Core EM - Emergency Medicine Podcast

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...

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....

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...

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 CSF Analysis & Microbiology Bacterial MeningitisOpening Pressure:<170H2​OColor:Gram Stain:60%–80%7%–41%Cell Count:>10002000/mm3>80%Glucose:<40<0.30.4Protein:>200Cytology:Viral MeningitisOpening Pressure:Color:Gram Stain:Cell Count:<300/mm3<20%Glucose:Protein:<200Cytology:Fungal MeningitisOpening Pressure:Color:Gram Stain:Cell Count:<500/mm3Glucose:Protein:>200Cytology:Neoplastic (Cancer-related) MeningitisOpening Pressure:Color:Gram Stain:Cell Count:<300/mm3Glucose:Protein:>200Cytology:Positive Management Protocol Stats & Clinical Pearls: Austrian Syndrome 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/SCAPE.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)...

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

We review BRUEs (Brief Resolved Unexplained Events). Hosts: Ellen Duncan, MD, PhD Noumi Chowdhury, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/BRUE.mp3 Download Leave a Comment Tags: Pediatrics Show Notes What is a BRUE? Cyanosis or pallor Irregular, absent, or decreased breathing Marked change in tone (hypertonia or hypotonia) Crucial Caveat: BRUE is a diagnosis of exclusion. If the history and physical exam reveal a specific cause (e.g., reflux, seizure, infection), it is not a BRUE. Risk Stratification: Low Risk vs. High Risk Risk stratification is the most important step in management. While only 6-15% of cases meet strict “Low Risk” criteria, identifying these patients allows us to avoid unnecessary invasive testing. Low Risk Criteria To be considered Low Risk, the infant must meet ALL of the following: Age: > 60 days old Gestational Age: GA > 32 weeks (and Post-Conceptional Age > 45 weeks) Frequency: This is the first episode Duration: Lasted < 1 minute Intervention: No CPR performed by a trained professional Clinical Picture: Reassuring history and physical exam Management for Low Risk: Generally do not require extensive testing or admission. Prioritize safety education/anticipatory guidance. Ensure strict return precautions and close outpatient follow-up (within 24 hours). High Risk Criteria Any infant not meeting the low-risk criteria is automatically High Risk. Additional red flags include: Suspicion of child abuse History of toxin exposure Family history of sudden cardiac death Abnormal physical exam findings (trauma, neuro deficits) Management for High Risk: Requires a more thorough evaluation. Often requires hospital admission. Note: Differential Diagnosis: “THE MISFITS” Mnemonic T – Trauma (Accidental or Non-accidental/Abuse) H – Heart (Congenital heart disease, dysrhythmias) E – Endocrine M – Metabolic (Inborn errors of metabolism) I – Infection (Sepsis, meningitis, pertussis, RSV) S – Seizures F – Formula (Reflux, allergy, aspiration) I – Intestinal Catastrophes (Volvulus, intussusception) T – Toxins (Medications, home exposures) S – Sepsis (Systemic infection) Workup & Diagnostics Step 1: Stabilization ABCs (Airway, Breathing, Circulation) Point-of-care Glucose Cardiorespiratory monitoring Step 2: Diagnostic Testing (For High Risk/Symptomatic Patients) Labs: VBG, CBC, Electrolytes. Imaging: CXR: Evaluate for infection and cardiothymic silhouette. EKG: Evaluate for QT prolongation or dysrhythmias. Neuro: Clinical Pearl: Only ~6% of diagnostic tests contribute meaningfully to the diagnosis. Be judicious—avoid “shotgunning” tests in low-risk patients. Prognosis & Outcomes Recurrence: Approximately 10% (lower than historical ALTE rates of 10-25%). Mortality: < 1%. Nearly always linked to an identifiable cause (abuse, metabolic disorder, severe infection). BRUE vs. SIDS: These are not the same. BRUE: Peaks < 2 months; occurs mostly during the day. SIDS: Peaks 2–4 months; occurs mostly midnight to 6:00 AM. Take-Home Points Diagnosis of Exclusion: You cannot call it a BRUE until you have ruled out obvious causes via history and physical. Strict Criteria: Stick strictly to the Low Risk criteria guidelines. If they miss even one (e.g., age < 60 days), they are High Risk. Education: For low-risk families, the most valuable intervention is reassurance, education, and arranging close follow-up. Systematic Approach: For high-risk infants, use a structured approach (like THE MISFITS) to ensure you don’t miss rare but reversible causes. Read More

Lessons from Rwanda’s Marburg Virus Outbreak and Building Resilient Systems in Global EM. Hosts: Tsion Firew, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Marburg_Virus.mp3 Download Leave a Comment Tags: Global Health, Infectious Diseases Show Notes Context and the Rwanda Marburg Experience The Threat: Marburg Virus Disease is from the same family as Ebola and has historically had a reported fatality rate as high as 90%. The Outbreak (Sept. 2024): Rwanda declared an MVD outbreak. The initial cases involved a miner, his pregnant wife (who fell ill and died after having a baby), and the baby (who also died). Healthcare Worker Impact: The wife was treated at an epicenter hospital. Eight HCWs were exposed to a nurse who was coding in the ICU; all eight developed symptoms, tested positive within a week, and four of them died. The Turning Point: The outbreak happened in city referral hospitals where advanced medical interventions (dialysis, mechanical ventilation) were available. Rapid Therapeutics Access: Within 10 days of identifying Marburg, novel therapies (experimental drugs and monoclonal antibodies) and an experimental vaccine were made available through diplomacy with the US government/CDC and agencies like WHO, Africa CDC, CEPI and more. The Outcome: This coordinated effort—combini...

