
195 episodes

Core EM - Emergency Medicine Podcast Core EM
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4.5 • 199 Ratings
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Core EM is dedicated to bringing Emergency Providers all things core content Emergency Medicine. In the true spirit of Emergency Medicine our content is available to anyone, anywhere, anytime.
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Hyperkalemia
We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)
Hosts:
Brian Gilberti, MD
Jonathan Kobles, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3
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Tags: Renal Colic
Show Notes
Introduction
* Background
Physiology:
Normal range and the significance of deviations (>5.5 mEq/L)
Epidemiology:
Prevalence of hyperkalemia in the ER
ESRD missed HD → ECG, monitor
Causes / Risk Factors
Causes
Kidney Dysfunction, Medications, Cellular Destruction, Endocrine Causes, Pseudohyperkalemia
High-Risk Medications:
Antibiotics: Bactrim, antifungals
Calcineurin inhibitors
Beta-blockers
ACE/ARB
K+ Sparing diuretics
NSAIDs
Digoxin
SUX – high risks in neuromuscular disease
Lab errors, hemolysis in samples
VBG vs Chem accuracy
When to repeat a hemolyzed sample
2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).
Clinical Presentation / eval
Symptomatic vs. Asymptomatic:
“First symptom of hyperkalemia is death”
If severe, ascending muscle weakness → paralysis
Point at which patients experience symptoms depends on chronicity
>7 mEq/L if chronic and can be lower if acute
Hyperkalemia can be a cause of non-specific GI symptoms
EKG Changes:
ECG findings may be the first marker the ER doc gets that something is wrong
Typical changes:
Peaked T-waves, shortened QT
Lengthening of PR interval and QRS duration
Bradycardia / Junctional rhythm
Hyperkalemia can produce bradycardia without other ECG findings
Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), -
Vasopressors
We go over the essential and complex topic of vasopressors in the ED.
Hosts:
Brian Gilberti, MD
Catherine Jamin, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3
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Tags: Critical Care
Show Notes
Introduction
* Host: Brian Gilberti, MD
* Guest: Catherine Jamin, MD
* Associate professor of Emergency Medicine at NYU Langone Health
* Vice Chair of Operations
* Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine
* Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED
What Are Vasopressors and When to Use Them
* Two primary mechanisms to increase blood pressure:
* Increasing systemic vascular resistance via vasoconstriction
* Increasing cardiac output via augmenting inotropy and chronotropy
* Indicators for vasopressor use:
* MAP 65
* Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min
* Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic)
* Pros: Can be infused peripherally via large bore IV
Vasopressin
* Mechanism: Activates V1a receptors causing vasoconstriction
* Dose: Fixed, non-titratable dose of 0.04 units/min
* Situational Preference: Second-line in septic shock
* Concerns: Potential for peripheral ischemia
Phenylephrine
* Mechanism: Stimulates alpha-1 receptors causing vasoconstriction
* Starting Dose: 100 mcg/min, titrate to MAP >65
* Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation
* Concerns: Increases afterload, can worsen low cardiac output states
Epinephrine
* Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors
* Starting Dose: 5-10 mcg/min, titrate to MAP >65
* Situational Preference: Anaphylactic shock, septic cardiomyopathy
* Limitations: Can induce tachycardia, may elevate lactate levels
Escalation Strategy in Refractory Shock
* Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine
* Consider POCUS, lactate, central venous saturation, and acid-base status -
Septic Joint in Children
We discuss the diagnosis and management of septic arthritis in the pediatric population.
Hosts:
Brian Gilberti, MD
Ellen Duncan, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Joint_in_Children.mp3
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Tags: Infectious Diseases, Pediatrics
Show Notes
General
Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis
Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition.
Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint.
Workup
Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain.
Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation.
Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach.
The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000.
1 criterion met = 3% probability of septic arthritis
2 criteria met = 40% probability of septic arthritis
3 criteria met = 93% probability of septic arthritis
4 criteria met = 99+% probability of septic arthritis
If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available.
Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies.
Management -
Podcast 186.0: Hypocalcemia
A quick primer on hypocalcemia in the ED.
Hosts:
Joseph Offenbacher, MD
Audrey Bree Tse, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3
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Tags: calcium, Critical Care, Endocrine
Show Notes
Swami’s CoreEM Post
Hypocalcemia Repletion:
* IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq
* For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours
* For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve
References:
* Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298.
* Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209.
* Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis
* Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166.
* Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53.
* Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/
* Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163.
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Podcast 185.0: Anticoagulation Reversal
How and when to reverse anticoagulation in the bleeding EM patient.
Hosts:
Joe Offenbacher, MD
Audrey Bree Tse, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3
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3 Comments
Tags: Anticoagulation, Critical Care, Resuscitation
Show Notes
Coagulation Cascade:
Algorithm for Anticoagulated Bleeding Patient in the ED:
Indications for Anticoagulation Reversal:
References:
Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001
Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008.
Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643
Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317.
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Episode 184.0 Ludwig’s Angina
A primer on this airway/ ID/ ENT emergency.
Hosts: Joe Offenbacher MD, A Bree Tse, MD
https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3
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2 Comments
Tags: Airway, ENT, Infectious Diseases
Show Notes
References:
Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168.
Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327.
Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074.
Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254.
http://www.emdocs.net/ludwigs-angina-2/
Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163.
Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306.
Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506.
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Customer Reviews
The Best Emergency Medicine Podcast!
Excellent coverage of both pediatric and adult emergency medicine topics. Artfully designed with a strong foundation in evidence based medicine.
Anticoagulant reversal bad sound
As previously mentioned, great content, but the sound quality was incredibly quiet on this episode. Such that I couldn’t listen to it in the car. Keep up the good work otherwise.
Can’t hear it
I have my volume turned all the way up and still can’t hear what they’re saying