Lymph node, spleen. Structure, function, development

  • The date: 04.03.2020

The spleen is located on the path of blood flow from the aorta to the hepatic portal vein system and performs the functions of immune control. Blood is deposited in the spleen (up to 16%) and erythrocytes are destroyed. In the embryo in the spleen, erythrocytes and leukocytes are formed, which enter the portal vein through the splenic vein.

Through the gate of the spleen, the splenic artery enters, which branches into trabecular arteries, passing into the pulp arteries, which branch out in the red pulp. The artery passing through the white pulp is called the central one. In the red pulp, the central artery branches out in the form of a brush into tassel arterioles. At the end of the brush arterioles there is a thickening - an arterial sleeve, clearly pronounced in pigs. The sleeves function as sphincters that block the blood flow, since contractile filaments are found in the endothelium of ellipsoid or sleeve arterioles. This is followed by short arterial capillaries, most of which flow into the venous sinuses (closed circulation).Some arterial capillaries open into the reticular tissue of the red pulp (open circulation), and then into the venous capillaries. Blood from the venous capillaries is delivered to the trabecular veins and then to the splenic vein.

The number of venous sinuses in the spleen of animals of different species is not the same: for example, there are many of them in rabbits, dogs, guinea pigs, less in cats, cattle and small ruminants. The part of the red pulp located between the sinuses is called the splenic, or pulp, strands. The beginning of the venous system is the venous sinuses. In the areas of transition of sinuses into veins, there are similarities of muscle sphincters, when opened, blood flows freely through the sinuses into the veins. Conversely, the closure (by contraction) of the venous sphincter leads to an accumulation of blood in the sinus.

Blood plasma penetrates the sinus membrane, which contributes to the concentration of cellular elements. When the venous and arterial sphincters are closed, blood is deposited in the spleen. When the sinuses are stretched, gaps are formed between the endothelial cells through which blood can pass into the reticular tissue.

Relaxation of the arterial and venous sphincters, as well as contraction of the smooth muscle cells of the capsule and trabeculae, lead to the emptying of the sinuses and the release of blood into the venous bed. The outflow of venous blood from the spleen pulp occurs through the vein system. The splenic vein exits through the portal of the spleen and flows into the portal vein.

The spleen is covered with a serous membrane, from which trabeculae extend deep into the organ - layers of loose fibrous connective tissue containing smooth muscle cells.

The basis of the spleen is reticular tissue in the form of a sponge filled with parenchyma - white and red pulp (Fig. 87, 88).

Figure: 87.

/ - shell; 2 - trabecula; 3 - venous sinuses; 4 - ellipsoidal macrophage sleeve; 5 - brush arterioles; 6 - central artery; 7-white pulp; 8- red pulp; 9- pulp artery; 10- splenic vein; // - splenic artery; 12 -trabecular artery and vein

Figure: 88.

7 - capsule; 2- trabecula; 3- red pulp; 4 - white pulp

The white pulp is built from lymphoid tissue collected around the arteries in balls called lymphatic follicles of the spleen, or splenic bodies. The number of follicles in different animals is different. For example, in cattle there are many follicles; pigs and horses have few.

In lymphatic follicles, 4 zones are distinguished: periarterial, center of reproduction, mantle, marginal.

Periarterial zone is thymus dependent. It occupies a small area of \u200b\u200bthe follicle near the artery and is formed mainly from T-lymphocytes and interdigitating cells that adsorb antigens. T-lymphocytes, having received information about the state of the microenvironment, migrate to the sinuses of the marginal zone through the capillaries.

Breeding center, or light center, reflects the functional state of the follicle and can change significantly in infectious diseases. The breeding center is a thymus-independent site and consists of reticular cells and an accumulation of phagocytes.

Figure: 89.

/ - venous sinus; 2 - endothelium; 5 - macrophage; 4- macrophage that has absorbed leukocytes;

5 - monocyte

Mantle zone surrounds the periarterial zone, the light center and consists of densely spaced small B-lymphocytes and a small number of T-lymphocytes, plasma cells and macrophages. The cells adjacent to each other form, as it were, a crown, stratified by circular reticular fibers.

Regional, or marginal zone is a transitional area between the white and red pulp, consists mainly of T- and B-lymphocytes and single macrophages, surrounded by marginal, or marginal, sinusoidal vessels.

The red pulp of the spleen makes up 75 ... 78% of the mass of the organ, consists of reticular tissue with cellular elements of the blood, which impart a red color to the parenchyma. The red pulp contains numerous arterioles, capillaries, venules and peculiar venous sinuses (Fig. 89). Various cellular elements are deposited in the cavity of the venous sinuses. Areas of red pulp located between the sinuses are called bullet-paired strands, which contain many lymphocytes and the development of plasma cells occurs. In the red pulp there are macrophages - splenocytes, which carry out phagocytosis of destroyed erythrocytes. As a result of the breakdown of hemoglobin, bilirubin and transferrin containing iron are formed and released into the blood. Bilirubin enters the liver and is part of the bile. Transferrin from the bloodstream is captured by macrophages, which supply the developing erythrocytes with iron.

The spleen is an unpaired organ located in the abdominal cavity on the greater curvature of the stomach, in ruminants - on the scar. Its shape varies from flat elongated to round; in animals of different species, the shape and size may be different. The color of the spleen - from intense red-brown to blue-violet - is due to the large amount of blood it contains.

Figure: 212. Palatine tonsils:

AND - dogs, B - sheep (according to Ellenberger and Trautman); and - pits of the tonsils; b - epithelium; in - reticular tissue; d - lymphatic follicles; d - loose connective tissue; e - glands; f - bundles of muscle fibers.

The spleen is a multifunctional organ. In most animals, this is an important organ of lymphocyte formation and immunity, in which, under the influence of antigens present in the blood, cells are formed either that produce humoral antibodies or participate in cellular immunity reactions. In some animals (rodents), the spleen is a universal organ of hematopoiesis, where cells of lymphoid, erythroid and granulocytic germs are formed. The spleen is a powerful macrophage organ. With the participation of numerous macrophages, it destroys blood cells and especially erythrocytes ("graveyard of erythrocytes"), the decay products of the latter (iron, proteins) are again used in the body.


Figure: 213. Cat spleen (according to Ellenberger and Trautnan):

a - capsule; b - trabeculae; in - trabecular artery; r - trabecular vein; d - light center of the lymphatic follicle; e - central artery; f - red pulp; s - the vascular vagina.

The spleen is the organ of blood deposition. The depositing function of the spleen is especially pronounced in horses and ruminants.

The spleen develops from clusters of rapidly multiplying mesenchymal cells in the dorsal mesentery. In the initial period of development, the formation of a fibrous frame, vascular bed and reticular stroma from the mesenchyme occurs in the anlage. The latter is colonized by stem cells and macrophages. Initially, it is the organ of myeloid hematopoiesis. Then there is an intensive invasion of lymphocytes from the central lymphoid organs, which are initially located evenly around the central arteries (T-zone). B-zones are formed later, which is associated with the concentration of macrophages and lymphocytes on the side of the T-zones. Simultaneously with the development of lymph nodules, the formation of the red pulp of the spleen is also observed. In the early postembryonic period, an increase in the number and volume of nodules, the development and expansion of centers of reproduction in them is noted.

Microscopic structure of the spleen. The main structural and functional elements of the spleen are the musculoskeletal system, represented by the capsule and the trabecular system, and the rest of the intertrabecular part is the pulp, built mainly of reticular tissue. Distinguish between white and red pulp (Fig. 213).

The spleen is covered with a serous membrane that grows tightly with the connective tissue capsule. From the capsule to the inside of the organ, there are crossbeams - trabeculae, which form a kind of reticular frame. The most massive trabeculae are at the gate of the spleen, they contain large blood vessels - trabecular arteries and veins. The latter belong to the veins of the muscleless type and on the preparations quite clearly differ in structure from the artery wall.

The capsule and trabeculae are composed of dense fibrous connective and smooth muscle tissue. A significant amount of muscle tissue develops and is contained in the deposit type spleen (horse, ruminants, pigs, carnivores). The contraction of smooth muscle tissue helps to push the deposited blood into the bloodstream. In the connective tissue of the capsule and trabeculae, elastic fibers predominate, allowing

the spleen to change its size and withstand a significant increase in its volume.

White pulp (pulpa lienis alba) macroscopically and on unstained preparations is a collection of light gray rounded or oval formations (nodules), irregularly dispersed throughout the spleen. The number of nodules in different animal species is different. In the spleen of cattle there are many of them and they are clearly delimited from the red pulp. Less nodules in horse and pig spleen.

With light microscopy, each lymph nodule is a formation consisting of a complex of cells of lymphoid tissue located in the adventitia of the artery and numerous hemocapillaries extending from it. The artery of the nodule is called central. however, it is more often located eccentrically. In a developed lymph node, several structural and functional zones are distinguished: periarterial, light center with a mantle zone and a marginal zone. The periarterial zone is a kind of clutch consisting of small lymphocytes closely adjacent to each other and interdigitating cells. Lymphocytes in this zone belong to the recirculating T-cell pool. They penetrate here from the hemocapillaries, and after antigenic stimulation they can migrate into the sinuses of the red pulp. Interdigitating cells are special process macrophages that absorb antigen and stimulate blast-transformation, proliferation and transformation of T-lymphocytes into effector cells.

The light center of the nodule in structure and functional purpose corresponds to the follicles of the lymph node and is a thymus-independent site. There are lymphoblasts, many of which are at the stage of mitosis, dendritic cells that fix the antigen and preserve it for a long time, as well as free macrophages containing absorbed decay products of lymphocytes in the form of stained bodies. The structure of the light center reflects the functional state of the lymph node and can change significantly with infections and intoxications. The center is surrounded by a dense lymphocytic rim - the mantle zone.

A marginal zone is located around the entire nodule. which contains T- and B-lymphocytes and macrophages. It is believed that functionally this zone is one of the areas of cooperative interaction of different types of cells in the immune response. The B-lymphocytes located in this zone as a result of this interaction and stimulated by the corresponding antigen proliferate and differentiate into antibody-forming plasma cells that accumulate in the cords of the red pulp. The shape of the splenic nodule is maintained by a network of reticular fibers - in the thymus-independent area, they are located radially, and in the T-zone - along the long axis of the central artery.

Red pulp (pulpa lienis rubra). An extensive part (up to 70% of the mass) of the spleen, located between the lymph nodes and trabeculae. Due to the content in it of a significant amount of erythrocytes, it has a red color on unstained preparations of the spleen. It consists of reticular tissue with free cellular elements in it: blood cells, plasma cells and macrophages. In the red pulp, there are numerous arterioles, capillaries and peculiar venous sinuses (sinus venosus); a wide variety of cellular elements are deposited in their cavities. The red pulp is rich in sinuses at the border with the marginal zone of lymph nodes. The number of venous sinuses in the spleen of animals of different species is not the same. There are many of them in rabbits, guinea pigs, dogs, less in cats, cattle and small ruminants. Areas of red pulp located between the sinuses are called splenic. or pulp cords, which contain many lymphocytes and the development of mature plasma cells occurs. Macrophages of the pulp cords carry out phagocytosis of damaged erythrocytes and participate in the exchange of iron in the body.

