Emergency Medical Minute

Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: Psychedelics are being studied for their therapeutic effects in mental illnesses, including major depressive disorder, post-traumatic stress disorder, anxiety, and many others Classic psychedelics include compounds like psilocybin, LSD, and ayahuasca MDMA and ketamine are often included in psychedelic research, but have a different mechanism of action than the others Their mechanism of action involves agonism of the 5HT2A receptor, among others Given their resurgence, there is an increase in recreational use of these substances A recent study assessed the risks of recreational users developing subsequent psychotic disorders Individuals who visited the ED for hallucinogen use had a greater risk of being diagnosed with a schizophrenia spectrum disorder in the following 3 years Hazard ratio (HR) of 21.32 After adjustment for comorbid substance use and other mental illness, the hazard ratio was 3.53 - still a significant increase compared with the general population They also found an elevated risk for psychedelics when compared to alcohol (HR 4.66) and cannabis (HR 1.47) The study did not assess whether patients received antipsychotics or other treatments in the ED References Lieberman JA. Back to the Future - The Therapeutic Potential of Psychedelic Drugs. N Engl J Med. 2021;384(15):1460-1461. doi:10.1056/NEJMe2102835 Livne O, Shmulewitz D, Walsh C, Hasin DS. Adolescent and adult time trends in US hallucinogen use, 2002-19: any use, and use of ecstasy, LSD and PCP. Addiction. 2022;117(12):3099-3109. doi:10.1111/add.15987 Myran DT, Pugliese M, Xiao J, et al. Emergency Department Visits Involving Hallucinogen Use and Risk of Schizophrenia Spectrum Disorder. JAMA Psychiatry. 2025;82(2):142-150. doi:10.1001/jamapsychiatry.2024.3532 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Ricky Dhaliwal, MD Educational Pearls: What factors are considered in a COVID-19 infection? The viral load: Understood as the impact of SARS-CoV-2 viral particles infecting host cell tissue itself (utilizing ACE-2 receptors). Pro-Inflammatory Response: Post-infection, the body's downstream systemic cytokine release (can be both normal or hyperactive, aka “cytokine storm”). What cardiac impacts have been observed with COVID-19? Arrhythmias: The mechanism of COVID-19 infection and arrhythmias is believed to be multifactorial. However, evidence suggests T-cell-mediated toxicity and cytokine storm may contribute to cardiac myocyte damage, precipitating proarrhythmias instead of direct viral entry. Bradycardia: Increased prevalence in patients with severe COVID-19 infection, but not associated with increased adverse outcomes. Atrial Fibrillation: Most common cardiac complication and risk factor for worsened outcomes in patients with COVID-19. Biggest associated risk is strokes, and may require heightened monitoring and anticoagulation therapy to mitigate stroke risk. Fibrosis of Cardiac Tissue: Similar to arrhythmias, believed to be inflammation-mediated in COVID-19. Fibrosis of cardiac tissue increases the risk that any arrhythmias that develop during infection may persist after the infection has resolved. Ventricular damage: Also inflammation mediated by an active infection and contributes to myocarditis. No evidence suggests that COVID-19 vaccination contributes to myocarditis.  Sinus node dysfunction induced by inflammation that may lead to or be similar to Postural Orthostatic Tachycardia Syndrome (POTS).  Big takeaway? Patients who have had or currently have COVID-19 are at an increased risk of developing arrhythmias and sustaining them post-infection. However, a majority of patients will recover. Due to atrial fibrillation being the most prevalent arrhythmia associated with COVID-19 infection, increased monitoring and potential anticoagulation therapy are required.  References Gopinathannair R, Olshansky B, Chung MK, Gordon S, Joglar JA, Marcus GM, et al. Cardiac Arrhythmias and Autonomic Dysfunction Associated With COVID-19: A Scientific Statement From the American Heart Association. Circulation. 2024 Nov 19;150(21):e449–65. Khan Z, Pabani UK, Gul A, Muhammad SA, Yousif Y, Abumedian M, et al. COVID-19 Vaccine-Induced Myocarditis: A Systemic Review and Literature Search. Cureus. 14(7):e27408. Summarized by Dan Orbidan, OMS1 | Edited by Dan Orbidan & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/

Contributor: Aaron Lessen, MD Educational Pearls: What is a Rescue Inhaler? A rescue inhaler is a medication for people with asthma to quickly reverse the symptoms of an asthma attack. Historically albuterol (Short Acting Beta Agonist (SABA)) monotherapy has been the mainstay rescue inhaler. This is because albuterol works fast and is relatively cheap. What are Combination Rescue Inhalers? Combination rescue inhalers contain a fast-acting bronchodilator as well as an inhaled corticosteroid (ICS) The steroid helps to reduce some of the chronic airway inflammation that is worsening the asthma attack and can help to prevent future attacks Examples include budesonide-formoterol and albuterol-budesonide Global Initiative for Asthma (GINA), states that combination therapy is now the preferred reliever for adults and adolescents with mild asthma What are the drawbacks of Combination Rescue Inhalers? These inhalers are generally more expensive than just using a SABA inhaler which can be a barrier for some people Improper use can also lead to conditions like thrush due to the addition of the steroid References Krings JG, Beasley R. The Role of ICS-Containing Rescue Therapy Versus SABA Alone in Asthma Management Today. J Allergy Clin Immunol Pract. 2024 Apr;12(4):870-879. doi: 10.1016/j.jaip.2024.01.011. Epub 2024 Jan 17. PMID: 38237858; PMCID: PMC10999356. Papi A, Chipps BE, Beasley R, Panettieri RA Jr, Israel E, Cooper M, Dunsire L, Jeynes-Ellis A, Johnsson E, Rees R, Cappelletti C, Albers FC. Albuterol-Budesonide Fixed-Dose Combination Rescue Inhaler for Asthma. N Engl J Med. 2022 Jun 2;386(22):2071-2083. doi: 10.1056/NEJMoa2203163. Epub 2022 May 15. PMID: 35569035. Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Geoff Hogan MD Educational Pearls: Penicillin allergies are relatively uncommon despite their frequent reports 10% of the population reports a penicillin allergy but only 5% of these cases are clinically significant 90-95% of patients may tolerate a rechallenge after appropriate allergy evaluation Penicillin Allergy Decision Rule (PEN-FAST) on MD Calc Useful tool to assess patients for penicillin allergies Five years or less since reaction = 2 points (even if unknown) Anaphylaxis or angioedema OR Severe cutaneous reaction = 2 points  Treatment required for reaction (e.g. epinephrine) = 1 point (even if unknown) A score of 0 on PEN-FAST indicates a less than 1% risk of a positive penicillin allergy test A score of 1 or 2 indicates a 5% risk of a positive penicillin allergy test A low score on PEN-FAST should prompt clinicians to proceed with the best empiric antibiotic for the patient's infection References Broyles AD, Banerji A, Barmettler S, et al. Practical Guidance for the Evaluation and Management of Drug Hypersensitivity: Specific Drugs [published correction appears in J Allergy Clin Immunol Pract. 2021 Jan;9(1):603. doi: 10.1016/j.jaip.2020.10.025.] [published correction appears in J Allergy Clin Immunol Pract. 2021 Jan;9(1):605. doi: 10.1016/j.jaip.2020.11.036.]. J Allergy Clin Immunol Pract. 2020;8(9S):S16-S116. doi:10.1016/j.jaip.2020.08.006 Piotin A, Godet J, Trubiano JA, et al. Predictive factors of amoxicillin immediate hypersensitivity and validation of PEN-FAST clinical decision rule [published correction appears in Ann Allergy Asthma Immunol. 2022 Jun;128(6):740. doi: 10.1016/j.anai.2022.04.005.]. Ann Allergy Asthma Immunol. 2022;128(1):27-32. doi:10.1016/j.anai.2021.07.005 Shenoy ES, Macy E, Rowe T, Blumenthal KG. Evaluation and Management of Penicillin Allergy: A Review. JAMA. 2019;321(2):188-199. doi:10.1001/jama.2018.19283 Trubiano JA, Vogrin S, Chua KYL, et al. Development and Validation of a Penicillin Allergy Clinical Decision Rule. JAMA Intern Med. 2020;180(5):745-752. doi:10.1001/jamainternmed.2020.0403 Summarized & edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Travis Barlock, MD Educational Pearls: Key clinical considerations when managing heart transplant patients due to their unique pathophysiology 1. Arrhythmias A transplanted heart is denervated, meaning it lacks autonomic nervous system innervation The lack of vagal tone results in an increased resting heart rate Adenosine can be used since it primarily slows conduction through the AV node  Atropine is ineffective in treating transplant bradyarrhythmia because its mechanism is to inhibit the vagus nerve - but the heart lacks vagal tone Allograft rejection can also cause tachycardia Consult transplant surgery - treatment is usually 500 mg methylprednisolone 2. Rejection Transplant patients are administered immunosuppressants Clinical presentation of acute rejection looks similar to heart failure with increased BNP, increased troponin, and pulmonary edema  Cardiac allograft vasculopathy is a form of chronic rejection Patients will not report chest pain due to denervated heart Symptoms are usually weakness and fatigue 3. High risk of infection due to immunosuppression Increased risk of infections which includes CMV, legionella, tuberculosis, etc Immunosuppressants have side effects such as acute kidney injury or pancytopenia 4. Radiographic Cardiomegaly A study found that radiographic cardiomegaly does not connote heart failure They hypothesized it is instead the result of a mismatch between the size of the transplanted heart and the space in the thoracic cavity  References Murphy JD, Mergo PJ, Taylor HM, Fields R, Mills RM Jr. Significance of radiographic cardiomegaly in orthotopic heart transplant recipients. AJR Am J Roentgenol. 1998 Aug;171(2):371-4. doi: 10.2214/ajr.171.2.9694454. PMID: 9694454. Park MH, Starling RC, Ratliff NB, McCarthy PM, Smedira NS, Pelegrin D, Young JB. Oral steroid pulse without taper for the treatment of asymptomatic moderate cardiac allograft rejection. J Heart Lung Transplant. 1999 Dec;18(12):1224-7. doi: 10.1016/s1053-2498(99)00098-4. PMID: 10612382. Pethig K, Heublein B, Wahlers T, Dannenberg O, Oppelt P, Haverich A. Mycophenolate mofetil for secondary prevention of cardiac allograft vasculopathy: influence on inflammation and progression of intimal hyperplasia. J Heart Lung Transplant. 2004 Jan;23(1):61-6. doi: 10.1016/s1053-2498(03)00097-4. PMID: 14734128. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Taylor Lynch, MD Educational Pearls: Pediatric febrile seizures are defined as seizures that occur between the ages of six months to five years in the presence of a fever greater than or equal to 38.0 ºC (100.4 ºF). It is the most common pediatric convulsive disorder, with an incidence between 2-5% What are the types of seizures? Simple: Tonic-clonic seizure, duration

Contributor: Aaron Lessen, MD Educational Pearls: Point-of-care ultrasound (POCUS) is used to assess cardiac activity during cardiac arrest and can identify potential reversible causes such as pericardial tamponade Ultrasound could be beneficial in another way during cardiac arrest as well: pulse checks Manual palpation for detecting pulses is imperfect, with false positives and negatives Doppler ultrasound can be used as an adjunct or replacement to manual palpation for improved accuracy Options for Doppler ultrasound of carotid or femoral pulses during cardiac arrest: Visualize arterial pulsation Use color doppler Numerically quantify the flow and correlate this to a BP reading - slightly more complex Doppler ultrasound is much faster than manual palpation for pulse check Can provide information almost instantaneously without waiting the full 10 seconds for a manual pulse check The main priority during cardiac arrest resuscitation is to maintain quality compressions If pulses are unable to be obtained through Doppler within the 10-second window, resume compressions and try again during the next pulse check References Cohen AL, Li T, Becker LB, Owens C, Singh N, Gold A, Nelson MJ, Jafari D, Haddad G, Nello AV, Rolston DM; Northwell Health Biostatistics Unit. Femoral artery Doppler ultrasound is more accurate than manual palpation for pulse detection in cardiac arrest. Resuscitation. 2022 Apr;173:156-165. doi: 10.1016/j.resuscitation.2022.01.030. Epub 2022 Feb 4. PMID: 35131404. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/

