Metabolic Disorders

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


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo

Emily Groopman, MD, PhD

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


Jeanmonod R, Asuka E, Jeanmonod D. Inborn Errors of Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:

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

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


Note: This transcript was partially completed with the use of the Descript AI

Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and this episode focuses on the management of children with metabolic disorders who present to the emergency department. I know that this is a subject that makes us all a little bit nervous, and you’re just hoping that the parents have a good laminated sheet to tell you everything that you need to do.

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

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

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

Take it away, Emily.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This has been Brad Sobolewski. See you next time.


Vitamin K Deficient Bleeding (Hemorrhagic disease of the newborn)

Newborn infants need intramuscular injections of Vitamin K in order to produce critical clotting factors. If they don’t get it they can have potentially life threatening bleeding.


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


  • American Academy of Pediatrics, Committee on Fetus and Newborn.  Controversies Concerning Vitamin K and the Newborn.  Pediatrics 2003 July; 112(1):191-2.
  • Ross, JA, Davies SM. Vitamin K prophylaxis and childhood cancer. Med Pediatr Oncol. 2000 Jun;34(6):434-7.
  • Cornelissen, M., et al.  Prevention of vitamin K deficiency bleeding: efficacy of different multiple oral dose schedules of vitamin K.  Eur J Pediatr.  1997 Feb; 156(2):126-30.
  • Greer, FR, et al. Improving the vitamin K status of breastfeeding infants with maternal vitamin K supplements. Pediatr. 1997 Jan;99(1).
  • Kher P, Verma RP. Hemorrhagic Disease of Newborn. [Updated 2023 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from:


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. Today, we’re gonna talk about vitamin k deficient bleeding, also known as hemorrhagic disease of the newborn. This is a bleeding disorder that manifests in the first few days to weeks of life after delivery. Under the umbrella are a whole range of hemorrhagic diseases, but the most important is vitamin k deficient bleeding.

I’ll get into why in a moment. Vitamin k itself is a fat soluble vitamin mainly synthesized by gut bacteria. Newborns have minimal vitamin k reserves in a sterile gut. And there’s insufficient placental transfer and breast milk is deficient in vitamin K, so that’s why infants need vitamin K at birth. Without it, they can’t produce clotting factors 2, 7, 9, and 10.

You need all those. In brand newborns, the levels are about 20 percent or less of adult values, but within a month after birth, they arise to within normal limits. Other causes of hemorrhagic disease of the newborn include hereditary clotting factor deficiencies such as hemophilia A or B. And the most common item on the differential, especially for late onset, which we’ll talk about in a moment, is trauma, non accidental or accidental trauma. So why am I covering this topic?

Well, a lot of people out there are actually refusing vitamin k for their newborns. Why? Well, families state that they have concerns about the preservative in the injection, maybe that it could cause autism. It doesn’t. The pain from the injection could be harmful to the infant.

They perceive that the intramuscular vitamin k is a vaccine. It’s not. The dose of intramuscular vitamin K is too high. It isn’t. A potential for adverse reactions to an injection like anaphylaxis.

Anaphylaxis can happen after IV infusion and it’s been rarely reported after I’m injection, like winning the Powerball odds. The injection is perhaps a potential entry for germs, that the intramuscular vitamin K causes cancer. So there was 1 study published in the British Medical Journal in 1990. It raised that concern, suggesting that the risk of cancer was doubled in babies that receive vitamin K after birth. Many studies since then in Europe and the United States have refuted this claim and there is absolutely no association between vitamin k and cancer.

Other concerns about vitamin K include that vitamin K may overwhelm the newborn’s immune system. There’s just a general desire to be natural and perhaps a belief that oral vitamin k prenatally to the mother is more effective, but it isn’t. Furthermore, parents who refuse IM vitamin k tend to refuse other preventative measures, including the Hep B vaccine at birth, prophylaxis against gonococcal ophthalmia, which is really bad, and subsequent routine vaccination. Approximately 1 half of the severe cases of vitamin k deficient bleeding are associated with parental refusal vitamin k during the birth and hospitalization. So hemorrhagic disease of the newborn vitamin k deficient bleeding can be categorized into 3 groups based on the age of onset.

Early occurs within the first 24 hours after birth and it’s generally due to maternal medicines that block vitamin k action. Uh, most commonly, these are anti epileptics like phenytoin, phenobarbital, carbamazepine or primidone. They could also be anticoagulants, coumadin, aspirin or even some antibiotics like cephalosporins. The incidence in infants who have not received vitamin k prophylaxis in parents that are on these medicines could be 6 to 12 percent. Classical vitamin k deficient bleeding happens within 1 week of neonatal life, the second through the seventh day.

With vitamin k, the risk is 0.01 percent. If babies are exclusively breastfed and they don’t get vitamin k at birth, that increases the risks. Late onset is from 8 days up to 6 to 12 months. And this is generally exclusively breastfed babies and babies with diarrhea, cholestasis or malabsorption because vitamin k absorption is dependent on bile. The risk is about 1 in 15000 to 1 in 20000 births.

Most common symptom of late onset is intracranial bleeding with a mortality of 20 to 50 percent and all the associated morbidity of an intracranial hemorrhage. The reason for the increased risk in exclusively breastfed infants, I. E. Even those who don’t get any solids or anything else, is because there’s only marginal levels of vitamin K in breast milk. Other causes of late onset, cystic fibrosis, celiac, chronic diarrhea, alpha 1 antitrypsin deficiency, and forms of hepatitis.

So if you suspect vitamin k deficient bleeding, take a good history. These are some of the points in the history that could lead to you making the diagnosis. So take a history of the drugs that mom was on during pregnancy, especially anticonvulsants. Preterm babies are at a higher risk. Breastfed or bottle fed?

Again, bottle- or formula fed infants are at a lower risk because fortified feedings have higher levels of vitamin K. Where was the delivery? Home delivered infants don’t have access to immediate vitamin k prophylaxis at the same rates that hospitalized infants do. So physical findings that you might see in a patient with vitamin K deficient bleeding include cephalohematoma, intracranial bleeding, intrathoracic bleeding, like hemoptysis or associated respiratory distress, intra abdominal bleeding, so you can see melena, hematemesis, you know, isolated GI bleed. You know, you could also think intussusception and mccals.

Skin, you’ll see petechiae on the mucous membranes. You’ll see hemorrhage or petechiae inside the mouth, on the gums, in the nose, excessive bleeding after circumcision, bleeding from the umbilical cord stump after it’s cut and if the umbilical cord falls off, bleeding from vaccine sites. And I mentioned it before and I’ll say it again, but intracranial bleeding is the worst possible outcome. It’s associated with late onset vitamin k deficient bleeding, and it presents with a floppy baby, lethargy, feeding difficulties, bulging fontanels, poor respiratory effort, altered consciousness, convulsions or pallor. These are sick looking babies.

So in evaluation, you wanna get a CBC. Uh, vitamin k deficient bleeding will have normal platelet levels. Thrombocytopenia actually suggests a maternal immune thrombocytopenia in a newborn. They can make antibodies to platelets which can cross the placenta. Clotting profile, the INR will be greater than 4, because again those factors are needed for proper blood clotting.

