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Fishhook injuries are common, surprisingly nuanced, and honestly a little intimidating until you've removed a few. In this first episode of our Minor Procedures series, we'll reel in the essentials of pediatric fishhook removal, helping you take the bait on four classic removal techniques, procedural planning, anesthesia strategies, and post-removal management. We'll discuss when to pull back, when to advance, when not to get hooked on a single technique, and how to avoid turning a simple procedure into the one that got away. Along the way we'll cover sedation, antibiotics, wound care, and practical pearls to help you land these cases with confidence. Learning Objectives Compare and select among the four major fishhook removal techniques based on hook characteristics, depth of penetration, and anatomic location. Apply evidence-based approaches to analgesia, anxiolysis, procedural sedation, and post-removal management for pediatric fishhook injuries. Identify situations requiring escalation of care, including ocular involvement, contaminated water exposure, tendon or joint involvement, and circumstances where routine management may not be sufficient. References Gammons MG, Jackson E. Fishhook removal. Am Fam Physician. 2001;63(11):2231-2236. Prats M, O'Connell M, Wellock A, Kman NE. Fishhook removal: case reports and a review of the literature. J Emerg Med. 2013;44(6):e375-e380. doi:10.1016/j.jemermed.2012.11.058 Doser C, Cooper WL, Ediger WM, et al. Fishhook injuries: a prospective evaluation. Am J Emerg Med. 1991;9(5):413-415. doi:10.1016/0735-6757(91)90204-w Transcript This episode used an AI-generated transcript created in Descript as an initial draft. The transcript was subsequently edited, expanded, and refined by the author with assistance from OpenAI's ChatGPT (GPT-5.5). Final editorial decisions and content responsibility remain with the author. Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski, and today we're gonna start a new series on minor procedures. These are the types of procedures that we perform all the time in the emergency department. They're not the subject of multicenter trials or big keynote lectures, but these are the things that patients and families remember, and trust me, they will remember them whether you do them well or not. First up, fishhook removal. So I'm hoping to reel in some listeners with this one, and so hopefully you'll take the bait, and by the end of this episode you'll understand exactly what angle I'm coming from. And hopefully I'm just not trying to make a bass of myself. So anyway, fishhook removal sounds really simple until you actually start doing it. There's not just one technique. There are four classic approaches, and I'll talk about them all, and which one you choose depends on the hook, whether there's a barb, how deep it is, where it's located, your personal experience with different techniques. Fishhook injuries in children are usually minor and most commonly involve the hands and head, though I've seen them stuck in other body parts as well. Most can be managed in the emergency department or urgent care setting with local anesthesia and basic equipment Of course, if there's concern for tendon involvement, joint penetration, neurovascular compromise, if it's anywhere near the eyeball, you should stop and rethink your plan. You know, so ortho, if it's embedded deeply in a joint, um, anything that involves the eye itself isn't necessarily an emergency department procedure, and I'm not talking about the eyebrow, I'm talking about the globe. Fortunately, that's very rare, but that's definitely an ophthalmology conversation. And so before you even think about removing, you need to understand the hook. Is this a single hook or is this a treble hook? A treble hook is a type of fishing hook that has three individual hooks and barbs arranged in a triangular formation, and they're all fused to a single shank and eye. The eye is where the line gets tied to the hook. Is it freshwater or saltwater? How long has it been there? Is it an old rusty one that was sitting in your garage? Was it underwater for a few hours and then it got hooked in the skin? And honestly, how cooperative is the kid gonna be? Because unlike actual fishing, this is one of the procedures where patience beats blunt force. So the simplest technique is retrograde removal. This is exactly what families think you're gonna do before you walk in the room. You know, just pull it out the way it went in. But that's not how hooks are designed. They have the barb. They're designed to stay in the fish. So most of the hooks that I've removed are barbed hooks, and so you can't just back them out. If you try to pull a hook out the way it came in, it's gonna catch and tug on the tissue, it's gonna lead to more pain, bleeding and tissue distortion and not really gonna get you anywhere. So just pulling it out doesn't work, and family probably would have already tried that at home. The technique I end up using most often is advance and cut. And it kind of sounds wrong the first time you explain it to a family because your solution to removing the hook is to continue to advance the hook, but mechanically, this makes the most sense. So you advance the point of the hook through the skin until the barb exits completely, then use either really good trauma shears or heavy wire cutters to cut the hook in between the shank and the barb. If it's in a location where you have, uh, enough room, I like to hold a hemostat real close to the skin, grabbing the hook. Then I cut near the barb, get the pointy part out of the way, remove the hemostats, and then back it through the skin. This is considered the most reliable technique, and in most reviews it's described as being nearly universally successful, even for larger hooks. In children, I think this needs to be the go-to technique because success matters. You just gotta get it done on the, the first attempt. Kids don't tolerate multiple failed attempts very well. Um, obvious downside is that you create a second puncture wound, but in practice, that puncture is usually controlled and much less traumatic than repeated unsuccessful pulling. Depending on where the skin's at, you may actually need to put a little bit of tension or pressure against the skin to get that hook to poke through. Ultimately, this advance and cut method is the one that you should spend the most time learning and teaching to your trainees. The string yank technique is the one that often is seen at summer camps and on YouTube videos. You loop string or heavy suture or even fishing line around the bend of the hook, apply downward pressure to the shank to disengage the barb, and then pull quickly in line with the shaft of the hook. When it works, it yanks it out almost instantly. That's why the YouTube videos are popular. One second there's a fishhook in the finger, and the next there isn't. The advantage is that this can sometimes just be performed without anesthesia and can even be done at home. The disadvantage is obvious if you work with children. This requires cooperation. Younger kids, anxious kids, a treble hook, something that's deeply embedded, like this isn't gonna work all that well, and it's, again, less reliable with bigger and deeply embedded hooks. The last technique is needle cover. This one gets less attention. It seems elegant, but in practice it's actually pretty hard to do, especially in smaller kid parts. You insert an 18-gauge needle alongside the entry tract until the bevel of that needle covers the barb, and then pull both out together The advantage is that you avoid creating a second puncture wound, and you can minimize tissue trauma. The disadvantage is it's really complex technically. Maintaining alignment of both the hook and needle can be tricky because they sort of like roll and move around. And if you want to do this one, it's probably easier for smaller and medium-sized hook rather than larger embedded or treble hooks. And as you might imagine in the literature, there's not really any randomized trials comparing these techniques. Most of what we know comes from prospective observational studies, case series, procedural experience, and expert review. Advance and cut seems to have the broadest success across scenarios. String yank does earn some points for field use and avoiding local numbing. Needle cover is hard to do, but if the parent is absolutely adamant that you don't create a second hole, then that's probably your best option. And as with any procedure, you should probably be facile in multiple techniques in case the first one doesn't work. You don't just want to stand there and flounder. Anyway, most fishhook removals in children can be done with local anesthesia alone. One percent Lido with or without epi is usually enough. Depending on the location, you may need to do a digital block or a field block instead of just injecting directly around the hook because local infiltration itself can distort the anatomy and actually make removal harder. So that's why I like blocking the digit or doing a little bit of a field block around it. If you have time, a topical anesthetic before local infiltration can be a nice gesture. LMX or EMLA can be really helpful, especially for really anxious kids or kids who are escalating before you even start setting up. They take about forty to sixty minutes. About forty-five minutes is probably ideal. So if you can get that put on in triage, that's actually a, a great technique. So if you know you're going to inject to numb to get the fishhook out, and you need a little bit of extra time to get child life or other personnel in the room, by all means, put a topical anesthetic there. It only absorbs into the outer two millimeters, but it'll help with the poke, not necessarily the burning that happens once the lidocaine is in the tissue. And now that we've talked about pain, I think it's also important to talk about anxiolysis. Most kids that have embedded fishhooks don't need full procedural sedation. If it's right next to the eye, like in the eyelid, then that might be beneficial, especially in a preschool-aged kid or younger. Plenty of them do need some anxiolysis. Um, intranasal or oral midazolam is probably, uh, the most popular option. It's got rapid onset in about twenty minutes, no IV, some amnesia. Recent pediatric data suggests that point four or point five milligrams per kilogram may perform better than lower doses, uh, for the intranasal. If you've got nitrous oxide, that's another nice option for cooperative kids. It provides anxiolysis and analgesia with rapid recovery and a very low rate of adverse respiratory events. Fishhook removal is actually one of those procedures where nitrous can feel disproportionately helpful because the procedure itself is often quick, and the hardest part is just reducing the fear and helping the kid hold still for about thirty to sixty seconds. I think ketamine still has a role. I alluded to when I might use that earlier. Occasionally, you walk into the room and then there's a deeply embedded treble hook, a really anxious child, a failed attempt prior to you being there. And ultimately, yes, IV procedural sedation with ketamine should be on the table, and it's as always an excellent option. And never, ever underestimate distraction. Hopefully, you work in a place where there are child life specialists because they are wonderful. They are magic. But you've got videos, you know, music, VR, parents. I mean, sometimes the difference between success and failure is a working iPad. And then finally, the question of antibiotics. So fishhook removal does not automatically equal a course of antibiotics. A prospective series of one hundred fishhook injuries found prophylactic antibiotics were unnecessary for uncomplicated soft tissue injuries that didn't involve the cartilage or tendon. So if you've got a contaminated wound, a delayed presentation, you know, it was already in an established infection, though I've never actually seen someone impale a fishhook into an area of cellulitis. There's tendon involvement, joint involvement, or, you know, gross water exposure. Well, then maybe consider antibiotics. Freshwater injuries do raise concern for organisms like Aeromonas. Saltwater injuries introduce concern for Vibrio species and occasionally Mycobacterium marinum enters the conversation or the tissue. Um, saltwater injuries are often treated with doxycycline plus a third-generation cephalosporin. You recognize the doxy decisions in younger children require some additional consideration. Freshwater injuries could push you towards broader Gram-negative coverage, but, but honestly, for most fishhook injuries, especially in healthy children, you're just dealing with skin flora. So once I get the hook out, I make sure there's no other retained foreign bodies, like little pieces of the hook or little pieces of the barb. I irrigate with saline or tap water, maybe a hundred mLs for a smaller hook, more for bigger hooks or grossly contaminated wounds. Make sure that there's full neurovascular function and normal range of motion. Antibiotic ointment, simple dressing, update their tetanus shot if it's not been within five years, and explain to the family that the good news is that this is really a forgiving injury most of the time. Once the hook is out, these generally heal really well. We don't need to suture them back up. We're not worried about long-term damage. Tell the parents to watch out for increasing redness, worsening pain, pus drainage, fever, or other systemic symptoms, trouble moving the area, especially if it was around a digit, you know, numbness or anything else that makes you concerned that infection has started instead of healing. Families will almost always ask jokingly when they can fish again. Honestly, usually pretty quickly. Just don't put the wound under water until it's healed, and don't stand directly behind whoever is casting. And now for some take-home points. Fishhook removal is a simple and straightforward procedure where technique really matters. You have to know what type of hook is embedded in the skin. Retrograde does work for superficial or barbless hooks, but most fishhooks that I've seen have barbs because they are designed to stay in the fish. Advance and cut is probably the most broadly successful technique. String yank works if you're a YouTuber. Needle cover is really, I think, only for those scenarios where the family does not want a second hole. It's really actually hard to do. Local anesthesia is enough for most kids, so injecting with lidocaine. If you have time, LMX or EMLA helps with the poke a little bit. Routine antibiotics are not usually necessary. And if there's ocular involvement or if it's in a joint, call an ophthalmologist or an orthopedist. Honestly, this is one of those procedures that's really satisfying once you get comfortable with it. I love doing it with our residents and trainees. Families come in expecting something dramatic, and by the time they leave, they're surprised by how straightforward it was. And I guarantee that this is a story that they will tell for years and years. And if you do a good job and make it a good experience and perhaps even a lighthearted one, they are going to remember that. And yeah, you'll be part of somebody's fishing story. So I hope you did enjoy this first episode on minor procedures. I'm gonna do additional ones like these along the way because, you know, I think that they don't get a lot of love when it comes to traditional education. If you've got any ideas for future procedures or topics, please send them my way. As the kids would say, like, rate, and review. If you leave a review on your favorite podcast site, that would really help other people discover the show. I podcast because I think it's a great way to teach, and I've been doing so since 2013. And yes, you can remove a fishhook. Don't let this straightforward procedure become the one that got away. For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.
Croup is a clinical syndrome of upper airway obstruction defined by barking cough, stridor, and hoarseness. Management hinges on severity assessment, universal corticosteroid use, and selective epinephrine. The key clinical task is distinguishing typical croup from high-risk mimics that require urgent airway intervention. Learning Objectives Differentiate croup from other causes of pediatric upper airway obstruction using key historical and physical exam features. Apply a severity-based approach to croup management, including appropriate use of corticosteroids and nebulized epinephrine. Recognize clinical features that suggest alternative or life-threatening diagnoses requiring escalation of care. References Cooke A, Conway S, Griffin L. Croup: Rapid Evidence Review. Am Fam Physician. 2026;113(3):254-258. Gates A, Johnson DW, Klassen TP. Glucocorticoids for Croup in Children. JAMA Pediatr. 2019;173(6):595-596. doi:10.1001/jamapediatrics.2019.0834 Bjornson CL, Klassen TP, Williamson J, et al. A Randomized Trial of a Single Dose of Oral Dexamethasone for Mild Croup. N Engl J Med. 2004;351(13):1306-1313. doi:10.1056/NEJMoa033534 Bjornson CL, Johnson DW. Croup. Lancet. 2008;371(9609):329-339. doi:10.1016/S0140-6736(08)60170-1 Bjornson C, Russell K, Vandermeer B, Klassen TP, Johnson DW. Nebulized Epinephrine for Croup in Children. Cochrane Database Syst Rev. 2013;(10):CD006619. doi:10.1002/14651858.CD006619.pub3 Transcript This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content. Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski. And today we're gonna talk about croup. We're gonna focus on diagnosis, severity based management, and how to differentiate it from scarier high risk conditions that may present similarly, but behave very differently. So croup is best understood as a clinical syndrome of upper airway obstruction caused by inflammation at the level of the larynx and subglottis. So in most cases this is viral laryngotracheitis, most commonly due to parainfluenza virus. But as you'd expect multiple viruses can cause it. The subglottis is the narrowest portion of the pediatric airway. So even small amounts of edema create large increases in airway resistance. So that's why the clinical picture is so consistent. You've got inspiratory stridor, hoarseness, and that characteristic barking cough, which either sounds like a seal or a dog, and yes, of course, I know the difference between the two coughs because I was a biology major. This is primarily a disease of children between six months and three years of age with a peak incidence in the second year of life. It's really, really common, like one and a half percent of all ED visits, maybe 350,000 visits a year, and 85% of these kids have mild disease. Hospitalization is rare. The range is variable, about two to 8% of cases, and return visits occur in about three to 5%. Fewer than 1% of children, a lot fewer, require intensive care or airway intervention. Honestly, most kids do really well. The ones who don't can get sick very quickly, and that's been my clinical experience. In the Northern Hemisphere, we see croup throughout the fall and winter, usually starting in around November and sort of tapering off by April. But that being said, I've seen croup-like symptoms every month of the year over the past couple of decades. Croup is absolutely a classic clinical diagnosis. A typical case begins with 12 to 48 hours of viral prodrome, you know, body aches, fever, congestion, cough, followed by often abrupt nighttime onset of barky cough and stridor. Symptoms fluctuate, and they're generally worse with agitation and get better when the kid is calm. That variability is the key feature. So what you'll have is a child who wakes up after sleeping for a few hours with a barky cough and then noisy stridor. This freaks parents out, and this is not hyperbole. There's this little center in the back of your brain that's like, please don't stop breathing and die. So appropriately, they're worried about the kid, they call emergency medical services, they bring them to the emergency department, and by and large, by the time they get there, the stridor has resolved. The kid is calm, and parents will say, I swear he looked a lot worse at home. Trust me, we believe you parents, this is what croup does. When I'm taking a history of croup, I get all of these details. Are there any sick contacts? If the parents are worried about a foreign body inhalation or ingestion, then I'm worried about a foreign body inhalation or ingestion. Listen to the lungs, inspect their airway. Always check the ears for concomitant otitis and I'll feel their trachea. I'll actually grab and hold the trachea and move it. Kids with croup really don't have a painful trachea. Kids with bacterial tracheitis, aside from looking more toxic, actually have a lot of pain when they move their trachea. Testing for croup is generally unnecessary. Labs and viral studies do not change management, and imaging is really reserved for atypical presentations or when you're considering an alternative diagnosis like a foreign body. If you do get an X-ray, what you're looking for is the classic steeple sign on the AP view. It is seen in croup, but it's not 100% sensitive nor specific. Once you've made the diagnosis of croup, it's important to assess severity, and remember that I said that most kids are mild. So mild croup is defined by the absence of stridor at rest. So they may have some stridor when they're upset or even a little bit of hoarseness or noise. It's important to listen to many, many children with croup to get a sense of this. Moderate croup includes stridor at rest with mild to moderate retractions. So at rest means that the child is in a position of comfort. They're calm with a parent, and they've generally been that way for about 10 to 15 minutes. Sometimes that's how long it can take for the stridor to dissipate once you get the kid calm. Severe croup, which is fortunately rare, involves marked work of breathing, agitation, fatigue, need for oxygen, altered mental status, and this aligns with the Westley croup score. It formalizes stridor, retractions, air entry, cyanosis, and mental status. But really, in practice, most of us get very good at bedside assessment of croup. Management of croup starts with corticosteroids. This is one of the highest-yield interventions that we have in pediatric emergency medicine. Every child with croup should receive dexamethasone. Typically 0.6 milligram per kilogram as a single dose up to a maximum of 10 milligrams. Some places will use 0.15 milligram per kilogram. Locally, we often give the IV formulation orally. It's 10 milligrams per mL. Tastes bad, but pairs reasonably well with apple juice. The oral suspension is 1 milligram per mL, tastes terrible, and pairs nicely with being spit on the ground by toddlers. The evidence behind dexamethasone is very robust. The main benefit is that it reduces return visits and hospital readmissions by about half, and those return visits include doctor's offices and emergency departments. In a Cochrane review of 1,679 children, glucocorticoids reduce return visits or readmissions with a risk ratio of 0.52, so that translates to a number needed to treat of seven. I've certainly seen seven or more croup kids during one shift, so for every seven children treated with dexamethasone, one return visit is prevented. Symptom improvement begins within about two hours and lasts at least 24 hours, but maybe up to a couple of days. Hospital length of stay for kids that get steroids is reduced by an average of 15 hours as well. Serious adverse events are rare. It's well tolerated, and other than the taste, kids do fine with it. And importantly, the benefit is consistent across all severities of croup, mild, moderate, and severe. So when you explain this to families who are very scared about their kids, but now their kid is looking better and you're only giving them a single medicine, not doing any tests or X-rays or anything, I think you have to frame the medicine in terms of what it's going to do for them over the next couple of days. So one way of explaining this to families would be to say something like this is a steroid called dexamethasone. It reduces the swelling in your child's airway that's causing the barky cough and noisy breathing. Most children start feeling better within a couple of hours, and the benefit lasts at least a full day, if not longer. Without this medicine, about one in five children need to come back because symptoms get worse again. You really get two bad days with croup in most cases. With this medicine, the risk of returning drops to about one in 10, so it cuts the chance of coming back in half. We can expect your child's cough to start improving over the next day or two. Most children are feeling a lot better within 48 hours, though a little bit of hoarseness and cough can last for a week to about 10 days. So it's possible that when your child goes to sleep later tonight, they may experience that barking cough and noisy breathing again. They're almost certainly going to be upset. The steroid blunts enough of the swelling so that you are much more likely to have them free of distress and stridor, that noisy breathing, once you get them calm. So if they're upset, get them calm, and if in about 10 minutes the stridor and noisy breathing get better, that's the dexamethasone doing its job and you can safely stay home. For children with moderate or severe croup, we're gonna use nebulized racemic epinephrine. It works fast by reducing airway edema by constricting inflamed blood vessels. You'll see improvement in stridor and work of breathing often within 30 minutes. The effect is transient and largely gone by about two hours, and you need to do a structured reassessment at about 30 minutes after the racemic epinephrine. If the child's clearly better, continue that observation for up to two hours. If they're unchanged or worse, repeat the epinephrine and start thinking more carefully about your diagnosis and disposition. Because it's got such a short duration, that two hours after treatment is the most common time period, though some institutions and some children will need to be observed a little bit longer. If they remain well appearing with no stridor at rest, normal oxygenation, minimal work of breathing, and they can tolerate oral fluids, they can be discharged. If symptoms recur, they require repeated epinephrine, or they fail to improve, then you may have to escalate care and consider admission. Honestly, with croup, supportive care is still one of the most important things. You gotta keep kids calm by minimizing agitation. Parents are experts at this with their own children. Agitation worsens airway obstruction. Airway resistance is fourfold greater when the kid's upset. Give oxygen if the kid's hypoxic. Fortunately, this is rare. Antipyretics and fluids are great, do them. Humidified air has not been shown to provide meaningful benefit, and obviously we should avoid sedatives because they can suppress respiratory drive without improving airway patency. Many parents will say that their kid was better when they were exposed to cool air or mist in the shower. Those can help, but honestly, don't stick your kid's head in the freezer if it upsets them. Keep them calm, hold them, and comfort them. Alright, croup, barking cough, stridor, variable symptoms, easy, right? There are some other diagnoses that can mimic this or overlap that you shouldn't miss. Spasmodic croup is a related phenotype. You've got sudden nighttime onset, often minimal prodrome, and recurrent episodes. These kids are typically well between episodes, and the pattern becomes more apparent over time. Some kids will bark with every mild cold or stuffy nose up until about eight or nine, but they usually don't have stridor and respiratory distress. Bacterial tracheitis is progression to a more severe and dangerous airway infection. These children often start with viral symptoms and then rapidly worsen. They've got a high fever, they appear toxic. Most importantly, they fail to respond to standard croup therapy. Toxic appearance plus lack of response should immediately shift your diagnostic reasoning. These kids may have a lot of pain when you grab and move their trachea. The cough can be more junky because again, they've got purulent mucus in their trachea. Epiglottitis is defined by the absence of barking cough and the presence of drooling, dysphagia, and tripod positioning. These children are very anxious, they're very ill, their airway is at risk, and so your immediate priority is keeping them calm and having the airway managed in the safest environment, generally the operating room. Deep neck space infections, including retropharyngeal cellulitis and abscesses and peritonsillar abscesses, present with fever, neck stiffness, sometimes even torticollis, and lymphadenopathy. Kids won't really have a barky cough and the exam localizes to the neck rather than the airway alone. Acute foreign body aspiration presents with sudden onset symptoms, no viral prodrome, no barking cough, and sometimes some asymmetric exam findings. The diagnosis is frequently missed when clinicians anchor too early on croup. If you have an esophageal foreign body, remember that 70% of these get stuck at the thoracic inlet. So always think about a kid who sounded like they had croup and got croup treatments, but also has some swallowing issues and is the right age to put things in their mouth. This is when you see coins and button batteries and other things stuck not in the upper airway, but in the esophagus right behind it. Alright, now when it comes to disposition, most kids with croup are gonna be sent home. Children who improve, they have no stridor at rest, minimal work of breathing, can be discharged home with clear return precautions. Those with persistent symptoms, need for repeated racemic epinephrine, hypoxia, or concerning features should be admitted. For kids who continue to worsen despite standard therapy, escalation includes high-flow nasal cannula, noninvasive ventilation as a bridge. Heliox can be used as a temporizing measure to reduce work of breathing. Fortunately, needing to intubate a child with croup is rare, but when it's needed, it can be challenging due to subglottic narrowing. You need the best proceduralists, and you should downsize your endotracheal tube by 0.5 to 1 millimeter smaller than usual. And I'll reiterate this again. The natural course of croup is really favorable for most kids. The fear's not gonna go away for the parents, this is a scary diagnosis, but I think with some reassurance, we can help them understand that this is something that is unlikely to cause significant problems and will get better. Most kids improve significantly within 48 hours, though like any other respiratory illness, symptoms can persist for a week or so. Severe outcomes are fortunately rare, and they almost always occur in children whose severity or alternative diagnosis was not recognized early. So again, here's my take-home points. Croup is a clinical diagnosis. Severity determines your management. Steroids, dexamethasone, should be given to all patients. Racemic epinephrine is used for moderate to severe disease with mandatory reassessment and observation. And most importantly, always reassess the diagnosis when the presentation does not fit the expected patterns. Things can get rough when you're barking up the wrong tree and thinking it's croup when it's actually something else. Well, I hope you enjoyed this episode on honestly one of the most classic conditions that we see in the pediatric emergency department. If you've got any feedback on the episode, send it my way. As the kids would say, like, rate, and review. I would love it if you left a review on your favorite podcast site. It helps more people find the show. I do this as a labor of love because I enjoy teaching, and I think that this is a wonderful way to reach my colleagues and learners. If you've got suggestions on other topics or episodes, I'd love to hear them. For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.
Episode 217: Testicular Cancer Dr. Arreaza: Welcome to Rio Bravo qWeek Podcast. Today we are discussing testicular cancer, a topic that may not appear frequently in primary care but is extremely important to recognize early. We are joined by Brandon Noorvash and Dr. Ebenezer Dadzie. Please introduce yourselves. Brandon: Thank you, Dr. Arreaza. My name is Brandon Noorvash. I am a third-year medical student at Western University of Health Sciences with a strong interest in urology. Ebenezer: Thank you for having us. My name is Dr. Ebenezer Dadzie, and I am a PGY-1 resident in the Clinica Sierra Vista Family Medicine Residency Program. Dr. Arreaza: Testicular cancer represents about 1-2% of cancers in men, but it is the most common cancer in men between the ages of 15 and 40. The good news is that it is also one of the most curable cancers in medicine, especially when detected early. Let's start with a quick question for our listeners. If a 25-year-old man presents with a painless lump in his testicle, what diagnosis should immediately come to your mind? Ebenezer: Testicular cancer should always be high on the differential. While benign conditions can cause scrotal swelling, a painless testicular mass should be considered cancer until proven otherwise. Dr. Arreaza: I agree. Especially if we perform a physical exam and find that the mass is attached to the testicle. Why is this such an important diagnosis for primary care physicians to recognize, what do you think, Brandon? Brandon: Testicular cancer typically affects young, otherwise healthy men, and early detection dramatically improves outcomes. Patients may delay seeking care because the lump is painless or because they feel embarrassed discussing symptoms. However, when diagnosed early, the 5-year survival rate exceeds 95%, and in localized disease it approaches 99%. Dr. Arreaza: Exactly, the survival is incredible and it gets even better with early detection. How common is testicular cancer? Ebenezer: In the United States, approximately 10,000 new cases are diagnosed each year, with around 500 deaths annually. The relatively low mortality reflects how effective current treatments are, especially chemotherapy for germ cell tumors. Dr. Arreaza: Let's talk about risk factors. What should clinicians know about risk factors for testicular cancer? Who is at risk? Brandon: The most important risk factor is cryptorchidism, or undescended testicle. Men with a history of cryptorchidism have about a 4-to-8-fold increased risk of developing testicular cancer. Ebenezer: Other risk factors include family history, personal history of testicular cancer, infertility, testicular atrophy, and certain genetic conditions such as Klinefelter syndrome. However, many patients who develop testicular cancer have no clear risk factors. Dr. Arreaza: Brandon, you recently saw a patient with testicular cancer during your rotation. Can you briefly tell us about that case? Protected health information is not being revealed, so patient confidentiality is being respected during this discussion. Dr. Arreaza: I think we all were pleasantly surprised to know that lung metastasis did not place the patient in a higher risk category. On the other hand, nonpulmonary visceral metastases (such as liver, bone, or brain) define poor-risk disease in nonseminoma and intermediate-risk disease in seminoma. Dr. Arreaza: And of course, if the patient presents with sudden severe pain, we should always think about testicular torsion, which is a surgical emergency. What should clinicians focus on during the physical exam? Ebenezer: Testicular tumors typically feel firm, irregular, non-tender, and located within the testicle itself. Brandon: A helpful exam pearl is transillumination. Fluid-filled structures like hydroceles will transilluminate, whereas solid tumors do not. Dr. Arreaza: I have to admit I've never done a transillumination in a scrotum before. Brandon/Ebenezer: I've done it. I had to clean my pen light afterwards. Arreaza: Once you suspect testicular cancer, what is the next step in evaluation? Ebenezer: The first diagnostic test is a scrotal ultrasound. Ultrasound is highly sensitive and can determine whether the mass is intratesticular, which is highly suspicious for malignancy. Dr. Arreaza: US and tumor markers. Let's talk a bit more about tumor markers. Why are they useful in testicular cancer? Brandon: Tumor markers help with diagnosis, staging, and monitoring response to treatment. Ebenezer: Alpha-fetoprotein, or AFP, is typically elevated in non-seminomatous germ cell tumors, particularly yolk sac tumors. An important point is that pure seminomas do not produce AFP. Brandon: Beta-hCG can be elevated in both seminomas and non-seminomatous tumors, although the levels are often higher in the non-seminomatous types. Ebenezer: LDH is less specific but can reflect tumor burden and disease activity, so it's useful for monitoring progression or response to treatment. Dr. Arreaza: So, tumor markers are not only diagnostic tools, but they also help guide staging and follow-up care. That's an important board question. Why don't we perform a biopsy in a testicular mass? Ebenezer: Testicular masses suspicious of cancer are not biopsied because biopsy can disrupt lymphatic drainage and potentially spread tumor cells. Instead, the standard treatment is radical inguinal orchiectomy, which both removes the tumor and establishes the diagnosis. Dr. Arreaza: Brandon, can you briefly explain the two main categories of testicular cancer? Brandon: Let's start with the germ cell tumors. They are broadly divided into seminomas and non-seminomatous germ cell tumors (NSGCT). Seminomas tend to grow more slowly and are highly sensitive to radiation therapy. Ebenezer: Non-seminomatous tumors include embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma. These tumors tend to be more aggressive but are still highly responsive to treatment. Dr. Arreaza: How are patients staged once the diagnosis is made? Ebenezer: Staging typically includes a CT scan of the chest, abdomen, and pelvis to evaluate for metastasis, especially to the retroperitoneal lymph nodes, which are the most common site of spread. Dr. Arreaza: And how is testicular cancer managed? Brandon: The initial step is almost always radical inguinal orchiectomy. Depending on staging and tumor type, treatment may include active surveillance, chemotherapy, radiation therapy, or retroperitoneal lymph node dissection. Ebenezer: One reason outcomes are so favorable is that germ cell tumors respond extremely well to cisplatin-based chemotherapy. Dr. Arreaza: Let's talk about prognosis. 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: Honda K, Kawai T, Taguchi S, Shiratori T, Miyakawa J, Nakamura Y, Kaneko T, Suzuki K, Suda S, Kamei J, Kakutani S, Niimi A, Yamada Y, Urakami S, Fukuhara H, Nakagawa T, Kume H. Impact and Risk Factors of Diagnostic Delay in Patients With Testicular Cancer: A Multicenter Retrospective Study. Int J Urol. 2025 Nov;32(11):1593-1601. doi: 10.1111/iju.70187. Epub 2025 Jul 28. PMID: 40726135; PMCID: PMC12586796. https://pubmed.ncbi.nlm.nih.gov/40726135/ Singla N, Bagrodia A, Baraban E, Fankhauser CD, Ged YMA. Testicular Germ Cell Tumors: A Review. JAMA. 2025;333(9):793–803. doi:10.1001/jama.2024.27122 https://jamanetwork.com/journals/jama/article-abstract/2829847?utm_source=openevidence&utm_medium=referral Chavarriaga J, Nappi L, Papachristofilou A, Conduit C, Hamilton RJ. Testicular cancer. Lancet. 2025 Jul 5;406(10498):76-90. doi: 10.1016/S0140-6736(25)00455-6. Epub 2025 May 29. PMID: 40451233. https://pubmed.ncbi.nlm.nih.gov/40451233/ Tateo V, Thompson ZJ, Gilbert SM, Cortessis VK, Daneshmand S, Masterson TA, Feldman DR, Pierorazio PM, Prakash G, Heidenreich A, Albers P, Necchi A, Spiess PE. Epidemiology and Risk Factors for Testicular Cancer: A Systematic Review. Eur Urol. 2025 Apr;87(4):427-441. doi: 10.1016/j.eururo.2024.10.023. Epub 2024 Nov 13. PMID: 39542769. https://pubmed.ncbi.nlm.nih.gov/39542769/ Langn RC, Puente MEE. Scrotal Masses. Am Fam Physician. 2022 Aug;106(2):184-189. PMID: 35977130. https://pubmed.ncbi.nlm.nih.gov/35977130/ Xu P, Wang J, Abudurexiti M, Jin S, Wu J, Shen Y, Ye D. Prognosis of Patients With Testicular Carcinoma Is Dependent on Metastatic Site. Front Oncol. 2020 Jan 10;9:1495. doi: 10.3389/fonc.2019.01495. PMID: 31998648; PMCID: PMC6966605. https://pubmed.ncbi.nlm.nih.gov/31998648/
Episode 216: Fibromyalgia Overview Reitta Wyllie and Tejasvi Ayaggari (medical students) discuss with Dr. Arreaza the presentation, diagnosis and management of fibromyalgia, a commonly unrecognized disease that may impact patient's quality of life if left untreated. Written by Reitta Nash, MSIV, American University of the Caribbean. Additional commentary provided by Dr. Tejasvi Ayyagari. Edits 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. Introduction Fibromyalgia is a chronic pain condition that affects millions of people worldwide, yet it remains one of the most misunderstood disorders in medicine. Patients often experience widespread pain, fatigue, sleep disturbances, cognitive difficulties, and a host of other symptoms that significantly impact daily functioning and quality of life. TJ: It's common, but I feel it is mostly misunderstood and sometimes goes undiagnosed. Reitta: Yes, despite its prevalence, fibromyalgia has historically been met with skepticism, delayed diagnosis, and stigma. Today, we'll break down what fibromyalgia is, what we know about its underlying mechanisms, how it's diagnosed, and how it's managed using evidence-based approaches. What is fibromyalgia? Fibromyalgia is a chronic pain disorder characterized by widespread musculoskeletal pain, accompanied by symptoms such as fatigue, non-restorative sleep, cognitive dysfunction often referred to as “fibro/brain fog,” and mood disturbances. TJ: Unlike inflammatory or autoimmune diseases, fibromyalgia does not cause structural damage to joints or muscles, nor does it produce objective findings on imaging or routine laboratory testing. Instead, it is considered a centralized pain disorder, meaning pain processing within the central nervous system is altered. Arreaza: Many years ago, I had a patient who had fibromyalgia in Germany. He shared how hard it was for him to get diagnosed and treated because many countries fail to recognize fibromyalgia as a disease. However, Germany is not one of them. The German Association of the Medical Scientific Societies (AWMF) has established specific diagnostic criteria for fibromyalgia syndrome (FMS). Also, the World Health Organization recognizes fibromyalgia as a chronic condition, and it is included in the International Classification of Diseases 10th edition (ICD-10). Reitta: The American College of Rheumatology (ACR) recognizes fibromyalgia as a distinct clinical diagnosis, affecting approximately 2–4% of the population, with a higher prevalence in women, though it can affect individuals of any sex or age. Historical Perspective Fibromyalgia was once referred to by terms such as fibrositis, a name that implied inflammation of connective tissue. However, as research failed to demonstrate inflammatory changes, the terminology evolved. In 1990, the American College of Rheumatology introduced the first formal diagnostic criteria, which focused heavily on tender point examination. Over time, these criteria were revised as understanding of the condition improved. Modern diagnostic criteria no longer rely on tender points and instead emphasize symptom severity and widespread pain distribution, reflecting a more patient-centered and clinically practical approach. What causes fibromyalgia? The exact cause of fibromyalgia is not fully understood, but current evidence supports a multifactorial, neurobiological model. The American Academy of Family Physicians identifies a spectrum of chronic overlapping pain conditions that frequently coexist with fibromyalgia, including IBS, TMJ pain, vulvodynia, Chronic fatigue syndrome, interstitial cystitis, endometriosis, chronic tension headaches, migraine, and chronic low back pain. These functional somatic conditions may represent a single disorder manifesting as pain in different body regions at different times over the life span. _____________________ References: Aaron RV, Ravyts SG, Carnahan ND,et al. Prevalence of depression and anxiety among adults with chronic pain: a systematic review and metaanalysis‑analysis. JAMA Netw Open. 2025;8(3):e250268. doi:10.1001/jamanetworkopen.2025.0268. PMID: 40053352. Bradley LA. Pathophysiologic mechanisms of fibromyalgia and its related disorders. J Clin Psychiatry. 2008;69(Suppl 2):6‑14. PMID: 19962493. doi:10.4088/JCP.v69s02102. Häuser W, Ablin J, Fitzcharles MA, et al. Fibromyalgia. Am Fam Physician. 2023;107(2):158‑166. Häuser W, Fitzcharles MA. Facts and myths pertaining to fibromyalgia. Nat Rev Rheumatol. 2018;14(9):525‑535. PMID: 38607678; doi:10.1038/s41584‑018‑0084‑4. Kleykamp BA, Ferguson MC, McNicol E, et al.The prevalence of psychiatric and chronic pain comorbidities in fibromyalgia: An ACTION systematic review. Semin Arthritis Rheum. 2021;51(1):166‑174. PMID: 33383293. doi:10.1016/j.semarthrit.2020.10.006. Magen E, Tolkin L, Aamar S, et al.Endocrine comorbidities in fibromyalgia. Clin Endocrinol (Oxf). 2025;[Epub ahead of print]. doi:10.xxxx/clinend.2025.xxxxx. Mohabbat AB, Wilkinson JM. Central sensitization: When it is not “all in your head.” Am Fam Physician. 2023;107(1):92‑96. Moscati A, Faucon AB, ArnaizYépez‑Yépez C, et al.Life is pain: Fibromyalgia as a nexus of multiple liability distributions. Am J Med Genet B Neuropsychiatr Genet. 2023;192(2):134‑148. doi:10.1002/ajmg.b.32911. Rivera FA, Munipalli B, Allman ME, et al.A retrospective analysis of the prevalence and impact of associated comorbidities on fibromyalgia outcomes in a tertiary care center. Front Med (Lausanne). 2023;10:1184734. doi:10.3389/fmed.2023.1184734. Sleurs D, Tebeka S, Scognamiglio C, Dubertret C, Le Strat Y. Comorbidities of selfreported fibromyalgia in United States adults: A ‑reported fibromyalgia in United States adults: A crosssectional‑sectional study from the NESARC‑III. Eur J Pain. 2020;24(9):1687‑1698. doi:10.1002/ejp.1619. Winslow BT, Vandal C, Dang L. Fibromyalgia: Diagnosis and management. Am Fam Physician. 2023;107(2):158‑166. PMID: 36791450. Wolfe F, Clauw DJ, Fitzcharles MA, et al. Revisions to the American College of Rheumatology fibromyalgia diagnostic criteria. Arthritis Care Res (Hoboken). 2023;75(12):2029‑2039. PMID: 41097025. doi:10.1002/acr.24963. Wolfe F, Clauw DJ, Fitzcharles MA, et al.Revisions to the American College of Rheumatology fibromyalgia diagnostic criteria. Arthritis Care Res (Hoboken). 2023;75(12):2029‑2039. PMID: 41097025. doi:10.1002/acr.24963. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
Contributor: Travis Barlock, MD Educational Pearls: Foul-smelling urine and cloudy urine are commonly misinterpreted as indicators of a UTI. However, these findings alone are not diagnostic. Criteria for UTI: Presence of localized urinary symptoms: Suprapubic pain Dysuria Hesitancy Urgency Urinalysis with WBC > 10 Urine culture with > 100,000 CFU/mL Colonization differs from infection - many patients harbor asymptomatic bacteria but do not have a true infection. Consequences of overtreatment One review showed 45% of patients treated with antibiotics for a presumed UTI actually had asymptomatic bacteriuria and were incorrectly treated. Unnecessary antibiotic treatment can have deleterious effects on the gut microbiome, increasing the risk of multidrug-resistant infections. Another problem with overdiagnosing UTI is missing the real diagnosis by explaining symptoms away as "just a UTI." Be mindful of the risk of overtesting versus not testing at all. Clinicians must navigate a balance between moving patients efficiently through the ER and testing appropriately when a UTI is truly suspected. References: Baghdadi JD, Korenstein D, Pineles L, et al. Exploration of primary care clinician attitudes and cognitive characteristics associated with prescribing antibiotics for asymptomatic bacteriuria. JAMA Netw Open. 2022;5(5):e2214268. doi:10.1001/jamanetworkopen.2022.14268 Colgan R, Williams M. Acute uncomplicated urinary tract infections in adults. Am Fam Physician. 2024;109(2):167-174. Accessed February 21, 2026. https://www.aafp.org/pubs/afp/issues/2024/0200/acute-uncomplicated-utis-adults.html#afp20240200p167-ta1 Summarized by Ashley Lyons OMS3 | Edited by Ashley Lyons & Jorge Chalit OMS4 Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf
The Podcasts of the Royal New Zealand College of Urgent Care
If we suspect a subcutaneous foreign body, we need to know where it is, what it is and how long it has been there. This requires a good history, a thorough examination and appropriate imaging. With this information, we can plan the best way to remove, which might involve referral. Check out the paper mentioned from the American Family Physician Chan C, Salam GA. Splinter removal. Am Fam Physician. 2003 Jun 15;67(12):2557-62. PMID: 12825845. Retained foot FB paper mentioned Chandrashekara CM, George MA, Al-Marboi BS. Neglected Foreign Body, the Cause of Navicular Osteomyelitis in A Paediatric Foot: A Case Report. J Orthop Case Rep. 2013 Jul-Sep;3(3):26-9. doi: 10.13107/jocr.2250-0685.111. PMID: 27298914; PMCID: PMC4719251. Retained FB in groin paper mentioned Yhoshu E, Chaudhary G, Gupta MK. Retained wooden foreign body in groin in a child: A case report and review of literature. Afr J Paediatr Surg. 2020 Jul-Dec;17(3 & 4):127-130. doi: 10.4103/ajps.AJPS_22_20. PMID: 33342850; PMCID: PMC8051621. Case of penile FB paper mentioned Kaneko T, Sakamoto A, Yoshida T, Yanagida K, Yoshimura I, Hagiwara K, Kimura M, Yamada Y, Nakagawa T. Penetrating penile injury due to the splintering of the floorboards in the gymnasium. IJU Case Rep. 2021 May 4;4(4):221-223. doi: 10.1002/iju5.12290. PMID: 34258532; PMCID: PMC8255285. www.rnzcuc.org.nz podcast@rnzcuc.org.nz https://www.facebook.com/rnzcuc https://twitter.com/rnzcuc Music licensed from www.premiumbeat.com Full Grip by Score Squad This podcast is intended to assist in ongoing medical education and peer discussion for qualified health professionals. Please ensure you work within your scope of practice at all times. For personal medical advice, always consult your usual doctor
Un nouvel épisode du Pharmascope est disponible! Dans ce 172e épisode, Nicolas, Olivier et Amélie discutent d'un problème très commun… L’hypothyroïdie! Cette première partie est consacrée à l'évaluation, le diagnostic et la prise en charge de l’hypothyroïdie. Les objectifs pour cet épisode sont les suivants: Discuter de l'évaluation et du diagnostic de l’hypothyroïdie Discuter des de la prise en charge et des différents traitements de l'hypothyroidie Discuter des caractéristiques pharmacologiques de la lévothyroxine Ressources pertinentes en lien avec l'épisode Jonklaas J, et coll; American Thyroid Association Task Force on Thyroid Hormone Replacement. Guidelines for the treatment of hypothyroidism: prepared by the american thyroid association task force on thyroid hormone replacement. Thyroid. 2014 Dec;24(12):1670-751. Chaker L, et coll. Hypothyroidism. Nat Rev Dis Primers. 2022 May 19;8(1):30. doi: 10.1038/s41572-022-00357-7. Wilson SA, Stem LA, Bruehlman RD. Hypothyroidism: Diagnosis and Treatment. Am Fam Physician. 2021 May 15;103(10):605-613. Chaker L, Papaleontiou M. Hypothyroidism: A Review. JAMA. 2025 Sep 3. Hollowell JG, et coll. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab. 2002 Feb;87(2):489-99. McCormack JP, Holmes DT. Your results may vary: the imprecision of medical measurements. BMJ. 2020 Feb 20;368:m149. Pollock MA, et coll. Thyroxine treatment in patients with symptoms of hypothyroidism but thyroid function tests within the reference range: randomised double blind placebo controlled crossover trial. BMJ. 2001 Oct 20;323(7318):891-5. Chen Y, Tai HY. Levothyroxine in the treatment of overt or subclinical hypothyroidism: a systematic review and meta-analysis. Endocr J. 2020 Jul 28;67(7):719-732. Roos A, et coll. The starting dose of levothyroxine in primary hypothyroidism treatment: a prospective, randomized, double-blind trial. Arch Intern Med. 2005 Aug 8-22;165(15):1714-20. da Rocha BS, et coll. Effects of timing and scheduling in levothyroxine adherence to hypothyroidism control: Meta-analysis with trial sequential analysis of Randomized Clinical Trials. Endocrine. 2025 Jul;89(1):52-61.
Episode 212: Managing HFpEFHyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. 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.Treatment of HFpEFArreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.Jordan: And that's worth repeating, because people still think of these as “diabetes drugs.” They're not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.Dr. Arreaza: They're also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That's excellent for a disease where we historically had almost nothing that worked.Jordan: They're also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what's next?Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.Dr. Arreaza: Something to remember: HFpEF patients don't tolerate congestion well, and being “a little wet” is not benign. Let's move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it's worth talking through how these drugs actually work in the kidney.Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.Dr. Arreaza: So let's talk about CKD, because this is where people panic.Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they're recommended even in advanced stages. They reduce progression to kidney failure by about a third.Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That's not kidney injury, that's physiology.Dr. Arreaza: And what about potassium creeping up?Mike: You adjust the dose or add a potassium binder. You don't just automatically stop the drug.Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn't always permanent. What about cardiorenal syndrome? That's where things get uncomfortable.Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.Dr. Arreaza: So we are cautious, but we don't avoid it.Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.Dr. Arreaza: Alright. Let's move on. What about mineralocorticoid receptor antagonists… MRA?Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.Mike: And you have to watch potassium and kidney function carefully, especially if they're already on an ACE inhibitor or ARB.Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It's not first-line for HFpEF, but in select patients, it's reasonable.Dr. Arreaza: Now let's clarify one of the biggest sources of confusion: beta blockers.Jordan: Beta blockers are not a treatment for HFpEF itself. They're only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.Jordan: But, and this is critical, you also don't stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?Mike: Continue it at the same dose or reduce it slightly if they're really unstable. Once they're euvolemic and stable, you can carefully titrate up.Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.Jordan: Don't forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn't change hard outcomes. Lifestyle is the main treatment. Dr. Arreaza: And when should you refer to cardiology?Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.Dr. Arreaza: So, it has been a great discussion. What is the takeaway?Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.Jordan: And it's understanding the physiology, so you don't withhold life-saving therapies out of fear.Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Jordan/Mike: Thanks! 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:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
Episode 211: Understanding HFpEF. Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF. Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and edits 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.What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let's start at the beginning. What is HFpEF?Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms.Dr. Arreaza: And this is where people get fooled by the ejection fraction.Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow.Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you're over-relying on echo reports without thinking clinically.Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It's not usually the primary cause; it's more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let's contrast this with HFrEF. How are these two different?Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction.Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn't relax, even though the EF looks reassuring on paper.Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems.Dr. Arreaza: And then there's the gray zone: heart failure with mildly reduced EF, or HFmrEF. That's an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF?Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart. Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can't pump effectively.Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think?Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don't just “burn out” and turn into HFrEF.Jordan: They're generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that's not the natural progression.Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working.Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis?Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different.Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures.Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF.Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it.Jordan: Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis.Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now?Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it's still rising.Dr. Arreaza: Why is that?Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks.Mike: HFpEF is the heart failure epidemic of the 21st century. It's honestly the cardiology equivalent of type 2 diabetes.Dr. Arreaza: Let's talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk?Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk.Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium.Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up.Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don't know what happened to her. What's the pathophysiology of COVID and heart failure?Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF.Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you've got a perfect storm for heart failure.Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years?Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense.Jordan: HFpEF is messy. It's not one disease. It's stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can't fix all of that.Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example. They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output.Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics.Dr. Arreaza: The miracle drug for HFpEF! Alright, let's wrap up.Mike: Bottom line: HFpEF is common, complex, and dangerous: even if the EF looks “normal.”Jordan: And if you're relying on ejection fraction alone, HFpEF will humble you every time.Dr. Arreaza: If you liked this episode, share it with a friend or a colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.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:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
HelixTalk - Rosalind Franklin University's College of Pharmacy Podcast
In this episode, we review the clinical presentation, diagnosis, and treatment of uncomplicated urinary tract infections. Key Concepts Uncomplicated urinary tract infections (UTI) are defined as an infection localized to the bladder without any systemic signs or symptoms of infection in someone who is not immunocompromised, pregnant, catheterized, and has normal urologic anatomy. UTIs are most commonly seen in younger women. E. coli is by far the most common urinary pathogen. Symptoms alone drive most of the diagnosis of UTI; however, urinalysis and urine culture can be helpful in some circumstances. Nitrofurantoin (Macrobid) is recommended for men and women for first-line therapy in most patients. Fosfomycin, Bactrim, pivmecillinam, and certain B-lactams can be considered in certain circumstances. Women are usually treated for 3-5 days and men 5-7 days. Some evidence suggests inferior clinical outcomes for B-lactam; however, the amount of data in general is lacking for B-lactams. Recommended B-lactams (aside from pivmecillinam) include amoxicillin/clavulanate, cephalexin, cefadroxil, cefpodoxime, and cefdinir. References Nelson Z, Aslan AT, Beahm NP, et al. Guidelines for the Prevention, Diagnosis, and Management of Urinary Tract Infections in Pediatrics and Adults: A WikiGuidelines Group Consensus Statement. JAMA Netw Open. 2024;7(11):e2444495. Published 2024 Nov 4. doi:10.1001/jamanetworkopen.2024.44495 Gupta K, Hooton TM, Naber KG, et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. Clin Infect Dis. 2011;52(5):e103-e120. doi:10.1093/cid/ciq257 Kurotschka PK, Gágyor I, Ebell MH. Acute Uncomplicated UTIs in Adults: Rapid Evidence Review. Am Fam Physician. 2024;109(2):167-174. https://www.wikiguidelines.org/
During this episode I discuss Bell's Palsy. From its incidence, to average recovery times, to the medications used during the recovery process and much more. I also discuss how I approach Bell's Palsy in clinical practice. Enjoy!Episode Resources Khan AJ, Szczepura A, Palmer S, et al. Physical therapy for facial nerve paralysis (Bell's palsy): An updated and extended systematic review of the evidence for facial exercise therapy. Clin Rehabil. 2022;36(10):1339-1355. doi:10.1177/02692155221102985.Kim SJ, Lee HY. Acute peripheral facial palsy: Recent guidelines and a systematic review of the literature. J Korean Med Sci. 2020;35(30):e245. doi:10.3346/jkms.2020.35.e245.de Almeida JR, Guyatt GH, Sud S, et al. Management of Bell palsy: clinical practice guideline. CMAJ. 2014;186(12):917-922. doi:10.1503/cmaj.131801.Dalrymple SN, Row JH, Gazewood J. Bell palsy: rapid evidence review. Am Fam Physician. 2023;107(4):415-420.
Alex and Venk discuss the fundamental differences of caring for people during an in-flight emergency: what changes with oxygen and pressure, what is available to you, what are the expectations, and more. Both have been teaching about this scenario to others and have been present for several such encounters. They bring their expertise and the available literature to establish this level-setting chapter of the Always on EM Podcast. By the end of this, hopefully, you'll have zero hesitation standing with confidence that you can provide assistance in any event that arises and be as well prepared as anyone to do it. So, buckle up, put your seatbacks up, stow your laptops, and tune in to this high-flying chapter of Always on EM! CONTACTS X - @AlwaysOnEM; @VenkBellamkonda YouTube - @AlwaysOnEM; @VenkBellamkonda Instagram – @AlwaysOnEM; @Venk_like_vancomycin; @ASFinch Email - AlwaysOnEM@gmail.com REFERENCES & LINKS Kim Y, Bae SC, Song YS. Exploring the potential of telehealth in-flight medical emergencies. Digit Health. 2025 Mar 13;11:20552076251326666. doi: 10.1177/20552076251326666. PMID: 40093698; PMCID: PMC11907535. Hawati SM, Binobaid F, Alsaeigh A, Alameer W, Al Ajmi AM, Alghamdi MK, Alqarni AA, Al-Harthi SN, Almelaifi A, Al Shehri AA. Assessing Emergency Medicine, Family Medicine, and ICU Doctors' Knowledge, Confidence, and Attitude in Managing In-Flight Medical Emergencies in the Kingdom of Saudi Arabia Hospitals: A Cross-Sectional Study. Cureus. 2025 Feb 1;17(2):e78359. doi: 10.7759/cureus.78359. PMID: 40046350; PMCID: PMC11880637. Hu JS, Smith JK. In-flight Medical Emergencies. Am Fam Physician. 2021 May 1;103(9):547-552. PMID: 33929167. Martin-Gill C, Doyle TJ, Yealy DM. In-Flight Medical Emergencies: A Review. JAMA. 2018 Dec 25;320(24):2580-2590. doi: 10.1001/jama.2018.19842. PMID: 30575886.
Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: CYP enzymes are responsible for the metabolism of many medications, drugs, and other substances CYP3A4 is responsible for the majority Other common ones include CYP2D6 (antidepressants), CYP2E1 (alcohol), and CYP1A2 (cigarettes) CYP inducers lead to reduced concentrations of a particular medication CYP inhibitors effectively increase concentrations of certain medications in the body Examples of CYP inducers Phenobarbital Rifampin Cigarettes St. John's Wort Examples of CYP inhibitors -azole antifungals like itraconazole and ketoconazole Bactrim (trimethoprim-sulfamethoxazole) Ritonavir (found in Paxlovid) Grapefruit juice Clinical relevance Drug-drug interactions happen frequently and often go unrecognized or underrecognized in patients with significant polypharmacy A study conducted on patients receiving Bactrim and other antibiotics found increased rates of anticoagulation in patients receiving Bactrim Currently, Paxlovid is prescribed to patients with COVID-19, many of whom have multiple comorbidities and are on multiple medications Paxlovid contains ritonavir, a powerful CYP inhibitor that can increase concentrations of many other medications A complete list of clinically relevant CYP inhibitors can be found on the FDA website: https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers References Glasheen JJ, Fugit RV, Prochazka AV. The risk of overanticoagulation with antibiotic use in outpatients on stable warfarin regimens. J Gen Intern Med. 2005;20(7):653-656. doi:10.1111/j.1525-1497.2005.0136.x Lynch T, Price A. The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects. Am Fam Physician. 2007;76(3):391-396. PAXLOVID™. Drug interactions. PAXLOVIDHCP. Accessed March 16, 2025. https://www.paxlovidhcp.com/drug-interactions Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Contributor: Meghan Hurley, MD Educational Pearls: Gastroenteritis clinical diagnoses: Diarrhea with or without vomiting and fever Vomiting in the absence of diarrhea has a large list of differential diagnoses, so the combination of diarrhea and vomiting in a patient is helpful to indicate the gastroenteritis diagnosis Symptom timeline is usually 1-3 days, but can last up to 14 days – diarrhea persists the longest Treatment for mild to moderate dehydration: oral or IV rehydration Begin orally to avoid unnecessary IV in a pediatric patient Administer ODT Ondansetron (Zofran) to prevent vomiting Meta-analysis showed that 2-8 mg orally, based on body weight, decreased vomiting quickly Wait 15-20 minutes for the medication to take effect Use streamlined method for oral rehydration: Fluids such as over-the-counter Pedialyte, Infalyte, Rehydrate, Resol, and Naturalyte may be used If patient weighs less than 10kg: administer 5mL of fluid per minute for 20 minutes If patient weighs 10kg or more: administer 10mL of fluid for 20 minutes If the patient can keep the fluid down, double the fluid volume and repeat If the patient once again keeps the fluid down, double the fluid volume and repeat If successful with each attempt, the patient may be discharged home Can prescribe ODT Zofran for 1-2 days at home If the patient vomits more than once during this oral rehydration process, intravenous rehydration must be initiated References Churgay CA, Aftab Z. Gastroenteritis in children: Part II. Prevention and management. Am Fam Physician. 2012 Jun 1;85(11):1066-70. PMID: 22962878. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
Understanding Hodgkin's Lymphoma, featuring pathophysiology and most common symptoms of Hodgkin's Lymphoma, as well as proposed pathophysiology. Includes classification, diagnosis (with Reed Sternberg Cells), and treatment options. Consider subscribing on YouTube (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=1Patreon: https://www.patreon.com/rhesusmedicineBuy Us A Coffee!: https://www.buymeacoffee.com/rhesusmedicineTimestamps: 0:00 What is Hodgkin's Lymphoma? 2:04 Hodgkin's Lymphoma Classification3:20 Signs and Symptoms of Hodgkin's Lymphoma5:00 Hodgkin's Lymphoma Causes & Pathophysiology6:10 Hodgkin's Lymphoma Diagnosis 7:45 Reed-Sternberg Cells9:10 Hodgkin's Lymphoma Staging (Lugano and Ann Arbor)10:05 Hodgkin's Lymphoma TreatmentReferences:BMJ Best Practice (2024) - “Plantar Fasciitis”. Available at https://bestpractice.bmj.com/topics/en-gb/487Weerakkody Y, Rizk M, Bell D, et al. Plantar fasciitis. Reference article, Radiopaedia.org https://doi.org/10.53347/rID-22645Wearing, S - Musculoskeletal Key (2016) - “Anatomy of the Plantar Fascia”. Available at https://musculoskeletalkey.com/anatomy-of-the-plantar-fascia/Clinical Knowledge Summaries (2020) - “Plantar Fasciitis”. Available at https://cks.nice.org.uk/topics/plantar-fasciitis/Am Fam Physician 2019;99(12):744-750. Available at https://www.aafp.org/pubs/afp/issues/2019/0615/p744.htmlPlease remember this podcast and all content from Rhesus Medicine is meant for educational purposes only and should not be used as a guide to diagnose or to treat. Please consult a healthcare professional for medical advice. #medicalmnemonic #medicalmnemonics #rhesusmedicine #studymedicine #studygram #medstudent #medicalschool
Understanding Plantar Fasciitis, the most common cause for heel / foot pain. Includes most common causes and risk factors, as well as multiple treatment options for plantar fasciitis.Consider subscribing on YouTube (if you found any of the info useful!): https://www.youtube.com/channel/UCRks8wB6vgz0E7buP0L_5RQ?sub_confirmation=1Patreon: https://www.patreon.com/rhesusmedicineBuy Us A Coffee!: https://www.buymeacoffee.com/rhesusmedicineTimestamps:0:00 What is Plantar Fasciitis?0:34 Plantar Fasciitis Pathophysiology1:25 Plantar Fasciitis Symptoms2:16 Plantar Fasciitis Causes and Risk Factors3:23 Plantar Fasciitis Diagnosis4:31 Plantar Fasciitis TreatmentLINK TO MNEMONICS:https://www.youtube.com/watch?v=p-XE7PiwGgE&list=PLGNSE_HvIV4t7a33bbHN1fq-j_tge0GmpLINK TO SOCIAL MEDIA: https://www.instagram.com/rhesusmedicine/References:BMJ Best Practice (2024) - “Plantar Fasciitis”. Available at https://bestpractice.bmj.com/topics/en-gb/487Weerakkody Y, Rizk M, Bell D, et al. Plantar fasciitis. Reference article, Radiopaedia.org https://doi.org/10.53347/rID-22645Wearing, S - Musculoskeletal Key (2016) - “Anatomy of the Plantar Fascia”. Available at https://musculoskeletalkey.com/anatomy-of-the-plantar-fascia/Clinical Knowledge Summaries (2020) - “Plantar Fasciitis”. Available at https://cks.nice.org.uk/topics/plantar-fasciitis/Am Fam Physician 2019;99(12):744-750. Available at https://www.aafp.org/pubs/afp/issues/2019/0615/p744.htmlPlease remember this podcast and all content from Rhesus Medicine is meant for educational purposes only and should not be used as a guide to diagnose or to treat. Please consult a healthcare professional for medical advice. #medicalmnemonic #medicalmnemonics #rhesusmedicine #studymedicine #studygram #medstudent #medicalschool
Episode 182: HPV VaxFuture Dr. Zuaiter and Dr. Arreaza briefly discuss HPV infection but pocus on the prevention of the infection with the vaccine. Dr. Arreaza mentions that HPV vaccine is also recommended by ASCCP to medical professionals. Written by Amanda Zuaiter, MS4, Ross University School of Medicine. Edits 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.Human Papilloma Virus (HPV).According to the World Health Organization, cervical cancer is the 4th most common cancer affecting women globally. Annually, there are over 600,00 new cases and more than 300,000 deaths. The leading cause of cervical cancer is HPV. HPV, or human papillomavirus, is a prevalent virus that is spread through close skin-to-skin contact, mainly by sexual intercourse. It is the most common sexually transmitted disease in the United States. The term STI and STD are used indistinctively, but some people make a difference, such as Dr. Cornelius Reitmeijer. STI refers to sexually transmitted infection, which can be asymptomatic, and STD stands for sexually transmitted disease, which are the signs and symptoms caused by the multiplication of the infectious agent and disruption of bodily functions. STI is the preferred term, as recommended by experts during the last few years. Low risk vs High risk HPV.There are over 200 strains of HPV which fall into two categories: low risk and high risk. The low-risk types, HPV 6 and 11, cause warts around the genitals, anus, mouth or throat. The high-risk types, HPV 16 and 18, are linked to cervical, vaginal, anal, and other cancers. Persistent infection with high-risk HPV types is the primary cause of cervical cancer, accounting for 70% of cervical cancer cases. While often asymptomatic, persistent HPV infections can develop into papular lesions which can cause bleeding and pain or cause sore throat and hoarseness if warts develop in the throat.Not all warts will turn into cancer, but the risk of a wart turning into cancer is higher than normal skin or mucosa that has not been infected by HPV.Even though cervical cancer is the most well-known condition linked to HPV, it's important to note that HPV isn't just a women's health issue. It can also cause cancers in men, such as throat, penile and anal cancers. Men, however, are not screened for HPV if they have no signs or symptoms of infection.HPV Prevention: General measures that can be taken are maintaining a healthy immune system by exercising regularly and a balanced diet and quitting smoking.Male circumcision has been shown to reduce the risk of penile cancer in men and their sexual partners may have a lower risk of cervical cancer. Screening: Women should undergo regular pap smears with HPV screening. Pap smear screening begins at the age of 21 and is recommended every 3 years. From ages 30-65, co-testing should be done every 5 years, according to the guidelines by the American College of Obstetrics and Gynecology. Also, HPV test self-collection is now available in the US since May 2024, and it is useful especially in rural areas.The most effective ways to prevent the transmission of HPV is to practice safe sex, using condoms, and getting vaccinated. HPV vaccine. For medical providers: It was announced only to ASCP (American Society for Colposcopy and Cervical Pathology) members in the middle of the pandemic. On February 19, 2020, ASCCP recommended HPV vaccination for clinicians routinely exposed to the virus.This recommendation encompasses the complete health care team, including but not limited to, physicians, nurse practitioners, nurses, residents, and fellows, as well as office and operating room staff in the fields of obstetrics and gynecology, family practice, gynecologic oncology, and dermatology. Let's remember that in 2018, the FDA a supplemental application for Gardasil 9 to include persons aged 27 to 45 years old. The ASCCP letter states “While there is limited data on occupational HPV exposure, ASCCP, as well as other medical societies, recommend that members actively protect themselves against the risks” among medical providers. For patients: The vaccine is given to prevent the types of HPV that are most likely to cause cancer and other health problems. It works by training the immune system to recognize and fight HPV before an infection can take hold. Gardasil-9® is the brand name that is offered in the US. The 9 means it targets 9 strains of the virus (6, 11, 16, 18, 31, 33, 45, 52, and 58). It's important to note that the vaccine is preventative, and it is not considered a treatment. This means it's most effective when given BEFORE any exposure to HPV, ideally during adolescence. The HPV vaccine is recommended for boys and girls ages 11-12 but can be started as early as the age of 9. We need to be prepared to manage vaccine hesitancy because some parents may be concerned when you explain the vaccine to them. A study done in Scotland found that there were NO cases of invasive cervical cancer in adults who received any doses of the HPV vaccine at 12 to 13 years of age. To get to that conclusion, they reviewed the cancer data of 447,845 women who were born between 1988 and 1996. The data demonstrated that the HPV vaccine prevents invasive cervical cancer, especially when given between 12 to 13 years of age. When the vaccine is given later in life, it tends to be less effective. AmandaHow is HPV vaccine given?The vaccine schedule is as follows: -For ages 9-14, two shots are given with the second dose 6-12 months after the first. -For those ages 15-26, three shots are given. After the first shot, the second is given after 1-2 months, and the third shot 6 months after the first. This is the same schedule for immunocompromised people regardless of their age. -People over the age of 26 can still receive the vaccine, as the FDA has approved the vaccine for individuals up to the age of 45. With that being said, those over the age of 26 may not fully benefit from the vaccine due to the fact they may have already been exposed to HPV. Still, vaccination can provide protection against other strains of the virus.Other HPV Vaccine considerations:Is HPV vaccine effective?-Studies have shown that the HPV vaccine is nearly 100% effective at preventing cervical pre-cancers caused by HPV 16 and 18.Are boosters needed?-The vaccine provides protection for at least 10 years and boosters are not required. The vaccine is recommended for boys too, as they are also at risk for HPV causing cancers, and administration of the vaccine helps to reduce the spread of the virus. It is safe to administer the HPV vaccine with all other age-appropriate vaccinations. What if my patient misses a dose?-If a dose is missed, it can be resumed at any time without restarting the series. There are no known severe side effects or reactions to the vaccine. The vaccine can be given even if the person has already been exposed to HPV as it can protect against the other types of HPV.Conclusion: HPV is a common cause of cervical cancer, and the benefits of the HPV vaccine are profound. Countries with high vaccination rates have already seen significant drops in HPV infections, genital warts, and cervical pre-cancers. Vaccination protects individuals and helps achieve herd immunity, benefiting entire communities.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:Sabour, Jennifer, “The Difference Between STD and STI,” Verywell Health, August 22, 2024, https://www.verywellhealth.com/std-vs-sti-5214421. ASCCP Letter, February 19, 2020, https://www.asccp.org/hpv-vaccinationBarry HC. Scottish Screening: No Cases of Invasive Cervical Cancer in Women Who Received At least One Dose of Bivalent HPV Vaccine at 12 or 13 Years of Age. Am Fam Physician. 2024 Aug;110(2):201-202. PMID: 39172683. https://pubmed.ncbi.nlm.nih.gov/39172683/World Health Organization. “Cervical Cancer,” March 5, 2024, www.who.int/news-room/fact-sheets/detail/cervical-cancerACOG, “Cervical Cancer Screening FAQ,” www.acog.org/womens-health/faqs/cervical-cancer-screening. Accessed January 9, 2025.ACOG, “HPV Vaccination FAQ,” www.acog.org/womens-health/faqs/hpv-vaccination. Accessed January 9, 2025.Cox, J. Thomas and Joel M Palefsky, UpToDate, www.uptodate.com/contents/human-papillomavirus-vaccination, accessed January 9, 2025.National Cancer Institute. “HPV and Cancer.” National Cancer Institute, 18 Oct. 2023, www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-and-cancer .Theme song, Works All the Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
Dr. Adela Cope breaks down pelvic inflammatory disease, tubo-ovarian abscess, ovarian torsion, ectopic pregnancy and more in this densely packed chapter of Always on EM. Tune in as Alex and Venk also try to figure out which one has the correct mental model of PID and who will ask the first stupid question. CONTACTS X - @AlwaysOnEM; @VenkBellamkonda YouTube - @AlwaysOnEM; @VenkBellamkonda Instagram – @AlwaysOnEM; @Venk_like_vancomycin; @ASFinch Email - AlwaysOnEM@gmail.com LEARN MORE ABOUT RESIDENCY: https://youtu.be/gCQ0zimhhhY?si=NpsyTruGM9N_UpVM https://college.mayo.edu/academics/residencies-and-fellowships/emergency-medicine-residency-minnesota/ REFERENCES: Williams T, Mortada R, Porter S. Diagnosis and Treatment of Polycystic Ovary Syndrome. Am Fam Physician. 2016;94(2):106-113 Rutz M, Boulger C. Early Pregnancy. Sonoguide - American College of Emergency Physicians. Accessed 8/20/2024 (https://www.acep.org/sonoguide/basic/early-pregnancy) Rodgers SK, et al. A lexicon for first-trimester US: Society of radiologists in ultrasound consensus conference recommendations. Radiology. 2024; 312(2):e240122 Kreisel K, Flagg EW, Torrone E. Trends in pelic inflammatory disease emergnecy department visits, United STates, 2006-2013. Am J Obstet Gynecol 2018;218:117e1-e10 Adhikari S, Blaivas M, Lyon M. Role of bedside transvaginal ultrasonography in the diagnosis of tubo-ovarian abscess in the emergency department. JEM 2008. 34(4):429-433 Mohseni M, Simon LV, Sheele JM. Epidemiologic and clinical characteristics of tubo-ovarian abscess, hydrosalpinx, pyosalpinx, and oophoritis in emergency department patients. Cureus. 2020;12(11):e11647 CDC sexually transmitted infections treatment guidelines, 2021 - Pelvic Inflammatory Disease (PID) accessed 8-20-24 Linden JA. et al. Is the pelvic examination still crucial in patients presenting to the emergency department with vaginal bleeding or abdominal pain when an intrauterine pregnancy is identified on ultrasonography? A randomized tli. Annals of Emerg Med 2017(70):825-834 Stein JC, et al. Emergency physician ultrasonography for evaluating patients at risk for ectopic pregnancy: A Meta-Analysis. Annals of Emerg Med. 2010;56:674-683 Robertson JJ, Long B, Koyfman A. Emergency Medicine Myths: Ectopic pregnancy, evaluation, risk factors, and presentation. JEM. 2017(53)6819-828 Brown J, Fleming R, Aristizabal J, Rocksolana G. Does pelvic exam in the emergency department add useful information? West J Emerg Med. 2011;12(2):208-212 Lee R, Dupuis C, Chen B, Smith A, Kim YH. Diagnosing ectopic pregnancy in the emergency setting. Ultrasonography. 2018;37:78-87
João Mendes e Caio Bastos discutem um caso clínico apresentado pelo Frederico Amorim. Já sabe que vem surpresa né? Referências: 1. Mercado MG, Smith DK, Guard EL. Acute Kidney Injury: Diagnosis and Management. Am Fam Physician. 2019;100(11):687-694. 2. Bhatla A, Menez S, Feldman L. Things We Do For No Reason™: Routine renal ultrasound testing for patients presenting with or developing acute kidney injury in the hospital. J Hosp Med. Published online June 27, 2024. doi:10.1002/jhm.13446 3. Foreman JW. Fanconi Syndrome. Pediatr Clin North Am. 2019;66(1):159-167. doi:10.1016/j.pcl.2018.09.002 4. Douvris A, Zeid K, Hiremath S, et al. Safety Lapses Prior to Initiation of Hemodialysis for Acute Kidney Injury in Hospitalized Patients: A Patient Safety Initiative. J Clin Med. 2018;7(10):317. Published 2018 Oct 1. doi:10.3390/jcm7100317 5. Luciano RL, Moeckel GW. Update on the Native Kidney Biopsy: Core Curriculum 2019. Am J Kidney Dis. 2019;73(3):404-415. doi:10.1053/j.ajkd.2018.10.011 6. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract. 2012;120(4):c179-c184. doi:10.1159/000339789 7. Kellum JA, Romagnani P, Ashuntantang G, Ronco C, Zarbock A, Anders HJ. Acute kidney injury. Nat Rev Dis Primers. 2021;7(1):52. Published 2021 Jul 15. doi:10.1038/s41572-021-00284-z
Episode 173: Acute OsteomyelitisFuture Dr. Tran explains the pathophysiology of osteomyelitis and describes the presentation, diagnosis and management of acute osteomyelitis. Dr. Arreaza provides information about Written by Di Tran, MSIII, Ross University School of Medicine. 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.What is osteomyelitis?Osteomyelitis, in simple terms, is an infectious disease that affects both bone and bone marrow and is either acute or chronic. According to archaeological findings of animal fossils with a bone infection, osteomyelitis was more than likely to be known as a “disease for old individuals”.Our ancestors over the years have used various vocabulary terms to describe this disease until a French surgeon, Dr. Nelaton, came up with the term “Osteomyelitis” in 1844. This is the beauty of medical terms, Latin sounds complicated for some people, but if you break up the term, it makes sense: Osteo = bone, myelo = marrow, itis = inflammation. So, inflammation of the bone marrow.Traditionally, osteomyelitis develops from 3 different sources:First category is the “hematOgenous” spread of the infection within the bloodstream, as in bacteremia. It is more frequent in children and long bones are usually affected. [Arreaza: it means that the infection started somewhere else but it got “planted” in the bones]Second route is “direct inoculation” of bacteria from the contiguous site of infection “without vascular insufficiency”, or trauma, which may occur secondary to fractures or surgery in adults. In elderly patients, the infection may be related to decubitus ulcers and joint replacements.And the third route is the “contiguous” infection “with vascular insufficiency”, most seen in a patient with a diabetic foot infection.Patients with vascular insufficiency often have compromised blood supply to the lower extremities, and poor circulation impairs healing. In these situations, infection often occurs in small bones of the feet with minimal to no pain due to neuropathy.They can have ulcers, as well as paronychia, cellulitis, or puncture wounds.Thus, the importance of treating onychomycosis in diabetes because the fungus does not cause a lot of problems by itself, but it can cause breaks in the nails that can be a port of entry for bacteria to cause severe infections. Neuropathy is an important risk factor because of the loss of protective sensation. Frequently, patients may step on a foreign object and not feel it until there is swelling, purulent discharge, and redness, and they come to you because it “does not look good.”Acute osteomyelitis often takes place within 2 weeks of onset of the disease, and the main histopathological findings are microorganisms, congested blood vessels, and polymorphonuclear leukocytes, or neutrophilic infiltrates.What are the bugs that cause osteomyelitis?Pathogens in osteomyelitis are heavily depended on the patient's age. Staph. aureus is the most common culprit of acute hematogenous osteomyelitis in children and adults. Then comes Group A Strep., Strep. pneumoniae, Pseudomonas, Kingella, and methicillin-resistant Staph. aureus. In newborns, we have Group B Streptococcal. Less common pathogens are associated with certain clinical presentations, including Aspergillus, Mycobacterium tuberculosis, and Candida in the immunocompromised.Salmonella species can be found in patients with sickle cell disease, Bartonella species in patients with HIV infection, and Pasteurella or Eikenella species from human or animal bites.It is important to gather a complete medical history of the patient, such as disorders that may put them at risk of osteomyelitis, such as diabetes, malnutrition, smoking, peripheral or coronary artery disease, immune deficiencies, IV drug use, prosthetic joints, cancer, and even sickle cell anemia. Those pieces of information can guide your assessment and plan.What is the presentation of osteomyelitis?Acute osteomyelitis may present symptoms over a few days from onset of infection but usually is within a 2-week window period. Adults will develop local symptoms of erythema, swelling, warmth, and dull pain at the site of infection with or without systemic symptoms of fever or chills.Children will also be present with lethargy or irritability in addition to the symptoms already mentioned.It may be challenging to diagnose osteomyelitis at the early stages of infection, but you must have a high level of suspicion in patients with high risks. A thorough physical examination sometimes will show other significant findings of soft tissue infection, bony tenderness, joint effusion, decreased ROM, and even exposed bone. Diagnosis.As a rule of thumb, the gold standard for the diagnosis of osteomyelitis is bone biopsy with histopathology findings and tissue culture. There is leukocytosis, but then WBC counts can be normal even in the setting of acute osteomyelitis.Inflammatory markers (CRP, ESR) are often elevated although both have very low specificity. Blood cultures should always be obtained whenever osteomyelitis is suspected. A bone biopsy should also be performed for definitive diagnosis, and specimens should undergo both aerobic and anaerobic cultures. In cases of osteomyelitis from diabetic foot infection, do the “probe to bone” test. What we do is we use a sterile steel probe to detect bone which is helpful for osteomyelitis confirmation.Something that we can't miss out on is radiographic imaging, which is quite important for the evaluation of osteomyelitis. Several modalities are useful and can be used for the work-up plan; plain radiographs often are the very first step in the assessment due to their feasibility, low cost, and safety. Others are bone scintigraphy, CT-scan, and MRI. In fact, the MRI is widely used and provides better information for early detection of osteomyelitis than other imaging modalities. It can detect necrotic bone, sinus tracts, and even abscesses. We look for soft tissue swelling, cortical bone loss, active bone resorption and remodeling, and periosteal reaction. Oftentimes, plain radiography and MRI are used in combination. Treatment:Treatment of osteomyelitis actually is a teamwork effort among various medical professionals, including the primary care provider, the radiologist, the vascular, the pharmacist, the podiatrist, an infectious disease specialist, orthopedic surgeons, and the wound care team.Something to take into consideration, if the patient is hemodynamically stable it is highly recommended to delay empirical antibiotic treatment 48-72 hours until a bone biopsy is obtained. The reason is that with percutaneous biopsy ideally done before the initiation of antibiotic treatment, “the microbiological yield will be higher”.We'll have a better idea of what particular bugs are causing the problem and guide the treatment appropriately. The choice of antibiotic therapy is strongly determined by susceptibilities results. The antibiotic given will be narrowed down only for the targeted susceptible organisms. In the absence of such information, or when a hospitalized patient presents with an increased risk for MRSA infection, empiric antibiotic coverage is then administered while awaiting culture results. It should be broad-spectrum antibiotics and include coverage for MRSA, broad gram-negative and anaerobic bacteria. For example, vancomycin plus piperacillin-tazobactam, or with broad-spectrum cephalosporin plus clindamycin. Treatment will typically be given for 4 to 6 weeks.The duration between 4-6 weeks is important for complete healing, but a small study with a small sample showed that an even shorter duration of 3 weeks may be effective, but more research is needed. In certain situations, surgery is necessary to preserve viable tissue and prevent recurrent infection, especially when there are deep abscesses, necrosis, or gangrene, amputation or debridement is deemed appropriate. If the infected bone is completely removed, patients may need a shorter course of antibiotics, even a few days only. Amputation can be very distressing, especially when we need to remove large pieces of infected bone, for example, a below-the-knee amputation. We need to be sensitive to the patient's feelings and make a shared decision about the best treatment for them.In patients with diabetes, additional care must be taken seriously, patient education about the need for compliance with treatment recommendations, with careful wound care, and good glycemic control are all beneficial for the healing and recovery process. Because this is a very common problem in the clinic and at the hospital, we must keep our eyes wide open and carefully assess patients with suspected osteomyelitis to detect it promptly and start appropriate treatment. Adequate and timely treatment is linked to fewer complications and better outcomes._________________________Conclusion: Now we conclude episode number 173, “Acute Osteomyelitis.” Future Dr. Tran explained the pathophysiology, diagnosis, and management of osteomyelitis. A bone biopsy is the ideal method of diagnosis. Delaying antibiotic treatment a few days until you get a biopsy is allowed if the patient is stable, but if the patient is unstable, antibiotics must be started promptly. Dr. Arreaza mentioned the implications of amputation and that we must discuss this treatment empathically with our patients. This week we thank Hector Arreaza and Di Tran. Audio editing by Adrianne Silva.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:Bury DC, Rogers TS, Dickman MM. Osteomyelitis: Diagnosis and Treatment. Am Fam Physician. 2021 Oct 1;104(4):395-402. PMID: 34652112.Cunha BA. Osteomyelitis in elderly patients. Clin Infect Dis. 2002 Aug 1;35(3):287-93. doi: 10.1086/341417. Epub 2002 Jul 11. PMID: 12115094.Fritz JM, McDonald JR. Osteomyelitis: approach to diagnosis and treatment. Phys Sportsmed. 2008 Dec;36(1):nihpa116823. doi: 10.3810/psm.2008.12.11. PMID: 19652694; PMCID: PMC2696389.Hatzenbuehler J, Pulling TJ. Diagnosis and management of osteomyelitis. Am Fam Physician. 2011 Nov 1;84(9):1027-33. PMID: 22046943.Hofstee MI, Muthukrishnan G, Atkins GJ, Riool M, Thompson K, Morgenstern M, Stoddart MJ, Richards RG, Zaat SAJ, Moriarty TF. Current Concepts of Osteomyelitis: From Pathologic Mechanisms to Advanced Research Methods. Am J Pathol. 2020 Jun;190(6):1151-1163. doi: 10.1016/j.ajpath.2020.02.007. Epub 2020 Mar 16. PMID: 32194053.Momodu II, Savaliya V. Osteomyelitis. [Updated 2023 May 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532250/Royalty-free music used for this episode: Trap Chiller by Gushito, downloaded on Nov 06, 2023, from https://www.videvo.net
