Core EM - Emergency Medicine Podcast

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 rodenticides Examples: brodifacoum, bromadiolone, difenacoum, chlorophacinone Much more potent + far longer acting than warfarin MOA: inhibits VKORC1 → ↓ vitamin K recycling → impaired γ-carboxylation ↓ factors II, VII, IX, X + proteins C/S Highly lipophilic → extensive tissue/fat sequestration + slow redistribution Effect can persist weeks-months; occasionally much longer Not dialyzable Exposure: large acute ingestion OR repeated low-dose exposure Source may be unclear, concealed, or initially unknown Presentation Often delayed + insidious Severe coagulopathy may precede obvious bleeding Early: epistaxis, gingival bleeding, bruising/ecchymoses, hematuria Classic clue: well-appearing pt + extraordinarily abnormal coagulation studies Severe bleeding: RP hemorrhage, ICH, spinal hemorrhage, tamponade, major GI/GU bleeding RP bleed → flank/back pain ± CVA tenderness Labs & Diagnosis PT/INR: profoundly elevated, sometimes beyond assay range aPTT: may also be markedly prolonged with severe factor depletion CBC/plts: often initially preserved unless major blood loss/other process LFTs: often relatively normal Profound INR + no warfarin + preserved liver function → think superwarfarin CT based on bleeding site; CT A/P for suspected RP hemorrhage Confirm: specialized serum/blood testing for long-acting anticoagulants, typically chromatography/mass spec Do NOT delay resuscitation/treatment for confirmatory testing Elevated INR: Differential Superwarfarin exposure Warfarin toxicity Severe vitamin K deficiency: malnutrition, malabsorption, prolonged abx Liver failure/cirrhosis DIC Acquired factor deficiency/inhibitor Helpful discriminators Liver dz → abnormal hepatic profile/clinical context DIC → ↓ plts, ↓ fibrinogen, ↑ D-dimer No warfarin + massive INR + relatively normal LFTs/plts → superwarfarin rises on the differential ED Management Major/Life-Threatening Bleeding Goal: replace factors NOW + restore endogenous synthesis 4F-PCC = preferred factor replacement Fast, predictable correction Small volume No thawing/type matching FFP if PCC unavailable Slower + large volume/TACO risk Give IV vitamin K concurrently PCC = immediate bridge; vitamin K = sustained factor synthesis Recheck INR + clinical bleeding response Repeat PCC generally not routine; reassess before redosing No Major Bleeding, Critical INR Vitamin K is primary therapy High-dose PO vitamin K often preferred when clinically stable Avoid unnecessary PCC/FFP if no major bleeding Serial INR monitoring essential Poison Control Call early Helps with: Confirmatory testing Vitamin K dosing Duration of therapy Monitoring/taper strategy Outpatient planning The Long Game This is NOT standard warfarin toxicity Vitamin K requirements may persist for months Discharge only when bleeding controlled + clinically stable on oral regimen Close serial INR follow-up mandatory Slowly taper vitamin K under laboratory guidance Stopping too early → rebound INR elevation + recurrent bleeding Take Home Points Massive unexplained INR + relatively normal liver function → think superwarfarin Major bleeding → 4F-PCC + IV vitamin K Expect prolonged vitamin K therapy + meticulous INR follow-up Read More

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 petechiae Strawberry tongue Perioral 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) — MDCalc One 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 increase in Colorado/Minnesota in late 2022 (MMWR). Keep it in mind when a child isn’t following the typical strep course or just looks sicker than expected. The spectrum STSS, necrotizing fasciitis, meningitis, bacteremia, peritonitis. Increasingly common and worth highlighting: bone and joint disease — septic arthritis, osteomyelitis — often traveling with pyomyositis. The trap — nonspecific early presentation Symptoms are often nonspecific: fever, “not acting like themselves,” localized pain. Septic joint/osteo may show a limp or focal pain — but not always. When your gut fires, cast a wide net. Workup Blood cultures, CBC, chemistries, CRP, ESR. Imaging — tailor to the suspected site: Suspected joint → start with X-ray + ultrasound. Worried about osteomyelitis or pyomyositis → MRI (the recommended modality for pyomyositis per IDSA SSTI). Management Broad-spectrum: vancomycin + piperacillin-tazobactam (concordant with IDSA SSTI). In shock / STSS: ADD clindamycin or linezolid for toxin suppression — this is on top of vanc/zosyn, not a coverage swap. (IDSA: penicillin plus clindamycin for documented GAS necrotizing infection; consider IVIG in STSS.) The Kawasaki overlap Meaningful overlap between iGAS and Kawasaki disease. Proposed mechanism: strep superantigens activate a shared inflammatory (T-cell) pathway that may contribute to KD; some data suggest kids with iGAS may be at higher risk of developing Kawasaki. Get rheumatology involved early — they’ll want those inflammatory markers and can help sort KD from mimics. Take-Home Points Adult tools don’t translate to peds. Centor was built for ≥16 and is unreliable in young kids — diagnose on exam, the eponyms, and testing. Low threshold to swab the febrile kid with abdominal pain or headache. The bounce-back is a triage problem — carrier (2–20%) vs. new infection vs. true failure. True failure is usually the shield effect (beta-lactamase co-colonizers, not resistance) → switch to amox-clav or a first-gen cephalosporin. Treatment prevents rheumatic fever, NOT PIGN — and impetigo can cause PIGN too. iGAS is rising and hides behind nonspecific symptoms. When your gut fires, work it up broadly and escalate to MRI for osteo/pyomyositis. Treat with vanc + pip-tazo, and in shock add clindamycin/linezolid for toxin suppression. Keep Kawasaki in the differential and call rheum early. Links & References Calculators Centor Score (Modified/McIsaac) for Strep Pharyngitis — MDCalc Guidelines Shulman ST, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update. IDSA / Clin Infect Dis. 2012;55(10):e86–e102. — IDSA · Full text Stevens DL, et al. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update. IDSA / Clin Infect Dis. 2014;59(2):e10–e52. (necrotizing infection, STSS, clindamycin adjunct, MRI for pyomyositis) — IDSA · Full text Gewitz MH, et al. Revision of the Jones Criteria for the Diagnosis of Acute Rheumatic Fever in the Era of Doppler Echocardiography. AHA / Circulation. 2015;131:1806–1818. — Circulation · ACC “10 Points to Remember” CDC Group A Strep Disease Surveillance and Trends (invasive disease rising since 2014; 2023 20-year high) MMWR — Increase in Pediatric Invasive Group A Streptococcus Infections, Colorado and Minnesota, Oct–Dec 2022 Diagnosing Acute Rheumatic Fever (clinician guidance) Read More

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 Classifications Vague, 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 culture execution whenever urinalysis metrics display significant inflammatory profiles or clinical suspicion of UTI is high. 4. IMAGING MODALITIES & ALGORITHMIC CLINICAL SELECTION Non-Contrast CT Diagnostics Gold standard; diagnostic sensitivity and specificity parameters exceed 95% for stones >2 mm. Provides precise quantification of stone diameter (mm), exact localization (proximal, mid, or distal ureter), and degree of secondary hydronephrosis. Excellent structural visualization for detecting or ruling out alternate retroperitoneal, vascular, or intra-abdominal pathologies. Contrast-Enhanced CT Protocols Indicated when alternative intra-abdominal surgical pathology is highly suspected over isolated renal colic. Retains diagnostic capability to identify urinary tract stones >3 mm even within contrast-enhanced phases. NCCT Structural Architecture Limitations Standard stone protocol CT scans are executed in a prone position without IV contrast enhancement. It does not opacify the ureteral lumen. Presents a cumulative radiation exposure penalty when utilized serially across recurrent ED presentations. POCUS / Radiology Ultrasound Direct stone visualization capabilities are modest, operating at approximately 50% to 60% sensitivity, and is highly dependent on anatomical positioning at the extreme proximal ureter or the UVJ. Secondary obstruction tracking: Demonstration of hydronephrosis operates at a high sensitivity of approximately 80%. POCUS Clinical Utility Metrics Eliminates ionizing radiation exposure and allows immediate, rapid real-time execution directly at the patient’s bedside. Confirmation of significant hydronephrosis within a classic clinical presentation yields high post-test probability for stone presence while lowering suspicion for vascular catastrophes like a AAA. KUB Radiography Extremely poor overall diagnostic sensitivity, hovering around 57%. Fails to image radiolucent configurations (pure uric acid matrices) or small stones measuring <5 mm. Avoided in acute ED diagnostic pathways; selectively considered as a low-radiation tracking step in pediatric cohorts or pregnant populations. 5. Ultrasonography versus Computed Tomography for Suspected Nephrolithiasis Core Trial Architecture Large-scale multi-center randomized controlled trial assessing POCUS first vs. Radiology US first vs. NCCT first pathways in acute ED cohorts. Primary Clinical Outcomes No statistically significant variations in missed high-risk alternative diagnoses (AAA, appendicitis, bowel ischemia, or adnexal torsion rates remained rare at ~0.4%). No differences noted in serious adverse event rates, subjective pain-control scores, return ED visits, or overall hospitalization frequencies. Radiation Modulation Impact An ultrasound-first initial strategy reduced cumulative, downstream radiation exposure by approximately 50%. Algorithmic Selection Guidelines Establishes the clinical premise that raw diagnostic sensitivity does not automatically equate to superior clinical utility or better patient outcomes. An ultrasound-first diagnostic pathway paired with selective escalation to NCCT is safe and indicated for recurrent, young, clinically stable cohorts. 