Circulation. The complexity of the structure and multifunctionality of the spleen can be understood only in connection with the peculiarities of its blood circulation.

Arterial blood is directed to the spleen through the splenic artery. which through the gate enters the organ. Branches extend from the artery that go inside the large trabeculae and are called trabecular arteries. In their wall there are all the membranes characteristic of muscular-type arteries: intima, media and adventitia. The latter grows together with the connective tissue of the trabecula. From the trabecular artery, arteries of small caliber depart, which enter the red pulp and are called pulp arteries. Elongated lymphatic sheaths are formed around the pulp arteries; as they move away from the trabecula, they enlarge and take a spherical shape (lymph node). Inside these lymphatic formations, many capillaries leave the artery, and the artery itself is called central. However, the central (axial) location is present only in the lymphatic sheath, and in the nodule it is eccentric. Upon leaving the nodule, this artery splits into a series of branches - brush arterioles. Oval clusters of elongated reticular cells (ellipsoids, or sleeves) are located around the terminal sections of the brush arterioles. In the cytoplasm of the endothelium of ellipsoid arterioles, microfilaments are found, which are associated with the ability of ellipsoids to contract - a function of peculiar sphincters. The arterioles then branch out into capillaries. some of them flow into the venous sinuses of the red pulp (closed circulation theory). According to the theory of open circulation, arterial blood

from the capillaries out into the reticular tissue of the pulp, and from it seeps through the wall into the sinus cavity. Venous sinuses occupy a significant part of the red pulp and can have different diameters and shapes depending on their blood supply. The thin walls of the venous sinuses are lined with an intermittent endothelium located on the basal lamina. Reticular fibers run along the surface of the sinus wall in the form of rings. At the end of the sinus, at the site of its transition to the vein, there is another sphincter.

Depending on the reduced or relaxed state of the arterial and venous sphincters, the sinuses can be in different functional states. When the venous sphincters contract, the blood fills the sinuses, stretches their wall, while the blood plasma goes through it into the reticular tissue of the pulpal cords, and blood cells accumulate in the sinus cavity. In the venous sinuses of the spleen, up to 1/3 of the total number of erythrocytes can be retained. When both sphincters are open, the contents of the sinuses enter the bloodstream. Often this happens with a sharp increase in oxygen demand, when the sympathetic nervous system is excited and the sphincters relax. This is also facilitated by the contraction of the smooth muscles of the capsule and trabeculae of the spleen.

The outflow of venous blood from the pulp occurs through the vein system. The wall of the trabecular veins consists only of the endothelium, which is closely adjacent to the connective tissue of the trabeculae, that is, these veins do not have their own muscular membrane. This structure of the trabecular veins facilitates the expulsion of blood from their cavity into the splenic vein, which exits through the gate of the spleen and flows into the portal vein.

SPLEEN [lien (PNA, JNA, BNA)] - an unpaired parenchymal organ located in the abdominal cavity, performing immunological, filtration and hematopoietic functions, taking part in the metabolism, in particular iron, proteins, etc. S. does not belong to the number of vital organs, but due to the listed functional features, it plays an essential role in the body.

COMPARATIVE ANATOMY

The shape, size, and ratio of structural elements of S. in animals belonging to different taxonomic groups are extremely diverse. S. in reptiles is reduced, in nek-ry fish and amphibians it is presented in the form of separate clusters of lymphoid tissue located under the serous membrane of the stomach or intestines. S. in birds is a separate small organ, distinguished by a variety of forms. In mammals, the shape, size, and weight of S. are highly variable. The fibrous membrane and trabeculae of S. rabbit, guinea pig, rat, and humans are less developed than the spleen of dogs and cats, which is characterized by a powerful development of connective tissue. Trabeculae in S. of animals are much richer in smooth muscle cells than in the human spleen, and peritrabecular nerve plexuses present in S. of a pig and dog are absent in S. of a person. A sheep and a goat have a relatively short S. of a triangular shape; in cattle and a pig, S. has a wide, short, "tongue-like" shape.

EMBRYOLOGY

S. is laid in the form of an accumulation of mesenchymal cells in the thickness of the dorsal mesentery at the 5th week of intrauterine development. At the 6th week, S.'s primordium begins to separate, the first blood islands are formed in it. In a 7-week embryo, S. is clearly delimited from the stomach, surrounded by a single-layer (coelomic) epithelium. At 9-10th week S. is included in hematopoiesis carried out by hl. arr. extravascularly. The main product of growing hematopoiesis is erythrocytes, granulocytes, megakaryocytes; less intense lymphocytopoiesis. The intraorgan vascular bed is organized, primary arteries, veins, sinuses and a delicate network of reticular fibers in the gate area are formed. From the 7th to the 11th week of intrauterine development, S.'s length increases 7-9 times, and the transverse size - 9 times.

The most characteristic in the subsequent stages of embryonic development of S. is the intensified formation of its musculoskeletal elements - the reticular stroma, the system of vascular trabeculae, and collagen structures.

By the 13-14th week of intrauterine development, the venous sinus system differentiates. From the 15-16th week, the number of formalized limf, follicles increases, and gradually the foci of erythro- and myelopoiesis are reduced, "lymphocytopoiesis intensifies. By the 25-26th week, the predominant component of S. is lymphoid tissue (see). By 26 -28-th week in the red pulp already formed cystocular arterioles. By 28-32 weeks

S. ceases to function as an organ of myelopoiesis and is structurally formed as a lymphoid organ, although in the postnatal period the formation of follicles is still continuing. By the time the fetus is born, the capsule, vascular trabeculae and newly formed avascular trabeculae S. form a single system associated with the system of venous sinuses and containing reticular, collagen, elastic, and muscle components.

Formation of complex angioarchitectonics of S. begins with the intensive development of veins. The primary splenic vein - the inflow of the portal vein (see) - starts from the plexus located on the upper surface of C .; it is further joined by the primary intraorgan veins. S.'s arteries differentiate later.

ANATOMY

At newborn S. in 85% of cases it has a lobed structure, a rounded shape and pointed edges; its weight (weight) is from 8 to 12 g, dimensions are from 21 X 18 X 13 to 55 X 38 X 20 mm. In childhood, S. has the shape of a regular tetrahedron; later it becomes more elongated, sometimes bean-shaped. S.'s weight increases intensively; by 5 years it reaches 35-40 g, by 10 years 65-70 g, by 15 years 82-90 g, by 20 years 150-200 g. On average, the length of S. in adults is 80-150 mm, width is 60-90 mm, thickness 40-60 mm; weight 140-200 g.

Distinguish the outer convex diaphragmatic surface S. (facies diaphragmatica), adjacent to the costal part of the diaphragm (see), and the visceral surface (facies visceralis), facing other organs of the abdominal cavity. The anterior part of the visceral surface adjacent to the stomach (see) is called the gastric surface (facies gastrica), the posterior-inferior area adjacent to the left kidney (see) and the adrenal gland (see) is called the renal surface (facies renalis). On the border of the front and rear sections of the lower surface of S., the gate of the spleen (hilus lienis) is distinguished - the place of entry into the organ of the arteries and nerves and exit from it veins and limf, vessels (S.'s vascular pedicle). Colon surface S. (facies colica) - a triangular section of the visceral surface, to which from below adjoin the left bend of the colon (see Intestine) and the tail of the pancreas (see). The lower, or anterior, pole of C. (anterior end, T.) is somewhat pointed; the posterior, or upper, pole (posterior end, T.) is more rounded. The blunt lower edge, formed by the diaphragmatic and renal surfaces, faces the left kidney. The pointed edge, formed by the gastric and diaphragmatic surfaces, is often scalloped.

S. is directed by the longitudinal axis from behind and from top to front and down parallel to the course IX - XI of the left ribs, so that its projection field on the side wall of the chest is between the iX and XI ribs, in front reaching the anterior axillary line, 30-40 mm behind to the spine. Topographic-graphical-anatomical position of S. depends on the type of physique: in people with a high and narrow chest, it is located lower and vertically, in people with a wide chest, higher and horizontally. The size, position, filling of the stomach and transverse colon significantly affect the position of C.

Newly formed # primary lymph, follicles are small, diam. 0.2-0.3 mm, accumulation of lymphocytes. The volume of the follicle as it matures increases 2-3 times, the central artery moves to the periphery. The light central zone of lymph, the follicle (center of reproduction, embryonic center) contains reticular cells, lymphocytes, lymphoblasts, macrophages; high mitotic activity is noted in it. The structure of this zone reflects the functional state of the body and can change significantly during intoxication and infections. On the periphery of the follicle in the so-called. the mantle zone contains a dense layer of medium and small lymphocytes (Fig. 3). The reverse development of lymph, follicle begins, according to Jager (E. Jager, 1929), with atrophy or hyalinosis of its internal capillary network. Gradually, the follicle atrophies, is replaced by connective tissue.

Between the free cells of the white pulp (lymphocytes, monocytes, macrophages and an insignificant amount of granulocytes) there are reticular fibers, to-rye perform a supporting function. It is believed that they consist of a substance synthesized by reticular cells.

The marginal zone - a poorly discernible part of S.'s tissue - surrounds the white pulp and lies on the border with the red pulp. Many small arterial branches flow into this zone from the white pulp. It primarily accumulates damaged and defective cells, foreign particles. With hemolytic anemias, damaged erythrocytes are concentrated and phagocytosed in this zone.

The red pulp, which accounts for 70 to 80% of S.'s weight, consists of the reticular skeleton, sinuses, arterioles, capillaries, venules, free cells and various deposits. Macrophages of the red pulp, in addition to the supporting function, can carry out phagocytosis (see). These properties are not possessed by the cells lining the walls of the sinuses, similar in morphology. They are located on the basement membrane, which has many small holes, through which the cellular elements of the red pulp can freely pass. Free cells are located between the reticular fibers of the red pulp: lymphocytes (see), erythrocytes (see), platelets (see), macrophages (see), plasma cells (see).

The walls of the venous sinuses consist of a reticular syncytium, the nucleus-containing parts of which, oriented along the length of the sinus, are interconnected by thin bridges, which together creates a kind of lattice with numerous lumens.

In the peri-arterial plexuses of the red pulp, the nerves are more numerous than in the paravenous. Terminal nerve trunks penetrate the walls of the sinuses and arterial sleeves.

In the circumference of limf, follicles, networks of limf, capillaries begin. The diverting limf, vessels from the trabeculae and fibrous membrane follow to the regional (celiac) limf. nodes.

