PEM Currents: The Pediatric Emergency Medicine Podcast

Hair-thread tourniquet syndrome can progress from swelling and pain to ischemia and significant tissue injury if the constricting fiber is not completely released. In this episode of PEM Currents: The Pediatric Emergency Medicine Podcast, we review a stepwise approach to hair-thread tourniquet release, including chemical depilation, mechanical removal, and incisional release. We also discuss anesthesia, assessment of reperfusion, wound care, antibiotic use, and when to involve a surgical specialist. Learning Objectives After listening to this episode, you should be able to: Recognize hair-thread tourniquet syndrome, including cases in which the constricting hair or thread is deeply embedded or no longer visible. Select an appropriate release technique based on the constricting material, integrity of the skin, depth of the tourniquet, and degree of tissue injury. Describe chemical, mechanical, and incisional techniques for complete release of a hair-thread tourniquet. Select appropriate anesthesia and post-procedure care, including assessment of reperfusion, wound care, indications for antibiotics, and situations requiring surgical consultation. References Alruwaili N, Alshehri HA, Halimeh B. Hair tourniquet syndrome: Successful management with a painless technique. International Journal of Pediatrics and Adolescent Medicine. 2015;2:34-37. Arkoubi AY, Salati SA. Hair-Thread Tourniquet Syndrome: A Comprehensive Review. Cureus. 2024;16(5):e60832. doi:10.7759/cureus.60832. Barton DJ, Sloan GM, Nichter LS, Reinisch JF. Hair-thread tourniquet syndrome. Pediatrics. 1988;82(6):925-928. Bean JF, Hebal F, Hunter CJ. A single center retrospective review of hair tourniquet syndrome and a proposed treatment algorithm. J Pediatr Surg. 2015. Claudet I, Pasian N, Maréchal C, Salanne S, Debuisson C, Grouteau E. Hair-thread tourniquet syndrome. Arch Pediatr. 2010;17:474-479. Gottlieb M, Holladay D, Spearman D. Current approach to the evaluation and management of hair-thread tourniquets. Pediatr Emerg Care. 2019. Kudzinskas A, Reed A, Mahdi M, Tyler M. Evaluation of depilatory agents in the treatment of hair-thread tourniquet syndrome. J Emerg Med. 2021. Loiselle JM, Cronan K. Hair Tourniquet Removal. In: Henretig FM, King C, eds. Textbook of Pediatric Emergency Procedures. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:1065-1068. Martonovich N, Khatib M, Assaf M. Hair tourniquet syndrome: A retrospective study. Pediatr Dermatol.2023;40(1):125-128. doi:10.1111/pde.15151. O’Gorman A, Ratnapalan S. Hair tourniquet management. Pediatr Emerg Care. 2011;27(3):203-204. Prabhakar H, Rath S, Kalaivani M, Bhanderi N. Adrenaline with lidocaine for digital nerve blocks. Cochrane Database Syst Rev. 2015;(3):CD010645. Peckler B, Hsu CK. Tourniquet syndrome: a review of constricting band removal. J Emerg Med. 2001;20(3):253-262. Strahlman RS. Toe tourniquet syndrome in association with maternal hair loss. Pediatrics. 2003;111(3):169-170. Wiltrakis SM, Jaggi P, Lu L, Jain S. Optimizing antibiotic treatment of skin infections in pediatric emergency and urgent care centers. Pediatrics. 2022. Additional Resource Cheetham A. Management of Hair-Thread Tourniquet Syndrome. PEMBlog. September 1, 2026. The article includes a treatment algorithm, procedural techniques, and illustrations of hair-thread tourniquet release. ⁠Read the PEMBlog article Transcript This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content. Welcome to PEM Currents, the Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re going to talk about hair-thread tourniquet syndrome. This is an uncommon problem, but one where recognizing it quickly and completely releasing the constriction can prevent significant tissue injury. Hair-thread tourniquet syndrome occurs when a strand of hair, thread, or another thin fiber becomes tightly wrapped around an appendage. Toes are the most commonly affected site overall, but fingers and genitalia, including the penis, clitoris, and labia, can also be involved. Human hair is the most common constricting material, but synthetic fibers, thread, and even thin elastic bands have all been described. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf The pathophysiology is a progressive cycle. The constricting band first impairs lymphatic and venous outflow. The appendage becomes edematous, which makes the band even tighter and causes it to become more deeply embedded. Eventually arterial blood flow can become compromised, resulting in ischemia, tissue necrosis, and potentially loss of the appendage. And if the process has been going on for a while, granulation tissue or re-epithelialization can actually grow over the constricting fiber, making it even harder to identify. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf So prompt and complete release of that constricting fiber is the mainstay of treatment. Fortunately, despite how concerning some of these can look, most can be managed without an operation. In the largest single-center series, about 94% were managed nonoperatively. Let’s start with recognition and assessment. Classically, you’re looking for a circumferential groove with distal edema, erythema, pain, and sometimes cyanosis. But the hair or thread itself may not be obvious. It can be incredibly fine, buried within edematous tissue, or completely covered by granulation tissue or new epithelium. So if you have an edematous toe or finger with a circumferential groove, the fact that you can’t see a hair doesn’t rule out a tourniquet. Take a close look at the entire circumference of the appendage with good lighting and magnification. Assess distal perfusion, including color and capillary refill, and look at the degree of soft-tissue injury. On a finger, assess motor and sensory function when possible. You also want to determine, as best you can, whether you’re dealing with actual hair or synthetic thread, because that becomes important when deciding how you’re going to release it. The treatment approach is stepwise and depends on the depth and visibility of the constricting fiber, the condition of the skin, the degree of tissue injury, and whether the constrictor is hair or thread. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf For an appropriate hair tourniquet, a chemical depilatory is a great place to start. This is painless, noninvasive, and successful in roughly two-thirds of cases after one or two treatment cycles. Over-the-counter depilatory creams contain thioglycolate, which disrupts the chemical bonds in hair keratin. Apply the cream directly over the area of constriction and allow it to sit for about three to ten minutes. Then completely remove the cream, wash the area thoroughly with water, and reassess. You may need forceps to remove residual pieces because the hair frequently breaks apart rather than coming off as one intact strand. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf There are some important limitations. Depilatory cream only works on hair. It does nothing to cotton, rayon, polyester, or other synthetic fibers. You also shouldn’t use it on mucosal surfaces or over broken or ulcerated skin, and obviously avoid it in a patient with a known allergy to the product. So chemical depilation is not the universal first step for every hair-thread tourniquet. It’s an excellent first option when you’re dealing with hair and the skin is intact. If the constricting fiber is superficial enough that you can grasp it, if you’re dealing with synthetic thread, or if depilation fails, move to mechanical release. The simplest technique is to identify the free end with fine forceps or a hemostat and gently unwind the fiber. If you can see the constrictor but can’t easily unwind it, carefully pass a blunt probe or metal ear curette underneath it, usually approaching from the dorsal surface. Once you know the probe is between the skin and the constricting fiber, cut the fiber against the probe with fine-tipped scissors or a scalpel, then unwind and remove all of the remaining material. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf Another described option is a cutting suture needle. Pass the curve of the needle beneath the constricting fiber, then lift and use a gentle sawing motion to divide the band. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf Regardless of which mechanical technique you use, be careful about declaring victory after removing one piece of hair. There may be multiple strands, and a deeply embedded portion can remain even after the obvious part has been removed. Now we get to the more difficult situation. The fiber is deeply embedded, you can’t completely visualize it, there’s significant tissue injury or severe edema, or you’ve attempted another removal technique and the appendage still isn’t adequately reperfusing. At that point, you need to definitively release the constriction. Management of Hair-Thread Tourniquet Syndrome – PEMBlog.pdf Before we talk about that technique, let’s talk about anesthesia. For a digital or ring block, plain lidocaine is a reasonable default. There’s good contemporary evidence that lidocaine with epinephrine can be safely used in healthy, well-perfused digits, so this isn’t about going back to the old teaching that epinephrine can never be used in a finger. The problem is that those studies don’t specifically address the situation we have here: an appendage whose perfusion may already be compromised by a constricting tourniquet. And there’s another practical consideration. Return of perfusion is one of the things we’re going to use to determine whether our procedure actually worked. So in a digit that is already potentially ischemic, where I want to reassess perfusion immediately after re

Calcium channel blocker ingestions can cause profound bradycardia, hypotension, conduction abnormalities, and shock, and even a single tablet can be dangerous in a young child. In this episode of PEM Currents, we review the recognition and management of pediatric calcium channel blocker toxicity, including differences between dihydropyridine and non-dihydropyridine agents, high-dose insulin therapy, calcium and vasopressor support, and when to consider VA-ECMO. Learning Objectives After listening to this episode, learners should be able to: Recognize the clinical manifestations of calcium channel blocker toxicity and distinguish the typical effects of dihydropyridine and non-dihydropyridine agents. Describe the initial evaluation and management of a child with suspected calcium channel blocker toxicity, including the roles of calcium, atropine, high-dose insulin therapy, and vasopressors. Identify children who require prolonged observation, ICU admission, or escalation to advanced therapies such as VA-ECMO. References Management of calcium channel blocker toxicity in the pediatric patient. J Pediatr Pharmacol Ther. 2019;24(5):378-386. Are one or two dangerous? Calcium channel blocker exposure in toddlers. J Emerg Med. 2007. Intravenous lipid emulsion treatment for calcium-channel blocker intoxication: pediatric case series and review of the literature. Pediatr Emerg Care. 2022. Audette M, Comstock G. Is beta blocker toxicity associated with hypoglycemia? J Med Toxicol. 2026;22(3):357-363. doi:10.1007/s13181-026-01134-8. Script This is the original script for the episode, written by Drs. Robbie Daulton and Brad Sobolewski 1. Why CCBs Are So Dangerous Calcium channel blockers are an increasingly prescribed drug class which includes amlodipine, verapamil, diltiazem, and nifedipine. Unlike some of the ingestions we cover in this series, there’s no single reliably curative reversal agent. For non-dihydropyridine agents like verapamil and diltiazem especially, a single adult tablet can be lethal to a toddler; that’s exactly why they sit on the “one pill can kill” list. The sleepy, bradycardic toddler with altered mental status can look like sepsis or a metabolic problem well before it looks like a toxic ingestion, which is why this presentation is a challenge to identify. 2. How Kids Present The presentation depends heavily on which calcium channel blocker we’re talking about. Nausea and vomiting are the most common early complaint across all of these agents, so don’t be reassured by a benign-sounding chief complaint. Dihydropyridines, think amlodipine and nifedipine, are selective for vascular smooth muscle at therapeutic doses, so they mostly cause peripheral vasodilation and reflex tachycardia. But in overdose, that selectivity is lost, meaning you can see cardiogenic or distributive shock. Non-dihydropyridines, verapamil and diltiazem, hit the heart directly, meaning they can cause primarily cardiogenic shock. They slow the sinus node and block AV conduction, leading to sinus bradycardia, first-degree or higher-grade AV block, and sometimes a junctional escape rhythm, with a QRS that usually stays narrow since CCBs spare intraventricular conduction. 3. Pharmacology Pearls Calcium channel blockade doesn’t stop at the heart and vessels. These L-type channels also exist on pancreatic beta cells. Blockade suppresses insulin secretion and worsens peripheral insulin resistance. Cardiac myocytes become relatively starved of a key fuel during this stress state. High-dose exogenous insulin restores myocardial glucose uptake and improves contractility, aiding in cardiogenic shock states. 4. Work Up and Treatment Remember, if you have a child who presents with concerns for a CCB, it is important to urgently contact the Poison Control Center. Start with the fundamentals: ABCs, IV or IO access, glucose check, and a bedside EKG looking for that bradycardia and AV block. If the child is in shock, get a bedside echo early. Distinguishing cardiogenic from a distributive picture changes your resuscitation, and it’s a particularly important step for dihydropyridine overdoses where peripheral vasodilation, not pump failure, may be driving the hypotension. Send a blood gas with lactate (this will help distinguish from DKA), a basic metabolic panel, and an ionized calcium. A chest X-ray is worth getting if there’s evidence of severe toxicity or pulmonary edema, and an abdominal X-ray can help if you’re worried about a pill bezoar, especially with sustained-release products. For decontamination, activated charcoal can be considered if you’re early and the airway is protected. You can consider whole bowel irrigation, especially when faced with sustained-release products or when tablets are radiographically visible. For the shock itself, start with fluids and IV calcium repletion as a temporizing bridge. Atropine may be required for symptomatic bradycardia. The cornerstone for inotropic support needed in cardiogenic shock is high-dose insulin therapy: a bolus of 1 U/kg of regular insulin, followed by an infusion, paired with dextrose and glucose monitoring. Insulin can cause hypoglycemia, hypokalemia, and an increased volume/solute load, meaning frequent lab and volume status monitoring is important. For refractory cases, the Poison Center may recommend norepinephrine, or methylene blue, hydroxocobalamin, and angiotensin II. Glucagon appears in older references, but the evidence behind it is thin and inconsistent. Consider VA-ECMO for refractory cardiogenic shock or cardiac arrest despite maximal medical therapy. If you need to intubate, avoid benzodiazepines and barbiturates since they’ll exacerbate the hypotension. Pre-treat anticipated bradycardia with atropine and favor rocuronium over succinylcholine. 5. Who Goes Home, Who Gets Admitted Disposition hinges on the agent and the formulation. Any reported ingestion of a non-dihydropyridine, verapamil or diltiazem, in a toddler warrants an ED visit. Asymptomatic children after a confirmed immediate-release ingestion still need at least six hours of monitoring. Any exposure to a sustained-release or extended-release product requires longer observation, up to twenty-four hours. Anyone symptomatic, hemodynamically unstable, or on calcium, insulin, or vasopressor support needs an ICU bed. 6. Three Take-Homes Think calcium channel blocker whenever you see bradycardia, hypotension, +/- hyperglycemia. A single non-dihydropyridine tablet in a toddler is a genuine “one pill can kill.” It deserves an ED evaluation and a call to the Poison Center. Fluids and calcium buy you time, but early high-dose insulin euglycemic therapy is your cornerstone treatment for refractory cardiogenic shock. Vasopressors should be considered a helpful adjunct, with VA-ECMO kept in reserve for refractory shock or arrest.  

