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Core EM - Emergency Medicine Podcast

Core EM - Emergency Medicine Podcast

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  • 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 mins
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