Noncardiogenic Pulmonary Edema

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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