Each of us has experienced inflammation of one kind or another. And if its serious forms, such as pneumonia or colitis, happen in special cases, then such minor troubles as a cut or abrasion are commonplace. Many do not pay attention to them at all. But even the most minor injuries can cause exudative inflammation. In fact, this is such a state of the affected area, in which specific fluids collect in it, and then seep through the walls of the capillaries to the outside. This process is quite complex, based on the laws of hydrodynamics and can lead to complications in the course of the disease. In this article, we will analyze in detail what causes exudative inflammation causes. We will also consider the types (outcomes for each of them are unequal) of this kind of inflammatory processes, and along the way we will explain what they depend on, how they proceed, what treatment they require.

Inflammation - good or bad?

Many will say that, of course, inflammation is evil, because it is an integral part of almost any disease and brings suffering to a person. But in fact, in the process of evolution, our body for many years developed the mechanisms of inflammatory processes in itself so that they would help to survive the harmful effects, which are called irritants in medicine. They can be viruses, bacteria, any skin wounds, chemicals (for example, poisons, toxins), adverse environmental factors. Exudative inflammation should protect us from the pathological activity of all these irritants. What it is? If you do not go into details, it is quite simple to explain it. Any irritant, once in the human body, damages its cells. This is called an alteration. It starts the inflammatory process. Its symptoms, depending on the type of irritant and the place of its introduction, may differ. Among the common ones are:

• rise in temperature either throughout the body, or only in the damaged area;
• swelling of the affected area;
• soreness;
• redness of the injured area.

These are the main signs by which you can understand that exudative inflammation has already begun. The photo above clearly demonstrates the manifestation of symptoms - redness, swelling.

On some vessels, fluids (exudate) begin to accumulate. When they penetrate through the walls of the capillaries into the intercellular space, the inflammation becomes exudative. At first glance, this seems to be an aggravation of the problem. But in fact, the release of exudate, or, as doctors say, exudation, is also needed. Thanks to it, very important substances enter the tissues from the capillaries - immunoglobulins, kinins, plasma enzymes, leukocytes, which immediately rush to the focus of inflammation in order to eliminate irritants and heal damaged areas there.

Exudation process

Explaining what exudative inflammation is, pathological anatomy (the discipline that studies pathological processes) pays special attention to the process of exudation, the “culprit” of this type of inflammation. It consists of three stages:

1. There has been an alteration. She launched special organic compounds - (kinins, histamines, serotonins, lymphokines and others). Under their action, the channels of microvessels began to expand, and as a result, the permeability of the walls of the vessels increased.
2. In wider sections of the channels, the blood flow began to move more intensively. There was a so-called hyperemia, which, in turn, led to an increase in blood vessels (hydrodynamic) pressure.
3. Under the pressure of fluid from microvessels, exudate began to seep into the tissues through enlarged interendothelial gaps and pores, sometimes reaching the size of tubules. The particles that make it up moved to the focus of inflammation.

Types of exudates

It is more correct to call the exudate fluids leaving the vessels into the tissues, and the same fluids released in the cavity - effusion. But in medicine, these two concepts are often combined. The exudative type of inflammation is determined by the composition of the secret, which can be:

• serous;
• fibrous;
• purulent;
• putrid;
• hemorrhagic;
• slimy;
• chile;
• chyle-like;
• pseudochylous;
• cholesterol;
• neutrophilic;
• eosinophilic;
• lymphocytic;
• mononuclear;
• mixed.

Let us consider in more detail the most common types of exudative inflammation, its causes and symptoms.

Form of serous exudative inflammation

In the human body, the peritoneum, pleura, and pericardium are covered with serous membranes, so named from the Latin word "serum", which means "serum", because they produce and absorb fluids that resemble or are formed from blood serum. The serous membranes in the normal state are smooth, almost transparent, very elastic. When exudative inflammation begins, they become rough and cloudy, and serous exudate appears in tissues and organs. It contains proteins (more than 2%), lymphocytes, leukocytes, epithelial cells.

The causes of exudative inflammation can be:

• injuries of various etiologies (violations of the integrity of the skin, burns, insect bites, frostbite);
• intoxication;
• viral and bacterial infections (tuberculosis, meningitis, herpes, chickenpox and others);
• allergy.

Serous exudate helps to remove toxins and irritants from the focus of inflammation. Along with its positive features, there are also negative ones. So, if serous exudative inflammation occurs, respiratory failure may develop, in the pericardium - heart failure, in the meninges - cerebral edema, in the kidneys - renal failure, in the skin under the epidermis - exfoliation of it from the dermis and the formation of serous blisters. Each disease has its own symptoms. Of the general ones, one can distinguish a rise in temperature and pain. Despite the seemingly very dangerous pathology, the prognosis in the vast majority of cases is favorable, since the exudate resolves without leaving traces, and the serous membranes are restored.

fibrous inflammation

As noted above, all types of exudative inflammation are determined by the composition of the secret released from the microvessels. So, fibrous exudate is obtained when, under the influence of inflammatory stimuli (trauma, infection), an increased amount of fibrinogen protein is formed. Normally, an adult should have 2-4 g / l. In damaged tissues, this substance turns into the same protein, which has a fibrous structure and forms the basis of blood clots. In addition, in the fibrous exudate there are leukocytes, macrophages, monocytes. At some stage of inflammation, necrosis of tissues affected by the irritant develops. They are impregnated with fibrous exudate, as a result of which a fibrous film forms on their surface. Microbes actively develop under it, which complicates the course of the disease. Depending on the localization of the film and on its features, diphtheria and croupous fibrous exudative inflammation are distinguished. Pathological anatomy describes their differences as follows:

1. Diphtheria inflammation can occur in those organs that are covered with a multilayer membrane - in the throat, uterus, vagina, bladder, and gastrointestinal organs. In this case, a thick fibrous film is formed, as if ingrown into the shell of the organs. Therefore, it is difficult to remove, and leaves ulcers behind. Over time, they heal, but scars may remain. There is another evil - under this film, microbes multiply most actively, as a result of which the patient has a high intoxication with the products of their vital activity. The most famous disease of this type of inflammation is diphtheria.
2. Croupous inflammation is formed on mucous organs covered with a single layer: in the bronchi, peritoneum, trachea, pericardium. In this case, the fibrous film turns out to be thin, easily removed, without significant defects in the mucous membranes. However, in some cases, it can create serious problems, for example, with inflammation of the trachea, it can make it difficult for air to enter the lungs.

Exudative purulent inflammation

This pathology is observed when the exudate is pus - a viscous greenish-yellow mass, in most cases having a characteristic odor. Its composition is approximately the following: leukocytes, most of which are destroyed, albumins, fibrin threads, enzymes of microbial origin, cholesterol, fats, DNA fragments, lecithin, globulins. These substances form purulent serum. In addition to it, purulent exudate contains tissue detritus, live and / or degenerated microorganisms, purulent bodies. Purulent inflammation can occur in any organs. The "culprits" of suppuration are most often pyogenic bacteria (various cocci, E. coli, Proteus), as well as Candida, Shigella, Salmonella, Brucella. Forms of exudative inflammation of a purulent nature are as follows:

1. Abscess. It is a focus with a barrier capsule that prevents pus from entering neighboring tissues. In the cavity of the focus, purulent exudate accumulates, entering there through the capillaries of the barrier capsule.
2. Phlegmon. With this form, there are no clear boundaries at the focus of inflammation, and purulent exudate spreads into neighboring tissues and cavities. Such a picture can be observed in the subcutaneous layers, for example, in adipose tissue, in the retroperitoneal and perirenal zones, wherever the morphological structure of tissues allows pus to go beyond the focus of inflammation.
3. Empyema. This form is similar to an abscess and is observed in the cavities, next to which there is a focus of inflammation.

If there are many degenerative neutrophils in the pus, the exudate is called purulent neutrophilic. In general, the role of neutrophils is to destroy bacteria and fungi. They, like brave guards, are the very first to rush at the enemies that have penetrated our body. Therefore, at the initial stage of inflammation, most neutrophils are intact, undestroyed, and the exudate is called micropurulent. As the disease progresses, leukocytes are destroyed, and in pus most of them are already degenerated.

If putrefactive microorganisms (in most cases anaerobic bacteria) enter the inflammatory focus, the purulent exudate develops into putrefactive. It has a characteristic odor and color and contributes to the decomposition of tissues. This is fraught with high intoxication of the body and has a very unfavorable outcome.

Treatment of purulent inflammation is based on the use of antibiotics and ensuring the outflow of secretions from the focus. Sometimes this requires surgery. The prevention of such inflammation is the disinfection of wounds. Treatment of this pathology can have a favorable outcome only with intensive chemotherapy with simultaneous surgical removal of rotting fragments.

Hemorrhagic inflammation

In some very dangerous diseases, such as smallpox, plague, toxic influenza, hemorrhagic exudative inflammation is diagnosed. The reasons for it are the increasing permeability of microvessels up to their ruptures. In this case, the exudate is dominated by erythrocytes, due to which its color varies from pink to dark red. The external manifestation of hemorrhagic inflammation is similar to hemorrhage, but, unlike the latter, not only erythrocytes are found in the exudate, but also a small proportion of neutrophils with macrophages. Treatment of hemorrhagic exudative inflammation is prescribed taking into account the type of microorganisms that led to it. The outcome of the disease can be extremely unfavorable if therapy is started out of time and if the patient's body does not have enough strength to resist the disease.

Catarrh

A feature of this pathology is that the exudate with it can be serous, purulent, and hemorrhagic, but always with mucus. In such cases, a mucous secretion is formed. Unlike serous, it contains more mucin, the antibacterial agent lysozyme, and A-class immunoglobulins. It is formed for the following reasons:

• viral or bacterial infections;
• exposure to the body of chemicals, high temperatures;
• metabolic disorders;
• allergic reactions (for example, allergic rhinitis).

Catarrhal exudative inflammation is diagnosed with bronchitis, catarrh, rhinitis, gastritis, catarrhal colitis, acute respiratory infections, pharyngitis and can occur in acute and chronic forms. In the first case, it is completely cured in 2-3 weeks. In the second, changes occur in the mucosa - atrophy, in which the membrane becomes thinner, or hypertrophy, in which, on the contrary, the mucosa becomes thickened and can protrude into the cavity of the organ.

The role of mucous exudate is twofold. On the one hand, it helps fight infection, and on the other hand, its accumulation in the cavities leads to additional pathological processes, for example, mucus in the sinuses contributes to the development of sinusitis.

Treatment of catarrhal exudative inflammation is carried out with antibacterial drugs, physiotherapeutic procedures and folk methods, such as heating, rinsing with various solutions, ingestion of infusions and decoctions of herbs.

Exudative inflammation: characterization of specific exudative fluids

Above mentioned chylous and pseudochylous exudates that appear with injuries of the lymphatic vessels. For example, in the chest, this may be when ruptured. Chylous exudate is white in color due to the presence of an increased amount of fat in it.

Pseudochylous also has a whitish tint, but it contains no more than 0.15% fat, but there are mucoid substances, protein bodies, nucleins, lecithins. It is observed in lipoid nephrosis.

White color and chyle-like exudate, only it is given color by decomposed degenerate cells. It is formed during chronic inflammation of the serous membranes. In the abdominal cavity, this happens with cirrhosis of the liver, in the pleural cavity - with tuberculosis, pleural cancer, syphilis.

If there are too many lymphocytes in the exudate (more than 90%), it is called lymphocytic. It is released from the vessels when cholesterol is present in the secret, by analogy it is called cholesterol. It has a thick consistency, yellowish or brownish color and can be formed from any other exudative fluid, provided that water and mineral particles are reabsorbed from the cavity in which it accumulates for a long time.

As you can see, there are many types of exudates, each of which is characteristic of a certain type of exudative inflammation. There are also cases when, in any one disease, mixed exudative inflammation is diagnosed, for example, serous-fibrous or serous-purulent.

Acute and chronic forms

Exudative inflammation can occur in acute or chronic form. In the first case, it is an instant response to a stimulus and is designed to eliminate this stimulus. There can be many reasons for this form of inflammation. Most common:

• injury;
• infections;
• violations of the work of any organs and systems.

Acute exudative inflammation is characterized by redness and swelling of the injured area, pain, fever. Sometimes, especially due to infection, patients have symptoms of autonomic disorders and intoxication.

Acute inflammation takes a relatively short time, and if the therapy is carried out correctly, it is completely cured.

Chronic exudative inflammation can last for years. It is represented by purulent and catarrhal types of the inflammatory process. At the same time, tissue destruction develops simultaneously with healing. And although in the stage of remission chronic inflammation of the patient almost does not bother, it can ultimately lead to exhaustion (cachexia), sclerotic changes in the vessels, irreversible disruption of the organs and even to the formation of tumors. Treatment is mainly aimed at maintaining the remission phase. In this case, great importance is attached to the right lifestyle, diet, strengthening the immune system.

Serous inflammation. It is characterized by the formation of exudate containing up to 2% protein, single polymorphonuclear leukocytes (PMNs) and desquamated epithelial cells. Serous inflammation develops most often in the serous cavities, mucous membranes, pia mater, skin, less often in the internal organs.

The reasons. The causes of serous inflammation are diverse: infectious agents, thermal and physical factors, autointoxication. Serous inflammation in the skin with the formation of vesicles is a characteristic sign of inflammation caused by viruses of the Herpesviridae family (herpes simplex, chicken pox).

Some bacteria (mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella) can also cause serous inflammation. Thermal, less often chemical burns are characterized by the formation of blisters in the skin filled with serous exudate.

With inflammation of the serous membranes, a cloudy fluid accumulates in the serous cavities, poor in cellular elements, among which deflated mesothelial cells and single PMNs predominate. The same picture is observed in the soft meninges, which become thickened, swollen. In the liver, serous exudate accumulates perisinusoidally, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule. Serous inflammation of parenchymal organs is accompanied by degeneration of parenchymal cells. Serous inflammation of the skin is characterized by the accumulation of effusion in the thickness of the epidermis, sometimes exudate accumulates under the epidermis, exfoliating it from the dermis with the formation of large blisters (for example, with burns). With serous inflammation, vascular plethora is always observed. Serous exudate helps to remove pathogens and toxins from the affected tissues.

Exodus. Usually favorable. The exudate is well absorbed. The accumulation of serous exudate in parenchymal organs causes tissue hypoxia, which can stimulate the proliferation of fibroblasts with the development of diffuse sclerosis.

Meaning. Serous exudate in the meninges can lead to disruption of the outflow of cerebrospinal fluid (CSF) and cerebral edema, pericardial effusion makes it difficult for the heart to work, and serous inflammation of the lung parenchyma can lead to acute respiratory failure.

fibrinous inflammation. It is characterized by an exudate rich in fibrinogen, which is converted into fibrin in the affected tissue. This is facilitated by the release of tissue thromboplastin. In addition to fibrin, PMN and elements of necrotic tissues are also found in the composition of the exudate. Fibrinous inflammation is more often localized on the serous and mucous membranes.

The reasons. The causes of fibrinous inflammation are diverse - bacteria, viruses, chemicals of exogenous and endogenous origin. Among bacterial agents, the development of fibrinous inflammation is most favored by diphtheria corynebacterium, shigella, mycobacterium tuberculosis. Fibrinous inflammation can also be caused by Frenkel's diplococci, pneumococci, streptococci and staphylococci, and some viruses. Typically, the development of fibrinous inflammation during autointoxication (uremia). Development of fibrinous

inflammation is determined by a sharp increase in the permeability of the vascular wall, which may be due, on the one hand, to the characteristics of bacterial toxins (for example, the vasoparalytic effect of diphtheria corynebacterium exotoxin), on the other hand, to a hyperergic reaction of the body.

Morphological characteristic. A light gray film appears on the surface of the mucous or serous membrane. Depending on the type of epithelium and the depth of necrosis, the film can be loosely or firmly associated with the underlying tissues, and therefore there are two types of fibrinous inflammation: croupous and diphtheritic.

Croupous inflammation often develops on a single-layer epithelium of the mucous or serous membrane, which has a dense connective tissue base. At the same time, the fibrinous film is thin and easily removed. When such a film is separated, surface defects are formed. The mucous membrane is swollen, dull, sometimes it seems that it is, as it were, sprinkled with sawdust. The serous membrane is dull, covered with gray fibrin filaments resembling a hairline. For example, fibrinous inflammation of the pericardium has long been figuratively called a hairy heart. Fibrinous inflammation in the lung with the formation of croupous exudate in the alveoli of the lobe of the lung is called croupous pneumonia.

