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LITERATURE
Anatomy of Pleura:
When the primordial bronchial buds first appear they and the
trachea lie in a median mass of mesenchyme, cranial and dorsal to the
peritoneal cavity. The mass of the mesenchymal tissue is the future
mediastinum and separates the two pleura cavities. As the growing primordial
lung buds bulge into the right and left pleural cavity. They carry with them a
covering of the living mesothelium, which becomes the visceral pleura. As the
separate lobes evolve they retain the mesothelial covering.
The parietal pleura are supplied by the somatic nerves. These are:
(1) Inter costal nerves, supply the costal pleura and parietal pleura and
peripheral part of the diaphragmatic pleura.
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(2) Phrenic nerve supplies the mediastinal and central portion of the
diaphragmatic pleura. These somatic nerves are pain sensitive and
innervates the part of the pleura supplies by inter costal nerve is
referred to the adjacent chest wall and the pleura supplied by the
phrenic nerve referred to ipsilateral shoulder.
The parietal pleura receives its blood supply from the systemic
capillaries. Small branches of the inter costal arteries supply the costal pleura
whereas mediastinal pleura is supplied principally by the pericardiophrenic
artery. The diaphragmatic pleura are supplied by the superior phrenic and
musculophrenic arteries. The veins drain mostly into the azygos and internal
thoracic veins. The visceral pleura are supplied mainly by the branches of the
bronchial artery which divides into a network of much dilated capillaries
[Hayek 1960; Harris et al 1977].
Lymphatic Drainage:
The lymphatic vessels of the costal pleura drain ventrally toward the
nodes along the internal thoracic artery and dorsally toward the internal inter
costal lymph nodes near the heads of the ribs. The lymphatics of the mediastinal
pleura pass to the tracheobronchial and mediastinal nodes, where as the lymphatics
of the diaphragmatic pleura pass to the parasternal, middle phrenic and posterior
mediastinal nodes [Bernauddin et al 1980]. The lymphatics of the visceral pleura
drain sub–pleurally into interlober vessels then to hilar nodes [Burke et al 1966].
Applied Anatomy:
regular transfer of low protein fluid parietal pleura to visceral pleura, the
driving force being approximately 19mmHg.
Pleural Effusion:
(1) Hydrostatic gradient between the capillaries of parietal and visceral pleural.
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(2) Lymphatic system absorbing fluid and proteins in the pleural space.
The factor that alters the equilibrium between the formation and
absorption pleural fluid results in pleural effusion. The factors that alter the
equilibrium are [a] an imbalance between the hydrostatic and oncotic pressure in
the pleural capillaries, [b] alteration in the permeability in the pleural
capillaries, [c] impaired lymphatic drainage and [d] abnormal sites of entry
[Bensons, 1996]. As a result of the factors altering the dynamics of pleural fluid
formation the pleural effusion fluid can be either a transudate or an exudate.
For many years pleural fluid protein level of more than 3g% was
used frequently to separate exudates from transudates [Carr et al, 1958].
However Light and his colleagues [1972] found 18% of total misclassification
rate when the pleural fluid protein concentration of more than 3g% was used.
The works done by Light, Macgregor, Luchsinger and Ball [1972] showed that
simultaneously obtained pleural fluid and serum protein and LDH values
correctly classify 99% of cases into exudates or transudates. Light criteria
includes:
(1) Pleural fluid protein divided by serum protein greater than 0.5.
(2) Pleural fluid LDH divided by serum LDH greater than 0.6.
(3) Pleural fluid LDH greater than two– thirds the upper limit of normal
for the serum LDH.
(ii) Infections:
(a) Pneumonia, abscess.
(b) Tuberculosis.
(c) Fungal and actinomycotic disease.
(d) Subphrenic abscess.
(e) Hepatic amoebiasis.
Symptoms:
Physical Examination:
Inspection: Pleural effusion can increase the relative size of the hemithorax
on the same side of effusion. The intercostal spaces may be bulged or indrawn
depending on the intra pleural pressure. The intercostal space may be
retracted, if intrapleural pressure is decreased, during the inspiration.
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Palpation: Apex beat or trachea may be shifted to the opposite side depending
on the size of the effusion[Munro et al 1995]. Tactile vocal fremitus is either
diminished or absent in areas of the chest where pleural fluid separates the
lung from chest wall.
Percussion: The percussion note over the pleural effusion can be dull or stony
dull, The dullness is maximum at the lung bases where the thickness of the
fluid is greatest. Shifting of dullness to percussion is a definite indication of
presence of the free fluid in the pleural cavity.
Radiology:
In Postero–anterior Projection:
Lateral costophrenic angle is obliterated.
Density of the fluid is higher laterally curves gently downward and
medially with smooth meniscus shaped upper border to terminate at
the mediastinum.
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In Lateral Projection:
The upper surface of the fluid density is semicircular high anteriorly
and posteriorly. Curving smoothly downward to its lowest part in the
midway between the sternum and posterior chest wall (Fraser et al
1999).
In Lateral Projection:
Fluid accumulation may be localized in the space between the lung
base and diaphragm and some times may spilled to obliterate the
posterior costophrenic angle.
Massive effusion:
Atypical effusion:
Red blood cells: Hemorrhagic effusion is usually associated with exudates but
about 15% transudates also may have a hemorrhagic pleural fluid [Light
1973].
While Blood Cell Counl: Most transudates usually have a WBC count <
1,000/cm 3 . Whereas the exudates have a WBC count above 1,000/cm 3 [Light
1972] Parapneumonic effusion have a WBC count > 10,000/cm in the pleural
fluid [Light 1973].