The ratio of the structural components of S. changes with age. By the end of the first year of life, the amount of white pulp doubles, reaching an average of 21% of the total weight of C. (in a newborn, about 10-11%). Red pulp is also noticeably reduced (from 86 to 75%). At the age of 5, the white pulp is 22%, but then, by the age of 15, its weight decreases to 14-16%, remaining approximately at the same level until the age of 50, and by the age of 60-70 it again decreases to 7%. The maximum number of limf, follicles per 1 cm 2 of S.'s area (in a newborn) sharply decreases already in the first year of life, when the number of mature follicles increases and atrophic follicles appear. The diameter of limf, S.'s follicles of the newborn is from 35 to 90 microns, and in the 2nd year of life - from 160 to 480 microns. Already in the first years of life, S.'s connective tissue reaches significant development - by the age of 12, the thickness of the fibrous membrane increases 10 times, the number of collagen, reticular and elastic fibers increases.

At the age of 20 to 40 years, S.'s micro-architectonics relatively stabilizes. In the future, signs of aging appear - varicose veins. polychrome coloration, violation of clear orientation of fibers, their fragmentation. In limf, follicles, the walls of blood vessels thicken, capillaries close, the central artery narrows. With age, there is a partial atrophy of lymph, follicles and connective tissue develops in their place. Deposits of fibrin, fibrinoid, or hyaline in the central arteries appear by age 10. After the age of 50, these substances are found in all links of the vascular bed of C. After 60 years, individual thickened elastic membranes and trabecular arteries split, and after 70 they are often fragmented.

NORMAL AND PATHOLOGICAL PHYSIOLOGY

For a long period of time, S. was considered a "mysterious" body, since its normal functions were not known. Actually, and still cannot be considered that they have been fully studied. Nevertheless, in the crust, time already much about S. can be considered established. So, a number of basic fiziol is described. functions Participation in cellular and humoral immunity (see), control over circulating blood corpuscles, hematopoiesis (see Hematopoiesis), etc.

The most important function of S. is immune. It consists in the capture and processing of harmful substances by macrophages (see. System of mononuclear phagocytes), purification of the blood from various foreign agents (bacteria, viruses). S. captures and destroys endotoxins, insoluble components of cell detritus in burns, trauma, and other tissue damage. S. actively participates in the immune response - her cells recognize antigens foreign to this organism and synthesize specific antibodies (see).

The sequestration function is carried out, in particular, in the form of control over circulating blood cells. First of all, this applies to erythrocytes, both aging and defective. Fiziol. the death of erythrocytes occurs after they reach about 120 days of age, pathologically altered - at any age. It has not been clarified exactly how phagocytes distinguish between senescent and viable cells. Apparently, the nature of the biochemical and biophysical changes occurring in these cells matters. For example, there is an assumption, according to S.'s rum, cleans the circulating blood from cells with a changed membrane. So, with hereditary microspherocytosis, erythrocytes cannot pass through S., they stay in the pulp for too long and die. It has been shown that S. has a better ability than the liver to recognize less defective cells and functions as a filter. In the spleen, granular inclusions (Jolly's bodies, Heinz's bodies, iron granules) are removed from erythrocytes (see) without destroying the cells themselves. Splenectomy and S.'s atrophy lead to an increase in the content of these cells in the blood. The increase in the number of siderocytes (cells containing iron granules) after splenectomy is especially clearly detected, and these changes are persistent, which indicates the specificity of this function of C.

Splenic macrophages reutilize iron from destroyed erythrocytes, converting it into trans-ferrin, i.e. the spleen takes part in iron metabolism.

S.'s role in the destruction of leukocytes has not been studied enough. There is an opinion that these cells in fiziol. conditions die in the lungs, liver and C .; platelets (see) in a healthy person are also destroyed by hl. arr. in the liver and C. Probably S. also takes another part in thrombocytopoiesis, since after splenectomy about S.'s damage, thrombocytosis occurs and the ability of platelets to agglutination increases.

S. not only destroys, but also accumulates blood corpuscles - erythrocytes, leukocytes, platelets. In particular, it contains from 30 to 50% and more circulating platelets, to-rye, if necessary, can be thrown out into the peripheral bed. With patol. states, their deposition is sometimes so great that it can lead to thrombocytopenia (see).

In case of violation of the outflow of blood S. increases, for example, with portal hypertension (see), and, according to some researchers, can accommodate a large amount of blood, being its depot (see Blood depot). Reducing, S. is capable of throwing the blood deposited in it into the vascular bed. In this case, S.'s volume decreases, and the number of erythrocytes in the blood increases. However, normal S. contains no more than 20-40 ml of blood.

S. participates in the exchange of proteins and synthesizes albumin, globin (the protein component of hemoglobin), factor VIII of the blood coagulation system (see). S.'s participation in the formation of immunoglobulins is important, a cut is provided by the numerous cells producing immunoglobulins (see), probably of all classes.

S. takes an active part in hematopoiesis, especially in the fetus (see). In an adult, it produces lymphocytes and monocytes. S. is the main organ of extra-medullary hematopoiesis in violation of normal processes of hematopoiesis in the bone marrow, eg, with osteomyelofibrosis, hron. blood loss, osteoblastic cancer, sepsis, miliary tuberculosis, etc. There are indirect data confirming the possibility of S.'s participation in the regulation of bone marrow hematopoiesis. S.'s influence on erythropoiesis is tried to be confirmed on the basis of the fact of the appearance of reticulocytosis after removal of normal S., for example, when it is damaged. However, this may be due to the fact that S. delays the early release of reticulocytes. The mechanism of an increase in the number of granulocytes after splenectomy remains unclear - either more of them are formed and they quickly leave the bone marrow, or they are less actively destroyed. The pathogenesis of thrombocytosis developing in this case is also unclear; most likely, it arises due to the removal of these cells from the S. depot. These changes are of a transient nature and are usually observed only during the first month after splenectomy.

S. probably regulates the maturation and release of erythro- and granulocytopoiesis cells from the bone marrow, the production of platelets, the process of denuclearization of maturing erythrocytes, and the production of lymphocytes. It is quite probable that lymphokines synthesized by C's lymphocytes can have an inhibitory effect on hematopoiesis (see Mediators of cellular immunity).

Data on changes in certain types of metabolism after splenectomy are contradictory. The most characteristic change in the liver after splenectomy is an increase in the level of glycogen in it. The enhancement of the glycogen-fixing function of the liver, which occurs after splenectomy, is also persistently maintained when the liver is influenced, leading to a weakening of this function (poisoning with phosphorus and carbon tetrachloride, the introduction of dinitrophenol, thyroxine in the experiment). Similar changes are noted in patients with nek-ry hron. liver diseases. At the same time, the development of fatty liver infiltration is inhibited, the level of ketone bodies and cholesterol in the liver decreases. Experiments with S.'s removal from parabiotic animals allow us to conclude that humoral factors are produced in S., the absence of which causes an increased fixation of glycogen and, thereby, influences the processes of fat accumulation in this organ for the second time.

S. plays a large role in the processes of hemolysis (see). In patol. conditions, it can delay and destroy a large number of altered erythrocytes, especially with some congenital (in particular, microspherocytic) and acquired hemolytic (including autoimmune nature) anemias (see. Hemolytic anemia). A large number of erythrocytes lingers in S. at stagnant plethora, polycytemia (see). It has also been established that the mechanical and osmotic resistance of leukocytes decreases when they pass through the S. So, G. Lepehne found even phagocytosis of leukocytes in S. at inf. hepatitis. According to Hermann (G. Gehrmann, 1970), destruction of platelets in S. is also possible, in particular at idiopathic thrombocytopenia (see).

S.'s dysfunction is observed at nek-ry patol. conditions (severe anemia, nek-ry inf. diseases, etc.), as well as with hypersplenism.

Cytolytic diseases that solve an independent nosology (for example, hereditary and acquired hemolytic anemias, idiopathic thrombocytopenic purpura, immune leukolytic conditions) should not be classified as hypersplenism. S. at the same time is only a place of destruction of blood corpuscles and can play an essential role in the production of antibodies. Splenectomy is often beneficial. Excessive destruction of erythrocytes is accompanied by the development of generalized hemosiderosis (see), including the spleen. With hereditary and acquired disorders of lipid metabolism (see. Thesaurismosis), accumulation of a large amount of lipids is noted in the spleen, which leads to splenomegaly (see).

Decreased S.'s function (hyposplenism) is observed with S.'s atrophy in old age, with starvation, hypovitaminosis. It is accompanied by the appearance in erythrocytes of Jolly's bodies and target erythrocytes, siderocytosis.

PATHOLOGICAL ANATOMY

With the functional and morphological features of the spleen, in particular with belonging to the organs of immunogenesis, the variety of its structural changes is associated with many patol. processes.

In a macroscopic examination of S. (measurement of dimensions, weighing, an incision along the long axis through the gate and transverse cuts into plates 10-20 mm thick) pay attention to the state of the walls and lumen of the vessels of S. gate, capsules, color and texture of tissue, the presence of focal changes (hemorrhages, necrosis, scars, granulomas, etc.). The increase in S.'s sizes and its weight (more than 250-300 g) is usually associated with patol. changes, to-rye, however, can be observed in the non-enlarged organ. S.'s color and consistency depend on blood filling; they change with pulp hyperplasia, deposition of amyloid, various pigments, fibrosis, S.'s defeat at acute and hron. infections, anemias, leukemias, malignant lymphomas, histiocytosis. For microscopic examination, take pieces from various parts of the spleen, fix them in formalin and (or) zenkerformol, Carnoy's liquid; embedding in paraffin is recommended.

The most frequent manifestation of S.'s dystrophy is hyalinosis of small arteries and arterioles (see. Arteriolosclerosis), which is usually observed normally at the age after 30 years; less often, hyaline is deposited in the form of lumps in limf, follicles and red pulp. Mucoid and fibrinoid swelling of S.'s connective tissue (see. Mucous dystrophy, Fibrinoid transformation), primarily of the walls of the venous sinuses and small vessels (up to their fibrinoid necrosis), the prolapse of protein precipitates in the centers of lymph, follicles are noted as a regularity of the disease in achuto. As a result, coarsening of the walls of S.'s sinuses occurs, the peri-arterial, so-called. bulbous, sclerosis, most pronounced in systemic lupus erythematosus (see).

S.'s amyloidosis is usually observed with general amyloidosis (see) and takes second place in frequency after kidney amyloidosis. Sometimes in diseases causing secondary amyloidosis (tuberculosis, hron. Purulent processes), only C amyloidosis can be observed. Lymph, follicles when amyloid is deposited in them on a cut through the organ have the appearance of vitreous bodies, similar to sago grains. In these cases, they speak of the "sago" spleen. S.'s weight in such cases is increased slightly. Diffuse prolapse of amyloid in the walls of the sinuses, blood vessels and along the reticular fibers is accompanied by an increase in S.'s weight (up to 500 g); its tissue is dense, greasy, yellowish-red in color ("greasy", "ham" spleen). A combined deposition of amyloid in lymph, follicles and red pulp is also possible.

