friends that we make after they graduate or like when they don't kind of live in the same cities as us anymore like they once did at the start of university I was just wondering Christina or if anyone else has any advice on like how to stay in touch or how important it is to stay in touch with your friends even when you feel like you don't have time to. Yeah honestly planning time with your friends it's more of like an essential thing than it is like an optional thing. You might think that you've got exams coming up you're super busy you, you don't have time, but it'll take a toll on your mental health if all you're doing 24-7 is just studying and spending at the library. And it can even, you know, sometimes if you're studying with friends who are in your year group at your med school, it can kind of be a social study event. You can study together, help each other learn things. But yeah, I really wouldn't feel bad about spending time with friends or getting a coffee with someone going for a meal. It might not feel like a big event or a big deal at the time, but it just helps with your mental well-being and it's just super important. Yeah, and I suppose it is easier to coordinate all of that if your friends are medics who are on the same course as you kind of doing the same things as you're doing um so it's a bit funny actually I don't have many non-medic friends like I actually in third year of fourth year when people graduated I didn't notice it as much most of my friends are medics um but what I would say is for the odd people that I do know is just try to make the most of social media as much as you can like you definitely have them on Instagram and on Snapchat so whenever they've got like a story that they're doing something cool or they're traveling just try to reply to like to them as much as you can and just show them that you're still there you're still thinking of them um whenever their birthday pops up on Facebook like drop them a message like just remind them all the time that like you're there and you want to stay in contact amazing um Charlotte yeah I think like for me so now like all of my friends have left university basically other than other than one because most of my friends were non-medics so they all left at the end of their third year or their fourth year and now because I took the year out and now I'm in final year all my medic friends have left too so uni this year is very very different to how uni has been before and staying in touch with everyone is it can be difficult but one thing I've noticed is all the time that I've got back from not you know not seeing friends as much like I'm kind of trying to pump that time into keeping in contact with everyone just it's just in a different format now so I walk back and forth to the hospital every day that you know it's like a half an hour 40 minute walk that's a great amount of time to call a friend um and just you know hear about how their week's going how it's been like settling into the kind of doctor life for them all which I think has been an adjustment for everyone obviously um and then I think like one thing that really helped. So I saw a friend on the weekend who I'd not seen for a whole year, which is just far too long to go without seeing someone who's really important to you. But we've kept in contact every week with just like sending regular voice notes to each other. And I think like that thing of being able to hear someone's voice and like just like their intonation and the way they talk about things and hearing them laugh and all of that, I think makes you feel so much more connected sometimes than just a message would. So I'd say like try different things, different things work with different friendships. And then the other thing is just plan dates to see each other really far in advance. There's a kind of big group of us who are like medics and we've realised that the next time we can all get together with everyone's rotas is Christmas. And that feels like a long time away, but if we don't get it in the diary now, then the next time after that will be even further away. So yeah, plan early and just find your different ways of keeping in touch with different people I think um and I know when we were kind of like thinking about the podcast Judy you said some really interesting things about like appreciating how friendships might change which I thought I yeah really resonated with me but Judy I just wanted to ask as well you've kind of seen this from both sides So you've studied in like an entirely different country and moved countries. So like your perspective on this is like, you're bound to be like the expert in it by this stage. So I just wanted to kind of ask how, like even being so far away, how has that changed perspective? So I do like definitely feel like this is my area because like I I um I moved from Ireland to England and I moved to England from England to Poland so like I'm like constantly trying to stay in touch with my Irish friends and my English friends and when I'm there I'm trying to stay in touch with my Polish friends so um I had to quite get quite good at um keeping in touch with everyone. And I think what Charlotte was talking about earlier, I did mention like kind of like understanding and anticipating like a change in friendship dynamics. Like we get so used to seeing people like every day that when they aren't there, there's like this sudden like feeling of like loss. But I think if we have like a realistic idea of like, OK, so I'm not going to be able to knock on your door it's not going to be as easy for us to plan things and just kind of understanding that just because they're a little bit further away doesn't mean that they've necessarily like that they necessarily care less about you or anything like that but I think when you have those expectations and you sort of have an idea of how it's going to be, it might make the process a little bit easier. Another thing, and I think I do this all the time, is to reach out shamelessly.
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I'm Stephen Morrissey, Managing Editor of the New England Journal of Medicine, and I'm talking with Margaret Somerville and Nicola Biller-Andorno about their clinical decisions article on physician-assisted suicide. Dr. Somerville is an ethicist at McGill University in Montreal, and Dr. Biller-Andorno is an ethicist at the University of Zurich, who's currently a Commonwealth Fund Harkness Fellow at the Harvard School of Public Health in Boston. Thank you both for joining us today. I'll direct questions to each of you, and I hope you'll respond to one another's statements as in a debate. First, Dr. Somerville, in your essay, you write that you do not support assisted suicide because it's incompatible with the essential role of physicians as healers. But what about patients with terminal illnesses where there's no hope for a cure? Why in those cases not allow physicians to assist in ending their lives if it would ease their suffering? which I regard as the same thing in terms of the ethics and law that should govern them, shows, I believe, that the damage that we do to the institution of medicine and indeed the damage we do to the institution of law in their capacity carrying of the value of respect for life and the danger of abuse regarding these procedures as ethical and making them legal is so great that we shouldn't do that. Dr. Biller-Andoner, what are your thoughts on the conflict between the role of a physician as a healer and the act of prescribing lethal medication to end a patient's life? Well, I think if physicians can offer a cure and if a patient wants a cure, that's great. But I do think there are two important limitations to the role of a physician or to the duty of a physician to heal. And I think one is there is no unconditional duty to heal. I think all medical interventions need to be legitimized through the will of a patient, at least if the patient's competent. And then I think healing is really just one element in what a patient does. I think there are other tasks, such as alleviating suffering and accompanying those who medicine cannot cure. And I think it's also a very special obligation to also not abandon those who cannot cure anymore. And I can easily imagine situations in which patients with very serious diseases consider physician-assisted suicide the best option that's available to them. And some of these patients may have experienced a lot of medical care in the past and may just not want any more of it. And I think in such cases, I don't think there is a duty with a conflict with a duty to heal, but rather I think the physician in that case would provide the kind of support to a dying patient that the patient has in fact requested. To continue along that line, Dr. Biller-Andorno, you say in your essay that there's a broad consensus about the importance of palliative medicine and hospice in helping to care for patients at the end of their lives. Yet you believe that for a subset of patients, those services are not sufficient. Why do you feel that robust palliative care is unable to address the medical and emotional needs of all patients? Well, first of all, I think palliative care has advanced greatly over the past decades. And I also think it has a very important influence and beneficial influence on helping us understand how a peaceful death is possible in very different settings, in the hospital, in the hospice, or at home. And I very much admire that work, and I think it's made a huge difference to a lot of people. At the same time, I think some people may not choose to spend their last days in a state of dependency, of being intensely cared for. And I don't see why we have to tell these people that they absolutely have to accept that. And I think a key idea is that we all strive for an authentic death. That is, we all want to die in a way that is in harmony with the values and preferences that we've embraced during our adult lives, most of our adult lives. And for some, this may mean to patiently wait for death to come. And for others, it may mean to set the scene themselves to determine when they die, how they die, etc. And I don't think we should make a judgment on what is the better way to die. For some people, I think what they perceive as a loss of autonomy and possibly a loss of dignity while receiving end-of-life care is so threatening to them, they prefer to avoid that. And I think we should actually respect that. What you're suggesting there, though, is what we call radical autonomy. And that's the value on which the case for physician-assisted suicide and euthanasia is based. And what that says is that my wishes dominate every other consideration. And the case against that is that we don't die as an individual. We die as a member of a family, as a member of a group, as a member of society, and that therefore how we die matters to all of those entities. And what we're talking about here is doctors inflicting death, to put it in very blunt terms, doctors killing their patients when you're talking about euthanasia. And we have to look at the impact of that, not just on the individual who, as you say, might want it, but on all of those other institutions and society itself. And so what we end up with is a conflict between respect for the value of radical autonomy, that what I say goes and I can have exactly what I want as compared with maintaining the value of respect for life. And the difference between the pro and anti-euthanasia groups is that the pro-euthanasia people give priority to the value of autonomy. The anti-euthanasia people give priority to the value of respect for life. And doctors are among the most important people in carrying that value of respect for life. I think there is a subtle but very important difference between active euthanasia and assisted dying. I think it's very important to appreciate that assisted dying really is a manifestation of the will of the patient, and I think the danger of abuse is much less than in the case of active euthanasia, where, as you're saying, one person is really effectively killing another person. I think this distinction should be maintained, and I would argue very differently if we were talking about active euthanasia. Yeah, although I don't agree with that, because I think what you can see in the jurisdictions that have allowed this, that you see what's called the logical slippery slope, that once you allow one thing, then the next thing does follow. Well, I think in those countries that you just mentioned, I think the idea was from the very outset not to exclude active euthanasia. But if you look at another country, such as Switzerland, which has this tradition of assisted use, sort of allowing that under certain circumstances, there's never been a strong push towards active euthanasia. But those two practices have actually been kept quite separate. And I think there's no slippery slope that can be perceived at the moment of Switzerland really drifting towards active euthanasia, nor in fact towards significant expansion of its physician-assisted suicide practices. If you're talking about radical autonomy, even if you think physician-assisted suicide should be permitted, of course considerations about family, about physicians do play a role. And I'm sure all patients who have actually chosen that option have given a lot of consideration of how to involve their families, if they should involve their families, how to make sure that their families don't suffer unnecessarily, et cetera. And I also think you cannot actually force or compel a physician to perform assistance in issues that, if this goes against a physician's religious beliefs or moral judgments? Well, we're seeing, what we see in the jurisdictions that have legalized these procedures, and maybe Switzerland is different, is that there is this expansion of what we call the logical slippery slope, and there's also the expansion of what's called the practical slippery slope. And what the practical slippery slope is is the abuse of these procedures. And there's very strong evidence that the abuse consists of using it for vulnerable, old, fragile people and disabled people. And that's one of the big worries. And as well, I mean, even if you look at the Oregon situation, which is the United States, and you look at the work of Dr. Kathleen Foley from Memorial Sloan Catering and Dr. Herbert Hendon, they did a book on this. And what you can see is that there are cases where the people are doubtful about whether they want to commit suicide. They're encouraged by their relatives. And I think that once we step over that line and once we allow physicians to be complicit in this, then it's very difficult to stop it. But I don't think that even the failure of being able to stop it is the main problem. I think the main problem is having physicians involved in people helping people to kill themselves or, in the case of euthanasia, killing those people. That's the main problem.
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And that's what we're thinking of doing. Dr. Biller-Andorno, to return to the point that Dr. Samuel raised about possible abuses, which is a concern that opponents of physician-assisted suicide have often raised. If patients do choose to end their lives for the wrong reasons, financial considerations, being a burden to family members, overwhelming depression, what sort of safeguards do you see that could prevent that sort of abuse of physician-assisted suicide? I think for the time being, these concerns have not really materialized, at least not in the programs that have been documented in the literature. I think right now, physician-assisted suicide rather seems to be an option realized by those who are very aware of the options, who are ready to make their case or ready to present their case to committees, etc. So to those who are actually highly educated and privileged. But I think abuse is certainly a valid concern. However, I think that those who are desperate, those who cannot afford to continue to pay for their care, those who have no place to go once the hospital has dismissed them, I think those people will actually find other ways to end their lives. So I'd rather like to think that we have a societal responsibility to make sure the more vulnerable members of our communities, in fact, feel appreciated and feel supported rather than banning a practice that might be appealing to those who are disadvantaged in a society. On the other hand, I think it's important to closely monitor the practice of physician-assisted suicide, including the motivation of those who are up for it. I absolutely think we have to have a very close look at this. And I also think we need appropriate procedural rules that need to be followed to aim to maximize voluntariness, and that is certainly have a very robust informed consent procedure, making sure that the wish to be assisted in dying is stable, to make sure it's very clear that you can withdraw at any time, to try to involve family members to avoid conflict, for instance. I think all of this, as it's been spelled out, for instance, in various programs in Washington and Oregon, needs to be heeded very carefully. As to the fact that you think that procedural rules will safeguard the use of these procedures, that's simply not true. In one study done in Belgium, in the Flanders region of Belgium, they surveyed physicians to ask them if they participated in either euthanasia or physician-assisted suicide. And of the physicians who had participated, they resurveyed them to ask them had they always done so in accordance with the procedural guidelines and the rules that were surrounded these procedures. And 32% of the physicians said they had carried out euthanasia without following the guidelines. So the fact that people who advocate this say, well, we can safeguard it, that is simply not true in practice, and we've got exactly the same results from the Netherlands. That, again, is two countries who allow both active euthanasia and physician-assisted suicide. But at the same time, I think, you know, if you establish a program, I think certainly this is going to be a learning process, and certainly there may be cases of abuse. There may certainly be a potential to improve rules and procedures. But I also think we have to see this in light of the alternatives. And I think that is the number of people who would just go out and kill themselves in some other way. In Switzerland, for instance, the number of cases of physician-assisted suicide has risen some, but not immensely, but the total number of suicides has remained stable. So there's reason to think that some of the suicides that would have happened otherwise in an uncontrolled way, so to speak, in a non-physician assisted way, may have now been channeled towards the physician. I mean, one of the things that people worry about with this is the message that we're giving in general in the society that suicide is an appropriate response to suffering. The people who work to try to prevent suicide are extremely worried about that. Also, disabled people are very, very worried because people who are then seen as a good act to help this person who's got a certain condition to kill themselves, disabled people say, well, I'm like that. I've got that condition. Do you think it's a good thing to help me to kill myself? I mean, those are the sorts of worries. These are the wider implications of legalizing this. I think these are very legitimate worries, but at the same time, I think these are really issues that need to be debated in the various political fora and that really call for public education. And I don't think you could, for instance, say we prohibit all genetic tests because genetic information Thank you. to help those people who think use that is the best possible option that's available to them, to offer them all the help that's available for sure, to show them alternatives, to make them be very aware that there are people out to help them. But if they reject that, to also help them comply with their wish if that's what they really want. But you see, there's a difference between somebody doing an act as an act of desperation when they don't know what else to do and they've done it all by themselves and they commit suicide as compared with a societally sanctioned physician involvement legalized in our law agreement that yes your life's not worth living we'll help you to kill yourself yourself. There you've got the ethics of complicity of both the medical profession and the law and society. And that's a hugely different situation from a spontaneous and sad act by an individual where if at all we can help to prevent it, all of us try to prevent the suicides. I mean, when you have somebody brought into an emergency room and they've tried to commit suicide, people don't stand back and say, oh, you're exercising your right to commit suicide, so we won't do anything. They go into full-speed action to try to save that person's life. And we're reversing that. To end by bringing it back to physicians, a question for each of you. Dr. Somerville, would you accept assisted suicide if someone other than a physician were responsible for it? No, I wouldn't, because I believe that in society we need to maintain this very fundamental value of respect for life and authorizing someone to help somebody else to kill themselves necessarily infringes that value. Respect for life operates at two levels. It's a respect for every individual human life and respect for human life in general in the society. And even if you could say, which I wouldn't, that authorizing this would not offend the individual's right because, as Dr. O'Donohue is saying, the individual gives their informed consent, etc., you would still be offending the value of respect for life at the societal level and you wouldn't be able to maintain it. And just as we've realized that we've got a physical ecosystem that we have to protect and hold on trust and hand on to future generations, we've got what I call a metaphysical ecosystem. That is all the values, principles, beliefs that are necessary to be maintained to have a society in which reasonable people would want to live. And of those values, I think respect for life is probably the single most important. So therefore, no matter who was doing it, it would still offend that value of respect for life. I just think it's even worse when it's physicians doing it because we regard physicians as healers, as those people who, particularly in a secular society, carry the value of respect for life, not just for themselves and those dear to them, but for the society as a whole. So I still would not agree with that, although I think if it is legalized, it should not be physicians who do it. And finally, Dr. Biller-Andorno, in constituencies where physician-assisted suicide is legal, what happens if patients are unable to find a local provider who will agree to assist? Is there any compulsion to bring perhaps unwilling physicians into the process? No, I don't think you can compel physicians to provide assistance against their own will, against their own moral judgment or religious belief. Because I think how you think about assisted suicide very much hinges on your very personal convictions about what is a good death. Is life and death given by God, for instance? Is this something you can take in your own hands? I think these are very individual considerations that you cannot, that mean you cannot really compel a physician to act either way. But I do think that you can require physicians who are unwilling to provide suicide assistance to refer patients to colleagues or to programs that are willing to evaluate the patient. And from what we know so far, programs or organizations that are well regulated have been able to find a sufficient number of physicians who are willing to engage. So I think there shouldn't be an issue of availability. I don't think legalizing physician-assisted use means that the respect for life is not being heeded or that certain life is not considered worth living.
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And I think what it wants to achieve is a peaceful death, a death that the individual can actually readily accept. And I think we can provide sufficient safeguard to maintain that as a practice that actually is quite in accord with our legal frameworks. And finally, I also think we shouldn't think of physician-assisted suicide as being against palliative care. I think we should rather think of this as a continuum, as a spectrum of options that are available to a dying patient. I think physician-assisted suicide may be one end of the spectrum, and I think it should be seen together with all the other alternatives that are available. And I think the challenge is to really make sure we work together to make sure the patient can actually have as much of their preferences heeded at the end of life as they really want to. Thank you, Dr. Biller-Andorno. Thank you, Dr. Somerville.
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🎵 Welcome back to the Curbsiders. This is the internal medicine podcast that uses expert interviews to bring you clinical pearls and practice changing knowledge. This is Paul Williams here by myself, plus or minus a couple of cats. I'm here to introduce an episode about primary care of the refugee patient. This is an episode we did as a live event at the Penn State Hershey Medical Center for their Grand Rounds, and we had the pleasure of talking to Dr. Tanuja Devaraj. As you'll hear in the recording, she got a just beautiful introduction from the staff there at Penn State, but you don't get to hear it, so I'd like to repeat it. Dr. Devaraj is a general internist at Penn State Hershey Medical Center. She completed her residency at the Primary Care Social Internal Medicine Residency at Montefiore in New York. Her professional interests include refugee and immigrant health, medical education, and health advocacy. Her interest in refugee health began as a medical student in Philadelphia, where she led a refugee health partnership working with Burmese and Bhutanese community in advocacy, education, and health care. She's continued to pursue her interest in migrant health in residency in the Bronx. She completed asylum evaluations, provided primary care for a large immigrant population, and did clinical training in Uganda. As an internist at Penn State, she works with the Bhutanese refugee population in the primary care setting and works on resident training in refugee health. She is a fantastic speaker on the topic, an undoubted expert, and was just a pleasure to talk to. And so without wasting any more time, I'm going to present our episode on primary care of the refugee patient. So I think we should bring our guest up, Paul. What do you think? I think that sounds great. So as we said up top, I'm not going to repeat the bio because the bio that was done was already outstanding. So let's please bring up Dr. Dhanusha Devaraj to talk to us about refugee health. You can applause again. That'd be nice. There you go. Hi, everyone. Thank you for having me. It's a pleasure. We're excited to talk to you. So before we get to talking about the main topic, refugee health, we're going to ask you some easier questions or maybe not easier questions. These actually seem to cause people more stress, but we're going to do it anyway. So can you give the audience a one-liner about yourself and definitely include something outside of your job as a doctor? So one-liner, I'm a 32-year-old woman. I'm also an identical twin. My twin is here in the family medicine department. Grew up in India, have lived all over. I would say I have a passion for medicine, health equality, people in general, cultures, and traveling. All right. That was great. The question that brings probably the most anxiety that we often ask, so I'm going to ask you for a book recommendation, fiction, nonfiction, doesn't have to be medically related, but something that doctors should read for whatever reason. So I was thinking about this last night, and I actually have two. One relevant for this topic, and one in general that I found very helpful throughout medical school in being a well-balanced physician. So the first one is Full Catastrophe Living by John Kabat-Zinn. It's a guide to practicing mindfulness, and it's also the guide for mindfulness-based stress reduction that we use for patients, individuals who are coping with stress, chronic pain, and I think it's helpful in being a mindful doctor and also having this as a tool for patients. The second one is a fictional book about a couple that is a refugee, supposedly from Syria, but they don't actually disclaim. It's called Exit West by Moshin Hamid. And I think it gives you a very magical, fictional, but realistic view and storyline between what it means to be a refugee. Excellent. Oh, yes. What's your favorite failure? This is not in the script, but I love this question, and I know you didn't prepare for it at all, so it's perfect. If you can recall your most memorable patient complaint and what you learned from that. So either a favorite failure or a patient complaint. I think we need to get your favorite patient complaint one of these days, Stuart. We're going to Tunisia now. I mean, the failure is very easy to remember because I don't think a lot will forget it. And this was when I was at MS3, a medical student, just starting my clinical rotations in internal medicine. And I had a very challenging and disheartening experience where a hospitalist said that I wasn't fit to be a doctor. I will never forget that and that was yeah a challenging experience and luckily it's not true but yeah I think what I learned from that is what it means to be a mentor and a teacher and I think I'll always remember that working with medical students and residents is the impact that we have and remembering about constructive learning and positive feedback. And to be fair, that was the example of a bad mentor, right? Did they give you any constructive, did they even give any specific examples? Was it like at all meaningful feedback or was just like, yeah, I don't think this is going to work out for you, full stop, no embellishment? I think it was more of a personality or a cultural mismatch. Like I think she just didn't like the way I presented or the way I was in rounds. And it was not her style of working and practicing. And, and I just started clinical rotations. Yeah. Well, and shout out to that person now, as you give this your first grand round. So before we move on, I would like to say, so we're talking about your training. What is so far in your training and in your time as an attending, what's the best advice that you've received that you would like to leave the audience with? I would say two things. So we had a course in clinical reasoning at Montefiore, which I learned a lot from. And something I really took away from that and remember is don't anchor when you're taking a history and forming a differential. Always be thorough. Think about all the possibilities and keep thinking about the possibilities before anchoring. And I think it's done a lot as we copy-paste in our EMR. Patients get labeled with diagnoses that are not actually true. And I try to remember that. Yeah. Something that Uncle Bob, Bob Centaur said, I think I've said this on multiple shows, but he said, we were talking about pneumonia and he said, when the emergency department tells him a patient has pneumonia, he assumes it's not correct. And then he tries to convince himself, you know, maybe if it is pneumonia, he tries to find evidence that it might be. So I think that's a good way to avoid the anchoring bias, especially with all the handoffs that there are nowadays in medicine. Should we do Picks of the Week? Yeah, absolutely. So for the audience, if you've listened to our podcast, the Picks of the Week on the pre-recorded podcast episode is a little bit different than the way we do it on Grand Rounds. So Grand Rounds, I ask for a Pick of the Week from Paul and Matt, and they'll give me one. And so, for example, the one that Paul gave to me was Ad Astra. And so what my job is is to match it with something eclectic to see if I know them very well. So it's either Ad Astra or the 1998 film Lost in Space. Well, yeah, it's a real head-scratcher. Yeah, Lost in Space, which sank beneath the critical waves immediately because it was awful. So I think I'm going to stay with my pick of the week. And we'll burn through since I'd like to actually get to the meat of the talk. But if you like science fiction and you have a complicated relationship with your father, add Astra. And by the way, I was talking to my mom about this. If you like science fiction, by definition, you probably have a complicated relationship with your father. So add Astra might be the movie for you. No comment. Okay. And then Matt, he sent me Snuff by Terry Pratchett. So you can either pick that one or this wonderful Lego set that I picked for no apparent reason whatsoever. Dude, I would go with the Lego set. So I'll say a word about Terry Pratchett. The Terry Pratchett Discworld series is, it's like fantasy, mystery. It's also the main character, Sam Vimes, it becomes very more, he's a lovable curmudgeon.