Diphtheritic inflammation develops in organs covered with stratified squamous epithelium or a single-layer epithelium with a loose connective tissue base, which contributes to the development of deep tissue necrosis. In such cases, the fibrinous film is thick, difficult to remove, and when it is rejected, a deep tissue defect occurs. Diphtheritic inflammation occurs on the walls of the pharynx, on the mucous membrane of the uterus, vagina, bladder, stomach and intestines, in wounds.

Exodus. On the mucous and serous membranes, the outcome of fibrinous inflammation is not the same. On the mucous membranes, fibrin films are rejected with the formation of ulcers - superficial with lobar inflammation and deep with diphtheria. Superficial ulcers usually regenerate completely, while deep ulcers heal with scarring. In the lung with croupous pneumonia, the exudate is melted by proteolytic enzymes of neutrophils and absorbed by macrophages. With insufficient proteolytic function of neutrophils, connective tissue appears at the site of the exudate (exudate is organized), with excessive activity of neutrophils, it is possible to develop an abscess and gangrene of the lung. On serous membranes Fibrinous exudate may melt, but more often it undergoes organization with the formation of adhesions between serous sheets. There may be a complete overgrowth of the serous cavity - obliteration.

Meaning. The value of fibrinous inflammation is largely determined by its type. For example, in diphtheria of the pharynx, the fibrinous film containing pathogens is tightly associated with the underlying tissues (diphtheritic inflammation), while severe intoxication of the body with corynebacteria toxins and decay products of necrotic tissues develops. With tracheal diphtheria, intoxication is slightly expressed, however, easily rejected films close the lumen of the upper respiratory tract, which leads to asphyxia (true croup).

Purulent inflammation. It develops with the predominance of neutrophils in the exudate. Pus is a thick creamy mass of yellow-green color with a characteristic odor. Purulent exudate is rich in proteins (mainly globulins). Formed elements in purulent exudate make up 17-29%; these are living and dying neutrophils, a few lymphocytes and macrophages. Neutrophils die 8-12 hours after entering the focus of inflammation, such decaying cells are called purulent bodies. In addition, in the exudate, you can see elements of destroyed tissues, as well as colonies of microorganisms. Purulent exudate contains a large number of enzymes, primarily neutral proteinases (elastase, cathepsin G and collagenase), released from the lysosomes of decaying neutrophils. Neutrophil proteinases cause the melting of the body's own tissues (histolysis), increase vascular permeability, promote the formation of chemotactic substances and enhance phagocytosis. Pus has bactericidal properties. Non-enzymatic cationic proteins contained in specific granules of neutrophils are adsorbed on the bacterial cell membrane, resulting in the death of the microorganism, which is then lysed by lysosomal proteinases.

The reasons. Purulent inflammation is caused by pyogenic bacteria: staphylococci, streptococci, gonococci, meningococci, Frenkel diplococcus, typhoid bacillus, etc. Aseptic purulent inflammation is possible when certain chemical agents (turpentine, kerosene, toxic substances) enter the tissues.

Morphological characteristic. Purulent inflammation can occur in any organs and tissues. The main forms of purulent inflammation are abscess, phlegmon, empyema.

Abscess - focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A granulation sac is formed around the abscess.

tissue, through the numerous capillaries of which leukocytes enter the abscess cavity and partially remove decay products. The abscess that produces pus is called pyogenic membrane. With a long course of inflammation, the granulation tissue that forms the pyogenic membrane matures, and two layers are formed in the membrane: the inner one, consisting of granulations, and the outer one, represented by mature fibrous connective tissue.

Phlegmon is a purulent diffuse inflammation, in which purulent exudate diffusely spreads into tissues, exfoliating and lysing tissue elements. Usually, phlegmon develops in tissues where there are conditions for easy spread of pus - in fatty tissue, in the area of ​​\u200b\u200btendons, fascia, along the neurovascular bundles, etc. Diffuse purulent inflammation can also be observed in parenchymal organs. In the formation of phlegmon, in addition to anatomical features, an important role is played by the pathogenicity of the pathogen and the state of the body's defense systems.

There are soft and hard phlegmon. Soft phlegmon characterized by the absence of visible foci of necrosis in the tissues, with hard cellulitis in the tissues, foci of coagulation necrosis are formed, which are not subjected to melting, but are gradually rejected. Phlegmon of adipose tissue is called cellulite, it has a limitless distribution.

Empyema is a purulent inflammation of hollow organs or body cavities with accumulation of pus in them. In body cavities, empyema can form in the presence of purulent foci in neighboring organs (for example, pleural empyema with lung abscess). Empyema of hollow organs develops when the outflow of pus is disturbed during purulent inflammation (empyema of the gallbladder, appendix, joint, etc.). With a long course of empyema, the mucous, serous, or synovial membranes become necrotic, and granulation tissue develops in their place, as a result of which adhesions or obliteration of cavities are formed.

Flow. Purulent inflammation is acute and chronic. Acute purulent inflammation tends to spread. Delimitation of the abscess from the surrounding tissues is rarely good enough, and progressive fusion of the surrounding tissues may occur. An abscess usually ends with spontaneous emptying of pus into the external environment or into adjacent cavities. If the communication of the abscess with the cavity is insufficient and its walls do not collapse, a fistula is formed - a channel lined with granulation tissue or epithelium, connecting the abscess cavity with a hollow organ or body surface. In some cases, pus spreads under the influence of gravity along the muscle-tendon sheaths, neurovascular bundles, fatty layers to the underlying sections and forms accumulations there - swells. Such accumulations of pus are usually not accompanied by noticeable hyperemia, a feeling of heat and pain, and therefore they are also called cold abscesses. Extensive streaks of pus cause severe intoxication and lead to depletion of the body. In chronic purulent inflammation, the cellular composition of exudate and inflammatory infiltrate changes. In pus, along with neutrophilic leukocytes, a relatively large number of lymphocytes and macrophages appear, and infiltration by lymphoid cells predominates in the surrounding tissue.

outcomes and complications. Both outcomes and complications of purulent inflammation depend on many factors: the virulence of microorganisms, the state of the body's defenses, the prevalence of inflammation. With spontaneous or surgical emptying of the abscess, its cavity collapses and fills with granulation tissue, which matures with the formation of a scar. Less often, the abscess becomes encapsulated, the pus thickens and may undergo petrification. With phlegmon, healing begins with the delimitation of the process, followed by the formation of a rough scar. With an unfavorable course, purulent inflammation can spread to the blood and lymphatic vessels, while bleeding and generalization of infection with the development of sepsis are possible. With thrombosis of the affected vessels, necrosis of the affected tissues may develop, in case of their contact with the external environment, they speak of secondary gangrene. Long-term chronic purulent inflammation often leads to the development of amyloidosis.

Meaning. The value of purulent inflammation is very high, as it underlies many diseases and their complications. The value of purulent inflammation is determined mainly by the ability of pus to melt tissues, which makes it possible to spread the process by contact, lymphogenous and hematogenous.

Putrid inflammation. It develops when putrefactive microorganisms enter the focus of inflammation.

The reasons. Putrefactive inflammation is caused by a group of clostridia, anaerobic infection pathogens - C.perfringens, C.novyi, C.septicum. In the development of inflammation, several types of clostridia are usually involved in combination with aerobic bacteria (staphylococci, streptococci). Anaerobic bacteria form butyric and acetic acids, CO 2 , hydrogen sulfide and ammonia, which gives the exudate a characteristic putrid (ichorous) odor. Clostridium enters the human body, as a rule, with the earth, where there are a lot of bacteria themselves and their spores, so most often putrefactive inflammation develops in wounds, especially with massive wounds and injuries (wars, disasters).

Morphological characteristic. Putrefactive inflammation develops most often in wounds with extensive crushing of the tissue, with disturbed blood supply conditions. The resulting inflammation is called anaerobic gangrene. The wound with anaerobic gangrene has a characteristic appearance: its edges are cyanotic, there is a gelatinous swelling of the tissue. Cellulose and pale, sometimes necrotic muscles bulge out of the wound. When feeling in the tissues, crepitus is determined, the wound emits an unpleasant odor. Microscopically, serous or serous-hemorrhagic inflammation is first determined, which is replaced by widespread necrotic changes. Neutrophils that enter the focus of inflammation quickly die. The appearance of a sufficiently large number of leukocytes is a prognostically favorable sign, indicating the attenuation of the process.

