PEM Currents: The Pediatric Emergency Medicine Podcast

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.

In this episode we dive into the resurgence of Mycoplasma pneumoniae—an atypical bacterial cause of community-acquired pneumonia that’s making waves in pediatric emergency medicine. We’ll cover its clinical presentation, epidemiology, diagnostic approach, and management, including why standard beta-lactam antibiotics won’t work. Plus, we’ll discuss whether M. pneumoniae even needs to be treated in the first place! Learning Objectives Describe the clinical presentation, epidemiology, and complications of Mycoplasma pneumoniae infections in pediatric patients, including its atypical manifestations. Differentiate Mycoplasma pneumoniae pneumonia from typical bacterial and viral pneumonia based on history, physical exam findings, and diagnostic testing. Assess the current evidence for antibiotic treatment of Mycoplasma pneumoniae and justify treatment decisions based on patient presentation, severity, and potential complications. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo References Vallejo, Jesus G. “Mycoplasma Pneumoniae Infection in Children.” UpToDate, 1 Nov. 2024, www.uptodate.com/contents/mycoplasma-pneumoniae-infection-in-children. Garcia T, Florin TA, Leonard J, Shah SS, Ruddy RM, Wallihan R, Desai AP, Alter S, El-Assal O, Marzec S, Keaton M, Yun KW, Leber AL, Mejias A, Cohen DM, Ramilo O, Ambroggio L; Children’s Hospitals Initiative for Research in Pneumonia (CHIRP). Clinical Features and Management Strategies in Children With Mycoplasma Pneumoniae. Pediatr Emerg Care. 2025 Feb 17. doi: 10.1097/PEC.0000000000003338. Epub ahead of print. PMID: 39960098. Gao L, Sun Y. Laboratory diagnosis and treatment of Mycoplasma pneumoniae infection in children: a review. Ann Med. 2024 Dec;56(1):2386636. doi: 10.1080/07853890.2024.2386636. Epub 2024 Aug 3. PMID: 39097794; PMCID: PMC11299444. Shah SS. Mycoplasma pneumoniae as a Cause of Community-Acquired Pneumonia in Children. Clin Infect Dis 2019; 68:13. “Mycoplasma Pneumoniae Infections Have Been Increasing.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 18 Oct. 2024, www.cdc.gov/ncird/whats-new/mycoplasma-pneumoniae-infections-have-been-increasing.html. Transcript Note: This transcript was partially completed with the use of the Descript AI  Welcome to PEMCurrents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re focusing on a pathogen that has been making waves in pediatric emergency departments across the country. Mycoplasma pneumoniae. Whether you know it or not, you’ve likely seen a surge where you work. Patients are presenting with community acquired pneumonia that isn’t responding to standard beta lactam antibiotics, or with parents who are just concerned that their child has walking pneumonia. That’s because mycoplasma pneumonia is just a little bit different than most of the pathogens that we deal with in children. So let’s dive in. So, what is it? Microbiology lecture. Warning, med school trigger. Uh, so Mycoplasma pneumoniae is a small, obligate intracellular bacterium and it lacks a cell wall. So that’s why it doesn’t respond to beta lactam antibiotics like penicillin and amoxicillin and cephalosporins. Instead, it requires macrolides, tetracyclines, or fluoroquinolones for treatment. It’s spread via respiratory droplets and thrives in crowded environments such as schools and daycare centers. It binds to the epithelial cells in the upper and lower respiratory tract, triggering an immune response that leads to mucosal damage, increased mucus production, and impaired gas exchange. So mycoplasma pneumonia infections have been on the rise, especially in children. After a lull during the COVID 19 pandemic, cases reemerged in 2023 and continued to climb into 2024. Historically, mycoplasma pneumonia has been most common in children aged 5 to 17 years and young adults. But what’s new is that we’ve seen a striking increase in infections among children aged 2 to 4. Per the CDC, diagnosed mycoplasma infections increased steadily through the summer of 2024, peaking in August for 2 to 4 year olds and 5 to 17 year old age groups. There’s also been an increase in diagnosis in those under 12 months of age. This is all notable because these infections have historically been thought to affect school aged children much, much more than younger children. All right, let’s talk about clinical features. So the incubation period for mycoplasma pneumonia can be around two to three weeks. Symptoms often start gradually, with fever, headache, malaise, and sore throat, preceding the onset of a persistent dry cough. Unlike classic or typical bacterial pneumonia, which has abrupt onset in focal lung findings, mycoplasma pneumonia patients often present with a prolonged worsening cough that can persist for weeks to months. The name walking pneumonia was coined because people with this mild form of respiratory infection can still walk around and do their normal activities. It’s attributed to, but not exclusive to, mycoplasma disease. Now some patients can develop severe pulmonary complications, fortunately those are rare. These include respiratory failure, pleural effusions, necrotizing pneumonia, and pyema. Beyond the lungs, mycoplasma pneumonia is a weird bug, and it can also cause some extra pulmonary manifestations. So you can get mucocutaneous disease, including erythema multiforme. and mycoplasma induced rash and mucositis, also known as RIME, and even Stevens Johnson syndrome. Patients can get joint pain, you can have a hemolytic anemia due to IgM antibodies causing an autoimmune hemolysis, or even neurological complications such as meningoencephalitis, seizures, transverse myelitis, or even Guillain Barre syndrome. Alright, so making the diagnosis starts with having a firm understanding of bacterial versus viral etiologies of pneumonia. And generally, we should make this diagnosis clinically. So typical bacterial pneumonia, like streptococcus pneumoniae, is more likely when symptoms such as fever, chills, cough, and focal chest pain start abruptly. These patients often have respiratory distress or tachypnea and focal lung findings like rails or crackles or decreased breath sounds. A typical bacterial pneumonia, like mycoplasma pneumonia, presents with a gradual onset of fever, headache, malaise, sore throat, followed by the worsening non productive cough. It’s often accompanied by wheezing and or rails, and fever and illness are typically milder. than in the classic bacterial pneumonia. Now viral pneumonia, which is also all over the place, and due to RSV, parainfluenza, influenza, adenovirus, and more, is more common in children under 5 years of age. The cough develops gradually following an upper respiratory tract infection, and lung findings are diffuse and bilateral, often with wheezing. Think of viral pneumonia like bronchiolitis, but in a preschooler instead of a baby. And so while mycoplasma pneumonia is often a clinical diagnosis based on presentation, there is some confirmatory testing. PCR testing of the nasopharynx, or throat, is highly sensitive and specific. You can get serology, which will detect IgM and IgG antibodies. It’s useful, but it takes longer to result. The caveat of these serologic tests is that There’s probably a lot of seropositivity without symptoms in the general population. So basically, many people could have positive mycoplasma without symptoms. There are no distinguishing features on blood labs like CBC and blood culture, which are generally not necessary in these patients unless they’re critically ill. And the chest x ray findings, if you need them, will typically show bilateral patchy infiltrates, though some cases can have unilateral lobar consolidations. So as you might imagine, chest x rays aren’t as useful as you’d think in diagnosing mycoplasma. When it comes to management, first and foremost, supportive care. Treat fever, ensure adequate hydration, and provide respiratory support as needed, like if kids need oxygen, that sort of stuff. Cough suppressants and cough medicines are generally ineffective and no better than honey, and really not recommended in many age groups, but if you’ve got a middle schooler or teenager and parents want to try it, eh, have at it. Or don’t. Before I talk about antibiotics, I do want to bring up the question as to whether or not we actually have to treat mycoplasma in the first place. Studies supporting antibiotic treatment of documented mycoplasma pneumoniae in children are limited. Supports provided predominantly by in vitro studies, a randomized trial in military recruits, and some observational studies in which inclusion of mycoplasma pneumoniae specific therapy was associated with a decreased risk of treatment failure. So, whether that’s a change in antimicrobial therapy or a hospital admission, or length of stay in children with community acquired pneumonia, but they didn’t have etiologic data in that study. There was a systematic review of 17 studies, including 4, 294 patients, where they found insufficient evidence for the efficacy of antimicrobial treatment of mycoplasma pneumonia, lower respiratory tract infection in children less than 17 years of age. There was publication bias, heterogeneity, and lack of blinding. We also don’t know whether administration of antibiotics decreases the incidence or severity of associated mucocutaneous disease. And I’m not even going to get into pans or pandas here. I can’t bear it. So, yes, I’m going to talk about antibiotics. But consider this scenario, you’ve got a kid, cough and wheezing, you think it’s a virus, maybe it actually is mycoplasma, there’s a good chance they’ll be fine anyway, even if you don’t treat it. So yes, think of mycoplasma pneumoniae, but don’t make it your sole focus when you’re really just dealing with viral pneumonia in a lot of kids. Okay, the first line treatment is azithromycin. The ZBA is actually all right, so it’s 10 milligram per kilogram in one dose, max dose of 500 milligrams. That could be orally or IV on the first day, and then five milligram per kilogram in one dose. Maximum dose of 250 