Contributor: Travis Barlock, MD Educational Pearls: What is Hoover's sign used to identify? This physical exam maneuver differentiates between organic vs. functional (previously known as psychogenic) leg weakness. Organic causes include disease processes such as stroke, MS, spinal cord compression, guillain-barre, ALS, and sciatica, among others In Functional Neurologic Disorder, the dysfunction is in brain signaling, and treatment relies on more of a psychiatric approach How is Hoover's Sign performed? Place your hand under the heel of the unaffected leg and ask the patient to attempt to lift the paralyzed leg. If the paralysis is due to an organic cause, then you should feel the unaffected leg push down. This is due to the crossed-extensor reflex mechanism, an unconscious motor control function mediated by the corticospinal tract. If you don't feel the opposite heel push down, that is a positive Hoover's Sign. How sensitive/specific is it? An unblinded cohort study in patients with suspected stroke found a sensitivity of 63% and a specificity of 100% Fun Fact There's also a pulmonary Hoover's sign, named after the same doctor, Charles Franklin Hoover, which refers to paradoxical inward movement of the lower ribs during inspiration due to diaphragmatic flattening in COPD. References McWhirter L, Stone J, Sandercock P, Whiteley W. Hoover's sign for the diagnosis of functional weakness: a prospective unblinded cohort study in patients with suspected stroke. J Psychosom Res. 2011 Dec;71(6):384-6. doi: 10.1016/j.jpsychores.2011.09.003. Epub 2011 Oct 6. PMID: 22118379. Stone J, Aybek S. Functional limb weakness and paralysis. Handb Clin Neurol. 2016;139:213-228. doi: 10.1016/B978-0-12-801772-2.00018-7. PMID: 27719840. Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: CYP enzymes are responsible for the metabolism of many medications, drugs, and other substances CYP3A4 is responsible for the majority Other common ones include CYP2D6 (antidepressants), CYP2E1 (alcohol), and CYP1A2 (cigarettes) CYP inducers lead to reduced concentrations of a particular medication CYP inhibitors effectively increase concentrations of certain medications in the body Examples of CYP inducers Phenobarbital Rifampin  Cigarettes St. John's Wort Examples of CYP inhibitors -azole antifungals like itraconazole and ketoconazole Bactrim (trimethoprim-sulfamethoxazole) Ritonavir (found in Paxlovid) Grapefruit juice Clinical relevance Drug-drug interactions happen frequently and often go unrecognized or underrecognized in patients with significant polypharmacy A study conducted on patients receiving Bactrim and other antibiotics found increased rates of anticoagulation in patients receiving Bactrim Currently, Paxlovid is prescribed to patients with COVID-19, many of whom have multiple comorbidities and are on multiple medications Paxlovid contains ritonavir, a powerful CYP inhibitor that can increase concentrations of many other medications A complete list of clinically relevant CYP inhibitors can be found on the FDA website: https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers  References Glasheen JJ, Fugit RV, Prochazka AV. The risk of overanticoagulation with antibiotic use in outpatients on stable warfarin regimens. J Gen Intern Med. 2005;20(7):653-656. doi:10.1111/j.1525-1497.2005.0136.x Lynch T, Price A. The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects. Am Fam Physician. 2007;76(3):391-396. PAXLOVID™. Drug interactions. PAXLOVIDHCP. Accessed March 16, 2025. https://www.paxlovidhcp.com/drug-interactions Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Educational Pearls: Physiologic stimulation of ventilation occurs through changes in levels of: Arterial carbon dioxide (PaCO2) Arterial oxygen (PaO2) Hypercapnia is an elevated level of CO2 in the blood - this primarily drives ventilation Hypoxia is a decreased level of O2 in the body's tissues - the backup drive for ventilation Patients at risk of hypercapnia should maintain an O2 saturation between 88-92% Normal O2 saturation is 95-100% In patients who chronically retain CO2, their main drive for ventilation becomes hypoxia An audit was performed of SpO2 observations of all patients with a target range of 88–92% at a single hospital over a four-year period This found that excessive oxygen administration was more common than insufficient oxygen and is associated with an increased risk of harm Individuals at risk of hypercapnia include but are not limited to patients with COPD, hypoventilation syndrome, or altered mental status References Homayoun Kazemi, Douglas C. Johnson, Respiration, Editor(s): V.S. Ramachandran, Encyclopedia of the Human Brain, Academic Press, 2002, Pages 209-216, ISBN 9780122272103, https://doi.org/10.1016/B0-12-227210-2/00302-2. O'Driscoll BR, Bakerly ND. Are we giving too much oxygen to patients at risk of hypercapnia? Real world data from a large teaching hospital. Respir Med. 2025 Mar;238:107965. doi: 10.1016/j.rmed.2025.107965. Epub 2025 Jan 30. PMID: 39892771. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen, MD Educational Pearls: Quick background info Cardiac arrest is when the heart stops pumping blood for any reason. This is different from a heart attack in which the heart is still working but the muscle itself is starting to die. One cause of cardiac arrest is when the electrical signals are very disrupted in the heart and start following chaotic patterns such as Ventricular tachycardia (VTach) and Ventricular fibrillation (VFib) One of the only ways to save a person whose heart is in VFib or VTach is to jolt the heart with electricity and terminate the dangerous arrhythmia. A recent study in the Netherlands looked at how important the time delay is from when cardiac arrest is first identified to when a defibrillation shock from an Automated External Defibrillator (AED) is actually given. Their main take-away: each minute defibrillation is delayed drops the survival rate by 6%! These findings reinforce the importance of rapid AED deployment and early defibrillation strategies in prehospital cardiac arrest response. References Stieglis, R., Verkaik, B. J., Tan, H. L., Koster, R. W., van Schuppen, H., & van der Werf, C. (2025). Association Between Delay to First Shock and Successful First-Shock Ventricular Fibrillation Termination in Patients With Witnessed Out-of-Hospital Cardiac Arrest. Circulation, 151(3), 235–244. https://doi.org/10.1161/CIRCULATIONAHA.124.069834 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Ricky Dhaliwal, MD Educational Pearls:  Ketorolac and ibuprofen are NSAIDs with equivalent efficacy for pain in the emergency department Oral ibuprofen provides the same relief as intramuscular ketorolac IM ketorolac is associated with the adverse effect of a painful injection IM ketorolac is slightly faster in onset but not significant Studies have assessed the two medications in head-to-head randomized-controlled trials and found no significant difference in pain scores IM ketorolac takes longer to administer and has a higher cost Ketorolac dosing Commonly given in 10 mg, 15 mg, and 30 mg doses However, higher doses are associated with more adverse effects Gastrointestinal upset, nausea, and bleeding risk Studies have demonstrated equal efficacy in pain reduction with lower doses References Motov S, Yasavolian M, Likourezos A, et al. Comparison of Intravenous Ketorolac at Three Single-Dose Regimens for Treating Acute Pain in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2017;70(2):177-184. doi:10.1016/j.annemergmed.2016.10.014 Neighbor ML, Puntillo KA. Intramuscular ketorolac vs oral ibuprofen in emergency department patients with acute pain. Acad Emerg Med. 1998;5(2):118-122. doi:10.1111/j.1553-2712.1998.tb02595.x Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen, MD Educational Pearls: Colchicine is most commonly used for the prevention and treatment of gout There is research investigating the anti-inflammatory and cardioprotective effects of colchicine  This drug has a narrow therapeutic index: a small margin between effective dose and toxic dose Colchicine overdoses can be unintentional or intentional and are associated with poor outcomes Phase 1: 10 - 24 hours after ingestion Patient looks well but may have mild symptoms mimicking gastroenteritis Phase 2: 24 hours - 7 days after ingestion Multiple organ dysfunction syndrome (MODS) Phase 3: recovery is usually within a few weeks of ingestion Treatment for colchicine overdose Treat early and aggressively Gastrointestinal decontamination with activated charcoal and orogastric lavage  Dialysis and ECMO for MODS treatment References Finkelstein Y, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y. Colchicine poisoning: the dark side of an ancient drug. Clin Toxicol (Phila). 2010 Jun;48(5):407-14. doi: 10.3109/15563650.2010.495348. PMID: 20586571. Gasparyan AY, Ayvazyan L, Yessirkepov M, Kitas GD. Colchicine as an anti-inflammatory and cardioprotective agent. Expert Opin Drug Metab Toxicol. 2015;11(11):1781-94. doi: 10.1517/17425255.2015.1076391. Epub 2015 Aug 4. PMID: 26239119. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Travis Barlock, MD Educational Pearls: What is Portal Vein Thrombosis? The formation of a blood clot within the portal vein, which carries blood from the gastrointestinal tract, pancreas, and spleen to the liver Not only can this cause problems downstream in the liver, but the backup of venous blood can cause ischemia in the bowels How does it present? Similar to acute mesenteric ischemia: Sudden onset of abdominal pain, nausea, vomiting, and fever How is it diagnosed? Abdominal CT or MRI with contrast What causes it? Cirrhosis Coagulopathy (Factor V Leiden mutation, Prothrombin gene mutation, Antiphospholipid syndrome, Protein C, protein S, antithrombin III deficiency, etc.) Oral Contraceptive Pills (OCPs) Cancer such as hepatocellular carcinoma How is it treated? Aggressive fluid resuscitation Antibiotics. Be sure to cover enteric gram-negative bacteria and anaerobes Heparin, same dosing as a bolus for a DVT Endovascular treatment, such as a thrombectomy with IR Surgical evaluation if there has been tissue death in the mesentery References Hilscher, M. B., Wysokinski, W. E., Andrews, J. C., Simonetto, D. A., Law, R. J., & Kamath, P. S. (2024). Portal Vein Thrombosis in the Setting of Cirrhosis: Evaluation and Management Strategies. Gastroenterology, 167(4), 664–672. https://doi.org/10.1053/j.gastro.2024.05.017 Intagliata, N. M., Caldwell, S. H., & Tripodi, A. (2019). Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis. Gastroenterology, 156(6), 1582–1599.e1. https://doi.org/10.1053/j.gastro.2019.01.265 Ju, C., Li, X., Gadani, S., Kapoor, B., & Partovi, S. (2022). Portal Vein Thrombosis: Diagnosis and Endovascular Management. Pfortaderthrombose: Diagnose und endovaskuläres Management. RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin, 194(2), 169–180. https://doi.org/10.1055/a-1642-0990 Summarized by Jeffrey Olson MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: Acute mountain sickness (AMS) is the term given to what is otherwise colloquially known as altitude sickness High altitude cerebral edema (HACE) is a severe form of AMS marked by encephalopathic changes Symptoms begin at elevations as low as 6500 feet above sea level for people who ascend rapidly May develop more severe symptoms at higher altitudes The pathophysiology involves cerebral vasodilation Occurs in everyone ascending to high altitudes but is more pronounces in those that develop symptoms The reduced partial pressure of oxygen induces hypoxic vasodilation in the brain, which results in edema and, ultimately, HACE in some patients Symptomatic presentation Headache, nausea, and sleeping difficulties occur within 2-24 hours of arrival at altitude HACE may occur between 12-72 hours after AMS and presents with ataxia, confusion, irritability, and ultimately results in coma if left untreated Clinical presentation may be mistaken for simple exhaustion, so clinicians should maintain a high index of suspicion Notably, if symptoms occur more than 2 days after arrival at altitude, clinicians should seek an alternative diagnosis but maintain AMS/HACE on the differential Treatment and management AMS Adjunctive oxygen and descent to lower altitude Acetazolamide is used as a preventive measure but is not helpful in acute treatment +/- dexamethasone HACE Patients with HACE should receive dexamethasone to help reduce cerebral edema Immediate descent to a lower altitude References Burtscher M, Wille M, Menz V, Faulhaber M, Gatterer H. Symptom progression in acute mountain sickness during a 12-hour exposure to normobaric hypoxia equivalent to 4500 m. High Alt Med Biol. 2014;15(4):446-451. doi:10.1089/ham.2014.1039 Levine BD, Yoshimura K, Kobayashi T, Fukushima M, Shibamoto T, Ueda G. Dexamethasone in the treatment of acute mountain sickness. N Engl J Med. 1989;321(25):1707-1713. doi:10.1056/NEJM198912213212504 Luks AM, Beidleman BA, Freer L, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention, Diagnosis, and Treatment of Acute Altitude Illness: 2024 Update. Wilderness Environ Med. 2024;35(1_suppl):2S-19S. doi:10.1016/j.wem.2023.05.013 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Meghan Hurley, MD Educational Pearls: Gastroenteritis clinical diagnoses: Diarrhea with or without vomiting and fever Vomiting in the absence of diarrhea has a large list of differential diagnoses, so the combination of diarrhea and vomiting in a patient is helpful to indicate the gastroenteritis diagnosis Symptom timeline is usually 1-3 days, but can last up to 14 days – diarrhea persists the longest Treatment for mild to moderate dehydration: oral or IV rehydration Begin orally to avoid unnecessary IV in a pediatric patient Administer ODT Ondansetron (Zofran) to prevent vomiting Meta-analysis showed that 2-8 mg orally, based on body weight, decreased vomiting quickly Wait 15-20 minutes for the medication to take effect Use streamlined method for oral rehydration: Fluids such as over-the-counter Pedialyte, Infalyte, Rehydrate, Resol, and Naturalyte may be used If patient weighs less than 10kg: administer 5mL of fluid per minute for 20 minutes If patient weighs 10kg or more: administer 10mL of fluid for 20 minutes If the patient can keep the fluid down, double the fluid volume and repeat If the patient once again keeps the fluid down, double the fluid volume and repeat If successful with each attempt, the patient may be discharged home Can prescribe ODT Zofran for 1-2 days at home If the patient vomits more than once during this oral rehydration process, intravenous rehydration must be initiated References Churgay CA, Aftab Z. Gastroenteritis in children: Part II. Prevention and management. Am Fam Physician. 2012 Jun 1;85(11):1066-70. PMID: 22962878. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen, MD Educational Pearls: If a patient sustains a cut, the provider has several options on how to close the wound. If they choose to suture the wound closed, it involves needles both in the form of injecting numbing medication (lidocaine) as well as with the suture itself. Other techniques are “needleless,” like closing the wound with adhesive strips (Steri-Strips) or skin adhesive (Dermabond). But which method is best? A recent study looked to compare guardian-perceived cosmetic outcomes of pediatric lacerations repaired with absorbable sutures, Dermabond, and Steri-Strips. It also assessed pain and satisfaction with the procedure from both guardian and provider perspectives. Participants: 55 patients were enrolled; 30 completed the 3-month follow-up. Cosmetic Ratings (Median and IQR): Sutures: 70.5 (59.8–76.8) Dermabond: 85 (73–90) Steri-Strips: 67 (55–78) (P = 0.254, no statistically significant difference) Satisfaction and Pain: No significant differences in guardian or provider satisfaction Pain levels were comparable across all methods Even though there was no statistically significant difference in guardian-perceived cosmetic outcomes, the Dermabond did have the highest ratings at the end of the study. References Barton, M. S., Chaumet, M. S. G., Hayes, J., Hennessy, C., Lindsell, C., Wormer, B. A., Kassis, S. A., Ciener, D., & Hanson, H. (2024). A Randomized Controlled Comparison of Guardian-Perceived Cosmetic Outcome of Simple Lacerations Repaired With Either Dermabond, Steri-Strips, or Absorbable Sutures. Pediatric emergency care, 40(10), 700–704. https://doi.org/10.1097/PEC.0000000000003244 Summarized by Jeffrey Olson MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: Serotonin syndrome occurs most commonly due to the combination of monoamine oxidase inhibition with concomitant serotonergic medications like SSRIs Examples of unexpected monoamine oxidase inhibitors Linezolid - a last-line antibiotic reserved for patients with true anaphylaxis to penicillins and cephalosporins Methylene blue - not mentioned in the podcast due to its uncommon usage for methemoglobinemia Other medications that can interact with SSRIs to cause serotonin syndrome Dextromethorphan - primarily an anti-tussive at sigma opioid receptors that also has serotonin reuptake inhibition Clinical presentation of serotonin syndrome Altered mental status Autonomic dysregulation leading to hypertension (most common), hypotension, and tachycardia Hyperthermia Neuromuscular hyperactivity - tremors, myoclonus, and hyperreflexia Hunter Criteria (high sensitivity and specificity for serotonin syndrome): Spontaneous clonus Inducible clonus + agitation or diaphoresis Ocular clonus + agitation or diaphoresis Tremor + hyperreflexia Hypertonia, temperature > 38º C, and ocular or inducible clonus Management of serotonin syndrome Primarily supportive - benzodiazepines can help treat hypertension, agitation, and hyperthermia. Patients often require repeated and higher dosing of benzodiazepines Avoid antipyretics to treat hyperthermia since the elevated temperature is due to sustained muscle contraction and not central temperature dysregulation In refractory patients, cyproheptadine (a 5HT2 antagonist) may be used as a second-line treatment Patients with temperatures > 41.1º C or 106º F require medically induced paralysis and intubation to control their temperature References Boyer EW, Shannon M. The serotonin syndrome [published correction appears in N Engl J Med. 2007 Jun 7;356(23):2437] [published correction appears in N Engl J Med. 2009 Oct 22;361(17):1714]. N Engl J Med. 2005;352(11):1112-1120. doi:10.1056/NEJMra041867 Dunkley EJ, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. 2003;96(9):635-642. doi:10.1093/qjmed/hcg109 Ramsay RR, Dunford C, Gillman PK. Methylene blue and serotonin toxicity: inhibition of monoamine oxidase A (MAO A) confirms a theoretical prediction. Br J Pharmacol. 2007;152(6):946-951. doi:10.1038/sj.bjp.0707430 Schwartz AR, Pizon AF, Brooks DE. Dextromethorphan-induced serotonin syndrome. Clin Toxicol (Phila). 2008;46(8):771-773. doi:10.1080/15563650701668625 Thomas CR, Rosenberg M, Blythe V, Meyer WJ 3rd. Serotonin syndrome and linezolid. J Am Acad Child Adolesc Psychiatry. 2004;43(7):790. doi:10.1097/01.chi.0000128830.13997.aa Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/