We review the diagnosis, risk stratification, & management of acute pulmonary embolism in the ED. Hosts: Vivian Chiu, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Pulmonary_Embolism.mp3 Download Leave a Comment Tags: Pulmonary Show Notes Core Concepts and Initial Approach Definition:DVTIncidence & Mortality:Mantra:risk stratifyresuscitate with precisionRisk Factors: Clinical Presentation and Risk Stratification Presentation:Acute/Subacute:DyspneaChronic:Pulmonary Infarction Signs:High-Risk Red Flags:hypotension

We break down pneumothorax: risks, diagnosis, and management pearls. Hosts: Christopher Pham, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax.mp3 Download Leave a Comment Tags: Chest Trauma, Pulmonary, Trauma Show Notes Risk Factors for Pneumothorax Secondary pneumothoraxPrimary spontaneous pneumothorax Symptoms & Differential Diagnosis Diagnostics Bloodwork:EKG:

Angioedema – Recognition and Management in the ED Hosts: Maria Mulligan-Buckmiller, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Angioedema.mp3 Download Leave a Comment Tags: Airway Show Notes Definition & Pathophysiology Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability. Triggers increased vascular permeability → fluid shifts into tissues. Etiologies Histamine-mediated (anaphylaxis)Bradykinin-mediatedIdiopathic angioedema Clinical Presentations SwellingRespiratory compromiseAbdominal manifestations

Granulomatosis with Polyangiitis (GPA) – Recognition and Management in the ED Hosts: Phoebe Draper, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/GPA.mp3 Download Leave a Comment Tags: Rheumatology Show Notes Background Red Flag Symptoms: Workup in the ED: Management: Stable patients:Unstable patients: Conditions that Mimic GPA:

We discuss capacity assessment, patient autonomy, safety, and documentation. Hosts: Anne Levine, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Capacity_Assessment.mp3 Download Leave a Comment Show Notes The Importance of Capacity Assessment Defining Capacity Real-World ED Examples The 4 Pillars of Capacity Assessment UnderstandingSample prompts:

We dive into the recognition and management of blast crisis. Hosts: Sadakat Chowdhury, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Blast_Crisis.mp3 Download Leave a Comment Tags: Hematology, Oncology Show Notes Topic Overview Pathophysiology & Associated Conditions Risk Factors Clinical Presentation

We explore the expanding field of Geriatric Emergency Medicine. Hosts: Ula Hwang, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Geriatric_Emergency_Medicine.mp3 Download Leave a Comment Tags: Geriatric Show Notes Key Topics Discussed Challenges in Geriatric Emergency Care Adapting Clinical Approach Identifying High-Risk Geriatric Patients

We discuss the injuries sustained from smoke inhalation. Hosts: Sarah Fetterolf, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Smoke_Inhalation.mp3 Download Leave a Comment Tags: Environmental, Toxicology Show Notes Table of Contents 00:37 – Overview of Smoke Inhalation Injury 00:55 – Three Key Pathophysiologic Processes 01:41 – Physical Exam Findings to Watch For 02:12 – Airway Management and Early Intervention 03:23 – Carbon Monoxide Toxicity 04:24 – Workup and Initial Treatment of CO Poisoning 06:14 – Cyanide Toxicity 07:19 – Treatment Options for Cyanide Poisoning 09:12 – Take-Home Points and Clinical Pearls Physiological Effects of Smoke Inhalation: Thermal Injury:Chemical Irritation:Systemic Toxicity:

We discuss the evaluation of and treatment options for acute back pain. Hosts: Benjamin Friedman, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Back_Pain.mp3 Download Leave a Comment Tags: Musculoskeletal, Orthopaedics Show Notes **Please fill out this quick survey to help us develop additional resources for our listeners: Core EM Survey** Clinical Evaluation: Primary Goal:Red Flags: Assessment:Additional Tools: Imaging Guidelines: Routine Imaging:ACEP Recommendations:Advanced Imaging: Treatment Options: Evidence-Based First-Line:

We discuss the impact of family presence during resuscitations. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Family_Presence_During_Resuscitation.mp3 Download Leave a Comment Tags: Critical Care, Pediatrics Show Notes Overview Historical Context:Current Practices in Pediatrics:Common Concerns & Myths: Evidence from the Literature New England Journal of Medicine study on Family Presence During Cardiopulmonary Resuscitation (Jabre et al., 2013):

We discuss the recognition and treatment of necrotizing fasciitis. Hosts: Aurnee Rahman, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Necrotizing_Fasciitis.mp3 Download Leave a Comment Tags: Critical Care, General Surgery Show Notes Table of Contents 0:00 – Introduction 0:41 – Overview 1:10 – Types of Necrotizing Fasciitis 2:21 – Pathophysiology & Risk Factors 3:16 – Clinical Presentation 4:06 – Diagnosis 5:37 – Treatment 7:09 – Prognosis and Recovery 7:37 – Take Home points Introduction Definition Types of Necrotizing Fasciitis Type I (Polymicrobial)

We sit down with one of our toxicologists to discuss acetaminophen toxicity. Hosts: Marlis Gnirke, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acetaminophen_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Table of Contents 0:35 – Hidden acetaminophen toxicity in OTC products 3:24 – Pharmacokinetics and toxicokinetics 6:06 – Clinical Course 9:22 – The antidote – NAC 11:02 – The Rumack-Matthew Nomogram 17:36 – Treatment protocols 22:34 – Monitoring and Lab Work 23:23 – Considerations when treating pediatric patients 23:57 – IV APAP overdose, fomepizole 25:42 – Take Home Points Acetaminophen vs. Tylenol: The importance of recognizing that acetaminophen is found in many products beyond Tylenol.Common medications containing acetaminophen, such as Excedrin, Fioricet, Percocet, Dayquil/Nyquil, and others.The risk of unintentional overdose due to combination products. Prevalence of Acetaminophen Toxicity: