Exudate happens. Exudation and exudates

Exudation is the exit of the liquid part of the blood through the vascular wall into the inflamed tissue. The liquid leaving the vessels - exudate - impregnates the inflamed tissue or accumulates in the cavities (pleural, peritoneal, pericardial, etc.).

Depending on the characteristics of the cellular and biochemical composition, the following types of exudate are distinguished:

1. Serous exudate, almost transparent, is characterized by a moderate protein content (3-5%, mainly albumins), low specific gravity (1015-1020), pH in the range of 6-7. The sediment contains single segmented nuclear granulocytes and desquamated cells of the serous membranes.

Serous exudate is formed with inflammation of the serous membranes (serous pleurisy, pericarditis, peritonitis, etc.), as well as with burn, viral or allergic inflammation. Serous exudate is easily absorbed and leaves no traces or forms a slight thickening of the serous membranes.

2. Fibrinous exudate is characterized by a high content of fibrinogen, which, upon contact with damaged tissues, passes into fibrin, as a result of which the exudate thickens. Fibrin falls on the surface of the serous membranes in the form of villous masses, and on the surface of the mucous membranes - in the form of films. In connection with these features, fibrinous inflammation is divided into diphtheritic (tightly sitting films) and croupous (loosely sitting films). Croupous inflammation develops in the stomach, intestines, bronchi, trachea. Diphtheritic inflammation is characteristic of the esophagus, tonsils, and oral cavity. Fibrinous inflammation can be caused by pathogens of dysentery, tuberculosis, diphtheria, viruses, toxins of endogenous (eg, with uremia) or exogenous (sublimate poisoning) origin.

The prognosis of fibrinous inflammation is largely determined by the localization and depth of the process.

On the serous membranes, fibrin masses partially undergo autolysis, and most of them are organized, that is, they grow into connective tissue, and therefore adhesions and scars can form that disrupt the function of the organ.

On the mucous membranes, fibrinous films undergo autolysis and are rejected, leaving a defect in the mucous membrane - an ulcer, the depth of which is determined by the depth of fibrin precipitation. Healing of ulcers can occur quickly, but in some cases (in the large intestine with dysentery) it is delayed for a long time.

3. Purulent exudate is a turbid inflammatory liquid of a greenish hue, viscous, containing albumins, globulins, fibrin filaments, enzymes, tissue proteolysis products and a large number of polymorphonuclear leukocytes, mostly destroyed (purulent bodies).

Purulent inflammation can occur in any tissue, organ, serous cavities, skin and proceed as an abscess or phlegmon. The accumulation of purulent exudate in the body cavities is called empyema.

The etiological factors of purulent inflammation are diverse, it can be caused by staphylococci, streptococci, meningococci, gonococci, mycobacteria, pathogenic fungi, etc.

5. Putrefactive exudate (ichorous) develops with the participation of pathogenic anaerobes in the inflammatory process. Inflamed tissues undergo putrefactive decomposition with the formation of foul-smelling gases and a dirty green exudate.

6. Hemorrhagic exudate is characterized by the content of a different number of erythrocytes, as a result of which it acquires a pinkish or red color.

Any type of exudate can take on a hemorrhagic character, it depends on the degree of permeability of the vessels involved in the inflammatory process. Exudate mixed with blood is formed during inflammation caused by highly virulent microorganisms - the causative agents of plague, anthrax, smallpox, toxic influenza. Hemorrhagic exudate is also observed in allergic inflammation, in malignant neoplasms.

7. Mixed forms of exudate - serous-fibrinous, serous-purulent, serous-hemorrhagic, purulent-fibrinous and others - occur when a secondary infection is attached, with a decrease in the body's defenses or the progression of a malignant tumor.

With inflammation of the mucous membranes, an exudate is formed with a high content of mucus, leukocytes, lymphocytes and desquamated epithelial cells. Such an exudate, as it were, flows down the mucous membrane, therefore inflammation is called catarrhal (katarrheo - flow down). These are catarrhal rhinitis, gastritis, rhinosinusitis, enterocolitis. By the nature of the exudate, they speak of serous, mucous or purulent catarrhs. Usually inflammation of the mucosa begins with serous catarrh, which then becomes mucous and purulent.

Exudation is one of the signs of venous hyperemia and at the same time determines the nature of tissue changes in the focus of inflammation.

