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They calculated projected clinical benefits including primary transmission, quality-adjusted life years saved, and mortality. They also calculated the cost of HIV care and PrEP as well as incremental cost-effectiveness ratios over the same 10-year period. They found that after calculating 10-year clinical outcomes, total primary transmissions were highest for no PrEP usage and lowest for the long-acting PrEP usage. The authors found that at a range of willingness-to-pay thresholds between $50,000 and $300,000 per quality, cabotagravir for PrEP among those with high risk for HIV would only provide good value for money if its annual price was less than $6,600 higher than generic oral PrEP. The authors conclude that long-acting cabotagravir would only provide a good value for the money if its annual price was less than generic oral PrEP, which is less than half of cabotagravir's current cost. According to the authors of the accompanying editorial from the State University of New York at Albany and Emory University, this analysis yields important findings about the economic aspects of long-term injectable PrEP and sets the groundwork for addressing pressing questions related to policy, programs, and social justice related to HIV management and prevention. Real-world evidence on inactivated COVID-19 vaccines against the Delta variant of SARS-CoV-2 is limited, leaving an important gap in the evidence base to inform immunization programs around the world. The last article I'll highlight in this podcast helps to fill this gap. To estimate inactivated vaccine effectiveness against the Delta variant, the authors of this article conducted a retrospective cohort study based on the first outbreak of this variant in mainland China that occurred in Guangdong between May and June 2021, and included 10,805 laboratory-confirmed adult cases and their close contacts. Participants were categorized as unvaccinated, partially vaccinated, meaning one dose, and fully vaccinated with two doses. Of these individuals, 1.3% developed infection, 1.2% developed symptomatic infections, 1.1% had pneumonia, and 0.2% developed severe illness. The researchers estimated that effectiveness of full vaccination against infection was 51.8%, against symptomatic infection was 60.4%, and against pneumonia was 78.4%. Most important, full vaccination was 100% effective against severe illness. By contrast, the effectiveness of partial vaccination was far lower, for example, only 11.6% effective against pneumonia. Further evidence that efforts must be made to ensure full vaccination of target populations. Also new is the latest Annals on Call podcast. This episode features a discussion of the risk of recurrent venous thromboembolism following subsegmental pulmonary embolism. And that brings us to the end of the February 1st Annals of Internal Medicine podcast. I hope I've piqued your interest in going to annals.org to take a closer look at some of the new articles I've mentioned. Stay well and please return in two weeks for more Annals Highlights. Thanks to Beth Jenkinson and Andrew Langman for their technical support.
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I'm Joan Stevenson, editor of JAMA's Medical News and Perspectives section. Today, this JAMA Evidence Podcast will focus on the process of diagnosis. Our guest expert is Dr. Gordon Guyatt. Dr. Guyatt, why don't you introduce yourself to our listeners? I'm a professor of medicine and of clinical epidemiology and biostatistics at McMaster University in Canada. I work clinically as a hospitalist and spend much of my time on research and education-related activities. Dr. Guyot, can you briefly describe the two complementary approaches to diagnosis? One approach can be termed pattern recognition. The clinician takes a history, looks the patient over, does a targeted physical examination, and the diagnosis is clear. So, for instance, a patient presents with a three-day history of pain associated with vesicles appearing in a particular dermatome and the lesions do not cross the midline, the diagnosis of herpes zoster is secure. On the other hand, patients may present with problems that are much more difficult to diagnose, in which case the clinician has to generate a differential diagnosis and estimate the probabilities associated with each item in that differential diagnosis and then undertake further testing to try and narrow the differential diagnosis and ultimately come to a definitive diagnosis. So, for instance, a patient presents with nonspecific fatigue, there will be many possible diagnoses that enter the physician's mind, and that requires a subsequent investigation where, as new information comes in, the probabilities change, and ultimately, hopefully, the clinician arrives at the right diagnosis. In many physicians' practices, the patient's diagnosis is usually self-evident. So how do we know when to go to the effort of making a formal diagnosis on probabilistic grounds? Well, my first comment would be to congratulate all those physicians in whom the patient's diagnosis is usually self-evident. These are clearly exceptional diagnosticians. However, if there was a suggestion that I would have to the situations when you're pretty sure, perhaps on pattern recognition basis, but not absolutely sure, and you don't know whether to start generating a differential with probabilities and further investigation, what I would suggest that clinicians do is look at the consequences of a mistake. So, for instance, let's say one has a middle-aged individual who presents with a 30-pound weight loss over the last six months, feeling very fatigued and generally unwell, and a physical examination reveals a hard, knobbly liver. Well, there's a very, very, very high likelihood that one is looking at a malignancy, either a primary in the liver or, more likely, a primary somewhere else that has spread to the liver. However, one would probably be making a mistake to announce to the patient at that moment that that is the diagnosis because the consequences of being wrong and telling someone they have cancer when they do not have cancer would be very unpleasant for both the patient and physician. And thus, in that situation, when the consequences of believing your pattern recognition are potentially damaging, it's probably worthwhile to adopt a probabilistic approach and conduct further investigation. How can a clinician estimate pre-test probabilities? Well, one way to do it is on the basis of past experience. So I'm a general internist, and when I get called to the emergency room to see a patient who is short of breath, I know that pneumonia and heart failure are at the top of the list. Chronic obstructive lung disease and asthma are high on the list, and pulmonary embolus is something that I have to think about but that is lower on the list. And it's simply seeing many, many patients that has led me to that way of thinking about pretest probabilities. However, we can all be misled by our experience. We are all subject to making inferences that may not be accurate. And another way to get at pretest probabilities is to use the literature. So studies that explicitly look at differential diagnosis, they take a patient presenting with syncope or presenting with headache or presenting with fatigue. They follow patients up with detailed investigations and sometimes long-term follow-up. And at the end, they say 20% of the patients had this diagnosis, 15% this diagnosis, and so on. So for instance, one of the things that I bear in mind when I'm seeing an older patient over 65 with anemia and I wonder about how likely it is that this is iron deficiency, my pre-test probability before other information is available will be around 35% because a study that was actually conducted in my own community found that of such individuals, 35% that is of older people presenting with anemia, 35% of them ended up having iron deficiency. Dr. Guy, would you please describe the concepts of test threshold and treatment threshold, and what determines these different thresholds? Well, one can think of any patient, their probability of having a particular condition. So a patient presents with dyspepsia, and depending on the nature of the presentation of the patient, it could be gastroesophageal reflux, it could be an ulcer, it could be a cancer, it could be nonspecific dyspepsia where investigation would not reveal a particular biologic explanation. So one has this pretest probability and one has to decide what to do. If the probability of a particular diagnosis is sufficiently low, below the test threshold as we say, one would not pursue that particular diagnosis. If the diagnosis is sufficiently clear, the probability is extremely high. Above the treatment threshold, we would not do any further testing and we would simply treat the patient. If the probability is between the test threshold and treatment threshold, then we would conduct further investigations. What determines these thresholds? Well, if the test is very invasive on the test threshold end, that will tend to raise the test threshold in that we are disinclined, we are less inclined to do tests that are very invasive, such as a pulmonary angiography. The other thing is the consequences of missing the particular diagnosis. And if the consequences are, if we miss the diagnosis, it would be a very bad thing. That will lower the test threshold. We have to be very sure before we conclude that the patient doesn't have the condition of interest. On the other hand, the same factors affect the treatment threshold, but differently. The more invasive the test, the more we will lower the treatment threshold and be ready to treat rather than test further because of the possible adverse consequences of the test. And the other thing is the consequences of a false positive. If we treated the patient, if the treatment is particularly toxic, that is going to raise the treatment threshold, we have to be very sure before we abandon further testing. What if I were a physician who sees patients intermittently and episodically over the years? How would I organize my practice so that I can take advantage of that fact in revisiting old diagnoses and making new ones in those patients and in others like them? Well, the big advantage to me of seeing patients repeatedly over years is that one understands their values and preferences well. And in terms of the test and treatment thresholds that I just described, the test and treatment thresholds are actually going to differ between patients. So consider the patient presenting with dyspepsia and the choice being whether to go and do an endoscopy or give the patient a trial of an anti-acid drug such as an H2 antagonist or a proton pump inhibitor. There may be some patients whose values are such that they definitely want to know what is going on. They are unsatisfied by the uncertainty that comes when you don't do an invasive test, and they are ready to undergo an endoscopy. There may be other patients for whom the endoscopy is much more aversive and who are much more ready to tolerate some uncertainty in whom a trial of an acid-suppressing intervention would be what would be best for those individuals. Is there anything else that JAMA-evidenced users should know about diagnosis? Well, potentially there's a lot that they could know. So within the User's Guide to the Medical Literature, there are chapters on differential diagnosis, which I alluded to in how one gets one's pre-test probabilities. There's a chapter on diagnostic tests, which deals with risk of bias in diagnostic tests. And there are chapters on advanced topics in diagnosis, including, and particularly most important, likelihood ratios, which are a very powerful way to interpret diagnostic test results, and clinical prediction rules, which are more and more available, and again are another tool for generating pretest probabilities. Also, JAMA users may be very interested in the rational clinical examination. All items of clinical examination are best conceptualized as diagnostic tests, and the rational clinical examination is extremely powerful in providing you with the evidence and guidance for how to use items of physical examination in making diagnoses or leading you toward diagnoses and delivering optimal patient care. Thank you, Dr. Guyatt, for this overview of the process of diagnosis. This has been Joan Stevenson of JAMA interviewing Dr. Gordon Guyatt about the process of diagnosis for JAMA evidence.
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The Radiology Review is pleased to offer the Board Exam Study Guide, Episodes 1-101, available for purchase as a book on Amazon or in Kindle version. Welcome to the Radiology Review Podcast, your on-the-go source for radiology education with your host, Dr. Matt Covington, a board-certified radiologist. Please follow the podcast on Twitter at RadRevPodcast. Send emails to theradiologyreview at gmail.com or visit the website theradiologyreview.com. Welcome back to the Radiology Review Podcast. This is an educational episode focusing on theranostics in nuclear medicine, and I will begin the episode with questions and answers that are general to theranostics in nuclear medicine. Afterwards, I will focus on questions and answers specific to lutetium dotatate therapy, for which the current trade name that is often used is lutathera. I then plan to release specific episodes on PSMA-based theranostics, and we will also go back to the original theranostic agent, radioactive iodine. Before I get into the questions and answers on this episode, I first want to read a portion of an email that I got titled, Thanks from Australian Residents. And this email was final board exams and the material you released, hours we spent driving with you in our ears, made all the difference. We're happy to say that many of us passed with the help of your teaching. We look forward to being ongoing listeners in the years to come. Keep up the amazing work in helping generations of trainees to prepare to succeed. Thank you so much, Daniel and Ray, for this message. One of the greatest privileges of this podcast is having a reach that extends well beyond my location in Salt Lake City, Utah, and provides an educational forum that allows future radiologists like you to prepare to succeed while you do things like commute, exercise, or do other things where a book or screen is not generally possible. I also want to remind listeners that there is a discount code section on my website, theradiologyreview.com, where you can frequently find discos for things like board preparation and educational resources in radiology. Without further ado, let's get into the questions and answers for this episode. First question, what is meant by the term theranostics. A theranostic agent generally means using a radioactive imaging agent and paired or identical therapeutic agent that both have uptake at the same molecular target, receptor, or process for use in both therapy and diagnostics. Therefore, the combination of therapy and diagnostics has been made theranostics. Next, what are some of the most common theranostic agents in clinical use? Perhaps the most established example of a theranostic agent is iodine-131. One can perform imaging on a gamma camera and treat thyroid disorders with iodine-131. Therefore, this is both a therapy and diagnostic agent, and therefore this is a theranostic agent. Agents such as iodine-131 allow you to first image to confirm if the intended target shows uptake and then confidently treat the patient with a therapeutic dose of iodine-131 with good assurance that the therapy will localize to the affected tissue since this was first confirmed on imaging. Thereafter, one can image post-therapy to confirm uptake in the intended target and thereafter image for surveillance of disease. All of this is provided with iodine-131, a theranostic agent. In this example, the gamma rays emitted by I-131 allow imaging, and the beta particle of I131 allows therapy. More recent theranostic agents are lutetium-177-dotatate, which is a therapeutic agent that has been paired with copper-64-dotatate or gallium-68-dotatate, both of which can be used in PET-CT imaging because copper-64 and gallium-68 are both positron emitting, and then the therapy can be provided with lutetium-177, which emits a beta particle. This theranostic pair can be used for various somatostatin positive malignancies to include various neuroendocrine tumors. Another example is lutetium-177-PSMA paired with F18 or gallium-68-PSMA, which can be used for the diagnosis and treatment of metastatic prostate cancer in certain scenarios. Next question. What radioactive particles are typically used in nuclear medicine therapies? Hopefully this is an easy answer to reach for you, and the answer I'm looking for is alpha and beta particles, both of which are used in most current nuclear medicine therapies. For example, I-131, Y-90, and lutetium-177 all use beta particles. Radium-223 and actinium-225, for which there is currently a lot of enthusiasm for new theranostic agents, are examples of current and emerging radionuclides that use alpha particles for therapy. Next, considering alpha and beta particles, which particle is larger? The answer I am looking for is definitely the alpha particle, which contains two protons and two neutrons and is therefore a helium nucleus. The alpha particle is larger than a beta particle, which for therapy purposes are electrons. Alpha particles are something like 8,000 times larger than beta particles. Next question. Which particle travels a greater distance in human soft tissues, alpha particles or beta particles? The answer is that beta particles travel a greater distance in soft tissue than alpha particles. Beta particles are smaller and highly energetic, allowing them to penetrate around 3 to 4 millimeters in human soft tissues. In comparison, the much larger alpha particle only travels something like 50 to 100 micrometers or 0.05 to 0.1 millimeter in human soft tissue. So the alpha particle is much larger and also travels a much, much shorter distance in human soft tissue than does a beta particle. One could ask themselves, which particle is superior for nuclear medicine therapies? The answer I have arrived at, for now at least, is it depends. Alpha particles undoubtedly cause more local damage and are more lethal in the local environment in which they deposit. The short traveling range also can limit off-target radiation exposure, which can spare things such as adjacent normal bone marrow or normal lung from radiation exposure. On the other hand, beta particles can travel further and in some instances this may be beneficial to kill a larger area of tumor than merely the region where the particle deposits, which could be particularly helpful for things like tumor heterogeneity, wherein part of a tumor may take in the particle and part of the tumor may not. Therapies based on beta particles in theory could kill portions of the tumor that does take in the beta particle as well as portions of adjacent tumor that does not. Therapies based on beta particles are also sometimes easier to produce. A final point, many nuclear medicine therapeutic agents deliver some dose to the bone marrow, as well as organs like the liver, kidneys, bladder, and possibly the colon as part of the excretion of the agent. Therefore, many therapies require adequate renal and liver function levels, adequate blood counts, such as white blood cell count, red blood cell count, hemoglobin, and platelet levels, as well as frequent urination and defecation during therapy to minimize toxicity that can result from the therapy. Now let's transition specifically into questions and answers on lutetium-177 dotatate. First, lutetium-177 dotatate can be used for treatment of certain somatostatin-positive neuroendocrine tumors. What are the most common sites of neuroendocrine tumors? Gastrointestinal sites are most common, and in order of gastrointestinal prevalence, it is the small intestine, followed by the rectum, followed by the colon, followed by pancreas, followed by appendix, and finally the stomach.
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And the gastrointestinal sites are most common in general, followed by the respiratory system. Note that five-year survival is higher for small intestine neuroendocrine tumors at about 70% compared to rectal neuroendocrine tumors at about 30% for 5-year survival. Next question. True or false? Lutetium-177-dotatate is considered a peptide receptor radionuclide therapy, and this is often abbreviated PRRT. The answer here is true. PRRTs, or peptide receptor radionuclide therapies, involve a radiopharmaceutical connected to a peptide that binds a specific receptor to selectively target and treat cancerous cells. As mentioned, lutetium-177-dotatate emits a beta particle, which is a high-energy electron, which kills tumor cells via free radical formation following receptor binding and internalization into the cell. Gamma rays are also released, which can be imaged using a gamma camera. Next, what receptor type does lutetium-177-dotatate bind to? Lutetium-177-dotatate is a radiolabeled somatostatin analog that binds to somatostatin receptors with highest affinity binding for somatostatin type 2 receptors. Next, what types of neuroendocrine tumors does lutetium-177-dotatate currently have approval to treat? Lutetium-177-dotatate is currently FDA-approved for treatment of somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors, which is often abbreviated GEP for gastroenteropancreatic, GEP-NETs for neuroendocrine tumors. Next, what is the typical dose and duration of treatment of lutetium-177 dotatate for gastroenteropancreatic neuroendocrine tumors? Currently, a fixed dose of a 200-millicurie intravenous infusion of lutetium-177-dotatate is given every eight weeks for a total of four doses. If toxicity develops, the interval may be extended to 16 weeks from every eight weeks between treatments in certain cases. The intention of this is to allow additional time between therapies for toxicities to resolve. Next, true or false, you can treat a patient with lutetium-177 dotatate while currently taking long-acting somatostatin analogs need to be discontinued for at least four weeks prior to initiating lutetium-177 dotatate therapy. Next, true or false? Short-acting somatostatin analogs must only be discontinued 24 hours prior to initiating lutetium-177-dotatate therapy? The answer here is true. Short-acting octreotide only needs to be discontinued at least 24 hours prior to initiating lutetium-177 dotatate therapy. Next, what is guidance for use of octre 24 hours after each lutetium-177 dotatate dose. However, octreotide LAR must not be administered within 4 weeks of each subsequent lutetium-177 dotatate dose. Remember that lutetium-177 dotatate is administered every eight weeks for a total of four doses. Short-acting octreotide may be administered for symptomatic relief during lutetium-177 dotatate therapy, but must be discontinued at least 24 hours before each lutetium-177 dotatate dose. After completion of all doses of lutetium-177 dotatate therapy, octreotide LAR may be given every four weeks until disease progression or for up to 18 months following treatment. Next, true or false, amino acid solutions are given prior to lutetium-177-dotatate infusions? The answer is true. An intravenous solution of amino acids containing L-arginine and L-lysine is given 30 minutes prior to lutetium-177-dotatate can both induce nausea and vomiting, so antiemetics are typically given prior to starting the amino acid infusion. Next, why are IV amino acids started 30 minutes prior and continued throughout and following lutetium-177-dotatate infusion. Lutetium-177-dotatate is renally excreted. The amino acid infusion is given to protect the kidneys from excessive radiation dose and lowers radiation dose to the kidneys by up to about 50% through reducing the tubular reabsorption of lutetium-177-dotatate. Next, what are potential treatment and management steps for cases of lutetium-177 extravasates, first stop the injection and remove the IV catheter. Keep the IV catheter and infusion materials, such as tubing, to allow measurement of residual activity to determine the absorbed dose. That was extravasated. Elevate the affected arm to accelerate dispersion and prevent stagnation in tissue. In certain cases, aspiration of extravasated fluid, a saline flush, application of a warm compress, or heating pad may be used to increase blood flow and promote dispersion of extravasated lutetium-177 dotatate. Finally, treat symptomatically for inflammation or pain. Next, what radioprotection measures are taken during lutetium-177 dotatate treatment? During administration of lutetium-177 dotatate, isolate the patient and ensure radiation emission limits to others are not exceeded during and following the lutetium-177 dotatate administration. This often requires initial isolation for something like four to five hours. Patients should stay well hydrated and urinate as often as possible in a designated hospital toilet that is appropriately isolated. The patient should not be discharged until it is deemed safe to leave the designated area or hospital, according to institutional or government policies. After leaving the hospital, a patient should continue to stay hydrated, urinate frequently, and defecate at least daily, using laxatives as needed. Close contact with others should be restricted per institutional radiation safety protocols. Prior to discharge, the nuclear medicine physician must outline radio protection rules to others. Next, what lab tests are typically monitored before and after lutetium-177 dotatate treatment? Lab tests that are typically monitored include kidney and liver function tests and a complete blood count before and every four weeks during treatment to be continued at least three months following the last infusion of lutetium-177 dotatate and every six months thereafter to assess for any potential delayed adverse reactions. Last and final question for this episode. If toxicity sufficient for dose modification occurs, how is this handled? General principles include first withholding lutetium-177 dotatate therapy and thereafter monitoring relevant labs every two weeks. If toxicity resolves within 16 weeks of the previous injection, lutetium-177 DotaTape therapy may be continued, though it would be continued at half dose. If dose-limiting toxicity recurs at half dose, treatment should cease. If the initial dose-limiting toxicity does not resolve after 16 weeks of the most recent prior injection, therapy should not be reinitiated. A few final points. A negative pregnancy test needs to be confirmed for individuals of childbearing potential prior to lutetium-177-dotatate administration. Patients should not breastfeed during lutetium-177-dotatate treatment and for something like two and a half months following the final treatment infusion. Effective birth control should be used during and for at least four months for males and seven months for females following the final infusion of lutetium-177 dotatate. During treatment, patients should be monitored for evidence of neuroendocrine tumor release, which includes symptoms like flushing, diarrhea, hypotension, and bronchoconstriction, and symptoms should be treated with fluids, corticosteroids, electrolytes, and possible intravenous somatostatin as clinically indicated. Patients also need to be monitored for evidence of hypersensitivity reactions, including anaphylaxis, during and for at least two hours after completion of infusion. If hematologic or other toxicity occurs, such as renal or hepatic toxicity, treatment may need to be withheld or restarted at a lower dose. Finally, as a special disclaimer, this information is for educational purposes only. Please refer to institutional guidelines, society guidelines, and the FDA label for any question on clinical use of lutetium-177 dotatate or other nuclear medicine therapies. Again, this information is for educational purposes only and is intended merely for board preparation purposes. That is enough for now. I hope this information is helpful for many of you. A free downloadable study guide on this topic is available at my website, theradiologyreview.com, so check that out. Also, remember to check out the discount code section of my website. While you are there, you may also want to check out articles of interest to radiologists and nuclear medicine professionals at the Radiology Review Insider with my most recent post on supplemental breast cancer screening, a topic for which I am deeply invested and which I feel is deeply important. So if you would like to learn more about supplemental breast cancer screening, check out my post at the Radiology Review Insider or listen to the podcast episode on supplemental breast cancer screening. Keep up the good work and study hard. Remember, you have to study really hard to succeed on radiology board exams.
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I will catch you on the next episode. Content of this podcast is provided for informal educational purposes only for radiology trainees and radiologists. Medical practitioners, please make your own independent assessment before suggesting a diagnosis or recommending any course of treatment. This podcast should not be used for self-diagnosis or self-treatment and is not a substitute for independent professional medical care. Please consult your own physician regarding any diagnosis, imaging interpretation, or course of treatment. What's better than listening to the Radiology Review? Nothing! Well, true. But you could buy our book, The Board Exam Study Guide, Episodes 1-101, available for purchase as a book on Amazon or in Kindle version.
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The Curbsiders podcast is for entertainment, education, and information purposes only, and the topics discussed should not be used solely to diagnose, treat, cure, or prevent any diseases or conditions. Furthermore, the views and statements expressed on this podcast are solely those of the host and should not be interpreted to reflect the official policy or position of any entity, aside from possibly cash, like moral hospital, and affiliate outreach programs, if indeed there are any. In fact, there are none. Pretty much, we are responsible if you screw up. You should always do your own homework and let us know when we're internists. So, Paul, good luck, buddy. No, thanks, man. Appreciate it. I am anticipating you're going to be doing this one, but really, I mean, you're the one with the bringing the framework for this one who chased down all the, you know, all the great reading that we were able to do before this. This is going to be a really fun episode. I mean, this is like the definition of high yield, Paul. This is, we see this all the time. And actually I thought this was like a pretty basic topic, but then like reading through it, it gets deep and there's a lot of really interesting stuff to dig into. I mean, I, you know, all respect owed to our former guests, but I think even without recording this one yet, this is probably our best episode. So I'm pretty, pretty excited for what's about to happen. This is like, this is going to be your equivalent of slam dunking and breaking the backboard. Is that? Yeah, for sure. Okay. For those who are not Paul Williams fans before, this is the one where I win them over. So get ready to get charmed. Okay, Paul. So I like this character that you play because in real life, you will rarely, if ever, say anything that's not extremely humble. And now you're calling your shot like Babe Ruth. It's going to fall apart pretty quick, I'm a doctor, I'm a doctor Thank you. Well, I do want to just say that I am not an expert on Udima, so I'm just here to play the fool and add in youthful references. So you guys are fully the experts on this. I like the implied insult there. That's strong work, Ben. We thank you in advance for the youthful references. Yes. Paul and I, our youth is long in the rearview mirror at this point. We're just on a freight train headed towards death. So with that. All right, Paul. So let's get into, actually, why don't we do some picks of the week? I really, I have a pick of the week, Paul, that I wanted to, my pick of the week is peppermint tea, Paul, which I'm drinking right now. I've never had it before. And a couple of movies recently mentioned peppermint tea. And I was like, I think I'm going to try that. But in all seriousness, Paul, I'm trying to think if I read any books lately that I would actually recommend to the audience. Uh, it's, I've been in a little bit of a dry spell book wise. So I I've read some things, but nothing, nothing pertinent. And, uh, Oh, I know what I want to recommend Paul Return of the Living Dead I watched it this weekend and it's it's a funny movie it is it is really the some of the biggest performances I've ever seen Paul it's not a subtle film no it's not not a subtle film really tight 90 minutes maybe maybe 93 minutes, just really wacky stuff, ends with a bang, literally. Yeah, check it out, Return of the Living Dead. I believe it was filmed in 1985. I was three years old, which is why I've never seen it before now. I feel like that was a staple of my youth, I think. So make some peppermint tea, watch Return of the Living Dead, and just think about Paul's punk rock youth, as he said to me when I told him I was watching it. So Beth, you want to give a pick of the week? I do have a pick of the week. And usually I wait to recommend a book. I want to finish it before I recommend it. So this one, I'm actually only halfway through, but I think it's pretty fun. So I'm going to recommend it anyway. It's The Medical Detectives by, and I'm sure I'm going to mispronounce his name, Bertrand Ruach, or Ruach, or something French that I can't pronounce. It's a kind of collection of his essays where he wrote about medical mysteries in the mid-century era. And it's just a really interesting little time capsule of medicine at that time. It's kind of like the big hits of internal medicine, like med ed things that we learn about. Like there's a trichinosis case and there's anthrax and there's all kinds of other schistosomiasis. That one had a really horrific treatment. Some of this I'm like, oh gosh, like you hear about these historic treatments. They gave him potassium antimony tartrate, which sounds horrible. It apparently made him throw up at some point. And yeah, it makes me very happy that we've progressed a little bit, but recommend it for a little bit of a time capsule. Sounds fantastic. And of course, we're going to want to pick from Paul before we get into the main topic. This one might not be so earth shattering. Now that we're not a monoculture and everyone's interests are so niche, I don't know if everyone's aware of royal blood or not as a band and this might be a little bit of a late recommendation but royal blood they're an english group it's a twosome it's a bass player and a drummer out of england and the the bass player uses like effects pedals and loops and studio chicanery to sort of cause this wall of sound they're great they put out a couple of good albums but their most recent one typhoons, came out earlier this year. And they are mostly straight ahead rock, but this most recent album actually is a little bit dancier, which I'm kind of liking. The guy has perfect pitch. The instrumentation is fantastic. The drummer is a human metronome. And then you throw in some disco and some falsetto, and I'm actually fairly happy. So if that sounds vaguely appealing to you, I would recommend the Royal Blood album, Typhoons, which out, I want to say in March or April, I think of this year. Paul, between you and Elena, I'm building up a list of things that I have to check out on Spotify so that I can become much cooler in my musical tastes. But this one, I think I would like. I think you would like this one. Yeah. And their first album for sure. But I think if, yeah, I think you'd probably enjoy all their stuff actually from your official postage right from your computer. That way you can spend more time running your business and less time running to the post office. Did you know that stamps.com has been around for more than 20 years now and they've helped over 1 million small businesses? And let me tell you why. That's because stamps.com gives you access to all the post office and UPS shipping services that you're going to need right from your home computer, and you don't even need any special equipment. All you need is a computer and a standard printer. With Stamps.com, you can get discounts that aren't available anywhere else, like up to 40% off USPS rates and 76% off UPS rates. Whether you're running an office that sends invoices or maybe you have a side hustle like the curbsiders and once in a while you have to send things to your listeners or your customers, well, Stamps.com has you covered and you can be up and running in minutes. As I told you, you don't need special equipment. Save time and money this year with stamps.com and sign up with promo code curb for a special offer that includes a four-week trial, free postage, and a digital scale with no long-term commitments or contracts. Just go to stamps.com, click the microphone at the top of the page, and enter code curb. This podcast is sponsored by BetterHelp Online Therapy. You know, we talk about BetterHelp a lot on this show. And this month, we're discussing some of the stigmas around mental health. Because as I've mentioned before, I've been a customer of BetterHelp for long before they were even a sponsor on the show.
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At this point, I am ready to talk about it on a podcast that is listened to internationally, which is good. So I've made some progress and I've come to look at therapy as a tool that we should be utilizing before things get worse so that we can avoid those lows. What's great about BetterHelp is that it's customized online therapy that offers video, phone, and even live chat sessions with your therapist. So you don't have to see anyone on camera if you don't want to. And it's much more affordable than in-person therapy and you can be matched with a therapist in under 48 hours. Give it a try and see why over 2 million people have used BetterHelp Online Therapy. This podcast is sponsored by BetterHelp and Curbsiders listeners get 10% off their first month at betterhelp.com slash curb. That's B-E-T-T-E-R-H-E-L-P dot com slash curb. All right. So with that, Beth, will you take us to a case from Cashlack Memorial, which almost certainly has a clever name. Yes. And this is one of my recent favorites, I have to say. Lynn Fadima. Lynn Fadima. Great last name. Ms. Fadima, yes, is a 50-year-old female with a past medical history of type 2 diabetes complicated by peripheral neuropathy, chronic low back pain, hypertension, and obesity. And she's here in your clinic to establish care. Her primary concern is lower extremity swelling. It's been ongoing for years, but it seems like it's worse now. She's reporting that she can't really wear the shoes she likes anymore. You know, she can't wear pretty shoes because of this. Her legs are feeling tight and uncomfortable, and she wants to know what you think is going on with her legs. So, Dr. Paul Williams, expert guest, please take us through what's the pathophysiology here? It's probably a helpful way to actually figure out how we can actually help poor Ms. Fadima. Maybe one of the names I'm most ashamed of writing in my history with curbsiders. But I think a good way to think about things that actually cause edema. So when you think about edema in general, basically your body's waging a war. There's hydrostatic pressure. So everything's trying to force stuff out of the vessels. And then you have oncotic pressure trying to sort of suck everything back in. And there's this delicate balance there. And happily for homeostasis, most of the time things are where they belong and the fluid is in the vessels and not just kind of floating around the interstitium where it does not belong. And that's when you have excess flow of the interstitium, that is by and large edema. And we'll sort of get into the very specific causes of it. So anytime I'm looking at someone with edema, there's something that has caused imbalance. And I think it's helpful to probably break it up mechanistically what we think is happening here. So is there an increase in the hydrostatic pressure? And usually I think about that in terms of is there venous hypertension? So is there something that's causing the pressures within the vessel to be higher? And lots and lots and lots of stuff can do that. Most of the stuff that you think of right out the gate, but classically right-sided heart failure, I think you can see that with, or even venous insufficiency, but something that's causing the pressure in the veins to be higher than it should be. And then it pushes out the fluid and the fluid just doesn't make its way back in. I think another mechanism to think about is endoluminal obstruction, which is another way that you can actually cause venous hypertension. So really, these two are related. So if you have something blocking the lumen of the vessel, impeding venous return, and whether that thing is a clot or extrinsic compression, like a popliteal cyst or a tumor or even pregnancy, something's keeping the venous return from happening the way that it's supposed to. So again, this results in venous hypertension. So you're just seeing the fluids not going where they want to be. And then I think lastly, the other side of this is the oncotic pressure component. And again, I think we all know this stuff, but we may not think about it. When we see some with oral extremity edema, we may just kind of knee-jerk, start for osom osomite, which we'll talk to. But things that would cause decreased oncotic pressure are things that cause your lower protein state. So nephrotic syndrome, classically, someone who has protein energy malnutrition, certainly you can see decreased oncotic pressure because lower albumin, liver failure because of the decreased synthesis. So all those things can lead to a lower oncotic pressure. So as opposed to the increased hydrostatic pressure or the fluids being pushed out, you just don't have the stuff that you need in the vessel to suck the fluid back in. So that's my very basic way of thinking about it. And then I think probably a third thing as I'm thinking about it is just leaky capillaries. And probably the prototypic example would be burns can do that and just cause inflammation. But anything that would cause inflammation at a local site, whether it be infection, would cause a little bit of vasodilation, things become a little bit more permeable. I think we've all seen, I'm talking too much now, but we've all seen dependent edema in the summertime. The patient comes in, it's August, it's hot outside, and they're like, my legs are swelling up. And I think that's in part because you're seeing increased vasodilation from the warmer weather. Things are a little bit leakier, and as a result, you end up with edema. So that's my basic breakdown of how I start to think about things mechanistically. High pressures, like high hydrostatic pressures from various reasons or low oncotic pressures or this leaky capillaries. I do think there's like take cirrhosis. I think they have a little bit of both going on. For sure. So I think it's, they're not going to always cleanly fit into one bucket. And that was one of the big take-homes was that from some of these review articles, they're like, often patients have more than one reason to have edema. Right. Yeah, exactly. And there's the other component is interstitial pressure, right? Like, so the thing that's kind of also helping to keep fluid in the vessels, but you just typically don't see changes in that so much. So maybe with inflammation, you might see it. And I think we can talk about the Cardi B tweet, which I love. So, you know, decreased cabin pressure could also indirectly cause decreased interstitial pressure. But that's not one that we think of as much from a mechanistic standpoint. So this Cardi B tweet, Paul, you kind of glossed over it, but basically she's tweeting out a picture of her swollen feet and ankles after a plane flight. And how exactly does the physiology work there? Yeah, no, thanks so much for asking. I had to actually redact some portions of the tweet because this is a family program after all. But Cardi B says, look how small my feet get every time I take flights. My stomach even gets more puffy. And then she goes on to say why she skipped a show and then she was angry that some people accused her. So anyway, you don't have to look into it. But I love this as an example and the fact that she includes it because it has a lot of the underlying pathophysiology that might cause edema. So think about all the things that you need to actually allow venous return to happen. So part of that is the activity of your muscles, right? Like the venous is a passive system. Like all you've got are valves in place. So you need the muscles contracting to actually kind of work the venous circulation back where it belongs. And when you're on those long flights, your calf muscles aren't working. You just, you don't, you don't get that. So as you're sitting for long periods of time, you're not, you're not contracting the muscles. And as a result, you have venous stasis. So that's one. Two is just, Cardi B probably has a much nicer airplane seat than you or I are used to, but I would still, you're sitting and you actually have extrinsic compression of the venous return, right?
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You have extrinsic compression, you're causing venous hypertension. Reason number two, why poor Cardi B is experiencing edema. And then reason number three, and I think this is true, I've not been able to find papers to back me up on this, but you're in the air, you have lower cabin pressure. I think everyone's feet get a little bit swollen. Like I feel like I know even I get kind of achy just sort of being up there, even if I'm trying to make a conscious effort to sort of contract and walk around. And it still, things just kind of hurt. And I think that's because the cabin pressure is lower when you're actually at altitude. And as a result, this is one of the rare instances where it's almost your interstitial pressure is a little bit less. And so as a result, things are a little bit leakier and you get a little bit of puffiness that way. So I think she has three good pathophysiologic reasons to have edema just because she's flying around. So it's a pity Cardi B. I hope that she feels better, but I appreciate her tweet because it helped make a couple of teaching points. I love it, Paul. This is the kind of thing you get in a Paul Williams. If you hear a Paul Williams talk, he will include some really well-crafted slides with clever teaching points like that. So Paul, this is, so Ms. Fad a little bit before we started recording, but I think it be keying you in on what the diagnosis might be here? chronic edema and chronic bilateral edema specifically. And I think that, unfortunately, that gives us the broadest possible differential. It'd be for better or for worse if she came in with a hot, red, angry leg, which we'll talk about later on. That would probably narrow things down a lot. But it still gives us a differential to work with. In terms of who this patient is, she's over the age of 50. And right away, for me, that makes me think more about chronic venous insufficiency because that is just a disease that becomes more prevalent the older that you get. And so you asked, so actually, let me flip it to you, Matt. So when you, because I feel like we see this a lot. So when you see someone that you suspect might have chronic lower extremity edema, like what kind of questions are you asking them and how are you differentiating that from the other sort of more actionable causes? Well, like you, I definitely, acute versus chronic is the first step because if it's acute, you really have to go down the DVT pathway, which we can talk about later. But for chronic edema, I do. One of the simple questions is like just asking them, does it get better overnight? You know, when they tend to be recumbent, as long as they're not sleeping in a recliner, when they're recumbent, if it's better in the morning, you know, that's much less worrisome. That would make me think this is like dependent edema or something related to venous insufficiency versus if it doesn't, then something like a lymphedema that doesn't change throughout the day. So I find that helpful. And then whether or not it's painful because certain conditions are painful and certain conditions are not. So those are useful things to know. Of course, as an internist, someone who almost became a geriatrician, I love blaming medications for things. So I also will commonly look at the medications. She has hypertension. So you know, we're going to talk about calcium channel blockers, and she's got chronic back pain and neuropathy. So you know, we're going to want to know if she's on gabapentinoids ball. And those are some of the things. And then like just kind of trying to think like, do I think she has cardiopulmonary disease or do I think she has cirrhosis? Those would be some of the big ones in if she's still having menstruation, you could ask about that as well. What am I missing? What other things are you going to ask about? No, you're doing great. And I think that the organ systems that we think about primarily when we worry about scary causes of edema are cardiac, nephrogenic, and hepatic. I think those are kind of the three biggies, and we can talk about the workup. But I think the cardiac is the one that you can't miss. So your usual, you can't miss any of them, or at least you shouldn't. So you ask about your symptoms of heart failure. Is the patient having orthopnea? Are they having proxismal nocturnal dyspnea? Like, do they have progressive dyspnea on exertion? All those things. Like, I think you have to ask those questions, even if you don't have high suspicion. It would be embarrassing to miss someone who has no onset heart failure. And that's the patient where you might get the echo. You know, this is a patient we mentioned in her medical history that she has a history of obesity. And that can, in and of itself, predispose you to chronic venous insufficiency. You can have actually external compression just from abdominal pannus sometimes. But then also, you think about other comorbidities. This is someone who has a risk for diastolic dysfunction, impossible HFPEF. This is someone who may even potentially have risk for perhaps undiagnosed obstructive sleep apnea. So other historical things that you might ask about are, you might do your might do your stop bang. So, you know, are you snoring? Do you have daytime somnolence? Would all be reasonable questions to ask because it's actually a pretty common cause of lower extremity edema is undertreated or undiagnosed OSA. And then I think other stuff, you know, in terms of historical context, because I'm not sure we're going to talk about this elsewhere, like this is a patient who has a background of diabetes, and we don't know what medications she's on, but some of them might contribute. But if you worry about something like nephrotic syndrome, like you could ask about, and I'm Dr. Joel Toft, told us that the way he asked about foamy urine is it doesn't go down on one flush, which I thought was hilarious because, you know, like there's bubbles. When people urinate, there's some bubbles in the water, but he's like, it's so foamy that sometimes it doesn't all go down in one flush, which is hopefully something I will never experience personally, Paul. So I think that's- If you would, I hope that you would do us and our listeners a favor and report back. Like, I just, I think you owe it to our audience. I'll live tweet it, Paul, if you're not- Can you make a TikTok video of the flush? That's a great idea. Yeah. Beautiful. With like a Doja Cat song in the background. That's perfect. Yeah. Okay. So we talked about, does it improve overnight? Is it painful? Drugs, systemic diseases like heart, liver, kidney. We talked about sleep apnea, pulmonary hypertension. We talked about potentially tying it to menstruation. And then the one thing I guess we missed was like history of malignancy or trauma, especially I would think of that if this was a unilateral, but you know, you could think of that still because you can get bilateral compression if they have an abdominal pelvic malignancy. For sure. Or take, for instance, someone who has, and again, you can, I'm always good at spitballing worst case scenarios, but if someone has an IVC filter that is clotted off, certainly like that, you could get bilateral edema from that. So you can't rule out DVT just because it's bilateral, for sure. But now we're sort of in zebra land. I think the one statistic that I think is useful is that 30% of the adult population has a diagnosis of venous insufficiency. 1% has heart failure. So just remember, common things being common. One of the reasons to not do the shotgun, everyone gets an echocardiogram and a 24-hour urine protein is because you can get lower extremity edema because about a third of the population does just because of venous insufficiency. So again, I think if there's any takeaway point from the entire episode, it's going to be sort of be thoughtful and deliberate about how you're working this up and how you're treating it.
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I think my workup would probably be different if this was a 30-year-old patient with minimal past medical history as opposed to Ms. Fadima, Yeah. I would hope that you do a good JVD examination. I hope that you would look for the lateral displaced PMI and so forth and so on. You're going to look at the legs. That's always a great place to start. I think there's a lot of hay made about pitting versus non-pitting edema, or at least we report it. So maybe actually, so since I'm talking probably a little bit over much, Matt, so how do you conceptually, what's the difference and how does that help us? Is that something that you worry too much about? Yeah, I think I put a little bit of stock in it. Certainly, some conditions are non-pitting, and some of those are like lymphedema versus chronic venous insufficiency or heart failure. I think chronic venous insufficiency and heart failure are more likely to have some pitting components to them. Lymphedema can have pitting early on, but once it's more sort of fully out there, lymphedema and another condition that looks similar to it, lipedema, neither one of those is pitting once they're kind of fully formed. So I think it's useful in that setting. The thyroid, the changes that go along with thyroid disorder are fortunately rare for the patient. So I'm not sure that I've confidently seen that in my career. You've not seen pre-tibial myxedema? Yeah. One thing that I would just comment on with the exam, I've just noticed if you take care of geriatric patients and you're feeling for edema, if you just gently press enough that you blanch your thumbnail and hold for five seconds, it's not painful for the patient in most cases, and you can still check for pitting. But when I see people just go in there, they just mash as hard as they can on the shins. And some of these patients, it can be painful. It's painful, yes. Or they're on blood thinners and they're going to get bruising from it. So please be kind to your patient when you're testing for edema. But I would pay attention to pitting edema over the shins. And then I would also check on the tops of the feet. And then, Paul, you'll tell us a little bit about stemmer sign as well, you know, if we're thinking about lymphedema as a cause, because that can help differentiate between like a chronic venous insufficiency and something like lymphedema. But that's how I check for edema. Probably something I should have mentioned up top is another cause of edema, as you mentioned, is that you don't have the lymphatic return in lymphedema. There's some reason for it most of the time. You can have idiopathic lymphedema and there's classifications for that. But more often than not, there's a secondary cause that is something is impeding lymphatic return. And that can be radiation or it can be extrinsic compression or it can be tumor or it can be surgical disruption. There's lots and lots of stuff that can do it. And lymphedema behaves a little bit differently in part because there are chronic changes over time that you don't see with just the venous hypertension edema. So like you, lymphedema, you actually leak proteins as well. And as a result, there's sort of chronic inflammation and underlying fibrosis. And as a result, the skin and the tissue underneath becomes thicker as opposed to just sort of swollen with fluid, which is one of the ways that you can actually differentiate. So you can use that to your advantage to figure out what's happening. And lymphedema, and maybe we can even talk a little bit about management after this, but lymphedema, you can assess for it by looking for something called stemmer sign, which is a fun little trick where basically you just try to pinch the skin at the base of the toes. If you can grab it, if you can actually pinch and pull up, then you're probably dealing with a good old-fashioned bread-and-butter edema as opposed to lymphedema where you can't actually get a hold of the skin to pull it up because you can't tent it because the skin itself is sort of fibrotic and thickened from these chronic changes over time. And that's called Stemmer's sign. So impress your million-year-old attendings by doing that on the next toe that you see and they'll love you forever. The rest of the examination, not the rest, but I think a lot of the examination basically has to do with figuring out what might actually be causing underlying edema. If it's not dependent on edema, if it's dependent on edema just sort of being the edema that happens if you let your legs hang down for a long two-period time, or if it's not chronic venous insufficiency, what else could it be? And I think that's where the physical examination is most helpful. I think poking and prodding at the legs, other than trying to differentiate between lymphedema and chronic venous insufficiency may not be super duper helpful, but I think most of the exams should be focused on underlying etiology is kind of how I think about it. As you develop your differential, that should define your examination. We should not be doing the same exam on every single patient. But I just want to define for our listeners also, or at least talk about briefly, is the lipedema, which is not a term that I had known much about or thought much about. And I think that we've all seen this. And this is basically pathologic accumulation of adipose tissue in the lower extremities, and sometimes the upper extremities too. What's characteristic about this is the feet are spared. So you see relatively skinny feet, but then you see a lot of adiposity coming up both the extremities. I think that I've seen a ton of this and just didn't have the language to describe it. And this is a fairly good mimic of edema, and it's not. It's actually adipose tissue. So I think just being aware that this exists and kind of being mindful of it and sort of knowing your terms is probably helpful when you're examining the patient. And I think, truth be told, these patients will not be presenting with a complaint of swelling of lower extremities. Like this is not going to be a change in anything for them. But I think it's just something to be mindful of as you're doing your physical examination. Let's talk about the workup here. So let me give you a little bit more of the history that we get from Ms. Fadima. So she reports that her legs have been like this for years. She doesn't have symptoms of heart failure. She doesn't snore. She's somewhat ambivalent about daytime somnolence, which I think that's pretty common when you're suspecting sleep apnea and the patient isn't really giving you anything, but you're still want to suspect it just because it's so common. But you're kind of sleepy, aren't you? I mean, as you're nodding aggressively asking. You're asking leading questions. So she says, yeah, maybe my legs improve with elevation. She does notice that they're worse at the end of the day. And delving further into the history, Paul, it's getting interesting. She takes metforminin piaglitazone for her diabetes the latter was maybe supposed to help her liver paul amlodipine 10 milligrams for her high blood pressure gabapentin 300 milligrams three times a day for her neuropathy probably for her chronic back pain too right paul i'm sure yeah trying true and naproxen 500 milligrams twice a day for her low back pain. She does note that she sometimes takes an extra dose when it really bothers her. Now, Paul, I'm going to ask you a question, which this is the thing where I say something that's totally wrong and you correct me. So, Paul. This is my favorite rhetorical device. Great. So, Paul, none of these medications are a problem for her edema. Am I correct? Unfortunately, Matt, that is incorrect. And in fact, her medication list is just an absolute nightmare if you're trying to tease out what a potential cause of lower-issue edema might be. So whoever wrote this case is an absolute monster. That was you, I believe. Yeah. She also just finished a dose of steroids for a cold two weeks ago. Oh, yes. I forgot about that. Right. Because Paul's- Also, her chemotherapy. Yeah. I forgot about that.
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Yeah. Yeah, Z-Pak and a prednisone taper. Yeah, absolutely. Okay. Better safe than sorry, especially in your diabetic patients. You really want to make sure you load them up with steroids to calm down that inflammation. All right. Yeah. So her medication list, I'm not saying it's bad. I'm just saying that there's a lot of potential culprits when we're talking about someone who has lower extremity edema. So the glitazones, we don't see too, too much. But I think there is some people think they might be helpful for the metabolic associated fatty liver disease. So not uncommon. But unfortunately, they do cause or can cause fluid retention. So possibly a cause of etiology. Let's talk about the naproxen next. All the NSAIDs can, again, cause you to hang on to excess fluid. So certainly, possibly, we could blame them. Also, maybe, who knows? Let's be mean. They're giving her renal failure. Why not? I think the amlodipine is the one that I think we all feel comfortable. Like if you asked any resident about what blood pressure medication might cause artemis edema, like they all know amlodipine and it does tend to be dose dependent. It does tend to be worse in older patients than younger patients. So for someone, you can get away with the lower doses, but as you crank up the doses, you're more likely to have this lower artemis edema. Do you remember how that works, Matt? Not to put you on the spot. Yeah, I do. I do. So it is a vasodilator. And so you're basically causing almost like causing increased pressure in the capillary. So more fluid leaks out. That's my understanding of it. So if the afferent is dilated, puts more fluid into the capillaries and it leaks out. So one of the mechanisms that I believe the great Tony Brew was recommending in his tutorial is that if you give something that dilates the efferent arteriole, then you can kind of keep the pressure lower in the capillaries and maybe mitigate this problem. So that would be something like an ACE inhibitor or an angiotensin receptor blocker. And those could potentially be paired with these more so than what often happens, Paul, is giving diuretics for this condition. You're so smart, Matt. That was magnificent. Yeah, exactly. It's pre-capillary arterial or dilation, but it doesn't actually do anything to the venules. So exactly right. So you have this increased flow. The veins don't have the capacity to kind of suck it back up. And as a result, you have the edema. Exactly right. And this is not a sodium problem. Like it's not even really a volume problem. So things like diuretics are not going to really fix it at all. So mechanistically, they just don't make sense. And I think anecdotally, in my own experience, I've seen people try this and I've not seen it work too. So the medication that seems to make a difference are your ACEs or your ARBs because they also cause post-capillary dilation. And as a result, you sort of mitigate the problem to some extent is my understanding of things. So with the rest of her meds here, I mean, it's going to be hard, right? Because she has chronic pain from two different sources. She has neuropathy. She has chronic back pain. And what about the gabapentin? We mentioned the NSAIDs. So NSAIDs, and I believe it's actually through a sodium retention, the NSAIDs can cause some edema. But what about the gabapentinoids? And are those a problem? This is not something that I was commonly taught. But recently, I think we saw this on Twitter, a bunch of people were talking about this. And of course, all the review articles mention it as well. Yeah. And I've seen this in actually clinical practice slightly before the Twitter buzz and far before this episode. But yeah, I've seen the gabapentinoids unfortunately also can cause large-shrimpy edema. Again, they are dose-dependent. And again, your older patients are going to be more prone to that side effect than your younger patients. So it's just something to be aware of. In my own practice at CashLack North Northeast, I fixed someone's edema just by stopping their pregabalin. Like they've been on pregabalin for chronic pain, probably not entirely appropriately, happily not prescribed by me, but I was like, please stop taking that, and her edema got better. And because it wasn't treating her pain anyway, that was kind of a moot point. So just, yeah, I think it's an important one to be mindful of because like you, I was not, I don't think taught that in my trainings, and I think it's probably more common than we recognize. I hate food waste, so I love this product. Here's how it works. They are a grocery delivery service offering an entire line of sustainable groceries that taste delicious and reduce waste just by embracing the natural imperfections in food. 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Join the movement at imperfectfoods.com and use the code curb. Hey listeners, it's time to get excited because guess what? ACP's internal medicine meeting 2022 is taking place in Chicago, Illinois in person from April 28th to April 30th, 2022. It is going to be fantastic. We'll be there in person. That's right. You can hug Paul. Hashtag hug Paul. Come on, get it trending, people. Our team will be choosing from more than 200 scientific and practice-related sessions. There's also hands-on activities in the Clinical Skills Center. There's workshops, two keynote speakers, StorySlam, and the in-person exhibit hall and networking events. We'll be there. We'll be recording. We'll be mixing it up. Come and find us. Hug Paul. Grab some CME and mock credit. There's tons of opportunities for live question and answer with their expert faculty. And with registration, you get a couple different options. With the standard registration, you get 30 days post-meeting on-demand virtual access, or you can choose premium access and keep that for up to one year post-meeting access. So you can go through all these scientific sessions because as I've said before, you might be overwhelmed by how much great content there is, so you're going to want that extended access so you can get to everything. And let's say you're making a mistake and you're not going to go live. Well, virtual access is also available for select live stream and recorded sessions, so check that out on the site. For early bird discount, register before January 31st and use the code IM22CURB. Visit annualmeeting.acponline.org to learn more. That's annualmeeting.acponline.org to learn more and use the code IM22CURB when you register. So Paul, we've been talking about the medications here, and I just wanted to throw you a little bit of a curveball in the history. So we're kind of leaning in, okay, maybe this is medication-induced right now, but let's say Ms. Fadima, what if she had bilateral, circumferential erythema and edema of the lower extremities? Most certainly, and again, I'm going to use this device, which I find very helpful. Almost certainly, this is bilateral cellulitis, which I believe is very common. Is that true? Yeah, no, it's all of that other than your description was incorrect.
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Yeah, no, I think we've made this point a bunch of times on the show. But with chronic venous insufficiency, it's a spectrum, right? So you can have someone who comes in with swelling of the legs that's cyclic and maybe worse in the summertime and it bothers them. And you try to talk them into compression stockings, which are awful, but we'll get into it. And that's really the worst of it. But then you also have the more severe end of the spectrum where you have chronic venous stasis changes. You can see changes in the skin itself. You can have stasis dermatitis where the legs become kind of red and shiny and kind of hot and even look a little bit like they're either infected or like a DVT, but it's bilateral and kind of there all the time. And certainly, I think we've all seen super infection with that because you're also prone to ulceration. I think if you're not careful and if someone who say, for instance, has a background of diabetes neuropathy, who maybe starts with a foot infection that then ascends, like there's lots of ways this can go south, but typically not bilaterally. It's not impossible, but it's also not the most likely thing. So I think the two points to be made here is bilateral cellulitis is very uncommon. And then what is unfortunately common is to have bilateral skin changes that just look sort of chronically inflamed and red and angry. And I'm not sure, Matt, do you have any tips or tricks for differentiating between an infected leg and sort of a chronic venous stasis changes? Like how do you approach that? Because I feel like we see this all the time where the patients, maybe the leg looks worse, but it's hard to tell. It is hard to tell. I think if it's very symmetric bilateral, especially if it's non-tender, but it's just warm and red and they have this chronic swelling, then I'm not, you know, if it's not tender and it's just warm, red, swollen, and it's chronic, I'm much less concerned. And I'm more going to try to decongest them, you know, use some compression therapy, maybe some topical steroid for inflammation that's going on. These are things that I would anecdotally do that I believe do work and just kind of counsel them. We're going to get into the treatment in a minute here, but that's how I would approach it. If you look at the medial malleolus area, that patients tend to form ulcers or tend to have like pigmentation changes there. You know, that's an area where, again, I would think that makes me think venous insufficiency if I see hyperpigmentation or ulceration in the medial malleolus, that's really keying me in on that as the diagnosis. We should probably get into a little bit of like what might the treatment be for her right away. I think you could tell her the treatment for that. And then we can talk about maybe if this was a chronic venous insufficiency or if this was a lymphedema, how it might be different. So what would you do for her? For her, I mean, I would stop the medications that I could is probably the first thing that would look like. So I would probably try to decrease her dose of amlodipine because I just feel like we see that one so often as a corporate medication. And it's worth noting, and I think this is even in Tony's tutorial as well, like it can augment the changes that you see that are seasonal. So in the warmer weather, you might actually see even more edema if someone is on a calcium channel blocker. So it may just make preexisting stuff worse. So I think it's worth probably scaling back that and trying a different agent or an additional agent if you can. And stop the NSAIDs, go to topical, because as I think we're finding out, they're just better for everything anyway. And if you can get away from the gabapentin, great, but you may not be able to, and that's okay. The other thing, you'd mentioned compression, and it's probably worth mentioning that even if she was having recurrent infections from her chronic venous stasis, actually, the recent landmark trial that showed compression is probably our best bet in terms of preventing that from happening. But then it's also the thing that's going to help the most in terms of relieving symptoms. So I would advise poor Ms. Fadima to elevate as much as possible. I would probably order compression stockings. These are usually the way that you order these. They have different levels of pressure depending on what condition you're trying to treat. So for venous insufficiency, you want 30 to 40 millimeters of mercury at the ankle. And then the other caveat is if you think there's arterial insufficiency, so if you're worried for any arterial disease, don't go compressing. That's a bad idea. But for venous insufficiency, you want the 30 to 40 at a level that the patient will tolerate. And then we talked before, I would personally not start a diuretic for this patient, at least not empirically, in the absence of any kind of volume overload from heart disease or renal failure or anything like that, because I just don't think mechanistically doesn't make sense. There's no evidence for it. And I think you just increase the risk of things like electrolyte abnormalities without any real benefit. Yeah. I think part of the other counseling, weight loss would help in many cases. It could help with the edema. As we mentioned, the calf is the peripheral heart of the leg. So the muscle pump from exercise can help even if they're just doing exercises in, even if they're wheelchair bound doing exercises or not very mobile, they could try some of these exercises. So those are some of the things. And then just telling them it's probably going to be worse when it's hot out. If you eat a giant sodium load, it might worsen your edema. Just kind of giving some of that expectation counseling. And then Paul, as always telling them, like, I don't think this is cancer. I don't think you're going to die from this. You know, that's often useful. That's a lot of the times that's what patients want to hear when they have this. But what workup might you do? Let's say we stop the meds, but the edema is still there, Paul. And now you're thinking you're not as sure of the diagnosis. Maybe this could be chronic venous insufficiency. Are there labs or imaging studies that you might get for her at this, maybe not at the first visit because we thought we had such a slam dunk reason, and she wasn't giving us any worrisome symptoms? What labs might you do or imaging? Yeah, I will say I'm not going to be able to give you a straightforward algorithm, and obviously you have to look at the the patient in front of you. And I think we alluded to this earlier, because Ms. Fadima is a little bit older and multi-morbid, I would probably be a little bit more aggressive and a little bit earlier with my workup than I would with somebody else. So I think for her, given the fact that she has her underlying diabetes, I probably would check a protein creatinine ratio in her urine and make sure that she's not spilling and it's not nephrotic syndrome, even though we're not seeing the periorbital edema. And see also another excellent tutorial by Tony Brew. I would check a TSH just because one of these days maybe it'll actually help me make the diagnosis of lower extremity edema. But it's because you're supposed to. But I don't think it's terribly high yield. I think higher yield is probably a comprehensive metabolic panel is probably my go-to. And this is personal practice. This is not any guideline driven stuff, by the way, but I feel like that would help give you an albumin. So if their albumin comes back and I have patients like this, if it comes back at 1.3 and say they're a post bariatric surgery patient, that points you down a different pathway. It would also give you a sense of their renal function as well, because it's going to give you either being on the creatinine and just make sure that you're not missing renal diseases and etiology for a cause of volume overload. I also think for her, depending on what the stop bang is like, if you have high suspicion for sleep apnea, obviously polysomnography should be part of the workup.
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I think I'd do my initial workup, see what there is to see. What do you think about a BNP? Because I saw a BNP listed as Yeah. failure, there is some prognostic value to it. You know, you got to be more worried about patients with a high BNP. I'm not hinging the entire diagnosis on that, but sometimes I think it can be helpful. I'm not sure what you feel about that, Paul. And this is now we're in like non-expert opinion, but for me, I, it's almost like ordering an outpatient troponin for me. Like I just, I just tend not to do it because I, yeah, it's, I'm not sure it's all that helpful. Okay. And then Paul, how often are you ordering like pelvic imaging, you know, concern? Like if someone, if you do this whole workup and then you're still not convinced that it just doesn't seem like chronic venous insufficiency, it's not lymphedema, you know, are you ever doing the CT abdomen pelvis? Or like if you think ovarian cancer, you're looking for like transvaginal ultrasound. Is that something that you're doing? Yeah, I've done – and I'd be curious to hear your answer too. I've done pelvic imaging where it just doesn't smell right. And then if you – especially certainly if you have a patient with a prior history of malignancy, you know, I think specifically something about it, someone who maybe has a history of prostate cancer would get pelvic imaging from me too. It's sweet. But it's, there are certain patients and I think age is probably the biggest thing, you know, it's unusual for someone in their seventies or even the sixties to suddenly develop lower extremity edema that you just don't have a good explanation for. Like, that's just not how this chronic venous insufficiency behaves. So I think you have to, again, look at the patient in front of you, but if you're worried about underlying malignancy and they have the right background gestalt for it, I would certainly consider it if the workup was initially negative. We, let's say we even got abdominal imaging and she doesn't have like a lymphadenopathy that's bulky or, you know, a gigantic uterus with fibroids or something that's like compressing her, her venous return. So Paul, we've done all those things. And now Paul, I know, you know, we're going to talk about some horse chestnut seed extract. So tell me exactly. You know, we're going to talk about some horse chestnut seed extract. So tell me exactly. You know we're going to talk about some more chestnut seed extract. Paul, this is, when I read this, I was like, this was probably what I was most excited to talk about on this episode because I just wanted to find out if you've ever actually done this or if you were aware of this, like prior to, you know, developing this lower extremity talk that you've been giving. Matt, it's so weird that I get the chance to do this to you and perhaps we can cut this out but i'm gonna leave it up to you this came up at acp buddy like this is um this is one of those like uh i don't remember at all yeah it's i think this was a recap i i don't want to screw up which of our excellent guest correspondents did it but this actually came up in a recap i almost have perfect recall of the show paul you know like i almost did every episode 17 times but yeah no i i'm% sure we talked about this before. So to answer your question, yes, I've heard of it. I have not had the wherewithal to actually order it. How about you? No. As I said, last week when I was doing some pre-reading for this, that's the first time that I remember coming across it. But it is really recommended only for short-term use, Paul. And there's a lot of practical things that I think are the reason why. But it's a 300 milligrams twice a day dose, which gives you 50 milligrams of Eshin, whatever that is, Paul. And I was looking up, apparently they think for, and this is for chronic venous insufficiency. That's what we're talking about using it for. You can give it in the short term, maybe while you're starting to put into place some of these lifestyle things, some of the compression, just to give you like a little bit of a boost. That's how it seems like it'd be used, Paul. And it inhibits the activity of elastase and hyaluronidase. And both of those are thought to somehow play a role in venous insufficiency. The downside is it's an inhibitor of the SIP system, which means that it's going to wreak havoc with, potentially wreak havoc with other medications that the patient may be on. But what is more concerning is that it can have additive effects to anticoagulants and antiplatelets, Paul. Great. So, you know, for a lot of our patients in internal medicine, they're older, they're on antiplatelets, they're on anticoagulants. I'm not going to be throwing a lot of horse chestnut seed extract at them. But Paul, the Memorial Sloan Kettering Cancer Center, they have actually a really great integrative medicine where they talk about all the different herbs and medicinal supplements that are not traditional Western medicine. And looking this up, apparently there's been some case reports of people taking horse chestnut seed. And I don't think this was the extract. I think they were maybe just eating the actual seeds because there's at least one case report of someone who had a bezoar from this. Oh, nice. And another person had their kidney rupture. Oh, jeez. And then there was one case report of pericarditis. But, you know, I feel like probably lots of people are like trying this for their edema. We're not even hearing about it. I mean, listen. And there's no like epidemic of pericarditis from horse chestnut seed extract. So, or bezoars. If I stopped a medication every time it made someone's kidney rupture, I'd have to stop everyone's medications. It's just, you know, you can't make an omelet, a few eggs, et cetera, et cetera. So anyway, if anyone wants the citations, we'll link to the Memorial Sloan Kettering and they have these case reports in there. I thought that was just hilarious. Not that this happened to patients, but I was just like, oh yeah, let's look up the side effects. It's going to be like heartburn or something like that. And I'm like, kidney rupture? I'm like, are you kidding me? Yeah, well, you know. Yeah. So horse chestnut seed extract, that's maybe something. But Paul, what if we actually thought she had actual, maybe she had a prior pelvic surgery or inguinal lymph node dissection or pelvic radiation. Let's say pelvic radiation, Paul. She had bilateral lymphedema of her lower extremities. What might the therapy look like there? Yeah, lymphedema is tough. It's frustrating for patients. I think it's sometimes frustrating for caregivers and providers too. And I think the takeaway I would ask our listeners for lymphedema is like this is not not a one person show, like there should be a team managing the patient's lymphedema. And there are multidisciplinary lymphedema clinics available. I mean, obviously, the availability is going to vary, but sort of associated with larger medical centers, at least they probably exist where they will go for physical therapy and sort of manual assistance with the lymphatic drainage and then also, you know, vascular doctors to make sure everything is optimized the way they can and help prevent recurrence of infection, which unfortunately is a common problem for patients living with lymphedema. So I just, above and beyond sort of checking in very often, I think probably the best service we can provide our patients with lymphedema is to get them to one of these specialized centers if available because it is just such a... It's called complex decongestive physiotherapy, Paul. Complex decongestive physiotherapy. So it is, you know, it's not just a clever name. It is, it requires a lot. And really like the principle is they're trying to get the limb size down enough, and then they will put the patient in compression. This does work. Unfortunately, I believe the patient just has to keep doing it.
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And he got hooked up. He went to the lymphedema clinic. He had really horrible, very longstanding lymphedema. And the goal was just to get him like to be able to, he was having trouble just getting up and getting out of the chairs because the limbs were so heavy. And they were just, they were working and able to get him one of these devices. And, but it's, it's still tough, but he was pleased with the results. And it's, he's meeting with a physiotherapist more so than a physician at most of these visits who's doing, who's doing the work. Um, and your job is like doing the, obviously I'll get some of this, but doing a good exam, checking between the toes, making sure that you're actually treating aggressively for tinea pedis and just preventing any super infection. But, but yeah, it's, it's, yeah, it's a great service if you can, if you can connect your patient to it. Yeah. So essentially meticulous skincare for any of these patients with chronic edema, because as we said, they are going to be prone to infections. So Paul, with Miss Fadima, let's say that we've stopped her medications. I believe you wrote in the case that, so she hates us now, but her edema does get better. And we gave her some of these basic things to do. And it turns out she just had chronic venous insufficiency. She stopped the meds. Her legs are no longer swollen. She decides she still wants you as her Dr. Paul. But Beth, will you read us? Let's do another case, which is going to be a quicker case. And we'll talk about a different type of edema. Well, after we helped Ms. Lynn Fadima, she changed her mind. She doesn't hate us anymore. So much so that she told her brother that we're really great. And she wanted to come down to, he wanted to come down to the clinic. And he's seeing you in your office. He's 64 years old. He has diabetes, also with neuropathy. He has hypertension. He's on lisinopril for that, thankfully. He has obesity, and he also has tobacco use disorder. And he's presenting with left calf swelling that's been ongoing for two days, and he's feeling a pulling sensation that he hasn't ever felt anything like before. So, uh-oh. How is this case different? All right. How is this case different? The case is different because now I think we're in the land of this is acute unilateral lower extremity edema. And this is a completely different animal than what we've been talking about before. So, you know, chronic stuff just overall is less acutely scary. Acute edema, the thing that you can't miss is DVT. I think that's probably the most dreaded diagnosis. And unfortunately, other things that you might worry about, things like cellulitis of the lower extremity, even to some extent, like a ruptured popliteal cyst, all those things can happen acutely. But clinically, I think it's really hard to differentiate those things. And so I really think you're stuck mostly worrying about DVT and sort of working that up. And then once that comes back negative, fingers crossed, hopefully, then you can sort of work up the other stuff. But for this patient, you have someone who has diabetes, which means they're at risk for lower extremity infections. So again, you'd sort of do your exam between the toes and we'll get to the examination and workup. But he also has his tobacco use, which raises the possibility of occult malignancy. It also just increases yours for DVT overall. So I think you have lots of or a few things that could be happening here with Cal, but I think the thing that you can't miss, the thing you have to worry about most is DVT in this patient. I agree. And I was trying to, for a patient like this, Paul, what I struggle with is DVT versus cellulitis. I think probably a lot of people do. But with cellulitis, I mean, it can be painful, red, swollen, same as the DVT. Yeah. areas where there's a bit of a pattern where it's not quite clear where the cellulitis starts and ends, but that doesn't help you too much. I mean, if someone has a superficial venous thrombophlebitis, sometimes it's kind of obvious they had an IV in that site recently, or you can palpate something very superficial. That's different. But a lot of the times, I'm worried, is this DVT or cellulitis? Those are my two because either one, I'm going to have to prescribe a medicine at that visit. The other possible thing that I've seen, and it's less common, but you should think about it, is a ruptured Baker's cyst where they had a Baker's cyst that ruptured and it kind of spills all this fluid into the leg and the leg becomes acutely like red, warm, and painful. If they have a history of osteoarthritis and you're lucky enough to have like prior imaging or just knowledge that they had that cyst there, then that's a possible thing. But you're still going to get the ultrasound imaging in that case. So those are kind of the three big things, the superficial venous thrombophlebitis that you can try to differentiate, the cellulitis, and the ruptured Baker's cyst, but you're probably going to have to get some imaging. I know that we're both point-of-care ultrasound enthusiasts. I can tell you that my vascular exam is one of my weaker exams personally, but even the people who are really good at it tell me that they would not rule out a diagnosis based on a change. The D-dimer, I don't feel would help me, cellulitis, because any infection, you can get an elevated D-dimer. So in my practice, I'm mostly, maybe I'll get a D-dimer if I think there's going to be a delay in the ultrasound and I want to figure out if I'm going to empirically treat somebody. But most of the time, I don't empirically treat for just simple DVT and I'm getting an ultrasound as quickly as I can, like a formal ultrasound as quickly as I can. Yeah. So for him, we'll image him. I think we probably should mention, you mentioned sort of the three most common causes of unilateral or extremity edema. I think we can talk about some other ones too, especially, I think you named the big players for acute unilateral edema. If this were chronic, I think that changes the differential a little bit. And I think we touched on that at the beginning. Again, things that cause decreased muscle tone, like things like stroke or MS or L5 radiculopathy can also cause anything that causes flaccidity can cause chronic large-stromed edema. Acutely, you'd hate to miss compartment syndrome. That would be embarrassing, but hopefully you've taken a history and would figure that part out. And then there's May-Thurner syndrome, which I feel obligated to mention just because every cardiologist loves it, and I still don't entirely know why. Are you familiar with this, Matt? I'm familiar. I mean, it's compression of the veins up in the pelvis. And I know that I think classically it's like one of the arteries is compressing the iliac vein, but I think you can also get like in pregnancy, if there's a gravid uterus, it can sort of mimic that or other malignancies or other lesions in the pelvis can mimic that. So I don't remember which side it is. It is classically- It's classically, the left vein is compressed by the right iliac artery. And it's, by the way, this is really common. Like it doesn't necessarily lead to pathology. It's often found, you can see it in autopsies all the time. And it doesn't necessarily mean this person's having recurrent left lower extremity DVTs, but that can be a manifestation of it. So if you have a younger female patient in her second or third decade of life who has chronic left lower extremity edema or is having recurrent DVTs on the left-hand side, like that should prompt you at least to think about Mather-Nurse syndrome. So it's interesting. It's actually fairly common, but what's common is the fact that it exists, not the pathology that you associate with it. That pathology actually doesn't happen all that often. if you do find the DVT, you want to make sure you see the top of the clot.
