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 ...
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    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
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    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...
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  • Episode 224: Kidney Stones

    Episode 224: Kidney Stones
    Jun 8 2026
    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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  • Episode 223: Thyroid Storm

    Episode 223: Thyroid Storm
    May 15 2026
    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” hyperthyroidismWarm, moist skin Precipitating Events: Infection, trauma, or surgeryParturitionAbrupt cessation of antithyroid medications Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of Thyroid Storm25–44: Suggestive of impending storm< 25: Storm unlikelyNote: 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 hypercalcemiaElevated 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: PropranololMechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃.Dosing: PO: 60–80 mg every 4–6 hoursIV: 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 (Thionamides) Agent of Choice: Propylthiouracil (PTU) preferred over Methimazole in life-threatening storm.Mechanism: Blocks synthesis of new hormone and inhibits peripheral T₄-to-T₃ conversion (decreases T₃ by ~45% in 24 hours).Dosing: 200–250 mg PO every 4 hours Step 3: Inhibition of Hormone Release (Iodine) Agents: Potassium iodide (SSKI) or Lugol’s solutionCritical Timing: Must wait at least 60 minutes AFTER thionamide administration.Rationale: Immediate iodine administration provides substrate for new hormone synthesis (Wolff-Chaikoff effect bypass), potentially worsening thyrotoxicosis. Step 4: Inhibition of Peripheral Conversion & Adrenal Support Agent: Glucocorticoids (Hydrocortisone)Mechanism: Inhibits peripheral T₄ to T₃ conversion and treats potential relative adrenal insufficiency.Dosing: 300 mg IV loading dose, followed by 100 mg IV every 8 hours IV. Supportive Care & Avoidance Measures Hyperpyrexia Management: Acetaminophen is the standard of careAvoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels Volume Resuscitation: Aggressive IV fluids; patients are often profoundly dehydratedMay require 3–5 liters of isotonic crystalloid per 24 hours Take Home Points I. Diagnostic Essentials Clinical Diagnosis: Based on hyperpyrexia, cardiovascular dysfunction, and altered mentation.Key Differentiator: Altered mentation (agitation, delirium, psychosis) is often the sole finding distinguishing “storm” from “compensated” thyrotoxicosis.Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of storm.25–44: Suggests impending storm.< 25: Storm unlikely.Note: High sensitivity, low specificity (e.g., hyperthyroid + flu can score > 45). Triggers: Infection, trauma, parturition, or abrupt cessation of antithyroid drugs. II. The Four-Step Blocking Strategy Beta Blockade (Propranolol): Dose: 60–80 mg PO q4–6h or 0.5–1 mg IV over 10 min.Action: Blocks symptoms and inhibits peripheral T4 to T3 conversion.Caution: Avoid in acute decompensated heart failure with systolic dysfunction. Thionamides (PTU): Dose: 200 to 250 mg every four hours. (note: some resources suggest a loading dose beforehand)Action: Preferred over methimazole; blocks new hormone synthesis and peripheral T4 to T3 conversion. Iodine (SSKI/Lugol’s): Timing: Must wait ≥ 60 minutes AFTER thionamide dose.Action: Blocks hormone release.Pitfall: Early iodine provides substrate for new hormone synthesis, worsening the condition. Glucocorticoids (Hydrocortisone): Dose: 300 mg IV load, then 100 mg IV q8h.Action: Blocks conversion and provides adrenal support. III. Critical Supportive Care Hyperpyrexia: Use Acetaminophen. NEVER Use Aspirin: Displaces thyroid hormone from binding proteins, acutely increasing free T4/T3 levels. Volume: Aggressive fluid resuscitation; patients may require 3–5 L/day due to profound dehydration. Read More
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    9 min
  • Episode 222: Local Anesthetic Systemic Toxicity (LAST)

    Episode 222: Local Anesthetic Systemic Toxicity (LAST)
    Apr 7 2026
    We discuss this ominous complication of providing local anesthesia. Hosts: Elaine Jonas, MD Brian Gilberti, MD 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”...
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  • Episode 221: High-Output Heart Failure