Episode 168: UTI in MalesFuture Dr. Tran gives a summary of UTIs in Males, including epididymitis, orchitis, urethritis, prostatitis, and pyelonephritis. Diagnosis and treatment were briefly described and some differences with female patients were mentioned by Dr. Arreaza. Written by Di Tran, MS-3, Ross University School of Medicine. 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.WHAT ARE URINARY TRACT INFECTIONS?Urinary Tract Infection (UTI) is an infection of any part of the urinary tract system. It may involve any part of the renal system, the kidneys, the ureters, the bladder, the prostate, and the urethra. Different from men, a woman may get a UTI more easily due to their anatomical difference. A woman's urethra is shorter and lies close in proximity to both the vagina and the anus, which allows easy access for bacteria to travel up to the bladder.UTI is further subdivided into two different categories, depending on where the infection takes place within the urinary tract:Lower Tract Infection – cystitis and urethritis when the infection occurs on the bladder and the urethra, respectively. Common infections are a result of bacteria migrating from the skin (and also from sexual organs) to the urethra and ending up in the bladder.In males, other forms of lower tract infection can result in prostatitis, epididymitis, and orchitis.Upper Tract Infection - aka pyelonephritis, is a more concerning infection that involves the upper parts of the urinary system, in other words, the ureters, and kidneys.AGE DIFFERENCES IN UTI FOR MEN:For men, the incidence of UTI increases with age. Dr. John Brusch reports UTI rarely develops in young males and the prevalence of bacteriuria is 0.1% or less. Men who are 15-50 years of age often have urethritis due to sexually transmitted infection (STI), mainly by Neisseria gonorrhoeae and Chlamydia trachomatis. Symptoms include frequency, urgency, and dysuria (most common).Men who are 50 years or older, especially those with prostatic hyperplasia, will have signs and symptoms of incomplete bladder emptying, hesitancy, slow stream, difficulty initiating urination, and dribbling after urinating. Due to the enlargement of the prostate gland, there will be partial blockage of urine flow from the bladder, which in turn, creates a reservoir where bacteria can grow and cause an infection. The most common offending microorganism for this age group is Escherichia coli.Interestingly, while UTIs are rare among men under 60, by the age of 80, both women and men have similar incidence rates. The bladder tends to have a higher residual volume in older males because the prostate grows no matter what, it´s just a part of aging for males. Some may end up with more or less lower urinary tract symptoms, but the prostate is enlarged in general.Other risk factors for UTI in males are men who are not circumcised, urethral strictures, fistulas, hydronephrosis (or dilated ureters overfilled with urine due to failure of drainage to the bladder), and the use of urinary catheters. DIFFERENT TYPES OF UTIs IN MALES:EPIDIDYMITIS:The infection starts from the retrograde ascending route from the prostatic urethra, backing up to the vas deferens, and eventually ending in the epididymis.In men who are younger than 35 years of age, the usual pathogens are C. trachomatis and N. gonorrhoeae (sexually transmitted).In men who are older than 35 years of age, the usual offending agents are Enterobacteriaceae and gram-positive cocci (E. coli as mentioned previously).ORCHITIS:This unique UTI is caused by viral pathogens, such as mumps, coxsackie B, Epstein-Barr (EBV), and varicella (VZV) viruses. Several studies have shown that patients having orchitis have a history of epididymitis. Fortunately, this infection is uncommon, and it was the main reason to develop the MMR vaccine. It is caused by viruses other than mumps, so you can still have orchitis even if you are vaccinated. Antibiotics are not prescribed for viral orchitis.BACTERIAL CYSTITIS:Having a similar pathophysiology of ascending infection mechanism, male patients in this category often present frequency, urgency, dysuria, nocturia, and suprapubic pain. On a side note, having hematuria is concerning, especially without symptoms, because it's automatically a red flag that should prompt an immediate evaluation in search of other causes besides infection, such as underlying malignancy. Possible etiologies are calculi, glomerulonephritis, and even schistosomiasis infection that can ultimately result in squamous cell carcinoma of the bladder. Arreaza: Let me share a little anecdote about hematuria. One Sunday when I was a resident I woke up with hematuria. Of course, I immediately went to urgent care, knowing hematuria means trouble in men. I had a urine dipstick test, which was normal. The first thing the nurse practitioner asked me was, “Did you eat any beets?”, and I never eat beets, but that day I had a full bag of beet chips. So, yes, that was the cause of my pseudo-hematuria. Lesson learned: Always ask about beets when you have a patient with painless hematuria with a normal dipstick. PROSTATITIS:This is an infection of the prostate gland. The most common offending agent is E. coli. Acute prostatitis will present with signs of “acute” infection, such as fever, chills, and suprapubic pain. On rectal exam, we will find a prostate that is warm, swollen, boggy, and very tender. Make sure you perform a gentle prostate exam as you may spread bacteria to the blood and cause bacteremia and potentially sepsis. Patients are normally very sick and it is not your typical cystitis, but it is more severe. Chronic Prostatitis can arise from different causes, ranging from retrograde ascending infection, “chronic” exposure to urinary pathogens, and even autoimmune etiologies. The majority of patients often are asymptomatic. URETHRITIS:This infection is further classified into two groups, gonococcal and non-gonococcal. For gonococcal urethritis, N. gonorrhoeae is the most common pathogen. Agents of non-gonococcal urethritis include C. trachomatis, Ureaplasma, trichomonas, and Herpes Simplex Virus (HSV). Patients often present symptoms of dysuria, pruritus, and purulent penile discharge.PYELONEPHRITIS:Following a retrograde ascending mechanism, an infection may travel from the bladder and make its way to the kidney, causing damage and inflammation to the renal parenchyma. According to Dr. John Brusch, E. coli is responsible for approximately 25% of cases in males. Pyelonephritis presents with chills, fever, nausea/vomiting, flank pain/costovertebral angle tenderness, and dysuria. Other findings include pyuria and bacteriuria. Pyelonephritis is a common cause of sepsis. Diagnosis of UTIs.URINE STUDIES: Urine culture remains the gold standard for diagnosis of UTI. Other studies include suprapubic aspiration, catheterization, midstream clean catch, and Gram stain. Imaging studies are not always needed, but you may order plain films, ultrasonography, CT scans, and MRIs. It will depend on the severity of your case and your clinical judgment.UTIs in women: In males, we should perform urine culture and susceptibility studies. However, in women, urine studies are not needed all the time, they should be reserved for women with recurrent infection, treatment failure, history of resistant isolates, or atypical presentation. This is done to confirm the diagnosis and guide antibiotic selection.Interestingly, in a recent evidence review, published in the American Family Physician journal, women can self-diagnose their uncomplicated cystitis. All that is needed is having typical symptoms (frequency, urgency, dysuria/burning sensation, nocturia, suprapubic pain), without vaginal discharge. If you have those elements, you have enough information to diagnose, or even the patient can self-diagnose, an uncomplicated UTI without further testing, but in males, you should ALWAYS perform urine studies.TREATMENTS:Men with UTI should ALWAYS receive antibiotics, with urine culture and susceptibility results guiding the antibiotic choice. Laboratory results will help us determine the best treatment plan. UTIs are often treated with a variety of antibiotics. Dr. Robert Shmerling, of Harvard Medical School, states that most uncomplicated lower tract infections can be eradicated with a week of treatment with antibiotics. Common antibiotics for UTI are fluoroquinolones, trimethoprim-sulfamethoxazole (TMP-SMZ), minocycline, or nitrofurantoin.On another hand, if it's an upper tract infection or prostatitis, the course of treatment can be extended for longer periods. For those patients who are hemodynamically unstable or have severe upper UTI, hospital admission is required to monitor for complications and IV antibiotics.UTIs in males are less frequent than UTIs in females, except when patients are 80 years and older when the incidence is similar in both sexes. UTIs in males must prompt further evaluation because if left untreated, they can have detrimental effects on your patients' health. As a take-home point, UTI in males is less common than in females, and it requires urine studies or other studies to identify the etiology and guide treatment. Antibiotics are always used, and you may guide your treatment depending on the results. Imaging is not always needed, but use your clinical judgment to make a more specific diagnosis and detect complications promptly. __________Conclusion: Now we conclude episode number 168, “UTI is Males.” Future Dr. Tran described the different anatomical areas that can be infected in males with UTI. She reminded us that UTIs in males always need to be treated with antibiotics and urine cultures are done to guide treatment. Dr. Arreaza mentioned a few differences in the diagnosis and treatment of UTIs in females. For example, women can self-diagnose an uncomplicated cystitis, and urine studies or antibiotics are not always needed in women. This week we thank Hector Arreaza and Di Tran. Audio editing by Adrianne Silva.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:Shmerling, R. H. (2022, December 5). Urinary tract infection in men. Harvard Health Publishing. https://www.health.harvard.edu/a_to_z/urinary-tract-infection-in-men-a-to-z.Brusch, J. L. (2023a, March 27). Urinary tract infection (UTI) in males. emedicine.medscpae.com. https://emedicine.medscape.com/article/231574-overview.Kurotschka PK, Gágyor I, Ebell MH. Acute Uncomplicated UTIs in Adults: Rapid Evidence Review. Am Fam Physician. 2024;109(2):167-174. https://www.aafp.org/pubs/afp/issues/2024/0200/acute-uncomplicated-utis-adults.htmlRoyalty-free music used for this episode: Tropicality by Gushito, downloaded on July 20, 2023, from https://www.videvo.net/royalty-free-music/
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: September 27, 2018 When is eye pain an ophthalmological issue, and when is it a neurologic issue? This week, neuro-ophthalmologist and glaucoma specialist Dr. Ahmara Ross simplifies ocular pain for the day-to-day neurologist. Produced by James E Siegler and Ahmara Ross. Music by Yan Terrien, Unheard Music Concepts, Steve Combs, and Scott Holmes. Sound effects by Mike Koenig, Daniel Simion. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. Be sure to follow us on Twitter @BrainWave saudio for the latest updates to the podcast. REFERENCES Fiore DC, Pasternak AV, Radwan RM. Pain in the quiet (not red) eye. Am Fam Physician 2010;82(1):69-73. PMID 20590074Friedman DI. The eye and headache. Continuum (Minneap Minn) 2015;21(4 Headache):1109-17. PMID 26252594Lee AG, Al-Zubidi N, Beaver HA, Brazis PW. An update on eye pain for the neurologist. Neurol Clin 2014;32(2):489-505. PMID 24703541Waldman CW, Waldman SD, Waldman RA. A practical approach to ocular pain for the non-ophthalmologist. Pain Manag 2014;4(6):413-26. PMID 25494693 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
Episode 162: Early-Onset Sepsis Dr. Kooner explains how to diagnose early-onset sepsis by using clinical evaluation and clinical tools. Dr. Schlaerths describes the signs and symptoms of sepsis in neonates, and Dr. Arreaza adds comments about GBS bacteriuria. Written by Lovedip Kooner, MD, editing Hector Arreaza, MD, and comments by Katherine Schlaerth, MD. Rio Bravo Family Medicine Residency Program.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.Introduction:Neonatal sepsis is defined as pathogenic bacterial growth from blood or cerebral spinal fluid culture within the first 28 days of life. Neonatal sepsis can be divided into two categories: early-onset sepsis (EOS) and late-onset. EOS is neonatal sepsis within 72 hours or 7 days after birth, depending on the specialist. How common is early-onset sepsis (EOS)?According to the CDC, the infant mortality rate rose for the first time in 20 years in the USA. In the U.S., the incidence of EOS is 0.5 in 1,000 live births and carries a mortality rate of about 3%. What causes EOS?Most infections are due to ascending lower vaginal tract flora. Other causes include intra-amniotic infections and maternal hematogenous spread of systemic infections. Group B streptococcus (S. agalactiae) accounts for about 1/3 of the infectious organisms, followed by E. coli which accounts for about 1/4, and Viridans streptococci account for about 1/5 of infections. Cases of E. coli are seen more often with prolonged rupture of membranes and intrapartum antibiotic exposure. Other notable infections are Listeria monocytogenes, coagulase-negative staphylococci (CoNS), herpes simplex virus, and enteroviruses. The role of GBS.Approximately 30% of women have vaginal and rectal GBS colonization and 50% will transmit it to the newborn. Without maternal antibiotic treatment, 1-2% of those infants will develop EOS. The American College of Obstetricians and Gynecologists (ACOG) recommends universal culture-based screening for GBS at 36-37 weeks and 6 days regardless of mode of delivery. GBS bacteriuria: Treat it (symptomatic and asymptomatic) if >105 CFU/mL. Do not treat it in asymptomatic patients if GBS 18 hours, intrapartum fever, or GBS positive in previous pregnancy.Nucleic acid amplification test: NAAT in pregnancy is not recommended to determine colonization status. However, if NAAT is obtained in the intrapartum period, give IAP if positive. But, you must also give IAP if negative + mentioned risk factors (18h, Maternal fever >100.4F)What is considered adequate intrapartum antibiotic prophylaxis? Penicillin and ampicillin are the recommended antibiotics for prophylaxis. Cefazolin can be given if there is a penicillin-allergy with a low risk for anaphylaxis. Clindamycin and vancomycin are reserved for cases of maternal penicillin allergy. Specifically, clindamycin can be used only if GBS is known to be sensitive to clindamycin. Vancomycin must be used if GBS is resistant to clindamycin. Do not use erythromycin. You will Administered at least 4 hours before delivery.IAP is believed to reduce neonatal GBS disease by: (1) temporarily reducing maternal vaginal GBS colonization; (2) preventing colonization of the fetus or newborn's surfaces and mucous membranes; and (3) achieving antibiotic levels in the newborn's bloodstream sufficient to surpass the minimum inhibitory concentration (MIC) for eliminating group B streptococci.Diagnosis of EOS:Clinical presentation: Tachycardia, tachypnea, temperature instability, supplemental oxygen requirement, and lethargy. Hypoglycemia should not be considered a sign of EOS.Diagnosing early-onset sepsis is achieved through blood or cerebrospinal fluid (CSF) cultures. Not effective methods for diagnosing EOS include laboratory tests, such as a complete blood cell count or C-reactive protein (CRP), as well as surface cultures, gastric aspirate analysis, or urine culture.Most infants will generally show signs of EOS GBS infection within the initial 24 hours of birth, with approximately 85% exhibiting symptoms during this timeframe.Waiting for cultures and/or signs can delay lifesaving treatment.Management:According to the American Academy of Pediatrics (AAP), the management of term and late-term infants is undertaken via the clinical condition assessment, the categorical risk factor assessment, and the multivariate risk assessment. As a part of the 2015 AAP guidelines, the Categorical Risk Factor Assessment is more of an algorithmic approach based on the presence or absence of specific risk factor threshold values such as:Ill-appearing infant. Mother diagnosed with chorioamnionitis.Mother GBS positive with inadequate intrapartum prophylaxis.ROM >18 hours.Birth before 37 weeks of gestation.Antibiotics are not always needed, and they can even cause damage. Information taken from the American Academy of Pediatrics, “Management of Neonates Born at ≥35 0/7 Weeks' Gestation With Suspected or Proven Early-Onset Bacterial Sepsis,” published on December 1, 2018:(1) Any newborn infant who is ill-appearing or (2) when the mother has a clinical diagnosis of chorioamnionitis -> laboratory testing must be ordered, and empirical antibiotic therapy should be started.(3) A mother who is colonized with GBS and who received inadequate intrapartum antibiotic prophylaxis, with a duration of ROM being >18 hours or birth before 37 weeks' gestation -> laboratory testing should be ordered.(4) A mother who is colonized with GBS who received inadequate IAP but with no additional risk factors -> observation in the hospital for ≥48 hours.______________________________Conclusion: Now we conclude episode number 162, “Early-onset Sepsis Introduction.” Dr Kooner explained the role of GBS in the pathophysiology of EOS, Dr. Schlaerth discussed the importance of clinical evaluation and Dr. Arreaza explained that GBS screening in the third trimester is not needed when there is a GBS positive urine culture early in pregnancy. Don't miss part 2 of this discussion. By the way, we do not recommend using feces to prevent or treat sepsis, we just shared anecdotal information to end with a funny note.This week we thank Hector Arreaza, Lovedip Kooner, and Katherine Schlaerth. Audio editing by Adrianne Silva.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:Neonatal Early-Onset Sepsis Calculator by Kaiser Permanente, available at: https://neonatalsepsiscalculator.kaiserpermanente.org/.Espinosa K, Brown SR. Neonatal Early-Onset Sepsis Calculator. Am Fam Physician. 2021;104(6):636-637.https://www.aafp.org/pubs/afp/issues/2021/1200/p636.html.Puopolo KM, Benitz WE, Zaoutis TE; COMMITTEE ON FETUS AND NEWBORN; COMMITTEE ON INFECTIOUS DISEASES. Management of Neonates Born at ≥35 0/7 Weeks' Gestation With Suspected or Proven Early-Onset Bacterial Sepsis. Pediatrics. 2018 Dec;142(6):e20182894. doi: 10.1542/peds.2018-2894. PMID: 30455342. https://pubmed.ncbi.nlm.nih.gov/30455342/.Briggs-Steinberg C, Roth P. Early-Onset Sepsis in Newborns. Pediatr Rev. 2023 Jan 1;44(1):14-22. doi: 10.1542/pir.2020-001164. PMID: 36587021. https://pubmed.ncbi.nlm.nih.gov/36587021/.Flannery DD, Puopolo KM. Neonatal Early-Onset Sepsis. Neoreviews. 2022 Nov 1;23(11):756-770. doi: 10.1542/neo.23-10-e756. PMID: 36316253. https://pubmed.ncbi.nlm.nih.gov/36316253/.Polin RA; Committee on Fetus and Newborn. Management of neonates with suspected or proven early-onset bacterial sepsis. Pediatrics. 2012 May;129(5):1006-15. doi: 10.1542/peds.2012-0541. Epub 2012 Apr 30. PMID: 22547779. https://pubmed.ncbi.nlm.nih.gov/22547779/.Royalty-free music used for this episode: Good Vibes_Adventure Time by Simon Pettersson, downloaded on July 20, 2023, from https://www.videvo.net/
Kaue, Ingrid e Luísa conversam sobre os riscos da hipocalemia e como fazer reposição de potássio: classificação da hipocalemia, quais os riscos, reposição enteral, reposição venosa e quando usar diuréticos poupadores de potássio, tudo neste episódio. Referências: Ferreira JP, Butler J, Rossignol P, et al. Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(22):2836-2850. doi:10.1016/j.jacc.2020.04.021 Kim GH, Han JS. Therapeutic approach to hypokalemia. Nephron. 2002;92 Suppl 1:28-32. doi:10.1159/000065374 Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000;160(16):2429-2436. doi:10.1001/archinte.160.16.2429 Kim MJ, Valerio C, Knobloch GK. Potassium Disorders: Hypokalemia and Hyperkalemia. Am Fam Physician. 2023;107(1):59-70. Asmar A, Mohandas R, Wingo CS. A physiologic-based approach to the treatment of a patient with hypokalemia. Am J Kidney Dis. 2012;60(3):492-497. doi:10.1053/j.ajkd.2012.01.031 Grobbee DE, Hoes AW. Non-potassium-sparing diuretics and risk of sudden cardiac death. J Hypertens. 1995;13(12 Pt 2):1539-1545. Ferreira JP, Butler J, Rossignol P, et al. Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol. 2020;75(22):2836-2850. doi:10.1016/j.jacc.2020.04.021 Goyal A, Spertus JA, Gosch K, et al. Serum Potassium Levels and Mortality in Acute Myocardial Infarction. JAMA. 2012;307(2):157–164. doi:10.1001/jama.2011.1967 Macdonald JE, Struthers AD. What is the optimal serum potassium level in cardiovascular patients?. J Am Coll Cardiol. 2004;43(2):155-161. doi:10.1016/j.jacc.2003.06.021
Contributor: Ricky Dhaliwal, MD Educational Pearls: Croup Caused by: Parainfluenza, Adenovirus, RSV, Enterovirus (big right now) Age range: 6 months to 3 years Symptoms: Barky cough Inspiratory stridor (Severe = stidor at rest) Use the Westley Croup Score to gauge the severity Treatment: High flow, humidified, cool oxygen Dexamethasone 0.6 mg/kg oral, max 16mg Severe: Racemic Epinephrine 0.5 mL/kg Consider heliox, a mixture of helium and oxygen Very severe: be ready to intubate Bronchiolitis Caused by: RSV, Rhinovirus Symptoms are driven by secretions Symptoms: Cough Wheezing Dehydration (often the symptom that makes them look the worst) Age range: 2 to 6 months Treatment: Suctioning Oxygen IV fluids Nebulized hypertonic saline DuoNebs? No. Asthma Caused by: Environmental factors Viral illness with a predisposition Treatment: Beta agonists Steroids Ipratropium Magnesium (relaxes smooth muscle) References Dalziel SR, Haskell L, O'Brien S, Borland ML, Plint AC, Babl FE, Oakley E. Bronchiolitis. Lancet. 2022 Jul 30;400(10349):392-406. doi: 10.1016/S0140-6736(22)01016-9. Epub 2022 Jul 1. PMID: 35785792. Hoch HE, Houin PR, Stillwell PC. Asthma in Children: A Brief Review for Primary Care Providers. Pediatr Ann. 2019 Mar 1;48(3):e103-e109. doi: 10.3928/19382359-20190219-01. PMID: 30874817. Midulla F, Petrarca L, Frassanito A, Di Mattia G, Zicari AM, Nenna R. Bronchiolitis clinics and medical treatment. Minerva Pediatr. 2018 Dec;70(6):600-611. doi: 10.23736/S0026-4946.18.05334-3. Epub 2018 Oct 18. PMID: 30334624. Smith DK, McDermott AJ, Sullivan JF. Croup: Diagnosis and Management. Am Fam Physician. 2018 May 1;97(9):575-580. PMID: 29763253. Westley CR, Cotton EK, Brooks JG. Nebulized racemic epinephrine by IPPB for the treatment of croup: a double-blind study. Am J Dis Child. 1978 May;132(5):484-7. doi: 10.1001/archpedi.1978.02120300044008. PMID: 347921. https://www.mdcalc.com/calc/677/westley-croup-score Summarized by Jeffrey Olson | Edited by Meg Joyce & Jorge Chalit, OMSII
In this first clinical spotlight episode, Dr. Jessica Klain and I discuss a case of transient global amnesia. We review the current practice guidelines for differential diagnosis and management, and discuss how our opinions differ from a paper that we reference: Sealy D, Tiller RJ, Johnson K. Transient Global Amnesia. Am Fam Physician. 2022 Jan 1;105(1):50-54. PMID: 35029951.
