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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.
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.
How that comes about, I think, can come about in a number of ways. And so when MGB offered substantial raises that made us the highest paid residents in the country, when they offered retirement benefits, when we had unlimited fertility benefits, and a whole host of kind of different improvements in our salary and our benefits, that didn't seem to be enough. 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.
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.
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. And they felt, and I heard this from my own residents, that we know you know what we struggle with, but we also worry that you're not able to effectively communicate that to those that have the power to change these things. 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.
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.
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. During that conversation, Lisa, you know, I raised what I thought were some of the potentials that might happen should unionization come to pass. 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.
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.
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.
With less than three years to go, these two MDGs are seriously off-target for many countries. Among the 75 so-called countdown countries that have 98% of all maternal deaths and deaths among children younger than 5 years of age, only 17 are on track to reach the MDG4 target for child mortality, and only 9 are on track to reach the MDG5 target for maternal mortality. 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.
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.
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.
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.
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. You know, I didn't even put that in the script. 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.
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.
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. So pulling up our extrahepatic biliary obstruction schema, the question that I'm asking myself is what could happen inside the lumen of that bile duct, the wall of the bile duct, or the external environment that the bile duct sits in, what could happen that will cause obstruction and bleeding to jaundice? 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.
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.
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 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.
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. Radiologists do not always report visualized Tarlov cysts, or they may report an imaging study as normal, despite the presence of Tarlov cysts, as in the case of this patient's initial MRI scan. 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.
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.
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.
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. And that affected the relationship that I have with them, of course. 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.
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.
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.
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. Tachycardia, hypotension, hypoxemia, and fever developed, and he was admitted to the coronary care unit. 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.
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.
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.
We have to make sure that our patients understand what's been accomplished here. And there's still a long ways to go. Patients have to think about taking these drugs, that they're willing to come in for whether it's every month or every two weeks for an infusion or eventually a sub-Q injection, whether they are willing to tolerate the side effects which occur in some people, and whether or not the improvement that has been statistically demonstrated is going to actually have a sufficient impact on their lifestyle and their families to justify the investment in time and ultimately the investment in money. 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.
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.
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. It's not just do you have amyloid, it's how much. 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.
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 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.
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. A 35-year-old pregnant woman with new hypertension, a case record of the Massachusetts General Hospital by Ann Klebanski and colleagues. 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.
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.
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.
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. So you have two on dad's chromosome 16, two alpha genes, and you have two on chromosome 16 from your mom. 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.
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.
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. Think of it more as something you want to do for beta thalassemia. 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.
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.
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. It's like working hard on something it normally does not work hard on, which is making red cells. 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?
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.
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 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.
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. Whereas if you said, look, this evidence of difference is evidence of some problem that we can fix. 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.
Hello, and welcome to this JAMA Editor's Audio Summary for our August 23, 2016 issue. This is Dr. Phil Fontanarosa, Executive Editor of JAMA. This issue of JAMA includes three research reports, a scholarly special communication article, and four interesting viewpoints. Let's start with the research reports. The value of integrated team-based delivery models, incorporating physical and mental health care in a primary care setting, is not established. In this retrospective cohort study, Dr. Reese Brennan and colleagues from Intermountain Health Care in Salt Lake City, Utah, evaluated the association between receipt of primary care in practices that integrated team-based care with measures of health care quality, utilization, and cost. Based on their analysis of more than 113,000 patients enrolled in 102 primary care practices in an integrated health care system, including 27 practices with team-based care and 75 practices with traditional practice management, the authors found that compared with traditional care practice models, receipt of care in integrated team-based practices was associated with higher rates of some measures of health care quality, such as adherence to a diabetes care bundle and documentation of self-care plans, lower rates of some measures of acute care utilization. Such as emergency department visits and hospital admissions, and lower actual payments received by the health care delivery system, indicating lower health care costs. In an insightful editorial, Dr. Thomas Schwenk from the University of Nevada discusses resource utilization and costs of integrated behavioral and primary care health systems. One of the most difficult challenges in acute care medicine, such as in the emergency department, is the lack of a system. The lack of a system is the evaluation of children with fever, especially when evaluating febrile infants, and differentiating those with viral infection from those with serious bacterial infection. Two articles in this issue of JAMA represent a potentially important advance, the potential of genetics, specifically RNA expression profiling, to help in the evaluation of febrile children. In one study in this issue of JAMA, Dr. Mahajan and colleagues assessed the association between RNA and febrile infants. The results of the evaluation of RNA bio-signatures and bacterial infection in 279 randomly selected febrile infants 60 days of age and younger, median age of 37 days, who presented to emergency departments over two years. Of these infants, 89 had bacterial infections, including 32 with bacteremia and 58 with urinary tract infection. Sixty-six genes were identified that best discriminated the infants with. Among infants in the validation test set, the sensitivity was 87% and the specificity was 89% for identifying bacterial infection. In a subset of infants with bacteremia, the sensitivity and specificity in the validation test set were 94% and 95%, respectively. In another study in this issue, Dr. Herberg and colleagues determined whether RNA expression measured by microarray. In the validation set, the sensitivity was 100% and the specificity was 96%. In another study in this issue, Dr. Herberg and colleagues determined whether RNA expression measured by microarray. In another study in this issue, Dr. Herberg and colleagues determined whether RNA expression In a thoughtful editorial, Dr. Howard Bauchner, editor-in-chief of JAMA, reviews some of the important developments over the past four to five decades involving the evaluation of infants and children with fever and discusses the promise and potential of the techniques evaluated in these preliminary genetic studies for improving the care and outcomes for febrile children. A comprehensive special communication article in this issue of JAMA addresses the important topic of the high cost of prescription drugs in the United States. These rising costs are a major concern and a major factor in health care expenditures for patients, health care organizations, and insurers. In a scholarly review of the literature, Drs. Aaron Kesselheim, Jerry Avorn, and Amit Sarpatwari examined determinants of U.S. drug prices, justification for the pricing decisions, and consequences for patients' investments. The evidence reviewed suggests that some of the key factors contributing to the high prices of prescription drugs include market exclusivity, which is awarded at the time of the U.S. Food and Drug Administration approval of the product, combined with drug coverage requirements imposed on government payers. The authors found no evidence of an association between research and development costs and drug prices.
No population has been harmed more by the COVID-19 pandemic than patients residing in nursing homes and long-term care facilities. The mortality from COVID-19 infection has been extremely high in these places. Once COVID-19 vaccines became available, it was up to a small team at the CDC to determine how to get the vaccine from the factories where it was made and injected into patients and staff at more than 13,000 facilities across the United States. In the end, they were able to deliver more than 5.2 million doses of vaccine to some of the most vulnerable people in the United States by combining the coordination of local health departments, delivery services such as FedEx and UPS, pharmacies such as Walgreens and CVS, and the companies that made the vaccine. Given the extreme requirements for cold storage for these vaccines, moving them was no easy feat. Neither was it easy to find an army of pharmacists to figure out how to process the vaccines once they got to their destination. In today's JAMA Clinical Reviews podcast, we tell the story of how the CDC pulled all this off. From the JAMA Network, this is JAMA Clinical Reviews, interviews and ideas about innovations in medicine, science, and clinical practice. Here's your host, Ed Livingston. Let's start by having you tell us your name and title. Sure. My name is Ruth Link-Gellis, and I'm an epidemiologist at the Centers for Disease Control. And what unit are you working in within the CDC? Right now, I am on the Vaccine Task Force, and I'm leading the rollout planning for long-term care for COVID-19 vaccination. Can you tell me a little bit about that task force and what their work is and how they're going about it? Sure. So the task force was set up by the CDC. And I'm a member of the CDC's vaccine task force. And I'm a member of the CDC's vaccine task force. So the task force was set up in the spring when it became clear that vaccines were in sight for COVID-19. And the task force's basic responsibilities are to sort of design the implementation, distribution, administration systems for COVID-19 vaccines. So everything from working with the manufacturers to understand cold chain and make sure that state and local jurisdictions have the capability to distribute vaccines, all the way through reporting administration data for the vaccines back to the CDC. And then we also have the ability to report the vaccine back to the CDC and then reporting it publicly on our website. So this is an enormously complicated endeavor. You have to coordinate the people who make it, the people who distribute it, the people who are going to give it across a very large country. So could you give us a little bit of insight as to how that process worked? Yeah, it is, I think, one of the more complicated endeavors we've ever undertaken as a country. The two vaccines that were first off the line, Moderna and Pfizer, that folks are probably pretty familiar with at this point, are the two vaccines that were first off the line, are from a distribution and logistics standpoint, some of the hardest vaccines to work with. They require negative 20 and negative 80 cold chain storage for one. And for two, I think just by virtue of being new and designed so relatively quickly, we have dealt with issues of vaccine hesitancy throughout the country. So our task force is divided into sort of units, and each unit focuses on a specific piece of this problem. There's an implementation of the vaccine, a presentation unit that works very closely with state and local health departments. So thinking through everything from how to target disproportionately affected populations to how to actually run a mass vaccination clinic and sort of giving technical advice to state and local jurisdictional health departments for that. And then there's another unit that deals just with the distribution and administration data. So thinking through sort of the logistics around cold chain, these thermal shippers that have been used for the Pfizer vaccine, to ensure negative 80 cold chain is managed, reporting data back. So there's just a massive amount of data coming back into CDC.
So Pfizer and Moderna make a bunch of vaccines. What's the first step? Does somebody from the CDC call up their CEO and say, we've got to push this stuff out across the country. What do you recommend? We know that ultimately a couple of pharmacy chains were selected to facilitate this process. Did somebody call up the CEO of CVS or Walgreens and say, hey, look, we're trying to figure out how to do this. How did it actually work? Talking about sort of the general population distribution of vaccines, we've been able to do a lot of the work that we've been doing with the vaccine first. It's been really an iterative approach with the pharmaceutical companies and then also distributors like McKesson that are doing a lot of the actual distribution. And then also with UPS and FedEx who are doing the real delivery of the vaccine. And so it's been, I think, conversation after conversation or Zoom call after Zoom call to make sure that sort of every piece of the puzzle is nailed down so that we're not wasting any vaccine. For long-term care specifically, I think we identified the vaccine as a vaccine. And so we had a lot of discussions with the state health departments that we needed additional strategies and plans to ensure that staff and residents in long-term care had access to vaccine. These are obviously some of the most hardest hit individuals during the pandemic. And it's an incredibly complicated space to vaccinate folks who are bedbound or homebound, medically fragile residents. And then the staff have historically lower rates of vaccination versus other healthcare personnel. So back in June, we started, thinking through the best methods for getting vaccine into these facilities. Pretty clearly onsite vaccination support was needed. So we started working with CVS and Walgreens who already provide onsite vaccination services in many long-term care facilities throughout the country through collaborations with long-term care pharmacies, including Omnicare and PharmErica. So the program was really designed to leverage this sort of depth of knowledge and expertise that the pharmacies bring. And so we started working with CVS and Walgreens to provide on-site vaccine support. And so we started working with CVS and Walgreens to provide on-site vaccine support. And so we started working with CVS and Walgreens to provide on-site as well as to access their network of actual pharmacists that could do the onsite vaccination. So we ended up with about 70,000 facilities enrolled in the program. So you can imagine the number of pharmacists needed to actually implement onsite vaccination at that many separate facilities. So that was done, again, kind of an iterative approach, working with both pharmacies throughout the summer and into the fall to understand sort of how their logistics and infrastructure are going to be used to get the vaccine. And so we started working with implementation works and then working with state health departments to understand sort of the scope of their needs. And then in October, we had facilities themselves actually sign up to participate in the program. It was really built to allow some flexibility for implementation. So states signed off on all the facilities that would receive vaccine. They selected which vaccine, so Moderna or Pfizer, and then they determined the start date of the program. And they could launch it either just for skilled nursing facilities first or skilled nursing facilities and assisted living and some other categories of facilities that were eligible. This planning went through the summer and into the fall, basically right up until vaccine became available in mid-December when we launched the program. So there was sort of a jumpstart in that there had been programs in place for vaccinating these populations in the past so that you could build upon that. Is that correct? Yeah. So, you know, I think it's a good question. I think it's a good question. I think it's a good question. Many of these facilities have sort of on-site flu vaccination for their residents. So it's not a completely unfamiliar concept to do these on-site vaccinations. I think the difference here is, you know, flu vaccine is kind of administered throughout the fall. Staff can get it off-site pretty easily. Residents might get a dose in the hospital before coming to the long-term care facility. So it's a little bit less volume all at once.
And so we were able to get the most vulnerable people in the pandemic to really get them vaccinated all at once as quickly as possible. And I think that was the big challenge that we designed the program to overcome. So we're talking about long-term care facilities. We're including so-called nursing homes. And nursing homes are where most of the deaths have been. Some of the most dramatic events within the pandemic have been large numbers of deaths in nursing homes. Could you go over the terminology for me? When you say long-term care facilities, what kinds of facilities are we talking about? So I think, you know, long-term care facility, generally the way that we use it is kind of an umbrella term that includes skilled nursing facilities or nursing homes, which are actually registered and licensed by CMS, the Centers for Medicare and Medicaid Services, at the federal level. And that's about 15,000 nursing homes nationwide. And then the rest of the facilities are sort of these other groups of facilities that are licensed by the CDC. And so I think that's a really good way to at the state level. And those licenses and the definitions and vocabulary that states use to define them vary quite a bit state to state. But broadly, it includes assisted living facilities, which are generally facilities where folks don't need quite the level of nursing care that they would get in a nursing home, but they do need help with medication management, activities of daily living, eating, bathing, things like that. Then there's also residential care homes, which are smaller homes often aimed at nursing homes. And so we're talking about a lot of those facilities. And then there's also the H.U.D. 202 facilities. And these are H.U.D. subsidized facilities for individuals 62 plus, medically fragile individuals 62 plus, and then there's also the H.U.D. 202 plus. So these are folks who, if they could afford it, would be in a higher level assisted living facility and for whom there were real concerns around equity. And so bringing on-site services made a lot of sense. In the report that's in the February 25th, 2021 issue of JAMA, you described the first wave of vaccinations that your group achieved. So could you tell us what was the target population for that vaccination effort and how did that work? How did it roll out? Yeah, so those were the nursing homes or the skilled nursing facilities that I mentioned. So there's about 15,000 of those nationwide. We had about 13,500 that registered for the program. And so these are, you know, sort of the highest level of care. These folks are often on ventilators, IV medications, all kinds of things. They're staffed around the clock. I think to a lot of folks, they would actually look like a hospital, but they're long-term care facilities. So folks spend quite a lot of time in these facilities. And so we're looking at a lot of those facilities. Since they were the hardest hit, they were the first targets of the program. So many states chose to start with just the skilled nursing facilities and wait until later in January to start in the assisted living and other facilities. So we targeted those 13,500 first in many states. And our target was really to get through first clinics in those states within the first four to five weeks after starting the program. So in states that chose Pfizer, we had about 15,000 firsts. And so we had about 15,000 firsts in those states. In states that chose Pfizer, we started December 21st. In states that chose Moderna, we started December 28th. Unfortunately, right in the middle of the holidays, which I think kind of affected the first couple of weeks of rollout and unfortunately meant that a lot of both staff and residents were not in the facilities at the time. So I think, you know, we saw a little bit lower uptake right at the beginning. But uptake really took off the first week in January. And by the end of January, we were really through with the vast majority of first clinics in these facilities.
