PEM Currents: The Pediatric Emergency Medicine Podcast

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

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

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

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

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

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

Penetrating neck injuries in children are rare—but when they happen, the stakes are high. In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the clinical pearls behind “no-zone” management, how to distinguish hard and soft signs, when to image versus operate, and why airway always comes first. Get ready for a focused, evidence-based deep dive into pediatric neck trauma. Learning Objectives Understand the shift from zone-based to “no-zone” management in pediatric penetrating neck injuries and describe the rationale behind this transition. Apply ATLS principles to the initial assessment and stabilization of children with penetrating neck injuries, including decisions regarding imaging and airway management. Evaluate clinical findings to determine the need for operative intervention versus observation in stable pediatric patients with soft versus hard signs of vascular or aerodigestive injury. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo@med-mastodon.com References Stone ME Jr, Christensen P, Craig S, Rosengart M. Management of penetrating neck injury in children: A review of the National Trauma Data Bank. Red Cross Annals. 2017;32(4):171–177. doi:10.1016/j.rcsann.2017.04.003 Callcut RA, Inaba K. Penetrating neck injuries: Initial evaluation and management. UpToDate. Waltham, MA: UpToDate Inc. [Accessed June 24, 2025]. Available from: https://www.uptodate.com Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 4o AI Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and in this episode we are diving into a high-stakes but fortunately rare topic in pediatric trauma — penetrating neck injuries. Now these injuries make up less than 1% of all pediatric trauma, but when they occur, they demand precision and vigilance in terms of diagnosis and management. As you know, the neck packs some vital organs, vessels, the airway, esophagus, and nerves into a tiny little area, so even a seemingly minor wound can injure multiple structures. Now you remember — way back when — where you learned about the zones of the neck, and this is the traditional teaching, which chopped the neck up into three zones. You’ve got Zone I, which is the area between the clavicle and cricoid. You’ve got the subclavian arteries and vein, the carotid, and the apices of the lungs. Zone II, the cricoid to the angle of the mandible — this includes the carotids, jugulars, the vagus nerve, the trachea, and the esophagus. And then you have Zone III, which is the angle of the mandible to the base of the skull — you’ve got the distal carotid, the vertebral artery, and cranial nerves IX through XII. Now, you may recall some teaching that you got in medical school or residency where the management was dictated by which zone was injured. And admittedly, a lot of this evidence is in adults, and more penetrating trauma is seen in adults as well. But now practice is leaning towards the “no zone” approach, where imaginary lines on the skin surface are not dictating management as much as presentation, symptoms, and deciding when to go to the OR versus using CT angiography. So let’s talk about mechanisms of injury for a minute. Toddlers can injure their neck when they fall with something in their mouth, like pencils or chopsticks. School-age kids may take a bike handlebar to the neck, or they’re trying to run or jump over a fence and they get impaled on that — that sounds painful. Adolescents, unfortunately, are subject to assaults, stabbings, and gunshot wounds, as well as clothesline-type injuries or other high-velocity injury where the neck is injured as they’re riding a bike. So low-velocity mechanisms dominate pediatric penetrating neck injuries. Force matters, because depth and tissue cavitation decide the overall injury pattern. In terms of assessing the patient with a penetrating neck injury, it all starts with the ABCs. Is the patient’s airway patent? Are they protecting and maintaining it? Look for signs such as hoarseness, stridor, aphonia (they can’t talk at all), a bubbling wound, or an expanding hematoma. For breathing, patients should be breathing comfortably with no distress. Look for any signs of asymmetry on chest rise, feeling of crepitus or subcutaneous air, or diminished breath sounds — obviously the latter two indicating a pneumothorax or even hemothorax. For circulation, if the wound is bleeding, apply direct pressure. Some surgeons will use a Foley balloon tamponade method if they need to stop bleeding before going to the operating room. Patients will need large bore IVs and fluids — and especially blood product resuscitation. Only immobilize the C-spine if a patient has neurologic deficits or a high injury mechanism. Think — somebody that was riding their bike and clotheslined the fence. Neck collars hide neck wounds and hamper airway management unless they’re strictly needed. You may have also heard of hard signs and soft signs in terms of the parlance of managing penetrating neck injury. In general, hard signs mean go to the operating room. Soft signs need a CT angiogram and observation. So here are some hard signs: • Active arterial bleeding — blood spurting out of the patient • Expanding or pulsatile hematoma • Airway compromise, stridor, or other signs • Air bubbling from the neck wound • Shock that is unresponsive to fluids • Any focal neurologic deficit Soft signs include: • Minor oozing • A small and stable hematoma • Mild dysphonia or dysphagia • Subcutaneous air without any respiratory distress • Mild voice changes • Just a little bit of hemoptysis A large pediatric series showed that 50 to 70% of children with hard signs did need operative repair. Most with only soft signs were managed safely with imaging and serial exams. So I alluded to this paradigm at the beginning of the episode — the “no zone” strategy. For stable children with no hard signs, CT angiography is the gold standard. It has a sensitivity of 95 to 99% for major vascular injury. You’re able to visualize the trachea, esophagus, spine, and any foreign bodies. Make sure you always get a chest X-ray as well, since penetrating neck injuries can injure the apices of the lungs or thoracic structures. Also, if the CTA is negative but you still have suspicion for injury to the aerodigestive tract, you can do a water-soluble contrast esophagram or flexible endoscopy. Plain films — yes, you can assess the C-spine and look for radiopaque foreign bodies, but again, if you truly have a child that is stable and has no hard signs, CTA is the gold standard. If you follow this, you can cut non-therapeutic neck explorations in half without missing any injuries. So this should be part of your protocol. If you do have a neck wound that you have to manage before the surgeons can get to it: direct pressure first. The Foley balloon tamponade method is where you take an 18 to 20 French catheter, place it into the wound, inflate the balloon with 10 to 15 milliliters of water, and then clamp it. I wouldn’t necessarily do this in a Level 1 trauma center — I have surgeons available — but it might be useful if you have to transport a kid quickly to a trauma center. Never, ever, ever pull an impaled object out of the neck in the emergency department. These should be removed in the operating room. Now, superficial injuries with the platysma intact get routine closure. Anything deeper deserves imaging. So here’s some pediatric-specific pearls, again, because these are really rare. Kids have a small airway, and soft tissues swell quickly, so there’s a low threshold for securing the airway. If you’re concerned about the airway, make a plan to do it right now. Kids have low blood volume and don’t tolerate hemorrhage as well. They’ll underreport pain, especially younger ones — so rely on the exam and parental observations. Definitely use Child Life to help keep them calm. And unfortunately, some neck wounds are self-inflicted, so make sure you address mental health concerns after the child is stabilized. Alright. So let’s bring it all home. What are some key take-home points? 1. Penetrating neck trauma is fortunately rare in kids — far less than 1% of all pediatric trauma — but still high-risk. 2. Males predominate. The younger the child, the higher the risk of aerodigestive injury. 3. Hard signs → go straight to the OR. 4. Soft signs → CT angiography and observation. 5. Hard vs soft signs reliably stratify risk. 6. CTA + chest X-ray is first-line in stable, hard-sign-negative children, which limits unnecessary surgical exploration. 7. Esophageal injuries are sneaky — you may need endoscopy or contrast studies if CTA is equivocal. 8. In terms of immediate management: airway beats everything. • People talk about the triple setup: RSI, extraglottic rescue, surgical airway kit. 9. Children with concerning but non-operative injuries need serial examinations — these are very powerful. • Observation is a test. Check neurovascular status every 2 to 4 hours for at least a day. 10. If there’s an impaled object — leave it, transport intact, and remove it in the OR. 11. If you’re working in the community or not at a Level 1 pediatric trauma center — focus on careful airway management and immediate transport. That’s all for this episode. I hope you found it useful — especially since these injuries are less common, but can be incredibly impactful. If you enjoyed the content, or want to hear something different about pediatric trauma, reach out and let me know — I’ll take an email, a comment on the blog, a social media message. And please — as my 13-year-old would encourage me to say — like, rate, and review. It he