At a number of diseases in S., xanthoma cells scattered diffusely or lying in the form of clusters are found (see. Xanthomatosis). They are formed when lipid metabolism is disturbed due to the accumulation of lipids in macrophages. Thus, with diabetes mellitus, atherosclerosis, and familial xanthomatosis, cholesterol is excessively deposited in S.'s macrophages (and other organs); cells similar to xanthoma, sometimes. occur with idiopathic thrombocytopenic purpura; massive accumulation of certain types of lipids is observed in S. with thesaurismosis, which leads to the formation of cells characteristic of this or that form of the disease - Gaucher and Pick cells, to the development of significant secondary changes in S. and an increase in its size (see Gaucher disease, Niemann - Pick's disease).

S.'s hemosiderosis - excessive deposition of hemosiderin in it - is a manifestation of general hemosiderosis (see), and is observed at hemochromatosis (see), diseases and patol. states accompanied by increased hemolysis, violation of iron utilization, especially with hemolytic, hypoplastic and iron-refractory anemias (see), leukemia (see), malaria (see), relapsing fever (see), sepsis (see), hron. eating disorders (dyspepsia, diseases of the stomach and intestines). With hemosiderosis S. has a rusty-brown color, sometimes slightly increased. In the red pulp with gistol. research reveals numerous siderophages, in the endothelium of the sinuses, the walls of blood vessels, trabeculae, S.'s capsule - hemosiderin deposits (printing. Fig. 3). Local hemosiderosis of S. is often found in areas of hemorrhage. In their centers and in extensive foci of necrosis, crystals of hematoidin can be detected (see. Bile pigments). At malaria in S. there is a delay of hemomelanin, to-rye during recovery can disappear. Deposition in S. of coal pigment, which penetrates hematogenously from the lungs, is also possible. With morfol. research it is necessary to take into account the possibility of loss at fixing S.'s tissue in solution of formalin so-called. formalin pigment settling diffusely in the tissue in the form of brown grains.

Often in S. there are foci of necrosis (see). Small foci usually arise due to toxic effects in infections, large foci are due to circulatory disorders.

Circulatory disorders in S. come to light quite often. Active hyperemia is found in acute infections and is characterized by congestion of the pulp arteries. With general venous plethora due to S.'s heart failure it is increased, dark red, its weight is 300-400 g. Histologically, blood overflow of S.'s stretched sinuses is determined (printing. Fig. 4), atrophy of limf, follicles of varying degrees. With prolonged stagnation of blood, fibrosis of the pulp cords is noted (cyanotic induration of the spleen). Portal hypertension (see) developing with cirrhosis of the liver, sclerotic narrowing or thrombosis in the portal vein system, obliterating phlebitis of the hepatic veins, leads to the development of significant changes of the same type in S. and its pronounced increase (cirrhotic splenomegaly, thrombophlebitic splenomegaly). S.'s weight can be increased to 1000 g or more, its tissue is fleshy, the capsule is thickened, often contains extensive fibro-hyaline areas ("glazed" spleen), S.'s adhesions with surrounding tissues are possible. S.'s surface on a cut is motley due to focal hemorrhages, the presence of multiple dense nodules of orange-brown color. With gistol. the study reveals stagnation of blood, however, less pronounced than with general venous plethora, uneven expansion of the venous sinuses with distinct endothelial hyperplasia, multiple hemorrhages of various ages, reduction of lymph. follicles with proliferation of connective tissue in their area (spleen fibrosis), fibrosis of the pulp cords. In S.'s tissue, areas of sclerosis, impregnated with iron and often calcium salts, are revealed - Gandhi-Gamna's nodules, or sclero-pigmented nodules (printing. Fig. 5). Iron impregnation in the area of \u200b\u200bscars also occurs at hron. leukemias, hemolytic anemias, thesaurismosis, etc. A decrease in S.'s blood supply is observed with massive acute or prolonged repeated blood loss (see), hypoplastic anemia (see).

Inflammatory changes in S. (splenitis) are constantly found at inf. diseases. Their nature and intensity depend on the characteristics of the pathogen and immunol. the state of the body.

Productive inflammation in S. with the formation of granulomas of various structures and development of splenomegaly can be observed with tuberculosis (see below), sarcoidosis (see), brucellosis (see), tularemia (see), visceral mycoses (see), leprosy ( cm.). The sizes of granulomas vary: in their outcome fibrosis occurs. S., as a rule, is amazed at miliary tuberculosis; similar changes can be detected in children with post-vaccination complications with generalization of the process. At early congenital syphilis in S. pale treponemas, acute inflammation, sometimes nice paired gummas are found; with visceral syphilis, gums in the spleen are rare.

Hyperplasia of S.'s lymphoid tissue reflects its participation in the body's immune reactions during antigenic irritation of various origins (see.Immunomorphology). The presence of large limf, follicles with light tsentralsh, abundance of plasmablasts and plasma cells in S.'s tissue (see), proliferation of histiocytes (see) and macrophages (see) are characteristic of a humoral immune response; often this is accompanied by hyperplasia of the endothelium of the sinuses, tissue dysproteinosis (printing. Fig. 6 and 7). With a cellular immune response, an increase in the number of lymphocytes in T-dependent zones of S. without their plasmatization, the appearance of large basophilic cells-immunoblasts, a macrophage reaction is found. The reaction of the immune response mainly according to the humoral type is observed in S. at the majority of acute infections, according to the cellular type - at inf. mononucleosis, transplant rejection, nek-ry hron. infections. A mixed type of immune response is common histologically. Hypoplasia of the white pulp up to its complete aplasia is observed with immunodeficiency syndromes, starvation, corticosteroid treatment, and after radiation therapy. Significant atrophic changes in the white and red pulp are observed during intensive treatment of malignant tumors and leukemias with antineoplastic agents, massive S. amyloidosis, and widespread sclerotic changes. With osteomyelofibrosis, marble disease, cancer metastases to the bone marrow in S., regenerative growths of hematopoietic tissue are often revealed - foci of extramedullary hematopoiesis (printing. Fig. 8).

Cadaveric changes in S. arise early due to the proximity to the intestine - autolysis of cells of the red pulp, stroma, and somewhat later of the white pulp occurs.

SURVEY METHODS

Into the wedge. apply percussion and S.'s palpation to practice (see. Palpation, Percussion), laparoscopy (see. Peritoneoscopy), X-ray and radioisotope research, splenomanometry, S.'s puncture biopsy, adrenaline test (see).

S.'s percussion is carried out in a vertical or horizontal (on the right side) position of the patient. Dullness over the upper edge of S. along the anterior axillary line is differentiated with a pulmonary sound, approximately along the edge of the costal arch or 10-20 mm higher than it, with a tympanic sound over the stomach. The upper border of dullness over the S. runs almost horizontally, the lower - from behind and from above, down and forward. With a high standing, the upper outer surface of S. can be at the level of the VIII rib, with a low one - at the level of the XII rib. More often S. is located between the IX and XI ribs.

Determination of S.'s size according to MG Kurlov is carried out in the patient's lying position with incomplete turn on the right side, if possible without displacing the pelvis. Percussion along the tenth intercostal space starting from the spine and along the borders of dullness determine the long size C. If * C. protrudes from the hypochondrium, then the length of its protruding part is taken into account. S.'s width is determined by percussion from above from the anterior axillary line towards the posterior axillary line. The results of the study are recorded in the form of a fraction, in a cut, the length is indicated in the numerator, and the width of C is indicated in the denominator. With an increase in C, the length of its protruding part is indicated in front of the fraction, for example. 6 22/11 cm.

S.'s palpation is performed in a horizontal position of the patient on the back and in the right lateral position. With a deep breath, the increased S. descends and "rolls over" through the examiner's fingers. With a significant increase in S., its lower edge descends into the abdominal cavity and it is possible to probe the characteristic notch on it, its front surface, to determine its consistency and soreness. Normally S. is not palpable.

Laparoscopy in the absence of adhesive process makes it possible to examine S., edges are normally bluish-red; on its surface you can see scars, retractions and other patol. changes.

Roentgenol. S.'s research is carried out in a vertical and horizontal position of the patient. At fluoroscopy, the area of \u200b\u200bthe left half of the diaphragm is examined, noting its mobility, the abdominal organs bordering on S., the left lung. The conditions of S.'s research can be improved by introducing gas into the large intestine and stomach. Overview images are performed in frontal and lateral projection. By special methods rentgenol. researches are computed tomography (see. Computer tomography), celiacography (see) and lienography (see), diagnostic pneumoperitoneum (see) and pneumoren (see), supplemented by tomography (see). In differential and topical diagnosis of isolated S.'s defeat an important role belongs to arteriography (see), computed tomography, diagnostic pneumoperitoneum.

Obtaining a radionuclide image of S. is based on the property of cells of the macrophage system to absorb damaged erythrocytes or colloids from the blood. For research, erythrocytes labeled with 51 Cr, 99m Tc or 197 Hg are used (see Radiopharmaceuticals). On a scan (see. Scanning) or a scintigram (see. Scintigraphy) S.'s area with a uniform accumulation of radionuclide in the norm is 35-80 cm 2; at S.'s diseases the accumulation of the radionuclide is uneven, the area of \u200b\u200bthe spleen increases.

S.'s puncture is shown in those cases when the reason for its increase is not established. Contraindications to puncture are hemorrhagic diathesis (see), severe thrombocyte (see). Before puncture with the help of percussion and palpation determine S.'s size and position, carry out X-ray and radioisotope research. S.'s puncture is performed without anesthesia in the position of the patient on his back or on his side. For puncture, thin needles are used, usually used for intramuscular injections. The needle should be free of barbs at the end, and the syringe should be absolutely dry. The needle is injected into S. to a depth of 20 mm, a punctate is obtained, which is subjected to cytological examination (see). Complications of S.'s puncture can be capsule and parenchyma ruptures accompanied by intra-abdominal bleeding.

PATHOLOGY

S.'s pathology includes malformations, injuries (open and closed), S.'s diseases and tumors.

Developmental defects

S.'s developmental defects include its complete absence, dystopia, wandering S., a change in shape and the presence of additional S. Complete absence of S. (asplenia) is extremely rare and is usually combined with malformations of the heart and vascular system. Wedge, the diagnosis of asplenia is difficult. In these cases, radiography and computed tomography are not always informative, since the effect of S.'s absence can be due to her dystopia or displacement. Directed radioisotope research plays an important role in establishing the correct diagnosis. However, in patients with congenital heart defects, S. may be functionally defective - unable to accumulate a radiopharmaceutical. It is also observed in those cases when S. has an irregular shape with the presence of deep cutouts or is unusually elongated (the so-called tailed spleen), sometimes reaching with one pole of the pelvic cavity. In some cases, lobular S. (consisting of many shares) occurs. These malformations usually do not require treatment.

As a result of ectopia or dystopia, S. can change its position in the abdominal cavity and be, for example, in the retroperitoneal space, in an umbilical or diaphragmatic hernia (splenic hernia), between the bottom (fornix) of the stomach and the dome of the diaphragm, in the right half of the abdominal cavity, what is observed at transposition of organs (see).

