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|Latin||cavum pleurae, cavum pleurale, cavitas pleuralis|
|Latin||cavum pleurae, cavum pleurale, cavitas pleuralis|
In human anatomy, the pleural cavity is the potential space between the two pleurae (visceral and parietal) of the lungs. A pleura is a serous membrane which folds back onto itself to form a two-layered membrane structure. The thin space between the two pleural layers is known as the pleural cavity and normally contains a small amount of pleural fluid. The outer pleura (parietal pleura) is attached to the chest wall. The inner pleura (visceral pleura) covers the lungs and adjoining structures, via blood vessels, bronchi and nerves.
In humans, there is no anatomical connection between the left and right pleural cavities. Therefore, in cases of pneumothorax, the other lung will still function normally unless there is a tension pneumothorax or simultaneous bilateral pneumothorax, which may collapse the contralateral parenchyma, blood vessels and bronchi.
The visceral pleura receives its blood supply from the bronchial circulation, which is the same as the lungs. The parietal pleura receives its blood supply from the intercostal arteries, which is the same as the overlying body wall.
The costal and cervical portions and the periphery of the diaphragmatic portion of the parietal pleura are innervated by the intercostal nerves. The mediastinal and central portions of the diaphragmatic pleura are innervated by the phrenic nerves. The visceral pleura covering the lung itself receives its innervation from the autonomic nervous system.
Initially the intraembryonic coelom is one continuous space. During development this space partitions to form the pericardial, pleural and peritoneal cavities. The diaphragm and the paired pleuropericardial membranes separate the coelomic cavity into four parts. From the splanchnopleura (the visceral mesodermal layer) develops the visceral pleura and from the somatopleura (parietal mesodermal layer) develops the parietal pleura.
The pleural cavity, with its associated pleurae, aids optimal functioning of the lungs during breathing. The pleural cavity also contains pleural fluid, which allows the pleurae to slide effortlessly against each other during ventilation. Surface tension of the pleural fluid also leads to close apposition of the lung surfaces with the chest wall. This relationship allows for greater inflation of the alveoli during breathing. The pleural cavity transmits movements of the chest wall to the lungs, particularly during heavy breathing. This occurs because the closely apposed chest wall transmits pressures to the visceral pleural surface and hence to the lung.
Pleural fluid is a serous fluid produced by the serous membrane covering normal pleurae. Most fluid is produced by the parietal circulation (intercostal arteries) via bulk flow and reabsorbed by the lymphatic system. Thus, pleural fluid is produced and reabsorbed continuously. In a normal 70 kg human, a few milliliters of pleural fluid is always present within the intrapleural space. Larger quantities of fluid can accumulate in the pleural space only when the rate of production exceeds the rate of reabsorption. Normally, the rate of reabsorption increases as a physiological response to accumulating fluid, with the reabsorption rate increasing up to 40 times the normal rate before significant amounts of fluid accumulate within the pleural space. Thus, a profound increase in the production of pleural fluid—or some blocking of the reabsorbing lymphatic system—is required for fluid to accumulate in the pleural space.
A pathologic collection of pleural fluid is called a pleural effusion. Mechanisms:
Pleural effusions are classified as exudative (high protein) or transudative (low protein). Exudative pleural effusions are generally caused by infections such as pneumonia (parapneumonic pleural effusion), malignancy, granulomatous disease such as tuberculosis or coccidioidomycosis, collagen vascular diseases, and other inflammatory states. Transudative pleural effusions occur in congestive heart failure (CHF), cirrhosis or nephrotic syndrome.
Localized pleural fluid effusion noted during pulmonary embolism (PE) results probably from increased capillary permeability due to cytokine or inflammatory mediator release from the platelet-rich thrombi.
When accumulation of pleural fluid is noted, cytopathologic evaluation of the fluid, as well as clinical microscopy, microbiology, chemical studies, tumor markers, pH determination and other more esoteric tests are required as diagnostic tools for determining the causes of this abnormal accumulation. Even the gross appearance, color, clarity and odor can be useful tools in diagnosis. The presence of heart failure, infection or malignancy within the pleural cavity are the most common causes that can be identified using this approach.
Microscopy may show resident cells (mesothelial cells, inflammatory cells) of either benign or malignant etiology. Evaluation by a cytopathologist is then performed and a morphologic diagnosis can be made. Neutrophils are numerous in empyema. If lymphocytes predominate and mesothelial cells are rare, this is suggestive of tuberculosis. Mesothelial cells may also be decreased in cases of rheumatoid pleuritis or post-pleurodesis pleuritis. Eosinophils are often seen if a patient has recently undergone prior pleural fluid tap. Their significance is limited.
If malignant cells are present, a pathologist may perform additional studies including immunohistochemistry to determine the etiology of the malignancy.
Chemistry studies may be performed including pH, pleural fluid:serum protein ratio, LDH ratio, specific gravity, cholesterol and bilirubin levels. These studies may help clarify the etiology of a pleural effusion (exudative vs transudative). Amylase may be elevated in pleural effusions related to gastric/esophageal perforations, pancreatitis or malignancy. Pleural effusions are classified as exudative (high protein) or transudative (low protein).
In spite of all the diagnostic tests available today, many pleural effusions remain idiopathic in origin. If severe symptoms persist, more invasive techniques may be required. In spite of the lack of knowledge of the cause of the effusion, treatment may be required to relieve the most common symptom, dyspnea, as this can be quite disabling. Thoracoscopy has become the mainstay of invasive procedures as closed pleural biopsy has fallen into disuse.
Diseases of the pleural cavity include: