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Core EM - Emergency Medicine Podcast

Core EM - Emergency Medicine Podcast

著者： Core EM
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Core EM Emergency Medicine PodcastCore EM 衛生・健康的な生活 身体的病い・疾患
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  • Episode 228: Tickborne Illnesses

    Episode 228: Tickborne Illnesses
    2026/10/19
    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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    1分未満
  • Episode 227: Diarrhea

    Episode 227: Diarrhea
    2026/09/24
    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 bowel. Small, painful, frequent stools suggest colon.Volume status: urine output, dark concentrated urine, dry mucous membranes, orthostatic symptoms.Exposures: recent foods, travel, sick contacts, occupation (animal or sewage contact), recent antibiotics or hospitalization.Timing after ingestion: <6 hours suggests a preformed toxin (Staph aureus, Bacillus cereus), 8–16 hours suggests Clostridium perfringens, and >16 hours suggests viral or other bacterial causes.High-risk hosts: pregnancy → Listeria, cirrhosis → Vibrio, hemochromatosis → Yersinia (both siderophilic).Exam: volume status plus a real abdominal exam. A soft belly does not end the evaluation. Who Gets Testing Ask first whether the result will change anything. If the patient is going home on supportive care, a stool study often just generates a callback.Test when the patient is likely to be admitted or is higher risk: febrile, hypovolemic, elderly (roughly >70), known cardiac disease, immunocompromised, IBD, or pregnant.Bloodwork is not routine. Send a BMP and CBC for significant hypovolemia, persistent vomiting, bloody stool, or the elderly and comorbid.Routine cultures cover Salmonella, Campylobacter, Shigella. Ask the lab specifically for Vibrio, Yersinia, Aeromonas, or Listeria.Know your multiplex GI PCR panel. At many shops it already includes C. diff, so ordering it separately is redundant. One call to your lab settles this.Bloody stool → send Shiga toxin. Bloody but fecal WBC negative → consider amoebiasis.Bloody diarrhea plus anemia, thrombocytopenia, or a rising creatinine → think HUS, especially in young children.Antibiotics or hospitalization within 3 months → C. diff moves up the differential.Neutropenic patient on active chemotherapy → consider typhlitis (enterocolitis of the cecum).CT only for peritoneal signs or focal tenderness. It is not part of the routine workup. Management Oral rehydration solution is the mainstay for anyone tolerating PO — water, salt, sugar. Preferred over sports drinks and flavored electrolyte powders, which are not ORS-formulated. A commercial ORS packet is ideal, and the home recipe works when you do not have one. One liter of water, six level teaspoons of sugar, half a teaspoon of salt.IV fluids for severe hypovolemia, intractable vomiting, or if labs are being drawn anyway.Most non-bloody, non-traveler’s diarrhea does not need antibiotics.Suspected Shiga toxin E. coli: no antibiotics. Lysing the organism releases toxin and raises HUS risk.When empiric coverage is warranted: azithromycin for severe inflammatory diarrhea, fever, dysentery risk, or fluoroquinolone resistance. Otherwise cipro or levofloxacin, and IV ceftriaxone if PO is not tolerated.Traveler’s diarrhea: most cases are self-limited. Reserve antibiotics for moderate to severe illness, and reach for azithromycin given widespread quinolone resistance in South and Southeast Asia.Confirmed C. diff: oral vancomycin 125 mg four times daily for 10 ...
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    15 分
  • Episode 226: Superwarfarin Toxicity

    Episode 226: Superwarfarin Toxicity
    2026/08/11
    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 rodenticidesExamples: brodifacoum, bromadiolone, difenacoum, chlorophacinoneMuch more potent + far longer acting than warfarinMOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation↓ factors II, VII, IX, X + proteins C/SHighly lipophilic → extensive tissue/fat sequestration + slow redistributionEffect can persist weeks-months; occasionally much longerNot dialyzableExposure: large acute ingestion OR repeated low-dose exposureSource may be unclear, concealed, or initially unknown Presentation Often delayed + insidiousSevere coagulopathy may precede obvious bleedingEarly: epistaxis, gingival bleeding, bruising/ecchymoses, hematuriaClassic clue: well-appearing pt + extraordinarily abnormal coagulation studiesSevere bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleedingRP bleed → flank/back pain ± CVA tenderness Labs & Diagnosis PT/INR: profoundly elevated, sometimes beyond assay rangeaPTT: may also be markedly prolonged with severe factor depletionCBC/plts: often initially preserved unless major blood loss/other processLFTs: often relatively normalProfound INR + no warfarin + preserved liver function → think superwarfarinCT based on bleeding site; CT A/P for suspected RP hemorrhageConfirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass specDo NOT delay resuscitation/treatment for confirmatory testing Elevated INR: Differential Superwarfarin exposureWarfarin toxicitySevere vitamin K deficiency: malnutrition, malabsorption, prolonged abxLiver failure/cirrhosisDICAcquired factor deficiency/inhibitor Helpful discriminators Liver dz → abnormal hepatic profile/clinical contextDIC → ↓ plts, ↓ fibrinogen, ↑ D-dimerNo warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential ED Management Major/Life-Threatening Bleeding Goal: replace factors NOW + restore endogenous synthesis4F-PCC = preferred factor replacement Fast, predictable correctionSmall volumeNo thawing/type matching FFP if PCC unavailable Slower + large volume/TACO risk Give IV vitamin K concurrentlyPCC = immediate bridge; vitamin K = sustained factor synthesisRecheck INR + clinical bleeding responseRepeat PCC generally not routine; reassess before redosing No Major Bleeding, Critical INR Vitamin K is primary therapyHigh-dose PO vitamin K often preferred when clinically stableAvoid unnecessary PCC/FFP if no major bleedingSerial INR monitoring essential Poison Control Call earlyHelps with: Confirmatory testingVitamin K dosingDuration of therapyMonitoring/taper strategyOutpatient planning The Long Game This is NOT standard warfarin toxicityVitamin K requirements may persist for monthsDischarge only when bleeding controlled + clinically stable on oral regimenClose serial INR follow-up mandatorySlowly taper vitamin K under laboratory guidanceStopping too early → rebound INR elevation + recurrent bleeding Take Home Points Massive unexplained INR + relatively normal liver function → think superwarfarinMajor bleeding → 4F-PCC + IV vitamin KExpect prolonged vitamin K therapy + meticulous INR follow-up Read More
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    14 分
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