Pulmonary & Critical Care Medicine: Pleural Diseases Surinder K Jindal, PS Shankar
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The Pleura

PS Shankar MD FRCP FAMS DSc (h.c.Gul) DSc (h.c.NTR) DSc (h.c.RGUHS) DSc (h.cTU) D. Litt (Hampi)
Rajiv Gandhi University of Health Sciences Bengaluru, Karnataka, India


Pleural cavity is a thin walled space between visceral and parietal pleurae of each lung. The parietal pleura lines the inner surface of the chest wall and the visceral pleura envelopes the surface of the lungs. The pleural space contains a small amount of transudative fluid and it is not static. The space becomes real when fluid or air separates the layers of the pleura.
An abnormal accumulation of fluid in the pleural space may occur from increased formation, decreased clearance, or obstruction to the clearance pathways. Air can enter the pleural space either from the lung parenchyma and airways or from outside. Pleura can get thickened, or calcified. It can be the seat of diffuse or solitary primary tumors, or drug induced diseases.
The pleural space is a thin, fluid-filled cavity between visceral and parietal pleurae of each lung. Pleura is lined by serous membrane which folds back onto itself to create a double-layered pleural sac. Parietal pleura is attached to the chest wall and the visceral pleura covers the lungs. There is no connection between the right and left pleural cavities. As the pleurae adhere to each other so closely, the pleural cavity may be considered a potential space which becomes real when there is accumulation of fluid or air resulting in pleural effusion or pneumothorax, respectively.
The pleurae help in optimal functioning of the lungs during respiration. Small amount of serous fluid found in the pleural cavity acts as a lubricant and facilitates the pleurae to slide against each other during respiration. Pleural cavity can become seat of diseases due to pleural effusion or pneumothorax and the pleura can develop fibrosis, plaques, calcification, or tumors.
The pleural cavity is a thin-walled space between visceral and parietal pleurae of each lung. The pleurae are serous membrane which form a two layered membranous pleural cavity. The outer or parietal pleura is attached to the chest wall and lines the inner surface of the chest wall, cervical tissues, mediastinum, and diaphragm. There is a connective tissue layer with collagen and elastic fibers underneath it. The inner or visceral pleura, envelopes the surface of the lungs including the interlobar fissures. It sends prolongations into the parenchyma of the lung. The right and left pleural cavities are separate and do not have any communication.1
The serous membranes with a single layer of nucleated, flat mesothelial cells enclose the pleural space approximately 10–20 µ wide. Normally, each pleural space contains 10 mL of transudate of low protein content and cell concentration. The space becomes real when fluid (pleural effusion) or air (pneumothorax) separates the layers of the pleura.
The visceral pleura receives its entire blood supply from the branches of pulmonary arteries and they terminate in a capillary network. The pleura around the hilum is supplied by the bronchial arteries.2 The branches of the intercostal arteries and internal mammary artery supply the parietal pleura. The venous drainage is largely through pulmonary veins from the visceral pleura and the drainage from the parietal pleura is to the systemic veins. The lymphatic drainage from the visceral pleura is to the hilum. The intercostal, parasternal, and paravertebral lymphatics drain the costal pleura and the drainage from diaphragmatic and mediastinal pleura is to the posterior mediastinal lymph nodes.
The intercostal nerves innervate the parietal pleura overlying costal, cervical, and peripheral portions of the cupola of the diaphragm. The pleura overlying mediastinal and central portions of the cupola of the diaphragm is supplied by the phrenic nerves. The visceral pleura overlying the lungs receive autonomic nerve supply, and there is no sensory nerve supply. The parietal pleurae are sensitive to pain. The pleuritic pain probably originates in the endothoracic fascia rich in intrapleural nerves.3
The pleural fluid is not static and it is produced continuously and reabsorbed mainly through the subpleural capillaries and pleural lymphatics. Most of the fluid is produced by the parietal circulation formed by the intercostals arteries and it gets absorbed by the lymphatic system. The intracellular junctions offer 3a gap for diffusion of solutes and molecules. The stomata in the parietal pleura offer exit points for pleural fluid, protein, and cells. These stomata have connection with lymphatics lacunae, which lead to collecting lymphatics. The pleural fluid has been considered as interstitial fluid of the parietal pleura. There is a pressure gradient from pleural interstitium to the pleural space. The parietal pleura is supplied by vessels under systemic pressure and the pressure in the pleural space is subatmospheric. Normally, a few milliliters of fluid is always present in the pleural cavity. Large amount of fluid can accumulate in the pleural cavity when the rate of production of the fluid exceeds the rate of reabsorption.4
A low protein filtrate from systemic vessels reaches the parietal pleural interstitial space where it gets concentrated and gets leaked through the mesothelium into the pleural space. The visceral pleura does not play an important role in the formation of pleural fluid and protein as the microvessels are situated at a greater distance from the mesothelium compared to those of the parietal pleura. Moreover, the filtration pressure is low in the vessels of the visceral pleura. They drain into low pressure pulmonary veins. The filtered liquid probably gets absorbed into the lower pressure vessels. However, the formation and removal of pleural fluid is a slow process.
An abnormal accumulation of fluid in the pleural space occurs from increased formation, decreased clearance, or obstruction to the clearance pathways. All the three mechanisms may play a role. There can be an increased rate of formation of fluid from an increased microvascular hydrostatic pressure, decreased microvascular oncotic pressure, decreased pressure in pleural space (atelectasis), and an increased microvascular permeability (inflammation of vessels, malignancy) and movement of fluid from the peritoneal to pleural space through either diaphragmatic defects or diaphragmatic lymphatics.
