Core EM - Emergency Medicine Podcast

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 

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.

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 bowel tissue. Hirschsprung-associated Enterocolitis: Complication of Hirschsprung’s disease involving blockage and infection. Intussusception: Older infants might only show altered mental status instead of the typical intermittent pain and lethargy. Symptoms: Common symptoms include bilious emesis (green vomit) or hematemesis (vomiting blood). Emergency Response: Urges early mobilization of pediatric surgery and radiology teams upon suspicion of these conditions. Toxins Includes intentional or unintentional ingestion. One pill killers include: calcium channel blockers (CCB), tricyclic antidepressants (TCA), opiates, sulfonylureas, Class 1 antiarrhythmics, antimalarials, camphor, oil of wintergreen. Seizures The second ‘S’ in the mnemonic refers to seizures, which can be triggered by various conditions such as hypoglycemia, sepsis, inborn errors of metabolism, and trauma. First-Line Treatment: Actively seizing patients should initially be treated with benzodiazepines. Second-Line Medications: Includes fosphenytoin, phenobarbital,