It’s a question nearly as old as time — or at least as old as Lactated Ringer’s solution: which fluids serve our critically ill children best? Plenty of studies have taken a swing at this, with a variety of results but never quite settling the debate.  Concerns about normal saline largely stem from its supraphysiologic chlorine content, which has been thought to cause hyperchloremic metabolic acidosis, kidney injury, coagulation abnormalities, and potentially worsened systemic inflammatory response (Weiss 2017). Prior studies have explored clinical differences between fluids with some showing increased rates of acute kidney injury and small increased need for renal replacement therapy with normal saline as compared to balanced fluids (Sankar 2023, Long 2025). Still, many of these studies were hampered by small sample sizes and the lingering sense that we were all waiting for another trial to settle the debate. Despite these prior papers, there is still uncertainty. Enter the PRoMPT BOLUS trial — fashionably late, but hopefully worth the wait (Balamuth 2026).  Let’s take a minute to review the insights generated from the PRoMPT BOLUS study:

PRoMPT BOLUS: Methods

• The authors of this study used a pragmatic, open-label, randomized trial to compare balanced crystalloid vs 0.9% saline.
• This study put the MULTI in multicenter with 47 sites throughout the US, Canada, Australia/New Zealand, and Costa Rica – basically a world tour! 
• 9,041 patients, ages 2 months to <18 years with suspected sepsis requiring more than one fluid bolus were enrolled and continued on the same fluids for at least 24 hours
• The primary outcome was Major Adverse Kidney Events within 30 days (MAKE30)
  • Mortality
  • Need for renal replacement therapy
  • Persistent kidney dysfunction up to 30 days

PRoMPT BOLUS: Results

• The primary outcome evaluating for major adverse kidney events within 30 days found no clinically significant difference in these events between balanced fluids and saline.
  • Balanced fluids: 3.4%
  • Saline: 3.0% 
• Secondary outcomes showed no meaningful differences between: 
  • Hospital length of stay
  • Hospital-free days
  • Safety events including thrombosis or cerebral edema
• Where the fluids did part ways was in the laboratory values: 
  • Normal saline was associated with hyperchloremia and hypernatremia
  • Balanced fluids was associated with hyperlactemia

The labs noticed. Clinically, not so much.

PRoMPT BOLUS: Discussion

• This was a large study that showed there was no notable benefit with the use of balanced fluid over 0.9% saline when looking at effects on renal function.
• Electrolyte differences (notably hypernatremia and hyperchloremia) were observed but did not translate into differences in clinical outcomes. 
• The authors acknowledge that a key limitation is the early definition of septic shock, which may have overcaptured patients based on vital signs rather than laboratory data — casting a slightly wider net in the name of early enrollment.
• This early enrollment may have also contributed to the low incidence of adverse events, suggesting the study population may have been somewhat less sick than anticipated
• While subgroup analysis of the more severely ill patients suggested a possible benefit of the balanced fluids, the study was not powered to make definitive claims

Will this change practice? 

This was a well-designed study that prioritized large-scale enrollment while minimizing disruption to usual care. The lack of clinically significant differences suggests that fluid choice can reasonably be individualized. If I’m faced with a patient who is already hypernatremic or hyperchloremic, I’ll still lean toward a balanced solution such as Lactated Ringer’s solution.

That said, real-world decision-making is as much about logistics as it is about physiology. One of the main practical limitations of balanced fluids is medication compatibility. We love Ceftriaxone (“Cef-kill-it-all”) in pediatrics, but it’s a classic example of an incompatibility that often necessitates a second IV if using LR for fluid resuscitation. When IV real estate is at a premium in small patients, thinking about compatibility becomes less of a pharmacologic detail and more of a daily survival strategy. For me, this translates to a simple cognitive shortcut during resuscitation: fewer line-management decisions, less mental bandwidth consumed, and a quicker reach for 0.9% normal saline for my initial bolus solution in most pediatric patients.

Moral of the Morsel

• The Nephrons Stayed Neutral! Balanced fluids compared to normal saline did not meaningfully reduce mortality, renal replacement therapy, persistent kidney dysfunction, hospital length of stay, or hospital-free days compared with normal saline.
• The Labs Had Drama, the Patients Did Not! Normal saline was associated with more hyperchloremia and hypernatremia, while balanced fluids were associated with more hyperlactemia — but these lab differences did not translate into meaningful clinical outcome differences.
• Fluids are Easy! Lines are Hard. Fluid choice can be individualized: balanced fluids may make sense in patients who are already hypernatremic or hyperchloremic, but in real-world pediatric resuscitation, medication compatibility and limited IV access may make normal saline the simpler first-bolus choice.

References: 

1. Weiss SL, Keele L, Balamuth F, et al. Crystalloid Fluid Choice and Clinical Outcomes in Pediatric Sepsis: A Matched Retrospective Cohort Study. J Pediatr. 2017;182:304-310.e10. doi:10.1016/j.jpeds.2016.11.075
2. Sankar J, Muralidharan J, Lalitha AV, et al. Multiple Electrolytes Solution Versus Saline as Bolus Fluid for Resuscitation in Pediatric Septic Shock: A Multicenter Randomized Clinical Trial. Crit Care Med. 2023;51(11):1449-1460. doi:10.1097/CCM.0000000000005952
3. Long B, Gottlieb M. Balanced Crystalloids for Pediatric Sepsis and Septic Shock. Acad Emerg Med. 2026;33(1):e70115. doi:10.1111/acem.70115
4. Balamuth F, Weiss SL, Long E, et al. Balanced Fluid or 0.9% Saline in Children Treated for Septic Shock. N Engl J Med. Published online April 24, 2026. doi:10.1056/NEJMoa2601969

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So much of what we see in the pediatric emergency department is “just a virus.”  These kiddos, big and small, are going through their first few chapters of life and getting knocked in the teeth by all sorts of bugs for the first time.  While viral infections are often an annoyance, they can still lead to chaos and consequences! We have a good idea of common presentations for viruses such as Mumps, Influenza, and even Measles, but there is one virus that can look like, well, basically everything.  Let’s take a moment and enter the lion’s DEN to indulge in another tasty morsel about a virus that simply refuses to stay in its lane: aDENovirus.  