The PT will be more than 4 times normal. That’s increased due to decreased activity of factor 7. The PTT will also be increased due to decreased activity of factors 2, 9, and 10. The clotting time will be increased due to clotting factor deficiencies, but fibrinogen levels will remain normal. Protein induced by vitamin k antagonists, PIVCA, I guess.

There’s an estimation you can get a lab on that. Any amount of PIVCA is abnormal and indicates vitamin k deficiency. This disappears around day 5 after the administration of vitamin k, but this lab is not part of the routine ED evaluation. Imaging is targeted at the differential diagnosis in the site of bleeding. So get a chest x-ray or an ultrasound, determine if there’s bleeding in the body cavities, you know, the chest or the abdomen.

Um, CT and MRI are most useful to evaluate for intracranial hemorrhage. So treatment. Uh, vitamin k at birth. I think I mentioned that before. So for an infant that’s greater than 1500 grams, so most of the babies that you’ll be taking care of, 1 milligram I’m Less than 1500 grams, 0.3 mgs per kg up to 0.5 mg per kilogram I’m Intravenous vitamin K is not recommended for prophylaxis in preterm infants.

The form that we now give is vitamin K1, It’s a naturally occurring fat soluble form of vitamin k. So before the introduction of vitamin k 1, long before any of us trained, they used vitamin k 3. K3 was a synthetic water soluble derivative. And in higher doses, it was associated with kernicterus hemolytic anemia and hyperbiliruminemia. So vitamin K1, current version, very safe.

Again, in the US, intramuscular vitamin K at birth is recommended. There are no known toxicity or side effects associated with vitamin K1. Now in some parts of Europe, they’ll do oral regimens at birth, at 2 to 4 weeks, and at 6 to 8 weeks. Uh, they can be weekly or even daily. There’s no licensed oral form for newborns in the US.

Some have given infants the injectable liquid by mouth, but it’s not observed and that’s an unstudied intervention. There’s no safety or efficacy data available on that route of administration. In countries that have gone to oral prophylaxis, failures, even with good compliance, have been reported. Failures have not been reported with routine I’m prophylaxis. So based on the available observational evidence, a single I’m dose of vitamin k appears to be more effective in preventing late onset vitamin k deficient bleeding versus oral regimens.

So maternal dietary changes have little effect overall on vitamin K status of the newborn. There was 1 smaller study that showed that 5 milligrams a day or 800 percent of the recommended daily allowance may raise infant serum levels to near formula fed infants in moms that are breastfeeding. But there’s no FDA approved multivitamin that contains that amount of vitamin K. So if you have a baby with hemorrhagic disease of the newborn, in early and classic forms, the treatment is oral vitamin K, 2 milligrams dose, repeated at 2 to 4 weeks and 6 to 8 weeks. And so again, these are milder forms of bleeding.

All breastfed babies with diarrhea and malabsorption situations require an additional postnatal dose of vitamin K to prevent late onset vitamin K deficient bleeding. For the late form of the disease, oral vitamin K is not as efficacious as parenteral. Hence, the 0.5 to 1 milligram single I’m dose should be administered. A presumptive diagnosis of vitamin k deficient bleeding should be made in an infant presenting with bleeding or neurologic symptoms, and either a prolonged PT and or INR, a history of not receiving vitamin k prophylaxis at birth. You should immediately give them 1 to 2 milligrams IV or sub q.

The vitamin k dose should normalize the coagulation profile within 2 to 3 hours. Infants may need resuscitation with blood products if they’ve lost more than 20 percent of their blood volume. And remember, a newborn can become hypotensive by bleeding enough inside their brain. And also, babies may need 10 to 20 ml per kilo of fresh frozen plasma. I’m going to leave you with a quote from Stanford University and Lucille Packard Children’s Hospital.

So the success of vitamin K prophylaxis has been so dramatic that many practitioners have actually never seen an infant afflicted with hemorrhagic disease of the newborn or vitamin k deficient bleeding. Now, it’s a popular trend in some areas to refuse prophylaxis in an effort to keep things natural for the infant. However, it’s important to keep in mind that the infants most at risk for the classic form of the disease are healthy babies who are exclusively breastfed. So we need to work closely with the parents who refuse vitamin k to help them understand the need for prophylaxis and the severity of the disease. The benefit of using I’m vitamin k injection should be explained to parents.

For those that refuse injection, counseling about the adverse effects of vitamin k deficient bleeding should be explained. The alternate oral dose of 2 milligrams should be recommended in the parents that strictly refuse I’m along with a repetition of that dose at 2 to 4 and then 6 to 8 weeks of age. Alright. So that’s all that I’ve got for this episode on vitamin k deficient bleeding AKA hemorrhagic disease of the newborn. Hopefully, you will feel armed to discuss vitamin k refusal with parents, as well as understand the different forms of the disease, including early, which is related to maternal medicines, classical, which is exclusively breastfed infants who don’t get vitamin k at birth, and the late form, which is the most dire and presents often with intracranial hemorrhage. If you have ideas for other episodes or topics you’d like to suggest, send them my way. I will take your feedback via email, a comment on PEMBLOG, a direct message on a social media platform, a snail mail.

However you wanna get feedback in my direction, let me know. Encourage your colleagues to listen to the podcast as well. More listeners means more learning. And, hey, I know that this can be a tough tough topic to discuss with some parents. I think we’re all better armed to have those conversations if we practice them beforehand.

So hopefully, this episode will prepare you for the next time you meet a newborn whose parents are using vitamin k. For PEM currents, the pediatric emergency medicine podcast, this has been Brad Sobolewski. See you next time.

Infectious Diseases


This episode will help you recognize cellulitis and even differentiate it from erysipelas which is totally a different thing. You’ll also learn about treatment, whether or not a blood culture is necessary, and a whole lot more.


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Chen AE, Carroll KC, Diener-West M, Ross T, Ordun J, Goldstein MA, Kulkarni G, Cantey JB, Siberry GK. Randomized controlled trial of cephalexin versus clindamycin for uncomplicated pediatric skin infections. Pediatrics. 2011 Mar;127(3):e573-80. doi: 10.1542/peds.2010-2053. Epub 2011 Feb 21. PMID: 21339275; PMCID: PMC3387913.

Daniel J. Pallin, William D. Binder, Matthew B. Allen, Molly Lederman, Siddharth Parmar, Michael R. Filbin, David C. Hooper, Carlos A. Camargo, Clinical Trial: Comparative Effectiveness of Cephalexin Plus Trimethoprim-Sulfamethoxazole Versus Cephalexin Alone for Treatment of Uncomplicated Cellulitis: A Randomized Controlled Trial, Clinical Infectious Diseases, Volume 56, Issue 12, 15 June 2013, Pages 1754–1762,

Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.

Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis 2014; 59:e10.


