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Iron poisoning can be deceptive. Early symptoms can look like routine gastroenteritis, children may appear to improve during a latent phase, and significant toxicity can progress to metabolic acidosis, shock, and hepatic injury. In this episode of PEM Currents, we review the recognition and management of pediatric iron toxicity, including when to obtain a serum iron level, the role of abdominal radiographs and whole bowel irrigation, indications for deferoxamine, and disposition. Learning Objectives After listening to this episode, learners should be able to: Recognize the clinical stages of pediatric iron toxicity and identify features concerning for significant systemic toxicity. Use the estimated elemental iron dose, serum iron concentration, and abdominal radiography to evaluate a child with a suspected iron ingestion. Describe the emergency management of iron toxicity, including supportive care, whole bowel irrigation, indications for deferoxamine, and appropriate disposition. References Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-570. Halil H, Tuygun N, Polat E, Karacan CD. Minimum ingested iron cut-off triggering serious iron toxicity in children. Pediatr Int. 2019;61(5):444-448. Klein-Schwartz W, Oderda GM, Gorman RL, Favin F, Rose SR. Assessment of management guidelines: acute iron ingestion. Clin Pediatr (Phila). 1990;29(6):316-321. Banner W Jr, Tong TG. Iron poisoning. Pediatr Clin North Am. 1986;33(2):393-409. Script This is the original script for the episode, written by Drs. Robbie Daulton and Brad Sobolewski 1. Why Iron Matters Iron is one of the most dangerous toxic ingestions we see in young children. It’s found in prenatal vitamin and iron supplements, and the small, often candy-like tablets make exploratory toddler ingestions particularly concerning. Historically, iron was a leading cause of death from unintentional pediatric drug ingestion. What makes iron especially important in the ED is that early toxicity can look just like gastroenteritis, with vomiting, diarrhea, and abdominal pain. If you’re not thinking about an ingestion, it can be easy to miss. 2. How Kids Present: The Five Stages Iron follows a staged, sometimes deceptive, clinical course, although not every child progresses through every stage. Stage one begins 30 minutes to six hours after ingestion with vomiting, diarrhea, abdominal pain, and sometimes GI bleeding from direct mucosal injury. This is the stage that can easily be mistaken for gastroenteritis. Stage two, from about six to 24 hours, is the trap. GI symptoms may improve and the child may appear better, even as systemic toxicity progresses. Stage three, typically 12 to 24 hours after ingestion, is characterized by shock and metabolic acidosis. Children may be hypotensive, tachycardic, lethargic, and poorly perfused. Stages four and five occur later. Hepatic failure can develop over the next several days, while GI strictures and obstruction can occur weeks later. The pattern to remember is early GI symptoms, apparent improvement, and then unexplained shock and metabolic acidosis. That should make you think about iron toxicity even if the ingestion wasn’t clear from the history. 3. Pharmacology Pearls Iron causes toxicity in two ways. First it directly injuries the GI mucosa, causing the early vomiting, diarrhea, abdominal pain. Once absorbed, free iron overwhelms the body’s binding capacity (specifically ferritin and transferrin) and causes cellular and mitochondrial injury, contributing to metabolic acidosis, vasodilation, and shock. Serum iron typically peaks two to six hours post-ingestion, which is why the serum iron concentration should be measured four to six hours after ingestion. With enteric-coated or extended-release preparations, absorption can be delayed, so a repeat level may be necessary. 4. Working It Up and Treating It Start with the basics: ABCs, early IV or IO access, and aggressive treatment of shock. These children may need significant fluid resuscitation and vasoactive support. The most useful diagnostic test is a serum iron level drawn four to six hours after ingestion. Under 350 micrograms per deciliter is associated with minimal toxicity, 350 to 500 with mild to moderate toxicity, above 500 with serious systemic toxicity, and above 1,000 with severe toxicity and increased risk of mortality. But treatment decisions should be based on the entire clinical picture, not just the iron level. Check electrolytes, an anion gap, blood gas, lactate, liver enzymes, and coagulation studies to assess the severity of systemic toxicity. An abdominal X-ray can be helpful because many iron tablets are radiopaque. A positive film confirms tablets are present and can help guide decontamination, but a negative X-ray does not exclude an iron ingestion. Like all other periodic table elements, activated charcoal does not bind iron. If tablets are visible on imaging, whole bowel irrigation should be considered. For serious toxicity, including shock, metabolic acidosis, altered mental status, or a serum iron level above 500, consider IV deferoxamine. Hypotension can occur with rapid administration, so make sure the child has adequate volume resuscitation. Most importantly, treat the patient, not the iron level. Aggressively resuscitate shock, reassess frequently, and involve Poison Control early for any child with significant symptoms or a potentially toxic ingestion. 5. Who Goes Home, Who Gets Admitted For disposition, start with the estimated elemental iron dose, not the total tablet or iron salt weight. Less than 20 milligrams per kilogram is generally low risk, while 40 milligrams per kilogram or more should raise concern for significant toxicity. Newer pediatric data suggest serious toxicity may occur at lower doses, but the reported dose is imperfect, so symptoms and the serum iron concentration matter more than any single cutoff. Pay attention to what was actually ingested. Prenatal vitamins often contain substantial amounts of elemental iron, commonly around 27 to 65 milligrams per tablet, while multivitamins often contain little or no iron. A toddler can therefore reach a toxic dose with only a handful of prenatal vitamins. An asymptomatic child more than six hours after a low-risk ingestion with a reassuring serum iron level can typically go home. Children with significant symptoms or ongoing fluid requirements should be admitted. Hemodynamic instability or the need for deferoxamine warrants ICU-level care. Discuss significant ingestions with Poison Control. After significant toxicity, counsel families that GI strictures can develop weeks later and present with recurrent vomiting or obstruction. 6. Three Take-Homes Iron poisoning is deceptive. Early vomiting and diarrhea can look like gastroenteritis, and apparent improvement during the latent phase does not mean the child is in the clear. Obtain a serum iron level four to six hours post-ingestion. It’s your most useful test, but interpret it alongside the clinical picture. Activated charcoal does not bind iron. Consider whole bowel irrigation when tablets are visible on imaging, and treat serious toxicity, including shock, metabolic acidosis, altered mental status, or an iron level above 500, with aggressive supportive care and deferoxamine.

