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But it's this idea of as we age, we have a deregulated ability to do nutrient sensing. Basically, our bodies are not able to tell as we age if we have an abundance of food or if we have not enough food. And this goes along with a lot of data in mice and in some primates of caloric restriction. So having less food for a portion of your life increases lifespan in a lot of animal models. So there are a lot of different host factors that are implicated as a possibility in this. Some of them are things you've definitely heard of, like insulin, right? Or IGF-1, insulin growth factor one. There are a lot of others, like mTOR, AMPK. Sirtuins are in AMPK. These are all various fancy names for factors that our body uses to help signal to our brain when there is food that needs to be digested versus when our nutrient stash is very low. So we need to engage in catabolism, like break down our own stores instead of building a bunch of muscle and fat. So there's evidence to suggest that states of anabolic signaling, that is our body saying, hey, we've got a lot of food. We need to build up stores. That process accelerates aging, at least in mice. And so manipulating this signaling so that a mouse's metabolism thinks it's living under limited nutrients by manipulating some of these factors can extend longevity. Interesting. So that's what is meant by caloric restriction is manipulating the factors, not straight up caloric restriction? No, straight up caloric restriction means straight up caloric restriction. Okay. This is trying to get at a way of can we trick our bodies into thinking that we're living calorically restricted, but we don't want to live calorically restricted. What is the mechanism for caloric restriction increasing longevity? And what is caloric restriction mean? Great questions. So caloric restriction in animal models means reducing an animal's nutrient intake to about 30 to 40% of what is typically considered necessary for the amount of calories that a mouse needs. So it's very, very restricted. I want to be extremely clear on here that I am not by any means recommending this for human beings. This could be very dangerous. Okay. But in mice, restricting them to that very small amount of calories, 30 to 40% of what would normally be needed, does increase lifespan. And it also increases the age at which animals are able to reproduce, if that makes sense. It increases how long you are reproductively viable? Well, no, because these animals tend to not be able to reproduce while they're living under caloric restriction. But then they get to an age where normally, like a normal mouse at, say, this many months of life would no longer be able to reproduce. This mouse who's been calorically restricted now can reproduce if you start feeding them. Okay, but if the mouse is only consuming 30 to 40% of what is considered necessary for it to live, how is it living? Well, so that is the idea behind all of these factors. Basically, the thought is that in so doing, in restricting these calories, you're altering the way that the body is metabolizing everything in a way that is promoting catabolism. So that breaking down of our own body stores rather than anabolism, the building up of our muscles, the building up of fat stores, right? So that's the idea behind why caloric restriction works. We know from animal model studies from a long, long time ago that restricting animals' diets makes them live a longer time. These genes and these factors and these hormones that have been identified seem to be the possible mechanistic way that caloric restriction manifests. So if we could directly affect those, mTOR or insulin or what have you, then we could trick our bodies into breaking down stores rather than building fat. And that might make us live longer. That's the theoretical idea behind it. Interesting. Yeah. It kind of it reminds me of going back to the evolutionary hypotheses, the germ soma theory, where it's like like the germ line is always favored, but maybe here's the exception where if the soma line can't support the germ line, then the soma line has to be favored first. Yes, exactly. I think that that is a good way to kind of, yeah, piece those together. Interesting. Okay. There's a few more, but I will say I'm not going to go into quite as much detail because from what I read, the topics that I've already covered are maybe the ones where we're a little bit farther along in that we have data from animal models and from cell models to show that manipulating these various things, be they nutrient sensing or protein stability, can affect aging. The other ones are a bit more theoretical still, at least from what I read. And apologies if someone has some great data that I didn't see on these last few topics. Send it our way if you do. I would love to read it. So another possibility is the idea of mitochondrial dysfunction. So our mitochondria are often called the powerhouse of our cells. They do a lot for our bodies. And the idea is that over time, just like our DNA in our nucleus, these mitochondria can just sort of not function as well anymore. This is thought to be very related to things like oxidative stress over time. That's all I got for you on mitochondrial dysfunction related likely to the process of aging. Okay. There's also just the idea of cellular senescence in general, cells going quiescent over time. A lot of our cells in our body are not dead, but they no longer divide. They're no longer active. So there's a large thought that just this entire process of cells kind of turning off a lot of their activity then relates to aging. And it's likely protective to, right, like reduce the amount of DNA damage that might occur through the process of replicating cells that don't need to be replicated, et cetera. So this might be something that's more related to protection against aging rather than involved in the process of aging, like protective against it? Yeah, yeah. Okay. Then there's the idea of stem cell exhaustion, which I, again, didn't get that much into detail of, but the idea that our stem cells are the ones that aren't able to keep up the way that they need to, to be able to produce more cells correctly. Like the basal layer of our skin cells are stem cells that can become any various type of cell. But as insults occur to these stem cells, then hence the process of aging. And finally, there is also this thought of defective or diminished cell-to-cell communication. And there's a lot that probably goes into this. One that I think is interesting, and I didn't, I will, full disclosure, actually read any papers by him, but I watched a TED Talk of this researcher named Michael Levin, who is a researcher at Tufts University and does really interesting research on cell-cell communication from a bioelectric field perspective. It's very, very interesting. But there's also a lot of other ways that our cells communicate with each other besides potentially a bioelectric field. But I will link to that TED Talk because it's fascinating. And it's likely that this process over time also becomes defective and is involved in the process of aging. That was like a very fast speed through. And I know that I left a lot of detail out. I will cite a couple of papers, one from 2013 that's a few years old now, but another that is a summary of a 2021 symposium of gerontologists that has a lot more detail on these nine different processes and where we kind of stand in terms of in vitro cell data, animal model data, and human data. But the thing is, I think it's very clear just by going over all those various processes that these are all very interconnected. Right. Especially when we talk about humans, it's not one single piece. All of these processes are likely at play, and we are not at a point where we can say that we have an answer or a drug or an intervention at all that can prolong our life in any meaningful way. We don't even have one that could likely prolong our health, at least not yet. So really, for me, what it comes down to is that forever is a very, very long time. So do I think it's possible that humans will ever unlock the many locks between us and immortality? No, I will say no. Yeah, it doesn't seem likely. It doesn't. Do I think that it could be theoretically possible, this concept of immortality? I kind of don't, Erin. Do you? No.
Yeah. I, maybe. Maybe. I similarly doubt it. I mean, and I think that's a thing too, is that immortality is not what people are working on. Exactly. It's how it's being sold. Yes. And one of the things that I think is really interesting in reading from the gerontology perspective is that I do think that a lot of the research into these questions of like, how does aging happen? And can we manipulate those processes? This research can be used to improve the lives of humans. And I do think that it could potentially increase our health span and delay the onset of all these various aging Ooh, that's such a good point. And aging itself is not considered a disease. So you cannot study it from a, like, applying for NIH grants perspective or from a drug development perspective. You cannot study it in the same way that you can study diseases. Oh, that is very interesting. It really is. Because it also means that the funding is not actually being directed towards aging. The funding from the government is being directed towards addressing these diseases that we think maybe could be preventable, right? But if we think that these are interrelated diseases that are all part of the process of aging, then wouldn't it make more sense to address them from a wider perspective by addressing these underlying mechanisms rather than addressing cardiovascular disease or diabetes itself and cancer itself? Let's think about these things that underpin both of those or all of those. And so I think that that's kind of the argument of a lot of the people who do this type of research. And I think it's really valid. And maybe that's the gap that some of these biotech companies are filling by directing their funding to address that. I don't know. Maybe that's an optimistic view, but maybe. That is, that's a really good point. And I mean, I know that like a lot of epidemiological studies will look at all of these things together, but it just, there are so many different avenues of research. Yeah. And it does seem like aging is super multifactorial. A lot of these diseases are super multifactorial, but some of the factors, like they are like siloed diseases. Exactly. That's, yeah. I also think it's important to point out, like you mentioned, Erin, there are a lot of other, in my mind, ethical and moral concerns related to this idea of pursuing an increased lifespan or healthspan in thinking about the state of our planet and climate change and how we've impacted our planet with the lifespans that we currently have. And also in, like you said, where is this development and technology going to go? Who is going to benefit from it? Because the increase in lifespan that we've seen in the last 50 to 100 years hasn't been even across the board. And people who are wealthy live much longer than people who are not wealthy. And so that is likely going to continue to be true, especially if all of the research being done on this is from a capitalistic perspective of companies trying to make money off of it. I don't know. Yeah. I mean, anti-aging is one of the world's biggest industries. Yeah, definitely. It really is. And I'll repeat again, not a single anti-aging product has been shown to actually slow, stop, or reverse aging in any capacity. Yeah. Diet and exercise, Erin. Diet and exercise. Yeah. Listeners, do you think you'd want to live forever? I'm curious. I'm curious. And if so, why? Or why not? Or why not? Yeah. Should we do sources? Yeah. and the Evolution of Aging. There is a book by Shefferson et al., or a bunch of editors, titled The Evolution of Senescence in the Tree of Life, and that's from 2017. And then the book that I already mentioned by Stephen Cave, Immortality, The Quest to Live Forever, and How It Drives Civilization. And those are both really, I just really enjoyed the Stephen Cave book as an interesting one to mention is a paper from 2021 called Longevity Leap, Mind the Healthspan Gap. And then there was, there's a bunch more. music for this episode and all of our episodes. Thank you to the Exactly Right Network, of whom we're proud to be a part. And thank you to you, listeners. I really hoped that you liked this one. Yeah. Yeah, I hope so, too. And a special thank you to our patrons, as always. Thank you so much for supporting us. Yeah. Well, Erin, happy 100. Happy 100. And until next time, wash your hands. You filthy animals. you
Hello and welcome back to Doctor Informed. You're listening to Season 2, Episode 7. This is a podcast brought to you by the BMJ and sponsored by Medical Protection. Doctor Informed is primarily for those doctors working in hospitals, taking you beyond medical knowledge and talking about all those things that you need to know to be a good doctor, but which don't involve medicine. I'm Clara Munro, a general surgical registrar in the northeast of England, and I work as a freelance clinical editor at the BMJ. In our new season of Doctor Informed, we will be discussing topics relevant to hospital doctors, those often not covered formally in teaching, which can, and today I hope will, inspire some debate amongst doctors. Today we will be talking about grit, what it is, how it relates to medicine, and whether we should be considering using grit scoring when recruiting doctors, either to medical school or to specialty. The definition of grit was developed by Angela Duckworth, an American psychologist and researcher. Grit refers to the combination of passion and perseverance for long-term and meaningful goals. It is the ability to persist at something you feel passionate about, even when doing so can seem hard. Both in the UK and right around the world right now, many doctors are choosing to leave the profession. In the wake of the pandemic, we're seeing more and more reports of poor well-being amongst healthcare professionals with burnout high. What can grit tell us about this? Do we all just need more grit? Or are even the grittiest people limited when faced with a pandemic, waiting lists or failing health systems. Can understanding grit help support clinicians better? I'm thrilled today to be joined by our panel and our expert joining us is Simone Betchen, a neurosurgeon working in Brooklyn, New York, who has researched extensively on this subject. Thank you, Clara. I've been here for about 16 years now. And as a female neurosurgeon, I am in the great minority here in the United States, where about 7% of neurosurgeons at this point are female. I had the distinct pleasure many years ago now to seeing Angela Duckworth talk about grit in person and at that point afterwards I was thinking what I had been through through my training as a medical student and then as a resident in neurosurgery and even as an attending as years went on and then what all of us as physicians have to go through to get to where we are and started to think about the question of grit in medicine. My focus was also looking at grit and gender and so I called up Professor Duckworth and I said, you know, what do you think? And she had never been able to find a difference really meaningfully between men and women in even the most difficult fields, but sent me on my way and has given me great advice and had a lot of meaningful conversations with her about grit and medicine since then. So I did publish a paper several years ago now looking at grit in surgeons. The punchline really being that there was no difference in gender between men and women surgeons. This is amongst about 1,100 surveys. The interesting point, and I think we can probably dig into it a little more later, of what we did see was that while there was a correlation with burnout, and I think that's something that's been documented and discussed in the past, interestingly, women had the same grit scores as men, but higher burnout rates. And so I think when you're thinking about medicine and burnout, as you talked about in the introduction, it's interesting to think about, you know, it's not grit alone, but what else could it be? And, you know, we had our own hypotheses of what those things might be that were also protective or predictive of burnout that we can dig into later. Well, I can't wait to talk about this. And I'm really pleased to be joined by the rest of our panel today and we have some familiar faces. We're joined again by Declan. Declan would you like to remind our listeners about yourself? Yes hiya I'm Declan Murphy I'm a current academic ophthalmology trainee up in the north of England. I find this topic absolutely fascinating i think particularly around um you know the concerns with the nhs and the workforce problems as well that we're having um so i'm really really interested and really excited to have a discussion about it and after a bit of a break i am thrilled aisha is back with us on the podcast aisha for those of our listeners who have not been with us from the beginning, shocking, would you like to reintroduce yourself? Yeah, sure. Thanks, Clara. And thanks for having me again. So hi, everyone. My name is Ayesha Ashmore. I am an Aabza and Ghani Raj in the East Midlands and super interested in this topic as well. It's caused lots of contentious arguments in my household. So I'm interested to see where this discussion takes us. Excellent. up by discussing what people are talking about on the wards or what has been in the news recently. I can't take credit for this one, but one of our other panellists drew my attention to the story of Daymar Hamlin, a defensive back who plays for the NFL American football team Buffalo Bills. In a high profile matchup against the Cincinnati Bengals, the young player, born 1998, which makes me feel very old, collapsed on the pitch whilst playing, having had a cardiac arrest. Did anyone else see this story? Has anyone else read about this? Yeah, I saw it. that this might be related to the COVID vaccine. And that's why we're seeing so many, you know, young professionals, athletes collapsing everywhere. So nothing's changed. Yeah, I thought it was really interesting as well. I'm looking at the tweets. So one, the Georgia Congresswoman, Marjorie Taylor Greene tweeted, before the COVID vaccines, we didn't see athletes dropping dead on the playing field like we do now. Time to investigate the COVID vaccines. That tweet has been viewed around, well, over a million times a day for the last three days since it went up, which shocks me that we're still getting this level of misinformation. Declan, you're a football fan. What do you think about this? First of all, I'm not a football fan. You're not? Or an American football fan. I'm pretty sure this was American football. It was, yeah. I am, however, a basketball fan, even though I'm about 5'7". So I have some interest in sports, yes. I think it's really interesting. I think there's a couple of things. I think firstly, if, you know, the classic discrepancy between cardiac arrest and heart attack, you know, that's been going on forever and clearly we're not doing something well enough to inform the public. I'm always of the opinion that, you know, the general public aren't stupid. We're perhaps just not communicating that well enough to them. So I think there's that part of the thing where actually we as a medical profession have to take some responsibility, as well as the journalists also have to, in terms of how they actually are communicating with the public. Because it's a very basic concept and I refuse to believe that the public aren't able to understand that. So I think, yeah, that's one interesting then you have the other side of thing the misinformation um where you know clearly there are groups who are knowingly you know attributing these things to covid for example and then you have the public who again i feel aren't stupid but perhaps haven't been um kind of educated in how to critically appraise information. And again, I think in some ways, that's kind of our responsibility as medical professionals, always just educate as full stop. So it's really interesting. And these things pop up every single time there's something, you know, in the news about a health related thing to any celebrity. I think Rod Gilbert is in the news at the moment with his prostate cancer and there's a lot of kind of lack of understanding about that as well so yeah I mean I just kind of looked at it and I was like well we really need to start educating people better and the medias that we use to educate people need to be you know aligned with what you know helps people to understand things um but yeah the whole misinformation side of thing as well is just I don't know how I don't know how to solve that problem sadly I think it's quite a lot to do with us as medical professionals there's been like this massive push to go jargon free but there hasn't been like a kind of quality control for the jargon free language that we. So I think because there isn't this kind of standard on how to use non-medical language, we ourselves as medics may be getting it wrong when we're describing things not using medical language. And then that's being propagated.
So, you know, don't have, not the qualifications, but haven't been educated in that field and are thrown about these terms, which, you know, very much sounds like they have a legitimate understanding, but really don't. So it's very difficult for the general public to be able to, you know, decide, you know, what the truth is. If people start using sports terms, I would have no idea if they were accurate or not, I'm going to be completely honest. Interestingly, this is a sort of aside, but stemming from what you've said, Declan, when you guys write letters to patients after clinic, do you write it to the patient or do you write it to their general practitioner, their family doctor, with the patient copied in? It depends on the consultant you're working for doesn't it I don't know I always wrote to the patient I mean I didn't really care what who the consultant was um to be to be honest I know I'm such a rebel um but yeah I think it's it there was a time when I was about 14 and i remember going my dad had an ogd this is very off topic so i don't i'm an ophthalmologist now i can't remember what's a supple gastro do it had an ogd a thing down the throat anyway you'll know this a camera test of the gullet yeah exactly that um and it was just when they came to explain his results, it was so terribly explained to him that he had absolutely no idea. And maybe I was a bit older. Maybe I was like 17, 18. I might have just started med school. But I remember being like, can you please explain that again? Because that makes absolutely no sense. And I think that's always stuck in the back of my mind of like, you actually have to be able to communicate what the hell's going on to these people. So even if the consultant wanted X, Y, Z put in, I would also add on, you know, this is what it means in real terms. But I think maybe that's just me where, you know, I do try to be patient focused. I can't be. No, I actually found out the other day that it is the NHS standard now to write your letter. We should all be writing the letters to the patients in a jargon-free way to summarise the consultation, which I've always tried to do, but a bit like you, Aisha, sometimes my boss is like, why are you doing that? Write it to their GP. Is there a standard, Simone, in the US? Do you write letters to patients or do you write it to the family doctor? So with the electronic medical record,'s a little bit of a pre-populated situation which I'm sure is similar and our letters do go to the primary to the referring doctors and they are available on the portal for the patients to log into and then they the patients will get a separate patient summary at the time that's written more that skips a lot of the details and is more of an action plan diagnosis focus that they would get at the time of a visit that's i quite like that i think that's quite a good model because, yeah, the criticism from consultants, maybe this is what they said to you, Aisha, is I've been referred this patient so I'm going to write to the doctor in doctor language to the person that's referred them. But sometimes I think when those patients get copied in and there's all these, you know, Declan is a doctor and he doesn't even know what OGD means so how can we expect patients to remember I'm just in awe of this online portal and here I am with my little dictaphone recording tape we are about 30 years behind I think well it's a difficult thing to do though isn't it I think And it's also hard because you do need to use specific terms to communicate to other physicians. And I mean, simplifying some of them succinctly is not easy. I mean, I remember doing a couple of things for the BMJ and trying to write for, even from like an ophthalmology perspective, trying to write for a general doctor is is difficult so it's pretty challenging with the time constraints and stuff that you have as well isn't it to actually be able to do that and in medical school we're not taught how to write when you know and it's it's a skill that really does take training um so yeah it's a challenging one well interesting stuff uh now we are all warmed up in our discussion. I am keen that we move on to the nitty gritty of our topic. Sorry, the MPS Foundation could fund it. The MPS Foundation is a global not-for-profit research initiative backed by 130 years of healthcare expertise from medical indemnity leaders, Medical Protection Society Limited. Our aim is to make the world safer for patients and clinicians in hospital and outpatient practice and dental care environments. Applications are now open. We're looking for proposals that are original, evidence-based and focused on applied research. Find out more at thempsfoundation.org and apply for a grant. The MPS Foundation. Transforming the future. Okay, back to the show. Simone, as our experts today, I want to start with you. Could you tell us a little bit more about what is grit and what grit isn't? I think grit, you summarised great in your introduction. It is the passion and perseverance, really for long periods of time and often without the positive reinforcement or feedback that we might seek as individuals when pursuing something difficult. So it really has nothing to do with talent or with luck or with our intentions or our wishes it's more of you know our ability to continue on a goal and a path making progress over time and is this something that you I mean you mentioned how you got into talking or thinking about grit and that you went to see one of Professor Angela Duckworth's lectures. Is grit something that you now use when you think about yourself or you think about your trainees or your colleagues that you work with? So honestly, I think more about it with my children a lot of the time and how I can instill, you know, grit in them. I think one of the things when we think about grit is we automatically think it's just part of us or not. But like many things in our personality, it is mutable. And there is a lot of evidence that grit changes over time. We know that older people have more grit than younger people, for instance. That's, you know, been well documented over the years. So I think about it when you think about studying it and who the proper comparison is, right? So, you know, you talk about your trainees and your colleagues and you think about grit. And is your comparison your next door neighbor who isn't in medicine? Or your comparison your other colleagues that are in medicine are the other people within your own specialty so I think about it like that and I think about it when it relates to burnout but I certainly don't think about it as far as screening for people for any type of positions. I think that's interesting that you mentioned that grit is something that you have or you haven't got grit. Because I think my immediate assumption was this is testing for something that is part of your personality. But what I'm hearing from you is that actually grit is something that you can almost train into people. Is that what you think? I do think it is something that people can get better at. And I think you also have to think of when it's time to quit something, right? I mean, if you're pursuing a goal and, you know, we're all successful doctors here, but there was a point where we gave something up, something else up in our lives so that we could make that decision to go into medicine, right? So whether it was, you know, sports or another academic career that you may have been interested in and working towards, we all do have to know when to pull back and to change course. Yeah, grit is absolutely something that can change over time. Angela's book, she talks about how she makes her kids do one hard thing every day. And that's how she thought about instilling grit in someone. I think there's a lot of connections, obviously, between grit and things like Carol Dweck's, you know, growth mindset that she and others have talked about at length and, you know, instilling in children in school. And they're very similar, right, with these social science abstract ideas. And I do think that they're changeable. And I do think we can do things to fortify our grit or to, you know, Professor Duckworth is really well known for having developed the grit scale that takes about three minutes and it's available online. Anyone can take it and you can get your instance score as a feedback. Of course, as with any of these social science scales, you have to understand the drawbacks of them. The GRIT scale was really developed for research. It wasn't developed as a screening tool.
If you can't measure it, it's very, very hard to talk about it. We like to put numbers and values on things. And this is another way we can put a number or value to a personality trait or an idea. But you can think about it. We're more as people than what a piece of paper tells us, right? And it's great for self-reflection. It's great for research. It may even be great for screening people who might be predisposed to burnout or, you know, think about how we can make people grittier as a way to protect them from burnout. But it's very hard to use one of these subjective measurements to screen people for job applications or trainees into medicine or anything else because it is subjective. And also, I think because it's pretty easy for many people to give dishonest answers, right? You know, you have to really be willing to be honest with yourself to measure a lot of these traits. So when it's that easy to fake, you shouldn't be using it to screen people for a job position or a career goal. So we can't use the score to choose the grittiest people, but it does give us an idea when we're researching or targeting people for help understood Aisha I saw you nodding when Simone mentioned about grit also being about when to give up if you had to give up on something in the past because of medicine oh god where where do we start with that question Clara have you ever done something really hard and just had to think, do you know what, Aisha, can't do this, just going to have to pop this in the bin? Well, it's funny that you mention that because I did my grit score today and I got my husband to do his grit score. Amazing. And we both did it without knowing about grit and then we compared our results. And your husband is a general surgeon? Vascular surgeon. Vascular surgeon, apologies. And my score was higher than his, which has caused mainly, this is what's caused the contention in our household today. We're going to have a divorce on our hands. Well, maybe. Because he says that actually, like he said, Simone, you can fake it, can't you? And I think that my personal kind of life and grit score is very different to my medical life and grit score. So in my personal life, I can't have a hobby for more than one second. Whereas in a professional life, I will spend three years trying to get a paper published if that's what what what's needed and it's so and it's so funny because in one in one aspect of my personality I'll just give up immediately and um in another I won't and and so my husband was was raging at the fact that he's gone through this difficult um process of getting a vascular surgery number and has persevered for like his entire life to get there. And I've got a higher grit score. Do you think he has a higher grit score in his personal life? Yeah, definitely. That's interesting. That's really interesting, isn't it? How about you, Declan? I'm assuming you haven't done your grit score. It's all right. I didn't do mine either. I just now made it kind of standard of homework for this podcast. podcast yeah I did have about a five second brief look at what the grit score was um but no I haven't done mine I feel like you can you can have a grit score to an extent but there's many many other factors which are also contributing so I'm probably going to be leaving medicine pretty soon and you know I haven't done my grit score but i'd argue it's pretty damn high yeah um and you know i tend to persevere whatever but yeah it's it's a it's a difficult one because yeah i think it's it's also knowing um i think it's recognizing you know your own your own mental health and stuff as well um and and whether whether it's worth worth broad context of your life, really. Also, I guess I didn't quite understand when you're saying you can use your grit score to know when to quit. Am I interpreting that right? As in, you know, some of the high grit score can persevere through challenges and achieve, you know, highly kind of alongside those challenges. But I guess where does it come into play when you're then thinking about using it to quit, Simone, if you don't mind me asking? Of course, I don't think you can use it like that. I think that, like any personality trait, some of your greatest strengths can also be your greatest weaknesses, right? So if you dig in your heels, and you're going for something that's just not working out you you still need to have the self-recognition of when to quit I don't think the grit score has anything to do with that I just think that there are times when grit isn't the be-all end-all for your you know long-term goals and do you perhaps think people with the highest grit scores do you kind of find the find it challenging to quit because you can sometimes go for too much? Which just just kind of reflecting when, you know, people get in their kind of very competitive specialties, which I feel pretty much all of us are in that sometimes it can be a lack of the recognition of, you know, factors and people persevere regardless it's a great question Declan and I think it just speaks to how there's not one thing that we can use to make decisions or determine who we are as people or how we act do I think that the grittiest people don't know when to quit I don't that's generally true. I don't know that there's ever been any evidence to show that people with really high grit scores don't know when to make the decision to move on. But I do know that all of us in life have made that decision to give up on things, no matter how gritty we are, right? we've all made choices to give something up and I think as Aisha clearly pointed out she's really gritty in her medical life and maybe in her personal hobbies you know she's just not as gritty and maybe her husband is you know a little bit more balanced or different has a different approach and I think that that's probably true for all of us, which takes me back to, you know, it depends what your reference is. You know, what exactly are you talking about and who are you comparing yourself against? One of my questions, which I think you've sort of asked there, Dachlan, was, is there such a thing as being too gritty? Like, is it something that we, you know, we see as being good? You know, grit is good. It helps you stick at things. But also, can it get you stuck in a job that you hate or a specialty that you hate because you think, well, I've said I'm going to carry on doing this, so I'm going to dig my heels in. You know, does it equate to stubbornness?? I mean I don't think it's the same thing as stubbornness I think it's different I don't know that there's a correlation between stubbornness and grit there is a correlation between grit and success which is very hard to define but there have been attempts to study that and there is a high correlation but it's not the only factor. There certainly are gritty people that can end up not being successful. Is it because they end up too gritty and they're stubborn and don't know when to quit? That's a great hypothesis about maybe why those, that percentage of people doesn't end up, you know, quote unquote successful. Well, I guess when I was thinking about this topic, when I first saw grit, I thought, oh, tough and stubborn. Those are the words that I equated it to. And then I think the more I've read about it, the more I've understood that maybe there's there's many more facets to it. But I think almost, you know, I know that you're saying that grit score in the in the sense that you've looked at it in the past and the score that Professor Duckworth developed isn't for selection. But I was thinking that actually, you know, all the things that any of us do to get into medical school kind of proves the grittiness already. I mean, medical school is already a sort of a grit test in itself. It's like, can you jump through all of these hoops to prove that actually you want to stick at something when it's hard, you know, when all of your friends are going out and getting drunk and you're having to wake up at 9am the next morning to go to a lecture. Does that actually prove that you have some perseverance or are committed to something? So actually, you know, are we kind of selecting for grit already? And then those that are relatively successful, all of these other factors are coming into play? Oh, 100%. We're pre selected in medicine, of course.
And there's such nuanced conversations about, you know, do different specialties have different grit? I mean, it's really hard to compare when you're at such a high level at the beginning point. And I think that, you know, the scale was just used to try to study it and give a scientific measurement to a trait that is otherwise hard to define. Simone, when I was doing my background reading about you, and I know that you've touched on this earlier, but I noticed that you were involved in a subject which is very close to my heart, which is women in surgery. And one of my first thoughts was, is grit gendered, which I know pertains to the research that you did. One of the things I wondered is, do men generally have more grit than women? And historically, is this where there are more men in sort of successful or inverted commas, high powered professions? or is this less about grit and more about sort of preexisting patriarchal structures or something else entirely? I think a lot about female surgeons and we can talk about, Clara, we could talk about female surgeons for hours, but our study, not that it's the end to the story, but really demonstrated that within surgeons at least, and there's been other studies that have mimicked these findings in residents and in other medical specialties, that men and women have the same grit scores. They're not significantly different. I think that the point in me doing the study was that maybe not so much, or hopefully less so now than when I went into training, but certainly when I interviewed for residencies, I was inappropriately asked many times if I was tough enough to do neurosurgery. And I think that while tough and grit are not exact synonyms, there are nuanced differences. I do think that there is a preconceived notion in the society here in the U.S. and probably globally, given the numbers are similar for female surgeons around the globe, that women are lacking some kind of, whether you call it grit or toughness or ability to, you know, be successful in a surgical residency and a surgical career. Hopefully the data, you know, we have shows that that's not the case. Women are just as gritty as men. So I don't think it has anything to do with that. I think also that, interestingly, what we saw, and I know that the data prove it out in many other places, is that burnout in women in medicine and surgery specifically is much higher than in men. And if your grit's the same, but your burnout and the rates of which you're leaving your career or higher you know that becomes a much more interesting question and is it that women are more likely to report burnout than men which is possible you know certainly there are you know gender and cultural differences about who reports what kind of symptoms and then then second of all, if grit is the same, then what else is protective of burnout? Because if we can figure out how to protect people against burnout, then we can screen them and hopefully change things before burnout occurs instead of waiting for it. We kind of hypothesized some kind of success, however you define that, might be protective, but we don't have any answers. Yeah, I'd be curious to see if anyone else has ideas of what they think might be protective of burnout besides grit as far as personality traits. I was going to ask you, Aisha, because you work in Ops and Gynae, and I feel like whenever people talk about women not being tough, somebody just has to say childbirth. I'm sure that you have tons of experience with that. Do you have any thoughts on, you know, if women are as gritty as men, why is it that women report more burnout? Or what could we do to protect people that report more burnout it's interesting because like obs and gynae in the uk has one of the highest attrition rates um within the special within different um specialties and one of the reasons for it is burnout um normally secondary to like litigation and things because um there's in obstetrics in particular particular you get quite a lot of um incidents which end up in litigation um and i don't know if there's um any evidence to what i'm saying here but one of the protective factors for myself and the people i work with um within my own training program is having peers and peer support and being able to reflect amongst our group that actually these are normal things to happen within training and to be able to almost have kind of an echo chamber and be able to bend a bit but then also take some constructive steps as to actually is there anything that I could have gone better it's true reflection really and then to be able to take it forward knowing that actually it's not just me and I think it's actually helped a lot of people get through difficult parts of trading, particularly when things have gone really badly wrong, which is the nature of Ops & Gynae. That would certainly lend to your hypothesis, wouldn't it, Simone, that if you've got fewer women in a specialty and those women have a higher rate of burnout, if they've got less peer support or less, you know, I guess peer support in the sense that people that look like them or people that are like them, perhaps that's a reason. Declan, as somebody who's in the process of leaving the NHS and has had a degree of burnout, but is obviously incredibly gritty, is there that uh that might have have been a protective factor for you i i mean i think what ayesha says is is amazing i think ophthalmology and academia in itself are both incredibly isolating and there's so few people who are doing the same thing that you're doing that it's it's very very challenging to actually get somebody that understands what you're going through. You know, you can't speak to consultants because they're typically big, big dog professors on their own who, you know, can't quite relate to those challenges anymore. You can't speak to your peers because, you know, you're basically doing two jobs and trying to achieve the same clinically as them at the same time. Can't speak to allied healthcare professionals because they're just like, research, why waste your time doing that? So I actually think that's an absolutely huge one. Yeah, so I think that probably would have helped me. But I mean, ultimately, it's the whole system, which is the reason why I'm leaving. But yeah, I think what Ayesha said would probably be the key thing that probably would have helped me stay in a little bit longer. I also think there's like a massive lack of mentoring that, like back in the day, which is what I hear from my consultants all the time, you would have like someone who, you know, a senior person who would kind of take you under their wing, you know, would support you through training and kind of prevent all of these issues from arising or not arising, but having an effect as an effect as it may be doing now. And I think there's just a complete lack of mentoring within our training programmes nowadays. I wouldn't know who to turn to from the consultant who to go to um for that level of support yeah absolutely and I mean I personally feel like almost the opposite um I mean I remember raising a few concerns about different things and you feel quite isolated as a junior because you know you you rotate quite frequently so the consultants aren't in my personal opinion, don't appear as invested in you as they may be in the rest of the team that they have to spend the time with. So it's a very isolated position to be as a junior doctor, I think, at the moment now. Because the consultants have a pretty rubbish job, generally, as it is. They're trying to, you know, keep everything great in the whole team. And then you have the, you know, F1 SHOs and registrars who are doing a hell of a lot of the groundwork, but really don't know where to turn. So I do think that's a major, major factor. Simone, you talked about grit not being this kind of unchanging entity that somebody just possesses or doesn't possess, that it changes it with time and place, I imagine, and job. And we talked about things you can do to increase somebody's grit. I think that the interaction is probably difficult to measure or to, you know, say that this one thing takes credit for it. You know, the relationship between things like resilience, success, grit and burnout are interesting. Certainly Certainly we've seen correlations. The question is, is there a causation there, right? We're always careful as doctors and scientists as thinking about is correlation the same as causation. And so I do wonder if, you know, burnout separate from your grit can then in a flywheel kind of circle back and impact your level of grit. So if you do have a certain level of burnout, does that then impact your willingness to persevere and persist on this goal for a long time? If you don't have success, does that come back and tell you that your grit should go down?
I tend to think that if it's time to quit something or something's not going right, you need other personality traits that come in that will tell you that this is more stubbornness than grit and it's time to move on to something else. So I think it's a self-awareness. So maybe it's that, you know, that you're a mindfulness almost that you need that can counteract when the grid is not your friend anymore. I'm really glad that you brought up the word resilience because it's a word that's come up on this podcast loads. We've had loads of discussion about it. And one of the studies that I came across when I was reading this which I will link in the show notes and this is a 2017 study by Laura Halliday, Abigail Walker, Stella Vig, John Hines and John Bracknell suggested that grit could be used to sort of target for want of a better term individuals who need more support and that could be done in the form of resilience training. And I know, as I say, that that's a bit of trigger word for some of us on this podcast. But taking aside what people think about resilience training and how it can be sort of weaponized as an intervention, what do people think about using these grit scores as a way of sort of helping people by supporting them better, I suppose? I mean, I'd be interested in hearing what people as trainees, you know, earlier on in their career feel, because I do think that if we're going to use it as a screening in the aims of helping and not as a way to weed certain people out, you know, there has to be obviously the same kind of privacy that you get from any other medical examination or data that people get. So there has to be obviously a protection and a privacy issue with the data. And then if we think about as an institution or a health service that we're going to help to build people, protect them against burnout or build resilience or grit, then there has to be, before you actually screen for that, there has to be a program in place that is going to be proven to be beneficial. Because if we're going to use it, then we have to be able to help them, right? We can't just get this data and say, boy, you might be at risk for burnout or, you know, you need to work on something. You know, so I think you need to have a plan in place first. Yeah. But I'd be interested to hear what some of the other folks think on the panel about whether that's even a good idea or if that's kind of crossing a line for them. I'm not sure, you know, because it almost feels like you're setting up like a two-tier system based on a score so that some people get some support, which can either be seen as they're getting lots of extra help or it could be seen as, oh, you're not good enough, so you're getting extra help. And then like the rest. And I think it does the opposite of leveling the playing field I think it makes it completely uneven and I don't I don't think I would like that as a trainee no I mean you wouldn't you wouldn't like it if you were in the like no grit group or the low grit group would you I don't know I don't think I'd like it any any of those groups to be honest because you can argue like each each group has its own benefit don't know. I don't think I'd like any of those groups, to be honest, because you can argue, like, each group has its own benefit, don't you think? What do you think, Declan? Yeah, I mean, you may have swayed me. I honestly thought, hmm, that might be a good idea. As long as, like Simone said, there's an actual, you know, reasonable evidence-based plan for those who are struggling, because then it would at least, you know, show that they're at least trying to care about us and, you know, trying to quantify in a certain way to find those who are most at risk. But like Aisha said, that will come with a million challenges and I think, yeah, there would be conflict between different trainees, different allied healthcare professionals, why the doctor's getting it, but we're not. We're doing X more hours than them, if that's the case. I think it would be difficult to roll out. But, I mean, generally, it would be nice to see that, as an organisation, the NHS are trying to use some sort of evidence to intervene to those who may be most at risk. As we've kind of already talked about, it's not just about your grit score, it's your personality as a whole. So how can you, you know, stratify risk based on just a grit score? Yeah, I mean, they may well add additional things in, I guess, to make it a bit more, yeah, a bit more thorough. I'm curious, would you be in favor then of having, if there was a proven training or program that could build things like grit and resilience, would you be interested in having it then available on just a, if you want it, you can go and do it basis or a mandatory, everybody has to go and do this because it's that important for us. And so there's no two tier system between the haves and the have nots. No, I mean, I was just gonna say, we've discussed resilience, resilience training we have in the NHS. And I imagine that there is, you know, something similar in a lot of other places and I think that the criticism certainly from people that I've spoken to you on this podcast and off this podcast and I think I heard someone say recently resilience training in the way that we have it at the moment particularly with the NHS being in the situation it is is asking a person to run into a burning building waiting for them to catch fire and then once they've caught fire bringing them out and saying here's how you can put the fire out but by the way now you have to go back in the building again and that's why a lot of people feel actually we're not fixing the systemic problems that have created you know that have meant that person is now on fire we are just fixing the individual and making it and making it an individual problem when actually a lot of this is systems-based. So I can totally see where the idea of resilience training comes from and that there is a lot of good in it. But I think I can also see the frustration when there's a systems-based problem and somebody saying, you know, I don't think a training program is going to sort this out I guess my final question was going to be whether we call it grit or whether we call it resilience or whether we call it toughness or stubbornness whatever the name is for it is actually one of the issues that a lot of healthcare systems whether they're public or private have relied on any healthcare practitioners grittiness for too long and actually we're getting kind of to the end of people's gritty tethers now when it comes to you know wide scale burnout and and generally poor well-being and the professions? Yes, absolutely. I mean, there's those different factors that come into it, you know, economic, you know, we aren't getting paid as much as we once were and we can't afford to live on the salaries that we're on. And then you go and you have increasing amount of challenges at work and you feel devalued on our role. You could argue is less respected and whether it be by the public or not so I think there's an accumulation of all of those and I mean for me anyway you know having been someone who I would probably say is fairly gritty and throughout medical school in the early parts of my career I'm at the end of my tether and there are other alternatives which which give you you a better work-life balance and you need to focus on your own well-being. So yeah, I completely agree. I'm very much at the tether of my grit. Simone, you said something right at the beginning which I just wanted to circle back to you to sort of, you know, come full circle so to speak is one of, in your definition of grit, one of the things that you said was that it's the being able to continue even when you're not getting that validation. You know, somebody saying, well done you, keep going. And I actually wondered if maybe that is one of those protective factors that we were talking about from burnout is actually somebody saying to you, you've done a good job, keep going, you know, in whatever format comes public or personal. I don't know if that's something that you think protects you, Aisha, from feeling burnt out. Definitely. I mean, so, funny story, but at the beginning of my training, every cesarean section I went to, I fainted in. Every one of them. I spent most of that year lying on the floor on the board.
You're going you're like don't don't let this like completely destroy you because it was um because I was like god how am I ever going to do this specialty like I have to be able to stay upright um and it it was it was them saying you're doing a good job you know you're good at every every other part of your job this is just a little hiccup. You'll get through it. And eventually I did. But yeah, I definitely think that was something that kept me in training and managed and kept me going through to SD5 now. Even when all those systems-based things, even when the house is on fire, that still keeps you going. That's really interesting. Grit is not the be-all end-all. There are other things that are very important to us as physicians and as people. And while we are already self-selected as a pretty gritty crowd, obviously things like integrity, honesty, you know, hardworking, tolerance, kindness. These are all important factors for being a good citizen, a good human being, and certainly a good physician as well. And I think making any overreaching statements that grit is, you know, the most important thing that we look for is saying too much. You know, it happens to be the topic we're talking about today, but I, you know, I don't want anyone to walk away thinking it's the only personality trait that should be looked at or cared about or thought about when we think about who we are and what's protective of our own personal, you know, burnout and whether it's grit or a combination of things. And I think that both Aisha and Declan have made really good points that for them, things that are protective are having potentially mentors and peers. And those are things that, you know, are very hard to measure. We had toyed with the idea of success. So I think that there's, this obviously is multifactorial. It's not really easy to pick out one thing. And I think we each as individuals will need to do our own self-exploration about what it is that, you know, we think makes us grittier or less gritty or will protect us against burnout because it's probably a little bit different for everyone. I think that's a really good note, probably the most positive note to leave this podcast on. So thank you so much for joining us for this episode. And thank you for listening to Doctor Informed. That's all we have time for today. We're really keen to hear from our listeners. For ideas of future discussions and reflections on the topics we've discussed today, please get in touch. If you like our show, I'd love it if you could support us by leaving a review wherever you got your... If you like our show, I'd love it if you could support us by leaving a review wherever you get your podcasts or share with the people you know tell your friends about it that really helps people find us if you'd like to hear other episodes please subscribe to doctor informed on spotify apple podcast or wherever you get your podcast from and you'll be notified when our next episode is up. Until then, goodbye from us.
Hola y bienvenidos a In Conversation With, un podcast de The Lancet Regional Health Europe. Es noviembre del 2023 y soy Daniela Marí, Senior Editor de The Lancet Regional Health Europe. Y este mes estoy encantada de estar acompañada por mi amiga, Daniela. Thank you. la presentación y pronóstico de la condición post-COVID-19 fue publicada en nuestro issue del mes de octubre. Muchas gracias, doctora, por acompañarnos. Muchas gracias, Daniela, por la invitación. Pero antes de que hablemos sobre el estudio, me gustaría que primero platicáramos sobre qué es la condición post-COVID-19, Síndrome Crónico COVID, Long COVID. Pero long COVID, but it is not until October 2021, more than a year after the first cases, that the World Health Organization does not issue a definition through the Delphi method of what is then called post-COVID-19 condition. for which it should be redefined or profiled. For example, our group believes that it is very important to separate those patients who have had sequelae of a serious infection by SARS-CoV-2, which have often required an entry in a critical unit, from those patients who have had a milder infection and who persist with symptoms in the three months. Because probably the physiopathology and the evolution of these two patients ¿Y qué tan común es esta condición? The 11% of patients who have had an acute infection by SARS-CoV-2 will have long COVID or persistent COVID. This prevalence can vary according to the SARS-CoV-2 variant and the vaccine status. It seems that with Omicron it could be 5% according to a study published by Perlis, a large cohort of the United States. But there are several factors that influence this percentage, such as the vaccine status of the population in the post-pandemic era. Thank you. ¿Por qué ha sido tan difícil definir y diagnosticar esta condición? for several reasons. The first is that the symptoms are very unspecific. There are more than 200 described symptoms that affect all organs and systems. Not all patients have the same symptoms or the same evolution. Another reason is that we still do not know the physiology well. Although in the last year we have advanced, there have been many advances and it is not yet known well. Different hypotheses are being taken. One is viral persistence, whether it is a living virus or viral particles that produce a persistent antigenic response. Another is inflammation or alterations caused by SARS-CoV-2 in the different components of the immune system. Alterations have been described in different cytokines or cells of the immune system, such as monocytes, natural killer, lymphocytes T, which are present in these patients. The autoimmunity, disengaged by the virus, or already present previously and not manifested before the infection by SARS-CoV-2. The reactivation of other viruses, especially of the Herpes family. Also the microvascular dysfunction. For example, the group of Dr. Petrorius has described aggregates of amyloid plaques in patients with COVID-persistent. Alterations in the intestinal microbiota or endocrine metabolic alterations such as cortisol decrease, described by Dr. Iwasaki's group recently. Finally, but not least, the absence of biomarkers. We do not have any biomarker that helps us in the diagnosis or that is useful to evaluate the effectiveness of the different treatment studies. ¿Y dado que hay tantas hipótesis sobre la fisiopatología, ¿existe algún tratamiento para esta condición? No. There are different clinical trials in progress that mainly evaluate drugs that act on viral persistence or inflammation, but we do not have results yet. The fundamental problem of these studies and clinical trials is the lack of a specific biomarker to evaluate efficacy. Most endpoints are clinical based on symptom scales or life quality scales. Thank you. Well, we started with a single consultation attended by the doctors of the Infectious Diseases Service, but we quickly saw that due to the multi-organic effect, this attention should be multidisciplinary. the of affected people of COVID Persistent of Catalonia who have helped us both in the assistance part and in the research. The joint work with the affected people is fundamental for this and for other pathologies. The structure of our unit is dynamic, we have been including actions according to the needs that we have been observing, but we have also stopped doing things that did not make much sense. And very important, in the last year and a half, Thank you. and we already know that we have several guides that are very good, but these guides must be executed and applied according to the real resources available in each area. Equity in the patient's care is fundamental. In our unit we have seen about 1,500 patients, but we are unable to follow up on all of them, so collaborative work with primary care is essential. Thank you. Reino Unido o Alemania hay un mayor conocimiento y conciencia social y médica del COVID persistente. Uno de los retos que representa esta enfermedad es el estigma, el estigma de las personas que la padecen. Muy bien, ahora sí vamos a entrar al estudio. ¿Cuáles fueron los objetivos de este estudio? Teníamos varios objetivos en este estudio. Uno de ellos era caracterizar los pacientes. Lo que observábamos en la práctica clínica es que no todos los pacientes se comportan de la misma manera, no todos tienen los mismos síntomas y es por esta razón que hicimos un análisis no supervisado por clústeres de este estudio y qué lo diferencia de otros estudios sobre long COVID? of clusters per symptoms, what we saw is that the different clusters, the different groups, the symptoms were additive. That is, cluster 2 had more symptoms than 1 and 3 more than 2. The most frequent symptoms in the three clusters were fatigue, neurocognitive affectation and dysthymia. These groups that we found are very similar to those described in the Recovery cohort, with the difference that in this American cohort there is one more cluster that predominantly has an effect on the level of the olfactory. As for the factors associated with the cure of long COVID, the male sex, a higher level of study, was related to a higher probability of healing, as well as the presence in the unit of critics, a fact that undoubtedly emphasizes the need to differentiate the post-care intensive syndrome of the long COVID. Cephalia, tachycardia, myalgias, neurocognitive affectation in acute stage of infection were also related to a higher probability of curing. It should be noted that only 7.6% of our patients were considered cured after two years of follow-up. It is clear that our study has certain limitations and the main thing is that our unit is hospitalary is por el que el porcentaje de curación que nosotros decidimos es tan bajo. Pero aún así, el porcentaje tan bajo de recuperación es muy importante porque dado que las infecciones por SARS-CoV-2 continúan, y aunque por diferentes factores, la incidencia de long COVID en la actualidad es menor, continúan habiendo nuevos casos que se suman a un porcentaje no despreciable de pacientes ya diagnosticados y que no se han curado y persisten con ciertas limitaciones. Los sistemas de salud europeos deben prepararse para atender a miles de pacientes. Es sin duda un reto para todos los sistemas sanitarios. Y hablando de esto, justamente, que los sistemas de salud se tienen, according to the World Health Organization, around 36 million people in the European region of the UN have experienced long COVID in the first three years of the pandemic. This means that one in 30 Europeans have experienced long COVID. How do the findings of this study fit with these numbers? Muchos pacientes con COVID persistente no están diagnosticados, ya sea porque no han consultado los centros médicos o los que lo han hecho no han sido diagnosticados por el gran desconocimiento que hay aún de esta entidad. La formación a todo el personal sanitario es fundamental, así como la divulgación no de esta enfermedad para aumentar la conciencia social. Bueno, y quiero aprovechar que estamos platicando con la directora de una unidad de Long COVID para preguntarte un poco sobre cuáles crees que sean las cuatro áreas que tendríamos que priorizar en cuanto al estudio de Long COVID. La primera, sin duda, es la prevalencia real. Tenemos que saber a qué nos enfrentamos, cuál, what is the real number of patients who suffer from long COVID. The second is the physiopathology.
The third is treatment. Clinical trials are fundamental to treat persistent COVID. The United States has invested a lot of money in this. I think Europe should do the same. And finally, prevention. Vaccination or acute infection treatment can prevent the development of long COVID. Although COVID-19 is no longer an emergency, Y creo que con esta última frase tan importante podemos terminar nuestro episodio. Muchas gracias de nuevo por esta conversación sobre Long COVID y por hablarnos sobre los hallazgos del estudio y sobre todo por explicarnos por qué long COVID es un problema de salud pública al que hay que darle prioridad. Muchas gracias por la oportunidad y muchas gracias por ayudar a incrementar este conocimiento de long COVID. Thank you, Dr. Mateo, and thank you for listening to this episode of In Conversation Week. Remember that you can subscribe to In Conversation Week from The Lancet Regional Health Europe, wherever you usually listen to your podcasts. you
Hello and welcome to the latest Lancet podcast. I'm Richard Lane and it's Thursday, May the 27th. In this week's podcast, we're discussing renal medicine as we publish two papers that form a short clinical series ahead of the European Renal Association, European Dialysis and Transplant Association, ERA, EDTA, Congress in Madrid coming up in early June. Sorry, that's a bit of a mouthful. Let's hear from our guest interviewee for this podcast. Hello, my name is Daniel Aflisa. I'm Professor of Internal Medicine at the Saarland University and the Saarland University Medical School in Germany. I'm not an author of these two papers, but I will be chairing the joint Lancet-ERA-EDTA Symposium at the ERA-EDTA Congress in Madrid on Sunday, June 4th at 15 o'clock. The first series paper looks at managing people who have acute kidney injury. Would you mind describing more about acute kidney injury because it is a multifaceted clinical condition, isn't it? And what sort of people are potentially at risk? Indeed, the acute kidney injury has mostly several causes. In previous times, acute kidney injury was related to primary kidney diseases or kidney diseases due to, for example, systemic diseases like vasculitis. However, in recent times, we have more and more patients getting acute kidney injury because of systemic infections, sepsis, or large surgical interventions or surgical procedures, like procedures at the heart or lungs or something. So actually, in these patients, there is a lot of comorbidities present like cardiovascular diseases or other diseases which can lead to high risk for acute kidney injury in such patients. And who are most at risk of getting acute kidney injury and why is prevention so important? Why are prevention measures so important when we're looking at acute kidney injury? From large epidemiological studies we know that the highest risk have patients who have already some kind of kidney injury, so chronic kidney disease, for example, with high proteinuria, loss of protein in the urine. So these patients have usually an additional triacondycinase, so they get acute kidney injury and acute kidney failure. Identification of such high-risk patients or high-risk individuals is very important in order to reduce the risk for acute kidney injury after or during such procedures like surgical procedures or heart catheters, for example. And in terms of the things to avoid, the key negative measures associated with acute kidney injury, perhaps you could discuss the importance of these for clinicians. Volume depletion in the kidney obviously is one, low blood pressure is another and also toxicity in the kidney. Can you just run through these key negative aspects that need to be prevented? The kidney is very sensitive to blood pressure decrease or volume depletion. So during such procedures like, for example, heart catheter or open surgical interventions at the heart, blood pressure drops or volume depletion can occur. And this may lead to profound kidney injury. A second important point is toxicity, such for example toxicity of certain drugs or interventions. And in terms of positive clinical intervention the sort of things clinicians are looking for are volume and replacement, the use of saline solutions although it's controversial is it with some of these crystalline solutions that are available as well and obviously avoiding kidney toxicity. That's true. One of the most important measures is to keep the blood pressure constant during such interventions and also to have an appropriate or ideal volume management including also vasopressor drugs. So this is very important in order to prevent further injury to the kidney. One problem is however which, which was shown in recent large intervention studies, that the use of saline might be problematical because large amount of saline, sodium chloride solutions, may be also toxic in some circumstances and may also lead to kidney injury. There are several large studies on the way, which be published in a few years to resolve this issue and to show if sodium chloride should be replaced by other buffered crystalline solutions. And a key, the key point I guess of paper one in this pair of series papers is about awareness isn't it? About raising awareness for prevention efforts in relation to acute kidney injury where does awareness need to be raised obviously if you work in internal medicine or renal medicine you're probably aware of these things presumably the call for awareness it goes more broadly does it into other parts of medicine primary care nursing and elsewhere yes I think that the awareness for the possibility of acute kidney injury should be much broader than also for a nephrologist or even doctors of internal medicine. A large part of the population has, for example, chronic kidney disease or reduced kidney function that they are not aware of, even not their doctors. So we have to make these patients and their physicians aware that there might be a problem. And if such patients or such individuals have these mentioned intervention, large procedures, surgical procedures, they can get further injury to their kidney and then they develop progressive chronic kidney disease. So this is a very important point and goes beyond internal medicine and beyond surgery. The second paper in the series looks in much more focus at post-transplantation and obviously kidney transplantation is quite widespread now particularly in developed medical settings with a high success rate and good patient outcomes but this is very much looking at preservation of the graft. So is the point here that although transplantation, renal transplantation is successful, we still need to do better in terms of understanding how to preserve the graft function. Is that right? That's absolutely correct. Actually, the survival rates one year after transplantation for kidney transplant is extremely high and improved in the last two decades. It's now up to 95%. This is probably because of the used quadruple therapy or immune suppression. However, the Cinderella of transplantation is long-term outcome, the long-term preservation of transplant function. Here we have to do much research to improve. The paper alludes to obviously recent developments in key specialties, molecular immunology, computational biology and others that are potentially making the path ahead easier, better for preservation of graft function after transplantation. Can you elaborate here? We know from several studies that the loss of transplants, the long-term loss, is mostly related to what we call or describe as a chronic rejection of the transplant. So it's a pure, almost pure immunological process and we now learn to understand how this happens. We learn to understand which cells are involved in this process, how this chronic rejection takes place. With the implication being, therefore, that we can better manage the potential of graft rejection in the future. Yes, that's true. And there are several ways which are already tested, like, for example, application of co-stimulatory blockade or even application of bone marrow transplantation in addition to kidney transplantation to induce immune tolerance. So in terms of the longer-term outlook for reducing graft-versus-host disease to a minimum, do you think that is a realistic possibility? Well, actually, the risk of graft-versus-host disease is extremely low in kidney transplantation. What the problem is, if we use the bone marrow in addition to kidney transplant, then it could happen that we induce also graft-versus-host disease. And there are ways to induce immune tolerance with this approach, but the problem of inducing graft-versus-host disease remains as with bone marrow transplantation. And here we have to find new venues to make or to induce immune tolerance for the kidney graft, but not to induce graft-versus-host disease. But looking back overall on these two papers that we've discussed, what are your reflections on the path ahead over the next 5-10 years for the management of kidney disease, both in terms of preventing it, and then obviously after transplantation and the outcomes thereof? I think with respect to acute kidney injury, we have to find reliable biomarkers for patients at risk. So biomarkers which can tell us which patients will clearly be at risk to develop acute kidney injury to minimize the co-risk when other things like interventions, surgeons, surgical interventions are planned. With respect to transplantation, I think that the most promising way is indeed to try to induce immune tolerance in order to reduce or eliminate the need for the also nephrotoxic immune suppression in order to allow also chronic survival of transplant more than 15 or 20 years. It's been a fascinating discussion. Professor Fleischer on the line. Many thanks indeed for joining the Lancet podcast. You're welcome.
Hello once again listeners, welcome to the Lancet Gastroenterology and Hepatology podcast in conversation with. I'm Hugh Thomas, the Deputy Editor. In this episode we'll be discussing a health policy piece that appears in our June issue, discussing the landscape of public health policies related to non-alcoholic fatty liver disease or NAFLD in the Americas. Corresponding author on the paper is Dr Juan Pablo Arab. He's an Associate Professor of medicine at the Catholic University of Chile School of Medicine with interests in clinical and translational research and epidemiology of non-alcoholic fatty liver disease and alcohol-related liver disease. He's also the director for living donor liver transplantation at his institution. Dr. Arab, thank you very much for joining us and welcome to the podcast. Thank you. Thank you for inviting me and hello everyone. So obviously NAFLD has been getting a lot of attention in the past decade, so we barely need to go over that. And of course, a lot of the research, perhaps it's fair to say, has been conducted in Europe and North America particularly. In terms of the situation in the broader Americas, what's the kind of the current situation there? So non-alcoholic fatty liver disease or NAFLD represent the most common liver disease globally. And NAFLD is considered the hepatic manifestation of metabolic syndrome, obesity, and type 2 diabetes mellitus. So NAFLD prevalence has been increasing due to its relation to these worldwide obesity and diabetes epidemics. NAFLD affects around 25% of the general population, so one out of four people may have NAFLD. And the higher prevalence of NAFLD is found in Middle East, around 32%, and South America, around 30% prevalence. So on the other side, Africa have the lowest prevalence of NAFLD, it's around 13%. And there are high risk groups, for example, up to 70% of patients with overweight and obesity have NAFLD, 65% of patients with type 2 diabetes, and 90% of morbidly obese patients. And there are other comorbidities associated with NAFLD, such as dyslipidemia, hypertension, or coronary artery disease. But worryingly, NAFLD prevalence could increase by up to 18 percent by 2030. And this is due to the sedentary lifestyles, obesity, and increasing prevalence of type 2 diabetes globally. And NAFLD constitutes the second leading cause of liver transplantation in several high-income countries, including the USA. Now, we need to know that most risk factors for NAFLD are modifiable. For example, the International Diabetes Federation has said that 80% of type 2 diabetes cases are preventable with healthy diet and physical activity. Thus, the early identification and treatment of individual components of metabolic syndrome are critical in preventing both cardiovascular and liver-related mortality. But unfortunately, the dietary patterns in the Americas, including high intake of fried foods, corn syrup, red and processed meats, refined grains, snacks, sauces, and soft drinks, promote the development and progression of NAFLD. So globally, in the Americas, it's around 30% prevalence of NAFLD. When we talk about these NAFLD-related public health policies, what are the sort of things that we're talking about? And how are they being used to improve NAFLD and related comorbidities? This is a great question. And probably one of the main problems or difficulties is to measure the health care and economic burden of NAFLD and this is due to its underdiagnosed and complex relationships with other disease. Since several factors promote NAFLD development and its severity, public health policies aiming at this risk factor or the consequence of NAFLDs are key. So public health policies can start from child care environment strategies, such as nutrition standards for food or beverage, or direct food and beverage policies strategies, such as taxes on unhealthy food, licensing restrictions, menu and calorie labeling, nutritional standards for food, and portion size restrictions. Also messaging and marketing strategies, such as healthy food marketing and promotion, or toying ban in children's restaurant meals. Another important strategies are physical activity interventions, such as street-scale and community-scale land use design and transportation and recreational trial networks. The school environment strategies, for example, having clear rules for food and exercise in schools, or also the healthcare environment, such as insurance coverage for weight management, counseling, pharmacotherapy, or even bariatric surgery are also needed to tackle this disease. Finally, we need to address the comorbid conditions strongly related to NAFLD development and progression. For example, diabetes, obesity, dyslipidemia, hypertension, cardiovascular disease, alcohol consumption, cirrhosis, and hepatocellular carcinoma. So if we tackle the risk factor and we have policies aiming the consequence of NAFLD, we can reduce the impact of the disease burden. Fantastic. So moving then onto your study, how did it come about and how did you conduct it? So this is interesting because the American region is characterized by key social, cultural, ethnic and economic difference. I mean, not all the same in America are the same, are very different. So these differences are reflected in different health problems on the region. Similarly, there are large differences in governance across the region, so there was no comprehensive information about public health policies on NAFLD-related conditions in the Americas. Thus, we aimed to assess the presence of different public health policies on NAFLD-related conditions and scientific guidelines across 17 countries in America. We also evaluated the burden of disease related to NAFLD in terms of prevalence and mortality of chronic liver disease due to NAFLD and the incidence of NAFLD-related hepatocellular carcinoma. So for this, we constructed a questionnaire to assess the presence of public health policies for NAFLD and related conditions in each country. We also assess the main healthcare specialties involving the management of patients with NAFLD, scientific guidelines, awareness, and monitoring mechanisms available in each country. The information was gathered using an electronic form, and we recruited participants through the American Association for the Study of the Liver Disease and the Latin American Association for the Study of the Liver. We selected hepatologists who were actively involved in the special interest group on NAFLD. We also used available data sources such as the World Bank Open Data Source, the World Health Organization Global Information System, the Global Burden of Disease Database, and the International Registry on Organ Donation and Transplantation. All this updated to 2019 to get all this data. Great. And what were your key findings then? So considering a population of more than 900 million people, we found a median prevalence of chronic liver disease due to NAFLD of 13.6%. The highest burden of chronic liver disease due to NAFLD was in Cuba, Ecuador, and Mexico. And the lowest burden disease was observed in Argentina, Canada, and Peru. The median mortality due to NAFLD chronic liver disease was 2.5 per 100,000 inhabitants, and the mortality due to NAFLD-related chronic liver disease was highest in Mexico, Honduras, and Guatemala. The lowest mortality rates were in Paraguay, Canada, and Uruguay, and the highest incidence of NAFLD-related hepatocelular carcinoma was observed in Canada, the USA, and Honduras. In this study, none of the 17 included countries had established national public health policies to decrease NAFLD specifically, and only one country, which was Brazil, so 6% of our sample, had public health policies to prevent cirrhosis. There was heterogeneity in the existence of public health policies to prevent NAFLD-related conditions, such as diabetes, 88% of the countries, hypertension, 82% of the countries, cardiovascular diseases, 82% of the countries, obesity, only 53% of the countries, and dyslipidemia, only 35% of the countries. So there were few efforts to monitor disease burden due to NAFLD, no registries, and also scarce effort to raise awareness in the Americas. The countries with the highest number of public health policies were Brazil, Colombia, and Mexico. However, there is a crucial lack of planning and implementation of public health policies in the Americas, and we found that even high-income countries such as the USA or Canada have no established national public health policies addressing NAFLD. This funding is concerning due to the high burden of NAFLD in the region that I told you, up to 30%. So regarding national guidelines on NAFLD and related conditions, only 35% of the countries have published national clinical guidelines for NAFLD. And four out of six with the national guidelines were those with the highest number of public policies. So Brazil, Colombia, Mexico, and Argentina. And finally, regarding management of patients with NAFLD, awareness and monitoring, the foremost, especially in charge of the diagnosis of NAFLD, were gastroenterologists and hepatologists, followed by internal medicine specialists, then diabetologists, and then primary care providers.