So we'll be pretty much done with the program. And what we saw, I think, was kind of as expected. Hesitancy was a real concern. We saw about 80% uptake in residents in these facilities, but unfortunately under 40% uptake in staff in the facilities. So definitely a lot of work to be done on the hesitancy side of things to really bring up those coverage rates. How many doses of vaccine have you administered? At this point in the entire program, I think we're at about 5.2 million doses, of which about 3.6 million are first doses, and the rest are second doses. Pretty much all we see in the press are complaints about the vaccine rollout being chaotic. People who believe they should get vaccinated can't get access to it. It's just one series of bad news stories after another. But we haven't heard much about these nursing homes, these skilled nursing facilities. They've been covered nationally. You've got, you hit them all. You've had this huge success in getting the most vulnerable population there is vaccinated, and yet there's not a lot of talk about that. How do you react to that? Yeah, I mean, I think everyone is understandably exhausted and frustrated after a year plus of living under a pandemic. You know, I think everyone sees vaccines as a light at the end of the tunnel. And so there's this real urgency that certainly we feel at CDC, and I know state and local health departments are feeling it too, to really move vaccine out as quick as possible. And I think, you know, a lot of people have pictures of like Dodger Stadium and the mass vaccination events happening there. And that's really not what long-term care vaccination is. It's really medically very fragile individuals. And so, you know, it's not, you know, it's not, you know, it's not even a centralized location in a facility. It's going room to room to room. So sort of methodically going through the facility and vaccinating everyone. And so it does just take more time, I think, than some of the sort of mass vaccination events that we see states holding. So I think, you know, there's understandably some frustration that it takes longer. And I think there was hope at the beginning that it would, by a lot of health departments and governors, that it would happen, you know, within a matter of a week or two. But, you know, I think getting the vast majority of these facilities done within four to five weeks is really quite an accomplishment that, you know, I think in the end we're pretty proud of. I think these five plus million doses that are out there now make up about somewhere between 10 and 15 percent of all immunizations given nationally. And the pharmacies are continuing to administer about 100,000 doses a day through this program. So we are still making a lot of progress and really actually seeing an uptick even in new first doses being given at second and third clinics. So even making some progress, I think, on the hesitancy side of things. Well, one of the reasons we wanted to publish this in JAMA and do this interview is that, as you pointed out earlier, this is the most important population of all. These are the people who die. And throughout the whole pandemic, it's been very clear that the mortality is exceptionally high in older patients and especially those who are very ill, who are in nursing homes and these other long-term care facilities. And the mortality is not that high. And it's not that high for everyone else. And yes, the disease has terrible consequences for people, but it's just absolutely devastating in long-term care facilities. What we know about the vaccines is that they prevent clinical disease. We don't know if they prevent infection or transmission, but they prevent clinical disease. So the effect that this vaccine should have in reducing mortality in these facilities should be huge, absolutely huge. This was a really important story from our perspective. This got done. The rest of the population, even though everybody wants to get vaccinated yesterday, it's less important than in the one that you've covered. It just seems like an absolutely remarkable achievement and an important one.
And it was quite an achievement. It's a big logistic problem that you overcame. It's really been a massive team effort, not just at CDC, but state and local health departments coordinating locally with the facilities. And I think it's been a really important step for the public to be able to get vaccinated. And I think it's been a really important step for the public to be able to get vaccinated. And I think it's been a really important step for the public to be able to get vaccinated. And really doing everything they can to ease some of the hesitancy concerns, especially among staff. The pharmacies, it's a big lift. I think each of them have 10 or 12,000 pharmacists each working on this. So I think it's been sort of a massive nationwide team effort. And also, I think, honestly, quite fulfilling for a lot of folks working on the response to actually start seeing vaccine getting out there and getting in people's arms this quickly at these rates after we've kind of lost our lives. And I think it's been a really important step for the public to be able to get vaccinated. And I think it's been a really important step for the public to all been through this last year of misery. Now, you've mentioned that you had 13,500 nursing homes and skilled nursing facilities that were part of the initial wave. And then there are also assisted living facilities, residential care, intermediate care, HUD 202 facilities. Where are you with the rest of it? Yeah, so we have about 55,000 sort of those other facilities that you mentioned. And they are, you know, we have about 55,000 of those other facilities that you mentioned. And they are I think we're today at about 85% complete with the first clinics in those facilities. A lot of states waited until sort of mid or late January to start those. They really wanted to focus in on getting the skilled nursing facilities done first. So the second part of the program has lagged a little bit because of that. But we're making really great progress through it. As I said, about 85% done with first clinics and well underway with second clinics, and even starting third clinics in those facilities in a lot of states. So we're making really great progress I think, as it goes on, we're seeing, as I said, about 100,000 doses a day given through the program. And I think we'll continue to see that for probably the next couple of weeks until we really start wrapping things up in late February and March. Is there a next step after you get all that done for your group? Or is this it? There is, I think, going to always be a next step for COVID-19 vaccination and long term care. So the next thing on our radar is facilities like these, have a lot of turnover. I think the estimates are about 30% turnover every month for residents. So you know, as soon as that third clinic takes place, coverage in these facilities will start to drop as new residents and new staff come into the facilities. So our focus is shifting away from sort of the strike teams getting in and doing as much vaccination as quickly as possible to sort of maintaining coverage in the facilities. So we're, we're working through the federal retail pharmacy program to get more of that coverage. So we're working through the federal retail pharmacy program to get more of that coverage. So we're, we're working through the federal vaccine out to long term care pharmacies. And then a lot of states have their own plans and are working directly with local pharmacies to ensure that these facilities have an ongoing and sustainable supply of vaccine. One of the things that you mentioned was that there was a fairly low staff participation rate in getting vaccinated. That has been observed before, been observed with the flu. Can you speak to that? And do you have any thoughts about what should be done to encourage staff to get more of the vaccine? Yeah, I think there's a lot of work to be done. I think there's a lot of work to be done. I think staff or even make staff be vaccinated against diseases that they could transmit to vulnerable populations.