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, Brad Sobolewski discusses advanced imaging in pediatric emergency care with Dr. Jennifer Marin (jennifer.marin@chp.edu) 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. Learning Objectives Demonstrate the ability to use shared decision-making strategies when discussing imaging options with families of pediatric patients presenting to the Emergency Department. (Bloom’s: Apply; Kirkpatrick Level 2 – Learning) Evaluate the risks and benefits of ultrasound, CT, and MRI for common pediatric emergencies and identify appropriate imaging modalities based on clinical guidelines discussed in the podcast. (Bloom’s: Analyze; Kirkpatrick Level 3 – Behavior): Assess the impact of implementing strategies for reducing low-value imaging in the pediatric emergency department on patient care outcomes, including diagnostic accuracy, radiation exposure, and healthcare costs. (Bloom’s: Evaluate; Kirkpatrick Level 4 – Results) Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo@med-mastodon.com References Marin JR, Lyons TW, Claudius I, et al; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Section on Radiology; American College of Emergency Physicians Pediatric Emergency Medicine Committee; American College of Radiology. Optimizing Advanced Imaging of the Pediatric Patient in the Emergency Department: Policy Statement. Pediatrics. 2024;154(1):e2024066854. doi:10.1542/peds.2024-066854. PubMed Marin JR, Lyons TW, Claudius I, et al; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Section on Radiology; American College of Emergency Physicians Pediatric Emergency Medicine Committee; American College of Radiology. Optimizing Advanced Imaging of the Pediatric Patient in the Emergency Department: Technical Report. Pediatrics. 2024;154(1):e2024066855. doi:10.1542/peds.2024-066855. PubMed Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 4o AI Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and in 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 kn

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. Learning Objectives Describe the classic and atypical clinical presentations of Parvovirus B19 infection in pediatric patients, including erythema infectiosum, arthropathy, transient aplastic crisis, and chronic anemia in immunocompromised hosts. Understand the epidemiology and transmission timeline of Parvovirus B19, especially its seasonal peaks and viral shedding period. Recognize key diagnostic features that help differentiate Parvovirus B19 from other viral exanthems and systemic illnesses. Formulate an evidence-based management plan for patients with suspected or confirmed Parvovirus B19, including those with underlying hemolytic disease or immunocompromise. Counsel families and caregivers—including pregnant household contacts—on the risks, exposures, and infection control considerations related to Parvovirus B19. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo@med-mastodon.com References 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 Transcript 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 infecti

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. Learning Objectives Compare the clinical presentation of bacterial infections in unvaccinated and undervaccinated children versus fully immunized children in the Emergency Department Assess the need for empiric antibiotics and diagnostic testing in an unvaccinated or undervaccinated child presenting with fever without source Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo References 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 Transcript 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 appea

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! Learning Objectives Describe the clinical presentation, epidemiology, and complications of Mycoplasma pneumoniae infections in pediatric patients, including its atypical manifestations. Differentiate Mycoplasma pneumoniae pneumonia from typical bacterial and viral pneumonia based on history, physical exam findings, and diagnostic testing. Assess the current evidence for antibiotic treatment of Mycoplasma pneumoniae and justify treatment decisions based on patient presentation, severity, and potential complications. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo References 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. Transcript 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