For example, Brazil, Chile, and Mexico have a wide range of healthcare providers to manage NAFLD. By contrast, Haiti and Honduras have only one healthcare provider for patients with NAFLD. Moreover, only five countries, so 29% of our sample, have referral algorithms for diagnosis and management of patients with NAFLD. and 13 countries performed disease donor liver transplantation in 2019 with a median disease donor transplant rate of only 1.7 per million inhabitants. So countries with the highest transplantation rate were USA, Canada, Argentina, and Brazil, and notable three of these countries without liver transplantation were available. Also were the countries with the lower number of public health policies on NAFLD-related conditions. These were Honduras, Haiti, and Guatemala. Just five countries out of 17 had national campaigns to raise awareness and inform the population about NAFLD. And seven countries, so 41%, have a registry of disease burden due to NAFLD. This is important because basically, if we are not worried about NAFLD and we are not developing guidelines, patient awareness or campaigns, we will not have more complex things such as liver transplantation for these conditions. Sure. Thank you so much for summarizing that. I mean, I think it's really clear that there are some big holes, some bigger than others in certain countries, but on the whole, a lot more work to do. How does that public health policy landscape then, how does that contrast with other regions? So this lack of NAFLD public health policies was also described in Europe in an European study in 2020, in which none of the 29 include countries had written strategies or action plans for NAFLD. And as far as I know, there is no additional studies covering other regions of the world. So basically, the lack of awareness in NAFLD and public health policies is a global issue. Interestingly, in our study, national clinical guidelines addressing NAFLD were reported only in 35% of the countries, which is low and concerning, but it's comparable with the European study. They have 34% and we have 35%. The development of NAFLD clinical guidelines is not trivial and must be encouraged since the adequate diagnosis, surveillance, and management of this patient with NAFLD could help to stop the progression of the disease. Sure. I mean, I think you also touched on it a little bit there, but what are the real kind of implications of your findings? What do we actually really need to do to improve the situation and get things better? So the main implication is that public health policies are urgently needed to address this public health problem globally, not only in the Americas. And a barrier to access to healthcare systems such as living in rural areas or poverty and low availability of liver transplantation in several countries in the Americas also contribute to increasing the burden of novelty. Other several barriers to access could be associated, for example, with substantial socioeconomic inequalities, which are very present in the region of the Americas, and it are very different, especially in Latin American countries. Which are the solutions? Well, multiple aspects could be developed to improve the prevention, screening, and treatment of NAFLD. The development of a written national plan to decrease NAFLD could have an impact and is easy to do, similar to other public health issues such as alcohol consumption. Indeed, the development of national plan could reflect the commitment of the countries to reduce the health consequences of NAldi. These policies could be established as separate documents or include broader public health policies, including clear responsibilities, objectives, strategies, strategies, and who needs to take care of what, you know, because this is not only for doctors. It's the food company, it's the beverage company, it's the alcohol company. So we need to have multiple stakeholders. And the other thing which is very important is how we prepare for NAFLD. This is the new epidemic. So this is a relevant aspect and contributes to preventing and managing the burden of NAFLD. So it is crucial to increase awareness about NAFLD and advocate to the development of public health policies for NAFLD, which could be facilitated by frameworks, especially designed for this purpose. So in conclusion, our study shows that there is absence of public health policies addressing NAFLD and there is low awareness of NAFLD and its consequences in the Americas. Thank you. a clear call for action and encourage the development of national policies against NAFLD and national guidelines to decrease the burden of NAFLD. Obviously, each country needs to tailor their own public health policies. Mediterranean diet is not for everyone, you know, because they will need to adapt that to the cultural issues, ethnic issues and socioeconomic issues. Dr. Arab, thank you very much for giving us that fantastic overview of your study there and really some strong messages to end on, I think. Thank you very much for the invitation and I invite everyone to read our article if you have done it. Thank you very much. Take care. Bye-bye. You can read the health policy piece on NAFLD in the Americas online now at thelancet.com. Thank you to Dr. Arab and thank you for listening to this episode of the Lancet Gastroenterology and Hepatology Podcast in conversation with. Remember, you can subscribe to him in conversation with wherever you usually get your podcasts.
From the JAMA Network, this is the JAMA Network Open Editor Summary, a discussion of the most important articles published in the latest issue of JAMA Network Open. Here are your hosts, Fred Rivara and Steve Finn. Hello, podcast listeners. This is Fred Rivara, Editor-in-Chief of JAMA Network Open. And here, as always, is my friend and colleague and Deputy Editor, Steve Finn. We'll talk with you today on Veterans Day, November 11th, 2020, here in the United States. And we're going to talk with you about COVID, sort of a year review of what we've published in COVID. I just looked at some of the statistics on the Johns Hopkins website in the Institute for Health Metrics and Evaluation. And as of today, there are 51 million cases of COVID in the world, which includes 1.2 million deaths. In the United States, there are 10 million cases. And as of today, 240,688 deaths. Texas, which is one of our largest states in the United States, has so many cases of COVID that if it was a country in the world, it would be the 11th ranked country in terms of the number of cases. So we're really seeing multiple hotspots here in the United States. And our Institute for Health Metrics and Evaluation here at the University of Washington projects that if nothing changes by January 1st, there'll be 328,000 deaths in the United States from COVID. So we all are feeling this, and across all the globe, we are feeling this. Now, we at the Journal have been seeing this. We have had a marked increase in the number of papers submitted to our journal, and most of that has really been due to COVID. In the first nine months of 2020, we received 7,055 manuscripts, and 41% of those were COVID-related papers. Our acceptance rate overall is now 17%. For COVID papers, it's 8%. So we're being pretty careful about what we've accepted. I'm going to talk with you today about some highlights of the papers that we have accepted. The first one we'll talk about is a paper that discusses a problem that we in the United States are really very concerned about, which is the whole problem of increased incidence and increased death rates in Black people and low-income people in the United States. Steve, do you want to just maybe talk about that for a second? Yes, Fred. The first paper is by Adhir Kari and his colleagues, and they looked at the prevalence of COVID and COVID-related deaths in counties according to their income and found that non-white residents and in the poorer counties, there was an eight-fold greater infection rate and a nine-fold higher mortality rate in counties that were not predominantly white. And just to put that into perspective, the higher rate was over 30 deaths per 100,000 versus three per 100,000. So massive differences, and they persisted, as you well know. Right. And we have a call for papers right now on systemic racism and health. And I think that the conclusions around the country are that what's happened here with our problems with racism and poverty in the United States is that these populations have a much higher rate of comorbidities, diabetes, heart disease, and that's really what's causing this increased death rate. In terms of the increased infection rate, I think these individuals live in more crowded housing. Some of them are doing essential jobs, whether it be working in hospitals or driving buses or working in grocery stores, and so their exposure to COVID is higher and they can't prevent that exposure and not work. Yes. I mean, there are some counties which the serologic evidence of infection is as high as 70%. Wow. That's really amazing. I know that people talk a lot about some of the ultra conservative Jewish communities in New York City where they have very high rates of COVID. And speaking of these counties, we've published another paper, which was an interesting study. It compared border counties in Iowa to border counties in Illinois. And the reason that this was of such interest was that the two states had quite different approaches to shutdowns and uses of masks. Iowa, the governor there, really did not have a stay-at-home order, did not emphasize the use of masks, while in Illinois, there was an emphasis on staying at home and use of masks. And what they found is that in these counties where it's just really separated by the border, there was a much higher rate of COVID in Iowa than Illinois, and 30% of the cases in Iowa in these border counties. So, Fred, one of the other studies that we published, as you know, had to do with pooling of specimens, both to make testing more affordable, but also an acknowledgement of the limited testing supplies that exist in many places. And that continues to be the case. As you well know, this country has lagged seriously in testing. It's amazing this day and age, it still does. Yeah. But the idea of pooling, of course, is that if you put several samples together and the entire sample is the entire test specimen is negative, you can make the assumption that each of those individual samples was negative. But if it's positive, then you need to go back and rerun each of the contributing specimens. And obviously, as the number of specimens in a testing sample grows, the likelihood that it becomes positive grows with that. And one of the papers we published looked at the optimal way in which to combine these specimens in pooled specimens. And they found that you could reduce the number of individual tests by 84% by pooling samples of up to 13 patients, which would make a huge economic sense, particularly in places where frequent testing is being performed. As I went back and looked at that article, one of the assumptions was that you could do that if the prevalence of COVID in the community was 1%. Well, you know, you mentioned Texas. You know, we now have states, which Texas is one, with prevalence rates of up to almost 20% now in terms of testing. So I don't know how relevant at this point in time in our country, this notion of pooling really is anymore. Well, one area where it might be relevant is the next article we want to talk about, which is college campuses. So we had this really, I think, very important article that was published early on here. And it looked at what's the optimal testing for colleges to employ when they bring back their students. And this came out in the late summer before college students came back on campus. And they tried to look at, you know, colleges need to stay open because students need to be educated, but also financially they have to stay open. And so these individuals undertook a modeling process where they tried to figure out what would be the optimal testing frequency for colleges to employ. And what they found is that, you know, depending upon what the effective reproduction number is, is that screening college students every two to five days is probably the best strategy, the most cost-effective strategy. And I know that a lot of colleges now are, in fact, testing students. They test them all when they come to campus, and some of them then keep those students in quarantine and then retest them 14 days later when they first come to campus, and then are retesting them weekly or randomly sampling students to test weekly. So there is a lot of testing on college campuses, and most college campuses which have done that have very few cases of COVID. You know, and I wonder whether our nation's schools, K-12 schools, ought to adopt the same kind of a testing strategy. Yes. But as you know, there's a great deal of variability across college campuses. And when you don't follow those strict protocols, it's clear that those colleges become hotbeds for infection. And as you well know, at our own university, we had an outbreak of COVID that affected, I think, more than 100 students related to fraternities and sororities. Yes. I mean, it is a problem. And, you know, my daughter works as a college counselor at a school back in New Hampshire. And, you know, she says it's tough on the students because on the one hand, they don't want to get sick. They want the college to stay open. But on the other hand, you know, there are 19, 20, 21-year-olds that want to hang out with friends. And it's really tough, and particularly if they're telling these kids to stay in their rooms. You know, the dining halls are closed. The students pick up their meals at the dining hall, and then they're supposed to go back to their rooms to eat. So it really is a big problem of knowing what to do. But one of the other studies that was really important, I think, was our study on a randomized controlled trial of hydroxychloroquine.
Yeah, actually it was of chloroquine, which is, you know, a closely related compound. And this was early on when there was a lot of hype, as many people will remember, about chloroquine and hydroxychloroquine from the highest quarters of our nation. But there were very few studies done. And there were some early studies that were small and not well done, to be honest, that gave what appeared to be signals of efficacy. And there was a lot of enthusiasm. And we published a study, a randomized control trial from Brazil. And they took what would now be thought of as very high doses of chloroquine. But again, I think in the early days, we didn't know much about dosing. We didn't know much about toxicity. And they didn't want to underdose the drug and base the doses on some theoretical evidence of what might be effective. And they started a randomized control trial. They were going to randomize a couple hundred patients, but by the time they got to 81, they realized that actually those patients were doing worse than the patients who were not randomized to chloroquine. The trial was complex. In those days, patients were basically getting everything that was thought to be possibly effective. So they were getting azithromycin and oseltamivir. But even so, the mortality rate of the high dose was huge. It was almost three times higher than the controls. And the trial was stopped. And as we know, subsequently, multiple other trials have also been conducted. And we now know that both hydroxychloroquine and chloroquine have no effect and actually may be harmful. Right. And it really, I mean, I think this was a triumph of science here, you know, where the use of this clearly was ahead of the science. And then when the science was conducted, it really showed that the drug was not effective under any circumstances, whether it be prophylactically, treatment of myopatients, treatment of severe patients, and then the fact that it could be harmful. And we're seeing this with other drugs too, as you know, tocilizumab, you know, there's remdesivir, which for which there was huge excitement, which, you know, may be somewhat effective, but, you know, I think there's a lot of rethinking about the role of remdesivir and antibodies. So, you know, right now we're still in a situation with the exception of corticosteroids in severely ill patients, which do appear to lend some benefit. We still don't have effective therapies. Right. I mean, it's ironic that, you know, a drug that is used a lot for a lot of other diseases, dexamethasone, is the one thing that has shown to be effective. It's been available for a long time. It's relatively safe, used in short terms, and it's cheap. And one of the other things that we've all seen across the world is the psychological impacts of COVID on people living in cities during lockdowns, people in schools not being able to go to school, but also among healthcare workers. And we were one of the first people to publish a survey of healthcare workers. This is a study that came from China, 1,257 healthcare workers in 34 hospitals in China. And it found out that 50% of these individuals had symptoms of depression, 45% had anxiety, 35% had insomnia, and 70% had varied degrees of distress. You know, this was, I think, a very important study early on. It's actually had 481 citations so far by other papers. There have been subsequently a lot of other studies which essentially said the same thing. And, you know, I think that's reassuring, though, is that healthcare workers, if they are using proper PPE, for the most part, have had very low rates of hospital-acquired infection, that most of the healthcare workers who have been infected have acquired their disease in the community and not in the hospital. Well, I think that, you know, there's many other papers that we have. Please go to our website, JAMAnetworkopen.com, and you can see all of these papers here. Just type in COVID at the top in the search bar. You can see all the papers we publish. We are continuing to publish these papers. We publish five days a week. Thank you for listening to this podcast. You can go to jammanetworkaudio.com and listen to all the podcasts produced by the JAMA Network. Thanks very much. Take care and be safe.
Hello and welcome to the Lancet podcast. Richard Lane here on Friday, October the 14th. This week, a themed issue on surgery and I'm delighted to be joined to discuss this as I was last year by one of my colleagues, Dr. Bill Summerskill. Bill, welcome. A great issue and a variety of content. Perhaps we could kick off, I think, with the editorial, which I know you had a lot to do with. This is looking at the fundamental issue, really, isn't it? A key issue with surgery, and that is the whole business of risk in the non-cardiac setting. What was the sort of thrust for the editorial? Well, this was looking at outcomes in England, Richard, and it showed that really for the general surgical patient, the non-cardiac surgery patient, that increasing age and comorbidity really results in serious risks. And there's what's regarded as a forgotten group, these people who have greater than 5% risk of death from surgery. One might think that that would be a very high-risk group of particular individuals, but in fact, just somebody who's aged 50 or over and has one coexisting condition, such as diabetes, would be put into this category, as would someone who is aged 50 but having to have an emergency surgery. So it's looking at how non-cardiac surgery can be made more safe, the same way that we have worked on improving outcomes in cardiac surgery. It looks at the fact that surgeons don't operate in isolation but are parts of complex teams and hospitals are complex organisations. One of the great aids is having the good anaesthetic support and intensive care unit care for a patient afterwards. So that's another issue that comes up and of course has enormous resource implications for the UK because to offer the safest service, one would want to be able to analyse the risk of a patient during their entire journey through hospital, which means having the personnel available to do that, the diagnostic facilities to support it, rapid access to operating theatres rather than having to wait until late at night, and a choice of different levels of post-operative care. Do you get a sense in this country, and maybe beyond as well, that we are moving forward in this area because the criticism has been historically, and this journal has written about it extensively, that one of the problems with surgery is that there hasn't been the evidence base from randomised trials that you would have with, say, the use of a drug as an intervention. With surgery, it's always been more ad hoc and there's been great heterogeneity with the approach of different surgeons working in the same areas. Do you think we're making progress? I think we are making progress, Richard, on a number of counts. And that's why we shouldn't be too alarmed by this report. We should be alarmed by the findings. But actually, this is how change begins, with a report that identifies a problem. What would be alarming would be if the report was not acted on appropriately. To really improve care, it's looking at the different components of care. Now, this is stopping the heart during surgery, and that's a common procedure. It's done in cardiac bypass surgery, it's done in the pulmonary arteries and that is kind of a myth-busting paper that shows that actually you don't necessarily have to keep circulation going to the brain when the body is cold, providing it's for limited periods of time. Other papers in the series look at surgery for refractory epilepsy, the types of people in whom you get good results for that, and then one looking at just the kind of risk factors that might underlie the Royal College of Surgeons report of mortality in non-cardiac surgery. This report, which comes to us from the Lebanon, actually uses data from the United States and shows that anemia, no matter how mild, is actually associated with a far greater risk of morbidity and mortality afterwards. And then the final paper, which is a debate-stimulating paper, looks at the variation of surgical care at the end of life. We know that there's an enormous variation in medical care at the end of life. And I believe that in the United States, there's a figure of about one in five people will end their life in a high dependency unit. And here they found widespread variation amongst people on Medicare as to the number of procedures and the timing of procedures towards the end of life. I suppose where the role of evidence comes in is not to hamper individual care, but to help to give us some understanding about when these interventions are going to be most valuable for people. Thank you, Bill, for that overview. And of course, I will just also ask you, we publish a series in the issue which has obviously a strong surgical theme, and that is to do with transplantation. Can you just give us a very brief overview of these papers? There's a lovely collection of three papers in the green section of the journal on transplantation. But actually, the great introduction to that comes from a piece in the perspective section where it goes back to the origins of organ transplantation. And for anyone interested in the history of medicine, this takes us back to 1894 and a surgeon called Otto Lanz. And the whole proposal of what then would be quite fantastic, that one could transplant organs in the body. And that actually accompanies our whole change from the view of the health of the body as a complete whole with certain balances, onto a more contemporary vision of replaceable parts. In the series, there are three papers. The first one looks at a perennial problem with transplantation, which is how does one achieve self-sufficiency of organ donation? That's also a point that comes up in one of the editorials on a report launched by Nuffield. The other two series papers look specifically at kidney transplantation. One of them is really, I suppose, dedicated to keeping the transplanted kidney healthy. How to do that? And the other one, keeping the transplanted recipient healthy, being aware of the fact that cardiovascular disease is such a problem in people who receive a kidney transplant and ways to minimize that. But you know, throughout the whole issue, I think there are pieces that people are going to find interesting. I was fascinated by the technology section, which shows just how high technology is transforming surgery. And surgery is such a big part of our Thank you. and the importance of surgery and its renaissance as a serious research discipline from which we hope to be able to report more and more research developments in the future. Many thanks indeed, Bill, for that really superb overview of the issue. And it is a terrific issue. And as Bill says, most of us have connections with surgery in one way or the other. So I think it's a particularly important themed issue that will be relevant to many people, core Lancet readers and listeners to the podcast as well, who may not be Lancet subscribers. It's a terrific issue. Do enjoy reading it. But in the meantime, many thanks to Bill and to you all for listening. We'll see you next time.
Hello and welcome to our latest podcast for the Lancet Digital Health. I'm Christina Wayman and I'm delighted to be joined today by Professor Søren Brunac to talk about his work that has been published today in the Lancet Digital Health, which is on the development of a model that can use long-term disease history and acute admission data to predict mortality in patients admitted to intensive care units. Professor Brunac, thank you so much for joining me today. Thank you for calling me. So what inspired you and your group at the University of Copenhagen to embark on your project, which has been published today in the Lancet Digital Health? And can you tell us a little bit more about predicting outcomes in patients who are admitted to intensive care? Yeah, first of all, this is a difficult task because the patients are so different. It's a very heterogeneous patient group. So there is a large mortality, of course, in the group. And it's also important because decisions are made at intensive care on whether to continue the treatment. It's costly and so on. So in my group we have this general interest in patient histories and their sort of diagnosis as they have been given over many years and this is clearly a type of health data that are underutilized today. These disease histories are collected in registries and people are doing a lot of nice research on them, but these data are not really used at the bedside. So that's one of the motivations for this study. Can we extract information from the previous history that actually can can add for example to survival predictions and of course also many many other things but it is a key problem I think in healthcare today that we are not good at exploiting the data we actually have on the patient because they're hidden in some database, but could they actually be plugged in via, say, a social security number, be plugged in in a sort of individual level way in an algorithm, we would be able to do much better, I think. And this is also what this work is showing, that there's actually a lot of information in relation to survival prediction in these historic data. That's great. Thank you. Can you tell us a little bit more about the machine learning model that you developed and validated to predict in-hospital mortality? Yeah, so we are using a machine learning model that actually is quite simple. It's what is called a feed-forward neural network that is trained with backpropagation, as it's called, and it is shown and depicted in figure one in the paper. So there will be an input layer that receives the encoding of the previous disease history and also encodings of all the vitals and other features that are picked up during the first 24 hours of admission. So we are essentially in the input layer in the network combining different time scales because we have the fine-grained data for the 24 hours, but then we have tested up to 20 years of prehistory on the other side. So we are really aggregating timescales in the information we plug into the neural network. And then all these features, they are fed to so-called hidden units that are connected to the input features. And then the whole idea with this architecture is that the hidden units are then connected to an output unit that will give you a survival score. And everything is connected. Every feature is connected to every hidden unit. And that means that you can pick up any correlations. You might have the age or you might have a specific laboratory value, bilirubin or something like that. And then that can be analyzed in relation to how correlated it is to a previous diagnosis. That could be lung cancer or it could be also or something that might have happened 10 years ago or 15 years ago. So this relatively simple architecture is actually quite powerful because it can pick up any correlations. It's mathematically proven that such an architecture can pick up any correlation that you have between the input features. So one should also remember that this is, of course, not a network that picks up dynamics. It receives the disease history. It receives the data from the 24 hours, and then it gives a survival score. So it's just a static model that then can be compared, for example, to the conventional survival scores that are used in intensive care today. For example, the SAPS score. So the comparison we are making in the paper is really between these traditional scores that are based on data from 24 hours and a little bit of disease history with going sort of all in to the previous disease history of the patient. So the architecture is quite simple and not a complicated dynamic neural network. So how will your model predicting outcomes for patients in ICU shape clinical research and approaches to emergency patient therapy? I think that this kind of work will really emphasize the value of disease history information. Actually, when the patient arrives at the doorstep of the ward, one can already, based on the previous disease history, without measuring anything on the patient, actually produce a score from these disease history data. And that is new. And of course, that concept can be used in intensive care, can also be used if you are having a baby and you would predict a risk of, for example, having sexual or something. So the disease history is something that actually can be used in many different contexts. But here we are, of course, using it in intensive care. So I think that's mainly what we add here. Of course, there's a lot of work being done on how one measures all kinds of high-frequency data in intensive care and converts that into survival scores and so on. But here, the main message in this paper is that there is actually a lot of gold in the prehistory and the history of the patient. So from your model, there are many variables that can be considered important when a patient is admitted to intensive care. These include previous admission, laboratory test results and severity of disease and others as well. Which did you find to be the most predictive of both positive outcomes and negative outcomes in patients? Yeah, we've made a quite detailed analysis of that. And there we are also helped by the fact that we are using a quite simple neural network architecture. So it's actually easier to interpret and explain. That's a hot area in machine learning. One would like to sort of convert the black box into something that you understand. And in figure four, we try to rank those features that actually are most important for the network and not surprisingly the age of the patient is really the most important. If you're old, the chance of you dying is higher. If you're younger, it is lower. But even a feature like the age, you can try to look into where are the nonlinear correlations between age and other features. And this is also shown in figure 4, that there are some diagnoses where the age is sort of correlated with those diagnoses in relation to the prediction, for example, metastatic cancer. But then there's the length of stay is also important. There's the urinal output. If it's low, then, of course, it's not surprising that the chance of you dying is higher. So in figure four we sort of show across these ten most important features whether they are dragging you towards survival or non-survival as the feature is high or low. But there's also serum urea, there's bilirubin that I already mentioned and so on, minimum serum creatine, and these are sort of the highest ranking ones. One should, of course, not forget many of the other ones, but they are most sort of bang for the buck here in terms of the error that you make in the network if you remove them. So it's a nice way of also giving something back to the clinicians. Are there correlations they did not think of? And in the paper, we also describe some of these correlations to previous diagnoses that maybe were unexpected. So what are the future implications of your study? How would you like for your research to be taken moving forward? Yes, I think that this discrimination we often make with health data between live patient record data and data that are being transferred to research registries that might in the end and maybe some years into the future, I predict that it will go away because we will use and need to use a lot of the data that we see in the research registries today directly at the point of care. And as I said before, this is just one example. I mean, that's also what irritates people, patients often in healthcare, at least in my country, that the hospital system cannot remember the past of the patient. The patient or the family, they have to describe the prehistory to the doctor. And of course, if you are not having any family to follow you, you are often in a bad situation. So if you can pull it out of a database, then you could maybe also democratize healthcare in that sense that actually it doesn't really matter whether your daughter or son will go with you to the hospital or you come alone because the information needed will actually be pulled out of a database.
So what are some of the unanswered questions then regarding your model that you see as, say, 24 predictions every 24 hours and dynamically based on the high-frequency data that you pick up on the intensive care award, make a more dynamic prediction that could be used in decision support. Of course, then the disease history would not change. It's the same, but there would come a new prediction after one and a half days and two days and so on. And I think that's really also what is needed in these wards that you simply during the admission you plug the data into the algorithm. So that's one of the perspectives and we are also working along those lines because we have all these dynamic data in the work we publish here in Lancet Digital Health. We stop after 24 hours, we plug the data into the algorithm, but of course we have the high frequency data for the entire admission and we think we can squeeze more out of that and I think also many other groups work across along these lines. Well thank you so much for joining me today and to discuss your fascinating study that you're publishing with us in the Lancet Digital Health and thank you to our listeners for tuning in today. Thanks very much. Goodbye.
Hello out there. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, the Journal of the American Medical Association. And this week I'm going to tell you about this February 25, 2009 issue of JAMA. As usual, I will start with the cover, which this week features a painting by Sean Scully, who was born in 1945, and bless him, he's still alive. This painting is called The Wall of Light Black. It was painted in 1998, and it's an American painting. However, Mr. Scully was born in Ireland and then moved to the United States. This is not one of my favorite art paintings, but hey, different strokes for different folks. The first article deals with evidence underlying the ACC AHA practice guidelines. Clinical practice guidelines typically include ratings or categorizations that reflect the objective quality of the evidence supporting the guideline recommendations. Thank you. to September 2008 to assess the evolution of the guidelines and the distribution of recommendations across class and levels of evidence. In their analysis, the subset of guidelines with at least one revision or update by September 2008, the authors found that current recommendations were largely based on lower levels of evidence or expert opinion and reflected a lower level of certainty or class compared with earlier guideline versions. In an editorial, Drs. Torrance Schoenefeld and Robert Senter from the University of Alabama in Huntsville discuss potential bias and other limitations in the guideline development process and in the utility of practice guidelines in clinical practice. The JAMA patient page has information for your patients about evidence-based medicine. The second article deals with diabetes and perinatal depression. Individuals with diabetes have an increased risk of depression compared with the general population. In a retrospective cohort study of low-income women who gave birth in 2004 to 2006, Dr. Kathy Becks-Kozamanil from Harvard Medical School and colleagues examined the association between pre-existing diabetes and perinatal and postpartum depression. In this sample of low-income women who were continuously enrolled in Medicaid for six months prior to delivery and through the first postpartum year, the authors found that compared with women without diabetes, women with pre-pregnancy or gestational diabetes had a significantly increased risk of experienced depression during pregnancy and postpartum. The third article deals with assessing antiretroviral therapy after incarceration. The United States prison system may offer the first opportunity for some individuals at high risk of human immunodeficiency virus, that's HIV of course, infection, to receive screening and treatment. However, the likelihood that treatment will continue after prison release is not known. To address this question, Professor Jacques Balagian from the University of Texas in Galveston and his colleagues reviewed medical and drug assistance program records for 2,115 Texas prison system inmates who received antiretroviral therapy, that's ART, while incarcerated and who were released between January 2004 and December 2007. The authors found that only 5.4% of inmates filled the prescription for ART within 10 days of release, potentially averting a clinically significant treatment interruption, and only 30% fill the prescription within 60 days. The Clinician's Corner is a commentary on promoting more conservative prescribing. It's well known that patients may be at risk of medication-related harm if physicians do not adhere to appropriate prescribing practices. However, guidelines for effective evidence-based prescribing are lacking. To address this deficiency, Drs. Gordon Schiff from Harvard Medical School and William Galanter of the University of Illinois in Chicago present a set of principles that may guide clinicians in evidence based prescribing. These principles include consideration of alternatives to pharmaceutical treatment of disease, heightened vigilance for adverse effects, a cautious embrace of new drugs, rational drug utilization, and addressing barriers that interfere with conservative prescribing. There are three commentaries in this issue. The first deals with professional monopolies in medicine. This one was written by Drs. Mark Bayer-Loker and Dr. Alan Detsky, both from the University of Toronto. The second, defining and improving survival rates from cardiac arrest in United States communities. This one by Drs. Mickey Eisenberg and Dr. Bruce Psady from the University of Washington School of Medicine. And the third, The Feminization of Medicine and Population Health. This one was by Dr. Susan Phillips and Ms. Emily Austin, both from Queen's University, Kingston, Ontario, Canada. And A Peace of my mind, this one written by Dr. Ranjana Srivastava from Melbourne, Australia, quote, it's hard to believe that in this modern age, when there are seemingly inexhaustible ways of achieving a given outcome, we all draw a blank at Mr. V. And the title of this one is Dying to Talk. And medical news and perspectives. Although the United States Food and Drug Administration stood by its approval of ezetimib, simestatin, after reviewing data showing it reduces levels of low-density lipoprotein cholesterol, whether the drug actually improves clinical outcome remains unknown. The next article is growth in health care spending slows but still outpaces the rate of inflation. And the health agencies update sexually transmitted infections, tainted diet drugs, antipsychotic risks, and imported drugs. And from the Centers for Disease Control and Prevention, multi-state outbreaks of salmonella infections associated with live poultry in the United States in 2007, and outbreak of Listeria myonocytogenes infections associated with pasteurized milk from a local dairy, Massachusetts, 2007. We also have an editorial in this issue thanking and having great appreciation to the JAMA's peer reviewers and authors. This one was written by Dr. Phil Fontanarosa, the Executive Deputy Editor of JAMA, and me. And the readers respond, how would you manage a 76-year-old patient with multiple medical problems and recurrent clostridium difficile colitis? Go to www.jama.com to read the case and submit your response, which may be selected for online publication. The submission deadline is February 25th. And author in the room, we invite you to join Dr. Stephen Schroeder, March 18th, from 2 to 3 p.m. Eastern Time, when he will discuss smoking cessation in patients with psychiatric illness. That's it for this week. Thank you for listening. Please let me know if you have suggestions to make this podcast more educational or interesting to you. This is Dr. Kathy DeAngelis, Editor-in-Chief of JAMA, speaking to you from beautiful and frigid downtown Chicago, where the wind blows mightily, but our patients are always our top priority.
Welcome. This is Howard Bauchner, editor-in-chief of JAMA, doing my second podcast. Thank you so much for joining me. I'd like to highlight three papers that appear in JAMA this week. The first is on the effect of bronchoalveolar lavage in children with cystic fibrosis. The second is clinically relevant changes in family history of cancer over time. And the final paper appears in a clinician's corner and is entitled Novel Therapies for Septic Shock Over the Past Four Decades. With respect to the first paper, which focused on determining if bowel-directed therapy for pulmonary exacerbations in children with cystic fibrosis during the first five years of life provides better outcome than current standard practice. This study highlights the importance of randomized clinical trials. The study was conducted in the Australia-Asian Cystic Fibrosis BAL Clinical Trials Group. It involved eight cystic fibrosis centers. It was conducted between 1999 and 2009. In the study, 84 children were assigned to bowel-directed therapy and 86 to standard care. The general sense was that the more information provided by bowel with more aggressive directed therapy towards pseudomonas would potentially eradicate it so that at five years of age there would be a difference in pseudomonas coverage between the two groups. However, as is often the case, the more information garnered in the bowel group did not result in a lower prevalence of pseudomonas aeruginosa infection at age five years. In addition, in reviews of CT scans of the lung, there was no less structural damage in the intervention group. This study, once again, highlights the importance of randomized clinical trials and equally is important that more information, often with additional aggressive therapy, does not necessarily lead to better outcomes. The second study is fascinating. It's entitled The Clinically Relevant Changes in Family History of Cancer Over Time. It was conducted by Dr. Zygos and colleagues. I recall fondly when I was a medical student and then a resident, constantly being pimped about the importance of family history. I would often shake my head and go, well, is it really changing what I'm doing? And this paper and other recent research really indicates that knowledge of family history and equally as important, knowledge of changes in family history, likely impacts on screening for different types of diseases. This was a descriptive study examining baseline and follow-up family history from participants in the Cancer Genetics Network. There were over 10,000 participants in the study. The principal findings were as follows. For colorectal cancer, breast cancer, and prostate cancer, between the ages of 30 and 50 years of age, there was a significant change in family history, which would result in changes in screening for each of those disorders. The authors, as well as an accompanying editorial, highlights the importance of obtaining accurate family histories over time. This should be easier now than in the past because of electronic medical records, which should make it somewhat easier for the primary care physician and other clinicians to obtain accurate family histories. Other data now also suggest that family history impacts on other types of screening. For example, the rates of celiac disease in families can be significant. A family history of celiac disease probably suggests that other members in that family should be screened. Sudden cardiac death is another entity in which a positive family history would indicate screening. So whereas in the past I was unsure about the clinical significance of family history, both this article and other data that have emerged over the last decade suggest that an appropriately obtained family history could very well change the type of care that we deliver. And the last article that I would like to talk about is entitled Novel Therapies for Septic Shock Over the Past Four Decades. In this paper, which is presented as a grand rounds, characteristics of patients with severe sepsis or severe shock are presented. It's quite clear that therapies for septic shock have changed dramatically over the last four decades, and these authors review the over three dozen phase three clinical trials that have been conducted in patients with sepsis and septic shock. The reviews include trials that have examined endotoxin antagonists, intravenous immunoglobulins, high and low dose steroids, a nitric oxide synthase inhibitor, inflammatory modulating agents, and anticoagulants. Certainly none of these therapies are a panacea or a cure-all for septic shock, but a great deal of research has been conducted in this area, and Drs. Suffredini and Munford are to be congratulated for an excellent review on the last four decades of novel therapies for septic shock.
Hello and welcome to the latest episode of The Lancet Neurology, In Conversation With. I'm Sarah Passy, a Senior Editor at The Lancet Neurology. For our December podcast, I'm delighted to be joined today by Professor Rustam Al-Johi Salaman, who is Professor of Clinical Neurology at the University of Edinburgh and Honorary Consultant Neurologist in NHS Lothian, and whose meta-analysis entitled Effects of Oral Anticoagulation in People with Atrial Febrileation after Spontaneous Intracranial Hemorrhorrhage, or cockroach, was published online in October and is a now December issue. Russ, it's lovely to see you again and to speak with you today about your work. So first of all, can you please introduce yourself for our listeners and tell them a little bit about your work? Well, thank you very much, Sarah. It's a pleasure to be with you. And hello to everybody out there in cyberspace. Thanks for tuning in. So Cockroach is not only a bad acronym, Sarah, it's also an example of team science in modern research. So I'm really grateful to all the collaborators from either the completed or the ongoing randomized control trials who are all individually struggling to recruit enough patients to address the dilemma about whether to start or avoid oral anticoagulation for atrial fibrillation after intracranial hemorrhage. But collectively, even though each trial is a struggle in itself, collectively we'll have over 2,000 patients' worth of data when cockroach is all said and done in years to come, which will give us a really good shot at answering this question overall. Brilliant. So your paper was published online first, just in time for the World Stroke Congress, at which you presented the data from the Cockroach meta-analysis. Could you tell us about some of published in parallel with the conference. And that requires a huge amount of organisation from authors and editors, as well as very swift peer review. So thanks to you and the peer reviewers for making me burning the midnight oil come good in time for the conference. And I think it's that sort of thing, breaking results published at the same time, that really make these international conferences exciting, because it gives you the opportunity not only to hear practice changing research but also to have all the evidence there in a publication alongside it and there were a few other examples of people doing this at the conference as well as some examples of really exciting trials where we wished we could see all the data in full to fully interpret them but we don't yet have the full publications. So I suppose a big headline from the conference is the commission itself. So the Lancet Neurology World Stroke Organization Commission. So it might be worth talking about that if that's okay. Yeah, of course. Yeah. So I think it's really addressing the issue about the future burden of stroke. And we all know that survival after stroke is improving. And although outcomes for individual patients are getting better, the aging population, the expansion of the world's population means that the burden overall is going to rise. So although we've got a lot to celebrate about treatment of stroke, and that's mainly ischemic stroke, not yet intracerebral hemorrhage, there's actually a huge burden that we need to address. So the projection from the commission that stroke mortality is going to increase by 50% in absolute terms. That's huge. More than 6.5 million people per year in 2020 to almost 10 million a year by 2050. It's absolutely huge with corresponding increases in the disability adjusted life years as well. But the thing I like about these commissions and why it's important to hear about at the conference is it's not just quantifying the problem epidemiologically and in public health terms, it's making recommendations that are practical solutions. And it'll come as no surprise that the four pillars I agreed with, all about adequate surveillance, good prevention of stroke, which after all, as we all know, is the main thing we should focus on far better to prevent a severe disease than to try to improve it when it's happened. So surveillance, prevention, further improvements in acute care, and obviously, importantly, in rehabilitation to improve life after stroke. So I think your readers will find lots of valuable nuggets in there that they're very likely to agree with and they can use with policymakers, health services and their other stakeholders in their own countries to campaign to reduce the future burden of stroke on everyone. Yeah, brilliant. Yeah, it's really important commission. Really pleased with it. So let's move on to your article now. Could you tell our listeners about the Cockroach Project and how did it begin and why? So cockroach, as I mentioned earlier, is about oral anticoagulant drugs, but it's also about other classes of antithrombotic drug, antiplatelet drugs. And clearly, we worry more about the risks of bleeding with oral anticoagulation than we do with antiplatelet drugs. But it is a concern for both. And I guess all of this started back in, for me anyway, in the early 2010s, when, like many other stroke physicians, I was wrestling with the everyday clinical dilemma of a patient in front of me who has a history of bleeding and of clotting, and wanting to work out what to do about either of these classes of antithrombotic drug. And it's something we see in other contexts as well, with thrombolysis as well, where we worry about bleeding. So there are many different types of drug where this dilemma arises. I think that the fundamental, that the eureka moment for me was moving from a natural human position of worry about bleeding, what I call haemophobia, where none of us likes the sound, the sight, the thought of blood. And we're especially hemophobic about blood when bleeding has already occurred, and quite understandably. So it's the severity of bleeding and the way we feel about it that then makes everybody very nervous about using drugs that might increase the risk of bleeding to prevent clotting events. And so that's why I sought to do a randomized control trial, first of all, in a high-risk population, at high risk of clotting, of the lower-risk type of drug, antiplatelet drugs. And that was the RESTART trial, which we started in 2013 and was published in The Lancet in 2019. That was antiplatelet drugs after intracerebral hemorrhage in a high-risk population of people who'd already been on an antithrombotic drug because they'd had some kind of clotting disease like a myocardial infarction or ischemic stroke. So that, if you like, is where the issue started, focused on a bleeding disease and the lower risk type of drug, whilst also trying to keep a real world perspective, much like the Lancet's Commission on Stroke does, about what the fundamental underlying drivers of these diseases are, clotting and bleeding. We have to keep in perspective that aging, high blood pressure, alcohol misuse, cigarette smoking, poor diet, lack of exercise, salting one's food, all these things, interstroke has shown that those are the major risk factors for both bleeding and clotting diseases. So that's why I was concerned not just about the risk of bleeding again for these conditions, but also that we might be, perhaps by omitting antithrombotic drugs, missing an opportunity to prevent clotting problems that these patients are surely at high risk of. So whilst doing these trials, we've also been putting the observational epidemiological evidence in place to really get a good assessment of what the bleeding and clotting risks are for survivors of brain haemorrhage. So the whole story has kind of evolved in the intervening 15 years or so, but it started with restart and epidemiological research and then Cockroach arose later. Great, thank you. So could you outline for our listeners the key messages of Cockroach meta-analysis that we've just published? Sure. Well, Cockroach, just in case anybody's wondering what the acronym stands for, stands for the Collaboration of Controlled Randomised Trials of Long-Term Oral Antithrombotic Agents After Spontaneous Intracranial Hemorrhage. And if anybody can actually spot the letters that create COCROACH there, they've done really well as listeners, but you do need to see it written down. And the reason we chose this acronym was because it's been so difficult to do these trials. And our strapline, if you like, is you can't crush a cockroach. We are determined to resolve these therapeutic dilemmas, even though the individual trials are difficult to do. And that's where an individual patient data measure analysis really makes a difference. So the idea was hatched when I got a group of trialists together in this area in 2017 at the European Stroke Organization Conference. And we agreed to collaborate, thought ahead to how this would be done.
And what we've done in this first iteration of COCKROACH is bring together the four available completed randomized control trials of oral anticoagulation for atrial fibrillation after intracranial hemorrhage. There are several others ongoing, another five or so, that are either still following up participants or still recruiting, but the results of those trials won't be known for another four or five years. So in order to inform doctors and patients around the world about whether they should be taking part in the ongoing trials, we thought we should summarize all the available data from the four completed trials to date now, and then pause complete recruitment to the ongoing trials, and then do a further iteration of this in years to come. So hopefully I'll be back in less than a decade anyway to talk about that, Sarah. And the headline finding from this individual patient data meta-analysis is that although the effects of oral anticoagulation are uncertain on our primary outcome of any stroke or cardiovascular death, and they're uncertain overall as well as in individual subgroups, oral anticoagulation does definitely reduce the risk of ischemic major adverse cardiovascular events for intracranial hemorrhage survivors with atrial fibrillation. And that's a significant finding both clinically and statistically in the meta-analysis that wasn't shown individually by any of the trials until this meta-analysis was done. So what we can say to patients and their carers is we know oral anticoagulation has a really powerful effect for reducing the risk of stroke and other major adverse cardiovascular events in atrial fibrillation, whether somebody's never had an ischemic stroke before or if they've had an ischemic stroke. And now we can say we also know that it has the same benefit for patients with atrial fibrillation after intracranial hemorrhage too. But what we're still not sure about is the overall balance of bleeding and clotting, although it's important to note that amongst our secondary outcomes were hemorrhagic major adverse cardiovascular events, and there wasn't a statistically significant increase in them. And also that the overall effects on functional outcome remain uncertain. And doctors will be concerned about that. Going back to where I started with this on haemophobia, people are worried about bleeding because bleeding in the brain is the most severe type of stroke. So even though there might be numerically fewer bleeds during follow-up than there are ischemic strokes, any increase in a small number of bleeds versus a large reduction in a larger number of ischemic strokes has an unknown effect on functional outcome overall, because it may only take a few severe bleeding events to outweigh the reduction in ischemic events. But we really don't know what the answer to that is. And I think that's the most intriguing issue about this question. And I hope we'll be able to address that in the final iteration of this meta-analysis. Yeah. So it's important for these trials to finish recruitment and get the data out so we can quickly make progress with treatment of any disease, whether it's COVID or intracranial hemorrhage. So yes, I'm afraid this is another systematic review and meta-analysis that concludes that more trials are needed. But at least the good news about this one is that those trials are ongoing and they will be completed. The only uncertainty is how well they will recruit. And I think Cockroach really should indicate to all clinicians that there is every reason to keep randomizing and randomize as many people as possible so that we're not only confident in the overall effects of these drugs when the final meta-analysis is done, but we can also do precision medicine and work out what the effects are in subgroups of people. And that requires enormous numbers of people to be recruited to these trials. So yes, the messages keep on recruiting, but with good reason and evidence for why. And the final caveat to all of that, of course, is the correspondence in the Lancet from the Enrich AF trial about one of those subgroups that you might also want to discuss? Yeah, we can do if you like. Yeah, so the Enrich AF, they wrote in the Lancet, didn't they, about there was a one subgroup that stopped recruiting. Yeah, absolutely. So Ashkan Shwamanesh, who's the chief investigator of the Enrich AF trial, which is an international main phase trial addressing exactly the same dilemma as our individual patient data measure analysis. That's run from PHRI at McMaster in Canada, and more than 20 countries internationally are taking part. And they're looking at a doxaban or avoidance of oral anticoagulation, which could include anti-bladder therapy or nothing for intracranial hemorrhage survivors. And they've recruited well over 700 patients now, so they're the biggest ongoing trial in this area. And clearly, safety needs to be very carefully monitored in randomized control trials by data monitoring committees. And this is one of these rare examples where a data monitoring committee has watched the emerging data, and they haven't stopped the trial overall. They've looked at benefits and harms in subgroups and they've decided that two subgroups of patients should no longer continue oral anticoagulation and should not continue to be enrolled in the trial. And those two subgroups were people with low bar intracerebral hemorrhage, which has a higher risk of recurrent hemorrhage than non-lobar locations. And secondly, those with convexity subarachnoid hemorrhage, that spontaneous bleeding in the subarachnoid space, not due to an aneurysm, probably due to cerebral amyloid angiopathy, which also has a high risk of future intracranial hemorrhage. We don't know what the data show. It's just that the Data Monitoring Committee has given this advice. But they're obviously highly respected and trusted groups of individuals and will have made this decision with good reason within the ENRICH-AF trial itself. But it does create a dilemma for us because should we not even randomize these patients in the ongoing trials in order to be really confident about what the effects are, given that we're not actually able to see the data? And as far as I know, the data monitoring committees of the ongoing trials have not forbidden inclusion of this group of patients, and these people are still being randomized in the other ongoing trials. And I think, you know, I have to respect those data monitoring committees' decisions and they may have more information about what was found in Enrich AF than others do in the public domain, but they would have considered this carefully. And I think that is a one potential option for these patients in future to continue to be randomized in the other ongoing trials pending the Enrich AF result, because the decision was made on only a couple of hundred patients. We had just over a hundred patients in the cockroach individual patient data meta-analysis in this group, and we didn't see overall any evidence of harm in the two trials that could provide data on this, PsoStart and Apache AF. So that's the other advantage of having this IPDMA coincidentally being brought together and being published at the same time as the letter in The Lancet expressing the data monitoring committee's decision about the subgroup in Enrich AF because it allows us to see all the available data from published trials about this alongside a data monitoring committee decision in one trial. So this is the best we can get short of data monitoring committees of all similar trials sharing their emerging data and doing individual patient data meta-analyses as the trials go on. Imagine how complex that would be to do. But, you know, arguably, ethically for patients worldwide, if we could have a way across all data monitoring committees of monitoring all the emerging data as it's accrued, whilst you might compromise the ultimate size of individual trials, you would have in real time almost the combined evidence about safety of an intervention from all ongoing trials at one time and I think that's logistically very challenging to do and does compromise the integrity to a degree of individual trials but for me that would be if you like the idealistic version of this individual patient data matter analysis. So let's move on to the future. So obviously we know there's going to be another iteration of Cockroach in about five, six years' time, we hope. But what about the field? Where do you see the most important movement in the next few years? And also for yourselves, what are you up to? Well, the first question is easier to answer probably, Sarah. I'm a firm believer that in medical research, we need to be safeguarding its future by bringing on early and mid-career researchers. I feel very passionately about that. And I think a key thing about this area is that daring to go into it and ask the question, can we test antithrombotic drugs after intracerebral hemorrhage? It was a really difficult thing for me to do. I lost a lot of hair in the process. And I'm really grateful to more than 100 sites in the UK for completing Restart because it showed us surprising evidence of safety of antiplatelet drugs after ICH.
So those people who've set their own trials in motion are definitely part of the future story here. The second is thinking hard about this balance between bleeding and clotting events and the beneficial and adverse effects of treatment is something doctors have always struggled with. But there are many other contexts in which these dilemmas arise, whether it's, for example, after subdural hemorrhage, not just after the types of bleed that we see in stroke services, the neurosurgeons will be concerned about this too, whether it's people with microbleeds on MRI at times when we're considering thrombolysis and various other antithrombotic strategies in the future, and so on and so on. Of course, it doesn't always start with bleeding. There's also the issue of what happens if bleeding occurs after an ischemic event whilst on antithrombotic drugs. So I think I see us maybe daring to confront more of these dilemmas in other areas and a growth of interest in this area amongst the stroke research workforce that we need to safeguard for the future. And as to what I'm up to, well, I'm doing that sort of thing, really. I really want to bring on the next generation of stroke researchers. But the thing that's really going to keep me occupied until my retirement and lead to me losing the rest of my hair is the definitive main phase trial to follow restart, which I finally got funding for of antiplatelet therapy after any intracerebral, any spontaneous intracerebral hemorrhage, not just in the high risk group that was recruited to restart. So we're intending to recruit more than 4,000 patients to that starting in 2024 and maybe having the results available for the European Stroke Organization Conference in 2030 all being well. So I've made a note in my diary for a parallel submission of aspiring for about January or February 2030, if that's okay, Sarah. I'll pop it in my diary. Thanks so much for the advance notice of that. So thank you so much, Rustam, for such an interesting discussion today. There's so much else we could have talked about, but we just don't have the time. So you can read Professor Salman's article online now at thelancet.com. Thank you for listening to this episode of The Lancet Neurology in conversation with. And remember that you can subscribe wherever you usually get your podcasts
Hello, and welcome to Gemma Network Open Live. I'm Seth Truger, Digital Media Editor at Gemma Network Open. Of course, if you're following along live, please send us your questions or comments on Twitter at Gemma Network Open, or in the comment box on Facebook or YouTube Live. Today, we are talking about an interesting paper, the comparison of cardiac advance associated with zithromycin versus moxicillin, And we've got first author Dr. Hari Patel with us. Welcome, Dr. Patel. Thank you, Seth. Thanks for having me. Can you just start off by telling us in the audience a bit about who you are and what prompted you to do this study? Yeah, absolutely. So I'm an outcomes researcher and a pharmacist by training. I work for my own consulting company at the moment, which focuses on generating real-world evidence. But at the time when I did this research, it was actually part of my PhD dissertation at the university. And then the research was partly motivated by the fact that there was a lot of conflicting evidence and different studies that examined the same exact research question. So for the longest time, azithromycin was considered to be the safest drug or safest macrolide. But in 2012, there was a study that showed there was an increased risk among patients who were prescribed azithromycin. What this study found was that there was an increased risk of death as well. And then soon after this study, the FDA issued a warning, which cautioned the use of azithromycin. And then over the course of eight years, like I said, there's been several observational studies that looked at this, and they found either an increased risk or no risk with azithromycin. So based on this, what we did was we asked ourselves three questions. First, we asked if there was a change in cardiac risk factors among patients who receive azithromycin before and after the FDA warning. And what we found was there was no increase in the prevalence or decrease in the prevalence. So saying that the FDA warning didn't have any impact on the way azithromycin is prescribed. Secondly, we looked at a risk prediction model to help us identify some of the baseline comorbid conditions and especially specific QT prolonging medications that increase the risk of cardiovascular events with azithromycin. And then lastly, in this third paper, we examined the risk of cardiac events among azithromycin and amoxicillin users. And what we found was that in a large, so what we did was we used a large claims database to conduct a retrospective cohort study. And we used high dimensional propensity scores to control for confounding and we included almost 2 million patients who were prescribed azithromycin and matched those patients against amoxicillin users. And then we looked at the occurrence of cardiac events either arising from a hospitalization or an emergency room visit. And we looked at this risk at a 5-day, 10-day, and a 30-day period after patients had started on therapy. And we looked at several subgroups. We looked at patients who were elderly, patients who had cardiovascular disease. And we looked at patients who had the predictors based on our prediction model from the previous analysis. And so what did we find? We found that there is no increased risk in the overall population. But if you're going to be prescribed azithromycin with another QT prolonging medication, then you're going to experience at least a 40% increased risk in cardiac events. Yeah. So great. Thanks. That was a wonderful overview. But to hit some of the key points there, so you use the Truven market scan database, which is a really good database. It's got a ton of data. As you said, you were able to suss out about 2 million moxilin uses and 2 million patients who got azithromycin, which is a ton of data. As you said, you were able to suss out about 2 million moxillin uses in 2 million patients who got azithromycin, which is a ton of patients, 2009, 2015. You looked at all the different outcomes of syncope, palpitations, long QT syndrome, ventricular arrhythmias, cardiac arrest, and death. And then the three time points, 5, 10, 30 days. It's pretty impressive. I was honestly, one of the things that was most impressive is even that pretty expansive definition of outcomes, which includes, you know, just symptoms like palpitations, there were really small rate of events. It was less than 1500 or fewer than 1500 events, which was, I think if your math was right, or if I got your math right, it was 3.4 per 10,000, which is really exactly. Yeah. So, and then the reason why that number is low is you have to keep in mind that these conditions led to a hospitalization or ER visit. So, if you're taking azithromycin, you may experience palpitation and it may self-resolve and you could have other symptoms that you may experience. But if you haven't gone to the doctor or if you haven't gone to see an ER doctor, for instance, then we wouldn't be able to capture this. So what we're looking here is a very serious set of conditions that led to a hospitalization among azithromycin and amoxicillin users. That makes a lot of sense. And I also found it interesting that not only are the rates pretty similar, but the most common events that you found were syncope and palpitations. Syncope made up, I think, 70% of the event. Exactly. So 70% of the patient had syncope, 30% had palpitation out of those 1500 cardiac events that we had measured. Yeah. Interesting. And, you know, as you said, all the differences you found were not significant. The odds ratios were at five days, 1.08 at 10 days, 1.05 and 30 is 0.98. And they all crossed one, although the five day and 10 day were pretty close to one. And I think, you know, it would not be unfair to interpret this as a trend towards an increase, but with 2 million in each group and only, you know, 700 events in each group, that seems like a, a pretty low risk. If there's any there, even, you know, being, I'd say as a bias towards finding a difference as you can. Yeah, no, absolutely. I think you make a good point in terms of the risk is definitely rare, but among the patients who are prescribed these QT prolonging medications, that's a preventable risk that we want to highlight from this study is that if clinicians, especially even pharmacists who can counsel patients or monitor patients who are going to be taking these medications together. So let's prevent the risk that where we can. Yeah. And looking at the table, which unfortunately we can't show because it's too big, there's too much data here. The list of the QT prolonging drugs to me was really fascinating. It was, it looks like most of them are antidepressants. That's right. So there's over 200 medications that have either known possible conditional risk of QT prolongation and majority of them are falling into the category of antidepressants. So not all the antidepressants could be on the list, but the ones that have been previously linked with QT prolongations are the ones we had included in our study. That makes sense. That's also, I think, a useful category to just kind of think about, you know, if I'm going to prescribe somebody azithro or moxil moxilin, thinking instead of what are the QT-prolonging antidepressants look, are they on an antidepressant? All right, now is the T-prolonging one. Exactly. Replace typical questions with easy questions. Right. And then so one thing that's interesting to me, I think we all agree there's a lot of azithromycin that's prescribed, and a lot of it is probably prescribed for subclinical reasons, politely. But in 2019, the new pneumonia guidelines came out from the IDSA and ATS, and basically essentially replaced a lot of the most common indications for azithromycin, which was just for uncomplicated outpatient community-acquired pneumonia, with moxicillin. So So I think that could potentially provide a good natural experiment if a lot of people who otherwise would have gotten azithromycin are going to be getting moxicillin, theoretically, if people actually follow the guidelines. No, absolutely. I would love to set up that natural experiment, right? I mean, we're not going to find a better comparison.
Yeah. And I think, you know, forensic scores are great and you guys have a lot of data and a huge database, but, you know, there's so much potential for clinical nuance that just doesn't get into those databases that it's really hard to say. Absolutely. Yeah. I mean, one of the limitations is that, you know, we don't have the clinical severity of these infections or even the conditions for which these medications are prescribed, which could potentially, you know, result in residual confounding, as you mentioned. Yeah, and you know, I would say, you know, from my kind of initial gut is that people who get azithro instead of moxilin, where both would theoretically be appropriate, are probably more likely to be people we think are more sick. So even if they don't tick boxes that end up in a database that end up being more sick, there might be some nuance there. Who knows? I don't know. We'll see. But again, I think if nothing else, the low rate of events I found pretty reassuring here, which is great. Yeah, no, overall, like the message I would leave with is that it's a safe therapy. I think the risk, again, it's three to four in 10,000 prescriptions of azithromycin. But what's important is that one in five patients who receive azithromycin are on these QT prolonging medications. So that's where we want to drive the point home is that, you know, let's be careful when we're prescribing azithromycin if you especially have another medication that's going to prolong the QT interval. Yeah. And of course, when we say, you know, when you say it's safe, which I totally agree, it's in the appropriate patients from this cardiac arrhythmia point of view, you know, antibiotics, inappropriate antibiotic use exposes both patients and the community to all sorts of side effects. You know, some was between one and six and one in 10 people get diarrhea, one in six to one in 10 get yeast infections i mean stuff that's just really unfortunate plus the more serious things like c diff and of course antibiotic resistance over time as we you know quickly approach the post-antibiotic era yeah yep great well that brings us about to the end of the time anything else you wanted to add here no so i mean i just want to reiterate the point that you know if you're going to be taking azithromycin, more than likely you're going to be safe. But as a patient or a provider, if you happen to see those other QT prolonging medications, be careful. Let's try to avoid if we can. Let's monitor the patients who really need to be on these medications together. Certainly sounds very reasonable. So thanks again for this great work and thanks for joining us today. Great. Thanks for having me. Great. So that wraps things up for this episode. Of course, you can get this paper and more at jamminatworkopen.com where everything is free and open access. We've got new papers coming out every weekday morning at 10 a.m. Central Time and join us again next week on September 29th, 3 p.m. Central for another episode of J&O Live. Take care and stay safe.
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 JAMA Editor's Audio Summary for our December 10, 2019 issue. This is Howard Bauchner, Editor-in-Chief. I hope all of you are beginning to enjoy the holiday seasons, starting with the original research reports. The first, red blood cell storage and multiple organ dysfunction. Increased storage time of red blood cells may impair their oxygen delivery or adversely affect immune, endothelial, and hemostatic function. Spinella and colleagues randomized over 1,500 critically ill children and found that the use of fresh red blood cells compared with standard issue red blood cells did not reduce the incidence of new or progressive multiple organ dysfunction syndrome. The median age of the 1,538 patients was 1.8 years. The median storage duration was 5 days in the fresh group versus 18 days in the standard issue group, P of less than 0.001. There were no significant differences in new or progressive multiple organ dysfunction syndrome between fresh, 20.2%, and standard issue red blood cell groups, 18.2%, with an unadjusted absolute risk difference of 2%, minus 2.0 to 6.1 of P.33. The prevalence of sepsis was 25.8% in the fresh group and 25.3% in the standard-issue group. In an editorial, McQuilton and Cooper discuss the safety of international red blood cell transfusion practices for critically ill children. On to the second original research report, a genetic cause of amyloid cardiomyopathy. Hereditary transthyretin amyloid cardiomyopathy associated with a particular genetic variant, the TTRV122I genetic variant, is primarily found in individuals of African ancestry. Damrauer and colleagues conducted cross-sectional and case control studies of 3,724 and 2,307 individuals of respectively African and Hispanic Latino ancestry and found that this variant was significantly associated with heart failure. Overall, there were 1,376 cases of heart failure. The particular variant was associated with higher rates of heart failure. In the cross-sectional cohort, 44% in the carriers versus 30% in the non-carriers for an adjusted odds ratio of 1.7 and a P.006. In the case control study, it was 2.6% in the carriers versus 1.8% in the controls. Again, a significant difference. The authors conclude, among individuals of African or Hispanic Latino ancestry enrolled in two academic medical center-based biobanks, the TTRV1 to 2i genetic variant was significantly associated with heart failure. On to the third original research report, fertility treatment and cancer risk in children. Fertility treatment may increase the risk of cancer in children by mechanisms associated with fertility drugs or assisted reproductive technology. Hargrave and colleagues conducted a retrospective cohort study of over a million children born in Denmark and found an increased risk of childhood cancer associated with the use of frozen embryo transfer, but not with other fertility treatments. As already mentioned, compared to children born to fertile women, the use of frozen embryo transfer was associated with an elevated risk of childhood cancer, 14 cancer cases, a hazard ratio of 2.43, an incidence rate difference of 26.9 per 100,000, mainly due to an increased risk of leukemia and sympathetic nervous system tumors. The authors conclude, among children born in Denmark, the use of frozen embryo transfer compared with children born to fertile women was associated with a small but statistically significant increased risk of childhood cancer. This association was not found for the use of other types of fertility treatment examined. On to the clinical review and education section, and there's a recommendation statement and an evidence report from the U.S. Preventive Services Task Force. Starting with the recommendation statement, screening for abdominal aortic aneurysm. Risk factors for abdominal aortic aneurysm include older age, male sex, and smoking. The U.S. Preventive Services Task Force recommends one-time screening for abdominal aortic aneurysm with ultrasound in men age 65 to 75 years who have ever smoked. This is a B recommendation, but there are three other specific recommendations within this report. The task force recommends that clinicians selectively offer screening for abdominal aortic aneurysm with ultrasound in men 65 to 75 years who have never smoked rather than routinely screening all men in this group, a C recommendation. The task force recommends against, against routine screening for AAA with ultrasound in women who have never smoked and have no family history of AAA, a D recommendation. The task force concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for AAA with ultrasound in women aged 65 to 75 years who have ever smoked or have a family history of AAA, an I statement. Accompanying the task force recommendation statement is an evidence report, Outcomes of Screening for Abdominal Aortic Aneurysm. AAAs are often asymptomatic with slow expansion until possible rupture. Gerges, Blake, and colleagues reviewed 50 studies with over 300,000 participants and found that one time AAA screening in men aged 65 years or older was associated with a decrease in AAA-related mortality and rupture rates, but was not associated with all-cause mortality. There are two other articles in the Clinical Review and Education section. On to the first, Clinical Management of Constipation. Causes of constipation include motor disorders of the colon, defecation disorders, and adverse events associated with the use of drugs. This JAMA Insights article by Wald reviews treatment options for individuals with chronic idiopathic constipation, irritable bowel syndrome with constipation, and opioid-induced constipation. And the second short and related article in this section, Opioid-Induced Constipation. In the Shama Clinical Guidelines Synopsis of a 2018 guideline developed by the American Gastroenterological Association, Rao and colleagues discussed the medical management of opioid-induced constipation. Before wrapping it up, I want to mention that there's an audio author interview. Pascal Carrion, who's the author of The Viewpoint, Improving the System to Support Clinical Well-Being and Provide Better Patient Care, discusses this report with me in a 20-minute podcast. In addition, as always, I've interviewed a member of the U.S. Preventive Services Task Force, in this case, Michael Barry, who discusses with me the task force recommendation statement entitled, Screening for Abdominal Aortic Aneurysm, U.S. Preventive Services Task Force Recommendation Statement. It's a helpful podcast because he walks through it quite systematically. Screening for men who smoke, screening for men who don't smoke, screening for women who do smoke, and then screening for women who do not smoke. And wrapping it up with the rest of the content, and as I've already mentioned, there is a viewpoint that reflects the recent report from the National Academy of Medicine by Carrion, Cassell, and Zhao entitled Improving the System to Support Clinician Well-Being and Provide Better Patient Care. The second viewpoint entitled, Is Transcultural Psychiatry Possible? by Greenard, Kane, and Correll. And the third by Cohen and Torres, The Potential of Object Relations Theory for Improving Engagement with Health Apps. And the fourth by Gelid and Good, Adelamumab and the Challenges for Biosimilars. There's a piece of my mind hiding in plain sight. And two research letters. The first, Primary Care Spending in the Commercially Insured Population. And the second, Hepatitis C Virus Antibody Testing Among 13 to 21-Year-Olds in a Large large sample of U.S. federally qualified health centers. Thanks so much for listening. This is Howard Bauchner with JAMA. For more podcasts, visit us at jamanetworkaudio.com. You can subscribe to our podcasts on Stitcher and Apple Podcasts. Thank you.