Adenovirus: The Basics

• Adenovirus is a double-stranded DNA virus that causes a wide range of clinical symptoms from snotty sniffles to disseminated ICU-level chaos
• Adenovirus does not follow a seasonal pattern and is prevalent year-round [1]
• Infections occur worldwide and affect individuals of all ages, with higher burden in neonates, young children, and the immunocompromised

• Part of the Adenoviridae family and Mastadenovirus genus, there are more than 100 serotypes grouped into seven subspecies (A-G), each responsible for distinct clinical syndromes [1,3]
  • Respiratory disease: Types 1–5, 7, 14, 21, 55 
  • Severe respiratory infections: Types 3, 7, 14 
  • Epidemic keratoconjunctivitis: Types 8, 37, 53, 54, 64 
  • Gastroenteritis: Types 40, 41

• Transmission occurs via respiratory droplets, direct contact or fomites, and fecal-oral
  • Highly transmissible:  daycares, military facilities, college dorms, hospitals, and transplant units
• Community outbreaks of adenovirus-associated pharyngoconjunctival fever have been attributed to water exposure from contaminated swimming pools [1-2]

Adenovirus Presentation: The Clinical Chameleon

• Adenovirus doesn’t pick a system… it picks all of them.
• Common Things are Common – Adenovirus is known to cause [2,4]:
  • URI (pharyngitis, tonsillitis, coryza)
  • Follicular conjunctivitis / Keratoconjunctivitis
  • Otitis media
  • Gastroenteritis
  • Croup
  • Bronchiolitis
  • Fever greater than >104°F, and lasting longer than 5 days

• Less commonly, but typical of Adenovirus – Think severe cases and disseminated disease [4]:
  • Hemorrhagic cystitis
  • Pneumonia
  • Bronchiolitis obliterans
  • Seizures
  • Meningitis / Encephalitis
  • Hepatitis
  • Myocarditis / Pericarditis / Cardiomyopathy

• High-risk players:
  • Neonates
  • Immunocompromised (transplant, oncology, etc.)

Adenovirus: Diagnostic Approach

Testing is not routinely required for mild disease but can be considered in:

• Severe illness (hospitalization, ICU-level care)
• High-risk populations
• Outbreak settings
• Screenings of high-risk transplant populations or in patients with prolonged fever >7 days (practice varies)

Preferred Diagnostic Modality: PCR

• Polymerase chain reaction is the gold standard due to high sensitivity and specificity
• Specimen selection typically varies by syndrome:
  • URI or Conjunctivitis: Nasopharyngeal/throat swab or conjunctival swab
  • Gastroenteritis: Stool
  • Hemorrhagic cystitis: Urine
  • Pneumonia: BAL, sputum, tracheal aspirate
  • Meningitis/Encephalitis: CSF
  • Hepatitis/Myocarditis: Blood or tissue

(As always) If you are going to test, know what to do with the results!

• Negative PCR: Generally rules out infection at respective site
• Positive PCR: Must be interpreted cautiously due to:
  • Prolonged viral shedding and symptomatic carriage (especially stool, upper respiratory tract)
• Key distinctions:
  • Blood viral load: Rising/high levels → concern for invasive disease
  • Tissue/CSF PCR: Indicates true active infection 

Adenovirus: Management

Like nearly all viruses the management of Adenovirus is supportive care

• Oral +/- IV fluids (re)hydration, antipyretics, and analgesics
• Tender loving care

Most infections in immunocompetent patients are self-limited

• In certain cases of severe illness or in immunocompromised individuals anti-virals may play a role
• Cidofovir is the most commonly used agent, though there is major concern for nephrotoxicity and myelosuppression [1]
• Other alternative therapies include brincidofovir, topical ganciclovir (ocular disease), and ribavirin
  • These medications typically have limited availability, limited roles, and inconsistent benefits

Adenovirus Vaccination

• It exists! A live oral vaccine (protective against serotypes 4 and 7) has only been approved for military personnel ages 17 years to 50 years [1,5]
• Adenovirus vaccination has been highly effective in preventing community outbreaks in these populations

Moral of the Morsel:

• Everything is Adenovirus!  Adenovirus causes a broad spectrum of disease, from mild URI to fatal disseminated infection
• The Kawasaki Imitator!  Adenovirus is known to cause prolonged fever for up 5 to 7 days with a lot of the same C.R.A.S.H. and BURN signs and symptoms
• Conjunctivitis or Chlorine?  Community and home pool exposure can be a source of adenovirus induced pharyngoconjunctival fever
• Wash Yo’ Hands! Infection control is critical due to environmental persistence and outbreak potential

References                 

1. “Adenovirus Infections”, Red Book: 2024–2027 Report of the Committee on Infectious Diseases, Committee on Infectious Diseases, American Academy of Pediatrics, David W. Kimberlin, MD, FAAP, Ritu Banerjee, MD, PhD, FAAP, Elizabeth D. Barnett, MD, FAAP, Ruth Lynfield, MD, FAAP, Mark H. Sawyer, MD, FAAP
2. “Adenovirus Infections”, American Academy of Pediatrics. American Academy of Pediatrics Section on Infectious Diseases. June 2022. William Otto, MD, FAAP
3. Greber, U.F. (2020), Adenoviruses – Infection, pathogenesis and therapy. FEBS Lett, 594: 1818-1827.
4. Shieh WJ. Human adenovirus infections in pediatric population – An update on clinico-pathologic correlation. Biomed J. 2022 Feb;45(1):38-49. doi: 10.1016/j.bj.2021.08.009. Epub 2021 Sep 10. PMID: 34506970; PMCID: PMC9133246.
5. Lyons A, Longfield J, Kuschner R, Straight T, Binn L, Seriwatana J, Reitstetter R, Froh IB, Craft D, McNabb K, Russell K, Metzgar D, Liss A, Sun X, Towle A, Sun W. A double-blind, placebo-controlled study of the safety and immunogenicity of live, oral type 4 and type 7 adenovirus vaccines in adults. Vaccine. 2008 Jun 2;26(23):2890-8. doi: 10.1016/j.vaccine.2008.03.037. Epub 2008 Apr 10. PMID: 18448211.

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The febrile neonate has long been the ultimate anxiety generator in the pediatric emergency department.  Fever in this age group may be the only sign of invasive bacterial infections (IBI), such as bacteremia or bacterial meningitis, which can be, well… anxiety generating. Historically, the reflex has been simple: Fever + neonate => Lumbar puncture for everyone. Antibiotics for everyone. Admission for everyone. As our guidelines evolve and, ideally, vaccinations improve, our risk stratifications change. Recent data evaluating the Pediatric Emergency Care Applied Research Network (PECARN) prediction rule suggests that a significant proportion of neonates may be safely identified as very low risk for bacterial meningitis, potentially allowing clinicians to avoid routine lumbar puncture in carefully selected patients [Burstein, 2026]. Let’s take a minute to digest a tasty morsel on the question is: do all febrile neonates need an LP?

Febrile Neonates and Lumbar Punctures: Basics

• Historical perspectives:
  • Risk stratification of febrile infants has evolved over decades:
    • Rochester criteria
    • Boston criteria
    • Philadelphia criteria
  • More recent strategies (including PECARN) focus specifically on invasive bacterial infections (IBI) rather than the broader category of serious bacterial infection, reflecting the much lower morbidity associated specifically with urinary tract infections.
  • This shift aligns with the 2021 guideline from the American Academy of Pediatrics (AAP), which emphasizes risk stratification using inflammatory markers (IM). [Pantell, 2021]
• Invasive Bacterial Infection risk remains real in neonates!
  • Febrile infants ≤28 days have approximately 4–5% risk of invasive bacterial infection
  • Bacterial meningitis occurs in ~0.7% of cases¹
• Clinical exam alone is unreliable!
  • Neonates with invasive infections often initially appear quite well
  • Laboratory risk stratification very important in this group
• Bacteriology is changing [Pantell, 2021]
  • Group B Strep leads to rapid and progressive illness, even when lab studies were unexciting.
  • Listeria monocytogenes – needs to be considered, but better regulations on food safety and education has reduced its impact.
  • Escherichia coli is now the most common organism found in infants 1 to 60 days of life.
  • Decision models that were constructed based on prior infection epidemiology (Gram-positive predominance previously; Gram-negative prevalence today) can lead to errors. 
• Testing has evolved [Pantell, 2021]
  • The WBC count, ANC count, Band count, and Urinalysis were the prior tools of risk stratification.
    • The WBC count performs poorly (and is the “Last Bastion of the Intellectually Destitute”).
    • These are less useful with E. coli being the most prevalent pathogen in this age group.
  • Other Inflammatory Markers (IM) are now more useful.
    • No single IM on its own is reliable enough for risk stratification so combinations of them are advocated for.
    • ANC count is still used as it is more available than procalcitonin.
      • >4,000 (or >5,200) is abnormal (depending on the reference you are using)
      • < 1,000 is also concerning for evolving sepsis.
    • C-reactive Protein
      • Produced by the liver in response to infections (and several other conditions)
      • Widely available and even as a point-of-care test 
      • >/= 20 mg/L is abnormal for this guideline.
    • Procalcitonin
      • Produced rapidly in response to infection and tissue injury.
      • Found to be more specific for bacterial infections than any other IM currently used.
      • Currently considered the most accurate IM for risk stratification … but…
      • It is not as readily available in all hospitals and may not be available at all hours.
      • >0.5 ng/mL is abnormal for this guideline.
    • Specific Pathogen Detection is also improving.

Febrile Neonates and LPs: PECARN Rule

• Low risk is defined by: [Burstein, 2026; Kuppermann, 2019; Mahajan, 2016]
  • Negative urinalysis
  • Procalcitonin ≤0.5 ng/mL
  • Absolute neutrophil count ≤4000/mm³
  • *No CSF data required to apply the rule
• Large international cohort evaluation
  • A pooled analysis of 1537 well-appearing febrile neonates ≤28 days from four international cohorts was performed. [Burstein, 2026]
  • Infection prevalence:
    • Invasive Bacterial Infection: 4.5%
    • Bacteremia: 3.8%
    • Meningitis: 0.7%
• Rule performance was strong
  • Sensitivity                               94.2%
  • Specificity                                41.6%
  • Negative Predictive Value      99.4%
• Key Clinical Takeaways: [Burstein, 2026]
  • 41% of infants were classified as low risk
  • No cases of bacterial meningitis were misclassified as low risk
  • Missed infections were bacteremia without meningitis

Febrile Neonates and LPs: Potential Real-World Impact

• If lumbar punctures had been avoided in low-risk infants:
  • >600 LPs would have been avoided in the cohort
  • No meningitis cases would have been missed [Burstein, 2026; Searns, 2026]

• Procalcitonin matters:
  • Is one of the most accurate biomarkers for serious invasive bacterial infection in young infants.
  • It outperforms traditional inflammatory markers. [Kuppermann, 2019; Mahajan, 2016]

• But caution is still warranted
  • Important limitations:
    • Only well-appearing infants were studied
    • Preterm infants excluded
    • Requires procalcitonin laboratory availability
    • HSV infection still mandates LP, if suspected
    • Data derived largely from high-income healthcare systems [Searns, 2026]
  • Age still matters
    • Editorial notes that misclassified infections occurred in infants 8–21 days old. [Searns, 2026]
    • Suggests that the youngest neonates may still warrant extra caution.

Febrile Neonate and LP: Why This Matters?

• >70,000 infants are evaluated annually for fever in the first months of life in the United States.
• If PECARN-based stratification were widely adopted, the editorial suggests tens of thousands of lumbar punctures, hospitalizations, and antibiotic exposures could be avoided every year. [Searns, 2026]
• Pediatric medicine is gradually progressing toward “safely doing less” by balancing the risks of invasive testing against the rare but devastating possibility of missed invasive bacterial infection. [Searns, 2026]
• Remember though, the acceptable risk of missing infection varies between clinicians and families.
• Shared decision-making will likely be key moving forward.