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Because in those cases, patients might be candidate for intervention and they're at higher risk for, you know, the phlegmasia complications, things like that. Yeah. And I made the joke, but the reason they love it is because they can actually do something about it. Okay. There you go. There you go. So that's another one of the acute causes. And then the other chronic causes, Paul, so the acute causes, cellulitis, DVT, and then the chronic causes, lymphedema, lipoedema should be put in there too. Great. And then this thing, complex regional pain syndrome, which I don't quite understand that well, I believe that can be unilateral as well. Yes. Yes. So that would be another thing if you're working the algorithm there. And then sometimes I find that if people have had a surgery on one side versus the other, they might have venous insufficiency on that side, not necessarily lymphedema. Great point. Yeah. Especially the patients who've had older cabbages where they actually did vein harvesting from the cap. I feel like you can see venous insufficiency there as a result too. That's a great point. Right. So I usually just ask like, have you had surgeries on this leg? Has this ever been ultrasounded before? And sometimes if it's an older person, they'll be like, oh yeah, this has been swollen like this for decades and I've had ultrasounds before or their caregiver who's there with them will tell you that. And then I don't necessarily go working it up. But this is a little bit of a, I think, easier algorithm in some sense than the chronic bilateral venous insufficiency, which really requires a much bigger history and potential workup. For the patient like Calpheedema, with acute unilateral, it's a much quicker workup, but a little bit more scary, at least in the first 24 hours until you conclude things. So anything else that you wanted to talk about, Paul? I mean, it's been a whirlwind tour and I'm not sure, I don't know what we missed. I feel like it's been, Absolutely. I don't know what to do about and seems to be, I found one paper on it from 1999 in the American Journal of Kidney Diseases. And even the authors were like, I'm not sure if this is actually a thing or not. So like I, you'll see, you might read about that, but I'm not sure that would not be the first thing to think about in terms of a differential for, for bilateral large-term edema. Yeah. I think one thing that, you know, that, that you just reminded me of is, which is maybe pertinent to the idiopathic edema is that patients who have had edema, they've often tried diuretics. Either they got them from a prior physician or they got them from a friend or family member. And some of the articles did mention that if patients are taking diuretics inappropriately because they think it's going to help them, they can become chronically volume depleted and their renin-aldosterone angio system can be ramped up and they can actually be retaining salt and water kind of paradoxically despite taking the diuretics. So I generally try to tell patients like, listen, like diuretics, they're great if you have high blood pressure and we need it for that. Or if you have cardiopulmonary disease that like requires diuretic therapy to kind of help your heart and lungs work better. Yes. in your edema. So I really don't think this, and sometimes if a patient's really insistent and I'm not sure, maybe they had that grade one diastolic dysfunction, Paul, maybe I'll give them like a brief trial of it and I'll check their electrolytes. And then we decide if it actually helped them or if there were any harmful effects and we stop it. But, you know, I don't like set it and forget it and give all my patients with chronic edema diuretic therapy. I feel like that's a, you know, we should not be doing that. And as I mentioned, Paul, to me, this is kind of like the azithromycin of lower extremity edema. You know, it's kind of akin to that because I find myself mostly talking about why they don't need diuretics when people come into my office with edema, not necessarily. That's like the hardest part of it for me, actually, sometimes. Yes, it's right. I think that's the trap we fall into a lot of the times where we're sort of doing stuff for the illusion of actually doing stuff and it may not actually help. And I feel like there's a lot of things in medicine that we're prone to. And I think this is one of those cases where you just kind of want to, you desperately want to help the patient. It comes from a good place, but this is probably not the right way to do it a lot of the time. Yeah. So, so with that, I think we should probably get to the outro, Paul. Sure. This has been another episode of the Curbsiders bringing you a little knowledge food for your brain hole. Yummy. Great. Consistent is your byword. Get your show notes at thecurbsiders.com. And while you're there, sign up for our mailing list to get our weekly show notes in your inbox. Plus, twice each month, you'll get our new Curbsiders Digest. Do you get it? Digest. Recapping the latest practice-changing articles, guidelines, and news in internal medicine. And we're committed to providing you with high-value, practice-changing knowledge. And to do that, we really want your feedback. So please subscribe, rate, and review the show on Apple Podcasts. We actually read them and, you know, maybe once in a while we'll read them on air because sometimes they're funny. And sometimes they hurt our feelings. Yeah, that too. So you can contact us at thecurbsiders at gmail.com. A reminder that this and most episodes are available for free CME credit for all healthcare professionals through VCU Health at curbsiders.vcuhealth.org. A special thanks to our writer and producer and guest expert for this episode, Dr. Paul Nelson-Williams. Thank you and goodbye.
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From the JAMA Network, this is JAMA Internal Medicine Author Interviews, conversations with authors exploring the latest clinical research, reviews, and opinions featured in JAMA Internal Medicine. I am Dr. Robert Steinbrook, Editor-at-Large at JAMA Internal Medicine. I'm here with Dr. Aaron Kesselheim from the Brigham and Women's Hospital and Harvard Medical School in Boston, and Dr. Jay Crossan, Chairman of the Medicare Payment Advisory Commission, also known as MEDPAC. MEDPAC is a nonpartisan legislative branch entity that provides the U.S. Congress with analysis and policy advice on the Medicare program. We will be discussing the research article in JAMA Internal Medicine that Dr. Kesselheim wrote with four of his colleagues. The study analyzes a proposed Medicare policy to shift the coverage of certain drugs from Medicare Part B to Part D and the likely effects on total drug spending as well as out-of-pocket costs for Medicare beneficiaries. Medicare Part B primarily covers physician-administered drugs and biologic agents. With Dr. John Christensen, Dr. Crossan wrote a commentary for JAMA Internal Medicine about Dr. Kesselheim's study. The commentary also discusses recent proposals that MedPAC has made about Medicare Part B and Part D costs. Dr. Kesselheim and Dr. Crossan, welcome to the JAMA Internal Medicine Podcast. Thank you. Thank you. Before we discuss the study, can each of you state in a few sentences why total Medicare spending and patient cost sharing for prescription drugs are such important policy issues. What problems do the United States need to solve? Dr. Kesselheim, could you go first? Sure. Well, first of all, it's a pleasure to be here. Thank you so much for hosting this. And I would say, first of all, that prescription drugs are one of the most important medical interventions we have. I was just in clinic this morning, and we were talking about prescription drugs all morning. And they can be transformative in the life of patients and are an important part of a clinical treatment plan. So trying to ensure that patients can get prescription drugs is a fundamental policy issue. But unfortunately, there's been a substantial problem over the last few years with very expensive prescription drugs that make it challenging for patients to be able to afford them. And the increasing prices of prescription drugs have put strains on payers and forced them to cut back medical services in other fields as well. So I think that the reason that this is an important issue is because we want to ensure that pharmaceutical drugs are priced at a level that is a reasonable approximation of the value that they provide so that they can be reasonably available to the patients who need them. And unfortunately, in the United States, we don't do that. We have prices that are set by the pharmaceutical manufacturers at whatever the market will bear. And in many cases, that leads to drug prices that are well beyond their value and far beyond what is paid in other countries for those products. Dr. Crossan? Yes. I mean, I think the larger perspective here has to do with total Medicare spending. At the commission, we try to adhere to three basic principles. One is to make sure that providers of Medicare services to beneficiaries are paid fairly, that we protect the interests of beneficiaries as best we can, but we also take care to watch the total Medicare spending over time as it impacts the federal budget and the fiscal health of the Medicare program. As Dr. Kesselheim mentioned, Medicare spending is projected to rise, and particularly because of increased drug costs. Medicare spending is projected to reach about $1 trillion in 2022, CBO projection. Another way of looking at it is that from 1970 to 2030, we're going to go from 20 million Medicare beneficiaries to 80 million. But at the same time, we will go from about 4.5 workers per beneficiary paying into the trust fund to 2.5. On the beneficiary side, about 60% of the average beneficiary income, senior's income, comes from Social Security. And about 24% of that is the cost of Part D and Part B premiums and cost sharing. And that's gone up from about 7% in 1980. So not only does the increased cost of Medicare, and particularly drug costs, impact the potential health of the Medicare program, but the ability for Medicare beneficiaries to have adequate income to live. Yes, there are some very important questions here and issues for the future. Dr. Kesselheim, can you briefly summarize your study and the main findings and how the research contributes to the discussion about the high cost of prescription drugs? Sure. So very broadly speaking, there are two main parts of the Medicare program that pay for prescription drugs. There's the Medicare Part B program, which primarily covers physician-administered drugs and biologic agents, as you mentioned. And then there's the Medicare Part D program that covers outpatient drugs sold in a retail setting. But the important issue is that the system for paying for drugs in those two different settings is much different. Medicare Part B, the cost of drugs is set based on their average sales price in other settings. And so basically what the pharmaceutical manufacturer sets and is able to get in other settings, whereas Medicare Part D, the cost of the drugs is maintained by individual Medicare Part D plans that use various strategies to negotiate prices and as a result might be able to achieve more savings. And so what we did was we took a cohort of the 75 drugs that lead to the most amount of spending in Medicare Part B and modeled what would happen if they were instead paid through the Medicare Part D program, taking into account the average rebates that drugs provide. And so what we found is, indeed, that if you were to take that step for these drugs, that you'd find a substantial reduction in the amount of money that Medicare would spend for them. And that's, I think, the good news is we found anywhere from about a 7% to 18% or so decrease in the spending overall on these products. However, there are different systems for the amount of out-of-pocket costs that patients are responsible for in Medicare Part B and Part D. So what we found was that in general, out-of-pocket costs might go down, but there is a minority of patients, anywhere from about 20% to 30% of patients, for whom we might expect the out-of-pocket costs to go up if a switch was made from the Medicare Part B model to the Medicare Part D model. And so what we found was that, again, there might be cost savings overall, but that there would be this fraction of patients that might have to encounter more out-of-pocket costs as a result of the shift. And another major finding that we had was that we compared the amount that Medicare Part B spends on these out-of-pocket costs as compared to a group of other high-income countries and found that the amount that Medicare Part B spends basically across the board on these products was substantially more than what these drugs are priced at in other countries. We are paying a lot more than other countries are paying for these same products. So it's a complex matter. It's not simply do one thing and there's one direct result. There can be a variety of impacts depending on where one is in the system. Dr. Crossan, can you summarize what you learned from the study and how these findings contribute to the discussion about Medicare Part B and Part D? Yeah, thank you. I was very pleased to read Dr. Kesselheim's studies. I think it's a valuable contribution. The context here, and people may not realize this or think about it all the time, is that the Medicare program generally pays directly to providers for services to Medicare beneficiaries and sets prices. Congress sets the prices for the Medicare program. That's not true for drugs, neither in Part B nor in Part D. As Dr. Kesselheim just pointed out, these two programs are really different from the way Medicare normally pays and, for various reasons, are quite complex. What that means is that if Congress or CMS sets out to try to change the way Medicare pays for drugs through Part B or Part D, there are not uncommonly complications. In other words, in setting any policy to change a complex payment system of this kind, there are trade-offs. Sometimes there are winners and losers, as was pointed out in the study. But in addition, because of the complexity, even with the best thought-out plans, there may be unforeseen consequences. And I think that's not only true of this particular proposed change, but I think it will be true virtually for any idea or set of ideas that come forward to change the cost of Medicare drugs. So, Dr. Kesselheim, what is the status of the proposed Medicare Part B to Part D shift, and how does that fit into what the Centers for Medicare and Medicaid Services has said that it might be doing? Well, this shift was most recently proposed in this context over the summer when the current administration released its blueprint for how it might try to reduce drug prices.
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And I think that currently they've put out a request for information on the blueprint and on other aspects of this. So they're, as we sit here today, I think still gathering information from stakeholders about what they think about this particular idea, but also on a number of other ideas that were part of that blueprint and have been mentioned in other contexts as well. So is it fair to say that this proposal is still under active discussion and it's part of the various options that the Department of Health and Human Services and CMS are considering? Yes, I think that is fair to say. Dr. Crossan, MedPAC has made a variety of very interesting proposals about ways to approach Part B and Part D costs. And could you highlight one of those that you are most hopeful that Congress and Medicare will move forward on? Sure. And we'll focus on Part B because, as Dr. Kesselheim has pointed out in his article, that's a particular area of rising costs because of the new biopharmaceuticals that are coming online virtually every month. So as you say, MedPAC has made a number of proposals over the last few years on both Part B and Part B, but particularly on the Part B side in our June report, and again, this is, as I said earlier, necessarily complex. We have suggested that Congress essentially change the way physicians are paid for the provision of Part B drugs. And we've suggested that rather than the physicians purchasing the drugs and then being reimbursed by Medicare based on the average cost of drugs, that in some ways, similar to Part D, that there be an intermediary purchasing program set up, which we call the drug value program. In that, Medicare would contract with private vendors to negotiate prices. The physicians would get reimbursed the negotiated price plus a fee for administration. But the key element here is that these vendors would have significantly important negotiating strengths to deal with the pharmaceutical companies. And we've recommended, for example, that together with the physicians who would be working with these vendors, the vendors would develop a formulary that would give them negotiating leverage with respect to the pharmaceutical companies. And we have even proposed that for the single source, very high cost drugs, that in the case of extreme drug costs, that the vendors collectively be given the ability to use binding arbitration. And we have gone even further and suggested that the model, this sounds a little funny, but that the model would be based upon baseball arbitration. That is, in this case, the vendors together and the pharmaceutical company would each submit a bid to the arbitration panel. But the arbitration panel could only find for one side or the other, there would be no middle ground. That's been used successfully in some parts of the country with respect to health care costs, and it creates an incentive for both parties to be reasonable. So that's a very interesting proposal. Just one point of clarification. Would this program to go forward require Congress to enact new legislation? Oh, absolutely, because it would fundamentally reshape the Part B payment process. To conclude our discussion, I wanted to ask each of you about your crystal ball for 2019. Do you see new federal initiatives to control the cost of Medicare Part B and Part D? Do you think that 2019 will be the year of some new things happening? Dr. Kesselheim first. I am hopeful that 2019 will see some things moving in this area. I mean, I think, first of all, when you poll people, about 75% of people believe that prescription drug prices are too high, and that makes it a Republican and Democratic issue. So I don't think this is a partisan issue, and I think that there are a lot of people who are suffering because of increases in drug prices for essential medications that they can't afford. So I do think that there's going to be a lot of political pressure on Congress and the executive branch to do something, and so I am hopeful that something will come up. And what exactly that will be, I mean, I think we'll see. I think that there's also been talk about trying to set up a plan to better negotiate prices in Medicare Part D as well to try to ensure, again, that prices are more closely related to the value that they offer rather than to what the pharmaceutical manufacturers think that they can get, the maximum amount that they think that they can get from the market. And actually, some people have suggested this arbitration mechanism as well in the Medicare Part D space. And I would say that I think that it's an interesting idea, although oftentimes arbitrations happen behind closed doors and are open to being affected by the political process. So I would hope that if there is an arbitration process in Medicare Part B or Part D, that it would be transparent and might even allow for third party bids about what the price should be and would be done in a way that might be accountable to the patients who are going to be relying on it. Thank you. Those are interesting considerations. Dr. Crossan, your crystal ball for 2019. Yeah, I wish I had one. So I agree that I think we're going to see at least bipartisan interest in this regard, whether the ideas will be consonant. I'm not certain about that. In addition to the idea of Medicare directly negotiating, which I think has been on the table, I think there's been some thoughts about linking Part B, at least, payments to some sort of foreign benchmark. There's the issue of reimportation potential from Canada or other countries. And I think what I said earlier is going to apply here, and that is that there is no easy fix to a problem this difficult, particularly because Part B and Part D are complex payment mechanisms, and you either have to start by making modest adjustments to them or fundamentally overturn them. And in so doing, there are going to be significant fallouts in terms of the unintended consequences and the complexity and the need for, and I think we would hope that this would be the case, that Congress moves forward and then within a period of time watches to see the impact and then comes back and changes and fixes things so that over time we have a better program. Of all these ideas, I would come back and say as a starting point that our 2016 MedPACs, 2016 recommendations for improving Part D by strengthening Part D plans, but also putting them under some increased pressure by reducing reinsurance. And then on the Part B side, the DVP program are good starting points. Thank you, Dr. Kesselheim and Dr. Crossan for an excellent discussion of what I think is fair to say, one of the most important health policy topics for the federal government and the public. And it will be interesting to see what happens as the year goes forward. This is Dr. Robert Steinbrook, Editor-at-Large at JAMA Internal Medicine. I hope you have enjoyed this JAMA Internal Medicine podcast. Thanks for listening.
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I'm Rachel Gottbaum, and this is Intention to Treat from the New England Journal of Medicine. Remember the beginning of this pandemic? Now to growing concerns about the deadly coronavirus officially hitting the U.S. Here's what we know. Fast-breaking developments in the coronavirus emergency in the U.S. and around the world. The number of cases soaring just today. Tonight, the Christmas surge is here as we witness the darkest days of the pandemic. A record number of Americans have become infected and lost their lives to COVID. The single-day death toll soaring above the grim benchmark. And then a major medical breakthrough. The very first COVID vaccines. Breaking news. Pharmaceutical giant Pfizer just announced moments ago that its coronavirus vaccine is 95% effective. It comes just as the U.S. recorded the deadliest day of the pandemic in six months. Well, we're getting Moderna's phase three interim results, 94.5% efficacy for their COVID-19 vaccine. But did we expect too much from these vaccines? Let's talk now about breakthrough COVID cases. That's when people contract the virus after vaccination. They are extremely rare, but in Napa County, what appears to be the Bay Area's first fatal breakthrough COVID-19 infection has happened. The new CDC internal report not only acknowledges that so-called breakthrough infections are rising, but that they may be as transmissible as unvaccinated cases. And what about all these boosters? You know, more than 100 million Americans have now received their first booster shot, but 91 million people who are eligible have yet to get the additional shot. So based on the new booster is ready. Health officials on Long Island say not many people. The pandemic is over. We still have a problem with COVID. We're still doing a lot of work on it, but the pandemic is over. Well, the pandemic is definitely not over. But what about the future? Can we do better with our COVID vaccines? And if so, how much better? And how do we make sense of these short-acting boosters and what we can really expect moving forward? I'm Rachel Gottbaum, and you're listening to Intention to Treat from the New England Journal of Medicine. To get some answers to these questions, I'm joined by NEJM Editor-in-Chief, Dr. Eric Rubin. Hi, Eric. Thanks so much for joining us. Great to be here, Rachel. Thanks. We're also going to bring in Eric's colleague at the FDA Vaccine Advisory Committee, Dr. Paul Offit. Dr. Offit is Director of the Vaccine Education Center at Children's Hospital of Philadelphia. Paul, thank you so much for being here. It's my pleasure. Thanks for asking. Let's first talk about where we are before we discuss if we can actually do better. Well, I think we're doing great. I mean, if you look at where we were in 2020, we didn't have monoclonal antibodies. We didn't have vaccines. We didn't have antivirals. All we had was barrier protections, you know, sort of isolate, quarantine, test, close schools, close businesses, restrict travel. That's how bad things were. And you'd have 3,000 people dying a day, 4,000 people dying a day. we were bad off. And we were a blank slate. We had no population immunity when that virus first rolled into this country. Now we do. We have probably 90% to 95% population immunity. We have drugs that can treat people at high risk. We have monoclonal antibodies for people who are immune compromised. And we have vaccines as our ticket out of this pandemic. So we're in much, much better shape. So Eric, what are your thoughts? Remember that at the beginning of the epidemic, when we first used vaccines, they were remarkably effective, not only at preventing death and preventing severe disease, as Paul already said, but they really prevented infection and transmission of disease. So there was a time when it looked like we might be able to really control disease to a much greater extent. That doesn't appear to be the case now. The vaccines do help prevent severe disease. They are stopping people from dying, and that's very important. But at the same time, we've had to lower our expectations thus far. Yes. Let's talk about these lowering of expectations because, Paul, in one of your recent perspective articles for NAJM, you talk about an over-promising with these vaccines and a stirring up of confusion. What did we need to do differently? I think there was a false hope in a sense that was created by those original studies back in December of 2020. I mean, what you found was you found 95% protective efficacy against all manner of illness, mild, moderate, severe illness. There's no way that was going to last. I mean, those were relatively short studies. They were done over only a period of three months. This is a short incubation period mucosal infection. You're not going to be protected against mild disease for very long. It's true really of all short incubation period mucosal infections, whether it's flu or parainfluenza virus or rotavirus. You can get excellent protection, I think probably fairly long-term against severe disease, but you're not going to get long-term protection against mild disease. And that's what happened. Six months later, if you look at the studies that were done, protection against severe disease was holding up, but protection against mild disease wasn't. And that was also true a year later. And I think we created this unrealistic expectation. To me, the seminal moment came when thousands of men got together in Provincetown, Massachusetts to celebrate the July 4th holiday. 79% were vaccinated. 346, despite being vaccinated, got COVID. Four were hospitalized. Four of 346. That was a hospitalization rate of 1.2%. That was a vaccine working very well. The remaining 342 had mild or asymptomatic infection, which the CDC labeled as breakthrough infections. That was the wrong word. Breakthrough implies failure. That's not a failure. That was a moment to celebrate that vaccine. Here were people who, because they were vaccinated and then exposed to the virus, only suffered a mild illness. And I think we lost that opportunity and created this unrealistic notion that we could somehow in any long-term manner protect against mild disease, which is just not possible. The only attainable goal of this vaccine is keep people out of the hospital, keep them out of the intensive care unit, and keep them from dying. So Eric, let me get to you for a minute. Did you somehow think we were going to do better with these vaccines? Paul is clear that they will probably never be long durability with them. What's your experience? Well, first, let me add something to what Paul said, which is that there is this annoying thing called evolution. So not only is the immunity short-lived to many of these infections, but the virus has changed and it continues to change. And it's changing because of vaccines and because of the amount of infection out there that's applying some sort of evolutionary pressure to select for these new mutants. So there's sort of a double whammy here, our lack of ability to produce long-lasting immunity using vaccines and natural infection, and the fact that the virus keeps changing. If we keep on doing the same thing, we're very likely to come up with the same sorts of answers. Chasing after each new viral variant is likely to, at best, continue what we're doing right now. It's not likely to make a breakthrough for preventing infection for any persistent amount of time, I think. So Eric, what would you like to see? I would love to see more effort put into different modalities. Some of them are being tried, although they're not being tried at the scale or with the pace that the original vaccines were when they were developed. There certainly are efforts, for example, to try to produce mucosal vaccines. Perhaps they would make a difference. Perhaps they would give us more protection against infection. So far, I'm afraid the results haven't been glowingly positive. Here's how I see this. If you want to try and protect against a mild infection or try and decrease transmission, you need high levels of neutralizing antibodies, especially now with these more contagious variants, which have, if anything, shorter incubation periods. So the only way to get sort of long-lived protection against mild illness is to have long-lived induction of antibodies. And that is not something I can think of a way to do, unless you're trying to just goose several times a year, which I don't think is a viable public health strategy. To me, what makes sense is focus on the goal. The goal is prevent serious illness.
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I don't see how you can reasonably try and prevent against mild disease for any length of time for a short incubation period disease, knowing that neutralizing antibodies are not going to be long-lived. And I can't think of a strategy that would allow that to happen. The only other way that this could happen is if this becomes a longer incubation period disease, like measles or rubella or smallpox, the kind of diseases you really can eliminate from the face of the earth because they are long incubation. So Paul, do we need to change our expectation here? about being in crowds over the winter and indoors over the winter, that you're less likely to transmit, less likely to get mild disease. I just think that's a little misleading. And I think that's caused a fair amount of disappointment. Very early on, actually, you know, six months, eight months into this, having a vaccine, people would say, look, I mean, I got two doses of the vaccine and then I still got infected. And I do think if you could go back in time and sort of do this all over again, I wish we could have set more reasonable expectations for what this vaccine can and can't do. What would we have said then? We would have said that the goal of this vaccine is to prevent serious illness. The goal of this vaccine is to keep you out of the hospital, keep you out of the ICU, and keep you out of the morgue. That is the goal. You may still get a mild illness. You still may get two doses or three doses or four doses, and you still may get a mild illness. You may feel terrible, but you're not going to need oxygen. You're not going to need to go to the hospital. And that's the goal of this vaccine. It would have been more realistic to, I think, have offered that rather than this sort of notion of COVID zero. So Eric, are you as pessimistic as Paul that we're not going to get real durability and we're going to have mild disease, as you guys call it. But what that means is we're going to be infectious and we're going to be living with this. What's your take on it? Well, I have to agree with Paul. We have many years of experience with trying to develop vaccines, and these are the characteristics of the vaccines we get. Having said that, we don't right now harness every part of the immune system. Cell immunity, for example, perhaps it could make a difference. Mucosal immunity, which certainly is induced by some other vaccines, might be an addition. It may be impossible. It may be this is the best we can do. I wouldn't give up yet, but I do think that we're not going to know unless we make some sort of investment in continuing research and development. Remember that things that prevent disease are far better than things that treat disease. So I think we underinvest in vaccines in general, and this is one where I would continue to be spending some money. Paul, you talked about repeated boosters is not a viable public health option. We've had editorials from colleagues who have agreed and said we shouldn't be getting these even once a year. That's the current state of things. So where do we go here? Right. So on September 1st, the CDC recommended that everybody over 12 years of age receive a bivalent vaccine booster dose. I guess I would argue that if you look at their data, the CDC data or data recently published by the United Kingdom, the question was, does a booster dose benefit people in terms of preventing hospitalization? Yes, that was true for a third dose. It was true to a lesser extent with the fourth dose. But if you look at who benefited, it wasn't everybody. The people who benefited primarily were those who were elderly, those who lived in nursing homes, those who were immune compromised, and those who had high-risk medical conditions. So focus on them. So essentially, there is no magic bullet. I'd like you to speak about how we should be thinking about this and how providers should be thinking about this. You know, I started as a Red Sox fan in the 1960s, and optimism does eventually pay off oftentimes. So I'd go back to where we started with what Paul said. We have had a huge success here, not just vaccines, but of course, a lot of people have been infected. And therefore, the prevalence of immune individuals is very high. So we're really starting from a pretty good place. Paul? Right. I think moving forward, given that we have a high level of population immunity, given that we have vaccines and monoclonals and antivirals, which can help save our lives, to me, the critical thing that has to happen moving forward is a collaboration between two groups. One is CDC epidemiologists in collaboration with immunologists and academic centers to answer the question, for how long are you protected against severe disease based on how many doses of the vaccine you've gotten, based on which vaccines you've gotten, based on what your medical background is? How often do you need to get a booster dose? Is it a year later? Is it two years later? Is it five years later? So that's what you need to define. I think Paul makes an important point that I want to make very explicit. While we've invested a lot in developing vaccines, rolling them out, and other public health measures, one place we have continued to fall short is in surveillance. We really don't know who's getting infected, how many people are getting infected, and that problem has been compounded because of home testing, lack of reporting systems. We really need some sort of systematic surveillance. I think the important point is, I don't think we know. We don't know the answer to boosting without data. We're going to have to have a good idea of what's happening and what's working at any given time to inform those decisions. So, Paul, do you envision the future of COVID to be like the flu in terms of having an annual tailored shot for each strain moving forward? Is that how you see this happening? I guess I'm going to make the following predictions, which is probably a terrible thing to do, because if you make predictions about SARS-CoV-2, you're always wrong, but I'm going to try anyway. I assume this virus is going to be circulating for years, if not decades. I assume that if the entire world were vaccinated and the virus still never mutated, that it would still circulate in the community and still cause mild disease in many and severe disease in some. And so the goal then is to focus on those who are most at risk for severe disease and make sure that we can, you know, keep them as immune as possible over time. But we will settle in to where we are with flu. You know, two years before SARS-CoV-2 came into the United States in, say, January 2020, two years before that, we had 800,000 hospitalizations from influenza and 60,000 deaths. I mean, if we masked in social distance and were a little more careful about interacting with people during the winter, we could have dramatically lowered those numbers. We didn't. We accepted those. And I think at some level, we're going to get to the point with this virus where we grandfather in, if that's the right term, a certain amount of disease and hospitalization and death. I don't know what those numbers are, but I suspect that's likely to happen. Well, thank you both very much. It sounds like what we're working on now is not going to get us long-term durability, which is what I think a lot of people had hoped for. Then again, we may need to rethink how we see these vaccines. Paul Offit is the director of the Vaccine Education Center at Children's Hospital of Philadelphia. And he's also on the FDA's Vaccine Advisory Committee with Eric Rubin, who is editor-in-chief of the New England Journal of Medicine. Thank you both very much for coming in. Thanks, Rachel. Thank you. You're listening to Intention to Treat from the New England Journal of Medicine. Next time, we'll hear from OBGYN specialists practicing in states where providing needed medical care can mean a criminal indictment and where patients are being put at risk. We can't function like this. We can't function in fear. We can't be fearful that every time we provide indicated abortion, we could potentially go to jail. And so I think we're all bracing for an increase in maternal death. And the fact that we think we won't be able to change the law until women die seems absurd. I'm Rachel Gottbaum. you
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Hello out there. This is Dr. Kathy DeAngelis, the editor-in-chief of JAMA, the Journal of the American Medical Association. And this week I'm going to tell you about the December 17, 2008 issue. And as usual, we'll start with the art on the cover. And this issue has one of my very favorite artists, Giuseppe Accombaldo, who lived from 1527 to 1593. Now, that's kind of interesting. He lived a long time ago, but I consider him to be pretty much of a modern artist, our own modern artist, because this gentleman had an incredible imagination. And if you look at the painting, you'll see that it looks like a man's face, but it's made of trees and leaves and fungus and that sort of thing. And he did the Four Seasons. That's probably his most famous set of art. And this one is Winter. The first article is Feeding Guidelines and Mortality of ICU Patients. Early nutritional support for patients in the intensive care unit, or the ICU, is associated with reduced mortality rates, but early initiation of nutritional support is not universally practiced. In a cluster randomized trial, Dr. Gordon Doig from the University of Sydney and his colleagues investigated whether evidence-based feeding guidelines that were implemented using a multifaceted practice change strategy and educational outreach could improve feeding practices and reduce ICU mortality. The authors found that ICUs in the intervention hospitals successfully implemented the evidence-based nutritional support guideline, but this was not associated with reductions in hospital mortality compared with ICUs in the control group hospitals. In an editorial, Naomi Jones and Dr. Darren Honeykand from Queen's University, Kingston, Ontario, discuss the nutritional treatment of ICU patients and the complexities of guideline implementation. The second article deals with low glycemic index versus high fiber diet in diabetes. Some data suggests that a low glycemic index diet may improve glycemic control and have beneficial effects on cardiovascular risk factors. But questions remain regarding the diet's effectiveness for patients with type 2 diabetes. Dr. David Jenkins from the University of Toronto School of Medicine and his colleagues randomly assigned patients with type 2 diabetes controlled by oral medications and no clinically significant cardiovascular, renal, or liver disease to receive either low glycemic index or high cereal fiber dietary advice and assess the effects on glycemic control and cardiovascular risk factors. The authors found that six months treatment with low glycemic index diet was associated with a moderate reduction in hemoglobin A1c and an increase in high density lipoprotein cholesterol levels compared with the high cereal fiber diet. That's promising. The third article deals with mortality in cancer patients with pre-existing diabetes. Some cancers are more common in persons with diabetes, but the association of pre-existing diabetes with long-term all-cause mortality in cancer patients is not clear. Bethany Barone from Johns Hopkins School of Public Health and her colleagues conducted a systematic review of the literature and meta-analysis to address this question and found that compared with normal glycemic individuals, persons with diabetes at the time of cancer diagnosis had an increased risk of long-term all-cause mortality across all types of cancer. And the JAMA patient page has information for your patients about colon cancer. The fourth article is a review and deals with smoking and colorectal cancer. Whether cigarette smoking is associated with an increased risk of colorectal cancer has been a subject of controversy. In a systematic review and meta-analysis of data from observational studies, Eduardo Boteri from the European Institute of Oncology in Milan, Italy, and his colleagues assessed the relationship of smoking with colorectal cancer incidence and mortality. Comparing smokers with non-smokers, the authors found the excess risk of colorectal cancer was 1.18, that's a confidence interval of 1.11 to 1.25, The fifth article is the clinician's corner. Has this pubertal girl been sexually abused? And this is part of the Rational Clinical Exam series. Dr. Molly Curtin-Burkoff from the University of North Carolina School of Medicine and her colleagues conducted a systematic literature review to determine the diagnostic utility of genital examination findings to identify non-acute sexual abuse in pre-puberty girls. The authors found that the presence of vaginal discharge and hymenal transections, deep notches, or perforations raise the suspicion of sexual abuse. However, these findings cannot independently confirm or exclude sexual abuse as a cause of genital trauma in young girls. This issue, we have two commentaries. The first by Mr. Benjamin Fellett and Dr. Carrie Gross from the Yale University School of Medicine and deals with access to experimental drugs for terminally ill patients. The second commentary is a JAMA classic celebrating 125-year anniversary of JAMA. This one is by Dr. Carol Jenny from Brown University School of Medicine. Medicine discovers child abuse. Now that's something I wish we had never discovered. The medical news and perspectives. All smokers should receive a pneumococcal vaccination to protect against infection according to a new recommendation from advisors to the United States Center for Disease Control and Prevention. Economics may play a role in crowding and boarding in emergency departments. 1,000 Genomes Project promises closer look at variation in the human genome, and medical student enrollment is up but still falls short of meeting the need. And in the Centers for Disease Control and Prevention, anaplasma phagocytophilium transmitted through blood transfusion, Minnesota, 2007. Federal air travel restrictions for public health purposes in the United States, June 2007 to May 2008. And a piece of my mind, a testy experience. This one's by Dr. Carolyn Welbury from Georgetown University, and it deals with anxiety over recertification exam. I think many of us can read this and identify very closely. This young physician was very concerned about having probably failed her recertification exam and was very relieved when she passed by a mile. I guess we never get over test anxiety, no matter how well experienced we are. The readers respond, how would you manage a 41-year-old woman with recurrent uterine fibroids? Go to www.jama.com, read the case, and submit your response, which may be selected for online publication. Submission deadline is December 31, 2008. 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, the Editor-in-Chief of JAMA, speaking to you from beautiful and cold downtown Chicago, where the wind blows mightily, but the patients are always our top priority.
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Hey folks, just a quick reminder that this podcast is not meant to be used for medical advice, just good old-fashioned education. Hello, Clinical Problem Solvers. Welcome. My name is Robby Jihah, and I'm a clinician educator at UCSF. We have the whole crew here today, Arsalan, Charmaine, and Reza. Hey, Arsalan, what's good with you? Robbie, I'm feeling really good. You know, it's been a little bit since we recorded, and it's always a treat hanging out with you guys. So I'm loving it. Sharmeen, how are you doing? I'm doing great. It's good to be back. Per Reza's advice, I'm drinking my Persian black tea now. Your mom would be so proud of you, Sharmeen. I know. You know, I try very, very hard. How are you doing, Reza? Sharmeen, I'm doing quite great. I'm very excited for tonight's episode. Let's see what Robby has in store for us. Well, Reza, the reason you have no idea is because we have a clinical unknown for you. And as a reminder for the audience, this is a case that Reza has not seen or heard about before. The goal is to capture the entire spectrum of clinical reasoning. We'll hear Reza's problem representations. We'll hear him deploy some diagnostic schema and share a few illness scripts along the way. The goal for you folks, again, listen and think in parallel and pause whenever you need to and think along with us. So without further ado, let's jump right in. So today we have a 48 year old man who presents with muscle aches, fatigue, and a new rash. Two weeks ago, he had a mild cough, which was followed by rhinorrhea. The cough slowly went away and was followed by general malaise and fatigue. He also had subjective fevers, nausea, with occasional non-bloody, non-bilious emesis. These symptoms were actually gradually improving, but on the day of presentation, he noticed a rash on his chest and his back. The rash was completely asymptomatic, but it prompted him to seek care. His two children were home and were sick with a URI two weeks prior to the onset of his symptoms. He had no shortness of breath, no abdominal pain, no changes in bowel habits, or really any other complaints. So we have this middle-aged man who's presenting with myalgias, fatigue, and a new rash. What's most bothersome to this patient is his rash. And my approach to rash is to first actually see the patient's rash and then ask questions. When you have rash and fever, you can think of life-threatening causes like Rocky Mountain spotted fever or staph infection, but I don't think that is the case here because it seems overall the patient is actually improving. It seems like he had a viral syndrome two weeks ago, which his kids may have had as well. So there might be something within the family that's going around. Now my mind is trying to link the rash to the preceding viral syndrome. And one way to link the two together is through a viral exanthem. The thing that makes that less likely is usually you have the rash when you actually have the fever in the viral syndrome. So at this juncture, we're going to get more information from Robbie, but I really want to see this rash. I want to know if the rash blanches or not. And if this gentleman actually has muscle weakness. Reza, that's awesome. Are there any cannot miss diagnoses when you're dealing with the rash? There are a lot of can't miss diagnoses when you deal with rash and fever. I mentioned a few of them, like Rocky Mounted Spotted Fever is one't miss, or a staph or strep infection. Also, I would include in that category, meningococcemia. And these patients would have the rash, the fever, and signs of meningitis. So I would think about those four. And here, we're also told that he's having some nausea and some emesis. I think this is secondary to whatever systemic process is happening in this patient. Other considerations, actually, that you can't miss include dress syndrome. So this is a patient who is on antibiotic or allopurinol or an anti-epileptic and develops LFT abnormalities or rash, fever, and some lip swelling or facial swelling. But there are many, I think, causes of rash that can be life-threatening. And it really depends on whether the patient has a fever, do they have a blistering skin condition like, you know, toxic epidermal necrolysis, for example, or a severe drug reaction. So you mentioned the blanching and non-blanching rash on the exam. What else are you going to look for on exam to help narrow your differential diagnosis? Well, the blanching and non-blanching, the reason that that is an important distinction to make is because if the rash blanches, it tells me that the process is due to vasodilation. And that actually usually is a reassuring sign. If the rash doesn't blanch, then that tells me that red blood cells have extravasated from the vessel. And it makes me concerned for a vasculopathy like a vasculitis. And the way you can tell if a rash blanches or not is you can take a clear ruler or like a clear plastic and push it over the rash and see if it blanches. Other stuff, Charmaine, I'm going to look for an exam. I am definitely going to evaluate for a nuchal rigidity. I'm going to listen for any type of heart murmur that might exist. I would do an abdominal exam. And of course, we would need his vital signs. All right, let me give you folks some more data. The patient had a history of focal epilepsy that was diagnosed several years prior and was actually fairly refractory to anti-epileptics. He actually acquired inpatient EEG during which all his anti-epileptics were discontinued for four days but was otherwise on these medications for over a year. This EEG occurred one month prior to his initial presentation. His medications include valproic acid, lamotrigine, and levotiracetam. He does not smoke and does not use any illicit substances. He has no travel outside California and is sexually active with his wife of 20 years. On his exam, his vitals were normal. He appeared well. His HNT exam was completely normal. He had no cervical lymphadenopathy. His cardiac, pulmonary, and abdominal exams were completely normal. And on his trunk, there was an erythematous, confluent macular rash over his chest and his upper back. Labs were obtained, and CBC and DIF, renal panel were both normal. In terms of his LFTs, his AST was 120, his ALT was 277, his ALKFOS was 194, his total bilirubin was 0.6, and his direct bilirubin was 0.2. The INR was 1, albumin was 4, a UA and a test x-ray were both negative. A respiratory viral panel was obtained and revealed a human rhino slash enterovirus. His HIV was neg, a monospot was negative, and a CMV IgM was negative. Hep serologies were also obtained and were also negative. So we got a lot more information here, and let's just try to tackle this one bit at a time. So what's striking here is that he's been on several anti-epileptic agents. And Arsalan, back to your question of life-threatening causes of rash, one of those include severe drug reactions, whether it's SJS, Stephen Johnson syndrome, and toxic epidermal necrolysis, or DRESS syndrome, or acute generalized exanthomatous pustulosis, AJAP. So him being on all these medications makes me concerned for a possible drug reaction, even if he stopped these medications for four days. So I would go through each of those, and maybe we can address each of those possibilities in real time. Could this be SJS or TN? We were told the patient has no mucosal ulcerations, and his rash is not consistent with that diagnosis. So then we can ask the question about AJEP, or acute generalized exanthomatous pustulosis. This usually develops within a day of initiation of antibiotics. And we were not told that this patient was started on any new medication. And the rash is not pustular based on the physical exam. So I think AGEP is less likely. One diagnosis we really need to consider here is DRESS syndrome.
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And we were given the diff, which was normal. And so the patient does not have an eosinophilia. but the LFT abnormalities and the rash itself and the anti-epileptic agents makes that a consideration. Those patients often also have facial edema. And a quick trick to know if someone has swelling when you're looking at their lips is just look at their driver's license or some kind of photo identification and compare how they appear in the photo to how they appear before your eyes. Now we get into the social history. And back to your question again, Arsalan. Other life-threatening causes of fever and rash definitely includes sexually transmitted diseases. And here, I'm happy that they sent the HIV. Mono and CMV. CMV is fair game here because he has kids and kids can be infected by CMV and pass it on to their parents. And these patients can present with sort of a hepatocellular pattern of liver inflammation, which this patient has. And they can also have a viral exanthem, which this patient has, but they're often more sick. They're fatigued. They have fever, and this patient is afebrile for now, but CMV is another possibility in the differential diagnosis. As far as interpreting his labs, as I mentioned, he has an elevated AST, ALT, and alkaline phosphatase, all consistent primarily with a hepatocellular pattern of inflammation. His albumin is normal, which suggests that this has not been a chronic inflammatory process. The negative UA is helpful because with DRESS, you can also get an interstitial nephritis. So those patients may have a pyuria, but here we're told there's no white cells. And the check sex ray is important because we are given upper respiratory symptoms to, it essentially rules out or makes a pneumonia very unlikely. The positive result here is the human rhino and enterovirus. Can that explain his rash? Well, it certainly can explain his upper respiratory symptoms. Whether it can explain the rash, to be honest with you, it's not on my illness script for those upper respiratory viruses to cause this type of rash on the patient's chest and back. Something else I thought about, and I keep going back to Arsalan's question, was if you have someone who's traveled, thinking about diseases like measles is important, but we were not given any travel history. So to summarize, we have a middle-aged man who two weeks prior to this presentation had some type of what appears to be a viral upper respiratory syndrome with two kids that were sick. And then two weeks later, he presents with this macular rash over his chest and back. And this is all in the backdrop of him being on several medications that are known culprits for drug reactions and hypersensitivity reactions. And his labs revealed a hepatocellular pattern of liver inflammation with a slightly elevated alkaline phosphatase. So right now where I'm leaning in my differential diagnosis is either some type of drug reaction leading to a hypersensitivity reaction and also hepatocellular inflammation or some type of viral syndrome that we haven't identified. I think that's less likely, though, because usually the exanthem with viruses happens during the infection. Raz, that's amazing. And I'm having some technical issues, so sorry if you already talked about this. But the fact that he's been on this anti-epileptic for about a year, does it, in your mind, make a drug-related process more likely, less likely? How are you incorporating that? You know, Sharmin, I think that when you start these agents, probably your highest risk for a reaction is early on in taking these medications. That being said, I imagine you can still have a reaction while being on these medications for a long term. And I'm using analogic reasoning here where I know ACE inhibitors, you can develop angioedema at any moment. So I imagine any of these medications can lead to some type of reaction at any moment. I may be wrong. That's awesome, Rez. Great discussion. I am eager to see how this case continues to unfold. I have no questions right now. All right, let me give you some more information. So he was diagnosed with a nonspecific viral illness and discharged with return precautions. A scheduled phone follow-up two days later, his symptoms had improved and his rash had resolved. However, two days later, he developed high fevers measured up to 102 degrees Fahrenheit at home. A pruritic macular rash developed on his chest, back, and thighs. He also felt that his face and hands were swollen. He was asked to present again to urgent care where his temperature was measured at 102 degrees Fahrenheit, his heart rate was 112, his blood pressure was 116 over 80, and he was breathing comfortably at 16 breaths per minute, satting at 98% on room air. He appeared ill and had a slightly plethoric face. HENT exam was otherwise normal. He had no palpable lymphadenopathy. And jumping to skin exam, 50% of his body surface area was involved with a bright pink circular papules that coalesced into larger plaques that were most prominent on the trunk, forearms, and legs. Both hands had some edema and erythema without focal synovitis. There was no mucosal involvement and the rest of his exam was normal. So, you know, the decision to discharge this patient was not a wrong decision because this patient was afebrile and recently had a viral syndrome and had what appeared to be a benign rash and didn't have any concerning findings like fever or blisters or mucosal sloughing. So I totally agree with the decision to discharge this patient. Now, however, we're dealing with a different case. And the high fever is concerning in the setting of a rash that sort of covers more than 50% of his body. And the question is, is whether this rash is related to his prior presentation, or whether it's a separate process altogether, or whether it's one process that has had two steps in its manifestations, where we saw the early phase a couple days ago, and now we're seeing the second phase. You can see right away, vital signs are vital, and this patient's tachycardia and fever suggests inflammation. In the setting of rash, actually, I'm quite concerned. And his face is swollen. He has a plethoric face. And I would make sure that his airway is not compromised and that he's breathing okay. And now I'm trying to link this almost full body rash. It's greater than 50%. So I don't think it meets the criteria for erythroderma. But now we want to unify sort of inflammation, full body rash, and this sort of plethoric phase. It's really important that they evaluated his mucosal services to make sure that there's no ulcerations, because that would make us concerned for SJS and TEN. With a swollen face and these sort of confluent erythematous lesion, I am still concerned for some type of drug reaction, in particular, the drug reaction with eosinophilic systemic symptoms. So I think repeating the CBC with a diff and sending a urinalysis would be important here. What else can lead to fever and rash? I think we talked about some of the viruses, but I don't associate those with a plethoric phase. And he doesn't have travel outside of the US, nevertheless, I would make sure that his vaccines are all up to date. So what I think we need to do here is repeat some of the labs to see what might be driving his inflammatory process. And at this juncture, I would stop his medications, but I would get a neurologist involved and an allergist. And the reason for that is because we know it's been so difficult to control his epilepsy. And the last thing I want to do is cause a seizure in this guy. But at the same token, I wouldn't want to add fuel to fire by continuing medications that may be driving his presentation. As you mentioned, an allergist, as I was hearing about this, I was thinking I would get a dermatologist involved as well. But an allergist, is there a specific, is that for dress in particular? You know, RC, I am post-call. No, I'm not. I think a dermatologist is totally appropriate. And I really appreciate you making that point. I think that's an excellent point. The allergist was more so because I'm thinking that the anti-epileptics may be at play here. And I want them to tell me how concerned I should be. So I think their involvement might be helpful. But I think getting our neurologists and our dermatologists involved would be very nice as well. All right. So Reza, you asked and you shall receive.
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The upper limit of normal was 500. The hemoglobin and platelets were normal, as was the renal panel and AUA. The ALT was 178, AST 475, and ALKFOS 194. And as a general reminder, these are slightly more elevated than they were before. A T-billy and direct bilirubin are both still normal. The INR is 1, and the albumin is 3.7. A CK was normal, blood cultures were negative, and a ferritin was 437. A CT chest abdomen pelvis revealed mild hepatosplenomegaly, no lymphadenopathy, and no radiographic evidence of portal hypertension. Hand x-rays to assess for synovitis only showed soft tissue edema and no underlying bony pathology. So here we're now dealing with, I would say his salient features include an eosinophilia, a confluent erythematous rash that's covering more than 50% of his body, his history of epilepsy, taking multiple anti-epileptic drugs, and his sort of inflamed state. So those are the salient features of this case. And here, once again, we have hepatocellular inflammation, which would be consistent with a diagnosis of DRESS. His ferritin of 437 just is consistent with inflammation. It doesn't clue us into a specific cause. His CT scan showing a mild hepatosplenomegaly would also be in line with DRESS syndrome. And I will say, like, what else is on our differential diagnosis? I keep coming to DRESS. Could this be a lymphoma? It certainly can. A lymphoma can cause eosinophilia. You can get mild hepatosplenomegaly even without lymphadenopathy, and you can get a perineoplastic rash in the setting of underlying malignancy. But I think that's less likely. And I would put probably the most likely diagnosis here being the drug reaction with eosinophilic and systemic symptoms due to one of his anti-epileptics. And back to Charmaine's excellent question. Usually you see this type of reaction after two to six weeks on an anti-epileptic or antibiotic or medication. But I imagine you can see it at any point while these patients are on the meds. And some things you have to worry about with DRESS is, is the myocardium involved? So making sure he's not having any kind of cardiac symptoms. Is the kidneys involved? You can check the UA that Robbie had given us to see if there's any evidence of interstitial nephritis. All this stuff is important because it determines how you treat such a patient. Are they going to need steroids or not? For this patient with this hepatocellular inflammation, this erythematous rash and fever, I would favor administering steroids. And I think at this juncture, Arsalan, I would get my allergist involved because I am concerned for a drug-related hypersensitivity reaction. DXRXEDU in the house. Follow me on Twitter, please. That means that you didn't get the answer. I appreciate you. That's his follow on Twitter. That's right. That's his handle on Twitter. Thank me to me for that useless elaboration. So dermatology was consulted and made a diagnosis of drug-induced hypersensitivity syndrome, otherwise known as DRESS. The diagnosis was rendered owing to the classic appearance of the rash, along with the facial swelling, coupled with a transaminitis in the face of a very common offending agent, which was the lamotrigine. He was started on high-dose steroids as well as topical steroids, which over the course of two days resulted in a rapid improvement of the rash and the LFT abnormalities. Neurology was consulted, and lamotrigine was placed on his allergy list with plans to follow up to further titrate his other anti-epiloptic medications. He is currently undergoing a slow prednisone taper. So Reza, I'm curious to hear your reflections on this case. Well, first of all, Robbie, thanks so much for preparing and presenting this case. That was a wonderful exercise, and primarily because I finally got the diagnosis right. I'm just joking. I want the audience to know that Charmaine and Arsalan were also unaware of this case ahead of time, so all their questions were genuine and, I think, on point. I think Charmaine raised a great question. Like, if someone is on an anti-epileptic for a whole year, what's the likelihood of them developing DRESS? And I would say early on, it was difficult to separate his viral syndrome, if he really did have a viral syndrome, from his rash. So that was challenging for me to do, to know if his current presentation is related to what had occurred two weeks prior to the rash. The other challenging part of this case, which may have led to a delay in diagnosis for me and maybe the treatment team, was his lack of eosinophilia when he first presented. And he didn't have that facial swelling. So I'd be interested to know from you, Robbie, one, is like the likelihood of developing this type of reaction when you're on these agents for a whole year? And two, like not having the eosinophilia, like what is a test characteristic of that? Because by the way, eosinophilia is in the name of the syndrome. So Raz, let me answer those two questions. And I was lucky enough that our amazing dermatology colleagues were armed with at least a hypothesis about what happened here. And the one thing that I learned from them is that, yes, we have this classic association with the drugs causing this hypersensitivity syndrome being on board on the order of weeks. But there are exceptions to those rules. It's not unheard of that somebody has been on medications for a longer period of time, as you alluded to. But they also hypothesized that the four-day hold of those medications during the inpatient EEG monitoring may have been enough of time for that time point to have been considered a re-trigger. So they're not really sure. But hypothesize that may be one way to understand why it happened now. As to the eosinophilia question, they taught me that DRESS was actually recently renamed to DIS, which clearly doesn't lend itself to an acronym. Robby, you couldn't let me have one minute of joy that I got the diagnosis. You did. You did. You did. You did. This is really just renaming DRESS to reflect the fact that up to a third of people don't have eosinophilia. And so they don't want us to shy away from the diagnosis when eosinophilia is absent. And that can occur in up to one third of of the patients. And so DIS stands for drug-induced hypersensitivity syndrome. So that's how they explain those two questions. A reflection? Yeah, just a question for you guys. So like DRESS or DIS is associated with like high morbidity and mortality. What complications do you guys have in the back of your mind when you're worried about DRESS, if you can just reemphasize that for the audience? The cutaneous manifestations of DRESS are a signal to the diagnosis, but unlike SJS and TEN, are rarely the source of morbidity. What you have to worry about DRESS is the visceral complications. And there are really three organs that can go down that can cause a lot of problems. The liver, the kidney, the heart. The liver is the most common organ, and occasionally cases of acute liver failure from Dress have been described, but these are rare. Acute kidney injury can occur, requiring renal replacement therapy, which also tends to recover. The cardiac manifestations of Dress can also be fairly morbid, and a layer of challenge is that they can also be delayed. So it's not unheard of that patients get a cardiomyopathy weeks into their DRESS syndrome. So to summarize, it's really the visceral manifestations, unlike SJS and TEN, it's not the skin, liver, kidney, and heart. Awesome. All right, folks, thanks for tuning in. We still have to decide what schema we're going to use for this episode, so stay tuned. We'll probably keep that a surprise for you. Make sure to check them out on clinicalproblemsolving.com. Any questions, please email us at theclinicalproblemsolvers at gmail.com. And don't forget to follow us on Twitter at CPSolvers. And thank you again for tuning in. That's a wrap.
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Hello out there. This is Dr. Kathy DeAngelis, the Editor-in-Chief of JAMA, the Journal of the American Medical Association. And this week, I'm going to tell you about the November 12, 2008 issue. And as always, I'll start with the cover. And this one's a doozy. It's a painting by Ernst Ludwig Kirchner, who lived from 1880 to 1938. My goodness, it almost looks like a Maxine painting. But it's Irma Schilling, Painting of a Sick Woman, A Lady with a Hat. It's 1913, and it's German. This painting is not to my taste, but I would never second-guess Dr. Southgate. She is, after all, the guru. And the first article is a JAMA Express, and it deals with vitamins E and C and cardiovascular disease prevention. This is one of two articles in this issue that will have been presented on November 11th at the American Hospital Association late-breaking trials. In the randomized and placebo-controlled Physician's Health Study, Professor Howard Sesso from Harvard Medical School and his colleagues assess the individual effects of vitamin E, 400 IU every other day, and vitamin C, 500 milligrams a day, supplements on the risk of major cardiovascular disease, or CVD. The CVD events among 14,641 male physicians who were 50 years or older and at low risk of CVD at baseline. The authors report that compared with placebo, neither vitamin E nor vitamin C supplementation reduced the risk of major cardiovascular events during a mean follow-up of eight years. And the second JAMA Express deals with aspirin and atherosclerosis in type 2 diabetes. To assess the efficacy of low-dose aspirin for primary prevention of cardiovascular events among patients with type 2 diabetes, Dr. Hisao Ogawa from Kumamoto University in Japan and his colleagues from 163 institutions in Japan randomly assigned patients with type 2 diabetes and no history of atherosclerosis disease either to low-dose aspirin therapy, 81 or 100 milligrams per day, or to a non-aspirin control group. During a median 4.37 years of follow-up, the investigators found that low-dose aspirin therapy was not associated with a significant reduction in the risk of cardiovascular events. In an editorial, Dr. Antonio Nicolucci from Conservo Mario Negri South Research Institute in Italy, of course, discusses the role of aspirin in the primary prevention of cardiovascular disease. The third article deals with non-fasting triglycerides and ischemic control. Elevated levels of non-fasting triglycerides are associated with an increased risk of ischemic heart disease. The role of triglycerides in the risk of ischemic stroke is not clear. Therefore, Dr. Jacob Freiberg from Copenhagen University Hospitals in Denmark and his colleagues hypothesized that increased levels of non-fasting triglycerides increased the risk of ischemic stroke and tested their hypothesis in an analysis of data from a population-based cohort study of Danish adults. In prospective and cross-sectional analysis of the study data, the authors found that increased non-fasting triglyceride levels were associated with higher risk of ischemic stroke. And the fourth article, extensively drug-resistant TB in the United States. Emergence of extensively drug-resistant tuberculosis, or XDR-TB, is a global public health concern. To examine the epidemiology and clinical course of XDR-TB, Dr. Sarta Shah from the CDC and colleagues analyzed TB cases that were reported in the United States from 1993 to 2007. The authors report risk factors, clinical features, and survival rates for XDR-TB compared with multidrug-resistant TB and drug-susceptible TB cases. Among the authors' findings is that 83 cases of XDR-TB have occurred in the United States since 1993. Recent declines in annual cases parallel improvements in TB and HIV-AIDS control. The fifth article deals with depression screening on cardiovascular care, and it is a clinical review for the clinician's corner. Several practice guidelines recommend that patients with cardiovascular disease be evaluated for depression. Thank you. Hospital in Montreal, Canada, and his colleagues systematically reviewed the literature on the accuracy of depression screening and cardiovascular care and the effects of depression treatment on cardiac outcomes. The authors found that depression screening tools have reasonable accuracy and that treatment of depression is associated with modest improvement in depressive symptoms but does not improve the cardiac outcomes. And the JAMA patient page has information for your patients about depression. This issue has three commentaries. The first is by Dr. Vladimir Hrshinsky from the University of Western Ontario in Canada, and it deals with shifts in thinking about dementia. Thank you. protection. And the third commentary deals with translating new medical therapies into societal benefits, the role of population-based outcome studies, and this was written by Drs. Christopher Booth and William McKillop from Queen's University in Ontario, Canada. And the medical news and perspectives, studies illuminating how a gene-regulating process called methylation can sometimes play a role in cancer, are just beginning to lead to clinical applications. The GAO, FDA oversight to produce is poor. Now there's something interesting. And the CDC, more teens must be vaccinated. Officials recommend extending testing for chronic hepatitis B virus infection. And the Nobel Prize honors HIV-HPV discoveries. And from the Capital Health Call, IT bill is criticized, influenza pandemic, hospital infections, and ALS Registry. And from the Centers for Disease Control and Prevention, an update on measles in the United States from January through July 2008, and state-specific influenza vaccination coverage among adults in the United States from the 2006-2007enza Season. And a piece of my mind, this one by Dr. Sarah Schenck from Newark, Delaware. Quote, and then I see it. There is stool everywhere on his sheets, his VA pajamas, even his socks. That's from A Lesson Learned by Accident. And the last two sentences, I think, tell us more about medicine and why we all went to become physicians. Quote, You mean you went to medical school to clean sheets? And her response, No, I went to medical school to take care of patients. Think about that one for a while. In fact, read the entire piece of my mind. And author in the room teleconference, we invite you to join Rita Redberg, a physician from California, on November 19th from 2 to 3 p.m. Eastern time, when she will discuss stress testing to document ischemia before PCI. And readers respond, how would you manage a 24-year-old woman with intractable seizures since age 10? Go to www.jama.com, read the case, and submit your response, which may be selected for online publication. The submission deadline is November 26th. 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, the Editor-in-Chief of JAMA, speaking to you from beautiful downtown Chicago, where the wind blows mightily, but our patients are always the top priority.
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Hello and welcome to the latest podcast for The Lancet Oncology. Richard Lane here with you on Tuesday, December the 4th. In this month's podcast, we're looking at the COBOLT trial published December the 4th, which is looking at ultrasound-guided breast conserving surgery. To find out more, I interview one of the authors of the paper, Dr. Nicole Krekkel. I'm a resident in plastic surgery and also a PhD student at the VU Medical Centre in Amsterdam, Department of Surgical Oncology. Dr. Krekor, many thanks indeed for talking to the Lancet Oncology. You're one of the authors of a paper published in the Lancet Oncology, and this is looking specifically at breast conserving surgery for breast cancer treatment. What are the main problems of breast conserving surgery? So, in words, the background to this study. We have performed a randomized controlled clinical trial to evaluate the intraoperative use of ultrasonography as a method to guide the excision of palpable breast cancer in breast conserving surgery. And to further explain this, in daily practice, the excision of a palpable breast cancer is guided by preoperative diagnostic imaging and the surgeon's ability to feel the tumor during the surgery, thus by the intraoperative tactile skills of the surgeon. And this is a somewhat blind approach of what we call palpation-guided surgery, and this is known to be highly inaccurate, with studies worldwide reporting positive resection margins in up to 41 of patients. And moreover, a surgeon tends to over-excise normal breast tissue, healthy tissue, in an effort to attain negative margins, resulting in needlessly large excision volumes. Previous retrospective evaluation of over 700 breast conserving procedures in the Netherlands showed that breast cancers are incompletely excised by palpation in over 20% of patients with excision volumes that are over 2.5 times as large as they should be. Consequently, there is a higher rate of additional interventions required, such as boost radiotherapy, re-excision, or even a mastectomy, to obtain definite negative margins. And also, the cosmetic results following the treatment are highly unsatisfactory. Ultrasonography is a method to continuously visualize the tumor during the excision, thereby offering the possibility for the surgeon to excise the tumor under direct vision. The technology of high-frequency real-time-time ultrasoundography has steadily improved in recent years, resulting in increased sensitivity and greater portability of the ultrasound and even availability of ultrasound in the operating theater. And thereby, ultrasound-guided surgery has been introduced as well into breast cancer surgery as a method of excising non-palpable breast cancers, so breast cancers that we cannot feel. Tell us about the methodology used in this study. We performed a comparative randomized clinical trial including patients with palpable invasive breast cancer amenable for breast-conserving surgery. Patient recruitment was between October 2010 and the trial was closed in March 2012, and six medical centers in the Netherlands participated in the trial. And the patients were randomly assigned by computer-generated random allocation stratified by study center into either ultrasound-guided surgery or palpation-guided surgery. The primary outcomes were surgical margin involvement, classified as tumor-free, focally positive or positive, and excess healthy tissue resection, which was defined by a calculated resection ratio, or CRR, which was calculated by, derived from the excision volumes and tumor diameters, and in an ideal situation, the CRR is one, implying optimal volume resection and the CRR of 2 implies that the volume resection was twice as large as it should be. Moving on to the results, I mean as you said from the key objectives there, how did this intraoperative ultrasound improve the accuracy among patients given that form of surgery? Our trial clearly demonstrated that ultrasound-guided surgery significantly improves surgical accuracy in terms of margin status and the extent of healthy breast tissue reception, thereby reducing the need for additional treatment and possibly improving cosmetic outcomes. A total of 134 patients were randomly assigned to either ultrasound-guided surgery, and that were 65 patients, or palpation-guided surgery, and that was 69 patients. And a dramatic difference in margin involvement was seen, with only two patients having tumor-involved margins in the ultrasound group compared to 12 patients in the palpation-guided surgery group, which was 3% versus 17%, and statistically significant. And ultrasound-guided surgery also resulted in reduced excision volumes with a median of 38 cc volume resection in the ultrasound group versus 58 ccc in the palpation group with a CRR, calculated resection ratio of 1 in the ultrasound group, which implies optimal volume resection versus 1.7 in the palpation group, which is almost twice as large as it should be. Very important findings, obviously, for clinicians clearly and, of course, for for patients. I mean in terms of summarizing the messages to breast cancer patients I mean clearly there's a benefit in terms of the surgical technique but also the cosmetic outcome must be important given the quality of life issues associated with breast cancer treatment. Yes by allowing continuous intraoperative tumor visualization ultrasound guided surgery can significantly lower the rate of tumor-involved margins following palpable breast cancer excision, thus reducing the need for additional interventions, including re-excision and even mastectomies. In addition, through the achievement of optimal resection volumes, ultrasound guided surgery can significantly reduce unnecessary healthy breast tissue resection and may therefore contribute to improved cosmetic results and quality of life of breast cancer patients. Our study follow-up will, of course, focus on cosmetic results and quality of life for patients, and these results are expected in the coming years. Thank you very much indeed. And final question, obvious final question really, that is what happens next. Important findings here. The numbers of patients in your trial aren't enormous. So do you think more research needs to be done to back these findings up or are there implications, do you think, for changing surgical practice for breast cancer patients based on just these findings? Although our power analysis showed that our groups of patients are sufficient to prove the efficacy of ultrasound-guided surgery, of course, further research would strengthen our own study and would therefore strongly be recommended. However, we still feel that surgeons should be encouraged to learn the skills needed to perform intraoperative ultrasound-guided surgery and to gain personal competence in the use of ultrasound for breast cancer excisions. And it should be noted that in our experience, surgeons can easily learn the skills needed to perform ultrasound-guided surgery with a relatively short training period of up to eight procedures. And of course, an ultrasound device should be present in the operating room, but in most clinics, an ultrasound is already available for other procedures. It looks like a very important future way of doing this type of surgery. Do you think in years to come this will become a standard surgical technique for breast conserving surgery? I think so. I think it should be stated in the guidelines to use some form of visualization during the surgery. And ultrasonography is logically a very simple and easy way to visualize a tumor during the surgery. And I think it's the best way to improve surgical accuracy of palpal breast cancer excision. So if you ask me, I should recommend it as the standard in the future. It's fascinating. Well, we'll follow this one very carefully. But in the meantime, that's a fascinating study. Many thanks indeed for talking about it. That's Dr. Nicole Krekkel on the line from the VU University Amsterdam in the Netherlands. Many thanks indeed for talking to the Lancet Oncology. You're welcome. And thanks to you all for listening. See you next time.
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From the JAMA Network, this is JAMA Author Interviews, conversations with authors exploring the latest clinical research, reviews, and opinion featured in JAMA. I'm Dr. Gregory Kerfman, the executive editor of JAMA, and in this JAMA Author Interview, I'll be speaking with Dr. Ai-Min Lee. Dr. Lee is Professor of Medicine at Harvard Medical School and Professor of Epidemiology at the Harvard T.H. Chan School of Public Health. Along with her co-authors, Sarah Ketel and Charles Matthews, she has written a viewpoint article, now available online at geminetwork.com, which is entitled Fitness Trackers to Guide Advice on Activity Prescription. Thank you very much for joining us, Dr. Lee. Thank you so much for hosting me, Dr. Kaufman. I'm very pleased to be speaking with you today on physical activity and health. Well, thank you. And Dr. Lee, can you please begin by describing the current clinical practice guidelines for physical activity to promote optimal health? Before I begin describing the clinical practice guidelines, I'd like to give a little perspective on physical activity guidelines. Now, many of our listeners probably are aware that physical activity guidelines have changed over the years and sometimes change by quite a bit. I think this is very appropriate because the evidence base that we have on physical activity and health has grown exponentially over time. And of course, it is appropriate to change guidelines when evidence changes. Currently, many professional societies, organizations do give their own guidelines on physical activity. And these guidelines are all based on the current federal guidelines for physical activity. The latest federal guidelines that we have are the 2018 Physical Activity Guidelines for Americans. These guidelines say that for adults to get substantial health benefits, they should engage in moderate intensity physical activity, such as brisk walking, for 150 minutes a week or 75 minutes a week in vigorous intensity physical activity, such as brisk walking for 150 minutes a week or 75 minutes a week in vigorous intensity physical activity, such as jogging or some combination of the two that results in equivalent energy expenditure. And on top of that, muscle strength exercises on two days of the week. Now, people might ask, what is moderate intensity physical activity? What is vigorous intensity physical activity? And of course, there are technical definitions for this, but a very good rule of thumb is when you are physically active at a moderate intensity level, you can feel yourself breathing a little bit harder, your heart rate going up a little bit faster, and importantly, you cannot sing. You may be able to carry on a conversation, but you cannot sing. So that's moderate intensity. If you can sing, that is light. Now, if you are physically active at a vigorous intensity level, you can neither sing nor can you carry on a conversation. So just one additional bit of context, these federal guidelines that were developed in 2018 were based on literature and evidence from studies that used predominantly self-reports of physical activity because at that time the state of the art for physical activity studies was to use self-reports from participants. At that time, we didn't have devices that could track physical activity, or I should say we didn't have many published studies that used devices to track physical activity. Well, thank you very much for that, Dr. Lee. And in your article, you suggest an alternative for quantifying physical activity, and that is the use of fitness trackers. And I wonder if you could describe some of these devices and explain how they work. So fitness trackers are a group of devices that, as its name suggests, tracks fitness or more precisely tracks our physical activity. These devices all have something in common. They contain a unit called an accelerometer and as the name suggests, the accelerometers measure our body movements or more precisely accelerations. So these fitness trackers are things like the smart watches that many people wear. You can use your phone as well, provided you're carrying your phone. There is a ring that people can wear to track your physical activity as well. So these are commercial products. The research devices that we use also are pretty much the same. In addition, we have a device that has a sticky back and we paste it to the thigh or to the lower back or to the ankle. But they all contain accelerometers which measure our body accelerations. These accelerations are then translated by means of algorithms. And the algorithms differ depending on the manufacturer of the device, and they're not always publicly available. The research devices do have open source software, and some of these can be viewed by researchers. So these algorithms take the signals and then translate them into different physical activity metrics. For example, time spent in moderate intensity physical activity, time spent in vigorous intensity physical activity, or I think the most useful, at least currently, and interpretable metric is the metric of steps taken per day. Now, the newer versions of these devices also contain a sensor that can estimate heart rate, and this heart rate is factored into the algorithm that translates the acceleration signals in order to interpret the signals into different physical activity metrics. For individuals who want to measure their daily physical activity, are there advantages to using a fitness tracker? And I wonder if you recommend a specific type of tracker to your patients? So I like the way you phrased the question. You said for people who want to measure their physical activity, and that's exactly it because we are all different. Some people obsessively measure it and some people don't. So for the people who don't, I think, you know, that's probably not very much use asking them to get a tracker because they might use it and then it'll sit in their drawer for the rest of their lives. But for people who do want to measure their physical activity, I think there are big advantages to using a fitness tracker. And again, as I mentioned previously, I think the most interpretable unit, the one that is most intuitive to both patients and clinicians, is the metric of steps taken per day. The advantage is that this is something that's very objective. You don't have to do a lot of work. Your device tracks this for you. This can be something that you and the patient use to monitor progress, monitor how they are keeping up with a plan that you provide for the patient. And studies have shown that seeing this metric does increase step count. Studies have suggested that if you provide step counters to outpatients, they do increase the number of steps that they take to about an additional 2,500 steps per day. In terms of what tracker to use, I think that again depends on patient preference. There are three main types. So the watch, I think, is what most people use. You can also use your phone and there is a ring that you can wear. I don't see very many people using the ring. People use the watch a lot, but some people don't like wearing watches. I actually think it's harder to carry your phone. So your phone will only track your physical activity if you carry it. And a study that we've conducted has shown that steps are actually tracked a little less well by the phone among women compared to men, which sort of makes sense, right? Because men wear pants most of the time with pockets that can incorporate a phone. I'm wearing pants now, but my pockets are too small for my phone. So I'm actually carrying my phone in my hand. So if I don't carry my phone, it's not going to track my physical activity level. So first, the device should match patient preference. And second, that's also the affordability factor. I think that many smartwatches that are reasonably priced and many people can afford that. The phone, again, you know, you can have cheaper phones, more expensive phones. Most phones nowadays have accelerometers in them. All right. Well, that's very interesting. And I wonder if, in the light of these new devices, if you believe that the next update of the physical activity clinical practice guidelines will actually include fitness tracking, such as measuring step counts, as part of the guidelines? So not only do I think the next iteration of guidelines will include step counts, I think they should include step counts because I think guidelines should be driven by the evidence that is available. And in the last few years, the evidence based on step counts and health has really grown tremendously. The use of fitness trackers is already very ubiquitous nowadays, and the step count metric is very commonly used by many people. So I think this is an objective measure. It's not something that your patients have to think too hard about. It's a measure that keeps, at least it keeps me honest. It's not like I can overestimate my physical activity. It can provide motivation for many people and it's simple to monitor and use. So I, for one, would very much like to see our next iteration of guidelines include a step count metric. Having said that, we spoke earlier about patient preferences and some people do not want to monitor their step counts.
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They know, for example, after dinner every night, I'll go for a half-hour walk. Or they know I'm going to play tennis twice a week. Or they know, you know, I swim in the weekends. So for these people, they might prefer to monitor time instead. I personally believe that we should keep the time metric, but we should also add additional metrics like the step count metric as evidence becomes available. So if you were to recommend a daily step count to promote health to your patients, what number would you suggest? So the first thing I would say to that is that when we get fitness trackers, many of the trackers have as a default goal 10,000 steps per day. And we really do not need 10,000 steps a day to be healthy. For many people, this is a very large and probably inaccessible number. Having said that, the step goal that I would set, well, these days of personalized medicine, I think it's important to set a goal depending on where your patient is at. And I think of this step goal as sort of a tiered way of looking at it. So you know your patient. What's your patient like? Is this a patient who does really not very much? If so, then I would set a goal that is a little bit of a challenge, but also achievable because you want to empower the patient to be able to achieve this first step. My first step would probably be to say, try to increase your step count by 2,000 steps a day. So 2,000 steps is approximately one mile. This sounds like a lot, but remember that the fitness trackers counts all steps. It's not that the patient has to go out and walk a mile continuously. If I go make myself a cup of coffee, those step counts count. If I go out and get my mail, those step counts count. So to get an additional 2,000 steps a day, I think is really quite doable for many people. Now, the next tier would be if your patient is already doing something but would like to achieve optimal health benefits or substantial health benefits. Then for that I would say if the patient is younger than 60 years of age, a step goal of 9,000 steps per day is reasonable. And if the patient is 60 years or older, a step count of 7,000 steps per day is reasonable. Now, when I say per day, sometimes people say, oh, I only got 4,000 steps today and I feel bad. I didn't make my goal. Now, of course, our lives differ from day to day. But if on average over the week, you can get those 7,000 or 9,000 steps per day, that would be great. Now, there's, of course, a category of our patients who already do 10,000 and more, and they may feel, what, you know, is this not good for my health? I would say that, you know, more power to you. If you can get 10,000 steps or more, that's fantastic. Go for it and keep at it. All right, that's great. And I think from a public health perspective, one of the most important points that you make in your viewpoint article for JAMA is that any level of physical activity above sedentary behavior may promote health. And I wonder if you could comment on this very important point. I agree. That's a totally important point because too many people in the world, in the US, are not physically active. And perhaps they don't start because they feel like it's just too difficult. The large body of knowledge that we have on physical activity and health, and particularly with the newer devices that can measure even low levels of physical activity. They very encouragingly show us that there's a dose-response relationship between physical activity and health. And for many outcomes, more specifically, this dose-response relationship is what I call curvy-linear, meaning if you do some physical activity, you get some health benefit. If you do more physical activity, you get more. And then it tapers off at a certain point because obviously we can't live forever. And in fact, the dose response curve, you see that the biggest bang for your buck actually occurs among those who move from doing nothing to doing just a little bit more. So I think the body of knowledge that we have now is so encouraging because it shows that, you know, any little bit that you do is helpful and that there is no amount that we would say that's too little to have health benefits. Well, Dr. Lee, thank you very much for your insightful discussion of physical activity tracking in health promotion. To follow this and other JAMA Network podcasts, please visit us online at jamanetworkaudio.com. This JAMA author interview was produced by Daniel Morrill. I'm Dr. Gregory Kerfman, and thanks for listening.
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Okay, welcome to episode 86 of the Divine Intervention Podcast. In today's episode, I'm going to essentially discuss how to be an excellent intern. There are many facets to being an excellent intern, but this is just basically like a general overview of your job descriptions as an intern, especially for a medicine intern or a transitional year intern. I'll talk about some key things, expand on some key things, and just essentially like mention some high yield key things you should do as an intern, right? And really like these are born from my experiences being an intern, from mistakes I have made as an intern, from good things I've identified in other people doing well as interns, from mistakes I've identified from other people that have made mistakes as interns, right? So I will just sort of talk through these things in no particular order. And hopefully this should be a relatively short podcast and we'll get through this. So what's your job description as an intern? First thing is to show up on time for stuff, right? So the thing is you always want to be early, right? Don't build a reputation as a person that is always late, because the thing is, you'll get noticed, and then ultimately, you'll get into trouble with that, right? In fact, people think of it as like a professionalism issue, right? And professionalism, once that word becomes dangled around you as a deficiency you have, that can raise some very serious problems in residency, right? Because the thing is, reputation really does matter a lot in residency. And the reputation you build early on is the thing that may ultimately stick with you for the rest of residency, believe it or not, right? Because the thing is, you may do so many good things in the middle of residency, in the end of residency, but really it's the reputation that you acquire early that will ultimately stick, right? So remember this when you're starting out an intern year. Essentially, just work on building, you know, a strong, solid reputation with your other residents, with nurses, with your attendants, with the support staff. And really, if you establish this good reputation, it will follow you through, even if you make some mistakes along the way after that initial good reputation that you have built up. So you should sort of establish a rule for yourself that you try to get to things like five minutes ahead of time. Because really, if your program director notices that you are always early, you're always present at things, you'll be in your program director's good books. And this is basically like, you know, pretty much establishing a savings account that you can withdraw on, you can draw on in the future when you get into trouble, for some troubles you may face down the line in residency. Second thing is to sort of work hard in everything you do, right? Again, don't be known as the lazy resident because again, if you acquire a reputation as a person that does not do their job, it's a very surefire way to destroy yourself in residency. So really don't be the person that pawns off admissions on other people. Don't pawn off work on other people because really if you acquire that reputation, people will retaliate and you really will not like the outcome. I mean, the unfortunate situation in many hospitals, in many residency programs, is that hospitals are like a cesspool of gossip. Okay? So, don't let bad information, bad information like, oh, this person doesn't do their job, spread about you. Because again, that can put you into trouble that you do not envisage because once like really like literally it's your job so you might as well just do your job right work hard do your job so avoid this just don't be lazy because i mean you know what you signed up for even as a college student going into med school? So just freaking do your job and you will not get into trouble. Because the thing is, once a rumor starts spreading that you are lazy, it is a very hard reputation to repair, okay? And the problem is if it gets into the ears of the wrong people, so basically like people in charge, like program directors, directors of medical education and whatnot, you can actually begin to have troubles in residency that are more far-reaching than you could ever imagine, okay? I guess next thing is obviously, right, you want to see your patients in the morning, pray around and around on your patients. That's kind of obvious. I won't say more than that. Another thing is you want to get good at coming up with assessment and plans, right? I mean, as a medicine intern, that is like almost like the bane of your existence, right? You want to come up with assessments for problems and plans. And I mean, this may be something I may talk about in the future in a more expansive podcast. But really, how do you identify your problem? How do you make a problem list? It's actually quite easy. The way you make a problem list is one, you identify lab derangements, right? What, and usually Epic or CERN or PowerChart or whatever you use will blank out these things in red, right? If there are lab derangements that are like serious, they should make its way to your problem list. If there are chief complaints that are serious, if the patient's chief complaint should certainly make its way to your problem list. Is there a test that was done like a chest x-ray or an echo or whatever that identified a problem? That should make its way to your problem list. Are there super deranged vitals like sinus tachycardia or whatever? That should make its way to your problem list. Are there chronic problems the patient has at home that they are bringing with them to the hospital like diabetes, like heart failure? That should make its way to your problem list. Are there chronic problems the patient has at home that they are bringing with them to the hospital, like diabetes, like heart failure, that should make its way to your problem list. That is essentially your problem list. And then literally for each problem that you write down, the next thing you want to do is to say, okay, how will I assess this problem, right? So if, for example, it's a pneumonia and you're like, oh, you know what, I'll assess this with a decrement in the white count, with a clinical improvement in the patient's symptoms, with an improvement in how their chest x-ray looks every morning. Like, ask yourself, how will you assess these problems? How do you plan to fix this problem? So what are the interventions, right? Are you giving antibiotics? Are you sending them to the cath lab? What's your intervention for the problem? And then how will you track the resolution of that problem? If you basically answer those questions for each of those problems you identified, you've essentially made up your plans for your problems. And really, if you're very systematic in this format, in setting up your assessment and plan, you will be an intern that misses very few things with regards to a patient's hospital course. And then you also want to, if there is some kind of outpatient follow-up that's needed for the patient's problem, you also want to kind of, you know, focus on that in your assessment and plan. Don't forget to continue home medications, right? That's important, right? So you don't want a patient to be on like a chronic med at home and then you don't do a med rec. So you don't continue those medications in the hospital. And then the problems they came into the hospital with you add more new problems to that. That's not necessarily a prudent. Right. And then another thing with regards to discharge summaries, discharge summaries. Again, this is a freestyle podcast. Discharge summaries. I'll encourage you to start writing them when you admit the patient, okay? And then update them every day. If you do that, your discharge summary can take like a minute, two minutes to write. But if you don't and you wait, you're kind of like moseying, lazing about, and you wait till the patient is leaving the hospital to write your discharge summary, then it can become a one or two hour ordeal, right? Especially for patients with like prolonged stays in the hospital, like 30, 40, 50 day stays in the hospital. That can make your life profoundly miserable, right? And then one other rule is starting low and going high. This is basically a medication rule. So I will encourage you, start and up titrate as needed. It generally does not make any sense to try to go for the highest nuclear dose of a particular medication. That's not particularly smart because if the patient has an unwelcome side effect, trust me, you probably would not want to experience that if you can avoid it. So start at a low dose.
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And then you definitely want to learn how to read EKGs and chest x-rays. That's just an important thing you want to do as an intern. You also want to get good at presenting your patients. Again, I will encourage you, build a standardized approach. In fact, you know what, let me just combine this with another thing I guess I want to talk about. And that's like note writing, presenting, all that stuff. The key principle here is you want to develop a standardized approach to things you do in residency, like tasks that you repeat every day in residency. try to develop approaches to those tasks. Because the thing is, when you develop an approach or like an algorithm in your mind, or like a template in your mind that you use for like abstracting information from a patient, rounding in the morning, writing your HPIs, writing discharge summaries, admitting patients to the floor, admitting patients to the ICU. If you can come up with a standardized approach, one, it makes you very efficient, and two, it makes that process almost mindless, right? Because the thing is, if you gain a reputation as an efficient intern that is also accurate, it builds a lot of goodwill with your seniors, with your attendants, and with your program director, okay? That's the kind of good attention you want to attract as an intern. And again, you can do this by developing approaches to all these things. Like literally, I mean, I'm a transitional year resident. I have approaches to how I write discharge summaries, to how I write HPIs, to how I come up with assessment and plans, to how I round on patients in the morning, to how I do my pre-rounding, to how I do my presentations, I have approaches to how I do tasks that I repeat often, right? It is one thing that has helped me tremendously as an intern. Now, next thing is, right, I mean, obviously, you're going to admit patients as an intern. That's your job. And then you also want to sort of learn how to put in the right orders. In fact, if I were you, this is one thing I would focus on very early in intern year, like knowing how to put in the right orders for common things. Right. So like like medical admit orders, ICU admit orders like CWA protocol orders, opioid withdrawal power plans, blood transfusion orders, orders for pressers, orders. Thank you. orders for like blood draws, orders for CBCs, for BMPs, for cultures like respiratory cultures, blood cultures, for consults. I will encourage you to figure out how to put in those orders because trust me, putting in orders is actually maybe one of your top three responsibilities as an intern. And if you can get very accurate at doing this, it will make your work really fast because you don't need to keep asking, oh, how do I put in this order? How do I do i do this how do i do that so ask your seniors early and often how they put in certain orders so that you know exactly like literally like what you type into the order screen so you know what you are ordering for specific situations now if you know that um i mean there are even other sets that you can create or other sets that already exist right so like other sets for B, for example, those are things you'll sort of want to be able to conglomerate into like a power plant for yourself. Because think about it, right? You can save your, if you do the work once of sort of like grouping all the Hep B labs together and all the Hep C labs together and all the HIV labs together, you can just literally click on two things and you have all those labs ordered instead of, for example, having to order like the HB surface antigen and the HB core antibody and the HB surface antibody and all that individually as you're putting in orders. Right. These are all things that can save you time and make you super efficient as an intern. Now, your next task as an intern is to do well in your interning exams and your boards. So you may see divine here, you go with the whole test taken again. The thing is, many people think that studying in residency should not be a thing. Well, think again. You could not be further from the truth. Let me tell you why. And I will give you some very good, very compelling reasons why you should study in residency. The first thing is you want to be competent. Okay. The thing is many people think that, oh, you get competent just from seeing patients. That is not true. You can actually learn a lot from literally studying. Okay. Because the thing is when attendants begin to see as a person that has a good knowledge base that is competent, guess what? You become more trusted and you become less babied if such a word exists. If you want to be independent in residency, you can actually acquire a lot of independence if people know that you are competent. And trust me, competence comes from seeing patients and also from learning your craft by literally studying, okay? The worst thing that can happen to you as an intern or as a resident is to cause patient harm because you have like a lapse in your knowledge, right? I mean, classic example is like screwing up a code because you don't know your ACLS algorithms. Again, do people make mistakes? Of course, you can make mistakes, right? But egregious mistakes, common things that pretty much everyone knows, but you don't know because you're not spending time to attend to your knowledge base, that can put you in trouble very quickly, right? It can put you into the bad book of your program director, right? It can also be a source of lawsuits, not just in residency, but even as an attendant in the future. And again, just remember, it's your job, right? Like literally, it's your freaking job. You might as well get good at your craft. This is something you're going to do for the rest of your life, right? I mean, if you're a transitional year intern going into like another specialty, that's a different story. But regardless, this is your job. This is what you're going to do for the rest of your life. You might as well spend the time in a controlled environment to learn your craft really well. And the thing is, studying also helps you with exams, right? Because the thing is, say for example, right? You study routinely, you do well on your in-training exams. The thing is, that will help you buy a lot of goodwill. And it actually gets unnecessary attention off your back. Let me give you an example, right? say, for example, you're doing super well on your in-training exams. The thing is, you may actually be able to get away with stuff that other people may get in trouble for. But if you sort of look at it on the flip side, if you perform poorly on your in-training exams, you essentially attract attention that is not the good kind. You basically put yourself on your program director's radar because your program director begins to see you as a person that is at risk for failing exams in the future. So you essentially come under their watch light. And to be honest, this is the last thing you want to do. You don't want to come under the watch light of a program director. And this is something you may say, Devine, come on, it's not a big deal. It's something you may not understand now, but when you get into residency, you will understand the peril of coming under a program director's watch light. It's something you will understand when you start residency. The thing is, when you come under a program director's watch light, or you come under the watch light of other attendings of your seniors, little things that others may do that may not attract as much pushback will attract a lot of pushback if you're on people's watch list. It basically makes your residency experience very uncomfortable. And you will essentially be in a situation where you're trying to go above and beyond and trying to prove yourself because you've just established this bad reputation as a person that is at risk for not doing well on exams. You essentially begin to walk on eggshells. And that residency is already stressful enough. You don't want to put yourself under this cloud. Now, next thing is you want to be humble as a resident. Don't be proud. Don't be egotistical. Don't be the person that everyone says, oh, this guy has a big ego. Be humble. Try not to stir up jealousy on your own. I mean, obviously, some of this is out of your control because some people are just jealous. But be a teachable person. Don't be the person that always boasts. Don't disclose your test scores ever.
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I scored in the 99th percentile, in the 95th percentile on my engineering exam. Don't disclose your test scores ever. Don't be the source of that information. If other people hear from other people, fine, whatever. But do not disclose your USMLE scores. No, just your scores are for you. They are for program directors. They are not for public knowledge. You don't need to disclose your test scores to other people. Don't be the person that answers every single question and money report. Because the thing is, if you're proud, you will attract attention. And again, the attention you attract will not be the good kind. Because the thing is, medical professionals in general are very competitive people. So if they see that you're succeeding so heavily and they're not, and you're boasting about it, the thing is that jealousy can spur co-residents to basically turn against you and start doing things that can undermine you and pull you down. Okay. So again, be careful. If you're humble, you will very likely not get into these kinds of troubles. Okay. And I mean, the unfortunate thing is sometimes you may be super humble, but some people are just super jealous by nature. Some people just do not like seeing other people succeed and they're not succeeding. So in view of this, be careful in residency. I'm not saying be suspicious and be like always, oh, I'm watching out. People are out to get me. No, no, no. That's not what I'm saying. You don't need to be suspicious, but be cautious. Okay. Think twice before you trust people because people can stab you in the back. Okay. So be very careful. Be very careful in residency. Okay. In every organization, not everyone is going to be your friend. I mean, even the Bible says this, that a man's enemies are members of his household. If you look it up, I believe it's a verse in the book of Proverbs, okay? So just be careful, okay? Not everyone is out for, not everyone is pleased with your successes, okay? So just be careful in residency. Now, next thing is you want to be an excellent communicator, Okay. Communication is extremely important in residency. In fact, I will probably make a podcast that is targeted specifically towards communication as a resident. The thing is, if you're a good communicator, you can prevent many patient care errors. If you pass along information, you know, in a clear, succinct manner, right? Many conflicts, believe it or not, that arise in residency, many patient care errors that arise in residency, all arise from a failure of communication. So as an intern, try to always keep your attendance, always keep your seniors in the loop, okay? Don't be the person that acquires a reputation as, oh, he did not hand off correctly. He did not pass along this information really well. Remember if and then statements when you're doing handoffs. Like, if this happens, this is what you should do. That's a very good means of practicing a good communication. And again, if you're an excellent communicator, it will attract attention to you, but it will attract the good kind of attention. I mean, one thing that a senior of mine thought me that has helped me a lot is like touching base with nurses in the morning. Right. So, for example, in the morning after I like see a patient and I know what I'm doing for that patient for that day, guess what I do? I walk to the nurse and say, so for Mr. X, this is what I plan to do today. He's going for this at this time. This is what I plan to do today, blah, blah, blah. And I asked the nurse literally, like, are there any concerns you have? They voiced those concerns and we walked together to deal with those concerns. And then I ask, is there anything you need from me for this patient? If they need it from you, you fix it right there and there. The reason I do this is it basically prevents you from getting unnecessary pages during the course of the day from nurses. It's a very useful skill. In fact, I'm very thankful to my senior that actually taught me that. Your next responsibility as an intern is to do research. If you don't do research, you will very likely not be able to get into fellowship and you will just basically limit your career options if you don't have good research on your books next thing is don't lie okay the thing is if you lie people will not trust what you say if people don't trust what you say they will essentially begin to question and recheck your every move okay and trust is one thing you definitely want to build as a resident now next, next thing is document, document, document. This is something that you will understand the importance of when you start residency. The thing is, people cannot lie or argue against records that have been kept. If you are called for an emergency situation on the floor or something unusual happens during the course of the day, just go ahead and write a brief note, write your reasoning, write how you assess the situation, write down what you did in clear terms, okay? Because again, it's in the medical record. If something is documented, you likely will not get into trouble, especially if you explain a good reason why you did certain things, okay? Document, document, document. The brief note is your friend. It is extremely, extremely, extremely important. Now, next task as an intern, right, is you want to stay under the radar, but you don't want to be seen as a person that is completely quiet. Because the thing is, if people see you as a person that just keeps withdrawing into your shell, people can begin to pick on you and you can also get into trouble that way. You certainly do not want to do that. You want to fly under the radar, but you want to be a person. Remember, medicine is a team sport. You want to fly under the radar, but you also want to run interference with your co-residents. Basically, you want to put yourself out enough to be like, oh, people know you, but you don't want to put yourself out too much to where people think you're egotistical, but you also don't want to pull yourself back too much to where people think you're a weirdo and you're not a team player. Because again, that can begin to bring up issues for you in residency. Now, next thing you want to do in residency as an intern is to amass political capital. Basically, this is like gaining goodwill. And there are many ways you can gain goodwill. And I'll say probably the easiest way to gain goodwill is to respect your nurses. The thing is, if you do simple things like greeting nurses, touching base with your nurses in the morning, responding to your pages in a timely fashion, right? Coming when a nurse, like if a nurse like pages you on or calls you and says that they are concerned about a patient and they want you to come and assess the patient, go and assess the patient. The thing is, if you do these little things here and then really to be, to be honest with you, these things are not hard. They are very easy. And the thing is, this goodwill will essentially spread around the hospital like wildfire, and it will make it possible for you to get things done for your patients quickly. And the thing is, nurses will be willing to go to bat for you. Other residents will be willing to go to bat for you because they know that you've established goodwill. So basically, the way you establish goodwill is by doing good deeds that you never know where you would need. Let me just put it this way because, I mean, I'm a Christian and I don't do good deeds with the expectation of a return. But remember, the Bible says that you reap what you sow, right? If you sow good deeds, you reap goodwill in return, okay? So just sort of keep those things at the back of your mind, okay? You will make your residency experience miserable if the nurses hate you, okay? And at the end of the day, again, remember, these people you're working with are all your colleagues. They're one big family, so act appropriately. And also, it's probably a good practice to collect phone numbers. Because those people are usually the gateway to their respective subspecialties. Another thing you want to do, make your attendance life easier, make your seniors life easier. I mean, there are basic things, right, that you can do well as an intern, like Scott work. You can do Scott work very well. I mean, you've been a medical student for years, right? You can do Scott work really well.
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Make your attending's life easy. And again, these are just all means of acquiring goodwill, okay? Although, don't try to be so independent that you are then handling dangerous situations on your own without putting your attendant and your senior in the loop that can get you into trouble really quickly. Okay. So if you need help, literally ask for help. And again, avoid professionalism issues. Um, professionalism is probably something I should essentially make a podcast on in the future. It's just one of those terms that if it's dangled along with your name, that you have professionalism issues, that is something that is very hard to repair in a residency. I'll just put it that way. And again, try to avoid problems with your program director. Just try not to get in their bad books. The program director can make your life profoundly miserable. So really, your goal every single day is to just get in your good books. And again, I've talked about many things you can do that can help you get in your program director's good books. It's not like your program director sets out to make your life miserable. No. For the most part, under most circumstances, program directors actually work in your best interests. So make their job easier by just doing the right thing. If you do the right thing, you'll be in the good books. If you do the wrong thing, you'll be in their bad books. Okay. So don't be in their bad books because at the end of the day, they can make decisions that can have telling consequences for your future as a resident. Now, when you start a new rotation, meet your senior, meet your attending and set expectations early. Ask them, what are your expectations of interns or whatever under these circumstances like what are specific things you love people to do and then every week ask for feedback do you think i'm meeting expectations this is essentially like a nice way to almost control the narrative you'll get in your evaluations at the end of uh at the end of a rotation yeah i really want to try to keep this uh to 30 minutes or less. I'm going to sort of speed up here a little. Another important thing is sort of set up social needs of your patients early, right? So classic things you'll probably see if you work at any big hospital is like getting patients placed for like endocarditis, like after they clear the blood infection and then they need like IV antibiotics for a long while. If a patient has osteo and they need to get to a facility to get like IV antibiotics or a person needs to go to rehab after the hospital stay. These are things you want to sort out early, right? Placement comes first. Just one of those things you want to live like. In fact, I'll tell you this. When you are meeting a patient as part of your workup of a patient, ask yourself, are there any social needs that may impact this patient's stay? If you identify social needs, literally, once you're done with the admission, go meet social work and begin to tee these things up from the get-go, okay? It can make you very efficient and it can actually reduce a patient's length of stay in the hospital. Remember, pre-certs, getting placed, all that stuff, insurance approvals take time. So start them early so that while you are taking care of the medical problems of a patient, you are also taking care of the social problems of a patient so that as the medical problems are resolving, the social problems have already been resolved and they can get out of the hospital as quickly and efficiently as possible. Now, also you want to get good at like some basic procedures like intubation, placing arterial lines, placing central lines. If you're really gung-ho, maybe getting good at placing gambros. Those are things you use for like temporary dialysis. Those are things you, especially intubations, right? You want to get good at intubations. It's one thing that may save your butt, especially if you have like a crashing patient in the future. And this last rule is something I've read a lot on SDN and is a useful rule to know. Remembering that they can always hurt you more. They can always hurt you more, right? So what does this mean? Basically, if something happens, don't be the person that always complains, right? If something is not egregious, if something is something you can tolerate and just deal with and doesn't affect your life significantly, to be honest, don't complain against your seniors. Don't complain against your attendants. I'm not encouraging bad behavior here. Right. Again, in fact, this basically what I'm saying now does not reflect the views of any residency program I'm associated with. But basically, I'll just tell you this. Don't be the person that always complains. OK, don't be the person that always complains. If your master repetitions, the person that always complains, people can begin to turn against you. And whether you like it or not, as an intern, you have a lot less power than a second year. And a second year has a lot less power than a senior resident. And a resident has a lot less power than an attendant. So again, don't be... Basically, develop some sort of thick skin. Again, if something really bad is happening, and this is affecting a patient, affecting you personally, obviously you should report those things. Again, I'm not saying to keep these things in, but don't be the person that, oh, you report every single thing. You just basically build a bad reputation and basically, let's just say you may have certain unforeseen consequences from being the person that just does not get along and always reports everything. Like every little thing that happens gets under your skin. Do not acquire that reputation. So I think I've probably said enough. And this is, this, you know, looks like a pretty good stopping point for me. If you have any questions, feel free to reach out. I'll try to make more residency-focused podcasts in the future. And again, as I round up, I want to mention that I offer one-on-one tutoring for the USMLE Step 1, Step 2CK, Step 2CS, and Step 3 exams. I have tutored thousands of people that have done super well on these exams. Talk about like 90th, 95th percentile sort of scores. I also tutor for the preclinical med school exams, the third year shelf exams, the internal medicine in training exam and the internal medicine board exams, believe it or not. And I also have admissions committee experience with a top three medical school. I've been on an admissions committee before. So I actually prepare like ERAS applications for med students applying to residency and AMCAS applications for college students applying to med school. Like I can do mock interviews, I can help with personal statements and all that stuff. And on the offhand, you have a friend or relative that needs tutoring in organic chemistry. I also offer tutoring for those for organic chemistry as a discipline. So I hope you have a wonderful day. I think this is probably like a record for me. This is like the third podcast I believe I'm making today. Today is obviously a day off. So I'm trying to like make the most of my free day and by churning out as many podcasts as possible. So have a wonderful week ahead. I wish you the very best and God bless. And the match is actually coming up this week. So I'm everyone i hope you all match if you don't match remember it's not the end of the world uh there's the soap there's a scramble it's an anxiety provoking process but you know pray okay i'm a christian i believe in prayer pray okay seek good advice and you know just try to play your cards right and learn from your mistakes and um you, I wish you all the very best. If you're ever in any like tenor situation, you can reach out and I can try to draw from my wealth of experience to, you know, try to guide you in the right direction. So have a wonderful week. God bless. I'll see you in the next podcast. Thank you.
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So, I ended up actually doing a stress test on him, and it was grossly abnormal. Did an angiogram, and he had a proximal LAD significant lesion. And he ended up getting stent. Now, this is a 36-year-old, right? So, you're like, man, he's got no risk factors. So, you know, always trust yourself in what you're hearing. Hi guys. California. Dr. Patel is a longtime friend and mentor. He's an excellent educator, and I'm so glad to have him on the show. We'll be discussing the evaluation of the patient with chest pain, and we spent a lot of time on this episode talking about the ins and outs of cardiac imaging and cardiac stress testing. Thank you. I think don't exactly know what to do with. And we asked Neil all about these topics and get pretty detail-oriented here. I think you'll find it very informative. So without further ado, here's Dr. Neil Patel. Hi, Neil. How's it going? Hey, how are you guys doing? Neil Patel here. Doing great. Just me. I'm the only one doing great, apparently. Tony doesn't want to say hi. Okay. Okay, deal. So I know we're going to talk about, obviously, we're going to talk about chest pain today. One of the biggest things, if you look at, you know, whatever, anything that we do, right, people's symptoms and what people are complaining of and we're worried about X, Y, and Z, just to kind of put a couple of numbers, right? So of all the chest pain that comes to the ER, maybe 10% is actual ACS, right? So acute coronary syndrome, things that need to be acted upon in some way, shape, or form, whether it be testing, whether it be adjusting medications, whether it be an angiogram. And, you know, so, but that number is a lot, so although 10% doesn't seem like a lot, but the number of visits in the ER per year are enormous for chest pain, and that's obviously a very common complaint. People are just worried, you know, chest pain, and it's an assumption that everything comes, that's got to be heart- related. But I do think that when it comes to us as physicians, regardless of the symptom, you know, history and history and history are such a huge thing. And, you know, we all learn that in med school. And I think sometimes it gets lost because obviously your days or everyone's days are laid out differently once you kind of branch off into your realms. And sometimes you don't have time, you don't necessarily to kind of dig into that. But if you get someone, right, 58, diabetic, high blood pressure, obesity, and they're having some symptoms that are concerning. See, when we talk about low, intermediate, high risk, the way I kind of approach these people is kind of what's their risk factors for having CAD, right? If this is a 26-year-old with nothing going on, fully active, chances of him having obstructive CAD, right? Critical narrowing causing heart blockage is probably extremely low. Just by the fact that you can get older, age alone carries a very powerful predictor. So the person who's 56 versus the person who's 86, right? 56 depends on what you're hearing, what else is kind of going on. That person is probably intermediate risk, especially in this setting, right? Diabetes, hypertension, obesity. And you want to ask yourself, well, okay, so they have intermediate risk for CAD, but is what they're complaining of, is their symptom actually related to CAD, right? There's two different questions, right? One is to say, we kind of get these consults all the time. This person's intermediate risk and patient's having chest pain. So then I go to talk to them. I had a patient today and she was 67. She was a smoker. She was diabetic, which by the way, smoking and diabetes by and far are the two big things that you kind of, when you kind of got to really press hard because they carry, they carry, it's just very powerful predictors of development of plaque and calcium and CAD. And so then she's starting to tell me her story. She goes, yeah, you know, I get this chest pain. Every time I move my right arm and I lift it above my head, my chest hurts. Now, you know, so you say to yourself, well, is that really, you know, related to a blockage, you know, a critical blockage? You say to yourself, well, the heart, like any other muscle, when it's active, when the heart rate goes up, when it's stressed, it's going to need more blood. If there's a real blockage there, there should hopefully be some degree of exertional component, right? So I think that people may or may not be familiar with the whole diamond Forrester model. And they say, well, what is the characteristic? Was it provoked by stress? And then did it go away? And we can talk about the models, although I'll tell you to look at it differently, which is the models are nice, but when you break the models down, all of them come down to history, physical, right? They say, do you have a history of a stroke? Do you have a history of smoking? Do you have a history of high blood pressure? Do you have a history of CAD? And then you say, well, what was it that you were doing when your symptoms came on? And then you say, well, what are your symptoms? And so the person that I saw today, that's not related to her probability of having CAD. Moving your arm and reproducing the pain, yet while she walks up a hill, she doesn't get the pain. I was like, look, you have risk factors for developing CAD. Chances are you probably have CAD because you're smoke. You have all these things. You have the setup for it. But what you're complaining of does not seem to be bothering me. And that sometimes is hard for people to do because it's kind of like committing and then you're worried like, oh man, but if I send them out and they have a heart attack, like what's going to happen, right? You're worried about, you know, nowadays we're worried about a lot of things. We're worried about legality, right? We're worried about, oh, we don't want to just send them out. And then this person should just get a stress test. But I think it matters, you know, you find out what's triggering it, really what's the problem. And then you say to yourself, well, how active are they in their day? And I don't necessarily ask people, can you climb up a flight of steps? I know we always talk about Mets, and we say, can you climb up a flight of steps with the groceries? Oh, you can? Okay, then you're four Mets. The way I word it is, what's the most physically active thing you do in your day? When you leave it open-ended, you'd be surprised. People are like, oh, I walk into the end of the driveway and get my mail. If you ask them, are you physically active? They would have answered yes, and they wouldn't necessarily be wrong. But if you ask them, hey, what exactly do you do? You might get some interesting answers, things know, things that you're just like, wait a minute, that does not have anything to do with it. So, you know, my first approach is kind of verifying their history, kind of getting a sense for who they are, kind of getting a sense for how active they are, and say, okay, one bucket. Do you think that there's some chance that they have CAD? If so, what are the reasons? You say to yourself, okay, totally fine. But now you say to yourself, well, what are their symptoms? And outside and respective of their risk factors, you say to yourself, well, what is triggering the pain? What does the pain sound like? And based on that, I'm going to try to combine the two and say, are they low, intermediate, or high risk? So let me give you another example. I had a 36-year-old come into my office who said, never smoked, no high blood pressure, no high cholesterol, no family history of CAD. But he's like, man, Doc, you know, he's like, every time I have to run up this hill, I get this chest pressure right in the middle of my chest, right in the middle.
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If I'm doing everything else, it's okay. But every single time I'm going up there. So for him, I said, okay, well, look, his risk factors, not really that much, right? He's 36. Age doesn't really count. He's got no other history. He's got no cholesterol. I double-checked his lipids. I said, you know, you're not eating, you know, you're definitely not smoking. He's like, no, no alcohol use. I said, okay, and no other illicit drug use, which, by the way, illicit drug use accelerates CAD, so cocaine and methamphetamines, so just to keep that in the in my background mind because we see a lot of that too so then we say but his history forget how old he is forget his risk factors you hear the story and you're like man this is like really it sounds really bad right I think all three of you would probably agree right despite his age I'm running uphill and I just get this mid-cernal chest pressure and pain that just won't go away until I stop. So I ended up actually doing a stress test on him and it was grossly abnormal. Did an angiogram and he had a proximal LAD significant lesion. And he ended up getting stent. Now this is a 36-year-old, right? So you're like, man, he's got no risk factors. So always trust yourself in what you're hearing, right? And of course, you can only go by what patients tell you, but that's true for any disease, right? You can ask as many questions as you want, but if either they interpret it differently or they are not forthcoming with a lot of the information, it's kind of hard for you to kind of help them out. But for the most part, you want to kind of narrow down. When do you get this? What are you doing? And how does it affect your life? And then you can definitely make a decision as to where you should go. So I'll tell you that the low-risk people, so young people, no risk factors, even middle-aged people with no real risk factors, you got to kind of say to yourself, well, you know what? Let me see what the story sounds like, and then maybe I'll do some stress testing. If you look at the intermediate group, they're the people that, as with most testing, definitely can be encouraged to get some type of testing, and we'll talk about that. And the high-risk people is, oh, I've had a heart attack before. I've had strokes before. I still smoke. My A1C is 10. My blood pressure is 180. And yeah, every time I walk across my living room, I get winded and I get this tightness. No pain, but I get this tightness or this shortness of breath, that person's clearly at high risk of having something that's unstable or having a high critical lesion that probably is there and should be looked at. And when you look at risk and benefits of all these procedures, when you have someone who's high risk, the risk and benefit, the benefits tend to outweigh the risk because you're preventing another heart attack or you're helping them feel better if you do the angiogram and you find something. In the intermediate group, you're just trying to say, well, who do I need to really take care of it and who do I not? So getting back to our patient, you know, 58, diabetic, high blood pressure, obesity, family history. So for about four weeks, intermittent chest pain, for example. And we always talk about characteristic and we say, oh, sharp, most likely is not cardiac related. Or we say, stabbing pain or electric pain is most likely not cardiac. And that is probably true for a majority of people. But in this person, you know, I don't think it's wrong to stress this person because it's not really sure. Maybe that person's not giving you a full story. They're not really giving you a full idea. Like, yeah, when I walk, when I do this. So for the intermediate people, I would say, you know, stress testing is totally appropriate. And so the main ones that we have, so you could do a treadmill stress test, which I think all of us are familiar with. So EKG, put them on a treadmill, and we look for any ischemic changes, provided that their baseline EKG is normal. So if you're going to send someone for a treadmill stress test, make sure their EKG is normal, meaning there's no LVH. There's no ST changes that are already present. Arresting ST changes don't really mean much. That's why we end up calling them non-specific. So someone who's asymptomatic and you see that, that doesn't necessarily mean that they have some critical lesions sitting there, especially if you're asymptomatic. So you just say to yourself, okay, ST changes with symptoms, different story. And because you don't know, you kind of have to err on the side of caution. So that's just kind of this kind of case you're talking about, intermediate risk, person comes in, they've been having symptoms intermediately for like a month or two. And then what if they have like T-wave inversions on there? That's like the bane of my existence. Like everyone always has some T-wave inversion somewhere. Yeah, no, I agree probably say that, you know, in this person, I probably would say, yeah, you know, again, that kind of pushes you more to kind of look further, right? You say to yourself, okay, are you going to necessarily, you know, send them to the ER based on that? No. Are you going to send them, you know, based on the, you know, you're going to send them to the ER if you feel that they're having actual pain right now that's concerning. For example, if you had pain in T-wave inversions, for sure. You've got to send them. That kind of makes sense. But if it's asymptomatic and you have these changes, it's kind of hard to say. It's kind of hard to say, but that just gives you another sign that this could be, that this is more likely than knees testing because it's combining everything, right? Everything you know, your history, your physical, and kind of the EKG, which is also an important part. And those are okay for, if they have those and we're sending them for an exercise test, that's not a, for an exercise EKG test, the T-wave inversionsions are okay you know i personally would would do that with imaging just because so you know a lot of times this is what happens right you get an abnormal stress test with some subtle sd changes but no chest pain and the person walked for like like five stages you know they went for 15 minutes you're like well what this mean? So I usually say repeat those people with some type of imaging because the EKG can have many false positives specifically in females. Now we don't know if it's the estrogen or kind of just the way the leads are, but they tend to get a lot of false positives, especially inferiorly. And those people I tend to say, you know what, just like even from the right from the beginning, I don't send them just for a treadmill. I say, just do a treadmill with imaging. And the reason to do treadmill is that it kind of gives you more information about them as an individual. How much are they really walking? You know, what happens to their blood pressure? And, you know, if this And if this is truly exertional, chances are most people that get on the treadmill don't push themselves as much in their everyday as they do on the treadmill, right? Because that treadmill goes up. Every three minutes, it goes up higher and faster. And still, just for you guys, when you tell people this, usually by stage three, people are still walking. It's a brisk walk. It's an uphill walk. But people have this perception that I'm going to be put on the treadmill and I got to start running right away. And that's just not the case. First stage, anyone should be able to coast through. Second stage, people should be able to coast through. And third stage is kind of different. But if you can finish stage three, you know that you've given us a really good, for most people, not like the ultra young people who are fit, but if you can finish stage three, in my book, you've done quite a bit of exertion and we should be able to get the information that we need. So that's the usual exercise treadmill. That's what we're looking for.
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I personally would probably just send him with something with imaging like Echo. Still make him walk if he can walk because I want to know how much he can do. Can you get good enough windows on a stress echo for someone who's that obese though? You'd be surprised. Sometimes imaging is worse in the thinner people because there's more rib space. Air is a complete enemy of the ultrasound. There tends to be actually we've had plenty of thin people where the imaging is horrible and we've had plenty of thin people where the imaging is horrible. And we've had plenty of obese people where the imaging is perfect. So what we usually do is we always do a baseline echo before we start. And that's true for me even where I was in fellowship. So you'll know whether this is going to work or not. And your sonographer should be able to tell you, look, we're not going to be able to get any images. And if that ends up being the case, you can change them to, like, nuclear imaging. So for CED, how do you feel that stress echo compares with MPS or new med stress tests in general? Yeah, yeah. So echo imaging is more specific, and nuclear perfusion scan, or MPI, as we call it, microcordial perfusion imaging, is more sensitive. But there's also radiation involved. So it kind of depends, right? If it's someone who's in their 40s, no real reason to kind of subject them to radiation, especially if they have good imaging on their echo. There's just not a point. But sometimes you need to do those things, and that kind of is variable. So those are the people that can walk. So let's talk about that for a second. So what about people who can't walk, right? Someone who's got a knee replacement coming up. You don't know if they can do four meds. You want to give them some type of cardiac clearance. They're older. You're not really sure if they're, you know, having any issues, but you want to kind of work them up before they, before you clear them for surgery. You know, they can get a, you know, dobutamine echo, right? So they just lay there. We give them dobutamine, increase their heart rate. We see what happens to their heart under the stress. That's one option. The other option is that you give them, you know, vasodilator. So regadensin or adenosine nuclear imaging, and you see if there's any areas that, that are not getting enough flow. And I will say that, you know, out of both have a little bit of their drawbacks. You give someone dobutamine, you can provoke arrhythmias, which still should be short-lived, but it's always nerve-wracking to see that. With the adenosine, although it's short-term, people feel nauseous, headaches, shortness of breath because of the way that their adenosine and regadenosine work in the lungs and then other receptors in the body. And again, also short-lived. So ordering either one for people who can't walk is totally appropriate. Again, realizing that nuclear imaging is more sensitive, but echo imaging is more specific. We see a lot more, for whatever reason, at CashLac, most of our patients seem to be getting nuclear medicine scans. We do a lot of MPS. I'll be honest, where I was at for training, we had really good echo, but our nuclear lab was also very well known. And the head of our nuclear lab has written many, many books and is well-renowned in nuclear imaging, so we trusted their reads. So I think it matters, you know, kind of institutionally, what are your drawbacks? Kind of getting a sense or a feeling like, you know, how often is something called abnormal? You know, if everything is called abnormal all the time, that kind of decreases my confidence in using that modality. So it kind of depends on your institution. If you find that all the myocardial perfusions are maybe abnormal or artifact or subtle ischemia, that's not really helpful to you guys, right? It's kind of, is it there or is it not there? And sometimes you do have to call what you see. But if you see a pattern, like it's happening all the time, then it's kind of like, well, maybe I need to do a different imaging technique. And it's good that we have more than one, right? Maybe if you just had one, then you're kind of stuck with all these reads and you're like, what's going on? I don't really know. So equally in fellowship, we use both. Although I will say that maybe it was, I don't know, maybe a lot of the people just believe individual subsections. Like for example, people who had renal transplants, every time they were listed, they got a dobutamine echo. That was just what those surgeons did. But if anyone had like a orthopedic surgery coming up, everyone got a nuclear stress test, you know, for like clearance. So, you know, people have their own, right? The ordering physicians also should know that they have more than one option. But sometimes what happens is that you develop your own practice and you say to yourself, well, I've always ordered this and I trusted it. I'm just going to stick with it. But I will caution you to remember that we do have to think of things like radiation. We can't just say, just get it done and whatever. We really shouldn't be doing that. We should be trying to do the right thing for the patient. So a 40-year-old who always has chest pain should not constantly be getting nuclear stress tests. That's just my opinion. It just doesn't make any sense. And just to quantify it for the listeners, I had looked this up and I was kind of alarmed because I had never really quantified this before. But basically, every year, just walking around, just for solar radiation, get about like one millisievert of radiation and the American College of Radiology recommends that you try to limit your lifetime radiation dose to 100 millisieverts so I guess if you live 100 years you shouldn't have any stress if you plan to live 100 years you shouldn't have any like any sort of radiation from cardiac imaging or whatever right but for a chest x-ray is 0.02 millisieverts and a nuclear medicine uh like a thallium stress test is 29 millisieverts right maybe 25 if you uh depending on depending on the source that you look at and assessed to maybeessna maybe is about 12. So that's anywhere from like 500 to 1,000 depending on what numbers you use. But it could be up to 1,000 times the amount of radiation you get from a chest X-ray. And that's important. And it's the same thing with CAT scans, right? Sometimes we come down to CAT scans and MRIs and we say, you know, what's better? And I think sometimes, you know, we get people all the time in the ER that come in through chest pain who always get ruled out for PE. You know, we had that in residency. You know, you come in and it's like, I'm just going to rule you out for PE. And it's hard, man. I mean, you know, to make that distinction and say, wait a minute, like, you know, is this really needed? A lot of it is also fear, like not knowing, right? But I think that that kind of sometimes limits us in our confidence in using our history ability and our physical. And there's a reason why that's taught in medical school, right? Or I hope it still is, right? History and physical, history and physical. And you learn that in residency or you should because that in general shouldn't steer you wrong. If you just start choosing people in buckets, that will steer you wrong. For example, there was a patient who came in hypoxic to 74%, had some shortness of breath, and was diagnosed with COPD and sent upstairs. You get an echo, the RV is completely blown out. I said, you got to rule them out for PE. You would think that would have been done with someone that hypoxic, and it wasn't, and she had a saddle embolus. Sometimes you just think, you know what, this person is this. You got to got to take the extra few minutes to kind of dig in and kind of be able to make your right call. But anyway, but yeah, the radiation dose is enormous.
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I was going to say, one thing that I always tell my trainees is understanding the difference between ACS and CAD. And I think one of the problems that we have with a lot of these patients that are admitted for chest pain rule-outs is that the residents that we train, oftentimes on admission, they'll order that MPI or MPS, I guess, depending on where you're training, what it's called. And this patient may not have a pre-existing history of CAD, but they're coming in with some, you know, their intermediate risk. And so they're already ordering this test at this point that they've already received five, six ad nauseum times at this point. And I think it's important to understand that most lesions that actually cause ACS may not be, they may not be significant lesions seen on coronary angiography. There's a couple of articles that I have saved from the 90s and 80s. I think they're great articles that basically show that the majority of our MIs come from previously non-critically stenotic lesions. So it's important to understand that those plaques that rupture are likely your smaller plaques, not your larger plaques that cause stable disease, stable symptoms. And when your patients present to the ED with these stable symptoms, understanding that it may not be, you may not have to continue to order these same tests. You actually said it perfectly right. That, you know, the future MIs tend to come with the ones that are like 50%, you know, and 60%, not the ones that are necessarily 80%. They tend to give you your chronic stable angina, you know? What do you think about endovascular ultrasound to identify those non-critically stenotic lesions? Yeah, I mean, I would say we don't do it routinely because it adds to procedure time. And some of them, depending on what you use, may need extra contrast. And so I think we tend to do it in the settings of, is the stent properly deployed? Okay, so it doesn't seem to add any prognostic value? No, not really, because when you go to secondary prevention for MI, you're still going to do your aspirin, statin, lower the blood pressure. You're still going to do those regardless of what you see there, right? There's no additional pill or intervention that we do saying that, oh, this one's 50%. It's going to cause an MI. So we should add this medication, right? Those medications have already been added on. The question is, is there anything else added? And I usually tell people that, you know, you do what you can do, right? So control your cholesterol, control your weight, control eating habits, control your diabetes, control your hypertension. And you're doing that and stay active and you're doing what you can do, right? Blood flow is the most powerful way to kind of keep arteries open. No, it's the best way to keep your arteries open is to keep the blood flowing. And so that's why sometimes we have some stenosis that we see on angiogram that we don't intervene on because we see that there's enough flow. And so then we just say to the patient, I say to him, exercise, you know, just keep exercising. As long as you're not feeling anything, you're totally fine and that should take care of itself. So, yeah, I agree that not everyone necessarily needs a stress test. Some people just need their medication adjustment. Is their blood pressure 180? Is their heart rate resting at 90? Do they need long-acting nitroglycerin? Not necessarily that everyone needs to have a stress test, especially if their troponins are negative, right? They come in with a story that sounds real, but their troponins are negative. I first look at their meds. I first say, hey, you know, what can we do to alter that? Because we know that medication is also very powerful. Lifestyle modification is very powerful. It's not necessary that everyone needs a stent. We know that from the COURAGE trial that not everybody, the people who were getting stents for the 50-60% lesions weren't necessarily having better outcomes. And that was one of the main studies that kind of showed power of medical therapy. Obviously, if you have 80% lesion and you're having symptoms, that makes sense. But what about the asymptomatic patient that has a 50% lesion? That should not be fixed with a stent. That you're going to kind of stick with medication and trying to alter other parameters. Because you got to remember calcium hardening of the heart arteries is not unique to the heart. That hardening is happening everywhere in the body. Things that cause strokes, things that cause claudication or peripheral vascular disease, that's all part of the same game. So you've got to kind of also sometimes step back and say, well, everything kind of needs to be altered here. It's not just this. I know we mentioned one thing, so the stress testing, we talked about that, and we mentioned CAT scans. So coronary CT seems to be a pretty big thing that people are maybe utilizing or not utilizing so much. So I'll tell you that the person where it's not appropriate is the low risk. To say that I just want to know doesn't really help you. And the CAT scans have a lot more radiation than obviously your x-rays and things like that. But it has a slightly less than your myocardial perfusion. Yeah, I think when I was looking this up, it seems like they're getting better at lowering the radiation dose, but it was predicting anywhere from like 3 to 14 millisieverts if you're getting a coronary CT angiogram and about 1 millisievert if you're getting just a coron coronary artery calcium score yeah so what's the difference so the CAC score the calcium score is just straight non-contrast you're just looking at how much calcium is there and they have a way to kind of compute what your total number is um and usually we say you know above 100 uh you know you should try to have um risk factor cetera. But above 400 is definitely considered high. However, knowing that there's calcium in the LAD, knowing that there's calcium elsewhere, what do you do with that information? So I will tell you that when we ordered it, or at least when I ordered it and some of my colleagues from cardiology ordered it, all we're looking for is osteoproximal disease, right? Someone whose story is intermediate, you're not really sure, but you're not convinced that they need an angiogram, like an actual invasive procedure that carries the risk of dissection and things of that nature. You say to yourself, maybe they can get a coronary CT. And as long as there's not proximal disease, you know, like I said, left main disease or proximal LAD, you're just going to treat them medically. But what happens is that if you're not in tune to that in terms of what you're looking for, you're going to get a result back that says has calcium X, Y, and Z. And then you're going to say, oh my God, you know, like, like we need to go look at this further. So I wouldn't necessarily just order it on. So again, low risk probability, absolutely not. And it's definitely also not indicated for high risk, again, based on history and physical because we've had a couple of cases where the coronary calcium was read as like 500 or 600. Literally, they've gotten a cath, not much of anything. Now, I don't know. We could never figure those out. We can never figure out why that would have been like, we expected definitely to find, you know, something, but it's happened on more than one occasion. And so it kind of goes to the point, which is like, know your test, know what you're looking for, and then say, is it okay for this patient to get it? That's sitting in front of me, you know, try not to do it the other way around, which is like, know your test, know what you're looking for, and then say, is it okay for this patient to get it that's sitting in front of me? You know, try not to do it the other way around, which is symptom, I'm going to get this test because you're going to have many issues with that. And just the other caveat to the coronary CT, two things, BMI, we have a cutoff, you know, greater than 35, the imaging gets kind of dicey. And number two is if they're not in a sinus rhythm or a regular rhythm, it almost doesn't help because they have to gate it.
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It's just not going to be as accurate. So that's the calcium scoring. But when we do CT angio, we do a calcium score first. And if there isn't significant amount, then we inject the dye and we run them again. And then we say for sure, you know, calcium score and CT angio zero for calcium, no obstructive CAD. What is the negative predictive value for the CAC score? So if you have a CAC score of zero, how prognostic is that? Oh, that's very good. That's it. You're done. You're done. You don't need to do any more further testing. Their chest pain, et cetera, that is not related to their... Yeah. So a lot of the times when we get that, we do that. Like last week, I ordered... I got three results back, and all three of those people that I sent them for, all of them were zero. That's exactly why I sent it to them. You know what I mean? That was why I, why I wanted it because I wanted to know that it was zero because their story didn't sound real, but they kept coming in with the symptoms. Now, of course you can tell them that you may still have the symptoms, but at least you know that it's not from blocked arteries. You know what I mean? And sometimes that is helpful for the patient. So, yeah. And the reason why I asked that there was an article, it's a favorite of mine that I talk with some of the trainees about. It's from Jack Cardiovascular Imaging from 2015. It's actually, the title is wonderful. A 15-year warranty period for asymptomatic individuals without coronary artery calcium, a prospective follow-up of 9,715 individuals. I think it's a wonderful trial because I've shown this to a few patients. The CAC score of zero said, hey, look, you're good for 15 years. Goodbye. Yeah, you know, I remember that study. 15 just seems like a lot. It does seem like a lot, but man, it makes people happy, at least the patients. And when they come back with chest pain in two years, then we can reevaluate them and find out if the study is maybe not appropriate. Exactly. So we can talk about this. So I will say that most nuclear scanning is good for one to two years. One year in the diabetic, meaning if it's normal, and then two years if it's a non-diabetic. I would probably also say around two years for exercise treadmills and echo imaging. So that's roughly roughly my cutoff because now obviously if it's a 26 year old and somehow they get a cac score of zero uh then that's good for at least five or six years in my mind i mean even probably more than that because unless they're not 15 unless they're altering their you know environment in the sense of they start smoking two packs a day, they start drinking, they start doing drugs, things like that. Then obviously that's something that needs to be considered. But you have to remember that when you're doing stress imaging, you're looking at functional testing. When you're doing coronary CT, you're looking at anatomical imaging. And just because you find calcium on a CAC score doesn't mean it's functionally significant. So we've seen that too, where we get referrals for someone who's got a high CAC score and the symptoms are kind of like not much of anything. So either we'll put them on a treadmill to make sure that if that stuff is real, it's not causing any issues or depending on, on the, on the circumstance, we may get a nuclear stress test just to say, look, not an issue. Um, we'll just, again, continue to treat them with, um, statin and aspirin and, um, and other, other, uh, uh, modification. And, and, and talking about that, uh, coronary CT, um, the anatomical versus the functional imaging, that was last year, 2015, there was the PROMIS trial where they basically looked at that. And I've heard that that's controversial among cardiologists because basically the study showed that there was no difference in long-term outcomes between either doing like a nuclear medicine stress test versus this CT coronary angiogram. And some people read that as a positive towards CT coronary angiogram because maybe it's less radiation and maybe shorter hospital stays. And some people said, well, we don't need to be doing this, um, this study yet because it's not, it's no better than what we already have. So. Yeah, I agree. But I think that, I think that anything that can get people the information they need without putting them at risk and radiation to me is a risk, you know, for the course of someone's life. I think it is a good thing. The only thing is that like not every site has a coronary CT and not everyone's software is gated for it and not everyone can read it. So I think, you know, if it was widespread, the nuclear cameras and echo imaging is widespread. And I think that has something to do with it. Coronary CT I think is useful in the right people because sometimes you say to yourself, like, like I said, I had a few people that I did it and it didn't sound real and it came back zero. But, you know, that's how I'm at a place where they can do that. But there's many, many, many places where they don't have that. And so it's not necessarily that some of these people don't want to do it. It's just how do you get away from what the institution provides you? You can't. And so, you know, if you guys have it at your hospital, then you can start to have discussions on like, you know, who's appropriate and who's not appropriate. But again, it still comes down to intermediate and what are you looking for, right? If you're looking to just get them, you know, anatomically and say, look, this is not CAD, then that may be appropriate. If you're looking to risk stratify someone, so if someone sounds like they're intermediate, so you have a 58-year-old diabetic, hypertension, et cetera, although they're intermediate because of their other risk factors, but they got no calcium at all, that helps you. That helps you that their risk of CV events in the next year are a lot lower than the normal person with their risk factors because it tells you that that's not the case. Or you have the opposite. You think that someone's a 34-year-old, early heart disease in the family, smokes, et cetera, has some chest pain, a little worried, and you find that they do have some calcium in the arteries, that person may get appropriately put on statin ahead of time. You know what I mean? You can probably bump them up in their risk level and maybe more aggressive with what you're doing with them instead of just telling a normal 34-year-old like you normally would, which is like eat right and exercise. So I think as far as the cardiac imaging, the only one we haven't really touched on is MRI, which I have not really seen much of. Yeah, so I think that too also comes down to whether the radiologists or the cardiologists at your institution are okay with reading them and are they trained in it because clearly it's not, it's not, clearly it's not that easy. But I don't usually order looking for obstructive CAD. I've never ordered a cardiac MRI for that. The reasons to order for me is cardiomyopathy in a young patient, making sure that there isn't anything else for someone who has hypertrophic cardiomyopathy and you need to know how thick the walls are because your echo imaging wouldn't give it to you or if there's a concern for anomalies you know congenital or not or history of V so a lot of more like physical structural issues with the heart as opposed to obstructive CAD is where I start to use MRI you know cardiac sarcoid you know, you're looking for VT and you're wondering if it's really related to this and looking for a scar. So that's where I usually use cardiac MRI. I personally have not ordered it for any other functional testing at all. And I would probably say that most people haven't either. Yeah. And I, I think it's expensive and yeah, I'm looking it up here and up here and it's pretty expensive. Although I guess if you want to have coronary artery disease, I guess San Diego is the best place to have it. It's cheaper there than Baltimore. Don't ask why, I have no clue. Okay. So San Diego, the price for cardiac MRI is $650 to $1,700.
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Minneapolis, it's $3,400. Yeah, that's almost as much as the insurance payment for left heart cath. How much is that at cash lack? Free. It's about two weeks. It's about two weeks. Yeah. Time is money. And just a brief, you know, we talk about all these scores, like Timmy and Hart score. If you look at them, the reason why they really kind of change things is that they incorporate biomarkers, right? Yeah. For troponin. So clearly if your history and your story, you're worried, to me it kind of makes sense, right? If you get a positive troponin, you're going to take that more seriously. And you're going to say, yeah, we should probably get cardiology involved to say, what do you think? Should we do something or not? Clearly if the troponins keep going up, that obviously is an indication or a consideration for calf in the right people. If it stays flat, you can argue that, you know what, I can risk stratify them with a stress test to see if this is truly a problem because there's obviously a slew of reasons why someone's troponin can be elevated. It's not just from ACS. It's not just from obstructive CAD. Trauma, myocarditis, aortic stenosis, hokum, all these things can cause you to spill a little bit of troponin. So remember, always take the information you have from the patient, but then also say, yeah, they're set up for CAD, but is that what's causing their symptom that they're having? And to make the connection can be sometimes difficult. But I think that sometimes people don't pay attention they just they just assume that it's related right uh you know as soon as they hear chest pain that's it you know yeah like there's certain patients they have a baseline troponin elevation and abnormal ekg and they take an aspirin and their timmy score is going to come back high but right it's going to come back high to the. Exactly. Yeah. What are they telling you? They basically looked at like physical exam and clinical impression versus if you add to those things the heart and TIMI score. And for patients, what was helpful was for patients when they're first evaluated in like an emergency setting with chest pain, they use the same number, similar number that you said, Neil. about, they said about 13% of patients would, would have chest pain in that setting. And then they calculated the likelihood ratios based on the heart and Timmy score. And for patients with a high heart score or a high Timmy score, you know, those patients should be admitted for further workup, obviously. And, and for patients with a low score, that's pretty reassuring. Those patients probably need, they can either be sent home or have just a short course, maybe two troponins, you watch them overnight or something. But the intermediate folks were kind of in that gray zone where we're going to be thinking about stress testing. And I think that's probably helpful for people that don't have their 10,000 hours like you do of evaluating patients with chest pain. No, it is totally helpful. And I hope I didn't make it sound like they're not useful at all. But what I was trying to get at was that essentially that score is telling you what the most important things are when you talk to them. And EKG and biomarkers and things like that. But I'll say that when you're talking to them, the symptoms that I really pay attention to, jaw pain, bilateral arm pain, those things bother me. I had a patient who had a negative dobutamine stress test who the PCP appropriately referred because he said she keeps having exertional chest pain. I talked to her. She goes, yeah, every time I walk up the hill, it goes into my jaw. I calfed her despite a negative dobutamine stress echo. And man, she had proximal LAD. She had distal left main. She ended up getting a bypass surgery. So when you hear those things, that's kind of where I get a little bit more suspicious. And if you look at the sensitivity and specificity of all these stress tests, correct me if I'm wrong, but I think it's in the 60% to 70%, maybe 80% for certain tests, but it's not like 95% sensitive and specific. But I think that comes down to who's being referred, right? Like you can drop your sensitivity and specificity if you say send the four of us you know there's no risk factors and no chest pain and you send us well that's obviously going to drop those numbers well i i do smoke but you know that's the e-cigarettes yeah so i think that i think that's the you know i think that's where that comes down to okay and but those numbers can shift if applied to the right patient. Because if you send five people to stress testing and you send them and they were all intermediate and they were having relatively typical symptoms, most chances are they're going to come back positive. So you would say to yourself, look, my specificity and sensitivity are really high. But that's because you chose the right test based on what you were hearing and not just sending them. And so, you know, I agree that those numbers are there and that's probably going to stay because, you know, you don't always have control over what other people are thinking. But again, I think that you still have to just kind of use it and say, how can I, how can I, these are the, this is all this testing that's available to me. How do I make it work for me? Right. So I think we've definitely taken a lot of your time and I think we should just kind of like recap. So maybe, maybe your take home points, if you could give us those and then we can we can close out here so you can go back to your go back to your fancy life in southern california yeah yeah so i would say you know uh although this sounds cliche but the most important thing that we can probably do is is history and physical absolutely when you're when you're worried that someone's symptoms are related to obstructive CAD, you got to come down to what are they telling me? When is it? And rely on what you've learned before, right? Is it exertional? You know, all those scores are important, right? Diamond and Forrester, it's important to know those things, not because you're going to write that in your note, but you're going to say to yourself, these are the things that I'm looking for. And then I think the second thing is knowing who to test with a stress test and who is not going to be that helpful. Remember, intermediate people are the ones that really help you to say, I need to do something more versus I don't need to do anything. And that's like the non-invasive testing. And number three is, you know, don't be afraid to kind of stick with what your initial plan is. You know, if someone comes back, has a negative stress test, but you're still worried about them, talk to the cardiologist, right? Don't let that skew you. I think sometimes we get a negative result and we say, oh, great, keep going. But like I said, that one patient that I was talking about, that PCP, didn't give up and that was good because it prevented a really potentially disastrous situation. So always trust what you're hearing and always take the extra couple of minutes to kind of dive in if you have to because that will make a huge difference. Great. Thank you so much. Yeah, thank you guys. I think I feel a lot more comfortable now with this cardiac imaging. Yeah, I know. Hopefully, that'd be great. Yeah. but I think not. Let me just take a quick look here. Yeah, because we can always just kind of chronologically readjust things in post. Yeah, absolutely. The most important article is the patient satisfaction with coronary CT angio. Yeah, that's such a, yeah. Absolutely most important. You could probably just talk about coronary CT and CAC scores for, I mean,'s so many articles right now. Yeah, just forget that. Yeah, I think people are trying to prove it one way or another. So that's why they're trying to push through. I saw some interesting, the MESA study, like the multi-ethnic study of atherosclerosis.