Hi, and welcome to In Conversation With, a podcast from The Lancet Microbe. I'm Senior Editor Rebecca Barksby, on this episode I'm talking to Dr. Erika Furmeister about how access to safe water and sanitation is associated with antibiotic resistance. Dr. Erika Furmeister is an Assistant Professor in Environmental and Occupational Health Sciences and Environmental Engineering at the University of Washington in the United States. Her main area of research is on the environmental transmission of pathogens. But the topic of our conversation today is a paper by Dr. Vermeister and colleagues entitled Evaluating Community Water and Sanitation Access and the Global Burden of Antibiotic Resistance Using Human Fecal Metagenomes from 26 Countries, an Ecological Study. This paper was published in The Lancet Microbe in June 2023. Welcome Erica, it is a pleasure to have you on this podcast to talk about your paper. So I wanted to start by asking you to clarify what you mean by water and sanitation and how are these connected to antibiotic resistance? Thanks Rebecca for having me. Yes, so water and sanitation have very specific definitions. They are set by the Joint Monitoring Program for Water Supply and Sanitation, which is a WHO UNICEF program that monitors progress towards global drinking water, sanitation, and hygiene goals. These goals are set by, it's called the Sustainable Development Goals. There's 17 of them that are adopted by the UN member states, and goal six is for clean water and safe sanitation. So towards these goals, there's different definitions of safe water and safe sanitation. So improved water is defined as a water source that's protected from contamination. It could be like a protected well or sandpipe. Improved sanitation is sanitation that separates human waste from human contact. So examples of that are like a flush or pour flush pit latrine, a ventilated improved pit latrine. These are kind of the older definitions that were for the Millennium Development Goals, and now we've moved to what's called safely managed sanitation and safely managed drinking water. Safely managed water is defined as an improved source that's accessible on premises, available when needed, and free from contamination. And then safely managed sanitation is improved sanitation where excreta are safely disposed of on-site or traded off-site. And so we use the older definitions because progress towards safely managed sanitation, essentially the data isn't there yet because these are newer definitions. So we went with improved water and improved sanitation for our paper. And then your question of how does this relate to antimicrobial resistance? So antibiotics are excreted in human waste in urine and feces, and so that applies selective pressure for the development of resistance. Also in human waste, we can have the excretion of antimicrobial resistance genes or resistant organisms, especially in people who are taking antibiotics. And so if you think about how transmission occurs, like similar to enteric pathogens, if we don't have barriers in place, a new host can ingest antimicrobial resistant genes or antimicrobial resistant bacteria. So improved drinking water and sanitation act as barriers essentially to prevent transmission of antimicrobial resistant genes and antibiotic resistant bacteria. There's also one another way in which they're linked and that's people who don't have access to improved drinking water and sanitation tend to have a higher burden of infectious diseases and therefore tend to consume more antibiotics. Sure. So with that background, could you please describe your study design of your paper? Yeah, so we were interested in this link between the burden of antimicrobial resistance in the human gut and access to improved drinking water and sanitation. So for the first part, this burden of antimicrobial resistance, we decided to look at publicly available human fecal metagenomes. What's a metagenome? It's basically all the sequencing data that comes from when you extract all the DNA that's in a fecal sample. So if you extract the DNA and then sequence that, you get your human fecal metagenome. And so we looked for publicly available sequencing data from primarily low and middle income countries. We also included some higher income countries in there. And then authors of the paper contributed additional metagenomes. In total, we got around 1,600 metagenomes from 26 countries. And then for the second part of what we were looking at, which is improved water and sanitation, we used publicly available household data sets that are from MIX, which stands for Multiple Indicator Cluster Survey, which is a UNICEF program, and then DHS, which stands for demographic and health survey, which is a USAID program. And both of them collect country-level data generally on well-being, but these surveys are also used to monitor progress towards those development goals that I talked about in my previous question. And so there are household data sets where there are questions on what type of drinking water source do you have and what type of sanitation do you have. So we looked at the location of where these fecal metagenomes are from and looked at the same geographic location in these surveys and linked them up to define basically the percentage of people in a defined area that have access to improved drinking water and sanitation. So those are kind of the two pieces that we looked at. We have this household survey data that tells us the fraction of people who have improved drinking water and sanitation. We have these fecal metagenomes that we align to databases of antimicrobial resistance genes to calculate abundance of resistance genes. And then we use generalized linear models to model the association between the two. We also looked at some other things like what are the most abundant families of bacteria? What's the relative abundance of different antimicrobial resistance genes by drug class, all in WHO-defined regions around the world. So before we go on to what your main findings were, could we just go back to the metagenomes? Because you used metagenomes that were all publicly available online. Was that just through searches on databases? Yeah, so we searched the SRA, the Sequence Read Archives, and took metagenomes that are available through that. Yeah. Okay, so now that we've established your methods for your paper, could you please go through your main findings? Yes. So when we look at the abundance of resistance genes by region, we found the highest abundance of antimicrobial resistance genes in Africa and Southeast Asia. When we looked at association between access to improved drinking water and sanitation and abundance of ARGs, we found that with basically higher access, so more access to improved drinking water and sanitation, the lower abundance of antimicrobial resistance genes, and this is controlling for region and population density. This is an interesting finding because if you look at the association between improved sanitation with antimicrobial resistance genes alone and improved drinking water and antimicrobial resistance genes alone, there wasn't a significant association. So it's really the combined access to improved drinking water and sanitation where we see this lower abundance of antimicrobial resistance genes in the fecal metagenomes. So how can these findings be used to inform future policy or research? Yeah, so for policy, there are national action plans for combating antimicrobial resistance. And right now, even outside of these national action plans, I'd say the primary method of combating antimicrobial resistance is through stewardship, which is essentially through education, reducing demand and usage of antimicrobials and making sure it's like appropriate prescriptions for antimicrobials. And that's great. But there's also other ways to think about combating antimicrobial resistance. And so our results suggest that we should be including community-level drinking water and sanitation in these plans to combat AMR. And providing improved drinking water and sanitation is beneficial for many other reasons, like other health benefits. It's also important to have, you know, we have the right to safe water and to have a dignified place to use the restroom. So I think, you know, outside of our findings, it is not a bad thing to be providing improved water and sanitation. But yes, so we think that they should be included in these national action plans for combating AMR. And if you look at the current national action plans, very few of them mention water and sanitation. Some mention water and sanitation in the context of healthcare settings, which is also great. But what we really are interested in is including WASH in communities. Yeah. And then in terms of future research areas. So this was an observational analysis of secondary data. And so it would be good to look at this causal if there's a causal relationship through more carefully designed studies that are specifically for this purpose of looking at the association between abundance of resistance genes, or just you could also look at antimicrobial resistance in a different way and access to improved drinking water and sanitation. So you looked at the available metagenomes, but a lot of the research that we see currently is wastewater surveillance. But that wasn't something you looked at. Could you expand on why? Yeah, so wastewater surveillance is great, definitely supportive of that. However, especially in low and middle income settings, not everyone is connected to sewer systems.
And, you know, 1,800 or 1,600 metagenomes is also not representative of everybody. So I think it's just important to think about what is the question you're trying to ask. And we definitely do need more representative sampling from low and middle income countries. Yeah. I mean, as you say, improving access to water and sanitation has got so many other health benefits, not just the ones you're talking about in your paper. How do we improve that access? Because it can't, it must be quite a difficult thing to actually do. Yes, that is true. We have been trying to figure this out for decades, right? Like it's not a new problem. We have known that water and sanitation are important for health for a very long time. I think the question is like, how can we do that in an economically feasible way? And that includes investment from governments and a lot of different parties. I think people want improved water and sanitation. It's how do we have enough money to provide it for everyone? Yeah. Yeah. Just like all health interventions, I think. So what is next for your research, both related to this paper and outside of this paper? Yeah that's a good question. So I just started as a faculty member at UW and so one thing that we're working on is some of the topics that you've mentioned today which is wastewater surveillance for antimicrobial resistance. So we're looking at ways of sequencing resistance genes so that we can tell what allele or like what version of the gene we have present in our sample. And then one, just one final question. Your paper is described as an ecological study. Could you please elaborate on what that actually means? Yes, good question. An ecological study is when we have this aggregate exposure measurement. So we have aggregate measures of wash. And that's why it is an ecological observational study. So finally, could you tell us what were the limitations of this study? Yes. So to me, the main limitation is that it's an observational analysis. There's data limitations in that the data that we have on antibiotic usage is not great. You know, how do you measure that? We don't have data on safely managed sanitation. As I mentioned before, it's still a relatively new definition, and therefore we haven't implemented surveys in every country to measure progress towards safely managed sanitation. And the quality of improved water and sanitation can vary substantially, and we're trying to capture that with these survey questions. But, you know, these are just, I would say, pretty like shallow questions. And we can't really capture the nature of what is the quality of the improved water and sanitation. So definitely data limitations are a big part of what I would say are the main limitations to this analysis. Yeah. Yeah. In the surveys, when they're asked about antibiotic use or health kind of seeking behavior, do you know if they have any part of it that looks at where the antibiotics are sourced from? I'm only asking because we were at a talk recently about substandard and falsified medicines in low and middle income countries. I was just wondering whether, do they collect data on where they get the antibiotics from? No, and they don't even really collect data on, you know, if they're using antibiotics. like, I believe it's DHS. They ask the question as it pertains to like, if you're reporting an illness, then I believe the follow up question is like, have you used any treatment methods? So yeah, like, there are not antimicrobial usage questions included in these surveys. Because I think one issue is that a lot of times people don't necessarily know what they're taking or like you know where it came from it's like oh that's you know that's just like the thing that I get from my neighbor when I feel sick or yeah it's I would say there's a lot of like casual or maybe the word is unregulated use. So you are the first author on this paper, but you are not alone. You have got a lot of people on there with you from a lot of countries, it seems. So could you tell me about your research group, where you're all from, what your backgrounds are and how you came together to get this paper sorted? The co-authors of this paper are a collection of authors that have worked together before, are interested in this topic, particularly those who are even authors of some of the studies that we found through our search of publicly available metagenomes. So we have authors from around the world, from Peru, Ecuador, India, Kenya, Ethiopia, the UK, and the United States. Excellent. A true international collaboration. Thank you very much for joining us on this episode of In Conversation With. I think your paper is really interesting. It adds a different element to antimicrobial stewardship, less about reducing the use of antibiotics, but making sure that antimicrobial resistant genes aren't circulating as much in the environment and in water. So I think it's an exciting study. It's great to have it with us. And I'm so glad that you came on the podcast. Thank you so much for having me, Rebecca. I really appreciate the opportunity to chat about this paper. Great. Thank you so much. You can read the paper by Dr. Fairmeister and colleagues online now at thelancet.com. Thank you to Dr. Fairmeister and thank you for listening to this episode of In Conversation With The Lancet Microbe. You can subscribe to the In Conversation With series wherever you usually get your podcasts. you
Hi, and welcome back to Sharp Scratch. You're listening to episode 69, Can You Learn Empathy? This is a podcast brought to you by the BMJ and sponsored by Medical Protection, where we talk about all the things you need to know to be a good doctor, but that you might not necessarily get taught in medical school. I'm Pat, I'm the editorial scholar here at the BMJ, and I'm also a medical student at Anglia Ruskin University. And today I'm very pleased to be joined by our good friends Lily and Izzy. Lily, would you like to introduce yourself? Yeah, hi, I'm Lily. I am a final year in East London at Barts and I literally have, I have this week left of medical school organised placement and then I'm done. It's all just finals and like my elective and stuff so I'm in a weird a weird headspace nice to see you guys yeah that's crazy because yeah you're starting in August right yeah so we start at the end of August and then yeah I start F1 on the 1st of August I guess so it's like the final year is perfectly a year oh gosh, gosh. I'm in shock. When do you finish at uni? So, yeah, I'm also a final year. I'm at Nottingham. I have another four weeks of organised placement. Then my exams are March and April. And then I have elective TTP, which is like our transition to placement practice module. And then, yeah, doctoring life, if I pass my finals. Which you will, of course. I mean, mine's not dissimilar. I started my final year, though, at the beginning of July, so I'm feeling a bit hard done by it. Wow. It's just been going on so long. Yeah I think Barts might have a short year because technically I've organised teaching it's August to February, March and then after that it's just exams and elective and a huge gap which in theory should be on a holiday but due to the rising heating costs I can't afford it. I just turned off the heating, I can't afford heating I just have like blankets on. Well yeah always nice to have you guys back and I'm also excited to introduce our expert guest today Dr David Jeffery. David would you like to introduce yourself? Hi I'm David I'm a retired palliative care doctor and former academic mentor at Dundee Medical School involved in student support. And when I finished that job, I went and did a PhD exploring empathy in medical students and that finished in 2018. Yeah, I actually, I'm just halfway through the book that you wrote based on your thesis and, you know, I'm very intrigued by some of the points in there so yeah very looking forward to our conversation today. So empathy is ingrained into the brains of medical students from the very beginning is the cornerstone in medical school interviews you know there will always be an MMI station or panel question asking you to provide an example in showing empathy or explaining the difference between empathy and sympathy. So I thought in this episode we could delve a little bit deeper into the phenomenon of empathy. You notice our empathy increase or decrease over the course of our training, anything that may act as a barrier to empathy and what may enhance one's empathy. I know the definition of empathy is drilled into most medics' minds, but I guess just a quick reminder of what empathy is. It could be encapsulated as standing in the person's shoes and understanding things from their position. So Lydia and Izzy, as you both mentioned earlier, you're both final year medical students. And I suppose, just reflecting on your medical school career, do you think you've noticed any differences in, I suppose, the empathy that you express? I don't know. I mean, I remember one of my first lectures, the dean of our medical school said, we always find that by fifth year, the students have less empathy than they did when they were first year. And I remember thinking, that's a bit strange. I won't do that. And I mean, comparing back to my first year, I mean, mean I don't think I see much I hope I don't see much difference but I wonder if you did it on like a scale like did a like validated method of screening of working out actually the actual levels of empathy whether they would have changed because I think I view a lot of things with a very different perspective now than I did back in the day but I mean I think of it less as putting myself into someone else's shoes I think and I think of I think of it more as a understanding someone else's perspective but not saying oh I know how that feels it's I can understand how that might feel because otherwise there's a danger, I guess, of taking it away from the patient and putting it onto yourself, which I think is probably something that I've noticed a lot more, especially after my psychiatry placement, the language you used there was really important. So that's just like a five years of empathy in a minute. yeah yeah I find this question so difficult I was listening to your lecture about empathy I think about your PhD when you did it at Dundee and I listened while I ran this morning and you said something about how you noticed that the clinical students finished the degree feeling more empathetic and I don't know if I feel that way I think yeah with some patients I think I now I have more of a kind of long longer experience now with medicine I definitely feel kind of a stronger sense of understanding what's going on for them and being able to really kind of delve into their life story so in in that case, I do have moments, especially in A&E, which is my placement at the moment, where I feel real connection that I don't think I could have felt in first year. However, me and my friends talking about this, maybe last year, about how a patient coming with abdominal pain in first year, my initial perspective would have been like, oh gosh, that's awful. I wonder what it is what it is whereas now it's okay that's most likely not that awful let's hope it's let's rule out the bad things and it probably won't be bad so there's kind of a I kind of come from a slightly different perspective now which I tried to kind of fight I don't want to be assuming patients are I don't want to be assuming patients are... I don't want to assume patients' pain is disproportionate to the pathology. But I wonder if medicine kind of teaches you to expect that. So they're the two kind of opposing people in my brain. Yeah, definitely. And yeah, I guess, David, you mentioned that you did a PhD on empathy in medical students. What were your findings in terms of do medical students' empathy decline throughout the training or do they just kind of stay the same or fluctuate? Well, I think it's a difficult thing. I think one of the problems that I struggle with is that you were mentioning before about empathy scales and measuring empathy. I think empathy is such a complex construct or experience that it's kind of artificial to measure it. You know, what are you actually measuring when you try and have a scale? You might be empathetic one day, you might be moving house and not feel empathetic the next day. You're the same person. So the main sort of change that I saw with students was at the beginning, they were kind of fixated with either you were, you know, I am empathetic or I'm not empathetic. But by the end, by the time they were doing their final years, they could see empathy more as a relational thing between two people. This was something between two individuals. It was a relational construct. It was something that, it wasn't something I had or you hadn't. It would depend it too. It depends on really whether, does the patient want you to be empathetic? You know, will the patient, does they want, do they want to disclose this stuff to you? Do they want to share feelings? So measure, I have problems with the measuring of scales and most of the work done on empathy has been on a thing called the Jefferson Physician Empathy Scale. And there have been hundreds of studies of measuring that. And that does show a dip in empathy. But certainly my study, just as you both have been saying today, you felt empathetic all the way along. Certainly some students identified barriers that made them hide their empathy. They still felt they wanted to connect with patients but their work environment kind of stopped them doing it. I don't know if that's your experience. That's why I struggle to put it into words so much. I was saying scales of empathy because it's so, so qualitative as opposed to quantitative. Can you measure it honestly? Yeah, as you said, how do you measure empathy? And also your empathy or just emotions could change, fluctuate every day, right? Depending what you're experiencing on the day.
And that really isn't great because you need to show communication skills in OSCEs. But because I have an agenda of my own that I need to get through, I need to do this task, this task, this task in 10 minutes and do it well. I sometimes, you know, you need to remember that the patient also has their own agenda, which in order to realise, you kind of have to be empathetic. Because a lot of it, they drill into us, you know, ideas, concerns and expectations, which is, you know, the pinnacle of trying to get to the bottom of what the patient actually wants from the consultation. And're not going to understand the patient enough I don't think if you don't actually explore that with them and sometimes I find that when I'm in a rush with these OSCEs or if for instance I know that my own GP's in a rush I can notice it myself like when I'm the patient I can spot it because instead of like open questions it's closed questions just trying to get to the bottom of a point as opposed like the medical side of it as opposed to you know the whole biopsychosocial I can put it into both see both perspectives from there and ideally by the time my OSCE is coming a month in a bit, I'll have worked this one out. I think David made a good point that the context in which you come from will make a massive difference. If you're moving house or you're going through a life event and things are stressful anyway, you go into work or you go into placement and it is just a bit harder to kind of grab that sense of deep understanding with a patient you don't really have the emotional resources to do that and then on the flip side when you wake up and you have an incredible day you're having an amazing week and the sun is shining and you stroll into work you feel like the most empathetic person in the world you feel like Mother Teresa like you feel like you could solve everyone's problems and I wonder if trying to find a way to be baseline empathetic even if you're having a bad day I think that's kind of the the kind of life's work of a doctor I wonder yeah like on yeah going on to the point about the baseline of empathy, do you think most medical students come in with a certain level of empathy? And do you think throughout medical school, do you think we get, like, be given, you know, different skill set or tools to enhance that empathy? Well, I think, as David said, it is relational. It's a thing that you do. And in some cases you perform, being a bit more cynical. So I think it's hard to kind of say that a person is or isn't empathetic. And then it's hard, like, I mean, as we've kind of all now expressed, it's a really hard concept to measure and grasp and kind of have a concrete idea of whether it increases or decreases and I wonder if we actually posed it as David does as something which you can learn and practice and co-construct with patients that becomes more doable and more feasible whereas I think lots of medical students have this idea that if they are not inherently empathetic whatever that means they're never going to be there there's no point I'm going to be a surgeon instead I'm not good with people they kind of forget the concept as a whole which I think is a failing of medical school although it's actually medical school trying to encourage empathy they kind of almost discourage it and people who it doesn't come naturally to them and if we kind of I wonder if expressed it as a like a practice I wonder if we'd be better able as teaching to teach students how to do it just as a side note I'm sure there are some lovely empathetic surgeons out there but I think I'd agree with that it can be taught learned I think you probably do have to have a baseline level to be able to learn it maybe I don't know David correct me if I'm wrong but I'd say that you know the fact that all the medical schools are jumping towards MMI style of interview is because you can get role plays in there and you can see how someone interacts with a situation that they don't expect or know how to deal with. And so whilst they're thinking about how do I solve this problem, which has been faced with me because, you know, role plays can come in all weird and wonderful varieties. I think to be able to have this baseline level of empathy that you don't have to really think about is a key I guess attribute of successful interview candidate but I think I think everyone has the capacity I don't think it is something that I don't know I could I really do believe that everyone has the capacity to be empathetic and I think interviews have a get a snapshot so you're right the people who are the best at practicing or performing or doing empathy, whether that's real or not, they will get the offer for the medical school place, yes. But I don't think that means the people who get rejected don't have the capacity. They just haven't been given the tools and the space and the encouragement. Well, I think one of the things that was interesting, I think that Izzy was talking about OSCEs and certainly the students I spoke to in my study all felt that OSCEs were an act. I mean, you're often with a simulated patient who's acting and you under pressure of time are acting as well. So this kind of sort of fake empathy of you know nodding forward and saying the right things and holding the hand and so on and this wasn't real empathy at all and the other pressure that was on was assessment because the students I spoke to felt very strongly that as soon as they felt they were being assessed, their empathy went out the window. They started to think, am I doing the right thing? Am I doing this? How do I get these marks? So kind of if you've engendered in your medical school a competitive, stressful sort of culture, that isn't going to work to help people's empathy. And I think the thing that does help that you've both alluded to really, and I think particularly Lily was saying there is that what students I found really valued was having the chance to be with the patient, see them perhaps reflect afterwards with an experienced clinician without being assessed. know we would talk to someone who wasn't saying going to give you a mark out of it or or humiliate you afterwards but to try and encourage you and so on i think that's one of the most powerful ways of increasing uh your your empathy um particularly in areas of emotional regulation, particularly when it comes down to sharing emotions with patients. They found that if they could talk to someone else afterwards, they found that very, very helpful. I think I actually really struggle to remember the OSCEs, that they're actors. I think I'm just trying to think of myself in my OSCEs and I think of the probably from last year's easiest memories and I actually I think I think of them as real as real patients and I kind of forget that they're acting so I wonder if that kind of that and I do my OSCEs are by far my best exam I wonder if that kind of helps me um i kind of lose the connection between fake and real i don't know i'm the opposite oscars my worst exam because i get overwhelmed with this this is assessed this is not a normal clinical environment i'm not comfortable here and it reflects i think um so i'm looking forward to that coming up no i think that think that's a really common experience. And I get really nervous and I definitely don't, I don't think I perform exams as well. But I think that's a really common experience. I think OSCEs are a bit arguable. I think also this kind of idea of forced empathy, whether or not it is actually forced, could reflect know practice as a doctor when you're older or in your career David where you find people who um you know have lived experience of a condition um and this whole debate around lived experience you know is it valuable to have lived experience as a doctor does it make your practice better and I'd say well you can you you definitely be able to be able to have more empathy but not everyone actually uses it as empathy and sometimes it turns into this is about me I understand where it's coming from and it adds a different dimension certainly to your practice which can or cannot be beneficial but when I'd say you base your practice around the fact you have lived experience is that empathy or is that making you just giving yourself a unique selling point a USP and turning it actually into more of a force thing, because you feel like you have to keep up pretenses. I don't know if you've thought about cases like that, David, or if it's just medical students, but I think in the near future, that's something that's going to become very evident as more and more people, you know, begin to open up in the medical world about health conditions and things.
But the key thing you're saying is I think that the hallmark of empathy is that your attention is other-directed. It's directed at the other person. You're interested in the other person's perspective, and it's not self-directed. So that if you're retaining a self-directed view about your own illness and stuff like this, you could end up burdening the patient with your story of your own illness. So you're quite right with that. They have to be careful. But the key is that your perspectives are interested in the other person. It's not about me. It's about you. How do you feel? Because in empathy, you're trying to see it from their point of view, not how I would feel in their situation, because that leads to distress and burnout. What you've got to try and achieve is having the imagination to see what's it like for this person. And clearly that can be very difficult. The students identified many different types of patients, particularly you mentioned there mental health patients, obese patients, alcoholics, whole groups of people who they found it quite difficult to empathise with. And I think this is a place where the humanities can help a lot. I think within reading, drama and so on, that you can get insights from other things that can inform your imagination. David, a bit of your work found that students found a barrier to empathy was kind of time and feeling like to be a good, efficient clinician, you can't really be too empathetic. And I found that point so resonant. I once had a doctor say to me a couple of years ago, an amazing doctor, and he said, notice how the patient makes you feel because that will make you a better doctor and i thought that was just such a great kind of argument against people who would argue that you can't be empathetic and be a good efficient doctor um in that actually if you can be aware of your own emotions which requires you to also be listening to the patient properly and notice how they make you feel, do they make you feel worried and sad and actually a bit alarmed? And actually that's a really good indicator of how unwell they are. And that therefore will make you a better clinician because you have got to the point quicker. So I understand how they feel that and I would feel the same, but I think that's actually, like you say, it's a bit of a fallacy. Yeah, I think time, I mean, there's a huge problem between empathy and efficiency, if you like. But in fact, if you do spend that time, I think if you find that if you spend that time with patients, it's a tremendous investment, particularly the first assessment. If it's that first crucial meeting with someone, you just get that instinctive thing, can I get on with this person? Will I disclose stuff? And if you invest that time in the first place, then people will accept that maybe at other occasions you are rushed and you've got to be a bit shorter, but they know that you're the sort of doctor who will sit and listen to them. Of course, if you don't spend the time and you maintain what's called professional detached concern, in other words, you just stick to the cognitive stuff and don't go into emotions, you will never see that world. So there are some doctors who would never be aware of some of the aspects of suffering and existential distress that patients have because they never explore that. What do you think of doctors who can perform empathy so well that actually is patients do respond really well to those doctors? Because they definitely exist, but the patients can't tell that that doctor doesn't actually feel empathetic maybe it's not that common patients are actually intuitive but there definitely are doctors like that would you say that's kind of i don't know what you what would you think about that no i i think it's got i mean it's a difference which some people have aligned this to surface acting and deep acting. And that surface acting is where you don't feel the emotions or even a taste of the emotions of the patient. I'm not suggesting you feel all the suffering of a patient, but you kind of get a sample of it. But in surface acting, you're not doing that. You're doing as you're behaving as you are doing in an acting sort of way. And then there's deep acting in which actors actually feel the emotions. I would disagree. I think patients are highly sensitive to when a doctor cares about them or not, and as to whether they're being authentic or not. And not just doctors. I think outside when you meet people you can tell whether someone's interested and they're going to help you and want to do something and that you matter to them you know whether it's in the supermarket or the bank or anywhere you can just look at people and get a sense of whether they're going to connect with you so I'm not sure that faking it is actually going to fool many patients I think they're going to connect with you. So I'm not sure that faking it is actually going to fool many patients. I think they're very, very quickly onto that. I think also this whole era of COVID medicine, where a lot of things are over the telephone, a massive part of, you know, one of the first things we were taught in medical school was non-verbal communication. Telephone appointments take all of that out. So I was saying that sometimes I feel, oh, I like, oh, that doctor was a bit, you know, a bit rushed or seemed a bit harsh. I wonder if I'd had exactly the same conversation with them face to face over a video I would have had that same feeling because you can't tell if they're looking at the computer the whole time or if they're sitting there open you know in that three for tea like position which just makes you think actually what you know what is this pandemic doing to people's empathy what actually effect will it have on medical students coming through who have all these different experiences for instance my I've had two GP placements one in October 2020 and one in October 2021. I definitely saw about, in the first one, about 90% of the consultations were telephone. This one may be about 60%, the most recent one. But it still means that I've got a very different experience with general practice to someone who trained five years before me and would have seen hundreds of patients probably across the eight weeks. I could probably say I've probably seen about 25 in GP, which is just so different. I think that's a great point, Izzy. I definitely found on my recent GP placement, probably 70% were on the phone. My one thing is that although it's harder, it's definitely harder, it's also definitely not impossible. And there is absolutely a way to have an empathetic telephone conversation. But kind of, as you say, it is harder and it requires the clinician to really think about what their tone of voice is implying and pauses and what questions do you ask and how much time you give them I think I mean I'm sure you'd agree it is possible it's just harder and I think I got better as I went and actually towards the end I could really I really could connect with a patient over the phone having never seen their face they've never seen mine no body language at all but I could get that connection was at the beginning I found that harder. Well we'll discuss a little bit more about empathy in medical students but that'll be right after this message from our sponsor. it pays to be with Medical Protection. There's our free membership during your medical school years, our wealth of training resources to help you become the best doctor you can be, and our international experience that protects you during your elective, no matter how far from home you end up. In fact, there are many reasons why our members worldwide trust us to support and protect them throughout their careers. And if you're looking for one more, every week one lucky new joiner wins £183. That's the average student weekly spend. Just join for free and you're automatically entered into the draw. That's why UK medical students choose to be part of medical protection. You can are some barriers to empathy in our working environment? Lily's comments about learning how to empathise over the telephone because in a previous life I was a GP before I specialised in palliative medicine. You've done everything. I got booted out of everything, don't I? I was GP for something like 20 years, I found telephone conversations one of the hardest things to do with patients. And that it's only when you really knew patients well that I felt confident with dealing things over the phone, that I really needed to see people. And it was just interesting that you could develop this experience, Lily, with using the phone. And it's interesting, too, that patients want face-to-face consultations in spite of these telephone ones.
And obviously there are huge, gosh, huge political and philosophical impacts on who we think is worthy, which I don't need to go into today. But even like a tiny example of of like we had we did an ortho ward round when I was on Jerry's and the little old lady who never complains that's the patient that you listen to you give more painkillers to because she was an easy patient in inverted commas she was didn't make you feel kind of pressured and I think it's so it's sad but it does the patients that complain the most or the patients that are the most complicated they're often the patients I think I notice especially in hospital healthcare professionals are less likely or they're more reluctant to give them that time which is required to be empathetic um for me that's a really big kind of it's like an emotional barrier i guess it's not even anything to do with time yeah i think if we just butt in there i think that part of being empathetic is to strive to be non-judgmental you know and as you say it is it sometimes very difficult. One other way that people have approached it in the past that sometimes some of these patients that you're describing, Lily, were called heart sink patients. You know, people came with multiple diffuse symptoms which didn't really sort of fit in with anything that you knew. But sometimes sitting and discussing that with colleagues in a quiet way and reflecting on why does that make us feel uncomfortable, what's going on in the sort of balance group type thing, that can be very helpful in sorting that out. I think always sharing it with other people. I think it's one of the things in palliative medicine, we always worked as a team and we always discussed things and shared difficult problems. And that made those sort of situations a little bit easier. And people would have suggestions. We had a psychologist on our team and he would sometimes sit down, obviously he saw patients, but he'd sometimes sit down with us and suggest ways in which we might move forward in a consultation when we got stuck, as you were saying? I think that's a really great solution I don't think in my professional life I have ever seen a doctor discuss with other doctors or other healthcare professionals about their own reaction to a patient and why is it that it makes it yeah why are they complicated why are we reluctant to treat this patient or maybe reluctant to investigate things um i've only ever seen really very concrete dilemmas like oh this patient smokes they need oxygen let's get people involved to figure that out never have i seen actually we don't know what the issue is can we explore it i've never seen that done but i'd love to see that done the concept, isn't it? Yeah, but MDTs, I mean, the only ones I've ever watched are ones with concrete, like, yes, they might be complicated patients, but they're complex, like physiologically or like biologically, maybe even complex social problems, but we still, they're still kind of graspable, aren't they? I've never seen someone actually say, I don't know what it is about this patient that is making this difficult. People don't want to admit that. It's interesting, there's a French philosopher, Ricoeur, who actually looked at this and he said, we've got to try and move away from the idea of the competent doctor and the vulnerable patient and accept that both parties are vulnerable you know we all have we're all vulnerable and sometimes the more senior you are the more lonely and vulnerable you can feel you know so some of these guys in the very tops of things are actually very lonely people too and you need to remember that I think that's why because if you are going to engage in the emotional side of patients and feel some of their suffering you've just got to have someone that you can share that with and unload to you can't do it I mean all other specialties that involved with that like social services or counselling or nursing even, they all have nominated supervisors that they can talk. I mean, supervisor sounds an awful word, but they all have people that they can go and reflect with. So I think the things you were saying are very pertinent with that. And I think the things you were saying, Lily, about having a supportive team and colleagues you can go to in the firm is vital. It doesn't have to be a name tutor. It can be an informal thing. But you need to identify these people. Seeing your first death always encouraged you need to talk it out. You need to explore it with others. I didn't do that. And that's I regret because I thought oh I don't need to I'm fine and I was fine and then I wasn't and it's like it's because you know dying is that something you can empathise with? I don't that's maybe an exception I don't know. I used to work as a carer in my holidays like a nursing care assistant in a care home and I think how they treated death was so much more reflective of kind of who we need to be as people so what happened on the first time I saw one of our residents I didn't see them die but then be dead um the like ritual is that every carer who has worked with that resident takes turns and they go in either alone or with someone else and they get a bit of time. Most people actually talk to the person, which is kind of interesting. And they might stroke their hair. It's quite interesting. And then afterwards, in the handover, we all talk about that person who's died and we reflect on how it made us feel. And usually there's carers who are really affected. And then that enables us. So it's only about like half an hour and then we can then do the rest of our shift. And we're still really good carers who are really clinically competent. But actually, we can then do that job better and kinder and happier. And that's just so vastly different to how it's treated in medicine. I wonder if we just took half an hour when someone dies to kind of talk about it and let people kind of grieve in their own way. I don't know. I think that would, because really the empathy there is then for the family. That's like a really important aspect of death. I think we'd be better able to do that if we had ourselves reflected on the death already. And I think the ambulance service are one that are notoriously good for that because, you know, when you've watched documentaries about, you know, paramedics and, you know, they show like, obviously the extremes of their job, you know, not every day is going to be like that they show they show the highlights but they do usually come back to this point where they say you know there's been a maybe a a road traffic collision with multiple victims and you know some of the staff are told you you need to come to this meeting later so we can talk through it and that's something that I've seen in multiple trusts have that from when I've been watching this these series and things and so it's not impossible yeah I agree having a hot debrief is so important and I really like the example that you've given Lily with a I guess just having a closure and with that person that you've cared for I guess that will have been um shadowing doctors when you go and certify a death sometimes you don't even know the patient or um yeah or or sometimes um you just don't have the time to have that half an hour or something to really summarize and collect your thoughts yeah i suppose that people would like to leave work at work right You don't want to bring all the emotions back home with you. Otherwise, that would be too much. And yeah, that might lead to burnout, as you mentioned, David. I think one of the things that's important is that from medical educators' point of view, that it's really important that when, as clinicians, we're having difficult conversations with families or dying patients, that with the patient's permission, you have students alongside you so that they see and they can involve and then discuss these things afterwards as well. So I think quite often there's a tends to be situations where, oh, I'm going to have this very difficult conversation with someone who's requesting euthanasia. I'll just do it myself rather than actually think, well, this would be really useful for this student to come alongside and be with me with this, you know. So I think there is that. But I think your points that Lily was making, it's so vital to have a chance to talk about it. And some of the students I talked to were so distressed when patients died and they hadn't had any chance to talk about it. Even when they went back and asked about it, kind of they were told to sort of man up. Come on, this is medicine. You know, we don't do this. I mean, one one student described described. It's unbelievable. This described a cupboard in the ward that people went into to cry so that no one would see them cry. I mean, I found that absolutely incredible.
I remember one thing you said again, David, in that lecture I watched was about how you noticed that, or even you noticed or someone had noticed that doctors who employ more empathy and give time to their patients more, their job is is more rewarding they have higher job satisfaction and they have less burnout so to kind of address pat's point about we worry that if we empathize too much and take all those things home we're going to burn out and yes there is a balance between those things but i wonder if actually the cure the like the healing salve of burnout might actually be kind of empathy. Yeah, I think it's clear that there's a study by someone called Jackson on oncologists. They looked at people who were a group of oncologists who really stuck to the chemotherapy regimes, discussions and so on. And another group who went in to talk about impending death and dying and went into the issues with the patients. And the group that connected emotionally had much less burnout and stress and much more measured job satisfaction than the group that kept that detached concern. So as long as, come back, as long as you've got some support, then I think that this, I don't know, it's a sort of myth that I don't know where it comes from, this idea that to connect emotionally with patients is a bad thing. I don't know where that's arisen from, but certainly using detached concern and detaching from patients is not a good coping mechanism. You end up with more burnout and lack of job satisfaction. I think that's a really good note to end on. Well, David, thank you very much for joining us today. Well, that's all we have time for today. If you would like to hear more other episodes, please subscribe to Sharp Scratch wherever you get your podcasts. And in two weeks time, you'll be notified of our next episode while you wait for the next one do check us out on social media we are bmj student on twitter facebook and instagram let us know what you think about the podcast using the hashtag sharp scratch i'd love to hear your ideas for what we should cover later in the season it's also really helpful to ask if you can leave a rating and a review on wherever you get your podcasts as it helps element students students to find a show. Until then, we're looking for new med students to come join the panel. If you're a regular listener of Sharp Scratch and interested in being featured on a podcast, you can fill in the short application form, which you can find a link for in the show notes. In the past, the panel has consisted of med students studying in the UK, but recording remotely meant that we can extend this opportunity to med students studying abroad too. So please apply if you're interested and we look forward to receiving your applications.
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. When someone doesn't seem to know what's happening, it may be thought that they have some sort of cognitive problem, especially if they're elderly. Hearing loss can also cause people to seem confused. When someone can't hear very well, they may invest so much energy in trying to understand what's being said to them that they may appear confused. They may spend so much energy just trying to listen to the words that they can't absorb them. In a new study published in the January 16, 2020 issue of JAMA Otolaryngology, Dr. Justin Golub from Columbia University spoke with Dr. Michael Johns, the online editor for JAMA Otolaryngology, about his research examining the relationship between hearing loss and cognitive decline. I'm Dr. Michael Johns, online editor for JAMA Otolaryngology Head and Neck Surgery. Joining us today, we have Dr. Justin Golub, otologist, neurotologist, and assistant professor of otolaryngology head and neck surgery at Columbia University. He has published a thought-provoking study in this week's JAMA Oto Online First entitled, Association of Subclinical Hearing Loss with Cognitive Performance. Welcome, Dr. Golub, and thank you for taking the time for this today. It's a pleasure to have you with us. Well, thanks, Mike. I'm happy to be here. I just had a cup of coffee and I'm ready to go. Excellent. The findings of your investigation are very intriguing and build upon this growing knowledge base regarding hearing loss and its associations with cognitive performance. Can you give the listeners some background on the topic and what led you to perform this particular study? Sure. Well, as you may know, age-related hearing loss is one of the most common things that Odell-Aaron-Gadges deal with, and we typically have thought of it as sort of a nuisance. And if people want, they can go on and they can get hearing aids and treat it. But if they don't want to treat it, it's not a big deal. But in the past decade or so, there's been more and more evidence showing that maybe age-related hearing loss actually is a problem. It's been independently associated with all sorts of bad things, depression, dementia, falls, hospitalizations. And if you think about it, it kind of makes sense. If you can't hear, then you're not going to be as aware of your environment, and you might be more prone to slipping and falling. And if you can't communicate with your loved ones and talk during Thanksgiving, you're more likely to be depressed. It just kind of makes sense. And studies, including by our own group, have shown actually a dose-dependent relationship, meaning that the more hearing loss you have, the stronger the association with all these bad things. So in one study by my collaborator at Johns Hopkins, Frank Lynn, and his group, the risk of incident dementia rose from about 1.9 times to 4.9 times as hearing loss increased from mild to severe, controlling for a bunch of confounders. In another study that we did in our group, people with mild hearing loss had on average a 2.5 drop on a common cognitive test called the digit symbol substitution test. But those who had severe hearing loss, they had over a six point drops. That's a big difference, six versus 2.5. And this was clinically significant. Sure. And it's basically been assumed that this relationship between worse hearing and worse cognition begins when people have hearing loss. And we typically define hearing loss in adults at about 25 decibels, which is sort of arbitrary. And no one really has ever looked at whether this relationship started earlier in those who have hearing better than a 25 decibel pure tone average. Got it. And so what was your key research question with this particular study? Yeah. So the question was whether the relationship between hearing and cognition begins kind of quote before people have hearing loss. In other words, does it exist among those who have normal hearing? And it's a little funny to phrase it this way because we're studying hearing loss in people who don't have hearing loss, but the definition of hearing loss, it's kind of arbitrary. So in kids, we define it usually as 20 decibels. We usually use the pure tone average as like the single number. So about 20 decibel pure tone average, which is the mean threshold at 500, 1,000, 2,000, and 4,000 hertz on a pure tone audiogram. And in adults, we define it at 25. But for example, last week, I had a cold and I probably had my hearing drop from like five to 15. You may hear my voice right now. I'm a little raspy because I'm still getting over a cold. Maybe I can fly out. You could scope me. But I was very disturbed by this. And actually in the past when I've had colds, I've gone to our audiologist and said, hey, you know, I feel like I'm deaf. Can you measure my hearing? And they measure it. And it's, and it's like pretty good. It's like 15 decibels, but I noticed a big difference. So it told me, you know, this whole definition of hearing loss, it's kind of arbitrary and people who are sensitive, they may actually really notice hearing loss when it's, you know, better than the average kind of arbitrary 25 decibel threshold. And it does have implications for hearing screening and early detection as well, huh? Perhaps. And you're studying a biological phenomenon, there's really no need to label an artificial threshold. So we wanted to look at the entire threshold appearing from perfect to severe without defining any strict cut points and the association with cognition, which is also, it's a continuous thing. It's not really categorical. You don't really have step declines in your cognition. It would gradually decline over time. Sure. Totally makes sense. So tell us about the methodology that you used in your data sources. Sure. So we used two really big US cross-sectional studies that had both a good hearing measure, in other words, audiometry. So they weren't just saying people, hey, do you think you have hearing loss? Agree. Medium agree. Disagree. They actually sat down, had an audiogram, and had pure tones done. And they also had high quality cognition data. They had a variety of cognitive tests. So we used two of these studies. One was the Hispanic Community Health Study. And you actually recently had Michelle Arnold on your podcast, great podcast, and talked about hearing aid use and the same thing. And then we also use something a little better known called the National Health and Nutrition Examination Study, or NHANES. And so we chose to use both of these, not because I like double the work, but we wanted to confirm that findings were in both studies and not just one. So if we found it, it wasn't just a fluke or something related to that particular patient sample. Got it. And so as a result of combining them, it was pretty big. There were almost 6,500 subjects and the mean age was 59. And then in terms of the actual statistical methods, we use the relatively common technique of multivariable regression, which basically allows us to correlate an exposure, which in this case was hearing as measured by pure tone average with an outcome, which was cognition. And we used a couple of different cognition tests. And we controlled for a bunch of potential confounders, including age, sex, education, and cardiovascular disease. So what did you find out? What did you learn? So we used a few types of regression, which was kind of the special sauce of this paper. I'm on this NIH training grant, so I got to learn how to do these very sophisticated things thanks to the help of my brilliant biostatistical colleagues. So the first thing we did is we used regular multivariable linear regression, which is what you see in like half of papers. This draws a straight line across all people on the x-axis. And so first we confirmed what people have found before, that as hearing gets worse, cognition gets worse, and we were able to draw a line through all levels of hearing loss. But the question is, is the relationship between hearing loss and cognition, is it really linear? So a lot of people think that it's not linear. It would basically be a horizontal line going from perfect hearing, zero to 25 decibels, meaning there's no relationship. And then once you reach hearing loss, that's when the relationship begins.
So in your head, you can imagine a graph that's a horizontal line to start. And then a threshold is hit where you get hearing loss. And then the line starts to go down. People kind of assume this. And I sort of thought this was the case too. So the first thing we did is we used this special regression technique called GAM regression, which sounds scary, but it's not. And it stands for generalized additive model regression. That sounds even more scary, but basically is very simple. The computer using techniques that are sophisticated for the podcast, I will refer to them as magic. It basically draws a curve through the points. So instead of a line, it's drawing a squiggly curve. So it's more sensitive to where the points really are rather than forcing a line. So the point of doing this is it can show you a nonlinear relationship. Maybe it's like exponential or something nonlinear. And in nature, things really aren't often linear. We just always do linear regression because it's easy, because it uses, you know, like ninth grade math. If you remember, Y equals MX plus B may cause some nightmares in listeners, but that is a line. And that's all regression does, just making a line. And so we found that in doing this GAM regression, the relationship actually existed in people who had normal hearing. So from going from zero decibel perfect hearing to 24 decibels of borderline hearing loss, there was a drop in cognition. And then going from 25 decibels on to say 100 decibels, there was also a drop in cognition. And this is multivariable. So we're controlling for age and various confounders. But wait, that's not all. So the weird thing, which is why I think this study is so interesting, is not only was there a relationship in people who had normal hearing, it actually seemed that the relationship was stronger in those who have normal hearing. So that means that the drop in cognition going from 0 to 25 decibels seemed to be a little bigger than the drop going from, say, 25 to 50 decibels. And we showed that in certain tests, that was significantly different, meaning that the relationship was significantly stronger among those with normal hearing compared to those with hearing loss. That's pretty interesting. So we have this association with subclinical hearing loss and cognitive performance. What are your thoughts about the association? The direct relationship, causation, are these just related or unrelated simultaneous decline in two systems? What do you think is happening? Yeah, great question. And that's, of course, what everyone wants to know. We found this cross-sectional association, but what does that mean? Everyone cares about the C word, causation. So first thing I have to say is this is a cross-sectional study, so it's hard to infer causation. So there's some theories that causally link worse hearing with worse cognition. So one theory is that people who have a lot of hearing loss, they have to spend a lot more mental energy decoding the words. And so they have less mental energy left at the end of the sentence to make memories. And people of hearing loss have told me this repeatedly. So they say, you know, I'm sitting in a restaurant, someone's across from me, and if I don't eat and I stare at their face and I really concentrate and I have my hearing aids on, I know what they're saying. I can tell the words. But the problem is I'm focusing so much on what the words are. By the time they're done talking, I don't have any mental capacity left to actually think about the content of the speech. And then as I start thinking about it, they're already two sentences ahead. And I just don't understand what people are saying. Now, it's also possible that there could be confounders, right? So confounders are a common cause. So for example, age is the ultimate confounder. Age can cause hearing loss. Age can cause cognitive decline. But we controlled for age and other potential confounders. So those shouldn't be explaining the relationship. The problem is you cannot control for everything. There's always a possibility of confounders that you don't know about, and so you can't control them. And that's why you really need randomized trials because it gets rid of confounders. The surprising thing about this study is that the relationship between hearing and cognition already began among people with non-perfect hearing. So people who had good hearing but not perfect hearing, their cognition was slightly worse, controlling for these confounders. And that is kind of unexpected. So this is the fun part about doing science. So I'm sitting here trying to write the discussion section of my paper, and I'm staring at the word processor like, wait, I don't, I don't know what to put here. So then I had to like stop and think about it for like a week. And as I'm like walking to work and driving, like what, what does this mean? And, and so, you know, if you think about it, I think, I think you can, it kind of can explain it. So like, let's say you're a college student and you're in a hard lecture and you're sitting next to someone who has just slightly better hearing than you. And it's hard to hear the professor because, you know, all you can hear are people tapping away at their smartphones on Twitter and Instagram and things I haven't heard of. Now, the person who has slightly better hearing is going to take a little more home from the lecture, all other things being equal between those two students. So, note, they both have normal hearing, but one just has a little better hearing. So you could see the person who has a little better hearing, they're at an advantage in that situation. And this is just an isolated example, but there's many situations in life where we're in a situation where there's stimulating stuff happening through speaking. You know, lectures, we go to lectures all the time, and people who can hear a little better, they're probably going to soak up a little more. And in a very simple way, they might be a little smarter as a result. So an analogy maybe is muscle mass. So if you have better muscle mass, even better than someone who's average, you'd probably be a better runner, right? And if you were a better runner, you may be a more fit individual. So in the sense of muscle mass for your overall fitness, better muscle mass is better beyond what's considered, you know, normal, the threshold between normal and pathological. Likewise, if you have better hearing, you may be a better hearer, if I can coin a word, and maybe a better listener, and maybe even a more cognitively fit individual. Yep. Got it. That makes sense. How should these new findings be applied now and or in the future? So that's a great question. So I love otolaryngology, and if I could redo residency, I would still do an otolaryngology residency. But I have to say the clinical research in otolaryngology is a little behind, say, other more mature and larger fields like cardiology. So I like to think of this analogy of hypertension. So both hearing loss and hypertension are kind of like silent disorders, pun intended for hearing loss, meaning people often don't know they have the symptoms. And this is true for most people with age-related hearing loss. The patients who come and see us, they're the rare ones who tend to be noticing it and bothered by it, and they actually come in the office. But for every person I see who has age-related hearing loss, there's probably another 10 who don't even realize they have it or don't care and never see someone for it. And so hypertension is kind of like this too. It's another disorder that used to be considered benign. And over time, it was realized that it was bad and we needed to control hypertension more aggressively. And so initially 140 was considered sort of the cut point between normal and hypertension. That was lowered and lowered and lowered. And the reason why is we realized that the better the hypertension control, the better the outcomes. And that data came from randomized controlled trials. And I think that's what we need in otolaryngology. If we're going to talk about, you know, lowering the threshold for hearing loss, we can't do that unless we have trials showing that we really need aggressive treatment for hearing loss. We're many steps behind that. We're just trying to get people who have severe hearing loss to where their hearing aids currently. Lots of implications from this. Early exposure to noise, concert attendance, loud headphone use. Any final message for our listeners? Absolutely.
And while this particular study is not longitudinal, it's not a randomized controlled trial, it does show among the first evidence that this association we've been seeing between hearing loss and cognition, it may begin among earlier forms of hearing loss than previously thought. Now, it's risky to make treatment recommendations based on preliminary data, but the thing about treating hearing loss is that it's very low risk and the potential benefit is high. You know, there's a little risk to getting and wearing a hearing aid. So these data suggest that maybe we should encourage adults, even with mild hearing loss, to pursue a hearing aid. And that seems kind of strange. I see a lot of adults who have a lot of hearing loss and they don't want to wear hearing aids. And the ones with mild hearing loss, I've been tending just to reassure them like most people do, and I don't really push hearing aids. So that seems kind of extreme. But if you take a step back, in children, we very much encourage children with mild hearing loss to wear hearing aids. And why this discrepancy? If it's good for our kids, why isn't it good for adults? So I think we need to really think about hearing loss as a bigger problem with adults that we need to treat earlier. Terrific conversation. Dr. Golub, thank you for joining us today and discussing this increasingly important issue of hearing impairment and cognitive decline absorb the conversation. This sort of redirected mental energy can lead to cognitive decline. Dr. Golub's research shows that there might be a relationship between very mild hearing loss and cognitive decline. If true, this is really important because noise is becoming more prevalent in our society, most especially by the ubiquitous use of earbuds and earphones that constantly bombard someone's eardrums. Ultimately, this will result in some element of hearing loss, and that hearing loss could prove to be an important cause for cognitive decline, even in young people. Being an observational study, this research is preliminary, but the results are interesting and merit further research. I'd like to thank Dr. Michael Johns from Otolaryngology for interviewing Dr. Justin Golub from Columbia University, and Dr. Golub for publishing his research in JAMA Otolaryngology. Thank you.
The following episode of Annals on Call is brought to you by Annals of Internal Medicine. For more episodes and links to CME and MOC, visit go.annals.org slash oncall. There was no good data that high-dose colchicine was any better than low-dose colchicine in treating acute gout. But the big difference between the American College of Rheumatology and the American College of Physicians guidelines, so to speak, is really what's the data showing that you need to treat to target. Welcome to Annals on Call, a podcast based upon articles from the Annals of Internal Medicine in which we discuss the implications of the article for you, the listener. This is Dr. Bob Centaur. I'm Professor Emeritus at the University of Alabama at Birmingham and former chair of the Board of Regents for the American College of Physicians. Today we're going to discuss the management of acute and recurrent gout, a clinical practice guideline from the American College of Physicians. This article appeared in the January 3rd issue 2017. There's an accompanying editorial titled, To Treat or Not to Treat, To Target, in Gout. Our guest today is Dr. Robert McLean, who is currently the president-elect of the American College of Physicians. He's a practicing rheumatologist and internist in Connecticut and on the teaching faculty at Yale University. He was a member of the ACP Guidelines Committee when this guideline was developed. The highlight for this you've already gotten a clue to from the intro. We're going to talk about the treatment of acute gout and the different options and work on understanding the controversy about how much we should give of uric acid lowering agents. I hope you enjoy this podcast. So welcome, Robert. Well, thank you, Bob. So what I want to do is I want to go through some of the recommendations of this guideline and get your opinions. And I'm really interested in what you actually do in your practice. So the first recommendation was that clinicians could choose either corticosteroids, nonsteroidals, or colchicine for acute gout. And in the corollary in recommendation number two, they talk about how clinicians should use relatively low-dose colchicine to what I was taught back in the 70s when you had acute gout. So patient comes in with gout and you're going to treat them. Tell me how you decide between these three drugs, which patient should get which ones, and when you're using colchicine, why we use this new strategy for colchicine. Sure. Well, thanks, Bob. So I think the first consideration to keep in mind is, does the person really have gout or not? And as you know, there were two clinical guidelines papers that came out. One was on management of gout, and the other was on diagnosis of gout. And for the most part, the information in the diagnosis of gout guideline is not nearly as controversial, but the guidelines committee wanted to address aiming it more at primary care, internal medicine audience of how do you really know someone has gout or not? And I think just to kind of cover that quickly, the gold standard really is do you see gout crystals that are being ingested by white cells in someone's synovial fluid. Sometimes it's not always easy to get synovial fluid. And so the reality of practice is that we sometimes empirically treat someone who has a big, hot base of the first big toe, what Hippocrates called pedagra. And we say this is gout until proven otherwise to some extent. And as long as they don't have some other major risk factors for an infection infection like a diabetic foot or something, most of the time we're usually pretty right with some of our clinical judgment. So on the assumption that someone has what looks like classical gout there or somewhere else that we have no reason to doubt it's something else, the question is how do we treat them? And going back and looking at the data and the studies, there was really, I think, a feeling that the data showed, when you look at high-quality data, that all three of the medications mentioned work well, NSAIDs, steroids, and colchicine. And there was nothing in terms of the data, head-to-head trials, that showed that anything was more effective than the other. There are clearly patient reasons that would make one choose one agent over another. Things like renal dysfunction or GI problems or GI bleeding may prevent you from being able to use NSAIDs. Steroids, if someone's diabetic or has other issues with steroid use, there might be issues with that. And some people may be intolerant of colchicine. But I think that the feeling was that for efficacy reasons, all of them were equally good. One of the points that was made in the explanation underneath the recommendations was that really all NSAIDs are really quite equal on this and probably for other things as well. There was no strong evidence that Indicin was any better than anything else. And I think we wanted to make the point specifically that it's not better because it's used a lot. And as you mentioned before, there's a lot of teaching that Indicin, because it seems to have a more rapid onset and is a fairly potent NSAID, works really well. But the problem is that it has probably the highest risk profile of any of the NSAIDs, whether it be renal dysfunction or GI upset or especially because it tends to cross the blood-brain barrier more than other NSAIDs. It has a really high incidence of either causing headache or kind of head fuzziness or neurologic dysfunction. And in my practice, I can't remember the last time that I actually used Indusyn. In fact, I probably haven't at all prescribed it. The only time I've probably used it is if some patient begged it that nothing else worked as well as Indusyn and I'd give them a low dose for just a few days. Back to the colchicine issue, the classical teaching, as you had mentioned, had been to use colchicine, kind of blast people hard with it. And the classical teaching was give one dose of colchicine, which is 0.6 milligrams an hour, until either their gout got better or they had diarrhea, whichever came first. And the problem with that was that virtually everyone would get diarrhea within three or four doses of an hourly colchicine. Some studies were done that actually showed that people did just as well by giving them two doses in the first day and then follow-up doses for a couple days or however long. We'll get to that in a few minutes. But you did not need to blast people with so much colchicine in the first day to the point where they got adverse effects like diarrhea. And that's where the recommendation to come, which was there was no good data that high-dose colchicine was any better than low-dose colchicine in treating acute gout. I'll stop there for a sec. Does that make sense? Absolutely. So let's go through each of these just to be a little bit more specific for the audience. What nonsteroidal do you usually use? If I came in with acute gout and saw you, I had pedagra, and I really wanted some help, what would you prescribe? If you had not taken anything yet, I would potentially have you take two Aleve twice a day. Okay. Aleve is? Naproxen. Naproxen. Aleve is the over-the-counter form. If for some reason the person had some prescription naproxen, I would usually use the 500 instead of the 375, which are the two prescription doses, and have them take 500 twice a day with food of naproxen. And if that really wasn't doing much over a day or two, I would have a very low threshold to add on steroids, or quite frankly, at the beginning, I actually use a lot of colchicine too. So if there was no contraindication to colchicine, I would actually give people colchicine at the recommended dose now, which is to give 1.2 milligrams as a starting loading dose, which is two tablets together. And then later in the day, I think the evidence or some of the studies showed you could take it even an hour or two later. I might give it several hours later so that they have a total of three doses in the first day, but I would not give it any higher than that. But one of the effective things about colchicine is that especially if you catch the gout episode or attack early, and I don't know that there's great, there's no evidence kind of showing this, but I think that our clinical judgment tends to show that gout really responds quickly, early gout to colchicine. And it almost can be a therapeutic trial that can really strongly suggest that what you had was gout.
So if you have somebody who has a hot pedagra-type toe and you you give them colchicine, and within 24 hours, they are dramatically better. You have virtually ruled out anything else. Okay, so just let me make sure I have this. So you like naproxen 500 twice a day, and you've had good success with that. Yes. You sometimes give 1.2 of colchicine, and then an hour or two or three later, 0.6, but that's all the colchicine for today. And if they respond to that, that tells you it's probably crystalline arthritis, either gout or pseudogout. Correct. When do you use steroids? And it was interesting to me in the table, where I am, we've always used prednisone, but you don't even list prednisone. You list prednisolone and methylprednisolone, at least the committee did, as the corticosteroids of choice. Right. Well, you know, the tricky things that we have with the Clinical Guidelines Committee, and this gets at one of the core issues that we deal with, is the Clinical Guidelines guidelines committee following the ACP's kind of protocol is to look at what the data shows. And so when the studies that have shown that steroids were effective used prednisolone or methylprednisolone, that is what we need to say works. Now, many people, at least in this country and different parts of the country, might use prednisone versus prednisolone, some of its clinical habit. But on the basis of what the studies actually showed, we're kind of, our hands are tied to show that. And that really gets it, as I say, one of the core issues here, which is what's the purpose of the guideline? Is it to give the best practice advice on what should be done, which may go in between what data shows, or is it to say this is what the best evidence-based studies show us works or doesn't work? And our guidelines committee has really kind of stuck to the latter. And that's where sometimes there are conflicts or differences of opinion that these guidelines come to. Because in some cases, there's not great data to tell us exactly what to do in a given clinical situation. And that makes it tricky and frustrating because somebody might read our guideline and say, well, this isn't really telling me exactly what I should do in a given situation. And the truth of the matter is that's because we may not have a study that gives us a great answer based upon what that clinical question is. So I've been told before that the advantage of prednisolone is that prednisone is a pro-drug that has be converted to prednisolone, and prednisolone is the active drug. I was always taught that it was fairly expensive, but as I read the table in the article, it's only 11 days for a 50-day supply of the 15-milligram dosage, and since you're giving 30 or 45 milligrams, how many days, if you were going to give prednisolone to a patient, how many days would you give it to them for gout? Yeah, you know, so whether it's prednisone or whether it's colchicine or the NSAIDs, there's not great data on how long to treat. I would say my personal practical advice would be to usually treat for a week or two with a tapering dose of the steroid. And some of that is more clinical judgment of what I've seen in practice. Many times people have been given things like the convenient Medrel dose pack that's used for so many things. They basically take 6, 5, 4, 3, 2, 1 with a rapid taper. Right. a 10 to 14 day course slowly tapering down and that's for example if it's their first episode of gout or they have it infrequently maybe once or twice a year and I'm not worried that they are really actively needing more prophylactic treatment if I'm going to be starting them on uric acid lowering therapy which is a whole nother issue. So with the prednisone so I like to treat for probably 10 to 14 days, gradually tapering. Similarly with colchicine, if I think someone has an isolated episode for whatever reason, I'll give them a week or two, usually closer to two weeks of colchicine. As we mentioned before, they take the loading dose the first day, and then I would typically have them take it once. I usually have them take it twice a day for maybe a week. Then I drop down to once a day for a week and then I would stop it. Great. So that's really helpful. Let's go to the third issue. And this is when do you put people on urate lowering therapy? What are the criteria? Because it's interesting here, the recommendation here, which is very clear, is you don't give it after the first attack or someone with infrequent attacks, although infrequent is not defined. Correct. the other things. And what I've been told is tophagous gout should get urate-lowering therapy, and kidney stones that have urate in them should get urate-lowering therapy. And that's not mentioned in here. Right. Well, so, yeah, so our goal here was to address gout. It was not to address uric acid kidney stones. So that was kind of off the table just in terms of the studies and the data that we looked at. Although I think to some extent there's a certain logic that if somebody has uric acid stones and presumably they have elevated levels of uric acid in their urine that you want their uric acid to be lower because of that. But to some extent from the joint standpoint, and similarly with tofacius gout, if someone has enough of a uric acid load within their body metabolically, what we tend to see is that frequently there is actually joint damage from TOFI. I think what's less certain from the standpoint of actually prospectively following groups of patients or any sort of trials is how much uric acid elevation do you need to get TOFI. We know that the higher the levels, the higher the risk. But one of the big mysteries that we really have is why is there not more gout? We know that there are millions and millions of people who have elevated uric acid levels. The definition of that we'll get to in just a minute. And why, if there's so many people who have elevated uric acid levels, isn't there more gout? And it really is a great mystery. So while it's a risk factor, it's not the only thing. And so the idea that has been promulgated based upon some observational retrospective data that lowering uric acid below a certain target is the optimal strategy is not really supported by strong prospective data. Now, and that's a difference where the ACP said the data is not there whereby we looked at a group of patients who were randomized to, you know, a certain strategy which was what we call treat to target, get the uric acid level below six is the number versus not treating them to target and just putting them on, you know, allopurinol or fibuxtastat at some dose, but not really worrying what the follow-up uric acid level is. We don't have data showing that one strategy is better than the other. And that's why, to some extent, we ended up being kind of vague and uncertain in that. Now, the rheumatology community has, for the past probably 10 years, gone on some assumptions that getting the uric acid level below 6 makes a lot of logical sense. And it does make a lot of logical sense. But the data showing it is retrospective and not as strong as one might actually think. Now, the good news is, I think with some of this controversy, and I think it may have been happening anyway, some better designed trials to answer some of these questions are in fact in the works. But the big difference between the American College of Rheumatology and the American College of Physicians guidelines, so to speak, is really what's the data showing that you need to treat to target. Now, one of the points that was made in the editorial that you had made reference to, to treat or not to treat, to target and gout, points at the fact that we have a certain amount of physiologic knowledge about uric acid. Now, we have a physiologic knowledge about a lot of things that don't necessarily prove to be true all the time. And one of the things that the Clinical Guidelines Committee is concerned about at times is making assumptions that certain treatments or interventions are necessarily good.
