In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, Brad Sobolewski discusses advanced imaging in pediatric emergency care with Dr. Jennifer Marin ([email protected]) from UPMC Children’s Hospital of Pittsburgh. They explore the evidence behind ultrasound, CT, and MRI, strategies to reduce low-value imaging, and the role of shared decision-making in selecting the appropriate diagnostic test.

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.

In this episode, we tackle the clinical mischief of Parvovirus B19, a common viral infection with a surprisingly wide range of manifestations—from the classic “slapped cheek” rash of erythema infectiosum to aplastic crises in children with hemolytic anemias and fetal hydrops in pregnant contacts. We’ll break down the virology, epidemiology, clinical presentation, and complications of Parvovirus B19. You’ll also learn how to manage exposures in the emergency department, especially when the child has a pregnant caregiver, and why isolation isn’t always necessary once the rash shows up.

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.

This episode of PEM Currents: The Pediatric Emergency Medicine Podcast focuses on the approach to unvaccinated or undervaccinated children aged 3–36 months presenting to the ED with fever. Host Brad Sobolewski reviews differences in immune response, risk for serious and invasive bacterial infections, and outlines evaluation strategies including labs, imaging, and empiric antibiotics. He highlights data showing increased interventions in this population and calls for local guideline development. The episode emphasizes thoughtful, individualized care in the context of rising vaccine hesitancy and declining immunization rates.

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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.

In this episode we dive into the resurgence of Mycoplasma pneumoniae—an atypical bacterial cause of community-acquired pneumonia that’s making waves in pediatric emergency medicine. We’ll cover its clinical presentation, epidemiology, diagnostic approach, and management, including why standard beta-lactam antibiotics won’t work. Plus, we’ll discuss whether M. pneumoniae even needs to be treated in the first place!

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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.

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the complex and often underrecognized issue of inhalant misuse. From the early days of glue sniffing to the recent rise of nitrous oxide misuse, fueled by brands like Galaxy Gas and viral trends on TikTok and Instagram, inhalant misuse has evolved into a growing concern among adolescents.

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:

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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.

In lieu of a traditional episode this holiday season I wanted to share a reading of the Pediatric Emergency Medicine version of a famous Christmas poem.

‘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!”

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore pertussis, also known as whooping cough – a disease that remains a public health challenge despite widespread vaccination efforts. We will review the clinical presentation, diagnostic strategies, management protocols, infection control practices, and vaccination updates. This episode also covers what healthcare providers need to know about post-exposure prophylaxis, respiratory precautions, and managing occupational exposures.

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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.

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, I explore the complexities of gastroesophageal reflux (GER) and gastritis in children and adolescents. I’ll make the important distinction between gastritis – which is diagnosed only via endoscopy – and dyspepsia, the term best used to describe the symptoms many patients experience. I’ll dive into the latest clinical practice guidelines and discuss evidence-based approaches to diagnosis and treatment.

Topics covered include:

Join me as I scope out the nuances of gastroesophageal reflux and gastritis and provide practical insights for clinicians in the emergency setting.

PEMBlog

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Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint Recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2018;66(3):516-554. doi: 10.1097/MPG.0000000000001889

Lightdale JR, Gremse DA; Section on Gastroenterology, Hepatology, and Nutrition. Gastroesophageal Reflux: Management Guidance for the Pediatrician. Pediatrics. 2013;131(5):e1684-1695. doi: 10.1542/peds.2013-0421

Tighe M, Afzal NA, Bevan A, et al. Pharmacological Treatment of Children with Gastro-oesophageal Reflux. Cochrane Database Syst Rev. 2014;2014(11):CD008550. doi: 10.1002/14651858.CD008550.pub2

Sintusek P, Mutalib M, Thapar N. Gastroesophageal Reflux Disease in Children: What’s New Right Now? World J Gastrointest Endosc. 2023;15(3):84-102. doi: 10.4253/wjge.v15.i3.84

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’s episode will focus on gastro esophageal reflux and gastritis in children and adolescents. Both conditions can present with similar symptoms. They do, though, have distinct pathophysiologies and management strategies.

So we’re going to discuss the evidence based approaches to diagnosis and treatment, and I will talk about why it is presumptive to call things gastritis before definitive diagnosis, even though I put it in the title of the episode. Alright, let’s scope things out. I’m going to begin by making a brief distinction between gastroesophageal reflux and gastroesophageal reflux disease.

