Core EM - Emergency Medicine Podcast

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 Evalua

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: Signif

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

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? BRUE stands for Brief Resolved Unexplained Event. It typically affects infants <1 year of age and is characterized by a sudden, brief, and now resolved episode of one or more of the following: Cyanosis or pallor Irregular, absent, or decreased breathing Marked change in tone (hypertonia or hypotonia) Altered level of responsiveness 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: Serious underlying conditions are identified in approx. 4% of high-risk infants. 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: Consider Head CT/MRI and EEG if there are concerns for trauma or seizures. 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—combining therapeutics, widespread testing, and years of investment in a resilient healthcare system—helped curb the fatality rate down to 23%. Barriers and Enablers in Outbreak Preparedness Fragmented Systems: Emergency and surveillance functions often operate in silos, leading to delayed or missed outbreak identification (e.g., inconsistent travel screening at JFK during early COVID-19 vs. African countries). Solution: Empowering Emergency Departments and the community as the sentinel site can bridge this gap. Limited Frontline Capacity and Protection: Clinicians are often undertrained and underprotected and are frequently not part of the decision-making for surveillance. Weak Governance and Accountability: Unclear command structures and lack of feedback discourage early reporting. Enabler: Strong governance and accountability in Rwanda helped contain the virus. Dependence on External Programs: Many low-income countries rely on outside sources for vaccines and therapeutics, slowing response. Solution: Invest in local production (e.g., Rwanda’s pre-outbreak investment in developing its own mRNA vaccines). Lack of Resource-Smart Innovation: Gaps exist in things like integrating digital triage tools and surveillance systems. Four Pillars of a Responsive and Equitable Emergency System Workforce: Invest in pre-service and in-service training, mentorship, and fair compensation to ensure a skilled, protected, and motivated team. Integration into the Health System: Emergency care (including pre-hospital services) must not operate in silos; it needs to be embedded in national health strategies and linked to surveillance, referral, and financing systems. Equity in Design and Policy: The system must address the needs and protection of vulnerable groups and work closely with policymakers. Data: Utilize real-time data and dashboards to provide a feedback loop between clinicians and policymakers, enabling tailored and innovative interventions. Advice for Clinicians in Global Health Work Start Small and Build Trust: Meaningful work requires humility and relationship over scale or visibility. Focus on local priorities and sustainable change through long-term partnership, not just presence. Avoid the “savior mindset”. Be T-Shaped: Be deep in one specialty (e.g., EM) but fluent across other critical areas like policy, finance, and data, as these drive decision-making. Focus on Knowledge Transfer: True impact means making yourself less essential over time. Prioritize mentorship, co-creation, and sharing leadership opportunities. Looking Ahead: Global Threats Shaping the Next Decade The future of EM will be shaped by the convergence of several complex challenges: Climate and Environmental Crisis: Extreme heat, floods, and vector-borne illnesses will strain emergency systems. Preparation: Invest in climate-resilient infrastructure for both EDs and the community. Outbreaks and Biosecurity: Future outbreaks will emerge faster than current systems can handle, coupled with challenges from anti-microbial resistance. Conflict, Displacement, and Urbanization: Mass migration and overcrowded cities will require new models of emergency care that are mobile, scalable, and inclusive. Preparation: Building resilient healthcare systems ready for crisis mental health and cross-border coordination. Digital Tools and AI: These can augment solutions, but investment is needed in data governance and ethical AI that preserves local control and adapts to local capacity. Read More

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 One Comment Tags: Pulmonary Show Notes Core Concepts and Initial Approach Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli. Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually. Mantra: “Don’t anchor on the obvious. Always risk stratify and resuscitate with precision.” Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy. Clinical Presentation and Risk Stratification Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse. Acute/Subacute: Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever. Chronic: Can mimic acute symptoms or be totally asymptomatic. Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion. High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes), requirement of vasopressors, or signs of shock → activate PERT team immediately. Crucial Mimics: Think broadly; consider pneumonia, ACS, pneumothorax, heart failure exacerbation, and aortic dissection. Workup & Diagnostics History/Scoring: Ask about prior clots, recent surgeries, hospitalizations, travel. Use Wells/PERC criteria to assess pretest probability. Labs: D-dimer: A good test to rule out PE in a patient with low probability. If suspicion is high, proceed directly to imaging. Troponin/BNP: Act as RV stress gauges. Elevated levels are associated with increased risk of a complicated clinical course (25-40%). Lactate: Helpful in identifying patients in possible cardiogenic shock. EKG: Most common finding is sinus tachycardia. Classic RV strain patterns (S1Q3T3, T-wave changes/inversions) are nonspecific. Imaging: CXR: Usually normal, but quick and essential to rule out other causes. CTPA: The usual standard and gold standard for stable patients. High sensitivity (> 95%) and can detect RV enlargement/strain. V/Q Scan: Option for patients with contraindications to contrast (e.g., severe contrast allergies). POCUS (Point-of-Care Ultrasound): Useful adjunct for unstable patients. Bedside Echo: Can show signs of RV strain (enlarged RV, McConnell sign). Lower Extremity Ultrasound: Can identify a DVT in proximal leg veins. Treatment & Management Resuscitation (Reviving the RV): Oxygenation: Give supplementally as needed (nasal cannula, non-rebreather, high flow). Intubation: Avoid if possible; positive pressure ventilation can worsen RV dysfunction. Fluids: Be judicious; even the smallest amount can worsen RV overload. Vasopressors: Norepinephrine is preferred as first-line for hypotension/shock. Anticoagulation (Start Immediately): Initial choice is UFH or LMWH (Lovenox). Lovenox is preferred for quicker time to therapeutic range, but is contraindicated in renal dysfunction, older age, or need for emergent procedures. DOACs can be considered for stable, low-risk patients as an outpatient. Escalation for High-Risk PE Systemic Thrombolytics: Consider for very sick patients with shock/cardiac arrest (e.g., Alteplase 100 mg over two hours or a bolus in cardiac arrest). High risk of intracranial hemorrhage; weigh risks versus benefits. PERT Activation: Engage multidisciplinary teams (usually including ICU, CT surgery, and interventional radiology). Interventions: Consult specialists for catheter-directed thrombolysis or suction embolectomy. Surgical embolectomy can also be considered. Bridge to Care: Activate the ECMO team early for unstable patients to buy valuable time. Prognosis & Disposition Mortality: Low risk < 1%; intermediate 3-15%; high risk 25-65%. Complications: 3-4% of patients develop Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Others may have long-term RV dysfunction and chronic shortness of breath. Recurrence: ∼ 30% chance in the next few weeks to months, if not treated correctly. Disposition: ICU: All high-risk and some intermediate-high risk patients. Regular Floor: Intermediate-low risk patients. Outpatient Discharge: Low-risk patients can be sent home on anticoagulation. Use PSI or HESTIA scores to risk stratify suitability, typically starting a DOAC. Shared Decision-Making: Critical to ensure care is safe and consistent with the patient’s wishes. Read More

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 pneumothorax Trauma: rib fractures, blunt chest trauma (as in the case). Iatrogenic: central line placement, thoracentesis, pleural procedures. Primary spontaneous pneumothorax Young, tall, thin males (10–30 years). Connective tissue disorders: Marfan, Ehlers-Danlos. Underlying lung disease: COPD with bullae, interstitial lung disease, CF, TB, malignancy. Technically, anyone is at risk. Symptoms & Differential Diagnosis Typical PTX presentation: Dyspnea, chest pain, pleuritic discomfort. Exam clues: unilateral decreased breath sounds, focal tenderness/crepitus. Red flags (suggest tension PTX): JVD Tracheal deviation Hypotension, shock physiology Severe tachycardia, hypoxia Differential diagnoses: Pulmonary: asthma, COPD, pneumonia, pulmonary edema (SCAPE), ILD, infections. Cardiac: ACS, CHF, pericarditis. PE and other acute causes of dyspnea. Diagnostics Bloodwork: limited role, except type & screen if intervention likely. EKG: reasonable given chest pain/shortness of breath. Imaging: POCUS (bedside ultrasound) High sensitivity (86–96%) & specificity (97–100%). Signs: Seashore sign: normal lung sliding. Barcode sign: absent lung sliding. Lung point: most specific for PTX. CXR Sensitivity ~70–90% for small PTX. May show pleural line, hyperlucency. CT chest (gold standard) Defines size/severity. Rules out mimics (bullae, pleural effusion, hemothorax). Guides intervention choice. Management First step for all: Oxygen supplementation (non-rebreather if possible). Accelerates resorption of pleural air. Stable vs. unstable decision point: Unstable/tension PTX Immediate needle thoracostomy (14-g angiocath, 2nd ICS midclavicular). Temporizing until chest tube/pigtail placed. Stable, small PTX (<2 cm on O₂) Observation, supplemental O₂, conservative management. Stable, larger PTX or symptomatic Chest tube or pigtail catheter insertion. Pigtail catheters: less invasive, more comfortable, similar efficacy for simple PTX. Large bore tubes: indicated if associated with blood, pus, large collections. Disposition Admit all patients with chest tubes; cannot be discharged with tube in place. Service responsible varies by hospital: trauma, CT surgery, MICU, etc. Level of care (ICU vs. floor) depends on stability: ICU if unstable course, intubated, shock physiology. Stepdown/floor if stable and straightforward. Take Home Points Always broaden differential in dyspnea/chest pain → don’t anchor on asthma/COPD. Exam findings + history (trauma, risk factors) crucial to raising suspicion. Ultrasound is more sensitive than CXR and highly specific when lung point found. Oxygen is first-line; intervention determined by size + stability. Pigtail catheters increasingly favored for simple, stable PTX. All patients with intervention require admission; service varies by institution. Read More

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) Associated with urticaria/hives, pruritus, and redness. Triggered by allergens (foods, insect stings, medications). Rapid onset (minutes to hours). Bradykinin-mediated Hereditary angioedema (HAE): C1 esterase inhibitor deficiency (autosomal dominant). Acquired angioedema: Associated with B-cell lymphoma, autoimmune disease, MGUS. Medication-induced: Most commonly ACE inhibitors; rarely ARBs. Typically lacks urticaria and itching. Gradual onset, can last days if untreated. Idiopathic angioedema Unknown cause; diagnosis of exclusion. Clinical Presentations Swelling Asymmetric, non-pitting, usually non-painful. May involve lips, tongue, face, extremities, GI tract. Respiratory compromise Upper airway swelling → stridor, dyspnea, sensation of throat closure. Airway obstruction is the most feared complication. Abdominal manifestations Bowel wall angioedema can mimic acute abdomen: Nausea, vomiting, diarrhea, severe pain, increased intra-abdominal pressure, possible ischemia. Key Differentiating Features Histamine-mediated: rapid onset, hives/itching, resolves quickly with epinephrine, antihistamines, and steroids. Bradykinin-mediated: slower onset, lacks urticaria, prolonged duration, less responsive to standard anaphylaxis medications. Diagnostic Approach in the ED Focus on airway (ABCs) and clinical assessment. Labs (e.g., C4 level) useful for downstream diagnosis (esp. HAE) but not for acute management. Imaging: only if symptoms suggest abdominal involvement or to rule out other causes. Treatment Strategies Airway protection is always priority: Early consideration of intubation if worsening obstruction or inability to manage secretions. Histamine-mediated (anaphylaxis): Epinephrine (IM), antihistamines, corticosteroids. Bradykinin-mediated: Epinephrine may be tried if unclear etiology (no significant harm, lifesaving if histamine-mediated). Targeted therapies: Icatibant: bradykinin receptor antagonist. Ecallantide: kallikrein inhibitor (less available). C1 esterase inhibitor concentrate: replenishes deficient protein. Fresh frozen plasma (FFP): contains C1 esterase inhibitor. Tranexamic acid (TXA): off-label, less evidence, considered if no other options. Complications to Watch For Airway compromise: rapid deterioration possible. Abdominal compartment syndrome from bowel edema (rare, surgical emergency). Take-Home Points Secure the airway if in doubt. Differentiate histamine-mediated vs bradykinin-mediated by presence/absence of hives/itching and speed of onset. Use epinephrine promptly if suspecting histamine-mediated angioedema or if uncertain. Consider bradykinin-targeted therapies for confirmed hereditary, acquired, or ACE-inhibitor–related angioedema. Recognize ACE inhibitors as the most frequent medication trigger; ARBs rarely cause it. Labs and imaging generally don’t change initial ED management but aid diagnosis for follow-up care. Read More

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 One Comment Tags: Rheumatology Show Notes Background A vasculitis affecting small blood vessels causing inflammation and necrosis Affects upper respiratory tract (sinusitis, otitis media, saddle nose deformity), lungs (nodules, alveolar hemorrhage), and kidneys (rapidly progressive glomerulonephritis) Can lead to multi-organ failure, pulmonary hemorrhage, renal failure Red Flag Symptoms: Chronic sinus symptoms Hemoptysis (especially bright red blood) New pulmonary complaints Renal dysfunction Constitutional symptoms (fatigue, weight loss, fever) Workup in the ED: CBC, CMP for anemia and AKI Urinalysis with microscopy (hematuria, RBC casts) Chest imaging (CXR or CT for nodules, cavitary lesions) ANCA testing (not immediately available but important diagnostically) Management: Stable patients: Outpatient workup, urgent rheumatology consult, prednisone 1 mg/kg/day Unstable patients: High-dose IV steroids (methylprednisolone 1 g daily x3 days), consider plasma exchange, cyclophosphamide or rituximab initiation, ICU admission Conditions that Mimic GPA: Goodpasture syndrome (anti-GBM antibodies) TB, fungal infections Lung malignancy Other vasculitides (EGPA, MPA, lupus) ANCA Testing Utility: C-ANCA/PR3-ANCA positive in 80-90% of GPA cases P-ANCA/MPO-ANCA more common in MPA Don’t delay treatment while awaiting results if suspicion is high Outcomes: Without treatment: Fatal within a year (renal failure, respiratory complications) With treatment: 5-year survival ~75-90%, but ~50% relapse rate Long-term rheumatology follow-up is essential Take-Home Points: Always include vasculitis in the differential for unexplained respiratory, renal, or systemic symptoms. Recognize pulmonary-renal syndromes early. Initiate high-dose steroids immediately for unstable patients without waiting for ANCA results. GPA is rare but life-threatening – early recognition saves lives. Read More

