PEM Currents: The Pediatric Emergency Medicine Podcast

In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we take a structured, evidence-based approach to the acute treatment of migraine in children and adolescents. From confirming the diagnosis and screening for concerning features to optimizing outpatient therapy and executing a protocolized emergency department strategy, this episode walks through what works. We review the role of NSAIDs and triptans, clarify how IV fluids and ketorolac fit into care, and provide a stepwise framework for dopamine antagonists, valproate bridge therapy, DHE protocols, steroids, discharge planning, and admission decisions. Practical dosing, reassessment timing, and family-centered communication strategies are emphasized throughout.

Learning Objectives

Recognize the clinical features of pediatric migraine and distinguish it from secondary causes of headache.

Implement a stepwise, evidence-based emergency department approach to acute pediatric migraine, including appropriate medication selection and timing of reassessment.

Develop safe discharge and follow-up plans by defining treatment endpoints, minimizing medication overuse, and identifying patients who require referral or inpatient management.

References
1. Oskoui M, Pringsheim T, Holler-Managan Y, et al. Practice Guideline Update Summary: Acute Treatment of Migraine in Children and Adolescents: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2019;93(11):487-499. doi:10.1212/WNL.0000000000008095.

2. Patterson-Gentile C, Szperka CL. The Changing Landscape of Pediatric Migraine Therapy: A Review. JAMA Neurology. 2018;75(7):881-887. doi:10.1001/jamaneurol.2018.0046.

3. Bachur RG, Monuteaux MC, Neuman MI. A Comparison of Acute Treatment Regimens for Migraine in the Emergency Department. Pediatrics. 2015;135(2):232-238. doi:10.1542/peds.2014-2432.

4. Ashina M. Migraine. The New England Journal of Medicine. 2020;383(19):1866-1876. doi:10.1056/NEJMra1915327.

5. Richer L, Billinghurst L, Linsdell MA, et al. Drugs for the Acute Treatment of Migraine in Children and Adolescents. The Cochrane Database of Systematic Reviews. 2016;4:CD005220. doi:10.1002/14651858.CD005220.pub2.

Transcript
This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered.

And today we’re gonna talk about the acute treatment of migraine headache in children and adolescents. This is bread and butter for the PED, requires precise diagnosis and evidence-based treatment. We’re gonna talk about making that diagnosis, red flags, outpatient and ED treatment, as well as some second-line agents, admission decisions, and a whole lot more.

So migraine in children is defined by three criteria, and at least five attacks lasting two to 72 hours. So you gotta have at least two of the following: pulsating or throbbing quality, moderate to severe intensity, aggravation by routine activity, and a unilateral location. Although in children, it’s often bilateral, plus at least one of nausea or vomiting and photophobia and/or phonophobia.

In children headaches are frequently bilateral, bifrontal, bitemporal. The duration might be shorter than adults, especially in kids under second or third grade. And you may have to infer whether or not they have photophobia from their behavior. Like does the child close their eyes or wanna go into a dark room?

In the emergency department, we’re often diagnosing based on pattern recognition plus exclusion of dangerous secondary causes. Or even more often than that, the patient comes in and says, I’ve got a migraine. Before I move on to treatments, let’s talk about some red flags where you might wanna pause and not just jump to migraine therapy.

And the mnemonic SNOOP can be helpful here. And it stands for S for systemic symptoms such as fevers, myalgia, weight loss, or another S, secondary risk factors such as an immune deficiency, cancer, pregnancy, N for neurologic signs, papilledema, focal deficit, confusion, seizures. O onset sudden, or thunderclap.

Migraines are often a little more gradual than that. The other O is older age, or technically younger age too, younger than five years or older than 50. Hopefully those patients are not coming into the pediatric emergency department. And then pattern changes, these new symptoms in a previously stable pattern.

Don’t ignore that. And precipitants, you know, is it worse with Valsalva, position change, or under significant exertion? If these signs are present, you’ll probably wanna take a pause and just not throw migraine treatment at the patient. If they’re stable, MRI is the preferred imaging modality, but a very sick patient, it’d be okay to get a head CT. If you’ve got a normal neurologic exam, there’s no red flags. Again, you don’t need routine imaging for migraine headaches.

So let’s talk about treatment. So hopefully patients have actually started to treat their headache before they arrive in the emergency department. If they haven’t, it’s a good idea to have some triage protocols in place.

So ibuprofen, 7.5 to 10 milligrams per kilogram, 10 milligrams per kilogram is superior to placebo and it’s superior to acetaminophen at two hours. So that’s what we would use. Early treatment’s critical. So ideally within the first hour of onset. So that’s why triage protocols help. We’ll give kids 10 mg per kg of ibuprofen and like 30 ounces of Gatorade.

Blue is often the first Gatorade choice, though that’s not an evidence-based statement. You can also use naproxen, but most of the studies are on ibuprofen. If NSAIDs fail, many adolescents and some older children will be prescribed triptans. The best evidence currently supports sumatriptan plus naproxen or zolmitriptan nasal spray.

Rizatriptan is FDA approved down to age six. Adolescents respond to these agents better than younger children, and the route matters. The nasal formulations help when nausea is prominent. Families should be counseled to treat early, use weight-appropriate dosing, and avoid using acute medications more than 10 days per month.

Often patients will have already taken an NSAID and a triptan before they get to the ED, and that’s where we get into the treatment of refractory migraine. Now this is most of the patients that I will see, and before we push medications, let’s briefly review ED treatment goals. You either want the patient headache free.

Back to their baseline or mild descending pain. So a pain score of one to three. If you don’t reach one of those endpoints and it’s not agreed upon with the patient and their family, you’ve not completed treatments. You should do a reassessment within one hour after each intervention. And let’s face it, if you’re not reassessing within an hour and defining treatment goals, you’re not practicing protocolized migraine care.

So in the emergency department, many of you may be familiar with the migraine cocktail. So what is that? In general, it’s a dopaminergic agent such as prochlorperazine or metoclopramide plus ketorolac, plus IV fluids. Let’s take a look at all three of those components and see if you can guess which one is actually the one that can abort the migraine.