So, reflux itself is a common physiologic process, especially in infants, that usually resolves by 12 to 18 months, when the gastroesophageal sphincter gets tighter, and kids spend more of their life on it. upright. Gastroesophageal reflux disease is when the patients have severe symptoms that persist and cause long term issues.

Now, either way, this is due to reflux of the stomach contents into the esophagus. Now, gastroesophageal reflux is incredibly common in infants with up to 50 percent of b cells. babies under three months regurgitating daily. This typically peaks at about four months of age and improves as the infant grows.

Gastroesophageal reflux disease is less common, but still affects about 10 percent of children and up to 10 to 20 percent of adolescents. Adolescents with GERD often present similarly to adults with heartburn and regurgitation as the primary complaints. Now there are some risk factors for GERD.

Gastroesophageal reflux and reflux disease in children. A main one is neurological impairment. So kids with cerebral palsy or other neurologic disorders have delayed gastric emptying and poor esophageal motility, increasing the risk of GERD. Children with respiratory conditions and chronic lung disease like asthma are more prone to GERD as well.

And reflux itself can exacerbate the existing respiratory symptoms either through microaspiration or vagal mediated bronchospasm. Prematurity and congenital conditions like esophageal atresia also obviously increase the risk. So gastroesophageal reflux and reflux disease result from transient relaxation of the lower esophageal sphincter.

That allows acidic gastric contents to flow back into the esophagus. Now, the lower esophageal sphincter is supposed to prevent this reflux from happening. In GERD, the sphincter relaxes too frequently or incompletely, which can lead to symptoms building up over time. Other factors like delayed gastric emptying and abnormal esophageal motility can worsen problems in general.

And the presentation for GERD varies by age. Infants will have frequent spitting up or vomiting after feeds, irritability during or after feeds, especially in the more significant cases where the esophagus is irritated. Uh, infants may start to refuse to feed due to the discomfort. They can have poor weight gain or even failure to thrive in more severe cases.

And they can have Sandefur syndrome, which is the arching of the back and dystonic posturing that occurs during or after feeds as a response to discomfort from acid reflux. This is sometimes misidentified as seizures. In older children and adolescents, heartburn is the most common symptom. It’s a burning sensation in the chest or epigastrium, and that is the classic symptom in this age group.

You can also see regurgitation, acid or food regurgitating into the mouth, leading to a sour taste. uh, ill defined epigastric or chest pain, and it’s often worse by eating or lying down after meals. And some other symptoms that you gotta think about in reflux, chronic cough, hoarseness, or even asthma like symptoms.

These extra esophageal manifestations can occur due to irritation of the upper airways by the gastric contents. Now, in the pediatric emergency department, the diagnosis of reflux is primarily clinical. You just got to take a good history and do a physical examination, especially when the symptoms are typical, like regurgitation, heartburn, or epigastric pain in an older child or adolescent.

You want to take a good history on feeding or dietary habits. In infants, you want to know the amount and frequency of feeding, especially because baby stomachs are small and no newborn stomach can hold six ounces. So, the parents may say, well, he Doesn’t ever seem full. Well, baby doesn’t know how to be full.

So really, you need to learn how much a baby can take and follow weight gain appropriately. Overfeeding a baby will lead to increased spitting up and reflux. You should also ask about older children and adolescents eating trigger foods like spicy things, caffeinated beverages, and acidic beverages like pop.

These can all exacerbate reflux. You want to ask about nocturnal symptoms. So if the kid has symptoms that are worse at night or immediately upon waking up, this may indicate reflux exacerbated by lying down, especially after meals. Red flags that you should always ask about include hematemesis, melana, dysphagia, and Unintentional weight loss, these all need further investigation for complications like esophagitis or another diagnosis such as EOE or peptic ulcer disease.

If any of those red flags are present, you should definitely consider a further diagnostic workup. Again, otherwise the diagnosis is based on history and physical examination. So if you see failure to thrive or poor weight gain, again, vomiting blood or passing black tori stools, signs of esophagitis such as painful swallowing or difficulty swallowing.

They need more workup often via GI. So diagnostic testing centers around endoscopy. That’s the gold standard and ultimately getting a camera in there. Taking a look for strictures or ulcers and taking a biopsy of the esophageal and gastric mucosa will make the diagnosis and evaluate for other things like eosinophilic esophagitis or helicobacter pylori infection.

