After listening to this episode, learners should be able to:

1. Recognize the clinical manifestations of calcium channel blocker toxicity and distinguish the typical effects of dihydropyridine and non-dihydropyridine agents.
2. Describe the initial evaluation and management of a child with suspected calcium channel blocker toxicity, including the roles of calcium, atropine, high-dose insulin therapy, and vasopressors.
3. Identify children who require prolonged observation, ICU admission, or escalation to advanced therapies such as VA-ECMO.

1. Management of calcium channel blocker toxicity in the pediatric patient. J Pediatr Pharmacol Ther. 2019;24(5):378-386.
2. Are one or two dangerous? Calcium channel blocker exposure in toddlers. J Emerg Med. 2007.
3. Intravenous lipid emulsion treatment for calcium-channel blocker intoxication: pediatric case series and review of the literature. Pediatr Emerg Care. 2022.
4. Audette M, Comstock G. Is beta blocker toxicity associated with hypoglycemia? J Med Toxicol. 2026;22(3):357-363. doi:10.1007/s13181-026-01134-8.

This is the original script for the episode, written by Drs. Robbie Daulton and Brad Sobolewski

Calcium channel blockers are an increasingly prescribed drug class which includes amlodipine, verapamil, diltiazem, and nifedipine. Unlike some of the ingestions we cover in this series, there’s no single reliably curative reversal agent. For non-dihydropyridine agents like verapamil and diltiazem especially, a single adult tablet can be lethal to a toddler; that’s exactly why they sit on the “one pill can kill” list. The sleepy, bradycardic toddler with altered mental status can look like sepsis or a metabolic problem well before it looks like a toxic ingestion, which is why this presentation is a challenge to identify.

The presentation depends heavily on which calcium channel blocker we’re talking about. Nausea and vomiting are the most common early complaint across all of these agents, so don’t be reassured by a benign-sounding chief complaint.

Dihydropyridines, think amlodipine and nifedipine, are selective for vascular smooth muscle at therapeutic doses, so they mostly cause peripheral vasodilation and reflex tachycardia. But in overdose, that selectivity is lost, meaning you can see cardiogenic or distributive shock.

Non-dihydropyridines, verapamil and diltiazem, hit the heart directly, meaning they can cause primarily cardiogenic shock. They slow the sinus node and block AV conduction, leading to sinus bradycardia, first-degree or higher-grade AV block, and sometimes a junctional escape rhythm, with a QRS that usually stays narrow since CCBs spare intraventricular conduction.

Calcium channel blockade doesn’t stop at the heart and vessels. These L-type channels also exist on pancreatic beta cells. Blockade suppresses insulin secretion and worsens peripheral insulin resistance. Cardiac myocytes become relatively starved of a key fuel during this stress state. High-dose exogenous insulin restores myocardial glucose uptake and improves contractility, aiding in cardiogenic shock states.

Remember, if you have a child who presents with concerns for a CCB, it is important to urgently contact the Poison Control Center.

Start with the fundamentals: ABCs, IV or IO access, glucose check, and a bedside EKG looking for that bradycardia and AV block. If the child is in shock, get a bedside echo early. Distinguishing cardiogenic from a distributive picture changes your resuscitation, and it’s a particularly important step for dihydropyridine overdoses where peripheral vasodilation, not pump failure, may be driving the hypotension.

Send a blood gas with lactate (this will help distinguish from DKA), a basic metabolic panel, and an ionized calcium. A chest X-ray is worth getting if there’s evidence of severe toxicity or pulmonary edema, and an abdominal X-ray can help if you’re worried about a pill bezoar, especially with sustained-release products.

For decontamination, activated charcoal can be considered if you’re early and the airway is protected. You can consider whole bowel irrigation, especially when faced with sustained-release products or when tablets are radiographically visible.

For the shock itself, start with fluids and IV calcium repletion as a temporizing bridge. Atropine may be required for symptomatic bradycardia. The cornerstone for inotropic support needed in cardiogenic shock is high-dose insulin therapy: a bolus of 1 U/kg of regular insulin, followed by an infusion, paired with dextrose and glucose monitoring. Insulin can cause hypoglycemia, hypokalemia, and an increased volume/solute load, meaning frequent lab and volume status monitoring is important. For refractory cases, the Poison Center may recommend norepinephrine, or methylene blue, hydroxocobalamin, and angiotensin II. Glucagon appears in older references, but the evidence behind it is thin and inconsistent.

Consider VA-ECMO for refractory cardiogenic shock or cardiac arrest despite maximal medical therapy.

If you need to intubate, avoid benzodiazepines and barbiturates since they’ll exacerbate the hypotension. Pre-treat anticipated bradycardia with atropine and favor rocuronium over succinylcholine.

Disposition hinges on the agent and the formulation. Any reported ingestion of a non-dihydropyridine, verapamil or diltiazem, in a toddler warrants an ED visit.

Asymptomatic children after a confirmed immediate-release ingestion still need at least six hours of monitoring. Any exposure to a sustained-release or extended-release product requires longer observation, up to twenty-four hours.

Anyone symptomatic, hemodynamically unstable, or on calcium, insulin, or vasopressor support needs an ICU bed.

1. Think calcium channel blocker whenever you see bradycardia, hypotension, +/- hyperglycemia.
2. A single non-dihydropyridine tablet in a toddler is a genuine “one pill can kill.” It deserves an ED evaluation and a call to the Poison Center.
3. Fluids and calcium buy you time, but early high-dose insulin euglycemic therapy is your cornerstone treatment for refractory cardiogenic shock. Vasopressors should be considered a helpful adjunct, with VA-ECMO kept in reserve for refractory shock or arrest.

After listening to this episode, learners should be able to:

1. Recognize the clinical stages of pediatric iron toxicity and identify features concerning for significant systemic toxicity.
2. Use the estimated elemental iron dose, serum iron concentration, and abdominal radiography to evaluate a child with a suspected iron ingestion.
3. Describe the emergency management of iron toxicity, including supportive care, whole bowel irrigation, indications for deferoxamine, and appropriate disposition.

1. 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.
2. 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.
3. 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.
4. Banner W Jr, Tong TG. Iron poisoning. Pediatr Clin North Am. 1986;33(2):393-409.

This is the original script for the episode, written by Drs. Robbie Daulton and Brad Sobolewski

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.

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.

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.

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.

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.

1. 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.
2. Obtain a serum iron level four to six hours post-ingestion. It’s your most useful test, but interpret it alongside the clinical picture.
3. 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.

By the end of this episode, listeners should be able to:

1. Compare the composition and physiologic effects of 0.9% saline and balanced crystalloids used for pediatric fluid resuscitation.
2. Summarize the design and major findings of the PRoMPT BOLUS trial.
3. Describe important limitations of PRoMPT BOLUS when applying its results to children with septic shock.
4. Apply current evidence and 2026 Surviving Sepsis Campaign recommendations when selecting crystalloid fluids for pediatric septic shock.

1. 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.
2. 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.

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 seventy-five percent of crystalloid as the assigned fluid rather than requiring exclusive use of one fluid. That could reduce the ability to detect a small treatment effect, but it also makes the study more reflective of real clinical practice.

The investigators themselves described the trial as a comparison of predominant rather than exclusive use of balanced crystalloids versus saline. Finally, the trial was open label, so clinicians knew which fluid the child was receiving. That introduces the possibility of treatment bias, though the primary outcome relied on relatively objective measures.

A substantial proportion of children also did not have a measured baseline creatinine, so baseline kidney function sometimes had to be imputed using age- and sex-based values. That’s worth remembering because persistent kidney dysfunction was part of the primary composite outcome. Taken together, I think PRoMPT BOLUS makes the bedside decision simpler.

Balanced fluids remain a completely reasonable and defensible choice. They cause less hyperchloremia, and there’s no reason to abandon them if they’re already part of your usual resuscitation fluid strategy or your order sets. At the same time, the largest pediatric randomized trial now shows no improvement in major kidney or mortality outcomes compared with normal saline.

So if you use saline at your local hospital, that’s okay too. The 2026 Surviving Sepsis Campaign still conditionally favors balanced crystalloids, but that recommendation is based on very low-certainty evidence. So PRoMPT BOLUS adds important randomized data suggesting that for most children with septic shock, either crystalloid strategy is reasonable.

The practical takeaway is that the choice of crystalloid is probably less important than getting the resuscitation itself right. Give 10 to 20 mLs per kilo when a fluid bolus is indicated, reassess frequently, watch for improvement in perfusion and for signs of fluid overload, and move to vasoactive support when fluid alone is not correcting the shock.

Balanced crystalloids will produce less hyperchloremia. Normal saline will produce more. In PRoMPT BOLUS, that biochemical difference did not translate into a difference in kidney injury, dialysis, or mortality. For most children with septic shock, balanced fluids are fine, normal saline is fine, and timely, thoughtful resuscitation matters much more than which bag is hanging.

I hope you found this episode on fluids for sepsis in children helpful and that you’ll be able to take this knowledge back to the bedside the next time you work in the emergency department. If you’ve got other topics you want me to cover, especially as they relate to practice-changing research in pediatrics, like the PRoMPT BOLUS trial from the Pediatric Emergency Care Applied Research Network, PECARN as we call it, let me know.

Send it my way. If you have time to leave a review on your favorite podcast site, please do so. It helps other people find the show, and definitely share this with your colleagues. I think this study and perhaps this podcast episode could be a great combo for an upcoming journal club. For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.

1. Recognize the evaluation and management of embedded earlobe earrings, including indications for local anesthesia, incision, and removal techniques.
2. Differentiate uncomplicated earlobe piercings from cartilage piercings that require additional concern for perichondritis, Pseudomonas infection, and possible ENT consultation.
3. Apply evidence-based post-procedure care, including appropriate wound management, antibiotic selection, and counseling to help prevent future embedded earrings.

1. Timm N, Iyer S. Embedded earrings in children. Pediatr Emerg Care. 2008;24(1):21-24.
2. 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.
3. Kim MM, Goldman RD. Ear-piercing complications in children and adolescents. Can Fam Physician. 2022;68(9):661-663.

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 gently spread the tissue with a mosquito hemostat until the hardware comes into view.

Notice that I said spread, not dissect. You’re not hunting for the earring. You’re simply opening the tissue until you see the hardware, enabling yourself to grab it. Once you can see metal, you’re almost done. Hold one side steady and separate the backing from the post. Don’t just grab one piece and pull because the whole earring will usually rotate within the earlobe instead of coming apart.

I also keep gauze or a surgical towel underneath the ear while I’m working. The little backings seem to launch themselves across the room every single time you let go, and I’d rather catch one than spend five minutes looking under the stretcher.

Occasionally, you’ll inherit a child who’s already had one or two unsuccessful attempts. Maybe the parents tried at home, maybe the pediatrician tried, maybe another emergency department tried. Every failed attempt makes the next one more difficult. If you’re not making progress, ask yourself, “Am I pulling in the right direction? Do I actually know where the backing is, or am I just fishing for it? Would a tiny posterior incision solve this? Do I need another pair of hands or somebody more experienced?”

Most of the time, changing your approach works better than just yanking harder. Once the earring’s out, I always look at both pieces. Is the backing intact? Is the decorative front intact? Is the post complete?

If something doesn’t look right, especially when you compare it, hopefully, to the other earring that they brought or at least a picture of it, I’ll go back and explore the wound. The last thing you want to do is leave a small piece of metal behind. Once I know everything is out, I put the earring and the backing into a specimen cup and hand it back to the family.

They almost always appreciate getting the jewelry back, especially if it has sentimental value. Then I’ll irrigate the wound with about one hundred to two hundred milliliters of saline. I’m not trying to pressure irrigate it like a contaminated laceration. I just want to wash away dry drainage, debris, and any small blood clots around the piercing tract.

After that, I make sure the bleeding is stopped and that the earlobe still has good color and perfusion before the child leaves. One other question that comes up pretty often, should you close the incision? Most of the time, I don’t. These are really small incisions, usually only a millimeter or two, and it’s okay to allow them to heal by secondary intention.

If there’s any contamination or early infection, I don’t want to trap that underneath a closed wound. Every once in a while, though, I’ll have to make a larger incision, maybe because the backing was deeply embedded or it’s larger or the tissue was particularly swollen. If that incision is more than two or three millimeters, I’ll have a conversation with the family about the trade-off between cosmesis and infection risk.

In some of those cases, I’ll loosely approximate the incision with one or two absorbable sutures, something like 5-0 fast-absorbing gut. If I do that, I’ll only close the incision I created. I still leave the original piercing tract open because I want any residual pus to have somewhere to go. That’s also one of the advantages of making the incision on the back of the earlobe.

If you decide to leave it open or even if you only loosely close part of it, any resulting scar is usually much less noticeable than it would be on the front. Whether I suture or not, I make sure we’ve got good hemostasis and that the earlobe still has good color and perfusion, and then I’ll put some antibiotic ointment and a bandage on it and call it a day.

Honestly, if there’s no cellulitis, no abscess, and the child is otherwise healthy, I generally don’t prescribe oral antibiotics. Topical antibiotic ointment and routine wound care are usually enough. Redness by itself does not equal infection. These ears are inflamed and swollen simply because the earring has been buried in the tissue.

If there’s expanding cellulitis, significant purulent drainage, an associated abscess, fever, or if the child is immunocompromised or has something like diabetes, then I’ll start some oral antibiotics. My first choice is usually cephalexin because these are uncomplicated skin and soft tissue infections caused by methicillin-sensitive staph or streptococci that cause common skin infections.

If the kid has a history of MRSA, there’s a high local prevalence of community-associated MRSA, the family’s had MRSA, or the infection is frankly purulent, then I’ll switch to clindamycin or trimethoprim-sulfamethoxazole, depending on local resistance patterns.

Let’s come back to cartilage one more time.

There, you’re primarily worried about perichondritis, where Pseudomonas aeruginosa is the major pathogen. These patients usually warrant ENT involvement, and antibiotic selection changes substantially, often requiring antipseudomonal coverage. That’s a separate entity from the routine embedded earlobe earring.

Families will also ask, “Can we just put it back in?” Eh, not so fast, right? That piercing tract isn’t really a piercing anymore. It’s a wound. Let it heal completely. If they decide to pierce it again, I’d recommend choosing a slightly different location once everything is healed. You should also talk to families about how to keep this from happening again.

Most of the time, this isn’t because the family did something wrong. Sometimes it just happened. But there are a few things that probably would help. Avoid spring-loaded piercing guns if possible. Don’t clamp the backing tightly against the earlobe. Leave just a little room for swelling. Keep new piercings clean while they’re healing.

And if they notice the backing start disappearing beneath the skin, don’t wait several days hoping the swelling will go down and it’ll just work itself out. These are much easier to remove when they’re only partially embedded than when the skin has completely grown over the hardware.

All right, a few take-home points.

First, figure out which part of the earring is actually embedded before you start yanking on anything. Give your local anesthetic, lido with epi, time to work. I usually wait at least five minutes, but more often seven to ten. And most uncomplicated earlobe piercings don’t need oral antibiotics after removal.

And again, this was really an episode about earlobe embedded earrings. If you’re dealing with cartilaginous piercings that get stuck or infected, think Pseudomonas, think perichondritis, and early ENT involvement.

Honestly, I really enjoy this procedure. It’s quick, it’s satisfying, and families are incredibly appreciative when you’re done. The ear looked terrible when they walked in, they thought their child might need surgery, and then 15 minutes later, they’re walking out with a Band-Aid, their earring in a specimen cup, and the popsicle color of their choice.

These are the fun procedures. So I hope you enjoyed this installment in our minor procedures series.

I’ve already got several more procedures on my list, and I’ll be working through them over time. If there’s one that you’d like me to cover, let me know. As the kids would say, like, rate, and review. If you leave a review on your favorite podcast platform, it really does help other clinicians discover the show, which I appreciate because it helps teach more people good stuff.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

1. Recognize the clinical features and epidemiology of Cyclospora cayetanensis infection in children, including when to suspect the diagnosis in patients with prolonged watery diarrhea.
2. Select appropriate diagnostic testing for cyclosporiasis and identify the limitations of routine stool cultures, ova and parasite examinations, and gastrointestinal pathogen panels.
3. Apply evidence-based treatment and supportive care for pediatric cyclospora infection, including appropriate antimicrobial therapy, hydration, and follow-up considerations.

1. Stobbe M. Outbreak of diarrhea-causing parasite grows to more than 1,000 cases. ABC News. Published July 8, 2026. Accessed July 10, 2026.  
2. 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.  
3. Giangaspero A, Gasser RB. Human cyclosporiasis. Lancet Infect Dis. 2019;19(7):e226-e236. doi:10.1016/S1473-3099(18)30789-8.  
4. Pyzocha N, Cuda A. Common intestinal parasites. Am Fam Physician. 2023;108(5):487-493.  
5. Centers for Disease Control and Prevention. Clinical care of cyclosporiasis. Updated March 8, 2024. Accessed July 10, 2026. 

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 searching for an answer for a week or two. They’ve been told it’s viral. They’ve been waiting for it to improve, and then you finally make the diagnosis within a day or two of starting the right antimicrobial, the kid’s turning the corner. If the kid has a true sulfonamide allergy, things are a little more complicated, and I mean a true allergy, not just the parent who says, “Well, my mother was allergic to sulfa, so we’ve always avoided it.”

There really isn’t a perfect alternative. At this point, I’m probably talking to ID. Nitazoxanide’s been used, ciprofloxacin’s been used, but we generally try to avoid fluoroquinolones in children. Neither has been shown to work as well as trim-sulfa. And if you’ve got somebody who’s immunocompromised with Cyclospora, which fortunately I’ve never seen, I’d be calling ID.

Of course, don’t forget everything else that goes along with taking care of prolonged diarrhea. Oral rehydration is still the goal whenever possible. Some kids are gonna need IV fluids because by the time they get to you, they’ve been losing fluid for days. Replace electrolytes if they’ve been really sick.

And if the illness has dragged on for a couple of weeks, don’t forget the nutritional burden. Sometimes they’ve lost enough weight that getting them eating and drinking normally again becomes part of an ongoing treatment plan. The good news is that most otherwise healthy children recover completely.