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But I would highly recommend the Discworld series and the City Watch or Night's Watch series, which Snuff is part of. But I build Legos with my kids every day. We have so many Legos. That's like a main activity in my house. So I will choose Legos. Excellent. I just want to point out that the whole reason I picked it out is because Watto is included in the Lego set. So I have succeeded in making you choose something that includes Watto. Okay. And then my pick of the week is this doctor puppet. So I brought it to work actually on Thursday and had the residents present to the puppet. It was the most, it was the strangest rounds we've ever had. I see a meeting with human resources, with human resources in your future. We should, we should start to move it. Yeah, we should because next one was a plague mask. We're going to skip that one. All right, Paul, why don't you start us off with a case from Cashlack? I would love to. This is what we're all here for. So let's talk about the case of a 35-year-old woman from Mali. She presents to your clinic, which is a primary care clinic, initially with a concern of loss of appetite. She's here for primary care, and your job is to obtain a migrant history. And this revealed that she is an undocumented immigrant. She has fled her country from persecution and is trying to seek asylee status. And so I think while we're waiting for our translator to show up and while we're trying to sort of wrap our heads around all that means, I think it's probably helpful to start even just with some basic definitions. So if you could even just help us differentiate what is the difference between a refugee versus an asylee versus an asylee seeker versus a migrant, if you could help us with that to start. Sure. So a refugee is anyone who has fled their country due to persecution or war or violence. Once they have fled to a neighboring country, they are granted refugee status by the UNHCR or by the host country. And they're protected legally to have basic rights to shelter, education and health care. It's a temporary resettlement until they get assimilated or resettled into the host country or a third country, commonly the U.S., yeah. An asylee is someone who is also fleeing the country for fear of persecution, but that hasn't been granted that sanction or protection yet, and they are in their host country going through a prolonged legal process trying to obtain refugee status or permanent resident status. A migrant is someone like myself or anyone who migrates to a foreign country in order for educational or economic or family opportunities. Paul, you have crack at where do you want to go from here with this? So let's start with the population that you have some familiarity with. And obviously, this is a big question, and we can sort of get to more granular details as we go through cases. But our patient's from Mali, but you have specific familiarity with the Bhutanese population. So I wonder if you wouldn't mind just giving us a little bit of background about them before we kind of get into the meat of the case. Yeah, all of us here have probably met our Nepali-speaking Bhutanese population. Often they introduce themselves as Nepali, but they're actually a refugee population, and there's a large community of them in the Harrisburg area. I worked with this population in Philadelphia when I was in medical school, and a lot of them have migrated to Hershey or to other areas, again, for community reasons or for job reasons. And they're a refugee population from Bhutan. They moved to Bhutan in the 1600s. They're predominantly Hindu. They've lived there for many, many years. But in the 1990s, as part of a nationalistic and ethnic conflict and cleansing in Bhutan. They were forced to leave Bhutan. Their rights to citizenship were taken away, and so they lived in Nepal in refugee camps. So most of our patients, the wait to get in or come to the U.S., which I think the U.S. started accepting refugees from Bhutan in 2005, have been in those camps for 10, 15, 20 years. The younger generation typically born in the refugee camps. And they come to larger cities like Philadelphia to resettle and then often migrate depending on where opportunity lies. And so Pennsylvania actually has the largest Bhutanese refugee population. We have around 9,000. And the U.S. till now has resettled 90,000 from Bhutan. We were actually talking a lot about Bhutan and the whole situation last night. And one of the things that I brought up to Matt, that Bhutan is actually the only country in the world that has a ministry of happiness. And the only reason why I bring this up is not to be funny or anything, but even in a country that's labeled as having one of the highest standards of living for their citizens, there are still segments of the population that are either disenfranchised from being involved with that government or are otherwise disadvantaged in some way, shape, or form. This is what happened with the Nepalese-speaking Bhutanese in the 90s and early 2000s. So just bear that in mind that oftentimes what you hear in media may not reflect the actual situation on the ground. And we should always kind of question what we're told when something like this happens. And so just think about it. And that's actually the current king of Bhutan. I can't pronounce his name because it's like very, very long, but that's him and his wife right there. Well, with that said, Tanuja, we are going to be getting into what, as a primary care doc, what would be our roles when we're meeting patients who are refugees. I think it's worth touching on what happens before somebody comes to the U.S., what basic things in broad strokes is, what basic medical care or medical screenings are done? Because I think everyone just kind of probably thinks, okay, you should check patients for tuberculosis. Is that like a major concern when people are migrating or I'm probably using the wrong terms, but forgive me. That's fine. No, you did fine. So yeah, again, like I said, it's a really long process to be accepted as a refugee to resettle in a host country or third country. And six months prior to them migrating to a country, there is a visa medical examination and there's like clinics or doctors that have official guidelines and what they need to examine for. And it's the initial checkpoint or exam is a very like broad generalized exam, making sure that there's no active TB or like schizophrenia or like obvious and glaring illnesses that prevent someone from successfully migrating and also to protect like the population from transmitting infectious disease. So it's a very general physical and mental exam. They don't screen for latent TB or chronic diseases or anything like that. It's just looking for if they have obvious illnesses at that point. What exactly happens to them if they have these illnesses? So most patients are, not patients, or individuals at that point, are eligible for treatment and following their treatment with the DOT and then rechecking them several months later and seeing if they have been cleared and are still accepted to the host country. It's very rare that someone gets rejected based on their health condition. And at this point, they're living in a refugee camp and the host country is kind of helping them through the paperwork to see if they're going to be given refugee status. Am I understanding that right? Yes. Okay. So I think we want to spend most of our time talking about when you're actually seeing patients in the primary care office. What would a first visit look like? So it depends on what context you're seeing the patient. So once they arrive, the CDC has guidelines for an initial domestic medical examination. And if you are, I think Jefferson, where I went to medical school, was one of the clinics doing those initial domestic medical examinations. And then a lot of them are just Department of Health clinics or physicians who have partnered, and this is what they do. And that's very different from the setting that we see patients in, which is not the initial exam or the initial checkpoint, but people who have resettled for a couple years often lost a care after this initial checkpoint and coming to you for just routine primary care. So at this, the CDC has a nice guideline on their website about what the initial checkpoint includes, and this is, again, more targeted at, like, making sure that we protect public health and transmission of infectious diseases. So it's looking for latent TB or active TB. HIV is no longer recommended pre-departure, but it is recommended post-arrival.
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And then you can consider a CBC, a BMP with glucose to look for chronic illness or diseases, and then updating their vaccinations as well. So that's the major coverage at the initial exam. And so this is, just so I'm understanding, this is the initial domestic exam before they're still seen in your primary care office. Is that correct? So can you take on face value that all that stuff's going to be done? I guess when you're meeting the patient, what can you assume 100% for sure is done and what things do you have to sort of reinvent? Because my understanding is there's some variability among the initial domestic examination. Yeah. So I think these are guidelines and recommendations and they're not always consistently implemented. And they should have a record of what's been done, but I almost never get the records from patients, and it's really hard to know what has been done. So I keep in mind what's recommended, and I actually repeat, and most providers do who do primary care for this population will try to get records, and what they can't confirm will repeat a lot of these tests or initial preventive screenings. Paul and I were talking about this yesterday. I thought it was interesting from vaccination specifically. This is just like something that I thought was very practical knowledge. They were like, for most of the vaccinations, if there's any question, just repeat them. Specifically hepatitis B and varicella, they're like check titers before you just like revaccinate with those. So I guess I'm not sure if you're doing that in your practice, but I thought that was insanely practical to know that. Yeah, I would agree with that. Like Tdap and MMR for adults, most patients have received those prior to departure just because of the programs and healthcare opportunities in their refugee camps. But hepatitis B is not often given. Varicella is not often given. Pneumovaxes, flu shots are, yeah. Who's providing the healthcare in these refugee camps? So a lot of times they're like UN aid organizations providing health care. The host country itself, you know, they try to provide education and basic health care as well. So it's a combination. Yeah. When you say host country, I want to make sure I'm understanding. So let's say when I was in residency, I had some friends from Syria and there was some some of their family members were in like Jordan in camps, but then is that considered the host company country or is the host country, whatever country they're trying to get into, uh, for more permanent settlement or is it, they might have multiple host countries. It's multiple. So the, so Jordan may is their initial host country because they're essentially providing them a safe, um the war or violence that they're fleeing from. And then because, like for Nepal example, it's a poor country itself, so it's not able to assimilate these individuals. So then they're looking for a third country to migrate to. Yeah. So you mentioned, I mean, this is primary care just in general, but in terms of not being able to get a patient's prior medical records like that, just feel, I don't think I've ever seen them ever. They're, they're my white whale. But, but I feel like that's a reasonable segue to talk about other barriers that you sort of, you might run into this initial encounter and just in general, in terms of taking care of this patient population. So I feel like language is probably an obvious one and the records are one, but what other things should you be mindful of during your first visit as you take care of these patients? Yeah, like you said, the social economic determinants are kind of obvious ones like language, culture, access to insurance, and navigating the healthcare system. But I think good particular examples is often when after their initial domestic examination, they have welfare or health coverage for eight months as part of their resettlement into the U.S. And after that, there's a huge period where people become uninsured or don't know how to apply for Medicaid or how to get insurance. And so there is a lot of fragmented and interrupted care in the initial arrival and by the time you see the patient. So the first encounter is usually that they have really uncontrolled chronic medical conditions or have been out of care for a long time. And so that's, I think, your first barrier is keeping that in mind. They might come to you with eight different complaints, and that's how the typical presentation is. And the other common barrier is people don't have a concept of primary care and continuity care because that's not something that they had access to in refugee camps. So their health belief is you go to the doctor when you're sick or when you have a physical complaint or a problem. So I think being aware of that, they may not understand that you want to see them every three months for their diabetes or they need to take the medication daily for a chronic illness and keeping that in mind and doing a lot of education and teach back when you first meet these patients. Speaking of communication, all the papers that you had sent us mentioned how important it is to use official interpreters, not to use family members as interpreters. And I know it's always more, it's like convenient to use and very tempting to use family members as interpreters, but especially all the papers were suggesting definitely use official interpreters. And even when you do that, there's certain understandings of diseases like high blood pressure. My blood pressure is only high when I exercise, or my blood pressure is only high when I'm in pain. And maybe you can give an example from the Bhutanese population. Are there any chronic diseases that we commonly treat where there's like a barrier where the way that they think about the disease is different than how Western medicine would think about it? Yeah, and I don't know if there's like one particular example or this is the belief of hypertension, but I think every individual is a little different and they have their own interpretation. I had a patient the other day that she was having a chronic cough. So I stopped her ACE inhibitor and she didn't actually have high blood pressure. And I said, let's, you know, see you the next visit. And then she said, well, I said, did you stop it? And she's like, I did for some time, but my neck started hurting. And I think that was related to my blood pressure. So I restarted the Lisinopril and then her cough got worse. And so it's just telling her, no, this is what blood pressure means and I don't think it's related to your neck pain. They may not believe you, but trying to find a common ground to say, let's try this again. Let's stop the Lisinopril. I think in reading this, reading about this, it's not an area of health that I really have any, I have really practiced minimally and I hadn't thought about it, but I think it just gave some good practical tips just in any of our patients, probably just asking them like, what's your understanding of like what diabetes means or what high blood pressure means. And, you know, their understanding of the need to take a blood pressure medication every day is probably good to assess because it seems like that's where a lot of these things trip up. Like a lot of just the practical aspects of things, particularly with refugee health, kind of model some of the things we see with patients who are born in this country. Yeah, I think it's not that who cares what I think because I'm not the expert here. But in terms of like, I think, well, as we'll discuss moving forward, it sounds like the therapeutic relationship is going to be really important in terms of, I mean, any patient relationship, particularly with this patient population in terms of establishing trust and sort of treating not just the chronic diseases, but maybe even some of the past traumas. And before we get there, though, I just didn't want to miss a chance to talk about the migration history, which is an element of the social history that I have virtually no experience with. So I wonder, I just don't want to lose that thread while we're still sort of meeting this patient for the first time. So if you wouldn't mind just telling me how to approach the migration history and how you might even sort of prepare for it before talking to the patient. Yeah, so a lot of times you may not be able to prepare for it, just as an example of this patient who you don't know that, you know, they're, you don't know that they're seeking a Sally status, they're just coming to you for routine primary care. But as in our situation, like we are familiar with this population and just knowing a little bit of their background, culturally, religious background, and the politically what they've been through and their experience in the refugee camps, I think helps you prepare for understanding what you're walking into.
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The UNHCR has a lot of information about refugee camps and their challenges in those camps and the health challenges that they face as well. So I think just knowing who you're getting to know is important. And then I guess the next part of it is taking a migration history. So I think this is the key component of your social history, and you can weave it into your social history when you're getting to know a patient. And it's just starting very broadly and open-ended, asking about where the patient was born, and if you know that they're a refugee, what year did they migrate to the refugee camps, how long did they live in the refugee camps, what was life like, and what was their access to education or to food security, to health care, just to kind of understand what went on in their life there. For a lot of people, that's, again, 10, 20 years. And then I always ask about migration to the U.S. or where you're interviewing them. A lot of times you get separated from families, and that will give you insight into family structure and who's in the household. And a lot of time there's economical and physical and emotional strain in the migration process as well, if it's not a peaceful or easy migration. And then I think the next phase you ask about is their settlement process to see how is it going living in the U.S.? Do you feel well adjusted? What are some of the things that are hard? What are some of the things that you're enjoying or you like being here and getting that part of it. And then the tricky part I think it weaves into is the past medical history. When you ask someone what medical problems they have, they may say, oh, nothing, I was fine. And the answer is not what you're looking for. And so asking it in a different way, were you taking any medications before? When was the last time you saw a doctor? Did you have any surgeries? And weaving into those different parts of the history in that direction. So from a practical standpoint, during this process, during the resettlement process, in the United States, who covers the cost of medications, health care, etc.? So do they have access to medications and do they have to pay for it? Where does it come from? During the initial process, do you mean? Yeah. So during the initial process, screening, oh, you've got diabetes, let's start you on something. Who covers that? So they have, I mean, it's like Medicaid. They have medical assistance for the first eight months as part of their resettlement process. So that's through the government. That's through federal government, not through state? Through federal government. And then after that, they would have to apply for medical assistance, which might be very complicated for someone who's not a native speaker and doesn't have great resources at their disposal. Exactly. That was some of the advocacy work that we did as medical students in Philly was having, I mean, after the ACA, there were more and more opportunities for having access to insurance. And then after Pennsylvania passed the Medicaid expansion, that also made things easier. So we were just in the community setting up just workshops to help people fill out these applications and get insurance because, yeah, a lot of people aren't insured. And depending on the state you're in, you may not be able to get that insurance. So some states don't even allow them to apply for Medicaid if they're not like a citizen or something? No, they're eligible to apply for Medicaid because they now usually have a permanent resident or green card status and they're in their process of getting citizenship. But this is the same for any underserved population. If Medicaid expansion hasn't been applied, then there's a very small percentage of people who are eligible for Medicaid. So let's return to our patient. And to recall, because we went a long way. So this is a 35-year-old patient from Mali who's reporting a loss of appetite. And so with some exploration, it sounds like maybe this is possibly due to patients' underlying depression. Maybe there's some post-traumatic stress from a traumatic migration process and the loss of her children. And so as you uncover and explore all this, I wonder if you wouldn't mind talking broadly about how commonly you see mental health issues among refugees and sort of what are the more common mental health disorders that you uncover as you're doing this kind of exploration? Yeah, I think mental health is one of the most common chronic medical problems that you will see in your clinic setting. And that includes anxiety, adjustment disorder, depression, and PTSD. There's different studies out there in the literature, and some say the rates of PTSD in this population is as high as 30%, and depression is also as high as 30%, and the rates of suicide is twice that of a U.S.-born individual. So there is a huge mental health impact due to their history of losing their nationality from their country of origin and their country of birth. Process of migration is itself a very stressful and traumatic experience. And then just waiting in a limbo period until they come to another country and then assimilating here, especially in our older population, if you've met anyone like over 40 or 50 who... Careful. That's easy with the older population. Well... But older for our refugee population, I mean, because they're... You'll see the younger population are well assimilated because they take ESL, they learn English, and can work and have kids and have a reason and purpose to be assimilated into our culture. But the older population who have lived in a very rural setting, especially the Bhutanese population, who don't know how to read and write in their own language, find it very, very hard to adjust to this, yeah, environment. I think I went on a tangent. I'm not sure what we were talking about. And I'm glad that you sort of talked to the Bhutanese patient population. Are there any barriers that are unique to the treatment of these underlying disorders with UG populations or the Bhutanese? I know that access to sort of mental health services just in general in this country is kind of a nightmare. So for this population, are there any additional barriers? Yeah, I think for any individual who's not from a Western culture, the definition of depression and anxiety or the terminology may not even exist. And so the expression of these mental health concerns is not your typical presentation. Your patient's not saying, you know, I feel sad, I feel low, I'm not able to get to work, or I'm not able to get to these things. The presentation is usually somatic symptoms of headache or fatigue or abdominal pain, insomnia. I think maybe we can read the next case and kind of expand this discussion a little bit more. So the other case that we had was a 40-year-old woman with a history of diabetes, high blood pressure, chronic pain. She's coming for establishing primary care. She's a Bhutanese refugee. She's been here for five years, recently relocated from Virginia because the public health assistance coverage was not great there. She's got high blood sugar, high blood pressure, and hasn't been on any medications in the past month transitioning to Pennsylvania. She's got chronic pain all over her back and all through her legs. And when reading this case, again, I was trying to make parallels between patients that I've cared for just kind of in primary care and the refugee population. There was a woman I was caring for for several years for chronic pain. And after knowing her for three years, seeing her once a month or once every three months, like very frequently for just always, there was always somatic complaints. One day she just started telling me that her husband used to beat her. He died young. She had a child that died. And she just started just telling me all these things that just sort of like, you know, just sort of tied. I suspected were driving some of the somatic complaints, these just very like major past traumas that she had been through. Have you noticed that in the refugee population, this sort of thing is something that people are telling you about? And do they have any insight into that these things may be related to their symptoms? Or is it just something that you sort of have to guide them towards understanding, which is probably very hard to do? I mean, I don't think it's common that patients connect their physical complaints to a history of trauma or torture or just to the stress of assimilation and migration. And I think that's true for any of our patients with a history of trauma, wherever they're born or wherever they're from. I think it's good to, people are more comfortable with their physical complaints.
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And then over time and over building a relationship, you work with the patient to explore their prior stressors and trauma and their current stressors and to see if we can make that connection. But I think the most therapeutic thing is validating and building that relationship. Are you using any specific screening tools when you're talking to patients, particularly about PTSD or when you're trying to elicit a history about trauma or torture, or do you just sort of use your own questions? I know there are some tools, but I have no experience using them. Yeah, the tools that are available is the Harvard Trauma Questionnaire and the Hopkins Symptom Checklist, which I haven't used, but it's validated in different cultures and different languages for refugee population. You have to purchase them. They're not always easily available. So you can use the, I use the PCL-5, which was developed for veterans. And it's a guide to the PTSD diagnosis as per the DSM-5, which I think is a pretty good tool. And I also use the GAD-7 and the PHQ-9, but just modifying the questions and doing the questions a little bit with the patient to get that information. Yeah. There's also a one-question abbreviated PTSD screener from the PCL-5 that you can use, but I don't know if it's validated in refugee populations. It is in veterans. Yeah. This might be the place for this, and it's probably an uncomfortable discussion a little bit. And, you know, we talked sort of before this. So rather than me dancing circles around it, in terms of eliciting a history of past trauma or even potentially torture, which is certainly a concern in patient populations and refugee populations, is there, I'd like to hear sort of what the general recommendations are, but then I think more importantly, your specific approach and how you address that, kind of, if at all. Again, the general recommendation is that all refugees are recommended to be screened for trauma. And the CDC has a simple, like, two question steps that you can do. And one is, have you ever experienced violence or trauma in the former country that you resided in? If you did, would you like to talk about it? And leaving it open-ended. And I think Jama had a good article about questions that you can ask about trauma or witnessing trauma or torture. In practice, again, if you're not their initial physician or you're not at their initial checkpoint, this may feel out of context when you're seeing a patient in clinic for the first time. They're coming to you with headache, back pain, A1C of 11. They haven't had insurance or medications for a while. And so that's their agenda. So understanding what their priority is and your priority in the first few visits is establishing care, building that relationship. And then I think in practice, if you, you should be screening for anxiety and depression and mental health as we do for all of our primary care patients. And if there are signs of anxiety or depression or signs of PTSD with nightmares or hypervigilance and you're managing these mental illnesses, then eventually asking them about prior trauma and prior stress that they've experienced, I think is very valid and very helpful in caring for these patients. she had high blood glucose and hypertension. So of course, we're going to want to address that. We're going to want to address her pain complaints. And help me out just recapping the initial labs that we were going to do, maybe like a CBC, BMP. And then we were going to make sure her vaccines are up to date, check a varicella and hepatitis B titer if we're unsure about those ones. Apparently, they're very expensive to just give. And then are we giving her albendazole? We didn't talk about that, but that's something I'm dying to give a patient albendazole. I have not had the occasion. So most refugees should be empirically treated prior to their migration to the U.S. And I don't empirically treat for helminths or schistosomasomas or Strongylides. And we have our ID expert in the audience. So I do tests. You do a stool test for ONP and for Schisto only if they're in an endemic area where they have frequent contact with water-rich areas. And then Strongy, you do the serologic testing as well if they come from an endemic area. My favorite, what was terrifying about that one, they were just like, oh yeah, a lot of the worms will just like die off once they're out of the native population and stop getting like the life cycle. But Strongyloides can just like, it's all in one, it's all in the same person. So that will not go away if they have it. So you have, and the serology is much more sensitive than the stool. Than the stool. And strongyloides is important, or the reason we fear it is if patients become immune compromised and they have a chronic infection, the hyperinfection syndrome can be very, with the high mortality. Okay. And I think the only other thing we would be doing, STI testing, testing for sexually transmitted infection, make sure they don't have like super gonorrhea or something like that. The special super gonorrhea screening test. Yeah. Yeah. And then anything else I'm missing for that exam before we go for audience questions, just kind of recap like what we'd be doing at that first primary care visit, or at least the first few primary care visits? I think that's everything. The two things that I will emphasize that I think that's unique for refugee populations and especially our Bhutanese population is the chronic illnesses present differently and often present at a younger age. It's not uncommon to see a 35-year-old thin woman with raging diabetes or uncontrolled hypertension. So it's a little different from our population and what the USPTF recommends. So I would definitely check an A1C and a lipid profile for younger refugee populations. And I think there's hepatitis B and hepatitis C, less so for our Bhutanese population, but populations from sub-Saharan Africa or the Hmong population in Thailand or the Burmese population, the rates of hepatitis B and C, very high. And this is your chance to prevent HCC. So always screen and link to care. And with these chronic diseases that you're seeing, so I think we've used raging as a descriptor a couple of times for the diabetes, is that an acute recognition of a chronic problem or how much of that is a component of sort of westernization? And I guess along with those, they come here and then just eat the garbage that is available. So I guess, what is the role of anticipatory guidance also in terms of sort of, does it differ at all from general primary care with refugees in terms of how you counsel about how to eat and what to eat? That was a lot of questions stacked together. Yeah, I would say, so I think there's definitely, after they move here, they're at increased risk for obtaining or assimilating to hypertension, diabetes. But it's actually in the trend globally due to globalization and rapid urbanization, the rates of chronic diseases in their native countries are very, very high. So depending, Iraq is an example, very high rates of diabetes and hypertension, South Asia, and even sub-Saharan Africa. When I was in Uganda, you know, you're seeing AIDS and then you're also seeing uncontrolled diabetes. So I think this double burden of disease and rise in non-communicable diseases in the global setting is a true and real thing. That question just reminded me of one of the cases in one of the papers mentioned that there was a patient with uncontrolled diabetes, and the fix was that she had been through starvation, and they just had to kind of guide her towards better foods. She wasn't willing to cut down on portions because it was a whole thing of having been through starvation. She just, you know, that was something that probably would have never occurred to me to even think about when I was trying to counsel somebody. So something else to think about. Should we take audience questions, Paul? Or do we have, Stuart, you want to? So if anybody would like to ask questions, either you can yell them out or you can come down to the bottom of the steps here. Also, we are happy to end early and just hang out if there's no specific questions. Or Stuart can do a couple minutes of stand-up, which... Please don't let that happen. I beg of you. Somebody ask a question. One of the things that I'm noticing when I have a refugee population patients, they come in as families. They'll be not just one patient, but actually several people all with different complaints. And they'll often schedule all at the same time.
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We do it with all our patients. You will get buy-in. And I think over time you will be able to establish that individual relationship with your patient, and I think that's important to talk to the patient directly without family members being there. Any other questions? Are there any other resources that you use to prepare? Obviously, you're familiar with the Nepalese population, Bhutanese, but are there other resources that you use to prepare when you know somebody's coming in from refugee from another country or home country you may not be familiar with? Yeah, there's multiple resources. So the UN Refugee Organization or the UNHCR has important information about the number of refugees, the life in refugee camps, the health issues. The CDC has a nice country profile for each refugee population. I also use the WHO and the Lancet in understanding epidemiology and global burden of disease. There's a good Lancet tool that gives you a little pictogram of what the most prevalent conditions are and what's the highest burden of disease, there's a good Lancet tool that gives you a little like pictogram of what the most prevalent conditions are and what's the highest burden of disease in that population. Yeah. Okay. Well, we can end a little bit early unless anyone else has any burning questions. And maybe we should do an outro. All right. Yeah, sure. For form's sake. So this has been another episode of The Curbsiders. We're going to give you a little knowledge food for your brain hole. Yummy. Thank you, Stuart. I'm glad to see you so directly engaged in front of the audience. Get your show notes at thecurbsiders.com forward slash podcast and sign up for our mailing list at thecurbsiders.com forward slash knowledge food to get our weekly show notes in your inbox. That's right, Paul, because we're committed to providing you with practice-changing, high-value knowledge. I just flipped that. And to do that, we need your feedback. So please subscribe, rate rate and review the show on iTunes or contact Matt directly at thecurbsires at gmail.com special thanks to our social media team Hannah R. Abrams on Twitter Beth Garbs Garbatelli on Instagram I still don't even know what that is and Chris the Chew Man Chew on Facebook until next time I've been Stuart Kent Brigham and I would like to thank Stuart for composing our music and Claire Morgan at Notterly for editing our audio and until next time, I've been Stuart Kent Brigham. And I would like to thank Stuart for composing our music and Claire Morgan at Notterly for editing our audio. And until next time, I've been Dr. Matthew Frank Watto. Thank you so much for the opportunity to be on Curbsiders. I listen to you guys often. And until, I guess, maybe next time, I've been Dr. Tanuja Devaraj. Strong work. And I remain Dr. Paul Nelson-Williams. Thank you. Okay. We have a pun. Oh, God. You can just applaud. We don't need this. Yeah, yeah. Not yet. So what does this keyboard and Paul have in common right now? Yeah. There's no escape. Great stuff. Now you can take a bow.
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Welcome, my name is Devine. This is episode 468 of the Devine Intervention Podcast. In today's podcast, I'm going to be continuing the rapid review series for the USMLE Step 2 CK and Step 3 exams. This is going to be series 98. So let's go ahead and jump right into it. So what if they give you a question about a patient, they tell you that for the last two hours, he has been having a very severe headache. And they tell you that he has vision loss in both eyes. In fact, it is mentioned that he has lost vision in the outer half of both eyes. If you see something like that, what should you be thinking about? Well, I would hope that you'd be thinking about some kind of stroke. In fact, if you wanted to maybe be smarter about localizing it, I would think about an anterior communicating artery stroke. The person basically has bitemporal hemianopsia. So what's the deal there? Well, the deal here is that this person probably had some kind of aneurysm in the circle of Willis. And then that aneurysm ruptured. And then as a result of that, you had like bleeding in the anterior part of the brain. You have like a bitemporal hemianopsia. In fact, if you even have just an aneurysm of the anterior communicating artery, that can certainly compress the optic chiasm and you can get a bitemporal hemianopsia. Remember, when a person has a bitemporal hemianopsia, the high-yield thing to know is that you're going to lose your outer visual field in both eyes, your outer visual field in both eyes. So like the outer half in both eyes. That's going to be bitemporal hemianopsia. So now the big question then begs, who are the people that typically get aneurysms in the circle of Willis? Well, I mean, normal people can get aneurysms in the circle of Willis. But our friends at the USMLEs, they also love, if you know certain diseases that have these associations. So like, for example, people that have Marfan's. Marfan's is associated with people having aneurysms in the circle of Willis. Autosomal dominant polycystic kidney disease is also associated with people having aneurysms in the circle of Willis. All these things can cause aneurysms. And again, these aneurysms can pop and that can cause a lot of problems. Now, what if they give you a question about a 29-year-old male and they tell you that he is brought to the hospital by his wife because for the last two days, he has been having very severe headaches. He has been having some visual difficulty. He has been having neck stiffness. And then they give you a bunch of vital signs. You notice that his temperature is like one or two degrees Fahrenheit. His blood pressure is like 90 over 60. He's tachycardic. He's tachypneic. And he has a fever, as I've already mentioned. And then they say, which of the following is the most appropriate empiric therapy for this patient's presentation? I really hope in that situation you're saying, oh, divine, I think it would be wise for me to give this person some element of ceftriaxone and some element of vancomycin. And I'll say plus or minus steroids in this circumstance. So what's the deal there? So this person sounds an awful lot like they have bacterial meningitis. I know you may be like, but Devine, could it not be viral? Could it not be fungal? Could it not be TB? Again, if we're just going with most common presentation that underlies what I just said, bacterial meningitis is the thing that makes the most sense. One thing I'm going to comment on here is we live in a world, especially of USMLE takers, where people are so focused on getting the exact, or what is the exact? What is that one thing here that tells me, oh, this is exactly what's going on? That's not a wise way to take the USMLE exams. The USMLE exams are almost like based on probabilities. That's one way I like to think of the USMLEs. I think of it as a probability-based exam. You ask yourself with the question that has been given, what is the most likely thing that is being tested here? What is the thing of highest probability that's being tested with this question that is placed right before me, right? You see a person with crazy high fevers, no core rigidity, youngish person, acute presentation. Again, it's almost certainly like if they had to make you like play odds, you're playing the lottery. I would probably put my money on bacterial meningitis because it's just the thing that makes the most sense in this circumstance. So in this circumstance, I would certainly be giving this person a combination of ceftriaxone, vancomycin, and steroids. That's what I'd be doing, like CVS. Just remember CVS, like the drugstore chain. So why that? Well, the thing is, the most common cause of meningitis is going to be strep pneumo. Strep pneumo is the most common cause of meningitis. So we're going to give ceftriaxone because it's going to cover it very beautifully. But another thing we do is we're going to say, okay, let's go ahead and give Venk because Venk can also cover staph aureus. Although also don't forget that ceftriaxone can also cover nitrate meningitis because yes nitrile meningitis is not necessarily the most common cause of meningitis, but it's pretty common as well. So you want to basically cover all your bases when you're giving a person empiric therapy. That's why we give ceftriaxone, vancomycin, and we give steroids. Ceftriaxone and van will pretty much cover most of the notable gram positives and gram negatives that can cause meningitis. And then steroids are generally indicated when you're worried about strep pneumo meningitis. When you're worried about strep pneumo meningitis, you got to add steroids in those circumstances. And then obviously, as you then get like a lumbar puncture and you get like gram stain results and CSF culture results, you can then reorganize your therapy accordingly. But empirically, believe it or not, you will get questions on your exams where you have to treat a disease empirically. Empiric treatment of meningitis, very, very high yield to know. In general, you want to do ceftriaxone and vancomycin. They may not throw in steroids as part of the answer, but for sure, you want to give ceftriaxone and vancomycin. Now, remember, the empiric treatment of meningitis is different if you're talking about like a neonate or you're talking about a person over age 50. When you're dealing with a neonate or a person over age 50, then in addition to giving ceftriaxone and vancomycin, you also have to give ampicillin. Because people that are neonates, people that are over age 50, they are predisposed to getting meningitis from listeria. Listeria, the most effective drug for covering listeria infection is ampicillin. So it's pretty helpful in those circumstances to give those people ampicillin just to empirically cover listeria because listeria meningitis, I believe, has a really bad mortality if you pretty much don't treat it and treat it on time. So it's just one of these weird things that you kind of need to keep in mind for your test. Okay. Now, what if they give you a question about a child and they tell you that this child, you know, for the past seven days, this child has been having like really high fevers. And they tell you that this child has also been having like some chest pain. In fact, over the last two days, the child has been having chest pain. And they tell you that, oh, that you listen to the child's chest and you hear a holosystolic murmur. You hear a holosystolic murmur at the apex. You're like, hmm, holosystolic murmur at the apex. You're like, hmm, that's kind of weird. And then they also tell you that in the Q-stem that this child has cervical lymphadenopathy. And what they tell you that this child does not have any edema of the throat, doesn't have any infiltrates or exudates on the throat.
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If you see, and you know, they will say like in the question that, oh, at a doctor's visit like a month ago, there was no murmur heard in this child's chest, right? And then you may see, they may give you a picture of like the tongue in this child or whatever. When you put all these things together, what are you thinking about? I really hope you're saying, oh, Devine, this sounds an awful lot like Kawasaki's disease. Maybe like, wait, what? In fact, I kind of want to break down this topic because it's something that people could really whiff on on exams. And I wouldn't want you to whiff on this stuff. But they could give you a question about a child with just this disparate set of symptoms. You see cervical lymphadenopathy. You see these very high fevers that have been going on for a couple of days. You notice that the child may have like even some valvular issues like mitral regurg, you may notice that they may have like coronary artery aneurysms. You can even see this right upper quadrant pain because sometimes in Kawasaki's disease, the inflammation spreads to the right upper quadrant. And when it spreads there, you can basically have like edema of the wall of the gallbladder. That's what's called gallbladder hydrops. That can certainly happen. And then, remember, these people can also have a rash on their palms and soles, although they won't always mention it like that. They can turn that rash to edema. They can say, oh, this person has edema of the hands and feet. When you see stuff like that, you want to think about Kawasaki's disease. You want to think about Kawasaki's disease. Now, what are some things that you could have conflated this with? Well, one of the things you could have conflated this with is rheumatic fever. Just be careful. Just be careful, right? Rheumatic fever, right? Usually they would have given you some kind of group A strep antecedent in the question. Group A strep usually causes some kind of pharyngitis. So you're going to see like some throat findings, like literally inside the throat. That's just something I want to keep in mind. I will tell you some information about a rapid strep test. Another way you could have also screwed this up is thinking about mono, right? Because people are like, oh, mono, mono, divine right upper quadrant, maybe hepatitis something, something, megaly. Yes, it could also be mono. But again, mono causes a pharyngitis. Mono causes lymphadenopathy, which this child had. But, you know, this child did not have pharyngitis. And again, I didn't really mention anything about an age or a situation where the child could have kissed someone. Like mono is going to be something that you're going to be seeing in a teenager or older on your exams. So say, for example, a person is like five or six years old. I will probably not pick mono for that person. It doesn't really make sense to pick that kind of answer. There has to be some very significant extenuating circumstances in a question for you to go down that pathway. So Kawasaki's disease. So what are some big things to keep in mind with Kawasaki's disease? Well, people that have Kawasaki's disease, typically you're going to see them, they're going to have like fever for a couple of days. You're going to see them have, sometimes they can have cardiac abnormalities that can be actually a presentation. Believe it or not, an MI can be a presentation of Kawasaki's disease. I'm going to say that again. An MI in a little child can be a presentation of Kawasaki's disease. Be very, very careful about that. Be very, very careful about that. An MI can be a presentation of Kawasaki's disease in a little child. So you see a little child with an MI and you see the child has like a fever with the MI. One of the first things I want you to think about is Kawasaki's disease. Or you see a child that has a fever, they have an MI, and you see like mitral problems, like mitral insufficiency that develops acutely, I also want you to think about Kawasaki's disease, okay? I know some of these things I'm saying may sound like unusual presentations, but I promise you these are very high yield presentations to know for the purposes of your exams. Now, Kawasaki's disease, what are some other things to know here? Well, again, as I've said, these people can have coronary artery aneurysms. In fact, this is one of the reasons why these people get aspirin and IVIG, okay? This is one of the reasons why these people get aspirin and IVIG, right? Aspirin and IVIG, aspirin and IVIG, aspirin and IVIG. Because Kawasaki's disease is an example of a kind of a vasculitis, right? And remember, they also have like a rash on the palms and soles. Now, one thing I also want to bring up here, and honestly, I don't know why this is the case, but this is something you definitely need to know for exams, is that Kawasaki's disease has a pretty solid association with thrombocytosis. I'm going to say that again. Kawasaki's disease has a pretty strong association with thrombocytosis, with thrombocytosis, with thrombocytosis. That is super, super, super high yield to know for purposes of the USMLE exams. People can have Kawasaki's and have thrombocytosis. Why? Honestly, I've not really found a good explanation in all my reading, but that's something that I would strongly encourage you to know for exams, strongly encourage you to know for exams. Now, one thing I want to comment on here is what are some causes of acute mitral regurg? Because the pattern of development of acute mitral regurg, sorry, the pattern of development of mitral regurg can tell you certain things on your exams. In fact, let's discuss mitral regurgiton from a few different perspectives. Because it's one of these things that, it's just one of these like innocuous concepts, just kind of pops up out of the blue on exams. And people kind of shake with those things. I don't want you to be one of those people. So if you see acute mitral regurgiton, especially in a very young child, and you notice that you have a fever, one of the things I want you again to think of is, I certainly, certainly, certainly want you to think of either rheumatic fever or Kawasaki's disease. But again, I've already explained to you how you can differentiate rheumatic fever from Kawasaki's disease. Now, if you see a person develop acute mitral regurg, and the person has like a bad medical history, right? And you see that this mitral regurg develops like super suddenly, like literally within like a few hours, you see them develop pulmonary edema. I want you to think of that person having an MI. So what exactly is happening there? Well, the thing that's happening is that they have a papillary muscle rupture. They've literally ruptured their papillary muscles. They've literally ruptured it, right? And sometimes on exams, instead of calling it a papillary muscle rupture, they'll call it rupture of the cordy tendini. They'll call it rupture of the cordy tendini. Rupture of the cordy tendini. Those are structures that support the papillary muscles. So if those things rupture, they're going to have this acute onset mitral regurgitation. Again, it's just one of these weird things you want to keep at the back of your mind for exams. And then if you see a person develop chronic mitral regurg, you notice that man, over time, person is developing mitral regurg, developing mitral regurg. Then I want you to think of that person having some kind of dilated cardiomyopathy, dilated cardiomyopathy, dilated cardiomyopathy. So why does dilated cardiomyopathy cause mitral regurg that is chronic? Well, the thing is dilated cardiomyopathy will cause mitral regurg that is chronic because, again, what exactly does it do? Basically, what it's going to do is you're going to have a dilation of the left ventricle. When you dilate the left ventricle, you're essentially going to pull the mitral valve leaflets apart.