The leading factor in exudation is an increase in vascular permeability in the area of inflammation. The increase in vascular permeability occurs in two phases. The first phase is early, immediate, develops after the action of the altering agent and reaches a maximum within a few minutes. This phase is due to the action of histamine, leukotriene E4, serotonin, bradykinin on venules with a diameter of not more than 100 microns. The permeability of capillaries remains virtually unchanged. An increase in permeability in the territory of venules is associated with a contraction of vascular endotheliocytes, rounding of cells, and the formation of interendothelial gaps through which the liquid part of blood and cells exits. The second phase is late, slowed down, develops gradually over several hours, days and sometimes lasts up to 100 hours. This phase is characterized by a persistent increase in vascular permeability (arterioles, capillaries, venules) caused by damage to the vascular wall by lysosomal enzymes, active oxygen metabolites, prostaglandins, leukotriene complex (MPC), hydrogen ions.

In the mechanisms of development of exudation, in addition to increasing vascular permeability, a certain role belongs to pinocytosis - the process of active capture and passage through the endothelial wall of the smallest droplets of blood plasma. In this regard, exudation can be considered as a kind of microsecretory process provided by active transport mechanisms. Activation of pinocytosis in the endothelium of microvessels in the focus of inflammation precedes an increase in the permeability of the vascular wall due to the reduction of endotheliocytes.

Of great importance in the development of exudation belongs to osmotic and oncotic factors.

In the tissues of the focus of inflammation, osmotic pressure increases, while the osmotic pressure of the blood remains practically unchanged. Hyper-osmia of tissues is due to an increase in the concentration of osmo-active particles in them - ions, salts, organic compounds with a low molecular weight. Factors causing hyperosmia include increased dissociation of salts due to tissue acidosis (lactic acidosis type A), release of potassium and its accompanying macromolecular anions from cells, increased breakdown of complex organic compounds into less complex, finely dispersed ones, as well as compression and thrombosis. lymphatic vessels that prevent the removal of resins from the focus of inflammation.

Simultaneously with an increase in osmotic pressure, an increase in oncotic pressure is also observed in the tissues of the focus of inflammation, while oncotic pressure in the blood decreases. The latter is due to the release from vessels into tissues, first of all, of finely dispersed proteins - albumins, and as the permeability of the vessel increases - globulins and fibrinogen (Serov V.V., Paukov V.S., 1995).

In addition, in the tissue itself, under the influence of lysosomal proteases, the breakdown of complex protein macromolecules occurs, which also contributes to an increase in oncotic pressure in the tissues of the inflammation focus.

The factor contributing to exudation is an increase in hydrostatic pressure in the microvasculature and the filtration area of the liquid part of the blood.

The biological meaning of exudation as a component of inflammation lies in the fact that together with the exudate, immunoglobulins, active complement components, plasma enzymes, kinins, biologically active substances are released into the altered tissue, which are released by activated blood cells. Entering the focus of inflammation, they, together with tissue mediators, provide opsonization of the pathogenic agent, stimulate phagocytic cells, participate in the processes of killing and lysis of microorganisms, provide wound cleansing and subsequent tissue repair. In the exudate, metabolic products, toxins, toxic pathogenicity factors that have come out of the blood stream, i.e., are found. the focus of the focus of inflammation performs a drainage function. Due to the exudate, the blood flow first slows down in the focus of inflammation, and then the blood flow completely stops when the capillaries, venules and lymphatic vessels are compressed. The latter leads to the localization of the process and prevents the dissemination of infection and the development of a septic state.

At the same time, the accumulation of exudate can lead to the development of severe pain due to compression of nerve endings and conductors. As a result of compression of parenchymal cells and disturbances in their microcirculation, disorders of the functions of various organs may occur. When exudate is organized, adhesions can form, causing displacement, deformation and pathology of the functions of various structures. In some cases, the course of the inflammatory process is complicated by the flow of exudate into the alveoli, into the body cavity and leads to the development of pulmonary edema, pleurisy, peritonitis, pericarditis.

Serous exudate can be observed with streptococcal, staphylococcal infections, tuberculosis, syphilis and rheumatism. Serous exudate is light yellow, transparent, contains about 3% protein. Serous-fibrinous exudate differs from serous exudate by the presence of fibrin bundles.

For serous exudate of streptococcal and staphylococcal origin the presence of neutrophilic granulocytes is characteristic in the complete absence or presence of single lymphocytes and mesotheliocytes.

