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

Hosts:
Christopher Pham, MD
Brian Gilberti, MD

• 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.

• 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.

• Bloodwork: limited role, except type & screen if intervention likely.
• EKG: reasonable given chest pain/shortness of breath.

Angioedema – Recognition and Management in the ED

Hosts:
Maria Mulligan-Buckmiller, MD
Brian Gilberti, MD

Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability.

Triggers increased vascular permeability → fluid shifts into tissues.

• 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.

• 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

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

Hosts:
Phoebe Draper, MD
Brian Gilberti, MD

• 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

• Chronic sinus symptoms
• Hemoptysis (especially bright red blood)
• New pulmonary complaints
• Renal dysfunction
• Constitutional symptoms (fatigue, weight loss, fever)

• 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)

• 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

• Goodpasture syndrome (anti-GBM antibodies)
• TB, fungal infections
• Lung malignancy
• Other vasculitides (EGPA, MPA, lupus)