General doctrine of inflammation. Exudative inflammation. Pathological anatomy: Exudative inflammation Exudative changes

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The exudative phase of inflammation can have the following types:

Serous inflammation (exudate contains protein and does not contain blood cells);

Fibrinous inflammation (exudate contains a significant amount of fibrin precipitated on the tissue);

Purulent inflammation (exudate contains a large number of leukocytes, mostly dead leukocytes);

Hemorrhagic inflammation (there are many red blood cells in the exudate);

Ichorous inflammation (putrefactive flora settles in the exudate).

During the development of the exudation phase, various metabolic disorders occur at the site of inflammation. In the area of ​​inflammation:

a) - gas exchange changes, which is accompanied by an increase in oxygen consumption by tissues and a decrease in the release of carbonic acid by tissues, as a result of which the respiratory coefficient of tissues (the ratio of CO2 to O2) decreases. This indicates a disruption of oxidative processes in the area of ​​inflammation.

b) - carbohydrate metabolism is disrupted, which leads to an increase in glucose content. Increased glycolysis promotes the accumulation of lactic acid in the area of ​​inflammation.

c) - the content of free fatty acids increases, which is due to increased lipolysis processes. At the same time, ketone bodies accumulate in the tissues.

d) - protein metabolism is disrupted, which is manifested by the accumulation of polypeptides in tissues, the appearance of albumosis and peptones.

e) - mineral metabolism is disrupted. There is an increased concentration of K+ in the exudate, and this contributes to an even greater release of the liquid part of the blood into the tissues and an increase in their swelling.

In the absence of a delimiting shaft, diffuse suppuration of loose tissue occurs (phlegmon). Pus along the interstitial spaces can spread to neighboring areas, forming so-called leaks and edema abscesses. When pus accumulates in the natural cavities of the body, empyemas are formed (empyema of the pleura, gallbladder, etc.).

To assess the phenomena that occur during inflammation, one should distinguish between those that are protective (adaptive) in nature and those that are pathological (destructive) in nature, thereby determining the harmful effects of inflammation.

Inflammation is the response of the mesenchyme to damage.

Purpose of inflammation:

1) isolation of the damaging factor

2) destruction of the damaging factor

3) creating optimal conditions for recovery.

Phylogenetically, inflammation is a younger reaction than damage and compensation, since many factors are involved in its implementation - cells, blood vessels, nervous and endocrine systems.

The etiology of inflammation coincides with the etiology of damage. That is, inflammation is caused by 7 groups of factors: physical, chemical, toxins, infection, dyscirculation, neurotrophic, metabolic.

Pathogenesis

Consists of 3 sequential processes (phases).

Ι Alteration

ΙΙ Exudation

ΙΙΙ Proliferation

Ι ALTERATION PHASE

Plays a decisive role in the development of inflammation. Without alteration (damage) to cells and tissues, inflammation does not occur. Why?

Because when cells are damaged (dystrophy, necrosis), lysosomes containing proteolytic enzymes leave the cells. These enzymes, after the breakdown of lysosomes, cause the appearance of inflammatory mediators, which trigger the exudation phase.

Inflammatory mediators are active biological products. Currently, many mediators are known. But a special place is occupied by such mediators as HISTAMINE and SEROTONIN.

Mediators are secreted by 5 cells - mast cells, granulocytes, platelets, lymphocytes, macrophages. But a special place in this series is occupied by LABROCYTES (mast cells), which produce large amounts of histamine and serotonin.

Inflammatory mediators cause an increase in the permeability of microvasculature vessels - therefore, they initiate the 2nd phase of inflammation - exudation.

ΙΙ EXUDATION PHASE

The site of action is the microvasculature.

Dynamics ---- 7 successive stages (processes):

1) reaction of blood vessels and blood

2) increased permeability

3) plasmorrhagia

4) emigration of blood cells

5) phagocytosis

6) pinocytosis

7) formation of exudate and infiltrate

1) Reaction of blood vessels and blood -

Under the influence of mediators (histamine, serotonin), a short-term spasm of arterioles and precapillaries initially occurs, followed by LONG-TERM paralytic dilatation of arterioles and the development of arterial hyperemia, which is manifested by redness and warming of the inflammation. Arterial congestion contributes to the development of lymphostasis, lymphothrombosis and lymphatic edema - the release of lymph into the area of ​​inflammation. Under the influence of mediators, blood viscosity increases and blood clots form in the venules. This leads to venous congestion, which gives the inflammation site a bluish tint and causes hypoxic damage.

2) Increased permeability.

Under the influence of mediators and hypoxia, the capillary wall becomes loose due to damage to the endothelium and loosening of the basement membrane. This causes an increase in the permeability of the capillary wall.

3) Plasmorrhagia

As a result of increased permeability of the capillary walls, there is an increased outflow of plasma from the lumen of the capillaries into the area of ​​inflammation (plasmorrhagia).

4) Emigration of blood cells.

Movement of granulocytes, lymphocytes, monocytes into the zone of inflammation through the capillary wall (leukodiapedesis). The transition of these cells occurs in 2 ways - a) interendothelial and b) transendothelial (through the endothelium). Granulocytes and monocytes migrate interendothelially. Transendothelial - lymphocytes. The reason for migration is chemotaxis - the attraction of leukocytes by decay products that accumulate in the area of ​​inflammation. Chemotaxis can be carried out by proteins, nucleoproteins, kinins, plasmins, complementary factors and other substances that appear at the site of inflammation.