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And over time, that can present as mitral regurg. Okay, mitral regurg can be a presentation of dilated cardiomyopathy on exams. And again, remember our friends at the USMLEs, they can give dilated cardiomyopathy many different names. They can call it eccentric hypertrophy on exams. They can call it chronic volume overload on exams. Again, remember, this is one of the hallmarks of the USMLEs these days, is taking what you know and just being more descriptive or putting it in other terms, right? There's nothing wrong with memorizing stuff, but make sure you understand and can reason through stuff. And not just understand or reason through stuff, but ask yourself, what is the story behind this thing? Many people will be well served to learn things in the story format on USMLE exams. Like as they are studying, they are learning the story behind the pathology. When you learn the story behind the pathology, then it will be very easy for you to recognize those things on exams. That's just the truth. But let's go ahead and continue. So as I wrap up today, one thing I think I want to focus on is to discuss some of the uses of aspirin on exams. Because sometimes people wonder, when can I use aspirin on the USMLE exams? Believe it or not, there are actually a myriad of weird associations with aspirin that I would say will be pretty helpful for you to know for your test, right? So the first one we've kind of talked about, you can use aspirin for Kawasaki's disease. You know, in general, you'll try to avoid giving aspirin to little kids. But in Kawasaki's disease, you throw that rule out the window. You can give aspirin to little kids that have Kawasaki's disease. Now, what's the second association with Kawasaki's disease? When a person has an ischemic stroke that is not of a cardiac origin, because remember, you can get ischemic strokes on USMLE exams in general for two major reasons. You can get it from the carotids, or you can get it from the heart. Usually, people that get the heart, which is less common, are people that have e-fib or have had a recent MRI. But if you have like an ischemic stroke because of a carotid problem, one of the treatments you should strongly consider is aspirin. Obviously, if you are less than four and a half hours from symptom onset and it's an ischemic stroke, the first thing you're going to give is TPA, kind of like the smart play. But once you're done giving TPA, in terms of what the person should be on long-term, I'll strongly encourage you to consider putting those people on aspirin. Strongly consider people putting those people on aspirin. When people have ischemic strokes, they need to be on antiplatelet agents. When they have ischemic strokes of carotid origin, which again is the most common kind of ischemic stroke, go ahead and put those people on antiplatelet agents like aspirin or clopidogrel or dipyridamol. Usually aspirin is the go-to on exams. But remember, if a person has a stroke from a cardiogenic source, let's say they have AFib or they have mitral stenosis or they have whatever, please do not put them on an antiplatelet agent Put them on an anti-coagulant, something like Warfarin, something like Apixaban, something of that nature. Just be wise, be smart, okay? It seems like a subtle difference, but it's a common difference I've seen many, many students kind of basically mess up on exams. You don't want to be one of those people. Now, what's the third use of aspirin? The third use of aspirin is in peripheral arterial disease. Actually, every single person that has peripheral arterial disease has to be on aspirin. Because again, peripheral arterial disease is basically like atherosclerosis. Atherosclerosis of a person's lower extremity vessels. That's more of a thrombotic phenomenon. Those people certainly should be on an antiplatelet agent like aspirin. And remember, when you've had an MI, one of the first drugs you're supposed to get is aspirin. It's one of the drugs you get in the acute phase of an MI. But also after a person has had an MI and they get a stent placed in their hearts, they need to be on dual antiplatelet therapy. That dual antiplatelet therapy is usually going to be aspirin and some other drug, typically something like clopidogrel, a P2Y12 inhibitor. Now, another thing to keep in mind with aspirin for exams is that you can use it as a clamsia prophylaxis, right? So if a woman has had like a clamsia in a previous pregnancy, you're like, hmm, gee, I don't want this woman to have this problem again in future pregnancies. When she gets pregnant again, go ahead and put her on aspirin. Go ahead and put her on aspirin. And then don't forget that aspirin can cause tinnitus. Aspirin can absolutely positively cause tinnitus. It can cause tinnitus. That's something you want to keep in mind on exams. And then what are the acid-base anomalies you can get when you take aspirin or you overdose on aspirin? Well, the acid-base anomalies you can get is you can get a respiratory alkalosis and a metabolic acidosis at the same time. Many people, for purposes of their USMLE exams, actually many resources have thought people this, is this whole concept of, in fact, I may have thought this in the past, but this is something that I've pretty much kept solidly in mind for years, that those two problems show up at the same time, right? Many people learn that, oh, wait, you get the respiratory alkalosis first, and then you get the metabolic acidosis later. That is not true, Okay. Because you see some people, they'll get these arrow questions involving acid-based problems and aspirin. And then they'll only pick the answer that shows respiratory alkalosis alone. And then they won't pick the one that reflects respiratory alkalosis and metabolic acidosis. Please, let me tell you right now, both of those problems crop up when you have aspirin toxicity, right? It revs up your respiratory rate. So you're going to blow CO2. You're going to get a metabolic, sorry, a respiratory alkalosis from that. But you're also going to get a metabolic acidosis for two reasons. One, aspirin is literally known as acetylsalicylic acid. Okay. It's an acid. So just based on acid base, you know right off the bat, you're going to get a high anion gap metabolic acidosis. But that's not all. Aspirin is also an uncoupling agent. It kind of works like dinitrophenol. It's an uncoupling agent of the electron transport chain. So basically, you will not be able to make ATP. You're pretty much wasting that proton gradient that you have in your inner mitochondrial, in your intermembrane space of your mitochondria. So basically, yes, you're doing everything. Most of your electron transport chain is happening. But basically, aspirin uncouples that process. And when it uncouples that process, you pretty much just generate a lot of heat. So your body is going to start depending a lot on glycolysis to give it any kind of useful energy like ATP. So you're going to be making a lot of lactic acid. can certainly cause you to become acidotic. Okay. So please aspirin, please. I want you to disband this from your mind of, Ooh, respiratory alkalosis first metabolic acidosis down the line. No, it's respiratory alkalosis and metabolic acidosis at the same time. I'm going to say that again at the same time. That's pretty high yield to know for, for exams. That's pretty, pretty high yield to know for, for exams. Okay. So I think I'm going to go ahead and stop here. I think those are, well, I guess maybe let's throw in one more aspirin factoid here, right? So you see a person that, you know, they've been taking aspirin for like pain or whatever. And then you notice that, you know, they've been having asthma style symptoms. They've been having nasal polyps. This is pretty easy, right? This is aspirin induced asthma. I believe these days it's called aspirin exacerbated respiratory disease. Well, what's the pathophase behind that?
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It's an irreversible inhibitor of COX-1 and COX-2. Well, guess what? If you shut down COX-1 and COX-2, then arachidonic acid needs to be useful in life. So how is it going to get useful? It's going to get useful by getting shunted down the lipo-oxygenase pathway into making leukotrienes. Well, leukotrienes, they can cause bronchospasm, they can cause asthma-like symptoms, right? So that's actually the pathophase behind aspirin-exacerbated respiratory disease. Because basically, by shutting down the cyclooxygenase pathway, then the only fit for arachidonic acid is like, okay, I'm going to go down the lipo-oxygenase pathway, and you're going to make all these leukotrienes, again, which can cause a lot of airway problems that can certainly cause asthmatic symptoms. Aspirin exacerbated respiratory disease has a classic association with nasal polyposis. Okay. Has a pretty strong association with nasal polyposis. Right. And again, by the way, if you ever see nasal polyposis, okay, let me take a step back real quick. So that aspirin exacerbated respiratory disease, how can you treat it? Well, obviously a wise thing is to probably stop taking aspirin. It's probably not a smart idea. That's one. But the second thing I would say to keep in mind there is maybe using a leukotriene antagonist, like a leukotriene receptor blocker, something like Montelukast or Zafrelukast. Or you can use a lipoxygenase inhibitor like Xyluton, for example, Z-I-L-E-U-T-O-N. Those are very effective therapies for managing aspirin exacerbated respiratory disease. Okay. And then with nasopolyposis, I don't know, just all these higher things just kind of flying into my brain. But nasopolyposis, remember your exams, think of aspirin exacerbated respiratory disease. Think of cystic fibrosis. Cystic fibrosis is a very common cause of nasopolyposis on exams. And then also think of just chronic rhinosinusitis with nasal polyposis. That's also something that causes nasal polyposis on exams. We treat that with inhaled corticosteroids. And then a fourth cause of nasal polyposis on exams, believe it or not, is Wagner's granulomatosis. Remember, Wagner's, these days, we call it GPA. Granulomatosis with polyangiitis. That can also present with a nasal polyposis. Just something you want to keep at the back of your mind for exams. Something you certainly want to keep at the back of your mind for exams. And then don't forget that aspirin can also precipitate gout attacks. Why? Because it can raise your uric acid levels. So if a person has a history like gout, aspirin is not maybe the smartest idea in those people. It's only if they really, really need that aspirin for like a really, really big reason. Like say, for example, they've had like an MI, for example. And remember as well, aspirin is the drug we use for pericarditis in people that have had MIs. For the first six months after you've had an MI, you cannot take any other instead but aspirin, but aspirin. But aspirin. Why? Because again, you can have a pretty high risk of myocardial rupture. So again, just be smart. Be wise. Aspirin is the NSAID you can take for pericarditis. Really, again, for the first six months after an MI, don't go taking any other kind of NSAID like ibuprofen. You're just going to rupture your myocardium. And that's going to be a very very bad thing okay so i think i'm going to go ahead and stop here again thank you for joining me um for those of you that are studying for step two step three or step one i have a bunch of classes that are coming up actually starting like two more yeah tomorrow right so i have a test taking strategies class uh it's two and a half hours long it's for step one all the way to step three um that's tomorrow on friday i have a a biostatistics class. If you struggle with biostats, you're taking step one to step three. That class is exactly what you need. On Saturday, I have a five-hour class that covers quality improvement, social sciences, healthcare systems, ethics, and whatnot. Let me tell you this. These classes are not lectures. They are all based on stories. They are all based on scenarios. They are all based on clinical presentations because that's exactly the way your USMLE exams will be, right? So that's one benefit of my review courses, I would say, is you're not just learning the concept, but you're learning the story. You're learning the context behind that concept. It's a much more efficient, much more effective way to learn and prepare for exams. And then if you're taking step two or step three, next week, Monday, Tuesday, Thursday, and Friday, it's a four-day course. I am actually going to be having the 20-hour step two, step three review. It's also helpful for people that are preparing for shelf exams. So if you're interested in any of these courses, just shoot me an email and I'll give you some more information. They're all held over Zoom. Most of them are in the evening, so you should be able to partake of them. And then I also offer one-on-one tutoring for Step 1, Step 2, Step 3, pre-clinical med school exams, 30-day shelf exams. I also help people with ERAS applications, so personal statements, recommendation letters, editing those things, editing applications, editing supplemental applications, doing mock interviews. I do all those things with people. And I have these podcasts on the major apps, you know, Apple Podcasts, Google Podcasts, and Spotify. I have them on those major platforms. I have a YouTube channel called Divine Intervention USMLE Podcasts and Videos. That's where I post the videos that I make. So you can go ahead and check those out. And then, you know, many of you know I'm a Christian. So I do have another website called DivineInterventionLifeLessons.com. DivineInterventionLifeLessons.com. DivineInterventionLifeLessons.com. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. Many people have said that, oh, Divine, I love these little life lessons you put at the end of some of your podcasts. So I decided to basically make a separate website where every week I post like two podcasts, about 10 to 20 minutes long, where I address a life lesson from a biblical perspective. Again, many people have listened to those, found those to be extremely helpful. So go ahead and check those out. So I'll see you in the next podcast. The one thing I'll just say to you today is whenever you face a tough circumstance, so think of this as a mini life lesson. Whenever you face a tough circumstance, be quiet and try to be constructive. Be measured in your steps. Because usually when people face chaos, when people face catastrophe or disaster, they start doing a lot of irrational things. But I promise you, even in a situation of chaos, even in a situation of disaster, you can make good, wise choices. Take a step back. Be patient. Be calm. Be gentle when a tough circumstance comes and then think, process, ask yourself, okay, what is the rational approach in this situation? What do I do? Many times quietness and even just doing nothing is the best move in a chaotic circumstance. Sometimes just doing nothing. Because when you do nothing and take a step back, it then causes you to ponder the situation rationally and begin to do like just wise, wise things, right? Begin to do just wise things. I mean, you see this in many situations of life where catastrophe happens and people just like, I must do something, I must do something. But in those things they do end up adding to the problem instead of actually like solving the problem. So again, just realize the importance, recognize the importance of stopping, looking, listening, thinking in the course of a bad situation. Okay, well, I'm going to stop blabbering for now. I'll see you in episode 469. Bye for now. God bless you.
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I'm Jan Engmeyer with JAMA Evidence. Today we'll hear from Dr. Richard Bedlak about carpal tunnel syndrome, a topic discussed in Chapter 10 of the Rational Clinical Examination. Welcome to the podcast, Dr. Bedlak, and please introduce yourself to our listeners. Well, thanks for having me, Jan. My name is Dr. Richard Bedlak. I'm a neurologist and a specialist in neuromuscular medicine at Duke University and the Durham VA Medical Center in Durham, North Carolina. Thank you for joining us. What causes carpal tunnel syndrome and what are some of the more common signs and symptoms? So Jan, within the wrist, there's a small space which is deep to something called the transverse carpal ligament and between the rigid carpal bones. This is called the carpal tunnel, and through it passes the median nerve and some flexor tendons. Carpal tunnel syndrome occurs when the median nerve gets compressed in this small space, and common symptoms of carpal tunnel syndrome include wrist pain, which sometimes radiates approximately up the forearm, as well as intermittent hand numbness, especially in the thumb, index, and middle fingers. The most common sign is sensory loss over the median nerve dermatome, which involves the thumb, the forefinger, and the middle finger. In more severe cases, there can be weakness of the median innervated abductor pollicis brevis and opponent's muscles as well. What is the prevalence of carpal tunnel syndrome in the general population? Jan, it turns out to be pretty common. So one half of 1% of the population reports that they were diagnosed with carpal tunnel syndrome to aid in diagnosis? And which findings favor the electrodiagnosis of carpal tunnel syndrome and which findings seem to argue against it? That's an excellent question. So, Jan, it turns out there's three parts of the history and exam for clinicians to remember. First, they can ask their patients to use something which is called a CATS hand diagram. This is a drawing of the palmar and dorsal hand surfaces. And on this diagram, patients should color in the location of their pain and numbness. Symptoms involving the fingertips and or the thumb side of the hand are highly supportive of carpal tunnel syndrome with a likelihood ratio of 2.4. Symptoms involving only the ring and little fingers and the ulnar side of the hand argue strongly against carpal tunnel syndrome with a likelihood ratio of 0.2. Second, clinicians can test the sensation of their patient's hands to see if there's median dermatomal sensory loss. This can be accomplished by pressing a clean, sharp pin against the palmar surface of the index and the ipsilateral little fingers. Diminished pinprick sensation in the index finger compared to the little finger, which is called hip algesia, is strongly supportive of carpal tunnel syndrome with a likelihood ratio of 3.1. Finally, clinicians can test their patient's thumb abduction strength. To do this, they should have the patient raise their thumb perpendicular to the palm so that it's directly over the middle of the palm. The clinician will then attempt to press the thumb back down into the center of the patient's palm. This maneuver isolates the abductor pollicis brevis, which is innervated by the median nerve. Weakness in this muscle is supportive of carpal tunnel syndrome with a likelihood ratio of 1.8, and normal strength in this muscle makes carpal tunnel syndrome less likely with a likelihood ratio of 0.5. Is there anything else you would like to tell our listeners about the clinical examination for carpal tunnel syndrome? Jan, I'd just like to say that given how common carpal tunnel syndrome appears to be, I think it's important for clinicians to be aware of it and to remember the three key parts of the history and clinical exam that are helpful in making a diagnosis. Now, there are many other questions and exam maneuvers that are sometimes employed. For example, Phalen's test and looking out for a Tenel sign, but these don't appear to be nearly as useful. For confusing cases or those that don't respond to conservative therapy, nerve conductions can be useful for confirming the diagnosis. Well, thank you very much, Dr. Bedlak, for this helpful synopsis of diagnosing carpal tunnel syndrome. Additional information about this topic is available in Chapter 10 of the Rational Clinical Examination. This is Jan Engmeyer talking with Dr. Richard Bedlak about carpal tunnel syndrome for JAMA Evidence.
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From the JAMA Network, this is the JAMA Medical News Podcast, discussing timely topics in clinical medicine, biomedical sciences, public health, and health policy, featured in the Medical News section of JAMA. How can machine learning reduce diagnostic errors and amplify the reach of precision medicine? Is it possible for machine learning to identify both typical and atypical disease patterns? In what ways can medical imaging reveal novel phenotypes and help us develop new metrics for patient outcomes? I'm Dr. Kirsten Bibbins-Domingo, and I'm the Editor-in-Chief of JAMA and the JAMA Network. This conversation is a part of a series of videos and podcasts hosted by JAMA in which we explore the rapidly evolving intersection of AI and clinical practice. I'm joined today by Dr. Rima Arnault. She's a practicing cardiologist and an associate professor of medicine, radiology, and pediatrics at the University of California, San Francisco. She's also a faculty member at the Baker Computational Health Sciences Institute, the UCSF-UC Berkeley Joint Program in Computational Precision Health, and the Center for Intelligent Imaging. Welcome, Dr. Arno. Thanks for having me. Wonderful. I hope we can do this interview on a first-name basis, if that's okay with you. Wonderful. So, Rima, you're a cardiologist, and I know you're in clinical practice. You focus on patients. You also focus on imaging, echocardiograms, and other types of images. And then there's this intersection of AI. So I'd love you to tell me how AI got to be part of the research you're doing as it relates to your clinical practice. Believe it or not, it started when I was a trainee in the bench science doing basic science. And I got to see that the genotype is only as good as the phenotype that you can map it to. Both in the research lab and in the clinical world, so much of phenotyping is measured using imaging. It is at once an extremely data-rich and valuable source of phenotyping and also very difficult to do correctly. So we watch scalability and reliability of the genomics half of the equation taken off. And phenotyping is still an artisan craft. You know, we have answers for the genome. How big is the genome? What's the structure of the genome? You know, chromosomes, genes, coding, non-coding regions, SNPs. Ask those questions about the phenome, and we still don't have clear answers. So I became really interested in what we could do to make phenotyping, and specifically image-based phenotyping, more accurate, more reliable, and scalable. A scale and an ability to match what we were doing on the genomic side. And that's how I got into this. People are doing a lot with phenotyping around structured data, you know, lab values and numbers. They're doing a lot with text. And imaging to me felt like that final frontier. In the basic science lab, imaging was the bread and butter of phenotyping. And during my clinical training, I fell in love with clinical imaging as well. So everything just pointed to this idea that we need to get better with image-based phenotyping. Wonderful. So you really have come at a time when the capabilities in computation, in the advances in artificial intelligence, combined with imaging, and I understand imaging from people who think about this in the AI sphere as this extraordinary collection of data to describe a thing that we perceive as an image, and in the case of echocardiograms, moving images. You now have the ability to describe all of the patterns you're seeing and all the data that describe those in a way we couldn't before because of the computational capacity. Yeah. We now have that ability, but we need to work to make it a reality. Wonderful. So tell me a little bit about the area you work in. What are the types of phenotypes that you're interested in? I'm an echocardiographer. So really it's anything that we would care about as a cardiologist. So ruling out structural disease, valve disease, wall motion abnormalities. When patients get echocardiograms or when they get any imaging really, physicians look at the entire picture. We're not focused on one phenotype or the other. We have to look and figure out everything that may be wrong with the patient, whether it's the indicated cause or whether it's something incidental or surprising. So we want to train computers to assist us with that comprehensive task. Right. And I've heard this described as it's as challenging to understand what's normal as it is to understand those outlier patterns. How do you think about using all of the tools that are available to you now with AI in echocardiography. Where do you see the most promise in helping clinicians do their job better? That really comes down to individual use cases. And even within echocardiography alone, there are myriad use cases. Some are to assist screening processes. So physicians who may be out in the community screening for disease, especially diseases that may be rare. So they don't see them very often. They're not sure what they're seeing when it comes across. We have a screening project, a screening use case that we do, which pertains to detection of congenital heart defects from fetal screening ultrasound. That's the 20-week ultrasound that's recommended for every pregnancy worldwide. And we find a big gap and kind of a diagnostic paradox because congenital heart disease is at once the most common birth defect, but it's also still very rare in the population. It makes it hard for physicians to build and maintain their skills at CHD detection, especially with an imaging modality as noisy and difficult as ultrasound. It's such a great example, what you're talking about, because it is so critically important, devastating, obviously, to a pregnant person and to plan for the future for if there are treatments for a baby born with a congenital heart disease. You're talking about fetal ultrasound, so a very specific area that somebody needs to be technically good at detecting something that is rare, but extremely consequential. Yes. And because it's rare, you can easily lose skills in sort of that detection, which I'm sure is not something that is in every cardiologist portfolio. Exactly. So this is where something can really help make that detection not only more accurate for a particular clinician, but I hear you saying it also could potentially scale to be able to make it available to patients who may not be coming to UCSF to see you in your clinic. Yes, exactly. And the other challenge about this problem is that expert centers are few and pregnancies happen everywhere on earth. Yes. And so one really needs to create a solution, as you said, that is scalable to all the locations where pregnancies happen, whether it's a tertiary care center or a small rural clinic. Yeah, it's such a great example. So much of the details in your example I really like because I think it's clear that you would want to be accurate and have tools that help you in the accuracy. But the scalability, I think, is also a very nice angle to what you're talking about. We recently interviewed Atul Butte, who talks about scalable privilege. Yes. When he talks about the potential with AI. And I think it's a very good example. And I hear that when I hear you talk about what gets you excited about detecting congenital heart disease. That's such a great term, scalable privilege. And we think about that a lot as well in terms of how we're going to design a solution for the patients and providers that need the most help. These issues of equity are not just about the patient cohort and how to include the right amount of patients. It's really also comes to bear on a technical level. Some of our work, one of the unglamorous parts of data science is we have to figure out what kinds of machines, how many clinics, how many sonographers are operating out there so that we tailor our solution appropriately. It's not just about the fancy neural networks where the rubber meets the road is in the clinics. One of our recent papers, we have started to study this. We find a vast diversity in the types of imaging data, the amount of imaging data, even the protocols that are performed for fetal screening ultrasound across the world. And this is an area with clear clinical guidelines. So we have to design a solution that overcomes that variability. We're very aware as well that in so many places in the community, they're not going to have the latest high quality ultrasound machines. In fact, the WHO says about a third of the world lacks prenatal care altogether. So we really thought about those issues of access and bias in the way that we designed our solution in the hopes that it'll be implementable, truly implementable worldwide.
