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1. Episode 982: Epistaxis Management10.11.2025 (00:06:23)

   Contributor: Meghan Hurley, MD Educational Pearls: 1. Initial Assessment Start with a physical examination: Determine if the bleed is anterior or posterior. Perform a primary survey: assess airway, breathing, and circulation (ABCs). Airway compromise = intubation immediately. If the patient is stable, have them blow out any clots, then re-examine the nares. 2. Topical Medications Anesthetics: provide local anesthesia and pain relief. Lidocaine Tetracaine Vasoconstrictors: reduce bleeding. LET (Lidocaine, Epinephrine, Tetracaine) is ideal because it provides anesthesia and vasoconstriction. Cocaine pledgets (less common). Tranexamic acid (TXA). Oxymetazoline (Afrin). Cautery (Chemical): If an anterior bleed is visualized, silver nitrate can be applied for cauterization 3. Technique Tips Use a nasal speculum. Spread up and down rather than side to side to avoid injury to the septum. Place LET-soaked gauze in the nares. Apply a nasal clamp for ~15 minutes to compress the vessels. Note that pledgets may cause upper lip numbness 4. Reassessment After 15 minutes, remove materials and inspect for a source of bleeding. If still bleeding and a source is identified, cauterize the site. Observe for 15 minutes to monitor for recurrence of bleeding. 5. Packing If the above measures fail to control bleeding: Anterior packing: Nasal tampon (Merocel) Convenient for outpatient removal. Balloon device Inflate the anterior balloon for compression. Posterior packing:  More complex, should consult ENT for additional assistance. 6. Disposition & Follow-Up Although rare, toxic shock syndrome is a possible complication of nasal packing. Antibiotic prophylaxis is controversial, but may be considered in high-risk patients. Outpatient follow-up if stable: Tampon: The patient can remove it at home. Balloon: Return to ED for removal. 7. Risk Factors for Epistaxis & Prevention Deviated septum, dry environments, and anticoagulant use Advise on humidifier use, nasal saline, and medication review to minimize future episodes. References: Tunkel DE, Anne S, Payne SC, et al. Clinical Practice Guideline: Nosebleed (Epistaxis). Otolaryngology–Head and Neck Surgery. 2020;162(1_suppl):S1-S38. doi:10.1177/0194599819890327   Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

2. Episode 981: Electrical Burns03.11.2025 (00:03:41)

   Contributor: Travis Barlock, MD Educational Pearls: Quick Statistics on Electrical Burns: Electrical burns compose roughly 2 to 9% of all burns that come into emergency departments. The majority of patients who receive electrical burns are male, typically aged 20's to 30's, accounting for 80 to 90% of all electrical burn victims. The majority of burns are linked to occupational exposure. The upper extremities are more commonly impacted by electrical burns, accounting for 70 to 90% of entry points into the body during an exposure. What are some of the key considerations in electrical burns? Unlike chemical or fire/heat related burns, electrical burns have the potential to cause significant internal damage that may not be physically appreciated externally. This damage can include, but is not limited to: Cardiac dysthymias (PVCs, SVT, AV block, to more serious ventricular dysrhythmias such as ventricular fibrillation or ventricular tachycardia). Deep tissue injury resulting in rhabdomyolysis from the initial surge of electricity Rare cases of compartment syndrome What are the treatment considerations for patients who suffer electrical burns? Remembering that cutaneous findings associated with burns may underestimate the severity of the injury, with deeper structures being more likely to be involved as the voltage of the burn injury is directly correlated to severity. Manage the patient's airway, breathing, and circulation as always, and conduct further workup into potential cardiac involvement with EKGs, as well as analysis of the extremities where entry occurred for muscle breakdown and compartment syndrome. Clinical Pearl on Voltage and Current: Voltage can be thought of being equivalent to pressure in a fluid/liquid system. Higher voltages are equivalent to higher pressures, but the ultimate damage delivered to the system is from the rate of delivery/speed of the electrical energy surging (current) through the body. Current is dependent on the tissue it is travelling through, with different tissues having differing electrical resistances. Tissues like the stratum corneum of the skin and the human bone confer the most resistance (thus lower current) whereas skeletal muscle confers lower electrical resistance (thus higher current) due to water and electrolyte content, which is why injuries like rhabdomyolysis are possible and increase with increasing voltage. References Khor D, AlQasas T, Galet C, et al. Electrical injuries and outcomes: A retrospective review. Burns. 2023;49(7):1739-1744. doi:10.1016/j.burns.2023.03.015 Durdu T, Ozensoy HS, Erturk N, Yılmaz YB. Impact of Voltage Level on Hospitalization and Mortality in Electrical Injury Cases: A Retrospective Analysis from a Turkish Emergency Department. Med Sci Monit. 2025;31:e947675. doi:10.12659/MSM.947675 Karray R, Chakroun-Walha O, Mechri F, et al. Outcomes of electrical injuries in the emergency department: epidemiology, severity predictors, and chronic sequelae. Eur J Trauma Emerg Surg. 2025;51(1):85. doi:10.1007/s00068-025-02766-1 Faes TJ, van der Meij HA, de Munck JC, Heethaar RM. The electric resistivity of human tissues (100 Hz-10 MHz): a meta-analysis of review studies. Physiol Meas. 1999;20(4):R1-10. doi:10.1088/0967-3334/20/4/201 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate

3. Tox Talks 2025 Recap 1, Digoxin and Beta Blockers29.10.2025 (00:57:21)

   Contributors: Preeya Prakash MD, Adam Greenhaw PharmD, Travis Barlock MD, and Jeffrey Olson MS4 In this episode, cardiologist Preeya Prakash and medical student Jeffrey Olson listen in as two cases are presented from EMM's recent event, Tox Talk 2025. Talk 1- Digoxin Overdose Dr. Adam Greenhaw presents a case of a Digoxin overdose along with many pearls. During the studio listen in, Dr. Prakash helps to answer the questions of: How does digoxin work? Why might a patient still be on digoxin in 2025? What are the EKG findings of digoxin toxicity? Is there any utility in atropine for bradycardia caused by digoxin? Should you use calcium to treat hyperkalemia in the setting of a digoxin overdose? If/when might a cardiologist get involved in a patient with a digoxin overdose? Talk 2- Propranolol Overdose Dr. Travis Barlock presents a case of a beta blocker overdose as well as many associated pearls. During our studio listen in, Dr. Prakash helps to answer the questions of: What are the different beta blockers and how do they work? If you are worried about a propranolol overdose, what medications do you want on hand? What POCUS cardiac view can give you the most information for different scenarios? Why or why not might transcutaneous or intravenous pacing be a good idea for a beta blocker overdose? If/when might you want a cardiologist to get involved in a patient with a beta blocker overdose? References Alahmed AA, Lauffenburger JC, Vaduganathan M, Aldemerdash A, Ting C, Fatani N, Fanikos J, Buckley LF. Contemporary Trends in the Use of and Expenditures on Digoxin in the United States. Am J Cardiovasc Drugs. 2022 Sep;22(5):567-575. doi: 10.1007/s40256-022-00540-x. Epub 2022 Jun 24. PMID: 35739347; PMCID: PMC10263277. Chan BS, Buckley NA. Digoxin-specific antibody fragments in the treatment of digoxin toxicity. Clin Toxicol (Phila). 2014 Sep-Oct;52(8):824-36. doi: 10.3109/15563650.2014.943907. Epub 2014 Aug 4. PMID: 25089630. Hack JB, Wingate S, Zolty R, Rich MW, Hauptman PJ. Expert Consensus on the Diagnosis and Management of Digoxin Toxicity. Am J Med. 2025 Jan;138(1):25-33.e14. doi: 10.1016/j.amjmed.2024.08.018. Epub 2024 Sep 11. PMID: 39265879. Krenz JR, Kaakeh Y. An Overview of Hyperinsulinemic-Euglycemic Therapy in Calcium Channel Blocker and β-blocker Overdose. Pharmacotherapy. 2018 Nov;38(11):1130-1142. doi: 10.1002/phar.2177. Epub 2018 Oct 4. PMID: 30141827. Patocka J, Nepovimova E, Wu W, Kuca K. Digoxin: Pharmacology and toxicology-A review. Environ Toxicol Pharmacol. 2020 Oct;79:103400. doi: 10.1016/j.etap.2020.103400. Epub 2020 May 7. PMID: 32464466. Rotella JA, Greene SL, Koutsogiannis Z, Graudins A, Hung Leang Y, Kuan K, Baxter H, Bourke E, Wong A. Treatment for beta-blocker poisoning: a systematic review. Clin Toxicol (Phila). 2020 Oct;58(10):943-983. doi: 10.1080/15563650.2020.1752918. Epub 2020 Apr 20. PMID: 32310006. Produced by Jeffrey Olson, MS4 Donate: https://emergencymedicalminute.org/donate/