Episode 156: Obesity, Fertility, and PregnancyFuture Dr. Hamilton defines obesity and explains the pathophysiology of obesity and its effects on fertility and pregnancy. Dr. Arreaza adds some input about the impact of epigenetics on newborn babies. Written by Shelby Hamilton, MS3, American University of the Caribbean School of Medicine. Editing 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 of obesityObesity is a multifactorial chronic disease that is increasing in prevalence across the globe. It can be defined as a body mass index (or BMI) greater than 30 kg/m2. According to the CDC from 2017-March 2020, the prevalence of obesity in United States adults was 41.9%.Classification of obesity by BMI.Obesity can further be divided into three classes: class I which is a BMI between 30-34.9; class II which is a BMI between 35-39.5; and class III which is a BMI greater than 40. We recommend avoiding the term “morbid obesity” because of the negative connotation of the word “morbid.” Class III or severe are better terms in those cases. This classification is based on the individual risk of cardiovascular disease. One of the greatest health consequences affecting individuals with obesity is the cardiovascular effects including hypertension, dyslipidemia, and coronary artery disease. Other effects include insulin resistance and diabetes, cholelithiasis, non-alcoholic fatty liver disease, osteoarthritis, and even depression.How Does Obesity Affect Fertility?Obesity can have an extensive effect on the overall health of an individual. In addition to these commonly discussed effects, obesity can also influence a person's fertility. This is especially observed in women with polycystic Ovary Syndrome (PCOS) who have a greater BMI and also have symptoms of anovulation. Excess adipose tissue plays a role in the effects that obesity has on fertility. White adipose tissue can secrete a specific group of cytokines known as ‘adipokines'. These adipokines include leptin, ghrelin, resistin, visfatin, chemerin, omentin, and adiponectin. With a greater percentage of adipose tissue, there are higher rates of hypothalamic gonadotropin hormonal dysregulation, which can be combined with insulin-related disorders, low sex hormone binding proteins, and high levels of androgens. The combination of these factors can result in decreased ovarian follicle development and decreased progesterone levels.Hormonal changesObesity is an endocrine disorder. One specific adipokine that affects the hypothalamic-gonadotropin axis is chemerin. Chemerin impairs the release of follicle-stimulating hormone (FSH) from the pituitary gland. This reduction in FSH release consequently leads to anovulation, meaning that no egg will be released from an ovarian follicle, contributing to infertility. Shelby: Another adipokine affecting fertility is adiponectin. The receptors of adiponectin are predominantly expressed in reproductive tissues, including the ovaries and endometrium. In individuals with a greater BMI, a decrease in adiponectin secretion has been observed, resulting in decreased stimulation of its receptors, especially in the endometrium, which has been linked to recurrent implantation failure. Adiponectin has also been shown to affect glucose uptake in the liver. With reduced adiponectin levels, there is reduced hepatic glucose uptake, leading to insulin resistance. As tissues become less sensitive to insulin, the body compensates by secreting higher amounts of insulin, leading to hyperinsulinemia. Higher levels of circulating insulin have also been proven to cause hyperandrogenemia in women by blocking the hepatic production of sex hormone-binding globulin. Insulin can also act on the IGF-1 receptors in the theca cells, increasing steroidogenesis, and thus, increasing androgens. With hyperandrogenemia, there is also increased granulosa cell apoptosis as well as increased peripheral conversion of androgens into estrogen. This creates negative feedback to the hypothalamic-pituitary axis to decrease the release of gonadotropins such as FSH which are critical in ovulation.Leptin is another adipokine that is shown to be increased in obesity. Studies on mice have shown that leptin impairs the development of ovarian follicles, resulting in a decrease in ovulation. In these studies, it was also observed that leptin reduces the production of estriol by the granulosa cells in the ovarian follicles as well as increases the rate of apoptosis in granulosa cells, both of which affect ovulation. Leptin decreases hunger, but persons with obesity may be resistant to its effects and that's why they have higher levels than a person with normal weight. They have high levels of leptin but are still hungry because they have leptin resistance.Studies have also shown that the fatty acid composition of follicular fluid found in ovarian follicles also plays a role in fertility. In individuals with a high BMI, this fluid contains high levels of oleic acid, which can cause embryo fragmentation after fertilization occurs. Stearic acid is another fatty acid found in elevated levels in the follicular fluid of women with a greater BMI, which can also affect the quality of the embryo while in the blastomere stage.The bottom line is obesity decreases fertility. It does not mean that patients with obesity will not get pregnant, but it can make it harder to get pregnant. Female patients who are losing weight must be warned about their improved fertility once they start to lose weight.What effect does obesity have on pregnancy?While obesity may make it more difficult for a woman to get pregnant, it is not impossible. However, there are potential risks both to the mother's health as well as the baby's health. Therefore, it is very important to monitor these patients even more carefully.Women who have a greater BMI pre-pregnancy are at a greater risk of developing gestational hypertension. Gestational hypertension is defined as blood pressure greater than 140/90 on more than one reading in the second half of pregnancy. Hypertension during pregnancy can also have serious complications such as kidney failure, stroke, myocardial infarction, or even heart failure. Gestational hypertension can also result in preterm birth or low birth weight.Treatment of mild hypertension in pregnancyRecent studies published in the AFP Journal support the treatment of mild hypertension in pregnancy. It states that “evidence and expert opinion support treating mild chronic hypertension in pregnancy with approved antihypertensives, with a strength of recommendation: B”. There was a randomized control trial with about 2,000 women who were randomized to receive antihypertensive treatment vs no treatment. The treatment group had a lower incidence of preeclampsia with severe features, preterm birth, placental abruption, and neonatal or fetal death. There was not an increase in fetal growth restriction or maternal or neonatal complications. So, it is advisable to treat chronic, mild hypertension in pregnancy, according to the AFP Journal.PreeclampsiaPreeclampsia is another condition that is at a higher risk in women with obesity, which is a more serious manifestation of hypertension in the second half of pregnancy. Along with high blood pressure, there are also effects on the kidneys and liver. Hypertension accompanied by proteinuria is indicative of preeclampsia and should be taken seriously. Preeclampsia can become eclampsia, where the patient also experiences seizures. There is also the risk for stroke, HELLP syndrome, placenta abruption, preterm birth, and fetal growth restriction.Gestational diabetesAnother risk is gestational diabetes. Elevated blood glucose during pregnancy can result in a larger baby and delivery by cesarean. There may also be a greater risk of the mother and child developing diabetes mellitus later on in life.OSAWomen with a greater BMI may also be at risk of developing obstructive sleep apnea during pregnancy. Not only can this result in fatigue but can also contribute to the development of gestational hypertension and preeclampsia.Effect of obesity on the fetusAs mentioned, there are some risks to the fetus in women with a greater pre-pregnancy BMI. There is a greater risk for these babies to be born with birth defects such as congenital heart defects and neural tube defects. Another risk previously discussed is macrosomia, or large for gestational age. Larger babies are also at increased risk for shoulder dystocia during delivery as well as resulting clavicle fractures, brachial plexus injuries, and nerve palsies. Preterm birth is another risk, which also increases the risk of short-term and long-term health complications. Lastly, a higher BMI is directly correlated with the risk of spontaneous abortion or stillbirth.SummaryAs the prevalence of obesity increases, it is important to discuss the health risks that are associated with this disease. In our patients of childbearing age and who may be hoping to conceive, it is even more important to discuss how a higher BMI may affect fertility and pregnancy. While discussing these topics with patients, it is important to try our best to build rapport with the patient so that the discussion is seen more as one of concern and support rather than one of criticism regarding their weight. We may want to help by not only telling patients to “lose weight” or “diet”, but we can also provide them with resources regarding dietary adjustments and ways they can incorporate physical activity into their lives without just telling them to eat less and move more. Stay tuned for our episode on the management of obesity in pregnancy.ConclusionNow we conclude episode number 156, “Obesity, fertility, and pregnancy.” Future Dr. Hamilton explained how obesity affects the hormonal regulation of fertility. She also explained the obstetrical risks associated with obesity. Primary care professionals need to educate our patients about the benefits of preconception weight control. Dr. Arreaza explained that hypertension is a common condition in pregnant patients with obesity and mentioned the benefits of treating mild hypertension in pregnancy. We hope to bring you an episode on the management of obesity in pregnancy soon, so stay tuned! This week we thank Hector Arreaza and Shelby Hamilton. Audio editing by Adrianne Silva.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:Gautam, D., Purandare, N., Maxwell, C., Rosser, M., O'Brien, P., Mocanu, E., McKeown, C., Malhotra, J., & McAuliffe, F. (2023) The challenges of obesity for fertility: A FIGO literature review. International Journal of Gynecology & Obstetrics, 160(S1), 50-55. https://doi.org/10.1002/ijgo.14538Pandey, S., Pandey, S., Maheshwari, A., & Bhattacharya, S. (2010). The impact of female obesity on the outcome of fertility treatment. Journal of Human Reproductive Science, 3(2), 62-67. https://doi.org/10.4103/0974-1208.69332.Perreault L. Obesity in adults: Prevalence, screening, and evaluation. In: UpToDate, Pi Sunyer FX (Ed) Wolters Kluwer. https://www.uptodate.com (Accessed on October 6, 2023).Obesity and Pregnancy FAQ, The American College of Obstetricians and Gynecologists (ACOG), https://www.acog.org/womens-health/faqs/obesity-and-pregnancy, Accessed on October 10, 2023.Adult Obesity Facts, Centers for Disease Control and Prevention (CDC), https://www.cdc.gov/obesity/data/adult.html, Accessed on October 7, 2023. Dresang L, Vellardita L. Should Medication Be Prescribed for Mild Chronic Hypertension in Pregnancy?. Am Fam Physician. 2023;108(4):411-412. Royalty-free music used for this episode: "I Think We Have a Chance." downloaded on November 11, 2023, from https://www.videvo.net/.
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: October 14, 2018 There is nothing mysterious about the chemistry of the cerebrospinal fluid. Cells. Protein. Glucose. But the interplay of these unique components can give you incredible insight into the state of the central nervous system. This week, we revisit a prior episode where Dr. Mike Rubenstein reviews his approach to interpreting CSF results. And then we have an update at the end regarding recent advances in CSF analysis. Produced by James E Siegler and Michael Rubenstein. Music by Steve Combs. Sound effects by Mike Koenig and Daniel Simion. Voiceover by Patrick Green (German). BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. If you like what you hear, let us know, and rate the show! REFERENCES Deisenhammer F, Bartos A, Egg R, et al. Guidelines on routine cerebrospinal fluid analysis. Report from an EFNS task force. Eur J Neurol 2006;13(9):913-22. PMID 16930354Frederiks JA, Koehler PJ. The first lumbar puncture. J Hist Neurosci 1997;6(2):147-53. PMID 11619518Messacar K, Schreiner TL, Van Haren K, et al. Acute flaccid myelitis: a clinical review of US cases 2012-2015. Ann Neurol 2016;80(3):326-38. PMID 27422805Nagel MA, Cohrs RJ, Mahalingam R, et al. The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features. Neurology 2008;70(11):853-60. PMID 18332343Seehusen DA, Reeves MM, Fomin DA. Cerebrospinal fluid analysis. Am Fam Physician 2003;68(6):1103-8. PMID 14524396Shah KH, Edlow JA. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. J Emerg Med 2002;23(1):67-74. PMID 12217474 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
Episode 147: Routine Prenatal CareWritten by Elika Salimi, MSIV. Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Comments and editing 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._____________________Elika: So, we're going to talk about some general principles of prenatal care and some of the most important diagnostic methods that we mainly use for taking care of pregnant women. I will forewarn you that there will be a ton of details in this talk, and I do recommend possibly taking notes as things can get easily confusing. This way you can have something to refer back to whenever you have a pregnant patient of your own.Arreaza: You can also download the episode notes from our website.Elika - So your patient is pregnant and she comes to you for care. How do we go about it? Well, this is assuming she had it at home urine pregnancy positive test and we got a blood hCG on her and everything's good and we know she's pregnant. Ok so now what happens next?Arreaza – We need to confirm the patient wants to keep the pregnancy.Elika - First, we're going to talk about the frequency of the check-ups. In this case, we are talking about a situation where the mother is coming to her appointments as she was supposed to but we all know that sometimes that doesn't happen if everything is going as it is supposed to then typically we get the initial examination at about 10 weeks of gestation and then until the 28th week there should be monthly visits, then from the 28th through the 36th there should be biweekly visits, and from the 36th week until birth, the visits are every week.Areaza – What´s next?Elika - Now I'd like to note that during the prenatal period, informed consent is very important and it should be obtained during this time because you want to prevent and manage any ethical conflicts that might exist between the mother and possibly the healthcare providers because we all know that any pregnancy can become high-risk at some point and pregnant individuals should be informed about the potential need for a c-section for example and be encouraged to discuss any concerns ahead of time. Elika - Now while we're talking about ethics, if the doctor finds him/ or herself in a situation where the patient is asking for something that the Dr does not feel comfortable with such as a certain type of treatment or a certain method of delivery or if they're, let's say, desiring an abortion and the doctor doesn't do abortions, then in this case you would refer the patient to a physician that is comfortable with the patient's desired outcome or treatment. And this is perfectly legal and fine just as long as you help the patient find somebody else. Arreaza – Abortion is legal in most states, but check your local regulations.Elika - So as mentioned earlier, the initial visit occurs at about 10 weeks of gestation. We start with checking their personal and family history and finding out about any previous pregnancies including at what GA baby born and weight if they know, any complications, gestational diabetes or preeclampsia, any history of postpartum hemorrhage requiring blood transfusion, any abortions (if present at what GA), and the method of deliveries, whether it was vaginal or a cesarean and what kind of C-section they had done. These are very important for you to obtain from your patient. You will also assess for depression and domestic partner violence.Arreaza – In California, we have a wonderful service called CPSP: Comprehensive Perinatal Services Program. What comes next? Elika - Upon receiving the history, we will do the gynecological examination and send in some samples. We will also send her to do some lab work. Now what do those labs entail? Well, we are going to get a CBC such as screening for anemia, we will also do TSH but only in people who have possible signs of thyroid disorder so not everybody needs to get this. And, we are going to send for a blood typing to find out about their ABO group and the Rhesus status. We will also obtain a urine analysis to screen for proteinuria and asymptomatic bacteriuria because in pregnancy, unlike outside of pregnancy, you do need to treat asymptomatic bacteriuria. We will also ensure that the mother is on prenatal vitamins, so folic acid, if not already, and iron, if indicated, and vitamin B6 if the patient has signs of nausea or hyperemesis gravidarum and this can be combined with doxylamine. Usually, pregnant women don't get a glucose screening test at the first visit unless let's say they have high risk of diabetes or they there was glucose in the urine. Arreaza – I like the topic of diabetes in pregnancy. So, in a high-risk population, we want to make sure a pregnant patient does not have diabetes, or pregestational diabetes.Elika - We will also screen for STI's including HIV, syphilis, hepatitis B, Hep C, and we also check for gonorrhea and chlamydia (pap) screening particularly in those under 25, or over 25 with high risk of infection. We will also test for rubella and varicella. Some places also order a QuantiFERON gold for tuberculosis. There are certain women that have indications for third-trimester screening for STI's on top of the ones that they already got in their first trimester. Those include chlamydia, gonorrhea, HIV, syphilis, and Hep B, and C but each of those have its own indications so for the purposes of time I will let you look that up on your own.Arreaza – Summary: Physical exam and labs to rule out preexisting conditions that may interfere with pregnancy, either infectious or metabolic, to mention some diseases. Elika - And finally, we will do an ultrasound assessment to get a more accurate reading of the fetus's gestational age.Arreaza – What comes after the first trimester?Elika- So like I mentioned they're going to need to be following up and some particular things need to be done at specific weeks. So we are going to discuss those. At every follow visit you need to obtain: the patient's weight, BP and other vitals, fetal heart sounds, the baby's measurement from the mother's pubic symphysis up until the fundus of the uterus, as well as a urine analysis to check for any glucose or protein in the urine because we are always concerned of possible preeclampsia or gestational diabetes. Another examination that I should mention is a Doppler ultrasound and this is usually indicated if there is suspected fetal growth restriction or if there's pregnancy-induced hypertension or if there's suspected fetal deformities or there is growth discordance in multiple pregnancies.Now we are going to discuss assessing for any abnormalities in the fetus. All pregnant women regardless of age should be offered noninvasive and aneuploidy screening test before 20 weeks of gestation. The 1st trimester combined screening occurs at about 10 to 13 weeks gestation, where we can order some blood tests for the mom such as the amount of hCG in maternal serum, as well as PAPP-A, on top of nuchal translucency that will see on the ultrasound. There is also the triple screen at 15-20 weeks which consists of ordering hCG, alpha-fetoprotein aka AFP, and estriol then there's also the quad screen test at 15-22 weeks gestation that consists of hCG, AFP, Estriol and Inhibin A. We also have the cell free fetal DNA testing that can occur after 10 weeks gestation at which the fetal DNA is isolated from the maternal blood specimen for genetic testing and this one actually happens to be the most sensitive and specific screening test for common fetal aneuploidies, and it is used for secondary screening after the ultrasound.Arreaza – Actually that test is done in all our patients on Medi-Call (cfDNA).Elika - If any of the screening tests are abnormal then we can provide counseling to mothers for more invasive diagnostic tests such as chorionic villus sampling, amniocentesis, and cordocentesis. At that point, you want to refer the patient to perinatology. Finally, in general an anatomical scan occurs ~18-22 weeks. Arreaza – Excellent, we have done the non-invasive genetic screening. What's next? Elika - Now we are going to talk about what happens in the third trimester specifically and what test you need to order. In the third trimester, you will order a CBC again, particularly at 24 weeks you want to do a repeat hemoglobin. We will also do the indicated repeat STI checks. We are also going to do gestational diabetes screening with the oral glucose test that I briefly mentioned earlier at around 24-28 weeks. This is usually done with a 50g 1 hr glucose tolerance test and if abnormal then a 100g 3 hour glucose test. You will also be repeating the Rh antibody just to make sure that the mother is still Rh negative because at 28 weeks, Rh negative mother should be administered RhoGAM 300 mcg intramuscularly and they need to get it again within 72 hours of delivery. Don't forget to give a TDAP vaccine at 27 weeks. And at 36 weeks you need to be obtaining a GBS culture (vaginal and rectal) for the patient just to make sure that there is no colonization because if there is then the patient is going to need GBS prophylaxis at admission because colonization by these bacteria can cause chorioamnionitis and neonatal infection such a sepsis. Overall when third trimester approaches you're going to make sure the plans for delivery have been properly scheduled or discussed with the patient and typically around 34 weeks you also want to check with your patient to see if they desire sterilization and obtain a consent if they will be having a C-section and they want to be sterilized after that. In those not requesting sterilization, it is a good idea to discuss what they want to do after this pregnancy for birth control since it is not safe to get pregnant again for another year. From 36 weeks' gestation, use Leopold maneuvers for assessment of fetal presentation but I'll let you look that up on your own. At this time, you may also use ultrasound as needed to confirm fetal lie and placental position.Patients with maternal conditions such as gestational diabetes or gestational hypertension/pre-eclampsia, or fetal condition such as heart defects or fetal growth restriction need to get biweekly NST/BPP tests at clinic in the third trimester because there is an increased risk of fetal hypoxic injury or death. An NST is basically a non-stress test that measures fetal heart rate reactivity to fetal movements. BPP /biophysical profile is a noninvasive test that evaluates the risk of antenatal fetal death usually after the 28th gestational week and what it consists of is the ultrasound assessment of fetal movement, fetal tone, fetal breathing, and amniotic fluid volume or we can also perform a contractions stress test that basically measures fetal heart rate reactivity in response to uterine contractions. Arreaza – I like talking about obesity. Weight gain is expected during pregnancy. Patients with normal weight are expected to gain 25-35 pounds. Patients with obesity are recommended to gain 11-20 only.Summary: Now I know that this was very extensive talk with a ton of details but if you took notes and refer back to it then I think things will somewhat make more sense and come together that way. The best thing we can do is try to adhere to guidelines to make sure that we don't miss anything. Sometimes it could be particularly difficult to manage patients that don't or can't come to their appointments regularly and you may sometimes have to give them bad news and what not so overall it is not always happy moments we face but the best we can do is try to give them the best care possible to avoid complications and have the patient deliver a healthy baby. Thank you for listening to me once again and hopefully I'll be back again soon on another talk on an OB/GYN related topic soon. Thank you very much. _____________________Conclusion: Now we conclude episode number 147, “Routine Prenatal Care.” Future Dr. Salimi gave an excellent summary of the care provided during the different trimesters of pregnancy. Remember to collect a detailed history, perform a comprehensive physical exam, and order the labs to rule out pre-existing conditions that could interfere with pregnancy or detect complications early to start timely interventions or refer to a higher level of care. This week we thank Hector Arreaza, Elika Salimi, and Verna Marquez. Audio editing by Adrianne Silva.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:AAP, ACOG. Guidelines for Perinatal Care. American College of Obstetricians and Gynecologists Women's Health Care Physicians; 2017Zolotor AJ, Carlough MC. Update on prenatal care. Am Fam Physician. 2014; 89(3): p.199-208. pmid: 24506122.World Health Organization. WHO Recommendations on Antenatal Care for a Positive Pregnancy Experience. World Health Organization; 2016Workowski KA, Bachmann LH, Chan PA, et al. Sexually Transmitted Infections Treatment Guidelines, 2021. MMWR. Recommendations and Reports. 2021; 70(4): p.1-187. doi: 10.15585/mmwr.rr7004a1Murray ML, Huelsmann G, Koperski N. Essentials of Fetal and Uterine Monitoring. Springer Publishing Company; 2018Royalty-free music used for this episode: Space Orbit by Scott Holmes, downloaded on July 20, 2022 from https://freemusicarchive.org/music/Scott_Holmes/.