With serous tuberculous pleurisy Mycobacterium tuberculosis does not penetrate into the pleural cavity, there are no tuberculomas on the pleura. In this case, the exudate contains a different number of lymphocytes, mesotheliocytes, fibrin; Mycobacterium tuberculosis is not detected.

With tuberculous pleurisy with tuberculomas on the pleura in the exudate, their elements are detected (epithelioid and giant cells of Pirogov-Langhans against the background of lymphoid elements) or elements of cheesy decay, neutrophilic granulocytes and Mycobacterium tuberculosis.

With tuberculous or syphilitic exudative pleurisy lymphocytes predominate in the exudate not in all periods of the disease. So, with tuberculous pleurisy in the first ten days of illness, the exudate contains up to 50-60% of neutrophilic granulocytes, 10-20% of lymphocytes and many mesotheliocytes.

As the disease progresses, the number of lymphocytes increases, while the number of neutrophilic granulocytes and mesotheliocytes decreases. The long-term predominance of neutrophilic granulocytes is a poor prognostic sign; it may indicate the transition of serous tuberculous pleurisy to tuberculous empyema. In tuberculous pleurisy, neutrophilic granulocytes of the exudate do not phagocytize Mycobacterium tuberculosis, while in pleurisy caused by pyogenic flora, phagocytosis of neutrophilic granulocytes is often observed.

With tuberculosis degeneratively altered neutrophilic granulocytes with wrinkled, fragmented and rounded nuclei appear in the exudate. Such cells are difficult to distinguish from true lymphocytes. In addition, tuberculous exudate always contains erythrocytes, sometimes there are so many of them that the exudate is hemorrhagic in nature.

Tuberculosis is characterized by a pronounced leukolysis, primarily of neutrophilic granulocytes. The predominance of lymphocytes in the exudate may be due to their greater persistence. Not always a large number of lymphocytes in the exudate coincides with lymphocytosis. In some cases, with tuberculosis, an increase in the number of eosinophilic granulocytes in the exudate and in the blood is pronounced. It is also possible that they are absent in both effusion and blood.

With a protracted form of tuberculous pleurisy plasma cells are found in the exudate. A diverse cellular composition of the serous fluid in tuberculosis can be observed only at the beginning of the disease, and during the peak of the disease, as a rule, lymphocytes predominate.

Eosinophilic exudate

With exudative pleurisy, the number of eosinophilic granulocytes in the serous fluid sometimes reaches 97% of the cellular composition. Eosinophilic exudate can be observed with tuberculosis and other infections, abscesses, injuries, multiple cancer metastases to the lungs, migration of ascaris larvae to the lungs, etc.

The nature of eosinophilic exudate is:

serous;
hemorrhagic;
purulent.

An increase in the number of eosinophilic granulocytes in the exudate can be combined with an increase in their content in the blood and bone marrow, or is observed with a normal amount of eosinophilic granulocytes in the blood.

Purulent exudate

Purulent exudate by origin and clinical manifestations is different. Most often, purulent exudate develops secondarily (the lungs or other organs are primarily affected), but it can also be primary in inflammatory processes in serous cavities caused by various pyogenic microorganisms.

Exudate may be transitional from serous to purulent. With repeated punctures, stages of the development of the process can be observed: first, the exudate becomes serous-fibrinous or serous-purulent, and then purulent. At the same time, it becomes cloudy, thickens, acquires a greenish-yellow, sometimes brownish or chocolate color (due to the admixture of blood).

Enlightenment of the exudate with repeated punctures and a decrease in the number of cells in it indicates a favorable course.

If the exudate from the serous transparent becomes purulent, cloudy, and the number of neutrophilic granulocytes in it increases, this indicates the progression of the process. There is no decay of neutrophilic granulocytes at the beginning of the inflammatory process, they are functionally complete, actively phagocytize: bacteria are visible in their cytoplasm.

As the process grows, degenerative changes in neutrophilic granulocytes appear in the form of toxogenic granularity, hypersegmentation of the nuclei; the number of stab neutrophilic granulocytes increases. Usually a large number of neutrophilic granulocytes in the exudate is accompanied by leukocytosis with the appearance of other forms in the peripheral blood.

