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.

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!

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 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.

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/

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.

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.

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.

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 this episode is all about eCPR, an emerging, resource intensive, but life saving technique that can be activated in situations  where there was a witnessed out of hospital cardiac arrest with continuous CPR in process or an in hospital cardiac arrest.

Now, I know that this isn’t readily available, but it is becoming more common in large children’s hospitals, and I thought that this would be a good time to share an overview.  So, eCPR, extracorporeal cardiopulmonary resuscitation, is an advanced medical procedure used in cases of cardiac arrest where traditional CPR has failed.

Refractory CPR is a situation where the team has not obtained return to spontaneous circulation in 30 minutes. Now, some centers are using 15 minutes in their guidelines, but 30 is what I’m familiar with. And here’s a basic overview of the eCPR process. So first, the patient has ongoing, high quality CPR.

Some sample objective markers of high quality CPR could include an end tidal CO2 greater than 10 millimeters of mercury, and or pH greater than 7, and or intermittent organized breathing. cardiac rhythms. If the patient meets criteria, then the multidisciplinary ECMO, extracorporeal membrane oxygenation team, is activated.

The patient will undergo cannulation, where large catheters are inserted into an artery and vein, like the femoral, to connect them to the heart lung machine.  ECMO will take over the function of the heart and lungs, circulating and oxygenating the blood externally.  The patient will remain on ECMO while the underlying causes of the cardiac arrest are addressed.

These could include severe sepsis. asthma, heart failure, and more.  If the patient’s heart function recovers, they’re gradually weaned off of ECMO. If not, further interventions, including potential transplantation, may be considered.  eCPR is typically performed in specialized centers with highly trained personnel in well coordinated teams.

It is a last resort for patients who would otherwise have a very low chance of survival. Now the evidence behind the benefits of eCPR are encouraging. There are some observational studies and meta analyses which generally support its use, showing increased survival rates in cases of refractory cardiac arrest.

One of the landmark studies, the ARREST trial, compared traditional CPR with early eCPR in adults and found significantly improved survival rates among those treated with eCPR.  Now, this study did take place in a single center with a mature eCPR system already in place. So eCPR itself is not a standalone intervention.

It’s part of a comprehensive system of care that requires robust infrastructure and and coordination.  When we turn the focus to pediatric patients, the data is unsurprisingly more limited, but compelling. For instance, eCPR is well established as a bridge therapy in pediatric patients with congenital heart disease and increasingly used in in hospital cardiac arrests. 

One review of pediatric eCPR cases demonstrated a 73 percent survival rate, and the majority of these survivors maintained their pre arrest neurological baseline.  And ultimately,  Most of the data thus far is in in hospital arrest. And that makes sense. It’s easier,  if easy is a relative term, to coordinate ECMO initiation when the patient is already in the hospital.

It’s much more logistically difficult when the patient arrests out of the hospital and then presents to the emergency department with CPR ongoing via EMS personnel and then to get transitioned to ECMO.  And because this process is so resource intensive,  It’s important to consider the risks, which are significant.

The process of cannulation itself, which again involves placing large bore catheters in arteries and veins to connect to the ECMO circuit, can lead to complications such as distal ischemia, thrombosis, and hemorrhage.  Maintaining the ECMO circuit requires continuous monitoring on anticoagulation, adding additional layers of complexity and the concern of intracranial hemorrhage. 

So again, that’s why eCPR is reserved for specific cases where the potential benefits clearly outweigh the risks and the patient meets the standardized criteria accepted by the facility in which it’s deployed. Now, where I work, we have eCPR available, but you may work at a place in which it’s not yet available or currently being developed.

The first and most obvious step is that the facility has to have an established ECMO center.  Then developing an eCPR program involves building a comprehensive system of care that extends out into the community as well. So we need to include pre hospital providers, the emergency medicine teams. ECMO proceduralists, the ECMO perfusionists, and intensive care unit clinicians.

One of the key lessons from existing eCPR programs is the importance of rigorous training and simulation. So for instance, large scale simulation programs have been shown to improve adherence to activation protocols and reduce activation times. Of course, both of those are critical to the success of eCPR. 

These simulations focus on the coordination of care across multiple divisions within the hospital, ensuring that everyone involved knows their role and can act swiftly when times of the essence.  Looking forward, the future of eCPR is bright, but it needs to be available in more centers. We need to refine our systems of care and develop more precise inclusion criteria.

And to spread what has already been learned, about the rigorous simulation and systems based training. And of course, there needs to be more data on outcomes in pediatrics.  Future prospective studies should focus on outcomes across a broad array of pediatric patients. This will provide the evidence needed for institutions to support the monumental financial and resource cost to set up eCPR programs in the first place. 

Well, that’s all for this episode on extracorporeal cardiopulmonary resuscitation, eCPR.  I hope that it provided a basic overview and some context. for this emerging therapy.  eCPR is becoming more readily available, and we should all have an understanding of why it is such a pivotal therapy for in and out of hospital cardiac arrest in children. 

If you have any feedback on this episode, or the show in general, send them my way. I’ll take an email, a direct message on X, or you can, as the kids say, send Like, rate, and leave a review,  or if you found the content helpful, just share it with a colleague.  And most of all, thank you for listening. I have been producing this podcast for a dozen years, and I continue to enjoy sharing new knowledge with all of you. 

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

Cervical Spine Injuries are fortunately rare in children. this episode is all about learning when to suspect them, how to immobilize the C-spine properly, and which imaging test to choose. It was inspired by a hot-off-the-presses publication from the Pediatric Emergency Care Applied Research Network (PECARN) focused on clinical decision rules for cervical spine imaging in children.

Here is the aforementioned PECARN paper:

Leonard, J. C., Harding, M., Cook, L. J., Leonard, J. R., Adelgais, K. M., Ahmad, F. A., Browne, L. R., Burger, R. K., Chaudhari, P., Corwin, D. J., Glomb, N. W., Lee, L. K., Owusu-Ansah, S., Riney, L. C., Rogers, A. J., Rubalcava, D. M., Sapien, R. E., Szadkowski, M. A., Tzimenatos, L., Ward, C. E., Yen, K., Kuppermann, N. (2024). PECARN prediction rule for cervical spine imaging of children presenting to the emergency department with blunt trauma: a multicentre prospective observational study. Lancet Child & Adolescent Health. https://doi.org/10.1016/S2352-4642(24)00104-4.

@PECARNTeam on X

Also maybe watch this music video that details how to clear the C-spine

…also maybe watch this music video that details how to clear the C-spine

Leonard, J. C., Harding, M., Cook, L. J., Leonard, J. R., Adelgais, K. M., Ahmad, F. A., Browne, L. R., Burger, R. K., Chaudhari, P., Corwin, D. J., Glomb, N. W., Lee, L. K., Owusu-Ansah, S., Riney, L. C., Rogers, A. J., Rubalcava, D. M., Sapien, R. E., Szadkowski, M. A., Tzimenatos, L., Ward, C. E., Yen, K., Kuppermann, N. (2024). PECARN prediction rule for cervical spine imaging of children presenting to the emergency department with blunt trauma: a multicentre prospective observational study. Lancet Child & Adolescent Health. https://doi.org/10.1016/S2352-4642(24)00104-4.

Sasser SM, Hunt RC, Faul M, Sugerman D, Pearson WS, Dulski T, Wald MM, Jurkovich GJ, Newgard CD, Lerner EB; Centers for Disease Control and Prevention (CDC). Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage, 2011. MMWR Recomm Rep. 2012 Jan 13;61(RR-1):1-20. PMID: 22237112.

Leonard JR, Jaffe DM, Kuppermann N, Olsen CS, Leonard JC; Pediatric Emergency Care Applied Research Network (PECARN) Cervical Spine Study Group. Cervical spine injury patterns in children. Pediatrics. 2014 May;133(5):e1179-88. doi: 10.1542/peds.2013-3505. PMID: 24777222; PMCID: PMC9923608.

Baker C, Kadish H, Schunk JE. Evaluation of pediatric cervical spine injuries. Am J Emerg Med. 1999 May;17(3):230-4. doi: 10.1016/s0735-6757(99)90111-0. PMID: 10337876.

