Serous fluid accumulates in the pleural cavities (pleural fluid), peritoneal cavity (ascitic fluid), in the pericardial cavity (pericardial fluid) and is removed by puncture or incision of these cavities. To prevent clotting, you can add a 5% sodium citrate solution to the test liquid (2-5 ml of solution per 100 ml of liquid) or rinse the walls of the vessel into which the serous liquid will be collected with this solution. For testing, all collected serous fluid is sent to the laboratory in clean containers. Depending on the mechanism of formation, two types are distinguished serous fluid- transudate and exudate.

Transudate

Transudate (non-inflammatory fluid) appears in case of disorders of general and local circulation (right ventricular failure of the heart, portal hypertension due to portal vein thrombosis, cirrhosis of the liver, adhesive pericarditis, etc.), a decrease in oncotic pressure in the vessels (hypoproteinemia of various origins), disturbances in electrolyte metabolism ( most often with an increase in sodium concentration, an increase in aldosterone production), etc. Transudate is usually light-colored yellow, transparent, its relative density ranges from 1005-1015 (determined in the same way as the relative density of urine, i.e., by a urometer). The amount of protein in the serous fluid is determined by the turbidity formed when sulfosalicylic acid is added or by the Brandberg-Roberts-Stolnikov method. The transudate contains from 5 to 10 g/l of protein.

Exudate

Exudate is an inflammatory fluid. Serous exudate is light yellow in color and transparent. In all other cases, the exudate is cloudy, and its color depends on the nature (bloody, purulent, etc.). The relative density of the exudate is 1.018 and higher. It contains from 30 to 80 g/l of protein.

It is not always easy to distinguish between transudate and exudate, since there are liquids that are similar in their properties to both exudate and transudate, and exudate with a low relative density and a relatively low protein content. To differentiate these liquids, the Rivalta reaction is used.

Methodology. A narrow cylinder with a capacity of 200 ml is filled with water, add 2-3 drops of ice acetic acid and stir. Then, add 1-2 drops of the test liquid from a pipette into the resulting weak solution of acetic acid and watch on a black background for the appearance of a cloud-like cloudiness, reminiscent of cigarette smoke. In the exudate, the turbidity increases as the drop descends and reaches the bottom of the cylinder ( positive reaction), in the transudate, slight turbidity dissipates and disappears before reaching the bottom of the cylinder (negative reaction).

After settling the serous fluid delivered for examination for

After 1-2 hours, the sediment is collected with a glass tube for centrifugation (as when examining urine). If there is a lot of liquid, then the sediment is collected in several centrifuge tubes (up to 10). After centrifugation for 5-10 minutes at 1500-3000 rpm, all the resulting sediments are poured into one test tube and centrifuged again. As a result, a concentrated sediment is obtained, from which native preparations are prepared for microscopic examination.

If there are fibrinous bundles, shreds or clots in the liquid, then their quantity and volume are described in the analysis. The bundles and scraps are selected with a narrow spatula and a needle from the liquid poured into a Petri dish, and then pieces are split off from them to prepare native preparations, since the formed elements are usually found in the bundle. The bundle placed on a glass slide is stretched with a needle and spatula. Otherwise, the result will be a thick preparation, unsuitable for microscopic examination (the shaped elements will be indistinguishable in it).

After microscopic examination, native preparations are stained according to Romanovsky - Giemsa or Pappenheim. Painting time - no more than 5 minutes. In the presence of serous fluid of pus, smears are prepared from the sediment for Ziehl-Neelsen and Gram staining.

Types of exudate

Depending on the type of pathological process, different types of exudate are distinguished.

Serous and serous-fibrinous exudate

Serous and serous-fibrinous exudate is observed with staphylococcal, streptococcal infections, tuberculosis, syphilis, rheumatism. Fibrinous clots are usually present in serous-fibrinous exudate. Microscopy reveals no large number cellular elements. Lymphocytes predominate. Sometimes a significant number of either neutrophilic granulocytes, or monocytes, or macrophages, or eosinophilic granulocytes, or all of these elements in any ratio is detected. In prolonged forms of pleurisy, the cytogram is characterized by the presence of plasma cells. Often, at the beginning of tuberculous pleurisy, a variegated cytogram pattern is revealed (eosinophilic and neutrophilic granulocytes, histiocytes, elements of tuberculoma, etc.), due to which it sometimes has to be differentiated from lymphogranulomatosis.

Serous-purulent and purulent exudate

Serous-purulent and purulent exudate is cloudy, thick, green-yellow, sometimes brownish or chocolate-colored; observed with bacterial infection. Cytograms are characterized a large number neutrophilic granulocytes, often with degenerative changes, the presence of macrophages, single giant cells of foreign bodies and detritus.

Putrid exudate

Putrid exudate is different putrid smell, greenish color. Cytograms contain a large amount of detritus of disintegrated cells, needles fatty acids, sometimes crystals of hematoidin and cholesterol are found, as well as many microorganisms, including anaerobic ones.

Eosinophilic exudate

Eosinophilic exudate is characterized by a large number of eosinophilic granulocytes, which can reach more than 90% cellular composition effusion. It is sometimes observed with tuberculosis or other infections, abscess, trauma, multiple metastases of cancer in the lungs, migration of roundworm larvae into the lungs, etc. By nature, eosinophilic exudate can be serous, hemorrhagic and purulent.

Hemorrhagic exudate

Hemorrhagic exudate appears with mesothelioma, cancer metastases, hemorrhagic diathesis, and chest wounds. When infection penetrates into the cavity with hemorrhagic exudate, it can turn into purulent-hemorrhagic. An admixture of pus in the exudate is detected using Petrov's test: when water is added, the sterile exudate becomes clear due to hemolysis of red blood cells, and the infected remains cloudy due to the presence of leukocytes.

At microscopic examination pay attention to red blood cells. If the bleeding has already stopped, then only old forms of red blood cells with various signs their death (microforms, “mulberries”, shadows of erythrocytes, poikilocytes, schizocytes, vacuolated, fragmented erythrocytes, etc.). The appearance of unchanged red blood cells against the background of old, changed ones indicates re-bleeding. The presence of only unchanged red blood cells indicates fresh bleeding. When hemorrhagic exudate transforms into purulent or another form, corresponding cellular elements appear. During the period of resorption of hemorrhagic exudate, sometimes up to 80% of its cellular elements are eosinophilic granulocytes, which is a favorable sign.

Cholesterol exudate.

Any encysted exudate that persists for a long time (several years) can turn into cholesterol. Cholesterol exudate is thick, yellowish or brownish in color, with a pearlescent sheen, sometimes chocolate-colored (depending on the number of disintegrated red blood cells). On the walls of a test tube moistened with exudate, casts of cholesterol crystals in the form of tiny sparkles are macroscopically visible. Microscopic examination reveals fatty-degenerated cells, cellular decay products, fat droplets and cholesterol crystals.

Milky exudate.