Note: This transcript was partially completed with the use of the Descript AI

 Welcome to another episode of PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today’s episode is all about cellulitis. What is it? Well when a break in the skin occurs, normal skin, flora, and bacteria can enter the subcutaneous tissue, where they do not belong, and they can also invade the lymphatic system.

And although this podcast episode is entitled cellulitis, I’m also going to talk about erysipelas. The two terms are not interchangeable. but both manifest as areas of skin, erythema, edema, and warmth. Cellulitis involves the deeper dermis and subcutaneous fat. Whereas erysipelas involves the upper dermis and there’s a more clear demarcation between the involved and uninvolved tissue.

There’s a fun fact, since the ear doesn’t have deep or dermal tissue, it’s always. ear-a-sipelas. I’ll pause for laughter. Anyway, a skin abscess, which is not the focus of this episode, is a collection of pus deep within the dermis or subcutaneous space. Impetigo, also not included in this episode, is a very superficial infection with that honey crusted drainage. There are also bullous versions. So cellulitis tends to develop in a bit more of an indolent fashion over a few to several days, whereas erys syphilis is more acute. You get systemic symptoms faster, such as fever. Chills, severe malaise, and headache. These can precede the onset of the local skin changes and start just in a matter of hours.

Clinically, for both, you’ll see areas of skin erythema. edema and warmth. You can also see petechiae and hemorrhage, as well as superficial bulla, vesicles, or even echemosis. Sometimes you also see regional lymphangitis or enlargement of the regional lymph nodes. If you’ve got a lot of edema surrounding the hair follicles, you can see some dimpling in the skin.

This creates an orange peel texture appearance, peau d’orange. I hope I pronounced that right. I took Spanish in high school. Anyway, the skin is warm to the touch, it’s uncomfortable, it hurts with movement, and some patients can describe an itchiness or a tight feeling in addition to the pain. You may see fever and other systemic symptoms, and cellulitis and erysipelas, especially in children, are nearly Always unilateral.

Bilateral red limbs? That’s probably something different. Complications that you should be aware of include bacteremia, endocarditis, septic arthritis, or osteomyelitis. Full blown sepsis and toxic shock syndrome. Fortunately, those are rare. So, in general, mild cellulitis has no systemic features in a patient with no significant comorbidities.

Moderate cellulitis has moderate swelling and tenderness with some systemic features like fever or tachycardia. Severe cellulitis has severe swelling and tenderness. really affecting function. It’s a larger body surface area, and you’ve got marked systemic features. So fever or hypothermia, extreme tachycardia, tachypnea, altered consciousness, a very unwell appearance, or even hypotension.

So what causes it? Well, bacteria, and the most common etiology. Staphylococcus aureus is actually an infrequent cause of cellulitis in children. But it can be seen more often in penetrating wounds. Methicillin resistant Staphylococcus aureus classically causes abscess formation. So you won’t really see that as the cause of isolated cellulitis or erysiplas in children.

So how do you make the diagnosis? Well, it’s clinical, right? Look for areas of skin that are erythematous, edematous, warm, and painful. Labs or imaging are not routinely necessary. If you think that there’s an abscess, you can diagnose it clinically by a localized area of induration or fluctuance or use an ultrasound.

Cellulitis can look like a cobblestone street on sonogram. And you should consider whether or not an abscess is present if you see significant induration, so thickening or hardening of the soft tissues, of greater than three centimeters or non uniform induration. The lesion’s been present greater than two to three days and changing or getting worse, and there’s a history of a previous incision and drainage in that patient.

And so do you need labs? Nah, not really. And the vast majority of patients of CBC or other labs will not aid in making the diagnosis of cellulitis. What about blood culture? Every febrile kid with cellulitis needs a blood culture, right? Not so fast, right? A blood culture can cost more than $200-300.

If you’re sending the kid home. Well, you definitely shouldn’t be sending a blood culture because if you’re worried about bacteremia and sepsis, that kid needs to stay in the hospital. And think about the risk of a false positive versus the risk of a true positive. So if the risk of a contaminant culture is greater than the risk of actually catching a bacteria, then don’t send it.

The cost of false positive cultures, repeat visits, length of stay, could be in the thousands of dollars. And so a lot of the previous studies on getting blood cultures were done in the immediate post Haemophilus influenzae B and Prevnar vaccine era. And we do now live in an era where these invasive organisms are fortunately not as big of a concern.

Vaccinate your children, people. But we do deal with MRSA. But still, for mild and moderate cellulitis, MRSA’s not really the etiology. And so even if a kid has a fever, But they look better after a dose of acetaminophen or ibuprofen. You don’t routinely need a blood culture. Now you could even admit a kid for IV antibiotics, maybe they’re dehydrated or they can’t take PO for some reason, without sending a blood culture.

So, admission does not mandate a blood culture. As always, you want to check with your local recommendations and follow algorithms present at your institution. So, what about disposition? So, with prompt identification and treatment with a correct antibiotic, which I’ll get to in a few minutes, patients can see an improvement in their signs and symptoms within about 48 hours.

The treatment failure rate is low, less than 1 out of 7, but probably a bit lower than that, with initial appropriate antibiotic treatment. Overall Cellulitis has a really good treatment prognosis. So when do you want to think about admission to the hospital or short stay unit versus discharge? Right, so you should probably admit a patient to the hospital if they have significant systemic symptoms.

You’re concerned about SIRS or sepsis. Again, fever alone does not necessitate admission. Especially if the kid looks better after antipyretics. If you are concerned that the child may need subsequent or future I& D, like they’re forming a phlegmon, they have a deeper infection, like necrotizing fasciitis, or they need sub sexually consultation, these are probably reasons to admit the patient to the hospital.

Now, some facilities have a short stay unit, like in their emergency department. So, if you don’t meet inpatient admission criteria, you’re likely to improve within 28 hours. Maybe the kid failed initial outpatient treatment with 48 hours of appropriate antibiotics, and they need just a day of IV. They’ve got a rapidly expanding lesion, but it’s probably IND.

The kid has a lot of pain. They can’t tolerate oral antibiotics, or they’re less than six months of age. You know, maybe that’s a patient you observe for just 24 hours in a short stay. And fortunately, cellulitis in children under the age of 2 months of age is rare, but those kids should probably be admitted for IV antibiotics as well, and you should get a blood culture in those situations. One example would be neonatal mastitis, a skin infection of the breast tissue.

Alright, so let’s talk about antibiotics. And generally, your best choice for the majority of children is cephalexin. You’d think because MRSA is everywhere. You want to avoid first generation cephalosporins, but it’s still mostly beta hemolytic strep.

And studies, including Chen et al., showed no difference between cephalexin and clindamycin. And what about length of treatment? Well, for mild cases, five days is probably just as good as ten days. But if you have moderate or severe symptoms, a week and a half is a good idea. You’ll see a lot of places start cephalexin plus clinda, or cephalexin plus trimethoprim sulfamethoxazole.

It’s still often done out in the community. A representative randomized control trial from Palin from 2013 showed that the addition of TrimSulfa did not improve outcomes in a very large cohort that contained lots of children. So the bottom line is, even in patients where you think they might have MRSA nasal carriage?