So it seems like that should be a they're not getting vaccinated. Yeah. So, you know, you mentioned historically staff in long term care have had lower rates of flu vaccination. So we knew, knew going in that this would be would be a problem. And I think, you know, there's a number of systemic barriers to vaccination amongst these staff. They are often lower paid than other healthcare personnel and sometimes work multiple jobs. There is often a lack of paid time off. So for COVID vaccine in particular, we heard a lot of concern around side effects and them needing to take time off. So I think there are, you know, in addition just to the hesitancy, there are some pretty significant systemic barriers to high vaccination coverage in this population. And then I think for COVID in particular, being the first people recommended to be vaccinated, there was definitely an increased amount of hesitancy and some sort of sentiment of wanting to wait and see others get vaccinated and make sure that folks felt safe. We are seeing a pretty nice uptick, about 20 to 30% increase in first doses at second clinics. So those are either new residents or staff or folks who were initially vaccinated. And I think that's a big part of the reason why we're seeing so much hesitancy. So I think that's a big part of the reason why we're seeing so much hesitancy. Which is great. And CDC also has a long-term care facility toolkit with information aimed specifically at staff and then also residents and their families. And we've done a number of other outreach fireside chats to facilities themselves to try to talk through some of the issues around hesitancy. I think, you know, you mentioned thinking through a mandate and there's been a lot of research into that. And I think, you know, it needs to be done sort of delicately. I think sometimes from what I've read that some of the mandates can backfire depending on kind of how they're rolled out and how they're implemented and communicated with staff. So I think there's a lot more work to be done to try to understand sort of the behaviors behind hesitancy and then really try to mitigate some of the systemic barriers to vaccination. So the population that you vaccinated has the highest mortality and as a consequence should have the greatest response. So I think that's a really important thing to think about. And I think that's a really important thing to think about. So I think that's a really important thing to think about. Is your group the one collecting the data on mortality in these populations? And if so, when will we know if there has been an effect to reduce mortality in this group as a result of your vaccination efforts? Yeah, there's a number of groups that are already working on this. So we're, you know, obviously collecting a lot of the uptake information. There's a surveillance system at CDC that looks specifically at COVID cases and deaths in long-term care. And so we're obviously collecting a lot of the uptake information. So we're obviously collecting a lot of the uptake information. There's a surveillance system at CDC that looks specifically at COVID cases and deaths in long-term care. They're already well underway with some studies to try to understand the early impact of vaccine. And then state and local health departments are also working on their own analyses, working very closely with the facilities in their jurisdictions to understand what's going on. So no one is as eager as our team to see the impact from this program and vaccination more widely. So we're hopeful that in the next couple of weeks, we'll start seeing some of that data come out. So you're at the tip of the spear. This has been a pandemic like none we've seen in our lifetimes. There will be more pandemics in the future. I think everybody recognizes that it's inevitable. There's a new vaccine technology that can be implemented very quickly and tailored to almost any pathogen with vaccination development almost immediately. And that technology will involve the complexities of distribution that you've encountered. And so whatever you're doing, you're going to be able to do it. And so whatever you've done here will be the map for future efforts to try to control pandemics as they move through our community.
Yeah, it's a great question. I think, you know, we can't overestimate the complexities of vaccine distribution in a country as large. And diverse as the United States. We look to other countries and certainly we've seen rollout in, for example, Israel and very high coverage very quickly. But of course, other countries have different health care systems than ours. So I think, you know, we work within the health care system that we have. And we need to be able to leverage sort of all public, public health and private organizations to try to get vaccine out there. So I think our program was this really nice blend of a public private partnership. That worked really well. And so I think we can probably leverage some ideas from that. And we're trying to now with the retail pharmacy program to get vaccine out more widely into pharmacies nationwide. So I think that's one of the big takeaways. And then the other big takeaway from all of this is sort of the importance of data. I wasn't around for H1N1, but hearing stories about sort of how it was managed 10 years ago. How a pandemic and vaccine rollout was managed versus how it's being managed now. I think we've made. Tremendous strides in sort of our ability to understand where vaccine is going and just being able to track it and see where we have pockets of vaccine hesitancy or pockets of disadvantaged groups that aren't getting access to vaccine and try to pivot quickly and fill those gaps. And I think so from that perspective, I think it's kind of an exciting time to be in public health. And as I'm sure we're all aware, this is not going to be the last pandemic probably in our lifetimes. But I think it'll be really exciting. It's really exciting to see the next time around. Hopefully we'll have made equivalent leaps and bounds in our ability to run these programs and get vaccine out there smoothly and quickly. The rest of the world will be rolling out vaccine efforts similar to what we've just accomplished here. What advice do you have for them? Yeah, I mean, I guess I would circle back to data being the most important piece here. You know, as much as you can understand your highest risk populations before you start vaccine rollout. I think that makes everything. Go more smoothly. I think, you know, in our program, we had great data for skilled nursing facilities going into the program. But that was just a tiny subset of those that we knew needed vaccine. And there there really wasn't great data on assisted living and others in the program. And that created complexities for us with rollout. So, you know, as much as other countries are able to get that kind of information ahead of time and sort of methodically plan out first group, second groups, third groups to get vaccine. I think that makes everything. Go more smoothly. A small group of highly dedicated professionals at the CDC executed an incredibly complex plan to deliver millions of doses of vaccine to the most vulnerable patients there have been in the COVID-19 pandemic. Those living in nursing homes and long term care facilities. They did this by coordinating the efforts of several major organizations that had the capacity to take on certain parts of the effort. CVS and Walgreens for pharmacy support. Medex and UPS for logistics and package delivery. And local health departments who understood the local needs of their populations and how to get the vaccine to the right places. To me, the complexity of what happened here parallels that of the space program. But instead of having hundreds of thousands of people working on a hard problem, there were only a small group of very capable professionals at the CDC who identified key partners and were able to get them all to work together for a common purpose. What they did was astonishing. They got the vaccine out to more than 13,500 of the 15,000 nursing homes and long term care facilities in the US and got nearly 80% of all patients in these facilities vaccinated and about 40% of the staff. They gave more than 5.2 million doses of vaccine in a little over a month's time. A truly remarkable achievement. A remaining issue that needs to be addressed is why so few staff were vaccinated. This is a known problem.
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. I'm back after being away for a week and I'm here with probably my favorite guest, Zeke Emanuel. Zeke is the Diane S. Levy and Robert M. Levy University Professor, Professor of Healthcare Management, University of Pennsylvania, where he's Vice Provost for Global Initiatives and Chair of the Department of Medical Ethics and Health Policy. Welcome, Zeke. It's great to be here, and thanks for the flattering comment. I won't take it to heart, but I'll tell my mom to listen. Oh, you can take it to heart. So it'll be wide-ranging, Zeke, but let's start, you know, before we came on, I mentioned, have we become immune to the number of deaths? 170,000 deaths, 1,000 a day to the end of the year gives us 300,000, and then the estimate is that about 50% more are COVID related, but not COVID counted. That brings us almost to a half a million deaths. Have we just become immune to it? Yes. I do think the fact that we're not shocked every day that we're losing a thousand people, that somehow we can dismiss it as all the, just the elderly or something, which is totally false, has made us somewhat immune. And we know that something happens over and over again. You sort of block it out. But to put it in context, half a million deaths is a little under a increase in 20 percent of all deaths every year. So we have about 2.7, 2.8 million deaths in the United States. And again, even among those deaths, 75% of them are in people over 65, they're seniors. But 500,000 is a very whopping chunk of that from one illness that began killing Americans in late February. And I do think we've lost sight of how powerful that is. As you said, 1,000 people a day is a plane full of 300 people, three of them dropping out of the air every day. That would shock us if we actually stepped back, or 1,000 people dying from a hurricane. That's a shocking number. I see the number every morning, and I'm just amazed. As I said, I think we've become almost immune to it. I also think early in this epidemic, people had no idea. When I began talking months ago about, we're going to have a quarter of a million deaths by November, people were like, no, you're exaggerating. And it's like, that's easily going to be the number by November 1st, election day. So many different issues have come up. Schools have become a nightmare. We published an important article, schools closed, mortality went down. Parents are divided. It's been difficult for teachers. I fully recognize it. But everyone keeps saying the same thing for young children, first grade, second grade, third grade, fourth grade, not to be in school. Kind of zooming education just may not work very well. What's your sense? Will we ever get back to school this year? Physically get back to school? First of all, Howard, I like to put this in context of, you know, it's not like the United States is the only country confronting the issue of school openings. Lots of other countries have done school openings, you know, whether it's Finland or Belgium or the Netherlands, New Zealand, certainly. So you have a lot of experience about opening schools and it can be done safely. We've had one major other country that has opened and it's not gone well. How much that was schools, how much that was other things happening in the environment, that's Israel. So we can do it well. But before you can do it, you have to have a low rate of transmission in the community.