There are three types of such exudate.

Chylous exudate appears when a significant amount of lymph enters the serous cavity from large lymphatic vessels. This liquid contains a large number of small droplets of fat, which is stained red by Sudan III and black by osmium. When standing in the liquid, a creamy layer forms and floats to the top.

To clarify the liquid, add 1-2 drops of caustic alkali with ether to the exudate. Depending on the cause that caused the rupture of the lymphatic vessel, the cellular elements of the exudate may be different. If a tumor has grown into a vessel and destroyed it, then tumor cells can be found in the fluid.

Chyle-like exudate observed with intensive breakdown of fatty degenerated cells. Microscopic examination reveals an abundance of fatty degenerated cells, fatty detritus and fatty droplets of various sizes. There is no microflora. Chyle-like exudate is observed in chronic purulent pleurisy, atrophic cirrhosis of the liver, malignant neoplasms etc.

Pseudochyle exudate macroscopically also resembles milk, but particles suspended in the exudate are not stained by Sudan III and osmium and do not dissolve when heated. Microscopy reveals mesotheliocytes and single fat droplets. Pseudochyle exudate occurs in lipoid and lipoid-amyloid degeneration of the kidneys.

Guide to practical exercises in clinical laboratory diagnostics/ Ed. prof. M.A. Bazarnova, prof. V.T. Morozova.- K.: Vyshcha School, 1988.- 318 p., 212 ill.

Transudate is usually a colorless liquid (non-inflammatory effusion) that accumulates in body cavities, tissues, and subcutaneous fat due to edema.

Effusion appears in the following diseases:

• cirrhosis;
• dropsy;
• heart failure.

Transudate is formed due to sweating of the liquid part of the blood serum. The effusion may contain impurities of pigments: blood, bile. At various diseases non-inflammatory effusion accumulates in different parts of the body.

Thus, it is formed in the pleural cavity, pericardium, and peritoneum during heart failure and cirrhosis. With varicocele, it accumulates in the lining of the testicles. Sometimes infection is possible with subsequent development of pleurisy and peritonitis.

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Reasons

The reasons for the accumulation of transudate in the body are as follows: disorders of lymphatic drainage, blood circulation (systemic and local), metabolic processes, thinning of capillary walls.

In addition to liver cirrhosis, dropsy and heart failure, nephrotic syndrome can lead to this pathology, endocrine disorders, such as ovarian fibroma, myxedema, chronic glomerulonephritis, amyloid lipoid nephrosis, venous thrombosis, portal hypertension and other pathologies.

Composition of the transudate

Non-inflammatory liquid is characterized by colorlessness and transparency, less often a cloudy color or a pale yellow tint of the liquid.

Relative density – 1.006-1.012, protein content – ​​up to 3%, Rivalta test negative, number of leukocytes in 1 µl – less than 1000, ratio of effusion protein to serum protein – less than 0.5, ratio of effusion LDH to serum LDH – less than 0.6 .

What is the difference between transudate and exudate?

The difference from exudate is that the density of transudate is less, it accumulates without inflammatory processes in the tissues and it contains much less protein (up to 2-3%), and there are no enzymes characteristic of plasma at all.

The accumulation of transudate is most often painless and is not associated with an increase in temperature. But sometimes the qualitative differences between exudate and transudate disappear.

Then the most important diagnostic criterion is the clinical picture of the disease, a complex of anatomical and bacteriological changes.

Pathological processes occurring in the body can lead to fluid accumulation. Its collection and examination are of great importance at the diagnostic stage. The goal here is to find out whether the extracted material is exudate or transudate. The results of such an analysis make it possible to identify the nature of the disease and choose the right treatment tactics.

Exudate- a liquid whose origin is associated with ongoing inflammatory processes.

Transudate- effusion formed for reasons unrelated to inflammation.

Comparison

Thus, by determining the type of liquid, important conclusions can be drawn. After all, if the punctate (material extracted from the body) is an exudate, then inflammation occurs. This process is accompanied, for example, by rheumatism or tuberculosis. Transudate indicates circulatory problems, metabolic problems and other abnormalities. Inflammation is excluded here. This fluid collects in cavities and tissues, say, in heart failure and some liver diseases.

It must be said that the difference between exudate and transudate is not always visible. Both can be transparent and have a yellowish tint. However, the exudate often has a different color and is also cloudy. There are quite a few variations of this liquid. The serous variety is especially close in its characteristics to transudate. Other samples are more specific. For example, purulent exudate is viscous and greenish, hemorrhagic - with a red tint due to the large number of red blood cells, chylous - contains fat and resembles milk when visually assessed.

When comparing the density of exudate and transudate, lower parameters are noted for punctate of the second type. The main distinguishing criterion is the protein content in liquids. As a rule, the exudate is very saturated with it, and the amount of this substance in the transudate is small. The Rivalta test helps to obtain information regarding the protein component. Drops of the test material are added to the container with the vinegar composition. If, falling, they turn into a cloudy cloud, then there is an issue with exudate. Biological fluid the second type does not give such a reaction.

More detailed information about the difference between exudate and transudate is reflected in the table:

Prevention

Part X. Study of exudates and transudates Exudate

Exudate

Exudate (exsudatum; lat. exsudare - to come out, to be released) - liquid, rich in protein and containing formed elements of blood; formed during inflammation. The process of moving exudate into surrounding tissues and cavities of the body is called exudation, or sweating. The latter occurs following damage to cells and tissues in response to the release of mediators.

Depending on the quantitative protein content and the type of emigrated cells, serous, purulent, hemorrhagic, and fibrinous exudate are distinguished. There are also mixed forms exudate: serous-fibrinous, serous-hemorrhagic. Serous exudate consists predominantly of plasma and a small amount shaped elements blood. Purulent exudate contains disintegrated polymorphonuclear leukocytes, cells of the affected tissue and microorganisms. Hemorrhagic exudate is characterized by the presence of a significant admixture of red blood cells, and fibrinous exudate is characterized by the presence of a significant admixture of red blood cells. great content fibrin. The exudate may resolve or undergo organization.

Transudate

Transudate (Latin trans - through, through + sudare - ooze, leak) is a non-inflammatory effusion, edematous fluid that accumulates in body cavities and tissue crevices. Transudate is usually colorless or pale yellow, transparent, less often cloudy due to the admixture of single cells of deflated epithelium, lymphocytes, and fat. The protein content in the transudate usually does not exceed 3%; they are serum albumins and globulins. Unlike exudate, transudate does not contain enzymes characteristic of plasma. The relative density of transudate is 1.006–1.012, and that of exudate is 1.018–1.020.

Differential diagnosis of exudate and transudate

Sometimes the qualitative differences between transudate and exudate disappear: the transudate becomes cloudy, the amount of protein in it increases to 4–5%). In such cases important to differentiate fluids, it is necessary to study the entire complex of clinical, anatomical and bacteriological changes (the presence of pain in the patient, elevated temperature body, inflammatory hyperemia, hemorrhages, detection of microorganisms in liquid). To distinguish transudate from exudate, the Rivalta test is used, based on their different protein content.

