Inflammation

Inflammation is a complex compensatory-adaptive reaction of the body to the impact of pathogenic factors of the external or internal environment, occurring locally or with general damage to all organs and tissues.

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What causes inflammation?

The causes of inflammation can be varied. Environmental factors include: microorganisms, mechanical, chemical and physical irritants (injuries, burns, frostbite, exposure to strong acids and alkalis, pesticides, etc.).

The most common causes of endogenous effects are: the body's own vasoactive mediators - histamine and serotonin, which form allergic reactions; or toxic products of incomplete metabolism in diseases and damage to parenchymatous organs (for example, the liver, pancreas, etc.).

All types of inflammation can be combined with each other (for example, peritonitis - as a local purulent inflammation of the peritoneal cavity; and a general inflammatory reaction in the form of alteration or exudation in all organs and tissues - as a manifestation of intoxication from the main process). Or have a transitional phase of the process - alteration into exudation, then into suppuration and proliferation, as a stage of the regenerative process, which is characteristic of all types of inflammation.

The basis of any type of inflammation is: capillary permeability, with the exudation of plasma and various protective blood cells; local or general changes in the metabolism and function of organs and tissues; regenerative elements of proliferation (reproduction and replacement).

Morphologically and clinically, there are 4 types of inflammation

Alterative inflammation

Alteration - damage to tissue and cells - can be considered as a result of the direct action of a pathogenic factor and general disturbances that occur in the damaged tissue.

In all cases of inflammation, alteration is the first phase of the process. Morphologically, this type of inflammation can be defined as edema and swelling of tissues and cells. Formed elements of the blood, with the exception of erythrocytes, do not exude from the capillaries during alteration. The period of edema and swelling of tissues is considered a reversible stage of alterative inflammation. But the reversibility of alteration in most cases is limited to two weeks. If the process is not stopped during this time, irreversible tissue changes develop in the form of necrobiosis, dystrophy, connective tissue degeneration.

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Exudative inflammation

Unlike alterative inflammation, with exudative inflammation, the vascular reaction is observed not only in the venous part of the capillaries; but also in the arterial part, with vascular dilation and increased permeability. This leads not only to abundant exudation of blood plasma and its free accumulation. In the subcutaneous tissue, intermuscular spaces, serous cavities, organs, etc., but also to the release of leukocyte elements of the blood into the exudate. Small, formed elements of the blood mainly exude: eosinophils and lymphocytes. The appearance and growth of neutrophils in the exudate, as a rule, indicates the transition of exudative inflammation to purulent.

Clinically, exudative inflammation is accompanied by: pronounced edema of soft tissues (e.g., subcutaneous tissue); free accumulation of exudate in serous cavities; oozing into hollow organs (e.g., into the tracheobronchial tree in bronchitis and pneumonia). In most cases, the fact of exudation itself does not present any difficulties for diagnosis. The complex problem is identifying the cause of its development and differential diagnosis with purulent inflammation.

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Proliferative (productive) inflammation

It is formed in two forms: reproduction (restoration) of the atypical, with the outcome in degeneration.

• 1) In the form of reproduction (restoration) - as a stage of completion of other types of inflammation, with the formation of scars that undergo reorganization, up to complete resorption.
• 2) Typical proliferative inflammation, usually developing with chronic exposure to a pathogenic agent. In practice, this is a protective reaction of tissues aimed at limiting the irritant (foreign body, parasites, chronic infection, for example, rheumatoid). The basis of proliferation is the proliferation of young cells of local connective tissue, as well as cambial cells of blood vessels, i.e. histiogenic and hematogenic reactions are formed, which are accompanied by: tissue proliferation, development of granulomas, coarse deforming scars (in parenchymatous organs it manifests itself in the form of sclerosis, fibrosis and cirrhosis with diffuse proliferation of connective tissue).

Purulent inflammation

Morphologically, it is characterized by: the formation of a liquid transudate containing proteins, fibrin threads, disintegrated cellular elements of the blood; the presence of tissue detritus; dead and viable microorganisms. Such an inflammatory product is called "pus".

Purulent inflammation develops only in the presence of pathogenic microflora, which is the trigger for the body's reaction to both exogenous and endogenous infections. The process of purulent inflammation is staged. The initially introduced microflora is inert in itself, in addition, it is exposed to the body's protective factors (phagocytosis, complement fixation reaction, etc.) and can be destroyed by them. This period occurs in the form of alteration. Clinically, it may not manifest itself in any way (incubation period) or manifest itself slightly: itching, slight painful irritation in the form of distension, unclear hyperemia. Palpation reveals: local pastosity; seals, as a rule, are absent; slight local increase in skin temperature, moderate pain. No changes in the general condition are noted.

The second stage - infiltration, is essentially a phase of exudative inflammation. It is formed when microflora begins to develop in the focus, releasing toxins that cause a neuro-reflex reaction with the release of inflammation mediators, determining the formation of a typical vascular reaction. Due to the increased permeability of the vessels, the plasma effusion is massive, with formed elements of blood.