Exodus. Usually unfavorable, which is associated with the massiveness of the lesion and a decrease in the resistance of the macroorganism. Recovery is possible with active antibiotic therapy in combination with surgical treatment.

Meaning. It is determined by the predominance of anaerobic gangrene in mass wounds and the severity of intoxication. Putrefactive inflammation in the form of sporadic cases can develop, for example, in the uterus after a criminal abortion, in the colon in newborns (the so-called necrotizing colitis of newborns).

Hemorrhagic inflammation. It is characterized by the predominance of erythrocytes in the exudate. In the development of this type of inflammation, the main significance belongs to a sharp increase in the permeability of microvessels, as well as negative neutrophil chemotaxis.

The reasons. Hemorrhagic inflammation is characteristic of some serious infectious diseases - plague, anthrax, smallpox. With these diseases, erythrocytes predominate in the exudate from the very beginning. Hemorrhagic inflammation in many infections can be a component of mixed inflammation.

Morphological characteristic. Macroscopically, areas of hemorrhagic inflammation resemble hemorrhages. Microscopically, a large number of erythrocytes, single neutrophils and macrophages are determined in the focus of inflammation. Significant tissue damage is characteristic. Hemorrhagic inflammation can sometimes be difficult to distinguish from hemorrhage, for example, with hemorrhage into the abscess cavity from an arrosed vessel.

Exodus. The outcome of hemorrhagic inflammation depends on the cause that caused it, often unfavorable.

Meaning. It is determined by the high pathogenicity of pathogens that usually cause hemorrhagic inflammation.

Mixed inflammation. It is observed in cases when another type of exudate joins. As a result, serous-purulent, serous-fibrinous, purulent-hemorrhagic and other types of inflammation occur.

The reasons. A change in the composition of the exudate is naturally observed during inflammation: the formation of serous exudate is characteristic for the onset of the inflammatory process, later fibrin, leukocytes, and erythrocytes appear in the exudate. There is also a change in the qualitative composition of leukocytes; neutrophils are the first to appear in the focus of inflammation, they are replaced by monocytes and later by lymphocytes. In addition, in the case of a new infection joining an already ongoing inflammation, the nature of the exudate often changes. For example, when a bacterial infection is attached to a viral respiratory infection, a mixed, more often mucopurulent exudate is formed on the mucous membranes. And, finally, the addition of hemorrhagic inflammation with the formation of serous-hemorrhagic, fibrinous-hemorrhagic exudate can occur when the body's reactivity changes and is a prognostically unfavorable sign.

Morphological characteristic. It is determined by a combination of changes characteristic of various types of exudative inflammation.

Outcomes, meaning mixed inflammation are different. In some cases, the development of mixed inflammation indicates a favorable course of the process. In other cases, the appearance of a mixed exudate indicates the addition of a secondary infection or a decrease in the body's resistance.

Catarrh. It develops on the mucous membranes and is characterized by an abundant release of exudate flowing down from the surface of the mucous membrane, hence the name of this type of inflammation (Greek katarrheo - I drain). A distinctive feature of catarrh is the admixture of mucus to any exudate (serous, purulent, hemorrhagic). It should be noted that mucus secretion is a physiological protective reaction, which is enhanced in conditions of inflammation.

The reasons. Extremely diverse: bacterial and viral infections, allergic reactions to infectious and non-infectious agents (allergic rhinitis), the action of chemical and thermal factors, endogenous toxins (uremic catarrhal colitis and gastritis).

Morphological characteristic. The mucous membrane is edematous, plethoric, exudate flows from its surface. The nature of the exudate can be different (serous, mucous, purulent), but its essential component is mucus, as a result of which the exudate takes the form of a viscous, viscous mass. Microscopic examination in the exudate determines leukocytes, desquamated cells of the integumentary epithelium and mucous glands. The mucous membrane itself has signs of edema, hyperemia, is infiltrated with leukocytes, plasma cells, there are many goblet cells in the epithelium.

Flow catarrhal inflammation can be acute and chronic. Acute catarrh is characteristic of a number of infections, especially for acute respiratory viral infections, while there is a change in the types of catarrh - serous catarrh is usually replaced by mucous, then - purulent, less often - purulent-hemorrhagic. Chronic catarrhal inflammation can occur both in infectious (chronic purulent catarrhal bronchitis) and in non-infectious (chronic catarrhal gastritis) diseases. Chronic inflammation in the mucous membrane is often accompanied by a violation of the regeneration of epithelial cells with the development of atrophy or hypertrophy. In the first case, the shell becomes smooth and thin, in the second it thickens, its surface becomes uneven, it can swell into the lumen of the organ in the form of polyps.

Exodus. Acute catarrhal inflammations proceed 2 3 weeks and usually come to an end with full recovery. Chronic catarrhal inflammation is dangerous by the development of atrophy or hypertrophy of the mucous membrane.

Meaning. It is ambiguous due to the variety of reasons that cause it.

Exudative inflammation: serous, fibrinous (croupous, diphtheritic), purulent (phlegmon, abscess, empyema), catarrhal, hemorrhagic, mixed. Outcomes of exudative inflammation

Types of exudative inflammation: 1) serous, 2) fibrous, 3) purulent, 4) putrefactive, 5) hemorrhagic, 6) mixed, 7) catarrhal

Exudative inflammation is inflammation in which exudative processes predominate. Occurrence conditions:

• 1) the impact of damaging factors on the vessels of the microvasculature;
• 2) the presence of special factors of pathogenicity (pyogenic flora, isolation of chemotaxis); distinguish between independent and non-independent types of exudative inflammation. Independent species occur on their own, and non-independent species join them. Independent include serous inflammation, fibrinous and purulent. To dependent - catarrhal, hemorrhagic and putrefactive inflammation.
• 1) Fibrinous inflammation: the exudate is represented by fibrinogen. Fibrinogen is a blood protein that, going beyond the blood vessels, turns into insoluble fibrin. Intertwining fibrin threads form on the surfaces of the organs of the film - grayish, of various thicknesses. Occurs on the mucous membranes, serous membranes, as well as on the skin.
• 2) With purulent inflammation, the exudate is represented by polymorphonuclear leukocytes, includes dead leukocytes, destroyed tissues. Color from white to yellow-green. ubiquitous localization. The reasons are varied; First of all - coccal flora. The pyogenic flora includes staphylo- and streptococci, meningococci, gonococci and coli - intestinal, Pseudomonas aeruginosa. One of the pathogenicity factors of this flora are the so-called leukocidins, they cause an increase in the chemotaxis of leukocytes on themselves and their death.
• 3) Catarrhal inflammation - mucus is mixed with the exudate. There is a drain of exudate from the inflamed surface. Typical localization - mucous membranes. The outcome of catarrhal inflammation is the complete restoration of the mucosa. In chronic catarrhs, atrophy of the mucous membrane is possible (atrophic chronic rhinitis).
• 4) Hemorrhagic inflammation is characterized by the admixture of red blood cells to the exudate. The exudate becomes red, then, as the pigments are destroyed, it becomes black. It is typical for viral infections, such as influenza, measles, natural (black) smallpox, with endogenous intoxications, for example, intoxication with nitrogenous slags in chronic renal failure. It is typical for pathogens of especially dangerous infections that are strong in virulence.
• 5) Putrid (gangrenous) inflammation occurs due to the attachment of putrefactive flora, primarily fusospirochetal, to the foci of inflammation. It is more common in organs that have a connection with the external environment: putrefactive gangrene of the lung, limbs, intestines, etc. Decaying tissues are dull, with a fetid specific odor.
• 6) Mixed inflammation. They talk about it when there is a combination of inflammation (serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic).
• 7) Productive (proliferative inflammation) - the proliferation phase predominates, resulting in the formation of focal or diffuse cellular infiltrates, which can be polymorphic-cellular, lymphocytic-cell, macrophage, plasma-cell, giant-cell and epithelioid-cell. One of the main conditions for the development of proliferative inflammation is the relative stability of damaging factors in the internal environment of the body, the ability to persist in tissues.

It is characterized by the predominance of the exudation phase and the accumulation of exudate in the focus of inflammation. Depending on the nature of the exudate and the localization of the process, there are: 1) serous 2) fibrinous 3) purulent 4) putrefactive 5) hemorrhagic 6) mixed 7) catarrhal (feature of localization of the process on the mucous membranes).