Immunocompromised patients are the group that worries us the most. Their symptoms can become prolonged. They can relapse. Sometimes they require longer admissions or even secondary prophylaxis. One question that occasionally comes up is whether you need to repeat stool testing after treatment. In general, you don’t.

If the kid’s symptoms have resolved, then you don’t need to prove microbiologic cure. Treat the patient, not the PCR. If the kid feels better, you don’t need to prove that the pathogen is gone. So let’s get back to that hypothetical scenario we started with, that kid in July that’s had watery diarrhea for 10 days.

The stool culture was negative. They’re starting to lose weight. The parents are frustrated. Everyone keeps telling them it’s a virus. Maybe it is another virus. Maybe it’s two illnesses in a row. But this is the patient where you have to take a step back and consider just one more test instead of offering more reassurance.

That’s what Cyclospora is. Of course, you shouldn’t suspect it in every single child with prolonged diarrhea, but be aware of whether or not there’s an outbreak and test for it. Before wrapping this episode up, here’s a few more things I’d like you to remember. One, if watery diarrhea has lasted more than a week, especially during the summer months, make sure Cyclospora is somewhere on your differential.

Second, remember my comparison. Greasy diarrhea, think Giardia. Swimming pool exposure and profuse watery diarrhea, think Cryptosporidium. Prolonged watery diarrhea during the summer, think Cyclospora. Third, don’t let a negative routine ova and parasite examination or stool molecular pathogen panel falsely reassure you.

Make sure your laboratory is actually testing for Cyclospora, and remember that not every GI PCR panel includes it. Finally, once you make the diagnosis, treatment is pretty straightforward. Trimethoprim-sulfamethoxazole for most patients. Kids will start feeling better in 24 to 48 hours. Cyclospora isn’t the first diagnosis that comes to mind when a kid has diarrhea, and it shouldn’t be.

Viral gastro is still far more common. But when the diarrhea has been going on for 10 days, the stool studies are negative, the kid’s starting to lose weight, and the family says, “I thought we were finally getting better,” that’s when you have to stop and think about Cyclospora. It’s the child with the diarrhea that lingered.

If you enjoyed this episode, as the kids would say, like, rate, and review. Leaving that review on your favorite podcast platform really does help other people discover the show, and I’ve been fortunate to be teaching through this podcast since 2013 because of listeners like you. If you got ideas for future episodes or topics you’d like me to cover, I’d love to hear them.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

1. Compare and select among the four major fishhook removal techniques based on hook characteristics, depth of penetration, and anatomic location.
2. Apply evidence-based approaches to analgesia, anxiolysis, procedural sedation, and post-removal management for pediatric fishhook injuries.
3. 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.

1. Gammons MG, Jackson E. Fishhook removal. Am Fam Physician. 2001;63(11):2231-2236.

2. 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

3. 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

This episode used an AI-generated transcript created in Descript as an initial draft. The transcript was subsequently edited, expanded, and refined by the author with assistance from OpenAI’s ChatGPT (GPT-5.5). Final editorial decisions and content responsibility remain with the author.

Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I'm your host, Brad Sobolewski, and today we're gonna start a new series on minor procedures. These are the types of procedures that we perform all the time in the emergency department. They're not the subject of multicenter trials or big keynote lectures, but these are the things that patients and families remember, and trust me, they will remember them whether you do them well or not.

First up, fishhook removal. So I'm hoping to reel in some listeners with this one, and so hopefully you'll take the bait, and by the end of this episode you'll understand exactly what angle I'm coming from. And hopefully I'm just not trying to make a bass of myself. So anyway, fishhook removal sounds really simple until you actually start doing it.

There's not just one technique. There are four classic approaches, and I'll talk about them all, and which one you choose depends on the hook, whether there's a barb, how deep it is, where it's located, your personal experience with different techniques. Fishhook injuries in children are usually minor and most commonly involve the hands and head, though I've seen them stuck in other body parts as well.

Most can be managed in the emergency department or urgent care setting with local anesthesia and basic equipment Of course, if there's concern for tendon involvement, joint penetration, neurovascular compromise, if it's anywhere near the eyeball, you should stop and rethink your plan. You know, so ortho, if it's embedded deeply in a joint, um, anything that involves the eye itself isn't necessarily an emergency department procedure, and I'm not talking about the eyebrow, I'm talking about the globe.

Fortunately, that's very rare, but that's definitely an ophthalmology conversation. And so before you even think about removing, you need to understand the hook. Is this a single hook or is this a treble hook? A treble hook is a type of fishing hook that has three individual hooks and barbs arranged in a triangular formation, and they're all fused to a single shank and eye.

The eye is where the line gets tied to the hook. Is it freshwater or saltwater? How long has it been there? Is it an old rusty one that was sitting in your garage? Was it underwater for a few hours and then it got hooked in the skin? And honestly, how cooperative is the kid gonna be? Because unlike actual fishing, this is one of the procedures where patience beats blunt force.

So the simplest technique is retrograde removal. This is exactly what families think you're gonna do before you walk in the room. You know, just pull it out the way it went in. But that's not how hooks are designed. They have the barb. They're designed to stay in the fish. So most of the hooks that I've removed are barbed hooks, and so you can't just back them out.

If you try to pull a hook out the way it came in, it's gonna catch and tug on the tissue, it's gonna lead to more pain, bleeding and tissue distortion and not really gonna get you anywhere. So just pulling it out doesn't work, and family probably would have already tried that at home. The technique I end up using most often is advance and cut.

And it kind of sounds wrong the first time you explain it to a family because your solution to removing the hook is to continue to advance the hook, but mechanically, this makes the most sense. So you advance the point of the hook through the skin until the barb exits completely, then use either really good trauma shears or heavy wire cutters to cut the hook in between the shank and the barb.

If it's in a location where you have, uh, enough room, I like to hold a hemostat real close to the skin, grabbing the hook. Then I cut near the barb, get the pointy part out of the way, remove the hemostats, and then back it through the skin. This is considered the most reliable technique, and in most reviews it's described as being nearly universally successful, even for larger hooks.

In children, I think this needs to be the go-to technique because success matters. You just gotta get it done on the, the first attempt. Kids don't tolerate multiple failed attempts very well. Um, obvious downside is that you create a second puncture wound, but in practice, that puncture is usually controlled and much less traumatic than repeated unsuccessful pulling.

Depending on where the skin's at, you may actually need to put a little bit of tension or pressure against the skin to get that hook to poke through. Ultimately, this advance and cut method is the one that you should spend the most time learning and teaching to your trainees. The string yank technique is the one that often is seen at summer camps and on YouTube videos.

You loop string or heavy suture or even fishing line around the bend of the hook, apply downward pressure to the shank to disengage the barb, and then pull quickly in line with the shaft of the hook. When it works, it yanks it out almost instantly. That's why the YouTube videos are popular. One second there's a fishhook in the finger, and the next there isn't.

The advantage is that this can sometimes just be performed without anesthesia and can even be done at home. The disadvantage is obvious if you work with children. This requires cooperation. Younger kids, anxious kids, a treble hook, something that's deeply embedded, like this isn't gonna work all that well, and it's, again, less reliable with bigger and deeply embedded hooks.

The last technique is needle cover. This one gets less attention. It seems elegant, but in practice it's actually pretty hard to do, especially in smaller kid parts. You insert an 18-gauge needle alongside the entry tract until the bevel of that needle covers the barb, and then pull both out together The advantage is that you avoid creating a second puncture wound, and you can minimize tissue trauma.

The disadvantage is it's really complex technically. Maintaining alignment of both the hook and needle can be tricky because they sort of like roll and move around. And if you want to do this one, it's probably easier for smaller and medium-sized hook rather than larger embedded or treble hooks. And as you might imagine in the literature, there's not really any randomized trials comparing these techniques.

Most of what we know comes from prospective observational studies, case series, procedural experience, and expert review. Advance and cut seems to have the broadest success across scenarios. String yank does earn some points for field use and avoiding local numbing. Needle cover is hard to do, but if the parent is absolutely adamant that you don't create a second hole, then that's probably your best option.

And as with any procedure, you should probably be facile in multiple techniques in case the first one doesn't work. You don't just want to stand there and flounder. Anyway, most fishhook removals in children can be done with local anesthesia alone. One percent Lido with or without epi is usually enough.

Depending on the location, you may need to do a digital block or a field block instead of just injecting directly around the hook because local infiltration itself can distort the anatomy and actually make removal harder. So that's why I like blocking the digit or doing a little bit of a field block around it.

If you have time, a topical anesthetic before local infiltration can be a nice gesture. LMX or EMLA can be really helpful, especially for really anxious kids or kids who are escalating before you even start setting up. They take about forty to sixty minutes. About forty-five minutes is probably ideal.

So if you can get that put on in triage, that's actually a, a great technique. So if you know you're going to inject to numb to get the fishhook out, and you need a little bit of extra time to get child life or other personnel in the room, by all means, put a topical anesthetic there. It only absorbs into the outer two millimeters, but it'll help with the poke, not necessarily the burning that happens once the lidocaine is in the tissue.

And now that we've talked about pain, I think it's also important to talk about anxiolysis. Most kids that have embedded fishhooks don't need full procedural sedation. If it's right next to the eye, like in the eyelid, then that might be beneficial, especially in a preschool-aged kid or younger. Plenty of them do need some anxiolysis.

Um, intranasal or oral midazolam is probably, uh, the most popular option. It's got rapid onset in about twenty minutes, no IV, some amnesia. Recent pediatric data suggests that point four or point five milligrams per kilogram may perform better than lower doses, uh, for the intranasal. If you've got nitrous oxide, that's another nice option for cooperative kids.

It provides anxiolysis and analgesia with rapid recovery and a very low rate of adverse respiratory events. Fishhook removal is actually one of those procedures where nitrous can feel disproportionately helpful because the procedure itself is often quick, and the hardest part is just reducing the fear and helping the kid hold still for about thirty to sixty seconds.

I think ketamine still has a role. I alluded to when I might use that earlier. Occasionally, you walk into the room and then there's a deeply embedded treble hook, a really anxious child, a failed attempt prior to you being there. And ultimately, yes, IV procedural sedation with ketamine should be on the table, and it's as always an excellent option.

And never, ever underestimate distraction. Hopefully, you work in a place where there are child life specialists because they are wonderful. They are magic. But you've got videos, you know, music, VR, parents. I mean, sometimes the difference between success and failure is a working iPad. And then finally, the question of antibiotics.

So fishhook removal does not automatically equal a course of antibiotics. A prospective series of one hundred fishhook injuries found prophylactic antibiotics were unnecessary for uncomplicated soft tissue injuries that didn't involve the cartilage or tendon. So if you've got a contaminated wound, a delayed presentation, you know, it was already in an established infection, though I've never actually seen someone impale a fishhook into an area of cellulitis.

There's tendon involvement, joint involvement, or, you know, gross water exposure. Well, then maybe consider antibiotics. Freshwater injuries do raise concern for organisms like Aeromonas. Saltwater injuries introduce concern for Vibrio species and occasionally Mycobacterium marinum enters the conversation or the tissue.

Um, saltwater injuries are often treated with doxycycline plus a third-generation cephalosporin. You recognize the doxy decisions in younger children require some additional consideration. Freshwater injuries could push you towards broader Gram-negative coverage, but, but honestly, for most fishhook injuries, especially in healthy children, you're just dealing with skin flora.

So once I get the hook out, I make sure there's no other retained foreign bodies, like little pieces of the hook or little pieces of the barb. I irrigate with saline or tap water, maybe a hundred mLs for a smaller hook, more for bigger hooks or grossly contaminated wounds. Make sure that there's full neurovascular function and normal range of motion.

Antibiotic ointment, simple dressing, update their tetanus shot if it's not been within five years, and explain to the family that the good news is that this is really a forgiving injury most of the time. Once the hook is out, these generally heal really well. We don't need to suture them back up. We're not worried about long-term damage.

Tell the parents to watch out for increasing redness, worsening pain, pus drainage, fever, or other systemic symptoms, trouble moving the area, especially if it was around a digit, you know, numbness or anything else that makes you concerned that infection has started instead of healing. Families will almost always ask jokingly when they can fish again.

Honestly, usually pretty quickly. Just don't put the wound under water until it's healed, and don't stand directly behind whoever is casting. And now for some take-home points. Fishhook removal is a simple and straightforward procedure where technique really matters. You have to know what type of hook is embedded in the skin.

Retrograde does work for superficial or barbless hooks, but most fishhooks that I've seen have barbs because they are designed to stay in the fish. Advance and cut is probably the most broadly successful technique. String yank works if you're a YouTuber. Needle cover is really, I think, only for those scenarios where the family does not want a second hole.

It's really actually hard to do. Local anesthesia is enough for most kids, so injecting with lidocaine. If you have time, LMX or EMLA helps with the poke a little bit. Routine antibiotics are not usually necessary. And if there's ocular involvement or if it's in a joint, call an ophthalmologist or an orthopedist.

Honestly, this is one of those procedures that's really satisfying once you get comfortable with it. I love doing it with our residents and trainees. Families come in expecting something dramatic, and by the time they leave, they're surprised by how straightforward it was. And I guarantee that this is a story that they will tell for years and years.

And if you do a good job and make it a good experience and perhaps even a lighthearted one, they are going to remember that. And yeah, you'll be part of somebody's fishing story. So I hope you did enjoy this first episode on minor procedures. I'm gonna do additional ones like these along the way because, you know, I think that they don't get a lot of love when it comes to traditional education.

If you've got any ideas for future procedures or topics, please send them my way. As the kids would say, like, rate, and review. If you leave a review on your favorite podcast site, that would really help other people discover the show. I podcast because I think it's a great way to teach, and I've been doing so since 2013.

And yes, you can remove a fishhook. Don't let this straightforward procedure become the one that got away. For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

1. Differentiate croup from other causes of pediatric upper airway obstruction using key historical and physical exam features.
2. Apply a severity-based approach to croup management, including appropriate use of corticosteroids and nebulized epinephrine.
3. Recognize clinical features that suggest alternative or life-threatening diagnoses requiring escalation of care.

1. Cooke A, Conway S, Griffin L. Croup: Rapid Evidence Review. Am Fam Physician. 2026;113(3):254-258.
2. Gates A, Johnson DW, Klassen TP. Glucocorticoids for Croup in Children. JAMA Pediatr. 2019;173(6):595-596. doi:10.1001/jamapediatrics.2019.0834
3. 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
4. Bjornson CL, Johnson DW. Croup. Lancet. 2008;371(9609):329-339. doi:10.1016/S0140-6736(08)60170-1
5. 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

This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content.

 Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. And today we’re gonna talk about croup. We’re gonna focus on diagnosis, severity based management, and how to differentiate it from scarier high risk conditions that may present similarly, but behave very differently.

So croup is best understood as a clinical syndrome of upper airway obstruction caused by inflammation at the level of the larynx and subglottis. So in most cases this is viral laryngotracheitis, most commonly due to parainfluenza virus. But as you’d expect multiple viruses can cause it. The subglottis is the narrowest portion of the pediatric airway.

So even small amounts of edema create large increases in airway resistance. So that’s why the clinical picture is so consistent. You’ve got inspiratory stridor, hoarseness, and that characteristic barking cough, which either sounds like a seal or a dog, and yes, of course, I know the difference between the two coughs because I was a biology major.

This is primarily a disease of children between six months and three years of age with a peak incidence in the second year of life. It’s really, really common, like one and a half percent of all ED visits, maybe 350,000 visits a year, and 85% of these kids have mild disease. Hospitalization is rare. The range is variable, about two to 8% of cases, and return visits occur in about three to 5%. Fewer than 1% of children, a lot fewer, require intensive care or airway intervention. Honestly, most kids do really well. The ones who don’t can get sick very quickly, and that’s been my clinical experience.

In the Northern Hemisphere, we see croup throughout the fall and winter, usually starting in around November and sort of tapering off by April. But that being said, I’ve seen croup-like symptoms every month of the year over the past couple of decades.

Croup is absolutely a classic clinical diagnosis. A typical case begins with 12 to 48 hours of viral prodrome, you know, body aches, fever, congestion, cough, followed by often abrupt nighttime onset of barky cough and stridor. Symptoms fluctuate, and they’re generally worse with agitation and get better when the kid is calm. That variability is the key feature.

So what you’ll have is a child who wakes up after sleeping for a few hours with a barky cough and then noisy stridor. This freaks parents out, and this is not hyperbole. There’s this little center in the back of your brain that’s like, please don’t stop breathing and die. So appropriately, they’re worried about the kid, they call emergency medical services, they bring them to the emergency department, and by and large, by the time they get there, the stridor has resolved. The kid is calm, and parents will say, I swear he looked a lot worse at home. Trust me, we believe you parents, this is what croup does.

When I’m taking a history of croup, I get all of these details. Are there any sick contacts? If the parents are worried about a foreign body inhalation or ingestion, then I’m worried about a foreign body inhalation or ingestion. Listen to the lungs, inspect their airway. Always check the ears for concomitant otitis and I’ll feel their trachea. I’ll actually grab and hold the trachea and move it. Kids with croup really don’t have a painful trachea. Kids with bacterial tracheitis, aside from looking more toxic, actually have a lot of pain when they move their trachea.

Testing for croup is generally unnecessary. Labs and viral studies do not change management, and imaging is really reserved for atypical presentations or when you’re considering an alternative diagnosis like a foreign body. If you do get an X-ray, what you’re looking for is the classic steeple sign on the AP view. It is seen in croup, but it’s not 100% sensitive nor specific.

Once you’ve made the diagnosis of croup, it’s important to assess severity, and remember that I said that most kids are mild. So mild croup is defined by the absence of stridor at rest. So they may have some stridor when they’re upset or even a little bit of hoarseness or noise. It’s important to listen to many, many children with croup to get a sense of this.

Moderate croup includes stridor at rest with mild to moderate retractions. So at rest means that the child is in a position of comfort. They’re calm with a parent, and they’ve generally been that way for about 10 to 15 minutes. Sometimes that’s how long it can take for the stridor to dissipate once you get the kid calm.

Severe croup, which is fortunately rare, involves marked work of breathing, agitation, fatigue, need for oxygen, altered mental status, and this aligns with the Westley croup score. It formalizes stridor, retractions, air entry, cyanosis, and mental status. But really, in practice, most of us get very good at bedside assessment of croup.