Monotherapy with cephalexin is fine. So, if you’re doing outpatient treatment or you’re transitioning patient to oral treatment after IV, the first line therapy is oral cephalexin. The dose is 50 mg per kg per day, divided every 8 hours or 3 times a day with a max of 500 mg per dose. If the patient has a true allergy to cephalosporins, you do oral clindamycin, 10 mg per kg per dose, every 8 hours, or 3 times a day, with a max of 1, 800 mg per day, or 600 mg per dose.

If you see treatment failure, that’s another reason to do clinda. So if the kid’s not getting better in 48 to 72 hours on cephalexin, you can do the same dosing of clinda that I just mentioned a moment ago. For inpatient treatment, first line therapy is intravenous cefazolin. So 20mg per kg per dose every 8 hours with a max of 1g per dose.

Cephalosporin allergy, you would use clindamycin. And yes, PO and IV clindamycin are bioavailable. But if you’re admitting somebody, there’s probably a reason that they may not be able to take PO. So if it’s IV, it’s 10mg per kg per dose every 8 hours with a max of 900mg. So it’s higher than the max for PO.

And so again, I will reiterate that 5 days for very mild cellulitis is totally okay. But you could do 10 if that’s what you do locally. Moderate and severe, you need 10 days. Some specific scenarios that you might want to deviate from cephalexin, so if there’s a mammalian bite, some don’t need prophylactic antibiotics, and I’ll admit, There’s no randomized controlled trials of dog bites.

I don’t think the IRB would approve that, but if you are concerned about infection, amoxicillin clavulonate, 22. 5 milligram per kilogram with a max of 875 milligram per dose, oral twice daily. If the kid looks well, And the degree of redness or symptoms is very mild, you could do five days, that’s totally okay.

If the child got an infection in a seawater or freshwater environment, there’s some different organisms like Aeromonas and Vibrio and other things that you want to consider. So you would still start with Cephalexin, but you would add Ciprofloxacin, 10 mg per kg, max 500 mg per dose, twice a day. Or Trimethoprim sulfamethoxazole twice a day with an overall treatment length of 5 to 10 days.

And if you definitely think that it’s methicillin resistant staphylococcus aureus that you’re treating, mild cellulitis, you could do trimethoprim sulfamethoxazole or clindamycin. If you’re sure it is moderate MRSA cellulitis, you could do a trial of oral antibiotics with close follow up or vancomycin IV.

And if they have severe cellulitis, Vancomycin IV, and if you have Staphylococcal Scalded Skin Syndrome, consider adding clindamycin. Switch to oral antibiotics as soon as the patient looks better. And there are some cases of cellulitis where you might need a specific subspecialist. So a general surgeon should be consulted if you have cellulitis of the breast, perianal tissues, perineal tissues, a complex of recurrent pilonidal abscess, Though you could drain these and have them follow up as an outpatient.

Or the cellulitis is just large and complex, or you think it’s going to need drainage in a day or two. ENT should see invasive neck cellulitis, especially with significant symptoms, or you’re concerned that it might be a deeper infection. ophthalmology and or ENT for orbital or periorbital cellulitis, orthopedics for septic arthritis, tenosynovitis or osteomyelitis, and dental or oral maxillofacial surgery for facial cellulitis due to dental infection where the kid might need to be admitted.

All right, so that’s all for this episode on cellulitis. Remember, most cases are mild or moderate, and the child will do incredibly well with oral antibiotic therapy, which should generally be cephalexin. You do not need labs, and especially a blood culture, for the vast majority of children with infections like cellulitis or erysipelas.

A fever does not mean you have to get a blood culture or admit the kid. If they haven’t started antibiotic therapy yet, and they look better after they defer vest with antipyretics, Start oral antibiotic therapy and develop a close follow up plan. Well, I hope this episode is useful. Ultimately, my goal is to deliver succinct evidence based information to help you on your next shift in the ED.

If there’s other topics that you want to hear about, send them my way. I’ll take an email. I’ll take a comment on the blog. I’ll take a direct message on Twitter or X or whatever it’s called. Leave a review on your favorite podcast site. That helps other people find it. And if more people can learn, I’m going to be happy about it.

Encourage your colleagues to listen and subscribe to the podcast. And thank you so much for your time and attention. I know you’re all busy out there. For PEM Currents, the Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you next time.



Laryngomalacia, is the most common cause of infant stridor. Early diagnosis is crucial as it can impact a child’s growth and development. Most infants get better on their own, but those with severe symptoms need surgical interventions like supraglottoplasty. Learn all about diagnosis and management of this common problem in this brief podcast episode.


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Klinginsmith M, Goldman J. Laryngomalacia. [Updated 2022 Jun 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from:

Hartl TT, Chadha NK. A systematic review of laryngomalacia and acid reflux. Otolaryngol Head Neck Surg. 2012 Oct;147(4):619-26.

Boogaard R, Huijsmans SH, Pijnenburg MW, Tiddens HA, de Jongste JC, Merkus PJ. Tracheomalacia and bronchomalacia in children: incidence and patient characteristics. Chest. 2005 Nov;128(5):3391-7.

Isaac A, Zhang H, Soon SR, Campbell S, El-Hakim H. A systematic review of the evidence on spontaneous resolution of laryngomalacia and its symptoms. Int J Pediatr Otorhinolaryngol. 2016 Apr;83:78-83.


Note: This transcript was partially completed with the use of the Descript AI

Welcome to another episode of PEMCurrents, the pediatric emergency medicine podcast. As always, I’m your host, Brad Sobelewski. Your time is valuable and was mine, and that’s why I release these brief episodes, focus on a single topic, get you in, get you out, teach you something. Today, let’s talk about The most common cause of noisy breathing in newborns and infants, laryngomalacia. You’ve all seen this, or should I say you’ve all heard this, And you will hear the symptoms of stridor and noisy breathing, often positional, and it can impact growth and development.

Now I always thought it was just because airways are small and they’re floppier and therefore noisier, but All infants have small airways and all of their cartilage is soft, so there’s more to the picture. So why does this happen? Well, it could be neurologic function. You could have abnormal tone of the laryngeal nerve. You might have an imbalance of demand supply during inhalation in some infants.

And reflux isn’t a direct cause, but approximately sixty percent of infants with laryngomalacia do also have gastroesophageal acid reflux disease. And we know that reflux can irritate and swell the upper airway, potentially worsening obstructive symptoms. So the incidence is unknown, but it’s probably about one in two to three thousand infants. But it might underestimate it because lots of mild cases don’t actually present clinically, and they’re not diagnosed endoscopically. In the past, we thought there was a male predominance, But it’s equally common in female infants, and black and Hispanic infants may have a higher risk compared with white infants.

Low birth weight has also been suggested to be a contributing factor. So when you’re looking at an infant with possible laryngomalacia, You need a very detailed birth history. So were there any surgical procedures or intubations? Parents need to give you information about breathing difficulties, Especially, noisy breathing or episodes of apnea, noisy breathing that worsens with feeding or while lying down may indicate laryngomalacia. You should also ask detailed questions about feeding habits, weight gain, or if the child’s experiencing failure to thrive.

