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Emergency Medical Minute

Emergency Medical Minute
Emergency Medical Minute
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  • Episode 974: ACE Inhibitor Angioedema
    Contributor: Ricky Dhaliwal, MD Educational Pearls: Angioedema in anaphylaxis Histamine and mast cell-mediated pathway Treatment: First line: epinephrine for vasoconstriction and bronchodilation Second line: H1 and H2 antihistamines such as Benadryl and famotidine ACE inhibitor-induced angioedema Different pathway from anaphylaxis ACE inhibitor-induced angioedema is mediated by bradykinins Therefore, anaphylaxis medications are not beneficial in patients with ACE inhibitor-induced angioedema Leading cause of drug-induced angioedema in the US Patients most commonly present with swelling of the lips, tongue, or face Treatment: Airway management: varies depending on the severity and progression of the presentation If awake nasointubation is required, LMX is a 5% lidocaine water-soluble solution that provides anesthesia to the oropharynx Medications: Icatibant is a synthetic bradykinin B2-receptor antagonist that can be used in acute treatment Tranexamic acid (TXA) inhibits the plasmin-dependent formation of bradykinin, but the data on this treatment are mixed and limited Fresh frozen plasma (FFP) is thought to degrade high levels of bradykinin with subsequent resolution of angioedema Discontinue ACE inhibitor References Bork K, Wulff K, Hardt J, Witzke G, Staubach P. Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy. J Allergy Clin Immunol. 2009 Jul;124(1):129-34. doi: 10.1016/j.jaci.2009.03.038. Epub 2009 May 27. PMID: 19477491. Bova M, Guilarte M, Sala-Cunill A, Borrelli P, Rizzelli GM, Zanichelli A. Treatment of ACEI-related angioedema with icatibant: a case series. Intern Emerg Med. 2015 Apr;10(3):345-50. doi: 10.1007/s11739-015-1205-9. Epub 2015 Feb 10. PMID: 25666515. Karim MY, Masood A. Fresh-frozen plasma as a treatment for life-threatening ACE-inhibitor angioedema. J Allergy Clin Immunol. 2002 Feb;109(2):370-1. doi: 10.1067/mai.2002.121313. PMID: 11842313. Pathak GN, Truong TM, Chakraborty A, Rao B, Monteleone C. Tranexamic acid for angiotensin-converting enzyme inhibitor-induced angioedema. Clin Exp Emerg Med. 2024 Mar;11(1):94-99. doi: 10.15441/ceem.23.051. Epub 2023 Aug 1. PMID: 37525579; PMCID: PMC11009700. Simons FE. First-aid treatment of anaphylaxis to food: focus on epinephrine. J Allergy Clin Immunol. 2004 May;113(5):837-44. doi: 10.1016/j.jaci.2004.01.769. Erratum in: J Allergy Clin Immunol. 2004 Jun;113(6):1039. Dosage error in article text. PMID: 15131564. Summarized by Meg Joyce, MS2 | Edited by Meg Joyce & Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/
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  • Emergency Medicine Cases with Dr. Barlock
    Contributors: Travis Barlock MD, Jeffrey Olson MS4 Feel free to use the cases below for your own practice. All of the scenarios are completely made up and designed to hit several teaching points. Case 1 25 M, presents to the ED with chest pain. Stabbing, started a few hours ago, substernal. Thinks it is GERD. After 2-3 minutes, pain worsens and radiates to the back. VS: BP 125/50 (Right arm 190/110). HR 120. RR of 18. Sat 98% on RA. Additional VS: Temp of 37.2, height of 6’5”, BMI of 18. PMH: None, doesn’t see a doctor. Meds: None FH: Weird heart thing (Mitral Valve Prolapse), weird lung thing (spontaneous pneumothorax), tall family members with long fingers and toes Physical Exam: Cards: Diastolic decrescendo at the RUSB, diminished S2. UE pulses are asymmetric, LE pulses are asymmetric, carotid pulses are asymmetric, BP is asymmetric MSK: Knees, elbows, and wrists are hypermobile. Imaging: CXR #1 normal, #2 widened mediastinum (no read yet but shows widened mediastinum), POCUS shows small effusion CTA/MRA doesn’t come back until after the case.  