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 One Comment Show Notes The Importance of Capacity Assessment Arises frequently in the ED, even when not formally recognized Carries both legal implications and ethical weight Failure to appropriately assess capacity can result in: Forced treatment without justification Missed opportunities to respect autonomy Increased risk of litigation and poor patient outcomes Defining Capacity Capacity is: Decision-specific: varies based on the medical choice at hand Time-specific: can fluctuate due to medical conditions, intoxication, delirium Distinct from competency, which is a legal determination Relies on a patient’s ability to: Understand relevant information Appreciate the consequences Reason through options Communicate a clear choice Real-World ED Examples Intoxicated patient with head trauma refusing CT Unreliable neuro exam Potentially time-sensitive intracranial injury Elderly patient with sepsis refusing admission due to caregiving responsibilities Balancing autonomy vs. beneficence Patient with gangrenous diabetic foot refusing surgery Demonstrates logic and consistency despite high-risk decision The 4 Pillars of Capacity Assessment Understanding Can the patient explain: Their condition Recommended treatments Risks and benefits Alternatives and outcomes? Sample prompts: “What are the options for your situation?” “What might happen if we do nothing?” Appreciation Does the patient grasp the personal relevance of the information? Sample prompts: “Why do you think we’re recommending this?” “How do you think this condition could affect you?” Reasoning Can the patient logically explain their choice? Must demonstrate a rational process, even if the outcome seems unwise Sample prompts: “What factors are you considering in making this decision?” “What led you to this conclusion?” Choice Is the patient able to clearly communicate a decision? Any modality acceptable: verbal, written, gestural Sample prompts: “We’ve discussed several options. What do you want to do?” “Have you decided what option is best for you?” Common ED Challenges & Solutions Time Pressure Capacity assessments can be time-consuming Yet, patients leaving AMA without proper evaluation are at higher risk: ↑ 30-day mortality ↑ 30-day readmission Communication Barriers Language differences → use certified interpreters Cognitive impairment or psych illness → clarify baseline status Noisy ED environment → relocate to quiet space Use simple language, avoid jargon Ethical Dilemmas Providers may disagree with patient choices Ensure decision-making process—not the choice itself—is being judged Use tools like the Aid to Capacity Evaluation (ACE) When uncertain, consult Psychiatry or Risk Management Best Practices in Documentation Clearly document: The patient’s understanding, appreciation, reasoning, and choice Information delivered: Condition Treatment recommendations Alternatives and risks Patient’s responses and logic Witnesses to the conversation Any discharge instructions, including: Follow-up plans Prescriptions provided Return precautions Also document: If patient refused treatment, document: That risks and benefits were clearly explained That refusal was voluntary If treatment was administered despite objection: Document rationale for presumed lack of capacity Legal/ethical justification for action Involvement of other services (e.g., Psychiatry, Risk) Read More

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 2 Comments Tags: Hematology, Oncology Show Notes Topic Overview Blast crisis is an oncologic emergency, most commonly seen in chronic myeloid leukemia (CML). Defined by: >20% blasts in peripheral blood or bone marrow. May include extramedullary blast proliferation. Without treatment, median survival is only 3–6 months. Pathophysiology & Associated Conditions Usually occurs in CML, but also in: Myeloproliferative neoplasms (MPNs) Myelodysplastic syndromes (MDS) Transition from chronic to blast phase often reflects disease progression or treatment resistance. Risk Factors 10% of CML patients progress to blast crisis. Risk increased in: Patients refractory to tyrosine kinase inhibitors (e.g., imatinib). Those with Philadelphia chromosome abnormalities. WBC >100,000, which increases risk for leukostasis. Clinical Presentation Symptoms often stem from pancytopenia and leukostasis: Anemia: fatigue, malaise. Functional neutropenia: high WBC count, but increased infection/sepsis risk. Thrombocytopenia: bleeding, bruising. Leukostasis/hyperviscosity effects by system: Neurologic: confusion, visual changes, stroke-like symptoms. Cardiopulmonary: ARDS, myocardial injury. Others: priapism, limb ischemia, bowel infarction. Rapid deterioration is common — early recognition is critical. Diagnostic Workup CBC with differential: assess blast % and cytopenias. Peripheral smear and manual diff: confirm immature blasts. CMP: screen for tumor lysis syndrome: Elevated potassium, phosphate, uric acid. Low calcium. LDH & uric acid: markers of high cell turnover. Coagulation studies (PT, PTT): assess for DIC. Definitive tests (done inpatient): bone marrow biopsy, flow cytometry. Emergency Department Management Resuscitation & ABCs: oxygen, IV fluids, vitals monitoring. Avoid aggressive transfusions: Risk of hyperviscosity with PRBCs and platelets. Initiate broad-spectrum antibiotics early: High suspicion for sepsis in functionally neutropenic patients. Consider antifungals for prolonged febrile neutropenia. Cytoreduction strategies: Hydroxyurea to lower WBCs quickly. Tyrosine kinase inhibitors (TKIs). High-dose chemotherapy. Early consultation with hematology/oncology is essential. Mutation testing may guide targeted therapy. Prognosis Without treatment: median survival ~3 months. With treatment: Potential survival >1 year. Best outcomes in patients who enter a second chronic phase and undergo allogeneic stem cell transplant. Ethical & Logistical Considerations Treatment may involve aggressive interventions with serious side effects. Important to assess: Patient goals of care. Capacity for informed consent. Resource limitations: Not all hospitals have oncology services. Patients may require transfer over long distances. Emphasize early, transparent discussions with patients and families. Top 3 Take-Home Points Recognize early: Look for cytopenias, leukostasis, and rapid clinical decline. Resuscitate appropriately: Start antibiotics; be cautious with transfusions. Call for help: Early hematology/oncology involvement is essential for definitive care. Read More

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 One Comment Tags: Geriatric Show Notes Key Topics Discussed Importance and impact of geriatric emergency departments. Optimizing care strategies for geriatric patients in ED settings. Practical approaches for non-geriatric-specific EDs. Challenges in Geriatric Emergency Care Geriatric patients often present with: Multiple chronic conditions Polypharmacy Functional decline (mobility issues, cognitive impairments, social isolation) Adapting Clinical Approach Core objective remains acute issue diagnosis and treatment. Additional considerations for geriatric patients: Review and caution with medications to prevent adverse reactions. Address functional limitations and cognitive impairments. Emphasize safe discharge and care transitions to prevent unnecessary hospitalization. Identifying High-Risk Geriatric Patients Screening tools: Identification of Seniors at Risk (ISAR) Frailty screens Alignment with the “Age-Friendly Health Systems” initiative focusing on: Mentation Mobility Medications Patient preferences (what matters most) Mistreatment (elder abuse awareness) Minimizing Hospital-Related Harms Involvement of multidisciplinary teams: Social workers and care managers for care transitions Geriatric-certified pharmacists for medication review Coordination with outpatient services post-discharge Implementing Geriatric Care in All EDs Basic geriatric care achievable even in resource-limited or rural EDs. Level 3 Geriatric ED Accreditation can be achieved through: Improved care transitions Staff education enhancements Age-friendly environments (comfort, nutrition, hydration) Future of Geriatric Emergency Medicine Vision: Universal integration of geriatric-focused care. Goals: Enhanced patient experience Improved care transitions Alignment of treatments with patient goals Broader enhancement of emergency care quality for all patient populations Read More

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: Direct upper airway damage from heated air or steam. Leads to swelling, inflammation, and possible airway obstruction. Chemical Irritation: Causes bronchospasm, mucus plugging, and inflammation in the lower airways. Increases capillary permeability, potentially causing pulmonary edema. Systemic Toxicity: Primarily involves carbon monoxide and cyanide poisoning. Clinical Signs and Symptoms: Physical Exam: Facial burns, singed nasal hairs Hoarseness, stridor (upper airway swelling) Carbonaceous sputum (lower airway edema) Systemic Symptoms: Headache, dizziness, nausea Syncope, seizures, altered mental status Airway Management Considerations: Not every patient requires immediate intubation. Intubation should be performed early if airway compromise is suspected, as swelling can rapidly progress. Close airway monitoring recommended for all patients. Carbon Monoxide Poisoning: Common cause of death post-smoke inhalation (50–75% of fire-related injuries). Hemoglobin affinity 250 times greater for CO than oxygen, impairing tissue oxygenation. Diagnosis: Carboxyhemoglobin level via VBG (ensure proper lab ordering). Pulse oximetry unreliable; falsely high readings. Treatment: Immediate high-flow oxygen administration. Consider hyperbaric oxygen therapy for severe cases to reduce delayed neurocognitive sequelae. Cyanide Poisoning: Blocks cytochrome oxidase in electron transport chain, halting aerobic ATP production. Patients present critically ill; notable features include: Elevated lactate levels (>8–10 mmol/L) Arterialization of venous blood Treatment: First-line therapy: hydroxocobalamin (Cyanokit) binds cyanide forming vitamin B12 for renal excretion. Alternative: Cyanide antidote kit (amyl nitrite, sodium nitrite, sodium thiosulfate); induces methemoglobinemia and requires monitoring. Important note: hydroxocobalamin turns blood and urine bright red; draw labs beforehand. Key Takeaways: Assess for airway compromise and signs of inhalation injury early. Maintain a high index of suspicion for CO and cyanide poisoning in smoke inhalation victims. Immediate, aggressive oxygen therapy and early antidote administration can significantly impact outcomes. Read More

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: Distinguish benign musculoskeletal pain from serious pathology. Red Flags: Look for indicators of spinal infection, spinal bleed, or space-occupying lesions (e.g., tumors, large herniated discs). Assessment: A thorough history and neurological exam (strength testing, gait) is essential. Additional Tools: Use bedside ultrasound for post-void residual assessment in suspected cauda equina syndrome Imaging Guidelines: Routine Imaging: Generally not indicated for young, healthy patients without red flags. ACEP Recommendations: Avoid lumbar X-rays in patients under 50 without risk factors, as they do not change management and may increase costs and ED time. Advanced Imaging: Reserve MRI for patients with red flags, neurological deficits, or suspected cauda equina syndrome; CRP may be a part of your calculus when evaluating for infectious causes of back pain Treatment Options: Evidence-Based First-Line: NSAIDs offer modest benefit. Skeletal muscle relaxants can be used but require caution due to side effects. Ineffective Therapies: Acetaminophen shows no benefit for back pain. Steroids are not recommended for non-radicular pain, with only limited benefit in sciatica. Topical treatments, lidocaine patches, and opioids are not supported by evidence and may pose additional risks. Alternative and Experimental Interventions: Nerve Blocks: Current evidence is limited; more research is needed on trigger point injections and erector spinae plane blocks. Severe Pain Management: A single opioid dose (preferably codeine or oral morphine) may be considered to facilitate discharge when necessary. Use diazepam sparingly for immediate mobilization. Onsite physical therapy in the ED can be beneficial when available. Preventing Chronic Pain: Research Focus: Ongoing studies are evaluating whether duloxetine (Cymbalta) can prevent the transition from acute to chronic back pain. Non-Pharmacologic Measures: Consider spinal mobilization, physical therapy, acupuncture, and cognitive behavioral therapy (CBT) as adjuncts in management. Take-Home Points: Most acute back pain is benign, but watch for red flags like IV drug use, anticoagulation, or neurological symptoms (e.g., weakness, bladder dysfunction) that may indicate serious conditions like spinal infections, bleeds, or cord compression. Avoid unnecessary lumbar X-rays in young, healthy patients without red flags—MRI is preferred only for those with risk factors, neurological deficits, or suspected cauda equina syndrome. Use NSAIDs and skeletal muscle relaxants for acute musculoskeletal back pain, as they offer modest benefits. Avoid opioids, acetaminophen, and steroids for non-radicular pain, as they lack evidence. For severe, uncontrolled pain, consider a single opioid dose (e.g., codeine) or diazepam sparingly Encourage patients to engage in non-pharmacologic therapies like yoga, massage, or cognitive behavioral therapy to aid recovery and prevent chronic pain. Read More

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: The conversation around allowing family members in the room during resuscitation events began gaining attention in 1987. Since then, the practice has been increasingly encouraged. Current Practices in Pediatrics: Family presence during pediatric resuscitations remains inconsistent, with healthcare provider acceptance ranging from 15% to 85%. Many subspecialists and consultants still request that families step out, often due to outdated concerns. Common Concerns & Myths: Interference in resuscitation → Studies show minimal disruption. Legal risks → No increased litigation risk has been demonstrated. Family trauma → Research suggests that presence may help with grieving and reduce PTSD symptoms. Evidence from the Literature New England Journal of Medicine study on Family Presence During Cardiopulmonary Resuscitation (Jabre et al., 2013): In a randomized controlled trial of 570 relatives, PTSD-related symptoms were significantly higher in family members who were not offered the opportunity to be present during resuscitation. 79% of relatives in the intervention group witnessed CPR compared to 43% in the control group. Family members who did not witness CPR had a higher likelihood of PTSD symptoms (adjusted OR 1.7, p=0.004). Anxiety and depression symptoms were also higher in those who did not witness CPR. Impact on Medical Teams: The study found no evidence that family presence affected resuscitation success rates, medical team stress levels, or led to legal consequences. Health professionals’ concerns over interference were largely unfounded. Guideline Support & Barriers to Implementation Professional recommendations from pediatric societies support family presence during resuscitations. Barriers include: Lack of institutional policies ensuring family inclusion. Lack of formal training for providers on how to support families during these critical moments. Final Takeaways Encouraging institutional policy changes and training providers is key to implementing family presence during codes. Medical teams should challenge outdated practices and prioritize family-centered care in the emergency department. Family-witnessed resuscitation does not increase stress, legal risk, or compromise medical care—but it can significantly improve bereavement outcomes. Read More

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 Necrotizing soft tissue infections can be easily missed in routine cases of soft tissue infection. High mortality and morbidity underscore the need for vigilance. Definition A rapidly progressive, life-threatening infection of the deep soft tissues. Involves fascia and subcutaneous fat, causing fulminant tissue destruction. High mortality often due to delayed recognition and treatment. Types of Necrotizing Fasciitis Type I (Polymicrobial) Involves aerobic and anaerobic organisms (e.g., Bacteroides, Clostridium, Peptostreptococcus). Common in immunocompromised patients or those with comorbidities (e.g., diabetes, peripheral vascular disease). Type II (Monomicrobial) Often caused by Group A Streptococcus (Strep pyogenes) or Staphylococcus aureus. Can occur in otherwise healthy individuals. Vibrio vulnificus (associated with water exposure) is another example. Fournier’s Gangrene (Subset) Specific to perineal, genital, and perianal regions. Common in diabetic patients. Higher mortality, especially in females. Pathophysiology Spread Along Fascia Poor blood supply in fascial planes allows infection to advance rapidly. Tissue ischemia worsened by vascular thrombosis → rapid necrosis. High-Risk Patients Diabetes with vascular compromise. Recent surgeries or trauma (introducing bacteria into deep tissue). Immunosuppression (e.g., cirrhosis, malignancy, or immunosuppressive meds). NSAID use may mask symptoms, delaying diagnosis. Clinical Presentation Early Signs & Symptoms Severe Pain out of proportion to exam findings. Erythema (often with indistinct borders). Fever, Malaise (systemic signs of infection). Rapid progression with possible color changes (red → purple). Bullae Formation (fluid-filled blisters) and skin necrosis/gangrene. Crepitus in polymicrobial cases (gas production in tissue). Late-Stage Signs Systemic toxicity: hypotension, multi-organ failure if untreated. Diagnosis Clinical Suspicion Is Key Pain out of proportion, rapid progression, systemic signs. The “finger test” (small incision to explore fascial planes). Surgical Consultation Early surgical exploration is often the definitive diagnostic step. Lab Tests LRINEC Score (CRP, WBC, Hemoglobin, Sodium, Creatinine, Glucose) to stratify risk. Not definitive but can guide suspicion. Imaging CT scan may reveal gas in tissues, fascial edema, or muscle involvement. Must not delay surgical intervention if clinical suspicion is high. Treatment Principles Immediate & Aggressive Surgical Debridement Often multiple surgical procedures are required as necrosis progresses. Debridement back to healthy tissue margins. Empiric Broad-Spectrum Antibiotics Cover gram-positive (including MRSA), gram-negative, and anaerobes. Examples include: Vancomycin or Linezolid (for MRSA). Piperacillin-tazobactam or Carbapenems (for gram-negative & anaerobes). Clindamycin (to inhibit bacterial toxin production). Adjust based on culture results later. Adjunct Therapies Hyperbaric Oxygen Therapy (if available) for resistant cases. Evidence is mixed; not universally accessible. Supportive Care Intensive monitoring, often in an ICU setting. Fluid resuscitation & vasopressors for septic shock. Prognosis & Disposition High Mortality Rate Influenced by infection site, patient’s baseline health, and speed of intervention. Importance of Rapid Intervention Early recognition, aggressive surgery, and antibiotics improve survival. Long-Term Considerations Patients may require extensive rehabilitation. Reconstructive surgery often needed for tissue deficits. Disposition Operative management is mandatory; patients do not go home. Critical care admission is typical for hemodynamic monitoring and support. Five Key Take-Home Points High Suspicion Saves Lives: Recognize severe pain out of proportion as a critical red flag. Know Your NF Types & Risk Factors: Type I polymicrobial vs. Type II monomicrobial, plus subsets (Fournier’s). Clinical Diagnosis Above All: LRINEC and imaging help, but timely surgical exploration is paramount. Combined Surgical & Medical Therapy: Early debridement + broad-spectrum antibiotics (including toxin inhibition) is lifesaving. Extended Recovery & Mortality Risks: High mortality if missed or delayed. Expect prolonged rehab and possible multiple surgeries. Resources & Further Reading LRINEC Score Calculator EMCrit – Necrotizing Fasciitis Read More

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 One 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: Widespread availability and under-recognition contribute to its prevalence. The potential for unintentional overdose when taking multiple medications containing acetaminophen. Pharmacokinetics and Metabolism: Normal metabolism pathways of acetaminophen and the role of glutathione. Formation of the toxic metabolite NAPQI during overdose situations. Saturation of safe metabolic pathways leading to hepatotoxicity. Pathophysiology of Liver Injury: How excessive NAPQI leads to hepatocyte death, especially in zone III of the liver. The difference between therapeutic dosing and overdose metabolism. Clinical Stages of Acetaminophen Toxicity: Stage 1: Asymptomatic or nonspecific symptoms (first 24 hours). Stage 2: Onset of hepatic injury (24-72 hours), elevated AST/ALT. Stage 3: Maximum hepatotoxicity (72-96 hours), signs of liver failure. Stage 4: Recovery phase, complete hepatic regeneration if survived. Antidote – N-Acetylcysteine (NAC): Mechanisms of NAC in replenishing glutathione and detoxifying NAPQI. The importance of early administration, ideally within 8 hours post-ingestion. NAC’s role even in late presenters and in fulminant hepatic failure. The Rumack-Matthew Nomogram: How to use the nomogram for acute overdoses to determine the need for NAC. Limitations in chronic overdoses and late presentations. Emphasis on obtaining accurate time of ingestion and acetaminophen levels. Treatment Protocols: Standard 21-hour IV NAC protocol and dosing specifics. Managing anaphylactoid reactions associated with IV NAC. Criteria for extending NAC therapy beyond 21 hours. Monitoring and Laboratory Work: Importance of trending AST/ALT, INR, creatinine, lactate, and phosphate. Use of the King’s College Criteria for potential liver transplant evaluation. Special Considerations: Adjustments in pediatric patients regarding NAC dosing volumes. Awareness of IV acetaminophen overdoses and their management. Emerging discussions on the use of fomepizole in massive overdoses. Take-Home Points: Comprehensive Medication History: Always inquire about all medications taken to assess for potential acetaminophen exposure. Early Recognition and Treatment: Due to often silent initial stages, maintain a high index of suspicion and measure acetaminophen levels promptly. Understanding Metabolism and Toxicity: Recognize how overdose alters metabolism, leading to toxic NAPQI accumulation. N-Acetylcysteine Efficacy: NAC is most effective when administered early but remains beneficial even in advanced stages. Proper Use of the Nomogram: Utilize the Rumack-Matthew Nomogram appropriately for acute ingestions and consult toxicology when in doubt. Monitoring and Continuing Care: Be vigilant in monitoring laboratory values and prepared to extend NAC therapy as needed. Consultation and Resources: Engage with poison control centers and utilize available resources for complex cases.   Resources Mentioned Rumack-Matthew Nomogram Rumack-Matthew Nomogram, credit: MDCalc King’s College Criteria King’s College Criteria for Acetaminophen Toxicity Use this tool to assess the need for liver transplant evaluation in cases of acetaminophen-induced hepatic failure. Includes criteria for pH, INR, creatinine, and more. Poison Control Center (available 24/7 for consultation): 1-800-222-1222   References Goldfrank’s Toxicologic Emergencies, 9th Edition was consulted for information on the pharmacokinetics and clinical presentation of acetaminophen toxicity. For more details, see: Nelson, L. S., Howland, M. A., Lewin, N. A., Smith, S. W., Goldfrank, L. R., & Hoffman, R. S. (Eds.). (2011). Goldfrank’s toxicologic emergencies (9th ed.). McGraw-Hill Education. Read More

We review Sexually Transmitted Infections and pertinent updates in diagnosis and management. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Sexually_Transmitted_Infections_2_0.mp3 Download Leave a Comment Tags: gynecology, Infectious Diseases, Urology Show Notes Table of Contents (1:49) Chlamydia (3:31) Gonorrhea (4:50) PID (6:14) Syphilis (8:08) Neurosyphilis (9:13) Tertiary Syphilis (10:06) Trichomoniasis (11:13) Herpes (12:49) HIV (14:10) PEP (15:13) Mycoplasma Genitalium (18:00) Take Home Points Chlamydia: Prevalence: Most common STI. High percentage of asymptomatic cases (40% to 96%). Presentation: Urethritis, cervicitis, pelvic inflammatory disease (PID), prostatitis, proctitis, pharyngitis, arthritis. Importance of considering extra-genital sites (oral and rectal infections). Testing: Gold Standard: Nucleic Acid Amplification Test (NAAT) via PCR. Sampling Sites: Endocervical or urethral swabs preferred over urine samples due to higher sensitivity. Triple-site testing (genital, rectal, pharyngeal) recommended for comprehensive detection. Treatment Updates: Previous Regimen: Azithromycin 1 g orally in a single dose. Current First-Line Treatment: Doxycycline 100 mg orally twice daily for 7 days. Alternatives: Azithromycin remains an option for patients unlikely to adhere to a 7-day regimen or for pregnant patients. Note: PID treatment differs and will be discussed separately. Gonorrhea: Presentation: Similar to chlamydia; can be asymptomatic. Symptoms include urethritis, cervicitis, PID, prostatitis, proctitis, pharyngitis. Testing: Gold Standard: NAAT. Sampling Sites: Endocervical swabs are more sensitive than urine samples. Triple-site testing is crucial to avoid missing infections. Treatment Updates: Previous Regimen: Ceftriaxone 250 mg IM plus azithromycin 1 g orally. Current Recommendation: Ceftriaxone 500 mg IM single dose. Adjusted due to rising azithromycin resistance and updated pharmacokinetic data. Co-Infection Considerations: High rates of chlamydia and gonorrhea co-infection (20% to 40%). CDC recommends empiric treatment for chlamydia when treating gonorrhea to prevent complications like PID and infertility. Pelvic Inflammatory Disease (PID): Etiology: Not solely caused by chlamydia and gonorrhea; about 50% of cases involve other pathogens like bacterial vaginosis (BV) organisms and anaerobes. Treatment Changes: Expanded Coverage Regimen: Ceftriaxone 500 mg IM once. Doxycycline 100 mg orally twice daily for 14 days. Metronidazole 500 mg orally twice daily for 14 days. Inclusion of metronidazole addresses anaerobic bacteria contributing to PID. Syphilis: Stages and Presentation: Primary Syphilis: Painless chancre on genitals. Treatment: Penicillin G 2.4 million units IM single dose. Secondary Syphilis: Rash (often diffuse), mucocutaneous lesions, nonspecific joint pain. Treatment: Same as primary syphilis. Latent Syphilis: Asymptomatic phase; divided into early (<1 year) and late (>1 year). Treatment for Late Latent: Penicillin G 2.4 million units IM once weekly for 3 weeks. Recommended when the timing of infection is unclear. Neurosyphilis: Can occur at any stage. Symptoms include visual changes, severe headaches, neurological deficits. Diagnosis: Requires lumbar puncture (LP) for confirmation. Treatment: Admission for intravenous penicillin G. Tertiary Syphilis: Rare, advanced stage with severe manifestations (e.g., gummas, cardiovascular complications, neurological signs). Treatment: Extended penicillin therapy similar to late latent syphilis. Trichomoniasis: Presentation: Often asymptomatic. In women: Vaginal discharge. In men: Urethritis. Testing: Shift from wet mount microscopy to NAAT for improved detection. Swab samples preferred over urine for higher sensitivity. Treatment Updates: Previous Regimen: Metronidazole 2 g orally in a single dose. Current Recommendations: Women: Metronidazole 500 mg orally twice daily for 7 days. Men: Single 2 g dose remains acceptable. Herpes Simplex Virus (HSV): Types and Transmission: HSV-1 and HSV-2: Both can cause oral and genital infections. Increasing crossover between oral and genital sites. Testing: Serum IgG testing not useful for acute diagnosis due to widespread prior exposure. Preferred Method: PCR testing from lesion swabs. Clinical Tip: If the lesion is characteristic, clinicians may start treatment without waiting for test results. Treatment: Preferred Medication: Valacyclovir (Valtrex) for ease of dosing. Dosage: Initial episode: 1 g orally twice daily for 7 to 10 days. Recurrence: 1 g daily for 5 days. Alternative: Acyclovir for cost considerations. Human Immunodeficiency Virus (HIV): Testing Limitations: Window Periods: Fourth-generation tests have a window period of 2 to 4 weeks. Negative results during this period may not rule out recent infection. Acute HIV Infection: Presents with flu-like symptoms: malaise, joint pains, fatigue. Diagnosis Challenges: Standard HIV tests may

We discuss migraines with one of the authorities in the field. Hosts: Benjamin Friedman, MD of Montefiore Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Migraines.mp3 Download Leave a Comment Tags: Neurology Show Notes Initial Approach to Diagnosing Migraines: Differentiating between primary headaches (migraine, tension-type, cluster) and secondary causes (e.g., subarachnoid hemorrhage). The importance of patient history and reevaluation after initial treatment. Recognizing the unique presentation of cluster headaches and their management implications. Effective Acute Migraine Treatments: First-line treatments including anti-dopaminergic medications like metoclopramide (Reglan) and prochlorperazine (Compazine), and parenteral NSAIDs like ketorolac (Toradol). The limited role of triptans in the ED due to side effects and less efficacy compared to anti-dopaminergics. The use of nerve blocks (greater occipital nerve block and sphenopalatine ganglion block) as effective treatments without systemic side effects. Treatments to Avoid or Use with Caution: Diphenhydramine (Benadryl): Studies show it does not prevent akathisia from anti-dopaminergics nor improve migraine outcomes. IV Fluids: Routine use is not supported unless the patient shows signs of dehydration. Magnesium: Conflicting evidence with some studies showing no benefit or even harm. Managing Refractory Migraines: Second-line treatments including additional doses of metoclopramide combined with NSAIDs or dihydroergotamine (DHE). Considering opioids as a last resort when other treatments fail. The potential use of newer medications like lasmiditan and CGRP antagonists. Preventing Recurrence of Migraines: Administering a single dose of dexamethasone (4 mg IV) to reduce the risk of headache recurrence after discharge. Prescribing NSAIDs or triptans upon discharge for outpatient management. Recognizing and addressing chronic migraine, and initiating preventive therapies like propranolol when appropriate. Key Takeaways Differentiate Primary from Secondary Headaches and Reassess After Treatment: Use patient history and reevaluation post-treatment to distinguish migraines from more serious conditions, reducing unnecessary imaging and procedures. First-Line Treatments Are Effective: Anti-dopaminergic medications and NSAIDs are the mainstay of acute migraine treatment in the ED. Reserve opioids for cases unresponsive to multiple lines of treatment. Avoid Unnecessary Interventions: Diphenhydramine and routine IV fluids do not have proven benefits and can be excluded to streamline care. Utilize Nerve Blocks for Refractory Cases: Greater occipital nerve blocks and sphenopalatine ganglion blocks are effective alternatives for patients not responding to medication. Prevent Recurrence with Dexamethasone and Outpatient Planning: A single IV dose of dexamethasone can help prevent recurrence. Provide prescriptions and consider preventive therapies to reduce future ED visits. Read More