4. Episode 980: Brain Injury Guidelines (BIG)27.10.2025 (00:03:17)

   Contributor: Aaron Lessen, MD Educational Pearls: Traumatic Brain Injuries are a frequent complaint in the Emergency Department and have increased in recent years. The American Association for Surgery of Trauma (AAST) has created Brain Injury Guidelines (BIG), in an attempt to categorize brain injuries and the level of treatment they require. They are… BIG 1 Normal neuro exam Not intoxicated Not on anticoagulation or antiplatelet medications Minimal findings on head CT No fracture Maximum of "trace" subarachnoid hemorrhage No intraventricular hemorrhage                             Monitor for 6 hours No need to repeat the head CT No need to consult neurosurgery BIG 2 Normal neuro exam Not on anticoagulation or antiplatelet medications Any of the following Intoxicated Slightly more findings on head CT Non-displaced skull fracture 4-8 mm bleed (subdural, epidural, intraparenchymal (max two locations)) Maximum of "localized" subarachnoid hemorrhage No intraventricular hemorrhage     Hospitalize No need to transfer No need to repeat the head CT No need to consult neurosurgery BIG 3 Abnormal neuro exam On anticoagulation or antiplatelet medications Intoxicated Significant findings on head CT Displaced skull fracture >8 mm bleed (subdural, epidural, intraparenchymal (or more than 2 locations)) "Scattered" subarachnoid hemorrhage Intraventricular hemorrhage     Full treatment, admission to trauma center, neurosurgery evaluation References Joseph B, Friese RS, Sadoun M, Aziz H, Kulvatunyou N, Pandit V, Wynne J, Tang A, O'Keeffe T, Rhee P. The BIG (brain injury guidelines) project: defining the management of traumatic brain injury by acute care surgeons. J Trauma Acute Care Surg. 2014 Apr;76(4):965-9. doi: 10.1097/TA.0000000000000161. PMID: 24662858. Joseph B, Obaid O, Dultz L, Black G, Campbell M, Berndtson AE, Costantini T, Kerwin A, Skarupa D, Burruss S, Delgado L, Gomez M, Mederos DR, Winfield R, Cullinane D; AAST BIG Multi-institutional Study Group. Validating the Brain Injury Guidelines: Results of an American Association for the Surgery of Trauma prospective multi-institutional trial. J Trauma Acute Care Surg. 2022 Aug 1;93(2):157-165. doi: 10.1097/TA.0000000000003554. Epub 2022 Mar 28. PMID: 35343931. Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

5. Episode 979: Oral vs Temporal Thermometers20.10.2025 (00:03:13)

   Contributor: Taylor Lynch, MD Educational Pearls: A recent study published in a pediatric journal in April 2025 compared temporal and oral thermometers Paired temperature measurements (temporal and oral temperature within 30 minutes) were obtained from 1,412 pediatric patients 26% of patients had statistically different temporal and oral temperatures The temporal reading was always lower than the oral reading Children less than 12 years old were 2-3x more likely to actually have that statistical difference in temperatures The study also evaluated 1,000 adult patients 36% had a temporal temperature that was 0.5 degrees Celsius lower than the oral temperature Reasons for the statistical difference between the two types of thermometers: Environment: temporal thermometers are affected by ambient room temperature, diaphoresis, and inaccuracy in measuring temperature at the site of the temporal artery Physiologic: a patient with inadequate perfusion will not have an accurate temporal reading Impact: Obtaining an accurate temperature is crucial in patient care For example, in the setting of sepsis, temperature is a necessary component to identifying when a patient meets SIRS criteria References Salhi RA, Meeker MA, Williams C, Iwashyna TJ, Samuels-Kalow ME. Inaccuracy of Temporal Thermometer Measurement by Age and Race. Acad Pediatr. 2025 Apr;25(3):102620. doi: 10.1016/j.acap.2024.102620. Epub 2024 Dec 15. PMID: 39681266. Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

6. Episode 978: Delusional Parasitosis13.10.2025 (00:03:55)

   Contributor: Taylor Lynch, MD Educational Pearls: Delusional parasitosis is a subtype of the psychiatric condition delusional disorder Defined as a fixed, false belief of infestation by parasites or other organisms A somatic type of delusional disorder Primary delusional parasitosis Occurs in the absence of other psychiatric or medical conditions Secondary delusional parasitosis Causes include methamphetamine use disorder, schizophrenia, neurologic diseases, or medical conditions such as thyroid disease Pathophysiology Poorly understood Upregulation of striatal dopamine system is implicated Management Form a strong therapeutic alliance and do not discredit the patient immediately Perform a full physical exam This helps reassure the patient and strengthen the therapeutic alliance Some day there may be a patient in whom this is not a delusion Treatment & Management Discontinuation of substances if substance-induced Antipsychotic medications like risperidone or olanzapine References Lepping P, Russell I, Freudenmann RW. Antipsychotic treatment of primary delusional parasitosis: systematic review. Br J Psychiatry. 2007;191:198-205. doi:10.1192/bjp.bp.106.029660 Moriarty N, Alam M, Kalus A, O'Connor K. Current Understanding and Approach to Delusional Infestation. Am J Med. 2019;132(12):1401-1409. doi:10.1016/j.amjmed.2019.06.017 Skelton M, Khokhar WA, Thacker SP. Treatments for delusional disorder. Cochrane Database Syst Rev. 2015;2015(5):CD009785. Published 2015 May 22. doi:10.1002/14651858.CD009785.pub2 Summarized and Edited by Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

