Pathophysiology of Pleural Effusion in Pneumonia
Pleural effusion in pneumonia develops when the inflammatory process from underlying bacterial pneumonia disrupts the normal balance between pleural fluid formation and lymphatic drainage, leading to fluid accumulation in the pleural space. 1
Primary Mechanism
The pleural space normally contains only 0.3 ml/kg body weight of fluid, with lymphatic vessels capable of draining several hundred milliliters of extra fluid per 24 hours. 1 When inflammation from pneumonia extends to the pleural surface, it overwhelms this drainage capacity and triggers a cascade of pathophysiological changes. 1
The Three-Stage Progression
The development of parapneumonic effusion follows a predictable continuum: 1
Exudative Stage (Stage I): The inflammatory process associated with underlying pneumonia leads to accumulation of clear fluid with low white cell count, low LDH, physiological pH, and normal glucose in the pleural cavity. 1, 2 The fluid remains sterile at this point despite the adjacent infection. 2
Fibropurulent Stage (Stage II): Deposition of fibrin in the pleural space leads to septation and loculation formation. 1 White cell counts increase dramatically, LDH activity rises (>200 U/L), protein levels exceed 3 g/dL, pleural fluid pH falls below 7.20, and glucose levels drop. 2, 3 The fluid thickens and may become overtly purulent (empyema). 1
Organizational Stage (Stage III): Fibroblasts infiltrate the pleural cavity, converting fibrin strands into thick, non-elastic membranes (the "peel"). 1, 2 These solid fibrous pleural peels prevent lung re-expansion ("trapped lung"), impair lung function, and create persistent pleural space with ongoing infection potential. 1
Underlying Inflammatory Mechanisms
The presence of polymorphonuclear leukocytes, high LDH activity, and elevated protein levels in pleural fluid indicates acute inflammation from the adjacent pneumonic process. 2 The inflammatory cascade causes:
- Increased capillary permeability in pleural membranes 4
- Direct bacterial invasion from pneumonic lung tissue 5, 6
- Release of inflammatory mediators and cytokines 6
- Impaired fibrinolysis leading to fibrin deposition 1
Microbiology and Bacterial Factors
Nearly 50% of patients with acute bacterial pneumonia develop an accompanying parapneumonic effusion. 3 The most common causative organisms include:
- Streptococcus pneumoniae (currently the predominant pathogen) 1
- Staphylococcus aureus (particularly in infants under 6 months) 1
- β-hemolytic streptococci (Streptococcus pyogenes) 1
Bacterial virulence features and direct invasion contribute significantly to effusion development, though microbiological yields from pleural fluid are only around 56% due to prior antibiotic use. 1, 5
Clinical Implications
The rate of parapneumonic effusion complicating pneumonia ranges from 1% to 40% in hospitalized adults, with the majority resolving with appropriate antibiotic therapy alone. 1, 3 However, a small fraction develops complicated parapneumonic effusions requiring drainage. 3
Key Diagnostic Indicators of Complicated Effusions:
- Pleural fluid pH <7.00 (immediate drainage indicated) 3
- Pleural fluid glucose <40 mg/dL 3
- Pleural fluid LDH >1000 IU/L 3
- Positive Gram stain 3
- Presence of septations or loculations on imaging 5
Important caveat: The longer drainage is delayed in complicated parapneumonic effusions, the more difficult tube drainage becomes due to progressive fibrin deposition and loculation formation. 3 Early identification through diagnostic thoracentesis is critical when fluid thickness exceeds 10 mm on decubitus radiographs. 3