Contributor: Aaron Lessen, MD Educational Pearls: Many patients present to the ED with elevated BP Many are referred from outpatient surgery centers or present after an elevated measurement at home Persistent questions on the best way to treat these patients The AHA published a scientific statement on the management of elevated BP in the acute care setting Hypertensive emergencies: SBP/DBP >180/110–120 mm Hg with evidence of new or worsening target-organ damage Includes aortic dissection or subarachnoid hemorrhage  Require aggressive treatment Asymptomatic markedly elevated inpatient BP: SBP/DBP >180/110–120 mm Hg without evidence of new or worsening target-organ damage AND asymptomatic elevated inpatient BP: SBP/DBP ≥130/80 mm Hg without evidence of new or worsening target-organ damage No benefits to urgent treatment in the ED, but there are harms to treating patients in this manner These patients do not require IV medications  Provide reassurance and instructions on following up with their PCP to manage their BP in the outpatient setting Removed the term “hypertensive urgency” References Bress AP, Anderson TS, Flack JM, et al. The Management of Elevated Blood Pressure in the Acute Care Setting: A Scientific Statement From the American Heart Association. Hypertension. 2024;81(8). doi:https://doi.org/10.1161/hyp.0000000000000238 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3  Donate: https://emergencymedicalminute.org/donate/  