Iron poisoning can be deceptive. Early symptoms can look like routine gastroenteritis, children may appear to improve during a latent phase, and significant toxicity can progress to metabolic acidosis, shock, and hepatic injury. In this episode of PEM Currents, we review the recognition and management of pediatric iron toxicity, including when to obtain a serum iron level, the role of abdominal radiographs and whole bowel irrigation, indications for deferoxamine, and disposition. Learning Objectives After listening to this episode, learners should be able to: Recognize the clinical stages of pediatric iron toxicity and identify features concerning for significant systemic toxicity. Use the estimated elemental iron dose, serum iron concentration, and abdominal radiography to evaluate a child with a suspected iron ingestion. Describe the emergency management of iron toxicity, including supportive care, whole bowel irrigation, indications for deferoxamine, and appropriate disposition. References Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553-570. Halil H, Tuygun N, Polat E, Karacan CD. Minimum ingested iron cut-off triggering serious iron toxicity in children. Pediatr Int. 2019;61(5):444-448. Klein-Schwartz W, Oderda GM, Gorman RL, Favin F, Rose SR. Assessment of management guidelines: acute iron ingestion. Clin Pediatr (Phila). 1990;29(6):316-321. Banner W Jr, Tong TG. Iron poisoning. Pediatr Clin North Am. 1986;33(2):393-409. Script This is the original script for the episode, written by Drs. Robbie Daulton and Brad Sobolewski 1. Why Iron Matters Iron is one of the most dangerous toxic ingestions we see in young children. It’s found in prenatal vitamin and iron supplements, and the small, often candy-like tablets make exploratory toddler ingestions particularly concerning. Historically, iron was a leading cause of death from unintentional pediatric drug ingestion. What makes iron especially important in the ED is that early toxicity can look just like gastroenteritis, with vomiting, diarrhea, and abdominal pain. If you’re not thinking about an ingestion, it can be easy to miss. 2. How Kids Present: The Five Stages Iron follows a staged, sometimes deceptive, clinical course, although not every child progresses through every stage. Stage one begins 30 minutes to six hours after ingestion with vomiting, diarrhea, abdominal pain, and sometimes GI bleeding from direct mucosal injury. This is the stage that can easily be mistaken for gastroenteritis. Stage two, from about six to 24 hours, is the trap. GI symptoms may improve and the child may appear better, even as systemic toxicity progresses. Stage three, typically 12 to 24 hours after ingestion, is characterized by shock and metabolic acidosis. Children may be hypotensive, tachycardic, lethargic, and poorly perfused. Stages four and five occur later. Hepatic failure can develop over the next several days, while GI strictures and obstruction can occur weeks later. The pattern to remember is early GI symptoms, apparent improvement, and then unexplained shock and metabolic acidosis. That should make you think about iron toxicity even if the ingestion wasn’t clear from the history. 3. Pharmacology Pearls Iron causes toxicity in two ways. First it directly injuries the GI mucosa, causing the early vomiting, diarrhea, abdominal pain. Once absorbed, free iron overwhelms the body’s binding capacity (specifically ferritin and transferrin) and causes cellular and mitochondrial injury, contributing to metabolic acidosis, vasodilation, and shock. Serum iron typically peaks two to six hours post-ingestion, which is why the serum iron concentration should be measured four to six hours after ingestion. With enteric-coated or extended-release preparations, absorption can be delayed, so a repeat level may be necessary. 4. Working It Up and Treating It Start with the basics: ABCs, early IV or IO access, and aggressive treatment of shock. These children may need significant fluid resuscitation and vasoactive support. The most useful diagnostic test is a serum iron level drawn four to six hours after ingestion. Under 350 micrograms per deciliter is associated with minimal toxicity, 350 to 500 with mild to moderate toxicity, above 500 with serious systemic toxicity, and above 1,000 with severe toxicity and increased risk of mortality. But treatment decisions should be based on the entire clinical picture, not just the iron level. Check electrolytes, an anion gap, blood gas, lactate, liver enzymes, and coagulation studies to assess the severity of systemic toxicity. An abdominal X-ray can be helpful because many iron tablets are radiopaque. A positive film confirms tablets are present and can help guide decontamination, but a negative X-ray does not exclude an iron ingestion. Like all other periodic table elements, activated charcoal does not bind iron. If tablets are visible on imaging, whole bowel irrigation should be considered. For serious toxicity, including shock, metabolic acidosis, altered mental status, or a serum iron level above 500, consider IV deferoxamine. Hypotension can occur with rapid administration, so make sure the child has adequate volume resuscitation. Most importantly, treat the patient, not the iron level. Aggressively resuscitate shock, reassess frequently, and involve Poison Control early for any child with significant symptoms or a potentially toxic ingestion. 