So merely making assumptions based on what we assume is physiology or pathophysiology is something that we try to avoid. Now, the physiologic aspect of uric acid, which I'll touch on briefly, it's known that the solubility level for uric acid at normal pH and temperature is about 6.8. So presumably, if anyone has a uric acid level over 6.8, they are theoretically saturated or super saturated. And so the question is, why aren't more people walking around with a uric acid level of 7, 7.5, or 8? Why aren't they developing gout? Why isn't the uric acid precipitating out of the blood or out of the serum into joints or wherever? And the answer is we really don't know why, but it's not happening all that much. But we do seem to see that when people have higher uric acid levels, well, 10, 11, 12, they clearly have higher risks of gout. But as I say, so, but a retrospective trial had seemed to show that after people to put on medications for their gout, those who got the level over when they were followed over a six to 12 month period, if the levels achieved were under six, that was where the frequency of recurrent gout tended to level off. And that's where this magical number of 6.0 came from. It really came from one retrospective trial. And I think that we were not comfortable with that kind of relatively limited data, although it makes physiologic sense, at making a strong recommendation that this was the strategy that needed to be adhered to for everybody. So, first of all, when do you start your low-ring therapy just for gout alone? I didn't answer your question. So, back when I was a fellow, before we had this treat-to-target approach within the rheumatology community, the feeling was, you know, we don't know what makes people have gout or not. If, in fact, somebody has limited gout, they have one or two episodes a year, maybe it's precipitated by a heavy weekend of socializing and a little too much shellfish and alcohol, which seems to acutely raise your acid levels, whatever it was, if somebody had a couple attacks a year, one or two, and it was well-controlled with whether colchicine or NSAIDs or steroids, so that within a week or two of treatment, you could get it under control. There was nothing that suggested back in the early 1990s when I was a fellow that people necessarily needed to be on long-term uric acid lowering therapy if you were able to control a couple of attacks fairly easily. If you were not able to control it with as-needed treatments for a week or two and they were having recurrent attacks or they had TOFI, which really demonstrated that their uric acid body burden was significant and potentially doing damage to joints, then the feeling back then was to treat them. At this point, I tend to have a low threshold if someone has more than one or two attacks a year to put them on uric acid lowering therapy. Now, some of it also depends on what is their uric acid level. So if somebody has had gout and I, uh, that had one attack and I measure their uric acid level several weeks later when they are back to their relative equilibrium of uric acid, then I'll have a better sense of what their risk factors might be for future episodes. And I also may, it's a great opportunity to look at their uric acid level and say, is there something else that we might try to do to make it lower, which we have a general feeling is probably a better thing. So for example, are they drinking too much? Maybe are they on a thiazide diuretic? So some other optional blood pressure medication might be an alternative. Are they truly eating a lot of shellfish or, you know, the bad diet foods that tend to, we think, raise your acid levels, although data is not incredibly strong in how much diet impact can have. But that's also because I think some of those trials just haven't really been done well or designed well. But population studies looking at people with larger BMIs and who have certain dietary habits do tend to suggest at an epidemiologic level that those things are associated with higher uric acid levels. So if someone has more than, and the guidelines came down on that, we decided that if in fact someone has more than two episodes per year or problematic gout, as I mentioned reasons before, that at that point is worth having a discussion with the patient about potentially going on treatment. Part of the issue is if you're going to put someone on uric acid lowering therapy, they got to take the pill every day. So you're committing the person to a medication to take every day, potentially indefinitely, as opposed to episodic treatment. And I think in this day and age, everyone seems to agree that I think we need to have more patient involvement in that decision of whether to commit to that. So when you do that, I assume you try allopurinol because it's so much less expensive than the newer agents. Correct. And the way the table in the guideline says you're going to start at 50 to 100 milligrams per day and then increase, but I'm trying to understand, the rheumatologist would tell me, and I've talked to some of the rheumatologists at my institution, and they're going to increase until they get the uric acid below six. Right. If you follow this guideline, are you just going to say, okay, now I have you on 100. If you have two more episodes in the next year, then we'll go up to 200? Yeah, again we just i think the problem is the reality there's no there's no data on really on how to guide us and so the feeling was if in fact you put someone on you know kind of the starting dose of 100 milligrams say uh and then you have tapered them off of the prophylactic treatment which everyone should get put on when they are started on these uric acid lowering therapies. Because people do need to realize, and I think most people tend to learn this, although I still see patients where they got treated inappropriately because they got started on something like allopurinol, but they were not also covered with either a little bit of steroid or NSAIDs or colchicine as a prophylactic because when you are interfering with uric acid metabolism when you're starting one of these medications, you actually physiologically seem to free up uric acid crystals into the circulation, which can precipitate a flare. So we want to cover people with a prophylactic treatment, and studies do suggest that that clearly decreases the rate of gout flares when you're starting the treatment. So after they had been on the treatment, allopurinol, say 100 milligrams for a month or so, I would then stop the prophylactic treatment, the colchicine or the low-dose steroid or whatever, and then the guideline would essentially say, see if they have any recurrent attacks on that dose of allopurinol, that the data to monitor uric acid levels down to a certain target was just not there. Now, as I say, the rheumatologists are not comfortable with that and would say that based upon their experience that people clearly do better if their uric acid level is below six. The teaching has been, there again without necessarily great data, that if someone has TOFI, their uric acid body burden is even higher and you might want to treat to an even lower target. There's no prospective data suggesting that. It would be interesting to see with the technology we have now, and I'm not sure if anyone is looking at this, whether in fact MRIs looking at joints and changes in joints as you lower uric acid levels will help support the fact that we truly decrease the risk of joint damage by pushing the uric acid level lower. We don't know that yet, and that's kind of why we're limited in what we're saying that the evidence shows us to do. So this has been great. Let me see if I can summarize this last part. I was always taught to give 0.6 of colchicine daily when I started allopurinol, and as you suggested, for a month to make sure that the allopurinol does not induce an attack. Does that sound right? Yes, it does.
That's correct. That would be just for someone who has recurrent attacks. I believe that many people would have a different decision if someone had many TOFI or had kidney stones, that they'd work much, much harder to get the uric acid below six because you're trying to decrease crystallization and melt the TOFI. What you've done is you've actually taken these guidelines and given us some real good ideas about how to put the guidelines into practice, what we absolutely know, and where it's fuzzy. And I think it's important for all of us physicians to understand where the data are fuzzy. And it's very clear to me that I'm looking forward to the studies of whether lowering uric acid below a certain level is a way to prevent recurrent gout. So it's time for Bob's Pearls. What did I get out of doing this podcast and reading these articles? First, I have a much better understanding of how to treat acute gout. I had always used indomethacin as my non-steroidal. From now on, I'm going to use naproxen either at 375 milligrams if I'm doing over-the-counter therapy or 500 milligrams, and each of these would be twice a day. For steroids, I'm going to give a week at a solid dose, maybe 20 milligrams of prednisone or 20 milligrams of prednisolone, and then taper slowly over the following week. But the big thing I learned was that I was doing colchicine all wrong. I've avoided colchicine for many years because of the diarrhea. The data that supported this guideline shows that you can give 1.2 milligrams as a loading dose and then later on within about two or three hours give another 0.6 milligrams. That will not lead to many side effects and then you follow that up with 0.6 milligrams twice a day for the next week to two weeks. I also better understand the controversy about how to treat recurrent gout. Recurrent gout is defined as two or more episodes. We're struggling because we don't have great data on whether we should treat a target or not. The American College of Rheumatology and many gout specialists believe that we should get the uric acid below six and we should measure the uric acid as we start uric acid lowering therapy. The American College of Physicians suggested that in the absence of data, we should give 100 milligrams of allopurinol and then if they have two more episodes of gout, increase the allopurinol, but not recheck the uric acid. Because we don't have any data, we can't say whether one group is right or one group is wrong. We also heard that studies are in plans to try to do a better job of elucidating this important question. What the editorial told us was that regardless of strategy, very few people with recurrent gout are taking uorg slash oncall. Participant statements on this podcast reflect the views of the participants and not necessarily those of the Journal or the American College of Physicians, unless so identified. The information contained in the podcast should never be used as a substitute for clinical judgment.
You're listening to Sharp Scratch, episode 45, New Life. This is a podcast brought to you by the BMJ and sponsored by Medical Protection, where we bring together medical students, junior doctors and expert guests to discuss all the things that you need to know to be a good doctor that you might not get taught in medical school. I'm Nikki and I'm the editorial scholar here at the BMJ and I'm also a medical student at the University of Manchester and I'm excited to be joined today by my good friends Chidera and Anna. Anna do you want to introduce yourself? Yeah hi everyone my name's Anna I'm a final year medical student at King's College London and I'm very excited to be here talking about new life because I'm also president of a society called the British Undergraduate Society for Obstetrics and Gynaecology. So yeah, it's an area of interest of mine. Amazing, thanks for joining us Anna. And Chidera? Hi, I'm Chidera, I'm a junior doctor, very junior doctor, working at Imperial Healthcare Trust. I'm currently working in the neurosurgery department, but I do remember a very long Obst and Gynae placement at university, actually, that I did really enjoy. Amazing. And I'm delighted to also be joined today by our expert guest, Professor Lucy Chappell. Lucy, do you want to introduce yourself to our listeners? Thanks, Nikki. I'm Lucy Chappell, I'm an NIHR Research Professor of Obstetrics at King's College London and I'm a Consultant Obstetrician at Guy's and St Thomas' NHS Foundation Trust. It's great to be here today. Thank you so much for taking the time to join us. So essentially today we want to talk a bit about babies. I guess being present for a birth for the first time is probably quite a key moment in your career. On this podcast we like to talk a lot about things that you don't really learn at medical school and I suppose in some ways this topic is a bit of an exception because at med school they do try to teach you what you need to know to be a good doctor in the realm realm of births but after all there is still like a bit of a gap between learning all of the right things and then experiencing it for the first time so Anna and Chidera I know you've both spent some time on obs and gynae and you'll definitely know a little bit more than me because I haven't had an obs and gynae block yet so I'll be asking you both lots of my questions in a bit partly so I can save this episode up to listen back to next year when I go back before my Obst and Gynae block. But first of all, Lucy, do you still remember the first time that you were present for a birth? I remember my undergraduate block really well because it was that block that made me fall in Obst and Gy gyne and I remember it for several reasons um most of all because it was the first time I encountered a different approach to what you might call patients because pregnant women are generally not patients they are well women who um come into contact with the healthcare system at a really pivotal moment in their life. But they're not there for a disease. They're there usually because they're well and having a baby, although some pregnant women do have medical complications. So I remember my births, but I also remember some really phenomenal teachers who transformed my career path because they got got me seeing medicine a bit differently and and women differently and that's why I'm where I am today. Oh that's amazing so going back to that first block and you were talking a bit about like all of the amazing things that you saw do you still do you remember how you felt seeing those things and do you still get those same emotions now? Yes every birth that I am part of I still get that sense of usually excitement although I do look after a group of women with high-risk medical problems so it isn't always and we can talk a bit more about that but I've always said that if I stop feeling that anticipation and that surge of adrenaline, then it's probably time to stop obstetrics. I should still feel a sense of what that woman is going through. It is one of the biggest days of her life. And if you ever become immune to that, then you've got to re-examine your relationship with obstetricsrics as a specialty because you need to be present for that woman and that family in with that frame of mind professional but just it still moves me every time and I'm fine with that. That's really amazing way to think about it I think I guess you must have also in your time seen lots of medical students have their first experience with birth like what is that generally like for people? I think the experience is very varied as medical students and doctors we are privileged to be there at some really major moments whether it's birth or death and those are extraordinary moments um so for birth uh there is such a wide range of births and I think um how it's done is crucial um so both integrating the medical student into that journey now even, even as junior doctors, you may often have snapshots of that woman's pregnancy journey. So when you turn up for the culmination of nine months work, it can be quite hard to be parachuted into that. And particularly because sometimes we say quick, room seven, she's about to have a baby, then that's a few minutes in what is a nine-month journey. So there is still something very special about that moment when a baby is born, whether vaginally or by cesarean or by whatever method, but it's got to be seen in the bigger context for that woman. So I think what I see from medical students is both depends on that context and how much they understand the wider context, but also their personal journey and what they bring to it, both in terms of sort of from the medical perspective, what, you know, where they want to be in, you know, and particularly, are they interested in pregnancy and the birth journey, but also often their personal journey. And I think we should recognise that we're all humans. And that's what I bring to it. I've had three babies. So of course, I, you know, there's no doubt that I bring my personal journey, and we all do, whether that relates to birth or illness or death or any other part of medicine. Anna and Chidera do you guys remember the first birth that you were present for? Yeah so it was in fifth year which at Cambridge is when we do sort of all of our women's health and I mean it was um like you were saying um I was on the ward and I'd been on the obstetrics ward for maybe three or four days and had not been lucky enough to be around when somebody gave birth it was a bit of a potluck and I know some of the other students had literally um done night shifts just to hope that they could catch someone um when they deliver and one of the nurses basically just pulled me into this room with a woman who was screaming and swearing quite loudly at her husband and just generally into the environment. And when the baby eventually arrived, it was actually, I think, a pretty smooth birth. She'd been admitted because I think she was slightly overweight and had some gestational diabetes. But otherwise, the birth itself actually went really well. I don't think she required anything extra. And I don't know why, but as soon as the baby cried, I started crying. And I had that for the rest of my placement, like even for cesareans. As soon as I heard the baby cry, I would burst into tears. So I'm not sure what that means for any potential future obstetric career. But yeah, it was really, really emotional. Yeah, that was my next question. I was going to ask you how it made you feel, but you've touched on the crying and you said that carried on throughout the whole placement every single time no genuinely what about you Anna yeah I definitely got teary the first time I saw a birth um but I was quite I guess um to dare just did the air quotes around lucky as well I was very lucky in that I actually had seen um births before I went to medical school um so my mum was training to be a midwife around the time that I was doing my GCSEs um and that was how I managed to get work experience in the hospital um and it was on an obstetric ward and I still remember the consultant um bringing me into theatre to see a section list and the first time I honestly still get emotional thinking about it I was getting emotional just hearing Lucy talking about her still getting emotional because it's just so amazing like and now that's such a long time ago like that person who was born is walking around in the world somewhere. And I always will have been there when they took their first breath. Like, I just think it's amazing.
They don't do that anymore, unfortunately. But it was definitely something that appealed to me about Kings. That's really nice. And yeah, I didn't want to be one of those people who was like very set on a specific specialty. I tried to keep an open mind. But yeah, then when I did my obs and gynae block during um I did it at KCH actually Lucy um and yeah I don't think I'm ever going to be able to do anything else so some things just pull you back in yeah Lucy what are your thoughts on the um block that Anne was talking about where you're paired with a woman for the full nine months and I think there's a lot to be said for that concept in pregnancy, but also in other areas. And it's a bit like either seeing cross-sectional data or longitudinal data. And not that pregnant women are data, they are human beings. But the point is, is that you get a very different perspective when you've seen someone through that journey. And one of the things that as a consultant, one of the realisations that dawns on you when you start doing your own antenatal clinics is that you're going to follow those women through a pregnancy. And you take a sort of responsibility for helping her, guiding her through that journey, that if you are just seeing people on a one-off, you might fix the here and now, but you don't have the umbrella view of how can you help. So not only do you see her through a pregnancy, she can come back for another one. And when you first see the women, as a new consultant, when you first see the women who you've already seen through one pregnancy, that's also really special because you start to get a window into their lives in a way that I know that those in primary care often do. And that people in GPs often talk about the privilege of sharing much more than a snapshot outpatient clinic appointment, but a nine-month journey where women start to tell you things that you don't hear otherwise. And you have to make space in a consultation to hear what the women might tell you about. And this goes back to my undergraduate experience of when the consultant obstetrician and gynecologist introduced me to the idea of what was said in a consultation, but also what was left unsaid, that you may or may not want to explore. And why this matters is that pregnancy care is about more than just this sort of tight clinical model. It's about the much wider psychosocial issues that a woman might be facing interaction with with a family so her partner her the rest of her children and it brings the realization that when we do a consultation or when we're at a birth that's just one tiny part so so a really good example is the woman's expectations of a birth. And there is a lot sort of fueled by media, friends, other experiences. And women may come with either a very sort of loose expectations. So understanding that there is quite a lot of uncertainty during birth. But sometimes, as a result, I think of the messages that we out, they come with a with quite a tight and narrow expectation. And then it's hard if they don't, those expectations aren't met. So we want to provide a high quality maternity service in the UK. And there is much more that we can do and that we are striving to do for that to happen. But for women understanding what we and they can control about a birth and also what is that uncertainty and what is controllable is maybe important. I think I've strayed from your original question, Nikki, but it took me off on some forks in the road. All really valuable, valuable things to think about, though, I think, for our listeners. So by complete chance today, because of timetables and everyone's availability, we have a fab but all female panel. But I did think it would be interesting to get a male medical student's perspective on all of this as well. So had a little chat with Ollie who's a med student at the University of Leeds. So I spotted you on Twitter because you'd tweeted a little bit about life as a male medical student on an obs and gynae block and that you thought it was it felt a little bit pointless. You've told me that since then your views have changed a bit but just talk me through what your initial thoughts were when you wrote that. So a little bit on the background of that tweet I'd just finished my first sort of four days on OBS and gynae block in a district general hospital up here in Yorkshire where I'm studying and in that first four days on the gynaecology side of things I'd spent more time outside consultation rooms, outside rooms on the wards and I wasn't really feeling very good about the placement as a whole. That's through no fault of anybody, that's just the way things go occasionally. And it's something that I was very much aware of going in to my obs and gynae block that a lot of male students, especially that I'd spoken to previously, had found that when they were on their block, they'd spent a lot of time outside of the consultation room, outside of bays on the ward, just because patients didn't feel comfortable with them being present. And so I did what I probably sometimes do a bit too much of, which is tweet about it. And the wording in my tweet was pretty clumsy. I said that life as a male medical student on an obs and gynae block feels quite quite pointless and while I regret tweeting it in those kind of terms the conversation that that stimulated was really really interesting and sort of attracted attention from both professionals working within obstetrics and gynaecology both medical and midwifery but also from patients and partners of patients who have been seen through those services and who have accessed those services. So when you said that you spent a lot of time on the corridors and outside was that because patients weren't giving consent for you to be present in consultations or? Yeah predominantly because patients were offered the obviously made it very clear who I was whenever I was with other healthcare professionals in clinic. And a lot of patients made it very, very clear that they weren't comfortable with a student present. So I understand why that was the case. But I was kind of conflicted in the sort of I need to be able to see what I need to see in order to achieve the goals that placement set out for me but similarly you the last thing anyone with the best with the best intentions in the world best will in the world wants to do is to make any patient feel uncomfortable or their presence to be seen as something that makes people uncomfortable so definitely i completely understand where you're coming from with that you mentioned that the responses to your tweet you learned a lot from the responses from a variety of different people can you talk us through a couple of like the highlights of things you mentioned the patients for example had responded to you so a lot of patients or yeah it was a mixture of patients who had had quite varied experiences with healthcare professionals and I think when I tweeted I hadn't quite appreciated the extent to which some patients fear and have trepidation when it comes to seeing medical professionals, and especially when it comes to female patients with gynaecological or obstetric problems, seeing, bring themselves in for what they know and what they anticipate is going to be quite an invasive invasion of their personal space invasion of their bodies by somebody else who they may not have ever met before um and a lot of the more poignant responses for me were when ladies responded that in they would in the same situation refuse a male medical student to be present because of past experience they'd had with men, both in medical contexts and outside medical contexts. It shocked me to think that they'd had experiences with male medical practitioners who had made them feel that uncomfortable, that violated, that they then had that impact moving forward to any future medical care they had. Okay, so Lucy, what are your reflections on listening to that? That's hard to hear on a number of fronts. And I think it reminds us how as a community, there are many reasons to try and address several of the issues that Ollie raises. We need a diverse workforce in obstetrics and gynacology who serve the needs of the women that we see. And what Olly raises is how we can and should all contribute to that. So I understand the perspective of the women who have had previous negative experiences with a man, either in a personal context or a professional one. So we commit as healthcare professionals not to repeat that. And both that's not acceptable in any sense. But then it's wrong to sort of add insult to injury by saying, well, you know, men, it's, a man has to be there. So I respect the right of women to say no, but it leads me to say, how do we then enable Ollie and his colleagues to be present at a birth? And a lot to do is how I introduce or a midwife introduces Ollie. So I talk about colleagues when I talk about medical students.
Many doctors won't go on to be obstetricians and gynecologists, but they need that exposure as much as anyone who is and arguably more because if that is going to be your experience of birth. So to try and put myself in the woman's shoes and then say, how can I make this a more positive experience for women? We've been talking in this recording about the impact of seeing a birth. I would like to think I don't discriminate on sex or gender or ethnicity or any other characteristic. So just see people as a person with another label, whether, you know, and I think if we all take that approach across medicine, it will help. Definitely. Anna, what were your thoughts when you were listening to that? So I thought it was really interesting and particularly talking about sort of patient perspectives because I'm interested in knobs and gynae. I follow a lot of sort of patient advocacy groups and things on Twitter. And it is a really, I think, heated area in some respects. And there's a lot of debate and there's a lot of people who have been harmed by obstetric services. And that's just a fact that we know that. There was an embrace out this week, wasn it um and you know there's some big systemic issues um around race and i think that we have to be up front about that as healthcare professionals even healthcare professionals in training um and say you know what what can we do exactly as you're saying lucy like what can we do make people feel more comfortable? And actually it's something that we had a lot of discussion with, with the Ops and Gynae Society that I run amongst our committee. And one of the things that we have done is that we have made a commitment that every learning, like educational webinar we do, we always have a patient perspective as well as a professional perspective. If we can't find a patient perspective, then we won't do the session until we've found one. And I think people have really valued that. Our most recent series has been four webinars on different sort of pathologies of pregnancy. I suppose you would call it preeclampsia and things like that. And we always have a patient perspective. And a lot of the feedback we've got has been like, that's been really useful. So I suppose that I've kind of, it's a bit tangential really, but I suppose what I'm trying to say is that there are other ways to understand people's perspectives as well as actually being there in the room. Not that I'm saying we shouldn't enable people to be in the room, but i think that there's a lot of other resources and things out there that can help definitely what about you chidera what your thoughts i mean it is really interesting because as lucy said for someone i know ollie has an interest in surgery and and so do i so for me the obs and gynae placement will essentially be probably the only obstetric experience that I have ever and I'm incredibly grateful for it but I can understand from I guess the point of view of someone who has a very limited or restricted exposure during that period of time being a bit concerned because if that's if that's all you ever learn or at least are able to learn on ward, which we know is so much more valuable than what you can learn in a book, I can understand feeling frustrated. But on the other hand, you know, again, pregnancy is such a private and can be such a trying time that I can understand from the patient's point of view why they may be slightly more cautious about who they want in the room. So it is difficult, but I appreciate what Lucy said about, I guess, the senior in the room taking the time to frame it in such a way that, you know, at least the male medical students are getting a bit more exposure because I can remember when I was in medical school, it was a bit of a running joke that if you were a guy on an obs and gynae placement, you know, you might as well home because you won't see very much well you know and people wouldn't want you in the room so I think I guess advocating from the point of view of the consultant or the registrar on the ribbon doing as best you can to make it more comfortable I think is is really useful to maybe breaking what for some people may just be a slightly more superficial social stigma barrier as opposed I know for some people it may be on the basis of quite significant trauma but I know for me for example I might just be a little bit embarrassed about the you know a guy being there if I haven't got my trousers on or whatever and maybe someone framing that conversation when we start it in that way of introducing them as a professional colleague I think would really help me feel more comfortable about that person being there. So following on from that, Lucy, do you have any tips for medical students about gaining consent to be able to be able to observe? I think it's about how you approach it in terms of respecting both the healthcare professional colleagues and then particularly the woman's perspective. So rather, I mean, we slightly perpetuate this by the rushing students into birth rooms at the last minute. And I think approaching it from the, how can I gain this woman's trust and how can I show the healthcare professionals that seeing the birth is, it kind of is too much of a tick box because actually what you need to do is to, I think, try and sit with a woman. And that's a hard skill. And it's actually quite a hard skill for medics, particularly those of us who like stuff quickly. So to go and sit with a woman in labour is not a skill that we see developed. But if you're going to be part of a birth, then understanding the natural rhythm of labour, which is what the midwives do, is, I think, a good step. You can tick a birth by going to see a caesarean. And that's generally more straightforward. There's more people in it's it's an operation but I would I would argue that seeing a normal birth is is also a crucial part even if our cesarean section rate is going up and is you know 30 35 percent most babies are born and it's a very different process so I think taking the time to build the relationships with the healthcare professionals that allow you to find women who are comfortable, but also being prepared to sit in a room feels you're doing nothing. And sometimes doctors aren't very good at doing nothing. So it's slightly counterintuitive. We do stuff. Because, you know, if that's going to be one of only a few births you're going to see, that is your experience. It probably will stay with you for the rest of your life for the reasons that Anne and Dara talk about. But to work out how to make that experience count. Thank you. We'll discuss a little bit more about being present in a birth but that will be right after this. How much do you care about indemnity right now? Probably not a lot. You're still a few years away from really worrying about claims and complaints from patients but being part of medical protection is about a lot more than just indemnity. We can be there if something goes wrong but we're also here to help make sure things go Thank you. members benefit from our expert advice and support throughout their career. During your years at medical school your membership is completely free. You'll get training resources that can help you become an even better doctor plus a dedicated student team there for you when you need it most.
So I think I for the second birth that I saw when I had a little bit more time I met the lady during the ward round and then I came back and took a really long history and to be honest it kind of turned into a really long chat about you know how she had tried to conceive and previous experiences she's had and I think a previous miscarriage and to be honest I kind of I think just set myself up as like an emotional support dog slash medical student for the day um so I mean I'm someone who likes to get to know my patients and particularly support them emotionally now even now so and I still consider that a very valuable aspect of my job alongside doing I guess the more clinical things so I felt in a way still quite useful because um I think her husband kind of was coming and going throughout the day etc and so actually I was probably spent more time with her that day than he did and so I felt well at least she's not alone and from that point of view I felt like I was contributing something and hopefully she enjoyed or at least wasn't annoyed by me being there. Yeah I guess you're right a lot of the time the most useful thing a medical student can do is just sort of be there and listen I think that's something that we're always told patients value quite a lot because we have the time we're not needed to be physically doing other things so that's probably the most useful thing that we can do what do you think Anna? Yeah I totally agree like my experience is has been very similar to Chidera's like I spent a lot of time because I was interested in Ops and Gynae I spent a lot of time on the ward kind of the the healthcare professionals got to know me they would see me coming um and I would spend a lot of time with the women even when I was sort of going to c-section lists and things you know there's there's all that time while they're having the epidural and everything and I would spend time talking to them and talking to their partners if they were there and I never encountered anyone who had then subsequently felt uncomfortable with me being in the room which is really really nice I think that's probably probably an unusual experience but I was very lucky and yeah holding hands and holding retractors that's what medical students are good for right yeah even now I'm an SHO and I still think that's like 50% of my job it's great though at least you are useful the other really big thing that came up from sort of speaking to my course mates about this my friends who who are currently on OBS and Guiney blogs, is that students are often really worried that something might go wrong while they're in the room and sort of how that's handled. And are you supposed to pitch in? Like, is there anything you can do? Are you meant to stand back? Do you leave the room? Do you get a chance to debrief afterwards? Lucy, can you reflect a little bit on the practicality of and what like the logistical reality might be for a student? I think it's, I'm going to sort of take the scenario where it's not expected. And there are varying degrees of urgency. So, you know, everything varying from the situation where the fetal heart rate stays down and you're going to sort of, you know, drill for a fetal brachycardia and onwards. And then those with a bit less urgency. I think I'll tell a story from SHO days. So it was my first week as an SHO in Obzengaini and I was in a birth room and the midwife delivered the baby's head and then asked the mum to turn on to all fours and delivered the rest of the baby. And I sort of thought, didn't think much of it, but it transpired that the midwife had recognised shoulder dystocia. So the head delivering and the shoulders getting stuck. And as part of the manoeuvres had turned the women onto a force which can help relieve shoulder dystocia. I had done nothing. I'd stood at the side as an SHO. I hadn't even recognised it. And I was sort of, it went through a big thing of, you know, why hadn't I acted? You know, if somebody came to me and said, I just noted times for you, it'd be like, oh, joy. You know, so both knowing when to step in and offer help and knowing when to step back and just be observing, but you can still be useful. And I would just think of that teamwork and where you might be that cog in the team whilst recognising that it can be a tough experience for you because you may feel a bit as if you're not sure where to help. So you should have other experiences from other areas in medicine, emergency medicine or whatever else, where you can draw parallels and transferable skills. I think you're a useful part of the team and we can't shield medical students and junior doctors from all these tough times. So just seeing bits of them and gradually seeing more is really important. That would be my take on it. Yeah, amazing. amazing thank you chidera and anna do either of you guys have any advice on sort of how to reflect on a scenario like that if you're present if something goes wrong either in obstetrics or anywhere in medicine and sort of how like who you might debrief with how you might manage your own emotions in those situations well chidera probably has some better experiences than me given that she's an actual doctor but I actually was in an obstetric emergency I actually wasn't on obstetrics at the time I was on paediatrics and we were crash bleeped to theatre and it was just such a flurry of activity I think I didn't really know where to look Eventually another consultant obstetrician came up from clinic and that was when I was like, oh, something's happening here. And it's exactly as Lucy said, I was a runner. I went and got clothes for the neonate. I helped with the neonatal research because I was supposed to be on pediatrics. But I think I did do a lot of reflecting on that situation and particularly the leadership that was shown by the consultant obstetrician was something that I actually found really inspiring and I did follow the case up and both mum and baby had good outcome which was really nice to find out but yeah the leadership that was shown in that theatre is something that I have never forgotten and if I can at some point in my career be that person like that would be yeah it was a very it was a very stressful situation and it was stressful to be there but when I was yeah sort of debriefing with myself that was what really stood out to me like everything calmed down as soon as um the second consultant came in and started kind of taking the reins um so yeah I think but I think most universities provide um services and things and you can obviously access like the BMA's counselling service um and practitioner health and stuff if you're um struggling with experiences you've had I'm not so sure about sort of formal debriefing provided by the university haven't ever done that. I think Anna said something that really chimed which is about recognising your own emotional needs and the fact the same event may have a different impact for different individuals so just getting used to asking yourself how that's felt I think we've all gone home and walked out a situation where it may be that another healthcare professional hasn't even recognised your need, but needing a safe way to unburden. We've all had flatmates who have probably been a bit surprised by our stories, particularly if they're not in medicine. But just finding those routes to tell a story. It's very interesting that there's a long tradition of telling birth stories anyway. And so what you're doing is often telling a story from a healthcare professional point of view, a medical student or junior doctor, just reliving, talking through. But look at what Anna's reflected on. She's reflected on the leadership that was shown as part of that emergency situation. So taking something from it that is a sort of positive, you know, a positive in what is a tough situation. Chidera, what about you? Have you got any experiences or tips on how to reflect and debrief? so I would say when it comes to these sort of things just speaking generally of any sort of I guess experience exposure that you may have to unfortunately a poor outcome um I like team debriefs I think they're useful just so that because I think it's very easy often to leave a situation thinking I should have done x I should have done y and actually I've always found team debriefs are quite good for setting everybody's mind at ease because you suddenly realize that everybody around the room is feeling that they maybe did not contribute x or did something wrong and I think just that in the moment or maybe five minutes later in a coffee room is really useful. I think particularly if you're at a hospital or a trust that has a really strong mess culture, that again has been really useful for debriefs for me. Particularly in F1, our mess culture was quite strong and the F1 group was really quite tight.
And again, that's really useful. And I guess what Anna said about debriefing with yourself is actually really useful. So I don't know if you know, but in Foundation, we use something called Horus. We fill in all of the little things that we have to get ticked off. But there is a reflection panel on there. And actually, you have no requirement to do reflections, but it's a really nice structure because it asks you specific questions about sort of what you think you could have done, what you've learned describing the scenario. And even just the structure of that has helped me with my reflections in terms of teasing out areas where maybe I felt uncomfortable, didn't entirely understand why or entirely know how to fix that for next time. So I think debriefing with friends, debriefing with your team, particularly if you have a senior or a mentor that you're close to. But actually taking the time to really think through yourself is really helpful as well. Thank you. Lucy, yeah. I just want to touch on an area that I don't know, Nicky, whether you'd plan to talk about it, but the real tragedies. And because it's almost like a sort of, you know, not quite an unspoken taboo, but I look after women who have a stillbirth and sometimes present. It is one of the toughest things that that I do and it is normal to be emotional to have emotions and to have a very strong response to the very tough times you know this isn't like the expected death of someone who's elderly, where for many reasons, somebody may die in more expected peaceful circumstances. There is rarely anything that is, you know, it is really anything other than a tragedy, particularly for the individuals. We can learn to respond professionally. There's been debates in the BMJ about is it okay to cry in front of a patient or a woman and we can come back to that. But one of the reasons I'm an obstetrician and that I feel so strongly about what I do is how you can make a difference to those women, particularly for the care at the time of their loss and also for me, care in future pregnancies so one of the most important parts of my my role is that if if they are going through a tough time I make that I try and do everything I can to make a positive contribution at what is a very difficult time and that I also get get what is often the joy of a woman taking a baby home next time. So it is a difficult topic and we often shield medical students from it. But sometimes if medical students join me in clinic, I do a clinic where a lot of women have had a previous pregnancy loss. And I've had students with me when a woman has sometimes just opened up about what that's like. And I wouldn't shy away from it because although it is a tough discussion, it's extraordinarily, you feel as if, again, an incorporated part of a woman's journey. But last week I saw somebody and she's just had her second baby and the joy of her holding a baby in her arms and taking it home this time is just phenomenal. It's why I do my job and I still get choked up about it because it's so special. Yes, that's amazing. I actually really wanted to get a patient experience and their opinion for the episode and with the BMJ patient editor team we did a call out for anyone who'd given birth with a medical student in the room we were looking for someone who'd given birth with a medical student in the room and we ended up getting a few responses saying they couldn't remember if a medical student had no one who said that they specifically remembered that wanted to contribute so i wonder if that kind of answers my question of that having us there is probably the least of some of their worries and they've got more important things to worry about so if you ever feel invasive perhaps that's a good thing to think about. Okay panel so what would your tips be if a medical student is feeling nervous before starting their OBS and gynae block? Me next year when I'm about to start and I'm listening back, what are you going to tell me? I think I would embrace the block as an extraordinary opportunity to get an insight into one of the most special parts of a woman's life and just not just the woman but her wider family and to think about this as an extraordinary part of medicine because she doesn't have a disease and to reframe pregnancy not in illness terms not in disease terms but as an event in a woman's life that then puts that whole and to try and tune into that experience and to seek out those bits of of particularly maternity rather than gynecology but to focus on maternity and birth about understanding that that the range of women's perspectives and that to know that this will be the one of the most special times in the woman's life and you're going to be allowed into that part so so to understand it in in that context would be my suggestion I think just speaking more broadly about my experience doing my obstetrics and gynecology block, which was also combined with some sexual health as well, is that really like lean into it because there really is something for everyone. You know, even if you know you're not going to be an obstetrics and gyne doctor, there's, you know, perinatal psychiatry. There's a lot of in um both benign and malignant gynecological disease and i think if you try hard enough you really can find something that that is interesting to you um i mean i love obs and gynae so i'm probably the wrong person to talk to about this and to daryl what about you what tips would you give um i mean to echo the other two, I think regardless of whether you have an interest in obstetrics or gynaecology or not, I mean, I think often as med students or doctors, we talk about the privilege that we have of having insight into our patients' lives. And I think for me, you know, I've known I wanted to be, for example, a neurosurgeon since I I started medical school but I still think the opportunity to see someone having a child particularly their first child is a privilege that as a medical student or as a doctor or as a healthcare professional is unmatched so I think it's something to be excited for and as Anna said to lean into because it's I think it's a privilege that you are unlikely to match ever again really just want to pick up on what you said to Gerard because you you've just encapsulated beautifully why all medical students should embrace it which is that I would love that any doctor is is all very likely apart from the geriatricians, to have pregnant women in their normal, as part of their practice. So we, I have to call the neurosurgeon sometimes. And there are very few doctors, you know, that I don't. So pregnant women are not scary. And will be much less scary if you as Anna says wonderful phrase lean into the to the attachment so that you don't leave obstetrics and gyne still scared of pregnant women because our experience as obstetricians is is that many other doctors are now that's partly from sort of lack of familiarity but we're here to be that bridge so whether you know if you've got a woman who needs neurosurgery I'm there to help you because you're going to do your bit and I can do mine but if you've if you've had a positive experience during OBS and gynae that will help you so so you know there are very few doctors who who won't need that experience just to remind them that pregnant women are just human beings then, bye from us. Bye.
The U.S. Health Resources and Services Administration defines health equity as the absence of avoidable differences among socioeconomic and demographic groups or geographic areas in health status and health outcomes, such as disease or mortality. The COVID-19 pandemic, which has disproportionately affected Black, Latinx, and Indigenous Americans, is the latest manifestation of the failure to achieve health equity in the United States. I'm Stephen Morris, the managing editor of the New England Journal of Medicine, and I'm talking with Michelle Evans, a senior investigator and the deputy scientific director at the National Institute on Aging and a member of the journal's editorial board. As part of the journal's series on the fundamentals of U.S. health policy, Dr. Evans has written a perspective article about health equity in the United States. Dr. Evans, as you write in your article, Black, Latinx, and Indigenous Americans are dying from COVID-19 at disproportionately high rates. So what has the pandemic taught us about health inequities and access to care in this country? Well, I think, unfortunately, it uncovers something that those of us in the medical profession face every day, that individuals from minority backgrounds are at greater risk. The COVID pandemic really is sort of the superimposition of an acute medical problem or acute condition with high virulence upon pre-existing poorly managed severe chronic disease. So it's health inequities that sort of have permitted this acute infection to really exploit existing susceptibilities among Blacks, Latinx, and Indigenous populations whose baseline medical health conditions frequently include diabetes, systemic arterial hypertension, asthma, and obesity. So these medical vulnerabilities driven by social and political determinants of health unfortunately created a conducive environment for infection and transmission that has resulted in disparate infection, hospitalization rates, as well as the significantly disproportionate mortality rates that we're seeing. How have health policies widened or failed to close the gaps in health status and health outcomes among minority patients in the United States? Well, I think one of the issues certainly has been the availability of healthcare access, because what is sort of most important in terms of susceptibility is it's not only that we just have a higher prevalence of these chronic diseases, but it's also the severity of the disease and disparities in disease control and management. So hypertension is more frequently corrected and managed appropriately in 60% of whites with hypertension compared to less than 50% of African Americans and Hispanics. And that relates to the higher uninsured rate as well as the fact that many minorities have no usual source of care that ultimately impedes their access to high-quality care. And much of this is related to low levels of economic viability in our economy. African Americans, Hispanics, and indigenous Americans are frequently segregated in either low-paying occupations such as service industry. They also occupy jobs that perhaps are in the new gig economy that don't even have health insurance linked to their job. And many of these low-paying jobs, particularly now in the pandemic, many of these workers have been left out of the economic picture altogether with higher unemployment rates. And the fact that we link insurance to employment, again, increases the inaccessibility of healthcare access to these populations. So looking at that sort of more general public policy area, in your article you talk about the effects of childhood poverty on health, educational attainment, employment opportunities, income, and you write that nearly three-quarters of children living in poverty are non-white. So what kinds of general public policies would begin to address intergenerational poverty and children's health? Well, I think the government has made some start in terms of the earned income tax credit, the Supplemental Nutritional Assistance Program, the National School Lunch Program, as well as the Temporary Assistance to Needy Families and other excellent family support programs that do lift children from poverty. However, there are gaps that remain in the support network for children. And this is continued in terms of educational opportunities. For example, we know that low economic conditions in the family is associated with poor health outcomes, but also with poor educational outcomes. So if we look here in the terms of the pandemic, we're looking at, for example, in the city of Baltimore, almost 40% of households have no laptop. And if you're a child and your school has gone completely remote, that may mean that you're winding up trying to do your homework on your parents' cell phone, if they even have cell phone access. So a simple thing like changing the digital divide, making sure that children nationwide have access to internet. We frequently think that maybe it's the rural areas of the country that do not have access to the internet. However, in an urban eastern city like Baltimore, we have limited internet accessibility for a large number of poor children that will ultimately result in even furthering the existing low and limited educational opportunity for them. You also mentioned in your article inadequate diversity among health care professionals as another contributor to these disparities. To what extent is the resolution of that going to wait for answers to these economic and education policy questions, and how much can be accomplished through more targeted attempts now to recruit non-white health professionals? I think there's no new information about the underrepresentation of minorities in STEM. NSF's post-secondary education data from 2016 shows that only 22% of those who received bachelor's degrees in science and engineering were underrepresented minority students. Only 9% of science and engineering doctorate degrees were awarded to underrepresented minority students. This is not new information. We need to do better in terms of focusing at the undergraduate level at building the pipeline. The AAMC, in their most recent set of data for the matriculation year of 2019-2020, shows us that over 21,000 matriculants, only 230 of them were indigenous Americans. That's 1.1%. Only 95 of them were Native Hawaiians or Pacific Islanders. Those are numbers we can start to do something about now. And it's critically important that we do this because at this rate, we're never going to achieve a diverse physician workforce. Whites comprise about 60% of the U.S. population, and about 56% of practicing physicians are white. So whites have a significantly increased chance of finding a culturally concordant physician. And while I feel that most physicians give great care, the best care they are able to deliver in the setting in which they are practicing, regardless of a patient's racial and ethnic group, there are several studies that suggest racial concordance between physicians and their patients is a significantly influential factor in health outcomes as well as in success of disease management and control. Recent work that was published this month in PNAS by Brad Greenwood and I believe Rachel Hardiman showed that racial concordance is a critical factor in childbirth, which is an area of persistence and in some communities a worthening health disparity. They showed that newborn physician racial concordance is associated with a significant improvement in survival for black infants in Florida. The result was even more pronounced in medically complicated childbirth situations as well as in hospitals that deliver more black neonates. So we have to take this seriously, and the reason why I circle back to childhood poverty here is that's where we must start. If we are starting with keeping children in poverty and not raising them up from poverty, we are just reigniting health disparities and health inequities from one generation to the next. So we have to really consider a comprehensive view of how we will address this problem from the aspect of diversity among health professionals, but even in terms of national security, because the military has problems nationwide with the unevenness of our healthcare system. The Heritage Foundation reported in 2017 that among the 71% of citizens who were between the ages of 17 to 24 and eligible to serve in the military, 32% of those were ineligible because of health-related conditions, including obesity, asthma, and mental health conditions, which says to me, at least, that we have a nationwide problem with dealing with health in children, adolescents, and young adults. You also say in your article that, like biomedical research, health policy needs to embrace ethical tenets, respect for persons, beneficence, justice. So what would policy reform that focuses on those ethical tenets look like? Well, I think we need, as a nation, to reflect on what are the important tenets of being an American? What are the things that we respect? And we respect equity. We respect equality. And how can we purport to live up to the foundational tenets of our country if we are unable to respect one another's rights? And I certainly believe that health care is a right. Health equity is all about providing the opportunity for everyone to be as healthy as they possibly can be. And we cannot continue to abridge that right. There are many ways to get to that point, but I think we all must embrace as the goal to achieve health equity. I'm not a health policy expert, but as a physician and a citizen, I believe that policy reform should be aimed at that one universal goal, achieving health equity. Finally, what today can individual physicians do to promote health equity in their own practices and on a policy level? Well, I think the issue facing physicians is very complex.
Since there is such disparity in health, education, economic opportunity, clinicians must provide care that recognizes that equal treatment may not be enough to close the gap or to correct the systemic disadvantage that some of their patients face. The recognition of these special needs, personal targeting of those needs, and the provision of medical care and ancillary support is critical. The issues that physicians face in the care of disenfranchised and marginalized populations, they're complex problems. They're multidimensional problems. They're problems that hit back every day. For example, many believe that medical algorithms are critical to guide physicians in providing the best care possible. We as physicians come to define high-quality care sometimes by following evidence-based medical algorithms. So we also have to think that these disease-based medical algorithms must be adjusted for the social and political determinants of health. If these algorithms are applied too rigidly without considering the contextual nature of the care you're providing, they may, in fact, for some patients, reduce the overall quality of the outcomes that we're seeking to provide. And this is a major challenge because it's not that physicians do not wish to understand how race, how poverty, how literacy, immigration status, housing, density, occupation. They want to understand how these play a role in the disease process and in the context of the treatment plan. But physicians are also faced with the length of patient encounters that have become so short and often so rushed because of patient volume and paperwork and other factors that may be out of their control, but may perhaps be in the control of the major medical systems for which they work. So this is a situation where physicians, as well as major academic medical centers, health insurance providers, need to work together to understand that there needs to be personalization of care, just as in the enormous expansion of genomic understanding of how to best treat tumors on an individualized basis. We need to understand how to best treat patients on an individualized basis, understanding the context in which they live, the context in which they suffer from and are burdened by health disparities and health inequities. Thank you, Dr. Evans.
Hello, and welcome to this JAMA Editor's Audio Summary for our April 23rd, April 30th, 2014 issue. This is Jeffrey Saver, Associate Editor of JAMA. This issue of JAMA is a special issue devoted to neurology, co-edited with my colleague Roger Rosenberg. It emphasizes the advances in therapeutics as well as diagnostics occurring in neurology. Included in the issue are five original contributions, three randomized trials, one national quality improvement project, and one population-based observational study. The first of the randomized trials in the issue is on ambulance-based thrombolysis and its effect on time to treatment in acute ischemic stroke. We know that the benefit of tissue plasminogen activator as a treatment for acute ischemic stroke is highly time dependent. In this study, Emiger and colleagues analyzed whether having a mobile hospital on wheels, a mobile ambulance containing a CAT scan, and a neurologist, and laboratories for doing blood work at the scene could accelerate the start of tissue plasminogen activator in acute stroke patients. In the PHANTOM-S trial, they, in alternate randomized weeks, had patients follow the standard here in Berlin of being brought by ambulance to the nearest stroke center, or in the intervention weeks, having the mobile ambulance go out to the scene to evaluate the patient on site. They found that there was a substantial time reduction that occurred during the weeks in which the mobile ambulance was deployed, and it was especially notable when the ambulance was available for direct response. Among the patients in whom the mobile CT ambulance was deployed, the alarm to treatment time, the time from the call to the EMS service to the delivery of TPA, was shortened by 25 minutes. There was no increase in the frequency of intracerebral hemorrhage among patients treated in the field, and weeks in which the ambulance with the CAT scanner was deployed saw a higher number of patients treated with TPA in addition to the greater frequency of TPA treatment. In a second study analyzing accelerating the start of TPA therapy, Dr. Greg Fonaro and colleagues from the National American Registry Get With The Guidelines Stroke analyzed the effectiveness of an intervention that targets stroke program to accelerate TPA treatment. Ten care strategies for faster door-to-needle times for TPA administration were disseminated to hospitals participating in Get With The Guidelines stroke throughout the United States. And the effectiveness of the intervention was analyzed in a before and after paradigm, comparing the pre-period from 2003 to 2009 with the post-period from 2010 to 2013. Among the over 60,000 TPA-treated patients, there was a marked acceleration in the proportion of patients meeting the national quality improvement target of a door-to-needle time under 60 minutes. The improvement per year in meeting this goal was 1.4% per year in the pre-intervention period and 6.2% per year in the post-intervention period. Overall, the door-to-needle time declined from 77 minutes in the pre-intervention period to 67 minutes in the post-intervention period, suggesting that there was a substantial acceleration in treatment as a result of the intervention nationally. In another randomized trial in this neurology theme issue of JAMA, Chamberlain and colleagues reported on the administration of lorazepam versus diazepam as anticonvulsant therapies for pediatric status epilepticus. These agents had previously been compared in adult patients, but this was the first major trial to analyze their relative effectiveness in the pediatric age group. They, at 11 U.S. academic centers, enrolled 273 patients, 140 to diazepam and 133 to lorazepam. The primary outcome was a cessation of status epilepticus for 10 minutes without recurrence within 30 minutes. And this outcome was achieved with comparable frequency in the two groups, 72% in the diazepam group and 73% in the lorazepam group. Adverse effects, including the need for assisted ventilation, also occurred at comparable frequencies between the two groups, except there was more sedation in the lorazepam group. The authors concluded that among pediatric patients with convulsive status epilepticus, treatment with lorazepam does not improve efficacy or safety compared with treatment with the older standard agent of diazepam. In another randomized trial in this issue, the Nordic investigators report the results of acetazolamide as a treatment for preserving visual function in patients with idiopathic intracranial hypertension or pseudotumor cerebri in the IIH treatment trial. Acetazolamide has been a traditional component of the neurologic treatment for idiopathic intracranial hypertension for decades, but had never been subject to a well-done randomized clinical trial before. In the Nordic trial, 165 patients with idiopathic intracranial hypertension and mild visual loss were randomized. All of them received a background intervention of a low-sodium weight reduction diet. Patients received a dose of acetazolamide up to 4 grams per day or matched placebo for a six-month period. The primary outcome was the perimetric mean deviation, the average ability to detect targets in different parts of the visual field. And this did show a statistically significant benefit among patients in the acetazolamide group compared with placebo. There were also improvements in papilledema grade and in vision-related quality of life, as reported by patients. The authors conclude that acetazolamide and a low-sodium weight reduction diet compared with diet alone results in modest improvement in visual field function. The fifth original investigation in this neurology theme issue of JAMA comes from Salman and colleagues, and they analyzed the outcome after conservative management or interventional management for unruptured brain arterial venous malformations. The intervention in this study could be any combination of three treatments that actively alter the structure of the malformation, including endovascular embolization, neurosurgical excision, or stereotactic radiosurgery. This was an observational study using the Scottish National Registry and capturing the effect of these treatments in regular clinical practice among a large population with long-term follow-up, providing complementary information to the recent ARUBA trial, which was a randomized study with shorter-term follow-up and selective group of patients enrolled. Among the 204 patients followed in this study, 103 underwent interventional therapy and 101 underwent medical therapy. Patients were followed for an average of seven years, and the rate of progression to the primary outcome, which was deaf or sustained disability, was higher in the patients who received intervention versus the patients who received conservative management. The conservative management arm had a hazard ratio of 0.59, a 41% reduction in the primary outcome of death or disability. The benefit was sustained up to 12 years of follow-up. The authors conclude that among patients who are age 16 or older, in routine clinical practice, use of conservative management compared with intervention is associated with better outcome over 12 years of follow-up in patients with unruptured arteriovenous malformations of the brain. Also in this issue is an evidence-based review of the pharmacologic treatment of Parkinson's disease by Drs. Carnally and Lang, which provides an excellent up-to-date overview of management. In addition, the issue contains three viewpoints from neurologic leaders in American medicine. In the first, Callahan and colleagues discuss how neurologists can choose even more wisely, looking at the process of identifying priorities for waste reduction in neurologic care. In the second viewpoint, Birbeck and colleagues consider the global impact of neurologic disease and opportunities and challenges in advancing neurology worldwide. And in the last viewpoint, Timothy Pedley looks at neurology at the crossroads in the evolution of American medicine, considering changes in the support of federal science and in the delivery of healthcare and their impact on the practice of neurology. So that is an overview of the neurology theme issue of JAMA. This is Jeffrey Saver, Associate Editor of JAMA. For more podcasts, visit us online at jama.com.
Hello and welcome to the Lancet Psychiatry Podcast. Today we're going to be talking about an issue in global mental health which relates to a review we've just published. I'm joined by the author. Would you like to introduce yourself? Hi, yes. Niall, thanks very much for having me. My name is Gareth Nock here. I'm a psychiatrist at the Department of Psychiatry at Stellenbosch University in Cape Town. Okay, and could you just tell us what your paper is about? What's the title of it? Our paper is a systematic review of the effectiveness of traditional healers in treating mental illness and mental disorders. Okay, and that sort of brings up the first question, which I guess I have and a lot of other people would have, which is that psychiatry has had a really long, hard struggle over the past 100 years to be accepted and respected as this sort of modern, evidence-based medical specialty. So why the focus on traditional healers, which some would say is the exact opposite of that? Well, yeah, that's a very good question. The main motivation for this paper was that it turns out that people go to traditional healers a great deal. They're very widespread. In the developing world, certainly, where there's a great mental health treatment gap, so many people don't get treatment, conventional treatment, for psychiatric disorders, and many people then go to traditional healers for treatment. And also then in the developed world, in the UK, for example, many Muslim people go to see their Muslim clerics for traditional or faith healing. In the USA, there's Native American healing, which is very popular. And in fact, all over the world, it turns out that traditional healers are greatly used in mental health. And our review is part of a larger collaborative project funded by the National Institute of Health in the US, which is collecting data and working towards improved mental health care delivery, specifically in Africa, and specifically by collaborating with traditional healers. So we want to know, we wanted to know, what is the effectiveness, the current effectiveness of traditional healers in treating mental illness? I suppose the first question is what is tradition? So some people would say, for instance, homeopathy as being traditional healing, but I think that doesn't come under your definition, does it? Yes, exactly. So one of the challenges when we put together this review was in finding suitable definitions which we could use and keep it systematic and keep it as objective as possible. And the existing definitions of traditional healing, for example, by the World Health Organization, are actually not suitable. They concentrate on words like indigenous or on the fact that the healing must have a long history. And that really includes a whole sort of heterogeneous collection of healing methods, as you say, homeopathy, chiropractic, faith healing, all these things. It's just a huge array. And we wanted to focus on something which was sort of inherent to a particular class of healing. So the definition which we used in this review was any form of healing in which the healer makes explicit use of a sort of spiritual or religious or magical causation. And that, in fact, includes most of African traditional healing, as we know it here in Africa and South Africa. It also includes a huge number of traditional healers in South America, in North America, all over the world. And by virtue of being kind of religious or magical, they happen to also fit the World Health Organization definition by being quite local and culturally specific and also generally having a long history. But we didn't use that in our definition. So I suppose you could say our traditional healers are magico-religious healers. And that brings up a real issue when you're pulling all these studies into a systematic review framework, because one of the things you want to look at in a systematic review is quality. And that partly relies on the amount of money that's behind the study, the sort of logistics of it. But also, I think the idea of quality in most people's minds would include something like a randomized controlled trial. And when you're talking about the explicit use of these methods, that surely precludes the RCT as I think most people would understand it. Yes, no, certainly. So any of these traditional healing methods are extremely complex interventions. A complex intervention is an intervention which consists of many different parts which interact with each other in a sort of non-additive way. So we don't have the luxury of being able to pull out one aspect of sort of a magical religious healing encounter and test that one aspect. You have to go for the whole package, which is quite unlike testing drugs in psychiatry, which we can take out the effect and look only at the effect of the drug by comparing it to a placebo, which is what we do in an RCT. So a proper RCT is really impossible when testing such a complex intervention. The best we can do is try and find other interventions to compare it to, and it has been compared to. In some of our reviewed studies, they compared people going to traditional healers to people going to the local community clinic, sometimes comparing religious healers to lay psychotherapists. But certainly there's nothing approaching an RCT here. So our level of evidence, when looked at from the rigorous sort of viewpoint of psychiatry, is not very good. And one of the, well, it could be one of the joys or one of the disadvantages of mental health, which is that though there are certain sort of common experiences and factors all over the world, many experiences are different or experienced differently, expressed differently, depending on the culture in which an individual exists. And so when you're looking at the question of traditional healers, does the presentation of the patient come into this as well? What kinds of things would people be coming to these healers with? Would they be things which fit nicely into DSM or ICD, or is it less tangible and much broader than that? Well, yeah, absolutely. So the experience of mental illness or psychological symptoms is very different depending on one's culture, and the expression of it is markedly different between, for example, Western societies and more developing societies. Also behind that, the understanding of distress is very different. In Western society, we've got sort of an implicit mental and physical distinction on which psychiatry is largely based, and certainly the psychiatric diagnostic system. In most of the developing and traditional cultures, there's no distinction between the physical and the mental. So that comes through in the studies which we reviewed, in which very few of them had actually used psychiatric diagnoses. Some of them did. Some of them were studies were done by psychiatrists in a traditional setting. But the majority of them sort of grouped a whole lot of complaints together, and very often including quite a lot of somatic complaints, because certainly in many developing countries, somatization is a very common presentation of mental distress. So patient groups in these studies were often very heterogeneous. And what we had to do, we had to try and only include studies which gave us some sort of measurable psychological result. Even if half of the complaints were physical in nature, we still looked for a psychological result. And in other studies which just lumped all psychiatric complaints together, we had to make a generalization over all those psychiatric complaints. Now let's just talk about the type of treatment. And you've given the sort of broad definition. I think that the type of treatment is something which I guess clinicians get a bit worried about because every intervention, whatever type it is, whether it's a drug, whether it's a psychological intervention, whether it's a social intervention, whether it's a traditional intervention, does have the potential for harm as well. And it would be interesting to know a bit more about the sort of diversity, the types of treatments, and whether there are any treatments which on the face of it might have some adverse effects as well. Yeah. All the magical religious healing traditions which we included in our review, they're actually all, from a broad perspective, are remarkably similar. I noticed when I was preparing this review and I had my papers on the desk in front of me, when I came in in the morning and started reading a paper without looking at the title, it was difficult sometimes to tell whether I was reading about traditional healing in Africa or reading about it in Indonesia. The overall template is very much the same in that there's a supernatural sort of causation usually which is sought. There's some form of divination. There's explanation. And then there's usually some form of a ritual or ceremony which is used to promote healing or promote personal transformation. That's the basic template. And then even where physical means of treatment are used, for example, if they use herbs or sometimes starvation, which again comes to harm. Even where these physical treatments are used, they've more than often, more than not, got a symbolic or magical or religious meaning behind them. That's the form of treatment which usually happens.
In the African set, there's quite frequent chaining up, starvation, sometimes beating, and this happens probably all over the world. I can't remember the exact numbers, partly because there have been no surveys of how often these sorts of harms occur. In our review, we didn't look at any harms because there's not enough surveys to actually do a review. They do occur, and part of the broader project, the collaborative project which this review is a part of, we'll look at those harms and we'll look at, when we look at collaborating between traditional healers and conventional care, we'll look at ways of trying to minimise those harms and bring them down. And that's going to be, I think, one of the big challenges for global mental health, where clearly we want to build services from the grassroots, but there will, unfortunately, as you suggest, be times when that clashes with ideas about universal human rights. And I foresee those as being really quite difficult negotiations, maybe. Absolutely. We've also done the second, well, following on from our review, we've been looking at some qualitative data from interviews with traditional healers and with conventional psychiatric nurses in three African countries. And we found that although both sides are very, very keen to work with each other, each side is fairly stubborn about what they believe they can do for the other patients and what the other side can't do. So, for example, most of the African traditional healers in our focus groups firmly believe that mental health care is outside the remit of conventional psychiatry because they believe it's got a supernatural cause. And as a consequence of that, they are very reluctant perhaps to take advice from conventional psychiatrists, although they also do try not to harm the patient. The general feeling is that the traditional healers are extremely sincere in wanting the best for their patients. So let's just return to your review now, and if you could just give me the main findings. Now, as I understand, the data wasn't really suitable for a meta-analysis. Yeah, that's right. We eventually found 32 papers which looked at a quantitative outcome of mental illness being treated by traditional healers. And we rated those by quality in an objective way. The general quality then wasn't that good, but we can still draw some conclusions, partly because we have to. We have two options. One is to draw some conclusions on imperfect data, and the other option is to have no idea whatsoever what the effectiveness is. What we tended to find is that for the more minor or common mental disorders, such as minor depression, anxiety, somatization, and the sort of traditionally neurotic disorders, we found that there was a tendency that most people who attended the traditional healer found the intervention to be useful and helpful in many ways. What was interesting is that very often with that helpfulness and usefulness and the benefit they get from that intervention, the patients didn't necessarily report an improvement in psychiatric symptoms. So this, in a way, is quite different to traditional psychiatry where we're very much focused on symptoms. These patients were saying they felt a lot better, but, for example, their sleep might not have improved or even perhaps their mood might not have improved. And it seems that what the healers are doing in this case is they're providing, they're giving ritual and ceremony which provides meaning and explanation about what's happened. It puts the illness and puts the suffering in context, which people find very useful in many ways. We also found that expectation and belief is obviously very, very important here. Three studies which we reviewed measured expectations before the healing intervention and then measured the subjective outcomes after the healing intervention. And without fail, obviously, there was a huge correlation between pre-healing expectations and actual outcome. And certainly the use of ritual and ceremony and the fact that the healers are sanctioned by society increases the degree of expectation and belief in the positive outcome, which is really useful in terms of the healing intervention. So in terms of the more minor mental disorders, we found that the interventions from traditional healers were helpful, certainly for those who believed in the healers and chose to go to them. But for psychosis, what we call psychotic disorders, not much of an effect? Not so much. So there were a number of papers which looked mostly at psychotic disorders, schizophrenia and mania, and they tended to find that although there was often an improvement or some improvement in symptoms, that improvement typically took about two to three months and was difficult really to separate out from the natural course of illness. One of the other papers looked specifically at Tourette's syndrome and OCD. And both of these are, you know, both compulsions and obsessions and tics are very, are quite neuropsychiatric in character and not particularly amenable to a psychosocial intervention. And this paper found out that there was almost no effect from traditional healers in Bali in treating these very sort of neuropsychiatric symptoms. So traditional healers really should be viewed as a useful psychosocial intervention for people who believe in them. And they really can be quite useful when there's an expectation and belief. And that prompts me to speculate, if you'll bear with me here, that you mentioned that effect on depression and anxiety and so on, that kind of level and type of disorder. And it just put me in mind of this thing which is quite commonly talked about in people who deal with psychological treatment research, which is the sort of dodo hypothesis, they all have won and all shall have prizes. I think that's from Alice in Wonderland, the notion that what label you put on the intervention doesn't matter that much. What matters is the therapeutic alliance. And I just wonder if a bit of that might be coming through here. Absolutely. Absolutely. So another finding from this review is that it seems that amongst the heterogeneity that we find of the different sort of healing traditions and amongst individual healers, even in the same village, there's a lot of variability. Two of the studies found that one or two of the healers themselves were actually getting much better results than other healers in apparently the same village. So some individuals seem to be much more able to form a good therapeutic alliance and get much better results. And clearly the analogy here, or there's strong analogies to psychotherapy and in fact any psychiatric encounter where one belief and expectancy in the outcome is really, really important. That includes trust in the healer and where social sanction might be an important part in traditional healing. For psychiatrists, it might be having your certificates on the wall, for example, to increase belief and expectation. And then also the individual qualities of the healer or psychiatrist or psychotherapist are very, very important. There's a lot of analogies between a traditional psychotherapy, therapeutic intervention, and then traditional healing. And I think one of the great areas of interest over the years and decades to come will be looking for those points of commonality and to find out what traditional healing might tell us in high-income countries who maybe don't use these methods so much. What it can tell us about psychotherapies which are established and new psychotherapies and really looking for common mechanisms and factors. Absolutely, yes. When I was reading through these papers and digesting them, I kept notes about what can psychiatry in a way learn, what can psychiatry be reminded of from these studies of traditional healers. None of the traditional healing observations here are new to psychiatry, But the fact that these psychosocial interventions get such good results for psychosocial problems and people continue to go to them and invest so much value in these healers just goes to show how important nonspecific interventions are. So that will be the non-drug interventions, the power of the interaction in psychiatry. Thank you very much, Gareth. I think that's a good point for us to end on today. Just to say that that paper on traditional healers and mental health is free to download from the Lancet Psychiatry website. So for now, thank you very much again, Gareth, for joining us. And thank you to you, the listener, for downloading this podcast. I hope that you'll join us again next time. Thank you. Bye-bye.
This is the JAMA Editor's Audio Summary from the JAMA Network. Hi, this is Eric Peterson, Corresponding Editor for JAMA, and welcome to the first edition of the 2014 year. This edition starts off with a bang with many, many great articles. The first of these studies is the TeamAD VA Cooperative Randomized Trial. This is an interesting study comparing vitamin E and memantine in treatment of patients with mild to moderate Alzheimer's disease. The study compared, in addition to acetylcholinestase inhibitor, whether the addition of these other two drugs, alone or in combination, could improve functional status. The study found that vitamin E was effective in reducing functional decline in patients with early Alzheimer's disease. Amantine, in contrast, had no effect on functional decline. Next, we have actually three studies that were presented as late-breaking clinical trials at the recent American Heart Association meetings. The first of these is a study by Kim et al. looking at a very large out-of-hospital cardiac arrest population treated in Seattle. This study looked at over 1,300 patients with cardiac arrest and compared whether giving pre-hospital cold saline could improve the outcome of these patients relative to starting hypothermia within hospital. The study found that the pre-hospital intervention was effective in reducing core temperatures for these patients. However, the study had no impact on survival or cognitive improvement. The study also found that the intervention was complicated by increasing rates of pulmonary edema requiring diuretic use. Overall, the study does not support the idea that pre-hospital infusions of IV saline can improve outcomes in patients with cardiac arrest. In an editorial, Granger and Becker praised the authors for carrying out such a large and well-conducted study. They both, however, raised the questions about what we do and don't know about hypothermia in cardiac arrest patients and urged strongly the need for further randomized studies to define when and where hypothermia can improve outcomes. A second study of out-of-hospital cardiac arrest compared whether mechanical chest compressions versus manual chest compressions resulted in better outcomes. This study by Rubertson and colleagues looked at over 2,500 patients without a hospital cardiac arrest. They found that mechanical chest compressions did not improve outcomes relative to manual chest compressions, looking at four-hour survival. A final late-breaking randomized trial was presented by Heldman and colleagues. This study compared two forms of stem cells, mesenchymal stem cells versus bone marrow mononuclear cells, in the treatment of ischemic cardiomyopathy. The study was a phase one trial and compared 65 patients treated with mesenchymal stem cells, bone marrow cells, as well as placebo, and then looked at effects up to one year out after treatment. Given the relatively limited sample size, the study was not able to definitively determine whether one type of stem cells was more effective than the other, but does lead us towards carrying out larger phase II and Phase III studies with these agents. This issue of JAMA also contains a very interesting clinical review written up by Yanoski and Yanoski looking at issues of long-term treatment for obesity. The authors identified up to 20 clinical studies as well as one meta-analysis which look at various therapies useful in the treatment of long-term obesity. The authors review the evidence supporting the use of medications as a means of altering the course of patients with obesity. They identify where there's drugs that are effective in helping patients lose weight, but also identify areas where we need more information. This edition of JAMA also contains an important viewpoint by the director of the CDC, Thomas Frieden, and colleagues. As we all know, high blood pressure is a major problem in the U.S. The viewpoint points out that protocol-driven treatments for hypertension are a critical pathway to actually improving the outcomes of patients with high blood pressure. The authors identify the challenges in managing and controlling blood pressure in the U.S., as well as describe ways in which the Million Hearts Campaign and other strategies have been successful in better managing blood pressure on a national level. I hope you all enjoy this first edition of JAMA for 2014. This has been Eric Peterson, Corresponding Editor for JAMA. Have a good day. For more JAMA Network podcasts, visit us online at jama.com.