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They excluded like patients over 75 or whatever, but it was, I thought it was interesting. So that, that's one way that like for some of my patients, if they're really like, I don't think I need a statin and if I feel strongly that they are high risk, you know, that might be for an asymptomatic patient, I might be using the CAC score sometimes to try to get those people, like, you know, recategorize them. Yeah. Yeah, and I guess a couple of brief questions that I do have here. What's your take on CAC scoring asymptomatic diabetic patients? And if they have a low CAC score about even considering stopping a statin? Yeah, I'll say that I personally don't do that. CAC scores for asymptomatic patients, I don't do it. It actually falls in one of those, when you're talking about the use criteria, appropriate use criteria, that actually falls under inappropriate. So despite their diabetes, because the secondary or primary prevention with statin is so powerful that I would have such a hard time stopping that unless they were like, there's some other issue, like totally intolerant. But then at that point, even if you didn't have a CAC score, you'd probably still stop it, right? Like you can't tolerate a medication, you can't tolerate the medication. So usually asymptomatic patients, I don't. They have to be giving me something to make me want to do that. And again, the risk versus the benefit of knowing versus the risk of radiation. Right. I think the way that I interpret it myself is that even with a negative CAC score, if someone has a history of diabetes, it doesn't mean that they're not going to be at risk for developing. Absolutely. They're still at risk for developing coronary artery disease. Okay. And then another question I had was, and this is going to be brief too, what knowledge or what information do you have about using PCSK9 inhibitors for statin intolerant patients that are at intermediate or high risk for coronary artery disease? We don't have that yet. And I think partly because of the expense. Yeah, it's about $600 per injection. Yeah, so I don't have any personal experience with that. So unfortunately, I won't be able to comment on that. But it shows promise, but it's like anything else, right? The cost is what it comes down to. It's very important that it works, but if you can't afford your medication, what good is it? There's a lot of talk about Diamond Forrester versus Timmy and Hart. So Timmy and Hart score, my understanding is that it's basically just looking at or understanding what the risk for MACE is. So it's a little different than Diamond Forrester. It's looking at the risk for having underlying coronary artery disease. And again, I just want to make sure that I'm teaching this correctly, but my understanding, again, is the difference between ACS and CAD. That with a low TIMI or heart score doesn't necessarily mean that they don't have CAD. It's just low risk for MACE or ACS. Yes, that's absolutely true. So I actually use, well, so we don't, again, we don't, once you use these enough, you don't necessarily just say, I'm going to use this score, right? You're doing it all the time. When you're talking to the patient, you're putting them through that score in your head. You're asking them the triggers. You're asking what it sounds like. You're thinking, you know, so I think when you, when you talk to residents, I think you teach it just like that. Know these things, but what's more important is know what's the, what's the components of each, because when you know the components, you're going to ask that in your history and you're going to say to yourself, this is what I think it is. So I agree. ACS, I mean, um, CAD does not mean ACS. Exactly. I actually had a, I recently saw a 72-year-old gentleman. He was a retired marathon runner. It sounds like the typical person who would have CAD at an earlier age. So he was a retired marathon runner, and he was, I think, I don't know, some sergeant in the Marines. He was still working out, and for about four weeks before I saw him, he started having this unstable angina-type picture, progressive stable angina. He had angina before, but he never did. And his EKG was completely unremarkable. His troponins were negative. His Hart and Timmy scores were otherwise unremarkable. I still sent him over to the ER, and surprisingly, within about 24 hours of admission, he started popping troponins. Yeah. Yeah, so, you know, again, it kind of just harkens to the point that you really have to rely on your clinical consult, and you can't just use these algorithms. No. Because these algorithms will lead you into this clinical quagmire, and yeah, so history and physical is an important thing. Yeah, we had a patient who went, I think, seven stages on Bruce and then started having some chest pain and had a proximal LAD lesion. So don't be fooled by, oh, he got five stages. His chest pain that he's having can't be real because these people just have a higher tolerance. You know, they just have a higher tolerance and sometimes they need to get to that high level before they feel anything different. So yeah, I remember that patient ran for seven minutes and then all of a sudden he's like, yeah, now I'm starting to feel it. But imagine anyone else probably would have stopped at stage five and have been like, what's the point? You know, but we were like, you know what? Just keep going. Just keep going. Just keep going. Lucky enough. Lo and behold, that's where it was. So I totally agree. You know, negative stress tests. If you're still worried because you keep hearing something that's not right, talk to the cardiologist, figure it out. What's happening. Excellent. Well, yeah. Thanks for coming. That's all I have. Thank you so much. Thank you guys for having me. to leave us a review. You can contact us on our pages on Facebook, LinkedIn, Google+, or follow us on Twitter at The Curbsiders. Until next time, I've been Dr. Tony Sedari. I've been Dr. Matthew Watto. I've been Dr. Stuart Kent Brigham. Wait, is that your middle name?
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Welcome to the September 20, 2016 Annals of Internal Medicine podcast. I'm Dr. Christine Lane, Annals Editor-in-Chief, and I'll be sharing some highlights about new articles published since our last podcast. The first article I'd like to bring to your attention identifies three objective criteria that can quickly identify patients with out-of-hospital cardiac arrest who have little chance of survival and can therefore be considered for organ donation. Using data from two registries and one trial in Paris, France, researchers found that there is essentially no chance of survival in patients whose out-of-hospital cardiac arrest is not witnessed by emergency medical services personnel who have non-shockable initial cardiac rhythm and in whom spontaneous circulation does not return before receipt of a third, Thank you. to save the life of a person with an out-of-hospital cardiac arrest. Clinical decision rules, known as termination of resuscitation rules, help to identify cases where further resuscitation is futile, thus avoiding ambulance transport and its associated costs. These rules do not, however, take into consideration the potential utility of transporting dead patients to the hospital for organ donation. For organ donation after cardiac death to be considered, patients must have zero chance of survival, be legally eligible to donate, and be rapidly transported to an appropriate hospital under continuous resuscitative maneuvers. The most important thing is to establish criteria for identifying patients with no chance of survival during the first minutes of CPR. Thus, the authors of this article believe that their findings could help to identify eligible organ donors. In an accompanying editorial, Drs. Joanna Hart and Scott Halpern raise some caution regarding implementation of these criteria. They write, quote, one of the main contributions of the current work is to highlight the need for additional evidence prior to establishing standards of care for facilitating organ donation following out-of-hospital cardiac arrest, end quote. They note at least three areas of investigation that are needed. First, researchers should seek to quantify the potential unintended consequences for patients, families, and society of preserving organ donation for patients through ongoing resuscitation. Second, studies are needed to describe the center or physician attributable variability that may influence survival rates among cardiac arrest patients. And third, real-world experience is needed to accurately quantify the marginal increase in transplanted organs resulting from donation protocols. Chronic constipation is defined by a patient having no more than two complete bowel movements per week with hard stools, frequent straining, and the sensation of incomplete evacuation. Most chronic constipation is functional, which means it is not caused by any physical illness and is associated with decreased quality of life. Laxatives produce only temporary relief and nearly half of patients are dissatisfied with their traditional therapies. Some have recommended the use of acupuncture for chronic constipation. However, the evidence for the therapeutic effects of acupuncture on constipation has been limited. An article published online first on September 13th provides some evidence on this topic. Researchers randomly assigned about 1,000 patients to 28 sessions of acupuncture at traditional acupoints or sham acupuncture at non-acupoints over eight weeks. They found that the patients in the treatment group had increased complete spontaneous bowel movements during the eight weeks of treatment and improved quality of life. These effects persisted throughout the 12-week follow-up. The researchers conclude that acupuncture could be a valuable therapeutic option for patients with chronic severe functional constipation. The aim of cardiovascular disease screening is to improve the health of an already healthy population and reduce the risk factors for cardiovascular disease. Primary care physicians who play a central role in cardiovascular disease prevention cite inconsistency in published recommendations as one of the reasons for not using cardiovascular disease prevention guidelines or global risk assessment tools. A systematic review published September 13th evaluates current guidelines for screening and risk assessment for primary prevention of cardiovascular disease in apparently healthy people. The reviewers identified 21 guidelines, 17 of which were rigorously developed on cardiovascular screening interventions that would be done within a cardiovascular health check program. Recommendations from 16 of the 17 rigorous guidelines supported cardiovascular disease risk assessment. Most guidelines recommended integrating age, sex, smoking, blood pressure, and lipid levels into assessment by using prediction models. However, there was no consensus on which prediction model to use. Guidelines on total cardiovascular risk differ about when to initiate statin treatment. Most guidelines agreed on the need to consider ethnicity as a risk factor for cardiovascular disease. Other areas of agreement included a consensus on the limited role of novel biomarkers and markers of subclinical atherosclerosis, a conservative approach to aspirin use, and the importance of addressing lifestyle factors. The diversity in cardiovascular disease guidelines may partly reflect the uncertainty of the benefits of screening. The authors of this article advise physicians to assess the strength of the recommendations and the level of evidence to decide which of the recommendations they should implement for a particular patient. Many U.S. policymakers believe that increased integration between hospitals and physicians will foster better quality hospital care and potentially lower health care spending. The logic behind this notion is that when physicians are more substantially influenced by the hospitals in which they work, they are less likely to focus on generating revenue to maintain their own independent practice and more likely to focus on patient care. Further, as hospitals respond to external pressures to improve quality, they believe that having a physician workforce that is tightly integrated with the hospital will make it easier to incentivize clinicians to focus on quality. The tightest form of integration is hospital-physician employment relationships have increased in recent years, and advocates believe that such a trend should lead to greater care coordination, more closely aligned incentives, and ultimately better patient care. An article published online first on September 20th explores whether this is actually the case. The researchers compared quality of care over time in 803 U.S. hospitals that switched to a physician employment model to about 2,000 matched hospitals that maintained traditional models of hospital physician affiliation. In 2003, approximately 29% of hospitals employed members of their physician workforce, a number that rose to 42% by 2012. Up to two years after conversion, the authors found no association between switching to an employment model and improvement in any of four primary composite quality metrics. The authors conclude that physician employment by hospitals is unlikely to be sufficient by itself to improve the quality of care hospitals provide. To evaluate an association between maternal H1N1 influenza vaccination during pregnancy and offspring congenital malformation, authors of an article published online first on September 20th took genetic and shared environmental factors into account. Congenital malformation was observed in 5% of prenatally vaccinated and 4.8% prenatally unexposed offspring. Taking intrafamilial factors into consideration, H1N1 vaccination during pregnancy did not appear to be linked to overall congenital malformation in offspring, although risk increases for specific malformations could not completely be ruled out. GRADE is an approach used by many clinical guideline developers to systematically rate the quality of evidence and strength of recommendations for a particular clinical area. An Ideas and Opinions Commentary, published online first on September 20th, discusses some limitations of the GRADE methods and suggestions for improving assessment methods. If you practice hospital medicine, I want to remind you that this summer, Annals launched a new feature, Annals for Hospitalists, that aims to simplify your search for information that matters most to you. Developed by and for hospitalists in collaboration with the University of Michigan Hospital Medicine Program, Annals for Hospitalists provides highlights from Annals of Internal Medicine and ACP Journal Club of information that is most relevant to hospitalists. In addition, a monthly commentary, Inpatient Notes, provides unique perspectives on contemporary topics in hospital medicine. The author of this month's Inpatient Notes is Dr. Jeffrey Barnes from the University of Michigan. Dr. Barnes discusses the expanded options for oral anticoagulation, an important topic for hospital medicine physicians as initiation of anticoagulation is among the most common tasks hospitalists perform. If you're a hospital medicine physician, I encourage you to go to annals.org and register to receive the monthly Annals for Hospitals email alerts and read the inpatient notes commentary. Check out this new feature and let us know what you think. The articles that appear in the September 20th print issue were all initially published online first and have been highlighted in prior podcasts. Briefly, some of the topics covered in this print issue include special shoes for knee osteoarthritis, familial clustering of staph infections, strategies to improve diabetes care, and binge eating disorder. And the second issue of the month also includes ACP Journal Club. Read it for summaries of recent articles that your internal medicine colleagues rated to be of high quality and high clinical relevance. This month's summaries address cervical cancer, cerebrovascular disease, depression, insomnia, aortic stenosis, hypertension, venous thromboembolism, and type 2 diabetes. September 20th also brings the latest episode of The Consul Guys. Go to annals.org or the iPad edition to view this episode on atrial fibrillation, a reminder that you can earn CME credit with each Consul Guys episode. That's all for this podcast. Thanks for listening.
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Thanks to Beth Jenkinson, Megan Caffrey, and Andrew Langman for their technical support.
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Hello and welcome to the podcast for the October 2008 issue of the Lancet Infectious Diseases. Richard Lane here with TLID's editor John McConnell. Welcome John and a few items to cover this week. Let's start with something that always seems topical and that's flu vaccination but specifically this is quite interesting. It's actually discussing the value of stockpiling flu vaccinations in preparedness for a pandemic flu. Tell me more. Yes, Richard. Well, what's happened in the past few years is that people have been working on vaccines specifically against the avian influenza H5N1 strain. And research and development has reached the stage where vaccines have started to be produced, which appear to be cross-reactive against several different H5N1 strains. It appears now that it may well be worth stockpiling some of these vaccines and being prepared to give them to certain key workers in anticipation of a flu pandemic. And is this, do you think, part of a proper, if you like, you know, organised strategy for preparedness for pandemic flu? Or is it scaremongering? It does smack of scaremongering a bit. Well, I think it's a reasonable arm of the preparedness strategy to consider, because what we have to remember is that we won't have a vaccine precisely matched against the pandemic strain until several months after that pandemic strain has emerged, because you can't produce a precise vaccine until you know what type of virus you're dealing with. So these vaccines which are being worked on at the moment are, as I've said already, appear to be cross-reactive against quite a broad range of flu virus, flu H5N1 virus strains. So they won't produce perfect protection against the H5N1 strain, assuming that turns out to be the pandemic strain. They won't produce perfect protection, far from it. But there's a very good argument for saying that if you give this vaccine in anticipation of a pandemic, then the people who've received the vaccine will have some level of protection, however imperfect it might be, and therefore will be protected to some degree against the pandemic flu strain. I think the way that this has to be used is that not rather than giving it to the whole population, which I don't think would be either practical or cost effective, is perhaps thinking about giving it to key workers, healthcare personnel, exactly what they call first responders, so that they have some level of protection if they are exposed to a pandemic strain. In the meantime, we might buy some time for ourselves in order to develop a vaccine precisely against the pandemic strain which does emerge. And imperfect though that sounds, is there enough evidence to back up the fact that some protection would become available? The only evidence you can really accumulate is immunological evidence. So all you can do is you can immunise these people, you can give them the vaccine and you can see if they develop any sort of meaningful immune response against them. What of course you can't do is you can't experiment by exposing them to flu virus strains. That would be rather unethical. This is an example of a vaccine trial where you have to rely on immunological markers. You can't actually rely on protection against illness or death as your endpoints. And the final thing, just picking up on how and who should be targeted by this type of campaign. You mentioned frontline healthcare workers. Would you also include other vulnerable groups like elderly people, etc.? I'm not sure I would because there's a whole debate going on anyway about whether the elderly are really protected against seasonal flu by the current vaccines as well as they are supposed to be. So and I'm not also not entirely convinced that it's the elderly that will be most at risk in the event of a pandemic. The evidence from previous pandemics is that in some cases it's actually young people who are more at risk. And it does very much depend upon what the hemagglutinin and neuraminidase types are that are in whichever pandemic strain turns up and causes the pandemic. Thanks, John. Moving on, you've got a review about tumour necrosis factor, TNF, and this is to do with the emergence over the past decade of human monoclonal antibodies as a strategy for dealing with a variety of diseases, obviously particularly in relation to their immunological function. Can you just outline briefly how these agents operate. This review is about TNF antagonists. TNF is a key factor in the immunological reaction. So it's involved in the development and modulation of inflammatory cells. So what TNF antagonists can do is that they appear to have therapeutic value, quite considerable therapeutic value in inflammatory diseases such as various types of arthritis and psoriasis. So in the last 10 years or so, these TNF antagonists have been used for treatments of arthritis and psoriasis. However, because TNF is itself key in the immune process, if you in some way turn down that immune process, then you may run the risk that the immunity won't work so well against infection. So the key issue here is that it appears that people using TNF antagonists have a greater risk for the re-emergence, particularly of latent tuberculosis. And this can be something like 10 or 20 times higher risk of latent tuberculosis re-emerging in people who are using these drugs than it is in untreated people. So this is a real genuine risk, and there have been many cases in K-series of tuberculosisculosis, latent tuberculosis emerging in people who are taking TNF antagonists. So do the authors of this review have any sort of conclusions or recommendations for what we need to do? They've actually compared the various different types of drugs and they've found that the risk of re-emergence is quite considerably greater for some types of drugs than it is for others. So, for example, there's a TNF antagonist called infliximab, and it appears that the risk of tuberculosis in somebody taking infliximab is considerably greater than it is in another different type of TNF antagonist called etanacept. So finally on this one John, if we know this, and it's obviously an important observation, what do we need to do to prevent it happening? Well the first and essential thing to do of course is to screen people for latent tuberculosis infection before they start taking these drugs. And it is possible to screen them by, you can do chest x-ray, you can give them a tuberculin skin test. They're quite crude and imperfect ways of detecting latent TB. There are some more precise immunological tests, but they're not yet in particularly widespread use. But you certainly need to screen people, and if they are showing any indication that they have a latent TB infection then you can treat them with antibiotics before they are given their TNF antagonists. And finally John let's end with the front of your journal, the Leading Edge, this month's editorial and this is looking again at the ever topical issue of hospital acquired infections. I read today in a UK national newspaper that the UK government has met its target on reducing MRSA in hospitals. So what's your editorial saying? This very issue was one of the topics addressed in this Leading Edge editorial. So the UK government had set itself the target of reducing MRSA, particularly in hospitals in England and Wales, by 50% over four years. So one of the topics we discuss is how they appear to have actually moved the goalposts in achieving this target. But, you know, you could reasonably argue that they're only a few months off the target they originally set themselves, and they've done quite well. And let's hope that they maintain the momentum in reducing the incidence of MRSA infections. One of the other triggers was a new initiative in the United States where patients who are getting Medicare payments or patients getting Medicare payments for their care in hospitals, the hospitals which are caring for these, which are taking the Medicare payments, will not receive additional funding if the patient gets a particular type of hospital, particular types of hospital-acquired infections while they are under hospital care. So this is really a way of encouraging hospitals to take much greater care in preventing the acquisition of hospital-acquired infections. It's a financial incentive to do something about the growing concern with hospital-acquired infections. It is very much a United States initiative at the moment and similar initiatives are only really going to work in healthcare settings where individuals pay for their care or, as in Medicare, the state pays for an individual's care and you don't have universal health insurance as we do in the UK. But I think providing a financial incentive to hospitals to do something about healthcare-associated infections is a way of tackling the problem that needs to be explored. And I'm sure this very issue is going to be discussed at an upcoming conference in two months' time. Nice Q2. Something you're organising, John. Tell us about the conference. Well, yes, Richard. The Lancet Infectious Diseases is organising a conference on healthcare-associated infections, which is going to be in London on December the 11th and 12th of this year.
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Great. We look forward to that. John, many thanks indeed. Those were some of the highlights from the October 2008 issue of The Lancet Infectious Diseases. Thanks for listening. See you next month.
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Hello, Richard Lane here with the Lancet podcast on Friday, May the 25th. This week's feature is about repetitive strain injury, or RSI, the topic of a seminar in this week's issue. In a moment, we'll be hearing from one of the authors of this seminar about a condition which affects millions of people worldwide. Before that, a quick canter through some other highlights from this week's issue. We have editorials about international health regulations, another one about hypertension, and drugs for tuberculosis. This week's clinical update in the comments section is about cholecystitis, advocating early surgery to benefit patients and reduce healthcare costs. The European Union Clinical Trials Directive, three years on, is assessed in World Report. There are research articles about aspirin use and preeclampsia. This study was published online a week ago. Fortification of cereals to reduce anemia among Kenyan children. And an analysis of the impact of global fund grants in countries with varying incomes and health infrastructures. And there is a review about the alarming rise in incidence of type 2 diabetes among young people. The authors of the review conclude that urgent action is required on all fronts to stem the tide of type 2 diabetes and its associated complications. But back to our main feature, RSI. This is the subject of this week's seminar, and although it's a condition affecting millions of people worldwide, the reality is there is very little scientific evidence to guide us concerning prevention and treatment. Earlier I spoke to one of the authors of the seminar, Professor Moritz van Tulder from VU University Medical Center in Amsterdam. and there doesn't seem to be consensus about the best diagnostic tests as well. So it seems to be a complex problem, but it does affect a lot of people and obviously mostly workers or it's mostly work-related condition and therefore it's also associated with high costs of sick leave. Estimates vary from about 10% of the workers that may have RSI complaints up to as high as 40% in some specific working populations. So it does affect a lot of people and again it's difficult to come up with one figure. I think the most important message is that it does affect a lot of people and especially workers. The majority of RSI problems are in the elbow, the wrist and hands, maybe even the fingers, but sometimes also neck and shoulder pain is included. And especially at the elbow, wrist and hand, I think it's often associated with pressure on the nerves. The physical risk factors at work are repetitive movements, maybe jobs where you have a poor posture that needs a lot of strength. So it seems to be associated with physical risk factors at work, but also psychosocial factors, maybe a high workload, a high level of stress. Job dissatisfaction is sometimes seen as a risk factor for RSI. It may happen in any job. And again, as long as it's associated with repetitive movements, high physical or psychosocial workload, and the risk factors that I just mentioned. They're not really gold standard interventions that are very effective for RSI, and again, it may vary if you have problems with the elbow or the wrist or hand. If you look at the evidence from scientific research, then it seems some interventions are effective for short-term pain relief, for example, for elbow complaints or corticosteroid injections for carpal tunnel syndrome. And for neck pain, for example, and shoulder pain, exercises seem to be the most effective. But there are still many other treatments or interventions that are commonly used in daily practice that are not really strongly supported by scientific evidence, not necessarily meaning that they are not effective. They're not large, high-quality studies that have supported their effectiveness. So I think it's especially important to do more high-quality research to find out which interventions or treatments are the most effective maybe not for all patients with RSI but specifically looking at subgroups that may benefit more from specific intervention than from other interventions. Professor Moritz van Tulde concluding this week's podcast. Thanks for listening. See you next week.
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Hello and a very warm welcome to the first ever podcast for The Lancet Oncology. I'm Richard Lane and I'm with TLO editor Dr David Collingridge. Welcome David and we're going to discuss some highlights from the March 2008 issue of The Lancet Oncology. Let's start with a very interesting research article and this is looking at the whole issue of insurance status, health insurance status, ethnicity and cancer risk. Before we talk about the current study in the Lancet Oncology, what have we known about this topic up until now? Several studies to date have suggested that people from ethnic minorities are more likely to be diagnosed with advanced stage cancer. Equally, previous studies reported that health insurance status is an important factor in receiving cancer prevention and screening as well as diagnostic services and treatment. So individuals without insurance or they're underinsured tend to have less access to screening, they present with more advanced disease and they consequently have limited treatment options and poor outcomes. It's also important to acknowledge that while ethnicity and insurance are critical factors, they're not the only factors influencing cancer outcomes. So for example, socioeconomic status, level of education, residence in a nursing home or in a rural location, distance to the nearest hospital or biological differences in susceptibility to cancer and other comorbidities also influence risk. But ultimately, of course, having the financial capacity to access healthcare is fundamental. Just before we go into the details of the study, can you just remind us as to why early detection is so important? Well, for most types of cancer, early detection is associated with a better outcome. So, for example, for patients with colon cancer, a diagnosis of a stage 1 cancer is associated with a five-year disease-specific survival of over 90%. Whereas if a patient is diagnosed at stage 3 survival drops to about 40%. And if the diagnosis is made very late at stage 4 disease, metastatic disease, survival drops below 10%. And also it's important to realise, isn't it, that insurance, health insurance status and ethnicity are not necessarily independent of each other. That's exactly right. There's a lot of data now indicating that patients with cancer from ethnic minorities are more likely to be uninsured or underinsured. So David, the current study, can you just summarise, this is obviously a very large piece of research in the United States, can you just summarise how this study was actually done? Well, Michael Halpern and colleagues are all from the American Cancer Society in Atlanta, in Georgia, and they identified nearly 4 million patients diagnosed with one of the 12 most common cancers in the US between 1998 and 2004 using the US National Cancer Database. This particular database is a hospital-based registry that includes about 75% of all cancer cases in the States. They then calculated the odds ratios to compare cancer stage diagnoses across different ethnic populations and across the major categories of health insurance in the States. The major categories include, for example, private insurance, which mainly covers working adults less than 65 years of age, Medicare, which is a government-run entitlement for the majority of retired people aged 65 years or older, but also for younger people who have a chronic disability. There's also Medicaid, which is a government-funded scheme for people with low incomes or low-value assets. And finally, of course, there's the category of people who have no insurance at all. In terms of the results, they seem pretty clear, don't they? I.e., for the non-white population and for people who are either under-insured or not insured at all, the risk of cancer is increased. Can you put some numbers on that? The results are very, very clear, actually, in this paper. Uninsinsured or Medicaid insured patients are significantly more likely to present with advanced stage disease compared with privately insured patients. For example, the odds ratio for a stage 3 or 4 disease at diagnosis for uninsured or Medicaid insured patients with colon cancer was 2.0 or 1.6 respectively, and the comparable odds ratio to melanoma, who are higher still, at 2.0 and 3.3, respectively. So the data are very clear-cut. The data also clearly show that black and Hispanic patients had an increased risk of advanced stage disease and diagnosis compared with white patients. Interestingly, patients in receipt of Medicare had similar odds ratios to those calculated for privately insured patients. So the conclusions are truly limited to just the uninsured, the underinsured and the ethnic minorities. In terms of the implications of these study findings, David, what can happen now? Do you think that there's sufficient evidence here to really influence policies, if you like, in the way that the American health insurance world is set out? Well, this is a really interesting and really quite difficult question, actually. But the results very clearly showed the most prominent odds ratios were associated with cancers that are easily screened. So there's a clear message here about the need for improved access to screening and diagnostic services, which needs to be considered within the context of insurance coverage. But equally, the finding that Medicaid-insured patients did no better than uninsured patients suggests, at least superficially, that giving some help, a safety net if you will, is not an effective strategy. But what the study doesn't tell us is the proportion of patients who became eligible for Medicaid because of their cancer diagnosis versus those in receipt of Medicaid before their diagnosis and this confounds the interpretation somewhat. Plus there are other problems with over interpreting the Medicaid data. For example some patients can find it difficult to find a healthcare provider willing to accept Medicaid payments and other patients can find the process of means testing difficult and this can influence their long-term eligibility for Medicaid. However overall Michael Halpern's study does clearly emphasise a need for effective and affordable insurance and effective infrastructure for the underinsured and uninsured otherwise about 47 million people in the states will remain marginalised and continue to face a potentially lethal barrier to accessing healthcare. Moving on David, another interesting study, this is looking at children who have had cancer in childhood being followed up in adulthood and it's a Dutch study. What kind of proportion of people are we talking about or children who have cancers are we talking about who actually need to be followed up in adulthood? It's a very surprisingly high number actually. 75% of children with cancer will become long-term survivors and many will experience late effects resulting from their cancer treatment. These effects range from cosmetic complications that might have physical or psychological consequences to complications from their radiation treatment, neurological sequelae, orthopaedic endocrine deficiencies, infertility, cardiac damage or second malignancies. In fact, about 10% of childhood cancer survivors die of a late effect within 20 years of their original treatment. So there is a clear need for long-term monitoring. And how generally is long-term follow-up done? Well, up to now, about 90% of childhood survivors continue to be monitored into adulthood in paediatric clinics. Most long-term follow-up programmes consist of a paediatric oncologist or sometimes another survivor focus specialist along with one or more specially trained nurses in collaboration with a network of specialists as required. Most long-term follow-up teams will monitor the patient for cancer recurrence, they will manage any persistent long-term effects of the initial treatment, they will screen for any late effects and any subsequent cancers, they will address psychosocial needs of the family and the patient and provide counselling and education to optimise health and quality of life. But clearly though, a paediatric environment is not right for adult assessments and patients are often lost to follow-up because as an adult they no longer live near the original hospital that they had their treatment and equally other problems may restrict the effectiveness of the current follow-up system. For example many institutions do not have the resources to support long-term follow-up and some oncologists regrettably do not refer their patients to long-term follow-up, even if the programme exists. So in terms of this study, this is looking at what they call a shared model. Can you just define the main objectives of this Dutch study? Well, Ria Blauwbroek and colleagues from the Netherlands decided to investigate the feasibility of, as you say, this shared care approach to long-term follow-up. And to do this, they invited a random selection of adult survivors of a childhood clinic who had been treated at that clinic at least five years previously and were not involved in any follow-up programme. And they then assessed them by their own long-term follow-up processes. But one year later, the survivors were asked to see their family doctor who had been already made aware of the medical history of the patient, and given any specific instructions as necessary, along with specific assessment forms to complete and return to the paediatric clinic. And then finally, two years after this, the survivors returned to the long-term follow-up clinic for another assessment. Now the main endpoints of the study were to assess the satisfaction of the patients and the family doctors to this shared care concept.
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And in terms of results we see some pretty high satisfaction levels don't we? Yes the results were very good actually in this model. 92% of survivors agreed to participate, 98% of family doctors really wanted to be involved, and 90% of doctors returned the appropriate data to the long-term follow-up clinic. Plus, 88% of survivors and 82% of family doctors were satisfied with the shared care model. What's interesting is in the link comment that accompanies this paper, written by Kevin Offinger from the Memorial Sloan Kettering Cancer Centre in New York. This commentary suggests the study actually has very few flaws and it clearly demonstrates the shared care model to be a feasible one and would most likely be cost effective in comparison to the current approach. The challenge now of course is to see whether this can be put into practice in large scale environments and the numbers here are relatively small, and of course we are talking about a Dutch setting, but you've clearly said that, yes, we need larger studies, don't we, to try and replicate these encouraging findings. Exactly. Yeah, fantastic. Okay, David, would you just briefly remind us of some other highlights from the March issue of The Lancet Oncology? Elsewhere in the issue, the leading edge this month, the editorial, reflects on the cases of two patients in the UK who have been denied an opportunity to self-fund an additional chemotherapeutic drug on top of the regimen provided by the UK National Health Service. Now in essence, the UK Ministry of Health believes patients in the UK should either self-finance their entire treatment or be happy with the options available through the NHS. Now we argue in this editorial that the approach does not allow sufficient compassion for patients with cancer and it does not give the health service sufficient flexibility to be part of a solution to patients' problems rather than an obstacle. Elsewhere in the issue, Wasaburo Kozumi and colleagues from Japan present data from a Phase 3 trial called SPIRITS. This particular study was designed to assess a new chemotherapy regimen for advanced gastric cancer. This cancer is the second most deadly type worldwide and highly prevalent in East Asia and Japan. Now despite numerous trials in this area, median survival is still less than 12 months. It really is a terrible disease. Now the spirits trialists investigate the use of cisplatin, which is commonly used in this setting in other countries, in combination with S1. S1 is an oral drug that comprises Tegafor, a prodrug of fluorouracil, and potassium oxonate. The control arm of the trial was S1 alone, which is a standard first-line treatment in Japan. The results show that for patients in Japan, so patients of East Asian descent, the median survival can exceed one year, and this is quite a finding. And finally, David, you've got a review. This is looking at paediatric leukaemias. Yes, we have a review this month by Chin Hon Pui and Scott Howe from St Jude's Children's Hospital in the States, who highlight the challenges that still exist for treating paediatric acute lymphoblastic leukaemia and acute myeloid leukaemia, and in particular the need to eliminate relapse without the use of cranial irradiation, along with the need for more effective treatments for relapsed or refractory CNS disease. They also discuss one of the other areas of great challenge in treating these diseases, and that's how to effectively treat children with CNS relapse after a short period of remission or after cranial irradiation. And those were some highlights from the March issue of The Lancet Oncology, our first podcast for TLO. Many thanks, David. Thanks, everyone, for listening. See you next month.
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This is the New England Journal of Medicine COVID-19 update for December 21st, 2022. I'm Stephen Morrissey, Managing Editor of the Journal, and I'm talking with Eric Rubin, Editor-in-Chief, and Lindsay Baden, Deputy Editor. Eric and Lindsay, I'd like to start with an announcement. In the midst of the holiday season, we'll be taking next week off. And given that, I thought that we should get an idea of where we stand at the end of the year, particularly when it comes to vaccines. Several countries, including the United States, have moved to using bivalent vaccines. So what are these vaccines and how do they differ from the earlier versions? Steve, all of the widely used bivalent vaccines are similar in many respects. All of them are mRNA-based and all include the original viral sequence that was derived from the spike protein of a viral isolate from the beginning of the outbreak in Wuhan. However, in addition, the vaccines contain a second sequence derived from Omicron variants. There are two different flavors, a bivalent vaccine containing sequences derived from a BA1 isolate and another based on a BA4 or BA5 isolate. In the U.S., we're only using the latter, while both types are a couple of important points. One is how the vaccine or the immunogen is delivered, which is the vaccine platform. And the speed of development, manufacturing, scale up of protein and viral vector delivered immunogens are just different than what we see with mRNA technology. That's an important consideration as we move forward and think about which types of vaccines or immunogens can be scaled up rapidly in response to a rapidly changing environment, as we've seen with the emergence of Omicron a year ago. In addition, you point out the insert, or what is the immunogen, and how do we manipulate that insert or immunogen to bring out immunity against the target of interest? In this case, it's the emergence of Omicron, whether it's BA11 or BA.4.5. And how can we leverage these technological platforms to be responsive in a kinetically appropriate fashion for how the virus is evolving? I do want to point out that there have been multiple types of bivalent vaccines that have been designed, manufactured, and even studied, such as for the beta variant, the delta variant, as well as BA1, BA4, 5. And how these different types of immunogens have behaved individually and together has allowed us a better understanding of their safety, their manufacturability, as well as the immunogenicity or the immune responses they can elicit. And as someone who's been involved in some of these studies, it's been remarkable the speed with which these types of immunogens can be designed based upon circulating sequences and vaccines potentially delivered to the clinic. Overall, the implications of these concepts, as you have alluded to, speak to how do we have technologies that we can use to be responsive to changes in the pathogens that we are trying to respond to. In this case, the emergence of the Omicron variants a year ago and having vaccines that are deliverable to the community that are likely to elicit more favorable immune responses. I think it's important to point out that the idea of multivalency or combinatorial vaccines is not a new one. And in fact, many of the vaccines we use routinely have combinations of antigens. The annual influenza vaccine contains either three or four antigens, each one derived from a different viral variant. The pneumococcal vaccine, which is directed against a bacterial pathogen, Streptococcus pneumoniae, contains as many as 23 different antigens from different strains. On top of that, we have vaccines that combine antigens from completely different viruses like MMR. So we know that the concept of delivering multiple antigens at once works. This isn't new. So there's every reason to think that this should be an effective way of protecting against disease. And the COVID vaccines we're using now, these bivalent vaccines, how well do they work? I think that before we give a score to these, we need to think about what the important goals are for these vaccines. When the mRNA vaccines were first introduced, they were incredibly effective at preventing infection and probably at limiting transmission. However, as COVID-19 has gone on, with the appearance of new variants, the vaccines have become progressively less able to prevent infection and mild to moderate disease. They do seem to retain the ability to protect against hospitalization and death, though. So our goalposts have moved, and I think that it would be great if the newer vaccines produced at least some short-term protection against infection. So the goalposts have moved. And while I think it would be great if the newer vaccines produced at least some short-term protection against infection, at this point, the priority is to stop people from dying and to free up hospital beds. This means that it takes a while to assess vaccines because it takes a while for those endpoints to be measurable. Our initial yardstick for the performance of a new COVID vaccine is its ability to induce protective antibodies. By that criterion, the bivalent vaccines have had some success. They certainly are able to induce better neutralizing antibody titers against a variety of strains. However, this success is being challenged as new, more divergent strains started to appear. For example, today we published a small study of the ability of serum derived from individuals who received either one or two monovalent boosters or one bivalent booster. To summarize the results, the bivalent booster resulted in better neutralization against BA1 and BA5, even then two monovalent boosters. But it's important to remember that BA1 has disappeared and BA4, BA5 are almost gone. These have been replaced by more divergent viruses. In this study, while titers were fairly high against the two viruses I just mentioned, they did decline a fair amount against strains like BQ11 and XBB, which are now circulating. So what does this mean clinically? It's still fairly early to measure the effectiveness of these vaccines in preventing infection. And when we get those numbers, they will be a little bit difficult to interpret because the population that's being vaccinated is very heterogeneous in terms of their prior vaccination history, the timing of those vaccines, and the incidence of infection in those individuals. Unfortunately, hospitalization and death rates have fallen, so it will take longer until we have a good sense of whether or not these vaccines prevent the worst outcomes. It's likely that when we do get those numbers, unfortunately, they'll be useful only for strains that have already been replaced by new strains. So we're constantly going to be playing catch up as long as we have a similar vaccination strategy. Eric, I think you raised an important point about moving goalposts and yardsticks that we use to measure success or failure. As we think about what success looks like for vaccination and our prevention strategies, we have to carefully reflect on goals that we had two and a half years ago when we had initial efforts to control the spread of SARS-CoV-2. There, our initial assessments were in part related to what technologies we had available in our understanding of viral infection. And preventing mild to moderate infection was an important goal and ultimately preventing hospitalization. Two and a half years later, where we are now, infection is rampant in our communities, but hospitalizations remain low in comparison. Although they are increasing this winter, in part related to more vulnerable individuals getting infected, in part related to other viruses that are circulating. But what we are seeing in our hospitals, and this will be a challenge as we measure efficacy and success, is in patients who are admitted to the hospital and have COVID. Are they admitted due to COVID and COVID-associated illness? Or are they admitted for another medical condition and happen to have COVID? And we are seeing both scenarios play out. That will be a challenge as we try to understand the benefits of vaccination and prevention strategies, as well as the burden of illness. And the burden of illness will be difficult to assess, as you know, as our testing approaches change, particularly with the increase in home testing, which is terrific, but the inability to easily track individuals diagnosed that way. Another goalpost that we are reflecting on, or yardstick, and I think is important for us to think carefully about is how do we measure protection in the lab in vitro? Antibody titers, neutralizing antibody, as you point out, when we look at sero studies after vaccination or from individuals previously infected, and we look at how it neutralizes VA1, VA45, BQ1, XBB, we are inferring that neutralization is the signature of protection. It may well be a marker of protection. It may well be important to protection. But there likely are many other aspects of the immune response that afford protection and ameliorate illness and severe illness. And I think in the U.S. currently, hybrid immunity, either vaccine-induced or infection-induced, is widespread and likely to diminish severity of illness in the future.
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And this is the nature of what we have to deal with as infectious diseases spread into different communities. So I think, Eric and Steve, it's very important that we think carefully about the goalposts and yardsticks we use to determine what is beneficial and how much illness we are seeing, because circumstances have changed and may be different between different, very important communities. Eric, you said that we're constantly playing catch up. Are there vaccine strategies that might allow us to get ahead of the game? I think the answer is we don't know, but there are some things to consider. For example, we're looking at using antigens that are relatively close to one another right now, but it might be that more divergent antigens from more distantly related viruses can induce broader immunity than these rather closely related sequences that are being used right now. And there is some evidence for that in small studies. Also, it could be that different routes of administration can induce different types of immunity that give something that gives better protection or perhaps even broader protection. We've talked a lot in the past about using mucosal vaccines, but different methods of delivering those vaccines might also make a difference, not only the route of administration, but the method of delivering those. That's pretty speculative. We don't really have any evidence for that right now. But I think that Lindsay just made a very important point, which is thinking about the population that is receiving those vaccines. In China, there's a relatively low rate of prior infection, in fact, an extremely low rate nationwide. And that means everyone there is naive to infection and vaccines have to do a very different job than they do in most of the rest of the world, where the rates of prior infection and what Lindsay referred to as hybrid immunity are going to be very, very high. So we really should be thinking about vaccines for most of the world that work well on the background of prior infection, as opposed to what we were looking at before, which is still the situation in China, looking you ask us, broader immunity. One strategy, which are the approach to the bivalent or multivalent vaccines, are you take antigens or spike proteins that are as divergent as possible, and you use them to bring out broader immunity because the immunogens look very different. Another strategy is to look for conserved epitopes or regions of the viral coat that don't change across the species of influenza or SARS-CoV-2 and are exposed, thus vulnerable to attack. So there are different scientific strategies, and it's encouraging to see different strategies being pursued for the respiratory viruses of import, as they may enable us to develop vaccines that are broader and in the immunity they elicit to the circulating strains and to potentially future strains if truly conserved epitopes can be identified. What also is important here, as Eric alluded to, is compartment. Does the mucosal compartment behave the same as the systemic compartment? Is one more important for severity of illness than the other for transmission? And do we need to understand the biology in the different compartments? And much science is going on in these arenas that can allow us to exploit the differences to enhance immunity where we need it to have a salutary effect on illness, which I think we've achieved, and to improve the effect we can have on transmission, which needs much more work. And one last element that we all have been thinking about is the durability of the immune response. And that is something we've learned with the current vaccine strategies, particularly the mRNA strategies. The responses don't seem to be as durable as we would like, whether it's due to the vaccine, the immunogen, the change in the virus. There are many questions here that have to be understood. But there may well be strategies where we look at different vaccine platforms to see if they can bring out immune responses that may be more durable or broader. Science needs to be done here for us to understand the potential. But we have many more tools now than we did a year ago or two years ago. And I'm certain we will see data emerging that will help inform these different approaches and combination of approaches. To pick up on your last point, Lindsay, I think it's really important to think about the fact that we're using already very different tools than we did only a few years ago. We've learned a lot over the decades that we've been making vaccines. However, I'm not sure all the same rules will apply as we look at different vaccines and different ways of delivering them. So although I know that there is a feeling among some in the community that we're doing about as well as we can, I'm not sure that that's fair. I think that we might be able to do better and we'll learn about that as we try these new approaches. Nonetheless, from everything you say, it's clear that making vaccines that have lasting effects is going to be challenging. So, is there any good news we can take into the new year? I think there are several good stories. Remember that we're doing a lot better. Hospitalizations have fallen dramatically. Death rates have dropped dramatically. There are still populations that we need to reach in order to further improve. And there might be technologies that we can improve on that will also bring these numbers down. And I don't think that addressing the issue of infection is out of reach. It's something that I think is still on the radar. But clearly, we know a lot more about the pathogenesis of this disease, and we're learning more about what immunity means. Lindsay already alluded to the fact that there are lots of different kinds of immunity, and we've been measuring antibodies largely. We have measured other sorts of immunity, but we don't really understand what those numbers mean right now. And I think we're going to learn more about that. And as we do learn more, I think there will be dividends to come. And I keep in mind that while we're discussing vaccines, treatments have improved markedly. There are now good outpatient treatments. There are more on the way. And I think that we're going to continue to be able to decrease the morbidity of disease and the mortality induced by disease in the coming year. Steve, I actually view this whole discussion as good news. I would look at it the other way around. In the three years since this virus emerged, and it was three years ago, it was December of 19 when it was first emerging, and January when the world really appreciated it. In this three years, we have been able to define the pathogen, define the pathogenesis of illness, understand immune dysregulation, understand viral parameters, and develop multiple countermeasures. Vaccines, treatments like monoclonal, small molecules, as Eric mentioned. We've also been able to not only deploy these interventions to communities that need them, we've also been able to respond to viral evolution. It's not a static problem. And the ability to identify escape mutants and other aspects of viral pathogenesis that's emerging under selective pressure in real time, I think is terrific and allows us to then adapt our therapies to be appropriate to changes in the pathogen. I think it's remarkable that all this has occurred in the last three years or two years in particular in relation to treatments. However, it's still incredibly frustrating, the burden of infection that is going on globally as well as domestically, and that we have to continue to respond in a way that's proportionate and appropriate to the diseases that SARS-CoV is causing. But I actually am full of hope that scientific progress enables us to be responsive and to go to scale as quickly as we have done. It doesn't mean there aren't plenty of challenges. But as we go into the new year, I think we should be inspired with what science can do for us if we allow it. Over the three years that the epidemic has been around, the world has changed. And mostly it hasn't changed for the better. Now we are much more restricted in the kinds of things we can do. We've had these large economic shocks to the world associated with lockdowns and the social costs and consequences of those lockdowns. But it's really important to reflect on how much better things are now. Two and a half years ago, everyone was staying home. Businesses were shut down. You had to walk around on the street with a mask on. Now, people are getting together for the holidays in ways that they hadn't been able to do for years. There are good tests available for those who are at particular risk that can make any gathering much safer. And when people get sick, there are better treatments for them. So I think the news is good. It could be better, but that's hopefully what the new year will bring us, some improvement on what's already a much better situation. Eric, if we're expressing our hopes, I would also hope that we can apply what we've learned and the technologies that have been developed to the other respiratory pathogens we're facing.
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If we put our efforts in the right direction, we can tackle so many more pathogens that cause so much illness. So again, I am full of hope, but I think there are miles to go before we sleep, as I've said before. And there are many, many more medical problems we can solve with the kind of focus and energy that we have brought to responding to SARS-CoV-2. Thank you, Lindsay. Thank you, Eric.
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Hi, and welcome back to Sharp Scratch. You're listening to episode 70. There's no pill for homelessness. 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 who discuss all the things you need to know to be a good doctor, but that you might not get taught so much at medical school. I'm Pat, I'm the editorial scholar here at the BM the BMJ and I'm also a medical student at Anglia Ruskin University. Today I'm very pleased to be joined by our friends Lily and Kaode. Lily, would you like to introduce yourself? Yeah, hi, I'm Lily. I'm a final year medical student in East London and I'm just revising for my final exams, which are in two weeks. And then I'm basically done. I have elective, which is insane. So that's very exciting. Yeah, time flies so quickly. I know, it's insane. Have you received your allocations as well? Oh yeah, we get them in two weeks. In two weeks, okay. Yeah, on the 10th of March, I have my final ever written exam of medical school. I get told where I'm going to be for the next two years. I have my UCL intercalation graduation. Anything else? Maybe that's it. And there are some personal things as well. Lots of anniversaries on that day. It's so weird. Oh my God, that's so much. But very exciting at the same time. It's exciting. Yeah. Yeah, nice to have you back with us. And Kayode, would you like to introduce yourself? Hello, I'm Kayode. I am a final year medical student at the University of Dundee. It's not so sunny today, but it's snowing, which I wasn't expecting. I'm not happy about this because it just delayed everything this morning. I couldn't walk as quickly as I wanted to. For some reason, the snow trucks seem to like, oh, I don't know if you can tell, the sun is shining on my face now. They seem to just neglect my streets, but every other street around me gets like gritted and everything. Just my streets, my specific street gets left icy and I live on top of a hill and I'm always scared I'm going to just slide down which has happened before in the past so yeah I wasn't expecting this to know otherwise I'd have put the grit myself because I bought some last year because I was like I'm not having this anymore but yeah other than that I'm I'm a-okay I've already done my finals. Same position as Lily, waiting to hear back from allocations, which I'm surprisingly nervous for. I usually don't care about stuff like this until the day of it. I was like, oh my God, this is happening today. But I've been, yeah, all over the place this week. It's kind of refreshing. Fingers crossed that you guys get your first rotation. And yeah, thanks for joining us. I'm also delighted to introduce our expert guest today, Dr. Andrew Moskrop. Andrew, would you like to introduce yourself? Hiya. So, yeah, my name's Andrew. Gosh, I've done my finals and my first rotations, and I'm just sort of having palpitations at the sort of the flashbacks to that. So I currently work as a GP here in Oxford at a practice that works with people who are homeless in the city and yeah I've been doing that for the past few years. Yeah thank you for joining us today. There is often a debate whether medicine is an art or a science. Our curriculum tends to favour the science bit. We bury our heads in the pathophysiology of diseases and management algorithms and guidelines a lot but are we treating the symptoms or the cause? We are taught a holistic approach to medical history and examination you know with the social history of the patient embedded in the algorithm when we're taking history. Although there are caveats to this there's increasing research suggesting that your postcode has more of an impact on your health than your genetic code. What can doctors do to better address the true cause of people's ill health? So I thought in this episode, we could talk a little bit about whether our medical education is teaching enough about social determinants of health and whether there's a disconnect between our undergrad training and actual clinical practice. So, Kaode and Lily, well, you know, we're taught to elicit social history when we're taking a full medical history. How much do you learn about social determinants of health at med school? Oh, I'm not sure how much we get explicitly taught. I'm sure we've had at least one lecture with a nice slide that has social determinants of health on it. But I don't know whether I think the people that tend to be more aware of that stuff are people who just naturally have an interest and kind of passion for that sort of thing and also there's a difference between naming social determinants of health like tokenistically like a list and actually be able to have a conversation where you fully understand the scope and the depth of how people's lives can affect their health and I don't think that all medical students could do that but I would challenge most medical students to be able to list three things that would affect health that aren't necessarily just organic problems if that makes sense yeah yeah I think I saw you nodding there when you when Lily was mentioning you know people when people are interested in it then you know they kind of can link between the social determinants of health and um about one day taking a history yeah definitely i think it's one of those annoying things where attempts can be made to teach these things but it's one of those things that you find not that many people engage in i know for um my job so in my unit we do two general practice um placements in one in fourth year one in fifth year and for each of those placements we have to do like a poster about like um one pages that we've seen and sort of like describe their life story and look at the data surrounding their postcode and everything and i think some people really engage with it some people not so much and And I don't know, I think attempts are made to teach these things, but I don't know if they're taken very seriously because like you said in your introduction, people focus a lot on the science because that's what you're ultimately going to be mostly examined on and they sort of forget about all the social stuff. I think it probably can't be taught in a lecture format which is tricky because I don't think medical students would respond very well to being given like a seminar or like being split into tutorial groups like you do for like social science degrees but again I think medical students approach most of medical school as what is examinable material and what can I tokenistically learn to pass, which I don't blame them for because you have to pass these exams and they're really hard. But if we teach everything in that way and we kind of put that onus on exams, things like this, which aren't necessarily to try and get one more mark on the exam, they're just to yourself a better and more rounded doctor they will always fall to the wayside won't they yeah I agree um I mean personally I'm interested in kind of surgery determines health side of things and that's how I kind of learn more about it rather than learning it from lectures I suppose um I think we can talk a little bit more about this later. But Andrew, I know you've written about this gap between the undergraduate education and actual clinical practice. Yeah, so in your opinion, do you think that this connect between the undergraduate precepts and actual clinical practice? Well, it's kind of interesting, because, you know, sort of hearing you guys, I mean, it totally resonates to my experience 20 years ago, like, you know, when I was sort of finishing up at medical school and, you know, like what you're saying about sort of how it's really not that examinable or at least not quite as readily as, say, naming the bones of the fingers or, you know, whatever else might be sort of at stake and sort of more, you know, easily accessible in an exam format, you know, like which drug to use for which problem, all that kind of stuff. These things definitely are sort of rather more complex. That's, you know, that's, there's no question. And I also recall sort of, it was definitely sort of fairly selective in terms of who actually bothered to engage with these issues at med school and who didn't. And I'm sure that actually at the time I didn't particularly.
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At the same time it's kind of a bit of a shame that things haven't quite sort of moved on as they might because I think that our understanding of the importance of these things probably has sort of progressed and it's sort of a shame that by the sounds of it medical schools haven't quite found a means of making that apparent in the curriculum and in the teaching because you know these things aren't really just a sort of or they shouldn't be merely a peripheral interest of those that sort of happen to find it moderately interesting, because all of our patients will be impacted to some greater degree or other by what we sort of term the social determinants of health. They're tremendously important. tremendously important. I mean, like, you know, even to the extent that some authors would sort of claim that, you know, deprivation, for example, can have as big an impact on your health as smoking or obesity. You know, the things that we would sort of consider to be, you know, that's what we work with in terms of health care. And this is, you know, what's important to us in terms of sort of understanding patients' risks and their likely outcomes and so on and so forth. Actually our social circumstances should be really right up there. So it's kind of unfortunate to hear that that hasn't quite gathered the pace that it might have done. Like when Andrew was talking it made me think a bit more about the teaching that we get in my medical school. And I would say, actually, in hindsight, we probably don't get that much teaching on it, but we get a lot of assessment on it, at least within my medical school anyway. The importance of these topics is there, but I think the delivery and ensuring that people understand and learn more about it isn't quite there. I think universities or at least my university does the central teaching on social determinants of health well in that like we're all aware of them and we're taught them and I actually do think that at least my university people are able to research and kind of find the right articles and evidence to back up claims but what I think is missing is which I think maybe relates a bit too much to our empathy episode is the kind of emotional education for me the biggest moments of really absorbing the impact of people's lives on their health has been on our GP placements so we do them every single year at my university and it's always the home visits and it's visiting people's houses where all the mum and the dad and their six children all live in one room and they have maybe have one living room but it's kind of we had there was one family where their daughter was autistic so their entire flat was covered in crayon on all the walls um which they couldn't move out because they were renting and they wouldn't be allowed to get their deposit back. And they all slept in one bedroom. And for me, those moments are the real, like, I remember all of them so distinctly in my mind. And they're the things that I really hang on to. Whereas I think that isn't centralised. You can't, like, mandate that every medical student goes and visits a poor family that like just is ridiculous um and that's kind of just happened by chance I don't know if every medical student gets that eventually but kind of ties into what you're saying is that eventually once you're a doctor you cannot avoid those patients in those situations so you do you will just willingly or unwillingly have an emotional education in how patients' lives can be so different to the lives that we think people just live. I wonder how we can introduce that emotional education into university. I don't know how we'd do that. Yeah, I think in addition to that, as you mentioned, the kind of social circumstances of patients or the people around them can have such an influence on the health of the patient. Andrew, with your background in general practice as well as working with a vulnerable group of people, do you see kind of these healthcare managers kind of play out in the community? I think that's important and it certainly is a big part of my work. You know, I'm sort of thinking about sort of seeing homeless people. You know, there's all sorts of, and certainly if they're sort of homeless on the street, there's all sorts of ways in which that might impact how I choose to treat them. So, you know, I don't give them 56 tablets of whatever medication it is because they've got nowhere to put it. And I certainly don't give them a pile of medications that might have a street value because it makes them more vulnerable. So, you know, it certainly sort of impacts what I do. But at the same time, you know, those sorts of things in which we accommodate someone's social circumstances into our management plan, whilst really helpful for the individual, it is, I think, to some extent, it is kind of slightly accepting of the status quo. And are we okay with that? You know, like, so am I, you know, am I okay with the fact that, you know, these patients are homeless? Well, I'm not really. So, and if I'm not, then, you know, I've got to gotta kind of I don't think it's enough for me just to sort of you know practice in a way that sort of recognizes it but also to sort of do something to sort of advocate uh for for some kind of change and I guess that and I suppose maybe that's maybe that's the significant difference between uh you know people's attitudes towards this because as you say people very often do sort of incorporate this into management plans but then you know is that where it ends um and perhaps for some people it is um for others it might not be um but you know like i guess you know you can't sort of resolve these issues in the course of your clinical practice but you can sort of, you know, advocate and support, you know, perhaps policy changes that might sort of alter things. And you're quite right, not everyone sort of wants to get political about this. But at the end of the day, you know, it is politics that shape people's context and, as a consequence, shape the presentations that we're met with be that six kids in a single room or whatever. I think you said really beautifully there about kind of standing in the patient's shoes and thinking about say it was a homeless person kind of adapting the management plan to their circumstances and I'm just thinking if it would help to have kind of representation of doctors from that kind of background to truly understand what circumstances people are going through. And it just happens that one of my friends at med school, they kind of come from that background. And I interviewed her about what was she going through when she was in that circumstance. My name is Maz Sadler and I am a fourth year medical student at Anglia Ruskin. I was homeless sporadically for six years between the ages of 14 and 19. It's quite difficult to condense because it's quite, with every person who has an experience of homelessness, it's really multifaceted. There's so many layers to it. it you know you don't just wake up in the morning and then your landlord kicks you out and I mean obviously that's how it happens for some people but with so many others there's like such an array of socioeconomic factors from a healthcare perspective I think we sometimes as medics get frustrated when we see any patient repeating health behaviors that we know like have a negative impact on them you know say if you have an alcoholic who who has dreadful liver disease and they keep coming in over and over again and they don't stop drinking or if you have a diabetic who continues to not manage their diabetes well you know there's all sorts of frustrations that I think we allow ourselves to fall into but with homelessness specifically there's this kind of societal stigma that they are people who just will not help themselves who won't do what it takes and what's necessary to get out of that situation um but when you are homeless your priorities just completely shift like it took me a good five years to be able to shift away from seeing each day as an individual unit that had no relationship to the rest of time because when you're homeless all you see is like the day in front of you you see yeah you just see where am I going to get food today am I going to be able to have a shower today like if you're female you know am I going to be able to get tampons am I going to be able to have a shower today? Like if you're female, you know, am I going to be able to get tampons? Am I going to be able to, you know, wash? Can I afford clothes? All these things like it's it's a very much a survival mindset. And I suppose, you know, with your experience, especially now you're kind of close to the end of medical school. And so I suppose how what kind of things would you want your fellow medics to understand when it comes to proposing a management plan?
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I think that understanding the contributing factors and going out of your way to understand the contributing factors as a doctor can be just as important as treating the disease in front of you, especially, you know, if, especially if you're in a kind of like more community facing role, like maybe GP or something like that. If you have somebody who, you know, is returning with the same issues or you suspect there might be something else going on, like, I think it's really important to not only involve yourself kind of more in what's contributing to this, but also seek help from others in the community, you know, the social workers and the mental health support workers and all these MDTs that can really provide more holistic, well-rounded support to that person. I also think that there's a real fear of judgment. Okay, so say a man is homeless and he's had a sore on his leg for six months and if he'd got it seen six months ago it would have been fine but now it's you know it's septic and it's terrible and the longer you leave it the worse it gets well saying to a patient well why didn't you come in six months ago I mean first and foremost it doesn't help the situation in front of you now and it's not really our place to judge anybody's situation but that will make that person and anybody that they tell about it less likely to seek help in future so I think it's really important to just bear in mind kind of however busy and stressed you are and however frustrating the case in front of you may seem like nobody nobody wants to be in that situation and nobody would choose it for themselves you know like this this misconception that homeless people are lazy and they choose to be that way because they can't be bothered to get a job is just so outrageous to me because, you know, I would do anything in my power to avoid ever returning to that situation. And I'm very lucky in that I was only in it for a relatively short time compared to some other people. And I had the benefit of my education and my friends to help me get out of it where a lot of people aren't that fortunate so I think I'd really like to see medics have a level of compassion for everybody generally of course but for people who find themselves in living in circumstances that that you just think to yourself okay would I choose this for myself if not then they probably haven't either this is probably they're probably a victim of circumstance and so my job here is to treat the person that I see in front of me without judgment first and foremost and secondly establish is there anything that I can do more holistically to help this person's situation and if not I might see them again in two weeks and that's okay because they need my help again in two weeks and I might see them again a week after that and that's okay because they need my help again a week after that our job is to just kind of be there and do what we need to do non-judgmentally without, because lecturing people never got the point across, right? If you're not willing to help in a meaningful way, it's just, you know, it's just words, it's just noise. Yeah, Andrew, I know that you work with people, a lot of people like homeless people as well. I don't know if anything that was said in the clip is kind of similar to the things that you see in practice. That was really interesting. And I was kind of amazed that this person is now a colleague of yours. You know, that's kind of great because I think in lots of ways, not least obviously, because her life clearly significantly altered and she sounds as though she's very much happier about that now, understandably. I guess the other neat thing about it is that it suggests that there's perhaps a growing diversity of medical students. I don't think that predictably we've been very good on that in the past. There tends, there tends to be sort of a fairly, we're pretty homogenous actually as a sort of profession in terms of social class, ethnicity. You know, we tend to sort of, you know, like, you know, patterns sort of get repeated. It's kind of like very often medical students, their parents were doctors, this kind of stuff. And it's nice to sort of hear that actually maybe some barriers to entry into medical school are being at least challenged. So that was kind of encouraging. It was fascinating too to sort of hear her talk about how in her situation she had wholly different priorities from those that might have been those of her caregivers. And I think she's quite right to sort of point out how, you know, people in that situation, they can be really frustrating to deal with. You know, it can look like as though they're sort of thoughtlessly just participating in sort of self-inflicted harm, whether that's through alcohol and, you know, the consequence of liver disease that she sort of mentioned too, whether it's sort of drug use or whatever. And, you know, and so it's important to sort of, I think, acknowledge there are frustrations about that and try and sort of put them to one side and sort of recognise where the patient's at. And you don't even need to be sort of homeless to sort of find yourself caught in that trap of self-defeating behaviours you know like and if we allow ourselves to sort of get annoyed with people because they're continuing to smoke and drink too much then we're going to be engaging in an awful lot of victim blaming which as was pointed out in that clip is sort of unhelpful really it doesn't sort of actually bring about behaviour change and it's really the wholly sort of wrong approach. Yeah, I think there was loads to take away from that clip. I found it very moving. Yeah, and not least, definitely my biggest thing was actually kind of, which is, this is obvious, but there isn't this dichotomy between medical students or doctors and patients in terms of, it's not always us as the kind of like traditional like white saviors kind of like trying to solve people's problems and actually as Andrew has said medical students and doctors are becoming more diverse and kind of the more that we challenge the traditions and stereotypes of medicine we're going to have a more diverse workforce which will be able to engage and empathize with our patients better which will only create better health outcomes and then also I think the other thing is that yes other than kind of political activism and advocacy as you said Andrew in terms of what doctors can actually do in their day-to-day jobs to make some sort of difference. I think as the clip says if we come into situations compassionately and we take a moment before we see our patients to remind ourselves that whatever they come in with we need to be safe and non-judgmental and welcoming and not focus on a behaviour and actually focus on the person in front of you and what their life is like, I think we can have more constructive conversations and appointments with patients that actually produce real benefit for their health, which at the end of the day is our job. Because I think if you kind of go about your day, focus on how stressed you are and how busy you are and how many patients you have. You don't go into situations with that mindset. And understandably, you don't have time or you think you don't have time to kind of access that compassionate part of you. You think all you have time to do is treat their broken hand in A&E. And actually, if you just give yourself 10 seconds, you might have a more honest conversation with the patient and actually make a bigger difference in the long run if they feel they can come to doctors and talk to them and share earlier rather than later, which I think is the entire goal of medicine eventually is to be improving patients' outcomes in the long term rather than in the short term. And I think that's important. And even though, as we were saying, there are a whole bunch of social factors that are playing out, some of which are unalterable by us at least, I think how we deal with people is really important because even within the NHS, and if you're going on to a career in the NHS, you're already off to a good start in terms of your impact upon health inequalities because the great thing about the NHS is you don't have to pay for it, so finances and people's social circumstances don't act as a barrier to the same way that they might in, say, a private healthcare system. So that's great. If you're playing a part in that, that's wonderful. But it's important to recognise that even within the NHS, people who are poorer, people who have poorer education, they tend to do worse. They have worse outcomes from care. They've got less satisfaction. They wait longer for appointments at their GP practice. They wait longer in A&E and they wait longer for routine surgery appointments. And so I sort of suspect that there's something going on there. And, you know, and that doesn't, that shouldn't be a consequence of being poor or having sort of like fewer educational opportunities, opportunities.
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And so I think that if we can acknowledge their context and actually not allow that to prejudice against people unthinkingly because we're sort of stressed and we're having a difficult day, et cetera, et cetera, if we can actually sort of overcome that, even though they might be frustrating to deal with because some of this might seem like as though they've brought it on themselves through alcohol or whatever, you know, if we can get over that, then I think we sort of go further towards actually reducing some of the disparities, some of the inequalities in outcomes from health experiences and healthcare experiences. We'll discuss more about the wider implications of health inequality in the system, but that'll be right after this message from our sponsor. 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't blame them, so why not join them? Visit medicalprotection.org to find out more. Okay, back to this show. navigating the healthcare structure. Just to give a really extreme example, so I volunteer at a prison and then you can see people, kind of the same people going through the revolving doors of prison. And sometimes, you know, when you offer to help them, they could just feel very, well, even the patients or the people themselves just feel frustrated and helpless because of this kind of labyrinth that they have to navigate. It's tricky isn't it because I guess that you know I guess what we've got to acknowledge too is you know there's going to be a bunch of people for whom we are the system you know that's what we sort of represent and unfortunately those that it might well be the very people that we're trying to understand and engage with. You know, if you sort of think about, you know, the sort of breadth of patients that we might encounter, there'll be those whom we find it very easy to work with. They may well be graduates and they may well have a similar sort of education and social background to ourselves. But then there's going to be an awful lot of other people who may have an awful lot of health needs and maybe even greater health needs who are you know for whom that's not going to be true they won't have gone to university they won't have had the educational privileges that we've had and we might represent something that's intimidating to them you know going to see their GP might feel a little bit like going to the job centre where they're going to get berated about their behaviour or something like this. It might feel like just yet another engagement that they've got with an authority figure. So they might actually be on their guard and somewhat wary about having conversations with us. So I think we to be kind of in tune with that if we can as well. And it's true not just in general practice but in hospitals too. You know, by the time we've been shoved out the end of medical school, you know, like hospitals are our home. We're totally familiar with this environment. And yet for an awful lot of people, it's going to be absolutely intimidating. You know, it's full of like really well-educated people who are doing really, you know, sophisticated technical tasks. And it might be, you know, if you're homeless, that's a world away from your day-to-day experience. And it's pretty wacky to find yourself in there. And I think that, so recognising that is kind of important. So yeah, just sort of, you know, being aware of what we might represent to the patients that we're dealing with can be kind of important. Yeah, I was going to say the same thing, which is that part of this challenge is recognising that we also make the system that we're in. And the harsh reality, which is not acceptable, is that there are patients that you leave longer in A&E and you see them later and there are patients that you give appointments later to in GP and that is awful and completely speaks to our prejudices and kind of what we think is an acceptable patient and who deserves care and the quiet nice grateful patient often doesn't align with the patient who needs our care the most. I think that's a again that is just is just a challenge that is so in the scope of this podcast, we're not able to solve that problem, but we just choosing people to go into medical school and then cultivating a culture of doctors who are not prejudiced and who are aware of this sort of thing and do treat everyone equally, inverted commas, is going to be the like challenge of medicine I think for a very long time and one other small point is that the NHS is not free for everyone and we have to accept that we actually have a really unequal system in that people who come to this country who aren't citizens they do not get free health care and that is I think something we can actually challenge as doctors in our workplaces get rid of the posters in A&E I think we can actually do quite a lot to challenge that specific problem which I think would make such a difference to so many patients who do not get the health care that they deserve. I was literally literally in my mind because I was literally like I literally made notes about like yeah, immigration checks like when you're registering for a GP and stuff and I've always found that weird and odd. Like, what? Yeah, sorry, Pat. No, sorry. I was going to say, since there was a charity called Doctors of the World, they were doing a campaign about doctors are not border guards, right? Like, you know, they're coming in to take a box to say that, yeah, they're, I don't know, from the EU or have permanent residency here before treating them. Yeah, that was a great campaign. I tried to do my elective with them, but because of COVID, it was too difficult. But yeah, they're an amazing organisation to follow if you're interested in that sort of thing. I think we have to just cultivate a more compassionate environment, which actually also involves funding and staffing and making the work environment better for staff so that we can actually do our jobs, which is treating patients properly rather than 70% of our job, which is treating the initial problem but ignoring everything else because you don't have time or money. And if we the NHS properly and we fund the welfare state everyone's health will get better but I mean I'm probably not going to be the one to actively change that but what we can do is kind of yeah do some sort of advocacy and activism but if anyone is listening and wants to become the next prime minister then that would be really useful. Lily there's nothing stopping you from becoming the next prime. I think you can do it. I would vote for you. I wouldn't vote for me. I'd vote for you as well. Actually, I'd make you my health secretary. Yeah. But I think also, you don't have to just sort of have a position of power. I mean, as you say, sort of calling out some of the BS, like, you know, if it's sort of posters in A and E departments that are sort of distinguishing some patients that can and can't access care, you know, that's clearly nonsense. And it's clearly within your power to sort of react to that. So, you know, I think that there are things that you can do as well as as you say like sort of uh being mindful of uh of how you sort of engage uh with patients and you know i guess i would say don't be sort of afraid of like you know going a bit of extra uh distance for for people we don't just have to sort of treat everyone equally i think we can sort of treat people according to need and i guess that sometimes that means that uh some people get a little bit more. I guess the important thing is that we sort of actually get the balance right so that we don't sort of, you know, sort of deliver more care to those people who have less need and that we do sort of try and deliver more care to those people who who have greater need.