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I think that that's a really important goal. We keep our use cases in mind, our patients in mind. And it's one thing to be at the bleeding edge of the AI development. And in order to get these solutions to work for a task as challenging as fetal diagnostic ultrasound, we absolutely have to do those things. But we also can't forget the implementation challenges and making sure that we can implement in diverse healthcare settings, as is our goal. Wonderful. So there are advances like with the foundation models and generative AI. How do you see those playing out and their applications to cardiovascular disease or to imaging? I think on the imaging side, what foundation models are able to generate with respect to imaging still needs a little work to be adaptable to medical imaging. So what are some of the things to think about with foundation models going forward? One is their size. If you want to be able to deploy a foundation model quickly or in a low resource setting, do you have to stand up an entire supercomputer basically to manage and operate this, right? And that gets into issues of access and equity and using these models in research or for medical use cases. Related to that is also whether or not these models will increase the diversity of research or reduce it. So on the increase side, you know, we'll have these pre-trained foundation models that people can borrow off the shelf, fine tune for their task. And that's a tide that can rise all boats and increase the amount of research going on. At the same time, if these foundation models are relatively few, is everyone building research solutions off of a small handful of foundation models, which, you know, each have their own biases and constraints? Do we end up then constraining the solutions that we build on top of those models? So these are all things that need to be studied. And additionally, of course, foundation models have been demonstrated to have an ability to hallucinate. So to make up information that sounds plausible, but is factually untrue. And that's a problem, no matter what you're using these models for. It's an active area of research across several industries. So tell me a little bit about, you've talked a lot about sort of your vision as a researcher, how you got interested, where you see the potential going. Tell us a little bit about like the day to day. So, you know, we've already had the ability for our, you know, ECG reader to tell me what the readout is. I'm a general internist. I use that. I know to be trained not to over rely on that, to also think through how I'm trained to read ECGs. That's where I encounter sort of cardiovascular tests that have this interpretive component to it. What should be the standard in the workflow of what the average cardiologist is thinking about with these tools that improve our ability to interpret images, to detect signal from noise? But we also know there are things like automation bias. We know that these models are not perfect. How do we think about integrating the human knowledge with the additional knowledge that we get that's coming from these very powerful tools? Yeah, this is a whole area of research around implementation and also human algorithm interaction. I don't think we've solved these things by and large for the application of AI into our daily clinical workflow. I'm sure I can see use cases where AI can be helpful, automating some of the tedious measurements we do in cardiac imaging, for example. And you're right. There's been research. I think we talked about this a couple of weeks ago, where when the computer says something, humans are likely to believe it because it's appeared to us on a computer screen and it may or may not be true. And that's really, I'd say that's almost more about the human and how they interact with computers than the algorithm itself. But if you're going to apply algorithms of any kind, artificial intelligence or otherwise, in high stakes settings, these are things that we need to evaluate. I think that's really exciting. And I think this is a theme we've come to again in a few of our conversations where we have to make these models and machines work better, but we also have to understand the intersection with humans and understand how humans interact with other types of information in order to make ultimately a decision that's for the patients. I also really like in your story that you are focused on clinical applications, but it started with this discovery. And I'm guessing that as you understand patterns of disease with echo, as you look at echocardiography, there's the potential to discover things you haven't thought about before with the human heart, right? It's not just the congenital heart disease that we know and diagnosing that better, but also patterns that we may not have described before. Exactly right. And that's something that's very exciting to me. How do we take standard image-based phenotypes, information we already know exists within imaging, such as measurements, wall motion, and other things like that, and make it more accurate, reliable, and scalable? But you're right, there's this whole other layer after that. What information is contained in the image that's more than meets the human eye, right? That's very exciting. Is there a way to automate that discovery and automate the validation of potential image-based phenotyping? I think one of the first things that needs to happen is we need to have models that learn clinically relevant features within imaging. Make sure that if they are classifying heart disease, you can interrogate that model and know that it looked at the heart and not some funny text in the upper left corner of the picture, because some of the early machine learning models did just that. Otherwise, you might think you have a novel phenotype, and really it's just an artifact. Well, this is a very exciting time for this field. Arima, it's been such a pleasure speaking with you today. I'm really looking forward to more work from you and what you find in your work and certainly its application to the care of patients. And I really think our talk today really exemplified many of the themes of accuracy, but also scalability. And it's really been such a pleasure. Likewise. Thank you so much. Yeah. A lot of what we've discovered that pertains to one use case is really applicable to other use cases. So we're really trying to build a base of knowledge that then helps us with use cases across imaging modalities and across the lifespan. Wonderful. Thank you for listening. We welcome comments on this series. We also welcome submissions in response to JAMA's AI and Medicine Call for Papers. We hope you'll join us for future episodes of the AI and Clinical Practice series. Subscribe to the JAMA Network YouTube channel and follow JAMA Network podcasts wherever you get your podcasts. Until next time, stay informed and stay inspired.
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Hey everybody, welcome back to another episode of the USMLE Guys podcast. My name is Dr. Paul. Today we're doing another high-yield USMLE Step 1 drill session. If you're enjoying the drill sessions and you'd like to learn more about how you can work with us to pass your USMLE Step 1 exam, don't forget to visit our website at usmleguys.com. Now let's get started with today's drill session. Parasympathetic. The nicotinic ACH receptors are what type of channels? Ligand-gated sodium-potassium channels. The micturition center that regulates bladder function is located in which structure? The pons. Stimulation of the M3 receptor will lead to which action in the detrusor smooth muscle? Contraction. Inhibition of the M3 receptor is desired when a patient has which typegency incontinence. Beta 3. Inhibition of which alpha receptor can help to decrease urinary obstruction? Alpha 1. Which G protein class is associated with the alpha 1 receptor? GQ. Which G protein class is associated with the alpha-2 receptor? GI Which G protein class is associated with the beta-1 receptor? GS Which G protein class is associated with the beta-2 receptor? GS Which G protein class is associated with the beta-3 receptor? GS Which G protein class is associated with the M1 receptor? GQ Which G protein class is associated with the M2 receptor? GI Which G protein class is associated with the M3 receptor? GQ Which G protein class is associated with the D1 receptor? GS Which G protein class is associated with the D2 receptor? GI Which G protein class is associated with the H1 receptor? GQ Which G protein is associated with the H2 receptor? GS Which G protein is associated with the V1 receptor? GQ Which G protein is associated with the V2 receptor? GS. Which adrenergic receptor increases lipolysis, thermogenesis in skeletal muscle, and increases bladder relaxation? Beta 3. Which dopamine receptor relaxes vascular smooth muscle? D1. Which vasopressin receptor increases water permeability and reabsorption? V2. Which adrenergic receptor increases heart rate, lipolysis, renin release, and cardiac contractility? Beta 1. Which cholinergic receptor decreases heart rate and atrial contractility? M2. Which cholinergic receptor increases gut peristalsis and exocrine gland secretions? M3. Which neurotransmitter modulates the release of norepinephrine from a sympathetic nerve ending? Norepinephrine. It does it itself. What is the precursor of dopamine in the noradrenergic axon? Tyrosine. Which cholinomimetic agent stimulates muscarinic receptors in the airway when inhaled. Which cholinomimetic is exactly the same structurally as acetylcholine but is resistant to acetylcholine esterase? Which direct cholinomimetic agent is used to treat urinary retention? Bethanacol Which direct cholinomimetic agent is useful in Sjogren's syndrome? Pylocarpine Which cholinomimetic agent is useful long-term for myasthenia gravis? Pyridostigmine. Which antidote for anticholinergic toxicity can freely cross the blood-brain barrier? Thizostigmine. Which anticholinesterase is an effective tool in managing postoperative neurogenic ileus and urinary retention? Neostigmine. Donepazil, rivastigmine, and galantamine are all effective for which condition? Alzheimer's disease. With pralidoase poisoning. Atropine. Which two effects does atropine have on the eyes? It causes pupil dilation and cycloplegia. Which two effects does atropine have on the airway? Bronchodilation and decreased secretions. What is the main effect atropine will have on the stomach? Decreased acid secretion. What does atropine do to gut motility? It decreases it. What does atropine do to urinary urgency if a patient has cystitis? It decreases it. Atropine can cause acute angleosure glaucoma in the elderly due to causing which effect? Madriasis. Describe the action of albuterol on beta-2 versus beta-1 receptors. Activity is greater on beta-2 than beta-1. What are the effects of isoproteranol on beta-1 vs. beta-2 receptors? They are equal. Describe the effects of norepinephrine on alpha-1 versus alpha-2 versus beta-1 receptors. Alpha-1 is greater than alpha-2 is greater than beta-1. What are the two effects that can result from mixing beta blockers with cocaine? Unopposed alpha-1 activation can result in extreme hypertension and coronary vasospasm. What is the drug of choice for hypertension in pregnancy? There are a few we can use, but alpha-methyldopa is typically the drug of choice. What are the possible adverse effects of alpha-methyldopa? Direct Coombs positive hemolysis, drug-induced lupus, and hyperprolactinemia. What does the administration of phenoxybenzamine prior to pheochromocytoma surgery achieve? It prevents a hypertensive crisis by preventing catecholamine release. What is the most worrisome adverse effect of prescribing prazosin? First dose orthostatic hypotension. Which alpha-2 selective drugs used for depression can increase both appetite and serum cholesterol. Mirtazapine. What is the drug of choice for controlling the symptoms of hyperthyroidism? Propranolol. Which two beta blockers are effective at decreasing AV node conduction velocity in supraventricular tachycardia? Metoprolol and Esmolol Which class of medication is effective as prophylaxis against variceal bleeding. Beta blockers. Which beta blocker used in glaucoma can decrease the production of aqueous humor? Timelol. Phosphodiesterase 5 inhibitors exert their effects by decreasing the hydrolysis of what? C. GMP. Which nonspecific phosphodiesterase inhibitor can cause cardiotoxicity? D. Theophylline. What is the mechanism of action of the phosphodiesterase 4 inhib inhibitor raflumilast. It increases cyclic AMP in neutrophils, granulocytes, and bronchial epithelium. For which condition is the phosphodiesterase-3 inhibitor milrinone used? Acute decompensated heart failure with cardiogenic shock. The puffer fish, which contains the tetrodotoxin, binds to which type of channels in the nerve tissue? Fast voltage-gated sodium channels. What is the mechanism of action of the ciguatoxin? It opens sodium channels and causes depolarization. Which criteria is used to reduce harmful polypharmacy in geriatric populations? Beer's criteria. What is the treatment for acetaminophen toxicity? N-acetylcysteine What does the administration of N-acetylcysteine achieve in acetaminophen toxicity? It replenishes glutathione. What is the treatment for benzodiazepine toxicity? Flumazenil. What are the two treatment options for arsenic poisoning? Dimer caprol and succimer. What are the treatment options for copper toxicity? Penicillamine and Triantine What is the treatment for digitalis toxicity? Digoxin-specific antibody fragments What is the agent used to reverse a heparin overdose? Protamineaprone. What is the treatment protocol for cyanide poisoning? Hydroxocobalamin, nitrates, and sodium thiosulfate. What are the two treatments for mercury poisoning? Dimer caprol and succimer. What is the treatment protocol for methemoglobin toxicity? Methylene blue and vitamin C. What is the treatment for opioid overdose? Naloxone. What is the purpose of giving sodium bicarbonate in salicylate poisoning? To alkalinize the urine. What's the purpose of giving sodium bicarbonate in TCA poisoning? It stabilizes the cardiac cell membrane. What is the treatment protocol for beta blocker toxicity? Atropine, glucagon, and saline. What is the treatment for immediate reversal of warfarin toxicity? FFP or PCC. What is the treatment for a delayed reversal of warfarin toxicity? Vitamin K. What is the cardiovascular side effect associated with doxorubicin or donorubicin use? Dilated cardiomyopathy.
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Diphenhydramine. Name three classes or specific drugs that can cause SIADH. Carbamazepine, cyclophosphamide, and SSRIs. Halothane, amanita phylloides, valproic acid, and acetaminophen can all cause damage to which organ? The liver. Which two steps can minimize the risk of pill-induced esophagitis? Upright posture and adequate water ingestion with the drugs. What is the major side effect seen with quinine or quinidine? Synchonism. Isoniazid and phenytoin are known to precipitate which problem? Peripheral neuropathy. Which drug is associated with causing yellowing of the vision? Digoxin. What is the visual problem associated with isoniazid? Optic neuritis. What is the major adverse effect of ifosfamide or cyclophosphamide use? Hemorrhagic cystitis. What can be given to prevent hemorrhagic cystitis in someone treated with cyclophosphamide or ifosfamide? Mesna. What is the most common side effect associated with the use of ACE inhibitors? Dry cough. Which side effect is associated with busulfan, amiodarone, bleomycin, nitrofurantoin, methotrexate, and carmustine? Pulmonary fibrosis. Which vitamin is linked to idiopathic intracranial hypertension? Vitamin A. Which movement disorder is associated with the use of metoclopramide and antipsychotics? Tardive dyskinesia. Which drug is linked to gray baby syndrome? Chloramphenicol. In enzyme kinetics, Vmax is directly proportional to what? Enzyme concentration. In enzyme kinetics, Km is inversely related to what? The affinity of the enzyme for its substrate. Most enzyme reactions follow which type of curve? Hyperbolic. On the Lineweaver-Burke plot, Vmax is higher the closer you are to which value on which axis? 0 on the y-axis. On the Lineweaver-Burke plot, Km is higher the closer you are to which value on which axis. Zero on the x-axis. What is an irreversible competitive inhibitor's effect on Vmax? It decreases it. What is a reversible competitive inhibitor's effect on Vmax? Unchanged. What is an irreversible competitive inhibitor's effect on KM? What is a reversible competitive inhibitor's effect on KM? It increases it. What does the presence of a reversible competitive inhibitor do to potency? Decreases it. What does the presence of an irreversible competitive inhibitor do to efficacy? Decreases it. Can a reversible competitive inhibitor be overcome by increasing the concentration of substrate? Yes. Can an irreversible competitive inhibitor be overcome by increasing the concentration of substrate? No. What is the effect on Vmax in the presence of a non-competitive inhibitor? It gets decreased. What is the effect on Km in the presence of a non-competitive inhibitor? It's unchanged. What pharmacodynamic change occurs in the presence of a non-competitive inhibitor? Efficacy is decreased. What is the bioavailability of an IV dose of a drug? 100%. How can we calculate volume of distribution? By taking the amount of drug in the body and dividing it by plasma drug concentration. Defects in the function of which three organs can impair drug clearance? The heart, kidneys, and liver. 3. state? 4 to 5. Which type of elimination does alcohol, aspirin, and phenytoin undergo? 0 order. Which type of elimination is directly proportional to the drug concentration? 1 order. The maximal effect a drug can produce is known as its what. Efficacy. Potency refers to what with respect to a drug. The amount needed for a given effect. How is the therapeutic index calculated? By taking the median toxic dose divided by the median effective dose. Which type of therapeutic index indicates a safer drug? A higher therapeutic index. The higher the index, the safer the drug. What is the treatment for acetaminophen toxicity? N-acetylcysteine. What does the administration of N-acetylcysteine achieve in acetaminophen toxicity? It replenishes glutathione. What is the treatment for benzodiazepine toxicity? Flumazenil. What are the two treatment options for arsenic poisoning? Dimer caprol and succimer. What are the treatment options for copper toxicity? Penicillamine and triantine. What is the treatment for digitalis toxicity? Digoxin-specific antibody fragments. What is the agent used to reverse a heparin overdose? Protamine sulfate. What are the three options to treat iron toxicity? What is the treatment protocol for methemoglobin toxicity? Methylene blue and vitamin C. What is the treatment for opioid overdose? Naloxone. What is the purpose of giving sodium bicarbonate in salicylate poisoning? To alkalinize the urine. What's the purpose of giving sodium bicarbonate in TCA poisoning? It stabilizes the cardiac cell membrane. What is the treatment protocol for beta blocker toxicity? Atropine, glucagon, and saline. What is the treatment for immediate reversal of warfarin toxicity? FFP or PCC. What is the treatment for a delayed reversal of warfarin toxicity? Vitamin K. What is the cardiovascular side effect associated with doxorubicin or donorubicin use? Dilated cardiomyopathy. What can be given to manage the development of Redman syndrome associated with vancomycin use? Diphenhydramine. Name the six pharmacologic causes of cutaneous flushing. Which endocrinopathy can be precipitated by the use of lithium or dimeclocycline? Diabetes insipidus. Name three classes or specific drugs that can cause SIADH. carbamazepine, cyclophosphamide, and SSRIs. Halothane, amanita phylloides, valproic acid, and acetaminophen can all cause damage to which organ? The liver. Which two steps can minimize the risk of pill-induced esophagitis? Upright posture and adequate water ingestion with the drugs. What is the major side effect seen with quinine or quinidine? Synchonism. Isoniazid and phenytoin are known to precipitate which problem? Peripheral neuropathy. Which drug is associated with causing yellowing of the vision? Digoxin. What is the visual problem associated with isoniazid? Optic neuritis. What is the major adverse effect of ifosfamide or cyclophosphamide use. Hemorrhagic cystitis. What can be given to prevent hemorrhagic cystitis in someone treated with cyclophosphamide or ifosfamide? Mesna. What is the most common side effect associated with the use of ACE inhibitors? Dry cough. Which side effect is associated with busulfan, amiodarone, bleomycin, nitrofurantoin, methotrexate, and carmustine? Pulmonary fibrosis. Vitamin A. Tardive dyskinesia. Which drug is linked to grey baby syndrome? Chloramphenicol. Thank you guys for sticking around until the end. I hope you found that to be useful. If you'd like to learn how we can help you prepare for and pass your USMLE Step 1 exam, don't forget to head over to our website, usmleguys.com, to learn how you can work with us today. I'll see you guys on the next episode.