Contributor: Megan Hurley MD Educational Pearls: What is the mediastinum? The thoracic cavity is separated into different compartments by membranes The lungs exist in their own pleural cavities, and the mediastinum is everything in between The mediastinum extends from the sternum to the thoracic vertebrae and includes the heart, the aorta, the trachea, the esophagus, the thymus, as well as many lymph nodes and nerves. What is a pneumomediastinum? Air in the mediastinum How can pneumomediastinum be categorized? Traumatic Ex. Stab wound to the trachea Ex. Boerhaave's Syndrome of the esophagus, possibly from an endoscopic procedure. This mechanism in particular is a higher risk of infection because not only air but food can accumulate in the mediastinum Ex. Intubation with a bougie These will likely need surgical repair Nontraumatic Ex. Forceful inhalation causing microperforations in the trachea. Possibly while inhaling something like drugs Ex. Bad asthma for similar reasons Ex. Gas forming bacteria What happens if you use positive pressure ventilation on a patient with a hole in their trachea? The positive pressure will force extra air into the mediastinum The air will move between the layers of subcutaneous tissue and can track up into the neck and face regions recognized as crepitus on exam This can also cause a tension pneumomediastinum in which the air pressure in the compartment constricts the heart, impeding its ability to fill during diastole These patients can undergo bronchoscopy because that procedure does not require positive pressure and will not worsen the condition. Endoscopies do require positive pressure so endoscopies are not an option How is a tension pneumomediastinum treated? By inserting a needle into the space from below the xiphoid process to allow the air to escape, similar to a pericardiocentesis As a temporizing measure, if the hole is high enough in the trachea, the intubation can be continued by deliberately pushing the endotracheal tube into the right main bronchus, creating a seal, and only ventilating the right lung while the patient heads to surgery. This is called right-mainstemming. References Clancy DJ, Lane AS, Flynn PW, Seppelt IM. Tension pneumomediastinum: A literal form of chest tightness. J Intensive Care Soc. 2017 Feb;18(1):52-56. doi: 10.1177/1751143716662665. Epub 2016 Aug 3. PMID: 28979537; PMCID: PMC5606356. Grewal, J., & Gillaspie, E. A. (2024). Pneumomediastinum. Thoracic surgery clinics, 34(4), 309–319. https://doi.org/10.1016/j.thorsurg.2024.06.001 Underner, M., Perriot, J., & Peiffer, G. (2017). Pneumomédiastin et consommation de cocaïne [Pneumomediastinum and cocaine use]. Presse medicale (Paris, France : 1983), 46(3), 249–262. https://doi.org/10.1016/j.lpm.2017.01.002 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Ricky Dhaliwal MD Educational Pearls:  Etomidate was previously the drug of choice for rapid sequence intubation (RSI) However, it carries a risk of adrenal insufficiency as an adverse effect through inhibition of mitochondrial 11-β-hydroxylase activity A recent meta-analysis analyzing etomidate as an induction agent showed the following: 11 randomized-controlled trials with 2704 patients Number needed to harm is 31; i.e. for every 31 patients that receive etomidate for induction, there is one death The probability of any mortality increase was 98.1% Ketamine is preferable due to a better adverse effect profile Laryngeal spasms and bronchorrhea are the most common adverse effects after IV push Beneficial effects on hemodynamics via catecholamine surge, albeit not as pronounced in shock patients 2023 meta-analysis compared ketamine and etomidate for RSI Ketamine's probability of reducing mortality is cited as 83.2% Overall, induction with ketamine demonstrates a reduced risk of mortality compared with etomidate The dosage of each medication for induction Etomidate: 20 mg based on 0.3 mg/kg for a 70 kg adult Ketamine: 1-2 mg/kg (or 0.5-1 mg/kg in patients with shock) Patients with asthma and/or COPD also benefit from ketamine induction due to putative bronchodilatory properties References  Goyal S, Agrawal A. Ketamine in status asthmaticus: A review. Indian J Crit Care Med. 2013;17(3):154-161. doi:10.4103/0972-5229.117048 Koroki T, Kotani Y, Yaguchi T, et al. Ketamine versus etomidate as an induction agent for tracheal intubation in critically ill adults: a Bayesian meta-analysis. Crit Care. 2024;28(1):1-9. doi:10.1186/s13054-024-04831-4 Kotani Y, Piersanti G, Maiucci G, et al. Etomidate as an induction agent for endotracheal intubation in critically ill patients: A meta-analysis of randomized trials. J Crit Care. 2023;77(April 2023):154317. doi:10.1016/j.jcrc.2023.154317 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen MD Educational Pearls: Pregnant patients at high risk of cardiac arrest, in cardiac arrest, or in extremis require special care A useful mnemonic to recall the appropriate management of critically ill pregnant patients is TOLDD T: Tilt the patient to the left lateral decubitus position This position relieves pressure exerted from the uterus onto the inferior vena cava, which reduces cardiac preload If the patient is receiving CPR, an assistant should displace the uterus manually from the IVC towards the patient's left side O: Administer high-flow adjunctive oxygen  L: Lines should be placed above the diaphragm Lines below the diaphragm are ineffective due to uterine compression of the IVC May consider humeral interosseous line vs. internal jugular or subclavian central line D: Dates should be estimated > 20 weeks, can consider a resuscitative hysterotomy (previously known as perimortem c-section) to improve chances of survival The uterus is palpable at the umbilicus at 20 weeks and 1 cm superior to the umbilicus for every week thereafter D: Call the labor and delivery unit for additional help References ACOG Practice Bulletin No. 211 Summary: Critical Care in Pregnancy. Obstetrics & Gynecology. 2019;133(5) Fujita N, Higuchi H, Sakuma S, Takagi S, Latif MAHM, Ozaki M. Effect of Right-Lateral Versus Left-Lateral Tilt Position on Compression of the Inferior Vena Cava in Pregnant Women Determined by Magnetic Resonance Imaging. Anesth Analg. 2019;128(6):1217-1222. doi:10.1213/ANE.0000000000004166 Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac Arrest in Pregnancy. Circulation. 2015;132(18):1747-1773. doi:doi:10.1161/CIR.0000000000000300 Singh, Ajay; Dhir, Ankita; Jain, Kajal; Trikha, Anjan1. Role of High Flow Nasal Cannula (HFNC) for Pre-Oxygenation Among Pregnant Patients: Current Evidence and Review of Literature. Journal of Obstetric Anaesthesia and Critical Care 12(2):p 99-104, Jul–Dec 2022. | DOI: 10.4103/JOACC.JOACC_18_22  Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Travis Barlock MD Educational Pearls: What is the ST segment? The ST segment on an ECG represents the interval between the end of ventricular depolarization (QRS) and the beginning of ventricular repolarization (T-wave).  It should appear isoelectric (flat) in a normal ECG. What if the ST segment is elevated? This is evidence that there is an injury that goes all the way through the muscular wall of the heart (transmural) This is very concerning for a heart attack (STEMI) but can be occasionally caused by other pathology, such as pericarditis What if the ST segment is depressed? This is evidence that only the innermost part of the muscular wall of the heart is becoming ischemic This has a much broader differential and includes a partial occlusion of a coronary artery but also any other stress on the body that could cause a supply-and-demand mismatch between the oxygen the coronaries can deliver and the oxygen the heart needs This is called subendocardial ischemia What else should you look for in the ECG to identify subendocardial ischemia? The ST-depressions should be at least 1 mm The ST depressions should be present in leads I, II, V4-6 and a variable number of additional leads. There is often reciprocal ST elevation in aVR > 1 mm The most important thing to remember when you see subendocardial ischemia is…history Still, keep all cardiac causes on your differential, such as unstable angina, stable angina, Prinzmetal angina, etc. Also consider a wide array of non-cardiac causes such as severe anemia, severe hypertension, pulmonary embolism, COPD, severe pneumonia, sepsis, shock, thyrotoxicosis, stimulant use, DKA, or any other state that lead to reduced oxygen supply to the subendocardium and/or increased myocardial oxygen demand. References Birnbaum, Y., Wilson, J. M., Fiol, M., de Luna, A. B., Eskola, M., & Nikus, K. (2014). ECG diagnosis and classification of acute coronary syndromes. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc, 19(1), 4–14. https://doi.org/10.1111/anec.12130 Buttà, C., Zappia, L., Laterra, G., & Roberto, M. (2020). Diagnostic and prognostic role of electrocardiogram in acute myocarditis: A comprehensive review. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc, 25(3), e12726. https://doi.org/10.1111/anec.12726 Cadogan, E. B. a. M. (2024, October 8). Myocardial Ischaemia. Life in the Fast Lane • LITFL. Retrieved December 7, 2024, from https://litfl.com/myocardial-ischaemia-ecg-library/#:~:text=ST%20depression%20due%20to%20subendocardial,left%20main%20coronary%20artery%20occlusion. Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Alec Coston MD Educational Pearls: Causes of seizures in a fairly well-appearing child with diarrhea: Electrolyte abnormalities: hypocalcemia, hyponatremia Also hyperkalemia which causes arrhythmias and syncope - can appear like seizures Hypoglycemia If the child has diarrhea and appears very sick, differential diagnosis may include: Hemolytic uremic syndrome (HUS): simultaneous occurrence of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury Typically caused by Shiga-like toxin producing Escherichia coli (also known as EHEC, or enterohemorragic E. coli) One of the main causes of acute kidney injury in children Toxic ingestions such as salicylates, lead, or iron In this case, the child had a seizure but appeared well and was afebrile: Consult with neurology led to a diagnosis of benign convulsions with mild gastroenteritis (CwG) First identified in 1982 in Japan Viral gastroenteritis with diarrhea and convulsions but does not include fever, severe dehydration, or electrolyte abnormalities Uncommon illness caused by rotavirus and norovirus pathogens Criteria for discharge is similar to a febrile seizure - the patient had one seizure that lasted less than 15 minutes and he quickly returned to his baseline, so he was able to be safely discharged home This diagnosis does not predispose him to epilepsy later in life References Lee YS, Lee GH, Kwon YS. Update on benign convulsions with mild gastroenteritis. Clin Exp Pediatr. 2022 Oct;65(10):469-475. doi: 10.3345/cep.2021.00997. Epub 2021 Dec 27. PMID: 34961297; PMCID: PMC9561189. Mauritz M, Hirsch LJ, Camfield P, et al. Acute symptomatic seizures: an educational, evidence-based review. Epileptic Disorders. 2200;1(1). doi:https://doi.org/10.1684/epd.2021.1376 ‌Noris, Marina*; Remuzzi, Giuseppe*, †. Hemolytic Uremic Syndrome. Journal of the American Society of Nephrology 16(4):p 1035-1050, April 2005. | DOI: 10.1681/ASN.2004100861    Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen MD Educational Pearls: Induction agent selection during rapid sequence intubation involves accounting for hemodynamic stability in the post-intubation setting Many emergency departments use ketamine or etomidate A recent study sought to explore the rates of post-induction hypotension of ketamine compared with propofol Single center retrospective cohort study of patients between 2018-2021 Ketamine and propofol were both significantly associated with post-induction hypotension Ketamine adjusted odds ratio = 4.50 Propofol adjusted odds ratio = 4.88 50% of patients became hypotensive after induction with either propofol or ketamine These findings suggest post-induction hypotension is mainly due to sympatholysis rather than the choice of agent itself References Tamsett Z, Douglas N, King C, et al. Does the choice of induction agent in rapid sequence intubation in the emergency department influence the incidence of post-induction hypotension?. Emerg Med Australas. 2024;36(3):340-347. doi:10.1111/1742-6723.14355 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen MD Educational Pearls: Can opioids cause cardiac arrest? Opioids can cause respiratory suppression and the subsequent low oxygen levels can lead to arrhythmias and eventually cardiac arrest. In 2023, 17% of out-of-hospital cardiac arrests (OHCA) were attributable to opioids. Given that this is a rising cause of cardiac arrest, should we just treat all cardiac arrest with naloxone (Narcan)? Naloxone is correlated with an increased chance of return of spontaneous circulation (ROSC) Additionally, a wide variety of individuals can be exposed to opioids and therefore opioid overdose should be considered in all cases of OHCA But does naloxone improve neurologic outcomes? Yes, naloxone, especially when given early on in the resuscitation can improve neuro outcomes What is the dose? 2-4 mg IN/IV depending on access. High suspicion for opioid overdose consider going with an even higher dose such as 4-8 mg IN/IV References Orkin, A. M., & Dezfulian, C. (2024). Recognizing the fastest growing cause of out-of-hospital cardiac arrest. Resuscitation, 198, 110206. https://doi.org/10.1016/j.resuscitation.2024.110206 Quinn, E., & Du Pont, D. (2024). Naloxone administration in out-of-hospital cardiac arrest: What's next?. Resuscitation, 201, 110307. https://doi.org/10.1016/j.resuscitation.2024.110307 Saybolt, M. D., Alter, S. M., Dos Santos, F., Calello, D. P., Rynn, K. O., Nelson, D. A., & Merlin, M. A. (2010). Naloxone in cardiac arrest with suspected opioid overdoses. Resuscitation, 81(1), 42–46. https://doi.org/10.1016/j.resuscitation.2009.09.016 Wampler D. A. (2024). Naloxone in Out-of-Hospital Cardiac Arrest-More Than Just Opioid Reversal. JAMA network open, 7(8), e2429131. https://doi.org/10.1001/jamanetworkopen.2024.29131 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/