The fluid can accumulate in the pleural space in situations like congestive heart failure (increased pulmonary venous pressure), cirrhosis of the liver, nephritic syndrome, severe hypoproteinemia (decreased colloid osmotic pressure), pneumonia, inflammation, infarction, immunologically related diseases and malignancy (increased capillary permeability), collapse (increased intrapleural negative pressure), and mediastinal involvement of carcinoma (decreased lymphatic drainage). Systemic venous hypertension causes a decreased clearance of fluid from pleural space. Malignant involvement of the pleural lymphatics is associated with blockage of the lymphatic drainage system.
Pleura can become seat of inflammation (pleurisy), collection of fluid (pleural effusion), or air (pneumothorax). It can also become seat of fibrosis, thickening, and malignancy. The inflammation of the pleura begins as an acute fibrinous (dry) pleurisy. It is secondary to the underlying diseases of the lung such as tuberculosis, pneumonia, infarction, or bronchogenic carcinoma.4
A collection of fluid in the pleural space is referred to as pleural effusion. The condition develops generally due to an underlying lung disease or systemic disease. The accumulation of fluid as a result of increased transudation is referred to as hydrothorax. Collection of pus, blood, or chyle is referred to as empyema, hemothorax, or chylothorax, respectively, and the term pleural effusion is not applied to these conditions. Empyema thoracis is a pyogenic infection of the pleural cavity with purulent effusion. It may occupy whole (total) or part (encysted) of the space.
Pleural effusion may develop in malignant diseases and it may be exudative, bloody, chylous, or transudative fluid. The condition becomes a morbid problem in advanced cancer. Though all types of lung cancer can lead to pleural effusion, adenocarcinoma appears to be the most common pulmonary malignancy to involve the pleura, due to its peripheral location and tendency for blood vessel invasion and tumor embolization to the visceral pleura. Metastatic breast malignancy is commonly noted with lymphangitic spread and the effusion may be ipsilateral, contralateral, or even bilateral. Among lymphomas, Hodgkin's disease is the leading cause of malignant pleural effusion and is associated with intrathoracic lymph node involvement.
The presence of air in the pleural space is referred to as pneumothorax. Air (gas) can enter the pleural space either from the lung parenchyma and airways (internal) or from outside (external). The condition can occur suddenly as in spontaneous pneumothorax. It can be primary when it occurs in patients without antecedent lung diseases or secondary when it occurs in patients with underlying lung diseases.
Connective tissue diseases are characterized histologically by inflammation and fibrinoid necrosis of collagen and blood vessels and clinically by manifestations affecting different systems such as skin, joints, vessels, muscles, and viscera. Lungs and pleura may get affected in the process. Pleural involvement is noted frequently in rheumatoid arthritis and systemic lupus erythematosus among connective tissue diseases, and it develops due to an immunologic abnormality.
The pleura may get thickened over the convexity of the thorax and sometimes in the interpleural fissure. Pleural thickening may be either localized or generalized. When the thick layer of fibrous tissue limits the expansion of the chest wall, it is referred to as fibrothorax.5
Localized pleural thickening is noted in the inferior portions of the thoracic cavity as it forms the earliest site of pleural fluid accumulation from pleural inflammation. It leads to an obliteration of the costophrenic angle on the radiograph. A generalized pleural thickening involving the entire hemithorax may occur following intense pleural inflammation from large collections of pus, blood, or fluid that are not resolved properly. In all these situations, there are collections of pus, blood, or serous fluid, respectively, in the pleural cavity. It is followed by deposition of the layers of fibrin on the visceral pleural surface to result in a fibrinous envelope surrounding the effusion. There is an inflammatory reaction following invasion of capillaries and organization of fibrous tissue.
Inhaled asbestos fibers from industrial or environmental exposure can cause fibrotic changes in both lung parenchyma in the form of interstitial fibrosis and the chest wall pleura either in the form of circumscribed pleural plaque(s) or diffuse pleural thickening. Pleural plaques and pleural thickening appear to be the most common radiographic abnormalities of asbestos exposure. Asbestos-induced pleural fibrosis is a progressive disease. Pleural plaques and pleural fibrosis are two separate pathologic entities.
Extensive calcification is often noted in old hemothorax, tuberculous pleurisy, empyema, or chronic spontaneous pneumothorax. There is deposition of calcium in the peel lying in the pleural space but no calcification of the pleura itself.
Primary tumors of the pleura may be diffuse or solitary. Mesotheliomas are the examples of diffuse pleural malignancies. Solitary pleural tumors may be benign or malignant.
A relatively small number of drugs can induce adverse reactions on the pleura. A drug is considered causal when a pleural disease develops following its administration, resolves on its discontinuation, and recurs on reexposure. Drug-induced pleural disease may be in the form of pleuritis, pleural effusion, and/or pleural thickening. In many instances, it occurs in the absence of parenchymal 6infiltrates. Drug-induced pleural disease is a rare occurrence compared to drug-induced parenchymal lung disease. The treatment consists of withdrawal of offending agent and administration of systemic corticosteroids for refractory cases.
Pleura can be a seat of inflammation, infection, and malignancy. There can be accumulation of fluid in the form of transudate or exudate. Pneumothorax can develop secondary to an underlying lung disease or without an antecedent lung disease. Pleura can be involved in rheumatoid arthritis or systemic lupus erythematosus. Pleura may get thickened with thick layer of fibrous tissue. Pleura can be a seat of pleural plaques, calcification, or mesothelioma.
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