Clinically, this stage is characterized by: increased pain, which becomes bursting; expansion and increase of edema; appearance of bright hyperemia with blurred edges. In the depth of the edema, a painful compaction is palpated - elastic, often round or oval in shape.

The third stage is suppuration; vascular reactions are sharply expressed. Vessels become empty and thrombosed, mainly venous trunks, with blood flow in the infiltrate tissues being cut off (Arthus phenomenon). They become necrotic, and a pyogenic capsule is formed around them. Granulations and scar tissue from fibroblasts grow around it from healthy tissues. A restrictive barrier is formed, determining the course of the purulent process. It can proceed in the form of an abscess, when the delimitation is sufficient; or phlegmon - when the delimitation is either weak or absent altogether. Thus, an abscess is a delimited typical purulent inflammation, and phlegmon is an undelimited typical purulent inflammation. General manifestations of purulent infection depend on the nature of the microflora, since gram-positive microflora gives more local manifestations, and gram-negative - causes a greater degree of intoxication.

The second important point is the tension of microflora in the focus, and the critical number is up to myriads per cm3 of tissue. With a lower tension of microflora, the process proceeds as a local one. Greater tension causes a breakthrough of microflora into the blood, with the development of: with preserved resistance of the organism - purulent-resorptive fever; in cases of its decrease and immunodeficiency - intoxication syndrome.

The third point is determined by the prevalence of the focus of purulent infection and its delimitation. Abeceding forms of purulent inflammation, as a rule, proceed as a local process; and phlegmonous ones are prone to intoxication. But its localization should also be taken into account, for example, with a relatively small brain abscess, severe functional disorders are formed.

The fourth point and, perhaps, the leading one is the state of the macroorganism. The presence of: vitamin deficiency, alimentary exhaustion, malignant tumors, diabetes, immunodepression - determine the decrease in the natural resistance of a person to the effects of pathogenic microflora. This significantly aggravates both the local manifestation of inflammation and the general reaction of the body to purulent inflammation. The general response to purulent infection according to the state of reactivity of the body can be of three types.

1. Normergic - with preserved resistance and normal immunity, i.e. in a practically healthy person, when an adequate protective reaction to purulent inflammation is formed according to the type of local and general manifestations, depending on its nature.
2. Hypoergic (up to anergic) is caused by a decrease in resistance due to the pathological conditions listed above. Figuratively speaking, the body simply has nothing to fight the infection with and the possibility of its generalization is formed, but there is no response protective action to pronounced purulent inflammation (blood reactions in the form of leukocytosis, as well as the development of local restrictive barriers are not observed).
3. The hyperergic reaction occurs in the form of autoallergy, since modern microflora in most cases is allergen-active and causes a general reaction with the release of a large amount of histamine and serotonin, up to the development of anaphylactic shock, even with “small” abscesses.

Clinically, in a normergic state of the body, general manifestations of purulent infection give 4 pictures.

• Purulent (infectious) toxicosis. This is a typical reaction of the body to "minor" forms of purulent inflammation with preserved reactivity of the body. It is formed when the microflora tension in the inflammation focus is less than the critical number (10 myriads per cm3). In this case, the release of microflora into the bloodstream does not occur, and the process occurs in the form of local purulent inflammation. The general reaction is manifested by headaches, malaise, weakness. Body temperature is maintained at a subfebrile level (37.0-37.5 degrees). In the blood, there is a slight increase in leukocytes, there is a leukocyte, a shift in the formula to the left, but the leukocyte intoxication index is normal, ESR is accelerated. Organ function is not impaired.
• Purulent-resorptive fever. It develops frequently and complicates up to 30% of all purulent-inflammatory diseases. It is caused by the tension of microflora in the lesion above 10 myriads per cm3 ^, which determines the periodic release of microflora into the blood directly from the abscess, or through the lymphatic system. But if the body's resistance is preserved, it is destroyed in the blood by cellular elements.

Clinically, purulent-resorptive fever is accompanied by: high body temperature with a daily range of up to one degree; chills with profuse sweating, especially when microflora enters the blood; weakness, malaise. Blood tests reveal: high leukocytosis, increased ESR; in the leukocyte formula, a shift to the left, a slight increase in the intoxication index and an increase in the fraction of medium molecules. Functional changes in the internal organs are not particularly pronounced, with the exception of tachycardia.

• Intoxication syndrome
• Bacterial shock. In literary sources, many authors understand bacterial shock as intoxication syndrome, which is fundamentally wrong. The issue was discussed at an international conference in Chicago (1993), and the decision made on this issue does not differ from our opinion.

Bacterial shock develops only when the blood-brain barrier is broken, mainly during superinfection with viral passage, which determines the role of toxin penetration. In this case, the functions of the cerebral cortex are blocked with a violation of the central regulation of the activity of all internal organs, including vital ones. Intensive edema of the brain develops according to the type of exudative inflammation, up to the wedging of the medulla oblongata into the foramen magnum. A distinctive clinical feature is a sudden loss of consciousness against the background of a purulent-inflammatory disease with complete areflexia - there are not even convulsions. Death in such patients occurs quickly, within an hour. Resuscitation measures are futile.