In children with septic shock, does the choice between balanced crystalloids and 0.9% saline actually matter? This episode reviews the composition and physiologic differences between commonly used crystalloids, summarizes the 2026 PRoMPT BOLUS trial, and discusses how its findings fit with the updated Surviving Sepsis Campaign pediatric guidelines. We also consider the trial’s limitations and what the results mean for fluid selection at the bedside. Learning Objectives By the end of this episode, listeners should be able to: Compare the composition and physiologic effects of 0.9% saline and balanced crystalloids used for pediatric fluid resuscitation. Summarize the design and major findings of the PRoMPT BOLUS trial. Describe important limitations of PRoMPT BOLUS when applying its results to children with septic shock. Apply current evidence and 2026 Surviving Sepsis Campaign recommendations when selecting crystalloid fluids for pediatric septic shock. References Weiss SL, Peters MJ, Oczkowski SJW, et al. Surviving Sepsis Campaign International Guidelines for the Management of Sepsis and Septic Shock in Children 2026. Pediatr Crit Care Med. 2026. Published April 1, 2026. Jointly issued by the Society of Critical Care Medicine and Infectious Diseases Society of America. Recommendation 24 suggests balanced/buffered crystalloids over 0.9% saline for children with septic shock requiring fluid boluses (conditional recommendation, very low certainty), while recognizing 0.9% saline as a suitable alternative and preferred in selected situations such as hyponatremia or concern for increased intracranial pressure. Balamuth F, Weiss SL, Long E, et al. Balanced Fluid or 0.9% Saline in Children Treated for Septic Shock. N Engl J Med. 2026. Published April 24, 2026. PRoMPT BOLUS was a large pragmatic randomized trial comparing balanced crystalloids with 0.9% saline in children treated for suspected septic shock and found no reduction in major adverse kidney events within 30 days with balanced fluids. 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 which fluid we should use when managing a septic pediatric patient. So when we resuscitate a child with septic shock, the major decision is usually not whether to give crystalloid, but which crystalloid to give. And for a long time, there’s been a gradual shift towards balanced fluids such as Lactated Ringer’s or Plasma-Lyte, largely because they are more physiologic and produce less hyperchloremia than normal saline. The question’s always been whether those biochemical differences actually translate into better clinical outcomes. That is the question that a study called PRoMPT BOLUS was designed to answer. So before getting into the trial, it’s worth briefly reviewing what these fluids actually contain. So normal saline is 0.9% sodium chloride. It contains one hundred and fifty-four milliequivalents per liter of sodium and a hundred and fifty-four milliequivalents per liter of chloride. The chloride concentration is substantially higher than plasma. Balanced crystalloids contain less chloride and have some other electrolytes and a buffer. Lactated Ringer’s contains approximately a hundred and thirty milliequivalents per liter of sodium, one hundred and nine of chloride, four of potassium, a small amount of calcium, and lactate as a buffer. Plasma-Lyte contains approximately one hundred and forty of sodium, ninety-eight of chloride, five of potassium, magnesium, and acetate and gluconate as buffers. The concern with normal saline is that the large chloride loads can produce hyperchloremic metabolic acidosis. There’s also been concern about adverse effects on renal blood flow and kidney function. Balanced fluids are designed to more closely approximate plasma composition, so the hypothesis has been that they might reduce kidney injury. That hypothesis has been supported by physiologic data and by some adult studies, although pediatric evidence before PRoMPT BOLUS was limited and inconsistent. The 2026 Surviving Sepsis Campaign Pediatric Guidelines recommend crystalloids over albumin for initial resuscitation and conditionally suggest balanced or buffered crystalloids over 0.9% saline in children with septic shock who require fluid boluses. Importantly, that recommendation is based on very low-certainty evidence. Balanced options again include Lactated Ringer’s, Hartmann’s solution, or Plasma-Lyte. If balanced fluids are not readily available, saline remains an acceptable alternative. Saline may also be preferable in some specific situations like significant hyponatremia or concern for increased intracranial pressure. For children in resource-abundant settings, the general approach is still ten to twenty mLs per kilo per bolus with reassessment after each bolus, potentially up to forty to sixty mLs per kilo in the first hour if perfusion remains abnormal and there are no signs of fluid overload. Now, PRoMPT BOLUS, the full name of which is the Pragmatic Pediatric Trial of Balanced versus Normal Saline Fluid in Sepsis, was an international randomized pragmatic trial designed to specifically compare the two fluid strategies in children with suspected septic shock. The final trial enrolled nine thousand and forty-one children from two months to younger than eighteen years across forty-seven emergency departments in five countries. Children were randomized to predominantly balanced crystalloid or predominantly 0.9% saline, and the assigned fluid strategy was used for bolus and maintenance crystalloid during the initial treatment period. The balanced fluid arm was not a single product. Depending on the site, children could get Lactated Ringer’s, Hartmann’s solution, or Plasma-Lyte. That’s important when interpreting the study. PRoMPT BOLUS was really testing a strategy of predominantly balanced crystalloid versus a strategy of predominantly saline use rather than comparing LR versus saline alone, though LR was the most commonly used one. The primary outcome was something called MAKE30, M-A-K-E thirty, or major adverse kidney events within thirty days. This was a composite outcome that included death, new renal replacement therapy, or persistent kidney dysfunction. That choice of outcome is useful because the biologic rationale for balanced fluids has always centered largely on kidney protection. The investigators were therefore asking whether the lower chloride exposure associated with balanced fluids translated into clinically meaningful renal benefit. So what was the result? Well, the spoiler is that the answer was no. So MAKE30 occurred in three point four percent of children receiving balanced fluids and three percent receiving saline. The relative risk was one point one with a ninety-five percent confidence