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the complex and often underrecognized issue of inhalant misuse. From the early days of glue sniffing to the recent rise of nitrous oxide misuse, fueled by brands like Galaxy Gas and viral trends on TikTok and Instagram, inhalant misuse has evolved into a growing concern among adolescents. We’ll dive into the clinical presentations, including acute and chronic symptoms, the dangers of “sudden sniffing death,” and the specific risks associated with nitrites, hydrocarbons, and nitrous oxide. Learn how to recognize and manage cases in the emergency department, ask the right questions to uncover inhalant use, and provide critical resources for prevention and support. Whether you’re a seasoned pediatrician or new to emergency medicine, this episode offers essential insights into tackling this hidden epidemic. Learning Objectives By the end of this episode, listeners will be able to: Recognize the clinical signs and symptoms of inhalant misuse, including acute intoxication and long-term complications. Differentiate between the risks and toxic effects associated with specific inhalants, such as hydrocarbons, nitrites, and nitrous oxide. Formulate effective strategies for identifying, managing, and preventing inhalant misuse in pediatric patients. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo References Perry H, Burns MM. Inhalant misuse in children and adolescents. UpToDate. Ganetsky M (ed). Updated February 26, 2024. Accessed January 13, 2025. https://www.uptodate.com/contents/inhalant-misuse-in-children-and-adolescents Hogge RL, Spiller HA, Kistamgari S, et al. Inhalant misuse reported to America’s Poison Centers, 2001-2021. Clin Toxicol (Phila) 2023; 61:453. Marcus E. The next drug epidemic is blue raspberry flavored: How Galaxy Gas became synonymous with the country’s burgeoning addiction to gas. Intelligencer. Published January 6, 2025. Accessed January 13, 2025. https://nymag.com/intelligencer/article/galaxy-gas-flavored-nitrous-oxide-drug-epidemic.html Transcript Note: This transcript was partially completed with the use of the Descript AI  Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re diving into an important topic, inhalant misuse, with a special focus on nitrous oxide. Welcome Recently, there’s been a concerning rise in recreational use of nitrous oxide, often referred to as Galaxy Gas, which is actually a brand name, which has become synonymous with flavored nitrous oxide products. Even as that brand, Galaxy Gas, is being phased out of the market, its legacy persists, fueled in part by its viral presence on social media platforms like TikTok and Instagram. So, this episode is going to break down the symptoms, clinical presentations, and management of inhalant misuse in children and adolescents with a specific eye on how these trends are shaping a new wave of cases presenting to the ED across the globe. So, what are inhalants? Well, these are volatile substances that you’re not meant to breathe in. They produce vapors, which, when you inhale them, cause psychoactive effects. They include everyday household items like glue, paint thinner, and gasoline, as well as recreational substances such as nitrous oxide, often referred to as whippets or galaxy gas. Interestingly, when these are sold, either online or in physical stores, they’re marketed As additives to make your own whipped cream at home. The people that sell them in stores are told to specifically not refer to them as whippets or to refer to them as a drug. Oh no, they’re only for cooking. The customers and the people selling them know otherwise. Anyway, the recreational use of nitrous or whippets, it’s been around since the late 18th century, uh, when it was used in laughing gas parties among the immigrants. English elite. Fast forward to today, and nitrous remains one of the most commonly misused inhalants. It’s evolved from its medical and industrial applications to a recreational substance with a significant cultural footprint. And let’s face it, the prevalence of this inhalant misuse is concerning. In the US, about 11 percent of high school students have used inhalants at least once. And what’s striking is that inhalant use peaks in younger adolescents, particularly those in like 7th through 9th grades, middle schoolers. making it one of the earliest substances that are misused among young people. So, these inhalants are often used through sniffing, huffing, or bagging. Sniffing involves inhaling the fumes directly from the container. Huffing uses a cloth soaked with the substance. And bagging, or perhaps ballooning, involves inhaling fumes from a bag or balloon placed over the nose and mouth. So you decant the substance from the canister into a balloon, and then you inhale that into your mouth. The latter dramatically increases