The formation of transudate is most often caused by heart failure, portal hypertension, lymph stagnation, venous thrombosis, renal failure. The mechanism of transudate occurrence is complex and is determined by a number of factors: increased hydrostatic pressure of the blood and reduced colloid-osmotic pressure of its plasma, increased permeability of the capillary wall, retention of electrolytes, mainly sodium and water, in the tissues. The accumulation of transudate in the pericardial cavity is called hydropericardium, in abdominal cavity– ascites, in the pleural cavity – hydrothorax, in the cavity of the testicular membranes – hydrocele, in the subcutaneous tissue – anasarca. Transudate easily becomes infected, turning into exudate. Thus, infection of ascites leads to peritonitis (ascites-peritonitis). With prolonged accumulation of edematous fluid in the tissues, degeneration and atrophy of parenchymal cells and sclerosis develop. If the process progresses favorably, the transudate may resolve.

Ascites

Ascites is the accumulation of fluid in the abdominal cavity. A small amount of it may not produce symptoms, but an increase in fluid leads to distension of the abdominal cavity and the appearance of discomfort, anorexia, nausea, heartburn, side pain, and respiratory disorders.

Diagnostic paracentesis (50–100 ml) provides valuable information; use a 22 gauge needle; a puncture is performed along the white line 2 cm below the navel or with skin displacement in the left or right lower quadrant of the abdomen. A routine examination includes examination, determination of the content of total protein, albumin, glucose in the liquid, the number of cellular elements, cytological examination, culture; Sometimes amylase, LDH, triglycerides are examined, and culture is performed for Mycobacterium tuberculosis. Rarely, laparoscopy or even exploratory laparotomy is required. Ascites due to CHF (constrictive pericarditis) may require diagnostic catheterization of the right heart.

Table 24

Characteristics of peritoneal fluid in ascites of various origins

Transudate

Transudate (lat. (gapz - through, through + zibage - ooze, seep) - non-inflammatory effusion, edematous fluid that accumulates in body cavities and tissue crevices. Transudate is usually colorless or pale yellow, transparent, less often cloudy due to the admixture of isolated deflated epithelial cells, lymphocytes, fat. The protein content in the transudate usually does not exceed 3%; they are serum albumins and globulins. Unlike exudate, there are no enzymes characteristic of plasma.

Differences between exudate and transudate

The relative density of transudate is 1.006-1.012, and that of exudate is 1.018-1.020. Sometimes the qualitative differences between transudate and exudate disappear: the transudate becomes cloudy, the amount of protein in it increases to 4-5%). In such cases, it is important for the differentiation of fluids to study the entire complex of clinical, anatomical and bacteriological changes (the presence of pain in the patient, elevated body temperature, inflammatory hyperemia, hemorrhages, detection of microorganisms in the fluid). To distinguish transudate from exudate, the Rivalta test is used, based on their different protein content.

The formation of transudate is most often caused by heart failure, portal hypertension, lymph stagnation, venous thrombosis, and renal failure. The mechanism of transudate occurrence is complex and is determined by a number of factors: increased hydrostatic pressure of the blood and reduced colloid-osmotic pressure of its plasma, increased permeability of the capillary wall, retention of electrolytes, mainly sodium and water, in the tissues. The accumulation of transudate in the pericardial cavity is called hydropericardium, in the abdominal cavity - ascites, in the pleural cavity - hydrothorax, in the cavity of the testicular membranes - hydrocele, in the subcutaneous tissue - anasarca. Transudate is easily infected, turning into exudate. Thus, infection of ascites leads to peritonitis (ascites-peritonitis). With prolonged accumulation of edematous fluid in the tissues, degeneration and atrophy of parenchymal cells and sclerosis develop. If the process progresses favorably, the transudate may resolve.

	Ultrafiltrate plasma	Transudat	Exudate	Plasma
Vascular permeability	Normal	Normal	Increased
Types of proteins	Albumin	Albumin
				No (fibrinogen)
Relative density
			Inflammation

At acute inflammation There is an immediate (but reversible) increase in the permeability of venules and capillaries, due to the active contraction of actin filaments in endothelial cells, leading to the expansion of intercellular pores. Direct damage to endothelial cells by toxic agents can lead to the same result. Large amounts of liquid and large molecular proteins can penetrate through vessels with impaired permeability. These changes in permeability are caused by various chemical mediators (Table 1).

Fluid exudation: the passage of large amounts of fluid from the bloodstream into the interstitial tissue causes swelling (inflammatory edema) of the tissue. An increase in the transfer of fluid from the microvasculature into the tissue due to an increase in vascular permeability is called exudation. The composition of the exudate approaches the composition of plasma (Table 2); it contains large amounts of plasma proteins, including immunoglobulins, complement, and fibrinogen, due to the increased permeability of the endothelium no longer preventing these large molecules from entering the tissue. Fibrinogen in acute inflammatory exudate is quickly converted into fibrin under the influence of tissue thromboplastins. Fibrin can be detected microscopically in the exudate in the form of pink threads or bundles. Macroscopically, fibrin is most clearly visible on the inflamed serous membrane, the surface of which varies from normal shiny to rough, yellowish, covered with a film and coagulated proteins.

Exudation must be distinguished from transudation (Table 2). Transudation - This is the process of increased transfer of fluid into tissues through vessels with normal permeability. The force under which fluid passes from the bloodstream into the tissues is due to an increase in hydrostatic pressure or a decrease in the osmotic pressure of plasma colloids. Transudate has a composition similar to that of plasma ultrafiltrate. In clinical practice, the identification of edematous fluid (transudate or exudate) has great diagnostic value, since it provides identification of the causes of disorders, for example, in the study of peritoneal fluid (with ascites).

Exudation reduces the activity of the damaging agent by:

Breeding it; - increasing lymph outflow; - flooding with plasma containing numerous protective proteins such as immunoglobulins and complement.

Increased lymphatic drainage facilitates the transport of damaging agents to regional lymph nodes, thereby facilitating a protective immune response. Sometimes, when infected with virulent microorganisms, this mechanism can cause their spread and the occurrence of lymphangitis and lymphadenitis.

Cellular reactions:

Types of cells involved: acute inflammation is characterized by active emigration of inflammatory cells from the blood to the area of ​​damage. Neutrophils (polymorphonuclear leukocytes) dominate in the early stage (in the first 24 hours). After the first 24-48 hours, phagocytic cells of the macrophage system and immunologically active cells such as lymphocytes and plasma cells appear at the site of inflammation. However, neutrophils remain the predominant cell type for several days.

Marginal position of neutrophils: in a normal blood vessel, cellular elements are concentrated in the central axial flow, separated from the endothelial surface by a zone of plasma (Fig. 3). This separation depends on the normal flow of blood, which occurs under the influence of physical laws, the influence of which leads to the accumulation of the heaviest cellular particles in the center of the vessel. Since the speed of blood flow in dilated vessels during acute inflammation is reduced, the distribution of cellular elements is disrupted.

Red blood cells form large aggregates ( "rouleau) (so-called “sludge” phenomenon).

Leukocytes move to the periphery and come into contact with the endothelium (margination, marginal standing), on which many of them adhere . This happens in result increase expression (appearance on the cell surface) of various adhesion molecules cells (MYSELF , cell adhesion molecules) on leukocytes and endothelial cells. For example, the expression of beta 2 integrins (CD11-CD18 complex), which include leukocyte function antigen-1 (LFA-1, leukocyte function antigen-1), is increased due to the influence of chemotactic factors such as C5a (the “anaphylatoxin”) of complement , and leukotriene B 4 LTB 4. The synthesis of complementary CAM molecules on endothelial cells is similarly regulated by the actions of interleukin-1 (IL-1) and TNF (tumor necrosis factor, which is also detected outside tumors; they include ICAM 1); , ICAM 2 and ELAM-1 (endothelial leukocyte adhesion molecule).

Emigration of neutrophils: adherent neutrophils actively leave blood vessels through the intercellular gaps and pass through the basement membrane, entering the interstitial space ( emigration). Penetration through the vessel wall lasts 2-10 minutes; in interstitial tissue, neutrophils move at speeds of up to 20 µm/min.

Chemotactic factors (table 1): active emigration of neutrophils and direction of movement depend on chemotactic factors. Complement factors C3a and C5a (forming in a complex anaphylatoxin) are powerful chemotactic agents for neutrophils and macrophages, like the leukotriene LTB4. The interaction between receptors on the surface of neutrophils and these “chemotaxins” increases neutrophil motility (by increasing the influx of Ca 2+ ions into the cell, which stimulates actin contraction) and activates degranulation. Various cytokines play an activating role in the development of the immune response.

Red blood cells enter the inflamed area passively, in contrast to the active process of emigration of leukocytes. They are pushed out of the vessels by hydrostatic pressure through widened intercellular gaps following the emigrating leukocytes ( diapedesis). In case of severe damage associated with impaired microcirculation, a large number of red blood cells can enter the site of inflammation (hemorrhagic inflammation).

Immune phagocytosis (B) is much more effective than nonspecific (A). Neutrophils have receptors on their surface for the Fc fragment of immunoglobulins and complement factors. Macrophages have the same properties.

1. Recognition - the first step of phagocytosis is recognition of the damaging agent by the phagocytic cell, which occurs either directly (upon recognition of large, inert particles) or after the agent is coated with immunoglobulins or complement factors (C3b) ( opsonization). Opsonin-facilitated phagocytosis is a mechanism involved in the immune phagocytosis of microorganisms. IgG and C3b are effective opsonins. Immunoglobulin, which has a specific reactivity towards the damaging agent (specific antibody) is the most effective opsonin. C3b is formed directly at the site of inflammation by activating the complement system. In the early stages of acute inflammation, before an immune response develops, nonimmune phagocytosis dominates, but as the immune response develops, it is replaced by the more effective immune phagocytosis.

2. Absorption - after recognition by a neutrophil or macrophage, the foreign particle is engulfed by a phagocytic cell, in which a membrane-bounded vacuole called a phagosome is formed, which, when fused with lysosomes, forms a phagolysosome.

3. Destruction of microorganisms - when the damaging agent is a microorganism, it must be killed before death of the phagocytic cell occurs. Several mechanisms are involved in the destruction of microorganisms.

PROLIFERATION

Proliferation(reproduction) of cells is the final phase of inflammation. Proliferation of cambial cells is observed at the site of inflammation connective tissue, B- and T-lymphocytes, monocytes, as well as cells of local tissue in which the process of inflammation unfolds - mesothelial, epithelial cells. In parallel, cellular differentiation and transformation are observed. B lymphocytes give rise to the formation of plasma cells, monocytes give rise to histiocytes and macrophages. Macrophages can be the source of the formation of epithelioid and giant cells (foreign body cells and Pirogov-Langhans type cells).

Cambial connective tissue cells can subsequently differentiate into fibroblasts that produce collagen protein and glycosaminoglycans. As a result, very often outcome inflammation, fibrous connective tissue grows.

REGULATION OF INFLAMMATION

Regulation of inflammation carried out with the help of hormonal, nervous and immune factors.

It is known that some hormones enhance the inflammatory response - these are the so-called

pro-inflammatory hormones (mineralocorticoids, pituitary somatotropic hormone, pituitary thyreostimulin, aldosterone). Others, on the contrary, reduce it. This anti-inflammatory hormones , such as glucocorticoids and adrenocorticotropic hormone (ACTH) from the pituitary gland. Their anti-inflammatory effect is successfully used in therapeutic practice. These hormones block the vascular and cellular phenomenon of inflammation, inhibit the mobility of leukocytes, and enhance lymphocytolysis.

Cholinergic substances , stimulating the release of inflammatory mediators, act similarly pro-inflammatory hormones, and adrenergic , inhibiting mediator activity, behave like anti-inflammatory hormones.

The severity of the inflammatory reaction, the rate of its development and nature are influenced by state of immunity. Inflammation occurs especially rapidly under conditions of antigenic stimulation (sensitization). In such cases they talk about immune, or allergic, inflammation.

Pleural effusion is the accumulation of pathological fluid in the pleural cavity during inflammatory processes in adjacent organs or layers of the pleura or when there is a violation of the relationship between the colloid-osmotic pressure of the blood plasma and the hydrostatic pressure in the capillaries.

Pleural fluid of inflammatory origin is exudate. The fluid accumulated as a result of a violation of the relationship between the colloid-osmotic pressure of the blood plasma and the hydrostatic pressure in the capillaries is a transudate.

After obtaining pleural fluid, it is necessary to determine, depending on the color, transparency, relative density, biochemical and cytological composition, whether the effusion is an exudate or a transudate.