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Hello and welcome to the latest podcast from The Lancet. It's April the 5th and my name is Francesca Towey. Today we're discussing a new article from the Global Burden of Disease Working Group who provide worldwide observational epidemiological data at global, national and regional levels. This latest study focuses on the smoking prevalence and the attributable disease burden from 1990 to 2015. And joining me is the senior author of the paper, Dr. Emanuela Gekidu from the Institute for Health Metrics and Evaluation in Seattle, USA. Welcome. Thank you very much. So to start, previous global burden of disease or GBD studies have included smoking prevalence. How does yours differ from these? Yes, it is true. All the previous GBV studies going back to the original one published in 1996 have included smoking because it is one of the leading risk factors. There are several improvements and advancements that the 2015 study has made. One of the main areas in which this study is better over previous studies is that we have included larger number of data sources. So the number of data sources has increased by almost 40% over the previous study that was published in 2013. In this study that was just published today, we have almost 3,000 country years of data. And having more data significantly improves our estimation and makes all of our numbers much more current and up-to-date. We have also made improvements in the analytical methods. In this paper, in addition to publishing on smoking prevalence, we have conducted new analysis where we look at smoking by levels of sociodemographic index, which is a measure of development. We also look at smoking across birth cohorts and we decompose the drivers of change over the past decade and we look at what is responsible for the trends we're seeing right now. You completed several analyses of smoking data in your study. Please can you briefly explain what these were and what were your main findings? So in this study we have looked at global, regional and national levels and trends of daily smoking and one of the big findings is that there has been a significant decline of more than 25% in the prevalence of daily smoking among men and women. But in 2015, the prevalence of smoking is still very high, with about one out of every four men smoking daily and about one out of every 20 women. We have also looked at deaths from smoking, and in 2015, we find that 6.4 million deaths, which is approximately 11% of all global deaths, so more than 1 in 10 deaths, were attributable to smoking. And half of those deaths occurred in only four countries, so China, India, the U.S., and Russia were responsible for half of the smoking deaths in the world in 2015. We have found that progress in using daily smoking has been heterogeneous, and while there have been some successes, there's still a long way to go. In this study, we have highlighted the countries with a large smoking population. So we have looked at where do most of the world's smokers live. And in this analysis, we found that there are three leading countries in terms of where currently daily smokers are living in the largest numbers. And those are China, Indonesia, and India. In this study, we also provided a new angle by looking at information on daily smoking for adolescents and we have a special focus on adolescents, specifically young people aged 15 to 19 because we wanted to look at what's happening in initiation. That's the age group that a lot of young people pick up smoking. And what we found was that despite global decreases, there are several countries that still have a high prevalence of daily smoking among adolescents. And this might be a good area for policies to target is to prevent initiation from happening. The next part of the analysis looked at patterns of daily smoking across birth cohorts, and we looked at this by level of development. And what we found was that male age patterns were consistent across levels of development, and they peak between ages 25 and 35 years. But the female age patterns varied across levels of development. And they peak around age 25 for high development areas, but they increase steadily until age 60 for low and middle development countries. Finally, we looked at the drivers of change in the tobacco epidemic and the attributable burdens due to smoking. And in terms of drivers of change, we looked at the daily smoking prevalence rate, the risk-deleted DALY rate, which is an analysis that looks at what would happen to burden of disease if there wasn't smoking. We looked at population growth and population aging. And while the drivers of change vary by sex and by level of development, population growth and population aging have offset reductions in smoking attributable valleys that have occurred due to reductions in smoking prevalence. So what this means is that these demographic forces with the population getting older and growing, they're poised to increase the burden of disease due to smoking globally, unless there's more progress in combating the smoking epidemic. How do you see your findings building on the global strategies that already exist to help reduce smoking and combat its negative health effects, such as WHO's Framework Convention on Tobacco Control and their 25 by 25 non-communicable disease targets. IHME is only one of several global partners working on tobacco to combat the tobacco epidemic and all of us are working together to achieve the same thing. We're hoping to eliminate death and disease burden caused by tobacco use. We hope that the results of our study can be used as an evaluation tool to see how well countries are doing in reducing the habit of daily smoking and where more could be done, which countries have achieved significant reductions and what has worked in those countries and how could other countries adopt these strategies so that more successes can be achieved globally. Clearly, the results of the GBD study are just the starting point and a lot more work needs to be done, but they can be used to measure progress by countries before and after the Framework Convention for Tobacco Control, FCTC, was entered into force. And in fact, there was a paper published a couple weeks ago, March 21st, by Gravely and colleagues in Lancet Public Health Online, which showed an association between implementation of the FCTC and a decline in smoking prevalence. So we see our work in this as part of a larger effort working together with WHO and other partners. At HME, we develop and we apply cutting-edge analytics and models to examining multiple sources of data and provide the clearest picture of the tobacco epidemic that is was that you only included smoking tobacco and didn't include smokeless tobacco or e-cigarettes. Are these products that you would include in of our study that in the GBD 2015 we have included tobacco only, and we have only looked at daily smokers because it is an important measure of tobacco use, and it is the risk factor that contributes the most to death and disease. That said, the tobacco pandemic is very complex. Some people only smoke occasionally, and there's tobacco products that are being used that are not smoked. In future iterations of the Global Burden of Disease, we do intend to include analysis on smokeless tobacco, which is of particular importance in certain parts of the world. Specifically, India comes to mind when thinking about smokeless tobacco and Southeast Asia in general, as well as some countries in Europe like Sweden. And so we hope that in future iterations of the GBD we'll be able to do a comprehensive analysis of the burden of disease due to smokeless tobacco. E-cigarettes are an emerging force and we do need to fully understand them. It is something that we would consider adding to future iterations of the whole burden of disease study. Our preliminary exploration to date has revealed that very little data are available to do a comprehensive assessment of the burden of e-cigarettes and what their contribution to the health of the populations that use them might be. And so we would encourage data collection efforts to include e-cigarettes, so that would be in population surveys and regular monitoring, so that we will have the ability to appropriately assess the prevalence of their use and also their contributions to the health of the population. Another part that is important here is secondhand smoke because it is also part of the tobacco epidemic and it does contribute significantly to death and disease. And IHME, with funding from Bloomberg Philanthropies and the Bill and Melinda Gates Foundation, are putting all of our team together and trying to enhance the analysis of the tobacco epidemic, expanded in the sense of including smokeless tobacco, potentially e-cigarettes, and fully capturing the burden of secondhand smoke. So an important part of how we do our work is our collaborator network, and especially for these new areas in which we hope to expand the global burden of disease, we see the GBV collaborator network as a very significant contributor. And we hope that through our extensive network of collaborators and the Global Tobacco Partners, we'll be able to keep all the tobacco analysis up to date, current and as relevant as it can be. Well, thank you very much for taking the time to talk to us today about your paper and thank you all for listening.
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Hey, Paul, I'm excited to tell you that we are launching a Curbsiders Patreon. Have you heard about this? I did because I work with you, but tell me more about it. All right, Paul. Well, we want to be able to keep offering this great free content, and we're doing things like upgrading our website. We offer transcripts now for episodes, recording new seasons of our miniseries, Teach and Addiction Medicine. The Digest is growing its staff. And Paul, now we're on video. People could see us as we're talking right here. What a treat for our listeners. That's right. So with Cash Slack admitting privileges, they're going to get all episodes ad-free. That's the whole back catalog plus future episodes. And twice monthly, there's going to be bonus episodes where me and you recap a show and answer some listener questions. So people should sign up today at patreon.com slash curbsiders. and you get a whole lot more of Paul, America's PCP. First one that came up. This is from 11 Hilarious Arthritis Puns. You know, Paul, apparently there is bipartisan agreement in Congress for medical cannabis that it should be allowed for the purpose of relieving arthritis pain. You know why? Tell me why. In other words, Paul, there is joint support for joint support for joint support. That's terrific. Okay, good. There we go. All right, Paul, welcome back to the Curbsiders. In person here, ACP Internal Medicine 2023. This will, of course, be released after the fact. But, Paul, today we're talking about wisely ordering autoantibodies. Certainly a topic that I could have used, and now I feel empowered. How about you? I feel much better about being more restrictive about my ordering. There'll still be the errand to ANA that I don't know what to do with, but I feel like I'm going to do better after this episode. And our guest, Dr. Matthew Carroll, we'll tell you a bit about him in a second. But Paul, what is it that we do on Curbsiders? Thank you for asking. We are the Internal Medicine Podcast. We use expert interviews to bring you clinical pearls and practice changing knowledge. And Matt, you're about to tell us about our excellent guests and a little bit about what we talked about. That's right. So Dr. Carroll is a rheumatologist. He went to Uniformed Services University. He worked as a medical officer and leader in the United States Air Force. He serves tours of duty in South Korea, United Kingdom, Saudi Arabia, Colorado, Kuwait, and Oman. In 2007, he completed his rheumatology fellowship and relocated to Kiesler Medical Center in Thank you. the program to meet the next accreditation standards. He initiated multiple clinical trials, led the IRB, and served as the designated institutional officer, the DIO. Upon retirement in 2017 from the military, he's working in Singing River Health System. He has been an ACP member since 1996, Paul, active in the Air Force chapter. He's been a part of the Board of Governors from 2002 to 2005. He's won a chapter laureate award in 2021, and he served as the Air Force ACP chapter governor from 2017 to 2021 and received the honor of Master American College of Physicians in 2022. So needless to say, we are thrilled to have such a great guest on this episode. A reminder that this and most episodes are available for CME credit for all health professionals through vcuhealth at curbsiders.vcuhealth.org. And with that, let's get on to the interview. Audience, this is going to be our take two because I forgot to press record. So we'll do it again. Okay. Matt, thank you for answering this question twice in a row. So welcome to the Curbsiders. Thank you. And give the audience a hobby or interest that you have outside of medicine. So I like to garden. I think that's kind of fun. It's a nice way to kind of relieve stress. And living in South Mississippi, it's kind of easy to almost get two seasons growing. I don't usually do successful in the fall, but I'll get some tomatoes and other veggies before the bugs get them. And then I like to run. So I think running is just a good way to offload stress and stay cardiovascularly fit and try to keep the cardiologist hungry. Hopefully it won't be stenting me at any point soon. And then my wife is, you know, certainly my better half. She keeps us busy. We've got young kids and we're running around taking care of them. And so I try to do, I'm a mad scientist for my kids. They're in middle school and, well, really upper elementary. So I just, I was a chemist. I was my bachelor's. Oh, nice. I dress up with white hair and a lab coat, and we just do cool experiments, and the kids like that, too. So a little bit of everything. You might need a YouTube channel with this. I thought about it. It just, I'm not as tech savvy. My wife's a lot smarter. She tried. And we almost did that with the pandemic. But I just try to stay busy in certain activities and areas. Because I think, as we all know, as the kids grow faster and life goes on, there's so much going on. Yeah. This touches on two things that Nat and I have talked about, and that the people who garden seem to be much better adjusted than people who don't. And then also, we were talking earlier about how running is more to prevent psychopathy than it is to actually make you feel good. Like, I don't know if like for me, it just keeps me dreaming lightly homicidal and I it's, it is stressful. And then, yeah, at least for me gardening, it's, you're gonna be thinner. Yeah. Sorry. Gardening. I still Paul audience. Eventually I will start a garden. Paul, same. I think it's in your near future. I think a yard is in your near future, Paul, with this upcoming move. I think a garden is in your future. This episode is brought to you by Grammarly. And I want to tell you about Grammarly Premium's advanced tone suggestions, because these are going to help you communicate more confidently. They're going to help you reframe things in a more positive way. And instead of sounding kind of meek in your suggestions, you're going to sound confident. You're going to be concise in your communication. That's why it's here to help you. It's a tool. It follows you all over the internet. When we write our show notes, when I write emails to guests of the show, I want to sound good. I want to get things right. And Grammarly helps me do that because it has tons of features like spelling, grammar, punctuation, and conciseness. And as I said, Grammarly Premium's tone suggestions help me balance that being direct and also being friendly, but still finding solutions. So the right tone, it can really move any project forward when you get it just right with Grammarly. Go to grammarly.com slash tone to download and learn more about Grammarly Premium's advanced tone suggestions. That's G-R-A-M-M-A-R-L-Y dot com slash tone. So Paul, do you want to ask anything? Sure. And you were giving us some excellent advice before we started recording. So now that we have actually started recording, I would love to hear that advice to its completion. Yeah. Well, first of all, again, thank you for having me here. It's really an honor to be on Podcasters and to just kind of hopefully provide a very informative session for all of us here, but certainly more importantly for the listening and viewing audience. I joked about earlier, patients and other docs will come to me sometimes and say, what wisdom do you have? What advice do you have? And I always kind of jokingly say, but it's partially true, is the gray hairs are getting deeper. It seems like, you know, we're going from a 64K down to a 32K down to a smaller and smaller, you know, memory. But the reality is, I think the takeaway is we are under a tremendous amount of stress every day as we see our patients with regard to trying to be productive for our views and get that next patient in and just move people through.
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And I've really been focusing on the past five or 10 years, and maybe if not a little bit longer, on the service aspect of it. I think in medicine, we're here to serve. We're here to give back to our community and build and nurture, especially in some of the turbulent times that we've seen. So I think just taking the time to know your patient, go that extra mile for your patient, not always easy. I mean, I certainly stumble on that journey, but it's a blessing to be able to take that one extra step and maybe get that medicine for a discount because you took the five minutes or your nurse took the five minutes to get them the medication card for the discount or we're ranging for transportation or something like that, which can be a real, you know, it takes some time. It takes valuable time from all your, you and your, all your staff. I think probably one of the best headspace adjustments I've made in my entire career is recognizing that the goal is to get patients towards a shared health goal as opposed to getting them to do the thing that I want them to do. And once you even make that adjustment, it like becomes much better. Yeah, early on, I used to take it personally if the patient didn't do the things that I was trying to arrange for them. And then I was like, oh yeah, that's because they didn't want to do that. I should probably find out what they want. And then if we're working together, it'll work better and I will be less frustrated with things. Or sometimes afford them. Yes. So I think we're in a good spot, Paul, to just jump into a case from cash lack. Paul, would you do the honors of reading it? Just because I think everyone loves to hear from America's PCP. Yeah. My soothing baritone. We're going to talk about Jocelyn, who is a 44 year old female. She has a history significant for chronic low back pain, migraine headaches, pure hypercholesterolemia, parentheses mild, a BMI of 29. She's coming to our primary care office for an initial visit. She's reporting joint pain in her knees and her hands. The pain has been present on and off for years, but it has gotten progressively worse over the past six months. She has stiffness in her knees and hands upon awakening. She works in an Amazon warehouse packing and stacking boxes. She states her energy level could be better, as is true for all of us. Her grandmother and her aunt have arthritis, but she's not sure what type, whether or not to take any medications for it. And so we have a picture here that I feel like comes up all the time in primary care, where is this an inflammatory arthritis? Because she has some of the things, is this simple arthralgia? And I guess the question for you, Matt, is how do we tease this out? And sort of what are you listening for in history to kind of help make that initial determination and sort of guide the rest of the visit? So I think a couple aspects here. One, obviously, there seems to be some chronicity to it. I think the case had mentioned that it was about six months in. So at least if you look at a bunch of different guidelines, it looks like we're past six weeks for a threshold where you might want to be considering more long-term potential for an autoimmune issue. The reality is this screams fibromyalgia to some extent, and there's other chronic pain syndromes that might be coming in here. But in an ideal way, if you could find some degree of synovitis or actual swelling in the joints on exam, that would probably be a little bit more of a tip-off. And I think also what we don't really have in this case, but I know it's a vignette, is just some other things to think about is, is there evidence of sclerodactyly? Is there evidence of Raynaud's or history of Raynaud's? Is there excessive dry eyes, dry mouth? Is there anything else that might really steer you toward like an ANA positive autoimmune condition? The five of those being lupus, immune, I'm sorry, idiopathic inflammatory myositis, Sjogren's, mixed connective tissue. And so I think irrespective, if you don't have any of the telltale signs for that, then it's probably worth saying, all right, look, you know, right now it may just be that you have something like fibromyalgia. Maybe any other additional screening that might be appropriate for that would be the next to consider and move on from there. Now, if symptoms develop and change, that's where you might want to reinvestigate what's kind of going on. And I think not to be too preachy, but a lot of us know in our day-to-day practice, medicine's an iterative process. You'll see somebody and your pre-test probability is low, but then six months later, they come in with evidence of digital pitting on their fingers or maybe new dry eyes, dry mouth, just something else that then says, hey, I didn't capture this before, but now maybe I need to reinvestigate and kind of go back through that. We did pre-test, here's the testing, here's the post-test, let's bring the post-test back for another pre-test and keep kind of doing that cycling. Yeah, and I guess part of the point is, like, you, these, I've seen patients present with, like, a new rheumatoid arthritis, and they were obviously inflamed, and they could barely move, and it was, like, really not subtle. Right. Some of the other patients, it took a while for things to really declare themselves. It sounds like that's what you're getting at, And you can kind of maybe tell by how bad the person looks in front of you. Exactly. And by the way, just again, gray hairs, remember? Thigh escleroderma. That was the one I think I missed. All right, sorry. But that aside, yes, absolutely. And usually the ones who are really more active with a lot more going on, they're going to declare themselves much earlier. It doesn't mean you can't have rheumatoid arthritis that's really kind of smoldering or say lupus that's smoldering over a period of time. So that's where that iterative process of kind of following up with the patient, seeing how you're doing, getting them back in a couple of weeks, trying a medicine that fails, maybe try the next step. And, you know, despite a lot of our advances in medicine and rheumatology certainly as well, we're still blessed with the follow-up aspect, you know, to get patients back and how are you doing? Have we made an improvement? Are we failing here? What's next? Yeah. And for someone like this who's coming in kind of largely undifferentiated, maybe we're waiting for something to declare itself, what other historical things are you asking about specifically at this initial visit to kind of at least get a sense of where you think things are going? Yeah, and I think a lot of that harkens back to what we had brought up before. So dry eyes, dry mouth, that's one that's kind of easily overlooked and that can be a little difficult to assess. I mean, there you might want to ask about how frequently do they use over-the-counter eye drops? Do they have to drink frequently at night? Do they drink frequently throughout the day? That may not per se diagnose them with obviously sick symptoms, but that might be suggestive of it. Certainly poor dentition as a consequence of months or years of sick symptoms. Sclerodactyly, Raynaud's is another big one. So I think for a lady in this population, certainly if she's, hey, I've had Raynaud's for five years, you know, and now you see some sclerodactyly on your exam, that's going to kind of be like, hey, there's more going on here that meets the eye. And sclerodactyly, like sort of the thickening of the skin, the fingers are curled a little bit. And that might be more of an advanced finding, but at least some sort of skin, loss of skin turgor is probably the better way to put that on there, or a better way to frame that. What else? Rashes, any rash that would be somewhat suspicious. Little challenge there is of course the malar rash, because a lot of times ladies in this age might have acne rosacea, or if they're darker complected, it might be difficult to diagnose.
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So that can be a challenge, but that might be a little tip off too. And I see that occasionally. That's a challenge where you get somebody with fatigue and achiness and they have what probably is acne rosacea, but is interpreted as a malar rash and then that ANA is fired. But again, I mean, you're seeing the patient, you're trying to interpret everything that's going on. And so I really don't try to, it's easy to be the Monday night quarterback and say, well, it's crazy to order that A&A, but that's what you were seeing at the time. So you kind of go with your suspicion. And then again, you update your post-test probability to be your pre-test again. Thank you. Podcasts, photos, and lecture slides that I know are building up in your email and on your phone. Glass also has a community library with fantastic pages from clinicians around the world. The community library is filled with dot phrase like clinical plans for common situations that you're going to encounter on the wards and in the clinic. So try Glass for yourself today by visiting glass.health to keep all your medical knowledge in one place. That's glass.health. And the pro version of Glass gives you access to their AI features and medical knowledge visualizations. You can get one month of Glass Pro free by signing up at glass.health and using asking, but synovitis, just talk me through a little bit of what you're looking for, what that feels like. I know everyone, well, it's some bogginess, and you're like, I still don't know what that means necessarily. And this patient specifically was saying joint pain in the knees and hands, and maybe there's some morning stiffness. We didn't get too deep into that yet. Yeah, no, and that's perfect. And that's a challenge, because I'll just tell you, even when I was a rheumatology fellow and we were on rounds, you know, the gray hairs at the time, right, the ones who taught us, they would be like, well, there's some trace synivibus. And then you're sitting there going, what does that mean? It's a challenge. And I guess it gets back to the old adage, you know it when you see it, right? So there's going to be some times where you're like, wow, those second and third MCPs are pretty obviously swollen. And there's a degree of bogginess and just a very easy elicitation of pain when you press on it. But it's the repetition in the exam that I think will help you over time realize, yeah, that's probably more tender than it is swollen versus obvious swelling and tenderness. But it is hard. It's a challenge even for a rheumatologist. I don't, and I'll speak for myself maybe, but it can be a challenge. So assuming you don't, I don't have rheumatoid arthritis. If I feel my own joints and then feel the patients and there's a little bit of a sponginess or give to it, then that's like sort of. Exactly. And you should be able to feel like between say the metacarpal and the phalange, you should be able to feel like a little going or an indentation. And sometimes you don't get that. Now it gets a little bit harder as we get older, of course, because if you've got osteoarthritis or other types of arthritis, there might be, well, osteoarthritis, I guess being the main one, the PIPs and DIPs may really have substantial changes to them that reflect chronic and rather than acute swelling. So no over chronic synovitis picture. And that's, you know, it is, it's tough. And how much stock do you put in the morning stiffness question? Is that, it's a challenge because in a perfect world, less than 30 minutes, you would think that's probably your typical wear and tear. I know my fibromyalgia patients can have morning sickness that lasts several hours. And so you sit there scratching your head going, okay, well, they've got what would technically fall into the range of an inflammatory arthritis. And yet they really don't have anything on exam. So again, that's where it, you know, you're looking at the whole picture. It can be very, it can be challenging, and it's challenging as a rheumatologist. It can be challenging certainly as an internist and a specialist. It's hard, and I think that's that iterative process of trying to keep gathering more information to help you uptake your predisposability. Okay. So let's say we conclude that she has morning stiffness that never quite goes away, and she doesn't have any joint deformities or active synovitis on our thorough joint exam. After talking with you, we think we got it down a little bit. Awesome. Let's say we even got x-rays. We don't see any erosions of the hands, the wrists, the knees yet. And we think this could maybe be early rheumatoid arthritis because she has this symmetric arthritis. It's involving the hands and she's got morning stiffness. She says maybe, you know, maybe she has a little fatigue. What, what would be like your initial tests that you would order after that? Like serologies? Well, upfront, you know, hopefully to kind of enter the 2010 classification criteria for RA, which again, you know, in rheumatology, we use a lot more classification criteria to help us with homogeneity from study standpoint. Like research, yeah. Yeah, exactly. But they certainly can help us in a quasi-diagnostic sense, but they're not diagnostic, and that's a talk for another day. If you have synovitis plus the history that's observed, let's assume that's kind of going on here. Now you're looking at an ESR CRP that would be potentially the next to assess inflammation and, and get, you know, the rheumatoid factor and anti-CCP and, and with the 2010 classification criteria, those are the ones that would be the next that if you're getting positives on those, so either low or high amounts of inflammation or, or a strong or weak positive rheumatoid factor or CCP, those would start to give you certain amounts of points that might push you more toward diagnosis of RA. Yeah. What about the, I mean, I've heard some people say they order like a CBC and a CMP. I have seen like elevated white count and some liver enzymes that are elevated. And, you know, I don't know if you throw urinalysis in, if you're ever considering, could this be an arthritis or just like your simple osteoarthritis, or is this like a inflammatory arthritis? What else do you order? Well, if I'm thinking RA, I usually limit it to those with some of the novel markers that we'll talk about here, depending on clinical suspicion. If I'm thinking more lupus, you know, or even Sjogren's, I'm thinking kind of more in that flavor of an autoimmune condition, urinalysis. Usually I get a urine protein creatinine ratio just to make it easy. And my lazy rheumatology ways, I guess, speaking for myself, not us as a community, I don't want to know if there's blood in the urine. And I don't mean that in a bad way. You don't want to get stuck with the cysts. Amen, amen. I was like, right, you know, it's like you're a 65-year-old lady who you're just like, oh, I know that there's, well, I'm not worried about the cyst though, more just the UTI. I guess that's the whole thing I should have said. I don't want to know anything about a UTI. Is there protein or not? And if there's a lot of protein, that's important. This past week, I ordered the UA and the urine protein creatinine for a patient that I was working up for this, and they had microscopic hematuria, no protein. So I'm like, darn it, now I've got to go. Exactly. And I'm just bringing that up in a humorous note. I mean, obviously, you get a urinalysis, and if there's blood and protein, sure, you work that as appropriate. For me, I guess I've just gotten kind of lazy in the sense that if I open the hood and I see that there's certainly like two grams of proteinuria, that's put me down more. I loop a Sjogren's kind of path there and then I'll get the UA, you know, and that might give me additional information about what else is kind of coming through, creinated red blood cells or something.