Catarrh . It develops on the mucous membranes and is characterized by an abundant release of exudate flowing from the surface of the mucous membrane (Greek katarrheo - flowing). A distinctive feature is the admixture of mucus to any exudate (serous, purulent, hemorrhagic).

Macroscopically - mucous membranes are full-blooded, edematous, exudate flows from the surface (in the form of a viscous, viscous mass). Microscopically - in the exudate there are leukocytes, desquamated epithelial cells, edema, hyperemia, infiltration of Le, plasma cells, there are many goblet cells in the epithelium. The change of serous catarrh is characteristic - mucous, then purulent, there is a gradual thickening of the exudate as inflammation develops.

Exodus. The acute course lasts 2-3 weeks and ends with complete recovery, often accompanied by acute respiratory viral infections. Chronic inflammation can lead to the development of atrophy or hypertrophy of the mucous membranes (Example: atrophy of the gastric mucosa in chronic gastritis).

Serous inflammation - develops on the serous membranes, mucous membranes, pia mater, skin, less often in the internal organs. The exudate contains at least 3-5% protein. If the protein is less than 2%, then this is not an exudate, but a transudate (for example, with ascites). The serous exudate contains single PMNs and single desquamated epitheliocytes. Turbid fluid accumulates in the serous membranes and serous cavities. The soft meninges become edematous. In the liver, serous exudate accumulates perisinusoidally, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule. Serous inflammation of parenchymal organs is accompanied by degeneration of parenchymal cells. In the skin, exudate accumulates under the epidermis, can exfoliate it from the dermis, with the formation of blisters (for example, with burns, or herpes).

Exodus. Usually favorable - resorption of exudate. A transition to purulent or fibrinous inflammation is possible. And tissue hypoxia in chronic course can stimulate the proliferation of fibroblasts and lead to the development of sclerosis. Perhaps the development of hyalinosis.

fibrinous inflammation. Occurs on the mucous membranes and serous membranes, less often in the interstitial tissue. In the exudate, a lot of fibrinogen is found, which turns into the affected tissue, under the action of tissue thromboplastin fibrin. In addition to fibrin, the composition of the exudate includes Le and elements of necrotic tissues. A grayish film appears on the surface of the mucous or serous membrane. There are croupous, diphtheritic and diphtheroid inflammation.

1. Croupous inflammation- develops on mucous membranes lined with multi-row - ciliated epithelium (trachea, bronchi), serous membranes (surfaces of the epicardium, pleura) and gives them a dull gray color. The films lie freely and can be easily removed. Only some cells of the mesothelium or epithelium are damaged. When the films are rejected, hyperemia is determined. Favorable outcome - resorption of exudate. Unfavorable - the formation of adhesions in the cavities, rarely complete overgrowth of the cavity with connective tissue - obliteration. With croupous pneumonia, carnification is possible (from the Latin caro - meat) - “meatification” of the lobe of the lung, as a result of the replacement of fibrin with connective tissue. Rejection of fibrin films in the form of casts from the trachea and bronchi in diphtheria leads to the development of asphyxia and is called true cereal. Fibrin films on the epicardium with fibrinous pericarditis resemble hair, the heart is figuratively called “hairy”.

2. Diphtheritic inflammation- usually observed on mucous membranes with glandular epithelium, and a loose connective tissue base, contributing to the development of deep necrosis (intestinal mucosa, endometrium). Necrotic masses are impregnated with fibrin. Fibrin films and necrosis extend deep beyond the epithelial layer. Thick films are tightly soldered to the underlying tissue, it is difficult to reject, when the films are rejected, a deep defect is formed - an ulcer that heals with the formation of a scar.

3.Diphtheroid (diphtheritic-like) inflammation- occurs on mucous membranes covered with stratified squamous non-keratinized epithelium (in the larynx, pharynx, tonsils, in the epiglottis and true vocal cords). The epithelium becomes necrotic, impregnated with fibrin. Fibrin films can penetrate to the basal layer of the epithelium. When such a film is removed, a surface defect is formed - erosion, which heals by epithelization.

Purulent inflammation - is characterized by the predominance of Le in the exudate. Pus is a thick, creamy yellow-green liquid with a characteristic odor. Purulent exudate is rich in proteins (mainly globulins). Formed elements from 17 to 29%, these are living and dead leukocytes, single lymphocytes and macrophages. Neutrophils in the focus of inflammation die after 8-12 hours. Dead white blood cells are called purulent bodies. In addition, in the exudate you can see elements of destroyed tissues, colonies of microbes, it contains many enzymes, neutral proteases (ellastase, cathepsin G and collagenases) released from the lysosomes of decaying neutrophils. Proteases cause the melting of the body's own tissues (histolysis), increase vascular permeability, promote the formation of chemotactic substances and enhance phagocytosis. Non-enzymatic cationic proteins of specific granules of neutrophils have bactericidal properties.

The reasons. The causes of the development of purulent inflammation can be various bacteria. Aseptic purulent inflammation is possible when certain chemicals enter the tissues (turpentine, kerosene, some toxic substances).

Purulent inflammation can develop in all tissues and organs. The main forms are abscess, phlegmon and empyema.

1. Abscess- focal purulent inflammation, characterized by tissue melting with the formation of a cavity filled with pus. A shaft of granulation tissue is formed around the abscess, with numerous capillaries through which Le enters the abscess cavity and partially removes decay products. The pus-producing membrane is called the pyogenic membrane (two-layer capsule). With a long course, the granulation tissue matures in the membrane, mature fibrous connective tissue is formed. Allocate spicy(two-layer capsule) and chronic abscess(the capsule has three layers).

2. Phlegmon- diffuse purulent inflammation, in which purulent exudate diffusely spreads into tissues, exfoliates and lyses tissue elements. Usually, phlegmon develops in tissues where there are conditions for easy spread of pus - in fatty tissue, in the area of ​​\u200b\u200btendons, fascia, along the neurovascular bundles, etc. Distinguish soft(absence of visible foci of necrosis in the tissues) and hard phlegmon(foci of coagulative necrosis, which do not melt, but are gradually rejected).

3. empyema- purulent inflammation in body cavities or hollow organs with accumulation of pus in them and preservation of the anatomical integrity of the organ. In body cavities, empyema can form in the presence of purulent foci in neighboring organs (for example: pleural empyema with lung abscess). Hollow organ empyema may develop in violation of the outflow of pus (for example: empyema of the gallbladder, appendix, joint). With a long course of empyema, the mucous, serous and synovial membranes become necrotic, and granulation tissue develops in their place, which leads to the development of adhesions and obliteration of the cavity.

Flow purulent inflammation can be acute and chronic. Acute purulent inflammation tends to spread. The demarcation of the abscess from the surrounding tissue is rarely good enough, and progressive tissue fusion may occur. Or the emptying of pus into the external environment or cavity. Possible education fistula- a channel lined with granulation tissue or epithelium, connecting the abscess with a hollow organ or body surface. If pus, under the influence of gravity, passively, along the muscular-tendon sheaths, neurovascular bundles, fatty layers, flows into the underlying sections and forms clusters there - sills . Due to the absence of hyperemia, feelings of heat and pain - called cold leaks. Extensive streaks of pus cause severe intoxication and lead to depletion of the body.

Outcomes and complications- With spontaneous and surgical emptying of the abscess, its cavity collapses and fills with granulation tissue, which matures with the formation of a scar. Petrification is possible with thickening of pus. With phlegmon, rough scars form. With an unfavorable course, bleeding, generalization of infection with the development of sepsis is possible. With thrombosis of blood vessels in the focus of inflammation, the development of a heart attack or gangrene is possible. With a long chronic course, the development of amyloidosis is possible. The value of purulent inflammation is determined by the ability of pus to melt tissues, which makes it possible to spread the process by contact, lymphogenous and hematogenous routes. Purulent inflammation underlies many diseases.

Putrid inflammation - characterized by putrefactive decomposition of inflamed tissues. As a result of entering the focus of one or another type of inflammation of putrefactive bacteria (clostridia, anaerobic infection pathogens - C. perfringens, C. novyi, C septicum), a combination with other types of bacteria is possible, causing tissue decomposition and the formation of foul-smelling gases (ichorous smell - associated with the formation of butyric and acetic acid, CO 2, hydrogen sulfide and ammonia). Such inflammation occurs when the earth gets into the wounds, which is typical for massive wounds and injuries during wars and disasters. It has a severe course, accompanied by the development of gangrene.