In addition to this, usually fixed, displacement of the organ, there is a so-called. wandering S., moving in the abdominal cavity because of the weakness of its ligamentous apparatus, for example, with splanchnoptosis (see), congenital absence of the mesentery of the stomach. Such a S. hangs on the vascular-ligamentous pedicle, extending from the horseshoe-shaped part of the duodenum, and can be twisted around its axis (S.'s volvulus); at the same time, patients complain of a feeling of pressure and abdominal pain of a transient nature. The repeated twisting of S.'s leg can cause a wedge, a picture of an acute abdomen (see). The S. is most often increased in size, dense, on a cut of dark red color with extensive foci of necrosis. The slowly developing volvulus leads to a kind of colliquation necrosis of S., sometimes to its fusion with the surrounding intestinal loops, and then intestinal obstruction (see). Surgical treatment - laparotomy is shown (see) followed by splenectomy (see).

Additional S. (from one to several hundred) is the most frequent anomaly in the development of this organ. Additional S. can be located at the gate of the main S. and along the splenic vessels, in the omentum, Douglas space. The identification of additional S. is possible using methods of radioisotope research. Clinically, this condition does not manifest itself. However, with a splenectomy carried out with to lay down. the purpose, for example, with autoimmune hemolytic anemia, lymphogranulomatosis, additional S. must be removed to prevent recurrence of the disease.

Damage

Submitted by SV Lobachev and OI Vinogradova, S.'s injuries occur on average in 22.2% of cases of all injuries of the abdominal organs. They are divided into open and closed. Open injuries are the result of wounds (gunshot, stab-cut, etc.), sometimes they can occur during surgery on the abdominal organs, for example, during operations on the stomach, pancreas, and colon.

Diagnosis of open injuries is usually not difficult - the localization of the entrance and exit holes of the wound, the direction of the wound channel, the nature of the wounding instrument matter.

Closed injuries of S. (blunt injury of S.) are possible upon impact in the region of the left hypochondrium, compression of the abdomen and lower parts of the chest, fracture of the ribs on the left as a result of a fall from a height, a blow by an air or water wave, a moving vehicle, etc. depends on the degree of S.'s mobility, the height of the diaphragm (when inhaling or exhaling), intra-abdominal pressure, the amount and degree of blood filling of the organ. With a sharp impact or compression, the S. bends in a horseshoe-like manner, its poles approach each other, as a result of which the capsule breaks along the diaphragmatic surface. On the visceral surface S.'s capsule bursts when striking in the area of \u200b\u200bthe IX-XI ribs, to-rye bend and put pressure on S. outside. When ribs are fractured, their fragments can damage S. and penetrate into its parenchyma. When falling from a height, with a sharp concussion, tears and tears of S.'s parenchyma are possible in the places of attachment of ligaments, adhesions and vascular pedicles, a rupture of the capsule in its weakest places.

In the diagnosis of closed injuries of S., the data of anamnesis, an assessment of the circumstances of the incident, the position of the injured and traumatic object, the nature and signs of damage on the victim's body (abrasions, bruises) are important.

The most characteristic symptoms of intra-abdominal bleeding (see) are dizziness, fainting, cold sweat. The pains are usually aching in nature, constant and accompanied by a feeling of bursting in the left hypochondrium, irradiate to the left shoulder and scapula, and intensify, as a rule, with a deep breath and cough. Nausea and vomiting are possible.

On examination, pallor of the skin and mucous membranes, dry and coated tongue are revealed; respiratory movements of the anterior abdominal wall, especially its left half, are weakened. The symptom of "vanka-stand up" is characteristic - the patient seeks to take a sitting position.

Palpation can determine the tension of the muscles of the anterior abdominal wall (see Muscle protection symptom) in the left abdomen and left hypochondrium. Shchetkin's symptom-<люмберга (см. Щеткина - Блюмберга симптом), как правило, слабо выражен. Положителен симптом Вейнерта - если исследующий охватывает обеими руками поясничную область пострадавшего с обеих сторон, то слева определяется резистентность тканей. Часто встречается симптом Куленкампффа - резкая болезненность при пальпации живота без напряжения мышц передней брюшной стенки. При перкуссии можно ошибочно определить увеличение границ С. в связи с наличием сгустков крови в ее области. Иногда наблюдается признак Питтса и Белленса - границы тупости, выявляемой при перкуссии передней брюшной стенки, перемещаются в правой половине живота при изменении положения тела больного и не изменяются слева, что связано со скоплением сгустков крови вокруг поврежденной С.

When a rectal examination (see) is determined by the soreness and overhang of the anterior wall of the rectum due to the accumulation of blood in the lower abdominal cavity. In this case, the patient may feel heaviness in the rectum and the urge to defecate. At a gynecological examination (see), the soreness of the posterior fornix of the vagina is noted, with puncture to-rogo often find blood. With rentgenol. a study reveals a change in the size and shape of S., signs of blood in the abdominal cavity (see. Hemoperitoneum), changes in neighboring organs. Subcapsular closed damages of S. are accompanied by an increase in all S. and its transverse size, an increase in the intensity of its shadow. The increase in these signs, found during repeated studies, precedes the rupture of the organ capsule. At rupture of S.'s capsule and internal bleeding it is possible by means of computed tomography to find directly the rupture line and indistinct blackout of the left subphrenic space, in which S.'s outlines, left kidney are lost. Darkening often extends to the left lateral canal of the abdominal cavity.

The so-called. S.'s secondary ruptures can be observed several hours or days after the injury as a result of damage to its parenchyma and the subsequent rupture of the capsule; thus there is a wedge, a picture of intra-abdominal bleeding.

With an unclear wedge, a picture that allows, however, to suspect S.'s damage, the most informative diagnostic method is laparoscopy, and if it is impossible or worsening of the patient's condition, diagnostic laparotomy (see).

In cases of difficult diagnosis of S.'s damage, observation of the patient is permissible within no more than two hours. Victims with concomitant injury and S.'s damage can enter the hospital in a state of shock (see) and acute blood loss (see), which requires resuscitation (see Resuscitation).

Treatment of open and closed S.'s injuries is, as a rule, operational. At open S.'s injuries it includes primary surgical treatment of a wound (see). Splenectomy is made more often (see), however, some surgeons in some cases carry out savings operations. For example, at single ruptures, small tears and cracks of S. with preserved blood circulation in the organ, suturing of S.'s wound is performed (splenorrhaphy); sutured with interrupted catgut sutures with hemming of a large omentum on the leg, which provides biol. tamponade (see) and conditions for the development of collateral circulation. After suturing S.'s wound and covering it with a large omentum, it is necessary to make sure that hemostasis is reliable, thoroughly dry the abdominal cavity and suture the operating wound. It is not necessary to tamp S.'s wound with gauze tampons, since after their removal secondary bleeding may occur. Gauze tampons can also promote suppuration with the subsequent development of peritonitis (see), and, in addition, after their removal, conditions are created for the eventration of the abdominal organs (see Eventration) and the formation of a postoperative hernia (see).

When the upper or lower pole of S. is torn off, it can be cut off, and the resulting defect can be sutured with mattress catgut sutures and covered with a large omentum on the leg in the same way as when closing a wound C. Wedge-shaped excision of a crushed section of S. is performed with single deep injuries with crushed edges. At the same time, the edges of the wound are economically excised and the defect is sutured with interrupted catgut sutures with suturing of a large omentum on the leg.

S.'s resection (splenotomy) can be performed in order to remove an unviable part of an organ, cut off with a cross section within healthy tissues. Mattress catgut sutures are applied to S.'s fabric, with a large omentum on the leg stitching to them.

The prognosis depends on the severity of the injury and the timeliness of surgical treatment.

Features of combat damage, staged treatment. Combat damage S. is divided into open and closed, to-rye can be single or multiple, isolated or combined.

Of the open injuries, gunshot wounds are more often observed - bullet and shrapnel (through, blind and tangential). Of all the wounds to the abdomen during the Great Patriotic War of 1941-1945. S.'s wounds were, according to I. M. Vorontsov, 5%, according to I. S. Belozor, - 7%. At the same time, shrapnel wounds prevailed over bullet wounds (70.8% and 29.2%, respectively), and blind wounds prevailed over through and tangential wounds. S.'s gunshot wounds are often accompanied by life-threatening bleeding. Closed injuries of S. are divided into two groups: with violation of the integrity of the capsule (superficial and deep cracks, marginal and central ruptures, crushing of the parenchyma and separation of part or the entire organ) and without violating the integrity of the capsule. With a safe S. capsule, formation of subcapsular superficial and deep (central) hematomas is possible, to-rye can cause secondary ruptures of S.'s capsule (two-stage rupture) with subsequent massive hemorrhage into the abdominal cavity.

S.'s injuries, combined with injuries of the left lower ribs, left lung, diaphragm, left kidney, liver and other internal organs, are among the extremely severe injuries.

The wounded, to-eye about S.'s damage, promptly performed surgical intervention, in the overwhelming majority of cases recover and after carrying out rehabilitation measures can return to duty.

Diseases

In patol. S.'s process is involved at many inf. diseases - typhoid and typhus (see. Typhoid fever, Epidemic typhus), sepsis (see), anthrax (see), inf. mononucleosis (see. Mononucleosis infectious), acute viral hepatitis (see. Hepatitis viral), inf. lymphocytosis (see Acute infectious lymphocytosis), cytomegaly (see), malaria (see), visceral leishmaniasis (see), tularemia (see), listeriosis (see), brucellosis (see), syphilis (see. ). The page is usually also amazed at systemic acute and hron. histiocytosis (see. Histiocytosis, Lettertera-Siwe's disease, Henda-Schüller's - Christian's disease).

Violation of the outflow of blood through the splenic vein leads to a progressive increase in C. With prolonged blockade of the outflow, bleeding from varicose-dilated collateral veins of the stomach, rectum, esophagus is possible. Acute obliteration of the portal vein trunk is accompanied by symptoms resembling intestinal obstruction. The diagnosis is established on the basis of a wedge, picture and splenoportography data (see). Operational treatment - the imposition of a splenorenal anastomosis (see), and with severe splenomegaly and cytopenia - splenectomy (see).

Thrombophlebitic splenomegaly, see Splenomegaly.

A splenic infarction can develop as a result of thromboembolism of the branches of the splenic artery or its local thrombosis in leukemia, collagen diseases, a number of infections, atherosclerosis, and also often in subendothelial infiltration of S.'s vessels with tumor cells in the terminal stage of hron. myeloid leukemia, lymphosarcoma, with tumor metastases. S.'s heart attacks are often observed with sickle-cell anemia (see), sometimes with Markiafava-Mikeli's disease (see. Hemolytic anemia) and periarteritis nodosa (see. Periarteritis nodosa). S.'s heart attacks with prolonged septic endocarditis (see) develop as a result of detachment of overlays on the aortic valve and embolism of S.'s vessels. Ischemic and hemorrhagic heart attacks of S. have a wedge-shaped or irregular shape (see. Heart attack). Multiple merging infarctions give S.'s tissue a spotted appearance - a "spotted" spleen. Often, at the same time, perisplenitis is noted (see) with the development of further fibrosis of the capsule and the picture of the so-called. glaze C. In this case, if the embolus is infected, an abscess develops in the infarction zone. In the terminal phase of uremia (see) in S. characteristic multiple white or yellowish color foci of necrosis appear. Similar changes can be found in generalized infections. There is no blockage of arterial vessels.

Wedge, the picture depends on the size of the heart attack. Diagnosis of small S.'s heart attacks is difficult due to scarcity a wedge. symptoms. With more extensive lesions as a result of the tension of the capsule, the development of perisplenitis, pains appear in the left hypochondrium, often radiating to the back and intensifying on inspiration. On the left, a pronounced phrenicus symptom is determined (see). In the perisplenitis zone, you can hear the rubbing noise of the peritoneum.

Treatment is aimed at eliminating the causes of the heart attack. Organization of S.'s infarction usually ends with the formation of a scar, occasionally a cyst is formed. At suppuration of S.'s infarction, splenectomy is shown.

Spleen abscess. Small, asymptomatic flowing abscesses of S. are often found at generalized not amenable to treatment inf. diseases. The group, which is most important in a wedge, in relation to the group, is represented by large isolated abscesses of S., to-rye can be observed at bacteremia against the background of endocarditis or salmonellosis; when infected with S.'s heart attacks, which are often observed in hemoglobinopathies, sickle-cell anemia; at infection of subcapsular hematomas, and also after to lay down. vascular embolization C. The reason for the development of an abscess C. Can serve as a breakthrough into it of a subphrenic abscess (see).

In a wedge, a picture, fever and pain in the upper left half of the abdomen and chest are usually observed (due to reactive pleurisy). The pain may radiate to the left shoulder. Quite often, muscle tension of the anterior abdominal wall and splenomegaly are detected. The friction noise of S.'s capsule is rarely heard. Radiography may reveal a darkening zone in the left upper quadrant of the abdomen, displacement of other organs, for example, the colon, kidney, stomach, displacement of the left dome of the diaphragm, as well as left-sided pleurisy.

When scanning S. and a liver abscesses to dia. 20-30 mm. S.'s abscess is also detected by ultrasound examination. The detection of nonvascularized tissue of an organ at arteriography against the background of the corresponding wedge, picture also testifies in favor of S.'s abscess. S.'s abscess can be complicated by hemorrhage into the abscess cavity, a breakthrough into the abdominal cavity, kidney, pleural cavity.

Treatment of S.'s abscess is usually carried out with broad-spectrum antibiotics. If antibiotic therapy is ineffective, splenectomy is performed.

The prognosis is determined, as a rule, by complications, such, for example, as the development of peritonitis (see) when S.'s abscess breaks out into the abdominal cavity or pleurisy (see) - when it breaks into the pleural cavity.

Spleen tuberculosis. More often S. is involved in the process with general miliary tuberculosis. ’Infection occurs both hematogenous and lymphogenous. Macroscopically, on the surface of the enlarged S.'s section, multiple gray or pale yellow millet tubercles sharply demarcated from the surrounding tissue are visible. Tuberculomas in S. are rare. The tubercles can be located both in the red and in the white pulp. They consist of epithelioid cells, Pirogov-Langhans cells, as well as plasma and lymphoid cells. In punctate, single epithelioid cells are usually detected; Pirogov-Langhans cells in punctate are rare (see. Tuberculosis).

Isolated S. tuberculosis often proceeds with a meager wedge, symptomatology. Splenomegaly of varying severity, ascites, low-grade fever are most often noted. In the blood, leukopenia (sometimes leukocytosis), lymphopenia are found, in some cases - neutropenia, thrombocytopenia (as well as thrombocytosis), anemia. Sometimes aplastic syndrome develops, with cut it is necessary to exclude tuberculous damage to the bone marrow. With rentgenol. examination of the abdominal cavity can reveal petrified foci in the area C.

Diagnosis of S.'s tuberculosis is difficult if there are no signs of fresh or previously existing tuberculosis of other organs. The diagnosis is based on the results of cytol. researches of punctate S., however, the only reliable criterion is the detection of mycobacteria of tuberculosis in a smear or sowing them from punctate. It should be borne in mind that with concomitant S.'s amyloidosis, its repeated punctures may turn out to be uninformative. If S.'s tuberculosis is suspected, but in the absence of reliable evidence, specific tuberculostatic therapy ex juvantibus is performed.

Spleen syphilis. At acquired primary syphilis S. has the usual sizes; with congenital and acquired secondary syphilis, it is increased due to hyperplastic changes in the red pulp; at S.'s tertiary syphilis hl is increased (sometimes significantly). arr. due to syphilitic cirrhosis of the liver, in S. growths of specific granulation tissue can come to light. Treatment is directed at the underlying disease (see Hepatolienal Syndrome, Syphilis).

Echinococcus of the spleen. Its hydatidous form (unicameral echinococcus) is more common, recognition of a cut presents well-known difficulties. In diagnostics, an important role is played by ultrasound (see. Ultrasound diagnostics) and computed tomography (see. Computed tomography). In some cases, rupture of the echinococcus bladder and seeding with daughter scolexes of the abdominal cavity is possible (see. Echinococcosis).

Spontaneous rupture of the spleen occurs at inf. mononucleosis, lymphosarcoma, myeloid leukemia. The cause of its development is the disintegration of a tumor, S.'s rapid increase and hyperextension of its capsule with splenomegaly. Wedge. the picture is characterized by sudden severe pain in the left hypochondrium, signs of irritation of the peritoneum, rapidly growing anemia.

Treatment is prompt. As a rule, splenectomy is performed, but recently, especially in children, partial resection and suturing of S.'s rupture (splenorrhaphy) have been used more often.

The prognosis depends on the underlying disease.

Tumors

S.'s primary tumors, both benign and malignant, are rare. From benign tumors in S. hemangioma (see), lymphangioma (see), fibroma (see), hamartoma (see) are found. Hemangioma can be single or multiple, of various sizes (from a small nodule to a large tumor with a diameter of 50-100 mm and more); it is located deep in the tissue and on the surface, has a cavernous or capillary structure. At thin-walled superficial hemangioma rupture of S.'s capsule with bleeding into the abdominal cavity is possible. Sometimes hemorrhages, thrombosis occur in the tumor, its organization is noted with deposits of calcium salts.

Lymphangioma occurs in the form of separate nodes, as well as conglomerates of cysts with transparent or turbid contents, to-rye penetrate S. and lead to an increase in its size. S.'s fibroma looks like a single small node and does not appear clinically. Hamartoma (splenoma), like fibroma, in most cases is found only at autopsy. It is small in size, usually located deep in the tissue of S., often encapsulated, built like the tissue of S. itself, but differs from it in the ratio of white and red pulp, in connection with which pulp and follicular forms are distinguished.

Among primary malignant neoplasms of S. in the first place are lymphosarcomas (see). Tumor growths can be nodular or diffuse; they consist of atypical lymphoid cells and cause a gradual increase in S.'s sizes. S.'s primary lymphosarcoma is differentiated with its secondary involvement in the process at other primary localizations of lymphosarcoma, hron. lymphocytic leukemia (see. Leukemias) on the basis of a wedge, picture, changes in blood and bone marrow. At S.'s primary lymphosarcoma, in contrast to hron. lympho-leukemia, low leukocytosis and lymphocytosis are observed.

Reticulosarcoma is less common (see), isolated cases of angiosarcoma (see) and fibrosarcoma (see) of the spleen are described.

At the beginning of development of a tumor of S. usually do not give a wedge, manifestations. Only in the process of growth of tumor nodes and an increase in the organ as a whole, patients feel heaviness, dull pain in the left hypochondrium.

Metastases in S. of cancer, melanoma, chorionepithelioma and other malignant tumors are rare.

Combined treatment of S.'s tumors (surgery and chemotherapy).

When indications for surgical intervention for this or that pathology S. use various approaches, for example, in case of S.'s injuries use the upper median, paramedial incisions or traisrectal incision, which can be extended downward, allowing to revise the abdominal organs in this area (see . Laparotomy). In case of combined damage with suspected injury to the organs of the thoracic cavity, a thoracoabdominal approach is indicated. For removal of S., which has normal dimensions, paracostal access is shown without dissection of the rectus abdominis muscle.

Bibliography:

Anatomy, physiology - Parin V.V.Selected works, vol. 1, p. 46, M., 1974; Physiology of the blood system, Physiology of erythropoiesis, ed. V.N. Chernigovsky, p. 256, L., 1979; Folkov B. and Neil E. Blood circulation, trans. from English, M., 1976; Chkholaria ND Blood vessels of the spleen, Tbilisi, 1965; Embryogenesis of human organs, ed. V. B. Suchkova, p. 123, Volgograd, 1974; Herrath E. Bau und Funktion der normalen Milz, B. 1958; Irino S., Murakami T. a. F and jiet a T. Open circulation in the human spleen, Arch, histol. jap., v. 40, p. 297, 1977; Miller J. F. a. o. Interaction between lymphocytes in immune responses, Cell. Immunol., V. 2, p. 469, 1971.