Management of croup starts with corticosteroids. This is one of the highest-yield interventions that we have in pediatric emergency medicine. Every child with croup should receive dexamethasone. Typically 0.6 milligram per kilogram as a single dose up to a maximum of 10 milligrams. Some places will use 0.15 milligram per kilogram.

Locally, we often give the IV formulation orally. It’s 10 milligrams per mL. Tastes bad, but pairs reasonably well with apple juice. The oral suspension is 1 milligram per mL, tastes terrible, and pairs nicely with being spit on the ground by toddlers.

The evidence behind dexamethasone is very robust. The main benefit is that it reduces return visits and hospital readmissions by about half, and those return visits include doctor’s offices and emergency departments. In a Cochrane review of 1,679 children, glucocorticoids reduce return visits or readmissions with a risk ratio of 0.52, so that translates to a number needed to treat of seven.

I’ve certainly seen seven or more croup kids during one shift, so for every seven children treated with dexamethasone, one return visit is prevented. Symptom improvement begins within about two hours and lasts at least 24 hours, but maybe up to a couple of days. Hospital length of stay for kids that get steroids is reduced by an average of 15 hours as well. Serious adverse events are rare. It’s well tolerated, and other than the taste, kids do fine with it. And importantly, the benefit is consistent across all severities of croup, mild, moderate, and severe.

So when you explain this to families who are very scared about their kids, but now their kid is looking better and you’re only giving them a single medicine, not doing any tests or X-rays or anything, I think you have to frame the medicine in terms of what it’s going to do for them over the next couple of days.

So one way of explaining this to families would be to say something like this is a steroid called dexamethasone. It reduces the swelling in your child’s airway that’s causing the barky cough and noisy breathing. Most children start feeling better within a couple of hours, and the benefit lasts at least a full day, if not longer.

Without this medicine, about one in five children need to come back because symptoms get worse again. You really get two bad days with croup in most cases. With this medicine, the risk of returning drops to about one in 10, so it cuts the chance of coming back in half.

We can expect your child’s cough to start improving over the next day or two. Most children are feeling a lot better within 48 hours, though a little bit of hoarseness and cough can last for a week to about 10 days.

So it’s possible that when your child goes to sleep later tonight, they may experience that barking cough and noisy breathing again. They’re almost certainly going to be upset. The steroid blunts enough of the swelling so that you are much more likely to have them free of distress and stridor, that noisy breathing, once you get them calm.

So if they’re upset, get them calm, and if in about 10 minutes the stridor and noisy breathing get better, that’s the dexamethasone doing its job and you can safely stay home.

For children with moderate or severe croup, we’re gonna use nebulized racemic epinephrine. It works fast by reducing airway edema by constricting inflamed blood vessels. You’ll see improvement in stridor and work of breathing often within 30 minutes. The effect is transient and largely gone by about two hours, and you need to do a structured reassessment at about 30 minutes after the racemic epinephrine.

If the child’s clearly better, continue that observation for up to two hours. If they’re unchanged or worse, repeat the epinephrine and start thinking more carefully about your diagnosis and disposition. Because it’s got such a short duration, that two hours after treatment is the most common time period, though some institutions and some children will need to be observed a little bit longer.

If they remain well appearing with no stridor at rest, normal oxygenation, minimal work of breathing, and they can tolerate oral fluids, they can be discharged. If symptoms recur, they require repeated epinephrine, or they fail to improve, then you may have to escalate care and consider admission.

Honestly, with croup, supportive care is still one of the most important things. You gotta keep kids calm by minimizing agitation. Parents are experts at this with their own children. Agitation worsens airway obstruction. Airway resistance is fourfold greater when the kid’s upset.

Give oxygen if the kid’s hypoxic. Fortunately, this is rare. Antipyretics and fluids are great, do them. Humidified air has not been shown to provide meaningful benefit, and obviously we should avoid sedatives because they can suppress respiratory drive without improving airway patency.

Many parents will say that their kid was better when they were exposed to cool air or mist in the shower. Those can help, but honestly, don’t stick your kid’s head in the freezer if it upsets them. Keep them calm, hold them, and comfort them.

Alright, croup, barking cough, stridor, variable symptoms, easy, right? There are some other diagnoses that can mimic this or overlap that you shouldn’t miss.

Spasmodic croup is a related phenotype. You’ve got sudden nighttime onset, often minimal prodrome, and recurrent episodes. These kids are typically well between episodes, and the pattern becomes more apparent over time. Some kids will bark with every mild cold or stuffy nose up until about eight or nine, but they usually don’t have stridor and respiratory distress.

Bacterial tracheitis is progression to a more severe and dangerous airway infection. These children often start with viral symptoms and then rapidly worsen. They’ve got a high fever, they appear toxic. Most importantly, they fail to respond to standard croup therapy. Toxic appearance plus lack of response should immediately shift your diagnostic reasoning.

These kids may have a lot of pain when you grab and move their trachea. The cough can be more junky because again, they’ve got purulent mucus in their trachea.

Epiglottitis is defined by the absence of barking cough and the presence of drooling, dysphagia, and tripod positioning. These children are very anxious, they’re very ill, their airway is at risk, and so your immediate priority is keeping them calm and having the airway managed in the safest environment, generally the operating room.

Deep neck space infections, including retropharyngeal cellulitis and abscesses and peritonsillar abscesses, present with fever, neck stiffness, sometimes even torticollis, and lymphadenopathy. Kids won’t really have a barky cough and the exam localizes to the neck rather than the airway alone.

Acute foreign body aspiration presents with sudden onset symptoms, no viral prodrome, no barking cough, and sometimes some asymmetric exam findings. The diagnosis is frequently missed when clinicians anchor too early on croup.

If you have an esophageal foreign body, remember that 70% of these get stuck at the thoracic inlet. So always think about a kid who sounded like they had croup and got croup treatments, but also has some swallowing issues and is the right age to put things in their mouth. This is when you see coins and button batteries and other things stuck not in the upper airway, but in the esophagus right behind it.

Alright, now when it comes to disposition, most kids with croup are gonna be sent home. Children who improve, they have no stridor at rest, minimal work of breathing, can be discharged home with clear return precautions. Those with persistent symptoms, need for repeated racemic epinephrine, hypoxia, or concerning features should be admitted.

For kids who continue to worsen despite standard therapy, escalation includes high-flow nasal cannula, noninvasive ventilation as a bridge. Heliox can be used as a temporizing measure to reduce work of breathing.

Fortunately, needing to intubate a child with croup is rare, but when it’s needed, it can be challenging due to subglottic narrowing. You need the best proceduralists, and you should downsize your endotracheal tube by 0.5 to 1 millimeter smaller than usual.

And I’ll reiterate this again. The natural course of croup is really favorable for most kids. The fear’s not gonna go away for the parents, this is a scary diagnosis, but I think with some reassurance, we can help them understand that this is something that is unlikely to cause significant problems and will get better.

Most kids improve significantly within 48 hours, though like any other respiratory illness, symptoms can persist for a week or so. Severe outcomes are fortunately rare, and they almost always occur in children whose severity or alternative diagnosis was not recognized early.

So again, here’s my take-home points. Croup is a clinical diagnosis. Severity determines your management. Steroids, dexamethasone, should be given to all patients. Racemic epinephrine is used for moderate to severe disease with mandatory reassessment and observation. And most importantly, always reassess the diagnosis when the presentation does not fit the expected patterns.

Things can get rough when you’re barking up the wrong tree and thinking it’s croup when it’s actually something else.

Well, I hope you enjoyed this episode on honestly one of the most classic conditions that we see in the pediatric emergency department. If you’ve got any feedback on the episode, send it my way.

As the kids would say, like, rate, and review. I would love it if you left a review on your favorite podcast site. It helps more people find the show. I do this as a labor of love because I enjoy teaching, and I think that this is a wonderful way to reach my colleagues and learners.

If you’ve got suggestions on other topics or episodes, I’d love to hear them.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

1. Recognize the clinical features of pediatric migraine and distinguish it from secondary causes of headache.

2. Implement a stepwise, evidence-based emergency department approach to acute pediatric migraine, including appropriate medication selection and timing of reassessment.

3. Develop safe discharge and follow-up plans by defining treatment endpoints, minimizing medication overuse, and identifying patients who require referral or inpatient management.

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.

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 with an IV. This often causes lots of angst, even in older teenagers.

The medication just does not get to the brain as effectively and fast enough if you take it by mouth. Many patients who get the dopaminergic agents, so prochlorperazine, will invariably feel jittery or anxious or like they gotta move or like they got ants in their pants. I tell them to expect this so they’re not surprised and worried when it happens.

I tell them that once they start feeling that way, it means the medicine is probably working. They need to hit the nurse button and we’re gonna get them up and have them take a walk. This fixes it for the majority of patients just getting up and moving.

In adult centers, even with the initial administration of the prochlorperazine or as sort of a reflexive response to any of those symptoms, they just give a slug of IV Benadryl.

There’s some studies in adolescents especially that this may decrease the effectiveness of the IV agents you’re giving in the first place, and it may also increase return rates to the ED. So I will use IV diphenhydramine if getting up and moving around isn’t working, or if the distress is significant, or if the patient clearly indicates they’ve needed it in the past.

So if after the migraine cocktail, the patient has met their pain goals and the reassessment is favorable, they can go home to outpatient follow-up. How about if the headache got better, but not all the way? It’s usually when the initial migraine cocktail didn’t achieve the pain endpoints fully, like it helped partially. If the dopamine blockade didn’t do anything, valproate is unlikely to rescue the case.

And so valproate works on GABA and it stabilizes some of these pain processes, but the dopaminergic agent needs to have done something first for valproate to work. Per the most common protocol, you give an initial dose of IV valproate, then you discharge the patient home on Depakote ER.

So oral valproic acid under 10 years old or under 50 kilograms, 250 milligrams PO twice a day for two weeks, or older than 10 or greater than 50 kilos, 500 milligrams twice a day for two weeks. This is the extended release and it’s most helpful if you give the first oral dose in the emergency department.

So that’s why it’s very important to build this protocol in advance. If you don’t have IV valproate, then don’t just give the patient oral valproate, and definitely don’t prescribe an oral course for discharge.

All right, well, what about DHE? Dihydroergotamine for refractory or status migrainosus?

Generally, this is only given at pediatric centers where you have neurology coverage. It’s contraindicated if you’ve had another dose of DHE within 14 days, or you’ve had any triptan of any sort within 24 hours, and you must obtain a pregnancy test in adolescent females before giving it.

The dosing for less than 30 kilograms is 0.5 milligram. At least 30 kilograms is one milligram. You give 50% of the dose over three minutes, then the remaining 50% over 30 minutes.

If this is gonna work, the patients are gonna start feeling wretched at first. They’re gonna get very nauseous and they’re gonna vomit. They’re gonna have flushing, and you’ll see transient hypertension.

Most of that resolves within the hour in most centers. If you’re committing to DHE, you’re kind of bringing the patient into the hospital anyway, though some facilities will have DHE done in the emergency department with close outpatient follow-up. Either way, it’s really best practice to involve child neurology if you’re giving DHE.

Alright, well what about steroids? They give those in grownups too, right?

Steroids really only have a role for recurrence prevention in children. So for kids that have a history of returning within 72 hours for rebound headache, you can give dexamethasone 0.6 milligram per kilogram IV dose, the max of 10 milligrams.

You do not discharge them home on a steroid prescription or a Medrol dose pack or something else, and this can cut the recurrence risk down a bit.

There’s other therapies out there like magnesium and ketamine. There’s just not enough evidence there. And the purpose of this episode is to discuss the therapies that have good evidence behind them and should be part of protocols across the country.

Some patients are unfortunately not responsive to emergency department therapy and need admission. The main inpatient therapy is the DHE protocol. If they’re not DHE eligible, they haven’t tolerated it well or it’s unavailable, admission’s unlikely to help them unless they just need some IV fluids to help them get back up on their feet.

You should consult neurology if the headache goals are not met after maximizing ED therapy for advice. And we should definitely avoid opioids. They don’t treat patients with migraines. They increase recurrence risk. They increase revisit rates. Again, the dopamine antagonist prochlorperazine, it’s superior for sustained relief when families ask about them, and fortunately they’re asking about opioids far less.

We use medications that treat the migraine pain pathways and signaling. We don’t just wanna mask the pain.

All right, so that’s all I’ve got on the acute management of migraine headaches, especially in the emergency department. Remember that migraine care in the ED should be protocolized and evidence-based. IV fluids are supportive.

Prochlorperazine is the first line, or you can use metoclopramide as well. Ketorolac is an adjunctive therapy. Valproate is next line. If you’ve gotta escalate, and DHE is specialized therapy, you can start in the ED, but most of these patients are getting admitted. Dexamethasone or steroids in children can reduce recurrence risk, but they’re not really part of the acute management.

You should definitely define the endpoints and structurally and systematically reassess patients at an hour. The goal is to get them feeling better to a defined endpoint and to restore function. There is evidence-based pediatric emergency migraine care. You should understand that, plus how to explain why these agents are being given and some of the side effects to patients and families.

I find that that approach increases your likelihood of buy-in and success.

Alright, so that’s it for this episode on the Acute Management of Migraine Headaches in Children and Adolescents. I hope you found it helpful and I can pretty much guarantee that you’re gonna see a patient with a migraine on your next shift.

If you’ve got any feedback or comments, send them my way. If you like this episode, leave a review on your favorite podcast site. It helps more people find the show. Or recommend it to a colleague. If there’s other topics that you’d like to hear, send them my way for the Pediatric Emergency Medicine podcast.

This has been Brad Sobolewski. See you next time.

1. 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.
2. 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.
3. Demonstrate effective, patient- and family-centered communication techniques for explaining the diagnosis of PNES and facilitating timely referral to appropriate outpatient therapy.

1. 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)
2. 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)
3. 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)
4. 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)

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 their airway, oxygenating, and hemodynamically stable, avoid repeated benzodiazepines. Avoid intubating them unless clearly indicated, and avoid reflexively loading them with antiseizure medications such as levetiracetam or valproic acid.

Take a focused history. You’ve gotta find out if they have a prior epilepsy diagnosis. Have they had EEGs before? What triggered today’s event? Do they have a psychiatric history? Does the patient have school stressors or family conflict? And then is there any recent illness or injury?

Only order labs and imaging when clinically indicated. EEG is not widely available in the Emergency Department.

We definitely shouldn’t say things like, “this isn’t a real seizure,” or use outdated terms like pseudo-seizure. Don’t say it’s all psychological, and please do not imply that the patient is faking.

If you see a patient and you think it’s PNES, you’re smart, you’re probably right, but don’t promise diagnostic certainty at first presentation. Remember, a sizable proportion of these patients actually do have epilepsy, and referring them to neurology and getting definitive testing can really help clarify the diagnosis.

Communication errors, especially early on, worsen outcomes.

One of the most difficult things is actually explaining what’s going on to families and caregivers. So here’s a suggestion. You could say something like:

“What your child is experiencing looks like a seizure, but it’s not caused by abnormal electrical activity in the brain. Instead, it’s what we call a functional seizure, where the brain temporarily loses control of movement and awareness. These episodes are real and involuntary. The good news is that this condition is treatable, especially when we address it early.”

The core treatment of PNES is CBT-based psychotherapy, or cognitive behavioral therapy. That’s the standard of care. Typical treatment involves 12 to 14 sessions focused on identifying triggers, modifying maladaptive cognitions, and building coping strategies.

Almost two thirds of patients achieve full remission with treatment. About a quarter achieve partial remission. Combined improvement rates reach up to 90 percent at 12 months.

Additional issues that neurologists, psychologists, and psychiatrists often face include safe tapering of antiseizure medications when epilepsy has been excluded, treatment of comorbid anxiety or depression, coordinating care between neurology and mental health professionals, and providing education for schools on event management.

Schools often witness these events and call prehospital professionals who want to keep patients safe. Benzodiazepines are sometimes given, exposing patients to additional risk. This requires health system-level and outpatient collaboration.

Overall, early diagnosis and treatment of PNES is critical. Connection to counseling within one month of diagnosis is the strongest predictor of remission. PNES duration longer than 12 months before treatment significantly reduces the likelihood of remission.

Video-EEG confirmation alone does not predict positive outcomes. Not every patient needs admission to a video-EEG unit. Quality of communication and speed of treatment, especially CBT-based therapy, matter the most.

Overall, the prognosis for most patients with PNES is actually quite favorable. There are sustained reductions in events along with improvements in mental health comorbidities. Quality of life and psychosocial functioning improve, and patients use healthcare services less frequently.

So here are some take-home points about psychogenic non-epileptic seizures, or PNES. Pseudo-seizure and similar terms are outdated and misleading. Do not use them. PNES are real, involuntary, brain-based events. Diagnosis relies on positive clinical features, what the events look like and when they happen, not normal lab tests or CT scans.

Early recognition and diagnosis, and rapid referral to cognitive behavioral therapy, change patients’ lives. If you suspect PNES, get neurology and mental health professionals involved as soon as possible.

Alright, that’s all I’ve got for this episode. I hope you found it educational. Having seen these events many times over the years, I recognize how scary they can be for families, schools, and our prehospital colleagues. It’s up to us to think in advance about how we’re going to talk to patients and families and develop strategies to help children who are suffering from PNES events.

If you’ve got feedback about this episode, send it my way. Likewise, like, rate, and review, as my teenagers would say, and share this episode with a colleague if you think it would be beneficial.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

After listening to this episode, learners will be able to:

1. 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.

2. 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.

3. Determine when consultation with orthopedics and infectious diseases is indicated, and recognize clinical features that warrant prolonged therapy or more conservative management.

1. 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

2. 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

3. 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

4. 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

5. 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

6. Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352-360. doi:10.1056/NEJMra1213956

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 Staphylococcus aureus, first-generation cephalosporins or antistaphylococcal penicillins remain the preferred parenteral agents. For oral therapy, high-dose cephalexin, 75 to 100 milligrams per kilogram per day divided every six hours, is preferred. Clindamycin is an alternative when beta-lactams cannot be used.

For clindamycin-susceptible MRSA, clindamycin is the preferred IV and oral agent due to excellent bioavailability and bone penetration, and it avoids the renal toxicity associated with vancomycin.

For clindamycin-resistant MRSA, vancomycin or ceftaroline are preferred IV agents. Oral options are limited, and linezolid is generally the preferred oral agent when transition is possible. Daptomycin may be used parenterally in children older than one year without pulmonary involvement, typically with infectious diseases and pharmacy input.

Beta-lactams remain the drugs of choice for Kingella kingae, Streptococcus pyogenes, and Streptococcus pneumoniae. Vancomycin has no activity against Kingella, and clindamycin is often ineffective.

For Salmonella osteomyelitis, typically seen in children with sickle cell disease, third-generation cephalosporins or fluoroquinolones are used. In underimmunized children under four years, consider Haemophilus influenzae type b, with therapy guided by beta-lactamase production.

Doxycycline has not been prospectively studied in pediatric acute hematogenous osteomyelitis. There are theoretical concerns about reduced activity in infected bone and risks related to prolonged therapy. While short courses are safe for certain infections, the longer durations required for osteomyelitis increase the risk of adverse effects. Doxycycline should be considered only when no other active oral option is available, typically in older children, and with infectious diseases consultation. It is not appropriate for routine treatment.

Many hospitals automatically consult orthopedics when children are admitted with osteomyelitis, and this is appropriate. Early orthopedic consultation should be viewed as team-based care, not failure of medical management.

Consult orthopedics when MRI shows abscess or extensive disease, there is concern for septic arthritis, the child fails to improve within 48 to 72 hours, imaging suggests devitalized bone or growth plate involvement, there is a pathologic fracture, the patient is a neonate, or diagnostic bone sampling or operative drainage is being considered. Routine surgical debridement is not required for uncomplicated cases.

Infectious diseases consultation is also often automatic and supported by guidelines. ID is particularly valuable for antibiotic selection, dosing, IV-to-oral transition, duration decisions, bacteremia management, adverse reactions, and salvage regimens. Even in straightforward cases, ID involvement often facilitates shorter IV courses and earlier oral transition.

Osteomyelitis is generally not contagious, and clustering is uncommon for Staphylococcus aureus. Kingella kingae is the key exception. It colonizes the oropharynx of young children and spreads via close contact. Clusters of invasive Kingelladisease have been documented in daycare settings.

Suspicion should be higher in children six to 36 months from the same daycare, with recent viral illness, mild systemic symptoms, refusal to bear weight, modest CRP elevation, and negative routine cultures unless PCR testing is used. Public health intervention is not typically required, but awareness is critical.

There is no minimum required duration of IV therapy for uncomplicated acute hematogenous osteomyelitis. Transition to oral therapy should be based on clinical improvement plus CRP decline. Many children meet criteria within two to six days.

Oral antibiotics must be dosed higher than standard outpatient regimens to ensure adequate bone penetration. Common regimens include high-dose cephalexin, clindamycin, or linezolid in select cases. The oral agent should mirror the IV agent that produced clinical improvement.

Total duration is typically three to four weeks, and in many cases 15 to 20 days is sufficient. MRSA infections or complicated cases usually require four to six weeks.

Early oral transition yields outcomes comparable to prolonged IV therapy with fewer complications. Most treatment-related complications occur during parenteral therapy, largely due to catheter-related issues.

Take-home points: osteomyelitis in children is a clinical diagnosis supported by labs and MRI. Empiric antibiotics should be guided by age, illness severity, and local MRSA prevalence. Early transition to high-dose oral therapy is safe and effective when clinical response and CRP support it. Orthopedics and infectious diseases consultation improve care and reduce variation. FAST MRI is changing how we diagnose osteomyelitis. Daycare clustering is uncommon except with Kingella kingae.

That’s all for this episode. If there are other topics you’d like us to cover, let me know. If you have the time, leave a review on your favorite podcast platform. It helps more people find the show and learn from it. For PEM Currents, this has been Brad Sobolewski. See you next time.

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.

• 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/

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 feedback on this episode or there's other common topics you'd like to hear about, send them my way. If you enjoyed this episode and think that other people should listen to it, share it with them. More listeners means more learners. And if you have a chance, leave a review or like the podcast on your favorite podcast site for PEM Currents, the Pediatric Emergency Medicine Podcast.

This has been Brad Sobolewski. See you next time.

Learning Objectives

By the end of this episode, you will be able to:

1. Define BRUE and contrast it with the older concept of ALTE.

2. Recognize evolving risk stratification criteria

3. Apply evidence-based strategies for evaluation and counseling of infants with BRUE, including safe discharge decisions and the role of home monitoring.

References

1. 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

2. 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).

3. 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).

4. 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).

5. 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).

6. 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

7. 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

Learning Objectives

1. 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.
2. 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.
3. 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

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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 antibiotics, and we shouldn't be treating viruses with antibiotics anyway, so get good at looking at ears and know what you're seeing. And have they taken similar antibiotics since then? Like. Different penicillins, Augmentin, or cephalexin. So if they said that they were allergic to amoxicillin, but then somehow tolerated Augmentin.

They're not allergic. If a patient had rash only, but no hive swelling or difficulty breathing, no reaction within the first hour. It occurred more than five years ago or before the kid was three. And especially if they tolerated beta-lactam antibiotics. Since then, they're a great candidate for de labeling and I would refer that kid to the allergy clinic.

Generally, they can get them in pretty darn quick. Alright, we're gonna wrap up this episode. Most kids labeled penicillin allergic or amoxicillin allergic, or not actually allergic to the medication. There are some scores like pen fasts that are validated tools to assess risk and support de labeling.

Direct oral challenge for most patients is safe, efficient, and increasingly the standard of care. There are allergy clinics like the Pats at Cincinnati Children's that can dela children in a single visit with oral challenges alone, needing no skin testing, and emergency departments can play a key role in identifying and referring these patients and possibly de labeling ourselves in the future.

Well, that's all for this episode on Penicillin Allergy. I hope you learn something new, especially how to assess whether an allergy label is real, how to ask the right questions and when to refer to an allergy testing clinic. If you have feedback, send it my way. Email, comment on the blog, a message on social media.

I always appreciate hearing from you all, and if you like this episode, please leave a review on your favorite podcast app. Really helps more people find the show and that's great 'cause I like to teach people stuff. Thanks for listening for PEM Currents, the Pediatric Emergency Medicine podcast. This has been Brad Sobolewski.

See you next time.

1. Apply an age-based approach to the differential diagnosis of limping in children.
2. Demonstrate diagnostic reasoning by integrating history, physical exam, imaging, and lab findings to prioritize urgent conditions like septic arthritis and SCFE.
3. Appropriately select and interpret imaging and lab studies, including understanding the utility and limitations of ultrasound, MRI, and the Kocher criteria.

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1. 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
2. UpToDate. Evaluation of limp in children. Accessed September 2025.
3. UpToDate. Differential diagnosis of limp in children. Accessed September 2025.
4. StatPearls. Antalgic Gait in Children. NCBI Bookshelf. Accessed September 2025.
5. Pediatric Emergency Care. “Approach to Pediatric Limp.” Pediatrics in Review. 2024.

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’t use the labs and values of Kocher criteria in the knee or elbow, or another joint. It is only the hip. And the four classic criteria are fever greater than 38.5 Celsius, non-weight bearing on the affected side, ESR, greater than 40. Or CRP greater than two and white blood cell count greater than 12,000, and you use them in combination to predict the likelihood of septic arthritis of the hip.

So if you have none of them, you have less than a 0.2% chance of septic arthritis. If you have one, you have 3%, two 40%. Three of them, 93% and all four, a 99 plus percent chance of having septic arthritis. So the more criteria that are positive, the higher the post-test probability of septic arthritis. And remember I mentioned this before, ultrasound isn’t part of that rule, so don’t let a small effusion sway you one way or the other.

Septic arthritis is a clinical diagnosis supported by aspiration of the hip. Ultrasound can help, but a normal scan doesn’t clear the joint, so some orthopedists will recommend not getting an ultrasound on intermediate risk cases and just going straight to joint aspiration if the concern’s high. So if the kid’s worried they stay, don’t discharge a maybe septic joint.

I think now’s a good time to come back to some of the common diagnoses that you’ll have on your differential, and I think an age-based schema makes sense here. In Kids Under three, you’re thinking toddlers fracture, septic, hip, developmental dysplasia of the hip, non-accidental trauma, leukemia and transient synovitis in kids three to 10 transient synovitis rules the day.

Injuries and trauma. Hopefully you have a good history. Septic arthritis, juvenile idiopathic arthritis, and leg calf, Perth’s disease, and then kids older than 10, you’ll start to see scfe. So slipped capital, femoral epiphysis, stress fractures, osteomyelitis, overuse injuries, and yes, still unfortunately, malignancy leg, Ewing sarcoma.

Thinking beyond the limb should remind you that systemic causes can lead to limp as well. Appendicitis can present as right hip pain or limp. Testicular torsion may cause abdominal pain and referred thigh pain. Leukemia obviously can present with limp, nighttime pain, and subtle systemic signs. Discitis may masquerade as refusal to walk or sit upright.

And any malignancy can present subtly. You can see bruising, fatigue, pal anemia, or bony tenderness. So red flags for a child with limp, so you’re calling orthopedics, admitting or escalating. Your plan is when the kid is ill appearing toxic or febrile. Your labs obviously suggest inflammation or infection.

You have septic, arthritis, osteomyelitis, or non-accidental trauma. At the top of your list, and you have diagnostic uncertainty on a child who isn’t improving. So you did a workup. It’s reassuring, and despite analgesia, reassurance and time, the kid still won’t walk well. Maybe that kid needs workup for osteomyelitis, so sometimes the best course of action is to admit them and get the MRI the next day.

All right. Here’s some take home points on the child with limp. Limping is due to pain, weakness, mechanical or neurologic causes. Think broadly in terms of your differential history, physical exam and observation, or more valuable than a dozen labs. Age-based differential diagnoses guide you and help you tailor your exam and questions accordingly.

So I think that’s a good schema to teach. Always start with plain films, especially if you suspect injury. The Kocher criteria are only valid for differentiating septic hip versus transient synovitis. Don’t use them in another joint. And septic arthritis is a clinical diagnosis, so if you’re worried and they have multiple factors, tap that joint.

If you’re concerned about the kid and they’re still not walking, it’s okay to admit, and again, don’t forget to check the feet. I’ve seen many kids that have been limping because there’s a splinter in the bottom of the foot. You can save yourself a lot of time and money by just yanking that little splinter.

Well, that’s all for this episode. I hope that this helps you evaluate limping kids with a bit more confidence, precision, efficiency, and ultimately lets you communicate rationale for testing and treatments better with families. If you’ve got ideas for other episodes, send them my way. If you wanna collaborate on making a podcast in the future, I’d love to do that as well.

If you like this episode of this show in general, share it with your colleagues and. If you have the time, leave a comment on the blog or like rate review the podcast. It helps more people find it and more people learn. If you notice that input adds on this, I’m not making a dime. I just wanna teach people stuff.

That’s all for this one, for PEM Currents, the Pediatric Emergency Medicine podcast. This has been Brad Sobolewski. See you next time.

1. Describe the pathophysiology of vaso-occlusive crises in children and adolescents with sickle cell disease and how it relates to clinical symptoms.
2. Differentiate uncomplicated vaso-occlusive crises from other acute complications of sickle cell disease such as acute chest syndrome, splenic sequestration, and stroke.
3. 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.

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1. Kavanagh PL, Fasipe TA, Wun T. Sickle cell disease: a review. JAMA. 2022;328(1):57-68. doi:10.1001/jama.2022.10233
2. 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
3. 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/
4. 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
5. 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
6. 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
7. 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
8. 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

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

1. Treat pain promptly and aggressively. Do not wait on labs.
2. Use IV opioids for moderate to severe pain and reassess often.
3. Lactated Ringer’s may be preferred for IV hydration, but avoid overload.
4. Labs and imaging should follow clinical appearance and local protocols. Reticulocyte count and hemoglobin trends are key.
5. Disposition should be based on pain control, potential complications, and social support.
6. Prevention matters—hydroxyurea and primary care follow-up reduce crises and admissions.

1. Understand the shift from zone-based to “no-zone” management in pediatric penetrating neck injuries and describe the rationale behind this transition.
2. Apply ATLS principles to the initial assessment and stabilization of children with penetrating neck injuries, including decisions regarding imaging and airway management.
3. 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.

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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

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, reach out and let me know — I’ll take an email, a comment on the blog, a social media message.

And please — as my 13-year-old would encourage me to say — like, rate, and review. It helps other people find the podcast. I just want people to learn, basically.

Share this episode and the podcast with the folks you work with — and not just physicians in the emergency department. I think we all deserve to learn about how we manage injuries in children.

For PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

1. Demonstrate the ability to use shared decision-making strategies when discussing imaging options with families of pediatric patients presenting to the Emergency Department. (Bloom’s: Apply; Kirkpatrick Level 2 – Learning)
2. Evaluate the risks and benefits of ultrasound, CT, and MRI for common pediatric emergencies and identify appropriate imaging modalities based on clinical guidelines discussed in the podcast. (Bloom’s: Analyze; Kirkpatrick Level 3 – Behavior):
3. Assess the impact of implementing strategies for reducing low-value imaging in the pediatric emergency department on patient care outcomes, including diagnostic accuracy, radiation exposure, and healthcare costs. (Bloom’s: Evaluate; Kirkpatrick Level 4 – Results)

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1. Marin JR, Lyons TW, Claudius I, et al; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Section on Radiology; American College of Emergency Physicians Pediatric Emergency Medicine Committee; American College of Radiology. Optimizing Advanced Imaging of the Pediatric Patient in the Emergency Department: Policy Statement. Pediatrics. 2024;154(1):e2024066854. doi:10.1542/peds.2024-066854. PubMed
2. Marin JR, Lyons TW, Claudius I, et al; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Section on Radiology; American College of Emergency Physicians Pediatric Emergency Medicine Committee; American College of Radiology. Optimizing Advanced Imaging of the Pediatric Patient in the Emergency Department: Technical Report. Pediatrics. 2024;154(1):e2024066855. doi:10.1542/peds.2024-066855. PubMed

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 today’s episode, we are diving into a critical topic that every clinician in the emergency department encounters: we are talking about advanced imaging. Wait, so is this like an upper-level college course?

No. Advanced imaging, according to the American Academy of Pediatrics, the American College of Emergency Physicians, and the American College of Radiology, refers to diagnostic modalities like ultrasound, computed tomography or CT, and magnetic resonance imaging or MRI that provide detailed visualization of the internal structures of our patients to aid in the evaluation and management of the kids that we see in the ED.

So it’s the name for all of the cool imaging studies that we order on all of our patients, and they are essential for doing our daily jobs and identifying serious conditions like traumatic brain injuries, appendicitis, and stroke. There’s also risks. We’re talking about radiation exposure, having to sedate patients, false positive results, incidental findings that we have to deal with, and the obvious increase in healthcare costs, and there certainly is a rise in CT and MRI use.

And how do we actually strike the right balance between obtaining essential diagnostic information and avoiding unnecessary imaging? So here to help us navigate these complex decisions is Dr. Jennifer Marin. She’s an emergency department director of imaging at UPMC, Children’s Hospital of Pittsburgh, my hometown, a Yinzer, and a leading voice in pediatric emergency imaging.

She’s been at the forefront of research into imaging optimization. Focusing a lot on when to image, when not to image, and how to communicate imaging decisions effectively with families. In this episode, which we recorded as a discussion on May 12th, 2025, we will explore the latest evidence and guidelines, discuss practical strategies for reducing low-value imaging, and highlight how shared decision-making can help ensure that every scan is the right scan.

Jen, let’s start broadly. What are the most common injuries or conditions in children that require advanced imaging in the ED? And what are some of the trends that you’re seeing regarding how often we’re performing these studies? You know, reordering more imaging just because it’s more readily available because our patients and families expect it.

Or is there something else going on here? Thanks, Brad, and thanks so much for having me. It’s an honor to be on your podcast. To answer your first question, I think really the most common things that we see patients being imaged for would be suspected appendicitis. The kid who comes in with belly pain, you don’t wanna miss an appendicitis.

So we’re doing a lot of abdominal ultrasounds in those cases. Head trauma, um, of course people don’t wanna miss a bleed. So we do imaging for closed head injury. Those patients with minor head trauma, cervical spine trauma, abdominal trauma. And then I would say also children who come in with headaches. Uh, and those who also have seizures, those would be probably the most common reasons why we image kids.

So these studies are all readily available. We can get them sort of whenever we want. Really. What are some of the trends that we’re seeing in terms of ordering practices? Yeah, there’s definitely been studies that have shown that over time we are using more advanced imaging modalities. And I, I like to say to the residents and trainees, if you build it, they will come. And so as we now have more availability of these tests, when I started training, we did not have 24 hour ultrasound. We certainly didn’t have MRI available in the ED. But now that we have 24 hour ultrasound, it’s much easier to just get the ultrasound, or at least that’s the perception, right?

So it’s relatively cheap when you talk about ultrasound compared to other advanced imaging modalities, it isn’t usually painful. It’s no radiation and it’s fairly quick. So I think that when we, our threshold to order tests like this have gone way down simply because of the availability. Do you feel like sometimes we just assume that a patient or family wants an imaging test in order to figure out what’s going on?

Sometimes we do think that. I think we think that probably more than they actually do. And I’ve actually started, instead of assuming that a family is expecting imaging, I’ve started asking, what are you worried about? And what do you think should be done? And a lot of times I’m very surprised when I explain to the families why imaging isn’t necessary, if in fact they are expecting it. Most of the time it’s very well received.

Right. And I feel like we used to see a kid who would come in with a day and a half, two days of pain, right? So it was a little bit easier. Um, but now they’ll come in with a few hours of pain. And the reality is that if you get an ultrasound in early appendicitis, you’re probably not even gonna see the appendix. And so the test really isn’t gonna be that useful. And I go into that a little bit with families and I think it really resonates with them and has them understanding why we’re not doing the ultrasound.