We discuss a new class of medications, Immune Checkpoint Inhibitors, and their side effects. Hosts: Avir Mitra, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Immune_Checkpoint_Inhibitors.mp3 Download Leave a Comment Tags: Oncology Show Notes Overview of Immune Checkpoint Inhibitors (ICIs) ICIs are a relatively new class of oncologic drugs that have revolutionized cancer treatment. Unlike chemotherapy, ICIs help the immune system develop memory against cancer cells and adapt as the cancer mutates. Since their release in 2011, ICIs have expanded to 83 indications for 17 different cancers, with approximately 230,000 patients using them. Mechanism of Action Cancer cells can evade the immune system by binding to T cell receptors that downregulate the immune response. ICIs work by blocking these receptors or ligands, preventing the downregulation and allowing T cells to proliferate and attack cancer cells. Common ICIs Risks and Toxicities of ICIs ICIs can lead to autoimmune attacks on healthy cells due to immune system upregulation. Immune-related adverse effects (irAEs) include colitis, pneumonitis, dermatitis, hepatitis, and endocrine issues (e.g., hypothyroid, hypocortisolemia, hypophysitis). These toxicities can present as infections, making diagnosis challenging in the emergency room. Management of ICI Toxicities in the ER Diagnosis: Look for signs that mimic infections (e.g., cough and fever in pneumonitis). Diagnostic Imaging in pneumonitis: If CXR is normal but suspicion is high, consider CT scans to differentiate conditions like pneumonitis from other issues such as malignancy-associated pleural effusion or acute pulmonary embolism. Treatment: The primary treatment for irAEs is steroids (e.g., prednisone 1 mg/kg). Start steroids early and hold the ICI to manage symptoms effectively and increase the likelihood of resuming ICI therapy later. Consider using antibiotics in combination with steroids if there is uncertainty about whether symptoms are due to infection or ICI toxicity. Coordinate care with the patient’s oncologist if possible Disposition Decisions Patient disposition (admit vs. discharge) should depend on clinical presentation and severity. Coordination with oncology is crucial; they are often comfortable with starting steroids even if there is a potential infection. Patients can be discharged if symptoms are mild, but sicker patients with more complex presentations may require admission. Take-Home Points ICIs are a new class of cancer drugs that effectively target cancer cells but come with unique immune-related toxicities. Diagnosing irAEs can be challenging due to symptom overlap with infections. The cornerstone of treatment is early administration of steroids and temporarily holding the ICI. Close collaboration with oncology teams is essential for optimal patient management. Read More

We discuss a case of ataxia in children and how to approach the evaluation of these pts. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ataxia_in_Children.mp3 Download Leave a Comment Tags: Neurology, Pediatrics Show Notes Introduction The episode focuses on ataxia in children, which can range from self-limiting to life-threatening conditions. Pediatric emergency medicine specialist shares insights on the topic. The Case An 18-month-old boy presented with ataxia, unable to keep his head up, sit, or stand, and began vomiting. Previously healthy except for recurrent otitis media and viral-induced wheezing. The decision to take the child to the emergency department (ED) was based on acute symptoms. Differential Diagnosis Common causes include acute cerebellar ataxia, drug ingestion, Guillain-Barre syndrome, and basilar migraine. Less common causes include cerebellitis, encephalitis, brain tumors, and labyrinthitis. Importance of History and Physical Examination A detailed history and physical exam are essential in diagnosing ataxia. Key factors include time course, recent infections, signs of increased intracranial pressure, and toxic exposures. Look for signs such as bradycardia, hypertension, vomiting, and overall appearance. Diagnostic Workup Initial tests include point-of-care glucose and neuroimaging for concerns about trauma or increased intracranial pressure. MRI is preferred for posterior fossa abnormalities, but non-contrast head CT is commonly used due to accessibility. Lumbar puncture may be needed if meningismus is present. Treatment Approach Treatment depends on the underlying cause: Acute cerebellar ataxia is self-limiting and typically resolves with time. Antibiotics are required for meningitis or encephalitis. Steroids may be useful for cerebellitis and acute disseminated encephalomyelitis (ADEM). Specialist consultations are necessary for severe diagnoses like intracranial masses. Outcome of the Case Study The child had a normal fast T2 MRI and improved during the ED stay. Diagnosed with a combination of cerebellar ataxia and labyrinthitis. Received myringotomy tubes and experienced no further neurologic changes or otitis media episodes. Take-Home Points Diverse Etiologies: Ataxia in children can have various causes that range from self-limiting to life-threatening Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures. Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting. Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities. Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention. Read More

We discuss the approach to diagnosing and managing hypernatremia in the emergency department. Hosts: Abigail Olinde, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hypernatremia.mp3 Download Leave a Comment Tags: Electorlye Show Notes Episode Overview: Introduction to Hypernatremia Definition and basic concepts Clinical presentation and risk factors Diagnosis and management strategies Special considerations and potential complications Definition and Pathophysiology: Hypernatremia is defined as a serum sodium level over 145 mEq/L. It can be acute or chronic, with chronic cases being more common. Symptoms range from nausea and vomiting to altered mental status and coma. Causes of Hypernatremia based on urine studies: Urine Osmolality > 700 mosmol/kg Causes: Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses Unreplaced GI Losses: Vomiting, diarrhea Unreplaced Insensible Losses: Burns, extensive skin diseases Renal Water Losses with Intact AVP Response: Diuretic phase of acute kidney injury Recovery phase of acute tubular necrosis Postobstructive diuresis Urine Osmolality 300-600 mosmol/kg Causes: Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea Partial AVP Deficiency: Incomplete central diabetes insipidus Partial AVP Resistance: Nephrogenic diabetes insipidus Urine Osmolality < 300 mosmol/kg Causes: Complete AVP Deficiency: Central diabetes insipidus Complete AVP Resistance: Nephrogenic diabetes insipidus Urine Sodium < 25 mEq/L Causes: Extrarenal Water Losses with Volume Depletion: Vomiting, diarrhea, burns Unreplaced Insensible Losses: Sweating, fever, respiratory losses Urine Sodium > 100 mEq/L Causes: Sodium Overload: Ingestion of salt tablets, hypertonic saline administration Salt Poisoning: Deliberate or accidental ingestion of large amounts of salt Mixed or Variable Urine Sodium Causes: Diuretic Use: Loop diuretics, thiazides Adrenal Insufficiency: Mineralocorticoid deficiency Osmotic Diuresis with Renal Water Losses: High glucose, mannitol Risk Factors: Patients with impaired thirst response or those unable to access water (e.g., altered or ventilated patients) are at higher risk. Important to consider underlying conditions affecting thirst mechanisms. Diagnosis: Initial assessment includes history, physical examination, and laboratory tests. Key tests: urine osmolality and urine sodium levels. Lab errors should be considered if the clinical picture does not match the lab results. Management Strategies: Calculate the Free Water Deficit (FWD) to guide treatment. Administration routes include oral, NGT, G-tube, or IV with D5W for larger deficits. Safe correction rate is 10-12 mEq/L per day or 0.5 mEq/L per hour to avoid cerebral edema. Address hypovolemia with isotonic fluids before correcting sodium. Monitoring and Follow-Up: Monitor sodium levels every 4-6 hours. Assess urine output and adjust free water administration as needed. Admission to ICU for symptomatic patients or those with severe hypernatremia (sodium >160 mEq/L). Decision to discharge vs admit is a complicated one that factors in symptoms, etiology, degree of hypernatremia, patient preference, access to follow up, etc. Take Home Points: Hypernatremia is a serum sodium level over 145 mEq/L, with symptoms ranging from nausea to coma. It is primarily caused by water loss exceeding intake due to various factors like sweating, vomiting, diarrhea, and renal issues. Correcting hypernatremia too quickly can lead to cerebral edema, so a safe correction rate is essential. Initial treatment involves calculating the Free Water Deficit and selecting the appropriate administration route. Monitor sodium levels frequently and decide on admission or discharge based on symptoms, sodium levels, and patient’s ability to follow up. Read More

We discuss an approach to the acutely agitated patient and review medications commonly used. Hosts: Jonathan Kobles, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Agitation.mp3 Download Leave a Comment Tags: Agitation, psychiatry, Toxicology Show Notes Background/Epidemiology •Definition and Scope: Agitation encompasses behaviors from restlessness to severe altered mental states. It’s a common emergency department presentation, often linked with acute medical or psychiatric emergencies. •Significance: Patients with agitation are at high risk for morbidity and mortality, necessitating prompt and effective management to prevent harm to themselves and healthcare providers. A Changing Paradigm in Describing Agitation •Terminology Shift: Move away from terms like ‘excited delirium’ due to their politicization and stigmatization. Focus on describing agitation by severity and underlying causes. Agitation as a Multifactorial Process •Complex Nature: Recognize agitation as a result of various factors, including medical, psychiatric, and environmental influences. Recognizing Agitation •Signs and Symptoms: Identify agitation early by monitoring for behaviors such as hostility, pacing, non-compliance, and verbal aggression. Initial Evaluation •Severity Assessment: Determine the severity of agitation and prioritize reversible causes and life-threatening conditions. •Diagnostic Steps: Perform vital signs check, blood glucose levels, ECG, and a targeted medical screening exam. Life Threats •Immediate Concerns: Identify and address immediate life threats such as hypoxia, hypoglycemia, trauma, and acute neurological emergencies. Forming a Differential Prior to Treatment •Prioritization: Severe agitation requires immediate treatment to facilitate further evaluation and reduce risk of harm. Physician/Staff Safety •Safety Measures: Ensure personal and team safety by maintaining a calm environment and preparing for potential violence. Multimodal Approach •Self-check In: Physicians should mentally prepare and approach the situation calmly to ensure effective management. •Verbal De-escalation: Use techniques focused on safety, therapeutic alliance, and patient autonomy to manage agitation non-pharmacologically. Medication Administration •Oral/Sublingual Medications: Consider oral medications for less severe cases to maintain patient autonomy and avoid invasive procedures. •IM or IV Medications: Use intramuscular or intravenous medications for rapid control in severe cases. Specific Medication Regimens •PO Regimens: •Medications: Antipsychotics like Zyprexa (olanzapine) 5-10 mg, benzodiazepines like Ativan (lorazepam) 1-2 mg. •Benefits: Empower patients with a sense of autonomy, avoid injection-related trauma. •Pharmacokinetics: •Olanzapine: Onset in 15-45 minutes, peak effect in 1-2 hours, duration 12-24 hours. •Lorazepam: Onset in 30-60 minutes, peak effect in 2 hours, duration 6-8 hours. •IV/IM Regimens: •Medications: Droperidol, haloperidol, midazolam, ketamine. •ACEP 2023 Guidelines: Recommend droperidol with midazolam or an atypical antipsychotic for severe agitation. •Pharmacokinetics (IM): •Haloperidol: IM onset in 15, time to sedation ~25 minutes, can last for 2 hours •Droperidol: IM onset in 5-10 minutes, duration 2-4 hours but can last as long as 12 hours •Midazolam: IM onset ~15 minutes, , duration 20 minutes – 2 hours. •Lorazepam: IM onset ~15-30 minutes, , duration up to 3 hours •Ketamine: IM onset in ~5 minutes, duration 5-30 minutes. Special Situations •Elderly/Dementia: Optimize environment, use non-pharmacologic measures, avoid benzodiazepines to reduce delirium risk. •Parkinson’s Disease: Avoid antipsychotics that can precipitate a Parkinsonian crisis. •Autism/Pediatrics: Engage caregivers, create a calming environment, avoid aggressive measures. •Alcohol Withdrawal: Utilize benzodiazepines and phenobarbital. Re-dosing and Physical Restraints •Re-dosing: Use the lowest effective dose, consider continuous monitoring, and reassess frequently. •Physical Restraints: Employ as a last resort, ensuring close monitoring for any adverse effects. Final Points •Clinical Leadership: Physicians should lead with clear communication, planning, and support for the team. •Continuous Learning: Regular debriefing and assessment after each incident to improve future responses.   Read More

