Podcasts about clinical features

Idiopathic intracranial hypertension (IIH) is characterized by symptoms and signs of unexplained elevated intracranial pressure (ICP) in an alert and awake patient. The condition has potentially devastating effects on vision, headache burden, increased cardiovascular disease risk, sleep disturbance, and depression.  In this episode, Teshamae Monteith, MD, FAAN speaks with Aileen A. Antonio, MD, FAAN, author of the article “Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Antonio is an associate program director of the Hauenstein Neurosciences Residency Program at Trinity Health Grand Rapids and an assistant clinical professor at the Michigan State University College of Osteopathic Medicine in Lansang, Michigan. Additional Resources Read the article: Clinical Features and Diagnosis of Idiopathic Intracranial Hypertension Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @aiee_antonio Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Monteith: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which appears in the June 2025 Continuum issue on disorders of CSF dynamics.  Hi, how are you? Dr Antonio: Hi, good afternoon. Dr Monteith: Thank you for being on the podcast. Dr Antonio: Thank you for inviting me, and it's such an honor to write for the Continuum. Dr Monteith: So why don't you start off with introducing yourself? Dr Antonio: So as mentioned, I'm Aileen Antonio. I am a neuro-ophthalmologist, dually trained in both ophthalmology and neurology. I'm practicing in Grand Rapids, Michigan Trinity Health, and I'm also the associate program director for our neurology residency program. Dr Monteith: So, it sounds like the residents get a lot of neuro-ophthalmology by chance in your curriculum. Dr Antonio: For sure. They do get fed that a lot. Dr Monteith: So why don't you tell me what the objective of your article was? Dr Antonio: Yes. So idiopathic intracranial hypertension, or IIH, is a condition where there's increased intracranial pressure, but without an obvious cause. And with this article, we want our readers---and our listeners right now---to recognize that the typical symptoms and learning about the IIH diagnostic criteria are key to avoiding errors, overdiagnosis, or sometimes even misdiagnosis or underdiagnosis. Thus, we help make the most of our healthcare resources. Early diagnosis and management are crucial to prevent disability from intractable headaches or even vision loss, and it's also important to know when to refer the patients to the appropriate specialists early on. Dr Monteith: So, it sounds like your central points are really getting that diagnosis early and managing the patients and knowing how to triage patients to reduce morbidity and complications. Is that correct? Dr Antonio: That is correct and very succinct, yes. Dr Monteith: And so, are there any more recent advances in the diagnosis of IIH? Dr Antonio: Yes. And one of the tools that we've been using is what we call the optical coherence tomography. A lot of people, neurologists, physicians, PCP, ER doctors; how many among those physicians are well-versed in doing an eye exam, looking at the optic disc? And this is a great tool because it is noninvasive, it is high resolution imaging technique that allows us to look at the optic nerve without even dilating the eye. And we can measure that retinal nerve fiber layer, or RNFL; and that helps us quantify the swelling that is visible or inherent in that optic nerve. And we can even follow that and monitor that over time. So, this gives us another way of looking at their vision and getting that insight as to how healthy is their vision still, along with the other formal visual tests that we do, including perimetry or visual field testing. And then all of these help in catching potentially early changes, early worsening, that may happen; and then we can intervene more easily. Dr Monteith: Great. So, it sounds like there's a lot of benefits to this newer technology for our patients. Dr Antonio: That is correct. Dr Monteith: So, I read in the article about the increased incidence of IIH, and I have to say that I completely agree with you because I'm seeing so much of it in my clinic, even as a headache specialist. And I had a talk with a colleague who said that the incidence of SIH and IIH are similar. And I was like, there's no way. Because I see, I can see several people with IIH just in one day. That's not uncommon. So, tell me what your thoughts are on the incidence, the rising incidence of IIH; and we understand that it's the condition associated with obesity, but it sounds like you have some other underlying drivers of this problem. Dr Antonio: Yes, that is correct. So, as you mentioned, IIH tends to affect women of childbearing age with obesity. And it's interesting because as you've seen that trend, we see more of these IIH cases recently, which seem to correlate with that rising rate of obesity. And the other thing, too, is that this trend can readily add to the burden of managing IIH, because not only are we dealing with the headaches or the potential loss of vision, but also it adds to the burden of healthcare costs because of the other potential comorbidities that may come with it, like cardiovascular risk factors, PCOS, and sleep apnea. Dr Monteith: So why don't we just talk about the diagnosis of IIH? Dr Antonio: IIH, idiopathic intracranial hypertension, is also called pseudotumor cerebri.  It's essentially a condition where a person experiences increased intracranial pressure, but without any obvious cause. And the tricky part is that the patients, they're usually fully awake and alert. So, there's no obvious tumor, brain tumor or injury that causes the increased ICP. It's really, really important to rule out other conditions that might cause these similar symptoms; again, like brain tumors or even the cerebral venous sinus thrombosis. Many patients will have headaches or visual disturbances like transient visual obscurations---we call them TVOs---or double vision or diplopia. The diplopia is usually related to a sixth nerve palsy or an abducens palsy. Some may also experience some back pain or what we call pulsatile tinnitus, which is that pulse synchronous ringing in their ears. The biggest sign that we see in the clinic would be that papilledema; and papilledema is a term that we only use, specifically use, for those optic nerve edema changes that is only associated with increased intracranial pressure. So, performing of endoscopy and good eye exam is crucial in these patients. We usually use the modified Dandy criteria to diagnose IIH. And again, I cannot emphasize too much that it's really important to rule out other secondary causes to that increased intracranial pressure. So, after that thorough neurologic and eye evaluation with neuroimaging, we do a lumbar puncture to measure the opening pressure and to analyze the cerebrospinal fluid. Dr Monteith: One thing I learned from your article, really just kind of seeing all of the symptoms that you mentioned, the radicular pain, but also- and I think I've seen some papers on this, the cognitive dysfunction associated with IIH. So, it's a broader symptom complex I think than people realize. Dr Antonio: That is correct. Dr Monteith: So, you mentioned TVOs. Tell me, you know, if I was a patient, how would you try and elicit that from me? Dr Antonio: So, I would usually just ask the patient, while you're sitting down just watching TV---some of my patients are even driving as this happens---they would suddenly have these episodes of blacking out of vision, graying out of vision, vision loss, or blurred vision that would just happen, from seconds to less than a minute, usually. And they can happen in one eye or the other eye or both eyes, and even multiple times a day. I had a patient, it was happening 50 times a day for her. It's important to note that there is no pain associated with it most of the time. The other thing too is that it's different from the aura that patients with migraines would have, because those auras are usually scintillating and would have what we call the positive phenomena: the flashing lights, the iridescence, and even the fortification that they see in their vision. So definitely TVOs are not the migraine auras. Sometimes the TVOs can also be triggered by sudden changes in head positions or even a change in posture, like standing up quickly. The difference, though, between that and, like, the graying out of vision or the tunneling vision associated with orthostatic hypotension, is that the orthostatic hypotension would also have that feeling of lightheadedness and dizziness that would come with it. Dr Monteith: Great. So, if someone feels lightheaded, less likely to be a TVO if they're bending down and they have that grain of vision. Dr Antonio: That is correct. Dr Monteith: Definitely see patients like that in clinic. And if they have fluoride IIH, I'm like, I'll call it a TVO; if they don't, I'm like, it's probably more likely to be dizziness-related. And then we also have patient migraines that have blurriness that's nonspecific, not necessarily associated with aura. But I think in those patients, it's usually not seconds long, it's usually probably longer episodes of blurriness. Would you agree there, or…? Dr Antonio: I would agree there, and usually the visual aura would precede the headache that is very characteristic of their migraine, very stereotypical for their migraines. And then it would dissipate slowly over time as well. With TVOs, they're brisk and would not last, usually, more than a minute. Dr Monteith: So, why don't we talk about routine imaging? Obviously, ordering an MRI, and I read also getting an MRV is important. Dr Antonio: It is very important because, one: I would say IIH is also a diagnosis of exclusion. We need to make sure that the increased ICP is not because of a brain tumor or not because of cerebral venous sinus thrombosis. So, it's important to get the MRI of the brain as well as the MRV of the head. Dr Monteith: Do you do that for all patients' MRV, and how often do you add on an orbital study? Dr Antonio: I usually do not add on an orbital study because it's not really going to change my management at that point. I really get that MRI of the brain. Now the MRV, for most of my patients, I would order it already just because the population that I see, I don't want to lose them. And sometimes it's that follow-up, and that is the difficult part; and it's an easy add on to the study that I'm going to order. Again, it depends with the patient population that you have as well, and of course the other symptoms that may come with it. Dr Monteith: So, why don't we talk a little bit about CSF reading and how these set values, because we get people that have readings of 250 millimeters of water quite frequently and very nonspecific, questionable IIH. And so, talk to me about the set value. Dr Antonio: Right. So, the modified Dandy criteria has shown that, again, we consider intracranial pressure to be elevated for adults if it's above 250 millimeters water; and then for kids if it's above 280 millimeters of water. Knowing that these are taken in the left lateral decubitus position, and assuming also that the patients were awake and not sedated during the measurement of the CSF pressure. The important thing to know about that is, sometimes when we get LPs under fluoroscopy or under sedation, then these can cause false elevation because of the hypercapnia that elevated carbon dioxide, and then the hypoventilation that happens when a patient is under sedation. Dr Monteith: You know, sometimes you see people with opening pressures a little bit higher than 25 and they're asymptomatic. Well, the problem with these opening pressure values is that they can vary somewhat even across the day. People around 25, you can be normal, have no symptoms, and have opening pressure around 25- or 250; and so, I'm just asking about your approach to the CSF values. Dr Antonio: So again, at the end of the day, what's important is putting everything together. It's the gestalt of how we look at the patient. I actually had an attending tell me that there is no patient that read the medical textbook. So, the, the important thing, again, is putting everything together. And what I've also seen is that some patients would tell me, oh, I had an opening pressure of 50. Does that mean I'm in a dire situation? And they're so worried and they just attach to numbers. And for me, what's important would be, what are your symptoms? Is your headache, right, really bad, intractable? Number two: are you losing vision, or are you at that cusp where your optic nerve swelling or papilledema is so severe that it may soon lead to vision loss? So, putting all of these together and then getting the neuroimaging, getting the LP. I tell my residents it's like icing on the cake. We know already what we're dealing with, but then when we get that confirmation of that number… and sometimes it's borderline, but this is the art of neurology. This is the art of medicine and putting everything together and making sure that we care and manage it accordingly. Dr Monteith: Let's talk a little bit about IIH without papilledema. Dr Antonio: So, let's backtrack. So, when a patient will fit most of the modified Dandy criteria for IIH, but they don't have the papilledema or they don't have abducens palsy, the diagnosis then becomes tricky. And in these kinds of cases, Dr Friedman and her colleagues, when they did research on this, suggested that we might consider the diagnosis of IIH. And she calls this idiopathic intracranial hypertension without papilledema, IIHWOP. They say that if they meet the other criteria for modified Dandy but show at least three typical findings on MRI---so that flattening of the posterior globe, the tortuosity of the optic nerves, the empty sella or the partially empty sella, and even the narrowing of the transverse venous sinuses---so if you have three of these, then potentially you can call these cases as idiopathic intracranial hypertension without papilledema. Dr Monteith: Plus, the opening pressure elevation. I think that's key, right? Getting that as well. Dr Antonio: Yes. Sometimes IIHWOP may still be a gray area. It's a debate even among neuro-ophthalmologists, and I bet even among the headache specialists. Dr Monteith: Well, I know that I've had some of these conversations, and it's clear that people think this is very much overdiagnosed. So, that's why I wanted to plug in the LP with that as well. Dr Antonio: Right. And again, we have not seen yet whether is, this a spectrum, right? Of that same disease just manifesting differently, or are they just sharing a same pathway and then diverging? But what I want to emphasize also is that the treatment trials that we've had for IIH do not include IIHWOP patients. Dr Monteith: That is an important one. So why don't you wrap this up and tell our listeners what you want them to know? Now's the time. Dr Antonio: So, the- again, with IIH, with idiopathic intracranial hypertension, what is important is that we diagnose these patients early. And I think that some of the issues that come into play in dealing with these patients with IIH is that, one: we may have anchoring bias. Just because we see a female with obesity, of reproductive age, with intractable headaches, it does not always mean that what we're dealing with is IIH. The other thing, too, is that your tools are already available to you in your clinic in diagnosing IIH, short of the opening pressure when you get the lumbar puncture. And I need to emphasize the importance of doing your own fundoscopy and looking for that papilledema in these patients who present to you with intractable headaches or abducens palsy. What I want people to remember is that idiopathic intracranial hypertension is not optic nerve sheath distension. So, these are the stuff that you see on neuroimaging incidentally, not because you sent them, because they have papilledema, or because they have new headaches and other symptoms like that. And the important thing is doing your exam and looking at your patients. Dr Monteith: Today, I've been interviewing Dr Aileen Antonio about her article on clinical features and diagnosis of idiopathic intracranial hypertension, which appears in the most recent issue of Continuum on disorders of CSF dynamics. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today. Thank you again. Dr Antonio: Thank you. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Spontaneous intracranial hypotension reflects a disruption of the normal continuous production, circulation, and reabsorption of CSF. Diagnosis requires the recognition of common and uncommon presentations, careful selection and scrutiny of brain and spine imaging, and, frequently, referral to specialist centers.  In this episode, Gordon Smith, MD, FAAN speaks with Jill C. Rau, MD, PhD, author of the article “Clinical Features and Diagnosis of Spontaneous Intracranial Hypotension” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Rau is an assistant professor of clinical neurology at the University of Arizona, School of Medicine-Phoenix in Phoenix, Arizona. Additional Resources Read the article: continuumjournal.com Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Full episode transcript available here Interview with Jill Rau, MD Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension, which she wrote with Dr Jeremy Cutsworth-Gregory from the Mayo Clinic. This article appears in the 2025 Continuum issue on disorders of CSF dynamics. I'm really excited to welcome you to the Continuum podcast. Maybe you can start by just telling our listeners a little bit about yourself? Dr Rau: Hi, thanks for having me. I'm really honored to be here, and I really enjoyed writing the paper with Dr Cutsforth-Gregory. I hope you guys enjoy it. I am the director of headache medicine at the Baba Bay Neuroscience Institute at Honor Health in Scottsdale, Arizona. I'm also currently the chair of the special interest group in CSF Dynamics at the American Headache Society, and I've had a special interest in this field since I first watched Dr Linda Gray speak at a conference where she talked about spinal CSF leaks and their different presentations. And they were so different than what I had been taught in residency. They're not just the post-LP headache. They have such a wide variety of presentations and how devastating they can be, and how much impact there is on someone's life when you find it and fix it. And I've been super interested in the field and involved in research since that time. And, yeah. Love it. Dr Smith: Well, thanks for sharing your story. And as I reflected on our conversation ahead of time and have been thinking about this issue… this is a cool topic, and every time I read one of these manuscripts and have the opportunity to speak with one of the authors, I learn a ton, because this was something that wasn't even on the radar when I trained back in the 1800's. So, really looking forward to the conversation. I wonder if you could really briefly just summarize or remind for everyone the normal physiology about CSF dynamics, you know, production, absorption, and so forth? Dr Rau: So, the CSF is the fluid that surrounds the brain and the spinal cord, and it's contained by the dura, which is like a canvas or a sac that covers that whole brain and spinal cord. And within the ventricles of the brain, the choroid plexus produce CSF. It's constantly producing and then being reabsorbed by the arachnoid granulations and pushed into the venous space, the cerebral sinuses, venous sinuses. And also some absorption and push into the lymphatics that we've just learned about in the past year. This is kind of new data coming out, so always learning more and more about CSF, but we know that it bathes the brain and the spinal cord, helps keep some buoyancy of the brain as well as pushing nutrients in and pulling out metabolic waste. And it sort of keeps the brain in the state of homeostasis that's happy. And so, when there's a disruption of that flow and the amount of fluid there, that disrupts that, that can cause lots of different symptoms and problems for people. Dr Smith: One of the many new things I learned is that even the name of this---spontaneous intracranial hypotension---is misleading. And I think this is clinically relevant, as we'll probably get to in a moment, but can you talk a little bit about this? Is this really like a pressure disorder or a volume disorder? Dr Rau: Yeah. It's almost certainly a volume disorder. We do see in some people that they have low pressure, and it's still part of the diagnostic criteria. But it's there because if you have a low pressure, if you measure an opening pressure and it's below six, if you're measuring it in the spine in the right place, then you have indication that there's low volume. But there's over 50% of people's opening pressure who have a spinal CSF leak, have all the symptoms and can be fixed. So, they have normal pressure in 50% of the people. So, it is an inaccurate term, hypotension, but it was originally discovered because of the thought that it was a low-pressure situation. Some of the findings would suggest low pressure, but ultimately, we are pretty sure it's a low-volume condition. Dr Smith: Another new thing that I learned that really blew me away is how bad this can be. I did a podcast with Mark Burish about cluster, and I was reminded many cluster patients are pushed to the point of suicidal ideation or committing suicide by the severity of pain. And this sounds like for many patients it's equally severe. Can you maybe paint a picture for our listeners why this is so clinically important? Dr Rau: A large number of people, even people who are known to have leaks because they've had them before or they've releaked, they have a lot of brain fog and cognitive impairment. They often have severe headaches when they're upright. So, orthostatic headache is probably the number one most common symptom, and those headaches are one of the worst headaches out there. When people stand up, their fluid is not supporting the brain and there's an intense amount of pain. And so, they spend a large portion of their lives horizontal. And there's associated symptoms with that, it's not just headache pain and brain fog. There's neck pain. There's often subsequent disorders that accompany this, like partial orthostatic tachycardia syndrome. We don't know if that's because of deconditioning or an actual sequela of the disease, but it's a frequent comorbidity. We have patients that have extreme dizziness with their symptoms, but many patients are limited to hours, if that, upright per day, combined, total. And so they live their lives, often, just in the dark, lots of photophobia, sensitive to the light, really unable to function. It's also very hard to find and so underrecognized that a lot of patients, especially if they don't have that really clinical symptom of orthostatic headache. So, it's often missed. So, they're just debilitated. You know, treatments don't work because it's not a migraine and it's not a typical headache. It's a mechanical issue as well as a metabolic issue and not found, not a lot helps it. Dr Smith: So, you know, I have always thought about this as really primarily an orthostatic symptom. I wonder if you can talk about the complexity of this; in particular, kind of how this evolves over time, because it's not quite that simple. And maybe in doing so, you can give our listeners some pearls on when they should be thinking about this disorder? Dr Rau: A large portion of people do have headache with spinal CSF leak, in particular, spontaneous intracranial hypertension- hypotension, excuse me. And that's something to be thought about, is that there are spontaneous conditions where people have either rupture of the dural sac, or an erosion of the dural sac, or a development of a connection between the dura and the venous system. And that is taking away or allowing CSF to escape. In these instances that patients have spontaneous, there may be a different presentation than if they have, like, a postdural puncture or a chronic traumatic or iatrogenic leak. And we're not sure of that yet, but we're looking into that. Still, the largest presentation is headache, and orthostatic headache is very dominant in the headache realm. But over time, patients' brains can compensate for that lack of CSF and start overproducing---or at least we think that's probably what's happening. And you may see a reduction in the orthostatic symptoms over time, and you may see an improvement in the radiographic findings. So, there are some interesting papers that have been published that look at these changes over time, and we do see that sometimes within that first three to four months; this is the most common time to see that change. Other patients may worsen. You may actually see someone going from looking sort of normal radiographically to developing more of a SIH-type of picture on the brain. And so it's not predictable which patients have gone from orthostatic to improvement or the other way around, both radiographically and clinically. So, it can be quite difficult to tell. So, for me, if I have a patient that comes to me and they're struggling with headache… if it's orthostatic, very clearly orthostatic: I lay down, I get considerably better or my headache completely goes away. And then when I stand up, it comes on relatively quickly, within an hour. And sometimes it's a worsening-throughout-the-day type of thing, it's lowest in the morning and it worsens throughout the day. These are the times that it's most obvious to think about CSF leak. Especially if that headache onset relatively suddenly, if it onset after a small trauma. Like I've had patients that say, you know, I was doing yoga and I did some twists and I felt kind of a pop. And then I've had this headache that is horrible when I'm upright but is better when I lay down ever since, you know, since that time. That's kind of a very classic presentation of spinal CSF leak or spontaneous intracranial hypotension. Maybe a less common presentation would be someone who comes to you, they've had a persistent headache for a couple years, they kind of remember it started in March of a couple years ago, but they don't know. Maybe it's, you know, it's a little better when they lay down. It may be a little worse when they're up moving around, but so is migraine, and it's a migrainous headache. But they've tried every migraine drug you can think of. Nothing is responding, nothing helps. I'm always looking at patients who are new daily, persistent headaches and patients who aren't responding to meds even if it's not new daily, but they have just barely any response. I will always go back and examine their brain imaging and get full spine to make sure I'm not missing. And you can never be 100% sure, but it's always good to consider those patients to the best of your ability, if that- have that in the back of your mind. Dr Smith: So obviously, goes without saying, this is something people need to have on their radar and think about. And then we'll talk more about diagnostic tools here in a second. But how common is this? If you're a headache doc, you see a lot of patients who have intractable headaches. And how often do you see this in your headache practice? Now you're- this is your thing, so probably a little more than others, but, you know, how common will someone who sees a lot of headache encounter these patients? Dr Rau: If you see a lot of headache, I mean, currently the thought is it's about 5 in 100,000. That was from a study before we were finding CSF venous fistulas. I think a lot of us think it's more common than that, but it's not super common. We don't have good estimates, but I would guess between 5 and 10 for 100,000 persons, not “persons who come to a tertiary headache clinic with intractable headaches”. So, it's hard to gauge how frequent it is, but I would say it's considerably more frequent than we currently think it is. There's still a group of people with orthostatic headaches that we can't find leaks on; that, once you treat other things that can cause or look for other things that can cause orthostatic headaches. So, there may be even still a pathophysiology out there that is still a leak type. Before 2014, we didn't even know about CSF venous fistulas. And now here we are; like, 50% of them are CSF venous fistulas. So, you know, we're still in a huge learning curve right now. Dr Smith: So, I definitely want to talk about the fistulas in a second. But before moving on, one of the things that I found really interesting is the wide spectrum of clinical phenotype. And we obviously don't have a lot of time to get into all of these different ones, but the one that I was hoping you might talk about---and there's a really great case, and you're on bunch of great case, a great case of this---is brain sagging dementia, not a term I've used before. Can you really briefly just tell our listeners about that, because that's a really interesting story and a great case in your article? Dr Rau: Yeah. So, brain sag dementia is a… almost like an extreme version of a spontaneous intracranial hypotension. Where there is clear brain sag in the imaging---so that's helpful---but the patients present kind of like a frontotemporal dementia. And when this was first started to being determined, you could turn the patient into Trendelenburg, and sometimes they would improve. There are some practitioners that have introduced fluid into the thecal sac and had temporary improvement. Patching has improvement, then they leak again, sometimes  not. But the clinical changes with this have been pretty tremendous to be able to identify that that's a real thing. And in some cases, out of Cedars Sinai, you know, who does a lot of the best research in this, they've had lots of cases where they can't find the leak, but there's clear brain sag that fits with our clinical picture of CSF leaks. So, we're on a learning curve. But yeah, this- they really present. They have disinhibition and cognitive impairment that is very similar to frontotemporal dementia. Dr Smith: Well, so let's talk about what causes this. You mentioned CSF venous fistulas. I mean, that was reported now just over a decade ago, it's pretty amazing. That accounts for about half of cases, if I understand correctly. What are the other causes? And then we'll talk more about therapy in a minute, but what causes this? Dr Rau: So, within the realm of spontaneous, you know, we say it's spontaneous. But the spontaneous cases we account for, they can be tears in the dura, which are usually sort of lateral tears in the dura. They can be little places that rubbed a hole, often on an osteophyte from the spine. They can come from these spinal diverticuli. So, I always describe it to my patients like those balls that have mesh and squishy, and you squeeze them in the- through the mesh, there's the extra little bubbling out. If you think of like the dura bubbling, out in some cases, through the framing of the spine, right where the spinal nerve roots come out, they should poke out like wires from the dura. But in many cases they poke out with this extra dura surrounding them, and we call that spinal diverticuli. And if you imagine like the weakening of where you squeeze that, you know, balloon through your fingers, in those locations, that's a very common place to find a CSF leak, and you can imagine that the integrity of the dura there may be less than it would be if it were not being expanded in that direction. And that's often the most common place we see these CSF venous fistulas. So, you can get minor traumas; like I said, it can be spontaneous, like someone just develops a leak one day. It can be rubbed off, and it can be a development of a connection between the dura and the venous system. There are also iatrogenic causes, but we don't consider them spontaneous. But when you're considering your patients for spontaneous cases, you should consider if they've ever had chronic---even long, long time ago---had any spinal implementation, procedures near the spine, spinal injections, LPs in the past, and especially women who've had epidurals in pregnancy. Dr Smith: All right, so we see a patient, positional severe headache, who meets the clinical criteria. Next step, MRI scan? Dr Rau: Yeah. So, the first thing is always to get the brain MRI with and without contrast. Most places will have a SIH or a spinal CSF leak protocol, but you should get contrast because one of the most pathognomonic findings on brain MRI is that smooth diffuse dural enhancement. And that's a really fantastic thing when you find it, because it's kind of a slam dunk. If you find it, then you will see other findings. It almost never exists alone. But if you see that, it's pretty much a spinal CSF leak. But you're also looking for subdural collections, any indication of brain sag. We do have these new algorithms that have come out in the past couple of years that are helpful. They're not exclusionary---you can have negative findings on the brain and still have spinal CSF leak---but the brain MRI is extremely helpful. If it's positive for the findings, it really does help you nudge you in the direction of further investigations and treatments. Dr Smith: And what about those further investigations and treatments, right? So, you see that there's findings consistent with low pressure, and I guess I should say low intracranial CSF volume. Be that as it may, what's the next step after that? Dr Rau: Depends on where you are and what you can do. I almost always will get a full spine MRI: so, C spine, T spine, and L spine separately. Not, you know, we don't want it all in one picture, because we want to get the full view. And you want to get that with at least T2 highly- heavily T2 weighted with fat saturation in at least the sagittal and axial planes. It's really helpful if you can get it in the coronal planes, but we have to have- often have good talks with your radiologist to get the coronal plane. I spoke about the spinal diverticuli earlier, and I want to clarify a little bit of something. The coronal image will show those really nicely. It's interesting, but 44% of people have those. So just having the spinal diverticuli does not indicate that you have a leak. But if you have a lot of those, there may be more likelihood of having leak than if you don't have any of those. So, I will get all of those and I will look at them myself, but I've been looking at them myself for a long time. But a lot of radiologists in community hospitals, especially not- nonneuroradiologists, but even neuroradiologists, this isn't something that's that everybody's been educated about, and we've been learning so much about it so rapidly in the past ten years. It's not easy to do and it's often missed. And if it's not protocoled properly, the fat saturation's not there, it's very hard to see… you can have a leak and not see it. Even the best people, like- it's not always something that's visible. And these CSF venous fistulas that we talked about are never visible on normal MRI imaging. Nonetheless, I will run those because if I can find a leak---and 90% of the ones that are found on MRI imaging are in the thoracic spine. So that's where I spend the most of my time looking. But if you find it, that's another thing to take to your team to say, hey, look, here it is, let's try and do this, or, let's try and do that, or, I've got more evidence. And there are other findings on the spine; not just the leak, but other findings, sometimes, you can see on spine that maybe help you push you towards, yes, this is probably a leak versus not. Dr Smith: So, your article has a lot of great examples and detail about kind of advanced imaging to, like, find the fistula and what not. I guess I'm thinking most of our listeners are probably practicing in a location where they don't have a team that really focuses on that. So, let's say we do the imaging of the spine and you don't find a clear cause. Is the next step to just do a blood patch? Do you send them to someone like you? What's the practical next step? Dr Rau: Yeah, if your- regardless of whether you find a leak or not, if your clinical acumen is such that you think this patient has a leak or I've treated them for everything else and it's not working and I have at least a high enough suspicion that I think the risk of getting a patch is lower than the benefit that if they got a patch and it worked, I do send my patients for non-directed blood patches, because it currently does take a long time to get them to a center that can do CT myelograms or any kind of advanced imaging to look for sort of a CSF venous fistula or to get treated outside of a nondirected patch. You know, sometimes nondirected patches are beneficial for patients, and there's some good papers out there that sort of explain the low risks of doing these if done properly versus the extreme benefit for patients when it works. And, I mean, I can't tell you how many people come in and tell me how their lives are changed because they finally got a blood patch. And sometimes it works. And it's life-changing for those people. You know, they go back to work. They can interact with their kids again. Before, they didn't know what was wrong, just had this headache that started. So it's worth doing if you have a strong clinical suspicion. Dr Smith: Yeah. I mean, that was great. And, you know, to go back to where we began, this is severe. It's something like 60% of patients with this problem have thought about suicide, right? And you take this patient and cure the problem. I feel really empowered having read the article and talked to you today. And so, I'm ready to go out and look for this. Thank you so much for a really engaging conversation. This has been terrific. Dr Rau: Thank you. I appreciate it. I enjoyed being here. Dr Smith: Again, today I've been interviewing Dr Jill Rau about her article on clinical features and diagnosis of spontaneous intracranial hypotension---which I guess I should say hypovolemia after having talked to you---which she wrote with Dr Jeremy Cutsworth-Gregory. This article appears in the most recent issue of Continuum on disorders of CSF dynamics. Please be sure to check out Continuum Audio episodes from this really interesting issue and other interesting issues. And thank you, our listeners, again for listening to us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