There are, of course, other causes of noisy breathing in infants that are on the differential. Unilateral vocal cord paralysis Often happens after surgery. So if the kid’s not had surgery, it’s pretty much less likely. Bilateral vocal cord paralysis, which is twice as worse, Prevents with biphasic stridor and may require tracheostomy if respiratory distress is significant. Laryngeal papillomatosis can cause a hoarse cry in upper airway obstruction, and it also appears in infancy.

Subglottic hemangiomas are fortunately rare, but they can cause Torrey Strider. Hemangiomas distributed like a beard are suggestive of this. Subglottic stenosis happens via scarring in the subglottic region due to a previous intubation. So stridor may be present in these infants, but it doesn’t typically change with position. And the child’s history would include a NICU stay and an intubation.

Tracheomalacia and bronchomalacia can coexist with a ringomalacia. Expiratory airway sounds are commonly heard in addition to the stridor, and diagnosis needs scope. We’ll talk more about those in a moment. Vascular ring is a rare cause of airway obstruction in infants, and you’d have feeding difficulties in stridor. The best way to diagnose this is through imaging like CT scans.

And finally, you should always think about foreign body aspiration Even in a child who is not eating solids yet. Remember, an older sibling could feed them something. I have seen this before. So an infant is in respiratory distress after being accompanied or the symptoms are persistent, you should always think about a foreign body, especially in the acute setting. The physical exam of a Child with possible laryngeal malaysia focuses on the airway and breathing naturally.

Make sure that the nasal passages are patent. You don’t wanna miss The oral cavity should be explored for cleft lip, cleft palate, glossoptosis, Pierre Robin sequence, or micronathia. Obviously, all of those facial and oral abnormalities can contribute to breathing and feeding difficulties. You wanna check out the neck for masses or vascular lesions. And many infants have hemangiomas, but I mentioned this before.

If you see them in a beard like distribution, worry about airway hemangiomas. So if you have an infant that has some intermittent, noisy breathing on inspiration, and sometimes it’s worse with feeding and when they lay down, you should really think about laryngomalacia. And if the infant is thriving and growing well, not having any apnea or color change, you can kinda wait it out. But if you wanna make the diagnosis definitively, you will need to have an otolaryngologist perform an awake, Flexible fiber optic laryngoscopy. That’s the primary diagnostic tool for infant stridor in general.

You get a comprehensive view of the oropharynx, the supraglottis, the glottis, the subglottic area, and the hypopharynx. For infants with laryngomalacia on scope will have some specific anatomical abnormalities. They’ll have shortened aryepiglottic folds, An omega shaped epiglottis and or redundant arytenoid tissue. And again, The awake flexible fiber optic laryngoscope is the gold standard for diagnosing laryngomalacia. The Kid is awake and breathing, and that allows you to assess the dynamic collapse of the supraglatic airway during respiration.

In the child with more severe symptoms or you’re worried about tracheomalacia, direct laryngoscopy including a diagnostic bronchoscopy in the OR under general anesthesia may provide a more comprehensive look at the Airway and the upper aerodigestive tract. So you’ll scope down to the main stem bronchi in this standpoint. Sometimes you get A triple scope, which is flexible laryngoscopy, bronchoscopy, and upper endoscopy. So three endoscopists together. I don’t know if there’s a discount.

And this is important when there’s severe symptoms or you have concern about synchronous airway lesions. Direct laryngoscopy can also be a prelude to surgical intervention if you need it. Speech therapists could be particularly valuable If there’s issues with swallowing or feeding, if you’re concerned about aspiration or swallowing deficits sometimes they’ll do a modified barium swallow study. Sleep studies can be particularly helpful to look at symptoms of obstructive sleep apnea, especially in older symptomatic infants. As I’ve alluded to before, fortunately, most children resolve on their own by about twelve to eighteen months of age.

So this management is conservative, includes upright feeding, antireflux therapy, so alterations to how you Feed, burp, and position. And no study has yet shown that proton pump inhibitors improve laryngomalacia symptoms, but they’re still widely used. What’s important to remember is that the majority of infants don’t need any intervention. However, there is a small proportion of infants that do have more severe symptoms, like poor weight gain, Feeding difficulties, obstructive sleep apnea, severe breathing symptoms, they’ll need a procedure called supraglottoplasty. And so how is that done?

Well, they could use lasers or cold steel or microdebridement, and it’s really tailored to the individual patient’s anatomy. So you could divide shortened area epiglottic folds. You can remove some redundant arytenoid mucosal tissue. You could do an epiglottopexy or a combination of some of these. And you really obviously don’t wanna scar the infant’s airway or cause glottic stenosis.

Supraglottoplasty is highly effective. Ninety five percent do great and see measurable and significant improvement in their laryngomalacia symptoms. Only about five percent need some sort of provision, And a higher risk of that is seen in patients that were under two months of age when they got the initial procedure or have neurologic or cardiac comorbidities. Neurologic comorbidities have the highest rate of revision surgery. Maybe up to three out of five patients will need a trach due to ongoing airway obstruction.

Aspiration after supraglottoplasty is the main risk, but it’s rare and not significantly associated with the procedure Self. And let’s not forget the main reason that most of you have heard of larynga Malaysia. It’s because a parent was worried about it. It can be scary to have a baby who is breathing noisily. The fear in the back of your head is that the baby could stop breathing and die.

It’s real. I’ve heard it personally. Ultimately, providing reassurance, guidance, close follow-up, and helping the parent understand what they’re doing well can go a long way into making sure that you’re not missing anything else and you’re appropriately monitoring the infant with potential laryngomalacia. Refer to ENT if you’re unsure of the diagnosis or if you feel that it will benefit the patient. It may seem a little barbaric, but an awake Bedside fiber optic scope isn’t actually that big of a deal.

Alright. So here’s some summary points. The majority of patients with Laryngomalacia will outgrow it by twelve to eighteen months. Diagnosis can be suspected clinically, but awake fiber optic Flexible laryngoscopy is definitive. Severe symptoms should be monitored and include recurrent cyanosis or respiratory distress, Apnea and failure to thrive.

These need further workup, including many times direct laryngoscopy and bronchoscopy to rule out other airway abnormalities. Surgery is generally only indicated in patients with severe laryngomalacia, and it’s called Supraglottoplasty. It’s generally well tolerated to highly effective. Patients with neurologic comorbidities or congenital cardiac disease and those less than two months of age are more likely to require revision surgery for relief of ongoing symptoms. Alright.

So that’s it for this episode. Hopefully, you learned something new about laryngomalacia. If you have any other suggestions for topics, send them my way. I’ll take emails, comments on the blog, direct messages on x or Twitter, threads, Facebook, whatever channels you wanna use. My goal is to make sure that you are ready for your next ED shift with up to date information that’s evidence based and ready to deliver to patients and families.

If you have the time, leave a review on your favorite podcast site. That helps with discovery so that more people can listen and learn. And share this episode in the show with your colleagues. I’d love to hear what they think as well. For PEM currents, the pediatric emergency medicine podcast, this has been Brad Sobolewski.