Also get a pH monitoring and impedance probe. This measures both acid and non acid reflux events. It’s kind of like a Holter monitor for reflux. This is obviously ordered by a gastroenterologist, but But the probe itself measures reflux, and then the patient can press a button for an event monitor. And this is particularly useful in children with atypical symptoms or extra esophageal manifestations like cough or asthma, and especially in those that have had a normal endoscopy.

Contrast radiography, like a barium swallow, has much lower sensitivity and specificity than scopes or, in certain situations, even impedance probes and pH monitors. Now, that being said, imaging can be helpful if you suspect hypertrophic pyloric stenosis or other causes of obstruction such as duodenal atresia or antral webs.

But again, you should suspect these based on a detailed history and physical. A management of gastroesophageal reflux is largely dependent on the severity of symptoms and the patient’s age. And most cases of GERD in a pediatric ED can be managed conservatively with feeding or lifestyle modifications and short term pharmacotherapy.

So in infants, you want to recommend smaller, more frequent feeds. Again, overfeeding is a common contributor to reflux in infants. Maybe parents will have to thicken the feeds, but I do not recommend this in the emergency department. Um, and this practice adds rice cereal to the formula or express breast milk that may reduce regurgitation.

Again, this should only really be done under supervision of the child’s pediatrician, keeping infants upright for a half hour after feeds, can let gravity be your friend and reduce reflux episodes. And in older Children and adolescents, the first and most important thing to do is to do dietary modifications like avoiding trigger foods, caffeine, chocolate, spicy foods and acidic beverages like pop.

Large fatty meals should also be avoided, especially in the two to three hours before bedtime. You should encourage older children to avoid lying down immediately after meals, and in some cases, elevating the head of the bed by 30 degrees can reduce night time symptoms. If you feel that you do need to do pharmacologic management, The most effective drugs are proton pump inhibitors like omeprazole and lansoprazole.

They can reduce gastric acid production and help heal the esophagus. A 4 8 week trial of PPIs is recommended for children with moderate to severe GERD, especially those with esophagitis. So you could start that in the emergency department if the symptoms are severe enough, provided that they have primary doctor follow ups.

You may need to wean these PPIs off if symptoms improve because long term use could be associated with risks such as malabsorption of calcium and magnesium or maybe even an increased risk of GI infections such as C. difficile. H2 blockers or H2 formatidine can be used as an alternative to PPIs in milder cases of GERD.

They start working faster. Again, the PPI’s take three to four days to start working. H2’s work immediately. They do reduce acid production to a lesser degree. In older children and adolescents, antacids can provide symptomatic relief of heartburn, but they don’t address underlying acid production. And then there’s things for infants like myelocon and gas drops.

And if you want to try them, go ahead, but they ain’t gonna stop the physiologic process of reflux. And I’ll touch on surgical management briefly before moving on to part two. In rare, severe cases where GERD is refractory to medical management, surgical interventions like fundoplication may be considered, especially in kids with neurologic impairments or life threatening aspiration.

All right, let us shift gears to gastritis. So gastritis is inflammation of the gastric mucosa and can result from infections such as H. pylori, H. pylori, medication overuse, particularly NSAIDs or other stressors. Children with gastritis often present with epigastric pain, nausea, and vomiting, particularly after meals.

And yes, these symptoms do overlap with gastroesophageal reflux and gastroesophageal reflux disease, but they are separate entities. Now there’s a big caveat here. I know that I’m using the word gastritis. And it’s even in the title of the episode. But technically, this diagnosis is only made after endoscopy and biopsy.

Trust me, I asked a gastroenterologist about this directly. So therefore, if you’re seeing this kid for the first time and there’s no established diagnosis, it’s more accurate, especially when an endoscopy has not yet happened, to diagnose them and label that diagnosis based on their symptoms, such as abdominal pain, nausea, early satiety, endoscopy.

Or, you can label it as dyspepsia, also known as indigestion. This refers to a condition characterized by discomfort or pain in the upper abdomen. Typically manifests as fullness, bloating, nausea, or burning in the stomach, especially after eating. And as noted throughout this episode, dyspepsia can be caused by several factors that overlap with GERD and even a kid who gets an ultimate diagnosis of gastritis, like overeating, spicy or fatty food, stress, or underlying conditions.

And technically, the most common cause is functional dyspepsia. Now, I know that’s a lot to digest, and you might be starting to churn, but let’s talk now about the relationship between eating and pain. A key feature of gastritis is the timing of pain. Pain in gastritis typically occurs shortly after eating, as food stimulates gastric acid production, which can irritate the inflamed stomach lining.

