Description

Accumulation of fluid in the pleural cavity

Pathophysiology

• Normally 1 to 15 mL of fluid in the pleural space
• Alterations in the flow and/or absorption of this fluid lead to its accumulation.
• Mechanisms that influence this flow of fluid:
  • Increased capillary hydrostatic pressure (i.e., congestive heart failure [CHF], overhydration)
  • Decreased pleural space hydrostatic pressure (i.e., after thoracentesis, atelectasis)
  • Decreased plasma oncotic pressure (i.e., hypoalbuminemia, nephrosis)
  • Increased capillary permeability (i.e., infection, toxins, connective tissue diseases, malignancy)
  • Impaired lymphatic drainage from the pleural space (i.e., disruption of the thoracic duct)
  • Passage of fluid from the peritoneal cavity through the diaphragm to the pleural space (i.e., hepatic cirrhosis with ascites)
• Two types of pleural effusion:
  • Transudate: Mechanical forces of hydrostatic and oncotic pressures are altered, favoring liquid filtration.
  • Exudate: Damage to the pleural surface occurs that alters its ability to filter pleural fluid; lymphatic drainage is diminished.
• Stages associated with parapneumonic effusions (infectious exudates):
  • See “Appendix, Table 3.”
  • Exudative stage
    • Free-flowing fluid
    • Pleural fluid glucose, protein, lactate dehydrogenase (LDH) level, and pH are normal.
  • Fibrinolytic stage
    • Loculations are forming.
    • Increase in fibrin, polymorphonuclear leukocytes, and bacterial invasion of pleural cavity are occurring.
    • Pleural fluid glucose and pH falls, whereas protein and LDH levels increase.
  • Organizing stage (empyema)
    • Fibroblasts grow.
    • Pleural peal forms.
    • Pleural fluid parameters worsen.