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Core EM - Emergency Medicine Podcast: Daily Summaries Delivered
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Core EM Emergency Medicine Podcast
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- 4 days ago12 min
Episode 229: Iron Poisoning
Iron overdose in the ED: five stages, elemental iron math, decontamination, and deferoxamine. Hosts: Brian Chastain, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Iron_Poisoning.mp3 Download Leave a Comment Tags: Toxicology Podcast Video Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 Iron Poisoning Stages at a Glance Stage Timing What’s happening 1 · GI 30 min–6 h D
- 1 weeks ago
Episode 228: Tickborne Illnesses
Tickborne illnesses in the ED: attachment time, the rash, the smear, prophylaxis, & treatment. Hosts: Samantha Nakos, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Tickborne_Illnesses_1_.mp3 Download Leave a Comment Tags: Babesiosis, Ehrlichiosis, Infectious Diseases, Lyme Disease, Tick-Borne Illnesses Podcast Video Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 Lyme, Anaplasmosis, Ehr
- Sep 24, 202614 min
Episode 227: Diarrhea
Acute diarrhea in the ED: stool testing, treatment, and a spotlight on Cyclospora. Hosts: Neya Vishwanath, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Diarrhea.mp3 Download Leave a Comment Tags: Gastrointestinal, Gastrointestinal Diseases Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below. Course Highlights: Credit: 12.5 AMA PRA Category 1 Credits™ Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. Cost: Free for NYU Learners $250 for Non-NYU Learners Click Here to Register and Begin Module 1 Framing the Patient Acute is <2 weeks, persistent is 2–4 weeks, chronic is >30 days. Most acute diarrhea is self-limited and needs only supportive care. Stool cultures are positive in only 2–6% of unselected patients. Yield rises with >4 stools/day and longer duration. The ED job is not to name the organism. It is to find volume depletion, rule out the dangerous mimic, and decide who needs testing, antibiotics, or admission. Don’t-Miss Mimics Diarrhea is a symptom, not a diagnosis. In anyone who looks sick, gastroenteritis is a diagnosis of exclusion. Abdominal catastrophes: mesenteric ischemia (pain out of proportion, vascular risk factors), early appendicitis, partial obstruction with overflow stool, diverticulitis. Systemic disease presenting through the gut: sepsis from another source, DKA, adrenal insufficiency. Fulminant C. diff or toxic megacolon: distension, fever, tachycardia, peritonitis. The diarrhea may actually stop as the colon dilates. GI bleeding masquerading as dark diarrhea, and in women of childbearing age, ectopic pregnancy. History & Exam Duration, frequency, and appearance. Watery and high-volume suggests small
- Aug 11, 202613 min
Episode 226: Superwarfarin Toxicity
Superwarfarin toxicity: recognition, reversal, and prolonged vitamin K therapy. Hosts: Mac Josh Reandelar, DO Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Superwarfarin_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Toxicology & Pathophysiology Long-acting vitamin K antagonists (LA-VKAs), developed as potent rodenticides Examples: brodifacoum, bromadiolone, difenacoum, chlorophacinone Much more potent + far longer acting than warfarin MOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation ↓ factors II, VII, IX, X + proteins C/S Highly lipophilic → extensive tissue/fat sequestration + slow redistribution Effect can persist weeks-months; occasionally much longer Not dialyzable Exposure: large acute ingestion OR repeated low-dose exposure Source may be unclear, concealed, or initially unknown Presentation Often delayed + insidious Severe coagulopathy may precede obvious bleeding Early: epistaxis, gingival bleeding, bruising/ecchymoses, hematuria Classic clue: well-appearing pt + extraordinarily abnormal coagulation studies Severe bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleeding RP bleed → flank/back pain ± CVA tenderness Labs & Diagnosis PT/INR: profoundly elevated, sometimes beyond assay range aPTT: may also be markedly prolonged with severe factor depletion CBC/plts: often initially preserved unless major blood loss/other process LFTs: often relatively normal Profound INR + no warfarin + preserved liver function → think superwarfarin CT based on bleeding site; CT A/P for suspected RP hemorrhage Confirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass spec Do NOT delay resuscitation/treatment for confirmatory testing Elevated INR: Differential Superwarfarin exposure Warfarin toxicity Severe
- Jul 14, 2026
Episode 225: Group A Strep
