PEM Currents: The Pediatric Emergency Medicine Podcast

Brad Sobolewski, MD, MEd
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  • Medicine
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PEM Currents: The Pediatric Emergency Medicine Podcast is an evidence-based podcast focused on the care of ill and injured children in the Emergency Department. The host is Brad Sobolewski, MD, MEd author of PEMBlog.com and a Professor of Pediatric Emergency Medicine at Cincinnati Children’s and the University of Cincinnati.

  1. Aug 5

    Minor Procedures: Embedded Earrings

    Embedded earrings are a common pediatric emergency department presentation that can usually be managed quickly and safely without procedural sedation. This episode reviews why earrings become embedded, how to distinguish uncomplicated earlobe cases from higher-risk cartilage piercings, step-by-step removal techniques, pain control strategies, and appropriate wound care, antibiotics, and follow-up. Learning Objectives Recognize the evaluation and management of embedded earlobe earrings, including indications for local anesthesia, incision, and removal techniques. Differentiate uncomplicated earlobe piercings from cartilage piercings that require additional concern for perichondritis, Pseudomonas infection, and possible ENT consultation. Apply evidence-based post-procedure care, including appropriate wound management, antibiotic selection, and counseling to help prevent future embedded earrings. References Timm N, Iyer S. Embedded earrings in children. Pediatr Emerg Care. 2008;24(1):21-24. Muntz HR, Pa-C DJ, Asher BF. Embedded earrings: a complication of the ear-piercing gun. Int J Pediatr Otorhinolaryngol. 1990;19(1):73-76. Kim MM, Goldman RD. Ear-piercing complications in children and adolescents. Can Fam Physician. 2022;68(9):661-663. 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. Today, we’re continuing our new series on minor procedures. These are the procedures we perform all the time in pediatric emergency departments. They’re not the subject of giant multicenter trials or big keynote lectures, but they are the procedures that families remember. If you make them quick, comfortable, and maybe even a little less scary, families and patients will remember that. And if the procedure turns into a wrestling match with three people trying to hold down a screaming child while you’re searching for an earring backing, they’re gonna remember that too. Today’s topic is embedded earrings. A kid walks into the emergency department holding one ear. The earlobe is swollen and red, and the parent says, “I can’t find their earring.” It didn’t disappear. The ear basically swallowed it, and the parents almost always feel bad. They think they did something wrong or they waited too long. Honestly, this happens all the time. The first one can be a little intimidating because the hardware isn’t always where you expect it to be, but after you’ve removed a few of these, you’ll realize they’re actually pretty straightforward. Most can be managed right in the emergency department or a well-resourced urgent care. One of the best studies on the topic actually came from Cincinnati Children’s. Tim and Iyer reviewed over 100 children who presented to our emergency department with embedded earrings over about a four-and-a-half-year period. The median age was eight years, and about 60% of the children were younger than 10. That fits with most of our clinical experience. Younger children are more likely to sleep on new piercings, play with their earrings, forget the aftercare instructions, or simply not notice that the backing has become too tight. Nearly 90% of embedded earrings involve the earlobe rather than the cartilage, and in about two-thirds of patients, it wasn’t the decorative front of the earring that got stuck, it was the posterior backing or clasp. That’s helpful because I, um, almost always start looking on the back of the ear, ‘cause usually they’ve taken off the front. About one-third of children had evidence of a localized infection when they presented. Usually, that meant tenderness, erythema, swelling, and maybe a little purulent drainage or crusting around the piercing. Doesn’t necessarily mean they need oral or systemic antibiotics, but it does mean they shouldn’t wait another week hoping the earring somehow works itself out. So why does this happen? It’s really a pressure injury. The backing gets tightened against the earlobe, either because it was applied too snugly when the ears were pierced or because the ear swells afterward and suddenly there’s no room for the tissue to expand. That constant pressure decreases blood flow, produces local inflammation, and eventually the skin begins to grow around the earring hardware. Kids speed the whole process along by twisting the earrings, playing with them, sleeping on them, bumping them during play, and not cleaning the piercing consistently while it’s healing. One thing that probably contributes as well is the spring-loaded ear piercing gun. These devices place the earring and immediately snap on the backing, and sometimes that backing ends up much tighter than it should be. If swelling develops over the next day or so, the backing can quickly become buried beneath the skin. It’s one of the reasons I generally recommend families avoid piercing guns and instead use a method that leaves just a little room for post-procedure swelling. When these patients show up in the emergency department, they almost always complain of pain, swelling, redness, and tenderness around the piercing site. Sometimes there’s drainage. Sometimes the parent says they can’t unscrew the backing anymore. Sometimes they tell you they can feel the earring in the earlobe, but you can’t actually see it. Now, I’ll get to the procedure technique in just a minute. But before I start talking about that, I do wanna separate earlobe piercings from cartilage piercing, ‘cause they’re really different problems. Once cartilage is involved, the stakes go up considerably. Cartilage has relatively poor blood supply, making it much more susceptible to perichondritis, chondritis, cartilage necrosis, and permanent cosmetic deformity. The bacteria may be different as well. We’ll come back to that later. For now, though, let’s stay with the earlobe because, frankly, that’s where almost all of these procedures occur. All right. Before you start any procedure, you wanna have everything ready. So I’ll have local anesthetic, so lidocaine or lidocaine with epi. Epi is totally fine in the earlobe. At least two mosquito hemostats, stuff to grab the earring, an 11 blade, gauze, saline, and a good light source. I think if there’s any chance I’ll need to make a small incision, I’ll prep the ear before I do anything with, uh, betadine or chlorhexidine. Once the ear starts bleeding a little or the child starts moving around, everything gets just a little harder to see and grab. Absolutely bring your child life specialist if you’ve got them and someone to hold, like a medic or a PCA. One of the interesting things about the Cincinnati study is that none of the 100 children required procedural sedation. None. And honestly, that fits with my experience. The overwhelming majority of these can be managed with local anesthesia alone. For the earlobe, I usually perform a small field block using one percent lidocaine with epinephrine, using a twenty-seven or thirty-gauge needle. Epi is perfectly safe in the earlobe and gives you a little hemostasis while you’re working. One thing I probably do differently from some people is I actually wait for the anesthetic to work a little longer. I don’t just block and immediately start. I’ll wait at least five minutes. Honestly, it’s usually closer to seven to ten minutes. During that time, I’m talking with the family, keeping child life involved, making sure all my equipment is ready, and just letting everybody settle down a bit. Those extra few minutes make the whole procedure a lot easier. And again, this is pediatrics, so never underestimate distraction. You’ve got videos, music, you know, stuffed animal, a toy. Parents should be there holding the child’s hand. You gotta coach the parents as well. And sometimes that’s really all you need, a good block and some distraction. Of course, some kids do need more. For an anxious child, you can use intranasal midazolam or oral midazolam. If your department has nitrous oxide, this is a great procedure for it because it’s usually pretty quick. You’re often treating anxiety more than pain. I have used ketamine a handful of times, and not because something went wrong, but just because you have an extremely anxious child, and you’re not gonna accomplish the procedure safely any other way. First, figure out what you can see and what you can feel. Sometimes both the decorative front and backing are still visible, but the ear is simply too swollen to separate them normally. Those are the easy ones. I’d grab each side with a mosquito hemostat, disengage the backing from the post, and remove the earring. More commonly, the backing is buried beneath the skin. The decorative front may still be attached, or the parents may have already removed it and left the backing sitting in the earlobe. I’ll gently compress the earlobe from the front while looking at the back. That pressure tents the skin enough to expose a few millimeters of metal through the original piercing hole, and that may be all that I need to grab the backing and remove it. If you still can’t see it, keep palpating. Usually, I can feel the hardware through the swollen tissue. Once you localize it, I’ll make a tiny incision on the back of the earlobe directly over it. And when I say tiny, I mean tiny, like a couple millimeters, just enough to expose the metal. But don’t be afraid of making that incision. It’s honestly usually the difference between wrestling with the earring for ten minutes and having it out within sixty seconds. From there, the rest is pretty straightforward. Whether the front is buried, the backing is buried, or neither side is visible, I gen