Subsequently, neutrophilic granulocytes disintegrate, while bacteria are detected intra- and extracellularly. With a favorable course of the disease and recovery, degenerative changes in neutrophilic granulocytes are weakly expressed, their number decreases, there is no decay, a significant number of histiocytes, mesotheliocytes, monocytes, and macrophages are found.

Putrid exudate

Putrid exudate of brown or greenish color, with a sharp putrid odor. Microscopic examination reveals detritus as a result of the breakdown of leukocytes, needles of fatty acids, and sometimes crystals of hematoidin and cholesterol. There are many microorganisms in the exudate, in particular anaerobes that form gases.

Hemorrhagic exudate

Hemorrhagic exudate appears with mesothelioma, cancer metastases, hemorrhagic diathesis with associated infection, chest injuries. The spilled blood is diluted with serous exudate and remains liquid.

For sterile hemothorax characterized by the presence of a transparent reddish effusion. The protein part of the plasma coagulates, and fibrin is deposited on the pleura. In the future, the organization of fibrin leads to the formation of adhesions. In the absence of complications, the reverse development of pleurisy occurs quickly.

For mild infection pleural fluid from hemorrhagic can go into serous-hemorrhagic or serous.

With complication of pyogenic infection serous-hemorrhagic exudate turns into purulent-hemorrhagic. The admixture of pus in the exudate is detected using Petrov's samples, which is as follows. Hemorrhagic exudate(1 ml) diluted in a test tube five to six times with distilled water. If there is only an admixture of blood in the exudate, then the erythrocytes are hemolyzed by water and it becomes transparent; if there is pus in the exudate, it remains cloudy.

Microscopic examination of the exudate look at the erythrocytes. If the bleeding has stopped, only old forms of erythrocytes with various signs of their death (microforms, "mulberries", shadows of erythrocytes, poikilocytes, schizocytes, vacuolized, etc.) can be detected in it. The appearance of fresh, unchanged erythrocytes against the background of old forms indicates re-bleeding. With prolonged bleeding into the pleural cavity, altered and unchanged erythrocytes are observed in the exudate. Thus, an erythrocytogram allows you to determine the nature of bleeding (fresh or old, repeated or ongoing).

For non-infectious hemothorax in the exudate, unchanged segmented neutrophilic and eosinophilic granulocytes can be detected. Their distinctive features in the period of suppuration are pronounced signs of degeneration and decay. The severity of these changes depends on the timing of bleeding and the degree of suppuration.

In the first days after bleeding, karyorrhexis and karyolysis are noted, as a result of which neutrophilic granulocytes become lymphocyte-like and can be mistaken for them.

Lymphocytes and monocytes more persistent and almost do not change in the exudate. In the period of resorption, macrophages, mesotheliocytes and plasma cells are found in the pleural fluid. In the period of exudate resorption, eosinophilic granulocytes appear in it (from 20 to 80%). This allergic reaction is a sign of a favorable outcome of the disease.

With the addition of a pyogenic infection exudate cytogram is characterized by an increase in the number of neutrophilic granulocytes with an increase in signs of degeneration and decay in them.

Cholesterol exudate

Cholesterol exudate is a long-term (sometimes several years) encysted effusion into the serous cavity. Under certain conditions (reabsorption of water and some mineral components of the exudate from the serous cavity, as well as in the absence of fluid inflow into a closed cavity), exudate of any etiology can acquire the character of cholesterol. In such an exudate, enzymes that destroy cholesterol are absent or contained in small quantities.

Cholesterol exudate is a thick yellowish or brownish liquid with a pearly tint. An admixture of disintegrated erythrocytes can give the effusion a chocolate tint. On the walls of a test tube moistened with exudate, macroscopically visible are casts of cholesterol crystals in the form of tiny sparkles. In addition to cholesterol crystals, cholesterol exudate reveals fat-degenerate cells, cellular decay products, and fat drops.

Chylous, chyle-like and pseudo-chylous (milky) exudate

Common to these types of exudate is the resemblance to diluted milk.

Chylous exudate due to the ingress of lymph into the serous cavity from the destroyed large lymphatic vessels or the thoracic lymphatic duct. The lymphatic vessel can be destroyed by trauma, tumor invasion, abscess, or other causes.

The milky appearance of the liquid is due to the presence of drops of fat in it, which is stained red with Sudan III and black with osmic acid. When standing in the exudate, a creamy layer is formed, floating up, and cellular elements (erythrocytes, leukocytes, among which there are many lymphocytes, mesotheliocytes, and in the presence of neoplasms, tumor cells) settle to the bottom of the tube. If you add one or two drops of caustic alkali with ether to the exudate and shake the test tube, the liquid becomes clear.