5. Who Goes Home, Who Gets Admitted For disposition, start with the estimated elemental iron dose, not the total tablet or iron salt weight. Less than 20 milligrams per kilogram is generally low risk, while 40 milligrams per kilogram or more should raise concern for significant toxicity. Newer pediatric data suggest serious toxicity may occur at lower doses, but the reported dose is imperfect, so symptoms and the serum iron concentration matter more than any single cutoff. Pay attention to what was actually ingested. Prenatal vitamins often contain substantial amounts of elemental iron, commonly around 27 to 65 milligrams per tablet, while multivitamins often contain little or no iron. A toddler can therefore reach a toxic dose with only a handful of prenatal vitamins. An asymptomatic child more than six hours after a low-risk ingestion with a reassuring serum iron level can typically go home. Children with significant symptoms or ongoing fluid requirements should be admitted. Hemodynamic instability or the need for deferoxamine warrants ICU-level care. Discuss significant ingestions with Poison Control. After significant toxicity, counsel families that GI strictures can develop weeks later and present with recurrent vomiting or obstruction. 6. Three Take-Homes Iron poisoning is deceptive. Early vomiting and diarrhea can look like gastroenteritis, and apparent improvement during the latent phase does not mean the child is in the clear. Obtain a serum iron level four to six hours post-ingestion. It’s your most useful test, but interpret it alongside the clinical picture. Activated charcoal does not bind iron. Consider whole bowel irrigation when tablets are visible on imaging, and treat serious toxicity, including shock, metabolic acidosis, altered mental status, or an iron level above 500, with aggressive supportive care and deferoxamine.

In children with septic shock, does the choice between balanced crystalloids and 0.9% saline actually matter? This episode reviews the composition and physiologic differences between commonly used crystalloids, summarizes the 2026 PRoMPT BOLUS trial, and discusses how its findings fit with the updated Surviving Sepsis Campaign pediatric guidelines. We also consider the trial’s limitations and what the results mean for fluid selection at the bedside. Learning Objectives By the end of this episode, listeners should be able to: Compare the composition and physiologic effects of 0.9% saline and balanced crystalloids used for pediatric fluid resuscitation. Summarize the design and major findings of the PRoMPT BOLUS trial. Describe important limitations of PRoMPT BOLUS when applying its results to children with septic shock. Apply current evidence and 2026 Surviving Sepsis Campaign recommendations when selecting crystalloid fluids for pediatric septic shock. References Weiss SL, Peters MJ, Oczkowski SJW, et al. Surviving Sepsis Campaign International Guidelines for the Management of Sepsis and Septic Shock in Children 2026. Pediatr Crit Care Med. 2026. Published April 1, 2026. Jointly issued by the Society of Critical Care Medicine and Infectious Diseases Society of America. Recommendation 24 suggests balanced/buffered crystalloids over 0.9% saline for children with septic shock requiring fluid boluses (conditional recommendation, very low certainty), while recognizing 0.9% saline as a suitable alternative and preferred in selected situations such as hyponatremia or concern for increased intracranial pressure. Balamuth F, Weiss SL, Long E, et al. Balanced Fluid or 0.9% Saline in Children Treated for Septic Shock. N Engl J Med. 2026. Published April 24, 2026. PRoMPT BOLUS was a large pragmatic randomized trial comparing balanced crystalloids with 0.9% saline in children treated for suspected septic shock and found no reduction in major adverse kidney events within 30 days with balanced fluids. Transcript This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content. Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski, and today we’re gonna talk about which fluid we should use when managing a septic pediatric patient. So when we resuscitate a child with septic shock, the major decision is usually not whether to give crystalloid, but which crystalloid to give. And for a long time, there’s been a gradual shift towards balanced fluids such as Lactated Ringer’s or Plasma-Lyte, largely because they are more physiologic and produce less hyperchloremia than normal saline. The question’s always been whether those biochemical differences actually translate into better clinical outcomes. That is the question that a study called PRoMPT BOLUS was designed to answer. So before getting into the trial, it’s worth briefly reviewing what these fluids actually contain. So normal saline is 0.9% sodium chloride. It contains one hundred and fifty-four milliequivalents per liter of sodium and a hundred and fifty-four milliequivalents per liter of chloride. The chloride concentration is substantially higher than plasma. Balanced crystalloids contain less chloride and have some other electrolytes and a buffer. Lactated Ringer’s contains approximately a hundred and thirty milliequivalents per liter of sodium, one hundred and nine of chloride, four of potassium, a small amount of calcium, and lactate as a buffer. Plasma-Lyte contains approximately one hundred and forty of sodium, ninety-eight