Moral of the Morsel

• Times are Changing: Evidence suggests that biomarker-driven prediction rules can identify neonates at extremely low risk for meningitis.
• Vigilance is still required! Prediction rules guide decisions — they don’t replace clinical judgment.
• New Febrile Neonate Evaluation Reflex: Every febrile neonate may not need a spinal tap; however, every febrile neonate deserves thoughtful risk stratification.

References

• Burstein B, Waterfield T, Umana E, Xie J, Kuppermann N. Prediction of Bacteremia and Bacterial Meningitis Among Febrile Infants Aged 28 Days or Younger. JAMA. 2026;335(5):425-433. doi:10.1001/jama.2025.21454
• Searns JB, O’Leary ST. Moving the Field Forward to Safely Do Less With Febrile Neonates. JAMA. 2026;335(5):405-406. doi:10.1001/jama.2025.23133
• Kuppermann N, Dayan PS, Levine DA, et al. A Clinical Prediction Rule to Identify Febrile Infants 60 Days and Younger at Low Risk for Serious Bacterial Infections. JAMA Pediatr. 2019;173(4):342-351. doi:10.1001/jamapediatrics.2018.5501
• Pantell RH, Roberts KB, Adams WG, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old. Pediatrics. 2021;148(2):e2021052228. doi:10.1542/peds.2021-052228
• Mahajan P, Kuppermann N, Mejias A, et al. Association of RNA Biosignatures With Bacterial Infections in Febrile Infants Aged 60 Days or Younger. JAMA. 2016;316(8):846-857. doi:10.1001/jama.2016.9207

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As Thanksgiving approaches in the US and the time of feasting nears, we gather together today to digest (pun intended) an uncommon cause of submandibular swelling in children. That is, of course, the Ranula. No, it’s not the bulging belly of a baby frog, as the name suggests; it’s a salivary pseudocyst in the floor of the mouth. Any swelling ABOVE the neck, such as periorbital cellulitis, Pott’s Puffy Tumor, or superior vena cava syndrome, gives us pause. But swelling OF the mouth or neck area? That quickly causes dry mouth and even a lump in the throat (literally and figuratively). I’m looking at you hereditary angioedema, mumps, and uvulitis! Today we dish up a serving of scrumptious salivary succulence. Be sure to scroll down for more on this juicy diagnosis of plunging ranula.

Plunging Ranula – Pathophysiology

• Best to first define terms, as the specific names denote the underlying pathophysiology
  • Ranula
    • Benign pseudocyst arising from the sublingual salivary gland from one of the many Ducts of Rivinus
  • Plunging Ranula 
    • Ranula that “plunges” below the mylohyoid muscle to the submandibular space and can occupy deeper spaces in the anterior cervical region
• Causes
  • Congenitally imperforate salivary gland duct
  • Direct trauma to the sublingual gland
  • Defect of mylohyoid muscle 
  • Herniation of sublingual gland through mylohyoid muscle

Plunging Ranula – Presentation

• Usually diagnosed in early adulthood between 2nd and 3rd decade, but can be diagnosed in children
• Unilateral, progressive, or recurrent painless neck swelling without associated oral swelling
  • Kids under 5 more commonly present with some combination of the following:
    • Lingual swelling
    • Snoring
    • Obstructive sleep apnea
    • Dysphagia
    • Failure to thrive
    • Upper airway obstruction

Plunging Ranula- Diagnosis

• Differential
  • Abscess
  • Thyroglossal duct cyst
  • Branchial Cleft cyst
  • Lymphatic malformation
  • Lipoma
  • Reactive lymph nodes
  • Lymphatic malignancy

• Clinical Diagnosis
  • Unilateral, painless, submandibular swelling without oral involvement likely signifies a ranula, but one must remain aware of other, more dangerous imitators
    • Imaging not needed, but is helpful to distinguish from other pathology

• Imaging
  • Ultrasound
  • Computed Tomography
  • Magnetic Resonance Imaging
  • The presence of a ‘‘tail sign’’ (indicating communication between the collapsed sublingual and submandibular space over the posterior edge of the mylohyoid muscle) supports the diagnosis of a plunging ranula. Will be seen on all imaging modalities.

Plunging Ranula- Treatment

• ENT consult/referral
  • Aspiration
  • Ablation
  • Transoral excision
  • Marsupialization

Moral of the Morsel

• More chilling than a polar plunge. A ranula is a benign pseudocyst arising from the submandibular salivary gland that can “plunge” into deeper neck spaces.
• Don’t get choked up. As always, we must stay vigilant, as ranulas in younger children can present with upper airway obstruction, dysphagia or even failure to thrive.
• Rethink, review, re-examine, and reduce radiation. Imaging is not necessary for diagnosis but may be helpful to distinguish from other pathology.
• Time to Dig Deeper. Other, more dangerous diagnoses, such as abscess and deep space infection must be considered.
• #Dispo. Outpatient ENT referral is the most common disposition from the ED.

References

• Kokong, D., Iduh, A., Chukwu, I., Mugu, J., Nuhu, S., & Augustine, S. (2017). Ranula: Current Concept of Pathophysiologic Basis and Surgical Management Options. World Journal of Surgery, 41(6), 1476–1481. https://doi.org/10.1007/s00268-017-3901-2
• Liman, A. R. U. A., Tuang, G. J., & Mansor, M. (2021). Plunging Ranula. In Ear, Nose and Throat Journal (Vol. 100, Issue 10_suppl, pp. 1004S-1005S). SAGE Publications Ltd. https://doi.org/10.1177/0145561320927828
• Lyly, A., Castrén, E., Aronniemi, J., & Klockars, T. (2017). Plunging ranula–patient characteristics, treatment, and comparison between different populations. Acta Oto-Laryngologica, 137(12), 1271–1274. https://doi.org/10.1080/00016489.2017.1357082

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As I sit in the ED at 3 am, enjoying my root beer slushy and contemplating the end of summer, I recall a recent article describing glycerol intoxication in children who consumed sugar-free slush beverages. Of all the things that children, ruled by their underdeveloped prefrontal cortices, put in their mouths (i.e. button batteries, lead foreign bodies, vape juice, detergent pods, ethanol, etc.), most would not expect a quintessentially summer beverage to lead to severe consequences. This serves as a reminder that we must “stay vigilant“, as the good Dr. Fox would say.  So, grab a slushy (preferably not sugar free), pull up a seat, and let’s go on a journey to learn more about glycerol intoxication – Beware the Slush!!!

