Nursemaid’s Elbow

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 antistaphylococcal penicillins remain the preferred parenteral agents. For oral therapy, high-dose cephalexin, 75 to 100 milligrams per kilogram per day divided every six hours, is preferred. Clindamycin is an alternative when beta-lactams cannot be used. For clindamycin-susceptible MRSA, clindamycin is the preferred IV and oral agent due to excellent bioavailability and bone penetration, and it avoids the renal toxicity associated with vancomycin. For clindamycin-resistant MRSA, vancomycin or ceftaroline are preferred IV agents. Oral options are limited, and linezolid is generally the preferred oral agent when transition is possible. Daptomycin may be used parenterally in children older than one year without pulmonary involvement, typically with infectious diseases and pharmacy input. Beta-lactams remain the drugs of choice for Kingella kingae, Streptococcus pyogenes, and Streptococcus pneumoniae. Vancomycin has no activity against Kingella, and clindamycin is often ineffective. For Salmonella osteomyelitis, typically seen in children with sickle cell disease, third-generation cephalosporins or fluoroquinolones are used. In underimmunized children under four years, consider Haemophilus influenzae type b, with therapy guided by beta-lactamase production. Doxycycline has not been prospectively studied in pediatric acute hematogenous osteomyelitis. There are theoretical concerns about reduced activity in infected bone and risks related to prolonged therapy. While short courses are safe for certain infections, the longer durations required for osteomyelitis increase the risk of adverse effects. Doxycycline should be considered only when no other active oral option is available, typically in older children, and with infectious diseases consultation. It is not appropriate for routine treatment. Many hospitals automatically consult orthopedics when children are admitted with osteomyelitis, and this is appropriate. Early orthopedic consultation should be viewed as team-based care, not failure of medical management. Consult orthopedics when MRI shows abscess or extensive disease, there is concern for septic arthritis, the child fails to improve within 48 to 72 hours, imaging suggests devitalized bone or growth plate involvement, there is a pathologic fracture, the patient is a neonate, or diagnostic bone sampling or operative drainage is being considered. Routine surgical debridement is not required for uncomplicated cases. Infectious diseases consultation is also often automatic and supported by guidelines. ID is particularly valuable for antibiotic selection, dosing, IV-to-oral transition, duration decisions, bacteremia management, adverse reactions, and salvage regimens. Even in straightforward cases, ID involvement often facilitates shorter IV courses and earlier oral transition. Osteomyelitis is generally not contagious, and clustering is uncommon for Staphylococcus aureus. Kingella kingae is the key exception. It colonizes the oropharynx of young children and spreads via close contact. Clusters of invasive Kingelladisease have been documented in daycare settings. Suspicion should be higher in children six to 36 months from the same daycare, with recent viral illness, mild systemic symptoms, refusal to bear weight, modest CRP elevation, and negative routine cultures unless PCR testing is used. Public health intervention is not typically required, but awareness is critical. There is no minimum required duration of IV therapy for uncomplicated acute hematogenous osteomyelitis. Transition to oral therapy should be based on clinical improvement plus CRP decline. Many children meet criteria within two to six days. Oral antibiotics must be dosed higher than standard outpatient regimens to ensure adequate bone penetration. Common regimens include high-dose cephalexin, clindamycin, or linezolid in select cases. The oral agent should mirror the IV agent that produced clinical improvement. Total duration is typically three to four weeks, and in many cases 15 to 20 days is sufficient. MRSA infections or complicated cases usually require four to six weeks. Early oral transition yields outcomes comparable to prolonged IV therapy with fewer complications. Most treatment-related complications occur during parenteral therapy, largely due to catheter-related issues. Take-home points: osteomyelitis in children is a clinical diagnosis supported by labs and MRI. Empiric antibiotics should be guided by age, illness severity, and local MRSA prevalence. Early transition to high-dose oral therapy is safe and effective when clinical response and CRP support it. Orthopedics and infectious diseases consultation improve care and reduce variation. FAST MRI is changing how we diagnose osteomyelitis. Daycare clustering is uncommon except with Kingella kingae. That’s all for this episode. If there are other topics you’d like us to cover, let me know. If you have the time, leave a review on your favorite podcast platform. It helps more people find the show and learn from it. For PEM Currents, this has been Brad Sobolewski. See you next time.    

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

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 antibiotics anyway, so get good at looking at ears and know what you're seeing. And have they taken similar antibiotics since then? Like. Different penicillins, Augmentin, or cephalexin. So if they said that they were allergic to amoxicillin, but then somehow tolerated Augmentin. They're not allergic. If a patient had rash only, but no hive swelling or difficulty breathing, no reaction within the first hour. It occurred more than five years ago or before the kid was three. And especially if they tolerated beta-lactam antibiotics. Since then, they're a great candidate for de labeling and I would refer that kid to the allergy clinic. Generally, they can get them in pretty darn quick. Alright, we're gonna wrap up this episode. Most kids labeled penicillin allergic or amoxicillin allergic, or not actually allergic to the medication. There are some scores like pen fasts that are validated tools to assess risk and support de labeling. Direct oral challenge for most patients is safe, efficient, and increasingly the standard of care. There are allergy clinics like the Pats at Cincinnati Children's that can dela children in a single visit with oral challenges alone, needing no skin testing, and emergency departments can play a key role in identifying and referring these patients and possibly de labeling ourselves in the future. Well, that's all for this episode on Penicillin Allergy. I hope you learn something new, especially how to assess whether an allergy label is real, how to ask the right questions and when to refer to an allergy testing clinic. If you have feedback, send it my way. Email, comment on the blog, a message on social media. I always appreciate hearing from you all, and if you like this episode, please leave a review on your favorite podcast app. Really helps more people find the show and that's great 'cause I like to teach people stuff. Thanks for listening for PEM Currents, the Pediatric Emergency Medicine podcast. This has been Brad Sobolewski. See you next time.