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I feel like, yeah, these initial tests, like this is invariably we'll come back with like an elevated set rate, but a normal CRP and maybe the rheumatoid factor is positive, but the CCP is negative. And you're like, oh, well, now, now, now what do I do with this? Which I guess is what we're going to be talking about the entire back half of this episode. We're on that right now. There's nothing in there about a CBC or whatever, but that does give you more credence, right? So you've got an elevated ESR, maybe a slightly elevated CRP, but the person's got a BMI of 30, and then you have some, you know, leukocytosis, and there's no other clear reason. You're like, all right, there might be some actual inflammation here that's not related to cystitis or steroid use or, you know, you name it. And then the CHEM-7, sure, that's probably not unreasonable to do. I'll do that based on what I think potentially is going to happen down the road with regard to treatments. Okay. Got it. That makes sense. Let's give you some labs here. So we have a mildly increased white count, NCRP. The kidney and liver functions are normal, or the liver tests. Sorry to our hepatology listeners. And rheumatoid factor is positive, but CCP, which is now, I'm told, ACPA for anti-citrullinated protein antibody or peptide antibody. ACPA, yeah. Anti-CCP or ACPA, you might see it, listeners. So let's say the CCP is negative, but the rheumatoid factor is positive. Matt, what do you think about those? Well, let's assume, again, she has synovitis. So at this point, if she's got true synovitis that you're like, those are definitely swollen, tender joints, and she's got at least more than 10, and she's had her symptoms for a couple of months now, obviously, and your ESR is elevated and your rheumatoid factor is elevated, I always have to look back at the guidelines. You're pretty much there at that point by saying, hey, I think you've got rheumatoid arthritis. And then if you feel that's within your wheelhouse, you can certainly start treatments for that. If not, send it over to rheumatology, obviously, just saying, here's what I found. And kind of yay or nay, you'd be the C-sign, so to speak, to give the thumbs up or thumbs down. And is the cutoff for rheumatoid factor somewhere around 30? Sure. It depends on your lab. I think mine is like 14. I, what would be helpful rheumatoid factor? That's a talk for another day too, is if you get this kind of rheumatoid factor of 17, you're kind of like, ah, you know, it's a low positive and I'm not really sure what to do there. Rheumatoid factor with the rheumatoid factor of 17 with a CCP of two 50. Okay. That's like, you know, slam dunk there. Rheumatoid factor of two 70. Okay. Well then there's a differential that goes with maybe hep C screening, hep B screening. Yeah. I don't know if we talked about your approach to imaging after this initial presentation. Is this someone that you would get x-rays of the hands and feet or wrists right away? We did give some x-rays. We jumped ahead of that just to, I guess, the way that the case was written was just to take that off the table. But yeah, when would you get those? Would you get those after or before the... I usually get them up front, in part because if you get some of that ambiguity and you see some evidence of interstitial lung disease on chest x-ray, obviously not the best tool for that. But if you do, that would be kind of saying, hey, you've got somebody who's got all these serologic findings, this historical stuff, and they've got interstitial lung disease. You're like, hmm, all right, this is starting to get a little suspicious. Or if you, and this may not happen per se within six to 12 months, but let's say you get hand x-rays at the start of this appointment, and you find there are actual erosions involving the MCPs or PIPs, kind of these periarticular erosions, you're there. I mean, essentially, that might be erosions, a positive rheumatoid factor, an ESR, all these clinical symptoms like that starting to pull you in there. My understanding is the erosions are a later finding. Like, if you're catching someone with early rheumatoid, you might not see those. Exactly, right. And that may be a distinction we'll talk about here is whether or not to get MRI. I don't want to get the cart before the horse, I guess. But yeah, absolutely. So you would hope, and the aspiration that we have as rheumatologists is to capture them early. And actually a lot of great, interesting stuff now trying to get people in the pre-RA phase. Capture them early, treat them aggressively, and never let those erosions come up. Like we never want to have a hand damage. The stuff that I trained with in the late 90s was you were guaranteed to go to just severe deformities and joint replacements. That error should never hopefully happen. And it remains a challenge now as a rheumatologist because I'll get patients come in and I'm like, I don't really know. Do you really have RA? Well, then CCP's, I'll repeat a CCP. Okay, it's positive. So the whole idea is we really want to keep people in remission and control and never let those erosions develop. Never let the lung stuff come up. Never go down that road. And this is one of the diseases where once you have it under control, you kind of keep your foot on the throat of the disease. You don't like just like say, let's see how you do off your medication. Right, exactly. And I tell patients, we don't know how to hit, and this is an 80s reference here, the eject button from the cassette player just yet, right? But we know how to hit pause. We're 80s, we're kids of the 80s. Yeah, so we're birds of a feather. That's good. So I know how to hit the pause button. I don't know how to hit eject. But there's very smart people trying to figure out how to hit the eject. Yeah. And maybe one day we'll be there. Yeah, so in this case, we gave, you know, she didn't have sign of itis by our exam, but I probably would send this patient because she's got enough features, a positive rheumatoid factor. I probably would send her to you to see see if you, what you think. And, uh, and maybe she is someone that's early. Maybe, maybe she's someone we caught, but this person has one, she's a positive rheumatoid factor, no sign of itis. The CCP was negative. What else can we do that might help us figure out? And what's the new stuff, the fancy stuff? Cause our listeners like to be well-informed Paul, right? Like they want to, they want to show off the leading edge of the blade. That's right. The tip of the spear, as we said. So what's the new stuff that Paul and I will try to remember these autoantibodies? Hey, everybody. This is Watto. I just wanted to break in here and set up this next section. We're going to talk about two newer tests that you might think about ordering for patients with suspected rheumatoid arthritis. As we get into, these can help you pick up some extra cases who are missed by the rheumatoid factor or the CCP testing, respectively. So these are 14-3-3-ADA protein. That's an inflammatory marker of sorts that you can send. And then finally, the second one is the anti-CAR-P antibodies. That's anti-carbamylated protein is what it stands for. And those can pick up another maybe 10 or 15% of patients that you might miss with the more traditional testing for RA. So with that, I just wanted to set up this next segment and let's get back to the show. Well, there's actually several.
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It's a citrullinated vimentin. I'll talk, I think, beyond this, but what I'm presenting here at the conference are two additional RA labs. One is what's called a 1433-ATA protein, and I believe that got its name because of the way it patterned out on a gel electrophoresis. The name is really kind of annoying, I guess, but the reality is it's an isoform. There's actually six or seven of them, these proteins that like to dimerize. It's the sixth of seven, and it's unique to brain and to synovium. Now, let me step back for a second. I guess I'm getting, again, the cart before the horse. As the trends in rheumatology have kind of gone for RA, we're trying to take the needle from the 90s, where it was established disease, to the 2010 the 2010s early disease to now pre-RA. So in that process, when you look at the RF and CCP specifically, for early RA, you're missing, for established RA, you're missing about 12% of patients with the RFs and CCPs. With the rheumatoid factor and CCP for early, you're missing about 28%. So there's a big gap there. And the whole idea, like I told you earlier, is we want to capture this very early. We never want erosions. We never want deformities. We don't want any of that at all. So these other proteins, these other labs might be helpful. Back on track, 1433-ADA is really an inflammatory marker. And so it's not an antibody. So that's kind of like an adjunct, maybe, if you want to think of it in the same family as the ESR and CRP. And so a value of 0.2 nanograms per milliliter or higher is considered positive. I will say when it's the 0.2, 0.3, 0.4, I'm like, what does that mean? Now, if they're 0.4 and they've got a rheumatoid factor of like 230, I think we're there. If they're more of an OA picture with 0.4, I'm like, I think we'll just watch and wait. I wouldn't diagnose it based solely on that. But the strength of that test comes in conjunction with other antibodies that you might have. And we do think that when you're rheumatoid factor and or CCP and or both positive, that adds another 15% that you're going to capture if that protein's positive too. 0.8 or higher is what really kind of sets the, you're like, you're there, you've got an abnormal test. And again, I wouldn't diagnose RA alone just based on that. And again, that's kind of staying within the 2010 classification criteria. But that can, again, be of help to you there. Did you mean if the CCP and the rheumatoid factor are negative, but you're still suspicious and the 14-33-ATA is positive, then that might capture extra people? Absolutely. So that's all I did is we're trying to capture extra. Yeah, I'm sorry. That's why I kind of gave that and or kind of thing. Yeah, so you're going to probably capture about 15% more people in that scenario there with that 14-3-8 of protein. And earlier disease too, which is nice because you'll capture them earlier. And it seems like this would be a send-out lab that I don't know if I haven't tried to order it. Maybe now I'll look into it. I know for me initially it was, let's see, so it rolled out in the mid-2010s. Working with Lab, they were pretty straightforward. I think it should be relatively easy if you work with your Lab department to get that kind of squared away. It's been around for almost about 8 to 10 years now or 7 to 10 years. I'm just late to hear about it. Well, I think we're still, it's kind of back back a couple years ago, it was a little bit more half-baked, and now we're getting to the near completion of it, right? So if you will, in the baking process. Sort of figuring out where to use it. Exactly. We've got to have a lot more studies roll out. And then on the carb P, so carb stands for carbamylation, but when you look at the likelihood ratio for the carb P, it's only, I think, about one or somewhere in there. It's really not as good. So with the CARB-P, if that's positive and everything else is negative, you might capture another 5% to 10% of patients with it. And my caution there is, again, we're not in the same arena as the 2010 classification criteria with these. A positive CARB-P, not a really convincing exam. It might be like something you want to watch or wait. This is the way I would take it as a rheumatologist. I think as an internist, if you were to get that test, you know, I don't know what to make of this, boom, send it over to rheumatology, let us figure it out. The reality is I would probably watch and wait somebody. But if you're RF positive at 100 and you've got a carb P that is anti-carb P that is like 40 units or whatever, you know, that's a positive test. I think anything over 20 or 25, then you're there. Like, I think at that point, you probably say, look, with the elevated ESR, the leukocytosis, your clinical history, and these other autoantibodies were probably there. Just the key takeaway is that the two of them, one, they're not within the confines of the current classification criteria, but they can still clinically educate us. And then two, the CARB-P, I don't think really has the strength that the 1433 has, and those are still not as good as the CCP. And I wonder, yeah, I wonder if these will be incorporated in future guidelines or just when this is written about in the future, there'll be more guidance on how to use these so we can make that earlier, that pre-RA diagnosis and use that to treat people early, prevent any kind of joint deformity from happening. Yeah, I don't know where that is in the process. I wouldn't be surprised if there, I mean, 2010 has been a while, but I still think those criteria are serving us well. I don't know how they're going to incorporate a lot of this new stuff. And there's still more antibodies beyond it, but those are the two more mainstream ones I think that are kind of out there. Yeah, given that I don't know what to do with the RF half the time, I think these will, I'll probably leave it to my friendly neighborhood rheumatologist, but just know that they exist. As you might know, Brooklinen was founded by a husband and wife duo, Rich and Vicky, back in 2014, almost 10 years ago now. And their mission is to provide customers hotel quality, luxury bedding, delivered directly to your door at a fair price. And these things are great. Wirecutter and Good Housekeeping have said that these are the best sheets. Plus, they have over 100,000 five-star reviews. And I can tell you my personal review. You know, my sleep plan, as I've talked about on the show before, my sleep has struggled, but I got a great bed now. I got great sheets from Brooklinen, and they are a huge upgrade from those old sort of scratchy cheap sheets that we had from one of the big box stores. My wife and I love them, and I won major points with the wife for bringing home Brooklinen sheets. 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So Paul, do you want to read this one? Sure. We're going to now be talking about Sharon, who is a 33 year old female. She has a history of rosacea, obesity with a BMI of 34 and low back pain. This should sound hauntingly familiar. She recently saw dermatology for hair loss. Her iron indices and thyroid testing were normal, but an ANA was positive at 1 to 80 with a speckled pattern. She's had Raynaud's phenomenon since she was a teenager. No cardiopulmonary complaints. She does not have dry eyes or dry mouth because we took a great history. On exam, she does not have synovitis in as much as we can tell. She does not have sclerodactyly. There is no objective muscle weakness. She does have mild erythema of the chin, the cheeks, and the nose, which include the nasolabial folds. So Sharon is coming to us with this now. The abnormal lab is really the thing that we're going to focus on, at least to start, of this abnormal ANA. And I think everyone at this table is probably even guilty. Well, we won't include you, Matt, but Matt Watto. I think we've probably at least checked one ANA that's come back sort of vaguely positive. We're like, oh no, now what? So I guess for you, what, what, what are we to do with this information? Um, and how would you explain it to the patient when she's coming to us? Like I've got subnormal lab. Does this mean I have lupus? Like where, what do we do with this? No. And that's really good. And you know, one last thought about the case we just talked about too, as you see your friendly neighborhood rheumatologist kind of doing some more of these tests, you'll eventually get that pickup into your practice. You know, that'll imprint on you about where to go. So for this case, I think, you know, as a rheumatologist, and I think you would hopefully feel comfortable doing this as an internist, but I get that. I mean, it can be challenging as an internist. Medicine is so broad and deep in many areas. You're really kind of done with her. I don't think there's any other testing that would need to be done. You've got a 1 to 80 speckle pattern. That's probably just reflective that she's a lady and a human on planet Earth. And you're going to have a positive ANA at 1 to 80 and probably about 20%, 15% of ladies, you know, that high. It's even higher for a 1 to 40, less for a 1 to 60. And the pattern kind of is insightful but not very specific at this point. And you really have a history and a physical that seem to go with some other alternative diagnosis. So you really at this point could pump the brakes and say, look, yeah, I know you've got that, but I'm not really convinced that's meaningful for where your disease is at this process. If anything new develops, then maybe it's worth repeating that down the road as clinically guided. I'm not saying to follow sequential ANAs, because sometimes the primary care docs will do that, or, you know, our allied health professionals, and you'll get this up and down in the ANA, which is not really helpful either just again that iterative process of okay we did this at time point a and this is what we were thinking at the time but now we're b three six twelve months down the road and there's new clinical symptoms then that's time to go back and maybe re-update what you're you know kind of doing test wise but i think here you could potentially stop and i i think the questions will go on we'll talk about the differences in the testing because that's certainly one place that the ANA testing is really, unfortunately, not very easy because of several different things and automation and a few other things we'll talk about. Because when you look at the workup for hair loss, which we talked about this on the show before, if it's non-scarring hair loss, to me, the ANA doesn't really have a role unless there's a lot of other features where you think lupus might be part of it. And I've seen some patients get, several patients get an ANA scent and it comes back like this. That was my impetus to put this case here. And then the rosacea thing too, you talked about a little bit early on that lupus commonly spares the nasolabial folds, but rosacea can do that as well. So how do you differentiate between those two? I read that maybe if the person has a lot of inflammatory symptoms of the eyes as well, that's more of a rosacea thing than a lupus thing, but I'm not sure what else you find helpful with the malar rash question. Time. Time? Yeah, just that iterative process again of watching your patient, how you're doing, and getting in a couple months maybe trying on trying on yeah on some acne rosacea therapy if you feel comfortable with that maybe getting sense on it you know whatever that whatever i think floats your comfort level and the busyness of your practice um you know it's easy to say well you should do everything and that's not the case it's just what you feel comfortable with and what you feel you know so i think here i'd give it more the tincture of time rather than trying to just over-diagnose something that may not be there. And I've now seen, I think, two patients who developed, they were in the hospital with like acute lupus and I saw the malar rash come out like over hours, certainly over days. And to me, that was like, you know, that was just very striking. I'm not sure if that's classic for it or if they can have this chronic, you know, malar rash that just doesn't go away or it's there for weeks weeks or for your sub acute for i'm sorry for your systemic lupus erythematosus so your sle yeah that one should that can be very acute that's a very quick on and off rash some of my less so my sub acute cutaneous lupus and then certainly more for my chronic cutaneous lupus you can get this kind of chronic malar rash that just so then it would be medically yeah so that you have a chronic malar rash? Yeah, that might really, that certainly seems to suggest that you're falling more in the chronic cutaneous lupus, which interestingly enough, only about 10% of patients actually have systemic lupus with it. So malar rash, 90% of them likely have lupus. Like at that point, you're there. Again, like with what you described. If you're more the chronic, that's, you know, that's still lupus, like skin lupus, and it's confusing, but it's really less likely to be global lupus or systemic lupus erythematosus. Okay. Okay, cool. Paul, you looked like you had a question in there. I might have, I might have talked over. No, no, you're great. No, more I thought I was, I was going to say, and we might be jumping ahead a little bit here. Most of the ANAs, I want to usually, you know, I'm very good at blaming myself and feeling guilty about things, but most of the sort of the randomly positive ANAs I've seen have been part of order sets. So if someone has an acute kidney injury or if someone has an acute liver injury or something along those lines, like it's one of the battery of tests that you just sort of click a bunch of buttons and then it kind of comes back vaguely positive and you're like, oh, no, now what? I guess so where to go from here, I guess, is do you have a differential for a patient who just has a positive ANA and nothing else, or is it just a matter of one of those things? I guess, how do you think about that broadly? Yeah, so two things real quick. One, there's always been a part of me that leans, and maybe, I don't know if it's because now I'm a specialist. I think if you're dealing with visceral organ involvement, and I'm going to speak for myself, and this is not per se global guidance from key opinion leaders, and I don't consider myself a key opinion leader. So if somebody comes in with proteinuria, right, checking an A&A there is probably not unreasonable because you want to make sure you can, I've had two or three cases throughout the years where they are pretty much just lupus nephritis and there's nothing else going on. So severe pleurisy, interstitial lung disease.