interval from point eight eight to one point four. There were also no significant differences in death, new renal replacement therapy, persistent kidney dysfunction, or hospital-free days. In practical terms, balanced crystalloids did not improve the major patient-centered outcomes the trial was designed to measure. There were clear biochemical differences between the groups. Hyperchloremia occurred in thirty-one point four percent of children receiving balanced fluids compared with forty-nine percent with saline. Hypernatremia was also less common with balanced fluids, one point eight versus three point one percent. Hyperlactatemia was slightly more common in the balanced fluid group, nineteen point eight compared with sixteen point seven percent. So the fluids behaved differently in the ways that you would expect physiologically. Balanced crystalloids clearly reduced hyperchloremia, but that difference did not translate into fewer major kidney events, less dialysis, shorter hospitalization, or lower mortality. There are several limitations to this study worth keeping in mind. The first is that this was a broad emergency department population with suspected septic shock, not a study limited to children with the most severe forms of shock. Only a minority of patients required vasoactive medications, and overall mortality was low. The results are therefore most applicable to the typical child with suspected septic shock receiving early ED resuscitation. They do not completely answer whether fluid composition might matter more in a smaller subgroup of children receiving very large fluid volumes or prolonged resuscitation. The second limitation is that the event rate for MAKE30 was lower than expected. When the trial was designed, investigators anticipated an event rate of about six percent in the saline group. The observed rate was closer to three percent. That means there were fewer outcome events than anticipated, which reduced the ability to detect a very small treatment effect. So the trial makes a large benefit from balanced fluids unlikely, but it can’t exclude a small or subtle difference. A third limitation is that the balanced fluid group included several different solutions. Lactated Ringer’s, Plasma-Lyte, and Hartmann’s are all considered under the umbrella of balanced crystalloids, but they’re not chemically identical. The study therefore supports the broader conclusion that a balanced fluid strategy is not superior to saline for most children in this setting, rather than providing equivalence between any single specific balanced solution and saline, even though Lactated Ringer’s is used far and away most often. The trial was also intentionally pragmatic, which means that there was some crossover between fluid types. Adherence was defined as receiving at least s

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

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

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

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

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

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

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

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

BRUE, Brief Resolved Unexplained Events, are a common and anxiety-provoking condition that presents to the Emergency Department. In this episode we explore the definition of BRUE, contrast it with ALTE, and walk through evidence-based approaches to risk stratification. We’ll explore the original AAP framework and two subsequent prediction models to see where the recommendations stand today. This is a classic example of scary event / well child that you will see in the Emergency Department. Learning Objectives By the end of this episode, you will be able to: Define BRUE and contrast it with the older concept of ALTE. Recognize evolving risk stratification criteria Apply evidence-based strategies for evaluation and counseling of infants with BRUE, including safe discharge decisions and the role of home monitoring. References Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief resolved unexplained events (formerly apparent life-threatening events) and evaluation of lower-risk infants: Executive summary. Pediatrics. 2016;137(5):e20160591. doi:10.1542/peds.2016-0591 Carroll AE, Bonkowsky JL. Acute events in infancy including brief resolved unexplained event (BRUE). In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025). Carroll AE, Bonkowsky JL. Use of home cardiorespiratory monitors in infants. In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025). Carroll AE, Bonkowsky JL. Sudden infant death syndrome: Risk factors and risk reduction strategies. In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025). Carroll AE. Patient education: Brief resolved unexplained event (BRUE) in babies (The Basics). In: UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025). Nama N, Neuman MI, Finkel MA, et al. Risk prediction after a brief resolved unexplained event. JAMA Pediatr. 2023;177(12):1263–1272. doi:10.1001/jamapediatrics.2023.4197 Nama N, Neuman MI, Finkel MA, et al. External validation of brief resolved unexplained events prediction rules for serious underlying diagnosis. JAMA Pediatr. 2024;178(4):398–407. doi:10.1001/jamapediatrics.2024.0114

Is that penicillin or amoxicillin allergy real? Probably not. In this episode, we explore how to assess risk, talk to parents, and refer for delabeling. You’ll also learn what happens in the allergy clinic, why the label matters, and how to be a better antimicrobial steward. Learning Objectives Describe the mechanisms and clinical manifestations of immediate and delayed hypersensitivity reactions to penicillin, including diagnostic criteria and risk stratification tools such as the PEN-FAST score. Differentiate between low-, moderate-, and high-risk penicillin allergy histories in pediatric patients and identify appropriate candidates for direct oral challenge or allergy referral based on current evidence and guidelines. Formulate an evidence-based approach for evaluating and counseling families in the Emergency Department about reported penicillin allergies, including when to recommend outpatient referral for formal delabeling. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski References Khan DA, Banerji A, Blumenthal KG, et al. Drug Allergy: A 2022 Practice Parameter Update. J Allergy Clin Immunol. 2022;150(6):1333-1393. doi:10.1016/j.jaci.2022.08.028 Moral L, Toral T, Muñoz C, et al. Direct Oral Challenge for Immediate and Non-Immediate Beta-Lactam Allergy in Children. Pediatr Allergy Immunol. 