See you next time.


Meckel Diverticulum

Meckel diverticulum is a congenital anomaly of the small intestine that can present with various clinical manifestations, including rectal bleeding and obstruction. Recognizing the characteristic features and understanding the differential diagnosis is crucial in managing patients with lower gastrointestinal bleeding. This episode will help you recognize and diagnose this surgical condition that you probably remember because the “rule of twos.”


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Dixon P & Nolan D. The Diagnosis of Meckel’s Diverticulum: A Continuing Challenge. Clin Radiol. 1987;38(6):615-9

Ghahremani G. Radiology of Meckel’s Diverticulum. Crit Rev Diagn Imaging. 1986;26(1):1-43

Weerakkody Y, Ranchod A, Yap J, et al. Meckel diverticulum. Reference article, (Accessed on 26 Oct 2023)

Sagar J, Kumar V, Shah DK. Meckel’s diverticulum: a systematic review. J R Soc Med. 2006 Oct;99(10):501-5.

An J, Zabbo CP. Meckel Diverticulum. [Updated 2023 Jan 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from:


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. Your time is valuable and so is mine. And that’s why I release these brief, succinct episodes focused on a single clinical topic, get you in, get you out, teach you something. Today I’m going to talk about Meckel diverticulum. If you haven’t seen it clinically, you have seen it on a test and it is absolutely something that you should be thinking about when you see a patient with bloody stools in the emergency department.

So Meckel diverticulum is a congenital abnormality of the small intestine and it’s the most common cause of significant lower GI bleeding in children. It arises from an incomplete involution of the vitelline duct during embryonic development. You didn’t think I’d say that during this podcast.

Typically occurring during the seventh week of gestation. It’s characterized by a blind ending true diverticulum, a pouch, that contains all of the layers typically found in the ileum. So especially relevant to board exams, Meckel diverticulum follows the rule of twos. So it affects approximately 2 percent of the population.

It’s located about two feet from the ileocecal valve. It’s usually about two inches long. Only about 2 percent of cases actually become symptomatic. It is most commonly diagnosed by the age of two years, with 45 percent of symptomatic cases occurring in this age group. It is two times as common in boys, and there are two types of epithelium found in the meckle diverticulum, gastric and pancreatic.

So the clinical presentation of Meckel can vary depending on the complications that arise. The most common presentation in children Under the age of five years is rectal bleeding, which may be intermittent or just massive, but the bleeding is usually painless. Other complications include obstruction due to intussusception or volvulus, which can lead to bowel ischemia or shock.

Diverticulitis and umbilical fistula can also occur, but that might typically be seen later in life. In approximately a third of cases, Meckel diverticulum may perforate, and traumatic rupture of one could actually occur following blunt trauma. Let’s move briefly into the differential diagnosis of GI bleeding in children.

So, upper GI bleeding is typically not bright red. Now you could have a briskly bleeding ulcer and a liver transplant patient, but that’s not something we typically see in pediatrics. So generally lower GI bleeding is bright red, hematochezia, whereas the upper GI bleeding is maroon or dark black, diverticular disease.

which is rare in children, could cause bright red bleeding. A vascular ectasia or angio dysplasia, which is really hard to diagnose unless you’re an endoscopist. You could have bright red blood from inflammatory bowel disease, infectious colitis, mesenteric ischemia or ischemic colitis, colorectal cancer or polyps, hemorrhoids, both internal and external.

Aortoenteric fistula, or vascular fistulas, which are pretty darn rare in children, and generally a complication of inflammatory bowel disease or previous surgery, a rectal foreign body, a rectal ulcer, which is often associated with HIV, syphilis, or other sexually transmitted infections, or an anal fissure.

So all of these things are on the differential for lower GI bleeding. It’s important to note that if you see diarrhea with blood, as opposed to just frank blood, you should be thinking about infectious problems, like STEC causing organisms, like E. coli 0157:H7 which can lead to hemolytic uremic syndrome, or inflammatory bowel disease, or other problems.

So the diagnosis of Meckel diverticulum is called a meckle scan. I wonder how it got its name. It’s a technetium 99 pertectinate scan, and it’s the classic test of choice for diagnosis. It’s a nuclear medicine study, and the radioactive tracer is taken up by the gastric mucosa, which is in the Meckel diverticulum.

Therefore, it’ll show up on the radiology picture. The sensitivity is reported to be about 60 percent in adults, but 85 90 percent in children. The uptake of the dye can be increased by giving cimetidine or glucagon. So the feeding artery of the Meckel diverticulum is an anomalous branch of the superior mesenteric artery.

It has a long and non branching course and it ends generally towards the right lower quadrant. So the MEKL scan will help you pick up where that gastric mucosa is and then the surgeons can figure out how the blood supply gets there. Ultrasound and CT are not really good at differentiating a Meckel diverticulum from normal bowel.

So, if you think that somebody has a Meckel diverticulum, Here are some following management steps. If the patient has signs of obstruction, insert a nasogastric tube for GI decompression. Give broad spectrum antibiotics to cover potential bacterial infection, especially if the patient is ill appearing.

Give IV fluids packed red blood cells to resuscitate. A CBC and type and screen are great lamps to get. If there’s brisk bleeding or the patient’s unstable, consider COAGs. And yeah, you’re gonna want to consult a surgeon because that is how you deal with asymptomatic Meckel diverticulum. So if you’ve got complications such as significant bleeding, bowel obstruction or perforation, emergent surgical removal is warranted.

This can be done via a laparoscopic or open approach. So I’m going to wrap this up here. Again, this is a brief episode. A Meckle diverticulum is a congenital anomaly of the small intestine that can present with various clinical manifestations, including rectal bleeding. and bowel obstruction. Recognizing the characteristic features and understanding the differential diagnosis is crucial in managing patients with lower GI bleeding.

The Meckel scan is the preferred diagnostic modality. It’s a nuclear medicine scan and prompt surgical consultation is necessary for symptomatic cases. All right, so that’s it for this brief episode. If there’s other topics you want to see me tackle, send them my way. I’ll take your suggestions via email. Direct message on X or Twitter, Facebook, Instagram, telepathy. Any feedback is good feedback. Until next time, for PEMCurrents: The Pediatric Emergency Medicine Podcast, this has been Brad Sobolewski. See you later. 

Choosing Wisely Infectious Diseases

Respiratory viral panels

Just because you can test for dozens of viruses with a single swab should you? Is this actually measuring a current infection, or a recent virus from which the child has since recovered. And what about the cost? Are these tests expensive (spoiler alert: They are!). Learn about the situations when we should get these panels, and how we can avoid overusing them when we shouldn’t in this tremendous discussion with Dr. Olivia Ostrow and Dr. Kelly Levasseur.

This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the the American Board of Internal Medicine Foundation, the goal of which is the spark conversations between clinicians and patients about what tests, treatments, and procedures are needed – and which ones are not.