6. IMAGING SELECTION MATRIX Indications Favoring an Ultrasound-First Approach Age parameters <35 years to mitigate lifetime cumulative radiation risks. Confirmed, well-documented history of recurrent nephrolithiasis presenting with identical symptoms to prior events. Hemodynamic stability paired with reassuring, classic clinical tracking. Indications Favoring Immediate NCCT Imaging Advanced age parameters. First-time presentation with zero history of stone disease. Atypical clinical presentation or diagnostic uncertainty. Persistent, unmitigated symptoms refractory to standard ED interventions. High pre-test probability of immediate surgical or urological decompression. 7. EMERGENCY PHARMACOTHERAPY & COLIC MANAGEMENT First-Line Analgesic Paradigms NSAIDs: Specifically Ketorolac (Toradol) titrated at 15–30 mg. High-Yield Data Marker: Multiple trials confirm IV NSAIDs provide equivalent pain reduction scores to titrated IV opioids in acute renal colic. Mechanism: Targets localized ureteral smooth muscle spasms and downregulates prostaglandin-mediated hyper-filtration and local tissue inflammation. NSAID Absolute/Relative Contraindications Significantly depressed GFR or active acute renal failure states. Active gastrointestinal hemorrhage risks or history of severe peptic ulcerations. Third-trimester pregnancy. Second-Line Analgesic Titration Intermittent titration of IV opioids (e.g., Morphine) indicated if the NSAID maximum ceiling effect is reached or if explicit contraindications prevent NSAID administration. Antiemetic Adjuvant Therapy Concomitant use of Ondansetron (Zofran) to manage reflex nausea and vomit-induced dehydration. Fluid Resuscitation Realities Targeted IV fluids to correct explicit volume deficits driven by emesis or reduced oral intake. Physiologic Caveat: Aggressive, high-volume fluid hydration does not accelerate stone transit speed or improve the spontaneous passage rate. 8. MEDICAL EXPULSIVE THERAPY (MET) CLINICAL PARAMETERS Pharmacologic Agent Tamsulosin (Flomax) dosed at 0.4 mg orally once daily for a maximum duration of 28 days. Target Efficacy Window Highly specific for distal ureteral stones measuring between 5 mm and 10 mm. Yields modest improvements in spontaneous clearance rates within this specific size band. Literature Controversies A 2015 Lancet randomized controlled trial demonstrated neutral primary endpoints. Subsequent large-scale meta-analyses and network meta-analyses identify a significant signal for benefit, particularly for combinations. Stones Measuring <5 mm MET is generally not indicated or cost-effective. Spontaneous passage rates are high, making the side effect profile of alpha-blockade unjustifiable. Side Effect Profile Orthostatic hypotension, transient dizziness, and retrograde ejaculation. 9. SPONTANEOUS PASSAGE PROBABILITIES Size-Dependent Passage Vectors Stones <5 mm: 70% to 90% spontaneous passage rate. Managed conservatively. Stones 5–10 mm: 50% to 60% spontaneous passage rate. Candidates for MET. Stones >10 mm: <10% spontaneous passage rate. Spontaneous transit is rare; requires urologic intervention. Anatomical Location Passage Vectors Distal Ureter (UVJ area): ~75% spontaneous passage likelihood. Mid-Ureter (Crossing point of iliac vessels): ~60% spontaneous passage likelihood. Proximal Ureter (UPJ to upper third): ~48% spontaneous passage likelihood. Transit Timeline Dynamics Mean passage window spans 2 to 4 weeks for complete structural clearance. Temporal Risk Threshold: Unremitting ureteral obstruction lasting >4 weeks carries an elevated risk of irreversible renal parenchymal injury, persistent AKI, and permanent loss of nephron function. 10. ADMISSION ARCHITECTURE & UROLOGIC CONSULTATION CRITERIA Mandatory Surgical Emergency Decompression Criteria Obstructed Urinary Tract + Concomitant Infection: Co-existence of an obstructing stone and upper tract infection (fever, systemic chills, pyuria, nitrites, leukocytosis) is a urologic emergency. It carries a high risk for rapid progression to pyonephrosis, perinephric abscess, overwhelming urosepsis, and cardiovascular collapse. Requires emergent urologic consultation for surgical retrograde stent placement or percutaneous nephrostomy tube insertion. Refractory Symptom Complexes Intractable pain scores or persistent emesis failing aggressive ED parenteral therapies. High-Risk Patient Anatomy / Physiology Solitary functioning kidney or renal transplant anatomy presenting with acute obstruction (high risk for sudden anuric renal failure). Complete clinical anuria. High-grade, progressive acute kidney injury (AKI) that fails to stabilize following targeted volume resuscitation. Acute obstructing ureterolithiasis manifesting within a pregnant patient. High Structural Stone Burden Stone diameter >10 mm. Spontaneous resolution is unlikely; needs shockwave lithotripsy, ureteroscopy, or specialized stenting. Prolonged Structural Symptoms Documented stone impaction or symptom tracking extending past a 4-week timeline without clear passage. 