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So what would you recommend to the listeners who may not know very much or don't know how to become more aware of things what would you recommend that they do like right now in this instance like after listening to this podcast what would you say they should do so i guess um i mean it depends because i guess everyone's sort of you know probably pretty busy preparing for various other things you know we heard lily at the outset sort of describe how uh much she had sort of going on uh in the near future and i'm sure that's true for a lot of medical students but i think sort of uh being aware of these issues and sort of gaining an understanding of how people's social context impacts their health and their health presentations i guess that's something that you can sort of do through reading but also just sort of thinking about it like when you're next sat in front of patients when you're next sort of sat in a clinic and you know my recollection of like sometimes sort of sitting in clinics you know be that in sort of GP surgeries or hospital outpatient appointments sometimes it could be a little bit dull but if you sort of take that that frame and sort of try and sort of think about sort of people's backstories and what might brought them here and like what some of the tensions might be in their sort of their context that, you know, and like whether actually the advice of the consultant or GP is going to be sort of manageable for them. You know, if you sort of think about those sorts of things and maybe sort of keep it on your mind, maybe it becomes a little bit more interesting and maybe you start to sort of engage in it a little bit more. Yeah, I think, I know earlier I joked that you can't have every medical student go into a really deprived environment intentionally. But actually, I wonder if making home visits a compulsory part of medical school would make such a difference, especially in East London. There's such a huge deprived community in East London that actually it amazes me that some medical students have managed to avoid that. And I think with, obviously, boundaries and appropriateness and professionalism, I wonder if having every medical student on every GP placement at some point encouraged to go on a home visit, I think that would probably go quite far to the emotional education part of it yeah I think that's a good idea instead of just seeing patients in you know kind of the sanitized area of hospital or in a clean hall without putting a background exactly and also people who are who get home visits at least in my experience there are they're a specific group and other than kind of people who are immobile or in nursing homes actually they often are more deprived and more isolated. Yeah it's a good reminder of what we said what Andrew said about what we can do in the medical capacity as well as kind of wider capacity say challenging the system as a medical student so yeah as we kind of close to the end of the episode is there there anything that you'd like to add my only thing to add is that i think the sun from scotland has come to london because my room is now sunny the sun is still very much here the like the reflection of the river the view from my room oh my god like it's a shame this is a podcast because it's beautiful and I think you guys should all be very very jealous but I guess my take home is treat the person in front of you and health is political again, another episode where I stopped myself from doing a fire and brimstone speech I'm very proud of myself but yeah I don't know how you can practice medicine without being somewhat political but that's just my opinion but yeah yeah for similarly um I think if you're able to which absolutely not everyone is integrating in something social sciencey is was made such a vast difference to my awareness of this sort of stuff. But in lieu of that, kind of accessing and looking for resources on that sort of thing, which sounds then completely vague. But even just like read, like Googling some of the journals that do kind of health policy science stuff and kind of reading a few of the ones that are about social determinants of health and poverty and deprivation and even like things like structural violence by paul farmer which i know he's very controversial at the moment although r.i.p um that's obviously an amazing article to read if you want some sort of introduction into how medicine is not just as clearly said it's like a political sterile environment it's actually the complete opposite i. I think we've talked about a few things that people can have on their mind. I would advocate for those social changes that get closer towards tackling the causation of a lot of people's health problems. Thinking about taxation, sickness benefits, unemployment benefits, housing policies, blah, blah, blah., in our day-to-day practice, I would encourage people to sort of ensure that we don't worsen inequalities through our interactions, that we're sort of mindful of the impact that we can make, make sure that we're not sort of being punitive towards people who live in difficult social circumstances by giving them a hard time about their, you know, their behaviour such as smoking and alcohol whilst supporting them to sort of make changes if that's what they want to do. Yeah, and hopefully then we can sort of actually sort of play a positive role. But remembering that it's not us as doctors that are going to fix health inequalities. It's going to sort of happen outside of us. Thank you very much for coming on to the episode and sharing your insights and expertise. Yeah, that's all we have time for today. We're also currently looking for a new Sharp Scratch panelistillian Kodate. We're so fun. Come and join us. Yes. So, yeah, if you'd like to represent the voice of medical students in future Shapscratch episodes, please visit the show notes and apply via the link. And if you'd like to hear other episodes, please subscribe to Shapscratch wherever you get podcasts. And in two weeks time, you'll be notified of our next episode. While you wait for the next 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 if you could leave us a rating and a review on wherever you get your podcasts as it helps elements students to find a show until then is goodbye from us
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Welcome. This is the New England Journal of Medicine. I'm Dr. Lisa Johnson. This week, April 28, 2016, we feature articles on transcatheter versus surgical aortic valve replacement, exazomib in myeloma, Ebola vaccine trials, and an experimental approach to treating Duchenne's muscular dystrophy, a review article on violence against health care workers, a case report of a woman with hemiplegia and aphasia during a transatlantic flight, and prospective articles on Tobacco 21 laws, on a moonshot to Malawi, and on colorectal cancer on the decline. Transcatheter or Surgical Aortic Valve Replacement in Intermediate-Risk Patients by Martin Leon from Columbia University Medical Center, New York Previous trials have shown that among high-risk patients with aortic stenosis, survival rates are similar with transcatheter aortic valve replacement, TAVR, and surgical aortic valve replacement. In this trial, 2,032 intermediate-risk patients with severe aortic stenosis at 57 centers were randomly assigned to undergo either TAVR or surgical replacement. The rate of death from any cause or disabling stroke was similar in the TAVR group and the surgery group. At two years, the Kaplan-Meier event rates were 19.3% in the TAVR group and 21.1% in the surgery group. In the transfemoral access cohort, TAVR resulted in a lower rate of death or disabling stroke than surgery, whereas in the transthoracic access cohort, outcomes were similar in the two groups. TAVR resulted in larger aortic valve areas than did surgery and also resulted in lower rates of acute kidney injury, severe bleeding, and new-onset atrial fibrillation. Surgery resulted in fewer major vascular complications and less paravalvular aortic regurgitation. In intermediate-risk patients, TAVR was similar to surgical aortic valve replacement with respect to the primary endpoint of death or disabling stroke. Neil Mote from Royal Brompton Hospital, London, writes in an editorial that there is a consistent message emerging from the three large trials published to date involving patients at high, intermediate, and very high risk. Transcatheter aortic valve replacement is non-inferior to surgery in terms of early and midterm mortality and is likely to be superior if the patient has vascular anatomy and vessels that are healthy enough to be treated with the use of a transfemoral approach. As with many trials involving new technologies, the findings have to be interpreted with the understanding that the technology in both groups has advanced since the design of the trial. The results of further trials are awaited with interest. Oral Ixazomib, Lenalidomide, and Dexamethasone for Multiple Myeloma by Philippe Moreau from the University Hospital Hôtel-Dieu, Nantes, France. In this Phase III trial, 722 patients who had relapsed, refractory, or relapsed and refractory multiple myeloma were randomly assigned to receive exazomib, an oral proteasome inhibitor, plus lenalidomide dexamethasone, exazomib group, or placebo plus lenalidomide dexamethasone, placebo group. Progression-free survival was significantly longer in the exazomib group than in the placebo group at a median follow-up of 14.7 months. Median progression-free survival, 20.6 months versus 14.7 months. A benefit with respect to progression-free survival was observed with the exazomib regimen as compared with the placebo regimen in all pre-specified patient subgroups. The overall rates of response were 78% in the exazomib group and 72% in the placebo group, and the corresponding rates of complete response plus very good partial response were 48% and 39%. The median overall survival has not been reached in either study group, and follow-up is ongoing. The rates of serious adverse events were similar in the two study groups. Thrombocytopenia of grade 3 and grade 4 severity occurred more frequently in the exazomib group. The addition of exazomib to a regimen control of a future outbreak. In this Phase 1 study, a single dose of a chimpanzee adenovirus 3, CHAD3 vaccine, was administered in 76 healthy volunteers in England. No safety concerns were identified at any of the dose levels studied. Four weeks after immunization with the CHAD3 vaccine, Zaire Ebola virus, Zeebov-specific antibody responses were similar to those induced by RVSV Zeebov vaccination, which was assessed in another Phase 1 trial. Zeebov neutralization activity was also similar with the two vaccines. Boosting with the modified vaccinia oncara MVA vector increased virus-specific antibodies by a factor of 12 and increased glycoprotein-specific CD8 T cells by a factor of 5. Significant increases in neutralizing antibodies were seen after boosting in all 30 participants. Virus-specific antibody responses in participants primed with CHAD3 remained positive six months after vaccination, but were significantly higher in those who had received the MVA booster. The CHA3 vaccine, boosted with MVA, elicited B-cell and T-cell immune responses to ZBOV that were superior to those induced by the CHA3 vaccine alone. Phase I trials of RVSV Ebola vaccine in Africa and Europe by Seleji Agnangi from the Centre de Recherche Médicale de l'Ambaréné, Gabon. Four Phase I studies assessed the safety, side effect profile, and immunogenicity of a recombinant vesicular stomatitis virus-based Ebola vaccine, RVSV-ZBOV, at various doses in 158 healthy adults in Europe and Africa. No serious vaccine-related adverse events were reported. Mild to moderate early-onset reactogenicity was frequent but transient. Fever was observed in up to 30% of vaccinees. Vaccine viremia was detected within three days in 95% of the participants receiving 3 million plaque-forming units or more. RVSV was not detected in saliva or urine. In the second week after injection, arthritis affecting 1 to 4 joints developed in 22 percent of participants in Geneva, with pain lasting a median of 8 days. Two self-limited cases occurred in 3% of participants in Hamburg, Germany and Califi, Kenya. The virus was identified in one synovial fluid aspirate and in two skin vesicles of two other vaccinees, showing peripheral viral replication in the second week after immunization. Zeebov glycoprotein-specific antibody responses were detected in all the participants, with similar glycoprotein-binding antibody titers but significantly higher neutralizing antibody titers at higher doses. Glycoprotein-binding antibody titers were sustained through 180 days in all participants. In these studies, RVSV-Zibov was reactogenic but immunogenic after a single dose and warrants further evaluation for safety and efficacy. Workplace Violence Against Healthcare Workers in the United States, a review article by James Phillips from Beth Israel Deaconess Medical Center, Boston. In January 2015, a surgeon at Brigham and Women's Hospital in Boston was shot and killed at work by the son of a deceased patient. Even though the event received substantial media coverage, reporters did not highlight the fact that although the murder of a health care worker is rare, episodes of workplace violence against medical providers happen daily across the country. Although the majority of these incidents of workplace violence are verbal, many others constitute assault, battery, domestic violence, stalking, or sexual harassment. This review focuses on our current knowledge about workplace violence in various health care settings, including the prevalence across professions, potential risk factors, and the use of metal detectors in preventing violence. Between 2011 and 2013, the number of workplace assaults averaged approximately 24,000 annually, with nearly 75% occurring in health care settings. Researchers have yet to discover statistically significant, universally applicable methods of risk reduction. To date, most research has been directed at quantifying the problem and attempting to profile perpetrators and their victims. The few studies that have focused on interventions to reduce violence have highlighted the unlikelihood of finding a simple, one-size-fits-all solution to prevent this violence. A 49-year-old woman with sudden hemiplegia and aphasia during a transatlantic flight. A case record of the Massachusetts General Hospital by Lee Schwamm and colleagues. A 49-year-old woman was brought to the emergency department two hours after the onset of hemiplegia and aphasia during a transatlantic flight. Two hours earlier, severe weakness developed on the right side, and she lost the ability to speak. The patient's husband alerted a flight attendant, and a passenger who was a physician informed the crew that they must transport her to a hospital within three hours to enable proper treatment. The pilot accelerated the aircraft to arrive in Boston within two hours after symptom onset. The patient was evaluated by emergency medical technicians on her arrival at the airport.
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The patient was brought to the emergency department. On the initial examination, the patient was alert and followed simple commands, but answered, yuck, to all questions. A diagnosis of acute ischemic stroke due to occlusion of the left middle cerebral artery was made. A bolus of tissue plasminogen activator was administrated 13 minutes after the patient's arrival at the hospital. Imaging studies were consistent with infarction involving the territory of the left middle cerebral artery. One hour after the patient's arrival, she was transported to an operating room for endovascular thrombectomy. The left internal carotid artery, anterior cerebral artery, and middle cerebral artery were successfully recanalized. Hints to the cause of this patient's stroke became available by the second hospital day. The CRISPR Way to Think About Duchenne's, a Clinical Implications of Basic Research article by Michelle Kalos from Stanford University, California. Today's hottest genome engineering method, CRISPR-Cas9, has recently been used to treat mouse models of the most common form of muscular dystrophy, Duchenne's muscular dystrophy. Three groups of investigators have recently described the use of CRISPR-Cas9 to remove a mutation in the gene encoding the dystrophin protein and thereby to affect the expression of the protein. The researchers used the CRISPR-Cas9 genetic engineering system to cut out the mutated part of DMD in the MDX mouse model of the disease, thereby allowing the synthesis of a shorter version of the dystrophin protein in muscle fibers and restoring partial muscle function. This type of approach could potentially remove disease mutations in about 80% of patients with Duchenne's, although it would require sequence-level knowledge of each patient's specific mutation and a customized strategy for its removal. Have Tobacco 21 Laws Come of Age? A Perspective Article by Stephanie Moraine from Baylor College of Medicine, Houston. On January 20, New Jersey Governor Chris Christie vetoed a bill passed with strong bipartisan support by his state legislature that would have raised New Jersey's minimum age of sale for tobacco products to 21. The veto is a setback in an otherwise accelerating movement toward dissemination of Tobacco 21 laws as a new tool for reducing young people's access to cigarettes and e-cigarettes. By March of this year, at least 125 localities and the state of Hawaii had adopted Tobacco 21 laws, and California was on the cusp of following suit. In September 2015, the first federal Tobacco 21 legislation was introduced. Are Tobacco 21 laws ready to go to scale, as these legislative developments suggest? These authors believe they are. Recent research has shown that laws raising the minimum age for purchase of tobacco products to 21 are effective, enjoy very high levels of public support, and have minimal economic impact in the short term. Over the longer term, the revenue loss from decreased smoking prevalence will be substantial. But allowing future generations to become addicted to nicotine in order to preserve tobacco revenue fails the red-face test as an argument against Tobacco 21. Moonshot to Malawi, a perspective article by Satish Gopal from the Malawi Cancer Consortium, Lilongwe. In his 2016 State of the Union address, President Barack Obama called for a moonshot to cure cancer. The announcement energized the cancer community to continue building on the remarkable collective progress made in recent years. The pace of that progress has been dizzying. But Dr. Satish Gopal now lives in Malawi, a small, resource-limited country in southern Africa with a population of 17 million. From there, it can be difficult to appreciate the tangible fruits of a decades-long international war on cancer. Despite small daily victories and immense Thank you. The neglect spans the continuum from awareness to prevention, diagnosis, treatment, and palliation. To his constant surprise, Dr. Gopal is often asked by clinicians, researchers, funders, and policymakers whether people get cancer in Malawi. They certainly do. Although it is preventable, cervical cancer is the leading cancer among Malawian women. No radiotherapy is available, and despite repeated demonstrations that cancer can be cured even here if old drugs are consistently available and properly used, they routinely stock out of generic chemotherapy medicines that were licensed in the 1960s or 1970s. Shooting for the moon in cancer science is important, but so is shooting for a world that is just and equitable. Colorectal cancer on the decline. Why screening can't explain it all. A perspective article by H. Gilbert Welch from the Department of Veterans Affairs Medical Center, White River Junction, Vermont. U.S. colorectal cancer incidence has dropped by more than 45% since its peak in the mid-1980s. More important, colorectal cancer mortality has fallen by more than half. These trends are often attributed to screening, but the magnitude of the changes alone suggests that other factors must be involved. Also, the timing of the trends isn't consistent with this explanation. Population-wide colorectal cancer screening has been slow to disseminate into clinical practice. If not screening, what explains the decrease in colorectal cancer mortality? These authors believe there are three categories of plausible explanations. First, the treatments available for colorectal cancer today are better than they were 30 years ago. Second, earlier detection of symptomatic disease and subsequent reductions in mortality can occur even in the absence of widespread screening. Finally, there could be fewer cases of colorectal cancer occurring in the first place. Our images in clinical medicine features a 78-year-old woman who had undergone coronary artery bypass graft surgery 30 years earlier and had a smoking history of 54 pack years who presented to the emergency department with shortness of breath and fatigue. The troponin level was within the normal range. There was no evidence of ischemic changes on electrocardiography. X-ray of the chest revealed a mediastinal hyaluron mass lesion on the left side. CT angiography of the chest revealed two partially thrombosed aneurysms of the saphenous vein grafts. The larger aneurysm arose from the superior graft that was anastomosed to the left anterior descending coronary artery, and the smaller aneurysm arose from the inferior graft, which was anastomosed to the diagonal artery. In view of the risks of undergoing surgery again and the absence of angina, the patient continued to pursue a conservative course, and the symptoms at presentation resolved. A 49-year-old woman presented to the dermatology clinic with an asymptomatic pigmented lesion on the ventral surface of her tongue. The lesion, which had been present for four months, was suggestive of oral melanoma. The patient reported no trauma and no alcohol or cigarette use. However, she did report that she had undergone a dental restoration procedure three months before the appearance of the lesion. Physical examination revealed an asymmetric brownish-gray pigmented macule measuring 1 cm by 1.2 cm in the greatest dimensions, with a central area of regression. No other cutaneous or mucosal abnormalities were found. The lesion was completely excised. Histopathological examination revealed dermis with fibrosis and an interstitial deposit of thin, elongated black pigment with no inflammatory cell infiltrate. No melanocytic hyperplasia or evidence of cancer, This concludes the summary of the April 28, 2016 issue of the New England Journal of Medicine. We're interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at NEJM.org. Thank you for listening.
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Okay, welcome. My name is Devine. I'm a resident. This is episode 206 of the Devine Intervention Podcast. And in this podcast, I'm going to begin a family medicine shelf exam rapid review series. I'll just be doing a bunch of cases that highlight topics and concepts that are commonly tested on the family medicine exam. It will be completely random. But hopefully as you listen to this series and as I build up this series, you'll find it to be very helpful for the exam. So let's just jump right into it. So the first thing I think I want to start with is talking through like an algorithm that's frequently tested on the family medicine shelf. And that is the algorithm that relates to a thyroid nodule, right? So if a person has has a thyroid nodule what is always your first step in diagnosis if you're pressing you know a physical exam you'll palpate a thyroid nodule what is always your first step in diagnosis well i would really hope that you're thinking that uh you'd want to go ahead and measure the tsh right because the thing is when you measure the tsh that will help you delineate between the person potentially having a hot nodule or a cold nodule okay a hot nodule or a cold nodule so you measure the tsh and basically the way i teach people this concept is essentially if the tsh is low you know you're dealing with a hot nod right? Because the algorithm can get complicated real fast if you try to overcomplicate things, right? So the best thing to just ask yourself is, is the TSH low? If the TSH is low, it's a hot nodule. If the TSH is not low, so any other results, be it normal, high, whatever, it doesn't matter, then it goes into the TSH, not low pile. So let's talk about the TSH low pile, right? So if the TSH is low kind of pile, right? Then we know we're dealing with a hot nodule, right? And once a person has a hot nodule, right? The thing is the chance of like thyroid cancer, because when you see a thyroid nodule, right? The thing that freaks you out is thyroid cancer, right the tsh is low you know it's a hot nodule super low risk of cancer so your next step in diagnosis on an mbm exam will be to order a ryu scan okay you want to be able to reinterpret those ryu scan results right so if for example a person you get a ryu scan and you find like a single hot spot on the ryu scan, that's going to be a toxic adenoma, right? That's pretty easy. But what if they told you that, oh, you see multiple hot spots? What are you thinking about under those circumstances? Well, I hope you're telling me that it's a toxic multi-nodular goiter, right? Okay. And then what if they tell you that there's diffuse, there's a diffusely increased uptake on the Ryus scan? What are you thinking about? Well, that'll be Graves' disease, right? That'll be Graves' disease, right? That'll be Graves' disease, right? So whenever you see those kinds of things, think about, again, those are kind of like the big things you want to keep at the back of your mind with a Raius scan. And I'll say some quick things at the end, but let me talk about like the other part of this algorithm, right? So the other part of the algorithm, if the TSH is not low, right, that means you have a cord nodule, right? The problem with cord nodules is most of them are benign, about 70% of them, 70, 75%, they're like colloid cysts in the thyroid. But you know, you can never be sure of that, right? So typically after that, you want to do like an FNA with ultrasound, right? So you can get like some thyroid tissue and send it off to a pathologist, right? And, you know, if you see a cancer, you want to know like some quick, for the family medicine shelf, you don't need, again, need to go all super in depth on these cancers, but you need to kind of know some of them, right? And like some key things, right? So say for example, right, they tell you that you see some of my buddies, my buddies from a pathology specimen of a cold thyroid nodule. What kind of cancer are you thinking about? Well, I hope you're thinking about papillary thyroid cancer. Remember, papillary thyroid cancer is popular. So it's the most common kind of thyroid cancer. And don't forget the biggest risk factor for that, which is a history of exposure to neck radiation, right? So remember, papillary thyroid cancer, it actually loves to spread through lymph nodes. The reason I'm saying that is there is another kind of thyroid cancer, follicular thyroid cancer, that loves to spread hematogenously. It doesn't spread via lymph nodes, right? So that's something you want to keep at the back of your mind for exams, right? So follicular thyroid cancer, hematogenous spread, but papillary thyroid cancer loves lymphatic spread. It has the best prognosis of all the thyroid cancers. It's associated with exposure to head and neck radiation. Another thing you may see on histology is the often anion nuclei, right? You may see the often anion nuclei, right? So those are the big things there. And then what if they give you a question about a person that has like a neck mass and then they tell you that or like the father the uncle or whatever like just a ton of family members dying of like some weird neck mass or maybe like this person has had like hypercalcemia for whatever bizarre reason or something um if you see like multiple family members with thyroid cancer right i would really hope you're thinking about one of the men syndromes right in this case it will be men2a or men2b right because they likely have medullary thyroid cancer, right? I would really hope you're thinking about one of the MEN syndromes, right? In this case, it will be MEN2A or MEN2B, right? Because they likely have medullary thyroid cancer. Remember, medullary thyroid cancer has a terrible prognosis and all people that have MEN2A, 2B, they need a prophylactic thyroidectomy at some point early in their lives because it's not a matter of if they will get thyroid cancer, it's just a matter of when they will get the thyroid cancer, right? So typically for those folks, you know, you go ahead and get a prophylactic thyroidectomy. This is medullary thyroid cancer here. And what is the key histologic finding on a biopsy in a person that has medullary thyroid cancer? Well, I hope you're telling me that you'll find amyloid in the thyroid gland, right? So if they say something about a person having like apple green birefringence on congol red staining from like a thyroid biopsy specimen, you want to think about medullary thyroid cancer, right? And remember that people that have medullary thyroid cancer, they can actually come in with like symptomatic hypocalcemia on an MBM exam because the tumor marker for medullary thyroid cancer is calcitonin. So that calcitonin, right, can calcitone down your blood calcium levels, right? So that can cause hypocalcemia. Or if they want to get like super sneaky, they can give you like an EKG on your family-made shelf in a person that has like a neck mass, and then you see like a prolonged QT interval, right? You should, again, think about hypocalcemia for medullary thyroid cancer under those circumstances, right? Now, I said that at the end, I will say some other things about our, well, let me say one more thing. So what if they tell you that, oh, from this thyroid nodule, you get a biopsy specimen of the thyroid and you see a lot of like lymphoid follicles. What are you thinking about under those circumstances? Well, I would hope you're thinking about a person having like Hashimoto's, right? Remember, the most common cause of hypothyroidism in the US is Hashimoto's, thyroiditis, right? Is Hashimoto's, thyroiditis. And those people who have very low levels of like, I mean, like they can have like a thyrotoxic phase, right? But usually they present with hypothyroid symptoms. And the hypothyroidism when you'll see on your exam, it will be something along the lines of like bradycardia, right?
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At least probably like 80% of the MBM questions I've seen on hypothyroidism, those people almost always have bradycardia, right? And you know, they will feel tired, they will gain weight, they will have like the pre-tibial myxedema and all that badness, right? And they may also have like cholesterol lab abnormalities, right? So if you see a ton of lymphoid follicles in the thyroid gland think about uh Hashimoto's thyroiditis um if you also do a biopsy though right let's say you see a person that has had like a long history of Hashimoto's thyroiditis and then you have like this rapidly expanding neck mass whenever you see stuff like that you obviously want to think about um like a thyroid lymphoma remember thyroid lymphoma is actually one of the neoplastic, like potential neoplastic complications of a person having a long history of Hashimoto's thyroiditis. And remember, sometimes your friends at the MBME, right, they play this game where they will not give you the name of something you're familiar with, right? So occasionally, instead of putting Hashimoto's thyroiditis, they can put lymphocytic thyroiditis as the answer choice on an exam. That's just code word for Hashimoto's thyroiditis, right? And then if they give you a question about a person that, you know, has hyperthyroid symptoms, like their TSH is low, but you get a RIO scan and you notice, you're like, hmm, I'm not seeing any optic whatsoever on a RIO scan. What pathology should you think about? So your thyroid gland will no longer be stimulated. So you will not have increased uptake. Another thing you may see that may cause those kinds of symptoms, although this person will have like a tender thyroid gland on an MBM exam, is the person having like a, like a dequervins or like the subacute thyroiditis, right? So if a person has hyperthyroid symptoms, they have a tender thyroid gland, right? But then you see no on a right-of-scan, that's pathognomonic for de Quervain's thyroiditis. So you may say, Devine, okay, well, how do I tell de Quervain's thyroiditis apart from a person exogenously taking thyroid hormone? Well, remember, I think I've said this in multiple podcasts in the the past, right? That there's this thing known as thyroglobulin. Thyroglobulin is like the C-peptide of the thyroid gland. So if a person's thyroid hormone is coming from the actual thyroid gland, the person's thyroid globulin levels will be elevated when they're in a state of thyrotoxicosis. But if the thyroid hormone is not coming from the thyroid gland, the thyroglobulin levels will be really low. So if a person is injecting thyroid hormone or, you know, taking like oral Synthroid or whatever, those people will not have elevated levels of thyroglobulin. But if a person has the equivalence thyroiditis, right, because remember, the equivalence thyroiditis is just generalized inflammation of the thyroid gland, right? So you have like release of preformed thyroid hormone. you see that right you should suspect um the person uh you know having a and again you also have a tender thyroid gland you should suspect that the quervins or thyroiditis are under those circumstances right um so those are kind of like some big things you want to keep in mind there and again remember your eminence syndromes they're just sort of kind of thyroid related. So let's talk about those, right? So remember, right, those things have autosomal dominant inheritance. There's MEN one where they will have like parathyroid, like primary hyperparathyroidism, right? So they can have hypercalcemia. They can have like pituitary adenomas, most commonly like a prolactinoma. But remember, those people can also have, so the prolactinoma, right, obviously will cause like gynecomastia, galactoria,oria infertility because prolactin is a suppressor of gnrh right and then um they can also have a pituitary another pituitary thing they can have right they can also have like a growth hormone secreting a tumor right so they can have like acromegaly right so like oh like the species between their teeth is increased they have frontal busing their. Their friends don't recognize them anymore. Their rings don't fit. Their hats don't fit. And they can get like a hypertrophic cardiomyopathy and die from that. Right. So that's probably that's actually the most common cause of death in people with macromegaly. Right. And then remember that they can also get pancreatic neuroendocrine tumors. They can get insulinomas. Right. They'll have like the classically described Whipple's triad, right? So like they'll have hypoglycemia, signs of hypoglycemia, and then their symptoms get better with glucose augmentation, right? Or they can get like a glucagonoma, right? So if you see a person that's like developing like new onset diabetes, right? They've never had a history of diabetes. And then weirdly they develop diabetes and you're like, hmm. And then this person has like a skin rash. Like a necrotic skin rash. Think about a glucagonoma. Under those circumstances. Right. So. The classically described. Necrolytic migratory erythema. Right. That's a pathognomonic thing. You may see on an MBM exam. And then. Also do not forget that. If a person has. Another pancreatic neuroendocrine tumor. I guess that can show up. Right. It's like like a gastrinoma, right? So those people can have like the Zollinger-Ellison syndrome. So, you know, you see these people that seem to have like these very virulent ulcers, right? Especially if you see ulcers in the jejunum of the small bowel, right? That's super unusual. That's not H. pylori. That's Zollinger-Ellison syndrome, right? And usually those people tend to have chronic diarrhea as well, right? And then I guess maybe the final pancreatic neuroendocrine tumor i should talk about here is the vipoma right remember vipomas tend to present with the wdha syndrome right where you have like watery diarrhea uh they will have like hypokalemia they will have achlohedra right again those are all classic things you may see with man1 and again um it's autosomal dominant inheritance man2a right you can the primary hyperparathyroidism, but those people can also have pheochromocytomas, right? So the pheos, right? You'll see like the episodic headache and hypertension. And obviously for that, you want to check the levels of metanephrines and catecholamines in the urine, right? You'll be elevated. And then you do like a CT scan of the abdomen or an MRI of the abdomen, or you do like the nuclear medicine test, which we classically call like an MIBG scan to establish other diagnosis, right? And then those people can also have a medullary thyroid cancer, which I've talked about already, right? And then MEN2B, right? Those people do not get calcium problems. They don't get the primary hyperparathyroidism, but they can get the pheochromocytoma, right? They can get the morphanoid habitus, right? So they can be like super tall and all that jazz, right? And then they can also have the pheochromocytoma right they can get the morphanoid habitus right so they can be like super tall and all that jazz right and then they can also have the pheochromocytomas right and then they can also have the mucosal neuromas like the growths on mucosal surfaces usually it's the lips on an mbm exam right so hopefully you feel comfortable with these thyroid pathologies again they are all high yield things that tend to pop up on exams right so that's something i definitely know if I were you preparing for any of these exams. And then one thing I found to be high-yield for these family medicine exams is knowing the cholesterol screening guidelines, right? So those are things that people, unfortunately, tend to not know very well. They're kind of detailed. So, you know, they're kind of one of those annoying things that you need to like sort of furnish in the back of your mind for exams, right?
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That's not always the case, right? So if a person has an LDL cholesterol, not total cholesterol, LDL cholesterol more than, you know, 190, right? So 190 or higher. So if it's 189, it doesn't fall. But 190 or higher, right? Go ahead and give those people a statin, right? And again, usually you give like high intensity statins like atorvastatin or rosovastatin, right? And then if a person has like a really bad like atherosclerotic cardiovascular disease, right? Like they have coronary artery disease, they've had stroke, they have peripheral arterial disease, whatever. For those people, they also deserve high intensity statins. And again, again, remember, atoverstatin and rosuvastatin are your high-intensity statins, right? And then if you have diabetes and your LDL cholesterol is more than 70, right, and you're basically between the ages of 40 to 75, the way I just think about it is, are you a diabetic? Is your cholesterol more than 70? Are you more than 40 years old? That's it. You get a high intensity statin as well. But if you're also over the age of 40 and your cholesterol is just above 70, right? But you notice that this person's ASCVD risk is more than 7.5%. So 7.5%. Those people also deserve a high intensity statins, right? So again, I'll reel them out., LDL greater than 190, so greater than or equal to 190, right? If you've had, like, really bad atherosclerotic cardiovascular disease, so that the classic ones on exams, MI, stroke, PAD, right? Or if you're a diabetic and your cholesterol is greater than 70 and you're over the age of 40, right? Your LDL cholesterol greater than 70 and you're over the age of 40, you also get a high-intensity statin then if you're over the age of 40, right? I mean, if you want to be more strict, like between 40 and 75, and you don't, again, you don't have diabetes, but your LDL cholesterol is over 70, but your ASCVD risk is more than 7.5%. Those people also deserve high intensity statins on an MBM exam, right? And that ASCVD score, you don't need to memorize how to calculate it is something that you would typically get on an mbme exam right and again remember your high-intensity statins are things like atover starting and resolver starting right and then um one other thing that your friends at the mbme love to test on exams are like these are vitamin defic, right? So let's maybe run through the vitamins. That's probably where I'll stop today because it's a fairly large topic, right? So let's maybe go through the B vitamins, right? So vitamin B1, right? So vitamin B1 is thiamine, right? So what are the high-yield things you want to keep at the back of your mind for your family medicine shelf with thiamine. The big ones you want to keep at the back of your mind, one, you want to think about like an alcoholic, right? So, alcoholics, right? They can get Wernicke-Korsakoff syndrome. Remember, Wernicke-Korsakoff syndrome arises because you have issues with transketolase. Transketolase is one of those key enzymes in the non-oxidative phase of the pentose phosphate pathway, right? So, transketase uses thiamine, vitamin B1 as a cofactor. So if you're an alcoholic, you know, you deplete your B1. If you deplete your B1, then you can get into trouble, right? Like having Wernicke-Korsakoff syndrome. And remember, Wernicke's, right, is the triad of a person having a confusion, right? Ophthalmoplegia. Ophthalmoplegia is just code word for any eye problem. And then ataxia, right? If you see that, that's reiki, that's reversible, right? You give IV thiamine for that and you give the thiamine before you give glucose, right? But if you take that thread and add on to it things like a person making stuff up, right? So like confabulations or the person having like disorganized movements like ataxia, then that's Corsacops. Corsacops is also treated with IV thiamine, but it's irreversible, right? It's irreversible. And then one other thing that you may see with thiamine problems on an exam is a person that has hyperemesis gravidarum, right? So if they describe a five-trimester pregnant woman vomiting a ton, those people actually have a pretty high risk of wernicke's. So those people actually deserve vitamin B1, like IV vitamin B1 when they come to the hospital, in addition to the anti-emetics that you're giving them, right? And usually on MBME exams, those people have a metabolic acidosis. They'll have like a hypokalemic, hypochloremic metabolic acidosis, sorry, hypokalemic, hypochloremic metabolic alkalosis. Whoops, I take that back. Metabolic alkalosis, right? Because you're vomiting stomach acid, right? So you become alkalotic from that. And also because you're vomiting a ton, right? You become volume depleted. So the activity of your urinary and your tensile and aldosterone system goes up, right? So aldosterone will dump all those protons at the level of the alpha-intercalated cell of the collecting of the distal nephron, right? So you get a metabolic alkalosis there. And you're hypochloreic right because you're vomiting hydrochloric acid literally right so those are the big things to know with thiamine and remember thiamine has that neuroanatomical association with hemorrhagic infarctions of the mammillary bodies right so that's something you want to keep in mind um and then having a thiamine deficiency right can also cause um wet berry berry right that's like a dilated cardiomyopathy again that you can find in a chronic alcoholic right because again if thiamine is not working you may say divine why is that well if thiamine doesn't work i don't know some key pathways in your body i don't know like maybe like uh like the pyruvate dehydrogenase complex is not going to work so your tc is basically the gateway to your tc cycle is shot right so you're not going to be able to make atp right and if you're not making atp right your cells will begin to feel they'll be essentially have like it's almost like a metabolic ischemia in a sense right so you get into trouble and you can get a dilated cardiomyopathy which is essentially wet berry berry it's called wet berry berry because if your heart doesn't work you have edema everywhere right now vitamin b2 uh riboflavin that's not really tested on the family med shelf so i'm gonna move on from that vitamin b3 is niacin right niacin certainly is tested right pellagra right pellagra right and there are many things that can cause pellagra in your test right so you know if you don't eat foods that are rich enough in b3 well you're kind of screwed there that's one but another thing that can kind of screw you over as well is if you have like carcinoid syndrome, right? Remember carcinoid syndrome is where you have like a GI mass that makes a ton of serotonin. Well, think about it. Serotonin is known as 5-HT for a reason, right? 5-hydroxytryptophan, right? So that means it's derived from tryptophan. Well, guess what? What do you think we use to make niacin? We also use tryptophan to make niacin, right? So if you shunt all your tryptophan towards making serotonin, well, you're going to get pellagra with that, right? Or if you have like heart knob disease where you have trouble reabsorbing like neutral amino acids like tryptophan at the level of the proximal convoluted tubule, right?
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And then what are the things you find with niacin deficiency aka pellagra right you know you have the four d's right so like diarrhea dermatitis dementia and death right so those are all things to keep at the back of your mind for exams um vitamin b5 pantheothenic acid that's step one so i'm going to skip that there's no vitamin b4 at least i don't think yeah i'm pretty sure actually i'm certain there's no vitamin b4 it's only if they discovered vitamin b4 and i'm not aware of it but vitamin b6 is definitely high you'll to know for exams right that's pyridoxal phosphate there are many different contexts that you could see this in on an mbm exam right so especially on a family medicine shelf right the probably the classic one would be like tb treatment right your doctor says oh you're taking isoniazid I would really love you to take this vitamin alongside, right? You're like, doc, I don't think you really know what you're talking about. Or maybe you read like Dr. Google and, you know, read some crap online. Well, fine. I wish you all the best with your cedaroblastic anemia, right? So what are the things that B6 can cause, right? So B6 can cause cedaroblastic anemia, right? Because remember, if you remember from step one, there's this enzyme known as ALAS, like ALS synthase, that's like the reclimiting enzyme of heme synthesis. Well, it needs B6 as a cofactor, right? So, you know, if your B6 is not working, if you don't have B6, because isoniazid depletes your B6, if your B6 is not working, right, then ALAS will not work, you won't make heme, so you get a titerobbroplastic anemia another thing that can also happen is you can also get seizures right from a b6 deficiency right so um because again remember glutamate is an excitatory neurotransmitter at least of the central nervous system like the brain and then gaba is the inhibitory neurotransmitter of the brain right so gaba is inhibitory kind of calms you down glutamate is super excitatory kind of spruces you up right so if you have like uh b6 deficiency there's this enzyme known as gad glutamate decarboxylase that will not work and gad converts glutamate to gaba right so if gad doesn't work because the cofactor is not around then your glutamate will rise your gaba will plummet and because you have high glutam much excitation, you can get seizures, right? And then you can also get like LFT abnormalities, right? Well, what's the cofactor used by your transaminases? It's vitamin B6, right? So if your vitamin B6 does not work, that explains why isoniazid is potentially hepatotoxic as well, right? So those are all things you want to keep in mind on exams. Vitamin B7, biotin, I'm going to skip that. That's more step one further. B8, there's no vitamin B8, at least as far as I know. But B9 folate, you know, kind of high yield to know, right? So if you're the kind of person that does a tea and toast diet, well, you well you can get a folate problem right and folate can cause a megaloblastic anemia right so the mcv will be more than 100 and those people can also get like hyperhomocysteinemia although remember that people that have a folate deficiency will not get methylmalonic acidemia right because remember it's b12 deficiency that's cobalamin it's b12 deficiency that will cause the methylmalonic acidemia, right? Because remember, it's B12 deficiency. That's cobalamin. It's B12 deficiency that will cause the methylmalonic acidemia in addition to the megaloblastic anemia and hyperhomocysteinemia. Because if you remember from step one, with your O-chain fatty acids, right? Like if you want to go from methylmalonyl-CoA to succinyl-CoA, you need methylmalonyl-CoA mutase for that to happen, right? So if you have a B12 deficiency, the enzyme methylmalonyl-CoA to succinyl-CoA, you need methylmalonyl-CoA mutase for that to happen, right? So, you know, if you have a B12 deficiency, the enzyme methylmalonyl-CoA mutase will not work because B12 is its cofactor. So you get a methylmalonic acidemia from that. And then remember, right, B12 can also cause all these other problems, right? Like subacute combined degeneration of the spinal cord. So like your dorsal columns, your corticospinal tract won't work. So those people have problems with like fine touch, vibration, proprioception. They will have like upper motor neuron symptoms kind of deal, right? You know, so those are things to keep in mind. And then remember, right, fully deficiency, right? Classic in people that are taking anti-epileptic drugs. And B12 deficiency, right? If you're a vegan, right? Like an unwise vegan, you you know you don't take like b12 supplements because remember b12 comes from animal products right uh remember fully it comes from fully age right so if you're taking if you're vegan you're not going to get a fully deficiency but you'll definitely get a b12 deficiency especially if you're like a prolonged like you're like a long-termer you're a long-termer vegan right so um let's see is there any other vitamin stuff i want to talk about or mineral stuff um if a person has like dysgousia so you know like impaired t sensation or a person has um alopecia right that's classic zinc deficiency and i mean there are many things that can cause zinc deficiency right like if you're on tpn for a long time right or if you have wilson's disease believe it or not right if you have wilson's disease and it's being treated and you're not supplementing zinc that can also cause problems because one of the treatments for wilson's disease is a copper chelator known as triantine so t-r-i-e-n-t-i-n-e um well in addition to being able to kill it uh copper it's actually pretty good at chelating zinc right so you can get a deficiency that way right um and then vitamin c deficiency right so the person will have like mucosal bleeds um they'll have uh because collagen doesn't work very well because remember from step one if you want to like hydroxylate like proline and lysine residues you kind of need vitamin c for that so you have like you know like a kind of like screwed up um collagen synthesis when you a vitamin C deficiency. So you essentially have like scurvy, you'll have like bleeding gums and all that crap. And then don't forget, right? If they give you a question about a person that has like a malabsorptive disorder, right? That's basically like a gateway to like fat soluble vitamin deficiency questions on exams, right? So like night blindness with like vitamin A deficiency or like osteoporosis or secondary hyperparathyroidism with a vitamin d deficiency right uh because remember right like if you have a fat malabsorption then by default you are not able to resolve your ade and k vitamins or vitamin e deficiency right that'll be like the person you have like acanthocytosis on a blood smear and you also have ataxia because again if you remember from step one um it's kind of phenomenal how step one actually is really helpful for step two like doing like knowing your step one material well really helps on step two at least in my experience um but i mean e deficiency can cause ataxia right because from step one if you remember your spinal cerebellar tracts uh the proper myelination of this of those tracts depends on our vitamin e right and then vitamin k they can get like all these vitamin k deficiency they can get all these bleeds so i guess your major question you may be like oh divine what are the things that can cause fat malabsorption well a bunch of stuff right so let's assume your terminal ileum has been reset then because you have crohn's disease well you're not going to be reabsorbing many fats that way. And that can also cause B12 deficiency, right? Or if a person has like cystic fibrosis on a family medicine shelf, if you have CF, right, your pancreas, right, you have like an endocrine and exocrine pancreatic defect, right, because your pancreatic secretions are very thick, right? So you're not making lipase, you know, so that can cause problems. Or. Or let's assume you have celiac disease. Celiac disease can also cause a fat malabsorption.
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Remember, you want to avoid bloating-containing foods in those people. And then if you've drunk alcohol for a pretty long portion of your life, and then they tell you that, oh, the person has had recurrent episodes of abdominal pain, that's chronic pancreatitis, right? Pancreas is shot, no more lipase, right? So you're kind of screwed from that perspective. So I think those are kind of like the key vitamins and minerals. You know, you want to commit to memory for your exams. One thing that just dropped in my mind, let me just see this for completeness sake, because again, the family medicine shelf covers like kids to adopt, right? So if you see a newborn with like big tongue, like a big tongue, beefy red tongue, has an umbilical hernia, has macroglossia, right? That's pretty classic for congenital hypothyroidism, right? And usually the most common cause there is like thyroid dysgenesis, right? So again, these are just all things you want to keep at the back of your mind. And I will try really hard. It's just, again, time. That's my big limiting factor here. But I'll try really hard to hopefully make some more family medicine related shelf podcasts as time goes on. But I'll just make them rapid review series. It will be a comprehensive library at the end. It will just take a while to to get to. Right. So I'm going to go ahead and pause here. Again, as I do at the end of every podcast, I do offer one-on-one tutoring for many exams. Step 1, 2CK, 2CS, Step 3, preclinical med school exams, 30-inch shelf exams. If you're a medicine resident, the ABI-M board exam, the medicine in training exam, or if you're a college student that needs tutoring for the MCAT, or you need tutoring for like general chemistry, organic chemistry, physics, biochemistry, histology, physiology. I tutor for all those things. And then I do like these booster courses. It's like 15 hours for step 2, CK step 3. It's like 20 hours for step 1. Where again, I review like the most knows. Like right before you take like your USMLE exams. Again, I've done it with a ton of people, super successful with that stuff. And then I do like comprehensive USMLE reviews. I just need a group of five to seven people. So if you have a group, you know, just reach out to me and I'll be happy to kind of give you some more details. And then again, as I've said in prior podcasts, I think that's maybe like episode 204 or something like that. There's this podcast I made recently on USMLE and the military. So the USMLE has started focusing these days on like military servicemen and women and also like geriatric folks. I'll make a geriatric podcast like actually very soon. But that stuff's tested on the exam. So please, before you take step 2CK or step 1 or step 3 i promise you you'll literally be shortchanging yourself if you do not listen to the podcast on like usmle and the military it's one of the more recent podcasts i made it's like some episode above 200 or something like that so um you know just listen to it get your free points and move on from that so um if you need details again on any of these things or let's say you're a med student applying to residency so like an eras application or college student applying to med school so like an amcas application uh so you know you need help with like editing your application editing your personal statements doing mock interviews rec letters again reach out to me um again i've done this with a ton of people more than 90 of the people i worked with have matched at their first choices. And I also have like admissions committee experience. I've been on the admissions committee of a top two med school for a year. So again, I have a lot of experience with this stuff. So, you know, if you need any of those things, either reach out to me through the website or you send me an email at divineinterventionpodcasts with an S at the end at gmail.com. So have a wonderful rest of your day. God bless you. I'll see you next time. Thank you.
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Welcome to the New England Journal of Medicine. I'm Dr. Michael Bierer. This week, June 4, 2015, we feature articles on high-flow oxygen in acute hypoxemic respiratory failure, follow-up of outcomes in type 2 diabetes, the promise and problems of precision medicine, the clinical genome resource, cancer-predictive Panels, and the Challenge of Regulating Genetic Testing, a review article on vasopressin antagonists, a clinical problem-solving article describing a disease in sight and out of mind, and perspective articles on Brazil's family health strategy and on a NICE delivery. Visit NEJM.org to view a video in clinical medicine demonstrating non-invasive positive pressure ventilation. In certain conditions, this technique offers the benefits of invasive ventilation with fewer of the risks that are associated with intubation rate primary outcome was 38% in the high-flow oxygen group, 47% in the standard group, and 50% in the non-invasive ventilation group. The number of ventilator-free days at day 28 was significantly higher in the high-flow oxygen group, 24 days, versus 22 in the standard oxygen group and 19 in the non-invasive ventilation group. The hazard ratio for death at 90 days was 2.01 with standard oxygen versus high-flow oxygen and 2.50 with non-invasive ventilation versus high-flow oxygen. In patients with non-hypercapnic acute hypoxemic respiratory failure, treatment with high-flow oxygen, standard oxygen, or non-invasive ventilation did not result in significantly different intubation rates. There was a significant difference in favor of high-flow oxygen in 90-day mortality. Michael Mathais from the University of California, San Francisco, writes in an editorial that he believes that high-flow oxygen therapy through a nasal cannula should be considered to be an effective and safe therapy for the treatment of spontaneously breathing patients with acute hypoxemic respiratory failure. Although additional trials are needed, high-flow oxygen should be used for the treatment of patients without hypercapnia and with acute severe hypoxemic respiratory failure in the emergency department, the intensive care unit, and hospital settings in which appropriate monitoring is available. Follow-up of glycemic control Outcomes in Type 2 Diabetes by Rodney Hayward from the Veterans Affairs Ann Arbor Healthcare System, Michigan. The Veterans Affairs Diabetes Trial previously showed that intensive glucose lowering, as compared with standard therapy, did not significantly reduce the rate of major cardiovascular events among 1,791 military veterans, median follow-up 5.6 years. The authors now report the extended follow-up of the study participants. The difference in glycated hemoglobin levels between the intensive therapy group and the standard therapy group averaged 1.5 percentage points during the trial and declined to 0.2 to 0.3 percentage points by three years after the trial ended. Over a median follow-up of 9.8 years, the intensive therapy group had a significantly lower risk of the primary outcome of the time to the first major cardiovascular event than did the standard therapy group, hazard ratio 0.83, with an absolute reduction in risk of 8.6 major cardiovascular events per 1,000 person-years, but did not have reduced cardiovascular mortality, hazard ratio 0.88. No reduction in total mortality was evident. After nearly 10 years of follow-up, patients with type 2 diabetes who had been randomly assigned to intensive glucose control for 5.6 years had 8.6 fewer major cardiovascular events per 1,000 person-years than those assigned to standard therapy, but no improvement was seen in the rate of overall survival. Ample evidence is available to implicate vasopressin, a small polypeptide that is synthesized in the hypothalamus and secreted from the posterior pituitary, in the pathogenesis of most hyponatremic disorders. As the most common electrolyte disorder, hyponatremia is consistently associated with increased mortality and morbidity. The treatment of hyponatremia has been plagued by a paucity of controlled studies and by a lack of reliable and safe approaches. Therefore, the regulatory approval of vasopressin antagonists represents a milestone in the field. The advent of the use of vasopressin antagonists has provided physicians with a new means of increasing the plasma sodium level in patients with hyponatremia. These agents appear to offer substantial advantages over previously available therapies that have been shown to have limited efficacy and unacceptable side effect profile, or both. This review summarizes the salient discoveries that culminated in the development of these drugs and focuses on what vasopressin antagonists do and do not do, side effects, emerging safety concerns, and important gaps in data. The authors attempt to reconcile the disparate recommendations for the use of vasopressin antagonists that are available in two guidelines. The review concludes with suggestions as to how and when vasopressin antagonists should be used and for how long. Insight and Out of Mind, a clinical problem-solving article by Nasia Safdar from the William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin. A 21-year-old man presented to the emergency department with fever and rash. His fever started approximately one week before presentation and was associated with chills, myalgia, nausea, and vomiting. He also had a headache without photophobia. On the day of admission, he woke up with a rash on his face, trunk, and extremities. The patient lived in the upper Midwestern United States, but one week before the onset of fever, he was in Southern California for four days, and he made a short trip to Tijuana, Mexico at that time. On examination, a generalized blanching morbilliform rash was present on his face, neck, trunk, and extremities, including the palms and soles. The rash was confluent on the trunk and arms. A petechial rash was also noted on his legs. The patient began to receive ceftriaxone and doxycycline empirically for coverage of bacterial and rickettsial infections, respectively, and was discharged while awaiting further test results. Then, IgM results and a PCR test of a nasopharyngeal swab were positive for measles. Around the time this patient traveled to California, there was an ongoing outbreak of measles in that state. The diagnosis of measles can be challenging for physicians and health care staff who may have never seen a patient with this infection. Although approximately 600 people had been exposed to the patient, no secondary cases of measles occurred. Precision Medicine. Personalized, problematic, and promising. A Sounding Board article by J. Larry Jameson from the University of Pennsylvania Perlman School of Medicine, Philadelphia. The growing recognition of precision medicine by clinicians, health systems, and the pharmaceutical industry, as well as by patients and policymakers, reflects the emergence of a field that is accelerating rapidly and will leave a major imprint on the practice of medicine. Arguably, the principles of precision medicine have been a cornerstone of medical practice since the earliest efforts to classify disease and prescribe a specific treatment on the basis of a diagnosis. What is new, however, is the pace of advances in diagnostic and treatment options. Precision medicine is a classic example of disruptive function. Increasingly, we must use informatics to assist us, not for replacing judgment, but for providing facts. Indeed, primary care providers may have the most challenging role in precision medicine. They stand on the front lines of the clinical care delivery system with a mandate to prevent disease, identify early signs of disease, and navigate referral paths that now have many more branches as a result of precision medicine. ClinGen, the Clinical Genome Resource, a special report by Heidi Rem from Harvard Medical School, Boston. On autopsy, a patient is found to have hypertrophic cardiomyopathy. The patient's family pursues genetic testing that shows a likely pathogenic variant for the condition on the basis of one study. Given the dominant inheritance of the condition and the risk of sudden cardiac death, other family members are tested. Several family members test negative and are told that they are not at risk, and those who test positive are told that they need to be regularly monitored for cardiomyopathy on echocardiography. Five years later, during a routine visit of one of the genotype-positive family members, the cardiologist queries a database for current knowledge on the genetic variant. The variant is now interpreted as likely benign by another laboratory. A newly available testing panel for additional genes that are implicated in hypertrophic cardiomyopathy is initiated on an affected family member, and a different variant is found that is determined to be pathogenic. Family members are retested, and one member who previously tested negative is now found to be positive for this new variant. An immediate clinical workup detects evidence of cardiomyopathy. The assignment of pathogenic status to genetic variants has been stymied by conflicting study results and lack of a publicly accessible database. Launched in April 2013, the publicly accessible ClinVar database, which is now part of the Clinical Genome Resource, serves as the primary site for deposition and retrieval of variant data and annotations.
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Advances in sequencing technology have made multi-gene testing, or panel testing, a practical option when looking for genetic variants that may be associated with a risk of breast cancer. In June 2013, the U.S. Supreme Court invalidated specific claims made by Myriad Genetics with respect to the patenting of the genomic DNA sequence of BRCA1 and BRCA2. Other companies immediately began to offer panel tests for breast cancer genes that included BRCA1 and BRCA2. The subsequent flourishing of gene panel testing services has generated much interest both within the clinical genetics community and in the popular press. These panels cover a total of more than 100 genes, and breast cancer is specifically mentioned as an indication for 21 of these genes. However, the fact that the technology is available does not necessarily mean that such tests are appropriate or desirable. In this article, an international group of cancer geneticists review the level of evidence for the association of gene variants with the risk of breast cancer. Variants that are predicted to truncate BRCA1 and BRCA2, together with a subset of missense variants, confer a high risk of breast cancer. PALB2 and perhaps P10 may also fall into this category, but the evidence is insufficient. It is difficult to draw firm conclusions from the data because of ascertainment bias and the lack of data from large populations. The FDA and Genomic Tests Getting Regulation Right A special report by Barbara Evans from the University of Houston Law Center, Houston. The FDA recently advanced two draft guidelines proposing a regulatory framework for laboratory-developed tests, a category that includes many but not all genomic tests. These recent initiatives kindled debate about the legal authority of the agency to regulate genomic testing, as well as about the potential effects that such regulation may have on discovery and innovation. There is little doubt that the FDA has ample power to impose at least some new regulatory requirements on genomic testing, enough in any event to make laboratory directors squirm. The question is not whether the FDA can regulate genomic testing, but whether the FDA can regulate it well. Does the FDA have the correct set of statutory powers to make genomic technologies safe and effective for consumers, persons undergoing testing, whether as patients, research participants, or direct purchasers, while still fostering innovation? These authors believe the answer is no. To press forward with the powers the FDA now has could subject genomic testing to counterproductive regulatory burdens that may, ironically, diminish consumer safety and chill innovation. Yet a relatively modest set of statutory reforms that builds on concepts the FDA already has developed for drugs and other medical devices could position the agency to play a crucial and constructive role. In an editorial, Elizabeth Phimister, an editor for the journal, writes that a goal of clinical genetics research is to determine the status for all variants in all disease genes in populations of different ancestries. Is the variant benign or pathogenic? If it is the latter, to what extent is it pathogenic? Another goal is to determine whether each pathogenic variant carries a risk in persons with sporadic disease that is equivalent to that in persons with familial disease, and whether the effect on risk varies across populations of different ancestries. Attempts to achieve these goals will require huge, well-annotated data sets. With the rapid accrual of genetic and genomic information, the realization of these goals should be straightforward. But there are substantive obstacles. One of these is missing metadata, such as a lack of information on family history or ancestry in genetic databases. Another obstacle is false information, such as benign variants being labeled as pathogenic in databases. That is why ClinVar is a welcome resource. ClinVar has a system to report where the claim originated and what level of review it underwent, and to distinguish the claims of single laboratories versus those of expert panels. To create an environment in which patients' medical care can be improved through knowledge of genetic status, there is a need for tools that access other types of data, such as medical records, and deep phenotype data, the collection of which depends on establishing and implementing systems for capturing and analyzing those data. Brazil's Family Health Strategy – Delivering Community-Based Primary Care in a Universal Health System, a perspective article by James Masinko from UCLA Fielding School of Public Health, Los Angeles. Brazil has made rapid progress toward universal coverage of its population through its national health system. Since its emergence from dictatorship in 1985, Brazil has invested substantially in expanding access to health care for all citizens. The system is financed primarily through taxes with contributions from federal, state, and municipal budgets. Health care management is decentralized, and municipalities are responsible for most primary care services, as well as some hospitals and other facilities. All publicly financed health services and most common medications are universally accessible and free of charge at the point of service for all citizens. An important innovation in the system has been the development, adaptation, and rapid scaling up of a community-based approach to providing primary health care, which relies on lay community health agents and interdisciplinary care teams to provide universal access to proactive first-contact care and public health interventions. The nucleus of each family health strategy team includes a physician, a nurse, a nurse assistant, and four to six full-time community health agents. Each community health agent is assigned to approximately 150 households, which agents visit at least once per month, irrespective of need or demand, and collect individual and household-level data. A Nice Delivery The Cross-Atlantic Divide Over Treatment Intensity in Childbirth A perspective article by Neil Shah from Beth Israel Deaconess Medical Center, Boston For generations, both British and American mothers have assumed that the safest way to give birth is to spend many hours, if not days, in a hospital bed under the supervision of an obstetrician. Now, new guidelines are challenging these deeply held beliefs. The UK's National Institute for Health and Care Excellence, NICE, has concluded that healthy women with low-risk pregnancies are safer delivering at home or in a midwife-led unit than in a hospital under an obstetrician's supervision. The New York Times editorial board and others wondered, are midwives safer than doctors? The safety argument against physician-led hospital birth is simple and compelling. Obstetricians who are trained to use scalpels and are surrounded by operating rooms are much more likely than midwives to pick up those scalpels and use them. For women giving birth, the many interventions that have become commonplace during childbirth are unpleasant and may lead to complications, including hospital-acquired infections. For babies, the interventions rarely appear to be helpful. Of course, there are caveats. The NICE guidelines apply to low-risk pregnancies only. Pregnancies in women who are obese or have diabetes, for example, are excluded. At its core, this debate is not about the superiority of midwives over doctors or hospitals over homes. It is about treatment intensity and when enough is enough. The images in Clinical Medicine features a 54-year-old woman who presented with five days of fever, cough, and rhinorrhea after returning to the United States from a missionary visit to the Philippines. She reported full vaccination as a child, including the measles vaccine, although records of dosing and strain were not available. Examination revealed an exanthem involving the head, neck, and shoulders with cephalocaudal spread, small white papules on buccal mucosa bilaterally, conjunctivitis with serous discharge, and cervical lymphadenopathy. Laboratory evaluation showed elevated aminotransferase levels, leukopenia, and thrombocytopenia. The patient was placed in an airborne infection isolation room immediately on suspicion of measles. Serologic testing revealed elevated anti-rubiola IgM titers, 4.4 times the upper limit of the normal range, and negative anti-rubiola IgG titers. This case highlights classic clinical features of measles, the need for clinical suspicion in travelers returning from high-risk areas, and the risk of inadequate immunity, even among immunized persons. The patient received supportive care, including vitamin A supplementation, for a diagnosis of measles, from which she had a full recovery. An 82-year-old man in Spain presented with a one-year history of swelling of his left ear with associated difficulty hearing. He had applied topical glucocorticoids for four months without response. On examination, the ear was enlarged, indurated, and erythematous with no associated lymphadenopathy. Biopsy revealed chronic inflammatory infiltration in the dermis with confluent epithelioid granulomas and a lymphocytic background. High magnification showed abundant intracytoplasmic amastigotes in dermal macrophages. Leishmania infantum was identified by means of culture and PCR assay. No visceral enlargement was noted on ultrasonography of the abdomen. The patient was treated with amphotericin B with complete resolution of the lesion after two months and recovery of hearing loss. This concludes the summary of the June 4, 2015 issue of the New England Journal of Medicine. We're interested in your feedback about our audio summaries. Any comments or suggestions may be sent to audio at nejm.org. Thank you for listening.
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Hello and welcome to the Lancet Gastroenterology and Hepatology podcast in conversation with. I'm Hugh Thomas, the Deputy Editor. In this episode, we'll be discussing a series appearing on our December issue, discussing the emergence of non-alcoholic fatty liver disease in sub-Saharan Africa and the challenges it presents. The first paper of the series outlines the epidemiology, risk factors, social determinants of health and current management of NAFLD in sub-Saharan Africa. The second paper of the series describes current issues and challenges in the management of the disease, as well as identifying research priorities. I'm joined today by Professor Wendy Spearman, corresponding author on both papers. Professor Spearman is Head of the Division of Hepatology at the University of Cape Town and Head of the Liver Clinic and Liver Transplant Clinic at Cape Town's Khytoskia Hospital. Professor Spearman, thank you very much for joining us and welcome to the podcast. Good afternoon everyone and thank you Hugh on behalf of my co-authors. We really look forward to actually discussing our two new recent papers on non-alcoholic fatty liver disease. Great, so just to take us right to the very beginning of the story, what do we know about the burden of non-alcoholic fatty liver disease in sub-Saharan Africa? So non-alcoholic fatty liver disease, and I'm going to call this NAFL because it's a bit shorter, really is the leading cause of chronic liver disease globally and is estimated to affect approximately 25% of the world's population. And I think it's important to know what we mean by non-alcoholic fatty liver disease. So this is really defined as the presence of more than 5% of liver steatosis without causative factors such as alcohol, certain drugs, and also the absence of other liver diseases. And we really have the spectrum of histology from simple fat to non-alcoholic steatohepatitis to advanced fibrosis and cirrhosis. And this really, this burden of disease is really considerable. 3% to 5% of individuals with non-alcoholic fatty liver disease who develop non-alcoholic steatohepatitis, who've got one to two percent developing advanced fibrosis. And I think the important thing to realize, if you have NASH with advanced fibrosis, this can rapidly progress to end-stage liver disease and death and the risk of liver cancer. And another thing that's interesting is that liver cancer in non-alcoholic fatty liver disease can actually develop in the absence of cirrhosis. So I think we need to remember that NAFLD not only causes liver disease, but also can actually promote the progression of other diseases, particularly alcohol-related liver disease, and in sub-Saharan Africa, viral hepatitis, hepatitis B and C. And then we have numerous extrahepatic manifestations of NAFLD, such as cardiovascular disease, cerebrovascular, chronic kidney disease. So you can really realize the impact this has in terms of disease and also socioeconomic burden within countries such as sub-Saharan Africa. And although liver-related mortality is increased, cardiovascular disease remains the leading cause of death in these patients with NAFLD and advanced fibrosis. So unfortunately, despite the increasing prevalence associated morbidity and mortality with long-term healthcare costs and consequent economic burdens, NAFLD is really seldom considered as a complication of the metabolic syndrome. So if we look in sub-Saharan Africa, we've got really evolving economies, increasing urbanization, and we have this transition from infectious disease burden of TB, HIV, malaria, to really increasing burden of non-communicable diseases. And it's estimated that the prevalence is about 13.5% in the general population. But the data is really quite scarce, as I'll show you when we discuss the individual regions, but it ranges from about 9% in Nigeria to 20% in Sudan. So if we think about the really increasing burden of communicable diseases in sub-Saharan Africa, particularly this rising prevalence of obesity and type 2 diabetes, this is probably a real underestimation, particularly because there's overlapping challenges of increasing urbanisation and food insecurity. And food insecurity is really quite an interesting concept. The WHO and the United Nations General Assembly have recently identified food insecurity as a global health risk promoting metabolic risk. And if we look at the component of the metabolic syndrome, this is really core to the development of non-communicable diseases and the development of NAFLD. And so NAFLD really represents the liver component of the metabolic syndrome and is part of a multi-system disease. And so if we look at metabolic syndrome in sub-Saharan Africa, it actually ranges between 11% and 23%, depending on how you diagnose it. The prevalence of the metabolic syndrome, which is driving NAFLD, is higher in women than in men. It also tends to be greater in semi-urban and urban areas compared to rural areas. And of note in southern Africa, the prevalence of metabolic syndrome is the highest and that really compares well with the higher rates of obesity here that are seen compared to eastern, western and central sub-Saharan Africa. So if we look really at a meta-analysis which looks at the relationship between food insecurity and metabolic risk factors in sub-Saharan Africa, this really corroborates a high pool prevalence estimate of key metabolic risk factors amongst food insecure participants, with the most prevalent risk factors being high lipids, hypertension, overweight, obesity, and diabetes. And importantly, the increasing number of metabolic diseases are associated with an increased risk of progressive liver disease, Duchenne-Daffy-Dee, and a reduced survival. So I think what I've shown is really that there's really this interaction between non-communicable diseases, this rising obesity and diabetes prevalence, which has an impact with NAFLD. And unfortunately, NAFLD is really not considered as a liver component of this metabolic syndrome. Okay, so now we understand the burden a little bit better. What do we know about the factors thatden of Disease 2017 study, it showed really between 1980 and 2014 that the age-standardized body mass index increased in men from 21 to 23 and women from 21.9 to about 25. And then really concerningly in children, the increasing prevalence of overweight and obesity was really problematic. And this has been driving the adult obesity and adolescent obesity, which really is under-recognized, I think. And then very importantly, if we look at obesity, we look at visceral obesity, so the central obesity, and that's surrogate markets of waist circumference. And this has been shown to be a key risk factor for the complications of metabolic syndrome, so a stronger association of NAFLD than BMI alone, and a greater risk for national fibrosis. Looking at diabetes, once again, between 2017 and 2045, Africa is really projected to have the highest relative increase worldwide in diabetes, increasing from about 16 million in 2017 to as high as 41 million in 2045. So really a significant problem. And we see if we look at the pool prevalence of undiagnosed diabetes amongst adults, it's about 3.8%. And if you look in the different regions in Western Sub-Saharan Africa, 4.7%, Eastern 4.4%, Northern 4.2%, and Southern Sub-Saharan Africa, 1.46%. So we see this variation across the different regions, but overall, this rising prevalence of obesity and diabetes. And then dyslipidemia or elevated cholesterol levels are also a leading contributor in terms of cardiovascular disease. And in fact, the overall pool prevalence was about 25% in the general African population. So once again, another thing, we seem to often underestimate this burden of non-communicable diseases within Africa. Once again, hypertension is a problematic and chronic kidney disease. And we have this bi-directional effect with NAFLD driving these non-communicable diseases and non-communicable diseases driving the prevalence of metabolic syndrome and NAFLD. So really this sort of circle of interactions that we need to actually address to break cycles of burden of disease. Yeah, and one of the aspects that your series really discusses is that the burden is not homogenous either between regions or between areas within countries and specific settings. For instance, you mentioned the urban versus rural divides. Is that accurate? Is that a fair assessment? Yeah, I think that that is. So if we look at southern sub-Saharan Africa, here we're looking at NAFLD having an age standardised prevalence of about 11.4%. So it's increased really from 1990 from 3.7 million per million to 8.1 million in 2017. So this rapid rise in terms of NAFLD numbers, once again, it really corresponds with the prevalence of type 2 diabetes, particularly in South Africa, where the prevalence has increased from about 4.8% in men to 7.7% in women. And so we see this rising prevalence of type 2 diabetes.