2024;35(3):e14096. doi:10.1111/pai.14096 Castells M, Khan DA, Phillips EJ. Penicillin Allergy. N Engl J Med. 2019;381(24):2338-2351. doi:10.1056/NEJMra1807761 Shenoy ES, Macy E, Rowe T, Blumenthal KG. Evaluation and Management of Penicillin Allergy: A Review.JAMA. 2019;321(2):188–199. doi:10.1001/jama.2018.19283 Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 5 AI  Welcome to PEM Currents, the Pediatric Emergency Medicine podcast. As always, I'm your host, Brad Sobolewski, and today we are taking on a label that's misleading, persistent. Far too common penicillin allergy, it's often based on incomplete or inaccurate information, and it may end up limiting safe and effective treatment, especially for the kids that we see in the emergency department. I think you've all seen a patient where you're like. I don't think this kid's really allergic to amoxicillin, but what do you do about it? In this episode, we're gonna break down the evidence, walk through what actually happens during de labeling and dedicated allergy clinics. Highlight some validated tools like the pen FAST score, which I'd never heard of before. Preparing for this episode and discuss the current and future role of ED based penicillin allergy testing. Okay, so about 10% of patients carry a penicillin allergy label, but more than 90% are not truly allergic. And this label can be really problematic in kids. It limits first line treatment choices like amoxicillin, otitis media, or penicillin for strep throat, and instead. Kids get prescribed second line agents that are less effective, broader spectrum, maybe more toxic or poorly tolerated and associated with a higher risk of antimicrobial resistance. So it's not just an EMR checkbox, it's a label with some real clinical consequences. And it's one, we have a role in removing. And so let's understand what allergy really means. And most patients with a reported penicillin allergy, especially kids, aren't true allergies in the immunologic sense. Common misinterpretations include a delayed rash, a maculopapular, or viral exum, or benign, delayed hypersensitivity, side effects, nausea, vomiting, and diarrhea. And unverified childhood reactions that are undocumented and nonspecific. Most of these are not true allergies. Only a very small subset of patients actually have IgE mediated hypersensitivity, such as urticaria, angioedema, wheezing, and anaphylaxis. These are super rare, and even then they may resolve over time without treatment. If a parent or sibling has a history of a penicillin allergy, remember that patient might actually not be allergic, and that is certainly not a reason to label a child as allergic just because one of their first degree relatives has an allergy. So right now, in 2025, as I'm recording this episode, there are clinics like the Pats Clinic or the Penicillin Allergy Testing Services at Cincinnati Children's and in a lot of our peer institutions that are at the forefront of modern de labeling. Their approach reflects the standard of care as outlined by the. Quad ai or the American Academy of Allergy, asthma and Immunology and supported by large trials like Palace. And you know, you have a great trial if you have a great acronym. So here's what happens step by step. So first you stratify the risk. How likely is this to be a true allergy? And that's where a tool like the pen fast comes. And so pen fast scores, a decision rule developed to help assess the likelihood of a true penicillin allergy based on the patient's history. The pen in pen fast is whether or not the patient has a self-reported history of penicillin allergy. They get two points if the reaction occurred in the past five years. Two points if the reaction is anaphylaxis or angioedema. One point if the reaction required treatment, and one point if the reaction was not due to testing. And so you can get a total score of. Up to six points. If you have a score of less than three. This is a low risk patient and they can be eligible for direct oral challenge. A score greater than three means they're higher risk and they may require skin testing. First validation studies show that the PEN FFA score of less than three had a negative predictive value of 96.3%. Meaning a very, very low chance of a true allergy. And this tool has been studied more extensively in adults, but pediatric specific adaptations are emerging, and they do inform current allergy clinic protocols. But I would not use this score in the emergency department just to give a kid a dose of amoxicillin. So. For low risk patients, a pen fast score of less than three or equivalent clinical judgment clinics proceed with direct oral challenge with no skin testing required. The protocol is they administer one dose of oral amoxicillin and they observe for 62 120 minutes monitoring for signs of reaction Urticaria. Respiratory symptoms or GI upset. This approach is safe and effective. There was a trial called Palace back in 2022, which validated this in over 300 children. In adolescents. There were no serious events that occurred. De labeling was successful in greater than 95% of patients. And skin tested added no benefit in low risk patients. So if the child tolerates this dose, then you can remove that allergy immediately from the chart. Parents and primary care doctors will receive a summary letter noting that the challenge was successful and that there's new guidance. Children and families are told they can safely receive all penicillins going forward. And providers are encouraged to document this clearly in the allergy section of the EMR. So you're wondering, can we actually do this in the emergency department? Technically, yes, you can do what you want, but practically we're not quite there yet. So we'd need clearer risk stratification tools like the Pen fast, a safe place for monitoring, post challenge, clinical pathways and documentation support. You know, a clear way to update EMR allergy labels across the board and involvement or allergy or infectious disease oversight. But it's pretty enticing, right? See a kid you diagnose otitis media. You think that their penicillin allergy is wrong, you just give 'em a dose of amox and watch 'em for an hour. That seems like a pretty cool thing that we might be able to do. So some centers, especially in Canada and Australia, do have some protocols for ED or inpatient based de labeling, but they rely on that structured implementation. So until then, our role in the pediatric emergency department is to identify low risk patients, avoid over document. Unconfirmed reactions and refer to allergy ideally to a clinic like the pets. So who should be referred and good candidates Include a child with a rash only, especially one that's remote over a year ago. Isolated GI symptoms. Parents unsure of the details at all. No history of anaphylaxis