So fluids are commonly given in pediatric migraine, but they alone do not treat it. They’re helpful. Many patients have been throwing up or a bit dehydrated, but there are small randomized trials that show essentially no meaningful pain reduction in patients that get IV fluids alone. Well, what about ketorolac?

Toradol, like that’s the first thing you give to a kid with a kidney stone, right? It does help, but it’s really adjunctive. So the main first-line agents for refractory or status migrainosus in the emergency department are the dopamine antagonists, and the first-line treatment for most patients is prochlorperazine or Compazine.

The dose is 0.15 milligram per kilogram IV. The max is 10 milligrams. This is the backbone of ED migraine care. And why do they work? Well, migraines aren’t just some random vascular headache. This is an inherited disorder with central pain pathways gone awry. Dopamine plays a large role in that pain, nausea, hypersensitivity, amplification of symptoms and more that, frankly, I won’t get into this podcast because molecules hurt my head.

The dopamine antagonists treat the headache, they reduce the nausea, and they just tamp down this process. Overall, the response rates approach 85%. Some studies have suggested that the response rate is about 77% at an hour and 90% at three hours. If you add the ketorolac and IV fluids, you get your response rate up to about 93 to 94%.

These agents really do work well together. There have been randomized trials comparing IV prochlorperazine versus ketorolac. 85% of prochlorperazine patients achieved headache relief versus only 55% of ketorolac patients. So ketorolac helps, but really it’s the prochlorperazine. Metoclopramide, or Reglan, is used in a lot of centers as well.

There are some smaller studies in children and adolescents that show that prochlorperazine is more effective, but if kids have an adverse reaction, more on that in a moment, or they prefer metoclopramide because they’ve responded to it in the past, it’s okay to go with it as well.

Right. So what does it actually look like when you give the migraine cocktail to a patient?

I think it’s important to explain to patients and families what to expect, and if this is a teenager, I’m talking to them directly. I mean, they’re getting the medication first and foremost. I tell them that the most effective way to treat their headache is with an IV. This often causes lots of angst, even in older teenagers.

The medication just does not get to the brain as effectively and fast enough if you take it by mouth. Many patients who get the dopaminergic agents, so prochlorperazine, will invariably feel jittery or anxious or like they gotta move or like they got ants in their pants. I tell them to expect this so they’re not surprised and worried when it happens.

I tell them that once they start feeling that way, it means the medicine is probably working. They need to hit the nurse button and we’re gonna get them up and have them take a walk. This fixes it for the majority of patients just getting up and moving.

In adult centers, even with the initial administration of the prochlorperazine or as sort of a reflexive response to any of those symptoms, they just give a slug of IV Benadryl.

There’s some studies in adolescents especially that this may decrease the effectiveness of the IV agents you’re giving in the first place, and it may also increase return rates to the ED. So I will use IV diphenhydramine if getting up and moving around isn’t working, or if the distress is significant, or if the patient clearly indicates they’ve needed it in the past.

So if after the migraine cocktail, the patient has met their pain goals and the reassessment is favorable, they can go home to outpatient follow-up. How about if the headache got better, but not all the way? It’s usually when the initial migraine cocktail didn’t achieve the pain endpoints fully, like it helped partially. If the dopamine blockade didn’t do anything, valproate is unlikely to rescue the case.

And so valproate works on GABA and it stabilizes some of these pain processes, but the dopaminergic agent needs to have done something first for valproate to work. Per the most common protocol, you give an initial dose of IV valproate, then you discharge the patient home on Depakote ER.

So oral valproic acid under 10 years old or under 50 kilograms, 250 milligrams PO twice a day for two weeks, or older than 10 or greater than 50 kilos, 500 milligrams twice a day for two weeks. This is the extended release and it’s most helpful if you give the first oral dose in the emergency department.

So that’s why it’s very important to build this protocol in advance. If you don’t have IV valproate, then don’t just give the patient oral valproate, and definitely don’t prescribe an oral course for discharge.

All right, well, what about DHE? Dihydroergotamine for refractory or status migrainosus?

Generally, this is only given at pediatric centers where you have neurology coverage. It’s contraindicated if you’ve had another dose of DHE within 14 days, or you’ve had any triptan of any sort within 24 hours, and you must obtain a pregnancy test in adolescent females before giving it.

The dosing for less than 30 kilograms is 0.5 milligram. At least 30 kilograms is one milligram. You give 50% of the dose over three minutes, then the remaining 50% over 30 minutes.

If this is gonna work, the patients are gonna start feeling wretched at first. They’re gonna get very nauseous and they’re gonna vomit. They’re gonna have flushing, and you’ll see transient hypertension.

Most of that resolves within the hour in most centers. If you’re committing to DHE, you’re kind of bringing the patient into the hospital anyway, though some facilities will have DHE done in the emergency department with close outpatient follow-up. Either way, it’s really best practice to involve child neurology if you’re giving DHE.

Alright, well what about steroids? They give those in grownups too, right?

Steroids really only have a role for recurrence prevention in children. So for kids that have a history of returning within 72 hours for rebound headache, you can give dexamethasone 0.6 milligram per kilogram IV dose, the max of 10 milligrams.

You do not discharge them home on a steroid prescription or a Medrol dose pack or something else, and this can cut the recurrence risk down a bit.

There’s other therapies out there like magnesium and ketamine. There’s just not enough evidence there. And the purpose of this episode is to discuss the therapies that have good evidence behind them and should be part of protocols across the country.

Some patients are unfortunately not responsive to emergency department therapy and need admission. The main inpatient therapy is the DHE protocol. If they’re not DHE eligible, they haven’t tolerated it well or it’s unavailable, admission’s unlikely to help them unless they just need some IV fluids to help them get back up on their feet.

You should consult neurology if the headache goals are not met after maximizing ED therapy for advice. And we should definitely avoid opioids. They don’t treat patients with migraines. They increase recurrence risk. They increase revisit rates. Again, the dopamine antagonist prochlorperazine, it’s superior for sustained relief when families ask about them, and fortunately they’re asking about opioids far less.

