10th January 2024

Background

Epidemiology

Pleural effusions are a common pathology seen in respiratory medicine, with approximately 200,000 new cases in the UK each year with over 50 underlying aetiologies spanning a breadth of medical specialities. Pleural effusions can largely be categorised into 2 forms: transudative and exudative. The most common underlying cause of a transudative pleural effusion is heart failure, whereas the most common cause of an exudative effusion is pneumonia.

Pathophysiology

In normal physiological circumstances, the volume of pleural fluid is carefully governed by a balance between liquid into the pleural space (via the parietal pleura) and liquid outflow (via the parietal and visceral pleura). A small amount of fluid (estimated at 10-20mL, or 0.3mL/kg) is always present within the space to allow effective ventilation of the lungs. Several mechanisms help maintain this tightly controlled volume: Starling forces at the visceral pleura, lymphatic drainage at the parietal pleura and “electrolyte-coupled liquid absorption” via the mesothelium on both visceral and parietal pleura.

Pleural effusions result from either increased pleural fluid production or impaired absorption via a) a change in the transpleural pressure balance and subsequently Starling’s forces, b) impairment of the lymphatic system or c) change in mesothelial permeability.

Transudates 

Transudative pleural effusions result from increases in the systemic capillary pressure in the setting of congestive cardiac failure. This increased capillary pressure changes hydrostatic and oncotic pressures across the pleura, thus altering the normal equilibrium seen, i.e., Starling’s forces. This alteration results in pleural fluid production exceeding its absorption and resultant accumulation. As the mesothelium remains largely unaltered, protein and cell leakage into the fluid is minimal.

Transudative pleural effusions secondary to chronic liver disease and nephrotic syndrome also result from a change in Starling’s forces at the capillary membrane, but in these cases, it is a reduction in oncotic pressure from hypoalbuminaemia. This drives the balance in favour of hydrostatic pressure, and subsequently, fluid is moved into the pleural space.

Exudates 

Exudative pleural effusions are either a result of impaired protein and cell removal from the pleural space (via the lymphatic system) or from increased permeability of the mesothelial membrane to water and small solutes. This results in fluid accumulation that is high in cell number and protein within the pleural space.

Specifically, in parapneumonic exudative effusions (the most common form of exudative pleural effusion) it is the direct result of inflammatory-mediating cytokines and cells interacting with the mesothelial membrane, which increase its permeability to cells and protein. At times, this inflammatory-mediated damage to the mesothelium can be so significant that bacteria can enter the pleural space, resulting in the formation of an empyema (pleural infection).