5) Phagocytosis

Phagocytosis is the capture and consumption of microbes and foreign bodies. There are 2 types of phagocytes - a) microphages (neutrophils) - they are capable of destroying only microbes, b) macrophages (monocytes) - they are able to capture small particles (microbes) and large particles - foreign bodies. The phagocytic function of macrophages is provided by lysosomal enzymes, of microphages - by cationic proteins (proteolytic enzymes) and atomic oxygen, which is formed during the process of peroxidation. Phagocytosis of microbes can be complete (complete destruction of microbes) or incomplete (the microbe is not destroyed and is carried by phagocytes throughout the body). Reasons for incomplete phagocytosis: 1. immunodeficiency, caused by many factors, including the immunodeficiency virus, 2. characteristics of the microbe (phagocytes cannot destroy the tuberculosis bacillus because it has a thick, waxy shell).

6) Pinocytosis

Capture of tissue fluid that contains antigen by macrophages, in the cytoplasm of which an information complex is formed. Composition of the information complex: transformed antigen + information ribonucleic acid. The information complex is transmitted through cytoplasmic contacts to the B lymphocyte. A B lymphocyte turns into a plasma cell. The plasma cell produces antibodies specific to this antigen. Specific antibodies bind to this antigen, which increases the phagocytic reaction to destroy the antigen by 100 times.

7) Formation of exudate and infiltrate.

At the end of the exudation phase, exudate and infiltrate are formed. Exudate in its usual form is a liquid containing decay products of tissues and cells. It accumulates in the stroma and cavities. Its composition is complex, but unlike tissue fluid it contains more than 2% proteins. Therefore, it is an opaque, cloudy liquid. Whereas transudate is a clear liquid. In cases where the cellular component predominates over the liquid, the exudate receives a special name - infiltrate. Infiltrate is more typical of chronic inflammation.

ΙΙΙ PROLIFERATION PHASE

Completion of the inflammatory process. The inflammation zone is separated from the surrounding tissue. The processes of proliferation predominate over the processes of alteration and exudation. They multiply: 1) cambial mesenchymal cells, 2) adventitial cells, 3) endothelium, 4) reticular cells, 5) B- and T-lymphocytes, 6) monocytes.

During reproduction, differentiation and transformation of cells occur.

As a result

Mesenchymal cambial cells develop into epithelioid cells (resembling squamous epithelial cells), histiocytes, macrophages, fibroblasts and fibrocytes;

B lymphocytes - into plasma cells

Monocytes - into epithelioid cells and macrophages.

As a result, all these cells perform the function of cleansing and restoring the activity of the microvasculature. And this allows you to start the recovery processes in full.

The inflammatory response manifests itself differently at different age periods. It develops in full in adulthood. In other age groups it has its own characteristics.

Thus, in fetuses and newborns, alteration and proliferation predominate over exudation, and there is also a tendency to generalization. This is explained by the imperfection of protective and immune mechanisms during this period of life. In old age, there is a decrease in reactivity and prolonged inflammatory processes due to a relative decrease in defense mechanisms.

Regulation of inflammation.

Inflammation is regulated by the endocrine and nervous systems. Both systems can increase or decrease the severity of inflammation.

Endocrine system

There are 2 known groups of hormones:

1) pro-inflammatory

2) anti-inflammatory.

1) Pro-inflammatory (increase inflammation) - somatotropic hormone, aldosterone.

Mechanism of action: increase the osmotic pressure of tissue fluid due to the accumulation of sodium in it. As a result, plasmorrhagia (exudation) increases.

2) Anti-inflammatory (reduce inflammation) - glucocorticoids, ACTH.

Mechanism of action: blocking the transition of lymphocytes to mast cells (mast cells), which produce inflammatory mediators. A logical chain of events arises: no mast cells - no inflammatory mediators - no exudation - no inflammation.

Nervous system

There are also 2 groups of factors -

1) pro-inflammatory

2) anti-inflammatory

1) Pro-inflammatory - cholinergic substances.

Mechanism of action: an increase in cGMP (a universal mediator), which activates the production of inflammatory mediators, which intensifies the inflammatory process.

2) Anti-inflammatory - adrenergic factors.

Mechanism of action: they increase the amount of cAMP (a universal mediator), which blocks the production of inflammatory mediators, resulting in a weakening of the inflammatory process.

Clinical and morphological signs of inflammation.

There are 5 of them: 1) redness - caused by arterial plethora

2) increased temperature - due to arterial plethora

3) swelling - due to exudation

4) pain - caused by the action of mediators on nerve endings

5) dysfunction is caused by damage to structures, which triggers inflammation.

Types of inflammatory response .

1. Adequate(or normergic reaction) is characterized

directly proportional relationship between the strength of the damaging factor and the strength of inflammation.

2. Inadequate characterized by a discrepancy between the strength of the damaging factor and the severity of inflammation.

This may be a hypoergic reaction (weakened)

Hyperergic reaction (intensified)

- Hypoergic the reaction may be

1) reaction of the strength of the immune system - when a strong damaging factor is reflected with less losses with moderate inflammation.

2) a reaction of immune weakness - when a weak damaging factor leads to severe damage (dystrophy, necrosis), and the inflammatory reaction is almost absent (this is evidence of the body’s defenselessness, and it accompanies serious diseases, such as blood diseases).

- Hyperergic the reaction always reflects increased sensitization of the body. It may be the result of impaired humoral and cellular immunity. And it always accompanies immune inflammation.