On episode #78 of the Infectious Disease Puscast, Daniel and Sara review the infectious disease literature for the weeks of 3/27/25 – 4/9/25. Hosts: Daniel Griffin and Sara Dong Subscribe (free): Apple Podcasts, RSS, email Become a patron of Puscast! Links for this episode Viral Demise of the Milwaukee protocol for rabies (CID) A natural experiment on the effect of herpes zoster vaccination on dementia (Nature) Taking a shot at dementia(microbeTV: TWiV) Recommendations from the 10th European Conference on Infections in Leukaemia for the management of cytomegalovirusin patients after allogeneic haematopoietic cell transplantation and other T-cell-engaging therapies (LANCET: Infectious Diseases) Epstein-Barr virus exposure precedes Crohn`s disease development (Gastroenterology aga) Bacterial Blujepa (gepotidacin) approved by US FDA for treatment of uncomplicated urinary tract infections (uUTIs) in female adults and paediatric patients 12 years of age and older (GSK) GSK wins FDA nod for first oral UTI antibiotic in almost 30 years(BioSpace) Efficacy and safety of individualised versus standard 10-day antibiotic treatment in children with febrile urinary tract infection (INDI-UTI): a pragmatic, open-label, multicentre, randomised, controlled, non-inferiority trial in Denmark (LANCET: Infectious Diseases) Frequency and severity of Myasthenia Gravis exacerbations associated with the use of ciprofloxacin, levofloxacin, and azithromycin (Muscle & Nerve) The cost of blood cultures: a barrier to diagnosis in low-income and middle-income countries (LANCET: Microbe) Rethinking blood culture (LANCET: Microbe) Trends in Anaplasmosis Over the Past Decade: A Review of Clinical Features, Laboratory Data and Outcomes(CID) Fungal The Last of US Season 2 (YouTube) Cracks in the curriculum: the hidden deficiencies in fungal disease coverage in medical books (OFID) Kazachstania slooffiae fungemia: a case report and literature review on an emerging opportunistic pathogen in humans (OFID) Plasma microbial cell-free DNS metagenomic sequencing for diagnosis of invasive fungal diseases among high risk outpatient and inpatient immunocompromised hosts (CID) Parasitic Fatal Case of Splash Pad–Associated Naegleria fowleri Meningoencephalitis — Pulaski County, Arkansas, September 2023 (CDC: MMWR) Notes from the Field: Fatal Acanthamoeba Encephalitis in a patient who regularly used tap water in an electronic nasal irrigation device and a continuous positive airway pressure machine at home — new Mexico, 2023 (CDC: MMWR) Malaria (NEJM) Miscellaneous FDA grants marketing authorization of first home test for chlamydia, gonorrhea and trichomoniasis (FDA) Music is by Ronald Jenkees Information on this podcast should not be considered as medical advice.