We have to get the rate of transmission down, the number of new cases down, and then we can talk about it. There are places in the United States where you can discuss reasonably reopening in-person education. You've come from one of them, Maine. I think there are over a seven-day period, there are like 11 cases of COVID in the state. All right. That means that you're having, call it, two new cases per 100,000 people per day. That's a number that you can open schools with, especially if you have a testing capacity that has, you know, a positivity rate under three, certainly under five. Yes. And I think those are the numbers we need to have to talk about reopening schools. So New York City, it turns out, yeah, it could reopen given the numbers of new cases and testing percentage positivity. The problem in New York is you don't have the infrastructure. You don't have outdoor spaces where you can hold classrooms and space people out. And that, I think, makes it hard in the city. Probably in the surrounding suburbs, it's going to be doable. Lots of Connecticut, Vermont, New Hampshire, as we said, Maine. You can open schools in, if not all, every county or every school, a lot of those areas. On the other hand, clearly Texas, which leads the list again at nearly 200 cases per 100,000 over a seven-day period, it makes no sense to open up in-person education. So I think that's a serious problem. So the first question any parent ought to ask is, what's the daily transmission rate per 100,000 in our community? Is it low enough that we can safely reopen schools? The early experiences with colleges haven't gone very well. Many have retreated from in-person opening. Some delayed the decision, then some opened, and the early experience hasn't gone well. I think some college communities are saying a little nervous about bringing 19, 20, 21-year-olds and how responsibly they'd behave. Any sense about colleges, Zeke? Yeah, well, I've spent a lot of time advising both my own and other colleges. And the problem is what students do, especially if they're off campus, but how much socializing they're doing, how adherent to the safety practices, wearing face masks, staying six feet apart, they are. And it does appear that they're not actually adhering to them, whether it's at fraternities, sororities, or other parties or bars that are near campus. It does seem that the necessary rules to keep the COVID transmission to a minimum just aren't being adhered to. And that's the real problem. They're not being socially responsible. I have talked to my alma mater, Amherst College, about reopening. They're going to reopen with about half the students on campus. They tested the faculty and staff and almost a thousand tests, all negative. But they're worried about a few students who are renting houses off campus to avoid the strictures of living on campus. And that is the worry, that they're going to throw parties there. And I think that's a very sad commentary on how we've not inculcated the right to live on campus. And that is the worry, that they're going to throw parties there. And I think that's a very sad commentary on how we've not inculcated in people's social responsibility, responsibility for others actually adhering to rules, that we expect those kind of behaviors. I don't know. It's a little sad that that's what our image of college life is and therefore what we've communicated to students about their responsibility. What's gone well? What's gone well? Look, I think we have to be wildly impressed by the vaccine action. The number of shots on goal, as you say, you know, number of potential candidate vaccines, vaccines that rapidly entered humans trial that we're now got. I think it's seven in phase three trial. That is pretty impressive. You have to be wowed by the scientific prowess that represents.
They got it up and running in March and quickly were able to generate thousands upon thousands of people randomized and get evidence right away of what's working, what's not working. And I do think in certain pockets of the country where the governors, the mayors have spoken with one voice, a consistent voice, I think people wearing masks, adhering to social distancing, you have seen, and New York is a very good example, you've seen a dramatic decline and a persistent decline. You haven't seen a second bounce. We will see a second bounce. That's inevitable. But I do think that it shows that the public health measures work. You don't need magic pharmaceutical or vaccine yet. You can get the numbers down low with the public health measures, and they can stay low. You need good leadership for that. You need consistent messaging, but the public is willing to listen. And I think that's been a positive sign. And I will say we've learned a lot about the negative effects of opening indoor dining, indoor bars, indoor gyms right away. And I think one of our problems is we got into this open closed, you know, no, it's phased opening and only some things are going to be open. Not every non-essential business is going to be open. And I think in many places we lost sight of that. I heard a statistic from the public health person in Los Angeles saying that the day they opened indoor dining and bars, they have 10 million residents in LA. 500,000 of them went to restaurants, bars, and other locations. And it's like, you want to know why you had a resurgence? You know, it doesn't take a genius to figure it out there. Those should be among the last places open. And yet, for all sorts of reasons, quite understandable, but not good, they were among the first to be reopened. And that was a mistake. The other thing that I actually think we've done well, because the epidemiology was so clear by March or April, you really have to protect the elderly. It's unbelievable. I mean, their mortality rate, once you're 65, 70, 75, or 80, is just enormous. And I do think we've done a really good job in protecting the elderly over the last couple months. And I think you see it in the ratio of number of cases to deaths, which is much lower than it had been. So I do think that is the one thing that we've learned and we've done relatively good at. But the number of cases in the young people has gone up. Yeah, it's skyrocketing. Yeah. Yeah. I do think that is true. We did learn who was vulnerable and I think moved relatively expeditiously in that direction. I want to go back to vaccines. We've published a major study from China, phase three. There's been others in the other major journals, the more experimental vaccines. They're all early optimism by everyone. You and Paul Offit, who I've also interviewed, had a piece in the New York Times a few weeks ago about the so-called October surprise. I've interviewed Steve Hahn, who I was incredibly impressed with, about the mechanism for vaccine approval, whether or not EUA, emergency use authorization, will be used, how transparent they will be with the data. Will they allow the external advisory board to really drive the final decision by the FDA? How are you thinking about it? Well, I have great respect for Steve Hahn. I think he is a man who wants to do the right thing. I think he's under tremendous pressure from everyone, as you might imagine. And I think until you've sat in the decision-making chair of a federal bureaucrat who has to make a critical decision, you can't understand all the political pressures. But, you know, there are literally lives at stake in whether you approve something or not. There's the trust in the vaccine process. There's all the political pressure that's going to be brought to bear on him. I don't envy him one iota.
And I'm feeling better about it. Knowing how much pressure there can be, I can't say that I'm 100% confident that there's going to be no shenanigans here. But with his hand on the tiller and being forewarned about what might happen if the science doesn't drive this, I'm hoping he's able to resist. If there are political pressures, I'm hoping he can resist them and that a decision about a vaccine in October before the election will be based upon evidence and nothing else. You're an ethicist by training. I think sometimes people forget that because you live in a world of health policy. You've raised concerns about ethical distribution of vaccines both in the United States and around the world. It's been a remarkable phenomena of development. I think the U.S.'s commitment is up to $5, $10, or $15 billion in procuring early delivery of vaccines, supporting the development of the ability to produce it before we even know if it's going to be successful. It's very different than any other time in my life around vaccine development, procurement, distribution. First, let's talk about the U.S. What do you think will happen in the U.S. if there is a successful vaccine? Then let's talk about the world. Well, look, I think inevitably, Howard, one of the problems is you're not going to have enough vaccine out of the box. So even with the advanced purchases, even with some of the vaccines being relatively easy to produce, you're only going to have tens and maybe under optimal circumstances, 100 million doses, call it before the end of the year. 100 million doses is really good, but it still represents a third of the population of the United States. It's not enough for herd immunity, even under the more recent revised calculations, which I have to say I'm somewhat skeptical of, where we only need 45 to 50 percent of the population vaccinated for herd immunity. So you're going to have to prioritize, and I think that's going to be a difficult, ethical decision. One thing I would say is that in that prioritization, we have to keep our eye on the ball. And I think people are misinterpreting the ball here. So the primary goal is, I think, to reduce premature mortality of people. Now, a lot of people assume, oh, well, that means healthcare workers get it first, and then the people who are at highest risk get it first. That may not be true. That may not be the best way to reduce premature mortality. It may be better to, for example, immunize people who are at high risk of transmitting the virus, both because of jobs, living situations, and other circumstances. And that, I think, we have to leave an open mind and look at some detailed modeling about what the best way is to reduce the premature mortality. And that, we should not rush to an assumption about, it's high-risk people that need to get the vaccine first. So I do think that's going to be critically important in thinking about who gets the vaccine initially. And it may or may not be healthcare workers. Certainly at Penn, we've seen the transmission among healthcare workers now that everyone knows how to Don and Doff PPE. It's basically gone to zero, both acquisition from patients and colleagues. So I don't know that frontline healthcare workers ought to be necessarily at the highest priority given they can don it off PPE effectively. Payment going to be an issue in the US, Zeke? Well, the government has said it's going to pay for it. So it's acquiring all the doses and going to distribute them. That's like what we did under H1N1. I might say that just having the vaccine and actually having it produced is not, that's necessary, but not sufficient. You actually have to put it in vials. You have to fill, finish it in a sterile fashion. You actually have to have enough syringes and needles.