milligrams for the next four days. If azithro is unavailable, or in the case of an allergy, you could use doxycycline two to four mgs per kg per day, orally or iv. in one or twice daily dosing. The max daily dose is 200 milligrams, and it’s done for seven days. Compared with other tetracycline antibiotics, doxy is much less likely to cause permanent tooth discoloration in young children, and it can be given safely for less than 21 days to children of all ages. Tetracycline for kids greater than eight years of age, and azithromycin are also options, but azithromycin has lots of GI side effects. For immunocompromised children, especially with previous exposure to macrolides, fluoroquinolones like levofloxacin are an alternative initial agent. Fluoroquinolones are bacteriocidal rather than bacteriostatic, and the dosing for levofloxacin varies according to age. So greater than six months but less than five years. Levofloxacin is 8 10 mg per kg per dose orally or IV every 12 hours. The max total daily dose is 750 mg and you treat for 7 10 days. For kids older than 5 years, you do Levofloxacin 10 mg per kg per dose once per day orally or IV. And that max dose is again, 750 milligrams per day for seven to 10 days. All right, so let’s talk about some take home points. So mycoplasma pneumonia is back with a vengeance after the COVID 19 pandemic, and it is affecting younger children more than ever before, especially kids, two to four years of age. For most patients, it is a clinical diagnosis. You should think about it, though, in kids with classic presentations, or in a child who has failed treatment with beta lactams for a presumed community acquired pneumonia. And don’t fear the Z Pak, right? If you diagnose mycoplasma pneumonia, macrolides and zithromycin are the first line treatment. Fluoroquinolones are good for immunocompromised children. Mycoplasma can cause extrapulmonary disease. So, go online and look up some pictures of the mucocutaneous manifestations. There are also hematologic and neurologic complications. And keep an eye on outbreaks and community trends. The epidemiology is shifting, and infections are rising, so your hospital should have a local plan to deal with infection in your community. Thank you so much for listening to this episode. If you found it helpful, let me know. Leave a review, send a message on social media or email, and share it with your colleagues and learners. And as always, as my 13 year old would say, don’t forget to like and subscribe. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.

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

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

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore pertussis, also known as whooping cough – a disease that remains a public health challenge despite widespread vaccination efforts. We will review the clinical presentation, diagnostic strategies, management protocols, infection control practices, and vaccination updates. This episode also covers what healthcare providers need to know about post-exposure prophylaxis, respiratory precautions, and managing occupational exposures. Learning Objectives Understand the clinical progression of pertussis through its three distinct stages and identify key symptoms, including age-specific presentations in infants and older children. Implement effective management strategies for pertussis, including supportive care, appropriate antibiotic regimens, and post-exposure prophylaxis for contacts and healthcare providers. Promote pertussis prevention by understanding vaccination schedules (DTaP vs. Tdap), addressing vaccine hesitancy, and adhering to infection control protocols in clinical settings. Connect with Brad Sobolewski PEMBlog: PEMBlog.com Blue Sky: @bradsobo X (Twitter): @PEMTweets Instagram: Brad Sobolewski Mastodon: @bradsobo How about a fun AI song about whooping cough? YouTube Shorts TikTok References StatPearls Lauria AM, Zabbo CP. Pertussis. [Updated 2022 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519008/ AAP Pediatrics in Review Heather L. Daniels, Camille Sabella; Bordetella pertussis (Pertussis). Pediatr Rev May 2018; 39 (5): 247–257. https://doi.org/10.1542/pir.2017-0229 UpToDate Yeh S et al. Pertussis infection in infants and children: Clinical features and diagnosis. UpToDate. Available at: https://www.uptodate.com. Accessed December 3, 2024. MMWR Seither R, Yusuf OB, Dramann D, et al. Coverage with Selected Vaccines and Exemption Rates Among Children in Kindergarten — United States, 2023–24 School Year. MMWR Morb Mortal Wkly Rep 2024;73:925–932. DOI: http://dx.doi.org/10.15585/mmwr.mm7341a3 Transcript Note: This transcript was partially completed with the use of the Descript AI Welcome to PEM Currents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobolewski, and today we’re talking about pertussis, a disease that is challenging clinicians and public health officials alike. Despite being vaccine preventable, Pertussis is on the rise, yet again, fueled by declining vaccination rates, waning immunity, and