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If you're starting to destroy organs, probably not bad as a specialist to maybe consider checking it. I think, though, the pitfall, as you very astutely bring up, Paul, is that you might get this ANA of 1 to 80 speckle pattern, then you're like, well, what does that mean? And again, rheumatology can kind of help you there, but that's neither here nor there. I think the bigger takeaway, probably, for our listening audience is the ANA testing has kind of evolved over the years as technology has evolved. And there's really two different kind of flavors. And it's important for you to know which one you're dealing with to give you further insight. The first is the indirect immunofluorescence. And there you've got a cell that's lining a slide. And it's usually what's called a human epithelial cell. You wash the patient's blood over it. You tag whatever antibodies hang behind after you've washed it. And then there's a fluorescein molecule that lights up. And essentially now there's a technician looking at that slide saying that's a speckled pattern and based on the dilutions you're at 1 to 80. So this case seems to obviously suggest that they did an indirect immunofluorescence or IIF. In the mid to late 2000s and more so that you might, is you'll get to these what are called solid phase assays, and those are a similar concept in the sense that you have a bead or you've got a plate or a well, and there's some sort of antibody, or I'm sorry, there's some sort of antigen, so it's an autoantigen that you would have at the bottom of that, either recombinant, purified, you name it, however they put it in there. It's attached to the well. Same thing, put the blood in there, label it with another immunoglobulin. It used to be enzymatic. Now it's a lot more color-based and lasers and a bunch of stuff to capture that data much quicker than just looking at color changes. But the concept is that there's some sort of antibody, again, sticking to that. Those are quicker to do, but they don't always, they enhance the specificity, but they really forfeit a little bit of the sensitivity. Indirect immunofluorescence gives you more sensitivity, but not the specificity. And trying to understand between which of those your lab is getting will probably help you down the road. Again, I think the easy way is if you're getting a titer and a pattern, most likely going to be indirect immunofluorescence. And at that point, you're kind of like, I know it's going to pick up stuff, but it doesn't really help me rule in disease. And so that's why I think here you can kind of pump the brakes and say, okay, it was one to 80, one to 640 speckle pattern. Okay. Different story. Maybe at that point now you need to start getting some of the extractable nuclear antigen, like a DNA and a Smith and all the other ones that kind of make up the alphabet soup of rheumatology. Yeah. Sometimes there's the reflex. You can order an A&A with reflex to the extractable nuclear antigens. Is there an absolute titer value that raises your eyebrows? I know this is probably not a fair question to ask, but like 1 to 80, 1 to 40, you can be like, especially if there's nothing else going on here, but is there just a number in and of itself where you're like, okay, this is probably significant? It's more shades of gray. I think as you hit 1 to 320, you're like, well, okay, something's going on there. And then 1 to 640 or higher. But I've seen that also with patients who have Hashimoto's. And so you do a big old workup, you find out the DNA is negative, Smith's negative, everything else is negative as part of that workup is we'll get somebody, 1 to 640 ANA speckled pattern, some other pattern. And you do the rest of the workup with the extractable nuclear antigens and you find out, oh, that's negative. And it turns out they have actually Hashimoto's. So I think the higher the number, certainly the more serial dilutions that you need, obviously the AKA the higher the titer, a little bit more important that is suggestive of, but it may not always go with a rheumatologic autoimmune illness. It could be again, thyroid or hepatitis or something different in that. Something's not necessarily all of it. Gotcha. Keep your differentials broad. Sure. Yeah. And you mentioned earlier that there's, there's the ones, the diseases that commonly have a positive ANA and you said there's about five of them. So I just wanted to recap and I'm trying to find him. I know I had it out here. I think the gray hairs receded. So, so scleroderma, Sjogren's, my, oh my, my, my professor, my hair, right. Mixed connective tissue, lupus, idiopathic inflammatory myositis. Holy cow, right? Good. Okay, yeah. And lupus can be drug-induced or the systemic type. Yeah, more systemic. But yeah, drug-induced lupus can certainly be a cause of ANA. I've never made the diagnosis of mixed connective tissue disease. Usually that seems like that's a rheumatologist. Like you send them where they've got some other, that's like a little bit of what? It is. Is it usually scleroderma, lupus, like Sjogren's? Yeah, usually high titer ANA with a strong positive anti-RMP or U1 RMP. Okay. And then there you've got a little like, yeah, it's the smorgasbord of some sclerodactyly and maybe some myositis and maybe a little interstitial lung disease. Okay. Well, that sounds like that's mixing in with connective tissue. And your slides had, I thought this was helpful. So a positive ANA, but no rheumatologic disease would be maybe autoimmune hepatitis, autoimmune thyroid disease, PBC, idiopathic pulmonary hypertension, and multiple sclerosis. So those are some things you could think about that would have that. I think I've actually seen recently since I've seen a patient with Hashimoto's that was really like not yet treated and new and they had a high positive ANA and I wonder if that's what it was from. I think they were still seeing rheumatology to sort it out, but that seems like that could have been it. So, okay, so this is helpful. So the positive ANA 1 to 80 is like, but it depends on what else is going on clinically, like most of what we've talked about so far. One of the few patterns, I meant to bring this up earlier, one of the few patterns that really may be a little bit more telltale is if you're getting an anti-centromere pattern. So let's say you get a 1 to 640 for the titer and an anti-centromere pattern, and especially if you have some evidence of, like if you have sclerodactyly, you're kind of there, but let's say they've got history of renotes with maybe some digital infarcts or something else strange. And you're like, yeah, there's something that's, that's strange things are afoot, you know, at that point. But, and again, any questions, Hey, room, how can we help you? What's going on here? And that's the limited form of scleroderma that is associated with that. Okay. So we have, we we've given our differential diagnosis for the ANA, both the non-rheumatologic causes and the rheumatologic causes. We talked a little bit about how there's the immunofluorescent version. That's where you get the titer and the pattern. And then there's the newer ones, which could be molecular or enzyme linked. Yeah, they've got a whole bunch of those. There's many different flavors of that. Okay. So, uh, we talked about, I think, I think we talked a little bit about like what to do now when this person, when this person comes to you that had an ANA that you just don't, you're not really convinced they have any rheumatologic disease going on. You said you can sort of let time be the arbiter to steal a phrase from our friend, Elliot Tapper.
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Paul, how do you handle this? Or do you have any other questions about this area before we move on a little bit? No, I mean, I would probably handle it. Surprisingly, actually, like the case where I would tell the patient, I'm not sure I would have checked this in the first place. I don't think there's anything to worry about here. And we can just sort of watch things for right now is probably how I would leave things be. And we tried to, it seems like Raynaud's is pretty common and you can have Raynaud's. I know, you know, my wife gets Raynaud's and she doesn't have lupus. So it's kind of just depends. And how do you talk to somebody? So they have the positive ANA, they have, just with Raynaud's in general, is there anything that heightens your concern about that condition? Well, again, it gets back to a lot of the history and physical exam, right? So let's say you have Raynaud's and sclerodactyly, right, or some evidence of loss of skin turd or distal to the MCP joints, right? That's going to be a tip-off of like, hey, there's probably a little bit more happening here. Digital infarcts, pitting, loss of pulp at the end of the fingertips. What else? Dry eyes, dry mouth might be another kind of tip-off or maybe show grins. It gets back to a lot of the history and physical about what else might be out there. For us and for those in the audience who might be skilled at doing it, nail fold capillaroscopy can be very helpful. So if you take a look at the nail fold capillaries and kind of usually I get a derm light and try to take a look with one of the derm light things. The old school way was taking some, Oh, interesting. that's worth. Abnormal changes there. That can be a little problematic, I think. I'm trying to think of this as an internist. That might be a little problematic if you're not doing that all the time. And to be honest with you, if you're busy in my clinic, I'm not really kind of routinely doing it unless I have a high suspicion. I'll go run back and grab my DermLite. So I think that would be another tip off, but another high positive ANA. So I think if you've got somebody who has Raynaud's symptoms and a strong positive ANA, that may not per se relate to something from a systemic autoimmune standpoint. They might have Hashimoto's or whatever, but that might give you a little bit more of, hey, there could be something more happening here and maybe worth further investigating. Again, I think it gets back to your Raynaud's with a strong positive ANA, say 1 to 1280, but there's really no sclerodactyl. There's nothing else going on. You may be going, okay, well, these might be two different processes. And maybe the Raynaud's is just by itself, but the ANA is due to something different. Right. And I think as clinically driven, you might go, okay, well, you do have the non-scarring alopecia, you've got scarring alopecia, you've got dry eyes, dry mouth, you've got whatever that might steer you more toward extractable nuclear engines or no, your TSH was, you know, 12. Okay. Maybe now it's time for us to get, you know, maybe you're there, you have Hashimoto's or something. So we would, we probably wouldn't be shotgunning the, if we're, if we're ordering an A and a, it should be done, I guess, kind of to summarize what my take-home is. And Paul, I'd love to hear if you have anything to add to this take-home is, you know, try to recognize, do they fit into any of these buckets or do they have features of multiple things? In case I think mixed connective tissue disease but that would make me want to get an ANA is there a diagnosis here that the ANA might help us sort of support like be further evidence that that's what might be going on here don't just order the ANA for the patient that says I have fatigue and and in that case it may not be helpful and there's either a reflex or maybe a second round test could be where you get all these Right. you have a positive a and a and everything you don't have to send those from the start which i think a lot of people sometimes do maybe because they come in a panel or something i do actually sometimes because i try to adjust my thinking a little bit and i'd love to hear your thoughts on this as to actually having a differential diagnosis i think to your point like i think we sometimes fall into the trap of this feels kind of roomy so you just do the a and a and then it comes back sort of weird like so i think like this sounds like lupus so i might check like an a and a and a double-stranded DNA. Like I prefer to have a differential in mind rather than just sort of checking for something, quote something, you know, rheumatologic, because I think that's where I've got myself into trouble with sort of nonspecific tests and then a nonspecific differential. Yeah. Yeah. And I, one last, no, these are great thoughts. And if I may interject, I don't want to dissuade anybody in the audience listening to this from doing what they think is clinically relevant, right? So if that's in your differential and you're pretty strongly convinced that it could be there, then go ahead and get it, right? But it's always, I guess, the key at the end of the day, and which I hope this certainly podcast does, and maybe the lecture here and any other articles that come out in the future, just, you know, in Seattle's, you know, just kind of, it's an iterative process and know why you're getting the test, right? And I know we talked a little bit about the indirect immunofluorescence and the solid phase assays, and I don't think even, it's important to know what tests you're doing, but it all gets back to the test, right? If the test has inherent limitations, that's going to limit what you're going to take away from it. But there's a little bit of time that can be built into some of this. I never want us to miss somebody who we could have caught earlier, but I think the converse, the current switch has flipped the other way, that ANAs are just, and I think it's less internist and I'm not trying to point fingers. It just, there's a lot of ANAs being ordered and people really don't know why they're doing it. And just cool to pump the brakes. What are we, what's the differential here? Lupus is really low. Okay, ANA is probably not needed. Or ANA was one to 40. We're like done. I think at this point we can kind of move along. Yeah. And, uh, just for the audience, uh, as a note, when we were saying idiot, idiopathic inflammatory myopathies or myositis, that's, it used to be called polymyositis and now it's recognizing it's a bunch of different things. It's actually six, it's several different flavors. We did an episode on that. So they can, they can refer back to, uh, last summer, summer 2022, we did an idiopathic inflammatory myopathy, myopathy, myosit you can go back to that. So we'll, I think we should be wrapping up here. So probably this is a great time to ask you for some take-home points. I know you kind of just gave us some great take-home points, but from the overall episode, we talked about the patient with possible rheumatoid arthritis, and then we talked about the patient with a positive ANA. What, maybe one or two take-home points on those topics? Yeah. So one, it's always your pre-test for suspicion, right? And your pre-test suspicion is always updated by your history, your physical, and any other data that you're gathering. And it may be that even with some scant labs that you do, like, hey, this person just seems like maybe they have inflammation. We get an ESR, CRP, and a CBC. And they all show some degree of inflammation, which may or may not be related to BMI or something different.
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And then, of course, that's the global point of how you want to keep updating your pre-test probability for your future test to help you get that diagnosis. But then, of course, knowing the strengths and weaknesses of the test is always key. And I don't think as an intern or even a subspecialist, you have to know all the nitty-gritty details about indirect immunofluorescence versus solid-phase assays. Because to be honest with you, as a rheumatologist, I understand some of that, but at a very cursory high level, it's not delve into the weeds. It's just, what's my lab getting back to me as a result? And what are some of those strengths and those strengths and weaknesses from a global perspective right my solid phase assays are going to bring up a lot more information as compared to maybe the indirect and then you might figure out over time that your practice you might want to have some degree of a lot of labs are now going to this reflex that if the a and a is positive over a certain threshold it will screen for the other extractive yeah to help you yeah so it really i mean i think I think it's the essence of medicine is we treat our patients. We don't treat numbers. We don't treat antibodies. They're there to help us, but we treat our patient. Paul and I lament about this a lot of the time. Just give me a black and white answer. Tell me yes or no. What should I do? But it's never that easy. That's why internal medicine is interesting. And that's, I guess that keeps us all in job. So thank you so much for all your time today. You're presenting so much at this meeting, you still said yes to this interview. So thank you. That was awesome. A great opportunity. Lots, lots of people are going to hear this andiders, bringing you a little knowledge food for your brain. Oh, yummy. Great. Still hungry for more? Join our Patreon and get all of our episodes ad-free, plus twice-monthly bonus episodes at patreon.com slash curbsiders. You can find show notes at thecurbsiders.com, and while you're there, sign up for our mailing list to get our weekly show notes in your inbox, including our Curbsiders Digest, which recaps the latest practice-changing articles, guidelines, and news in internal medicine. And we're committed to high value practice changing knowledge, and we want your feedback. So please subscribe, rate, and review the show on YouTube, Spotify, Apple Podcasts. You can send an email to askcurbsiders at gmail.com. Reminder that this and most episodes are available for CME through vcuhealth at curbsiders.vcuhealth.org. Wanted to give a special thanks to our producer for this episode, Dr. Beth Garbs-Garbatelli, and to our whole Curbsiders team. Our technical production is done by Podpaste. Elizabeth Proto runs our social media. Chris the Chew Man Chew is the moderator for our Discord, and Stuart Brigham composed our theme music. And with all that, until next time, Paul, I've been Dr. Matthew Frank Watto. And Matt, as always, our main Dr. Paul Nelson-Williams. Thank you and goodbye.
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Hello and welcome to the February 1st, 2022 Analysts of Internal Medicine podcast. I'm Dr. Christine Lane, Analyst Editor-in-Chief, with a quick overview of the new material you'll find if you go to analyst.org. I know how busy our listeners are, so let's get right to the new articles. First is a case control study that found that despite a very low absolute risk, there is an increased relative risk of carditis associated with BNT162b2 vaccination, more commonly referred to as the Pfizer-BioNTech COVID vaccine. Case reports of carditis after vaccination have accrued globally, but careful study of whether these case reports represent a true association has been lacking. Researchers from the University of Hong Kong studied 160 patients with carditis, the cases, and 15,033 patients without carditis, the controls, to examine the potential risk of carditis associated with vaccination with two different COVID vaccines, the Pfizer-BioNTech or the Corona vaccines. The researchers matched each case patient with 10 control patients based on age, sex, and date of hospital admission. Among the 160 carditis cases, 20 occurred with Pfizer-BioNTech and 7 with Corona vaccination. Patients who received the Pfizer-BioNTech vaccine were three times more likely to experience carditis than unvaccinated patients. Patients who received Coronavac had a similar risk as unvaccinated patients to experience carditis. The researchers observed that carditis associated with the Pfizer vaccine mostly occurred in men and after the second dose. Cumulated incidence of carditis after vaccination was 0.57 per 100,000 doses of the BNT162b2 vaccine and 0.31 per 100,000 doses of Coronavac, demonstrating very low absolute risk of carditis after either vaccination. Of note, none of the 20 case patients with carditis after vaccination required ICU care or died, while of the 133 patients with carditis not associated with vaccination, 14 required ICU care and 12 died. Next is the latest update of the American College of Physicians' Rapid Living Practice Points on the antibody response to SARS-CoV-2 after initial infection and protection against reinfection. In a systematic review that summarizes evidence on which the ACP based its recommendations, researchers from the Portland VA Research Foundation identified studies on the risk of reinfection and duration of protection following SARS-CoV-2. They found strong evidence that the immunity afforded by recent infection conferred substantial protection against symptomatic reinfection with the alpha variant of COVID-19 for at least seven months. However, the durability of protection in the setting of the Delta and Omicron variants is unknown. Based on the evidence in this updated review and prior versions of the review, ACP advises against using SARS-CoV-2 antibody tests for diagnosis of SARS-CoV-2 infection. ACP also advises against using SARS-CoV-2 antibody tests to predict the degree or duration of natural immunity, particularly in light of different variants. The authors note that these practice points do not evaluate vaccine-acquired immunity or cellular immunity. Vaccination is currently the best clinical recommendation for preventing infection, reinfection, and serious illness from SARS-CoV-2 infection and its variants. Additionally, a previous practice point concerning the use of antibody tests to estimate community prevalence of SARS-CoV-2 infection has been retired due to limited relevance as vaccinations Thank you. how long it lasts, and the role of variants. In light of these evidence gaps, it is important that individuals and communities continue to use all available tools, especially vaccination, to help slow and reduce further spread. The next article concerns two relatively common conditions, chronic kidney disease and gout. Chronic kidney disease is a common comorbidity in patients with gout. The American College of Rheumatology recommends allopurinol to lower serum urate levels to below 0.36 millimoles per liter for patients experiencing gout flares, TOFI, or radiographic joint damage. Lowering serum urate levels is also thought to be beneficial to reduce the progression of chronic kidney disease. The two recent randomized controlled trials suggested that allopurinol was associated with a two-fold increased risk for death in patients with renal disease who did not have gout. Researchers studied electronic health records for 5,277 adults in the United Kingdom with gout and moderate to severe chronic kidney disease to examine the relationship of allopurinol initiation, allopurinol dose escalation, and achieving target serum urate level after allopurinol initiation to all-cause mortality. Mortality over five-year follow-up and propensity score match cohorts was examined for each dose stage strategy. The data showed that neither allopurinol initiation nor achieving target serum urate level with allopurinol nor allopurinol dose escalation were associated with an increased risk for death in patients with gout and concurrent chronic kidney disease. According to the authors, these findings should alleviate concern about utilizing allopurinol in this patient population. There is much concerted effort to promote racial ethnic diversity in the U.S. physician workforce. Despite these efforts, a brief research report published on January 25th found that marked disparities in racial ethnic representation persist in internal medicine residency programs. A racially and ethnically diverse physician workforce could improve access to care, communication, patient satisfaction, and health outcomes, particularly for underserved, marginalized patient groups. Despite this need, members of racially, ethnically minoritized groups are still underrepresented. These include those identifying as American Indian or Alaska Native, Native Hawaiian, other Pacific Islander, Black or African American, and Hispanic, Latino, or of Spanish origin. Researchers from the University of Washington School of Medicine studied data from the American Association of Medical Colleges to elucidate trends in representation for internal medicine residency applicants and matriculants who identified as underrepresented in medicine. Between 2010 and 2018, a total of 214,656 individuals applied to internal medicine residency programs and 87,489 matriculated. Of those, 13.2% of the applicants and 10.6% of the matriculated students identified as a member of a race or ethnicity underrepresented in medicine. In examining disaggregated matriculant data for those underrepresented groups, only the proportion of matriculants who are Hispanic, Latino, or of Spanish origin significantly changed. For every year studied, a greater proportion of white persons were represented among matriculants compared with applicants. According to the study authors, diversifying internal medicine residencies will require dramatic, innovative approaches before, during, and after the application process. The next article provides an interesting historical perspective on the impact of pandemics. The authors report a study of continuous monthly mortality data for more than 100 years in Switzerland, Sweden, and Spain, and found that excess deaths associated with the COVID-19 pandemic reached greater peaks than those of other periods of excess deaths since 1918. Switzerland, Sweden, and Spain are particularly suitable for an overtime perspective of pandemic-related excess mortality because they have reliable continuous data on death counts and were militarily neutral during both world wars. So excess mortality could not be attributable to war-related deaths. Historical data may help to support pandemic planning. In collaboration with the Swiss Federal Statistical Office, researchers from the universities of Zurich, Bern, and Oslo estimated age-specific monthly excess deaths from all causes for Switzerland, Sweden, and Spain for 2020 to 2021 and other pandemic periods since the end of the 19th century in chronologic order. The authors collected data from monthly all-cause-related deaths from each country's statistical office and used yearly data on population size and age structure to account for demographic shifts over time. They found that for all three countries, 2020 marked the highest number of excess deaths since 1918. However, excess deaths in 1918 were estimated to be six to seven times higher than in 2020. The relative excess deaths in 2020 was 12.5% in Switzerland, 8.5% in Sweden, and 17.3% in Spain. The researchers speculate that excess mortality in 2020 might have been even higher if not for worldwide public health interventions. Next is a case report of electrocardiographic artifacts synchronized with cardiac rhythm that suggested a pathological condition in a healthy patient. The authors describe how identifying and repositioning the suspect electrode and repeating the electrocardiogram produced an accurate reading. Pre-exposure prophylaxis, or PrEP, holds great promise for reducing HIV infection, but adherence over the long term can be difficult to achieve. A long-acting injectable PrEP regimen with cabatogravure could improve adherence to PrEP, but the drug is much more expensive than currently available daily oral regimens. Researchers from Harvard Medical School used the cost-effectiveness of preventing AIDS complications model to simulate a population-prescribed PrEP with risk factors for HIV similar to the participants of the major trial of cabotagravir.
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