Contributor: Aaron Lessen MD Educational Pearls: A study evaluated the patient-care impact and financial costs of holding patients in the ED, a nationwide issue Prospective, observational study of acute stroke management Conducted at a large urban, comprehensive stroke center The study evaluated patients in multiple categories:  admitted to med/surg admitted to med/surg but held in the ED admitted to the ICU Admitted to ICU but held in the ED Examined the amount of time nurses and providers spent with each patient This was analyzed in conjunction with the knowledge of each providers' salaries and the overhead costs of the med/surg unit, ICU, and ED  Conclusions: Patients who required med/surg inpatient care but who were held in the ED resulted in a doubled daily cost $1856 for med/surg inpatient boarding vs $993 for med/surg inpatient care Patients who required ICU care but who were held in the ED also resulted in an increased daily cost, but this difference was not as large $2267 for ICU inpatient boarding vs $2165 for ICU care Holding in the ED negatively impacts patients since they receive less time from providers Holding also results in increased financial costs References Canellas MM, Jewell M, Edwards JL, Olivier D, Jun-O'Connell AH, Reznek MA. Measurement of Cost of Boarding in the Emergency Department Using Time-Driven Activity-Based Costing. Annals of emergency medicine. Published online May 1, 2024. doi:https://doi.org/10.1016/j.annemergmed.2024.04.012 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen MD Educational Pearls: Aortic injury occurs in 1.5-2% of patients who sustain blunt thoracic trauma Majority are caused by automobile collisions or motorcycle accidents Due to sudden deceleration mechanism accidents Clinical manifestations Signs of hypovolemic shock including tachycardia and hypotension, though not always present Patients may have altered mental status Imaging Widened mediastinum on chest x-ray, though not highly sensitive CT is more sensitive and specific, and signs of thoracic injury include an intimal flap, aortic wall outpouching, and aortic contour abnormalities In hemodynamically unstable or otherwise unfit for CT patients, transesophageal echocardiogram may be used Four types of aortic injury (in order of ascending severity) I: Intimal tear or flap II: Intramural hematoma III: Pseudoaneurysm IV: Rupture Management Hemodynamically unstable: immediate OR for exploratory laparotomy and repair Hemodynamically stable: heart rate and blood pressure control with beta-blockers Minor injuries are treated with observation and hemodynamic control Severe injuries may receive surgical management Some patients benefit from delayed repair An endovascular aortic graft is a surgical option Mortality 80-85% of patients die before hospital arrival 50% of patients that make it to the hospital do not survive References Fox N, Schwartz D, Salazar JH, et al. Evaluation and management of blunt traumatic aortic injury: a practice management guideline from the Eastern Association for the Surgery of Trauma [published correction appears in J Trauma Acute Care Surg. 2015 Feb;78(2):447]. J Trauma Acute Care Surg. 2015;78(1):136-146. doi:10.1097/TA.0000000000000470 Lee WA, Matsumura JS, Mitchell RS, et al. Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg. 2011;53(1):187-192. doi:10.1016/j.jvs.2010.08.027 Osgood MJ, Heck JM, Rellinger EJ, et al. Natural history of grade I-II blunt traumatic aortic injury. J Vasc Surg. 2014;59(2):334-341. doi:10.1016/j.jvs.2013.09.007 Osman A, Fong CP, Wahab SFA, Panebianco N, Teran F. Transesophageal Echocardiography at the Golden Hour: Identification of Blunt Traumatic Aortic Injuries in the Emergency Department. J Emerg Med. 2020;59(3):418-423. doi:10.1016/j.jemermed.2020.05.003 Steenburg SD, Ravenel JG, Ikonomidis JS, Schönholz C, Reeves S. Acute traumatic aortic injury: imaging evaluation and management. Radiology. 2008;248(3):748-762. doi:10.1148/radiol.2483071416 Summarized by Jorge Chalit, OMS3 | Edited by Meg Joyce & Jorge Chalit Donate: https://emergencymedicalminute.org/donate/  

Laboring Under Pressure Episode 4: Obstetric Emergency in South Africa with Dr. Meghan Hurley Contributors: Meghan Hurley MD, Travis Barlock MD, Jeffrey Olson MS3 Show Pearls Map of South Africa Referenced South Africa Geography Lesson There is a big disparity between Cape Town and its neighbor Khayelitsha. Cape Town is the legislative capital and economic hub of South Africa, known for its infrastructure, tourist attractions, and developed urban areas. Khayelitsha Township is a large informal settlement on the outskirts of Cape Town, with limited infrastructure and services compared to the city center. Many residents live in informal housing. This disparity is the lasting effect of how land was divided up and populations were moved around during Apartheid. Apartheid was a policy of segregation that lasted from 1948 to 1994. How does medical education work in South Africa? Medical education in South Africa typically follows a 6-year undergraduate program directly after high school Registrars our the equivalent of Resident in America. They are graduated doctors who work in hospitals under the supervision of senior doctors as they progress toward becoming specialists. Pearls from the case and the discussion afterward Whole blood from a draw can be used instead of urine on a POC pregnancy test. Wait a little bit longer before making a determination because blood is more viscous. Although the casettes are not approved for whole blood several studies have shown this to be efficacious. Free fluid in the abdomen and a pregnancy of unknown location is a rupture ectopic until proven otherwise. Appendicitis can present on the left side. Most commonly from an extra appendix, but can also result from situs inversus or mid-gut malrotation. This presentation can also be the result of an atypically large appendix. Fever is common in appendicitis (~40%) and becomes less common with older patients. Don't be falsely reassured by a normal hemoglobin in acute bleeding because patients bleed whole blood and the hemoglobin concentration is not affected. These patients should be resuscitated with whole blood. Give rhesus factor negative blood to female patients of childbearing age to prevent them from developing antibodies to the rhesus factor which can lead to Rh disease in future pregnancies. Rhogam can be given in cases of ruptured ectopic pregnancies to lower the risk of alloimmunization. Blood transfusions carry the risk of lung and heart injury from the extra volume. The treatment for this condition is to diurese the patient. Other topics discussed include the complications of working in a South African township hospital at night, the epidemiology of burns, and the importance of global health.   References Akbulut S, Ulku A, Senol A, Tas M, Yagmur Y. Left-sided appendicitis: review of 95 published cases and a case report. World J Gastroenterol. 2010 Nov 28;16(44):5598-602. doi: 10.3748/wjg.v16.i44.5598. PMID: 21105193; PMCID: PMC2992678. Barash, J. H., Buchanan, E. M., & Hillson, C. (2014). Diagnosis and management of ectopic pregnancy. American family physician, 90(1), 34–40. Fromm C, Likourezos A, Haines L, Khan AN, Williams J, Berezow J. Substituting whole blood for urine in a bedside pregnancy test. J Emerg Med. 2012 Sep;43(3):478-82. doi: 10.1016/j.jemermed.2011.05.028. Epub 2011 Aug 27. PMID: 21875776. Moris, D., Paulson, E. K., & Pappas, T. N. (2021). Diagnosis and Management of Acute Appendicitis in Adults: A Review. JAMA, 326(22), 2299–2311. https://doi.org/10.1001/jama.2021.20502 Sowder AM, Yarbrough ML, Nerenz RD, Mitsios JV, Mortensen R, Gronowski AM, Grenache DG. Analytical performance evaluation of the i-STAT Total β-human chorionic gonadotropin immunoassay. Clin Chim Acta. 2015 Jun 15;446:165-70. doi: 10.1016/j.cca.2015.04.025. Epub 2015 Apr 25. PMID: 25916696.   Produced by Jeffrey Olson, MS3 | Edited by Jeffrey Olson and Jorge Chalit, OMSIII

Contributor: Taylor Lynch, MD Educational Pearls: What is neutropenic fever? Specific type of fever that is seen in cancer patients and other patients with impaired immune systems These patients are highly susceptible to infection Typically occurs 7-10 days after the last chemotherapy dose, this is when the immune system is the weakest It is useful to know the specific type of malignancy. For example, heme malignancies (ALL, AML, etc.) have more intense chemo and are at higher risk of neutropenic fever To qualify as a neutropenic fever, a patient must have one recorded temperature greater than 38.3 degrees C or be over 38 degrees C for one hour. The severity of the neutropenic fever is established by the absolute neutrophil count. Abs neutrophil count under 1500 is mild, less than 1000 is moderate, less than 500 is severe. Also look at monocytes (cell that becomes a macrophage). Less than 200 is very concerning What is the workup and treatment? Obtain a panculture (culture blood from both arms and all indwelling lines), obtain urine culture, and get a chest x-ray. Do not preform a rectal exam or obtain a rectal core temperature. This could cause bacteremia. Treat with Cefepime (broad range and includes pseudomonas but not MRSA). If there is concern for MRSA add vancomycin. Admit with Neutropenic precautions (gowns, gloves, mask, positive pressure room) References Peseski, A. M., McClean, M., Green, S. D., Beeler, C., & Konig, H. (2021). Management of fever and neutropenia in the adult patient with acute myeloid leukemia. Expert review of anti-infective therapy, 19(3), 359–378. https://doi.org/10.1080/14787210.2020.1820863 Zimmer, A. J., & Freifeld, A. G. (2019). Optimal Management of Neutropenic Fever in Patients With Cancer. Journal of oncology practice, 15(1), 19–24. https://doi.org/10.1200/JOP.18.00269 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce & Jorge Chalit, OMS3  

Contributor: Jorge Chalit-Hernandez, OMS3 Typically presents with biliary colic Right upper quadrant abdominal pain lasting more than 30 minutes and subsiding over several hours Often associated with fatty meals but not always Must rule out other causes of pain Peptic ulcer disease - typically presents with epigastric pain Pancreatitis - pain that radiates to the back or family history of pancreatitis Laboratory workup  LFTs including ALT, AST, and alkaline phosphatase are within the reference range Lipase and amylase within the reference range Imaging workup RUQ ultrasound is unremarkable Upper endoscopy with ultrasound can help rule out peptic ulcer disease and small stones HIDA scan may show a reduced gallbladder ejection fraction below 30-35% or it may be normal  Opiates may give false-positive results Opiates can sometimes make biliary colic worse due to their contractile effect on the sphincter of Oddi Some patients may benefit from surgical intervention i.e. cholecystectomy Classic biliary-type pain (best predictor of response to cholecystectomy) Pain for > 3 months duration Positive HIDA scan References Alhayo S, Eslick GD, Cox MR. Cholescintigraphy may have a role in selecting patients with biliary dyskinesia for cholecystectomy: a systematic review. ANZ J Surg. 2020;90(9):1647-1652. doi:10.1111/ans.16003 Arshi J, Layfield LJ, Esebua M. Mast cell infiltration and activation in the gallbladder wall: Implications for the pathogenesis of functional gallbladder disorder in adult patients. Ann Diagn Pathol. 2021;54:151798. doi:10.1016/j.anndiagpath.2021.151798 Carr JA, Walls J, Bryan LJ, Snider DL. The treatment of gallbladder dyskinesia based upon symptoms: results of a 2-year, prospective, nonrandomized, concurrent cohort study. Surg Laparosc Endosc Percutan Tech. 2009;19(3):222-226. doi:10.1097/SLE.0b013e3181a74690 Joehl RJ, Koch KL, Nahrwold DL. Opioid drugs cause bile duct obstruction during hepatobiliary scans. Am J Surg. 1984;147(1):134-138. doi:10.1016/0002-9610(84)90047-3 Mahid SS, Jafri NS, Brangers BC, Minor KS, Hornung CA, Galandiuk S. Meta-analysis of cholecystectomy in symptomatic patients with positive hepatobiliary iminodiacetic acid scan results without gallstones. Arch Surg. 2009;144(2):180-187. doi:10.1001/archsurg.2008.543 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Taylor Lynch MD Supraventricular tachycardias (SVTs) arise above the bundle of His The term SVT includes AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia, atrial fibrillation, atrial flutter, and multifocal atrial tachycardia  AVNRT is the most common form of SVT Paroxysmal Spontaneous or provoked by exertion, coffee, alcohol, or thyroid disease More common in women (3:1 women:men ratio) HR 160-240 Narrow complex with a normal QRS Unstable patients receive synchronized cardioversion at 0.5-1 J/kg Valsalva maneuver is attempted before pharmaceutical interventions Increases vagal tone at the AV node to slow conduction and prolongs its refractory period to normalize the conduction Traditionally, patients are asked to bear down, but this only works in 17% of patients REVERT trial assessed a modified valsalva that worked in 43% of patients Adenosine Slows conduction at the AV node by activating potassium channels and inhibiting calcium influx Extremely uncomfortable for most patients Not commonly used anymore Nondihydropyridine calcium-channel blockers are preferred A 2009 RCT investigated low-infusion CCBs compared with adenosine bolus The study found a conversion rate of 98% in the CCB group vs. adenosine group at 86.5% The main adverse effect of CCB is hypotension, which a slow infusion rate can mitigate Diltiazem dose is 0.25 mg/kg/2min and repeat at 0.35 mg/kg/15 minutes or slow infusion at 2.5 mg/min up to a conversion or 50 mg total References 1. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): A randomised controlled trial. Lancet. 2015;386(10005):1747-1753. doi:10.1016/S0140-6736(15)61485-4 Belz MK, Stambler BS, Wood MA, Pherson C, Ellenbogen KA. Effects of enhanced parasympathetic tone on atrioventricular nodal conduction during atrioventricular nodal reentrant tachycardia. Am J Cardiol. 1997;80(7):878-882. doi:10.1016/s0002-9149(97)00539-0 Lim SH, Anantharaman V, Teo WS, Chan YH. Slow infusion of calcium channel blockers compared with intravenous adenosine in the emergency treatment of supraventricular tachycardia. Resuscitation. 2009;80(5):523-528. doi:10.1016/j.resuscitation.2009.01.017 Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in Circulation. 2016 Sep 13;134(11):e234-5. doi: 10.1161/CIR.0000000000000448]. Circulation. 2016;133(14):e506-e574. doi:10.1161/CIR.0000000000000311 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen, MD Educational Pearls: Pediatric case study where the child's tongue was stuck in the opening of a hard plastic drink lid Entrapment restricts circulation which causes fluid to build and the tongue becomes more edematous with time There is a risk of ischemia with prolonged entrapment Initially tried 2% viscous lidocaine for analgesia and lubricant The ER recognized that this mucosal, edematous tongue could benefit from the trick for ostomies and rectal prolapses → table sugar! Sugar granules absorb water which decreases tissue edema This option avoids sedation and aggressive treatment References A Young Girl with Tongue Swelling Jarjour, Jane et al. Annals of Emergency Medicine, Volume 84, Issue 3, 317 - 318 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Megan Hurley, MD Educational Pearls: Fevers Tylenol Up until 20 weeks NSAIDs are ok but after 20 weeks they are contraindicated Can limit the amount of amniotic fluid produced Can lead to growth restriction Can cause premature closure of the ductus arteriosus Cough Cough drops Humidifier Guafenesine and dextromethorphan (Mucinex) is not well studied but is probably ok with caution in certain circumstances such as post-tussive emesis causing poor PO intake and weight loss Congestion Flonase (Fluticasone nasal spray) Nasal rinses Humidifier 1st generation anti-histamines (Diphenhydramine, Doxylamine, etc.) However, these tend to have more side effects such as fatigue, drowsiness, and dizziness Concider switching to a 2nd generation (Cetirizine, Loratidine, etc.) during the day Disease specific treatments Flu (A and B) gets tamiflu (Oseltamivir) Covid gets paxlovid (Nirmatrelvir/ritonavir) Antibiotics for suspected pneumonia Additional recommendations Elevating the head of bed Nasal strips Stay well hydrated Tea Ice chips Echinacea Zinc Rest Avoid NSAIDs Pseudophedrine Afrin (Oxymetazoline) Combined meds in general References Antonucci, R., Zaffanello, M., Puxeddu, E., Porcella, A., Cuzzolin, L., Pilloni, M. D., & Fanos, V. (2012). Use of non-steroidal anti-inflammatory drugs in pregnancy: impact on the fetus and newborn. Current drug metabolism, 13(4), 474–490. https://doi.org/10.2174/138920012800166607 Black, E., Khor, K. E., Kennedy, D., Chutatape, A., Sharma, S., Vancaillie, T., & Demirkol, A. (2019). Medication Use and Pain Management in Pregnancy: A Critical Review. Pain practice : the official journal of World Institute of Pain, 19(8), 875–899. https://doi.org/10.1111/papr.12814 D'Ambrosio, V., Vena, F., Scopelliti, A., D'Aniello, D., Savastano, G., Brunelli, R., & Giancotti, A. (2023). Use of non-steroidal anti-inflammatory drugs in pregnancy and oligohydramnios: a review. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians, 36(2), 2253956. https://doi.org/10.1080/14767058.2023.2253956 Summarized by Jeffrey Olson MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3  