  2. Jul 20

    Cyclospora

    Cyclospora is an uncommon but important cause of prolonged watery diarrhea in children, particularly during the summer months and during foodborne outbreaks. This episode reviews the epidemiology, clinical presentation, diagnostic pitfalls, treatment, and practical emergency department approach to recognizing and managing pediatric cyclosporiasis.   Learning Objectives Recognize the clinical features and epidemiology of Cyclospora cayetanensis infection in children, including when to suspect the diagnosis in patients with prolonged watery diarrhea. Select appropriate diagnostic testing for cyclosporiasis and identify the limitations of routine stool cultures, ova and parasite examinations, and gastrointestinal pathogen panels. Apply evidence-based treatment and supportive care for pediatric cyclospora infection, including appropriate antimicrobial therapy, hydration, and follow-up considerations. References Stobbe M. Outbreak of diarrhea-causing parasite grows to more than 1,000 cases. ABC News. Published July 8, 2026. Accessed July 10, 2026.   Bilung LM, Tahar AS, Yunos NE, et al. Detection of Cryptosporidium and Cyclospora oocysts from environmental water for drinking and recreational activities in Sarawak, Malaysia. Biomed Res Int. 2017;2017:4636420. doi:10.1155/2017/4636420.   Giangaspero A, Gasser RB. Human cyclosporiasis. Lancet Infect Dis. 2019;19(7):e226-e236. doi:10.1016/S1473-3099(18)30789-8.   Pyzocha N, Cuda A. Common intestinal parasites. Am Fam Physician. 2023;108(5):487-493.   Centers for Disease Control and Prevention. Clinical care of cyclosporiasis. Updated March 8, 2024. Accessed July 10, 2026.  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. It’s July and a seven-year-old comes into your emergency department with 10 days of watery diarrhea. They were seen earlier in the week and told it was probably viral gastroenteritis. Maybe they got a prescription for ondansetron, maybe they didn’t. Stool cultures have already come back negative. Mom tells you, “Every time I think he’s finally getting better, the explosive diarrhea comes right back.” So what’s going on? Today we’re talking about Cyclospora. Honestly, it’s one of those organisms that most of us forget about until summer rolls around, or since medical school. We don’t diagnose it every week, and depending on where you practice, you may go years without seeing a case. But then an outbreak happens, and maybe just a handful of sporadic cases show up, and suddenly you’re reminded that not every child with prolonged diarrhea has viral gastroenteritis. Cyclospora cayetanensis is a coccidian protozoan that’s transmitted through contaminated food or water. In the United States, it’s most commonly associated with imported fresh produce, things like cilantro, basil, lettuce, salad mixes, and berries. Unlike bacterial food poisoning, everyone at the picnic usually isn’t sick, so it often presents as an isolated illness because the exposure happened days earlier and may have involved only one particular food item. Families are often trying to remember the one thing that they ate that made everybody sick. Honestly, sometimes it’s simply the salad they bought at the grocery store a week ago. One thing that’s helped me remember these organisms over the years is that they each sort of develop their own personality. You know, it’s often confused with Giardia and Cryptosporidium. So if the diarrhea is greasy, think Giardia. If it’s profuse, watery diarrhea after swimming, think Cryptosporidium. If it’s prolonged, watery diarrhea during the summer, think Cyclospora. Now, obviously there are exceptions, but I think that’s a pretty useful framework, especially when you’re seeing patients one after another in a busy ED. One of my favorite pearls about Cyclospora, and I think it’s probably the one fact that’s most worth remembering because it explains how it sort of works. Unlike Giardia or Cryptosporidium, the oocysts that are passed in stool aren’t immediately infectious. They actually have to spend days to weeks out in the environment before they mature enough to infect somebody else. So Cyclospora isn’t really spread by the kids sitting next to them at daycare. It’s spread by the salad they both ate last week. I think that’s a lot easier to remember than trying to memorize the organism’s life cycle. The incubation period averages about seven to 10 days, so by the time symptoms begin, families usually don’t remember exactly what their kid ate. They’re certainly not connecting today’s diarrhea with the salad they had a week ago. The diarrhea itself is usually watery, sometimes pretty high volume, sometimes even explosive. One thing that’s a little deceptive is that it tends to wax and wane. Parents will tell you, “Yesterday I thought we had finally turned the corner,” and today they’re right back where they started. Along with the diarrhea, you’ll often see abdominal cramping, bloating, nausea, fatigue, maybe even a low-grade fever, and if this has been going on for a while, some weight loss or poor weight gain. Most of these kids don’t walk in looking critically ill. They walk in because they’re still having diarrhea when everyone expected them to be over it. That’s really the patient where Cyclospora should come to mind. And of course, not every child with prolonged diarrhea has it. Giardia is still incredibly common, especially after untreated water exposure, camping, or daycare. Again, those kids have greasy, foul-smelling stools with bloating and flatulence. Cryptosporidium is the swimming pool organism. Those oocysts are remarkably resistant to chlorine, so swimming pools, splash pads, and water parks should all get your attention. Those patients usually have profuse watery diarrhea, but in otherwise healthy children, it tends to run its course over a couple weeks. Cyclospora is different because it just hangs around. That’s really what makes me think about it. It’s not necessarily how sick the kid is, it’s that they’re still sick when they should actually be getting better. So aside from when you’re in the middle of an outbreak, when should you actually suspect it? It’s really when a few things start lining up. The diarrhea has lasted more than a week. Maybe it got a little better and then came back. The kid has lost some weight or looks a little dehydrated. It’s summertime. The bacterial stool studies are negative. Maybe there’s a history of travel. Maybe there isn’t. Maybe there’s a history of eating fresh produce. Maybe there isn’t. At some point, you have to stop saying, “Eh, it’s probably still viral,” and start asking yourself whether you’re dealing with something else. One teaching point that’s worth repeating, partly because it shows up on board exams and partly because it explains the epidemiology, is that Cyclospora isn’t spread directly from person to person. Fresh stool isn’t immediately infectious because those oocysts still have to sporulate in the environment before they can infect the next person. So let’s say you’re thinking about Cyclospora. What do you actually order? A routine stool culture isn’t gonna help you. Even a routine ova and parasite examination may not be enough. That’s an easy mistake to make because a lot of us were taught persistent diarrhea, send culture and O&P or a stool molecular pathogen panel. Many labs don’t specifically look for Cyclospora unless you ask them to or order it specifically. So there’s gastrointestinal PCRs for it, but you have to order them separately. So you can actually get back a negative O&P and feel reassured when in reality no one’s really tested for Cyclospora. If your hospital has a multiplex GI PCR panel that includes it, that’s probably what you should order first. If you don’t, you probably have to order it separately. Another board pearl. So if you’re taking a board exam and they describe a child with prolonged watery diarrhea during the summer, maybe after eating fresh produce, and then they casually mention that the routine ova and parasite examination was negative, don’t let that throw you off. That’s actually the clue. The organism may still be there, the lab just wasn’t sent to look for it. If your lab is using microscopy, Cyclospora can be identified with a modified acid-fast stain. The oocysts are a little larger than Cryptosporidium, and one interesting feature is that they stain variably. Some stain bright red, while others hardly stain at all, giving them that classic ghost organism appearance, which I think is just, like, cool. And because oocyst shedding is intermittent, collecting two or three stool specimens over several days can improve the diagnostic yield if you still have a high index of suspicion. The good news is that once you make the diagnosis, treatment is actually pretty straightforward. Trimethoprim-sulfamethoxazole remains the treatment of choice. In adult-sized patients, that means trimethoprim one hundred and sixty milligrams plus sulfamethoxazole eight hundred milligrams, just one double-strength tablet, orally twice a day for seven to ten days. For kids greater than two months of age to eighteen years, it’s eight to ten milligrams per kilogram trimethoprim and forty to fifty milligrams per kilogram sulfamethoxazole per day orally in two divided doses for seven to ten days. Most children begin feeling noticeably better within twenty-four to forty-eight hours. Honestly, this can be a pretty satisfying infection to treat because families have often been sea