The Choosing Wisely recommendation: Do not obtain comprehensive viral panel testing for patients who have suspected respiratory viral illnesses

The Choosing Wisely Pediatric Emergency Medicine Recommendations

The Choosing Wisely Campaign Toolkit

Bonus Resource: The Dialogue Around Respiratory Illness Treatment (DART) program which is designed to support antibiotic stewardship


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


  1. Gill, PJ, Richardson, SE, Ostrow O. Testing for respiratory viruses in children: to swab or not to swab. JAMA Pediatr. 2017;171(8):798-804
  1. Noël KC, Fontela PS, Winters N, et al. The clinical utility of respiratory viral testing in hospitalized children: a meta-analysis. Hosp Pediatr. 2019;9(7):483-494
  1. Parikh K, Hall M, Mittal V, et al. Establishing benchmarks for the hospitalized care of children with asthma, bronchiolitis, and pneumonia. Pediatrics. 2014;134(3):555-562
  1. Innis K, Hasson D, Bodilly L, et al. Do I need proof of the culprit? Decreasing respiratory viral testing in critically ill patients. Hosp Pediatr. 2021;11(1):e1-e5
Choosing Wisely

Constipation: Diagnosis, X-Rays, and more

Where else is the poop going to be? Constipation is by and large a clinical diagnosis. This episode reviews how to make the diagnosis, red flags, and why X-Rays don’t necessarily help assess stool burden adequately in most children.

This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the the American Board of Internal Medicine Foundation, the goal of which is the spark conversations between clinicians and patients about what tests, treatments, and procedures are needed – and which ones are not.

The Choosing Wisely recommendation: Do not obtain abdominal radiographs for suspected constipation

The Choosing Wisely Pediatric Emergency Medicine Recommendations

The Choosing Wisely Campaign Toolkit


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Anwar Ul Haq MM, Lyons H, Halim M. Pediatric Abdominal X-rays in the Acute Care Setting – Are We Overdiagnosing Constipation?. Cureus. 2020;12(3):e7283. Published 2020 Mar 15. doi:10.7759/cureus.7283

Beinvogl B, Sabharwal S, McSweeney M, Nurko S. Are We Using Abdominal Radiographs Appropriately in the Management of Pediatric Constipation?. J Pediatr. 2017;191:179-183. doi:10.1016/j.jpeds.2017.08.075

Berger MY, Tabbers MM, Kurver MJ, Boluyt N, Benninga MA. Value of abdominal radiography, colonic transit time, and rectal ultrasound scanning in the diagnosis of idiopathic constipation in children: a systematic review. J Pediatr. 2012;161(1):44–50.e502. DOI:

Freedman SB, Rodean J, Hall M, et al. Delayed diagnoses in children with constipation: multicenter retrospective cohort study. J Pediatr. 2017;186:87-94.e16. DOI:

Freedman SB, Thull-Freedman J, Manson D, et al. Pediatric abdominal radiograph use, constipation, and significant misdiagnoses. J Pediatr. 2014;164(1):83-88.e2

Hoskins B, Marek S. Things We Do for No Reason: Obtaining an Abdominal X-ray to Assess for Constipation in Children. J Hosp Med. 2020;15(9):557-559. doi:10.12788/jhm.3387

Kearney R, Edwards T, Braford M, Klein E. Emergency provider use of plain radiographs in the evaluation of pediatric constipation. Pediatr Emerg Care. 2019;35(9):624-629. DOI: 10.1097/PEC.0000000000001549

McSweeney ME, Chan Yuen J, Meleedy-Rey P, Day K, Nurko S. A Quality Improvement Initiative to Reduce Abdominal X-ray use in Pediatric Patients Presenting with Constipation. J Pediatr. 2022;251:127-133. doi:10.1016/j.jpeds.2022.07.016

NICE. Constipation in children and young people: diagnosis and management.  NICE. Clinical guideline [CG99] Published: 26 May 2010 Last updated: 13 July 2017. Available online at 

Pensabene L, Buonomo C, Fishman L, Chitkara D, Nurko S. Lack of utility of abdominal x-rays in the evaluation of children with constipation: Comparison of different scoring methods. J Pediatr Gastroenterol Nutr. 2010;51(2):155-159. DOI:

Reuchlin-Vroklage LM, Bierma-Zeinstra S, Benninga MA, Berger MY. Diagnostic value of abdominal radiography in constipated children: a systematic review. Arch Pediatr Adolesc Med. 2005;159(7):671-678. doi:10.1001/archpedi.159.7.671

Rome IV Criteria:

Rothrock SG, Green SM, Hummel CB. Plain abdominal radiography in the detection of major disease in children: a prospective analysis. Ann Emerg Med. 1992;21(12):1423-1429. doi:10.1016/s0196-0644(05)80053-8

Tabbers MM, DiLorenzo C, Berger MY, et al. Evaluation and treatment of functional constipation in infants and children: Evidence-based recommendations from ESPGHAN and NASPGHAN. J Pediatr Gastroenterol Nutr. 2014;58(2):258-274. DOI:

Choosing Wisely Neurology

Do we need labs or a head CT after simple febrile or unprovoked seizures?

Labs or CT scans are not necessary to provide additional diagnostic information or reassurance for most children who recover completely following simple febrile seizures or unprovoked first time generalized seizures. The rate of abnormalities on these studies is very low, and the cost and downsides are too high to justify ordering them on a regular basis.

This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the the American Board of Internal Medicine Foundation, the goal of which is the spark conversations between clinicians and patients about what tests, treatments, and procedures are needed – and which ones are not.

The Choosing Wisely recommendation: Do not order laboratory testing or a CT scan of the head for a patient with an unprovoked, generalized seizure or a simple febrile seizure who has returned to baseline mental status

The Choosing Wisely Pediatric Emergency Medicine Recommendations

The Choosing Wisely Campaign Toolkit


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


American Academy of Pediatrics, Subcommittee on Febrile Seizures. Neurodiagnostic evaluation of the children with a simple febrile seizure. Pediatrics. 2011;127(2):389-394. DOI:

Brugman J, Solomons RS, Lombard C, Redfern A, Du Plessis AM. Risk-Stratification of Children Presenting to Ambulatory Paediatrics with First-Onset Seizures: Should We Order an Urgent CT Brain?. J Trop Pediatr. 2020;66(3):299-314. doi:10.1093/tropej/fmz071

Expert Panel on Pediatric Imaging, Trofimova A, Milla SS, et al. ACR Appropriateness Criteria® Seizures-Child. J Am Coll Radiol. 2021;18(5S):S199-S211. doi:10.1016/j.jacr.2021.02.020

Fine A, Wirrell EC. Seizures in Children. Pediatr Rev. 2020;41(7):321-347. doi:10.1542/pir.2019-0134

Hirtz D, Ashwal S, Berg A, et al. Practice parameter: Evaluating a first nonfebrile seizure in children. Report of the Quality Standards Subcommittee of the American Academy of Neurology, the Child Neurology Society, and the American Epilepsy Society. Neurology. 2000; 55(5):616-623. Reaffirmed October 17, 2020

Jaffe M, Bar-Joseph G, Tirosh E. Fever and convulsions: indications for laboratory investigations. Pediatrics. 1981;67(5):729 –731

Maytal J, Krauss JM, Novak G, Nagelberg J, Patel M. The role of brain computed tomography in evaluating children with new onset of seizures in the emergency department. Epilepsia. 2000;41(8):950-954. doi:10.1111/j.1528-1157.2000.tb00277.x

McKenzie KC, Hahn CD, Friedman JN; Canadian Paediatric Society, Acute Care Committee. Emergency management of the paediatric patient with convulsive status epilepticus. Paediatr Child Health. 2021;26(1):50-57

NICE. Epilepsies in children, young people and adults; Evidence reviews underpinning recommendations. NICE guideline NG217. 2022. Accessed online at 

NICE. Epilepsies in children, young people and adults. NICE guideline NG217. 2022. Accessed online at 

Reinus WR, Wippold FJ, 2nd, Erickson KK. Seizure patient selection for emergency computed tomography. Ann Emerg Med 1993;22:1298-303.