Contributor: Travis Barlock MD Educational Pearls: Assessment of head and neck vascular injury due to blunt trauma Symptomatic patients require screening head and neck CT angiography EAST guidelines include the following criteria for a screening CT angiography in blunt head trauma: Unexplained neurological deficits Arterial nosebleed GCS < 6 Petrous bone fracture Cervical spine fracture Any size fracture through the transverse foramen LeFort fractures type II or type III EAST guidelines include a grading scale for vascular injury: Grade I: Luminal irregularity or dissection with 25% luminal narrowing, intraluminal thrombus, or raised intimal flap Grade III: Pseudoaneurysm Grade IV: Occlusion Grade V: Transection with free extravasation References Bensch FV, Varjonen EA, Pyhältö TT, Koskinen SK. Augmenting Denver criteria yields increased BCVI detection, with screening showing markedly increased risk for subsequent ischemic stroke. Emerg Radiol. 2019;26(4):365-372. doi:10.1007/s10140-019-01677-0 Biffl WL, Moore EE, Offner PJ, et al. Optimizing screening for blunt cerebrovascular injuries. Am J Surg. 1999;178(6):517-522. doi:10.1016/s0002-9610(99)00245-7 Kim DY, Biffl W, Bokhari F, et al. Evaluation and management of blunt cerebrovascular injury: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2020;88(6):875-887. doi:10.1097/TA.0000000000002668 Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

Contributor: Aaron Lessen, MD Educational Pearls: Hemothorax: blood in the pleural cavity, most commonly due to chest trauma Treatment: thoracostomy tube for blood drainage helps to avoid clotting, scarring, and infection A recent study looked at patients with hemothorax who either received or did not receive thoracic irrigation with saline Evaluated incidence of secondary intervention, such as video-assisted thoracoscopic surgery (VATS), for persistent hemothorax Patients who received irrigation had a slight decrease in secondary intervention frequency Multi-center study - all patients who had the irrigation procedure were at two centers Study limitation: variability in approaches at each location could be a confounder Technique that could potentially prevent future complications References Carver TW, Berndtson AE, McNickle AG, et al. Thoracic irrigation for prevention of secondary intervention after thoracostomy tube drainage for hemothorax: A Western Trauma Association multi-center study. J Trauma Acute Care Surg. Published online May 20, 2024. doi:10.1097/TA.0000000000004364 Yi JH, Liu HB, Zhang M, et al. Management of traumatic hemothorax by closed thoracic drainage using a central venous catheter. J Zhejiang Univ Sci B. 2012;13(1):43-48. doi:10.1631/jzus.B1100161 Summarized by Meg Joyce, MS | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/

Contributor: Taylor Lynch, MD Educational Pearls: When it comes to hypoglycemia, the age dictates possible causes Neonate: Hormonal deficiency Congenital Adrenal Hyperplasia (21-hydroxylase deficiency, 11β-hydroxylase deficiency) Primary or Secondary Adrenal Insufficiency leading to cortisol deficiency  Hypopituitarism Inborn errors of metabolism Systemic infection (Under 30 days old should trigger a full infectious workup) Toddler Accidental ingestions Sulfonylureas such as glipizide or glyburide Older children Addison's Disease (Hypocortisolism) Accidential or intentional ingestions Exogenous insulin How is it diagnosed? Child or infant Glucose

Contributor: Kiersten Williams MD, Travis Barlock MD, Jeffrey Olson MS2 Show Pearls Hypertensive disorders of pregnancy are one of the leading causes of maternal mortality worldwide. Hypertension (HTN) complicates 2-8% of pregnancies The definition of HTN in pregnancy is a systolic >140 or diastolic >90, measured 4 hours apart There is a range of HTN disorders Chronic HTN which could have superimposed preeclampsia (preE) on top Gestational HTN in which there are no lab abnormalities PreE w/o severe features Protein in urine Urine protein >300 mg in 24 hours Urine Protein to Creatinine ratio of .3 +2 Protein on urine dipstick PreE w/ severe features Systolics above 160 mmHg Diastolics above 110 mmHg Headache, especially not going away with meds, or different than previous headaches Visual changes, anything that lasts more than a few minutes RUQ pain, which could present as heartburn Pulmonary edema Low platelets, if

Contributor: Sean Fox, MD Educational Pearls: Newborns may lose up to 10% of their birth weight in the first week of life Weight loss is greatest in exclusively breastfed infants Should regain birth weight by age 2 weeks Newborns should gain an average of 30g (1 oz) per day in the first 3 months of life Some will gain more and some will gain less Infants double their birth weight by 6 months of life and triple their weight by 12 months A 1-year-old should weigh on average 10 kg (22 lbs) A 3-year-old should weigh on average 15 kg (33 lbs) 2-year-olds are between 10-15 kg on average Weight assessment can help determine causes of forceful vomiting Not all “projectile” vomiting is due to pyloric stenosis Some infants may experience vigorous vomiting from overfeeding Weight estimates can also provide information for quick decisions on medical management for children coming via EMS  Helps to prepare medications and dosages based on predicted average weight References Crossland DS, Richmond S, Hudson M, Smith K, Abu-Harb M. Weight change in the term baby in the first 2 weeks of life. Acta Paediatr. 2008;97(4):425-429. doi:10.1111/j.1651-2227.2008.00685.x Grummer-Strawn LM, Reinold C, Krebs NF; Centers for Disease Control and Prevention (CDC). Use of World Health Organization and CDC growth charts for children aged 0-59 months in the United States [published correction appears in MMWR Recomm Rep. 2010 Sep 17;59(36):1184]. MMWR Recomm Rep. 2010;59(RR-9):1-15. Macdonald PD, Ross SR, Grant L, Young D. Neonatal weight loss in breast and formula fed infants. Arch Dis Child Fetal Neonatal Ed. 2003;88(6):F472-F476. doi:10.1136/fn.88.6.f472 Paul IM, Schaefer EW, Miller JR, et al. Weight Change Nomograms for the First Month After Birth. Pediatrics. 2016;138(6):e20162625. doi:10.1542/peds.2016-2625 Summarized & Edited by Jorge Chalit, OMS3 Special thanks to the Carolinas Medical Center for their contribution to this episode  

Contributor: Travis Barlock, MD Educational Pearls: SVT: supraventricular tachycardia Pharmacotherapy for SVT includes drugs that block the AV node, such as adenosine EKG criteria before adenosine administration in SVT Regular rhythm Monomorphic: ​​all QRS complexes are identical If the EKG is polymorphic, with QRS complexes displaying changing morphologies, it is unsafe to administer adenosine  Adenosine can worsen polymorphic VTach and lead to VFib References Ganz, Leonard I., and Peter L. Friedman. “Supraventricular Tachycardia.” New England Journal of Medicine, vol. 332, no. 3, 19 Jan. 1995, pp. 162–173, https://doi.org/10.1056/nejm199501193320307. Smith JR, Goldberger JJ, Kadish AH. Adenosine induced polymorphic ventricular tachycardia in adults without structural heart disease. Pacing Clin Electrophysiol. 1997;20(3 Pt 1):743-745. doi:10.1111/j.1540-8159.1997.tb03897.x Viskin, Sami, et al. “Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy.” Circulation, vol. 144, no. 10, 7 Sept. 2021, pp. 823–839, https://doi.org/10.1161/circulationaha.121.055783. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3  

