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Core EM - Emergency Medicine Podcast

Core EM - Emergency Medicine Podcast

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 Core EM Emergency Medicine PodcastCore EM Disturbo fisico e malattia Igiene e vita sana
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  • Episode 230: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

    Episode 230: Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
    Nov 2 2026
    DRESS in the ED: Diagnosing this delayed drug reaction behind rash and shock & how to manage. Hosts: Nir Lavi-Romer, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/DRESS.mp3 Download Leave a Comment Tags: Allergy + Immunology, Critical Care, Dermatology, DRESS, Rash 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 DRESS vs SJS/TEN vs Anaphylaxis at a Glance DRESSSJS/TENAnaphylaxisOnset after drug~2–8 wks; hrs–days on re-exposure~1–3 wksMin–hrsSkinDiffuse, infiltrated erythema; blisters rareDusky lesions → blisters, sloughingUrticaria, flushingNikolskyNegPosNegMucosaMild, if anySevere, hemorrhagicAngioedemaBig cluesFacial edema, lymphadenopathy, eos, organ injuryEpidermal detachmentWheeze, ↓BP, GI sxResponse to epiNoneNoneExpected Background Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): drug exposure → rash + systemic involvement (liver, kidneys, lungs, heart, pancreas)Systemic dz is what makes pts critically ill → think ICU. Mortality up to ~10% in retrospective series; 1.7% in a prospective multinational registry (SEAIC 2020)Eosinophilia not universal → also called drug-induced hypersensitivity syndrome (DIHS)Rare, but can’t-miss Pathophysiology Type IV, T-cell–mediated delayed hypersensitivity; Th2 cytokines (IL-5) recruit eosinophils (SEAIC 2020)Not IgE-mediated → don’t expect an anaphylaxis-style response to epiExact cause unclear. Two leading contributors: Genetics: HLA polymorphisms, e.g., HLA-A*31:01 w/ carbamazepine DRESS (CPIC 2018)Herpesvirus reactivation (HHV-6, HHV-7, EBV, CMV) in up to ~75%; cause vs consequence still unsettled The Culprit Drugs 200+ drugs implicated; a short list does most of the damage: Allopurinol, vancomycin, TMP-SMX & other sulfasAromatic antiepileptic drugs (AEDs): phenytoin, phenobarbital, carbamazepine, lamotrigineLess common: NSAIDs, antiretrovirals, ACEi, CCBs, atypical antipsychotics Latency: classically 2–8 wks after starting the drug; re-exposure → hrs to days (SEAIC 2020)Med rec has to look back: SEAIC treats any drug started <6 mo & stopped <14 d before onset as a compatible suspect Clinical Presentation Rash: itchy morbilliform eruption → diffuse, confluent, infiltrated erythema, often >50% BSA; can be tender. Blisters & sloughing rareFacial edema: classicLymphadenopathy (LAD), feverMucosa: mild, ~half of pts, usually 1 site (mouth/pharynx)Organs: liver most common (~75%) & the leading cause of death; kidney (esp. allopurinol), lungs, heart (myocarditis), pancreas (SEAIC 2020)Sick end of the spectrum: shock, hypoxemia, AMS, multi-organ failure Diagnosis Clinical Dx Built on hx (new drug, wks back) + exam. Labs & biopsy support it; neither should hold up tx Sorting the Dangerous Rashes Anaphylaxis: min–hrs after exposure; urticaria, angioedema. No response to epi → reconsiderStevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN): blisters, sloughing, severe hemorrhagic mucosal dz, Nikolsky posPemphigus vulgaris: flaccid bullae; Nikolsky & Asboe-Hansen posNecrotizing soft tissue infection: pain out of proportion, crepitusNikolsky: pressure on skin → epidermis shears/sloughsAsboe-Hansen: pressure on a bulla → fluid spreads laterally past its borderPoints to DRESS: delayed onset after a new drug, facial edema, LAD, no blistering/sloughing, mild mucosal dz Labs Gauge severity/end-organ damage, not the dx. Can be normal early → don’t use to excludeSEAIC admission panel: CBC w/ diff (eos, atypical lymphs), LFTs/INR, Cr + UA, lipase, CK, troponin (SEAIC 2020)Delphi: ECG for all; troponin/BNP only if cardiac involvement suspected (Delphi consensus 2024). Crashing pt → send the full panel up frontDelphi grades severity on liver, kidney & blood derangement; any other organ involved = severe (Delphi consensus 2024) RegiSCAR Score Quantifies suspicion (MDCalc): <2 excluded, 2–3 possible, 4–5 probable, >5 definite (SEAIC 2020)Early on, eos may not have appeared & a course ≥15 d can’t be confirmed (scores −1) → a low ED score doesn’t exclude Management Stop the Drug, Hold New Ones Stop every possible culpritCareful adding drugs to a sick pt; SEAIC specifically avoids empiric abx (esp. amoxicillin) & NSAIDs acutely (SEAIC 2020)Aromatic AED cross-reactivity 40–80% → avoid phenytoin, phenobarbital, lamotrigine, oxcarbazepine; benzos considered safe Resuscitate ABCs first, like any crashing ptEpi for any concern of ...
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    10 min
  • Episode 229: Iron Poisoning