We use medications that treat the migraine pain pathways and signaling. We don’t just wanna mask the pain.

All right, so that’s all I’ve got on the acute management of migraine headaches, especially in the emergency department. Remember that migraine care in the ED should be protocolized and evidence-based. IV fluids are supportive.

Prochlorperazine is the first line, or you can use metoclopramide as well. Ketorolac is an adjunctive therapy. Valproate is next line. If you’ve gotta escalate, and DHE is specialized therapy, you can start in the ED, but most of these patients are getting admitted. Dexamethasone or steroids in children can reduce recurrence risk, but they’re not really part of the acute management.

You should definitely define the endpoints and structurally and systematically reassess patients at an hour. The goal is to get them feeling better to a defined endpoint and to restore function. There is evidence-based pediatric emergency migraine care. You should understand that, plus how to explain why these agents are being given and some of the side effects to patients and families.

I find that that approach increases your likelihood of buy-in and success.

Alright, so that’s it for this episode on the Acute Management of Migraine Headaches in Children and Adolescents. I hope you found it helpful and I can pretty much guarantee that you’re gonna see a patient with a migraine on your next shift.

If you’ve got any feedback or comments, send them my way. If you like this episode, leave a review on your favorite podcast site. It helps more people find the show. Or recommend it to a colleague. If there’s other topics that you’d like to hear, send them my way for the Pediatric Emergency Medicine podcast.

This has been Brad Sobolewski. See you next time.

Psychogenic nonepileptic seizures (PNES) are common, often misunderstood, and increasingly encountered in pediatric emergency care. These events closely resemble epileptic seizures but arise from abnormal brain network functioning rather than epileptiform activity. In this episode of PEM Currents, we review the epidemiology, pathophysiology, and clinical features of PNES in children and adolescents, with a practical focus on Emergency Department recognition, diagnostic strategy, and management. Particular emphasis is placed on seizure semiology, avoiding iatrogenic harm, communicating the diagnosis compassionately, and understanding how early identification and referral to cognitive behavioral therapy can dramatically improve long-term outcomes.

Learning Objectives

Identify key epidemiologic trends, risk factors, and semiological features that help differentiate psychogenic nonepileptic seizures from epileptic seizures in pediatric patients presenting to the Emergency Department.

Apply an evidence-based Emergency Department approach to the evaluation and initial management of suspected PNES, including strategies to avoid unnecessary escalation of care and medication exposure.

Demonstrate effective, patient- and family-centered communication techniques for explaining the diagnosis of PNES and facilitating timely referral to appropriate outpatient therapy.

References

Sawchuk T, Buchhalter J, Senft B. Psychogenic Nonepileptic Seizures in Children-Prospective Validation of a Clinical Care Pathway & Risk Factors for Treatment Outcome. Epilepsy & Behavior. 2020;105:106971. (PMID: 32126506)

Fredwall M, Terry D, Enciso L, et al. Outcomes of Children and Adolescents 1 Year After Being Seen in a Multidisciplinary Psychogenic Nonepileptic Seizures Clinic. Epilepsia. 2021;62(10):2528-2538. (PMID: 34339046)

Sawchuk T, Buchhalter J. Psychogenic Nonepileptic Seizures in Children - Psychological Presentation, Treatment, and Short-Term Outcomes. Epilepsy & Behavior. 2015;52(Pt A):49-56. (PMID: 26409129)

Labudda K, Frauenheim M, Miller I, et al. Outcome of CBT-based Multimodal Psychotherapy in Patients With Psychogenic Nonepileptic Seizures: A Prospective Naturalistic Study. Epilepsy & Behavior. 2020;106:107029. (PMID: 32213454)

Transcript
This transcript was generated using Descript automated transcription software and has been reviewed and edited for accuracy by the episode’s author. Edits were limited to correcting names, titles, medical terminology, and transcription errors. The content reflects the original spoken audio and was not substantively altered.

Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we are talking about psychogenic non-epileptic seizures, or PNES. Now, this is a diagnosis that often creates a lot of uncertainty in the Emergency Department. These episodes can be very scary for families and caregivers and schools.

And if we mishandle the diagnosis, it can lead to unnecessary testing, medication exposure, ICU admissions, and long-term harm. This episode’s gonna focus on how to recognize PNES in pediatric patients, how we make the diagnosis, what the evidence says about management and outcomes, and how what we do and what we say in the Emergency Department directly affects patients, families, and prognosis.

Psychogenic non-epileptic seizures are paroxysmal events that resemble epileptic seizures but occur without epileptiform EEG activity. They’re now best understood as a subtype of functional neurological symptom disorder, specifically functional or dissociative seizures. Historically, these events were commonly referred to as pseudo-seizures, and that term still comes up frequently in the ED, in documentation, and sometimes from families themselves.

The problem is that pseudo implies false, fake, or voluntary, and that implication is incorrect and harmful. These episodes are real, involuntary, and distressing, even though they’re not epileptic. Preferred terminology includes psychogenic non-epileptic seizures, or PNES, functional seizures, or dissociative seizures.

And PNES is not a diagnosis of exclusion, and it does not require identification of psychological trauma or psychiatric disease. The diagnosis is based on positive clinical features, ideally supported by video-EEG, and management begins with clear, compassionate communication.

The overall incidence of PNES shows a clear increase over time, particularly from the late 1990s through the mid-2010s. This probably reflects improved recognition and access to diagnostic services, though a true increase in occurrence can’t be excluded. Comorbidity with epilepsy is really common and clinically important. Fourteen to forty-six percent of pediatric patients with PNES also have epilepsy, which frequently complicates diagnosis and contributes to diagnostic delay.

Teenagers account for the highest proportion of patients with PNES, especially 15- to 19-year-olds. Surprisingly, kids under six are about one fourth of all cases, so it’s not just teenagers.

We often make the diagnosis of PNES in epilepsy monitoring units. So among children undergoing video-EEG, about 15 to 19 percent may ultimately be diagnosed with PNES. And paroxysmal non-epileptic events in tertiary epilepsy monitoring units account for about 15 percent of all monitored patients.