Contributor: Aaron Lessen, MD Educational Pearls: How does an automated blood pressure cuff work? Automated blood pressure cuffs work differently than taking a manual blood pressure. While taking a manual blood pressure, one typically listens for Korotkoff sounds (turbulent flow) while slowly deflating the cuff. An automatic blood pressure cuff only senses the pressure in the cuff itself and specifically pays attention to oscillations in the pressure caused by when the pressure of the cuff is between the systolic (heart squeezing) and diastolic (heart relaxed) pressures. These oscillations are at a maximum when the pressure in the cuff matches the mean arterial pressure (MAP) and therefore the machines are most accurate at reporting the MAP. The machines then use the MAP and other information about the oscillations to estimate the systolic and diastolic pressures, which are less accurate. What should you do if you need more accurate systolic and diastolic blood pressures? Take a manual blood pressure. Get an arterial-line (a-line), which provides continuous data for the blood pressure at the end of a catheter. What happens if the cuff is too big or too small for the patient? If the cuff is too small it will overestimate the pressure. If the cuff is too large it will underestimate the pressure. What should you do if the cuff cycles a bunch of times before reporting a blood pressure? It probably isn't very accurate so consider another method. Bonus fact! The MAP is not directly in the middle of the systolic and diastolic pressures but is weighted towards the diastolic pressure. The MAP can be calculated by adding two-thirds of the diastolic pressure to one third of the systolic pressure. For example if the BP is 120/90 the MAP is 100 mmHg. References Benmira, A., Perez-Martin, A., Schuster, I., Aichoun, I., Coudray, S., Bereksi-Reguig, F., & Dauzat, M. (2016). From Korotkoff and Marey to automatic non-invasive oscillometric blood pressure measurement: does easiness come with reliability?. Expert review of medical devices, 13(2), 179–189. https://doi.org/10.1586/17434440.2016.1128821 Liu, J., Li, Y., Li, J., Zheng, D., & Liu, C. (2022). Sources of automatic office blood pressure measurement error: a systematic review. Physiological measurement, 43(9), 10.1088/1361-6579/ac890e. https://doi.org/10.1088/1361-6579/ac890e Vilaplana J. M. (2006). Blood pressure measurement. Journal of renal care, 32(4), 210–213. https://doi.org/10.1111/j.1755-6686.2006.tb00025.x Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3  

Contributor: Megan Hurley, MD Educational Pearls:  Heat cramps Occur due to electrolyte disturbances Most common electrolyte abnormalities are hyponatremia and hypokalemia Heat edema Caused by vasodilation with pooling of interstitial fluid in the extremities Heat rash (miliaria) Common in newborns and elderly Due to accumulation of sweat beneath eccrine ducts Heat syncope Lightheadedness, hypotension, and/or syncope in patients with peripheral vasodilation due to heat exposure Treatment is removal from the heat source and rehydration (IV fluids or Gatorade) Heat exhaustion Patients have elevated body temperature (greater than 38º C but less than 40º C) Symptoms include nausea, tachycardia, headache, sweating, and others Normal mental status or mild confusion that improves with cooling Treatment is removal from the heat source and hydration Classic heat stroke From prolonged exposure to heat Defined as a core body temperature > 40.5º C, though not required for diagnosis or treatment Presentation is similar to heat exhaustion with the addition of neurological deficits including ataxia Patients present “dry” Exertional heat stroke Prolonged exposure to heat during exercise Similar to classic heat stroke but the patients present “wet” due to antecedent treatment in ice baths or other field treatments Management of heat-related illnesses includes: Cooling Rehydration Evaluation of electrolytes Antipyretics are not helpful because heat-induced illnesses are not due to hypothalamic dysregulation References Casa DJ, McDermott BP, Lee EC, et al. Cold water immersion: the gold standard for exertional heatstroke treatment. Exerc Sport Sci Rev 2007; 35:141. Ebi KL, Capon A, Berry P, et al. Hot weather and heat extremes: health risks. Lancet 2021; 398:698. Epstein Y, Yanovich R. Heatstroke. N Engl J Med 2019; 380:2449. Gardner JW, JA K. Clinical diagnosis, management, and surveillance of exertional heat illness. In: Textbook of Military Medicine, Zajitchuk R (Ed), Army Medical Center Borden Institute, Washington, DC 2001. Khosla R, Guntupalli KK. Heat-related illnesses. Crit Care Clin 1999; 15:251. Lipman GS, Gaudio FG, Eifling KP, et al. Wilderness Medical Society Clinical Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. Wilderness Environ Med 2019; 30:S33. Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce, MS1  

Contributor: Taylor Lynch, MD Educational Pearls: What is Central Cord Syndrome (CCS)? Incomplete spinal cord injury caused by trauma that compresses the center of the cord More common in hyperextension injuries like falling and hitting the chin Usually happens only in individuals with preexisting neck and spinal cord conditions like cervical spondylosis (age-related wear and tear of the cervical spine) Anatomy of spinal cord Motor tracts The signals the brain sends for the muscles to move travel in the corticospinal tracts of the spinal cord The tracts that control the upper limbs are more central than the ones that control the lower limbs The tracts that control the hands are more central than the ones that control the upper arm/shoulder Fine touch, vibration, and proprioception (body position) tracts These sensations travel in separate tracts in the spinal cord than the sensation of pain and temperature Their pathway is called the dorsal column-medial lemniscus (DCML) pathway This information travels in the most posterior aspect of the spinal cord Pain, crude touch, pressure, and temperature tracts These sensations travel in the spinothalamic tract, which is more centrally located These signals also cross one side of the body to the other within the spinal cord near the level that they enter How does this anatomy affect the presentation of CCS? Patients typically experience more pronounced weakness or paralysis in their upper extremities as compared to their lower extremities with their hands being weaker than more proximal muscle groups Sensation of pain, crude touch, pressure, and temperature are much morelikely to be diminished while the sensation of fine touch, vibration, and proprioception are spared What happens with reflexes? Deep tendon reflexes become exaggerated in CCS This is because the disruption in the corticospinal tract removes inhibitory control over reflex arcs What happens to bladder control? The neural signals that coordinate bladder emptying are disrupted, therefore patients can present with urinary retention and/or urge incontinence What is a Babinski's Sign? When the sole of the foot is stimulated a normal response in adults is for the toes to flex downward (plantar flexion) If there is an upper motor neuron injury like in CCS, the toes will flex upwards (dorsiflexion) How is CCS diagnosed? CCS is mostly a clinical diagnosis These patient also need an MRI to see the extent of the damage which will show increased signal intensity within the central part of the spinal cord on T2-weighted images How is CCS treated? Strict c-spine precautions Neurogenic shock precautions. Maintain a mean arterial pressure (MAP) of 85-90 to ensure profusion of the spinal cord Levophed (norepinephrine bitartrate) and/or phenylephrine can be used to support their blood pressure to support spinal perfusion Consider intubation for injuries above C5 (C3, 4, and 5 keep the diaphragm alive) Consult neurosurgery for possible decompression surgery Physical Therapy References Avila, M. J., & Hurlbert, R. J. (2021). Central Cord Syndrome Redefined. Neurosurgery clinics of North America, 32(3), 353–363. https://doi.org/10.1016/j.nec.2021.03.007 Brooks N. P. (2017). Central Cord Syndrome. Neurosurgery clinics of North America, 28(1), 41–47. https://doi.org/10.1016/j.nec.2016.08.002 Engel-Haber, E., Snider, B., & Kirshblum, S. (2023). Central cord syndrome definitions, variations and limitations. Spinal cord, 61(11), 579–586. https://doi.org/10.1038/s41393-023-00894-2 Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMSIII  

Contributor: Megan Hurley, MD Educational Pearls: Initial assessment of patients with severe burn injuries begins with ABCs  Airway: consider inhalation injury Breathing: circumferential burns of the trunk region can reduce respiratory muscle movement Circulation: circumferential burns compromise circulation Exposure: Important to assess the affected surface area Escharotomy: emergency procedure to release the tourniquet-ing effects of the eschar  Differs from a fasciotomy in that it does not breach the deep fascial layer PEEP = positive end-expiratory pressure The positive pressure remaining in the airway after exhalation Keeps airway pressure higher than atmospheric pressure Common formulas for initial fluid rate in burn shock resuscitation Parkland formula: 4 mL/kg body weight/% TBSA burns (lactated Ringer's solution) Modified Brooke formula: 2 mL/kg/% (also lactated Ringer's solution) Less fluid = lower risk of intra-abdominal compartment syndrome Lactated Ringer's solution is preferred over normal saline in burn injuries Normal saline is avoided in large quantities due to the possibility of it leading to hyperchloremic acidosis References Acosta P, Santisbon E, Varon J. “The Use of Positive End-Expiratory Pressure in Mechanical Ventilation.” Critical Care Clinics. 2007;23(2):251-261. doi:10.1016/j.ccc.2006.12.012  Orgill DP, Piccolo N. Escharotomy and decompressive therapies in burns. J Burn Care Res. 2009;30(5):759-768. doi:10.1097/BCR.0b013e3181b47cd3  Snell JA, Loh NH, Mahambrey T, Shokrollahi K. Clinical review: the critical care management of the burn patient. Crit Care. 2013;17(5):241. Published 2013 Oct 7. doi:10.1186/cc12706 Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit

Contributor: Taylor Lynch, MD Educational Pearls: What is NMS? Neuroleptic Malignant Syndrome Caused by anti-dopamine medication or rapid withdrawal of pro-dopamenergic medications Mechanism is poorly understood Life threatening What medications can cause it? Typical antipsychotics Haloperidol, chlorpromazine, prochlorperazine, fluphenazine, trifluoperazine Atypical antipsychotics Less risk Risperidone, clozapine, quetiapine, olanzapine, aripiprazole, ziprasidone Anti-emetic agents with anti dopamine activity Metoclopramide, promethazine, haloperidol Not ondansetron Abrupt withdrawal of levodopa How does it present? Slowly over 1-3 days (unlike serotonin syndrome which has a more acute onset) Altered mental status, 82% of patients, typically agitated delirium with confusion Peripheral muscle rigidity and decreased reflexes. AKA lead pipe rigidity. (As opposed to clonus and hyperreflexia in serotonin syndrome) Hyperthermia (>38C seen in 87% of patients) Can also have tachycardia, labile blood pressures, tachypnea, and tremor How is it diagnosed? Clinical diagnosis, focus on the timing of symptoms No confirmatory lab test but can see possible elevated CK levels and WBC of 10-40k with a left shift What else might be on the differential? Sepsis CNS infections Heat stroke Agitated delirium Status eptilepticus Drug induced extrapyramidal symptoms Serotonin syndrome Malignant hyperthermia What is the treatment? Start with ABC's Stop all anti-dopaminergic meds and restart pro-dopamine meds if recently stopped Maintain urine output with IV fluids if needed to avoid rhabdomyolysis Active or passive cooling if needed Benzodiazapines, such as lorazepam 1-2 mg IV q 4hrs What are active medical therapies? Controversial treatments Bromocriptine, dopamine agonist Dantrolene, classically used for malignant hyperthermia Amantadine, increases dopamine release Use as a last resort Dispo? Mortality is around 10% if not recognized and treated Most patients recover in 2-14 days Must wait 2 weeks before restarting any medications References Oruch, R., Pryme, I. F., Engelsen, B. A., & Lund, A. (2017). Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatric disease and treatment, 13, 161–175. https://doi.org/10.2147/NDT.S118438 Tormoehlen, L. M., & Rusyniak, D. E. (2018). Neuroleptic malignant syndrome and serotonin syndrome. Handbook of clinical neurology, 157, 663–675. https://doi.org/10.1016/B978-0-444-64074-1.00039-2 Velamoor, V. R., Norman, R. M., Caroff, S. N., Mann, S. C., Sullivan, K. A., & Antelo, R. E. (1994). Progression of symptoms in neuroleptic malignant syndrome. The Journal of nervous and mental disease, 182(3), 168–173. https://doi.org/10.1097/00005053-199403000-00007 Ware, M. R., Feller, D. B., & Hall, K. L. (2018). Neuroleptic Malignant Syndrome: Diagnosis and Management. The primary care companion for CNS disorders, 20(1), 17r02185. https://doi.org/10.4088/PCC.17r02185 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII  

Contributor: Travis Barlock MD Educational Pearls: Recent study assessed outcomes after ROSC with epinephrine vs. norepinephrine Observational multicenter study from 2011-2018 285 patients received epineprhine and 481 received norepinephrine Epinephrine was associated with an increase in all-cause mortality (primary outcome) Odds ratio 2.6; 95%CI 1.4-4.7; P = 0.002 Higher cardiovascular mortality (secondary outcome) Higher proportion of unfavorable neurological outcome (secondary outcome) Norepinephrine is the vasopressor of choice in post-cardiac arrest care References Bougouin W, Slimani K, Renaudier M, et al. Epinephrine versus norepinephrine in cardiac arrest patients with post-resuscitation shock. Intensive Care Med. 2022;48(3):300-310. doi:10.1007/s00134-021-06608-7 Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit  