Leonard JC, Browne LR, Ahmad FA, Schwartz H, Wallendorf M, Leonard JR, Lerner EB, Kuppermann N. Cervical Spine Injury Risk Factors in Children With Blunt Trauma. Pediatrics. 2019 Jul;144(1):e20183221. doi: 10.1542/peds.2018-3221. PMID: 31221898; PMCID: PMC6615532.

Leonard JC, Jaffe DM, Olsen CS, Kuppermann N. Age-related differences in factors associated with cervical spine injuries in children. Acad Emerg Med. 2015 Apr;22(4):441-6. doi: 10.1111/acem.12637. Epub 2015 Mar 16. PMID: 25779934.

Leonard JC, Kuppermann N, Olsen C, Babcock-Cimpello L, Brown K, Mahajan P, Adelgais KM, Anders J, Borgialli D, Donoghue A, Hoyle JD Jr, Kim E, Leonard JR, Lillis KA, Nigrovic LE, Powell EC, Rebella G, Reeves SD, Rogers AJ, Stankovic C, Teshome G, Jaffe DM; Pediatric Emergency Care Applied Research Network. Factors associated with cervical spine injury in children after blunt trauma. Ann Emerg Med. 2011 Aug;58(2):145-55. doi: 10.1016/j.annemergmed.2010.08.038. Epub 2010 Oct 29. PMID: 21035905.

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 this episode is all about cervical spine injuries in children. Now, fortunately, cervical spine injuries in kids are rare. They only happen in about 1- 2 percent of pediatric blunt trauma injuries.

But, In children with cervical spine injuries, at least one in five have permanent neurologic deficits, and serious cervical spine injuries, there’s a 7 percent mortality rate. So severe mechanisms are the scenarios where you are most likely to see a C spine injury in kids. So these are motor vehicle collisions with a patient ejected from the car, motor vehicle collision with death of another occupant, and Intrusion into the patient’s passenger compartment of greater than 12 inches at the roof and or greater than 18 inches at any site. So you got to ask the prehospital personnel about the injury and the crash scene fall of a distance greater than 10 feet or two to three times the child’s height diving into a body of water and an axial load. So force applied to the top of the head and acceleration deceleration Injury of the head.

So you hit your head on a dashboard during a head on collision. A clotheslining force. So that’s caused by a rope, a cable, or another object exerting traction on or striking the neck while the body is in forward motion. And certain sports do have a higher association with cervical spine injuries like football, hockey, wrestling, bicycling, trampoline use or riding ATVs. Infants can get a cervical spine injury during breech delivery or, unfortunately, during non accidental trauma as well. Axial injuries, occiput to C2, are much more commonly seen in children under the age of eight – it’s three quarters of all cervical spine injuries. These are most often due to motor vehicle collisions and falls.

Kids this age are more susceptible because of their big lollipop heads. You know, they have a giant head size related to their body size and they have loose joints and ligaments overall. Their C spine fulcrum is higher at birth, it’s at C2 to C3, as opposed to C5 to C6, which is the usual position in older children and adolescents just through the process of normal growth.

The most common injuries seen in these younger patients are growth plate fractures and ligamentous injuries. It’s particularly difficult to diagnose cervical spine injuries in kids under three because they can’t give you an accurate history and cooperate with the exam. Older children, so older than eight, so middle schoolers and up, have a higher likelihood of injuries in the C3 to C7 range.

This makes up about half of the injuries. And these happen during motor vehicle collisions and sports. You more often will see vertebral body and arch fractures as opposed to the growth plate fractures and ligamentous injuries in the younger children. And overall, C spine injury can occur through a lot of different mechanisms including flexion, extension, vertical compression, rotation, or combination of all of the above.

And though we’re talking about injuries to the vertebra, the cervical spine, spinal cord injuries themselves happen either due to direct compression, or disruption of the cord itself by a fracture, fragment, or a sublux vertebra. Let’s go ahead and pivot to initial management. And we need to suspect cervical spine injuries in any patient with multisystem blunt force trauma.

You want to limit spine motion during your primary survey, the ABCs, or the rapid cardiopulmonary assessment. Someone can hold c spine, and we’ll talk about more about maintaining and clearing the c spine in a little bit. You’ll do jaw thrust alone as an airway maneuver. No head tilt. Orotracheal intubation with video laryngoscopy is ideal.

C spine injuries themselves can impact airway maintenance and or patency. So if you have an unstable injury above C3, you can actually have respiratory paralysis. A lower cervical injury could impact the phrenic nerve. The cervical spinal column injury itself may be associated with airway obstruction from retropharyngeal hemorrhage, edema, or maxillofacial trauma.

You should also consider the possibility of quote unquote spinal shock. This is due to the loss of sympathetic output and vasodilatation. So you could worry about this in a bradycardic and hypotensive patient, but in multisystem trauma hypotension is more likely hemorrhage. than it is spinal shock.

Resuscitate with volume and blood. When evaluating the cervical spine in particular, if you can get details on the mechanism, that’s fantastic. You’ve got some specific injury patterns that you should be on the lookout for. So a patient that has hyperflexion can have a vertebral body wedge fracture and disruption of the posterior elements.

A hyperextension Extension injury will compress the posterior elements and disrupt the anterior longitudinal ligament. This is the hangman’s fracture, the posterior neural arch of C1 or the pedicles of C2. Axial load can cause burst fracture, so someone that dives into a pool. A rotational injury will disrupt the facets.

This is more common in combination with an extension or flexion injury, not just rotation alone. And then there’s the specific Atlanto Axial Rotary Subluxation Pattern. It’s often minor trauma in younger children, where C1 and C2 essentially get stuck on each other in a rotary position, and the kid can’t turn their neck.

Children will have some localized cervical pain, muscle spasm, decreased neck range of motion. They may or may not have neurological symptoms, even if they’ve resolved. These can include paresthesias, numbness, or weakness. The distribution of these neurologic symptoms is really variable, and it can range from involvement of single dermatomes to dramatic neurologic deficits including quadriplegia.

The ability to walk does not completely exclude a C spine injury. And interestingly, even children with no symptoms can have a cervical spine injury. There is a retrospective review of children just before the turn of the millennium that found that even 10 percent of that population with cervical spine injury were initially asymptomatic.

Finally, there are some children that you need to be aware are more predisposed to cervical spine injury than others. And this includes children with Down syndrome, clipple feel, osteogenesis imperfecta, marfans, Ehlers Danlos, chronic steroid use, rickets, and more. When it comes to physical examination of a child with a suspected cervical spine injury, remember, immobilize the c spine, either by hand, so another team member holding inline c spine, or by placing a collar, like an Aspen or Miami.

The ABCs are, as always, incredibly important. An axial injury, occiput to C2, causes abrupt cessation of respiration, so that patient will be apneic. A patient who is hypoventilating may have injuries of the spinal cord at the level of diaphragmatic control, so C3, C4, C5. And hypotension, bradycardia, or temperature instability can result from hemorrhagic and or spinal shock.

When examining the neck, you want to maintain in line stabilization. You have to palpate, but don’t press too hard on the spinous processes for local tenderness, muscle spasm, or obvious deformity. Either start at C7 and work your way up, or find C1 and work your way down. Be deliberate about touching each cervical vertebrae.

Tell younger children to use their words. Yes if it hurts, no if it doesn’t. Don’t shake their head. They always do this. A child with midline cervical tenderness. is more likely to have a cervical spine injury than a child with paraspinous muscular tenderness or spasm. Infants and toddlers who can’t cooperate can actually be cleared without imaging after minor trauma if they have a normal neurologic examination that includes mental status and GCS 15 and no other life threatening injuries.

It’s really hard to know if an 18 month old has C spine pain or not. In my experience, doing a neurologic exam is really difficult in the resuscitation area, especially when a patient is supine and has an immobilized c spine. The overall Glasgow Coma Scale and evaluation of tone, strength, sensation, and reflexes constitutes a complete neurologic exam.

50 percent of all children with cervical spine injuries will have some sort of neurological deficit. And yes, doing a neuro exam is hard, and it takes practice. Part of that is learning ways to get patients to participate when they are uncomfortable or scared. And subtle findings are fortunately most common, but harder to elicit.

An isolated sensory deficit is the most common neurological finding in cervical spine injury. Ipsilateral posterior spinal column and contralateral anterior column are tested via light touch. The anterolateral spinal column is tested with pinprick or pain. The ipsilateral posterior spinal column is tested with position sense, so moving that toe, and dysesthesia will localize to the central cord.