We discuss an approach to the critically ill infant. Hosts: Ellen Duncan, MD, PhD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/The_Critically_Ill_Infant.mp3 Download Leave a Comment Tags: Pediatrics Show Notes The Critically Ill Infant: THE MISFITS Trauma ‘T’ in the mnemonic stands for trauma, which includes both accidental and intentional causes. Considerations for Non-accidental Trauma: Stresses the importance of considering non-accidental trauma, especially given that it may not always present with obvious external signs. Anatomical Vulnerabilities: Highlights specific anatomical considerations for infants who suffer from trauma: Infants have proportionally larger heads, increasing their susceptibility to high cervical spine (c-spine) injuries. Their liver and spleen are less protected, making abdominal injuries potentially more severe. Heart 5 T’s of Cyanotic Congenital Heart Disease: Introduces a mnemonic to help remember key right-sided ductal-dependent lesions: Truncus Arteriosus: Single vessel serving as both pulmonary and systemic outflow tract. Transposition of the Great Arteries: The pulmonary artery and aorta are switched, leading to improper circulation. Tricuspid Atresia: Absence of the tricuspid valve, leading to inadequate development of the right ventricle and pulmonary circulation issues. Tetralogy of Fallot: Comprises four defects—ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta. Total Anomalous Pulmonary Venous Connection (TAPVC): Pulmonary veins do not connect to the left atrium but rather to the right heart or veins, causing oxygen-rich blood to mix with oxygen-poor blood. Other Significant Conditions: Ebstein’s Anomaly: Malformation of the tricuspid valve affecting right-sided heart function. Pulmonary Atresia/Stenosis: Incomplete formation or narrowing of the pulmonary valve obstructs blood flow to the lungs. Left-sided Ductal-Dependent Lesions: Conditions such as aortic arch abnormalities (coarctation or interrupted arch), critical aortic stenosis, and hypoplastic left heart syndrome are highlighted. These generally present with less obvious cyanosis and more pallor. Diagnostic and Management Considerations: Routine prenatal ultrasounds detect most cases, but conditions like coarctation of the aorta and TAPVC might not be apparent until after birth when the ductus arteriosus closes. Emphasizes the importance of a thorough physical exam: checking for murmurs, assessing hepatosplenomegaly, feeling for femoral pulses, measuring pre- and post-ductal saturations, and taking blood pressures in all four limbs. Treatment Recommendations: Early initiation of alprostadil (a prostaglandin) for patients with suspected ductal-dependent lesions to maintain ductal patency. Preparedness for potential complications from alprostadil treatment, such as apnea and hypotension, which may necessitate intubation and hemodynamic support. Endocrine Focuses on acute salt-wasting crisis in undiagnosed Congenital Adrenal Hyperplasia (CAH). Electrolyte imbalances: ↓Na, ↑K, ↓HCO3, ↓Glu. Treatment: hydrocortisone (25mg for babies, 50mg for kids, 100mg for adults). Metabolic Electrolyte abnormalities such as hypoglycemia (values: <60 in infants, <40 in neonates). Broad differential. Rule of 50s for correction: D% x #ml/kg fluid = 50. Inborn Errors of Metabolism Major classes include organic acidurias (profound anion gap metabolic acidosis) and urea cycle defects (hyperammonemia) Recommendation: Draw gas and ammonia level. Sepsis Emphasized as a critical condition in the differential diagnosis for ill infants, though placed later in the mnemonic for easier recall. Presentation and Diagnosis: Sepsis in infants often presents nonspecifically, making early detection challenging. Immediate drawing of blood cultures upon suspicion of sepsis. Initial Treatment: Prompt initiation of antimicrobials and fluids. Use of vancomycin for gram-positive and MRSA coverage, a third-generation cephalosporin or pip-tazo for broad bacterial coverage, and acyclovir for HSV. (tailor based on age and institutional guidelines) Supportive Care: Highlights the necessity of fluid resuscitation to stabilize the patient. Formula Formula-Related Electrolyte Imbalances: Incorrect mixing of infant formula can cause hypo- or hypernatremia. Consequences of Electrolyte Imbalances: Both conditions can lead to severe outcomes including altered mental status, seizures, coma, and potentially death. Management Strategies: Treatment varies based on the sodium levels: Symptomatic hyponatremia is treated with hypertonic saline. Hypernatremia requires fluid resuscitation. Intestinal Catastrophe Specific Conditions: Malrotation with Midgut Volvulus: Twisting of the intestines that can obstruct blood flow. Necrotizing Enterocolitis (NEC): Can occur in both full-term and preterm infants, involves inflammation and bacterial infection that can destroy bowe

We review Acute Respiratory Distress Syndrome Hosts: Sadakat Chowdhury, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ARDS.mp3 Download Leave a Comment Tags: Critical Care, Pulmonary Show Notes Definition of ARDS: Non-cardiogenic pulmonary edema characterized by acute respiratory failure. Berlin criteria for diagnosis include acute onset within 7 days, bilateral pulmonary infiltrates on imaging, not fully explained by cardiac failure or fluid overload, and impaired oxygenation with PaO2/FiO2 ratio <300 mmHg, even with positive end-expiratory pressure (PEEP) >5 cm H2O. Severity based on oxygenation (Berlin criteria): Mild: PaO2/FiO2 200-300 mmHg Moderate: PaO2/FiO2 100-200 mmHg Severe: PaO2/FiO2 <100 mmHg Epidemiology: Occurs in up to 23% of mechanically ventilated patients. Mortality rate of 30-40%, primarily due to multiorgan failure. Differentiation from Cardiogenic Pulmonary Edema: Chest CT shows diffuse edema and pleural effusion in cardiogenic edema; patchy edema, dense consolidation in ARDS. Ultrasound may show diffuse B lines in cardiogenic edema; patchy B lines and normal A lines in ARDS. Pathophysiology: Exudative phase: Immune-mediated alveolar damage, pulmonary edema, cytokine release. Proliferative phase: Reabsorption of edema fluid. Fibrotic phase: Potential for prolonged ventilation. Etiology: Direct lung injury (pneumonia, toxins, aspiration, trauma, drowning) and indirect causes (sepsis, pancreatitis, transfusion reactions, certain drugs). Diagnostics: Comprehensive workup including imaging (chest X-ray, CT), laboratory tests (complete blood count, basic metabolic panel, blood gases), and specialized tests depending on suspected etiology. Management Strategies: Steroids: Beneficial in certain etiologies of ARDS, with specifics on dosing and duration. Fluid Management: Conservative fluid strategy, diuresis guided by patient condition. Ventilation: Non-invasive ventilation (NIV) preferred in specific cases; mechanical ventilation strategies to ensure lung-protective ventilation. Proning: Used in severe ARDS to improve oxygenation. Inhaled Vasodilators: Used for refractory hypoxemia and specific complications like right heart failure. Extracorporeal Membrane Oxygenation (ECMO): Considered for severe ARDS as salvage therapy. Supportive Care: Includes monitoring and management of complications, nutrition, and physical therapy. Ventilation Specifics: Tidal volume and pressure settings aim for lung-protective strategies to prevent ventilator-induced lung injury. Permissive hypercapnia, plateau pressure, PEEP, and ventilation mode adjustments based on patient response. ARDSnet Table: ventilator_protocol_2008-07 Read More

We review Nitrous Oxide Toxicity: Symptoms, diagnosis, and treatment overview Hosts: Stefanie Biondi, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nitrous_Oxide_Toxicity.mp3 Download Leave a Comment Tags: Toxicology Show Notes Patient Case Illustration Hypothetical case: 21-year-old male with no previous medical history, experiencing a month of progressively worsening numbness, tingling, and weakness. Initially starting in his toes and spreading to his hips, and later involving his hands, the symptoms eventually escalated to the point of immobilization. Despite initially denying drug use, the patient admitted to using 40-60 canisters of nitrous oxide (whippets) every weekend for the last three months. Background and Recreational Use of Nitrous Oxide Nitrous oxide, a colorless, odorless gas with anesthetic properties. Synthesized in the 18th century. Its initial medical purpose expanded into recreational use due to its euphoric effects. Resurgence as a recreational drug during the COVID-19 lockdowns. Accessibility and legal status. Public Misconceptions and Health Consequences There are widespread misconceptions about nitrous oxide Particularly the belief in its safety and lack of long-term health risks. Contrary to popular belief, frequent use of nitrous oxide can lead to significant, sometimes irreversible, health issues. Neurological Examination and Diagnosis Key components of the examination include assessing strength, sensation, cranial nerves, and proprioception, with specific abnormalities such as symmetrically decreased strength in a stocking-glove pattern, upgoing Babinski reflex, and positive Romberg sign being indicative of potential toxicity. Physical Exam Findings: Upper vs Lower Motor Neuron Lesions Localize the Lesion- Differential Diagnoses for Extremity Weakness Localize the Lesion- Differential Diagnoses for Extremity Weakness Localize the Lesion- Differential Diagnoses for Extremity Weakness MRI Findings and Subacute Combined Degeneration The MRI displayed symmetric high signal intensity in the dorsal columns, a diagnostic feature identified as the inverted V sign or inverted rabbit ear sign. Significance of the Inverted V Sign: This MRI sign is pathognomonic for subacute combined degeneration, indicating it is a distinct marker for this condition. T2 Weighted Axial Images: The inverted V sign is observed in T2 weighted axial MRI images, which are used to evaluate the presence and extent of demyelination within the spinal cord. Interpretation of Hyperintense Signals: Hyperintense signals on T2 weighted images generally indicate demyelination, where the protective myelin sheath around nerve fibers is damaged or destroyed. Anatomical Location: The dorsal columns, located anatomically dorsal (toward the back) within the spinal cord, will appear toward the bottom of the screen in an axial (cross-sectional) view on the MRI. Demyelination Appearance: Demyelination in the dorsal columns, typically situated in the thoracic spine, manifests as an upside-down V shape on the MRI, correlating with the described inverted V or rabbit ear sign. Pathophysiology of SCD due to Nitrous Oxide Nitrous Oxide’s Effect on Vitamin B12: Nitrous oxide inactivates vitamin B12 by oxidizing a cobalt component within the molecule, rendering the vitamin functionally ineffective despite adequate consumption and absorption. Impact on Methionine Synthase: The oxidation of vitamin B12 by N2O prevents it from activating methionine synthase, an enzyme critical for important biochemical processes. Folate to Tetrahydrofolate Conversion: Inactive methionine synthase cannot convert folate into tetrahydrofolate, which is necessary for DNA synthesis. This disruption can lead to megaloblastic anemia, a condition associated with N2O-induced subacute combined degeneration. Conversion of Homocysteine to Methionine: Methionine synthase is also responsible for converting homocysteine to methionine. Methionine is essential for the maintenance of myelin integrity, the protective sheath around nerve fibers. Demyelination and Neurological Symptoms: The inability to maintain myelin integrity due to disrupted methionine production leads to the demyelination of dorsal columns and peripheral motor/sensory nerves, characteristic of N2O-SCD. Normal B12 Levels with Functional Deficiency: Blood levels of vitamin B12 can appear normal in individuals affected by N2O exposure, as the issue lies in the vitamin’s inactivation rather than its absence, creating a functional deficiency. Diagnosis of N2O-SCD: To diagnose N2O-induced SCD, healthcare providers need to check for elevated levels of methylmalonic acid and homocysteine. These substances are typically metabolized with the help of vitamin B12, and their elevated levels indicate a functional deficiency of B12 due to N2O exposure. Treatment and Management Lack of Standardized Treatment: There is no universally accepted treatment protocol for N2O induced

We review threatened abortion and the complexities in its care. Hosts: Stacey Frisch, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Threatened_Abortion.mp3 Download One Comment Tags: OBGYN Show Notes Background Defined as vaginal bleeding during early pregnancy (before 20 weeks) with a closed cervical os, no passage of fetal tissue, and IUP on ultrasound Occurs in 20-25% of all pregnancies. Initial Assessment and Management Priority is to assess patient stability, establish good IV access, FAST may be helpful in identifying some ruptured ectopics early Broad differential diagnosis is crucial to avoid mistaking conditions like ectopic pregnancy for other emergencies. Importance of a detailed history and physical examination. Diagnostic Approach Essential tests include HCG level, urinalysis, and possibly CBC + blood type/Rh status. Rhogam’s use is well-supported in second and third trimester bleeding; however, data is less robust for first trimester bleeding in preventing sensitization Importance of interpreting b-HCG with caution and understanding HCG discriminatory zones. Use of ultrasound imaging, both bedside and formal, to assess the pregnancy’s status. Patient Counseling and Management Open and honest communication about the prognosis of threatened abortion. Addressing psychosocial aspects, including dispelling guilt and myths, and screening for intimate partner violence and mental health issues. Recommendations against bedrest and certain activities Lack of evidence supporting restrictions on sexual activity. Standard pregnancy guidelines: avoiding smoking, alcohol, drug use, and starting prenatal vitamins. Follow-up and Precautions Adopting a wait-and-see approach for stable patients, with scheduled follow-ups for ultrasounds and beta-HCG tests. Educating patients on critical warning signs that require immediate medical attention. Emphasizing the importance of returning to the hospital if experiencing significant bleeding or other severe symptoms. Take Home Points Threatened Abortion is defined as Experiencing abdominal pain and/or vaginal bleeding during early pregnancy (before 20 weeks), characterized by a closed cervical os and no expulsion of fetal tissue. In these cases, it is important to assess patient stability promptly. Keep your differential broad in these cases. The evaluation will in most cases involve a combination of labs and ultrasound imaging. Understand that the Rhogam certainly has a role in second and third trimester vaginal bleeding in the Rh-negative patient, and that there is a dearth of good data on its role in the first trimester – it will ultimately be a decision that is made by you, OBGYN, and the patient. Approach the interpretation of HCG levels with caution and remember that ectopic pregnancies might not adhere to conventional HCG levels. Established follow up and discharge instructions are crucial. Manage stable patients with a watchful waiting approach, scheduling subsequent visits for continuous ultrasounds and HCG testing. Clearly outline the importance of immediate medical attention for symptoms such as intense bleeding, significant abdominal pain, fever, or feelings of insecurity at home. Finally, we play an important role wherein we must ensure that the patient is medically stable and psychosocially safe. Here, compassionate communication is crucial when discussing what the diagnosis might entail, alleviate any feelings of blame or shame, and remain vigilant for signs of intimate partner violence or mental health issues. As emergency medicine physicians, it’s crucial for us to approach these cases with a comprehensive mindset. Read More