Contributor: Taylor Lynch, MD Educational Pearls: Opioid Epidemic- quick facts Drug overdoses, primarily driven by opioids, have become the leading cause of accidental death in the U.S. for individuals aged 18-45. In 2021, opioids were involved in nearly 75% of all drug overdose deaths The rise of synthetic opioids like fentanyl, which is much more potent than heroin or prescription opioids, has played a major role in the increase in overdose deaths What is Narcan AKA Naloxone? Competitive opioid antagonist. It sits on the receptor but doesn't activate it. When do we give Narcan? Respiratory rate less than 8-10 breaths per minute Should you check the pupils? An opioid overdose classically presents with pinpoint pupils BUT… Hypercapnia from bradypnea can normalize the pupils Taking other drugs at the same time like cocaine or meth can counteract the pupillary effects Basilar stroke could also cause small pupils, so don't anchor on an opioid overdose How does Narcan affect the body? Relatively safe even if the patient is not experiencing an opioid overdose. So when in doubt, give the Narcan. What if the patient is opioid naive and overdosing? Use a large dose given that this patient is unlikely to withdraw 0.4-2 mg every 3-5 minutes What if the patient is a chronic opioid user Use a smaller dose such as 0.04-0.4 mg to avoid precipitated withdrawal How fast does Narcan work? Given intravenously (IV), onset is 1-2 min Given intranasal (IN), onset is 3-4 min Given intramuscularly (IM), onset is ~6 min Duration of action is 60 mins, with a range of 20-90 minutes How does that compare to the duration of action of common opioids? Heroine lasts 60 min Fentanyl lasts 30-60 min, depending on route Carfentanyl lasts ~5 hrs Methadone lasts 12-24 hrs So we really need to be conscious about redosing How do you monitor someone treated with Narcan? Pay close attention to the end-tidal CO2 to ensure that are ventilating appropriately Be cautious with giving O2 as it might mask hypoventilation Watch the respiratory rate Give Narcan as needed Observe for at least 2-4 hours after the last Narcan dose Larger the dose, longer the observation period Who gets a drip? If they have gotten ~3 doses, time to start the drip Start at 2/3rds last effective wake-up dose Complications Flash pulm edema 0.2-3.6% complication rate Might be from the catecholamine surge from abrupt wake-up Might also be from large inspiratory effort against a partially closed glottis which creates too much negative pressure Treat with BIPAP if awake and intubation if not awake Should you give Narcan in cardiac arrest? Short answer no. During ACLS you take over breathing for the patient and that is pretty much the only way that Narcan can help Just focus on high quality CPR References https://nida.nih.gov/research-topics/trends-statistics/overdose-death-rates#:~:text=Drug%20overdose%20deaths%20involving%20prescription,of%20deaths%20declined%20to%2014%2C716. Elkattawy, S., Alyacoub, R., Ejikeme, C., Noori, M. A. M., & Remolina, C. (2021). Naloxone induced pulmonary edema. Journal of community hospital internal medicine perspectives, 11(1), 139–142. https://doi.org/10.1080/20009666.2020.1854417 van Lemmen, M., Florian, J., Li, Z., van Velzen, M., van Dorp, E., Niesters, M., Sarton, E., Olofsen, E., van der Schrier, R., Strauss, D. G., & Dahan, A. (2023). Opioid Overdose: Limitations in Naloxone Reversal of Respiratory Depression and Prevention of Cardiac Arrest. Anesthesiology, 139(3), 342–353. https://doi.org/10.1097/ALN.0000000000004622 Yousefifard, M., Vazirizadeh-Mahabadi, M. H., Neishaboori, A. M., Alavi, S. N. R., Amiri, M., Baratloo, A., & Saberian, P. (2019). Intranasal versus Intramuscular/Intravenous Naloxone for Pre-hospital Opioid Overdose: A Systematic Review and Meta-analysis. Advanced journal of emergency medicine, 4(2), e27. https://doi.org/10.22114/ajem.v0i0.279 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSII

Contributor: Taylor Lynch MD Educational Pearls: Anticholinergics are found in many medications, including over-the-counter remedies Medications include: Diphenhydramine Tricyclic antidepressants like amitriptyline Atropine Antipsychotics like olanzapine Antispasmodics - dicyclomine Jimsonweed Muscaria mushrooms Mechanism of action involves competitive antagonism of the muscarinic receptor Symptomatic presentation is easily remembered via the mnemonic: Dry as a bone - anhidrosis due to cholinergic antagonism at sweat glands Red as a beet - cutaneous vasodilation leads to skin flushing Hot as a hare - anhidrotic hyperthermia Blind as a bat - pupillary dilation and ineffective accommodation Mad as a hatter - anxiety, agitation, dysarthria, hallucinations, and others Clinical management ABCs Benzodiazepines for supportive care, agitation, and seizures Sodium bicarbonate for TCA toxicity due to widened QRS Activated charcoal if patient present < 1 hour after ingestion Temperature monitoring Contact poison control with questions Physostigmine controversy Acetylcholinesterase inhibitor Black box warning for asystole and seizure Contraindicated in TCA overdoses Crosses blood-brain barrier, so useful for TCA overdoses Indicated only in certain anticholinergic overdose with delirium Disposition Admission criteria include: symptoms >6 hours, CNS findings, QRS prolongation, hyperthermia, and rhabdomyolysis ICU admission criteria include: delirium, dysrhythmias, seizures, coma, or requirement for physostigmine drip References 1. Arens AM, Shah K, Al-Abri S, Olson KR, Kearney T. Safety and effectiveness of physostigmine: a 10-year retrospective review. Clin Toxicol (Phila). 2018;56(2):101-107. doi:10.1080/15563650.2017.1342828 2. Nguyen TT, Armengol C, Wilhoite G, Cumpston KL, Wills BK. Adverse events from physostigmine: An observational study. Am J Emerg Med. 2018;36(1):141-142. doi:10.1016/j.ajem.2017.07.006 3. Scharman E, Erdman A, Wax P, et al. Diphenhydramine and dimenhydrinate poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2006;44(3):205-223. doi:10.1080/15563650600585920 4. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson "loco" weed abuse in adolescents. Pediatrics. 1979;63(4):520-523. 5. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2007;45(3):203-233. doi:10.1080/15563650701226192 Summarized by Jorge Chalit, OMSIII | Edited by Jorge Chalit  

Contributor: Aaron Lessen, MD Educational Pearls: How fast does cellulitis recover? A recent prospective cohort study took a look at this question. The study included 300 adults with cellulitis (excluding those with peri-orbital cellulitis or abscesses) in two emergency departments in Queensland, Australia. They collected data from initial and follow-up surveys at 3, 7, and 14 days, and compared clinician and patient assessments at day 14. Improvement was fastest between day 0 and day 3, with gradual progress thereafter. At day 14, many still had skin redness and swelling, though warmth had often resolved. Clinicians reported higher cure rates than patients (85.8% vs. 52.8%). Conclusion: Cellulitis symptoms improve quickly at first but continue to linger for many patients. Patients and doctors often have different views on when cellulitis is fully cured. How should we counsel patients? Even on antibiotics, the margins of the cellulitis may continue to spread a small amount. Skin warmth should be the first symptom to go away. It takes time to get better. Only about 50% of patients believed their cellulitis was cured at 2 weeks. References Nightingale, R. S., Etheridge, N., Sweeny, A. L., Smyth, G., Dace, W., Pellatt, R. A. F., Snelling, P. J., Yadav, K., & Keijzers, G. (2024). Cellulitis in the Emergency Department: A prospective cohort study with patient-centred follow-up. Emergency medicine Australasia : EMA, 10.1111/1742-6723.14401. Advance online publication. https://doi.org/10.1111/1742-6723.14401 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII

Contributor: Aaron Lessen MD Educational Pearls: A recent study assessed EMS treatment of high blood pressure in the field 2404 patients randomized to prehospital treatment (1205)  vs. usual care (1199) Included patients with prehospital BP greater than 150 mm Hg The treatment arm's BP goal was 130-140 mm Hg The primary efficacy outcome was functional status 90 days out Stroke was confirmed by imaging upon hospital arrival On arrival, the mean SBP of the treatment arm was 159 mm Hg compared with 170 mm Hg in the usual care group No significant difference in functional outcomes between the treatment group and the usual care group (Common Odds Ratio of 1.00, 95% CI = 0.87-1.15) Post-imaging analysis revealed 46.5% of the undifferentiated patients had a hemorrhagic stroke Prehospital reduction in BP did reduce the odds of poor functional outcome in hemorrhagic stroke patients alone (Common Odds Ratio 0.75, 95% CI 0.60-0.92) Those with ischemic stroke had increased odds of poor functional outcome (Common Odds Ratio 1.30, 95% CI 1.06-1.60) Bottom line: it is challenging to identify the stroke type in the prehospital setting and therefore not necessarily helpful to treat the blood pressure References 1. Ren X, Zhang C, Xu P, et al. Intensive Ambulance-Delivered Blood- Pressure Reduction in Hyperacute Stroke. New England Journal of Medicine. 2024;390(20):1862-1872. doi:10.1056/NEJMoa2314741 Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit  

Contributor: Taylor Lynch MD Educational Pearls: Overview: Sympathomimetic drugs mimic the fight or flight response, affecting monoamines such as dopamine, norepinephrine, and epinephrine Limited therapeutic use, often abused. Types: Amphetamines: Methamphetamine, Adderall, Ritalin, Vyvanse MDMA (Ecstasy) Cocaine (Both hydrochloride salt & free based crack cocaine) Theophylline (Asthma treatment) Ephedrine (For low blood pressure) BZP, Oxymetazoline (Afrin), Pseudoephedrine (Sudafed) MAO Inhibitors (treatment-resistant depression) Mechanisms: Act on adrenergic and dopaminergic receptors. Cocaine blocks dopamine and serotonin reuptake. Methamphetamines increase stimulatory neurotransmitter release MAO Inhibitors prevent neurotransmitter breakdown. Symptoms: Agitation, tachycardia, hypertension, hyperactive bowel sounds, diuresis, hyperthermia. Severe cases: Angina, seizures, cardiovascular collapse. Diagnosis: Clinical examination and history. Differentiate from anticholinergic toxidrome by diaphoresis and hyperactive bowel sounds. Tests: EKG, cardiac biomarkers, chest X-ray, blood gas, BMP, CK, coagulation studies, U-tox screen. Treatment: Stabilize ABCs, IV hydration, temperature monitoring, benzodiazepines. Avoid beta-blockers due to unopposed alpha agonism. Whole bowel irrigation for body packers; surgical removal if packets rupture. IV hydration for high CK levels. Observation period often necessary. Recap: Mimic sympathetic nervous system. Key symptoms: Diaphoresis, hyperactive bowel sounds. Treatment: Supportive care, benzodiazepines. Use poison control as a resource. References: Costa VM, Grazziotin Rossato Grando L, Milandri E, Nardi J, Teixeira P, Mladěnka P, Remião F. Natural Sympathomimetic Drugs: From Pharmacology to Toxicology. Biomolecules. 2022;12(12):1793. doi:10.3390/biom12121793 Kolecki P. Sympathomimetic Toxicity From Emergency Medicine. Medscape. Updated March 11, 2024. https://emedicine.medscape.com/article/818583-overview Williams RH, Erickson T, Broussard LA. Evaluating Sympathomimetic Intoxication in an Emergency Setting. Lab Med. 2000;31(9):497-508. https://doi.org/10.1309/WVX1-6FPV-E2LC-B6YG Summarized by Steven Fujaros | Edited by Jorge Chalit, OMSIII