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Accumulation of fluid in the pleural cavity
- 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.