You want to ask detailed questions about the timing in pain in relation to meals. Again, that pain is mostly shortly after eating. The foods that cause more symptoms are the ones you’d expect. Spicy, fatty, acidic, or caffeinated items. A detailed dietary history is one of the first steps to making the diagnosis.

You also want to take a detailed history of medication use, especially NSAIDs. Chronic NSAID use for often comorbid symptoms such as headache can damage the gastric mucosa leading to gastritis. The red flag symptoms, as expected, are similar to GERD. Look for signs of GI bleeding, such as hematemesis or melanoma.

or somebody who appears pale, dehydrated, in severe pain, or worse, even in shock. So if you think a kid has dyspepsia, or maybe even eventually gastritis, it’s the history and physical alone which will make the diagnosis. Now a GI cocktail, which is antacid plus viscous lidocaine, could modify the patient’s current symptoms and help sort of convince them where the pain is coming from.

It has been called into question recently by the adult literature. And probably with good cause, as In an older adult with GI symptoms, you should be worried about myocardial infarction or other causes and if you alleviate or mask the pain then you may be moving yourself away from a more important diagnosis.

There also is the worry about rapid systemic absorption of the lidocaine. In general, I’ve not found them to be incredibly helpful in children, but if you’re not worried about other causes, and you need to modify the kid’s pain to sort of help them convince that it’s their stomach and esophagus as a source of the pain, then it could be worth trying.

I mentioned again that the diagnosis is based on history and physical. If they’ve been dealing with chronic symptoms, And there’s an abrupt worsening, or again, the child has red flag symptoms, then you probably do want to get some labs, such as the CBC, check the HNH, lipase, renal panel, liver profile, and ESR and CRP.

Like a kid with normocytic anemia and an ESR of 140, that ain’t gastritis. I’d be worried about inflammatory bowel disease, for instance. Plain films are generally not helpful unless you suspect obstruction or foreign body ingestion. And then, only a radiopaque foreign body. A CT scan can show some signs of liver disease or pancreatitis, but the HNP followed by targeted labs is a more safe and judicious approach.

Now, ultrasound is useful if you suspect gallbladder disease, but the patient needs to be NPO for six to eight hours before the procedure. This will that the gallbladder is distended, which improves the accuracy of the ultrasound in visualizing gallstones or sludge or other abnormalities. So, a kid with mild symptoms, and you want to rule out gallbladder disease?

Like, you can totally order this as an outpatient. You don’t need to make them wait in the ED for six to eight hours. Have a detailed discussion with the patient and family and do shared decision making in terms of interventions, the GI does, and again, these will be the gold standards. Endoscopy, upper GI and endoscopy is the gold standard for diagnosing gastritis.

You see direct visualization of the gastric mucosa and you take biopsies, which can rule out helicobacter pylori or eosinophilic esophagitis or eosinophilic gastritis. Non invasive H. pylori testing, like stool antigens or a urea breath test, can be helpful for diagnosing H. pylori, especially in cases of chronic or recurrent symptoms.

But, being on a PPI can make these tests less accurate. So really, scope is still the way to go. In the end, the most common diagnoses are All of these kids with gastritis like symptoms are going to end up is functional dyspepsia. This is chronic or recurrent pain and discomfort centered in the left upper abdomen without any identifiable structural or biochemical abnormalities upon medical examination.

Gastritis is, once again, inflammation of the stomach lining, which is only truly identified with endoscopy and biopsy. And yes, I called this episode gastroesophageal reflux and gastritis because it’s a colloquial term, but it’s important to make the distinction that ultimately these kids should be labeled as their symptom or dyspepsia in the ED and then followed up with their primary doctor or GI if necessary.

And many of us will ask about H. pylori. And it’s more common in adults, but it’s actually pretty rare in kids. So unless someone living in the home with a kid has an active infection is being treated. it’s probably not going to be H. pylori in the kid. And still, GI would recommend that we don’t start empiric antibiotic treatment in the emergency department anyway, because it’s best to diagnose that with a scope.

So in the odd, rare scenario where you have a family member being treated for H. pylori and a kid with symptoms, I wouldn’t actually start them on a PPI and instead refer to GI for definitive diagnosis. Other things on the differential include peptic ulcer disease, Again, that’s something that really you’ll pick up on endoscopy, but a kid looks like they’re bleeding out, I’d be worried about it, and they are coming in.

It’s also worth mentioning that gastroparesis and delayed gastric emptying can also cause symptoms of dyspepsia. So what are some other important causes of abdominal pain that you should differentiate from dyspepsia and gastritis? And by differentiate, I mean both ask the right questions and tell the family that you are not worried about them.