There are 2 types of hyperergic reaction -

1) immediate type hypersensitivity \GNT\

2) delayed-type hypersensitivity\HRT\

1) Immediate-type hypersensitivity occurs immediately after exposure to an antigen (drugs, pollen, foods and other allergens). It is characterized by acute inflammation with the development of an alterative-exudative reaction. Inflammation is triggered by humoral factors - antibodies, immune complexes, antigens.

2\ Delayed-type hypersensitivity - observed when cellular immunity is impaired (aggressive action of T-lymphocytes and macrophages). The inflammatory reaction occurs one day after exposure to the antigen. Example: inflammation of the skin one day after the administration of tuberculin.

Terminology. Classification .

Inflammation of an organ or tissue is indicated by the ending -it. It is added to the name of the organ or tissue. Examples: myocardium—myocarditis; endocardium - endocarditis, etc.

There are also special terms: pneumonia - inflammation of the lungs, empyema - purulent inflammation of the cavities, etc.

Classification. It is carried out according to 3 principles -

Duration of flow

By causal factors

According to pathomorphology

According to the flow, there are 3 types of inflammation -

• Ø acute - up to 3 weeks
• Ø subacute - up to 3 months
• Ø chronic - longer than 3 months.

According to the causative factors, there are:

• banal (nonspecific) inflammation
• specific inflammation (inflammation due to tuberculosis, syphilis, leprosy, rhinoscleroma, glanders).

According to pathomorphology (basic principle), 3 types of inflammation are distinguished depending on the predominance of one of the main components of inflammation -

1) alternative

2) exudative

3) proliferative (productive).

1) ALTERNATIVE INFLAMMATION

With this type of inflammation, damage to the organ parenchyma predominates. The vascular reaction is weakly expressed. The degree of damage is very diverse and ranges from ordinary dystrophy (mild damage) to necrosis (necrotic damage). Pathomorphology depends on the degree of damage.

Outcome - small lesions heal completely - scar tissue forms in place of large lesions. The meaning depends on the localization and severity of the process.

2) EXUDATIVE INFLAMMATION

It is characterized by the predominance of the exudation reaction during inflammation with the formation of effusion, which determines the entire picture of inflammation.

According to the characteristics of the exudate, 7 types of exudative inflammation are distinguished -

A. Seroznoe

B. Fibrinous

V. Purulent

G. Glinostnoe

D. Hemorrhagic

E. Catarrhal

G. Mixed.

A. Serous inflammation

Features of inflammation. Exudate is a liquid containing 3-8% albumin. There are few cells. The course of inflammation is acute. Hyperemia is well expressed. The porosity of the capillaries is moderate. Localization - serous cavities (cardiac, abdominal, pleural), meninges, stroma of the liver, myocardium, kidneys.

Appearance of the exudate: slightly cloudy, straw-yellow liquid.

Reasons: thermal, chemical, infections, etc.

The outcome is favorable: complete resorption. Rarely - sclerosis - more often in the liver, kidneys, myocardium.

B. Fibrinous inflammation

The exudate contains a lot of fibrin. Damage to capillaries with this type of inflammation is significant. Serous and mucous membranes are most often affected, less often the stroma of organs.

There are 2 types of this inflammation:

1) lobar

2) diphtheritic

1) Croupous inflammation. The word croup (crow-crow, croaking, wheezing like a crow) emphasizes the predominant localization of the process (for example, the mucous membrane of the trachea, bronchi). It is characterized by the formation of a fibrinous gray-yellow film. The film is loosely bound to the surface by necrotic mucous or serous membrane. When the film is peeled off, a surface defect is revealed.

2) Diphtheritic inflammation. It is characterized by deep necrotic changes in the mucous and submucosal layers. Fibrin loss occurs both in depth and on the surface. The fibrinous gray-yellow film is tightly fused to the underlying tissues, and when it is rejected, a deep defect is formed.

Diphtheritic (meaning leathery) inflammatory process is observed not only with diphtheria (disease). This is a broader concept, since diphtheritic inflammation occurs in various types of pathology.

Causes of fibrinous inflammation:

Bacteria: streptococci, staphylococci, bacilli - tuberculosis, diphtheria, etc.

Uremia (renal failure) - endogenous poisoning with the development of fibrinous pericarditis (hairy heart), fibrinous pleurisy, etc.

Exogenous poisoning.

Course: 1) acute 2) chronic

Outcome: small defects on the mucous membranes heal, in place of large ones, scar tissue forms with the possible development of stenosis, for example, of the trachea and bronchi; Fibrous adhesions always form on the serous membranes, which can lead to adhesive disease when localized in the abdominal cavity and intestinal obstruction.

B. Purulent inflammation

Pus is a thick, viscous, gray-green liquid. The purulent exudate contains many globulins, fibrin and, most importantly, neutrophils.

Types of purulent inflammation.

1) Phlegmon is a diffuse abscess. Characterized by the spread of pus through the intermuscular spaces, fatty tissue, fascia, tendons

2) Abscess - limited purulent inflammation. There is pus in the abscess cavity; the abscess wall is formed by a pyogenic membrane.

Localization varies: skin, head, kidneys, liver, lungs and other internal organs.

3) Empyema - purulent inflammation of the cavities: pleural, abdominal, joints.

4) Furuncle - purulent inflammation of the hair follicle.

5) Carbuncle - purulent inflammation of a group of hair follicles.

6) Paronychia - purulent inflammation of the periungual bed.

7) Panaritium - purulent inflammation of the finger.