of chloride, five of potassium, magnesium, and acetate and gluconate as buffers. The concern with normal saline is that the large chloride loads can produce hyperchloremic metabolic acidosis. There’s also been concern about adverse effects on renal blood flow and kidney function. Balanced fluids are designed to more closely approximate plasma composition, so the hypothesis has been that they might reduce kidney injury. That hypothesis has been supported by physiologic data and by some adult studies, although pediatric evidence before PRoMPT BOLUS was limited and inconsistent. The 2026 Surviving Sepsis Campaign Pediatric Guidelines recommend crystalloids over albumin for initial resuscitation and conditionally suggest balanced or buffered crystalloids over 0.9% saline in children with septic shock who require fluid boluses. Importantly, that recommendation is based on very low-certainty evidence. Balanced options again include Lactated Ringer’s, Hartmann’s solution, or Plasma-Lyte. If balanced fluids are not readily available, saline remains an acceptable alternative. Saline may also be preferable in some specific situations like significant hyponatremia or concern for increased intracranial pressure. For children in resource-abundant settings, the general approach is still ten to twenty mLs per kilo per bolus with reassessment after each bolus, potentially up to forty to sixty mLs per kilo in the first hour if perfusion remains abnormal and there are no signs of fluid overload. Now, PRoMPT BOLUS, the full name of which is the Pragmatic Pediatric Trial of Balanced versus Normal Saline Fluid in Sepsis, was an international randomized pragmatic trial designed to specifically compare the two fluid strategies in children with suspected septic shock. The final trial enrolled nine thousand and forty-one children from two months to younger than eighteen years across forty-seven emergency departments in five countries. Children were randomized to predominantly balanced crystalloid or predominantly 0.9% saline, and the assigned fluid strategy was used for bolus and maintenance crystalloid during the initial treatment period. The balanced fluid arm was not a single product. Depending on the site, children could get Lactated Ringer’s, Hartmann’s solution, or Plasma-Lyte. That’s important when interpreting the study. PRoMPT BOLUS was really testing a strategy of predominantly balanced crystalloid versus a strategy of predominantly saline use rather than comparing LR versus saline alone, though LR was the most commonly used one. The primary outcome was something called MAKE30, M-A-K-E thirty, or major adverse kidney events within thirty days. This was a composite outcome that included death, new renal replacement therapy, or persistent kidney dysfunction. That choice of outcome is useful because the biologic rationale for balanced fluids has always centered largely on kidney protection. The investigators were therefore asking whether the lower chloride exposure associated with balanced fluids translated into clinically meaningful renal benefit. So what was the result? Well, the spoiler is that the answer was no. So MAKE30 occurred in three point four percent of children receiving balanced fluids and three percent receiving saline. The relative risk was one point one with a ninety-five percent confidence interval from point eight eight to one point four. There were also no significant differences in death, new renal replacement therapy, persistent kidney dysfunction, or hospital-free days. In practical terms, balanced crystalloids did not improve the major patient-centered outcomes the trial was designed to measure. There were clear biochemical differences between the groups. Hyperchloremia occurred in thirty-one point four percent of children receiving balanced fluids compared with forty-nine percent with saline. Hypernatremia was also less common with balanced fluids, one point eight versus three point one percent. Hyperlactatemia was slightly more common in the balanced fluid group, nineteen point eight compared with sixteen point seven percent. So the fluids behaved differently in the ways that you would expect physiologically. Balanced crystalloids clearly reduced hyperchloremia, but that difference did not translate into fewer major kidney events, less dialysis, shorter hospitalization, or lower mortality. There are several limitations to this study worth keeping in mind. The first is that this was a broad emergency department population with suspected septic shock, not a study limited to children with the most severe forms of shock. Only a minority of patients required vasoactive medications, and overall mortality was low. The results are therefore most applicable to the typical child with suspected septic shock receiving early ED resuscitation. They do not completely answer whether fluid composition might matter more in a smaller subgroup of children receiving very large fluid volumes or prolonged resuscitation. The second limitation is that the event rate for MAKE30 was lower than expected. When the trial was designed, investigators anticipated an event rate of about six percent in the saline group. The observed rate was closer to three percent. That means there were fewer outcome events than anticipated, which reduced the ability to detect a very small treatment effect. So the trial makes a large benefit from