You're going to need two doses separated by three to four weeks. And I think there could be a lot of bottlenecks there. And I don't think as far as we can tell, and we did a report for the Center for American Progress on this, that the administration has well worked out each one of the potential steps. So that worries me as well, that we're going to find ourselves, yes, we can produce the vaccines, but guess what? Getting them into vials, shipped out, distributed, and into people's arms. Each one of those steps are prone to a bottleneck. WHO is trying to raise $15 to $20 billion for world purchase of vaccines and then sort through an ethical approach to distribution. Right. Let's put the money aside. Let's say you could give the WHO a billion doses, 500 million doses. Where do we go from there? Well, you know, they seem at the moment to be under extreme pressure to distribute it based upon population, to make sure that every country gets it. And that does fulfill one important ethical principle, which is equal concern for countries. But it fails the principle I mentioned before that you really want to minimize premature deaths on the notion that that is a total deprivation and you can't compensate people for it. And it's very severe. So if you want to minimize the harm of premature death, you don't actually distribute it evenly among countries. You concentrate on countries that at the moment when you have the vaccine have severe hotspots and where the vaccine is going to make the biggest difference in terms of reducing premature death. So I think I see a tension in their current thinking from where what I think the ethical approach is. Will the U, Germany, Japan, the wealthy countries get vaccine first? Almost inevitably, they're going to get vaccine first. I think the real question is, is there going to be enough extra to make sure that it's fairly and equitably distributed, that there's enough for low and middle income countries? Now, the negative thing is that there's a lot of pressure for vaccine nationalism. We saw this, you know, and the United States on this is not unique. France, when Sanofi announced that it was going to send the first doses to the United States, France went berserk. The French population went berserk. You know, wait, this is a French company. We've supported you all these years and now the U.S. is going to get the fruits here.. So we need to recognize this as a very common human instinct, and I think that there are actually good ethical reasons for it. On the other hand, there is this effort by the WHO, Gavi, and CEPI to create this pool of money. They will be able to buy some vaccine. In addition, some major vaccine manufacturers, such as AstraZenecaeneca have pledged to distribute the vaccine fairly and equitably. And so I do think we have a reasonably good chance of having a fair number of doses that will be distributed among low and middle income countries that, you know, left to market forces would not be available. China's played an interesting role. We published a phase two study about a week or 10 days ago. It's more of a traditional vaccine. It appeared to have lower adverse events than the other vaccines. They're moved rapidly into phase three, given their population. I suspect they may easily report out phase three data first. The Chinese always seem to have an interesting world policy. They've invested around the world in different ways. Can you imagine them being the world provider of vaccine? Well, again, part of the issue of traditional vaccines is the production process, a little more challenging than the RNA vaccines. And so that may turn out to be a rate limiting factor. But I think, frankly, they're more likely to use it in a political fashion. And I think we should see that for what it is. As you know, Howard, one of the things I like to do is read and think about history. One of the great American achievements, maybe one of the greatest in the 20th century, and we had a number of them, was landing a man on the moon.
And I think we need to have that expansive view on this vaccine issue because it really has to be a worldview. Remember, we can immunize the United States, but it ain't returning to normal if the rest of the world doesn't have vaccine. Right. I mean, you can see what's happened in New Zealand. Right. They were in some ways sterile. They had more than 100 days of no. Right What do you get? It comes in from outside because the rest of the world isn't that way. If we want to return to normalcy, where normalcy includes air travel, it includes communication with other countries, really open borders, you got to get this vaccine around the world and not just to the United States or not just to a handful of developed countries. And I think that's got to be our approach and that's got to be our direction. It's going to be good for us and good for the world. And sort of having a very narrow minded self-interest, I think, is not going to be good for the United States. Bob Redfield, Tony Fauci, many others have really talked about the tremendous concerns about the fall. I mean, we're still at 40, 50, 60,000 cases nationwide per day. I mean, Bob couldn't have been clearer. And Tony, social distance masks, we have to get under 10,000 cases per day throughout the U.S. I know there's pockets. Flu comes in the fall. We have to have a massive flu vaccination campaign. Any sense, any crystal ball of how it's going to play out in the fall, Zeke? I agree with them. I've been worried about the fall from day one. And I think our early evidence that when you open up indoor bars, indoor restaurants, et cetera, that you get these resurgences has to make you worried about the fall when things get cold. Forget flu for a second. When things get cold, now add on flu, another respiratory virus, and you have a serious problem. And add on the fact that we have a vaccine, but in a typical year, only 45% of adults get vaccinated. And our usual, many of our usual sites of vaccination, the workplace, schools are going to be absent. We're not going to be able to vaccinate people through those mechanisms. It is really worrisome. We could use, right? We have flu vaccine is available today. I know because on Monday I got my shot, right? Two days ago, I got my flu vaccine. We could have used, if we have thought about it, this moment early in the late summer, early fall to try out a new vaccine strategy, our expanded vaccine access. If the administration had planned, okay, in March, we're going to have a vaccine sometimes. We're going to have to actually, because we're going to administer to hundreds of millions of Americans, we're going to have to have a new administration infrastructure. Let's test it out and give it a dry run on flu. We haven't done that, but we should begin doing that because it's going to be necessary. I have long been an advocate of mandatory vaccination. Certainly for under 18, we can mandate flu vaccines, I think, relatively easily. I think even for adults, and presumably a lot of employers will require this. It'll enhance the number who get it. But given the unemployment rate and other things, it still won't be universal. We do need to have everyone get a flu vaccine if they can and expanded vaccination infrastructure. The sort of patchwork we've had a few people at CVS and Walgreens and Walmart, some at the doctor's office, some at that's's just going to make it hard, especially in COVID where we need to give people too. And we know a lot of people will forget or a lot of people will ignore it, not have the time, whatever it is. Drug stores, grocery stores, drive up vaccination. We have drive up testing. I mean, when you think about a different type of delivery system, and I like the idea, try it for flu. If it works, you can then duplicate it later on.