First, pancreatitis. So the pain in pancreatitis is typically more severe, constant, can radiate to the back, unlike the more intermittent pain of gastritis. Patients will have more nausea and vomiting and some systemic signs like fever or tachycardia. Elevated lipase can make the diagnosis, though Ultrasound or CT can show some pancreatic inflammation.

Gallstones can be seen in adolescence. Pain in the right upper quadrant or epigastric pain. It’s often described as colicky, worsened by fatty meals. Ultrasound, as I noted before, is the diagnostic test of choice. And peptic ulcer disease from duodenal ulcers improves with food, but then worsens several hours later.

Whereas gastric ulcers may worsen shortly after eating, similar to gastritis. Endoscopy will make the diagnosis. And then there’s celiac disease. So celiac disease can cause dyspepsia symptoms as well. Celiac disease is a true autoimmune disorder triggered by the ingestion of gluten. It’s a protein found in wheat, barley, and rye.

In individuals with celiac disease, gluten intake leads to an immune mediated inflammatory response that damages the small intestine’s mucosal lining, specifically the villi. It kind of blunts them down. This impairs nutrient absorption and can lead to a variety of GI symptoms. So if somebody says, I’m not eating gluten because I don’t feel like it or because I want better hair.

Maybe I should try that. That’s not celiac disease. Celiac disease is an immune process. So dyspepsia is a symptom that can occur in celiac disease, and so if you take a history that things worsen upon eating gluten, or what happens if the patient has eliminated gluten from their diet, which is something that I’ve seen many families do on their own.

And it’s not within the scope of this episode, but the anti tissue transglutaminase antibodies, TTG, IgA, that’s the most sensitive and specific initial test for celiac. All right, let’s start to talk about now the management of dyspepsia and gastritis. Dietary and lifestyle changes are the first line treatment.

They can significantly improve symptoms. It’s important that we communicate to patients and families how optimistic we are that these can make a difference. So avoid trigger foods, spicy and fatty foods, acidic foods and beverages like citrus fruits and carbonated drinks. Caffeine and chocolate, and even dairy products if you suspect lactose intolerance.

You want to encourage eating of small, frequent meals. That allows you to digest the gastric contents a little more efficiently. Chew your food thoroughly. Don’t swallow things like a snake. That reduces the swallowing of air and aids digestion. And avoid late night eating, especially two to three hours before bedtime.

No bedtime snacks for these kids. Kids should stay well hydrated, adequate water intake, and limit sugary drinks like juice and pop that can irritate the stomach. Gatorade. That’s a big offender that I’ve run up against. Stress management is really important because stress can exacerbate symptoms, deep breathing, meditation, biofeedback, regular physical activity promotes healthy digestion, and avoiding secondhand smoke because tobacco smoke can irritate the stomach lining.

If you want some symptomatic relief, you can use antacids. They neutralize stomach acid and provide quick relief from symptoms. So Tums, or calcium carbonate, you chew it and it neutralizes existing stomach acid. It’s quick, short term relief. If you take way too many of them, you can get constipation or hypercalcemia.

Maalox, which is aluminum hydroxide and magnesium hydroxide, it’s two antacids, and it can balance side effects maybe, I don’t know. That also provides symptomatic relief. It’s a little bit gritty, but you drink it. And there are pediatric formulations. If you take a lot of it, magnesium can cause diarrhea, and aluminum can cause constipation.

I don’t know if those balance out at all. I haven’t tried it. Then you have your H2 receptor antagonists, or H2 blockers. These medications reduce stomach acid production by blocking histamine receptors in the stomach lining cells. So you’ve got things like famotidine or pepsid. Runitidine or Zantac was commonly used, but it’s been withdrawn from the market due to some safety concerns.

Lomatidine will decrease acid secretion, and it’s effective for mild to moderate symptoms, and it starts shortly after taking it, and is generally well tolerated. The next step up are proton pump inhibitors. These are more potent acid suppressants, and they block the enzyme responsible for acid secretion itself, as opposed to just the pump.

You’ve got drugs like Prilosec, which is Omeprazole, Prevacid, which is Lansoprazole, or Nexium, Esomeprazole. They all work fine and there’s some pediatric formulations which you can look up and sometimes insurances will take one and not the other, again, beyond the scope of this episode. These are prescribed for more severe symptoms or when H2 blockers are ineffective.