Causes: most often pyogenic microorganisms (all types of coccal infections), tuberculosis bacilli, fungi, chemical agents.

Course - 1) Acute 2) Chronic.

Acute inflammation occurs in the form of diffuse or limited inflammation. In severe cases, the process spreads over large areas and can cause death from intoxication and multiple organ failure.

Chronic occurs over a long period of time with the development of fibrosis around the purulent process. It gives complications such as chronic fistula tracts, extensive leaks of pus, intoxication, wound exhaustion, amyloidosis.

G. Putrefactive inflammation

It develops when a putrefactive infection enters the area. It is characterized by increased necrobiotic processes and the formation of foul-smelling gas.

D. Hemorrhagic inflammation

Occurs when red blood cells penetrate into the exudate. This indicates severe damage to the microvasculature. It is observed in severe forms of influenza, smallpox, anthrax, and plague.

E. Catarrhal inflammation.

This is an inflammation of the mucous membranes with the formation of mucus and its accumulation in exudate. The composition of the exudate is different, but it always contains mucus.

Forms of catarrhal inflammation (catarrh) -

1) serous

2) slimy

3) purulent.

1) Serous. A cloudy exudate is characteristic. The mucous membrane is swollen, full-blooded. It is observed with a viral respiratory infection in the respiratory system and with cholera in the mucous membrane of the small intestine.

2) Mucous. Characterized by the presence of a large amount of mucus. The exudate is viscous and is located on the hyperemic mucosa. Localization - respiratory and digestive organs.

3) Purulent. Severe purulent inflammation followed by erosive and ulcerative processes, as well as fibrosis and deformation.

The course of catarrhal inflammation is acute and chronic.

The outcome of acute inflammation depends on the form of catarrh - with serous and mucous catarrh, complete recovery occurs, with purulent inflammation - cicatricial and ulcerative processes with stenosis and deformation.

Chronic catarrh occurs as follows:

1) atrophic catarrh with the development of atrophy (decrease) in the thickness of the mucosa. 2) hypertrophic catarrh - with thickening of the mucosa due to the proliferation of parenchymal and mesenchymal structures.

In this case, organ function is impaired with the development of chronic gastritis, enteritis, colitis, bronchitis, emphysema and pneumosclerosis.

G. Mixed inflammation.

Options: serous-purulent, serous-fibrinous, purulent-fibrinous and others.

It usually develops when, in the course of inflammation, a new infection occurs, or the reactive, protective forces of the body change significantly.

Each of us has encountered 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 people don’t pay attention to them at all. But even the most minor injuries can cause exudative inflammation. In essence, this is a condition of the affected area in which specific liquids collect in it and then seep out through the walls of the capillaries. 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 look in detail at the causes of exudative inflammation. We will also consider the types (outcomes for each of them are not equal) of this kind of inflammatory processes, and along the way we will explain what they depend on, how they proceed, and what treatment they require.

Is inflammation bad or good?

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 has developed mechanisms of inflammatory processes for many years so that they help survive harmful influences, in medicine called irritants. They can be viruses, bacteria, any skin wounds, chemicals (for example, poisons, toxins), unfavorable environmental factors. Exudative inflammation should protect us from the pathological activity of all these irritants. What it is? Without going into details, it is quite simple to explain. Any irritant entering the human body damages its cells. This is called alteration. It starts the inflammatory process. Its symptoms, depending on the type of irritant and the location of its introduction, may differ. Among the common ones are:

• a rise in temperature either throughout the body or only in the damaged area;
• swelling of the sore spot;
• 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.

At some point, fluids (exudate) begin to accumulate in the vessels. When they penetrate through the walls of the capillaries into the intercellular space, the inflammation becomes exudative. At first glance, this appears to be making the problem worse. But in fact, the release of exudate, or, as doctors say, exudation, is also necessary. Thanks to it, very important substances enter the tissues from the capillaries - immunoglobulins, kinins, plasma enzymes, leukocytes, which immediately rush to the source of inflammation to begin eliminating irritants and healing damaged areas.

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. An alteration has occurred. She put special organic compounds into work - (kinins, histamines, serotonins, lymphokines and others). Under their influence, the microvascular beds began to expand, and as a result, the permeability of the vessel walls increased.
2. In wider sections of the riverbeds, the blood flow began to move more intensely. So-called hyperemia arose, which, in turn, led to an increase in blood (hydrodynamic) pressure in the vessels.
3. Under the pressure of fluid from microvessels, exudate began to seep into the tissue through enlarged interendothelial gaps and pores, sometimes reaching the size of tubules. The particles that make it up moved to the site of inflammation.

Types of exudates

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

• serous;
• fibrous;
• purulent;
• putrid;
• hemorrhagic;
• mucous;
• frail;
• chyle-like;
• pseudochyleous;
• cholesterol;
• neutrophilic;
• eosinophilic;
• lymphocytic;
• mononuclear;
• mixed.

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

A form of serous exudative inflammation

In the human body, the peritoneum, pleura, and pericardium are covered by 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 their normal state are smooth, almost transparent, and very elastic. When exudative inflammation begins, they become rough and cloudy, and serous exudate appears in the tissues and organs. It contains proteins (more than 2%), lymphocytes, leukocytes, and epithelial cells.