Like the AMA essentially is closed. You can't do it at work. No one's coming to work. And then you have 30 million unemployed. So workplaces aren't going to do it. You can't get to the doc's office without PCR testing. So that won't be an effective model. When you say a new system, what do you envision, Zeke? I'll make you vaccines are. No, I don't want to be vaccinated. Just think about the mayor of a city, right? You bring in the heads of your healthcare systems. You bring in your pharmacies. You carve up the city and you basically say, all right, guys, you're responsible for these blocks, right? We don't really care whether they're your patients or not. You create an electronic platform so everyone can report. And then you get the city covered by the infrastructure you have. And I think that would be the important approach. You know, lots of other countries actually have people go to people's houses to give vaccines. And I do remember my father as a pediatrician in the 60s doing that, going to kids who couldn't come in for whatever reason and give vaccines, go to their house and make a house call and give vaccines. I think we need to think about that model today, especially because it's the second shot that really worries me. Getting people in the first time, sure. But the second, you know, maybe they get a little pain, it's inconvenient. All sorts of things can make it hard to get that second shot. And so we need to marshal all the resources, have them in an organized fashion and assign responsibilities and make sure that they get the people vaccinated who they're responsible for. But I think breaking it up by geography, assigning geographies to whether it's health system or stores or whatever, pharmacies is probably the way I would go at the local level. Nationally, they're not going to have responsibility. They're going to basically have the, we can supply you and we can make sure that the supplies get to you. But the federal government doesn't have the capacity to actually administer this. It's interesting. I always thought that the hardest medical job in America was to be FDA director. I thought for the last couple of months, it was probably Dr. Fauci's position. I think the hardest medical job in America for the last six months has been being a mayor of a big city. I feel for every one of the mayors who were thrust into these enormously complicated decisions with experts disagreeing, not a lot of certainty about what to do. I really feel like the mayors of the major cities, it's been a very, very difficult six months, and they're not going to have a lot of money come the fall, which will be an issue. Right. And Howard, they control some variables, but they don't control a lot of the big variables. So you're responsible without all of the capacity to answer like getting PPE, getting ventilators, hospital surge capacity. So I do think it's been a very challenging time. I want to return to one or two scientific questions. So, you know, the recovery trial really championed steroids. Now there's a number of other steroid trials that will be reported out in the coming days, which is good. Remdesivir had some positive effects, not overwhelming. And I think there'll be some additional remdesivir trials, many other trials ongoing. But the new kid on the block was this morning, yesterday, and the day before, convalescent plasma, 30,000, 35,000 patients treated with it. It went up on a preprint server. And then, according at least to a report this morning, Drs. Collins and Fauci have expressed their concern that the observational data is not very clear. A sense of convalescent plasma, how this is just playing out, Zeke? It shows you can get a lot of people, but not have a well-designed study. I have to agree with Dr. Fauci. I just don't understand the study. You have no placebo control group here. So what are we supposed to make of this?
And so the impact, you don't know how to understand it because how you decide or how it was decided when people get it is very subjective. And one of the subjective factors may be who's likely to do better and who's likely to do worse. And you can't control for that. And so I think the data are very hard to interpret. And it's certainly, I think, impossible to make a definitive judgment on whether to recommend this stuff if it were free, all right, but it isn't free. It's expensive, hospital-based. I have to say one of the things that does concern me, Howard, about a lot of the opening trials is that they're not easy things to administer or cheap, right? We're going to now have monoclonal antibodies. Right. Great. Hard to produce, hard to produce in large quantities like remdesivir, and they're going to be pretty expensive and institutional-based therapies. We need things that are much cheaper. If we get dexamethasone early on and it does have kind of the similar effects as it did on critically ill patients. That's a cheap oral medication. That's a very different scenario. But I think one of the disappointing factors to me is a lot of these early trials are going to report very expensive interventions that have to be administered in hospitals, maybe financially lucrative, but is not the kind of thing that can be scaled effectively or easily, it seems to me. And certainly, it can't be used in the prophylactic or for mild cases. Right. The other issue is that many of them are struggling to enroll patients. And so many of them may end up reporting preliminary results that are underpowered, which will even make it more difficult to really understand the true impact for various reasons. Knowing what recovery did in the UK and the fact that we're underpowered on these trials when we have thousands of patients a day throughout the country, that's disappointing. See, last question. It's more of a political question. I don't think you'll be shy about it. This would have been difficult regardless of who was president. You know, we're a country that has free speech and we champion it and people are allowed their opinions. But we haven't allowed good public health measures and science to win out, or it's been a struggle. Let's put it that way. I mean, for the first time about a month ago, we finally saw a fair amount of the leadership, both Democrat and Republicans, masking, finally saying it needed to change. Bob Redfield on my show couldn't have been clearer. We have to socially distance. We really have to mask for six weeks. We have to get the number of daily cases down or the fall will be a nightmare. Virtually all of the medical leadership has now spoken with a single voice, but we have struggled with the public. Is there a way to change that? I think there is a way to change it. But and, you know, the CDC has known about public health communication well before COVID. They knew what worked. They had proven what worked. They had a whole manual on it, and we violated almost every one of their requirements. You have to be consistent, speak with one voice, and repeat the message over and over, and make sure that all the people who are looked up upon by society, whether they're political leaders, they're sports stars, they're movie celebrities, they're business leaders, they have to speak with the same voice and you have to get them together. The effort to create a common message and to get every leader to speak and reinforce that common message, whether it's by Instagram or tweeting, we didn't do that. Could we do that? Well, we certainly are going to have to do it around vaccination. And I think we're going to have to, I hope that with the change in leadership, we'll be able to get that done with the federal government leading and someone at the White House calling every celebrity, athlete, business leader, everyone they can think of to reinforce that message and reinforce it over and over. I mean, one of the other things we know from communications studies is that one message isn't enough.
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.
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.
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. This young man has a progressive, severe, subacute illness affecting multiple systems. 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.
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.
From the JAMA Network, this is the JAMA Editor's Summary, a review of important research and review articles appearing in the latest JAMA issue. Hello, and welcome to this edition of the JAMA Editor's Summary podcast for the November 8, 2022 issue. I'm Dr. Kirsten Bibbins-Domingo, Editor-in-Chief of JAMA and the JAMA Network. Let's start with the original research reports, of which there are three. Two reports were published online simultaneous with presentations of the results at the European Society for Intensive Care Medicine at the end of October and now appear in print in this week's issue. They are part of JAMA's Caring for the Critically Ill Patient section. The first, from Dr. Bernard and colleagues, on behalf of the exact investigators, examines the effect of lower versus higher oxygen saturation targets on survival to hospital discharge among patients resuscitated after out-of-hospital cardiac arrest. The administration of a high fraction of oxygen following return of spontaneous circulation and out-of-hospital cardiac arrest may increase reperfusion brain injury. This randomized clinical trial was designed to examine whether targeting a lower oxygen saturation in the patient's life-threatening condition may be a good idea. In the early phase of post-resuscitation care for out-of-hospital cardiac arrest, improved survival at hospital discharge. This multicenter, parallel group, randomized clinical trial enrolled unconscious adults with return of spontaneous circulation and a peripheral oxygen saturation of at least 95% while receiving 100% oxygen. The trial was conducted in Australia between December 17th and August 12th, 2019. The trial was conducted in Australia between December 17th and October 12th, 2019. with data collection from ambulance and hospital medical records. The trial enrolled 428 of the planned 1,416 patients and was stopped because of the pandemic. Patients were randomized by paramedics to receive oxygen titration to achieve an oxygen saturation of at least 90 to 94% for the lower target or 98 to 100% for the higher target. The trial was conducted in Australia between December 17th and August 12th, 2019. The trial was conducted in Australia between December 17th and August 12th, 2019. The trial was conducted in Australia between December 17th and August 12th, 2019. The findings do not support use of an oxygen saturation target of 90 to 94% in the out-of-hospital setting after resuscitation from cardiac arrest. The editorial from Drs. Elmer and Guyette places these findings in context of other trials comparing lower versus higher oxygen saturation targets that have been primarily conducted in the ICU setting. The pathophysiological sequelae of the out-of-hospital setting and the out-of-hospital setting may have been very similar in the in the minutes after return of spontaneous circulation. The editorialists highlight that the out-of-hospital environment has unique limitations and complexity that requires rigorous study to extrapolate intervention from the out-of-hospital setting to the out-of-hospital setting. The editorialists highlight that the out-of-hospital setting and complexity that requires rigorous study to extrapolate interventions primarily tested during intensive care, such as has been done in the EXACT trial. The second original research report is from Dr. Fernando and colleagues and examines the association of extracorporeal membrane oxygenation, or ECMO, with new mental health diagnoses in adult survivors of critical illness. ECMO is used as temporary cardiorespiratory support in critically ill patients, but little is known about long-term psychiatric sequelae among survivors after ECMO. These authors use a population-based retrospective cohort study in Canada to examine the association of ECMO survivorship and post-discharge mental health diagnoses among adult survivors of critical illness. Their primary outcome was a composite of new mental health diagnosis following the discharge, and the composite included mood disorders, anxiety disorders, post-traumatic stress disorder, schizophrenia, other psychotic disorders, other mental health disorders, and social problems. The authors found that among adult survivors of critical illness, receipt of ECMO, compared with ICU hospitalizations without ECMO, was significantly associated with a modestly increased risk of negative effects of ECMO. The authors found that among adult survivors of critical illness, receipt of new mental health diagnosis, or social problem diagnosis, after discharge.