(4) Protein:
LDH level in pleural fluid. An LDH level of greater than upper two thirds of
that of the normal serum level or greater than 200 IU is associated with an
exudates pleural effusion. [Light et al, 1972] and the transudates have an
LDH level less than that. A pleural fluid LDH to serum LDH ration of greater
than 0.6 is associated with an exudative effusion and a ratio less than 0.6
indicates a transudative effusion [Light et al 1972].
(6) Cholesterol:
(7) Bilirubin:
(8) Albumin:
(9) Glucose:
JC et al 1968 & Yamanotoz S et al 1976) & most of the pleural fluid cultures
are negative for tubercle bacilli (Bueno CE et al 1990). Occasionally
tubercular empyema occurs due to rupture of caseous or lung cavity (Berger
HW et al 1973). Although tuberculosis is considered a chronic illness,
tubercular pleuritis most commonly manifest as acute illness. Most of the
patients have nonproductive cough, pleuritic chest pain and are febrile.
Sometimes the onset is less acute with mild chest pain, low grade fever, non–
productive cough, weight less and easy fatiguability (Moudgil H et al).
Laboratory Investigation:
Blood: ESR is elevated and most of the patients do not have Leukocytosis.
Sputum: Zhiel Neelsen stain of sputum for acid fast bacilli in most of the
patients is negative.
Pleural Biopsy:
primary tumour of pleura [mesothelioma] and other small number of cases are
caused by sarcoma, malignant melanoma (Anderson et al 1974).
Pleural Biopsy:
Parapneumonic Effusion:
Laboratory Investigations:
Pleural Biopsy:
Empyema:
Laboratory Investigation:
Pleural Biopsy:
Hydrothorax:
Rheumatoid Disease:
pleural effusion that characteristically have low pleural fluid glucose level.
They occur in about 3 % of patients with active rheumatoid disease and are
more common in man than woman. Although pleural effusion usually
unilateral, but they can be bilateral in 20% cases. Pleural fluid is exudative
and may appear turbid due to presence of cholesterol crystals or high
cholesterol level [chyliform effusion], low pleural fluid glucose of less than
45mg/dl, high LDH level of >700 IU/L and high rheumatoid factor titers.
Cellular elements are mostly polymorphs. Pleural biopsy has a limited role in
the diagnosis of rheumatoid pleural disease although the specimen may show
rheumatoid nodule diagnostic of rheumatoid pleurisy (Walker W C et al 1967
& Horler A R et al 1959).
Laboratory Investigations:
Serum Protein and Serum Albumin: The term protein is derived from
"proteios" which means holding first place. As the name indicate these group
of compound is the most important of cell components present abundantly in
cytoplasm and the cell walls.
protein.
Classification:
Fibrous Protein: They are highly complex and fibrillar proteins. Major types
of fibrous proteins are collagen, elastin, keratin, actin and myosin. These
fibrillar proteins have got the properties capable of stretching and recoil to
their natural length also has a tendency to creep.
Nucleo proteins: Contains highly basic amino acids and nucleic acids.
Plasma Proteins:
(b) Globulin
(c) Fibrinogen
Albumin:
Globulin:
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Types:
Fibrinogen:
serum except in that the low molecular weight proteins such as albumin are
present in greater quantities in the intrapleural fluids Protein. Normally
pleural fluids contains about 3.5 to 4.5 gm/dl of albumin. (Light RW et al
1990)
hepatic cirrhosis and ascites. The pleural fluid in this condition originates in
the peritoneal space and escapes across the diaphragm to enter into the pleural
space [Johnston and Loo 1964]. In ascites with pleural effusion the pleural
fluid protein is higher than the ascitic fluid protein [Lieberman et al 1966] but
still does not cross the transudative level.
Serum LDH:
Lactate Dehydrogenase:
Enzyme Isoforms:
infarction is suggested. This method has been largely superseded by the use of
Troponin I or T measurement.
Hemolysis:
Tissue Turnover:
Other uses are assessment of tissue breakdown in general; this is
possible when there are no other indicators of hemolysis. It is used to follow–
up cancer patients, as cancer cells have a high rate of turnover, with destroyed
cells leading to an elevated LDH activity.
served better than the pleural– fluid protein level in differentiating exudates
form transudates. The study by Light et al [1972] showed that most of the
exudates [71 %] had pleural LDH concentration above 200U/L where as none
of the transudates had a values higher that that. It was also observed that only
2% of the transudates had a pleural fluid to serum LDH ratio more than 0.5.
Whereas 86% of exudates exceeded this value. Using various combination of
parameters pleural– fluids to serum protein ratio, pleural fluid LDH level and
pleural fluid to serum protein ratio, pleural fluid found that the combination
of pleural–fluid to serum protein ratio of greater than 0.5, pleural–fluid LDH
level greater than 200U/L and pleural–fluid to serum LDH ratio greater than
200U/L and pleural–fluid to serum ration greater than 0.6 was most suitable to
differentiate the transudates from exudates. It appears that combination of all
these parameters will be more helpful in differentiation.
served better than the pleural– fluid protein level in differentiating exudates
form transudates. The study by Light et al [1972] showed that most of the
exudates [71 %] had pleural LDH concentration above 200 U/L where as none
of the transudates had a values higher that that. It was also observed that only
2% of the transudates had a pleural fluid to serum LDH ratio more than 0.5.
Whereas 86% of exudates exceeded this value. Using various combination of
parameters of pleural fluids to serum protein ration of.5, pleural–fluid LDH
level greater than 0.6U/L ill and pleural–fluid to serum LDH ratio greater than
200U/L and pleural–fluid to serum ration greater than 0.6 was most suitable to
differentiate the transudates from exudates. It appears that combination of all
these parameters will be more helpful in differentiation.
usu
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