Episode 181: Cannabinoid Hyperemesis SyndromeFuture Dr. Johnson explains the pathophysiology, assessment, and management of Cannabinoid Hyperemesis syndrome. Dr. Arreaza adds some insights on the topic.  Written by Tyler Johnson, MSIV, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific-Northwest. Editing and comments by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Definition Cannabinoid hyperemesis syndrome (CHS) is a syndrome of cyclic abdominal pain, vomiting, or nausea in older adolescents and adults who have chronic ϲаnոаbis use.The term “marijuana” is considered racist by some people. In the 1930s, American politicians popularized the term “marijuana” in the U.S. to portray the drug as a “Mexican vice” and to have a justification to persecute Mexican immigrants. Epidemiology The overall prevalence of cannabinoid hyperemesis syndrome is unknown due to a lack of definitive criteria or diagnostic tests. It occurs in a population that may not disclose substance use. One study conducted in 2015 in a United States urban emergency department not named, found one-third of patients with near-daily cannabis use met criteria for having had CНЅ in the prior six months.Why are rates of CHS increasing?Between 2005-2014 hospitalizations cyclic vomiting syndromes increased by 60 %. concurrent cannabis use in hospitalized patients increasing from 2 to 21 percent. 7 years after the commercialization of cannabis in Canada, the Canadian health services found a 13-fold increase in cyclic vomiting syndromesPotential correlations for the increase in CHS are increased legalization and commercialization of cannabis, higher tetrahydrocannabinol concentrations in cannabis products, and increased recognition of the syndrome.Legal status of Cannabis in the USCannabis is legal in 24 states: Alaska, Arizona, California, Colorado, Connecticut, Delaware, Illinois, Maine, Maryland, Massachusetts, Michigan, Minnesota, Missouri, Montana, Nevada, New Jersey, New Mexico, New York, Ohio, Oregon, Rhode Island, Vermont, Virginia, and Washington. It is also legal in Washington, D.C. Cannabis is approved for medical use in 38 states.Federal level: Cannabis is a Schedule I drug, under the Controlled Substance Act (added in 1970) in the group of Hallucinogenic or psychedelic substances. Tetra-hydro-cannabinol (THC, a “mind-altering substance in cannabis”) is on the same list. However, cannabidiol (CBD, derived from hemp or non-hemp plants) was removed from the Controlled Substances Act in 2018. CBD is FDA-approved (under the name of Epidiolex®) to treat rare seizure disorders. CBD is still on the list of controlled substances in some states. I see THC as a problem.THC increased concentration As recreational Cannabis becomes more normalized, innovators look to find new ways to differentiate their product and increasing THC has become a common way to perform this similar to alcohol content in the beer, wine, and liquor industry. An article by Yale School of Medicine titled “Marijuana: Rising THC Concentrations in Cannabis Can Pose Health Risks” states, “In 1995, the average THC content in cannabis seized by the Drug Enforcement Administration was about 4%. By 2017, it had risen to 17% and continues to increase. Beyond the plant, a staggering array of other cannabis products with an even higher THC content like dabs, oils, and edibles are readily available—some as high as 90%.”Recently, cannabis-infused water started to be sold in some grocery stores.Pathophysiology of CHSIt is not entirely understood. Some suggest multifactorial involving cannabinoid metabolism, exposure dose and tolerance modifying receptor regulation, complex pharmacodynamics at Cannabinoid receptors, and even changes in genetics and cannabinoid variation in plants. CB1 receptors are involved in gastric secretion, sensation, motility, inflammation, and lipogenesis. The activation of CB1 and CB2 receptors has been suggested as the possible cause of CHS.Risk FactorsCHS can occur after acute or acute on chronic use but many report daily 3-5x cannabis use cannabis use over one year and many over at least two years. Median age 24 years. Interesting factsMedical visits for inhaled cannabis are more likely associated with CHS while edibles are more likely for acute psychiatric reactions.Also, CHS is a paradoxical effect since cannabis and cannabinoid receptor agonists are known antiemetics (as seen in nabilone and dronabinol (synthetic analogs of THC)) and prescribed by some physicians to combat chemotherapy effects.Clinical Features of CHSCyclical pattern with abdominal pain, severe nausea, and vomiting up to 30 episodes daily. Pain is intense and even referred to as “scromiting” due to its intense nature, causing patients to scream and vomit concurrently.Typically, it presents with 2 or more episodes over a 6-month period with no symptoms in between. It starts within 24 hours of last cannabis use (differentiating from cannabis withdrawal) and occurs at day or night. There is a gradual symptom resolution of nausea and vomiting after several days of cannabis cessation. Some patients had symptoms 2 days to 2 weeks after cessation. Diagnosis of CHSClinical diagnosisRule out neurological symptoms such as migraine headaches, acute abdomen, motion sickness, and medications, such as recent antibiotics and chemotherapy.Often the diagnosis is discovered with a thorough history reporting a decrease in symptoms with hot showers/baths.Management of CHS AcuteRehydrate with Fluids Dopamine Antagonists– Droperidol (0.625 or 1.25mg) /Haloperidol (0.05 to 0.1mg/kg with max dose of 5mg initially) favored over typical antiemetics like Zofran or Reglan.If needed, combine with an antiemetic like metoclopramide IM or ondansetron IV and consider patients' dehydration status likely requiring US-guided IV.Topical capsaicin cream 0.025 – 0.1% on the abdomen. Long term97% resolution of symptoms completely in a systematic review of patients who stopped cannabis use.Reinforce it may take several weeks of abstinence for symptoms to resolve and symptoms can worsen if cannabis is resumed. It is unknown if a reduction in use can prevent recurrence.Approaches in the clinicEducate patients on the etiology of their symptoms with complete cessation of cannabis use.Consider referral to counseling for cannabis use disorder and abstinence support for treatment-seeking cannabis users. Approach topics such as changing one's environment, seeking social support, and using self-help techniques to non-treatment-seeking individuals.Consider referring patients with polysubstance use and significant comorbidities to a supervised withdrawal management setting. Conclusion: Cannabis use is increasing with legalization and commercialization across the United States. With increased use, Cannabinoid hyperemesis syndrome incidence increases. Often it can be diagnosed with a thorough history including chronic cannabis consumption and symptomatic relief by showers. Physicians will need to develop counseling approaches to better understand CHS patients and how to approach an often-difficult topic.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Angulo MI. Cannabinoid Hyperemesis Syndrome. JAMA. 2024;332(17):1496. doi:10.1001/jama.2024.9716. Link: https://jamanetwork.com/journals/jama/fullarticle/2824833#:~:text=Cannabinoid%20hyperemesis%20syndrome%20(CHS,last%20less%20than%201%20week.Backman, Isabella, Marijuana: Rising THC Concentrations in Cannabis Can Pose Health Risks, Yale School of Medicine, August 30, 2023. https://medicine.yale.edu/news-article/not-your-grandmothers-marijuana-rising-thc-concentrations-in-cannabis-can-pose-devastating-health-risks/Buchanan, Jennie A and George Sam Wang, Cannabinoid Hyperemesis Syndrome, Up To Date, updated July 17, 2024. https://www.uptodate.com/contents/cannabinoid-hyperemesis-syndromeTheme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Warning: This post discusses statistics about extreme pain that may be distressing. While cluster headaches are a neglected, high-impact issue, understanding their true burden requires appreciating the intensity of suffering involved. The pain often reaches levels far beyond typical human experience, making subjective accounts a valuable datapoint until we have robust methods for quantifying pain intensity. For further context, links to firsthand accounts are provided in the footnote[1]. You no longer have a headache, or pain located at a particular site: you are literally plunged into the pain, like in a swimming pool. There is only one thing that remains of you: your agitated lucidity and the pain that invades everything, takes everything. There is nothing but pain. At that point, you would give everything, including your head, your own life, to make it stop. - Yves, cluster headache patient from France (from Rossi et al., 2018) Key [...] ---Outline:(01:11) Key takeaways(03:57) 1. Introduction(04:00) 1.1. Clinical Features and Pain Comparisons(07:22) 1.2. Treatment and Prevention(10:02) 1.3. The Heavy-Tailed Valence Hypothesis and Existing Metrics(14:49) 1.4. Goal(16:14) 2. Methods(17:43) 2.1 Prevalence(19:17) 2.2 Frequency(22:21) 2.3 Duration(23:53) 2.4 Intensity(25:58) 2.5 Burden Metrics(29:01) 3. Results(29:10) 3.1. Global Burden of Cluster Headache Pain(32:05) 3.2. Reweighting of Extreme Pain(39:41) 3.3. Ceiling Effects(43:34) 4. Recommendations and Conclusions(48:31) AcknowledgementsThe original text contained 26 footnotes which were omitted from this narration. --- First published: November 1st, 2024 Source: https://forum.effectivealtruism.org/posts/geh2g2nKb7Kkp26ze/quantifying-the-global-burden-of-extreme-pain-from-cluster --- Narrated by TYPE III AUDIO. ---Images from the article:Apple Podcasts and Spotify do not show images in the episode description. Try Pocket Casts, or another podcast app.

Beyond the Digest are bonus episodes to the DermSurgery Digest that include reviews of interesting and relevant articles in dermatologic surgery literature. This episode features articles from the Journal of the National Comprehensive Cancer Network(JNCCN), the Journal of the American Academy of Dermatology (JAAD) and JAMA Dermatology. Articles include:Mohs Micrographic Surgery in the Surgical Treatment Paradigm of Melanoma In Situ and Invasive Melanoma: A Clinical Review of Treatment Efficacy and Ongoing Controversies. JAADEstablishing Consensus for Mohs Micrographic Surgery Techniques in the Treatment of Melanoma in Situ for Future Clinical Trials: A Modified Delphi Study. JNCCNRecurrence Rate of Small Melanoma In Situ on Low-Risk Sites Excised With a 5-mm Excisional Margin. JAMA DermatologyRecurrence Rate of Melanoma In Situ Excised With a 5-mm Excisional Margin. JAMA DermatologySubcutaneous Injection of Tranexamic Acid Reduces Postoperative Bleeding Following Mohs Micrographic Surgery: A Single Institution Cohort Study. JAADHistopathological Discrepancy of Biopsy Specimens Compared to Subsequent Mohs Surgery or Wide Local Excision Specimens. JAADExtramammary Paget Disease. Part I. Epidemiology, Pathogenesis, Clinical Features, and Diagnosis. JAADExtramammary Paget Disease. Part II. Evidence-based Approach to Management. JAADBeyond the Digest contributors to this episode include: Dermatologic Surgery Digital Content Editor Naomi Lawrence, MD; Beyond the Digest Co-host Yesul Kim, MD; Tara Jennings, MD; Sydney Proffer, MD; and Katie Shawan, MD. Your feedback is encouraged. Please contact communicationstaff@asds.net.

Eosinophilic Esophagitis (EoE) is increasingly recognized as a major cause of swallowing difficulties in children and adults. It affects about one in 2,000 people. But the differences in EoE presentation and outcomes by ethnicity and race remain understudied. Dr Evan Dellon from the University of North Carolina School of Medicine at Chapel Hill is here to explain EoE and discuss the recent findings of a study he co-authored, “Clinical Features and Treatment Response to Topical Steroids in Ethnic and Racial Minority Patients With Eosinophilic Esophagitis.”  We focus on what patients need to know about the main findings, as well as tips for patients to begin discussing their symptoms and treatment options with their provider. This episode is brought to you by Sanofi Regeneron.   

Drs Michelle Kittleson and Ilan Wittstein unravel the complexities of stress cardiomyopathy, discussing the challenges in diagnosis and insights into management strategies. Relevant disclosures can be found with the episode show notes on Medscape (https://www.medscape.com/viewarticle/997319). The topics and discussions are planned, produced, and reviewed independently of advertisers. This podcast is intended only for US healthcare professionals. Resources Takotsubo Cardiomyopathy: Review of Broken Heart Syndrome https://pubmed.ncbi.nlm.nih.gov/32039951 Takotsubo Cardiomyopathy Following Cardiac Surgery https://pubmed.ncbi.nlm.nih.gov/26661572/ Stress Cardiomyopathy in Critical Care: A Case Series of 109 Patients https://pubmed.ncbi.nlm.nih.gov/36331975/ Immune Checkpoint Inhibitor-Associated Myocarditis: Manifestations and Mechanisms https://pubmed.ncbi.nlm.nih.gov/33645548/ Acute Stress Cardiomyopathy: Heart of Pheochromocytoma https://pubmed.ncbi.nlm.nih.gov/32988608/ Takotsubo Cardiomyopathy: Pathophysiology and Role of Cardiac Biomarkers in Differential Diagnosis https://pubmed.ncbi.nlm.nih.gov/29081904/ Short- and Long-Term Incidence of Thromboembolic Events in Takotsubo Syndrome as Compared With Acute Coronary Syndrome https://pubmed.ncbi.nlm.nih.gov/30987433/ Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy https://pubmed.ncbi.nlm.nih.gov/26332547/ Withdrawal of Pharmacological Treatment for Heart Failure in Patients With Recovered Dilated Cardiomyopathy (TRED-HF): An Open-Label, Pilot, Randomised Trial https://pubmed.ncbi.nlm.nih.gov/30429050/ Comparison of Complications and In-Hospital Mortality in Takotsubo (Apical Ballooning/Stress) Cardiomyopathy Versus Acute Myocardial Infarction https://pubmed.ncbi.nlm.nih.gov/32762963/ Gender Differences in Patients With Takotsubo Cardiomyopathy: Multi-Center Registry From Tokyo CCU Network https://pubmed.ncbi.nlm.nih.gov/26317750/

Authors:  Sebouh Bazikian - MS4 at Keck School of Medicine of University of Southern California Gowri Gowda - PGY1 at the University of California Davis Integrated Vascular Surgery Program Steven Maximus- Vascular surgery attending at the University of California Davis, Director of the Aortic Center   Resources:  Rutherford's 10th Edition Chapters: 88, 89, and 91 The North American Symptomatic Carotid Endarterectomy Asymptomatic Carotid Atherosclerosis Study Audible Bleeding's eBook chapter on cerebrovascular disease Houston Methodist CEA Dissection Video: Part 1: https://www.youtube.com/watch?v=wZ8PzhwmSXQ Part 2: https://www.youtube.com/watch?v=E_wWpRKBy4w   Outline:  1. Etiology of Carotid Artery Stenosis Risk factors: advanced age, tobacco use, hypertension, diabetes. Atherosclerosis as the primary cause. Development of Atherosclerotic Disease and Plaque Formation LDL accumulation in arterial walls initiating plaque formation. Inflammatory response, macrophage transformation, smooth muscle cell proliferation. Role of turbulent blood flow at carotid bifurcation in plaque development. Clinical Features of Carotid Artery Stenosis Asymptomatic nature in many patients. Symptomatic presentation: Transient ischemic attacks, amaurosis fugax, contralateral weakness/sensory deficit. Carotid bruit as a physical finding, limitations in diagnosis. Importance of Evaluating CAS Assessing stenosis severity and stroke risk. Revascularization benefits dependent on stenosis severity. Classification of Stenosis Levels Clinically significant stenosis: ≥ 50% narrowing. Moderate stenosis: 50%–69% narrowing. Severe stenosis: 70%–99% narrowing. Stroke Risk Associated with Carotid Stenosis Annual stroke rate: ~1% for 50-69% stenosis, 2-3% for 70-99% stenosis. Diagnosis and Screening No population-level screening recommendation. Screening for high-risk individuals as per SVS guidelines. Carotid Duplex Ultrasound as primary diagnostic tool. Additional tools: CT angiography, Magnetic Resonance Angiography. Handling of 100 cm/sec, Internal/Common Carotid peak systolic velocity Ratio > 4. Revascularization Criteria Symptomatic Patients: 50-69% or 70-99% stenosis, life expectancy at least three or two years, respectively. Asymptomatic Patients: 70% stenosis, considering life expectancy. Surgical Indications and Contraindications Indications: symptomatic patients, life expectancy considerations. Contraindications: Stenosis