the fact that people can’t stop coughing on each other. In this episode, we’ll go over clinical presentation, diagnosis management, infection control, and post exposure protocols. So pertussis, or whooping cough, is caused by Bordetella pertussis, a gram negative coccobacillus. It definitely spreads via respiratory droplets, and has no environmental or animal reservoirs, making humans the sole carriers. The incubation period averages about 7 to 10 days, and the disease progresses through some distinct clinical stages, which I will go over in a moment. Pertussis has been recognized since the 16th century. I was not practicing medicine back then. Um, with the first documented epidemic occurring in Paris in 1578. Bordetella pertussis was isolated in 1906 by Belgian researchers, Jules Bordet and Octave Gengou, I hopefully I pronounced them right, but they’re long gone, so they won’t be mad at me,, leading to the development of a whole cell pertussis vaccine in the 1940s. Introduction of the DTP, the diphtheria tetanus pertussis vaccine, dramatically reduced disease incidence overall. In the 1990s, we got the acellular pertussis vaccine, the DTaP, which replaced the whole cell formulation due to concerns about some side effects. So pertussis remains endemic in many regions of the world despite vaccination efforts. During the 23 24 school year, DTaP coverage among kindergartners in the United States dropped to 92. 3%, which is below the 95 percent threshold needed for herd immunity. That is is why we’re seeing an outbreak now. This is a pretty troubling trend that began during the COVID 19 pandemic and has just gotten worse since. The exemption rate for vaccines rose to 3. 3 percent. This is the highest on record. Non medical exemptions accounted for over 93 percent of these exemptions. And 14 states in the U. S. have reported exemption rates exceeding 5 percent. Idaho is leading at 14. 3 percent. So the implications of these declining vaccination coverage rates are significant and that’s why we’re seeing more and more outbreaks, especially putting our vulnerable populations at highest risk. Alright, let’s get back to the clinical presentation. Wait, what’s that sound? Hold on. Coughing. Yeah, so that’s the whoop and the cough of pertussis. And I’d wager that many of you have not yet heard that clinically, so that’s why I included it on this episode. So here’s the stages of disease. First is the catarrhal stage, which lasts one to two weeks. You have rhinorrhea, mild cough, and a low grade fever, if any. You are highly contagious during this phase, but it’s often unrecognized as pertussis. Then, in the next two to eight weeks, you have the paroxysmal stage. You have these severe paroxysms of coughing, the inspiratory whoop right beforehand, post tussive emesis. Infants, especially under six months of age, may present atypically with just apnea, cyanosis, or bradycardia. for that. Following that, you have the convalescent stage, which lasts weeks to months. You have gradual resolution of symptoms, though residual cough may persist. That’s why they call it the 100 day cough. Aside from coughing forever, there’s some important complications you need to be aware of. And they can be severe, especially, as I noted earlier, in young infants. So respiratory complications include apnea, secondary bacterial pneumonia, and pulmonary hypertension. Children encephalopathy, often due to hypoxia. And the mechanical complications can include rib fractures, subconjunctival hemorrhage, and even rectal prolapse due to intense coughing and valsalva. Greater than 50 percent of kids under 12 months of age with pertussis could require hospitalization. 50 percent of those kids will have apnea, 20 percent will have pneumonia, and up to 1 percent will die. Encephalopathy occurs in about 20 percent of mortality cases, probably due to hypoxia, or maybe the toxin produced by the bacteria itself. So, making the diagnosis of pertussis starts with high index of clinical suspicion. Early diagnosis, as you’d suspect, is critical to limiting disease spread and initiating treatment. So, PCR testing, which is widely available now, has high sensitivity in the first three to four weeks and is the preferred diagnostic test. Culture is the old gold standard, but it’s slower and less sensitive. It can take up to a week to grow. CBC might show significant lymphocytosis, um, most often in infants, but it ain’t going to make the diagnosis of pertussis for you. And a chest x ray will just show you some non specific findings, such as peribronchial thickening in severe cases. And unless you’re worried about concomitant bacterial pneumonia, you probably don’t need a chest x ray to make the diagnosis of pertussis. You can get an isolated pertussis PCR, or Or it can come as part of a respiratory panel. But remember those comprehensive viral respiratory panels cost 1, 600. So if you’re just worried about pertussis, don’t get the whole panel. So management starts with supportive care. Infants with apnea, cyanosis, or feeding difficulties should obviously be