Inflammation

Inflammation is a complex compensatory-adaptive reaction of the organism to the effect of pathogenic factors of the external or internal environment, which proceeds locally or with a common lesion of all organs and tissues.

[1], [2], [3], [4], [5], [6], [7], [8]

What causes inflammation?

The causes of inflammation can be diverse. Factors of the external environment are: microorganisms, mechanical, chemical and physical stimuli (trauma, burns, frostbites, the impact of strong acids and alkalis, pesticides, etc.).

The causes of endogenous effects are most often: own vasoactive mediators - histamine and serotonin, which form allergic reactions; or toxic products of incomplete metabolism in diseases and injuries of parenchymal organs (for example, liver, pancreas, etc.).

All kinds of inflammation can be combined (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 transient phase of the process - an alteration to exudation, then to suppuration and proliferation, as a stage of the regenerative process, which is typical for all types of inflammation.

At the heart of any kind of inflammation lies: the permeability of capillaries, with the sweating of plasma and various protective uniform elements of blood; local or general changes in metabolism and function of organs and tissues; regenerative elements of proliferation (reproduction and substitution).

Morphologically and clinically distinguish 4 types of inflammation

Alterative inflammation

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

In all cases of inflammation, alteration is the first phase of the process. Morphologically, this kind of inflammation can be defined as swelling and swelling of tissues and cells. Uniform elements of blood, with the exception of red blood cells, do not sweat when altered from capillaries. The period of swelling and swelling of tissues is considered a reversible stage of alterative inflammation. But the reversibility of the alteration in. Most cases are limited to two weeks. If during this time the process does not stop, irreversible tissue changes in the form of necrobiosis, dystrophy, connective tissue degeneration develop.

[9], [10], [11], [12], [13]

Exudative inflammation

Unlike the alterative, with exudative inflammation, the vascular reaction is noted not only in the venous part of the capillaries; but also in the arterial, with the expansion of the vessels and the increase in their permeability. This leads not only to an abundant sweat 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 blood into the exudate. Sweat mainly small, uniform elements of blood: eosinophils and lymphocytes. The appearance and growth of neutrophils in the exudate, as a rule, indicates the transition of exudative inflammation into purulent inflammation.

Clinically, exudative inflammation is accompanied by: marked edema of soft tissues (eg, subcutaneous tissue); free accumulation of exudate in serous cavities; sweating in the hollow organs (for example, in the tracheobronchial tree with bronchitis and pneumonia). In most cases, the very fact of exudation for diagnosis is not difficult. A complex problem is the identification of the cause of its development and differential diagnosis with purulent inflammation.

[14], [15], [16], [17], [18], [19], [20], [21], [22]

Proliferative (productive) inflammation

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

• 1) In the form of reproduction (recovery) - as a stage of completion of other types of inflammation, with the formation of scars, which are subject to reorganization, up to complete resorption.
• 2) Typical proliferative inflammation, usually developing with chronic exposure to a pathogenic agent. Practically it is a protective reaction of tissues aimed at delimiting the stimulus (foreign body, parasites, chronic infection, for example, rheumatoid). The proliferation is based on the multiplication of young cells of local connective tissue, as well as cambial cells of blood vessels, i.e. Histiogenic and hematogenous reactions are formed which are accompanied by: tissue growth, development of granulomas, coarse deforming scars (in the parenchymal organs it is manifested as sclerosis, fibrosis and cirrhosis due to diffuse germination of the connective tissue).

Purulent inflammation

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

Purulent inflammation develops only in the presence of pathogenic microflora, which is the starting point of the body's reaction to the effect of both exogenous and endogenous infection. The process of purulent inflammation is a stage. Primarily introduced microflora itself is inert, in addition, it is exposed to the influence of protective factors, the body (phagocytosis, complement fixation reaction, etc.) and can be destroyed by them. This period takes the form of an alteration. Clinically, it may not manifest itself (the incubation period) or manifest itself insignificantly: itching, minor pain irritation in the form of raspiraniya, fuzzy hyperemia. When palpation is determined: local pastoznost; seals, as a rule, no; slight local increase in skin temperature, moderate soreness. There are no changes in the general condition.