Okay, but what is PNES?

Well, it’s best understood as a disorder of abnormal brain network functioning. It’s not structural disease. The core mechanisms at play include altered attention and expectation, impaired integration of motor control and awareness, and dissociation during events. So the patients are not necessarily aware that this is happening.

Psychological and psychosocial features are common but not required for diagnosis and may be less prevalent in pediatric populations as compared with adults. So PNES is a brain-based disorder. It’s not conscious behavior, it’s not malingering, and it’s not under voluntary control.

Children and adolescents with PNES have much higher rates of psychiatric comorbidities and psychosocial stressors compared to both healthy controls and children with epilepsy alone. Psychiatric disorders are present in about 40 percent of pediatric PNES patients, both before and after the diagnosis. Anxiety is seen in 58 percent, depression in 31 percent, and ADHD in 35 percent.

Compared to kids with epilepsy, the risk of psychiatric disorders in PNES is nearly double. Compared to healthy controls, it is up to eight times higher.

And there’s a distinct somatopsychiatric profile that strongly predicts diagnosis of PNES. This includes multiple medical complaints, psychiatric symptoms, high anxiety sensitivity, and solitary emotional coping. This profile, if you’ve got all four of them, carries an odds ratio of 15 for PNES.

Comorbid epilepsy occurs in 14 to 23 percent of pediatric PNES cases, and it’s associated with intellectual disability and prolonged diagnostic delay. And finally, across all demographic strata, anxiety is the most consistent predictor of PNES.

Making the diagnosis is really hard. It really depends on a careful history and detailed analysis of the events. There’s no single feature that helps us make the diagnosis. So some of the features of the spells or events that have high specificity for PNES include long duration, so typically greater than three minutes, fluctuating or asynchronous limb movements, pelvic thrusting or side-to-side head movements, ictal eye closure, often with resisted eyelid opening, ictal crying or vocalization, recall of ictal events, and rare association with injury.

Younger children often present with unresponsiveness. Adolescents more commonly demonstrate prominent motor symptoms. In pediatric cohorts, we most frequently see rhythmic motor activity in about 27 percent, and complex motor movements and dialeptic events in approximately 18 percent each.

Features that argue against PNES include sustained cyanosis with hypoxia, true lateral tongue biting, stereotyped events that are identical each time, clear postictal confusion or lethargy, and obviously epileptic EEG changes during the events themselves.

Now there are some additional historical and contextual clues that can help us make the diagnosis as well. If the events occur in the presence of others, if they occur during stressful situations, if there are psychosocial stressors or trauma history, a lack of response to antiepileptic drugs, or the absence of postictal confusion, this may suggest PNES.

Lower socioeconomic status, Medicaid insurance, homelessness, and substance use are also associated with PNES risk. While some of these features increase suspicion, again, video-EEG remains the diagnostic gold standard.

We do not have video-EEG in the ED. But during monitoring, typical events are ideally captured and epileptiform activity is not seen on the EEG recording. Video-EEG is not feasible for every single diagnosis. You can make a probable PNES diagnosis with a very accurate clinical history, a vivid description of the signs and appearance of the events, and reassuring interictal EEG findings.

Normal labs and normal imaging do not make the diagnosis. Psychiatric comorbidities are not required. The diagnosis, again, rests on positive clinical features. If the patient can’t be placed on video-EEG in a monitoring unit, and if they have an EEG in between events and it’s normal, that can be supportive as well.

So what if you have a patient with PNES in the Emergency Department?

Step one, stabilize airway, breathing, circulation. Take care of the patient in front of you and keep them safe. Use seizure pads and precautions and keep them from falling off the bed or accidentally injuring themselves. A family member or another team member can help with this.

Avoid reflexively escalating. If you are witnessing a PNES event in front of you, and if they’re protecting their airway, oxygenating, and hemodynamically stable, avoid repeated benzodiazepines. Avoid intubating them unless clearly indicated, and avoid reflexively loading them with antiseizure medications such as levetiracetam or valproic acid.

Take a focused history. You’ve gotta find out if they have a prior epilepsy diagnosis. Have they had EEGs before? What triggered today’s event? Do they have a psychiatric history? Does the patient have school stressors or family conflict? And then is there any recent illness or injury?

Only order labs and imaging when clinically indicated. EEG is not widely available in the Emergency Department.

We definitely shouldn’t say things like, “this isn’t a real seizure,” or use outdated terms like pseudo-seizure. Don’t say it’s all psychological, and please do not imply that the patient is faking.

If you see a patient and you think it’s PNES, you’re smart, you’re probably right, but don’t promise diagnostic certainty at first presentation. Remember, a sizable proportion of these patients actually do have epilepsy, and referring them to neurology and getting definitive testing can really help clarify the diagnosis.

Communication errors, especially early on, worsen outcomes.

One of the most difficult things is actually explaining what’s going on to families and caregivers. So here’s a suggestion. You could say something like:

“What your child is experiencing looks like a seizure, but it’s not caused by abnormal electrical activity in the brain. Instead, it’s what we call a functional seizure, where the brain temporarily loses control of movement and awareness. These episodes are real and involuntary. The good news is that this condition is treatable, especially when we address it early.”

The core treatment of PNES is CBT-based psychotherapy, or cognitive behavioral therapy. That’s the standard of care. Typical treatment involves 12 to 14 sessions focused on identifying triggers, modifying maladaptive cognitions, and building coping strategies.

Almost two thirds of patients achieve full remission with treatment. About a quarter achieve partial remission. Combined improvement rates reach up to 90 percent at 12 months.

Additional issues that neurologists, psychologists, and psychiatrists often face include safe tapering of antiseizure medications when epilepsy has been excluded, treatment of comorbid anxiety or depression, coordinating care between neurology and mental health professionals, and providing education for schools on event management.

Schools often witness these events and call prehospital professionals who want to keep patients safe. Benzodiazepines are sometimes given, exposing patients to additional risk. This requires health system-level and outpatient collaboration.

Overall, early diagnosis and treatment of PNES is critical. Connection to counseling within one month of diagnosis is the strongest predictor of remission. PNES duration longer than 12 months before treatment significantly reduces the likelihood of remission.

Video-EEG confirmation alone does not predict positive outcomes. Not every patient needs admission to a video-EEG unit. Quality of communication and speed of treatment, especially CBT-based therapy, matter the most.

Overall, the prognosis for most patients with PNES is actually quite favorable. There are sustained reductions in events along with improvements in mental health comorbidities. Quality of life and psychosocial functioning improve, and patients use healthcare services less frequently.

So here are some take-home points about psychogenic non-epileptic seizures, or PNES. Pseudo-seizure and similar terms are outdated and misleading. Do not use them. PNES are real, involuntary, brain-based events. Diagnosis relies on positive clinical features, what the events look like and when they happen, not normal lab tests or CT scans.

Early recognition and diagnosis, and rapid referral to cognitive behavioral therapy, change patients’ lives. If you suspect PNES, get neurology and mental health professionals involved as soon as possible.

Alright, that’s all I’ve got for this episode. I hope you found it educational. Having seen these events many times over the years, I recognize how scary they can be for families, schools, and our prehospital colleagues. It’s up to us to think in advance about how we’re going to talk to patients and families and develop strategies to help children who are suffering from PNES events.

If you’ve got feedback about this episode, send it my way. Likewise, like, rate, and review, as my teenagers would say, and share this episode with a colleague if you think it would be beneficial.

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

Osteomyelitis in children is common enough to miss and serious enough to matter. In this episode of PEM Currents, we review a practical, evidence-based approach to pediatric acute hematogenous osteomyelitis, focusing on diagnostic strategy, imaging decisions including FAST MRI, and modern antibiotic management. Topics include age-based microbiology, empiric and pathogen-directed antibiotic selection with dosing, criteria for early transition to oral therapy, and indications for orthopedic and infectious diseases consultation. Special considerations such as MRSA, Kingella kingae, daycare clustering, and shortened treatment durations are discussed with an emphasis on safe, high-value care.

Learning Objectives
After listening to this episode, learners will be able to:

Identify the key clinical, laboratory, and imaging findings that support the diagnosis of acute hematogenous osteomyelitis in children, including indications for FAST MRI and contrast-enhanced MRI.

Select and dose appropriate empiric and pathogen-directed antibiotic regimens for pediatric osteomyelitis based on patient age, illness severity, and local MRSA prevalence, and determine when early transition to oral therapy is appropriate.

Determine when consultation with orthopedics and infectious diseases is indicated, and recognize clinical features that warrant prolonged therapy or more conservative management.

References

Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2021 guideline on diagnosis and management of acute hematogenous osteomyelitis in pediatrics. J Pediatric Infect Dis Soc. 2021;10(8):801-844. doi:10.1093/jpids/piab027

Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America: 2023 guideline on diagnosis and management of acute bacterial arthritis in pediatrics. J Pediatric Infect Dis Soc. 2024;13(1):1-59. doi:10.1093/jpids/piad089

Stephan AM, Platt S, Levine DA, et al. A novel risk score to guide the evaluation of acute hematogenous osteomyelitis in children. Pediatrics. 2024;153(1):e2023063153. doi:10.1542/peds.2023-063153

Alhinai Z, Elahi M, Park S, et al. Prediction of adverse outcomes in pediatric acute hematogenous osteomyelitis. Clin Infect Dis. 2020;71(9):e454-e464. doi:10.1093/cid/ciaa211

Burns JD, Upasani VV, Bastrom TP, et al. Age and C-reactive protein associated with improved tissue pathogen identification in children with blood culture-negative osteomyelitis: results from the CORTICES multicenter database. J Pediatr Orthop. 2023;43(8):e603-e607. doi:10.1097/BPO.0000000000002448

Peltola H, Pääkkönen M. Acute osteomyelitis in children. N Engl J Med. 2014;370(4):352-360. doi:10.1056/NEJMra1213956

Transcript
This transcript was provided via use of the Descript AI application

Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re covering osteomyelitis in children. We’re going to talk about diagnosis and imaging, and then spend most of our time where practice variation still exists: antibiotic selection, dosing, duration, and the evidence supporting early transition to oral therapy. We’ll also talk about when to involve orthopedics, infectious diseases, and whether daycare outbreaks of osteomyelitis are actually a thing.

So what do I mean by pediatric osteomyelitis? In children, osteomyelitis is most commonly acute hematogenous osteomyelitis. That means bacteria seed the bone via the bloodstream. The metaphysis of long bones is particularly vulnerable due to vascular anatomy that favors bacterial deposition.

Age matters. In neonates, transphyseal vessels allow infection to cross into joints, increasing the risk of concomitant septic arthritis. In older children, those vessels involute, and infection tends to remain metaphyseal and confined to bone rather than spreading into the joint.

For children three months of age and older, empiric therapy must primarily cover Staphylococcus aureus, which remains the dominant pathogen. Other common organisms include group A streptococcus and Streptococcus pneumoniae.

In children six to 36 months of age, especially those in daycare, Kingella kingae is an important and often underrecognized pathogen. Kingella infections are typically milder, may present with lower inflammatory markers, and frequently yield negative routine cultures. Kingella is usually susceptible to beta-lactams like cefazolin, but is consistently resistant to vancomycin and often resistant to clindamycin and antistaphylococcal penicillins. This has direct implications for empiric antibiotic selection.

Common clinical features of osteomyelitis include fever, localized bone pain, refusal to bear weight, and pain with movement of an adjacent joint. Fever may be absent early, particularly with less virulent organisms like Kingella.

A normal white blood cell count does not exclude osteomyelitis. Only about one-third of children present with leukocytosis. CRP and ESR are generally more useful, particularly CRP for monitoring response to therapy.

No single CRP cutoff reliably diagnoses or excludes osteomyelitis in children. While CRP is elevated in most cases of acute hematogenous osteomyelitis, the Pediatric Infectious Diseases Society and the Infectious Diseases Society of America note that high-quality data defining diagnostic thresholds are limited. A CRP above 20 milligrams per liter is commonly used to support clinical suspicion, with pooled sensitivity estimates around 80 to 85 percent, but no definitive value mandates the diagnosis. Lower values do not exclude disease, particularly in young children, as CRP is normal in up to 40 percent of Kingella kingae infections.

CRP values tend to be higher in Staphylococcus aureus infections, especially MRSA, and higher levels are associated with complications such as abscess, bacteremia, and thrombosis, though specific cutoffs are not absolute.

In summary, CRP is most useful for monitoring treatment response. It typically peaks two to four days after therapy initiation and declines rapidly with effective treatment, with a 50 percent reduction within four days seen in the majority of uncomplicated cases.

Blood cultures should be obtained in all children with suspected osteomyelitis, ideally before starting antibiotics when feasible. In children, blood cultures alone can sometimes identify the pathogen.

Plain radiographs are still recommended early, not because they’re sensitive for acute osteomyelitis, but because they help exclude fracture, malignancy, or foreign body and establish a baseline.

MRI with and without contrast is the preferred advanced imaging modality. MRI confirms the diagnosis, defines the extent of disease, and identifies complications such as subperiosteal abscess, physeal involvement, and concomitant septic arthritis. MRI findings can also guide the need for surgical consultation.

Many pediatric centers now use FAST MRI protocols for suspected osteomyelitis, particularly from the emergency department. FAST MRI uses a limited sequence set, typically fluid-sensitive sequences like STIR or T2 with fat suppression, without contrast. These studies significantly reduce scan time, often avoid the need for sedation, and retain high sensitivity for bone marrow edema and soft tissue inflammation.

FAST MRI is particularly useful when the clinical question is binary: is there osteomyelitis or not? It’s most appropriate in stable children without high concern for abscess, multifocal disease, or surgical complications. If FAST MRI is positive, a full contrast-enhanced MRI may still be needed to delineate abscesses, growth plate involvement, or adjacent septic arthritis. If FAST MRI is negative but clinical suspicion remains high, further imaging may still be necessary.

The Pediatric Infectious Diseases Society and the Infectious Diseases Society of America recommend empiric antibiotic selection based on regional MRSA prevalence, patient age, and illness severity, with definitive therapy guided by culture results and susceptibilities.

Empiric therapy should never be delayed in an ill-appearing or septic child. In well-appearing, stable children, antibiotics may be briefly delayed to obtain imaging or tissue sampling, but this requires close inpatient observation.

For children three months and older with non–life-threatening disease, empiric therapy hinges on local MRSA rates. In regions with low community-acquired MRSA prevalence, generally under 10 percent, reasonable empiric options include cefazolin, oxacillin, or nafcillin.

When MRSA prevalence exceeds 10 to 20 percent, empiric therapy should include an MRSA-active agent. Clindamycin is appropriate when local resistance rates are low, while vancomycin is preferred when clindamycin resistance is common or the child has had significant healthcare exposure.

For children with severe disease or sepsis, vancomycin is generally preferred regardless of local MRSA prevalence. Some experts recommend combining vancomycin with oxacillin or nafcillin to ensure optimal coverage for MSSA, group A streptococcus, and MRSA. In toxin-mediated or high-inoculum infections, the addition of clindamycin may be beneficial due to protein synthesis inhibition.

Typical IV dosing includes cefazolin 100 to 150 milligrams per kilogram per day divided every eight hours; oxacillin or nafcillin 150 to 200 milligrams per kilogram per day divided every six hours; clindamycin 30 to 40 milligrams per kilogram per day divided every six to eight hours; and vancomycin 15 milligrams per kilogram every six hours for serious infections, with appropriate monitoring.

Ceftaroline or daptomycin may be considered in select MRSA cases when first-line agents are unsuitable.

For methicillin-susceptible Staphylococcus aureus, first-generation cephalosporins or antistaphylococcal penicillins remain the preferred parenteral agents. For oral therapy, high-dose cephalexin, 75 to 100 milligrams per kilogram per day divided every six hours, is preferred. Clindamycin is an alternative when beta-lactams cannot be used.

For clindamycin-susceptible MRSA, clindamycin is the preferred IV and oral agent due to excellent bioavailability and bone penetration, and it avoids the renal toxicity associated with vancomycin.

For clindamycin-resistant MRSA, vancomycin or ceftaroline are preferred IV agents. Oral options are limited, and linezolid is generally the preferred oral agent when transition is possible. Daptomycin may be used parenterally in children older than one year without pulmonary involvement, typically with infectious diseases and pharmacy input.

Beta-lactams remain the drugs of choice for Kingella kingae, Streptococcus pyogenes, and Streptococcus pneumoniae. Vancomycin has no activity against Kingella, and clindamycin is often ineffective.

For Salmonella osteomyelitis, typically seen in children with sickle cell disease, third-generation cephalosporins or fluoroquinolones are used. In underimmunized children under four years, consider Haemophilus influenzae type b, with therapy guided by beta-lactamase production.

Doxycycline has not been prospectively studied in pediatric acute hematogenous osteomyelitis. There are theoretical concerns about reduced activity in infected bone and risks related to prolonged therapy. While short courses are safe for certain infections, the longer durations required for osteomyelitis increase the risk of adverse effects. Doxycycline should be considered only when no other active oral option is available, typically in older children, and with infectious diseases consultation. It is not appropriate for routine treatment.

Many hospitals automatically consult orthopedics when children are admitted with osteomyelitis, and this is appropriate. Early orthopedic consultation should be viewed as team-based care, not failure of medical management.

Consult orthopedics when MRI shows abscess or extensive disease, there is concern for septic arthritis, the child fails to improve within 48 to 72 hours, imaging suggests devitalized bone or growth plate involvement, there is a pathologic fracture, the patient is a neonate, or diagnostic bone sampling or operative drainage is being considered. Routine surgical debridement is not required for uncomplicated cases.