7. Episode 977: Amyloid Therapy and Stroke-like Events06.10.2025 (00:03:03)

   Contributor: Aaron Lessen, MD Educational Pearls: The cause of Alzheimer's disease is multifactorial, but the most widely suspected mechanism is the amyloid cascade hypothesis: Beta-amyloid proteins accumulate in the central nervous system, forming plaques that impair neuronal function. In recent years, advances have led to the development of targeted therapies with monoclonal antibodies. These drugs: Work by degrading amyloid plaques Slow the rate of cognitive decline and disease progression Have major side effects, most notably the development of amyloid-related imaging abnormalities (ARIA) ARIA may present as edema, effusion, or microhemorrhages, which are only detectable on MRI Symptoms can include headache, vertigo, or focal neurologic deficits that mimic stroke For patients presenting to the emergency department with stroke-like symptoms, it is important to consider whether they have a history of Alzheimer's disease and whether they are taking these medications. This guides decisions about imaging and treatment: The work-up may require MRI, which can delay thrombolytic or endovascular therapy in patients with true strokeConversely, treating a patient with ARIA using thrombolytics increases the risk of bleeding and other complications References Ebell MH, Barry HC, Baduni K, Grasso G. Clinically Important Benefits and Harms of Monoclonal Antibodies Targeting Amyloid for the Treatment of Alzheimer Disease: A Systematic Review and Meta-Analysis. Ann Fam Med. 2024 Jan-Feb;22(1):50-62. doi: 10.1370/afm.3050. PMID: 38253509; PMCID: PMC11233076. Ma C, Hong F, Yang S. Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules. 2022 Feb 11;27(4):1210. doi: 10.3390/molecules27041210. PMID: 35209007; PMCID: PMC8876037. Perneczky R, Dom G, Chan A, Falkai P, Bassetti C. Anti-amyloid antibody treatments for Alzheimer's disease. Eur J Neurol. 2024 Feb;31(2):e16049. doi: 10.1111/ene.16049. Epub 2023 Sep 11. PMID: 37697714; PMCID: PMC11235913. Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

8. Episode 976: Improvised Burr Hole in an Epidural Hematoma29.09.2025 (00:04:18)

   Contributor: Alec Coston, MD Case Report Summary: A 17-year-old female involved in a motor vehicle collision presented to a rural emergency facility via personally operated vehicle. During workup and initial CT scan, the patient began rapidly decompensating with CT revealing a 1.5cm epidural hematoma with 7mm of midline shift. The patient went from being able to walk and talk to being obtunded with a blown left pupil and unresponsive. Following intubation, the patient was being prepared for transport but potential delays required immediate emergency evacuation of the hematoma via a Burr Hole. A traditional Burr Drill was not immediately available at the facility, so an improvised Burr Drill using an Intraosseous (IO) drill was used. 35mL of blood was removed from the hematoma and the patient immediately improved from a GCS of 3 to GCS of 8. The patient was transferred to a higher level of care facility, extubated the following day, and made a full neurological recovery.  Educational Pearls: What is an epidural hematoma? An epidural hematoma is a collection of blood between the dura mater (outermost layer of the meninges) and the skull, whereas a subdural hematoma is a collection of blood between the dura mater and arachnoid mater. Both can be life threatening depending on location and size. Epidural hematomas tend to be arterial, and are typically secondary to trauma and can rapidly expand, but with timely recognition and evacuation of the bleed, favorable outcomes are often possible. What are typical intracranial pressures and at what levels do they become pathologic? Typical intracranial pressure (ICP) varies by age, but past infancy and early childhood, adolescents and adults have a value typically between 8-15mmHg. Values exceeding 20mmHg become pathologic and rise exponentially with increased volume. Initial symptoms may include headache, nausea, and vomiting, but with increased pressures may progress to more life threatening symptoms such as loss of consciousness, cranial nerve palsies, pupillary constriction or dilation (sign of herniation), and respiratory irregularities. What is the takeaway in timing of epidural hematomas? Older studies show that evacuation of a hematoma with lateralizing features before the two hour mark of coma symptom onset is correlated with decreased mortality (ranging from 15-17%), but beyond 2 hours the mortality increases to well over 50%. Though mortality statistics have grown more variable, early targeted evacuation of epidural hematomas still remains critical for improved patient outcomes. In austere conditions with limited resources, improvisation with interosseous drills and needles can improve patient outcomes and achieve the target therapy for epidural hematomas. References Haselsberger K, Pucher R, Auer LM. Prognosis after acute subdural or epidural haemorrhage. Acta Neurochir (Wien). 1988;90(3-4):111-116. doi:10.1007/BF01560563 Hawryluk GWJ, Nielson JL, Huie JR, et al. Analysis of Normal High-Frequency Intracranial Pressure Values and Treatment Threshold in Neurocritical Care Patients: Insights into Normal Values and a Potential Treatment Threshold. JAMA Neurol. 2020;77(9):1150-1158. doi:10.1001/jamaneurol.2020.1310 Pisică D, Volovici V, Yue JK, et al. Clinical and Imaging Characteristics, Care Pathways, and Outcomes of Traumatic Epidural Hematomas: A Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury Study. Neurosurgery. 2024;95(5):986-999. doi:10.1227/neu.0000000000002982 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

9. Episode 975: Nursemaid's Elbow22.09.2025 (00:03:45)

   Contributor: Aaron Lessen, MD Educational Pearls: What is a Nursemaid's Elbow? A condition in which an elbow gets partially pulled out of place (a radial head subluxation) Usually happens in kids under 5 because the ligaments around their elbow are still loose. A common situation is when an adult pulls a child up by the hand or swings them by the arms. The sudden tug causes the radius to slip out of its normal spot at the elbow joint. How are they identified? These don't normally need an xray The child will often hold their arm close to their side and refuse to use it There's usually no swelling or obvious deformity. Treatment? Reduce the radial head subluxation. There are two possible techniques: Flexion and supination. Start with the arm extended and pronated. Then supinate the forearm. Then bend the elbow up all the way. Hyper-pronation. One hand stabilizes just above the child's elbow, the other holds the wrist. Start with the arm extended. Hyperpronate the forearm. Listen/feel for a click The child is normally back to normal quickly, if not get the xray Which is better? Hyperpronation (Aksel, 2025) 10% first attempt failure rate Flexion-pronation has a 25% first attempt failure rate References Aksel G, Küka B, İslam MM, Demirkapı F, Öztürk İ, İşlek OM, Ademoğlu E, Eroğlu SE, Satıcı MO, Özdemir S. Comparison of supination/flexion maneuver to hyperpronation maneuver in the reduction of radial head subluxations: A randomized clinical trial. Am J Emerg Med. 2025 Feb;88:29-33. doi: 10.1016/j.ajem.2024.11.026. Epub 2024 Nov 18. PMID: 39579408. Ulici A, Herdea A, Carp M, Nahoi CA, Tevanov I. Nursemaid's Elbow - Supination-flexion Technique Versus Hyperpronation/forced Pronation: Randomized Clinical Study. Indian J Orthop. 2019 Jan-Feb;53(1):117-121. doi: 10.4103/ortho.IJOrtho_442_17. PMID: 30905991; PMCID: PMC6394198. Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