Differential diagnostic differences between pleural exudate and transudate

Signs	Exudate	Transudate
Onset of the disease		Gradual
Presence of pain in chest at the beginning of the disease	Characteristic	Not typical
Increased body temperature	Characteristic	Not typical
Presence of general laboratory signs of inflammation (increased ESR, “biochemical inflammation syndrome”*)	Characteristic and very pronounced	Not typical, sometimes general laboratory signs of inflammation may be present, but, as a rule, they are mild
Appearance of liquid	Cloudy, not entirely transparent, intense lemon-yellow color (serous and serous-fibrinous exudate), often hemorrhagic, may be purulent, putrefactive with unpleasant smell	Transparent, slightly yellowish, sometimes colorless liquid, odorless
Change in appearance of pleural fluid after standing	It becomes cloudy, more or less abundant fibrin flakes fall out. Serous-purulent exudate is divided into two layers (upper - serous, lower - purulent). Effusion clots when standing	Remains transparent, no sediment is formed or it is very delicate (in the form of a cloud), there is no tendency to coagulate
LDH	> 200 U/l or > 1.6 g/l
Pleural fluid protein/blood plasma protein
Pleural fluid LDH/blood plasma LDH
Glucose level		> 3.33 mmol/l
Pleural fluid density	> 1.018 kg/l
Effusion cholesterol/serum cholesterol
Rivalta test**	Positive	Negative
The number of leukocytes in pleural fluid	> 1000 in 1 mm 3
Number of red blood cells in pleural fluid	Variable
Cytological examination of pleural fluid sediment	Neutrophilic leukocytosis predominates	A small amount of desquamated mesothelium

Notes:

* biochemical inflammation syndrome - increased blood levels of seromucoid, fibrin, haptoglobin, sialic acids - nonspecific indicators of the inflammatory process;

** Rivalta test is a test for determining the presence of protein in pleural fluid: water in a glass cylinder is acidified with 2-3 drops of 80% acetic acid, then the test pleural fluid is dripped dropwise into the resulting solution. If it is an exudate, then after each drop in the water there is a cloud in the form of cigarette smoke, but with a transudate there is no such trace.

After determining the nature of the effusion (exudate or transudate), it is advisable to take into account the most common causes of exudate and transudate, which to a certain extent facilitates the further differentiation of pleural effusions.

The nature of the exudate is determined not only by the variety of causes, but also by the ratio of accumulation and resorption of the effusion, the duration of its existence:

• moderate effusion and good resorption - fibrinous pleurisy;
• exudation exceeds absorption of exudate - serous or serous-fibrinous pleurisy;
• infection of the exudate by pyogenic microflora - purulent pleurisy (pleural empyema);
• the rate of resorption exceeds the rate of exudation - the formation of adhesions during resorption;
• carcinomatosis, pleural mesothelioma, pulmonary infarction and trauma, pancreatitis, hemorrhagic diathesis, overdose of anticoagulants - hemorrhagic effusion;
• the predominance of allergic processes - eosinophilic exudate;
• trauma to the thoracic duct due to tumor or tuberculous lesions - chylous exudate;
• chronic long-term course exudative pleurisy, in particular, with tuberculosis - cholesterol effusion.

Causes of pleural effusion (S. L. Malanichev, G. M. Shilkin, 1998, as amended)

Type of effusion	Main reasons	Less common causes
Transudate	Congestive heart failure	Nephrotic syndrome(glomerulonephritis, renal amyloidosis, etc.); cirrhosis; myxedema, peritoneal dialysis
Inflammatory and infectious exudates	Parapneumonic effusion; tuberculosis; bacterial infections	Subphrenic abscess; Intrahepatic abscess; Viral infection; fungal infections
Non-infectious inflammatory exudates	Thromboembolism pulmonary artery	Systemic connective tissue diseases; pancreatitis (enzymatic pleurisy); reaction to medicines; asbestosis; post-infarction syndrome Dressler; “yellow nails” syndrome*; uremia
Tumor exudates	Cancer metastases; leukemia	Mesothelioma; Meigs syndrome"
Hemothorax	Injury; cancer metastases; pleural carcinomatosis	Spontaneous (due to hemostasis disorders); rupture of a vessel in pleural adhesions during spontaneous pneumothorax; rupture of aortic aneurysm into the pleural cavity
Chylothorax	Lymphoma; injury to the thoracic lymphatic duct; carcinoma	Lymphangioleiomyomatosis

Notes:

* “Yellow nails” syndrome is a congenital hypoplasia of the lymphatic system: thickened and curved yellow nails, primary lymphedema, less often exudative pleurisy, bronchiectasis are characteristic.

** Meigs syndrome - pleurisy and ascites in ovarian carcinoma.

Tuberculous pleurisy

Tuberculosis is a common cause of exudative pleurisy. More often, tuberculous pleurisy develops against the background of any clinical form pulmonary tuberculosis (disseminated, focal, infiltrative), bronchoadenitis or primary tuberculosis complex. IN in rare cases tuberculous exudative pleurisy may be the only and primary form of pulmonary tuberculosis. According to A.G. Khomenko (1996), there are three main types of tuberculous pleurisy: allergic, perifocal and pleural tuberculosis.

Allergic pleurisy

Is hyperergic. It is characterized by the following clinical features:

• acute onset with chest pain, high temperature body, rapid accumulation of exudate, severe shortness of breath;
• rapid positive dynamics (exudate resolves within a month, rarely longer);
• increased sensitivity to tuberculin, which causes a positive tuberculin test;
• eosinophilia in peripheral blood and a significant increase in ESR;
• the exudate is predominantly serous (in the early stages it can be serous-hemorrhagic), contains a large number of lymphocytes, sometimes eosinophils;
• frequent combination with other manifestations caused by hyperergic reactivity - polyarthritis, erythema nodosum;
• absence of Mycobacterium tuberculosis in pleural effusion.

Perifocal pleurisy

Inflammatory process in the pleural layers in the presence of pulmonary tuberculosis - focal, infiltrative, cavernous. Perifocal pleurisy occurs especially easily when the pulmonary tuberculosis focus is subpleural. Features of perifocal pleurisy are:

• long-term, often recurrent course of exudative pleurisy;
• the formation of a large number of pleural adhesions (adhesions) in the resorption phase;
• serous nature of the exudate with a large number of lymphocytes and a high content of lysozyme;
• absence of mycobacteria in the exudate;
• the presence of one of the forms of tuberculosis of the lungs (focal, infiltrative, cavernous), which is diagnosed using an x-ray method after preliminary pleural puncture and evacuation of exudate;
• sharply positive tuberculin tests.

Pleural tuberculosis

Direct damage to the pleura by the tuberculosis process may be the only manifestation of tuberculosis or be combined with other forms of pulmonary tuberculosis. Pleural tuberculosis is characterized by the appearance of multiple small foci on the pleural layers, but the presence of large foci with caseous necrosis is possible. In addition, exudative inflammatory reaction pleura with accumulation of effusion in the pleural cavity.

Clinical features of pleural tuberculosis:

• long-term course of the disease with persistent accumulation of effusion;
• the exudate can be serous with a large number of lymphocytes and lysozyme (with the development of pleurisy due to seeding of the pleura and the formation of multiple foci) or neutrophils (with caseous necrosis of individual large foci). With widespread caseous lesions of the pleura, the exudate becomes serous-purulent or purulent (with a very extensive lesion) with a large number of neutrophils;
• Mycobacterium tuberculosis is detected in pleural effusion, both by microscopy and by culture of the exudate.