And this is a podcast, so I can’t make you conjure up a table in your head, but I think it is important to remember where some deficits will come from if you have injuries at particular levels. And so if you have an injury at C2 to C3, you may just see apnea. C3 and C4 control the diaphragm, so you want to make sure the patient is spontaneously breathing.

C5 is flexion of the biceps. with the palm up, or supinated. C6 is extension of the wrist. C7 is extension of the elbow. L2 through L4 are extension of the knee. L5 is dorsiflexion of the great toe. And S3 and 4 is rectal tone. So absence of rectal tone is a poor prognostic sign, but it’s also not sensitive for cervical spine injury.

In a child with a GCS of 15 with no active neurological complaints, I would argue that a digital rectal exam is pretty invasive, and just squeezing the buttocks together is probably a good proxy. A child with altered mental status, or decreased responsiveness, or high index of suspicion for cervical spine injury should get a digital rectal examination.

And yes, on board exams! You have these spinal cord injury syndromes. They show up again and again and again. I’ve actually rarely seen them in pediatric practice, fortunately. But for completeness, here they are. Anterior cord syndromes are from hyperflexion, and you’ll see paralysis and loss of pain sensation without loss of light touch or proprioception.

Central cord syndromes are from hyperextension, and you’ll see weakness that is greater in the upper as opposed to the lower extremities, and transient burning sensation of the hands and fingers. Brown Sequard syndrome, which is cord hemisection, will lead to ipsilateral paralysis, loss of proprioception, and loss of light touch, and a contralateral loss of pain and temperature sensation.

And then Horner syndrome is disruption of the sympathetic chain. So you’ll see ipsilateral ptosis, meiosis, and anhydrosis. Okay, so let’s say the ABCs are normal, GCS is 15, and there are no focal neurologic findings. How do we attempt to clear the C spine? So for this, you’re gonna need another team member.

So have the patient lie supine. Have your assistant hold inline C-spine mobilization. They’re gonna be standing above the patient’s head, and then you’ll remove the anterior front portion of the collar. Reach behind their neck, inside the back portion of the collar, and feel very intentionally. See one all the way down to C seven.

Or the reverse, C7 all the way up to C1, asking the patient at each one if there is pain. And again, tell them to use their words, yes or no, and not nod or shake their head. And they’ll still mess this up. At each cervical vertebrae, feel for any swelling or step off. So one that feels kind of more in than the rest.

If there is pain at any cervical vertebrae, replace the collar. And then you’ll move on to imaging, which we’re going to talk about in just a moment. If there is absolutely no pain in C1 through C7, You can have your teammate release inline c spinal mobilization and then ask the patient to actively flex, extend, and rotate to the left and right, all at 45 degrees.

If they have no pain in the midline with any of these movements, then the cervical spine is clinically cleared. But if they have pain or decreased range of motion in any direction, replace the collar and move on to imaging. No matter where you work, you should apply clinical decision rules with an imaging algorithm for anybody with suspected cervical spine injuries.

Now in grown ups, you’re probably familiar with the Canadian C spine rule. It’s a highly sensitive rule that is designed to prevent missing cervical spine injuries while limiting the amount of unnecessary radiologic examinations. This Canadian C spine rule does not apply to children under 16 years of age.

In many settings in adults, plain radiographs have actually been abandoned in favor of CT scans. And a negative CT scan, if you rule in via the Canadian C spine rule, is generally sufficient to clear the majority of C spine injuries and allows for collar removal. In children, though, we prioritize limiting radiation risk.

And so it’s recommended, based on recent evidence from the Pediatric Emergency Care Applied Research Network, PCARD, that we have a three tiered decision rule. So the highest risk patients, these patients have a risk of cervical spine injury of about 12%, are going to recommend immediate medical attention.

CAT scan. These patients will have altered mental status, A GCS of three to eight or unresponsive on the AVPU alert, voice pain, unresponsive, mnemonic. Highest risk patients also include those with any abnormality of the airway, breathing, or circulation. and somebody with a focal neurological deficit. And then there’s an intermediate risk group that has a just under 4%, specifically a 3.

6 percent chance of a cervical spine injury. And these are patients that it is recommended to get a plain x ray. These are patients with posterior neck pain, altered mental status, but a GCS of greater than eight. Or patients with a substantial head or torso injury and substantial means that they’re going to require an intervention or observation in the hospital.

And then there’s a low risk group with a risk of cervical spine injuries of 0. 2 percent or less. And these patients generally don’t need any imaging. And so this is, uh, Assuring through meticulous investigation that none of the following risk factors are present. So neck pain or midline posterior neck tenderness, decreased range of motion or pain with range of motion on flexion, extension, or rotation to the left and right, torticollis, altered mental status so a GCS of 14 or less, any focal neurologic finding and remember sensory deficits are the most common in cervical spine injuries, Any substantial coexisting injuries, so especially torso injuries or child abuse injuries.

Any relevant predisposing condition like Down syndrome. And high risk mechanisms. Diving, hanging, an axial load force, a clothes lining force, or a motor vehicle collision with significant intrusion, ejection from the vehicle, or a death in the vehicle. So again, if the child is negative for all of those, you don’t have to place a collar.

And you don’t need any imaging, and that includes an x ray or a CT scan. The goal of using this high intermediate, low tiered approach is to cut the rate of CAT scans in children by greater than 50%. And so the Pediatric Emergency Care Applied Research Network is actively working on that, initially in an ED setting, with future work in the pre hospital setting.

And so hopefully that helps you understand when to get imaging. But what about the actual imaging choices themselves? Plain x rays are the initial choice in children with normal mental status, but cervical spine tenderness. They’ve got adequate sensitivity to exclude unstable c spine injuries. There are two view x ray series of the neck, that’s an AP and a lateral, or a three view series, cross table lateral, AP, and when obtainable, then open mouthed odontoid.

Multiple views, as you’d expect, are more sensitive, like 90%, as opposed to a single view, which is only 79%. Some children are chunky, and it’s hard to see all seven cervical vertebrae, but you do need to see that for a complete set of film. Some of you might work at a place where they get the swimmer’s view, where they grab both patients hands or wrists, and then pull down to try to get the shoulders out of the way to show C7.

If you have a high suspicion for cervical spine injury, don’t do this. Flexion extension views have fallen out of favor in my practice environment because CT is readily available. The FlexX views are still used in some situations, and they could show some ligamentous disruption. This is where the patient actively flexes and extends with X rays taken.

Never do passive flexion of a suspected C spine injury. CT or CAT scans, by default, get axial images. computed axial tomography. Then the computer is going to do fancy sagittal, coronal, and 3D reconstruction, which is totally cool. CT scans are indicated in any child with altered mental status, a GCS of 3 to 8, or unresponsive on the AFPU.

Also, in children with an abnormal airway breathing and or circulation. and orifocal neurologic deficit. The risk of radiation is the primary concern here, and radiology departments should follow the ALERA, or as low as reasonably acceptable, principle. A C spine CT delivers substantially more radiation to the skin, thyroid, and spinal cord, up to 10 50 percent more.

Children younger than 5 years of age are more prone to radiation induced malignancies due to the increased radio sensitivity of certain organs and a longer latency or life period to develop a cancer. Calculating the lifetime risk of getting cancer from CT scans is hard to do, which is great because we’re not just like scanning people for no reason and seeing if they get cancer later.

The best current estimate is that the estimated lifetime cancer mortality risk attributable to the radiation exposure from a CT for a one year old is approximately 0. 07 to 0. 18%. So not zero, but pretty low. The risk of radiation exposure exceeds the benefit of CT imaging in the majority of children evaluated for C spine injury.

So most of them don’t have a very low GCS, or abnormal ABCs, or focal neurologic deficits. That’s why PCARN is doing this work. Many adult centers will readily get CT scans in adults with suspected c spine injuries. These are just not necessary in the majority of children. Either nothing or plain x rays are sufficient.

And what about MRI? It’s becoming increasingly available. In anybody with an abnormal neurologic examination, or when imaging of the spinal cord or other soft tissues is paramount, MRI can be very helpful. For It is superior to CT for visualizing soft tissues and identifying intervertebral disc herniation, ligamentous injuries, and spinal cord edema, as well as hemorrhage, compression, and transection type injuries.