  3. Jun 4

    Minor Procedures: Fishhook Removal

    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

  4. Apr 15

    Croup

    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 b

  5. Mar 2

    Migraines

    In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we take a structured, evidence-based approach to the acute treatment of migraine in children and adolescents. From confirming the diagnosis and screening for concerning features to optimizing outpatient therapy and executing a protocolized emergency department strategy, this episode walks through what works. We review the role of NSAIDs and triptans, clarify how IV fluids and ketorolac fit into care, and provide a stepwise framework for dopamine antagonists, valproate bridge therapy, DHE protocols, steroids, discharge planning, and admission decisions. Practical dosing, reassessment timing, and family-centered communication strategies are emphasized throughout. Learning Objectives Recognize the clinical features of pediatric migraine and distinguish it from secondary causes of headache. Implement a stepwise, evidence-based emergency department approach to acute pediatric migraine, including appropriate medication selection and timing of reassessment. Develop safe discharge and follow-up plans by defining treatment endpoints, minimizing medication overuse, and identifying patients who require referral or inpatient management. References 1. Oskoui M, Pringsheim T, Holler-Managan Y, et al. Practice Guideline Update Summary: Acute Treatment of Migraine in Children and Adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2019;93(11):487-499. doi:10.1212/WNL.0000000000008095. 2. Patterson-Gentile C, Szperka CL. The Changing Landscape of Pediatric Migraine Therapy: A Review. JAMA Neurology. 2018;75(7):881-887. doi:10.1001/jamaneurol.2018.0046. 3. Bachur RG, Monuteaux MC, Neuman MI. A Comparison of Acute Treatment Regimens for Migraine in the Emergency Department. Pediatrics. 2015;135(2):232-238. doi:10.1542/peds.2014-2432. 4. Ashina M. Migraine. The New England Journal of Medicine. 2020;383(19):1866-1876. doi:10.1056/NEJMra1915327. 5. Richer L, Billinghurst L, Linsdell MA, et al. Drugs for the Acute Treatment of Migraine in Children and Adolescents. The Cochrane Database of Systematic Reviews. 2016;4:CD005220. doi:10.1002/14651858.CD005220.pub2. Transcript This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered. And today we’re gonna talk about the acute treatment of migraine headache in children and adolescents. This is bread and butter for the PED, requires precise diagnosis and evidence-based treatment. We’re gonna talk about making that diagnosis, red flags, outpatient and ED treatment, as well as some second-line agents, admission decisions, and a whole lot more. So migraine in children is defined by three criteria, and at least five attacks lasting two to 72 hours. So you gotta have at least two of the following: pulsating or throbbing quality, moderate to severe intensity, aggravation by routine activity, and a unilateral location. Although in children, it’s often bilateral, plus at least one of nausea or vomiting and photophobia and/or phonophobia. In children headaches are frequently bilateral, bifrontal, bitemporal. The duration might be shorter than adults, especially in kids under second or third grade. And you may have to infer whether or not they have photophobia from their behavior. Like does the child close their eyes or wanna go into a dark room? In the emergency department, we’re often diagnosing based on pattern recognition plus exclusion of dangerous secondary causes. Or even more often than that, the patient comes in and says, I’ve got a migraine. Before I move on to treatments, let’s talk about some red flags where you might wanna pause and not just jump to migraine therapy. And the mnemonic SNOOP can be helpful here. And it stands for S for systemic symptoms such as fevers, myalgia, weight loss, or another S, secondary risk factors such as an immune deficiency, cancer, pregnancy, N for neurologic signs, papilledema, focal deficit, confusion, seizures. O onset sudden, or thunderclap. Migraines are often a little more gradual than that. The other O is older age, or technically younger age too, younger than five years or older than 50. Hopefully those patients are not coming into the pediatric emergency department. And then pattern changes, these new symptoms in a previously stable pattern. Don’t ignore that. And precipitants, you know, is it worse with Valsalva, position change, or under significant exertion? If these signs are present, you’ll probably wanna take a pause and just not throw migraine treatment at the patient. If they’re stable, MRI is the preferred imaging modality, but a very sick patient, it’d be okay to get a head CT. If you’ve got a normal neurologic exam, there’s no