Limping is a common complaint in pediatric emergency care, but the differential is broad and the stakes are high. In this episode, we walk through a detailed, age-based approach to the evaluation of the limping child. You’ll learn how to integrate the Kocher criteria, when imaging and labs are truly necessary, and how to avoid being misled by small joint effusions on ultrasound. We also highlight critical mimics like appendicitis, testicular torsion, and malignancy—and remind you why watching a child walk is one of the most valuable parts of the exam. Whether it’s transient synovitis, septic arthritis, or something much more concerning, this episode gives you the tools to manage pediatric limps with confidence. Learning Objectives Apply an age-based approach to the differential diagnosis of limping in children. Demonstrate diagnostic reasoning by integrating history, physical exam, imaging, and lab findings to prioritize urgent conditions like septic arthritis and SCFE. Appropriately select and interpret imaging and lab studies, including understanding the utility and limitations of ultrasound, MRI, and the Kocher criteria. Connect with Brad Sobolewski Mastodon: @[email protected] PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski References Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662-70. doi:10.2106/00004623-199912000-00002 UpToDate. Evaluation of limp in children. Accessed September 2025. UpToDate. Differential diagnosis of limp in children. Accessed September 2025. StatPearls. Antalgic Gait in Children. NCBI Bookshelf. Accessed September 2025. Pediatric Emergency Care. “Approach to Pediatric Limp.” Pediatrics in Review. 2024. Transcript Note: This transcript was partially completed with the use of the Descript AI and the Chat GPT 5 AI Welcome to PEM Currents, the Pediatric Emergency Medicine podcast. As always, I’m your host, Brad Sobolewski, and in this episode we’re gonna tackle the evaluation of a child presenting with limp. We’ll cover, age-based differential diagnosis. How to take a high yield history and do a detailed physical exam, imaging strategies, lab tests, and when to worry about systemic causes. We’ll also talk about the Kocher criteria for septic arthritis and how to use and not misuse ultrasound when you’re worried about a hip effusion. After listening to this episode, I hope you will all be able to apply an age based. Approach to the differential diagnosis of limp in children. Demonstrate diagnostic reasoning by integrating history, physical exam, imaging, and lab findings to prioritize urgent conditions like septic, arthritis, and scfe, and appropriately select and interpret imaging and lab studies, including understanding the utility and limitations of ultrasound MRI and the Kocher criteria. So let me start out by saying that a limp isn’t a diagnosis, it’s a symptom. It can result from pain, weakness, neurologic issues, or mechanical disruption. So think of limping as the pediatric equivalent of chest pain. In adults. It’s common, it’s broad, and it’s sometimes could be serious. And the key to a good workup is a thought. Age-based approached and kids under three think trauma and congenital conditions between three and 10 transient synovitis range Supreme and over 10 think SCFE and systemic disease. And your differential diagnosis always starts with history. So you gotta ask the family, when did the lymph start? Was it sudden or gradual? Is there a preceding viral illness or an injury? Is the limp worse in the morning? Does it get better with activity? Do the kid complain of pain or are they just favoring one leg? And then are there any systemic symptoms such as fever, rash, weight loss, fatigue, or joint swelling elsewhere? And you wanna find out whether or not the kid is actually bearing any weight at all. Have they had recent travel or known tick exposure? Are they potty trained and are they having accidents now? Have they had any prior episodes of joint swelling or limping like this in the past? And don’t forget a developmental history, especially in kids under preschool age. Most children begin to stand at nine to 12 months. Cruise at 10 to 12 months and walk independently by 12 to 15 months. A child who has never walked normally may have a neuromuscular or congenital problem. When you are evaluating limp, obviously you wanna watch the kid walk, get them outta the exam room if needed. First of all, your exam room is small. Kid may feel confined and they might be more willing to take some steps. If you have ’em out in the hallway, obviously have the caregiver nearby and a toy, a phone, some object of enticement. You wanna watch their stance phase, or they just avoiding bearing weight on one limb. When they’re standing the swing phase, do they hold that leg stiff? Does it bend normally? And are they in balance? Are they symmetric? And again, don’t just settle for a few steps. Try to get ’em walking at least 10 to 15 feet if possible, and if they’re refusing to walk in, the ED asks parents for a video. You wanna examine every joint head to toe, and even if the child only complains about one area, palpate every limb. I usually start distally so at the fingertips or toes and really systematically work my way up watching for any signs of pain, you check range of motion and observe resistance to movement log. Roll the hips externally and internally rotate them as well. See if you can feel an A fusion, you know, squeeze the calf to localize pain. And in a kid with limp, you always gotta check the feet too, right? Look for puncture wounds on the plantar surface. Splinters, ingrown, toenails, cellulitis, or even, you know, gravity dependent swelling or petechiae. And certainly your systemic exam should include the abdomen. You know, look for signs of appendicitis or sous irritation, testes for testicular torsion. And you wanna look at the skin diffusely to make sure there’s no petechiae, target shape, rashes, or bruising. Now for most kids with limp, I find that the history and physical exams sort of guide where you’re going, right? If they had a fall or an injury, well, you’re just looking at a kid who may have sprained or broken something, and you can really target towards imaging as your workup. You know, there’s some kids though that may benefit from labs and in general, they depend on the scenario. So if you see A C, B, C, well you’re gonna get leukocytosis, but C, B, C. In the context of limp is most useful when you’re considering a differential. So if you see blasts, well, you know you’ve got a new malignancy. If you have a general elevation of the white count and use it in context with the Kocher criteria, it could be more valuable. So A CBC alone is not gonna get you the cause it supports your differential. ESR and CRP are often ordered and they’re just general inflammatory labs. CRP rises and falls faster than ESR, and they co vary and either can be used in prediction rules. I’ll talk about that in a little bit if you think the kid’s bacteremic, yeah. Get a blood culture. If you’re in an endemic area and you’re considering Lyme on the differential, you can send off serology. And let’s be honest, a NA