With widespread caseous necrosis of the pleura, disintegration of large tuberculous foci on the pleura and blockade of exudate resorption mechanisms, purulent tuberculous pleurisy (tuberculous empyema) can develop. At the same time, in clinical picture very dominant pronounced syndrome intoxication: body temperature rises to 39 C and above; severe sweating appears (heavy sweats at night are especially typical); patients lose weight. Characterized by shortness of breath, significant weakness, pain in the side, severe leukocytosis in the peripheral blood, increased ESR, and often lymphopenia. Pleural puncture reveals purulent exudate.

Tuberculous pleural empyema can be complicated by the formation of a bronchopleural or thoracic fistula.

When diagnosing tuberculous pleurisy, anamnesis data (presence of pulmonary tuberculosis or other localization in the patient or immediate family), detection of Mycobacterium tuberculosis in exudate, identification of extrapleural forms of tuberculosis, specific results of pleural biopsy and thoracoscopy data are of great importance. Characteristic features pleural tuberculosis during thoracoscopy are millet-like tubercles on the parietal pleura, extensive areas of caseosis, and a pronounced tendency to form pleural adhesions.

Parapneumonic exudative pleurisy

Bacterial pneumonia is complicated by exudative pleurisy in 40% of patients, viral and mycoplasma - in 20% of cases. Streptococcal and staphylococcal pneumonia are especially often complicated by the development of exudative pleurisy.

The main characteristic features of parapneumonic exudative pleurisy are:

• acute onset with severe chest pain (before the appearance of effusion), high body temperature;
• predominance of right-sided effusions;
• a significantly higher frequency of bilateral effusions compared to tuberculous exudative pleurisy;
• development of exudative pleurisy against the background of diagnosed pneumonia and a radiologically determined pneumonic focus in the lung parenchyma;
• high frequency purulent exudates with a large number of neutrophils, however, with early and adequate antibacterial therapy the exudate may be predominantly lymphocytic. In a number of patients, hemorrhagic exudate is possible, in isolated cases - eosinophilic or cholesterol effusion;
• significant leukocytosis in the peripheral blood and an increase in ESR by more than 50 mm h (more often than with other etiologies of pleurisy);
• rapid onset of a positive effect under the influence of adequate antibacterial therapy;
• detection of the pathogen in the effusion (by inoculating the exudate on certain nutrient media), the mycoplasma nature of exudative pleurisy is confirmed by an increase in the titers of antibodies to mycoplasma antigens in the blood.

Exudative pleurisy of fungal etiology

Pleural effusions of fungal etiology account for about 1% of all effusions. Fungal exudative pleurisy develops mainly in persons with a significant impairment of the immune system, as well as those receiving treatment with immunosuppressants, glucocorticoid drugs, and in patients suffering from diabetes mellitus.

Exudative pleurisy is caused by the following types of fungi: aspergillus, blastomycetes, coccidoides, cryptococci, histoplasma, actinomycetes.

Fungal exudative pleurisy is similar in course to tuberculosis. Typically, pleural effusion is combined with fungal infection of the lung parenchyma in the form focal pneumonia, infiltrative changes; abscesses and even decay cavities.

Pleural effusion in fungal exudative pleurisy is usually serous (serous-fibrinous) with a pronounced predominance of Lymphocytes and eosinophils. When a subcapsular abscess breaks into the pleural cavity, the effusion becomes purulent.

The diagnosis of fungal exudative pleurisy is verified by repeated detection of fungal micelles in pleural fluid, in sputum, also by repeated isolation of a fungal culture when inoculating exudate, pleural biopsy, sputum, pus from fistulas. According to K. S. Tyukhtin, S. D. Poletaev from exudate, fungal cultures are isolated from blastomycosis in 100% of patients, cryptococcosis - from 40-50%, coccidioidomycosis - from 20% of patients, and when pleural biopsy specimens are cultured - in almost all cases.

In addition, serological methods for studying blood serum and exudate are of great importance in the diagnosis of fungal exudative pleurisy - high titers of antibodies in the complement fixation reaction, agglutination-precipitation with antigens of certain fungi. Antibodies can also be detected using immunofluorescence and radioimmunological methods. Positive skin tests with the introduction of allergens of the corresponding fungus can have a certain diagnostic value.

Aspergillus pleurisy

Aspergillus exudative pleurisy most often develops in individuals with medical artificial pneumothorax (especially in the case of bronchopleural fistula formation) and in patients who have undergone lung resection. Pleural fluid may contain brown lumps in which aspergillus is found. The presence of calcium oxalate crystals in the effusion is also characteristic.

The diagnosis is confirmed by the identification of aspergillus in the pleural caustic culture when inoculated on special media, and the detection of anti-aspergillus in the pleural effusion using the radioimmunological method.

Blastomycosis pleurisy

Blastomycosis exudative pleurisy in its clinical picture resembles tuberculous pleurisy. Infiltrative changes are often observed in the lung parenchyma. Lymphocytes predominate in the exudate. Microscopic analysis can detect the typical yeast fungi Blastomyces dermatitidis; culture of pleural fluid for blastomycosis is always positive. Pleural biopsies reveal non-cheesy granulomas.

Coccidioidal pleurisy

Exudative pleurisy in coccidioidosis in 50% of cases is accompanied by infiltrative changes in the lungs, erythema nodosum or multiforme, and eosinophilia in the peripheral blood. Pleural effusion is an exudate, it contains many small lymphocytes and a high level of glucose is determined; eosinophilia of the effusion is not typical.

Pleural biopsy reveals caseous and noncaseating granulomas. Culture of pleural biopsies for coccidiosis gives a positive result in 100% of cases, and culture of effusion - only in 20% of cases. All patients had a positive skin test for Coccidioides immitis. After 6 weeks from the onset of the disease, antibodies are detected in a titer of 1:32 using the complement fixation reaction.

Cryptococcal pleurisy

Cryptococcusneotormans is ubiquitous and lives in soil, especially if it is contaminated with pig excrement. Exudative pleurisy of cryptococcal origin often develops in patients suffering from hematological malignancies, and is usually one-sided. In most patients, along with pleural effusion, damage to the lung parenchyma is detected in the form of interstitial infiltration or nodular formation. Pleural effusion is an exudate and contains many small lymphocytes. High levels of cryptococcal antigens are found in pleural fluid and serum. Cryptococcal genesis of pleurisy is confirmed positive result culture of pleural fluid and pleural or lung biopsies for cryptococci.

Histoplasmic pleurisy

Hystoplasma capsulatum is ubiquitous in soil and rarely causes pleural effusion. Typically, exudative pleurisy caused by histoplasma has a subacute course; at the same time, changes in the lungs are detected in the form of infiltrates or subpleural nodes.

Pleural effusion is an exudate and contains many lymphocytes. A pleural biopsy reveals a noncaseating granuloma. The diagnosis is verified by obtaining a histoplasma culture by inoculating pleural fluid, sputum, pleural biopsy, as well as by bacterioscopy of biopsy material. There may be high titers of antibodies to histoplasma in the blood of patients, which is determined by immunoelectophoresis.