That’s a wonderful point. And I don’t think there’s any such thing as a perfect test. There’s almost nothing that’s a binary yes-no. There’s false positives and false negatives for everything. And if you are born with your appendix behind your cecum, no ultrasonographer in the universe is going to be able to get it to come out to take a picture. Do you think that medical-legal concerns also play a role?

Is it different in taking care of children versus adults? I think medical-legal implications do play a role, and there’s been studies on that, but it’s mostly in the general EM literature, not as much in pediatrics. But I think that it’s something that is probably there that we think about. Nobody wants to miss an appendicitis. Nobody wants to miss a head bleed, right? We don’t wanna miss anything. And I think that when we’re faced with a child who has one of these diagnoses, that’s where we need to weigh the risks and benefits. And in some cases have a conversation with the family because sometimes it’s clear-cut that they need imaging. Other times it’s clear that they don’t need imaging, but there’s a lot of gray.

And you mentioned in your intro, shared decision-making, and I think that shared decision-making plays a really important role with imaging in a lot of these scenarios.

So I’m gonna shift gears just a tiny bit. You talked a few moments ago about some of the more common conditions in which we get imaging. I’m gonna ask specifically about CT scans and radiation. And it’s a topic that comes up again and again and we’re learning more and more over time about the risks of radiation, particularly in growing children where we really don’t understand the long-term risks. Can you talk about safer alternatives? How we should approach the risk of CT scan with families and some of the decisions around that?

Absolutely. So there is a risk of radiation. We know this. What we don’t know is what exactly is that risk. And a lot of the studies that have been done were done on patients who received imaging on much older equipment. And the equipment that we use now is much more sophisticated, much more high-tech, and does have the ability to deliver much lower radiation doses. So the explanation that I give to families, especially when I’m in a shared decision-making situation or in a scenario where I’m recommending a CT and the family is a bit hesitant, you know, I’ll say the benefits of this scan very likely outweigh any of the risks.

We don’t know what that risk is. We know that any radiation can be potentially harmful, but when you’re getting imaged at a children’s hospital, for example, and this is a kid who’s not getting imaged every month or every year like some of our adult patients are, then the risks really are generally outweighed by the benefits when you have a high pretest probability of disease.

CT does get the lion’s share of concerns about risk and advanced imaging. But there’s two other modalities that we’re talking about today. Really, on one end we’ve got ultrasound, which there’s no ionizing radiation whatsoever. It’s readily available and it’s first line for things like appendicitis, kidney stones, and soft tissue infections. And then at the other end we have MRI, and it’s not just set it and forget it. Now we have rapid protocols and other things. Can you talk specifically about some of these Rapid MRI protocols and how they may supplant CT scans?

Yes, so Rapid MRI protocols have really exploded, I would say in the last decade. We actually have four different rapid protocols depending on the scenario, depending on the imaging question, and it’s a wonderful test. I think that there are limitations to it, right? So one is going to be the speed with which you can get it, and our MRI scanners, you know, we don’t have an infinite number, and so we are competing with other patients around the hospital who need MRIs and sometimes kids have to wait two, three plus hours to get it.

The other thing though that’s important is a lot of times, you know, the CT gives us good information and it’s fast, but it may not be the best test. And so MRI is going to give us more information depending on the scenario. So I’m thinking about maybe a seizure patient, where an MRI might be a better test than a CT. And so getting the CT is to some extent, only delaying the inevitable because the patient’s ultimately going to need the MRI.

So what I initially learned about MRI, it was like this two hour long test. You had to lay in this big machine. It made a ton of noise. You had to put headphones on. When you talk about rapid MRI, like how fast can these patients be in and out of the scanner?

So these tests are very fast. They’re not as fast as CT scans. You can get a head CT probably in under two minutes, but you can get a rapid MRI in five to seven minutes. In some cases, if you’re doing a shunt protocol, for example, some of them take a little bit longer, 10 minutes, 12 minutes. But still, to your point, Brad, it’s not this hour long scan that we’re used to seeing and most patients tolerate it well.

But – and I’ll go back to your earlier question – one of the limitations of MRI is you can get a scan down to three minutes, but if you’re a 19-month-old who doesn’t want to lay still, it’s not going to happen. So that risk of sedation really becomes something to consider when we’re getting a rapid MRI in a particular age group.

Locally, we will not do MRIs on ED patients below six years of age.

When I started residency way back in the day, I said to one of my mentors, ‘What am I gonna do about two-year-olds?’ And I was told, ‘Nothing.’ And that has held true all throughout my career.

Yes, and so thinking about these imaging modalities, I keep coming back to the fact that most of the time when we’re ordering one, it’s because we’re thinking about what’s next from a management standpoint for the patient. That often involves our subspecialty colleagues, whether that’s our surgeons, our subspecialist surgeons, or other pediatric subspecialties. How are we collaborating with these pediatric specialists to ensure that we’re triaging and effectively making decisions and integrating these decisions into the overall treatment plan for the children we’re caring for in the emergency department?

Subspecialists are key, right? And I think that getting multidisciplinary collaboration when we are figuring out what is the best imaging strategy for X is critical. We have clinical effectiveness guidelines, as I’m sure many know, and many pediatric emergency departments have these. These are multidisciplinary guidelines that have been put together that really take into account all the relevant stakeholders and what’s the best imaging test to get the answer that we’re interested in.

We’ve collaborated with general surgery, radiology, and all different specialties depending on the scenario, so that we’re imaging in the right way and not having to redo the study. We have different protocols like for kidney stones, where we do a very low dose CT, and we have parameters around which we decide whether to do that CT in lieu of ultrasound for certain patients.

None of that would be possible without earlier collaboration with all the relevant stakeholders first.

You think about all the different points in your system where the decision could go wrong. You just mentioned a CT protocol for stones. You could order another version of a, you know, abdominal CT and get a study that also looked at the kidneys but wasn’t specific for it. And they’re all on that giant menu. So you have to think from top to bottom in your system and get everybody involved and on board. And I would agree with you completely that I found that’s the only way to drive decisions toward the preferred imaging modality. Everybody that’s a stakeholder has to agree. And you can’t just snap your fingers and make that happen.

And we are working in children’s hospitals with tons of resources, world experts, and the availability of tests. But the majority of our patients do not initially seek care in our facilities. We know that nine out of ten children that go to the ER do not go to children’s hospital ERs. And I think some of the concern about low-value imaging or imaging with high risks has to be directed at our children who may receive imaging outside of children’s hospitals.

So what can pediatric emergency medicine physicians specifically do to reduce the use of low-value imaging being performed at non-children’s hospitals?

You’re absolutely right, Brad. And I always say that I do not envy my emergency medicine colleagues, particularly those practicing in community settings. We really do have so many resources at our disposal, and it is very hard for them to know everything about kids and adults while practicing in locations where they don’t have these consultants available 24/7.

I think it’s very important, almost an obligation, for us to provide outreach and education to our community ED colleagues so that they are given the tools needed to provide the right imaging to the right patient at the right time.

So I’ll give you a couple of examples. At UPMC, we have many hospitals as part of our system, but only one pediatric children’s hospital. And so we routinely do outreach with our community providers. There’s an education series, a lecture series, and I had the opportunity to give a talk on this very topic to those providers. It was all these medical directors at other hospitals who then had the opportunity to cascade down the message about low-value imaging, when to image, when not to image. We provided resources, which I’ll talk about in a little bit, and, you know, hopefully that will lead to less low-value imaging in the community setting.

Another recommendation that I have is regarding transport calls. We all take transport calls when we’re practicing at the ‘mothership.’ Patients are getting transferred, and I think having a conversation with the doc at the point of care, even if imaging has already been done — and maybe it was low-value or could have been avoided — I think it’s important to talk to the provider and say, ‘Hey, you know what? Just so you know, next time you have a kid like this, don’t feel like you have to image them. We are happy to take this kid without imaging.’

It’s going to save time, it’s going to save us having to upload the disc that may or may not be corrupted. It’s going to save the patient, potentially, another scan because they were moving all over the table because the techs at the referring hospital aren’t used to trying to manage a wriggling infant.

I almost empower them to not necessarily do imaging because I think that there is this common misconception in the community setting that you can’t transfer a patient unless you know what the diagnosis is or unless you have imaging available. And that’s really not the case at all.

Talking about some of the resources in the guidelines that we published, the policy statement and technical report that we published in Pediatrics and in some other journals, statements on advanced imaging in children who present to the emergency department. It was authored by the American Academy of Pediatrics, the American College of Emergency Physicians, and the American College of Radiology. Those statements were published, and one of the documents that I think is very useful is the supplement to the technical report, which includes several publicly available clinical effectiveness guidelines from various children’s hospitals all over the country.

These can be used at the point of care to help with decision-making so that we’re providing high-value care and performing high-value imaging.

Before we bring this episode to a close, there’s one other subject I wanted to talk a little bit more about, and it’s incidental findings. You know, it’s when we get a study right, and we discover something that we weren’t expecting to see. I think, colloquially, it’s gotten the name ‘Incidentaloma.’ How do you suggest we approach when we discover something that we weren’t expecting to see? What does that mean for patients and families? And is there a cascade of decisions that happen because of that that could have been avoided?

Absolutely. Yeah. I don’t think we talk about these enough because we don’t have to deal with them in the ED. So an incidental finding is something that a radiologist sees on the imaging study that means nothing. It doesn’t cause the patient any harm, and it’s certainly not the reason for their symptoms. But when you tell someone that they have a nodule, let’s say, on their lung from a CT PE study, that then sparks what we call ‘care cascades.’

And they have to follow up on that. It’s an extra visit, time off work, time out of school, an extra cost, anxiety-provoking. And maybe they need to follow it up every three months. It’s a real burden on families and on the healthcare system more broadly and probably something that doesn’t get enough attention in emergency medicine.

So, I would encourage folks when they’re ordering tests, particularly if the pretest probability is very low, to think about the risks, including incidental findings and how they’re really not insignificant.

Before we end our conversation, what final words of advice do you have for someone who’s going to have a shift soon after they listen to this episode? What’s one thing that they can take to the bedside in an upcoming discussion with a patient and their family?

Understanding that imaging isn’t always necessary to make a diagnosis, and that’s something that I think today’s trainees need to hear, and also some of the families need to hear. There’s so much information available online, as you know, and Facebook groups and resources and ‘My friend, my grandmother,’ etc., and it can be overwhelming.

Taking the time to explain to families, especially those who are expecting imaging or have questions about imaging, why we aren’t doing imaging and the risks associated with it, which are very real — I think that that carries a lot of weight.

What about other healthcare teams that interface with our patients when they may be requesting tests that we’re concerned pose additional risks or costs to patients? How do we have a collaborative discussion with them when there’s a difference of opinion about what best to do for a patient?

Yes. I think you answered it, actually, Brad — having a collaborative discussion. A lot of times when we consult a service, it’s a resident who might be at another hospital. They have to come to our hospital. They’re just reflexively asking for imaging. I say to the resident, ‘I’m going to call that resident back.’ And I’ll say, ‘You know what? I would really love for you to just see the patient before we talk about getting a CT because I don’t think the kid needs a CT.’

Most of the time, that works really well. Sometimes they’ll say, ‘Well, here’s why I want the CT,’ and I’ll say, ‘Oh, that’s really helpful. We’ll go ahead and get it.’ So I think having a conversation and questioning in a very respectful way can be eye-opening on both sides.

And that is a conversation that is best had by voice or face-to-face. It can be uncomfortable to feel like you’re going to have a disagreement with somebody. But ultimately, everybody’s goal is the same — just to do what’s right for the kid and their family.

And the other people that are really smart and amazing and wonderful are radiologists. We should always be willing to call them on the phone. They’re not just the test referral center. You don’t just put in the test and get it. Sometimes we should be calling them and saying, ‘Here’s the problem I have at hand. What’s the best way that we can safely image this child?’

Jen, thank you so much. Tons of fascinating information. As I mentioned before, I will put links to all of these excellent resources in the show notes. I hope that in listening today, you will come up with some new ways to approach these issues with patients and families, as well as the folks we collaborate with. And don’t be afraid to have those discussions with folks calling in from other institutions. We all have the same goal. And ultimately, it’s on us working in pediatric emergency departments to disseminate that best information.

Jen, thank you very much.

Brad, thank you so much. It was such an honor. I had a really nice time. Thank you.

Alright, that’s all for this episode. I hope you now understand what the term ‘advanced imaging’ encompasses — ultrasound, CT, MRI — the radiologic studies that we use to make diagnoses every day in the emergency department on children. Sometimes these tests are necessary; sometimes they’re not. We have to collaborate with patients, families, our radiology colleagues, the other specialists we collaborate with, and providers working at community EDs to decide whether to image and, if we do, to get the right test that will get us the most accurate results with the least risk.

So if you liked this episode, share it with a colleague, leave a review on your favorite podcast site, or send me a comment via email, on the blog, or via social media.

For PEM Currents: The Pediatric Emergency Medicine Podcast, I’m Brad Sobolewski. See you next time.

• Describe the classic and atypical clinical presentations of Parvovirus B19 infection in pediatric patients, including erythema infectiosum, arthropathy, transient aplastic crisis, and chronic anemia in immunocompromised hosts.
• Understand the epidemiology and transmission timeline of Parvovirus B19, especially its seasonal peaks and viral shedding period.
• Recognize key diagnostic features that help differentiate Parvovirus B19 from other viral exanthems and systemic illnesses.
• Formulate an evidence-based management plan for patients with suspected or confirmed Parvovirus B19, including those with underlying hemolytic disease or immunocompromise.
• Counsel families and caregivers—including pregnant household contacts—on the risks, exposures, and infection control considerations related to Parvovirus B19.

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Jordan, Jeanne A. “Treatment and Prevention of Parvovirus B19 Infection.” UpToDate, Jun. 14, 2024. https://www.uptodate.com/contents/treatment-and-prevention-of-parvovirus-b19-infection

Edwards, Morven S. “Clinical Manifestations and Diagnosis of Parvovirus B19 Infection.” UpToDate, Jun. 14, 2024. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-parvovirus-b19-infection

Macri, Angela, and Crane, Jonathan S. “Parvoviruses.” StatPearls, NCBI Bookshelf, Jun. 28, 2023. https://www.ncbi.nlm.nih.gov/books/NBK482245/

Kostolansky, Sean, and Waymack, James R. “Erythema Infectiosum.” StatPearls, NCBI Bookshelf, Jul. 31, 2023. https://www.ncbi.nlm.nih.gov/books/NBK513309/

“Parvovirus B19 Infection and Pregnancy.” Centers for Disease Control and Prevention. https://www.cdc.gov/parvovirusb19/pregnancy.html

Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 4o AI

Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we are covering Parvovirus B19—a common but clinically diverse viral infection that you will definitely encounter in pediatrics, and not just in the form of a rash. Parvovirus B19 is best known for causing fifth disease, but in certain patients it can lead to some serious complications like aplastic crises, fetal hydrops, or chronic anemia.

So as you can see, this virus does a lot of stuff. But what is it? Well, let’s get nerdy. It is a non-enveloped, single-stranded DNA virus in the Parvoviridae family. There are some forms of parvo that infect other mammals, but Parvovirus B19 is only for humans, and it loves erythroid progenitor cells. It was discovered by accident back in 1975, so a little bit before I was born, and it was labeled B19 because of the sample number in a Hepatitis B screening panel. Since then it has been identified as the cause of several syndromes. I’ll go over those as we move along here.

Parvovirus B19 is spread via respiratory droplets, much less commonly by blood products or vertical transmission. The incubation period is typically four to fourteen days. Viremia peaks at days five through ten after exposure, and that’s when the patient is most contagious. The classic rash and joint symptoms appear later, and at that point, the patient is actually no longer infectious. So that detail’s key—because when a kid shows up with a slapped cheeks rash, you no longer need to isolate them.

So the classic presentation that’s on every board exam ever is called erythema infectiosum, or fifth disease. This is the most well-known manifestation, seen primarily in school-aged children, especially in the spring and early summer. Again, it’s also known as fifth disease—this is one of the six classic childhood exanthems. These are a group of viral rash-causing illnesses that were originally numbered in the late 19th and early 20th centuries based on their order of description.

So: first disease was measles or rubeola, which obviously we don’t see as much anymore. Second disease was scarlet fever from group A Streptococcus. Third disease was rubella, or German measles. Fourth disease was Dukes’ disease, now believed to be a misclassified form of scarlet fever or staphylococcal scalded skin syndrome. Fifth disease is erythema infectiosum caused by Parvovirus B19. Sixth disease is roseola infantum, caused by HHV-6, and sometimes HHV-7.

Honestly, fifth disease is a historical happenstance—and I just think it’s fun to know that. Sometimes I share it with patients and families.

Here’s how it typically plays out. Phase one is the viral prodrome. This occurs during peak viremia. About 50% of symptomatic patients experience nonspecific flu-like symptoms: low-grade fever, malaise, myalgias, headache, coryza, nausea, and sometimes even diarrhea. This lasts about two to three days.

Phase two is the classic rash. This appears two to five days after the prodrome. You get an erythematous malar rash with circumoral pallor—the classic slapped cheeks appearance. You can also see a lacy, reticular rash on the trunk and extremities, which follows the slapped cheek rash about one to three days later. This rash can fade within a week or two, or it can wax and wane for weeks, especially worsening with sun, exercise, or stress. By the time the rash appears, viremia has resolved and the patient usually feels well.

Only about 25% of infected individuals will have this classic rash syndrome. Another 50% will only have mild flu-like illness, and 25% remain completely asymptomatic.

Let’s talk about the joint symptoms. These are seen in about one out of ten children. More commonly, adults—especially women—have joint symptoms, affecting up to 60% of them. Typically, joint symptoms are symmetric and affect the small joints of the hands, wrists, knees, and feet. The joint pains can last about one to three weeks. Chronic arthropathy occurs in a very small subset of patients and can last for months or more. Importantly, there’s no joint destruction—it hurts, but the joints are fine afterwards.

A serious manifestation of Parvovirus B19 infection that you do not want to miss is called transient aplastic crisis. This occurs when Parvovirus B19 halts erythropoiesis in patients with underlying hemolytic disorders like sickle cell disease, thalassemia, or hereditary spherocytosis. In one study of just over 300 patients with homozygous sickle cell disease, Parvovirus B19 infection caused transient aplastic crisis about 80% of the time.