We review a general approach to syncope in children. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Syncope_in_Children.mp3 Download Leave a Comment Tags: Cardiology, Pediatrics Show Notes Initial Evaluation and Management: Similar initial workup for children and adults: checking glucose levels for hypoglycemia and conducting an EKG. The history and physical exam are crucial. Dextrose Administration in Children: Explanation of the ‘rule of 50s’ for determining the appropriate dextrose solution and dosage for children. ECG Analysis: Importance of ECG in diagnosing dysrhythmias like long QT syndrome, Brugada syndrome, catecholamine polymorphic V tach, ARVD, ALCAPA, and Wolff-Parkinson-White syndrome. Younger children’s dependency on heart rate for cardiac output and the risk of arrhythmias in kids with congenital heart disease. Condition Characteristic ECG Findings Congenital/Acquired Long QT Syndrome (LQTS) Prolonged QT interval Congenital/Acquired Wolff-Parkinson-White Syndrome (WPW) Short PR interval, Delta wave Congenital Brugada Syndrome ST elevation in V1-V3, Right bundle branch block Congenital Atrioventricular Block (AV Block) PR interval prolongation (1st degree), Missing QRS complexes (2nd & 3rd degree) Congenital/Acquired Supraventricular Tachycardia (SVT) Narrow QRS complexes, Absence of P waves, Tachycardia Congenital/Acquired Ventricular Tachycardia Wide QRS complexes, Tachycardia Congenital/Acquired Arrhythmogenic Right Ventricular Dysplasia (ARVD/C) Epsilon waves, V1-V3 T wave inversions, Right bundle branch block Congenital Hypertrophic Cardiomyopathy (HCM) Left ventricular hypertrophy, Deep Q waves Congenital Pulmonary Hypertension Right ventricular hypertrophy, Right axis deviation Acquired Athlete’s Heart Sinus bradycardia, Voltage criteria for left ventricular hypertrophy Acquired Catecholaminergic Polymorphic VT (CPVT) Bidirectional or polymorphic VT, typically normal at rest Congenital Anomalous Origin of Left Coronary Artery from Pulmonary Artery (ALCAPA) May be normal, signs of ischemia or infarction in severe cases Congenital History Taking: Key aspects include asking about syncope with exertion, syncope after being startled, and syncope after pain or emotional stress. Prolonged loss of consciousness may indicate seizures, and emotional stress and pain can trigger breath-holding spells. Breath-Holding Spells: Clarification of misconceptions about breath-holding spells, discussing their causes and characteristics, like cyanotic and pallid types. Association with iron deficiency and the fact that most children outgrow these spells by age 8. Physical Examination and History: A cardiac exam is vital, with specific signs to look for, like murmurs in hypertrophic cardiomyopathy. History can help identify the etiology of syncope, such as vasovagal responses or orthostatic hypotension. Vasovagal Syncope: Common in kids, especially teenagers, typically presenting with a prodrome of lightheadedness, diaphoresis, and pallor. Normal glucose and EKG are expected in these cases. Additional Lab Tests: Pregnancy tests in reproductive-age women, and checking for less common causes like pulmonary embolism, subarachnoid hemorrhage, and toxic exposures. Take Home Points: Immediate assessments for syncope in children should include a FS to evaluate for hypoglycemia and an ECG to evaluate any cardiac rhythm or conduction abnormalities. Apply the “Rule of 50s” for hypoglycemic patients to suggest which fluids should be used. Refer to our table for ECG findings to look out for when reviewing ECG tracings for these patients. Pay particular attention to clues in the history that would suggested HCOM or seizures. Breath-holding spells usually resolve by eight HCOM murmurs will increase with Valsalva maneuver Always keep your differential broad when approaching these patients given the heterogeneity of potential pathology that could lead to this chief complaint Read More

We go over the treatment of rapid atrial fibrillation (afib with RVR). Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Rapid_Atrial_Fibrillation.mp3 Download One Comment Tags: Cardiology Show Notes Understanding AF with RVR Categories General AF with RVR: Definition and basic understanding. Rapid AF with Pre-excitation: Characteristics and complications. Chronic AF in Critical Illness: Identification and special considerations. Stability Assessment in AF with RVR ACLS Protocols: Distinction between unstable and stable patients. Unstable Patients: Immediate need for synchronized cardioversion, standard dose at 200 J for adults. Stable Patients: Rate vs. rhythm control strategies, consideration of underlying etiology. Limitations in Chronic AF: Challenges in patients with AF secondary to critical illness. ACLS Guidelines and ECG Findings Tachycardia with a Pulse Approach: Initial assessment guidelines. ECG Interpretation: Irregularly Irregular Rhythm: Absence of discernible P waves. Ventricular Rate: Typically over 100 bpm. QRS Complexes: Usually narrow, alterations in the presence of bundle branch block or ventricular rate-related aberrancy. Identifying Pre-Excitation Syndromes: Signs of shortened PR interval and slurred QRS, indication of Wolff-Parkinson-White Syndrome. AF with Pre-Excitation (WPW Syndrome) Risk Assessment: Dangers of using AV nodal blockers (BB/CCB, digoxin, adenosine). Alternative Management: Utilization of procainamide or amiodarone for stable patients, synchronized electrical cardioversion for unstable patients. Treatment Approaches for AF Types General Rapid AF: First Line Agents: Metoprolol vs. Diltiazem. Metoprolol Considerations: Dosing (5 mg every 10-15 minutes, max 15 mg), benefits in CAD and HF, limitations in asthma/COPD patients. Diltiazem Advantages: Faster action, suitability in asthma/COPD, typical dosing (0.25 mg/kg initial, followed by 0.35 mg/kg if needed). Critically Ill Patients: Tailoring treatment to underlying pathology, avoiding typical AF pharmacologic treatments. Systematic Evaluation of Tachycardia Causes (TACHIES Mnemonic) Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals (WPW), Embolus, Sepsis. Application of the mnemonic for a comprehensive approach to differential diagnosis. Ultrasound in Diagnostic Assessment Application in Undiagnosed Tachycardia: Identifying EF, pericardial effusion, valvular pathology, and signs of pulmonary embolism. Fluid Status Evaluation: Use of ultrasound for assessing b-lines in lung scans. Management of Chronic AF with HD Instability Assessment of Hemodynamic Impact: Effects of extreme tachycardia on cardiac output, preload and afterload considerations. Chronic vs. Paroxysmal AF: Differentiation in clinical presentation and treatment response. Approaches in Complex AF Cases Addressing RVR of Unclear Etiology: Targeted therapies based on suspected underlying causes. Medication Strategies: Amiodarone: Bolus and drip approach, slow AV nodal without significant impact on contractility. Esmolol: Titration for heart rate control, short-acting nature allowing for rapid cessation if adverse effects are observed. Comprehensive Patient Disposition Considerations: Hemodynamic stability, underlying cause, comorbidities, outpatient follow-up feasibility. Decision-Making Process: Balancing acute management with long-term treatment strategies. Take Home Points Differentiation in AF with RVR Types: It’s essential to distinguish between primary AF with RVR, chronic AF with RVR related to other health issues, and new-onset AF (NOAF) with RVR in critically ill patients, as each type necessitates a unique approach to treatment. ACLS Guidelines for AF with RVR: The ACLS guidelines provide a treatment framework, particularly recommending immediate synchronized cardioversion for unstable patients. However, these guidelines may have limited effectiveness for chronic AF with RVR patients suffering from underlying critical illnesses. ECG Diagnosis in AF: Identifying AF on an ECG is crucial, with key indicators being an irregular rhythm without clear P waves and a ventricular rate exceeding 100 bpm. Accurate ECG interpretation guides effective treatment planning. Special Cases like WPW Syndrome: WPW syndrome and similar conditions require careful treatment consideration, as standard AF treatments can worsen these conditions. Alternatives like procainamide or amiodarone are often more appropriate. Patient-Centered Management of AF with RVR: Management should account for the patient’s overall health, underlying conditions, the chronicity of AF, and other comorbidities. Drugs like metoprolol and diltiazem offer benefits and risks, demanding personalized treatment plans. Pathophysiology in Critical AF Patients: Understanding the underlying pathophysiology in critically ill patients is vital. Tachycardia in these cases might be compensatory, necessitating an investigation into

We discuss Electrical Storm (VT storm) and how to care for the very irritable heart. Hosts: Brian Gilberti, MD Reed Colling, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Electrical_Storm.mp3 Download Leave a Comment Tags: Cardiology Show Notes Background/Overview of VT: Definition: What makes it a storm Three or more sustained episodes of VF, VT, or appropriate ICD shocks in a 24-hour period Pathophysiology: Understanding the origin and mechanism Sympathetic drive/adrenergic surge Underlying pathology: Sodium channelopathies, infiltrative disease like cardiac sarcoidosis, etc. RF’s / trigger / population (reversible cause in ~25% of patients) MI Electrolyte Derangements (emphasis on potassium and magnesium) New/worsening heart failure Catecholamine Surge Drugs (stimulants, cocaine, amphetamines, etc) QT Prolongation Thyrotoxicosis Clinical Presentation: Symptoms of VT: spectrum of symptoms – from palpitations to syncope to cardiac arrest Differentiating VT from other potential ER presentations. Diagnostics in ER: Electrocardiogram (ECG): Recognizing VT patterns. Monomorphic vs polymorphic (Torsades) may change management Wide QRS Fusion best Capture beats Concordance AV-dissociation Lab tests: Potassium, magnesium, troponins, TFTs, etc. Acute Management in the ER: Hemodynamically stable vs. unstable V Unstable = cardioversion Sedation Catecholamine surge should be considered No ideal agent Etomidate or propofol can be considered Ketamine may worsen irritability Pharmacological treatments: Amiodarone Class III antiarrhythmic Most studied in VT storm First line Beta Blockers Propranolol B1 and B2 activity Non-pharmacological approaches: Immediate synchronized cardioversion IABP / ECMO considered for HD unstable patient Cath lab if ischemic etiology suspected Stellate Ganglion Block Take Home Points Definition: VT Storm is commonly defined as three or more sustained episodes of ventricular fibrillation, ventricular tachycardia, or appropriate ICD shocks within a 24-hour period. Varied Presentation: Patients may experience a range of symptoms from palpitations to severe hemodynamic instability. ECG and Diagnosis: Initial ECG may not show VT; continuous cardiac monitoring or device interrogation may be required for diagnosis. VT Identification: Look for wide QRS, rate over 100, fusion beats, capture beats, and AV dissociation to identify VT. Management in Hemodynamic Instability: Cardiovert if the patient shows signs of hemodynamic instability. Sedation Considerations: Be cautious with sedation, especially with ketamine, as it may worsen cardiac irritability in these already adrenergic state patients. Medication Choices: Typically, amiodarone and propranolol are used to manage VT Storm. Cardiology Involvement: Involve cardiology early on, as treatment may extend beyond medications. Read More

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma) Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3 Download 2 Comments Tags: Renal Colic Show Notes Introduction Background Physiology: Normal range and the significance of deviations (>5.5 mEq/L) Epidemiology: Prevalence of hyperkalemia in the ER ESRD missed HD → ECG, monitor Causes / Risk Factors Causes Kidney Dysfunction, Medications, Cellular Destruction, Endocrine Causes, Pseudohyperkalemia High-Risk Medications: Antibiotics: Bactrim, antifungals Calcineurin inhibitors Beta-blockers ACE/ARB K+ Sparing diuretics NSAIDs Digoxin SUX – high risks in neuromuscular disease Lab errors, hemolysis in samples VBG vs Chem accuracy When to repeat a hemolyzed sample 2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA). Clinical Presentation / eval Symptomatic vs. Asymptomatic: “First symptom of hyperkalemia is death” If severe, ascending muscle weakness → paralysis Point at which patients experience symptoms depends on chronicity >7 mEq/L if chronic and can be lower if acute Hyperkalemia can be a cause of non-specific GI symptoms EKG Changes: ECG findings may be the first marker the ER doc gets that something is wrong Typical changes: Peaked T-waves, shortened QT Lengthening of PR interval and QRS duration Bradycardia / Junctional rhythm Hyperkalemia can produce bradycardia without other ECG findings Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017) Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998) ECG changes are not linear, there is no exact association between K+ levels and ECG changes ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs) Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms BRASH Syndrome Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels. Labs Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice) Consider evaluation for adrenal insufficiency Waiting for labs may not be an option Renal dysfunction + consistent ECG findings → prompt treatment before chem results Realistically 2 hours to get back chemistry in most settings ≈ eternity Management in the ER Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia A. Acute Management Strategies: Cardiac protection with calcium 1g over 5-10 mins Lasts 30-60 mins, may have to redose Dose considerations if on digoxin AEs: Calciphylaxis and hypercalcemia Fast pushes can result in hypotension, arrhythmia Calcium chloride vs calcium gluconate Caution in patients taking Digoxin IVF choice – NS vs LR Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL Shifting potassium: insulin/glucose 5 units vs 10 units 5 similar effect, less hypoglycemic episodes (LaRue 2017) If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume Decrease but about 0.5-1.2 mEq/L Effect starts 10-20 mins after administration and can last 4-6 hours Albuterol 10-20 mg over 10 mins (NB: higher dose than for asthma) Peak effect at 90 mins Decreases by 0.5 – 1.0 mEq/L alone With insulin, ~1.2 mEq/L, additive effect Bicarbonate Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift. Removal: Lokelma (Sodium Zirconium cyclosilicate) Luckily residents have never had to use Kayexalate Can start working in 1-2 hours of administration 0.37 mEq/L reduction at 4 hours after 10 g Not a magic bullet in patients who need dialysis Diuretics No studies that demonstrate effectiveness in this ED setting May be effective in patients with normal renal function If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K Nephron BOMB Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex) Thiazide (500-1000 mg IV chlorothiaz

We go over the essential and complex topic of vasopressors in the ED. Hosts: Brian Gilberti, MD Catherine Jamin, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3 Download Leave a Comment Tags: Critical Care Show Notes Introduction Host: Brian Gilberti, MD Guest: Catherine Jamin, MD Associate professor of Emergency Medicine at NYU Langone Health Vice Chair of Operations Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED What Are Vasopressors and When to Use Them Two primary mechanisms to increase blood pressure: Increasing systemic vascular resistance via vasoconstriction Increasing cardiac output via augmenting inotropy and chronotropy Indicators for vasopressor use: MAP <65, systolic BP <90, or significant drop from baseline BP Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients) Commonly Used Vasopressors in the ED Norepinephrine Epinephrine Vasopressin Phenylephrine Norepinephrine Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy) Starting Dose: 10 mcg/min, titrate to MAP >65 Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic) Pros: Can be infused peripherally via large bore IV Vasopressin Mechanism: Activates V1a receptors causing vasoconstriction Dose: Fixed, non-titratable dose of 0.04 units/min Situational Preference: Second-line in septic shock Concerns: Potential for peripheral ischemia Phenylephrine Mechanism: Stimulates alpha-1 receptors causing vasoconstriction Starting Dose: 100 mcg/min, titrate to MAP >65 Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation Concerns: Increases afterload, can worsen low cardiac output states Epinephrine Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors Starting Dose: 5-10 mcg/min, titrate to MAP >65 Situational Preference: Anaphylactic shock, septic cardiomyopathy Limitations: Can induce tachycardia, may elevate lactate levels Escalation Strategy in Refractory Shock Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine Consider POCUS, lactate, central venous saturation, and acid-base status Peripheral Pressors Can safely be administered peripherally via large bore IVs in proximal upper extremity Sites: Cephalic or basilic veins Adverse Events: Low at 1.8% based on meta-analysis Actions in case of extravasation: Phentolamine injection, nitroglycerin paste Push-Dose Pressors Primarily Phenylephrine (peri-intubation, during procedures) Also Epinephrine for peri-code situations Doses: Epi – 5-20 mcg every 2-5 min Take-Home Points Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine. Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65 Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock. Vasopressin is commonly the second we reach for in most of these scenarios Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient Additional References Importance of RUSH (Rapid Ultrasound in SHock) exam for diagnosis and treatment planning: https://emcrit.org/rush-exam/ Read More