wheezing her hives, and no recent serious cutaneous reactions. I would avoid referring and presume that this allergy is true. If they've had recent anaphylaxis, they've had something like Stevens Johnson syndrome dress, or toxic epidermolysis necrosis. Fortunately, those are very, very rare with penicillins and there's a need for penicillin during the ED visit without allergy backup. So even though we don't have an ED based protocol yet. De labeling amoxicillin or penicillin allergy can start with good questions in the emergency department. So here's one way to talk to patients and families. You can say, thanks for letting me know about the amoxicillin allergy. Can I ask you a few questions to better understand what happened? This is gonna help us decide the safest and most effective treatment for your child today, and then possibly go through a process to remove a label for this allergy that might not be accurate. You wanna ask good, open-ended questions. What exactly happened when your child took penicillin or amoxicillin? You know, look for rash, hives, swelling, trouble breathing, or anaphylaxis. Many families just say, allergic, when the reaction was just GI upset, diarrhea or vomiting, which is not an allergy. How old was your child when this happened? Reactions that occurred before age of three are more likely to be falsely attributed. How soon after taking the medicine did the reaction start? Less than one hour is an immediate reaction, but one hour to days later is delayed. Usually mild and probably not a true allergy. Did they have a fever, cold or virus at that time? Viral rashes are often misattributed to

Limping is a common complaint in pediatric emergency care, but the differential is broad and the stakes are high. In this episode, we walk through a detailed, age-based approach to the evaluation of the limping child. You’ll learn how to integrate the Kocher criteria, when imaging and labs are truly necessary, and how to avoid being misled by small joint effusions on ultrasound. We also highlight critical mimics like appendicitis, testicular torsion, and malignancy—and remind you why watching a child walk is one of the most valuable parts of the exam. Whether it’s transient synovitis, septic arthritis, or something much more concerning, this episode gives you the tools to manage pediatric limps with confidence. Learning Objectives Apply an age-based approach to the differential diagnosis of limping in children. Demonstrate diagnostic reasoning by integrating history, physical exam, imaging, and lab findings to prioritize urgent conditions like septic arthritis and SCFE. Appropriately select and interpret imaging and lab studies, including understanding the utility and limitations of ultrasound, MRI, and the Kocher criteria. Connect with Brad Sobolewski Mastodon: @[email protected] PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski References Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-70. doi:10.2106/00004623-199912000-00002 UpToDate. Evaluation of limp in children. Accessed September 2025. UpToDate. Differential diagnosis of limp in children. Accessed September 2025. StatPearls. Antalgic Gait in Children. NCBI Bookshelf. Accessed September 2025. Pediatric Emergency Care. “Approach to Pediatric Limp.” Pediatrics in Review. 2024. Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 5 AI Welcome to PEM Currents, the Pediatric Emergency Medicine podcast. As always, I’m your host, Brad Sobolewski, and in this episode we’re gonna tackle the evaluation of a child presenting with limp. We’ll cover, age-based differential diagnosis. How to take a high yield history and do a detailed physical exam, imaging strategies, lab tests, and when to worry about systemic causes. We’ll also talk about the Kocher criteria for septic arthritis and how to use and not misuse ultrasound when you’re worried about a hip effusion. After listening to this episode, I hope you will all be able to apply an age based. Approach to the differential diagnosis of limp in children. Demonstrate diagnostic reasoning by integrating history, physical exam, imaging, and lab findings to prioritize urgent conditions like septic, arthritis, and scfe, and appropriately select and interpret imaging and lab studies, including understanding the utility and limitations of ultrasound MRI and the Kocher criteria. So let me start out by saying that a limp isn’t a diagnosis, it’s a symptom. It can result from pain, weakness, neurologic issues, or mechanical disruption. So think of limping as the pediatric equivalent of chest pain. In adults. It’s common, it’s broad, and it’s sometimes could be serious. And the key to a good workup is a thought. Age-based approached and kids under three think trauma and congenital conditions between three and 10 transient synovitis range Supreme and over 10 think SCFE and systemic disease. And your differential diagnosis always starts with history. So you gotta ask the family, when did the lymph start? Was it sudden or gradual? Is there a preceding viral illness or an injury? Is the limp worse in the morning? Does it get better with activity? Do the kid complain of pain or are they just favoring one leg? And then are there any systemic symptoms such as fever, rash, weight loss, fatigue, or joint swelling elsewhere? And you wanna find out whether or not the kid is actually bearing any weight at all. Have they had recent travel or known tick exposure? Are they potty trained and are they having accidents now? Have they had any prior episodes of joint swelling or limping like this in the past? And don’t forget a developmental history, especially in kids under preschool age. Most children begin to stand at nine to 12 months. Cruise at 10 to 12 months and walk independently by 12 to 15 months. A child who has never walked normally may have a neuromuscular or congenital problem. When you are evaluating limp, obviously you wanna watch the kid walk, get them outta the exam room if needed. First of all, your exam room is small. Kid may feel confined and they might be more willing to take some steps. If you have ’em out in the hallway, obviously have the caregiver nearby and a toy, a phone, some object of enticement. You wanna watch their stance phase, or they just avoiding bearing weight on one limb. When they’re standing the swing phase, do they hold that leg stiff? Does it bend normally? And are they in balance? Are they symmetric? And again, don’t just settle for a few steps. Try to get ’em walking at least 10 to 15 feet if possible, and if they’re refusing to walk in, the ED asks parents for a video. You wanna examine every joint head to toe, and even if the child only complains about one area, palpate every limb. I usually start