    Episode 229: Iron Poisoning
    Oct 26 2026
    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 StageTimingWhat’s happening1 · GI30 min–6 hDirect corrosive GI injury; abd pain, vomiting2 · Latent6–24 hGI sx improve; iron redistributing into tissues3 · Shock / acidosis6–72 hProfound metabolic acidosis → shock, MSOF4 · Hepatotoxicity12–96 hHepatotoxicity → fulminant liver failure5 · GI scarring2–8 wksGastric outlet obstruction, GI tract scarring The Case 31M w/ hx depression, anxiety; found minimally responsive at home by familyEMS: HR 67, SpO2 96% on 2 L NC, BP 46/21; withdraws to pain, not opening eyes → 2 L IVF + push-dose epi en routeED: BP ↑ to 90/61, other VS unchanged; dried vomit on lips/shirt; breathing comfortably, protecting airwayPOC VBG: pH 7.24, pCO2 33, pO2 25, HCO3 14, lactate 2.5ECG: NSR, otherwise unremarkable → get an ECG in any possible toxic ingestionAdditional 30 mL/kg bolus + norepi gttFamily arrives → bottle of iron pills under the pt’s bed Pathophysiology Free iron = multisystem oxidative injuryPrimary mechanism: free radical generation + lipid peroxidation → damages cellular and mitochondrial membranes throughout the bodyProfound metabolic acidosis via 2 routes: uncoupled oxidative phosphorylation → anaerobic metabolism → lactate; Fe³⁺ reacts w/ water → releases 3 H⁺ → excess acidDirect mucosal necrosis in the gut (corrosive injury)Negative inotrope on the myocardium → hypotension, cardiogenic shock in large ingestions Clinical Stages Classic progression after large ingestions; stages overlap and pts can present anywhere along the timelineStage 1, GI (30 min–6 h): direct GI tract injury; abd pain, vomiting. Persistent vomiting = very sensitive indicator of a serious ingestionStage 2, latent (6–24 h): GI sx improve, but iron is redistributing into the tissues → ongoing damageThe latent-phase trap: pts look like they’re turning the corner right before they crump. Contrast: pts never symptomatic >6 h after ingestion are unlikely to develop toxicity (AAPCC 2005); GI sx that improve ≠ never symptomaticStage 3, shock (6–72 h): tissue iron → profound acidosis → shock, MSOFStage 4, hepatotoxicity (12–96 h): hepatotoxicity → fulminant liver failureStage 5, GI scarring (2–8 wks): gastric outlet obstruction, GI tract scarring from the initial corrosive injury Diagnosis / Workup Imaging Emergent plain-film abd XR in any suspected iron ingestion → intact adult iron tabs are radiopaqueConfirms pills still in the stomach/GI tract → helps decide on WBINegative XR ≠ no ingestion: chewables, liquid formulations and already-dissolved tabs often don’t show up Serum Iron Draw 4–6 h post-ingestion for regular formulations, ~8 h for extended releaseOften hard to interpret → time of ingestion and formulation frequently unknown>500 mcg/dL → serious systemic toxicity>1,000 mcg/dL → very significant mortality Elemental Iron Math Toxicity tracks the elemental iron dose, not the mass of the pill SaltElemental FePer 325 mg tabFerrous sulfate~20%~65 mgFerrous fumarate~33%106 mgFerrous gluconate~12%~36–38 mg <20 mg/kg elemental Fe → usually asymptomatic20–60 mg/kg → GI sx likely; systemic toxicity possible, esp. at the upper end>60 mg/kg → threshold for serious toxicity, possible deathAAPCC out-of-hospital guideline: refer to an ED for ≥40 mg/kg elemental Fe (adult ferrous salt formulations) or severe/persistent sx; any self-harm ingestion → ED regardless of amount (Manoguerra 2005)AAPCC: children’s chewable vitamins w/ iron, and unintentional carbonyl iron or polysaccharide-iron complex ingestions → home obs w/ f/u Management Decontamination Activated charcoal: no role. Iron is a metal → doesn’t bind; ↑ aspiration and other complicationsWhole bowel irrigation (WBI) = main decontamination strategy, esp. w/ pills on XR → flush tablets before further GI injury and systemic absorptionPEG-ELS (polyethylene glycol electrolyte solution) until rectal effluent is clear; large volume → often via NG tubePEG-ELS rates: 1.5–2 L/h adolescents/adults (as on air); peds 500 mL/h (9 mo–6 y), 1 L/h (6–12 y) (AACT/EAPCCT 1997)AACT...
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    12 min
  • Episode 228: Tickborne Illnesses