the risk of asphyxia. The mechanism of action is rapid and profound. These substances are absorbed through the lungs and distributed to the brain, where they act on GABA and glutamate receptors. The primary effects are euphoria, dizziness, and disorientation. They’re felt within seconds and last 15 to 30 minutes or less. And. Patients that use these will repeatedly use it throughout the day. You can either get one little individual canister of nitrous, or a big canister which costs about 120 to 120. Repeated use can sustain that intoxication. So the symptoms of inhalant misuse are important to recognize. So first and foremost are the neurological symptoms. Euphoria, ataxia, disorientation, and slurred speech are common in acute intoxication. Chronic misuse can be devastating and unfortunately we don’t know how much, or how long, or how frequent leads to these symptoms. But nevertheless, they’re pretty darn bad. It includes cerebellar dysfunction, peripheral neuropathy, and toxic leukoencephalopathy, which manifests as white matter degeneration visible on MRI. Basically, misuse of this stuff can paralyze you. The cardiovascular symptoms include sudden sniffing death syndrome, which is the generation of a fatal arrhythmia, which is particularly dangerous with halogenated hydrocarbons. Pulmonary symptoms include hypoxia, reactive airway dysfunction, and in severe cases, pulmonary edema or even a pneumothorax. Glue sniffer’s rash is a hallmark skin finding. It presents as erythema and inflammation around the mouth and nose. and nose. Chronic users may also see weight loss, abdominal pain, nausea and vomiting, and metabolic abnormalities like hypokalemia and acidosis, especially if they’re misusing toluene, which is fortunately less common. Further complicating matters is that each inhalant has its own special risks. Hydrocarbons, again found in solvents and glue, can lead to cranial neuropathy, cerebellar dysfunction, and cardiac arrhythmias. Chronic misuse of these results in profound hypokalemia and metabolic acidosis. Nitrous oxide, so whippets or galaxy gas, interferes with vitamin B12 metabolism, so it can lead to polyneuropathy, myelopathy, and hyperhomocystinemia, which increases the risk of venous thromboembolism. Nitrites, which are known as poppers, can cause intense vasodilation and methemoglobinemia. with symptoms ranging from headache to cyanosis and seizures. So management, unfortunately, of inhalant intoxication is primarily supportive. Stabilization, you have to ensure that the patient is removed from the exposure source and administer 100 percent oxygen if they’re hypoxic. If the patient is unconscious and in a tachyarrhythmia, the treatment is electricity! Amiodarone or lidocaine on the palsgar rhythm and avoid catecholamines like epinephrine unless the patient’s in cardiac arrest. For nitrous oxide neurotoxicity, administer high dose vitamin B12 intramuscularly or subcutaneously. I would consult a toxicologist because I know that this is rare. And if you have a patient with methemoglobinemia, chances are you’re actually taking a board test, but you would treat that with IV methylene blue. In cases of toluene misuse, monitor and correct the electrolyte imbalances carefully, avoid dextrose, which can actually worsen the hypokalemia. Again, I would call a toxicologist for help from this, because fortunately, it’s very rare. And listen, this problem isn’t going anywhere. So pediatricians, Educators and parents all play a crucial role in prevention. Frankly, these should not be so accessible. They should not be able to be sold easily online or in physical smoke shops. Also, we need to advocate for federal regulation on these as controlled substances, because currently right now they’re not. Everybody knows the dance that the retailers play in saying, Oh yeah, you can use these to make whipped cream at home, but they are marketed with with flavoring in brightly colored containers and they are very attractive to young children. They’re piggybacking off the same strategies that made vaping and vape cartridges so popular. Students should be educated about the dangers of inhalants. That means both local advocacy in schools and in medical care settings, but also using some of the same techniques that made getting high off these popular, like social media. We’ve got to reduce access. and curiosity. Schools should definitely replace solvent based products with safer alternatives and monitor students for signs of misuse. For those already misusing inhalants, referral to a substance use disorder program is essential. Chronic complications often resolve with cessation, but addressing coexisting mental health problems and comorbidities such as depression and suicidality is equally important. Okay, I know that that was just a whiff of a topic that you ma