Presenting symptoms are those of anemia: pallor, fatigue, tachycardia, weakness. You’ll often see a hemoglobin drop of greater than 30% from baseline, an undetectable reticulocyte count, and possibly leukopenia and thrombocytopenia. This often requires hospitalization and transfusion—in one series, 87% of children with transient aplastic crisis required packed red blood cell transfusions.

In immunocompromised children, B19 can also cause chronic infection, with persistent viremia and pure red cell aplasia. You’ll see this in transplant patients, patients with leukemia, or advanced HIV. These patients don’t get rash or joint symptoms—those are immune-mediated—and these kids have compromised immune systems. Diagnosis is confirmed with PCR, often as part of a viral panel, or via characteristic bone marrow findings. Treatment is with IVIG and, if possible, reduction of immunosuppression, though this can be tricky. These patients often need admission and careful care.

Let’s talk about fetal infection. Parvovirus B19 is not routinely screened for in pregnancy, but vertical transmission can cause hydrops fetalis, stillbirth, and severe fetal anemia. The risk is highest in the second trimester. The overall rate of fetal loss after maternal infection is around 2 to 6%, but it may be higher depending on timing and fetal response.

Now, let’s talk about a wonderfully named manifestation: papular purpuric gloves and socks syndrome. This is why pediatrics is great—we have the best names for things. This is a rare manifestation of Parvovirus B19, often seen in adolescents or young adults. You get painful, pruritic petechiae and purpura of the hands and feet, with a sharp demarcation at the wrists and ankles. You may also see mucosal erosions. You’re probably thinking, this sounds like mycoplasma or other viral illnesses—and it does. But unlike fifth disease, patients are contagious when this rash appears.

Finally, let’s talk about some rare neurologic complications. These include encephalitis, Guillain-Barré syndrome, and brachial plexopathy. One review identified about 129 cases of parvovirus-related neurologic complications between 1970 and 2012, with encephalitis making up about two-thirds of those cases. These are rare, but something to keep in mind—especially if you’re in a large academic children’s hospital.

So how do we diagnose Parvovirus B19? It’s usually a clinical diagnosis—especially in cases of typical erythema infectiosum. In more complicated cases or in immunocompromised children, you can check IgM antibodies (which appear about 7 to 10 days after exposure and peak at 2 to 3 weeks). IgG indicates past infection. PCR is most useful in immunocompromised patients or when evaluating possible fetal infection.

Management of erythema infectiosum is supportive care only—antipyretics, hydration, and reassurance. The rash can be itchy; use moisturizers or antihistamines like cetirizine. Explain to families that the rash may last for days to weeks and can worsen with sunlight. I’ve seen a lot of visits in urgent care where this is the main concern during outbreaks.

For joint symptoms, use NSAIDs. A patient with transient aplastic crisis will likely need hospitalization and red blood cell transfusion, especially if unstable. In immunosuppressed patients with chronic infection, treat with IVIG and carefully consider immunosuppressive management.

What if the child has a pregnant caregiver? The child is most contagious **before** the rash appears—during the viral prodrome—so it’s easy to mistake for another virus. Once the rash appears, the child is no longer infectious. If a pregnant household contact was exposed during the contagious period—especially in the first or second trimester—they should contact their OB provider for serologic testing (IgG and IgM). If seronegative, serial ultrasound may be recommended to monitor for fetal hydrops.

Isolation of the child is not necessary after the rash appears. If they are in the viremic phase, then hand hygiene and respiratory precautions are important to limit household spread.

Take-home points: Parvovirus B19 can cause a range of presentations—from slapped cheeks to life-threatening anemia. It’s a clinical diagnosis, especially in typical cases. If you’re not familiar with the rash, look it up—so you’ll recognize it in the ED. In patients with red cell disorders or immunosuppression, use PCR or serology. Don’t miss a transient aplastic crisis in a child with sickle cell. And remember: once the rash appears, the child is no longer contagious. The virus spreads during the early, flu-like phase.

Thank you for listening to this episode. If you found it helpful, let me know. Leave a review, shoot me a message on social media or email, and share it with your colleagues and learners. And as my 13-year-old would like to remind me: like and subscribe.

For PEM Currents, this has been Brad Sobolewski. See you next time.

• Compare the clinical presentation of bacterial infections in unvaccinated and undervaccinated children versus fully immunized children in the Emergency Department
• Assess the need for empiric antibiotics and diagnostic testing in an unvaccinated or undervaccinated child presenting with fever without source

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Curtis M, Kanis J, Wagers B, et al. Immunization status and the management of febrile children in the pediatric emergency department: what are we doing? Pediatr Emerg Care. 2023;39(1):1-5. doi:10.1097/PEC.0000000000002864

Finkel L, Ospina-Jimenez C, Byers M, Eilbert W. Fever without source in unvaccinated children aged 3 to 24 months: what workup is recommended? Pediatr Emerg Care. 2021;37(12):e882-e885. doi:10.1097/PEC.0000000000002249

Herz AM, Greenhow TL, Alcantara J, et al. Changing epidemiology of outpatient bacteremia in 3- to 36-month-old children after the introduction of the heptavalent-conjugated pneumococcal vaccine. Pediatr Infect Dis J. 2006;25(4):293-300. doi:10.1097/01.inf.0000207485.39112.bf

Kaufman J, Fitzpatrick P, Tosif S, et al. Faster clean catch urine collection (Quick-Wee method) from infants: randomised controlled trial. BMJ. 2017;357:j1341. doi:10.1136/bmj.j1341

Kuppermann N, Fleisher GR, Jaffe DM. Predictors of occult pneumococcal bacteremia in young febrile children. Ann Emerg Med. 1998;31(6):679-687. doi:10.1016/S0196-0644(98)70225-2

Rutman MS, Bachur R, Harper MB. Radiographic pneumonia in young, highly febrile children with leukocytosis before and after universal conjugate pneumococcal vaccination. Pediatr Emerg Care. 2009;25(1):1-7. doi:10.1097/PEC.0b013e318191dab2

Trippella G, Galli L, De Martino M, Lisi C, Chiappini E. Procalcitonin performance in detecting serious and invasive bacterial infections in children with fever without apparent source: a systematic review and meta-analysis. Expert Rev Anti Infect Ther. 2017;15(11):1041-1057. doi:10.1080/14787210.2017.1400907

Van den Bruel A, Thompson MJ, Haj-Hassan T, et al. Diagnostic value of laboratory tests in identifying serious infections in febrile children: systematic review. BMJ. 2011;342:d3082. doi:10.1136/bmj.d3082

Note: This transcript was partially completed with the use of the Descript AI

 Welcome to PEM Currents: The Pediatric Emergency Medicine P odcast. As always, I’m your host, Brad Sobolewski, and this episode is gonna focus on a challenging yet. Unfortunately, timely clinical question, what do we do with the UN or under vaccinated child who presents to the emergency department with fever? So what are we gonna go over in this episode?

Well, we’re gonna compare the clinical presentation of bacterial infections in unvaccinated and unvaccinated children versus fully immunized children in the emergency department, and we will assess the need for empiric antibiotics and diagnostic testing in this challenging population. Now, before you listen to this episode, I will presume that you are all familiar with the recommended child and adolescent immunization schedule for children ages 18 and younger in the United States or wherever you live.

So I’ll pause for a moment so that you can review that. Great. Welcome back, and there’s a few definitions that I will use. Unvaccinated or unm. Immunized means that you have no vaccines. Unvaccinated or under immunized means that you have some but not all of your vaccines, and you should always verify vaccine status via history EMR records and state registries.

So I think the first important question to answer is, when is a child immunocompetent? And honestly, competency is sort of on a sliding scale, and a child is immunocompetent if they have a normally functioning immune system capable of mounting an effective response to infections. So this means you have intact, innate and adaptive immunity with functioning neutrophils, macrophages, T cells, and B cells.

You don’t have. Severe combined immunodeficiency like a primary immunodeficiency or a secondary immunodeficiency. You’re on chemo or you’re severely malnourished. Immunocompetent kids respond to vaccines completely immunized, so greater than two doses of PCV and HIB should be immunocompetent against those bugs.

Unvaccinated or under vaccinated children are functionally immunocompromised in specific clinical scenarios such as fever without source. And it can be hard to figure out what immuno competency by disease and vaccine status really means. And so I do encourage you to be familiar with some of the information provided by the CDC as long as it’s still online.

So how common is it for children to be unvaccinated in the United States? Unfortunately. It’s getting more common. So as of the 2023-24 school year, about 3.3% of US kindergartners had an exemption from one or more required vaccines. That data is up versus 2022. 2023 translates to about 80,000 kids in the United States, and vaccination coverage varies across states.

So in the 2023-24 school year. MMR coverage was 79.6% in Idaho, and 98.3% in wild, wonderful West Virginia. 14 states reported exemption rates greater than 5% and in generally 95% vaccination rate for diseases needed for herd immunity. And we often wonder is the question of, well, is your kid’s vaccines up to date?

A good enough question, and let’s be honest, many of us just rely on adult caregivers to give us this information. Is your kid up to date on shots? Yeah, sure. I’ve had a few where up to date meant we were up to date in our decision to stop vaccinating them three years ago. EMR confirmation and state records are better and all 50 states, district of Columbia and some US territories do have immunization information systems.

And I’d encourage you to be familiar with and sign up for accounts on all of the different states that you work in. So for me, that’s Ohio, Kentucky, and Indiana. How often do we see UN or under vaccinated kids in the ed? And unsurprisingly, this number is not known. I asked some ID experts and we haven’t broadly assessed our rate, and we could do this, but it would take really a manual query of state vaccine records for any patient that doesn’t have vaccine status in the EMR.

And it would be timely and laborious though. Interesting. In Indiana, Curtis et al did a retrospective review of almost 800 well-appearing febrile children three to 36 months throughout 2019, presenting in one Indiana pediatric emergency department, and they were really looking at vaccine status. They excluded children with complex chronic illnesses like sickle cell disease, congenital heart disease, immunodeficiency, trach vent, et cetera, and they also excluded kids with an ill appearance or hemodynamic instability during that encounter.

They learned that 91.5% of their patients were fully vaccinated, five and a half percent were under vaccinated, and 3% were unvaccinated. Does that data match what you’ve seen and Yes, we don’t know the true scope of the problem. I. But I think perhaps a more important question is whether or not unvaccinated or unvaccinated children are more at risk for non-vaccine preventable illnesses.

Clearly they’re at risk for vaccine preventable illnesses ’cause they don’t have the vaccine. And so in this episode, I’m gonna focus mainly on children three to 36 months of age with fever for less than five days. And I will say that the approach to an unvaccinated febrile child may differ from fully immunized children due to an increased risk of occult bacteremia and invasive bacterial infections.

The child’s immune system matures both with and without vaccines. Maternal immunity wanes by about three to six months until 36 months to maybe five years. The adaptive immune system is still developing. And kids are less capable of mounting an effective response to encapsulated bacteria like streptococcus pneumonia.

Haemophilus influenza type B RIA meningitis. By age five, we have developed more robust natural immunity from subclinical exposures to bacteria cumulatively. And so as long as you have a working immune system and a spleen that does what it’s supposed to do, different pathogens become more relevant, so you lose risk to encapsulated bacteria and you’ll see more mycoplasma pneumonia, streptococcus pyogenes.

And others, and at least for the context of this episode, I’m gonna be talking about fever without a source. And now maybe we’re excluding fever for an hour, which we’ve all seen in the emergency department, but it really means. When a complete history and physical examination cannot identify a specific source of fever greater than 39 centigrade or 102.2 Fahrenheit in a previously healthy otherwise well-appearing child.

Now, that threshold for 39 degrees could also be extrapolated to 40 degrees, and it’s relevant to literature and both the pre PCV and HIB era and in the post PCV and HIB era. But for simplicity’s sake, and based on the evidence that we do have, I’ll set that threshold at 39 degrees Celsius for this episode.

These children are at risk for occult infection such as UTI bacteremia and occult pneumonia. However, the majority of children who are well appearing and have no identifiable source of infection do have a self-limited viral illness. And in all of these kids, you gotta assess vaccine status, travel history, sick contacts, any immune compromise, and any symptoms of localizable bacterial infection to evaluate the risk of serious illness.

So serious bacterial infection defined as any bacterial infection requiring medical intervention, but it may not invade sterile sites. It’s like a UTI pneumonia skin and soft tissue infections like cellulitis and abscess. An invasive bacterial infection is a subset of serious bacterial infection where the bacteria gets into sterile body sites like blood and CSF.

It’s bacteremia, meningitis, osteomyelitis, septic arthritis, and. Let’s be honest, fever is still the most common complaint for infants and children brought to the ed. It’s greater than 6% of all ED visits. Most of these kids under 36 months will have some clinically apparent source of infection, even like a obvious URI or otitis media, and about one out of five of these children though a source cannot be identified during the h and p.

Certainly any child who’s ill appearing or has unstable vitals should be managed for presumed sepsis or septic shock, and that’s not the focus of this podcast episode in well Appearing Children with Fever. The main goal is to determine the risk of a clinically occult bacterial infection. I. So with that, let’s run through a few of these common bacterial infections.

So let’s start with urinary tract infections. So this is the most common occult bacterial infection in febrile infants and young children. And children under the age of two. Fever may be the only symptom. The prevalence is roughly eight to 10% in young children with fever. Greater than 39 Celsius. Risk factors include age, female sex circumcision status.

You should definitely use UTI calc. To help estimate the risk and the presence of another infection, like URI. Acute otitis media or gastro doesn’t completely rule out UTI, but in select scenarios like bronchiolitis with RSV, it does reduce the risk a bit. Females, three to 24 months with fever greater than 39 and no source, the risk could be as high as about 5%.

Uncircumcised. Males with high fever and no source probably have a similar risk to females, but circumcised males have a risk of 2% or under. You should also think about testing if there’s been fever for greater than 48 hours. If there’s history of UTI or any known GU anomaly, even like hypos, SPADs, and you can cath, you can clean catch, you can use the quick wee maneuver or even a super pubic aspiration which parents don’t like.

Alright, let’s talk about occult bacteremia. And honestly, when we talk about this topic, it’s the thing that we worry the most about. It’s the presence of bacteria in the blood of a febrile, well appearing child in the absence of an identifiable focal bacterial source of infection. So in the pre HIB and Prevnar era, this was like three to 11% of febrile children.

Streptococcus pneumonia made up 73 to 90% of these, and HIB made up eight to 22%. Hib was way more likely to cause meningitis. In fact, in 5% of bacteremia, kids with hib, they had meningitis. Really high rate. In the post vaccine era, the rate of occult bacteremia is. Point two five to 1%, so it’s less than 1%. A third of these are e coli.

A third are non-vaccine serotype, streptococcus pneumonia, and the other third are staph aureus, salmonella species, RIA meningitis, and strep pyogenes. Interestingly, both then and now, 95% of occult bacteremia is caused by strep pneumo resolve without IV antibiotics. These are all well appearing kids in which this happens, so we actually probably never know that some of these kids have it.

There’s a higher risk of occult bacteremia in children younger than four months of age, children with high fever, 39 or 40, and unvaccinated, and we’ll talk about labs in a little bit, but elevated white count A and C procalcitonin band count. These are all things that can be used to assess the risk. In preparation for this episode, I had the pleasure of talking to some folks that practiced in the pre HIB and Prevnar vaccine era, and what they told me was interesting.

They said that. Ultimately you could reduce a kid’s fever and that still didn’t reduce the risk of them having bacteremia. So they still had to work these kids up. But if the kid looked great after they responded to Antipyretics, well, they probably didn’t have meningitis. I. And so I alluded to this a couple minutes ago, but, uh, let’s talk about lab characteristics for oc cult bacteremia in the post vaccine era.

Let’s start with the CB, C and differential. And yes, we all know that CBC is not a good indicator of whether the child has a bacterial infection or not, but in this specific population, based on the available research, a white blood cell count greater than 15,000 does have a sensitivity of 72%. And a specificity of 55%.

This is based on one study from Hertz in, uh, pediatric infectious disease, and in their study though, the rate of a true positive blood culture was 1.6% and the contaminant rate was 1.8%. Interesting. A NC per Cooperman, etal and Annals of Emergency Medicine in 1998 of greater than 10,000 was a slightly better indicator and absolute band count of greater than 1500.

It’s also been suggested. None of these are perfect. So what about procalcitonin? And I know it’s not available everywhere, but it probably does have a better. A test characteristic than white blood cell count and a NC. Generally, the threshold is set at 0.5 nanogram per milliliter, but some sites suggest the threshold of greater than two and trella in the expert.

A review in of anti infectious therapy journal in 2017 noted that it had a sensitivity of 82%, specificity of 86%, and a positive likelihood ratio of six. And Van den Bruel in BMJ 2011 found procalcitonin to have better specificity than white blood cell count. Now let’s talk about pneumonia. So most children but bacterial pneumonia have some sort of abnormality.

On exam. In pro-vaccine era studies, 20 to 40% of three to 36 month old with fever greater than 39, and no clinical evidence of pneumonia, but with a white blood cell count greater than 20,000 actually had low bar or segmental pneumonia on a chest x-ray. In a study published in pediatric emergency care in 2009, Rutman and colleagues in a retrospective cohort of children less than five found that in comparison, occult pneumonia was identified more often.

Pre PCV. Then post PCV, so about 15% to 9% in kids younger than two, though the rate was higher. Pro-vaccine era, 17% and post vaccine era at 10%. So in the UN or under vaccinated kid with a temp greater than 39. If you get a white blood cell count and it’s greater than 20,000, you should get a chest x-ray, even if the kid has a normal lung exam.

And now let’s talk about blood cultures and. How many of you have heard from a nurse? Well, while, I’m getting the line. Why don’t I just draw a blood culture? So it’s either okay in these children to send it right away or to hold it until you get the labs back. And I think I would consult local practice variation, um, and what your colleagues do and the risk of contamination will not increase while the blood culture sits if it was obtained correctly.

And every hospital’s lab is different, but some of the bacteria that are considered common contaminants include bacillus. corynebacterium, cutie bacterium acnes, which was p acnes and micrococcus. Other contaminants include staphylococcus epidermis and the reins group. As long as the patient doesn’t have any risk of endocarditis, any other bug that grows.