The second stage - infiltration, in fact, is a phase of exudative inflammation. It is formed with the onset of development in the focus of microflora, releasing toxins, which cause a neuro-reflex reaction with the release of mediators of inflammation that determine the formation of a typical vascular reaction. By increasing the permeability of blood vessels, the effusion of the plasma is massive, with uniform elements of blood.

Clinically, this stage is characterized by: increased pain, they become bursting; expansion and increase of edema; the appearance of bright hyperemia with blurred edges. In the depth of the edema palpable painful compaction - elastic, more often, round or oval.

The third stage is suppuration; vascular reactions with it is pronounced. Vessels empty and thrombosed, mostly venous trunks, with the flow of blood in the tissues of the infiltrate (Arthus phenomenon) turned off. They are necrotic, around them a pyogenic capsule is formed. Around it from healthy tissues granulation and scar tissue from fibroblasts grow. A restrictive barrier is formed that determines the course of the purulent process. It can flow in the form of an abscess, when the delineation is sufficient; or phlegmon - when the delimitation is either weak or nonexistent. Thus, the abscess is a delimited typical purulent inflammation, and phlegmon is not a delimited typical purulent inflammation. The general manifestations of a purulent infection depend on the nature of the microflora, since the gram-positive microflora gives more local manifestations, while the gram-negative microflora causes more intoxication.

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

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

The fourth moment and, perhaps, the leading is the state of the macroorganism. Presence: avitaminosis, alimentary depletion, malignant tumors, diabetes mellitus, immunodepression - determine the decrease in human natural resistance to the effects of pathogenic microflora. This greatly burdens both the local manifestation of inflammation, and the general reaction of the body to purulent inflammation. The general response to a purulent infection on the state of the organism's reactivity can be of three kinds.

1. Normaergic - with preserved resistance and normal immunity, i.e. In a practically healthy person, when an adequate protective reaction to purulent inflammation is formed by the form of local and general manifestations, depending on its nature.
2. Hypoergic (up to anergic) is due to a decrease in resistance due to the pathological conditions listed above. Figuratively speaking, the body already has nothing to fight with the infection and the opportunity for its generalization is being formed, but the reciprocal protective effect on the expressed purulent inflammation (blood reactions in the form of leukocytosis, as well as the development of local restrictive barriers are not noted).
3. Hyperergic reaction occurs in the form of auto-allergy, as the modern microflora in most cases is allergenoactive 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, with the normal state of the body, the general manifestations of a purulent infection are 4 pictures.

• Purulent (infectious) toxicosis. This is a typical reaction of the body to "small" forms of purulent inflammation with the preserved reactivity of the organism. It is formed when the strain of microflora in the focus of inflammation is less than the critical number (10 myriads per cm3). At the same time, ejection of microflora into the bloodstream does not occur, and the process proceeds in the form of local purulent inflammation. The general reaction is manifested: headaches, malaise, weakness. The body temperature is kept at the level of the subfebrile condition (37.0-37.5 degrees). There is a slight increase in leukocytes in the blood, there is a leukocyte, a shift of the formula to the left, but the leukocyte index of intoxication is normal, the acceleration of the ESR. Function of organs is not broken.
• Purulent-resorptive fever. It develops frequently and complicates up to 30% of all purulent-inflammatory diseases. It is caused by the strain of microflora in the focus above 10 myriads per cm ³, which determines the periodic ejection of microflora into the blood directly from the abscess, or through the lymphatic system. But with the preserved resistance of the organism, it is destroyed in the blood by cellular elements.

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

• Syndrome of intoxication
• Bacterial shock. In literary sources, many authors under the bacterial shock understand the syndrome of intoxication, which is fundamentally wrong. The issue was discussed at an international conference in Chicago (1993), and the decision taken on this issue does not disagree with our opinion.

Bacterial shock develops only when the blood-brain barrier breaks through, mainly during superinfection with the viral passage, which determines the role of toxins penetration. At the same time, 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 development of cerebral edema according to the type of exudative inflammation, up to the medulla oblongata in the large occipital opening. A distinctive clinical feature is a sudden loss of consciousness against the background of a purulent-inflammatory disease with complete areflexia - there is not even a convulsion. Death in such patients occurs quickly, within an hour. Resuscitation measures are unpromising.