and rheumatoid factor are really only useful if there’s a chronic history and you can have about 15% of kids with a false positive a NA anyway, and they’re not really helpful in acute limp. So get them if rheumatology recommends them, but otherwise, they’re not really a useful part in the initial differential diagnosis. And again, I alluded to Lyme a moment ago, but if Lyme arthritis is your top diagnosis, especially with a known rash. You can start treatment while serologies are pending. That’s totally okay. So in conjunction with Labs, imaging is generally recommended in most kids with Limp, and I would say in most cases you start with plain films. Sometimes it’s easy, right? They hurt in one particular occasion. You take a picture, you see a fracture, but two views, the affected and unaffected side can be really helpful, especially in cases of SCFE or in subtle or perhaps occult toddler’s fracture. If you’re not sure where the problem is, you can’t isolate it on your exam or history. Consider imaging the entire leg. I mean, that’s when you’re looking at like the hip femur, knee tib fib, even the ankle and foot. It’s not that much radiation. Ultrasound is useful for seeing joint effusions, especially of the hip. It’s fast, generally painless and radiation free, but not all effusions are infected. Ultrasound is not part of the Kocher criteria. I’ll get back to that in a minute. And a normal ultrasound or an ultrasound without effusion doesn’t rule out septic arthritis. And then we’ve got MRI, which is definitely best for detecting osteomyelitis, discitis, and soft tissue abscesses. Among other diagnoses in kids under five, you’re probably gonna need to sedate them, which can delay diagnosis. So in general, you’re admitting those kids and then they can get a sedated MRI later the next day. But if radiology has it available and you’ve got the right protocol and the kids’ the right age, you can get it in the emergency department. But these are often more subtle situations. So if you’re really suspicious for septic arthritis, don’t wait around for an MRI contact ortho and tap that hip. And speaking of septic arthritis, let’s talk about the Kocher criteria. K-O-C-H-E-R. These are four classic criteria, and they are only validated for differentiating septic arthritis and transient synovitis of the hip. So you can’t use the labs and values of Kocher criteria in the knee or elbow, or another joint. It is only the hip. And the four classic criteria are fever greater than 38.5 Celsius, non-weight bearing on the affected side, ESR, greater than 40. Or CRP greater than two and white blood cell count greater than 12,000, and you use them in combination to predict the likelihood of septic arthritis of the hip. So if you have none of them, you have less than a 0.2% chance of septic arthritis. If you have one, you have 3%, two 40%. Three of them, 93% and all four, a 99 plus percent chance of having septic arthritis. So the more criteria that are positive, the higher the post-test probability of septic arthritis. And remember I mentioned this before, ultrasound isn’t part of that rule, so don’t let a small effusion sway you one way or the other. Septic arthritis is a clinical diagnosis supported by aspiration of the hip. Ultrasound can help, but a normal scan doesn’t clear the joint, so some orthopedists will recommend not getting an ultrasound on intermediate risk cases and just going straight to joint aspiration if the concern’s high. So if the kid’s worried they stay, don’t discharge a maybe septic joint. I think now’s a good time to come back to some of the common diagnoses that you’ll have on your differential, and I think an age-based schema makes sense here. In Kids Under three, you’re thinking toddlers fracture, septic, hip, developmental dysplasia of the hip, non-accidental trauma, leukemia and transient synovitis in kids three to 10 transient synovitis rules the day. Injuries and trauma. Hopefully you have a good history. Septic arthritis, juvenile idiopathic arthritis, and leg calf, Perth’s disease, and then kids older than 10, you’ll start to see scfe. So slipped capital, femoral epiphysis, stress fractures, osteomyelitis, overuse injuries, and yes, still unfortunately, malignancy leg, Ewing sarcoma. Thinking beyond the limb should remind you that systemic causes can lead to limp as well. Appendicitis can present as right hip pain or limp. Testicular torsion may cause abdominal pain and referred thigh pain. Leukemia obviously can present with limp, nighttime pain, and subtle systemic signs. Discitis may masquerade as refusal to walk or sit upright. And any malignancy can present subtly. You can see bruising, fatigue, pal anemia, or bony tenderness. So red flags for a child with limp, so you’re calling orthopedics, admitting or escalating. Your plan is when the kid is ill appearing toxic or febrile. Your labs obviously suggest inflammation or infection. You have septic, arthritis, osteomyelitis, or non-accidental trauma. At the top of your list, and you have diagnostic uncertainty on a child who isn’t improving. So you did a workup. It’s reassuring, and despite analgesia, reassurance and time, the kid still won’t walk well. Maybe that kid needs workup for osteomyelitis, so sometimes the best course of action is to admit them and get the MRI the next day. All right. Here’s some take home points on the child with limp. Limping is due to pain, weakness, mechanical or neurologic causes. Think broadly in terms of your differential history, physical exam and observation, or more valuable than a dozen labs. Age-based differential diagnoses guide you and help you tailor your exam and questions accordingly. So I think that’s a good schema to teach. Always start with plain films, especially if you suspect injury. The Kocher criteria are only valid for differentiating septic hip versus transient synovitis. Don’t use them in another joint. And septic arthritis is a clinical diagnosis, so if you’re worried and they have multiple factors, tap that joint. If you’re concerned about the kid and they’re still not walking, it’s okay to admit, and again, don’t forget to check the feet. I’ve seen many kids that have been limping because there’s a splinter in the bottom of the foot. You can save yourself a lot of time and money by just yanking that little splinter. Well, that’s all for this episode. I hope that this helps you evaluate limping kids with a bit more confidence, precision, efficiency, and ultimately lets you communicate rationale for testing and treatments better with families. If you’ve got ideas for other episodes, send them my way. If you wanna collaborate on making a podcast in the future, I’d love to do that as well. If you like this episode of this show in general, share it with your colleagues and. If you have the time, leave a comment on the blog or like rate review the podcast. It helps more people find it and more people learn. If you notice that input adds on this, I’m not making a dime. I just wanna teach people stuff. That’s all for this one, for PEM Currents, the Pediatric Emergency Medicine podcast. This has been Brad Sobolewski. See you next time.

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

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

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, Brad Sobolewski discusses advanced imaging in pediatric emergency care with Dr. Jennifer Marin ([email protected]) from UPMC Children’s Hospital of Pittsburgh. They explore the evidence behind ultrasound, CT, and MRI, strategies to reduce low-value imaging, and the role of shared decision-making in selecting the appropriate diagnostic test. 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: @[email protected] 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 know, I’ll say the benefits of this scan very likely outweigh any of the risks. We don’t know what that risk is. We know that any radiation can be potentially harmful, but when you’re getting imaged at a children’s hospital, for example, and this is a kid who’s not getting imaged every month or every year like some of our adult patients are, then the risks really are generally outweighed by the benefits when you have a high pretest probability of disease. CT does get the lion’s share of concerns about risk and advanced imaging. But there’s two other modalities that we’re talking about today. Really, on one end we’ve got ultrasound, which there’s no ionizing radiation whatsoever. It’s readily available and it’s first line for things like appendicitis, kidney stones, and soft tissue infections. And then at the other end we have MRI, and it’s not just set it and forget it. Now we have rapid protocols and other things. Can you talk specifically about some of these Rapid MRI protocols and how they may supplant CT scans? Yes, so Rapid MRI protocols have really exploded, I would say in the last decade. We actually have four different rapid protocols depending on the scenario, depending on the imaging question, and it’s a wonderful test. I think that there are limitations to it, right? So one is going to be the speed with which you can get it, and our MRI scanners, you know, we don’t have an infinite number, and so we are competing with other patients around the hospital who need MRIs and sometimes kids have to wait two, three plus hours to get it. The other thing though that’s important is a lot of times, you know, the CT gives us good information and it’s fast, but it may not be the best test. And so MRI is going to give us more information depending on the scenario. So I’m thinking about maybe a seizure patient, where an MRI might be a better test than a CT. And so getting the CT is to some extent, only delaying the inevitable because the patient’s ultimately going to need the MRI. So what I initially learned about MRI, it was like this two hour long test. You had to lay in this big machine. It made a ton of noise. You had to put headphones on. When you talk about rapid MRI, like how fast can these patients be in and out of the scanner? So these tests are very fast. They’re not as fast as CT scans. You can get a head CT probably in under two minutes, but you can get a rapid MRI in five to seven minutes. In some cases, if you’re doing a shunt protocol, for example, some of them take a little bit longer, 10 minutes, 12 minutes. But still, to your point, Brad, it’s not this hour long scan that we’re used to seeing and most patients tolerate it well. But – and I’ll go back to your earlier question – one of the limitations of MRI is you can get a scan down to three minutes, but if you’re a 19-month-old who doesn’t want to lay still, it’s not going to happen. So that risk of sedation really becomes something to consider when we’re getting a rapid MRI in a particular age group. Locally, we will not do MRIs on ED patients below six years of age. When I started residency way back in the day, I said to one of my mentors, ‘What am I gonna do about two-year-olds?’ And I was told, ‘Nothing.’ And that has held true all throughout my career. Yes, and so thinking about these imaging modalities, I keep coming back to the fact that most of the time when we’re ordering one, it’s because we’re thinking about what’s next from a management standpoint for the patient. That often involves our subspecialty colleagues, whether that’s our surgeons, our subspecialist surgeons, or other pediatric subspecialties. How are we collaborating with these pediatric specialists to ensure that we’re triaging and effectively making decisions and integrating these decisions into the overall treatment plan for the children we’re caring for in the emergency department? Subspecialists are key, right? And I think that getting multidisciplinary collaboration when we are figuring out what is the best imaging strategy for X is critical. We have clinical effectiveness guidelines, as I’m sure many know, and many pediatric emergency departments have these. These are multidisciplinary guidelines that have been put together that really take into account all the relevant stakeholders and what’s the best imaging test to get the answer that we’re interested in. We’ve collaborated with general surgery, radiology, and all different specialties depending on the scenario, so that we’re imaging in the right way and not having to redo the study. We have different protocols like for kidney stones, where we do a very low dose CT, and we have parameters around which we decide whether to do that CT in lieu of ultrasound for certain patients. None of that would be possible without earlier collaboration with all the relevant stakeholders first. You think about all the different points in your system where the decision could go wrong. You just mentioned a CT protocol for stones. You could order another version of a, you know, abdominal CT and get a study that also looked at the kidneys but wasn’t specific for it. And they’re all on that giant menu. So you have to think from top to bottom in your system and get everybody involved and on board. And I would agree with you completely that I found that’s the only way to drive decisions toward the preferred imaging modality. Everybody that’s a stakeholder has to agree. And you can’t just snap your fingers and make that