We’re talking staph aureus, strep pneumonia, strep pyogenes, enterococcus, e coli. These are all probably true pathogens. Let’s say a blood culture is sent and then it comes back positive. So these kids should, in most cases, especially if it’s suspected to be a real pathogen, be reevaluated in the emergency department.

If kids are febrile at reevaluation, there’s a 40% chance of persistent bacteremia. And if they’re ill appearing about a one in 25 or 4% chance of meningitis. So these kids, if they’re ill appearing in febrile still, they need a full sepsis evaluation plus an LP iv antibiotics and admission. I. If they’re afebrile reevaluation, probably only about a 9% chance of persistent bacteremia.

And though we don’t know the exact numbers, that risk might be a little bit higher in unvaccinated children. So you can repeat the blood culture in labs and these well appearing kids, but you don’t necessarily have to tap them a positive blood culture for nisia meningitis, HIB gram-negative rods, or other pathogens.

Well, these always deserve a full sepsis workup. LP IV antibiotics and admission. If the kid’s afebrile and well appearing and they’re more than three months of age and they’re positive for e coli or staph aureus, they might not need an LP consult your local practice variations. Um, and any kid with group B streptococcus bacteremia, who’s three to six months of age definitely needs an LP and admission, and that only scratches the surface.

Admittedly, um, this can be a complex topic, so I would consult your local ID recommendations and hospital practice to determine what you should do based on what grows in your culture. I think now that we’ve talked about occult infections in some of the labs, you may be wondering, broadly speaking, do UN or under vaccinated children actually have more stuff done to them in the ed?

And the answer is probably, but we actually don’t know the broad answer. And so going back to that original study from Indiana, these kids that were. Not fully immunized, so UN or under vaccinated, were 83% more likely to get an intervention and 99% more likely to receive an antibiotic prescription, a discharge.

So this included all sorts of interventions, like blood testing, urine studies, chest radiographs. So ask yourself, what do you do if a kid is on or under vaccinated? Has a fever greater than 39, and is three to 36 months of age, are you working ’em up? What do your colleagues do? Do you have a practice guideline where you work?

In fact, is there a consensus guideline for the management of the UN or under vaccinated child with fever? And the answer to that unfortunately is no. No, there is not. Not from the A A P, not from the Infectious Disease Society of America, not in Red Book, not anywhere. So I’m gonna suggest one possible way to work these kids up with the caveat being that again, there’s no consensus, so.

For a child with fever greater than 39 degrees centigrade, who is well appearing, but unvaccinated or under vaccinated, who is between three to 36 months of age, you might want to consider getting procalcitonin CBC with differential urinalysis and urine culture if they meet the risk factors. And again, I would use UTI calc for that.

Any viral detection assays that you deem necessary. And you can draw blood culture and send immediately or send after the procalcitonin or CB, C results. So if the white blood cell count is greater than 20,000, regardless of the physical exam, you should get a two of you chest x-ray to assess for occult pneumonia.

If the procalcitonin. Is greater than 0.5. The white blood cell count is greater than 15,000. The a NC is greater than 10,000 and or the absolute band count is greater than 1,500. Then you should send the blood culture if you haven’t already done so and give empiric antibiotics against streptococcus pneumonia.

For most patients, this should be ceftriaxone 50 milligram per kilogram intramuscular. This depot version of antibiotics will provide coverage for 24 hours. It’s not the same as giving an IV dose. So yes, this is an IM dose. If they have an allergy to cephalosporins, you can give Clindamycin 10 milligram per kilogram iv followed by the first oral dose.

Eight hours later. Add UTI. Treatment is warranted based on your testing. If all of those labs. Are below those thresholds, then antibiotics are not recommended unless the urinalysis says otherwise. So after the labs are back, you reassess the patient. Are they well appearing? Are they well hydrated and demonstrating good oral intake?

Do they have a parent, guardian or caregiver that has no significant social barriers and. Can they follow up with their primary care doctor or at your facility within 24 to 48 hours? If yes to all of those, you can send them home. If not, eh, you should probably admit them to the hospital. I. Now again, this is just one way to consider working up the unvaccinated or unvaccinated child age three to 36 months of age, who is well appearing with fever greater than 39 degrees Celsius for less than five days.

This is not the official recommendation of my hospital or any that I know of, and I hope this inspires you to develop your own practice patterns and perhaps more importantly, have conversations locally where you work about better defining. How we evaluate and manage these children because unfortunately.

Their ranks are increasing. Well, I hope you found this episode on the approach to the unvaccinated and unvaccinated child with fever in the ed thought provoking. I hope it helps sharpen your thinking and clinical decision making and inspires you to have conversations locally about your practice patterns in these vulnerable children.

If you enjoyed the episode, be sure to like, subscribe, leave a review wherever you get your podcasts. Billy helps other folks find the show. You got feedback. Send it my way. I’ll take it over social media. I’ll take it via comments. I’ll take it via email, as always, for PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.

• Describe the clinical presentation, epidemiology, and complications of Mycoplasma pneumoniae infections in pediatric patients, including its atypical manifestations.
• Differentiate Mycoplasma pneumoniae pneumonia from typical bacterial and viral pneumonia based on history, physical exam findings, and diagnostic testing.
• Assess the current evidence for antibiotic treatment of Mycoplasma pneumoniae and justify treatment decisions based on patient presentation, severity, and potential complications.

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Vallejo, Jesus G. “Mycoplasma Pneumoniae Infection in Children.” UpToDate, 1 Nov. 2024, www.uptodate.com/contents/mycoplasma-pneumoniae-infection-in-children.

Garcia T, Florin TA, Leonard J, Shah SS, Ruddy RM, Wallihan R, Desai AP, Alter S, El-Assal O, Marzec S, Keaton M, Yun KW, Leber AL, Mejias A, Cohen DM, Ramilo O, Ambroggio L; Children’s Hospitals Initiative for Research in Pneumonia (CHIRP). Clinical Features and Management Strategies in Children With Mycoplasma Pneumoniae. Pediatr Emerg Care. 2025 Feb 17. doi: 10.1097/PEC.0000000000003338. Epub ahead of print. PMID: 39960098.

Gao L, Sun Y. Laboratory diagnosis and treatment of Mycoplasma pneumoniae infection in children: a review. Ann Med. 2024 Dec;56(1):2386636. doi: 10.1080/07853890.2024.2386636. Epub 2024 Aug 3. PMID: 39097794; PMCID: PMC11299444.

Shah SS. Mycoplasma pneumoniae as a Cause of Community-Acquired Pneumonia in Children. Clin Infect Dis 2019; 68:13.

“Mycoplasma Pneumoniae Infections Have Been Increasing.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 18 Oct. 2024, www.cdc.gov/ncird/whats-new/mycoplasma-pneumoniae-infections-have-been-increasing.html.

Note: This transcript was partially completed with the use of the Descript AI

 Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re focusing on a pathogen that has been making waves in pediatric emergency departments across the country. Mycoplasma pneumoniae. Whether you know it or not, you’ve likely seen a surge where you work.

Patients are presenting with community acquired pneumonia that isn’t responding to standard beta lactam antibiotics, or with parents who are just concerned that their child has walking pneumonia. That’s because mycoplasma pneumonia is just a little bit different than most of the pathogens that we deal with in children.

So let’s dive in. So, what is it? Microbiology lecture. Warning, med school trigger. Uh, so Mycoplasma pneumoniae is a small, obligate intracellular bacterium and it lacks a cell wall. So that’s why it doesn’t respond to beta lactam antibiotics like penicillin and amoxicillin and cephalosporins. Instead, it requires macrolides, tetracyclines, or fluoroquinolones for treatment.

It’s spread via respiratory droplets and thrives in crowded environments such as schools and daycare centers. It binds to the epithelial cells in the upper and lower respiratory tract, triggering an immune response that leads to mucosal damage, increased mucus production, and impaired gas exchange. So mycoplasma pneumonia infections have been on the rise, especially in children.

After a lull during the COVID 19 pandemic, cases reemerged in 2023 and continued to climb into 2024. Historically, mycoplasma pneumonia has been most common in children aged 5 to 17 years and young adults. But what’s new is that we’ve seen a striking increase in infections among children aged 2 to 4.

Per the CDC, diagnosed mycoplasma infections increased steadily through the summer of 2024, peaking in August for 2 to 4 year olds and 5 to 17 year old age groups. There’s also been an increase in diagnosis in those under 12 months of age. This is all notable because these infections have historically been thought to affect school aged children much, much more than younger children.

All right, let’s talk about clinical features. So the incubation period for mycoplasma pneumonia can be around two to three weeks. Symptoms often start gradually, with fever, headache, malaise, and sore throat, preceding the onset of a persistent dry cough. Unlike classic or typical bacterial pneumonia, which has abrupt onset in focal lung findings, mycoplasma pneumonia patients often present with a prolonged worsening cough that can persist for weeks to months.

The name walking pneumonia was coined because people with this mild form of respiratory infection can still walk around and do their normal activities. It’s attributed to, but not exclusive to, mycoplasma disease. Now some patients can develop severe pulmonary complications, fortunately those are rare.

These include respiratory failure, pleural effusions, necrotizing pneumonia, and pyema. Beyond the lungs, mycoplasma pneumonia is a weird bug, and it can also cause some extra pulmonary manifestations. So you can get mucocutaneous disease, including erythema multiforme. and mycoplasma induced rash and mucositis, also known as RIME, and even Stevens Johnson syndrome.

Patients can get joint pain, you can have a hemolytic anemia due to IgM antibodies causing an autoimmune hemolysis, or even neurological complications such as meningoencephalitis, seizures, transverse myelitis, or even Guillain Barre syndrome. Alright, so making the diagnosis starts with having a firm understanding of bacterial versus viral etiologies of pneumonia.

And generally, we should make this diagnosis clinically. So typical bacterial pneumonia, like streptococcus pneumoniae, is more likely when symptoms such as fever, chills, cough, and focal chest pain start abruptly. These patients often have respiratory distress or tachypnea and focal lung findings like rails or crackles or decreased breath sounds.

A typical bacterial pneumonia, like mycoplasma pneumonia, presents with a gradual onset of fever, headache, malaise, sore throat, followed by the worsening non productive cough. It’s often accompanied by wheezing and or rails, and fever and illness are typically milder. than in the classic bacterial pneumonia.

Now viral pneumonia, which is also all over the place, and due to RSV, parainfluenza, influenza, adenovirus, and more, is more common in children under 5 years of age. The cough develops gradually following an upper respiratory tract infection, and lung findings are diffuse and bilateral, often with wheezing.

Think of viral pneumonia like bronchiolitis, but in a preschooler instead of a baby. And so while mycoplasma pneumonia is often a clinical diagnosis based on presentation, there is some confirmatory testing. PCR testing of the nasopharynx, or throat, is highly sensitive and specific. You can get serology, which will detect IgM and IgG antibodies.

It’s useful, but it takes longer to result. The caveat of these serologic tests is that There’s probably a lot of seropositivity without symptoms in the general population. So basically, many people could have positive mycoplasma without symptoms. There are no distinguishing features on blood labs like CBC and blood culture, which are generally not necessary in these patients unless they’re critically ill.

And the chest x ray findings, if you need them, will typically show bilateral patchy infiltrates, though some cases can have unilateral lobar consolidations. So as you might imagine, chest x rays aren’t as useful as you’d think in diagnosing mycoplasma. When it comes to management, first and foremost, supportive care.

Treat fever, ensure adequate hydration, and provide respiratory support as needed, like if kids need oxygen, that sort of stuff. Cough suppressants and cough medicines are generally ineffective and no better than honey, and really not recommended in many age groups, but if you’ve got a middle schooler or teenager and parents want to try it, eh, have at it.

Or don’t. Before I talk about antibiotics, I do want to bring up the question as to whether or not we actually have to treat mycoplasma in the first place. Studies supporting antibiotic treatment of documented mycoplasma pneumoniae in children are limited. Supports provided predominantly by in vitro studies, a randomized trial in military recruits, and some observational studies in which inclusion of mycoplasma pneumoniae specific therapy was associated with a decreased risk of treatment failure.

So, whether that’s a change in antimicrobial therapy or a hospital admission, or length of stay in children with community acquired pneumonia, but they didn’t have etiologic data in that study. There was a systematic review of 17 studies, including 4, 294 patients, where they found insufficient evidence for the efficacy of antimicrobial treatment of mycoplasma pneumonia, lower respiratory tract infection in children less than 17 years of age.

There was publication bias, heterogeneity, and lack of blinding. We also don’t know whether administration of antibiotics decreases the incidence or severity of associated mucocutaneous disease. And I’m not even going to get into pans or pandas here. I can’t bear it. So, yes, I’m going to talk about antibiotics.

But consider this scenario, you’ve got a kid, cough and wheezing, you think it’s a virus, maybe it actually is mycoplasma, there’s a good chance they’ll be fine anyway, even if you don’t treat it. So yes, think of mycoplasma pneumoniae, but don’t make it your sole focus when you’re really just dealing with viral pneumonia in a lot of kids.

Okay, the first line treatment is azithromycin. The ZBA is actually all right, so it’s 10 milligram per kilogram in one dose, max dose of 500 milligrams. That could be orally or IV on the first day, and then five milligram per kilogram in one dose. Maximum dose of 250 milligrams for the next four days. If azithro is unavailable, or in the case of an allergy, you could use doxycycline two to four mgs per kg per day, orally or iv.

in one or twice daily dosing. The max daily dose is 200 milligrams, and it’s done for seven days. Compared with other tetracycline antibiotics, doxy is much less likely to cause permanent tooth discoloration in young children, and it can be given safely for less than 21 days to children of all ages.

Tetracycline for kids greater than eight years of age, and azithromycin are also options, but azithromycin has lots of GI side effects. For immunocompromised children, especially with previous exposure to macrolides, fluoroquinolones like levofloxacin are an alternative initial agent. Fluoroquinolones are bacteriocidal rather than bacteriostatic, and the dosing for levofloxacin varies according to age.

So greater than six months but less than five years. Levofloxacin is 8 10 mg per kg per dose orally or IV every 12 hours. The max total daily dose is 750 mg and you treat for 7 10 days. For kids older than 5 years, you do Levofloxacin 10 mg per kg per dose once per day orally or IV. And that max dose is again, 750 milligrams per day for seven to 10 days.

All right, so let’s talk about some take home points. So mycoplasma pneumonia is back with a vengeance after the COVID 19 pandemic, and it is affecting younger children more than ever before, especially kids, two to four years of age. For most patients, it is a clinical diagnosis. You should think about it, though, in kids with classic presentations, or in a child who has failed treatment with beta lactams for a presumed community acquired pneumonia.

And don’t fear the Z Pak, right? If you diagnose mycoplasma pneumonia, macrolides and zithromycin are the first line treatment. Fluoroquinolones are good for immunocompromised children. Mycoplasma can cause extrapulmonary disease. So, go online and look up some pictures of the mucocutaneous manifestations.

There are also hematologic and neurologic complications. And keep an eye on outbreaks and community trends. The epidemiology is shifting, and infections are rising, so your hospital should have a local plan to deal with infection in your community. Thank you so much for listening to this episode. If you found it helpful, let me know.

Leave a review, send a message on social media or email, and share it with your colleagues and learners. And as always, as my 13 year old would say, don’t forget to like and subscribe. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

We’ll dive into the clinical presentations, including acute and chronic symptoms, the dangers of “sudden sniffing death,” and the specific risks associated with nitrites, hydrocarbons, and nitrous oxide. Learn how to recognize and manage cases in the emergency department, ask the right questions to uncover inhalant use, and provide critical resources for prevention and support. Whether you’re a seasoned pediatrician or new to emergency medicine, this episode offers essential insights into tackling this hidden epidemic.

By the end of this episode, listeners will be able to:

• Recognize the clinical signs and symptoms of inhalant misuse, including acute intoxication and long-term complications.
• Differentiate between the risks and toxic effects associated with specific inhalants, such as hydrocarbons, nitrites, and nitrous oxide.
• Formulate effective strategies for identifying, managing, and preventing inhalant misuse in pediatric patients.

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Perry H, Burns MM. Inhalant misuse in children and adolescents. UpToDate. Ganetsky M (ed). Updated February 26, 2024. Accessed January 13, 2025. https://www.uptodate.com/contents/inhalant-misuse-in-children-and-adolescents

Hogge RL, Spiller HA, Kistamgari S, et al. Inhalant misuse reported to America’s Poison Centers, 2001-2021. Clin Toxicol (Phila) 2023; 61:453.

Marcus E. The next drug epidemic is blue raspberry flavored: How Galaxy Gas became synonymous with the country’s burgeoning addiction to gas. Intelligencer. Published January 6, 2025. Accessed January 13, 2025. https://nymag.com/intelligencer/article/galaxy-gas-flavored-nitrous-oxide-drug-epidemic.html

Note: This transcript was partially completed with the use of the Descript AI

 Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re diving into an important topic, inhalant misuse, with a special focus on nitrous oxide. Welcome Recently, there’s been a concerning rise in recreational use of nitrous oxide, often referred to as Galaxy Gas, which is actually a brand name, which has become synonymous with flavored nitrous oxide products.

Even as that brand, Galaxy Gas, is being phased out of the market, its legacy persists, fueled in part by its viral presence on social media platforms like TikTok and Instagram. So, this episode is going to break down the symptoms, clinical presentations, and management of inhalant misuse in children and adolescents with a specific eye on how these trends are shaping a new wave of cases presenting to the ED across the globe.

So, what are inhalants? Well, these are volatile substances that you’re not meant to breathe in. They produce vapors, which, when you inhale them, cause psychoactive effects. They include everyday household items like glue, paint thinner, and gasoline, as well as recreational substances such as nitrous oxide, often referred to as whippets or galaxy gas.

Interestingly, when these are sold, either online or in physical stores, they’re marketed As additives to make your own whipped cream at home. The people that sell them in stores are told to specifically not refer to them as whippets or to refer to them as a drug. Oh no, they’re only for cooking. The customers and the people selling them know otherwise.