balanced fluids unlikely, but it can’t exclude a small or subtle difference. A third limitation is that the balanced fluid group included several different solutions. Lactated Ringer’s, Plasma-Lyte, and Hartmann’s are all considered under the umbrella of balanced crystalloids, but they’re not chemically identical. The study therefore supports the broader conclusion that a balanced fluid strategy is not superior to saline for most children in this setting, rather than providing equivalence between any single specific balanced solution and saline, even though Lactated Ringer’s is used far and away most often. The trial was also intentionally pragmatic, which means that there was some crossover between fluid types. Adherence was defined as receiving at least seventy-five percent of crystalloid as the assigned fluid rather

Embedded earrings are a common pediatric emergency department presentation that can usually be managed quickly and safely without procedural sedation. This episode reviews why earrings become embedded, how to distinguish uncomplicated earlobe cases from higher-risk cartilage piercings, step-by-step removal techniques, pain control strategies, and appropriate wound care, antibiotics, and follow-up. Learning Objectives Recognize the evaluation and management of embedded earlobe earrings, including indications for local anesthesia, incision, and removal techniques. Differentiate uncomplicated earlobe piercings from cartilage piercings that require additional concern for perichondritis, Pseudomonas infection, and possible ENT consultation. Apply evidence-based post-procedure care, including appropriate wound management, antibiotic selection, and counseling to help prevent future embedded earrings. References Timm N, Iyer S. Embedded earrings in children. Pediatr Emerg Care. 2008;24(1):21-24. Muntz HR, Pa-C DJ, Asher BF. Embedded earrings: a complication of the ear-piercing gun. Int J Pediatr Otorhinolaryngol. 1990;19(1):73-76. Kim MM, Goldman RD. Ear-piercing complications in children and adolescents. Can Fam Physician. 2022;68(9):661-663. Transcript This transcript was generated using Descript and subsequently reviewed and lightly edited for spelling, grammar, and clarity. Minor inaccuracies may remain, and the audio recording should be considered the definitive version of this content. Welcome to PEM Currents: The Pediatric Emergency Medicine Podcast. As always, I’m your host, Brad Sobolewski. Today, we’re continuing our new series on minor procedures. These are the procedures we perform all the time in pediatric emergency departments. They’re not the subject of giant multicenter trials or big keynote lectures, but they are the procedures that families remember. If you make them quick, comfortable, and maybe even a little less scary, families and patients will remember that. And if the procedure turns into a wrestling match with three people trying to hold down a screaming child while you’re searching for an earring backing, they’re gonna remember that too. Today’s topic is embedded earrings. A kid walks into the emergency department holding one ear. The earlobe is swollen and red, and the parent says, “I can’t find their earring.” It didn’t disappear. The ear basically swallowed it, and the parents almost always feel bad. They think they did something wrong or they waited too long. Honestly, this happens all the time. The first one can be a little intimidating because the hardware isn’t always where you expect it to be, but after you’ve removed a few of these, you’ll realize they’re actually pretty straightforward. Most can be managed right in the emergency department or a well-resourced urgent care. One of the best studies on the topic actually came from Cincinnati Children’s. Tim and Iyer reviewed over 100 children who presented to our emergency department with embedded earrings over about a four-and-a-half-year period. The median age was eight years, and about 60% of the children were younger than 10. That fits with most of our clinical experience. Younger children are more likely to sleep on new piercings, play with their earrings, forget the aftercare instructions, or simply not notice that the backing has become too tight. Nearly 90% of embedded earrings involve the earlobe rather than the cartilage, and in about two-thirds of patients, it wasn’t the decorative front of the earring that got stuck, it was the posterior backing or clasp. That’s helpful because I, um, almost always start looking on the back of the ear, ‘cause usually they’ve taken off the front. About one-third of children had evidence of a localized infection when they presented. Usually, that meant tenderness, erythema, swelling, and maybe a little purulent drainage or crusting around the piercing. Doesn’t necessarily mean they need oral or systemic antibiotics, but it does mean they shouldn’t wait another week hoping the earring somehow works itself out. So why does this happen? It’s really a pressure injury. The backing gets tightened against the earlobe, either because it was applied too snugly when the ears were pierced or because the ear swells afterward and suddenly there’s no room for the tissue to expand. That constant pressure decreases blood flow, produces local inflammation, and eventually the skin begins to grow around the earring hardware. Kids speed the whole process along by twisting the earrings, playing with