Glycerol Intoxication Syndrome – What is Glycerol?

• Glycerol is also known as glycerin
  • Natural compound in lipids
  • Endogenous metabolite in mammals
• When consumed by mouth, it is easily absorbed from the GI tract
  • First pass metabolism through the liver
• The body uses glycerol to make ATP through glycolysis
• Can be substituted for use in gluconeogenesis and lipogenesis
• Excretion
  • Glycerol is oxidized and exhaled as carbon dioxide
  • Only very little excreted in the urine or stool
  • After high doses, it can be detected in the urine soon after administration

Glycerol Intoxication Syndrome – Glycerol Uses

• Can have therapeutic use
  • Oral or IV administration
  • Mobilizes edema by inducing an osmotic gradient
  • Reduces intraocular pressure in glaucoma
• Used as a food additive
  • Approved by the European Food Safety Authority
  • In the past, has not been shown to cause significant clinical symptoms of intoxication or toxicity
  • You can find glycerol in flavored drinks, sauces, breads/rolls, breath mints/gum, and edible ices
  • Prevalent in sugar-free ice beverages
    • Helps maintain appropriate texture in the absence of sugar and high fructose corn syrup
  • Dose of glycerol required to cause adverse effects is 125 mg/kg
    • Toddler need only consume as little as 50 – 220 mL of a slush beverage to experience symptoms
    • Of note, standard size for this drink in the UK is 500 mL! (Probably same or higher in the US)

Glycerol Intoxication Syndrome – Symptoms

• Hypoglycemia
  • 2025 case series from the UK with 21 children referred to a metabolic service after being diagnosed with slush ice drink related hypoglycemia
  • Tested for genetic syndromes which could cause similar symptoms to Glycerol Intoxication Syndrome (GIS)
  • 14/21 had no inborn genetic errors
  • All children had consumed a slush beverage within 60 minutes of symptom onset
• GIS symptoms
  • Altered level of consciousness (94%)
  • Pseudohypertriglyceridemia (89%)
  • Hypoglycemia (95%, median BGL 21.6 mg/dL)
  • Lactic Acidosis (94%, median 4.3 mmol/L)
  • Hypokalemia (75%, median 2.7 mmol/L)
  • Tonic-clonic seizure (1 patient)

Glycerol Intoxication Syndrome – Differential Diagnosis

• Genetic/Metabolic
  • Glycerol Kinase (GK) Deficiency
  • Fructose-1,6-diphosphatase (FDP) deficiency
  • Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency
• Toxicologic
  • Methanol Toxicity
  • Ethylene Glycol Toxicity
  • Ethanol Toxicity
  • Isopropanol Toxicity
• Infectious
  • Sepsis/Septic Shock
  • Acute Gastroenteritis
  • Bacterial Meningitis

Glycerol Intoxication Syndrome – Diagnosis

• Diagnosis is difficult in the ED
• Signs and symptoms can be non-specific
• Keep a broad differential, but a thorough history can help unveil this diagnosis
• Children should be admitted to the appropriate service
  • Toxicology and Genetics consults should be considered
• Diagnostic testing
  • Look for hypoglycemia, metabolic acidosis, and glyceroluria
  • Urine glycerol level not frequently considered/ordered in ED, but can be obtained after admission
  • Negative biochemical/enzymatic or genetic testing for inherited metabolic diseases

Glycerol Intoxication Syndrome – Treatment, Management, and Disposition

• Hypoglycemia- give dextrose, both bolus and continuous dosing
• Acidosis- treat with fluids and dextrose to improve acidosis
• Electrolyte abnormalities- replete potassium as needed
• Patients with refractory hypoglycemia, severe acidosis, profound electrolyte abnormalities and altered mental status should be admitted to the ICU
• Well-appearing patients can be admitted to the general floor
  • Consultation with appropriate subspecialty services should be considered
• Children should refrain from drinking sugar-free slush ice beverages in the future

Moral of the Morsel

• Glycerol is Global! It is a common food additive, which is generally safe and most children who ingest it in normal dietary quantities suffer no adverse effects.
• Ask about Ingestions! Staying vigilant and eliciting an excellent history (recent slushy ingestion) is important to relate the non-specific GIS symptoms to slushy ingestion.
• Totally NOT Sweet! GIS presents with hypoglycemia, altered mental status, and metabolic acidosis, which overlaps with many other diagnoses.
• Treat and Replete! Treatment of GIS requires dextrose, fluids, electrolyte repletion, supportive care, and frequently, admission.

References

Brothwell, S. L., Fitzsimons, P. E., Gerrard, A., Schwahn, B. C., Stockdale, C., Bowron, A., Anderson, M., Hart, C. E., Hannah, R., Ritchie, F., Deshpande, S. A., Sreekantam, S., Watts, G., Yap, S., Mundy, H., Veiraiah, A., Collins, A., Cozens, A., Morris, A. A., & Crushell, E. (2025). Glycerol intoxication syndrome in young children, following the consumption of slush ice drinks. Arch Dis Child, 110, 592–596. https://doi.org/10.1136/archdischild-2024-328109

Mortensen, A., Aguilar, F., Crebelli, R., di Domenico, A., Dusemund, B., Frutos, M. J., Galtier, P., Gott, D., Gundert-Remy, U., Leblanc, J. C., Lindtner, O., Moldeus, P., Mosesso, P., Parent-Massin, D., Oskarsson, A., Stankovic, I., Waalkens-Berendsen, I., Woutersen, R. A., Wright, M., … Lambrée, C. (2017). Re-evaluation of glycerol (E 422) as a food additive. EFSA Journal, 15(3). https://doi.org/10.2903/J.EFSA.2017.4720