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So a real problem of diabetes and obesity. And then in southern sub-Saharan Africa, we have this added problem of HIV infection and its therapies and the metabolic consequences are potentially additive factors. And that will really drive further problems relating to non-alcoholic fatty liver disease. So probably out of all the regions, southern sub-Saharan Africa leads the pack in terms of the burden of disease. But we're seeing this really throughout sub-Saharan Africa. In western sub-Saharan Africa, it's increased from 8.4 million in 1990 to 23 million. River prevalence now at 8%. And what we're seeing here, increasingly obesity and type 2 diabetes. But importantly, we see this rising in the urban areas rather than predominantly in the rural areas. In central sub-Saharan Africa, the age standardized prevalence is about 7.5%. Obesity here is less prevalent, but we have seen a significant increase in countries like Burundi, rising from 2.6% to 5.4%, and in DR Congo, rising from 4.4% to 6.7%. And once again here in central Sub-Saharan Africa, it is the urban-based individuals with this rising metabolic syndrome, which is driving the problem of NAFLD. Typically here in Central Sub-Saharan Africa, they've actually formally looked at the local traditional diets, which tend to be protective, much more vegetarian. And once they move into the urban area, there's increase of calorie-dense diets. Eastern Sub-Saharan Africa, once again, this rise, it's now an age-standard prevalence of 7%, rising from about 7.1 per million in 1990 to 18 per million in 2017. And once again, we see here the rise in diabetes, obesity, but definitely sort of urban-based rather than rural. So I think what we're seeing, certainly southern sub-Saharan Africa, very high prevalence of diabetes, obesity driving the NAFLD, but we see this increasing urbanisation and effects on non-communicable diseases throughout sub-Saharan Africa and something that probably hasn't been addressed adequately. Yeah, and then you certainly, one of the things you touch upon in the series as well is the recognition of the NAFLD burden and of the related comorbidities is pretty poor across sub-Saharan Africa. Is that correct as well? I think absolutely. And I think once again, it comes down to the fact that non-alcoholic fatty liver disease is really not considered a complication of the metabolic syndrome, despite the increasing prevalence of these comorbidities that I've described. And unfortunately, there are really no published national clinical guidelines on NAFLD in sub-Saharan Africa. So we have a number of comprehensive national guidelines, protocols, and treatment algorithms for the management of the non-communicable diseases. Unfortunately, effective implementation of these protocols is lacking. Unfortunately, compounding this is that none of these guidance documents on type 2 diabetes, obesity, dyslipidemia or hypertension include the burden of fatty liver disease or even mention fatty liver disease that should be considered as part of the complications. So I think most primary healthcare doctor will know with type 2 diabetes, you're going to look for the risk of cardiovascular disease, chronic kidney disease, diabetic retinopathy. But really, very few of them will think about looking at that liver, and that's really problematic. And as I've mentioned, this bidirectional effect of the metabolic risk factors both driving NAFLD and NAFLD driving the severity of the non-communicable diseases. And I think that's really important if we think that non-alcoholic fatty liver disease has associated with about an almost 1.5 fold increased risk of incident chronic kidney disease. We know that hypertension is poorly managed in sub-Saharan Africa, so this feeds into one another. And then in terms of diabetes, it's really been clearly shown that NAFLD is associated with two times higher risk of developing diabetes, depending on the severity of NAFLD at higher risk. But importantly, if you get the diabetes under control, the NAFLD improves as well. So we really need to be addressing this at a primary healthcare level. And I think there are a number of ways that we can actually address that. And one of the things is to actually recognise, both from national departments of health and from international aid agencies, the sort of changing healthcare landscape in sub-Saharan Africa with this hybrid of communicable disease now sort of converging with increasing non-communicable diseases. And so one really needs a transition from a system that's focused on infectious diseases to a much more integrated system at all levels of care, but particularly at primary healthcare. So I think this is something that needs to be addressed and there are ways that we can actually approach this. So are there any specific mechanisms that you suggest in your series to improve this recognition? Yes, so there's been this sort of idea of actually changing the name of non-alcoholic fatty liver disease to metabolic dysfunction associated fatty liver disease. And I think that's going to make a major difference in the understanding of both healthcare workers in terms of policymakers and also the general public. And really what we look at with this new proposed definition is that you have evidence of liver steatosis by astrology or imaging or biomarkers or scores. And in addition to that, you have one of the following three. So being overweight or obese, presence of type 2 diabetes, evidence of metabolic dysregulation with at least two metabolic risk factors. And what we're looking at here is a rise in the lipid levels, hypertriglyceremia, glucose intolerance, insulin resistance. So really looking, specifically identifying what are those metabolic risk factors. So I think the difference here, you're basing this diagnosis on positive diagnostic criteria that are really central to the metabolic syndrome, does not exclude alcohol, and you can coexist with other liver diseases. Because we know in reality, liver disease, chronic liver disease, it tends to be multifactorial. It's really not a single agent. And I think it also avoids the sort of stigmatization that is associated with non-alcoholic fatty liver disease. And I think when we'll be able to bring this to healthcare workers, to the general public and raise the awareness. And I think particularly, I mean, COVID-19 has raised the sort of general awareness and sort of knowledge of healthcare workers around the risk of metabolic risk factors in terms of outcomes for COVID-19 and non-alcoholic fatty liver disease and obesity. So I think we're in a setting where we can really sort of leverage on this increased awareness of what the problems are relating to obesity, diabetes, and hypercholesterolemia. I think, you know, we need to educate the healthcare workers, general public around multi-system impact of metabolic risk factors. And we really need to task shift away from the, looking away from GIT and hepatologists actually being concentrating their management of NAFLD to primary healthcare level. And I think what one then needs to be able to do is to recognize which of those individuals are at risk of having advanced disease, cirrhosis and complications, and then having a very clear referral pathway from primary healthcare to secondary to tertiary level. And they're really quite simple point of care tests that you can look at, which are very well known, the APRI score, the FIB score, the NAPLD activity score. And these are all available on your cell phone. You just plug in the numbers and they can have very clear, simple guidelines to decide who actually needs to move up the level of care. And I think importantly, what we've shown is that if you have these higher scores, it's quite important to combine this with imaging and ultrasound, but important something that will give you more impact in terms of fibrosis scoring. And here we look at the FibroScan. The FibroScan will be able to give you an actual figure for the fibrosis. Some of it can actually even measure the amount of fat. And I think what's important is that actually can be done by nurses. Community healthcare workers can be trained. It's really quite a simple technique and will enable you to identify those who are more likely to have advanced fibrosis complications and then one can refer them upwards. So I think there are lots of simple things that we can do, but it does depend on this being recognised by departments of health, by policy makers, and also providing funding at primary healthcare level to expand beyond infectious diseases. Great. I think also one key message that comes out of your series is that you, I mean, you mentioned that the management of non-alcoholic liver disease should be centred on prevention. I was just wondering if you could expand a little bit on the kind of the policies and strategies that that could involve. Yes, I think that's extremely important. So we all know they're quite sort of sophisticated medications that are becoming available to manage non-alcoholic fatty liver disease. But in reality, in sub-Saharan Africa, that's going to be outside the price range of what we are going to be able to afford.
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So what we really want to do is prevent the development. So I think we need to look at lifestyle changes. We need to look at diet. We need to look at weight loss. And I think what has been shown, despite all the other medications, that sustained weight loss has the best benefits in terms of improving the stages of NAFLD in terms of degree of fat, degree of inflammation and fibrosis. And really, when it's not looking at massive weight loss, it's really just losing 5% to 7% of your weight over a period of time. What you don't want is very rapid weight loss, as this can actually aggravate steatosis and steatohepatitis. But I think we need to actually look at that. And in terms of exercise as well, one needs to actually be sure that one's actually having a regular exercise program with both aerobic and resistance training. And so what we know is that many of our patients being overweight have difficulty doing aerobic exercises. And what one then can actually look at as looking resistance training, and that can be quite easily done at home. And once again, I think we need to sort of look at what we've been doing during COVID-19, during those lockdowns, doing home exercises. We've gotten to that kind of pattern of behavior and we need to leverage on that. I think importantly, one needs to look at control of diabetes. We need to look at control of dyslipidemia. And there's often a concern about the use of statins and potentially being hepatotoxic, but really there's no contraindication to starting statin if it's needed for control of dyslipidemia. So I think we need to go back to the basics, making sure that when actually in terms of diabetes, do we have the ability to actually monitor, do home monitoring of glucose? One tends to forget that this can often be quite expensive. You need access to the strips, you need access to the machines, and they need to be calibrated regularly. So I think we need to get back to basics just to look after in terms of diabetes, hypertension, dyslipidemia, and then bring in this sort of liver health approach where you're looking at liver as a whole, looking at your non-communicable diseases, particularly in sub-Saharan Africa, viral hepatitis. So really have these programs, sort of know your status like we do with HIV. So know your HIV, hepatitis B and C status. So we have a holistic approach to the problems that are developing within sub-Saharan Africa. So just looking ahead to the next few years then, what are going to be the key issues and problems that are facing countries in sub-Saharan Africa with respect to NAFLD? I think if we look at sort of the key challenges, I think what will be the key challenges really will relate to us being able to actually recognise the real burden of disease, both in terms of communicable and non-communicable diseases. We need to recognise that, unfortunately, there's this rising prevalence of obesity and type 2 diabetes. And I think one needs to also recognise that Africans tend to be 10 times younger when they present with these non-communicable diseases. So they're going to have a significant impact in terms of socioeconomic factors in sub-Saharan Africa. And I think if we increase the infrastructure at the primary healthcare level, this must be combined with adequate resources to actually deal with this. You can't just add this added work to nurses, to primary care, healthcare physicians. So one really needs to actually look at how we're going to improve the infrastructure, support this from national departments of health. And I think importantly, if we look at sub-Saharan Africa, much of the infectious diseases treatment is dependent on international aid. And we need to look and see how we can actually harness that to be more holistically in terms of primary health care. And then I think if we look at COVID-19, I think we need to leverage what we've learned. Look at the role of telehealth, telementoring, develop these programs, particularly the Project ECHO programs, which have been run very effectively dealing with all of these diseases, but plus the non-communicable diseases, and really apply this in our setting here in sub-Saharan Africa, where we have very limited access to human resources. And this problem of actually very sort of this brain drain where very competent individuals actually leave the country. And we need to really be positive. We have a lot to offer. We can actually harness what we have, but we need to use this effectively. And then I think one needs to remember that everything ultimately comes down to education, education of the public, education of healthcare workers, and education of our policymakers to realise that this is something that we need to address very actively. Professor Spearman, thank you very much for that comprehensive dive into your two series papers and really for providing us a much needed overview of the NAFLD situation in sub-Saharan Africa. Thank you. Thank you. You can read the series on NAFLD in sub-Saharan Africa online now at thelancet.com. Thank you to Professor Spearman and thank you for listening to this episode of the Lancet Gastroenterology and Hepatology podcast, In Conversation With. Remember, you can subscribe to In Conversation With wherever you usually get your podcasts.
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Hello and welcome to a special episode of The Lancet Voice for Black History Month here in the UK. I'm Jessamy Baganal. And I'm Gavin Cleaver. We've got a packed show today and we're also joined on hosting and discussion duties by two of the founding members of The Lancet's Group for Racial Equality, Senior Executive Editor at The Lancet, Dr Pamela Das, and Senior Editor at The Lancet Global Health, Mandy Baudgler. First, for this Black History Month podcast, Jessamy and I spoke with Dr Kevin Fenton, who's the Director of PHE London and an important figure in the capital's COVID response. Okay, Kevin Fenton, thank you so much for joining us today on this Black History Month podcast. There's a profile of you in this week's issue of The Lancet as well, but we thought it would be great to kind of flash that out by having a bit of a chat with you. And so thank you so much for joining us. Great, thank you. It really is a pleasure to be here with you and such an honour to be featured in this edition for Black History Month, which is such an important time of reflection, of also thinking to the future as well. So this is an excellent opportunity to continue the conversation. Kevin, you've had such an amazing and varied career. And I was reading your profile before this interview. You did your PhD on the variation of STIs across racial and ethnic groups, which I believe was sort of stimulated by your experience of HIV and AIDS. I just wondered whether you might tell us about that time in your life. And then, you know, after that, there's sort of, there's been a lot of parallels drawn between HIV and COVID-19. And I wondered what your reflections were on it. Yeah. So, you know, when I arrived in the UK, when I came back to the UK in the early 1990s and completed my master's degree in public health. I wanted to continue my post-grad training in public health, but I had a love for academia and academic research. And one of the first opportunities I had was to work with Professor Dame Anne Johnson at the University College London at UCL. And with Dame Anne, I was able to do my PhD, which, as you say, looked at the University College London at UCL. And with Dayman, I was able to do my PhD, which, as you say, looked at the realities and contexts and drivers of variations in rates of HIV and STIs across racial and ethnic groups in the UK. And this was important at that time for a number of reasons. It was a time before the availability of highly effective antiretroviral therapies. It was a time when we were seeing increases in HIV rates among especially black Africans, many of whom had migrated here from sub-Saharan Africa and who were either diagnosed with HIV or acquired their infection here in the United Kingdom. And it was also a time when we were grappling with high rates of bacterial STIs among some minority groups, which had been described for decades previously. So I was really keen to take my initial training and to ask, well, why are we seeing these differences? And why, for some communities, these disproportionate rates were being described year on year, and yet our prevention and treatment efforts were not getting ahead of the epidemic curves. And what were the implications for emerging communities, such as Britain's Black African communities, when it came to understanding the impact on these diseases and the role that their social, cultural, behavioral context would play on the epidemiology. So it was a really interesting piece of work that really looked at both the epidemiological data, we looked at qualitative research as well to try and understand the context. So I think from that experience, it provided my first entry into research on health inequalities, on policy for tackling inequalities. And it also provided me with tools, which I subsequently used in my work in the US when I became the chief of the syphilis elimination effort to help to bring that lens of health equity to our work on programming. And then in my subsequent work globally, working on HIV, and even when I returned to the UK to focus on non-communicable diseases as PHE's National Director for Health and Wellbeing. So that early academic work, I think, set the foundation not only for my academic training and expertise in addressing and understanding inequalities, but it also fundamentally shaped the passion that I bring to my public health practice in looking at things through a lens of equity. Yeah, that's brilliant. And I mean, what a crucial sort of foundation really for what we're experiencing now. And I just wondered whether you had any insight, you know, about those parallels between HIV and COVID-19. Absolutely. You know, as an infectious disease epidemiologist and as a public health specialist and as a public health leader, somebody who's done more than two decades of working in HIV, you can't but help to drive the parallels between the two infectious diseases. On the one hand, we're bringing all of the tools and learning that we have about how do you manage an infectious disease and how do you drive rates of infection down in the absence of an effective vaccine or effective cure, and the role that behavioral, sociological, political, structural factors play in helping you to control an epidemic, in addition to mobilization of the communities. And in many senses, it reminds me of the very early days of the HIV pandemic, when all we had were the tools of community engagement, education, promoting behavioral change, but also in the early days of HIV, addressing stigma, discrimination, fear, which are a key part of how people and communities are responding to COVID today. Similarly, as we think about the tools which are required for effective control of the COVID epidemic, I hearken back to our learning from HIV, where we learnt about the importance of using a combination prevention approach, recognising that no single measure is going to be enough to control HIV and the spread in a community. But you need to think about ways in which you are educating and building awareness, the ways in which you promote basic prevention measures, and then how you layer onto that the sort of biomedical approaches for HIV, which are helpful in reducing transmission. So a clear part of the learning for COVID is ensuring that we're maximizing the use of every tool. A third key lesson is really understanding that infectious diseases are not randomly distributed in the population, but they do both cause inequalities and they can exacerbate inequalities. And we saw this with HIV and we've seen it with STIs, and we certainly have seen it with COVID as well. And these inequalities are not just by race, ethnicity, but they are seen by gender, by geographic area of residence, by socioeconomic deprivation, and by the prevalence of risk factors, including poorly controlled non-communicable diseases such as diabetes, heart disease, et cetera. So we know those factors drive inequalities. And therefore, I think the lesson from HIV is being not only mindful about the likelihood of COVID also driving inequalities, but with the knowledge that we have to be armed and forewarned and forearmed in terms of getting ahead of the curve, which involves engaging communities, delivering culturally competent interventions, ensuring that you're focusing on issues such as stigma and trust because that will determine how communities engage with messages and how communities who are at risk will be willing to take up some of the prevention messages which are necessary. So a lot of learning from HIV that we bring into COVID, and we're seeing this across the world as HIV leaders are sort of comparing and contrasting and thinking about how we bring the learning from one pandemic to another, but also keeping our eye on the prize for both, because there's now emerging evidence that as a result of COVID, that in many areas across the world, we're seeing a resurgence in HIV as treatment services, as preventive services for HIV take a hit. And so therefore, we need to manage both and learn from each other. Yeah. I mean, you talked a lot about inequalities there. And I just wonder, you were saying that you went on to take this sort of chief role in CDC as chief of the National Syphilis Elimination Effort. And you sort of did a lot of work about inequalities there. And we're running up to the sort of the election. I just wondered whether you could tell us about that work and also what's happened to inequalities over the last 15 years in the US? So I arrived in the United States for my CDC career at a really interesting time. It was the last four years of the Bush presidency and the first four years of the Obama presidency. So I had the privilege of serving under two different administrations who had, I think, very different approaches to both understanding and responding to the epidemic and I think my role both as the chief of the syphilis elimination effort and then when I was promoted to become the national director for HIV, viral hepatitis, STD and TB prevention at the CDC meant ensuring that we were working together to deliver the evidence to inform policy actions and then to identify areas where we could make the greatest difference on arresting these epidemics in the country.
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We also used a number of approaches given the inequalities to not only ensure we were delivering high quality prevention programs, but to really began to deliver targeted interventions with communities in order to address these inequalities. So with the syphilis elimination effort, working together with black community leaders, working together with LGBTQI leaders because of the high rates that we saw, especially among gay and bisexual men, in driving the resurgence of syphilis at that time. For our work on HIV, novel work in our Act Against AIDS initiative, which was the first targeted initiative for African Americans addressing HIV, which really drove to the heart of the factors which were driving the epidemic and the need for a broader coalition of communities to come together to work with us to control the epidemic. And again, that thinking was also used in our work with tackling viral hepatitis. And we were able to develop the first national strategy to eliminate viral hepatitis in the United States. And that really led to our work with Asian Pacific Islander communities, as well as older populations because of the concentration of the epidemic. So we use a number of their approaches, which were built upon principles of equity, but integrated that with what CDC does really well, which is evidence-based policymaking, delivering high-quality prevention programs, and evaluating their impact, and combining that new approach to help to tackle some of the inequalities that we've seen. So what has happened subsequently? Well, you know that you've seen so much happening in the U.S., both politically and socially, in terms of the context within which these epidemics are occurring. And I think the US is certainly at a really interesting time now, where as choices are made at the election, which will determine the path for not only the response to COVID, but I'm sure for the other infectious diseases as well. To bring us a bit more up to date, I suppose, you've been working at PHE London, and this year you led the review, PHE's review, of the impact of COVID-19 on BAME groups. Tell us a little bit about the experience of leading that review and how serious, of course, the impact has been. So, you know, it was a real privilege to have been asked to lead that review. It was an important time in the epidemic because we're still in the middle of the first wave when we were asked to look at the disproportionality in risks and outcomes of Covid. I had only started in the job on the 1st of April so I was asked to lead this work nearly two to three weeks into my new role as a regional director for London. And it was a time when I think there was a lot of concern and fear and anxiety within the community because visually on television you were seeing reports of people who were negatively impacted by the disease and of people who were dying from the disease and the images for example of healthcare workers at the time really visually could see that disproportional representation of BME individuals as those stories were being told and shared so there was something about the the zeitgeist, the national mood at the time of deep concern about the impact of this first wave, the fear and anxiety as we were in the midst of a lockdown at that time, because it was still in April, May, when we were doing the work, about how were we going to protect these communities and what lessons should should be learning to take this work forward. So that provides a bit of the context in which the work was done. We brought together a fantastic team of PhD scientists who did both phenomenal work on looking at the epidemiological data that we had available to us at the time to begin to provide a sort of objective national picture on what our surveillance data could tell us about the likelihood of being diagnosed with COVID, the likelihood of progressing to severe disease and of dying with the disease at that time. And then we also worked with our scientists to combine the epidemiological work with a deeper insight through an extensive stakeholder engagement exercise. So over a six-week period we were able to engage more than 4,000 individuals, colleagues working nationally, regionally, locally in government, those working in royal colleges, people working in the faith communities, local government, people and colleagues in the devolved nations, community organizations from all over the country. And the idea here was both to inform people of the work that we were doing in PHE, but to provide a safe space for people to reflect on their experience on the epidemic, to share what they were learning from their own communities and sectors, and to begin to think about what would a change in our response look like to protect communities moving forward. So the work resulted in two reports which were published. And clearly, there was a lot of interest in both the findings of the epidemiological as well as the stakeholder engagement report. And there were seven recommendations which arose from this work. And those recommendations were really focused to guide the system and system actors to focus on some of the most impactful things that could be done as we emerged from the first wave of the pandemic and as we prepared for potentially subsequent waves in the future. So there were focused recommendations which were able to guide where we needed to intervene in order to limit the impact on BME communities. And many of the recommendations were absolutely clear. We needed better data to understand the impacts of the epidemic and how our prevention programs were being delivered. We needed more culturally competent messaging using channels and messengers that resonate to community organisations. We needed organisations to really take a look at how they were delivering their programmes and ensuring that they were accountable and the quality of their programmes to address inequalities were robust. And of course we needed better data on testing and contact tracing so we could really understand how these interventions were being applied to especially minority communities to ensure that we were able to track the interventions. And then finally, we also really wanted to say that as we emerged from wave one and we started the process of recovery, that we looked at recovery through an equity lens because the impacts of lockdown and the first wave of the pandemic were unequal and for many communities they would have fallen further behind so as we are looking at recovery and as we're preparing for a second wave to be deliberate in thinking of equity in our approaches so those recommendations were as true yesterday as they are today. And in fact, they really have guided a lot of the work we've done in PHE. You know, system partners, including the NHS, have certainly moved forward in thinking about what the NHS does in terms of protecting its staff and their local communities. And PHE has been working with local authorities, and local authorities across the country have been doing phenomenal work in both implementing these recommendations but also looking at their programming on addressing inequalities. So our hope is that as we are now in the second wave and as we prepare for any further escalation of the epidemic, now that we know better, we are doing better. And part of that doing better is that we're engaging with our communities, really looking at our data, ensuring that we're protecting the most vulnerable and ensuring that we're maintaining that sort of rigor in responding in ways more effectively and earlier to prevent that disproportionality again this time around. Yeah, so perhaps we go into that in a little bit more detail. How important is this current moment and the kind of, I suppose, post-pandemic rebuilding effort to kind of ensure an equitable United Kingdom in the future? Well, we're now grappling with the re-emergence of infection and ensuring that we mitigate harms in this second wave and what is absolutely clear is that the epidemic is evolving differently in different parts of the country so we see the real escalation of the epidemic which has been described in the northwest and the northeast of the country London has perhaps an immediate intermediate pattern where we're not seeing the sort of exponential rise at this time in part because we were so severely affected in wave one of the epidemic but we are being very vigilant in the city and are working with political leaders to ensure that we are proactive in both protecting Londoners but also engaging with businesses and other leaders across the city to ensure that we protect the economy as much as we can. So we're seeing different patterns of the re-emergence of the disease across the country. And I think that sort of leads us into three key areas. The first is the importance of a more local response that is going to be required, one that fully engages our local partners and local authorities, players working at the regional level to understand what works best for those regions when it comes to controlling the epidemic, building upon the assets that they have and ensuring that they're aligned closely with national efforts. Second, I think it really then speaks to if you have a disproportionate impacts geographically, how do you mitigate those impacts economically and socially? So all of these interventions represent a trade-off between your desire to control the infectious disease, the spread of the infectious disease, but also the limitations that it places on society, your ability to mix socially the kinds of businesses which are viable under these restrictions, the impacts that it's likely to have on individuals, whether on your physical or mental health and well-being, and of course the sustainability of the NHS. So that balance is one that we have to tread very carefully at any given time and it's never easy.
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And I think moving forward as we move beyond the second wave we'll be having to think through at a regional level what it means for restarting economies, re-engaging and supporting communities and rebuilding and building that better as we emerge from that as well. And then finally I think as we are in the second wave we are armed with better knowledge, better capabilities and better awareness in terms of how to manage the infection and its impact. So we now have better treatments. We understand now how to manage people with severe disease. We are likely to have a vaccine available in short order. And we begin thinking about the implementation of the vaccine and how we protect those in greatest need, but also think about the population scale-up of that approach. So as we are moving through the second wave, the contexts are going to be very, very different to where we were in wave one. And I think this means we need to take the public along with us. We need to work seamlessly and effectively from national, regional to local. We need to thirdly support local knowledge and understanding of communities because that link with local communities, that trust with local communities is going to be extremely important as we move through the second wave. And as we emerge from this, to ensure that as we are rebuilding that that sense of community of place-based approaches to building resilience and recovery are core part of the work that needs to be done so I think there are many implications from this work as we are emerging in the second wave that I think will fundamentally shift our approach to both public health in this country but hopefully the ways in which we engage and work from national to local. Yeah, so you mentioned public trust there, and it does seem that in some countries, it's been kind of a struggle, as you mentioned, to take the public with you in some cases. So what are your thoughts on the kind of maintaining public trust in public health going forward? So I think, you know, this pandemic is a once in a lifetime event, hopefully. You know, we're learning so much now, both in terms of our response to emergencies and planning for emergencies, response to pandemics. We're learning more about information and how information flows, especially in this digital age. We're learning about the importance of trust and the compact that we have as public servants between how we serve the public, how we engage the public. We're learning more about how we communicate and communicate effectively, both with each other as well as as public servants with the people and the communities we serve. And trust is certainly, and trust in government is certainly going to be a key part of how we move forward in all of this. Clear lessons from the first wave and certainly in the second wave is the importance of clear and consistent communication so that people understand both where we are in the epidemic, why we're being asked to do the things that we're doing, and where possible for evidence on the effectiveness of the sacrifices that people are making, that they can begin to see that being played out. We also are learning about the importance of transparency in all of this, transparency in decision making, transparency and equity in how decisions are made and applied, whether at the national or sub-regional level, and there are many lessons there for all of us. And then finally, we're hearing about the importance and learning about the importance of capturing the voices of a diverse range of players and partners to truly understand the impacts and the solutions to this epidemic. That a recognition that local partners must be working in partnership with regional and national partners, that local communities have an equally important voice in helping us to understand how messages and how interventions are landed and are going to be successful, especially with the most vulnerable. So it's not that we didn't know these lessons before. I mean, you know, we've been, these are core tenets of public health practice. I think the pandemic has certainly brought it to a fore. There are lessons that we will continue to learn. And I can see evidence of us improving almost on a daily basis as these lessons are learned and shared and practices reviewed and policies developed. And it will require us to continue to be agile and to continue to be honest that there are times when we will get things right. And there are times when things won't go as we had planned. But we are all working towards the same vision and we're all working and have the same hopes. And I think that is part of the honesty that we will need to be successful as we emerge through this second wave and beyond. So it was wonderful to speak with Kevin. What an inspiring figure. And I'm joined by Dr. Pamela Das, Senior Executive Editor at The Lancet. And Pam has written the profile of Kevin that's in this week's issue of The Lancet. So, Jessamy, Pam, Kevin does have a lot to say. And he's been so important to London during this pandemic. But also, he does seem to have just a clear vision, you know, a really just one of those people that has a very strong academic understanding of the research and kind of the relationships between different aspects of public health, which gives him, you know, a vision for what is happening and what needs to happen, which I think is, well, rare based on all of the events, you know. Yeah, I absolutely agree. He is really exceptional. He seems to be an expert in every area from community engagement to, you know, knowing the latest research and how that's going to change practice. I mean, he must have such a sharp mind and be also very politically astute. I mean, one thing I wasn't able to really get into with him, but maybe he was very careful. You know, he's obviously had to work in some very difficult areas over the years, e-cigarettes being one. But I think, you know, that also shows what kind of character he is to balance that, you know, that political with the science and be quite astute in what he does. Yeah, a remarkable, very, very remarkable. One of the truly great black figures in medicine in the UK over the last century was Dr Harold Moody, a figure whose life is underrepresented in the history books. I spoke with historian Stephen Bourne to find out more about Dr Moody, his life and his legacy. Stephen Bourne, thank you so much for joining us today here on The Lancet Voice. You've written a book about Dr. Harold Moody. So perhaps we're doing this for Black History Month, talking about the history of black people in the UK, especially in the medical field, of course. Tell us a little bit about what makes Dr. Moody such an important figure. I would put Dr. Harold Moody up there in the top 10, the top five. He's probably one of the most ignored and overlooked historical figures, black or white, in this country. And he was, in fact, described many years ago by the black historian Edward Scobie, who wrote a very early book about black people in Britain called Black Britannia in 1972. I mean, I've had a copy for many years, but he was the one that actually described Dr. Harold Moody as Britain's Dr. Martin Luther King. And that is something that I would agree with. And yet it's Dr. Martin Luther King who is embedded and has been embedded in our school curriculum for many, many years. Dr. Howard Moody doesn't even get a mention. So I've worked hard at local level, community level, because I live in the same sort of, grew up in Peckham where Dr. Harold Moody was based. And I'm also, you know, part of that local community. I've tried very hard to raise his profile, but we can come back to that later on if you like. But yeah, in my estimation, he is very, very important. So maybe you could give us like a quick potted history, I guess, of Dr. Harold Moody's work in the UK and what makes him so important. Yes, he was born in Jamaica, Kingston, Jamaica, in 1882. He was one of six children. His mother wanted all of her children to have an education and to go far, which they all did. Harold travelled to England in 1904 in the Edwardian period to study medicine, to train as a doctor at King's College, which was then in Lincoln's Field before it moved to South London. And he qualified, but had difficulty because of the racism of the times, had difficulty in finding a place in a hospital. So he set up his own practice in Queens Road, Peckham. Actually, it was Kings Road first, and then across the road, he moved his family, once he'd married and had a family of his own, across the road to Queens Road, Peckham, which is where he had his surgery from 1913 onwards. He was a very popular GP, greatly loved and respected in the local community of Peckham and the Olkent Road. The working class patients that came to him loved him.
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He was very good with children, particularly, and he wouldn't charge poor families for his help, particularly if it involved children. And this, of course, was all before, long before the NHS in 1948. During the First World War, black soldiers who joined to fight with the British got to hear about him. Not all of them, but some got to hear about him. And if they had problems on the front line or in the army, they would contact him. And that was really the kind of beginnings of his work as a campaigner, as an activist, which much later in 1931 led to him being the founder of the League of Coloured Peoples, which was based at his home in Queens, I mean, his home in Queens was also his surgery, but it also became the base of the League of Coloured Peoples, which was one of the first black-led organisations set up in this country. By no means the first, but one of the first to really have an impact and to have an influence. And he was the president until he died after the war. And so by the time of the Second World War, when the Second World War broke out in 1939, he was established. He was known to the government, to the Ministry of Defence, to the Colonial Office particularly. He would write letters to the Times newspaper. So he would go out of his way, in addition to being a full-time GP, to help any black person in need. People would go to him for help, advice, support, whether they had issues with housing or employment. And his influence was great enough so that in the Second World War, when his son, Joe Moody, who'd been educated in a public school, was officer material for the army, when Joe applied to join the army as an officer, to train as an officer, they turned him down, saying that the actual wording was, we cannot have officers of non-European descent. In other words, black men were discriminated against. So, of course, Dr. Moody waded in, fought that particular colour bar, as it was known then, and won his argument. And his son was admitted into the army in 1940. But unfortunately, the army, the military and the government said to Dr. Moody, we will lift this ban on black men in the army for the duration of the war. But Moody fought tooth and nail for that ban to be lifted forever. And I think by the end of the war, it had been because I don't think they ever reinstated it. So he was very influential in many, many ways. So you've written a book as well about Black Britain in wartime that I think features Dr. Harold Moody. So tell us a little bit about that and some of the takeaways, I guess, from researching that book. Well, I've written a book which was recently published called Under Fire, Black Britain in Wartime 1939-45. And that is a chronology of the Second World War, but from a kind of Black British perspective. So I start in 1939, the outbreak of war, the colour bars, it was the London Blitz. And I mean, Howard Moody, Dr. Howard Moody is a presence throughout the book. So there's a chapter about him at the beginning of the book because of his leadership of the black community at that time. And then I come back to him throughout the war, so to speak, and then end with a lengthy quote from a broadcast, the script of a broadcast that he did for the BBC radio in 1945 for VE Day, talking about the contribution that men and women of colour from across what was then the British Empire and looking forward to the future. He made this broadcast in a BBC Empire Service series called Calling the West Indies. So this would have been heard not in Britain, but across the Caribbean. And he'd made earlier broadcasts in this programme as well. So he was reaching out to his brothers and sisters, if you like, in Jamaica, where he had come from, and Barbados and Trinidad, across the Caribbean by making broadcasts to them. So he was known at the BBC. And in fact, in 1940, when a BBC broadcaster, this is radio, used the N-word, Harold Moody wrote to the Director General and was given a full apology, which is kind of interesting when you think how the BBC fudged it this year when somebody used the N-word on a BBC television programme. The BBC kind of stalled. But in 1940, they did apologise to Dr Moody, who then published this in the League of Coloured People's newsletter, which was published throughout the war. You mentioned the League of Coloured People's. What's the importance of them? What are some of their successes? They're very important because they were an action group that was made up of a lot of kind of distinguished, if you like, or eminent black people in Britain, including Dr. Cecil Belfield-Clark, who was from Barbados and had, like Dr. Moody, a surgery in Newington near the Elephant Castle. And he worked there, had that surgery for 45 years. Can you imagine? 1920 to 1965 when he retired. He kept that surgery open all through the Blitz. That story's in the book Under Fire as well. Incredible. And there were others, George Arthur Roberts, who was a Trinidadian who volunteered for the British Army in World War I, but settled in Camberwell after the First World War and became active in the League from its inception in 1931. And then during the Second World War, George Arthur Roberts joined, because he was too old for active service, he joined the London Fire Brigade and served as a fire officer all through the war. And Stella Thomas from West Africa, who became one of the first black women magistrates in West Africa. So there were intellectuals, there were people from the arts like Robert Adams, an actor from Guyana, who were the founder members. And most of them kind of stayed with it throughout the 1930s. But they were very influential. They were like an influential pressure group, if you like. How important do you think kind of an understanding of Dr. Moody's legacy is to the current moment, given we've had such a major year for this understanding of race relations? I cannot endorse him enough as an important British historical figure. He really is very important and we do need to understand his life and his legacy much better than we do. It shocks me that in spite of my own efforts to raise his profile, he's still not taught in schools. It needs to change. Hopefully it will change with the Black Lives Matter campaign. He is included, thankfully, in Patrick Vernon and Angelina Osborne's new book, 100 Great Black Britons as one of the top 100 along with Mary Seacole and many many others well 98 others to be exact so that's good that places him correctly where he should be but we cannot underestimate his legacy He was like Dr. Martin Luther King in America, considered by some more radical black people in Britain in the 1930s as a bit of an Uncle Tom, someone who was too friendly with the English. But that was his way of doing it. He was a devout Christian. He would go to the Camberwell Green Congregational Church in Wren Road, opposite Camberwell Green Park, and preach every Sunday. So he had a kind of Christian ideology, a Christian outlook. There was a faith that meant a lot to him. But maybe because he died too soon, that legacy got forgotten very quickly. He went on a tour of the Caribbean and America in the winter of 46, 47. This is a man who is over 60. But his plan was to raise funds for a colonial centre for African and Caribbean people in London. And he couldn't get very much. I mean, very few would support him. He burned himself out so that by the time he returned home in the spring of 1947, he was a dying man. He had influenza. It killed him in April 1947. But his funeral in May 1947 at the Camberwell Green Congregational Church, thousands attended, apparently, according to the newspaper reports. He was, as I say, say greatly loved but so quickly forgotten and so I the more I found out about him and realized there was very little in the public domain about him the more I wanted to do something so one of the things I did for example apart from putting him in my book under fire about 13 years ago I was friends with his niece, Cynthia Moody. Cynthia was lovely, and Cynthia was the custodian of Harold's brother's artwork, Ronald Moody. Ronald Moody was Harold's younger brother, who was a sculptor. Cut a long story short, Cynthia contacted me and said that Ronald's bronze portrait of Harold Moody had come up for auction in New Zealand. What do you think?
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And actually, I don't think they paid a huge amount for it. It was doable, thank goodness. And so the bronze portrait came back where it should have been because it kind of mysteriously vanished in the 1960s and then suddenly turns up in New Zealand, but we won't go into that. And I said to Southern Council, now that we have this bronze portrait of Harold back, please don't put it in a cupboard in a back street somewhere in one of your offices. Let's have it on full display in Peckham Library, which is very close to where Queen's Road is and where he lived and worked. And so that is now, thanks to myself and Cynthia Moody, now displayed. And what Cynthia did, she pointed out to the National Portrait Gallery who also have a bronze portrait of Howard Moody by Ronald Moody, his brother, but the National Portrait Gallery were of the understanding that they had the first copy and Cynthia said no, Southwark Peckham Library in Southwark have the first copy, you the second copy there is a difference between first and I don't understand art but apparently we have the more important copy and Cynthia Point because she knows she's the custodian of Ronald's artwork and she knew this so the National Portrait Gallery were a bit miffed I think well it's been a pleasure to chat about Dr. Moody's life with you, Stephen. And hopefully, you know, hopefully people listen to this podcast will, will, will take an interest in Dr. Moody's life. So it can become kind of more widely known because yes, when I was looking into it, I was amazed how few resources there were to learn about Dr. Moody relative to the importance of his life. I would highly recommend Under Fire, my book. Not because it's my book. Well, yes, because it's my book. I'm a shameless book plugger. I never used to be. When I started writing books 30 years ago, I didn't realise that I would have to be very bold and start waving them in the air and plugging them. So yes, I would start with Undefined because it gives you a good snapshot of his life in the Second World War. And then there will be references in the book to other sources, not just mine, but hopefully there will be more about him in the future. Let's keep our fingers crossed, not just by me, but by other people. And let's hope that he is taught in schools alongside Dr. Martin Luther King, because I think they make a very interesting comparison. Absolutely. Well, Stephen Bourne, thank you so much for speaking with me today. Thank you. So I really enjoyed speaking with Stephen. He's quite a character and it's wonderful to have this kind of repository of knowledge about the life of Dr Moody. You know, what really struck me in the podcast was the similarities between Harold Moody and Fenton as people and their backgrounds. So similar, both humble Christian backgrounds, clearly both high academic achievers, kind, compassionate, respectful, very well liked wherever they go. And a sort of way of working for the communities they chose to serve by working with them. I just find that really inspiring. You know, it's so great to highlight the achievements of these individuals to health and society more broadly. I mean, that's the great thing about Black History Month. It really is a celebration of their contribution. You know, to me, they were all heroes or were, sorry, Kevin still is, heroes of their time. I think, you know, Harold and Mary during the war and during those very difficult times in the last century. And then Kevin being faced with his second pandemic, not just one, but two, and being really on the front lines of that. I mean, it just shows, you know, their courage and an innovative leadership, I think, despite those challenges of discrimination and prejudice that they were all clearly up against. Finally, then, I spoke with Trevor Stirling, who is the chair of the Mary Seacole Trust, about the work that the Mary Seacole Trust does and about how they carry on Mary Seacole's legacy. Trevor, thank you so much for joining me today. An absolute pleasure. Thank you for the invitation. No problem at all. So perhaps we could kick off by you just telling us a little bit about the kind of the work of the Trust, like what are some of your aims and goals and what do you do? So the Mary Seacole Trust, its initial guise was the Mary Seacole Memorial Statue of Appeal and it was responsible for the erection of a statue of Mary Seacole back in 2016 following a 14-year campaign to raise the funds and the statue of Mary was to become the first bronze statue of a named black female anywhere in this country. We were determined that that would be a springboard and certainly not the end of the journey and therefore we subsequently changed the name of the charity to the Mary Seacole Trust and we created a broader set of legacy projects, one of which is education for example, so we work with the Florence Nightingale Museum and they now have a permanent installation and exhibition of Mary Seacole, which we funded. We run a competition with schools, which we're particularly excited about. It's going into its third year, where we ask young people to identify their modern-day Mary, having identified Mary's various attributes. And we have a diversity and leadership programme. But above all, we not only spend time promoting Mary and indeed promoting issues and challenges around social injustice, but we maintain Mary's beautiful statue, which is at St Thomas' Hospital. So lots of work with young people? Very much so. I mean, we do work at a leadership level, so that's the top of the challenge pyramid, if you like. But at the bottom, the next generation coming through, it's important that we inspire them if we're going to improve the future. So working with leaders as well as working with young people using Mary as a role model. So tell us a little bit about your background and I guess how you came to the Mary Seacole Trust and the statue. Well I'm a lawyer. I am involved with major trauma so those that suffer a serious injury through negligence or another. I help them with their rehabilitation and with recompense. My background actually is perhaps not untypical. My parents are from Jamaica, came here in the late 1950s. They're part of the Windrush generation. I underachieved in many ways, leaving school at 16 or or 17 stumbled across the law and whilst working I started initially pretty much as a post clerk but I worked my way up and I became a partner the youngest and first ever black partner of the firm I was then at age 28 and I've gone on to deal with some of the perhaps most significant group actions and actions in this country, including the Croydon tram, which I mentioned because the inquest is about to start. So my career has been one of starting with underachievement, trying to break through the barriers that were in my way, both as a child but also as an adult and now my aim is to try and help pull others through and that's where Mary Seacole and the Trust is a wonderful vehicle and I got involved by chance actually as we were working towards the final stage of the campaign for the statue simply because my son and I were watching old histories and after that jovial episode involving Florence and Mary I said that I wanted to try and get involved in raising awareness of Mary and found out about their campaign and have been active ever since. That's very inspiring. What a wonderful career and story. Moving on to talking about Mary herself, I think, what do you think that her relevance is to modern Britain, kind of her legacy? Well, I think she's become even more relevant and even more significant since the tragic incident involving George Floyd and his death and of course since the greater prominence around the Black Lives Matter movement. Why is she relevant? Because she has all of those characteristics which epitomise those who have historically been discriminated against in some way or another. And she is a collection of those characteristics. If you take the time she went to the Crimean War, she was a woman. She was a woman of age. She was a woman of color. Yet she broke through all of those stereotypical barriers. She was a traveler. She was an entrepreneur. She was an author. She was a traveler she was an entrepreneur she was an author she was a healer and so her importance of somebody who can break through those barriers and obstacles and do it for the right reasons not do it because it will make you famous or successful in the broader sense but do it because it's about being caring and being compassionate and that's what she did when she went out to the Crimea.
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Obviously black history is far deeper in British history. It is part of British history and Mary is a reminder of the existence of black contribution prior to Windrush because of course she was at the Crimean War and we are dealing with Victorian times in the 1800s. So it serves as a really important reminder as to how deep black history is. And, of course, it goes back even further than Mary Seacole. So it's, as you mentioned there, it's been a tumultuous year for racial injustice around the world. What does that mean to you? What does that mean to the Mary C. Cole Trust? How do you look at the events of 2020? We're starting with George Floyd. George Floyd was only a little bit younger than I. And the reality is that if I happened to be in another land at this time, I could have been George Floyd with a knee on my neck. There is too much discrimination that still exists and racism. And unfortunately, people like me personally, a black man, often are the victims of it through no fault of our own. And it's important this year that it isn't just a year, but that this is the start of something far deeper and meaningful in terms of long-lasting change. And I think that what we have seen is a collection of people from all different backgrounds. We saw that through the protests. From all different backgrounds, from across the world, that are starting to want to work together to bring about meaningful change. And the Mary Seacole Trust would very much want to be a part of that, using Mary as a role model, but also using our collective thoughts to try and bring about structural change to defeat racism once and for all. What do you think are some of the biggest challenges and inequalities facing Britain at the moment? Britain's main problem, I think, is that it doesn't fully accept its history. It has, as you would imagine, having established a successful empire, much to say in terms of its success. That does mean that there is often not room for some of the truth which gave rise to that success. And of course I'm talking about slavery and I'm talking about some of the structural racism that followed on from slavery. You cannot have 400 years of slavery and all the structures that come about as a result of that and then expect that the moment slavery is abolished that everything will be just fine. It's important to acknowledge that part of history and it's important to be involved in dismantling some of the structures that came about as a result and I'm afraid to say that that's not happened and not happened quickly enough so one of the biggest challenges that is faced now in society is one acceptance and understanding of real British history and then to identify how we can address some of the structural changes and solutions needed to make sure there is long-lasting change. And there is a clear distinction between structural and simply racism, and I'm talking about structural, and that has to be addressed at all levels of our society. Trevor thank you so much for speaking with me today it's been a real pleasure it's been really genuinely wonderful and inspiring to to speak with you so good luck with the future work for the Mary Seacole Trust. It's wonderful to speak with Trevor Sterling there and some really interesting interesting thoughts about structural racism. So turning to you, Pam and Mandeep, now you're heading up the Lancet's internal task force for anti-racism, which is the Group for Racial Equality. Perhaps you could tell us a little bit about that and how that came about and maybe talk about some of your backgrounds and how you came to start this group as well. Well I guess I'm quite new to The Lancet. I've been here for well over a year and a half now but my background initially so I'm second generation Indian Punjabi Sikh born and raised in the UK, studied biochemistry at university, got into science publishing and kind of found that I wanted a bit more than that. So I went back to university after working for a few years and did a master's in philosophy, politics and economics of health. And that kind of led me into the whole global health field. I worked for WHO for a while, London School of Hygiene and Tropical Medicine and then yeah start of 2019 I found myself joining the Lancet Global Health as a senior editor and I guess since I've joined working with in the academic side of global health I really noticed how kind of some of the colonial attitudes still seem to persist in present day global health and so I really I guess I've been looking for an opportunity to explore this a bit further and also it kind of ties in quite nicely with the whole idea of the diverse the lack of diversity in publishing it's very noticeable so I very much felt like I'm in the minority while I've been here. So a very visible minority. And so I just guess it's been in the back of my mind for over a year that I need to do something about this. And then earlier this year with the events of the summer and the awful murder of George Floyd in the US, it kind of, that was kind of the spark that led to me talking to Pam. And then we kind of, this whole idea of having a task force, the group for racial equality came about and we invited a whole bunch of others who were thinking kind of with a similar experience and way of thinking. And we've kind of developed a programme of work in the last couple of months that will address both cultural awareness internally and also kind of addressing racial and ethnic inequalities in medicine more broadly as well and health. And part of that work will also be to look through the Lancet's archives and so really in depth and explore how colonial history really influences global health today. Wow, that'd be interesting. Yes, that's going to be an uncomfortable process, I suspect. But I think Mandeep came up with a brilliant phrase at our first staff meeting where she said, to heal the past, you need to reveal it. And I think that is very true. We do need to reveal it. And I think this process and journey that we go on will be important, very important. So Pam, I was going to ask just generally about Grace, the group for racial equality at the Lancet. How's it been so far? What are some of the kind of aims and goals that you have moving forward? Well, we've met together as a group twice. We've got another meeting scheduled for next month. So in the few months that we've formed, I think we've done quite a lot, actually. I look back and I think, given that we're in a pandemic and we're all at home and we're not exactly feeling 100% about ourselves right now, that to start something as huge as this was going to be really hard. But I think, as Mandip said, I think we got the timing really right. The events to the summer, COVID as well, which has also put a spotlight on the disparities and race and ethnicity and discrimination. I think they've all come together at this perfect time where there's a sort of real momentum and a dialogue that really needs to happen. And so I feel we've really kind of capitalised on that by bringing together this group, this task force. As Mandeep says, we're going to be looking internally, i.e. at ourselves. So just a little bit about me. I, unlike Mandeep, I've been here nearly 20 years. I joined the Lancet in 2001 and I joined Lancet Infectious Diseases and it was just John McConnell and me for those six years. And the Lancet was very small. It was, I think, 40 people max. And that includes production, advertising, all the departments that we have today. So we were all on, you know, half a floor of an office. And yeah, it struck me in odd ways when I arrived because obviously I was the only Asian, but then we were a very small group. So I thought, well, you know, one out of 40 isn't that bad. But then as time went on and as we got bigger and expanded, I was still the only brown person in the group. So I did think, oh, well, you know, as one does when they sort of try to psychoanalyze it, they sort of think to themselves, oh, well, I must be really rather good at what I do because, you know, for the Lancet to have taken me on, you know, I'm, I'm very good at my job. And, um, and I just felt very privileged, very honoured, uh, and then put it out of my head. But then when Udani joined and, uh, I remembered I had somebody to talk to about it because I think that was the other thing. Who do I talk to about it at work work if you're the only one? You know, I talked to my parents or my friends or my parents' friends, but certainly never in the office.
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Udani's, you know, very lovely person anyway, but we hit it off quite quickly because we were the only two non-white people and we chatted about it. It was the first conversation I was able to have with another colleague about it. And so then, as I said, many years even after that passed and we were still the only two editors. And it's really, if I'm really honest, it's only in the last five years where we've really expanded the pool of non-white editors across all the teams. From a senior level, I still think that there's very few of us there. I was the only senior non-white person for maybe 17 years, really. If I think about it now, we have Rupert, we have Duke, you know, we have people in senior roles, but still very far from what we should have. And I think, you know, that diversity and contribute, you know, that diversity of our workforce, it simply doesn't reflect the diversity of the society we live in. And I think over the summer months, it was an opportunity for us to acknowledge as a group that we need to do better. We'll be looking at ourselves internally, looking at our recruitment processes, looking at the extent of the lack of racial and ethnic diversity in our workforce and our contributors. So, you know, that includes our authors, our peer reviewers, our international advisory boards. You know, we really need to look at everybody. And so that's one aim. The recruitment side of things, I think, is probably the most important aim of our group. But I see that as a very longstanding issue. I don't think we can do that on our own. We're going to have to work with HR, with human resources of Elsevier, as well as wonderfully now we have a new group, a new employee group, Embrace, to tackle the issues that we're also tackling. So we now have partners who have similar visions as us. And, you know, collectively, I think that's going to be much more powerful and a strong way of getting things done. And then externally, you know, I hope that we can still continue to use the pages of our journal to highlight the achievements and celebrate the diversity of minority groups, as well as highlight all the injustices that still continue to happen and ultimately create an advisory board who will be devoted to this issue alongside us and work together to put together a special issue on race and equality in science, health and medicine. So yes, so I think that we've got quite a few aims and objectives to look forward to. It sounds amazing and a really great programme of work and so kind of necessary. Obviously, there's so much that 2020 is going to change and there have been been periods historically where there's been a sort of refocusing on race and inequality. How do you see it panning out from here now? Do you think this is a turning point? I'd like to think it is. I think the pandemic is also an important factor in this. We already know that people from marginalised populations and from ethnic and racial groups are heavily impacted by the virus. And I don't think that's going to change. I think at the end, when we do come out of this, it will be those groups that are going to be left worse off. So I think, you know, we have a responsibility in many ways to do what we can now. It feels like a really important, important point in history. Yeah. So I do think it's, it is a turning point. Yeah, I agree with Pam on that. I think it is definitely, I mean, this year has been a year of change on so many different fronts. This change that we have started, especially on this issue of racial and ethnic diversity and equality, it's going to take a long time to actually see the results. Even with our programme of work internally, we're in it for the long haul. So we're looking to start this and see where it goes and keep it on the agenda. So it's excellent that we have Black History Month in October, but it's more than just one month. So we've got to keep celebrating and highlighting and just keep on banging the drum for this issue throughout the year. So once October's ended too. Thanks so much for listening to this special episode of The Lancet Voice to mark Black History Month. We hope it's kind of inspired you to look into some of these backstories and thank you for joining us. We'll see you again next time.
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Hello, and welcome to this week's Annals of Internal Medicine audio summary for our December 4th, 2007 issue. I'm Michael Berkowitz, Deputy Editor at Annals. We have another exciting issue for you this week, with articles on the use of telbivudine for the treatment of chronic hepatitis B, the three medications most responsible for emergency department visits by older adults, and the risk for fatal pulmonary embolism in patients with venous thromboembolism who discontinue their anticoagulants. I'll tell you about those articles, Thank you. But first, here's an in-depth summary of our feature articles. In 2002, Annals published a physician charter that proposed three fundamental principles of medical professionalism, dedication to patient welfare, respect for patient autonomy, and promotion of social justice in the health care system, and a set of specific commitments, for example, commitments to honesty with patients, improving quality of care, maintaining professional competence, and managing conflicts of interest, Thank you. Boston, report the results of a national survey assessing physicians' commitment to those standards first proposed in the Charter on Professionalism. The authors sent a survey to about 3,500 providers in three primary care and three non-primary care specialties, asking if they agreed that the charter commitments were important, and asking, with the use of patient scenarios and direct questions about past actions, if provider behaviors tracked their commitments commitments. A weighted 58% of providers who were sent the survey responded, and the study had three main findings. First, most respondents agreed that the commitments were important, with the exception that about 25% did not agree that respondents admitted to inappropriately revealing confidential information about a patient, and only 25% said that they had actively looked for racial or sex disparities in their practices, clinics, or hospitals. Finally, there seemed to be differences in behaviors by specialty, and no one came out looking lily white. If anything, anesthesiologists and pediatricians came out on top, being more likely to report an impaired colleague, accept new uninsured patients, and participate in quality improvement programs in the case of anesthesiologists, and being more likely to undergo competency assessments, report serious medical errors, and see patients who were unable to pay for services in the case of pediatricians. Internists tended to provide responses in the top half of the response distributions, but they were less likely than other providers in other specialties to provide care without reimbursement in settings serving poor and underserved patients. There were also differences by practice setting and reimbursement mechanisms, but to be clear, all of these differences were differences in proportions of providers who said that 4 and seeing which overlap and which do not. Based on these findings, the authors conclude that the professional aspirations embodied in the Charter on Professionalism are relevant and meaningful to physicians, even though professional behaviors don't always match attitudes and appear to vary by norm. They acknowledge that their measures are far from perfect and that the association between self-reported and actual attitudes and behaviors may be limited. They don't acknowledge that there are health system and other forces that keep even the best intention providers from acting on these professional ideals. Thank you. You imply in the paper's introduction that promoting professionalism among physicians is one way to improve the quality and efficiency of health care. In what ways would you say professionalism improves health care quality, and in what ways would you say it improves efficiency? I think that if you look back at the recent history of the U.S. healthcare system, you'll see that we've tried very hard to improve the functioning of the healthcare system through using regulatory means and through promoting competition in markets. We've done neither of them perfectly, and neither strategy has significantly improved the cost of care or the quality of care. That leads us to look for alternative ways of making the system function better. One of the reasons why markets don't function well is that there are asymmetries of knowledge between patients and providers of care, a fundamental flaw. And one of the reasons regulation doesn't function well is that there are just too many decisions made by doctors and patients and healthcare institutions every day for regulation to effectively control them. It would work much better if those who are most informed about decisions made decisions that were consistent with their patients' interests and with the interests of the larger society. It would become much more a self-regulating system than it is now. And ultimately, I think professionalism is about, in a major way, self-regulation in the patient's and society's interest. One of the primary findings of the paper is that professional behaviors don't match attitudes. So how confident are you about that finding, given that all your behaviors were self-reported and that there are selection and desirability and maybe other biases that could have inflated responses to both parts of the survey? You raise a very important point, which you mentioned in our studies, the fact that there is this thing called social desirability bias, and that not just physicians, but most people answering surveys don't like to admit to behaving or holding attitudes that may be considered against what are the prevalent norms in one's field or social reference group. So clearly, we might say, for example, that the level that we found that physicians support attitudinal norms about professionalism are probably likely to be overestimates. We've found that behaviors probably run along the same lines as that people may overestimate engaging in behaviors that are seen as positive, but at the same time they're likely to underestimate engaging in behaviors that are seen as counter to the norms. Now with that said, we've used a number of survey techniques to control for these things in that we allowed people to respond anonymously, which research in the survey field has shown that reduces this bias to some extent. Now we can't totally eliminate it, but we certainly believe that it's reduced given the way in which our study was conducted. And let me ask you another methodologic question, which is that your response rate was something like 58%. What implication does that have for the generalizability of the findings to physicians? Well, 58% in terms of surveyed physicians is a very good response rate. And it's getting harder and harder all the time to achieve those response rates. With that said, there's also no magic number. The issue is not the response rate. The issue is the extent to which the people who respond differ in any systematic way from the folks who don't. And as long as your responding group is big enough, in theory, you don't have a problem. We're very confident in what we've achieved, partly because of the high response rate and because of the fact that we didn't see differences in response by specialty, for example, which suggests at least along one variable, our respondents were similar to the population from which they were drawn. We found that physicians differ significantly on many of the attitudes and behaviors regarding professionalism by their specialty, and clearly that's something that I think we need to explore in the future, that there are really kind of systematic and predictable ways in which, for example, primary care doctors differ from other specialists such as anesthesiologists and or cardiologists. And I think the next step in the survey has to kind of begin to address those specialty-specific differences and what impact that might have on really the concept of professionalism within a specialty and between specialties as well. Cardiologists don't see the owning of an imaging facility and referring patients to that imaging facility as problematic nearly as often as other physicians do. So that the principle of putting patients' interests ahead of your financial interests, they're not as sensitive to that norm as some other specialties might be. Another thing that is interesting, though, is that cardiologists are more likely to report that they see uninsured patients, for example, than general internists are. And that may be because they see fewer of them in general, or it may be because they, in general, earn more money and feel less pressured and have more time. These are all speculative conclusions. But I think it highlights the fact that physicians are not all alike, that their circumstances, their training, and maybe their self-selection into professional areas affect their conformance to professional norms. And specialists were significantly more likely to report that they feel prepared to evaluate new clinical information. They were more likely to report impaired and incompetent colleagues than were primary care docs. Especially anesthesiologists. And I think those reflect the culture of these specialties. And also perhaps the risk for impairment, right, in some specialties. Absolutely. The ABIM charter and the questions in the survey reflect our modern preoccupations, for example, with improving health care quality and reducing disparities and managing conflicts of interest and errors. But I also wonder about a less modern and some people might even say a more heroic conception of professionalism that isn't addressed directly in the charter, in which doctors place patients' interests above all others. So that's embodied by classic images of a doctor sitting at a patient's bedside through the night waiting to make sure that they get better, or stories of physicians canceling important personal commitments to attend to emergencies.
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But I think that within the ABIM norms, there are questions about putting the interests of patients ahead of personal interests of physicians. On the behavioral side, they're not explicitly stated or as fully developed as one might like, but they definitely are there with respect to, for example, financial conflicts of interest and a willingness to see patients who are not insured and therefore can't pay, as well as a willingness to get involved in relationships with industries that might lead to biases in medical decision-making. But I would agree that we haven't explored that traditional notion of altruism and of putting patient interest ahead of professional interest as fully as we might. And we are, by the way, repeating this survey sometime next year, the end of next year. So we have an opportunity to expand on some of these dimensions. And I think this would be one that would be worth exploring. There's a parallel set of questions that have arisen very explicitly in some countries other than ours. Actually, a very interesting national experiment with that set of questions about professionalism that occurred as part of the SARS epidemic. Institute on Medicine as a profession is exploring the opportunity to do a similar survey in China. And in the pilot study that the Chinese developed based in part on our survey, they had a whole battery of questions about the willingness to care for SARS patients and what their respondents actually did during the SARS epidemic. So I think that is in some ways a paradigmatic instance of what you're talking about. The ultimate willingness to next step? What is the Institute on Medicine as a Profession or the American Board of Internal Medicine or we as individual providers do with this information? I think that one locus of activity should be the specialty society. I'd like to see other specialty societies besides the American College of Physicians and the American Board of Internal Medicine engage systematically in whatever assessment they think is appropriate for measuring the conformance of their members with professional norms and then to develop interventions that might improve that rate of conformance. So I think that's one locus of action. And I think our survey suggests that different specialty societies may emphasize different norms because their members will conform differently with different norms. The other thing where I think we collectively need to apply some effort is in public policies that can affect professionalism and organizational settings that can affect professionalism. Once you focus on professionalism as a kind of third force, aside from competition and regulation, in managing the healthcare system, it becomes reasonable to ask what mechanisms can be used to reinforce professionalism and almost to do an impact analysis when you're making policy or organizing your physician workforce, asking how will this affect professionalism. So it seems to us that large groups and prepaid group practice have certain advantages in terms of stimulating professionalism. Universities have certain advantages. And similarly, some other solo practice seems to have a lot of disadvantages. And we think that that's another reason to look at organizational setting and how you pay doctors may also have some impact. So I think that's especially society's public policy physician organization are all potential points of influence. Is the idea there that pay for performance wouldn't just be process measures such as HBA1C and clinical outcomes, but that physicians might be reimbursed for adherence to professional norms? I think we would need to do much better than we have in terms of measuring adherence to those norms. But yes, I could see that as one type of outcome if you can get consensus about which norms payers, employers, and physicians agree are core to appropriate functioning of the health system. This was really our first try, and we are going to be doing this survey again in about a year. We're going to be doing some additional work on the survey instruments, trying to refine it, make it a little more comprehensive, fix a few of the questions that didn't work so well. We're going to be fielding it among some of the same groups that we fielded at this time to get longitudinal data, as well as including some new specialties of psychiatry, I believe is one that we're going to focus on in the next round as well. And we should be in the field, I would guess, within the next year or so. But in addition, we also plan to do this study comparing doctors in the UK versus doctors in Scotland so that we'll be able to get both a U.S., non-U.S. comparison as well as a comparison looking at the differences in professionalism while taking into account the differences in the changes that have happened in England compared to Scotland and their health care reforms as well. And as I mentioned, we're talking about other international collaborations. We're having discussions with some collaborators in the Netherlands and in the EU and in China. I guess one of the questions that one could ask is whether professional norms and behaviors are attributes of Western culture uniformly, or whether they vary across nations and cultures within the West, and even across cultures West and East. So we're asking, I think, some more generic questions about the universality of professionalism as a concept. Dr. Campbell and Dr. Blumenthal, thanks so much for talking to me. You're very welcome. Listeners interested in thinking more about medical professionalism should consult the charter itself, an editorial accompanying this week's report entitled Medical Professionalism and the Parable of the Craft Guilds by Hal Sox, Annals Editor-in-Chief, and check out the website of the Institute for Medicine as a Profession, a nonprofit foundation and research institute affiliated with Columbia University that's focused on promoting professionalism in medicine. They're at www.imapny.org. Our other featured article this week is a college position paper on pay for performance that's being called an ethics manifesto by the college's Ethics, Professionalism, and Human Rights Committee. The paper raises the concern that pay-for-performance systems could create unacceptable conflicts of interest because rewards from favorable quality ratings could create provider incentives that conflict with what's important to and for our patients. Measuring hemoglobin A1c is a good example. Systems that reward good performance on such a highly specific measure could lead providers to give up on or refuse to accept new patients whose hemoglobin A1c is difficult to control. Such systems could lead providers to neglect other aspects of their patient's care, even if they don't deselect the patient from their practice, and to order tests or even give treatments that patients don't need to ensure that the measure meets the system's definition of quality so that the provider can maintain their income. The principles that emerge from these concerns are that pay for performance incentives should reward providers who care for more complicated and more vulnerable patients at least as much as they reward the care of less complicated patients. The paper makes the additional claim that measures of quality on which rewards are based need to incorporate domains of care quality that are important to patients and key to improving their health, such as provision of good counseling and good communication, continuity of care, maintaining patient confidentiality, and ensuring access. The authors make the case that ethical pay-for-performance systems need to develop broad and reproducible measures of these care elements and to recognize not just isolated care measures, but comprehensive care of the patient. Such systems need mechanisms to notify patients that incentives are in place, and they need to introduce administrative oversight of physicians, admittedly a potential burden to providers, the sole purpose of which would be to ensure that patients aren't fired from provider practices because the patients literally don't measure up, and to prevent providers from not accepting new patients who might make their quality measures worse. So these are great principles, and I'd vote for all of them in a minute if I were handed a ballot, but they also seem pretty abstract. So I went to the authors and asked for a little more detail about what they were trying to say and do. Lois Snyder is director of the Center for Ethics and Professionalism at the American College of Physicians, and Richard Neubauer is a member of the committee, a regent on the college's board of regents. He's chief of internal medicine at the Alaska Native Medical Center in Anchorage, Alaska, and he's a clinical assistant professor of medicine at the You bet. Thanks for having us. What does pay for performance look like in 2007 and 2008? Are there programs in place now in health systems or large practices or elsewhere that meet the committee's definitions of pay for performance? The committee used a broad definition of pay for performance, performance measurement tied to financial incentives to bring about clinician and systems change. Recent surveys suggest that there are now well over 100 pay for performanceperformance initiatives nationwide sponsored by a variety of health plans, employer coalitions, public insurance programs. For example, the Agency for Healthcare Research and Quality found that more than half of HMOs use pay-for-performance programs. And the Commonwealth Fund found that more than half of state Medicaid programs have one or more pay-for-performance programs, with nearly 85% expected to have them within the next five years. And I would add that there's also the so-called pay-for-reporting program that was recently started by CMS and Medicare over the past year, and that may evolve into a pay-for-performance program in the future. And also, England has put in place a pay-for-performance program that involves a very large number of performance measures.
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Let's say most internists are giving patients their flu shots and their Pneumovac shots, for example, or checking HbA1c levels in their patients with diabetes. Why is rewarding them for doing those things consistently and consistently well a problem? Okay, so the potential is that pay-for-performance programs that rely on a limited set of measures may have a number of unanticipated consequences. Most people agree that paying for higher quality can be valuable both economically and ethically. Reaching agreement on the details of how the program should work is a bit harder. The committee expressed in this paper their concern that medically appropriate care for individual patients should take precedence over other considerations and that incentives should encourage that. Potential pitfalls of pay-for-performance could include the selection of challenging patients, gaming the system to achieve good scores on a limited set of performance measures rather than focusing on the patient, and finally harm to the patient-physician relationship as another unintended consequence. The committee makes recommendations that sound like they might balance the potential adverse effects of pay-for-performance programs. What are those recommendations? Overall, the college wants to ensure that pay-for-performance programs help improve the quality of care in a manner that aligns with the goals of medical professionalism and also with the views of patients. Measures need to reflect what's important to patients, things like access and continuity of care with trusted physicians, effective communication, adequate time for office visits, coordination of care across settings and providers, the role of the family in care. There also needs to be transparency in these programs so that patients are aware of incentives, and there needs to be monitoring of programs to ensure that so-called challenging patients are not deselected or otherwise discriminated against. So in an ideal world, who do you think should be responsible for those actions, say notifying patients of incentives that might work against their interests or developing procedures to prevent patient deselection? That is not addressed specifically in this paper, but the college has said in the ACP Ethics Manual and other college policy that physicians should disclose potential conflicts of interest to patients and that purchasers and health plans should also disclose to patients any arrangements that may influence care. A particular problem in this specific area of pay for performance is that many physicians may not personally identify being paid for performance as a potential conflict of interest. A valuable outcome of addressing this issue prospectively could be that the public will better understand the incentives that may influence their care. So let's take that a little further. You acknowledge in the paper that notifying patients about incentives that work against their interests could increase the risk that patients won't trust their physician. But you say that secrecy and not being transparent has worse consequences. What consequences are you imagining? Well, of course, every payment system creates incentives and potential conflicts of interest. Patients should know the basis for health care recommendations they receive and whether contractual or other arrangements might influence clinician judgment to promote or limit treatment. We feel that trust is imperiled when potential conflicts of interest are not disclosed, leaving patients in the dark or leaving them to wonder if anything influenced their doctor's recommendations. The paper mentions developing objective measures of the values that you emphasize as a way of ensuring that a full range of values are represented in pay-for-performance programs. Let's take developing objective measures of continuity as a way of presumably preventing deselection of patients. Wouldn't that kind of measure penalize providers for non-adherent patients who disappear for long periods in much the same way that pay-for-performance programs might? Yeah, I think that's a very good observation. That's why these sorts of programs are very complicated. Patients often choose to refuse all sorts of recommendations from their physicians, and that's certainly their right. But at the end of the day, the sorts of measures that are going to reflect the best care, especially for patients with multiple chronic problems or the elderly, are very important. What we don't want, as we say in the paper, is the outcome where the patient died, but the electrolytes were in balance. Who does the committee intend as the audience for the paper? Who do you hope is going to read it and will take notice? We hope that physicians, patients, policymakers, payers, that they all read the paper, since all of them need to recognize and support the importance of the patient-physician relationship and the ethical obligations of physicians to their patients. And why is this a manifesto rather than a position paper or a recommendation statement? Yeah, while this is a position paper of the college, we purposefully chose the word manifesto in the title. The definition of a manifesto is a public declaration of principles, policies, or intentions. And we specifically wanted to focus attention on the fact that pay-for-performance programs need to adhere to basic ethical and professional standards that place the whole patient in the forefront, not just a few aspects of their care. I wonder if part of the problem lies in the language that we use. That is, pay for performance sounds venal as if it puts financial incentives first ahead of caring for the patient. I wonder if we talk more consistently about value-based purchasing, if that idea would more easily accommodate a range of values, including those that you emphasize in this week's paper. Do you think there's a difference between pay-for-performance and value-based purchasing? And do you think this paper might look different if the committee were addressing value-based purchasing of health care instead of pay-for-performance? Well, I think that the problem with pay-for-performance is that if it's grafted onto a dysfunctional payment system that doesn't recognize the care of the whole patient and continuity of care as one aspect of that, that's where the problem lies. You know, if we look at value-based purchasing in a global fashion, I think what that really means is trying to figure out what we want in our health care system, and our current payment system doesn't really address that. Well, and I would just add that I think you're absolutely right about the language, pay for performance, that pay for and performance don't really recognize the importance of what's going on here, the patient-physician relationship and the delivery of health care. And, in fact, patients would be rather surprised probably by the term pay for performance when their expectation is that their physician is doing for them, you know, the right thing in the first place. Why would they be paid extra to do a test that they should be getting anyway? So I think you're absolutely right. The language is perhaps part of the problem. One other additional thought on that, it's always seemed to me that the best way to improve physician performance on any specific set of things would be to give point-of-care feedback. In other words, if you knew that you're only meeting expected goals and how often you're doing hemoglobin A1C measurements 50% of the time, you would correct that as a caring physician. The problem is that we don't have the tools to know that in our practices. I'm not sure that paying for performance on that is the best way of changing that behavior. Are there initiatives that you're aware of that would allow individual providers or practices to monitor their own performance in that way? Well, I think the patient-centered medical home concept that the ACP is promoting is on the right track to getting to that answer. Well, and electronic medical records would go a long way toward collecting that information. And that is part of the patient-centered medical home concept. Ms. Snyder and Dr. Neubauer, thanks so much for talking to me. Thank you. Thank you. That was Lois Snyder, Director of the Center for Ethics and Professionalism at the American College of Physicians, and Richard Neubauer, a committee member and a regent on the college's Board of Regents, talking about the position paper they co-authored this week entitled Pay for Performance Principles that Ensure the Promotion of Patient-Centered Care, an Ethics Manifesto. Readers interested in pay for performance should also look at a perspective in this week's issue making the case that ventilator-associated pneumonia, which is out there as a possible quality measure for critical care patients, is an exceptionally bad pick for a quality measure because diagnosis is so imperfect and subjective. And you may also want to revisit a review of Pay for Performance entitled Pay for Performance and Accountability, Related Themes in Improving Healthcare by John Rowe, that's R-O-W-E, published just over a year ago in our November 7, 2006 issue. Other articles in this week's issue include an industry-funded randomized trial of telbivudine for the treatment of hepatitis B, E antigen chronic hepatitis, suggesting that telbivudine may provide greater viral suppression than the comparator drugs used in the trial, adefavir and lamivudine. Listeners interested in a more complete summary of this article can consult an audio summary that's on our annals.org website. We have a national surveillance study suggesting that warfarin, insulin, and digoxin are responsible for a third of visits to the emergency departments by the elderly for adverse drug events.