The causes of exudative inflammation can be:

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

Serous exudate helps remove toxins and irritants from the source of inflammation. Along with its positive functions, 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 - peeling it off from the dermis and the formation of serous blisters. Each disease has its own symptoms. Some common symptoms include 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 secretion released from the microvessels. Thus, 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 is also converted into protein, which has a fibrous structure and forms the basis of blood clots. In addition, the fibrous exudate contains leukocytes, macrophages, and monocytes. At some stage of inflammation, necrosis of the tissues affected by the irritant develops. They become saturated with fibrous exudate, resulting in the formation of a fibrous film on their surface. Microbes actively develop under it, which complicates the course of the disease. Depending on the location of the film and its characteristics, diphtheria and lobar 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 pharynx, uterus, vagina, bladder, and gastrointestinal tract. In this case, a thick fibrous film is formed, as if grown into the membrane of the organs. Therefore, it is difficult to remove, and leaves ulcers behind. They heal over time, but scars may remain. There is another evil - under this film microbes multiply most actively, as a result of which the patient experiences high intoxication with the products of their vital activity. The most famous disease of this type of inflammation is diphtheria.
2. Croupous inflammation forms on the mucous membranes of organs covered with a single-layer membrane: in the bronchi, peritoneum, trachea, pericardium. In this case, the fibrous film is thin, easily removable, without significant defects of the mucous membranes. However, in some cases it can create serious problems, for example, if the trachea is inflamed, 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 this: leukocytes, most of which are destroyed, albumin, fibrin threads, enzymes of microbial origin, cholesterol, fats, DNA fragments, lecithin, globulins. These substances form purulent serum. In addition to it, the purulent exudate contains tissue detritus, live and/or degenerated microorganisms, and purulent bodies. Purulent inflammation can occur in any organ. The “culprits” of suppuration are most often pyogenic bacteria (various cocci, E. coli, Proteus), as well as candida, Shigella, Salmonella, Brucella. The forms of exudative inflammation of a purulent nature are as follows:

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

If many degenerative neutrophils are present 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 enemies who 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, white blood cells are destroyed, and in the 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 one. It has a characteristic odor and color and promotes tissue decomposition. 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 lesion. Sometimes this requires surgery. Prevention of such inflammation is 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 flu, hemorrhagic exudative inflammation is diagnosed. The reasons for this are the increasing permeability of microvessels up to their rupture. In this case, red blood cells predominate in the exudate, 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 red blood cells 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 untimely and if the patient’s body does not have enough strength to resist the disease.

Catarrh

The peculiarity 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 chemicals and high temperatures on the body;
• metabolic disorders;
• allergic reactions (for example, allergic rhinitis).

Catarrhal exudative inflammation is diagnosed in 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 organ cavity.

The role of mucous exudate is twofold. On the one hand, it helps fight infection, and on the other, its accumulation in 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, ingesting infusions and decoctions of herbs.

Exudative inflammation: characteristics of specific exudative fluids

Mentioned above were chylous and pseudochylous exudates that appear as a result of injuries to the lymphatic vessels. For example, in the breast it can be due to a rupture. Chylous exudate is white in color due to the presence of an increased amount of fat in it.

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

The exudate is white and chyle-like, but its color is given by disintegrated degenerated 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 the exudate contains too many lymphocytes (more than 90%), it is called lymphocytic. It is released from the vessels when cholesterol is present in the secretion, by analogy it is called cholesterol. It has a thick consistency, yellowish or brownish color and can be formed from any other exudative liquid, 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 specific type of exudative inflammation. There are also cases when, for 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 intended to eliminate this stimulus. There can be many reasons for this form of inflammatory process. The most common:

• injury;
• infections;
• disruption of the functioning of any organs and systems.

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

Acute inflammation lasts a relatively short time, and if 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. In this case, tissue destruction develops simultaneously with healing. And although in the remission stage chronic inflammation hardly bothers the patient, it can ultimately lead to exhaustion (cachexia), sclerotic changes in blood vessels, irreversible disruption of organ function and even the formation of tumors. Treatment is aimed mainly at maintaining the remission phase. In this case, great importance is attached to a proper lifestyle, diet, and strengthening the immune system.

Inflammation is a local reaction of the body, which is aimed at destroying the cause of damage and restoring the body. Depending on its phase, there are 2 types: exudative and proliferative.

Exudative inflammation is characterized by the accumulation of fluid – exudate – in the body cavities and tissues.

Classification

Depending on the type of exudate and localization, the following types are distinguished:

1. purulent;
2. serous;
3. putrid;
4. catarrhal;
5. fibrinous;
6. hemorrhagic;
7. mixed.

Over the course of the inflammation, it can be acute or chronic.

It is localized more often in the mucous membranes, serous cavities (pleural, pericardial, abdominal), less often in the meninges, and internal organs.

Reasons for appearance

In types of exudative inflammation, the causes of development may differ.

Purulent inflammation caused by pyogenic microorganisms. These include staphylococci, streptococci, salmonella. In most cases, its development is provoked by the penetration of chemicals into tissues (kerosene, mercury, thallium).

Serous inflammatory process may appear as a result of exposure to infectious agents (mycobacteria, meningococcus), thermal and chemical burns, intoxication of the body with heavy metals or uremia and hyperthyroidism.

The putrefactive appearance appears when exposed to anaerobic microflora, namely clostridia. These microbes can enter the human body with soil. This type of inflammation is often found in war zones, disasters and accidents.

Catarrh occurs due to exposure to viral and bacterial agents, allergies, chemicals and toxins in the body.

Fibrinous is caused by the persistence of viruses, bacteria and chemical agents in the body. The most common pathogens are diphtheria bacillus, streptococci, and Mycobacterium tuberculosis.