Hello, and welcome to this author interview from the JAMA Network. This is Deanna Balandi with JAMA Neurology. Are more young people having strokes? Dr. Mary George and her colleagues at the Centers for Disease Control and Prevention in Atlanta looked at whether stroke hospitalization rates have continued to increase, and they looked at the prevalence of stroke risk factors among younger adults. Dr. George joins us along with Dr. James Burke of the University of Michigan, who wrote an accompanying editorial. So, Dr. George, let's jump right in with you and talk about how you conducted the study so we can get to your major findings. First, what kind of data did you use and who qualified as younger in your study? We used data from the National Inpatient Sample, which is part of the Healthcare Cost and Utilization Project sponsored by the Agency for Healthcare Research and Quality. And these are nationally representative data on hospitalizations from a stratified sample of about 20% of hospitals in the U.S. So the data allow us to calculate national estimates on hospitalization rates. We analyze stroke hospitalizations by stroke type, acute ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage. We calculated the hospitalization rates by age group, gender, and race ethnicity from 23 through 2012. Looking at the trends over time and the age groups that we used were 18 to 34, 35 to 44, 45 to 54, and 55 to 64 because we know age is an important risk factor for stroke. So now let's break down your findings a little bit. So first, how many more hospitalizations for acute ischemic stroke did you find in 2012 compared with 2003? So when we looked at the relative rate of increase, it ranged from 10% among non-Hispanic Blacks ages 45 to 54 to a 50% increase among some of the groups that were 35 to 44. What other kinds of increase in hospitalization rates for stroke did you see and for which other groups? So for ischemic stroke, with just a couple of exceptions up across ages 18 to 54, those rates increased. But with the age group 55 to 64, there were no increases except among Hispanics. It really had no change at all across the decade among those 55 to 64. What were some of the specific increases you saw among men? So among men, ages 18 to 34, a 15% increase. Among men, 35 to 44, a 40% increase. 45 to 54-year-olds, a 20% increase. How about for women? For women, the stroke rates are very small for women ages 18 to 34, but the relative increase was about 30%. For those 35 to 44, again, about a 30% increase. And among those ages 45 to 54, about a 20% increase. So you looked at stroke risk factors among these folks, too. Did you find more of these risk factors among people who were hospitalized with stroke? And what kinds of risk factors did you find? The risk factors were an interesting part of the study. Among those 18 to 34, the prevalence of hypertension among males increased from 1 in 3 to 40 percent over the decade, and among those younger women, increased from 1 in 4 to 1 in 3. Similarly, we found two-thirds of males and 57% of females ages 18 to 44 had hypertension. So very, very high rates of hypertension in this population. Another key finding was that about 30% of males and females ages 35 to 44 had diabetes and about 40% of males and females ages 35 to 44 had diabetes, and about 40% of males and females 45 to 54 had diabetes. We also noted that tobacco use nearly and obesity, and we looked at the changes in the prevalence of having at least three of those five traditional risk factors, we saw a near doubling of the prevalence of having at least three of those five risk factors over the decade. So what do your results mean? Well, I think identifying the high and rising prevalence of stroke risk factors among younger adults presenting with an acute stroke might prompt a sense of urgency among younger Americans, public. Burke, you wrote an editorial about the study, and you write that the evidence can seem pretty cloudy about whether or not there is, as you refer to it, a stroke tsunami amongst younger folks. And I was curious, in part, you say, because the magnitude of any increase that would be found could be due in part to the growth in the population of people 18 to 54 years old. So I guess I'm going to ask you the same question. Are more young people having strokes? Well, this is possibly the least satisfying answer I can give you, which is I don't think we really know. How come? Well, I mean, I think that the basic problem here is that while it seems like this should be a very easy problem, just count the number of strokes in a population over time, the tools that we have at our disposal for doing that counting have also been changing over this time. And if the tools for the counting are changing over time, it's hard to know if the count in 2003 means the same thing as the count in 2012. So what are the cautions you give about drawing conclusions from this study then? Well, there's a couple of specific things that changed over this interval that might lead to difficulty with interpretations of changes in counts over time. One of which is that the definition of ischemic stroke in TIA was evolving over the period of the study. So this sort of culminated in a scientific statement which redefined transient ischemic attack, TIA, from a time-based definition to a tissue-based definition, which means that if you had a positive MRI, a similar patient would have been called one thing, a TIA, in 2003, and a different thing, an ischemic stroke, in 2012. But during the period of the study, we know that TIAs were decreasing in terms of similar types of data. So it's possible that part of what we're seeing here is the same patients are just getting called different things. A second part of this is that the use of MRI increased substantially over the period of the study. And so MRI is an exquisitely sensitive test for picking up subtle ischemia. And it's possible that, again, the same patients may have been presenting in the earlier years of the study and not getting MRIs. But when you compare them to later years of the study, that subtle deficits, subtle strokes that might have otherwise been getting missed are now getting picked up. That would be still relevant and important. But from an interpretation perspective, it doesn't necessarily mean the stroke in the end is increasing. It just means that the pattern is the same and then we're catching more. And then the last part is that all of the data that we're basing this off of comes off of administrative coding. And so this is for hospital data, usually somebody buried deep in the basement of the hospital going through the charts and trying to assign diagnoses over time. There's been a big trend towards an increase in just more codes getting used per patient as there's been a big incentive for hospitals to code as many codes as possible so that it looks like your patients are as complicated as possible and also to use codes that are more likely to be highly reimbursed, for example, ischemic stroke as opposed to TIA. And those incentives were changing over the course of the study. So it's possible that some of what we're seeing here in terms of coding is a reflection of what's happening in the basement of the hospital amongst coders as opposed to what's happening in terms of the patients actually walking in the door of the hospital. Dr. George, what do you think about what Dr. Burke has said about the study? Well, I think there are some certain well-known limitations of using administrative data. There has been a lot of efforts over the period that we studied in terms of improving the quality of stroke care, which may lead to better diagnoses. I do think one of the limitations that we realize when we report on race is that the race data has to be taken with some caution because different states that contribute to this data do not always report race in the same way. So, Dr. Burke, how does the study contribute to this discussion about strokes in young people? I think right now it's hard to interpret. I think that what it does is it's waving a yellow flag at us, telling that there's a possible problem out there. And it's something that we probably should be focusing efforts to study. I think when I looked at these results, the thing that was really striking to me was I'm not sure what's truly happening with the trend. And I think from a societal perspective, that's a big problem.
I think that what this points to is the fact that I think our current systems for counting those strokes over time are not adequate to our needs. And we need to be thinking about better ways to count strokes so that we can have greater confidence about whether or not stroke is indeed increasing and whether or not we're actually facing a public health emergency here or whether or not we're seeing largely a reflection of changes in our measurement systems over time. So, Dr. George, what's next in terms of research in this area? One of the things I would say is that probably what was most concerning for me in this study is the rising rates and the very high rates of stroke risk factors among this young population. And we really need to do more work in prevention. So what's the takeaway, given the cautions that Dr. Burke has raised about the limitations of the data? I think the takeaway is that we are seeing some increases. They're not particularly in the 18 to 34-year-olds. Those rates are still pretty small, and the number of hospitalizations are pretty small. But we have now seen increases in the 18 to 44-year-olds over since 1996, very steady, straight increases. What we saw among 45 to 54-year-olds and among the 55 to 64-year-olds is that those stroke hospitalizations actually decreased from 95, 96 to 2003, 4, and then started to increase. So I think there has probably been some increase and that probably has something to do with the rising rates of risk factors. Well, thank you both for talking to us about your work. This is Deanna Balandi with JAMA Neurology. For more author interviews, please visit us online at jamanetworkaudio.com. You can also subscribe to podcasts at Stitcher and iTunes.
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 this interview, and these interviews are now called Conversations with Dr. Bauchner, and that's me, Howard Bauchner, Editor-in-Chief of JAMA, and I'm here with Jonathan Patz. Jonathan is a physician and is the Director of the Global Health Institute at the University of Wisconsin-Madison. He is a professor and the John P. Holton Chair in Health and the Environment, with appointments in the Nelson Institute for Environmental Studies and the Department of Population Health Sciences. For 15 years, Jonathan has served as the lead author for the United Nations Intergovernmental Panel on Climate Change, or often called the IPCC. He is recognized as one of the world's leaders in the effects of climate change on health. Jonathan, thanks so much for joining me today. Howard, it's a pleasure to be with you. So we're going to be discussing your viewpoint that is entitled, A Low-Carbon Future Could Improve Global Health and Save Money. Jonathan, before we get into the viewpoint, could you say a little bit about your two co-authors? I always want to make sure they get credit. Sure. Dr. Valerie Stull is a postdoc at the University of Wisconsin, and she's been studying the health benefits from a sustainable food system. Vijay Lame is a graduate from the University of Wisconsin, PhD, now working with the Natural Resources Defense Council, and his work addresses air pollution and health outcomes from that. Now, I want to read a very short segment from the viewpoint, then I want you to give the larger frame, and then we'll get into the details. The health benefits of low-carbon society should be central to policy debates on climate change. The enormity of such health benefits are illustrated by the discussion of three key sectors, energy, food, and transportation. Now, we'll return to each of those, energy, food, and transportation. But Jonathan, could you give our listeners the larger context, the bigger picture of what's at stake? One thing that's important to understand is that climate change, that we're now calling the climate crisis, is really happening. And there are many climate-sensitive diseases. So climate change is a health problem. But the context of this viewpoint is that the actions taken to stop climate change, which primarily means reducing our burning of fossil fuels, that those actions in themselves have immediate health benefits, especially when we think about what clean energy means for air quality and our health, what environmentally damaging food systems mean for the environment and our health, and how if we design cities more for people than for just automobiles, that we can promote physical fitness and have a huge benefit regarding chronic diseases. Do you think the evidence is in? Is the planet warming? Oh, yeah. There's no debate across the climate science community. The evidence is overwhelming. When the United Nations Intergovernmental Panel on Climate Change comes out with a new report about every five or six years, the certainty is more and more. So there's no debate amongst climate scientists. There's only debate amongst others that are not climate scientists. You and I have talked about this before. It's just hard for me to understand why we would ever risk being wrong about this issue. Well, this is where the precautionary principle comes out. You know, we never make decisions based on 100% certainty. But if the problem could be overwhelming, for example, a massive earthquake in San Francisco, we don't know when it's going to happen. Thank you. that the impacts could be overwhelming. And therefore, through the precautionary principle, we really need to start acting and we need to do something in a hurry regarding this. So let's talk about clean energy. What are the trends? What type of clean energy? Is it expensive? Oftentimes you hear, not in my backyard. What are the trends around clean energy? Well, the price of renewables has been dropping very fast. In fact, surprisingly fast. Solar energy has dropped 99% in price since the 1970s. And very recently, it's even in the last seven years, it's dropped 80% in price. So the trend for clean energy, you know, to get away from oil and gas, we're seeing a golden opportunity. We don't really need to wait around for clean energy options. And thinking about the World Health Organization statistic that 7 million people die prematurely every year from air pollution. This is where we've got incredible opportunities. In the United States alone, more than 64,000 people die every year from air pollution. So the trend in the price of renewables and battery technology is improving. This is incredible as far as health benefits, thinking about all of the health damages from air pollution. You raise a good point. We've published a number of papers about the relationship between air pollution and health. I travel oftentimes to Asia, quite frequently to China, and even China's come to recognize the cost of air pollution, both in terms of financial cost, as well as more importantly, the cost to human health. And I've been struck that when I first started going six or seven years ago, it was generally considered to be smog. That's changed. And it's really quite clear that they're acutely aware of the problem of air pollution throughout the country, but particularly in Beijing and Shanghai. And they've worked tirelessly beyond energy, you know, we have pollution from transportation. And a recent paper talked about diesel trucks and other dirty transportation sources. It's estimated that globally, at least from the year 2015, that 11% of the air pollution deaths come from transportation. And that's 385,000 deaths every year from emissions from transportation. The piece also focuses a bit on food and obviously the vegetable-based burgers that have been introduced. Oh, the Beyond Burger and the Impossible Burger. Thank you. They've actually become really quite popular. And it's interesting. I had interviewed Frank Yu about six months ago, and Frank mentioned that their effect on the individual human health was not as certain as what he thought would be the benefit of raising less cattle for the health of the planet. Could you just comment on the relationship between a low-carbon future and food? Sure, sure. You know, I pretty much agree with that statement. We need to think about our diet related to the health of us, but also the impact on the environment. And resource-intense animal-based foods, be it from the amount of feed required to feed cattle, to the water requirements and the land requirements. Animal-based food production, especially in wealthy countries where we have overconsumption of red meat, that's where we have some great opportunities to reduce the impact on the environment. Whether or not Beyond Burger or Impossible Burger has a difference in nutritional value compared to animal-based burger. The environmental benefits from switching more to a plant-based diet has a much less footprint on ecology. Thinking about food production needing to rise with the increased population, the emissions required for the fertilizer and the energy that goes into food production is enormous. Those emissions that also go to worming the planet simply from food production are not trivial. So we've talked a bit about food, which we just finished, and you had mentioned transportation, but I can't resist asking you a couple other questions. So I've just made you planetary czar for a few years. Where would you start in terms of trying to reduce fossil fuels and improve overall quality of the environment and health? What would be your priorities? Well, my main goal would be to get to a low-carbon economy. And how we do that, I don't claim to be the expert, but we need to put a price on the environmental and health damages of a high-carbon economy. So burning fossil fuels damages crops and ecosystems and our health through air pollution. Those numbers are not in the market. And just like we put a price on tobacco, and that had a good impact on reducing teen smoking, there needs to be some sort of fair price on carbon, and maybe that will bring in these health benefits. So I show a slide sometimes about the cost of clean energy. You know, if you wanted to invest in clean energy such that you would avoid emitting one ton of CO2 that warms the planet, well, that might cost. It might cost up to $30 to avoid emitting a ton. But every time you don't burn that coal and emit one ton of CO2, you also don't emit the other harmful pollutants like fine particles, PM2.5. And the effect on health is such that if you avoid emitting one ton of CO2, you also would avoid emitting those pollutants that on average globally equate to $200 in health benefit from avoided mortality and hospitalization.
So if we could change the metrics, change our goal, for example, from looking at just economic benefits to also including health benefits, I think that we would automatically trend towards a low-carbon society, and that means clean air, less food waste, and more plant-based diet, and alternative transportation that gets people out of just private motorized vehicles into well-designed cities that have decent mass transportation that promotes walking, is safe for biking. And when you look at the United States, where a majority of individuals don't even meet the minimum recommended levels of fitness and exercise, golden opportunities to reduce chronic disease through this low-carbon economy. I was about to ask what could individuals do, but you were very clear about that. One is take mass transportation or walk more. And I think you've already pointed out that the U.S. has become quite a sedentary population. I think everyone is well aware of the obesity rates in the adult population are above 50%, and the cost is enormous. Oh, absolutely. And some of these things, of course, are overlapping. When you think about the obesity epidemic, of course, there's the issue of food and getting to more plant-based diet and getting away from some of the unhealthy foods. But the other is how we design our cities. And I look at obesity as not a personal issue. It's a system-wide failure in both our food system and in our urban design. And we have designed, unintentionally, we have designed routine physical fitness for commuting. We've designed it out of our system and many places across the country. They vary in their bike friendliness and walk friendliness. And if you look at cities that have the most walkability and bike ability, those are the cities that have the lowest rates of obesity and diabetes. And of course, physical fitness goes beyond simply burning calories. There are wonderful chemicals that are released simply from contracting muscles, anti-cancer and immune-promoting chemicals that come from exercise. So if we can design our cities more for the alternative transportation and have safe walking and biking, and that also means efficient mass transit, I think we would do our own population a huge benefit, especially thinking about rates of obesity and sedentary lifestyle. What's interesting, I travel quite a bit to go to various meetings, and particularly in certain countries and in some cities in the U.S., these electronic scooters become quite popular and they look like fun. But then I realized if you're on one of those electronic scooters, you're not walking. So you're not getting quite as much exercise. So sometimes we create things that make life more convenient, but in other regards, they may make you less healthy. It's just this tension that I see all around. I think it's a great point. I think we really need to have a broad view of these things and look for unintended consequences. And I think you're right about like the Segway and the scooter, maybe less pollution, but indeed less opportunity for exercise. So we absolutely need a systems approach when we look at any of these alternatives. So you genuinely think linking this issue of energy and a cleaner planet to the health and economic benefits is the best way, in some regards, to sell it to the American population, the American people? It seems like outside the U.S., there's more of a conviction about some of these issues than there is in the United States. I have a simple message. And I think the first one is that people must recognize that the global climate crisis absolutely is a health emergency. It's not just about polar bears. It's not just an environmental issue. Climate change is a health problem. That's number one. And number two, and what this viewpoint gets to, is that the actions that we need to take to reduce greenhouse gas emissions that are causing the planet to heat up, these actions that we take have huge health benefits. That even for people that don't believe in the climate change science, and of course, it's not a matter of belief, it's a matter of science, but even for people that are denying that climate change is real, to reduce burning of coal and oil and design cities that promote physical fitness and to look towards a more plant-based diet, those actions that may be policies for climate change, in fact, have immediate health rewards and benefits, be it from cleaner air to healthier diets to exercise promoting neighborhoods and areas. These are just fantastic opportunities for health. So that's the key message, that the climate change is a health threat, but the actions necessary to get off of fossil fuels and get to a clean energy society have huge health benefits, and these benefits are today and tomorrow. I've been talking to Jonathan Patz, who is a physician, a professor, and the John P. Holton Chair in Health and the Environment with appointments in the Nelson Institute for Environmental Studies and the Department of Population Health Sciences. He's a faculty member at the University of Wisconsin-Madison, and he's authored a viewpoint for JAMA entitled, A Low-Carbon Future Could Improve Global Health and Save Money. I hope everyone reads it. As clinicians, if we can talk with our patients about some of these issues, there's so much to do in a visit with patients. But somehow, we really need to change the conversation in the United States and around the world, but particularly the United States. We still consume an enormous amount of the world's energy. And I think many people have been frustrated over the last three or four years with some of the national policies in the United States. Jonathan, I can't thank you enough for joining me today. Howard, thank you. It's a pleasure. Thanks so much for listening. For more podcasts, visit us at jamanetworkaudio.com. You can subscribe to our podcasts on Stitcher and Apple Podcasts.
Welcome back to Run the List, a medical education podcast in partnership with McGraw-Hill Medical. Our hosts are Dr. Naveen Kumar, Dr. Walker Redd, Dr. Emily is one of the core team members of the pod and one of the founders of the podcast back in 2019. As some of you may remember, last summer, July 1st, we started a partnership with McGraw-Hill Medical, which at the time we had hoped would elevate both the quality and almost the quantity of our episodes. And I think in the past season, we've achieved that. And so we're going to continue this partnership, keep the momentum going with what we've achieved this past season, be on the lookout for July 1st, this coming summer for season two, where we will cover some of our early episodes again with new content and hopefully improve quality as well. In the meantime, we're going to be chatting with Naveen about medical education, a topic very near and dear to our hearts and also to many of our listeners, and hopefully get some anecdotes from him and some pearls about being involved in medical education or even just bearing witness to the medical education wave that's currently happening, both in the classrooms and digitally. So with that, we'll run the list. Naveen, now that we have you here on the pod, when did you first become interested in medical education? Yeah, Blake, thanks so much for having me. Really fun to be on the other side of the microphone for this topic. You know, for me, the interest into medical education honestly started in college when I was a pre-medical student. And I was just so amazed by some of the professors who would teach us in these really large lecture halls and somehow have an ability to engage with us in a way that almost felt like they were just teaching us individually. I'm sure you've had that experience too, Blake, when you were in college. Oh, absolutely. Right? There's like a few teachers who just knew how to do this so well. And you would walk in knowing that for that hour, you were going to learn really effectively and in a way that was very engaging. And so I loved just being a part of that and seeing these professors teach in that way. And it was inspiring. And I looked at it and thought, you know what, it'd be really cool if I could get to some degree of that level when I was actually a physician myself. So that was college. And, you know, that appreciation for really great teachers just continued while I was in medical school. And obviously, like, you know, the content changes once you're in medical school. It becomes a little bit more specific. And the lecture halls get a little smaller. The class sizes are a little smaller. But just like in college, I saw those same really great teachers from time to time. And I was constantly amazed by how they were teaching content that was really complex, but they could deliver it in a way that seemed more simple and easy to understand in the larger groups. But then also, you know, in medical school, you do, as you know, Blake, a lot of small group work. And I loved how some of my best small group leaders were really flexible in the way they taught. And they were able to, you know, kind of pivot the session based on what us as the students were bringing up. But still at the end, they're able to bring us back. I'm thinking mainly to my like the case based tutorial sessions I would do as a first or second year student and just see how at the end, even though we had like a very winding path where like, you know, we were getting up and writing things on a chalkboard, looking things up on the Internet. During the session, we arrived at a place where we covered all the objectives that that small group leader had for us when we started out the case. So it was just kind of this continued exposure to really great teachers. And of course, it's not everyone, right? So I definitely saw my fair share of teaching that was not effective, but it was the really effective teachers that helped me get interested in pursuing a career in medical education. And then it really came together during my clerkship year when I was on the wards at the Brigham as a third year medical student back then. And I was just so impressed by watching my senior resident teach not only the interns, but also the medical students on her team. And it was just so impressive to see how she could run a team really effectively, provide really high level patient care, but also find time to teach during, before, after rounds in small tidbits. And this is like something I've taken for myself. The way I teach now is like trying to be very high yield. I think it's something we've discovered with our Run the List podcast is that you can teach very effectively in not a large amount of time if you're prepared and you have clear objectives. So by the time I got to clerkship and I saw this one senior resident I'm thinking about, I saw her as both a team leader, but also an educator. It was pretty clear that that was a pathway I wanted to go down. And I wanted to be just like that resident, but also those really impressive professors I had from before. Yeah, definitely. I like that you kind of all along from college in your narrative of your experiences now, you were very perceptive to the educators around you. And I think something that's interesting about medicine is that in high school or in college, we have these teachers in front of us at the blackboard or at the chalkboard, what have you. But in medicine, you could have people teaching you at kind of every level of the game, if you will. And so you could have residents that are teaching you as effectively or even more effectively at the bedside as a professor that you had during M1 or M2 at the whiteboard. So I really appreciate that. And that's something we're going to focus on in this episode and the next one in our second part is just kind of the different forms of education. But why don't we kind of start at the beginning? You know, I think of you as one of the core members of our team and someone who always knew they wanted to be a doctor, but also as a medical educator. It seems like you've kind of had this throughout, but maybe that's not the case. And so what advice do you have for students who are interested in med ed, whether they were thinking of that from the beginning or kind of came at it, you know, during M4 or even intern year? Yeah, Blake. So what I'll try to do during this first part of the medical education podcast series is I'm going to try to give some tips. So the first tip I want to give to those early listeners who are either students or maybe interns interested in getting medical education is to start early and often. And so what I mean by that, and I'll try to connect it to what I did as a third year student, is that I really pushed myself to teach whenever there was an opportunity. And so as a third year clerkship student, I found that generally towards the end of the week, usually on Fridays, the team would reserve some time for protected education led by someone on the team. And oftentimes that took the form of either the attending or the senior resident doing like a, you know, a 15 minute talk on a certain topic that came up during the week. And I found that as an opportunity where I could put myself in that situation and try to educate my team members, even though I knew I was a third year medical student, and you know how it is as a student, it's hard to teach above you. It's much easier to teach at your level or to those who are earlier in their career. But I found that putting myself in that position really helped me learn from an early stage how to become a more effective teacher. And so I think the take home point here is that especially when you're earlier on in your career, all of these opportunities to teach are going to be very stressful. And it will be easy to shy away from these opportunities or not seek them out to teach in front of your peers or again, like individuals who are more advanced in their training. Very easy to shy away from. But if you put yourself in that situation and you get up there and you get up to the chalkboard and you come prepared and you do your talk, you will learn so much about techniques on effective teaching, but also get really great feedback. Blake, you can probably attest to this. It's really easy to get good feedback when you're earlier in your career. I think it's harder, right? It gets harder as you move along. Very hard for me now as an attending to get feedback on my teaching from someone on my level, but very easy for me to give feedback to my student who just gave a 15 minute talk.
So that's third year. And then I want to think more about when I was a fourth year student. And this is when you start having the opportunity to actually take on more formal roles as a teacher. And so for me, that presented itself as a student tutor for a clinical skills course. And I imagine this is applicable in a lot of different medical schools where more senior medical students can actually fulfill a formal role in a course as a student tutor. And so what this looked like for me was I would teach in a small group setting where it definitely felt less pressure. And again, I was teaching a level below me to some degree. And so that gave me confidence that I could teach well and effectively. Also knowing that I was just in their shoes a few years ago, I think, right? That makes you a more effective teacher. And it was topics that I knew well. I knew the physical exam really well coming out of that clerkship year, how to take a history with a patient. These are all core skills that I had been practicing the whole year. And so I felt that I could teach it effectively. So that was a great way for me to become more involved formally in a course. Third year was more informal, pushing myself to teach my teams whenever I had the chance. And then fourth year was about starting to take on some more formal roles within the medical school curriculum. Yeah, I think that highlights kind of the what I was getting at earlier with medical education is that it could take many forms by many teachers, many kind of leaders on teams in the hierarchy of medicine. And so could you touch on, I guess, formal versus informal teaching in medical education? You know, we all, I guess, know of the formal teaching in the first year, year and a half, even two years, depending on the medical school and then maybe clerkship on the wards. But what about informal teaching and how that played a role in your experience? Yeah, absolutely. I think, you know, as a student, I was the recipient of a lot of informal teaching during any clerkship or clinical elective. And that gave me insight. We'll dive into this a little later about what I could do once I became an intern. And so a lot of this happened just kind of off the cuff. We came out of a patient room where there was a physical or within the patient room, there's a physical exam finding that the intern or the senior resident was demonstrating. You know, I remember being a clerkship student and being asked to listen to the heart on rounds, right? Like, I feel like a lot of med students have had this experience where you're told there's something and then you're on the spot to go and listen. And it's funny, right? Because one option is to pretend you heard something, right? Like no one actually knows if you actually heard it. But then if there are follow-up questions, you will not be ready to answer those if you didn't actually hear it. So I remember being put in that, in that, on the stage, listened. Sure enough, I heard a murmur. And then the next move was I, I couldn't tell if it was systolic or diastolic. And so it was so funny. I remember actually feeling the pulse. And then out of the corner of my eye, I could see my attending, like nodding his head, knowing that, okay, Naveen is now trying to distinguish this from a systolic and diastolic murmur. So I knew it was on the right path. And then sure enough, it was a diastolic murmur. And then based on the location, it seemed like it was an aortic insufficiency murmur. And I said that rounds and I got it right. And it felt so good. Oh, that's awesome. patients or clinical situations that arise while you're in the hospital. And as a student, you should be ready to receive that learning and see how your teachers are presenting that material so that when you are in that position, you can do the same for the next generation of learners. Yeah, absolutely. Would you say in your experience you had these kinds of opportunities come to you or kind of happen on the spot? I mean, I think you touched on both of them in your clinical skills course teaching, but then having to diagnose aortic insufficiency on the spot. So because medical education is so almost shape-shifting or hard to pin down because it happens in many forms, in many arenas, do you think that for your involvement in medical education in the past and currently, a lot of it has kind of been presented to you and you're like, yeah, sure, I'll do this, or you've had to seek it out or both? Yeah, this is exactly where I want to go. One of my tips is to say yes. And I think it's so important early on in your career, and this starts when you're a student, that when opportunities arise and, you know, leaders in medical education within your own institution, your own medical school come to you with opportunities to teach, you go for it. And it's always a lot of work to put together, let's say, a new talk on a certain topic. I find that, you know, to teach like half an hour, for me, honestly, it takes like, it takes several hours to put together that half an hour, 45 minute talk. But I've learned that once you've made that talk, you now have it and you have it for the rest of your life and you can teach it without, with edits as you, you know, as new information comes along, but that's your content and you can teach it so well because you made it yourself. So I think it's really important to say yes when you do have these formal opportunities to become involved in medical education. The other important piece of saying yes is that it helps you build a reputation. And so I tried to start doing this as a, like I said, a senior medical student by taking on more formal roles. I was starting to try to build my own reputation as a future educator. And it's so funny because, you know, I now work alongside folks in medical education who taught me and now we're peers, right? And it's been really hard for me to start calling them by their first name, but I've learned to be able to do that over time. And when it comes time for you, once you finish training and you're about to seek your first job, you now have individuals who have power and a position in medical education who know you as an educator so that when there's more formal leadership roles that come up, you're right there at the head of the potential applicants and they will actually come and seek you out. So I think when you were talking about looking for these opportunities, it hits home with me that yes, some of these things you're going to seek out for yourself, but if ever presented with the opportunity to become involved, go for it. Say yes. It's going to take time, but especially early in your career is very, very important to get involved. That is such a great tip. And I like how it kind of becomes circular where we're saying yes to something informally that maybe is presented to you can ultimately lead to something where people then seek you out because they know you as an educator. You know, because this first part is focused more on early trainees, you know, maybe upper year med students. It's interesting to me, especially doing this podcast with you all still as a medical student myself. It's like it's almost like a chicken and the egg where getting involved in medical education while you're still in the student phase feels kind of strange. You know, it's like, how do you find that as a student? And on top of that, because medical education is changing, like in't be an effective educator just because I'm so early in my training. But I feel that I want my students to look at it differently, which is that being a student, you're one of the best candidates to think about medical education because you know what you have been receiving and you can identify ways to do it better. So this idea of innovating is really important, and it's a great way to become involved as a medical student. And I think that starts with looking at your own curriculum and seeing if there's a gap there that needs to be filled. And then either formally or informally, getting a sense of, is there a need? You see the gap, but if you talk to your friends and peers, is there a true need for a change? I had a student who I worked with who did a wonderful job of going through this process of innovating by first doing a needs assessment amongst her entire class, identifying that there's a gap in the curriculum, namely global health during the clerkship years.
And so her process that I'll share, because I think there's some good takeaways here, is that she first, she identified the gap and she found a mentor, myself, to help guide her through this process. So I think that was key. Find the gap, find the mentor. Then after confirming that this was a true need by surveying her own student body, she then met with all the educational leadership of the clerkship year and she presented her idea formally. So she put together a really nice presentation and had it backed by data from her survey that this was a true gap in the curriculum. She then did her innovation, which was creating a global health didactic series that ran through the clerkship year between surgery, pediatrics, OB-GYN, internal medicine. And what I love that she did, and again, I don't want to toot my own horn, but this is what happens when you have a mentor is that you have a mentor who can push you a little further. And so, I was able to push the student to study the innovation and not just develop it. And so, she did a really nice job of creating surveys both before and after the curriculum. And she collected really, really good data that showed that it was a very effective curriculum that she innovated and introduced into the clerkship year. And then the final piece was that she wrote up her work, both as her main research project of her medical school career, but then she was successful in publishing this innovative curriculum in MedEd Portal, which is a great resource, great place to publish this type of work. So there's a lot of great learning points from what this student did, but it all starts with finding a gap, seeking a way to fill that gap, and doing it with the help of a mentor who can also help guide you through the scholarly process of hopefully publishing the hard work you've done. Wow, that's an amazing story and something that directly answers kind of what I was asking about innovating as a student for, I guess, your own class, but even future classes for medical education. So that kind of perfectly fits that question. I guess you gave so many tips. Maybe it'd be helpful to wrap up this first part of the two-part series and give us some pearls for early trainees, ways to get involved in medical education, and things to be mindful of because you are obviously advancing up the medical hierarchy and that transition to residency. Excellent. Yeah. So let's review my tips again. So number one, to start early and often. And remember, this can start absolutely as a medical student and it should start then. If you're interested in medical education, seek out those opportunities informally teaching on the wards versus formally becoming a student tutor in some of the clinical skills courses while you're still a medical student. So that again, start early and often. Second tip is, as we mentioned, say yes. So when opportunities arise, say yes and build your reputation as an educator, even as a student, but certainly once you enter residency. And number three is to practice your skills. And so what I meant by this, and we didn't get a chance to talk about this earlier, but I'll reflect on it now, is that it's really important to commit to teaching. I always found that sometimes, especially when I began as an educator, I would prepare teaching. And then when it was time for me to teach, I would get shy and I'd get nervous. And you can easily let that opportunity just slip. There's always reasons, especially in the hospital, right, where you push teaching to the next day because it's too busy. But what I did as an intern is I would informally teach my students, right? This was the kind of stuff that we talked about earlier, where you teach about the exam, or when you come out of room, you teach about, you know, a medication dose that you titrated. But then as a resident, it's time to start actually preparing for teaching. And what I found was helpful is that I would always start rounds with five minutes of teaching because I felt like if you didn't do it upfront, before you know it, the day has gone away from you. And it's really hard to stop the momentum of all the work that's building up to teach later in the day. So I always taught in the beginning and I would do five minutes. I'd come prepared. I knew what I wanted to teach. And then I felt like I could check that box that I taught my interns and I taught my students. And now let's move on to the patient care while still doing some more informal teaching throughout the day. So just to summarize again, that's this final tip is really to practice your skills both informally and formally within your role as a student, intern, or resident. Thank you.
Welcome to Deep Breath In, the podcast from the BMJ, sponsored by Medical Protection, where we tackle the everyday challenges of being a GP. And we've made it to the end of 2020, a year where as GPs we've had a front seat view of the impact that coronavirus has had on society, be it the patients who have died of the virus, those still suffering with symptoms months later, or those whose lives have been turned upside down from the economic and social impact and struggling with poverty, isolation and mental illness. But there have been some positives in 2020, unprecedented scientific effort to produce a vaccine and, well, I guess the launch of this podcast. And today we're celebrating the 19th episode with a classic end of year quiz featuring clinical pearls and some of the more surprising learning points from the B&J's education pages. We'll also hear from two past guests. Jud Brewer will give us some winter survival tips and we'll have an inspiring, thought-prov London and clinical editor for the BMJ. And today we're bringing you three podcast stars from across the BMJ's podcast series. I'll start with Kat from the Wellbeing podcast. Welcome Kat. Thanks Tom. Hi everybody, I'm Kat Chatfield. I'm a lapsed GP and I also host our Wellbeing podcast with my colleague Abby Rimmer. And the second star is Helen. Hi Helen, which podcast are you from? Talk Evidence. I think you're leaving that in Duncan the disrespect that I'm shown coming on this show um I'm Helen McDonald I'm the UK research editor for the BMJ and I'm an evidence-based medicine nerd um I do our talk evidence podcast and I won't forget who Jenny is because Jenny's with us every episode. Hi Jenny, how are you? I'm well Tom. I'm Jenny Rasanathan. I'm a family medicine doctor and clinical editor for the BMJ. It's so nice to be here again with you and with Kat and Helen. Yeah, no, it's great and thank you for coming on the podcast today. I thought we'd just start with a bit of self-reflection and maybe just ask you, for 2020, how has it changed you, do you think, or your outlook, or maybe your outlook on medicine? I'm not sure I've fully digested everything from 2020 yet in order to answer that question. I think we've been pushed to work in ways that people had kind of considered before but really didn't want to do in the numbers that we've seen globally. And now, you know, telemedicine, video consultations, different kinds of virtual engagements with patients is much more de rigueur. But I suppose many of us have gone through transitions from seeing patients in person to speaking with them remotely and back, hopefully, to seeing them in person. And I think the real takeaway for me is that there's very little substitute for the kind of empathetic exchanges and really kind of fulfillment and satisfaction that you can get from in-person patient encounters. Yeah, yeah, yeah. I'm definitely looking forward, fingers crossed, to more of that this year. Helen, I guess you've been watching this particularly from the evidence point of view on the talk evidence. what's uh what's been your perspective on this year you know one of the most interesting things i think i read it on twitter from ben goldacre at some point about midway through the first wave and he had written something like the the covid pandemic was making everyone more like themselves and and i thought that really kind of resonated with me. And I think the ways in which I've honed being more like myself have been talking. So we've done a lot of talking on Talk Evidence. We've quadrupled the number of episodes that we normally do. And largely what we've been talking about has been uncertainty and a willingness to share and be open and honest about the uncertainty that exists and the variety of ways in which you might act in line with some evidence supporting you. I think that has been a real theme. I think the other thing for me, which has been very satisfying, is the other thing I love to do is to create and to do new things. And everyone's been forced to innovate in the pandemic. And I think one of the things that I've most enjoyed in 2020 is trying to make our content live, which sounds very simple, but actually in publishing terms is quite difficult. So I've been working on our project to make living systematic reviews, in particular, a living systematic review of emerging treatments for COVID-19. And the idea there was really rather than to give people an answer today, to give people a sense of an evolving story of where we are in that journey. And I think that publication has been very helpful, because really, what it's done is to summarise that we've gone from not knowing towards some certainty that there are no really good treatments for COVID-19, perhaps, aside from steroids for severe disease. And I hope that that's really helped to support healthcare systems to avoid investing in treatments that don't have a solid evidence base. And I think because I didn't mention that I am, what did you call yourself Kat? Elapsed GP. Elapsed GP. I call myself a resting GP because I feel it's too early for me to have retired in my career and yet I don't have time to practice clinically at the moment. But I think GP is really at the core of how I think. And I think the other thing that I've enjoyed doing this year in talking to researchers is pushing people to think about people in the community, not just about people who've been admitted to hospital. When the evidence first started coming through, we saw lots of case series about people with severe disease. And it took a while to really learn about what was happening to the vast majority of people and I still think that's a big a big area around transmission in the community and understanding environmental and behavioural interventions and what's going on that that we still don't understand well. I think I saw that tweet as well going back to that and said something about the quiet hard workers who just get on with it and I thought yeah that's me. Is that you Tom? I know that's not true. So what are my noisy disruptive kind of work? I couldn't possibly say. Anyway Kat. Helen and Jenny is that your hard acts to follow? And then I think, you know, to see in the BMJ, the really kind of direct impacts of what we were publishing, you know, none of this kind of 17 years from research to bedside, it was all kind of happening so quickly and so fast. And to really think about how you could contribute in that way to the to the discussion and the debate and the resolving of some of the many uncertainties that that we had this year and then also the great joy for us of of being allowed to enable to start the well-being podcast which was a topic that was really really close to heart for a long time. And that we've done some kind of written stuff on in the BMJ, but being really allowed to dive into that and just everybody recognised that it was so critical for clinicians and for the whole, you know, everybody this year has had stress for their wellbeing. So I think that was a real opportunity. Yeah, so it's been kind of definitely lots to reflect on this year. Well we're going to sort of pivot now from a from an interesting chat about 2020 to the details of the NICE guidelines on hypothyroidism. Does that sound good? Smooth, smooth segue. Yeah. Sounds great. I think so. So we're going to do a quiz. So it's like a Christmas quiz, but we thought... Why do you pick this topic? Okay, well, I went right back to January. I was thinking, you know, let's try and do a quiz that's vaguely chronological. So we're going to start with, you know, those days back in January where, you know, a new nice guideline on hypothyroidism was kind of like a big event. So I'm going to ask you, that's the first quiz question. And we're going to just go through the quiz. A few questions, nothing too serious, I hope. But maybe some useful clinical nuggets there for us to, even you lapsed or was it sleeping GP you are, Helen? Resting. Resting, right. I'm not semi-conscious. I'm just resting. Poised. Well, by the end of this round, you might be. Well, maybe she's hypothyroid. Maybe. We need to replace that, you know? So, okay, some rules for the quiz. It's just a multiple choice, and it's kind of like fingers on buzzers, but of course there's no buzzers, so just sort of make a noise if you want to answer. I haven't really thought that through. Okay, so question one.
And there's four answers to choose from. Is it 25 micrograms? 100 micrograms? 1.6 micrograms per kilo? Or none of the above? Start lyothyronine. Oh, oh, oh. That's my line. I like that noise. I thought it was per kilo, but I can't remember if that's under 65 or over 65. So I'm going to go for C, the microgram per kilo. You're right. Yay! Top marks, Kat. Yeah, well done, Kat. Yes, one point to go. I mean, I have to admit that I see a lot of variation in that practice. Like you see some people, you know, who have always started on 25 micrograms, others, people just go for 100. So I thought it was quite useful to know. So question two. So when would you consider levothyroxine for adults with subclinical hypothyroidism? Again, this is according to the NICE guideline. So we've got three options this time. TSH of over 10 on two separate occasions, three months apart. If the patient has, sorry, option two, if the patient has thyroid antibodies, or option three, if the patient tells you that their friend who's a GP says they really should have it. Is that a trick question? I think more than one of those is true. I'm pretty sure it was the first option with a TSH level above 10 on two separate occasions separated by three months. Yes, that's right. And I feel guilty saying that, but at the same time, it was very much a conversation. And we talked about trying this as an option to alleviate some of the symptoms, which were consistent with hypothyroidism. And he got better. But every time I read the guidelines, I feel guilty and a bit ashamed of not following them. But do the guidelines sort of suggest that's not okay? I think that's okay isn't it? I mean we published also I'm more familiar with the rapid recommendations guidelines on this topic that we published although that was May 2019 so I really am stretching my memory somewhat here but I seem to remember that in that guidance if people had severe symptoms then that might be a circumstance in which you could consider a trial of the medication to see if it worked. Yeah and what was the other main difference in that the rapid recommendations? I forget, but it does vary a little bit from the NICE guide, doesn't it? I think there are two important differences. One is in terms of how, in terms of the information that they started with, the evidence that the NICE guidance looks at compared to the evidence that the rapid recommendations looks at is slightly different. And I just clicked these up because I seem to remember some controversy at the time around the differing recommendations. But in essence, the rapid recommendations predominantly uses a systematic review at its base, which is very heavily influenced by a large primary care trial that was done in over 65s. Whereas the NICE guidelines, I find the evidence a little bit harder to follow in that, but they look at a smaller subset of trials. So I think that's one reason which perhaps drives the differences. And then in terms of the recommendation, the rapid recommendation makes a strong recommendation against using thyroid hormone therapy for patients with subclinical hypothyroidism and they and they sort of pick a 20 rather than a 10 threshold as their degree of elevation that they consider it might be worth looking at. But they add some qualifications that the recommendation may not apply to those people who have severe symptoms, so the situation Jenny was mentioning, and to much younger adults, people who are pregnant and also people who are already taking treatment. So their guidance was very much centered around people who are at the beginning of the process trying to decide what to do whereas i think the nice guidance was a kind of consider so what might be in guideline sort of jargon a weak recommendation as opposed to a strong recommendation where strong recommendations are typically a standard of care whereas weak recommendations are much more discursive perhaps. Yeah thank you Helen that's incredibly helpful and yeah we'll need to make you our regular guideline untangling. I love a guideline. I haven't gone that deep into a comparison I I'm sure there are other things that you could pick up on. Well, I think that was enough for me. Was it enough? Anyway, let's move on to our next question. So this is about serial measurements. So before we get onto our COVID part of the quiz, I've got one more non-COVID thing just because, well, I guess it's nice to talk about something else. So just before the COVID first wave hit us, we published a paper from James McCormack and Daniel Holmes called Your Results May Vary, The Imprecision of Medical Measurements. This is all about the fact that levels of things that we measure, you know, like your haemoglobin or cholesterol or whatever, are always in flux, you know, from one day to the next or one month to the next. You know, lots of things influence the levels of these things in our blood. And, you know, it was a call really for clinicians to be aware of this problem and, well, consider it when, particularly when discussing these with patients. So I'm going to give you some examples of serial measurements. I want you to tell me if you think that the change in the results are likely to be a true difference, that's with a 95% confidence interval, in case you're wondering, or due to combined effects of this biological variation and analytic variation of what goes on in the lab. Did that all make sense? If you could see us on Zoom, everyone is looking very mystified and shaking their heads in disbelief that Tom has brought up such a ridiculous question. Well, particularly since the article has this really helpful tool that does it for you when you put the values in. So there's really literally no point in my brain knowing this information. Come on, do your question, Tom. We'll stop criticizing your quiz. Give us a go. The fact that there's a tool is the reason why we're having a question about it because it was easier to think about. Anyway, so I'm going to do one each. So we're going to go cat first. You can go first because you're so familiar with the tool. After that criticism, I should deserve to go first. So a total cholesterol from 5 to 4.5, would that be a true difference or not? I'm going to say that it's not a significant difference. You're right. One point for Kat. So, I won't ask you what you would have to go to. I don't know. For you to have a... Bonus point. How about bonus point, Tom? I'm going to say... Go on then. Just because it's simple, I'm going to say 5 to 4. Close. 4.12. 4.12. Tip of my tongue. Yeah, it's quite a big difference. I mean, one of the things in the paper is that often when you're seeing a patient and the cholesterol goes from 5 to 4.5, you know, you pat the patient and you go, oh, well done, you know, you've really done well with your diet haven't you and uh but actually you're just all you're seeing is noise so next question um jenny uh hemoglobin of 120 grams per liter to 110 what do you think true or have you got the tool out in front of you, Jenny? You said, from what to what? 120 to 110. She's cheating, isn't she? I am cheating. It really looks like she's typing it in. She's definitely typing it in. I'm using the tool because, because, number one, I wanted to try it out, but number two, these are not the usual units that I use. So it's very difficult for me to imagine what the correct reference range would be. I typically think about this in different units. But also they just kind of sound close enough, like 120 to 110. My guess would be that it's not significantly different. That's right. You're right. Yes. Well, for the bonus point, do you want to hazard a guess of what it would be? I feel like we have to continue with this bonus point thing now. Okay. There's a timer. What it would have to be? Okay. Oh, there's a timer. What? Well, according to this article, the difference would have to be some, I don't know, some percentage. It would have to be more than 6-10% different. Okay. So no, I suppose maybe less than 105?
I can't believe you didn't get this. It's 109.7. That's a big change. 120 to 109.7. That is a big change. So I chose those because that's the difference between not anemic and anemic in a woman. For those normal reference. Okay. Helen, you put us out of our misery and let's finish this round. TSH from 7 milliunits per litre. Oh, not the TSH again. Say that again. 7 milliunits per litre to 4. I'm going to buck the trend. I'm going to say I think that's a meaningful difference. No, it's not. No. But you can still go for your bonus point if you want. So what would the difference be? It's going to be quite big then, isn't it? I don't know. Let's go like one under that. Three. I think it must be there or thereabouts. Yeah. No, it's 3.78. I have to say, Tom, I enjoyed talking to James McCormack more about the concept behind this article in a bar in Copenhagen than I did being quizzed on it. Because I was very interested in the principle and despite being an EBM nerd, I am not a mathematician. It's a really interesting principle. I mean, those are huge changes that might appear on, you know, intuitive, you know, when you just get them and you're intuiting, is this a significant change? Am I going to change a management plan? To really understand that they don't represent anything more than normal statistical, biological and analytical variation is really important. I think one of the things James asked for, wasn't it, was that the kind of confidence interval or meaningful differences should be better shown on blood test results and the like, which I think would be very useful. Yeah, he would say, you know, just show it as like a blob, like a ballpark figure. So rather than, you know, giving this very precise value, which is really misleading. Jenny? No, just to say on that point, that is when our decision-making conversations with patients really center on what the number is, we're doing all of us a disservice. You know, it's very easy to focus on the fact that, oh, your cholesterol is now 4.5. Congratulations. Or when we're making decisions based on, and he talks about this in the article, you know, your hemoglobin A1c being 6.2 when it very well could be 6.5 in that moment or even higher. And even moments where we see perceived change, depending on the variation at that time, if the first reading was artificially low and the second reading was artificially high, you know, we could be going in the wrong direction of what we are seeing by those discrete numbers. Yeah. I think the only, well, one caveat which one of the peer reviewers picked up on, which I thought was a good point, was that they have selected this 95% confidence interval. And I guess the peer reviewer's point was in practice, you don't tend to wait till you're 95% sure to start investigating someone's anemia. 50% is probably good enough. And so that's why if you use the interactive tool, you can change that confidence interval. So you can actually select a value which you think is more maybe clinically relevant, perhaps. Yeah. So check out the... How certain do you have to be? That's the question. Yes. Yeah. Yeah. I'm not sure. As a patient, I want my doctor to be waiting till that point. Right. Shall we go on? So we're going to go on to COVID now with the next question. So we've reached March. We've reached March. But don't worry, we're not only two twelfths of the way through the quiz. Well, there aren't many topics for the rest of the year, let's face it. Yeah. Okay. So which method of estimating oxygen saturation during a remote assessment was quickly binned after initially being embraced in the early days of the pandemic honk honk Helen that was my reindeer noise I thought it was a cat cat did Father Christmas I don't think reindeer is actually reindeers actually honk. Were you going to give us options? Sorry, have I honked too soon? Well, if you don't need them, go for it. Isn't it that Roth score? It is, yes. Can you tell us more about the Roth score? No. I don't think we should spend time on it. Well, no, let's not spend too long on it. But I remember at the time, because everything was so urgent, wasn't it? And people were so terrified of face-to-face appointments that this went around very quickly on Twitter as a great way you could check someone's SATs without having to put a SATs probe on them. So you had to... What was it? Starting from 1 to 30... Yeah, count from 1 to 30 on your native language during a single exhalation. The time taken to reach that point is your counting time. And if it was under 8 seconds, then apparently that's associated with low SATs. But it was completely discredited. So don't do it. That was in that great article by Trish Greenhalgh, and she was one of our very first guests on Deep Breath In. She was, the very first. It was so great to hear her early wisdom in those days talking about what works, what doesn't work, giving us confidence that we would be okay seeing and talking to people remotely provided we're that way. Yeah, it was great. So I guess if you want to hear more about the Roth score, then go and listen to episode one. And that means we can move on and talk about something else. Okay, question five. Let me start that again. Question five. If you have four vaccinators giving a COVID vaccine every eight minutes... Oh, Lord. How long would it take you to vaccinate 100 patients? Oh, this is maths. Shall I give you some multiple choice? So option one, 100 minutes. Option two, 200 minutes. Option three, 250 minutes. I'm pleased to say I'm not even going to engage with this question. I'm just going to guess. I'm going to go in the middle. Honk, honk. I think it's 200. Right. Yes. Well done. And you've caught up. You're on two points now. Well, let's not talk more about the maths behind it, but who's excited about the vaccination programme? It's actually started in the UK. Yeah, I was excited to hear Claire Girarda talking about it the other day and she talked about how her local convent because they were all over 80 all of the nuns came along at once to be vaccinated and the waiting room was just full of nuns and full habits and wimpled kind of sitting socially distanced even though they're all in the same bubble in the waiting room and that was just such a lovely mental image that kind of made me feel very positive about the vaccine. I think one reflection I have on the role out of the vaccine program obviously I am not a vaccinator but I have been watching my partner who is a GP locally where I am in Bath doing his extensive preparations and e-learning modules before his vaccinating session yesterday. And I think one of the things that from an evidence point of view, I still found slightly worrying was just the lack of very clear evidence setting out what is currently uncertain about this vaccine. So there was an awful lot of information that key consenters could give, was my understanding, you know, how messenger RNA works and all these kind of scientific details. And I think that's wonderful. But there seemed to be less emphasis on just being clear how long we know this might last for, like how far the evidence stretches. And in terms of saying this vaccine is safe, instead perhaps saying this vaccine is safe insofar as we know. And it's effective insofar as we know. And this is how far into the future we can kind of reasonably project at the moment. There's no reason to think that it isn't going to be safe. And we hope that that immunity is going to last. But there is still, I think, quite a degree of a leap of faith, which is not to say I'm sceptical about vaccines because I'm not in any way. But I do think it's important that the conversations that I had are honest about what we know, because that's where we did a really lovely episode with Talk Evidence last week around trust in public messaging.
But why is it that that doesn't happen? It just seems maybe as GPs, you know, we're used to having those conversations where you say, I just don't know, but, you know, this is what we could do. Is there something different about the way other people think? Well, when I talked to Baruch Fischhoff, who's a professor in this kind of risk communication, particularly at public health messaging level, I don't know if we included this extract in the interview, but we were kind of talking about the different languages that people use and the language that politicians are sort of trained to use and the kind of language that the press like to message in is quite different from an information sharing language, which health care professionals might be more familiar with. So I think we have to try and separate when we're trying to share facts and information, including uncertainties and limitations of it, and when we're actually trying to persuade people to alter their behaviour and perhaps accept a vaccination and being clear with the patient actually what our role is there to do, whether we are there to give information and or whether we are there to also try and persuade them to take one path or another. We had a similar conversation about this during one of our episodes for Deep Breath In when we were talking about vaccinations. We were talking about the flu vaccination and the flu experience in New Zealand this year and having a conversation more generally about what is our role as a GP with respect to vaccines where actually the data may or may not paint a convincing or clear picture. And I think that was certainly true of the flu vaccine and also for these mRNA based vaccines for. In this case, because we just don't have enough history since their development, we don't have that kind of log of experience yet. But it, I think, prompted us all to think more about that role. Is it to explain those areas of uncertainty or to persuade? And I think a lot of us are biased around wanting to persuade and give people the vaccine. And maybe it is just about, as you were saying much more eloquently than me, just having that conversation about what we know, what we don't know, insofar as we know what we know right now. Yeah, I'm a believer in when you are open about that, but then say, but my kind of considered opinion, as you would repeat, my opinion is that I will have the vaccine and I'd recommend you do then then people tend to um I'd be more likely to to follow that that recommendation than if you're just trying to bulldoze the conversation and also I think the thing with bias is that it's dangerous when it's unconscious. So, you know, if you're aware of your bias and you are explicit about it with yourself and with your patients and say, you know, I am biased towards an interventional biomedical model, you know, I'm biased to have a high level of faith in some of this science. But with these caveats around the data and the uncertainty and blah, blah, blah. i think i think it's we're doing people a service if we all kind of surface that bias and express it clearly because it affects our decision making it affects the way we share information it affects the tone in which we present things um and i think you know if we can get patients to talk about their biases and which may often be experiences or kind of experiences of friends and relatives, then we will end up having a better conversation collectively about this and what we should do and surfacing those uncertainties. Kat, I wanted to ask you a bit more about the kind of wellbeing side of things as well, because I think for GPs, or for me at least this year, the first wave was actually sort of the quietest I've ever been as a GP in terms of workload. But now this winter and January, February seems like it's going to be perhaps the busiest because we've got the vaccination programme in addition to, you know, higher than ever levels of demand so uh where do you where do you see this ending up or what can we do about that yeah that's a really difficult question tom i mean i think what we've heard repeatedly this year i think from the well-being podcast is that all of the things that you think work probably do work so all the things around um trying to make a mental separation between your work time and your home time is very important and it's particularly challenging i think for a lot of people to do i mean if you're going into a and you're face to face, you will have some kind of transition between your work life and your personal life. But if you don't, or even if you do have that space to kind of consciously create a kind of transition ritual almost, where you are kind of able to let go of all of the pressures that you're facing at work and try to kind of not carry them into the other areas of your life you know that's that's very important for people and we've heard a huge range of different interesting experts talking about this from kind of people who specialize in mental health in the army talking about you know how you have rest and recuperation when you're being deployed in a combat zone or to how you transition back from spending six months as a medic in Antarctica and how that time to kind of adjust to normal life is important so I think paying attention to the things that you can control is really important you know you can't control the pressures you can't control the vaccination schedule and you the experience at work. But you can control how you respond to it and the time that you give yourself. So I think that transition seems to be increasingly important. And I think we're really aware of that as GPs. We all know kind of, you know, the branch of the consultation that's housekeeping. And perhaps we need to be more conscious of that than ever. Like, how do we housekeep ourself and our emotions um so i think that's critical and i think also you know some of the mindful mindfulness techniques are important so i think they kind of the when you're doing that housekeeping in between consultations taking those few seconds to ground yourself um there's things you know rituals like what can i see what can i smell what can i taste what can i hear just kind of really centering yourself in the moment so that you're not constantly being overwhelmed with the anxiety about what's to come or what has been but really just kind of working in the moment and dealing with what do i have to do right here right now because you can nearly always manage to do the thing that you have to do right here, right now. It's the pressure and awareness of all the other stuff that's really, really difficult. So I think those are two kind of really small things that people have found effective. Well, a couple of things you mentioned there very much remind me of a guest we had on one of our early podcasts, Brewer who is a well we're about to hear a clip from him so I better get this right because he'll probably hear what I'm about to say a neuroscientist but also a psychiatrist and he does a lot of work around mindfulness and burnout and anxiety and I loved his expression that about you can sneeze on somebody's brain from anywhere in the world and just be mindful of who's around you, like online, on Twitter. And I think I was certainly getting a lot of, you know, feeling very anxious at times because of all of the other people's anxieties being sort of transferred onto me. And he said, you know, stop watching the news, which I did. And that really helped. So we got him back on, actually. Yeah, we got him back on to give us some more tips to how GPs can survive, I suppose, or avoid the burnout over the next few months. So shall we have a listen to Judd again? And that interview is coming up after this from our sponsor. When you're a GP, you're not just nine to five. Being a GP is part of who you are, whatever the time of day. So when it comes to your indemnity, you need someone you can turn to at any time. Medical protection is always here for you with expert medico-legal advice including 24-7 in an emergency. We don't just cover patient claims, we're also here to provide support and legal representation when it comes to GMC inquiries, coroner inquests, criminal investigations and more. Online we offer risk prevention courses and webinars to keep you up to date with current news, risks and legislation. We also go the extra mile when it comes to your well-being. With a free counselling service and e-care app, we're helping members take positive steps to better mental and physical health. It's the protection your career deserves all in one place. And if you're about to qualify or have recently qualified, we can help you take the next step in your career with savings on membership for newly qualified GPs. To find out more visit medicalprotection.org. So how can we stave off burnout? Well, I think of three key things to start with. One is know its causes. Like any good physician, we want to diagnose the problem.
One is a lack of autonomy and the second one is uncertainty. So often it feels like we don't have control over what's going on right now. Just being able to see that very clearly is going to help us work with that and I'll talk about that in a minute. The second is uncertainty. There's a huge amount of uncertainty happening right now. We're in the middle of a pandemic. We're in the middle of trying to roll out vaccines for this pandemic. There are tons of pieces of uncertainty that are happening right now. So simply being able to recognize, you know, is this something related to my autonomy? Is this something related to uncertainty? So we can clearly diagnose what the cause is around, you know, one aspect of burnout. Step two, once we know its causes, is to treat the causes. Something very, very simple. This is, many folks probably are aware of the serenity prayer. A lot of my patients use this in trying to work with their addictions. It basically says, you know, God grant me the serenity to accept the things I cannot change, the courage to change the things I can, and the wisdom to know the difference. The reason I'm focusing on this is because this helps with both the autonomy and the uncertainty. We spend a lot of time trying to change things that we can't. We beat our heads against the wall. We spend a lot of energy doing a lot of work that's not actually productive. So it's really important to be able to treat those causes. Oh, is this something I can actually change? Great. That gives us the courage and the wisdom to be able to focus on things that we can change and then let go of the things that we can't. Number three, physician, heal thyself. So we all know the things that are going to make us healthy. These are things that we tell our patients all the time. So make sure you eat healthy food, make sure you exercise, make sure you get enough sleep, and make sure you reduce your stress. This is a duh for all of us. Yet we can know this intellectually, yet not implement this for ourselves. So what I'm going to focus on here is a slightly different approach. Now our brains, from a neuroscientific standpoint, our brains really focus on doing behaviors that are rewarding. So what I'm going to suggest is that we reflect back on times when we actually did these things. So when we went to bed instead of checking our social media feed or our Twitter feed, when we actually took the extra 15 minutes to cook a healthy meal as compared to getting takeout, when we actually took 20 minutes to do a short stint of exercise, go for a walk, meditate, pray, whatever it is that helped us de-stress. Now, what I'm focusing on here is reflecting on these things. In the moment when we have an opportunity to choose between getting takeout and cooking healthy food, what we need to do is reflect back on our previous experience and ask, what was it like when I did X versus Y? So our brains can clearly see the difference in terms of what is more rewarding. I don't know anybody that says, you know, I wish I didn't spend that extra 15 minutes to do that stress reduction thing because now I feel less stressed and that's terrible. No, they say, boy, it was worth that extra 15 minutes. It was certainly worth that, you know, extra 15 minutes of sleep when I turned off my phone and went to sleep. So reflecting back on these things when we have these choice points can help us be able to remember how rewarding those things are. And that recollection of the reward is what actually can help drive us into doing that behavior again. And then it becomes a virtuous cycle. So those are the three steps. Know the causes, autonomy, uncertainty, treat those causes. Remember, whatever works for you. I love the serenity prayer. Accept the things we can't change. Change the things that we can and really use our noggins to know the difference between those two. And then heal thyself. Remember what it's like when we do take care of ourselves. Use that recollection to help drive that forward in a virtuous way. very pleased to have been saying the same thing or in line at least that's very gratifying to feel that I have learned something from all our amazing guests this year I just want to reflect on the kind of take care of yourself and being healthy thing I think obviously it is incredibly important and it is genuinely true that sleep and exercise and food and good healthy food will help our mental health and our well-being but But I think also there is this kind of slight, I don't know what to call it, shaming around well-being. Like, you know, if what you need right now is to climb into bed with a tub of ice cream and watch back-to-back episodes of Friends for three hours, then that's okay. Like, it's all right to listen to your body telling you or your mind telling you what you need to feel better right now and obviously if those are very damaging habits in the long term around food or addiction substances alcohol you know then then we need to be cautious around that but I think you know there is this idea that what what you need to do is go and um kind of do yoga and meditate and clear your mind rather than you know clear your mind by playing a video game or or something else so it is really about I think understanding what works for you and what's effective stress reduction and escapism and not blaming or judging yourself. I think that's such a good point, Kat. The thing that came to mind for me listening to Judd, who's always so great, is what about when you're feeling too down to actually push yourself to do those things? If you can say, remember that time when I chose to do X healthy, quote unquote, behavior instead of Y less healthy behavior and how great that felt. And then there's something that's so stressful or so crippling from an anxiety perspective, or if your mood is just not there, what do we what do we do how can we advise patients i i feel like this is for me so much of the challenge how do you encourage people to build that internal motivation even when they can have that positive reflection and i think you know you don't have to answer that i just think but you know but i think you know when you are feeling that when you are feeling that anxious or overwhelmed like having a shower is a huge achievement and i sort of think you know being being kind to yourself and not setting goals that are overwhelming or unreachable i think this is less talking about patients who are depressed and anxious because I think it's a slightly different approach but clinicians particularly we may have this tendency to be very competitive with ourselves or other people and like oh I'm going to run a marathon or I'm going to you know meditate every day for half an hour and be really really good at it. So I think it's just about reducing those expectations and recognising that everything you can do that has a positive impact on your wellbeing is a step in the right direction. And that can be really, really small. And sometimes it's not putting pressure on yourself and saying, well, you know, I've cooked from fresh every night for the last three weeks. And actually today I'm going somebody else do it and we're gonna have takeout and we're gonna not worry about any of that isn't there also something just around what's humanly possible I mean a lot of this stuff around autonomy the kind of dick tats that come it's not only taking away your autonomy but often it's also providing with an awful lot of extra work. And I think people's own personal thresholds for either absorbing work or very rapid task switching or changing and doing something totally new, that differs. There's loads of stuff going on in people's general lives that also probably affects their ability to deal with those things.
