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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 1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN). Glucose: Low (200 mg/dL). Cytology: Negative. Viral Meningitis Opening Pressure: Normal. Color: Clear or bloody. Gram Stain: Negative. Cell Count: Slightly elevated (200 mg/dL). Cytology: Negative. Neoplastic (Cancer-related) Meningitis Opening Pressure: Normal. Color: Clear or cloudy. Gram Stain: Negative. Cell Count: Elevated (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 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 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 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 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