Hemorrhagic inflammation - characterized by a predominance of red blood cells in the exudate. It often develops in severe infectious diseases (influenza, anthrax, plague, etc.) accompanied by a pronounced increase in microvascular permeability and negative chemotaxis. Runs hard and hard. Macroscopically, areas of hemorrhagic inflammation resemble hemorrhages. Microscopically in the focus of inflammation: a large number of erythrocytes, single neutrophils and macrophages. Significant tissue damage is characteristic. The outcome depends on the pathogenicity of the pathogen and the reactivity of the organism, often unfavorable.

Mixed inflammation - develops when another type of exudate joins. For example: Serous-purulent; Serous-fibrinous; Purulent-hemorrhagic and other possible combinations.

Topic 6. Inflammation

6.7. Classification of inflammation

6.7.2. Exudative inflammation

Exudative inflammation characterized by the predominance of the reaction of the vessels of the microvasculature with the formation of exudate, while the alterative and proliferative components are less pronounced.

Depending on the nature of the exudate, the following types of exudative inflammation are distinguished:

-serous;
- hemorrhagic;
- fibrinous;
-purulent;
- catarrhal;
- mixed.

Serous inflammation

Serous inflammation characterized by the formation of exudate containing 1.7-2.0 g/l of protein and a small number of cells. Flow serous inflammation is usually acute.

The reasons: thermal and chemical factors (burns and frostbite in the bullous stage), viruses (for example, herpes labialis, herpes zoster and many others), bacteria (for example, mycobacterium tuberculosis, meningococcus, Frenkel diplococcus, shigella), rickettsia, allergens of plant and animal origin, autointoxication (for example, with thyrotoxicosis, uremia), bee sting, wasp, caterpillar, etc.

Localization . It occurs most often in serous membranes, mucous membranes, skin, less often in internal organs: in the liver, exudate accumulates in perisinusoidal spaces, in the myocardium - between muscle fibers, in the kidneys - in the lumen of the glomerular capsule, in the stroma.

Morphology . Serous exudate is a slightly cloudy, straw-yellow, opalescent liquid. It contains mainly albumins, globulins, lymphocytes, single neutrophils, mesothelial or epithelial cells and looks like a transudate. In the serous cavities, macroscopically, exudate from transudate can be distinguished by the state of the serous membranes. With exudation, they will have all the morphological signs of inflammation, with transudation - manifestations of venous plethora.

Exodus serous inflammation is usually favorable. Even a significant amount of exudate can be absorbed. Sclerosis sometimes develops in the internal organs as a result of serous inflammation in its chronic course.

Meaning determined by the degree of functional impairment. In the cavity of the heart shirt, the inflammatory effusion impedes the work of the heart; in the pleural cavity, it leads to compression of the lung.

Hemorrhagic inflammation

Hemorrhagic inflammation characterized by the formation of exudate, represented mainly by erythrocytes.

With the flow is acute inflammation. The mechanism of its development is associated with a sharp increase in the permeability of microvessels, pronounced erythrodiapedesis and reduced leukodiapedesis due to negative chemotaxis in relation to neutrophils. Sometimes the content of red blood cells is so high that the exudate resembles a hemorrhage, for example, with anthrax meningoencephalitis - “the red cap of the cardinal”.

The reasons: severe infectious diseases - influenza, plague, anthrax, sometimes hemorrhagic inflammation can join other types of inflammation, especially against the background of avitaminosis C, and in persons suffering from pathology of the hematopoietic organs.

Localization. Hemorrhagic inflammation occurs in the skin, in the mucosa of the upper respiratory tract, gastrointestinal tract, lungs, and lymph nodes.

Exodus hemorrhagic inflammation depends on the cause that caused it. With a favorable outcome, complete resorption of the exudate occurs.

Meaning. Hemorrhagic inflammation is a very severe inflammation, which often ends in death.

fibrinous inflammation

fibrinous inflammation is characterized by the formation of exudate rich in fibrinogen, which in the affected (necrotic) tissue turns into fibrin. This process is facilitated by the release of a large amount of thromboplastin in the necrosis zone.

Flow fibrinous inflammation is usually acute. Sometimes, for example, with tuberculosis of the serous membranes, it is chronic.

The reasons. Fibrinous inflammation can be caused by pathogens of diphtheria and dysentery, Frenkel's diplococci, streptococci and staphylococci, mycobacterium tuberculosis, influenza viruses, endotoxins (with uremia), exotoxins (mercuric chloride poisoning).

Localized fibrinous inflammation on the mucous and serous membranes, in the lungs. A grayish-whitish film appears on their surface (“membraneous” inflammation). Depending on the depth of necrosis and the type of epithelium of the mucous membrane, the film can be connected with the underlying tissues either loosely and, therefore, easily separated, or firmly and, as a result, separated with difficulty. There are two types of fibrinous inflammation:

-croupous;
-diphtheritic.

Croupous inflammation(from scot. group- film) occurs with shallow necrosis in the mucous membranes of the upper respiratory tract, gastrointestinal tract, covered with prismatic epithelium, where the connection of the epithelium with the underlying tissue is loose, so the resulting films are easily separated along with the epithelium even when deeply impregnated with fibrin. Macroscopically, the mucous membrane is thickened, swollen, dull, as if sprinkled with sawdust, if the film is separated, a surface defect occurs. The serous membrane becomes rough, as if covered with hair - fibrin threads. With fibrinous pericarditis in such cases, they speak of a “hairy heart”. Among the internal organs, lobar inflammation develops in the lung with lobar pneumonia.

Diphtheritic inflammation(from Greek. diphtera- leathery film) develops with deep tissue necrosis and impregnation of necrotic masses with fibrin on mucous membranes covered with squamous epithelium (oral cavity, pharynx, tonsils, epiglottis, esophagus, true vocal cords, cervix). The fibrinous film is tightly soldered to the underlying tissue; when it is rejected, a deep defect occurs. This is due to the fact that squamous epithelial cells are closely related to each other and to the underlying tissue.

Exodus fibrinous inflammation of the mucous and serous membranes is not the same. With croupous inflammation, the resulting defects are superficial and complete regeneration of the epithelium is possible. With diphtheritic inflammation, deep ulcers form, which heal by scarring. In the serous membranes, fibrin masses undergo organization, which leads to the formation of adhesions between the visceral and parietal sheets of the pleura, peritoneum, pericardial shirt (adhesive pericarditis, pleurisy). In the outcome of fibrinous inflammation, complete infection of the serous cavity with connective tissue is possible - its obliteration. At the same time, calcium salts can be deposited in the exudate, an example is the “shell heart”.

Meaning fibrinous inflammation is very large, since it forms the morphological basis of diphtheria, dysentery, and is observed during intoxication (uremia). With the formation of films in the larynx, trachea, there is a danger of asphyxia; with rejection of films in the intestine, bleeding from the resulting ulcers is possible. Adhesive pericarditis and pleurisy are accompanied by the development of pulmonary heart failure.

Purulent inflammation

Purulent inflammation characterized by a predominance of neutrophils in the exudate, which, together with the liquid part of the exudate, form pus. The composition of pus also includes lymphocytes, macrophages, necrotic cells of local tissue. In pus, microbes called pyogenic are usually detected, which are located freely, or are contained inside pyocytes (dead polynuclear cells): it's septic pus capable of spreading infection. However, pus without microbes exists, for example, when turpentine is administered, which was once used to “stimulate protective reactions in the body” in debilitated infectious patients: as a result, developed aseptic pus .

Macroscopically pus is a cloudy, creamy liquid of a yellowish-greenish color, the smell and consistency of which varies depending on the aggressive agent.

The reasons: pyogenic microbes (staphylococci, streptococci, gonococci, meningococci), less often Frenkel diplococci, typhoid bacillus, mycobacterium tuberculosis, fungi, etc. It is possible to develop aseptic purulent inflammation when certain chemicals enter the tissue.

The mechanism of pus formation associated with adaptation polynuclear cells specially to antibacterial control.

Polynuclear cells or granulocytes actively penetrate into the focus of aggression, thanks to amoeboid movements as a result of positive chemotaxis. They are unable to divide because they are the final cell of the myeloid series. The duration of their normal life in the tissues is no more than 4-5 days, in the focus of inflammation it is even shorter. Their physiological role is similar to that of macrophages. However, they absorb smaller particles: this microphages. Neutrophilic, eosinophilic and basophilic intracytoplasmic granules are a morphological substrate, but they reflect different functional characteristics of granulocytes.

