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Core EM - Emergency Medicine Podcast

Core EM - Emergency Medicine Podcast

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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 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
  • Episode 225: Group A Strep

    Episode 225: Group A Strep
    2026/07/14
    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 petechiaeStrawberry tonguePerioral pallor Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes.Extrapharyngeal clues: kids commonly present with abdominal pain or headache even when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache. Diagnosis / Workup Centor / Modified (McIsaac) Score Centor Score (Modified/McIsaac) — MDCalcOne point each: fever, tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough. The Modified (McIsaac) version adds age.Developed and validated in adults (≥16). It is not reliable in young children — don’t lean on it in peds the way you would in an adult.For reference, McIsaac culture-positive probabilities: ~2.5% (0 criteria), 6.5% (1), 15% (2), 32% (3), 56% (4). Testing Rapid PCR — high sensitivity and specificity; increasingly the front-line test.Rapid antigen detection test (RADT) — highly specific but less sensitive. Per IDSA, a negative RADT in a child/adolescent should be backed up with a throat culture (culture is the more sensitive gold standard). Backup culture is not required in adults. Who not to test Generally don’t test/treat children <3 — acute rheumatic fever is rare in this group.Exception: the symptomatic young child with a close contact recently diagnosed with strep. Management First-line: amoxicillin 50 mg/kg once daily, max 1 g/dose. GAS stays beta-lactam susceptible (penicillin and amoxicillin remain treatments of choice per IDSA 2012).IM penicillin G / benzathine (bicillin) for kids who can’t tolerate oral meds — one shot, done.Return to school: after one full day of treatment (~12–24 h), provided afebrile and feeling well.Contact prophylaxis: Pharyngitis — routine prophylaxis of asymptomatic contacts is not standard; consider it for households with recurrent infection or a history of rheumatic fever.Invasive GAS — more aggressive. Prophylaxis is recommended for household contacts who are immunosuppressed, pregnant, post-recent-surgery, or have an open wound (CDC). The Bounce-Back / Treatment Failure The kid who finishes amox and is back a week later. Sort into three buckets: Chronic carrier — GAS carriage in children runs 2–20%. Carriers test positive but are asymptomatic, with low risk of transmission or complications. Don’t chase them.New infection.True treatment failure → ask why: The shield effect — the throat is co-colonized with beta-lactamase producers (Staph aureus, H. influenzae, Moraxella) that degrade amoxicillin before it can act, effectively shielding the GAS.This is NOT true resistance — the strep is still beta-lactam susceptible; the neighbors are the problem.Fix: switch to a beta-lactamase–stable agent — amoxicillin-clavulanate or a first-generation cephalosporin. Complications Suppurative: peritonsillar abscess, sinusitis, meningitis, bacteremia.Non-suppurative: Acute rheumatic fever — typically 1–5 wks post-infection; Jones criteria (AHA 2015 revision · ACC summary · CDC).Post-infectious glomerulonephritis (PIGN) — several weeks out; hematuria / “Coca-Cola” urine. Note strep impetigo can also seed PIGN. The pearl: we treat strep to prevent rheumatic fever — but treatment does NOT prevent PIGN. Invasive Group A Strep (iGAS) Why it’s on the radar Rates have been climbing since 2014, and preliminary 2023 data hit a 20-year high (CDC). A CDC/ABCs analysis flagged a roughly 3-fold pediatric...
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  • Episode 224: Kidney Stones

    Episode 224: Kidney Stones
    2026/06/08
    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 ClassificationsVague, 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 & Asymptomatic Dynamics Silent intrarenal or ureteral stones found incidentally.Longitudinal tracking demonstrates up to 33.3% of initially asymptomatic cohorts convert to fully symptomatic renal colic within a multi-year tracking window. 2. EXCLUSION DIAGNOSES & CRITICAL PATHWAY RED FLAGS Vascular Mimics: AAA rupture/expansion. This is a mandatory exclusion pathway in elderly cohorts presenting with acute flank or back pain. Physical tracking requires active exploration for an expansile, pulsatile abdominal mass.Gynecologic Emergencies: Ruptured ectopic pregnancy. Demands universal screening protocols via rapid beta-hCG testing in all female patients of childbearing potential presenting with lower abdominal/pelvic localization.Infectious Upper Tract Decompensation: Acute uncomplicated pyelonephritis. Differentiated via persistent high spikes, high fevers, systemic shaking chills, and profound pyuria.Genitourinary Structural Crises: Acute testicular torsion. Mandates a thorough, explicit scrotal/testicular structural exam if the flank pain radiates into the scrotum.Gastrointestinal and Adnexal Torsional Confounds: Acute appendicitis variants, acute mesenteric/bowel ischemia, and ovarian torsion syndromes. 3. LABORATORY TESTING & PHYSIOLOGIC EVALUATION Urinalysis Interpretation Nuances Microscopic or gross hematuria presents in approximately 66% to 90% of acute cases.Critical Pathological Caveat: Complete absence of hematuria documented in 20% to 33.3% of confirmed, acute obstructing ureteral stones.Diagnostic rule: A pristine urinalysis with zero red blood cells is entirely insufficient to exclude acute ureterolithiasis. Urinary pH as a Composition Clue Consistently low urinary pH parameters (pH < 5.5) point strongly toward a uric acid crystalline composition.Elevated urinary pH parameters (pH > 7.5) indicate the presence of urease-producing microbial pathogens, pointing toward a struvite infection stone. Infectious Screening Metrics Active tracking for marked pyuria, positive leukocyte esterase, and bacterial nitrites to rule out an obstructed, infected upper urinary tract system. BMP Immediate quantification of baseline serum creatinine to establish accurate eGFR values.Targeting detection of post-renal AKI from bilateral obstruction, unilateral obstruction in a single functioning kidney, or severe volume depletion. CBC Evaluation for marked leukocytosis.Physiologic Nuance: Mild-to-moderate white blood cell count elevations frequently represent non-specific stress demargination driven by severe pain and repetitive vomiting.High-grade white blood cell shifts demand immediate exclusion of systemic bacteremia or an infected, obstructed urinary system. Adjunctive Lab Pathways Rapid qualitative urine hCG testing.Reflex urine ...
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