Tolins ML. TOXCARD: TOXIC ALCOHOL POISONING. emDocs.net. February 21, 2017. Accessed August 20, 2025. https://www.emdocs.net/toxcard-toxic-alcohol-poisoning/

Younes, M., Aquilina, G., Castle, L., Engel, K. H., Fowler, P., Frutos Fernandez, M. J., Gundert-Remy, U., Gürtler, R., Husøy, T., Manco, M., Mennes, W., Moldeus, P., Passamonti, S., Shah, R., Waalkens-Berendsen, I., Wölfle, D., Wright, M., Cheyns, K., Mirat, M., … Fürst, P. (2022). Follow-up of the re-evaluation of glycerol (E 422) as a food additive. EFSA Journal, 20(6). https://doi.org/10.2903/j.efsa.2022.7353

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We have previously discussed how knowing some basic pediatric topics can help you deliver excellent care to the patient you see in the Emergency Department. Sure, maybe you don’t want to remember all of the various infant formulas out there, but a little bit of understanding to serve you and your patients well. Similarly, a knowledge of some basic pediatric milestones and growth parameters can be very useful to you! Along with assisting you in recognizing issues like failure to thrive, familiarity with what infants should and should be doing can help you find those clues when searching through the giant haystack on subtle presentations. Another example of that is primitive reflexes. What appears to be an exaggerated moro reflex may not be that simple. Let’s take a minute to digest a morsel on Infantile Spasms:

Infantile Spasms: Basics 

• Also known as, “Infantile Epileptic Spasms Syndrome” or IESS (Zuberi 2022)
• Often used interchangeably with West Syndrome, although strictly speaking, West Syndrome is the triad of 1. Infantile spasms 2. Developmental regression and 3. Hypsarrhythmia on EEG (Wheless 2012)
• Seizure disorder of early infancy (Smith 2025, Wheless 2012)
  • Presents anywhere from the first week of life up to around 5 years old (Smith 2025),
  • Usually seen between 3 and 7 months
  • 90% of cases are seen in the first year of life (Wheless 2012) 
• Presentation ranges from subtle to the more obvious “jack knife” movements (Smith 2025, Wheless 2012)
• Infantile spasms are associated with future cognitive and motor delays; early identification and treatment improves outcomes (Widjaja 2014)

• Etiologies include:
  • Structural abnormalities of the brain, such as cortical dysplasia (Smith 2025, Pellock 2010)
  • Genetic abnormalities,
    • Trisomy 21 (Smith 2025, Pellock 2010)
    • Infantile spasms are also closely associated with tuberous sclerosis (Smith 2025)
  • Metabolic abnormalities, such as infantile hypoglycemia (Smith 2025, Pellock 2010)
  • Infections, including meningitis, encephalitis, and congenital infections – think TORCH (Smith 2025, Riikonen 1993)
  • Injuries and insults to CNS development in the perinatal and postnatal periods, such as hypoxic-ischemic encephalopathy (Smith 2025, Pellock 2010)
  • Anywhere from 10-40% of children will have no identifying cause (called cryptogenic infantile spasms) (Smith 2025, Wheless 2012, Pellock 2010)

Infantile Spasms: Clinical Features 

• Sudden, brief, clustered spasms (Zuberi 2022, Pellock 2010) 
• Often see flexion and extension movements of the head, neck, trunk, and extremities (Zuberi 2022, Pellock 2010)
  • Think: bending forward at the waist, throwing arms to the side, bending at the knee, throwing the head backwards, stiffening of the arms and legs (Boston Children’s Hospital, 2023)
  • Sometimes referred to as “jack knife” movements (Smith 2025)
• Symptoms can also be much more subtle and include frequent blinking or abnormal eye movements, head bobbing, or changes in breathing pattern (Smith 2025, Wheless 2012)
• Sometimes, signs of developmental regression start around the first noted spasms: the infant no longer rolls from front to back or back to front, they’re less socially interactive, or they’re fussy and more irritable (Smith 2025, Wheless 2012, Zuberi 2022)

Infantile Spasms: Differential 

• Other seizure types 
• Brain injuries, brain masses, CNS infections  
• Startle reflex 
• Esophageal reflux 
• Benign myoclonus 

Infantile Spasms: Evaluation and Diagnosis 

• EEG
  • Looking for the characteristic hypsarrhythmia pattern: high voltage spikes and slow waves (Zuberi 2022)
• MRI
  • Looking for structural abnormalities (Smith 2025, Pellock 2010)
• Blood, urine, and sometimes CSF testing
  • Looking for specific metabolic and genetic markers of disease (Smith 2025)
  • You’re friendly pediatric neurologist and geneticist can help with the specific tests: there’s a lot! 
• Admission to expedite the evaluation is completely reasonable… since… early diagnosis will help lead to early treatment.

Infantile Spasms: Treatment 

• Most importantly: earlier initiation of treatment can help prevent developmental regression (Widjaja 2015) 
• Treatment plans vary: options include ACTH, steroids, and anti-epileptics 
  • ACTH: adding supplemental corticotropin decreases the amounts of corticotropin-releasing hormone in the body, which is thought to trigger spasms (Smith 2025) 
  • Steroids: high dose oral prednisolone; also helps lower amounts of corticotropin-releasing hormone (Wheless 2012)
  • Vigabatrin: inhibits the enzyme that attacks GABA, so increases CNS GABA levels (Smith 2025)
    • Most helpful when infantile spasms are secondary to tuberous sclerosis (Wheless 2012)
• Other medications include our more typical anti-epileptics: levetiracetam, valproic acid, topiramate (Pellock 2010, Song 2017)
• Ketogenic diets are sometimes utilized (Song 2017)
• Rarely, when indicated: surgical removal of structural CNS lesions (Wheless 2012)

Infantile Spasms: Prognosis 

• The best prognosis occurs when treatment is initiated within 1 month of symptom onset (Widjaja 2015, Pellock 2010)
• Mortality varies wildly, and is often based on etiology: 3 to 33% (Smith 2025)
• Spasms are associated with other seizure disorders and psychomotor developmental delay or regression (Smith 2025)
  • Infants have a higher risk for cognitive and motor delays, autism spectrum disorder, among others (Wheless 2012) 
  • Parents sometimes note regression of developmental milestones such as rolling, sitting, crawling, babbling, and social smiles (Smith 2025)
• Spasms can sometimes improve or go away completely with treatment, only to be replaced with different types of seizure activity in the future (Smith 2025)

Moral of the Morsel 

• Keep your eyes open for it! Infantile spasms are a rare form of infantile epilepsy, but do present to our EDs.
• Videos can be very helpful! As the family if they have any videos of the concerning events.
• It can be subtle! While the jack-knife is a bit more obvious, be alert to the subtle presentations too.
• Got MRI and EEG? Yes, admission to help obtain MRI imaging and EEG is often your best course of action when concerned about possible infantile spasms!

