Core EM - Emergency Medicine Podcast

Episode 215: Marburg Virus and Global EM

Sat, 01 Nov 2025

Lessons from Rwanda’s Marburg Virus Outbreak and Building Resilient Systems in Global EM.

Hosts:

Tsion Firew, MD

Brian Gilberti, MD

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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.

Episode 214: Acute Pulmonary Embolism

Thu, 02 Oct 2025

We review the diagnosis, risk stratification, & management of acute pulmonary embolism in the ED.

Hosts:

Vivian Chiu, MD

Brian Gilberti, MD

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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.

Episode 213: Pneumothorax

Mon, 01 Sep 2025

We break down pneumothorax: risks, diagnosis, and management pearls.

Hosts:

Christopher Pham, MD

Brian Gilberti, MD

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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.

Episode 212: Angioedema

Sat, 02 Aug 2025

Angioedema – Recognition and Management in the ED

Hosts:

Maria Mulligan-Buckmiller, MD

Brian Gilberti, MD

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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.

Episode 211: Granulomatosis with Polyangiitis

Tue, 01 Jul 2025

Granulomatosis with Polyangiitis (GPA) – Recognition and Management in the ED

Hosts:

Phoebe Draper, MD

Brian Gilberti, MD

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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.