MRI is actually less sensitive than CT for detection of fractures of the posterior elements of the c spine and injuries to the cranial cervical junction. So it’s not perfect. Even fast protocols for MRIs are tough to get in children under the age of 6 years, they require sedation. And spinal cord injury without radiographic abnormality, C.

Wura, was defined way back in 1982, and I was 4 or 5 years old when this happened. And this was objective signs of myelopathy as a result of trauma in the absence of findings on plane radiographs, flexion extension radiographs, and cervical CT. CWRA is kind of a moot point when you have an imaging modality that uses fancy magnets to jiggle water molecules and take a cool picture.

You can demonstrate injury to the spinal cord and spinal ligaments. And so in anybody with a localizable neurologic sign or symptom, I’m not saying you have to get it in the ED because that’s just not practical, but these patients will, upon admission or shortly after their initial assessment, need an MRI at some point.

And though this episode is focused on cervical spine injuries, it goes without saying that if somebody has thoracic or lumbar spine pain, they should get plain imaging of that, or if they have substantial multisystem trauma and you’re getting a CT scan of the chest or abdomen, that is obviously going to include those bones as well.

Now moving on to disposition. Any patient with a cervical spine injury or a neurologic deficit They’re getting admitted to the hospital. And this obviously includes patients who need surgery, like unstable fractures and those sort of things. That’s a spine or neurosurgery operation. Patients with stable fractures, so an isolated spinous process, or transverse process fractured, identified by CT, will have a rigid cervical collar applied, so an aspen or vista, With trauma and spine follow up within a week.

Kids wear this collar 24 7. So again, you’ve got an isolated, stable fracture, no displacement, no neurologic symptoms, no other injuries, that kid could go home and they’re going to wear that collar 24 7. You have to teach them how to take care of it. If you have a negative x ray, but persistent midline c spine pain, we also recommend keeping the kid in the cervical collar and follow up at a trauma or spine center within a week.

Could you get a CT scan in those situations? Yes, but still most pediatric trauma centers will void the ionizing radiation of the CT scan and keep the patient in the collar until trauma follow up. Okay, so let’s wrap up this episode. Fortunately, cervical spine injuries in children are rare. You should learn how to clinically clear a C spine and know that it takes two people to do it correctly.

Practice your neurologic examination in children who are being evaluated for traumatic injuries. Know which mechanisms are more likely to cause C spine injuries. And make sure that you’re using a clinical decision rule with an imaging algorithm for kids with suspected C spine injuries. Highest risk patients should get CT scans.

They have a 1 in 8 chance of a c spine injury, altered mental status, GCS 3 to 8, unresponsive, abnormal ABCs or focal neurologic deficit. Patients that are intermediate risk have a less than 1 in 25 chance of a c spine injury and that’s when we would get a plain x ray. So they have Posterior midline neck pain, altered mental status, but a GCS of greater than 8, or some substantial comorbid head or thoracic injury that requires management or admission to the hospital.

Patients with no findings will have a less than 0. 2 to 0. 3 percent chance of a cervical spine injury and don’t need any imaging at all. So this is a patient with no midline neck pain, no pain on neck range of motion, Normal mental status, normal neurologic exam, no comorbidities, and no high risk mechanisms.

I encourage you all to take a look at the new publication from the PCAR Network in Lancet Child and Adolescent Health. I’ve provided a link in the show notes. This is the state of the art paper on the use of decision rules for cervical spine imaging in children. To learn more about the Pediatric Emergency Care Applied Research Network, or PCARN, check out PCARN.

org. You can also follow them on x at pkarn team. If you’ve got feedback on this episode, send it my way. Email, direct message on x, a comment on the blog, I’d love to hear it. Hopefully you found this information useful and you can take it back to your next shift. Overall, that’s the goal of this podcast.

Encourage your colleagues to listen and subscribe. Hopefully they will find it helpful as well. And please let me know if there are any topics specifically related to trauma and injuries in children that you think that I should cover. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski.

See you next time.

Febrile Seizures are among the most common neurological problema in young children, occurring in 1 out of 50 children between the ages of 6 months and 5 years of age. This episode of PEM Currents: The Pediatric Emergency Medicine Podcast is a Question and Answer style exploration of some of the most common learning points in this incredibly important topic.

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Xixis KL, Samanta D, Smith T, et al. Febrile Seizure. [Updated 2024 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448123/

Feenstra B, Pasternak B, Geller F, et al. Common variants associated with general and MMR vaccine-related febrile seizures. Nat Genet 2014; 46:1274.

Mullan PC, Levasseur KA, Bajaj L, Nypaver M, Chamberlain JM, Thull-Freedman J, Ostrow O, Jain S. Recommendations for Choosing Wisely in Pediatric Emergency Medicine: Five Opportunities to Improve Value. Ann Emerg Med. 2024 Feb 11:S0196-0644(24)00017-9. doi: 10.1016/j.annemergmed.2024.01.007. Epub ahead of print. PMID: 38349290.

Guedj R, Chappuy H, Titomanlio L, De Pontual L, Biscardi S, Nissack-Obiketeki G, Pellegrino B, Charara O, Angoulvant F, Denis J, Levy C, Cohen R, Loschi S, Leger PL, Carbajal R. Do All Children Who Present With a Complex Febrile Seizure Need a Lumbar Puncture? Ann Emerg Med. 2017 Jul;70(1):52-62.e6. doi: 10.1016/j.annemergmed.2016.11.024. Epub 2017 Mar 2. PMID: 28259480.

Shinnar S, Hesdorffer DC, Nordli DR Jr, Pellock JM, O’Dell C, Lewis DV, Frank LM, Moshé SL, Epstein LG, Marmarou A, Bagiella E; FEBSTAT Study Team. Phenomenology of prolonged febrile seizures: results of the FEBSTAT study. Neurology. 2008 Jul 15;71(3):170-6. doi: 10.1212/01.wnl.0000310774.01185.97. Epub 2008 Jun 4. PMID: 18525033.

Murata S, Okasora K, Tanabe T, Ogino M, Yamazaki S, Oba C, Syabana K, Nomura S, Shirasu A, Inoue K, Kashiwagi M, Tamai H. Acetaminophen and Febrile Seizure Recurrences During the Same Fever Episode. Pediatrics. 2018 Nov;142(5):e20181009. doi: 10.1542/peds.2018-1009. Epub 2018 Oct 8. PMID: 30297499.

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. This episode is all about febrile seizures, one of the most common neurological problems that you will see in the emergency department in children. And you know what? I’m going to structure this episode like a bit of a question and answer session.

I’ll ask a question, and then I’ll answer it. So the first and perhaps most important question is, What are febrile seizures and how common are they? Well, they are the most common neurologic disorder of infants and young children, and they happen in about 2 to 4 percent of children between the ages of 6 months and 5 years of age.

I’ll tell parents that they happen in about 1 out of 50 kids. It’s associated with fever, but in a child without evidence of intracranial infection. They are not considered a form of epilepsy. They peak between 12 and 18 months of age, the male to female ratio is 1. 6 to 1, and there is a higher prevalence reported in certain regions like Japan’s Mariana Islands.

A febrile seizure, very simply, is a convulsion associated with a temperature greater than 38 degrees Celsius. The child does not have any acute systemic metabolic problems like hypoglycemia or hyponatremia, and you don’t have to test for those. We’ll talk about that later. And they have no history of previous afebrile seizures.

So why do they happen? Well, they’re likely related to a vulnerability of the developing nervous system to the effects of fever. The neurons that generate these seizures aren’t completely myelinated until age 6. And these neurons that are undermyelinated are more hyper excitable by cytokines during fever in these younger children who get sick more often.

And of course, underlying genetic susceptibility plays a role. And so other risk factors include a high fever, A viral infection, certainly particular viruses. A recent immunization. Hmm. Family history of febrile seizures. Prenatal exposure to nicotine. Atopic diseases. And maybe iron deficiency anemia. And so check this out.

Febrile seizures are due to the degree of fever, not the rate of temperature rise, even though we see them as the temperature is increasing rapidly in the early parts of the illness. And this has been known since the 1950s. The majority of children have febrile seizures on the first day of illness. In some cases, it’s actually their first manifestation of illness.