Episode 139: What is PCOS Future Dr. Salimi explains the pathophysiology, signs, and symptoms of PCOS. Diagnostic criteria and the basics of treatment are also discussed. Dr. Arreaza adds some comments about the treatment of obesity. Written by Elika Salimi, MS3, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. 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.Hello there! My name is Elika and I am a third-year medical student at Western University of Health Sciences. Today I will be talking to you about polycystic ovary syndrome AKA PCOS.Do you have a female patient in her reproductive years with irregular menstrual cycles, or no menstrual cycles at all? Is she unable to conceive a child? Did she have an unexpected diagnosis of diabetes? Does she have more acne than she would like, or has hair in unwanted or unexpected areas such as her chin?Does she have a hard time losing weight? If you answered YES to many of these questions, it is possible that your patient is suffering from polycystic ovary syndrome also known as PCOS, which is one of the most common endocrine disorders in women. Pathophysiology:The exact pathophysiology behind this syndrome is unknown; however, per the American College of Obstetricians and Gynecologists committee, some studies have shown a strong association between PCOS and obesity. In a woman with obesity disorder, the excess adipose tissue ends up increasing peripheral estrogen synthesis and as a result, there is a decrease in peripheral sensitivity to insulin which means many of these women tend to have hyperinsulinemia. To be more detailed, it is important to mention that during these anovulatory cycles, the increase in estrogen, which is also unopposed estrogen with a lack of progesterone, can lead to endometrial hyperplasia and consequently increase the risk of endometrial carcinoma.Clinical Features: Unless there is a clear history and physical or if perhaps there was an incidental ultrasound finding of polycystic ovaries, the diagnosis of PCOS is not exactly black-and-white. That is why it is important to increase awareness so that women can put the pieces of the puzzle together and come in to get evaluated. Multiple cysts in ovaries can present in patients without PCOS, and they are common in teenagers. To use the multiple cysts as part of the diagnosis, the patient has to be 2 years after menarche (AAFP). Some of these clinical symptoms typically start during adolescence displaying menstrual irregularities such as she could've had her period and then stopped getting it or she has a very delayed onset of her menstrual cycle. It is also possible to have spotty menstrual cycles also known as breakthrough bleeding or menorrhagia. And very important to many women, she could be infertile or have difficulties conceiving.She could also have diabetes because of insulin resistance that comes with the metabolic syndrome that develops with PCOS, which is also increased if she has obesity. This obesity disorder going hand in hand with the metabolic syndrome, can also increase the risk of having sleep apnea, which could affect the quality of her sleep, finding herself more fatigued than she should be after adequate hours of rest. Other symptoms include skin conditions such as hirsutism which is basically male pattern hair growth in women in areas such as the upper lip, chin, around the umbilicus, back, or even buttocks. She could also have male pattern hair loss on the head or too much acne or oily skin or acanthosis nigricans which are these brown/velvety hyperpigmented streaks on the neck or axilla, or groin. She could also find herself more depressed or anxious.Diagnosis:The diagnostic criteria and treatments are mainly addressed in the Journal of Clinical Endocrinology & Metabolism, an evidence-based guideline for the assessment and management of polycystic ovary syndrome, and the American Family Physician Journal:The diagnosis of PCOS requires the presence of at least two criteria that are not due to any other endocrine disorder such as thyroid disease or hyperprolactinemia, or other. 1) Periods of oligo-ovulation and or anovulation which means she's either having very low ovulatory cycles or she's not ovulating at all. 2) hyperandrogenism and this could be based on her clinical features or laboratory studies showing elevated testosterone levels or LH to FSH ratio and 3) Seeing enlarged and/or polycystic ovaries on a pelvic ultrasound. This means that the pelvic ultrasound shows an ovarian volume of equal to or greater than 10 mL and/or there's multiple cystic follicles that are about 2 to 9 mm in one or both of her ovaries which also usually tend to have a string of pearls appearance.So, if you have 2 out of the 3, you have PCOS. There are ways to confirm that there is in fact hyperandrogenism by doing lab studies and this could mean that her testosterone levels are elevated, or her androstenedione is elevated as well as elevated dehydro-epi-androsterone sulfate (DHEAS) and of course we need to rule out pregnancy and other endocrine disorders as I mentioned earlier. However, if the clinical picture of hyperandrogenism is there then that fulfills the diagnostic criteria for PCOS even if the serum antigen levels are normal. This also applies to an elevated LH:FSH ratio of typically greater than 2 to 1 which is also a characteristic finding of most patients with PCOS but this is not exactly necessary for diagnosis. We also don't need to find cystic follicles in order to diagnose PCOS. Treatment: In family medicine practices and even OB/GYN practice for PCOS the most common recommendation for all patients is to encourage them to increase their physical activity (exercise) and eat healthy and try to consider behavioral modifications to have a target BMI of ideally less than 25 kg/m² because this can reduce estrone production in adipose tissue.Then we are thinking about ways to treat patients who are not planning to conceive versus those that are. For those patients that are not planning to conceive the goal is to regulate their menstrual cycles and irregularities as well as their hyperandrogenism and to treat the comorbidities as well to overall improve their quality of life.The first line treatment for hyperandrogenism to try to regulate menstrual cycle abnormalities is combined oral contraceptives also known as birth control pills. This also reduces endometrial hyperplasia which in turn can decrease the risk of endometrial carcinoma as mentioned earlier and it can reduce menstrual bleeding and you can reduce acne and try to assist with the hirsutism as well. As mentioned earlier, PCOS can also go hand-in-hand with insulin resistance or hyperinsulinemia and therefore we can also use metformin that can improve menstrual irregularities but also address the metabolic side of this as well. Summary: Diet, exercise, combined oral contraceptives, and metformin.Some other more controversial medications to treat hyperandrogenism could be potassium-sparing diuretics such as spironolactone that also inhibits 17-a-hydroxylase or finasteride which is a 5-alpha-reductase inhibitor and flutamide which is an androgen receptor blocker. The mentioned examples are typically for those people that can't really tolerate combined oral contraceptives. Other things to consider for those that are suffering from obesity syndrome are to possibly consider bariatric surgery if of course the criteria are met, and this is on a case-by-case basis. Bariatric surgery may be an answer to many of our metabolic problems that's why it is now called metabolic surgery. For patients who are planning to conceive the goal is to manage their comorbidities such as weight loss but also to try to induce ovulation.Now the first-line therapy for inducing ovulation is a medication called letrozole which is an aromatase inhibitor that in turn reduces estrogen production stimulating FSH secretion and ultimately inducing ovulation, not to get too heavily into the weeds of how these medications work, but basically it improves pregnancy and live birth rate outcomes in patients who are infertile because of the fact that they have anovulatory cycles or a.k.a. they are not ovulating.Then we also have clomiphene which is just an alternative to letrozole and has a different mechanism of action but it also stimulates ovulation by more particularly causing a pulsatile secretion of GnRH and in turn increasing FSH and LH as well, and this medication might be actually preferred over metformin monotherapy in women that are suffering from obesity syndrome who also have anovulatory infertility. However, apparently, clomiphene can cause more chance of multiple gestations versus letrozole.Also, letrozole is preferred over clomiphene to induce ovulation because of a higher rate of live births, but we have the risk of multiple pregnancies with both these methods. Let's talk about the second-line therapies.As mentioned earlier we have this 2 to 1 ratio of FSH to LH in women with PCOS or at least a good amount of them. We said that that is not required to diagnose this disorder but we can also give women exogenous FSH plus human menopausal gonadotropin, but this is really a second-line treatment for ovulation induction and typically we go for second-line treatments if first-line therapies aren't successful. But I will mention that using this exogenous gonadotropin is very expensive and it requires you to have access to specialized healthcare facilities and constant ultrasound monitoring so this may just not be feasible for many people but if you have the resources and it's affordable for you then exogenous gonadotropins are actually preferred over clomiphene and metformin therapy.Metformin can also use as a second-line monotherapy for fertility treatments and this in combination with clomiphene can increase pregnancy rates, especially in women who are suffering from obesity disorder, and of course, this is first-line therapy for insulin resistance.Now if we're talking about an invasive type of procedure for infertility it would be laparoscopic ovarian drilling which basically, we use a laser beam or surgical needle to reduce ovarian tissue to decrease its volume and try to reduce androgen production. Doing this can cause a hormone shift that can induce FSH secretion and ultimately improve ovarian function as well. This is also a second-line treatment for ovulation induction, but it can be performed as a first line if other indications for laparoscopy are present. Third-line therapy would be in vitro fertilization which means that basically we take mature eggs from ovaries and then we fertilize them with sperm in a lab and then the fertilized egg or the embryo is transferred to a uterus to be implanted.For the management of hirsutism, the first-line therapy is usually non-pharmacological and that's electrolysis or light-based hair removal with laser or photo-epilation. For acne, we can consider benzoyl peroxide or topical antibiotics if necessary.Final thoughts: Now I know that was a ton of information but ultimately, we are trying to make women more aware of PCOS and let them know that they are not alone, also we are trying to reduce complications such as cardiovascular problems, diabetes, endometrial cancer, infertility or even pregnancy loss. The best we can do is try to educate more women because many are suffering from this condition and they have no idea. Again, my name is Elika Salimi, and I am a third-year medical student. If you have any questions, you can reach me at elika.salimi@westernu.edu.___________________________Conclusion: Now we conclude episode number 139, “What is PCOS.” Future Dr. Salimi explained that patients with Polycystic Ovary Syndrome present with: Hyperandrogenism, Oligo-ovulation or anovulation, and multiple cysts in ovaries. If your patient meets 2 out of the 3 criteria, then you can confidently give the diagnosis of PCOS. Dr. Arreaza reminded us that by treating obesity you are also treating PCOS. This week we thank Hector Arreaza and Elika Salimi. Audio editing by Adrianne Silva.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:American College of Obstetricians and Gynecologists' Committee on Practice Bulletins—Gynecology..ACOG Practice Bulletin No. 194: Polycystic Ovary Syndrome..Obstet Gynecol.2018; 131(6): p.e157-e171.doi:10.1097/AOG.0000000000002656Hoeger KM, Dokras A, Piltonen T.Update on PCOS: Consequences, Challenges, and Guiding Treatment.The Journal of Clinical Endocrinology & Metabolism.2020; 106(3): p.e1071-e1083.doi:10.1210/clinem/dgaa839Williams T, Mortada R, Porter S.Diagnosis and Treatment of Polycystic Ovary Syndrome..Am Fam Physician.2016; 94(2): p.106-13.pmid: 27419327.Legro RS, Arslanian SA, Ehrmann DA, et al.Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline.J Clin Endocrinol Metab.2013; 98(12): p.4565-4592.doi:10.1210/jc.2013-2350.International evidence-based guideline for the assessment and management of polycystic ovary syndrome 2018.https://www.monash.edu/__data/assets/pdf_file/0004/1412644/PCOS_Evidence-Based-Guidelines_20181009.pdf
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: October 5, 2017 Dr. David Coughlin returns for this week's Teaching Through Clinical Cases to discuss the management of a delirious patient with a hyperkinetic movement disorder. Produced by James E Siegler. Music by Hyson, Josh Woodward, Komiku, and Peter Rudenko. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. REFERENCES Ables AZ, Nagubilli R. Prevention, recognition, and management of serotonin syndrome. Am Fam Physician 2010;81(9):1139-42. PMID 20433130 Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352(11):1112-20. PMID 15784664 Dosi R, Ambaliya A, Joshi H, Patell R. Serotonin syndrome versus neuroleptic malignant syndrome: a challenging clinical quandary. BMJ Case Rep 2014;2014:bcr2014204154. PMID 24957740 Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM 2003;96(9):635-42. PMID 12925718 Lappin RI, Auchincloss EL. Treatment of the serotonin syndrome with cyproheptadine. N Engl J Med 1994;331(15):1021-2. PMID 8084345 Mills KC. Serotonin syndrome. Am Fam Physician 1995;52(5):1475-82. PMID 7572570 Pedavally S, Fugate JE, Rabinstein AA. Serotonin syndrome in the intensive care unit: clinical presentations and precipitating medications. Neurocrit Care 2014;21(1):108-13. PMID 24052457 Radomski JW, Dursun SM, Reveley MA, Kutcher SP. An exploratory approach to the serotonin syndrome: an update of clinical phenomenology and revised diagnostic criteria. Med Hypotheses 2000;55(3):218-24. PMID 10985912 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: May 14, 2020 Can you hear that too? You can't? Well, that doesn't mean I'm having auditory hallucinations. It could just be tinnitus, which describes the irritating sound of ringing, buzzing, clicking, or hissing that affects 10% to 20% of the world's population. But is this a ringing in the ears or a ringing in the brain? Produced by James E Siegler. Music courtesy of Andrew Sacco, Jon Watts, Kai Engel, Lovira, Patches, and Kevin McLeod. Unless otherwise mentioned in the podcast, no competing financial interests exist in the content of this episode. Sound effects by Mike Koenig and Daniel Simion. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. Be sure to follow us on Twitter @brainwavesaudio for the latest updates to the podcast. REFERENCES Arenberg IK, Countryman LF, Bernstein LH, Shambaugh GE Jr. Van Gogh had Menière's disease and not epilepsy. JAMA 1990;264(4):491-3. PMID 2094236 Crummer RW, Hassan GA. Diagnostic approach to tinnitus. Am Fam Physician 2004;69(1):120-6. PMID 14727828 Dobie RA. A review of randomized clinical trials in tinnitus. Laryngoscope 1999;109(8):1202-11. PMID 10443820 Han BI, Lee HW, Kim TY, Lim JS, Shin KS. Tinnitus: characteristics, causes, mechanisms, and treatments. J Clin Neurol 2009;5(1):11-9. PMID 19513328 Langguth B, Kreuzer PM, Kleinjung T, De Ridder D. Tinnitus: causes and clinical management. Lancet Neurol 2013;12(9):920-30. PMID 23948178 Lockwood AH. Tinnitus. Neurol Clin 2005;23(3):893-900, viii. PMID 16026681 Lockwood AH, Salvi RJ, Burkard RF, Galantowicz PJ, Coad ML, Wack DS. Neuroanatomy of tinnitus. Scand Audiol Suppl 1999;51:47-52. PMID 10803913 Mattox DE, Hudgins P. Algorithm for evaluation of pulsatile tinnitus. Acta Otolaryngol 2008;128(4):427-31. PMID 18368578 Palomar García V, Abdulghani Martínez F, Bodet Agustí E, Andreu Mencía L, Palomar Asenjo V. Drug-induced otoxicity: current status. Acta Otolaryngol 2001;121(5):569-72. PMID 11583387 Sullivan M, Katon W, Russo J, Dobie R, Sakai C. A randomized trial of nortriptyline for severe chronic tinnitus. Effects on depression, disability, and tinnitus symptoms. Arch Intern Med 1993;153(19):2251-9. PMID 8215728 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.
Season 2, Episode 3: "What's That Smell?" For transcripts, follow the link here Please support our show! Please consider a tax-deductible donation to our podcast via the Foundation for Delaware County, a 501c3 organization. Every purchase of RWQ merch also helps support our show! Please rate and review us on Apple Podcasts–and tell your friends about us! Medical References Egan ME, Lipsky MS. Diagnosis of vaginitis. Am Fam Physician. 2000 Sep 1;62(5):1095-104. PMID: 10997533. del Mármol, J., Yedlin, M.A. & Ruta, V. The structural basis of odorant recognition in insect olfactory receptors. Nature 597, 126–131 (2021). https://doi.org/10.1038/s41586-021-03794-8 https://m.youtube.com/watch?v=snJnO6OpjCs Dr. Jen Gunter's blog https://vajenda.substack.com/ Historical References Farmer, Ashley D. Remaking Black Power: How Black Women Transformed an Era. Chapel Hill: University of North Carolina Press, 2017. Kettler, Andrew. “Race, Nose, Truth: Dystopian Odours of the Other in American Antebellum Consciousness.” Patterns of Prejudice 55, no. 1 (2021): 1–24. doi:10.1080/0031322X.2021.1898811. Lydia E. Pinkham Medicine Company. [Lydia E Pinkham's Vegetable Compound and other remedies]. [Ephemera]. 11779.F. Available through: Adam Matthew, Marlborough. Popular Medicine in America, 1800-1900, http://www.popularmedicine.amdigital.co.uk.udel.idm.oclc.org/Documents/Details/PM_11779_F_7 [Accessed January 31, 2023]. C. 1876 Reinarz, Jonathan. Past Scents: Historical Perspectives on Smell. Urbana, Il: University of Illinois Press, 2014.
Episode 132: Harm Reduction and Reproductive HealthMeghana explains how to implement harm reduction strategies in at-risk populations such as unhoused patients and injected drug users. Dr. Arreaza adds comments about PrEP for HIV and Expedited Partner Therapy (EPT) Written by Meghana Munnangi, MPH, third-year osteopathic medical student, College of Osteopathic Medicine of the Pacific Western University of Health Sciences. 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.Arreaza: It can be frustrating for physicians trying to change “risky” behaviors in their patients and turn those behaviors into “healthy” behaviors. Doctors deal with this issue every day, but after reading more about the principle of harm reduction, I'm feeling more prepared to help our patients reduce their risks.What is harm reduction?Meghana: Harm reduction is a set of evidence-based interventions that arose within the public health community to reduce the harms associated with risky health behaviors. Most commonly, harm reduction refers to the policies and programs that aim to minimize the negative impacts associated with substance use disorder. The goal is to “meet people where they are” and to provide compassionate, judgment-free interventions and resources to at-risk populations.Examples of people who are part of the “at-risk population.”Some examples are injection-drug users and sex workers. With America experiencing the largest substance use and overdose epidemic we have ever faced, it is exceedingly important we provide services such as clean needle exchange, overdose reversal training, safer sex kits, and more to prevent unnecessary injury, disease, and death. Arreaza: In some countries where prostitution is legal, women are required to have regular check-ups to continue work. I see that as a harm-reduction strategy. I disagree with having sexual workers, but if we are unable to eliminate them, then harm reduction may be the way to go. Why is harm reduction important in medicine?Meghana: Healthcare providers have a unique opportunity to improve the quality of life and limit the negative outcomes associated with risky health behaviors by incorporating harm reduction strategies into their practice. Harm reduction interventions not only decrease health risks in an individual but also in the community. Examples of harm reduction strategies. Meghana: Studies have shown that areas that have introduced clean needle exchange interventions have lower HIV seroprevalence compared to areas that do not have similar interventions [1]. It is critical as health care providers to respect our patient's choices and provide supportive care that will not deter patients from accessing care in the future. Patients who engage in risky activities often face stigma and are treated poorly by the medical system making behavioral changes even more difficult [2]. Understanding that many patients may not be willing to change their behaviors and using a practical approach to medical counseling can strengthen physician-patient relationships. Arreaza: I can think of another example. Pre-exposure prophylaxis for HIV in patients who have multiple sex partners. You wish those patients would have more insight into the risks associated with having multiple sexual partners, but if you cannot change them, you can still reduce the risk.What is harm reduction in the context of the reproductive health field?Meghana: Within Harm Reduction programs, there are many important strategies targeted toward improving sexual and reproductive health. Individuals who inject drugs and sex workers have limited access to family planning services and HIV testing. Studies have shown that individuals with substance use disorder have higher rates of unintended pregnancies, pregnancy-related mortality and morbidity, and lower rates of contraceptive use compared to the general population [3,4]. Harm reduction within the reproductive health field must include expanding access to condoms, contraceptive methods, STI and HIV testing, and prenatal care. Reproductive health harm reduction strategies can reduce rates of STIs, HIV, and unintended pregnancies. In addition to expanding access to condoms, STI screening, treatment, and partner therapy must be offered and encouraged to all patients. Arreaza: As a reminder to our listeners, Expedited Partner Therapy (EPT) consists in treating the partner(s) of a patient with chlamydia or gonorrhea. You, as a physician, treat a patient with STI, but you also give a prescription or medication to that patient, and he/she takes the prescription or medication to his/her partner(s) without me (the doctor) seeing the partner in the clinic or hospital. This is a harm-reduction strategy. It is permissible in 46 states in the US and potentially allowable in Alabama, Kansas, Oklahoma, and South Dakota. It is prohibited in 0 states. Meghana: Regarding birth control, a recent study by Dr. Frank and Dr. Morrison from the University of Michigan suggests that long-acting reversible contraceptives (LARCs) such as the Intrauterine Device (IUD) or the “Implant” should be offered and easily accessible to women with substance use disorder [5]. In America, around 45% of all pregnancies are unintended, and among women with substance use disorders, this number is doubled [6,7]. More so, women with substance use disorders are 25% less likely to use any form of contraception and are more likely to use less effective methods [5]. Patient autonomy is important.Meghana: Autonomy is one of the fundamental principles of ethics in medicine, so it is important that all contraceptive decisions are made without any form of coercion. Also, all discussions must take into consideration previous trauma, such as intimate partner violence. Contraceptive counseling should be comprehensive, and patients should be educated on all methods, including emergency contraception and barrier methods. Patients should not be coerced into choosing a LARC simply because they engage in risky health behaviors and should be offered the same methods as the general population [8]. Arreaza: Let's remember to offer Nexplanon to unhoused patients. On the topic of emergency contraception, you can listen to episode 129. Now, please give us a conclusion.“If you can't fly then run, if you can't run then walk, if you can't walk then crawl, but whatever you do you have to keep moving forward.”― Martin Luther King Jr.Meghana: Overall, family physicians are in a unique position to incorporate harm reduction strategies into their practice to improve the quality of life of their patients and to improve health outcomes in their community. Reproductive health harm reduction strategies should be considered and offered to all patients who engage in risky health behaviors. Individuals with substance use disorder and sex workers should be routinely tested for STIs, including HIV and Hepatitis C, as well as offered pregnancy testing and prenatal care if needed. Comprehensive contraceptive counseling, including condom use and emergency contraception, should be discussed with all patients, and conversations should be stigma-free and collaborative. Incorporating reproductive health interventions into already existing harm reduction programs is key to improving the overall health and well-being of our most vulnerable communities. _____________________Conclusion: Now we conclude episode number 132, “Harm Reduction and Reproductive Health.” Meghana gave us an excellent introduction to the principles of harm reduction in medicine. Applied to reproductive health, we can reduce risk by improving access to condoms, HIV and STI tests, and birth control methods, especially IUD and subdermal implants. Dr. Arreaza also reminded us of strategies such as pre-exposure prophylaxis for HIV (PrEP) and Expedited Partner Therapy for STIs. This week we thank Hector Arreaza and Meghana Munnangi. Audio editing by Adrianne Silva.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:Amundsen EJ. Measuring effectiveness of needle and syringe exchange programmes for prevention of HIV among injecting drug users. Addiction. 2006;101:911–2. Available at: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1360-0443.2006.01519.x?sid=nlm%3ApubmedNyblade L, Stockton MA, Giger K, et al.; Stigma in health facilities: why it matters and how we can change it. BMC Med. 2019;17(1):25. Available at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6376713/.Woodhams E. Partners in contraceptive choice and knowledge. November 18, 2021. Available at https://picck.org/enduring-sud/.Patel P. Forced sterilization of women as discrimination. Public Health Rev. 2017;38:15. Available at https://publichealthreviews.biomedcentral.com/articles/10.1186/s40985-017-0060-9Frank CJ, Morrison L. Harm reduction for patients with substance use disorders. Am Fam Physician. 2022;105(1):90-92. Preview available at https://www.aafp.org/pubs/afp/issues/2022/0100/p90.html.Heil SH, Jones HE, Arria A, et al.; Unintended pregnancy in opioid-abusing women. J Subst Abuse Treat. 2011;40(2):199-202. Preview available at https://pubmed.ncbi.nlm.nih.gov/21036512/.Terplan M, Hand DJ, Hutchinson M, et al.; Contraceptive use and method choice among women with opioid and other substance use disorders: a systematic review. Prev Med. 2015;80:23-31. Preview available at https://www.sciencedirect.com/science/article/abs/pii/S0091743515001140?via%3DihubBaca-Atlas MH, Nimalendran R, Baca-Atlas SN. Applying Harm Reduction Principles to Reproductive Health. Am Fam Physician. 2023 Jan;107(1):Online. PMID: 36689956. Available at https://www.aafp.org/pubs/afp/issues/2023/0100/letter-reproductive-health.html.Royalty-free music used for this episode: “Gushito - Burn Flow." Downloaded on October 13, 2022, from https://www.videvo.net/
The controversy surrounding whether to collect urine cultures and which empiric treatment to prescribe in patients with uncomplicated UTI has left many clinicians unsure of the right approach. In this the first episode of a podcast series, we'll discuss the definition of clinical cure and dive into the evidence behind grey areas in the diagnosis and management of uncomplicated UTI. Disclaimers: This presentation is sponsored by GSK. The speakers are GSK paid healthcare providers. The content is intended to support disease state education and is considered nonpromotional. The content and views expressed therein do not necessarily reflect the views, policies, or position of Pri-Med. This program is limited to Health Care Professionals (HCPs) only. GSK complies with all state and federal laws including transparent reporting and disclosure of payments and transfers of value to HCPs. References: Gupta K, Hooton TM, Naber KG, et al.; Infectious Diseases Society of America; European Society for Microbiology and Infectious Diseases. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. Clin Infect Dis. 2011;52(5):e103- e120. doi: 10.1093/cid/ciq2572. Anger J, Lee U, Ackerman AL, et al. Recurrent uncomplicated urinary tract infections in women: AUA/CUA/SUFU guideline. J Urol. 2019;202(2):282-289. doi: 10.1097/JU.00000000000002963 Houlbar M, Meng L. SHC Clinical Pathway: Inpatient Management of Urinary Tract Infections – Adult Patients. Stanford Antimicrobial Safety and Sustainability Program. November 2017. https://med.stanford.edu/content/dam/sm/bugsanddrugs/documents/c linicalpathways/SHC-UTI-Inpatient-Guideline.pdf. Accessed November 30, 2022. Hooton TM, Gupta K. Acute simple cystitis in women. UpToDate. Updated March 15, 2021. Accessed November 9, 2022. https://www.uptodate.com/contents/acute-simple-cystitis-in-women Colgan R, Williams M. Diagnosis and treatment of acute uncomplicated cystitis. Am Fam Physician. 2011;84(7):771-776. Shafrin J, Marijam A, Joshi AV, et al. Impact of suboptimal or inappropriate treatment on healthcare resource use and cost among patients with uncomplicated urinary tract infection: an analysis of integrated delivery network electronic health records. Antimicrob Resist Infect Control. 2022;11(1):133. Published 2022 Nov 4. doi:10.1186/s13756-022-01170-3 Daneman N, Chateau D, Dahl M, et al. Fluoroquinolone use for uncomplicated urinary tract infections in women: a retrospective cohort study. Clin Microbiol Infect. 2020;26(5):613-618. doi:10.1016/j.cmi.2019.10.016 Bratsman A, Mathias K, Laubscher R, Grigoryan L, Rose S. Outpatient fluoroquinolone prescribing patterns before and after US FDA boxed warning. Pharmacoepidemiol Drug Saf. 2020;29(6):701-707. doi:10.1002/pds.5018 FDA Drug Safety Communication. FDA. 2019. Accessed October 10, 2022 https://www.fda.gov/drugs/drug-safety-and-availability/fda-warns[1]about-increased-risk-ruptures-or-tears-aorta-blood-vessel[1]fluoroquinolone-antibiotics Nicolle LE; AMMI Canada Guidelines Committee*. Complicated urinary tract infection in adults. Can J Infect Dis Med Microbiol. 2005;16(6):349- 360. doi:10.1155/2005/385768
Welcome to the 2 View - Episode 24 Welcome to Episode 24 of “The 2 View,” the podcast for EM and urgent care nurse practitioners and physician assistants! Show Notes for Episode 24 of “The 2 View” – New street drug xylazine/"tranq," app for EM coding changes, FPL injuries, hemorrhoids. Molnupiravir Butler CC, Hobbs FDR, Gbinigie OA, et al. Molnupiravir plus usual care versus usual care alone as early treatment for adults with COVID-19 at increased risk of adverse outcomes (PANORAMIC): an open-label, platform-adaptive randomised controlled trial. Lancet. PubMed. NIH: National Library of Medicine, National Center for Biotechnology Information. Published January 28, 2023. Accessed February 21, 2023. https://pubmed.ncbi.nlm.nih.gov/36566761/ Molnupiravir. COVID-19 Treatment Guidelines. NIH. Last Updated: September 26, 2022. Accessed February 21, 2023. https://www.covid19treatmentguidelines.nih.gov/therapies/antivirals-including-antibody-products/molnupiravir/ Easy Emergency Medicine Coding Calculator American Medical Association. 2023 Emergency Medicine Coding Guide. MDCalc. Accessed February 21, 2023. https://www.mdcalc.com/calc/10454/2023-emergency-medicine-coding-guide CPT Evaluation and Management (E/M) Code and Guideline Changes. Ama-assn.org. AMA: American Medical Association. Accessed February 21, 2023. https://www.ama-assn.org/system/files/2023-e-m-descriptors-guidelines.pdf Graham. 2023 Emergency Medicine Level of Service/Billing Guidelines Overview. Published December 31, 2022. Accessed February 21, 2023. https://www.youtube.com/watch?v=WuV8O3SuXJI The Center for Medical Education. Documentation Changes that Can Help Your Practice. Published August 16, 2022. Accessed February 21, 2023. https://www.youtube.com/watch?v=gHLBjzQt4vo Xylazine DEA Joint Intelligence Report. The Growing Threat of Xylazine and its Mixture with Illicit Drugs. U.S. Department of Justice Drug Enforcement Administration. Dea.gov. Published October 2022. Accessed February 21, 2023. https://www.dea.gov/sites/default/files/2022-12/The%20Growing%20Threat%20of%20Xylazine%20and%20its%20Mixture%20with%20Illic it%20Drugs.pdf FDA warns about the risk of xylazine exposure in humans. Fda.gov. FDA. Published November 8, 2022. Accessed February 21, 2023. https://www.fda.gov/media/162981/download Hoffman J. Tranq dope: Animal Sedative Mixed with Fentanyl Brings Fresh Horror to U.S. Drug Zones. The New York Times. Published January 7, 2023. Accessed February 21, 2023. https://www.nytimes.com/2023/01/07/health/fentanyl-xylazine-drug.html. National Institute on Drug Abuse. Xylazine. National Institute on Drug Abuse: Advancing Addiction Science. Published April 21, 2022. Accessed February 21, 2023. https://nida.nih.gov/research-topics/xylazine Overdose C on O. Toxicity of Xylazine and How It Impacts People Who Use Drugs by Dr. Joseph D'Orazio. Published June 15, 2022. Accessed February 21, 2023. https://www.youtube.com/watch?v=Rqpf0jIuyCo Flexor Pollicis Longus and Other Thumb Injuries Gault D. A review of repaired flexor tendons. J Hand Surg Br. ScienceDirect. Published October 1987. Accessed February 21, 2023. https://www.sciencedirect.com/science/article/abs/pii/0266768187901811 Urbaniak JR. Repair of the flexor pollicis longus. Hand Clin. Europe PMC. Published February 1, 1985. Accessed February 21, 2023. https://europepmc.org/article/med/3912396 Hemorrhoids Procedure Review: Thrombosed Hemorrhoids. EM:RAP. EM:RAP.ORG. Published April 2018. Accessed February 21, 2023. https://www.emrap.org/episode/emrapliveapril/procedurereview Zuber TJ. Hemorrhoidectomy for Thrombosed External Hemorrhoids. Am Fam Physician. AAFP. Published 2002. Accessed February 21, 2023. https://www.aafp.org/pubs/afp/issues/2002/0415/p1629.html 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!