But then I think it comes back to that that's why it's so important that we work in teams so even in the in the community when you can feel quite isolated as a GP you know you have got a team around you because I think that threshold changes on a daily basis so some days you can be the one that soaks it all up and you can work late and you had a particularly good night's sleep or you're particularly feeling strong today and other days you just can't do it but we don't necessarily allow our workload to flex across the team and I think if we got better at kind of having those conversations with each other that say do you know what today I'm really today is a hard day I really can't do it today today could you pick up some of this slack and then I will in turn do that for you tomorrow I think some of the structures and ways in which we work as GPs are not very amenable to doing that and I think if we can build in some of that flexibility which which you can see more in some hospital teams or very functional hospital teams obviously very dysfunctional teams as well then I think we would see a kind of greater sense of collective well-being so it's not just about individual well-being it's about collective well-being. Yeah and that might have got harder this year for GPs I feel like we're more and more you're in your room you know from the moment you get in till when you leave because you're not going outside the room so much to get your patients and can't go in the communal areas um so yeah that's um it gets harder uh just going back to to judd's uh point there about uh i mean i did think it was useful to raise your sort of conscious you know to have a conscious thought when you're about to do something, because I find myself all the time, and maybe what he's talking about is maybe on the milder level of stress and burnout is when, you know, it's, you meant to go to bed half an hour ago, but you've been scrolling Twitter or, you know, as an example, quite useful to have that moment of awareness and how will I feel at the end of this? And actually, I only spoke to him yesterday, but I've tried that already and it seemed to help. And I got to bed early last night and, you know, yeah, it seems a useful little trick as part of the armoury, I suppose, rather than the whole picture picture I should say Judd's got a very good free course for burnout for GPs on his website which I've also done a little bit of it's a similar style of his videos and yeah you'll be very sad to hear that we're at that stage already, is the lateral flow test game. So I only heard this week that we're, in practices England at least going to get lateral flow tests so we can test staff I think twice a week from the new year. So I thought what better way to end the podcast than the lateral flow test game where we can think about how accurate these tests are and what mistakes we might make in using them. And this has been something which there has been a lot in the BMJ about in recent weeks. So we've got this interactive on bmj.com, which has been on there for a while as part of the COVID testing article where you can plug in your pre-test probability along with the sensitivity and specificity of the tests that you're doing and you can get some answers about the likelihood of false positives and false negatives and so on. So we're going to do that with the lateral flow test. Now, sorry, I feel like I'm just talking all the time. So I lost my train of thought. Okay. Let me start again. Not start again. Let me carry on. So with these lateral flow tests, there's some controversy around what the real world sensitivities are versus what they are in the studies. So when we're doing this game, shall we use the sensitivities as performed by NIHR nurses or the Boots Test Centre employees? Boots Test Centre. I'm sorry. I definitely go Boots. I agree with Kat. Well, that's good because that's the only one I've worked out the answers for. See, all of our brains think the same. We've all been influenced, GP brainwashed into the real world. Absolutely. So that's a sensitivity just so you can do the WAFs in a moment. Only 58% with the lateral flow tests for detecting COVID. So let's start with an example of let's take an asymptomatic person in a fairly high prevalence area. And maybe it's a health worker, maybe flouting the rules a bit. And maybe have a pre-test probability, you reckon, of around 1% of having COVID, even though they don't have any symptoms. Which may or may not be accurate, but 1% is the smallest you can put in the calculator. So how many false negatives would you expect? How many false negatives would you expect if you test 100 people? Is the answer A, 0, B, 3, or C, 10? Buzz in when you're ready. Can't you tell us in the calculator? So, sorry, I should put you out of your misery. The answer is zero. I was just about to say it's zero because if it's a pre-test probability of 1%, that means that you're estimating only one person in 100 to be positive right? That's right. And so a test of 58% that would still more than likely give you that one positive test. That's right. So Helen I'm going to look to you now because I'm sure you've talked about this on Talk Ev but uh but we've talked about testing a lot but my understanding is then that so obviously over 100 people that's kind of okay but as you get to larger numbers which we will be doing so if you do a thousand tests then you're going to detect six people but have four but miss four approximately and I guess that's the the concern isn't it that we're going to be falsely reassuring lots of people through this. Yeah it's kind of a mixture between a kind of mass public health intervention so these kind of small numbers start to have big implications for people's lives in absolute terms and around the prevalence area that you're testing in. Those are kind of the two key points that I think John Deeks, who we've spoken to a lot about testing on this programme, who is well worth following on Twitter if you allow yourself to ever read it again, following the wellbeing section. He's well worth listening to worth listening to okay so the second question the last question in the quiz uh just to end on a high um so we'll take someone with classic covid symptoms then so they've got fever myalgia and nosmia and they've you know the whole household of covid so you reckon their pre-test probability is really high and I'm going to estimate that 90%. So then how many false negatives would you expect if you test 100 people in that? And there's three options. 5, 25 or 38. 5, 25 or 38. And actually whoever gets this right will win the quiz. Oh, really? You've got a one in three chance. It's like finals again. I feel like I had a better than one in three chance at finals, I have to say. It's the higher one isn't it yes it's just that option c 38 yes yes you're right 38 so you you'd get detect 52 true positives but 38 people are told they are negative for covid even though they they have it so um i guess so, which is why I think they're not recommended for use in people with symptoms. But my take home word there, if you've got a member of staff who has some symptoms and quiz. And the final scores are, well, I guess I've already told you that Helen has won our quiz with three points. Yay! Woo! Thanks, guys. Thank you very much. I'm sure you've... It's been fun, hasn't it? It's been good. We should do this again. But maybe not for another year. It's definitely been thought-provoking. I could have done with a lot less maths. And if you want to hear that next year, then you can subscribe to the Prevent channel. And please leave us a nice review on iTunes. And next episode, I think, will be about vaccines. So another reason I hope to subscribe. So as we end 2020, there's obviously so much to look back on and so much to take stock of. And we thought, who better to do that than one of our past guests and the past president of the RCGP, Iona Heath. And in the episode we had on the fear, she definitely left us with a lot of food for thought and a lot of really useful wisdom about general practice and the role of fear in our lives this year.
In any festive message, there's an imperative to find some hope for the new year to come, which is not easy in our current circumstances, but I'm going to try. 2020, the dread year of pestilence, has been awash with fear and all practising clinicians recognise the power of fear to generate irritability and anger. The fears have been multiple and multifarious, encompassing death, suffering, loss of livelihood, sanity, love and the loved, disruption of plans, futures, education, employment and careers. For frontline health professionals, there may also be the fear of failing patients in the face of a horrible and unfamiliar disease while feeling exhausted and vulnerable. Fear is intensely personal and different people with different stories and different contexts can have very different vulnerabilities to each modality of fear. As a result fear may not be shared and the extent of fear may not be understood or even recognized which makes the resulting irritability and anger seem inexplicable and unwarranted. There seems little doubt that fear and anger have played out in the hostility and insult that have become the hallmark of a polarising scientific debate about the best ways to manage COVID-19. Much policy has been very understandably driven by fear and yet fear is a very blunt instrument with which to batter people into conforming to public health advice. We already know this through our experience of lifestyle advice, screening and preventive medication. And now we begin to see fear being used to promote the new vaccines, when surely this is a huge opportunity to recast vaccination as an act of social solidarity, were it not for a lingering feeling of huge financial imperatives lurking behind all official advice. Different people inevitably respond very differently to the same dose of fear. Some have become quite simply terrified, have not left their home for months and may never recover their confidence. Others, perhaps with less reason to be fearful in the short term, try to cling on to normality. The effect is hugely destructive of any sense of community or solidarity. So where is hope? We must find it by recognising that fear underpins anger and polarisation, and by reiterating that the emollient for both fear and anger is kindness. We need to remember that our responsibility is not to exacerbate fear through false certainty, to acknowledge the extent, the importance and the creativity of uncertainty, and to rebuild the tradition of academic debate that is based on mutual respect rather than the angry certainties that have characterised 2020. I wish you all happy festivities without fear and anger and underpinned by kindness. Thank you.
Hello and welcome to the February 4th, 2020 Annals of Internal Medicine Highlights Podcast. I'm Dr. Christine Lane, Annals Editor-in-Chief, to give a quick summary of the new material you'll find if you go to annals.org. I'll start with articles published online first on January 28th. Heart failure affects 26 million people globally and is a leading cause of hospitalization among older adults. Yet, despite dozens of studies on methods for reducing re-hospitalizations in older patients with heart failure, the great majority of patients still receive usual care, which is careful medication and reconciliation, an outpatient follow-up appointment, and some education. The first article I'll mention explores whether more intensive transitional care service interventions could be a way to reduce re-hospitalizations and improve patient outcomes. Researchers from Stanford University created a micro-simulation model using clinical trial, registry, and hospital data to assess the cost-effectiveness of three types of post-discharge heart failure transitional care services. The interventions assessed included disease management clinics, nurse home visits, and nurse case management, and the patients studied were those with heart failure who were aged 75 at the time of hospital discharge. The researchers found that all three transitional care interventions examined were more costly but also more effective than standard care, with nurse home visits dominating the other two interventions. Compared with standard care, nurse home visits increased quality-adjusted life years and cost, resulting in an incremental cost-effectiveness ratio of $19,570 per QALY gained. Of note, according to the researchers, each of the transitional care interventions studied resulted in important improvements in health outcomes, and the differences among them were modest. The authors suggest that it is highly unlikely that standard care post-discharge management is more cost-effective than any of the transitional care services they studied. An accompanying editorial notes that transitional care services are not yet standard because initiating them can be complicated and include upfront costs that must be shouldered by health care providers and may not be reimbursed by payers. Next is a case report from a physician who was a passenger on a recent airline flight when he responded to a flight attendant's request for a doctor on board. The flight attendant suspected that a young male passenger was having a stroke, which would require an emergency landing. A medical emergency during a commercial airline flight may require an unplanned landing, which disrupts travel plans and can be very costly. Therefore, it is important to know the difference between a true medical emergency and something that does not require an unplanned aircraft landing. The author found the plane passenger suffering from sudden onset ear pain, slurred speech, drooling, and a complete right-sided facial droop. The man had lost his forehead wrinkles and could not close his right eye, but had no mental symptoms and still had his physical strength. When the man reported that he had recently recovered from a cold and that his symptoms began during ascent, the author determined that there was no reason to deter the plane. The man's symptoms were caused by declining atmospheric pressure in the cabin, causing a relative increase in middle ear pressure from a blocked eustachian tube that was transmitted to the branches of the seventh nerve as they ran through his middle ear. This condition, known as facial barotrauma, can occur during ascent in scuba divers, during flight, during land travel at high altitudes, after certain operations on the middle ear, and with some structural disorders of the middle ear. The paralysis usually resolves within 15 to 30 minutes after maneuvers to reduce middle ear pressure, such as yawning, swallowing with pinched nostrils, and the Valsalva maneuver. Breathing oxygen-enriched air improves tissue oxygenation, which also helps. Next is a commentary on the quality of nutrition research by Dr. Ross Prentice of the University of Washington. Dr. Prentice notes the limitations of much currently available nutrition research and offers suggestions for improving the quality of evidence related to the health effects of what we eat. The authors of the second commentary published on January 28th attempt to answer the question, who owns sepsis? They note that critical care physicians founded the Surviving Sepsis Campaign, promulgated the Surviving Sepsis Campaign guidelines, popularized the principles of early recognition and bundled care, and spearheaded the latest overhaul of sepsis definitions. Yet they note an underappreciated consequence. The critical care perspective on sepsis is born of the experience of treating the sickest subset of patients. The authors believe that the next step is to better address the full spectrum of illness encompassed by sepsis. They believe that expanding the circle of sepsis stakeholders will help bring more awareness and balance to the plurality of patients with sepsis who are diagnosed and treated outside of intensive care units. Fueling controversy over the high cost of prescription drugs in the U.S. has been a substantial contribution of the federal government to the development of many products. A quarter of new drugs over the past decade had key late-state contributions from publicly funded research, most commonly by the National Institutes of Health, prompting concern that Americans are paying twice for these expensive medications. Senators and other policymakers have proposed NIH should more actively work to ensure fair pricing of drugs developed with its support. Critics had noted that such an intervention was attempted in 1989, but NIH stopped it just five years later because of concerns that it chilled government-industry collaboration. The authors of a 3rd January 28th commentary review this episode to better understand the rationale for the fair pricing condition and the impact of its removal. They then offer recommendations on how NIH can incorporate a reasonable pricing condition for drugs developed with taxpayer money that preserves necessary incentives for bringing these drugs to market. The final January 28th article presents the International Committee of Medical Journal Editors' recommendations for the disclosure of authors' interests when submitting manuscripts to medical journals. Moving to material published on February 4th. The Advisory Committee on Immunization Practices released its 2020 Recommended Immunization Schedule for Adults with changes to the administration of the influenza, human papilloma virus, hepatitis A, hepatitis B, meningococcal B, and pneumococcal conjugate vaccines. The schedule, which can be complex and challenging to implement, features revised content, format, and graphics to make it easier to follow. The complete schedule, including changes in the vaccine notes section, was published online at annals.org on February 4th. The schedule is streamlined for ease of reference. Physicians should pay careful attention to the details found in the vaccine notes section as they clarify who needs what vaccine, when, and at what dose. In addition to changes in the administration of some vaccines, the 2020 schedule includes new instructions for shared clinical decision-making for several vaccines. The study reported in the next article described trends in primary care visits among adults enrolled in a large national commercial insurer. The researchers found that rates of primary care visits decreased by 24 percent from 2008 to 2016, and the proportion of adults with no primary care visit in a year increased from 38% to almost 50%. Specialist visit rates remained essentially unchanged, of care. The author of an accompanying editorial suggests that declines in primary care visits may be an unintended consequence of money-saving efforts of large companies. Thank you. settings and may result in serious injury. Up to 1 million hospitalized patients fall each year, and as many as one-third of those falls are considered preventable. Preventing in-hospital falls has been a Joint Commission National Patient Safety Goal. The use of bedside sitters to provide patients at risk for falls with constant supervision is a practice rooted in tradition, but their use is expensive. Determining how effective they are for preventing falls is important for patients and providers. Researchers from the West Los Angeles Veterans Affairs Medical Center reviewed published evidence about the effect of sitters and alternatives to sitters on patient falls in adults in acute care hospitals. Of 20 studies meeting inclusion criteria, only two added sitters to usual care and had conflicting results. 18 studies compared alternatives to sitters. From those, the investigators found moderate certainty evidence that interventions that included video monitoring decreased sitter use without adversely affecting fall rates when compared to the use of sitters. They found little convincing evidence that close observation units or nurse assessment tools were effective alternatives. While there is a lack of evidence to support the use of one-to-one bedside sitters, the rationale for their use to prevent falls might be sufficiently compelling that it is premature to conclude that their use should be abandoned. Most of the articles in the February 4th print issue were initially published online first and discussed in prior podcasts. New material in the issue includes an On Being a Doctor essay, a Beyond the Guidelines Grand Rounds, and In the Clinic review. In Beyond the Guidelines, two experts in transgender medicine discuss appropriate care for transgender women with anxiety and hypertension. The experts and the patient agree that her case should be managed in primary care and that the topic of caring for transgender patients should be included in general medical training. This is an important point as transgender patients face discrimination in the healthcare setting and may not have access to medical professionals who can provide competent care.
Go to annals.org, the print issue, for current advice on preventing, diagnosing, and treating this very common condition. And the latest Annals on Call podcast features the topic of GLP-1 inhibitors in the management of patients with type 2 diabetes. That brings me to the end of this podcast. Thanks for listening, and I encourage you to go to annals.org to take a look at some of the articles I've mentioned. As always, there are many opportunities to earn CME and MOC credit if you do. Thanks to Beth Jenkinson and Andrew Langman for their technical support.
Hello, and welcome to this JAMA Editor's Audio Summary for our January 19th, 2016 issue. This is Howard Bauchner, Editor-in-Chief of JAMA. Death, dying, and the end of life. That is our theme for this week. There are two original research reports, eight viewpoints, three pieces from a piece of my mind, two accompanying editorials, and two research letters, both of which focus on where and how physicians die. Let's start with the original research reports, Healthcare and Costs Related to Cancer Deaths in Seven Countries, in an analysis of administrative and registry data from seven developed countries, the United States, Belgium, Canada, England, Germany, the Netherlands, and Norway. Beckelman and colleagues examined patterns of care, healthcare utilization, and expenditures over the 180-day and 30-day periods before death for patients aged 65 years or older who died of cancer in 2010. Among the authors' findings was that the end-of-life care was less hospital-centric in the Netherlands and the United States than in the other countries. The United States and the Netherlands had the lowest proportion of decedents die in acute care hospitals, 22.2% and 29.4%. A higher proportion of of life were higher in the United States, Norway, and Canada, intermediate in Germany and Belgium, and lower in the Netherlands and England. Intensive care unit admission was far more common in the United States, 40.3%, compared to the other countries, approximately 18%. Many of these findings will come as a surprise to all of us. I was particularly struck that end-of-life care appears to be less hospital-centric in the United States. In many regards, this may reflect how palliative care is structured in various countries. In the United States, this occurs outside of the hospital, whereas in other countries, it may occur within the hospital. On to the second original research report, Family Perspectives on Aggressive End-of-Life Cancer Care. Patients with advanced stage cancer often receive aggressive medical care at the end of life despite evidence that aggressive treatment does not improve quality of life, patient outcomes, or caregiver bereavement. Wright and colleagues surveyed over 1,100 family members of Medicare patients who died with advanced stage lung or colorectal cancer to assess the association of aggressive end-of-life care with family members' perceptions of the quality of care and whether the care was consistent with patients' preferences for end-of-life care. Overall, 51% of families reported excellent end-of-life care. The authors found that family perceptions of better end-of-life care was associated with earlier hospice enrollment, 59% versus 43%, avoidance of intensive care unit admission in the 30 days before death, 52% versus 45%, and death occurring outside the hospital, 57% versus 42%. In many regards, this article provides a clear message. Early hospice enrollment, avoidance of intensive care unit admission if possible, and death occurring at home are associated with a good death. Now on to the eight viewpoints. The first is entitled Responding to Patients Requesting Physician-Assisted Death. The second is entitled Why Physicians Should Oppose Assisted Suicide. These two viewpoints represent polar opposites in representing two very different views about whether or not physicians should participate in the death of their patients. At JAMA, we felt it was important to represent both views of this rather complicated and difficult discussion, that is, whether or not physicians should ever actively participate in the death of their patients. The next three viewpoints also focus on physician-assisted dying. Koltfelter and Adashi described the recent changes in law in California in a viewpoint entitled, The Liberty to Die, California Enacts Physician Aid in Dying Law. The second of the three viewpoints is entitled, Physician-Assisted Death in Canada. H.M. Choninoff summarizes the recent changes that are being mandated in Canada because of a recent Supreme Court decision. The Supreme Court in Canada reasoned that an outright, quote, prohibition deprives some individuals of life as it has the effect of forcing them to take their own lives prematurely for fear that they would be incapable of doing so when they reached the point where suffering was intolerable. The court also suggested an individual's response to a grievous and immediate medical condition is critical to their dignity and autonomy. In this viewpoint, Dr. Charnonoff describes the recent Supreme Court decision in Canada and how the medical community is responding to it. The final viewpoint focused on physician-assisted dying is by Larry Gostin and A.E. Roberts. These authors summarize the emerging law in four states with respect to physician-assisted dying. They also emphasize that in all four states, physicians can opt out of physician-assisted dying. The final three viewpoints focus on different issues. The first by Derek Angus and Bob Truong, entitled Towards Better ICU Use at the End of Life. The second by Ota Gidi, A Policy Prescription for Hospice Care. And the last by Moore, Rubin, and Halpern entitled The Problems with Physician Orders for Life-Sustaining Treatment. In a departure from our usual content, rather than a single article focused on a piece of my mind, there are three. These important narratives described issues related to death, dying, and end of life. The first is entitled, What Would Mom Want? The second, A Final Course. And the third, Hope is the Thing with Feathers. I do want to emphasize the two research letters. The first, Association of Occupation as a Physician with Likelihood of Dying in the Hospital. And the second, End of Life Care Intensity for Phys intensity for physicians, lawyers, and the general population. Both of these research letters emphasize that, indeed, physicians do not die very differently from other people in the United States of similar socioeconomic status. Finally, I'd like to comment on the two editorials that summarize the issue. The first is by Atul Gawande and is entitled Quantity and Quality of Life, Duties of Care in Life-Limiting Illness. Dr. Gawande not only summarizes the many pieces in this issue, but also adds his own comments about the issues related to death, dying, and end-of-life care. He concludes, the evidence indicates that the medical profession is harming vast numbers of patients by neglecting this goal and that this is not just a U.S. phenomena but a global one. People everywhere have essential needs aside from just living longer. Medical practices, research, and policies must ensure that clinicians have the skills to understand those needs and have the capabilities to serve them for patients with life-limiting illness. Everyone dies. Death is not an inherent failure. Neglect, however, is. And the last editorial is entitled Death, Dying, and End-of-Life Care by Phil Fontanarosa and me. We write, in 2014, approximately 2.6 million people died in the United States and approximately 55 million people died worldwide. Death is inevitable, but people die for many different causes and in many different environments. Most individuals at the end of life want to be surrounded by family, in familiar settings, Thank you. thereby improving the quality of end-of-life care as well as the quality of death and dying. Virtually every physician has emotionally painful and poignant stories about how medicine failed their own family members, friends, or colleagues during the final stages of life. In some ways, this is not surprising. Death always engenders great emotion, and recollections may not be accurate. Yet it is concerning when physicians, who know the healthcare system far better than Thank you. I believe that the political climate has changed dramatically over the last three or four years. And in the United States, we can now have an appropriate and important discussion about how to die well, both in the United States and around the world. We hope you like this theme issue entitled Death, Dying, and End of Life. Thanks for listening. This is Howard Bauchner with JAMA. For more podcasts, visit us online at jama.com.
Okay, welcome. My name is Devine. I am a resident and this is episode 143 of the Devine Intervention Podcast. In this podcast, I will be essentially giving a comprehensive biostats review for the USMLE exams. I will say essentially this podcast, if you're taking any exam of step one, step two, CK or step three, I strongly recommend that you make sure you go through this podcast. I'm actually attaching slides and I would highly recommend that you download the slides and maybe annotate them as I go along. But this will be a very, again, like I said, very comprehensive review. The only thing I really would not talk about in this podcast is bias. Bias is something I think probably deserves its own podcast. So I'll probably make a podcast in the future relating to that. And just as a pro tip for people taking the USMLE exams, whenever you get the drug ad questions, you should always leave them for last in the block. I would just say for the great majority of people, it usually makes no sense for them to try to do those drug ad questions first. Once you see it, just mark it, just mark those questions and move on, come back to them later. And then the other thing I want to say with regards to biostats is do not, because I see many people, they're just like, oh, biostats is a plug and play science. And they say, oh, yeah, I've memorized all the formulas. And then you're like, man, why are you doing so poorly on these biostats questions? The thing is, to be perfectly honest, it's not very common for you to have to do extensive math to arrive at the answers to most USMLE biostats questions. Most of them just kind of depend on having a thorough understanding of what's going on, like having a thorough understanding of the concepts, usually that gets you all of the way there for the most part with many of these questions. Because most times they ask you about relationships, they ask you about patterns, things that are not necessarily abstractable by just memorizing the formulas. So you will notice today, in fact, to be honest with you, and again, I'm not saying this from a point of pride. I'm just telling you what I do. I essentially never set up two by two tables for most biostats questions. Don't get me wrong. For some biostats questions, you know, you do need to, you know, do some math, right? Things like likelihood ratios and stuff like that. But for like maybe like 95% of biostats questions I do, I usually do not do any kind of math or set up like a two by two table or anything like that. Most times if you kind of like understand the concept and really know like, like not just like, oh, I know the formula, like really understand what the concept speaks. Typically the answers are pretty obvious on MBME exams, right? So my goal with this podcast is to teach you how to think about biostats. I essentially want you to feel like, oh, biostats is pretty easy. I actually feel like I have like a very good solid understanding of this. And for people that are taking the step three exam, especially, you better know your biostats. I will say probably like one out of every like five or six questions you'll meet on day one of your exam is going to be a biostats question. So don't blow that stuff off. It's a recipe for disaster. And then this podcast, I will also say it's probably very useful for people that are taking like the internal medicine in training exam and the internal medicine board exam, because this, they tend to test a lot of these concepts relating to like biostats, biostats, biostats. They test them in very unique ways. And I think this podcast should also make you very well served to deal with those kinds of problems. So without further ado, I'm just going to go ahead and jump into it. And I love the way I structure this. I have like questions, like really like 90% of this presentation is based on questions. So again, by sort of walking through these questions, I really do think it will give you like really by the end of this podcast, I think you should have a very, very solid basis for biostats. The thing I will just say though is this is one of those podcasts you don't want to speed through. Again, I'm saying this as someone that watches many things at 2.5x speed or 2x speed sometimes. But really, for the most part, you probably don't want to speed through this so that you don't lose the thread of thought. OK, well, try to really make sure as you're going through these slides, try to make sure that you're really understanding what's going on. As you listen to me make annotations, and I think at the end, you should feel very comfortable with biostats. So let's jump right into it. So question one. So a new serum test is created to screen for peripheral arterial disease. The sensitivity of the test is 80%. The most accurate interpretation of this statement is, so a new serum test created a screen for peripheral arterial disease, sensitivity is 80%. The most accurate interpretation of this statement is what? So option A, patients with positive test results have an 80% chance of having the disease. Option B, in patients with negative test results, 80% do not have the disease. Option C, in patients who have the disease, 20% will have a negative test result. And then in option D, patients with negative test results have an 80% chance of not having the disease. So what do you think the right answer here is? I will pause if I were you. So the right answer here is actually option C, right? The right answer here is option C, right? And if you kind of think about it right like the thing is again like i said earlier answering mbma questions for the most part especially the biostats questions i mean yeah you can do math to get to the answers but most times you you don't really need math to answer these questions many times you just need to think and you can usually finagle your way to the right answer. And sometimes, like even with knowing the formulas, I see some people, they're like, how do I even set up the math in the first place? If you don't have the understanding, it'll be hard for you to set up the math. Or if you set up the math, you set it up wrong. Okay. So just something to keep in mind, right? So the thing is sensitivity. When you're dealing with the concept of sensitivity, you're essentially trying to answer this question. You're essentially asking yourself, of all the population with a given disease, what percent have positive test results? That's literally all sensitivity deals with. Of all the population with a given disease, what percent have positive test results? Once you figure out that percent, you've essentially figured out your sensitivity. The thing is, the other percent that you don't detect that truly have disease, those will obviously be your false negatives, right? And if you notice, the second word in false negative is negative, but the word in front of it is false. So that means that if it's a negative that is false, that means it is in fact true, right? It's in fact a positive, right? So one thing I recommend, especially to people that I tutor one-on-one, I tell them to consider using like this second to first word mantra to keep things straight, okay? And another thing you want to remember here is that when a test is highly sensitive, it tends to have a low false negative rate. You kind of see the way that ends match with that. So looking at the other answers. Right. So answer choice is wrong. Right. Because he says, oh, patient with positive test results have an 80 percent chance of having the disease. That's essentially describing the positive predictive value, which I will get to in a bit. Option B says in patients with negative test results, 80% do not have the disease, right? Again, that's essentially expressing the negative predictive value. So I'll talk about that in a bit. And then option D says patients with negative test results have an 80% chance of not having the disease. Again, that's just almost like moving the words around for option B. Okay. So again, BioStats, I promise you, it sounds nebulous, but it's not hard if you just really try to understand what's going on. Now, the next question. So, a study is done on a thousand patients with a history of glioblastoma, so GBM.
100 patients have a positive ST test, and 900 have a negative ST test. Brain imaging with biopsy, so this is obviously like a gold standard test, is done on all these patients, and 30 recurrences of GBM are found. 10 patients with positive ST tests have GBM and 20 patients with negative ST tests have GBM. Which of the following best represents the sensitivity of ST tests? So I'll just read this real quick again. So study 1,000 patients that have a history of GBM. Neoceram test, the serum test is ST. You do it to screen for recurring GBM, right? 100 patients, they have a positive ST test, 900 have a negative ST test, and then you do like a gold standard test, right? So like brain imaging with biopsy, and you do it on all these patients, and you'll find 30 recurrences of GBM. And of those 30 recurrences, you notice that 10 patients with positive ST tests have GBM, like the GBM recurrence, and 20 patients with negative ST tests have the GBM recurrence, right? And then I'm asking for the sensitivity of the ST tests here, right? So option A is 92%, option B is 35%, option C is 75%, and option D is 50%. So what do you think the answer to this is? So the best answer here is actually B, right? So the sensitivity here is actually 33, 33%. And I'll talk about, I guess I'll sort of go ahead and mention it now. So the thing is, you may say, but Devine, there's no 33% as an answer choice. So here's the deal, right? So don't blame me, blame the NBMA. The thing is, occasionally the NBMA actually like does this thing where they put answers that are not completely exact with the math. They just put inexact answers that are kind of close to what the real answer is, right? Whenever you see this happening, you're like, man, I've done this math twice. I'm still getting the same answer. Pick the answer that is closest to the answer you spit out from your math, okay? And again, this question sounds really hard and nebulous with all these numbers, but again, if you do simple math based on an understanding of the concept, it will save the day for you here, essentially, right? So the thing is, sensitivity essentially tries to answer the question, right? Again, like I said, of all the population with a given disease, what percent have positive test results? Right. What percent have positive test results? Right. So the total disease population is 30 people. Right. That's me very clear in the question. And then the number of those like the the number of those disease people, positive test results is 10. So like 10 of those people have like the positive ST test. So your sensitivity is essentially 10 over 30, which is 33%. Again, you can go ahead and plug this into a two by two table if you want. But again, I don't think that's absolutely necessary if you just understand the concept. This is essentially what I do like on my own on exams. And the answer here is 33%. Okay. So let's jump on to the next question, right? So we have a new serum test for GBM, okay, has a specificity of 90%. The most accurate interpretation of this statement is what? So option A says 90% of patients with GBM have positive test results. Option B says 10% of patients with GBM are missed by this test. Option C says 10% of patients without GBM have positive test results. Option D says 90% of patients without GBM have positive test results, right? So I'll let you mull over that for a second. So what do you think the answer is here? So the best answer here is actually C. Okay, again, simple math plus understanding is the way to go with biostats. And really just in general with any subject on the USMLEs, understanding is usually the way to go, right? So again, kind of like I talked about with sensitivity, specificity essentially answers this one question. This is how you should try to interpret sensitivity. Of all the population without a given disease, what percent have negative test results? Again, of all population, of all the population without disease, what percent have negative test results? That's literally all you need to worry about right so in the question i tell you that the specificity of this test is like 90 right so that means of all the people without gbm 90 tested negative right so that means there's this 10 that should have tested negative but they ultimately ended Essentially, these people are false positives, right? So that's why the right answer here is C, because option C says, oh, 10% of patients without GBM have positive test results, right? Those are your false positives, okay? And kind of like I said that, oh, a highly sensitive test has a low false negative rate, right? You see the ends kind of matched there. A highly specific test on the flip side also has a low false positive rate. You can see how I kind of highlighted both P's in the PowerPoint. Okay. So let's take a quick like sidebar here, right? You've probably heard of this spin and snout principle, right? So let's talk about it, right? So the thing is, if you have a test that's like, you know, super sensitive, like a very highly sensitive test, people that have disease, just sort of walk with me through my thought process here. If a test is highly sensitive, it means that people with disease should have a positive test result. That's what you'd expect, right? On the other the other hand if a test being highly sensitive like comes out with like a negative result so if the test result says oh negative then that means the disease should be absent right because again this is kind of building up on things i've sort of talked about already right if the test is negative the disease should be absent that essentially tells you like essentially you're dealing with a low false negative rate. Right. So a negative test should help you rule out disease. That's where the snout principle comes from, that if a test is highly sensitive, that's the SN. Right. It should help you rule out disease. Right. But if you look at things from the other perspective, right, if a test is like highly sensitive, then that means people without disease should have a negative test result. Right. Now, the thing is, if you are like, oh, OK, this test is, you know, very specific people without disease, negative test result. If you get a result that is positive from this highly specific test, then that means that disease should be present because this highly specific test has a low false positive rate, right? So a positive test should help you rule in disease. That's where the spin principle comes from. So for a very specific test, that's the S. If positive, that's the P, should rule in disease, okay? Unlike the Snell principle where the S is a highly sensitive test, that's the S. If negative, that's the N, should help you rule out disease. And this kind of leads into my next point of like screening versus like confirmatory tests. The thing is, again, if you have a test that has very high sensitivity, like I said earlier, again, you may say, Devan, you're repeating yourself over and over again. Repetition always helps. Trust me. So in tests with high sensitivity, people that have disease, they should have positive test results. So a high sensitivity test, it actually makes a very good screening test. Because you don't want to inadvertently miss out on people that have disease. So take, for example, if you're screening for HIV, you want a test that is very high sensitive, right? So that you don't miss out on anyone that has HIV, right? Because imagine what will happen if you miss out on a person that truly has HIV. They go out into the world, have sex with other people, give those other people HIV, right? That's not good, right? So you want to try to prevent that. That's why you use high sensitivity tests for screening, right? That's why essentially for HIV, we use the ELISA test. The ELISA test is extremely sensitive for the detection of HIV. But if you have a test with very high specificity, people without disease should have negative test results, right? That's what you expect. So the thing is, these high specificity tests, they're actually awesome at confirmation. They are very good confirmatory tests, right?
So the thing is, these tests that are, again, very highly specific, they're good at labeling people without disease so that if you get like, you're like, oh, this test is very specific. It's a high specificity test. If you get a positive result, right? And you know, by definition already, I'm at this point home over and over again, you know, by definition that a high specificity test has like a very low false positive rate. If you get a positive result from a very specific test, then that patient very likely has the disease, right? So this is why if a person has a positive ELISA test for HIV, you don't run out into the room and tell the patient, oh, you've got HIV. Well, you should probably say it in a more patient-centered fashion, maybe a more subtle tone of voice, but that's a different story for another day. But after you do the EL ELISA test you don't tell your patients the results just yet right you the next thing you go you do is you tell the you you do a western blot right to confirm all right the western blot you do them after a positive ELISA right uh because again there is nothing that feels as terrible as telling the patient oh i'm sorry you have HIV and then you go and do the western blot and you're like oh crap, this patient doesn't have HIV, right? You would not want to do that. That kind of looks like a lawsuit waiting to happen. So you don't want to do that, right? So although I guess with that said, remember the Western blood is no longer what we do in most places to confirm HIV, at least in the US. Okay, so let's jump to the next question, right? So question four. So which of the following points best represents the region of the graph with the highest positive predictive value for the detection of type 2 diabetes mellitus? So I'll encourage you to look at the graph and then tell me what you think. What is the region on the graph that represents the highest positive predictive value for the detection of type 2 diabetes? Okay, so the right answer here is actually D, right? So the thing is, these questions, they're like super, super, super annoying, right? But let me just essentially tell you the trick that you should follow, right? The thing is, you should always try to have a frame of reference. When you have a frame of reference, these questions are cake, right? So here's what you should always think about. The region that has the highest positive predictive value will be the region that has the highest specificity, Okay? And that will essentially correspond to the region where you do not miss a single person that does not have disease. I'll repeat that again. The region of the graph that has the highest positive predictive value is the region that has the highest specificity. You see how the P's match? The P in PPV, the P in specificity. And I mean, think about it, right? You say that a test has like, for example, 100% specificity if all the people that don't have disease get a negative test. So you're essentially looking for the region on the graph where you do not miss out on anybody that has a negative test. And if you look at this graph, right, on slide 10, right, you see that there's the part of people that don't have disease. So the right answer here should be C. Because again, if you look at this graph, right, you notice that the blue, like the blue line sort of tells you, okay, these are all the people that do not have disease, right? They don't have any disease, right? And if you look at A, like B, if you look at B, B, the point B on the graph, you know, it has most of the people that don't have disease, but it doesn't have all of those people. But if you look at C, everything to the left of C includes everyone that does not have disease. Right. So that is the region of the graph where you have the highest specificity. So that's the region of the graph where you should have the highest positive predictive value. Okay. That is essentially the region of the graph where you absolutely do not miss out on anyone that does not have disease. Okay. Again, remember positive predictive value essentially means the percent of people with positive tests that have disease. Okay. So positive predictive value means of people right so you it's like it's basically like the question you answer when a patient like meets you and says like let's say you you give a positive test result to a patient if the patient asks you but doc um how sure are you that this result is correct essentially that patient is asking you about your positive about the positive predictive value of the test. Like, oh, okay, of all the people that have positive test results, what percent of them are correct? Which of them actually are like real true positives, right? If you see that, you're dealing with a positive predictive value, okay? So again, very, very high yield to make sure you understand these things. And kind of like a quick sidebar, so that you don't, again, mix this up on exams, let me try to buttress this point. The sensitivity of a test, right, I said this earlier, represents the percent of people with the disease that have positive test results. The sensitivity of a test is the percent of everyone that has disease that they get tested, they get positive test results. Positive predictive value of a test is the percent of people that have positive test results that have disease, okay? That's the percent of people with positive test results that have disease, okay? Do not mix this up. Percent of people with positive test results that have disease. So let's jump to the next question. So question number five. So which of the following points best represents the region of the graph with the highest negative predictive value for the detection of type 2 diabetes mellitus? All right. So which of the following points best represents region of the graph with the highest NPV for detecting type 2 DM? So the answer here is B. Okay. The answer here is B. All right. So remember, again, this question is super annoying, but again, not very hard. Right. Because essentially, the thing you're looking for in the graph is the region with the highest NPV, right, is the region that will have the highest sensitivity, right? Is the region that will have the highest sensitivity, kind of see how the ends match, right? So that's essentially the region of the graph that does not miss anyone with disease, right? Once you remember this, you're pretty much set, right? So if you look at this graph, right, you see the red line kind of shows all the people that have disease. If you chose C, yeah, you will miss very few people that have disease, but you are still, you're missing some people. We want like the part of the graph where you don't miss anybody at all that has a disease. That's where option B comes in because everything to the right of option B, those people all have disease. I really hope this makes sense, right? Again, remember, NPV is essentially like the percent of people with negative tests, right, that do not have disease, okay? Those are things, again, you want to keep in mind. And again, you see this next sidebar, again, please don't mix this up, right? If you notice, I'm kind of like trying to draw parallels and keep things as uniform as possible, right? Specificity, I already talked about this earlier, is the percent of people without disease that have a negative test result. That's it, right? But NPV is different. NPV is the percent of people with negative test results that don't have disease, okay? Those are two things. They sound very similar, but they are very different. And you can already begin to opine that your friends at the MBME want to write questions where they mix and match those words around to try to mess with your head. Do not fall for that. Remember divine saying, do not fall for that, okay? Make sure you really understand what these terms mean. So let's jump to the next question, right? So we have a clinical trial is conducted to measure the effectiveness of the IM test. So it's a test, I'm calling it IM test, as a screening tool for the detection of testicular cancer. So 500 IM tests are obtained. 20 men have positive IM tests and are found by testicular biopsy to have testicular cancer. 180 men have positive IM tests and are negative for testicular cancer by biopsy. 290 men have negative IM tests and are negative for testicular cancer by biopsy.
What is the negative predictive value of this test for the detection of testicular cancer? So I'll let you mull over that for a second and then we'll talk about the answer. So the correct answer here is actually A. The correct answer is A, right? So again, you see people, they see these questions, tons of numbers, they begin to hyperventilate. You do not need to do that. Again, the key thing is ask yourself, what is the quantity that's being tested? In this question, it's a negative predictive value. And then the next thing is you define it like you use like the logical definition you have. You sort of write that out and then say, OK, so what are the numbers I need to fulfill this definition I just wrote out? Right. You bring out the numbers you need. And many times this should get you to to your answer. Right. So notice there are all these numbers in the question. Right look at, like, again, I can already imagine people like setting up these two by two tables. Again, you don't need to do any of that crap, right? You really can reason through these things and make your life a lot easier and go through questions a lot faster, right? So if you look at it, like I said earlier, negative predictive value is of the people that have negative tests, what percent don't have disease? That's essentially all you're trying to do. The percent of people with negative test results that don't have disease. So all you need to do is ask yourself, oh, okay, who are the people that had negative test results? Well, there's 300 of them. So that's in your denominator, right? And then of those people that had negative test results, how many of them do not have testicular cancer? It's 290 of those people. It's 290 because the question clearly says 290 men have negative IM tests, but they are negative for testicular cancer by biopsy. Biopsy is like a gold standard test here. So you essentially just do like 290 over 300, and that's 97%. And that's it. Notice I did not set up any two by two table or anything like that. And you may say, Divine, no, that's not how it works on exams. I promise you, if you really dedicate yourself to understanding these things, this is how these questions work on MBME exams. So let's jump to the next one. So if the cutoff for a positive IM test result for the detection of testicular cancer is 5, which of the following best represents the outcome of adjusting the test cutoff value to 1? So if the outcome for a positive IM test result for the detection of testicular cancer is 5, which of the following best represents the outcome of adjusting the test cutoff value to Y. So option A says PPV would increase, so positive predictive value. So PPV would increase, but NPV would decrease. Option B says specificity would decrease, but sensitivity would increase. Option C says PPV and NPV would both increase. Option D says sensitivity and specificity will both increase. So let's move over that for a second. You can pause, try to work it out. OK, so let's talk about this. Right. So, again, like I said, define the quantity that's being tested, right? And then essentially like come up with your own answer in your mind first before you then start looking at the answers. Because the thing is, I see many people make this mistake on exams and it's usually like, it's essentially not a great way to take tests in general. But looking at the answer choices first before you look at a question, it just begins to mess your mind up. It begins to sway your mind in like every which direction, and then you end up getting confused, right? And then you start making assumptions when you're reading the question. So this is where you need to be careful, right? Like analyze what is being tested in the question, and then you go after your answer, right? So, look at this question, for example, right? Like, the prior cutoff is 5, right? So, it's like, oh, if you have an IM test value above 5, you have testicular cancer, right? Think about it. If you bring it down to 1, right? You're essentially being like, you're essentially setting yourself up for a situation where you would catch every single person that has testicular cancer. It's like if whatever love value just rises a smidge, just goes like above one by any stretch, you're like, boom, you have testicular cancer. So the thing is, you will essentially not miss anyone with testicular cancer. So if you think about it, if you're not missing out on anyone that has disease, that means your sensitivity must be going up, right? Your sensitivity has to be going up. And the thing is, whenever your sensitivity is going up, then you already know right off the bat that your NPV will go up. I already talked about this earlier. Remember the ends match. As your sensitivity is going up your mpv is going up right and the thing is as your sensitivity is going up believe it or not your specificity comes down okay so your sensitivity and specificity typically go in opposing directions although that's not always true but that's beyond the scope of our discussion here today and then ppv and mpv they typically also go in opposing directions. So the right answer to this question is actually B, because the specificity is decreasing, but the sensitivity is actually going up. Because you're essentially not missing out on anyone that has testicular cancer. Yes, you may say divine, but by lowering it to one, you know, yes, you're catching everyone that has testicular cancer, but you're also like catching a lot of people that, a lot of people that do not have testicular cancer. That is absolutely right, right? That is absolutely right. Right. You also get a lot of false positives. So I know some people may already begin to get a little confused with what I just said. Remember what I said earlier? I said that if a test is very sensitive, if you have a high sensitivity test, it has a very low false negative rate. A high sensitivity test has a very low false negative rate. You would actually extend that knowledge a little bit further and tell yourself that a high sensitivity test has a very low false negative rate, but it also has a very high false positive rate. If you're a test that is super sensitive, you're also going to catch a lot of people that the test calls them positive, but they actually do not have disease. Okay. So that's kind of like the trade-off for getting a very high sensitivity test. That is why whenever you do a screening test that is highly sensitive, you also want to do a confirmatory test that is highly specific so that you can weed out that big number of false positives that you're getting from being able to catch every single person that has disease. Because a highly specific test has a very low false positive rate. So you're essentially using the low false positive rate benefit of a high specificity test to counter the high false positive rate side effect that you get with a high sensitivity test. I really hope this makes sense. Again, I'm taking my time because biostats is like a sore spot for many people. So I want to make sure that you're essentially an expert by the time you're done with this podcast. Okay, so now let's jump to the next one, right? So a medical student at Johns Hopkins, that was actually my alma mater for medical school. So a medical student at Johns Hopkins invents a drug that improves survival in patients with glioblastoma multiforme, right? So GBM, by seven years, right? Which of the following changes will be seen a few years after the drug is approved by the FDA, right? So option A, the sensitivity of screening tests for detecting GBM will decrease. Option B, the prevalence of GBM will increase in the population. Option C, the positive predictive value of GBM detection tests will decrease. Option D, the incidence of GBM would increase in the population. Option E, the specificity of screening tests for detecting GBM would increase. And then option F says the negative predictive value of GBM detection tests would increase, right? So I'll give you some time to sort of think about that. So pause the recording and then try to come up with an answer. So let's walk through this, right? So we invented this drug, right, that improves survival in patients with GBM. So it doesn't cure. So read your questions carefully on the exam. I'm not saying that we're curing anything. No.
I mean, as some of you already know, GBM is a horrible disease, right? Like most people that get GBM, the median survival is like 14 months. It's like the worst possible kind of brain cancer a person can have. So the thing is, you've invented this drug. By essentially inventing this drug that improves survival, you will effectively keep more people that have already been diagnosed with GBM alive. Like they've been diagnosed with GBM, but they're able to live longer because of this drug. So the thing is, you know they've been diagnosed with gbm you're keeping them around for longer the prevalence of gbm in the population would increase right the prevalence would in fact go up right because if you think about it even if you get like a new person that gets diagnosed with gbm let's say oh ideally they would die with like ordinarily i'm not saying ideally i will you i never never want anyone to die, but pardon my English there, right? But, like, let's say usually people that get GBM die in six months, right? What if you give them a drug and then they are living like seven years or thereabouts, then that tells you that, okay, like the number of people with GBM will begin to accumulate because, yes, you are not changing the number of new people. Like, it's not like, oh, you are reducing the incidence of gbm no people will still get gbm at the same rate but when they get gbm they live longer than they used to live before so the prevalence actually goes up right and the thing is as prevalence goes up the positive predictive value actually goes up as well okay so as prevalence goes up, the PPV actually goes up. So that's why option C is actually wrong. And the thing is, remember I just told you in the previous question that PPV and NPV are inversely related to each other. As the PPV goes up, the NPV should go down. So that's why option F is wrong. And again, remember, when you change the prevalence of a test, it doesn't really do anything to the sensitivity or specificity of that test. Right. So that's why options in here, you know, flat out wrong. Really, the only things that can change the sensitivity or specificity of a test is if you like change the actual test. So let's say like the previous question, I think it was like a question or two ago where i actually like changed the cutoff value for the test okay so again you'll still be diagnosing gpm at the same rate so the incidence really does uh stay the same and kind of like as a sidebar right again um you may ask like divine why does the positive predictive value increase when the prevalence increases well stick, stick with me here for a second, right? The thing is, let me just give you a simple scenario that should clear this up pretty easily for you. So think of it. If you have a patient, you know, they come into the ED in December and they have, you know, like fevers and rhinorrhea. So like runny nose and they have like myalgia. So like everywhere hurts, right? They likely have the flu. Right. The thing is, if you did a flu swab on these people and it came back as negative, would you really believe those results? You probably would not because you're like, come on, man, this thing looks like classic, classic, classic influenza. Right. So the thing is, the prevalence of the flu goes up in December. Right? So if a test result is negative, you don't believe it. That's like an easy way to remember that the negative predictive value actually goes down, right? But if the test is positive, you're like, oh yeah, yeah. I mean, I kind of knew this before I even did the test that you for sure have the flu, right? So you are more likely to believe the results of a positive test, right? You are more likely to believe the results of a positive test, right? So that's the thing. If you're taking it another way, like you are less likely to believe the results of a negative test during a high prevalence period for a disease, okay? So again, stated another way, right? If a disease is common, you are more likely to believe that the result of the test is positive, okay, again, I know I'm repeating things different ways, but again, I just want you to feel super grounded in biostats by the end of this podcast. And again, as I kind of alluded to in the question, right, incidence, it's the number of new cases of a disease that, you know, have been diagnosed within a specific time period. So new cases, new cases, that's the name of the game, right? And then prevalence is essentially the number of people that are alive at a given time period. So you define the time period and say, oh, how many people are alive that have a certain disease, right? At that time period, that's the prevalence. So let's go ahead and jump to the next question. Okay, so question nine. So an M2, so like a second year med student. So an M2 researcher at the Gifted Medical Student Institute plans to study the effects of consuming high amounts of kale on the development of pheochromocytoma. He plans to publish the results of his study prior to graduation. Which of the following study designs presents the most appropriate means of completing the study? So option A says a randomized control trial. Option B says a prospective cohort study. Option C says a crossover study. Option D says a case control study. And option E says a case report. So pause. Try to come up with an answer. Okay, so let's walk through this, right? So if you think about this, the phenomenon that this researcher is trying to, you know, work on is super, super, super rare, right? It's super rare um i mean like feels as more as common as feels are in exams they actually know that common in the real world i mean like i remember like uh at most of these major medical centers they may see like one a year or one in two three years right so feels are very uncommon okay and the thing is this is a second year med student so he probably has like you know like two three years before he graduates so the thing is um if this student said oh you know what i want to you know do the high impact study do like a prospective cohort study or do like a randomized control trial the thing is it will literally take this patient like 60 plus years to get like me if not more to get results of from this study because again fuels are super rare and chances are before you find a person that consumes kale and you're able to then establish that oh you know what yeah this kale really played a big role in this person getting a few chromocytoma again that would literally take like a ton of time right that this med student not have. So the thing is, the concept here you want to understand is if you're trying to study like quantities that are rare, like rare phenomena, you almost always want to do case control studies on MDME exams. Okay? Because the thing is, when you then get somewhere, you essentially like, you know, you take people that have pheochromocytoma, you take people that don't have pheochromocytoma, but are very like similar in characteristic, right? So like they have similar ages, similar like environment they lived in, like similar comorbidities and all those things. And then you ask them, you look back to the exposure to kale in the past, right? The thing is, when you, you know, do this study, you can then use that as the basis for like a more detailed study, like a randomized control trial or like a cohort study, right? The thing is, many times doing case control studies provides the impetus for you to generate a new research question that you can then pursue with a more formal, a more rigorous study design, like a randomized control trial or like a prospective or cohort study. So the best answer to this question is actually option D. So again, case control studies, again, you need two groups, right? And they need to have similar characteristics, right? So group one, they should have the disease in question. Group two should not have the disease, right? And then you just go back in time and ask them about the exposures, right? The thing is, you can already begin to imagine that there'll be a lot of recall bias, right, with these case control studies. And again, you want to make sure that you remember, and I'll talk about this later, you want to remember that the data you get from case control studies, for the most part, are odds ratios. I'll talk about odds ratios in a bit.
So we have a professor and two medical students that undertake a case control study over the course of a year and publish their results in a high impact journal. So let's say like New England Journal or JAMA or whatever, right? Now, which of the following best represents an example of a possible conclusion from their study? Okay. Which of the following best represents an example of a possible conclusion from their study? So option A says, duloxetine decreases pain scores in patients with fibromyalgia. Okay. Option B says, a combination of sofosbuvir and ledipazvir cures hep C with high fidelity. Option C says asbestos exposure causes mesothelioma. Option D says orsodial administration improves survival in patients with primary biliary cholangitis. So if I really pause and try to come up with an answer. So let's talk about this, right? So if you notice, so the right answer here is option C. I'll just say that right off the bat. The thing is, if you think about it, right, like the researchers, they essentially like to look at people with mesothelioma. Like if you're looking at option C, they essentially took people with mesothelioma and then compared them to people without mesothelioma, right? And then they likely, you know, determined that, you know what, oh, there are all these people that have mesothelioma. They seem to have like a history of asbestos exposure. Maybe they worked in shipyards or whatever, right? And then based on that, you can then say, OK, let me do like a prospective cohort study of some sort. Right. Right. The thing is, you may say, but Devine, why are options A, B and D wrong? The thing is, those other answer choices are wrong because they essentially involve interventions, right? I mean, look at this for a second. Option A says, duloxetine decreases pain scores in patients with fibromyalgia. Well, how did you determine that? You must have given patients the duloxetine and then measured something, measured pain scores, okay? Or like combining sofosbuvir and ledipazvir cures hep C. Well, the thing is, you must have combined, you must have given those people hep, not giving them hep C, that'd be weird, right? You would have given those people those drugs and then determined that, oh, like did some blood tests and determined, oh, yeah, these people have actually cleared their viral load, right? Also dial, same deal, right? So those options A, B, and D all involve interventions, right? So chances are they are likely wrong, right? So again, notice this is a question that's like, oh, everyone knows what a case control study is, right? But I'd be willing to opine that a decent number of you may have struggled with this kind of question, right? So again, it's very important. You need to try to understand, like if there's any one thing you take away from me rambling, I mean, I would want you to take away biostats from this. But if there's one thing you can take away that would really help you, like literally for the rest of your test-taking life, and even just in patient care, is to try to make sure you understand concepts. The thing is, if you understand concepts, you typically will do very well on exams, regardless of how difficult the questions may seem, okay? So that's just something I want to leave with you that will really, I feel like you can almost like change the course of your test-taking life, like going forward, if you can really like abide by this principle. So again, kind of like to summarize here, right? Again, the case control studies, the cohort studies, they deal with exposures, right? But randomized control trials, they deal with interventions, okay? And if you notice, I put the word detour here. I just used it to remember to talk about what these studies are, right? So case control studies, right? Again, like I said, I already described them. People with disease, people without disease, right? And then that have similar characteristics, and then you look back in time and say, oh, okay. Ask them about the exposure. See if there are any, like, exposures they were enriched for in the past, right? A cohort study is where, you know, you identify two groups of people. One group has a risk factor. The other group does not have the risk factor. And then you just follow them in time to see if they develop a certain outcome, right then you calculate a relative risk and all that stuff from from there right and then a randomized control trial is you take an intervention okay you give it to one group and then you give the intervention to one group and then give like placebo to the other group and then you try to compare outcomes okay so again those are kind of important things to know so let let's jump to the next question, right? So the average normal CD4 count is a thousand per millimeter cubed of blood with a standard deviation of a hundred per millimeter cubed. Which of the following best represents the normal percentage of individuals who will be measured to have a CD4 count greater than 1200 per millimeter cube of blood? Option A says 2.51%. Option B says 95%. Option C says 5%. Option D says 16%. And option E says 68.2%. So pause, try to come up with an answer. Okay, so let's talk about this, right? So really the big thing you want to realize with this question is that 95% of the population, right, for a population that has a normal distribution, they should fall within two standard deviations of the mean, right? So the standard deviation here is 100, right? And the population mean and the mean is like, is 1000, right? So two standard deviations below the mean, that's two times 100. So two standard deviations below that's 800, two standard deviations above that's 1200, right? So that means 95% of the population falls within CD4 count number between 800 per millimeter cubed of blood and 1200 per millimeter cubed of blood right so that means five percent must fall outside of this range five percent must fall uh outside of the range so five percent must be like between less than 800 like have like less than 800 uh uh with regards to cd4 count or greater than 1200 right so because we have two groups that can fall under this 5% category, you essentially need to split that 5% in half, right? So that means there must be 2.5% that has a CD4 count less than 800, and then there must be 2.5% that has a CD4 count greater than 1,200. Again, make sure, I promise you, they test this stuff all the time on US time on usml you better make sure you understand what i just talked about so let's talk about uh uh we'll take a quick sidebar here and talk about like p values right so the thing is p values right to essentially use them to express like a probability that oh you know what the results i'm getting from this study i did are entirely by chance, okay? Obviously, you want that p-value to be as low as possible, right? Because the lower the number is, then the more, you know, confident you feel, like, oh, yeah, you know what? Because think about it, right? It's like, if the results, I mean, let's take it to an extreme. Let's say the results are, like, you're like, man, the results of this study I did, you know, the results could have, this results could have been obtained by chance, like 50% of the time. And obviously that study is never going to get published, right? It's going to get like the, once the person that reads the, let's say like the paper reviewer is reading whatever article or whatever you wrote, they'll just toss it in the trash within like five minutes, right? You don't want to do that. But compared with a person that says, oh, you know what? There's like a 1% chance that the results I got from this study were obtained by chance, right? People will feel a lot more, you know, confident with that, right? Because you're like, yeah, 50% chance versus 1% chance, right? That makes you feel a lot better because you're like, okay, that means there is a 99% probability that, oh, these results were not obtained by chance versus the other one where it's like, oh, a 50% probability where these results were not obtained by chance, right?
So the thing is, the lower your p-value, the more confident you are in the results of a test, okay? So if you have like a p-value of like 0.05, that is not as good as a P value of 0.01, because the 0.01 P value means that there is one chance in a hundred that the study results, you get them by chance versus the one that's like 0.05, where it's like for one, you have like a one in 20 chance where the results of the test, you are getting them by like the results you're observing from the study, like due to chance. Okay, so again, very high yield to understand those. And the thing is, if you're not told, basically like the p-value you should always use on MBME questions is 0.05. It's only if they give you a different p-value. If they don't give you any p-values, you don't see any p-values in the question, always use 0.05 because that's what's most commonly used in the scientific community. Okay, so let's go to question 12, right? So question 12 says, four separate drug trials are conducted to test the relative effectiveness of four different 3-beta-hydroxysteroide dehydrogenase agonists in raisin libido. The mean libido levels in the study with confidence intervals are graphed below. Which of the following statements are true? Okay, so you look at the graph, you can see on the x-axis, we have like four drugs, drug 1, 2, 3, and 4. On the y-axis, we have libido, right, low at the bottom, high at the top. And we're essentially, again, comparing average libido levels three months after treatment with these different drugs. So here are your answer choices, right, on the next slide, right? So option A says drug one is more effective than drug two. Option B says drugs three and four are similar in effectiveness. Option C says drug four is more effective than drug two and option d says drug drugs one and four show similar effectiveness so what do you think the answer here is okay so let's talk about it right so the thing is you kind, you kind of want to, again, realize this like general principle, right? With these are confidence intervals. The thing is, whenever you have two confidence intervals cross each other, right? So if like the lines overlap, then that means there is no significant difference between those two things, okay? Again, these scenarios are like super common on the USMLE exams. So really statements A, B, and D should be correct here, right? Because statement A says drug one is more effective than drug two. If you notice, drug one causes, gives rise to a higher libido like value than drug two and their lines do not intersect, okay? So drug one really is in fact more effective than drug two. Option B says drugs three and four are similar in effectiveness. Again, if you notice, drugs 3 and 4, their lines, their confidence interval lines cross each other, right? So that tells you that there are no significant differences between drugs 3 and 4. And then option D says drugs 1 and 4 show similar effectiveness. Again, the lines cross for drugs 1 and 4, so there are no significant differences between both. The effectiveness is essentially the same. Now, the thing is, they can test this in a graphical format, but they can also test it by giving you just numbers. The thing is, they can give you confidence intervals. They can give you confidence intervals of like relative risks or odds ratios or like absolute risk reductions and things like that. Whenever you see those things, you want to be careful. Here's the principle. Whenever you have a biostats quantity that is driven by ratios, that's essentially like a ratio, right? So like odds ratio, relative risk. The thing is, if the confidence interval crosses one, then you have results that are not significant. So the p-value for those kinds of studies should be greater than 0.05. On the other hand, if you have a quantity that's driven by differences, right? So like the difference between two means, for example, right? Or something like absolute risk reduction. The thing is, the results will be non-significant, right? So you have like p-value greater than 0.05 if the results of your confidence interval crosses 1. So you may say, Devine, why is that the case? Well, here's the thing. If, for example, you have a confidence interval of a relative risk that crosses 1, that means for a relative risk to be one, it means that the risk, like the risk in your numerator divided by the risk in your denominator is the same. Because the only way you can get the number one from dividing two things is if those two things are the same, right? So that's why if you have like a ratio driven biostats quantity, if the confidence crosses one then that quantity uh there's no sign there are no significant differences between the two things you're trying to measure right now for a difference right if the confidence interval crosses zero there are also no significant differences so why is that again walk me here for a second the only way the difference between two two between two numbers ends up being zero is if those two numbers are the same, right? It's like you can't get zero from doing two minus three, no. But you can get zero from doing two minus two, right? So if the confidence interval for like a difference between two things crosses zero, it tells you that those two quantities must be the same, okay? So that's why confidence interval for difference-driven quantities, difference-driven biostats quantities, when they cross zero, it tells you that you have results that are not significant. So let's go on to the next question, right? So we have a study that is done to assess the relationship between vaping in college. And by the way, vaping is a terrible idea. I mean, I'm sure studies are going to come out relatively soon about people getting like really bad lung injury. I've certainly seen a lot of that on the news recently. Okay, so a study is done to assess the relationship between vaping in college and the future need for lung transplant, right? The study yielded a relative risk of 3.5 with a p-value less than 0.05. Which of the following represents a possible 95% confidence interval from this study? So option E says 0.5 to 3.5. Option B says 2 to 4.5. Option C says 3.5 to 6. Option D says 3.9 to 7.1. And then option E says 0.71 to 3.68. So pause and try to come up with an answer. Okay, so let's talk about this, right? So the thing is, if you look at options A and E, options A and E are clearly wrong, right? Because notice the confidence interval for options A and E include one, right? But this study is measuring a relative risk, right? And remember, relative risk is a ratio, okay? The relative risk is a ratio, right? So you cannot have like significant results and have the confidence interval cross one. That's just flat out wrong, right? If you also look at options A and C, options A and C are also wrong because if you notice, the relative risk that we sort of got from the study begins or ends the confidence interval. This is literally not possible. If you ever get results from a test, the confidence interval includes the result of that test, but it does not start. This is why it's called a confidence interval in the first place. You take that value you get from the test and then use use your z scores and i'll talk about that in a bit you use your z scores to say oh uh this is the range lower than this number i got from the test this is the range higher than this number i got from the test okay so results that you obtained from a study have to be within a confidence interval they cannot begin or end the confidence interval right and then d is clearly wrong again because again it it does not include the value you got from the study right like the value you got from the study is like a freaking 3.5 you can have a uh you can have a um a confidence interval that's like 3.9 to 7.1 uh where's the value from your study it's not there it's not within range so it cannot be cannot be correct okay so the right answer here is actually option B. Okay. 2 to 4.5, because that includes the number you get from your study. Okay. And the confidence interval does not cross 1. Okay. So let's go on to the next question.