Like, they’re just a little bit congested, and then they’re convulsing. And then they find out that they’re febrile. The degree of fever associated with febrile seizures is variable, and it depends on the kid’s threshold convulsive temperature. So everybody has a little bit of a different set point. But most often, the fever is greater than 39 degrees Celsius, but 25 percent of febrile seizures do occur between the temperatures of 38 and 39.

In a study of just over 100 children, the temperature of febrile seizures was significantly higher than the mean temperature of fevers in children that did not have seizures, so 104 versus 103. 3. The seizure threshold is lower in infants. who have more febrile illnesses. So viral infections are often associated with high fever in kids, you know that.

One of the most classic viruses associated with febrile seizures is HHV 6. So human herpes virus 6. Another common one is influenza, specifically influenza A. So HHV 6 is the cause in one third of all first time febrile seizures in U. S. children under 2 years of age. The mean maximum fever in infants with a primary HHV 6 infection is generally 39. 5 Celsius, so 103 Fahrenheit or higher. So the incidence of febrile seizures associated with primary HHV 6 infection is estimated as high as 36 percent in 12 to 15 month olds. Other common causes include adenovirus RSV, HSV, CMV, HHV 7, and in Asia, influenza A is number one. The type of viral infection is not important in predicting the future recurrence of febrile seizures or whether or not the child will have a complex febrile seizure.

In kids up to two and a half years of age, breastfeeding may be a preventative factor for febrile seizures. Vaccines don’t cause autism, but they might cause febrile seizures. So the risk of febrile seizures is increased after administration of diphtheria, tetanus, toxoid, and whole cell pertussis, along with measles, mumps, rubella, and MMR with varicella vaccines.

The absolute risk is small, and genetic susceptibility likely plays a role in seizures after vaccines. The risk of a future febrile seizure with a subsequent vaccine is generally lower than the risk of the disease that you are vaccinating against. In drug company sponsored studies, the absolute risk of a febrile seizure after an MMRV vaccine is about 3 to 4 febrile seizures for every 100, 000 children receiving the vaccine.

So again, pretty darn low. So how do we categorize febrile seizures? We all know that there’s simple, That may not be the best terms, but that’s what we’ve got. So the focality, in a simple febrile seizure, they are generalized. A complex febrile seizure is focal, so the shaking is limited to one limb or one side of the body.

The duration, the duration for simple febrile seizures is less than 15 minutes, though 10 minutes has been proposed. Complex febrile seizures, on the other hand, are longer than 15 minutes. A simple febrile seizure is limited to a single episode in a 24 hour period, whereas complex febrile seizures, there is a recurrence of more than once in that 24 hour period.

Overall, 80 percent or more febrile seizures are simple, and 20 percent are complex. Ultimately, though, the history that you get may not be reliable. Both the motor movements and characteristics of the seizure, as well as the duration, are really hard to assess in a patient’s home. Obviously, you should ask about immunization status and whether or not the child has any underlying medical or neurologic problems or developmental delay.

And let’s be honest, the term simple sort of undersells how scary this is for families. There’s nothing simple about watching their child have convulsions and looking like they were gonna die. And why does the complex heterogeneity? Think about it this way. Two one minute seizures occurring an hour apart in a well appearing febrile child seem different than focal one sided convulsions or febrile status epilepticus.

More research is needed. So what’s the recurrence risk after febrile seizures? This is an important thing that we talk to families about. So the overall recurrence rate is approximately 30 to 35%. I will tell parents it’s a one in three chance. If you have two or more febrile seizures, you have a 50% chance of subsequent events.

The subsequent seizure is almost always similar to the first. So 95% of initial simple febrile seizures have recurrent, simple febrile seizures. And interestingly, they’re usually about the same length as well. The risk of recurrence is much higher in children under 12 months of age. So, though it’s one third overall, it’s about 50- 65 percent in children under 12 months of age when they have their first febrile suture.

In older children, like preschool and above, the risk is less than 20 percent. In a study published by Berg in Archives of Pediatrics and Adolescent Medicine in 1997, when I was a freshman in college, they looked prospectively at 428 children with a first febrile seizure. They noted that 17 percent had one recurrence, 9 percent had two recurrences, and 6 percent had three or more.

Three quarters of these recurrences were within one year of the initial seizure, and almost all were within two years. They found four factors for increased recurrence risk. Young age, history of febrile seizures in a first degree relative, lower degree of fever while in the emergency department, and brief duration between the onset of fever and the initial seizure.

Kids with all four of those had a 70 percent risk of recurrence, none of them only 20%. Complex features on the initial seizure were not associated with the risk of recurrence. Other factors that have been reported regarding recurrence in the literature include abnormal development before the first febrile seizure, recurrence of seizures within the same illness, children with one recurrence, and of course children who have had an unprovoked seizure after a febrile seizure are more likely to have future febrile seizures.

So what’s the risk of epilepsy following a febrile seizure? Well, 1% One out of a hundred human beings have epilepsy. If you have one simple febrile seizure, your risk of epilepsy is somewhere between 1 and 1. 5 percent. So it really doesn’t go up significantly. In a normal child with a simple febrile seizure, that risk is only slightly above that of the general population.

So they don’t really need a neurologic workup. Complex febrile seizures or a child with abnormal developmental history, or a child with a family history of epilepsy, have a risk of epilepsy development of about 5 to 10 percent after a febrile seizure. Some other factors related to the risk of epilepsy, if that first seizure is complex, the risk of epilepsy is about 18 times that of simple febrile seizures.

If the child has focal seizures, prolonged seizures, and repeated episodes within 24 hours during the same illness, the risk of epilepsy is 2%, 7%, 20 percent and 50 percent was 3, or all of those risk factors. One cohort study of almost 200 children with febrile seizures found the risk of epilepsy was highest in the first five years and appeared to decrease over time.

And other risk factors for epilepsy that have been identified in independent studies include Todd’s paralysis, short fever duration before the seizure, late onset of febrile seizures over three years of age, and multiple febrile seizure recurrences. There’s a tenfold increase. So what’s the evaluation and management for simple febrile seizures?

I joke that it’s discharge home, but really, Choosing Wisely recommends that we do not order laboratory studies or CT scans for a patient with a simple febrile seizure who has returned to baseline mental status. Labs just aren’t necessary. This postictal period is usually brief, so 20 to 30 minutes or up to 2 hours.

I think 2 hours is too long. And if the kid returns to a neurologic baseline, they’re unlikely to have a metabolic or structural abnormality that you’re going to need to identify. So in that child who has recovered with a normal neurological examination, You don’t need labs. They’re painful, they can give you erroneous or unexpected or irrelevant results, and they’re expensive.

So really focus on targeted testing. If you think they’re at risk for a UTI, well, yeah, get a urine. Go after COVID and flu if you think the swabs are beneficial or strep, but otherwise, you can avoid labs. In general, I think parents are most worried that their child’s gonna have a brain tumor or something wrong inside their head, and naturally, their minds will gravitate towards getting a CT scan.

These are expensive studies with a large amount of radiation, and in the absence of concerning signs on history in the exam, the rate of scarring abnormalities, mass, stroke, or other problems is really, really low, so like less than 1%. So in general, you don’t need a CT scan to show that the brain looks normal.

Children with recurrent febrile seizures or epilepsy following febrile seizures benefit more from MRI and EEG. What about complex febrile seizures? How do we evaluate and manage them? So again, focal onset greater than 15 minutes and or recurrent within 24 hours. The majority of children who develop complex febrile seizures will do so with their first seizure.

Todd’s paresis, so transient hemiparesis following a febrile seizure, usually of a complex or focal type, is rare and happens in about 1. 5 to 2 percent of cases. Prolonged or focal febrile seizures have a higher likelihood of meningitis or structural abnormalities, but still that risk is low. And so even in complex febrile seizures, if the child recovers, EEG or MRI may be the only test, if any, that they need.

You should develop a specific plan for each patient with each patient. A pediatric neurologist. So in terms of lumbar puncture, yes, you can get an LP and CSF studies to exclude meningitis or encephalitis in a child with a complex febrile seizure. The literature has long told us that in children older than 6 months of age who are completely vaccinated, you do not need to get an LP and CSF.

to rule out meningitis in a child with a simple febrile seizure. Admittedly, 25 percent of children with meningitis will have seizures at or before the initial presentation, but almost all of these kids will also have other signs and symptoms of meningitis, like altered consciousness, nuclear rigidity, a petechial rash.

So if you have a child with a complex febrile seizure, but they don’t have any other signs of meningitis, you don’t necessarily need to tap them. If febrile seizures occur after the second day of illness, if you have febrile status epilepticus, these should be other considerations as to whether or not an LP is needed.

But overall, the yield of LP is very low. Now note that pleocytosis can be seen in epileptic seizures, but it’s actually rare in febrile seizures without meningitis. So what does the AAP say? Well, they say that LP should be performed when there are meningeal signs or symptoms or other clinical features that suggest possible meningitis or intracranial infection.

Yeah, you should consider it in infants between 6 and 12 months of age if the immunization status for Hib or strep pneumonia is deficient or undetermined. So, 3, Strep pneumos, and two or three HIBs. And you should also consider an LP when the patient is on antibiotics, because antibiotic treatment could mask the signs and symptoms of meningitis.

This is perhaps the most nuanced scenario. If a child has a complex febrile seizure, and fortunately it’s a rare one that you’ll see, but you should consider, maybe they’re on otitis media, and then they have a febrile seizure, and it’s complex, probably tap that kid. In a study from Kim published in Pediatrics in 2010, they looked at 526 children with complex febrile seizures.

Almost two thirds of this population got lumbar punctures and only three had meningitis, all with a reason to suspect it. So one was clinically non responsive, one had a bulging fontanel and apnea, that’s a bad combo, and one was well appearing but had a positive blood culture for strep pneumonia and they didn’t do an LP, so they just presumed that they have meningitis?

I’m squinting. You can’t see that on the podcast, but that kid probably didn’t have meningitis. Another relatively large cohort of children with complex febrile seizures, published in 2017, showed that the incidence of bacterial meningitis in 839 patients with complex febrile seizures was 0. 7%, and none of them had HSV.

All five of those patients with meningitis had a concerning exam, and four out of five were less than 12 months of age. So, if somebody with a complex febrile seizure is going to have meningitis, there’s going to be other stuff going on. Simple febrile seizures do not require neurology consults or admissions.

They can be discharged home. Previously healthy and developmentally and neurologically normal children with two brief self resolved seizures within a 24 hour period, so technically a complex febrile seizure, can be discharged home with as needed neurology referral if the family and you are comfortable with that plan.

For Febrile status epilepticus, you should stop the seizure with medicines and admit to neurology in the PICU. And complex febrile seizures with focal features, strongly consider admission and always discuss with child neurology. And so briefly, let’s talk about that neurology referral and follow up.

Neurology will often see children in the near term with complex febrile seizures who you felt are safe for discharge but need evaluation. EEG itself is not useful in determining the risk of recurrent febrile seizures. If you’re looking for epilepsy, abnormalities are more likely to be seen on EEG when it’s performed shortly after the seizure, so less than 10 days, and when convulsions are of a longer duration and have focal features.

In children with focal complex febrile seizures, neurology is almost always going to get an MRI as well, and in children under 6, they’re probably going to need general anesthesia to do that. Alright, so what about the management of febrile status epilepticus? So originally this was defined as greater than 30 minutes.

It’s back down to 15 minutes, but there’s a current movement to define status epilepticus as greater than 5 minutes. And 5 minutes is a really long time to watch a kid seize, so I get it. In 1 third of febrile status epilepticus, the actual seizure duration is underestimated in the emergency department.

And the clinical clues that a seizure has ended are often subtle. So a child that is no longer seizing will have closed eyes and deep breathing. If the eyes are persistently open and deviated, even if there’s no limb convulsions or stiffening, they may have ongoing focal seizures. It’s really hard to figure this out.

I’ve also seen kids that are febrile having rigers, or just from a sympathetic surge after a seizure. So, response to painful stimuli, closed eyes, regular breathing. These are all subtle findings along with your vitals like capnography that can help you figure out if that kid is still seizing. In a wonderfully named study called Febstat, which was initially published back in 2008 as a multi center perspective cohort of 119 children one month of five years with febrile status, they noted that the median duration of seizures was 68 minutes.

They were convulsive in all but one child. They were continuous in half and intermittent in the other half. Two thirds of these status. Patients were partial. It was the first febrile seizure for 3 out of 4 children in the study. And HHV 6 was the most common identified infectious etiology. There was also a higher than expected family history of epilepsy in this population.

So if the seizure is going on longer than 5 minutes, start with an IV benzodiazepine if you can. So diazepam or lorazepam. Buckle midazolam or rectal formulations like diastat are alternatives if you don’t have an IV. If that first benzodiazepine doesn’t work, give it again at five minutes. If that doesn’t work five minutes later, give a second line drug.

Generally, levotiracetam or Keppra is the first choice for second line, but you could use fosfenitoin or valproate if you’ve got them. So are febrile seizures associated with an increased risk of mortality? This is very pertinent to familial concerns. Early reports actually suggest that febrile seizures were associated with an increased risk of sudden death later on.

We found that that’s probably not true and that small excess in mortality is really restricted to complex febrile seizures. These patients have pre existing neurologic abnormalities. Those are the ones that are really most at risk. Alright, well what about prescribing preventative medicines or rescue drugs?

I don’t think that children that have a single simple febrile seizure need to be prescribed rectal diastats. But if they’ve had a prolonged febrile seizure, including febrile status epilepticus, or have had multiple febrile seizures, prescribing diazepam rectal gel or midazolam nasal spray in an older child who is an appropriate size could be a good idea.

One dose administered rectally or nasally will not lead to respiratory depression. And so in general, if you’ve got a child that’s at risk for a prolonged future febrile seizure, are good candidates for rescue meds. through a process of shared decision making. Now, you could prevent the risk of subsequent febrile seizures by putting a kid on prophylactic anti epileptic medications.

Most febrile seizures are benign and the side effects of the AEDs generally outweigh the benefits. So you don’t need to put somebody on phenobarbital to stop them from having another febrile seizure. So the use of antipyretics, so acetaminophen, ibuprofen, at the first sign of fever does not prevent a recurrence of febrile seizures in a child that’s had one before.

Morata and colleagues did a single center perspective randomized control trial back in 2018 that noted that regular antipyretics may reduce the recurrence of febrile seizures during the same fever episode, so during that illness. But other studies, including one from Rosenblum back in 2013, which was a meta analysis of three RCTs of acetaminophen, ibuprofen, and diclofenac, starting antipyretics, at the onset of illness could not reduce the rate of recurrent febrile seizures compared with placebo.

Why don’t antipyretics work? Well, they facilitate heat loss, but they don’t inhibit heat production, or lower the threshold convulsive temperature during the initial stage of fever that triggers a seizure. Now, interestingly, phenobarbital can actually treat fever and seizures, but, you know, there’s side effects, so it’s not recommended.

Okay. So is there anything else on the differential? If you’re sure it’s a febrile seizure and you know what you’re doing, generally, you’re right. But, kids can have shaking chills, which are involuntary movements in febrile children that are fine, rhythmic, and oscillatory movements about a joint. They rarely involve the facial or respiratory muscles.

They usually involve both sides of the body simultaneously, and they are not associated with the loss of consciousness, and they are suppressible by touch. So shaking chills can easily be differentiated from fevers. Children with breath holding spells, the cyanotic or pallid types, will sometimes have stiffening or convulsing when they lose consciousness.

And yes, I’ve seen kids with colds and fever who have breath holding spells. And then there’s genetic epilepsy plus febrile seizures, which you are not going to diagnose in the ED. These are autosomal dominant seizures. mutations of sodium and calcium channels that lead to seizures with fever in early childhood that continue beyond six years of age.

And then there’s Dravet syndrome. So, Dravet syndrome is also known as severe myoclonic epilepsy of infancy. It will often resemble complex febrile seizures under one year of age. It’s a de novo mutation, so not inherited, of a voltage gated sodium channel in more than 80 percent of the patients with it.

So that’s why phosphenytoin doesn’t work in Dravet syndrome. And if you’ve heard of Dravet, probably the only thing you remember is that phosphenytoin doesn’t work. And I’ve been told by a wise pediatric neurologist where I work that Any female patient under 12 months of age with complex febrile seizures has Dravet syndrome until proven otherwise.