11. OUTPATIENT DISCHARGE MATRICES & SAFETY NETTING Discharge Criteria Checklists Pain score controlled with oral medications; tolerating adequate PO oral fluids; stable renal function panel; zero systemic or local signs of infection. Outpatient Prescribing Packets Scheduled or high-dose PRN oral NSAIDs plus short-course rescue oral opioids for breakthrough colic episodes. Tamsulosin 0.4 mg once daily if stone localization is distal and diameter measures 5–10 mm. Oral anti-emetics for home management. Discharge Guidance and Counseling Vigorous oral hydration to maintain constant, high volumetric urine throughput. Provide a urine strainer to capture the stone matrix for metabolic and chemical composition testing. Explicit Return Precautions Instruct the patient to return to the ED for temperature spikes, shaking chills, or unmanageable pain spikes. Instruct the patient to return for relentless vomiting preventing fluid retention. Clinical Follow-up Tracking Ensure structured outpatient urology follow-up within a 1- to 2-week window. 12. CLINICAL PEARLS & QUICK-REFERENCE SUMMARY NOTES The Hematuria Diagnostic Confound: Up to 33% of patients with a confirmed obstructing stone will exhibit a completely normal urinalysis with zero RBCs. Never drop nephrolithiasis from the differential based on a negative dipstick. Leukocytosis Interpretation: Severe colic and violent vomiting induce physiological demargination. Treat the overall clinical presentation and temperature curve; do not over-interpret an isolated WBC. Hydrative Fluid Mechanics: Fluids address dehydration from emesis. Over-hydrating a patient in acute colic does not push the stone out faster and may worsen pain by increasing renal capsular hydrostatic pressure. The 4-Week Functional Boundary: Ureteral obstruction lasting longer than 4 weeks requires specialized intervention to prevent permanent nephron damage. Size and Anatomy Rules: A 3 mm stone at the UVJ passes spontaneously in ~90% of cases. An 11 mm stone in the proximal ureter has a <10% clearance rate and requires early urologic involvement. Read More

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” hyperthyroidism Warm, moist skin Precipitating Events: Infection, trauma, or surgery Parturition Abrupt cessation of antithyroid medications Burch-Wartofsky Point Scale (BWPS): ≥ 45: Highly suggestive of Thyroid Storm 25–44: Suggestive of impending storm < 25: Storm unlikely Note: 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 hypercalcemia Elevated 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: Propranolol Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃. Dosing: PO: 60–80 mg every 4–6 hours IV: 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 solution Critical 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 care Avoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels Volume Resuscitation: Aggressive IV fluids; patients are often profoundly dehydrated May 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

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” murmur, acute right heart strain. Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or seizure activity. VI. Post-Resuscitation & Complications Observation: At least 2 hours after a CNS-only event. At least 4–6 hours after a CV event. Lipid Complications: Lab Interference: Lipemia interferes with hemoglobin, creatinine, and electrolyte measurements (draw labs before ILE if possible). Pancreatitis: Rare, delayed complication of high-dose ILE. Fat Embolism/Overload: Rare pulmonary complications. VII. Clinical “Red Flags” for Toxicity Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.” Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise. Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given. Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2​ is as vital as the lipid itself. Read More

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 flow velocities across the AV access if applicable. Laboratory Evaluation: BNP/NT-proBNP: Often markedly elevated (e.g., >70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL. Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb<7–8 g/dL) or myeloproliferative markers. Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis). 7. Management Strategy: A Stepwise Approach Phase 1: Immediate Stabilization (Volume Offloading) Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide). Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion. Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially. Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse. Phase 2: Targeted Therapy (Etiology Specific) Anemia: Transfuse to goal Hgb>7–8 g/dL to reduce demand. Beriberi: High-dose IV Thiamine (100–500 mg). Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole). Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases) Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites. Flow Reduction (Banding): Surgical narrowing of the fistula to target flow <600 mL/min. RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery). Ligation: Complete closure of the AVF. Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas). 8. Key Clinical Takeaways The “Normal EF” Trap: Do not be reassured by an EF of 55–65%; in the context of pulmonary edema and high CO, this is potentially HOHF. Pulse Pressure: Look for a wide pulse pressure (e.g., 180/60) as a marker of low SVR. ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid. Read More