Anyway, the recreational use of nitrous or whippets, it’s been around since the late 18th century, uh, when it was used in laughing gas parties among the immigrants. English elite. Fast forward to today, and nitrous remains one of the most commonly misused inhalants. It’s evolved from its medical and industrial applications to a recreational substance with a significant cultural footprint.

And let’s face it, the prevalence of this inhalant misuse is concerning. In the US, about 11 percent of high school students have used inhalants at least once. And what’s striking is that inhalant use peaks in younger adolescents, particularly those in like 7th through 9th grades, middle schoolers. making it one of the earliest substances that are misused among young people.

So, these inhalants are often used through sniffing, huffing, or bagging. Sniffing involves inhaling the fumes directly from the container. Huffing uses a cloth soaked with the substance. And bagging, or perhaps ballooning, involves inhaling fumes from a bag or balloon placed over the nose and mouth. So you decant the substance from the canister into a balloon, and then you inhale that into your mouth.

The latter dramatically increases the risk of asphyxia. The mechanism of action is rapid and profound. These substances are absorbed through the lungs and distributed to the brain, where they act on GABA and glutamate receptors. The primary effects are euphoria, dizziness, and disorientation. They’re felt within seconds and last 15 to 30 minutes or less.

And. Patients that use these will repeatedly use it throughout the day. You can either get one little individual canister of nitrous, or a big canister which costs about 120 to 120. Repeated use can sustain that intoxication. So the symptoms of inhalant misuse are important to recognize. So first and foremost are the neurological symptoms.

Euphoria, ataxia, disorientation, and slurred speech are common in acute intoxication. Chronic misuse can be devastating and unfortunately we don’t know how much, or how long, or how frequent leads to these symptoms. But nevertheless, they’re pretty darn bad. It includes cerebellar dysfunction, peripheral neuropathy, and toxic leukoencephalopathy, which manifests as white matter degeneration visible on MRI.

Basically, misuse of this stuff can paralyze you. The cardiovascular symptoms include sudden sniffing death syndrome, which is the generation of a fatal arrhythmia, which is particularly dangerous with halogenated hydrocarbons. Pulmonary symptoms include hypoxia, reactive airway dysfunction, and in severe cases, pulmonary edema or even a pneumothorax.

Glue sniffer’s rash is a hallmark skin finding. It presents as erythema and inflammation around the mouth and nose. and nose. Chronic users may also see weight loss, abdominal pain, nausea and vomiting, and metabolic abnormalities like hypokalemia and acidosis, especially if they’re misusing toluene, which is fortunately less common.

Further complicating matters is that each inhalant has its own special risks. Hydrocarbons, again found in solvents and glue, can lead to cranial neuropathy, cerebellar dysfunction, and cardiac arrhythmias. Chronic misuse of these results in profound hypokalemia and metabolic acidosis. Nitrous oxide, so whippets or galaxy gas, interferes with vitamin B12 metabolism, so it can lead to polyneuropathy, myelopathy, and hyperhomocystinemia, which increases the risk of venous thromboembolism.

Nitrites, which are known as poppers, can cause intense vasodilation and methemoglobinemia. with symptoms ranging from headache to cyanosis and seizures. So management, unfortunately, of inhalant intoxication is primarily supportive. Stabilization, you have to ensure that the patient is removed from the exposure source and administer 100 percent oxygen if they’re hypoxic.

If the patient is unconscious and in a tachyarrhythmia, the treatment is electricity! Amiodarone or lidocaine on the palsgar rhythm and avoid catecholamines like epinephrine unless the patient’s in cardiac arrest. For nitrous oxide neurotoxicity, administer high dose vitamin B12 intramuscularly or subcutaneously.

I would consult a toxicologist because I know that this is rare. And if you have a patient with methemoglobinemia, chances are you’re actually taking a board test, but you would treat that with IV methylene blue. In cases of toluene misuse, monitor and correct the electrolyte imbalances carefully, avoid dextrose, which can actually worsen the hypokalemia.

Again, I would call a toxicologist for help from this, because fortunately, it’s very rare. And listen, this problem isn’t going anywhere. So pediatricians, Educators and parents all play a crucial role in prevention. Frankly, these should not be so accessible. They should not be able to be sold easily online or in physical smoke shops.

Also, we need to advocate for federal regulation on these as controlled substances, because currently right now they’re not. Everybody knows the dance that the retailers play in saying, Oh yeah, you can use these to make whipped cream at home, but they are marketed with with flavoring in brightly colored containers and they are very attractive to young children.

They’re piggybacking off the same strategies that made vaping and vape cartridges so popular. Students should be educated about the dangers of inhalants. That means both local advocacy in schools and in medical care settings, but also using some of the same techniques that made getting high off these popular, like social media.

We’ve got to reduce access. and curiosity. Schools should definitely replace solvent based products with safer alternatives and monitor students for signs of misuse. For those already misusing inhalants, referral to a substance use disorder program is essential. Chronic complications often resolve with cessation, but addressing coexisting mental health problems and comorbidities such as depression and suicidality is equally important.

Okay, I know that that was just a whiff of a topic that you may be only a little bit familiar with. But trust me, you’ve probably met a patient That’s huffing or inhaling, and you just haven’t known it. So it starts with asking patients about what they’re doing. A good old heads exam. So when asking patients about inhalant misuse, it’s important to create a non judgmental and supportive environment.

Start with broad, open ended questions, and normalize them. Say that this is something that you ask all patients about. Ask about substance use, like vaping or alcohol, and then introduce inhalants by mentioning specific examples, such as sniffing glue, huffing spray paint, or using nitrous oxides like whippets or galaxy gas.

Again, normalize that conversation by acknowledging curiosity or peer influence, especially on social media. And, if they do disclose use, ask gently about frequency, Context and any symptoms like dizziness, headaches, or worse, emphasize that your goal is to support their health, not to judge or punish and provide reassurance and resources if needed.

Thank you for listening. Inate misuse is often overlooked, especially in pediatric emergency care settings, but if you’re vigilant and you’re informed, you can better serve our patients and manage complications. If you found this episode helpful, well let me know about it. Leave a review on your favorite podcast site that helps people discover the show, or you can reach out and contact me directly via email or social media.

Share it with your colleagues and learners and subscribe for more episodes. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

‘Twas the night before Christmas, and I’m working a shift, The symptoms were varied, the pace was quite swift. The screens glowed with orders, the rooms filled with care, In hopes that discharge summaries soon would be there.

The nurses were moving with hustle and speed, While families recounted each child’s urgent need. And I at my computer, my coffee in hand, Prepared for the onslaught that none could have planned.

When out in the lobby there arose such a clatter, I sprang from my chair to see what was the matter. Away to the triage I flew like a flash, Dodging spilled apple juice and a child with a rash.

The ambulances were wailing, the scene quite a sight, As the complaints rolled in on this hectic night. When what to my weary eyes did appear, But a febrile infant, his parents in fear.

A nursemaid’s elbow in need of a tug, And a kid with a cough wrapped tight in a hug. A forehead lac with blood streaming red, And a teen who proclaimed, “I think I’m half-dead!”

With quick-thinking teamwork, the cases we tamed, And I whistled and shouted and called them by name: “Now flu! Now croup! Now migraines and pain! On seizures! On sepsis! That ankle is sprained!

To the trauma bay stat, through triage with speed, Move quickly, move calmly, and meet every need!” As the snow flakes that fall when wild winter winds fly, We hustled and triaged as new patients arrived.

And then, in a twinkling, I heard down the hall, The sound of retching – a vomiting call. Ondansetron ordered, the nurse prepping the dose, I saw a pale toddler, looking morose.

He was sick from his tummy to the tip of his nose, And the sounds of his misery steadily rose. His eyes were all sunken, his cheeks far too pale, But a popsicle bribe led to a triumphant exhale.

The shift rolled along with splints left and right, Broken forearms galore on this holiday night. And ketamine laughter soon filled the air, As a lac repair finished with great skill and care.

Abdominal pains brought more to the bays, With parents repeating, “He’s been sick for days.” A scan ruled out danger, the appendix intact, While the next patient arrived with an asthma attack.

The hours wore on, the crowd didn’t cease, Yet amidst all the chaos, we found moments of peace. A mom’s grateful smile, a child’s sleepy yawn, Reminded us why we keep carrying on.

So I sat at the computer and typed one last note, Cleared my inbox of tasks and the orders I wrote. And I heard myself whisper as I turned off the light, “Merry Christmas to all, and to all a calm night!”

1. Understand the clinical progression of pertussis through its three distinct stages and identify key symptoms, including age-specific presentations in infants and older children.
2. Implement effective management strategies for pertussis, including supportive care, appropriate antibiotic regimens, and post-exposure prophylaxis for contacts and healthcare providers.
3. Promote pertussis prevention by understanding vaccination schedules (DTaP vs. Tdap), addressing vaccine hesitancy, and adhering to infection control protocols in clinical settings.

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StatPearls Lauria AM, Zabbo CP. Pertussis. [Updated 2022 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519008/

AAP Pediatrics in Review Heather L. Daniels, Camille Sabella; Bordetella pertussis (Pertussis). Pediatr Rev May 2018; 39 (5): 247–257. https://doi.org/10.1542/pir.2017-0229

UpToDate

Yeh S et al. Pertussis infection in infants and children: Clinical features and diagnosis. UpToDate. Available at: https://www.uptodate.com. Accessed December 3, 2024.

MMWR

Seither R, Yusuf OB, Dramann D, et al. Coverage with Selected Vaccines and Exemption Rates Among Children in Kindergarten — United States, 2023–24 School Year. MMWR Morb Mortal Wkly Rep 2024;73:925–932. DOI: http://dx.doi.org/10.15585/mmwr.mm7341a3

Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEM Currents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobolewski, and today we’re talking about pertussis, a disease that is challenging clinicians and public health officials alike. Despite being vaccine preventable, Pertussis is on the rise, yet again, fueled by declining vaccination rates, waning immunity, and the fact that people can’t stop coughing on each other.

In this episode, we’ll go over clinical presentation, diagnosis management, infection control, and post exposure protocols. So pertussis, or whooping cough, is caused by Bordetella pertussis, a gram negative coccobacillus. It definitely spreads via respiratory droplets, and has no environmental or animal reservoirs, making humans the sole carriers.

The incubation period averages about 7 to 10 days, and the disease progresses through some distinct clinical stages, which I will go over in a moment. Pertussis has been recognized since the 16th century. I was not practicing medicine back then. Um, with the first documented epidemic occurring in Paris in 1578.

Bordetella pertussis was isolated in 1906 by Belgian researchers, Jules Bordet and Octave Gengou, I hopefully I pronounced them right, but they’re long gone, so they won’t be mad at me,, leading to the development of a whole cell pertussis vaccine in the 1940s. Introduction of the DTP, the diphtheria tetanus pertussis vaccine, dramatically reduced disease incidence overall.

In the 1990s, we got the acellular pertussis vaccine, the DTaP, which replaced the whole cell formulation due to concerns about some side effects. So pertussis remains endemic in many regions of the world despite vaccination efforts. During the 23 24 school year, DTaP coverage among kindergartners in the United States dropped to 92.

3%, which is below the 95 percent threshold needed for herd immunity. That is is why we’re seeing an outbreak now. This is a pretty troubling trend that began during the COVID 19 pandemic and has just gotten worse since. The exemption rate for vaccines rose to 3. 3 percent. This is the highest on record.

Non medical exemptions accounted for over 93 percent of these exemptions. And 14 states in the U. S. have reported exemption rates exceeding 5 percent. Idaho is leading at 14. 3 percent. So the implications of these declining vaccination coverage rates are significant and that’s why we’re seeing more and more outbreaks, especially putting our vulnerable populations at highest risk.

Alright, let’s get back to the clinical presentation. Wait, what’s that sound? Hold on. Coughing. Yeah, so that’s the whoop and the cough of pertussis. And I’d wager that many of you have not yet heard that clinically, so that’s why I included it on this episode. So here’s the stages of disease. First is the catarrhal stage, which lasts one to two weeks.

You have rhinorrhea, mild cough, and a low grade fever, if any. You are highly contagious during this phase, but it’s often unrecognized as pertussis. Then, in the next two to eight weeks, you have the paroxysmal stage. You have these severe paroxysms of coughing, the inspiratory whoop right beforehand, post tussive emesis.

Infants, especially under six months of age, may present atypically with just apnea, cyanosis, or bradycardia. for that. Following that, you have the convalescent stage, which lasts weeks to months. You have gradual resolution of symptoms, though residual cough may persist. That’s why they call it the 100 day cough.

Aside from coughing forever, there’s some important complications you need to be aware of. And they can be severe, especially, as I noted earlier, in young infants. So respiratory complications include apnea, secondary bacterial pneumonia, and pulmonary hypertension. Children encephalopathy, often due to hypoxia.

And the mechanical complications can include rib fractures, subconjunctival hemorrhage, and even rectal prolapse due to intense coughing and valsalva. Greater than 50 percent of kids under 12 months of age with pertussis could require hospitalization. 50 percent of those kids will have apnea, 20 percent will have pneumonia, and up to 1 percent will die.

Encephalopathy occurs in about 20 percent of mortality cases, probably due to hypoxia, or maybe the toxin produced by the bacteria itself. So, making the diagnosis of pertussis starts with high index of clinical suspicion. Early diagnosis, as you’d suspect, is critical to limiting disease spread and initiating treatment.

So, PCR testing, which is widely available now, has high sensitivity in the first three to four weeks and is the preferred diagnostic test. Culture is the old gold standard, but it’s slower and less sensitive. It can take up to a week to grow. CBC might show significant lymphocytosis, um, most often in infants, but it ain’t going to make the diagnosis of pertussis for you.

And a chest x ray will just show you some non specific findings, such as peribronchial thickening in severe cases. And unless you’re worried about concomitant bacterial pneumonia, you probably don’t need a chest x ray to make the diagnosis of pertussis. You can get an isolated pertussis PCR, or Or it can come as part of a respiratory panel.

But remember those comprehensive viral respiratory panels cost 1, 600. So if you’re just worried about pertussis, don’t get the whole panel. So management starts with supportive care. Infants with apnea, cyanosis, or feeding difficulties should obviously be admitted to the hospital. They may need oxygen and or nutritional support.

And you definitely have to watch those kids very closely for the complications such as hypoxia and secondary infections. Remember, a tiny baby with pertussis can go apneic at a moment’s notice even without a persistent cough. Antibiotics reduce transmission. But do not significantly alter disease progression once the paroxysmal stage begins.

So again, you are treating with antibiotics to prevent more people from getting sick, more so than shortening the duration of illness. The main antibiotic that we use is azithromycin. For infants under 6 months of age, that’s 10mg per kg daily for 5 days. For children older than 6 months of age, 10mg per kg, max of 500mg on day 1, followed by 5mg per kg per day, max of 250mg on days 2 through 5.

That is the same dosing that you can give to a grown up. An alternative treatment, you would be trimethoprim sulfamethoxazole for patients who are allergic to macrolides. Post exposure prophylaxis is recommended for household contacts, so the people that the index patient lives with, any high risk individual, and infant, pregnant women, or immune compromised individuals that have been in any sort of contact with the person with pertussis, and and a health care worker exposed without appropriate PPE.

Again, pertussis spreads through respiratory droplets. So this necessitates strict infection control. So that starts in triage. So if you think that a patient has pertussis, then they need to be place on droplet precautions as soon as they are assessed. You wear a surgical mask and eye protection, so goggles or a face shield, and you want to maintain these precautions for five days after starting effective antibiotics or for 21 days if the patient is untreated.

As a clinician, Just ask yourself, did you wear appropriate PPE, mask and goggles? Don’t get lazy. Was the exposure prolonged or close? And rely on infection control in your institution to help decide whether or not you need post exposure prophylaxis. If you’re vaccinated and you wore PPE, you don’t need anything.

Unless you have symptoms. If you’re vaccinated and you did not wear PPE, then prophylaxis is recommended. If you’re unvaccinated and not up to date, well then what are you doing in healthcare? And immediate prophylaxis and vaccination update are required. And, okay, ’cause I just mentioned it. Let’s talk about vaccines.

So first I wanna talk about DTaP, dt, lowercase a uppercase p and t dap. Uppercase T D A P. So DTAP contain higher concentrations of diphtheria and pertussis antigens. It’s used for children under seven years of age. TDAP contains lower antigen concentrations and it’s designed for adolescents and adults to reduce reactogenicity.

There is no standalone pertussis vaccine. I’ve had patients say, well, I don’t want tetanus. Just give me the pertussis one. Well, tough Schenectes. We do not have a pertussis vaccine. alone. It’s only available in combination with diphtheria and tetanus toxoids, DTaP or Tdap. The combined vaccine boosts efficacy and ensures broader protection against all of the included infections.

Now the routine vaccination schedule, which if you are a pediatric resident, you know, like the back of your hand, the DTAP is administered at 2, 4, 6, and then between 15 and 18 months with a booster at 4 to 6 years. The Tdap is one dose at 11 to 12 years and then during every pregnancy to confer passive immunity to the newborns.

And again, depending on when you’re listening to this, you may be in the midst of a pertussis outbreak. And if you listen to this a few years later, after the original publication date in the fall of 2024, and you’re seeing another pertussis outbreak, well, dang it, we haven’t done our job. We need to strengthen school vaccination requirements.

We need to educate parents about vaccine safety and the risks of exemptions. And we need to broadly improve and ensure access to vaccinations through our community clinics. Thanks. Alright, so that’s it for this episode on Pertussis, which remains a significant public health challenge due to its severe complications in young patients and the ongoing decline in vaccination coverage.

Healthcare providers play a vital role in diagnosing and managing it, preventing its spread, and educating patients and families about the benefits of vaccination. Infection control practices and post exposure protocols are critical for protecting both clinicians and close contacts and other exposures.

Thank you so much for listening to this episode. I hope you found it educational and informative. If there’s other topics that you want to hear about, let me know. I’m on X, I’m on Blue Sky, I’m on Mastodon, I take emails, you can leave a comment on the blog, you can leave a review on your favorite podcast site, any feedback is good feedback, and encourage your colleagues to listen, and as the kids say, like and subscribe, I told my 12 year old I would say that at the end of the episode.

For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski, see you next time.