10. Episode 974: ACE Inhibitor Angioedema15.09.2025 (00:05:03)

    Contributor: Ricky Dhaliwal, MD Educational Pearls: Angioedema in anaphylaxis Histamine and mast cell-mediated pathway Treatment: First line: epinephrine for vasoconstriction and bronchodilation Second line: H1 and H2 antihistamines such as Benadryl and famotidine ACE inhibitor-induced angioedema Different pathway from anaphylaxis ACE inhibitor-induced angioedema is mediated by bradykinins Therefore, anaphylaxis medications are not beneficial in patients with ACE inhibitor-induced angioedema Leading cause of drug-induced angioedema in the US Patients most commonly present with swelling of the lips, tongue, or face Treatment: Airway management: varies depending on the severity and progression of the presentation If awake nasointubation is required, LMX is a 5% lidocaine water-soluble solution that provides anesthesia to the oropharynx Medications: Icatibant is a synthetic bradykinin B2-receptor antagonist that can be used in acute treatment Tranexamic acid (TXA) inhibits the plasmin-dependent formation of bradykinin, but the data on this treatment are mixed and limited Fresh frozen plasma (FFP) is thought to degrade high levels of bradykinin with subsequent resolution of angioedema Discontinue ACE inhibitor References Bork K, Wulff K, Hardt J, Witzke G, Staubach P. Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy. J Allergy Clin Immunol. 2009 Jul;124(1):129-34. doi: 10.1016/j.jaci.2009.03.038. Epub 2009 May 27. PMID: 19477491. Bova M, Guilarte M, Sala-Cunill A, Borrelli P, Rizzelli GM, Zanichelli A. Treatment of ACEI-related angioedema with icatibant: a case series. Intern Emerg Med. 2015 Apr;10(3):345-50. doi: 10.1007/s11739-015-1205-9. Epub 2015 Feb 10. PMID: 25666515. Karim MY, Masood A. Fresh-frozen plasma as a treatment for life-threatening ACE-inhibitor angioedema. J Allergy Clin Immunol. 2002 Feb;109(2):370-1. doi: 10.1067/mai.2002.121313. PMID: 11842313. Pathak GN, Truong TM, Chakraborty A, Rao B, Monteleone C. Tranexamic acid for angiotensin-converting enzyme inhibitor-induced angioedema. Clin Exp Emerg Med. 2024 Mar;11(1):94-99. doi: 10.15441/ceem.23.051. Epub 2023 Aug 1. PMID: 37525579; PMCID: PMC11009700. Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. 2004 May;113(5):837-44. doi: 10.1016/j.jaci.2004.01.769. Erratum in: J Allergy Clin Immunol. 2004 Jun;113(6):1039. Dosage error in article text. PMID: 15131564. Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

11. Emergency Medicine Cases with Dr. Barlock09.09.2025 (00:53:02)

    Contributors: Travis Barlock MD, Jeffrey Olson MS4 Feel free to use the cases below for your own practice. All of the scenarios are completely made up and designed to hit several teaching points. Case 1 25 M, presents to the ED with chest pain. Stabbing, started a few hours ago, substernal. Thinks it is GERD. After 2-3 minutes, pain worsens and radiates to the back. VS: BP 125/50 (Right arm 190/110). HR 120. RR of 18. Sat 98% on RA. Additional VS: Temp of 37.2, height of 6'5", BMI of 18. PMH: None, doesn't see a doctor. Meds: None FH: Weird heart thing (Mitral Valve Prolapse), weird lung thing (spontaneous pneumothorax), tall family members with long fingers and toes Physical Exam: Cards: Diastolic decrescendo at the RUSB, diminished S2. UE pulses are asymmetric, LE pulses are asymmetric, carotid pulses are asymmetric, BP is asymmetric MSK: Knees, elbows, and wrists are hypermobile. Imaging: CXR #1 normal, #2 widened mediastinum (no read yet but shows widened mediastinum), POCUS shows small effusion CTA/MRA doesn't come back until after the case.  ECG: Sinus Tach Labs: NT-proBNP 500 pg/mL D-Dimer: 7000 ng/L CBC: Hemoglobin: 13.5 g/dL, WBC: 20,000/µL, Platelets: 250,000/µL Chem 7: Na 138, K, 5.7, Cl 102, Bicarb 17, BUN 45, Creatinine: 3.5 mg/dL, Glucose: 180 LFTs: Albumin 2.4, Total protein 5.5, ALP: 140, AST: 3500, ALT: 2800, TBili: 3.2, DirectBili: 2.4, Ca: 7.8 LDH: 2200 PT: 20.5, INR: 2.2, Fibrinogen: 170 5th gen High-Sensitivity Troponin: Lactate: 7 mmol/L VBG: pH 7.22, paCO2 28, bicarb 15 Notes: Can have patient crash somewhere in middle and show 2nd xray   Case 2:  A 67-year-old female is brought to the ED by her daughter due to progressive weakness, confusion, and fatigue that have worsened over the past week. Unable to get out of bed and has become increasingly lethargic. Also having some nausea, constipation. The daughter denies any preceding illness, recent trauma, or travel. Does not know her meds but will head home to get them after talking with you.  VS: BP 88/55 mmHg, HR 110, RR 20, O2 Sat 98% on room air. Additional VS: Temp 36.8°C. PMH: Hypertension, osteoarthritis, and depression. Physical exam: General: Thin, somnolent but arousable. HENT: Dry mucous membranes Neuro: Confused, A&Ox1 (self), hyporeflexia Labs (Includes many that would not return in the ED in case you want to take this case forward to the floor) CBC: WBC 9,500, Hb 16.5, Hct: 50%, Platelets 220,000 Chem7: Na 129, K 2.1, Cl 95, HCO3 34, Creatinine 1.6, BUN 40, Glucose 115 LFTs: normal Magnesium: 1.1 Calcium: 10.8 mg/dL (corrects to 12.8) iCal: 3.2 Phosphate: 2.3 mg/dL Albumin: 2 BUN:Cr ratio: 25 VBG: pH: 7.49, PaCO2 45, HCO3: 34 Lactate: 2.8 Serum Osmolality: 276 mOsm/kg (Osmolal gap of 2) Urine Osmolality: 550 mOsm/kg Urine Sodium (UNa): 10 mEq/L (low). Urine Potassium (UK): 25 mEq/L (elevated). Urine Chloride (UCl): 12 mEq/L (low). Urine Magnesium (UMg): 20 (Elevated). Urine Calcium (UCa): 50 in 24 hrs (Low) 100 cc of urine with foley FeNa Plasma renin activity: 15 mg/mL/hr (elevated), Aldosterone: 25 ng/dL (Elevated), ADH: Elevated, Diuretic screen: Positive for thiazides PTH: 8 (low), HsTrop: 32, Cortisol and ACTH: Normal. EKG: Hypokalemia features CXR: Normal Renal US: shows stones Improves with fluids Note: Can have daughter return with med list at some point including HCTZ, ibuprofen, and sertraline   Case 3: Patient Presentation EMS Report: A 27-year-old male involved in a high-speed motorcycle collision is brought to the emergency department by EMS. The patient was found unconscious at the scene with evidence of severe thoracic and extremity trauma. He was intubated en route for airway protection due to altered mental status (GCS 7).  VS: HR 130, BP 90/60, RR: bagging at 12 bpm, satting 88% on 100% FiO2  Primary Survey Airway: Endotracheal tube in place. Breathing: Decreased breath sounds on the left side with visible chest asymmetry and paradoxical chest wall movement. Circulation: Mottled extremities noted, with significant deformity of the right thigh. Pulses are diminished in the right leg Disability: GCS remains 7 (E1 V2 M4). Pupils equal and reactive. Exposure: Full-body examination reveals an open fracture of the right femur, multiple abrasions, and bruising over the chest wall. Vent alarms Peak Inspiratory Pressure (PIP) 40 cm H₂O (elevated) Plateau Pressure (Pplat) 35 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 55 mmHg High-Pressure Alarm Triggering frequently Glucose 120 CBC: Hgb 8.9, Hct 27, WBC 14.2, platelets 220,000 VBG: pH 7.28, pCO2 33, bicarb 18, lactate 4.5 CXR with tension pneumothorax  Patient improves after chest tube, pigtail catheter, or needle decompression. Ready to be transferred upstairs and O2 starts tanking again Vent alarms- second episode Peak Inspiratory Pressure (PIP) 35 cm H₂O (elevated) Plateau Pressure (Pplat) 30 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 20 mmHg HR: 140, satting 84%, temp 38.5,  ABG: pH 7.32, pCO₂ 30 mmHg, pO₂ 60 mmHg on 100% FiO₂, HCO₃⁻ 18 mmol/L (hypoxemia and metabolic acidosis). D-dimer: Elevated Thrombocytopenia: Platelets 90,000/µL. US shows blown right ventricle ECG shows new RBBB CT PE: Ground glass opacities, consolidation, centrilobular nodules, septal thickening, and fat-attenuating lesions. Note: Management is largely supportive care so once the diagnosis is made, end the case.   References Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1;67(9):1959-66. PMID: 12751658. Coelho SG, Almeida AG. Marfan syndrome revisited: From genetics to the clinic. Rev Port Cardiol (Engl Ed). 2020 Apr;39(4):215-226. English, Portuguese. doi: 10.1016/j.repc.2019.09.008. Epub 2020 May 18. PMID: 32439107. Palmer BF. Metabolic complications associated with use of diuretics. Semin Nephrol. 2011 Nov;31(6):542-52. doi: 10.1016/j.semnephrol.2011.09.009. PMID: 22099511. Reed MJ. Diagnosis and management of acute aortic dissection in the emergency department. Br J Hosp Med (Lond). 2024 Apr 30;85(4):1-9. doi: 10.12968/hmed.2023.0366. PMID: 38708978. Roberts DJ, Leigh-Smith S, Faris PD, Blackmore C, Ball CG, Robertson HL, Dixon E, James MT, Kirkpatrick AW, Kortbeek JB, Stelfox HT. Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review. Ann Surg. 2015 Jun;261(6):1068-78. doi: 10.1097/SLA.0000000000001073. PMID: 25563887. Rothberg DL, Makarewich CA. Fat Embolism and Fat Embolism Syndrome. J Am Acad Orthop Surg. 2019 Apr 15;27(8):e346-e355. doi: 10.5435/JAAOS-D-17-00571. PMID: 30958807.   Produced by Jeffrey Olson, MS4 Special thanks to Evan Fisch MD Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/   Donate: https://emergencymedicalminute.org/donate/

