要約

Pleuritis is defined as inflammation of the pleura. The pleural space, as a thin fluid-filled space between the lung and the thoracic cavity, enables the smooth frictionless movement of the lung during respiration. It is lined by 2 layers of pleura: the visceral (covering the lung) and the parietal (covering the thoracic cage). Pain receptors are present on the parietal pleura. Irritation and inflammation of the pleura presents with symptoms of sharp lancing, fleeting pain in the chest that is exacerbated by deep breathing, coughing, sneezing, or Valsalva (forced expiration against a closed airway) and Mueller manoeuvres (reverse of Valsalva manoeuvre).

It is important to evaluate and exclude potentially life-threatening conditions such as pulmonary embolism, acute coronary syndrome, aortic dissection, and pneumothorax during evaluation. Pneumonia must also be considered. Though not causes of pleuritis per se, conditions such as pericarditis, perforated viscus, and costochondritis should be considered in the differential diagnosis when patients present with chest pain that is pleuritic in nature.

Pathophysiology

The pleural space is a potential space that can be filled with a variety of substances including transudative fluid, exudative fluid, pus, blood, air, or chyle. The pleural lining consists of a single layer of mesothelial cells supported by connective tissue. This layer not only acts as a mechanical envelope but also serves a biological role. It regulates diffusion of substances into the pleural space and plays an integral role in inflammatory responses to stimuli such as infection, traumatic injury, or introduction of foreign substances such as air, blood, or asbestos. Mesothelial cells recognise invasion of the pleural space and initiate recruitment of cells through co-ordinated expression of cytokines, chemokines, and vascular adhesion molecules. [1] Prompt resolution of the inflammation may allow the pleural surface to return to normal with no sequelae. However, prolonged inflammation will result in distortion of normal structure by fibrosis, adhesions, and scarring. Resolution of inflammation is directed by initiation of neutrophil apoptosis by mesothelial cells. [2]