red flags. Again, you don’t need routine imaging for migraine headaches. So let’s talk about treatment. So hopefully patients have actually started to treat their headache before they arrive in the emergency department. If they haven’t, it’s a good idea to have some triage protocols in place. So ibuprofen, 7.5 to 10 milligrams per kilogram, 10 milligrams per kilogram is superior to placebo and it’s superior to acetaminophen at two hours. So that’s what we would use. Early treatment’s critical. So ideally within the first hour of onset. So that’s why triage protocols help. We’ll give kids 10 mg per kg of ibuprofen and like 30 ounces of Gatorade. Blue is often the first Gatorade choice, though that’s not an evidence-based statement. You can also use naproxen, but most of the studies are on ibuprofen. If NSAIDs fail, many adolescents and some older children will be prescribed triptans. The best evidence currently supports sumatriptan plus naproxen or zolmitriptan nasal spray. Rizatriptan is FDA approved down to age six. Adolescents respond to these agents better than younger children, and the route matters. The nasal formulations help when nausea is prominent. Families should be counseled to treat early, use weight-appropriate dosing, and avoid using acute medications more than 10 days per month. Often patients will have already taken an NSAID and a triptan before they get to the ED, and that’s where we get into the treatment of refractory migraine. Now this is most of the patients that I will see, and before we push medications, let’s briefly review ED treatment goals. You either want the patient headache free. Back to their baseline or mild descending pain. So a pain score of one to three. If you don’t reach one of those endpoints and it’s not agreed upon with the patient and their family, you’ve not completed treatments. You should do a reassessment within one hour after each intervention. And let’s face it, if you’re not reassessing within an hour and defining treatment goals, you’re not practicing protocolized migraine care. So in the emergency department, many of you may be familiar with the migraine cocktail. So what is that? In general, it’s a dopaminergic agent such as prochlorperazine or metoclopramide plus ketorolac, plus IV fluids. Let’s take a look at all three of those components and see if you can guess which one is actually the one that can abort the migraine. So fluids are commonly given in pediatric migraine, but they alone do not treat it. They’re helpful. Many patients have been throwing up or a bit dehydrated, but there are small randomized trials that show essentially no meaningful pain reduction in patients that get IV fluids alone. Well, what about ketorolac? Toradol, like that’s the first thing you give to a kid with a kidney stone, right? It does help, but it’s really adjunctive. So the main first-line agents for refractory or status migrainosus in the emergency department are the dopamine antagonists, and the first-line treatment for most patients is prochlorperazine or Compazine. The dose is 0.15 milligram per kilogram IV. The max is 10 milligrams. This is the backbone of ED migraine care. And why do they work? Well, migraines aren’t just some random vascular headache. This is an inherited disorder with central pain pathways gone awry. Dopamine plays a large role in that pain, nausea, hypersensitivity, amplification of symptoms and more that, frankly, I won’t get into this podcast because molecules hurt my head. The dopamine antagonists treat the headache, they reduce the nausea, and they just tamp down this process. Overall, the response rates approach 85%. Some studies have suggested that the response rate is about 77% at an hour and 90% at three hours. If you add the ketorolac and IV fluids, you get your response rate up to about 93 to 94%. These agents really do work well together. There have been randomized trials comparing IV prochlorperazine versus ketorolac. 85% of prochlorperazine patients achieved headache relief versus only 55% of ketorolac patients. So ketorolac helps, but really it’s the prochlorperazine. Metoclopramide, or Reglan, is used in a lot of centers as well. There are some smaller studies in children and adolescents that show that prochlorperazine is more effective, but if kids have an adverse reaction, more on that in a moment, or they prefer metoclopramide because they’ve responded to it in the past, it’s okay to go with it as well. Right. So what does it actually look like when you give the migraine cocktail to a patient? I think it’s important to explain to patients and families what to expect, and if this is a teenager, I’m talking to them directly. I mean, they’re getting the medication first and foremost. I tell them that the most effective way to treat their headache is

  6. Jan 29

    Psychogenic Nonepileptic Seizures (PNES)