Resources 

• Smith MS, Matthews R, Rajnik M, et al. Infantile Epileptic Spasms Syndrome (West Syndrome) [Updated 2024 Feb 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. 
• Wheless JW, Gibson PA, Rosbeck KL, et al. Infantile spasms (West syndrome): update and resources for pediatricians and providers to share with parents. BMC Pediatr. 2012 Jul 25;12:108. doi: 10.1186/1471-2431-12-108. PMID: 22830456; PMCID: PMC3411499.
• Widjaja E, Go C, McCoy B, et al. Neurodevelopmental outcome of infantile spasms: A systematic review and meta-analysis. Epilepsy Res. 2015 Jan;109:155-62. doi: 10.1016/j.eplepsyres.2014.11.012. Epub 2014 Nov 22. PMID: 25524855.
• Pellock JM, Hrachovy R, Shinnar S, et al. Infantile spasms: a U.S. consensus report. Epilepsia. 2010 Oct;51(10):2175-89. doi: 10.1111/j.1528-1167.2010.02657.x. PMID: 20608959.
• Riikonen R. Infantile spasms: infectious disorders. Neuropediatrics. 1993 Oct;24(5):274-80. doi: 10.1055/s-2008-1071556. PMID: 8309517.
• Zuberi SM, Wirrell E, Yozawitz E, et al. ILAE classification and definition of epilepsy syndromes with onset in neonates and infants: Position statement by the ILAE Task Force on Nosology and Definitions. Epilepsia. 2022 Jun;63(6):1349-1397. doi: 10.1111/epi.17239. Epub 2022 May 3. PMID: 35503712.
• Boston Children’s Hospital. Infantile Spasms. Boston Children’s Hospital. Updated July 2023. Available from: https://www.childrenshospital.org/conditions/infantile-spasms
• Song JM, Hahn J, Kim SH, et al. Efficacy of Treatments for Infantile Spasms: A Systematic Review. Clin Neuropharmacol. 2017 Mar/Apr;40(2):63-84. doi: 10.1097/WNF.0000000000000200. PMID: 28288483.
• Mackay MT, Weiss SK, Adams-Webber T, et al. Practice parameter: medical treatment of infantile spasms: report of the American Academy of Neurology and the Child Neurology Society. Neurology. 2004 May 25;62(10):1668-81. doi: 10.1212/01.wnl.0000127773.72699.c8. PMID: 15159460; PMCID: PMC2937178.

The post Infantile Spasms appeared first on Pediatric EM Morsels.

Kids have big heads relative to their bodies. Unfortunately with relatively big heads comes many traumatic injuries – think pediatric facial fractures, nasal fractures, tongue lacerations, ear lacerations, and dental injuries. The eye tends to unfortunately bear the brunt of some trauma, too. I’m looking at you hyphema and traumatic glaucoma!

There are also some injuries that may be difficult to appreciate on first glance at a patient. There may be other larger, more distracting injuries that have pulled your attention. Vigilance is key, as is a very thorough physical exam to ensure you don’t miss these crucial diagnoses, such as nasal septal hematomas, frenulum tears, open globe injuries (which can be subtle), and mandible fractures. One particularly elusive injury presents with a “White Eye” Blowout since there is no outward indication of soft tissue injury. This is a complication of orbital floor fractures when soft tissue gets trapped by the fracture fragments. Let’s talk further about the “White Eye” Blowout.

White Eye – Basics

• Orbital floor blowout fractures comes from increased pressure to the eye from blunt direct injury [Balaraman 2021, Amarath-Madav 2022, Hakkou 2024]  
  • Increased pressure causes bowing and breaking of thin orbital floor bone 
  • In kids, this often causes linear rather than comminuted fractures 
  • Kid bones are still somewhat elastic, and the intact side of the bone springs back, acting like a trap door 
  • Soft tissue can get caught in this trap door 
• Pediatric facial fractures <15% of all facial fractures [Jordan 1998, Joshi 2011]  
  • Orbital blowout fractures 20% of pediatric facial fractures (range 7-41%) 
• Often in adolescents, but can happen in younger children 
• Usually during sports, from a fall, or during an assault 
• “White eye” blowout fractures, in particular, show no other outward signs of injury! 

White Eye – Presentation and Exam

• After an injury to the face or head, often a sports injury
• Patient may not have outward signs of soft tissue injury such as ecchymosis, tissue edema, or conjunctivitis (Hence, “white eye”) [Balaraman 2021]
• But they do have:
  • Restricted upward gaze
  • May have nausea or vomiting, which is also common with head injuries
  • Diplopia
  • Lack of enophthalmos
  • Eye pain
• May have unexplained bradycardia (oculo-cardiac reflex) 
  • Be vigilant! Symptoms can mimic typical head trauma and increased ICP, and this is easily missed on initial exam [Tarbet 2021]  
• One study showed up to 33% of pediatric cases were missed or misdiagnosed

White Eye – Diagnosis

• Have a high suspicion with a good physical exam with unilateral restriction of gaze 
• Non-contrast CT scan (need high resolution) [Amarath-Madav 2022]  
  • May only see a very subtle fracture line 
  • Look for entrapped tissue  
  • Look at coronal or sagittal views 
• Tear drop sign when entrapped tissue is seen herniating through fracture [Hakkou 2024] 