admitted to the hospital. They may need oxygen and or nutritional support. And you definitely have to watch those kids very closely for the complications such as hypoxia and secondary infections. Remember, a tiny baby with pertussis can go apneic at a moment’s notice even without a persistent cough. Antibiotics reduce transmission. But do not significantly alter disease progression once the paroxysmal stage begins. So again, you are treating with antibiotics to prevent more people from getting sick, more so than shortening the duration of illness. The main antibiotic that we use is azithromycin. For infants under 6 months of age, that’s 10mg per kg daily for 5 days. For children older than 6 months of age, 10mg per kg, max of 500mg on day 1, followed by 5mg per kg per day, max of 250mg on days 2 through 5. That is the same dosing that you can give to a grown up. An alternative treatment, you would be trimethoprim sulfamethoxazole for patients who are allergic to macrolides. Post exposure prophylaxis is recommended for household contacts, so the people that the index patient lives with, any high risk individual, and infant, pregnant women, or immune compromised individuals that have been in any sort of contact with the person with pertussis, and and a health care worker exposed without appropriate PPE. Again, pertussis spreads through respiratory droplets. So this necessitates strict infection control. So that starts in triage. So if you think that a patient has pertussis, then they need to be place on droplet precautions as soon as they are assessed. You wear a surgical mask and eye protection, so goggles or a face shield, and you want to maintain these precautions for five days after starting effective antibiotics or for 21 days if the patient is untreated. As a clinician, Just ask yourself, did you wear appropriate PPE, mask and goggles? Don’t get lazy. Was the exposure prolonged or close? And rely on infection control in your institution to help decide whether or not you need post exposure prophylaxis. If you’re vaccinated and you wore PPE, you don’t need anything. Unless you have symptoms. If you’re vaccinated and you did not wear PPE, then prophylaxis is recommended. If you’re unvaccinated and not up to date, well then what are you doing in healthcare? And immediate prophylaxis and vaccination update are required. And, okay, ’cause I just mentioned it. Let’s talk about vaccines. So first I wanna talk about DTaP, dt, lowercase a uppercase p and t dap. Uppercase T D A P. So DTAP contain higher concentrations of diphtheria and pertussis antigens. It’s used for children under seven years of age. TDAP contains lower antigen concentrations and it’s designed for adolescents and adults to reduce reactogenicity. There is no standalone pertussis vaccine. I’ve had patients say, well, I don’t want tetanus. Just give me the pertussis one. Well, tough Schenectes. We do not have a pertussis vaccine. alone. It’s only available in combination with diphtheria and tetanus toxoids, DTaP or Tdap. The combined vaccine boosts efficacy and ensures broader protection against all of the included infections. Now the routine vaccination schedule, which if you are a pediatric resident, you know, like the back of your hand, the DTAP is administered at 2, 4, 6, and then between 15 and 18 months with a booster at 4 to 6 years. The Tdap is one dose at 11 to 12 years and then during every pregnancy to confer passive immunity to the newborns. And again, depending on when you’re listening to this, you may be in the midst of a pertussis outbreak. And if you listen to this a few years later, after the original publication date in the fall of 2024, and you’re seeing another pertussis outbreak, well, dang it, we haven’t done our job. We need to strengthen school vaccination requirements. We need to educate parents about vaccine safety and the risks of exemptions. And we need to broadly improve and ensure access to vaccinations through our community clinics. Thanks. Alright, so that’s it for this episode on Pertussis, which remains a significant public health challenge due to its severe complications in young patients and the ongoing decline in vaccination coverage. Healthcare providers play a vital role in diagnosing and managing it, preventing its spread, and educating patients and families about the benefits of vaccination. Infection control practices and post exposure protocols are critical for protecting both clinicians and close contacts and other exposures. Thank you so much for listening to this episode. I hope you found it educational and informative. If there’s other topics that you want to hear about, let me know. I’m on X, I’m on Blue Sky, I’m on Mastodon, I take emails, you can leave a comment on the blog, you can leave a review on your favorite podcast site, any feedback is good feedback, and encourage your colleagues to listen, and as the kids say, like and subscribe, I told my 12 year old I would say that at the end of the episode. For PEMCurrents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski, see you next time.