Chylus-like exudate appears as a result of abundant breakdown of cells with fatty degeneration. In these cases, there is a history of purulent pleurisy, and puncture reveals a coarse thickening of the walls of the pleural cavity. A chyle-like exudate occurs in atrophic cirrhosis of the liver, malignant neoplasms, etc. Microscopic examination reveals an abundance of fatty degenerate cells, fatty detritus and fat drops of various sizes. Microflora is absent.

Pseudo-chylous exudate macroscopically it also resembles milk, but the particles suspended in it are probably not fatty, since they do not stain with sudan III and osmic acid and do not dissolve during heating. Microscopic examination occasionally reveals mesotheliocytes and fat droplets. Pseudo-chylous exudate is observed in lipoid and lipoid-amyloid degeneration of the kidneys.

Contents of cysts

Cysts can occur in various organs and tissues (ovaries, kidneys, brain, etc.). The nature of the contents of the cyst even one organ, such as the ovary, can be different (serous, purulent, hemorrhagic, etc.) and, in turn, determines its transparency and color (colorless, yellowish, bloody, etc.).

Microscopic examination usually reveals blood cells (erythrocytes, leukocytes), epithelium lining the cyst (often in a state of fatty degeneration). There may be crystals of cholesterol, hematoidin, fatty acids. In the colloid cyst, a colloid is found, in the dermoid - flat epitheliocytes, hair, crystals of fatty acids, cholesterol, hematoidin.

Echinococcal cyst (bladder) contains a transparent liquid with a low relative density (1.006-1.015), which contains glucose, sodium chloride, succinic acid and its salts. The protein is detected only when an inflammatory process develops in the cyst. To detect succinic acid, the liquid of the echinococcal bladder is evaporated in a porcelain cup to the consistency of syrup, acidified with hydrochloric acid and extracted with ether mixed equally with alcohol. Then the ethereal extract is poured into another cup. The ether is removed by heating in a water bath. In this case, succinic acid crystallizes in the form of hexagonal tables or prisms. The formed crystals are examined under a microscope. If the liquid contains protein, then it is removed by boiling, adding 1-2 drops of hydrochloric acid. The reaction for succinic acid is carried out with a clear filtrate.

Cytological diagnosis of echinococcosis it is possible only at the stage of an open cyst with a spontaneous outpouring of its contents into organs that communicate with the external environment (most often with a breakthrough of the echinococcal bladder into the bronchus). In this case, microscopic examination of sputum from the bronchus reveals characteristic hooks of echinococcus and fragments of a parallel striated chitinous membrane of the bladder. You can also find a scolex - a head with two rims of hooks and four suckers. In addition, fat degenerated cells and cholesterol crystals can be detected in the test material.

Depending on the causes of inflammation and the development of the inflammatory process, the following types of exudates are distinguished:

serous,

fibrinous,

hemorrhagic.

Accordingly, serous, fibrinous, purulent and hemorrhagic inflammation is observed. There are also combined types of inflammation: gray-fibrinous, fibrinous-purulent, purulent-hemorrhagic. Any exudate after its infection with putrefactive microbes is called putrefactive. Therefore, the allocation of such exudate to an independent rubric is hardly advisable. Exudates containing a large number of fatty droplets (chyle) are called chylous, or chyloid. It should be noted that the entry of fat droplets is possible in the exudate of any of the above types. It can be caused by the localization of the inflammatory process in the places of accumulation of large lymphatic vessels in the abdominal cavity and other side effects. Therefore, it is also hardly advisable to single out the chylous type of exudate as an independent one. An example of a serous exudate during inflammation is the contents of a bladder from a burn on the skin (burn of the II degree).

An example of fibrinous exudate or inflammation is fibrinous deposits in the pharynx or larynx in diphtheria. Fibrinous exudate is formed in the large intestine with dysentery, in the alveoli of the lungs with lobar inflammation.