    Episode 228: Tickborne Illnesses
    Oct 19 2026
    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, Ehrlichiosis & Babesiosis at a Glance LymeAnaplasmosisEhrlichiosisBabesiosisOrganismB. burgdorferi (spirochete)A. phagocytophilumE. chaffeensisB. microti (protozoan)VectorI. scapularisI. scapularisLone star tickI. scapularisAttachment to transmit≥36–48 hCan be <24 hNo dataMostly >48 hKey clueEM rash↓WBC, ↓plt, ↑LFTs↓WBC, ↓plt, ↑LFTsHemolysis, ↓pltSmear—Morulae in neutrophilsMorulae in monocytesIntra-RBC parasites, Maltese crossConfirmClinical (EM)Smear, PCRSmear, PCRSmear, PCRTreatDoxy × 10–14 dDoxy × 10 dDoxy until ≥3 d afebrileAtovaquone + azithro × 7–10 d Background Ixodes scapularis (deer tick) = primary US vector for Lyme, anaplasmosis, and babesiosis; I. pacificus on the West Coast. Ehrlichiosis → lone star tick (Amblyomma americanum), not the deer tick (CDC MMWR 2016)Why attachment time matters: B. burgdorferi lives in the tick midgut → multiplies and migrates to the salivary glands only after feeding starts → built-in delay Single infected nymph: 0 of ~90 animals infected at 24 h, ~10% by 48 h, ~70% by 72 h (Eisen 2018)Anaplasma can transmit w/in 24 h. Babesia ≈ Lyme, not faster: earliest 36 h, mostly after 48 h. True speedster = Powassan virus (w/in 15 min). Attachment time by hx is often unreliable (IDSA Lyme 2020) Regional variation: US Lyme = B. burgdorferi; Europe = mostly B. afzelii, B. garinii → different clinical picture. Systemic sx w/ EM more common in the US: ~65% vs ~37% in Europe (IDSA Lyme 2020) Lyme: The Rash and the Serology Erythema Migrans EM in ~70–80% of infections; appears at the bite site 3–30 d post-bite (avg ~7 d) (CDC)Usually not a bull’s-eye → most early EM is uniformly redExpanding erythematous patch + endemic area = Lyme until proven otherwise Serology 2-tier: EIA or IFA → IgM/IgG Western blot (or modified 2-tier: 2 EIAs, no blot)Early localized dz → often seronegative (as few as ~20% positive w/in 1 wk of noticing EM) → EM in an endemic area = clinical dx, per IDSA (IDSA Lyme 2020) The Other Three: Labs and the Smear Babesiosis Hunt for hemolytic anemia: ↓Hgb, ↑LDH, ↓haptoglobin, reticulocytosis; ↓plt and ↑LFTs commonSmear: intraerythrocytic parasites. Maltese cross (tetrad) = pathognomonic but infrequent; ring forms more common. PCR more sensitive than smear (IDSA Babesiosis 2020) Anaplasmosis & Ehrlichiosis Near-identical presentations. Classic triad: leukopenia, thrombocytopenia, transaminitisSmear: morulae → Anaplasma in neutrophils, Ehrlichia in monocytes. Smear is insensitive → whole-blood PCR confirms (CDC MMWR 2016) Management Post-Bite Prophylaxis (Lyme) High-risk bite only → all 3: Ixodes tick, highly endemic area, attached ≥36 h (by engorgement or hx); give w/in 72 h of removal (IDSA Lyme 2020)Doxycycline 200 mg PO × 1 (adults); 4.4 mg/kg PO × 1, max 200 mg (kids)Landmark RCT: 482 pts w/ I. scapularis bites → EM 0.4% doxy vs 3.2% placebo, efficacy 87% (Nadelman 2001)Kids <8: doxy traditionally avoided (tooth staining), but a relative CI only → benefit wins. No staining seen w/ short courses; CDC/AAP: doxy = drug of choice for tickborne rickettsial dz at any age (CDC MMWR 2016) Active Disease Early localized Lyme: Doxycycline 100 mg PO BID × 10–14 d (CDC: shorter end preferred; IDSA: 10 d)No 1st-gen cephalosporins (e.g., cephalexin) → ineffective vs B. burgdorferiEM vs cellulitis unclear → cefuroxime 500 mg PO BID × 14 d covers both. If using amoxicillin-clavulanate, dose it TID (500/125 mg) to match the TID amoxicillin regimen (CDC EM Treatment)Anaplasmosis: same doxy dose × 10 d (covers incubating Lyme). Ehrlichiosis: same dose until ≥3 d afebrile, usually 5–7 d total (CDC MMWR 2016)Babesiosis: Atovaquone 750 mg PO BID + azithromycin 500 mg day 1, then 250 mg daily × 7–10 d (IDSA Babesiosis 2020) Severe Babesiosis Inpatient: Atovaquone 750 mg PO BID + azithromycin 500 mg IV daily → all-PO once sx subside, 7–10 d total. Alternative: IV clindamycin + PO quinine (CDC Babesiosis)Consider RBC exchange transfusion for parasitemia...
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