Pleurisy: Symptom or Condition?

Jennifer Confer, PharmD, BCPS; Jennifer Egbert-Kibler, PharmD


US Pharmacist 

In This Article

Anatomy and Physiology

To comprehend pleurisy and associated pleuritic pain, the anatomy and physiology of the lung and its nerve innervations must be understood. The lungs, chest wall, and rib cage are lined with two continuous layers of epithelium known as the parietal pleura and the visceral pleura (FIGURE 1). The parietal (outer) pleura is the epithelial lining covering the chest wall, rib cage, and mediastinum; the visceral (inner) pleura covers the total surface of the lung.[1,2] The parietal pleura is innervated with somatic pain receptors supplied by the phrenic nerve; the pain signals are rapidly transmitted, leading to pain that is sharp and localized. In contrast, the visceral pleura has an autonomic nerve supply that develops from internal organs; pain sensations, if any, are transmitted slowly and are characterized as dull, achy, and slightly localized.[2]

Figure 1.

Pleurae of the lungs.

Between the parietal and visceral pleurae is the pleural space, which contains a serous fluid. Pleural fluid is produced by pleural vessels through negative pressure created upon inspiration. Fluid then exits through the parietal lymphatic system and is absorbed by the visceral pleura in a continuous manner. Pleural fluid provides lubrication between the chest wall and lung, allowing the lungs to slide effortlessly during inspiration and expiration.[2] If the smooth surfaces of the pleurae become inflamed or if the pleural space is increased or decreased, a pleural rub—a squeaking or grating sound made when the pleural linings rub together—results. This classic feature of pleurisy, detected by lung auscultation, can help the clinician identify the cause of the chest pain.[3]

During normal inspiration of the lungs, negative pressure is created in the pleural space as the thoracic cavity expands. When excess fluid accumulates in the pleural space, the negative pressure is diminished, altering the lung's capacity to expand fully during inspiration. Untreated, this leads to an inadequate exchange of oxygen and carbon dioxide.[2,4]

Three mechanisms are thought to cause pleural effusion (the accumulation of excess fluid in the pleural space).[2,4] In the first mechanism, increased production of fluid by parietal cells in the pleural space surpasses the ability of the lymphatic system to remove the fluid. By another mechanism, pleural fluid accumulates when an increased drainage of fluid into the pleural space occurs due to backflow from the lungs or liver. This can be seen in patients with congestive heart failure, in which the heart is unable to maintain cardiac output, leading to pulmonary congestion. This congestion within the pulmonary circulation can cause fluid to leak from the alveoli into the pleural space. In the third mechanism, a reduction in drainage of fluid from the pleural space secondary to an obstruction may prevent the fluid from being reabsorbed into the bloodstream.[2,4] An obstruction of this type could result when a tumor invades the pleura.


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