12. Episode 973: Meningitis Retention Syndrome08.09.2025 (00:02:16)

    Contributor: Travis Barlock MD Educational Pearls: Meningitis retention syndrome is a relatively novel and rare clinical condition Aseptic meningitis + acute urinary retention One study reports an incidence of about 8% in patients with acute aseptic meningitis Clinical presentation Typical meningeal symptoms including fever, stiff neck, and headache Urinary retention occurs about one week after initial symptoms Potential pathophysiology Immune-mediated dysfunction of the central nervous system Detrusor muscle underactivity from inflammation of the spinal cord Management Supportive care Bladder decompression References Hiraga A, Kuwabara S. Meningitis-retention syndrome: Clinical features, frequency and prognosis. J Neurol Sci. 2018;390:261-264. doi:10.1016/j.jns.2018.05.008 Pellegrino F, Funiciello E, Pruccoli G, et al. Meningitis-retention syndrome: a review and update of an unrecognized clinical condition. Neurol Sci. 2023;44(6):1949-1957. doi:10.1007/s10072-023-06704-0 Summarized & Edited by Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/

13. Episode 972: Hepatic Encephalopathy03.09.2025 (00:03:59)

    Contributor: Alec Coston, MD Educational Pearls: Hepatic encephalopathy (HE) is defined as a disruption in brain function that results from impaired liver function or portosystemic shunting. Manifests as various neurologic and psychiatric symptoms such as confusion, inattention, and cognitive dysfunction Although ammonia levels have historically been recognized as important criteria for HE, the diagnosis is ultimately made clinically. An elevated ammonia level lacks sensitivity and specificity for HE Trends in ammonia levels do not correlate with disease improvement or resolution A 2020 study published in the American Journal of Gastroenterology evaluated 551 patients diagnosed with hepatic encephalopathy and treated with standard therapy Only 60% of patients had an elevated ammonia level, demonstrating the limitations of ammonia levels However, a normal ammonia level in a patient with concern for HE should raise suspicion for other pathology. In patients with cirrhosis presenting with neuropsychiatric symptoms, consider HE as the diagnosis after excluding other potential causes of altered mental status (i.e., Seizure, infection, intracranial hemorrhage) The primary treatment is lactulose Works by acidifying the gastrointestinal tract. Ammonia (NH₃) is converted into ammonium (NH₄⁺), which is poorly absorbed and subsequently eliminated from the body Also exerts a laxative effect, further enhancing elimination References: Haj M, Rockey DC. Ammonia Levels Do Not Guide Clinical Management of Patients With Hepatic Encephalopathy Caused by Cirrhosis. Am J Gastroenterol. 2020 May;115(5):723-728. doi: 10.14309/ajg.0000000000000343. PMID: 31658104.\ Lee F, Frederick RT. Hepatic Encephalopathy-A Guide to Laboratory Testing. Clin Liver Dis. 2024 May;28(2):225-236. doi: 10.1016/j.cld.2024.01.003. Epub 2024 Jan 30. PMID: 38548435. Vilstrup, Hendrik1; Amodio, Piero2; Bajaj, Jasmohan3,4; Cordoba, Juan1,5; Ferenci, Peter6; Mullen, Kevin D.7; Weissenborn, Karin8; Wong, Philip9. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study Of Liver Diseases and the European Association for the Study of the Liver. Hepatology 60(2):p 715-735, August 2014. | DOI: 10.1002/hep.27210 Weissenborn K. Hepatic Encephalopathy: Definition, Clinical Grading and Diagnostic Principles. Drugs. 2019 Feb;79(Suppl 1):5-9. doi: 10.1007/s40265-018-1018-z. PMID: 30706420; PMCID: PMC6416238. Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons & Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/