happen. And we are working in children’s hospitals with tons of resources, world experts, and the availability of tests. But the majority of our patients do not initially seek care in our facilities. We know that nine out of ten children that go to the ER do not go to children’s hospital ERs. And I think some of the concern about low-value imaging or imaging with high risks has to be directed at our children who may receive imaging outside of children’s hospitals. So what can pediatric emergency medicine physicians specifically do to reduce the use of low-value imaging being performed at non-children’s hospitals? You’re absolutely right, Brad. And I always say that I do not envy my emergency medicine colleagues, particularly those practicing in community settings. We really do have so many resources at our disposal, and it is very hard for them to know everything about kids and adults while practicing in locations where they don’t have these consultants available 24/7. I think it’s very important, almost an obligation, for us to provide outreach and education to our community ED colleagues so that they are given the tools needed to provide the right imaging to the right patient at the right time. So I’ll give you a couple of examples. At UPMC, we have many hospitals as part of our system, but only one pediatric children’s hospital. And so we routinely do outreach with our community providers. There’s an education series, a lecture series, and I had the opportunity to give a talk on this very topic to those providers. It was all these medical directors at other hospitals who then had the opportunity to cascade down the message about low-value imaging, when to image, when not to image. We provided resources, which I’ll talk about in a little bit, and, you know, hopefully that will lead to less low-value imaging in the community setting. Another recommendation that I have is regarding transport calls. We all take transport calls when we’re practicing at the ‘mothership.’ Patients are getting transferred, and I think having a conversation with the doc at the point of care, even if imaging has already been done — and maybe it was low-value or could have been avoided — I think it’s important to talk to the provider and say, ‘Hey, you know what? Just so you know, next time you have a kid like this, don’t feel like you have to image them. We are happy to take this kid without imaging.’ It’s going to save time, it’s going to save us having to upload the disc that may or may not be corrupted. It’s going to save the patient, potentially, another scan because they were moving all over the table because the techs at the referring hospital aren’t used to trying to manage a wriggling infant. I almost empower them to not necessarily do imaging because I think that there is this common misconception in the community setting that you can’t transfer a patient unless you know what the diagnosis is or unless you have imaging available. And that’s really not the case at all. Talking about some of the resources in the guidelines that we published, the policy statement and technical report that we published in Pediatrics and in some other journals, statements on advanced imaging in children who present to the emergency department. It was authored by the American Academy of Pediatrics, the American College of Emergency Physicians, and the American College of Radiology. Those statements were published, and one of the documents that I think is very useful is the supplement to the technical report, which includes several publicly available clinical effectiveness guidelines from various children’s hospitals all over the country. These can be used at the point of care to help with decision-making so that we’re providing high-value care and performing high-value imaging. Before we bring this episode to a close, there’s one other subject I wanted to talk a little bit more about, and it’s incidental findings. You know, it’s when we get a study right, and we discover something that we weren’t expecting to see. I think, colloquially, it’s gotten the name ‘Incidentaloma.’ How do you suggest we approach when we discover something that we weren’t expecting to see? What does that mean for patients and families? And is there a cascade of decisions that happen because of that that could have been avoided? Absolutely. Yeah. I don’t think we talk about these enough because we don’t have to deal with them in the ED. So an incidental finding is something that a radiologist sees on the imaging study that means nothing. It doesn’t cause the patient any harm, and it’s certainly not the reason for their symptoms. But when you tell someone that they have a nodule, let’s say, on their lung from a CT PE study, that then sparks what we call ‘care cascades.’ And they have to follow up on that. It’s an extra visit, time off work, time out of school, an extra cost, anxiety-provoking. And maybe they need to follow it up every three months. It’s a real burden on families and on the healthcare system more broadly and probably something that doesn’t get enough attention in emergency medicine. So, I would encourage folks when they’re ordering tests, particularly if the pretest probability is very low, to think about the risks, including incidental findings and how they’re really not insignificant. Before we end our conversation, what final words of advice do you have for someone who’s going to have a shift soon after they listen to this episode? What’s one thing that they can take to the bedside in an upcoming discussion with a patient and their family? Understanding that imaging isn’t always necessary to make a diagnosis, and that’s something that I think today’s trainees need to hear, and also some of the families need to hear. There’s so much information available online, as you know, and Facebook groups and resources and ‘My friend, my grandmother,’ etc., and it can be overwhelming. Taking the time to explain to families, especially those who are expecting imaging or have questions about imaging, why we aren’t doing imaging and the risks associated with it, which are very real — I think that that carries a lot of weight. What about other healthcare teams that interface with our patients when they may be requesting tests that we’re concerned pose additional risks or costs to patients? How do we have a collaborative discussion with them when there’s a difference of opinion about what best to do for a patient? Yes. I think you answered it, actually, Brad — having a collaborative discussion. A lot of times when we consult a service, it’s a resident who might be at another hospital. They have to come to our hospital. They’re just reflexively asking for imaging. I say to the resident, ‘I’m going to call that resident back.’ And I’ll say, ‘You know what? I would really love for you to just see the patient before we talk about getting a CT because I don’t think the kid needs a CT.’ Most of the time, that works really well. Sometimes they’ll say, ‘Well, here’s why I want the CT,’ and I’ll say, ‘Oh, that’s really helpful. We’ll go ahead and get it.’ So I think having a conversation and questioning in a very respectful way can be eye-opening on both sides. And that is a conversation that is best had by voice or face-to-face. It can be uncomfortable to feel like you’re going to have a disagreement with somebody. But ultimately, everybody’s goal is the same — just to do what’s right for the kid and their family. And the other people that are really smart and amazing and wonderful are radiologists. We should always be willing to call them on the phone. They’re not just the test referral center. You don’t just put in the test and get it. Sometimes we should be calling them and saying, ‘Here’s the problem I have at hand. What’s the best way that we can safely image this child?’ Jen, thank you so much. Tons of fascinating information. As I mentioned before, I will put links to all of these excellent resources in the show notes. I hope that in listening today, you will come up with some new ways to approach these issues with patients and families, as well as the folks we collaborate with. And don’t be afraid to have those discussions with folks calling in from other institutions. We all have the same goal. And ultimately, it’s on us working in pediatric emergency departments to disseminate that best information. Jen, thank you very much. Brad, thank you so much. It was such an honor. I had a really nice time. Thank you. Alright, that’s all for this episode. I hope you now understand what the term ‘advanced imaging’ encompasses — ultrasound, CT, MRI — the radiologic studies that we use to make diagnoses every day in the emergency department on children. Sometimes these tests are necessary; sometimes they’re not. We have to collaborate with patients, families, our radiology colleagues, the other specialists we collaborate with, and providers working at community EDs to decide whether to image and, if we do, to get the right test that will get us the most accurate results with the least risk. So if you liked this episode, share it with a colleague, leave a review on your favorite podcast site, or send me a comment via email, on the blog, or via social media. For PEM Currents: The Pediatric Emergency Medicine Podcast, I’m Brad Sobolewski. See you next time.

In this episode, we tackle the clinical mischief of Parvovirus B19, a common viral infection with a surprisingly wide range of manifestations—from the classic “slapped cheek” rash of erythema infectiosum to aplastic crises in children with hemolytic anemias and fetal hydrops in pregnant contacts. We’ll break down the virology, epidemiology, clinical presentation, and complications of Parvovirus B19. You’ll also learn how to manage exposures in the emergency department, especially when the child has a pregnant caregiver, and why isolation isn’t always necessary once the rash shows up. 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: @[email protected] 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 infection. Management of erythema infectiosum is supportive care only—antipyretics, hydration, and reassurance. The rash can be itchy; use moisturizers or antihistamines like cetirizine. Explain to families that the rash may last for days to weeks and can worsen with sunlight. I’ve seen a lot of visits in urgent care where this is the main concern during outbreaks. For joint symptoms, use NSAIDs. A patient with transient aplastic crisis will likely need hospitalization and red blood cell transfusion, especially if unstable. In immunosuppressed patients with chronic infection, treat with IVIG and carefully consider immunosuppressive management. What if the child has a pregnant caregiver? The child is most contagious **before** the rash appears—during the viral prodrome—so it’s easy to mistake for another virus. Once the rash appears, the child is no longer infectious. If a pregnant household contact was exposed during the contagious period—especially in the first or second trimester—they should contact their OB provider for serologic testing (IgG and IgM). If seronegative, serial ultrasound may be recommended to monitor for fetal hydrops. Isolation of the child is not necessary after the rash appears. If they are in the viremic phase, then hand hygiene and respiratory precautions are important to limit household spread. Take-home points: Parvovirus B19 can cause a range of presentations—from slapped cheeks to life-threatening anemia. It’s a clinical diagnosis, especially in typical cases. If you’re not familiar with the rash, look it up—so you’ll recognize it in the ED. In patients with red cell disorders or immunosuppression, use PCR or serology. Don’t miss a transient aplastic crisis in a child with sickle cell. And remember: once the rash appears, the child is no longer contagious. The virus spreads during the early, flu-like phase. Thank you for listening to this episode. If you found it helpful, let me know. Leave a review, shoot me a message on social media or email, and share it with your colleagues and learners. And as my 13-year-old would like to remind me: like and subscribe. For PEM Currents, this has been Brad Sobolewski. See you next time.