White Eye – Treatment

• Previous thought was conservative management for 4-6 months [Jordan 1998]  
  • “Watch and wait”
  • Some recommended waiting for 2 weeks before operating
  • This is sometimes the treatment for adults who don’t get entrapment of tissue as often 
  • This is another example of the anatomy and physiology of children mandating a different approach.
• Now urgent or emergent surgery is recommended for children [Jordan 1998, Egbert 2000]  
  • Pediatric patients were found to rarely have spontaneous resolution 
  • Some had permanent motility restriction when surgery was delayed 
  • Usually go to OR with 24 hours 
  • Emergent OR for surgical management if showing signs of oculo-cardiac reflex bradycardia 
• Often mesh is placed to prevent re-herniation of inferior rectus, fat, and other soft tissue [Balaraman 2021, Hakkou 2024]

White Eye – Complications

• Oculocardiac or oculovagal reflex (OCR) = bradycardia + nausea, vomiting [Balaraman 2021, Amarath-Madav 2022]  
  • Also known as the Dagnini-Aschner reflex, or “Aschner reflex” 
  • Trigeminal-Vagus nerve reflex arc is triggered by stretch receptors of short and long ciliary nerves 
  • The trigeminal sensory nucleus is activated, and sends impulses to the visceral motor nucleus and subsequently the vagus nerve 
  • Vagus nerve stimulation acts on the SA and AV nodes, causing bradycardia, which can be profound 
  • Worsened by upward gaze, puts pressure and stress on the trapped soft tissue 
  • A literature review showed that 77% who presented with this OCR had orbital floor fractures
    • 70% had muscle entrapment 
• Nausea and vomiting 
• Diplopia (20%)  
  • *Usually* resolves after surgical reduction of entrapped tissue 
  • Can persist for weeks to months after surgery 
• Permanent or long term ocular mobility problems  
  • Balaraman reported one case where diagnosis was delayed 9 days  
    • Diplopia resolved after 45 days 
    • Had permanent residual restriction of upward gaze [Balaraman 2021] 
• Permanent vision disturbances 
• One case report of a Volkmann’s type of contracture of the inferior rectus muscle [Smith 1984] 
• Delayed release and prolonged tissue incarceration could reduce perfusion to the muscle and cause scarring [Balaraman 2021] 
• Periorbital edema 
• Parasthesia of maxillary portion of trigeminal nerve [Amarath-Madav 2022]  
  • Thought to be from irritation of infraorbital nerve when fracture disrupts infraorbital canal  

Moral of the Morsel

• Have a KEEN EYE for subtle exam findings! Symptoms of a white eye orbital blowout fracture can be subtle and easily missed. 
• Do a double-take to avoid double vision! Prompt diagnosis is key to avoid long term issues like diplopia, restricted upward gaze, and muscle scarring. 
• Don’t cry- look for the teardrop sign! High resolution CT scan is best for diagnosis. Fractures are hard to see, but look for the entrapped soft tissue. 
• Be still my heart! The oculocardiac reflex can cause severe and life-threatening bradycardia. Pay attention to the vital signs. 
• Cut to cure! Prompt surgical intervention relieves entrapped tissue and reduces complication rates. 

REFERENCES

• Jordan DR, Allen LH, White J, Harvey J, Pashby R, Esmaeli B. Intervention within days for some orbital floor fractures: the white-eyed blowout. Ophthalmic Plast Reconstr Surg. 1998;14(6):379-390. doi:10.1097/00002341-199811000-00001 {PMID 9842557}
• Joshi S, Kassira W, Thaller SR. Overview of Pediatric Orbital Fractures. Journal of Craniofacial Surgery. 2011; 22 (4): 1330-1332. doi: 10.1097/SCS.0b013e31821c9365.
• Balaraman K, Patnaik JSS, Ramani V, et al. Management of White-Eyed Blowout Fracture in the Pediatric Population. J Maxillofac Oral Surg. 2021;20(1):37-41. doi:10.1007/s12663-020-01393-0 {PMID 33584039}
• Egbert JE, May K, Kersten RC, Kulwin DR (2000) Pediatric orbital floor fracture: direct extraocular muscle involvement. Ophthalmology 107(10):1875–1879 {PMID: 11013191}
• Smith B, Lisman RD, Simonton J, Della RR (1984) Volkmann’s contracture of the extraocular muscles following blowout fracture. Plast Reconstr Surg 74(2):200–216 {PMID: 6463145}
• Amarath-Madav R, Adamkiewicz D, Bigler D, Yu JC, Lima MH. White-Eyed Orbital Blowout Fracture With Oculocardiac Reflex Secondary to Extraocular Entrapment in a Pediatric Patient. J Craniofac Surg. 2022;33(7):e767-e771. doi:10.1097/SCS.0000000000008713 {PMID: 36109010}
• Hakkou Z, El Zouiti Z, Elayoubi F, Tsen AA. Pediatric trapdoor fracture of the orbital floor with Tear-Drop sign: A case report. Radiol Case Rep. 2024;20(3):1403-1405. Published 2024 Dec 19. doi:10.1016/j.radcr.2024.11.068 {PMID: 39898335}
• Tarbet C, Siegal N, Tarbet K. White-eyed blowout fracture with muscle entrapment misdiagnosed as increased intracranial pressure: An important clinical lesson. Am J Emerg Med. 2021;48:375.e1-375.e3. doi:10.1016/j.ajem.2021.03.060 {PMID: 33867194}
• Prasad C, Arulmozhi M, Balaji J, Nisha MPN. White-Eyed Blowout Fracture. Ann Maxillofac Surg. 2020;10(1):217-219. doi:10.4103/ams.ams_150_19 {PMID: 32855945}
• Yew CC, Shaari R, Rahman SA, Alam MK. White-eyed blowout fracture: Diagnostic pitfalls and review of literature. Injury. 2015;46(9):1856-1859. doi:10.1016/j.injury.2015.04.025 {PMID: 25986667}

References

The post White Eye Blowout appeared first on Pediatric EM Morsels.