    Episode 221: High-Output Heart Failure
    Mar 24 2026
    We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure. Hosts: Nicolas Gonzalez, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3 Download Leave a Comment Tags: Cardiology 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 1. Core Definition & Hemodynamic Profile Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function. Hemodynamic Criteria: Cardiac Index (CI): >4.0 L/min/m2. Cardiac Output (CO): >8 L/min. Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state). The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses. 2. Pathophysiology: The Hemodynamic Paradox Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting). Effective Arterial Blood Volume: Paradoxically low despite high total CO. Neurohormonal Cascade: Activation of Renin-Angiotensin-Aldosterone System (RAAS). Increased Sympathetic Nervous System tone. Increased Antidiuretic Hormone (ADH) secretion. Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion. Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy. 3. Differential Diagnosis: Etiological “Buckets” Category A: Increased Metabolic Demand (Systemic) Hyperthyroidism/Thyrotoxicosis: Direct T3 effects: increased chronotropy/inotropy. Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation. Myeloproliferative Disorders: High cell turnover and increased oxygen consumption drive compensatory CO increase. Sepsis (Hyperdynamic Phase): Cytokine-mediated global vasodilation. Note: Often transient; may transition to sepsis-induced myocardial depression. Category B: Peripheral Vascular Effects (Shunting/Vasodilation) Arteriovenous Fistulas (AVF) / Malformations (AVM): Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population). Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation. Chronic Liver Disease (Cirrhosis): Formation of “spider angiomata” and internal AV shunts. Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide). Thiamine Deficiency (Wet Beriberi): Accumulation of pyruvate/lactate → systemic vasodilation. Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema. Chronic Lung Disease: Hypoxia/Hypercapnia-driven systemic vasodilation. Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output. Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma. 4. Special Focus: Hemodialysis Access-Induced HOHF Physiologic Phases of AVF Creation: Acute Phase: Immediate ↓ SVR. ↑ Stroke volume and Heart Rate (SNS-mediated). Endothelial shear stress → Nitric Oxide release → further arterial dilation. Subacute Phase (Days to 2 Weeks): RAAS-driven volume expansion. ↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP). Natriuretic peptide surge (BNP/ANP) peaks around Day 10. Chronic Phase (Weeks to Months): Adaptive hypertrophy. Decompensation occurs when dilation exceeds contractility limits. 5. Point-of-Care Physical Exam & Maneuvers Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF): Maneuver: Manually compress the AVF (or inflate cuff to >50 mmHg above SBP) for 30 seconds. Positive Result: Reflexive bradycardia or a transient rise in systemic BP. Significance: Confirms the shunt is a major contributor to the cardiac workload. Peripheral Pulse Assessment: Water Hammer Pulses: Rapid upstroke and collapse. Quincke’s Pulse: Visible capillary pulsations in the nail beds. Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries. Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs). 6. Diagnostic Workup (Technical Targets) POCUS / Echocardiography: Left Ventricle: Hyperdynamic function; EF typically >60%. Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2). IVC: Plethoric with minimal respiratory variation. Doppler: High ...
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  • Episode 220: Post-ROSC Care

    Episode 220: Post-ROSC Care
    Mar 3 2026
    We explore how to refine and optimize care in the vital minutes following ROSC. Hosts: Jonathan Elmer, MD, MS Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3 Download Leave a Comment 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 I. Phase 1: Stabilization (Minutes 0–10) The “Rearrest” Window & Pathophysiology High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC. Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside. Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse. Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations). Immediate Resuscitative Actions Vascular Access: Transition rapidly from IO to reliable IV access within 1–2 minutes. Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes. Vasoactive “Bridge”: Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration. Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing). Physician-Specific Task: Arterial Line: Goal: Placement within 5 minutes of ROSC. Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure. Utility: Immediate detection of rearrest and beat-to-beat titration of vasopressors. II. Phase 2: Diagnostic Workup (Minutes 10–40) Etiology Epidemiology ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates). Common Etiologies:Respiratory: COPD, pneumonia, mucus plugging. Cardiac: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure. Neurological: Intracranial hemorrhage (SAH/ICH), status epilepticus (4–5%). Metabolic: Dialysis-related disarray/hyperkalemia. Toxicology: Overdose accounts for ~10% of cases in urban centers. The “Broad Net” Strategy “Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers. Pan-Scan Protocol: Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis. Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest). Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility. Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia. III. Hemodynamic & Respiratory Targets Mean Arterial Pressure (MAP) Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion.Clinical Target: Aim for MAP >80 mmHg. The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence. Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow. Ventilation and Oxygenation PaCO2 Management: Target: High-normal to slightly hypercarbic (45–55 mmHg). Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%. PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral. IV. Neurological Prognostication & Communication The “Stunned” Brain Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail. Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury. Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours. Family Engagement Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation. Psychological Impact: Significantly reduces PTSD, anxiety, and depression in...
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