In lieu of a traditional episode this holiday season I wanted to share a reading of the Pediatric Emergency Medicine version of a famous Christmas poem. Transcript ‘Twas the night before Christmas, and I’m working a shift, The symptoms were varied, the pace was quite swift. The screens glowed with orders, the rooms filled with care, In hopes that discharge summaries soon would be there. The nurses were moving with hustle and speed, While families recounted each child’s urgent need. And I at my computer, my coffee in hand, Prepared for the onslaught that none could have planned. When out in the lobby there arose such a clatter, I sprang from my chair to see what was the matter. Away to the triage I flew like a flash, Dodging spilled apple juice and a child with a rash. The ambulances were wailing, the scene quite a sight, As the complaints rolled in on this hectic night. When what to my weary eyes did appear, But a febrile infant, his parents in fear. A nursemaid’s elbow in need of a tug, And a kid with a cough wrapped tight in a hug. A forehead lac with blood streaming red, And a teen who proclaimed, “I think I’m half-dead!” With quick-thinking teamwork, the cases we tamed, And I whistled and shouted and called them by name: “Now flu! Now croup! Now migraines and pain! On seizures! On sepsis! That ankle is sprained! To the trauma bay stat, through triage with speed, Move quickly, move calmly, and meet every need!” As the snow flakes that fall when wild winter winds fly, We hustled and triaged as new patients arrived. And then, in a twinkling, I heard down the hall, The sound of retching – a vomiting call. Ondansetron ordered, the nurse prepping the dose, I saw a pale toddler, looking morose. He was sick from his tummy to the tip of his nose, And the sounds of his misery steadily rose. His eyes were all sunken, his cheeks far too pale, But a popsicle bribe led to a triumphant exhale. The shift rolled along with splints left and right, Broken forearms galore on this holiday night. And ketamine laughter soon filled the air, As a lac repair finished with great skill and care. Abdominal pains brought more to the bays, With parents repeating, “He’s been sick for days.” A scan ruled out danger, the appendix intact, While the next patient arrived with an asthma attack. The hours wore on, the crowd didn’t cease, Yet amidst all the chaos, we found moments of peace. A mom’s grateful smile, a child’s sleepy yawn, Reminded us why we keep carrying on. So I sat at the computer and typed one last note, Cleared my inbox of tasks and the orders I wrote. And I heard myself whisper as I turned off the light, “Merry Christmas to all, and to all a calm night!”