Serous exudate. Its properties and formation mechanisms are given in § 126 and Table. 16.

fibrinous exudate. A feature of the chemical composition of fibrinous exudate is the release of fibrinogen and its loss in the form of fibrin in the inflamed tissue. Subsequently, the precipitated fibrin dissolves due to the activation of fibrinolytic processes. Sources of fibrinolysin (plasmin) are both blood plasma and the inflamed tissue itself. An increase in the fibrinolytic activity of blood plasma during fibrinolysis in lobar pneumonia, for example, is easy to see by determining this activity in the exudate of an artificial blister created on the patient's skin. Thus, the process of development of fibrinous exudate in the lung is, as it were, reflected in any other place in the patient's body, where an inflammatory process occurs in one form or another.

Hemorrhagic exudate It is formed during a rapidly developing inflammation with severe damage to the vascular wall, when erythrocytes enter the inflamed tissue. Hemorrhagic exudate is observed in smallpox pustules with the so-called black pox. It occurs with anthrax carbuncle, with allergic inflammation (Arthus phenomenon) and other acutely developing and rapidly occurring inflammatory processes.

Purulent exudate and purulent inflammation are caused by pyogenic microbes (strepto-staphylococci and other pathogenic microbes).

During the development of purulent inflammation, purulent exudate enters the inflamed tissue and leukocytes impregnate, infiltrate it, located in large numbers around the blood vessels and between the own cells of the inflamed tissues. The inflamed tissue at this time is usually dense to the touch. Clinicians define this stage of development of purulent inflammation as the stage of purulent infiltration.

The source of enzymes that cause the destruction (melting) of the inflamed tissue are leukocytes and cells damaged during the inflammatory process. Particularly rich in hydrolytic enzymes are granular leukocytes (neutrophils). Neutrophil granules contain proteases, cathepsin, chymotrypsin, alkaline phosphatase and other enzymes. With the destruction of leukocytes, their granules (lysosomes), enzymes enter the tissue and cause the destruction of its protein, protein-lipoid and other components.

Under the influence of enzymes, the inflamed tissue becomes soft, and clinicians define this stage as the stage of purulent fusion, or purulent softening. A typical and well-marked expression of these stages of development of purulent inflammation is inflammation of the hair follicle of the skin (furuncle) or the fusion of many boils into one inflammatory focus - carbuncle and acute diffuse purulent inflammation of the subcutaneous tissue - phlegmon. Purulent inflammation is not considered complete, “ripened” until purulent tissue fusion occurs. As a result of purulent fusion of tissues, a product of this fusion is formed - pus.

Pus It is usually a thick, creamy, yellow-green liquid with a sweetish taste and a specific odor. When centrifuged, the pus is divided into two parts:

sediment composed of cellular elements,

liquid part - purulent serum. When standing, the purulent serum sometimes coagulates.

The pus cells are called purulent bodies. They are blood leukocytes (neutrophils, lymphocytes, monocytes) in various stages of damage and decay. Damage to the protoplasm of purulent bodies is noticeable in the form of the appearance of a large number of vacuoles in them, violation of the contours of the protoplasm and erasure of the boundaries between the purulent body and its environment. With special stains in purulent bodies, a large amount of glycogen and fat droplets are found. The appearance of free glycogen and fat in purulent bodies is a consequence of a violation of complex polysaccharide and protein-lipoid compounds in the protoplasm of leukocytes. The nuclei of purulent bodies become denser (pycnosis) and fall apart (karyorrhexis). There are also phenomena of swelling and gradual dissolution of the nucleus or its parts in a purulent body (karyolysis). The disintegration of the nuclei of purulent bodies causes a significant increase in the amount of nucleoproteins and nucleic acids in the purulent.

Purulent serum does not differ significantly in composition from blood plasma (Table 17).

Table 17

Components	Serum of pus	blood plasma

Solids

Fats and lipoids with cholesterol
inorganic salts

The sugar content in exudates in general and in purulent exudates in particular is usually lower than in the blood (0.5-0.6 g/l), due to intensive glycolysis processes. Accordingly, there is much more lactic acid in the purulent exudate (0.9-1.2 g / l and above). Intensive proteolytic processes in the purulent focus cause an increase in the content of polypeptides and amino acids.

- inflammatory reaction of the pleura, proceeding with the accumulation of serous exudate in the pleural cavity. Symptoms of serous pleurisy are characterized by dull pain in the chest, dry cough, shortness of breath, cyanosis, tachycardia, signs of intoxication. Diagnosis of serous pleurisy is based on an assessment of the history, physical examination, thoracocentesis, laboratory examination of pleural effusion, ultrasound, radiography, pleuroscopy. Treatment of serous pleurisy includes etiotropic and symptomatic therapy, therapeutic pleural punctures, drainage of the pleural cavity, physiotherapy, exercise therapy, and massage.