Doctors Zieger, Vanden Bogard, and Vanderhoven provide the accompanying editorial. ECMO is associated with better survival rates among select critically ill patients, but half of patients who receive ECMO will die, and severe chronic diseases and severe chronic diseases will be reduced. The ART article includes a which some of the cells Jang Ho-ών purifies with street tissue fraction Tennessee 1. Hamlet's it Should be as weekly . However, the short and long-term physical and psychosocial outcomes of citizens water to stuck than are which makes the results of Fernando and colleagues of utmost relevance. They note the limitations in the current study, but comment that the importance of the question and these findings should encourage researchers to pursue more robust cost-effectiveness evaluations of ECMO for short-term and long-term outcomes in all health domains. This is essential information for treatment decisions, for informing patients and their relatives, for tailoring the post-ICU recovery trajectory to problems of this specific ICU patient group, and for determining what are acceptable outcomes, from whose perspective, and at what cost. In the third original research report, Dr. Fielding-Singh and colleagues examined the association between preoperative hemodialysis timing and postoperative mortality in patients with end-stage kidney disease. For patients with end-stage kidney disease treated with hemodialysis, the optimal timing of hemodialysis prior to elective surgical procedures is unknown. This retrospective study of more than 1 million Medicare beneficiaries examined one-, two-, or three-day intervals between the most recent hemodialysis treatments and the surgical procedure for the primary outcome of 90-day postoperative mortality. Longer intervals between hemodialysis and surgery were significantly associated with higher risk of postoperative mortality, mainly among those who did not receive hemodialysis on the day of surgery. However, the magnitude of the absolute risk difference was small, and the findings are susceptible to residual confounding. In the accompanying editorial, Dr. Blier states that the study of Fielding-Singh and colleagues provides some evidence that surgeries performed the day after hemodialysis or on the day of hemodialysis may be associated with better outcomes. The editorialist notes that performing surgeries on the day after a hemodialysis session causes less disruption in patient care and is likely to cause lesser delay in the evaluation of results. to be beneficial to patients overall. Let's turn to the viewpoints in the November 8th issue. Doctors Huang, Kesselheim, and Vokinger address the recent update to the essential medicines list. They argue that the update has resurfaced a long-standing tension with some medications on this list between high cost of these medications and the essential need for these medications for health systems and patients. They propose restructuring the list to formally remove considerations of cost and cost-effectiveness from the expert committee re-reviews of clinical effectiveness, safety, and public health value. Further, they call for chartering a new framework for pooled global negotiation and procurement of costly medicines eventually included in the list. Doctors Binger, Chen, and Harder authored a viewpoint on hospital ranking and health equity. These authors are from U.S. News & World Report, and the viewpoint summarizes why and how U.S. News & World Report has approached evaluating and publicly reporting hospital performance in various aspects of health equity. They further describe several novel equity measures published under the aegis of its best hospital rankings program. Doctors Mangione, Nicholson, and Davidson are current or former leaders of the U.S. Preventive Services Task Force. In their viewpoint, they write about addressing gaps in research to reduce disparities and advance health equity, and specifically on how the U.S. Preventive Services Task Force has incorporated the taxonomy of the National Academies on Science, Engineering, and Medicine with the goal of closing evidence gaps, clinical prevention. The Clinical Review and Education section of the November 8 issue of JAMA includes a review on the treatments of hypertension by Drs. Carey, Moran, and Welton. Hypertension affects approximately 116 million adults in the U.S. and more than 1 billion adults worldwide and is associated with increased risk of cardiovascular disease events, including coronary heart disease, and heart disease. The U.S. Preventive Services Task Force has also included a review on the treatments of heart failure and stroke, as well as death.
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.
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.
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. What role do you think that sort of individual experience plays in these situations? 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.
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.
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.
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.
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. And it does kind of go back to the, like, it's like making learning objectives when you're creating a talk. 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.
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.
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. And this runs you about $200 or there's a version where you can connect four microphones at a time, which is what we use. 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.
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.
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. And I guess all I'll say about that is like when you're naming your podcast, you just want to pick a website name that's easy to remember and type in. 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.
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.
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. When we're talking to our guests, I usually ask them to record themselves in QuickTime if they're on a Mac or Voice Recorder if they're on Windows, because both those programs are automatically loaded on Windows and Mac. 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.
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.
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.
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.
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 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.
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.
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.
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 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.
Yes. 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.
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.
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. So like I will, I will like consistently text my friends and like even one of my friends, she's just graduated and she's working as a doctor in Malta. And I texted her, I was like, I need to hear your your voice like we need to have a phone call like and I hope she's listening to this because she still hasn't called me back but yeah so like reaching out quite shamelessly because I feel like sometimes people have this idea that you know the phone goes two ways like if they wanted to text me they would don't do that just reach out because at the end of the day like they're your friend like when they see your message it might make their day um they're generally going to be happier to see your message so like don't sort of be in your head like oh like I haven't heard about from this person in such and such length of time maybe they no longer want to speak to me they most likely do um they're probably just busy um and I think with what Charlotte said about um making plans in advance um try to like make those plans but then also try to avoid flaking or changing at last minute because if that happens often um it can send out the message that perhaps you're not as interested in those plans you guys have made together, which is really sad because then the other party might stop being as enthusiastic to make plans. So I would say like really try to commit to the plans that you do have with people. And even if like schedules change, try to like let them know like far, far in advance and then offer like alternative dates. Because when you cancel something with someone, offering them alternative dates can be a way to show that you still genuinely care about the plans that you have made and that you are quite interested in like pursuing and continuing like in the planning aspect of it. And then finally, there is an app called How About. it basically it's like a calendar and like you have all your friends sort of plans for that month linked together so when you're trying to make a plan like you can see who's busy at what time and it just I think it saves a lot of back and forth and like the group chat and um so I'm trying to use it a little bit more um and see how my schedules merge with people's um it's so funny because one of my friends the year below she like knows my timetable like already um so she's like oh you have pharmacology now I'll see you later like she's very like so I think it is helpful to sort of have an idea of what that person's schedule looks like or feels like so you don't feel like you know they don't have time for you or anything of sort of that sort um but yeah that would be like my advice um thank you Julie for that amazing suggestion of that app I think I could do with it in planning future episodes of Sharp Scratch I'm very proud of us all for making it despite our busy schedules on this call this afternoon sadly I think that is all that we've got time for today but thank you so much to Judy and Charlotte for joining us thank you to our expert guest Christina as well it's been lovely to you on. And thank you to all our listeners for listening to this episode of Sharp Scratch. If you like our show, I would love it if you could support us by leaving a review wherever you get your podcasts or by sharing it with the people that you know. Telling your friends, probably your medic friends, about it really helps them to find the show. Please do keep in touch.
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.
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.
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. What we're doing there is we're moving past a two-and-a-half-thousand-year-old absolute basic norm of medicine that I will always care, I will cure where possible, I will never kill. 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.
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.
🎵 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.
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.
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. Maybe like someone sitting next to me right now, self-described curmudgeon anyway. 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.
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.

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