“When I draw the interprofessional team for the management of cardio-oncology patients, I always place nurses in the center of it, besides the patient, because nurses are the eyes and ears of interprofessional care 24 hours a day,” ONS member Anecita Fadol, PhD, FNP-BC, FAANP, FAAN, FHKAN, associate professor at the University of Texas MD Anderson Cancer Center in Houston, told Jaime Weimer, MSN, RN, AGCNS-BC, AOCNS®, oncology clinical specialist at ONS, during a conversation about getting to “the heart of the matter” of symptom management for the cardiovascular complications of cancer therapies. You can earn free NCPD contact hours after listening to this episode and completing the evaluation linked below. This episode is part of a series about cancer symptom management basics. We'll add a link to future episodes in the episode notes after the next episode airs. Music Credit: “Fireflies and Stardust” by Kevin MacLeod Licensed under Creative Commons by Attribution 3.0 Earn 1 contact hour of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at myoutcomes.ons.org by January 27, 2025. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of NCPD by the American Nurses Credentialing Center's Commission on Accreditation. Learning outcome: The learner will report an increase in knowledge related to cardiovascular complications associated with today's cancer treatments. Episode Notes Complete this evaluation for free NCPD. Oncology Nursing Podcast Episode 193: How Social Determinants of Health Affect Cardio-Oncology Survivorship ONS Voice articles: Nursing Considerations for ICI-Related Myocarditis Advanced Practice Nurses Are at the Heart of Patient Care in Cardio-Oncology Cardio-Oncology Program Monitors Heart Toxicities Throughout Survivorship Further Research Can Help Nurses Balance Cardiovascular Conditions With Cancer Treatments Clinical Journal of Oncology Nursing articles: Immune Checkpoint Inhibitor–Related Myocarditis: Recognition, Surveillance, and Management Cardio-Oncology: A Continually Evolving Subspecialty in Oncology Nursing Cardio-Oncology Health Disparities: Social Determinants of Health and Care for Black Breast Cancer Survivors Oncology Nursing Forum article: Mitigating Cardiovascular Dysfunction Across the Cancer Continuum ONS book: Cancer Basics (Third Edition) ONS course: Cancer Basics Learn more about the 48th Annual ONS Congress®. Journal of the American Heart Association article: Immune Checkpoint Inhibitor Myocarditis: Pathophysiological Characteristics, Diagnosis, and Treatment Circulation articles: Clinical Features, Management, and Outcomes of Immune Checkpoint Inhibitor–Related Cardiotoxicity Immune Checkpoint Inhibitor–Associated Myositis Cardio-Oncology: Vascular and Metabolic Perspectives: A Scientific Statement From the American Heart Association New England Journal of Medicine article: Fulminant Myocarditis With Combination Immune Checkpoint Blockade Lancet Oncology article: Cardiovascular Toxicities Associated With Immune Checkpoint Inhibitors: An Observational, Retrospective, Pharmacovigilance Study Journal of the American College of Cardiology article: Cardiovascular Disease Risk Among Cancer Survivors: The Atherosclerosis Risk In Communities (ARIC) Study American College of Cardiology Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes Advancing the Cardiovascular Care of the Oncology Patient Heart Failure Society of America 2022 American Heart Association/American College of Cardiology/Heart Failure Society of America Guideline for the Management of Heart Failure International Cardio-Oncology Society European Society of Cardiology Guidelines on Cardio-Oncology Joint National Committee Guidelines for the Management of Hypertension in Adults Attend the Cardio-Oncology Multidisciplinary Practice Virtual Environment on February 13, 2023. To discuss the information in this episode with other oncology nurses, visit the ONS Communities. To provide feedback or otherwise reach ONS about the podcast, email pubONSVoice@ons.org. Highlights From Today's Episode “The most commonly reported cardiovascular toxicities can be classified into five main categories: 1. Cancer treatment-induced hypertension; 2. Cardiomyopathy, left ventricular dysfunction, or heart failure; 3. Myocarditis; 4. Vascular toxicity; and 5. Arrhythmias and QTc prolongation. These cardiovascular toxicities can be caused by the different anti-cancer agents.” Timestamp (TS) 01:46 “Cardio-oncology is more complex than the straightforward cardiology practice. Because in terms of the cardiovascular complications, these symptoms can overlap. But on the other hand, it's a very interesting area of practice because, especially as a nurse, it's like you are a detective, looking into a case and trying to find out what is the main etiology.” TS 23:50 “Nurses have a critical role in identification, monitoring, and management of these treatment-related cardiovascular complications, both in the inpatient setting and the outpatient setting with our cancer survivors. So, a nurse should remember in nursing practice, before administering anticancer treatments. . . a comprehensive cardiovascular history and a full cardiovascular assessment should be performed.” TS 30:27 “When I have to draw the interprofessional team for the management of cardio-oncology patients, I always place nurses in the center of it, besides the patient. Because nurses are the eyes and the ears of the interprofessional care who is seeing the patient 24 hours a day. And early recognition—nurses can do it and monitor the response and all the other symptoms.” TS 36:42 “Nurses are very critical in the management of these patients. Nurses are the experts in terms of doing patient teaching because we have an intimate relationship with patients. In terms of the baseline cardiovascular disease in terms of patient teaching, it is very important for nurses to teach the patient aggressive management of the known cardiac risk factors. . . because these are the ones that could cause cardiovascular complications later on when patients are receiving anticancer treatments.” TS 39:05

The First Principles of Urinary Tract Infections that can get you through, well, any rotation to be honest: What is it, how do you get it, and what can you do about it? === Other Links === Check out our Notion document for First Principles, Free Anki flashcards, and Podcast: https://bit.ly/3dbWGBs Check out our Instagram: https://www.instagram.com/firstprinciplesofmedicine/ Go to http://www.oscer.ai/signup?promo_code=1PM to get a 3-month free Oscer Prime account. Oscer is a clinical reasoning platform powered by artificial intelligence that allows medical students to take histories from a database of over 200 simulated patients. You can use it to practice your history taking, master clinical skills, and perfect your diagnostic reasoning to score 100% for your clinical exams. Recorded 21 June 2022 Co-hosts: JT Yeung, Adian Izwan, Jason D'Silva, Daniel Bontempo. If you have any ideas or feedback, comment on this Notion document, or shoot us an email at firstprinciplesofmedicine@gmail.com === Timestamps === (01:28) First Principle - Anatomy (05:01) Second Principle - Body vs Bugs (09:27) Classification of UTIs (11:43) Predisposing Factors (14:35) Clinical Features (17:11) Management (17:52) Investigations (21:17) Patient Education (24:37) Summary - OSCE style

This week, Rob and Zach will be talking about Types of Headaches including Primary and Secondary Headaches. We will be discussing the following topics within this episode on Types of Headaches!Introduction to Types of HeadachesDefinition, Causes, Pathophysiology, Clinical Features, Diagnosis, Treatment of Secondary Headaches:Mass Occupying LesionsNon-Mass Occupying LesionsPathology Outside of the CNSDefinition, Causes, Pathophysiology, Clinical Features, Diagnosis, Treatment of Primary Headaches:MigrainesCluster HeadachesTension HeadachesTo follow along with Notes & Illustrations for our podcasts please become a member on our website! https://www.ninjanerd.org/podcast/types-of-headachesFollow us on:YouTube: https://www.youtube.com/ninjanerdscienceInstagram: https://www.instagram.com/ninjanerdlecturesFacebook: https://www.facebook.com/NinjaNerdLecturesTwitter: https://twitter.com/ninjanerdsciDiscord: https://discord.com/invite/3srTG4dngWTikTok: https://www.tiktok.com/@ninjanerdlecturesTMAC Fitness. 20 Minute Home Workouts Beginner and Advanced Workouts. No equipment. Each Workout Ends with a Meditation. Brand The Bone Coach Osteoporosis & Bone Health PodcastWorried about bone loss and fractures as you age? SUBSCRIBE NOW for Stronger Bones!

Episode 18 features Dr. April Schachtel and Dr. Katherine Stiff reviewing the following recent publications:“Atypical parakeratosis in nail unit squamous cell carcinoma” Prasad A, Shields BE, Xu YG, Aylward JL, Hinshaw MA. J Cutan Pathol. 2022 Jul;49(7):675-677.53."Evaluation of the Demographic and Clinical Features of Patients With Digital Myxoid Pseudocysts and Their Response to Treatment.” Güldiken G, Göktay F, Atış G, Güneş P. Dermatol Surg. 2022 Jun 1;48(6):625-630

Dr. Lauren Kim interviews Dr. Yeon Joo Jeong, Dr. Jong Eun Lee, and Dr. Minhee Hwang to discuss "Imaging and Clinical Features of COVID-19 Breakthrough Infections: A Multicenter Study" Imaging and Clinical Features of COVID-19 Breakthrough Infections: A Multicenter Study. Lee and Hwang et al. Radiology 2022; 303:682–692.

Episode 86: Abdominal Pain Case. Spikevax® is the brand name of the Moderna COVID-19, and it received full FDA approval in January 2022. Hepatitis B vaccine is now universally recommended to all adults between 19-59 years of age, or older than 60 with risk factors. Deidra Sieck presents a case of abdominal pain in pregnancy and differential diagnosis are discussed.  Introduction: Spikevax ® and Hepatitis B universal vaccination.  Written by Hector Arreaza, MD. Participation by Cecilia Covenas, MD.Spikevax®. This is the brand name given to the mRNA COVID-19 vaccine manufactured by Moderna. It was given full FDA approval for the prevention of COVID-19 in adults 18 years and older. This is the second vaccine approved by the FDA for the prevention of COVID-19 (the first vaccine was Comirnaty®, formerly known as Pfizer Vaccine.) The primary series of Spikevax for immunocompetent adults is comprised of 2 doses, 4 weeks apart. Immunocompromised patients receive a 3rd dose as part of the primary series, one month after the second dose. A booster shot of Spikevax is given at least 5 months after completing the primary series. Spikevax was also authorized for use as a “mix and match” single booster dose following completion of primary vaccination with a different COVID-19 vaccine. It means that recipients of the Pfizer and J&J vaccines who are 18 years and older may receive a single booster dose of Spikevax. The full FDA approval was granted to Spikevax on January 31, 2022.Did you know that Hepatitis B has killed 40 times more unvaccinated healthcare workers than HIV?  Yes, that's right. Hepatitis B is 50 to 100 times more infectious than HIV. It is transmitted by percutaneous or mucosal exposure to infected blood or other bodily fluids. As a reminder, immunizations against many diseases have been required for health care workers for decades, and hepatitis B is one of those required vaccines. That's not new, what's new is the new recommendation about universal Hep B vaccination. In November 2021, the ACIP (Advisory Committee on Immunization Practices from CDC) recommended universal adult Hepatitis B vaccination. After reviewing clinical evidence, the ACIP has unanimously voted to recommend the Hep B vaccine for all adults ages 19-59. Patients who should receive hep B vaccines are: all adults between 19 and 59 years of age, and adults older than 60 with risk factors for hepatitis B infection. However, adults older than 60 without risk factors may also receive hep B vaccines. Vaccinating against Hep B is done to decrease new infections, prevent transmission, and reduce health disparities. HHS has called for the elimination of viral hepatitis as a public health threat by 2030. There are some reasons to recommend universal Hep B vaccination for adults: many infected patients did not have any risk factors for infection and still got infected; almost 85% of adults in the U.S. fall into a higher-risk group, including patients with diabetes and kidney disease; hepatitis B cases in the U.S. rose by 11% between 2014 and 2018 despite having highly effective vaccines; Hep B is one of the primary causes of liver cancer, one of the deadliest cancers; universal vaccination of newborns started in 1991 in the U.S., so, many adults are not immune to Hep B, but now they can be vaccinated without the many restrictions imposed in the past.Remember, Spikevax is the new name for the Moderna vaccine; and you can start vaccinating all adults between 19 and 59 years of age against hep B, regardless of risk factors.This is Rio Bravo qWeek, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it's sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home.___________________________Abdominal Pain Case.  By Deidra Sieck, MS4, Ross University School of Medicine. Hosted by Hector Arreaza, MD.   Abdominal pain in pregnancy is quite common and has a wide differential. I want to begin with a case and then highlight a few of the “do-not-miss” diagnoses when a patient comes with the chief complaint of abdominal pain during her pregnancy. Case presentation: 23-year-old G2P1 at 32 weeks of gestation complains of 12 hours of right lower quadrant abdominal pain, anorexia, and nausea with vomiting. She denies vaginal bleeding or leakage of fluid from the vagina. Denies diarrhea or eating stale foods. No medical history and has been in good health. Denies dysuria and has had no previous surgeries. Her vital signs include a blood pressure of 100/70 mm Hg, heart rate of 105 beats per minute, and temperature of 101.5 F. On abdominal examination, bowel sounds are hypoactive. The abdomen is tender in the right lower quadrant to right flank with significant involuntary guarding. The cervix is closed. The fetal heart tones are in the range of 160 BMP (modified vignette from case files obstetrics and gynecology 5th ed.)What are some of the differentials that come to mind? The 6 differentials that should come to mind that are do not miss diagnoses include:  Placental abruptionAppendicitis Cholecystitis Ectopic Pregnancy Hemorrhagic cyst Ovarian TorsionI want to discuss each of these diagnoses and then devise a plan for the patient in this case. Placental abruptionThis is the most common cause of third trimester bleeding and is an obstetric emergency. It occurs during the second and third trimesters and is described as a midline persistent suprapubic pain. The pain is also accompanied by vaginal bleeding as well as an abnormal fetal heart rate tracing.  Mothers at risk have had a previous abruption, hypertension during the pregnancy, cocaine use, smoking, or preterm premature rupture of the membranes, or trauma as the most common cause of the abruption. This diagnosis is made clinically. The ultrasound is an unreliable modality to see the abruption. If the mother is stable and it is not a complete abruption, the mother usually delivers the baby very quickly vaginally. However, if the abruption is complete, the fetal heart tracing is category III, or the mother is hemodynamically unstable, it is best to deliver by c-section. Appendicitis. Appendicitis can occur any trimester during pregnancy and has been found to occur in 0.1-1.4/1000 pregnancies. The typical nonpregnant patient with appendicitis will come with complaints of right lower quadrant pain that may radiate to the right upper quadrant. This is usually associated with other complaints of nausea, vomiting, anorexia, or fever. [Anorexia: 80% sensitive, The sign of the hamburger] However, this diagnosis may be missed later in pregnancy because of an atypical presentation. As the gravid uterus grows, it can displace the appendix upward and lateral toward the flank. This leads to a presentation that appears to be more consistent with pyelonephritis, leading to a missed diagnosis. Because of the delay in diagnosis pregnant women are 2-3 times more likely to have a ruptured appendix, and the resulting peritonitis increases the likelihood of morbidity and mortality for the patient.  If appendicitis progresses to appendiceal rupture, there is a 30% chance of spontaneous abortion of the fetus. These patients need an ultrasound to make the diagnosis since they cannot have a CT scan in pregnancy despite a CT scan being the preferred modality in nonpregnant patients. The ultrasound should show a non-compressible, blind-ended tubular structure in the right lower quadrant with a maximal diameter greater than 6mm.After the ultrasound confirms the diagnosis, these patients should be taken immediately for an appendectomy. However, the decreased resolution of imaging seen with ultrasound can also lead to delays in these patients receiving the appendectomy.Cholecystitis. Cholecystitis is more common in pregnancy, with occurrence in 1/1600 pregnancies. This can occur anytime in pregnancy after the first trimester. Pregnant women are especially high risk of cholecystitis since they are female and fertile. The other two “f's” that are commonly listed as risk factors for cholecystitis include forty, and obesity. [the F word is banned in this podcast]. Pathophysiology: The increased progesterone and estrogen increase bile lithogenicity. Progesterone also decreases gallbladder contractility. This increase in gallbladder volume and decreased contractility lead to an increase in “biliary sludge” in the gallbladder. The biliary sludge acts as a precursor to gallstones and obstruction of the cystic duct or the common bile duct. The patient with cholecystitis typically comes with complaints of pain in the right upper quadrant which can be associated with nausea, vomiting, anorexia, and fever. This is the same presentation as a patient in pregnancy. The complication of missing this diagnosis includes secondary infection with enteric flora such as: E. coli, Klebsiella, and Enterococcus faecalis.  Fetal loss is seen in 3-20% of pregnancies complicated by cholecystitis. The diagnosis is made with a careful history as well as an ultrasound showing gallstones with dilation and thickening of the gallbladder and gallbladder wall. Treatment should be started with bowel rest, IV hydration, correction of electrolytes, analgesics. They should be given antibiotics if no improvement after 12-24 hours or are experiencing systemic symptoms. If the medical management does not work, these patients should have a cholecystectomy.  The cholecystectomy will most likely be laparoscopic due to the gravid uterus making it difficult to perform an open approach. If in the third trimester and the patient is stable, the surgeon may opt to wait until after delivery to remove the gallbladder.Ectopic pregnancy. This is the leading cause of maternal mortality in the first and second trimesters. It usually presents during the first trimester as pelvic or abdominal pain that is usually unilateral. The patient could also complain of nausea, vomiting, syncope, or vaginal spotting. The diagnosis is made using a serum hCG that meets the threshold and transvaginal ultrasound. The treatment can be surgical or medical. If the pregnancy is early, methotrexate can be used. However, the hCG needs to be trended and followed to zero. A D&C can also be used to treat ectopic pregnancy. Surgery is the first treatment in a patient that is hemodynamically unstable. This diagnosis is not likely in our patient.Ruptured corpus luteum or ruptured hemorrhagic cyst. The corpus luteum cyst is part of a normal endocrine function or a result of prolonged progesterone. In pregnancy, the corpus luteum produces progesterone until 7-10 weeks' gestation until the placenta can produce steroids including hCG and progesterone to maintain the pregnancy. However, intrafollicular bleeding can occur because of the thin-walled capillaries that invade the granulosa cells from the theca interna. If there is excessive hemorrhage, the cyst can enlarge and rupture. The patients presenting with this complaint present with unilateral cramping and lower abdominal pain 1-2 weeks before the rupture. If the corpus luteum becomes hemorrhagic, a hemoperitoneum can develop. These women should undergo an ultrasound, which will show free intraperitoneal fluid. This could also include some fluid around the ovary. The confirmatory method for diagnosis is laparoscopy. Culdocentesis is a procedure that checks for abnormal fluid in the space just behind the vagina. This area is called the cul-de-sac. During a culdocentesis, a long thin needle is inserted through the vaginal wall just below the uterus and a sample is taken of the fluid within the abdominal cavity.Once the bleeding is controlled, there is no further treatment needed. However, if the patient requires a cystectomy due to continued bleeding and the pregnancy is less than 10 weeks, she will need exogenous progesterone because of the loss of the corpus luteum. Ovarian Torsion. Pregnancy is a risk factor for ovarian torsion, especially around 14 weeks and after delivery. Torsion is most likely between 10-17 weeks, and more likely to happen in masses 6-8 cm in diameter. Pregnant and nonpregnant patients have the same presentation, suprapubic or lower quadrant pain, nausea, and vomiting, up to 20% can have a fever. Plan for the patient in the case:1. Ultrasound: Showed a non-compressible, blind-ended tubular structure in the right lower quadrant with a maximal diameter of 7mm.2. Appendectomy: Take the patient to the OR.____________________________Now we conclude our episode number 86 “Abdominal Pain Case.” We started by giving you an update on Spikevax®, formerly known as “the Moderna vaccine”. This is the newest COVID-19 vaccine fully approved by the FDA for patients 18 years and older. Also, Hepatitis B vaccination is now recommended universally to all adults 19-59 regardless of risk factors. Then, Deidra presented a case of a patient who was pregnant and had abdominal pain. Surprisingly, her diagnosis was appendicitis. This is a good reminder that pregnant and nonpregnant patients can get appendicitis. Even without trying, every night you go to bed being a little wiser.Thanks for listening to Rio Bravo qWeek. If you have any feedback about this podcast, contact us by email RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created for educational purposes only. Visit your primary care physician for additional medical advice. This week we thank Hector Arreaza, Cecilia Covenas, and Deidra Sieck. Audio edition: Suraj Amrutia. See you next week! _____________________References:Coronavirus (COVID-19) Update: FDA Takes Key Action by Approving Second COVID-19 Vaccine, US Food and Drug Administration, January 31, 2022. https://www.fda.gov/emergency-preparedness-and-response/coronavirus-disease-2019-covid-19/spikevax-and-moderna-covid-19-vaccine. ACIP fully recommends Spikevax, as CDC expands wastewater surveillance, University of Minnesota, Center for Infectious Disease Research and Policy (CIDRAP), February 04, 2022. https://www.cidrap.umn.edu/news-perspective/2022/02/acip-fully-recommends-spikevax-cdc-expands-wastewater-surveillance.  ACIP recommends universal hepatitis B vaccination for adults aged 19 to 59 years, Healio.com, https://www.healio.com/news/infectious-disease/20211103/acip-recommends-universal-hepatitis-b-vaccination-for-adults-aged-19-to-59-years. Landmark vote by CDC's Advisory Committee on Immunization Practices (ACIP) to recommend universal hepatitis B vaccination, Hepatitis B Foundation, November 4, 2021. https://www.hepb.org/news-and-events/news-2/the-cdcs-advisory-committee-on-immunization-practices-acip-voted-to-recommend-universal-hepatitis-b-vaccination/ Ananth, Cande Vanessa V, and Wendy L Kinzler. “Placental Abruption: Pathophysiology, Clinical Features, Diagnosis, and Consequences.” Edited by Charles J Lockwood, and Vanessa A Barss,  22 Feb. 2021, https://www.uptodate.com/contents/placental-abruption-pathophysiology-clinical-features-diagnosis-and-consequences.  Brooks, David C. Edited by Stanley W Ashley et al., Gallstone Disease in Pregnancy, 26 July 2021, https://www.uptodate.com/contents/gallstone-diseases-in-pregnancy.   H., De Cherney Alan, et al. “Chapter 25: Surgical Disorders In Pregnancy.” Current Diagnosis and Treatment: Obstetrics and Gynecology, McGraw Hill Medical Publishing Division, 2019.  “Obstetrics and Gynecology.” Case Files: Obstetrics and Gynecology 5th Edition, by Eugene C. Toy et al., McGraw-Hill Medical, 2016, pp. 135–144.  Rebarber, Andrei, et al. “Acute Appendicitis in Pregnancy.” Edited by Martin Weiser et al., Up To Date , 17 Sept. 2021, https://www.uptodate.com/contents/acute-appendicitis-in-pregnancy.  Runowicz, Carolyn D, and Molly Brewer. “Adnexal Mass in Pregnancy.” Edited by Barbara Goff and Alana Chakrabarti, UpToDate, 10 Feb. 2022, https://www.uptodate.com/contents/adnexal-mass-in-pregnancy.  Tulandi, Togas. “Ectopic Pregnancy: Clinical Manifestations and Diagnosis.” Edited by Deborah Levine et al., UpToDate, 18 Jan. 2022, https://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diagnosis.