Infectious diseases consultation is also often automatic and supported by guidelines. ID is particularly valuable for antibiotic selection, dosing, IV-to-oral transition, duration decisions, bacteremia management, adverse reactions, and salvage regimens. Even in straightforward cases, ID involvement often facilitates shorter IV courses and earlier oral transition.

Osteomyelitis is generally not contagious, and clustering is uncommon for Staphylococcus aureus. Kingella kingae is the key exception. It colonizes the oropharynx of young children and spreads via close contact. Clusters of invasive Kingelladisease have been documented in daycare settings.

Suspicion should be higher in children six to 36 months from the same daycare, with recent viral illness, mild systemic symptoms, refusal to bear weight, modest CRP elevation, and negative routine cultures unless PCR testing is used. Public health intervention is not typically required, but awareness is critical.

There is no minimum required duration of IV therapy for uncomplicated acute hematogenous osteomyelitis. Transition to oral therapy should be based on clinical improvement plus CRP decline. Many children meet criteria within two to six days.

Oral antibiotics must be dosed higher than standard outpatient regimens to ensure adequate bone penetration. Common regimens include high-dose cephalexin, clindamycin, or linezolid in select cases. The oral agent should mirror the IV agent that produced clinical improvement.

Total duration is typically three to four weeks, and in many cases 15 to 20 days is sufficient. MRSA infections or complicated cases usually require four to six weeks.

Early oral transition yields outcomes comparable to prolonged IV therapy with fewer complications. Most treatment-related complications occur during parenteral therapy, largely due to catheter-related issues.

Take-home points: osteomyelitis in children is a clinical diagnosis supported by labs and MRI. Empiric antibiotics should be guided by age, illness severity, and local MRSA prevalence. Early transition to high-dose oral therapy is safe and effective when clinical response and CRP support it. Orthopedics and infectious diseases consultation improve care and reduce variation. FAST MRI is changing how we diagnose osteomyelitis. Daycare clustering is uncommon except with Kingella kingae.

That’s all for this episode. If there are other topics you’d like us to cover, let me know. If you have the time, leave a review on your favorite podcast platform. It helps more people find the show and learn from it. For PEM Currents, this has been Brad Sobolewski. See you next time.

Night terrors are dramatic but benign episodes that can leave caregivers frightened and confused. In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we explore the clinical features of night terrors, how to differentiate them from other nocturnal events, and when to consider further evaluation such as polysomnography. We also discuss management strategies that center on sleep hygiene, reassurance, and safety, with a special look at the role of scheduled awakenings and when medication is appropriate.

Learning Objectives
By the end of this episode, listeners will be able to:

Describe the typical clinical presentation and age range of children with night terrors.

Differentiate night terrors from other parasomnias and nocturnal seizures based on clinical features and timing.

Discuss non-pharmacologic and pharmacologic management strategies for night terrors, including when to consider polysomnography.

References

Petit D, Touchette E, Tremblay RE, et al. Dyssomnias and parasomnias in early childhood. Pediatrics. 2007;119(5):e1016-e1025.

Morse AM, Kotagal S. Parasomnias of childhood, including sleepwalking. In: Chervin RD, ed. UpToDate. Hoppin AG, deputy ed. Waltham, MA. Accessed November 2025.

Van Horn NL, Street M. Night Terrors. Updated May 29, 2023. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2025 Jan–. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493222/

Transcript
This transcript was provided via use of the Descript AI application

Welcome to PEM Currents, The Pediatric Emergency Medicine Podcast. As always, I'm your host Brad Sobolewski. In this episode, we're talking about night terrors, also known as sleep terrors. A dramatic, confusing, and often terrifying experience for caregivers to witness. But they're usually benign and self-limited for the child.

Kind of like a lot of the things in childhood actually, what are we gonna talk about? Well, what are night terrors? How do we diagnose them? How to differentiate them from seizures or other parasomnias key counseling for parents in the emergency department, when to refer for sleep studies or neurology evaluation, and what role, if any, medications play.

So let's start with talking about what night terrors actually look like. They're part of a group of disorders called non REM parasomnias, which also includes sleepwalking and confusion arousals. They are not nightmares and they are not signs of psychological trauma. Children experiencing night terrors typically sit up suddenly during sleep, scream, cry or appear terrified. Show signs of autonomic arousal. So rapid breathing, tachycardia, sweating. They're confused or inconsolable for several minutes and they have absolutely no recollection of the event the next morning. These events usually occur in the first third of the night when children are in deep, slow wave sleep, so stage N three, and they can last five to 15 minutes, but trust me, they seem to last much longer to observers.

Night terrors occur most commonly between ages three and seven with a peak around five years of age. They're rare before 18 months and unusual after age 12. Preschool aged children are most affected because they spend more time in deep, slow wave sleep. They have more fragmented sleep architecture, and they may not have fully developed arousal regulation mechanisms.

Episodes can start as early as toddlerhood, especially if the child has a family history of parasomnias. So like sleep, walking night terrors or other things, sleep deprivation or stressful life events like starting daycare or a new sibling or a move, although less common, older children and even adolescents can experience night terrors, especially in the context of stress, sleep deprivation or comorbid sleep disorders like sleep apnea.

Why do they happen? Well, they're usually due to incomplete arousal from deep sleep, so the brain is essentially stuck between sleep and wakefulness. Factors that increase the risk of frequency of night terrors include again, sleep deprivation, recent illness, stress, or anxiety. Sleep disordered breathing, or a family history of parasomnias, there's a real strong genetic component.

Up to 80% of children with night terrors have a first degree relative with similar episodes. The diagnosis is entirely clinical and based on history. You should ask parents, what time of night did these episodes occur? Is the child confused, frightened, or hard to wake? Is there amnesia the next day so they don't remember the event?

And are the movements variable or stereotyped? Sometimes parents will video record these, and that can really help us clarify the episodes when we're in the emergency department. You definitely do not need labs or imaging in a typical presentation. I think parents are often seeking an explanation for why their child looks so freaky.

In my experience, just telling them that it's a night terror and that it's benign and providing reassurance on how healthy their kid is, is more than enough. Now, not all nighttime events are sleep terrors. You should consider neurology referral and video polysomnography or sleep studies with extended EEG when onset is very early, so younger than 18 months or late in childhood.