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 survivors’ families. Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome. Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization). Read More

We review diagnosing and managing bacterial meningitis in the ED. Hosts: Sarah Fetterolf, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Meningitis_2_0.mp3 Download Leave a Comment Tags: CNS Infections, Infectious Diseases, Neurology 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 Patient Presentation & Workup Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches. Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA. Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F. Physical Exam Findings: Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion). Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°). Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache). Imaging: Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax. CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy). Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement. CSF Analysis & Microbiology Bacterial Meningitis Opening Pressure: Elevated (Normal is <170 mm H2​O). Color: Cloudy or turbid. Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics. Cell Count: Very high (>1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN). Glucose: Low (<40 mg/dL); CSF/blood glucose ratio is <0.3–0.4. Protein: High (>200 mg/dL). Cytology: Negative. Viral Meningitis Opening Pressure: Normal. Color: Clear or bloody. Gram Stain: Negative. Cell Count: Slightly elevated (<300/mm3 WBC); dominated by lymphocytes (<20% PMN). Glucose: Normal. Protein: Moderately elevated (<200 mg/dL). Cytology: Negative. Fungal Meningitis Opening Pressure: Normal to elevated. Color: Clear or cloudy. Gram Stain: Negative. Cell Count: Elevated (<500/mm3 WBC). Glucose: Normal to slightly low. Protein: High (>200 mg/dL). Cytology: Negative. Neoplastic (Cancer-related) Meningitis Opening Pressure: Normal. Color: Clear or cloudy. Gram Stain: Negative. Cell Count: Elevated (<300/mm3 WBC). Glucose: Normal to slightly low. Protein: High (>200 mg/dL). Cytology: Positive (this is the key differentiator). Management Protocol Immediate Treatment: Early administration of antibiotics/antivirals is critical to reduce mortality. Antibiotics: Ceftriaxone 2g IV q12h + Vancomycin (or Rifampin in cephalosporin-resistant areas). Listeria Coverage: Add Ampicillin for patients > 50 years old. Antivirals: Acyclovir 10 mg/kg q8h. Steroids: Dexamethasone 10 mg IV q6h for 4 days (proven to reduce mortality and improve outcomes). Surgical Intervention: Neurosurgery performed an emergent EVD in the ED to relieve pressure from obstructive hydrocephalus. Post-Exposure Prophylaxis: Indicated only for N. meningitidis (not S. pneumoniae) for contacts < 24 hours from diagnosis. Regimens: Rifampin for 2 days, single-dose Ciprofloxacin, or IM Ceftriaxone (if pregnant). Stats & Clinical Pearls: Austrian Syndrome The Triad: Concurrent pneumonia, endocarditis, and meningitis caused by Streptococcus pneumoniae. Risk Factors: Asplenia (due to the spleen’s role in filtering encapsulated bacteria), alcohol use disorder, and immunosuppression. Mortality Rate: Extremely high at 28%; mortality is highest when there is CNS involvement. Incidence: Worldwide, S. pneumoniae is the leading cause of bacterial meningitis, accounting for 3,000–6,000 cases annually. Read More

We discuss the diagnosis and management of SCAPE in the ED. Hosts: Naz Sarpoulaki, MD, MPH Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SCAPEv2.mp3 Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care 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 The Clinical Case Presentation: 60-year-old male with a history of HTN and asthma. EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180. Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing. Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis). Differential Diagnosis for the Hypoxic/Tachypneic Patient Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis. Cardiac: CHF, ACS, Tamponade. Systemic: Anemia, Acidosis. Neuro: Neuromuscular weakness. What is SCAPE? Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload. Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload. Bedside Diagnosis: POCUS vs. CXR POCUS is the gold standard for rapid bedside diagnosis. Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones). Cardiac: Assess LV function and check for pericardial effusion. Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR. Management Strategy 1. NIPPV (CPAP or BiPAP) Start NIPPV immediately to reduce preload/afterload and recruit alveoli. Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation. Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13). 2. High-Dose Nitroglycerin The goal is to drop SBP to < 140–160 mmHg within minutes. No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously. IV Bolus: 500–1000 mcg over 2 minutes. IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required). Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues. 3. Refractory Hypertension If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator: Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid). Nicardipine: Effective alternative for rapid BP control. Enalaprilat: Consider if the above are unavailable. Troubleshooting & Pitfalls The “Mask Intolerant” Patient Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV). AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam). The Role of Diuretics In SCAPE, diuretics are not first-line. The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient. Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed. Disposition Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions. Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered. Take-Home Points Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR. NIPPV Immediately: Don’t wait. It saves lives and prevents tubes. High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose. Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask. Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase. Read More

We discuss the shift to prehospital blood to treat shock sooner. Hosts: Nichole Bosson, MD, MPH, FACEP Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Prehospital_Transfusion.mp3 Download Leave a Comment Tags: EMS, Prehospital Care, Trauma 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 What is prehospital blood transfusion Administration of blood products in the field prior to hospital arrival Aimed at patients in hemorrhagic shock Why this matters Traditional US prehospital resuscitation relied on crystalloid ED and trauma care now prioritize early blood Hemorrhage occurs before hospital arrival Delays to definitive hemorrhage control are common Earlier blood may improve survival Supporting rationale ATLS and trauma paradigms emphasize blood over fluid National organizations support prehospital blood when feasible EMS already manages high risk, time sensitive interventions Evidence overview Data are mixed and evolving COMBAT: no benefit PAMPer: mortality benefit RePHILL: no clear benefit Signal toward benefit when transport time exceeds ~20 minutes Urban systems still experience long delays due to traffic and geography LA County median time to in hospital transfusion ~35 minutes LA County program ~2 years of planning before launch Pilot began April 1 Partnerships: LA County Fire Compton Fire Local trauma centers San Diego Blood Bank 14 units of blood circulating in the field Blood rotated back 14 days before expiration Ultimately used at Harbor UCLA Continuous temperature and safety monitoring Indications used in LA County Focused rollout Trauma related hemorrhagic shock Postpartum hemorrhage Physiologic criteria: SBP < 70 Or HR > 110 with SBP < 90 Shock index ≥ 1.2 Witnessed traumatic cardiac arrest Products: One unit whole blood preferred Two units PRBCs if whole blood unavailable Early experience ~28 patients transfused at time of discussion Evaluating: Indications Protocol adherence Time to transfusion Early outcomes Too early for outcome conclusions California collaboration Multiple active programs: Riverside (Corona Fire) LA County Ventura County Additional programs planned: Sacramento San Bernardino Programs meet monthly as CalDROP Focus on shared learning and operational optimization Barriers and concerns Trauma surgeon concerns about blood supply Need for system wide buy in Community engagement Patients who may decline transfusion Women of childbearing age and alloimmunization risk Risk of HDFN is extremely low Clear communication with receiving hospitals is essential Future direction Rapid national expansion expected Greatest benefit likely where transport delays exist Prehospital Blood Transfusion Coalition active nationally Major unresolved issue: reimbursement Currently funded largely by fire departments Sustainability depends on policy and payment reform Take-Home Points Hemorrhagic shock is best treated with blood, not crystalloid Prehospital transfusion may benefit patients with prolonged transport times Implementation requires strong partnerships with blood banks and trauma centers Early data are promising, but patient selection remains critical National collaboration is key to sustainability and future growth Read More