Neutrophil polynuclear cells contain specific, optically visible, very heterogeneous granules of a lysosomal nature, which can be divided into several types:

Small granules, elongated in the form of a bell, dark in the electron microscope, which contain alkaline and acid phosphatases;
-medium granules, rounded, moderate density, contain lactoferrin
- bulk granules are oval, less dense, contain proteases and beta-glucuronidase;
- large size granules, oval, very electron dense, contain peroxidase.

Due to the presence of various types of granules, the neutrophil polynuclear is able to fight infection in various ways. Penetrating into the focus of inflammation, polynuclear cells release their lysosomal enzymes. Lysosomes, represented by aminosaccharides, contribute to the destruction of cell membranes and the lysis of some bacteria. Lactoferrin containing iron and copper enhances the action of lysozyme. The role of peroxidases is more important: by combining the actions of hydrogen peroxide and cofactors such as halogen compounds (iodine, bromine, chlorine, thiocyanate), they enhance their antibacterial and antiviral actions. Hydrogen peroxide is necessary for polynuclear cells for efficient phagocytosis. They can additionally produce it at the expense of some bacteria, such as streptococcus, pneumococcus, lactobacillus, some mycoplasmas that produce it. The lack of hydrogen peroxide reduces the lysing effect of polynuclear cells. In chronic granulomatous disease (chronic familial granulomatosis), which is transmitted by a recessive type only to boys, bactericidal failure of granulocytes is observed and then macrophages are involved in the capture of bacteria. But they are not able to completely resorb the lipid membranes of microorganisms. The resulting products of antigenic material cause a local necrotic reaction of the Arthus type.

Eosinophilic polynuclear cells capable of phagocytosis, although to a lesser extent than macrophages, for 24 to 48 hours. They accumulate in allergic inflammation.

Basophilic polynuclear cells . They share many functional properties with tissue basophils (mast cells). Unloading of their granules is caused by cold, hyperlipemia, thyroxine. Their role in inflammation is not well understood. In large numbers, they appear with ulcerative colitis, regional colitis (Crohn's disease), with various allergic skin reactions.

Thus, the dominant population in purulent inflammation is the population of neutrophilic granulocytes. Neutrophil polynuclear cells carry out their destructive actions in relation to the aggressor with the help of an increased outpouring of hydrolases into the inflammation focus as a result of the following four mechanisms:

At polynuclear destruction under the influence of an aggressor;
-auto-digestion of polynuclear cells as a result of rupture of the lysosomal membrane inside the cytoplasm under the action of various substances, for example, silicon crystals or sodium urates;
-release of enzymes by granulocytes into the intercellular space;
-by inverted endocytosis, which is carried out by means of invagination of the cell membrane without absorption of the aggressor, but by the outpouring of enzymes into it.

The last two phenomena are most often observed during resorption of the antigen-antibody complex.

It must be emphasized that lysosomal enzymes, if released, exert their destructive effect not only on the aggressor, but also on the surrounding tissues. Therefore, purulent inflammation is always accompanied histolysis. The degree of cell death in various forms of purulent inflammation is different.

Localization. Purulent inflammation occurs in any organ, in any tissue.

Types of purulent inflammation depending on the prevalence and localization:

-furuncle;
-carbuncle;
-phlegmon;
-abscess;
- empyema.

Furuncle

Furuncle- this is an acute purulent-necrotic inflammation of the hair follicle (follicle) and the associated sebaceous gland with its surrounding fiber.

The reasons: staphylococcus, streptococcus.

Terms contributing to the development of a boil: constant contamination of the skin and friction with clothing, irritation with chemicals, abrasions, scratches and other microtraumas, as well as increased activity of the sweat and sebaceous glands, beriberi, metabolic disorders (for example, diabetes mellitus), starvation, weakening of the body's defenses.

Localization: a single boil can occur on any part of the skin where there is hair, but most often on the back of the neck (in the back of the head), face, back, buttock, in the armpit and inguinal region.

The development of a boil begins with the appearance of a dense painful nodule with a diameter of 0.5-2.0 cm, bright red, rising above the skin in a small cone. On the 3-4th day, a softening area is formed in its center - a purulent “head”.

Macroscopically on the 6-7th day, the boil is a cone-shaped, towering above the surface of the skin, inflammatory infiltrate of a purple-cyanotic color with a yellowish-greenish apex (“head” of the boil).

Then the boil breaks through with the release of pus. At the site of the breakthrough, a greenish area of ​​necrotic tissue is found - the core of the boil. Together with pus and blood, the rod is rejected.

Exodus. With an uncomplicated course of the process, the cycle of development of the boil lasts 8-10 days. The skin tissue defect is filled with granulation tissue, which then matures to form a scar.

Meaning. The process of development of a boil can be accompanied by a pronounced local inflammatory reaction and relatively quickly end in clinical recovery. But with reduced resistance, a necrotic rod may melt and an abscess, phlegmon, may occur. A furuncle on the face, even a small one, is usually accompanied by rapidly progressive inflammation and edema, and a severe general course. In an unfavorable course, the development of fatal complications is possible, such as septic thrombosis of the sinuses of the dura mater, purulent meningitis and sepsis. In debilitated patients, the development of multiple boils is possible - this is furunculosis.

Carbuncle

Carbuncle- this is an acute purulent inflammation of several adjacent hair follicles and sebaceous glands with necrosis of the skin and subcutaneous tissue of the affected area.

A carbuncle occurs when pyogenic microbes enter the ducts of the sebaceous or sweat glands, as well as when they penetrate the skin through minor lesions, squeezing out a boil.

Terms development and localization the same as for the furuncle.

Macroscopically, the carbuncle is an extensive dense, red-purple infiltrate on the skin, in the center of which there are several purulent “heads”.

The most dangerous is the carbuncle of the nose and especially the lips, in which the purulent process can spread to the membranes of the brain, resulting in the development of purulent meningitis. Treatment operational; at the first symptoms of the disease, it is necessary to consult a surgeon.

Meaning. A carbuncle is more dangerous than a boil, it is always accompanied by a pronounced intoxication. With carbuncle, there may be complications: purulent lymphadenitis, purulent thrombophlebitis, erysipelas, phlegmon, sepsis.

Phlegmon

Phlegmon- this is a diffuse purulent inflammation of the tissue (subcutaneous, intermuscular, retroperitoneal, etc.), or the walls of a hollow organ (stomach, appendix, gallbladder, intestines).

The reasons: pyogenic microbes (staphylococci, streptococci, gonococci, meningococci), less often Frenkel's diplococci, typhoid bacillus, fungi, etc. It is possible to develop aseptic purulent inflammation when certain chemicals enter the tissue.

Phlegmon examples:

Paronychius- acute purulent inflammation of the periungual tissue.

Felon- acute purulent inflammation of the subcutaneous tissue of the finger. The tendon and bone may be involved in the process, purulent tendovaginitis and purulent osteomyelitis occur. With a favorable outcome, scarring of the tendon occurs and contracture of the finger is formed. With an unfavorable outcome, phlegmon of the hand develops, which can be complicated by purulent lymphadenitis, sepsis.

Phlegmon of the neck- acute purulent inflammation of the tissue of the neck, develops as a complication of pyogenic infections of the tonsils, maxillofacial system. Distinguish soft and hard phlegmon. Soft phlegmon characterized by the absence of visible foci of tissue necrosis, in hard cellulitis there is a coagulative necrosis of the fiber, the tissue becomes very dense and does not undergo lysis. Dead tissue can be sloughed away, exposing the vascular bundle, which can lead to bleeding. The danger of neck phlegmon also lies in the fact that the purulent process can spread to the tissue of the mediastinum (purulent mediastinitis), pericardium (purulent pericarditis), pleura (purulent pleurisy). Phlegmon is always accompanied by severe intoxication and may be complicated by sepsis.

Mediastenitis- acute purulent inflammation of the tissue of the mediastinum. Distinguish front and rear purulent mediastinitis.

Anterior mediastinitis is a complication of purulent inflammatory processes of the anterior mediastinum, pleura, neck phlegmon.

Posterior mediastinitis most often caused by the pathology of the esophagus: for example, traumatic injuries by foreign bodies (damage to the fish bone is especially dangerous), decaying cancer of the esophagus, purulent-necrotic esophagitis, etc.