This episode of PEM Currents: The Pediatric Emergency Medicine Podcast focuses on the approach to unvaccinated or undervaccinated children aged 3–36 months presenting to the ED with fever. Host Brad Sobolewski reviews differences in immune response, risk for serious and invasive bacterial infections, and outlines evaluation strategies including labs, imaging, and empiric antibiotics. He highlights data showing increased interventions in this population and calls for local guideline development. The episode emphasizes thoughtful, individualized care in the context of rising vaccine hesitancy and declining immunization rates. 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 appearing and have no identifiable source of infection do have a self-limited viral illness. And in all of these kids, you gotta assess vaccine status, travel history, sick contacts, any immune compromise, and any symptoms of localizable bacterial infection to evaluate the risk of serious illness. So serious bacterial infection defined as any bacterial infection requiring medical intervention, but it may not invade sterile sites. It’s like a UTI pneumonia skin and soft tissue infections like cellulitis and abscess. An invasive bacterial infection is a subset of serious bacterial infection where the bacteria gets into sterile body sites like blood and CSF. It’s bacteremia, meningitis, osteomyelitis, septic arthritis, and. Let’s be honest, fever is still the most common complaint for infants and children brought to the ed. It’s greater than 6% of all ED visits. Most of these kids under 36 months will have some clinically apparent source of infection, even like a obvious URI or otitis media, and about one out of five of these children though a source cannot be identified during the h and p. Certainly any child who’s ill appearing or has unstable vitals should be managed for presumed sepsis or septic shock, and that’s not the focus of this podcast episode in well Appearing Children with Fever. The main goal is to determine the risk of a clinically occult bacterial infection. I. So with that, let’s run through a few of these common bacterial infections. So let’s start with urinary tract infections. So this is the most common occult bacterial infection in febrile infants and young children. And children under the age of two. Fever may be the only symptom. The prevalence is roughly eight to 10% in young children with fever. Greater than 39 Celsius. Risk factors include age, female sex circumcision status. You should definitely use UTI calc. To help estimate the risk and the presence of another infection, like URI. Acute otitis media or gastro doesn’t completely rule out UTI, but in select scenarios like bronchiolitis with RSV, it does reduce the risk a bit. Females, three to 24 months with fever greater than 39 and no source, the risk could be as high as about 5%. Uncircumcised. Males with high fever and no source probably have a similar risk to females, but circumcised males have a risk of 2% or under. You should also think about testing if there’s been fever for greater than 48 hours. If there’s history of UTI or any known GU anomaly, even like hypos, SPADs, and you can cath, you can clean catch, you can use the quick wee maneuver or even a super pubic aspiration which parents don’t like. Alright, let’s talk about occult bacteremia. And honestly, when we talk about this topic, it’s the thing that we worry the most about. It’s the presence of bacteria in the blood of a febrile, well appearing child in the absence of an identifiable focal bacterial source of infection. So in the pre HIB and Prevnar era, this was like three to 11% of febrile children. Streptococcus pneumonia made up 73 to 90% of these, and HIB made up eight to 22%. Hib was way more likely to cause meningitis. In fact, in 5% of bacteremia, kids with hib, they had meningitis. Really high rate. In the post vaccine era, the rate of occult bacteremia is. Point two five to 1%, so it’s less than 1%. A third of these are e coli. A third are non-vaccine serotype, streptococcus pneumonia, and the other third are staph aureus, salmonella species, RIA meningitis, and strep pyogenes. Interestingly, both then and now, 95% of occult bacteremia is caused by strep pneumo resolve without IV antibiotics. These are all well appearing kids in which this happens, so we actually probably never know that some of these kids have it. There’s a higher risk of occult bacteremia in children younger than four months of age, children with high fever, 39 or 40, and unvaccinated, and we’ll talk about labs in a little bit, but elevated white count A and C procalcitonin band count. These are all things that can be used to assess the risk. In preparation for this episode, I had the pleasure of talking to some folks that practiced in the pre HIB and Prevnar vaccine era, and what they told me was interesting. They said that. Ultimately you could reduce a kid’s fever and that still didn’t reduce the risk of them having bacteremia. So they still had to work these kids up. But if the kid looked great after they responded to Antipyretics, well, they probably didn’t have meningitis. I. And so I alluded to this a couple minutes ago, but, uh, let’s talk about lab characteristics for oc cult bacteremia in the post vaccine era. Let’s start with the CB, C and differential. And yes, we all know that CBC is not a good indicator of whether the child has a bacterial infection or not, but in this specific population, based on the available research, a white blood cell count greater than 15,000 does have a sensitivity of 72%. And a specificity of 55%. This is based on one study from Hertz in, uh, pediatric infectious disease, and in their study though, the rate of a true positive blood culture was 1.6% and the contaminant rate was 1.8%. Interesting. A NC per Cooperman, etal and Annals of Emergency Medicine in 1998 of greater than 10,000 was a slightly better indicator and absolute band count of greater than 1500. It’s also been suggested. None of these are perfect. So what about procalcitonin? And I know it’s not available everywhere, but it probably does have a better. A test characteristic than white blood cell count and a NC. Generally, the threshold is set at 0.5 nanogram per milliliter, but some sites suggest the threshold of greater than two and trella in the expert. A review in of anti infectious therapy journal in 2017 noted that it had a sensitivity of 82%, specificity of 86%, and a positive likelihood ratio of six. And Van den Bruel in BMJ 2011 found procalcitonin to have better specificity than white blood cell count. Now let’s talk about pneumonia. So most children but bacterial pneumonia have some sort of abnormality. On exam. In pro-vaccine era studies, 20 to 40% of three to 36 month old with fever greater than 39, and no clinical evidence of pneumonia, but with a white blood cell count greater than 20,000 actually had low bar or segmental pneumonia on a chest x-ray. In a study published in pediatric emergency care in 2009, Rutman and colleagues in a retrospective cohort of children less than five found that in comparison, occult pneumonia was identified more often. Pre