Group A strep in the pediatric ED: from strep throat to invasive disease and toxic shock. Host: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Group_A_Strep.mp3 Download Leave a Comment Tags: Infectious Diseases, Pediatrics Show Notes Background Group A strep = Streptococcus pyogenes — gram-positive organism that colonizes the pharynx, but also the perianal and genital mucosa (worth remembering when the source isn’t the throat). Extremely common. The episode cites an estimated ~289 million cases/yr of strep pharyngitis in children 5–14 (NIH). For a U.S.-specific, verifiable anchor: the CDC estimates strep throat drives ~5.2 million outpatient visits/yr in people <65. No true beta-lactam resistance. GAS remains uniformly susceptible to penicillin and amoxicillin. Note this is not true for macrolides/clindamycin — roughly 1 in 3 invasive isolates are now erythromycin/clindamycin resistant. Pathophysiology — the throughline Exotoxins (superantigens) tie the whole spectrum together — they drive scarlet fever, streptococcal toxic shock syndrome (STSS), and are implicated in the Kawasaki overlap discussed below. The organism is the same from a sore throat to a life-threat; what changes is host response and toxin burden. Clinical Presentation Core findings: tonsillar inflammation/exudate, tender anterior cervical lymphadenopathy, fever. Classic strep tells to hunt for: Palatal petechiae Strawberry tongue Perioral pallor Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes. Extra
- Jun 8, 2026
Episode 224: Kidney Stones
A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED. Hosts: Brian Gilberti, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3 Download Leave a Comment Tags: Kidney Stones, Urology Show Notes 1. CLINICAL CORE & PHYSIOLOGIC FRAMEWORK Epidemiologic Risk Profiles Lifetime incidence parameters hover around 1 in 11, presenting with a prominent male sex skew. Peak demographic manifestation concentrated within the 30–60 age band. High-yield temporal parameter: 50% recurrence vector within a 5-year post-initial-insult window. Mineralogical Composition Vectors Calcium oxalate crystals represent the predominant structural matrix. Struvite configurations (magnesium ammonium phosphate matrix) account for 1–2% of cohorts. Struvite stones function explicitly as infection-driven configurations secondary to upper tract proliferation; higher distribution index noted in female cohorts. Etiological & Modifiable Relational Dynamics Profound systemic dehydration or low baseline fluid throughput states. High-sodium diet structures and heavy animal-protein consumption loads. Positive genetic/familial history variables. Relative risk modulation: Each variable independently operates to expand baseline risk by a factor of 2x to 3x. Pathophysiologic Symptom Complexes Acute, sudden-onset, maximum-intensity (10/10) unilateral flank pain. Classic structural radiation vector tracking downward toward the ipsilateral groin/genitourinary dermatomes. Distinctive behavioral marker: Renal colic pacing/writhing behavior with zero antalgic position availability. Concomitant autonomic triggers: Nausea and emesis manifest in 50% of acute presentations. Physical Exam Discordance Metrics Severe subjective distress contrasted with a characteristically soft, completely non-tender abdominal palpation exam. CVA tenderness is completely variable and lacks reliable negative predictive value. Atypical Presentation Classifications Vague, poorly localized abdominal pain presentations occurring in up to 20% of active cases. Isolated lower urinary tract irritative signs including acute frequency or severe urgency. Incidental
- May 15, 20269 min
Episode 223: Thyroid Storm
Diagnosis, workup, and the four-step treatment protocol for thyroid storm. Hosts: Annaliese Elam, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid_Storm.mp3 Download Leave a Comment Tags: Critica Care, Endocrine, Thyroid Storm Show Notes I. Pathophysiology & Diagnosis Definition: Life-threatening hypermetabolic state resulting from decompensated thyrotoxicosis. Hormonal Profile: Absolute levels of total T₄/T₃ often mirror uncomplicated thyrotoxicosis; storm is driven by rapid rate of rise, increased catecholamine sensitivity, or increased free T₄/T₃ concentrations. Clinical Presentation: Hyperpyrexia (e.g., 104.2°F) Tachycardia/Arrhythmias (e.g., 155 bpm) Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism Warm, moist skin Precipitating Events: Infection, trauma, or surgery Parturition Abrupt cessation of antithyroid medications Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of Thyroid Storm 25–44: Suggestive of impending storm < 25: Storm unlikely Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness. II. Laboratory & Ancillary Findings Thyroid Panel: Characteristically low TSH with elevated free T₄ and T₃. Metabolic Abnormalities: Mild hyperglycemia (catecholamine-induced insulin inhibition) Mild hypercalcemia Elevated LFTs and leukocytosis Cardiovascular: EKG may show sinus tachycardia or atrial fibrillation with rapid ventricular response. III. Management: The Four-Step Blocking Strategy Step 1: Sympathetic Blockade (Beta Blockers) Agent of Choice: Propranolol Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃. Dosing: PO: 60–80 mg every 4–6 hours IV: 0.5–1 mg over 10 minutes Critical Pitfall: Avoid in patients with acute decompensated heart failure with systolic dysfunction; risk of cardiovascular collapse. Step 2: Inhibition of Hormone Synthesis