Follow pediatric weight based dosing and know that it does take three to four days before the suppression starts working. Long term use could affect nutrient absorption of like magnesium or vitamin B12. And being on a PPI as opposed to being on an H2 blocker can, as I mentioned earlier, alter the results of an endoscopy.

So if you think a kid’s going to need a scope, don’t start a PPI. Or you can stop the PPI if they’re going to get a scope within the next one to two weeks. Let me talk about one more medication that I’ve used occasionally. And so it’s sucrophate or carophate. This kind of acts like a protective barrier over the stomach lining that can aid in healing.

It’s kind of like putting, like, spackle over the stomach. It just kind of blocks everything up and tamps down the symptoms. It’s a viscous, adhesive substance, and it can adhere to ulcer sites as well. This is really short term treatment for more severe pain. You would administer this on an empty stomach, usually an hour before meals, or when a child is having severe symptoms not around the time of meals.

If you use a lot of it, it can cause constipation or interfere with the absorption of other daily medications. So fortunately, most of the kids with dyspepsia, or kids that you think will ultimately be diagnosed with gastritis, will be able to be discharged home. So first and foremost, recommend dietary and lifestyle modifications.

For You could start a daily proton pump inhibitor and explain to the family that it takes three to four days before it starts working. If they want more immediate relief or the symptoms are mild, you consider using an H2 blocker instead. For mild intermittent symptoms, consider adding Tums if they like to chew a tablet or Maalox if they’d rather drink a liquid.

And for a step up to more severe symptoms, suggest the use of sucrophate and intermittently and judiciously. You should have the child follow up with their primary care doctor often after about 10 to 14 days on the acid blocking regimen that you prescribed. If they’re doing better and they’ve made diet and lifestyle modifications, the primary doctor at that point can discuss how long to maintain therapy and develop an exit strategy.

A trial of four to eight weeks would be reasonable. But if they’re not improving, And that could be a cause for referral to gastroenterology. It’s important in the ED to not over promise that, oh yeah, you’re going to see GI. Kids can get better on what we recommend. You should trust that. So don’t immediately refer to GI unless you’re worried about a bleeding ulcer or another diagnosis like inflammatory bowel disease or celiac or eosinophilic esophagitis because every time they swallow chicken and steak it gets stuck in their esophagus.

Remember, our community pediatricians, family medicine doctors, are brilliant. They can handle this problem. But if a child has those red flags, or if you’re concerned they need immediate intervention, by all means, get them to a pediatric center for admission and GI evaluation imminently. And again, I will say it yet one more time, because most of these kids have not yet had endoscopy with biopsy, I would not recommend using the diagnosis gastritis.

And I did put it in the title, but it’s what most people call it, and perhaps this was a bridge to education. Use symptoms as your diagnosis. Abdominal pain, nausea, early satiety, or probably most appropriately, call it dyspepsia. These kids are having indigestion. Don’t minimize it. It is having a significant impact on their daily lives.

They kept whining about it. They came to the ED. And it is tempting to call it gastritis because it seems more significant or impactful, but Avoiding making a presumptive diagnosis does not minimize the symptoms the child is having. Instead, use this as a teachable moment and link your interventions with your expected symptom improvement.

Alright, so we know that gastroesophageal reflux and gastritis are linked. really dyspepsia, are common yet distinct causes of GI symptoms in pediatric patients. Recognizing the key features of these conditions and differentiating them from other causes of epigastric pain, such as pancreatitis, gallstones, and ulcers, is crucial in providing appropriate management.

Thank you for listening to this episode. I hope you were able to pick up some new pearls that you can take back to your next clinical shift. If you have any feedback on this episode or would like to suggest content for a future episode, send it my way. I’ll take an email, a comment on the blog, a direct message on X or another social media platform.

And my kids will remind me to say, like, rate, and review. That’s so more people can find the show and continue to learn. For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

This episode of PEM Currents discusses ECPR (Extracorporeal Cardiopulmonary Resuscitation), an advanced procedure used in cases of cardiac arrest when traditional CPR fails. ECPR involves using ECMO (Extracorporeal Membrane Oxygenation) to take over heart and lung functions, offering a last-resort option that is becoming more common in large pediatric hospitals. While ECPR shows promise in improving survival rates, particularly in pediatric patients with conditions like congenital heart disease, it is resource-intensive and carries significant risks. Establishing an ECPR program requires robust infrastructure, multidisciplinary teamwork, and extensive training. The episode highlights the importance of understanding eCPR as a critical therapy for both in-hospital and out-of-hospital cardiac arrests.