We discuss the diagnosis and management of septic arthritis in the pediatric population. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Joint_in_Children.mp3 Download 2 Comments Tags: Infectious Diseases, Pediatrics Show Notes General Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition. Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint. Workup Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain. Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation. Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach. The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000. 1 criterion met = 3% probability of septic arthritis 2 criteria met = 40% probability of septic arthritis 3 criteria met = 93% probability of septic arthritis 4 criteria met = 99+% probability of septic arthritis   If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available. Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies. Management Empiric antibiotic therapy should target the most likely organisms and should not be delayed. Antibiotics may be narrowed once culture results are obtained. The choice of antibiotics is dependent on the age group, with specific combinations suggested for neonates, children between 1 month and 4 years, and children aged 5 and older. Cultures are only positive in 50-60% of cases. Synovial fluid PCR studies can help narrow antibiotic treatment. Take Home Points Limp in the pediatric population can commonly be transient synovitis but we should always consider septic arthritis Some clues in the history and physical that would point you towards septic arthritis include fever, refusal to bear weight, and limited range of motion on exam We are going to have to get labs, including CBC, inflammatory markers, and preoperative labs, along with an XR and possibly an ultrasound Kocher criteria is one tool that can help us determine if this is a patient that requires a joint tap. Arthrocentesis is the gold standard for diagnosis, but antibiotics should be started promptly if the diagnosis is suspected. The choice of antibiotics is dependent upon age group. Neonates get vanc/cefepime, kids 1-4 yo get vanc / ceftriaxone Older than 5 yo get vancomycin Add ceftriaxone to them if patient has sickle cell disease, are immunocompromised, or Lyme or STI are suspected Always cross check with institutional preferences / guidelines when choosing antibiotics Read More

A quick primer on hypocalcemia in the ED. Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3 Download 4 Comments Tags: calcium, Critical Care, Endocrine Show Notes Swami’s CoreEM Post Hypocalcemia Repletion: IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve References: Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298. ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209. Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166. Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53. Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/ Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163. Read More

How and when to reverse anticoagulation in the bleeding EM patient. Hosts: Joe Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3 Download 3 Comments Tags: Anticoagulation, Critical Care, Resuscitation Show Notes Coagulation Cascade:   Algorithm for Anticoagulated Bleeding Patient in the ED:     Indications for Anticoagulation Reversal:   References: Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001 Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643 Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317. Read More

A primer on this airway/ ID/ ENT emergency. Hosts: Joe Offenbacher MD, A Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3 Download 2 Comments Tags: Airway, ENT, Infectious Diseases Show Notes References: Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327. Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074. Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254. http://www.emdocs.net/ludwigs-angina-2/ Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306. Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506. Read More

A quick overview of pneumothorax for the EM physician: the what, why, diagnosis, and treatment. Hosts: Joe Offenbacher, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax_CoreEM_podcast.mp3 Download One Comment Tags: #pneumothorax #FOAMed Show Notes Shownotes: CoreEM Pulmonary Ultrasound Post References: Bense L, Lewander R, Eklund G, et al. Nonsmoking, non-alpha 1-antitrypsin deficiency-induced emphysema in nonsmokers with healed spontaneous pneumothorax, identified by computed tomography of the lungs. Chest 1993; 103:433. Bense L, Wiman LG, Hedenstierna G. Onset of symptoms in spontaneous pneumothorax: correlations to physical activity. Eur J Respir Dis 1987; 71:181. Brown SGA, Ball EL, Perrin K, Asha SE, Braithwaite I, Egerton-Warburton D, Jones PG, Keijzers G, Kinnear FB, Kwan BCH, Lam KV, Lee YCG, Nowitz M, Read CA, Simpson G, Smith JA, Summers QA, Weatherall M, Beasley R; PSP Investigators. Conservative versus Interventional Treatment for Spontaneous Pneumothorax. N Engl J Med. 2020 Jan 30;382(5):405-415. doi: 10.1056/NEJMoa1910775. PMID: 31995686. Chardoli M, Hasan-Ghaliaee T, Akbari H, Rahimi-Movaghar V. Accuracy of chest radiography versus chest computed tomography in hemodynamically stable patients with blunt chest trauma. Chin J Traumatol 2013; 16:351. Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database Syst Rev 2020; 7:CD013031. Ebrahimi A, Yousefifard M, Mohammad Kazemi H, et al. Diagnostic Accuracy of Chest Ultrasonography versus Chest Radiography for Identification of Pneumothorax: A Systematic Review and Meta-Analysis. Tanaffos 2014; 13:29. Gobbel Jr WG, Rhea Jr WG, Nelson IA, Daniel RA. Spontaneous pneumothorax. J Thorac Cardiovasc Surg 1963; 46:331. Lesur O, Delorme N, Fromaget JM, et al. Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax. Chest 1990; 98:341. Lichtenstein DA, Mezière G, Lascols N, et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005; 33:1231. Melton LJ 3rd, Hepper NG, Offord KP. Influence of height on the risk of spontaneous pneumothorax. Mayo Clin Proc 1981; 56:678. Ohata M, Suzuki H. Pathogenesis of spontaneous pneumothorax. With special reference to the ultrastructure of emphysematous bullae. Chest 1980; 77:771. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000; 342:868.   Read More

An interesting back story on this must-not-miss EKG finding in the ED! Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/CoreEM_Wellens.mp3 Download One Comment Tags: #FOAMed, #wellens, Cardiology, EKG, STEMI Show Notes Hosts: Joe Offenbacher MD, Audrey Bree Tse MD EKG Findings in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Table 1 in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. REFERENCES: de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Lee, M., & Chen, C. (2015). Myocardial Bridging: An Up-to-Date Review. Journal of Invasive Cardiology, 27(11), 521–528. https://lifeinthefastlane.com/ecg-library/wellens-syndrome/ Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14;2017:bcr2017222835. doi: 10.1136/bcr-2017-222835. PMID: 29246935; PMCID: PMC5753703. Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638–643. https://doi.org/10.1053/ajem.2002.34800 Tandy, TK; Bottomy DP; Lewis JG (March 1999). “Wellens’ syndrome”. Annals of Emergency Medicine. 33 (3): 347–351. PMID 10036351. doi:10.1016/S0196-0644(99)70373-2. (via Wikipedia) Read More

We discuss EM presentation, diagnosis, and management of subarachnoid hemorrhage. Hosts: Mark Iscoe, MD Brian Gilberti, MD Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SAH.mp3 Download One Comment Tags: Critical Care, Neurology, Subarachnoid Hemorrhage Show Notes Non-contrast head CT showing SAH (Case courtesy of Dr. David Cuete, Radiopaedia.org, rID: 22770)   Hunt-Hess grade and mortality (from Lantigua et al. 2015.) Hunt-Hess grade Mortality (%) 1. Mild Headache 3.5 2. Severe headache or cranial nerve deficit 3.2 3. Confusion, lethargy, or lateralized weakness 9.4 4. Stupor 23.6 5. Coma 70.5   Ottawa Subarachnoid Hemorrhage Rule, and appropriate population for rule application (from Perry et al. 2017) Apply to patients who are: Alert ≥ 15 years old Have new, severe, atraumatic headache that reached maximum intensity within 1 hour of osnet Do not apply to patients who have: New neurologic deficits Previous diagnosis of intracranial aneurysm, SAH, or brain tumor History of similar headaches (≥ 3 episodes over ≥ 6 months) SAH cannot be ruled out if the patient meets any of the following criteria: Age ≥ 40 Symptom of neck pain or stiffness Witnessed loss of consciousness Onset during exertion “Thunderclap headache” (defined as instantly peaking pain) Limited neck flexion on examination (defined as inability to touch chin to chest or raise head 3 cm off the bed if supine)   ___________________________ Special Thanks To: Dr. Mark Iscoe, MD (Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue) ___________________________ References: Bellolio MF, Hess EP, Gilani WI, et al. External validation of the Ottawa subarachnoid hemorrhage clinical decision rule in patients with acute headache. Am J Emerg Med. 2015;33(2):244-9. Carstairs SD, Tanen DA, Duncan TD, et al. Computed tomographic angiography for the evaluation of aneurysmal subarachnoid hemorrhage. Acad Emerg Med. 2006;13(5):486-492. Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737. Czuczman AD, Thomas LE, Boulanger AB, et al. Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap. Acad Emerg Med. 2013;20(3):247-256. Dugas C, Jamal Z, Bollu PC. Xanthochromia. [Updated 2020 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526048/ Goldstein JN, Camargo CA, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. 2006;26(6):684-90. Kumar A, Niknam K, Lumba-brown A, et al. Practice Variation in the Diagnosis of Aneurysmal Subarachnoid Hemorrhage: A Survey of US and Canadian Emergency Medicine Physicians. Neurocrit Care. 2019. Lantigua H, Ortega-Gutierrez S, Schmidt JM, et al. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015;19:309. Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666. Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions. Stroke. 1996;27(9):1558-63. Meurer WJ, Walsh B, Vilke GM, Coyne CJ. Clinical guidelines for the emergency department evaluation of subarachnoid hemorrhage. J Emerg Med. 2016;50(4):696-701. Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008;51(6):707-713 Perry JJ, Stiell IG, Sivilotti MLA, et al. High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study. BMJ. 2010;341:c5204. Perry JJ, Stiell IG, Sivilotti MLA, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343(jul18 1):d4277-d4277. Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-55. Perry JJ, Sivilotti MLA, Sutherland J, et al. Validation of the Ottawa Subarachnoid Hemorrhage Rule in patients with acute headache. CMAJ. 2017;189(45):E1379-E1385. Vermeulen MJ, Schull MJ. Missed diagnosis of subarachnoid hemorrhage in the emergency department. Stroke. 2007;38(4):1216-21. Read More

We discuss the (F)utility(?) of ED Utox screens with our very own Dr. Phil DiSalvo. Hosts: Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Urine_Drug_Screen_final.mp3 Download Leave a Comment Tags: Toxicology Show Notes Special Thanks To: Dr. Philip DiSalvo, MD Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue New York City Poison Control Center   References: Christian MR, et al. Do rapid comprehensive urine drug screens change clinical management in children? Clin Toxicol (Phila). 2017;57:977-980. Grunbaum AM, Rainey PM (2019). Chapter 7: Laboratory Principles. In Goldfrank’s toxicologic emergencies. New York, NY: McGraw-Hill Education. Moeller K, Kissack J, Atayee R, Lee K. Clinical Interpretation of Urine Drug Tests: What Clinicians Need to Know About Urine Drug Screens. Mayo Clinic Proceedings Review. Volume 92, Issue 5, p774-796, May 1, 2017. https://www.mayoclinicproceedings.org/article/S0025-6196(16)30825-4/fulltext Table 2: Approximate Drug Detection Time in the Urine Table 4: Summary of Agents Contributing to Results by Immunoassay Read More

EM management of the rare but potentially complicated precipitous vaginal breech delivery. Hosts: Audrey Bree Tse, MD Masashi Rotte, MD MPH https://media.blubrry.com/coreem/content.blubrry.com/coreem/Breesashi_Breech_CoreEM.mp3 Download One Comment Tags: Obstetrics, Precipitous Deliveries, Pregnancy Show Notes Frank Breech Presentation: Complete Breech Presentation: Incomplete Breech (“Footling”) Presentation:   Pinard Maneuver:   Mauriceau Maneuver: References: Cunningham FG et al. Breech Presentation and Delivery. Williams Obstetrics, 22nd ed. 2005. Desai S, Henderson SO. Labor and Delivery and Their Complications. Rosen’s Emergency Medicine, 8e. 2014. Chapter 181. Gabbe SG et al. Obstetrics: Normal and Problem Pregnancies, 2nd e. 1991. p.479. Stitely ML, Gherman RB. Labor with abnormal presentation and position. Obstet Gynecol Clin North Am. 2005; 32: 165. VanRooyen MJ, Scott J. Emergency Delivery. Tintanelli’s Emergency Medicine, 7th e. 2011. Chapter 105. http://www.emdocs.net/the-complicated-delivery-what-do-you-do/#:~:text=Deliveries%20that%20occur%20in%20the,in%20denial%20of%20their%20pregnancies. https://ranzcog.edu.au/womens-health/patient-information-resources/breech-presentation-at-the-end-of-your-pregnancy https://wikem.org/wiki/Breech_delivery Read More