- Apr 7, 2026
Episode 222: Local Anesthetic Systemic Toxicity (LAST)
We discuss this ominous complication of providing local anesthesia. Hosts: https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3 Download Leave a Comment Tags: Critical Care, Toxicology Show Notes I. Pathophysiology & Mechanisms Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption. Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue. Agent Profile: Bupivacaine (High Risk) Highly lipophilic with high protein binding. “Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole. Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility. Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin). Contributing Factors: Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity. Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold. II. Risk Assessment & Prevention Patient-Specific Risk Factors Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance). Body Composition: Low muscle mass/frailty (decreased volume of distribution). Organ Dysfunction: Hepatic: Reduced metabolism of amide LAs. Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold. Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade. Pregnancy: Increased sensitivity to cardiotoxicity. Procedural Risk Factors Vascularity of Site (Highest to Lowest Risk): Intercostal blocks (highest absorption rate). Caudal/Epidural. Interfascial plane blocks (e.g., TAP block). Psoas compartment/Sciatic. Brachial plexus. Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection. Prevention Mandates Weight-Based Dosing: Lidocaine (Plain): Max 4.5 mg/kg. Lidocaine (with Epi): Max 7 mg/kg. Bupivacaine: Max 2.5–3 mg/kg. Incremental Injection: 3–5 mL aliquots with frequent aspiration. Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase >10 bpmor SBP increase >15 mmHg). III. Clinical Presentation Neurologic Phase (Early to Late) Subjective: Metallic taste, tinnitus, circumoral numbness/tingling. Objective: Visual disturbances, agitation, confusion, tremors. Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea. Note: Early phases are often masked in patients receiving midazolam or propofol. Cardiovascular Phase Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase. Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks. Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole. Contractility: Profound, refractory hypotension and cardiogenic shock. IV. Immediate Management Algorithm Goal: Prevent hypoxia/acidosis and sequester the toxin. 1. Initial Actions Stop Injection: Immediately halt all LA administration. Call for Help: Specify “LAST Protocol” and “Intralipid Kit.” Airway Management: 100% O2. Hyperventilate slightly if needed to counter respiratory acidosis. Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST). 2. Seizure Control First-line: Benzodiazepines (e.g., Midazolam). Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression). Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity. 3. Lipid Emulsion Therapy 20% Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability). Bolus: 1.5 mL/kg IV over 1 minute. Infusion: 0.25 mL/kg/min immediately following bolus. If Instability Persists: Repeat bolus (up to 2 times). Increase infusion to 0.5 mL/kg/min. Upper Limit: ≈12 mL/kg total dose. 4. Modified ACLS Epinephrine: Use low doses (<1 mcg/kg) to avoid worsening arrhythmias and interfering with lipid rescue. Antiarrhythmics: Amiodarone is preferred. CONTRAINDICATED: Lidocaine: (Class Ib antiarrhythmic—will worsen toxicity). Vasopressin: Associated with poor outcomes in animal LAST models. Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression. Refractory Arrest: Early consultation for ECMO or Cardiopulmonary Bypass (CPB). V. Differential Diagnosis for the Peri-Procedural Patient High Spinal: Ascending sensory/motor block, profound sympathectomy (hypotension/bradycardia). Anaphylaxis: Urticaria, wheezing (rare with amides, more common with esters). Air/Gas Embolism: Sudden dyspnea, “mill-wheel” murmur, acute right heart strain. Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or
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