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Our CME article this week is an observational cohort study of about 2,000 patients with venous thromboembolism, suggesting that 4 to 9 percent will die from fatal pulmonary embolism in an average four and a half years after discontinuing anticoagulation. We have an update in oncology, the 9th of 10 updates appearing this year based on presentations given at the American College of Physicians annual Internal Medicine 2007 session held in April in San Diego. And finally, this month's In the Clinic supplement is a good one on heart failure. Well, that's it for today. Our theme music is by Brian Poole and Queezy Marles. Technical support for this summary was provided by Andrew Langman, Neil Cole, and Beth Jenkinson. Special thanks to Kevin Stahl and all our friends at WHYY, Public Radio and Television of Philadelphia, who helped produce these podcasts. Send feedback, suggestions, comments, and criticisms about this summary and the journal to podcast at annals.org. Check back in two weeks for a complete summary of our regularly scheduled December 18th, 2007 issue. I'm Michael Berkowitz, and thanks for listening.
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Welcome, listeners. This is Amalia Cochran. I am the web and social media editor for JAMA Surgery. I'm here today interviewing Dr. Guido Beldi, who is the senior author on a study entitled The Effectiveness of Prophylactic Intraperitoneal Mesh Implantation for Prevention of Incisional Hernia in Patients Undergoing Open Abdominal Surgery. Dr. Beldi, welcome. We're thrilled to have you here. Thank you very much. Welcome. What was your motivation and your team's motivation for choosing the research question that you did? This is rather twofold. One thing was that incisional hernia is really among the most frequent complication of any type of abdominal surgery. So the incidence is mostly, depending on how you assess it, more than 10%. And the other thing is we had some very good experience with the implantation of intraperitoneal meshes in patients we treat for incisional hernia. And therefore, we were thinking having this tool, we were using those meshes more than 10 years now, having this tool to use it in a prophylactic way in order to prevent this quite frequent complication. I agree. I don't do much general surgery myself. I'm a burn surgeon, but I recognize that ventral hernias are certainly one of the most common and most complicated things that we deal with in the world of general surgery. You all designed a very elegant clinical trial for this. What was the biggest challenge when you were designing the clinical trial itself? What was the hardest part of that? During the design, there were two aspects which were a bit difficult. We really wanted to include only a subset of patients which are really at high risk for having an incisional hernia. So we did not want to implant a mesh in all the patients, thereby we would have over-treated quite a lot of patients. And therefore we had to identify patients which are really at high risk using parameters which are present preoperatively and which are easily introduced. So we have the parameters of like a previous laparotomy being obese, having a male sex. And the last one, which was a bit the problem, which we found out later was that we had to include patients because of the risk profile with malignant disease. And because of including those patients, we then experienced that some patient died before they reached a point of follow-up, and therefore we had to increase a bit the sample size. I had noticed when I was looking at the study attrition, you all really did have excellent retention of your patients overall throughout the study period, with that one exception. And so I thought that that was particularly interesting. Yes. And this is also where we a bit changed our strategy that we still implant those meshes in patients, but in patients with like kind of pancreatic cancer, clad skin tumors, which do not have an average life expectancy of more than two, three, four years, we are not implanting the meshes in a prophylactic way unless there's an excessive risk or we have to redo surgery. But typically, this is not our population anymore because of the result of this study. Ah, that makes sense. One of the things that really struck me when I was carefully reading the study to prepare for our conversation today was when I looked at the hazard curves for the control group versus the mesh group. What stood out to me is that the control group had incisional hernia quite early and then it seemed to plateau off as opposed to the mesh group that was more consistent over time in the incidence of incisional hernia. Do you all have an explanation for why the control group tends to be earlier versus the mesh group being more balanced across time? We can only make presumptions about this earlier occurrence. We think that in the control group, there's like the tension and the pressure on the abdominal wall all over the incision will be quite high already from the beginning. And there's like no mesh taking off the pressure. Maybe this is the reason that we observe incisional hernia at the earlier time. But in the mesh group, it could be also that we have a later incidence because like in one patient, we had to explant the mesh at the later time point. There were some problems with a surgical site infection where it was not healing. And in another patient, there was a second operation about a year later. And in this patient, the surgeon used a resorbable suture to close it. And particularly in this patient, we had recurrence. Did you observe any particular learning curve or was that sort of an isolated incident of someone inadvertently using the resorbable suture? We used those measures before in many patients. And there was just a junior doctor not particularly familiar with the subject, but this was clearly an exception. If you're talking about a learning curve what we had to learn as well which was quite important and important occurrence was that we can treat surgical site infections in which we have a mesh exposed. This is like when talking about learning curve this was one of the important things we did not really write down because it's more just an observation. But what we observed is that even exposed meshes, they heal, but they tend to heal much longer, obviously, than in the control group in which there was no mesh present. This was one of the problems we described in this paper as well. Interesting. So that sounds like one of the ways that the study influenced your clinical practice in turn. Absolutely, yes. Was there anything that was particularly surprising to your team in the mesh group. We really thought this is like a non-resolvable mesh and therefore we should not have any kind of recurrence. But still, these are sometimes, because of the inclusion criteria, obese patients. And sometimes it was a bit difficult to implant the mesh and have a mesh with a sufficient size, in particular at the cranial and caudal endings. And this is where we observed our recurrences in the mesh group. Is there a single thing that you would consider to be the most important finding from the study? If you were making sure that our readers knew one thing from your study, what would that be? Mainly in Europe, people are very reluctant to use intra-abdominal meshes. Surgeons always feel that the incidence of fistula or intra-abdominal complications is much higher. And I think with this study, we could show that this is not the problem. The problem is, similar to the prophylactic use of preperitoneal meshes are surgical site infections. However, when one uses the intra-abdominal meshes, we only see late problems with surgical site infections, meaning that they do not heal. Whereas when one implants preperitoneal, pre-facial meshes, then the incidence of seroma or early surgical site infection is typically high compared to the control group. You mentioned that the study findings have impacted how your group manages patients who have surgical site infections after mesh implantation. Are there any other ways in which you and your colleagues are incorporating the study findings into your clinical practice? even in patients in which we have contamination in the abdominal cavity, because we learned also with this study that meshes heal despite local infection. It depends on the type of material, of course. We like polypropylene-based meshes, but in such circumstances, we continue using these meshes. And what is a next question that you and your team would like to answer regarding use of mesh or prevention of ventral incisional hernias? Is there another direction or extension of this study that you all are considering? We have observed that meshes work, that they can prevent incisional hernia. But the downside is always like the local problems with the surgical site infections that tend to heal longer. And therefore, we really think that it is necessary to identify novel mesh types, novel materials that allow an easier introduction of the mesh, like an easier application of the mesh, and also tend to have a lower inflammatory response. One of the important findings, which I did not allude to yet, was the identification that surgeons at the end of a long operation do not really like to extend their operation for another 15 to 20 minutes. So like the perfect mesh should be quite easy to implant, easier to be applied and reduce the workload at the end of an operation in order to guarantee its applicability for many patients and many situations. Dr. Beldy, I want to thank you for sharing your work with our readers and for taking some time with me this morning to do a little bit of a deep dive into your study. And I've enjoyed learning more about it. And thank you to you and your team. And also, Gemma Surgery readers, a thank you to all of you for listening to our podcast and for reading with us. Again, this is Amalia Cochran. I'm the web and social media editor for Gemma Surgery, and we look forward to speaking with you all again soon.
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This is Derek Paul, and welcome to the Anti-Racism in Medicine series of the Clinical Problem Solvers podcast, where, as always, our goal is to equip our listeners at all levels of training with the consciousness and the tools to practice anti-racism in their health professions careers. Today's episode is titled Dismantling Race-Based Medicine, Part One, Historical and Ethical Perspectives. And I am just beyond excited to be co-hosting this episode with two of my colleagues and anti-racism in medicine team members of people I admire a lot, learn a tremendous amount from every day, LaShira Lash-Nolan and Rohan Kazanchi. So I'll hand it over to Lash and Rohan to introduce themselves and today's guest, who many of you will know already, a critical race theory scholar, Professor Edwin Lindo. Amazing. Derek, it's so great to be here with you. Rohan, always a pleasure. Just to introduce myself, my name is LaShira Nolan. Most folks know me as Lash, and I'm an LA native now at Harvard Medical School, my second year where I'm serving as our student council president. I'm very passionate about this work. That's why I'm so blessed and excited to be a part of this team. I write about these issues a lot, speak on them often on panels and doing different presentations. And I'm just stoked for our conversation. Yeah, totally echo everything Lash said. I'm really excited to be here. Even more excited that Professor Lindo is joining us today. My name is Rohan Kazanchi. I'm currently an MD MPH student, getting my MD down at University of Nebraska Medical Center in Omaha, and doing my MPH this year at the University of Minnesota School of Public Health in Minneapolis. And completely echo what Lash said, I think we're all here because we care about these issues. These are our passions. These are our professional interests and, you know, the ways that we spend our personal lives outside of the classroom too. So I want to introduce the series that we're starting with today's episode. This is episode number one in a three-part series on dismantling race-based medicine. And our goal for this series is to answer fundamental questions. What is and isn't race? How have the ways our medical community defines race changed over time? And most importantly, how should we think about these issues in the context of ongoing discourse about racism in medicine and beyond? So today we're going to take a deep dive into the history of how racial categories have been defined in America. We'll talk about why it's important to distinguish between concepts like race, ethnicity, ancestry, and genetics. And we'll think about how the medical field's dark history of scientific racism plays into the broader struggle for racial and health equity. And I am so excited to introduce our esteemed guest, Professor Lindo. Edwin Lindo, JD, is a critical race theory scholar and educator who is an acting assistant professor in the Department of Family Medicine at the University of Washington School of Medicine, Assistant Dean for Social and Health Justice Office of Healthcare. Edwin teaches, presents, and writes on issues of racism within medicine and society. He's also the creator of the Praxis podcast, which I'm so lucky to have been a guest on. It's a vibe, y'all. Please check it out. And you can reach Edwin on Twitter via at Edwin Lindo. Edwin, thank you for being here with us. I get to, I had the honor of asking you our first question. I'm going to start off with a question that I think seems sort of easy, but it actually is more difficult. And that is, what is race? It's something that we are all, it's part of our lives from the moment we're born. Honestly, before the moment we're born is playing into our lives. But sometimes folks are a little later in life before they start thinking about it critically. So, you know, if you're new to this conversation, someone's having, you know, one of your students and they ask you, what is race? How do you think about it? Yeah. You know, I tell folks when we start talking about race, we start talking about racism. In many instances, it's like doing quantum physics because at its core, it doesn't actually make sense. And what I mean by that is we have something. So I'll get into the definition. You have folks like Dorothy Roberts and other critical race theory scholars that have guided us towards an enlightening definition of race being a socially, politically constructed taxonomy. And I use this definition a lot. And I go on to say, and it's based on perceived skin color and oftentimes culture with no scientific or biological determinacy of the physiology used for the purposes of allocating and or extracting resources from melanated black people when they were stolen and brought to this continent. If that's the beginning, then we really have to wrestle with that beginning, with the impetus of it. Now, we are in 2020 and folks say, well, and people always respond, well, great, Edwin, we should just get rid of the concept of race and we will be a unified human race and it's like wouldn't that be nice but that's not the world we live in race from the beginning was something that was created and I know we're going to talk more about that and it was created by we'll name very clearly. But we have to sit with the reality that medicine has grafted the social political endeavor of race to what is believed to be a physiological determinant, a biological identity. And the truth is that's just not accurate. And we know it's not accurate, and we'll talk more about that. But it's now our job to start ungrafting, removing that graft and saying, actually, there's a huge difference. One is the social construction. And social meaning is not just the white scientists that created the concept of race, but it's also us engaging with each other, right? That's why I don't think we need to get rid of race because it helps us identify with each other, understand what solidarity looks like, understand different struggles, understand culture, food, ceremonies, traditions, religious beliefs. And that's beautiful. We can embrace those differences and race helps us identify those. What it doesn't help with is identify how we are biologically different, yet people can't disassociate the two. And I think it's our job to say, it's okay that someone identifies as black, someone else identifies as brown, someone identifies as Asian. That's beautiful. It's unhelpful when folks start trying to identify how those different categories are physiologically different from each other. So long answer, but that's what and how I see race. Yeah, thank you for that. And that whole statement was a word. And now I'm just wondering if you could talk a little bit more about the history behind that. And we often hear people say that race is a social construct. And I'm wondering if you can also touch a bit more about what do we mean when we say that? And talking a little bit about how history and where we're at now kind of comes together to create this moment. Yeah. I mean, race is only a social political construct. Now that delves into a deeper question that I don't know as a society we're equipped yet to wrestle with, but there are some people that say, well, if it's a socially politically, a political construct that was created by white folks, then why are we still holding onto it? Why do we still identify with the colors that Johann Blumenbach and Carl Linnaeus created? That's a different conversation. I think it's a needed one. It's a different conversation because I'm going to start from the assumption that race is beneficial in the social endeavor and social project. Again, like I mentioned, to identify and engage with each other. But when we get to the question of what it means, it means that the project, I keep calling it a project because it isn't something that finishes, right? Race is changing, at least the way people view it. Mixed race, multiple races, single race folks. What does the identity mean? I think it depends on the consciousness that we're bringing forth to this conversation. But we are the ones that give value to the concept. And it could be a positive one, or it could be, as we've seen throughout time, an incredibly negative concept. And the reason I say in my definition that it was used for the purpose of allocating resources is that you have Johann Blumenbach, Carl Linnaeus in 1767 writing the book Systeme Naturae, and he literally created a taxonomy. There's an apex of the taxonomy and there's folks who are at the bottom of it.
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Black and Native folks, not getting many of them. European and Asian folks, Asian folks getting slightly more. White folks perceived as the most intelligent. You have Carl Linnaeus that says that they are intelligent, they are witty, or sorry, they are smart, they are imaginative, and they are governed by laws. That was the categories, the definitions associated with the color to perpetuate this racial taxonomy. And it's not an accident. What I mean by that is there was a vested interest in whiteness as a property right to ensure that certain racial categories were at the apex of this taxonomy and certain groups were at the bottom of it. What we need to sit with is how do we ensure that our social relationships around race are not the conversations that we have in the biological realm because they're not the same. And so you ask about the history. I am a believer that medicine is the reason we see the racism that we witness today. And there's a lot of physicians who are listening, a lot of clinicians that hear me when I give my talks and they say, Edwin, how dare you critique medicine? You're not even an MD. And I say, you don't have to be an MD to understand how racism works. And in observing it, what I've seen is that from the beginning, from Portuguese, the Portuguese coming to West Africa, using the term Negro, stealing and forcibly taking slaves into chattel slavery. You have the British, you have the Dutch, a number of other European countries that further endeavored in this project of slavery and chattel slavery. And I always ask the question, like, why? Why did this happen? And when you land in the United States in the 1619 project, or sorry, not project, but in 1619, when the first slaves were sold in the auction block guess what you had doctors that were at that auction that were hired by slave owners and they were effectively they were the the physical checkup for those slaves because they were they were paid to ask a. Are these people equipped to do the manual labor that we're expecting them to do? And to know that medicine played an integral role there and then pulled it even further and said, not only is our job to ensure that the slaves are fit, it is a conditioning of medicine. And people say, wait a minute, it was political, it was legal, it was economic. And I say, yeah, but all those things couldn't have existed until science and medicine let the world know that we were physiologically different people, right? Segregation doesn't exist unless white people think that black people are physiologically different, that they are inferior. And where do you think they got that idea from? They got it from science. They got it from doctors. And we have the evidence to prove it. Wow, Edwin, I appreciate this conversation so much. And what I'm sort of hearing you say is that human beings, we kind of, we develop race as a way to, as part of an important mechanism to subjugate people. And that medicine plays a role in sort of providing the various rationales for that, that are sort of now proved not to be the case, but about these ideas of biological inferiority, superiority in this way and that way. And that is, you know, a piece of how, an important piece of how you understand what it is that we're talking about here in the first place. I'm going to, if I may, quickly, I want to articulate some specificity. So I wouldn't say humans. So I focus my work in the United States. In the United States, it's white folks. There haven't been black folks or there haven't been Latino folks or there haven't been indigenous folks that use the concept of race to oppress any other group in the systematic way that white folks have done here. And I think that's important because there's many white folks say, oh, well, slavery existed across the globe. Yeah, but it was never actually based on the false articulation of physiological difference based on color. It was either you lost the war, it was religious persecution, but it wasn't race. And something about the United States, they said, oh, this is the thing. This is where we can gain and manage and hold the control of marginalization and oppression. Absolutely. And I want to touch on one of the points that you've made here, which is that, you know, folks say to you, you know, if race is not biological and it's not based in physiology, then it doesn't exist. So shouldn't we sort of act like it doesn't exist? Shouldn't we sort of perform colorblindness? And the problem with that, because there are all of these, because the social construct is extremely real and the implications are extremely real. The laws are extremely real. The genocides are extremely real. The enslavement is extremely real. The segregation is extremely real. And colorblindness also erases all of that. So, not just, you know, not just will we lose some of that richness that you were talking about, but it also does harm when we're colorblind to race. Hugely. I mean, absolutely. It's a huge impact on it to the extent that colorblindness, and this is actually at the heart of critical race theory, it is to critique racial liberalism that we see no color, things are fair. If you work hard enough, you'll make it. Stop harping on race as your oppressive variable that you can't control. And I push back and I say, yeah, if we actually treated everyone equal at this moment in time, and it's exactly what you're saying, it's an erasure of all the inequality and inequity that existed before this moment. And it's the same thing we're seeing with the allocation of scarce resources during the pandemic, right? We ask questions, who gets the ventilator? Who doesn't? It's someone who has a survivability that is better than the other person. Well, if you're coming with a pre-existing respiratory disease, your survivability is lower, but no one's considering that you have a pre-existing respiratory disease because you live on the South side of Chicago with the highest rates of asthma and you come into the hospital predisposed to this because of racial segregation, redlining, and systemic racism. So unless we consider that, then we're not actually treating everyone equal. We're just furthering the disproportionate impact that occurred in the past, blinding ourselves and saying, well, my job, and doctors do this all the time. My job is to treat everyone the same, Edwin. Why would you ask me to treat them differently? I said, because you already had. Professor Kimberly Crenshaw tells us when there is a disproportionate impact that harms people, there needs to be a disproportionate impact in the solution, which means we will be treating people differently, not because of the color of their skin, thinking there's a physiological difference, but because of how this country treats people who are of a darker hue. When we hold that, then it's, yeah, some groups do deserve more. And it's not deserve more so that they get extra. It's literally to just bring them to the starting line. Yeah. Edwin, I think this is really, really powerful. And I hope we can dive a little bit more into how to rectify, how to repair, how to reconcile with the harms that we've created, you know, in American society because of how we've stratified folks by these phenotypes, you know, that were rooted in medicine's perception of biology, but are just phenotypes, are our perceptions. So I kind of want to dive into that a little bit because I think you started there. And I think it's important for our learners and listeners who are thinking as, you know, future physicians, as future providers of healthcare, but maybe don't know the history of the role medicine played. How has medicine played a key role in defining this social and political characteristic of race throughout history? You know, thinking about folks like Linnaeus, like Morton, like Cartwright, these key examples of how medicine justified the subjugation of racial groups by attributing their, you know, by attributing their race to being associated with biological inferiority. Yeah, and it's, it runs deep. Again, going back to the early 18th century, going even before that, and I won't dig too far into it, but science and religion in the early 18th century and 17th century were like cousins. You couldn't read a scientific journal that didn't mention God. And so, religion was used in the medical sphere, in the scientific sphere to publish, to say, not only is this scientifically true, but the deity God has told us that these people should be subjugated to slavery, subjugated to differential treatment.
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Their lung capacity doesn't seem to be equal to mine. Yeah, let me work someone nearly to death and then ask to get their lung capacity measurement and compare it to mine when I'm just watching them. And then it becomes this false idea that there is innate physiological difference. And I mentioned this point because guess what? That data that he published researching his slaves was then used by life insurance companies to not give life insurance to black folks post-slavery and reconstruction saying, well, you are more likely to die because of poor lung strength and capacity. And therefore we're not going to give you life insurance. We then fast forward today and Lindy Baum at Penn has written extensively about this, Professor Lind Wendy Baum, about how even to this day, we have the spirometer machines that use race as a factor in calculating respiratory function. That's wild. Let's back up a little bit more before Samuel Cartwright. You mentioned Samuel Morton. You mentioned Samuel Cartwright or Samuel Morton. And there's even Josiah Knott. But these were folks who were polygenicists, physicians who studied at Penn and Harvard and were professors who believed that people of different races were of a different origin. And that's why they, in their mind, were able to rationalize that one group was inferior versus another. And you had evolution, a concept that existed that they didn't agree with for much of the time. And Darwin was like, no, you got to believe this because the evidence shows it. And their response is, well, I don't know. I don't know if your evolutionary theory is true. But what do we know about species of a different kind? They're unable to do what? They are unable to procreate. You can't make anything if you are of a different species. Well, we see the history. You had white slave owners that were having children by women on the plantation, black women. That completely destroyed this concept. But again, they knew that. They knew it. So they were willfully making up these things to maintain the power that they had. They finally accepted Darwin and evolutionary theory and said, yes, we'll accept it. However, Europeans are still evolutionarily wise, leaps and bounds beyond black folks and native folks. They even say in published pieces that black folks and native folks are just one step above the chimpanzee in the evolutionary chain and that Europeans are at least four evolutionary chains away. And therefore, we should hold the construct and the systems that we currently have. Again, a rationalization. We fast forward into the early 1900s and you had eugenicists, you had social anthropologists that were pathologizing black folks at the ends of Reconstruction, suggesting that black people had a predisposition to crime, to violent crime. In the 1920s and 30s, when this was at the forefront, you had Nazi Germany bringing over researchers to study how we, the United States, were doing such a good job of subjugating black people that they used those tactics to do the same things to Jewish people in Germany. That's how terrible this country has been, has continued to be. And yet we don't feel, we have to still make the argument for it. I'm getting tired of having to go up to argue with people that racism is not just something that I made up, but it happens every time in 2020. And the response, well, Edwin, what about heart disease? Or what about this comorbidity? It has higher rates in black people. Yes, it has higher rates in black people because we've subjugated black people through the arms of racism and strangled a community intentionally. And then you want to talk about gaslighting and then tell them there's something wrong about you that we can't figure out. No, 100 percent. I think that everything you're talking about is the experience that a lot of us have when we're sitting in lectures and we talk about all of these disparities, whether that's hypertension, diabetes, and they give us this graph. And clearly we see Latinx, Black, and Indigenous folks who are dying disproportionately from these diseases that are preventable, but there's no context given. And it kind of makes you feel like this is inherently wrong with this group. And I think a lot of our colleagues who don't get this education, they leave thinking exactly that. So, I mean, you got into this a little bit, but I'm wondering, you know, what are some ways that this is an example of this willful knowledge that these things are happening, but then choosing to ignore it in order to really maintain power? Yeah, that's the interesting thing about the scientific method in science is that it believes that it is apolitical. But the history and the data shows us that there is nothing apolitical about medicine. It has been political since day one for the purposes of holding power, maintaining power, excluding people from the spaces of power. And I do think when you talk about science, it's the same in law. People say, oh, Edwin, I'm not racist. This is just what the law tells us we have to do. The same in science. I went through the scientific method, Edwin, and I can't be racist because I use the subjective truth. I said, but the scientific method is only as good as the variables that you input into it. And if you aren't being critical of what you're imagining, the questions you're asking, what you're researching, who you're researching, how you're doing that research, then the biases, the history, the legacies, they seep in whether you wanted them to or not. And you're speaking of your colleagues or classmates, there's always someone who's like, well, I'll play the devil's advocate here. What about hypertension? They tell us that black people's response to channel blockers versus ACE inhibitors is different. And I'm like, yeah, well, what about the data that tells us if you use a dual therapy and you add a diuretic, that that difference disappears. So clearly it's not race. It's something else that we don't know, but we don't actually want to dig into it. There is something innate in this country that it wants to hold the fundamental physiological difference. And some people say, well, it's because our minds were tribal and we want to hold differences. And that's just, it's just tribalism, Edwin. And I'm like, no, it's not. There's people around the world throughout history that have lived without subjugating other people. That exists. It's a thing. What we're talking about is the property of whiteness. And that's the second time I've used that term. So I want to explain it to folks. There's an amazing critical race theory scholar named Professor Cheryl Harris who wrote the piece called Whiteness as Property. And she outlines and explains that a property right in legal terms is an expectation. That's all it is. It's an expectation to be able to do something. So with your land, if you own land, you have the expectation to put a fence up. You have expectation to own the air rights, the soil rights, to move soil, to sell part of the land, to put a sign up, you have an expectation to do a whole lot. Now, if we place that and transpose it onto whiteness, white folks have an expectation to walk into a bank and get a loan. They have expectation to walk through a store, a corner store and not get followed. They have an expectation to not get pulled over and killed by police. They have an expectation that they can go into any neighborhood they want to. But if they have that property right, that means it's at the exclusion of someone else's right. Because when I walk into a store, I keep my hands in my pocket. When I see blue and red lights, I make sure I slow down or I try to not bring attention to myself. If I am stopped, I've been explained by my dad that you keep your hands on the wheels, you put your hands on the side of the door and roll the window down. Why is this? Because I don't have the property right that white folks expect. How do we deconstruct that white folks shouldn't have a property right? that that property right is the privilege of whiteness. And in that privilege is actually at the exclusion, at the denigration and the dehumanizing of other communities, even when they say they don't want to be doing that. But it has to start from the beginning of, I don't actually think you are physiologically different than me. Because if we can't get over that hump, then we don't actually get to solidarity. Solidarity exists because you think that my liberation is attached to yours.
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And so I struggle when people are like, oh, that's the black struggle. That's the Latino struggle. That's the native struggle. I feel that conversation, unfortunately, adheres to the construct that these are different people. Yes, there's different experiences. There's different maneuvering through the world. But solidarity means that their freedom, their justice is attached to mine. And that's why I will fight. I will fight incredibly hard for it. Edwin. Oh, man, we should have had you on the podcast, you know, right away, because I think this is this is a absolutely fundamental conversation that we're having. And the point that you're making about needing to deconstruct these false beliefs about being physiologically and biologically different as sort of being foundational to so much of the rest of what happens. And I think what I'm understanding as we're having this conversation is that actually the racism in medicine isn't just a piece of the conversation. It is in some ways at the base of the conversation and what we're doing is extremely important for that reason. I also just have to appreciate you for talking too about your own personal experience, walking through this world, walking through this society, walking through the US know, the US, because I think, sometimes, even as we get deep into these conversations, whether it's on the data side, or it's more on, you know, we're the philosophical side, sometimes it's like, I know these things to be true, because I've lived them in my own body. And I've, and you're here, you're out. And sometimes you're out here trying to explain this to folks or convince them with data. When I know this to be true through my own lived experience, not just the ways that I may not have those property rights, but also I've seen the way this social construct plays out in different people relate to me in different ways in different spaces. And from being myself, I know that I am, you know, just as much as, just as worth just from being me. So I just appreciate you bringing that in. And I also wanted to make a pitch for a book. I think there are so many, we've already mentioned many great scholars. Isabel Wilkerson has a new book cast and she references and borrows from a lot of other folks who are scholars in the area, but I really like it because it's a very personal book that talks about her walking through the world. And she talks about some of these things that you've mentioned already about how preventing interracial relationships and marriages were so key to keeping racial caste systems. She talks about some of the things you mentioned in terms of the rise of the Third Reich in Nazi Germany, borrowing from some things that are already happening in the U.S. because they were so effective at disenfranchising and subjugating people. And she actually looks to she actually looks to at caste systems in India and she looks at, at how these, at how these ideas are related and, and not related. And I, I like edge cases because they sometimes help me understand what it is that, that, that we're saying. And one of the things that she says that I think was really interesting point to me and was about the way that sometimes the success of one person can actually be important to reinforcing the fact that racism doesn't exist, right? Like look at that person, whether it's, you know, Barack Obama is probably the biggest example. There's no racism. And I think that happens too in medicine a lot, both within the conversations on racism in medical education and the conversations that we have around racial disparities. And there's also, she referenced some interesting data about how racism plays out when you switch your social context and maybe you're a person who's now living and working in a predominantly white institution or, you know, sort of environment and how racism works on and weathers the body in that way. So I just want to make it, you know, I think that's a, these are important things for us to think about. And some people have the privilege of not thinking about them. And so if you're there, I would just encourage folks to sit down and do the work and put some time into those sources that we're going to share. We're going to share so much of your work after this and also some of the other scholars that are doing some of this important thinking. Yeah, I want to highlight two points because I have this conversation and oftentimes it's white folks, many non-black folks, many Latino folks like myself who are struggling. I have colleagues that are Latino that they're like, Edwin, I get you, but I don't really get it. And so there's two things. One is to get clarity on how unuseful or useless race is in the biological endeavor of studying the physiology, is that race changes the moment I change any nation-state's boundaries. That is, if I go to South Africa, my race is different than here in the United States. If I go to the Middle East to a country, my race is different. If I go to South America, my race is different. I go from mestizo to colored to Latino to Central American to indigenous. If that is the construct of race, how is it that we're using it in science? Because even us as society don't agree that there's a universal language of race yet we're going to take data points to say that someone's kidney responds differently to a white person's kidney and use race as the holding variable now some people say well then i'll stop using race in my data no that's not what i'm saying what i'm saying is we need to be precise in the way that we use race. That is, if we're going to study race, we should understand how race has affected health by the concept of racism causing that impact. So we should be studying racism as the risk factor that is harming our communities. That's point number one. Number two is, I was hearing you, Derek, and I still remember the conversations of someone's like, well, it improved to me that what you're saying is true. And I say for a couple of years now, I've decided to say, you know what? How about you prove to me that I'm biologically different? I need you to go do the research. I want you to go dig into those papers because you're really just responding to what you heard in class. And that was like two and a half slides. And more often than not, those slides are based on up-to-date. And if you go to up-to-date and you look at those peer-reviewed journals and you dig into it, these folks have no idea what they're talking about when it comes to race. Yet we're taking racial understandings, racial understandings of humanity based on scientists that have never had to study race. And they think they know what it is they're talking about. But I asked them, how many of you have defined race in your publications? 98% of them say, no, I never have. Great have great so if you haven't defined it then how the heck we know we're talking about the same thing because there's latinos who are in the caribbean there are latinos who are in central america and south america there are black folks who are caribbean west african south african canadian like who are we talking about because you're unclear and your lack of clarity is actually going to kill people. So we need to be intensely clear in what it is that we're talking about. And so I think if someone were to say, well, what would you encourage folks to do? I say, let's assume the position that science when it comes to race has been wrong. And let's start building from there. Yeah, Edwin, I think that's so excellent. And one other observation I'd make, you're talking about how across space, geographic space, race is defined differently. I think across time, race is defined differently too. And one of the examples that I often talk about is our own U.S. census has changed our racial categories repeatedly throughout history. Every 10 years, it seems like we get a new set of boxes to put people in. And I think that's so important because it shows that race is dynamic, right? Where you are in the world, where you are in U.S. history determines maybe what your race is. And, you know, speaks again to this point that racism, the experiences that people have because of their race are the risk factors, not race itself. And the burden of proof falling on us to prove this in spite of little evidence that proves the contrary. I absolutely think your point here is very strong, that as scientists and as clinicians, we need to be clear about what exactly we're talking about when we're defining these problems. Yeah. podcast team all the time is this starts in med ed. This starts with medical education, how we teach the future physicians of our country.
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I think a lot of folks can understand this notion that structural racism and structural determinants of health that kind of lie upstream of the way social determinants are distributed, right? These risk factors that we understand for chronic diseases, that's maybe more believable for folks, right? Policy shapes the way resources that are distributed across modern society. As a result, certain groups are disadvantaged, others are advantaged. But another myth that I think is harder to debunk for some folks is, oh, what about sickle cell? What about cystic fibrosis? What about diseases that seem to be linked to race because of ancestry or because of genetics? So the question that I would ask you to maybe answer for our listeners is, is race a good proxy for ancestry? Is race a good proxy for genetics? And can we kind of conclude based on the fact that the prevalence of sickle cell is greater in black populations or the prevalence of cystic fibrosis is greater in white populations that race is linked to these diseases? That's a great question. I'll answer it simply and then I'll answer it in a more complex way. No, they're not linked. The example I always give is if we put white folks in the exact same situation that they put black folks in, they would have all the comorbidities that we're witnessing in the research. Because it's about the conditions that existed and that were created to maintain power. If it was white folks that lived in most of the continent, the African continent, heading into South India and Eastern Europe, yet they would be the ones that have the highest rates of sickle cell trait, but they're not. And the reason there's a high concentration of black folks in the United States is because we stole them. We stole people from their land and brought them here. And we concentrated the populations in this country. But there's white Eastern Europeans that have high rates of sickle cell trait. I know white individuals that I've taught who came to me and said, Edwin, I went to my primary doc when I was a child. My parents were like, there's something wrong. And we think our child has sickle cell. And the doc was like, no, he doesn't. He's white and wouldn't do the test. And so they had to find another provider. This innate belief of physiological difference is killing people, black and white and everyone in between because of the lack of precision. You're asking the question about genetics and ancestry. I think if we're going to be precise in medicine, we have to focus on geography. Where are people from? Because geography explains a whole lot. It explains the environment. It explains nutrition. It explains the weather. It explains the evolutionary process. Regardless of the race, if we're actually trying to find out what the genetic differences are. But when I start seeing journals that say, oh, black people have a greater concentration of this allele and therefore their kidney is going to respond differently. And I'm like, that doesn't even sound right. Because if it's true, then that means all black people should have that allele. If race is the variable, but if only some black people have the allele, then it's not because of race. It's something else. What is the thing that those people with the same alleles have in common? Our eyes see race. Oh, well, they seem to be black. But there must be something. Maybe they're from a similar geographic region. Maybe it was the food that was eaten. Maybe it was the genetic response like sickle cell trait, which was a genetic evolution to malaria. The malaria belt across that region I just mentioned is the reason those folks in those regions have sickle cell trait. Put the malaria belt in any other part of the world, you would see the same response. So if we detach ourselves, and I always ask the question, and I ask particularly our white colleagues, why are you so attached to try to prove that I have a different bodily function than you do? What does that bring you? Does that add any value to this relationship? Does it add value to science? Because I haven't seen the value. Because more often than not, it's a inclination to get to the point of, well, there seems to be difference in outcomes. And we have many of our colleagues, and I forgot her name. If you know it, please shout it out. But where they call it the racial disparity complex, industrial complex, where, oh, let's study all the racial disparities that exist among comorbidities. Yeah, we know they're there. I want to know the question of how do we prevent them? How do we deconstruct racism causing these disparities? But then asking, going back to asking colleagues, how does this benefit the relationship of you trying to prove that I'm physically or physiologically different than you are? And it's hard for a good response to come. Sometimes it's, well, Edwin, I'm trying to do this to better science so we can provide better healthcare to these communities. I said, if that was true, then you're not listening to the community because the community is saying, we need jobs, housing, healthcare, and the police to stop killing us. Oh, I can't control that, Edwin. That's political. Oh, that's interesting, but you want to control genetics and you want to control other variables that are, you want to control race, which is almost humanly impossible to do because it doesn't it's not something you can so going back to the genetic part you know people will publish these disparity papers oh black people indigenous people latinx folks have higher rates of x and then towards the end of the discussion it's but we't know why, so we're going to assume that it's genetic. And I'm like, is there a class that folks take that they say, if you don't know the answer, let's just assume genetics? Because I'm going to say, I'm going to disabuse us of that class and tell you, if you don't know the answer, we're going to assume racism. Because I think if we start from there, then we can actually get to an interesting place. And I know it works because I had my research colleagues in the Department of Family Medicine when I gave a talk and I said that same thing. And the vice chair came up to me and was like, Edwin, so you're telling me that if it's not genetic and it's not physiological, it's something else. And I'm like, yeah. And he's like, and we don't know what that thing is yet. And I said, I mean, we do, but yeah. He's like, and if we find that thing, we could help solve the issues of these communities. And I said, yeah. And I said, and let's assume it's racism. And he's like, okay, I got to do some work for that because I don't know how that one works. But it's the logic steps that I think we've been conditioned with. And we do have to disabuse ourself and start from a place of maybe I don't know what I'm talking about. Maybe it's a shortcut that we use as clinicians, but it affects our decision-making. So, absolutely think these are really important points, and I'll throw it to Lash for the last word. Yeah, well, I can't agree more with everything that's been said today, and I just feel so blessed to be in community with these amazing scholars and folks that we have right now, y'all. The energy is definitely here. And I think like really what it comes down to for me is I've been listening to you is the same rigor that we approach all of medical school with, right? Like we're talking about the lungs, you're going to have a pulmonologist come. If we're talking about the heart, you're going to have a cardiologist come and teach me. So when we have conversations around race, don't send faculty a one pager and then have them give this lackluster discussion or presentation about this topic when there's clearly a rigor to it that is there and folks just aren't doing their research. So we can't continue to copy and paste. We can't continue to just say, all right, we're going to use this proxy. So I really hope that that's what folks get out of this. And it can't stop with just reading how to be an anti-racist. You got to, we can't spark notes this, right? And I think that's really what it comes down to. And all of these resources that you've given us today, Edwin, are definitely things that our learners can take away from this experience in this conversation.
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Yeah, that's a good question. I'm thinking where, there's so much, but I'm thinking where to start. And I actually think we have to start at home, meaning asking your classmates, our colleagues, what have you been taught at home that is allowing you to believe these things that so many of your other colleagues are telling you are not true? I think that's one, because it starts at home. It starts with the conditioning of stereotypes and the stereotypes coming from the racial definitions created by Carl Linnaeus. Two is, you mentioned research and work. I think that work is absolutely necessary. Reading the book is, as you said, not sufficient. I would actually ask that before you read the book, you start asking questions, that you start digging into concepts of race that is so beyond you. Because it is quantum physics. In many ways, it doesn't make sense. And that was his intention. When you have something that doesn't make sense, I mean, let's think about it. Racism is the real deadly consequence of a concept that is not real. That is race. It was made up. And so I get it when people are like, well, if you just stop talking about it, it will go away. It's like, no. Y'all, if I stop talking about it, the majority of people in this country, which are white, will make sure that we know that they're white. You know, when someone's like, Edwin, can you stop talking about race? And I'm like, what race are you? They're like, I'm white. Clearly, you are beholden to your race. Clearly, you want to hold on to it. We say we want to disassociate, but folks are wholly invested, especially when it comes to power. The third is, it is the institutions. I have colleagues that are specialists, family docs throughout the departments at UW Medicine. And I ask them, especially the family docs, if someone comes to you with a fractured femur, what would you do? Well, I check everything else. I'll make sure they're all right, but they're in emergency. So I'm going to transfer them to a specialist. I'm going to get a second opinion and I will transfer them to the surgeons, the orthopedic surgeons. I said, great. Why don't you just try to do it yourself? Oh, because I wasn't trained to do that, Edwin. I was trained to have the holistic approach to care. I said, yeah, that's great. Then why do you do that with race? When we talk about race, oh yeah, I can do this. I read a book. No, I think it's now time that the institutions, our colleagues say, this may be out of my league and I need to defer to my colleagues who have been trained in this work. And last year you were talking about this. We need the second opinions, right? We need the experts to come in who may not be physicians, who may be in sociology, who may be in history. And we start building this interdisciplinary network to address these things. The fourth thing, and I may be missing the numbers, but the fourth thing I would say is we have to put racism at the center of this conversation. If you're a primary doc, if you're a surgeon, if you're any other type of physician, if you're internal med, we have to, when our patient comes to the door, I want us to be conditioned to ask the question in our mind and hopefully at some point out loud of how is racism causing the outcomes that I'm seeing before me and my patient. Every primary doc should be asking the question, have you experienced racism to our melanated communities? And if so, what support are we going to provide them? Because the data shows us from David Williams, Professor David Williams at Harvard, who tells us a black man who has a graduate degree is on average going to die four years sooner than a white man who never graduated from high school because of racism. That a black man who lives to the middle age has a level of trauma almost equal to a white man who returned from Vietnam War with PTSD because of racism. If we aren't talking about racism, then we're not actually fulfilling our mission of practicing medicine. We're only doing part of it. And I think it's now time to say, we can't keep ignoring this. This is the issue. And let's address it. Because I would be clear that if we address racism, and it's not a prescription, but collectively as a system of medicine, if we address racism, we will address the majority of comorbidities and illnesses that we see among our patients, particularly our melanoma patients. But we have to stop being scared. We have to stop being scared of doing that. I think that is a perfect place for us to end. Professor Edwin Lindo, thank you for being on the podcast with us. Thank you. This has been an honor. Y'all are amazing. Keep doing the work. Always a pleasure. All right. I think that's cut. This is cool. This is a fantastic episode. Wow. Y'all are dope. Y'all are dope.
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Hello, and welcome to a very special episode of the Lancet podcast. From the Lancet offices in London, my name is Nikolaj Humphries. On July 10, 2012, we published a new global health series on family planning. This Lancet series reviews the evidence of the effects of population and family planning on people's well-being and the environment. The series appeared ahead of the London Summit on Family Planning, hosted by the UK government on Wednesday, July 11, 2012. The summit will bring together participants from across the world to mobilise global action supporting the rights of 120 million additional women and girls to access family planning without coercion or discrimination. The Lancet series amalgamates the latest thinking underpinning these crucial deliberations, showing how lack of access to family planning carries a huge price, not only in terms of women's and children's health and survival, but also in economic terms. We will now hear audio recorded at the launch of the family planning series. To start off, Professor and Chair of the Department of Maternal and Child Health at the University of North Carolina and leader of the series, Bert Peterson. When you look at the moment we're in, it's really potentially profound. At the dawn of the 21st century, global leaders gathered and they reviewed the principles and the shared purposes of the United Nations. And they declared, based on the Charter and the Universal Declaration of Human Rights, and I'll quote this, in applying these values to the new century, our priorities must be clear. First, we must spare no effort to free our fellow men and women from the abject and dehumanizing poverty in which more than one billion of them are currently confined. Let us resolve, therefore, and then they listed the eight Millennium Development Goals. And as we all know, these eight included not only poverty reduction and global partnerships for development, but also environmental sustainability, achieving universal primary education, empowering women, promoting gender equality, as well as the health goals, maternal health, reduction of child mortality, combating HIV, malaria, and other infectious diseases. And we're here today because although there was no Millennium Development Goal for family planning, we now have extensive and truly compelling evidence for the strong link between family planning and achieving these UN goals. And we likewise have a correspondingly compelling case for meeting unmet need for contraceptive information and services. With this evidence being compiled into a series in the Lancet, the world's leading journal for mental health, this series thus becomes the scientific and technical underpinning for the summit on family planning day after tomorrow, which aims to assure that an additional 120 million women in the world's poorest countries will have access to family planning information services and supplies by 2020. So what's new here? What's new is that we have now compiled evidence from existing studies and reported on new ones that in turn make the compelling case that meeting the unmet need for contraceptive information and services will not only improve the health of women, children, and families, and you'll hear in just a moment, for example, that meeting unmet need would prevent an additional 29 to 30 percent of maternal deaths. But you'll also hear about macroeconomic effects with improvements in the well-being of communities, nations, and even for the planet itself in terms of environmental sustainability. So let us be clear. Increasing access to family planning will not by itself enable us to cross the finish line. But let's be equally clear, and the evidence you're about to hear will make it clear, that meeting the great unmet need for contraceptive information and services will help us immensely in getting there. The bottom line, this is a rebirth, this is a reposition of family planning. The authors of the key scientific and technical papers are here to briefly highlight and discuss the evidence, and I want to thank them for getting us here. Having evidence is one thing, but harnessing that evidence and creating a highly effective tool for change in global health is quite another, and the Lancet is simply the best of the best at doing that and I want to thank Richard Horton and his outstanding team for the privilege of doing this together. It truly is a team effort and I'd be remiss if I didn't acknowledge Kathy VanCardi who at the UNC made this work. And I also want to thank PAI for the work they've done to help us prepare for this and for the launch. And last, but very importantly, the financial support from the Bill and Melinda Gates Foundation and from a generous gift by Dennis and Joan Gillings to the Gillings School of Global Public Health. Thanks to all for making this possible. Thank you very much. Thanks very much indeed. So what we're going to do is go down our list of speakers. We're going to speak for no more than three minutes each to explain the key points of their paper. So let me start off with Dr. Sajid Ahmed, who is the key author for the research paper in the book that you have in front of you for coming over here and showing a kid interested women's side. We examine the number of maternal deaths averted by contraceptive use in 172 countries globally and what we found our results shows that by contraceptive abuse 272 maternal deaths were aborted in the year we examined and this implies that in the absence of the contraceptive abuse maternal deaths would be 1.8 times higher than what we see today and this implies also that 38 maternal deaths could be prevented by every 100,000 women using a contraceptive method. And when you look at the association between the contraceptive prevalence rate and the percentage reduction in the maternal mortality, we can clearly see that the higher the maternal, higher the contraceptive use rate and higher the percentage reduction. And you can see the countries with the lower contraceptive prevalence rate, mostly in the sub-Saharan African countries, also has a very little reduction in maternal rate, maternal mortality by a contraceptive use. And one of the key interests to look at, if you fulfill the unmet needs of the contraceptive abuse, there's a number of the women who are not using the contraceptive method but wants to limit their birth and wants to limit their pregnancy or postpone their pregnancy. And that shows that we have a 358 for the 2008, 358,000 mortality not dead, and that could reduce down to the 254,000 if we fulfill the unmet needs and that simply translated that additionally 104,000 maternal death could be prevented if we fulfill the unmet needs of these women and and you can see that half of almost like a 60% of that maternal death would be in South-Saharan Africa. And when you consider the South Asia, that would be additional 40,000 maternal deaths could be prevented by a contraceptive view. So the key question is how the contraceptive view is reducing maternal mortality. There are at least four pathways to which contraceptive use really reduces maternal mortality. Number one is reducing exposure to the pregnancy and its complication. And also lowering the risk of the unsafe abortion, which is responsible for almost like a 30% of the maternal deaths globally. And during the the first pregnancy in the very young women when the pelvis is still not ready for delivery. And the last one is reducing the hazards associated with the high-risk pregnancy, those are too early, too late, too many, and too close when there is a very many pregnancy in a very short period of time. So in summary, the family planning provides the primary prevention. It's from the very early beginning, it's preventing the maternal mortality and this is the first paper showing for each country level of this 120, 172 countries, the number of maternal mortality that could be prevented by the contraceptive view. And countries with the low contraceptive views, predominantly in South and South Africa and some in South East Asia, also have high maternal mortality with weak health infrastructure and consider these countries with accelerated access to the contraceptive views in these countries will provide the greatest gain in the maternal mortality reduction. And I can see that we all know the vaccination prevents the child mortality and contraception prevents the maternal mortality. Vaccination saves children and contraception saves women. Thank you. Thank you very much, Saifuddin. Let's go straight to our next speaker, who is Dr. Alex Eze, and he's going to speak to us on global population trends and policy options. Thank you, Richard. Our paper focuses on global population trends and policy options. We started by actually highlighting the current patterns that various regions of the world experience and then zeroed in on the green areas which shows populations that are currently having negative population growth. In these countries, the total fertility rate is below replacement level. And also in the high rate areas, which is largely concentrated in sub-Saharan Africa, where the rate of growth is still over 2% and nearing 3% in some of these countries. Looking at these patterns shows a number of implications for the low fertility regions of the world, which is really the increasing rapid population aging that's occurring in these countries which places unsustainable burden on public pension and health care systems in these countries as well as potentially slowing economic growth.
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Going to the policy options, one of the things we noted is the fact that in the low-fidelity regions, policy efforts have been constrained by the reluctance to interfere with individual or personal decision-making that affects childbearing within these countries. And the key policy options in these regions that have been tried include bad bonuses,, subsidized childcare, paid parental leave, among others. For the high-facility regions, the major policy options is really the implementation of voluntary family planning programs. And this has been shown to reduce fertility by about 1.5 births per woman. It will address the high levels of a for family planning, which in South-Saharan Africa is at least one in four women, and improve the lives of women and children. And we have also argued in the paper that in addition to the implementation of voluntary family planning programs, there should also be efforts at improving access to health care and education. We reached the conclusion that for the high-fatality regions, we need to go beyond the reluctance, the reluctance of dealing with issues of below replacement fatality level. And we made the argument that addressing the challenges of high-fatality and rapid population growth in poor countries, as well as low- low fertility and negative population growth in rich countries, are fundamentally consistent and we should be able to deal with both. If you look at the, for the high fertility regions, we argue that we need to maximize the benefits of family planning. We argue that family planning programs provide a win-win solution. The welfare of individual women and children is improved and national economy and environment also benefit. The point we are making here that is central to all this discuss is really the choices that women make. In the high-fidelity country, in the low-fidelity countries, the challenge is that women are not able to achieve their desired family sizes because of the cost of childbearing. And if there are policies to address those, we can actually increase fertility in these countries. In the high fertility growth and high rapid growth countries, women are not able to achieve their desired family sizes because they don't have access to family planning programs. And if we can implement those programs, it can save the lives of women. Thank you. Thank you very much indeed, Alex. Hold your questions because we'll take questions after everybody's spoken. Our next speaker is John Cleland. John is a professor here at the London School of Hygiene and Tropical Medicine and he's the lead author of the paper on contraception and health. John. I don't have a PowerPoint, I'm sorry. This paper is about a huge, but largely acknowledged and under-recognised contribution that contraception makes to the survival of women, infants and children. And Dr. Ahmed has dealt very well with the benefits for women. I just add to that that about 100,000 women a year are dying unnecessarily from pregnancies that they didn't want to have, and that is a scandal. Another little nugget, roughly 50,000 women in the developing world die of unsafe abortion, and clearly contraception has the potential to virtually eliminate those. But let me concentrate on infant and child survival which hasn't been dealt with yet. Family planning affects survival of those groups of the population largely through its potential to widen the gap between one pregnancy and another. We know from really high quality evidence from the States and from many other countries that when a woman conceives within 18 months of an earlier pregnancy termination, or live birth typically, the risks of miscarriage, stillbirth, very early death in the first week of life, low birth weight and prematurity are significantly increased. And prematurity now is one of the major causes of undefined mortality. And we know that fetal growth is a huge determinant even of our survival in the middle age. So that link between birth spacing, pregnancy spacing, foetal growth and the state of health in which the foetus emerges into this world is crucially important. And it's largely because short intervals impugn fetal growth that we know that when children are born within two years of each other, that second child is 60% more likely to die before his or her first birthday than would have been the case had the interval been between three and five years. What's not so commonly recognised is that that effect of short intervals extends into the childhood years between age one and five, such that a short birth interval of less than two years between one birth and another raises the risk of child mortality by about 40%. And what's also not realised is that in high fertility countries most children have a younger sibling to compete with. And when a child receives a younger sibling within two years, the risk of that older boy or girl dying between age one and two is raised by about 40%. So you have a, in high fertility countries where most children born have both older and younger siblings, there's a double jeopardy that hugely raises the risk of under five mortality. Indeed, it's been estimated in high fertility countries, if all births were spaced by at least two years, infant mortality in the general population would fall by 10%, and child mortality between the age of one and five would fall by 20%. Why is this evidence being neglected by medics? Even, I hate to say it, but even the Lancet series on maternal survival, on neonatal health and child survival, have largely marginalized the huge role of contraception, both for the effects on the survival of women, which Dr. Ahmed's talked about, and the effects on neonatal infant and child health that I've tried to summarize for you. I think one reason is that the evidence has been produced by people like me, demographers, non-medical scientists, and published in non-medical journals. The second reason might be that family planning is regarded by many of my colleagues in the London School, dare I say it again, as a humdrum, prosaic, not very exciting intervention. They'd rather go for the more glamorous, high-tech interventions. And thirdly, there have been no randomised controlled trials. In fact, you can't do a randomised controlled trial of the effect on health of contraception. You can't allocate 5,000 women to use contraception and prevent the other 5,000. Such is the obsession with randomised controlled trials that I think family planning has suffered from not being part of that holy grail of scientific evidence. So I endorse exactly what Bert Peterson said. It's been vastly neglected, horrendously neglected for 15 years. It ought to be one of the priority interventions for maternal health, for neonatal survival, and infant and child health. And that's what this series is arguing for. I just want to make a few final points. First of all, this series is not about population control. It is about improving choices for women through better information services around contraception and family planning. As Jane pointed out, too often the debate in the past has stalled before it's even started because it's been catched perhaps inadvertently in terms of population control. That is not what this series is about. Indeed what this series shows is by improving choices through better information for women there are health dividends, economic dividends and environmental dividends through those better choices that women are empowered to make. And finally, it's very important also to stress, and I do want to draw your attention to the comments, which we haven't talked about. There is an extraordinary degree of consensus around these messages. If you look at the comments, we have pieces written by the Office of the Prime Minister in several African countries. We've got Ministers of International Development, Ministers of Health taking part and leading this debate around family planning. At the symposium this afternoon, we will have the Minister of Health from Ethiopia joining us also to talk about the importance of contraceptive information and services for his country. So this extraordinary degree of consensus across the scientific advocacy and political communities is very important as we approach the summit on Wednesday. We're on the cusp of what is a new social movement for family planning. And family planning for the last decade or so has been so neglected, so marginalized in global health. It's been the Cinderella of global health. And this is an opportunity to correct the mistakes of the past and to put us on a sustainable direction to improving the lives of women and children, as John pointed out. Okay, thank you very much indeed. Those were the closing remarks from our Editor-in-Chief, Richard Horton, from the launch of the Family Planning series. And that also closes this episode of The Lancet Podcast. We will be back next week with more from The Lancet. Goodbye.
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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 September 12, 2017 issue. This is Howard Bauchner, Editor-in-Chief of JAMA. Starting with the original research reports, the first two are originally randomized clinical trials, and in these two reports, they both represent long-term follow-up. The first, sentinel lymph node dissection for invasive breast cancer. Sentinel lymph node dissection, SLND, is non-inferior to axillary lymph node dissection in patients with invasive breast cancer followed up for a median of 6.3 years. But there remains concern about late recurrence. Giuliani and colleagues studied 891 women who had surgery for breast cancer and found that the non-inferiority of SLND for the outcome of overall survival persisted up to 10 years. In an editorial, Livingston and Lee suggest that less than perfect clinical trials may yield evidence to improve patients' quality of life without increasing their risk of mortality. They also explore the history of sentinel lymph node dissection and how the original research report published in JAMA approximately eight years ago transformed the care of women with invasive breast cancer. The second original research report, again, a long-term follow-up study, menopausal hormone therapy and long-term mortality. Randomized trials of hormone therapy have demonstrated adverse health outcomes in women treated for five to seven years. In a long-term study of over 27,000 post-menopausal women, Manson and colleagues found that hormone therapy was not associated with increased risks of all-cause, cardiovascular, mortality after cumulative follow-up of 18 years in an editorial McNeil supports the use of hormone therapy for women with troubling vasomotor symptoms premature menopause or early onset osteoporosis it's been my long-term belief that the original hormone replacement therapy papers published in JAMA over a decade ago transformed the way in which RCTs are conceived and reported. That is, it's important to focus not necessarily on single outcomes, but often on all-cause mortality. On to the third original research report, recurrence of reflux after anti-reflux surgery. Laparoscopic fundoplication creates a mechanical barrier to prevent the reflux of gastric contents into the esophagus. Marit, Uda, and colleagues conducted a population-based study of over 2,600 patients with laparoscopic anti-reflux surgery and identified risk factors for reflux recurrence. Of the 2,655 patients, 470 patients had reflux recurrence, 393 received long-term anti-reflux medications, and 77 underwent secondary anti-reflux surgery. Risk factors for reflux recurrence included female sex hazard ratio 1.57, older age hazard ratio 1.41, and comorbidity hazard ratio 1.36. The authors conclude among patients who underwent anti-reflux surgery by laparoscopy, 17.7% experienced recurrent gastroesophageal reflux requiring long-term medication use or secondary anti-reflux surgery. In an editorial, Speckler suggests that laparoscopic anti-reflux surgery may be an appealing option for young and otherwise healthy men. And on to the last original research report, CEP inhibitors and cardiovascular risk. Cholesterol ester transfer protein, CEP inhibitors, which reduce levels of low-density lipoprotein cholesterol, LDL-C, have not been shown to reduce the risk of cardiovascular events. To better understand this counterintuitive finding, Ferencz and colleagues conducted a genetic variability analysis of over 100,000 participants and found that the clinical benefit of lowering LDL-C can be attributed to a reduction in the number of lipoprotein particles containing apolipoprotein B, ApoB. In an editorial, Snyderman and Peterson suggest that lipid hypothesis should be reframed as the lipoprotein particle hypothesis given that ApoB, a measure of the total number of circulating atherogenic particles, appears to be a better marker of cardiovascular disease risk than LDL-C. I found this original research report to be a difficult read with complicated physiology, much genetics, and even more statistics. However, the editorial by Snyderman and Peterson is enlightening. On to the clinical review and education section, and there are two shorts. The first, acute diarrheal infection in adults. Oral rehydration is recommended for all patients with acute diarrhea, but indications for antibiotic use are less clear. In this JAMA clinical guideline synopsis, Ackrey and Davis discuss a 2016 guideline of the American College of Gastroenterology that is based on the presence of dysentery or fever, severity of illness, and history of foreign travel. And the second, antiphospholipid antibodies. This JAMA diagnostic test interpretation article by Gupta and colleagues presents the case of a 39-year-old man with a swollen leg, shortness of breath two are a privilege to have in JAMA. They represent the 2017 Lasker awardees. The first is entitled Preventing Cancer and Other Diseases Caused by HPV Infection, the 2017 Lasker-DeBakey Clinical Research Award. Congratulations to the authors Doug Lowy and John Siller, both of the NIH, who've been awarded this Lasker Prize. And the second goes to Cecile Richards and Planned Parenthood Federations ofes. It's entitled Diagnostic Errors and Diagnostic Calibration. Thanks for listening. This is Howard Bauchner with JAMA. For more podcasts, visit us at jamanetworkaudio.com. you
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Hello and welcome to the Lancet podcast for the October issue of the Lancet Infectious Diseases. I'm Richard Lane and I'm joined by TLID Senior Editor Pam Daz. Pam, the topics in two of the reviews in the October issue are being discussed at ICAC, that's the Interscience Conference on Antimicrobial Agents and Chemotherapy, which is taking place in San Francisco at the moment. What are they saying? Well, the first paper is on hand hygiene and preventing healthcare-associated infections. The World Alliance for Patient Safety, which was set up last year at WHO, made hand hygiene the global patient safety challenge for 2006. Now, the authors of this paper are experts in infection control and are leading this challenge. Indeed, the lead author, Didier Peté, has led much of the work in hand washing as one of the most important measures for preventing healthcare-associated infections. Now, there's a huge amount of literature out there supporting a strong correlation between hand hygiene and reducing healthcare-acquired infections. But still, non-compliance still remains a major problem in healthcare settings. So what this paper does is sum up all the published studies on hand hygiene in preventing healthcare associated infections. I understand that this is the first time this has been done and the authors review the evidence for hand transmission and microbial organisms during patient care and propose a model which should help develop strategies for educational purposes in the healthcare setting. I do recommend looking at this review, particularly for the pictures. They're all hand-drawn by Didier Petet's son and are really quite beautiful. Thanks for that, Pam. And the other review being discussed at ICAC is about quinolone resistance. What's that about? Well, quinolone resistance is a growing problem in treating gram-negative infections worldwide. Quinolones were introduced in 1962 in the form of naladixic acid, which is a synthetic agent. And then by modifying the quinolone molecule, by adding a fluorine molecule and an additional ring structure, yielded this new class of compounds, the fluoroquinolones, in the 1980s. Over the last 20 years since their introduction, resistance to these agents by gram-negative organisms has been common and widespread. Now, for a while, the main mechanism of resistance was known to be due to chromosomal mutations, which is common amongst many of the drug classes. But more recently, studies indicate that resistance can also be transferred on plasmids carrying the gene responsible, known as QNR. So what this paper describes is the epidemiology, the origins, mechanisms of action and resistance activity of QNR. The authors do point out that plasmid-mediated quinolone resistance is not good news. There is a good chance that these resistant genes that are carried can also be co-transmitted with other resistant elements and therefore will accelerate the pace of multi-drug resistance. With that in mind, the current clinical breakpoints, these are the points which are used to predict the clinical outcome of antimicrobial treatment, should be reconsidered in the light of this new mechanism of resistance. But there does seem to be still a lot more work needed to understand these genes. Thanks, Pam. And it's great to see there's some disagreement going on in your issue this month. And this is to do with the eradication of waterborne infections. Something that's being said in a news desk is rather different to what you're saying in your Leading Edge editorial. Yes, that's right. Professor Alan Fenwick from Imperial College and director of the Schistosomiasis Control Initiative recently wrote an article in Science back in August where he expressed a view that waterborne infectious diseases could be consigned to the history books. And the reason that is, is over the years, the continual donation of drugs and other inexpensive treatments by a number of very effective global health partnerships have been able to control many waterborne and vector-borne diseases. And that by scaling up this response over the next few years, we could actually see these diseases gradually disappearing. Now, on the one hand, he's right that treatment will substantially reduce disease morbidity. I'm not doubting that. But in terms of disease transmission, this will still continue. And so what the leading edge points out is just that, that actually we're not going to be able to confine these diseases to the history books till we actually tackle the root causes of these diseases, which are poor access to safe water and basic sanitation. So indeed, a new report from WHO and UNICEF, actually it's a second of their two reports on meeting the Millennium Development Goals for water and sanitation, actually is a bit of a grim read. It does say that the world is barely on track to reducing the proportion of people without sustainable access to safe drinking water and sanitation. The Leading Edge describes a number of things that need to be done if we're going to reverse the trend and really confine those diseases to the history books. And finally, Pam, it's good to see that you've got an infectious diseases perspective on the candidates for the upcoming WHO election. Yes, one of the biggest jobs in global health. There are 13 candidates in total that will be whittled down to five by early November and then on November 9th the new Director General will be elected. So in 2ID this month what we've done is we have profiled six of the 13 candidates who have a strong infectious disease background. We don't actually say who any of our favourites are, I don't think we actually know ourselves but it's interesting to see if one of them does get it. And of course, there's going to be plenty of coverage about the upcoming WHO elections, not just in the Lancet Infectious Diseases, but in the main Lancet Journal as well. Great. Many thanks, Pam. It's a great read this month's issue, the October issue of the Lancet Infectious Diseases. See you next month.
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Today on Sharp Scratch, you'll learn whether you ever really stopped being a doctor, how normal it is to want to leave medicine, and what actually is a portfolio career. You're listening to Sharp Scratch, episode 28, Leaving Medicine. This is a podcast brought to you by the BMJ and sponsored by Medical Protection, where we talk about all the things you might want to know to be a good doctor, but that you might not necessarily learn at med school. I'm Anna, and I'm a final year medical student at King's, and I'm also the editorial scholar here at at the BMJ and I'm absolutely delighted to be joined once again by my brand new friends Lily and Oki. Would you like to introduce yourselves? Yeah hi I'm Lily, I am currently intercalating in anthropology and have done three years of medicine prior. Hello I am Oki and I'm a third year medical student from Dundee. Brilliant, lovely to have you guys not with me because obviously social distancing etc. Obviously. But you know in the same virtual space as me and I'm also really really excited that today on Sharp Scratch we'll be joined by Dr Fiona Godley who I'm sure most of our listeners will know is not just the editor-in-chief of the BMJ but the first ever female editor-in-chief of the BMJ. Would you like to introduce yourself? Hi Anna, hi Lily, hi Oki, hi everyone. Yep that's me. I'm Fiona Godley, I'm editor-in-chief of the BMJ, yes, and I have been now for just over 15 years, since 2005. We're so grateful that... You sound impressed, Aki, at that. I'm impressed. 15 years! Too long, I'll say, too long. But yeah, it's so great for us to have you with us today, Fi, and hopefully you'll be able to give us some great insights into what we're going to be talking about. But also, hopefully this will be an opportunity for you to get a little insight into what we do at Sharp Scratch. So in our last episode, we talked about how useful it can be to have experience working outside of medicine before or maybe even during medical school. Today, we're talking about something that kind of has like similar themes, but is a bit different. So we're going to be talking about leaving clinical practice or even leaving the field of healthcare altogether. And I think we all know that increasingly doctors are looking at things like portfolio careers, combining clinical work with other things and some obviously do leave medicine altogether and pursue careers in other areas so I guess a lot of people I know who are no longer in clinical practice like still work in health adjacent fields um but not everyone so Lily okay we're all still at med school have you considered leaving medicine at all like in the time you've been at medical school yeah maybe 3 000 million times yeah okay good I'm glad it's not just me I was I like so sad. But I find that really sad to hear that you feel that way. I love a lot of it. I was so sad at the beginning because as I was actually saying earlier before we started recording, I studied history during my intercalated year and I was so sad at the beginning of that year that I was going to leave after my intercalated degree and I was going to go do a history master's and become a journalist and then by the end of the year I was like oh my god I can't sit here and just like talk about things that don't have any answer anymore I need to go back to my lovely comforting answerful world of medicine um so I think it's something that like it definitely almost everyone i've spoken to has been like there's been times where i've considered leaving medicine or leaving med school um so i think it's a really like relevant thing to talk about because we know that actually not that many people do leave medicine altogether certainly in med school like the dropout rates for medicine are really good compared to other courses and the attrition rate for doctors is nowhere near as bad as other professions like teaching and nursing but it does suggest that I mean if they're here the three of you I mean I've so long ago I can't remember I think I just felt you know pretty set on medicine and didn't didn't look elsewhere certainly not during my medical school although I did do history of medicine as my intercalated so I did sort of do a slightly less medical you know more artsy intercalated degree but it makes me wonder whether medical schools are doing enough to make you feel inspired and committed and you know excited and engaged at the moment. I would say for me it's more to do with imposter syndrome thinking oh am i actually good enough to be doing this right now rather than it just being oh i see so it's more of a self-doubting than a than a medicine isn't yeah kind of thing oh that's interesting that's really interesting which is completely different i great, Dr. Oki. I can't believe you would have self-doubt. And also, self-doubt is very healthy. Everyone should have some self-doubt. Sophie, I was wondering, maybe you would like to inspire us a little bit and tell us a little bit about your career and when you left clinical medicine. Yeah, so I mean, it's funny that here I am in this job, which is not clinical medicine. And yet I feel absolutely inspired and committed to and fascinated by and embedded in medicine. I don't feel, I mean, people will say I'm deluded, but I don't feel that I left medicine in the way that someone who's gone into something completely other might have done. And certainly to do this job, you couldn't, you have to be a doctor to be this, to be in this role. And we have, you know, on the BMJ, quite a few clinicians who have become editors, some of whom are still practicing. So my route was that I come from a very medical family and I'd always, as far as I can remember, wanted to do medicine and loved it pretty much. Right the way through, I did my training in London and Cambridge and then I did my SHO, as they were, jobs and then I was a medical registrar at the Whittington which is a very busy district general hospital in in North London and got my membership at the Royal College of Physicians and but it is fair to say that I remember wondering where I would go in medicine and I didn't want to specialise I loved general medicine and at the time I was doing this which was in mid to late 80s, general medicine was disappearing as a sort of a route. Everyone was having to decide to specialise. And I think at the time, kind of casualty acute medicine was a place for people who hadn't made it in surgery. And I didn't really feel like the place to be, although I loved working in casualty. It was a fascinating place to be. and I loved the whole sort of social if that's the right word side of hospitals the buzz and the interdisciplinary and the engagement so anyway I wasn't entirely sure of my route and also I was very interested in the kind of art side of things which is you know as I did my history of medicine degree and sorry I've got a dog coming trying to get in the joys of recording from home in addition I'd always had this sense of wanting to do something with the arts and I'd done my history of medicine degree and I wanted to write and I and someone saw the job advertised for the BMJ and the BMJ had decided they wanted to get some clinicians into the team, people who were still active and a bit of a younger kind of breed and so they set up this thing called the editorial registrar scheme and I was the second of those registrars and the idea was you'd come into the BMJ for a year and then go back into medicine but as it happened Trish Groves who was the first and I was the second, Louisa Dilner was the third, Alison Tonks who's also still with us, so the whole sequence of us who came and stayed and so the scheme in that sense was a bit of a, you know, not a failure but it didn't do what it was intended to do but it did recruit a whole load of clinically trained early specialty training clinicians and Cameron Abassi who's the BMJ's executive editor my deputy is also someone who came in through that route so it's been quite an interesting sort of sequence that has happened. And how did you feel about giving up seeing patients? Because, you know, I think a lot of people like myself included, that's a huge part of the reason why I didn't leave medicine, even though I've thought about it so many times is because I love seeing patients. And it's something that actually I've noted this year. I'm not a doctor, but I've noted this year being at the BMJ, which has been amazing. But I have missed seeing patients actually quite a lot more than I thought I was going to. So what was that like? Yeah, I agree.
