Noncardiogenic Pulmonary Edema

Noncardiogenic Pulmonary Edema is a topic covered in the 5-Minute Emergency Consult.

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Basics

Description

Noncardiogenic pulmonary edema (NCPE) is the accumulation of excess fluid and protein into the alveoli from factors unrelated to elevated hydrostatic pressure (pulmonary capillary pressure is normal)
  • Increased permeability:
    • Functional disruption of the capillary–alveolar membrane allows protein and fluid to move freely from the intravascular space into the alveolar space
  • Distinction between NCPE and cardiogenic pulmonary edema (CPE):
    • Pulmonary capillary pressure ≤18 mm Hg
    • Often apparent from the clinical circumstances
    • The concentration of protein in the alveolar fluid is identical to that of the intravascular space in patients with NCPE
    • Unlike in CPE, NCPE will not typically demonstrate cephalad redistribution of blood flow, pulmonary effusions, or cardiomegaly
  • Typically, onset of the edema is within 1–2 hr of the noxious insult
  • ∼250,000 cases occur each year in the U.S., with 46% mortality in severe cases
  • Mixed picture: Concomitant heart failure occurs in up to 20% of patients with acute respiratory distress syndrome (ARDS)

Etiology

  • ARDS is the leading etiology:
    • ARDS may be caused by:
      • Sepsis
      • Pneumonia
      • Trauma
      • Inhaled toxins and aspiration
      • Disseminated intravascular coagulation (DIC)
      • Pancreatitis
      • Near-drowning
      • S/p cardiopulmonary bypass
      • Transfusion-related acute lung injury (TRALI)
      • Major burn
      • Radiation pneumonitis
  • High-altitude pulmonary edema (HAPE)
  • Neurogenic pulmonary edema
  • Opioid overdose
  • Pulmonary embolus
  • Eclampsia
  • Re-expansion pulmonary edema after re-expansion of pneumothorax or drainage of large pleural effusion
  • Salicylate toxicity
  • Inhaled cocaine use
  • Uremia
  • Viral infections (i.e., hantavirus cardiopulmonary syndrome)

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Basics

Description

Noncardiogenic pulmonary edema (NCPE) is the accumulation of excess fluid and protein into the alveoli from factors unrelated to elevated hydrostatic pressure (pulmonary capillary pressure is normal)
  • Increased permeability:
    • Functional disruption of the capillary–alveolar membrane allows protein and fluid to move freely from the intravascular space into the alveolar space
  • Distinction between NCPE and cardiogenic pulmonary edema (CPE):
    • Pulmonary capillary pressure ≤18 mm Hg
    • Often apparent from the clinical circumstances
    • The concentration of protein in the alveolar fluid is identical to that of the intravascular space in patients with NCPE
    • Unlike in CPE, NCPE will not typically demonstrate cephalad redistribution of blood flow, pulmonary effusions, or cardiomegaly
  • Typically, onset of the edema is within 1–2 hr of the noxious insult
  • ∼250,000 cases occur each year in the U.S., with 46% mortality in severe cases
  • Mixed picture: Concomitant heart failure occurs in up to 20% of patients with acute respiratory distress syndrome (ARDS)

Etiology

  • ARDS is the leading etiology:
    • ARDS may be caused by:
      • Sepsis
      • Pneumonia
      • Trauma
      • Inhaled toxins and aspiration
      • Disseminated intravascular coagulation (DIC)
      • Pancreatitis
      • Near-drowning
      • S/p cardiopulmonary bypass
      • Transfusion-related acute lung injury (TRALI)
      • Major burn
      • Radiation pneumonitis
  • High-altitude pulmonary edema (HAPE)
  • Neurogenic pulmonary edema
  • Opioid overdose
  • Pulmonary embolus
  • Eclampsia
  • Re-expansion pulmonary edema after re-expansion of pneumothorax or drainage of large pleural effusion
  • Salicylate toxicity
  • Inhaled cocaine use
  • Uremia
  • Viral infections (i.e., hantavirus cardiopulmonary syndrome)

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