Pleural cavity

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Pleural cavity
The pleural cavity is the potential space between the pleurae of the pleural sac that surrounds each lung.
Details
Precursorintraembryonic coelom
Identifiers
Latincavum pleurae, cavum pleurale, cavitas pleuralis
MeSHD035422
TA98A07.1.01.001
TA23316
THH3.05.03.0.00013
FMA9740
Anatomical terminology

The pleural cavity, pleural space, or intrapleural space is the

membranes, and also to create a pressure gradient.[1]

The serous membrane that covers the surface of the lung is the

ribcage.[1]

Structure

In

tension pneumothorax, which may shift the mediastinum and the trachea, kink the great vessels
and eventually collapse the contralateral cardiopulmonary circulation.

The visceral pleura receives its blood supply from the

musculophrenic branches), or their anastomosis
.

The visceral pleurae are innervated by

cervcial cord. Only the parietal pleurae contain somatosensory nerves and are capable of perceiving pain
.

Development

During the third week of

gut tube
during the fourth week, with the splanchnopleure on the inner cavity wall and the somatopleure on the outer cavity wall.

The

parietal pleurae
.

The tissue separating the newly formed pleural cavities from the pericardial cavity are known as the pericardiopleural membranes, which later become the side walls of the

fibrous pericardium. The transverse septum and the displaced somites fuse to form the pleuroperitoneal membranes, which separates the pleural cavities from the peritoneal cavity and later becomes the diaphragm
.

Function

The pleural cavity, with its associated pleurae, aids optimal functioning of the lungs during

respiratory movements.[3] 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 ribs muscles to the lungs, particularly during heavy breathing. During inhalation the external intercostals contract, as does the diaphragm
. This causes the expansion of the chest wall, that increases the volume of the lungs. A negative pressure is thus created and inhalation occurs.

Pleural fluid

Pleural fluid is a

bulk flow and reabsorbed by the lymphatic system.[4] Thus, pleural fluid is produced and reabsorbed continuously. The composition and volume is regulated by mesothelial cells in the pleura.[5] In a normal 70 kg human, a few milliliters of pleural fluid is always present within the intrapleural space.[6]
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.

Pleural fluid circulation

The hydrostatic equilibrium model, viscous flow model and capillary equilibrium model are the three hypothesised models of circulation of pleural fluid.[7]

According to the viscous flow model, the intra pleural pressure gradient drives a downward viscous flow of pleural fluid along the flat surfaces of ribs.The capillary equilibrium model states that the high negative apical pleural pressure leads to a basal-to-apical gradient at the mediastinal pleural surface, leading to a fluid flow directed up towards the apex (helped by the beating heart and ventilation in lungs).Thus the recirculation of fluid occurs. Finally there's a traverse flow from margins to flat portion of ribs completes the fluid circulation.[8][9]

Absorption occurs into lymphatic vessels at the level of the diaphragmatic pleura.[10]

Clinical significance

Pleural effusion

A pleural effusion can form when fluid builds up in the pleural cavity (labelled as pleural space).
Main article: Pleural effusion

A pathologic collection of pleural fluid is called a pleural effusion. Mechanisms:

  1. Lymphatic obstruction
  2. Increased capillary permeability
  3. Decreased plasma colloid osmotic pressure
  4. Increased capillary venous pressure
  5. Increased negative intrapleural pressure

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.[11]

Transudate[12] Exudative causes[12]
* Congestive heart failure (CHF) * Malignancy

Pleural fluid analysis

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.[13]

Gross appearance

  • Clear straw-colored: If transudative, no further analysis needed. If exudative, additional studies needed to determine cause (cytology, culture, biopsy).
  • Cloudy, purulent, turbid: Infection, empyema, pancreatitis, malignancy.
  • Pink to red/bloody: Traumatic tap, malignancy, pulmonary infarction, intestinal infarction, pancreatitis, trauma.
  • Green-white, turbid: Rheumatoid arthritis with pleural effusion.
  • Green-brown: Biliary disease, bowel perforation with ascites.
  • Milky-white or yellow and bloody: Chylous effusion.
  • Milky or green, metallic sheen: Pseudochylous effusion.
  • Viscous (hemorrhagic or clear): Mesothelioma.
  • Anchovy-paste (or 'chocolate sauce'): Ruptured amoebic liver abscess.[12]

Microscopic appearance

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 pleural 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.[14]

If malignant cells are present, a pathologist may perform additional studies including immunohistochemistry to determine the etiology of the malignancy.

Chemical analysis

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

dyspnea, as this can be quite disabling. Thoracoscopy
has become the mainstay of invasive procedures as closed pleural biopsy has fallen into disuse.

Disease

Main article: Pleural disease

Diseases of the pleural cavity include:

See also

  • Coin test, medical diagnostic test for a punctured lung

References

  1. ^
    OCLC 780984149
    .
  2. OCLC 902010725
    .
  3. ^ Light 2007, p. 1.
  4. PMID 20956149
    .
  5. PMID 12503717
    .
  6. ISBN 978-0072827415
    .
  7. PMID 28523153
    .
  8. OCLC 949753083
    .
  9. PMID 15044678
    .
  10. PMID 30069369
    .
  11. S2CID 44337698
    .
  12. ^
    OCLC 78070199
    .
  13. OCLC 1239350014
    .
  14. ^ De Mais, Daniel. ASCP Quick Compendium of Clinical Pathology, 2nd. Ed. ASCP Press, Chicago, 2009.

Sources

External links
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