ICD-10

J90 Pleural effusion, not elsewhere classified

General information

Serous pleurisy, along with hemorrhagic and purulent pleurisy (pleural empyema), is a type of exudative pleurisy. The stage of serous effusion usually serves as a continuation of fibrinous (dry) pleurisy. Serous pleurisy in pulmonology is differentiated by etiology (infectious and aseptic), by course (acute, subacute and chronic), by the nature of distribution (diffuse and encysted). Infectious serous pleurisy among themselves are divided according to the type of causative agent of the inflammatory process (viral, pneumococcal, tuberculosis, etc.), aseptic - according to the type of underlying pathology (carcinomatous, rheumatic, traumatic, etc.).

Causes of serous pleurisy

Aseptic serous pleurisy may be due to malignant tumors of the lungs and pleura (pleural mesothelioma, lung cancer) or metastases of tumors of other organs; diffuse connective tissue diseases (rheumatism, rheumatoid arthritis, systemic lupus erythematosus); myocardial infarction, pulmonary infarction, pulmonary embolism, uremia, leukemia and other pathological processes.

The development of serous pleurisy may be the result of injuries and surgical interventions on the chest, taking certain medications (bromocriptine, nitrofurantoin). The provoking factors of serous pleurisy are frequent hypothermia, malnutrition, physical inactivity, overwork, stress, drug hypersensitization, a decrease in general and local reactivity.

Pathogenesis

Serous pleurisy is caused by a pathological protective reaction of the sensitized pleura to infectious-toxic irritation, which is expressed in excessive exudation and reduced absorption of fluid in the pleural cavity. The development of exudative inflammation in serous pleurisy is associated with an increase in the permeability of the blood and lymphatic capillaries of the lungs and pleura. Serous exudate is a clear yellowish liquid consisting of plasma and a small number of blood cells. Most often, a cloudy yellow serous effusion with fibrin flakes, an accumulation of lymphocytes, polymorphonuclear leukocytes, macrophages, mesothelial cells, and eosinophils is noted in the pleural cavity.

Infectious agents can penetrate into the pleural cavity from the primary foci by contact, lymphogenous or hematogenous routes and have a direct effect on the pleura or cause its sensitization with toxins and metabolic products. At the same time, the production of specific antibodies and biologically active substances is accompanied by local microcirculation disorders, damage to the vascular endothelium and the formation of exudate. The accumulation of serous exudate in the pleural cavity is observed in the acute stage of pleurisy, then the effusion can completely resolve, leaving fibrinous deposits (moorings) on the surface of the pleura that contribute to the development of pleurosclerosis. With pleurisy, a further change in the serous nature of the exudate towards purulent or putrefactive is possible.

Symptoms of serous pleurisy

Symptoms of serous pleurisy can complement the clinical manifestations of the underlying disease (pneumonia, tuberculosis, lung cancer, systemic vasculitis, etc.) or dominate over them. The initial stage of serous pleurisy is characterized by intense dull pain in the chest on the affected side, aggravated by inhalation; shallow, rapid breathing; dry cough, asymmetry of respiratory movements of the chest, pleural rub. With the accumulation of exudate in the pleural cavity, the pain gradually subsides, although it may persist, for example, with carcinomatous serous pleurisy. In some cases, polyserositis (pericarditis, pleurisy, and ascites) may develop.

There is heaviness in the side, shortness of breath begins to progress rapidly; with a large amount of effusion, cyanosis develops, tachycardia, swelling of the cervical veins, and sometimes swelling of the intercostal spaces. A patient with serous pleurisy is characterized by a forced position on the affected side. Increased pain during the recovery period may be associated with resorption of the serous fluid and contact of the pleural sheets or with suppuration of the exudate and the development of purulent pleurisy.

With serous pleurisy, there is an increase in intoxication, general weakness, an increase in body temperature to subfebrile, sweating, decreased appetite and disability. The severity of the general condition of a patient with serous pleurisy depends on the severity of intoxication and the rate of accumulation of free effusion. Serous pleurisy of tuberculous etiology is usually manifested by a more pronounced temperature reaction and intoxication.