Actinomycosis pleurisy

Actinomycetes are anaerobic or microaerophilic gram-positive bacteria that normally live in the oral cavity. Infection with actinomycetes usually occurs from infected gums, carious teeth, and tonsils of the patient himself. Actinomycosis is characterized by the formation of abscesses, the transition of the inflammatory process to chest wall with the formation of pleurothoracic fistulas. The formation of peripheral skin, subcutaneous and muscle abscesses is possible.

A characteristic feature of pleural exudate in actinomycosis is the presence of sulfur granules with a diameter of 1-2 mm - these are lumps of thin filaments of bacteria. The diagnosis of actinomycosis exudative pleurisy is established by identifying Actinomyces Israeli by inoculating pleural fluid on special media. You can also Gram stain smears of exudate and reveal thin, Gram-positive threads with long branches, which is characteristic of actinomycosis.

Most often, exudative pleurisy is observed with amoebiasis, echinococcosis, and paragonimiasis.

Amoebic pleurisy

The causative agent of amebiasis is Entamoeba histolytica. Amoebic exudative pleurisy occurs, as a rule, when an amoebic liver abscess breaks into the pleural cavity through the diaphragm. At the same time it appears sharp pain in the right hypochondrium and right half chest, shortness of breath, body temperature rises significantly, which is accompanied by chills. The patient develops purulent pleurisy. Pleural effusion is an exudate, has the characteristic appearance of “chocolate syrup” or “herring butter” and contains a large number of neutrophilic leukocytes, hepatocytes, as well as small solid insoluble particles of liver parenchyma. In 10% of patients, amoebas are found in the exudate. Using immunoradiological methods, high titers of antibodies to amoebas can be detected. Ultrasound and computed tomography of the liver can diagnose liver abscess.

Echinococcal pleurisy

Echinococcal exudative pleurisy develops when an echinococcal cyst of the liver, lung or spleen ruptures into the pleural cavity. Very rarely, a cyst develops primarily in the pleural cavity itself. At the moment of breakthrough, very sharp pain appears in the corresponding half of the chest, severe shortness of breath, and anaphylactic shock may develop in response to the arrival of echinococcal antigens. When a suppurating echinococcal cyst breaks into the pleural cavity, pleural empyema is formed.

A skin test with echinococcal antigen (Katsoni test) is positive in 75% of cases. Antibodies to echinococcal antigen are also detected in the blood using the complement fixation reaction (Weinberg test).

Paragonimiasis pleurisy

The development of exudative pleurisy is extremely characteristic of paragonimiasis. At the same time, many patients exhibit focal and infiltrative changes in the lungs. Characteristic features of paragonimimous exudative pleurisy are:

• long-term course with the formation of pronounced pleural adhesions;
• low content in the pleural exudate there is glucose and a high level of lactate dehydrogenase and IgE, and the IgE content is even higher than in the blood;
• severe eosinophilia of pleural fluid;
• detection of coated lung fluke eggs in pleural fluid, sputum, and feces;
• positive skin test with pulmonary fluke antigen;
• high titers of antibodies in the blood.

Endemic foci of infection are located in the Far East.

Pleurisy of tumor etiology

Among all pleural effusions, tumor effusions account for 15-20%. According to Light (1983), 75% of malignant pleural effusions are caused by lung cancer, breast cancer, and lymphoma. In the first place among all tumors causing the appearance of pleural effusion is lung cancer. According to N. S. Tyukhtin and S. D. Poletaev (1989), lung cancer (usually central) is diagnosed in 72% of patients with tumor pleurisy.

Second most common reason malignant exudative pleurisy - metastatic breast cancer, the third - malignant lymphoma, lymphogranulomatosis. In other cases we're talking about about pleural mesothelioma, ovarian and uterine cancer, cancer various departments gastrointestinal tract and tumors of other localizations.

The main mechanisms of formation of pleural effusion in malignant tumors are (Light, 1983):

• tumor metastases into the pleura and a significant increase in the permeability of its vessels;
• obstruction by lymphatic vessel metastases and sharp decline resorption of fluid from the pleural cavity;
• damage to the lymph nodes of the mediastinum and a decrease in the outflow of lymph from the pleura;
• obstruction of the thoracic lymphatic duct (development of chylothorax);
• the development of hypoproteinemia due to cancer intoxication and disruption of the protein-forming function of the liver.

Pleural effusion of a tumor nature has quite characteristic features:

• gradual development of effusion and other clinical symptoms (weakness, anorexia, weight loss, shortness of breath, cough with sputum, often mixed with blood);
• detection of a sufficiently large amount of fluid in the pleural cavity and its rapid accumulation after thoracentesis;
• detection using computed tomography or radiography (after preliminary removal of exudate from the pleural cavity) signs of bronchogenic cancer, enlarged mediastinal lymph nodes, metastatic lung disease;
• hemorrhagic nature of the effusion; with malignant lymphoma, chylothorax is often observed;
• pleural effusion meets all criteria for exudate and very often has low glucose levels (the lower the glucose level in the exudate, the worse the prognosis for the patient);
• detection of malignant cells in pleural effusion; it is advisable to analyze several samples of pleural fluid to obtain more reliable results;
• detection of carcinoembryonic antigen in the pleural fluid.

If there are no malignant cells in the pleural exudate and a tumor process is suspected, thoracoscopy with pleural biopsy and subsequent histological examination should be performed.

Pleurisy in malignant mesothelioma

Malignant mesothelioma is formed from the mesothelial cells lining the pleural cavity. People who work with asbestos for a long time are especially susceptible to the development of this tumor. The period between the development of the tumor and the time of onset of contact with asbestos ranges from 20 to 40 years.

The age of patients ranges from 40 to 70 years. Main clinical symptoms malignant mesothelioma are:

• gradually increasing pain of a constant nature in the chest without a clear connection with respiratory movements;
• paroxysmal dry cough, constantly increasing shortness of breath, weight loss;
• pleural effusion is the most common and early-onset sign of malignant mesothelioma;
• syndrome of compression of the superior vena cava by a growing tumor (swelling of the neck and face, dilatation of the veins in the neck and upper chest, shortness of breath); tumor growth into the pericardium and the walls of the heart cavities leads to the development of exudative pericarditis, heart failure, and cardiac arrhythmias;
• characteristic findings on computed tomography of the lungs are thickening of the pleura with an uneven, nodular internal border, especially at the base of the lung; in some cases, tumor nodes in the lungs are identified;
• features of pleural fluid: yellowish or serous-bloody color; has all the signs of exudate; decrease in glucose content and pH value; great content hyaluronic acid and the associated high viscosity of the liquid; a large number of lymphocytes and mesothelial cells in the exudate sediment; detection of malignant cells during multiple studies of exudate in 20-30% of patients.

To definitively verify the diagnosis, multiple biopsies should be performed. parietal pleura, thoracoscopy with biopsy and even diagnostic thoracotomy.