So that’s one special population with a complex febrile seizure, even two in a 24 hour period that deserves special workup. So let’s end with the last and perhaps most important question. How do we talk to families about febrile seizures? Well remember, they are scared, right? I would acknowledge that this was perhaps the most frightening thing they’ve ever seen their child do.

They are worried that it’s not going to stop and that their child would die. They may have felt helpless, but reinforce what they did right. Maybe they moved their child to the floor in the rescue position, or quickly called 911, or got help. All of these are active decisions that the family made to help their child, even if they could not have prevented the febrile seizure.

Define what a seizure is in ways they’ll understand, including how common febrile seizures are. Again, simple febrile seizures, 1 out of 50 children. Explain how the body protects itself during seizures. So there’s a sympathetic surge leading to increased heart rate. The skin will look pale due to peripheral vasoconstriction and shunting of blood to the core organs.

And when you’re seizing, you will close your glottis, your vocal cords, to prevent from aspiration, which leads to perioral cyanosis. So parents often will recall their child stiff, convulsing, and blue in the face. All of these are physiologic things that we expect during seizures, and I think it’s important to address how those were things that the body did You are certainly going to want to say whether or not the child had a simple or complex febrile seizure, because that will dictate what you do next.

Discuss the recurrence risk and what to do if it happens again, i. e., one third after you’ve had one, 50 50 chance after two or more, and you should always be evaluated by default. Talk about the use of antipyretics and their limited impact on recurrence. So they could reduce the risk during this illness, but they don’t necessarily reduce the risk in a future febrile illness.

And use lab tests, and especially CT scans of the brain judiciously. In a child who has recovered, is back to their baseline, has a normal neurologic exam, and no underlying neurologic problems, they’re unlikely to recover. to have any central nervous system abnormalities seen on imaging, nor any significant metabolic or infectious abnormalities seen on targeted lab testing.

So it’s A OK to not get any studies, but remember, you’re not doing nothing. You’re providing education and reassurance to a worried family. You can do this. If the child has recovered and you think it’s a simple febrile seizure, even if you’ve never seen one before, you’re gonna be right. You They’re that common.

I definitely recommend that you practice your speech or approach to febrile seizures before you go into the room if you haven’t done this before. So find an experienced senior resident, fellow, or attending and review it with them. You want to make sure that you can both give the family useful information.

but also not overwhelm them and anticipate what questions they might have. Well that’s it for this episode focused on febrile cedars. I hope you found it useful and will take the information back with you to your next shift in the emergency department. If you have suggestions for other topics that you’d like me to address in the future, send them my way.

I’ll take an email, a comment on the blog, a message on a social media platform of your choosing. My 12 year old told me that I should remind you to subscribe, and and review. Bottom line is I’m just happy if more people listen because that means more people learn and any feedback you can send in my direction, even if it’s in the form of a review, is very welcome.

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

This episode will help you better prepare for and manage children with inborn errors of metabolism in the Emergency Department. Consider it a supplement to what you remember from Biochemistry and the instructions on the family’s laminated care plan sheet. My special guest podcaster, Emily Groopman, is an actual Pediatric Geneticist in training and we hope that you will find this episode useful.

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Emily Groopman, MD, PhD is a first-year resident in the Combined Pediatrics-Medical Genetics Residency Program at Children’s National Hospital/NIH. She did her MD/PhD at Columbia University, where she investigated the diagnostic utility of exome sequencing for kidney disease. She is a member of the Clinical Genome Resource Inborn Errors of Metabolism (IEM) Clinical Domain Working Group, where as a biocurator she assesses the pathogenicity of variants in IEM-associated genes to facilitate expedited genetic diagnosis for IEMs. She aims to become a physician-scientist in pediatrics and medical genetics, engaging in bench-to-bedside research that utilizes multi-omics-based approaches to provide a molecular diagnosis and support personalized care for individuals with suspected rare genetic diseases and their families. You can contact her via email at [email protected].

Jeanmonod R, Asuka E, Jeanmonod D. Inborn Errors of Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459183/#

Rice GM, Steiner RD. Inborn Errors of Metabolism (Metabolic Disorders). Pediatr Rev. 2016 Jan;37(1):3-15; quiz 16-7, 47. doi: 10.1542/pir.2014-0122. PMID: 26729777.

Burton BK. Inborn errors of metabolism in infancy: a guide to diagnosis. Pediatrics. 1998 Dec;102(6):E69. doi: 10.1542/peds.102.6.e69. PMID: 9832597.

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 this episode focuses on the management of children with metabolic disorders who present to the emergency department. I know that this is a subject that makes us all a little bit nervous, and you’re just hoping that the parents have a good laminated sheet to tell you everything that you need to do.

Unfortunately, that’s not always the case. And, let’s face it, there are some great principles that you can apply across metabolic diseases to make sure that you are safely taking care of these children. And you’re thinking, hey! Brad’s not a pediatric medical geneticist. No, I’m not. So I called in a ringer.

Or, well, the ringer called me. So my special guest host on this episode is a trainee in pediatrics and medical genetics. Her name is Emily Groopman, and she’s a current resident at Children’s National Hospital. After doing her MD PhD at Columbia University, where she investigated the genetic diagnosis of kidney disease, she started her residency training with the long term goal of being a physician scientist caring for patients with rare genetic disorders.

She came to me with the idea for this episode based on a recognized need to reinforce key principles in the management of children with inborn errors of metabolism who present to the emergency department. I put a lot more information about Dr. Groopman and how to contact her in the show notes. But now I’m going to pass the mic.

Take it away, Emily.

Inborn errors of metabolism, or IEMs, refer to a diverse group of disorders that result from mutations in genes that are involved in pathways responsible for breaking down nutrients and generating energy. In other words, metabolism. While each of these conditions is individually rare, when considered as a group, they are IEMs occur in approximately 1 in 2, 500 births and can have severe health consequences, including ketoacidosis, cardiac arrhythmias, and encephalopathy.

Therefore understanding these diseases, their presentations and their evaluation is critical for emergency medicine providers. So first, a little bit about their etiology and epidemiology. IEMs are primarily caused, as I mentioned, by mutations in genes involved in metabolism. In other words, genes that include enzymes and other proteins that are involved in breaking down nutrients like carbs, proteins, and fats, and generating energy.

IEMs vary in their inheritance. Most IEMs are inherited in an autosomal recessive manner. Meaning that an individual must inherit two copies of the mutation, so one from each of his or her parents, to be affected. Since an individual must have two copies of the mutation to be affected, the parents and other family members who have one copy, which are known as carriers, will be unaffected.

So, importantly, you may not have a positive family history. Other factors, such as environmental influences, epigenetic changes, the microbiome, and additional genes, may also impact the penetrance of IEMs. In other words, whether or not individuals with a disease causing mutation manifest the associated genetic disease, and also the expressivity.

In other words, which features of the disease individuals with the mutation show for these conditions. Now, newborn screening, or NBS, includes testing newly born infants for certain IEMs.

Since which IEMs are tested for vary state by state, the tests used do not, and the tests do not have perfect sensitivity. And not all IEMs are included on NBS, NBS can miss individuals with IEMs. Therefore, and I want to stress this again, negative results on NBS do not rule out the possibility of IEM.

And it’s always worth considering IEM among children, including among older children and teens, who present with suggestive symptoms. So what’s the pathophysiology of IEMs? Now, IEMs result from disruption of major metabolic processes in our body. And these major metabolic processes include carbohydrate metabolism, protein metabolism, fatty acid oxidation, and glycogen storage.

And together, these processes help store us store nutrients from the food we eat and use it to generate energy. Now, carbs are our body’s preferred source of energy. When we eat, our bodies break down carbohydrates into glucose, which can be used by our cells to generate energy, aka ATP, via cellular respiration.

The glucose that is not immediately used to generate energy is stored in the liver and muscle cells as glycogen. When we’re between meals, in other words, we’re not eating, we’re not fasting, our bodies break down glycogen into glucose so that we can continue to generate the energy our cells need to function.

And altogether, we have enough stored glycogen to last for approximately 24 hours without food. Now, let’s say you fasted for that 24 hours, and at this point your glycogen stores will be depleted. At this point, our bodies have to shift to alternate pathways, first going down the hierarchy of gluconeogenesis, where you can make glucose from amino acids and other non sugar compounds, and then fatty oxidation.