14. Episode 971: Calcium Pretreatment for Diltiazem in AFib with RVR25.08.2025 (00:02:43)

    Contributor: Taylor Lynch, MD Educational Pearls: What is atrial fibrillation with rapid ventricular response (AFib with RVR) and how does it differ from atrial fibrillation (AFib)? AFib is an abnormal heart rhythm in which the heart has disorganized atrial electrical activity. This causes the atria to quiver with only select signals being conducted through the Atrioventricular (AV) Node to reach the ventricles and result in ventricular contraction. Often described as "irregularly irregular", a patient's EKG will present with no discernible P-waves, and irregular R-R intervals. AFib with RVR is distinguished from AFib when the patient's ventricular rate is greater than 100-110 beats per minute in AFib with RVR. What is the treatment for AFib with RVR? Diltiazem is considered one of the first line therapeutic agents in the treatment of AFib with RVR. Diltiazem inhibits L-Type calcium channels in the AV Node, reducing the amount of signals conducted to the ventricles, thus reducing the ventricular rate. Why pretreat patients receiving Diltiazem for AFib with RVR with calcium? While diltiazem inhibits cardiac calcium channels, it may also cause peripheral vasodilation, resulting in diltiazem-induced hypotension. A recent study found that this hypotension can be blunted by pretreating with 1-2g IV Calcium Chloride (IV Calcium Gluconate can be used in the ED). Calcium is thought to peripherally stabilize the vascular smooth muscle, preventing vasodilation without impacting the desired calcium channel blocker action at the AV node. Key takeaways? In combination with slower pushes of diltiazem for patients in AFib with RVR (AFib with ventricular rate >100-110 bpm) with borderline low blood pressures, 1-2 g of IV Calcium Gluconate can combat diltiazem induced hypotension peripherally without negating the cardiac effect of diltiazem to reduce the heart rate. References 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e1-e156. doi:10.1161/CIR.0000000000001193 Az A, Sogut O, Dogan Y, et al. Reducing diltiazem-related hypotension in atrial fibrillation: Role of pretreatment intravenous calcium. Am J Emerg Med. 2025;88:23-28. doi:10.1016/j.ajem.2024.11.033 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/

15. Episode 970: Fever Management22.08.2025 (00:02:06)

    Contributor: Aaron Lessen, MD Educational Pearls: Recorded March 2025 What is the best treatment for a fever? Tylenol? Ibuprofen? Combined? Alternating the two? The journal Pediatrics aimed to answer this question with a meta-analysis of 31 randomized controlled trials including 5,009 febrile children. Results showed that both combined and alternating acetaminophen/ibuprofen regimens were significantly more effective at reducing fever at 4 and 6 hours compared with acetaminophen alone, with numbers needed to treat (NNT) of 3 and 4, respectively. High-dose ibuprofen alone also offered modest benefit (NNT 8). What dose should I use? Oral acetaminophen 10 to 15 mg/kg Every 4–6 hours as needed Do not exceed 75 mg/kg/day (or 4,000 mg/day maximum for older/larger kids) Oral ibuprofen 5 to 10 mg/kg Every 6–8 hours as needed Do not exceed 40 mg/kg/day (or 2,400 mg/day maximum for older/larger kids) References De la Cruz-Mena JE, Veroniki AA, Acosta-Reyes J, Estupiñán-Bohorquez A, Ibarra JA, Pana MC, Sierra JM, Florez ID. Short-term Dual Therapy or Mono Therapy With Acetaminophen and Ibuprofen for Fever: A Network Meta-Analysis. Pediatrics. 2024 Oct 1;154(4):e2023065390. doi: 10.1542/peds.2023-065390. PMID: 39318339. Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/

16. Episode 969: Shoulder Reduction11.08.2025 (00:02:49)

    Contributor: Aaron Lessen, MD Educational Pearls: There are many techniques for reducing a shoulder dislocation A recent study discussed a new variation of closed reduction technique: wrist-clamping shoulder-lifting The patient is in a sitting position The provider holds the wrist of the injured arm with both hands and slowly rotates the arm to 90 degrees of abduction and 60 degrees of external rotation After this traction, the arm is slowly moved to 45 degrees of abduction and 60 degrees of external rotation The provider then secures the patient's wrist between the provider's knees and places their hand on the axilla to gently lift the shoulder upward for successful reduction There were 36 patients with shoulder dislocations in this study, and all 36 dislocations were successfully reduced with this technique There were no neurovascular complications or fractures No sedation or medication was required All procedures were performed by a single provider without assistance References Dai W, Liu L, Zong S, Zhou Y, Zheng J, Li X. An original closed reduction technique for acute shoulder dislocation: the wrist-clamping and shoulder-lifting. Int J Emerg Med. 2025 Mar 26;18(1):60. doi: 10.1186/s12245-025-00866-8. PMID: 40140973; PMCID: PMC11948627. Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

17. Episode 968: Heavy Metals04.08.2025 (00:02:50)

    Contributor: Megan Hurley MD Educational Pearls: Acute toxicity of heavy metals: Gastrointestinal upset is the most common presentation Chronic toxicity of heavy metals: Symptoms depend on the metal ingested Increased risk of cancer Altered mentation Developmental delays (in children) Kidney failure Four heavy metals that are tested for in a general panel and their sources: Lead Old paint (homes built before 1977) or some older toys Pipes of older homes or those with corrosive agents May obtain testing kits from home improvement stores to test water supply Mercury Previously in thermometers, although much less common now Compact fluorescent lightbulbs, LCD screens, and some batteries Large predatory fish like tuna, swordfish, dolphins, and shark Arsenic sources Most commonly found in pesticides Contaminated groundwater (especially private wells) Cadmiun sources Most commonly found in tobacco smoke Batteries Metal plating and welding Additional heavy metals that require specific testing Chromium, Nickel, & Thallium Thallium is found in rodenticides, pesticides, and fireworks Management of heavy metal toxicity depends on the intoxicant Generally, chelation therapy is used for acute and severe cases Arsenic: dimercaprol or DMSA Mercury: DMPS (chronic or mild) or DMSA (severe) Lead: succimer is first line, followed by dimercaprol or EDTA References Baker BA, Cassano VA, Murray C; ACOEM Task Force on Arsenic Exposure. Arsenic Exposure, Assessment, Toxicity, Diagnosis, and Management: Guidance for Occupational and Environmental Physicians. J Occup Environ Med. 2018;60(12):e634-e639. doi:10.1097/JOM.0000000000001485 Balali-Mood M, Naseri K, Tahergorabi Z, Khazdair MR, Sadeghi M. Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic. Front Pharmacol. 2021;12:643972. Published 2021 Apr 13. doi:10.3389/fphar.2021.643972 Kinally C, Fuller R, Larsen B, Hu H, Lanphear B. A review of lead exposure source attributional studies. Sci Total Environ. 2025;990:179838. doi:10.1016/j.scitotenv.2025.179838 Jannetto PJ, Cowl CT. Elementary Overview of Heavy Metals. Clin Chem. 2023;69(4):336-349. doi:10.1093/clinchem/hvad022 Järup L. Hazards of heavy metal contamination. Br Med Bull. 2003;68:167-182. doi:10.1093/bmb/ldg032 Zhang H, Reynolds M. Cadmium exposure in living organisms: A short review. Sci Total Environ. 2019;678:761-767. doi:10.1016/j.scitotenv.2019.04.395 Summarized & Edited by Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