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My Instagram

My Mastodon account @bradsobo

Gajkowski EF, Herrera G, Hatton L, et al. ELSO guidelines for adult and pediatric extracorporeal membrane oxygenation circuits. ASAIO J. 2022; 68:133–152. 

Stratton, M., & Edmunds, K. (2024). Extracorporeal Cardiopulmonary Resuscitation. Pediatric Emergency Care, 40(8), 618-622. 

ECC Committee, Subcommittees, and Task Forces of the American Heart Association. 2005 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2005;112(suppl):IV1–IV203. 

Yannopoulos D, Kalra R, Kosmopoulos M, et al. Rationale and methods of the advanced R2Eperfusion STrategies for refractory cardiac ARREST (ARREST) trial. Am Heart J. 2020;229:29–39. 

Bartos JA, Yannopoulos D. Starting an extracorporeal cardiopulmonary resuscitation program: success is in the details. Resuscitation. 2023; 187:109792.

Syphilis has gone by many nicknames over the years including “The Great Pretender” and “The Great Imitator.” Emily Labudde, MD, a Pediatric Emergency Medicine fellow at Children’s Healthcare of Atlanta and recent pediatric residency graduate from Cincinnati Children’s discusses the various manifestations of this sexually transmitted infection, and how we can’t miss this very treatable, but sneaky malady.

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Emily J. Labudde, Jane Lee; A Review of Syphilis Infection in Pediatric Patients. Pediatr Rev. July 2024; 45 (7): 373–380. https://doi.org/10.1542/pir.2023-006309

Centers for Disease Control and Prevention. “Sexually Transmitted Disease Surveillance 2021.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/std/statistics/2021/default.htm.

Centers for Disease Control and Prevention. “Sexually Transmitted Infections Treatment Guidelines 2021.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/std/treatment-guidelines/syphilis.htm.

Centers for Disease Control and Prevention. “Youth Risk Behavior Surveillance System.” Centers for Disease Control and Prevention, 2021. Available from: https://www.cdc.gov/healthyyouth/data/yrbs/index.htm.

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. Today’s episode is all about the great pretender, syphilis. And let’s face it, it’s not just a disease for Medieval royalty. It’s on the rise in the United States and abroad. So let’s talk about the manifestations and management.

And I’ve got a special guest host. This is Emily Labudde, originally from Detroit, at the time of recording this episode, a third year categorical pediatric resident at Cincinnati Children’s and a soon to be pediatric emergency medicine fellow in Atlanta. I’m going to pass the mic to you, Emily. My name is Emily Labudde, and I’m a third year pediatric resident at Cincinnati Children’s Hospital, and I’ll be starting fellowship in pediatric emergency medicine this summer at Emory University Children’s Healthcare of Atlanta.

Today’s podcast is going to cover acquired syphilis infection. Now, I know what you’re thinking. We don’t see a lot of syphilis in the pediatric ED. That’s what I thought, too, until I saw it, and with syphilis on the rise, it’s likely we’ll start to see more. I recently published a review article on syphilis in Pediatrics in Review, which you should check out.

It is far more detailed and also covers congenital syphilis, which is beyond the scope of this episode. At the end of this podcast, you should be able to appreciate the rising incidence of syphilis in the United States, especially amongst young people, recognize various signs and symptoms associated with different stages of syphilis infection, and identify the appropriate workup for possible syphilis infection, including co infections.

Syphilis is fondly referred to as the great imitator because of its various presentations. Headache? Could be syphilis. Rash? Could be syphilis. Weight loss? Could be syphilis. Epitrochlear lymphadenopathy? That’ll be on your boards. Definitely syphilis. I bet I could argue to have syphilis on every differential in some way, shape, or form.

But there are certain clues that can help guide you toward a more reasonable consideration of syphilis infection. Thank you, Jen. The U. S. is seeing a lot more cases of syphilis over the last decade or so. And, since we know from the CDC’s Youth Risk Behavior Survey that many American teens are having sex with less than optimal condom use and infrequent STI testing, pediatricians everywhere should be thinking more about acquired syphilis infection, not just congenital syphilis.

There are three stages of syphilis infection. Primary syphilis is often missed as it presents as a painless genital ulcer. Secondary syphilis causes systemic symptoms such as fever, anorexia, headache, malaise, lymphadenopathy, arthralgias, and rash, that classic rash on the palms and soles. It’s worth looking at a variety of pictures of this rash, some examples of which we have included in the show notes, as its appearance can vary, especially between different skin colors.