Welcome to Episode 14 of “The 2 View,” the podcast for EM and urgent care nurse practitioners and physician assistants! Show Notes for Episode 14 of “The 2 View” – Urticaria, Foreign Bodies, and a Special Interview Urticaria Bernstein JA, Lang DM, Khan DA, et al. The diagnosis and management of acute and chronic urticaria: 2014 update. J Allergy Clin Immunol. Published 2014. Accessed February 11, 2022. https://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Practice%20and%20Parameters/Urticaria-2014.pdf Radecki RP, MS. Does New IV Urticaria Medication Offer Benefits Over Current Treatments? ACEP Now. Published June 15, 2021. Accessed February 11, 2022. https://www.acepnow.com/article/does-new-iv-urticaria-medication-offer-benefits-over-current-treatments/ Safety of use of high dose antihistamines in difficult-to-control chronic urticaria patients. J Am Acad Dermatol. Published May 1, 2015. Accessed February 11, 2022. https://www.jaad.org/article/S0190-9622(15)00371-0/fulltext Sarti L, Barni S, Giovannini M, Liccioli G, Novembre E, Mori F. Efficacy and tolerability of the updosing of second-generation non-sedating H1 antihistamines in children with chronic spontaneous urticaria. Pediatr Allergy Immunol. Wiley Online Library. Published August 3, 2020. Accessed February 11, 2022. https://onlinelibrary.wiley.com/doi/10.1111/pai.13325 Schaefer P. Acute and Chronic Urticaria: Evaluation and Treatment. Am Fam Physician. Published June 2017. Accessed February 11, 2022. https://www.aafp.org/afp/2017/0601/p717.html Winters M. Clinical Practice Guideline: Initial Evaluation and Management of Patients Presenting with Acute Urticaria or Angioedema. AAEM - American Academy of Emergency Medicine. Published July 10, 2006. Accessed February 11, 2022. https://www.aaem.org/resources/statements/position/clinical-practice-guideline-initial-evaluation-and-management-of-patients-presenting-with-acute-urticaria-or-angioedema Foreign Bodies & Toxic Shock Syndrome Cone LA, Woodard DR, Byrd RG, Schulz K, Kopp SM, Schlievert PM. A recalcitrant, erythematous, desquamating disorder associated with toxin-producing staphylococci in patients with AIDS. J Infect Dis. NIH. PubMed.gov. Published April 1992. Accessed February 11, 2022. https://pubmed.ncbi.nlm.nih.gov/1552193/ Contou D, Colin G, Travert B, et al. Menstrual Toxic Shock Syndrome: A French Nationwide Multicenter Retrospective Study. Clin Infect Dis. Oxford Academic. Published January 15, 2022. Accessed February 11, 2022. https://academic.oup.com/cid/article-abstract/74/2/246/6255963 Parsonnet J, Hansmann MA, Delaney ML, et al. Prevalence of Toxic Shock Syndrome Toxin 1-Producing Staphylococcus aureus and the Presence of Antibodies to This Superantigen in Menstruating Women. J Clin Microbiol. NCBI. Published September 2005. Accessed February 11, 2022. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1234102/ Shands KN, Schmid GP, Dan BB, et al. Toxic-Shock Syndrome in Menstruating Women: Association with Tampon Use and Staphylococcus aureus and Clinical Features in 52 cases. N Engl J Med. Published December 18, 1980. Accessed February 11, 2022. https://www.nejm.org/doi/full/10.1056/nejm198012183032502?casa_token=GVNPVVA8uB4AAAAA:LQTf1B8PlxwffYbLmuOeWnteCLdkKtwEydZDKn2lYW-NoNe8953D58cgSMnWVnwbN136BWtd23zr Streptococcal Toxic Shock Syndrome: All You Need to Know. Cdc.gov. Published November 23, 2021. Accessed February 11, 2022. https://www.cdc.gov/groupastrep/diseases-public/streptococcal-toxic-shock-syndrome.html Toxic Shock Syndrome (Other Than Streptococcal) (TSS) 2011 case definition. Cdc.gov. Reviewed April 16, 2021. Accessed February 11, 2022. https://ndc.services.cdc.gov/case-definitions/toxic-shock-syndrome-2011/ Foreign Bodies Continued - Management Coskun A, Erkan N, Yakan S, Yıldirim M, Cengiz F. Management of rectal foreign bodies. World J Emerg Surg. Published March 13, 2013. Accessed February 11, 2022. https://wjes.biomedcentral.com/articles/10.1186/1749-7922-8-11 O'Malley G, O'Malley R. Body Packing and Body Stuffing. Merck Manuals Professional Edition. Reviewed/Revised May 2020. Accessed February 11, 2022. https://www.merckmanuals.com/professional/special-subjects/recreational-drugs-and-intoxicants/body-packing-and-body-stuffing Guest Interview: Kenny Walks Across America Facebook. Facebook.com. Accessed February 11, 2022. https://www.facebook.com/KennywalksacrossAmerica Kenny Walks Across America. Kenny Walks Across America. Accessed February 11, 2022. http://www.kennywalksacrossamerica.com Recurring Sources Center for Medical Education. Ccme.org. http://ccme.org The Proceduralist. Theproceduralist.org. http://www.theproceduralist.org The Procedural Pause. Emergency Medicine News. Lww.com. https://journals.lww.com/em-news/blog/theproceduralpause/pages/default.aspx The Skeptics Guide to Emergency Medicine. Thesgem.com. http://www.thesgem.com Trivia Question: Send answers to 2viewcast@gmail.com Be sure to keep tuning in for more great prizes and fun trivia questions! Once you hear the question, please email us your guesses at 2viewcast@gmail.com and tell us who you want to give a shout-out to. Be sure to listen in and see what we have to share!

Welcome to Ask Stago, the podcast dedicated to provide expert answers to your expert questions in hemostasis. In today episode, our expert guest, Dr Caroline Vayne from Tours University Hospital in France, gives us an overview on heparin induced thrombocytopenia. As usual, don't forget to send any question you may have to ask@stago.com, we will be glad to answer to it.   Learn more: Gruel Y, Vayne C, Rollin J, Weber P, Faille D, Bauters A, Macchi L, Alhenc-Gelas M, Lebreton A, De Maistre E, Voisin S, Gouilleux-Gruart V, Perrin J, Tardy-Poncet B, Elalamy I, Lavenu-Bombled C, Mouton C, Biron C, Ternisien C, Nedelec-Gac F, Duchemin J, De Raucourt E, Gouin-Thibault I, Rugeri L, Tardy B, Giraudeau B, Bejan-Angoulvant T, Pouplard C. Comparative Analysis of a French Prospective Series of 144 Patients with Heparin-Induced Thrombocytopenia (FRIGTIH) and the Literature. Thromb Haemost. 2020 Jul;120(7):1096-1107. doi: 10.1055/s-0040-1712957. Epub 2020 Jun 22. PMID: 32572863. Gruel Y, De Maistre E, Pouplard C, Mullier F, Susen S, Roullet S, Blais N, Le Gal G, Vincentelli A, Lasne D, Lecompte T, Albaladejo P, Godier A; Members of the French Working Group on Perioperative Haemostasis Groupe d'intérêt en hémostase périopératoire GIHP. Diagnosis and management of heparin-induced thrombocytopenia. Anaesth Crit Care Pain Med. 2020 Apr;39(2):291-310. doi: 10.1016/j.accpm.2020.03.012. Epub 2020 Apr 13. PMID: 32299756. Arepally GM. Heparin-induced thrombocytopenia. Blood. 2017 May 25;129(21):2864-2872. doi: 10.1182/blood-2016-11-709873. Epub 2017 Apr 17. PMID: 28416511; PMCID: PMC5445568. Rollin J, Pouplard C, Gruel Y. Risk factors for heparin-induced thrombocytopenia: Focus on Fcγ receptors. Thromb Haemost. 2016 Oct 28;116(5):799-805. doi: 10.1160/TH16-02-0109. Epub 2016 Jun 30. PMID: 27358188. Pishko AM, Cuker A. Diagnosing heparin-induced thrombocytopenia: The need for accuracy and speed. Int J Lab Hematol. 2021 Jul;43 Suppl 1:96-102. doi: 10.1111/ijlh.13564. PMID: 34288442. Tardy B, Lecompte T, Mullier F, Vayne C, Pouplard C. Detection of Platelet-Activating Antibodies Associated with Heparin-Induced Thrombocytopenia. J Clin Med. 2020 Apr 24;9(4):1226. doi: 10.3390/jcm9041226. PMID: 32344682; PMCID: PMC7230370. Cuker A, Arepally GM, Chong BH, Cines DB, Greinacher A, Gruel Y, Linkins LA, Rodner SB, Selleng S, Warkentin TE, Wex A, Mustafa RA, Morgan RL, Santesso N. American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia. Blood Adv. 2018 Nov 27;2(22):3360-3392. doi: 10.1182/bloodadvances.2018024489. PMID: 30482768; PMCID: PMC6258919. Vayne C, Rollin J, Gruel Y, Pouplard C, Galinat H, Huet O, Mémier V, Geeraerts T, Marlu R, Pernod G, Mourey G, Fournel A, Cordonnier C, Susen S. PF4 Immunoassays in Vaccine-Induced Thrombotic Thrombocytopenia. N Engl J Med. 2021 Jul 22;385(4):376-378. doi: 10.1056/NEJMc2106383. Epub 2021 May 19. PMID: 34010527; PMCID: PMC8174029. Pavord S, Scully M, Hunt BJ, Lester W, Bagot C, Craven B, Rampotas A, Ambler G, Makris M. Clinical Features of Vaccine-Induced Immune Thrombocytopenia and Thrombosis. N Engl J Med. 2021 Oct 28;385(18):1680-1689. doi: 10.1056/NEJMoa2109908. Epub 2021 Aug 11. PMID: 34379914. Kizlik-Masson C, Vayne C, McKenzie SE, Poupon A, Zhou Y, Champier G, Pouplard C, Gruel Y, Rollin J. 5B9, a monoclonal antiplatelet factor 4/heparin IgG with a human Fc fragment that mimics heparin-induced thrombocytopenia antibodies. J Thromb Haemost 2017; 15: 2065–75. Related podcast: Understand the sensitivity and specificity https://www.podcastics.com/podcast/episode/8-what-are-sensitivity-and-specificity-performances-of-a-diagnostic-assay-37747/   Content is scientific and technical in nature. It is intended as an educational tool for laboratory professionals and topics discussed are not intended as recommendations or as commentary on appropriate clinical practice.

Mark Gallant, DPT, OCS, FAAOMPT, joins our hosts Paul Mintken and Kory Zimney to talk through lateral hip pain. Dr. Mark works at Onward Richmond, an out of network practice in Richmond, Virginia focused on helping athletes heal quickly and perform better. Dr. Mark is also a graduate of Evidence In Motion's Orthopaedic Physical Therapy Residency and the Orthopaedic Manual Physical Therapy Fellowship. Here are some of the highlights: Alison Grimaldi's JOSPT article, "Gluteal Tendinopathy: Integrating Pathomechanics and Clinical Features in Its Management" on hip pain in 2015 is the key article that can give you a good foundation to learn more about lateral hip pain. Tissues take time to heal. Three visits is not always going give you the time to see your patients get better. The tendon is not going to heal if the patient doesn't eat proper nutrition, get proper sleep and have some sort of activity that they do. The lifestyle aspects are the best place to start. For runners suffering from, doing hip strengthening is not going to change running mechanics, so the first place to start with these active individuals is to look at their running mechanics. Mark Gallant's Clinical Pearl: Excessive data is the enemy. Doing a few tests really well, having a few manual therapy techniques you can do really well and having a few exercises that you can coach really well will be more productive than doing a mediocre job at everything.  Ad Info: Continue your learning past what you hear today, EIM offers certifications that elevate your clinical decision making and help get you to the next level of patient care and expertise. Get 5% off by letting your program advisor know you're a PT Elevated Podcast listener. Check out your program options here. The last episode of the season will feature questions and comments from you the listener. Send your questions, whether they be episode-specific, clinical or research-related to podcast@eimpt.com. Your question may be featured in the last episode, so include some info about you and your practice. We look forward to hearing your questions! More Links: Gluteal Tendinopathy: Integrating Pathomechanics and Clinical Features in Its Management Contact Mark Gallant @ZimneyKJ @PMintkenDPT @EIMTeam

What are the clinical features of body dysmorphic disorder? How can you body dysmorphic disorder? Tips for screening. Faculty: Robert Hudak, M.D. Hosts: Jessica Diaz, M.D. ; Flavio Guzman, M.D. Learn more about Premium Membership here Earn 1 CME: Obsessive-Compulsive and Related Disorders Body Dysmorphic Disorder: DSM- 5 Criteria and Clinical Features

What are the clinical features of hoarding disorder? How can you assess hoarding disorder? Tips for screening. What other comorbidities should you consider? Faculty: Robert Hudak, M.D. Host: Flavio Guzman, M.D. Learn more about Premium Membership here Earn 1 CME: Obsessive-Compulsive and Related Disorders Hoarding Disorder: DSM-5 Criteria, Clinical Features, Epidemiology, and Comorbidities

Metabolic Bone Diseases are commonly seen by General Practitioners in a Primary Care setting. In today's episode, our President Davog McCaffrey discusses the  Clinical Features, Investigations, Diagnosis and Management of 3 main Metabolic Bone Diseases - Osteoporosis, Osteomalacia and Paget's Disease. 