Diagnostics

For the diagnosis of serous pleurisy, a comprehensive examination is carried out with an assessment of the anamnesis, symptoms, and the results of various laboratory and instrumental studies. In the diagnosis of serous pleurisy, information about the patient's pathology is important: trauma, surgery, pneumonia, tuberculosis, rheumatism, tumors of various localization, allergies, etc. Physical examination reveals an increase in the volume of the chest on the side of the lesion, swelling of the intercostal spaces and swelling of the skin; limitation of respiratory excursion, characteristic of serous pleurisy. Percussion, with the accumulation of pleural fluid in a volume of at least 300-500 ml, a massive dullness of sound is detected, breathing over the zone of dullness is significantly weakened.

In case of serous pleurisy, ultrasound of the pleural cavity is performed, if a background pathology is suspected, an additional examination is used (ECG, hepatography, measurement of venous pressure, tuberculin tests, determination of serum enzymes and protein-sedimentary samples, and other tests). Differential diagnosis is necessary to distinguish between serous pleurisy and lung atelectasis, focal pneumonia, circulatory disorders accompanied by the formation of transudate (with pericarditis, heart disease, liver cirrhosis, nephrotic syndrome).

Treatment of serous pleurisy

In the treatment of serous pleurisy, it is necessary to take into account the general condition of the patient, the presence of an underlying underlying disease. Treatment of serous pleurisy is carried out in a hospital with the appointment of bed rest, a diet with fluid and salt restriction, and complex pathogenetic therapy.

After establishing the cause of serous pleurisy, additional etiotropic treatment may include tuberculostatic agents - with the specific nature of the disease; sulfonamides and broad-spectrum antibiotics - for nonspecific pneumonic pleurisy. With a significant accumulation of pleural exudate, causing respiratory and circulatory disorders, and also because of the threat of empyema, pleural puncture or drainage of the pleural cavity with fluid evacuation is carried out as an emergency. Then antibiotics can be injected into the cavity, and in case of serous pleurisy caused by pleural cancer, antitumor drugs.

Anti-inflammatory and hyposensitizing agents, glucocorticosteroids are shown. Symptomatic therapy of serous pleurisy includes cardiotonic and diuretic drugs. In the absence of contraindications, after resorption of the exudate, physiotherapy (ultrasound and electrophoresis with calcium chloride), active breathing exercises, and massage are prescribed to prevent pleural adhesions in serous pleurisy. With a persistent course of serous pleurisy, its surgical treatment may be required - obliteration of the pleural cavity, thoracoscopic pleurectomy, etc.

Forecast and prevention

The prognosis for serous pleurisy is largely determined by the nature and severity of the underlying disease: usually in the case of timely and rational treatment of pleurisy of infectious etiology, it is favorable. The most severe prognosis is associated with tumor pleurisy, indicating a far advanced oncological process. Prevention consists in the timely detection and treatment of the primary disease that caused the production and accumulation of exudate in the pleural cavity.

Hematogenous and histogenic nature of the liquid that is formed at the site of inflammation. Acute inflammation is characterized by the predominance of neutrophils in the exudate, for chronic - lymphocytes and monocytes, for allergic - eosinophils. Exudate formed during infectious diseases often contains the causative agent of the disease and therefore serves as material for microbiological diagnostics. The process of leakage of exudate from small blood vessels into tissues or body cavities during inflammation is called exudation. Exudation is a normal part of the defense mechanisms of the human body.

Literature

Krasilnikov A.P. Microbiological dictionary-reference book. - Minsk: "Belarus", 1986. - S. 343.

Wikimedia Foundation. 2010 .

See what "Exudation" is in other dictionaries:

Lat., from ex, and sudor, sweat. Exudation of liquid curdling substances in the body cavity. Explanation of 25,000 foreign words that have come into use in the Russian language, with the meaning of their roots. Michelson A.D., 1865. exudation of honey. education process... Dictionary of foreign words of the Russian language

EXUDATION- (exudation) slow release of fluid (exudate (exudatc)), containing proteins and leukocytes, through the walls of intact blood vessels; usually exudation occurs as a result of inflammation. Exudation is a normal component of protective ... ... Explanatory Dictionary of Medicine

- (exsudatio; ex + lat. sudo, sudatum to sweat) the process of moving a protein-rich fluid, often containing blood cells, from small veins and capillaries into the surrounding tissues and cavities of the body; manifestation of inflammation... Big Medical Dictionary