Hemorrhagic develops when a respiratory viral infection joins serous inflammation, causing changes in exudate and the release of streaks of blood, fibrin and red blood cells.

The mixed nature includes several causes of development and leads to the formation of hemorrhagic-purulent, fibrinous-catarrhal, and other types of exudate.

Forms of exudative inflammation and main symptoms

The most common type of inflammation is purulent. The main forms are abscess, phlegmon, pleural empyema.

1. An abscess is a limited inflammatory area in the form of a cavity in which pus collects.
2. Cellulitis is a diffuse diffuse process in which purulent exudate occupies an intermediate position between tissues, neurovascular bundles, tendons, etc.
3. Empyema is an accumulation of pus in an organ cavity.

Clinical symptoms of purulent inflammation are severe intoxication syndrome (fever, increased sweating, nausea, general weakness), the presence of pulsation in the area of ​​the purulent focus (fluctuation), increased heart rate, shortness of breath, and decreased physical activity.

Minor forms of the disease

Serous inflammation is accompanied by the formation in the body cavities of a turbid fluid consisting of a large number of neutrophils and deflated mesothelial cells. With the progression of inflammatory processes, the mucous membranes swell and plethora develops. When the skin is damaged, most often due to burns, bubbles or blisters form in the thickness of the epidermal layer. They are filled with cloudy exudate, which can peel off nearby tissues and increase the affected area.

The clinical picture depends on the localization of the inflammatory process. If there is fluid in the pleural cavity, chest pain, shortness of breath, and cough occur. Heart damage and accumulation of exudate in the pericardium provoke:

• the appearance of pain in its area;
• compression of nearby organs;
• development of heart failure;
• swelling of the veins of the cervical spine;
• shortness of breath;
• swelling in the limbs.

If the liver and kidneys are damaged, signs of acute liver and kidney failure may appear. Damage to the meninges develops meningitis, and unbearable headaches, nausea, and muscles become rigid.

Fibrinous form - characterized by the fact that the exudate contains a large amount of fibrinogen. Being in necrotic tissues, it is transformed into fibrin. The most common types of inflammation are lobar and diphtheritic.

With lobar, a loose film appears, located in superficial foci of necrosis. The mucous membrane develops into a thick, swelling structure covered with layers of fibrin strands. When it is separated, a shallow defect is formed. The affected organ is the lungs. The development of lobar pneumonia leads to symptoms such as cough with rust-colored sputum, shortness of breath, chest pain, and fever.

In diphtheria, a film forms in the deep layers of necrotic tissue. It is firmly fused with the surrounding tissues. When it is torn off, the defect reaches a large size and depth. The most commonly affected areas are the oral cavity, tonsils, esophagus, intestines and cervix. The main symptoms are pain depending on the site of inflammation (pain when swallowing, pain in the abdomen), abnormal bowel movements, and hyperthermia.

Putrefactive form - occurs when pyogenic bacteria migrate into an existing skin defect. Characterized by general symptoms of inflammation, as well as the release of an unpleasant odor.

Important! In the absence of antimicrobial therapy, putrefactive inflammation can lead to the development of gangrene, and subsequently to amputation of the limb.

Treatment tactics

Conservative treatment consists of eliminating the cause of inflammation. Since its development is most often caused by pathogenic microflora, basic therapy is based on antibacterial agents. The most effective antibiotics are penicillin (ampicillin, augmentin), cephalosporins (ceftriaxone, cefipime), sulfonamides (biseptol, sulfasalazine).

In addition to therapy aimed at eliminating the pathogen, anti-inflammatory treatment is carried out. To relieve pain and hyperthermic syndrome, NSAIDs (non-steroidal anti-inflammatory drugs) are used. These include ibuprofen, nurofen, aspirin.

Also, for purulent processes, surgical treatment is carried out.

The cavity of the abscess is opened with a scalpel, the purulent contents are expelled, then washed with antiseptics and antibiotics. At the end, drainage is installed and an aseptic bandage is applied.

When pus accumulates in the pleural cavity or pericardium, a puncture is performed to remove the purulent exudate.

Prevention

Preventive measures for various types of inflammatory processes include following all doctor’s recommendations, maintaining a healthy lifestyle and proper distribution of physical activity. In addition, you need to consume plenty of fruits and vitamins.

Topic 6. Inflammation

6.7. Classification of inflammation

6.7.2. Exudative inflammation

Exudative inflammation characterized by a predominance of the reaction of microcirculatory vessels 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.

Causes: 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 sting, caterpillar sting, etc.

Localization . It occurs most often in the serous membranes, mucous membranes, skin, less often in internal organs: in the liver, exudate accumulates in the 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 transudate. In serous cavities, exudate can be macroscopically distinguished from transudate by the state of the serous membranes. With exudation, they will have all the morphological signs of inflammation, with transudation - manifestations of venous congestion.

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

Meaning determined by the degree of functional impairment. In the cavity of the heart sac, inflammatory effusion complicates 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 predominantly by erythrocytes.

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

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

Localization. Hemorrhagic inflammation occurs in the skin, in the mucous membrane 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 that often ends in death.

Fibrinous inflammation

Fibrinous inflammation 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.

Causes. Fibrinous inflammation can be caused by pathogens of diphtheria and dysentery, Frenkel diplococci, streptococci and staphylococci, Mycobacterium tuberculosis, influenza viruses, endotoxins (for uremia), exotoxins (sublimate poisoning).

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

-lobar;
-diphtheritic.