PCV. Then post PCV, so about 15% to 9% in kids younger than two, though the rate was higher. Pro-vaccine era, 17% and post vaccine era at 10%. So in the UN or under vaccinated kid with a temp greater than 39. If you get a white blood cell count and it’s greater than 20,000, you should get a chest x-ray, even if the kid has a normal lung exam. And now let’s talk about blood cultures and. How many of you have heard from a nurse? Well, while, I’m getting the line. Why don’t I just draw a blood culture? So it’s either okay in these children to send it right away or to hold it until you get the labs back. And I think I would consult local practice variation, um, and what your colleagues do and the risk of contamination will not increase while the blood culture sits if it was obtained correctly. And every hospital’s lab is different, but some of the bacteria that are considered common contaminants include bacillus. corynebacterium, cutie bacterium acnes, which was p acnes and micrococcus. Other contaminants include staphylococcus epidermis and the reins group. As long as the patient doesn’t have any risk of endocarditis, any other bug that grows. We’re talking staph aureus, strep pneumonia, strep pyogenes, enterococcus, e coli. These are all probably true pathogens. Let’s say a blood culture is sent and then it comes back positive. So these kids should, in most cases, especially if it’s suspected to be a real pathogen, be reevaluated in the emergency department. If kids are febrile at reevaluation, there’s a 40% chance of persistent bacteremia. And if they’re ill appearing about a one in 25 or 4% chance of meningitis. So these kids, if they’re ill appearing in febrile still, they need a full sepsis evaluation plus an LP iv antibiotics and admission. I. If they’re afebrile reevaluation, probably only about a 9% chance of persistent bacteremia. And though we don’t know the exact numbers, that risk might be a little bit higher in unvaccinated children. So you can repeat the blood culture in labs and these well appearing kids, but you don’t necessarily have to tap them a positive blood culture for nisia meningitis, HIB gram-negative rods, or other pathogens. Well, these always deserve a full sepsis workup. LP IV antibiotics and admission. If the kid’s afebrile and well appearing and they’re more than three months of age and they’re positive for e coli or staph aureus, they might not need an LP consult your local practice variations. Um, and any kid with group B streptococcus bacteremia, who’s three to six months of age definitely needs an LP and admission, and that only scratches the surface. Admittedly, um, this can be a complex topic, so I would consult your local ID recommendations and hospital practice to determine what you should do based on what grows in your culture. I think now that we’ve talked about occult infections in some of the labs, you may be wondering, broadly speaking, do UN or under vaccinated children actually have more stuff done to them in the ed? And the answer is probably, but we actually don’t know the broad answer. And so going back to that original study from Indiana, these kids that were. Not fully immunized, so UN or under vaccinated, were 83% more likely to get an intervention and 99% more likely to receive an antibiotic prescription, a discharge. So this included all sorts of interventions, like blood testing, urine studies, chest radiographs. So ask yourself, what do you do if a kid is on or under vaccinated? Has a fever greater than 39, and is three to 36 months of age, are you working ’em up? What do your colleagues do? Do you have a practice guideline where you work? In fact, is there a consensus guideline for the management of the UN or under vaccinated child with fever? And the answer to that unfortunately is no. No, there is not. Not from the A A P, not from the Infectious Disease Society of America, not in Red Book, not anywhere. So I’m gonna suggest one possible way to work these kids up with the caveat being that again, there’s no consensus, so. For a child with fever greater than 39 degrees centigrade, who is well appearing, but unvaccinated or under vaccinated, who is between three to 36 months of age, you might want to consider getting procalcitonin CBC with differential urinalysis and urine culture if they meet the risk factors. And again, I would use UTI calc for that. Any viral detection assays that you deem necessary. And you can draw blood culture and send immediately or send after the procalcitonin or CB, C results. So if the white blood cell count is greater than 20,000, regardless of the physical exam, you should get a two of you chest x-ray to assess for occult pneumonia. If the procalcitonin. Is greater than 0.5. The white blood cell count is greater than 15,000. The a NC is greater than 10,000 and or the absolute band count is greater than 1,500. Then you should send the blood culture if you haven’t already done so and give empiric antibiotics against streptococcus pneumonia. For most patients, this should be ceftriaxone 50 milligram per kilogram intramuscular. This depot version of antibiotics will provide coverage for 24 hours. It’s not the same as giving an IV dose. So yes, this is an IM dose. If they have an allergy to cephalosporins, you can give Clindamycin 10 milligram per kilogram iv followed by the first oral dose. Eight hours later. Add UTI. Treatment is warranted based on your testing. If all of those labs. Are below those thresholds, then antibiotics are not recommended unless the urinalysis says otherwise. So after the labs are back, you reassess the patient. Are they well appearing? Are they well hydrated and demonstrating good oral intake? Do they have a parent, guardian or caregiver that has no significant social barriers and. Can they follow up with their primary care doctor or at your facility within 24 to 48 hours? If yes to all of those, you can send them home. If not, eh, you should probably admit them to the hospital. I. Now again, this is just one way to consider working up the unvaccinated or unvaccinated child age three to 36 months of age, who is well appearing with fever greater than 39 degrees Celsius for less than five days. This is not the official recommendation of my hospital or any that I know of, and I hope this inspires you to develop your own practice patterns and perhaps more importantly, have conversations locally where you work about better defining. How we evaluate and manage these children because unfortunately. Their ranks are increasing. Well, I hope you found this episode on the approach to the unvaccinated and unvaccinated child with fever in the ed thought provoking. I hope it helps sharpen your thinking and clinical decision making and inspires you to have conversations locally about your practice patterns in these vulnerable children. If you enjoyed the episode, be sure to like, subscribe, leave a review wherever you get your podcasts. Billy helps other folks find the show. You got feedback. Send it my way. I’ll take it over social media. I’ll take it via comments. I’ll take it via email, as always, for PEM Currents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.