Pathology - Abrikosov A.I. Private pathological anatomy, century. 1, p. 74, M. - L., 1947; Akimov V. I. and Kantor 3. M. Closed trauma of the abdomen, Kiev, 1963; Almazov V.A. and others. Leukopenia, p. 157, L., 1981; Askerkhanov R.P. About surgical approaches to the liver and spleen, Vestn. hir., t. 114, no. 4, p. 36, 1975; Bart I. Spleenka, trans. from Hungarian., Budapest, 1976; Berkutov A.N. and Zakurdaev V.E.Diagnosis of abdominal injuries, Voen.-med. zhurn., no. 12, p. 26, 1972; Borodin IF and Orlyanskaya VF Some questions of diagnosis and treatment of closed injuries of the spleen, Wedge, hir., No. 4, p. 29, 1980; Bugulov GK Subcutaneous injuries of the spleen, in the same place, p. 54; Geller LI Physiology and pathology of the spleen, M., 1964, bibliogr .; Glants RM and Rozhinsky MM Savings surgery of injuries of the spleen, M., 1973, bibliogr .; Gorshkov S. 3., Volkov V. S. and Kartashova T. I. Closed injuries of the spleen, Owls. med., no. 3, p. 28, 1978; Dymshits RA, etc. Spleen and erythropoiesis, Usp. fiziol. Sciences, vol. 4, no. 3, p. FROM, 1973; Zverkova AS About the role of the spleen in tumors and leukemias, Doctor, case, No. 7, p. 80, 1975; And in and sh-to about L. M. Closed trauma of the spleen, in the book: Traumatism. and will restore, hir. children age, ed. G. Ya. Epstein, p. 199, L., 1964; Karr Y. et al. Lymphoreticular diseases, trans. from English., M., 1980; Kassirsky I.A. and Alekseev G.A. Clinical hematology, p. 736, M., 1970; To and sh to about in-with to and y A.N., Tyut and L.A. N. and Che-emis and V.M. N. X-ray diagnostics of closed injuries and wounds of the abdominal organs, Military medical zhurn., No. 2, p. 22, 1982; To about m and s-sarenko V.P. Splenin, Kiev, 1961; Koretskaya T.I., Moskaleva G.P. and Gudim V.I., The role of the spleen in the regulation of erythropoiesis, Pat. fiziol. and experiment. ter., no. 4, p. 67, 1975; Lindenbraten LD and Naumov LB Methods of X-ray examination of organs and systems of a person, Tashkent, 1976; Meshkova VN Subcutaneous ruptures of the spleen based on materials from the surgical clinics of the Institute named after V.N. Sklifosovsky (from 1945 to 1958), Proceedings of the Institute of. Sklifosovsky, vol. 6, p. 70, M., 1961; The experience of Soviet medicine in the Great Patriotic War 1941 -1945, v. 12, p. 233, 507, M., 1949; Pathological anatomical diagnostics of human tumors, ed. N.A.Kraevsky, etc., M., 1982; Guide to Hematology, ed. A.I. Vorobyov and Yu.I. Lorie, p. 47, etc., M., 1979; Sikharulidze TS and Keleshe in and LF Damage to the spleen with combined trauma of the organs of the chest and abdominal cavities, Vestn. hir., t. 117, no. 10, p. 89, 1976; At t to and V. V. N. and Pakalns A. K. Diagnostics and treatment of closed injuries of the spleen, in the same place, t. 119, No. 10, p. 115, 1977; X e N and Mr. K., etc. Scanning of the spleen, Honey. radiol., vol. I, no. 11, p. 18, 1966; Surgical treatment of diseases of the blood system, ed. O.K. Gavrilova and D.M. Grozdova, M., 1981; Shcherb and t e N to about MK and Beresnev EA. Emergency X-ray diagnostics of acute diseases and injuries of the abdominal organs, M., 1977; F g e s e n O. u., Kretschmer H. Beziehungen zwischen Milz und Hamopoese, Z. ges. exp. Med., Bd 154, S. 36, 1971; G e d d e s A. K. a. Moore S. Acute (infantile) Gaucher's disease, J. Pediat., Y. 43, p. 61, 1953, bibliogr .; Die Milz, hrsg. v. K. Lennert u. D. Harms, B.- N. Y. 1970; Pathology, ed. by W. A. \u200b\u200bD. Anderson a. J. M. Kissane, v. 2, p. 1489, St Louis, 1977; Physiologie und Pathologie der Milz, hrsg. v. A. Hittmair, Basel-N. Y. 1955; R i nge 1 J. Infantilni forma Gaucherovy nemoci, Voj. zdra-votn. Listy, s. 541, 1954, bibliogr .; S o-d e m a n W. A. \u200b\u200ba. W. A. \u200b\u200bPathologie physiology, mechanisms, Philadelphia, 1974; The spleen, ed. by A. Blaus-tein, p. 45, N. Y. - L., 1963; S t and t-t e H. J. Hypersplenismus und Milzstruk-tur, Stuttgart, 1974; Williams W. J. a. o. Hematology, p. 611 a. o., N. Y. a. o., 1977.

V. G. Savchenko; I.I.Deryabin, A.I. Chalganov (military), L.M. Golber, G.I. Kositsky (normal and pathological physiology), G.A. operations), L.K.Semenova (an., hist., emb.), G.P. Filimonov (rent.), M.P. Khokhlova (pat.an.), I. Ya. Yakovleva (onc.) ...

Lymph node functions:

the hematopoietic function is antigen-dependent differentiation of lymphocytes;

barrier-protective function - nonspecific protection against antigens consists in their phagocytosis from the lymph by numerous macrophages and "coastal" cells; a specific protective function is the implementation of specific immune responses;

drainage function, the lymph nodes collect lymph from the vessels coming from the tissues. If this function is impaired, peripheral edema is observed;

the function of depositing lymph, normally a certain amount of lymph is retained in the lymph node and is turned off from the lymph flow;

metabolic function - participation in the metabolism - proteins, fats, carbohydrates and other substances.

Structure

The total number of lymph nodes in the human body is approximately 1000, which is about 1% of body weight. Their size is on average 0.5-1 cm. The lymph nodes are reniform, lie regionally in relation to the organs, in groups. From the convex surface of the lymph node, the carrying lymph vessels enter it, and from the opposite side, which is called the gate, the outgoing lymph vessels exit. In addition, the artery and nerves enter the gate of the lymph node, and the veins exit.

Lymph nodes are parenchymal zonal organs. They include the following structural and functional components:

trabeculae extending from the capsule, anastomosed with each other, they form a lymph node framework;

reticular tissue that fills the entire space between the capsule and trabeculae;

in the lymph node, two zones are distinguished: the peripheral cortical substance, and the central one - the medulla;

between the cortical and medulla - the paracortical zone or deep cortex;

sinuses - a set of lymph vessels through which lymph moves. The sequence of passage of lymph through the lymph node and the location of the sinuses is as follows: bringing lymph vessels - marginal or subcapsular sinus - intermediate cortical sinuses - intermediate cerebral sinuses - portal sinus - outflowing lymphatic vessel in the area of \u200b\u200bthe gate.

^ The cortical substance of the lymph node is represented by an accumulation of lymphoid tissue, which contains lymphoid follicles, or nodules, and an interfollicular plateau. Lymphoid nodules are round, up to 1 mm in size. Distinguish between primary without a reactive center, and secondary lymphoid follicles that have a reactive center (center of reproduction, light center).



Primary follicles are composed mainly of small "naive" B-lymphocytes associated with reticular and follicular dendritic cells. When the antigen enters, blast transformation of "naive" B-lymphocytes occurs, and secondary nodules are formed. They consist of a breeding center and a crown, or mantle, at the periphery. The crown is formed by small memory B-lymphocytes, as well as small "naive" lymphocytes of bone marrow origin. The reactive center at the height of the immune response is divided into dark and light zones. The dark area faces the paracortical area. Here, cells divide mitotically, move to a light, more peripheral zone, where more mature, migrating cells are located. The precursors of plasma cells leave the follicle through the lateral zones of the crown into the interfollicular plateau, and then move through the paracortical zone into the medulla (into the pulp), where they mature into plasma cells.

^ The paracortical zone or the zone of the deep cortex is located at the border of the cortical and medulla. It is the thymus-dependent zone (T-zone) of the lymph node. Contains mainly T-lymphocytes, however, plasmocytes migrating into the pulp cords of the medulla at different stages of development are found here. The entire paracortical zone can be divided into separate units. Each unit consists of a central and peripheral part. Blast transformation and multiplication of T-lymphocytes takes place in the center. On the periphery, there are postcapillary veins with high epithelium. Through them, the migration of lymphocytes from the blood to the lymph node and, possibly, back occurs.

^ The medulla consists of two structural and functional components: cerebral and pulp cords and cerebral intermediate sinuses. The cords are B-dependent. Here, the maturation of the precursors of plasmacytes migrated from the cortex into plasma cells occurs. Plasmocytes accumulating in the brain cords during the immune response secrete antibodies in the lymph. Outside, the cerebral sinuses are adjacent to the cerebral cords.

^ The structure of the lymph node sinuses

All lymph node sinuses are slit-like spaces that are lined with endothelium capable of phagocytosis. In addition to endothelial cells, rethelial cells are involved in the formation of the wall of the lymphatic sinuses. They have a process shape. In this case, the processes intersect all spaces of the sinus and, on the opposite side of it, form extensions in the form of areas, which, along with the littoral cells, form an intermittent lining of the sinuses. The basement membrane is absent in the lining of the sinuses. The processes of rethelial cells form a three-dimensional network that slows down the flow of lymph, which contributes to its more complete cleansing by macrophages. The network is also formed by reticular fibers running in different directions. There are many free macrophages and lymphocytes in the sinuses, which can be fixed in the network.

^ Blood supply to the lymph node

The blood vessels enter the gates of the node. Capillaries depart from the arteries into the capsule and trabeculae, as well as to the nodules. They have superficial and deep capillary networks. The capillary networks continue into the high-endothelial venules and then into the veins that exit through the gate of the node. Normally, blood never flows to the sinuses. With inflammation, trauma and other pathological conditions, a similar phenomenon is possible.