them, sleeping on them, bumping them during play, and not cleaning the piercing consistently while it’s healing. One thing that probably contributes as well is the spring-loaded ear piercing gun. These devices place the earring and immediately snap on the backing, and sometimes that backing ends up much tighter than it should be. If swelling develops over the next day or so, the backing can quickly become buried beneath the skin. It’s one of the reasons I generally recommend families avoid piercing guns and instead use a method that leaves just a little room for post-procedure swelling. When these patients show up in the emergency department, they almost always complain of pain, swelling, redness, and tenderness around the piercing site. Sometimes there’s drainage. Sometimes the parent says they can’t unscrew the backing anymore. Sometimes they tell you they can feel the earring in the earlobe, but you can’t actually see it. Now, I’ll get to the procedure technique in just a minute. But before I start talking about that, I do wanna separate earlobe piercings from cartilage piercing, ‘cause they’re really different problems. Once cartilage is involved, the stakes go up considerably. Cartilage has relatively poor blood supply, making it much more susceptible to perichondritis, chondritis, cartilage necrosis, and permanent cosmetic deformity. The bacteria may be different as well. We’ll come back to that later. For now, though, let’s stay with the earlobe because, frankly, that’s where almost all of these procedures occur. All right. Before you start any procedure, you wanna have everything ready. So I’ll have local anesthetic, so lidocaine or lidocaine with epi. Epi is totally fine in the earlobe. At least two mosquito hemostats, stuff to grab the earring, an 11 blade, gauze, saline, and a good light source. I think if there’s any chance I’ll need to make a small incision, I’ll prep the ear before I do anything with, uh, betadine or chlorhexidine. Once the ear starts bleeding a little or the child starts moving around, everything gets just a little harder to see and grab. Absolutely bring your child life specialist if you’ve got them and someone to hold, like a medic or a PCA. One of the interesting things about the Cincinnati study is that none of the 100 children required procedural sedation. None. And honestly, that fits with my experience. The overwhelming majority of these can be managed with local anesthesia alone. For the earlobe, I usually perform a small field block using one percent lidocaine with epinephrine, using a twenty-seven or thirty-gauge needle. Epi is perfectly safe in the earlobe and gives you a little hemostasis while you’re working. One thing I probably do differently from some people is I actually wait for the anesthetic to work a little longer. I don’t just block and immediately start. I’ll wait at least five minutes. Honestly, it’s usually closer to seven to ten minutes. During that time, I’m talking with the family, keeping child life involved, making sure all my equipment is ready, and just letting everybody settle down a bit. Those extra few minutes make the whole procedure a lot easier. And again, this is pediatrics, so never underestimate distraction. You’ve got videos, music, you know, stuffed animal, a toy. Parents should be there holding the child’s hand. You gotta coach the parents as well. And sometimes that’s really all you need, a good block and some distraction. Of course, some kids do need more. For an anxious child, you can use intranasal midazolam or oral midazolam. If your department has nitrous oxide, this is a great procedure for it because it’s usually pretty quick. You’re often treating anxiety more than pain. I have used ketamine a handful of times, and not because something went wrong, but just because you have an extremely anxious child, and you’re not gonna accomplish the procedure safely any other way. First, figure out what you can see and what you can feel. Sometimes both the decorative front and backing are still visible, but the ear is simply too swollen to separate them normally. Those are the easy ones. I’d grab each side with a mosquito hemostat, disengage the backing from the post, and remove the earring. More commonly, the backing is buried beneath the skin. The decorative front may still be attached, or the parents may have already removed it and left the backing sitting in the earlobe. I’ll gently compress the earlobe from the front while looking at the back. That pressure tents the skin enough to expose a few millimeters of metal through the original piercing hole, and that may be all that I need to grab the backing and remove it. If you still can’t see it, keep palpating. Usually, I can feel the hardware through the swollen tissue. Once you localize it, I’ll make a tiny incision on the back of the earlobe directly over it. And when I say tiny, I mean tiny, like a couple millimeters, just enough to expose the metal. But don’t be afraid of making that incision. It’s honestly usually the difference between wrestling with the earring for ten minutes and having it out within sixty seconds. From there, the rest is pretty straightforward. Whether the front is buried, the backing is buried, or neither side is visible, I gently spread the tissue with a mosquito hemostat until the hardware comes into view. Notice that I said spread, not dissect. You’re not hunti