18. Episode 967: Dilutional Hyponatremia28.07.2025 (00:02:58)

    Contributor: Taylor Lynch, MD Educational Pearls: Dilutional Hyponatremia: Occurs when there is an excess of free water relative to sodium in the body. Causes a falsely low sodium concentration without a true change in total body sodium. Commonly seen in DKA: Hyperglycemia raises plasma osmolality. Water shifts from the intracellular to extracellular space. This dilutes serum sodium, creating apparent hyponatremia. Corrected sodium calculation: Use tools like MDCALC, or apply this formula: Add 1.6 mEq/L to the measured sodium for every 100 mg/dL increase in glucose above 100. Clinical relevance: Considering corrected sodium in DKA is crucial, as the lab value may not be reflective of actual sodium depletion. True severe hyponatremia can lead to complications like seizures May require treatment with hypertonic saline. References: Fulop M. Acid–base problems in diabetic ketoacidosis. Am J Med Sci. 2008;336(4):274-276. doi:10.1097/MAJ.0b013e318180f478 Palmer BF, Clegg DJ. Electrolyte and Acid–Base Disturbances in Patients with Diabetes Mellitus. N Engl J Med. 2015;373(6):548-559. doi:10.1056/NEJMra1503102 Spasovski G, Vanholder R, Allolio B, et al. Diagnosis and management of hyponatremia: a review. JAMA. 2014;312(24):2640–2650. doi:10.1001/jama.2014.13773 Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

19. EMSAC 202426.07.2025 (00:11:51)

    Contributors: Col. (Dr.) Stacy Shackelford Dr. Sean Keenan Paramedic Alan Moreland Dr. Chris Tems Kara Napolitano From military-inspired trauma protocols to behavioral health alternatives and cardiac resuscitation, EMS is evolving fast. Our Medical Minutes from EMSAC highlight the growing need for prehospital providers to think critically, act quickly, and adapt to new approaches in trauma, crisis response, and patient advocacy. Educational Pearls: What was covered & recorded at EMSAC 2024 by EMM? Col. (Dr.) Stacy Shackelford, U.S. Air Force trauma surgeon and Director of the Joint Trauma System, emphasized the critical importance of early hemorrhage control and timely transfusions in prehospital trauma care. She highlighted military studies showing that interventions within 30 minutes can dramatically increase survival, underscoring the value of rapid response and frontline readiness. Dr. Sean Keenan, retired Army emergency physician and EMS doctor, introduced the concept of prolonged field care—managing critically injured patients in environments where evacuation is delayed. He discussed how this model, developed in the military, is now being taught to civilian EMS providers in rural areas. Paramedic Alan Moreland from Denver's STAR Program (Support Team Assisted Response) explained how alternative response teams, pairing paramedics with clinical social workers, are reshaping how we respond to behavioral health emergencies, reducing reliance on police or ambulance transport and focusing on trauma-informed care. Dr. Chris Tems, an emergency physician working with ECMO (extracorporeal membrane oxygenation), shared data on using ECMO for refractory cardiac arrest. With a survival rate of 87.5% in select emergency department cases, he highlighted ECMO's growing role in cardiac resuscitation for patients not responding to CPR. Kara Napolitano, of the Laboratory to Combat Human Trafficking, outlined the role EMS plays in recognizing human trafficking. She offered key indicators to look for and encouraged providers to stay alert to the signs of exploitation, emphasizing EMS's role in early intervention. Recorded by: Steven Fujaros, Brian Parga, & Ahmed Abdel-Hafiz Summarized by: Steven Fujaros

20. Episode 966: Acetaminophen Toxicity21.07.2025 (00:03:39)

    Contributor: Jorge Chalit-Hernandez, OMS4 Educational Pearls: What is the toxic dose of acetaminophen? 7.5 grams, in an adult. The safe daily limit is 4 grams in an adult with a normally functioning liver. This is equivalent to fifteen 500mg pills. What are the symptoms of acetaminophen toxicity? First 24 hours, symptoms are non-specific e.g. nausea, vomiting, lack of appetite. Can also be asymptomatic. 24-72 hours, hepatotoxicity occurs (causing yellow skin, pruritus, abdominal pain, bleeding, and confusion) Fulminant liver failure at 72-96 hours Liver function tests (LFTs) peak at 72-96 hours. When would you give activated charcoal? Within 4 hours of ingestion. The risk of activated charcoal is that it can be very dangerous if aspirated so use with caution with a poorly mentating patient When would you give N-acetylcysteine (NAC)? The peak absorption of acetaminophen occurs at about 4 hours with acute ingestions Use the Rumack–Matthew nomogram to plot the serum level of acetaminophen versus the time since ingestion to see if you are above the treatment line. If the ingestion time is unknown then just give it. How do you dose NAC? 3 bag system: First, a 150 mg/kg bolus is administered IV over 15-60 minutes (Bag 1), then a 50 mg/kg drip is administered over 4 hours (Bag 2), then a 100 mg/kg drip is administered over the following 16 hours (Bag 3). This is the Prescott Protocol that requires three bag of IV fluids 2 bag system: There is a simplified protocol that only requires 2 bags, 200mg/kg IV over 4 hours (Bag 1) followed by 100mg/kg over 16 hours (Bag 2) Less risk of anaphylactoid reactions with a 2-bag system due to the high rate of IV NAC given in the 3 bag system. What are the endpoints for stopping NAC? If the INR is If the acetaminophen level is References Hodgman MJ, Garrard AR. A review of acetaminophen poisoning. Crit Care Clin. 2012 Oct;28(4):499-516. doi: 10.1016/j.ccc.2012.07.006. PMID: 22998987. Rumack BH, Matthew H. Acetaminophen poisoning and toxicity. Pediatrics. 1975 Jun;55(6):871-6. PMID: 1134886. Sudanagunta S, Camarena-Michel A, Pennington S, Leonard J, Hoyte C, Wang GS. Comparison of Two-Bag Versus Three-Bag N-Acetylcysteine Regimens for Pediatric Acetaminophen Toxicity. Ann Pharmacother. 2023 Jan;57(1):36-43. doi: 10.1177/10600280221097700. Epub 2022 May 19. PMID: 35587124. Summarized by Jeffrey Olson, MS4 | Edited by Jeffrey Olson and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

21. Episode 965: Oxygen Administration in Trauma Patients14.07.2025 (00:02:10)

    Contributor: Aaron Lessen, MD Educational Pearls: Many trauma patients are placed on oxygen via non-rebreather A large, multicenter, controlled trial evaluated the outcomes of oxygen administration in trauma patients Patients were randomized to two groups 1. 8-hour restrictive oxygen strategy: only receiving oxygen when the patient's saturation dropped below 94% 2. 8-hour liberal oxygen strategy: 12-15 liters of oxygen per minute or fraction of inspired oxygen of 0.6-1.0 The study evaluated rates of death or major respiratory complications at 30 days There was no statistical difference between the two groups Therefore, there is no clear benefit to administering liberal amounts of oxygen to trauma patients, but there is also no clear harm Ultimately, trauma patients do not need to be on oxygen via non-rebreather unless they are hypoxic or short of breath References Arleth T, Baekgaard J, Siersma V, et al. Early Restrictive vs Liberal Oxygen for Trauma Patients: The TRAUMOX2 Randomized Clinical Trial. JAMA. 2025;333(6):479-489. doi:10.1001/jama.2024.25786 Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