( The spleen is a peripheral organ of the hematopoietic and immune systems. In addition to performing hematopoietic and protective functions, it participates in the death of erythrocytes, produces substances that inhibit erythropoiesis, and deposits blood. Spleen development. The spleen is laid on the 5th week of embryogenesis by the formation of a dense accumulation of mesenchyme. The latter differentiates into reticular tissue, grows with blood vessels, and is populated with hematopoietic stem cells. At the 5th month of embryogenesis, the processes of myelopoiesis are noted in the spleen, which by the time of birth are replaced by lymphocytopoiesis. The structure of the spleen. The spleen is covered from the outside with a capsule consisting of mesothelium, fibrous connective tissue and smooth myocytes. Crossbeams - trabeculae, anastomosed with each other, extend inward from the capsule. They also have fibrous structures and smooth myocytes. The capsule and trabeculae form the spleen's musculoskeletal system. It makes up 5-7% of the volume of this organ. Between the trabeculae is the pulp (pulp) of the spleen, the basis of which is the reticular tissue. Hematopoietic stem cells are found in the spleen in an amount of approximately 3.5 in 105 cells. Distinguish between white and red pulp of the spleen. The white pulp of the spleen is a collection of lymphoid tissue that is formed by lymph nodules (B-dependent zones) and lymphatic periarterial sheaths (T-dependent zones). When macroscopically examining sections of the spleen, the white pulp looks like light gray rounded formations that make up 1/5 of the organ and are diffusely distributed over the section area. The lymphatic periarterial sheath surrounds the artery after it leaves the trabecula. It contains antigen-presenting (dendritic) cells, reticular cells, lymphocytes (mainly T-helpers), macrophages, and plasma cells. Primary lymphatic nodules are similar in structure to those in the lymph nodes. This is a rounded formation in the form of an accumulation of small B-lymphocytes that have undergone antigen-independent differentiation in the bone marrow, which interact with reticular and dendritic cells. A secondary nodule with a germinal center and a crown occurs with antigenic stimulation and the presence of T-helpers. In the corona there are B-lymphocytes, macrophages, reticular cells, and in the germinal center - B-lymphocytes at different stages of proliferation and differentiation into plasma cells, T-helpers, dendritic cells and macrophages. The marginal, or marginal, zone of nodules is surrounded by sinusoidal capillaries, the wall of which is permeated with slit-like pores. In this zone, T-lymphocytes migrate along the hemocapillaries from the periarterial zone and enter the sinusoidal capillaries. Red pulp is a collection of various tissue and cellular structures that make up the entire remaining mass of the spleen, with the exception of the capsule, trabeculae and white pulp. Its main structural components are reticular tissue with blood cells, as well as sinusoidal blood vessels that form bizarre labyrinths due to branching and anastomoses. In the reticular tissue of the red pulp, two types of reticular cells are distinguished - poorly differentiated and phagocytic cells, in the cytoplasm of which there are many phagosomes and lysosomes. Between the reticular cells are blood cells - erythrocytes, granular and non-granular leukocytes. Some of the erythrocytes are in a state of degeneration or complete decay. Such erythrocytes are phagocytosed by macrophages, which then transfer the iron-containing part of hemoglobin to the red bone marrow for erythrocytopoiesis. The sinuses in the red pulp of the spleen represent part of the vascular bed, which originates from the splenic artery. This is followed by segmental, trabecular and pulp arteries. Within the lymphoid nodules, the pulp arteries are called central. Then come brush arterioles, arterial hemocapillaries, venous sinuses, pulpal venules and veins, trabecular veins, etc. In the wall of the brush arterioles there are thickenings called sleeves, sleeves or ellipsoids. Muscle elements are missing here. Thin myofilaments were found in the endothelial cells lining the lumen of the sleeves. The basement membrane is very porous. The bulk of the thickened sleeves are reticular cells with high phagocytic activity. Arterial sleeves are believed to be involved in filtering and detoxifying arterial blood flowing through the spleen. The venous sinuses form a significant part of the red pulp. Their diameter is 12-40 microns. The wall of the sinuses is lined with endothelial cells, between which there are intercellular gaps up to 2 microns in size. They lie on a discontinuous basement membrane containing a large number of holes with a diameter of 2-6 microns. In some places, the pores in the basement membrane coincide with the intercellular clefts of the endothelium. Thanks to this, a direct communication is established between the lumen of the sinus and the reticular tissue of the red pulp, and blood from the sinus can go out into the surrounding reticular stroma. Muscle sphincters in the sinus wall at the site of their transition to the veins are of great importance for the regulation of blood flow through the venous sinuses. There are also sphincters in arterial capillaries. The contraction of these two types of muscle sphincters regulates the blood flow to the sinuses. The outflow of blood from the microcirculatory bed of the spleen occurs through the system of veins of increasing caliber. A feature of trabecular veins is the absence of a muscle layer in their wall and fusion of the outer shell with the connective tissue of the trabeculae. As a result, the trabecular veins are constantly gaping, which facilitates the outflow of blood. Age-related changes in the spleen. With age, the atrophy of the white and red pulp is observed in the spleen, the number of lymphatic follicles decreases, the connective tissue stroma of the organ grows. Spleen reactivity and regeneration. The histological features of the structure of the spleen, its blood supply, the presence in it of a large number of large dilated sinusoidal capillaries, the absence of a muscular membrane in the trabecular veins should be taken into account in combat trauma. When the spleen is damaged, many vessels are in a gaping state, and the bleeding does not stop spontaneously. These circumstances can determine the tactics of surgical interventions. The spleen tissues are very sensitive to the action of penetrating radiation, to intoxication and infections. At the same time, they have a high regenerative capacity. Recovery of the spleen after injury occurs within 3-4 weeks due to the proliferation of cells of the reticular tissue and the formation of foci of lymphoid hematopoiesis. The hematopoietic and immune systems are extremely sensitive to various damaging influences. Under the action of extreme factors, severe injuries and intoxications, significant changes occur in the organs. In the bone marrow, the number of hematopoietic stem cells decreases, the lymphoid organs (thymus, spleen, lymph nodes) are emptied, the cooperation of T- and B-lymphocytes is inhibited, the helper and killer properties of T-lymphocytes change, the differentiation of B-lymphocytes is impaired.

The spleen lies along the blood vessels and is an organ that varies greatly in size. From the surface, the spleen is covered with a connective tissue capsule, which reaches its greatest thickness in the area of \u200b\u200bthe gate. The capsule contains smooth muscle cells, the number of which sharply increases in some representatives of the living world, including horses, predators, etc. The surface of the capsule is covered with mesothelium. All this creates a completely movable capsule structure. Numerous layers of loose unformed connective tissue - trabeculae depart from the capsule. These trabeculae contain numerous blood vessels, smooth myocytes. Trabeculae can anastomose with each other. The spleen stroma is formed by the reticular tissue. Distinguish between white and red pulp, the basis of which is the reticular tissue.

White pulprepresented by numerous lymphoid follicles scattered throughout the spleen. The white pulp makes up about one fifth of the mass of the spleen. The lymphoid follicles of the spleen are built from lymphoid tissue and are called malpighian bodies. The lymphoid follicles of the spleen differ in structure from the follicles of the lymph node. Each lymphoid follicle of the spleen contains a central artery, which, due to the corkscrew motion, can enter the cut several times. In the Malpighian body, 4 zones are distinguished, including the periarterial zone, the light center, the mantle zone, and the marginal zone. The light center (reactive center, multiplication center) and the mantle zone represent the B-zone, in which the antigen-dependent stage of B-lymphocyte maturation occurs. This zone is characterized by a specific microenvironment, including type 1 dendritic cells, macrophages, and a small number of T-lymphocytes. In the light center, blast transformation and multiplication of B-lymphocytes occurs, and in the mantle zone there is a cooperation of T- and B-lymphocytes and the accumulation of memory B-cells. The periarterial zone is the T-zone. Here, the antigen-dependent stage of maturation of T-lymphocytes occurs under the influence of a specific microenvironment (type 2 dendritic cells, macrophages, a small number of B-lymphocytes). This zone increases significantly with a cell-type immune response. The marginal zone is common for T and B lymphocytes. The marginal (marginal) sinuses are adjacent to it. In the marginal zone, cooperative interactions of T and B lymphocytes occur. In addition, T- and B-lymphocytes, as well as antigens, which are captured by macrophages, enter the white pulp through this zone. Plasma cells migrate through this zone into the red pulp. The cellular composition of this zone is represented by lymphocytes (mainly B-lymphocytes and plasma cell precursors), macrophages and reticular cells.

Red pulp represented by numerous blood vessels, including venous sinuses. Venous sinuses have a diameter of up to 40 microns and in structure resemble sinusoidal capillaries (lined with endothelium, which lies on an interrupted basement membrane). The red pulp also includes splenic cords containing erythrocytes, granular and non-granular leukocytes, plasmocytes at different stages of development, that is, destruction of old erythrocytes, maturation of plasma cells occurs here. It was found that blood cells from the capillaries enter the splenic cords, and then migrate through the gaps between the endothelial cells of the venous sinus wall into its lumen. This is facilitated by increased blood pressure due to its constant inflow and periodic contractions of smooth muscle cell bundles in the wall of the trabecular arteries and the spleen capsule.

The spleen is characterized by an abundant blood supply. About 800 ml of blood flows through the spleen every minute. The splenic artery enters the gate of the spleen, which splits into numerous trabecular arteries, the latter pass into the pulp arteries, in the adventitia of which there are accumulations of lymphoid tissue (lymphoid sheaths) belonging to the white pulp. The pulp artery enters the lymphoid follicle, acquires a corkscrew-like course and is called the central artery. In the malpighian follicle, the central artery provides numerous capillaries for nourishing its tissues. Coming out of the follicle, the central artery splits into many branches, which are called tassel arteries. The cystic arteries are surrounded by periarterial muffs composed of reticular cells, macrophages, and lymphocytes. At the ends of the brush arteries, sphincters are formed, consisting of clusters and reticular cells. The cystic arteries pass into capillaries, from which blood enters the venous sinuses. Sphincters are located at the ends of the venous sinuses. From the venous sinuses, blood enters the pulp veins, trabecular veins, and splenic veins. Trabecular veins and venous sinuses do not have a muscular membrane, therefore, if damaged, the vessels do not collapse, which leads to the development of parenchymal bleeding.

Distinguish open and closed blood supply spleen. When awake, blood flows in the spleen, without leaving the red pulp (closed blood supply). In a state of rest and rest, part of the blood is deposited, including in the venous sinuses, which creates conditions for the release of part of the blood into the red pulp, where the death of old erythrocytes occurs.

The spleen regenerates well both under physiological conditions and after injury. Under the experimental conditions, the possibility of complete restoration of the spleen was shown even after removal of 80-90% of its volume. However, the complete restoration of the shape and size of the spleen does not occur.

Spleen functions.

1. Hematopoietic function: the formation of T- and B-lymphocytes.

2. Immune function: due to lymphocytes, it participates in the regulation of the cellular and humoral immune response.

3.Depot of blood: due to the double system of sphincters.

4. Here the death of most red blood cells occurs.

6.Depot of blood stem cells.

B-lymphocytopoiesis.

In the bone marrow, from the progenitor cell of B-lymphocytes, B-lymphoblasts, B-prolymphocytes and B-lymphocytes are sequentially formed as a result of proliferation and differentiation. The formed B-lymphocytes from the bone marrow with the blood flow enter the peripheral organs of hematopoiesis, where they populate the B-zones. Under the influence of antigens, the antigen-dependent stage of B-lymphocyte formation is carried out here. In this case, blast forms are formed, and then plasma cells that produce antibodies.

T-lymphocytopoiesis.

Progenitor cells of T-lymphocytes and T-lymphoblasts from the red bone marrow enter the subcapsular zone of the thymus. In the thymus, proliferation and differentiation of T-lymphocytes occurs. In this case, the formation of T-prolymphocytes and T-lymphocytes occurs sequentially. The formed T-lymphocytes with the blood flow then enter the peripheral organs of hematopoiesis, where they populate the T-zones. An antigen-dependent stage of T-lymphocytopoiesis occurs in the T-zones.

Morphological features of the spleen in children

The spleen begins to function as a hematopoietic organ even in the embryonic period. However, the spleen of a newborn child has a number of significant morphological features.

First of all, a newborn child in the first years of life, as a rule, has several accessory spleens ranging in size from the head of a needle to the size of an average apple. In a newborn baby, the weight of the spleen is 8 - 12 grams. After the birth of the child, an increase in the mass of the spleen is noted, as a result of which by the age of 5 years this figure reaches 35 - 40 g, and by the period of puberty it is already 80 - 90 g. The capsule of the spleen of a newborn child is thin and built of very loose connective tissue containing single smooth muscle cells. Single weakly expressed, thin layers of connective tissue - trabeculae depart from the capsule. After birth, the spleen capsule gradually thickens, the number of elastic and muscle elements in it increases, and the trabeculae become wider. Finally, the capsule is formed by the age of 7 to 10 years, and the trabeculae by the age of 18 to 20.

The spleen of a newborn child contains few, immature lymphoid follicles, most of which are small with indistinct contours. Light centers in the lymphoid follicles are formed only by the end of the first year of a child's life. In 85% of newborns, the spleen has a lobular structure. After birth, the lobular nature of the structure of the spleen is gradually erased, an increase in the number of lymphoid follicles with pronounced light centers is noted. This process lasts up to 18 - 20 years.