Pleurisy with Meigs syndrome

Meigs syndrome is ascites and pleural effusion in malignant tumors of the pelvic organs (ovarian, uterine cancer). With tumors of this location, significant ascites develops due to peritoneal carcinomatosis and ascitic fluid leaks through the diaphragm into the pleural cavity. Most often, pleural effusion is observed on the right, but bilateral localization is also possible. Pleural effusion can also be caused by tumor metastases to the pleura.

Pleural effusion in Meigs syndrome is an exudate, and malignant cells can be found in it.

Pleurisy in systemic connective tissue diseases

Most often, exudative pleurisy develops with systemic lupus erythematosus. Damage to the pleura in this disease is observed in 40-50% of patients. Exudative pleurisy is usually bilateral, the exudate is serous, contains a large number of lymphocytes, lupus cells and antinuclear antibodies are found in it. A characteristic feature of exudative pleurisy in systemic lupus erythematosus is high efficiency glucorticoid therapy. Pleural biopsy reveals chronic inflammation and fibrosis.

In rheumatism, exudative pleurisy is observed in 2-3% of patients; the effusion is a serous exudate and contains many lymphocytes. Typically, pleurisy develops against the background of other clinical manifestations of rheumatism, primarily rheumatic carditis, and responds well to treatment with nonsteroidal anti-inflammatory drugs. Needle biopsy reveals the picture chronic inflammation pleura and its fibrosis.

Exudative pleurisy with rheumatoid arthritis characterized by a chronic relapsing course, serous lymphocytic exudate, contains rheumatoid factor in high titers (

Exudative pleurisy can also develop with other systemic connective tissue diseases - scleroderma, dermatomyositis. To make an etiological diagnosis of exudative pleurisy, diagnostic criteria for these diseases are used and other causes of pleural effusion are excluded.

Pleurisy in acute pancreatitis

Pleural effusion in acute pancreatitis or severe exacerbation chronic pancreatitis observed in 20-30% of cases. The pathogenesis of this effusion is the penetration of pancreatic enzymes into the pleural cavity through the lymphatic vessels through the diaphragm.

Pleural effusion corresponds to the signs of exudate, serous or serous-hemorrhagic, rich in neutrophils and contains a large amount of amylase (more than in blood serum). Pancreatogenic effusion is often localized on the left and tends to be chronic.

Pleurisy with uremia

Exudative uremic pleurisy, as a rule, is combined with fibrinous or exudative pericarditis. The exudate is serous-fibrinous, sometimes hemorrhagic, and contains few cells, usually monocytes. The level of creatinine in the pleural fluid is increased, but it is lower than in the blood.

Drug-induced pleurisy

Pleural effusion may appear during treatment with hydralazine, procainamide, isoniazid, chlorpromazine, phenytoin, and sometimes when taking bromocriptine. Leads to the appearance of effusion long-term treatment these drugs. Usually there is also drug-induced lung damage.

Empyema of the pleura

Pleural empyema (purulent pleurisy) is an accumulation of pus in the pleural cavity. Pleural empyema can complicate the course of pneumonia (especially streptococcal), spontaneous pneumothorax in penetrating chest wounds, pulmonary tuberculosis, and can also develop in connection with the transition purulent process With neighboring organs(in particular, when a lung abscess ruptures)

Pleural empyema is characterized by the following clinical and laboratory features:

• intense chest pain and shortness of breath appear;
• body temperature rises to 39-40°C, stunning chills and profuse sweating appear;
• swelling of the chest tissue on the affected side occurs;
• there are pronounced symptoms of intoxication, pain, general weakness, anorexia, myalgia, arthralgia;
• peripheral blood analysis is characterized by significant leukocytosis, shift leukocyte formula left, sharp increase ESR, toxic granularity of neutrophils;
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Chylothorax

Chylothorax is a chylous pleural effusion, i.e. accumulation of lymph in the pleural cavity. The main causes of chylothorax are damage to the thoracic lymphatic duct (during operations on the esophagus, aorta and trauma), as well as blockage of the lymphatic system and mediastinal veins by a tumor (most often lymphosarcoma). The development of chylothorax is also extremely characteristic of lymphangioleiomyomatosis.

Often the cause of chylothorax cannot be determined. This type of chylothorax is called idiopathic. According to Light (1983), idiopathic chylothorax in adults is most often the result of minor trauma to the thoracic lymphatic duct (during coughing, hiccups) that occurs after ingesting fatty foods. In rare cases, chylothorax develops with cirrhosis of the liver and heart failure.

The clinical manifestations of chylothorax are fully consistent with the symptoms of pleural effusion: patients complain of progressive shortness of breath and heaviness in the area of ​​the corresponding half of the chest. An acute onset of the disease is characteristic. Unlike pleural effusions of other nature, chylothorax, as a rule, is not accompanied by chest pain and fever, since the lymph does not irritate the pleura.

An objective examination of the patient reveals signs of pleural effusion, which is confirmed by x-ray examination.

The diagnosis of chylothorax is verified using pleural puncture. Chylothorax is characterized by the following properties of pleural fluid:

• the color is milky white, the liquid is not transparent, cloudy, odorless;
• contains a large amount of neutral fat (triglycerides) and fatty acids, as well as chylomicrons. It is generally accepted that chylothorax is characterized by a triglyceride content greater than PO mg%. If the triglyceride level is less than 50 mg%, then the patient does not have chylothorax. If the triglyceride content is between 50 and 110 mg%, it is necessary to determine lipoproteins in the pleural fluid using disc electrophoresis in polyacrylamide gel. If chylomicrons are found in the pleural fluid, then this is chylothorax.

Chylothorax is also characterized by the detection of a large number of drops of neutral fat (triglycerides) during microscopy of smears of chylous fluid after staining with Sudan.

With the long-term existence of chylothorax, especially when a large amount of lymph accumulates in the pleural cavity, it is necessary to frequently perform pleural punctures due to compression of the lung and displacement of the mediastinum. This leads to the loss of a large amount of lymph and exhaustion of the patient. This is due to the fact that about 2500-2700 ml of fluid containing large amounts of protein, fats, electrolytes and lymphocytes flows through the thoracic lymph duct every day. Naturally, frequent removal of lymph from the pleural cavity leads to a drop in the patient’s body weight and a violation of the immunological status.

As a rule, patients with pseudochylothorax experience thickening and often calcification of the pleura as a result long stay effusion in the pleural cavity. The lifespan of pleural effusion can range from 3 to 5 years, sometimes even longer. It is assumed that cholesterol is formed in the pleural fluid as a result degenerative changes erythrocytes and leukocytes. Pathological changes in the pleura itself disrupt the transport of cholesterol, which leads to its accumulation in the pleural fluid.

The clinical picture of pseudochylothorax is characterized by the presence of the physical and radiological symptoms of pleural effusion described above. The diagnosis is finally established using pleural puncture and analysis of the obtained pleural fluid. It is necessary to carry out differential diagnosis between chylous and pseudochylous effusion.

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