distally so at the fingertips or toes and really systematically work my way up watching for any signs of pain, you check range of motion and observe resistance to movement log. Roll the hips externally and internally rotate them as well. See if you can feel an A fusion, you know, squeeze the calf to localize pain. And in a kid with limp, you always gotta check the feet too, right? Look for puncture wounds on the plantar surface. Splinters, ingrown, toenails, cellulitis, or even, you know, gravity dependent swelling or petechiae. And certainly your systemic exam should include the abdomen. You know, look for signs of appendicitis or sous irritation, testes for testicular torsion. And you wanna look at the skin diffusely to make sure there’s no petechiae, target shape, rashes, or bruising. Now for most kids with limp, I find that the history and physical exams sort of guide where you’re going, right? If they had a fall or an injury, well, you’re just looking at a kid who may have sprained or broken something, and you can really target towards imaging as your workup. You know, there’s some kids though that may benefit from labs and in general, they depend on the scenario. So if you see A C, B, C, well you’re gonna get leukocytosis, but C, B, C. In the context of limp is most useful when you’re considering a differential. So if you see blasts, well, you know you’ve got a new malignancy. If you have a general elevation of the white count and use it in context with the Kocher criteria, it could be more valuable. So A CBC alone is not gonna get you the cause it supports your differential. ESR and CRP are often ordered and they’re just general inflammatory labs. CRP rises and falls faster than ESR, and they co vary and either can be used in prediction rules. I’ll talk about that in a little bit if you think the kid’s bacteremic, yeah. Get a blood culture. If you’re in an endemic area and you’re considering Lyme on the differential, you can send off serology. And let’s be honest, a NA and rheumatoid factor are really only useful if there’s a chronic history and you can have about 15% of kids with a false positive a NA anyway, and they’re not really helpful in acute limp. So get them if rheumatology recommends them, but otherwise, they’re not really a useful part in the initial differential diagnosis. And again, I alluded to Lyme a moment ago, but if Lyme arthritis is your top diagnosis, especially with a known rash. You can start treatment while serologies are pending. That’s totally okay. So in conjunction with Labs, imaging is generally recommended in most kids with Limp, and I would say in most cases you start with plain films. Sometimes it’s easy, right? They hurt in one particular occasion. You take a picture, you see a fracture, but two views, the affected and unaffected side can be really helpful, especially in cases of SCFE or in subtle or perhaps occult toddler’s fracture. If you’re not sure where the problem is, you can’t isolate it on your exam or history. Consider imaging the entire leg. I mean, that’s when you’re looking at like the hip femur, knee tib fib, even the ankle and foot. It’s not that much radiation. Ultrasound is useful for seeing joint effusions, especially of the hip. It’s fast, generally painless and radiation free, but not all effusions are infected. Ultrasound is not part of the Kocher criteria. I’ll get back to that in a minute. And a normal ultrasound or an ultrasound without effusion doesn’t rule out septic arthritis. And then we’ve got MRI, which is definitely best for detecting osteomyelitis, discitis, and soft tissue abscesses. Among other diagnoses in kids under five, you’re probably gonna need to sedate them, which can delay diagnosis. So in general, you’re admitting those kids and then they can get a sedated MRI later the next day. But if radiology has it available and you’ve got the right protocol and the kids’ the right age, you can get it in the emergency department. But these are often more subtle situations. So if you’re really suspicious for septic arthritis, don’t wait around for an MRI contact ortho and tap that hip. And speaking of septic arthritis, let’s talk about the Kocher criteria. K-O-C-H-E-R. These are four classic criteria, and they are only validated for differentiating septic arthritis and transient synovitis of the hip. So you can

Vaso-occlusive pain episodes are the most common reason children and adolescents with sickle cell disease present to the Emergency Department. Prompt, protocol-driven management is essential starting with early administration of IV opioids, reassessment at 15–30 minute intervals, and judicious hydration. Understanding the patient’s typical pain pattern, opioid history, and psychosocial context can guide more effective care. This episode walks through the pathophysiology, clinical presentation, pharmacologic strategy, discharge criteria, and complications to watch for helping you provide evidence-based, compassionate care that improves outcomes. Learning Objectives Describe the pathophysiology of vaso-occlusive crises in children and adolescents with sickle cell disease and how it relates to clinical symptoms. Differentiate uncomplicated vaso-occlusive crises from other acute complications of sickle cell disease such as acute chest syndrome, splenic sequestration, and stroke. Implement evidence-based strategies for early and effective pain management in vaso-occlusive crises, including appropriate use of opioid analgesia, reassessment intervals, and disposition criteria. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @[email protected] References Kavanagh PL, Fasipe TA, Wun T. Sickle cell disease: a review. JAMA. 2022;328(1):57-68. doi:10.1001/jama.2022.10233 Yates AM, Aygun B, Nuss R, Rogers ZR. Health supervision for children and adolescents with sickle cell disease: clinical report. Pediatrics. 2024;154(2):e2024066842. doi:10.1542/peds.2024-066842 Bender MA, Carlberg K. Sickle Cell Disease. In: Adam MP, Everman DB, Mirzaa GM, et al, eds. GeneReviews®. University of Washington, Seattle; 1993–2024. Updated February 13, 2025. Available from: https://www.ncbi.nlm.nih.gov/books/NBK1377/ Brandow AM, Carroll CP, Creary S, et al. American Society of Hematology 2020 guidelines for sickle cell disease: management of acute and chronic pain. Blood Adv. 2020;4(12):2656-2701. doi:10.1182/bloodadvances.2020001851 Brandow AM, Carroll CP, Creary SE. Acute vaso-occlusive pain management in sickle cell disease. In: Hoffman R, Benz EJ, Silberstein LE, Heslop HE, Weitz JI, Anastasi J, eds. UpToDate. UpToDate; 2024. Accessed July 2025. https://www.uptodate.com Glassberg JA, Strouse JJ. Evaluation of acute pain in sickle cell disease. In: Hoffman R, Benz EJ, Silberstein LE, Heslop HE, Weitz JI, Anastasi J, eds. UpToDate. UpToDate; 2024. Accessed July 2025. https://www.uptodate.com DeBaun MR, Quinn CT. Overview of the clinical manifestations of sickle cell disease. In: Hoffman R, Benz EJ, Silberstein LE, Heslop HE, Weitz JI, Anastasi J, eds. UpToDate. UpToDate; 2024. Accessed July 2025. https://www.uptodate.com McCavit TL. Overview of preventive outpatient care in sickle cell disease. In: Hoffman R, Benz EJ, Silberstein LE, Heslop HE, Weitz JI, Anastasi J, eds. UpToDate. UpToDate; 2024. Accessed July 2025. https://www.uptodate.com Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 4o AI Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. I’m your host, Brad Sobolewski. In this episode, we’re digging into a common but complex emergency department challenge: pain management for vaso-occlusive crises in children and adolescents with sickle cell disease. These episodes are painful—literally and figuratively. But with thoughtful, evidence-based care, we can make a big difference for our patients. Overview and Epidemiology Vaso-occlusive crises, or VOCs, are the most frequent cause of emergency visits and hospitalizations for individuals with sickle cell disease (SCD). They are responsible for more than 70 percent of ED visits among children with SCD and account for substantial healthcare utilization and missed school days. Most children with homozygous HbSS will experience their first painful episode before the age of 6. Recurrent VOCs are associated with higher risks of chronic pain, opioid use, and diminished quality of life. Why Do VOCs Happen? Sickle cell disease is caused by a point mutation in the beta-globin gene, leading to hemoglobin S. Under stress—such as infection, dehydration, or even cold exposure—red blood cells polymerize, sickle, and become rigid. These sickled cells obstruct capillaries and small vessels, leading to local tissue ischemia, inflammation, and pain. It’s not just about the blockage—the inflammatory cascade, endothelial damage, and cytokine release all contribute to the pain experience. What Does the Pain Feel Like? Ask kids and teens with sickle cell disease, and they’ll describe their pain as deep, throbbing, stabbing, or aching. It often feels bone-deep and can be relentless and exhausting. Many say it’s unlike any other pain—they may compare it to being “hit with a bat,” “bone being crushed,” or “something stuck inside my limbs trying to get out.” Common sites include: Long bones (femur, humerus) Lower back Chest (look out for acute chest syndrome) Abdomen Hands and feet (especially in younger children—think dactylitis) Clinical Presentation History Ask about typical pain patterns and how this episode compares to prior ones. Look for triggers: dehydration, weather changes, infection, stress. Document home medications, including opioid tolerance and response to prior ED treatments. Physical Exam Often nonspecific. Localized tenderness, guarding. May have fever if infection is present (but fever is not diagnostic of VOC). Look for signs of acute chest syndrome: tachypnea, hypoxia, chest pain. Vitals May show tachycardia from pain or dehydration. Febrile patients should be evaluated for sepsis or osteomyelitis. Pain scales Use age-appropriate tools: FLACC, Wong-Baker FACES, or numerical rating scales. Management: Treat Early, Treat Effectively Pain Medications Start early. Do not delay for labs. Aim for analgesia within 30–60 minutes of arrival. Mild pain (rare in ED): Acetaminophen or NSAIDs (e.g., ibuprofen, ketorolac). Moderate to severe pain: Opioids are first-line. Morphine IV: 0.1 mg/kg (max 10 mg) every 15–30 minutes as needed; consider PCA in admitted patients. Hydromorphone IV: 0.015 mg/kg if morphine does not work or if the patient has used it effectively in the past. Intranasal fentanyl: 1.5–2 mcg/kg as a bridge while waiting for IV access. Avoid codeine and meperidine due to poor efficacy and neurotoxicity risks. Reassess every 15–30 minutes until pain is controlled, then space doses out. Adjunctive Therapies Hydration: Lactated Ringer’s is associated with shorter hospital stays and lower readmission rates than normal saline. Avoid fluid overload; maintain euvolemia. Heat packs for local comfort. Distraction techniques, Child Life, music, games, screens. Anxiolytics may be considered for severe distress but use cautiously. Labs and Imaging Labs are not always needed if the child looks well and has an uncomplicated VOC. Follow local protocols. Consider: CBC and reticulocyte count: A low retic suggests aplastic crisis (often parvovirus B19). A high retic is appropriate in VOC, showing marrow response. Compare hemoglobin to baseline. BMP for renal function. LFTs or lipase if right upper quadrant pain. Chest x-ray if chest symptoms present. Blood cultures if febrile. Oxygen Only indicated if the patient is hypoxic. Transfusion Routine transfusion is not indicated for uncomplicated VOC. May be used in complications such as acute chest syndrome, stroke, or symptomatic anemia. Disposition: Discharge vs. Admission Discharge if: Pain is improved and manageable on oral medications. Tolerating oral intake. No concern for complications. Reliable follow-up and support available. Admit if: Persistent severe pain despite multiple IV doses. Need for frequent parenteral opioids. Acute chest syndrome, sepsis, or other complications. Poor outpatient support or unreliable follow-up. Complications to Watch For Acute chest syndrome: Chest pain, hypoxia, new infiltrate on chest x-ray. Splenic sequestration: Rapid hemoglobin drop, splenomegaly, signs of shock. Stroke: New neurologic deficits. Sepsis: Fever, tachycardia, especially in asplenic patients. Avascular necrosis: Recurrent or chronic hip or shoulder pain. Chronic pain: Increasing in frequency in adolescents and young adults. Prevention Hydroxyurea is the cornerstone of prevention. It increases fetal hemoglobin and reduces the frequency and severity of pain crises. It can be started as early as 9 months of age in children with HbSS or Sβ⁰-thalassemia. Other preventive strategies include: Staying hydrated. Avoiding extreme cold exposure. Keeping up with vaccines and penicillin prophylaxis. Addressing mental health and social stressors. Take-Home Points Treat pain promptly and aggressively. Do not wait on labs. Use IV opioids for moderate to severe pain and reassess often. Lactated Ringer’s may be preferred for IV hydration, but avoid overload. Labs and imaging should follow clinical appearance and local protocols. Reticulocyte count and hemoglobin trends are key. Disposition should be based on pain control, potential complications, and social support. Prevention matters—hydroxyurea and primary care follow-up reduce crises and admissions.

