Pleurisy is a symptom characterized by localized chest pain caused by a disease-causing inflammation of the pleura. Pleurisy can be caused by a primary pleural disease or secondary to a systemic illness. Hippocrates first described "pleuritis" in the 5 century B.C. as "pain in his side, fever and shivering" accompanied by "orthopnea" and tachypnea." Different types of pleuritis were described, including "bilious," "sanguineous," and "dry." Location of the pain was also used to describe pleuritis in these early texts, e.g., "pleuritis in the back," "extending along the spine and to the chest and groin," etc. The definition was then expanded by Galen, who tied Hippocrates' ideas on pleuritis to inflammation of the lining of the lungs. The lining of the lungs was referred to in these texts as the "hypezokos membrane." Galen also noted tachycardia in pleurisy and described it as a "hard pulse" that was noted to be "fast and frequent." In 1723, the term "pleurisy" came from an English translation of a text by Giorgio Baglivi in 1699. Baglivi also describes a "hardness of the pulse" as "an infallible sign of all pleurisies" and additionally mentions. "fever, spitting, and pain-in-the-side." The more recent definition of pleurisy was by Giambattista Morgagni in 1961, who performed post-mortem examinations on patients suffering from pleurisy. He defined "pleurisy" as disease-related primarily to the pleura and "peripneumony" as disease relating to the lung tissue. Through his work, he discovered that these were not distinct entities and re-termed this "pleuripneumony." Laennec, who invented the stethoscope, added egophony to the definition of pleurisy. Laennec also reclassified the terminology and referred to "pleuritic" to denote inflammation of the pleura and "pleurisy" to refer to the disease that caused the inflammation. Pleural Anatomy Two layers of pleura separate the lung and inner chest wall. Visceral pleura surrounding the lung tissue and is composed of a single mesothelial cell layer. They receive blood supply from the bronchial arteries supplying lung. The parietal pleura lines the inner chest wall, and in contrast to the visceral pleura, it contains stomata that drain pleural fluid to lymphatic capillaries in the loose connective tissue, which also contains systemic blood vessels and nerves. The lymphatics drain into their regional lymph nodes along the sternum or vertebra, and eventually into the thoracic and right lymphatic ducts. The lymphatics are 10um-12um in diameter, large enough to accommodate intact erythrocytes. The normal volume of pleural fluid is 0.1 to 0.2 mL/kg, with an influx of 0.5 mL/hr in adults. The maximal removal rate, calculated from instilling artificial pleural effusion into a bovine model, is 0.28 mL/kg/hr. Pleural fluid accumulates when the inflow exceeds removal (increased capillary plasma filtration) or if the rate of removal is impaired (blockage of lymphatic drainage). The normal amount of pleural fluid separates the two pleura by 10 to 20 micrometers, except at the hilum of the lung where they are contiguous. The parietal pleura has connective tissue and is innervated by sensory nerve fibers, while the visceral pleura lacks connective tissue and is innervated by the vagus nerve, hence insensitive to pain. The parietal pleura in the central diaphragmatic region is supplied predominantly by the phrenic nerve, the involvement of which may cause referred pain to the ipsilateral shoulder. The other areas of the parietal pleura are supplied by the intercostal nerves of the corresponding intercostal spaces. The primary function of the pleural membranes and pleural fluid is to allow for frictionless movement/sliding of the lung relative to the chest wall. On inspiration, a negative pressure caused by the outward movement of the chest cavity and the downward excursion of the diaphragm is transmitted to the pleural space leading to lung expansion. It generates a negative pressure relative to atmospheric pressure. This gradient allows atmospheric air to enter into the lungs.