    Psychogenic nonepileptic seizures (PNES) are common, often misunderstood, and increasingly encountered in pediatric emergency care. These events closely resemble epileptic seizures but arise from abnormal brain network functioning rather than epileptiform activity. In this episode of PEM Currents, we review the epidemiology, pathophysiology, and clinical features of PNES in children and adolescents, with a practical focus on Emergency Department recognition, diagnostic strategy, and management. Particular emphasis is placed on seizure semiology, avoiding iatrogenic harm, communicating the diagnosis compassionately, and understanding how early identification and referral to cognitive behavioral therapy can dramatically improve long-term outcomes. Learning Objectives Identify key epidemiologic trends, risk factors, and semiological features that help differentiate psychogenic nonepileptic seizures from epileptic seizures in pediatric patients presenting to the Emergency Department. Apply an evidence-based Emergency Department approach to the evaluation and initial management of suspected PNES, including strategies to avoid unnecessary escalation of care and medication exposure. Demonstrate effective, patient- and family-centered communication techniques for explaining the diagnosis of PNES and facilitating timely referral to appropriate outpatient therapy. References Sawchuk T, Buchhalter J, Senft B. Psychogenic Nonepileptic Seizures in Children-Prospective Validation of a Clinical Care Pathway & Risk Factors for Treatment Outcome. Epilepsy & Behavior. 2020;105:106971. (PMID: 32126506) Fredwall M, Terry D, Enciso L, et al. Outcomes of Children and Adolescents 1 Year After Being Seen in a Multidisciplinary Psychogenic Nonepileptic Seizures Clinic. Epilepsia. 2021;62(10):2528-2538. (PMID: 34339046) Sawchuk T, Buchhalter J. Psychogenic Nonepileptic Seizures in Children - Psychological Presentation, Treatment, and Short-Term Outcomes. Epilepsy & Behavior. 2015;52(Pt A):49-56. (PMID: 26409129) Labudda K, Frauenheim M, Miller I, et al. Outcome of CBT-based Multimodal Psychotherapy in Patients With Psychogenic Nonepileptic Seizures: A Prospective Naturalistic Study. Epilepsy & Behavior. 2020;106:107029. (PMID: 32213454) Transcript This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered. Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we are talking about psychogenic non-epileptic seizures, or PNES. Now, this is a diagnosis that often creates a lot of uncertainty in the Emergency Department. These episodes can be very scary for families and caregivers and schools. And if we mishandle the diagnosis, it can lead to unnecessary testing, medication exposure, ICU admissions, and long-term harm. This episode’s gonna focus on how to recognize PNES in pediatric patients, how we make the diagnosis, what the evidence says about management and outcomes, and how what we do and what we say in the Emergency Department directly affects patients, families, and prognosis. Psychogenic non-epileptic seizures are paroxysmal events that resemble epileptic seizures but occur without epileptiform EEG activity. They’re now best understood as a subtype of functional neurological symptom disorder, specifically functional or dissociative seizures. Historically, these events were commonly referred to as pseudo-seizures, and that term still comes up frequently in the ED, in documentation, and sometimes from families themselves. The problem is that pseudo implies false, fake, or voluntary, and that implication is incorrect and harmful. These episodes are real, involuntary, and distressing, even though they’re not epileptic. Preferred terminology includes psychogenic non-epileptic seizures, or PNES, functional seizures, or dissociative seizures. And PNES is not a diagnosis of exclusion, and it does not require identification of psychological trauma or psychiatric disease. The diagnosis is based on positive clinical features, ideally supported by video-EEG, and management begins with clear, compassionate communication. The overall incidence of PNES shows a clear increase over time, particularly from the late 1990s through the mid-2010s. This probably reflects improved recognition and access to diagnostic services, though a true increase in occurrence can’t be excluded. Comorbidity with epilepsy is really common and clinically important. Fourteen to forty-six percent of pediatric patients with PNES also have epilepsy, which frequently complicates diagnosis and contributes to diagnostic delay. Teenagers account for the highest proportion of patients with PNES, especially 15- to 19-year-olds. Surprisingly, kids under six are about one fourth of all cases, so it’s not just teenagers. We often make the diagnosis of PNES in epilepsy monitoring units. So among children undergoing video-EEG, about 15 to 19 percent may ultimately be diagnosed with PNES. And paroxysmal non-epileptic events in tertiary epilepsy monitoring units account for about 15 percent of all monitored patients. Okay, but what is PNES? Well, it’s best understood as a disorder of abnormal brain network functioning. It’s not structural disease. The core mechanisms at play include altered attention and expectation, impaired integration of motor control and awareness, and dissociation during events. So the patients are not necessarily aware that this is happening. Psychological and psychosocial features are common but not required for diagnosis and may be less prevalent in pediatric populations as compared with adults. So PNES is a brain-based disorder. It’s not conscious behavior, it’s not malingering, and it’s not under voluntary control. Children and adolescents with PNES have much higher rates of psychiatric comorbidities and psychosocial stressors compared to both healthy controls and children with epilepsy alone. Psychiatric disorders are present in about 40 percent of pediatric PNES patients, both before and after the diagnosis. Anxiety is seen in 58 percent, depression in 31 percent, and ADHD in 35 percent. Compared to kids with epilepsy, the risk of psychiatric disorders in PNES is nearly double. Compared to healthy controls, it is up to eight times higher. And there’s a distinct somatopsychiatric profile that strongly predicts diagnosis of PNES. This includes multiple medical complaints, psychiatric symptoms, high anxiety sensitivity, and solitary emotional coping. This profile, if you’ve got all four of them, carries an odds ratio of 15 for PNES. Comorbid epilepsy occurs in 14 to 23 percent of pediatric PNES cases, and it’s associated with intellectual disability and prolonged diagnostic delay. And finally, across all demographic strata, anxiety is the most consistent predictor of PNES. Making the diagnosis is really hard. It really depends on a careful history and detailed analysis of the events. There’s no single feature that helps us make the diagnosis. So some of the features of the spells or events that have high specificity for PNES include long duration, so typically greater than three minutes, fluctuating or asynchronous limb movements, pelvic thrusting or side-to-side head movements, ictal eye closure, often with resisted eyelid opening, ictal crying or vocalization, recall of ictal events, and rare association with injury. Younger children often present with unresponsiveness. Adolescents more commonly demonstrate prominent motor symptoms. In pediatric cohorts, we most frequently see rhythmic motor activity in about 27 percent, and complex motor movements and dialeptic events in approximately 18 percent each. Features that argue against PNES include sustained cyanosis with hypoxia, true lateral tongue biting, stereotyped events that are identical each time, clear postictal confusion or lethargy, and obviously epileptic EEG changes during the events themselves. Now there are some additional historical and contextual clues that can help us make the diagnosis as well. If the events occur in the presence of others, if they occur during stressful situations, if there are psychosocial stressors or trauma history, a lack of response to antiepileptic drugs, or the absence of postictal confusion, this may suggest PNES. Lower socioeconomic status, Medicaid insurance, homelessness, and substance use are also associated with PNES risk. While some of these features increase suspicion, again, video-EEG remains the diagnostic gold standard. We do not have video-EEG in the ED. But during monitoring, typical events are ideally captured and epileptiform activity is not seen on the EEG recording. Video-EEG is not feasible for every single diagnosis. You can make a probable PNES diagnosis with a very accurate clinical history, a vivid description of the signs and appearance of the events, and reassuring interictal EEG findings. Normal labs and normal imaging do not make the diagnosis. Psychiatric comorbidities are not required. The diagnosis, again, rests on positive clinical features. If the patient can’t be placed on video-EEG in a monitoring unit, and if they have an EEG in between events and it’s normal, that can be supportive as well. So what if you have a patient with PNES in the Emergency Department? Step one, stabilize airway, breathing, circulation. Take care of the patient in front of you and keep them safe. Use seizure pads and precautions and keep them from falling off the bed or accidentally injuring themselves. A family member or another team member can help with this. Avoid reflexively escalating. If you are witnessing a PNES event in front of you, and if they’re protecting

  7. 12/16/2025

    Osteomyelitis

    Osteomyelitis in children is common enough to miss and serious enough to matter. In this episode of PEM Currents, we review a practical, evidence-based approach to pediatric acute hematogenous osteomyelitis, focusing on diagnostic strategy, imaging decisions including FAST MRI, and modern antibiotic management. Topics include age-based microbiology, empiric and pathogen-directed antibiotic selection with dosing, criteria for early transition to oral therapy, and indications for orthopedic and infectious diseases consultation. Special considerations such as MRSA, Kingella kingae, daycare clustering, and shortened treatment durations are discussed with an emphasis on safe, high-value care. Learning Objectives After listening to this episode, learners will be able to: Identify the key clinical, laboratory, and imaging findings that support the diagnosis of acute hematogenous osteomyelitis in children, including indications for FAST MRI and contrast-enhanced MRI. Select and dose appropriate empiric and pathogen-directed antibiotic regimens for pediatric osteomyelitis based on patient age, illness severity, and local MRSA prevalence, and determine when early transition to oral therapy is appropriate. Determine when consultation with orthopedics and infectious diseases is indicated, and recognize clinical features that warrant prolonged therapy or more conservative management. References Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2021 guideline on diagnosis and management of acute hematogenous osteomyelitis in pediatrics. J Pediatric Infect Dis Soc. 2021;10(8):801-844. doi:10.1093/jpids/piab027 Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2023 guideline on diagnosis and management of acute bacterial arthritis in pediatrics. J Pediatric Infect Dis Soc. 2024;13(1):1-59. doi:10.1093/jpids/piad089 Stephan AM, Platt S, Levine DA, et al. A novel risk score to guide the evaluation of acute hematogenous osteomyelitis in children. Pediatrics. 2024;153(1):e2023063153. doi:10.1542/peds.2023-063153 Alhinai Z, Elahi M, Park S, et al. Prediction of adverse outcomes in pediatric acute hematogenous osteomyelitis. Clin Infect Dis. 2020;71(9):e454-e464. doi:10.1093/cid/ciaa211 Burns JD, Upasani VV, Bastrom TP, et al. Age and C-reactive protein associated with improved tissue pathogen identification in children with blood culture-negative osteomyelitis: results from the CORTICES multicenter database. J Pediatr Orthop. 2023;43(8):e603-e607. doi:10.1097/BPO.0000000000002448 Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352-360. doi:10.1056/NEJMra1213956 Transcript This transcript was provided via use of the Descript AI application Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re covering osteomyelitis in children. We’re going to talk about diagnosis and imaging, and then spend most of our time where practice variation still exists: antibiotic selection, dosing, duration, and the evidence supporting early transition to oral therapy. We’ll also talk about when to involve orthopedics, infectious diseases, and whether daycare outbreaks of osteomyelitis are actually a thing. So what do I mean by pediatric osteomyelitis? In children, osteomyelitis is most commonly acute hematogenous osteomyelitis. That means bacteria seed the bone via the bloodstream. The metaphysis of long bones is particularly vulnerable due to vascular anatomy that favors bacterial deposition. Age matters. In neonates, transphyseal vessels allow infection to cross into joints, increasing the risk of concomitant septic arthritis. In older children, those vessels involute, and infection tends to remain metaphyseal and confined to bone rather than spreading into the joint. For children three months of age and older, empiric therapy must primarily cover Staphylococcus aureus, which remains the dominant pathogen. Other common organisms include group A streptococcus and Streptococcus pneumoniae. In children six to 36 months of age, especially those in daycare, Kingella kingae is an important and often underrecognized pathogen. Kingella infections are typically milder, may present with lower inflammatory markers, and frequently yield negative routine cultures. Kingella is usually susceptible to beta-lactams like cefazolin, but is consistently resistant to vancomycin and often resistant to clindamycin and antistaphylococcal penicillins. This has direct implications for empiric antibiotic selection. Common clinical features of osteomyelitis include fever, localized bone pain, refusal to bear weight, and pain with movement of an adjacent joint. Fever may be absent early, particularly with less virulent organisms like Kingella. A normal white blood cell count does not exclude osteomyelitis. Only about one-third of children