FDA 连续批准2个血小板生成素受体激动剂术前治疗慢性肝病引起的血小板减少LANCET 使用阿司匹林预防Lynch综合征患者发生结直肠癌Science Advance 在体内将脾脏转化为类肝脏器官艾曲波帕（lusutrombopag）艾曲波帕（Lusutrombopag）是一种小分子的血小板生成素受体激动剂。2018年7月，FDA批准艾曲波帕.（lusutrombopag）治疗计划手术的、慢性肝病引起的血小板减少症。《L-PLUS2研究：艾曲波帕Lusutrombopag用于治疗正在接受侵入性治疗的慢性肝病患者血小板减少症》Hepatology，2019年10月 (1)该研究的目的是评价艾曲波帕用于慢性肝病合并血小板减少患者中，手术前提高血小板计数的疗效。这项全球性的、随机、双盲、安慰剂对照的第3期研究中，招募215名患者，患有慢性肝病且基线血小板计数

FDA 连续批准2个血小板生成素受体激动剂术前治疗慢性肝病引起的血小板减少LANCET 使用阿司匹林预防Lynch综合征患者发生结直肠癌Science Advance 在体内将脾脏转化为类肝脏器官艾曲波帕（lusutrombopag）艾曲波帕（Lusutrombopag）是一种小分子的血小板生成素受体激动剂。2018年7月，FDA批准艾曲波帕.（lusutrombopag）治疗计划手术的、慢性肝病引起的血小板减少症。《L-PLUS2研究：艾曲波帕Lusutrombopag用于治疗正在接受侵入性治疗的慢性肝病患者血小板减少症》Hepatology，2019年10月 (1)该研究的目的是评价艾曲波帕用于慢性肝病合并血小板减少患者中，手术前提高血小板计数的疗效。这项全球性的、随机、双盲、安慰剂对照的第3期研究中，招募215名患者，患有慢性肝病且基线血小板计数

This is a podcast article summary of "Histopathologic and Clinical Features in Patients with Diabetes and Kidney Disease" by Sarah F. Sanghavi and Charles E. Alpers.

Last week we finished up the Cluster B personality disorders, and we asked our listeners which cluster we should do next: A or C. And the winner is…Cluster A! Cluster A personality disorders are characterized as odd or eccentric personalities including that of schizoid personality disorder, schizotypal personality disorder, and the personality disorder we are covering today: Paranoid Personality Disorder. linktr.ee/blackbirdadvocacy References: https://www.merckmanuals.com/professional/psychiatric-disorders/personality-disorders/paranoid-personality-disorder-ppd Bouthier, M. and Mahe, V. (2019). Paranoid Personality Disorder and Criminal Offenses. Nestor, P.G. (2002). Mental Disorder and Violence: Personality Dimensions and Clinical Features. Johnson, J.G., et. al. (2000). Adolescent Personality Disorders Associated With Violence and Criminal Behavior During Adolescence and Early Adulthood. Coolidge, F.L. and Anderson, L.W. (2002). Personality Profiles of Women in Multiple Abusive Relationships Lee, R. (2017). Mistrustful and Misunderstood: A Review of Paranoid Personality Disorder.

Interview with Alan Braverman, MD, author of Clinical Features and Outcomes of Pregnancy-Related Acute Aortic Dissection

Interview with Alan Braverman, MD, author of Clinical Features and Outcomes of Pregnancy-Related Acute Aortic Dissection

A Very Brief Discussion On Bone Tumors,.. Their Risk Factors, Clinical Features, Investihations, Treatment Modalities & Follow Up Protocol... With Dr Rushit Shah Disclaimer : All the information provided by Health And Wellness Podcast and associated videos are strictly for informational purposes only. It is not intended as a substitute for advice from your health care provider or physician. The information provided and associated videos cannot be used to make a diagnosis or treat any health condition. This website contains general information about medical conditions and treatments. The information is not an advice, and should not be treated as such.The medical information on this website is provided “as is” without any representations or warranties, express or implied.

Dr. John Fleetham is joined by Dr. Christopher Chang to discuss the article “Clinical Features of 85 Fatal Cases of COVID-19 from Wuhan: A Retrospective Observational Study”.

Dr. David Lapides talks with Dr. Francesc Graus about his paper, "Clinical Features of Seronegative, but CSF Antibody-Positive, Anti-NMDA Receptor Encephalitis" You can read the article here:  https://nn.neurology.org/content/7/2/e659

Recent research suggests that loneliness is one more invisible symptom of MS. But social outreach and interaction have never been more accessible.  My guest is Mary Pettigrew, an MS Warrior and social media phenom. In 2014, Mary launched MSPals, a Twitter group that has evolved into a community of more than 5,000 followers. We're talking with Mary about the benefits of connecting online and the importance of finding your creative outlet. We're also talking about new research on the severity and impact of MS fatigue, along with a new smartphone app designed to improve MS fatigue. We'll tell you about a new way of treating spasticity, and we'll give you the details about a new study that's looking at TeleRehab. We'll even tell you how to sign up for the study! We have a lot to talk about! Are you ready for RealTalk MS?! ___________ Severity & Impact of MS Fatigue   2:06 MS TeleCoach App Designed to Improve MS Fatigue  4:31 A New Treatment to Manage Spasticity  6:45 The STEP MS TeleRehab Study  8:17 You Can Participate in the STEP For MS TeleRehab Study  10:23 My Interview with Mary Pettigrew, Founder of MSPals  11:58 ___________ SHARE YOUR FEEDBACK, QUESTIONS, AND IDEAS Email: jonstrum@RealTalkMS.com Phone: (310) 526-2283 ___________ LINKSIf your podcast app doesn’t allow you to click on these links, you’ll find them in the show notes in the RealTalk MS app or at www.RealTalkMS.com Download the RealTalk MS App for iOS Download the RealTalk MS App for Android Prevalence of Fatigue and Its Association with Clinical Features in Progressive and Non-Progressive Forms of Multiple Sclerosis Improving Fatigue in Multiple Sclerosis by Smartphone-Supported Energy Management: The MS TeleCoach Feasibility Study Supervised vs Telerehab Exercise program for People With Multiple Sclerosis: Eligibility & Study Sites iConquer MS Give RealTalk MS a Rating & Review ___________ Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 73 Hosted By: Jon Strum Guest: Mary Pettigrew Tags: MS, MultipleSclerosis, MSResearch, STEPMS, MSPals, RealTalkMS

Much existing propaganda claims that African Americans do not suffer from celiac disease. Even the Gluten Free RN was surprised to find out that her adopted daughter had a genetic predisposition to the disease back in 2006, as research available at the time regarded the HLA-DQ2 and HLA-DQ8 genes to be primarily Caucasian traits. And until we take steps to conduct a mass screening, we simply don’t know how common celiac disease is among people of African descent. Today, the Gluten Free RN is exploring celiac disease in the African American population. She covers a 2006 study out of Columbia University that assessed African American celiac patients, discussing the variety of ways the subjects presented with celiac disease and the potential reasons for their poor compliance with the prescribed gluten-free diet. Nadine also considers the prevalence of celiac disease on the continent of Africa, explaining why she believes the number of celiac patients will explode with the population’s growing exposure to wheat. Listen in for the Gluten Free RN’s insight on other health issues that may point to undiagnosed celiac disease and learn how we can prevent celiac disease among the African American population with access to testing, social support and gluten-free food! What’s Discussed: The 2006 Columbia University study of celiac disease in African Americans Identified nine patients with biopsy-proven celiac disease Presented with diarrhea, iron deficiency anemia and autoimmune disorders Why patients in the Columbia study demonstrated poor dietary compliance Expense, availability and palatability of gluten-free food Lack of symptoms at diagnosis, inaccurate dietary information Nadine’s prediction around the number of celiac patients in Africa Increasing exposure to wheat will cause explosion The statistics regarding the mortality burden of celiac disease Science Daily reported estimates of 42K child deaths every year in 2011 Majority from Africa and Asia The overlap between diabetes and celiac disease Every type 1 diabetic is HLA-DQ2/8 gene carrier The health issues that may indicate undiagnosed celiac disease Type 1 diabetes, cardiac issues, stroke and heart attack Obesity (stems from lack of nutrient absorption) How to prevent celiac disease among the African American population Access to testing, social support and gluten-free food Resources: Celiac Disease and How Gluten Affects Your Skin EP011 ‘Your Skin on Gluten’ on YouTube ‘Celiac Disease in African-Americans’ in Digestive Diseases and Sciences ‘First Global Estimates of Coeliac Disease and Its Mortality Burden’ in Science Daily Neurological Disorders Associated with Celiac Disease EP012 ‘Celiac Disease in the Developing Countries: A New and Challenging Public Health Problem’ in the World Journal of Gastroenterology ‘Systematic Review: Worldwide Variation in the Frequency of Coeliac Disease and Changes Over Time’ in Alimentary Pharmacology and Therapeutics ‘HLA Typing and Celiac Disease in Moroccans’ in Medical Sciences ‘A Historical Assessment of Sources and Uses of Wheat Varietal Innovations in South Africa’ in the South African Journal of Science University of Chicago: Celiac Disease Facts and Figures ‘Adult Coeliac Disease in South Africa: An Analysis of 20 Cases Emphasizing Atypical Presentations’ in the South African Medical Journal   ‘Epidemiological and Clinical Features in Immigrant Children with Coeliac Disease: An Italian Multicentre Study’ in Digestive and Liver Disease ‘Prevalence of Positive Coeliac Serology in a Cohort of South African Children with Type 1 Diabetes Mellitus’ in the South African Journal of Child Health ESPGHAN Goes Africa Course Connect with Nadine: Instagram Facebook Contact via Email ‘Your Skin on Gluten’ on YouTube Melodies of the Danube Gluten-Free Cruise with Nadine Books by Nadine: Dough Nation: A Nurse's Memoir of Celiac Disease from Missed Diagnosis to Food and Heal

Dr. Paul Wong:                  Welcome to the monthly podcast, On The Beat, for Circulation: Arrhythmia and Electrophysiology. I'm Dr. Paul Wong, editor in chief, with some of the key highlights from this month's issue. We'll also hear from Dr. Suraj Kapa, reporting on new research from the latest journal articles in the field. In our first article, Ratika Parkash and associates examined whether the outcomes following escalated antiarrhythmic drug therapy, or catheter ablation, depended on whether ventricular tachycardia with amiodarone refractory or sotalol refractory in patients with prior myocardial infarction in the VANISH study. At baseline, 169, or 65%, were amiodarone refractory, while the remaining were sotalol refractory. Amiodarone refractory patients had more renal insufficiency; 23.7% versus 10%. Worse, new ARC Heart Association class, 82.3% versus 65.5% class II or III; and lower ejection fraction, 29% versus 35%. Within the amiodarone refractory group, ablation resulted in a reduction of any ventricular arrhythmias compared to escalated drug therapy, with a hazard ratio of 0.53, P = 0.02. Sotalol refractory patients had trends towards higher mortality in VT storm with ablation, with no effect on ICD shocks. Within the escalated drug arm, amiodarone refractory patients had a higher rate of composite endpoint, with a hazard ratio of 1.94 and a P value of 0.01. In a trend toward higher mortality, hazard ratio 2.4, P = 0.07. While mortality was not different between amiodarone and sotalol refractory patients within the ablation treatment group. In our next study, Junaid Zaman and associates examined 57 cases in which local ablation of persistent atrial fibrillation terminated to sinus rhythm or organized tachycardia. The authors analyze unipolar electrograms collected during atrial fibrillation from multi-polar basket catheters to reconstruct isochronal activation maps for multiple cycles, and computational modeling and phase analysis were used to study mechanisms of map variability. At all signs of atrial fibrillation termination, localized, repetitive activation patterns were observed, 21% with complete rotational activity, 46% with partial rotational circuits, and 33% with focal patterns. In computer simulations incomplete segments of partial rotations coincided with areas of slow conduction, characterized by complex, multi-component electrograms. In our next article, Matthew Kalscheur and associates sought to use a novel machine-learning approach to predict outcomes following resynchronization therapy in the companion trial. The random forest algorithm resulted in the best performing model. In 595 CRTD patients in the companion trial, 105 deaths occurred, with a median follow-up of 15.7 months. The survival difference across subgroups differentiated by bundle branch block morphology and cure restoration did not reach significance, P = 0.08. The random forest model, however, produced quartiles of patients with an eight-fold difference in survival between those with the highest and lowest predictive probability for events, hazard ratio 7.96 with a P value of less than 0.0001. The model also discriminated the risk of composite endpoint of all cause mortality, or heart failure hospitalization, better than subgroups based on bundle branch block morphology and cure restoration. Future studies are needed to validate this model in other populations. In our next paper, Amr Barakat and associates examined the clinical outcomes of trans-venous lead extraction for CIED infection based on renal function. The authors examined 1,420 consecutive patients undergoing trans-venous lead extraction of infected CIEDs over a 14 year period. Groups with normal renal function, Group 1, consisting of 1,159 patients, Group 2, 163 patients with renal dysfunction not requiring dialysis, and Group 3, 98 patients on dialysis. Complete procedural success rates were comparable in the three groups: 94%, 96%, and 94% in Groups 1, 2 and 3, respectively. This was not statistically significant. The mortality rates were significantly higher in dialysis patients at one month. The procedure-related complication was 12.2% in dialysis patients versus 6.5% in Group 1 and 6.1% in Group 2. Other factors associated with mortality were lead material retention, functional New York Heart Association Class, and occurrence of procedural complications. In our next paper, Eric Johnson and associates studied the contribution of the current ITO, two left ventricular re-polarization in the human heart, since the current has been shown to have an important role in animal models. The authors found that using whole-cell voltage clamp recordings from myocytes, isolated from the left ventricle, non-failing human hearts, that there were two, distinct transient currents, ITO fast and ITO slow. The two currents have significantly different rates of recovery from inactivation and pharmacological sensitivities. ITO fast recovers in about 10 milliseconds, 100 times faster than ITO slow, and it's selectively blocked by KV4 channel toxin SNX 482. Using current clamp experiments, they found that regional differences in action potential wave forms, with a notch in phase one in the left ventricular subepicardial myocytes. In failing, left ventricular subepicardial myocytes, ITO fast was reduced, while ITO slow was increased. In addition, the notch and plateau potentials were depolarized, and action potential durations were prolonged, both statistically significantly. Slowing ITO fast inactivation results in a dramatic action potential shortening. The authors concluded that remodeling of ITO fast in failing, human left ventricular subepicardial myocytes, attenuates transmural differences in action potential wave forms. In our next paper, Ravi Vaidyanathan and associates examine the interaction between Caveolin 3 domain in the inward rectifier potassium channels. Although the IK1 current is mainly composed of Kir2.1, there are Kir2.2 and Kir2.3 heterotetromerisoforms that occur and modulate the IK1 current, but these have not been studied. Kir2.x isoforms have unique, subcellular co-localization in human cardiomyoctyes and co-immunoprecipitate with Cav3. Using induced pluripotential stem-cell-derived cardiomyocytes, the LQT9 Cav3 mutation, F97CCav3 resulted in actual potential prolongation. Based on the technique FRET, which is Fluorescent Resonance Energy Transfer, the authors calculated the distance between KR2.2 and cath ray proteins to be 6.61 nanometers. LQT9 is caused by Cav3 mutations. Prior work has shown that F97CCav3 mutation increases the late sodium current, and decreases KR2.1 current density by distinctive mechanisms. This study extends the authors' previous observations on the impact of LQT9 Cav3 mutation on Kir2.1 current, by demonstrating that mutation affects the Kir2.2 current. LQT9 causing Cav3 mutation differentially regulates current density and cell surface expression of Kir2.x homomeric and heteromeric channels. The authors show that the mutation does not affect Kir2.3 current, but the heterotetromer Kir2.2-2.3 demonstrated loss of function. Using the Li-Rudy [inaudible 00:09:45] model and myocyte mathematical model, the authors' data suggest that both loss of IK1 and increased sodium L are required for arrhythmia generation in LQT9. In our next study, Christophe Teuwen and associates use high resolution epicardial mapping electrodes, 128 or 192, with an inter-electrode distance of 2.0mm of the entire atrial surface in 164 patients. These patients were undergoing open-chest cardiac surgery. This study was designed to examine the conduction of atrial extrasystoles. The authors found that a higher degree of aberrancy was associated with a higher instance of conduction disorders. Most conduction disorders were provoked by atrial systoles emerging as epicardial breakthroughs. Atrial extrasystoles cause most conduction disorders in patients with left atrial dilatation or diabetes mellitus. In our next paper, Yuki Komatsu and associates examine 31 patients with idiopathic ventricular arryhthmias, using a two french microcatheter placed in a communicating vein between the great cardiac vein and small cardiac venous system, which passes between the aortic and pulmonary annulae, and is located in close associated with the left ventricular summit. They found that 14 patients had summit ventricular arryhthmias. The remaining 17 patients control group had ventricular arryhthmias originate from the right ventricular outflow track in the aortic cusps.  In patients with summit ventricular arryhthmias, the earliest activation during ventricular arryhthmias in the summit, preceded to cure as onset by 34 milliseconds. The summit ventricular arryhthmias exhibited inferior axes, negative polarity in lead one, deeper Q wave in AVL than AVR, nonspecific bundle branch morphology with an RS ratio in lead V1 of 0.67, distinguishing them from arryhthmias originating from the right ventricular outflow track or right ventricular cusp. Overall, ablation success was achieved in 10, or 71% of patients with summit ventricular arryhthmias, and 88% in the control group, P = 0.24. In our final paper, Deepak Padmanabhan and associates examine differences in mortality in patients with non-MRI conditional CID undergoing brain MRI compared to controls. Patients with CIDs undergoing brain MRI were compared with three control groups matched for age, sex, imaging year, and type of CID. These groups included 1) no CID and brain MRI, 2) CID in brain-computed CT, and 3) no CID in brain CT. They estimated all cause mortality at five years for CID MRI group, was not significantly different from patients who underwent CT, with or without a device. There was a significant increase in the mortality between CIED versus no CID MRI groups, hazard ratio 1.46 with a P value of 0.04. That's it for this month, but keep listening. Saraj Kapa will be surveying all journals for the latest topics of interest in our field. Remember to download the podcasts On the Beat. Take it away Saraj. Saraj Kapa:                          Thank you Paul, and welcome back to On the Beats where this month we'll be focusing on articles that are particularly hard-hitting, published across the literature in December of 2017. It's my pleasure to introduce 20 different articles that seem to have either particular interest or might change the field in the future. First, within the area of atrial fibrillation, we'll focus within the area of anticoagulation and stroke prevention. In the Journal of the American College of Cardiology, Vivek Reddy et al published on the five-year outcomes after left atrial appendage closure, from the Prevail and Protect AF trials. They included a total of 1,114 patients, with a total of 4,343 patient years of follow-up, randomized two to one to closure versus Warfarin. While ischemic stroke and systemic embolism of [inaudible 00:14:32] were numerically higher with closure, this did not reach statistical significance in terms of hemorrhagic stroke, unexplained death, and post-procedure bleeding favor left atrial appendage closure. These findings further support a role for left atrial appendage closure in the specific groups of patients enrolled in the Protect and Prevail Studies. Of course, we always need to understand, that extrapolation to patients who may not have met inclusion criteria will be difficult. In particular, given both trials had their own fundamental limitations in the Prevail study. There was a relatively low rate of [inaudible 00:15:09] in the Warfarin arm. And in turn, there was a relatively high complication rate in Protect AF with left atrial appendage closure. Part of the differences might be due to the fact that, with more experience, complication rates might decrease. Furthermore, a comparison with more novel agents, such as the new oral anticoagulants, remains to be seen. Next, within the realm of cardiac mapping and ablation for atrial fibrillation, we review an article by Vlachos et al published in the Journal of Cardiovascular Electrophysiology entitled Low-Voltage Areas Detected by High-Density Electroanatomical Mapping for Recurrence of Ablation after a Paroxysmal Atrial Fibrillation. They presented the results from a series of 80 patients undergoing ablation for paroxysmal atrial fibrillation, performing high-density voltage mapping to characterize the total area involved by low voltage. They demonstrated, when low voltage areas, defined as less than 0.4 millivolts, were seen in greater than 10% of the left atrial surface area, this served as an independent predictor of atrial fibrillation recurrence. These data support prior research, including that of MRIs, suggesting the characterization of the atrial substrate may correlate with likelihood of ablation success. Identifying methods however, to accurately and reproduce will identify these patients with more atrial substrate prior to ablation, remains to be seen. The importance of this, however, is our ability to better counsel patients on the likelihood of treatment success. Next within the realm of atrial fibrillation, we review elements of risk stratification managements. First, in the December issue of the Journal of American College of Cardiology, Takimoto et al published on how Eplerenone may reduce atrial fibrillation burden without preventing atrial electrical remodeling. In a randomized controlled ovine atrial tachy pacing model of atrial fibrillation. The authors provided daily, oral Eplerenone and compared this with a placebo. They showed that Eplerenone significantly reduced the rate of left atrial dilatation, with less smooth muscle actin protein, atrial fibril [inaudible 00:17:17]. Furthermore, Eplerenone further prolonged the time to persist in atrial fibrillation in 26% of animals. However, interestingly, Eplerenone did not prevent AF-induced electrical remodeling.  These data suggest that Eplerenone, or other medications that can be used to prevent or reverse structural remodeling, may offer an upstream therapy to reduce atrial fibrillation burden, and decrease likely the persistent atrial fibrillation. Giving the ever-growing population of patients suffering from atrial fibrillation, identifying upstream approaches to prevent it will be critical. Of course, these need to be taken with due consideration, however. Specifically, the model used here, namely that of an atrial tachy pacing model, might not be applicable to all human atrial fibrillation. Thus, whether or not such therapies actually offer benefit in clinical models, is as of yet unclear. Finally, from the realm of atrial fibrillation, we review the article by Rowin et al published in circulation entitled Clinical Profile of Consequences of Atrial Fibrillation Hypertrophic Cardiomyopathy. In patients presenting with hypertrophic cardiomyopathy, atrial fibrillation is known to be a significant co-morbidity. However, the implications of atrial fibrillation in terms of worsening of heart failure status, or long-term morbidity mortality are less clear. Rowin et al reviewed the natural history of atrial fibrillation amongst 1,558 patients, prospectively followed at a single center. Nearly 20% of the population developed atrial fibrillation with the majority having symptomatic paroxysmal atrial fibrillation. However, atrial fibrillation was not associated with any increase in cardiovascular mortality or worsening of heart failure status. Furthermore, mortality that was directly related to atrial fibrillation was nearly exclusively related to thrombolic stroke. Anticoagulation [inaudible 00:19:13] reduced this risk. The traditional scoring systems fared poorly in assessing the stroke risk of this population. About 121 patients underwent invasive rhythm control approaches, including 72 patients undergoing maze and 49 catheter ablation. The success rate of maze was significantly greater at around 75%. These data are important when counseling hypertrophic cardiomyopathy patients presenting with new-onset atrial fibrillation. While it is clear that paroxysmal atrial fibrillation has a significant impact on symptoms and quality of life, it does not cause worsened, overall, long-term outcomes. However, it does highlight the importance of anticoagulation in this population, nearly irrespective of the underlying risk score. In terms of rhythm control options, it appears that rhythm control options can be successful in these patients. Finding that catheter ablation is associated with a 40 to 50% success rate is in keeping with prior published data. Thus, consideration of when a patient needs to be referred to maze, needs to be considered in the clinical inpatient context. Changing gears, we will next review articles within the realm of ICDs, pacemakers, and CRT. In the New England Journal of Medicine this past month, Nazarian et al published on their experience regarding the safety of magnetic resonance imaging in patients with cardiac devices. They performed a prospective non-randomized study of the safety of, specifically, 1.5 tesla-strength MRI scans on legacy. In other words, not MRI conditionally-safe pacemakers and defibrillators. A total of 2,103 scans were done among 1,580 patients. They demonstrated no long term clinically significant adverse events. Nine patients did experience a reset to a backup mode, though eight of which were transients. The most common change seen acutely was a decrease in PVA amplitude in one percent of patients, and in a long term follow-up, 4% of patients experiencing a decrease in PVA amplitude, increase in atrial catheter sheer threshold, or increase in right or left ventricular capture threshold. However, none of these events were considered clinically significant. Furthermore, there was not a good [inaudible 00:21:23] group to know if this long term change in amplitudes or thresholds might have been seen in patients who had devices that were not exposed to MRI. These findings are complimentary to multiple, prior, published reports, indicating the safety of performing MRIs under clinical protocol in legacy pacemakers and defibrillators. It calls into question whether MRI conditional devices truly offer an additional safety factor furthermore, over legacy devices. Next we review an article by Lakkireddy et al published in Heart Rhythm entitled A Worldwide Experience, the Management of Battery Failures and Chronic Device Retrieval of the Nanostim Leadless Pacemaker. Lakkireddy et al reported their large multi-center experience on the overall risk of battery failure. Amongst 1,423 implanted devices there were 34 battery failures occurring, on the average, three years after implants. Furthermore, about 73 patients underwent attempted device retrieval, and this was successful in 90%, with the seven failures of retrieval being due to either inaccessibility of the docking button, or dislodgement of the docking button in one patient, in whom it embolized to the pulmonary artery. An additional 115 patients interestingly received an additional pacemaker after release of the device advisory. These data suggest that there may be as high as an overall 2% risk of battery failure with the Nanostim device, even late after implants. This highlights the need for close follow-up, even if the battery appears relatively stable up to two year after implants. Furthermore, almost 10% of devices cannot be successfully retrieved. However, in those patients, even with re-implantation of a separate device, there was no device-device interaction seen. Further innovation will be needed to optimize device longevity, and close follow-up of all patients undergoing implantation will be critical to understand the overall long term efficacy and safety when compared to other traditional devices. Finally, within the realm of device care, we focus on an article by Kiehl et al, again published in Heart Rhythm this past month entitled Incidence and Predictors of Late Atrial Ventricular Conduction Recovery Among Patients Requiring Permanent Pacemaker for complete heart block after cardiac surgery. They reviewed the likelihood of recovery of conduction in their retrospective cohort of 301 patients. Interestingly, 12% of patients had recovery of AV conduction on average six months after surgery. Those who did not recover tended to more likely have preoperative conduction abnormalities. Saraj Kapa:                          Findings that suggested a higher likelihood of long term conduction recovery included female sex and the existence of transient periods of AV conduction postoperatively. These data highlight that recovery of AV conduction is possible in a significant number of patients undergoing cardiac surgery. However, being able to predict long term recovery may assist in device selection, to avoid more costly device implantations that may not be needed over chronic follow-up. Prospective studies amongst larger numbers of patients are needed to better understand mechanisms of block, mechanisms of recovery, an optimal device in patient selection. Changing focus, we will next review two articles within the realm of supraventricular tachycardias. First we read an article by Han et al published in JACC Clinical Electrophysiology, entitled Clinical Features in Sites of Ablation for Patients With Incessant Supraventricular Tachycardia From Concealed Nodofascicular and Nodoventricular Tachycardias. Han and group describe three cases of concealed nodovascicular, nodoventricular re-entrant tachycardias, and focus on the different mechanisms of proving their participation in tachycardia. In all cases, atrial ventricular re-entering tachycardia was excluded. Successful ablation for these tachycardias occurred either at the slow pathway region, the right bundle branch, or the proximal coronary sinus. This is the first described case of incessant, concealed tachycardias related to these pathways. The importance of this article highlights an understanding the mechanisms proving the contribution to tachycardia, and the importance of recognition when performing electrophysiology studies, and being unable to reveal traditional mechanisms, which exist in most patients, such as atrial tachycardia, AVNRT or AVRT. Next we review an article by Guo et al published in Europace entitled Mapping and Ablation of Anteroseptal Atrial Tachycardia in Patients With Congenitally Corrected Transposition of the Great Arteries: Implications of Pulmonary Sinus Cusps. They reviewed three separate cases of anteroseptal atrial tachycardias in the setting of congenitally corrected transposition. They demonstrated that in these cases, there was successful ablation performed with the pulmonary sinus cusps. The result is successful and durable suppression. The reason this article is important lies in the fact that it's critical to understand both cardiac anatomy and cardiac nomenclature. The pulmonary valve in CCTJ is affectively the systemic ventricular arterial valve, given that the right ventricle is the systemic ventricle. Thus, mapping in this region of CCTJ abides the same principles as mapping the aortic valve in structurally normal hearts for similar tachycardias. However, understanding the nomenclature and that despite the variant anatomy, the utility of similar approaches to mapping of the systemic outflow are important when matching these complex, congenital anatomy or arrhythmia patients. Changing gears yet again, we review an article within the realm of sudden death and cardiac arrest. Baudhuin et al published in Circulation and Genetics entitled Technical Advances for the Clinical Genomic Evaluation of Sudden Cardiac Death. Baudhuin et al reviewed the utility of formal and fixed paraffin-embedded tissue, which is routinely obtained in an autopsy, to perform post-mortem, genetic testing. One of the main limitations to advising family members who have had prior family history of sudden death in closely related relatives, is that blood is often not available to perform DNA screening late after death. DNA however is often degraded in the tissues that are commonly available at autopsy, namely the formal and fixed paraffin-embedded tissues. The authors sought to evaluate if your next generation techniques could make these types of tissue adequate for diagnosis. They demonstrated amongst 19 samples, that performance characteristics were similar between whole blood and these tissue samples, which could be as old as 15 years. It can be critical to identify disease-causing mutations in family members, as individuals who might not yet be affected, but at risk, need to know about that overall risk. Given that decision to sequence might also not be universally applied at all centers, or in all situations, oftentimes these paraffin-embedded tissues might be the only available option, sometimes over a decade after death. This represents the first report of using next-generation sequencing approaches to successfully and accurately sequence for specific mutations using paraffin-embedded tissue. This may offer additional options to help family members achieve diagnoses for sudden death-inducing conditions. Within the realm of cellular electrophysiology, we review an article by Lang et al published in Circulation Research entitled Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart. Lang et al reviewed the effect of cell-cell coupling on the likelihood of triggered arryhthmias. In a [inaudible 00:28:45] model, they demonstrated the myocytes that are poorly synchronized with adjacent myocytes were more prone to triggered activity due to abnormal calcium handling when compared to myocytes with normal connection to adjacent cells. Thus, adequate coupling leads to voltage clamping during calcium waves, thus preventing triggering arrhythmias. While poorly coupled myocytes aren't able to to this due to a weakened currency, making them more prone arrhythmogenesis. These data highlight another critical cellular basis for arrhythmogenesis. In heart failure, while the focus for clinical management is typically areas of scar, there's clearly a role at the cellular level where cell-cell coupling abnormalities can lead to dynamic changes that can increase tendencies to arrhythmogenesis. The role in understanding the varying, arrhythmogenic risk based on varying factors, is important, and might have importance in the future advances in mapping technologies. Changing gears, we review an article published in the Journal of the American College of Cardiology by Mazzanti et al within the realm of genetic channelopathies entitled Hydroxyquinoline Prevents Life-Threatening Arrhythmic Events in Patients With Short QT Syndrome. They reviewed a cohort of 17 patients and demonstrated that hydroxyquinoline resulted in a reduction of arrhythmic events from 40% to 0% of patients. QTc prolongation was seen in all patients. These data clearly demonstrate that hydroxyquinoline plays a role in lowering the incidence of arrhythmic events in patients suffering from short QT syndrome. However, it's important to note that in many markets, quinoline has been difficult to access. In the specific case of QT syndrome thus, there's clearly a role for hydroxyquinoline. However, it also must be noted, the comparative efficacy with more commonly available drugs still needs to be evaluated. This past month has been of particular interest in the realm of ventricular arrhythmias, with multiple, potentially ground-breaking articles. One of the well-recited articles published this past month already is by Cuculich et al entitled Noninvasive Cardiac Radiation for Ablation of Ventricular Tachycardia published in the New England Journal of Medicine. Cuculich et al reported the first in-human data on the use of stereotactic body radiation therapy to perform noninvasive ablation of ventricular arryhthmias. Using a combination of noninvasive electrocardiographic imaging curing ventricular tachycardia, and stereotactic radiation, patients were treated with a single fraction of 25 [inaudible 00:31:15] while awake. A total of five patients were included with a mean ablation time of only 14 minutes. During the three months prior to treatment, there was a total of 6,577 VT episodes seen, and during a six week post-ablation period, considered a blanking period, there were 680 episodes. After this blanking episodes, there were only four episodes of VT seen over the ensuing 46 patient months. This study is important because it reflects the first in-human proof of concept that noninvasive ablation using radiation therapy traditionally as for treatment of solid tumors, may be affective in targeting cardiac tissue. Furthermore, modern techniques such as noninvasive electrocardiographic imaging might allow for a fully noninvasive experience for the patients. This is a vast advance seen within the realm of cardiac electrophysiology. In the early days, all we could do was map invasively and then have to go to much more invasive, open-heart surgery to treat arryhthmogenic substrates. Since the advent of catheter and radiofrequency ablation, surgical ablation is relatively fallen by the wayside, to a less invasive approaches. A completely noninvasive approach to successfully targeting tissue is potentially ground-breaking. However, there are several limitations in this study that can only be ascertained by reading the actual article. When we actually review the patients included, the long term follow-up was limited to only four patients, as one patient actually died within the blanking period, and in fact, this patient suffered from the largest burden overall of VT. Furthermore, amongst the remaining four patients, one required a redo ablation within the blanking period, and one had to be restarted on amioderone after the blanking period was over. Thus further data is really needed to clarify efficacy, given the overall success rate appears to be less than 50% on a per patient basis. Though on an overall episode basis, there was significant reduction. The exact type of radiation to be used also needs to be considered, within the realm of solid oncology. Stereotactic radiation is considered an older modality, with proton beam, and more recently, carbon beams offer more directed therapy. Thus, a lot more data is required to identify the promise of radiation therapy. Though again, this is a significant advance. Next, within the realm of invasive electrophysiology, we review an article by Turagam et al published in the JACC Clinical Electrophysiology entitled Hemodynamic Support in Ventricular Tachycardia Ablation: An International VT Ablation Center Collaborative Group Study. The utility of hemodynamic support during VT ablation is relatively unclear. Studies have been variable and limited. This group included 1,655 patients who underwent 105 VT ablations using hemodynamic support with a percutaneous ventricular assist device. Those undergoing support overall tend to be sicker, including lower ejection fractions and [inaudible 00:34:07] classes, and more VT events, including ICD shocks and VT storm. Hemodynamic support use interestingly, was an independent predictor of mortality with a hazard ratio of 5, though there was no significant difference in VT recurrence rates irrespective of the subgroup considered. These data indicate that, while patients are receiving hemodynamic support were overall sicker, there was no clear incremental benefit in use of hemodynamic support in terms of long term outcomes. In the area of substrate ablation, whether use of hemodynamic support to facilitate mapping during VT, actually alters outcomes remains to be seen. This study highlights the potential importance of randomized clinical approaches to better evaluate whether hemodynamic support truly alters the long term outcomes of the VT ablation. Next, we review an article by Munoz et al that focuses more on prediction of those patients who might be at risk for ventricular arrhythmias, again published in the last edition of JACC Clinical Electrophysiology and entitled Prolonged Ventricular Conduction and Repolarization During Right Ventricular Stimulation Predicts Ventricular Arrhythmias and Death in Patients With Cardiomyopathy. Munoz et al reviewed the relationship between paced QRS and pace Qtc and long term risk. A total of 501 patients with mean ejection fractions of 33% were included. Longer paced ventricular QRS and Qtc was associated with a higher risk of ventricular arrhythmia, and all caused death or arrhythmia, irrespective or ejection fraction. A paced QRS duration of 190 milliseconds was associated with 3.6 fault higher risk of arrhythmia, and a 2.1 fault higher risk of death or arrhythmia. These data suggest that findings during [inaudible 00:35:47] pacing and otherwise normal rhythm, including paced QRS and QTc may independently result in elevation of overall risk of ventricular arrhythmia and death. Physiologically these data make sense. In light of the fact that longer cure restorations are probably related to a greater degree of myopathy. While these data offer a prognostic indication, whether they alter outcomes or decision making regarding ICM implantation, remains to be seen. Next, also published in JACC Clinical Electrophysiology, Vandersickel et al reviewed a more cellular basis for toursades in an article entitled Short-Lasting Episodes of Toursades de Pointes in the Chronic Atrial Ventricular Model Have Focal Mechanism While Longer-Lasting Episodes are Maintained by Reentry. Vandersickel et al reviewed the mechanisms underlying toursades, and demonstrated that both focal and reentry mechanisms may exist. In five canines they used broadly distributed neuro electrodes to simultaneously map across the heart. They demonstrated that initiation and termination was always focal, but longer and non-terminal episodes always had reentry mechanisms. These data suggest that the mechanisms underlying toursades actually reflect a spectrum of potentially dynamic, electrophysiologic phenomenon the heart, including both focal and reentry activity. Understanding these mechanisms, and the fact that focal mechanisms almost universally underlie initiation may bring into consideration the optimal treatments whether in the form of pacing and defibrillation techniques or medication techniques for toursades. Finally, in the realm of ventricular arrhythmia, we review an article published in the last month's edition of Heart Rhythm by Penela et al entitled Clinical Recognition of Pure Premature Ventricular Complex-Induced Cardiomyopathy at Presentation. As we know, it's sometimes difficult to recognize patients when they present with frequent PVCs and a depressed injection fraction in terms of, whose injection fractions are purely caused by the presence of PVCs, and whose PVCs are only exacerbated by the presence of an underlying myopathy. The group included 155 patients and excluded all patients who did not normalize their elevated ejection fraction, or who had previously diagnosed structural heart disease, leaving a total cohort under consideration, of 81 patients. About 50% were diagnosed as having a PVC-induced cardiomyopathy on the basis of normalization of elevated function after PVC suppression. While the remainder was considered to have PVC exacerbated cardiomyopathy on the basis that things did not entirely resolve, and thus had an independent mechanism for nonischemic myopathy. Characteristics that suggested patients with a lower likelihood of EF normalization included those with longer intrinsic QRSs, above 130 milliseconds, a lower PVC burden of baseline, considered less than 17%, and larger [inaudible 00:38:33] greater than 6.3 cm. PVCs as a cause of [inaudible 00:38:35] are obviously a well-recognized treatable cause of myopathy, however again, it might be difficult to differentiate. Those patients whose PVCs are a result of the underlying myopathy versus those whose PVCs are the cause, and for whom ablation or suppression may reverse the myopathic process. The work of Penela et at offers an initial attempt at helping differentiate these processes, however validation of larger cohort is necessary. Next we review an article within the realm of syncopy entitled Prohormones in the Early Diagnosis of Cardiac Syncopy by Badertscher et al published in the Journal of the American Heart Association this month. They review the utility of circulating prohormones [inaudible 00:39:14] autonomic dysfunction or neurohormonal abnormalities, to differentiate cardiac from non-cardiac causes of syncopy in the emergency departments. They measured four novel prohormones in a multi-center study. In the emergency departments there is a specific protocol used to determine the perceived likelihood of the cause of syncopy to be cardiac versus non-cardiac. In addition to this, the prohormones are drawn. After this, everyone's final diagnosis was reached. Two independent cardiologists reviewed the cases to determine if it was a truly cardiac or non-cardiac cause of syncopy. Among 689 patients included, 125 overall were adjudicated as cardiac syncopy. Measure of the specific marker MR-proANP in combination with emergency department suspicion of syncopy, performed better than suspicion alone, to differentiate cardiac causes of syncopy. A combination of a circulating MR-proANP, less than 77, picomoles per liter, an [inaudible 00:40:17] probability of cardiac syncopy could be less than 20%, had a very high sensitivity negative predictive value of 99%. The significant resources are often used to manage patients with syncopy presenting to the emergency departments, and it's often extremely difficult at this stage to differentiate cardiac from non-cardiac causes of syncopy. And the amount of evaluation that can be done in the emergency department is often limited. Cardiac caused of syncopy are not good to miss, however, since these can include ventricular arrhythmias, and transient AV block, that might result in death as well. As is well-recognized, emergency department evaluation in clinical [inaudible 00:40:49] are limited in terms of their utility. This raises the utility of objective measures to help differentiates. These data suggest that circulating prohormones [inaudible 00:40:59] your hormonal function drawn during your emergency department evaluation, may be a useful adjunct to differentiate cardiac from non-cardiac syncopy. Whether they can be used to prospectively differentiate those patients requiring inpatient admission or now, however, remains to be seen. The last two articles we'll choose to focus on will fall under the realm of broader, other EP concepts. The first article we will review is by Varghese et al published in Cardiovascular Research entitled Low-Energy Defibrillation With Nanosecond Electric Shocks. Varghese et al reviewed the potential of low-energy nanosecond duration shocks for defibrillation in rapid hearts. In induced fibrillation examples, the repeated defibrillated nanosecond impulses as low as three kilovolts demonstrated effective defibrillation. The energy required is significantly lower than from monophasic shocks and longer pulse durations. Furthermore, there was no detectable evidence of electroporation, namely cardiac or so injury after defibrillation. Using nanosecond impulses, it may be feasible to defibrillate the heart with significantly lower energies. The implications for patients experiencing defibrillation, for example pain, is unclear without in-human studies. However, the ability to use lower energies could have implications in battery life. Further [inaudible 00:42:11] studies will be critical to study ambulatory efficacy as this research is performed in [inaudible 00:42:19] hearts. Finally, we review an article published in Circulation entitled Mortality in Supravascular Events After Heart Rhythm Disorder Management Procedures by Lee et al. Amongst three centers, a retrospective cohort study regarding the mortality and risk of supravascular events, was performed. They included a variety of heart rhythm [inaudible 00:42:40] procedures, including defibrillation threshold testing, lead extraction, device implant, and invasive electrophysiology studies and ablation procedures. Amongst 48,913 patients, 62,065 procedures were performed and an overall mortality of .36% was seen. Supravascular [inaudible 00:42:58] was lower at .12%. Interestingly, and expectedly, the highest risk was seen with lead extraction patients, with an overall mortality risk of 1.9%. Less than half of the deaths seen, however, were directly attributable to the procedure itself. The most common cause of procedural death was cardiac tamponade, largely seen amongst device implant patients. This is critical, as the number of ablation and other invasive electrophysiology procedures performed, is increasing. These data provide a large, contemporary experience regarding the overall risk attributable to a variety of heart rhythm disorder procedures. Interestingly, half of the procedure related deaths were associated with device implantation procedures. With the predominant cause being tamponade, highlighting the importance of early recognition of this treatable complication. Tamponade may not always be considered as a major issue after device implantation, however these data clearly suggest that it is. In addition, extraction, as expected, carried the highest incident of both supravascular events and mortality. Though, this is likely related to the higher rate of core morbidity in this population, including active infection. In summary, this month, we have reviewed 20 articles in various areas of electrophysiology published across the literature. Particularly high impact articles range from those reviewing experience regarding left atrial appendage closure and the efficacy of this, to the utility of using atrial fibrillation to predict risk and long term morbidity and mortality in hypertrophic cardiomyopathy, to further evidence regarding the safety of magnetic resonance imaging in legacy pacemakers and defibrillators, and novel considerations regarding supraventricular tachycardias and there diagnosis and management, especially invasively. Other potential groundbreaking articles included evidence that we can successfully use formal and fixed paraffin-embedded tissue that can be as old as 15 years, to successfully identify genetic mutations that might be responsible for sudden death. And evidence that using novel techniques, we might be able to perform completely noninvasive therapies for arrhythmias by using radiation therapies. However questions were also raised such as regarding the role of hemodynamic support for VT ablation. How to better differentiate those patients who will have recovery of AV conduction from those who won't, as they meet class I indications post cardiac surgery? And whether other factors such as right ventricular pacing during [inaudible 00:45:28] study might further differentiate patients at risk for ventricular arrhythmias in spite of a low ejection fractions. Many of the papers had to deal with tranlational work that still remains to be proven in terms of value at a clinical level, such as demonstrating mechanisms underlying trousades de pointes. Or the potential value of low-energy defibrillation with nanosecond electric shocks. Clinical protocols involving the use of prohormones in the early diagnosis of cardiac syncopy. How to differentiate PVC induced from other causes of myopathy, and how to manage, in the long term, these devices. Also, likely requires further study. Finally, covering all areas of electrophysiology, we reviewed one large article focusing on mortality in supravascular events after heart rhythm management disorder procedures at large. This article highlights the importance of considering institutional experience and reporting it to use as a benchmark to help better optimize our counseling of patients, as well as our procedures and protocols. I appreciate everyone's attention to these key and hard-hitting articles that we just focused on from this past month of cardiac electrophysiology across the literature. Thanks for listening. Now, back to Paul. Dr. Paul Wong:                  Thanks Seraj. You did a terrific job surveying all journals for the latest articles on topics of interest in our field. There's not an easier way to stay in touch with the latest advance. These summaries, and a list of all major articles in our field each month, can be downloaded from the Circulation Arrhythmia and Electrophysiology website. We hope you'll find the journal to be the go-to place for everyone interested in the field. See you next month.  

En el podcast de esta semana presentamos la información preliminar de los resultados del estudio OVIVA que busco comparar el uso de antibióticos endovenosos u orales en el tratamiento de osteomielitis y artritis séptica.   Referencias: Oral versus intravenous antibiotic treatment for bone and joint infections (OVIVA): study protocol for a randomised controlled trial  Matthew Scarborough y colaboradores. The OVIVA Trial: Oral versus intravenous antibiotics in the management of bone and joint infection - a multicentre open label randomised non-inferiority study. For bone and joint infections, oral antibiotics match IV, cost less  Francis Waldvogel, Gerald Medoff and Morton Swartz. Osteomyelitis: A Review of Clinical Features, Therapeutic Considerations and Unusual Aspects. New Eng J Med. Jan 22, 1970.    La Frase de la Semana: La tomamos del poeta y dramaturgo irlandés Oscar Wilde. Nacido el 16 de octubre de 1854 y fallecido el 30 de noviembre de 1900. “Sólo podemos dar una opinión imparcial sobre las cosas que no nos interesan, sin duda por eso mismo las opiniones imparciales carecen de valor”        

Posterior hip pain can have a number of causes, with referral from the lumbar spine, SIJ and hip, along with local structures such as the hip joint, gluteals, glute tendons, proximal hamstring tendons. How can you identify the structures involved in your patient's posterior hip pain? What tests can you perform in your objective assessment to assist your treatment? What is the best way to treat the glutes if they are the involved in your patient's pain? In episode 63 of the Physio Edge podcast, Benoy Mathew and David Pope explore how you can improve your diagnosis and results with posterior hip pain. You will discover: What are some of the common causes of posterior hip pain? Gluteal tendinopathy (GT) What area of symptoms will patients with GT report? What are the pattern of symptoms for GT? What tests can we perform to make GT more or less likely How can we treat GT? Deep gluteal syndrome (DGS) What is deep gluteal syndrome? What muscles can be involved in DGS? How can we differentiate it from Gluteal tendinopathy? What tests can you perform to confirm or exclude DGS? How does the treatment for DGS differ to GT? Benoy is presenting a free webinar with Clinical Edge on "How to assess & diagnose posterior hip and gluteal pain, that complements this podcast, and takes you through the common sources of hip pain, how to identify hip and lumbar spine red flags, and demonstrates exactly how you can perform an assessment to test and differentially diagnose the structures involved in your patients pain. CLICK HERE to enrol on this free webinar with Benoy Mathew Ben also presented a webinar with Clinical Edge on how to rehabilitate adductor and psoas related groin pain. The webinar helps you discover: Rehabilitation of adductor and psoas related groin pain Practical tips Common presentations Osteitis pubis, sports hernia, hip impingement Rehabilitation from initial stages to plyometrics CLICK HERE to watch the webinar "Rehab of adductor and iliopsoas related groin pain" with Benoy Mathew with a free trial Clinical Edge membership Links of Interest Download and subscribe to the podcast on iTunes Download your free podcast handout on how to assess and treat posterior hip pain Physio Edge podcast 053 Hip and groin pain part 1 - diagnosis, pathology and red flags with Benoy Mathew Physio Edge 054 Hip and groin part 2 - assessment and treatment with Benoy Mathew Download the free podcast handout for Physio Edge 054 Hip & Groin pain Part 2 Webinar on groin pain rehabilitation with Benoy Benoy Mathew on Twitter Benoy Mathew's website and courses Access to Ben's webinar on rehabilitation of hip and groin pain, along with all of the Clinical Edge webinars and videos with a free trial membership David on Twitter Review the podcast on iTunes Like the podcast on Facebook Free sports injury videos   Articles related to this episode: Franklyn-Miller et al (2009)- The Gluteal Triangle: a clinical patho-anatomical approach to the diagnosis of gluteal pain in athletes , BJSM. Open Access Link Grimaldi & Fearon (2015)- Gluteal Tendinopathy: Integrating Pathomechanics and Clinical Features in Management, JOSPT. Open Access Link Hernando et al (2016)- Evaluation and management of ischio-femoral impingement: a pathophysiologc, radiolgic and therapeutic approach to a complex diagnosis, Skeletal Radiol Martin et al (2016)- Deep Gluteal Syndrome, JHPS, Open Access Link Martin et al (2016)- Ishiofemoral Impingement and Hamstrings Syndrome, Distal Causes of Deep Gluteal Syndrome. Where do we go next? Clin Sports Med. Open Access Link Michel et al (2013)- Piriformis muscle syndrome: Diagnostic criteria and treatment of a mono centricseries of 250 patients, Annals of Physical and Rehabilitation Medicine The Copenhagen Hip and Groin Outcome Score (HAGOS): development and validation according to the COSMIN checklist Physical Examination of the Hip by Dr. Hal D. Martin