The speech given by Dr. Goldfrank at the 2020 NYU / Bellevue Emergency Medicine Graduation Ceremony https://media.blubrry.com/coreem/content.blubrry.com/coreem/Goldfrank_Graduation_Speech_2020.mp3 Download Leave a Comment Tags: Graduation. Goldfrank Show Notes Graduation 2020 Lewis R. Goldfrank, MD June 17, 2020 WELCOME TO THE GRADUATES Congratulations to a wonderful group of physicians. It is a pleasure to recognize your great accomplishments in the presence of your friends, families, loved ones and the residents and faculty who have learned so much from and with you. I would first like to recognize those of you who are members of the Gold Humanism Honor Society. There are a remarkable number of awardees in our graduating class of 2020. CLASS OF 2020 Joe Bennett (R) Max Berger (R) Ashley Miller (R) Leigh Nesheiwat (S) Kristen Ng (R) Emily Unks (S) AND Arie Francis (R) Nisha Narayanan (S) FUTURE PGY-4 Elena Dimiceli (S) Kamini Doobay (S) Mark Iscoe (R) FUTURE PGY-3 Stasha O’Callaghan (S) Nicholus Warstadt (S) FUTURE PGY-1 Aaron Bola (S) Alison (Ali) Graebner (S) Aron Siegelson (S) Melissa Socarras (S) Sarah Spiegel (S) Thomas Sullivan (S) Christy Williams (S) GOLD HUMANISM CORE VALUES Integrity, Excellence, Compassion, Altruism, Respect, Empathy, Service These are the values you want as a doctor for yourself or a loved one, to have outstanding listening skills with patients to be at your side during a medical emergency, to have exceptional interest in service to the community, to have the highest standards of professionalism to integrate a humanistic approach in patient care. These values are what brought all of you to NYU-Bellevue and that you have honed throughout your training. The remainder of this talk shows how all of you have been successful and demonstrated these values some of you were elected to the Gold Humanism—all of you have achieved humanistic success. Your personal efforts in the face of uncertainty of the evolution of the pandemic, the inadequate supplies, the hospital and governmental problematic decisions are remarkable. In our country, the President did not mourn the loss of more than a 100,000 human beings and the needs of society. Nor did he provide the leadership and moral support that the country desperately needed to optimally handle this unprecedented crisis. You, in contrast, demonstrate unflappable commitment to address and overcome obstacles to care for your patients, assist your peers, educate and care for your families and friends, while also caring for yourselves. This is a tribute to your humanism. You created essential ways to help patients who were isolated from families and friends during the critical phases of COVID-19. You utilized new tools to communicate your sorrow, your compassion and love, to maintain essential humanistic traditions of medicine while you could not talk, touch or utilize other essential skills to the fullest extent of a physician. When you recognized that all your knowledge of the social determinants of medicine was playing out as COVID-19 assaulted the poorest in our country, the people of color, the people with essential jobs without personal protective equipment, the people crowded in apartments and subways and buses, you spoke up and acted with appreciation and understanding of these disparities. You recognized that our system of using medicine to correct the societal social institutionally entrenched disparities was inadequate. George Floyd’s death, and that of Breonna Taylor and innumerable others document the racism in America that destroys a part of us each and every day and by extension reinforces and normalizes white privilege. The ever increasing body of video evidence of the horrors of systemic racism is indisputable. You recognized that the American system of criminalization of social determinants is unacceptable. You spoke up and demonstrated that you saw our blind spots on policing and race. You protested to demand change in America. Change for equity and justice must occur throughout our society. “Black Lives Matter” will only be realized when the social determinants are truly addressed through changes that impact every vulnerable person. We must recognize that person, institutional and societal failures will not be corrected by medicalizing or criminalizing of socially determined inequities. Racism is systemic. Today you are seeking to create essential changes in medicine that will only occur when all the workplaces and governmental sites across the country, are enriched to allow a full representation of all the voices of all the people. You are leaders in the response to COVID-19 and the fight against racism. You will not only be remembered for having been present, but particularly for how you have responded. Thank you for your courage, creativity, resiliency and ability to transition and advance under duress. It was a privilege to watch you demonstrate the importance of your core values and the impact that your training here at NY

An overview and management tips of hemoptysis in the ED. Hosts: Brian Gilberti, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hemoptysis.mp3 Download One Comment Tags: Critical Care, Pulmonary Show Notes OVERVIEW: Definition: expectoration/ coughing of blood originating from tracheobronchial tree Sources: Bronchial arteries (90%): under systemic circulatory pressure to supply supporting structures of the lung → heavier bleeding Pulmonary arteries (5%): under low pressure to supply alveoli → milder bleeding Nonbronchial arteries (5%): intercostal arteries, coronary arteries, thoracic/ upper/ inferior phrenic arteries Quantification: Mild: <20mL/ 24h Massive defined anywhere from >300mL-1L/ 24hr Mortality: 38% for massive (>500mL/ 24hr) vs 4.5% for nonmassive Etiology (in adults): Infectious (most common): Bronchitis PNA (necrotizing, lung abscess) TB Viral Fungal Parasitic Malignancy: Primary lung cancer vs metastatic disease Pulmonary: Bronchiectasis COPD PE/ infarction Bronchopleural fistula Sarcoidosis Cardiac: Mitral stenosis Tricuspid endocarditis CHF Rheumatological: Goodpasture Syndrome SLE Vasculitis (Wegener’s, HSP, Behcet) Amyloidosis Hematological: Coagulopathy/ thrombocytopenia/ platelet dysfunction DIC Vascular: Pulmonary HTN AA Pulmonary artery aneurysm Aortobronchial fistula Pulmonary angiodysplasia Toxins: Anticoagulation/ aspirin/ antiplatelets Penicillamine, amiodarone Crack lung Organic solvents Trauma: Tracheobronchial rupture Pulmonary contusion Other: bronchoscopy/ lung biopsy Pulmonary artery or central venous catheterization Foreign body aspiration Pulmonary endometriosis (catamenial hemoptysis) Idiopathic (up to 25% of cases) Pseudohemoptysis: Sinusitis Epistaxis Rhinorrhea Pharyngitis URI Aspiration GIB WORKUP: HPI: CP, SOB B symptoms: fever, weight loss, chills, night sweats Lymphadenopathy Timeframe: acute vs chronic Prior lung/ renal/ cardiac disease Recreational drug/ cigarette/ chemical exposures travel/ infectious exposure Medications Any other sites of bleeding Precipitating factors Description of blood clots Patients are unable to accurately estimate degree of bleeding PE: Petechiae, edema, ecchymosis, ulcers, clubbing (chronic lung disease) Cardiopulmonary Sputum samples Labs: CBC w/ diff, BMP, LFTs, coags, T&S ABG UA Infectious workup if suspected: cultures, grain stains Imaging: CXR: 20% will be normal. May see tumour, cavity, effusion, infiltrate, PTX. Early pulmonary hemorrhage may present as infiltrate CT: only for stable patients! May see bronchiectasis, cavitary lesions, acinar nodules, tumours CTA: bronchial arteries, aneurysms, PE ECHO: identify valvular abnormalities, signs of PE, aortic aneurysm Bronchoscopy: Not often performed in ED, but therapeutic & diagnostic Allows direct visualization of tumours, foreign bodies, granulomas, infiltration, as well as local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) MANAGEMENT: Goals: Control airway Protect healthy lung Identify and treat underlying cause Stabilize hemodynamics with volume resuscitation Provider precautions (respiratory & contact) ABCs, close monitoring Early airway management: massive hemoptysis, respiratory compromise, hypoxia, risk factors (elderly, AMS, coagulopathic) 2 x suction, preoxygenation, patient positioned upright, >8Fr ETT to facilitate suctioning/ bronch If bleeding side can be identified, consider “selective intubation” into nonbleeding lung to minimize further aspiration of blood and to provide ventilation Life threat = asphyxiation, not exsanguination. ~Only 150cc anatomic dead space in major airways 2 x large bore IVs MTP prn vs volume resuscitation “Bad lung down” in lateral position: theoretical belief to minimize reflux of blood into normal lung Correct coagulopathy Consider nebulized TXA for nonmassive hemoptysis (500mg w/ NS per neb) Double-blind, randomized controlled trial in 2018 Nebulized TXA (500mg TID) vs placebo (normal saline) in hemodynamically stable adult patients admitted with mild hemoptysis (<200 mL/ 24hr) and no respiratory instability Additional exclusion criteria included those with renal failure, hepatic failure, or coagulopathy Assessed mortality and hemoptysis recurrence rate at 30 days and 1 year 25 patients randomized to receive TXA nebs, 22 randomized to receive normal saline nebs Results: Resolution of hemoptysis within 5 days of admission was significantly higher in TXA-treated patients than placebo patients (96% vs 50%; P < 0.0005) Mean hospital length of stay was shorter for TXA group (5.7 +- 2.5 days vs 7.8 +- 4.6 days; P = 0.046) Fewer patients in TXA group required invasive procedures to control bleeding vs placebo group (0% vs 18.2%; P = 0.041) No side effects were noticed in either group Antibiotics if infectious Bronchoscopy: local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants) Rigid bronch for un

We go over the recent updates in the workup and management of pneumonia. Hosts: Brian Gilberti, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumonia_Updates.mp3 Download Leave a Comment Tags: Infectious Diseases, Pulmonary Show Notes 2007 Infectious Diseases Society of America/American Thoracic Society Criteria for Defining Severe Community-acquired Pneumonia Validated definition includes either one major criterion or three or more minor criteria Minor criteria Respiratory rate > 30 breaths/min PaO2/FIO2 ratio<250 Multilobar infiltrates Confusion/disorientation Uremia (blood urea nitrogen level > 20 mg/dl) Leukopenia* (white blood cell count , 4,000 cells/ml) Thrombocytopenia (platelet count , 100,000/ml) Hypothermia (core temperature , 368 C) Hypotension requiring aggressive fluid resuscitation Major criteria Septic shock with need for vasopressors Respiratory failure requiring mechanical ventilation A special thanks to our Infectious Diseases Editor: Angelica Cifuentes Kottkamp, MD Infectious Diseases & Immunology NYU School of Medicine Read More

Diagnosing and managing one of our critical diagnoses - posterior stroke. Hosts: Mukul Ramakrishnan, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/final_posterior_stroke_podcast_post_edit.mp3 Download 2 Comments Tags: Neurology, Posterior Stroke Show Notes See Dr. Newman-Toker demonstrate the HINTS exam here Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009 Nov;40(11):3504-10   Read More

We discuss one of the most complex problems we face – Homelessness Hosts: Kelly Doran, MD Audrey Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Homelessness.mp3 Download One Comment Tags: Social Emergency Medicine Show Notes Special Thanks To: Dr. Kelly Doran, MD MHS Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue ___________________________ References: Doran, K.M. Commentary: How Can Emergency Departments Help End Homelessness? A Challenge to Social Emergency Medicine. Ann Emerg Med. 2019;74:S41-S44. Doran, K.M., Raven, M.C. Homelessness and Emergency Medicine: Where Do We Go From Here? Acad Emerg Med. 2018;25:598-600. Salhi, B.A., et al. Homelessness and Emergency Medicine: A Review of the Literature. Acad Emerg Med. 2018;25:577-93. U.S. Department of Housing and Urban Development, Annual Homeless Assessment Report to Congress. Available at: https://www.hudexchange.info/resource/5783/2018-ahar-part-1-pit-estimates-of-homelessness-in-the-us/ U.S. Interagency Council on Homelessness. Home, Together Federal Strategic Plan to Prevent and End Homelessness. https://www.usich.gov/resources/uploads/asset_library/Home-Together-Federal-Strategic-Plan-to-Prevent-and-End-Homelessness.pdf Read More

We go into one of the more complex injuries – blunt neck trauma. Hosts: Audrey Bree Tse, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Blunt_Neck_Injuries.mp3 Download One Comment Tags: Trauma Show Notes Overview Blunt neck trauma comprises 5% of all neck trauma Mortality due to loss of airway more so than hemorrhage Mechanism MVCs with cervical hyperextension, flexion, rotation during rapid deceleration, direct impact Strangulation: hanging, choking, clothesline injury (see section on strangulation in this chapter) Direct blows: assault, sports, falls Initial Management/Primary Survey Airway Evaluate for airway distress (stridor, hoarseness, dysphonia, dyspnea) or impending airway compromise Early aggressive airway control: low threshold for intubation if unconscious patient, evidence of airway compromise including voice change, dyspnea, neurological changes, or pulmonary edema Assume a difficult airway Breathing Supplemental oxygen Assess for bilateral breath sounds Can use bedside US to evaluate for pneumothorax or hemothorax Circulation Assess for open wounds, bleeding, hemorrhage IV access Disability Maintain C-spine immobilization Calculate GCS Look for seatbelt sign Secondary Survey Evaluate for specific signs of vascular, laryngotracheal, pharyngoesophageal, and cervical spinal injuries with inspection, palpation, and auscultation Perform extremely thorough exam to evaluate for any concomitant injuries (e.g. stab wounds, gunshot wounds, intoxications/ ingestions, etc.) Types of Injuries Vascular injury Overview Carotid arteries (internal, external, common carotid) and vertebral arteries injured Mortality rate ~60% for symptomatic blunt cerebral vascular injury Mechanism Hyperextension and lateral rotation of the neck, direct blunt force, strangulation, seat belt injuries, and chiropractic manipulation Morbidity due to intimal dissections, thromboses, pseudoaneurysms, fistulas, and transections Clinical Features Most patients are asymptomatic and do not develop focal neurological deficits for days if Horner’s syndrome, suspect disruption of thoracic sympathetic chain (wraps around carotid artery) specific screening criteria are used to detect blunt cerebrovascular injury in asymptomatic patients (see below) Tintinalli 2016 Diagnostic Testing Gold standard for blunt cerebral vascular injury = MDCTA (multidetector four-vessel CT angiography) <80% sensitive but 97% specific Also images aerodigestive tracts and C-spine (unlike angiography) Followed by Digital Subtraction Angiography (DSA) for positive results or high suspicion Angiography is invasive, expensive, resource-intensive, and carries a high contrast load Management Antithrombotics vs. interventional repair based on BCVI grading system Involve consultants early: trauma surgery, neurosurgery, vascular surgery, neurology All patients with blunt cerebral vascular injury will require admission Tintinalli 2018 Pharyngoesophageal injury Overview Rare in blunt neck trauma Includes hematomas and perforations of both pharynx and esophagus Mechanism Sudden acceleration or deceleration with hyperextension of the neck Esophagus is thus forced against the spine Clinical Features Dysphagia, odynophagia, hematemesis, spitting up blood Tenderness to palpation SC emphysema Neurological deficits (delayed presentation) Infectious symptoms (delayed presentation) Diagnostic Testing Esophagography with water-soluble contrast (e.g. Gastrograffin) If negative contrast esophagography, obtain flexible endoscopy (most sensitive) Combination of contrast esophagography + esophagoscopy has sensitivity close to 100% Swallow studies with water-soluble agent MDCTA Plain films of neck and chest Findings such as pneumomediastinum, hydrothorax, or retropharyngeal air may suggest perforation but are not sensitive Management All pharyngoesophageal injuries receive IV antibiotics with anaerobic coverage Parenteral/ enteral nutrition NGT should only be placed under endoscopic guidance to avoid further injury Medical management vs. surgical repair depending on extent of injury Surgical repair for esophageal perforations or pharyngeal perforations >2cm Involve consultants early: trauma surgery, vascular surgery, otolaryngology, gastroenterology All patients with blunt cerebral vascular injury will require admission Laryngotracheal injury Overview Occurs in >0.5% of blunt neck trauma Includes hyoid fractures, thyroid/ cricoid cartilage damage, cricotracheal separation, vocal cord disruption, tracheal hematoma or transection Mechanism Assault, clothesline injuries, direct blunt force from MVCs compressing the larynx between a fixed object and the spine Clinical Features Patients are often asymptomatic at first and then develop airway edema and/or hematoma resulting in airway obstruction Children are at higher risk for airway compromise due to less cartilage calcifications Diagnostic Testing Flexible fiberoptic laryngoscopy (FFL) to assess airwa