ECG: Sinus Tach Labs: NT-proBNP 500 pg/mL D-Dimer: 7000 ng/L CBC: Hemoglobin: 13.5 g/dL, WBC: 20,000/µL, Platelets: 250,000/µL Chem 7: Na 138, K, 5.7, Cl 102, Bicarb 17, BUN 45, Creatinine: 3.5 mg/dL, Glucose: 180 LFTs: Albumin 2.4, Total protein 5.5, ALP: 140, AST: 3500, ALT: 2800, TBili: 3.2, DirectBili: 2.4, Ca: 7.8 LDH: 2200 PT: 20.5, INR: 2.2, Fibrinogen: 170 5th gen High-Sensitivity Troponin: Lactate: 7 mmol/L VBG: pH 7.22, paCO2 28, bicarb 15 Notes: Can have patient crash somewhere in middle and show 2nd xray   Case 2:  A 67-year-old female is brought to the ED by her daughter due to progressive weakness, confusion, and fatigue that have worsened over the past week. Unable to get out of bed and has become increasingly lethargic. Also having some nausea, constipation. The daughter denies any preceding illness, recent trauma, or travel. Does not know her meds but will head home to get them after talking with you.  VS: BP 88/55 mmHg, HR 110, RR 20, O2 Sat 98% on room air. Additional VS: Temp 36.8°C. PMH: Hypertension, osteoarthritis, and depression. Physical exam: General: Thin, somnolent but arousable. HENT: Dry mucous membranes Neuro: Confused, A&Ox1 (self), hyporeflexia Labs (Includes many that would not return in the ED in case you want to take this case forward to the floor) CBC: WBC 9,500, Hb 16.5, Hct: 50%, Platelets 220,000 Chem7: Na 129, K 2.1, Cl 95, HCO3 34, Creatinine 1.6, BUN 40, Glucose 115 LFTs: normal Magnesium: 1.1 Calcium: 10.8 mg/dL (corrects to 12.8) iCal: 3.2 Phosphate: 2.3 mg/dL Albumin: 2 BUN:Cr ratio: 25 VBG: pH: 7.49, PaCO2 45, HCO3: 34 Lactate: 2.8 Serum Osmolality: 276 mOsm/kg (Osmolal gap of 2) Urine Osmolality: 550 mOsm/kg Urine Sodium (UNa): 10 mEq/L (low). Urine Potassium (UK): 25 mEq/L (elevated). Urine Chloride (UCl): 12 mEq/L (low). Urine Magnesium (UMg): 20 (Elevated). Urine Calcium (UCa): 50 in 24 hrs (Low) 100 cc of urine with foley FeNa Plasma renin activity: 15 mg/mL/hr (elevated), Aldosterone: 25 ng/dL (Elevated), ADH: Elevated, Diuretic screen: Positive for thiazides PTH: 8 (low), HsTrop: 32, Cortisol and ACTH: Normal. EKG: Hypokalemia features CXR: Normal Renal US: shows stones Improves with fluids Note: Can have daughter return with med list at some point including HCTZ, ibuprofen, and sertraline   Case 3: Patient Presentation EMS Report: A 27-year-old male involved in a high-speed motorcycle collision is brought to the emergency department by EMS. The patient was found unconscious at the scene with evidence of severe thoracic and extremity trauma. He was intubated en route for airway protection due to altered mental status (GCS 7).  VS: HR 130, BP 90/60, RR: bagging at 12 bpm, satting 88% on 100% FiO2  Primary Survey Airway: Endotracheal tube in place. Breathing: Decreased breath sounds on the left side with visible chest asymmetry and paradoxical chest wall movement. Circulation: Mottled extremities noted, with significant deformity of the right thigh. Pulses are diminished in the right leg Disability: GCS remains 7 (E1 V2 M4). Pupils equal and reactive. Exposure: Full-body examination reveals an open fracture of the right femur, multiple abrasions, and bruising over the chest wall. Vent alarms Peak Inspiratory Pressure (PIP) 40 cm H₂O (elevated) Plateau Pressure (Pplat) 35 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 55 mmHg High-Pressure Alarm Triggering frequently Glucose 120 CBC: Hgb 8.9, Hct 27, WBC 14.2, platelets 220,000 VBG: pH 7.28, pCO2 33, bicarb 18, lactate 4.5 CXR with tension pneumothorax  Patient improves after chest tube, pigtail catheter, or needle decompression. Ready to be transferred upstairs and O2 starts tanking again Vent alarms- second episode Peak Inspiratory Pressure (PIP) 35 cm H₂O (elevated) Plateau Pressure (Pplat) 30 cm H₂O (elevated) EtCO₂ (End-Tidal CO₂) 20 mmHg HR: 140, satting 84%, temp 38.5,  ABG: pH 7.32, pCO₂ 30 mmHg, pO₂ 60 mmHg on 100% FiO₂, HCO₃⁻ 18 mmol/L (hypoxemia and metabolic acidosis). D-dimer: Elevated Thrombocytopenia: Platelets 90,000/µL. US shows blown right ventricle ECG shows new RBBB CT PE: Ground glass opacities, consolidation, centrilobular nodules, septal thickening, and fat-attenuating lesions. Note: Management is largely supportive care so once the diagnosis is made, end the case.   References Carroll MF, Schade DS. A practical approach to hypercalcemia. Am Fam Physician. 2003 May 1;67(9):1959-66. PMID: 12751658. Coelho SG, Almeida AG. Marfan syndrome revisited: From genetics to the clinic. Rev Port Cardiol (Engl Ed). 2020 Apr;39(4):215-226. English, Portuguese. doi: 10.1016/j.repc.2019.09.008. Epub 2020 May 18. PMID: 32439107. Palmer BF. Metabolic complications associated with use of diuretics. Semin Nephrol. 2011 Nov;31(6):542-52. doi: 10.1016/j.semnephrol.2011.09.009. PMID: 22099511. Reed MJ. Diagnosis and management of acute aortic dissection in the emergency department. Br J Hosp Med (Lond). 2024 Apr 30;85(4):1-9. doi: 10.12968/hmed.2023.0366. PMID: 38708978. Roberts DJ, Leigh-Smith S, Faris PD, Blackmore C, Ball CG, Robertson HL, Dixon E, James MT, Kirkpatrick AW, Kortbeek JB, Stelfox HT. Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review. Ann Surg. 2015 Jun;261(6):1068-78. doi: 10.1097/SLA.0000000000001073. PMID: 25563887. Rothberg DL, Makarewich CA. Fat Embolism and Fat Embolism Syndrome. J Am Acad Orthop Surg. 2019 Apr 15;27(8):e346-e355. doi: 10.5435/JAAOS-D-17-00571. PMID: 30958807.   Produced by Jeffrey Olson, MS4 Special thanks to Evan Fisch MD Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/   Donate: https://emergencymedicalminute.org/donate/
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  • Episode 973: Meningitis Retention Syndrome
    Contributor: Travis Barlock MD Educational Pearls: Meningitis retention syndrome is a relatively novel and rare clinical condition Aseptic meningitis + acute urinary retention One study reports an incidence of about 8% in patients with acute aseptic meningitis Clinical presentation Typical meningeal symptoms including fever, stiff neck, and headache Urinary retention occurs about one week after initial symptoms Potential pathophysiology Immune-mediated dysfunction of the central nervous system Detrusor muscle underactivity from inflammation of the spinal cord Management Supportive care Bladder decompression References Hiraga A, Kuwabara S. Meningitis-retention syndrome: Clinical features, frequency and prognosis. J Neurol Sci. 2018;390:261-264. doi:10.1016/j.jns.2018.05.008 Pellegrino F, Funiciello E, Pruccoli G, et al. Meningitis-retention syndrome: a review and update of an unrecognized clinical condition. Neurol Sci. 2023;44(6):1949-1957. doi:10.1007/s10072-023-06704-0 Summarized & Edited by Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/  
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  • Episode 972: Hepatic Encephalopathy
    Contributor: Alec Coston, MD Educational Pearls: Hepatic encephalopathy (HE) is defined as a disruption in brain function that results from impaired liver function or portosystemic shunting. Manifests as various neurologic and psychiatric symptoms such as confusion, inattention, and cognitive dysfunction Although ammonia levels have historically been recognized as important criteria for HE, the diagnosis is ultimately made clinically. An elevated ammonia level lacks sensitivity and specificity for HE Trends in ammonia levels do not correlate with disease improvement or resolution A 2020 study published in the American Journal of Gastroenterology evaluated 551 patients diagnosed with hepatic encephalopathy and treated with standard therapy Only 60% of patients had an elevated ammonia level, demonstrating the limitations of ammonia levels However, a normal ammonia level in a patient with concern for HE should raise suspicion for other pathology. In patients with cirrhosis presenting with neuropsychiatric symptoms, consider HE as the diagnosis after excluding other potential causes of altered mental status (i.e., Seizure, infection, intracranial hemorrhage) The primary treatment is lactulose Works by acidifying the gastrointestinal tract. Ammonia (NH₃) is converted into ammonium (NH₄⁺), which is poorly absorbed and subsequently eliminated from the body Also exerts a laxative effect, further enhancing elimination References: Haj M, Rockey DC. Ammonia Levels Do Not Guide Clinical Management of Patients With Hepatic Encephalopathy Caused by Cirrhosis. Am J Gastroenterol. 2020 May;115(5):723-728. doi: 10.14309/ajg.0000000000000343. PMID: 31658104.\ Lee F, Frederick RT. Hepatic Encephalopathy-A Guide to Laboratory Testing. Clin Liver Dis. 2024 May;28(2):225-236. doi: 10.1016/j.cld.2024.01.003. Epub 2024 Jan 30. PMID: 38548435. Vilstrup, Hendrik1; Amodio, Piero2; Bajaj, Jasmohan3,4; Cordoba, Juan1,5; Ferenci, Peter6; Mullen, Kevin D.7; Weissenborn, Karin8; Wong, Philip9. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study Of Liver Diseases and the European Association for the Study of the Liver. Hepatology 60(2):p 715-735, August 2014. | DOI: 10.1002/hep.27210 Weissenborn K. Hepatic Encephalopathy: Definition, Clinical Grading and Diagnostic Principles. Drugs. 2019 Feb;79(Suppl 1):5-9. doi: 10.1007/s40265-018-1018-z. PMID: 30706420; PMCID: PMC6416238. Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons & Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/  
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  • Episode 971: Calcium Pretreatment for Diltiazem in AFib with RVR
    Contributor: Taylor Lynch, MD Educational Pearls: What is atrial fibrillation with rapid ventricular response (AFib with RVR) and how does it differ from atrial fibrillation (AFib)? AFib is an abnormal heart rhythm in which the heart has disorganized atrial electrical activity. This causes the atria to quiver with only select signals being conducted through the Atrioventricular (AV) Node to reach the ventricles and result in ventricular contraction. Often described as “irregularly irregular”, a patient's EKG will present with no discernible P-waves, and irregular R-R intervals. AFib with RVR is distinguished from AFib when the patient’s ventricular rate is greater than 100-110 beats per minute in AFib with RVR. What is the treatment for AFib with RVR? Diltiazem is considered one of the first line therapeutic agents in the treatment of AFib with RVR. Diltiazem inhibits L-Type calcium channels in the AV Node, reducing the amount of signals conducted to the ventricles, thus reducing the ventricular rate. Why pretreat patients receiving Diltiazem for AFib with RVR with calcium? While diltiazem inhibits cardiac calcium channels, it may also cause peripheral vasodilation, resulting in diltiazem-induced hypotension. A recent study found that this hypotension can be blunted by pretreating with 1-2g IV Calcium Chloride (IV Calcium Gluconate can be used in the ED). Calcium is thought to peripherally stabilize the vascular smooth muscle, preventing vasodilation without impacting the desired calcium channel blocker action at the AV node. Key takeaways? In combination with slower pushes of diltiazem for patients in AFib with RVR (AFib with ventricular rate >100-110 bpm) with borderline low blood pressures, 1-2 g of IV Calcium Gluconate can combat diltiazem induced hypotension peripherally without negating the cardiac effect of diltiazem to reduce the heart rate.  References 2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(1):e1-e156. doi:10.1161/CIR.0000000000001193 Az A, Sogut O, Dogan Y, et al. Reducing diltiazem-related hypotension in atrial fibrillation: Role of pretreatment intravenous calcium. Am J Emerg Med. 2025;88:23-28. doi:10.1016/j.ajem.2024.11.033 Summarized by Dan Orbidan, OMS2 | Edited by Dan Orbidan and Jorge Chalit, OMS4 Get your tickets to Tox Talks Event, Sept 11, 2025: https://emergencymedicalminute.org/events-2/ Donate: https://emergencymedicalminute.org/donate/  
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