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And for a long time I said to people, you know, I'm a doctor, but I'm currently working as an editor. It took me about five years to stop saying that. Because a doctor is something kind of so substantial and so sort of concrete. And then I began to say I used to be a doctor and now I'm an editor. And then I stopped even bothering to say that. But the patient thing was interesting too because the joy of, it seemed to me, of clinical medicine is the sense of people coming to you at the most vulnerable and you being able to engage and help them. I mean, it sounds very cheesy, but... And also the very wide mix of people you meet through medicine, not necessarily the doctors so much, but the patients. And I really did miss that. And also the sort of physical activity of being a doctor, whereas being an editor, you're tending to sit at a desk. Oh, yeah, definitely. I have missed running around a hospital so much. I did miss all that. So there were a number of things that struck me in that first year. And when BMJ asked me to stay on for a second year and I got my register of rotation to keep the role open for me, which they did, I was sort of still thinking of going back to medicine and feeling rather bereaved of certain aspects of it. But by the time that second year had finished, I was really embedded in the journal and loved the breadth of it, the generalness of it, the academic stimulation. There was a social aspect in terms of all the different researchers and academics and clinicians you were dealing with at a distance, but still through the journal. So lots of travel, the journal allowed. Like, are your siblings still practicing? Like, did they ever make any comments about you not being a quote unquote real doctor anymore? Because I think that's something that people encounter. I was speaking to actually one of the clinical editors at the BMJ and they were saying, you know, I feel like I need to continue doing some locum shifts because otherwise all of my clinical colleagues are going to sort of think I'm not a real doctor anymore and all of this. And I just find it so interesting how much of our identities can be tied up in our professions. Yeah, I think that's true. I mean, one of the things is why does one want to be a doctor? I think, you know, when you say to people, I'm going to do medicine, they go, ooh, that's fantastic. You know, there's a kind of positive reinforcement reinforcement that goes on and so yes when you when you step away there are people who think well why would you do that what a complete you know what a waste of your training or but I think certainly for me I was the youngest of I am the youngest of four my three older siblings are all GPs so I'd already slightly taken a different route and that's one of the joys of medicine I think is that there are these very many different routes to stay within it and to contribute and be you know engaged so I went down the hospital route and did my membership and so that had set me apart a bit my dad had done I was a cancer specialist I think they sort of they kind of didn't really they they I mean they were slightly surprised I think but I think it was always like the sense that I would go back and then by the time I wasn't going to go back I was beginning to publish stuff and write stuff and so that brings you a bit of that feeling that just you know it shows people that it's real and you're actually doing something slightly useful and yeah. Lily and Oki what um if you both kind of considered leaving medicine why why did you stay like what were your pull factors like keeping you in medicine? I think a big one for me is probably pride the idea of having to tell people that yeah like what you were saying fee that I like let medicine go which is kind of seen as this like I don't know like palace I don't know I just think like when I tell people I'm a medical student they're're always like, wow, like without fail will always say something like, wow, or amazing or how or that's so hard. And the idea of losing that is like it's not the most significant thing, but it's like a big paranoia at the back of my mind, like telling my mum. But actually, in in reality I have stayed because I can't imagine doing anything else I don't know what my job as a doctor will look like I don't know if it will be look like me on the team in a hospital or as a GP or whether it becomes less than full time or public health or something like that but in reality, I can't imagine doing a job that isn't so directly useful and exciting. Yeah, I definitely get that. Because one of my friends who's a reg at the moment, he always says, if there's anything else in the world that you could do that would make you as happy as medicine, go do that instead instead. Obviously he's a bit negative. But I kind of like you Lily. I've thought about all the different careers. And I genuinely can't think of anything else. That would make me as happy. And also. Part of what I like about medicine. Is the amount of choice you have. So when people hear medicine. They think it's like quite a narrow pigeonhole that you're getting yourself into. But within medicine itself, there's so many different specialties. And then you can also do other things alongside medicine. So I quite like teaching. So as a doctor, I still get to teach. I enjoy doing research as well. As a doctor, I still get to do research. I like the clinical practice of it all. I get to do that as well. So medicine for me is just, it just ticks way too many boxes for me to leave because of not necessarily feeling good enough some days, if that makes any sense. Yeah, I definitely think the prospect of like being able to create your own career, which is like diverse and varied, that keeps me going. I think if I was looking at a trajectory of, yeah, I'm going to become a GP and do that for the rest of my life, perhaps I would struggle to motivate myself. But being like you were saying, like, oh, I could do a bit of teaching. I could do a bit of research. I could do some anthropology. Like that is exciting. And no other job allows you to do that, really. For me, there's also a bit of research I could do some anthropology like that is exciting and no other job allows you to do that really for me there's also a sense of like this maybe isn't a very nice thing to say but you know it people always tell you like how competitive it is to get into medical school and all of this and like I got into medical school like on my first attempt and I know that loads of people don't and it would just feel like I think there was always a sense of like it would be so pointless for you to give that up because someone who actually did want to go to medical school like could have had that place and you've just wasted that like I don't know I don't think that's a huge factor for me but there definitely is that guilt like and I guess when you become a doctor as well you're like oh you know the NHS has poured all this money into training me and now I'm going to give that up and not you know give back my service to to the NHS and to the people who have trained me I don't know if you agree with that Fi? Yeah no I absolutely do think that and um and and I think that's um in some in the same way that is quite it's it's a reasonable feeling isn't it to say, you know, you went to the trouble of all the work you did to get to medical school and people put their faith in you and have given you that training. I mean, but on the other hand, I would say if one had any doubt, you know, there are people who stay in medicine for the wrong reasons. But for that reason, they started doing it because their families wanted them to and they had, had you know anxieties about you know having a i don't know all sorts of of sort of reasons other than feeling they want to be a doctor themselves so i think it's important to balance that and the car it can take a lot of courage to move away from it from a from a role that you've taken on for the wrong reasons and i would applaud people who who do that you know what i mean um at the same time it's rather ironic that the thing we've we've set up at the BMJ of encouraging selected people to come um out of medicine to work on the BMJ you know we're sort of pulling we hope talented very like Anna very talented people out of medical um work stream into the BMJ but we do it because we think we are of medicine.
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Yeah. And I think that's where, I guess, Fi, you leaving clinical medicine, I suppose, may have had less of an impact on how you conceptualize your own identity in terms of the medical field, because the BMJ is so very kind of embedded into that whole world and it might be a bit different for people who leave and do something different which we're going to talk about in a little bit but what I've also found interesting is obviously at the moment the whole COVID-19 thing that's going on and all of these doctors have come out of retirement and they've fast-tracked final year medical students and i find that really interesting that even after you know you've done your service to the nhs and to your patients and you've retired people are still really really keen to come back and help when they're needed and it just makes me wonder whether you ever like actually stop being a doctor if you've trained and like become a doctor yeah it's interesting because I realize it's something we haven't perhaps looked at enough in this COVID thing period which is you know what is it is it that's led so many retired doctors to come back when we had prior to this had this sense that people were retiring early, they'd lost their mojo, they was feeling exhausted, burnout, you know, paperwork, overwork, all of that. And we talked about people, I mean, amongst my siblings, they retired pretty much bang on, you know, their 60th birthdays. And, you know, they've worked incredibly hard over the years and quite right too. And so I suppose it's really interesting. There's something about this COVID thing that re-inspires people. It's the national emergency, obviously, but it's also really acute clinical need. And also there's an element of sort of service and risk involved. I don't know. I'm really fascinated by it. And someone like Lily as an anthropologist, you could come in as a psychologist and examine this as a phenomenon. And we've also managed on the BMJ, just to give a plug for him, is to get Richard Lehman back out of retirement. Richard Lehman ran a fantastically successful column for us, looking at, you know, summarising and analysing research published in other journals. Very funny at times and critical and wonderful. But he stepped away a year or so ago. And when COVID came back, he's come back. So retirement is not you know i think there's a lot lots of ways in which people can come back into active service definitely i think it's just interesting how it seems like being a doctor like becomes so embedded into who you are and like i i already think that like as a med student maybe not so much in my first and second years but once i started seeing patients when i was in third year you know if someone asked like lily and oki if someone said to you describe who you are a medical student would be like one of the first things exactly exactly it's like one of the first things you would say and that's not to like impress people that's just because... It's just part of your identity. Yeah, it's become so much of what I have hung my identity on. I don't know whether that's healthy or not. Well, to be fair, we do spend most of our lives doing medicine. So makes sense for it to be something that um you identify with and some or something that you feel identifies you i used to think i was the anti-medic and i was like very cool until you are very cool until like my halfway ball um we had like um different categories for like um nominations for likeations. For like. Prizes and stuff. And one of the prizes was. The. Do you know. I study medicine. Prize. And I thought. No I didn't. I didn't win it. Thankfully. But. But I thought. No one would ever nominate me for this. But. Three of my friends did. And I was very shocked. And I'm like. Oh. Maybe. I am that person. So now I've decided to embrace it. Interestingly if people ask me oh what do you do I will always say I'm a student and they always say what do you study and I say medicine but it's not because it doesn't being a medical student isn't part of my identity because it absolutely is I haven't somehow escaped that but I think because it is such a strong identity it's such a strong marker people have like a real distinct sense of what a medical student is what a doctor is I really don't want people to think that I'm that person before knowing other things about me I guess um perhaps that's because I see like that image that people have in their brain as like a negative thing. I think that's part, yeah, this is something that I was going to, I wanted us to touch upon. It's like, it's kind of part of the fact that medicine as a profession, like you say, is so visible. Like it's not like doing, oh, but I can't even think, I can't even think of another job now. But you know, most people- There are no other jobs in the world. Most people, when you ask them- Alternative jobs. What they do, unless they're, you know, a doctor or a teacher or you don't have a clear sense of what their day-to-day life might be like unless you're in the same field, right? But I think because medicine as a profession is firstly so old and secondly, so visible in like the media, particularly recently, obviously, and, you know, shows like Scrubs and House and stuff have been massively, massively popular. And I think you're completely right. Like people have an idea of what that means. So you kind of get like your own identity is being sort of seen through the lens of other people who perhaps aren't exactly sure what you do but they feel like they have quite a clear sense of it from the media which is like a really weird position to be in because I completely get what you're saying like there's a reputation there and you're sort of like in so whether you want it or not yeah people have already made a decision about what type of person you are which is stressful yeah it's not it's not accidental i would i would lean away from thinking that this identity has kind of just come unsurprisingly out from medicine i would say that medicine is a field and the media and people themselves have can have deliberately idea of who a doctor is. And actually, for a lot of purposes, it's really useful for patients to think of a doctor as someone who's all-knowing, all-controlling. In a lot of cases, that's really helpful for a lot of patients. There's doctors in every single country in the world doing, you know, essentially at the basics of it, the same thing, right? So you kind of instantly have that connection and it's also a very historic profession. So we can look back on years and years of fascinating medical history and just feel like you're part of something bigger than you and I think that's what draws a lot of people to the profession yeah absolutely and I think you know if you leave it's like potentially like there are I guess there are some other professions where that's similar but I don't know medicine just seems like it it's very much its own thing like for you have more experience you know knowing people from other professions it makes me think also you know when you see politicians who have been doctors like Dr. Lim Fox and Dr. David Ernie they they continue to be um um you know seen as something in I mean a lot of a lot of politicians are lawyers aren't they or businessmen or and we don't sort of feel the need to say that all the time. So there's something additional that this confers on you. And it's a sort of assumption that there is some higher moral cause and some sort of larger, some sort of more ethical way of behaving. And that's good. That's true. I think at its best, that is absolutely true. Maybe a little bit spurious in some cases, but I agree with you. There is a sense of joining some greater good. And to leave that represents some kind of wrench or some kind of betrayal, even perhaps at its worst. Definitely. I guess the question leave medicine once you've joined the cult you can never leave well certainly the bmj we never let people leave the bmj anna so i'm afraid that's okay i'm okay with that okay cool so we're going to discuss um a slightly different situation where you might leave the health goes wrong, but we're also here to help make sure things go right too. We're the only medical defence organisation that protects doctors all over the world. From London to Brisbane, Cork to Cape Town, 300,000 members benefit from our expert advice and support throughout their career. During your years at medical school, your membership is completely free.
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And when it comes to your elective, you can trust in our international experience to protect you wherever you choose to go. It's no wonder that 90% of medical students in the UK choose to be part of medical protection. You can find out more at medicalprotection.org. Okay, back to the show. So Fi, obviously, as we've discussed, you stayed in a field that's, you know, like intimately allied to healthcare. And I think lots of people who leave clinical practice do actually stay in, you know, kind of adjacent fields. So lots of people start sort of medical companies, might work for charities that are sort of allied to health in some way. But there are some people who leave medicine entirely. So I spoke to someone who has done just that. So let's hear from them. Hi, everyone. So my name is Mayank Bhandari. I completed my medical training at UCL. I did a postgraduate qualification at the University of Cambridge and went on to do my foundation training in the East Midlands. I left medical training towards the end of FY2. So right now I work for McKinsey & Company, which is a global management consultancy firm that serves leading businesses, governments and non-governmental organisations across a range of industries and topics. So far, I've spent most of my time working for numerous global pharma companies on topics from AI and ML to marketing and sales strategies, tech and large-scale agile transformations. I've also spent a bit of time working on COVID-19 as well as with some of our private equity and transport and logistics clients. Leaving medicine is a question I get asked a lot and there's three main reasons for leaving clinical practice. So firstly, it was because I realised my excitement for healthcare was really about the potential we can make at a systemic level versus an individual patient. So having the opportunity, as I said, to work with global pharma companies, healthcare payers and providers, and NGOs has really fulfilled my desire to help at such a scale. Secondly, it was, in essence, to feed my intellectual curiosity about other industries outside of healthcare. So I'm a generalist at McKinsey, which means I'm able to work with pharma, medical products, clients within healthcare, but also across other industries like transport and logistics, consumer, banking, private equity, and so on. And that's something that I find very exciting. And thirdly, it was to really develop a robust business orientated approach to solving problems. It's a topic I've always been interested in from my time at university. I had a couple of startups and now I've really been able to throw myself in the deep end. The question around leaving the health sector, I don't really feel like I have. A lot of the work I do and my innate passion is for working on challenging problems or the ultimate aim of improving patient lives and I've had an opportunity to do that at McKinsey. I did not encounter any resistance at all to leaving clinical practice. If anything everyone was very very supportive from the get-go. It was challenging as I had over 15 interviews in the space of less than a month, but my clinical supervisor, education supervisor, that there's any kind of stigma associated with that um particularly going into something that's so different to medicine like finance or business and things like that. I actually have a friend who left medicine completely last year. So this friend was a first year at my uni and she was kind of like my daughter. And then she came to tell me, OK, I've got something to tell you. I was like, oh, what's going on? I thought something really bad was about to happen. And she said, oh, I've decided to sit my first year exams and then leave medicine. And she was really, really worried about telling me that. And I was like, why are you worried? Because I just replied, okay. And she was really confused. She thought I was going to tell her off and give her like a big lecture about it and stuff but i think it's important that she decided to that medicine wasn't for her in first year and i thought that was like a really brave thing for her to do and she's now studying geography which she's enjoying a lot more and it's what she wanted to do in the first place but her parents kind of pushed her into the medicine thing so i think it's good when people know themselves and know what's right for them and no one can tell you that apart from yourself regardless of what the prestige or whatever reason or other things that come with medicine i think that's really interesting okay and it seems to me that there's a broader sense about what education is about and what life is about, because surely there's gain in terms of the training, in terms of the experiences, in terms of the emotional development and personal development that come with being a doctor or training in medicine generally. And those assets, you know, to use that rather business term, will be transferable. You know, you will bring that experience to the next role you take on. So it's not like sort of just saying it never happened. It's saying all of that learning and training and experience is going to go into these other roles. So I think we should see it in a more positive sense than that. And it may be, who knows, that people who move into management management consultancy one of the other things medicine needs is people with good management experience and I was going to make the point earlier that there's in the portfolio that people might take on there is this additional very important role in medicine which is healthcare management and change management and those sort of things strategy that we hope many more doctors will begin to include within their kind of armamentarium of skills. Do we think it's generational? I don't have an answer to this but do you think we're seeing more I guess we're seeing portfolio careers now and as the world of every other job has changed for people to have multiple careers across their life whereas like in the olden days um people would do maybe one or two all their life that medicine is not immune to that mentality so I wonder if we're seeing that more of that now and especially as we're having more like millennial consultants and eventually we'll have Gen Z, loads of Gen Z doctors. I think we will see medicine has to shift dependent on the actual workforce. And if the workforce are a different age, a different generation, then that is what will happen. What is a portfolio career? It's where you like do, I guess, multiple different things. So, for instance, if you did like two days clinical work and two days working at a medical school and then one day doing research or something like that is a portfolio because you do like various different things. Ah, okay. I see. Right. Sorry, I should have explained that at the beginning. I've just been so like, because of all of the like BMJ stuff, people are very interested in like what their career is going to be like. So yeah, I know all of these words. I'm sorry. I should have explained that at the beginning. That's great. Sophie, what we usually like to do at the end of an episode of Sharp Scratch is to sum up our sort of top takeaways from the discussions that we've had. It's been really great to have you here with us today. So are there any sort of final thoughts on anything we've spoken about today that you'd like to leave our listeners with? It's been such a great discussion. It's really lovely to meet Lily and Oki and to talk to you, Anna. And just wanted to say to any listeners, if you want to, you know, engage with the journal, come and visit us. We really love to be, you know, involved with medical students Thank you. That's great, thank you so much Fi. Okay your second ever Sharp Scratch Sum Ups who wants to go first?
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Like Dr. House. Exactly. I think sitting in that identity and being like, actually, I am this person. I'm not just this person. I might change in the future. But actually, this is a really good identity for me to be right now may as well just go full out and get like a pretentious stethoscope with my name on it so I think my favourite thing about today has just been being able to draw you guys into all of my thoughts that I've been having about how much my identity is attached to being a medical student and how that fits with all of the other parts of my identity and to anyone who's listened to the tattoo episode you'll know that um I'm a little bit obsessed with how we form our identities and how we become parts of communities I find it really interesting so I'm sorry if you don't and I have made this another podcast that's all about that but um no I hope I hope people have found it interesting so that's all from us on sharp scratch today if you'd like to hear more from us, subscribe to Sharp Scratch wherever you get your podcasts. And in two weeks time, you'll get our next episode straight to your phone. While you wait for the next episode, check us out on social media. We're BMJ Student on Twitter, Facebook and Instagram. Let us know what you think about the podcast using the hashtag Sharp Scratch. We'd love to hear your ideas for what we should cover later in the season season it's also really helpful to us if you leave a rating and a review on apple podcasts or wherever you get your pods it helps other med students find the show until then it's goodbye from all of us you
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From the JAMA Network, this is Conversations with Dr. Bauchner, interviews featuring researchers and thinkers in healthcare about their publications in the latest issue of JAMA. Hello and welcome to Conversations with Dr. Bauchner. This is Howard Bauchner, Editor-in-Chief of JAMA, and I am joined by an old and dear friend and colleague, Howard Koh. Howard is the Harvey V. Feinberg Professor of the Practice of Public Health Leadership at the Harvard T.H. Chan School of Public Health and the Harvard Kennedy School. Welcome, Howard. Thank you so much, Howard. Before we start, I have to remind our listeners, Howard is a member of our editorial board and is one of the most decent human beings I know. But more importantly, for our listeners, Howard was my resident when I was a senior medical student at BUSM, and Howard gave me honors in medicine. And I was so proud of that honor. So Howard, for the last 30 or 40 years, I've been so grateful to you. Thanks, Howard. That's a great story. Thank you. All right. As a quick reminder, between 2009, 2014, Howard was the 14th Assistant Secretary for Health for the U.S. Department of Health and Human Services, having been nominated by President Barack Obama and confirmed by the U.S. Senate. We're here to discuss a very interesting and what may prove to be provocative viewpoint. It's entitled Sustainability, Business, and Health. Howard has two co-authors, and I'll let you first describe who they are, Howard. Sure. I had the pleasure of writing this viewpoint with Professor George Serafim of Harvard Business School and Dr. Amanda Richbeth, also of the Harvard Chan School of Public Health. I want to thank them for their collaboration. Howard, what's the basic premise of this viewpoint? Well, for a long time, the worlds of private business and public health have had a very contentious and checkered history. Everybody understands that. A lot of barriers to working together. But in a time of COVID, in particular, one sees that health and business are interdependent and are working together in ways that we've never seen before. For example, everyone knows that the safe reopening of society during COVID will require very intense interactions between the health and business sectors to keep our country healthy as we open up and get the economy going again. And in the time of COVID, we've already seen businesses stepping up in ways never imagined before. So this is a time where we need all sectors of society working together to get through this pandemic and also to promote the sustainable development goals put forward by the WHO in 2015. Now, much of the viewpoint is bound by these sustainable development goals. Can you talk a little bit about those so that people will know how you think of or see the interaction between government and business? Sure. So sustainability is a fascinating concept that's not that well understood. And when you look at the history in 1987, the UN World Commission on Environment and World Development, led by then Director General Groh Gruntland, put forward a landmark report talking about a vision of sustainable global development. In that report, they defined sustainability very simply as meeting today's needs without compromising the ability of future generations to meet their own needs. And a major theme through sustainability is focusing on the long term and not just the short term. So sustainability and sustainable global development became the foundation for the 2000 UN Millennium Development Goals for the world, the MDGs, and then in 2015, the UN Agenda for Sustainable Development, the so-called SDGs. So the SDGs really represent a global blueprint for the planet from now until 2030. They are achievable only through commitments of all sectors, and that has to include the private sector. We can't achieve these SDG goals through government and nonprofits alone. And I think, again, COVID reminds us of the importance of that theme. These sustainable development goals, they've matured over the decades because now they talk about the health of the planet, climate, poverty, working conditions, and then the greater world of cities and communities. Is it your sense that they've come to acknowledge to a greater extent the greater world in which we live in, Howard, and particularly more relevant for low and middle income countries? I think it's relevant for all of us in this country and everywhere around the planet. And what I particularly appreciate is that it respects the social determinants of health concept that everybody is starting to highlight in terms of making the world a healthier place. So the social determinants that we talk about all the time, I often define as saying that health is much more important than what happens to you in a doctor's office. It's where people live, labor, learn, play, and pray. So as you pointed out, Howard, the SDGs are highlighting the importance of healthy environments, healthy communities, the role of business, the critical role of education. We need the best interdisciplinary collaboration right now to make the world healthier. And we need the SDGs to help us get there and help us monitor progress from now until 2030. So that's the broader frame of the viewpoint. And then after that, you have different sections. And the first is the sustainability imperative, where you really begin to hone down on some of the approaches that are important for businesses. Could you talk about some of those with specifics? Sure. So given the contentious history of private business and public health, the business world is steadily realizing that they have to change the way they do business and the way they strategize about long-term goals. So for decades, their stated purpose was to appeal to shareholders only. But we all know that a focus on maximizing profits alone has driven up non-communicable disease, tobacco dependence, a major area for me throughout my career, for example, obesity, rising carbon emissions, social inequities, a whole host of challenges that everybody agrees, especially the business world, that has been driven often by a short-term focus on profits. So the result of that for business has been quite negative. There has been regular trackings of trust in CEOs worldwide for the last 20 years through the so-called Edelman Trust Barometer Report. And global public trust in CEOs is close to an all-time low. And this is not good for their long-term strategy, their long-term outcomes, and the way they are perceived by consumers and the public alike. If I can say a bit more on this one, Howard, another major theme that I learned through my business colleagues like Professor Serafin is that over the last 20 years, businesses have been increasingly reporting on their non-financial outcomes having to do with environment, social, and governance indicators, what are called ESGs. And so if you look worldwide, more and more companies are reporting on their ESG metrics and investors are looking at this as a way of judging whether they want to support companies that are having a positive social impact or not. So all those forces are coming into play. And that gets me to the major point put forward by my colleague, Professor John Quelch of the University of Miami, who points out that every business is a health business, whether they realize it or not. They impact the health of their employees, their consumers, their community, and the environment. So lately, more enlightened CEOs are taking that long-term sustainability approach going forward. Now, this is where I suspect some listeners will go, really? So let's talk about something that is so tangible. And you and I went back and forth with this viewpoint. I and Phil, who edit every viewpoint, had the same reaction, really. So let's focus in part on the United States because it's easier and I think people will understand the focus. Income disparity is remarkable in the U.S. Every metric indicates it's gotten phenomenally larger between the 0.1% or the 1% and the other 99% or the top 20% and the lower 80%. This is epitomized by CEO salaries. Why is it that companies who are so committed or theoretically committed to this simply don't raise the minimum wage? Yeah. So making changes for business by CEOs to move toward a more sustainable strategy that helps employees, consumers, community, and the environment are issues that can help them in terms of their trust levels, raising trust levels that are too low right now, as we just mentioned. It also helps for brand loyalty. It also helps support employees and retain them. And also consumers are having rising expectations for business. They are willing to pay more for products that are made by businesses promoting sustainability. And in fact, millennials and the younger generation is demanding this more and more. So businesses are following these pressures and responding to them in many ways. Now, with respect to your specific question about pay inequality, which is a hugely important issue and not an easy one, we are seeing some companies supporting efforts to raise the federal minimum wage beyond $7.25 an hour.
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And then more broadly, Howard, last summer in an announcement that got a lot of attention, the U.S. Business Roundtable, that's about 180 CEOs of the largest companies in the U.S., updated their statement of corporate purpose, saying that appealing to shareholders shouldn't be their only focus, but more broadly, they should be appealing to all stakeholders, to consumers, to suppliers, to community groups. And so that announcement has been met with mixed reactions. Some are enthused. Others are highly skeptical. We will have to see what the outcomes are. But the good news, I think, Howard, is that these issues are now on the table for debate. And COVID has accelerated the attention to how private business and public health can and should work together. Yeah, I think having them on the table for debate, I'm always struck just by, you know, let's just talk about coffee. So I often stop at Dunkin' Donuts for coffee. It's pretty inexpensive. I like a donut. I'm not a big fan of Starbucks, but it's a pretty good payer. It's my understanding it's a pretty good employer. People are willing to pay a little more because, you know, you're paying the person who's serving you the coffee a little more. But my understanding is it's a pretty good employer. So I think you're right. Some people have made a choice to be willing to pay a little more to know that the person working or waiting on them is getting a living wage. The other area that you mentioned under the sustainability imperative is around climate crisis. And I think there's no doubt left that there is a climate crisis. And for the people who still are somewhat disbelieving about it, I always comment, why would you risk being wrong? Being wrong threatens the future of the planet and the lives of your loved ones and potentially your children. So could you talk a bit about the climate crisis and how you see business interacting with that? Sure. I think the business world, in fact, I know the business world is paying very close attention to this. They also increasingly recognize that the climate crisis threatens their own business viability. So we're seeing, for example, sectors like the auto industry, all the major U.S. automakers moving steadily toward electric vehicles, not just Tesla, Ford and BMW and Honda and others. They've been pushed to make more fuel-efficient cars by the Obama administration. And then we've seen sustainability strategies within business that have pushed companies to get more of their energy from renewable sources and recycle non-hazardous waste at high levels. So business recognizes this and they're getting on the train. They know it's the future. Howard, the second section of the viewpoint is entitled Aligning Reporting Metrics and Investment. Now here you talk about metrics, how to hold people accountable. So could you work your way through what you've written in the viewpoint in this section? business and public health to work closer together, metrics have to be aligned and put out in easy to understand reports that appeal to investors who want to make money, but also appeal to the public health community that wants to see businesses doing their work in a socially conscious way. So he has pushed for in his research what are called impact weighted accounts. Now, we all know that businesses for a long time have been required to put forward standard profit and loss statements. And then I mentioned that they also report or last several decades, non-financial ESG metrics on environment, social and governance indicators. But to put them all together has been very difficult for somebody trying to get a quick and easy understanding of this. So through integrated reporting and so-called impact-weighted accounts that Professor Serafim has helped pioneer, there are now some early attempts to put all this information in apples-to-apples comparisons, make it quantitative, give companies credit when they are using their efforts to improve public health outcomes, dock them if their outcomes are hurting public health. And you can apply these metrics to all sorts of areas in terms of climate impact and community impact. One example that George has taught me is that for companies who really advocate to protect their employees through stress management or better access to nutrition, for example, at the work site, those efforts should be counted as positive aspects of the financial ledger, not negative aspects. So Professor Serafim and his colleagues are working on creating such integrated reports that could appeal to both a business audience and a health audience. Howard, why should a CEO buy in? They still are responsive or responsible to their stockholders. Those people want to see good return on their investment. And sometimes good return on their investment isn't so good for health. Right. So this is where the sustainability theme is major because the enlightened CEOs now know that they have to be effective, not just in the short term, but also the long term. That's what sustainability is all about. And also what's been fascinating about getting involved in this work, Howard, is learning from business professors like Mark Kramer and Professor Porter at Harvard Business School, saying that this might be a new strategy for CEOs that have to do with what they call shared value. In the past, when a business helped out a community, it was often viewed as simple philanthropy or more recently, corporate social responsibility. But according to Porter and Kramer, enlightened CEOs that promote sustainability strategies are really pushing for having positive social impacts as well as having their companies do well financially. So it's helping promote value on the business side as well as the social side. So that theme is catching hold. We see a number of organizations that have rallied around that, especially after the Business Roundtable announcement last year. So we have to watch this carefully and see how much this is going to impact the world of business and health going forward. Now, Howard, I know you well. We've been friends for a long time. I mean, you've had a four-decade commitment to public health. I don't think anyone would ever question your credentials. Do you think this can really work, Howard, or is it a bit of a pie in the sky and wishful thinking? Well, let's put it this way, Howard. We can't reach the SDGs through reliance on the health sector alone. We need more interdisciplinary efforts where all sectors of society get involved, especially in a time of COVID. To ignore the business sector is ignoring a huge part of daily life right now. We're witnessing the impact on business through this terrible health pandemic. So in my view, the only way we can make a healthier world is bring in colleagues and create non-traditional partners in housing and education and transportation and faith-based organizations. And yes, the world of business And that last sector, Howard, and we've talked about this a lot, is not easy to work with given the checkered history that we've encountered so far. But with sustainability, the SDGs, the ESGs, the forces on CEOs to change given their dropping public trust, and then the public support of companies who do the right thing. I mean, here I am, Howard, you know me well. I started my public health career as a tobacco control advocate. That's still probably my number one passion in the world of public health. So we saw in 2014 where CVS announced they were stopping selling tobacco. No one forced them to do that. They saw that as the right business decision, and it's been met with tremendous positive response. And if anything, their business has gone up since making that decision. So we need more business leaders to step up that way and make an impact on public health in as innovative ways as possible. It's interesting. I was talking to someone over the weekend, one of our associate editors, about the remarkable protests of the last 10 days, about the tragic history of slavery and racism in the United States. And he commented that what seemed so different to him was the multitude of people who were protesting, people of color, but people who were white, that it felt different. And he felt that that grew out of kind of a change in the educational system, that over the last two or three decades, our children have learned about these issues, and that it was manifest in these protests over the last 10 days. In some regards, I see an analogy to saying to businesses, it's got to be different. Absolutely. The enlightened CEO, they want to do work so that whenever they end their careers, they can look back and say, all right, I was able to be successful in the classic business way, but I made a difference in the world too. And we're seeing more examples of CEOs talking about these broad global themes and trying to align their companies to help promote the health of employees, consumers, communities, and the environment. None of this is easy. For every example that we cite, you can talk about many that go the other way. That's the way it's always been.
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Do this together. I'm hoping we can have a healthier society in the future. One last question, Howard. You worked in government for five years. Government has many levers. We've certainly seen they can spend money and then they make law. You were the Assistant Secretary of Health for U.S. Department of Health and Human Services from 2009 to 2014. How does government create the appropriate environment for business so that it's actually easier for business to think of sustainability? What's the role of government in this triangle between the public, government, and business? People have heard about the concept of public-private partnerships for a long, long time. But again, Howard, if we look at COVID alone, look at how all society and government had to rely on the private sector to get us through this initial phase of COVID. We had garment companies making face masks and other PPE. We had alcohol distilleries shifting production to make hand sanitizers. In a very well-publicized move, we had automobile companies working with ventilator industries to make more ventilators. And then a lot of attention to whether leading businesses were treating customers humanely through this crisis, deferring bill payments or expanding paid sick leave. So there is no doubt, especially in a crisis like this, that health and business are interdependent. We have to work together. And so if we can figure out ways that we can promote what's called a culture of health as the way everybody does business around here, that's what culture means, I'm really hoping that this could be an example of innovative partnerships for the future. I interviewed Mike Levitt, former governor of Utah, and then Don Berwick, and both of them commented that they didn't know, but they were thinking that this event was so traumatic, has created so much tumult in the world that there could be fundamental change afterwards. They weren't sure. Someone has written for us and will be published this week, a pandemic, 30 million to 40 million unemployed, and nationwide protests about racism. Each one of those would have been a remarkable year, but you've had all three in one year. What's your sense of how the pandemic could influence business? Well, we have seen so visibly in such a painful way the state of inequities in our society. And Howard, you know I'm a son of an immigrant family, so disparities and equity and rights has been a very important theme in my life personally and professionally. So in a time of crisis like this, where we need people to work together to promote health, and then we need to respond to the stark racial injustice that everybody has seen for themselves. We have to use this crisis as a way of doing better in the future. Addressing these issues are really making public health a reality for all people. You know, the WHO talks about the enjoyment of the highest attainable standard of health as one of the fundamental rights of every human being. I love that quote. I think about it almost every day. And Martin Luther King also said that he wanted all people to enjoy what he called the sunlight of opportunity. I love that quote too. And I think about that almost every day. So here's a time through the health crisis of our lives where people need to have opportunities for health equity, to enjoy the sunlight of opportunity, to reach the highest attainable standard of health. And in my view, the only way we can do it is to get beyond our health silo and work with other parts of society and really tackle the social determinants of health straight on. And I would like to think that this viewpoint with George Serafin and Amanda Richmuth was an opportunity to put that theme forward. This is Howard Bauchner, Editor-in-Chief of JAMA. I've been speaking to a colleague, a friend, a member of our editorial board, Howard Koh. Howard's the Harvey V. Feinberg Professor of the Practice of Public Health Leadership at the Harvard T.H. Chan School of Public Health, one of the preeminent thinkers in public health in the United States and around the world, with a four-decade commitment to improving the health of people in the United States. He's written a viewpoint for us entitled Sustainability, Business, and Health. Howard, thanks so much for joining me today. Howard, what a privilege. It's so great to work with you. And thank you so much for having me on. And for our listeners, for more podcasts, please visit us at jamanetworkaudio.com. You can subscribe and listen wherever you get your podcasts. Thanks so much and please stay healthy.
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Hello, and welcome to this author interview from the JAMA Network. This is Deanna Balandi with JAMA Internal Medicine. Historically, guidelines for screening and management of cervical cancer were simple and clear. But new guidelines have been issued, and some are wondering if they are too complicated. Here to talk about the complexities are Dr. Karen Smith-McCune of the University of California, San Francisco, and Dr. Sarah Feldman of the Harvard Medical School, Boston. Both have written viewpoints on the subject for JAMA Internal Medicine. Welcome, Drs. Smith-McCune and Feldman. Thank you. So tell me, Dr. Smith-McCune, could you describe the old guidelines and the recent changes for me? The new guidelines were developed in response to the fact that we've been able to really understand the role of human papillomavirus in the development of cervical cancer. And the guidelines were updated to incorporate HPV testing in cervical cancer screening. So in the new guidelines, we have the option of doing a pap with an HPV test. It's called co-testing for cervical cancer screening in women between the ages of 30 and 65. The new guidelines also are very clear about increasing the interval for any of the screening tests. So the interval for co-testing would be every five years, and this is a big change over the traditional annual pap test that we've all become very used to. The guidelines both recommend that if you're only going to do a pap test without the co-test, that shouldn't be done more often than every three years. And if you're going to do the co-test, you should do it every five years. So these represent significant changes in the periodicity of screening that are intended to acknowledge that doing these tests too often can be associated with harmful outcomes. So Dr. Feldman, what are some of the issues with the new guidelines? So to clarify, a program of prevention of cervical cancer includes both a set of guidelines for screening, which is evaluating asymptomatic women to see whether or not they're at risk for a particular illness, and then a separate set of guidelines, which are interventions to manage or evaluate women who've had abnormal tests. And so the screening guidelines are actually based on very, very good data, although they do suggest that there are several alternatives for screening that can be applied differently to different women depending on their setting, the availability of co-testing or pap alone, as well as their age and a number of other issues. And those screening guidelines are actually very good. And we know that if women test negative by whichever choice appropriate screening method is chosen as according to the guidelines, then they are probably pretty much low risk for cervical cancer as long as they're screened adequately and continue on the regimen recommended. On the other hand, patients who have abnormalities either of the HPV test or of the PAP test, sometimes it's much less clear what the appropriate next steps are. And so the second set of guidelines, which are management guidelines, attempt to try and tell clinicians what to do in the setting of abnormal PAPs or abnormal HPV tests. However, the data is much less clear, and the particular risk of any individual woman is much less clear once she's had some abnormalities. So the concern about the new guidelines, the management guidelines, is that they are often confusing for clinicians. They don't always clearly tell a clinician or a patient what their underlying risk is, which is conditional upon prior testing. So in other words, if a test has been abnormal in the past, it may affect the implications of a current test. If a patient's had abnormal HPV, that may have different implications than abnormal PAPs. And some of that is just not clear and very, very confusing to people in the community when they try and implement the management of abnormalities. So, Dr. Smith-McCune, what are the issues with the guidelines and the ability for physicians to implement them consistently? The problem comes from the availability of co-testing. When we did the PAP test alone, we had a very clear set of results that we've come to understand over 50 years of use. Now with co-testing, we have a new algorithm or a grid of results that can be quite complicated with two tests having the potential for several results. And that is what makes management algorithms very complicated. In my article, I actually address whether co-testing should be a preferred strategy. One of the guideline committees made that designation, and that tends to make clinicians want to adopt it because it seems to be the better one. But my issue with that designation is that it was actually based on weak evidence. It was considered a weak recommendation by the Guideline Committee itself. And this means that there's a lot of uncertainty surrounding the balance of benefits and harms and that decisions should be based largely on individual preferences and values. And this gets to clinicians' preferences and values. Once they see the guidelines for how to manage a woman who has an abnormal co-test result, they may choose to not go down that route at all and to stick with the pap alone every three years as a preferred option. So, Dr. Feldman, what are physicians supposed to do about it? Well, I think there are two options of what physicians can do. I mean, certainly one is to go and follow the management algorithms, which are complex, although there is an app that can be used to apply them. A simpler way of thinking about the new management guidelines are three things. First of all, I think there does need to be a lot greater transparency about the strength of the evidence for any particular choice. And I completely agree with Dr. Smith-McCune that there are many variables that come into deciding what's the right test in a particular situation. And they include everything from the strength of the particular evidence, the tests that are chosen, the patient's clinical history, her preference for frequency of testing, the physician's preference and ability to do the counseling and follow-up, and all these different issues. But one way that I think of simplifying it is that women who are appropriately screened starting at the age of 21, every three years with a PAP till age 30, should then elect with their provider to go either with a PAP every three years or co-test every five years, assuming all the results are normal. And they should continue with that pattern up to age 65 or so if all results are normal and their screening has been adequate. And that's, I think, been demonstrated in many studies to be a very good approach to screening, one of those two choices. There's a lot of evidence. However, my own thought is that if a patient has an abnormality or a distant history of abnormality, such as they tell you, you know, five years ago, I was treated with a loop. I don't know what for. So you know, probably they had some HPV infection at that point. You have to presume that. Then you start to think of them as a higher risk group. So people with a history of abnormals, people who have a currently abnormal set of test results, people with an uncertain history or inadequate screening, all of these people suddenly become, as much as we can tell from a variety of evidence, a higher risk group. That is higher than the completely asymptomatic low-risk screening group with all normal screens, according to the 2012 guidelines. And that higher risk group, I propose that we go with a simpler algorithm for follow-up once those people are appropriately managed and evaluated and then triaged according to their pathology results, which are really a better determinant of how high-risk or low-risk they are, to treatment or to close follow-up, whatever is appropriate. And then once they go back to the normal bucket group, I actually would suggest that until we have more information on primary HPV as a test, that we go to annual PAP screening for people who've been treated for high-risk abnormalities and are now back into the bucket of follow-up. Those people remain at higher risk than the completely negative group, and I'm suggesting that we just go with annual PAPs on those until we have more evidence and more clarity about the implications of an HPV test in that setting. How do you both feel about what, if anything, should be done about the new guidelines to simplify them? Well, I think that the guidelines for screening are simple with the one exception of the word preferred, which I agree should be omitted. But I think they're pretty simple. All women, regardless of sexual activity, should start at 21 every three years until 30, and at 30 have the option of every three years with Papillon or co-testing every five. So that's a pretty simple algorithm for primary screening. And I think that is simple. It's the management. And like I said, I think that we should think of women as either low risk, all negative screening, all adequate screening, or high risk, everybody else, inadequate screening or abnormal test results or unknown history. And those people I think of as higher risk.
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And similar to Dr. Smith-McCune, I think there should be options. I don't think it's a one-size-fits-all. I think we have to be considering some people will be PAP, some people will be HPV testing. I don't know. It's going to be different for different, and we should have a variety of options available. I like your idea about not repeating an HPV test on somebody who's shown to be high risk. We have done pretty well in monitoring that group and preventing them from getting cervical cancer in the age before HPV testing. And adding an HPV test to that group on top of an annual PAP does create a lot of anxiety in the patient's mind. If their PAP is normal, but they still have HPV, they get worried, the clinicians can get worried and start to do things that could be harmful. Thank you, Drs. Smith-McCune and Feldman for talking to us about your work. This is Deanna Balandi with JAMA Internal Medicine. For more podcasts, please visit us online at jamainternalmedicine.com.
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Welcome. This is the New England Journal of Medicine. I'm Dr. Michael Bierer. This week, March 19, 2020, we feature articles on discectomy or conservative care for sciatica, no sedation or light sedation in ventilated ICU patients, long-acting therapy to maintain HIV-1 suppression, and a screening program to eliminate hepatitis C in Egypt, a review article on hereditary angioedema, a case report of a man Thank you. forces, on opioid prescribing in the midst of crisis, and on the dishonesty of informed consent rituals. For more information on the ongoing coronavirus epidemic, including audio updates from NEJM Editor-in-Chief Eric Rubin and Deputy Editor Lindsay Baden, visit the COVID-19 Resource Center at nejm.org slash coronavirus. The treatment of chronic sciatica caused by herniation of a lumbar disc has not been well studied in comparison with acute disc herniation. In this single-center trial, 128 patients with sciatica that had lasted for 4 to 12 months and lumbar disc herniation at the L4, L5, or L5S1 level were randomly assigned to undergo microdiscectomy or to receive six months of standardized nonoperative care followed by surgery if needed. Among the patients assigned to undergo surgery, the median time from randomization to surgery was 3.1 weeks. Of the 64 patients in the non-surgical group, 34% crossed over to undergo surgery at a median of 11 months after enrollment. At baseline, the mean score for leg pain intensity was 7.7 in the surgical group and 8.0 in the non-surgical group. The primary outcome of the leg pain intensity score at 6 months was 2.8 in the surgical group and 5.2 in the non-surgical group. Secondary outcomes, including the score on the Owestree Disability Index and pain at 12 months, were in the same direction as the primary outcome. Nine patients had adverse events associated with surgery, and one patient underwent repeat surgery for recurrent disc herniation. In this single-center trial, involving patients with sciatica lasting more than four months and caused by lumbar disc herniation, microdiscectomy was superior to non-surgical care with respect to pain intensity at six months of follow-up. Andrew Schoenfeld from Brigham and Women's Hospital, Boston, writes in an editorial that discectomy was superior to non-operative care for the primary outcome of leg pain intensity at six months after enrollment. These findings may result from the fact that surgical intervention allowed for more rapid decompression of the compressed nerve root. Patients in the current trial who were assigned to undergo surgery received the intervention relatively quickly at a median of three weeks, and it is reasonable to conclude that expeditious removal of the nerve compression minimized the potential for long-term persistence of pain. In patients with disc herniation and persistent sciatica lasting four months or longer, it has been the editorialist's practice to provide information about the association between symptom duration and outcomes and to offer a decision regarding surgical or non-surgical treatment on the basis of the patient's preference. If the patient has no benefit from an appropriate course of non-operative care, they make a stronger recommendation for surgery. Viewed in this light, it is encouraging that the trial reported by Bailey and colleagues shows that surgical intervention still results in clinically meaningful improvement in patients with persistent sciatica. However, the trial does not help clinicians determine which patients are most likely to benefit from immediate surgical intervention or the duration of nonoperative care that is acceptable before surgery is recommended. Non-sedation or light sedation in critically ill mechanically ventilated patients by Henne Olsen from the Odense University Hospital, Svenborg Hospital, Denmark. In critically ill mechanically ventilated patients, daily interruption of sedation has been shown to reduce the time on ventilation and the length of stay in the ICU. In this randomized trial, 700 mechanically ventilated ICU patients were assigned to a plan of no sedation or to a plan of light sedation, that is, to a level at which the patient was arousable, defined as a score of minus 2 to minus 3 on the Richmond Agitation and Sedation Scale, RAS, with daily interruption. The mean RAS score in the non-sedation group increased from minus 1.3 on day 1 to minus 0.8 on day 7, and in the sedation group from minus 2.3 on day 1 to minus 1.8 on day 7. Mortality at 90 days was 42.4% in the non-sedation group and 37% in the sedated group, difference 5.4 percentage points. The number of ICU-free days and of ventilator-free days did not differ significantly between the trial groups. The patients in the non-sedation group had a median of 27 days free from coma or delirium, and those in the sedation group had a median of 26 days free from coma or delirium. A major thromboembolic event occurred in 0.3% of patients in the non-sedation group and in 2.8% of patients in the sedation group. Among mechanically ventilated ICU patients, mortality at 90 days did not differ significantly between those assigned to a plan of no sedation and those assigned to a plan of light sedation with daily interruption. In an editorial, Claudeérin from the Hôpital Édouard-Hériault-Lyon, France, writes that in adult patients admitted to the ICU. Sedation and analgesia are provided at the time of intubation and may be maintained for hours or days. The aim of sedation is to minimize oxygen consumption and facilitate a patient's ability to remain comfortably connected to a ventilator. Over the past two decades, it has been recognized that prolonged and deep sedation can increase the duration of mechanical ventilation, delay weaning, impair neuromuscular function, produce delirium, and have side effects specific to certain sedative drugs, such as prolongation of their effect after discontinuation because of pharmacokinetic changes. However, omitting sedation for mechanical ventilation is complicated by the reluctance of caregivers to nurse patients who are agitated or in pain. Intensivists have been attempting to define clinical situations in which the maintenance of deep sedation may be required and those in which a reduction of the level of sedation may be allowed. The results from the trial by Olson and colleagues are important because they arouse concern about omitting sedation in mechanically ventilated patients and reinforce the need to monitor sedation clinically with the aim of discontinuing it as early as possible or at least interrupting it daily. Such monitoring should be performed continuously, 24 hours per day, every day, on the basis of Nebraska Medical Center, Omaha. Simplified regimens for the treatment of HIV type 1 infection may increase patient satisfaction and facilitate adherence. In the Phase 3 ATLAS trial involving patients who had had plasma HIV-1 RNA levels of less than 50 copies per milliliter for at least six months while taking standard oral antiretroviral therapy, 616 participants were randomly assigned to either continue their oral therapy or switch to monthly intramuscular injections of long-acting cabotegravir, an HIV-1 integrase strand transfer inhibitor, and long-acting rilpivirine, a non-nucleoside reverse transcriptase inhibitor. At week 48, HIV-1 RNA levels of 50 copies per milliliter or higher were found in 1.6% of participants receiving long-acting therapy and in 1% receiving oral therapy, a result that met the criterion for non-inferiority for the primary endpoint. An HIV-1 RNA level of less than 50 copies per milliliter at week 48 was found in 92.5% of participants receiving long-acting therapy and in 95.5% of those receiving oral therapy, a result that met the criterion for non-inferiority for this endpoint. Virologic failure was confirmed in three participants who received long-acting therapy and four participants who received oral therapy. Adverse events were more common in the long-acting therapy group and included injection site pain, which occurred in 75% of recipients of long-acting therapy and was mild or moderate in most cases. 1% withdrew because of this event. Serious adverse events were reported in no more than 5% of participants in each group. Monthly injections of long-acting cabotegravir and rilpivirine were non-inferior to standard oral therapy for maintaining HIV-1 suppression. Injection-related adverse events were common but only infrequently led to medication withdrawal. Long-Acting Cabotegravir and Rilpivirine After Oral Induction for HIV-1 Infection by Chloe Orkin from Queen Mary University of London.
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At week 48, an HIV-1 RNA level of 50 copies per milliliter or higher was found in 2.1% of participants who received long-acting therapy and in 2.5% who received oral therapy, a result that met the criterion for non-inferiority for the primary endpoint. An HIV-1 RNA level of less than 50 copies per milliliter at week 48 was found in 93.6% who received long-acting therapy and in 93.3% who received oral therapy, a result that met the criterion for non-inferiority for this endpoint. Of the participants who received long-acting therapy, 86% reported injection site reactions, grade 3 or higher adverse events, and events that met liver-related stopping criteria occurred in 11% and 2% respectively who received long-acting therapy and in 4% and 1% who received oral therapy. Treatment satisfaction increased after participants switched to long-acting therapy. 91% preferred long-acting therapy at week 48. Therapy with long-acting cabotegravir plus rilpivirine was non-inferior to oral therapy with dolutegravir, abacavir, lamivudine with regard to maintaining HIV-1 suppression. Injection site reactions were common. Judith Currier from the UCLA Medical Center, Los Angeles, writes in an editorial that the monthly injectable treatment was non-inferior to continued daily oral treatment, and participants in both trials clearly preferred monthly injections over daily oral therapy. When approved by regulators, this major advance in treating HIV infection will provide a new option for a select group of patients who currently have viral suppression while taking ART and represents the first step toward making less frequent dosing of ART a reality. For many, freedom from the need for daily oral therapy is a major advance, even at the cost of having to receive monthly injections. That said, the overall effect that this new treatment approach has on the HIV epidemic will depend on our ability to address a few associated questions and challenges. Currently, most people living with HIV who are in care are seen in a clinic for monitoring every six months. Requiring monthly visits for injections will be challenging for busy HIV clinics. Plans to carefully monitor resistance as this treatment is rolled out will be needed. Long-acting injectable treatment has the potential to be a major advance in the treatment of HIV infection during pregnancy and in the postpartum period, as well as for children and adolescents, including those in low-resource settings. However, to date, studies involving these populations are lacking. The ATLAS and FLAIR trials are important milestones in the development of HIV therapeutics and represent major steps into the era of long-acting ART. Version 1.0 of long-acting ART holds promise for the millions of people living with HIV if we make addressing the challenges involved a priority. Hereditary Angioedema, a review article by Paula Busey from Icahn School of Medicine at Mount Sinai, New York. Hereditary angioedema is a rare, potentially life-threatening genetic disease that may include recurrent attacks of cutaneous angioedema, severe abdominal pain, and airway compromise. Over the past 40 years, scientific investigations have identified the fundamental defect of hereditary angioedema as a deficiency of functional C1 inhibitor protein, a protease inhibitor in the serpin superfamily, and have established that bradykinin is the biologic mediator of swelling. In 2000, hereditary angioedema with normal C1 inhibitor levels was described, for which molecular mechanisms are emerging. Despite progress in unraveling the pathophysiology of hereditary angioedema, a delay in proper diagnosis and a paucity of effective therapeutic approaches have hampered effective management of the disease until recently. Advances envisioned in 2008, however, have now been realized, with insights from basic research translated into novel therapies. Prophylaxis and treatment include C1 inhibitor replacement and inhibition of the calocrine and bradykinin pathways. This article reviews the progress made during the past decade in elucidating the pathophysiological mechanisms of hereditary angioedema and the subsequent development of targeted treatments for the disorder, with anticipated reductions in morbidity and mortality and an improved quality of life. A clinical vignette illustrates the profound effect of these treatments. A 64-year-old man with shortness of breath, cough, and hypoxemia, a case record of the Massachusetts General Hospital by Kerry Reynolds and colleagues. A 64-year-old man with a history of melanoma presented for evaluation of a mass in the left frontal and left parietal lobes. Four weeks earlier, the patient began to have clumsiness of the right upper arm as well as difficulty writing his name, holding a toothbrush, and coordinating activities with his right hand. MRI of the head showed focal hyperintensity in the left frontal lobe, which corresponded to a ring-enhancing lesion surrounded by edema. CT of the chest, abdomen, and pelvis revealed a solid, non-calcified nodule in the right upper lung that measured 2.2 centimeters in diameter. Metastatic melanoma was diagnosed, and the treatment included combination treatment with the immune checkpoint inhibitors ipilimumab and nivolumab. Fevers, dyspnea, and cough developed, and the patient presented to the emergency department. The oxygen saturation was 48% while the patient was breathing ambient air. CT of the chest showed bilateral airspace opacities. This patient's severe hypoxemia and diffuse inflammation of the lung were consistent with pneumonitis induced by immune checkpoint inhibitor therapy. Methylprednisolone was administered intravenously, and a decision to forego further therapy with a combination of ipilimumab and nivolumab was made. Screening and Treatment Programs to Eliminate Hepatitis C in Egypt A special report by Imam Waqed from the Menufia University, Shabin el-Kom, Egypt. In May 2016, the World Health Assembly set targets for the elimination of viral hepatitis, including reaching 90% diagnosis, 80% treatment coverage, and a 65% reduction in related mortality by 2030. When the targets were set, Egypt had the highest prevalence of HCV infection, a consequence of the prevalence of schistosomiasis and its mass treatment by unsafe intravenous injections in the 1950s to 1980s. With the decreasing cost of direct-acting antivirals in Egypt, from $1,650 for 12 weeks of sofosbuvir plus declatysvir in early 2015 to $85 for local generics in 2018, treatment of more patients and accelerated disease elimination became possible. In early 2018, the Egyptian government decided to embark on a massive effort to identify and treat all HCV-infected persons to achieve disease elimination over the shortest time period possible. These authors present the results of the national screening program. Although participation in screening was voluntary, turnout was very high. By screening 49.6 million persons over a period of seven months, the investigators managed to identify 2.2 million HCV seropositive persons and refer them for evaluation and treatment. The cost of identifying and curing a patient in the current campaign was $131, which clearly shows the magnitude of cost-saving by population screening. Universal Disease Screening and Treatment, the Egyptian Example, a perspective article by William Hazeltine from Access Health International, New York. Thirty years ago, chronic conditions such as diabetes, heart disease, and obesity accounted for less than 45% of the global disease burden. Today, they are the leading causes of death and disability worldwide. Although we are now able to treat many chronic and infectious conditions, few countries, rich or poor, have systematically tested and treated their people for the diseases that threaten them most. Now, however, the Egyptian government has provided an example of how routine testing and treatment for infectious and chronic diseases for an entire country can be achieved. Egypt has the highest rate of hepatitis C infection in the world. Ten years ago, it was estimated that nearly 15% of Egyptians were infected. In 2006, faced with evidence of rampant infection, Egypt's health ministry created the National Committee for the Control of Viral Hepatitis and appointed Dr. Wahid Das to run it. In 2018, Egypt launched the 100 Million Healthy Lives program. The goal was to screen all Egyptians 12 years of age or older for active hepatitis C virus replication, hypertension, diabetes, and obesity. Free treatment would be offered in government clinics for people who tested positive for hepatitis C, hypertension, or diabetes, and free counseling would be available for those considered obese. The program has become a permanent part of the Egyptian health system, and Egypt may soon be the first country to eliminate hepatitis C. Misdiagnosis, Mistreatment, and Harm When Medical Care Ignores Social Forces A perspective article by Seth Holmes from the University of California, Berkeley.
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Why should medical training focus on social factors, Goldfarb asked, when medicine's purpose is to cure individual patients? His essay assumed that one can effectively cure patients while ignoring the world in which they live. Unfortunately, that is an empirically untenable position. Social, political, and economic structures, those highlighted by Goldfarb, as well as structural racism, settler colonialism, other structures of marginalization, and the inequalities each of these produces, are injuring and killing people. To stop these processes, we need a range of community and team-based interventions, many of which occur beyond clinical practice, such as urban and regional planning to ensure the availability of safe housing and healthy food, and policy and systems changes to guarantee fair access to gainful employment and protection from environmental degradation. As clinicians, we endeavor to treat our patients' diseases and injuries, but when we dismiss social factors as peripheral, we not only miss opportunities to improve outcomes, we may in fact fail at medicine's core responsibilities to diagnose and treat illness and to do no harm. Once simple act of writing an opioid prescription has become fraught, physicians must check prescription monitoring databases to review patients' histories, make sure their prescription complies with state limits on dose or number of days supply, and consider any practice quality measures that might be affected. Beyond regulatory requirements, physicians must contend with growing stigma in the medical community against using opioids for pain management. Not surprisingly, there can be a palpable chill when a discussion about managing pain drifts toward opioids. Should I really start them? What if the patient demands more? What if I end up prescribing them long-term? Years of relaxed attitudes toward opioids have given way to an atmosphere of apprehension. In many ways, this caution is a positive development since 2011. As of 2018, the total volume of opioid prescriptions nationally had fallen by more than 40% from peak opioid around 2011. But like many other public debates, the opioid prescribing debate seems hopelessly polarized. Either opioids are industrially sponsored weapons of mass addiction, or they're a misunderstood last hope for alleviating suffering. The optimal use of these medications lies between these two poles. But where, exactly? There's no definitive answer, but there are persistent myths and misunderstand With his good left hand, he clutched his right to hold that injured arm in elbow flexion a little away from the body, with the forearm internally rotated. Looks like you dislocated the shoulder, Dr. Bivens said. They quickly agreed. Dr. Bivens should put it back. Enter the ritual paperwork. So we have a formal consent process. I consent, he replied. The nurse offered him a form and a pen. He gave her an exasperated look, nodding at his whole situation. Sometime later, a new patient popped up on Dr. Bivens' computer. Even as he clicked on her name, the chief complaint of seeking prescription refill was amended to high blood pressure. She'd just been to an occupational health clinic which had prescribed Hyzar DS, an antihypertensive combining Losartan 100 milligrams with hydrochlorothiazide 25 milligrams. Then the pharmacy told her a month's supply would cost $90. She was not optimistic Dr. Bivens could help, but in despair, she'd paid for one more $150 ED visit to find out. By splitting the Losartan hydrochlorothiazide pill into its components, Dr. Bivens got the monthly price down to $6. He printed two generic prescriptions with the associated coupons and returned triumphantly. He expected a hero's welcome but wasn't surprised to find her mostly just indignant. How could a medication that cost $90 a month now suddenly cost $6? We claim to have such deep respect for patient autonomy that we ritually inform people with acute orthopedic injuries of the obvious that the injury and stabilization efforts may have consequences. But in an era when medical bills bankrupt hundreds of thousands of families each year, we still routinely prescribe combined medications that we must know by now will cost patients ten times as much as the separate components. And when patients ask, what will it cost? We shrug helplessly. Our images in clinical medicine features a 19-year-old man with X-linked retinoscasis who presented with a three-day history of worsening vision in his right eye. He had received a diagnosis of X-linked retinoscasis at 5 years of age, when reduced visual acuity and macular cystic degeneration were noted in both eyes. At the current visit, the visual acuity was 20 over 70 in the right eye and 20 over 40 in the left eye. Examination of the right fundus showed prominent retinal corrugations radiating from the fovea and normal vasculature. Optical coherence tomography revealed a full-thickness retinal detachment and corrugation of deep layers of the retina, as well as diffuse retinoscasis. X-linked retinoscasis is an inherited retinal disease that occurs primarily in males. Because no retinal tears were observed, the patient was treated non-surgically. After a two-week course of daily oral acetazolamide, the retinal detachment resolved. The patient's visual acuity at follow-up had returned to a baseline of 20 over 40 in both eyes. A 49-year-old man with HIV infection presented to the HIV clinic with a several-week history of multiple, slow-growing, violaceous, ulcerated lesions on the gland's penis and external urethral meatus. He was sexually active with male partners and had not taken prescribed antiretroviral therapy for two years. Laboratory studies showed a CD4 cell count of 48 per cubic millimeter and an HIV viral load of 395,913 copies per milliliter. Tests for herpes simplex virus infection, syphilis, gonorrhea, and chlamydia were negative. An incisional biopsy was performed and a diagnosis of Kaposi's sarcoma was made. CT of the chest, abdomen, and pelvis did not show any extracutaneous involvement. Kaposi's sarcoma is a cancer caused by human herpesvirus 8, typically in the context of immunodeficiency. With treatment, the patient's penile lesions resolved completely. This concludes our summary. Let us know what you think about our audio summaries. Any comments or suggestions may be sent to audio at nejm.org. Thank you for listening.
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From the JAMA Network, this is JAMA Cardiology Author Interviews, conversations with authors exploring the latest clinical research, reviews, and opinion featured in JAMA Cardiology. Hello and welcome to this JAMA Cardiology podcast and thank you for joining us. I'm Anne-Marie Navar, Preventive Cardiologist at UT Southwestern Medical Center and an Associate Editor at JAMA Cardiology. I'm thrilled today to be talking about post-traumatic stress disorder and cardiovascular disease with two authors of a recent review published in JAMA Cardiology. Today we are joined by Dr. Chris O'Donnell, professor of medicine and member of the Boston VA healthcare system, as well as Dr. Murray Steen, a psychiatrist and professor at the University of California, San Diego, and the School of Public Health. He also is a staff psychiatrist at the San Diego VA. Dr. Steen, Dr. O'Donnell, thank you so much for joining us today. Thanks. Thank you. Dr. Steen, tell me a little bit about what set the stage for why this panel convened to write this review and talk about PTSD and cardiovascular disease. Tell us a little bit about the importance and the context for this review. It's been known for some time now that patients with post-traumatic stress disorder have a lot of health problems. And one of the sets of health problems that has become apparent that they suffer from frequently is cardiovascular disease. And I think we've been seeing this in our patients clinically. And then really over the past decade, the epidemiological research was showing these associations between PTSD and various forms of cardiovascular disease. And I think that is one of the factors that has led to this increase in research trying to figure out, is this a real association? Is it confounded in some way? And if it is a real causal association, what are the factors that are driving it and what can be done about it? So you bring up already a really important point, which is that the relationship between PTSD and cardiovascular disease can be really hard to untangle. Dr. O'Donnell, tell me a little bit about the types of studies that have been done in this area and how different people have approached untangling the interaction between these two. Thank you for asking that question. The evidence for the association of PTSD with cardiovascular disease risk factors and cardiovascular disease outcomes has been growing, particularly over the last decade or so. Several studies have been conducted, and these are described in Table 1 of the review, that show clear prospective associations in fairly large populations, both of veterans, combat-exposed veterans, and also in persons afflicted with PTSD that are civilian with risk factors such as hypertension, obesity, and type 2 diabetes, as well as incident coronary artery disease and heart failure. And these studies have been conducted generally in cohorts that were not necessarily designed to look at the exposure of PTSD and also at all of the confounders. So while there are some very interesting and provocative multivariable adjusted increases in risk, the confounders have often not been fully adjusted for. For example, lipid levels and lipid therapy have sometimes not been fully adjusted. Cigarette smoking as well. So it really provocatively provides observational prospective evidence of this association. And the question really remains, as Chris was mentioning, mainly from observational epi studies that weren't necessarily designed to try and look at the association. So they come from large observational studies like the Nurses' Health Study, where there have been questions asked about PTSD, and there's a fair bit of information about cardiovascular disease, as well as various lifestyle and other risk factors. And the majority of those studies, and we summarize them in table one of the manuscript, most of those studies do show moderately strong associations between PTSD, either in combat veterans or in civilian settings. Many of the civilian studies have been done in women and have focused in particular on sexual trauma, but the data do go beyond that. You do seem to find these moderately strong associations. The problem is, or one of the problems, is that most of the data are either cross-sectional or if they are longitudinal, there hasn't been multiple time points in the follow-up. And often there's one or two risk factors that are being evaluated. Sometimes it's just PTSD alone and its association. And rarely is there the opportunity to adjust for risk factors such as those that Chris was mentioning, things like lipid levels or hypertension or smoking. And so really knowing whether or not this is a causal association is something that we're not able to say yet. So in the absence of knowing whether this is causal or not, I think it's very clear from this review that this does appear to be a marker for people who are at increased risk of cardiovascular disease. This is part of a broader literature, some of which we've published in JAMA Cardiology. For example, we have a review earlier this year talking about adverse childhood experiences and later in life cardiovascular disease. So causal or not, it's clearly a marker for people who are at increased risk. Let's put on our clinician hats a little bit. And I'd like to hear from each of you, maybe first, Dr. Steen, from the psychiatry perspective, and then from Dr. O'Donnell, who's a cardiologist, how should clinicians be taking this research into their clinical practice? What do you want clinicians who are seeing patients to know, or how can we do better for these patients? Well, you know, the association of adverse childhood experiences, childhood maltreatment, with a whole host of adverse medical outcomes has been around for some time. And I think the review that you just cited focuses on some of the cardiovascular effects, or at least associations. And so clinically, I think the important thing to remember is that we should be asking our patients pretty routinely about things like childhood maltreatment because those sorts of experiences seem to have longstanding ripple effects in all dimensions of their health, including cardiovascular health. So knowing that somebody has had those kinds of experiences in childhood will make us want to look at their dietary habits because there's clearly an increase in obesity in individuals who've had that exposure and look to see, in fact, whether or not they also have comorbid mental health problems, which would not be limited to PTSD. They could be things like major depression would be even more apparent that we want to think about referring those folks for mental health treatment. I would add that this panel of co-authors that came together was convened a few years ago by the National Heart, Lung, and Blood Institute and included experts in cardiology as well as psychiatry and really a very multidisciplinary, impressive set of experts across the spectrum of clinical and research medicine. And I think the reason why there was even the desire to put this together is because the recognition that PTSD is prevalent. It's not heavily common, but it's in a 5% to 10% range across the lifespan of the population. And of course, cardiovascular disease is the leading cause of death in men and women. And so what I would say as a clinician cardiologist is that physicians in practice should be looking for this diagnosis having been made in their patients and or referral if there are symptoms that might suggest PTSD. And if that condition has been diagnosed, to be thinking very carefully about all of the major risk factors that we know and that we address to prevent cardiovascular disease, hypertension, lipids, cigarette smoking, et cetera. This may not be the only driver, but the recognition that there's emerging evidence of increased risk is important. And I guess I would finally add is whether there will be a time with more evidence accruing and maybe some more research coming, whether PTSD becomes a risk enhancer even in, for example, lipid guidelines or blood pressure guidelines. It isn't in there right now, and I'm not advocating that we have enough evidence to place it there, but we should certainly be thinking about that because, as you said, Anne-Marie, this is a marker and one that we can use to look carefully for increased risk and try to help prevent it. Really good points. And let me just ask Dr. Steen, as a psychiatrist, I'm sure talking to your patients about PTSD, mental health, and prior trauma experiences is probably as common for you as it is for a cardiologist to ask about smoking or blood pressure. But I think a lot of us aren't used to taking those types of histories. Can you give us some practical tips? What's some good language that we can use to elicit some of this history in a compassionate way? Yeah. And I think clinicians often are concerned that patients are going to be upset if they're asked these kinds of questions or they'll be seen by the patient as intrusive. And so I think you're right that at times that discourages us from asking those kinds of questions. But studies actually show that patients very much appreciate being asked about traumatic experiences in their past and see that as an opportunity to share with their physician events in their life that they feel have been important and have affected them. So it's pretty straightforward.
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