Pleural Effusion I: Introduction

Pleural effusion is the abnormal accumulation of fluid between the lungs and chest wall in the pleural cavity. Normally, this space contains only 5 to 15 mL of lubricating fluid. Effusion occurs when systemic factors or inflammation disrupt the balance of hydrostatic and oncotic pressures, causing excess fluid to leak into the pleural space from blood vessels or inflamed pleural membranes.

Transudative and exudative effusions are classified using Light's criteria, which measures protein and lactate dehydrogenase (LDH) levels in pleural fluid compared to serum. An effusion is exudative if pleural fluid protein/serum protein exceeds 0.5, pleural fluid LDH/serum LDH surpasses 0.6, or pleural fluid LDH exceeds two-thirds of the upper normal serum limit. Otherwise, it is transudative.

Transudative effusions result from systemic factors affecting blood vessel pressures. Congestive heart failure is the most common cause, where ineffective heart pumping increases venous pressure and fluid leaks into the pleural space. Liver cirrhosis reduces albumin production, lowering oncotic pressure. Nephrotic syndrome causes proteinuria, decreasing oncotic pressure and promoting fluid accumulation.

Exudative effusions develop from inflammation and increased permeability of pleural membranes. Common causes include pneumonia, which triggers inflammatory response; malignancy such as lung, breast, or mesothelioma; pulmonary embolism causing pleural irritation; connective tissue disorders like rheumatoid arthritis; and pulmonary infarction related to vasculitis or embolism.

In congestive heart failure, the heart cannot pump blood effectively, causing venous pressure to increase. This elevated pressure forces fluid to leak from blood vessels into the pleural space, creating a transudative effusion. This mechanism disrupts the normal hydrostatic-oncotic pressure balance that maintains the pleural cavity's small fluid volume.

Both conditions reduce oncotic pressure through different mechanisms. Liver cirrhosis decreases albumin production, lowering blood oncotic pressure and allowing fluid to shift into the pleural space. Nephrotic syndrome causes proteinuria, where excessive protein loss in urine reduces serum albumin and oncotic pressure, similarly promoting transudative fluid accumulation.

The pleural cavity is bounded by visceral and parietal pleural membranes. When these membranes become inflamed or their permeability increases due to infection, malignancy, or autoimmune disease, fluid with higher protein content accumulates in the pleural space. This increased vascular permeability allows fluid and proteins to leak from blood vessels into the pleural cavity.