Amidst the battle of the mental health crisis, major depressive disorder stands out as an all-too-common reality for many children and adolescents, but the forces of science and medicine can stand against this foe. Dr. Christopher Drescher, a clinical child psychologist, joins pediatric resident Dr. Daniel Allen and medical student Vuk Lacmanovic to remove the cape from this increasingly common condition and discuss its symptoms, diagnosis, and treatment. Specifically, they will: Define major depressive disorder (MDD) and recognize the common symptoms in both children and adolescents. Formulate a differential diagnosis for patients presenting with depressive symptoms. Recognize validated screening tools for depression in both children and adolescents. Review cognitive behavioral therapy and pharmacotherapy as treatment options. Review appropriate referral to a mental health specialist. Free CME Credit (requires sign-in): https://mcg.cloud-cme.com/course/courseoverview?P=0&EID=12493 References: Bhatia SK, Bhatia SC. Childhood and adolescent depression. Am Fam Physician. 2007 Jan 1;75(1):73-80. PMID: 17225707. Brent DA, Maalouf F. Depressive Disorders (in Childhood and Adolescence). In: Ebert MH, Leckman JF, Petrakis IL. eds. Current Diagnosis & Treatment: Psychiatry, 3e. McGraw-Hill; Accessed November 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2509§ionid=200807606 Clark MS, Jansen KL, Cloy JA. Treatment of childhood and adolescent depression. Am Fam Physician. 2012 Sep 1;86(5):442-8. PMID: 22963063. Fendrich M, Weissman MM, Warner V. Screening for depressive disorder in children and adolescents: validating the Center for Epidemiologic Studies Depression Scale for Children. Am J Epidemiol. 1990 Mar;131(3):538-51. doi: 10.1093/oxfordjournals.aje.a115529. PMID: 2301363. (PDF of CES-DC here) Forman-Hoffman V, McClure E, McKeeman J, Wood CT, Middleton JC, Skinner AC, Perrin EM, Viswanathan M. Screening for Major Depressive Disorder in Children and Adolescents: A Systematic Review for the U.S. Preventive Services Task Force. Ann Intern Med. 2016 Mar 1;164(5):342-9. doi: 10.7326/M15-2259. Epub 2016 Feb 9. PMID: 26857836. Hathaway EE, Walkup JT, Strawn JR. Antidepressant Treatment Duration in Pediatric Depressive and Anxiety Disorders: How Long is Long Enough? Curr Probl Pediatr Adolesc Health Care. 2018 Feb;48(2):31-39. doi: 10.1016/j.cppeds.2017.12.002. Epub 2018 Jan 12. PMID: 29337001; PMCID: PMC5828899. March JS, Silva S, Petrycki S, Curry J, Wells K, Fairbank J, Burns B, Domino M, McNulty S, Vitiello B, Severe J. The Treatment for Adolescents With Depression Study (TADS): long-term effectiveness and safety outcomes. Arch Gen Psychiatry. 2007 Oct;64(10):1132-43. doi: 10.1001/archpsyc.64.10.1132. Erratum in: Arch Gen Psychiatry. 2008 Jan;65(1):101. PMID: 17909125. Meister R, Abbas M, Antel J, Peters T, Pan Y, Bingel U, Nestoriuc Y, Hebebrand J. Placebo response rates and potential modifiers in double-blind randomized controlled trials of second and newer generation antidepressants for major depressive disorder in children and adolescents: a systematic review and meta-regression analysis. Eur Child Adolesc Psychiatry. 2020 Mar;29(3):253-273. doi: 10.1007/s00787-018-1244-7. Epub 2018 Dec 8. PMID: 30535589; PMCID: PMC7056684. Rachel A. Zuckerbrot, Amy Cheung, Peter S. Jensen, Ruth E.K. Stein, Danielle Laraque and GLAD-PC STEERING GROUP. Guidelines for Adolescent Depression in Primary Care (GLAD-PC): Part I. Practice Preparation, Identification, Assessment, and Initial Management. Pediatrics March 2018, 141 (3) e20174081; DOI: https://doi.org/10.1542/peds.2017-4081 Scott K, Lewis CC, Marti CN. Trajectories of Symptom Change in the Treatment for Adolescents With Depression Study. J Am Acad Child Adolesc Psychiatry. 2019 Mar;58(3):319-328. doi: 10.1016/j.jaac.2018.07.908. Epub 2019 Jan 8. PMID: 30768414; PMCID: PMC6557284. Sharma T, Guski LS, Freund N, Gøtzsche PC. Suicidality and aggression during antidepressant treatment: systematic review and meta-analyses based on clinical study reports. BMJ. 2016 Jan 27;352:i65. doi: 10.1136/bmj.i65. PMID: 26819231; PMCID: PMC4729837. Siu AL; US Preventive Services Task Force. Screening for Depression in Children and Adolescents: US Preventive Services Task Force Recommendation Statement. Pediatrics. 2016 Mar;137(3):e20154467. doi: 10.1542/peds.2015-4467. Epub 2016 Feb 8. PMID: 26908686. Weersing VR, Brent DA, Rozenman MS, Gonzalez A, Jeffreys M, Dickerson JF, Lynch FL, Porta G, Iyengar S. Brief Behavioral Therapy for Pediatric Anxiety and Depression in Primary Care: A Randomized Clinical Trial. JAMA Psychiatry. 2017 Jun 1;74(6):571-578. doi: 10.1001/jamapsychiatry.2017.0429. PMID: 28423145; PMCID: PMC5539834. Weersing VR, Shamseddeen W, Garber J, Hollon SD, Clarke GN, Beardslee WR, Gladstone TR, Lynch FL, Porta G, Iyengar S, Brent DA. Prevention of Depression in At-Risk Adolescents: Predictors and Moderators of Acute Effects. J Am Acad Child Adolesc Psychiatry. 2016 Mar;55(3):219-26. doi: 10.1016/j.jaac.2015.12.015. Epub 2016 Jan 18. PMID: 26903255; PMCID: PMC4783159. Xu Y, Bai SJ, Lan XH, Qin B, Huang T, Xie P. Randomized controlled trials of serotonin-norepinephrine reuptake inhibitor in treating major depressive disorder in children and adolescents: a meta-analysis of efficacy and acceptability. Braz J Med Biol Res. 2016 May 24;49(6):e4806. doi: 10.1590/1414-431X20164806. PMID: 27240293; PMCID: PMC4897997. Zhou X, Cipriani A, Zhang Y, Cuijpers P, Hetrick SE, Weisz JR, Pu J, Giovane CD, Furukawa TA, Barth J, Coghill D, Leucht S, Yang L, Ravindran AV, Xie P. Comparative efficacy and acceptability of antidepressants, psychological interventions, and their combination for depressive disorder in children and adolescents: protocol for a network meta-analysis. BMJ Open. 2017 Aug 11;7(8):e016608. doi: 10.1136/bmjopen-2017-016608. PMID: 28801423; PMCID: PMC5629731. Zhou X, Teng T, Zhang Y, Del Giovane C, Furukawa TA, Weisz JR, Li X, Cuijpers P, Coghill D, Xiang Y, Hetrick SE, Leucht S, Qin M, Barth J, Ravindran AV, Yang L, Curry J, Fan L, Silva SG, Cipriani A, Xie P. Comparative efficacy and acceptability of antidepressants, psychotherapies, and their combination for acute treatment of children and adolescents with depressive disorder: a systematic review and network meta-analysis. Lancet Psychiatry. 2020 Jul;7(7):581-601. doi: 10.1016/S2215-0366(20)30137-1. PMID: 32563306; PMCID: PMC7303954.
Drs. Bell and DeVine return for Part 4 of Perioperative Considerations, Management, and Process for patients on buprenorphine. This final (for now) episode discusses the ‘other' patient situations concerning perioperative times. How do you manage patients who have an undiagnosed opioid use disorder or are on very high doses of chronic opioids? What about patients who are opioid naive but who are high-risk for development of an OUD? These patients may be those who, personally, do not want opioids for any reason either due to a history of another substance use disorder or those who just do not want opioid exposure. Teaser- there will likely be a part 5 of this series of Perioperative Considerations… Below you will find the resources used for the development of this series. To learn more about the doctors as well as keep up with current happenings follow on twitter: @echocsct or email us with questions or feedback: theaddictionconnectionpodcast@gmail.com Part of the Ars Longa Media Productions. Articles for Perioperative Series: •Bentzley BS et al. Discontinuation of buprenorphine maintenance therapy: perspectives and outcomes. J Subst Abuse Treat 2015;52:48-57. •Buresh M, et al. Treatment perioperative and acute pain in patients on buprenorphine: narrative literature review and practice recommendations. J Gen Intern Med 2020;35(12):3635-3643. •Champagne K, et al. Patients on buprenorphine formulations undergoing surgery. Current Pain and Headache Reports 2022;26:459-468. •Engle AL, et al. The divided dose approach to perioperative buprenorphine management in patients with opioid use disorder. Journal of Opioid Management 2021;17(7):101-107. •Evans E, et al. Mortality among individuals accessing pharmacological treatment for opioid dependence in California, 2006-10. Addiction 2015;110:996. Goel A et al. The perioperative patient on buprenorphine: a systematic review of perioperative management strategies and patient outcomes. Can J Anaest 2019;66:201-17 •Greenwald M et al. Buprenorphine duration of action: mu-opioid receptor availability and pharmacokinetic and behavioral indices. Biol Psychiatry. 2007 Jan1;61(1):101-10. •Katz A, et al. Tobacco, alcohol, and drug use and willingness to change. J Hosp Med 2008;3:369-75. •Kubalanza K et al. Sublingual buprenorphine vs. morphine for acute pain. Am Fam Physician. 2012;86(7):682. •Liebschutz JM, et al. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized clinical trial. JAMA Intern Med 2014;174:369-76. •Machado FC et al. Transdermal buprenorphine for acute postoperative pain: a systematic review. Braz J Anesthesiol. Jul-Aug 2020;70(4):419-428. Pergolizzi J et al. Current knowledge of buprenorphine and its unique pharmacological profile. Pain Pract. Sep-Oct 2010;10(5):428-50.
Drs. Bell and DeVine return for Part 4 of Perioperative Considerations, Management, and Process for patients on buprenorphine. This final (for now) episode discusses the ‘other' patient situations concerning perioperative times. How do you manage patients who have an undiagnosed opioid use disorder or are on very high doses of chronic opioids? What about patients who are opioid naive but who are high-risk for development of an OUD? These patients may be those who, personally, do not want opioids for any reason either due to a history of another substance use disorder or those who just do not want opioid exposure. Teaser- there will likely be a part 5 of this series of Perioperative Considerations… Below you will find the resources used for the development of this series. To learn more about the doctors as well as keep up with current happenings follow on twitter: @echocsct or email us with questions or feedback: theaddictionconnectionpodcast@gmail.com Part of the Ars Longa Media Productions. Articles for Perioperative Series: •Bentzley BS et al. Discontinuation of buprenorphine maintenance therapy: perspectives and outcomes. J Subst Abuse Treat 2015;52:48-57. •Buresh M, et al. Treatment perioperative and acute pain in patients on buprenorphine: narrative literature review and practice recommendations. J Gen Intern Med 2020;35(12):3635-3643. •Champagne K, et al. Patients on buprenorphine formulations undergoing surgery. Current Pain and Headache Reports 2022;26:459-468. •Engle AL, et al. The divided dose approach to perioperative buprenorphine management in patients with opioid use disorder. Journal of Opioid Management 2021;17(7):101-107. •Evans E, et al. Mortality among individuals accessing pharmacological treatment for opioid dependence in California, 2006-10. Addiction 2015;110:996. Goel A et al. The perioperative patient on buprenorphine: a systematic review of perioperative management strategies and patient outcomes. Can J Anaest 2019;66:201-17 •Greenwald M et al. Buprenorphine duration of action: mu-opioid receptor availability and pharmacokinetic and behavioral indices. Biol Psychiatry. 2007 Jan1;61(1):101-10. •Katz A, et al. Tobacco, alcohol, and drug use and willingness to change. J Hosp Med 2008;3:369-75. •Kubalanza K et al. Sublingual buprenorphine vs. morphine for acute pain. Am Fam Physician. 2012;86(7):682. •Liebschutz JM, et al. Buprenorphine treatment for hospitalized, opioid-dependent patients: a randomized clinical trial. JAMA Intern Med 2014;174:369-76. •Machado FC et al. Transdermal buprenorphine for acute postoperative pain: a systematic review. Braz J Anesthesiol. Jul-Aug 2020;70(4):419-428. Pergolizzi J et al. Current knowledge of buprenorphine and its unique pharmacological profile. Pain Pract. Sep-Oct 2010;10(5):428-50.
EBB 244: Evidence on Artificial Rupture of Membranes, Assisted Vaginal Delivery, and Internal Monitoring. We are so excited to announce the upcoming release of a new Evidence Based Birth(R) Pocket Guide, all about Interventions! To give you a sneak peek to the Invention Pocket Guide, we are diving into the research and evidence on artificial rupture of membranes, assisted vaginal delivery an internal monitoring. Content note: Discussion of the benefits and risks of these interventions, including forceps and vacuum-assisted deliveries, which can be associated with birthing trauma for birthing people and babies, as well as the risk of mortality. Resources: Make sure you're on the Pocket Guide wait list by going here Amniotomy References: Kawakita, T., Huang, C-C, and Landy, H. J. (2018). Risk Factors for Umbilical Cord Prolapse at the Time of Artificial Rupture of Membranes. AJP Rep 8(2): e89-e94. https://pubmed.ncbi.nlm.nih.gov/29755833/ Simpson, K. R. (2020). Cervical Ripening and Labor Induction and Augmentation, 5th Edition. AWHONN Practice Monograph 24(4): PS1-S41. https://bmcpregnancychildbirth.biomedcentral.com/articles/10.1186/s12884-019-2491-4 Smyth, R. M., Markham, C. & Dowswell, T. (2013). Amniotomy for shortening spontaneous labour. Cochrane Database Syst Rev 6:CD006167. https://pubmed.ncbi.nlm.nih.gov/23780653/ Alfirevic, Z., Keeney, E., Dowswell, T., et al. (2016). Methods to induce labour: a systematic review, network meta-analysis and cost-effectiveness analysis. BJOG 123(9): 1462-1470. https://pubmed.ncbi.nlm.nih.gov/27001034/ de Vaan, M. D. T., ten Eikelder, M. L. G., Jozwiak, M., et al. (2019). Mechanical methods for induction of labour. Cochrane Database of Systematic Reviews 10: CD001233. https://www.cochrane.org/CD001233/PREG_mechanical-methods-induction-labour Simpson, K. R. (2020). Cervical Ripening and Labor Induction and Augmentation, 5th Edition. AWHONN Practice Monograph, 24(4), PS1-S41. https://nwhjournal.org/article/S1751-4851(20)30079-9/abstract Assisted Vaginal Delivery References: NHS article on forceps or vacuum delivery https://www.nhs.uk/pregnancy/labour-and-birth/what-happens/forceps-or-vacuum-delivery/ Bailey, P. E., van Roosmalen, J., Mola, G., et al. (2017). Assisted vaginal delivery in low and middle income countries: an overview. BJOG 124(9): 1335-1344. https://pubmed.ncbi.nlm.nih.gov/28139878/ CDC Wonder Database Feeley, C., Crossland, N., Betran, A. P., et al. (2021). Training and expertise in undertaking assisted vaginal delivery (AVD): a mixed methods systematic review of practitioners views and experiences. Reprod Health 18(1): 92. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8097768/ Crossland, N., Kingdon, C., Balaam, M. C. (2020). Women's, partners' and health care providers' views and experiences of assisted vaginal birth: a systematic mixed methods review. Reprod Health 17:83. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7268509/ Hook, C. D., Damos, J. R. (2008). Vacuum-Assisted Vaginal Delivery. Am Fam Physician 78(8): 953-960. https://www.aafp.org/afp/2008/1015/p953.html Tsakiridis, I., Giouleka, S., Mamopoulos, A., et al. (2020). Operative vaginal delivery: a review of four national guidelines. J Perinat Med 48(3): 189-198. https://pubmed.ncbi.nlm.nih.gov/31926101/ Verma, G. L., Spalding, J. J., Wilkinson, M. D., et al. (2021). Instruments for assisted vaginal birth. Cochrane Database Syst Rev. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD005455.pub3/full Internal Monitoring References: Euliano, T. Y., Darmanjian, S., Nguyen, M. T., et al. (2017). Monitoring fetal heart rate during labor: A comparison of three methods. J Pregnancy 2017: 8529816. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5368359/ Neilson, J. P. (2015). Fetal electrocardiogram (ECG) for fetal monitoring during labor. Cochrane Database Syst Rev 12: CD000116. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD000116.pub5/full Harper, L. M., Shanks, A. L., Tuuli, M. G., et al. (2013). The risks and benefits of internal monitors in laboring patients. Am J Obstet Gynecol 209(1): 38.e1-38.e6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3760973/ Bakker, J. J. H., Verhoeven, C. J. M., Janssen, P. F., et al. (2010). Outcomes after internal versus external tocodynamometry for monitoring labor. N Engl J Med 362(4): 306-13. https://www.nejm.org/doi/10.1056/NEJMoa0902748?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200www.ncbi.nlm.nih.gov Frolova, A. I., Stout, M. J., Carter, E. B., et al. (2021). Internal fetal and uterine monitoring in obese patients and maternal obstetrical outcomes. Am J Obstet Gynecol MFM 3(1): 100282. https://pubmed.ncbi.nlm.nih.gov/33451595/ Bakker, J. J. H., Janssen, P. F., van Halem, K. (2013). Internal versus external tocodynamometry during induced or augmented labor. Cochrane Database Syst Rev 8: CD006947. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD006947.pub3/full van Halem, K., Bakker, J. J. H., VerHoeven, C. J., et al. (2011). Does use of an intrauterine catheter during labor increase risk of infection? J Maternal Fetal Neonatal Med 25(4): 415-418. https://www.tandfonline.com/doi/abs/10.3109/14767058.2011.582905 For more information and news about Evidence Based Birth®, visit www.ebbirth.com. Find us on: TikTok Instagram Pinterest Ready to get involved? Check out our Professional membership (including scholarship options) here Find an EBB Instructor here Click here to learn more about the Evidence Based Birth® Childbirth Class.
Episode 116: Benefits of breastfeedingBy Timiiye Yomi, MD. Editing and comments by Hector Arreaza, MD.Dr. Yomi explains the benefits of breastfeeding for mother and baby. Three doctor listeners share their experiences with breastfeeding. 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.Breastfeeding is the process by which a child is fed breast milk. It is an ancient practice that dates to pre-historic times. The American Academy of Pediatrics recommends breastfeeding as the sole source of nutrition for babies for about 6 months and can be continued for as long as both mother and baby desire it, while the World Health Organization recommends exclusive breastfeeding for the first 6 months of life and up to 2 years with appropriate complementary foods.Human milk has many advantageous anti-infective and immunologic properties, making it the ideal nutritional source to optimize the infant's well-being. Of the over 130 million babies born every year in the world, only 42% of mothers breastfeed their newborn within the first hour of life, 38% practice exclusive breastfeeding, and over 50% breastfeed for up to 2 years. In this segment, we will be talking about the many benefits of breastfeeding to both children and mothers.Benefits to the baby: Breast milk has the right amount of nutrients and fluids needed for a baby's growth and development.It is easier to digest than formula, and breastfed babies have less gas, fewer feeding problems, and less constipation.It contains antibodies that protect infants from illnesses like otitis media, gastroenteritis, and respiratory illnesses like asthma and allergies, especially in children breastfed beyond 6 months. It reduces the risk of atopic dermatitis, NEC, Celiac Disease, Crohn's Disease and ulcerative colitis, Late-onset sepsis in the preterm infant, and childhood leukemia.Reduces the risk of childhood obesity, HTN, and type 1 and 2 diabetes Breastfed infants have a lower risk of sudden infant death syndrome (SIDS).Breastfed infants have been shown to have better cognitive development.Benefits to the mother:Promotes weight loss and some degree of contraceptive for mothersWomen who breastfeed longer have been shown to have lower rates of type 2 diabetes and high blood pressure, breast and ovarian cancer in premenopausal women, thyroid cancers, rheumatoid arthritis, and osteoporosisReduces the risk of post-Partum depressionBreastfeeding triggers the release of oxytocin that promotes uterine involution and may decrease the amount of postpartum hemorrhage.Additional benefits:Promotes mother-infant bonding Cheap and economical for families and societyConvenientIn summary, breastfeeding delivers a lot of health, nutritional and emotional benefits to both children and mothers. When not contraindicated, we encourage mothers to engage in this practice as it presents babies with a healthy start in life.The benefits of breastfeeding cannot be overstated. However, we recognize that some mothers have challenges breastfeeding. For those mothers, we say you are a great mother if you take good care of your baby, even if you cannot breastfeed him/her.Testimonials:Breastfeeding is highly recommended by healthcare professionals, and in most cases, it is a natural and smooth process. However, it is not always free of challenges. You will listen to testimonials about three different breastfeeding experiences. All these testimonials are anonymous and written by advanced-level healthcare providers. Their experiences fall on a spectrum ranging from positive and easy to negative and difficult.Testimonial #1: My grandma told me so.When I was pregnant with my first child, I was already keenly aware of the benefits of breastfeeding because by that time, I was established in my profession as a health care provider. I looked forward to breastfeeding my newborn. However, when my baby was born, I found that my breast anatomy made it extremely difficult for my baby to latch on. While it is possible for women to breastfeed with inverted nipples, for me and my baby, it did not work out. I felt like a failure as a new mother. When my grandma came to visit me and my newborn, I told her how frustrated I was with my body. She replied, “yah, sorry about that; you got those from me!” Yes, inverted nipples are a genetic trait, and 10-20% of women are born with inverted nipples. I had been feeling alone in my plight, but after talking with my grandma, I realized there were other women struggling just like me! Although I was very disappointed that I couldn't breastfeed, I didn't let that deter me from giving breast milk to my baby. Where there is a will, there is a way! I decided to bottle-feed my baby with my pumped breast milk. It was extra work and a bit time-consuming, but for me, the health benefits for both my baby and me were worth it. Thankfully, I am blessed with a supportive husband who took on the nighttime feedings while I pumped milk. I could only keep up this pumping routine for 3 months before my maternity leave ended. While I would have preferred my baby to receive breast milk for longer, I find peace in the saying, “something is better than nothing.” If only there had been wearable breast pumps back then, I'm sure I could have given my baby breast milk for much longer. Technology today is amazing! While I encourage all my patients to breastfeed, my personal experience has made me empathetic to the physical challenges and even heartache that women experience over breastfeeding. I always keep in mind that every woman and baby's situation is unique, and I also give myself grace for what I initially felt was a shortcoming as a new mother. Testimonial 2: Fed is best.I have been a breastfeeding advocate since medical school.Prior to the delivery of my first baby, I had my breast pump and bag ready. I had all the handouts about different breastfeeding techniques, positions, and all the available community resources. I had the tablets and teas that would stimulate milk production. I was ready!When I delivered my beautiful baby girl, she had trouble latching and it was very painful for me. All through that first night at the hospital, I requested the lactation coaches to come to the bedside to guide me, and they came by every shift. They even gave me all these extra syringes and tubes to feed my baby. We ended up feeding her with donor's milk at the hospital. We even fed her via a syringe the first few nights. I was never able to get her to latch. I drank my water and my tea, I took my tablets, and I was able to pump some milk,filling only 1/4 -1/2 of the bottle each time, only about 3-6 cc from each breast in a 20–30-minute session. My baby started to be fed with formula and my breast milk. I continued to pump during my lunch breaks when I returned to work. I did this until she turned 6 months old, then I stopped.My second baby was able to latch a few times in the hospital. I felt so relieved that I would be a successful breastfeeder, but she started to get jaundiced because of inadequate intake. We decided to give her donor milk again. At home, I still could not breastfeed, but I was able to pump. I even bought the hands-free Willow pump, thinking I could pump while charting or seeing patients, but it was not for me. My baby alternated feedings between breast milk and formula. I stopped pumping at 3 months.It was quite frustrating to not successfully latch and breastfeed. Somehow, I had this feeling as the song goes, “ I did my best, but I guess my best wasn't good enough”. Thankfully, one of my pediatric colleagues put my mind at ease. She said, “fed is best.” Indeed, my baby girls have grown to be beautiful, healthy babies, and our bond is strong. Now I counsel with grace and consideration. My mantra before was “breast is best”; now, it is “fed is best.”Testimonial #3: A mother of seven.I had seven babies, and each of them had different experiences with breastfeeding. I'd like to share with you how it went. Breastfeeding my first baby was relatively easy. He was a cooperative, calm infant and caught on quickly to the process. Baby number two was 6 weeks premature, so in the first week, he kept falling asleep, but as he got a bit older, things went well. Baby number 3 was born with a cleft lip and alveolar ridge, and breastfeeding was necessary. The breast tissue filled up the cleft in his lip, so he was able to grow normally until big enough for reparative surgery. He did have a bit of nipple confusion when I had to return to work. Baby three actually continued some token breastfeeding for a couple of weeks when his newborn sister was co-nursing. Because the breast is a demand-organ, increased suckling increases milk productivity, so neither child was deprived of milk. Baby four adapted well.Baby five was a somewhat slow learner but, with persistence, ultimately did well. Baby six also was an eager learner, but when she was 9 months, decided that she had had enough of breastfeeding, so we stopped. Baby seven adapted too well and breastfed for a couple of years. Several babies were breastfed during my pregnancies without issues. In my opinion, the first week is when you must teach a baby how to breastfeed, and it is generally the most difficult. If you can tough it through that first week, things become a lot easier. Babies have their own personalities and their own way of learning, so whereas one baby will prove a natural at the task, another may require a bit more patience. Breastfeeding and working can be challenging, but I was able to continue breastfeeding and return to work. It took determination and the reversal of day and night feeds. I didn't get much sleep at first, but the babies stayed so much healthier due to the immune benefits of breastfeeding, which meant less time off work with a sick child!If you have a “special needs” baby, and this includes premies and children with orofacial problems, breastfeeding prevents nutritional issues. Breastfeeding provided me with a special feeling of tranquility and peace, that's why it may reduce the risk of postpartum depression. Also, the luxury of being able to feed anytime, anywhere, was very helpful for me!All seven of our kids have advanced degrees, and several have their doctorates. I would like to think that breast milk played a role in their academic success. I think breastfed babies are smarter! ____________________________Conclusion: Now we conclude episode number 116, “Benefits of breastfeeding.” We hope your knowledge about breastfeeding was enriched by Dr. Yomi's presentation and that the testimonials gave you a broader perspective on the breastfeeding experience. This week we thank Hector Arreaza, Timiiye Yomi, Chelsea Dunn, Carmen Ruby, Anna Stewart, and three anonymous doctor mothers. Audio edition by Adrianne Silva.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! _____________________Links: Madore LS, Fisher DJ. The Role of Breast Milk in Infectious Disease. Clin Perinatol. 2021 Jun;48(2):359-378. doi: 10.1016/j.clp.2021.03.008. PMID: 34030819. https://pubmed.ncbi.nlm.nih.gov/34030819/American Academy of Pediatrics. (2021). Benefits of breastfeeding, Patient Care. Retrieved from https://www.aap.org/en/patient-care/breastfeeding/breastfeeding-overview/Westerfield KL, Koenig K, Oh R. Breastfeeding: Common Questions and Answers. Am Fam Physician. 2018 Sep 15;98(6):368-373. PMID: 30215910. https://www.aafp.org/pubs/afp/issues/2018/0915/p368.htmlRoyalty-free music used for this episode: Gushito, Latin Pandora by Videvo, downloaded on May 06, 2022, from https://www.videvo.net