22. Episode 964: Ketamine & Midazolam for Prehospital Seizure Management07.07.2025 (00:04:07)

    Contributor: Aaron Lessen, MD Educational Pearls: Prehospital seizures are typically managed with intramuscular midazolam (Versed) Seizures theoretically involve the NMDA pathway, and ketamine is a potent NMDA antagonist A recent retrospective cohort study analyzed a Florida EMS protocol that uses ketamine in seizures refractory to midazolam One group received two doses of midazolam for seizure control The other group received a dose of midazolam followed by a dose of ketamine After matching, 82% of the midazolam-only group patients had resolution of convulsions prior to ED arrival 94.4% of patients in the midazolam + ketamine group experienced resolution Absolute difference between groups was 12.4% (95% CI 3.1% to 21.7%) Limitations to the study include its prehospital setting and limited long-term follow-up References Zitek T, Scheppke KA, Antevy P, et al. Midazolam and Ketamine for Convulsive Status Epilepticus in the Out-of-Hospital Setting. Ann Emerg Med. 2025;85(4):305-312. doi:10.1016/j.annemergmed.2024.11.002 Summarized & Edited by Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

23. Episode 963: Antihypertensives and Emergency Room Considerations30.06.2025 (00:04:07)

    Contributor: Alec Coston, MD Educational Pearls: For patients presenting to the emergency room with hypertension, clinicians should determine if it is isolated and uncomplicated, or involves comorbidities with more complex underlying pathophysiology. For uncomplicated and isolated hypertension, first-line treatment is thiazide diuretics. How do thiazide diuretics work to treat hypertension? Thiazide diuretics work by blocking sodium and chloride resorption in the kidneys. "Where sodium goes, water follows," thus promoting diuresis and lowering blood pressure. Examples of thiazide diuretics and their benefits? Hydrochlorothiazide (HCTZ): First-line medication in uncomplicated and chronic hypertensive states. Cheaper and fewer significant adverse effects compared to chlorthalidone. HCTZ can be associated with decreased risk of stroke and myocardial infarction. However, for more complicated hypertension, especially in the setting of heart failure, Angiotensin Converting Enzyme (ACE) Inhibitors should be considered. How do ACE Inhibitors manage blood pressure? The body's kidneys drive the Renin-Angiotensin-Aldosterone-System (RAAS) to regulate blood pressure. It is easiest to understand RAAS as being pro-hypertensive as a response to decreased renal perfusion. As renal perfusion decreases, renin is released and activates angiotensin I, which is converted by ACE to Angiotensin II, which causes release of aldosterone. ACE Inhibitors prevent the conversion of Angiotensin I to Angiotensin II, thus decreasing the kidneys' production of Angiotensin II and Aldosterone levels. Why, in the context of heart failure, are ACE Inhibitors preferred? In heart failure, especially left-sided or left-ventricular heart failure, a vicious cycle can develop wherein the left ventricle fails to perfuse the kidneys due to over-dilation. The kidneys are hypoperfused and activate RAAS to try to retain volume and increase peripheral vasoconstriction, promoting renal perfusion. The increase in blood pressure puts further strain on the heart, thereby further decreasing cardiac output. The cycle develops, and extremely elevated blood pressures can develop. ACE Inhibitors can directly block this cycle, hence their preference in heart failure. Big takeaway? In uncomplicated hypertensive patients, consider thiazide diuretics. When comorbidities, especially heart failure, are introduced, then consider ACE Inhibitors. References Carey RM, Moran AE, Whelton PK. Treatment of Hypertension: A Review. JAMA. 2022;328(18):1849-1861. doi:10.1001/jama.2022.19590 Fan M, Zhang J, Lee CL, Zhang J, Feng L. Structure and thiazide inhibition mechanism of the human Na-Cl cotransporter. Nature. 2023;614(7949):788-793. doi:10.1038/s41586-023-05718-0 Hripcsak G, Suchard MA, Shea S, et al. Comparison of Cardiovascular and Safety Outcomes of Chlorthalidone vs Hydrochlorothiazide to Treat Hypertension. JAMA Internal Medicine. 2020;180(4):542-551. doi:10.1001/jamainternmed.2019.7454 Yu D, Li JX, Cheng Y, et al. Comparative efficacy of different antihypertensive drug classes for stroke prevention: A network meta-analysis of randomized controlled trials. PLoS One. 2025;20(2):e0313309. doi:10.1371/journal.pone.0313309 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

24. Episode 962: HEART Score23.06.2025 (00:04:16)

    Contributor: Taylor Lynch, MD Educational Pearls: How do we risk-stratify chest-pain patients? One option is the HEART score This score predicts a patient's 6-week risk of a major adverse cardiac event. Ex. Cath procedure, CABG, PCI, death H stands for History Ask 1) Was the patient diaphoretic? 2) Did they have nausea and/or vomiting? 3) Did the pain radiate down the right or left arm? 4) Was it exertional? Yes to one = one point. Two or more = two points. E stands for EKG One point for left ventricular hypertrophy, t-wave inversions, new bundle-branch blocks. No points for first degree AV block, benign early repolarization, or QT-prolongation Two points for ST-depression A stands for Age >65 gets two points 45-64 gets one point R stands for Risk factors Hypertension, hyperlipidemia, diabetes, obesity, family history, smoking, previous MI, previous CABG, stroke, peripheral arterial disease 1-2 risk factors get 1 point More than two risk factors gets two points T stands for Troponin 1-3x upper limit of normal gets one point >3x upper limit of normal gets two points This gives you a score between zero and ten 0-3 points, patients have a ~2% chance of an adverse event These patients likely go home 4-6 points, patients have a ~20% chance of an adverse event These patients get admitted or expedited outpatient stress test/echo 7-10 points, patients have a ~60% chance of an adverse event Admit and call cardiology. These patients likely get catheterized References Backus BE, Six AJ, Kelder JC, Bosschaert MA, Mast EG, Mosterd A, Veldkamp RF, Wardeh AJ, Tio R, Braam R, Monnink SH, van Tooren R, Mast TP, van den Akker F, Cramer MJ, Poldervaart JM, Hoes AW, Doevendans PA. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013 Oct 3;168(3):2153-8. doi: 10.1016/j.ijcard.2013.01.255. Epub 2013 Mar 7. PMID: 23465250. Laureano-Phillips J, Robinson RD, Aryal S, Blair S, Wilson D, Boyd K, Schrader CD, Zenarosa NR, Wang H. HEART Score Risk Stratification of Low-Risk Chest Pain Patients in the Emergency Department: A Systematic Review and Meta-Analysis. Ann Emerg Med. 2019 Aug;74(2):187-203. doi: 10.1016/j.annemergmed.2018.12.010. Epub 2019 Feb 2. PMID: 30718010. https://www.mdcalc.com/calc/1752/heart-score-major-cardiac-events Summarized by Jeffrey Olson, MS4 | Edited by Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

25. Episode 961: Cell Phone Sign16.06.2025 (00:01:45)

    Contributor: Aaron Lessen, MD Educational Pearls: A prospective study at the Mayo Clinic Rochester was conducted to examine whether patients actively using their phones on initial assessment in the ED was associated with higher discharge rates The study included 292 patients, and only about 15% of patients were on their phone The patients on their phone tended to be a younger demographic Scribes were trained to record the data during their shifts The results did show that patients on their phone have a higher rate of discharge 94% chance of discharge if the patient is on their phone 64% chance of discharge if the patient is not on their phone This concept can potentially contribute to improving triage decisions References Garcia SI, Jacobson A, Moore GP, Frank J, Gifford W, Johnson S, Lazaro-Paulina D, Mullan A, Finch AS. Airway, breathing, cellphone: a new vital sign? Int J Emerg Med. 2024 Nov 22;17(1):177. doi: 10.1186/s12245-024-00769-0. PMID: 39578750; PMCID: PMC11583604. Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/