• Negative pressure pulmonary edema (NPPE) is an uncommon, but well-recognized clinical entity that results from the negative intrathoracic pressure generated during spontaneous ventilation with concurrent upper airway obstruction.
• The pulmonary edema results from either:
  • "Pulling" of fluids from the pulmonary capillary bed into the alveoli (Starling forces), or
  • Injury to the pulmonary microvascular membranes from severe mechanical stress that results in capillary "leaking" of fluid.
• NPPE can result from laryngospasm or biting, commonly at induction or extubation, as well as from epiglottitis, tumors, obesity, hiccups, or obstructive sleep apnea.
• Clinical manifestations result from ventilation and perfusion difficulties (V/Q mismatching or shunt) with a frequent need for reintubation and temporary ventilatory support.

• Etiology
  • Laryngospasm
  • ETT biting
  • Airway trauma
  • Upper airway collapse
  • Bronchial obstruction
  • foreign body aspiration
  • Postoperative residual curarization (impairs the upper airway dilator muscle strength while preserving inspiratory muscle function)
• Patient characteristics
  • Young, healthy, athletic (capable of generating large negative intrathoracic pressures during an obstructive event)
  • Obstructive sleep apnea
• Surgical procedures
  • Oropharyngeal surgery, particularly for tumors or other potentially obstructing masses

• The pathogenesis of NPPE is related to the development of high negative intrapleural pressure by vigorous inspiratory efforts against an obstructed upper airway.
• 2 different mechanisms may explain the development of pulmonary edema during airway obstruction:
  • Starling forces: High negative intrathoracic pressures draw fluid out of micro-vessels into the peri-microvascular interstitium. Cardiogenic pulmonary edema states (CHF, fluid overload) have a similar presentation but result from positive capillary pressures that "push" fluid out of micro-vessels. During upper airway obstruction and forceful inspiration, pressure in the trachea and lower airways will decrease markedly (become more negative). The pressure in the pleural space decreases (becomes more negative) by exactly the same amount. The pressure in the pulmonary vessels decreases by much less, thus increasing the pressure difference between the inside and the outside of the capillaries and accelerating the formation of interstitial fluid.
  • Disruption of the alveolar epithelium and pulmonary microvascular membranes from severe mechanical stress occurs, leading to increased pulmonary capillary permeability and protein-rich pulmonary edema (this resembles non-cardiogenic pulmonary edema states such as acute respiratory distress syndrome).
  • Starling equation: Q = K [(P_mv - P_pmv) - (_mv - _pmv)], where
    • Q = Net transcapillary flow of fluid
    • K = Transcapillary permeability
    • P_mv = Hydrostatic pressure in microvessels
    • P_pmv = Perimicrovascular interstitium
    • _mv = Plasma protein osmotic pressure in the peripheral vessels
    • _pmv = Protein osmotic pressure in the perimicrovascular interstitium
• Respiratory dynamics:
  • Pulmonary edema is the pathologic accumulation of fluid in the lung interstitium, and later alveoli, producing impairment in gas exchange.
  • Pulmonary edema leads to V/Q mismatching since less alveoli are participating in gas exchange. The severity of V/Q mismatch correlates with the severity of the pulmonary edema.
  • Lung edema leads to decreased lung compliance, which leads to an increased work of breathing.

• Bite block to prevent biting on the ETT
• In patients prone to upper airway obstruction, consider prophylactic placement of an oral airway or nasal trumpet.
• Treat laryngospasm aggressively with positive pressure ventilation or succinylcholine.

• Cardiogenic pulmonary edema
• Neurogenic pulmonary edema
• Fluid overload
• Acute respiratory distress syndrome
• Non-cardiogenic pulmonary edema (e.g., acute respiratory distress syndrome).

• Cardiogenic Pulmonary Edema
• Non-Cardiogenic Pulmonary Edema
• Laryngospasm
• Postoperative Pulmonary Complications

518.4 Acute edema of lung, unspecified

J81.0 Acute pulmonary edema

Agnes Miller , MD

Kalpana Tyagaraj , MD