Did you know that the leading cause of monocular vision loss for people of all ages can only be prevented by intervening in early childhood? Amblyopia, or decreased vision from lack of visual stimulation, affects about 3-5% of children and can lead to permanent vision loss if not treated by the age of 8. Dr. Stephanie Goei, a pediatric ophthalmologist, joins medical students Lindsay Berman and Joanne Thomas to discuss detection, diagnosis, treatment, and prognosis of amblyopia in infancy and early childhood. Specifically, they will cover how to: Recognize common history and physical exam findings associated with amblyopia. Formulate a differential diagnosis for visual deficits in children. Appreciate the importance of vision screenings as part of regular wellness visits. Understand the initial diagnostic approach to amblyopia. Recognize when to refer patients with visual deficits to a pediatric ophthalmologist. Acknowledge how the approach to treatment of amblyopia depends on the specific etiology. Special thanks to Dr. Rebecca Yang for peer reviewing this episode. FREE CME Credit (requires free sign-up): Link Coming Soon! References: McConaghy JR, McGuirk R. Amblyopia: Detection and Treatment. Am Fam Physician. 2019 Dec 15;100(12):745-750. PMID: 31845774. Holmes JM, Lazar EL, Melia BM, et al.; Pediatric Eye Disease Investigator Group. Effect of age on response to amblyopia treatment in children. Arch Ophthalmol. 2011;129(11):1451–1457. American Academy of Pediatrics. Policy statement. Visual system assessment in infants, children, and young adults by pediatricians. January 2016. Accessed December 16, 2018. http://pediatrics.aappublications.org/content/137/1/e20153596 American Academy of Ophthalmology. Amblyopia PPP - 2017. November 2017. Accessed December 16, 2018. https://www.aao.org/preferred-practice-pattern/amblyopia-ppp-2017 Blair K, Cibis G, Gulani AC. Amblyopia. [Updated 2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430890/
www.tadeclinicagem.com.br/guia - Conheça o Guia TdC com 7 dias grátis Um serviço de revisão e atualização continuados em clínica médica. A informação que você precisa, do jeito que você prefere. Junte-se aos mais de 600 assinantes. Assine o Guia, ganhe tempo e atualize-se sem esforço. Referências EAU Guidelines. Edn. presented at the EAU Annual Congress Amsterdam, the Netherlands 2022.ISBN 978-94-92671-16-5 THOMAS C. MICHELS, MD, MPH, AND JARRET E. SANDS, DO. Dysuria: Evaluation and Differential Diagnosis in Adults; Am Fam Physician. 2015;92(9):778-788 James R. Johnson, M.D., and Thomas A. Russo, M.D., C.M. Acute Pyelonephritis in Adults; N Engl J Med 2018; 378:48-59 DOI: 10.1056/NEJMcp1702758 Current cilinical management of renal and perinephric abscesses; Department of Urology, AOUI, Verona - Italy. DOI: 10.5301/urologia.5000044 Stephen Bent, MD et al. Does This Woman Have an Acute Uncomplicated Urinary Tract Infection?. JAMA 2002, The Rational Clinical Examination Kalpana Gupta, MD, MPH. Acute simple cystitis in adult males; UpToDate 2022 Kalpana Gupta, MD, MPH. Acute complicated urinary tract infection (including pyelonephritis) in adults; UpToDate 2022 Thomas L Holland, MDVance G Fowler, Jr, MD. Clinical manifestations of Staphylococcus aureus infection in adults; UpToDate 2022
HEED THE REFERENCES: Anand Swaminathan, "REBEL Core Cast 47.0 Nausea and Vomiting", REBEL EM blog, January 13, 2021. Available at: https://rebelem.com/rebel-core-cast-47-0-nausea-and-vomiting/. Beadle KL, Helbling AR, Love SL, April MD, Hunter CJ. Isopropyl Alcohol Nasal Inhalation for Nausea in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2015; doi: http://dx.doi.org/10.1016/j.annemergmed.2015.09.031. Furyk, J. S., Meek, R. A., & Egerton-Warburton, D. (2015). Drugs for the treatment of nausea and vomiting in adults in the emergency department setting. The Cochrane database of systematic reviews, 2015(9), CD010106. https://doi.org/10.1002/14651858.CD010106.pub2 Mark Ramzy, "Aromatherapy vs Oral Ondansetron for Antiemetic Therapy Among Adult Emergency Department Patients", REBEL EM blog, December 3, 2020. Available at: https://rebelem.com/aromatherapy-vs-oral-ondansetron-for-antiemetic-therapy-among-adult-emergency-department-patients/. Phips, Ashley. (2015). Article Review: RCT of Antiemetic Efficacy in the ED. Available at http://www.emdocs.net/wp-content/uploads/2015/01/AntiemeticUseED-Phipps-.pdf Plewa, Young, Yerman. (20 July 2008). The vomiting patient in the ED: Evaluation and management. Emergency Medicine Reports. Available from https://www.reliasmedia.com/articles/13681-the-vomiting-patient-in-the-ed-evaluation-and-management Scorza K, Williams A, Phillips JD, Shaw J. Evaluation of nausea and vomiting. Am Fam Physician. 2007 Jul 1;76(1):76-84. PMID: 17668843. Wegrzyniak LJ, Repke JT, Ural SH. Treatment of hyperemesis gravidarum. Rev Obstet Gynecol. 2012;5(2):78-84. Yartsev. (2021). Deranged Physiology: Question 10 - Describe the physiology of vomiting. Available from https://derangedphysiology.com/main/cicm-primary-exam/past-papers/2010-paper-1-saqs/question-10p2#answer-anchor
Welcome to Episode 17 of “The 2 View,” the podcast for EM and urgent care nurse practitioners and physician assistants! Show Notes for Episode 17 of “The 2 View” – Monkeypox, A Typical NP/PA Day in the ER: Tips from the Heart, Timesavers, and Anaphylaxis. Monkeypox Lewis D. How PAs Can Avoid Malpractice: Go Back to Practice Basics. Medscape. Published May 23, 2022. Accessed May 30, 2022. https://www.medscape.com/viewarticle/974472 Monkeypox in Multiple Countries - Alert - Level 2, Practice Enhanced Precautions - Travel Health Notices. Centers for Disease Control and Prevention. Travelers' Health. Cdc.gov. Accessed May 30, 2022. https://wwwnc.cdc.gov/travel/notices/alert/monkeypox Monkeypox: public health advice for gay, bisexual and other men who have sex with men. World Health Organization. Who.int. Published May 25, 2022. Accessed May 30, 2022. https://www.who.int/news/item/25-05-2022-monkeypox--public-health-advice-for-gay--bisexual-and-other-men-who-have-sex-with-men Monkeypox Virus Infection in the United States and Other Non-endemic Countries – 2022. Centers for Disease Control and Prevention. HAN archive - 00466. Cdc.gov. Published May 20, 2022. Accessed May 30, 2022. https://emergency.cdc.gov/han/2022/han00466.asp Morgenstern J. Monkeypox. First10EM. Published May 19, 2022. Accessed May 30, 2022. https://first10em.com/monkeypox/ Rezaie S. Monkeypox…the basics. REBEL EM - Emergency Medicine Blog. Published May 26, 2022. Accessed May 30, 2022. https://rebelem.com/monkeypoxthe-basics/ Top Three Timesavers Heckerling PS, Tape TG, Wigton RS, et al. Clinical prediction rule for pulmonary infiltrates. Ann Intern Med. NIH National Library of Medicine: National Center for Biotechnology Information. PubMed.gov. Published November 1, 1990. Accessed May 30, 2022. https://pubmed.ncbi.nlm.nih.gov/2221647/ Mellick L. Ten Ways to Reduce a Dislocated Shoulder. Published August 13, 2015. Accessed May 30, 2022. https://www.youtube.com/watch?v=HtOnreM7heg Mellick L. The Davos Method of Shoulder Dislocation Reduction. Published May 2, 2016. Accessed May 30, 2022. https://www.youtube.com/watch?v=u2MsnjVNoPM UofSC Athletic Training. Spaso Technique for Glenohumeral Joint Reduction. Published October 11, 2020. Accessed May 30, 2022. https://www.youtube.com/watch?v=ei5Z62Whs1I Anaphylaxis? Roberts M, Sharma M. The 2 View. The Center for Medical Education. 14 - Urticaria, Foreign Bodies, and a Special Interview. 2 View: Emergency Medicine PAs & NPs. Published February 27, 2022. Accessed May 30, 2022. https://2view.fireside.fm/14 Tang AW. A Practical Guide to Anaphylaxis. Am Fam Physician. Published October 1, 2003. Accessed May 30, 2022. https://www.aafp.org/pubs/afp/issues/2003/1001/p1325.html Something Sweet Shoutouts to: Dr. Brendon Carmondy, who is the Assistant Director of the Emergency Department at Suburban Hospital in Maryland, and his entire team. Sierra Campus of the Hospitals of Providence in El Paso, TX, especially Dr. Madhu Achalla. 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!
The commonly seen diagnosis of Failure to Thrive is an easily preventable disease state but when ignored, it can lead to serious complications. Dr. Rebecca Yang and Dr. Kathryn McLeod joins medical student Sheenu Chirackel to discuss the evaluation and management for failure to thrive in childhood. Listen to this week's podcast to: Recognize common history and physical exam findings associated with Failure to Thrive Formulate a differential diagnosis for FTT Identify potential risk factors and causes for FTT Initiate appropriate therapy for FTT Special thanks to Dr. Rebecca Pierce for peer reviewing this episode FREE CME Credit (requires sign-in): https://mcg.cloud-cme.com/course/courseoverview?P=0&EID=10784 Thank you for listening to this episode from the Department of Pediatrics at the Medical College of Georgia. Remember that all content during this episode is intended for informational and educational purposes only. It should not be used as medical advice to diagnose or treat any particular patient. Clinical vignette cases presented are based on hypothetical patient scenarios. Thank you for your support! References: Berwick DM, Levy JC, Kleinerman R. Failure to thrive: diagnostic yield of hospitalisation. Arch Dis Child. 1982;57(5):347-351. doi:10.1136/adc.57.5.347 Bithoney WG, Van Sciver MM, Foster S, Corso S, Tentindo C. Parental stress and growth outcome in growth-deficient children. Pediatrics. 1995 Oct;96(4 Pt 1):707-11. PMID: 7567335. O'Brien LM, Heycock EG, Hanna M, Jones PW, Cox JL. Postnatal depression and faltering growth: a community study. Pediatrics. 2004 May;113(5):1242-7. doi: 10.1542/peds.113.5.1242. PMID: 15121936. Danner E, Joeckel R, Michalak S, Phillips S, Goday PS. Weight velocity in infants and children. Nutr Clin Pract. 2009 Feb-Mar;24(1):76-9. doi: 10.1177/0884533608329663. PMID: 19244151. Homan GJ. Failure to Thrive: A Practical Guide. Am Fam Physician. 2016 Aug 15;94(4):295-9. PMID: 27548594. Estrem HH, Pados BF, Park J, Knafl KA, Thoyre SM. Feeding problems in infancy and early childhood: evolutionary concept analysis. J Adv Nurs. 2017 Jan;73(1):56-70. doi: 10.1111/jan.13140. Epub 2016 Sep 23. PMID: 27601073. Larson-Nath, C., & Biank, V. F. (2016). Clinical review of failure to thrive in pediatric patients.Pediatric Annals, 45(2), e46-49. doi:http://dx.doi.org/10.3928/00904481-20160114-01 Cole, S. Z., & Lanham, J. S. (2011). Failure to thrive: An update. American Family Physician, 83(7), 829-834. Retrieved from https://www.proquest.com/scholarly-journals/failure-thrive-update/docview/2454417000/se-2?accountid=12365
Episode 90: Vaccines and Acne. Updates on pneumococcal and COVID-19 vaccines. Sarah explains the treatment of acne.New Pneumococcal Vaccine Recommendations. Written by Harkiran Bhattal, MS4, Ross University School of Medicine; Timiiye Yomi, MD; and Hector Arreaza, MD.During the recording, we used brand names because they are easier to use. We are not sponsored by the manufacturers of these vaccines. Terminology of pneumococcal vaccines: PCV13: Prevnar13®PPSV23: Pneumovax23®PCV15: Vaxneuvance® PCV20: Prevnar20®Tips about pneumococcal vaccines:-Prevnar13 is no longer used in adults. -Pneumovax23 is still being used in adults.-The two newer members of the pneumococcal vaccines are: Prevnar20® (PCV20) and Vaxneuvance® (PCV15). The following groups of patients are all adults 19-64 with underlying conditions OR >65 years old. Group A: Unknown or no prior doses of Prevnar13 or Pneumovax 23Option 1: Prevnar20 given as a single doseOption 2: Vaxneuvance followed by a dose of Pneumovax23 at least a year later (Consider >8 weeks in patients >19 at the highest risk)Group B: Previously received Pneumovax 23Give Prevnar20 or Vaxneuvance (at least 1 year since the last Pneumovax 23)Group C: Previously Received Prevnar13Give Pneumovax23 or Prevnar20 (if Pneumovax 23 is not available) >1 year since last dose of Prevnar13Group D: Previously completed series of Prevnar13 and Pneumovax23 in any orderNo additional doses are needed. Scenario 1: 68 yo M who has not previously received PCV or whose previous vaccination history is unknown (Group A). This patient should receive: 1 dose of Prevnar20 and be done, or Vaxneuvance followed by a dose of Pneumovax23. Scenario 2: 25 yo F with HIV not previously received PCV or whose vaccination history is unknown (Group A). This patient should receive: 1 dose of Prevnar20 and be done, or Vaxneuvance followed bya dose of Pneumovax 23 given 8 weeks later. This patient is in the highest risk group. Scenario 3: 50 yo M with chronic alcoholism who has not received any vaccine or unknown status (Group A). This patient should receive: 1 dose of Prevnar20 and be done, or Vaxneuvance followed by Pneumovax 23 one year later. Scenario 4: 43 yo M with previous Pneumovax 23 only (Group B). This patient should receive either: a single dose of Prevnar20 or Vaxneuvance and be done with either vaccine. Give either vaccine at least 1 year after Pneumovax 23. Scenario 5: 25 yo F with CSF leak and previously received Prevnar13 (Group C). This patient should receive Pneumovax23 or Prevnar 20 (if Pneumovax 23 is unavailable) at least one year after her las Pneumovax dose. Scenario 6: 35 yo M who previously completed Prevnar13 and Pneumovax in any order because he has a cochlear implant (Group D). This patient should NOT receive any additional dose. Research and MonitoringCDC and ACIP will continue to assess the safety of Vaxneuvance and Prevnar20 vaccines (the new kids on the block), monitor the impact of the implementation of new recommendations, and assess post-implementation effectiveness and recommendations as appropriate. Examples of risk factors to consider administration of pneumococcal vaccines: Chronic renal failure, HIV infection, alcoholism, cigarette smoking, chronic heart, liver, and lung disease. For a complete list of conditions, visit CDC.gov.___________________ A second booster shot of COVID-19 vaccines. By Hector Arreaza, MD.On March 29 and 30, 2022, CDC announced that a second booster dose of any mRNA COVID-19 vaccine may be given to certain individuals who are at risk of severe outcomes from COVID-19(1). Individuals who may choose to receive a second booster are: 1. People older than 12 years of age who have a moderate to severe immunocompromising condition. Remember, use Pfizer for older than 12 yo, and Moderna for older than 18 yo.2. People older than 50 years of age who are NOT moderately or severely immunocompromised.3. People 18-49 years of age who are NOT immunocompromised but received the J&J COVID-19 vaccine as both the primary and booster dose. When can you receive the second booster shot? At least 4 months after the first booster dose.Who is considered up to date? A person is considered up to date when he/she has received all recommended doses in their primary vaccine series, and a booster dose when eligible. A second booster dose is not required to be considered up to date at this time.Underlying medical conditions associated with higher risk for severe COVID-19 include: Cancer, obesity, cerebrovascular disease, diabetes mellitus, HIV, obesity, COPD, smokers, and chronic liver disease.Comment: Remember to give the second booster to your patients. ____________________Acne Treatment. By Sarah Park, MS3, University of California Los Angeles. Discussed with Hector Arreaza, MD. Definition: Acne vulgaris is a common inflammatory disorder of the pilosebaceous unit, which includes the hair follicle and sebaceous gland. It is characterized by chronic or recurrent development of papules, pustules, or nodules commonly on the face, chest, or upper back.(1,2) Acne affects nearly 50 million people in the U.S. per year and can cause significant psychological distress in those who are affected. It primarily begins at puberty when the production of androgens and/or sensitivity of androgen receptors increase, thereby commonly affecting adolescents and young adults.(2) Pathophysiology: The pathophysiology of acne involves four main processes: 1) sebum overproduction, 2) hyperkeratinization of the follicle, 3) bacterial colonization by Cutibacterium acnes, and 4) inflammation.(2,3) It can be classified as mild, moderate, or severe based on the extent and types of lesions.3Treatment: Treatment is selected based on the severity of the condition, patient preference, and tolerability. Acne treatment often requires long-term, consistent use of one or more medications.(3) The main objective of treatment is to decrease sebum production, get rid of extra keratin, treat infection and decrease inflammation. You can warn your patients that their skin may feel dryer and more scaly than usual, but that's part of the treatment. For mild and exclusively comedonal acne, topical retinoids like tretinoin are the treatment of choice(4), but topical retinoids can be used in any level of severity for maintenance. Examples: Adapelene, tazarotene, and tretinoin, For mild inflammatory papulopustular acne or mild mixed comedonal and papulopustular acne, topical retinoids may be used in combination with antimicrobial therapy (either combined with benzoyl peroxide or combined with benzoyl peroxide plus clindamycin or erythromycin). If patients cannot tolerate a topical retinoid, alternatives include salicylic acid and azelaic acid. Of note, oral or topical antibiotics should only be used in combination with benzoyl peroxide and retinoids for a maximum of 12 weeks. If unresponsive to these topical therapies, namely retinoids, benzoyl peroxide, and/or clindamycin, alternative therapies may be initiated. These include topical dapsone, minocycline, and clascosterone.Topical dapsone is an effective treatment for both inflammatory papulopustular and comedonal acne lesions. Topical minocycline is an alternative topical antibiotic used for specifically moderate to severe acne. And last but not least is topical clascosterone, a relatively new topical (specifically an androgen receptor inhibitor) approved by the FDA in 2020.(4)Treatment for moderate to severe acne: For moderate to severe acne vulgaris, management is systemic therapy. This includes oral antibiotics or hormonal therapies, often used in conjunction with topical therapy, or monotherapy with oral isotretinoin. 1. Oral antibiotics for acne vulgaris include doxycycline, minocycline, and sarecycline. Treatment should be limited to three to four months.(5)2. For female patients, hormonal therapy with oral contraceptives and/or spironolactone is also an option. A meta-analysis comparing oral contraceptive therapy and oral antibiotic therapy suggests similar efficacy for the treatment of acne. OCP treatment is often the first-line choice for hormonal therapy, especially for patients who desire the added benefit of contraception. Spironolactone is often used for patients who have contraindications to OCP therapy or prefer to avoid OCPs. Both methods work to inhibit acne by reducing the effects of androgen on the pilosebaceous unit.53. For severe, extensive, nodular acne vulgaris, oral isotretinoin is the drug of choice. It is given as a monotherapy and is often used when all other treatment modalities fail. Oral isotretinoin is the only medication that can permanently affect the natural course of acne by affecting all four factors in acne pathogenesis. Isotretinoin is most notably known for its teratogenic adverse effects and so is contraindicated in pregnant women and pregnancy must be avoided during therapy by using two forms of birth control.(5)Comment about isotretinoin use: Although prescribing isotretinoin (brand name Accutane®) is within the scope of family medicine, many providers choose not to prescribe it because of lack of training, monitoring hassles, fear of side effects, especially due to concerns with teratogenicity. Isotretinoin is an effective treatment for a condition that can not only disfigure and scar the face but can also cause significant psychosocial dysfunction. Dr. Van Durme recommended when you prescribe isotretinoin, you should have a regular schedule of monthly laboratory tests (including pregnancy test), then office visit, and then prescription, in that order. This schedule will improve the likelihood that side effects are managed promptly and medication is taken appropriately(7). If you would like more information about prescribing isotretinoin, visit https://ipledgeprogram.com.Conclusion: Use topical retinoids alone for mild cases of acne; topical retinoids combined with benzoyl peroxide or topical clindamycin or erythromycin for moderate cases; and topical retinoids combined with benzoyl peroxide and oral antibiotics in severe cases. Remember that isotretinoin is an oral treatment reserved for severe inflammatory papules and pustules with nodules. Treating acne effectively can certainly improve the quality of life of your patients. Now we conclude Episode 90 “Vaccines and Acne”. We gave you an update on pneumococcal and COVID-19 vaccines. Prevnar 20 seems to be the new star in the show. PCV15 is also useful but it needs to be followed by a shot of Pneumovax 23. Regarding COVID-19 vaccines, a second shot may be given to patients older than 12 who are immunocompromised or patients older than 50 who are NOT immunocompromised. Then we finished with a discussion about acne and we learned that topical is usually enough for mild cases, but oral therapy may be needed in moderate to severe cases of acne. Even without trying, every night you go to bed being a little wiser. Thanks for listening to Rio Bravo qWeek. Send us your feedback by email to RioBravoqWeek@clinicasierravista.org, or in 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, Timiiye Yomi, Amardeep Chetha and Sarah Park. Audio edition: Suraj Amrutia. See you next week! References:Kobayashi M, Farrar JL, Gierke R, et al. Use of 15-Valent Pneumococcal Conjugate Vaccine and 20-Valent Pneumococcal Conjugate Vaccine Among U.S. Adults: Updated Recommendations of the Advisory Committee on Immunization Practices — United States, 2022. MMWR Morb Mortal Wkly Rep 2022;71:109–117. DOI: http://dx.doi.org/10.15585/mmwr.mm7104a1 2. Pneumococcal Vaccination Timing for Adults, CDC. https://www.cdc.gov/vaccines/vpd/pneumo/downloads/pneumo-vaccine-timing.pdf, accessed on March 30, 2022. Interim Clinical Considerations for Use of COVID-19 Vaccines, Centers for Disease Control and Prevention, CDC.gov, https://www.cdc.gov/vaccines/covid-19/clinical-considerations/covid-19-vaccines-us.html#considerations-covid19-vax-booster, accessed April 5, 2022. Thiboutot, Diane, MD; and Andrea L Zaenglein, MD. Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris, UpToDate. Accessed on April 1, 2022. https://www.uptodate.com/contents/pathogenesis-clinical-manifestations-and-diagnosis-of-acne-vulgaris Leung AK, Barankin B, Lam JM, Leong KF, Hon KL. Dermatology: how to manage acne vulgaris. Drugs Context. 2021 Oct 11;10:2021-8-6. doi: 10.7573/dic.2021-8-6. PMID: 34691199; PMCID: PMC8510514. Oge' LK, Broussard A, Marshall MD. Acne Vulgaris: Diagnosis and Treatment. Am Fam Physician. 2019 Oct 15;100(8):475-484. PMID: 31613567. Graber, Emmy, MD, MBA. Acne vulgaris: Overview of management, UpToDate. Accessed on April 1, 2022. https://www.uptodate.com/contents/acne-vulgaris-overview-of-management Harris C. Clascoterone (Winlevi) for the Treatment of Acne. Am Fam Physician. 2021 Jul 1;104(1):93-94. PMID: 34264597. Acne vulgaris: Management of moderate to severe acne, UpToDate. Accessed on April 1, 2022. https://www.uptodate.com/contents/acne-vulgaris-management-of-moderate-to-severe-acne Van Durme DJ. Family physicians and accutane. Am Fam Physician. 2000 Oct 15;62(8):1772, 1774, 1777. PMID: 11057835. https://www.aafp.org/afp/2000/1015/p1772.html
Credits: 0.25 AMA PRA Category 1 Credit™ CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-266 Overview: ‘Tis the season for pediatric fevers! Join us to review a recent meta-analysis looking at 18 studies with patients younger than 2 years old who received acetaminophen or ibuprofen for fever or pain to determine if one medication should be recommended first, before the other. After this session, you'll be able to confidently advise parents of young children on how best to manage fever and/or pain at home with over-the-counter medications. Episode resource links: Long B, Gottlieb M. Ibuprofen vs. Acetaminophen for Fever or Pain in Children Younger Than Two Years. Am Fam Physician. 2022 Jan ;105(1):19. Wong T, Stang AS, Ganshorn H, Hartling L, Maconochie IK, Thomsen AM, Johnson DW. Combined and alternating paracetamol and ibuprofen therapy for febrile children. Evid Based Child Health. 2014 Sep;9(3):675-729. doi: 10.1002/ebch.1978. PMID: 25236309. Sullivan JE, Farrar HC. Fever and Antipyretic Use in Children. Pediatrics (2011) 127 (3): 580-587. (Reaffirmed 2016) Guest: Jillian Joseph, MSPAS, PA-C Music Credit: Richard Onorato
Credits: 0.25 AMA PRA Category 1 Credit™ CME/CE Information and Claim Credit: https://www.pri-med.com/online-education/podcast/frankly-speaking-cme-266 Overview: ‘Tis the season for pediatric fevers! Join us to review a recent meta-analysis looking at 18 studies with patients younger than 2 years old who received acetaminophen or ibuprofen for fever or pain to determine if one medication should be recommended first, before the other. After this session, you'll be able to confidently advise parents of young children on how best to manage fever and/or pain at home with over-the-counter medications. Episode resource links: Long B, Gottlieb M. Ibuprofen vs. Acetaminophen for Fever or Pain in Children Younger Than Two Years. Am Fam Physician. 2022 Jan ;105(1):19. Wong T, Stang AS, Ganshorn H, Hartling L, Maconochie IK, Thomsen AM, Johnson DW. Combined and alternating paracetamol and ibuprofen therapy for febrile children. Evid Based Child Health. 2014 Sep;9(3):675-729. doi: 10.1002/ebch.1978. PMID: 25236309. Sullivan JE, Farrar HC. Fever and Antipyretic Use in Children. Pediatrics (2011) 127 (3): 580-587. (Reaffirmed 2016) Guest: Jillian Joseph, MSPAS, PA-C Music Credit: Richard Onorato
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!