In other words, breaking down fatty acids into the compound acetyl CoA, which can be used to generate energy. Now importantly, fatty oxidation yields ketone bodies. And when the body is in a state that it’s relying primarily on fatty oxidation to generate glucose. You’ll need to get, you’ll accumulate high amounts of ketones leading to ketoacidosis, which is a metabolic emergency.

Now IEMs can disrupt any of these pathways and importantly can have severe health consequences. So what are you going to see? On clinical presentation. Now, first off, realize that most IEMs present with very nonspecific clinical features. You won’t be able to diagnose them on history and physical alone.

And biochemical testing is really needed in most cases to independently diagnose a specific IEM. Therefore, in the ED, the goal is really to recognize the science and symptoms on history and physical exam that are suggestive of metabolic disease. identifying which specific IEM the patient has is part of the later long term evaluation, typically with the help of your friendly geneticist.

It is not the job or the expectation of the EM provider. So what are some of these suggestive clinical features? They include neurologic dysfunction, which is one of the most common that includes things like developmental delay, regression, AKA loss of developmental milestones, hypotonia, encephalopathy, or seizures.

GI symptoms are the second most common, and they include vomiting, food intolerance, food aversion, GERD, refractory to normal antireflux measures, diarrhea, and dehydration. You should also think about IEM in cases where you have failure to thrive, exercise intolerance, or autonomic instability. Now, as I mentioned earlier, since these are autosomal recessive disorders, where you need to have two copies of the mutate, of a mutation to manifest disease, oftentimes family history is negative.

However, sometimes you might hear of siblings or other relatives who had early onset neurologic or GI dysfunction or died early in life, and this can often be attributed to sepsis or sudden infant death syndrome because the symptoms of these overlap with IEMs. You also might see a family history of multiple miscarriages and or constant infinity.

Now typically, IEMs involved in glucose, protein, or fat breakdown, which are, the formal term for them is called intermediary metabolism, will have a short asymptomatic interval. They would kind of like there’s a honeymoon period of days to weeks depending on the IEM after birth. And then they’ll present with acute metabolic decompensation in the neonatal period.

And these neonates typically present looking really, really unwell. So they’re lethargic, they might vomit, they’re hypotonic, hypothermic, they might have fever or seizures. And this is due to buildup of the toxic intermediates of the stalled metabolic pathway. Now the important thing for EM providers to know is that this can mimic the presentation of sepsis.

So you should consider IEM on your differential, especially when the ID workup is negative. And the neonate’s symptoms are refractory to standard measures. In these children, in children, IEMs can present with acute metabolic or neurologic decompensation, like vomiting, coma, or seizures, oftentimes precipitated by episode, things that are metabolically stressful.

So think infection, exercise, or change in diet. Now IEMs involving excretion pathways will generally present with symptoms related to the buildup of the toxic metabolites that cannot be excreted. Now, this, because this gets a lot of buzz, hyperammonemia is a very common feature of a number of different IEMs.

And so it’s important to know its presentation. Hyperammonemia presents with difficulty feeding, lethargy, altered mental status, seizures, vomiting, and vital symptoms of anomalies, most commonly loss of regulation or low core temperature. Now, in contrast, individuals with IEMs that involve pathways for accessing stored energy Can be asymptomatic or well appeared for long periods of time as long as they have a steady supply of energy.

So for instance, in infants who often follow a regular feeding schedule, they can slip under their radar as they’re getting enough energy and in a period in routine forms, and they don’t need to then have any kind of tapping into their stored energy. But again, metabolic GI illness, interrupt other interruptions in feeding schedule, intense exercise.

will result in symptoms. And depending on the specific IEM, these can range from severe metabolic decompensation like hypoglycemia or ketoacidosis, to more subtle features like muscle cramps. So to summarize, consider IEM for neonates with severe unexplained progressive or refractory illness shortly after birth, children who have severe neurologic or GI dysfunction, neglects associated with vomiting.

For metabolic stressors like fever or fasting, and children who are presenting with acidosis or hypoglycemia. Now, what should we do for evaluation and next steps in management? So, again, to reinforce, since IEMs have very specific non specific presentations, the goal in the ER is not to specifically diagnose the IEM.

Rather, it’s recognizing the child in front of you may have an IEM and do what you need to do to acute, for acute stabilization for their associated symptoms. So first, like pretty much many presentations, do ABC, get your PALS as indicated, and get IV access. Next, you want to stop the intake of potentially toxic compounds like protein, fat, glucose, and fructose, and this includes NG or G tube feeds if the child does have them.

Make them NPO and give IV, and give IV fluids with 10 percent dextrose, normal saline, or half normal saline. So D10NS or D10 half NS at one and a half times their maintenance rate. And the goal here is to give glucose, which is that, you know, number one, pure substrate for energy iteration metabolic pathways at a sufficient volume or rate so that this patient does not need to use the other metabolic pathways that might be causing their presentation.

Next, get stat labs, look at metabolic anomalies for blood labs. You want to get some lights, you can get a BMP or CMP glucose, LFT, CRP. CK, urea, and also assess their acid base status, so venous, capillary, or arterial blood gas, and also get COAGs. you want to look at their ammonia and lactate and importantly, if you can, , you want to get a plasma sample for some more sophisticated metabolic tests that can be done later.

So those would be a plasma sample for plasma amino acids, organic acids, acyl carnitine, other compounds, which your friendly geneticist, when you consult them will be incredibly happy you got. Now you also want to get some urine samples. You want to check the color and odor with a urine analysis. Look at the pH, whether there’s glucose, protein, ketones in there.

And you can also store some urine sample for downstream testing. As certain metabolic disorders, you want to look at organic acids in the urine. Now, if you end up needing to get an LP, you can also freeze some extra CSF for downstream testing. Aim for around two to five mils. And then, aside from these tests, There are some additional studies that might be indicated by clinical symptomatology.

So for instance, if they’re having cardiac issues, think about getting an EKG or an echocardiogram. If they’re encephalopathic, you want to consider neural imaging, CT or MRI. And importantly, call a stat genetics consult for further guidance or management. These patients typically do need to be admitted, even if it’s just for monitoring, and if they’re very much deranged in their ABCs, their mental status, they may need to be admitted to the ICU.

So you’ve done your initial workup, nothing’s really conclusive yet, and this patient’s still in the ED. your genetics consult hasn’t responded yet. What should you do? First, continue the glucose infusion. Then, once you get the go ahead from your genetics consult, send samples for specialized metabolic evaluation, including plasma amino acids and acyl carnitines, urine amino acids and organic acids, and whatever else your consult recommends.

Keep an eye on their labs. Again, your consult can give you some helpful tips on the frequency of monitoring, including their lights, glucose, lactate, acid base status, and ammonia. And importantly, if you’re at a referring facility, the most important things are really the basics. So get the ABCs, start D10.

If the patient has a metabolic plan, whether it’s in their electronic medical record and or in their carrier gibbous fans. Follow it. This was made by people who know them very well. If labs are very difficult to get, let’s say the kid’s a difficult stick, at least get a finger stick glucose, get IV access, and start those fluids, D10, either NS or half NS, at one and a half times maintenance.

An obtundate or somnolent child can still tolerate intraosseous access, especially if you put the lidocaine in, 0. 5 mg per kg, max 20 mg. You can use 1 or 2 percent Lido. this video. And really get that access in so you can start those fluids and stabilize the child. Make plans to safely transport the child to a tertiary care after stabilization.

and connect and contact genetics and the accepting ED as soon as you can. Emily, thank you so much. I really appreciate you sharing your knowledge and information and hopefully this was a helpful refresher and primer for the next time that you see a child with a metabolic disorder in the emergency department.

If there’s other topics that you want to hear on the podcast, reach out and let me know. I will take an email. I will take a direct message on X. I will take a comment on Facebook or the blog. If you have the time, leave a review. It helps more people find the show, and therefore more people learn about the care of ill and injured children in the emergency department.

And if you’re like Dr. Groopman, And you’re wondering, Hey, can I record a podcast? The answer is yes, you can. If there’s a topic that you’re interested in learning and teaching about, and it relates to the care of children in the emergency department, send it my way. For PEM Currents, the pediatric emergency medicine podcast.

This has been Brad Sobolewski. See you next time.