Penetrating neck injuries in children are rare—but when they happen, the stakes are high. In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the clinical pearls behind “no-zone” management, how to distinguish hard and soft signs, when to image versus operate, and why airway always comes first. Get ready for a focused, evidence-based deep dive into pediatric neck trauma. Learning Objectives Understand the shift from zone-based to “no-zone” management in pediatric penetrating neck injuries and describe the rationale behind this transition. Apply ATLS principles to the initial assessment and stabilization of children with penetrating neck injuries, including decisions regarding imaging and airway management. Evaluate clinical findings to determine the need for operative intervention versus observation in stable pediatric patients with soft versus hard signs of vascular or aerodigestive injury. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @[email protected] References Stone ME Jr, Christensen P, Craig S, Rosengart M. Management of penetrating neck injury in children: A review of the National Trauma Data Bank. Red Cross Annals. 2017;32(4):171–177. doi:10.1016/j.rcsann.2017.04.003 Callcut RA, Inaba K. Penetrating neck injuries: Initial evaluation and management. UpToDate. Waltham, MA: UpToDate Inc. [Accessed June 24, 2025]. Available from: https://www.uptodate.com Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 4o AI Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and in this episode we are diving into a high-stakes but fortunately rare topic in pediatric trauma — penetrating neck injuries. Now these injuries make up less than 1% of all pediatric trauma, but when they occur, they demand precision and vigilance in terms of diagnosis and management. As you know, the neck packs some vital organs, vessels, the airway, esophagus, and nerves into a tiny little area, so even a seemingly minor wound can injure multiple structures. Now you remember — way back when — where you learned about the zones of the neck, and this is the traditional teaching, which chopped the neck up into three zones. You’ve got Zone I, which is the area between the clavicle and cricoid. You’ve got the subclavian arteries and vein, the carotid, and the apices of the lungs. Zone II, the cricoid to the angle of the mandible — this includes the carotids, jugulars, the vagus nerve, the trachea, and the esophagus. And then you have Zone III, which is the angle of the mandible to the base of the skull — you’ve got the distal carotid, the vertebral artery, and cranial nerves IX through XII. Now, you may recall some teaching that you got in medical school or residency where the management was dictated by which zone was injured. And admittedly, a lot of this evidence is in adults, and more penetrating trauma is seen in adults as well. But now practice is leaning towards the “no zone” approach, where imaginary lines on the skin surface are not dictating management as much as presentation, symptoms, and deciding when to go to the OR versus using CT angiography. So let’s talk about mechanisms of injury for a minute. Toddlers can injure their neck when they fall with something in their mouth, like pencils or chopsticks. School-age kids may take a bike handlebar to the neck, or they’re trying to run or jump over a fence and they get impaled on that — that sounds painful. Adolescents, unfortunately, are subject to assaults, stabbings, and gunshot wounds, as well as clothesline-type injuries or other high-velocity injury where the neck is injured as they’re riding a bike. So low-velocity mechanisms dominate pediatric penetrating neck injuries. Force matters, because depth and tissue cavitation decide the overall injury pattern. In terms of assessing the patient with a penetrating neck injury, it all starts with the ABCs. Is the patient’s airway patent? Are they protecting and maintaining it? Look for signs such as hoarseness, stridor, aphonia (they can’t talk at all), a bubbling wound, or an expanding hematoma. For breathing, patients should be breathing comfortably with no distress. Look for any signs of asymmetry on chest rise, feeling of crepitus or subcutaneous air, or diminished breath sounds — obviously the latter two indicating a pneumothorax or even hemothorax. For circulation, if the wound is bleeding, apply direct pressure. Some surgeons will use a Foley balloon tamponade method if they need to stop bleeding before going to the operating room. Patients will need large bore IVs and fluids — and especially blood product resuscitation. Only immobilize the C-spine if a patient has neurologic deficits or a high injury mechanism. Think — somebody that was riding their bike and clotheslined the fence. Neck collars hide neck wounds and hamper airway management unless they’re strictly needed. You may have also heard of hard signs and soft signs in terms of the parlance of managing penetrating neck injury. In general, hard signs mean go to the operating room. Soft signs need a CT angiogram and observation. So here are some hard signs: • Active arterial bleeding — blood spurting out of the patient • Expanding or pulsatile hematoma • Airway compromise, stridor, or other signs • Air bubbling from the neck wound • Shock that is unresponsive to fluids • Any focal neurologic deficit Soft signs include: • Minor oozing • A small and stable hematoma • Mild dysphonia or dysphagia • Subcutaneous air without any respiratory distress • Mild voice changes • Just a little bit of hemoptysis A large pediatric series showed that 50 to 70% of children with hard signs did need operative repair. Most with only soft signs were managed safely with imaging and serial exams. So I alluded to this paradigm at the beginning of the episode — the “no zone” strategy. For stable children with no hard signs, CT angiography is the gold standard. It has a sensitivity of 95 to 99% for major vascular injury. You’re able to visualize the trachea, esophagus, spine, and any foreign bodies. Make sure you always get a chest X-ray as well, since penetrating neck injuries can injure the apices of the lungs or thoracic structures. Also, if the CTA is negative but you still have suspicion for injury to the aerodigestive tract, you can do a water-soluble contrast esophagram or flexible endoscopy. Plain films — yes, you can assess the C-spine and look for radiopaque foreign bodies, but again, if you truly have a child that is stable and has no hard signs, CTA is the gold standard. If you follow this, you can cut non-therapeutic neck explorations in half without missing any injuries. So this should be part of your protocol. If you do have a neck wound that you have to manage before the surgeons can get to it: direct pressure first. The Foley balloon tamponade method is where you take an 18 to 20 French catheter, place it into the wound, inflate the balloon with 10 to 15 milliliters of water, and then clamp it. I wouldn’t necessarily do this in a Level 1 trauma center — I have surgeons available — but it might be useful if you have to transport a kid quickly to a trauma center. Never, ever, ever pull an impaled object out of the neck in the emergency department. These should be removed in the operating room. Now, superficial injuries with the platysma intact get routine closure. Anything deeper deserves imaging. So here’s some pediatric-specific pearls, again, because these are really rare. Kids have a small airway, and soft tissues swell quickly, so there’s a low threshold for securing the airway. If you’re concerned about the airway, make a plan to do it right now. Kids have low blood volume and don’t tolerate hemorrhage as well. They’ll underreport pain, especially younger ones — so rely on the exam and parental observations. Definitely use Child Life to help keep them calm. And unfortunately, some neck wounds are self-inflicted, so make sure you address mental health concerns after the child is stabilized. Alright. So let’s bring it all home. What are some key take-home points? 1. Penetrating neck trauma is fortunately rare in kids — far less than 1% of all pediatric trauma — but still high-risk. 2. Males predominate. The younger the child, the higher the risk of aerodigestive injury. 3. Hard signs → go straight to the OR. 4. Soft signs → CT angiography and observation. 5. Hard vs soft signs reliably stratify risk. 6. CTA + chest X-ray is first-line in stable, hard-sign-negative children, which limits unnecessary surgical exploration. 7. Esophageal injuries are sneaky — you may need endoscopy or contrast studies if CTA is equivocal. 8. In terms of immediate management: airway beats everything. • People talk about the triple setup: RSI, extraglottic rescue, surgical airway kit. 9. Children with concerning but non-operative injuries need serial examinations — these are very powerful. • Observation is a test. Check neurovascular status every 2 to 4 hours for at least a day. 10. If there’s an impaled object — leave it, transport intact, and remove it in the OR. 11. If you’re working in the community or not at a Level 1 pediatric trauma center — focus on careful airway management and immediate transport. That’s all for this episode. I hope you found it useful — especially since these injuries are less common, but can be incredibly impactful. If you enjoyed the content, or want to hear something different about pediatric trauma