present with leukocytosis. CRP and ESR are generally more useful, particularly CRP for monitoring response to therapy. No single CRP cutoff reliably diagnoses or excludes osteomyelitis in children. While CRP is elevated in most cases of acute hematogenous osteomyelitis, the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America note that high-quality data defining diagnostic thresholds are limited. A CRP above 20 milligrams per liter is commonly used to support clinical suspicion, with pooled sensitivity estimates around 80 to 85 percent, but no definitive value mandates the diagnosis. Lower values do not exclude disease, particularly in young children, as CRP is normal in up to 40 percent of Kingella kingae infections. CRP values tend to be higher in Staphylococcus aureus infections, especially MRSA, and higher levels are associated with complications such as abscess, bacteremia, and thrombosis, though specific cutoffs are not absolute. In summary, CRP is most useful for monitoring treatment response. It typically peaks two to four days after therapy initiation and declines rapidly with effective treatment, with a 50 percent reduction within four days seen in the majority of uncomplicated cases. Blood cultures should be obtained in all children with suspected osteomyelitis, ideally before starting antibiotics when feasible. In children, blood cultures alone can sometimes identify the pathogen. Plain radiographs are still recommended early, not because they’re sensitive for acute osteomyelitis, but because they help exclude fracture, malignancy, or foreign body and establish a baseline. MRI with and without contrast is the preferred advanced imaging modality. MRI confirms the diagnosis, defines the extent of disease, and identifies complications such as subperiosteal abscess, physeal involvement, and concomitant septic arthritis. MRI findings can also guide the need for surgical consultation. Many pediatric centers now use FAST MRI protocols for suspected osteomyelitis, particularly from the emergency department. FAST MRI uses a limited sequence set, typically fluid-sensitive sequences like STIR or T2 with fat suppression, without contrast. These studies significantly reduce scan time, often avoid the need for sedation, and retain high sensitivity for bone marrow edema and soft tissue inflammation. FAST MRI is particularly useful when the clinical question is binary: is there osteomyelitis or not? It’s most appropriate in stable children without high concern for abscess, multifocal disease, or surgical complications. If FAST MRI is positive, a full contrast-enhanced MRI may still be needed to delineate abscesses, growth plate involvement, or adjacent septic arthritis. If FAST MRI is negative but clinical suspicion remains high, further imaging may still be necessary. The Pediatric Infectious Diseases Society and the Infectious Diseases Society of America recommend empiric antibiotic selection based on regional MRSA prevalence, patient age, and illness severity, with definitive therapy guided by culture results and susceptibilities. Empiric therapy should never be delayed in an ill-appearing or septic child. In well-appearing, stable children, antibiotics may be briefly delayed to obtain imaging or tissue sampling, but this requires close inpatient observation. For children three months and older with non–life-threatening disease, empiric therapy hinges on local MRSA rates. In regions with low community-acquired MRSA prevalence, generally under 10 percent, reasonable empiric options include cefazolin, oxacillin, or nafcillin. When MRSA prevalence exceeds 10 to 20 percent, empiric therapy should include an MRSA-active agent. Clindamycin is appropriate when local resistance rates are low, while vancomycin is preferred when clindamycin resistance is common or the child has had significant healthcare exposure. For children with severe disease or sepsis, vancomycin is generally preferred regardless of local MRSA prevalence. Some experts recommend combining vancomycin with oxacillin or nafcillin to ensure optimal coverage for MSSA, group A streptococcus, and MRSA. In toxin-mediated or high-inoculum infections, the addition of clindamycin may be beneficial due to protein synthesis inhibition. Typical IV dosing includes cefazolin 100 to 150 milligrams per kilogram per day divided every eight hours; oxacillin or nafcillin 150 to 200 milligrams per kilogram per day divided every six hours; clindamycin 30 to 40 milligrams per kilogram per day divided every six to eight hours; and vancomycin 15 milligrams per kilogram every six hours for serious infections, with appropriate monitoring. Ceftaroline or daptomycin may be considered in select MRSA cases when first-line agents are unsuitable. For methicillin-susceptible Staphyloco