Croupous inflammation(from Scottish crop- 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 with deep impregnation with fibrin. Macroscopically, the mucous membrane is thickened, swollen, dull, as if sprinkled with sawdust; if the film separates, 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 fused to the underlying tissue; when it is rejected, a deep defect occurs. This is explained by the fact that squamous epithelial cells are closely connected to each other and to the underlying tissue.

Exodus fibrinous inflammation of the mucous and serous membranes is not the same. With lobar inflammation, the resulting defects are superficial and complete regeneration of the epithelium is possible. With diphtheritic inflammation, deep ulcers are formed that heal by scarring. In the serous membranes, fibrin masses undergo organization, which leads to the formation of adhesions between the visceral and parietal layers of the pleura, peritoneum, and pericardial membrane (adhesive pericarditis, pleurisy). As a result of fibrinous inflammation, complete overgrowth 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 high, since it forms the morphological basis of diphtheria, dysentery, and is observed during intoxication (uremia). When films form in the larynx and trachea, there is a risk of asphyxia; When films in the intestines are rejected, 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 pus also includes lymphocytes, macrophages, and 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): this is septic pus capable of spreading infection. Nevertheless, there is pus without germs, for example, with the introduction of turpentine, which was once used to “stimulate protective reactions in the body” in weakened infectious patients: as a result, aseptic pus .

Macroscopically pus is a cloudy, creamy, yellowish-greenish liquid whose odor and consistency varies depending on the offending agent.

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

Mechanism of pus formation Connected with device polynuclear cells specially to antibacterial fight.

Polynuclear cells or granulocytes penetrate into the focus of aggression actively, 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 tissues is no more than 4-5 days; in the site of inflammation it is even shorter. Their physiological role is similar to macrophages. However, they absorb smaller particles: this microphages. Intracytoplasmic granules of neutrophils, eosinophils and basophils are a morphological substrate, but they reflect different functional characteristics of granulocytes.

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

Small granules, elongated bell-shaped, dark in an electron microscope, which contain alkaline and acid phosphatases;
-medium granules, rounded, of moderate density, contain lactoferrin
-bulky oval granules, less dense, contain proteases and beta-glucuronidase;
-large granules, oval, very electron dense, contain peroxidase.

Due to the presence of different types of granules, the neutrophil polynuclear cell is able to fight infection in different ways. Penetrating into the site 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 effect of lysozyme. The role of peroxidases is more important: combining the actions of hydrogen peroxide and cofactors such as halide compounds (iodine, bromine, chlorine, thiocyanate), they enhance their antibacterial and antiviral actions. Hydrogen peroxide is necessary for polynuclear cells for effective phagocytosis. They can additionally obtain it from certain bacteria, such as streptococcus, pneumococcus, lactobacilli, and some mycoplasmas that produce it. The lack of hydrogen peroxide reduces the lysing effect of polynuclear cells. In chronic granulomatous disease (chronic familial granulomatosis), transmitted by a recessive type only to boys, the bactericidal failure of granulocytes is observed and then macrophages are attracted to capture 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 during allergic inflammation.

Basophilic polynuclear cells . They share many functional properties with tissue basophils (mast cells). The unloading of their granules is caused by cold, hyperlipemia, and thyroxine. Their role in inflammation is not well understood. They appear in large quantities in ulcerative colitis, regional colitis (Crohn's disease), and 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 towards the aggressor through an increased outpouring of hydrolases into the site of inflammation as a result of the following four mechanisms:

At destruction of polynuclear cells under the influence of the aggressor;
-autodigestion of polynuclear cells as a result of rupture of the lysosomal membrane inside the cytoplasm under the influence of various substances, for example, silicon crystals or sodium urates;
-release of enzymes by granulocytes into the intercellular space;
-by knockover endocytosis, which is carried out by invagination of the cell membrane without absorbing the aggressor, but by pouring 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, have a destructive effect not only on the aggressor, but also on surrounding tissues. Therefore, purulent inflammation is always accompanied histolysis. The degree of cell death in different 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 location:

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

Furuncle

Furuncle is an acute purulent-necrotic inflammation of the hair follicle and the associated sebaceous gland with the surrounding tissue.

Causes: staphylococcus, streptococcus.

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

Localization: a single boil can occur on any area of ​​the skin where there is hair, but most often on the back of the neck (nape), face, back, buttock, armpit and groin area.

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 like a small cone. On the 3-4th day, a softening area forms in its center - a purulent “head”.

Macroscopically on the 6-7th day, the boil is a cone-shaped, rising above the surface of the skin, an inflammatory infiltrate of a purplish-bluish color with a yellowish-greenish tip (“head” of the boil).

The boil then bursts, releasing pus. At the site of the breakthrough, an area of ​​necrotic greenish tissue is found - the core of the boil. Together with pus and blood, the rod is rejected.

Exodus. In an uncomplicated course of the process, the development cycle 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 result in clinical recovery. But with reduced resistance, melting of the necrotic core may occur and an abscess and phlegmon may occur. A boil on the face, even a small one, is usually accompanied by rapidly progressing inflammation and swelling, and a severe general course. If the course is unfavorable, fatal complications may develop, such as septic thrombosis of the dural sinuses, purulent menigitis and sepsis. In weakened patients, multiple boils may develop - this is furunculosis.

Carbuncle

Carbuncle is an acute purulent inflammation of several nearby 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.

Conditions development and localization the same as with a boil.

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 carbuncle is 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 is surgical; At the first symptoms of the disease, you should consult a surgeon.