Purulent mediastinitis is a very severe form of purulent inflammation, accompanied by pronounced intoxication, which often causes the death of the patient.

Paranephritis - purulent inflammation of the perirenal tissue. Paranephritis is a complication of purulent nephritis, septic kidney infarction, decaying kidney tumors. Meaning: intoxication, peritonitis, sepsis.

Parametritis- purulent inflammation of the uterine tissue. It occurs with septic abortions, infected childbirth, the decay of malignant tumors. First, purulent endometritis occurs, then parametritis. Meaning: peritonitis, sepsis.

paraproctitis- inflammation of the tissue surrounding the rectum. It can be caused by dysentery ulcers, ulcerative colitis, decaying tumors, anal fissures, hemorrhoids. Meaning: intoxication, the occurrence of pararectal fistulas, the development of peritonitis.

Abscess

Abscess(abscess) - focal purulent inflammation with tissue melting and the formation of a cavity filled with pus.

Abscesses are acute and chronic. The wall of an acute abscess is the tissue of the organ in which it develops. Macroscopically, it is uneven, rough, often with torn structureless edges. Over time, the abscess is delimited by a shaft of granulation tissue, rich in capillaries, through the walls of which there is an increased emigration of leukocytes. Formed as if the shell of the abscess. Outside, it consists of connective tissue fibers that are adjacent to the unchanged tissue, and inside - of granulation tissue and pus, which is continuously renewed due to the constant supply of leukocytes from granulations. The abscess that produces pus is called pyogenic membrane.

Abscesses can be localized in all organs and tissues, but are of the greatest practical importance abscesses of the brain, lungs, liver.

Abscesses of the brain are usually divided into:

Peacetime abscesses;
wartime abscesses.

wartime abscesses are most often a complication of shrapnel wounds, blind injuries of the skull, less often through bullet wounds. It is customary to distinguish between early abscesses that occur up to 3 months after injury and late abscesses that occur after 3 months. A feature of wartime brain abscesses is that they can occur 2-3 years after injuries, and also occur in the lobe of the brain opposite the wound zone.

Peacetime abscesses. The source of these abscesses are:

-purulent otitis media (purulent inflammation of the middle ear);
-purulent inflammation of the paranasal sinuses (purulent sinusitis, frontal sinusitis, pansinusitis);
-hematogenous metastatic abscesses from other organs, including furuncle, facial carbuncle, pneumonia.

Localization. Most often, abscesses are localized in the temporal lobe, less often - the occipital, parietal, frontal.

The most common in the practice of medical institutions are brain abscesses of otogenic origin. They are caused by scarlet fever, measles, influenza and other infections.

A middle ear infection can spread:

By continuation;
- lympho-hematogenous way;
- perineural.

From the middle ear, the infection continues to spread to the pyramid of the temporal bone and causes purulent inflammation (osteomyelitis of the temporal bone), then the process passes to the dura mater (purulent pachymeningitis), pia mater (purulent leptomeningitis), later, with the spread of purulent inflammation to the tissue brain, an abscess is formed. With lymphohematogenous occurrence of an abscess, it can be localized in any part of the brain.

Meaning brain abscess. An abscess is always accompanied by tissue death and therefore the function of the area of ​​the brain in which the abscess is localized completely falls out. Purulent inflammation toxins have a tropism for neurons, causing their irreversible degenerative changes and death. An increase in the volume of an abscess can lead to its breakthrough into the ventricles of the brain and death of the patient. When inflammation spreads to the soft membranes of the brain, purulent leptomeningitis occurs. With an abscess, there is always a violation of blood circulation, accompanied by the development of edema. An increase in the volume of the lobe leads to dislocation of the brain, displacement of the trunk and infringement of it in the foramen magnum, which leads to death. Treatment of fresh abscesses is reduced to their drainage (according to the principle “ ubi pus ibi incisio et evacuo”), old abscesses are removed along with the pyogenic capsule.

lung abscess

lung abscess most often it is a complication of various pathologies of the lungs, such as pneumonia, lung cancer, septic heart attacks, foreign bodies, less often it develops with hematogenous spread of infection.

The significance of lung abscess is that it is accompanied by severe intoxication. With the progression of the abscess, purulent pleurisy, pyopneumothorax, pleural empyema, and pulmonary bleeding may develop. In the chronic course of the process, the development of secondary systemic amyloidosis and exhaustion is possible.

liver abscess

liver abscess- occurs most often in diseases of the gastrointestinal tract, which are complicated by the development of an inflammatory process in the portal vein. These are pylephlebitic liver abscesses. In addition, infection in the liver can penetrate the biliary tract - cholangitis abscesses. And, finally, it is possible to get an infection by the hematogenous route, with sepsis.

Causes of pylephlebitic abscesses liver are:

-intestinal amebiasis;
- bacterial dysentery;
-appendicitis;
- peptic ulcer of the stomach and duodenum.

Causes of cholangitis abscesses most often are:

-purulent cholecystitis;
-typhoid fever;
-purulent pancreatitis;
- disintegrating tumors of the liver, gallbladder, pancreas;
- phlegmon of the stomach.

Meaning process consists in severe intoxication, which leads to dystrophic changes in vital organs, it is also possible to develop such formidable complications as subdiaphragmatic abscess, purulent peritonitis, sepsis.

empyema

empyema- purulent inflammation with accumulation of pus in closed or poorly drained pre-existing cavities. Examples are the accumulation of pus in the pleural, pericardial, abdominal, maxillary, frontal cavities, in the gallbladder, appendix, fallopian tube (pyosalpinx).

Empyema of the pericardium- occurs either by continuation from adjacent organs, or when an infection enters the hematogenous route, or with a septic heart attack. This is a dangerous, often fatal complication. With a long course, adhesions occur, calcium salts are deposited, the so-called armored heart develops.

Pleural empyema- occurs as a complication of pneumonia, lung cancer, pulmonary tuberculosis, bronchiectasis, septic pulmonary infarction. The value is in severe intoxication. The accumulation of a large amount of fluid causes a displacement, and sometimes - a rotation of the heart with the development of acute heart failure. Compression of the lung is accompanied by the development of compression atelectasis and the development of pulmonary heart failure.

Empyema of the abdomen, as an extreme morphological manifestation of purulent peritonitis is a complication of many diseases. To the development of purulent peritonitis lead:

-wired (perforated) ulcers of the stomach and duodenum;
- purulent appendicitis;
-purulent cholecystitis;
- intestinal obstruction of various origins;
- intestinal infarction;
- disintegrating tumors of the stomach and intestines;
-abscesses (septic heart attacks) of the abdominal organs;
-inflammatory processes of the pelvic organs.

Meaning. Purulent peritonitis is always accompanied by a pronounced intoxication and, without surgical intervention, usually leads to death. But even in the case of surgery and successful antibiotic therapy, it is possible to develop adhesive disease, chronic, and sometimes acute intestinal obstruction, which, in turn, requires surgical intervention.

Catarrh(from Greek. catarrheo- flow down), or Qatar. It develops on the mucous membranes and is characterized by an abundant accumulation of mucous exudate on their surface due to hypersecretion of the mucous glands. The exudate can be serous, mucous, and desquamated cells of the integumentary epithelium are always mixed with it.

The reasons catarrh are different. Catarrhal inflammation develops with viral, bacterial infections, under the influence of physical and chemical agents, it can be of an infectious-allergic nature, the result of autointoxication (uremic catarrhal gastritis, colitis).

Catarrh may be acute and chronic. Acute catarrh is characteristic of a number of infections, for example, acute catarrh of the upper respiratory tract with acute respiratory infections. Chronic catarrh can occur both in infectious (chronic purulent catarrhal bronchitis) and non-infectious diseases. Chronic catarrh may be accompanied by atrophy or hypertrophy of the mucosa.

Meaning catarrhal inflammation is determined by its localization, intensity, nature of the course. The most important are catarrhs ​​of the mucous membranes of the respiratory tract, often taking on a chronic character and having severe consequences (emphysema, pneumosclerosis).

Mixed inflammation. In those cases when another type of exudate joins, mixed inflammation is observed. Then they talk about serous-purulent, serous-fibrinous, purulent-hemorrhagic or fibrinous-hemorrhagic inflammation. Most often, a change in the type of exudative inflammation is observed with the addition of a new infection, a change in the reactivity of the body.

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