Tertiary syphilis is rare, and you’re almost guaranteed not to see it in a pediatric ED as it develops decades after initial infection. It’s characterized by gummas, which are granulomatous soft tissue tumors seen most often in the liver, but also in the bone, brain, heart, skin, testis, and eyes, and end organ damage, particularly of the central nervous system.

At any stage, patients can develop neurosyphilis, that can present with vision changes, neuropathies, seizures, or altered mental status. You may have heard this once or twice before, but your history and physical exam are so important, especially when looking for an infection like syphilis that can present in many different ways.

A thorough review of systems can help guide your differential and can point towards co infections with other STIs. Brush up on your sexual history taking skills because they’re critical here. This includes all the details like who has what parts and where they put them. Teens are awkward and they get super nervous when you kick out mom and dad and ask them what they’ve been doing on the weekends, but you won’t fully understand your patient’s risks without asking these questions.

It’s good preparation prior to the physical exam, which, you guessed it, should be thorough. We’re talking full body skin exam, neuro exam, genital exam, and all of the lymph nodes. Now, it would be really nice if our patients came in saying, Hey, my partner has syphilis, please test me for syphilis. And, like we talked about, syphilis can look like a lot of different things, so it’s important to keep your differential broad.

Syphilis testing can be divided into two types, treponemal and non treponemal. You’ll want to start with a non treponemal test, such as an RPR or VDRL. The RPR or Rapid Plasma Reagent, which has now largely replaced the earlier VDRL or Venereal Disease Research. Laboratory Test is a non-specific serological test for syphilis that uses CARDIOLIPIN as antigen.

These are highly sensitive tests. But watch out for false positives. The RPR is also useful for post treatment monitoring. Trepanemal tests, such as the FTA ABS, are used as confirmation in the setting of a positive non trepanemal test. Patients with neurologic complaints should undergo CSF testing as well.

And, of course, where there’s one, there’s probably more. Use the information from your very thorough sexual history to test your patient for any other STIs they are at risk for. Patients with primary or secondary syphilis can be treated with a single dose of benzathine penicillin G or a 14 day course of doxycycline if your patient has a penicillin allergy.

For any patient with tertiary or neurosyphilis or a pregnant patient with any stage of infection, 10 to 14 days of penicillin G is the only option, even in penicillin allergic patients. So, if a patient has a severe penicillin allergy, have rescue medications available. Watch out for that Gerrish Herxheimer reaction, I know you haven’t heard those words since medical school, which can cause fever, headache, myalgias, or nausea and vomiting in the first 24 hours after treatment.

Last, but not least, remember that in some cases you’re telling your patient about their disease and possibly some dishonesty from their partner. Be sure to counsel them on sharing their results with all of their sexual partners, as well as your responsibility to inform the local health department for disease tracking purposes and the option for third party partner notification.

A few brief points on congenital syphilis, which is covered more in depth in the review article. We most often see this in infants born to mothers with poor prenatal care, as our OB colleagues do a great job screening for syphilis multiple times during pregnancy. Most infants with congenital syphilis are asymptomatic at birth, with appearance of hepatomegaly, jaundice, copious rhinorrhea, lymphadenopathy, and a similar maculopapular rash on their hands and feet that develop later in infancy.

Think about congenital syphilis in your little ones presenting like biliary atresia, who have a normal gallbladder treon ultrasound. Late congenital syphilis in children older than two can present with more severe features that are frequently tested on boards. Things like gummas, facial dysmorphias like saddle nose deformity and frontal bossing, sabershins, Hutchinson teeth, developmental delay, and hearing and vision concerns.

You’ll want to check a non trepanemal test in these kids, as maternal trepanemal antibodies can persist for over 15 months. Patients with congenital syphilis also receive treatment with penicillin G, 50, 000 units per kilo, frequency determined by their age. Thanks so much for listening, now get out there and practice your sexual histories.

Emily, thank you very much. Hopefully you all found this information helpful and we’ll be able to pick syphilis out of the lineup the next time you encounter it in the emergency department. If you want to learn how to produce a podcast episode, reach out to me, just like Emily did, and we will go through the entire process.

If you’ve got ideas for topics, send them my way. Any feedback that you have is greatly appreciated. Send me an email, leave a comment on the blog, a review on your favorite podcast site, or even a message through social media. And as my 12 year old would remind me to say, subscribe and share. For Pam Currens, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.