Riviello JJ Jr, Ashwal S, Hirtz D, et al; American Academy of Neurology Subcommittee; Practice Committee of the Child Neurology Society. Practice parameter: Diagnostic assessment of the child with status epilepticus (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2006;67(9):1542-1550 

Royal Children’s Hospital Melbourne. Afebrile Seizures. 2020. Accessed online at 

Sawires R, Buttery J, Fahey M. A Review of Febrile Seizures: Recent Advances in Understanding of Febrile Seizure Pathophysiology and Commonly Implicated Viral Triggers. Front Pediatr. 2022;9:801321. Published 2022 Jan 13. doi:10.3389/fped.2021.801321

Shah SS, Alpern ER, Zwerling L, Reid JR, McGowan KL, Bell LM. Low Risk of Bacteremia in Children With Febrile Seizures. Arch Pediatr Adolesc Med. 2002;156(5):469–472. doi:10.1001/archpedi.156.5.469

Subcommittee on Febrile Seizures; American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389-394. doi:10.1542/peds.2010-3318

Veerapandiyan A, Aravindhan A, Takahashi JH, Segal D, Pecor K, Ming X. Use of Head Computed Tomography (CT) in the Pediatric Emergency Department in Evaluation of Children With New-Onset Afebrile Seizure. J Child Neurol. 2018;33(11):708-712. doi:10.1177/0883073818786086

Young AC, Costanzi JB, Mohr PD, Forbes WS. Is routine computerised axial tomography in epilepsy worth while?. Lancet. 1982;2(8313):1446-1447. doi:10.1016/s0140-6736(82)91340-x
Yousefichaijan P, Dorreh F, Abbasian L, Pakniyat AG. Assessing the prevalence distribution of abnormal laboratory tests in patients with simple febrile seizure. J Pediatr Neurosci. 2015;10(2):93-97. doi:10.4103/1817-1745.159180

Choosing Wisely Psychiatry

Do we need labs to medically clear a patient for psych admission?

For most children requiring admission to an inpatient psychiatric facility laboratory studies are generally not required. Many of the children and adolescents being admitted already have an established mental or behavioral diagnosis, and a reassuring history and exam. The heterogeneity of clinical settings makes it challenging to establish processes that account for the needs of our patients while limiting the use of unnecessary resources broadly.

This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the the American Board of Internal Medicine Foundation, the goal of which is the spark conversations between clinicians and patients about what tests, treatments, and procedures are needed – and which ones are not.

The Choosing Wisely recommendation: Do not obtain screening laboratory tests in the medical clearance process of pediatric patients who require inpatient psychiatric admission unless clinically indicated

The Choosing Wisely Pediatric Emergency Medicine Recommendations

The Choosing Wisely Campaign Toolkit


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Thrasher TW, Rolli M, Redwood RS, et al. ‘Medical clearance’ of patients with acute mental health needs in the emergency department: a literature review and practice recommendations. WMJ. 2019;118(4):156-163

Donofrio JJ, Horeczko T, Kaji A, Santillanes G, Claudius I. Most routine laboratory testing of pediatric psychiatric patients in the emergency department is not medically necessary. Health Aff (Millwood). 2015;34(5):812-818

Chun TH. Medical clearance: time for this dinosaur to go extinct. Ann Emerg Med. 2014;63(6):676-677

Donofrio JJ, Santillanes G, McCammack BD, et al. Clinical utility of screening laboratory tests in pediatric psychiatric patients presenting to the emergency department for medical clearance. Ann Emerg Med. 2014;63(6):666-675.e663.

Santillanes G, Donofrio JJ, Lam CN, et al. Is medical clearance necessary for pediatric psychiatric patients? J Emerg Med. 2014;46(6):800-807

Santiago LI, Tunik MG, Foltin GL, Mojica MA. Children requiring psychiatric consultation in the pediatric emergency 

Berg JS, Payne AS, Wayra T, Morrison S, Patel SJ. Implementation of a Medical Clearance Algorithm for Psychiatric Emergency Patients. Hosp Pediatr (2023) 13 (1): 66–71

Choosing Wisely Radiology Respiratory

Do children with bronchiolitis, croup, asthma, or first-time wheezing need a Chest X-Ray?

For most children with children with bronchiolitis, croup, asthma, or first-time wheezing chest X-Rays are not necessary. These X-Rays are often obtained due to the possibility of missing pneumonia. But, these radiographs are hard to interpret, increase length of stay and the cost of care, and expose children to excess radiation.

This podcast episode is designed to disseminate the important work of Choosing Wisely, an initiative of the the American Board of Internal Medicine Foundation, the goal of which is the spark conversations between clinicians and patients about what tests, treatments, and procedures are needed – and which ones are not.

The Choosing Wisely recommendation: Do not obtain radiographs in children with bronchiolitis, croup, asthma, or first-time wheezing

The Choosing Wisely Pediatric Emergency Medicine Recommendations

The Choosing Wisely Campaign Toolkit


@PEMTweets on… sigh “X” (Twitter)

My Instagram

My Mastodon account @bradsobo


Shah SN, Bachur RG, Simel DL, Neuman MI. Does this child have pneumonia? The rational clinical examination systematic review. JAMA. 2017;318(5):462-471. PMID: 28763554.

Schuh S, Lalani A, Allen U, et al. Evaluation of the utility of radiography in acute bronchiolitis. J Pediatr. 2007;150(4):429-433. PMID: 17382126.

Ramgopal S, Ambroggio L, Lorenz D, Shah SS, Ruddy RM, Florin TA. A Prediction Model for Pediatric Radiographic Pneumonia. Pediatrics. 2022 Jan 1;149(1):e2021051405. doi: 10.1542/peds.2021-051405. PMID: 34845493

Florin TA, Carron H, Huang G, Shah SS, Ruddy R, Ambroggio L. Pneumonia in Children Presenting to the Emergency Department with an Asthma Exacerbation. JAMA Pediatr. 2016;170(8):803-805. https://doi:10.1001/jamapediatrics.2016.0310