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore pertussis, also known as whooping cough – a disease that remains a public health challenge despite widespread vaccination efforts. We will review the clinical presentation, diagnostic strategies, management protocols, infection control practices, and vaccination updates. This episode also covers what healthcare providers need to know about post-exposure prophylaxis, respiratory precautions, and managing occupational exposures. Learning Objectives Understand the clinical progression of pertussis through its three distinct stages and identify key symptoms, including age-specific presentations in infants and older children. Implement effective management strategies for pertussis, including supportive care, appropriate antibiotic regimens, and post-exposure prophylaxis for contacts and healthcare providers. Promote pertussis prevention by understanding vaccination schedules (DTaP vs. Tdap), addressing vaccine hesitancy, and adhering to infection control protocols in clinical settings. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo How about a fun AI song about whooping cough? YouTube Shorts TikTok References StatPearls Lauria AM, Zabbo CP. Pertussis. [Updated 2022 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519008/ AAP Pediatrics in Review Heather L. Daniels, Camille Sabella; Bordetella pertussis (Pertussis). Pediatr Rev May 2018; 39 (5): 247–257. https://doi.org/10.1542/pir.2017-0229 UpToDate Yeh S et al. Pertussis infection in infants and children: Clinical features and diagnosis. UpToDate. Available at: https://www.uptodate.com. Accessed December 3, 2024. MMWR Seither R, Yusuf OB, Dramann D, et al. Coverage with Selected Vaccines and Exemption Rates Among Children in Kindergarten — United States, 2023–24 School Year. MMWR Morb Mortal Wkly Rep 2024;73:925–932. DOI: http://dx.doi.org/10.15585/mmwr.mm7341a3 Transcript 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 recommend

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 […]

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 […]

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

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 […]

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 […]

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 […]