  8. 11/17/2025

    Night Terrors

    Night terrors are dramatic but benign episodes that can leave caregivers frightened and confused. In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the clinical features of night terrors, how to differentiate them from other nocturnal events, and when to consider further evaluation such as polysomnography. We also discuss management strategies that center on sleep hygiene, reassurance, and safety, with a special look at the role of scheduled awakenings and when medication is appropriate. Learning Objectives By the end of this episode, listeners will be able to: Describe the typical clinical presentation and age range of children with night terrors. Differentiate night terrors from other parasomnias and nocturnal seizures based on clinical features and timing. Discuss non-pharmacologic and pharmacologic management strategies for night terrors, including when to consider polysomnography. References Petit D, Touchette E, Tremblay RE, et al. Dyssomnias and parasomnias in early childhood. Pediatrics. 2007;119(5):e1016-e1025. Morse AM, Kotagal S. Parasomnias of childhood, including sleepwalking. In: Chervin RD, ed. UpToDate. Hoppin AG, deputy ed. Waltham, MA. Accessed November 2025. Van Horn NL, Street M. Night Terrors. Updated May 29, 2023. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2025 Jan–. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493222/ Transcript This transcript was provided via use of the Descript AI application Welcome to PEM Currents, The Pediatric Emergency Medicine Podcast. As always, I'm your host Brad Sobolewski. In this episode, we're talking about night terrors, also known as sleep terrors. A dramatic, confusing, and often terrifying experience for caregivers to witness. But they're usually benign and self-limited for the child. Kind of like a lot of the things in childhood actually, what are we gonna talk about? Well, what are night terrors? How do we diagnose them? How to differentiate them from seizures or other parasomnias key counseling for parents in the emergency department, when to refer for sleep studies or neurology evaluation, and what role, if any, medications play. So let's start with talking about what night terrors actually look like. They're part of a group of disorders called non REM parasomnias, which also includes sleepwalking and confusion arousals. They are not nightmares and they are not signs of psychological trauma. Children experiencing night terrors typically sit up suddenly during sleep, scream, cry or appear terrified. Show signs of autonomic arousal. So rapid breathing, tachycardia, sweating. They're confused or inconsolable for several minutes and they have absolutely no recollection of the event the next morning. These events usually occur in the first third of the night when children are in deep, slow wave sleep, so stage N three, and they can last five to 15 minutes, but trust me, they seem to last much longer to observers. Night terrors occur most commonly between ages three and seven with a peak around five years of age. They're rare before 18 months and unusual after age 12. Preschool aged children are most affected because they spend more time in deep, slow wave sleep. They have more fragmented sleep architecture, and they may not have fully developed arousal regulation mechanisms. Episodes can start as early as toddlerhood, especially if the child has a family history of parasomnias. So like sleep, walking night terrors or other things, sleep deprivation or stressful life events like starting daycare or a new sibling or a move, although less common, older children and even adolescents can experience night terrors, especially in the context of stress, sleep deprivation or comorbid sleep disorders like sleep apnea. Why do they happen? Well, they're usually due to incomplete arousal from deep sleep, so the brain is essentially stuck between sleep and wakefulness. Factors that increase the risk of frequency of night terrors include again, sleep deprivation, recent illness, stress, or anxiety. Sleep disordered breathing, or a family history of parasomnias, there's a real strong genetic component. Up to 80% of children with night terrors have a first degree relative with similar episodes. The diagnosis is entirely clinical and based on history. You should ask parents, what time of night did these episodes occur? Is the child confused, frightened, or hard to wake? Is there amnesia the next day so they don't remember the event? And are the movements variable or stereotyped? Sometimes parents will video record these, and that can really help us clarify the episodes when we're in the emergency department. You definitely do not need labs or imaging in a typical presentation. I think parents are often seeking an explanation for why their child looks so freaky. In my experience, just telling them that it's a night terror and that it's benign and providing reassurance on how healthy their kid is, is more than enough. Now, not all nighttime events are sleep terrors. You should consider neurology referral and video polysomnography or sleep studies with extended EEG when onset is very early, so younger than 18 months or late in childhood. So older than 12 or 13 episodes occur outside of the first third of the night. Again, find out when the kid went to bed. And do math. The first third of the night is the first 33% of their typical sleep time. The events are brief clustered or stereotyped. The movements are repetitive, focal or violent. If kid just moving just their right arm. That's not a night terror. Often the movements will look fearful and they'll be sort of disorganized. Rhythmic movements don't typically happen in night terrors, and there's a recent injury. The child has excessive daytime sleepiness, or there's some developmental regression or abnormality. All those are red flags. Differentiating from nocturnal frontal lobe epilepsy can be tricky. Nocturnal frontal lobe epilepsy events are usually short. Highly stereotyped. They have abrupt onset and offset, and they may include dystonic or tonic posturing. So if the family has a video of this, that can be really helpful using a good clinical history. Video recordings in EEG generally distinguish night terrors from these forms of epilepsy. But let's be honest, most of the kids you see in the ED with a typical presentation of night terrors are just night terrors. These events are really scary and we are gonna see them in the emergency departments, and so your first goal is to just reassure the family. The events are not harmful. The kid isn't aware that they had them, and the child suffers no ongoing psychological harm. That doesn't mean that the parent isn't freaked out or that nervousness doesn't linger. You wanna avoid sleep deprivation If possible, counsel families on age appropriate bedtimes and naps. Stick to a routine consistent bedtime routines. Reduce sleep fragmentation, which is a known risk factor for children with frequent or predictable night terrors. Try waking them 15 to 30 minutes before the usual episode happens. So I've seen lots of kids with frequent night terrors, and they usually happen around the same time at night. And you wanna do this, this 15 to 30 minute awakening before the usual episodes each night for about two to four weeks. That's labor intensive as a parent, but it can help these awakenings interrupt the sleep cycle and break the pattern. Keep kids safe. Use baby gates, door alarms. Make sure windows are locked, don't put younger kids in bunk beds and remove sharp obstacles or objects near the bed. So if they've got a pointy ended nightstand, oh, that's just something for the kid to fall into or smack against. Do we ever use medications for night terrors? Well, almost never. You know, pharmacologic therapy such as low dose benzodiazepines or tricyclic antidepressants is really only reserved for severe episodes. Kids with substantial risk for injury or disruption of the family life or school in a substantial way. I'm not gonna make that call in the emergency department. And these are sleep specialist referral guided therapies. You also wanna consider evaluating children for comorbid sleep disorders, especially in recurrent night terrors, like obstructive sleep apnea, restless leg syndrome. This may worsen the parasomnias. For kids in which you're unsure, polysomnography can be used. This is an overnight sleep study that monitors brainwaves via EEG, eye movements, muscle activity, heart rhythm, breathing effort, and airflow and oxygen saturation. But it's also done in a hospital and not during the kid's usual sleep routine. So most children that have night terrors, if you get the right history, you can make the diagnosis clinically and the kids don't need any expensive or expanded testing to get to the bottom of things. Alright, take home points for this brief episode. Night terrors are common, especially in preschool aged children. They occur in non REM sleep in the first third of the night. The episodes are very dramatic, but they're benign and children don't remember them. But trust me, parents do. The diagnosis is clinical. No labs or imaging are needed unless there's atypical features. You should reassure families, promote sleep hygiene and use scheduled awakenings for frequent and recurrent cases, and refer for sleep studies and or neurology of episodes or violent stereotyped, or suggest nocturnal seizures. Thanks for listening to this episode. I hope you found it educational about a topic that you will encounter in the emergency department. As with many things in children that are scary, there's a benign explanation and parents are just looking to know that their kid's gonna be okay. Often doing a thorough history in physical and really listening to the parents' concerns and then providing useful information is all you gotta do. That's why pediatrics is great. If you've got f

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PEM Currents: The Pediatric Emergency Medicine Podcast is an evidence-based podcast focused on the care of ill and injured children in the Emergency Department. The host is Brad Sobolewski, MD, MEd author of PEMBlog.com and a Professor of Pediatric Emergency Medicine at Cincinnati Children’s and the University of Cincinnati.

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