Meaning. A carbuncle is more dangerous than a boil and is always accompanied by severe 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 wall of a hollow organ (stomach, appendix, gall bladder, intestine).

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

Examples of phlegmon:

Paronychia- acute purulent inflammation of the periungual tissue.

Felon- acute purulent inflammation of the subcutaneous tissue of the finger. The process may involve tendon and bone, causing purulent tenosynovitis and purulent osteomyelitis. If the outcome is favorable, the tendon becomes scarred and a contracture of the finger is formed. If the outcome is unfavorable, phlegmon of the hand develops, which can be complicated by purulent lymphadenitis and sepsis.

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

Mediastenitis- acute purulent inflammation of the mediastinal tissue. Distinguish front and back purulent mediastinitis.

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

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

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

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

Parametritis- purulent inflammation of the periuterine tissue. Occurs in septic abortions, infected childbirth, and the disintegration of malignant tumors. First, purulent endometritis occurs, then parametritis. Meaning: peritonitis, sepsis.

Paraproctitis- inflammation of the tissue surrounding the rectum. Its causes may be dysenteric ulcers, ulcerative colitis, disintegrating tumors, anal fissures, hemorrhoids. Meaning: intoxication, the occurrence of perirectal fistulas, the development of peritonitis.

Abscess

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

Abscesses can be acute or chronic. The wall of an acute abscess is the tissue of the organ in which it develops. Macroscopically, it is uneven, rough, often with ragged, structureless edges. Over time, the abscess is delimited by a shaft of granulation tissue rich in capillaries, through the walls of which increased emigration of leukocytes occurs. A kind of abscess shell is formed. On the outside it consists of connective tissue fibers that are adjacent to unchanged tissue, and on the inside it consists of granulation tissue and pus, which is continuously renewed due to the constant supply of leukocytes from granulations. The membrane of an abscess that produces pus is called pyogenic membrane.

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

Brain abscesses are usually divided into:

Peacetime abscesses;
- wartime abscesses.

Wartime abscesses are most often a complication of shrapnel wounds, blind injuries to the skull, and less often penetrating bullet wounds. It is customary to distinguish between early abscesses, which occur up to 3 months after injury, and late abscesses, which occur after 3 months. The peculiarity of wartime brain abscesses is that they can occur 2-3 years after injury, and also occur in the lobe of the brain opposite the wounded area.

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 boils, facial carbuncles, pneumonia.

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

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:

To continue;
- lymphohematogenous route;
- perineural.

From the middle ear, the infection continues to spread to the pyramid of the temporal bone and causes purulent inflammation (temporal bone osteomyelitis), then the process moves to the dura mater (purulent pachymeningitis), soft meninges (purulent leptomeningitis), and subsequently, when purulent inflammation spreads to the tissue brain, an abscess forms. When an abscess occurs lymphohematogenously, it can be localized in any part of the brain.

Meaning brain abscess. An abscess is always accompanied by tissue death and therefore the entire function of the area of ​​the brain in which the abscess is localized is lost. Toxins of purulent inflammation have a tropism for neurons, causing their irreversible degenerative changes and death. An increase in the volume of the abscess can lead to its breakthrough into the ventricles of the brain and the death of the patient. When inflammation spreads to the soft membranes of the brain, purulent leptomeningitis occurs. With an abscess, there is always a circulatory disorder, accompanied by the development of edema. An increase in the volume of the lobe leads to dislocation of the brain, displacement of the brainstem and pinching of it in the foramen magnum, which leads to death. Treatment of fresh abscesses comes down 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 lung pathologies, such as pneumonia, lung cancer, septic infarction, foreign bodies, less often it develops with hematogenous spread of infection.

The significance of a lung abscess is that it is accompanied by severe intoxication. As the abscess progresses, purulent pleurisy, pyopneumothorax, pleural empyema, and pulmonary hemorrhage 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 can enter the liver through the bile ducts - cholangitis abscesses. And finally, it is possible to get an infection through 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 there are:

-purulent cholecystitis;
-typhoid fever;
- purulent pancreatitis;
- decaying tumors of the liver, gall bladder, pancreas;
- phlegmon of the stomach.

Meaning The process consists of severe intoxication, which leads to dystrophic changes in vital organs, and the development of such serious complications as subdiaphragmatic abscess, purulent peritonitis, and sepsis is also possible.

Empyema

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

Pericardial empyema- occurs either as a continuation from nearby organs, or when an infection occurs through the hematogenous route, or during a septic heart attack. This is a dangerous, often fatal complication. Over a long period of time, adhesions occur, calcium salts are deposited, and the so-called armored heart develops.

Empyema of the pleura- occurs as a complication of pneumonia, lung cancer, pulmonary tuberculosis, bronchiectasis, septic pulmonary infarction. The meaning is severe intoxication. The accumulation of a large amount of fluid causes displacement and sometimes 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 abdominal cavity, as an extreme morphological manifestation of purulent peritonitis is a complication of many diseases. The development of purulent peritonitis leads to:

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

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

Catarrh(from Greek katarrheo- I’m draining), 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.

Causes catarrhal inflammation are different. Catarrhal inflammation develops during viral and 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).

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

Meaning catarrhal inflammation is determined by its localization, intensity, and nature of the course. Catarrh of the mucous membranes of the respiratory tract, often becoming chronic and having serious consequences (pulmonary emphysema, pneumosclerosis), acquires the greatest importance.

Mixed inflammation. In cases where one type of exudate is joined by another, 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 when a new infection occurs or the body’s reactivity changes.