Core EM - Emergency Medicine Podcast copertina

Core EM - Emergency Medicine Podcast

Core EM - Emergency Medicine Podcast

Di: Core EM
Ascolta gratuitamente

Offerte di stagione | 0,99 €/mese per i primi 3 mesi

A seguire 9,99 €/mese – si applicano condizioni. Puoi disdire mensilmente.
Core EM Emergency Medicine PodcastCore EM Disturbo fisico e malattia Igiene e vita sana
Episodi
  • Episode 227: Diarrhea

    Episode 227: Diarrhea
    Sep 24 2026
    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 ...
    Mostra di più Mostra meno
    15 min
  • Episode 226: Superwarfarin Toxicity

    Episode 226: Superwarfarin Toxicity
    Aug 11 2026
    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
    Mostra di più Mostra meno
    14 min
  • Episode 225: Group A Strep

    Episode 225: Group A Strep
    Jul 14 2026
    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...
    Mostra di più Mostra meno
    Meno di 1 minuto
adbl_web_anon_alc_button_suppression_t1
Ancora nessuna recensione