So a study is done to assess the effectiveness of a new drug D for the treatment of GBM, right? So like glioblastoma multiforme. All patients enrolled in the study received the current standard of care. In addition to receiving standard of care, group A, so this is the experimental group, they received drug D. Group B received standard of care and the sham, Y. So that's essentially like a placebo, right? Of the 40 patients receiving D, so drug D, 8 die over the course of the study. On the other hand, of the 40 patients receiving Y, 20 die over the course of the study. So in this question, I'm asking, what is the number needed to treat for drug D? So option A is 2.7. Option B is 3.3. Option C is 13.3. Option D is 5.0. And option E is 15.5. So pause, try to come up with an answer. Okay, so let's talk through this, right? So really, if you ever want to calculate the number you need to treat, right, the big thing you want to remember is you essentially want to find the difference in risk between the patients that were exposed to some intervention and the patients that were not exposed, okay? So you take the difference and then the number you get from that difference, just divide it into one. That's all you literally need to do. Right? So if you notice, I'm not setting up any two by two table or any of that crap. I'm just, again, just reasoning through the concept and arriving at the answer. Right? So basically you ask yourself, what is the risk in people that have have um that got drugged what's the risk of like um of death in people that um um got drug d you take that risk what is the risk of death in people that got drug why you take that risk right drug why is the placebo it's the sham it's the sham drug right and then you take the difference between those numbers, divide it into one, and boom, you're home free, right? So basically, right, like the number you need to trade is like one divided by your absolute risk reduction, right? So it's like, again, 40 people got drug D, eight of them died. So like 20% of those people died, right? 40 people got drug Y in addition to standard of care, right? So the drug D people, right, also remember they also got standard of care, right? So, but 40 people got drug Y and 20 of them died within the period. So that's like 50%, right? So the risk difference is like 50 minus 20%, that's 30%, right? If you divide, 30% is like 0.3. If you divide that into one, then you're left with 0.33, right? You're left with 0.33, right? I mean, sorry, 1 divided by 0.3, that's 3.3. Whoops, sorry about that. That's 3.3, right? And that's the right answer. So the answer here is B, right? And if you understand the number needed to treat, you know the number needed to harm, right? It's essentially like the same calculation, right? But the thing that happens here is that like the rate of harm in the person that gets the drug um like the intervention tends to be higher than the rate of harm in the person that does not get the intervention right so let's say the intervention is like getting like i don't know let's say it's like a drug that ultimately gets pulled off the market so let's say like a thousand people you start them on a drug i mean yeah a thousand like a thousand people you get them into a study 500 of them you start them on a drug. I mean, yeah, like 1,000 people, you get them into a study. 500 of them, you start them on a drug. 500, you start on placebo. And then like 10% of the people in the group that get the drug die. And 1% of the people in the group that do not get the drug die, right? And that tells you that it's hazardous to take that drug, right? It's hazardous to take that drug. So like diethylstilbestrol, for example, is probably like a good example of stuff like that, right? So you may say, Devine, too many formulas to remember. Numbering it to harm, numbering it to treat, blah, blah, blah. How do I remember this? Let me actually give you one rule and then you're set. Essentially, take one and divide it by the difference between the risks for whatever two groups you're doing. Right. The only thing you just need to make sure you do is try to make sure that you put the higher numbered risk first before the lower numbered risk. So because you always want to get like a positive number from doing like your from doing your risk in exposed versus risk in unexposed. OK, again, very high yields to understand that. So, again, quickly as a sidebar here. Right. If you want to calculate relative risk, essentially, you know, just take the risk in people that are exposed divided by the risk in the people that are unexposed. Right. So, for example, right. So let's say you have like some kind of cohort study where you're comparing like smokers and non-smokers, right? And let's say you put 500, you have 500 people in the smoking group, 500 people in the non-smoking group, right? And let's say 100 people in that smoking group develop lung cancer, but 50 people in the non-smoking group develop lung cancer, right? Essentially, 20% of the people in the smoking group got lung cancer, 10% of the people in the non-smoking group got lung cancer, right? So if you take the relative risk, you divide the risk, you essentially say like risk in people that were exposed divided by risk in people that were unexposed, you get like 20% divided by 10%, which is essentially two, right? So basically, smoking gives you like a twofold increased risk of lung cancer compared with non-smokers. So again, I really hope you understand that relative risk. So let's jump to the next question. So if the presence of dysmorphic erythrocytes in the urine has a sensitivity of 90% and a specificity of 45% for the detection of IgA nephropathy, what is the likelihood ratio of having IgA nephropathy if the patient has dysmorphic erythrocytes detected on urinalysis? Option C, 4.55. Option D, 2.33. And option E, 1.67. So I'm sure this is probably the question that most people are like, I have no idea what's going on here. So let's sort of talk about likelihood ratios, right? So the thing is, they occasionally pop up on the USMLEs. So you kind of want to know about them. And many students, they kind of ask me, like many students I tutor, they ask me, Divine, when do I know when to use the positive likelihood ratio formula versus the negative likelihood ratio formula? So let me give you a rule that will make your life profoundly simple. Essentially, the thing you do here is if the patient has a positive result from a test, use the positive likelihood ratio formula. On the flip side, if a patient has a negative test result from a given test, okay? Use the negative likelihood ratio formula, right? So if you have to calculate here, essentially what you do is, since the patient, right, if you notice the patient had like positive test results, so because they tell you that, oh, she does, the patient actually does have dysmorphic erythrocytes detected on urinalysis, right? So this is one of those formulas that unfortunately, you do actually need to commit to memory for the exam, right. So to get the positive likelihood ratio, the thing you essentially do is you take the sensitivity and divide it by 1 minus specificity. So for this question, the sensitivity is like 0.9. You divide that by 1 minus 0.45. 0.45 is the specificity.
Okay. So let's, I guess, quick sidebar. Like what exactly do I mean by likelihood ratios? The thing is likelihood ratios, I can give like a very lengthy lecture on likelihood ratios. We clearly don't have that time because I'm already at like an hour and eight minutes. But again, this is, again, if you listen to this podcast, you'll be a biochem master by the end, right? So bear with me. I'll try to be done soon. There's probably like nine more slides remaining or something like that. So the thing is likelihood ratios. Whenever you calculate like a positive likelihood ratio, you're essentially telling yourself how much more likely, right? How much more likely is a phenomenon given a positive test result, right? How much more likely is a given phenomenon given a negative test result, right? So how much, sorry, how much less likely a phenomenon is when you have a negative test result, right? So again, it's kind of like if a person comes in, there's this example I love to give that let's say they tell you like when you're interviewing for med school that, oh, 100% of the, like 50, no, let's not say 100%. Let's say 50% of the students that come into this med school match into DERM, right? And then let's say you come into med school, you take Step 2CK, you get a, you get, you take Step 1, you get a 280, you get Step 2CK, you get a 280, right? Your chances of matching into DERM are a lot higher than, okay, let me put it this way. I think I said the first part wrong. So let's say, you know, you're interviewing for med school, they tell you that, oh, if you come to this med school, you have a 50% chance of matching into dermatology, okay? You come to this med school, 50% chance you're going into, you are gonna be able to, so let's say you applied to derm, your chances of matching are 50%, right? And then you come to that med school, you take step one, step two, so you can get two 80s on both, right? Clearly, your chances of matching into Durham with those kinds of scores are much higher than 50%. They are pretty more like 99 to 100%, right? Assuming you interview well and the other parts of your application are good and you're not like a robot or serial killer or something, right? So your likelihood ratio has adjusted like in the positive direction and it's very positive. If you calculate likelihood ratios for those, it'll probably be like some really high number, right? Because it's almost like certain, right? That, oh, you're going to match into them because you got those positive results, aka getting 280s on both USMLE exams. Okay, now let's go to question 16, right? So, in a study examining the relationship between exposure to ketamine and the subsequent development of neutropenia, medical records of 300 children were reviewed. 100 children who were exposed to ketamine were found to have neutropenia. 50% who were exposed to ketamine were found to not have neutropenia. 80 children who were not exposed to ketamine were found to not have neutropenia. And 70 children who were not exposed to ketamine were found to not have neutropenia. What is the odds ratio for this study? Option A, 3.29. Option B, 2.29. Option C, 5.67. Option D, 2.23. And option E, 7.16. So pause and try to come up with an answer. Okay, so let's talk about it, right? Let's talk about it, right? So the thing is, again, you may see this question and say, oh, Devine, this is a question that will easily take me five, 10 minutes on an MBA exam. It does not have to, okay? If you pay attention to the rule I'll give you, I'll give you like a slightly different formula. It's just a different way of thinking about odds ratios. It'll make your life supremely easy, right? You'll be like, whenever I see odds ratio questions, I can usually get done with them in like 30 seconds to a minute, okay? So I'll talk you through how I do that. So the thing is, odds ratio, right? So what does an odds ratio mean? It essentially compares the odds of a person with disease having been exposed to a given risk factor compared to the odds of a control being exposed to that same risk factor, right. So the thing is, my own formula for calculating odds ratio, I call it the logical people product divided by the weird people product. So I'll say that again. The logical people product divided by the weird people product. So what in the world do I mean by that? So here's what I define as my logic. These are the people that are logical, right? Because think about it. If you've been exposed to something bad, right? You should expect that you get disease from that thing, right? On the flip side, if you were not exposed, so let's say like, oh, if a person smokes, you should expect that it should be the ones getting lung cancer. If a person does not smoke, you should expect that they should be the ones not getting lung cancer, right? So basically, my logical people product are people that, you know, obey the classic norms that you expect, like logical norms, right? So they're exposed and they're affected, or they're unexposed and unaffected. You multiply those two numbers together. And then for my denominator, the weird people product, those are people that they're just super odd. It's like, let's say, for example, they smoked, but they didn't get lung cancer or they did not smoke and they got lung cancer. Right. So like exposed and unaffected. And then you multiply that by unexposed, but affected. Right. That's your weird people product. Right. So if you do that for this question right uh you essentially take a hundred a hundred right those are the people that were exposed to get the kid that were exposed to ketamine and got neutropenia multiplied by um multiplied by 80 right so those are the people that um they were not exposed to ketamine they did not have neutropenia and then you divide that by 70 right 70 represents the people who were they didn't get exposed to ketamine but unfortunately they they had a neutropenia and you multiply that by uh by 50 right 50 represents um the people that were exposed to ketamine but they actually did not get neutropenia so logical logical people product divided by weight people product, and that gives you an answer of 2.29. Okay, good. So let's go on to question number 17, right? So the mean block glucose level of a group of 81 medical students was 170 milligrams per deciliter with a standard deviation of 15 milligrams per deciliter. Calculate the 95% confidence interval and in words, interpret your results. So let's just sort of talk through this because I don't have multiple choice for this. I was kind of running out of time this morning when I was making these slides. So I started, you'll see at the end, I just summarized some high yield concepts that I just got really tired of making questions from them. Because really making these slides and making this podcast certainly takes a very like long Thank you. people teaching. I've done teaching for more than a decade. I just absolutely love it. I mean, personally, for me, teaching is the best job in the world. I don't know how anyone can ever hate teaching. But anywho, that's a conversation for a different day. So let's walk through this on the next slide. So the mean, the average in this question is 170 mgs per deciliter. The thing is, if you want to calculate confidence intervals, you need to calculate the standard error of the mean first. And the thing is, to calculate standard error of the mean, you typically take the standard deviation and divide it by the square root of your sample size. So you essentially take 15 and divide it by the square root of 81, which is our sample size, and we get 1.67.
Use two. It's an easier number to multiply by. So you take your, to get your confidence interval, you essentially take your mean, right? So like 170 plus or minus two times your standard error of the mean, which we already calculated as 1.67, right? So you essentially have like 170 plus or minus 3.34. 3.34 is 1.67 times 2, right? 1.6 times 2 is 3.2. 0.7 times 2 is 0.14, right? So 3.2 plus 0.14 is 3.34. That's how I do a lot of my mental math, right? So essentially, you have like 170 minus 3.34 or 170 plus 3.34. So your range is like 166.66 to 173.34, right? So how do you interpret this? And again, believe it or not, the NBME has been known to put questions that test confidence interval, and they essentially put interpretations of the confidence interval as answer choices and then they mix and match things and then you have to pick out the right interpretation right so for this study you can essentially say like 95 confidence that the real mean blood pressure of the medical student population right falls somewhere between 166.6 and 173.34, okay? Another way you can see this is that, oh, the mean blood pressure for any randomly selected group of 81 medical students will fall somewhere between, again, 166.66 and 173.34, okay? 95% of the time, if you essentially repeat the experiment on multiple locations, those are just two different ways of expressing the same thing. OK, again, make sure you know how to calculate confidence intervals and make sure you can interpret them in in words. OK, very important to know those things. So essentially done with the questions I have, I just want to summarize some highield concepts that I've just kind of run out of time to make questions out of. I love writing questions, but writing questions, especially writing good high-quality questions, takes ridiculous amounts of time. So I'm just going to do a quick summary here and then we'll be done, right? So remember your ROC curves, right? Classically, right? If you want to pick the best test, right? So the test with the highest combination of sensitivity and specificity, you want to pick a test that is on the uppermost left corner of the graph. And then your cohort studies, again, I already kind of talked about this. You look at two groups of people. They have different exposures. You follow them into the future for the development of an outcome. And you can actually have like a prospective cohort study or you can have one that's retrospective. The retrospective one, you take two groups of people. One got an outcome. One did did not get an outcome and then you look back to see what kinds of exposures they had right for some reason a retrospective cohort study looks an awful lot like a case control study okay but usually the case control study is used for like very rare phenomena versus cohort studies especially like the retrospective ones that are used for more common phenomena, right? The retrospective course studies are more for like common phenomena. And they tend to have like less recall bias in comparison with case control study. Although the odds ratio is usually pretty close to the relative risk when the prevalence of a disease is super, super, super low. I would encourage you to try to reason that out on your own. And then remember, if you're going like, oh, for a normal distribution, like one, two, or three standard deviations about the mean, you want to remember that 68% of the population fall within one standard deviation about the mean right uh you want to remember that 68 of the population for within the within one standard deviation of the mean 95 percent for within two standard deviations right and then 99.7 percent for within three standard activations right so again how you to know those and then if you essentially want to compare two groups of uh two groups of people with a test right uh you like the T test. Remember T for two, the T in T test for the T in two, right? But if you're comparing more than two groups, you want to use something called the F test. Sometimes they call it the ANOVA test on MBMEs, right? And then you want to also remember the differences between type one and type two errors, right? When you incorrectly reject the null hypothesis, so let's say the null hypothesis is actually true, but you actually end up rejecting it. That's a type 1 error. That's an alpha error. But on the flip side, if you incorrectly accept the null, so it's like, let's say like, oh, like you do a study and you say like, oh, smoking does not cause lung cancer. That is not true, right? That is false, right. So you're saying smoking does not cause lung cancer. You're accepting the null hypothesis and you are incorrectly accepting it. That's a type 2 error. That's a beta error. And remember that power is 1 minus beta. And beta errors have to do with power. And I'll talk about that in a second. Now, the thing is, whenever you have tight confidence intervals, your study is a lot more precise. When you have tight confidence intervals, your study is a lot more precise. But you should feel a lot less confidence, though, with the results of that study, right? Because you essentially have very little room for error. Because think about it, right? If, for example, a person offers, they'd say, oh oh you know what um do you want to take this bet this bet pays out a million dollars and in this bet um uh you're betting that the temperature of today is gonna fall somewhere between 101.1 and 101.3 you probably wouldn't want to take that bet because it's like there's there's a much larger range of temperatures that fall outside those parameters right so you'll likely get screwed versus someone that tells you oh you know what i'm gonna pay you off a million if um if you can predict the temperature for today and i'm uh if it falls between like 50 degrees and 150 degrees pay out a million. Obviously, you'll take that bet without thinking twice because you know your chances of success are a lot higher, right? So you feel a lot less confident in the results of a study when you have very narrow confidence intervals. I mean confidence, not confident. Confidence intervals, okay? Now, how can you increase power? This thing is, this slide is floridly high yield to know for the USMLE step one. If you're taking, not just step one, if you're taking any of the USMLEs and you don't know this concept on this slide, you're essentially shooting yourself in the foot, right? So let's talk about different means of increasing power, right? So one thing you can do is you can just recruit more people for a study, right? The more people you recruit, the more you more closely approximate the population you're trying to study, right? And the thing is, if you really do think about it, if you recruit more people for a study, if the effect size is small, you'll still be able to capture it because there's just so many people. I kind of think of it as like you like taking a dollar from every single person that walks by a street that you live on, right? Almost like a toll road. Toll roads are profitable because, yeah, it may be a dollar that they collect on each toll road, although that's not exactly true on the East Coast. The East Coast, they just gimp people up for money. But that's a different conversation for a different day. But if you're getting a dollar from every card that passes the toll road and a million cards pass that toll road a day, you've just made a million dollars, right? So the more people you recruit for a study, the more powerful your study becomes, right? Another way you can increase the power of a study is to essentially have a large difference between the two quantities you're trying to measure, right?
The other group, the average score is 100%. There's clearly a large difference. I mean, there is an obvious difference in those people, right? Like one group is clearly smart. The other group, you know, they need to study a little harder than they have, right? So if you have a large effect size, that can also increase the power of a study, right? And then another thing that can increase the power of a study is that if you have like many of your, like a lot of your data, sort of like clustering around like one central value, if you have that, it means your study is like you're super precise, like you're measuring things like really well. Because think about it, if you measure things really well, that means you are capturing any differences that exist at a high level, right? So whenever you have super precise measurements, you're increasing the power. You're also increasing the power of your study. In fact, if you have very accurate measurements, you're also increasing the power of your study. Remember, accuracy is very different from precision. Accuracy means how close are you to the true value. Precision means for the multiple values you measure, like let's say you measure the same thing over and over and over and over again. Do you get reproducible values, right? So do you measure something as 1.5 and then you measure it against like 1.49, you measure it again 1.48, you measure it again 1.51. That's a precise study. But if, for example, the true value of that test is 1.8, your measurements are precise, but they're not accurate because you're like way off from the true value. But let's say you measure a value that's like 1.79, right? And another one is 1.73. Another one is 1.85. Those values are not precise because they don't, you know, they don't cluster cluster around each other really well but they are accurate because they are very close to the true value um and again right again the more confident if you are more precise in your measurements chances are you like you made the measurements without leaving anything to chance so your p values are very low right so whenever you do a study and you have lower p-values, that makes your study have more power than one that has higher p-values. And then for the next slide, right? So this is, I believe, the second to the last, whoops, the third to the last slide, right? So this is another thing. It's kind of obvious, but people, for whatever bizarre reason, tend to get these wrong on the USMLEs. You need to remember that the fact that something is statistically significant, right, doesn't mean that it's clinically significant, right? So, like, it doesn't mean that, oh, a drug, I do my trial, my p-value is less than 0.05, so I'm going to bring this drug to market. No. It doesn't mean that it's clinically significant, right? So think about it. Let's say like, oh, you do a study, right? Or you do a randomized control trial. And the baseline blood pressure of people, blood pressures of people at the beginning of the trial is like 130 over 80. And then like two years after you've completed the trial, they've gotten this antihypertensive agent, their blood pressure is reduced to 129 over 79, right? And let's say, oh, you do like your calculations, you do your confidence intervals, you do your P, you get like significant results, P values less than 0.01. That's good. That's a statistically significant result, but that drug is useless because it's not clinically significant because it only lowered your systolic blood pressure by one in a two-year period and the systolic blood pressure by one in a two-year period. That's a useless drug, right? And then just, again, kind of like some basic things. Remember, right? Mean is the average. Median is the middle number, right? It's essentially like if you have like an odd numbered set of data, right? So let's say you have like seven values in a set. You parse three values at the beginning, three values at the end. The number in the middle is the median. And then the mode essentially represents the most frequent quantity in your data set. And the thing I'll tell you, if you're given a set of numbers, they very likely won't do this on an MBME because that's too easy. If you're given a set of numbers, arrange them in ascending or descending order before you start talking about like mean-median mode. And remember that the mean is affected by extreme values in the set, okay? So let's say a bunch of people, let's say like there are 10 people that take the USMLE Step 2 CK exam and nine of them get like two 10s, but one person gets like a 300. That's obviously gonna skew the results, right? That's gonna skew the mean. The mean will appear to be higher than it truly is. It won't be very representative of the population, right? Because there's this one person that just scored out of this world, okay? So that's something you absolutely want to make sure you keep at the back of your mind for exams. And then I'm going to the second to the last slide here, right? So if you have a normal distribution, right, you definitely want to remember that the mean, median, and mode are all the same. That's what makes it a normal distribution in the first slide here right so if you have a normal distribution right you definitely want to remember that the mean median and mode are all the same that's what makes it a normal distribution in the first place right and then remember that just remember this in like almost like ascending alphabetical order so like mean has ea precedes median that's ed which precedes mode right like od right so mean precedes medianes mode, right? That's the alphabetical order. If you remember that, that will help you remember what obtains with a negatively skewed or a positively skewed curve, right? Whenever you have a negatively skewed curve, it means like the kind of like the flat portion of the curve is off to the left, right? You'll just, again, just write your letters out, mean, median, mode, and then put a lot of less than signs in between so the mean is less than the median which is less than the mode positively skewed curve flat portion is on the right same thing write out mean median mode but put greater than signs between those so mean is greater than median which is greater than the mode and then sometimes your friends at the mbme can give you like you know they can give you like a curve that shows like a bimod distribution. And then they will give you answer choices that say which of the following phenomena best represents the curve shown above, right? And then they'll list like a bunch of like random crap like Hodgkin's lymphoma, something like Burkitt's lymphoma, slow and fast oscillators, blah, blah, blah. You certainly want to remember at least these two high yield examples of things that are associated with bimodal distributions, right? So what do I mean by bimodal? It means there are two things, almost like two peaks. There are two things that show up commonly. So like Hodgkin's lymphoma, for example, Hodgkin's lymphoma shows up in very young kids and then you don't see it for a long time again. And then there's this big uptick when people get older, okay? That's a bimodal distribution. Another common one is like suicide, right? Like suicide is very high in young people, but also very high in old people, right? It's lower in middle-aged people. That's another example of something that follows a bimodal distribution. And then like a lead time bias, essentially it's like kind of like thinking, it's like erroneous thinking. It's like, oh, survival has improved when, in fact, like the survival actually improved because you found the disease early, right? I kind of think of it like prostate cancer is a great example. It's like, oh, let's say you start, you know, you check a 40-year-old guy, you find prostate cancer, you detect it, you treat it, and then this 40-year-old guy dies at 85, and you're like, oh yes, by doing this test, I've improved survival in prostate cancer. No, that is not true. Chances are that guy may have lived to the age of like 85 without prostate cancer, without like necessarily dying from it, right? So don't mistake detecting something early for improved survival. That's classic lead time bias.
I'll likely make a future podcast that talks about lead time bias, and then we'll go from there. So as I do at the end of every podcast, I do offer one-on-one tutoring for many exams. So step one, 2CK, 2CS, step three, preclinical med school exams, third year clerkship self exams. If you're a medicine resident, the medicine in training exam, the medicine board exams, I do tutor a ton of people for those. And then if you're a college student and you need tutoring in like physics, gen chem, O chem, physiology, histology, biochemistry, I offer tutoring for all those things. And then the longitudinal tutoring that I offer for people starting out med school through their dedicated period and people that are starting third year through their dedicated period for Step 2CK. If you're interested in any of those things, reach out to me. It's something I've done with a decent number of people. And essentially all of them have been like wildly successful on their USMLE exams. And they've also crushed their preclinical and third year shelf exams. So if that's something you're interested in, just send me an email just in the heading, just write longitudinal tutoring. And again, I can try to point you in the right direction. Essentially what I do is I meet with these people like once or twice every week throughout their first and second years. And as I'm meeting them, I'm tutoring them for all their block exams. And but at the same time, I mean, I'm infusing them with step one knowledge and also like giving them like guided practice through like MBME style questions that ultimately like when they get to the dedicated periods, like they feel very confident and very ready for the exam right same thing with third years they start out and then i um i teach them like stuff that's uh pertinent to like i prepare them for their shelf exams and then they get to their dedicated periods they feel like super ready i mean there are people have tutored that have got into their dedicated periods and they're like i feel very ready for my exam. So if that's something you're interested in, reach out to me. Either send me an email, reach out through the website or send me an email. I'll actually list the email here, Divine Intervention Podcasts, with an S at the end at gmail.com. And then if you need one-on-one coaching or advising for like ERAS applications for med students applying to residency or AMCAS applications for college students applying to med school, feel free to reach out. Again, I have a ton of experience with this stuff. So like mock interviews, personal statements, the experiences section of these applications, stuff like that, writing rec letters. I can certainly help you out with any of these things. Again, I've done it with tons of people. I have a lot of admissions committee experience, so take that forward, you will. Okay, so I do hope you get something from this podcast. Please, please, please, if you're taking any USMLE exam, listen to this podcast. I promise you, it will help you a ton on the exam. So I wish you a wonderful rest of the day. Have a blessed rest of your day, and God bless you. I'll see you in episode 144. Thank you.
Hello out there. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, the Journal of the American Medical Association. And this week I'm going to tell you about the March 14, 2007 issue of JAMA. And this is a special theme issue on access to care. And when you're finished going through this journal, this particular issue, if you have any doubt that there is all kinds of inequities in access to health coverage, that means you better go back and read it twice. We start with the cover of JAMA, which is a painting of a mother protecting her child, much like physicians should be protecting their patients. This is a painting by Jean-Baptiste Camille Carreau. Of course, it's French, and it was painted around 1855. The first article has to do with financial barriers and outcomes after an acute myocardial infarction, or MI. Dr. Ali Rahimi and his colleagues from the Yale University School of Medicine determined the prevalence of self-reported financial barriers to health care services or medications, that's the avoidance due to cost, among 2,498 participants in a prospective observational study of acute MI and examined the association of these barriers with subsequent health outcomes. The authors report that 18.1% of patients mentioned financial barriers to health care services and 12.9% mentioned financial barriers to medication, even though 68.9% and 68.5% respectively were insured. Compared with patients without financial barriers, patients with financial barriers had a worse recovery, including higher rates of angina, poorer quality of life, and a higher risk of re-hospitalization. The second article has to do with high-deductible emergency department use and hospitalizations. Dr. James Warren and his colleagues from Harvard University School of Medicine assessed emergency department, that's ED visits, and subsequent hospitalizations before and after an employer-mandated switch from a traditional HMO plan to a high-deductible health plan. The authors found that among patients who switched to a high-deductible plan, emergency department visits and hospitalizations from the emergency department decreased from a baseline compared with control patients who remained in the traditional HMO. In an editorial, Drs. Corita Grudson and Bob Brook from the UCLA School of Medicine discuss issues to address before it can be concluded that efforts to control health care costs, such as high deductible health plans, are safe. And I advise you that if you are going to read this article, make sure you read the editorial that goes with it before you make any decisions about whether this is a safe or even a valuable method. The third article has to do with emergency Medicaid expenditures for immigrants. Undocumented or legal immigrants with less than five years of residence in the United States are excluded from Medicaid eligibility with the exception of limited emergency coverage, that's emergency Medicaid. Dr. Annette Dubard and Mark Massing from the University of North Carolina and the North Carolina Department of Health and Human Services examined 2001 through 2004 emergency Medicaid claims data for North Carolina. That's a state with a recent influx of immigrants. Among their findings were that 48,391 patients, 99% of whom were undocumented, received services reimbursed under emergency Medicaid. Childbirth and complications of pregnancy were the most common diagnoses. However, spending for patients who are elderly and disabled increased 98% and 82% respectively from 2001 through 2004. The next article has to do with insurance, care, and status after a health shock. In an analysis of 1997 through 2004 data from a prospective population-based survey, Professor Jack Hadley from the Urban Institute compared medical care use and short-term health changes among uninsured and insured non-elderly persons after a so-called health shock, that is, unintentional injury or onset of a chronic condition. Controlling for underlying medical conditions and baseline characteristics, the author found that uninsured persons who experienced a health shock received less medical care and had larger decreases in short-term health status than insured persons. The JAMA patient page has information for your patients about health care insurance. The clinician's corner in this issue is a special communication by Professor Michael Porter from the Harvard University Business School and Professor Elizabeth Teesburg from the University of Virginia Darden Graduate School of Business. Starting with the premise that a purpose of the health care system is not to minimize cost, but rather to improve health and health care value for patients. Doctors Porter and Teesburg describe a strategy for health care reform that is market-based and, importantly, physician-led. Their proposal for reform emphasizes three principles. Value for patients is the goal. Care is organized around medical conditions, not specialties or procedures. And care cycles and results, risk-adjusted outcomes and costs for each medical condition are measured. Now, this may seem like common sense, but I personally think that you should read this and perhaps even read their book. And if you don't come out believing that it's time for physicians to take back our medicine and take care of our patients, then I'd like you to call me and explain why you don't think that's true. We also have several commentaries. The first is an article by Dr. Arthur Garson from the University of Virginia School of Medicine and Dr. David Blumenthal from Harvard Medical School, and it has to do with state-federal partnerships. State-based health care reform initiatives suggest potential federal solutions. A second commentary has to do with universal coverage. Components of an equitable and efficient health insurance plan are discussed by Dr. Harold Luff from the UCSF School of Medicine. And the third commentary has to do with health disparities and access to health care. Ensuring universal access to health coverage through public health and social policies is discussed by Drs. Nicole Lurie and Tamara Dubowitz from the RAND Corporation. The final commentary has to do with access for patients with disabilities. Structural obstacles that compromise health care for patients with disabilities is discussed by Dr. Christy Kirshner and her colleagues from Northwestern University School of Medicine. There's also a research letter by Dr. Nicola Zetola from UCSF School of Medicine. There's also a research letter by Dr. Nicola Zetola from UCSF School of Medicine, and it has to do with association between rates of HIV testing and elimination of written consents in San Francisco. Medical news and perspectives deal with looming shortage of physicians raising concerns about access to care. The Poverty Shift May Burden Health System and Uwe Reinhardt, Ph.D., assessing United States insurance coverage. The Capital Health Call deals with the State of the Union Address, genetics bills, insuring insurance, and Medicare solvency. And from the Centers for Disease Control and Prevention, geographic disparities in diabetes-related amputations, Texas-Mexico border in 2003, the national, state, and urban area vacation coverage among children aged 19 to 35 months And finally, there's a very poignant piece of my mind. What makes a difference in which Dr. Perry Klassen, a physician from Oklahoma City, Oklahoma, discusses his own personal experience with colon cancer and his outcome, and he compares it with the outcome for one of his patients who has no insurance. Same diagnosis, quite a different outcome. And that's it for this week. Thank you very much for listening. Please let me know if you have suggestions to make this podcast more educational or interesting to you. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, speaking to you from beautiful downtown Chicago, where the wind blows mightily, but the patients are always our top priority.
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. Thank you so much for joining us. This is Charmaine. We have another edition of schema episode here for you. And as a reminder, our schema episodes are the episodes that we think about a couple of schemas, about like a systematic approach to a problem in the context of a case. And I'm here with some fabulous folks. Jack and his mustache penner are here. Dan Minter and his wonderful ID, fun facts. And the wonderful Anne-Marie Comfort and her very well-timed puns that I'm always so impressed with. Hey team, how y'all doing? I would say hello twice. one on my behalf and one on behalf of the hair on my upper lip. Hello, hello. And Marie, you all might remember our dear audience as her incredible discussion on our WDS episode. It's just here joining us on this schema episode. And Marie, do you want to reintroduce yourself to the audience? Hey everyone, I am so glad to be here. I'm a hospitalist on the East Coast, so bringing a little East Coast representation to this West Coast crew. And love clinical reasoning and love participating and helping to organize VMR. And so I am so happy to join today. Yeah, Anne-Marie has done the most incredible job leading our virtual morning report series. And you all, if you haven't joined, you're missing out. Come join us and nerd out on clinical reasoning on daily basis. So excited for you to join us, Anne-Marie. Welcome, AMK. This is awesome. We're super psyched to have you. I am so excited to be here. All right. Without further ado, I do have a case for you all. So this is a 70-year-old man who presented to emergency room for evaluation of one day of coughing up blood. Okay. Wow. So coming in strong already. So I'm sure a lot of us have been in scenarios where, you know, as we're doing our comprehensive review of systems, we ask about coughing up blood and invariably a patient may say yes to that. But I think that that underlies the fact that there's this huge range of hemoptysis ranging from like just a small speck of blood mixed in with sputum to just coughing up cups and cups and cups of frank blood. So when we're, you know, approached with this, before we really get into the diagnostic schema that I'm sure somebody in this, on this call will go through a little bit more, I like to think of like an initial triaging schema of, is this something that's immediately life-threatening where we need to, as Jack Penner and his mustache say, you'll put TX before DX, or is this something that we can sit and think about a little bit more and really go through the works of our diagnostic schema? So oftentimes you'll hear people talk about massive versus non-massive hemoptysis with a cutoff being something like 500 cc's. And really, if you identify massive hemoptysis, it's kind of like a five alarm fire because, you know, this is something that's immediately life-threatening to the patient. If that is the case, you know, certain things that you can do are, you know, make sure you get your ABCs, you know, that the airway is, you know, secured or, you know, at least being closely monitored if they're, you know, breathing okay and that they're not in circulatory collapse. And then often we talk a lot about positioning. I remember like in medical school and early in residency, this was like the most confusing, like my left versus right, like which side goes up, which side goes down. If you're bleeding into one lung and, or you have a good suggestion that one lung is kind of the problem spot, you want to put that side down so that you're not dripping blood from the bad lung into the good lung. So use gravity to your advantage. So to summarize, when we're initially triaging hemoptysis, we're going to want to first think from, you know, our sort of critical care resuscitation hats of, you know, do we have our airway breathing and circulation adequately addressed? Similarly, we're going to want to position the patient if we know or have a strong suspicion that they're bleeding from one lung, we're going to put that lung down. And then we're also going to think about, gosh, do we need to ask for help from anybody like pulmonologyology for possible bronchoscopic intervention, or from interventional radiology, like as if they need to embolize something empirically. Beautiful, Dan. So let me give you a little bit more information. In the morning, he was clearing up his throat and coughed up about one teaspoon of red liquid blood. He didn't notice any claws and there was no sputum mixed in there. And about five hours later, he coughed up another teaspoon of blood. And since then, he's been just kind of coughing up blood every couple of hours. He hasn't been experiencing any fevers, chills, lightheadedness, palpitations, or chest pain. He feels short of breath with exertion at baseline, which hasn't changed recently. He did notice a more bilateral ankle swelling over the past month. He has been more nauseous over the past month as well, without really any episode of vomiting, abdominal pain, or diarrhea. The nausea has limited his food intake, though. Additionally, he reported multiple episodes of dark-colored urine over the past month as well. He didn't report any rashes, muscle, or joint aches. Well, thank you, Dan, for going above the ID fellows call of duty and stabilizing the patient. Now that the patient is stabilized, I want to think about the hemoptysis schema. The pulmonary system deads ends in the alveoli. So if someone's coughing up blood, it either means that it's a mimic, like blood got there from either the GI system or upper respiratory tract. Usually I think about epistaxis as the number one cause or is true hemoptysis. And there's some sort of abnormal connection between a blood vessel and the lower respiratory tract, the trachea, bronchi, or alveolar. History and imaging helps me narrow down the differential. And also, I think about chest x-ray having a sensitivity about 50%. So in concerning cases, CT with contrast is going to be your go-to study. I'm going to focus on airway and alveolar processes and let Jack take vascular causes. So when I think about base rate, bronchitis is the most common cause, but usually this is small volume hemoptysis. Other airway causes I think about include bronchiectasis, foreign bodies, masses, or fistulas. Some parenchymal causes I think about are pneumonia, cavitary lung lesions, with TB being a leading cause worldwide. So definitely want to ask about those TB risk factors, lung abscesses, and perigomyosis and stranguloides. If I hear about red flag symptoms like immunocompromised, lung pathology, such as bronchiectasis, or an inflammatory signature, as in this case, like weight loss, night sweats, prolonged fevers, malignancy risk factors, or other organ dysfunction, I'm really concerned. Also, large volume or persistent hemoptysis also makes me consider a serious cause. Jack, I must ask you a question. What's in your differential for vascular causes? Well played, AMK, from the puns to the clinical teaching. Thank you for passing it off. You know, I think exactly as you said, like, if we think about our general framework, where there's some sort of abnormality between the parenchymal system and the vessel system, the question then in terms of what falls in the vascular DDX really hinges on the answer to the question of what are the vessels that either are going to be running through or around the pulmonary system? And whenever I think about vascular etiologies of disease processes, I sort of break it down to ask myself, which sort of vessel type am I going to be dealing with? Is this going to be an arterial cause, a capillary cause, or a venous cause? And the same framework can apply when we think about the vessels in and around the lungs. And so if we start then with the arterial system, right, we can think about the artery that is going to be running into and through the lungs, which is the pulmonary artery.
One, which we're probably going to see most often is going to be a pulmonary embolism. And you might be asking, wait a second, how do I get bleeding if there's an infarction in that area, right? Usually, we would expect no blood flow in an area where there's an embolism. And that is true. But if we have a pulmonary embolism that is there, eventually, that lung tissue can actually to infarct and that infarcted tissue can slough off into the airways and we can get some of this dead bloody tissue that the individual then coughs up. A much less common, but much more terrifying clinical manifestation may actually be a pulmonary artery aneurysm that then erodes into the bronchial tree. And so that is basically going to be a arterial bronchial connection where we're going to get basically arterial blood flow into the respiratory tree and you'll see massive amounts of hemoptysis. But the pulmonary artery isn't the only artery that exists around the lungs, right? There's actually three other types of arterial entities that we want to think about. The first is going to be, if we think about what's just above the lungs, is going to be thinking about the anominate artery, also known as the brachiocephalic artery. And we can actually get a tracheoanominate fistula where that artery erodes into the airway. And the most common setting we'll see that is in somebody who has a tracheostomy. If that tracheostomy tube gets placed a little bit too close to that artery, we can get an erosion of the artery into the trachea, and then that can lead to hemoptysis. The last two to think about is going to be an aortobronchial fissure, because again, we have a thoracic component of the aorta that is going to exist right around the lungs. And if somebody has a thoracic aortic aneurysm or has had prior interventions on their aorta, whether it was an open repair or an endovascular repair, we can ultimately get processes that erode into the bronchial tree again in the similar way that we saw with the tracheoprenominant fistula. The last one, if you want to call out a parlor trick, is going to be something like a Dulipoy lesion, which is going to be sort of the analogous to the Dulipoy lesion that we see in the GI tract, where there is a submucosal artery that has sort of eroded through the overlying epithelium, and it can then bleed into the airways. If we then follow the blood flow from the artery system to the capillary system, there's really two capillary processes that I want you to think about. The first is going to be diffuse alveolar hemorrhage, which oftentimes has its own DDX associated with it. But the three big categories we can think about in DAH is, is this capillaritis from an ANCA-associated vasculitis? Is this BLAM hemorrhage from elevated left-sided filling pressures, which we're going to sort of double-click on and talk about next? Or is it related to diffuse alveolar damage, and there's been so much pulmonary injury that the inflammatory process is also going to lead to some bleeding. And we'll often see this in the setting of ARDS. Lastly, is going to be the venous causes. And then the question is, well, wait a second, how do I get blood from my venous system ultimately into the airways? And the way that that happens is when there's a huge, huge traffic jam in the venous system. Most often, this is going to be from elevated left-sided filling pressures and congestive heart failure, particularly in individuals who have mitral valve disease, who can get a massively dilated left atrium and substantial pulmonary venous congestion. In that case, the hydrostatic pressures just lead to the development of pulmonary edema, and sometimes some blood can go with it. And then the other diagnosis, if we are worried about elevated venous pressure in the absence of heart failure, we're going to think about the very rare diagnosis of pulmonary venous occlusive disease or pulmonary capillary angiomatosis. You may have heard of either of those illnesses. They're quite rare diseases. So we're really going to focus our cognitive energy on thinking about congestive heart failure in this category of disease processes. But again, that is sort of like a really, really deep dive into the vascular causes of homunctasis. But in most cases, right, where we land in the venous system is going to depend on sort of contextualizing this patient. So I'm going to hand it over to Dan to think about how we can sort of put all of this in context. Well, that was amazing from both Anne-Marie and Jack and Jack's mustache. I loved that. So how do we connect this to the case? You know, when I think about trying to really frame our patient within the context of these various schema, I always try and go back to, you know, back to basics, like back to the problem representation, which again is going to be, you know, kind of a three component equation of who is our patient, like what contextual risk factors do they have? What is the timing? And what is the exact syndrome? So just kind of thinking that through right now, who is our patient? Well, we really don't know too much, you know, like Anne-Marie mentioned, like, you know, certain infections that are that are prevalent worldwide, like tuberculosis or strontulodiasis, we don't really know where this patient's from or what their risk factor is for. So I would certainly be really interested in delving deeper into that, as well as their other past medical history. What about the timing? It seems that at this point, we've been told that we have relatively acute onset of hemoptysis. And while that can be very stark and seem like a very punctuated time point, it may just be the tip of the iceberg. Maybe this is acute recognition of a more subacute to chronic problem. There is a little bit of hint of that as we talk about, you know, some of the lower extremity edema and maybe some weight loss and malaise. Lastly, let's just try and think as specific as we can what this patient syndrome is. So again, just kind of reviewing what we know, it seems that there's small volume hemoptysis, there's some nausea and some ankle swelling. You can do an individual schema for each of those and look for areas of overlap. While each of these are maybe intriguing lines of inquiry to follow, they're all relatively nonspecific. And I imagine that we're going to get some more specific and definitive data to base our decision making and sort of diagnostic process around in the future. So maybe we have more questions than answers, but it's, you know, it's an interesting diagnostic journey so far. Brilliant team. Here's more information for you all. For his past medical history, he had previously been diagnosed with heart failure with mildly reduced ejection fraction around 40%. He had hypertension, hyperlipidemia, type 2 diabetes, chronic kidney disease with a baseline creatinine of 1.8, and obstructive sleep apnea, for which he uses CPAP. He takes Lasix twice a day, Metope, Daily, Atorva, and Amlodipine. For his health, really good behavior and his social history. He was born and raised in the United States, no history of incarceration. He has a history of remote smoking. He smoked about a one pack per day for about 15 years. He quit 20 years ago. He rarely used alcohol, maybe one drink a month, and he did not use any other substances. Thanks so much for the updated info, Sharmini. This definitely helps expand my differential. When there is hemoptysis, one of the first things I'm going to do is look at the med list. And I don't see any anticoagulants or any antiplatelet agents, which helps me give a little bit of a sigh of relief. Other things I'm thinking about, as Jack mentioned, is that heart failure can increase venous pressures that can also lead to hemoptysis. I'd also want to go back and review the CKD history. How recently was it diagnosed? What was thought to be driving the CKD? Because that could certainly expand the differential. And then the great social history is also important. Smoking certainly increases the risk of cancer, which is always going to be on your differential with hemoptysis. Although, since it's a more distant history, I'm a little less concerned about that, but still concerned about that.
Awesome, Annemarie. And in terms of the CKD, it was largely contributed to his diabetes and hypertension. There was no biopsy done at the time. Next thing I'm going to share with you all is the exam and some basic labs. So on presentation, it was afebrile. He was like tacky to the low hundreds. Blood pressure was on 40s over 90s. He was satting about 96% on room air. He had an anecteric sclera. He had normal workup breathing. He had a bivalve crackles at the bases. He was tachycardic, regular rhythm, no murmurs, rubs, or gallops appreciated. He had 2 plus bilateral dorsal extremity edema up to the shins, and he had few scatters, palpable purpura mixed with patechiae on bilateral dorsal aspect of his feet and mid-shin. His labs, his CBC showed a white count of 11 with 98% neutrophils. No EOs were seen. His hemoglobin was 8. The last baseline we had in our system was about six months ago, and it was 9.5 at a time. And his platelets was in the 200s. That is close to his baseline. He had a sodium of 136, potassium of 4.5. His chloride was 106, bicarb of 21, BUN-77, creatinine of 3.7. His last creatinine was about a month ago, and it was 1.8. His glucose was 116. His FOS was slightly elevated at 4.6. Liver chemistries were within normal, and his COAG studies were all within normal as well. Thank you so much for this updated data, Sharmini. So, you know, I think in a case like this, where there are sort of increasing amounts of data that can be somewhat difficult to sift through, I think one of the things that I try to do for myself when I'm beginning to sort of frame the clinical syndrome that we're dealing with is to ask myself sort of two specific questions. One is, what are the dominant features of this patient's illness? Because you can imagine, we could list every single abnormality that we've come across so far, and it would take them probably one to two pages of paper. And so for us to be able to simplify that down to enhance our reasoning process, we're going to ask ourselves, what are the dominant features of the illness? And I think in this case, the dominant features of the illness are going to focus on the fact that we have an increased work of beaving and fibasal or crackles on exam. So there's some signature of a pulmonary disease process. And then on the labs, we have this pretty marked acute kidney injury with the creatinine up to 3.7 from the baseline of 1.8. And so there's also features of at least a renally focused process that we have here as well. But in addition to understanding the dominant clinical features, we also want to understand, are there any clinical features that are particularly characteristic of certain diseases? And in this case, we do have some findings here that I personally don't come across too often, which is the finding of the palpable purpura on the patient's lower extremities. And so I think if we sort of bring all of these three features together, we start to have an emerging picture of the problem that might be going on here, right? We have, again, the dominant features of pulmonary disease and renal disease. And then we have these skin findings sort of hanging on the outside. And so let's just talk through how we can sort of merge all of those together. I will say whenever we have two dominant organs involved, the question is, is organ one leading to a problem in organ two? Is organ two actually leading to a problem in organ one? Or is there a third scene of the crime that's actually causing the problems in both of the organs that we're seeing, right? So for example, if we think about the lungs, kidney and, and the skin findings that we have here, we can ask ourselves, is this a lung problem that's leading to a kidney problem, which many of us may have seen before in the setting of community-acquired pneumonia leading to an acute kidney injury in the setting of sepsis? The other hypothesis is actually, is this a kidney problem leading to a lung problem, right? If somebody has an acute renal failure, they could develop pulmonary edema. Or the third category that we mentioned, is there actually another scene of the crime that's leading to problems in both the kidneys or the lungs? And in that case, the palpable purpura may increase the probability of there being an underlying vasculitic process. And if we think about how vascularly rich the lungs and the kidneys are, we can see how a vascular problem could hit the lungs and also could hit the kidneys. That was awesome, Jack. You know, anytime I'm considering something in the kidney, I hearken back to, you know, Charmaine and Robbie on some earlier episodes as they take, you know, an anatomic journey flowing down the path of blood. And I think with, you know, kidney related stuff, you flow through the glomerulus, through the tubules, pass by the interstitium, I guess. And then, you know, there's vascular structures around the sides too. So I just kind of think anatomically, if we're going to frame a pulmonary renal syndrome, you know, sort of thinking by each component part. So maybe I'll tackle the glomerulus and the tubules, and I'll leave the interstitium and vascular parts to other folks. But if we consider, you know, what's, what are broadly speaking diseases that can affect both the glomeruli and the lungs? You know, I think of nephrotic syndromes and nephrotic syndromes. I'll leave nephrotic syndromes to the second part because it's a little bit more relevant. But, you know, if you have a nephrotic syndrome, there's certainly multiple ways where you can get your sort of lung pathology and kidney pathology. You can lose antithrombin three and get and become hypercoagulable and actually get pulmonary emboli. You could be sort of third spacing all throughout your body and get porofusions on top of renal disease. And you can also lose immunoglobulins and become qualitatively somewhat immunocompromised and then be more predisposed to pulmonary infections. But that's nephrotic syndrome. What about nephritic syndrome? This is kind of really where the money is, as Jack was sort of pointing out, if we think of, you know, causes of bleeding in both the kidneys and the lungs, you can kind of hone in on the small blood vessel. Oftentimes, you'll hear this referred to as a capillaritis. And it's just kind of a inflammation in all the small blood vessels throughout the body, but they kind of manifest or interact with the outside world at the interface of the lungs and the kidneys. My short list for causes of capillaritis that will cause a pulmonary renal syndrome include ankyloplasmic vasculitides, anti-GBM disease, systemic lupus erythematosus, cryoglobulinemia, and in the correct age group, henoxylin purpura. So just to kind of summarize, you know, out of nephrotic and nephritic syndromes, the ones that we're really going to refer to with, you know, the classic pulmonary renal syndromes of bleeding and glomerulonephritis is probably going to lie more on the nephritic end of the spectrum. Thinking again through ankylovasculitis, GBM disease, henoxylenpupira, lupus, and cryoglobulinemia. What do you think, Anne-Marie? I loved your journey along the stream of kidney ultrafiltrate. I won't call it urine yet, but I think we often sometimes forget about the interstitium and the vital role that it plays. So a lot of infections can affect the lung and then the renal interstitium. Just as a reminder, this space is really important. It helps support the nephrons, but then it also helps with oxygenation and hormone production. So some of the main infectious causes I think about are hantavirus, other hemorrhagic fevers, leptospirosis, legionella, malaria, CMV and immunocompromised folks, staph aureus, and some of your granulomatous pathogens like TB, Brucella, or fungal organisms. There's a lot of infections that can affect this space. Two autoimmune diseases that I also think about that can affect the interstitium are sarcoidosis and IgG4 disease.
And that's a great reminder because I always think about autoimmune and glomerular causes, but sometimes they can affect the interstitium too. In vascular causes, the main cause I think about is scleroderma, which can cause an interstitial lung disease and also sclerodermal renal crisis with schistocytes. It's important to recognize this because ACE inhibitors or ARBs are the treatment of choice and high dose steroids can actually worsen the disease. A few other rare things I want to throw out there that might come up on your medical trivia competitions that can also affect the kidneys and the lungs are some of the cystic diseases. Please do not hold me to this pronunciation, but Bert-Hogg-Dubé syndrome, which is a hereditary disease with benign skin lesions and kidney and lung cysts, autosomal dominant polycystic kidney disease, and a trivia favorite, lymphangioleomyomatosis. Jack, how are we going to connect it to the case? All right. Well, you know, I think at this point in time, right, we have to sort of take the next step forward and acknowledge that we have an enormous differential here. And we're going to have to sort of find ways to narrow that DVX so that we can make some progress going forward. And I think that that's going to involve two steps here, which is one, going to be characterizing the renal injury, and then two, characterizing the pulmonary disease that this patient has, as well as the underlying cause of the hemoptysis. And so to characterize the renal injury, we have to sort of ask ourselves, are we dealing with a pre-renal AKI, a post-renal AKI, or one of the causes of the intrarenal AKI? And if we think about how we're going to sort of figure that out, one is going to involve what is the predominant pulmonary syndrome, right? Because if we just have a run-of-the-mill community-acquired pneumonia that has some bronchitis associated with it, we might expect that the kidney injury gets better with tomorrow morning's lab, right? The patient gets some fluids, we give them some antibiotics, and we see that the kidney function starts to improve. We may see the kidney function plateau, which could suggest something like an acute tubular necrosis, which isn't oftentimes going to be on the hook with the pulmonary renal syndrome, but certainly can come to play in somebody who has had severe sepsis or prolonged hypotension in the setting of sepsis, right? But we also may see features that are going to help us prioritize an intrarenal AKI right off the bat. That could mean on the urinalysis, if we see things like proteinuria, hematuria, and white cells, it could mean that we see a sort of predominant signature of sterile pyuria on the UA, right? We see signs of inflammation with a kidney without a clear bacterial culprit, and that may help us prioritize interstitial causes. It doesn't seem like we have a great signature of disease for something like scleroderma up front, and we don't seem to have necessarily the anemia and thrombocytopenia like Anne Kay mentioned to sort of bring or to sort of invoke a vascular etiology of the patient's acute kidney injury. So I think really the two places we're going to look at is one, what does the UA show? And is that going to increase the probability of a glomerular disease process? Or two, what's the patient's renal function trend? If they get better with fluids and some underlying treatment of whatever we think the pulmonary process is, right, that's going to help us settle on the underlying etiology being a pre-renal syndrome, right? But as much as I would love our journey to end in the kidneys today, right, there's sort of three main tools that we could use to make progress is one, we can use cross sectional imaging with contrast to we can do diagnostic and therapeutic interventions with something like a bronchoscopy, or we can do another predominantly therapeutic, but also diagnostic intervention with the interventional radiologist. And so in this case, with a patient like this, who seems like they're stable enough, at least right now to get to the scanner, we're going to look at that cross-sectional imaging because it'll help us characterize the lung disease. Do we see features of a consolidated process, a nodular process, or a cavitary process on the CT scan? That might help us prioritize infection or underlying malignancy of the cause of the patient's hematosis, or a more diffuse process of ground glass opacities and diffuse consolidations, which may increase the probability of something like ARDS, diffuse alveolar damage, or diffuse alveolar hemorrhage, right? And then depending on those findings, right, it might help us decide, do we need to go to IR to focus on intervening on a potential bleeding vessel? Or do we need to go to bronchoscopy to figure out what has made its way into the airways? And then in addition to that, we're going to sort of get other general features to work out the patient's underlying acute kidney injury, right, knowing that the urine dipstick isn't going to be 100% perfect, right? So we might also quantify the degree of protein in the urine as well. But I think those are sort of the two places we're going to go. How do we understand the kidney injury better? And how do we understand the pulmonary process better? I just want to have all of you in real life with me at all times. You are just so, so, so good. So I have some more information for you all. And the creatinine got worse throughout the hospitalization. So it was like slowly getting worse up to mid-fours. And in the meantime, other labs, his CK was normal. BMP was in the 200s. His HIV, HCV screen were both negative. His UA showed specific gravity of 1.01. Didn't have any glucose, was one-paw dipstick, showed one-plus protein, three-plus blood. Negative nitrates and leukestrates showed about zero to five white blood cells per high power field and greater than 25 red blood cells per high power field. Spot protein to creatinine ratio was 800. Sputum cultures just showed oral flora. Block cultures were in no growth to date. We did the CT test without contrast that shows secretions in central airway, consolidations and patchy gland glass opacacities bilaterally with right greater than left, and with predominantly at the basis versus the apex. Kidney ultrasound didn't show any evidence of hydronephrosis. The pulmonary team was consulted and they did perform a bronchoscopy. BAL showed diffuse pink frothy bloody secretions throughout the entire tracheobronchial tree, worsened the bases, and increased bloody return from samples one to two to three. They showed about 70% segmented neutrophils, zero lymphocytes, 28% monos, and two EOs. So basically the EO count was very rare. AFB cultures and smear were negative. Bacterial fungal cultures were negative as well. Aspergillosis was also tested and it came back negative. Wow. That is so much information to go through. Maybe I'll just try and start at the top and work my way down. So just to summarize, it seems that from our urinalysis, we have evidence of what is likely an active urine sediment with protein and red blood cells, suggesting possibly a vasculitic process affecting the kidneys. You know, that fits in with how we've talked previously about the possibility of the pulmonary renal syndrome manifesting as vasculitis. If we turn our attention to the lungs, what can we gather from the available studies? It seems that our chest CT without contrast demonstrated ground glass opacities, as well as some consolidations. You know, when I think of ground glass, I think, you know, I'm a simple person. So I think blood, pus, or water, you know, we've already been considering, you know, sort of hemoptysis and sort of causes a diffuse alveolar hemorrhage. So that would be consistent with what we've been talking about so far. We have in this case, the benefit of our pulmonary colleagues performing a bronchoscopy, which is going to be one of the definitive tests to look for diffuse alveolar hemorrhage and really add the lungs to kind of our constellation of pulmonary renal syndrome. What they saw there, it seems very consistent. As they progressively lavaged the lungs, the return became more and more bloody. So that would suggest that what they're sucking out of the distal alveoli is in fact blood rather than some blood in the airway that then gets diluted with the lavage fluid.
We have radiographic and then also bronchoscopic evidence of a similar process affecting the lungs. So I think that we can say, as has been kind of hinted throughout this podcast, that this patient likely has a capillaritis affecting both the lungs and the kidneys and is suggestive of a small vessel vasculitis. That was great, Dan. I'm going to just make a confession that oftentimes when I hear like aliquots and all this like fancy stuff on bronc, it kind of confuses me. But I think the big picture is that we're seeing bleeding everywhere. That's even on the Bronc report. And when you see bleeding everywhere and it's getting subsequently blood urine samples, that points to an alveolar or capillary source like the capillaritis that we talked about in this case. But once we diagnose DAH, it's not enough to say there's diffuse alveolar hemorrhage. We need to know what's causing the diffuse alveolar hemorrhage so we can treat it. With DAH, most causes are autoimmune, but it's important not to miss your infectious causes like viruses and hemorrhagic fevers, atypical bacteria, and parasites, because you're going to be thinking about immunosuppression. And a lot of these cases, if you immunosuppress the patient and there's an infectious cause, it's actually going to get worse. Thankfully, we don't see any signs in the infectious studies here and no historic risk factors that would make us concerned about an infection. Charmaine, what happened next? You are amazing, as always. And we were thinking the same thing. So we had lower suspicion for infectious etiologies, and our attention was turned into autoimmune world. So we got some more labs, IgM, IgG, IgA levels were within normal. Complement levels, C3, C4 were within normal as well. ANA was 1 to 40 with nuclear speckled pattern. Anti-GBM IgG came back negative. The S-pep free light chains were unremarkable. The ANCA screen came back positive. NPO was greater than eight. Proteinase 3AB was less than one. And P-ANCA was one to 320. Right. Well, that is some very helpful data that we just got here. And I think, right, obviously one of the most glaring abnormalities that we have on the most recent labs that Charmaine gave us is the positive, the positive ANCA, as well as the positive NCO antibody. And if you're anything like me, ANCA's confuse you. I have feel like I have read about them a number of times. There's many different patterns. There's many different types, and it can be really difficult to sift through. Now, I am not a rheumatologist by any means, nothing close to it. I've just been very lucky to learn from some brilliant rheumatologists. And so I'm going to do my best to channel Dr. Sarah Goglin, one of the rheumatologists who I've had the privilege to learn from, who has also shared her wisdom and knowledge on a prior Clinical Unknown episode, and sort of try to share with you all what she has taught me about understanding ANCA antibodies. And so oftentimes when we hear about ANCA antibodies, it's in the setting of a concern for a small vessel vasculitis. But it's important to note that not all small vessel vasculinities like GPA, granulomatosis of polyangiitis, or MPA, microscopic polyangiitis, not all of the ANCA-associated vasculinities will have a positive ANCA titer. And the flip side is also true. Not all positive ANCA titers equal ANCA associated vasculitis. And so what we have to do is we have to contextualize the positive ANCA titer in the context of the patient's broader clinical syndrome and ask ourselves, are there features that suggest an ANCA associated vasculitis? And as Dan and Marie and Charmaine have all elaborated, we certainly have those features here. We have amonary renal syndrome, and we have cutaneous manifestations that might suggest an underlying small vessel vasculitis as well, right? So that fits here. And then in the setting of the positive ANCA titer, right, we also then are sort of know that we are maybe dealing with the ANCA-associated vasculitis disease process. The question then becomes, well, how do we sort of further understand which of the ANCA-associated vasculitides we have here? Are we dealing with granulomatosis with polyangiitis? Are we dealing with microscopic polyangiitis? Are we dealing with eosinophilic granulomatosis with polyangiitis? Or do we have a drug-induced ANCA-associated vasculitis from something like hydralazine, cocaine, or levamisol ingestion? For the drug-induced category, we don't necessarily see a prominent clinical signature of any of those drugs on board. We don't have the high amount of eosinophils in the periphery or on the bronchoscopy. So we can sort of move eGPA lower down on the list. And so the question then becomes, are we dealing with GPA here or MPA here? And to understand that, we can sort of double-click little bit more on understanding what these different ANCA antibodies mean and what the different titers show. And so when we think about ANCA antibodies overall, there are sort of two different things that we might hear labeled before ANCA. One is C-ANCA or P-ANCA, and the other one is PR3 positive or NPO positive. And these two concepts are sort of linked together. And we'll walk through right now how we can link them. So basically, when somebody has a positive ANCA, there's two ways to better characterize them. You can do them through an immunofluorescence assay to look at the pattern of the antibodies directed towards the neutrophil cytoplasm, which is what ANCA stands for. And we can use an ELISA to ask ourselves which antigens those antibodies are directed for. The immunofluorescence will give us a C-ANCA pattern or a P-ANCA pattern. And the ELISA will tell us, is it PR3 positive or MPO positive? In this case, we have an MPO positive titer, which is usually going to be associated with the P-ANCA pattern on immunofluorescence. A PR3 ELISA is usually going to be associated with a C-ANCA pattern on immunofluorescence. And that's important because more often than not, GPA is associated with the PR3 positive or C-ANCA pattern. And MPA is associated with the P-ANCA positive or the MPO pattern. And so in this case, if we sort of rewind to where we were, right, we have features of a small vessel vasculitis. We have the positive ANCA, which tells us that we're likely dealing with an ANCA-associated vasculitis. We don't have features of drug-induced or eosinophilic small vessel vasculitis. And then we have the MPO titer, which is going to be telling us that we're likely dealing with microscopic polyangiitis. I think that is sort of one way that we can think through this. Again, we're never going to settle on this diagnosis as generalist without the help of the rheumatologist, but we can go through the exercise of practicing interpreting these lab values so that we can make sure that we have at least as rich of an understanding as possible of the associated vasculitides. Jack, are you sure you're not a rheumatologist? Maybe the mustache is a rheumatologist. No comment. That was beautiful. So you're absolutely right. A patient was diagnosed with pancreas vas disease with the involvement of the kidney and lungs favored to be microscopic polyangiitis complicated by glomerulonephritis and diffuse alveoli hemorrhage. And he was started on pulsed steroids with peronatabra and the panel was for maintenance therapy with rituximab. Unfortunately, his course was complicated by development of multiple bloodstream infections, lung infections, skin and soft tissue infection that required a multiple hospitalization. As his health had deteriorated, he made a decision to transition to home hospice and passed away about six months after the vasculitis diagnosis was made. It's quite unfortunate in terms of the course. You know, I like to think about vasculitides. I like to think about glomerulonephritis and VAH. And in reality, you know, they're quite morbid diseases. And so any chance that we can get to catch these diseases earlier on to give patients the best chance we should take in.
And special shout out to Dr. Julia Armendariz who helped me with this case. Any thoughts, team? I would just say that I think this case really highlights how clinically rich learning from these cases can be, but also just how devastating the anxious associated vascular disease can be. I think if we sort of zoom out exactly what you said, Sharmin, and look at the fact that there was diffuse ovular hemorrhage, agglomerular nephritis, profound renal injury, like these can be, I think it can be very easy to sort of get enamored with the clinical elements of this case. And I just want to say thank you for bringing us back to the humanistic sides of a case like this too, which is that while the journey to the diagnosis can be educational, the journey after the diagnosis is oftentimes quite sad. I just second that, Jeremy. That was absolutely beautifully stated. And thank you so much for presenting this case. I never give up a chance to talk medicine with you all. Thanks so much. And Marie, Jack and Dan for such a wonderful discussion. And dear audience, we cannot wait to chat medicine next time with you all. Bye. Before you all log off, I just want everybody who's listening at home to join us and giving a huge round of applause to AMK for joining us on the Schema team. We are so stoked to have you. And thank you for hitting an absolute grand slam as we got to talk through this case. Looking forward. I know I speak for everybody who's listening when I say that we're looking forward to hearing you on more of these in the future. Believe. That's a wrap, folks.
From the JAMA Network, this is JAMA Dermatology Author Interviews. Conversations with authors exploring the latest clinical research, reviews, and opinions featured in JAMA Dermatology. Hello and welcome to this author interview from the JAMA Network. This is Dr. Adey Adamson, the web editor for JAMA Dermatology. Alopecia, or hair loss, is a common medical condition experienced by most people at some point during their lifetimes. There are many manifestations of hair loss, which include a variety of etiologies and patterns on the scalp, face, and body. Many forms of alopecia, such as alopecia areata, female pattern hair loss, and central centrifugal cicatricial alopecia, also known as CCCA, all share the commonality of decreasing hair density, which correlates with disease progression. To date, tools designed to quantify and assess hair loss are often made only for the assessment of one disorder at a time. For example, the severity of alopecia tool for alopecia areata. This is despite the fact that these tools primarily assess percent hair loss, which is a common outcome measure across different types of alopecia. Furthermore, these tools score alopecia by visual inspection, which may be cumbersome to do in a busy clinic and may not be highly reproducible, which is something important for clinical trials. In a new study in JAMA Dermatology, authors developed an automated algorithm which can be used as a single scoring system that measures percent hair loss, making it potentially useful across different types of hair loss. With me today is Dr. Elena Bernardis, who is a research assistant professor in the Department of Dermatology at the Perlman School of Medicine at the University of Pennsylvania in Philadelphia. She's also affiliated with the General Robotics Automation Sensing and Perception Lab at the University of Pennsylvania. She's the senior and corresponding author of this new study and is here to discuss the results and how they could potentially be applied to clinical practice as well as in clinical trial research. Welcome to the podcast, Dr. Mardaris. Thank you for inviting me. So would you mind telling the audience what your background is? Because you're not a clinician. It's not often that we have non-clinicians on the podcast. What is your role at the University of Pennsylvania? I have a PhD in computer and information science from Penn, where I specialized in computer vision. I started working in dermatology in 2013, and after working on acne and alopecia for four years at the Children's Hospital of Philadelphia, I joined the Penn faculty in 2018, where I started the computational dermatology lab. Our research lies at the intersection of computer vision and dermatology. So we create new AI algorithms for dermatological applications, both clinical and research. And is the study of the skin and the hair from your vantage point, what about that kind of interests you as a computer scientist? So I have been working on imaging and alopecia for almost 10 years now, despite the fact that I'm not a dermatologist. And it's important to me because hair loss impacts so many people. And if you had alopecia or know anyone who is affected by it, you know how profound that impact is. And what I find fascinating is that despite the common belief that it's all the same and there's nothing you can do about it, in reality, there are many types of alopecias with different causes from genetic to autoimmune disorders. And some are reversible. And at the minimum, they can be slowed down, especially if detected in the early stages. And it's also fascinating that there are still many unknowns leading to many active areas of dermatology research. So despite the staggering numbers, the technology to help quantify, diagnose, or treat alopecia patients is still very limited. And everything starts with having a system to quantify the hair loss. That's where computer vision comes in. I think that's very important and well said. Being able to quantify hair loss in patients can be a challenging task for dermatologists, especially because we see patients, you know, after two or three months, say after giving them a treatment. And it's hard to know sometimes, especially if Also, actually, the clinicians saw this. They could see that we encode what they see intuitively. So the idea is to teach the computer to see how a dermatologist sees. So in order to tackle this problem of trying to quantify hair loss in patients with different types of alopecia. What data did you have at your disposal in order to train these algorithms that you trained in order to automate this process of quantifying hair loss in the scalp? So we use a curated retrospective image data set collection that we put together over the course of many years. So while the data-driven learning approach is that you want as many labeled images as possible, in other words, we enrolled as many participants as we could from the alopecia clinics, both at CHOP and at Penn, and we labeled the photographs by integrating the information of what we learned from the dermatologists. And in your study, you focused primarily on three types of alopecia, alopecia areata, femur pattern hair loss, as well as central centrifugal cicatricial alopecia, which is also known as CCCA. Is there a reason why you only focused on those three types? Was it a matter of convenience or did it have to do where the pattern of the hair loss was located on the scalp? So there were also other kinds of alopecia that are included in the data set. But the reason we focus on these three is mainly because there are existing photographic scales for them. And also the photographic scales are on the same view, so we could easily compare them. The top views were used for comparing the alopecia scales that were the existing scales. But for our data set, we had multi-views. It wasn't just the top. We also had the lateral views and the back views. And so you were able to curate several hundred photos from various alopecias. And what was next? Did you have to have a group of dermatologists annotate these images in order to figure out some ground truth or where exactly in the scalp the alopecias were? Were they centrally in the scalp or were they on kind of the sides? How was the ground truth of what was hair loss assessed using computer vision? The ground truth was done over many years in different ways. We did have dermatologists also label what areas were hair densities, which ones were not. So labeling the data set took a long time to understand how to ask the dermatologist also to label. The majority was done by research assistants in my lab in the end. And where we did the scoring system analysis, so actually scoring with the traditional systems, research assistants did the scoring, but we also verified that their variability was comparable to the clinicians. We had three experts score a subset of the images just to make sure that the scores were similar, basically. And did you find relatively good concordance between the experts and those that were trained in order to do these scores that might not necessarily be dermatologists? Yes. And that's why we ended up using them. Of course, everyone was extremely highly trained in scoring. So once you labeled the images to help teach the algorithm how to recognize alopecia, then what? What was your goal once you had this data set that was labeled? So the focus of our algorithm presented in the article Hair Comb is that we want to quantify the hair loss. Because from a visual point of view, it's a definition of the common feature to all alopecia types. And the reason for calling it hair comb was because it combines hair formation at different levels. So we wanted to mimic the way a dermatologist would go about analyzing the scalp. So the idea of hair comb is that it combines two convolutional neural networks, one that learns coarse level of hair information. So the overall estimation of a person's hair loss, which is a measure relative to the person's baseline. It also means that the same hair density of two different people could mean completely different levels of alopecia. That was the part that was hard to label and how we had to figure out how to label the images in the beginning. And the other network that learns defined level of the hair information. So that goes down to the actual hair density per skin area. That's the basic idea of the algorithm. And how well did the algorithm do in measuring the percent hair loss when you tested it in the test set of images of hair loss after you trained the algorithm to do that task? So we trained the hair comb algorithm over 1,300 images with multi-views and tested over 200. And one thing to point out is what it was over a wide range of hair colors, skin and texture types, and also different types of alopecia. And on that set, it achieved 92% accuracy. And in terms of hair loss difference, so if you want a proxy for the salt score, it had only a seven percent error.
Yes. And it's also surprising that even when we used it on the interface that we later collected images from the public, it still performs also well. And that is surprising sometimes because despite the fact that we're such a visual photo-centric society, and people upload millions of selfies every week, when it comes to sending in images to an algorithm for clinical evaluation, we see a really high variability from blurry to the framing is completely off, even providing the guidelines. So it's nice to see that Haircom can handle most of it. And so the images that were solicited from the public, these were images through the patient portal, or were these actually solicited through people that weren't patients within the clinics at the University of Pennsylvania? So this was part of our piloting and testing the Tricky interface that runs the Haircombe algorithm in it. A good part of the participants that use Tricky were patients in the clinics, but we also had people from the public try to use it. So it was a mix. And can you explain to the audience what Tricky is? So Tricky is a system to help quantify the hair loss. So it's a way to allow everyone to use hair comb for measuring their hair loss. The idea is that the algorithm is integrated in it and it provides guidelines on how to take the photos and it outputs the density for you. And this is through a website or an app on a phone? The testing version was the web interface so that it could be used by anyone anywhere, including phones, but did not require any downloads. And so that was the interface or the portal that you used to get images from the public and then try this algorithm. And you found that to you somewhat surprised that it even performed really well in that way. So potentially this is an algorithm that could be used not only for, say, store-and-forward teledermatology, but also perhaps by providers in the clinic if they want to assess how a patient's doing in terms of hair loss over time. Is that fair? Exactly. The idea is that the dermatologist can use it to instantly quantify the hair loss while they're seeing the patient. And this relieves them from having to eyeball the alopecia or having to compare images or doing the measurements by hand. And it also can be used, it's not just confined to the clinics, it can be used at home for the teledermatology visits or for patients to take images to see how well they're doing during treatment. And there's also potential other applications in clinical trials as well for standardization. Do you see potential applications there as well? Yes, I hope so. The idea is that it can help both for the clinical side and the research side. One question that I had is some scales or some important features that we think about in alopecia include things like redness and erythema. And we also wonder about the loss of hair follicles. Do you think that there could be algorithms that may be able to also incorporate that into the scoring system? Yes. Of hair comb is to start with quantifying the hair loss. After that, we will be working on quantifying everything else, one thing at a time, basically. So the redness, where the scarring areas are, even like, for example, how many follicles you have per square area of skin. There's endless potentials here in terms of quantification. Anything else about your study that you found surprising or interesting that you may want to share with the audience? I guess how much I learned about alopecia. So not just that there are many types for starters, but the fact that some are curable. And for me, it was amazing to be working on images and seeing how the hair grows back, especially on the kids' images. So I really learned a lot. And I also learned to see some of the prognostic signs, the ones that you just mentioned, especially, for example, for alopecia areata. So another thing that I found very surprising is how hard it is to create labels that are meaningful from a clinical perspective. For example, how to deal with loose hair strands over the skin, which are obviously to anyone just scalp areas. That's not obvious from a pixel point of view. Or having the same densities have different meanings. For example, the fact that density itself is not a concept over one specific pixel, but it's an area. It's an exciting time in the treatment of patients that have alopecia, particularly those with severe disease like severe alopecia areata, where we've been able to bring back a lot of people's hair, not everyone, but a lot and way more than treatments of the past. So this is a really exciting area. And it's even more exciting that computer vision and artificial intelligence can be used in order to automate and standardize how we evaluate hair loss, particularly on the scalp. You raised an interesting point about hair loss or percent hair loss not being the same depending on who you are as a patient, how much it affects your quality of life, and where on the scalp it is. It may be a lot less distressing to have hair loss far on the crown of your scalp versus on the front or the side of your scalp, where it's more easily seen by others in society. Where the alopecia is on the scalp matters, as you just said. And right now, IRCOM just quantifies alopecia at each image that it's taken, and integrating that information is still left up to the clinician, though. So what's next in terms of the research topic in this area? So as I just mentioned, there are limits in quantifying alopecia from 2D images alone. And even when trying to match the guidelines, it is practically impossible to take the exact same view over time for tracking purposes or to compare between patients. And right now, this is still left up to the clinician. So in parallel, we have been moving towards 3D. We created a system that allows anyone to take a video taken from a handheld camera, like a cell phone, and it outputs a 3D model of the person's entire head, face, and scalp. This work was published earlier this year, and it was presented at the Augmented Virtual Reality Workshop at Computer Vision and Pattern Recognition Conference, which is the main computer vision venue of the year. So now we have a 3D model on one side and hair comb on the other, and the next step is to combine the two. This will allow to visualize the hair loss information over the entire scalp at once. And once it becomes doable in real time, especially with the advances in cell phone technology, one will be able to visualize the alopecia information, for example, on the phone screen in a mixed reality environment, superimposing it directly on the person. I want to thank you, Dr. Bernardus. This has been a truly fascinating discussion. This is Dr. Ade Adamsen, web editor for JAMA Dermatology. This episode was produced by Daniel Morrow at the JAMA Network. The audio team here also includes Shelley Steffens, Lisa Hardin, Audrey Foreman, and Mary Lynn Furkeluk. To follow this and other JAMA Network podcasts, please visit us online at jamanetworkaudio.com. Thank you for listening. Catch you on the next episode of the JAMA Dermatology Podcast.
This is an author interview from the JAMA Network. Hi, my name is James Meggs, and I'm an associate professor of medicine at Harvard Medical School and Massachusetts General Hospital. The objective of our study was to test the hypothesis that smoking cessation was associated with a protective effect reducing the risk for heart attack, stroke, and cardiovascular death over subsequent years following smoking cessation. We further sought to test the hypothesis that weight gain associated with smoking cessation does not weaken the cardiovascular protective benefits of stopping smoking. This study was a prospective observational cohort study conducted in the Framingham Heart Study, where we followed over 3,500 individuals for over 25 years for the occurrence of heart attack, stroke, and cardiovascular death. At every four year examination of these Framingham research subjects, we were able to weigh them, assess their smoking behavior, and then observe them for over the subsequent six years for the occurrence of a heart attack or stroke. We used a statistical method that allowed us to combine the experience over 25 years to estimate the six year relative risk reduction in cardiovascular events associated with smoking cessation. We further adjusted our prediction models for weight change that occurred in the four years following smoking cessation. What we found was that at baseline, early in the study, about 30% of individuals in the study were cigarette smokers, but by the end of the follow up, only about 12% were cigarette smokers. So over time in Framingham, individuals have been successfully stopping smoking. We also found that individuals who had quit smoking within the most recent four year period gained on average about two and a half kilograms. When we followed individuals forward over time, those who were still smoking, those who had never smoked, those who quit smoking in the last four years, and those who quit smoking more than four years ago, what we found was that relative to people who continue to smoke, those who quit smoking in the last four years had about a 50% relative risk reduction in the occurrence of cardiovascular disease, defined as heart attack, stroke, or cardiovascular death. Those who'd quit smoking more than four years ago also had about a 50% relative risk reduction in cardiovascular disease. Individuals who quit smoking gained on average about two and a half kilograms over four years. Individuals who quit smoking more than four years ago didn't have weight gain that was different from individuals who had never smoked and were continued to be followed. What we found when we adjusted the regression models predicting cardiovascular disease for weight gain that occurred after cigarette smoking was that there was no change in the benefit or beneficial relative risk reduction associated with smoking. That is to say, if we look at the risk associated with quitting smoking in the last four years, people were about 50% less likely to have a heart attack or a stroke or die from cardiovascular disease. If we accounted for the weight gain that occurred over the first four years of follow-up after stopping smoking, we still found about a 50% relative risk reduction in cardiovascular events. These results lead us to conclude that regardless of weight gain that may occur after cigarette smoking, smoking cessation is associated with a profound and pretty quick, very strong reduction in the chances of having a heart attack or stroke or dying from cardiovascular disease. The clinical application of this conclusion is doctors and patients can feel very comfortable that stopping smoking will confer protective benefits against cardiovascular disease, regardless if the patient gains some weight as a consequence of stopping smoking. The next steps in this research should focus on trying to apply what we've learned, particularly improving approaches to help patients quit smoking and to stay stopped. We understand well from decades of research that cigarette smoking is harmful to health and that stopping smoking is beneficial to health. What has been difficult to do is to translate that knowledge into changed behaviors on the part of doctors and patients so that ongoing research should focus on best approaches to help patients quit smoking cigarettes. For more JAMA Network podcasts, visit us online at jama.com.
Hello and welcome back to Sharp Scratch. You're listening to episode 87. It's not just you, medicine is weird. This is a podcast brought to you by the BMJ and sponsored by Medical Protection, where medical students, junior doctors and expert guests come together and discuss all the things you need to know to be a good doctor that you might not get taught in medical school. I'm Charlotte and I'm the editorial scholar here at the BMJ, looking after all the content the BMJ student will be producing this year. I've also just finished my fifth year as a medical student at the University of Oxford. Today we're joined by previous editorial scholar Anna. Anna, would you like to introduce yourself? Yes, hello everyone. Yeah, I'm Anna. I am now an FY2 doctor working in the northeast of England and I did Charlotte's job many moons ago now but really excited to be here to talk about this because it's something I've thought about quite a lot. Okay, it's great to have you with us Anna and we've also got one of our newer panellists joining us today. So Judy, would you like to introduce yourself? Hi, hello, my name is Judy. I'm a third year medical student at the University of Silesia and I'm really excited about this topic because, like Anna said, it's something that, you know, we kind of talk about a lot. Yeah, I think it'll be a really good discussion, hopefully. So medicine is a career unlike almost any other. As medical students and junior doctors, we've had a lot of experience with strange, surreal moments. The first time you ask a super invasive question to someone you've known for all of five minutes, the first time you make an incision in surgery, the first time you do an intimate examination, all of these things can be really strange as they kind of go against all of our social norms. And getting used to weirdness is really important but no one ever teaches you this in medical school in everyday life we follow like lots of rules that aren't written down anywhere but then when you start practicing medicine you have to kind of unlearn all these things that you know about how to behave and what what's kind of normal in any given situation so yeah Anna I know this is a subject you've thought a lot about before, as you just mentioned. Do you want to just quickly tell us a little bit about it before we get started? Yeah, sure. I mean, I haven't really thought about it in any kind of academic way, but it's something that, you know, you and I spoke about before, Charlotte. I have, it's conversations that I've had with one of my academic supervisors, who actually a psychologist by background and not a medic and quite interesting really. His initial work, like his PhD and stuff, was around the human-computer interface and then he sort of sidestepped into medical education, which I thought was quite fascinating. You know, what are the parallels there? Is the medic-patient interface a bit like the human-com computer interface but um I won't dwell on that too much um but yeah it's something that that he calls or sort of conceptualizes as as the deviancy of medicine which I think is maybe a really nice way of looking at it you know we at least you know my experience is I spent 18 years of my life learning how to behave in social situations. And then I went to medical school and they told me that that's not how we behave in these situations, which becomes such a huge part of your life. And then I think sometimes you can get a bit, well, I know personally, I can get a bit confused between what's a norm of one culture and what's a norm in another setting. And I think that can be really, really challenging as a med student. Yeah, I completely agree. So I thought we'd kind of start with that idea of like normalising stuff that isn't normal in one setting. And I know, Judy, you kind of wrote about some of this when we talked about this before. Yeah, definitely. definitely so with starting third year we have started an anatomy module and in our module we do dissections every week twice a week and sort of the first experience that I've had with the dissections was very surreal because you would expect we would be sort of told beforehand sort of, you know, you're going to see this and this is how you're going to feel and stuff like that. But we didn't get any of that. So when we walked into the labs for the first time, we were being told about what our exams would be like, how we would be marked. And he just sort of casually points at the table, oh's a specimen and I think I was just completely shocked um I knew it was something to expect but I didn't expect him to just sort of have it on there like very sort of casually um and I think my classmates were like that as well we were a bit surprised and I think maybe he did this on purpose to kind of try to get us used to the setting before sort of anything else because I feel like maybe he felt that talking about it for a very long time would maybe kind of work it up in our minds and make us more nervous than we would need to be so sort of from that very first introduction it was very much this is what we're going to be, this is what we're going to be doing. This is how we're going to be doing it. You know, we're going to get to work. It didn't really give us the time or the space to process what we were looking at and what we were sort of going to experience. And I would have moments in our classes while we are being taught about something, you know, quite in depth or quite detailed that I probably should be paying attention to where I kind of step away and I look at our specimen see I don't even know what to call it because I don't know what to sort of refer to our cadavers as and I think that's just that's a testament of how sort of I'm not really sure how to connect it in my mind yet but I would have moments where I would look at maybe fingernails or eyelashes and it all feels so real and I kind of have this moment of oh wow like this is a lot this is something that's you know it's kind of with medicine having to connect um professionalism and being emotional at the same time and sometimes we're're told, you know, don't be too emotional, don't get too attached to patients. But at the same time, we're told to be empathetic and be able to show empathy. So it's sort of being able to connect those two things in the same breath is quite difficult when we are kind of told things that are almost opposing to each other so that sort of was my main experience with a moment where I felt a bit sort of a little bit of dissonance with medicine. Yeah I really relate to that I think we had that we had our dissection in our first year and to for that to be one of the like very first things you do in medicine I think it really sets you up for like understanding how how strange and like different this degree and this profession is to other people's yeah I totally totally resonate with what you're saying particularly thing about the fingernails I mean I remember having a um so I went to King's and we have quite had quite a traditional curriculum I think quite to Oxford Charlotte. So, yeah, dissection was was one of the first things I did. And I think it is one of those, you know, points where you realize you're not the same as a psychology student. You're not the same as a history student. You know, you have this huge responsibility, I think, to use the donation that people have made to the best of your ability to learn. And I think it's interesting what you touched on, Judy, the, I guess the role of dissection being actually much more than simply learning anatomy.
And I think full body dissection has a greater role than than simply learning anatomy um but yeah I totally I remember the first time I went in the DR and um there's just like there was just like jars everywhere and I remember this woman um one of the techs like wheeling this cart um just of arms just of arms and I was like that's that is weird isn't it and I was just like this is so surreal I feel like I'm having an out-of-body experience but yeah I remember what you you know what you were saying about the fingernails I remember my it was very much framed as sort of being your first patient so that was kind of how I viewed that the the cadaver that we were working on and you know it is easy to like zone out when you're focusing on one specific part of anatomy and you know trying to do that dissection well um and you know focusing on that and sort of forget what the bigger picture is and I remember one moment that I had was when I saw that my cadaver's fingernails were painted pink and that just kind of you know it just brings you back into the sort of focus of like the magnitude of what you're doing and it's so against all of our instincts in a way you know I mean the Hippocratic Oath right when it was initially written you know way back in like Greek times first do no harm encompassed surgery because doctors at those times didn't do any surgery because that was you know there's a whole thing about you shouldn't cut into someone to relieve the kidney stone and stuff like that obviously we don't use that anymore but you know cutting into someone's body is even if you know that that's the right thing to do, is still weird. Like when I was on general surgery as an F1, we would often get the opportunity to go to theatre. And one of the things that obviously they would allow F1s to do would be to make some of the initial incisions and things like that. And also, you know, learning how to close the laparoscopic portholes and things like that at the end. It's still weird cutting into someone. Like even some of the surgery, like Regis said, like it still is, I still feel funny every time I do the initial incision. Like, because it's so against our instincts. Like we don't want to hurt people. And that is the most, you know, obviously they're under GA, you know, you're not hurting hurting them but there's something in your like lizard brain that's like no this is wrong um and I think yeah again that just kind of comes back to like the role of dissection is way more than just learning the anatomy yeah I agree and you'd like you mentioned surgery just then I was talking to a friend about this and we were saying like how weird it is the first time you go into surgery and it's such an unfamiliar and like uncomfortable environment to be in like you feel initially maybe quite stressed because everything is quite like regimented but then you get into this room and there's often like really like bouncy pop music playing whilst there's just like a person on the table and it's yeah it's such a weird feeling isn't it it's just it's really hard to like connect all of that in your head and be like okay this is normal but it's also not normal like I don't know it's really weird. And it comes back to that dichotomy that Judy was talking about you know for the people in that room you know the ODPs the scrub nurses the surgeons this is their day-to-day but you know, for the patient, it's, it's not, they're just, you know, this, this might be one of the scariest days of their lives. And I think that's something that I always try and come back to, like, particularly having, I've just finished working in general practice, you know, having an appreciation for the fact that whilst for you, you know, say, take something like diagnosing someone with type two diabetes, for you, you may do that every single day. And for you you know say take something like diagnosing someone with type 2 diabetes for you you may do that every single day and for you also it might not seem like that big a deal because like there's you know loads of things that you can do um in terms of like management of diabetes and stuff but for that patient that's that's a lifelong condition that they're going to live with and actually you know it's not just things like cancer or you know terminal illnesses that you need to approach as breaking bad news you know I always approach kind of any diagnosis as breaking bad news because it might come as a real surprise for people and I think that that just comes back to that idea of like our routine being very much out of the ordinary for you know most people who aren't doctors nurses whatever yeah and actually that um kind of leads us on really well to Patrick's voice note um so this week we've asked all our regular contributors to send in um some kind of voice notes about things that they found strange when studying medicine and we've chosen a few to talk about today. And so this is what Patrick has to say about how what is normal for you as a doctor might actually be really different to what's normal for a patient and then vice versa as well. Hi Charlotte, Patrick here, one of the final year students in Galway and one of the contributors to Sharp Scratch. So I had a strange experience where a junior doctor asked me to do a clinical exam of a man with rheumatoid arthritis on one of the wards and I was really enthusiastic because he you know apparently he had very classic signs and it would be great practice for my exams coming up so it wasn't really until I was sitting in front of him talking to him, you know, did I realize that what I was excited to see these classic findings like the ulnar deviation of the fingers and the swan neck deformity and all that, those kind of stuff is what made his life so difficult. And, you know, that's what made it difficult for him to put on his shoes and made it difficult for him to cook and meant that he was in pain every day. So I guess it just reminded me that, like, my reality of going on the wards and looking for patients with good clinical findings is really different to being a patient and having to live with those clinical findings. So I guess that was kind of a strange reminder to get. I think what he said is very relatable in terms of how when we see sort of the textbook examples, we are kind of excited to see it in real life. And sometimes we forget that this is actually impacting the way that people live. And I know like in med school, when we're taught about symptoms and sort of features to recognise, we are kind of taught very much, you know, this you look for this you look for this and sometimes I wonder in the classes that we have and the sort of seminars that we have if we were asked sort of at the end how do you think this these symptoms affect the person's life and even if it's not something that's sort of the curriculum, it sort of is good to kind of get medical students thinking about it because it's at the end of the day when we're doctors, we're not just going to be telling people what's wrong with them and sort of diagnosing them. We also have to have that level of empathy. So even if just asking at the end of a lecture or at the end of a seminar, you know, what do you think makes this patient's life more difficult based on what symptoms they're presenting? It kind of will help us to sort of bridge that gap of, you know, understanding what someone's living through versus reading about what someone's living through. I think it's a really, really lovely reflection from Patrick. And I think something that medical school curriculums are really, really crying out for is greater integration of patient and public involvement.
So when I was running the British Undergraduate Society for Obstetrics and Gynecology, you know, we recognised that actually a lot of these conditions within sort of obs and gynae, it can be very difficult for people to see those patients with those conditions, you educational event that we did and all of the feedback that we got from them was you know we love hearing from patients like it's so important to us to hear from patients about how this has impacted their lives and I think it's it's kind of interesting to me that this is considered quite a new area um yeah that's what I thought was really interesting as well like there's definitely moments where you kind of go into a clinic and you're like oh I hope I see like you said xyz today that'll make it a worthwhile day or I'll have learned something or seen something that I need for my exams or whatever but I think we sometimes fall into a trap of like forgetting that that that's a person whose life is full and complicated and you know like they're dealing with this and it feels really weird to look at it through that lens then I think um and it's kind of like accidental objectification of a person like just distilling them down into this one thing that I find really uncomfortable about it so yeah I really agree with Patrick that that's definitely like a moment of like dissonance in medicine I guess and I think although it's not to say that you shouldn't be excited about your clinical practice like that you you should be excited about your clinical practice but I think there is just having that awareness of what these things actually mean on a day-to basis and not just your kind of little snapshot of what you get in your sort of little short patient interaction that you have. And we'll talk a little bit more about like some of the strangest moments in medicine right after this message from our sponsor. Indemnity. You've probably not given it much thought, but it won't be long until the risk of claims and patient complaints becomes all too real. Thank you. during your medical school years, our wealth of training resources to help you become the best doctor you can be, and our international experience that protects you during your elective no matter how far from home you end up. In fact, there are many reasons why our members worldwide trust us to support and protect them throughout their careers. And if you're looking for one more, every week one lucky new joiner wins £200. That's the average student weekly spend. Just join for free and you're automatically entered into the draw. That's why UK medical students choose to be part of medical protection. You can't blame them, so why not join them? Visit medicalprotection.org to find out more. So I thought we could also maybe talk a bit about like work-life balance and like separation between different parts of your like personality or life in medicine um so one of the things that I always find like really really strange is in Oxford where all the medic like kind of parties happen um organized by like the clinical med soc um is on the actual hospital site so the building that all the parties in is like directly opposite the helipad um it's like a two minute walk from a and e and like the like opposite gyne like department and it's like really close to where we do all of our placements and i just find it so weird it's like a Friday night or a Saturday night and you're like dressed up in either some ridiculous outfit or something that you would never wear to the hospital normally and you're like suddenly in the place where you go every day of the week and act very differently and yeah I just that's like one of the things that always makes me feel like really strange about medicine is like where that separation is. Yeah I've had something similar in terms of not with sort of our hospital sites but with we have a study room in our dorms and usually when you go down there are students you know studying for tests and exams and stuff and it's quite the the atmosphere is very serious very sort of like grim and I think sometimes we I think last week we had a games night in the study rooms where we just kind of invited everyone from the dorms and it was just a bunch of young students and everyone was you know kind of in the party mood playing card games drinking everything and I kind of just looked around the room and I was like wow I can't believe this is the same room I was stressing over biochemistry so it's definitely a weird experience to sort of behold but I also think it's it's kind of a good thing at the same time sort of being able to have that seriousness but also having a the ability to sort of remove yourself and just kind of be able to kick back and relax because I feel like in medicine as a profession we are always kind of surrounded by the seriousness so being able to find that sort of area where we're able to just chill or just kind of let our hair down a bit is always nice yeah I agree the thing you said about like looking around the room is really funny so you know recently I had to read a whole year had to redo our OSCE um so they put us in isolation for like two, three hours before the OSCE. And we were isolating in that building where all the parties are. And I was like looking around thinking, how is this like, like what you're saying, Judy, like how on earth is this the same building? Like I'm so stressed. I'm sat here in my scrubs. I was just going to say, I really like those reflections on like physical places and how they can like have such a huge impact on you. I think the, you know, what you're saying about like hospitals and stuff, it kind of like resonates again, I guess, with that sort of idea of like what's normal for us is not normal for other people, because most people would only go to a hospital like if they were ill. And we go to a hospital all the time and it's something my partner who's not medical um I remember one sort of quick anecdote that kind of illustrates this we were in Brighton once and I was like oh god I really need a wee like really really need a wee um and I was like oh I can't really see anywhere where I can go to the toilet I was like is that the early the early pregnancy unit over there? I'll just pop in there and go to the toilet. And he's like, what are you talking about? You can't go in there. I was like, they're not going to, they're not going to not let me go to the toilet. Like, it's like an open reception. I can see some toilets. I'm just going to go in there. And obviously they did just let me go to the toilet. But that was only because I was like, I'm totally comfortable in this environment. Like, you know, if you weren't a med student or a doctor, like you simply would not do that. Um, so I think that that's, you know, that's, that's probably like part of this weirdness is the fact that like lots of people find hospitals very scary, which, you know, totally understandably, it's not a place that you associate good things happening in. But, you know, I, I now obviously having been a med student and then subsequently being a doctor in training, we're supposed to be called now, I feel really comfortable in hospital. I'm like, I know where everything is. Like, I know how things work. Yeah, things are a bit different kind of place to place. But ultimately, I know there's probably going to be a coffee shop somewhere. You know, there's certain things that you can expect in a hospital, I find quite comforting yeah I agree I definitely agree as well um I think what you were saying with um most people going to the hospital when they're sick um or just generally when they're not feeling well um uh and we kind of go to hospitals when we're perfectly fine um I just reminded me I was having a conversation conversation with one of my friends and they were like, oh, what are you up to? And I'm like, oh, I'm in hospital. And they were like, oh my God, are you okay? And I was like, yeah, I work here. And then it's kind of that weird experience of us being in a place where most people would sort of associate other things with. And I that's one of the things about medicine being able to sort of connect different emotions to different things at different times I don't know if that makes sense yeah definitely my um my husband every time I say I'm going to the hospital he goes oh no what's wrong I'm like not funny you're not funny. You're not funny. But yeah, he still finds that very funny. Yeah, my friend does that like genuinely. Like she forgets every single time and like I'll be texting her and she'll be like, wait, what? Like what Julie was saying. And it happens like, how long have I been doing placements? Like I've been doing placements for like two, three years now.
So we'll come back and discuss a little bit more about this with some more voice notes right after this advert I'm Dr Matt Morgan and alongside working as an intensive care consultant I work as part of the BMJ on examination team to support you in passing your medical exams. You can get access to our personalised revision resource online and in our app for years 1 to 3 totally free as well as a huge 40% discount on our medical student finals product. We'll help you pass your exams by making sure to maximise the best use of your time. We'll deliver you the most important questions, keep you on track with daily reminders and give you feedback to show how you're performing. We're committed to making revision easy, so start your journey to passing first time today by visiting onexamination.com to sign up or by downloading the One Examination app. Okay, so one of the other things that I think a lot of medical students find the weirdest bit about medicine is asking really invasive questions that you would never ask in any other situation like five minutes into knowing someone and I think that's something that you get used to quite quickly but it can feel weird at first and we have a voice note from Stan one of our other panellists about when this can be quite like an uncomfortable experience. So my clinical partner and I were taking a history from a man and towards the end of the conversation he mentioned that he had found a lump on his penis and so my clinical partner started asking him about this lump and when he got to the question of how big is it there was a pause on the phone and we didn't know what was happening but the patient then followed up with oh do you mean the lump so more of the story is always be clear with the questions you ask, especially if they're regarding someone's private parts. I mean, that is funny, isn't it? Yeah, I feel like that just captures it. That just captures the like awkwardness and like how easy it is to put your foot in it how like saying one sentence slightly differently to the way that like you would like mentally rehearsed it can like completely shift a conversation um but I did think that was quite funny from Stan yeah and it's again it again, it's like what's obvious to you as a medical, you know, I think that's probably been the kind of theme of this is like what's obvious to you as a medical professional and what's normal to you is not obvious and normal to the majority of your patient population. And I think you do always have to remember that. And, you know, I've been working in a place that has quite low health literacy and has um lots of problems with poverty and deprivation and and things like that and I think what's obvious to you is not obvious to the patients even in terms of you know what's the most important thing to be talking about um and I think it is a lot of medical practices about being mindful of that um and I think I've probably labored that point enough in this episode. But yeah, I think this is, you know, I remember when I was in third year and I was learning how to examine people, you know, physically lay your hands on someone who you've only just met, you know, someone comes in, you're immediately asking them about, you know, really, really personal personal stuff and that is a privilege and that is a responsibility um and I mean my approach to it is always to be extremely matter of fact because if you if you even start like hesitating or like you know sort of circling around it a bit then that's's gonna make everything more awkward. So, you know, just ask the questions because for the most part, people are expecting you to ask the questions. If they come in with a problem, an intimate problem, they are going to expect you to ask intimate questions. But I think it can be very, very hard when you're first learning. Yeah, I've definitely done that in OSCE practice is like go round and round, like trying to work out a way of like saying something that is the least awkward for me that I think will be the least awkward for the patient and realised like three minutes into me like babbling and like trying to come up with like a new way of phrasing something. The best way is to just be direct. And yeah, it can leave you like in just practising for OSCEs and just like laughing so much about how like awkward you can make something like just because it's new and it's scary and you're probably a bit nervous and it's such like an artificial environment really. It obviously becomes second nature quite quickly but to begin with it is really artificial. And you do have to be mindful about like the words that you're using. So I think yeah there is you know know some of these ideas around like how you phrase things what's the best way of speaking with you know the simplest language possible which can be really really hard when you know all of the like medical terminology and stuff and in one setting like when you're speaking to colleagues you probably do want to use some of that terminology particularly as a med student I think you're like you want to make sure people know that you know what those words mean but then then you have to switch to maybe speaking to people as I say who have got lower levels of health literacy and lower levels of literacy and you have to make sure that what they understand of what you're saying links to what you're saying which is not always as it seems. Yeah, I feel like a lot of this comes back to like the switch in like personality or language use or like so many of the things we've talked about have just been about like the, there's lots of aspects to being a medical student or a doctor and like turning those things on and then off in different settings is hard to get used to, I guess, at the beginning is kind of what we're saying. And Anna, what you mentioned earlier about, like, examinations and, like, actually, like, doing an examination, actually, like, touching someone, putting your hands on someone is a really, like, unnatural feeling. I started clinical placements in February 2021. So it was, like, right after I just had a year at home, like being, you know, you cross the street to be as far away from people as possible. And then suddenly being in an environment where like you actively were not supposed to be doing that was, it was really strange. It's just a really weird thing to get used to, I guess. I think sort of from listening to Stan's voice note and another thing that kind of I was thinking about that's weird with medicine is you kind of have to learn how to keep a really good poker face because you can't show your expression to certain things. And sort of when we're talking about awkward questions or sort of awkward misunderstandings, like in the situation that Stan was talking about, sort of you can't really like burst out laughing. You kind of have to carry on to sort of like stay as professional as you possibly can. And it's one of those things that I think, based on your reaction, makes such a big difference to the patients. Because I remember when I was getting my bloods done for being tested for iron deficiency anemia. And I think I was mentioning to the doctor, because at the time I wasn't't sure what I had I was mentioning some of my symptoms that my mum was with me I was quite young and she she mentioned one of my um quote-unquote symptoms which I don't think I don't think was a real symptom um but I remember the doctor started laughing and I was so embarrassed I was I I remember it so clearly and just from um and it wasn't really like a long like laugh or anything it was just like a little chuckle and I just I was like oh this is ingrained in my memory forever so it's so important how we react to those situations. I agree. The thing about having a good poker face, though, is so true. I think I have the kind of... I don't know.
I think on the flip side as well, not only just kind of working on our poker face, but also knowing the, like, social cues, like, sort of, like, trying not to sort of have a blank stare while we're talking to our patients so knowing when to kind of show emotion and when to not show emotion and it's just the back and forth like in like a space of 15 minutes is just it's a skill it's definitely a skill I admire in doctors because I'm just like wow how are you doing this especially when people tell you like awful things like this this is just my last point like people come in and they can tell you like the worst thing that you've ever heard has happened to them totally matter of factly and you yeah it's exactly as you say GD you do just have to sometimes I can't even figure out like how I'm supposed to respond because they're maybe like telling you something really really awful but in like a totally like jokey way and being like oh well you know this is what it is I'm just like yeah and I think what's hard about that as well is like the only other time that you'd probably hear something like that is from someone you're close to, like a family member or a friend. Exactly, where you'd respond totally differently. Yeah, you probably have like years of shared history. You know what they want you to say, or they know, you know that you're not going to be kind of overly scrutinised for your reaction to it like it's such a different setup um but yeah that's something that I imagine is quite hard to balance and something that probably happens fairly frequently as a doctor Anna I don't know but yeah all the time I mean I don't want to I don't want to put people off like it's a it's an enormous privilege being able to, you know, support people that like bad stuff has happened to. But I think particularly, you know, when you're from certain backgrounds as well, where maybe you have experienced less hardship in your life, which I certainly am. I think sometimes it can come as a shock and maybe not something that you were were expecting that much but it can be can be very difficult to respond to but on the other hand it is a fundamental part of being a doctor and it is nice to look back and think about times when you've dealt with that really well and that person will um you know probably remember that interaction forever because you got it right um and that's just as important and um just as important to reflect on those times when you felt that you did really well um as well as times when you felt that perhaps things might have gone differently had you phrased something differently or you know done something differently so I think that's just an important point to say as well at the end of all of this. Yeah I think that is actually such a good like take-home message like everything we've kind of touched on in this episode is that medicine is weird and it is all just like kind of a learning curve and that like some days will be easier than others but ultimately this is a whole new thing we're getting used to as medical students and new doctors. And also, like we said at the beginning, we're learning like whole new ways of behaving and interacting with people. Not just clinical facts and knowledge. It's this whole new culture of what it actually means to be a medical student or a doctor. And getting used to that can be really challenging sometimes. So, yeah. Thanks so much to our panellists for joining us and everyone at home for listening to this episode of Sharp Scratch. If you liked this episode, I'd love it if you could support us, leave a review wherever you get your podcasts and share with the people you know and tell your friends about it. That helps other people find the show too. If there's ever any topics you'd like us to cover or if you have any thoughts on this topic about how strange medicine can be at times do let us know we're on facebook twitter and instagram as bmj student um if you want to hear any other episodes from us um subscribe to sharp scratch wherever you get your podcasts and in two weeks time you'll get another episode from us we're talking all about fictional doctors next time um and the best medical tv shows so join us for that um and until then goodbye from us
In the January 8, 2014 issue of JAMA, we published a patient page on electronic cigarettes. At the time, what struck me about these devices were that they were simply a device that superheated fluids using an electric filament to create a vapor that delivers chemicals at high concentrations directly into the lungs. This seemed inherently dangerous to me, and when I discussed the potential hazards of e-cigarettes on social media, I was sharply criticized. The main criticism was that these devices were much safer than tobacco and should be viewed as a suitable alternative to smoking. But e-cigarettes are not safe. In November 2019, the CDC reported more than 2,000 cases of severe lung injury attributable to vaping. Most of the patients with this problem had exposure to tetrahydrocannabinol, and about two-thirds of patients had nicotine in their vaping devices. In recent reports, the CDC found vitamin E acetate in the THC vaping products that seems to be associated with the severe lung injury. In today's JAMA Clinical Reviews podcast, we discuss electronic cigarettes and vaping, their hazards, and the general problem of nicotine addiction. From the JAMA Network, this is JAMA Clinical Reviews, interviews and ideas about innovations in medicine, science's a medical student. Cara did a medical student rotation as a noun or a verb. E-cigarette use may often be referred to as Juuling or vaping. For today's Clinical Reviews podcast, we discuss electronic cigarette use with Dr. Suchitra Krishnansaran, a psychologist in the Department of Psychiatry at Yale University School of Medicine. Let's start with how they work. Technically, e-cigarettes are a very simple device. There is a receptacle which holds the e-liquid, a battery which charges a coil and then vaporizes the e-liquid, and then a mouthpiece where the user draws from the e-cigarette. But that's how they started. They were originally created to offer smokers a cleaner form of nicotine to help with their cigarette addiction. But they have evolved over the years to things which look nothing like a cigarette. There are, you know, cigarette-like products, which are called cig-a-likes. They are not very popular and not used very much. But then there are tank systems, which look like pens. You can get systems which look like cigars, which look like hookahs, which look like pipes. And then there are these devices called mods or modified devices, which look nothing like a cigarette. They come with various attachments, adjustments. They can be used for producing larger vape clouds. They are used recreationally by a lot of people in cloud competitions. And the most recent market entrants are these pod devices, which are, for an example of that, is a jewel. The pod devices contain the e-liquid in a little pod and are very small and very discreet. E-cigarettes vaporize a liquid that the user inhales, and the liquid, otherwise known as e-liquid or vape juice, comes in numerous varieties. Some varieties include nicotine. Others are flavored, often with fruit flavors. Popular flavors include mango, mint, cucumber, and there is a menu of how to create different flavors, but it's for edible products. So most of these chemicals and their use is for using edible products, not for inhalational exposure. So now the same formulas are being used to create flavors in these e-cigarettes and you're inhaling it. So I don't think, I mean, my guess is probably it's from a toxin perspective, definitely cigarettes are going to have more toxins than e-cigarettes. But I think the concern with e-cigarettes is we don't know what this long-term inhalational exposure or environmental exposure like you're talking about is really going to do. We are only now starting to understand what nicotine itself does. But what we do know from a lot of animal work and existing literature and emerging literature, I should say, is rapidly increasing in kids. However, when trying to convince people, especially kids, not to vape, it is important to honestly present the facts. When we first started going into schools to talk to them about e-cigarette use, we found that some of the schools had proactively taken their cigarette posters and converted them into e-cigarette posters. So there were posters everywhere in the school telling them, e-cigarettes cause lung disease, e-cigarettes cause oral cancers. I mean, there's all these pictures, but there was absolutely no evidence to support any of that information. And this is the pushback we got from a lot of the students when we went and say, you guys are telling us information which is not correct. So I learned that lesson a very long time ago that don't give them, don't try to scare them or use scare tactics. Present the facts to them. So that's what we try to do in all the schools. We don't go in and tell them this is going to cause cancer. Because although I know that is what turns kids away from doing things like this, since we don't have that information, we don't do that. And I'll tell you my own personal experience with my own son is I have, this is a weird thing, but I send him scientific papers to read. I've always sent him little science clips. I keep sending it to him. I don't know whether he reads them or not, but I do know they come up in conversations when I'm having conversations with him. So, yeah, he does read some of them. As Dr. Krishnan Saran alluded to, public interest in e-cigarette use has been focused on school-age children. The CDC recently published the results of the National Youth Tobacco Survey from 2018 and combined it with previous year's results to analyze the trends in teenage tobacco product use. The FDA considers e-cigarettes to be a tobacco product. Using this classification, the trends in tobacco product use among U.S. students in grades 6 through 12 were analyzed from 2011 through 2018. E-cigarettes are now the most popular tobacco product according to the 2018 survey results. Interestingly, there was a significant decrease in the rates of cigarette use and a significant increase in the rates of e-cigarette use. However, in part because these two trends were in opposite directions, the overall rate of use of any tobacco product has not changed significantly. Cigarette smoking is a very serious problem. I mean, it's one of our biggest public health concerns. We need ways to help smokers quit smoking, and there's absolutely no doubt that providing smokers with a cleaner form of nicotine patches? We spent years with a nicotine patch. Years. It is a totally non-addictive way of delivering nicotine because it does not produce the sharp increases, the peaks in blood nicotine levels. That's also the reason why many smokers don't like it as much. But still, we spent a lot of years developing the nicotine patch, developing the nicotine gum. We did trials with them, and then we showed they are effective. Okay, so nicotine patches work. What about verinacline, or what we also call Chantix? Medications like Chantix have proven efficacy and have been shown to work. Now, if somebody has tried everything and says, no, this is the only way that I want to go, I think physicians should support them in using e-cigarettes to quit smoking, not to use it as a tool to smoke or vape where they cannot smoke. So in other words, I'm saying don't support the idea of comorbid use where they're using cigarettes and e-cigarettes at the same time. The counseling should really be about using it to quit smoking completely and then wean yourself off the e-cigarettes too. Because, you know, as I said, nicotine addiction in itself, we have a lot of concerns about that too. So that is what I tell most people. Your next question I know is going to be to ask me, well, how do we wean people off e-cigarettes? Are there programs? And no, there aren't. We have not developed any of those yet. One of the big questions that comes up is, can e-cigarettes be used to help people stop smoking? A large clinical trial asking this question was published last year in the New England Journal of Medicine. I spoke with JAMA editor and Boston University professor Dr. George O'Connor, who wrote an editorial So that's a program they already have in place. In the context of this National Health Service Smoking Cessation Program, they instituted this pragmatic clinical trial where patients who sought care to help them quit smoking agreed to be randomized to either the usual care group, which is to say behavioral support with nicotine replacement therapy, offer the nicotine replacement therapy of their choice, which could be patches, gum lozenges, or a combination, or alternatively, the behavioral support plus e-cigarettes. And if they were randomized to the nicotine replacement therapy, conventional nicotine replacement therapy arm, they were given a three-month supply of the nicotine replacement therapy of their choice.
If they were randomized to the e-cigarette group, they were given a starter pack of second-generation e-cigarettes, which are the same kind of thing that are commonly used here in the United States. They were given a bottle of e-cigarette liquid with 18 milligrams per mil of nicotine, which is the usual place that a smoker would start who was trying to substitute electronic cigarettes. They were given a starter pack and a bottle and basically instructed in how to use electronic cigarettes as an alternative to smoking tobacco, again, along with the behavioral supports for quitting smoking tobacco. These groups were followed over time for 52 weeks, and whether or not they were smoking was validated by measuring by the detailed carbon monoxide measurements, compared to only 9.9, or about 10%, of the group in the conventional nicotine replacement therapy, a statistically significant difference, favoring more smoking cessation among those in the e-cigarette group as compared to the conventional nicotine replacement group. Sounds good. E-cigarettes can help people stop smoking. The 18% quit rate is high, and in other studies of e-cigarettes, when used to help stop smoking, the quit rates were only about half of that. But there are very important caveats regarding any potential benefit of e-cigarettes when used to help people stop smoking. At the 52 weeks, of those who had quit smoking tobacco in the electronic cigarette group, 80% of the patients were still using electronic cigarettes, whereas in the group that had been assigned to the conventional nicotine replacement therapy, the number that were still using conventional nicotine replacement was 9%. So in other words, the majority of patients who successfully quit smoking in the electronic cigarette group were still using electronic cigarettes at the end of the year, whereas those who quit smoking in the nicotine replacement group, while a smaller percentage, most of those were no longer still using nicotine replacement at the end of the year and had quit smoking. Think about this. If someone is smoking e-cigarettes to stop smoking, have they really stopped smoking? With the increasing number of people developing severe lung disease because of e-cigarettes, it's quite clear that long-term use of e-cigarettes is not benign. In fact, there are animal models that show that when nicotine is delivered this way, it can directly harm the lungs. So our point of raising this in the editorial was, if as shown in this study, electronic cigarettes as a smoking cessation, they lead to more success in smoking cessation, but the majority of people who use electronic cigarettes wind up smoking electronic cigarettes indefinitely, then we should not consider that necessarily a complete success. Because if there are long-term health effects, switching from tobacco to electronic cigarettes leaves the user on electronic cigarettes forever. There could be long-term health consequences of that. If not e-cigarettes, what should clinicians do to try to help patients stop smoking? There are a number of FDA-approved medications that can be used to assist with smoking cessation. There's the various forms of nicotine replacement therapy, patch gum, lozenge, for example. There's bupropion tablets and varenicline tablets. These appear to be safe. And the combination of bupropion with nicotine replacement therapy or use of varenicline, along with behavioral supports in some studies, have led to smoking cessation rates similar to those seen for the electronic cigarette intervention in this group. So that suggests the possibility that it may be that a better long-term outcome, conceivably, could derive from using these FDA-approved treatments, which lead to smoking cessation, and then using nothing at the end of the year, as opposed to e-cigarettes, which lead to an equal amount of smoking cessation, but long-term use of e-cigarettes at the end of the year. There you have it. There are lots of ways to help people stop smoking. Nicotine-containing e-cigarettes may or may not work. However, they do involve exposure to chemicals in the airways and lungs whose effects are unknown. Given the uncertainties, it is probably best for clinicians to suggest to their patients not to use e-cigarettes. That wraps up this episode of JAMA Clinical Reviews. A very special thanks to today's guest, Dr. Suchitra Krishnansaran, Dr. George O'Connor, and a special thanks to my co-producer of today's episode, Kara Borrelli, a medical student doing an elective rotation at JAMA. This episode also has CME, and you've already done most of the work towards earning credit for this activity. Thank you. and CME all in the same place. Look for it in the Apple Store. You can also find the entire array of JAMA Network podcasts at jamanetworkaudio.com. Today's episode was produced by Daniel Moore. Our audio team here at JAMA includes Jesse McCorders and Mike Lirkowitz, the Deputy Editor for Electronic Media here at the JAMA Network. Once again, I'm Ed Livingston, Deputy Editor for Clinical Reviews and Education for JAMA. Thanks for listening.
For several decades, studies of health care quality in the United States have documented suboptimal quality in a range of areas, examples of inappropriate care, and unexplained geographic variation in care. Although quality improvement efforts have led to progress in some areas, wholesale changes have been lacking. I'm Stephen Morrissey, Managing Editor of the New England Journal of Medicine, and I'm talking with Donald Berwick, President Emeritus and Senior Fellow at the Institute for Healthcare Improvement. As part of the journal series in honor of the 50th anniversary of the Institute of Medicine, now called the National Academy of Medicine, Dr. Berwick has co-authored a perspective article about the history of efforts to measure and improve healthcare quality in the United States. Dr. Berwick, prior to the 1980s, when interest in this area began to grow, what was known about the quality of the healthcare that was delivered in the United States? The history of studies of quality goes back actually to the turn of the 19th century. It was in the early 1900s that some really courageous people began looking, especially at the quality of surgical care, and they discovered a lot of variation and a lot of defects in care. But that information kind of remained closely held by the professional systems themselves that wasn't in the public's knowledge. Through the mid part of the century, there were further studies of variation in care, which, again, never reached public attention. It really was the 1980s, especially the Harvard Medical Practice Study that kind of cracked it open and began to show us how many problems there were, and especially the courageous work of Dr. Jack Winberg, who was the first really deep student of variability in practice, and then soon thereafter, important studies about safety in care, injuries to patients that were occurring because of mistakes in care. So how is healthcare quality now defined and measured? What fits under the umbrella of quality assessment, quality improvement? I see it in two steps. The first was the benchmark set in 2001 by the then Institute of Medicine, now the National Academy of Medicine's very important report called Crossing the Quality Chasm. I served on the committee that wrote that report. And in that report, we outlined six dimensions of quality, which have remained a pretty good framework for measurement and improvement. The six dimensions are safety, not injuring patients in care, effectiveness, adherence to science rather than unwarranted variation, patient-centeredness, which is sort of a shift of power to patients so care focuses on their needs, timeliness, which is avoiding unwanted delays, efficiency, which is avoiding waste, which is an element of quality, and equity, which probably should have been listed first. It's really racial and socioeconomic disparities in health. So that's six levels, safe, effective, patient-centered, timely, efficient, equitable care. You'll find that in the mission statements of many healthcare systems around the world today. Later on, in about 2005 or 2006, colleagues of mine at the Institute for Healthcare Improvement, Tom Nolan and John Whittington, set out what's now called the triple aim, which said that all of that that I just said refers to the quality of care when you're in the care system. They said there are two other objectives. One is improving the health of populations, which, of course, happens through social determinants of health in the public health sector, and also reducing per capita costs because health care, we now know, is extremely wasteful. We waste at least a third of the American health care expenditure on things that don't help anyone at all. So as AAAIM today, better care for individuals, better health for populations, and lower per capita cost represents another framework for the assessment and improvement of care. In your article, you describe roles that both government initiatives and non-governmental organizations have played in quality assessment and improvement. Have those efforts been synergistic, or has one approach generally been more effective than the other? Well, that's a matter of opinion. I think generally synergistic, but governmental approaches have tended to focus more on metrics. I call it outside-in quality, where accountability and pay for performance and public measurement are the tools that government tends to use to focus attention on what needs to be done. The private sector, especially professional societies that have taken this seriously, have also engaged in educational systems, networks, quality improvement collaboratives, which activate and support healthcare systems to change their processes and improve care. At best, they work together, but they don't always. Sometimes the surveillance systems actually chill investments in real change because people get frightened and they may even hide the data instead of trying to actually improve things. There have been important government efforts, though, to support improvement. When I was the administrator of the Centers for Medicare and Medicaid Services, for example, been mixed. Where has there been progress, and why is it, as you write, systemic improvement in quality of care has proven difficult to bring to scale? Well, it is a good news, bad news situation, I think. The good news is that awareness is there. As we said earlier, we now understand the patterns of a need for improvement of care much, much better than we did even 20 years ago. So there's a lot of knowledge. And we also have better theory. The reports from the National Academy of Medicine have emphasized the importance of what they call the learning healthcare system, or the use of systems thinking and awareness of interdependency. We really know a lot, a ton, about how to improve. And there are pockets of improvement. We have individual projects that have worked on healthcare infections, on pressure ulcers in patients confined to beds, on more patient-centered care, giving patients more control over their own care. I can, for almost every dimension of quality, we can name successes. The problem really is, well, there are a couple of problems. One is scale. We just haven't made the improvement of care a kind of consistent, effective process throughout the entire healthcare system. Why is an interesting question. I think it has to do in part with the buck doesn't stop anywhere. There's nobody, certainly in the United States, responsible for healthcare quality. We don't have an agency that oversees that or any particular form of national leadership for improvement. Second, the finance often controls, although reduction of waste is an element of quality, that's very important to understand. Higher quality and lower cost go together. That's what the AAA says. Healthcare organizations tend to focus on revenue and margin. And when things get tough, their attention is diverted from the kind of internal operational changes that are needed to actually improve quality. I personally believe that quality improvement is the best route to a sustainable, affordable healthcare system. But that, quote, business case is not widely embraced in healthcare leadership even today. I hope and think that will change, and there are counterexamples, but I think we have kind of a problem of leadership focus that still has not brought quality to the forefront. And in fact, in your article, you mentioned the reluctance of political leaders to fully endorse new payment models, to endorse the use of knowledge of what treatments work best as a national basis for coverage policies. How would greater acceptance of those kinds of reforms open the door to new opportunities to improve quality? At a national level, both in the public and private sector, it would help to establish goals. Back in the day when the President's Advisory Commission on Consumer Protection and Quality issued its report in the late 1990s, it was set out that we should aim for, say, a 50% reduction in safety problems in American healthcare. But that aim was never embraced as a matter of policy, never resourced, never linked to ongoing metrics. And without aims, it's really hard to improve. So I think that that kind of investment in setting goals would really help. We don't have a goal setting mechanism. I think also there's sort of a double edge to measurement. And when the system over relies on measurement, today there are thousands of metrics that are used, for example, applied to hospitals by government and private payers. You can't do that. You can't have these thousands and thousands of measures which erode the time of clinicians. They're actually distracting rather than helpful. And so some form of focus would be really important. From my belief system, where I work from, I actually don't think measurement holds the answer. I think the real approach is correctly outlined in the National Academy of Medicine's call for a learning healthcare system, which means supporting organizations to continually learn about how to do better. Who's doing best? How can I bring that into my system? And to have especially professional leadership for that so that physicians and nurses and others take the helm and set their own intentions toward the continuous improvement of care, which means changing the way they do their work over time. I'd much rather see that be done from inside the healthcare system, led by professionals than by auditors and measurers who think that if you just hold people's feet to the fire enough, that will do the trick.
So finally, in that regard, you say in your article that you support that call for a national independent, a political federal oversight agency for healthcare quality assessment and improvement. What are the barriers to bringing such a thing into existence? Well, first, I wouldn't so much emphasize oversight as transparency and support. I think that we don't need more pressure on the system. We need more leadership of the system. And there's a difference as to what the tone alley of that agency would be. The political problems with that are enormous. The healthcare system tries to do good work, but hospitals and clinicians don't really want another form of surveillance right now. They feel like they're working very hard and doing their best. And so far, their experience may not have been a real support from such an apparatus. I think we could change that, especially if this were clinically led as much as politically led. There are also resource implications because healthcare systems always feel pressed on money and their time and efforts are spent lobbying for payment. They don't particularly invest right now in the leadership of improvement. Right now, they're too worried about revenue and their income. We're also constrained by our payment system, the fee-for-service payment system, which sort of afflicts our country. It means that hospitals and doctors and others, in order to pay the bills, they need to keep the machines on. They need to keep working and working and working. And to get organized to improve, take some investment. You have to be able to get together and say, organize teams and insert metrics and learn from others. And I personally believe a more consolidated payment system, one that isn't hooked on fee-for-service, but rather involves global payments and population-based payments, will be more supportive of that kind of change. And yet we've seen that stall in this country. We talk a lot about value-based payment, which is sort of a way to think about that. But the progress has been very, very slow. Thank you, Dr. Berwick.
Hello and welcome to the May edition of the Lancet Neurology Podcast. My name is Nikolai Humphries. Today we'll be looking at a review published in the Journal on apathy in Parkinson's disease, clinical features, neural substrates, diagnosis and treatment. I am joined on the line by Paul Crack from Grenoble University Hospital. He is one of the authors. Hi Paul, welcome to the podcast. Hi Nicola, thank you for calling, good to be here. It's a pleasure to have you. Now, we are all familiar with the term apathy, but you use the term to describe a specific behavioural syndrome. I'm really interested about getting to the nub of that. Can you briefly describe the features of this syndrome? Yes, the term of apathy is indeed of common use in everyday English. But a patient, however, would never ever complain about being apathetic because in everyday language, apathy has a very negative connotation. Spontaneously, the patient will rather complain about fatigue. Physicians are using the term of apathy in order to describe a behavioral modification that's basically characterized by a decrease in motivation. Now, what does an apathetic syndrome look like? Well, a patient with apathy, first of all, has a loss of interest and drive. He will spend less time than usual with his favorite pastimes or hobbies. His flow of ideas has decreased. He has no spontaneous thoughts. His mind is empty, so he doesn't start new activities. And if apathy is severe, he actually doesn't start any activity at all, unless he's pushed to do so. And curiously enough, when he's pushed by his surroundings on a context such as a consultation, when stimulated to answer questions, he is able to do everything to behave normally. So if not specifically asking about symptoms of apathy, the physician can easily be misled and the apathy will remain completely unnoticed. The patient with apathy also has an emotional blunting. He feels less pleasure from activities that used to be his passions before. There's no more enthusiasm. The patient having less interest in social activities, he will progressively withdraw from social life. However, because of a lack of concern, he will not complain. So quite often, the apathetic patient doesn't even feel concern about his own state of inactivity. It's not sad. He feels unhappy only when realizing that people close to him are disappointed or start blaming him for his inactivity. That's about the typical situation we can observe in an apathetic patient. Thank you for that very vivid description. I think you explained how apathy affects the quality of life of patients, but could you also explain how it affects their caregivers. Yes, the patient himself, he may not spontaneously complain, but he feels no pleasure. He feels tired and that does indeed have an important impact on his quality of life. The Grenoble Group, we have recently looked at quality of life in patients after surgery when medication, anti-Parkinsonian medication, is sometimes withdrawn a lot, sometimes too much. And in that study, patients were divided into two groups, those who were apathetic and those who were not. The basic characteristics, motor improvement was perfectly identical among the two groups, but despite motor improvement, patients with apathy had absolutely no gain in quality of life. So this drastically illustrates that the non-motor behavioral symptoms of the disease are as important, if not more, than the motor science. The neurologist has to focus on both in order to improve the quality of life of his patients. The caregiver on his side is confronted with a person who can do everything that he used to do, but he doesn't anymore without any obvious explanation. If a wife or husband who used to be enthusiastic isn't anymore, then the caregiver doesn't understand. He can either feel guilty or start getting upset and blame the patient for his symptoms. Actually, I think apathy can be much more difficult to deal with the surroundings by the caregiver than for the patient himself. That's really, really interesting. I never really thought about it that way. Can you now shift towards Parkinson's? Now, apathy seems to be highly prevalent in Parkinson's disease and also other neurodegenerative diseases. Do we know why people with these disorders are so vulnerable to apathy? Yes, apathy is indeed highly prevalent in neurodegenerative diseases such as Parkinson's disease, which leads to a lack of dopamine and dysfunction of the so-called button-up mechanism of brainstem cortical activation in the early stages of this disease. But apathy is also frequent, for example, in Huntington's disease, which starts in the corded nucleus, which is part of the basal ganglia, and which holds a key position in the cortical-subcortical loops, which are involved in planning and execution of activities. Apathy is also extremely prevalent in progressive supralocal palsy. This is a disease which primarily affects the front lobe and thus it impairs the top-down mechanisms of cortical initiation and adaptation of behavior. Apathy is also frequent in Alzheimer's disease, so very, very frequent diseases which can affect the whole cortex, but also in diffuse white matter disease, in stroke or multiple sclerosis, which affect the fibers that link the different brain regions to each other. Or in non-degenerative psychiatric disease, such asathy, chronic depression, or the negative symptoms of chronic schizophrenia. Multivariate behavior is such a complex issue, and if only one of the brain structures involved in the cognitive or emotional aspects of multivariate behavior is impaired, this can lead to clinical features of apathy. So whether the disease starts in the cortex or in the basal ganglia or in the brain stem, we have an interruption of the cognitive and emotional corticobasal ganglia loops that are involved in our routine and pleasure behaviors. And this, to my mind, explains the vulnerability to such a complex clinical syndrome and also its frequency across various diseases. I'm reading in your review that you discussed the neural substrates of the various components of apathy. Could you give us an example of the type of pathology that might be associated with one of the subdomains of apathy? Sure. We can distinguish indeed emotional affective apathy, cognitive apathy or autoactivation apathy. Let's look more closely at the example of autoactivation apathy with a specific lack of initiation of activity. What is common to all the various components of apathy is a lesion or dysfunction in a loop involving the dorsolateral prefrontal cortex and the caudate nucleus. In autoactivation activity, in addition, there is a bilateral lesion or a dysfunction of the supplementary motor area where the initiation of behavior is started on a cortical level. A lesion affects bilaterally the internal globus pallidus, interrupting thus the outflow from the basal ganglia to the cortex. Are treatments available for the different components of apathy in patients with Parkinson's disease? Yes, indeed, we have different treatments available. The treatment in the de novo Parkinson's disease with a pure isolated apathy is not the same that in a patient who has apathy with emotional distress or in a patient with end-stage disease who has a severe executive syndrome. While in the de novo patient, we would start with a dopamine agonist with a preferential affinity to the myelimbic dopamine receptor in the nucleus accumbens, the so-called reward center, the patient with emotionally affective suffering should rather be treated with classical traditional antidepressants acting also on the serotonergic and noradrenergic systems, but which in just pragmatical approach may also be associated with dopamine agonist. And then finally, the patient with advanced disease suffering from dementia will be treated with acetilconilesterase inhibitors, which are less powerful and it is more difficult to repair the whole cortex rather than just replace the bottom-up activation with a dopamine agonist or levodopa. Also, some other drugs leading to powerful release of dopamine, such as amphetamines, are highly effective, but these are more difficult to handle. Although studies have shown a benefit in apathy, for example, in the context of apathy in Alzheimer's disease. You say that apathy can occur after deep brain stimulation in Parkinson's disease. This makes me wonder, can this post-operative apathy be reversed? Yes, provided we are talking about dopamine withdrawal apathy, which can occur with a considerable delay of several months or even years or so after surgery. And not talking about apathy in advanced PDE with severe diseasecutive syndrome or Parkinsonian dementia. So these are two different things. We have indeed performed a randomized controlled trial in withdrawal apathy occurring in the first year after surgery for Parkinson's disease using Piribenil, which is a D2, D3-stimulating dopamine agonist, and this has shown a significant benefit.

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