So older than 12 or 13 episodes occur outside of the first third of the night. Again, find out when the kid went to bed. And do math. The first third of the night is the first 33% of their typical sleep time. The events are brief clustered or stereotyped. The movements are repetitive, focal or violent.

If kid just moving just their right arm. That's not a night terror. Often the movements will look fearful and they'll be sort of disorganized. Rhythmic movements don't typically happen in night terrors, and there's a recent injury. The child has excessive daytime sleepiness, or there's some developmental regression or abnormality.

All those are red flags. Differentiating from nocturnal frontal lobe epilepsy can be tricky. Nocturnal frontal lobe epilepsy events are usually short. Highly stereotyped. They have abrupt onset and offset, and they may include dystonic or tonic posturing. So if the family has a video of this, that can be really helpful using a good clinical history.

Video recordings in EEG generally distinguish night terrors from these forms of epilepsy. But let's be honest, most of the kids you see in the ED with a typical presentation of night terrors are just night terrors. These events are really scary and we are gonna see them in the emergency departments, and so your first goal is to just reassure the family.

The events are not harmful. The kid isn't aware that they had them, and the child suffers no ongoing psychological harm. That doesn't mean that the parent isn't freaked out or that nervousness doesn't linger. You wanna avoid sleep deprivation If possible, counsel families on age appropriate bedtimes and naps.

Stick to a routine consistent bedtime routines. Reduce sleep fragmentation, which is a known risk factor for children with frequent or predictable night terrors. Try waking them 15 to 30 minutes before the usual episode happens. So I've seen lots of kids with frequent night terrors, and they usually happen around the same time at night.

And you wanna do this, this 15 to 30 minute awakening before the usual episodes each night for about two to four weeks. That's labor intensive as a parent, but it can help these awakenings interrupt the sleep cycle and break the pattern. Keep kids safe. Use baby gates, door alarms. Make sure windows are locked, don't put younger kids in bunk beds and remove sharp obstacles or objects near the bed. So if they've got a pointy ended nightstand, oh, that's just something for the kid to fall into or smack against. Do we ever use medications for night terrors? Well, almost never. You know, pharmacologic therapy such as low dose benzodiazepines or tricyclic antidepressants is really only reserved for severe episodes.

Kids with substantial risk for injury or disruption of the family life or school in a substantial way. I'm not gonna make that call in the emergency department. And these are sleep specialist referral guided therapies. You also wanna consider evaluating children for comorbid sleep disorders, especially in recurrent night terrors, like obstructive sleep apnea, restless leg syndrome.

This may worsen the parasomnias. For kids in which you're unsure, polysomnography can be used. This is an overnight sleep study that monitors brainwaves via EEG, eye movements, muscle activity, heart rhythm, breathing effort, and airflow and oxygen saturation. But it's also done in a hospital and not during the kid's usual sleep routine.

So most children that have night terrors, if you get the right history, you can make the diagnosis clinically and the kids don't need any expensive or expanded testing to get to the bottom of things. Alright, take home points for this brief episode. Night terrors are common, especially in preschool aged children.

They occur in non REM sleep in the first third of the night. The episodes are very dramatic, but they're benign and children don't remember them. But trust me, parents do. The diagnosis is clinical. No labs or imaging are needed unless there's atypical features. You should reassure families, promote sleep hygiene and use scheduled awakenings for frequent and recurrent cases, and refer for sleep studies and or neurology of episodes or violent stereotyped, or suggest nocturnal seizures.

Thanks for listening to this episode. I hope you found it educational about a topic that you will encounter in the emergency department. As with many things in children that are scary, there's a benign explanation and parents are just looking to know that their kid's gonna be okay. Often doing a thorough history in physical and really listening to the parents' concerns and then providing useful information is all you gotta do.

That's why pediatrics is great. If you've got feedback on this episode or there's other common topics you'd like to hear about, send them my way. If you enjoyed this episode and think that other people should listen to it, share it with them. More listeners means more learners. And if you have a chance, leave a review or like the podcast on your favorite podcast site for PEM Currents, the Pediatric Emergency Medicine Podcast.

This has been Brad Sobolewski. See you next time.

BRUE, Brief Resolved Unexplained Events, are a common and anxiety-provoking condition that presents to the Emergency Department. In this episode we explore the definition of BRUE, contrast it with ALTE, and walk through evidence-based approaches to risk stratification. We’ll explore the original AAP framework and two subsequent prediction models to see where the recommendations stand today. This is a classic example of scary event / well child that you will see in the Emergency Department.

Learning Objectives

By the end of this episode, you will be able to:

Define BRUE and contrast it with the older concept of ALTE.

Recognize evolving risk stratification criteria

Apply evidence-based strategies for evaluation and counseling of infants with BRUE, including safe discharge decisions and the role of home monitoring.

References

Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief resolved unexplained events (formerly apparent life-threatening events) and evaluation of lower-risk infants: Executive summary. Pediatrics. 2016;137(5):e20160591. doi:10.1542/peds.2016-0591

Carroll AE, Bonkowsky JL. Acute events in infancy including brief resolved unexplained event (BRUE). In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025).

Carroll AE, Bonkowsky JL. Use of home cardiorespiratory monitors in infants. In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025).

Carroll AE, Bonkowsky JL. Sudden infant death syndrome: Risk factors and risk reduction strategies. In: McMillan JA, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025).

Carroll AE. Patient education: Brief resolved unexplained event (BRUE) in babies (The Basics). In: UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed October 2025).

Nama N, Neuman MI, Finkel MA, et al. Risk prediction after a brief resolved unexplained event. JAMA Pediatr. 2023;177(12):1263–1272. doi:10.1001/jamapediatrics.2023.4197

Nama N, Neuman MI, Finkel MA, et al. External validation of brief resolved unexplained events prediction rules for serious underlying diagnosis. JAMA Pediatr. 2024;178(4):398–407. doi:10.1001/jamapediatrics.2024.0114